Flashcards in CSIM vascular Deck (107):
what are foam cells and when are they seen?
fat laden macrophages that are associated with atheroscelosis
what is it on a plaque that prevents thrombosis?
stroke an TIA can be due to atherosclerosis in which artery?
symptoms of PAD?
most are asymptomatic
- atypical exertional leg pain
- only 10-20% have intermittent claudication
- only a minority progress to rest pain / ulcers
investigations into claudication?
3 ways to do angiography?
where is claudication most common?
what ABPI is diagnostic of PAD?
what does an ABPI of 1.35 tell you?
calcification in the blood vessels
ABPI> 1.30 means the vessel is non-compressable
this can be due to:
- old age
- chronic renal insufficency
what is ABPI and what is a normal value?
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
features of critical limb ischaemia?
pain @ rest
doppler pressure < 50mmHg at ANKLE
when is critical ischaemia pain worst?
at night due to draining blood from feet
how long does IHD pain normally last?
a few minutes
if > 5 then think MI
if fleeting then unlikely to be angina
angina precipitaing factors?
exertion - most important
eating - blood drawn to GI system
extreme weather- very hot or cold
how is aortic dissection pain different to angina?
tearing pain with sudden onset
how is chostrochondritis pain different from angina
hurts to press on it
what blood test can be done to diagnose MI?
troponin T / I
what is troponin
protein released exclusively by cardiac muscle and rise significantly in cardiac muscle damage
what is metaclopramide?
anti - emetic often given with emetogenic drugs e.g. given with morphine
in suspected MI when should troponin be taken?
on admission and after 3 hours
how is troponin used to diagnose MI?
a rise of AT LEAST 10ng/l AND a 20% rise
what is junctional rhythm?
when the AV node takes over form the SA node
the rate of the AVN is ~40bpm so get bradycardia too
ECG: II, III and AVF ST elevation suggest what?
AV-F -> points to Foot
what is fundaparinux
the smallest LMWH
after a stent is put in following MI what drug therapy should they be on?
DUEL ANTI-PLATELET: aspirin and clopidigel for 1 year - to prevent stent thrombosis
why do we use anti platelets in the prevention of stroke / MI?
the acute formation of a clot is due to the activation of platelets on the rupture of a plaque
danger of statins
contraindicated in pregnancy and breastfeeding
effect of other NSAIDS on anti-platelet therapy?
decrease action of aspirin
possibly compete for a receptor?
complications of hypertension
dissecting aortic aneurysm
peripheral vascular disease
accellerated (malignant) hypertensioin
what are the causes of HF
due to LV systolic dysfunction:
- valve disease
causes of cardiomyopathy
clinical definition of MI?
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
there are two types of MI he said we need to know, what are they?
type 1 - occlusion of coronary artery due to atherosclerosis (the normal type)
type 2 - imbalance in O2 supply/demand -> ischaemia without definite CAD
what is the most common presentation to A&E?
first line ix in chest pain?
ECG- done before full history or examination
define typical angia?
1. crushing central chest pain
2. relieved by rest
3. relieved by GTN spray
2/3 is atypical angina
if there is reduced pain with GTN angina is confirmed T/F?
oesphageal spasm is relieved by GTN too
when is there ST elevation?
when there has been complete occlusion of the coronary artery
when should the troponin be done in relation to other management steps?
after ECG, history and examinatioin
what type of MI can AF lead to?
how long after infarct is high sensitivity troponin detectable?
what troponin level will be seen in an ST elevation MI?
very high, can be in the thousands
raised troponin is diagnostic of MI T/F? why?
other things raise it:
- post operation
- renal disease
what ix can rule out MI?
troponin taken 6 hrs later if not raised
use of anti platelets in in ACS?
high dose aspirin ASAP
clopidegril if not tolerated
what Ix is most useful for planning tx in ACS?
coronary angiogram, most people will have one
discharge planning following ACS?
anti-platelets and ACE inhibitors
Cholesterol and ciggs
diabetes and diet
exercise and education
diagnosis of acute coronary syndrome?
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
if suspecting ACS but ecg is normal, what ix to do next?
repete ECG in 30 mins
why does BP increase with age?
decreased elasticity of large arteries due to:
- increased calcium
- increased collagen
- decreased elastin
what % of hypertension is 'essential'?
common renal causes of hypertension?
endocrine causes of hypertension?
what does angiotensin II do?
makes adrenal glands release aldosterone
what does aldosterone do?
makes kidney reabsorb Na+
what BP makes you suspect phaeochromocytoma?
hypertension with postural hypOtentension
why do kidney US in hypertension
exclude polycystic disease
a shrunken kidney may suggsest renal artery stenosis
initial tests in those with hypertension?
test urine for presence of protein
take blood to measure glucose, electrolytes, creatinine
estimated glomerular filtration rate
examine fundi for hypertensive retinopathy
arrange a 12-lead ECG
ECG: what leads show the inferior heart border?
II, III and AVF
ECG: what leads show the lateral heart border?
I, V5 and V6
ECG: what leads show the anterior heart border?
V1 -> V4
ST elevation in I, V3, V4, V5, V6 indicates what?
anterior lateral STEMI
what hx is relevant in the assessment of dyslipidaemia?
symptoms of related conditions
- angina, claudication, dyspnoea
- thirst / polyuria
how does fat distribution effect risks associated with obesity?
central obesity is worse than peripheral
potentially because it drains straight to the liver
what stigmata of hyperlipidaemia?
Eyes – eyelids, cornea, retina
Achilles and digital extensor tendons
Knees and elbows
Palms and flexures
pathophys of hyperlipidaemia -> increased CV risk?
- 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
which are the major atherogenic lipoproteins?
these can all infiltrate the endothelium to get into the tunica intima
which lipoproteins are included in the total cholesterol blood test?
what is the triglyceride level used for?
calculating the LDL level
not considered directly atherogenic but is a RISK MODIFIER
should you fast for a cholesterol test?
what is the best marker for the risk of CV disease?
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
investigations to exclude secondary hyperlipaemias?
renal profile - exclude renal failure
liver profile - exclude cholestasis
TFTS - exclude hypOthyroidism
glucose / HbA1c - exclude diabetes
dipstick - exclude nephrotic syndrome
familial hyperlipidaemia: how is it passed on and how does it effect lipid profile?
reduce clearance of LDLs -> doubled LDLs from childhood
low fasting triglycerides
diagnosis of familial hyperlipidaemia?
genetic testing is necessary as there is an overlap in the LDL profile
who do we test for familial combined hyperlipidaemia?
moderate to severe mixed hyperlipidaemia
personal / family history of CVD or hyperlipidaemia
dont test children for this as it's not useful
how does remnant hyperlipidaemia lead to deranged lipid profile? and what is that profile?
reduced clearance of remnant
high total cholesterol
what does palmar xantholasma suggest?
pathognomic of remnant hyperlidipaemia
what is isolated hypertriglyceridaemia closely related to?
pancreatitis is a complication of which metabolic problem?
what does a raised CK tell you?
there has been muscle break down
NOT specific to cardiac muscle
what is the best marker for cardiac muscle death?
what drug class is amlodipine
what drug class is verapamil?
what is the first line tx for AF?
what is CHAD vasc used for?
calculating risk of stroke in AF patients
what is HAS BLED used for?
calculating 1 yr risk of bleeding in AF patients
what is amaurosis fugax?
transient (and painless) loss of vision- TIA of the retinal artery
from the greek for 'fleeting darkness'
what is the first line Ix if carotid bruit is heard?
what counts as 'sudden' death?
occurs within 1 hour of onset of symptoms
what is the most common cause of syncope in HCM patients?
vasovagal syndrome- this is just very common in general
most common cause of sudden death in the UK
coronary artery disease
what are the signs that are useful in predicting cardiac syncope?
Any sign of heart failure
Left ventricular dysfunction (best predictor)
Carotid sinus hypersensitivity (elderly)- rub the carotid bulb and see if they pass out
what investigations would you in suspected cardiac syncope?
MRI of heart for anyone with ?structural heart disease- better than echo
what re the red flags in cardiac syncope?
Any pre-existing cardiac history
Any malignant sounding family history
what does a slurring of the Q wave indicate?
a very short PQ interval indicates what?
how do channelopathies cause cardiac arrest?
cells are firing and resetting at different times which leads to polymorphic VT or VF
what happens in arrthymogenic right ventricular cardiomyopathy? what ECG does this give?
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
what is dilated cardiomyopathy and what are the two ways it can happen?
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
what is commotio cordis?
blow over the heart -> VF
what kind of ECG does long QT syndrome give?
where is there slow conduction in a post infarct heart?
around the scar
there is NO conduction where the scar is
Most LQTS involve problems with what channels?
what is first line imaging for PAD in whom revascularisation is being considered?
effect of NSIADs on platelets?
enhance effect of low dose aspirin
how do NSAIDs increase risk of MI?
worsen HF due to effect on prostaglandins - > sodium retention