Body Log

Question 1

Dehydration

Causes
Mode of action
Symptoms
Treatment

Answer 1

Causes: Hot humid weather, excessive sweating, vomiting, diarrhoea, burns

Mode of action: water loss causes increase in osmolarity and increase in ADH. This decreases plasma volume

Symptoms: olliguria, thirst, dryness

Treatment: fluids

Question 2

Oedema

What is it
Mode of action
Causes

Answer 2

Fluid retention, used to be called dropsy

MOA: hydrostatic pressure being more than osmotic pressure = water moves into interstitial space as there is presence of plasma proteins

Caused by damaged/ blocked lymphatics,

Question 3

Hyperthyroidism

What is it
Levels of antibodies

Answer 3

High levels of T3 or T4

Low TSH

Question 4

Hypothyroidism
What is it
Levels of hormones

Answer 4

Low T3 and T4

High TSH

Question 5

Parathyroid disease

What is it
Symptoms

Answer 5

Over production of PTH from a parathyroid tumour leading to high blood calcium

Causes symptoms of the brain, muscles and bones

Question 6

Liver fibrosis

Pathophysiology

Answer 6

Hepatic stellate cells lose their vitamin A storage capability and differentiation into myofibroblasts

Myofibroblasts synthesis and deposit collagen within the peri sinusoid always space resulting in liver fibrosis

Question 7

In which diseases are ANP and BNP released?

Answer 7

ANP- atrial natriuretic peptide released by atria
BNP- brain-type natriuretic peptide realised by ventricles

Left ventricular hypertrophy, mitral valve (BNP)
Congestive heart failure (ANP)

Question 8

Scurvy

Answer 8

Vitamin C deficiency

Prolyl hydroxylase cannot convert proline to hydroxyproline = reduced H bonds, less crosslinks, weakened structure

Signs and symptoms:
Gum disease
Bruising of skin
Poor wound healing
Bleeding

Question 9

Ectopic pregnancy

Answer 9

Implantation of embryo in Fallopian tube leads to rupture of tube= miscarriage and haemorrhage

Question 10

Placenta praevia

Answer 10

Implantation of embryo in lower segment of the uterine wall placenta blocks cervix
C-section required due to risk of haemorrhage

Question 11

Marfan’s syndrome

Answer 11

Autosomal dominant

Misfolding of fibrillin 1 gene leading to abnormal elastic connective tissue

Signs: very tall, long digits (arachnodactly), high arched palate, joint dislocation

Life expectancy: death round 40 years from aortic rupture (arteries too elastic causing catastrophic haemorrhage)

Question 12

Ellen’s-Danlos disease

Answer 12

Type 3 collagen deficiency leading to loss of structure

Presents as stretchy skin, unstable joints, easy bruising

Question 13

Allopecia areata/universalis

Answer 13

Autoimmune destruction of hair follicles

Can occur anywhere and everywhere

Worsened by stress

Psychosocial problems particularly for women

Question 14

Vitiligo

Answer 14

Autoimmune destruction of melanocytes leads to depigmentation

Psychosocial problems for dark-skinned people ( not very noticeable on fair skin)

Question 15

Psoriasis

Answer 15

Extreme overproduction of skin cells leading

Treat with steroids

Question 16

Malignant melonma

Answer 16

Aggressive skin cancer caused (usually) by excessive UV radiation causing mutations in the melanocytes

If UV penetrates the basement membrane - it metastasises (e.g. brain and liver) poor prognosis

Relatively rare in dark skinned races as melanin protects against UV radiation (evolutionary advantage)

Question 17

Osteogenesis imperfecta

Answer 17

Autosomal dominant
Type 1 collagen deformity/deficiency= COL1A gene mutation
major component in ground substance of bone

Severe cases: no conversion of foetal hyaline skeleton= incompatible with life

Most cases: repeated fractures lead to bowed long bones
Hearing loss
Short stature
Hypermobility (loose joints) and flat or arched feet
Poor teeth development
Blue sclera due to unknown cause- possibly thinning of cornea due to issues with collage that forms it

Question 18

Rickets

Answer 18

Vitamins D deficiency - not enough sunlight, dietary deficits or decreased ability to convert it
= less absorption of calcium by small bowl causing less rigid bones

Rickets in kids: bowed bones as there are still growing ( epiphyseal growth plates not yet closed after puberty), wears bones, ineffective mineralisation

Question 19

Achondroplasia

Answer 19

Autosomal dominant
Deformed fibroblast growth factor - mutation in FGF3 receptor gene leads to decreased endochondral ossification as FGF promotes collagen formation from cartilage
= short limbs, enlarged forehead, normal trunk

Question 20

Myasthenia Gravis

Answer 20

Autoimmune destruction of end plate ACh receptors by antibodies = reduced synaptic transmission- reduced endplate invaginations in synaptic clefts

30% reduction in receptor number sufficient for symptoms

Ptosis (drippy eyelids), fatigue, sudden collapse, intermittent muscle weakness

Treatment: immunosuppressive, AChE inhibitors

Question 21

Botulism

Answer 21

Botulinum toxin blocks ACh release at motor end plate-= non-contractile state of skeletal muscle- no muscle contraction

Stops facial muscle contraction preventing wrinkles
Treats muscle spasms (e.g cervical dystonia)

Question 22

Hypoparathyrodism

Answer 22

Lack of PTH= lack of calcium absorption= seizures

Question 23

Multiple sclerosis

Answer 23

Autoimmune destruction of myelin sheath and Schwann cells = decrease in conduction- loss of function

Treatment: B interferon or steroids

Question 24

Compartment syndrome

Answer 24

Trauma in one compartment could cause internal bleeding which exerts pressure on blood vessels and nerves

=deep constant poorly localised pain aggravated by passive stretch of muscle group
Paresthaesia (altered sensation)
Compartment feels tense and firm
Swollen shiny skin, sometimes obvious bruising
Prolonged capillary refill time

Treatment: fasciotomy subsequently skin graft

Question 25

Muscle hypertrophy

Answer 25

Overstretching- A and I bands can no longer re-engage | = new muscle fibrils are produced, new sacromere are added in the middle of the existing sacromeres

Question 26

Duchess muscular dystrophy

Answer 26

Most common muscular dystrophy X link recessive Mutation of dystrophin gene = excess calcium to enter muscle cell - calcium taken up my mitochondria - Water taken with it= mitochondria burst - muscles cells burst (rhabdomyolysis) - creatine kinase and myoglobin levels are extremely high in the blood Multiple skeletal muscle related symptoms and sings Muscle cells replace by adipose tissue

Question 27

Organophosphate poisoning

Answer 27

Inhibits the normal function of AChE= ACh activity at NMJ is potentiated ``` Multiple signs and symptoms Muscarinic symptoms S-Salivation L-lacrimation U-urination D- defecation G-GI cramping E-Emesis ``` ``` Nicotinic M- Muscle cramps T- tachycardia W-weakness T-twitching F-fasciculations ```

Question 28

Osteoarthritis

Answer 28

Age related Degeneration Mechanical failure of the articular cartilage- narrowing of the joint space- bone rubs against bone

Question 29

Rheumatoid Arthritis

Answer 29

Autoimmune disease Inflammation of synovial membrane = thickening of the joint capsule Subsequent damage to underlying bone and articular cartilage - both bone and cartilage disintegrate

Question 30

Osteoarthritic knee joint

Answer 30

Degeneration of the cartilage Narrowing of the joint space Growth of bony spurs (osteophytes)- causes inflammation and pain

Question 31

Osteomalacia

Answer 31

Osteomalacia: | Vitamins D deficiency = lower mineralisation, increased osteoid

Question 32

Osteoporosis

Answer 32

``` Primary type 1 (menopausal)- oestrogen no long mediating osteoclast function Type 2: old age- loss of osteoblast function- no remodelling, loss of oestrogen and androgen ``` secondary: Result of drug therapy Processes affect bone remodelling Metabolic bone diseases ( e.g. hyperparathyrodism) Risk factors: Insufficient calcium intake Lack of exercise Cigarette smoking

Question 33

Sentinel lymph nodes

Answer 33

First node to receive lymph form primary tumour Cancer cells travel through newly produced vasculature, interstitial space and lymph =swelling of lymph nodes

Question 34

Primary Lymphodema diseases

Answer 34

Congenital (Milroy’s disease) On sent within two years CauseL mutated FLT4 gene (VEGF-r) Small or missing endothelial cells in vessel wall Praecox (Meige’s disease) Onset: 2-35 years (familial: 1 in 3) Cause: currently unknown Tarda Onset after 35 years Cause currently unknown

Question 35

Secondary lymphoedema

Answer 35

Neoplasia Pelvic masses Infiltration of lymph node Surgery Node involvement Accidental Radiotherapy Nodal fibrosis- obstruction of vessel Autoimmune diease Rheumatoid arthritis Ezcema Infection Cellulitis - obstruction of vessel Filariasis- parasitic worm that invades and surveys in the lymphatic vessels

Question 36

Psoriasis

Answer 36

Extreme overproduction of skin cells- transit time is reduced= stratum corneum is produced in abundance as silvery scales every 2-3 days Treat with steroids

Question 37

hyperkertosis

Answer 37

Too much keratin put on the surface of skin (especially on the hands and feet)

Question 38

Multiple sclerosis

Answer 38

autoimmune destruction of myelin sheath and Schwann cells= decrease in conduction leading to loss of function Symptoms: fatigue, vision problems (diplopia), slurred speech (dysarthria), numbness and tingling sensations (paraesthesia), mobility issues (muscle spasms), urinary retention, constipation treat with B interferon or steroids