Clinical conditions

Question 1

How is collagen linked to scurvy disease?

Answer 1

Fibroblasts secrete procollagen that forms collagen
Vitamin c is require to produce pro collagen
Vitamin c deficiency leads to poor wound healing and impaired bone formation

Question 2

what is klinefelter syndrome and how is it caused?

Answer 2

triosomies 47,xxy

caused by meiotic non-disjunction

Question 3

what is mosacism and how is it caused?

Answer 3

presence of two or more cell lines/ chromosomal populations in cells of an individual
caused by mitotic non-disjunction in zygote

Question 4

what is Turner syndrome and why is significant?

Answer 4

monosomy 45,x

exception to be viable for life

Question 5

what is huntington disease?

Answer 5

CAG repeats in HTT gene leads to polyglutamine repeats in Huntington’s protein

Question 6

how is albinism inherited?

Answer 6

polygenic inheritance in a recessive manner

more than one gene responsible for presence of phenotype

Question 7

how does sickle cell anaemia form?

Answer 7

mutation in HBB gene coding for beta haemoglobin
Single base substitution from A to T
Mutation of glutamate to valine
changes negative charged residues to neutral and hydrophobic on surface
so aggregation of molecules, change in shape in RBC, more prone to lyse, more rigid and less flexible

Question 8

what causes Kwashiorkor?

Answer 8

insufficient protein intake
deficit in essential amino acids
young children displaced of breast milk

Question 9

what are the symptoms of kwashiorkor?

Answer 9

bilateral pitting oedema
hair changes
flacky appearance of skin
large, protuberant abdomen
anaemia- cant make haemoglobin
enlarged and fatty liver

Question 10

what causes marasmus?

Answer 10

insufficient energy intake resulting in negative energy balance
nutrient deficiencies
severe malnutrition in children

Question 11

what are the symptoms of marasmus?

Answer 11

muscle wasting
protuding ribs
diarrhoea or dehydration
-ve energy balance so fat store metabolism
muscle protein break down to release aa for gluconeogenesis

Question 12

what is lymphadenopathy?

Answer 12

swelling and enlarged lymph nodes
can cause pain
can occur in all the nodal regions or affect lymphatic organs

Question 13

what causes lymphadenopathy?

Answer 13

fighting infection- germinal centres fill with alot more lymphocytes
cancer metaphisise to lymph nodes via afferent lymphatics
lymphoma- malignancy(growth) of lymphoid tissue eg. hodgkins

Question 14

describe the role of sentinel lymph nodes in metastatic cancer?

Answer 14

first set of lymph nodes to recieve lymph from area of primary tumour and first to swell
help with detection

Question 15

describe the difference between primary and secondary lymphoedema?

Answer 15

primary- due to genetic inheritance to disease,
can onset within 2 years after birth(congenital) with age 2-35(praecox) or after 35 years(tarda),
absent or malformed lymph nodes/channels

secondary- due to cancer treatment, surgery, radiation therapy, infection and neoplasia,
obstruction of vessles, parasitic worms, pelvic masses

Question 16

what is the treatment for lymphoedema?

Answer 16

manual lymphatic drainage

Question 17

what is hyperkeratosis and how is it formed?

Answer 17

thickening of the outer layer of skin- large increase of keratin deposits(usually on palms)
can be painless
occurs due to inflammation and irritation in skin defences

Question 18

what is albinism and why does it increase risk of skin cancer?

Answer 18

inability to make normal amounts of melanin- lack melanin

decrease in protection against UV and sun

Question 19

what is the difference between psoriasis and eczema?

Answer 19

psoriasis- autoimmune disease, keratinised skin cells produce and replicate much faster, found on extensor parts of body, pitting in nail bed, dandruff, flares up due to stress, hormones and infection

eczema- chronic condition, dry, itchy skin and rash, found on flexor part of body, inflammatory response due to allergies and irritation

Question 20

what is vitiligo?

Answer 20

long term condition
pale white patches develop on skin caused by lack of melanin pigment in the skin
varies from person to person

Question 21

what is the difference between non-segmental and segmental vitiligo?

Answer 21

non segmental- symmetrical white patches appear on both sides of body, most common, auto-immune condition, t cells attack healthy melanocytes and kill them

segmental- the white patches only affect one area of the body, less common, ,caused by neuro chemicals released from nerve endings, melanocytes autolyse

Question 22

what causes or increases risk of vitiligo?

Answer 22

non- segmental - family members have it, autoimmune conditions family history, presence of another autoimmune disease, melanoma or cancer of the lymphatic system

segmental- stress triggers, skin damage or exposure to dermatologic toxins

Question 23

what is melanoma?

Answer 23

a type of skin cancer that can metastasise to other organs in the body
characterised by a new mole or change in a existing mole

Question 24

what causes malignant melanoma?

Answer 24

sudden intense sunlight when abroad especially in people with pale skin and freckles
skin cells develop abnormally due to UV exposure

Question 25

what is the difference between nodular and lentigo maligna melanomas?

Answer 25

nodular- changing lump on skin, black to red in colour, bleeding or oozing, develop on previously normal skin(head, neck, chest or back), faster-developing, grow downwards, more common lentigo maligna- flat, develop sideways, slight larger, darker than a freckle, affect older people more

Question 26

what causes psoriosis?

Answer 26

autoimmune disease flared up by hormones, stress or infection problems with immune system- t cells start to attack dividing cells

Question 27

what is psoriosis?

Answer 27

fast production and replacement of keratinised skin cells cells at surface lost very quickly red, flaky, crusty patches

Question 28

what is alopecia areata?

Answer 28

spot baldness hair lost from some(scalp) or all areas of body symptoms of psychosocial stress

Question 29

what causes alopecia areata?

Answer 29

systematic autoimmune disease body attacks own anagen(actively growing hair) and stops hair growth genetic association with family inheritance genetic risk factors with other autoimmune diseases eg type 1 diabetes, and celiac disease

Question 30

which vitamins can cause bone instability?

Answer 30

vitamin D3- produces calcitrol, important for calcium absorpotion vitamin C- synthesis of collagen vitamin K and B12- synthesis of bone proteins

Question 31

describe the features of bone affected by rickets and osteomalacia?

Answer 31

``` vitamin D deficiency poor calcium mobilisation low/ineffective mineralisation weakened bone development soft bones ```

Question 32

what is the difference between osteomalacia and rickets?

Answer 32

rickets- in children, impaired mineralisation of cartilage growth plates, bowled legs, bone deformities and impaired growth osteomalacia- impaired mineralisation of osteoid, increased osteoid, bone pain and tenderness

Question 33

causes of osteomalacia and rickets?

Answer 33

vitamin D deficiency | due to inadequate intake, malabsorption or lack of sunlight exposure

Question 34

describe the genetic basis of osteogenesis imperfecta?

Answer 34

mutation in COL1A gene | incorrect production of collagen 1 fibres

Question 35

decribe the phenotypic changes of osteogenesis imperfecta?

Answer 35

weak bones increased fracture risk shortened height and stature mainly neonates and children

Question 36

describe the radiological and structural changes in osteoporosis?

Answer 36

associated with aging incomplete filling of osteoclast resorption bays loss of bone tissue- higher risk of fracture irregular pattern trabecular and cortical bone very thin gaps in bone

Question 37

list the most common risk factors for osteoporosis?

Answer 37

secondary osteoporosis... drug therapy weightlessness(space travel), malnutrition and prolonged immobilisation- affect bone remodelling metabolic bone diseases eg hyperparathyroidism

Question 38

explain the importance of osteoporosis as a risk factor for fractures in elderly?

Answer 38

primary type 1- in postmenopausal women, increase in number of osteoclasts, loss of oestrogen primary type 2- in older men and women, loss of osteoblast function, loss of oestrogen and androgen

Question 39

outline the cause of achondroplasia?

Answer 39

inherited mutation in the FGF3 receptor gene FGF promotes collagen formation from cartilage endochondral ossification affected

Question 40

outline the characteristics of achondroplasia?

Answer 40

short stature but normal sized head and torso long bones cannot lengthen properly

Question 41

describe the pathophysiology of myasthenia gravis?

Answer 41

autoimmune disease- neuromuscular antibodies directed against ACh receptor- block little or no ACh receptors reduced number of endplate invaginations reduced synaptic transmission skeletal muscle weakness

Question 42

describe the clinical feature of myasthenia gravis?

Answer 42

ptosis- dropping of the eyelid

Question 43

state how neuromuscular transmission is disrupted in botulism?

Answer 43

toxin produced by clostridium botulinum bacteria | blocks neurotransmitter release at motor end plate

Question 44

state the consequences of botulism?

Answer 44

don't get muscle tone | non-contractile state of skeletal muscle- flaccid paralysis

Question 45

what are the uses of botulism?

Answer 45

clinically treats muscle spasm | cosmetically reduces appearance of wrinkles

Question 46

state how neuromuscular transmission is disrupted in organophosphate poisoning?

Answer 46

organophosphates inhibits function of ACh esterase(which is to stop signalling process by breaking down ACh) increased ACh activity at neuromuscular junction

Question 47

what are the symptoms of cholinergic toxidrome /organophosphate poisoning?

Answer 47

``` muscarinic symptoms SLUDGE Salivation Lacrimation Urination Defecation Gi cramping Emesis(vommiting) ``` ``` nicotinic symptoms weekdays MTWTF Muscle cramps Tachycardia Weakness Twitching Fasciculations ```

Question 48

explain the process and consequences of malignant hyperthermia?

Answer 48

severe reaction to anaesthetics- succinylcholine autosomal dominant inheritance- RyR1 gene males> females massive contraction fasciculation muscle rigidity- increase Ca2+ release excessive heat and metabolic acidosis increase muscle breakdown and hyperkalaemia(high blood k+ conc)

Question 49

describe the pathophysiology of Duchenne muscular dystrophy?

Answer 49

inherited by X linked recessive pattern- boys mainly mutation of dystrophin gene, so no dystrophin... excess Ca2+ enter muscle cell, taken up by mitochondria, water follows, mitochondria burst, muscle cell burst(rhabodomyolysis), creatine kinase and myoglobin in high conc in blood skeletal muscle symptoms and signs muscle cells replaced by adipose tissue

Question 50

what is troponin assay used for?

Answer 50

myocardial cell damage detection- cardiac ischaemia smallest change in troponin levels indicate cardiac muscle damage- not proportional to degree of damage must measure within 20 hours for accuracy

Question 51

how is collagen linked to scurvy disease?

Answer 51

fibroblasts secrete procollagen that forms collagen vitamin C is required to produce procollagen vitamin C deficiency so poor wound healing and impaired bone formation

Question 52

how is collagen linked to osteogenesis imperfecta?

Answer 52

abnormal type 1 collagen | manifests as blue sclera and bone malformation

Question 53

what is amyloidosis?

Answer 53

misfolding of proteins results in formation of amyloid fibres with infiltrate organs and can lead to disease eg alzheimers

Question 54

whats the difference between alpha and beta thalassemias?

Answer 54

a- decrease/absence of a chains in Hb, excess of b chains, form stable tetramers, symptoms before birth b- decrease/absence of b chains in Hb, excess a chains, unstable, symptoms after birth

Question 55

what is the cause and effects of ectopic pregnancy?

Answer 55

implantation at site not in uterine body- normally fallopian tube can be life threatening if not treating quickly- rupture fallopian tube or internal bleeding

Question 56

what is the cause and effects of placenta previa?

Answer 56

implantation in lower segment of uterine body- blocking cervical opening with the placenta c- section required can cause haemorrhage

Question 57

describe systemic sclerosis?

Answer 57

excessive accumulation of collagen in organs | leads to hardening and impaired function

Question 58

list the symptoms and signs of scurvy disease?

Answer 58

``` gum disease bruising of skin bleeding poor wound healing jaundice- yellowing of skin and eyes ```

Question 59

describe the cause Marfans syndrome?

Answer 59

autosomal dominant disorder fibrillin 1 gene is affected elastic tissue is abnormal

Question 60

describe the consequences of Marfans syndrome?

Answer 60

abnormally tall exhibit arachnodactyly- spider like and long fingers, long limbs frequent joint dislocation at risk of catastrophic aortic rupture- aortic eneurysm

Question 61

describe and explain ethlers-danlos syndrome?

Answer 61

deficiency in reticulin(type 3 collagen)- due to procollagen peptidase deficiency that causes tissues with high reticulin to rupture causes unstable joints, flat feet and stretchy skin

Question 62

why is acne caused?

Answer 62

blockage of pilosebaceous duct by sebum

Question 63

explain the cause and symptoms of acromegaly?

Answer 63

excess growth hormone in adults after puberty | periosteal growth leading to thickening of bones

Question 64

what is Barretts oesophagus- metaplasia?

Answer 64

Metaplasia- change of one type of differentiated cell to another acid reflux from stomach changes normal stratified squamous cells of oesophagus epithelium into simple columnar with a mucous secreting function

Question 65

describe and explain muscle atrophy?

Answer 65

destruction of muscle>replacement of muscle | due to denervation, misuse and age

Question 66

describe and explain muscle hypertrophy?

Answer 66

replacement of muscle>destruction of muscle increased work performed by muscle leads to more mitochondria, glycogen, blood supply and proteins in muscle

Question 67

describe the cause and effect of multiple sclerosis?

Answer 67

myelin sheath is removed from CNS axons and replaced by scar tissue (oligodendrocytes) Axonal destruction & overgrowth of glial tissue due to autoimmune attack(by T cells) conduction of nerve impulse slowed Relapsing and remission disease Pregnancy tends to reduce symptoms and relapse

Question 68

describe and explain the cause and consequences of tarui disease?

Answer 68

genetic defect phosphofructokinase-1 enzyme is deficient can's catalyse the reaction of fructose-6- phosphate to fructose-1,6-biphosphate inefficient pyruvate production lack of lactate formation

Question 69

describe what is meant by hypothyroidism?

Answer 69

underactive thyroid gland decrease in T3 and T4 levels increase in TSH

Question 70

what is Hashimotos?

Answer 70

hypothyroidism autoimmune disease blocking TSH receptors antibodies in blood; anti-TPO and anti-TG

Question 71

describe what is meant by hyperthyroidism?

Answer 71

overactive thyroid gland increase in T3 and T4 decrease in TSH

Question 72

what is grave's disease?

Answer 72

hyperthyroidism autoimmune disease activation of TSH receptors antibodies in blood; TSI and anti-TSH which increase t3 and t4

Question 73

what are the autoimmune features of graves disease?

Answer 73

exophthalmus- eyes putrude out antibodies deposit glucosaminoglycans thickening and redness of skin esp dorsal of foot due to antibodies

Question 74

how does TSI antibody cause hyperthyroidism?

Answer 74

mimics shape of TSH competes with TSH to bind to TSH receptor mimics TSH action causes excess T3 and T4

Question 75

how is hypo and hyper thyroidism diagnosed?

Answer 75

checking T4 and TSH levels

Question 76

describe the symptoms of hyperthyroidism?

Answer 76

``` goitre diarrhoea sweating weight loss heat intolerance ```

Question 77

why does goitre occur and what is it?

Answer 77

swelling of neck | follicles enlarge

Question 78

describe the symptoms of hypothyroidism?

Answer 78

``` goitre dry skin weight gain cold intolerance tiredness depression ```

Question 79

describe how hypothyroidism is treated?

Answer 79

oral thyroxine- increases T3 and T4 levels | increased iodine if necessary

Question 80

describe how hyperthyroidism is treated?

Answer 80

carbimazole- prevents iodine being incorporated with thyroglobulin and thyroidectomy radioactive iodine

Question 81

what factors increase the risk of malignant melanoma?

Answer 81

genetic mutation | heritable deposition

Question 82

What type of disease is sickle cel anaemia?

Answer 82

Autosomal recessive

Question 83

What’s the most suitable was to get a newborns HBB gene for a genetic test?

Answer 83

PCR(part of) newborns HBB gene

Question 84

Define lactic acidosis?

Answer 84

Build up of lactate in blood Due to anaerobic respiration in low oxygen levels so pyruvate is converted to lactate pH decreases, too much lactic acid

Question 85

Explain why lactic acidosis may occur?

Answer 85

In strenuous excercise Hearty eating Shock Congestive heart disease

Question 86

What is lactose intolerance?

Answer 86

Caused by lactase deficiency- not producing enough lactase Can’t digest lactose so it’s fermented by gut bacteria Produce acids that iritate GI causing cramps, bloating and diarrhoea Lactose in lumen of colon increases osmotic pressure, draw water out, diarrhoea

Question 87

Explain the biochemical basis of galactosaemia?

Answer 87

Deficiency in.. Kinase: rare, galactose build up Transferase: more common and serious, galactose and galactose-1-p build up, causes liver, kidney, brain and GI damage

Question 88

What are the symptoms of galactosaemia?

Answer 88

Conversions of galactose to galactitiol uses NADPH causes cataracts Galactose osmotic effects cause glaucoma Depleted NADPH Inappropriate disulphides bridge formation in proteins, loss of structure and function, aggregation, Heinz bodies Increase in intraoccular pressure

Question 89

Describe the clinical condition of glucose 6-phosphate dehydrogenase?

Answer 89

Inability to produce NADPH from NADP+ due to point mutation in gene coding for enzyme Low levels of NADPH Needed for reduction of oxidised glutathione back to active form- low levels Oxidative damage to cells RBC affected as only source of NADPH Haemoglobin form Heinz bodies Haemolytic anaemia

Question 90

How does a vitamin C deficiency lead to defected collagen tissue?

Answer 90

in post translational modification of collagen hydroxylation of lysine and proline by prolyl hydroxylase requires vitamin C as a cofactor hydroxylation increases H bonding- stabalises triple helix

Question 91

Describe the 4 blood groups?

Answer 91

``` AB- co dominant, universal reciever O- homozygous recessive, universal donor A- heterozygous dominant B- heterozygous dominant use I as genotype ```

Question 92

Describe what causes Ehlers-Danlos syndrome?

Answer 92

insufficient production of collagen type 4 | connective tissue has a higher ratio of elastin than collagen

Question 93

Describe the symptoms of Ehlers-Danlos syndrome?

Answer 93

stretchy skin joint hypermobility fragile skin that breaks and bruises easily

Question 94

what is compartment syndrome?

Answer 94

muscles of limbs are separated by fascia | a build up of pressure in one or more compartments can push on structures in other compartments and compromise them

Question 95

describe rhabdomyolysis?

Answer 95

muscle breakdown due to insufficient blood supply release myoglobin and creatine kinase into blood excreted via kidneys and makes urine dark

Question 96

what is the role of growth hormones(gh) on bone abnormalities?

Answer 96

in adults- no epiphyseal growth plates so high gh effects bone width not length, increasing periosteal growth excess gh- increase length of long bones, gigantism lack gh- decreased epiphyseal cartilage deposition, pituitary dwarfism

Question 97

what is the diagnosis clues of situs inversus and how is it caused?

Answer 97

heart on the right hand side of the body immotile cilia, as during embryogenesis left and right programming is modulated by motile cilia. if dont have motile cilia internal organs are on opposite sides

Question 98

why is mucus thick and sticky in cystic fibrosis patients?

Answer 98

CTFR protein dosent release chloride ions, osmotic ion so water doesnt get released from epithelial cells, decrease in water in mucus so more thick and less lubricating

Question 99

Describe how mutation can lead to hereditary spherocytosis?

Answer 99

Mutation in abjuring, spectrum, band 3, and band 4.1 Loss of functional RBC cytoskeleton Less efficient spherical shape Decrease in SA:volume More fragile, unable to buffer physical forces Osmotically fragile, shorter life cycle Increased rates of splenic destruction, causes haemolytic anaemia

Question 100

What are the symptoms of a defective mitochondrial fatty acid transport system?

Answer 100

Poor excercise tolerance | Large amounts of triacylglycerides in muscle cells

Question 101

When does conc of ketone bodies increase in circulation?

Answer 101

In starvation Untreated type 1 diabetes Can cause ketoacidosis, smell of acetone on breath by lungs excretion

Question 102

What triggers relapse of multiple sclerosis?

Answer 102

``` Infection Stress Heat Insomnia Poor diet Pack of sun exposure ```

Question 103

What are the main symptoms of muscular sclerosis?

Answer 103

``` Spastic paralysis of both legs Fatigue Vision problems Shakin or tingling of limbs Muscle spasms/stiffness/weakness Cognitive dysfunction Mental or sexual health issues Difficult eating or talking ```

Question 104

How is multiple sclerosis diagnosed?

Answer 104

``` Identify lesions(white areas on a t2 mri scan of brain and spinal chord) Has no cure ```

Question 105

What are the similarities between Gillian-barré syndrome and multiple sclerosis?

Answer 105

Similar initial symptoms like numbness, muscle weakness, pain and loss of balance and co-ordination Both autoimmune T cells destroy myelin sheath Delayed neurotransmission

Question 106

What are the differences between Gillian-Barré syndrome and multiple sclerosis?

Answer 106

GB is curable wheras MS isn’t GB symptoms are bilateral and effect both sides of body at same time GB also causes inability and difficulty in breathing- life threatening

Question 107

What’s a splenectomy and it’s effects?

Answer 107

Surgeons remove spleen Bone marrow and liver take over function of destroying old RBCs Increases risk of infection by encapsulated bacteria and malaria

Question 108

What is a splenomegaly?

Answer 108

Enlarged spleen due to response to localised infection(eg lymph nodes) or systemic infection(eg glandular fever or malaria)

Question 109

How do skeletal muscle respond to injury?

Answer 109

Connective tissue endomysium and perimysium divide and differentiate into myoblasts that fuse to form muscle fibres Satellite cells produce muscle fibres

Question 110

How does smooth muscle respond to injury?

Answer 110

Proliferation and differentiation of primitive smooth muscle into new muscle fibres

Question 111

Hep does cardiac muscle respond to injury?

Answer 111

Regenerates after injury in children | Can’t regenerate in adults- replaced by scar tissue

Question 112

What’s myopathy?

Answer 112

Disease of muscles that is not associated with the nervous system or emotional disorder

Question 113

What are some used of botulinum toxin covered by the NHS?

Answer 113

Sever underarm sweating Overactive bladder syndrome Blepharospasm- uncontrollable blinking

Question 114

What is muscle atrophy?

Answer 114

Wasting of muscle due to lack of use | Muscle shrinks as muscle fibres die

Question 115

What is muscle hypertrophy?

Answer 115

Increase size of muscle fibres due to excercise

Question 116

What is hyperplasia?

Answer 116

Increase in number of myofibrils in each muscle fibres due to exceed use

Question 117

When does muscle hypertrophy and hyperplasia occur?

Answer 117

Skeletal muscle- regular excercise they become stronger and larger Smooth muscle- during pregnancy due to growing fetid Cardiac muscle- to compensate for reduced blood flow

Question 118

Why does rhabdomyolysis occur?

Answer 118

Inherited Eg lactose dehydrogenase deficiency or duchenne muscular dystrophy Lipid lowering drugs eg statins

Question 119

Why is urine brown in rhabdomyolysis

Answer 119

Myoglobin and creative kinase in urine | A sign of kidney damage

Question 120

What is creatine kinase used for?

Answer 120

Blood assay to diagnose myocardial infarction, tissue damage, muscular dystrophy, rhabdomyolysis or kidney injury

Question 121

What are the consequences of rhabdomyolysis?

Answer 121

Myoglobin release- kidney damage Sodium release- tissue swelling and cell death as increases ca2+ conc outside sacroplasmic reticulum ATP release- loss of energy, Ca2+ influx, disintegrated cells Potassium release- electrolyte inbalance, prevents electrical conduction of cardiomyocyte, death

Question 122

How is lactate blood conc controlled

Answer 122

Heart concert it back to pyruvate and CO2 | Deliver and kidney convert it back to glucose in glucogenesis

Question 123

What is the consequence of lactose dehydrogenase deficiency

Answer 123

Pyruvate can’t be converted into lactate to regenerate NAD+

Question 124

Explain the key role of pyruvate dehydrogenase?

Answer 124

Converts pyruvate to acetyl coA Irreversible- release co2 Sensitive to B1 vitamin PDH Deficiency- pyruvate build up, lactic acidosis

Question 125

What is the normal temperature range, hypothermia and hyperthermia?

Answer 125

``` 40-42 hyperexia 42-38 hyperthermia 37.5- 36.5 normal 36.5-32 mild hypothermia 32-28 severe hypothermia <28 no vital signs ```

Question 126

What is therapeutic hypothermia?

Answer 126

Comatose cardia arrest- neuroprotective | Neonatal encephalopathy

Question 127

What is rigor?

Answer 127

Heat accompanied with shivering

Question 128

What is a febrile seizure?

Answer 128

Seizure associated w high temperature without any serious health issues Affects 6months- 5years

Question 129

What is normal pH and how is it measured?

Answer 129

PH 7.35-7.45 pH= -log[H+] Death <6.8 or >8 Acidosis if <7.35 causes headaches, confused, tremors, coma Caused by metabolic acidosis- lactic acid build up or respiratory acidosis- hypo ventilation

Question 130

What are the causes of oedema?

Answer 130

Increase in hydrostatic pressure Decrease In oncotic pressure in capillaries Increase in oncotic pressure in interstitium Impaired lymphatic drainage

Question 131

What are the symptoms of dehydration?

Answer 131

Adults: dry mouth, thirsty, fatigue, low urine output, concentrated urine Elderly: confusion, low bp Baby: sunken eye, cold skin

Question 132

What’s water intoxication?

Answer 132

Too much water Can cause reacted in [Na+] blood plasma Muscle weakness, seizure, coma, unconscious

Question 133

What is pheochromocytoma?

Answer 133

A tumour in chromaffin cells(adrenal medulla sympathetic post ganglionic neurones) resulting in increase adrenaline production

Question 134

What is refeeding syndrome?

Answer 134

Feeding too much too quickly after starvation- someone with marasmus or kwashiorkor Lack of nutrients and proteins for long time so live can’t synthesise albumina and lipoproteins, down regulating enzymes in urea cycle Proteins can’t be digester completely Toxic levels of ammonia build up in body

Question 135

Why is someone with refeeding syndrome at risk of cardiac arrhythmias?

Answer 135

``` High glucose consumption Cause high insulin spike Moves potassium into cells Hypokalemia Leading to cardiac arrhythmia ```

Question 136

Which step of collagen synthesis is affected in scurvy?

Answer 136

Hydroxyl action of proline and lysine groups

Question 137

What is osteoarthritis and it’s effects?

Answer 137

Age related mechanical failure of articulate cartilage Joint stiffness & pain Cartilage degenerates, narrowing of joint space and bone rubbing against bone

Question 138

Define and describe rheumatoid arthritis?

Answer 138

Autoimmune disease that attacks joints Inflammation of synovial membrane and thickening of joint capsules Damage to bone and cartilage Joint pain and stiffness- takes longer to relieve stiffness than in osteoarthritis Swelling and redness

Question 139

Describe the normal process of fracture repair?

Answer 139

Haematoma formation- inflammation, phagocytes and osteoclasts remove damage Fibrocartilogenous formation- soft callus, blood vessels infiltrate, granulation tissue develops, fibroblasts produce collagen, chondroblasts produce hyaline Bony callus formation- endochondral ossification, replace hyaline cartilage with cancellous bone, trabeculae develop Bone remodelling- cancellous bone to compact bone

Question 140

Describe how long bones develop?

Answer 140

Endochondral ossification Hyaline cartilage model Collar of cortical bone around shaft formed Nutrient artery penetrates cartilage and generates spiracles, supplying osteogenitor cells and generates primary ossification centres Cartilage forms epiphyseal growth plates Epiphysis develop secondary ossification centres and ossify

Question 141

What is compartment syndrome?

Answer 141

Muscles segregated into compartments by fascia Trauma to one compartment- internal bleeding- increased pressure- exerts pressure on other compartments Results in: deep constant pain, paresthesia, compartment feeling firm and tight , swollen red shiny skin

Question 142

A genetic defect in fibrilin1A causes what?

Answer 142

Abnormal elastic tissue | Elastin fibres made incorrectly

Question 143

A genetic defect in collagen1A1 gene causes what?

Answer 143

Osteogenesis imperfecta

Question 144

What does a genetic defect in FGFR3 cause?

Answer 144

Achondroplasia

Question 145

What is an example of a disease cause by triosomy?

Answer 145

Down syndrome | Triosomy 21

Question 146

What does a genetic defect in beta haemoglobin cause?

Answer 146

Sickle cell anaemia

Question 147

What can cause rhabdomyolysis?

Answer 147

Infection, toxins, statins, crush or blast injury, long term immobilisation like stroke Or inherited duchenne muscular dystrophy and lactate dehydrogenase deficiency

Question 148

What type of inheritance does haemophilia a follow?

Answer 148

X linked recessive

Question 149

What inheritance is sickle cel anaemia?

Answer 149

Autosomal recessive

Question 150

Describe Cushing’s syndrome?

Answer 150

Excess cortisol Excessive breakdown of proteins Weakened skin structure Striae formation

Question 151

How is ALT and AST used clinically?

Answer 151

Blood tests | If high in blood suggests liver damage such as viral hepatitis, autoimmune liver diseases or toxic injury

Question 152

what is hypoxia?

Answer 152

oxygen deprivation

Question 153

what are the 4 causes of hypoxia?

Answer 153

1 hypoxaemic- arterial content of O2 is low 2 anaemic- decreased ability of haemoglobin to carry O2 3 ischaemic- inturruption to blood supply 4 histiotoxic- inability to utilise oxygen in cells due to disabled oxidative phosphorylation enzymes

Question 154

what is phenylketonuria(PKU)?

Answer 154

``` phenylalanine metabolism defect autosomal recessive deficiency in phenylalanine hydroxylase accumulation of phenylalanine in blood accumulation of phenylketones ```

Question 155

what are the symptoms of phenylketonuria?

Answer 155

``` severe intellectual disability development delay microcephaly(small head) seizures hypopigmentation mental retardation ```

Question 156

what are the treatments for phenylketonuria?

Answer 156

strictly controlled low phenylalanine diet avoid artificial sweeterners avoid high protein food such as meat, milk and eggs

Question 157

what are the clinical signs of hypercholesterolaemia?

Answer 157

1 xanthelasma- yellow patches on eyelids 2 tendon xanthoma- nodules on tendon 3 corneal arcus- obvious white circle around eye

Question 158

what are hyperlipoproteinaemias?

Answer 158

raised plasma level of one or more lipoprotein classes caused by- overproduction or over removal 6 types

Question 159

what is the treatment for hyperlipoproteinaemias?

Answer 159

first; diet- reduced cholestrol and saturated lipid intake or increase fibre intake excercise, stop smoking drugs; satins- reduce cholestrol synthesis by inhibiting HMG-CoA reductase eg. atoravastatin bile salt sequeastrants- forces liver to produce bile acids using more cholestrol

Question 160

why does splenomegaly occur?

Answer 160

spleen growth... 1 back pressure- portal hypertension in liver disease 2 over work 3 extramedullary haemopoeisis 4 expanding as infiltrated by cells- cancel cells 5 expanding as infiltrated by other material- granulomas

Question 161

how do you examine the spleen?

Answer 161

start to palpate right iliac fossa feel for spleen edge to hit hand on inspiration(breath in) feel for splenic notch measure in cm from costal margin in mid clavicular line

Question 162

what is the main consequence that occurs due to splenomegaly?

Answer 162

hyperslenism low blood counts as pooling of blood occurs in the enlarged spleen risk of rupture of spleen as no longer protected by rib cage- avoid contact sports and vigorous excercise

Question 163

what causes hyposplenism?

Answer 163

lack of functioning spleen - splenectomy - sickle cell disease - gastrointestinal diseases eg. crohns disease - autoimmune disorders eg. rheumatoid arthiritis

Question 164

what will be seen on a blood film from someone with hyposlenism?

Answer 164

howell jolly bodies- red blood cells that contain DNA remnants because spleen is not functioning as normal so hasnt removed them

Question 165

what are patients with hyposplenism at risk of?

Answer 165

risk of sepsis from encapsulated bacteria | eg, streptococcis pneumonia, haemophilus influenza and meningocuccus

Question 166

what would expect the packed cell volume of an anaemic patient be?

Answer 166

depressed hematocit % | less RBCs

Question 167

what would expect the packed cell volume of an polycythemic patient be? how can u decide which type it is?

Answer 167

elevated hematocit % more RBCs ``` true= RCC elevated pseudo= RCC normal ```

Question 168

what is spondylolisthesis?

Answer 168

an anterior displacement of the vertebrae above on the vertebrae below caused by a disconnection of the vertebral body from the vertebral arch

Question 169

what symptoms can spondylolisthesis cause?

Answer 169

some people are assymptomatic most complain of some dicomfort raging from occassional lower back pain to incapacitating mechanical pain, sciatica from nerve root compression and neurodenic claudation

Question 170

what are5 red flag symptoms of cauda equina syndrome?

Answer 170

``` bilateral sciatica perianal numbness painless retention of urine faecal/urinary incontinence erectile dysfunction its a surgical emergency ```

Question 171

how does neurogenic claudication present?

Answer 171

pain in legs whilst walking

Question 172

what is neurological claudication?

Answer 172

compression of nerve roots, venous engorgement of nerve roots during excercise, reduced atrial flow, pain and paresthesia is relieved by rest and by spine flexion

Question 173

which vertebral level should a lumbar puncture needle be inserted? why?

Answer 173

L3/L4 | causa equina- mobile spinal roots, less chance of neurological damage

Question 174

what is sciatica?

Answer 174

pain caused by irritation or compression of one or more of the nerve roots that contribute to the sciatic nerve- L4-S3

Question 175

describe the 4 staged of intervertebral disc herniation?

Answer 175

1 disc degeneration; disc dehydrate and buldge with age 2 prolapse; nucleus pulposus slightly impinges into spinal canal 3 extrusion; nucleus pulposus breakes through annulus fibrosus 4 sequestration; nucleus pulposus seperates from main body of disc, enters spinal canal

Question 176

what is cauda equina syndrome?

Answer 176

usually secondary to prolapse disc | canal- filling disc compressing lumbar and sacral nerve roots

Question 177

what is the benefit of the transverse pericardial sinus?

Answer 177

seperates aorta and pulmonary trunk from benous inflow | allow surgeons to get behind aorta and pulmonary trunk, enables you to clamp aorta

Question 178

why does a sudden build up of fluid in pericardial sac prevent filling in diastole?

Answer 178

outer fibrous pericardium layer cant expand causing fluid to compress the heart

Question 179

what can be heard and felt over a stenosed vessel?

Answer 179

turbulent flow= noisy, korotkoff sounds | thrill- felt, bruit- heard

Question 180

what is the cardiac output of a 70kg man at rest?

Answer 180

5L/min | CO=SV X HR

Question 181

what causes the first heart sound?

Answer 181

in isovolumetric contraction | atrialventricular mitral valve shuts

Question 182

what causes the secound heart sound?

Answer 182

in isovolumetric relaxation | semilunar atrial valve shuts

Question 183

where can QRS be seen in cardiac cycle?

Answer 183

isovolumetric contraction, ventricle depolarisation

Question 184

where can p wave be seen in cardiac cycle?

Answer 184

atrial contraction, firing of SA node causes atrial depolarisation

Question 185

where can t wave be seen in cardiac cycle?

Answer 185

reduced ejection, ventricles repolarise

Question 186

what can cause pericardial collection or effusion?

Answer 186

viral and bacterial infection | stab wound

Question 187

what is pericardiocentesis?

Answer 187

a procedure to remove blood or fluid from pericardial sac

Question 188

what is a patient likely to have with a C4/5 prolapsed disk?

Answer 188

compression of c5 spinal nerve- emerge above | reduced sensation of later aspect of upper arm

Question 189

what is the most common sites for a herniation of an intervertebral disc?

Answer 189

L4/5 L5/S1

Question 190

what is a paracentral herniation?

Answer 190

slipped disc that compresses traversing nerve root- exits below

Question 191

what are the 4 signs of osteoarthritis on x ray?

Answer 191

Reduced joint space subchondral sclerosis bone cysts osteophytes

Question 192

why is posterior dislocation of the hip most common?

Answer 192

weak ischiofemoral ligament posteriorly

Question 193

what are the risk factors for primary osteoarthritis?

Answer 193

no known cause | age, female, ethnicity, genetics, nutrition

Question 194

what are the risk factors for secondary osteoarthritis?

Answer 194

obesity, trauma, malalignment, infection, inflammatory

Question 195

what are the symptoms of OA?

Answer 195

deep anchoring joint pain worsened with use, reduced ROM and crepitus(grinding), stiffness during rest, swelling and tenderness

Question 196

what is the pathology of OA?

Answer 196

exce4ssive loading of joint and damage to articular cartilage increased proteoglycan synthesis by chondrocytes flaking and fibrilation of cartilage erosion of cartilage- loss of joint space

Question 197

what does altered joint biomechanics lead to?

Answer 197

Vascular invasion and increased cellularity of subbchondralar bone(sclerosis) cystic degeneration of bone( cysts) osseous metaplasia of connective tissue(osteophytes)

Question 198

treatment of OA of hip?

Answer 198

weight loss activity modification stick/walker physiotherapy analgesia anti-inflammatory (NSAIDS eg. ibuprofen and COX-2 inhibitors) nutritional supplements corticosteroids injections viscosupplementation- hyaluronic injections surgery- total hip replacement

Question 199

why are intracapsular fractures of the neck of femur worse?

Answer 199

disrupt retinacular arteries(branches of circumflex femoral arteries) , artery of ligamentum terees cant supply demand avascular necrosis of bone increased risk w displaced fracture

Question 200

what is the treatment for a displaced intracapsular NOF fracture?

Answer 200

hemiarthoplasty- replace femoral head | total hip replacement

Question 201

what is an extracapsular NOF fracture?

Answer 201

interochanteric or subtrochanteric | intact retinacular artery supply

Question 202

Symptoms of hip/NOF fractures?

Answer 202

reduced mobility- inability to bear weight on limb | pain felt on hip, groin or knee

Question 203

what does a NOF fracture look like on examination?

Answer 203

hip shortened, aBducted and externally rotated

Question 204

whats the most common cause of hip dislocation?

Answer 204

can be congenital or due to trauma | knee hitting dashboard in road traffic collision

Question 205

what does a posterior hip dislocation look like on examination?

Answer 205

shortened, aDducted medial rotation(gluteus medius and minimus) sciatic nerve palsy maybe present

Question 206

what does a anterior hip dislocation look like on examination?

Answer 206

externally rotated abducted slightly flexed

Question 207

what does a central hip dislocation look like on examination?

Answer 207

fracture dislocation always femoral head palpable intrapelvic haemorrhage

Question 208

what are the complications of hip dislocation?

Answer 208

``` foot drop sciatic nerve injury post traumatic OA avascular necrosis infection ```

Question 209

how do you locate the correct site for gluteal intramuscular injection?

Answer 209

palm of hand on greater trochanter of femur thumb toward inguuinal region, index finger towards anterior superior iliac crest fingers make a V inject into gluteus medius

Question 210

what is a febrile seizure?

Answer 210

a convulsion in a young child caused by a spike in body temp often from an infection not in CNS

Question 211

when is the major peroid of congenital malformation in embryonic development?

Answer 211

embryonic peroid | 3-8 weeks

Question 212

what is situs inversus?

Answer 212

complete mirror image viscera | due to immotile cilia

Question 213

explain how acute inflammation can cause appendicitis?

Answer 213

``` accumulation of bacteria and exudate inflammed appendix blocked lumen faecolith- solid lumps of faeces increased pressure causes perforation(bursting) presents w abdominal pain ```

Question 214

explain how acute inflammation is linked to bacterial meningitis?

Answer 214

inflammation of meninges | compresses brain against skull

Question 215

describe what an abscess is?

Answer 215

accumulation of dead and dying neutrophils | with associated liquefactive necrosis

Question 216

describe the effects of an abscess?

Answer 216

compression of surronding structures | pain and blockage of ducts

Question 217

name 3 disorders of acute inflammation?

Answer 217

1 Hereditary angio-oedema 2 Alpha-1 antitrypsin deficiency 3 Chronic granulomatous disease

Question 218

what are the clinical signs of acute inflammation?

Answer 218

``` Rubor- redness Calor- heat Dalor- pain tumor- swelling loss of function ```

Question 219

what are the 3 nuclear changes seen under a light microscope during cell injury?

Answer 219

pyknosis- shrinkage of nucleus and chromatin karyorrhexis- fragmentation karyolysis- dillusion of nucleus

Question 220

what are the causes of infarction?

Answer 220

infarction= reduced arterial blood suplly, causes necrosis athlerosclerosis twisting compression occlusion by thrombosis or thromboembolism

Question 221

what is ischaemic- reperfusion injury?

Answer 221

blood flow returned to damage tissue that isnt necrotic yet, worsens damage

Question 222

what are the 4 types of hypoxia?

Answer 222

hypoxaemic- too low oxygen conc in arterials anaemic- haemoglobin cant carry oxygen ischaemic- interruption to blood supply histiotoxic- cant use oxygen, non functioning oxidative phosphorylation enzymes

Question 223

what type of hypoxia does carbon monoxide poisoning cause?

Answer 223

histiotoxic

Question 224

name the causes of cell injury?

Answer 224

``` hypoxia trauma radiation poisons alcohol drugs microorganisms hypersensitive or autoimmune reactions genetic abnormalities ```

Question 225

what is shock?

Answer 225

clinical syndrome caused by circulatory failure

Question 226

what process cuases swelling in acute inflammation?

Answer 226

net flow of fluid our of bloodvessels forming exudate in tissues

Question 227

explain how alcohol oxidation can cause liver damage?

Answer 227

build up of NADH- lactic acidosis, gout, hypoglyceamia | build up acetly CoA- fatty liver

Question 228

explain the mechanism of hangover?

Answer 228

limiting factor is aldehyde dehydrogenase excess alcohol consumption- build up of acetaldehyde acetaldehyde is toxic and longterm exposure causes hepatitis and cirrhosis

Question 229

describe and explain how alcohol dependence is treated?

Answer 229

disulfiram inhibits aldehyde dehydrogenase acetaldehyde not converted to acetate- accumulates gives hangover symptoms- discouraging alcohol consumption by classical conditioning

Question 230

which diseases can oxidative stress form?

Answer 230

``` cardiovascular rheumatoid arrthiritis alzheimers crohns COPD cancer parkinsons ```

Question 231

what are the 3 enzymes that could be deficient in galactosaemia?

Answer 231

galactokinase UDP- galactose epimerase uridyl transferase

Question 232

describe the pathophysiology of galactosaemia?

Answer 232

deficiency in enzymes increase aldose reductase activity build up of galacititol consume excess NADPH

Question 233

what are the symptoms of galactosaemia?

Answer 233

``` cataracts hepatomegaly and cirrhosis seizure, brain damage renal failure hypoglycaemia ```

Question 234

describe the pathophysiology of G6PDH deficiency?

Answer 234

decrease Glucose 6 phosphate dehydrogenase activity less NADPH need NADPH for GSSG(oxidised glutathione) to GSH(reduced glutathione) less GSH- cant protect against oxidative stress

Question 235

describe the symptoms of G6DPH deficiency?

Answer 235

oxidative stress lipid peroxidation- cell membrane damage, mechanical stress protein damage- aggregates of cross linked hb- heinz bodies haemolysis

Question 236

explain the clinical relevance of using creatinine as a marker?

Answer 236

creatine and creatine phosphate breakdown to release creatinine in muscle amount of creatinine in urine suggests an estimate for muscle mass can also indicate kidney function- urine

Question 237

describe the cause urea cycle defects?

Answer 237

autosomal recessive generic disorders deficiences in one of the enzymes- partial loss of function leads to... hyperammonaemia and accumulation of urea cycle intermediates

Question 238

how is urea cycle defects managed?

Answer 238

low protein diet | replace aa in diet w ketoacids

Question 239

what are the symptoms of a defective urea cycle?

Answer 239

ammonia toxicity children can die vomitting, lethargy, mental retardation, seizures, comma

Question 240

describe the heel prick test?

Answer 240

screening for every new born in the uk looks for genetic defects in amino acid metabolism like sickle cell disease, cystic fibrosis, congenital hypothyroidism, phenylketonuria, homocystinuria

Question 241

describe the pathophysiology of phenylketonuria(PKU)?

Answer 241

autosomal recessive- chromosome 12 deficiency in phenylalanine hydroxylase- cant convert phenylalanine to tyrosine accumulation of phenylalanine- transamination to phenylketones phenylketones accumulate in urine-musty smell

Question 242

describe the symptoms of PKU?

Answer 242

``` lack of tyrosine production- cant synthesise catecholamines hormones, melanin and proteins severe intellectual disability development delay microcephaly(small head) seizures hypopigmentation ```

Question 243

what is the treatment for PKU?

Answer 243

low phenylalanine diet high tyrosine diet avoid artificial sweetners avoid high protein food eg. eggs, meat and milk

Question 244

describe what homocystinurias is?

Answer 244

cant breakdown methionine excess homocysterine and methionine autosomal recessive- defect in crystathionine b synthase treat with low methionine diet, avoid milk, meat, cheese, eggs, nuts

Question 245

explain the process of paracetamol overdose?

Answer 245

produce NAPQI causes oxidative damage to hepatocytes- lipid peroxidation, damage to proteins and DNA treatment= acetylcysteine, replenishes GSH levels

Question 246

why during a myocardial infarction can a person feel pain from both sides sometimes?

Answer 246

cardiogenic fields from embryonic development are bilaterally symmetrical and are on both sides

Question 247

what feature of the left atrium can causes stasis of blood?

Answer 247

during atrial fibrillation blood collects in left auricle(small pouch formed from primitive atrium) whcih causes clotts

Question 248

describe the first and second heart sounds?

Answer 248

first sound- lup, louder and longer | second sound- dub, shorter and quite

Question 249

what causes the 3 shunts of the heart to shut at birth?

Answer 249

foramen ovale- as left atrial pressure exceed right atrial pressure ductus venosus- umbilical cord cut, no umbilical vein ductus arteriosus- first breath, increase oxygen pressure

Question 250

how do you classify congenital heart disease?

Answer 250

acyanotic... left to right shunts, obstuctive lesions blood in pulmonary circulation is full saturated so p02 is maintained eg. aortic stenosis, ASD, VSD cyanotic... complete right to left shunts systemic oxygen low eg. tetralogy of fallot, transposition of great arteries

Question 251

describe the haemodynamic effects of atrial septal defects?

Answer 251

1 increased pulmonary blood flow 2 RV volume overload 3 pulmonary hypertension- rare, pulmonary oedema 4 eventual right sided HF

Question 252

describe the haemodynamic effects of ventral septal defects?

Answer 252

1 left to right shunt 2 LV volume overload 3 pulmonary venous congestion 4 eventual pulmonary hypertension membranous portion of septum fails to develop properly so primary interventricular foramen still open

Question 253

Describe the pathophysiology and consequences of patent ductus arteriosus?

Answer 253

ductus arteriosus dosen't shut with first breath blood from aorta can enter pulmonary artery at high pressure high volume of blood at pulmonary artery, increases preload right sided heart failure- acyanotic blood fully saturated w oxygen

Question 254

describe atrial ventricular septal defects?

Answer 254

caused by inproper development of endocardial cushions hole in heart, with one common atriaventricular valve common in downs syndrome

Question 255

describe aortic/ pulmonary stenosis?

Answer 255

acyanotic semi lunar valves dont develop properly eg aortic valve is bicuspid hypertrophy and so heart failure

Question 256

describe coarctation of the aorta?

Answer 256

narrowing of the aorta radio femoral delay, strong radial pulse, weak femoral pulse high bp

Question 257

describe the pathophysiology of tricuspid atresia?

Answer 257

tricuspid valve fails to form blood cant flow from right atrium to ventricle r to l atrial shunt of entire venous return blood flow to lungs VSD oxygenated and deoxygenated blood mix in left side of heart so blood being pumped to rest of the body has low p02- cyanotic(r to l)

Question 258

describe the pathophysiology of transposition of the great arteries?

Answer 258

septum dosent spiral no oxygen- cyanotic aorta on right side(rv) and pulmonary trunk on left(lv) two circulations completely seperate, ASD and PDA shunts needed bidirectional shunting medical emergency, require prostagladins to maintai PDA to allow some oxygen in

Question 259

describe the group of cardiac defects present in tetralogy of fallot?

Answer 259

1 over riding aorta- very large, most blood passes through aorta 2 pulmonary stenosis- pulmonary valve and artery narrowed, less blood 3 ventricular septal defect- right must pass from right to left ventrical 4 right ventricle hypertrophy- generate more force to pump blood through stenosed pulmonary artery

Question 260

describe the pathophysiology of hypoplastic left ventricle?

Answer 260

``` mitral or artrial valves stenosed- less blood to LV underdeveloped Left Ventricle ascending aorta very small RV supports cirulation right to left shunt ```

Question 261

explain how alcohol metabolism can damage the liver?

Answer 261

acetaldehyde produced from alcohol by alcohol dehydrogenase is toxic increases acetyl coA, increase fatty acid synthesis and so TAG oxidation to acetaldehyde and then acetate produces NADH descreased NAD+/NADH ratio, favours formation of TAGs, reduced capactiy of liver to transport TAGs accumulate- fatty liver

Question 262

describe how disulfiram causes hangover symptoms?

Answer 262

inhitbits aldehyde dehydrogenase | acetaldehyde accumulation when drink alcohol

Question 263

what are the 2 features that make LDL associated with atherosclerosis?

Answer 263

long lived- not efficiently cleared by liver | more susceptible to oxidative damage

Question 264

Describe how raised serum LDL causes atherosclerosis?

Answer 264

oxidised LDL is recognised and engulfed by macrophages foam cells(macrophages containing lipids) accumulate in intima of blood vessels to form fatty streaks evolve into atherosclerotic plaques if plaques grow blocking lumen- angina if plaques rupture- thrombosis- stoke or MI

Question 265

describe what is familial hypercholestrolaemia?

Answer 265

absence or deficiency of functional LDL receptors elevated LDL and cholestrol in plasma signs... tendon xanthoma xanthelasma corneal arcus

Question 266

describe what is dyslipoproteinaemias?

Answer 266

defect in plasma lipoprotein metabolism primary- family inborn secondary- diet, drugs

Question 267

describe the classifications of hyperlipoproteinaemias?

Answer 267

raised level of one or more plasma lipoproteins type1- defective lipoprotein lipase, chylomicrons present type 11a- coronary artery disease association, defective LDL recpetor type 11b- coronay artery disease association type 111-raised IDL and chylomicrons, defective apoprotein, conory artey disease association type 1v- associated w coronary artery disease typev- raised chylomicrons and VLDL, associated w coronary artery disease

Question 268

describe the treatment of hyperlipoproteinaemia?

Answer 268

diet and life style modification reduce cholestrol and TAG intake statins- inhibit HMG coA reductase, reduce cholesterol synthesis, increase lipoprotein lipase expression

Question 269

what does deficiency in each of the lipid soluble vitamins cause?

Answer 269

A- dry eyballs, no tears D- rickets, weak/soft bones E- nerve and muscle damage, no protection against oxidative stress K- defected blood clotting

Question 270

why cant acetyl coA be converted to glucose in humans?

Answer 270

pyruvate dehydrogenase enxyme is irreversible so cannot form pyruvate and therefore cant be converted to glucose

Question 271

explain why defective lecithin-cholestrol acytltransferase enzyme is a problem?

Answer 271

LCAT usually maintains lipoprotein structure deficiency causes unstable and abnormal structure lipoproteins due to destruption in ratio of surface to core lipoproteins general failure in lipid transport, lipid deposits and athlerosclerosis

Question 272

why is the knee in flexion less stable?

Answer 272

curved surface of femoral chondyles and tibial plateau, small area of articulation can only get rotation when flexed- more movement

Question 273

what characteristic is seen with a superior gluteal nerve injury?

Answer 273

weakness is adductors of hip- gluteus medius and minimus | Trendelenburg Sign

Question 274

what is the clinical significance of the blood supply to the menisci?

Answer 274

from periphery blood supply decreases with age, centralminisci is avascular by aduthood impaired healing after trauma

Question 275

describe the mechanism of locking the knee?

Answer 275

internal(medial) rotation of femur 5 degrees on tibial plateau, cruciate ligaments tighten

Question 276

describe the mechanism of unlocking the knee?

Answer 276

popliteus contracts, rotates femur laterally

Question 277

what is the 'unhappy triad' of injuries?

Answer 277

ACL- anterior cruciate ligament MCL- medial collateral ligament medial miniscus

Question 278

describe a 'housemaids knee'?

Answer 278

pre-patellar bursitis, inflammation on front of knee, kneeling

Question 279

describe a 'clergymans knee'?

Answer 279

infra-patella bursitis, around tibical tibia, kneeling in a more erect position

Question 280

why is it more common for the patella to displace laterally?

Answer 280

q angle- direction of pull of quadracepts is lateral on patella

Question 281

how do you find the femoral pulse?

Answer 281

mid inguinal point- halfway between ASIS and pubic synthesis

Question 282

which 3 x rays do we use to view the knee?

Answer 282

anterior posterior lateral patella axial- skyline

Question 283

what are the common causes of femoral shaft fractures?

Answer 283

in young adults and children- high velocity trauma | site- proximal, mid shaft or suprachondylar

Question 284

what are common complications of femoral shaft fractures?

Answer 284

tense swollen thigh blood loss- hypovaleamic shock traction splint treeat with - surgical fixation

Question 285

what is the usual mechanism of injury for tibial plateau fractures?

Answer 285

high energy injury | axial loading with varus or valgus angulation

Question 286

describe the features of tibial plateau fractures?

Answer 286

``` articular cartilage of tibia damaged unichondylar(affect one condyle)- lateral tibial condyl more common or bicondylar(effect both condyles) post traumatic OA joint surface reduction instability ```

Question 287

what is the usual cause for patella fractures?

Answer 287

direct or indirect injury | patients aged 20-50 years

Question 288

on examination what is commonly seen for patella fractures?

Answer 288

palpable defect in patella | if extensor mechanism is disrupted the fracture completely splits patella- unable to do straight leg raise

Question 289

how are patella fractures treated?

Answer 289

if displaced- reduce and surgical fix | if undisplaced- splint and protect

Question 290

what is the difference between subluxation and dislocation?

Answer 290

subluxation is partial displacement | dislocation is complete displacement

Question 291

what is the most common cause of patella dislocatiojn?

Answer 291

usually lateral dislocation due to trauma- twistin action in slight flexion athletic teenagers

Question 292

describe the predisposing factors of patella dislocations?

Answer 292

``` weakness of quadriceps- VMO(vastus medicalis obliquus) ligamentous laxity(loose) shallow trochlear groove long patellar ligament previous dislocations ```

Question 293

what is the treatment of a patella dislocation?

Answer 293

reduce and immobolise | physiotherapy to strengthen VMO

Question 294

wwhat is the mechanism of injury in meniscal tearss?

Answer 294

most common knee injury | sudden twisting motion of wight bearing knee in high flexion

Question 295

how does a patient present with meniscal injuries?

Answer 295

intermittent, localised pain restricted motion swelling mechanical symptoms- locking, jamming, catching

Question 296

how do you treat a meniscal injury?

Answer 296

MRI- usually sagital if traumatic- mecisectomy or meniscal repair if degenerative/ chronic process- leave alone and rehabilitate

Question 297

what is the mechanism of injury for collateral ligament injuries?

Answer 297

contact/ direct blow- sporting injury medial collateral- valgus strain, more common lateral collateral- varus strain

Question 298

describe the presentation and treatment of collateral ligament injuries?

Answer 298

pain + instability associated w unhappy triad injuries brace and rehabilitate

Question 299

what is the mechanism, presentation and treatment of anterior cruciate ligament injury?

Answer 299

mechanism- non contact injury presentation- feel 'popping', swelling, recurrent instability(giving way), anterolateral rotatory instability, lachmans test treatment- rehabilitation and/or surgical reconstruction

Question 300

what is the mechanism, presentation and treatment of posterior cruciate ligament injury?

Answer 300

mechanism- 'dashboard injury', knne isflexed and experiences large force, fall onto knee, hyperextension treatment-brace and rehabilitation

Question 301

describe the mechanism of injury for knee dislocation?

Answer 301

uncommon high energy trauma must have 3 out of 4 ligaments ruptured

Question 302

describe a complication of knee dislocation?

Answer 302

popliteal artery tethered in popliteal fossa, angiogram (mra)to check for vascular injury

Question 303

what is an effusion?

Answer 303

accumulation of fluid

Question 304

describe acute knee effusions?

Answer 304

haemarthrosis- blood in the joint, due to ACL rupture | lipo- haemarthrosis- blood and fat in joint, fracture

Question 305

what is bursitis?

Answer 305

inflammation of bursae

Question 306

describe what a suprapatellar bursitis is?

Answer 306

common w knee effusion... | OA, rheumatoid arrthiritis, infection, gout

Question 307

describe what semimembranosus bursitis is?

Answer 307

popliteal(bakers) cyst | swelling in poploteal fossa

Question 308

what is Osgood-schlatters diseas(OSD)?

Answer 308

inflammation of apophysis of patella ligsment into tibial tuersosity pain and swelling- athletic teenagers rest and ice

Question 309

describe the typical symptoms of knee OA?

Answer 309

swelling stiffness knee pain

Question 310

describe knee OA?

Answer 310

high prevelance fluctuating symptoms-- provoked by activity, relieved by rest predispositions- age, sex(female), weight, post trauma treatment- strengthening excercises, analgeasia, weight loss, surgery

Question 311

describe the pathophysiology of septic arthritis?

Answer 311

invasion of joint space by micro-organism recent surgery? bacterial cause- most common= straphylcoccus aureus, articular cartilage damage risk factors- extreme age, diabetes mellitus, RA, immunosuppression, intravenouse drug use

Question 312

how does a patient present with septic arthritis?

Answer 312

``` pain swelling redness + warmth reduced ROM non wight bearing ```

Question 313

describe the treetment of septic arthritis?

Answer 313

aspirate to confirm diagnosis and define organism | antibiotics and surgical washout

Question 314

what is the tried of symptoms patients with septic arthritis present w?

Answer 314

fever pain reduced ROM

Question 315

what are the complications of chronic inflammation?

Answer 315

tissue destruction excessive fibrosis- deposits of collagen eg. gall bladder impaired function- eg. inflammatory bowel disease atrophy- eg. atrophis gastritis

Question 316

what is cirrhosis?

Answer 316

end stage liver damage | fibrosis and attempted regeneration

Question 317

whqt are the 4 causes of liver cirrhosis?

Answer 317

1 alcohol 2 hepatitis 3 drugs and toxins 4 fatty liver disease

Question 318

compare and contrast the 2 types of inflammatory bowel disease?

Answer 318

``` crohns... affects all of GI skip lesions- discontinous transmural- affects full thickness less like to rectal bleed ``` ``` ulcerative collitis... large bowel only continous mucosa and submucosa only more likely to have rectal bleeding ```

Question 319

describe the symptoms of anaemia?

Answer 319

shortness of breath, palpitations, headaches, claudation, angina, weakness, confusion

Question 320

describe the signs of anaemia?

Answer 320

pallor, tachycardia, systolic flow murmur, tachypnoa(high RR), hypotension

Question 321

define anaemia?

Answer 321

a haemoglobin concentration lower than normal range

Question 322

describe the causes of microcytic anaemia?

Answer 322

``` T halassamia A naemia of chronic disease I ron deficiency L ead poisoning S ideroblastic anaemia ``` small RBCs

Question 323

descrie the causes of normocytic anaemia?

Answer 323

anaemia of chronic disease blood loss sickle cell disease bone marrow failure

Question 324

describe the causes of macrocytic anaemia?

Answer 324

``` vitamin B12 deficiency folate deficiency liver disease alcohol toxicitiy myelodyplasia ```

Question 325

describe how b12 and folate deficiency causes megloblastic anaemia?

Answer 325

required for DNA synthesis so cytoplasm matures faster than nucleus cell division delays, cytoplasm just gets bigger, larger RBCs, large immature nucleus

Question 326

what can b12 and folate deficiency macrocytic anaemia develop into?

Answer 326

sub acute degeneration of the spinal chord pancytopenia all low blood count- neutropenia and thromboytopenia

Question 327

what does megaloblastic anaemia look like on a bloodfilm and investigations?

Answer 327

``` tear drops schistocytes macrocytic RBCs hypersegmented neutrophils low HB MCV raised low erythrocytes, reticulocytes, leukocytes and platelest raised serum ferritin, LDH and bilirubin ```

Question 328

describe percinicous anaemia?

Answer 328

decrease or abscent intrinsic factor, insufficient absorption of B12 reserves, autoimmune causes vitamin b12 deficiency

Question 329

describe how you treat b12 deficiency?

Answer 329

if percincous anaemia- hydroxycobalamine intramuscular for life(van cause hypokalaemia) other causes- oral cyanocobutamine change diet- eat meat, fish, milk, cheese and eggs

Question 330

describe how you would treat folate deficiency?

Answer 330

oral folic acid- in pregnancy too | change diet- eat more vegetables

Question 331

describe the causes of iron deficiency?

Answer 331

``` 1 insufficient iron from diet 2 malabsorption of iron 3 bleeding- heavy menstration 4 increased requirement- pregnancy 5 anaemia of chronic disease ```

Question 332

what are the epithelial changes you can get with iron deficiency?

Answer 332

angular cheilitis koilonychia(spoon nails) glossitis- glossy tongue with atrophy of lingual papillae

Question 333

describe the pathophysiology of anaemia of chronic disease?

Answer 333

inflammatory condition(eg. rheumatoid arthritis) causes immune cells to release cytokines(eg.IL6) cytokines inhibit erythropoeitin production by kidneys cytokines increase production of hepcidin by liver inhibits ferroportin decreases iron release from reticular endothelial system and decrease iron absorption in gut plasma iron reduced inhibition of erythropoeisis in bone marrow

Question 334

describe how iron deficiency anaemia is diagnosed?

Answer 334

``` low MCV-microcytic anaemia low MCHC low serum ferritin microcytic and hypochromic RBCs anisopoikocytosis- change in size and shape pencil cells target cells ``` reduced plasma ferritin

Question 335

describe how you treat iron deficiency?

Answer 335

``` diet alterations oral iron supplements intramuscular iron injedctions IV iron blood transfusion ```

Question 336

describe why excess iron is dangerous?

Answer 336

exceed binding capacity of transferrin- haemosiderin deposits in organs and promotes free radical formation... hydroxyl and hydroperoxyl radicals cause lipid peroxidation, damage to proteins and DNA

Question 337

describe the pathophysiology of hereditary haemochromatosis?

Answer 337

``` autosomal recessibe mutation in HFE gene loss of negative influences onf iron uptake- no hepcidin and increase affinity of transferrin receptor excess iron damage to organs ```

Question 338

describe the symptoms and tratment of heriditary haemochromatosis?

Answer 338

liver cirrhosis, diabetes mellitus,hypogonadism, cardiomyopathy, increased skin pigmentation venesection

Question 339

describer transfusion associated haemeosiderosis?

Answer 339

excess iron repeated blood transfusions, treat with desferriociamine slate grey colour of skin, same symptoms of HH

Question 340

which 2 enzymes can cause defects in red cell metabolism and there3fore anemia?

Answer 340

G6PDH deficiency- limits NADPH cant reform GSH, less protection against oxidative stress, heinz bodies, haemolysis, spleen destroys RBCs pyruvate kinase deficiency- final enzyme in glycolysis,, deficient in ATP cant do glycolysis, undergo haemolysis

Question 341

why are reticulocytes useful for evaluating anaemia?

Answer 341

immature RBCs- slightly larger than erythocytes so increase MCV shows if bone marrow is working- would ecpect an increase in number if bone marrow working to produce more RBCS

Question 342

if suffering from haemolytic anaemia what cells would you expect to see on a blood film?

Answer 342

schistocytes

Question 343

describe what causes sideroblastic anaemia?

Answer 343

iron is present but cant be incorporated into haemoglobin see ringed sideroblasts on blood film heriditary or accquired by myelodyplastic syndromes

Question 344

describe the causes of splenomegaly?

Answer 344

enlarged spleen 1 back pressure- portal hypertension in liver disease 2 over work 3 extramedullary haemopoeisis 4 expanding as infiltrated by cells- cancer 5 expandind as infiltrated by other cells- granulomas

Question 345

how would you exam splenomegaly?

Answer 345

palpate in right iliac fossa | measure and feel for splenic notch

Question 346

describe the risks of splenomegaly?

Answer 346

hypersplenism, low blood counts due to pooling of blood | risk of rupture- no longer protected by rib cage, avoid contact sports

Question 347

describe hyposplenism?

Answer 347

reduced spleen function increased risk of sepsis by encapsulated bacteria Holly jolly bodies(nuclear remenants in RBCs on blood film

Question 348

describe the causes of hyposplenism?

Answer 348

sickle cell anaemia GI disease splenectomy autoimmune disease

Question 349

describe what effect b12/folate deficiency has on the nervous system?

Answer 349

folate deficiency- in pregnancy causes neural tube defects vit b12 deficiency- associated w focal demyelination serious condition- subacute combined degeneratrion of the cord

Question 350

what is the normal range for blood pressure?

Answer 350

diastolic- 80-60 mmHg | systolic- 120-90 mmHg

Question 351

list the organs or tissues that can be damaged by hypertension?

Answer 351

``` heart- LV hypertrophy arteries- aneurysms kidneys- damage due to neuphrosclerosis retina- arteries narrow, haemorrhage brain- stroke, atherosclerosis ```

Question 352

list some modifiable risk factors for developing hypertension?

Answer 352

``` obesity high salt diet liw in fresh fruit and veg excess alcohol lack of excercise stress ```

Question 353

describe the effects of pherapeutic dose if adrenalin on vasomoto tone?

Answer 353

circulating adrenaline preferentially binds to B2 reeptors on smooth muscle- vasodialation noradrenalin from sympatheitc or higher dose of adrenaline(pherapeutic dose)- activates A1 receptors- vasoconstriction

Question 354

describe the drugs you can use to treat hypertension?

Answer 354

ACE inhibitors, Renin inhibitors or Angiotensin receptor bocker.... block actions of angiotensin II- stop vasoconstriction, stops aldosterone release and the reabsorption of Na and water angiotensinogin by renin to angiotensin 1 angiotensin I by ACE to angiotensin II diuretics... increase na and water excretion by inhibiting NA/CL cotransporter so reduce circulating volume vasodialators... L type calcium blockers- decrease Ca, relax a1 receptor blocker- reduce sypathetic

Question 355

describe the side effect of ACE inhibitors?

Answer 355

ACE also breakdown bradykinin(vasodialator) to peptide fragments causing vasoconstriciton if inhibited build up of peptide fragments, cough in lungs

Question 356

which electrode is the grounding electrode?

Answer 356

right leg electrode- black

Question 357

how many electrodes are there and how many leads/views are there in an ECG?

Answer 357

10 electrodes- 6 chest, 4 limbs | 12 views/leads- limb leads I, II, III, aVF, aVL, aVR, v1, v2, v3, v4, v5, v6

Question 358

what is the positive electrode for each of the leads?

Answer 358

``` I= leftarm II and III= left leg avL= left arm aVR= right arm aVF= left leg ```

Question 359

describe when you would get an upward deflection on an ECG?

Answer 359

wave of depolarisation towards + electrode | wave of repolarisation away from + electrode

Question 360

describe when you would get a downward deflectioon on an ECG?

Answer 360

wave of depolarisation away + elctrode | wave of repolarisation towards + electrode

Question 361

what does the amplitude of deflection depend on?

Answer 361

size of muscle changing potential how fast how directly wave is traveling towards electrode

Question 362

explain the shape of the ECG looking at the apex of the heart(lead II)?

Answer 362

p wave- atrial depolarisation QRS- ventricle depolarisatio q- left to right at right angle to left leg + electrode so small down wards r- depolarisation towards left leg s- depolarisation around apex Twave- repolarisation of ventricles wave of repolarisation away from + electrode so upward deflection

Question 363

describe what is meant by sinus rythm on an ECG?

Answer 363

if every QRS complex has a p wave before

Question 364

describe the abnormalities on a ventricular ectopic beats ecg?

Answer 364

wider QRS

Question 365

describe the abnormalities on a atrial fibbrulation beats ecg?

Answer 365

no p waves wavey baseline irregular R-R intervals

Question 366

describe the abnormalities on a ventricular fibrilation beats ecg?

Answer 366

no coordination | quiver wigley line

Question 367

describe the abnormalities on a first degree heart block ecg?

Answer 367

PR interval longer than 0.2 seconds

Question 368

what is a normal PR INTERVAL on an ECG?

Answer 368

0.12-0.2 secs

Question 369

describe the abnormalities on a second degree heart block- mobitz type 1 ecg?

Answer 369

successively longer PR intervals until one QRS is dropped

Question 370

describe the abnormalities on a second degree heart block- mobitz type 2 ecg?

Answer 370

PR intervals dont get longer, one QRS dropped

Question 371

describe the abnormalities on a third degree heart block ecg?

Answer 371

wide QRS | bradychardia

Question 372

describe the abnormalities on a bundle branch block ecg?

Answer 372

W or M shape | wide QRS with little notch

Question 373

describe the changes with hypokalaemia on an ECG?

Answer 373

``` low conc K+ extracellular- hyperexcitabilty increase amplitude and width of p wave longer PRI flattened and inverted t wave ST depression prominant u waves ```

Question 374

describe the changes with hyperkalaemia on an ECG?

Answer 374

high conc K+ extracellular- RMP less negative loss of p wave tall, tented t waves fiden QRS- sin wave

Question 375

where is the subtalar joint and whats its purpose?

Answer 375

between calcaneous and talus of foot | allow inversion and eversion

Question 376

how are the phalanges orientated in the foot?

Answer 376

first big toe only has 2 phalanges | all the rest have 3 phalanges

Question 377

what are the functions of the foot arches?

Answer 377

allow weight to be transferred around foot | gives stability

Question 378

why is the ankle more stable in dorsiflexion than plantarflexion?

Answer 378

trochlea of talus is wider anteriorly than posterior

Question 379

describe movement of the ankle joint?

Answer 379

only dorsiflexion and plantarflexion as ligaments limit movement medially and laterally and joint capsule weakest anterior and posterioir weaker ligaments laterally than medially(deltoid ligaments), inversion has greater mobility than eversion

Question 380

where does the sciatic nerve bifocate?

Answer 380

at apex of popliteal fossa into tibial nerve and common fibular nerve

Question 381

what are the 4 pilses of the lower limb and how do you examine them?

Answer 381

femoral artery- mid inguinal point, halfway between ASIS and pubis symphysis popliteal artery- bend knee, thumbs on tibial tuberosity, midline of popliteal fossa posterior tibial-posterior to medial malleoulus, invert foot dorsalis pedis- dorsum of the foot, lateral to tendon of extenser hallicus longus

Question 382

describe what is comp0artment syndrome?

Answer 382

muscle compartment seperated by fascia, trauma to a fascia compartment may lead to haemorrhage or oedema, causing a rise in intra-compartmental pressure

Question 383

describe the clinical signs of compartment syndrome?

Answer 383

severe pain in limb, excessive for degree of injury not relieved by analgesia pain worsened with passive stretch of muscles perform surgical decompression

Question 384

what are the short and long term consequences of compartment syndrom?

Answer 384

short term- decreased muscle perdusion, ischaemia, rhabdomyolysis, acute kidney injury longterm- necrotic muscle, volkmanns ischaemic contracture

Question 385

why is it important to consider combodities with a fracture patient?

Answer 385

can significantly impact healing time eg, someone with diabetes is double

Question 386

what makes an ankle fracture unstable?

Answer 386

if has ruptured of broken 1 bone and 2 ligaments

Question 387

descrie what a talus shift is?

Answer 387

disruption of any two medial or lateral ligaments ankle mortise is unstable and widens so talus can move medially or laterally unstable ankle fracture

Question 388

how do you treat stable ansd unstable ankle fractures?

Answer 388

stable- aircast boot or fibreglass cast, low case of secomndary complications, can weight bare safely unstable- surgical stabilisation

Question 389

whats the mechanism of injury for ankle fractures?

Answer 389

inversion or eversion

Question 390

describe what is a ankle sprain?

Answer 390

ligaments fail first partial or complete tear of one or more ligament usually anterior tibiotalar ligament inversion injury effecting plantar flexion and wightbearing

Question 391

in a severe ankle sprain why do you find sometimes an avulsion fracture of the fifth metatarsal tuberosity?

Answer 391

fibularis brevis tendon is attached to a tubercule on the base of the 5th metatarsal inversion injury- 5th metatarsal under tension and pull off fragment of bone

Question 392

describe an achilles tendon rupture?

Answer 392

middle aged explosive excercise, kicked on back of heel vascular watershed- thinner and less vascularity so more common site of injury

Question 393

describe signs and symptoms of achilles tendon rupture?

Answer 393

- sudden, sever pain at back of ankle - sound of loud pop - palpable depression in tendon - initial pain and swellin, bruising - cant stand on tiptoe thompson's test(simmonds) positive test for achilles tendon rupture- squeeze calf and foot dosent automatically plantarflex MRI or ultrasound

Question 394

how are achilles tendon ruptures treated?

Answer 394

conservatively

Question 395

describe the 4 lesser toe(little toes 2-5) deformities?

Answer 395

claw toe- neurological abnormality, can be a secondary condition to eg. diabetes or rheumatoid arrthritis hammer toe- idiopathic, zig zag bend, hallux valgus mallet toe- idiopathic, walk on nail curly toes- in children, normally go with age

Question 396

describe hallux valgus?

Answer 396

type of bunion- big toe deviation away from midline middle aged females, genetic factors, laxity and shoe wear(heels) unattractive, and can be painful treat- change shoes, surgery

Question 397

describe hallux rigidus?

Answer 397

type of bunion- OA of 1st MTPJ presents as pain and lump over joint conservative management, painkillers, steroid injections, activity modifications

Question 398

what are the 4 arthritis surgical treatments?

Answer 398

1 osteotomy- realignment 2 excisiion athroplasty- remove 3 arthrodesis- fusion 4 arthroplasty- replacement

Question 399

describe OA of ankle?

Answer 399

usually secondary- post traumatic or inflammatory | treat with athrodesis(fusion), can use arthroplasty(replacement)

Question 400

describe flat foot?

Answer 400

``` = pes planovalgus medial arch of foot collapsed foot ang;ed in valgus formation mainly assymptomatic children normal ```

Question 401

describe achilles tendonopathy?

Answer 401

degenerative, overuse and strain, obesity and diabetes pain and stiffness of achilles tendon- thickeni9ng and swelling worsened w activity

Question 402

what is the difference between fexible and rigid flat feet?

Answer 402

flexible- no medial arch, valgus formation when standing; on tip toes have medial arch and normal alignment rigid- tarsal coalition and abnormal, when on tip toes no medial arch and valgus alignment

Question 403

describe flat foot(planovalgus) adult onset?

Answer 403

change in foot shape, pain, middle aged females, tibialis posterior dyfunction treat- insoles, physiotherapy operation if dont get better- reconstruction

Question 404

describe how diabetes can cause foot problems?

Answer 404

loss of sensation die to peripheral neuropathy- continue to weight bear worsening problem ischaemia due to peripheral artery disease and microvascular disease immunosupression due to poor glyceamic control can lead to foot ulcers and infections

Question 405

describe charcot arthopathy?

Answer 405

associated with poorly controlled diabetes destruction of bone joints ans soft tissue, usually ankle and foot neuropathy- lack of pain so worsen injury soft bone and loss of bone stock rocker bottom could beseen

Question 406

how to treat and prevent diabetic foot problem?

Answer 406

diabetic foot screening- check feet, sensation, callouses and perfusion tight glyceamic control- prevent neuropathy and vascular disease, and maintain immune system

Question 407

what are the 5 important attributes for a normal gait?

Answer 407

``` stability in stance foot clearance during swing phase pre-positioning for initial contact adequate step length energy conservation ```

Question 408

how do we conserve energy with our gait?

Answer 408

minimise of excursion of centre of gravity control momentum transfer energy between body segments phasic muscle atrophy

Question 409

describe antalgic gait?

Answer 409

``` trys to reduce pain 'limp', uneven gait shorten stance phase on affected leg short swing phase on unaffected leg lack body weight shift to affected leg use walking stick on unaffected leg- to reduce weight on afffected leg ```

Question 410

describe trendelenburg gait?

Answer 410

hip aBductor weakness(gluteus medius and minimus) pain, neurological damge and trauma pelvis drops on unaffected side in stance phase can compensate- torso swings to affected side 'wadling'

Question 411

describe hemiplegic gait?

Answer 411

paralysis of one side of the body eg. from stroke, cerebral palsy or trauma spasticity(continous contraction) of affected side flexed upper limb, extended lower limb short step unaffected leg, circumduction affected leg

Question 412

describe diplegic gait?

Answer 412

``` spasticity of both lower limbs in cerebral palsy scissoring tight muscle groups- psoas, aDductors, hamstrings and calf ankles plantar flexed forefoot initial contact ```

Question 413

describe high steppage gait?

Answer 413

weakness of ankle dorsiflexion- 'foot drop' due to sciatica(L4 dorsiflex), common peroneal nerve palsy, neuromuscular disorders toes hanging down excessive hip flexion affected side foot slap

Question 414

describe parkinsonian gait?

Answer 414

``` neurological disorders- parkinsons reduction in dopamine short steps hard to initate movement- lean forward shuffling forward flexed no arm swing ```

Question 415

describe ataxic gait?

Answer 415

three causes... proprioceptive- loss of awareness of joints cerebellar disease-inherited, sensory or intoxication vestibular broad base 'reeling' inco-ordination arms balancing

Question 416

describe the difference of healing with primary or secondary intention?

Answer 416

primary- incised wound, opposed edges, minimal clott and granulation tissue, fibrous repair, less scar secondary- tissue loss, unapposed edges, alot of clott and granulation tissue, scar forms, takes longer

Question 417

describe the complications of fibrous repair?

Answer 417

excessive wound contraction from myofibroblasts loss of function overproduction of scar tissue- keloid scars fibrous adhesions form- block tubes disruption of tissue relationship with organs wound dehiscence- insufficient fibrosis

Question 418

what are the 3 functions of granulation tissue?

Answer 418

fills the gaps angiogenesis- cappilaries supply oxygen and nutrients contracts and closes- prevent infection

Question 419

describe alport syndrome?

Answer 419

``` inherited x linked disease type IV collagen abnormal chronic renal failure neural deafness eye disorders ```

Question 420

describe the pathophysiology of sickle cewll anaemia?

Answer 420

autosomal recessive, abnormal HbS mutate b globin, glutamine to valine now uncharged hydrophobic outer RBC low O2 state RBCs polymerise and form sickle shape, loose elasticity and deformable- vasoclusion acute chest pain

Question 421

describe the clinical manifestations of sickle cell anaemia?

Answer 421

vasooclusion causes acute chest pain, joint damage- avascular necrosis, chronic kidney damage anaemia- shorten RBC lidespan, haemolytic crisis 20-30 days Jaundice and gallstones- increased billirubin, chronic haemolysis splenic atrophy- infarction, infectrion by encapsulated bacteria end organ damage - O2 deprivation

Question 422

describe the difference between sickle cell disease and thalasseamia?

Answer 422

sickle cell- abnormal Hb due to mutation in b chain | thalassaemia- reduced Hb due to reduced epression in a or b chains

Question 423

explain the haematological abnormalities that come with alpha and beta thalasseamia trait?

Answer 423

heterozygous | can be assymptomatic, or mild anaemia

Question 424

explain the haematological abnormalities that come with alpha and beta thalasseamia major?

Answer 424

homozygous severe anaemia a- all genes in a deleted- tetramers of a globin, unable to deliver oxygen, excess y globin b- transfusion debendent

Question 425

describe the causes and consequences of heridetary spherocytosis?

Answer 425

autosomal dominant mutation in spectrin, ankyrin band 3 or protein 4.2 less flexible, form spherocyte, reduced lifepan consequences... anaemia, jaundice, howell jolly bodies, spleenomegaly

Question 426

what are the 4 main complications of heriditary spherocytosis?

Answer 426

megoblastic anaemia aplastic crisis haemolytic crisis pigment gall stones

Question 427

describe the causes and consewuences of pyruvate kinase deficiency?

Answer 427

inherited- autosomal recessive deficient in pk consequences... can catalyse last step of gycolysis no ATP, na/k/atpase pump stops and loose k+ watermoves out, cells shrink, cell death and haemolytic anaemia

Question 428

describe the causes and consequences of G6PDH deficiency?

Answer 428

x linked recessive inherited consequence... cant produce NADPH, less production against oxidative stress, dont maintain reduced glutathione, damaged rbc digest y spleen, increase billirubinb

Question 429

name the 4 types of myeloproliferative neoplasms?

Answer 429

1 polycytheamia vera- excess erythrocytes 2 essential thrombocytheamia- excess megakaryocytes and platelets 3 primary myelofibrosis- pancytopenia 4 chronic myeloid leukaemia- excess granulocytes

Question 430

describe the different types of polycytheamia vera?

Answer 430

relative- decrease in plasma volume absolute- increase in erythrocyte number primary- abnormality in bone marrow, mutation in gene for Janus kinase 2 secondary- increased erythropoeitin, csan be due to tumour, hypoxia or renal disease

Question 431

describe the clinical features of polycytheamia vera?

Answer 431

``` thrombosis haemorrhage headaches- dizziness plethora burning in hands and feet pruritus(itching) splenic discomfort gout arrthritis ``` manage by venesection and CVS RISKS

Question 432

DESCRIBE THE CUASES of essentialb thrombocytopenia?

Answer 432

primary- originates in bone marrow, mutations in JAK2 and CALK secondary- extrinsic stimulus redistributional- platelets move from splenic pool to bloodstream

Question 433

describe common symptoms of essential thrombocytopeni?

Answer 433

``` burning hands and feet thrombosis numbness of extremities headaches distribution in hearing and vision ```

Question 434

describe the causes and symptoms of myelofibrosis?

Answer 434

mutation, reactive bone marrow fibrosis, scar tissue mobolisation undergo extramedullary erythropoeisis splenomegaly, hepatomegaly tear drop rbcs fever, weight loss, bruiing ad fatique

Question 435

describe the causes and symptoms of chronic myeloif leukaemia?

Answer 435

unregulated growth og myeloid cells, accumulation of mature granulocytephilidelphia chromosome recipricol translocation clinical features high WBC count hyperviscous blood splenomegaly

Question 436

describe the function of JAK2 ?

Answer 436

tyrosine kinase receptor mutated in most myeloproliferative neoplasms multipotent stem cells survive longer and proliferate more eg. polycythemaia vera

Question 437

describe what is petechiae?

Answer 437

a symptom of severe thrombocytopenia(low platelets) | a small red or purple spot on the skin caused by a minor bleed from a broken capillary

Question 438

describe the function of tumour necrosis growth factors?

Answer 438

promotw fibroblast migration and proliferation

Question 439

describe the formation of scar?

Answer 439

bleeding and hoemeostasis inflammation - phagocutpsos of necrotic tissue debris proliferation- angiogensis, and granulation tissue remodelling- muturation of fibrose scar

Question 440

what 4 factors activate platelets?

Answer 440

collagen surfaces ADP thromboxane A2 thrombin

Question 441

describe the action of platelets?

Answer 441

adhesion- von willebrand factor on subendothelial basement membrane secrete factors from alpha and dense platelet granules that aid clotting aggregate to form platelt plug swell and change shape into sticky, spiny spheres

Question 442

how does aspirin decrease platelet aggregation?

Answer 442

inactivated cycloxygenase that makes thromboxane A2

Question 443

what triggers the intrinsic pathway?

Answer 443

exposed collagen surface with blood vessel daqage | contact activator

Question 444

what triggers the extrinsic pathway?

Answer 444

damaged endothelial release thromboplastin | tissue factor

Question 445

describe the different anti-coagulation tests?

Answer 445

APTT- intrinsic pathway, PT- extrinsic pathway, TCT- final step, fibrinogen to fibrin by thrombin

Question 446

describe the results of anti-coagulation tests?

Answer 446

prolonged APTT- deficiency in factor VIII, IIX, IX, XI, intrinsic pathway prolonged PT- deficiency in factor VII, extrinsic pathway prolonged PT + APTT- factors X, V, thrombin and fibronogen PT expressed as INR- INR above 1 slow clotting- warfarrin prolonged bleeding time- deficient platelt aggregation

Question 447

describe the pathophysiology of Von Willebrands disease?

Answer 447

``` inherited bleedind disorder, autosomal dominant VWF is deficient or abnormal can undergo normal functions.... - asist in platelet plug formation - stabalise factor VIII(8) ```

Question 448

describe the clinical manife3stations of Von Willebrands disease?

Answer 448

bleeding time and APTT raised- defected inntrinsic pathway spontaneous bleeding from muccous membrane decrease platelt function and adhesion excessive bleeding from wounds menorrhagia(heavy menstaul bleeding) normal no. of platelets but prolonged bleeding time

Question 449

describe the different types of Von Willebrands disease?

Answer 449

type 1+3- reduced quantity of circulating VWF | type 2- qualitive defects, multiple subtypes of VWF(2a) vWF expressed in normal amounts but dosent function properly

Question 450

describe the difference between haemophilia A + B?

Answer 450

haemophilia A... factor VIII(8) deficient intrinsic pathway life threatening bleeding, spontaneous haemorrage, trauma haemorrhage, petechaie absent both... X linked recessive(effects men more) prolonged PTT, normal PT ``` haemophilia B... factor IX(9) extrinsic pathway increased risk of bleeding treat with infusions of recombinant factor 9 ```

Question 451

describe thrombocytopenia?

Answer 451

deficiency in platelets in blood due to bleeding into tisues, bruising and slow clotting after injury - low platelet count - prolonged bleeding time - normal PT and APTT presents.. spontaneous mucosal bleeding, purpura, petechia

Question 452

describe thrombophillia?

Answer 452

inherited or accquired defects in homoestasis | increased risk of thrombosis (DVT)

Question 453

describe the pathophysiology of Disseminated Intravascular Coagulation (DIC)?

Answer 453

excess activation and consumptio of coagulation factors and platelets leading to multiple microthrombi forming in circulation RBC sheared and damage passing through occlused vessels- anaemia consumes platelts and fibrin activates fibrinolysis when actually need clott, haemorrhage- anaemia triggered by infection, malignancy and massive trauma

Question 454

describe the symptoms, signs & management of DIC?

Answer 454

``` symptoms and signs... haemorrhage, tissue hypoxia and infarction nucleated, immature RBCs schistocytes low platelets raised D dimers low fibrinogen at risk of gangrene and renal failure ``` treatment... treat underlying cause transfusion of platelts and clotting factors anticoagulants

Question 455

describe the causes of thrombocytopenia?

Answer 455

1 decreased production- marrow dysplasia/infiltration, infection, druga 2 increased consumption- immunological destruction, or non immune eg. DIC 3 sequestation- enlarged spleen 4 dillutional- massive blood transfusions

Question 456

describe how aspirins works?

Answer 456

irreversibly inactivates cyclooxygenase-1, so thromboxane A2 not made, decreased platelet aggregation, no platelt plug formed anti-coagulant used after MI or Stroke

Question 457

describe how Heparin works?

Answer 457

anti-thrombogenic forms irreversible complexes with antithrombin III, activating it, decrease thrombin formation uses... low MR, used against an to treat thrombosis iV or subcataneously given

Question 458

describe how Warfarin works?

Answer 458

interferes with vitamin K metabolism- factors II, VII, IX, X, protein C + S oral medication againnst and treat thrombosis

Question 459

name the natural anti-coagulants?

Answer 459

antithrombin III, protein C + S | work by opposing formation of fibrin

Question 460

describe how filters work to prevent thrombus formation?

Answer 460

pulmonary emboli specifically | put umbrella shape filter in inferior vena cava

Question 461

which 3 factors will increase the risk of thrombus forming?

Answer 461

Virchows triad 1 change in Vascular wall(endothelial damage) 2 change in blood flow(stasis, turbulent, laminar) 3 change in blood components(hypercoagulability)

Question 462

describe the stucture of a thrombi?

Answer 462

laminated structure | lines of Zahn- in arterial thrombi(blood flow)

Question 463

why do you have increased risk of DVT in lower limbs during pregnancy?

Answer 463

stasis due to pressure on large veins of pelvis by gravid uterus hypercoaguble blood blood isn't flowing so not laminated, no ligns of zahn

Question 464

describe the steps of thrombi formation?

Answer 464

1 platelets catch in crevices 2 platelets agggregate and stick on vessel wall 3 haemostasis fibrinogen binds platelets together and traps RBCs 4 more blood flows, platelets join and aggregate- white layer of platelets 5 RBCs get caught and aggregate- red layer of fibrin and RBCs 6 process repeats to form laminar

Question 465

describe the 5 outcomes of thrombosis?

Answer 465

1 lysis- breakdown of thrombus, most favourable- blood flow restablished 2 propagate- progressive spread of thrombus - distal in arteries, proximal in veins 3 organise- fibroblasts act on thrombus and lay down scar tissue, lumen still obstructed due to fibrotic scar 4 recanalisation- one or more channels fromed through thrombus, blood flow incompletely re-established 5 embolism- part of thrombus break off and travel through blood stream, lodging at a distant site

Question 466

describe what an embolism is?

Answer 466

sudden blocking of a vessel, at a distant site from origin | majority are thromboemboli

Question 467

describe the differences between arteriol and venous thrombi?

Answer 467

arterial. . - form due to endothelial injury or turbulent blood - lines of Zahn(blood flow continous) - painful - granular - lower cell content - emboli to distal smaller arteries can interfere with systemic circulation and brain(stoke) venous. .. - form due to stasis of blood(long haul flights) - DVT - painful, inflammation, thrombophlebitis - congestion - oedema - ischaemia - infarction - emboli to pulmonary circulation, pulmonary emboli

Question 468

describe what is a vegetation?

Answer 468

thrombus on cardia valve, easily embolise, normally on left side of heart due to greater pressure

Question 469

describe the clinical effects of thrombosis?

Answer 469

1 occlusion of artery- ischaemia and infarction 2 embolism 3 congestion and oedema in venous bed- pain and skin ulceration 4repeated miscariages- thrombus in uteroplacental vasculature- inherited thrombophilias

Question 470

describe the signs and symptoms of a sudden oclusion of an artery?

Answer 470

``` 6 Ps Pain Paralysis Paraesthesia Perishingly cold to touch Pallor Pulseless ```

Question 471

Describe why deep vein thrombosis ocurs?

Answer 471

find... D dimers in blood five signs of inflammation immobility- when calf muscle contracts it aids blood flow back to heart, no movement so stasis of blood -virchows triad, clott formation in lower limbs forms a pulmonary embolism

Question 472

describe the complications of athlerosclerotic plaques?

Answer 472

progressive narrowing of lumen- stenosis, intermittent claudation and angina haemorrhage into plaque- sudden expansion, occlusion of vessel or plaque rupture acute atherothrombotic occlusion- further thrombus formation embolisation- small infarcts claudation- stiffness of arteriol walls aneurysm formation- dilation of artery, adominal aorta

Question 473

describe the classic presentation of a patient with a ruptured abdominal aortic aneurysm (aaa)?

Answer 473

sudden onset abdominal pain radiating to back hypotension pulsatile abdominal mass

Question 474

describe the mechanism of statins?

Answer 474

inhibit HMG-coA reductase, less choolestrol produced by liver

Question 475

describe how to classify nerve injuries?

Answer 475

Seddon classification Neurapraxia- temporary block in conduction axonotmesis- axon divided neurotmesis- nerve divided

Question 476

describe wallerian degeneration?

Answer 476

recovery after axonotmesis and neurotmesis nerve injury 1 axon membran breaks apart- degeneration 2 myelin sheath degrades macrophages+schwann cells phagocytose 3 bands of bunger guide axon regeneration, schwann cells continue to proliferate and phagocytose 4 atrophy of innervated muscle

Question 477

describe clinical consequences of wallerian degeneration?

Answer 477

succsess- function restored failure- more common, unregulated regeneration of axons, traumatic neuroma, pain, no innervation of muscles, replaced by fibrous tissue and fat

Question 478

what are the most common sites for a slipped disc?

Answer 478

L4/5 (nerve L4) and L5/S1(nerve L5)

Question 479

what paraesthesia and myotome weakness would a patient with L4/L5 slipped disc have?

Answer 479

compression of L4 nerve root ankle dorsiflexion weakness medial lower leg L4 dermatome

Question 480

what paraesthesia and myotome weakness would a patient with L5/S1 slipped disc have?

Answer 480

L5 nerve root compressed ankle inversion and great toe extension weakness L5 dermatome, medial leg and first 3 toes

Question 481

what paraesthesia and myotome weakness would a patient with S1/S2 slipped disc have?

Answer 481

S1 nerve root compressed ankle plantarflexion and eversion weakness S1 dermatome, back of ankle and heel, last 2 toes

Question 482

describe periformis syndrome?

Answer 482

compression of sciatic nerve by periformis sciatic like symptoms... dull ache in buttock, pain when walking stairs, increased pain after long sitting, descrease ROM caused... spasm of periformis muscle due to overuse treat by activity modification, NSAIDs and physiotherapy

Question 483

if sciatic nerve was completely transected at buttocks which movements would be effected?

Answer 483

kneed flexion dorsiflexion and plantarflexion of ankle inversion and eversion of ankle ovements of toes

Question 484

describe meralgia paraethesia?

Answer 484

compression of lateral cutaneous nerve by inguinal ligament commonly due to pregnancy, obesity or tight tool belt around hip tendenerness, and reduced sensation around lateral thigh, aggrevated pain w walking and standing

Question 485

how do you treat compartment syndrome?

Answer 485

fasciotomy | urgent

Question 486

describe how a popliteal artery aneurysm can cause myoterm and dermatome symprtoms of tibial nerve?

Answer 486

enlarged popliteal artery compresses tibial nerve in popliteal fossa cant plantarflex ankle, reduced sensation of sole of foot and posterior leg

Question 487

describe damage to common peroneal nerve?

Answer 487

wraps around neck of fibular foot drop- paralysis of tibialis anterior muscles so cant dorsiflex, and extensors of toes, and lateral leg inversion of ankl loss of sensation of laterqal leg and dorsum of foot

Question 488

what are the nerve roots for the femoral ab=nd obturator nerve?

Answer 488

L2, 3, 4

Question 489

describe damage to superficial peroneal nerve?

Answer 489

fractures of proxiaml fibula, | loss of eversion of mid foot, loss of sensation over dorsum of foot

Question 490

describe damage to deep peroneal nerve?

Answer 490

common causes-motor neurone disease, diabetes, ischeamia, vasculitis, total knee replacement foot frop, cant extend toes, numb wenspace of first dorsum

Question 491

describe the causes of injury for saphenous nerve?

Answer 491

stripping and cutting of long saphenous vein | orthapeadic surgery near medial malleoulus and distal tibia

Question 492

whats the rate of axonal growth after division of a nerve?

Answer 492

1-3 mm/day

Question 493

if the tibial nerve was transected at popliteal fossa what position would the patients foot assume?

Answer 493

loss of ankle plantarflexion- paralysis of soleous and gastroceniumnius inversion partially lost- tibialis posterior paralysed unopposed pull of dorsiflexors and everters.... calcaneovalgus foot

Question 494

describe the haematological abnormalities seen with chronic kidney disease?

Answer 494

anaemia- blood loss of stones polycytheamia- renal tumour or tranplant neutropenia- immunosupression post transplant neutrophilia- infection, steroids thrombocytopenia- ureamia inhibits platelet production high platelets- inflammation

Question 495

describe why you could become anaemic with chronic kidney disease?

Answer 495

1 raised cytokines, anaemia of chronic disease, increase hepcidin inhibit ferroportin 2 reduced clearance of hepcidin, kidney malfunction 3 reduced erythropoeitin- kidney not secreting it 4 RBC damage sue to sheer stress, haemolysis in dialysis 5 ureamia, reduced lifespan of RBC

Question 496

describe how rheumatoid arthritis is linked to anaemia?

Answer 496

1 anaemia of chronic disease, cytokine release in inflammatory response 2 GI blood loss due to NSAIDs and steroids 3 autoimmuine haemolytic anaemia risk

Question 497

describe feltys syndrome?

Answer 497

triad of rheumatoid arthritis, neutropenia(low), splenomegaly(hypersplenism) decrease in neutrophils due to hypersplenism in rheumatoid arthrisis, bone maerrow failure- myeloid cells insensitive, dont stimulate GCSF

Question 498

describe how liver disease can cause anaemia?

Answer 498

- portal hypertension, splenomegaly, sequestion of cells in spleen and overdestruction, reduced RBc count - blood loss, deficiency in coagulation factors made by liver, endothelial dysfunction - blood loss, thrombocytopenia, defected platelet function as thrombopoeitin isnt made by liver

Question 499

describe how infection can cause haematological abnormalities?

Answer 499

``` neutrophilia- bacteria infection neutropenia- post viral infection lymphocytosis- viral infection in children lymphonpenia- HIV eosinophilia- parasite infection DIC- caused by sepsis haemolytic anaemia- malaria and gladular fever causes splenomegaly aplastic anaemia- viral hepatitis ```

Question 500

describe the pathophysiology of anaemia of chronic disease?

Answer 500

inflammatory conditions cause an increase in cytokine release by immune cells cause increase hepcidin production by liver inhibit ferroportin decreased iron release from reticuloendothelial system and decreased iron absorption from gut plasma iron reduced inhibit erythropoeitin release so inhibit erythroid proliferation, bone marrow shows lack of response- reduce RBC lifespan

Question 501

give examples of positive feedback?

Answer 501

fergson reflex in ovulation | blood clotting

Question 502

what can be used as contrast media and what are the criteria?

Answer 502

sodium iodide low osmolity, safe, chemically stable, water soluble, biologically inert, cost effective check kidney function

Question 503

what controls the 'biological clock'?

Answer 503

suprachiasmatic nucleus in hypothalamus | uses ques from environment- zeltgebers

Question 504

give exampls of circadian rhythms?

Answer 504

set point vary core body temp- changes with menstraution or over 24hrs melantonin- pineal gland, jet lag cortisol- changes throughout day, highest in the morning

Question 505

describe the differences and similarities between the endocrine and nervous system?

Answer 505

similarities... secrete, depolarise-excitable membranes, interactions with specific receptors, control homeostasis endocrine.... chemical hormones, slow, travel throug blood neurocrine.... chemical and electrical neurotransmitters and action potentials, fast, travel through axons and synapse

Question 506

describe how appetite is controlled?

Answer 506

arcuate nucleus in hypothalamus ghrelin peptide hormone activates excitary primary neurones stimulate apetitie- NPY and AgRP PYY, leptin, insulin and amylin activate inhibitory primary neurones supress apetite- POMC

Question 507

describe the role of ghrelin?

Answer 507

peptide hormone released from empty stomach promoting hunger by stimulating excitary neurones in arcuate nucleus inhibited by stretch of stomach

Question 508

describe the difference between DIC and thrombotic thrombocytopenic purpura?

Answer 508

DIC is due to excess thrombin but TTP is due to endothelial damage

Question 509

what is a direct consequence of alcohol that alters haematology?

Answer 509

toxicity of bone marrow with alcohol excess | pancytopenia

Question 510

which form of anaemia is associated with malaria?

Answer 510

haemolytic anaemia | splenomegaly- spleen destroys RBCs that contain parasite

Question 511

describe how the body adapts to anaemia?

Answer 511

increase 2,3DPG production, oxygen dissociation curve shifts to right so Hb gives up oxygen more readily increase erythropoeitin release more erythropoeisis in bone marrow, increase RBC count and oxygen carrying decrease blood viscosity, decrease TPR resistance, increase cardiac ouput

Question 512

describe how NSAIDs can cause anaemia?

Answer 512

drugs induce GI bleeding by... inhibiting COX 1 and COX 2 activity , and direct cytotoxic effects chronic blood loss as a side effect leading to anaemia

Question 513

how does iron deficiency cause changes to epithelial cells?

Answer 513

``` epithelial cells have a higher requirement for iron as they have a higher rate of mitosis changes... angular cheiltus(dry corners of mouth), glossitis(glossy tongur), koilonuchia(spoon nails) ```

Question 514

describe the causes of eosinophilia?

Answer 514

parasite infection autoimmuune disease allergic reaction haematoligica malignancy

Question 515

describe the causes of tachycardia?

Answer 515

1 ectopic pacemaker activity- due to ischeamia, damaged myocardium becomes depolarised and sponateously active over SAnode 2 after depolarisations 3 atrial flutter/ fibrilation 4 re-entry loop- conduction delay or accessory pathway

Question 516

describe the causes of bradycardia?

Answer 516

1 sinus bradycardia- sick sinus syndrome or extrinsic factors(eg. drugs) 2 Conduction block- problem at AV node and bundle of his or slowerconduction at AVN due to drugs

Question 517

describe how early after depolarisations can lead to arrythmias?

Answer 517

longer AP due to longer QT interval(time for depolarisation to repolarisation) longer QT so get oscillations

Question 518

describe how delayed after depolarisations can lead to arrythmias?

Answer 518

can trigger activity by having high intracellular calcium conc, selfperpetuating causing oscilations

Question 519

describe Wolff- Parkinsons- white syndrome?

Answer 519

re-entry loop due to an accsessory pathway between atria and ventricle causes superventricular tachycardia

Question 520

name the 4 classes of anti- arrhythmic drugs?

Answer 520

1 block voltage-sensitive sodium channels 2 antagonists of b-adrenoreceptors 3 block potasium channels 4 block calcium channels

Question 521

describe the mechanism of action of Lidocaine?

Answer 521

``` class 1-block open or inactive voltage sensitive sodium channels prefentially blocks damaged depolarised tissuechannels no effect on closed channels prevents automatic firing, shortens AP, slows conduction used after MI ```

Question 522

describe the mechanism of action of propanol and atenolol?

Answer 522

class 2- b-adrenoreceptor antagonsit blocks sympathetic action of b1 receptors at heart decrease slope of pacemaker potential(funny currents) at SAnode slows conduction at AVN prevent superventricular tachycardia after an MI reduce oxygen demand

Question 523

describe the mechanism of action of amiodarone?

Answer 523

type3 anti-arrythmic, has other actions not just to block potassium channels used to treat tachycardia in Wolf-parkinsons-white syndrome supress ventricular arythmias after MI

Question 524

why are drugs that block K channels not very good anti-arythmias?

Answer 524

prolong AP and QT- pro arythmic increases chance of early after depolarisations

Question 525

describe the mechanism of action of verapamil and diltaizem?

Answer 525

``` class4- block Calccium channels decrease slope of AP at SAN decrease Av node conduction slow conduction and HR decrease intropy ```

Question 526

describe the mechanism of anction of adenosine?

Answer 526

not a class produced endogenously but given as drug IV acts on A1(GCPRs) recptors at AVN enhances potassium conductance, hyperpolarises cell, heart stops so can recoordinate beat short halflife used to terminate reentrance superventricular tachycardias

Question 527

describe drugs with an intropic effect?

Answer 527

decrease or increase force of heart muscle contraction

Question 528

describe how do cardiac glycoscides increase intropy?

Answer 528

``` eg. digoxin stop na/k/atpase increase intracellular sodium concentration descrease NCX increase intracellular calcium conc increase force ``` increase vagal activity, slows AV conduction and HR

Question 529

describe how do b adrenoreceptor agonsits increase intropy?

Answer 529

eg. dobutamine and adrenaline | stimulate B1 receptors at SA and AV node

Question 530

describe how do calcium channel blockers decrease intropy?

Answer 530

L type ca channels | decrease ca intracellular, reduce workload

Question 531

describe how do b-adrenoreceptor antagonist decrease intropy?

Answer 531

block b1 receptors block cAMP, PKA less phosphorylation of VGCCs so less calcium stores reduce workload

Question 532

describe how you treat angina?

Answer 532

reduce workload of heart- beta adrenoreceptors and calcium channel antagonists, organic nitrates improve blood supply- calcium channel antagonists, organic nitrates

Question 533

describe how to treat hypertension?

Answer 533

vasodialation and decrease blood volume - calcium channel blockers, a1 receptor antagonists, ACE inhibitors

Question 534

name CVS conditions that increase thrombus formation?

Answer 534

atrial fibrilation valve disease- prosthetics acute MI

Question 535

explain the mechanism of action of organic nitrates to relieve angina?

Answer 535

reacts with thiols(-sh) in vascular smooth muscle releases NO which is a powerful vasodilator by lowering intracellular ca conc decrease pressure, lowers preload and workload of heart lowers oxygen demand and therefore decreases angina

Question 536

what does organic nitrates have thelargest pharmacological effect on?

Answer 536

veins, then arteries and then arterioles | as veins have less endogenous NO

Question 537

describe what is angina?

Answer 537

chest pain | oxygen supply to heart dosent meet demand, ischaemia of heart tissue

Question 538

what would you prescribe someone with Wolf-parkinsons-white syndrome?

Answer 538

potassium channel blocker eg. amiodarone | lengthens refractory period(inactive na channels) of myocytes to prevent re-entry loops

Question 539

describe the mechanisms of diuretics?

Answer 539

act on thick ascending limb of loop of henle to increase water and sodium loss from body to decrease blood volume lower preload and afterload of heart to reduce demand on heart

Question 540

what can beta blockers treat?

Answer 540

supravntricular tachycardia following an MI heart failure hypertension

Question 541

describe what a delayed PR interval suggests?

Answer 541

delayed conduction through AV node | in heart block, ischeamic heart disease and hypokalaemia

Question 542

describe the structure and behaviour of HIV?

Answer 542

ssRNA then converted to dsDNA to integrate into hosts genome binds to CD4 receptors ot T helper lymphoctytes and replicates inside cell- destroys cell, causes inflammation and spreads protein capsid- protection lipid envelope made from host cell membrane

Question 543

describe how HIV is spread?

Answer 543

``` contact of infected body fluids with mucosa; tissue/broken skin/ blood sexual contact(sexual assult), blood transfusion, breaks in mucosal membrane, contaminated needles, skin grafts and organ donations ```

Question 544

describe how HIV is managed?

Answer 544

``` life expectancy good serology and PCR diagnostic rapid testing and screening PEP- post ecposure prophylaxis PrEP- pre exposure prophylaxis condom usage 3 rounds of AVRs ```

Question 545

explain why you use 3 rounds of AVR to treat HIV?

Answer 545

RNA virus so has high mutation rate as RNA polymerase has higher error rate use 3 so less likely to develop resistance

Question 546

what factors affect HIV transmission?

Answer 546

type of exposure viral load condom use breaks in skin/ mucosa

Question 547

what is hepatitis?

Answer 547

inflammation of liver replication and destruction of hepatocytes results in end stage liver disease

Question 548

describe which hepatitis we are more concerned about?

Answer 548

Hep B and C | blood bourn and can become chronic infections

Question 549

describe the symptoms and signs of hepatitis?

Answer 549

``` itteric sclera- yellow eyes if viral hepatitis- intrahepatic jaundice abdominal pain fatigue anorexia/vomiting ``` hep c has no symptoms

Question 550

describe the difference between hepatitis B and C?

Answer 550

bboth blood bourne hep C= RNA virus hep B= DNA virus

Question 551

describe how you diagnose hep B?

Answer 551

serology look for surface antigen- HbsAg acute infection= surface antigen(HbsAg) and core antibody(HbcAb) IgM present cleared/past infection= negative for surface antigen, core and surface antibody(HbsAb) present chronic infection= surface antigen and core antibody IgG present vaccinated= positive for surface antibody

Question 552

define chronic hep B infection?

Answer 552

persistence of HbsAg- surface antigen after 6 months

Question 553

describe management for hepatitis?

Answer 553

Hep B- vaccination, no cure | Hep C- cure(anti-viral combo), no vaccination

Question 554

describe how you diagnose Hep C?

Answer 554

serology look for anti-Hep C antibody remains positive life long- thought can get reinfected viral PCR

Question 555

describe the outcome of hepatitis?

Answer 555

cure or chronic infection

Question 556

describe liver function tests?

Answer 556

-billirubin if raised... intrahepatic, prehepatic or extrahepatic jaundice -liver transaminase if raised ALT or AST... hepatocyte damage,intrahepatic problem if ALP raised... billary tract(delivery) problem -albumin if albumin decreased...severe liver disease, as liver synthesises it -coagulation clottin factors synthesised in liver check APTT INR and PT

Question 557

describe the different types of hepatitis?

Answer 557

viral hepatitis- 6 types, specifically focus on B and C, virus repkicated in hepatocytes alcohol hepatitis- excess alcohol results in liver disease and inflammation autoimmune hepatits- body attack its own liver

Question 558

describe the symptoms of HIV?

Answer 558

acute seroconversion stage... fever, malaise, weight loss, sores, rash recurrent and severe infections as CD4+ t cells drop

Question 559

describe the life cycle of HIV?

Answer 559

1 binding- HIV binds to surface receptors on CD4 cell(CCR5 or CXCR4) 2 fusion- HIV envolope fuses with CD4 membrane, releases its contents into host(RNA and RNA transcriptase) 3 reverse transcription- HIV RNA converts into DNA, enter CD4 nucleus 4 integration- ciral DNA mixes with host genome 5 replication- infected cell divides 6 assembly- new HIV proteins and RNA assemble 7 budding- newly formed immature HIV, moves out of CD4 and takes part of membrane with it

Question 560

describe the mechanism of action of HIV drugs?

Answer 560

CCR5 antagonists- prevent CD4 binding fusion inhibitorss non nucleoside reverse transcriptio inhibitors- stop viral DNA formation integrase inhibitors- inhibit genome integration protease inhibitors prevent budding

Question 561

describe HIV testing?

Answer 561

rapid testing serology PCR

Question 562

define aids?

Answer 562

CD4 count< 200 cells/ul

Question 563

which cells in the body express MHC class 1?

Answer 563

all nucleated cells | against intracellular microbes

Question 564

describe and differentiate between the different antibodies produces by helper T cells(CD4+)?

Answer 564

IgA- on mucosal surfaces IgM- primary response, t helper/thymus independent, first exposure, if dont have CD40L non-specific IgG- best response, secondary immune response, vaccinations, immune response from memory cells IgE- parasite response

Question 565

describe the function of activating niave T cells ?

Answer 565

extracellular microbes, when MHC class II on APCs binds to CD4+ on niave T cells they differentiate into T helper cells- Th17, Th2 or Th1

Question 566

describe the function of Th1?

Answer 566

intracellular microbes cause CD8+ to diffrentiate for cytotoxic t cell killing activate and recruite macrophages for phagocytosis activate B cells to secrete IgG and IgA uses IL-12

Question 567

describe the function of Th2?

Answer 567

extracellular pathogens increase number of eosinophils in parasite infections, use IL-5 activate B cells to produce antibodies(igE), IL-4 activates mast cells for local inflammation and allergies, IL-4

Question 568

describe the function of Th17?

Answer 568

extracellular pathogens recruit and activate neutrophils using IL-6 and IL-17

Question 569

what microbe would be displayed on MHC class I?

Answer 569

virus | present intracellular microbes to CD8+ cytotoxic T cells, usually undergo cell mediated immunity

Question 570

which cells in the body are CD4+?

Answer 570

naive T cells | they diffrentiate into T helper cells

Question 571

compare and contrast between cell mediated and humoral immunity?

Answer 571

cell mediated... action by complement, macrophages and cytotoxic T cells usually defence against intracellular microbes no antibodies CD8+ cytotoxic t cells ``` humoral response... action by antibodies, complement, and phagocytosis defence against extracellular microbe secrete antibodies- B cells CD4+ T helper cells ```

Question 572

describe how muscle cells increase their glucose supply during excercise?

Answer 572

upregulate GLUT4 receptors increase glucose uptake into cells during low energy signals(high AMP) so can produce more ATP energy

Question 573

what are the function of primary excitatory neurones in the arcuate nucleus?

Answer 573

stimulate appetite by releasing neuropeptide Y(NPY) and agouti related peptide(AgRP) activated by Ghrelin

Question 574

what is the function of a-MSH?

Answer 574

from POMC | at synapse acts on MC4 receptors to induce appetitie

Question 575

where are each of the hormones that control appetite released from?

Answer 575

Ghrelin- stomach wall PYY- small intestine Leptin- adipose Insulin- pancreas

Question 576

what is the function of secondary neurones in the arcuate nucleus?

Answer 576

co-ordinate a response to appetite via the vagus nerve

Question 577

what are the funtions of the hypothalamus-pituitary-axis(HPA)?

Answer 577

control of adrenal glands function of thyroid glands growth

Question 578

describe the route of hormones from the hypothalamus to the pituitary?

Answer 578

hypothalamus- axons- medial eminence- hypothyseal portal system- endocrine cells in anterior pituitary

Question 579

what type of hormone are insulin and glucagon?

Answer 579

``` peptide hormones water soluble insulin- tyrosine kinase receptor glucagon- GCPRs both extracellular, membrane receptors ```

Question 580

describe the clinical consequence of deficient or little insulin?

Answer 580

hyperglyceamia

Question 581

describe the endocrine function of the pancreas?

Answer 581

a cells secrete glucagon b cells secrete insulin delta cells secrete somatostatin

Question 582

describe the tests to diagnose diabetes?

Answer 582

fasting plasma glucose greater than 7.0mmol/l | oral glucose tolerence test, random plasma glucose greater than 11.1mmol/L

Question 583

describe the differences between type 1 aqnd 2 diabetes??

Answer 583

``` type 1 younger people absolute insulin deficiency autoimmune destruction of b cells, can synthesise insulin keto-acidosis treat w insulin injections ``` type 2 older people, obesity relative insulin deficience disorder in insulin secretion from b cells, or insulin resistance of tissues treat w drugs, excercise changes, and diet

Question 584

describe the pathophysiology of keto-acidosis?

Answer 584

in absence of insulin ketone bodies are produced low insulin... increase rate of lipolysis forms fatty acids= substrate for ketone formation activation of ketogenic enzymes, lyase hyperglyceamia, ketonaemia and acidosis

Question 585

explain the principle of measuring glycation of haemoglobin?

Answer 585

conc of HbA1c suggests how efficient control of blood glucose is in diabetes percentage of Hb glycosylated over 3 months due to RBC lifespan=120 days normal=4-6% high glucos is around 10%

Question 586

Name the microvascular complications of diabetes?

Answer 586

neuropathy nephropathy retinopathy

Question 587

Name the macrovascular complications of diabetes?

Answer 587

increased risk of stroke and MI | poor circulation to periphery- feet

Question 588

what is the triad of symptoms for diabetes?

Answer 588

polydipsia polyuria weight loss

Question 589

describe when you would do a stimulation blood test?

Answer 589

suspect hormone deficiency

Question 590

describe when you would do a suppression blood test?

Answer 590

suspect hormone excess

Question 591

describe why early diagnosis of prolactinoma is more common in women than men?

Answer 591

prolactin produced form anterior pituatary stimulate milk production and breast growth and inhibit LH, and FSH women miss their peroid and get breast milk- more obvious symptoms so present earlier men have testosterone symptoms which are less obvious

Question 592

describe the symptoms of prolactinoma?

Answer 592

prolactin secreting tumour- hyperprolactinaemia prolactin inhibits LH and FSH women menstraul disturbance, fertility problems, galactorrhea(milky nipple discharge) men low testosterone symptoms due to compression eg. visual field loss

Question 593

describe how to treatt a prolactinoma?

Answer 593

dopamine agonist to shrink tumour as dopamine(PIH) CANT OPERATE/SURGERY oral tablets... dopamine agonist

Question 594

describe the signs and symptoms of acromegaly?

Answer 594

large extremities- enlarged hands and feet | change in appearance- broad nose, thick lips, greasy skin

Question 595

describe diagnostic tests for acromegaly?

Answer 595

oral glucose tolerance test with GH response- hypertension and diabetes if fail to supress GH elevated IGF-1 elevated mean GH

Question 596

describe treatment for acromegaly?

Answer 596

surgical remove tumour reduce GH secretion with domamine agonists and somastatin aalogues block GH receptor radiotheray

Question 597

describe Cushings disease?

Answer 597

ACTH secreting anterior pituitary tumour | excess cortisol

Question 598

describe the symptoms and signs of Cushings?

Answer 598

``` round pink face and abdomen skinny, weak arm and legs purple/red striae on abdomen hypertension and diabetes osteoporosis(Thin bones) thin skin and easy bruising ```

Question 599

describe the causes of diabetes insipidus?

Answer 599

decrease in ADH/vasopressin making dilute urine as you cant resorb water in kidney, loose fluid vasopressin deficiency or resistance

Question 600

describe the two types of diabetes insipidus?

Answer 600

cranial DI... due to inflammation, irritation, malignancy or infection of pituitary so get vasopresson deficiency nephrogenic DI... kidney disease causes vasopressin resistance

Question 601

describe the consquences of diabetes insipidus?

Answer 601

severe dehydration hypernatraemia- increase in sodium reduced consciousness, coma and death

Question 602

what is pituitary apoplexy?

Answer 602

sudden vascular event in pituatary tumour leading to stroke haemorrhage and infarction sudden onset headache, double vision or visual field loss, cranial nerve palsy, hypopituitarism

Question 603

describe what is cervical spondylosis?

Answer 603

chronic age related degenerative osteoarthritis loss of disc height osteophytes facet joint arthritis

Question 604

describe the symptoms of cervical spondylosis?

Answer 604

radiculopathy- compresse nerve roots due to reduced space in intevertebral foramen(osteophytes)... pain and paraesthesia, myotomal weakness myelopathy- pressure on spinal nerves as narrowing of vertebral canal(osteophytes) ...gait dysfunction, muscle weakness, loss of balance, loss of bowel and bladder conrol

Question 605

describe the pathophysiology of a prolapsed disc?

Answer 605

tear in annulus fibrosis nucleus pulposus migrates through and into spinal canal compress spinal nerve

Question 606

what will a patient complain of with a left sided C5/6 prolapsed disc?

Answer 606

compression of C6 nerve root paraethesia and pain in C6 dermatome- anterior lateral forearm from neck into index finger and thumb weakness in elbow flexion, wrist extension and supination

Question 607

describe what is a jefferson fracture?

Answer 607

burst fracture in C1(atlas) due to axial loading fracture of anterior and posterior arches of atlas

Question 608

describe what is a hangmans fracture?

Answer 608

fracture through pars interarticularis of axial(C2) due to hyperextension of head on neck unstable, forward displacement of C1 and C2 on C3

Question 609

describe an odontoid process fracture?

Answer 609

hyperextension fraction | elderly patients falling

Question 610

describe the anatomy changed in cervical myelopathy?

Answer 610

thickening of ligamentum flavum osteophyte spinal chord signal change cervical chord compression due to spondylosis

Question 611

describe the symptoms of cervical myelopathy?

Answer 611

progessive disorder, clumsiness, loss of fine movement, loss of balance

Question 612

describe the difference between cervical myelopathy and radiculopathy?

Answer 612

myelopathy- compression of spinal chord | radiculopathy- compression/pinching of spinal nerve away from spinal chord

Question 613

what will a patient with a C4 myelopathy complain of?

Answer 613

neck pain C5 motor weakeness- shoulder abduction and other distal myotomes including trunk and lower limbd sensory numbness from shoulder distally

Question 614

what is the commonest cause of thoracic chord compression?

Answer 614

fractures and tumours

Question 615

what will a patient present with if they have thoracic chord compression at T10?

Answer 615

lower thoracic pain weakness of all muscles in the legs sensory- loss of sphincter control and numbness below umbilicus

Question 616

what is spondylodiscitis?

Answer 616

infection of spine | bacteria enters vertebral body nutrient artery, lodges at end plate and extends toweards disc

Question 617

if spondylodiscitis is left untreated what is the consequence?

Answer 617

epidural abscence and vertebral osteomyelitis

Question 618

describe what the function of divergence is in the brachial plexus?

Answer 618

to form divisions 3 posterior- supply extensors 3 anterior- supply flexors

Question 619

describe what the function of convergence is in the brachial plexus?

Answer 619

to form trunks | so that a muscle can be supllied by more than one spinal nerve root

Question 620

describe what erb's palsy is?

Answer 620

upper brachial plexus lesion superior trunk acts on sholuder and elbow

Question 621

describe what klumpke's palsy is?

Answer 621

lower brachial plexus lesion inferior trunk supplies more distal muscles- hand

Question 622

what occurs due to damage to the long thoracic nerve?

Answer 622

winged scapula | paralysis of serratus anterior muscle

Question 623

what conditions may lead to demyelination of nerve fibres?

Answer 623

multiple sclerosis- all CNS nerves Devics disease- optical and spinal chord of CNS Laundry-Guillain-Barre syndrome-PNS Charcot-Marie-Tooth disease

Question 624

give examples of classic ligand gated ion channel receptors?

Answer 624

nAchR- allows entry of Na+ | GABA- Cl- movemenr

Question 625

why do malignant neoplasms often have central necrosis?

Answer 625

inadequate perfusion as they outgrow their blood supply

Question 626

define a neoplasm?

Answer 626

abnormal cell growth which persists once the initial stimulus is removed

Question 627

what does bowel cancer screening programmes look for?

Answer 627

occult blood in stool(blood not visible by the naked eye)

Question 628

what are the 3 cancers routinely screened for in the UK?

Answer 628

cervical, breast, and bowel

Question 629

name the 3 clinical syndromes associated with mutations in DNA repair genes?

Answer 629

xeroderma pigmentosa familial breast cancer carcinoma hereditary non-polyposes colon cancer

Question 630

describe xeroderma pigmentosa?

Answer 630

reduced ability to repair after UV damage | more likely to develop skin cancer at a young age

Question 631

describe familial breast cancer carcinoma?

Answer 631

mutations in BRAC 1 or 2 | normally involved in repairing double stand DNA breaks

Question 632

describe hereditary non-polyposes colon cancer(HPNCC)?

Answer 632

mutation in gene that re pairs DNA mismatch colon cancer increased risk

Question 633

describe how proto-oncogenes can cause development of neoplasms?

Answer 633

mutated proto-oncogene forms a oncogene only one allele needs to be mutated gain of function mutation that drives proliferation and cell growth eg. RAS- abnormal restriction point, continuely progress through cell cycle eg. Her-2 - abnormal growth factor receptor, accelerated growtth, breast cancer

Question 634

describe how tumour suppressor genes can cause development of neoplasms?

Answer 634

normally inhibit tumour growth both alleles need to be mutated loss of function mutation eg. Rb gene- uncontrolled movement thorough cell cycle, familial retinoblastoma eg. P53- dont repair DNA or apoptosis, continue through cell cycle, Li-fraumeni syndrome

Question 635

what are the 6 Hallmark's of cancer?

Answer 635

``` 1 self sufficiency in growth signals 2 resistance to growth stop signals 3 cell immortilisation- telomeres 4 angiogenesis 5 resistance to apoptosis 6 ability to invade and produce metastases ```

Question 636

what is the epithelial to mesenchymal transition?

Answer 636

epithelial cell goes through changes to resemble a mesenchymal cell, allows them to cross basement membrane and invade

Question 637

describe the process of invasion of neoplasms?

Answer 637

1 altered cellular adhesion- decrease expression of E-cadherins(cell to cell) and integrin expression(cell to stroma matrix) 2 stromal proteolysis- increase MMPs and proteases degrade basement membrane and stroma(connective tissue) 3 increased mortility- actin cytoskeleton changes, propel

Question 638

describe the ways neoplasms metastasise?

Answer 638

1 haematogenesis spread- sarcomas spread to next capillary bed(usually liver or lungs) 2 lymphatic vessels- carcinomas spread to next lymph node 3 transcoelomic- fluid in body cavitoes, pericardial, peritoneal and pleural space

Question 639

which neoplasms spread to the bone and what do they cause?

Answer 639

breast, liver, kidney and thyroid- cause lytic lesions(destruct bone) prostate- sclerotic lesions(increase bone mass)

Question 640

what are the common sites of blood bourne metastasise?

Answer 640

travel through blood to liver, lungs, bone and brain

Question 641

describe lymphatic metastasise?

Answer 641

enter at afferent lymph vessels to periphery, spread inwards, replaced by cancer cells and connective tissue lymphodenopathy and blockage leads to lymphoedema

Question 642

describe the local effects of tumours?

Answer 642

``` compression of adjacent structures obstruction of tubes malignant- ulcerations leading to bleeding malignant- invade raised pressure ```

Question 643

describe the systemic effects of neoplasms?

Answer 643

increased tumour burden and cytokine release | reduce apetite, weight loss, malaise/lethargy, immunosupression, thrombosis, hormone production

Question 644

describe the causes of peripheral venous disease?

Answer 644

veins damages and walls weaken, varicose veins develop, valve cusps seperate, incompetent blood movement slow saphaneous veins

Question 645

describe symptoms and signs of peripheral venous disease?

Answer 645

``` veins tortous and twisted heaviness and acheing muscle cramps throbbing ezema haemorrhage ankle swelling ```

Question 646

describe what is superficial vein thrombophelebitis?

Answer 646

inflammatory process due to vein clott painful erythematouus after varicose veins increased risk of DVT

Question 647

describe how you would diagnose peripheral artery disease?

Answer 647

ankle brachial index measure BP og brachial artery and dorsalis pedis + posterior tibial artery divide ankle stystolic by brachial systolic if ABI<0.9

Question 648

what are the melanoma warning signs?

Answer 648

``` Asymmetrical Border irregularity(uneven, jagged, blurred) Colour irregularity(2 or more colours) Diameter large Evolving ```

Question 649

what are the differential diagnosis/possible disease that cause general hyperpigmentation?

Answer 649

``` Sunlight Pregnancy Addisons Renal failure Excess iron Drugs ```

Question 650

describe prevention of malaria?

Answer 650

Assess risk Bite prevention Chemoprophylaxis

Question 651

describe how a patient presents with malaria?

Answer 651

travel history, 6 day incubation jaundice, dark coloured urine, fever chils and sweats, head ache, splenomegaly, hepatomegaly, dry cough, back pain, fatigue, nausea and vomitting

Question 652

what species causes malaria?

Answer 652

plasmodium falciparum

Question 653

describe the investigations and treatment for malaria?

Answer 653

``` x3 blood film FBC, UandEs, LFTs, glucose and coagulation head CT? quinine doxycycline chloroquine ```

Question 654

what pathogen causes typhoid fever?

Answer 654

salmonella typhi salmonella e coli gram - bracillus

Question 655

describe how a patient with typhoid fever would present?

Answer 655

``` travel history(esp india/asia) abdominal cramps, tenderness, pink rash, spleen tip, headache, constipation, dry cough and bradycardia ingestion contaminated via faecal oral route ```

Question 656

describe investigations and treatment for typhoid fever?

Answer 656

LFTs and blood cultures | 3rd generation cephalosporins- ceftriaxone

Question 657

what causes legionnaire's disease?

Answer 657

legionella pneumocytes gram - bacilli air droplet mode of transmisiion from a water source(eg. shower) invades and replicates within macrophages

Question 658

describe investigations and treatment for legionnnaire's disease?

Answer 658

can cause acute lobar pneumonia but mainly nausea, headaches, muscle/chest pain and fever clarythromycin

Question 659

describe the cause of schistosomiosis?

Answer 659

helminths(parasitic worms) with travle history to tropical areas exposure to fresh water

Question 660

describe how a person with schistosomiosis might present?

Answer 660

high eosinophil blood count- acute infection fibrosis of liver and bladder- chronic infection presence og helminth eggs in stool and urine diarrhoea, coughs, rashes, muscle/abdominal/joint pain

Question 661

describe treatment for schistosomiosis?

Answer 661

steroids for inflammation | praziquantel

Question 662

describe the presentation of dengue fever?

Answer 662

travel history- mosquito bites, dengue virus | fever, back pain, head achre, fever and rash, muscle and joint pain

Question 663

describe the structure of SARS-COV-2?

Answer 663

``` very large genome +ssRNA coronviridae family- large, envoloped, pleomorphc spike glycoprotein(s) on surface lipid bilayer, membrane protein(M) envelope glycoprotein (E) nucleocapsid protein(N) ```

Question 664

describe how covid-19 enters and replicates?

Answer 664

1 virus spike glucoprotein(s) binds to ACE2 receptor 2 entry via receptor-mediated endocytosis 3 +ssRNA turns to -ssRNA template stand which makes new +ssRNA strands using RNA dependent RNA polymerase(RdRp) 4 +ssRNA assemble into nucleocaspid 5 +ssRNA form mRNA and translated into viral proteins

Question 665

describe the barriers of entry of corona virus via the respiratory route?

Answer 665

1- respiratory epithelial cells, thick glycocalyx and tracheobronchial mucus trap particles 2- cilliated respiratory epithelium, sweep mucus 3- lung secrete IgA, natural killer cells and macrophages

Question 666

why does coronavirus produce alot of varients?

Answer 666

constant replication- life cycle of approx 10hours viral RNA polymerase has high error rate and lack of proof reading- mutations forms resisitance

Question 667

describe control of blood pressure via the renin-angiotensin-aldosterone system(RAAS)?

Answer 667

low bp is detected by barorecptors that increase sympathetic tone renin released from kidneys angiotensinogen converts to angiotensin I ACE from lungs converts angiotensin I to angiotensin II works to... vasoconstrict arterioles pruduce aldosterone from adrenal cortex- increase Na/K/Atpase pumps to resorb water and Na into blood secrete ADH from posterior pituitary increase water resorption increase blood volume and pressure

Question 668

describe the action of aldosterone?

Answer 668

steroid hormone released from zone glomerulosa in adrenal cortex increases Na/K/ATPase activity increasing water resoprtion in blood RAAS increase blood volume

Question 669

how does aldosterone travel in blood?

Answer 669

steroid hormone= lipophilic | carrier protein= serum albumin

Question 670

how does cortisol travel in the blood?

Answer 670

steroid hormone=lipophilic | carrier protein= transcortin

Question 671

describe the action of cortisol?

Answer 671

increase protein breakdown(proteolysis) in muscle increase lipolysis of fat increase gluconeogenesis in liver -anti-inflammatory -resistant to stress -depression of the immune system produce by zone fasiculata in response to stress

Question 672

what hormones are produced by the adrenal cortex?

Answer 672

G salt - zone glomerulosa, mineral corticosteroids, aldosterone F sugar- zone fasiculata, glucocorticosteroids, cortisol R sex- zone reticularis, glucocorticosteroids, androgens

Question 673

describe the action of androgens?

Answer 673

released by zone reticularis, regulated by ACTH, CRH males DHEA- testerone females adrenal androgens- oestrogens also growth of pubic and axillary hair

Question 674

describe the structure and function of steroid hormones?

Answer 674

produced from cholestrol in the adrenal glands | lipid soluble, pass through lipid bilayer, bind to nuclear intracellular receptors to modulate gene transcription

Question 675

describe how ACTH can cause hyperpigmentation?

Answer 675

in Addisons disease decreased cortisol negative feedback on anterior pituitary reduced more POMC required to synthesis ACTH increase in ACTH forms a-MSH which stimulates melanin synthesis ACTH can also directly activate melanocortin receptors

Question 676

describe the pathophysiology of Cushing's syndrome?

Answer 676

excess cortisol due to .... -prescribe glucocorticosteroids for anti-infalmmatory eg. for asthma, inflammatory bowel disease, rheumatoid arthritis - benign pituitary adenoma secreting ACTH= cushing's disease -adrenal tumour secreting cortisol= adrenal cushing's - non pituitary-adrenal tumours producing ACTH= small cell lung cancer(rare) Pituitary tumour Adrenal tumour Ectopic ACTH

Question 677

describe the signs and symptoms of Cushing's syndrome?

Answer 677

``` purple striae acute weight gain 'buffalo hump' plethoric moon face abdominal obesity hyperglyceamia(bloods) and hypertension osteoporosis 'thin bones' thin skin and easy bruising ```

Question 678

describe the difference between Cushing's syndrome and Cushing's disease?

Answer 678

cushing's disease is specific to benign ACTH secreting pituitary adenoma cushing's syndrome is general chronic excess of cortisol

Question 679

describe the pathophysiology of Addison's disease?

Answer 679

autoimmune disease- thyroidtoxicosis or diabetes traditionally caused by turberculosis affects women more

Question 680

describe the signs and symptoms and treatment of addisons disease?

Answer 680

``` postural hypotension lethargy/fatigue weight loss anorexia hyperpigmentation hypoglyceamia nausea abdominal pain dizziness ``` treatment- hydrocortisone or fludrocortisone(steroid hormone therapy)

Question 681

what is addisons crisis?

Answer 681

hypotension, hypoglyceamia, dehydration, collapse, pigmentation, coma treat with IV fluid replacement and cortisol(hydrocortisone)

Question 682

describe signs of hyperaldosteronism?

Answer 682

hypertension left ventricular hypertrophy hypernatraemia hypokalaemia

Question 683

what is a phaeochromocytoma?

Answer 683

tumour of the chromaffin cells in the adrenal medulla catecholamines- noradrenaline and adrenaline secreted associated with sever hypertension

Question 684

what are the functions of angiotensin II?

Answer 684

``` sympathetic activity vasoconstriction posterior pituitary- ADH secretion kidney- Na/Cl reabsorption, K excretion- water retention adrenal gland-aldosterone secretion ```

Question 685

what is hyperaldosteronism?

Answer 685

excess aldosterone primary. .. defect in adrenal cortex, low renin levels secondary. .. overactivity of RAAS, high renin levels

Question 686

what is the clinical significance of the coracoclavicula lifament?

Answer 686

made up of conoid ligament and trapezoid ligament

Question 687

what is the clinical significance of the suprascapular notch?

Answer 687

suprascapular nerve passes through | innervates supraspinatous and infraspinatous

Question 688

what is the clinical significance of the sternocleidomastoid muscle?

Answer 688

pulls medical fragment upwards in a clavicle fracture

Question 689

explain the appearance of clavicular fracture on an xray?

Answer 689

lateral fragmment pulled down by weight of upper limb | medical fragement pulled up by sternocleidomastoid muscle

Question 690

explain why the humeral head is prone to dislocation?

Answer 690

small articulation and shallow glenoid fossa large femoral head highly mobile shoulder joint so less stable

Question 691

explain why anterior-inferior dislocation is the most common?

Answer 691

joint is weaker inferiorly- rotator cuff abscent

Question 692

what nerve is more at risk in dislocation of shoulder and why?

Answer 692

axillary nerve- supplies head of humerus as it wraps around neck

Question 693

name common complications of anterior-inferior shoulder dislocations?

Answer 693

rotator cuff muscle injuries damage to nerves recurrent dislocations hillsachs lesion- indentation of posterolateral humeral head bankart lesion- part of glenoid labrum torn off

Question 694

with damage to the axillary nerve whant range of adduction will be weakened?

Answer 694

weak deltoid muscle | 15-90degree abduction

Question 695

with damage to supraspinatous what movement is weakenes?

Answer 695

abduction above shoulder

Question 696

what syndrome can occur if the supraspinatous tendon is inflammed?

Answer 696

impingement syndrome calcification of supraspinatus tendon- inflammatory response and pain(tendinopathy) deposits of hydroxyapatite calcium crystals reduction of subacromial space

Question 697

what are the borders of the axilla?

Answer 697

anterior- pectoralis major and minor medial- serratus anterior posterior- scapularis, teres major lateral- intertubecular sulcus

Question 698

how do you test integrity of axillary nerve?

Answer 698

test sensation of deltoid- regimental badge

Question 699

what is the most common mechanism of injury for a clavicular fracture?

Answer 699

FOOSH mid clavicular fractures mainly manage conservatively- sling, analgeasia surgery may be necessary if complications occur

Question 700

name the 3 causes of shoulder impingement syndrome?

Answer 700

calcification of supraspinatus tendon- tendonapathy subacromial bursitis subachromial osteophytes all reduce the subacromial space

Question 701

describe what is adhesive capsulitis(frozen shoulder)?

Answer 701

inflammation of glenohumeral capsule- thickening and contraction formation of adhesions painful and reduced movement treatment= physiotherapy and analgeasia

Question 702

describe the X ray findings on shoulder osteoarthritis?

Answer 702

L oss of joint space O steophytes S ubchondral sclerosis S ubchondral cysts

Question 703

describe rotator cuff tears?

Answer 703

one of SITS muscles are torn acute due to trauma, see painful reduced ROM chronic due to degeneration with age, repetitive overuse , see loss of function chronic microtrauma

Question 704

describe causes of median nerve damage?

Answer 704

compression in carpal tunnel penetrating injury to wrist suprachondylar fracture

Question 705

describe the spleens role in the immune system?

Answer 705

removal of blood bourne pathogens- encapsulated bacteria antibody production- in acute phase IgM in long term production IgG splenic macrophages- removal of opsonized microbes and immune complexes

Question 706

describe what is SCID(sever combined immuno-deficiency)?

Answer 706

primary immune deficiency due to defective T cells, mean B cells cant activate

Question 707

give examples of supportive treatment for someone with immunodeficiencies?

Answer 707

prophylactic antibodies infection prevention nutritional support- vitamin A and D use UV-irradiated and CMV negative blood products only treat infections promptly and affectively

Question 708

what primary immunodeficiency is most associated with someone with reccurent viral infections?

Answer 708

``` T cell deficiency t cells cant be activated when presented with MHC class 1 microbes ```

Question 709

what is the most common cause of secondary immune deficiency worldwide?

Answer 709

malnutrition

Question 710

explain why elderly people are more at risk of shingles?

Answer 710

shingles is caused by reactivation Varicella Zoster virus lying dormant in dorsal route og ganglion in spine since the initial chicken pox infection elderly people develop multifactorial immunodeficiency(eg. diabetes and malnutrition) which reactivated latent VZV causing shingles

Question 711

describe common variable immunodeficiency(CVID)?

Answer 711

primary immune defect, where patient has B cells but can't produce antibodies antibody defect

Question 712

describe chronic granulomatos disease(CGD)?

Answer 712

primary immune defect- phagocytic defect phagocytes(neutrophils and macrophages) lack killing mechanism, defect of respiratory bursts- inneffective phagocytosis X linked

Question 713

what features of infection increase suspicion of immunodeficiency?

Answer 713

S evere P ersistent U nusual R eccurent

Question 714

describe Bruton's disease?

Answer 714

primary immune deficiency- antibody defect X linked defect in development of B cells have no B cells- cant produce antibodies

Question 715

describe IgA deficiency?

Answer 715

primary immune deficiency- antibody defect very low or undectable IgA levels present with symptoms when present with IgG subclass

Question 716

describe DiGeorge syndrome?

Answer 716

primary immune deficiency- T cell defect deletion on chromosome 22 causes hypoplastic thymus so no T cells can mature no thymus - T cells cant be made

Question 717

describe specific treatments for primary immuno deficiency?

Answer 717

regular immunoglobulin therapy- we want IgG>8g/L, life long | SCID- haemopoeitic stem cell therapy

Question 718

describe how age of symptom onset can indicate which primary immune deficiency is present?

Answer 718

age< 6months... phagocytic or T cell defect 6months< age< 5years... b cell- antibody or phagocytic defect age > 5 years... antibody/b cell/ complement defect

Question 719

describe the causes of secondary immune deficiency?

Answer 719

decrease production of immune components... - malnutrition - HIV - haematological malignancies and therapeutic treatment- chemotherapy and vascular catheter - splenectomy- encapsulated bacterio increase loss of immune components... - protein loosing conditions eg. nephropathy - burns

Question 720

describe what is meant by delivery system of viruses?

Answer 720

protexts virus and contains binding structures

Question 721

describe what is meant by payload of viruses?

Answer 721

contains genome and enzymes needed to replicate virus

Question 722

describe the structure of influenza virus?

Answer 722

orthomyxoviruses- spherical, envoloped, segmented, -ssRNA Genetic- 8genes encoding for 11 proteins surface antigens- haemagglutinin(H), Neuraminidase(N)

Question 723

describe and compare the different subtypes of influenza?

Answer 723

A; large host range in animals too, animal resevoirs, antigenic shift and drift, can cause large pandemics, younger adults too B; humans only, antigenic drift, severe disease, older adults, no pandemics C; human and swine(pig), antigenic drift, mild disease

Question 724

how is influenze virus transmitted?

Answer 724

respiratory route- coughing, sneezing and ihaling 1) small particle aerosols 2) large particles or droplets 3) particles lad on surfaces, indirect contact

Question 725

how does influenza virus replicate?

Answer 725

``` -ssRNA uses RNA dependent RNA polymerase(RdRp) to +ssRNA template strand to form alot of -ssRNA assemble into nucleocaspid mRNAs translate to form viral proteins ```

Question 726

how does influenza virus enter the cell?

Answer 726

``` Hemagglutinin protein(H) on virus binds to NANA residue(sialic acid) on a glycoprotein which acts as a receptor for virus enter by receptor mediated endocytosis ```

Question 727

how does influenza virus leave the cell?

Answer 727

Neuraminidase protein(N) cleaves sialic acid on NANA

Question 728

describe antigentic drift?

Answer 728

minor and gradual changes in H and N proteins of influenza virus causes seasonal epidemics no change in viral subtype random and small mutations

Question 729

describe antigenic shift?

Answer 729

dramatic and sudden changes in genes of H and N proteins infrequent- type A influenza only changes in subtype and H, N proteins, reassortants of different specials cause widerspread epidemics and pandemics

Question 730

what is haemolytic ureamic syndrome?

Answer 730

caused ny shiga toxin producing Ecoli | triad of acute renal failure, haemolytic anaemia, and thrombocytopenia

Question 731

describe the structure of E.coli?

Answer 731

6 strains gram -ve bracili found as normal microbiota of large bowel lactose fermenting, anaerobic Flagella(H), capsule(K), LPS(O), fimbriae(F)

Question 732

describe how E coli is identified?

Answer 732

MacConkey Agar- contains lactose and pH indicator, goes red with acid E.coli present- goes red/pink because ecoli is lactose fermenting(lactose energy sorce)so forms lactic acid, making low pH

Question 733

describe how e.coli is identified by serology?

Answer 733

look for O,H,K,F bacterial antigens

Question 734

describe what e.coli can cause?

Answer 734

due to virulence factors can cause intestinal infections- diarrhoea and extra- intestinal infections- UTIs, sepsis, neonatal meningitis, blood stream infections

Question 735

describe how e.coli can cause bacterial diarrhoeal illness?

Answer 735

enterotoxigenic e.coli(ETEC) produce heat stable toxin (ST) and heat labile toxin (LT) line of intestine secretes excess fluid-> watery diarrhoea and abdominal cramps

Question 736

describe what shiga toxin producing E.coli(STEC) causes?

Answer 736

Causes... haemorrhagic colitis and haemolytic uraemia syndrome b units of shiga toxins binf to GB3 on host, inhibit protein synthesis leding to cell death

Question 737

How does E.coli cause UTIs?

Answer 737

uropathogenic E.coli(UPEC)- gram -ve rods VIRULENCE FACTORS= adhesions of type 1 fimbriae allow entry and from IBCs, toxins LPS and HlyA, and iron aquisition where iron is limited in urinary tract produce their own UPEC travels from rectum to uretha to bladder, smaller journey for women- anatomical differences

Question 738

what is the treatment for e.coli UTIs?

Answer 738

trimethoprim

Question 739

what are the functions of the scapula?

Answer 739

protect the underlying neurovascular structures transmit forces from the upper limb into the axial skeleton attaches the upper limb to the trunk- shoulder girdle

Question 740

state three specific structures that add to stability of shoulder joint?

Answer 740

muscle tone; rotator cuff muscles, coracobrachialis, deltoid resist downward dislocation capsular and extracapsular ligaments glenoid labrum, deepen glenoid fossa

Question 741

what is the coracoacromial arch and what is its role in FOOSH?

Answer 741

osseo-ligamentous structure formed by inferior surface of acromion and coracoid process of scapula- coracoacromial ligament between prevents superior dislocation of humeral head fl=rom glenoid cavity

Question 742

what structures are damages in a surgical neck fracture of humerus?

Answer 742

fracture below the greater and lesser tubercles of the humerus axillary nerve and posterior circumflex humeral artery

Question 743

what are the main stages of frozen shoulder?

Answer 743

freezing- increasing pain, decreased range of motion frozen- extreme limited movement, significant pain thawing- slow improvement in ROM and reduce in pain

Question 744

what can damage to the anular ligament cause?

Answer 744

decreased stability of proximal radioulnar joint | subluxation or dislocation of radial head at elbow

Question 745

what does the rounded head of the capitulum of humerus allow?

Answer 745

pivot movement of proximal radioulnar joint | hinge movement of elbow joint

Question 746

what is the mechanism of injury of a suprachondylar fracture?

Answer 746

FOOSH- arm in extension | in children

Question 747

what are common complications of suprachondylar fractures?

Answer 747

damage to median or radial nerve cubitus varus angulation brachial artery at risk- volkmans isachaemic contractus, impaired blood supply, necrosis and fibrosis of forearm muscles

Question 748

describe the mechanism of injury for a pulled elbow(subluxation of radial head)?

Answer 748

ages 2-5 children longitudinal traction with arm extenden and foearm pronated(held up by arms/hands) radial head subluxed from annular ligament trweat by reversing the forces

Question 749

how does a patient present with pulled elbow?

Answer 749

pain, not using elbow | annular ligament around radius

Question 750

why does a pulled elbow usually occur as a pronated injury?

Answer 750

annular ligament more relaxed in pronation less secure joint- easier for sublaxation in supination annular ligament is taunt

Question 751

why are children prone to pulled elbows?

Answer 751

weaker annular ligament | as age the ligament strengthens

Question 752

what is the most common mechanism and type of elbow dislocation?

Answer 752

FOOSH arm in extended posterior lateral dislocations put back in place, and asses NV structures

Question 753

describe how a patient with radial head and neck fractures may present?

Answer 753

trauma, lateral elbow pain, restricted ROM | hard to identify on Xray- see fat pads/sail sign

Question 754

why does a radial head/neck fracture result in fat pads/sail sign?

Answer 754

haemarthrosis displaces fat | blood from radial head and fat leak into joint space

Question 755

delcribe elbow OA?

Answer 755

``` degenerative disease of articular cartilage, loss of cartilage leads to bone rubbing and pain with use L oss of joint space O steophytes S subchandral sclerosis S ubchondral cysts ``` treat- analgeasia, intra-articular injections and replacement

Question 756

describe elbow RA?

Answer 756

systemic inflammatory disease, autoantibodies attack synovium malaise, weight loss, low grade fever, morning stiffness L oss of joint space E rosion S soft tissue swelling S ee through bones(osteopenia)

Question 757

describe the pathophysiology of tennis elbow(lateral epichondyle)?

Answer 757

tendonopathy of common extensor origin- lateral epichondyle, particularly extensor carpi radialis brevis repetitive micro tears, overuse, repetitive wrist enxtension acute inflammation

Question 758

describe how a patient with tennis elbow would present and treatment?

Answer 758

present; 35-50 yrs old, pain in extensor origin(lateral epichondyle), on resisted wrist/finger extension w elbow extended treat; activity modification, conservative, physiotherapy and pain killers

Question 759

describe the pathophysiology of golfers elbow(medial epichondyle)?

Answer 759

tendonapathy of common flexor origin(medial epichondyle), micro trauma of flexor-pronator mass by repetitive wrist flexion and pronation overuse, acute inflammation

Question 760

descrie how a patient with golfers elbow present and treatment?

Answer 760

present; less common, pain over medial epichondyle, worse with wrist and forearm motion and gripping, heavy lifting treat; activity modification conservative, pjhysiotherapy and painkillers

Question 761

describe what is students elbow(olecranon bursitis)?

Answer 761

inflammation of olecranon bursa causing superficial swelling- dosent involve the joint, dosent effect ROM repeated minor trauma to elbow, ffriciton soft, cystic and transeliminating swelling

Question 762

describe treatment for student elbow?

Answer 762

``` conservative treatment rest, spontaneous solution antibodies if infected rarely drained aspirate bandage or compression ```

Question 763

describe what is and the presentation of cubital tunnel syndrome?

Answer 763

compression of ulnar nerve at cubital tunnel(lateral posterior arm) sensory symptoms seen first- numbness and tingling of ring and little thing - ulnar nerve supples flexor carppiulnaris, and half of flexor digitorum profundus

Question 764

what are rheumatoid nodules?

Answer 764

a manifestation of RA common in fingers, forearms and elbow in skin firm to touch and dont translluminate

Question 765

what is gouty trophi?

Answer 765

gout is main risk factor, gout= arthritis due to deposition of monosodium urate(MSU) crystals within joint, causes acute inflammation and tissue damage high uric acid levels in blood- hyperuricaemia

Question 766

describe the causes of carpal tunnel syndrome?

Answer 766

``` T rauma R heumatoid arthritis A cromegaly M yxoedema P regnancy ```

Question 767

what is the carrying angle and describe the significant differencre between women and men?

Answer 767

in full extension ulnar makes a valgus angle with humerus(dosent go directly straight down) men= 5-10degrees women= 10-15degrees women have larger carrying angles so the forearm can clear the hips in swinging movements whilst walking as women have a wider pelvis(hips)

Question 768

describe how you can test function of the median nerve and why it might be useful?

Answer 768

to check median nerve damage especially in suprachondylar fracture OK sign, if damged wont be able to make a rounded O

Question 769

compare and contrast cardiac and pleuritic pain?

Answer 769

``` cardiac pain... visceral afferent nerves deeper structures- heart central and dull worsened w excertion can be refered to jaw, arm and neck ``` ``` pleuritic pain... somatic afferent nerves chest wall, pericardium and parietal pleura localised, sharp worsened w chest movement ```

Question 770

describe pericarditis?

Answer 770

``` cardiac cause for chest pain- somatic; sharp, well localised pain inflammation of pericardium pericardial rub on examination typically viral infection ECG- ST elevation ```

Question 771

what conditions come under acute coronary syndromes?

Answer 771

unstable angina NSTEMI STEMI

Question 772

what is ischemic heart disease?

Answer 772

``` insufficient blood supply to heart muscle due to atherosclerotic disease of coronary arteries stable angina unstable angina NSTEMI STEMI ```

Question 773

describe the pathophysiology of stable angina?

Answer 773

asymptomatic atherosclerotic plaques form which are stable and fixed- stable occlusion of artery

Question 774

describe the pathophysiology of unstable angina?

Answer 774

stable atherosclerotic plaque turns unstable | platelet aggregation

Question 775

describe the risk factors for atherosclerotic plaque formation and therefore acute coronary syndromes?

Answer 775

modifiable: smoking, high fat diet, obesity, diabetes, hypertension, dyslipidaemia non-modifiable: increasing age, family history, male gender

Question 776

describe pathophysiology for myocardial infarction?

Answer 776

``` stable chronic occlusion plaque rupture thrombus formation sudden increase in occlusion of artery ischaemia and therefore infarction ```

Question 777

what is myocardial ischaemia?

Answer 777

either unstable angina or stable angina | metabollic demands of heart not met, causing pain, due to narrowing of the coronary arteries(atherosclerotic plaques)

Question 778

describe history, examination and investigations for stable angina?

Answer 778

history; pain increases with excertion(increased demand), dull chest pain releived by rest and may refer, quick episodes examination; normal or see risk factors for atherosclerosis(eg. high bp) investigations; troponin normal, ECG normal

Question 779

describe history, examination and investigations for unstable angina?

Answer 779

history; cardiac sounding chest pain atrest, sever and longer lasting, sweating and nausea examination; normal or pale, risk factors of atherosclerosis, comprimised cardiac function investigations; troponin normal, ECG St depression and T wave changes

Question 780

what can bbe used to relieve stable angina?

Answer 780

GTN spray ellievates myocardial ischaemia venodialation(systemic veins dialate) decreasing preload, filling, force of contraction and workload increasing blood supply and decreasing oxygen demand

Question 781

what factors can bring on angina?

Answer 781

increased workload and demand of heart excercise; faster heart rate, short diastole, coronary arteries cant fill, to meet demand eating; vasodialation of arteries in GI to aid digestion, decreases BP stimulating baroreceptors to increase HR Stress; sympathetic NS increases HR

Question 782

what is a myocardial infarction?

Answer 782

sudden occlusion of coronary artery, infarction of cardiac tissue

Question 783

describe signs and symptoms of an MI?

Answer 783

history; cardiac sounding chest pain at rest, crushing, severe and long lasting examination; sympathetic symptoms due to fall in CO, pale, failing heart Investigations; troponin increase(necrosis), ECG NSTEMI= ST depression and T wave inversion STEMI= ST elevation, overtime a pathological Q wave

Question 784

what is the difference between NSTEMI and STEMI?

Answer 784

NSTEMI- partial occlusion, sub-endocardial injury, ECG- t wave inversion and ST depression STEMI- complete occlusion, transmural injury, ST elevation, pathological Q waves

Question 785

why does a pathological Q wave occur in a STEMI?

Answer 785

dead muscle tissue- no AP ECG picks up action potential from opposite side- moving away from + electode q wave shows necrosis

Question 786

how do u manage myocaridal infarctions?

Answer 786

MONA Morphine- to ease pain Oxygen- maintain oxygen saturations when there is low CO Nitrates- venodialation to decrease workload and demand, decrease cardiac return nd increase blood flow Aspirin- anti platelet

Question 787

what surgical treatments can bused in coronary artery disease?

Answer 787

stents- placed to maintain blood flow through coronary artery invasive coronary angiogram- identifies coronary artery and see how occluded it is, uses X RAY and contrast

Question 788

what is a troponin assay?

Answer 788

hows to determine between myocardial ischaemia and infarction iinfarction- elevated troponin I and T, myocytes die

Question 789

what are the different causes of chest pain?

Answer 789

cardiac- acute coronary syndromes, pericarditis muscoskeletal- costochondritis and rib fracture GI- oesaphaguse reflux disease, peptic ulcer disease respiratory- pneumonia, pulmonary embolism, pleurisy

Question 790

what is the function of thyroid peroxidase?

Answer 790

regulates 3 major processes... 1) oxidation of iodide(as absorbed) to iodine- requires H2O2 2) addition of iodine to tyrosine on thyroglobulin 3) coupling of MIT or DIT to generate thyroid hormones

Question 791

dewcribe what is goitre?

Answer 791

enlargement of the thyroid gland due to hyper or hypo thryroidism overstimulated thyroid gland

Question 792

describe the causes of hypothyroidism?

Answer 792

``` failure of gland TSH or TRH deficiency iodine deficiency in diet radioactive iodine drugs autoimmune- Hashimotos ```

Question 793

what is a common complication of hypothyroidism in children?

Answer 793

cretinism | -dwarfed stature, mental deficiency, poor bone development, slow pulse, muscle weakness, GI disturbances

Question 794

what is a common complication of hypothyroidism in adults?

Answer 794

myxedema | -thick puffy eyes, muscle weakness, slowed speech, mental deterioration, intolerance to cold

Question 795

what are general symptoms of hypothyroidism?

Answer 795

``` obesity lethargy intolerance to cold bradycardia dry skin alopecia ```

Question 796

describe what is hashimoto's disease and how to treat ir?

Answer 796

autoimmune disease, destruction of thyroid follicules more common in women low T3 and T4, high TSH treatment; oral thyroid hormone

Question 797

describe what causes hyperthyroidism?

Answer 797

``` autoimmune- Grave's disease toxic multinodular goitre toxic adenoma excess T3/4 therapy drugs- amiodarone ```

Question 798

what are the general symptoms of hyperthyroidism?

Answer 798

``` weight loss irritability heat intolerance sweating tachycardia fatique and weakness buldging eyes- xathophalmus ```

Question 799

describe what is graves disease and how do you treat?

Answer 799

autoimmune- production of TSI which stimulates thyroid hormone stimulation outside normal negative feedback controle antibodies mimics actions of TSH- high T3/4 and low TSH treat- carbimazole

Question 800

what severe complications can occur with Hashimoto's?

Answer 800

myxoedema coma- in elderly, pericardial effusion

Question 801

what severe complications can occur with Grave's?

Answer 801

thyroid crisis- hyperexia, tachycardia, cardiac failure

Question 802

how do you scan a thyroid gland?

Answer 802

technetium-99m radioisotope scanning | low exposure to radiation due to short half life

Question 803

describe the embryonic development of the thyroid gland?

Answer 803

3-4 week gestation epithelial proliferation of floor of pharynx(base of tongue) first descends as diverticulum thru thyroglossal duct(connects thyroid gland to tongue) which then degenerates

Question 804

what do parafollicular cells produce and where r they found?

Answer 804

in thyroid gland | produce calcitonin

Question 805

what has a longer half life t3 or t4?

Answer 805

T4 longer half life T3 more biologically active T4 produced more than converted to T3 by liver and kidney

Question 806

how do thyroid hormones work?

Answer 806

T3+4 lipid soluble so can pass through plasma membrane must be transported in blood bound to thyroxine binding globulin (TBG) bind to nuclear receptors- increase transcription and gene expressions

Question 807

what condition can be treated by the drug carbimazole?

Answer 807

hyperthyroidism

Question 808

what type of hormone is TSH?

Answer 808

glycoprotein- 2 sub units(a + b)

Question 809

how is subclinical hyperthyroidism characterized?

Answer 809

low/undetectable concentration of TSH in serum, free T3/4 within normal range

Question 810

what would you expect to see in dietry iodine deficiency?

Answer 810

goitre low T3/4 high TSH

Question 811

what are the most common causes of goitre?

Answer 811

worldwide- iodine deficiency in diet | UK- multi nodular goitre

Question 812

describe thyroglossal cyst?

Answer 812

it is in the midline and moves up on tongue protusion

Question 813

describe what is heart failure?

Answer 813

a clinical syndrome airising from inability of heart to maintain CO to meet body demands leading to tissue hypoxia ad oedema reduced CO, tissue hypoperfusion, increased pulmonary pressures and tissue congestion

Question 814

what are the causes of heart failure?

Answer 814

ischeamic heart disease, hypertension, vascular disease, cardiomyopathies, arrhythmias all cause remodelling; loss of myocytes and fribrosis, changing ventricle shape and size and therefore function, impaired ventricular filling and ejection

Question 815

what is ejection fraction?

Answer 815

fraction ejected in a single heart beat of total volume available SV/EDV=ejection fraction

Question 816

what factors affect stoke volume?

Answer 816

preload- stretch on ventricle before contraction myocardial contractility afterload- TPR

Question 817

describe starlings law with regards to preload and SV?

Answer 817

the greater the EDV the greater the stretch- preload more stretch, greater contraction force, grearer SV ejected in systole(CO) up to a certain point

Question 818

how would you increase SV?

Answer 818

increase preload increase myocardial contractility decrease afterload

Question 819

what is the most common cause of heart failure?

Answer 819

ischaemic heart disease

Question 820

describe the pathophysiology of heart failure and how you determine between them?

Answer 820

either a... contractility(ejection) problem(systolic)- HFrEF; EF<40% filling(dialstolic) problem- HFpEF; EF>50%

Question 821

describe the pathophysiology of HFrEF?

Answer 821

``` ejection/contraction problem systolic can't pump with enough force as... -muscle walls thin/fibrosed - chamber space enlarged -abnormal or unco-ordinated myocardial contraction reduced ejection fraction<40% ```

Question 822

describe the pathophysiology of HRpEF?

Answer 822

``` Filling problem diastolic capacity for blood is reduced as... -ventricular chambers are too stiff - ventricular walls thickened(hypertrophy or remodelling) - space available reduced, decreased preload EDV reduced preserved ejection fraction>50% ```

Question 823

what type of heart failure is more common?

Answer 823

left ventricle HFrEF

Question 824

what are the symptoms of HFrEF and HFpEF?

Answer 824

same symptoms but different pathophysiologies dyspnoea(difficult breathing) and fatigue- due to tissue hypoperfusion increased tissue fluid retention

Question 825

why is it important to perform an echocardiogram and determine whether HFrEF and HFpEF?

Answer 825

confirms diagnosis identifies potential causes have implications for treatment options and prognosis

Question 826

what is the body neuro-humeral mechanisms in HF?

Answer 826

mechanism that leads to increased cardiac demand and further reduction in SV worsening the effect of a failing heart

Question 827

describe the mechanism of body neuro-humeral response to HF?

Answer 827

direct cardiotoxic effects from long-term activation of sympathetic NS and angiotensin II increasing cardiac work on already stuggling heart- further deterioration of CO increasing circulating volumes(Na and H2O retention) increased pressure within ventricles- failure to eject volume increased tissue fluid remaining in interstitial

Question 828

how does pulmonary oedema arise in HF?

Answer 828

left ventricular HF incresed pressure within LV- cant eject blood increases pressure in pulmonary circulation increased hydrostatic pressure at venule end of capillary bed gradient of hydrostatic and oncotic pressures- favour fluid in interstitium tissue fluid accumulates as pulmonary oedema

Question 829

how does peripheral oedema arise in HF?

Answer 829

right ventricular HF increased pressure within RV- cant eject bloos increased pressure in systemic circulation increase central venous and jugular venous pressure increased hydrostatic pressure at venule ends of capillary beds gradient of hydrostatic and oncoti pressure- favours fluid in interstitium tissue fluid accumulates as peripheral oedema

Question 830

describe how a patient with left ventricular HF presents?

Answer 830

-shortness of breath- breathlessness -basal pulmonary crackles -orthopnea(worsening of breathlessness when lying flat) -paroxysmal noctural dyspnoea(wake suddenly from sleep very breathless, want to open window) X ray accumulation of fluid

Question 831

describe how a patient with right ventricular HF presents?

Answer 831

- pitting peripheral oedema | - raised jugular pressure

Question 832

what is congestive heart failure?

Answer 832

both ventricle involved left sided HF usually causes right sided HF pulmonary and peripheral(lower limbs) oedema

Question 833

what are the causes of left sided HF?

Answer 833

``` previous MI volume overload due to mitral or aortic valve regurgitation dialated cardiomyopathy chronic hypertension sever aortic stenosis ```

Question 834

what are the causes of right sided HF?

Answer 834

left sided HF (increase in pulmonary pressures and therefore afterload of RV) secondary to chronic lung disease- pulmonary hypertension pulmonary valve stenosis

Question 835

what are the causes and consequences of reduced stroke volume?

Answer 835

reduced preload reduced myocardial contractility increased afterload heart failure

Question 836

describe the pharmacological management of heart failure?

Answer 836

``` ACE inhibitors diuretics Angiotensin receptor blockers furosemide beta blockers spironolactone digoxin renin inhibitors ```

Question 837

why do you give aspirin in an acute coronary syndrome?

Answer 837

anti-platelet drug | decreases thrombus risk so easier for blood to flow, reduces mortality

Question 838

why does peripheral oedema tend to reduce at night?

Answer 838

lying down central venous pressure evens out so less of an increase in hydrostatic pressure, reduced build up of tissue fluid

Question 839

whart happens to return of blood to heart when lying down?

Answer 839

increase venous return due to a decrease of effect of gravity, less pooling of blood

Question 840

why might a person with HF be short of breath when lying down?

Answer 840

increase pressure in pulmonary circulation due to lesser effects of gravity and increased preload, greater venous return to right heart, increase in hydrostatic pressure, greater pulmonary oedema

Question 841

what would you aspect with raised jugular venous pressure, fatique, angine and breathlessness?

Answer 841

right ventricular HF increase in right ventricle pressure- increase in systemic and central venous pressure- increases jugular venous pressure

Question 842

what vitamins effect bone stability?

Answer 842

vitamin D3- produces calcitriol(Ca absorption) vitamin C- sythesis of collagen vitamin K and B12- synthesis of bone proteins

Question 843

what family of viruses does EBV belong to?

Answer 843

human herpes virus

Question 844

what cell does EBV attack?

Answer 844

first epithelial cells, then B lymhocytes

Question 845

what infection does varicella-zoster virus cause?

Answer 845

chicken pox or shingles

Question 846

what are complications of EBV infection?

Answer 846

Burkitts lymphoma hodgkins lymphoma- reed steinberg cells gastic lymphoma

Question 847

what are the 3 types of viral infectio?

Answer 847

acute infection- multiple replications, death of hostg cell chronic infections- viral particles continue after period of illness, release of viral particles even without death of host cell, RNA viruses latent infections- DNA viruses or retroviruses, persistence of viral DNA, can lead to cancer

Question 848

what type of infection does EBV or VZV (herpes family) cause?

Answer 848

latent infection

Question 849

what are the likely causes of pharyngitis?

Answer 849

EBV or adenovirus or streptococcus pyrogenes

Question 850

what is common to see with an EBV infection?

Answer 850

``` splenomegaly sore throat pharyngitis tired, unwell head ache ```

Question 851

what would you see on investigation for an EBV infection?

Answer 851

increased WBCC- raised no. of lymphocytes

Question 852

what treatments are available for an influenza infection?

Answer 852

vaccinations antivirals neuraminidase inhibitors

Question 853

what can cause endocarditis?

Answer 853

viridans streptococci streptoccoci mutans straph aureus

Question 854

what micro-organism can cause glandular fever?

Answer 854

EBV

Question 855

describe the serology after a HEP B needle stick injury?

Answer 855

1 surface antigen(HbsAg) detectgable, rise in ALT 2 e-antigen seen, infectious 3 core antibody seen(IgM) due to core antigen (HbcAg 4 e- antibody 5 surface antibody(IgG) seen - clearance of virus IgG persists for life

Question 856

what does a streptococcus pyrogenes infection cause?

Answer 856

streptococcal pharyngitis | which is strep throat

Question 857

what are characteristics of streptococci?

Answer 857

gram + cocci | arranged in chains

Question 858

describe the clinical features of streptococcal pharyngitis?

Answer 858

children 5-15 years droplet spread sore throat, malaise, fever, head ache, swelling of tonsils scarlatinform rash

Question 859

why do we only give supportive treatment for strep throat(streptococcus pyrogenes)?

Answer 859

if left untreated, develop M protein specific antigen- gives immunity to group A streptococci antibodies dont helpt treat

Question 860

what is the main complication of streptococcal phyarngitis?

Answer 860

scarlet fever- rash and fever | when exotoxins s. pyrogenes present

Question 861

what are other complications of streptococcal phyarngitis?

Answer 861

supparative complications- can cause severe deep tissue infections with jhigh mortality, eg. peritonsillar cellulitis/abscess or retropharyngeal abscence acute rheumatic fever-inflammation of hearts, kjoints and CNS, caused by M protein binding to collagen or autoimmiune acute post-streptococcal glomerulonephritis- acute inflammation of renal glomerulus, antigen-antibody complexes

Question 862

what skin infections can streptococcus pyrogenes cause?

Answer 862

- impetigo; children, honey crusty lesions, self resolving - erysipelas; lymphatics and skin, face and lower limb, red hot lesions - cellulitis; deeper, skin and subcutaneous tissue, IV drug use or impaird lympathetic drainage - necrotising fasciitis; deep tissues, rapid necrosis, high fever, severe pain, high mortality

Question 863

what is toxic shock syndrome?

Answer 863

-blood stream and deep tissue infection of streptococcus pyrogenes endotoxin -bacteraemia -vascular collapse - organ failure very high and fast mortality

Question 864

what causes the severity of infection in toxic shock syndrome?

Answer 864

``` endotoxins release by bacteria trigger t cells(via MHC class II APCs) to give a non specific inflammatory response, leading to vascular collapse M protein fibrinogen complex formation ```

Question 865

which skin infection caused by streptococcus pyogenes can lead to glomerulonephritis?

Answer 865

inpetigo

Question 866

what antibodics are used to treat cellulitis?

Answer 866

flucloxacillin penicillin carbapenens

Question 867

what is the difference between tumour staging and grading?

Answer 867

staging is a measure of overall tumour burden | grading describes degree of diffrentiation

Question 868

why is radiation therapy given in fractional doses?

Answer 868

to reduce damage to normal tissue

Question 869

how does radiation therapy help cure cancer?

Answer 869

1 trigger apoptosis- free radical induced DNA damage, detected by cell cycle checkpints 2 interferes with mitosis- double strand DNA breaks, damage chromosomes, prevent complete M phase

Question 870

what are the effects of chemotherapy on the body?

Answer 870

``` hair loss pain trouble breathing weakened immune system-immuno comprimised constipation diarrhoea neuropathy bruising and bleeding rashes ```

Question 871

how is hormone therapy used to treatcancer?

Answer 871

selective oestrogen receptor modulators eg. tamoxifen | prevent oestrogen binding receptors- treats hormone positive breast cancer

Question 872

how is immunotherapy used to treat cancer?

Answer 872

target immune system to help fight cancer by recognising and attacking cancer cells immune checkpoint inhibitos

Question 873

what are the uses of tumour markers?

Answer 873

for diagnosis monitor tumour burden during tretment and follow up assess recurrence

Question 874

what is the aim of cancer screening?

Answer 874

attempts to detect cancers as early as possible when the chance of cure is highest

Question 875

what screening programmes are available in the UK?

Answer 875

breast screening- women 47-73 yrs old every 3 years cervical screening- women 25-64yrs every 3 yrs then every 5 bowel screening- at home testing, med and women, since 55

Question 876

where do the collateral ligaments of the wrist attach?

Answer 876

radial and ulnar styloid process

Question 877

what is the mechanism of injury in a scaphoid fracture?

Answer 877

FOOSH splits scaphoid into 3- distal 1/3, waist and proximal 1/3 waist fracture most common

Question 878

what is the most common carpal bone to be injured?

Answer 878

scaphoid- particularly waist

Question 879

what is a common issue with a scaphoid fracture?

Answer 879

retrograde blood supply of radial artery- if disrupted causes avascular necrosis of proximal part(on xray seen as hyperdense and sclerosis)

Question 880

how does a scaphoid fracture present?

Answer 880

FOOSH | pain and wrist swelling, pain in anatomical snuff box, pain pressing scaphoid tubercle

Question 881

what is the most common orthopaedic injury?

Answer 881

distal radius fracture

Question 882

describe what is a colles fracture?

Answer 882

most common distal radius fracture- extraarticulaf by FOOSH in pronation and extended distal fragment displaced dorsally- dinner fork deformaty post menapausal osteoporosis risk factor

Question 883

describe what a smiths fracture is?

Answer 883

distal radius fracture by FOOSH in supination(back of hand) in flexion distal fragment displaced volarly- garden spade deformity higher incidence of surgery

Question 884

what do you look for on X ray when you suspect a colles fracture?

Answer 884

6Ds Distal 2-3cm of radius Distal fragment displaced dorsally classic Dinner fork deformity

Question 885

how do you treat a distal radius fracture?

Answer 885

reduce, hold with cast, rehabilitate | smiths may need surgery

Question 886

what is seen in OA of the hand?

Answer 886

Heberden's nodules: presence of osteophytes causes bony swellings of DIPJs, only OA Bouchard's nodules: bony or cystic swelling of PIPJs, seen in other diseases too on X-ray see LOSS not systemic, disease of articular cartilage

Question 887

what is seen in RA of the hand?

Answer 887

swan neck; PIPJ extension +DIPJ flexion boutonniere(button pressin); PIPJ flexion + DIPJ extension radial deviation of wrist ulnar deviation of fingers from MCPJ on X ray see LESS systemic inflammatory disease- classicaly MCPJ and PIPJ

Question 888

describe what is psoriatic arthropathy?

Answer 888

autoimmune-HLA inflammatory and systemic arthritis affect joints and connective tissue dactylitis= swelling of whole digits enthesitis= inflammation of entheses(pain where tendons join bone eg. achilles) associated w psoarisi od skin and nails treat early and aggressively

Question 889

what is carpal tunnel syndrome?

Answer 889

pressure on median nerve in carpal tunnel palmar branch NOT involved caused by; pregnancy, RA, trauma/fracture, idiopathic and diabetes

Question 890

what are the symptoms for carpal tunnel syndrom?

Answer 890

-weak LOAF muscles(supplied by median nerve) Lateral 2 lumbricals Opponens pollicus Abductor pollicus brevis Flexor pollicus brevis -pain and paraethesia in median nerve sensory distribution -atrophy of thenar eminence muscles

Question 891

what is the guyons cannal?

Answer 891

where ulnar nerve travels | between hamate and pisiform

Question 892

wha diagnostic tests can you do for carpal tunnel syndrome?

Answer 892

tinnels test- tapping on median nerve phalens test- flexion of wrist to 90degrees and hold for 60 secs both trigger symptoms palmer abduction at thumb- as it is done by abductor pollicis brevis which is fully supplied by median nerve

Question 893

what is the treatment for carpal tunnel syndrome?

Answer 893

splinting analgesia steroid injection surgery

Question 894

how does compression of the ulnar nerve at guyons canal present?

Answer 894

loss of all intrinsic muscles of hand except LOAF ulnar paradox- ulnar nerve supplying half of flexor digitorum profundus and extensor carpi ulnaris already okay, still intact--> claw hand(contracting) deformity looks worse but acc isnt nearer the paw the worse the claw

Question 895

what is dupuytren's contracture?

Answer 895

``` thickening of palmar fascia- forms nodules and chords starts with little finger autosomal dominant inheritance cant extend finger- tough fibrous bands can be painful men 50-70 yrs old ```

Question 896

how do you treat dupuytrens contracture?

Answer 896

surgery, steroid injection, strectching excercise

Question 897

what clinical sign develops if injury to median nerve occurs at the elbow?

Answer 897

hand of benediction ask patient to make a fist- thumb, index and middle finger cant flex 3rd and 4th lumbricals lost 4th and 5th digits(unapposed ulnar half of flexor digitorum profundus and flexor carpi ulnaris) can flex due to ulnar nerve intact lost flexor digitorum superficialis and half of profundus

Question 898

why does hyperextension of MCP and hyperflexion of IP joints occur in median nerve damage?

Answer 898

extensor digitorum unapposed- hyper extend MCPJ | flexor digitorum profundus ulnar half unapposed, no lumbricals- hyperflexion of IPJ

Question 899

explain why claw hand is less pronounced in a proximal ulnar nerve lesion that a distal ulnar nerve lesion at wrist?

Answer 899

at a proximal lession loose both superficial and palmer branch of ulnar nevre, lossed innervation of ulnar half flexor digitorum profundus and flexor carpi ulnaris- cant flex, looks less worse at distal injury have ulnar 2 muscles intact so can flex digits but looks more worse even though less muscles are lost

Question 900

what soft tissue complications can occur after a colles fracture?

Answer 900

median nerve palsy and post traumatic carpal tunnel syndrome | tear of extensor pollicis longus tendon by attrition of tendon over sharp fragment of bone

Question 901

what are the bony attachments of the flexor retinaculum?

Answer 901

medially to pisiform and hook of hamate | laterally to tubercle of scaphoid and trapezium

Question 902

what is the use of metaphase spreads?

Answer 902

to find homologous pairs stains chromosomes do can distinguish by band pattern and size- in metaphase dark(AT) light(CG)

Question 903

what is rhe use of karyotyping?

Answer 903

to find homologous pairs of chromosomes(have same banding pattern) to see replicated/double chromosomes or missing ones chromosome analysis

Question 904

define between sister and non-sister chromatids?

Answer 904

sister chromatids- same alleles, from same chromosome non-sister chromatids- same homologous pair of chromosome, same genes different alleles homologous chromosomes- same DNA sequence, same genes

Question 905

where r the chromosomes during interphase?

Answer 905

chromosome territories

Question 906

describe the consequence of anaphase lag?

Answer 906

chromosomes missing and degraded from a daughter cell chromatids dont get pulled to poles, are in cytoplasm so one daughter cell will havr less chromosomes

Question 907

when does recombination occur?

Answer 907

prophase 1

Question 908

when does random assortment occur?

Answer 908

metaphase 1

Question 909

what can mitotic non disjunction lead to in a first post zigotic mitotic division?

Answer 909

triosomy | monosomy- not viable for life

Question 910

what can mitotic non disjunction lead to in a later post zigotic mitotic division?

Answer 910

mosacism | presence of 2 or more cell lines

Question 911

how many pairs of chromosomes are ther?

Answer 911

23 pairs | 46 chromosomes

Question 912

where does reduction of genetic material occur in meiosis?

Answer 912

meiosis 1

Question 913

what does non-disjunction on meiosis lead to?

Answer 913

myosomy and triosomy in gametes, faulty meiosis | miscarraiges, infertility, mental retardation

Question 914

why is an RNA primer needed in DNA replication?

Answer 914

to 'kickstart' replication DNA primase makes a short RNA primer as DNA polymerase can only extend a 3' end

Question 915

which direction does DNA polymerase read?

Answer 915

3' to 5'

Question 916

WHAT IS THe difference between a nucleotide and a nucleoside?

Answer 916

nucleotide has a ribose sugar, a nitrogen base and a phosphate a nucleoside has no phosphate

Question 917

what is the difference between ribose and deoxyribose?

Answer 917

ribose has OH on C2 | deoxyribose has H on C2

Question 918

what is the difference between euchromatin and hetrochromatin?

Answer 918

``` heterochromatin= tightly packed, genes not expressed, darker stained, inactive, solenoid euchromatin= loosely packed, genes expressed, light stained, beads on a string, active ```

Question 919

compare DNA and RNA?

Answer 919

DNA= deoxyribose sugar, double stranded, self replicating, bases= A,C,G,T, beta helix, UV damae RNA= ribose sugar, single stranded, synthesised from DNA, codes for proteins, bases= A, C, U, G, a helix, UV resistant

Question 920

what is DNA replication stress?

Answer 920

insufficient replication leads to replication fork slowing, stalling or breaking, miscoperation and proofreading of DNA polymerase, replication machinery defects

Question 921

name exogenous and endogenous sourced of DNA damage?

Answer 921

``` endogenous= free radicals, replication errors exogenous= ionising radiation, UV, alkylating agents, mutagenic chemicals, anti-cancer drugs, free radicals ```

Question 922

what is haemodynamic shock?

Answer 922

acute condition of inadequate blood flow throughout the body, decreased bp, innapropriately distributed tissue perfusion, general lack of O2 supply

Question 923

what are the 2 mechanisms of shock?

Answer 923

fall in cardiac output fall in total peripheral resistance both decrease BP

Question 924

describe the pathophysiology of cardiogenic shock?

Answer 924

acute heart failure to maintain cardiac output due to pump failure central venous pressure is normal or raised dramatic drop in arterial bp tissues poorly perfused- coronary arteries and kidneys

Question 925

waht are the causes of cardiogenic shock?

Answer 925

1) following a myocardial infarction- damage to left ventricle so cant pump out blood 2) serious arrhythmias 3) acute worsening heart failure

Question 926

why do you get small amounts of dark coloured urine in cardiogenic shock?

Answer 926

kidneys poorly perfused | reduced urine production

Question 927

what is the pathophysiology of mechanical shock?

Answer 927

cardiac tamponade= blood or fluid build up in pericardial space, comp0resses heart(fibrous sac), decreasing filling(limits EDV), affecting both sides of heart ventricles cant fill, decreased CO

Question 928

what causes mechanical shock?

Answer 928

massive pulmonary embolism

Question 929

how does a pulmonary embolism cause mechanical heart shock?

Answer 929

occludes large pulmonary artery occlusion of large pulmonary artery, increasing pulmonary arterial pressure so RV cant empty increasing central venous pressure so decreasing return of blood to left heart, decreasing filling of left heart decreases left arterial pressure- decrease BP shock

Question 930

how do you feel for ulnar nerve sensation?

Answer 930

touch along ulnar aspect/medial side of hand

Question 931

how do you feel for radial nerve sensation?

Answer 931

webspace between thumb and index on dorsum of hand- anatomical snuff box

Question 932

how do you feel for median nerve sensation?

Answer 932

finger tip of index finger

Question 933

how do you calculate heart rate?

Answer 933

HR=CO x SV

Question 934

how do you calculate blood pressure?

Answer 934

BP= CO x TPR

Question 935

how might an embolism reach the lungs?

Answer 935

deep vein thrombosis breaks off travels in venous system to right side of heart pumped out to lungs by pulmonary arteries

Question 936

describe the pathophysiology of hypovolaemic shock?

Answer 936

reduced blood volume normally due to haemorrhage, venous pressure falls, cardiac output falls(starling's law), arterial pressure falls detected by baroreceptors increases sympathetic stimulation, tachycardia and positive intropic effect(force of contraction), vasoconstriciton, venoconstriciton decreases CO

Question 937

describe frank-starlings law of the heart?

Answer 937

the more the heart fills, the more it stretches, the harder it contracts, the larger the stroke volume an increase in venous pressure will fill the heart more and therefore have a larger cardiac output INCREASE LEFT END DIASTOLIC PRESSURE INCREASES STROKE VOLUME

Question 938

what are the causes of hypovolaemic shock?

Answer 938

V for volume | decreased blood volume due to haemorrhage, sever burns or sever diarrhoea/vomitting

Question 939

how does a patient present with hypovolaemic shock?

Answer 939

tachycardia- sympathetic response weak pulse- decreased bp pale skin- peripheral vasoconstriction cold, clammy extremities- sympathetic response

Question 940

what is the compensatory response in hypovolaemic shock?

Answer 940

decreased blood pressurfe detected by baroreceptors increasing sympathetic response 1) tachycardia 2) increase intropy- force of contraction 3) peripheral vasoconstriction- venoconstriction

Question 941

describe the danger of decompensation in hypovolaemic shock?

Answer 941

``` peripheral vasoconstriction impairs tissue perfusion tissue damage due to hypoxia chemical mediator release- vasodilation TPR decreases dramatic fall in bp vital organs not perfused multi system failure ```

Question 942

describe the longer term responses to restore blood pressure in hypovalaemic shock?

Answer 942

renin-angiotensin-aldosterone system | anti-diuretic hormone

Question 943

describe distributive shock?

Answer 943

decrease in TPR low resistance shock due to excessive vasodialation

Question 944

what arfe the two causes of distributive shock?

Answer 944

toxic(septic) shock | anaphylactic shock

Question 945

describe cardiac arrest?

Answer 945

unresponsiveness associated with lack of pulse | heart has stopped

Question 946

what are the causes of cardiac arrest?

Answer 946

1) asystole- loss of electrical and mechanical activity 2) pulselessness electrical activity 3) ventricular fibrillation

Question 947

how do you treat cardiac arresst?

Answer 947

basic life support- chest compressions and external ventilation advanced life support- defibrillation, adrenaline- enhances myocardial function, increases peripheral resistance

Question 948

describe the pathophysiology of distributive shock by septic shock?

Answer 948

endotoxins released by circulating bacteria causes inflammatory response profound vasodilation dramatic fall in TPR and therefore decreased arterial pressure impaired perfusion of vital organs capillaries leaky- reduce blood volume increased coagulation and localised hypo-perfusion

Question 949

how does a patient present with septic shock?

Answer 949

infection, overwhelming inflammatory response tacchycardia due to sympathetic compensation to decrease bp warm and red extremities initially, later stages- vasoconstriction

Question 950

decribe the pathophysiology of anaphylactic shock?

Answer 950

severe allergic reaction release of histamine from mast cells- vasodilators drops arterial bp increased sympathetic response- increase CO impaired perfusion of vital organs mediators cause difficulty breathing

Question 951

how will a patient present with anaphylactic shock?

Answer 951

difficulty breathing collapsed rapid heart rate red, warm extremities

Question 952

how does a person with mechanical shock present?

Answer 952

dysponea- shortness of breath cold and clammy peripheries rapid heart rate- tachycardia

Question 953

what will happen if CD40L isnt present?

Answer 953

on t cells no CD40L only IgM produced

Question 954

what does presence of human chorionic gandotropin hormone in blood suggest?

Answer 954

malignant teratoma in testicles

Question 955

how is hodgkins lymphoma staged?

Answer 955

ann arbor staging

Question 956

what is tamoxifen used for and what are its major side effects?

Answer 956

oestrogen positive breast cancer | leads to endometrial hyperplasia

Question 957

what is the role of a her2 receptor in a normal cell?

Answer 957

growth factor receptor- receptor tyrosine kinase | proto-oncogene

Question 958

what medication is uesed for a HER2 positive tumour?

Answer 958

herceptin | attaches to her2 receptors on breast tumour cells, blocks growth signals, flags up tumour to cytotoxic t cells

Question 959

what tumour marker is present for large intestine/ GI adenocarcinomas?

Answer 959

carcinoembryonic antigen(CEA)

Question 960

what tumour marker suggests prostate malignancy?

Answer 960

prostate specific antigen (PSA)

Question 961

what tumour marker suggests malignant teratomas(testies)

Answer 961

human chronic gandotropin

Question 962

what tumour marker suggests ovarian malignancy?

Answer 962

cancer antigen 125(CA-125)

Question 963

what tumour marker suggests hepatocellular carcinoma?

Answer 963

alpha fetoprotein(AFP)

Question 964

what layers does a needle pass during a lumbar puncture?

Answer 964

``` skin subcutaneous fat supraspinous ligament interspinal ligament ligamentum flavum dura mater subdural space aracnoid mater ```

Question 965

how do you get tissue in the chest for diagnosis of malignancy?

Answer 965

if central- bronchoscope if peripheral- CT guided biopsy or take pleurafusions

Question 966

how can lung cancer be classified?

Answer 966

non small cell carcinomas(most common), either... 1) squamous cell carcinoma 2) adenocarcinoma 3) large cell carcinoma small cell carcinoma- more aggressive

Question 967

what lung malignancy molecular markers are common in non smokers?

Answer 967

ALK EGFR Ros1

Question 968

what are the different types of non small cell lung carcinomas?

Answer 968

adenomas squamous cell carcinoma lung cell carcinoma

Question 969

what mutation is most likely in smokers who have developed a non small cell lung carcinoma?

Answer 969

Kras

Question 970

mutations in oncogenes suggest what?

Answer 970

adenocarcinomas

Question 971

mutations in tumour supressor genes sugest what?

Answer 971

small cell carcinoma

Question 972

what oncogenes act as lung carcinoma molecular markers?

Answer 972

``` EGFR- transmembrane RTK detected by PCR ALK- young never smokers, RTK insulin receptors Ros1- RTK insulin receptors, crizontinib Kras- smokers, PCR detected BRAF- pcr detected ```

Question 973

what tumour suppressor gene mutation act as lung carcinoma molecular markers?

Answer 973

p53 mutations | RB1 and myc mutations

Question 974

what are the red flags for malignant melanomas?

Answer 974

abnormal shape- assymetrical | variable pigmentation

Question 975

what is the treatment for malignant melanomas?

Answer 975

systemic chemotherapy and radiation not useful need targeted therapies eg. Anti-BRAF immunotherapies eg. PDL1

Question 976

descrive how immunotherapies work?

Answer 976

tumour cells express PDL1/PDL1 cytotoxic cells also have PD1 receptor- so T cells cantg recognise tumour cells as foreign immunotherapies inhibit PD1 by binding to PD1 receptor on cancer cells(drugs have PDL) block receptor activation of host anti-tumour immune system drugs; nivolumab and atezolizumab

Question 977

how do cancer cells stay alive?

Answer 977

1) mutate proto-oncogenes to oncogenes 2) mutate tumour suppressor genes(BRCA1) 3) overexpress anti-apoptotic factors 4) inhibit pro-apoptopic signals(p53) 5) over express growth factors and receptors 6) mutate DNA repair mechanisms

Question 978

what is normal free plasma calcium concentration?

Answer 978

1.0-1.3mmol/L

Question 979

what is serum calcium levels?

Answer 979

2.2-2.26mM

Question 980

what are the 3 forms of calcium?

Answer 980

free ionized Ca2+ bound to serum proteins on anion site- albumin complexed with low Mr organic ions- citrate

Question 981

what are the 3 hormones the regulate calcium levels?

Answer 981

1 PTH- works on GI, released from cheif cells, increase Ca 2 calcitonin- works on bone, release by C cells, decrease Ca 3 Calcitriol(D3)- works on kidney, released by skin, icrease Ca

Question 982

what are the effects of PTH?

Answer 982

short term regulator to increase calcium with slight changes - GI, activates vit D and increase Ca uptakr - kidneys, decrease loss of Ca to urine, and increase resorption - bone, increase resorption(osteoclasts)

Question 983

what are the effects of calcitonin?

Answer 983

little effects on ca, try to decrease conc

Question 984

what are the effects of calcitriol?

Answer 984

long term increase of Ca - GI, increase absorbtion - kidney, increase ca resorption from urine - bone, increase resorbtion

Question 985

explain calcitriol formation?

Answer 985

cholestrol and UV forms active vitamin D3(precursor) in skin vitaamin D3 forms 25(OH)D in liver 1,25(OH)D then produced from 25(OH)D in kidney by renal C1 hydroxylase enzyme

Question 986

describe symptoms of hypercalcaemia?

Answer 986

stones- kidney stones(renal calculi) moans- depression, tiredness groans- abdominal pain, constipation

Question 987

descre severe hypercalcaemia?

Answer 987

serum calcium> 3.0mmol/L polyuria causes dehydration which then leads to lethargy, weakness, confusion and coma must rehydrate- treatment

Question 988

which cancers metatastise so the bone and cause lytic lesions and what does this cause?

Answer 988

breast, bronchus, kidney and thyroid | destruction of bone therefore hypercalcaemia

Question 989

what are the common sites fr bone metastasis?

Answer 989

vertebrae, pelvis, ribs, skull

Question 990

what are the causes of hypercalaemia?

Answer 990

- malignant osteolytic lesions from bone metastasise - multiple myeloma of lung, head and neck produce PTHrp, mimics effects of PTH - hyperparathyroidism

Question 991

what are the symptoms of hyperparathyroidism?

Answer 991

hypercalcaemia - moans, stones and groans

Question 992

describe primay and secondary hyperparathyroidism?

Answer 992

primary- one of 4 parathyroid glands develop an adenoma and secretes excess PTH, increases Ca secondary- all 4 parathyroid glands are hyperplastiv, vitamin D deficiency, decrease Ca

Question 993

explain hypercalcaemias actions on nerve impulses?

Answer 993

increase calcium, raises the threshold for nerve membrane depolarisation and therefore harder to develop an ation potential

Question 994

what is the effect of hypercalceamia on nerve impulses?

Answer 994

suppression of neural activity, lethargy, confusion and coma

Question 995

what is the effect of hypocalcaemia on nerve impulses?

Answer 995

more excitable nerves, tingling, muscle tetany and epilepsy

Question 996

describe when symptomatic hypocalcaemia is more common/cause?

Answer 996

after 6 hours of a total-thyroidectomy removal of parathyrod glands if serum calcium falls below 2.10mmol/L

Question 997

describe sensory symptoms of hypocalcaemia?

Answer 997

tingling around mouth and fingers- pins and needles

Question 998

describe motor symptoms of hypocalcaemia>

Answer 998

tetany of muscles | carpopedal spasm of hand

Question 999

descrieb the difference between osteomalacia and osteoporosis?

Answer 999

osteomalacia- rickets in children, vitamin D deficiency, normal structure bones, less mineralised, soft bones osteoporosis- structurally degraded, fully mineralised holes in bones

Question 1000

what type of hormones are calcitonin and PTH?

Answer 1000

peptide hormones

Question 1001

wjat is the function of lipoprotein lipase?

Answer 1001

on endothelial cells of blood vessels, break cobbvaelnt bonds of TAG releasing fatty acids(to tissues) and glycerol(to liver) requires ApoC-II

Question 1002

what are the 4 types of hormones?

Answer 1002

steroid hormones peptide hormones catecholamines thyroid

Question 1003

name all the fuel sources that can be used by the body?

Answer 1003

- glucose= prefered, little free glucose available - fatty acids= not in RBCs, brain and CNS, stored as TAG - amino acids= converted to glucose or ketone bodies - ketone bodies= from fatty acids, brain can use - lactate= anaerobic respiuration in muscle, cori cycle converts it back to glucose in liver

Question 1004

describe the features of metabolism up to starvation?

Answer 1004

- feed - initiallyu use glucose for fuel, make glycogen, incrwease fat sores - once glucose and fats no longer being absorbed, use glycogen stores, fatty acid release, preserve glucose for blood - no food, glycogen stores depleted, make glucose by gluconeogenesis for brain, fatty acid metabolism - starvation, fatty acid metabolism produces ketone bodies

Question 1005

name some anabolic hormones?

Answer 1005

promote fuel storage | insulin and growth hormone(protein synthesis)

Question 1006

name some catabolic hormones?

Answer 1006

promote release from stores and utilisation | glucagon, adrenaline, cortisol, growth hormone(increase lipolysis and gluconeogenesis)

Question 1007

what are anti-insulin effects of cortisol?

Answer 1007

cortisol released in starvation to prevent cells from using glucose, naming fatty acids to be preferentially metabolised

Question 1008

describe the metabolic response to starvation?

Answer 1008

decrease blood glucose levels release of cortisol and glucagon stimulates gluconeogenesis and glyconeogenolysis breakdown of protein and fat prefentially metabolism faty acids glycerol as substrat for gluconeogensis- kidneys start to contribute fatty acids for substrate of ketone bodies deplete fat stores protein used as fuel death- loss of muscle mass

Question 1009

describe 2 adaptations to starvation?

Answer 1009

brain uises ketone bodies as fuel, less glucose requirement | kidneys contribute to gluconeogenesis

Question 1010

describe why metabolic demand increases in pregnancy?

Answer 1010

mother has a net gain of 8kg | increase requirements and increasing demand of developing fetus and placenta

Question 1011

describe the two main phases of metabolic adaptation during pregnancy?

Answer 1011

anabolic phase - increase in maternal fat stores, small increase in level of insulin sensitivity, preparatory phase for increase in demand for rapid fetal growth in future catabolic phase- decreased insulin sensitivity, wincreased insulin resistance, increase in maternal glucose and free fatty acid conc, greater substrate for growth

Question 1012

what is the response to inulin in pregnancy?

Answer 1012

increase sensitivity due to progesterone and oestrogen causing hypertrophy and hyperplasia of b cells increase conc of insulin

Question 1013

describe placenta transfer?

Answer 1013

simple diffusion down conc grad | glucose as fuel transported by GLUT1

Question 1014

what is the fetal-placenta unit?

Answer 1014

fetus controls maternal metabolism endocrine unit- pestrogen and progesterone increase in importance as insulin increases anti-insulin effects(anti-insulin hormones produces) insulin/anti-insulin ratio falls

Question 1015

describe the actions of anti-insulin hormones in pregnancy?

Answer 1015

transient hyperglycaemia after meals because fo increased insulin resistance hypoglyceamia between meals/at night due to continous fetal withdrawal of glucose

Question 1016

name anti-insulin hormones?

Answer 1016

corticotropin releasing hormone human placental lactogen progesterone

Question 1017

what is gestational diabetes?

Answer 1017

pancreatic b cells do not produce sufficient insulin to meet increased requirement in late pregnancy increase in blood glucose

Question 1018

normally how does the mother adapr rp am increase requirement of insulin in pregnancy?

Answer 1018

hyperplasia and hypertrophy of b cell, increase insulin secretion to match demands

Question 1019

what are the 3 causes of gestational diabetes?

Answer 1019

1) autoantibodies similar to those in type 1 DM 2) genetic susceptibility similar to maturity onset diabetes 3) b cell dysfunction, obesity or chronic insulin resistance(majority)

Question 1020

what are complications of gestational diabetes?

Answer 1020

increase risk of miscarriage increase congenital malformation fetal macrosomia(larger body) shoulder dystocia

Question 1021

what factor is crucial in determining if a patient will develop gestational diabetes when pregnant?

Answer 1021

starting point in terms of insulin resistance before pregnancy risk factors; older ager(>25), high BMI, family history of diabetes or macrosomia

Question 1022

what is the management of gestational diabetes?

Answer 1022

insulin injections dietry modifications regular ultrasound scans

Question 1023

what is the basal metabolic rate?

Answer 1023

4kJ/min of energy

Question 1024

what contributes to daily energy expenditure?

Answer 1024

basal metabolic rate(BMR) diest induced thermogenesis(DIT) physical activity level(PAL)

Question 1025

what is the metabolic rate in a 100m sprint?

Answer 1025

200kJ/min, 30kJ total

Question 1026

what is the metabolic rate in a marothon?

Answer 1026

80kj/min, 10000kj total

Question 1027

where does energy come from in excercise?

Answer 1027

initial ATP limited stores only lasts 2 secs so must be rapidly re-synthesised creatine phosphate stores immediate energy long term supplied by glycolysis and oxidative phosphorylation

Question 1028

describe the use of muscle glycogen?

Answer 1028

in intense excercise, energy source | glycogenolysis by muscle glycogen phosphorylase glycosen to glucpse-6P to glycolysis and then into lactate

Question 1029

what is the cori cycle?

Answer 1029

``` liver egulates lactate glucose uptake (GLUT 4 and GLUT1)in muscles tranfromed to glucos in liver dor reuse ```

Question 1030

what can PCR be used for?

Answer 1030

specific single base mutations amplification of specific DNA sequence investigation of multiple base deletion mutation

Question 1031

what protein is commonly deficient in hereditary spherocytosis?

Answer 1031

ankyrin deficiency | leads to sphere shape RBC, lysis of RBC as they become less deformable, cannot squeexe between small capillaries

Question 1032

what order does a hisrtology/cytology report go in?

Answer 1032

``` clinical details macroscopic microscopic conclusion reported by: ```

Question 1033

what two things oppose clott formation?

Answer 1033

antithrombin 3 | d dimers

Question 1034

what is ventricular tachycardia?

Answer 1034

3 etopic beats in a row | can progress into ventricular fibrilation

Question 1035

which ion channel becomes inactive in cardiac myocytes in hyperkalaemia?

Answer 1035

voltage-gated sodium channels become inactive | high potassium causes a less negative membrane potential, slightly depolarised

Question 1036

what does the 4th aortic arch develop into?

Answer 1036

left- arch of aorta | right- right subclavian artery

Question 1037

what does the 6th aortic arch develop into?

Answer 1037

right and left pulmonary arteries

Question 1038

what does the 3rd aortic arch develop into?

Answer 1038

common carotids

Question 1039

how does ductus arteriosus close after birth?

Answer 1039

at first breath, increase in partial pressure of oxygen | becomes ligamentum arteriosum

Question 1040

how does foramen ovale close after birth?

Answer 1040

increase in venous return, increase in left atrium pressure, | becomes fossa ovalis

Question 1041

how does ductus venosus close after birth?

Answer 1041

umbilical chord cut, no umbilical vein flow | forms ligamentum teres

Question 1042

explain why tricuspid atresia is cyanotic?

Answer 1042

failure of tricuspid valcve to form must have a septal defect present so blood can flow between right atrium and ventricle oxygenated and deoxygenated blood mix

Question 1043

what do you give to delay the fusiomn of ductus arteriosus?

Answer 1043

prostagladins

Question 1044

when does central cyanosis occur?

Answer 1044

deoxygenated blood being pumped around the body paertial pressure in systemic circulation is low blue mucus membranes- lips

Question 1045

when does peripheral cyanosis occur?

Answer 1045

vasoconstriction- reduced perfusion | blue colouring of peripheries

Question 1046

how is sever hypertension defined?

Answer 1046

diastolic greater than 110 | or systolic greater than 180

Question 1047

what is normal heart rate?

Answer 1047

60to100 bpm

Question 1048

which leads look at the right coronary artery?

Answer 1048

anterior (V3 V4) | inferior (II, III, aVF)

Question 1049

which leads look at the left anterior descending coronary artery?

Answer 1049

septal(V1 V2)

Question 1050

which leads look at the left circumflex artery?

Answer 1050

lateral (I, aVL, V5, V6)

Question 1051

what is torsades des pointes?

Answer 1051

polymorphic ventricular tacchycardia ventricular fibrilation- QRS all look v different long QT intervals

Question 1052

what is ventricular tacchycardia?

Answer 1052

run of 3 or more consecutive ventricular ectopic beats

Question 1053

what is a mitral valve regurgitation heard as?

Answer 1053

holosystolic murmur between s1 and s2

Question 1054

what is the main cause of HFpEF?

Answer 1054

ventricular wall hypertrophy

Question 1055

describe valve insufficiency with regards to varicose veins?

Answer 1055

valve leaflets become pulled apart due to weakeness of vein walls resulting in retrograde blood flow through valve backflow of blood encourages varicose vrin formation

Question 1056

what are the complications of venous hypertension?

Answer 1056

- oedema - varicose eczema - lipodermatosclerosis - venous ulcerations

Question 1057

what causes the browny skin as a complication of varicose veins?

Answer 1057

macrophages oxidise iron from RBCs that have leaked from the blood vessels the oxidation causes iron to rust under the skin causing the brown stain

Question 1058

what is pericarditis characterized by?

Answer 1058

ST elevation in all leads | sharp, well localise, retrosternal chest pain

Question 1059

what type of shock does cardiac temponade cause?

Answer 1059

mechanical shock- heart cant fill

Question 1060

what are the main symptoms seen in anaphylactic shock?

Answer 1060

warm extremities, tachycardia, difficult breathing

Question 1061

how many kilojoules is there in one kilocalorie?

Answer 1061

4.2kJ

Question 1062

what is creatinine used to measure?

Answer 1062

released at constant rate when creatine phosphate is used by muscles for energy can be used to measure muscle mass and GFR- filtration rate of kidney

Question 1063

what is classified as obese?

Answer 1063

BMI over 30kg/m2

Question 1064

what is gibbs free energy change?

Answer 1064

energy change under standard conditions to form 1 mole of product, at 1 atm, 1mol conc and 273K

Question 1065

what causes secondary lactase deficiency?

Answer 1065

damage to small intestine

Question 1066

which reactions in glycolysis are irreversible?

Answer 1066

1, 3, 10

Question 1067

why are homocystinurea and marfans syndorme similar and different?

Answer 1067

homocystinurea- can be detected on a heel prick test | both present with skeletal deformities, connective tissue defects, and lens dislocation

Question 1068

describe the molecular basis for refeeding syndrome?

Answer 1068

enzymes in urea cycle have been down regulated in times of low protein intake so sudden high protein intake overwhelms them, ammonia build up, ammonia toxicity ammonia interferes with krebs cycle, blood brain barrier, pH in high concentrattions and protein synthesis

Question 1069

what signs and symptoms would you expect to see in a baby who has Von Ghierke's disease?

Answer 1069

protuberant abdomen due to hepatomegaly- gycogen cant be broken down in liver sweating and pallor relieved by feeding due to hypoglyceamia- glycogen not broken down to give glucose high blood fatty acid levels- gluconeogenesis

Question 1070

what classifies life threatening hypothermia?

Answer 1070

temp less than 28 degrees

Question 1071

what is the cause of multiple sclerosis?

Answer 1071

autoimmune degeneration of myelin in CNS axons probably against EBV loss of conduction velocity

Question 1072

If a patient has high cortisol, elevated ACTH, not supressed by high dose dexamethasone?

Answer 1072

ectopic tumours producing ACTH

Question 1073

if a patient has high cortisol, elevated ACTH, supressed by high dose dexamethasone?

Answer 1073

Cushings disease, benign pituatary adenoma secreting ACTH

Question 1074

if a patient has supressed ACTH, high cortisol and is taking glucocorticoids?

Answer 1074

exogenous cushings due to glucocorticoids

Question 1075

what do glucocorticoids do?

Answer 1075

steroids prescribed in asthma, inflammatory bowel disease, rheumatoid arthritis can cause cushings, high cortisol

Question 1076

if a patient has supressed ACTH, high cortisol and is not taking glucocorticoids?

Answer 1076

adrenal tumour produces cortisol- cushings syndrome

Question 1077

what haematological abnormality will be seen chronic alcohol dependence develops cirrhosis?

Answer 1077

thrombocytopenia, due to liver disease, splenomegaly and increased splenic pooling, reduced thrombopoetin production

Question 1078

why would you prescribe penicillin to a patient with sickle cell disease?

Answer 1078

to compensate for hyposplenism, spleen undergos atrophy due to vaso-occlusion as sickle cells block capillaries, ischaemia, infections to encapsulated bacteria

Question 1079

which endocrine gland secretes melatonin and what does it do?

Answer 1079

released from pineal gland | biological clock, helps with sleep, causes jet lag

Question 1080

what is commonly seen in a blood film og aqquired microangiopathic haemolytic anaemia eg. DIC?

Answer 1080

schistocytes | sheer stress, mechanical damage

Question 1081

what are 4 complications of hereditary spherocytosis?

Answer 1081

1 megaloblastic anaemia 2 aplastic criss 3 haemolytic crisis 4 pigmented gall stones

Question 1082

what are signs of DIC?

Answer 1082

``` nucleated RBCs blood cell fragments- schistocytes low platelets raised D dimers low fibrinogen ```

Question 1083

whzat is the term used to describe wide variation in size of erythrocytes?

Answer 1083

anisocytosis

Question 1084

what would be seen with dietry idodine deficiency?

Answer 1084

low T3 and T4 increased TSH goitre

Question 1085

what are symotoms of thalassaemia?

Answer 1085

hypochromic and microcytic RBCs anisopoikilocytosis(variation in size and shape of RBCs), frequent target cells# iron overload microcytic anaemia extramedullary haemopoeisis- splenomegaly, hepatomegaly, bone marrow widens jaundice

Question 1086

describe the steps of insulin synthesis?

Answer 1086

``` pre -proinsulin cleaved proinsulin folding in ER- align cysteine residues and disulphide bridge formation transport to golgi packaged into vesicles removal of c peptide, proteolysis ```

Question 1087

what can c peptide be used for clinically?

Answer 1087

released with insulin in equimolar amounts, can monitor endogenous insulin secretion

Question 1088

what would a patient with aldosterone secreting adrenal adenoma develop?

Answer 1088

mineralcorticoid excess, hypokalaemia upregulates Na/K/Atpase potasium out

Question 1089

what is the actiojn of carbimazole?

Answer 1089

treats graves disease inhibits thyroid peroxidase activity, dont idodinate tyrosines on thryoglobulin side effect- agranulocytosis

Question 1090

what is the net effect of parathyroid hormone on calcium and phosphate concentration?

Answer 1090

increased calcium conc, decreased phospjhate conc

Question 1091

what is feltys syndrome?

Answer 1091

neutropenia splenomegaly rheumatoid arthritis

Question 1092

what skin condition is seen with sever thrombocytopenia?

Answer 1092

petechaie

Question 1093

how is iron excess dangerous?

Answer 1093

promotes insoluble haemosiderin deposits in organs iron cant be excreted- iron exceeds binding capacity of transferrin iron promotes free radical formation- hydroxy and hydroperoxyl radicals cause damage by 1 lipid peroxidation, 2 damage to proteins, 3 damage to DNA

Question 1094

whats cushings reflex?

Answer 1094

rigid cavity, when there is increased intercranial pressure, impaired cerebral blood flow, increase sympahatic vasomotor activity - increases arterial BP - reflux bradychardiaa - irregular respiration

Question 1095

what symptoms and complicationas are seen with hereditary haemochromarosis?

Answer 1095

liver cirrhosis, diabetes mellitus, hypogonadism, cardiomyopathy, athropathy, increased skin pigmentation-brown skin elevated iron

Question 1096

what symptoms and complications are seen with transfusion associated haemosiderosis?

Answer 1096

liver cirrhosis, diabetes mellitus, hypogonadism, cardiomyopathy, athropathy, slate grey colour

Question 1097

what would be found in the liver function test of someone with acute liver failure?

Answer 1097

increased plasma AST and ALT | ALT and AST normally found at high conc in liver, increased plasma conc as enzymes leak our due to damage

Question 1098

what tumour can u absolutely not treat with surgery?

Answer 1098

prolactinoma

Question 1099

what drug is used to treat chronic myeloid leukaemia?

Answer 1099

tyrosine kinase inhibitor- imatinib

Question 1100

what vitamin supplement is given to a child with homocystinuria?

Answer 1100

vitamin B6 | deficient in cystathione beta synthase, cant metabolise methanione

Question 1101

what mode of drug action is metformin?

Answer 1101

decreases gluconeodenesis- lowers plasma glucose in tyoe 2 diabetes

Question 1102

what is a severe complication of marfans syndrome?

Answer 1102

aortic aneurysms

Question 1103

what foot condition is common in children?

Answer 1103

pes planus- flat feet

Question 1104

what is hallux valgus??

Answer 1104

medial deviation of 1st metacarpal joint and lateral deviation of halux

Question 1105

whats the function of bands of bunger?

Answer 1105

guide direction of axon regeneration

Question 1106

what is the most common tibial fracture?

Answer 1106

lateral tibial chondyle | anterior cruciate ligament

Question 1107

what test is used to assess the posterior cruciate ligament?

Answer 1107

drawers test

Question 1108

which ligament tear in your knee is most likely to give a popping sensation?

Answer 1108

cruciate ligaments

Question 1109

what deformity is common in a distal femoral fracture?

Answer 1109

distal fragment of the femoral shaft is pulled in to a varus deformity because of the adductors and gastrocenmius

Question 1110

why does a femoral shaft fracture present as swelling of thigh?

Answer 1110

blood vessels disrrupted, bleeding causing inflammation

Question 1111

what ligament does the lateral cutaneous nerve pierce?

Answer 1111

inguinal ligament

Question 1112

what is meralgia paresthetica?

Answer 1112

compression of lateral femoral cutaneous nerve

Question 1113

how does a NOF fracture present?

Answer 1113

adducted, shortened, internally rotated leg

Question 1114

what nerve is prone to damage in a posterior hip dislocation?

Answer 1114

sciatic nerve

Question 1115

where does referred pain of OA of hip present?

Answer 1115

knee

Question 1116

what fracture of femur is more common in women?

Answer 1116

intracapsular fracture, due to osteoporosis

Question 1117

what is spondylosis?

Answer 1117

osteoarthritis of intervertebral discs of cervical and lumbar spine

Question 1118

how does thalasseamia present on a blood film?

Answer 1118

hypochromic and microcytic red blood cells

Question 1119

why do you get splenomegaly in haemolytic anaemias?

Answer 1119

overworked spleen, breaks down RBCs fast

Question 1120

how does haemolytic anaemia occur in DIC?

Answer 1120

cells sheared on fibrin strands- microangiopathic anaemia

Question 1121

why are lay beliefs important?

Answer 1121

- understanding doctor-patient interactions - insight into lay coceptulisation, patients compliance and health seeking behaviours - better understand peoples deas bout health maintenace and disease prevention - why patients make certain decisisons

Question 1122

how do neutrophils leave blood vessles?

Answer 1122

degrade endothelial basement layer

Question 1123

when would endometrial hyperplasia become a problem?

Answer 1123

oestrogen acts unaposed.. - obest- androgens converted to oestrogen in adipose - tamoxifen use- SERM used after oestrogen positive breast cancer, antagonist of oestrogen in breast but agonist in endometrium - oestrogen secreting ovarian tumour

Question 1124

when would you measure jugular venous pressure?

Answer 1124

right sided heart failure

Question 1125

what are risk factors of cardiovascular disease?

Answer 1125

``` hypertension diabetes alcohol smoking obesity family history smoking inactivity ```

Question 1126

how do you measure bp?

Answer 1126

``` cuff above elbow sat comfortably in cubital fossa- brachial artery first korotkoff sound- systolic bp last korotkoff sound- diastolic bp ```

Question 1127

identify 2 common causes of aortic valve stenosis?

Answer 1127

congenital abnormality | rheumatoid fever

Question 1128

what disease can be diagnosed with the heel prick test?

Answer 1128

``` phenylketonuria(PKU) sickle cell disease congenital hypothyroidism cystic fibrosis median chain acetyl coA dehydrogenase deficiency ```

Question 1129

what must be given immediately after paracetamol overdose?

Answer 1129

acetylcysteine

Question 1130

how do free radical scavengers act as anti-oxidants?

Answer 1130

vitamin c and e | donate a hydrogen atom and its free electron to free radical in a non enzymatic reaction

Question 1131

what type of calcification can occur in athlerosclerotic plaques?

Answer 1131

dystophic calcification in the complicated plaque

Question 1132

what are the different types of calcification?

Answer 1132

dystrophic- localised in dying tissue, in atherosclerosis | metastatic- due to hypercalcaemia, generalised

Question 1133

what cellular accumulations are associated with alcohol hepatitis?

Answer 1133

mallorys hyaline

Question 1134

what cellular accumulations are associated with emphysema?

Answer 1134

uninhibited proteases

Question 1135

what cellular accumulation are associated with hereditary haemochromatosis?

Answer 1135

haemosiderin in organs- excess iron deposits

Question 1136

name the 3 types cell TB granuloma?

Answer 1136

langhans giant cells, lymphocytes, eptheloid histiocytes(macrophages)

Question 1137

what cancers do cytokeratins CK7+/CK20- indicate?

Answer 1137

tumour originated from lung, bowel, endometrium, ovary or thyroid

Question 1138

what cancers do cytokeratins CK7-/CK20+ indicate?

Answer 1138

tumour originated from large bowel, gastric carcinomas

Question 1139

what are the principal targets of cell injury?

Answer 1139

mitrochondria, proteins, nucleus, cell membranes

Question 1140

what is the key investigation for dianosing CES?

Answer 1140

whole spinal chord MRI

Question 1141

what are the investigation for diagnosing CES?

Answer 1141

whole spinal chord MRI rectal exam bladder scan

Question 1142

what are 4 consequences of undiagnosed Cauda equina syndrome?

Answer 1142

``` urinary incontinence loss of sensation of lower limb weak muscle movements in leg impetence- permanent erectile dyfuncton chronic pain ```

Question 1143

describe the difference between prokaryotes and eukaryotes?

Answer 1143

prokaryotes- one circular DNA plasmid, single strand free DNA, present cell wall, no carbohydrates in plasma membrane, 70s qribosome eukaryotes- many chromosomes, membrane bound nuclear envelope, abscent cell wall, carbohydrates in plasma membrane, 80S ribosomes

Question 1144

what colour does gram positive bacteria stain and why?

Answer 1144

purple- retain idoine | peptideoglycans in cell wall

Question 1145

explain ways that allow normal commensal flora to becom pathogenic?

Answer 1145

displacement from normal location to sterile areas normal flora overgrows if immunocomprimised normal flora can be depleted in antibiotic therapy

Question 1146

what is the role of opsonins?

Answer 1146

bind to microbial surfaces, allow enhanced attachment of phagocytes and clearance of microbes, increase recognition

Question 1147

give 3 systemic actions of macrophage derived cytokines (IL1/6)

Answer 1147

1 neutrophil mobilisation 2 hypothalamus increase body temp 3 increase CRP production in liver

Question 1148

what do proprioreceptors do?

Answer 1148

detect movement chaqnges

Question 1149

what is phaechromocytoma?

Answer 1149

tumour of the chromaffin cells in adrenal gland associated with hypertension secretes catecholamines

Question 1150

what is the mechanism of cell injury to hypoxia?

Answer 1150

1 cell deprived of oxygen 2 ATP production stops, glycolysis allows cells to keep going for a short while 3 membrane pumps stop working, so sodium and water seep into cell 4 cell swells 5 cell initiates stress response 6 PH drops due to lactic actic 7 calcium enters the cell and activated phospholipase, proteases, ATPase, endonucleases 8 organelles swell 9 enzymes leak out and attack cells 10 membrane starts to show blebbing 11 cell dies

Question 1151

what is antibiotic cross sensitivity?

Answer 1151

a hypersensitivity reaction to an antibiotic that is similar in structure to an antibiotic with a known allergy

Question 1152

how do free radicals damage cells?

Answer 1152

cross linking proteins breaking strands of DNA oxidation of membrane lipids

Question 1153

what is an effective way to treat an abcess?

Answer 1153

surgically, incision and drainage

Question 1154

which process in the cellular phase of acute inflammation requires energy?

Answer 1154

emigration of neutrophils is an active process

Question 1155

what is a sarcoma and how do they usually travel?

Answer 1155

stromal/connective tissue cell malignancy | via blood stream

Question 1156

what is a carcinoma and how do they iusually travel?

Answer 1156

epithelial cell malignancy | via lymphatics

Question 1157

what is an example of an ectopic tumour producing ACTH?

Answer 1157

small cell lung carcinoma | can lead to cushings syndrome

Question 1158

what is a retropharyngeal space infection usually secondary too?

Answer 1158

an upper respiratory tract infection

Question 1159

who is most common to get a retropharyngeal space infection?

Answer 1159

children, under the age of 5 | can develop into an abscess

Question 1160

what does a retropharyngeal abscess usually present as?

Answer 1160

``` visible buldge on oropharynx sore throat difficulty swallowing stridor reluctant to move neck high temp ```

Question 1161

why do we ask a patient to swallow if they have goitre?

Answer 1161

to localise the pathology to the thyroid gland | thyroid gland, hyoid bone and larynx move up when you swallow

Question 1162

why can goitre occu retrosternally?

Answer 1162

lower limit of the pretracheal fascoia extends into the thorax

Question 1163

what occurs in retrosternal extension of goitre?

Answer 1163

compression od strucutres | breathlessness, stridor, fascial oedema

Question 1164

whats the most common non traumatic cause of facial paralysis?

Answer 1164

inflammation of the facial nerve- Bells palsy

Question 1165

what is the most common cause of a neck lump?

Answer 1165

a swollen lymph node secondary to an infection