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4TH YEAR > CSIM vascular > Flashcards

CSIM vascular Flashcards

1
Q

what are foam cells and when are they seen?

A

fat laden macrophages that are associated with atheroscelosis

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2
Q

what is it on a plaque that prevents thrombosis?

A

fibrin cap

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3
Q

stroke an TIA can be due to atherosclerosis in which artery?

A

carotids

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4
Q

symptoms of PAD?

A

most are asymptomatic

symptoms:

  • atypical exertional leg pain
  • only 10-20% have intermittent claudication
  • only a minority progress to rest pain / ulcers
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5
Q

investigations into claudication?

A

APBI
Duplex ultrasound
angiography

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6
Q

3 ways to do angiography?

A

catheter
MRA
CTA

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7
Q

where is claudication most common?

A

calf
buttock
thigh

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8
Q

what ABPI is diagnostic of PAD?

A

0.9

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9
Q

what does an ABPI of 1.35 tell you?

A

calcification in the blood vessels

ABPI> 1.30 means the vessel is non-compressable 
this can be due to:
- old age
- chronic renal insufficency
- diabetes
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10
Q

what is ABPI and what is a normal value?

A

ankle brachial pressure index:
ratio of systolic BP in the ankle compared to the arm

the BP in the arm should be higher:
normal range = 0.91 - 1.30

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11
Q

features of critical limb ischaemia?

A

pain @ rest
gangrene
necrosis
doppler pressure < 50mmHg at ANKLE

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12
Q

when is critical ischaemia pain worst?

A

at night due to draining blood from feet

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13
Q

how long does IHD pain normally last?

A

a few minutes
if > 5 then think MI
if fleeting then unlikely to be angina

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14
Q

angina precipitaing factors?

A

EEEE

exertion - most important
eating - blood drawn to GI system
emotion
extreme weather- very hot or cold

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15
Q

how is aortic dissection pain different to angina?

A

tearing pain with sudden onset

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16
Q

how is chostrochondritis pain different from angina

A

hurts to press on it

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17
Q

what blood test can be done to diagnose MI?

A

troponin T / I

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18
Q

what is troponin

A

protein released exclusively by cardiac muscle and rise significantly in cardiac muscle damage

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19
Q

what is metaclopramide?

A

anti - emetic often given with emetogenic drugs e.g. given with morphine

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20
Q

in suspected MI when should troponin be taken?

A

on admission and after 3 hours

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21
Q

how is troponin used to diagnose MI?

A

a rise of AT LEAST 10ng/l AND a 20% rise

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22
Q

what is junctional rhythm?

A

when the AV node takes over form the SA node

the rate of the AVN is ~40bpm so get bradycardia too

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23
Q

ECG: II, III and AVF ST elevation suggest what?

A

inferior ischaemia

AV-F -> points to Foot

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24
Q

what is fundaparinux

A

the smallest LMWH

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25
Q

after a stent is put in following MI what drug therapy should they be on?

A

B-blockers
Statins
DUEL ANTI-PLATELET: aspirin and clopidigel for 1 year - to prevent stent thrombosis

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26
Q

why do we use anti platelets in the prevention of stroke / MI?

A

the acute formation of a clot is due to the activation of platelets on the rupture of a plaque

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27
Q

danger of statins

A

teratogenic

contraindicated in pregnancy and breastfeeding

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28
Q

effect of other NSAIDS on anti-platelet therapy?

A

decrease action of aspirin

possibly compete for a receptor?

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29
Q

complications of hypertension

A 
MI
stoke
hypertensive nephrosclerosis
dissecting aortic aneurysm
peripheral vascular disease
accellerated (malignant) hypertensioin
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30
Q

what are the causes of HF

A

due to LV systolic dysfunction:

  • cardiomyopathy
  • hypertension
  • IHD

other cause:

  • anaemia
  • hyperthyroidism
  • arrhythmia
  • valve disease
  • diastolic dysfunction
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31
Q

causes of cardiomyopathy

A

familial
alcohol
viral

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32
Q

clinical definition of MI?

A

evidence of myocardial necrosis (raised troponin)
AND AT LEAST ONE OF
- Symptoms of ischaemia
- ECG changes indicating ischaemia
- ECG evidence of necrosis: new pathological Q waves
- Imaging - new loss of myocardium, or new RWMA

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33
Q

there are two types of MI he said we need to know, what are they?

A

type 1 - occlusion of coronary artery due to atherosclerosis (the normal type)

type 2 - imbalance in O2 supply/demand -> ischaemia without definite CAD

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34
Q

what is the most common presentation to A&E?

A

chest pain

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35
Q

first line ix in chest pain?

A

ECG- done before full history or examination

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36
Q

define typical angia?

A
  1. crushing central chest pain
  2. relieved by rest
  3. relieved by GTN spray

2/3 is atypical angina

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37
Q

if there is reduced pain with GTN angina is confirmed T/F?

A

F

oesphageal spasm is relieved by GTN too

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38
Q

when is there ST elevation?

A

when there has been complete occlusion of the coronary artery

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39
Q

when should the troponin be done in relation to other management steps?

A

after ECG, history and examinatioin

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40
Q

what type of MI can AF lead to?

A

type 2

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41
Q

how long after infarct is high sensitivity troponin detectable?

A

~1hr

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42
Q

what troponin level will be seen in an ST elevation MI?

A

very high, can be in the thousands

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43
Q

raised troponin is diagnostic of MI T/F? why?

A

F

other things raise it:

  • sepsis
  • PE
  • post operation
  • AF
  • renal disease
44
Q

what ix can rule out MI?

A

troponin taken 6 hrs later if not raised

45
Q

use of anti platelets in in ACS?

A

high dose aspirin ASAP

clopidegril if not tolerated

46
Q

what Ix is most useful for planning tx in ACS?

A

coronary angiogram, most people will have one

47
Q

discharge planning following ACS?

A

AABCCDDEE

anti-platelets and ACE inhibitors
B blockers
Cholesterol and ciggs
diabetes and diet
exercise and education
48
Q

diagnosis of acute coronary syndrome?

A

at least two of:

  1. Chest pain (>20 mins and not relieved by rest or GTN)
  2. ECG changes consistent with ischaemia or
    necrosis (ST elevation or NEW LBBB)
  3. Elevation of cardiac markers
49
Q

if suspecting ACS but ecg is normal, what ix to do next?

A

troponin

repete ECG in 30 mins

50
Q

why does BP increase with age?

A

decreased elasticity of large arteries due to:

  • increased calcium
  • increased collagen
  • decreased elastin
51
Q

what % of hypertension is ‘essential’?

A

80%

52
Q

common renal causes of hypertension?

A

glomerulonephritis
diabetes
polycystic kidneys

53
Q

endocrine causes of hypertension?

A

steroid excess

54
Q

what does angiotensin II do?

A

vasoconstriction

makes adrenal glands release aldosterone

55
Q

what does aldosterone do?

A

makes kidney reabsorb Na+

56
Q

what BP makes you suspect phaeochromocytoma?

A

fluctuating

hypertension with postural hypOtentension

57
Q

why do kidney US in hypertension

A

exclude polycystic disease

a shrunken kidney may suggsest renal artery stenosis

58
Q

initial tests in those with hypertension?

A

test urine for presence of protein
take blood to measure glucose, electrolytes, creatinine
estimated glomerular filtration rate
cholesterol
examine fundi for hypertensive retinopathy
arrange a 12-lead ECG

59
Q

ECG: what leads show the inferior heart border?

A

II, III and AVF

60
Q

ECG: what leads show the lateral heart border?

A

I, V5 and V6

61
Q

ECG: what leads show the anterior heart border?

A

V1 -> V4

62
Q

ST elevation in I, V3, V4, V5, V6 indicates what?

A

anterior lateral STEMI

63
Q

what hx is relevant in the assessment of dyslipidaemia?

A

symptoms of related conditions

  • angina, claudication, dyspnoea
  • thirst / polyuria

risk factors

  • diet
  • alcohol
  • smoking
  • exercise

family history

64
Q

how does fat distribution effect risks associated with obesity?

A

central obesity is worse than peripheral

potentially because it drains straight to the liver

65
Q

what stigmata of hyperlipidaemia?

A

XANTHOLASMA

Eyes – eyelids, cornea, retina
Achilles and digital extensor tendons
Knees and elbows
Palms and flexures

66
Q

pathophys of hyperlipidaemia -> increased CV risk?

A
  • LDLs infiltrate the tunica intima causing it to expand (this is a fatty streak)
  • inflammation causes macrophage recruitment
  • macrophages take up lipids making FOAM cells
  • dying macrophage, mast cells and a fibrous, necrotic plaque make a complicated plaque
67
Q

which are the major atherogenic lipoproteins?

A

LDLs
IDLs
LP(a)

chylomycron-remnants

these can all infiltrate the endothelium to get into the tunica intima

68
Q

which lipoproteins are included in the total cholesterol blood test?

A

LDL
VLDL
IDL
HDL

69
Q

what is the triglyceride level used for?

A

calculating the LDL level

not considered directly atherogenic but is a RISK MODIFIER

70
Q

should you fast for a cholesterol test?

A

no

71
Q

what is the best marker for the risk of CV disease?

A

ratio of apolipoprotein b to apolipoprotein a

apoB is ‘BAD cholesterol’
apoA is ‘GOOD cholesterol’

therefore the higher the ratio of b : a the higher the risk

72
Q

investigations to exclude secondary hyperlipaemias?

A 
renal profile - exclude renal failure
liver profile - exclude cholestasis
TFTS - exclude hypOthyroidism
glucose / HbA1c - exclude diabetes
dipstick - exclude nephrotic syndrome
73
Q

familial hyperlipidaemia: how is it passed on and how does it effect lipid profile?

A

autosomal dominant
reduce clearance of LDLs -> doubled LDLs from childhood
low fasting triglycerides

74
Q

diagnosis of familial hyperlipidaemia?

A

genetic testing is necessary as there is an overlap in the LDL profile

75
Q

who do we test for familial combined hyperlipidaemia?

A

moderate to severe mixed hyperlipidaemia
AND
personal / family history of CVD or hyperlipidaemia

dont test children for this as it’s not useful

76
Q

how does remnant hyperlipidaemia lead to deranged lipid profile? and what is that profile?

A

reduced clearance of remnant
high total cholesterol
high triglycerides

77
Q

what does palmar xantholasma suggest?

A

pathognomic of remnant hyperlidipaemia

78
Q

what is isolated hypertriglyceridaemia closely related to?

A

diatebes

79
Q

pancreatitis is a complication of which metabolic problem?

A

severe hypertriglyceridaemia

80
Q

what does a raised CK tell you?

A

there has been muscle break down

NOT specific to cardiac muscle

81
Q

what is the best marker for cardiac muscle death?

A

Trop I

82
Q

what drug class is amlodipine

A

CCB

83
Q

what drug class is verapamil?

A

CCB

84
Q

what is the first line tx for AF?

A

B blockers

85
Q

what is CHAD vasc used for?

A

calculating risk of stroke in AF patients

86
Q

what is HAS BLED used for?

A

calculating 1 yr risk of bleeding in AF patients

87
Q

what is amaurosis fugax?

A

transient (and painless) loss of vision- TIA of the retinal artery

from the greek for ‘fleeting darkness’

88
Q

what is the first line Ix if carotid bruit is heard?

A

duplex US

89
Q

what counts as ‘sudden’ death?

A

occurs within 1 hour of onset of symptoms

90
Q

what is the most common cause of syncope in HCM patients?

A

vasovagal syndrome- this is just very common in general

91
Q

most common cause of sudden death in the UK

A

coronary artery disease

by far

92
Q

what are the signs that are useful in predicting cardiac syncope?

A

Any sign of heart failure
Left ventricular dysfunction (best predictor)

Carotid sinus hypersensitivity (elderly)- rub the carotid bulb and see if they pass out

ECG abnormalities

93
Q

what investigations would you in suspected cardiac syncope?

A 
ECG
Echo
Heart monitors
Genetic testing
MRI of heart for anyone with ?structural heart disease- better than echo
94
Q

what re the red flags in cardiac syncope?

A

Any pre-existing cardiac history

Any malignant sounding family history

95
Q

what does a slurring of the Q wave indicate?

A

WPW syndrome

96
Q

a very short PQ interval indicates what?

A

WPW syndrome

97
Q

how do channelopathies cause cardiac arrest?

A

cells are firing and resetting at different times which leads to polymorphic VT or VF

98
Q

what happens in arrthymogenic right ventricular cardiomyopathy? what ECG does this give?

A

clusters of fat and fibrous tissue get depositied in between cells (due to weakened connecting proteins between the cells) in response to stretch damage which occurs mostly in the RV and worsens with exercise

monomorphic VT / VF

99
Q

what is dilated cardiomyopathy and what are the two ways it can happen?

A

SAGGY HEART: the chamber dilates and scars form either due:

to an idiopathic/’poisoning’ process

Or due to the actual scar of the infarct plus super-added damage due to the neuro-hormonal response in chronic heart failure

100
Q

what is commotio cordis?

A

blow over the heart -> VF

101
Q

what kind of ECG does long QT syndrome give?

A

polymorphic VT

102
Q

where is there slow conduction in a post infarct heart?

A

around the scar

there is NO conduction where the scar is

103
Q

Most LQTS involve problems with what channels?

A

potassium

104
Q

what is first line imaging for PAD in whom revascularisation is being considered?

A

duplex ultrasound

105
Q

effect of NSIADs on platelets?

A

enhance effect of low dose aspirin

106
Q

how do NSAIDs increase risk of MI?

A

worsen HF due to effect on prostaglandins - > sodium retention

107
Q

an absolute risk reduction of 4% means you have to treat how many people to avoid one event?

A

25 - this is considered an okay number

4TH YEAR (12 decks)

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