*ILA*

Question 1

what is the structure of an artery (3)

Answer 1

inner intima
media
outer adventitia

Question 2

what are modifiable risk factors for atherosclerosis (6)

Answer 2

smoking, sedentary lifestyle, weight, hypertension, high cholesterol, diabetes

Question 3

what are non-modifiable risk factors for atherosclerosis (3)

Answer 3

age (more fatty streaks), family history, male gender (earlier fatty streak formation)

Question 4

what are examples of primary prevention (4) regarding atherosclerosis

Answer 4

stop smoking, exercise, diet, decrease alcohol intake

Question 5

what is secondary prevention and what is its aim

Answer 5

detecting during early disease development and aims to intervene before development of disease

Question 6

examples of secondary intervention for aatherosclerosis and what does each of them do (3)

Answer 6

aspirin (inhibits platelelt aggregation)
atorvastatin (reduces cholesterol levels)
atenolol (controls hypertension)

Question 7

what are the 2 tertiary preventative measures for atherosclerosis (surgical)

Answer 7

PCI- stents
CABG

Question 8

define a co-benefit of health and climate change

Answer 8

extra non-direct benefits from controlling climate change on health

Question 9

what are the 4 steps of atherosclerosis formation

Answer 9

1. endothelial lining damage
2. formation of fatty streaks in intima
3. inflammatory response where leukocytes attach the endothelial lining
4. platelet and plaque formation with a fibrous smooth muscle cap

Question 10

what can cause endothelial lining damage (2)

Answer 10

smoking, T2DM

Question 11

how can T2DM cause endothelial damage

Answer 11

poorly controlled diabetes mellitus can cause oxidative stress on vascular system= endothelial damage

Question 12

explain what happens at the fatty streak formation in atherosclerosis formation

Answer 12

low density lipoproteins enter the endothelium and r phagocytosed by macrophages and become foam cells

Question 13

what stage of atherosclerosis is reversible

Answer 13

fatty streak formation

Question 14

explain what happens when leukocytes attack the endothelial lining in atherosclerosis formation

Answer 14

foam cells recruit other inflammatory cells eg neutrophils, macrophages, lymphocytes

Question 15

where is the fibrous cap located in atherosclerosis

Answer 15

the fibrous cap cover the internal lumen side of the plaque

Question 16

what is a stable atherosclerotic plaque

Answer 16

non-ruptured

Question 17

what can atherosclerotic plaque rupture cause (3)

Answer 17

ischaemia, cerebrovascular thrombus and peripheral vascular disease

Question 18

what is anaphylaxis

Answer 18

Gell and Coombs IgE mediated hypersensitivity to an otherwise normal allergen

Question 19

what can trigger anaphylaxis 6

Answer 19

pollen, pets, dust, nuts, drugs (penicillins), contrast media
2 P, 2 D, C, N

Question 20

what r the risk factors of anaphylaxis 2

Answer 20

family history, atopic triad (asthma, allergic rhinitis, eczema)

Question 21

what are the two stages of anaphylaxis

Answer 21

sensitisation then secondary exposure

Question 22

what happens during the sensitisation stage of anaphylaxis (3)

Answer 22

1. 1st exposure to trigger
2. IgE forms against the antigen and binds via Fc to mast cell
3. this primes the antibodies in the body

Question 23

what happens in the secondary exposure stage of anaphylaxis

Answer 23

allergen binds to FAb region of IgE and this results in mast cell degranulation, releasing leukotrienes, tryptases and histamine

Question 24

explain why bronchospasm occurs in anaphylaxis

Answer 24

due to smooth muscle spasm

Question 25

what are the clinical signs of anaphylaxis (4)

Answer 25

bronchoconstriction, hypotension, tachycardia, central cyanosis

Question 26

what can anaphylactic shock be classed as

Answer 26

a medical emergency

Question 27

what is a sign of anaphylaxis exposure to an allergen (1)

Answer 27

deterioration after antigen exposure

Question 28

what is the step by step treatment of anaphylaxis (2)

Answer 28

ABCDE IM adrenaline 500mcg

Question 29

why is a second dose of adrenaline sometimes needed in anaphylaxis

Answer 29

adrenaline has a short half life so it may not have been effective as its concentration reduced too rapidly

Question 30

what test can confirm anaphylaxis and what does it read?

Answer 30

serum mast cell tryptase= specific reading for mast cell degranulation

Question 31

what is prevelance

Answer 31

number of cases at a given point in time

Question 32

what is incidence

Answer 32

number of new cases in a given time frame

Question 33

what two things will make an anaesthetic more effective

Answer 33

high protein binding highly lipid soluble

Question 34

why are anaesthetics high protein binding

Answer 34

binds to receptors so it has a longer effect

Question 35

why are anaesthetics highly lipid soluble

Answer 35

increases potency and can cross BBB early (2)

Question 36

why are two anaesthesias given to a patient for surgery

Answer 36

IV anaesthesia is given first to sedate patient (short half life) then followed by volatile anaesthesia to keep patient knocked out (longer half life)

Question 37

what happens to EC50 for competitive and non-competitive antagonists

Answer 37

comp= EC50 stays the same just a higher concentration is needed non-c= EC50 is decreased

Question 38

what is first pass metabolism/ first pass effect and give an example with its bioavailability after first pass metabolism

Answer 38

where a drug is metabolised which reduces the amount of active drug before it reaches the systemic circulation eg morphine undergoes phase 1 and phase 2 detoxification by the liver thats why bioavailability reduced to 50%

Question 39

what form is morphine excreted as and what is significant about this

Answer 39

morphine-6-glucuronide it's toxic to the body

Question 40

how is morphine prescribed in a patient with renal impairment

Answer 40

decreased morphine dose

Question 41

what r the names of factor 2 and 2a

Answer 41

2= prothrombin 2a= thrombin

Question 42

what r the names of factor 1 and 1a

Answer 42

1= fibrinogen 1a= fibrin

Question 43

when does the extrinsic pathway for the coagulation cascade occur and how

Answer 43

endothelial tissue injury exposed tissue factor in blood (factor 3)

Question 44

how is the intrinsic pathway activated

Answer 44

activated by vascular endothelium damage

Question 45

what is unique about the intrinsic pathway for coagulation cascade and why is this useful

Answer 45

has a + feedback loop which allows the fibrin plus to form quickly in the blood

Question 46

what is the blood test 1st line for DVT and GS/ diagnostic

Answer 46

positive D-Dimer test duplex doppler US

Question 47

what is d-dimer and what does it mean if there is a high d dimer value

Answer 47

product released when fibrin from a 2nd platelet plug is fibrinolysed If there r higher levels than normal of this product, it means there r higher levels of clot formation and degradation.

Question 48

how does heparin work

Answer 48

binds unselectively to antithrombin 3 which activates this and this inactivates certain factors in the coagulation cascade

Question 49

what factors does heparin work on

Answer 49

2 and 10

Question 50

state the half life and how fast heparin acts (general)

Answer 50

short half life acts rapidly

Question 51

how does warfarin act and what factors does it work on and what effect does this have

Answer 51

vitamin K antagonist prevents factors 2, 7, 9 and 10 being synthesised which prolongs prothrombin action

Question 52

state the half life and how fast warfarin acts (general)

Answer 52

longer half life slower onset

Question 53

what is INR

Answer 53

prothrombin time (measure time taken for a clot to form from a blood sample

Question 54

what does a high INR mean and what risk does this increase

Answer 54

blood takes too long to clot= increased risk of bleeding

Question 55

what r signs of a PE (6)

Answer 55

sudden onset chest pain syncope tachycardia ankle odema dyspnoea hemoptysis

Question 56

advice to reduce DVT on long haul flights (3)

Answer 56

compression stockings stay hydrated exercise legs regularly

Question 57

what is the term for transient visual disturbances and what causes this

Answer 57

amaurosis fugax mostly caused by carotid artery stenosis

Question 58

compare rhythms of atrial fibrillation and flutter

Answer 58

fibrillation is irregularly irregular flutter is regularly irregular

Question 59

what is cushings reflex

Answer 59

body's response to raised intercranial pressure

Question 60

what is the triad of presentation for cushings reflex

Answer 60

triad: hypertension bradycardia irregular respirations

Question 61

explain the pathophysiology of the cushings reflex 4

Answer 61

1. high intra-cranial pressure due to inflammation in the brain 2. this leads to poor cerebral perfusion and ischaemia of the brain 3. blood pressure increases due to arterial smooth muscle vasoconstriction to re-perfuse the brain 4. baroreceptors in the aorta detect the increase in blood pressure and initiate bradycardia to counteract the high blood pressure

Question 62

what causes raised intracranial pressure 3

Answer 62

ischaemic and haemorrhagic stroke, hypertension

Question 63

what are the two main physiological mechanisms of damage for AKI

Answer 63

reduction in GFR damage to glomeruli

Question 64

why are NSAIDs contraindicated for renal failure patients (what do they specifically do in their mechanism of action)

Answer 64

inhibits cox 1 and 2 which decreases prostaglandin secretion this decreases prostaglandin mediated vasodilation this decreases GFR= renal damage

Question 65

what is given with insulin to prevent hypoglycaemia

Answer 65

dextrose

Question 66

what are the complications of AKI 3

Answer 66

pulmonary/ peripheral oedema hyperkalaemia uremic pericarditis

Question 67

what is amaurosis fugax and what causes this 2

Answer 67

temporary/ transient visual disturbance loss of blood supply due to cartoid artery stenosis