OLT 1-3

Question 1

Function of muscle

Answer 1

• Motion of the body
• Movement of substances in the body
• Regulating organ volume
• Stabilising body position
• Thermogenesis

Question 2

Types of muscle

Answer 2

Cardiac
Smooth
Skeletal

Question 3

what is cardiac muscle

Answer 3

Cardiac muscle tissue forms most of the wall of the heart. It is striated and involuntary.
Cardiac muscle is branched
Allows conduction of electricity in multiple directions rapidly

Question 4

features of cardiac muscle

Answer 4

nucleus, branching cell and intercalated disc

Question 5

what is smooth muscle

Answer 5

Smooth muscle tissue is located in viscera. It is nonstriated and involuntary.
An example of smooth muscle are muscles in the respiratory tract that control broncho-constriction / dilation

Question 6

what is skeletal muscle

Answer 6

Skeletal muscle tissue is mostly attached to bones. It is striated and voluntary.
Responsible for body movement

Question 7

Skeletal muscle is covered by what three layers

Answer 7

◦ Epimysium, perimysium and endomysium

◦ These layers form tendons

Question 8

types of myscle fibres

Answer 8

• Slow Oxidative fibres (Red)- contract slow, resistant to tireing
• Fast Oxidative-glycolytic fibres- also red, can generate energy in addition to mitochondria= ability to maintain exercise for longer
• Fast Glycolytic fibers (White)- most powerful and rapid contractions, cant hold onto oxygen as much

Question 9

Effect of aerobic exercise on muscles

Answer 9

Exercise alters the size and ability of muscles
 Aerobic exercise:
 Greater resistance to fatigue
 Muscle cells form more mitochondria (store more oxygen)
 Improved digestion & elimination
 Cardiac hypertrophy

Question 10

Effect of resistance (isometric) exercise on muscles

Answer 10

Exercise alters the size and ability of muscles
 Resistance (isometric) exercise:
 Strong contraction against resistance
 Muscle enlarges – individual cells make more contractile elements

Question 11

types of Joints

Answer 11

◦ Nonsynovial or synovial joints
◦ Cartilage
◦ Ligament
◦ Bursa

Question 12

skeletal muscle movements

Answer 12

flexion-  bending at a joint anterior to the body
extension- straightening the joint towards the body
abduction- movement away from the midline
adduction- movement towards the midline
pronation
supination
circumduction
rotation
protraction
retraction
elevation
depression

Question 13

Examples of abnormalities of the Spine

Answer 13

Scoliosis

Herniated nucleus pulposus

Question 14

Common Congenital or Paediatric Abnormalities of the muscoskeletal system

Answer 14

 Congenital dislocated hip
 Talipes equinovarus (clubfoot)
 Spina bifida
 Coxa plana (Legg-Calvé-Perthes syndrome)

Question 15

joints of the shoulder

Answer 15

Glenohumeral joint
Rotator cuff (muscles and tendon )
Subacromial bursa
Acromion process
Greater tubercle of the humerus

Question 16

Abnormalities of the Shoulder joint

Answer 16

Atrophy
 	Dislocated shoulder
◦	Hunching of the shoulder forwards 
 	Joint effusion
 	Tear of the rotator cuff
 	Frozen shoulder—adhesive capsulitis
Subacromial bursitis

Question 17

Elbow joints

Answer 17

◦ Medial and lateral epicondyles

Question 18

Abnormalities of the Elbow

Answer 18

Olecranon bursitis
 	Gouty arthritis
 	Subcutaneous nodules
 	Epicondylitis—tennis elbow
◦	Lateral 
◦	Radiates down extensor surface

Question 19

joints of the wrist

Answer 19

Radiocarpal joint
Midcarpal joint
Metacarpophalangeal joints
Interphalangeal joints

Question 20

Abnormalities of the Wrist and Hand

Answer 20

• Ganglion cyst
• Colles’ fracture
• Carpal tunnel syndrome- pinched nerve
• Ankylosis- abnormal stiffening of joint
• Dupuytren’s contracture-
• Swan-neck and boutonniere deformities
• Ulnar deviation or drift
• Degenerative joint disease or osteoarthritis
• Acute rheumatoid arthritis

Question 21

Hip Joints

Answer 21

Acetabulum and head of femur
Anterior superior iliac spine
Ischial tuberosity
Greater trochanter of femur

Question 22

Landmarks of the Knee

Answer 22

Femur, tibia and patella
Suprapatellar pouch
Medial and lateral menisci
Cruciate ligaments
Prepatellar bursa
Quadriceps muscle

Question 23

Ankle and Foot joints

Answer 23

Tibiotalar joint
Medial and lateral
malleolus
Metatarsals

Question 24

Abnormalities of the Knee

Answer 24

	Mild synovitis
	Prepatellar bursitis
	Swelling of menisci
	Osgood-Schlatter disease
	Chondromalacia patellae

Question 25

Abnormalities of the Ankle and Foot

Answer 25

```  Achilles tenosynovitis  Chronic/acute gout  Hallux vagus with bunion and hammer toes  Callus  Plantar wart  Ingrown toenail ```

Question 26

Abnormalities Affecting Multiple Joints

Answer 26

``` Inflammatory conditions ◦ Rheumatoid arthritis ◦ Ankylosing spondylitis Degenerative conditions ◦ Osteoarthritis (degenerative joint disease) ◦ Osteoporosis ```

Question 27

what is scoliosis

Answer 27

Lateral curvature of the spine

Question 28

how to assess for spinal abnormalities

Answer 28

 Feel  Midline spinous processes T1 – T12  L4/5 most common site of problems  Exact site of any tenderness - bony or muscular  Move  Can patient twist around to look at you?  Flexion, extension & lateral flexion assess flexion, extension and lateral flexion

Question 29

how to assess for pelvic abnormalities

Answer 29

```  Look  Stance  Shortening?  Muscle wasting?  Feel  Tenderness – muscular e.g. strain of hamstrings  Move ```

Question 30

how to assess for abnormalities of the knees

Answer 30

Look  Effusion ( collection of fluid in joint)  Erythema  Deformity ``` Feel  Heat  Crepitus  Patellar movement  ? Ripple test ``` Move  McMurrays test- tests medial meniscus  Drawer test

Question 31

what is the mcmurray test

Answer 31

examiner applies one hand at knee along medial meniscus examiners other hand holds the foot and ankle externally rotate the foot and apply valgus stress at the knee slowly extend the knee

Question 32

what is the anterior drawer test

Answer 32

examiner srasps upper calf with both hands. fingers clasped behind the calf. both thumbs on the tibial plateau region. examiner pulls the tibia anteriorly in a sudden firm forward motion assess for laxity compare to laxity with the opposite knee

Question 33

how to assess for abnormalities of the ankles

Answer 33

``` Look  Swelling, deformity, erythema, bruising Feel  Ottawa ankle rules  Heat Move  Active, passive, resisted ```

Question 34

how to assess archilles tendon injury

Answer 34

```  “…felt like being shot…”  “…heard a snap and looked around…”  Minimal pain  May be a palpable gap  Active plantar flexion still possible  Thomson Test ```

Question 35

How to assess for abnormalities of the feet

Answer 35

``` Look  Swelling, deformity, erythema, bruising  Lymphangitis, wounds,  Toenails Feel  Ottawa ankle rules Move ```

Question 36

how to assess for head musculoskeletal injury

Answer 36

 Ears - ? Tophus  Eyes…?!  ‘Dry eyes’ - keratoconjunctivtis ```  Manidible Look  Symmetry  Swelling / deformity Feel  Tenderness – be specific – bony or soft tissue Movement ```

Question 37

how to assess for musculoskeletal injury of the neck

Answer 37

``` Look  Posture of head  Deformity? Feel  Tenderness – midline or soft tissue  Paraspinal area, trapezius, interscapular area Move  Flexion / extension  Rotation  Lateral flexion ```

Question 38

how to assess for musculoskeletal injury of the shoulder

Answer 38

``` Look  Normal deltoid contour?  Bruising / swelling Feel  Tenderness  Crepitus  Heat Move  Flexion, extension  Internal / external rotation  Abduction / Adduction ```

Question 39

how to assess for musculoskeletal injury of the elbow

Answer 39

```  Look  Deformity, swelling, redness  Feel  Tenderness, crepitus Move  Flexion / extension  Supination / pronation ```

Question 40

how to assess for musculoskeletal injury of the hand/ wrist

Answer 40

``` Look  Colour change  Swelling / deformity  Heberdens / Bouchards nodes?  Wounds / scars Feel  Tenderness  Parasthesia – constant / intermittent Move  Loss of function  Full grip  Pincer grip ```

Question 41

History taking specific to musculoskeletal system.

Answer 41

```  Presenting complaint  Past history – co-morbid factors  Past and current medication / drug use  Family and genetic history  Occupational, environmental and social history ```

Question 42

how to assess presenting musculoskeletal complaints

Answer 42

```  Pain? – site, nature, radiation, timing, etc.  Swelling / warmth  Stiffness  Locking  Time since onset  Mechanism of injury?  Other symptoms… ```

Question 43

how to assess past history in musculoskeletal assessment

Answer 43

 Previous trauma  Previous incident of same complaint  Co-morbid factors – psoriasis, diabetes, stroke, obesity, gout…  Drug History

Question 44

what family and genetic history to assess for in musculoskeletal assessment

Answer 44

 Osteoarthritis, osteoporosis, gout, and some cases rheumatoid arthritis are hereditary.  Osteogenesis imperfecta  Marfans syndrome

Question 45

Occupational, environmental and social history ( musculoskeletal assessment)

Answer 45

Occupational, environmental and social history

Question 46

musculoskeletal assessment- principles of examination

Answer 46

 General appearance  Cause no additional pain  Comparison of opposite sides  Examine joint proximal and distal to injury  Use standard terminology in describing positions and movement  Movements are always described from neutral position  LOOK  FEEL  MOVE

Question 47

Common Musculoskeletal Disorders

Answer 47

* Osteoporosis * Gout * Arthritis – O/A R/A

Question 48

structures in the long bone

Answer 48

cancellous bone, proximal epiphysis, articular cartilage, epiphyeal line, periosteum, compact bone, medullary cavity, diaphysis, distal epiphysis

Question 49

what do OsteoBlasts do

Answer 49

* Form bone, but cannot divide by mitosis. * Secrete collagen & other organic compounds * needed to build osseous tissue.

Question 50

what are osteocytes

Answer 50

• Prinicipal cells of bone tissue | No longer build bone

Question 51

what do osteoclasts do

Answer 51

• Settle on surface of matrix and responsible for resorbtion

Question 52

what is bone remodelling

Answer 52

* Bone is active and undergoes continual renewal * Osteoclasts responsible for bone resorbtion * Osteoblasts responsible for laying down new bone * Need to be in balance so that bone is continually renewed or remodelled * Parathyroid hormone, Calcitonin, Calcium levels and Vitamin D play a part in bone remodelling * Balance alters with age and osteoclasts outnumber osteoblasts as we age * Bones become more brittle * Imbalances result in increased loss of bone mass ( osteoporosis) * Inadequate mineralisation due to vitamin D deficiency (rickets, osteomalacia). * Excessive bone destruction and repair resulting in structural weaknesses (Paget’s Disease)

Question 53

what is Osteoporosis

Answer 53

• Defined as ‘porous bones’ • Loss of bone mass • Imbalance between octeoclasts and osteoblasts. • Manifests silently • May present as a fracture (Hip) • Bone becomes like fine china plate and minimal stress can cause a fracture - dowagers hump may be seen

Question 54

osteoporosis risk factors

Answer 54

• Risk factors: age, > females, males, post menopausal, sedentary lifestyle and calcium deficiency. • Affects 15% of women and 3% men in Australia • Pathogenesis is unclear Hormonal factors play a part

Question 55

osteoporosis diagnosis

Answer 55

``` • Bone Mineral Density Scan (BMD) • Dual-energy x-ray absorptiometry (DEXA) • Lab tests • Alk phos Osteocalcin (Gla protein) ```

Question 56

what is osteoarthiritis

Answer 56

 Non-inflammatory degenerative disease  Most commonly occurring form of arthritis  Leading cause of pain and disability in older adults  Begins with main load bearing joints – hips, knees – R.A. begins with smaller joints

Question 57

how does osteoarthiritis occur

Answer 57

* Inflammation of the joints often secondary to physical damage (loss of hyaline cartilage, as bones rub and damage= inflammation) * Reduced joint space & osteophyte formation * Damaged joint tries to heal itself * Creating osteophytes or spurs * Cartilage contains more water, less collagen * Cartilage becomes weak, rough, eroded * No longer protects the surface of the bone

Question 58

osteoarthiritis manifestations

Answer 58

* Gradual onset – progresses slowly * Localised joint pain * Pain may be associated with paresthesia * < ROM of joints * Enlarged joints

Question 59

Osteoarthritis - diagnosis

Answer 59

- Subjective history • X-rays of affected joints • MRI • Synovial fluid

Question 60

what is rheumatoid arthiritis

Answer 60

* Chronic systemic autoimmune disorder * Antibodies against IgG fragments * Inflammation in the joint * Abnormal healing responses lay down granulation tissue (pannus)

Question 61

rheumatoid arthiritis cause

Answer 61

* Cause not yet established… possibly * Behavioural – smoking * Environmental * Genetic * Combination * Defined as a systemic inflammatory disease * Main effect is the destruction of articular cartilage and underlying bone * Systemic effects include malaise, anorexia weight loss.

Question 62

Nursing care in Rheumatoid | Arthritis

Answer 62

* Nursing care centres on the chronic nature of the disease * Onset usually slow/gradual * Patients can suffer acute exacerbation * Medications * Improve functional ability * Involve the patient and family * Encourage self care

Question 63

what is gout

Answer 63

* Inflammatory response * Caused by reduced excretion of uric acid * Resulting in high levels of uric acid in the blood (hyperuriceamia) * Causes deposits of urates in connective tissue

Question 64

gout clinical manifestation

Answer 64

* Acute onset * Usually involves 1st metatarso-phalangeal joint * Attacks can be sporadic * Long term * Gouty arthritis * Tophi- white deposits of uric acid you can see around joints

Question 65

how is gout diagnosed

Answer 65

``` • Blood test o Uric Acid > o WCC > o ESR > (Acute attack) • 24hr Urine Specimen • Fluid aspirate from inflamed joint ```

Question 66

how is gout treated

Answer 66

* Medications * Nutrition * Lose weight if > * Fluid intake of >2L/day ( to help excrete uric acid) * Rest

Question 67

what is osteomylitis and who is at risk

Answer 67

* Infection of the bone * Bacteria infection * Older adults at > risk - < immune function

Question 68

osteomylitis manifestations

Answer 68

* Cardiovascular * GI * Musculoskeletal * Integumentary

Question 69

osteomylitis diagnosis

Answer 69

* Bone scans * MRI * Bloods * WBC * ESR * Biopsy

Question 70

osteomylitis treatment

Answer 70

* Medications * Antibiotic Therapy * Surgery * Debridement * Muscle flaps * ? amputation

Question 71

Complications of Musculoskeletal injuries

Answer 71

 Compartment Syndrome • Necrosis • Infection

Question 72

what is Compartment Syndrome

Answer 72

 Swelling inside the muscular compartment leading to decreased perfusion which in turn can lead to necrosis and muscle death.

Question 73

SITES OF COMPARTMENT SYNDROME

Answer 73

most common is the lower leg  anterior compartment  lateral compartment  deep posterior compartment. Increase in volume in compartment caused by  bleeding, infiltration of intravenous fluid or post-traumatic or ischaemic swelling. the two compartments of the forearm, the three compartments of the thigh abdomen after laparotomy for major trauma  abdomen difficult or impossible to close. open wound if the skin laceration is insufficient to decompress the oedema or if there is haemorrhage. Elsewhere: the feet of patients with diabetes and the lower limbs after malignant hyperthermia.

Question 74

steps of compartment syndrome

Answer 74

• 1. Pressure rise in compartment • 2. Decrease in perfusion & oxygenation • 3. Interstitial pressure overcomes intravascular pressure of capillaries ( don’t get blood supply!!!) • 4. Vessel walls collapse, causing impedance of blood flow • 5. Local tissue ischaemia • 6. Oedema (leading to pressure rise in compartment ) (Irreversible necrosis of muscle and nerve tissue within the compartment will begin occurring in less than 12 hours if no action is taken.)

Question 75

main signs of compartment syndrome

Answer 75

* PAIN: That is persistent, progressive and unremitting, is out of proportion to the injury, exacerbated by touch, stretching & elevation. * PALLOR: The limbs may be a pale or dusky colour. * PULSELESSNESS: By the time a limb has become pulseless it is an orthopaedic emergency. The pulse may be absent or diminished. * PARAESTHESIA: As the nerves become ischaemic, paraesthesia may occur within the affected compartments. * PARESIS: Report feelings of weakness in limb or it’s extremities

Question 76

how is necrosis a complication of muscoskeletal injury

Answer 76

 Usually secondary to compartment syndrome  Can be related to initial mechanism of injury. Blood supply is interrupted and the tissues die leading to necrosis.  Neurovascular injuries:  Permanent deficit due to initial trauma  Intra-operative damage to nerves and blood supply.

Question 77

how is infection a complication of muscoskeletal injury

Answer 77

* Open fracture - opportunistic infection to occur in the bone * Osteomyelitis * Osteomyelitis in compromised patients where there is disruption to skin integrity

Question 78

treatment for musculoskeletal injury pain

Answer 78

```  Appropriate pain relief should be administered as soon as possible  Splinting  Appropriate route for injury  Heat/cold  Elevation  Compression  Muscle relaxants  Traction ```

Question 79

4 main structures of the musculoskeletal system

Answer 79

* Bones * Muscles * Tendons * Ligaments

Question 80

4 types of musculoskeletal injury

Answer 80

 Strain  Sprain  Dislocation  Fracture

Question 81

sprain vs strain

Answer 81

 Sprain - partial or complete tearing of LIGAMENTS and tissues at the joint.  Strain - An extreme stretching or tearing of MUSCLE &/OR TENDON.

Question 82

dislocation?

Answer 82

 Dislocation - displacement or separation of a bone from its normal position at the joint.

Question 83

fracture?

Answer 83

 Fracture - a break or disruption in bone  Open - the skin is pierced by broken bone fragments  Closed - the broken bones do not penetrate the skin

Question 84

Recognizing Musculoskeletal Injury | General Injuries

Answer 84

```  Pain? – site, nature, radiation, timing, etc.  Swelling / warmth  Stiffness  Locking  Time since onset  Mechanism of injury?  Other symptoms… ```

Question 85

Recognition of Suspected Serious musculoskeletal Injury

Answer 85

* Significant deformity * Moderate or severe swelling and discoloration * Inability to move or use the affected part * Bone fragments protruding from the wound * Bones grating or a pop or snap heard by the victim * Loss of circulation in an extremity.

Question 86

signs and symptoms of sprains and strains

Answer 86

* Signs and Symptoms include | * Swelling, pain, redness, inability to bear weight on affected joint.

Question 87

treatment of sprains and strains

Answer 87

 R  I  C  E  Rest  Ice  Compression  Elevation

Question 88

signs of fractures

Answer 88

* Immediate localised pain * Decreased Function * Inability to weight bear or use affected part * Muscle spasm * Swelling, guarding, ecchymosis * Self splinting

Question 89

fracture classifications

Answer 89

```  Transverse  Oblique  Spiral  Comminuted  Segmental  Butterfly  Impacted ```

Question 90

describe the bone healing process

Answer 90

 Hematoma forms and fibrin network fills it  Cells grow along fibrin meshwork to form new tissue  Calcium salts deposited in new tissue  New tissue remodeled into normal shape

Question 91

fracture management treatment options

Answer 91

 Closed Reduction  Non Surgical  Manual Realignment  Plaster casting

Question 92

describe cast splintage

Answer 92

 Can be made of plaster or synthetic material  A backslab is used initially  Adequate padding over bony prominences  The joint above and below the # should be immobilised  Limb kept elevated  Regular neurovascular observations

Question 93

cast care advice

Answer 93

 Encourage patient movement of fingers and toes  Elevate the limb to help reduce pain and swelling.  DO NOT use anything to scratch under the cast.  NEVER allow the patient to cut or trim the cast  Avoid allowing the cast becoming wet.

Question 94

types of fracuture management options

Answer 94

 Surgical Intervention  Internal fixation  External Fixation

Question 95

fracture management- surgical intervention

Answer 95

* ORIF (Open Reduction, Internal Fixation) * Indications for internal * fixation are: * Failure of closed reduction * Unstable #’s * Pathological #’s * Fractures that generally unite poorly * Multiple fractures * Methods: * Screws & Plates * Steel Wires * Intra-Medullary nails

Question 96

describe external fixation for fracture treatment

Answer 96

 Transfixing screws are passed through the bone and are attached to an external frame.  Indications for external fixation include:  # ‘s associated with severe soft tissue injury  Severe multiple injuries  Pelvic # ‘s  Infected #’ ‘s

Question 97

function of the oral cavity

Answer 97

is the first part of the digestive tract. It is adapted to receive food by ingestion, break it into small particles by mastication, and mix it with saliva. The lips, cheeks, and palate form the boundaries.

Question 98

function of the tongue

Answer 98

Your tongue helps out, pushing the food around while you chew with your teeth. When you're ready to swallow, the tongue pushes a tiny bit of mushed-up food called a bolus (say: BO-luss) toward the back of your throat and into the opening of your esophagus, the second part of the digestive tract

Question 99

function of the pharynx

Answer 99

Also called the throat, your pharynx is the part of the digestive tract that gets the food from your mouth. Branching off the pharynx is the esophagus, which carries food to your stomach, and your trachea or windpipe, which carries air to your lungs.

Question 100

function of the Salivary glands (parotid, sublingual, submandibular)-

Answer 100

Parotid- These glands secrete a protein-rich fluid which is a suspension of alpha-amylase enzyme parotid glands produce a serous, watery secretion. submaxillary (mandibular) glands produce a mixed serous and mucous secretion. sublingual glands secrete a saliva that is predominantly mucous in character.

Question 101

function of the oesophagus

Answer 101

- The esophagus is a muscular tube that goes from your pharynx (throat) to your stomach. Food is pushed through your esophagus and into your stomach with a series of muscle contractions.

Question 102

function of the intestines

Answer 102

Small- Your small intestine also breaks down food using enzymes made in your pancreas and bile from your liver. The small intestine is the "work horse"' of digestion -- while food is there, nutrients are absorbed through the walls and into your bloodstream. Large- The large intestine is much broader than the small intestine and takes a much straighter path through your belly, or abdomen. The purpose of the large intestine is to absorb water and salts from the material that has not been digested as food, and get rid of any waste products left over.

Question 103

what are accessory organs

Answer 103

An organ that helps with digestion but is not part of the digestive tract. The accessory digestive organs are the tongue, salivary glands, pancreas, liver, appendix and gallbladder.

Question 104

pathophysiology of nausea and vomiting

Answer 104

Stimuli (environmental, psychological, physiological) Peripheral → Autonomic Nervous System ↓parasympathetic and ↑sympathetic activity (vagus [pneumogastric] nerve or vestibular nerve) Central: CNS -Medulla oblongata → vomiting centre & CTZ (chemoreceptor trigger zone- triggered by chemicals, contains dopamine and serotonin receptors- CTZ stimulates muscarinic receptors of vomiting centre, when muscarinic receptors of VC are stimulated this causes emetic reflex) Hormones – serotonin (5-HT) and dopamine (D2)

Question 105

how does motion sickness work

Answer 105

Motion causes stimulation of the labyrinth of inner ear (balance & movement perception) → vestibular nerve → CTZ → histamine release → release of serotonin and dopamine → Vomiting centre = N & V.

Question 106

role of diaphragm in nausea and vomiting

Answer 106

Motor response/act of vomiting – stimulation of phrenic nerve = contraction of abdominal muscles, parasternal intercostal muscles, and costal part of the diaphragm during vomiting = ↑ abdominal pressure and aid expulsion of gastric contents.

Question 107

causes of nausea and vomiting

Answer 107

Medications (e.g. opioids, chemotherapy, some antibiotics etc.) –including interactions & adverse reactions. Anaesthesia Pain, anxiety, unpleasant sight/smell/taste Symptoms associated with an underlying GI condition (e.g. bacterial/viral infection, bowel obstruction, constipation, GORD, gastroenteritis, diverticulitis, peritonitis etc.)

Question 108

treatment of nausea and vomiting

Answer 108

dopamine (D2) and serotonin (5HT) antagonists (A substance that acts against and blocks an action) (e.g. metoclopramide, ondansetron)

Question 109

examples of 5HT3 (serotonin) receptor antagonist antiemetic medications

Answer 109

ondansetron, dolasetron, tropisetron

Question 110

indications of 5HT3 (serotonin) receptor antagonists

Answer 110

N and V, GORD, hyperacidiy, peptic ulcer disease, gastric and duodenal ulcers, hypermotility, erosive osophagitis

Question 111

MOA of 5HT3 (serotonin) receptor antagonists

Answer 111

blocks seretonin 5HT3 receptos in the CTZ and vomit center, which are located in the medulla obongata. also blocks seretonin receptors peripherally (vagus nerve). this reduces communication with the vomit center and the chemoreceptor triggerzone (CTZ) therefore inhibiting the initiation of the vomiting reflex.

Question 112

adverse effects of 5HT3 (serotonin) receptor antagonists

Answer 112

headache, warm/ flushing sensation, constipation, xerostoma (dry mouth from decreased saliva production), irritation at injection site dizziness

Question 113

contraindications of 5HT3 (serotonin) receptor antagonists

Answer 113

- giving it with apomorphine ( lowers BP, LOC) - Not to be given concurrently with other serotonergic drugs as may cause seretonin syndrome - patients with congenital QT syndrome and patients with electrolyte abnormities, CHF, bradyarrhythmia

Question 114

Pathophysiology of GORD

Answer 114

– periodic relaxation of lower oesophageal sphincter = mucosa exposed to acid enzymes & become damaged = abnormal spaces in mucosal epithelium = overstimulation of nerve endings and peripheral sensation. --- • Symptoms of Mucosal Damage (Oesophagitis) • Exposure to acidic stomach contents • Very Common • Due to relaxation of the gastro-oesophageal sphincter

Question 115

Causes of GORD, what excabates it

Answer 115

Exacerbated by other gastrointestinal disorders (e.g. Hiatus hernia, central obesity, impaired gastric emptying). H-Pylori, medications that cause dyspepsia (indigestion) Other causes include– stress, high fat & spicy foods, NSAIDS, alcohol & caffeine.

Question 116

Clinical manifestations of GORD

Answer 116

Clinical manifestations – heartburn, regurgitation, belching, nausea, feeling bloated, angina type chest pain, cough, hoarse/sore throat, wheeze. ``` --- • Pain Epigastrium Chest Throat Jaw Arms • Dysphagia • Sweating • ```

Question 117

Treatment of GORD

Answer 117

Treatment /Management-: Pharmacological: Proton Pump Inhibitors (PPI’s) – e.g. omeprazole, pantoprazole etc. Non-pharmacological: diet –avoiding alcohol, caffeine, high fat & spicy foods ; stress minimisation and management --- • None- self limiting • Medication: Acid blocking medications (H2 -receptor agonists eg Ranitadine) Stomach acid production inhibitors (Proton Pump Inhibitors eg Omeprozole) • Diet • Smoking cessation Weight loss

Question 118

Complications of GORD

Answer 118

Complications: oesophagitis, oesophageal strictures, Barrett’s oesophagus (pre-cancerous changes to epithelium), gastro-oesophageal ulcers & bleeding, aspiration, sinusitis, adult onset of asthma.

Question 119

examples of Proton pump inhibitor medications (PPIs)

Answer 119

omeprazole, pantoprazole, esomeprazole

Question 120

indications of PPIs

Answer 120

GORD, Hyperacidity, peptic ulcer disease, gastric and duodenal ulcers, hypermotility, erosive osophagitis

Question 121

PPI MOA

Answer 121

Inhibits gastric acid secretion by inhibiting the K+/ H+ pump ( potassium pump) located on the apical membrane of the gastric pariental cells, inhibiting secretion of H+ acid into stomatch

Question 122

PPI adverse effects

Answer 122

headache, constipation/ diarrhoea, abdominal discomfort, flatulence, fever

Question 123

PPI contraindications

Answer 123

patients taking cilostazol ( as its an antiplatelet/ vasodilator) ppts with acute intestial nephritis if given with clopidrogel entric coated- must not be dissolved, halved or crushed

Question 124

what are Oesophageal varices

Answer 124

(dilation of distal oesophageal veins that connect portal & systemic circulations)

Question 125

Pathophysiology of oesophageal varices

Answer 125

Pathophysiology: Oesophageal varicose veins → direct result of liver dysfunction secondary to a clot or scarring = ↓blood flow to the liver → Blood flow therefore redirects to smaller vessels (e.g. such as those located in the lower aspect of the oesophagus)→ raised oesophageal venous pressure/portal HTN

Question 126

Clinical manifestations of Oesophageal varices

Answer 126

Clinical manifestations: Pain, Nausea, Haematemesis, +++ blood loss, Hypovolaemia, collapse, death (30-50% - 1st bleed) ``` --- • Pain • Nausea • Haematemesis (blood in vomit) • MASSIVE blood loss • Hypovolaemia • Collapse • DEATH ```

Question 127

complications of Oesophageal varices

Answer 127

Infection (e.g. bacterial peritonitis) Bleeding/haemorrhage Hepatic encephalopathy Oesophageal stricture (post banding or sclerotherapy)

Question 128

treatment of Oesophageal varices

Answer 128

Pharmacological – beta blockers (e.g. propranolol) to ↓ portal HTN & bleeding risk; Blood transfusion; vasoactive medications (vasopressin). Antibiotics (e.g. ceftriaxone) if bleeding present. Surgical: variceal banding; sclerotherapy, Balloon Tamponade (last resort) --- - Bleed first then varices • Pharmacological: Medication to reduce portal hypertension and prevent bleeding • Endoscopic: Variceal Banding – Elastic Band used to tie the point of bleeding Sclerotherapy – Drug injected into bleeding site • Balloon Tamponade: Emergency Proceedure Sengstaken tube/Minnesota Tube

Question 129

pathophysiology of pancreatitis

Answer 129

``` Pathophysiology: Inflammatory disorder (inflammation of the pancreas) - can be acute (short term) or chronic (persistent/ongoing inflammation) ``` Causes: alcoholism & smoking- most common- (acute /chronic), blocked biliary tract (acute) to strictures and pancreatic cysts (chronic) ``` --- Rare Tends to affect people >50 Causes • Alcoholism • Biliary tract obstruction • Peptic Ulcers • Trauma • Hyperlipidaemia • Medications ```

Question 130

clinical manifestations of pancreatitis

Answer 130

Upper abdominal pain (radiating towards the back) Nausea & vomiting Fever Tachycardia Steatorrhoea (fatty stools) – chronic.. ..monitoring withdrawal symptoms..

Question 131

complications of pancreatitis

Answer 131

``` Complications: Pancreatic cancer Infection Kidney failure Type 2 diabetes- cos effect on pancreas and beta cells ```

Question 132

treatment of pancreatitis

Answer 132

``` Treatment: Analgesia (e.g. Opioids) NBM IV Fluids Medications to manage alcohol withdrawal symptoms (e.g. diazepam) ``` often made nil by mouth --- Treatment o Analgesia  Opioids  NBM (nil by mouth) NG Suction (subjective data ascertain risk of vomiting meaning NG tube required)  IV Fluids (if actively vomiting or has been NBM for a while)  Medications eg. Antispasmotic, buscam, antimetics, antibiotics

Question 133

pathophysiology of diverticulitis

Answer 133

Pathophysiology: Development of diverticula (pockets/pouches) in the colon. Become inflamed & infected. 3 areas associated with the development of this condition. 1. structural abnormalities of the colonic wall 2. disordered intestinal motility 3. Low fibre diet (fibre deficiencies)

Question 134

clinical manifestations of diverticulitis

Answer 134

Clinical manifestations: Intermittent or constant abdominal pain (lower left quadrant) Fever N & V Constipation (most common) diarrhoea (less common)- some patients chop and change, but often one or other low fibre diet

Question 135

diverticulitis complications

Answer 135

Complications: Abscess, Fistula , Bowel obstruction, Bleeding, sepsis, Rare: pylephlebitis (inflamed thrombosis of portal vein) – complication secondary to intra-abdominal infection.

Question 136

diverticulitis treatment

Answer 136

Treatment: Pharmacological: double/triple antibiotic therapy (metronidazole, tazosin, ciprofloxacin, cephazolin), IVT, analgesia (opioids) Surgical: sever/life threatening Bowel resection (e.g. sigmoidectomy) ? Colostomy Open or laparoscopic Other: dietary changes (e.g. ↑fibre) often encourage patient to keep a diet diary ( as there are some foods that exacebate symptoms for patients)

Question 137

Peritonitis | (inflammation of the peritoneum) pathophysiology

Answer 137

Pathophysiology: Inflammation of the peritoneum (serous membrane that lines abdominal organs) Physiological response to a severe bacterial infection either via the bloodstream or as the result of the rupture of an abdominal organ. Life threatening - emergency

Question 138

clinical manifestations of peritonitis

Answer 138

``` Clinical manifestations: Feeling of bloating of fullness in abdomen Fever, anorexia, N & V, Oliguria / anuria Diarrhoea, fatigue, confusion, Presence of a paralytic ileus ```

Question 139

peritonitis complications

Answer 139

Complications: | Life threatening –sepsis, multi-organ failure, shock, hepatic encephalopathy.

Question 140

peritonitis treatment

Answer 140

Treatment: Multidisciplinary NBM (nil by mouth), NGT, Antibiotics (ceftriaxone/ cephazolin & metronidazole). IVT, analgesia (opioids), iDC (to monitor urine output- min req 30ml per hour average/ 0.5 ml per kilo per hour) , A-E. Surgery-resection (to remove infected tissue)

Question 141

malnutrition pathophysiology

Answer 141

■ Pathophysiology Inadequate nutrient intake, impaired nutrient absorption or loss of nutrients (short or long-term) that results in an imbalance between intake and the body’s protein and energy requirements = loss of tissue and functionality. glycogenesis/breakdown of fats/ketones/ ? metabolic acidosis

Question 142

malnutrition clinical manifestations

Answer 142

Fatigue, anorexia, muscle weakness & cramping, altered cognitive functioning –confusion/poor concentration, depressive symptoms, impaired healing, impaired thermoregulation etc. Pale oral mucosa, poor skin turgor, emaciated, brittle hair, pressure ulcers/chronic wounds, stunting (children)

Question 143

malnutrition management

Answer 143

Treat underlying cause, nutrient replacement Dietician referral oral, parenteral (e.g. NGT, PEG) or enteral nutrition (IV): temporary high cal food supplement. Development of healthy diet plan (e.g. small/frequent meals) Psychological /psychiatric assessment and support Speech therapist referral - assess for dysphagia - ? Need for NGT or PEG tube OT referral – assess home needs (meals on wheels, kitchen/eating aids etc.). Family involvement –as appropriate

Question 144

malnutrition complications

Answer 144

↓muscle & tissue mass; ↓mobility; convulsions ↑ risk of Diabetes, cardiovascular disease, kidney disease, infertility, stroke, pneumonia and other respiratory complications.

Question 145

Gastrointestinal: Age related changes

Answer 145

■ ↓ saliva production (1/3) ■ Gingiva retraction ■ Reduced oesophageal function (↓ propulsion, weaker gag reflex). ■ Gastric mucosa atrophies, ↓acid production, (atrophic gastritis due to ↓ digestion of proteins (e.g. intrinsic factor). Elderly at ↑risk of developing: Pernicious anaemia Gastric cancer ■ Atrophy of walls of small and large intestine. ↓motility Small intestine: ↓production of digestive enzymes Large intestine: formation of pockets (diverticuli) ■ No. of pancreatic secretory cells ↓ = ↓ digestion of fats. ■ Impact of long-standing/underying conditions: diabetes can = ↓ gastric emptying (approx. 50%) Helicobacter Pylori can cause gastric atrophy rather than aging (approx. 60%).

Question 146

What is the GI tract

Answer 146

‘….a long tube running from the mouth to the anus, which is divided into different organs: mouth, pharynx, oesophagus, stomach, small intestine and large intestine’

Question 147

What is the Upper GI tract

Answer 147

‘Mouth , the oesophagus and the stomach’

Question 148

What is the sphincter

Answer 148

• Specialised ring of circular muscle When contracted food cannot progress. • Sphincters located at at accessory organ ports Sphincters need to relax to allow accessory organ secretions to enter the GI tract • Sphincters allowing secretions into GI tract allow for digestive processes

Question 149

what happens in the mouth

Answer 149

Mix food and saliva to begin digestive process causes stimulation of chemoreceptors and olfactory nerves- encourage desire to eat and encourage uptake of nutrients 1.5 liters of saliva a day

Question 150

what does the pharynx do

Answer 150

Nasopharynx/oropharynx/laryngopharynx | Pharynx Leads to the oesophagus

Question 151

what is the oesophagus

Answer 151

* Hollow muscular tube * Approx. 25cm long * Sphincter at each end. Upper prevents air entering, lower prevents regurgitation from stomach * Upper third contains striated/ voluntary Muscle- innervated by motor neurons * Lower two thirds contain smooth muscle- innervated by parasympathetic nervous system * Peristaltic action for swallowing

Question 152

what is the stomatch

Answer 152

* Muscular organ * Stores/mixes food for correct absorption * Continues digestion- expels chyme into small intestime after * Major anatomical considerations

Question 153

sphincters of the stomatch

Answer 153

Oesophageal sphincter- allows food to be passed through stomach once it dilates Pyloric sphincter- relaxes and food is propelled through the gastro-duodenal junction into the duonenum

Question 154

functional areas of the stomatch

Answer 154

• Functional areas- these areas have glands producing different enzymes to aid with digestion Fundus (top of stomach) Antrum (bottom of stomach)

Question 155

how much can the stomatch expand

Answer 155

At rest- 50ml of fluid and is small but can expand to maintain 4L

Question 156

Upper Gastrointestinal: Age related changes

Answer 156

``` • Teeth >root cavities Enamel harder/brittle.. lead to increased root canities >loss of bone supporting teeth • Gums Gingiva retracts.. can lead to less bone supporting teeth or oral cavities.. can lead to pts needing dentures • Saliva tooth loss/fractures of teeth/dentures • Gums > periodontal disease • Saliva < ability to break down starches > swallowing time • Oesophageal Motility Discomfort > risk of aspiration • Stomach > gastric irritation ```

Question 157

what does the lower GI tract consist of

Answer 157

 Small intestine  Large intestine o Ancillary organs

Question 158

what do the Ancillary organs do

Answer 158

 Secrete substances that are required for digestion of chyme and therefore maintain a healthy GI tract  Connected to but does not form part of the GI tract: liver, pancreas, gallbladder

Question 159

what does the liver do

Answer 159

 Liver prouces bile= necessessary for the digestion and absorption of fat. Liver mainly processes nutrients absorbed from the small intestines, bile from liver secreted into the small intestine also plays an impotant role in digesting fat… Enzymes are secreted by the pancreas into the SI, there they continue breaking down food that has left the stomach

Question 160

what does the pancreas do

Answer 160

 Pancreas produces enzymes= responsible for digestion of carbohydrates, proteins and some fats These enymes are an alkaline fluid that neutralises the chyma

Question 161

what does the gallbladder do

Answer 161

 Gall Bladder stores bile when not being used. primary function is to store and concentrate bile yellow/ brown digestive enz prod by liver. The gallbladder is bart of the billary tract

Question 162

what does bile do

Answer 162

Bile helps the digestive process by breaking up fats, it alsodrains waste products from the liver and duodenum- part of the small intestine Secretions enter duodenum through ducts and different enzymes are released at different times at different places depending on the specific need of the GI tract at that specific time

Question 163

small intestine size

Answer 163

Small diameter- 2.5 cm | 5m long

Question 164

describe small intestine

Answer 164

3 structures  Duodenum  Jejenum  Ileum - All very similar - Illeal cecal valve controls flow of digestive material from the illium to the large intestine - Movements of the small intestine aid digestion and absorption, chyme stimulates movement, mixes scretions from the ancillary organs, peristalsis moves food to the lage intestines

Question 165

large intestine size

Answer 165

- Large diameter 7cm | - Short 1.5m long

Question 166

describe large intestine

Answer 166

- Cecum, appendix and colon divided into ascending transverse, descending and sigmoid colon, As well as rectum and anal canal are essential for understanding anatomy and physiology - Cecum receives chyme - 2 sphincters control how the chyme is moved through the large intestine. The illeocaecal valve allows chyme to move from the small to the large intestine and the O’bierne sphincter which controls movement from the colon to the rectum

Question 167

how does the anus and rectum work

Answer 167

- Complex - Multiple components - Aids defecation - Movement of faeces into sigmoid colon and rectum stimulate defecation/ rectal reflex - Controlled by anal sphincter which relaxes and creates urge to defecate.. which is controlled by the autonomic nervous system - Defecation reflex can be over ridden by the contraction of the external anal sphincter

Question 168

parts of anal/ rectal canal

Answer 168

```  Anal canal  Sphincters  Anal columns  Anorectal junction  Anal valve  Anal crypt  Rectum  Valves of Houston  Peritoneal reflection ```

Question 169

Oesophageal Disorders

Answer 169

``` - Dysphagia • Gasto-oesophageal Reflux Disease (GORD) (Heartburn) • Oesophageal Moniliasis (Infection) • Hiatus Hernia • Carcinoma • Oesophageal Perforation • Oesophageal Bleeding ```

Question 170

what is a hiatus hernia

Answer 170

``` • Hernation of a portion of the stomach through the oesophageal hiatus in the diaphragm • Disrupts the lower sphincter function • Impairs oesophageal Clearance • More common in women Most frequent in middle age onwards ```

Question 171

Hiatus hernia symptoms

Answer 171

``` • None • Gastric Reflux • Heartburn • Pain common after eating • Pain on bending • Pain when lying down Bleeding – Anaemia ```

Question 172

hiatus hernia treatment

Answer 172

``` • Lifestyle changes Losing weight Small meals Avoid bending from waist Sleeping well supported Smoking cessation Medication (see GORD) Surgery ```

Question 173

causes of oesophageal bleeding

Answer 173

* Oesophagitis- where stomatch acid has been exposed to esophagus causing inflammation. Prolonged exposure can cause erosion which can cause bleeding, if vessels become eroded can cause larger bleeds * Mallory Weiss Tear- small tear in the esophagus often caused by increased pressure in the esophagus caused by wrething and vomiting. Normally not a big problem unless you have clotting disorder caused by congenital disorder or alcoholism * Varices * Neoplasia/ growths in the oesophagus * Drugs: NSAIDS/ Aspirin / Alcohol

Question 174

what are varices

Answer 174

* Varicose veins that occur in GI tract * Account for 5-10% of all medical admissions * Mortality 30-50% on presentation of 1st bleed * Varices formed as direct result of liver dysfunction (as indicated with alcohol abuse) which resulting in raised oesophageal venous pressure causing the varicose veins

Question 175

oesophageal varices nursing interventions

Answer 175

``` • LOOK at your Patient • ABCDE • Blood Transfusion • Support • Monitor Observe patient Closely ```

Question 176

why do we vomit/ get nauseaus

Answer 176

• Defence mechanism – removes toxic or harmful substances from body – memory of previous encounters leads to avoidance • Medical interventions (e.g. surgery, chemotherapy, radiotherapy, drugs) can interfere with normal mechanisms

Question 177

Causes of N and V

Answer 177

``` • Forceful expulsion of gastric contents from the mouth • Caused by – powerful sustained contraction of abdominal muscles – descent of diaphragm – opening of gastric cardia • Involves co-ordination of – abdominal muscles – gastrointestinal muscles – respiratory muscles • Controlled by the Vomiting Centre ```

Question 178

Types of nausea and vomiting

Answer 178

* Post-operative nausea and vomiting (PONV) * Opioid-induced nausea and vomiting * Chemotherapy- and radiotherapy-induced nausea and vomiting * Nausea and vomiting in early pregnancy * Motion sickness and vestibular disorders

Question 179

• PONV - patient risk factors

Answer 179

``` • Incidence 20-37 % • Risk factors o Patient factors o Procedural factors o Anaesthetic factors o Post-operative factors ``` * Gender (female patients especially) * Age (peak 11-14 years) * Obesity * Migraine * Pre-operative eating patterns * Prior history of PONV or motion sickness * Anxiety * Gastroparesis (problem with muscles and nerves of the stomatch)

Question 180

• Consequences of PONV

Answer 180

``` • Practical consequences o Patient discomfort o Soiling • Medical complications o Wound dehiscence o Aspiration of vomit o Electrolyte imbalance and dehydration o Delayed oral therapy • Economic burden o Medical personnel time o Unplanned admission/delayed discharge o Bed blocking ```

Question 181

what is gastritis

Answer 181

 inflammatory disorder of the gastric mucosa’ (Craft and Gordon 2015 p 779)  Acute or Chronic  Acute erodes the surface epuithelium resulting in superficial damage  Chronic often affects the elderly, causes thinning and degeneration of the stomach wall  Acute gastritis commonly caused by ingestion of irritant e.g. NSAIDS or alcohol

Question 182

causes of gastritis

Answer 182

```  Acute gastritis commonly caused by ingestion of irritant e.g. NSAIDS or alcohol  Chronic Gastritis caused by:  Pernicious anaemia  Autoimmune disorders  Alcohol abuse  Peptic ulceration  Certain cancer  Chronic contains the antramoni and occurs 4 times more often than bundle gastritis  Antral- bottom, bundle top of stomatch ```

Question 183

gastritis symptoms

Answer 183

```  PAIN ( localised over stomatch)  Bloating  Nausea  Vomiting  Anorexia  Indigestion ```

Question 184

gastritis treatment

Answer 184

``` • Acute Episode:  Antiemetic  IV Fluids if Vomiting +++  Mouth Care  Analgesics • Medication:  Antacid  H2 blocker • If Helicobactor pylori found – antibiotic therapy • Dietary Advice ```

Question 185

what is a peptic ulcer

Answer 185

 Occurs in Stomach and Duodenum  Caused by damage to areas exposed to acid and pepsin containing secretions  Smoking and Stress increase acid production  Alcohol and coffee cause gastric erosion  Helicobactor Pylori (1982) significant cause of peptic ulcer disease

Question 186

symptoms of peptic ulcer

Answer 186

 Pain (Burning) Epigastrium Usually pain is localised  Dyspepsia  Duodenal Ulcer= usually pain 3-4 hours post meal  Gastric ulcer= pain 30-60min post meal  Belching

Question 187

peptic ulcer diagnosis

Answer 187

 Moved from Hospital care to Primary Care  Recognition of Helicobacter pylori 1982  H Pylori major factor in causing damage  H Pylori present in 90% of all patients with DU  Present in 75-80% patients with gastric ulcers  Diagnosis made from blood, biopsy or breath test  Endoscopy

Question 188

what is Helicobater Pylori

Answer 188

* The major cause of ulcers | * Second most common cause is NSAIDs

Question 189

peptic ulcer treatment

Answer 189

```  Eradication therapy if H Pylori detected – Antibiotic therapy  Antacid  H2 – Receptor antagonists eg Ranitadine  PPI eg Omeprazole  Discontinue NSAIDS/Aspirin  Dietary Advice  Smoking cessation Diarrhoea and constipation ```

Question 190

what is constipation

Answer 190

‘difficult or infrequent defecation’  Common complaint  Normal bowel habits – 1-3 times per day - once per week

Question 191

Causes of constipation

Answer 191

 Neurogenic disorders Large Intestine Neural pathways/neurotransmitters altered Parkinson's disease  Personal Habits Low fibre diet Highly refined (Processed) foods (white bread, snacks, cakes etc)  Sedentary lifestyle  Excessive use of antacids (Calcium carbonate)  Opioid Analgesics

Question 192

Problems with constipation

Answer 192

```  Serious  Can lead to perforation of the bowels Can cause death  Pain  Straining Cardiac issues Bradycardia (Valsalva manoeuvre) MI ```

Question 193

Assessment and Treatment of constipation

Answer 193

```  Subjective data Bowel habits Bristol Stool Chart  Objective data Abdominal Assessment PR exam Abdominal X-Ray/Barium Enema  Treatment Manage underlying disorder Increase fluid/fibre intake Laxatives/stool softeners/enemas ```

Question 194

what is diarrhoea

Answer 194

‘increase in the frequency of defecation and the fluidity and volume of faeces’ (Craft & Gordon 2015 p796)  More than 3 stools/day – Abnormal  Stool volume normal adult – 200grams/day

Question 195

types of diarrhoea

Answer 195

 Osmotic diarrhoea Produces large volumes Caused by:  Lactase and pancreatic enzyme deficiency  Excessive ingestion of synthetic sugars (artificial sweeteners)  Secretory diarrhoea Excessive mucosal secretion Caused by:  E-Coli  Clostridium Difficile (C-Diff)  Small volume diarrhea can also occur being caused by chromes disease, faecal impaction or ulcerative cholitis

Question 196

Problems with diarrhoea

Answer 196

 Acute or chronic  Pain is problematic If caused by bacterial infection can cause fever, cramping and bloody stool Steteral is fat in stool, lign of malabsorption syndrome, stool specimen must be taken to rule out any of these  Acute Fatigue, thirst, nausea, headache  Chronic Dehydration Electrolyte imbalance Excessive loss of potassium and sodium- can have systemic effects on ther systems

Question 197

assessment and treatment of diarrhoea

Answer 197

``` Assessment and treatment  Subjective data Bowel habits Bristol Stool Chart Exposure to contaminated food Travel  Objective data Abdominal Assessment Stool specimen Abdominal X-Ray  Treatment Fluid Resus Treat causal factors eg. Antibiotics for bacterial infection Nutritional support/balance ```

Question 198

difference between acute and chronic pancreatitis

Answer 198

``` Acute Mild disease Alcoholism /biliary tract obstruction Enzyme outflow blocked – leak into pancreatic tissue - Causes inflammation - Causing Systemic effects • Cardiac • Coagulation • Renal MODS ( multiple organ dysfunction syndrome) ``` ``` Chronic Due to structural and functional impairment Alcoholism Smoking Lesions caused by • Fibrosis • Strictures • Pancreatic cysts Risk Pancreatic Cancer ```

Question 199

assessment for treatment of pancreatitits

Answer 199

Subjective data • Pain • Time • Hx – Pain post eating Objective data • Lab tests • Pancreatic amylase- indicator for pancreatitis • Serum Lipase- indicator for pancreatitis • CRP (inflammatory marker may be indicative of systemic inflammation… although test not specific to pancreatitis)

Question 200

what is gantroenteritis and its causes

Answer 200

Inflammation of stomach and small intestine ``` Causes: • Bacteria • Viruses • Parasites • Toxins ```

Question 201

what are the primary mechanisms of gastroenteritis

Answer 201

2 primary mechanisms Production of exotoxins Invasion and ulceration of mucosa

Question 202

Explain the 2 primary mechanisms of gastroenteritis

Answer 202

2 primary mechanisms Bacteria/ virus cause inflammation and tissue damage Production of exotoxins- bacteria can produce and excrete an exotoxin that enters the gastric lumen causing damage and inflammation, exotoxins impair absorption and can cause secretions of significant amounts of electrolytes and water into bowel resulting in diarrhoea and fluid loss common bacterial endotoxins seen in clinical practice- staphylococcus, e coli and clostrium differseal Invasion and ulceration of mucosa- other bacteria such as salmonella and cert e coli strains directly damage the GI tissue causing ulceration of the small bowel and colon causing bleeding, fluid loss and as in exotoxin cause producing significant electrolytes and water into bowel resulting in diarrhoea

Question 203

gastroenteritis manifestations

Answer 203

``` GI Effects • Anorexia • Nausea & Vomiting • Abdominal Pain • Cramping • Diarrhoea • Loud bowel sounds/gurgling ```

Question 204

general effects of gastroenteritis

Answer 204

* Malaise/weakness * Muscle aches * Headache * Dry skin/mucous membranes * Poor skin turgor * Orthostatic hypotension * Tachycardia * > Temp/ pyrexia

Question 205

assessment and treatment for gastroenteritis

Answer 205

``` Diagnosis • Lab tests after 48hrs severe symptoms o U & E (urea and electrolytes) o Acid base • ABG’s • Stool Sample ``` ``` Treatments • Usually self limiting • Medications o AB’s – specific organism o Antidiarrheal drugs • Fluid Replacement therapy ```

Question 206

what is a stoma

Answer 206

Intestinal ostomy surgically created opening between intestine and abdominal wall – allows the passage of faecal material Name depends on location Ileostomy – ostomy made of ileum and small intestine Colostomy – ostomy made in the colon Can be temporary or permanent

Question 207

reasons for stomas

Answer 207

IBD (inflammatory bowel disease) • Ulcerative Colitis • Crohns (more common for these conditions to have ileostomy ) Cancers Tumors (more common for these conditions to have colostomy ) Bowel Obstruction- used for treatment

Question 208

care considerations for stomas

Answer 208

* Pre-operative education * Role of the stomal therapist * Check the stoma as part of the post op observations * Expect it to be red with moderate oedema and a small amount of bleeding * Stoma bag will be in situ * Bowel will be slow to regain normal peristalsis due to the anaesthesia.

Question 209

what do antiemetics do

Answer 209

* Symptom Control * Nausea Chemoreceptor trigger zone in the 4th ventricle, activated by CSF blood borne emetics, chemical toxins and drugs Also mediated by neurotransmitter 5HT which is released from afferent nerve pathw in stom and small in. it communicates with emetic center in medullar Chemoreceptor trigger zone doesn’t nduse vom, just relays messages to the emetic center via neurotransmitters such as acetyl choine, 5HT, histamine and dopamin

Question 210

Medications to control Nausea and Vomiting MOA

Answer 210

* Act principally by blocking neurotransmitters in emetic centre, the cerebral cortex, the CTZ or the vestibular apparatus ( VA is in the ear and it deals solely with balance so for example when we're looking at medications that are used to control the nausea that comes with seasickness that's where the vestibular apparatus comes into it ) * Dopamine antagonists * Muscarinic receptor antagonists * 5-HT3 –receptor antagonists

Question 211

Dopamine Antagonists examples

Answer 211

• Metoclopramide, prochlorperazine, domperidone

Question 212

Mechanisms of Hormone Regulation

Answer 212

```  Secretion Patterns  Diurnal Patterns  Pulsatile and cyclic Patterns  Dependent on Circulating substances  All hormone release operate within feedback loops to maintain internal environment  Triggers for hormone release  Chemical factors  Endocrine factors Neural control ```

Question 213

Regulation of Target Cell Sensitivity

Answer 213

 The sensitivity of a target cell to its hormone is related to the number of receptors per cell.  Target cells adjust to levels of hormones by increasing or decreasing the number of receptors upregulation and down regulation

Question 214

Protein Based Hormones moa

Answer 214

 First Messenger  Endocrine gland to target cell  Second Messenger  From receptor to cytoplasm and nucleaus

Question 215

 Function of Thyroxine

Answer 215

```  Regulates protein, fat and carbohydrate usage in all cells  Regulates metabolic rate of all cells  Controls body heat production  Increases blood glucose levels  Maintain growth hormone secretion ```

Question 216

Regulation of Thyroid Hormone Secretion

Answer 216

increased energy requirements -> hypothalamus releases thyrotrophin- releasing hormone-> anterior pituitary gland releases TSH-> thyroid gland to release thyroid hormone-> thyroid hormone targeting most body cells-> adequate levels of thyroid hormone in the blood

Question 217

what does the pineal gland do

Answer 217

 Melatonin – regulation of circadian rhythms

Question 218

what does the thymus gland do

Answer 218

 Development of T-lymphocytes

Question 219

what hormones to the testes and ovaries do

Answer 219

 Secrete hormones that have role in reproduction

Question 220

elimination of peptide hormones and catecholamines

Answer 220

 Degraded by enzymes in the blood or tissues |  Excreted by kidney and liver

Question 221

elimination of steroid hormones

Answer 221

 Bound to protein carriers and inactive in bound state  Unbound hormone conjugated in liver rendering them inactive  Excreted in bile or urine

Question 222

elimination of thyroid hormones

Answer 222

 Unbound hormone rendered inactive through removal of amino acids in tissues  Conjugated in the liver and eliminated in the bile

Question 223

reasons for hormone alterations

Answer 223

 Feedback systems that fail to function properly  Feedback systems that respond to inappropriate signals  Endocrine gland may fail to produce adequate amounts of hormone  Endocrine gland may produce and release too much hormone  Hormones may be degraded once in circulation  Hormones may be inactivated by antibodies prior to reaching target cell  Ectopic hormone production  Abnormal receptor function  Altered intracellular response to the hormone at the target cell

Question 224

Alterations to Pituitary Function

Answer 224

 Syndrome of inappropriate antidiuretic hormone secretion (SIADH)  Diabetes insipidus Nephrogenic Form – inadequate response of the renal tubules to ADH, such as pyelonephritis

Question 225

explain syndrome of inappropriate antidiuretic hormone secretion (SIADH)

Answer 225

 High levels of circulating ADH  Associated with symptoms of water intoxication (increase in water retention by the kidneys or increased total body water  hyponatraemia and concentrated urine  Diagnosis based on – low serum osmolality and hyponatraemia, urine hyper osmolality, urine sodium excretion matches intake, normal adrenal and thyroid function, absence of conditions that alter fluid volume status

Question 226

explain diabetes insipidus

Answer 226

 Insufficiency of ADH  polyuria and polydipsia |  Neurogenic Form – absence of ADH, damage to the hypothalamus, pituitary and can be seen with brain tumours

Question 227

Alterations to adrenal function

Answer 227

```  Hyperfunction  Hypofunction - Hyperaldosteronism - Hypercortisolism - Hypoadrenalism - Adrenal Crisis ```

Question 228

explain adrenal hyperfunction

Answer 228

 Hyperfunction  Hyperaldosteronism  Hypercortisolism

Question 229

explain adrenal hypofunction

Answer 229

 Hypofunction |  Hypoadrenalism

Question 230

Explain Hyperaldosteronism

Answer 230

 Excessive aldosterone secretion  Primary hyperaldosteronism  Excessive secretion from the adrenal cortex  Secondary hyperaldosteronism  Caused by extra-adrenal stimulus (RAAS)  Increased levels of aldosterone result in  Increased renal sodium and water reabsorption  hypervolaemia and hypertension  Renal excretion of potassium

Question 231

explain Hypercortisolism

Answer 231

 Excessive levels of serum cortisol  Chronic hypercortisolism leads to Cushing’s syndrome  Causes  Exogenous – administration of glucocorticoids (most common)  Endogenous – ectopic adrenocorticotrophic hormone secretion (adults), adrenal tumours (children)  Cushing’s Disease – excess production of ACTH from pituitary

Question 232

manifestations of Hyperaldosteronism

Answer 232

Manifestations – hypertension, hypokalaemia (assoc. with muscle weakness, cramping and headache)  Manage hypertension and hypokalaemia, correct underlying cause.

Question 233

manifestations of Hypercortisolism

Answer 233

- thin extremities, easy bruising, trunk obesity, pendulous abdomen, hyperpigmentation, puple striae, supraclavicular fat pad, moon face

Question 234

explain hypoadrenalism

Answer 234

 Primary adrenal insufficiency (Addison’s disease)  Hyposecretion of cortisol, aldosterone and androgens  Caused by autoimmune adrenalitis, adrenal infection, metastatic disease, adrenal haemorrhage, congenital adrenal hyperplasia, bilateral adrenalectomy.  Secondary adrenal insufficiency  Hyposecretion of pituitary ACTH hyposecretion of cortisol  Caused by exogenous treatment with glucocorticoid therapy which suppresses ACTH production

Question 235

hypoadrenalism manifestations

Answer 235

 Mild to moderate – weakness, fatigue, anorexia and weight loss  Moderate – nausea, vomiting, diarrhoea  Severe – hypotension leading to vascular collapse and shock

Question 236

explain adrenal crisis

Answer 236

 Life threatening condition develops from inadequate cortisol levels  Causes  Sudden cessation of glucocorticoids (steroids)  Illness  Infection  Trauma or surgery  Stressful periods  Early Intervention is essential – parenteral hydrocortisone

Question 237

alterations in pancreatic function

Answer 237

diabetes mellitus

Question 238

alterations of thyroid function

Answer 238

``` hyperthyroidism nodular thyroid disease thyroiditis thyrotoxic crisis hypothyroidism postpartum thyroiditis ```

Question 239

explain hyperthyroidism

Answer 239

 Graves’ Disease – autoimmune condition  An abnormal immune response triggers antibodies against the TSH receptor  Manifestations – Thyrotoxicosis (tachycardia, palpitations, nervousness, insomnia, heat intolerance, moist skin, tremor, lid retraction in the eye, increased SBP, increased cardiac contractility and weight loss)  Goitre – diffuse or enlarged gland caused by stimulation of thyroid cells increasing the size and vascularity of the thyroid gland.  Exophthalmos (protrusion of the eyeball), periorbital oedema, extraocular muscle weakness leading to diplopia – TSH receptors on tissue within the orbit

Question 240

what is Thyroiditis

Answer 240

 Thyroiditis – inflammation of the thyroid tissue due to viruses, trauma, medication or during the postpartum period

Question 241

what is Thyrotoxic crisis

Answer 241

 Thyrotoxic crisis – thyroid storm (rare but dangerous) | - hyperthermia, tachycardia, high output heart failure, agitation or delirium, nausea and vomiting or diarrhoea

Question 242

explain hypothyroidism

Answer 242

 Decreased production of thyroid hormone by the thyroid gland  Primary causes  Congenital defects  Defective hormone production  Loss of thyroid tissue after surgery or radioactive treatment  Primary hypothyroidism  Acute thyroiditis – bacterial infection  Subacute thyroiditis – nonbacterial inflammation  Autoimmune thyroiditis – Hashimoto disease  Painless thyroiditis

Question 243

alterations to parathyroid hormones

Answer 243

hyperparathyroidism | hypoparathyroidism

Question 244

explain hyperparathyroidism

Answer 244

 Hyperparathyroidism  Primary hyperparathyroidism – single parathyroid adenoma  Secondary hyperparathyroidism – compensatory response to chronic hypocalcaemia  Tertiary hyperparathyroidism – increase in number of parathyroid cells and loss of sensitivity to circulating calcium can autonomous secretion.

Question 245

explain hypoparathyroidism

Answer 245

 Damage to parathyroid glands during thyroid surgery

Question 246

pancreas endocrine function

Answer 246

 Produce hormones secreted into bloodstream  Involved in nutrient balance (blood glucose levels) and gastrointestinal functions  Insulin produced by beta cells  Glucagon produced by alpha cells Somatostatin by delta cells

Question 247

what is gluconeogenesis

Answer 247

the formation of glucose, especially by the liver from carbohydrate sources such as amino acids and the glycerol portion of fats

Question 248

what is Glycogenolysis

Answer 248

breakdown of stored glucose to increase the blood glucose levels

Question 249

what is Glucagon

Answer 249

hormone produced by the alpha cells, stimulating the breakdown of glycogen in the liver, the formation of carbohydrates in the liver and the breakdown of lipids in both the liver and adipose tissue

Question 250

3 main categories of diabetes mellitus

Answer 250

 Type 1 Diabetes Mellitus  Characterised by an absolute insulin deficiency  Type 2 Diabetes Mellitus  Insulin resistance with an accompanying deficiency in insulin production  Gestational Diabetes

Question 251

explain type 1 diabetes

Answer 251

 Autoimmune Destruction of the Beta (β) cells in the Islets of Langerhans  Severe or absolute lack of insulin caused by the loss of β cells  Slowly progressive autoimmune T-cell mediated disease that destroys the β cells  Concurrent abnormal production by alpha (α) cells with an increase production of glucagon.  Hyperglycaemia and ketonaemia can result from insulin deficiency however the excess of glucagon facilitates the other metabolic alterations seen in diabetes.

Question 252

clinical manifestations of type 1 diabetes

Answer 252

```  Classical Presentation  Polyphagia (increased hunger)  Polydipsia (increased thirst)  Polyuria (increased urine production)  Weight Loss  Ketoacidosis  Sweet Smelling Breath ```

Question 253

type 1 diabetes assessment and management

Answer 253

```  Urinalysis  Presence of classic signs and symptoms  Management Aim Avoid swings in insulin and glucose levels Mimic body’s natural patterns  Monitoring Blood Glucose Levels  Long Term – Glycolated haemoglobin A1c  The future Islet cell transplantation ```

Question 254

explain type 2 diabetes

Answer 254

 Currently around 1.7 millions Australians have diabetes (of which 85% have Type 2 diabetes)  280 Australian develop diabetes every day (1 every 5 minutes)  Total annual cost in Australia is approx. $14.6 billion  Fastest growing chronic disease in Australia  Fasting hyperglycaemia occurs despite insulin being available  Cellular Insulin resistance  No ketoacidosis  Gradual increase in hyperglycaemia  Metabolic Abnormalities  Insulin resistance  Increased glucose production by the liver  Impaired secretion of insulin by β cells ``` Type 2 – Risk Factors  History of diabetes in parents or siblings  Obesity  Physical inactivity  Race/ethnicity ```

Question 255

type 2 diabetes clinical manifestations

Answer 255

```  Slow onset  Hyperglycaemia – polyuria and polydipsia  Blurred vision  Fatigue  Paresthesia  Skin infections ```

Question 256

type 2 diabetes management

Answer 256

 Changes in diet and exercise |  Hypoglycaemic medication possibly in combination with insulin

Question 257

explain gestational diabetes

Answer 257

 Occurs during pregnancy and resolves once the infant and the placenta have been delivered  Glucose intolerance appears during pregnancy  New routine screening and screening of high risk women  Family history of diabetes  Some ethnic groups have a higher risk  Advanced maternal age  History of large babies  Prior history of gestational diabetes or polycystic ovary syndrome  Overweight prior to pregnancy (BMI >35)  Women on corticosteroids or antipsychotics

Question 258

complications of diabetes

Answer 258

```  Alterations in Blood Glucose  Alterations in cardiovascular system  Neuropathies  Increased susceptibility to infection  Peridontal disease ```

Question 259

4 metabolic problems of diabetic ketoacidosis

Answer 259

 Hyperosmolality from hyperglycaemia and dehydration  Metabolic acidosis from an accumulation of ketoacids  Extracellular volume depletion from osmotic diuresis  Electrolyte imbalances (potassium and sodium) from osmotic diuresis

Question 260

what increases risk of diabetic ketoacidosis

Answer 260

 Increased risk during physical or emotional stress – surgery, illness, infection, trauma, omitted insulin  Occurs in Type 1 Diabetes

Question 261

DKA – Manifestations and Treatment

Answer 261

 Manifestations – flushed skin, increased thirst, fruity breath, decreased BP, increased HR, Kussmauls Respirations, confusion, Nausea, vomiting, abdominal pain, fatigue, weight loss, blurred vision ``` Treatment  Immediate medical intervention  Primary Survey – Prioritise ABC  IV hydration  Regular Insulin  Potassium Replacement  Continuous cardiac monitoring ```

Question 262

Explain Hyperosmolar Hyperglycaemic State

Answer 262

 Plasma Osmolality >340 mmol/kg  Elevated Blood Glucose levels >33.3mmol/L  Altered Levels of consciousness  Precipitating Factors – infection, therapeutic agents or procedures, acute or chronic illness.  Hyperglycaemia  increased urine output  plasma volume decreases and glomerular filtration rate decreases  glucose is retained and water lost  increase in glucose and sodium lead to increased serum osmolality  severe dehydration  intracellular water reduced in all tissue including brain

Question 263

HHS – Manifestation and Treatment

Answer 263

 Manifestations - Flushed skin, increased thirst, decreased BP, increased HR, lethargic, nausea and vomiting, abdominal pain, fatigue, weight loss, malaise, extreme thirst, seizures ``` Treatment  Similar to DKA  Primary Survey – ABCDE  Intravenous fluid  Potassium replacement  Insulin administration ```

Question 264

Hypoglycaemia – Manifestations

Answer 264

``` Autonomic Nervous System • Hunger • Shakiness • Nausea • Irritability • Anxiety • Rapid Pulse • Pale, cool skin • Hypotension - sweating ``` ``` Impaired Cerebral Function • Strange or unusual feeling • Slurred Speech • Headache • Blurred Vision • Decreasing levels of consciousness • Difficulty in Thinking • Inability to concentrate • Seizures • Change in emotional behaviour • Coma ```

Question 265

Hypoglycaemia – Treatment

Answer 265

 Mild  15 g rapid acting or simple sugar (fruit juice, lollies, honey)  Followed by a meal with complex carbohydrates  Review diabetes management plan if occurring frequently  Severe  Blood glucose <3mmol/L  Conscious and alert – 10-15g of oral carbohydrate  Altered consciousness – parenteral glucose or glucagon

Question 266

Long-term complications of diabetes mellitus

Answer 266

Microvasculature  Neuropathies  Nephropathies  Retinopathies ``` Macrovascular  Coronary artery  Cerebrovascular  Peripheral arterial disease  Foot ulcers ```

Question 267

Diabetic Neuropathies

Answer 267

 Thickening of the walls of the nutrient vessels supplying the nerve  Demyelination process affecting the Schwann cell Somatic Neuropathy ```  Distal symmetric polyneuropathy  Autonomic Neuropathy  Disorders of vasomotor function  Decreased cardiac responses  Inability to empty the bladder  Gastrointestinal motility problems Sexual dysfunction  Kidney Enlargement  Nephron hypertrophy and Hyperfiltration ```

Question 268

Diabetic Nephropathies Risk Factors

Answer 268

– genetic or familial predisposition, elevated BP, poor glycaemic control, smoking, hyperlipidemia and increased albumin excretion.

Question 269

Diabetic neuropathies Affect on Glomeruli

Answer 269

 Capillary basement membrane thickening  Diffuse glomeruli sclerosis  Nodular glomerulosclerosis

Question 270

Diabetic Retinopathies

Answer 270

```  Abnormal retinal vascular permeability  Microaneurysm formation  Neovascularisation and associated haemorrhage  Scarring  Diabetic macular oedema  Retinal detachment ```

Question 271

discuss diabetic foot ulcers

Answer 271

 Sensory Neuropathy is a major risk factor  Impaired pain sensation, not aware of constant trauma to feet  Motor Neuropathy  Weakness of intrinsic muscles of the foot may result in deformities  Full foot exam at least once a year  Assessment of protective sensation, foot structure and biomechanics, vascular status and skin integrity

Question 272

diabetic infections

Answer 272

```  Soft tissue infections of the extremities  Osteomyelitis  Urinary tract infections  Pyelonephritis  Candidal infections of the skin and mucous surfaces  Dental caries  Periodontal disease  Tuberculosis ```

Question 273

diabetes nursing diagnosis

Answer 273

 Risk of impaired skin integrity related to diabetic neuropathies  Risk of Infection  Risk of injury related to neuropathies, visual deficit, hyperglycaemia  Risk of sexual dysfunction related to peripheral neuropathy  Risk of impaired coping related to the chronic nature of diabetes  Risk of knowledge deficit related to self care  Risk of falls related to neuropathies  Risk of feelings of powerlessness related to chronic nature of diabetes

Question 274

what is insulin

Answer 274

 Body’s main fuel storage hormone  Secreted in response to raised levels of glucose in the blood  Ensures tissues and cells have sufficient chemical substrates for energy, storage, anabolism and repair  Within 30-60 seconds of absorption of glucose after a meal insulin release is increased  Fall in blood glucose inhibits insulin secretion  Rapidly absorbed in the gut if given orally, with a half life of only a few minutes

Question 275

when is insulin replacement needed

Answer 275

 Human insulin has all the properties and actions of the natural hormone – synthetically engineered  Treatment of Type 1 diabetes and treatment of type 2 during emergencies, in stressful situations, during pregnancy or as an adjunct to oral hypoglycaemic agents

Question 276

insulin formulations

Answer 276

 Ultra Short Acting (or rapid acting)  Clear, onset of action 0-20 min, peak 60-90mins, Duration 3-5hrs  Apidra, Humalog, Novorapid  Short Acting  Clear, onset of action 30mins, peak 2-4hrs, Duration 6-8hrs  Actrapid, Humulin R, Hypurin Neutral  Intermediate Acting  Cloudy – gently shaken or rotated prior to use  Onset of action – 90mins, Peak 4-10hrs, Duration 12-24hrs  Protaphane, Humulin NPH, Hypurin Isophane  Long Acting  Have either no peak or only a slight peak, duration up to 24hrs  Lantus or Levemir

Question 277

different insulin dosing regimens

Answer 277

 Basal-bolus regimen |  Split mixed regimen

Question 278

describe the Basal-bolus dosing regimen

Answer 278

 Dose of short acting insulin given before each meal  Intermediate or long acting insulin at bedtime  Mimics the bodies natural rhythms of insulin release

Question 279

describe the split mixed insulin dosing regimen

Answer 279

 Total daily dose is estimated and split  One third short acting and two thirds intermediate or long acting.  Two thirds before breakfast and one third before evening meal

Question 280

insulin administration care considerations

Answer 280

 Obtain blood glucose level as ordered – to monitor response to insulin and adjust dose as required.  Always verify the name of the insulin being given – each insulin has a different peak and duration and the names can be confused  Gently rotate the vial containing the agent and avoid vigorous shaking – ensure uniform suspension of insulin

Question 281

when should you not use an insulin vial

Answer 281

Checks prior to Administration  Do not give insulin if:  The clear insulin has turned cloudy  The expiry date has been reached  The insulin has been frozen or exposed to high temperature  Lumps or flakes are seen in the insulin  Deposits of insulin are seen on the inside of the vial which cannot be dissolved with gentle shaking or rotation  The vial has been open for longer than a month.

Question 282

how is insulin prescribed

Answer 282

 Insulin should be prescribed on insulin chart with full dosage instruction

Question 283

how is insulin stored

Answer 283

 Vials and Pens are for individual patient use only  Unopened insulin should be stored in a fridge (2-8 deg C)  Insulin in use can be stored at room temperature (below 25 deg C) for up to 28 days  Label the date and time of opening when insulin is first used  Should be discarded if out of fridge for more than 28 days  Do not use if insulin has expired

Question 284

what type of diabetes can use oral hypoglycemics

Answer 284

Oral Hypoglycaemics- only for type 2 diabetes

Question 285

drug groups of oral hypoglycemics

Answer 285

 Biguanides  Sulfonylureas  Thiazolidindiones Choice of drug depends on;  Patients weight  Pancreatic, renal and liver function - Response to trialled medications

Question 286

example of a biguanide

Answer 286

metformin

Question 287

metformin MOA

Answer 287

 Mechanism of action  Increase glucose uptake and utilisation in skeletal muscle ( reducing resistance to insulin)  Reduce glucose production in the liver (gluconeogenesis)  Reduce low and very low density lipoproteins  Increase insulin sensitivity via increasing number of receptors and affinity for receptors  Does not affect β cells – does not increase insulin release and not as likely to cause hypoglycaemia.  Less likely to cause weight gain and improves lipid profile

Question 288

metformin Adverse Reactions and Administration

Answer 288

Absorbed after oral dose from length of GIT  Half life (5-10 hours)  Excreted unchanged in urine Adverse Reactions  GI upset – N&V, anorexia and diarrhoea (common)

Question 289

metformin contraindications

Answer 289

 Patients with GI problems, severe liver or kidney disease (increases risk for lactic acidosis which can be a fatal adverse effect)  Pregnancy category C – preferred to use insulin during pregnancy

Question 290

metformin dosage and administration

Answer 290

 Orally with meals |  500mg once or twice daily, max. 1gm three times daily.

Question 291

example of Sulfonylureas

Answer 291

 Glibenclamide, glipizide, glicazide, glimepiride

Question 292

what do Sulfonylureas do

Answer 292

 Enhance release of insulin from β cells in pancreas  Increase the cellular sensitivity to insulin in the body tissues.  Decrease glycogenolysis and gluconeogenesis  Reduce blood concentration in people with a functioning pancreas

Question 293

describe Glibenclamide

Answer 293

Glibenclamide  Inactivated in the liver  Elimination half life (2-10hours) – variable  Adverse Reactions  Hypoglycaemia and weight gain  GI effects (N&V, abdominal distress) - common

Question 294

Glibenclamide Dosage and Administration

Answer 294

 Average Dose 2.5-20mg/day before breakfast  Doses over 10mg daily – remainder taken in the evening  Dosage individualised based on blood glucose levels

Question 295

Glibenclamide administraion care considerations

Answer 295

 Monitor response carefully – blood glucose monitoring is the most effective method  Monitor individuals during times of trauma, pregnancy or severe stress – may need to arrange to switch to insulin coverage as it is easier to titrate.  Ensure that the individual is following diet and exercise modifications – increase effectiveness of the drug and decrease adverse effects.

Question 296

what is immunity

Answer 296

* Immunity is a protection from disease or more specifically infectious disease. * Immune Response is the collective and coordinated response of the cells and molecules that make up the immune system.

Question 297

• Two defence mechanisms that protect the body

Answer 297

* Innate immunity – early and rapid response | * Adaptive immunity -later but highly effective

Question 298

presence of innate vs adaptive immunity

Answer 298

• Innate immunity is something already present in the body. • Adaptive immunity is created in response to exposure to a foreign substance.

Question 299

specifity of innate vs adaptive immunity

Answer 299

I- Non-specific A- Specific

Question 300

response of innate vs adapt immunity

Answer 300

I- Fights any foreign invader A- Fights specific infection

Question 301

response time innate vs adaptive immunity

Answer 301

I- Rapid A- Slow (1-2 weeks)

Question 302

time span innate vs adaptive immunity

Answer 302

I- Once activated against a specific type of antigen, the immunity remains throughout the life. A- The span of developed immunity can be lifelong or short.

Question 303

inheritance innate vs adaptive immunity

Answer 303

I- • Innate type of immunity is generally inherited from parents and passed to offspring. A- Adaptive immunity is not passed from the parents to offspring, hence it cannot be inherited.

Question 304

decribe innate immunity

Answer 304

* Components – skin, mucous membranes, phagocytic leukocytes (neutrophils and macrophages), specialised lymphocytes (natural killer cells) plasma proteins (including the proteins of the complement system) * Rapid Response within minutes to hours * Aim to prevent establishment of infection, deeper tissue penetration of microorganisms

Question 305

describe adaptive immunity

Answer 305

* Components – two group of lymphocytes and their products (including antibodies) * Recognise numerous microbial and non-infectious substances and develop a specific response for each * Substances that illicit an adaptive response are called antigens * Develops a memory – so able to respond more rapidly and effectively on next exposure * Two type * Humoral Immunity * Cell mediated immunity

Question 306

humeral vs cell mediated immunity

Answer 306

Humoral Immunity • Mediated by antibodies produced by B lymphocytes • Antibodies secreted into circulation and mucosal fluid where they act to eliminate microbes or toxins. • Prevent organisms from colonising in body tissues Cell mediated Immunity • Defends against intracellular microbes such as viruses • Mediated by T lymphocytes • May active phagocytes to destroy microbes • Other mays kill host cell harbouring microbes

Question 307

phagocytic cells

Answer 307

macrophages, granulocytes and dendritic cells

Question 308

role of macrophages

Answer 308

* Engulf and kill invading microorganisms (innate response) * Dispose of pathogens and infected cells targeted for disposal (adaptive response) * Induce inflammation, scavenger cells

Question 309

role of granulocytes

Answer 309

* Neutrophils (phagocytosis –destroy them using degenerative enzymes –innate immunity), * basophils and eosinophils (role unclear)involved in allergic reactions

Question 310

role of dendritic cells

Answer 310

* Capture foreign agents and transport them to peripheral lymphoid organs * Antigen presenting cell (present molecule to B and T lymphocytes to initiate adaptive response)

Question 311

b lymphocytes role

Answer 311

• Only cells capable of producing antibodies (mediate humoral immunity)

Question 312

t lymphocyte role

Answer 312

* Cell mediated immunity * Helper T cells – help B lymphocytes produce antibodies and help phagocytic cells destroy ingested pathogens * Cytotoxic T cells – kill or lyse intracellular microbes

Question 313

natural killer cells role

Answer 313

* Innate immune response * First line of defence against viral infections * Also recognises and kills tumour cells, abnormal body cells and cells infected with intracellular pathogens

Question 314

what are Immunoglobulins

Answer 314

• Immunoglobulins – protein compounds found in body fluids produced by B lymphocytes

Question 315

types of immunoglobin

Answer 315

* IgG * IgA * IgM * IgD * IgE

Question 316

immunoglobin IgG

Answer 316

• Most abundant, most protective activity against infection