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2A content- Sameera > *ILA* > Flashcards

*ILA* Flashcards

1
Q

what is the structure of an artery (3)

A

inner intima
media
outer adventitia

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2
Q

what are modifiable risk factors for atherosclerosis (6)

A

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

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3
Q

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

A

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

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4
Q

what are examples of primary prevention (4) regarding atherosclerosis

A

stop smoking, exercise, diet, decrease alcohol intake

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5
Q

what is secondary prevention and what is its aim

A

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

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6
Q

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

A

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

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7
Q

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

A

PCI- stents
CABG

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8
Q

define a co-benefit of health and climate change

A

extra non-direct benefits from controlling climate change on health

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9
Q

what are the 4 steps of atherosclerosis formation

A
  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
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10
Q

what can cause endothelial lining damage (2)

A

smoking, T2DM

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11
Q

how can T2DM cause endothelial damage

A

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

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12
Q

explain what happens at the fatty streak formation in atherosclerosis formation

A

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

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13
Q

what stage of atherosclerosis is reversible

A

fatty streak formation

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14
Q

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

A

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

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15
Q

where is the fibrous cap located in atherosclerosis

A

the fibrous cap cover the internal lumen side of the plaque

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16
Q

what is a stable atherosclerotic plaque

A

non-ruptured

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17
Q

what can atherosclerotic plaque rupture cause (3)

A

ischaemia, cerebrovascular thrombus and peripheral vascular disease

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18
Q

what is anaphylaxis

A

Gell and Coombs IgE mediated hypersensitivity to an otherwise normal allergen

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19
Q

what can trigger anaphylaxis 6

A

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

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20
Q

what r the risk factors of anaphylaxis 2

A

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

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21
Q

what are the two stages of anaphylaxis

A

sensitisation then secondary exposure

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22
Q

what happens during the sensitisation stage of anaphylaxis (3)

A
  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
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23
Q

what happens in the secondary exposure stage of anaphylaxis

A

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

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24
Q

explain why bronchospasm occurs in anaphylaxis

A

due to smooth muscle spasm

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25
Q

what are the clinical signs of anaphylaxis (4)

A

bronchoconstriction, hypotension, tachycardia, central cyanosis

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26
Q

what can anaphylactic shock be classed as

A

a medical emergency

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27
Q

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

A

deterioration after antigen exposure

28
Q

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

A

ABCDE
IM adrenaline 500mcg

29
Q

why is a second dose of adrenaline sometimes needed in anaphylaxis

A

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

30
Q

what test can confirm anaphylaxis and what does it read?

A

serum mast cell tryptase= specific reading for mast cell degranulation

31
Q

what is prevelance

A

number of cases at a given point in time

32
Q

what is incidence

A

number of new cases in a given time frame

33
Q

what two things will make an anaesthetic more effective

A

high protein binding
highly lipid soluble

34
Q

why are anaesthetics high protein binding

A

binds to receptors so it has a longer effect

35
Q

why are anaesthetics highly lipid soluble

A

increases potency and can cross BBB early (2)

36
Q

why are two anaesthesias given to a patient for surgery

A

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

37
Q

what happens to EC50 for competitive and non-competitive antagonists

A

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

38
Q

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

A

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%

39
Q

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

A

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

40
Q

how is morphine prescribed in a patient with renal impairment

A

decreased morphine dose

41
Q

what r the names of factor 2 and 2a

A

2= prothrombin
2a= thrombin

42
Q

what r the names of factor 1 and 1a

A

1= fibrinogen
1a= fibrin

43
Q

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

A

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

44
Q

how is the intrinsic pathway activated

A

activated by vascular endothelium damage

45
Q

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

A

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

46
Q

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

A

positive D-Dimer test
duplex doppler US

47
Q

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

A

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.

48
Q

how does heparin work

A

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

49
Q

what factors does heparin work on

A

2 and 10

50
Q

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

A

short half life
acts rapidly

51
Q

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

A

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

52
Q

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

A

longer half life
slower onset

53
Q

what is INR

A

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

54
Q

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

A

blood takes too long to clot= increased risk of bleeding

55
Q

what r signs of a PE (6)

A

sudden onset chest pain
syncope
tachycardia
ankle odema
dyspnoea
hemoptysis

56
Q

advice to reduce DVT on long haul flights (3)

A

compression stockings
stay hydrated
exercise legs regularly

57
Q

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

A

amaurosis fugax
mostly caused by carotid artery stenosis

58
Q

compare rhythms of atrial fibrillation and flutter

A

fibrillation is irregularly irregular
flutter is regularly irregular

59
Q

what is cushings reflex

A

body’s response to raised intercranial pressure

60
Q

what is the triad of presentation for cushings reflex

A

triad:
hypertension
bradycardia
irregular respirations

61
Q

explain the pathophysiology of the cushings reflex 4

A
  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
62
Q

what causes raised intracranial pressure 3

A

ischaemic and haemorrhagic stroke, hypertension

63
Q

what are the two main physiological mechanisms of damage for AKI

A

reduction in GFR
damage to glomeruli

64
Q

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

A

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

65
Q

what is given with insulin to prevent hypoglycaemia

A

dextrose

66
Q

what are the complications of AKI 3

A

pulmonary/ peripheral oedema
hyperkalaemia
uremic pericarditis

67
Q

what is amaurosis fugax and what causes this 2

A

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

2A content- Sameera (21 decks)

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