Vascular disease

Question 1

3 stages of Atherosclerosis

Answer 1

1. Initiation: Foam cells > fatty streak
2. Transition: Fatty streak > fibrous cap (atheroma)
3. Progression: Unstable plaque > rupture > occlusion

Question 2

Vasodilatory factors and vasoconstriction factors

Answer 2

Vasodilation: NO, PGI2, COX

Vasoconstriction: ET-1, Angiotensin II, Thromboxane 2

Question 3

Order of Ix + Mx in carotid artery stenosis

Answer 3

1. Colour duplex ultrasound
2. CT/MRI angiography
3. Endarterectomy if over 70% stenosed

Question 4

Peripheral artery disease
Sx
Ix
Mx

Answer 4

Asymptomatic until 70% stenosed
Absent pulses + intermittent claudication (hypoxic), rest pain + ulcers = severe

1. Examine for absent pulses
2. ABPI to quantify
   <0.9 = PAD
   <0.4 = severe
   >1.3 = non-compressible / DM calcification
3. Duplex ultrasound is first imaging
4. MRI angiography is GOLD STANDARD

Clopidogrel + heparin
Angioplasty _/- stent OR bypass if surgery required

Question 5

6P’s of critical limb ischemia

Intermittent claudication vs critical limb ischemia

Answer 5

Pain, pallor, paralysis, paraesthesia, pulseless, perishing cold

Pain features: Critical limb ischemia hurts at rest and is worse at night, requiring patient to hang leg out of bed to drain blood! Claudication is only on movement

Pain location: Critical is feet or toes. Claudication is calf.

Gangrere or ulcers is only seen in critical

ABPI:
<0.9 = PAD
<0.4 = severe
>1.3 = non-compressible / DM calcification

ABPI or duplex ultrasound then angiography

Question 6

Metabolic syndrome

Answer 6

At least 3 of:

Mnemonic for criteria for Metabolic Syndrome: W.E.I.G.H.T.

WE = waist expanded (>35in F, 40in M)
IG = impaired glucose (>110mg/dl)
H = hypertension (BP >130/85)
H = HDL low (<50mg/dl F, <40mg M)
T = TGs > 150mg/dl

Question 7

3 features of typical angina

Answer 7

1. Constricting pain in chest/shoulders/arms/jaw
2. Comes on with exertion
3. Relieved with rest or GTN within 5 minutes

Question 8

First line Ix in suspected ACS

Answer 8

1. ECG!
2. CXR
3. Troponin. MAx sensitivity at 12-24hrs. Do one on admission and then again within 3 hours and look for rise of >10 or >20%

Question 9

MI = high troponin AND

Answer 9

Symptoms of ischemia
ECG changes in ST or new LBBB
New pathological Q waves
Imaging evidence of loss of myocardium

Question 10

Decubitus angina

Prinzmetals angina

Answer 10

Decubitus angina = Angina lying down

Prinzmetals angina = vasospasm of coronary artery causing angina like symptoms

Question 11

Type 1 MI

Type 2 MI

Answer 11

Occlusion (complete occlusion = Q wave and ST elevation)

HF or arrhythmias

Question 12

ACS algorithm

Answer 12

1. All get MONA until you get to ECG
2. ECG + troponin
   a. If STEMI or new LBBB then cath lab (alongside usual MONAC treatment)
   b. If unstable angina or NSTEMI do GRACE risk assessment:
   i. Low = 300mg clopidogrel and assess for need of coronary angiography via ischemic testing
   ii. High risk then fondaparinux/unfractionated heparin (if angiography soon, as fondaparinux lasts a while and harder to reverse), clopdogrel, highest risk also get a glycoprotein IIb/IIIa receptor antagonist and prepare for coronary angiography with view to PCI
3. Troponin again after 3 hours
4. Bloods, CXR, ABGs, Echo, CMRI, PCI

Question 13

Other causes of raised troponin

Answer 13

PE
sepsis
post-op
AF
LVF

Question 14

MI + ECG leads + Artery

Answer 14

II, III, aVF = Inferior = R coronary artery

V1-V4 = Anterior = L anterior descending

I, V5-V6 = Lateral = Circumflex artery

Question 15

TIMI

GRACE

Answer 15

TIMI: For NSTEMI 14day risk of death

GRACE: 6month death/MI risk - used to determine whether low risk - clopidogrel OR high risk - heparin/fondaparinux in unstable/NSTEMI patients

Question 16

ECG changes risk order

Answer 16

1. ST elevation with co-existing depression
2. ST depression
3. ST elevation
4. T wave inversion

Question 17

MI Mx

Answer 17

1. Aspirin 300mg, clopidogrel/tricagrelor AND fondaparinux
2. GP IIb/IIIa inhibitors in those with severe pain or DM Hx
3. HR >60 give B blocker
4. Nitrates if ongoing pain
5. Statins 80mg
6. ACE inhibitors

Question 18

Subsequent MI Mx - A3BCDE

Answer 18

A. Atorvastatin 80mg, ACE Inhibitor (LV dysfunction), Aspirin
B. Beta-blocker (if HR not too low) and blood pressure below <140
C. Clopidogrel
D. Diet and diabetes
E. Education + exercise

Question 19

Normal angina Mx

Answer 19

1. Lifestyle
2. Aspirin/clopidogrel
3. GTN for symptom relief + long acting nitrate (isorbide mononitrate)
4. B blocker (reduce cardiac load)
5. CCB
6. Statin

Question 20

Hypertension
NICE definition
Pathophysiology (3)

Answer 20

> 140/90 or ABPM >135/85

1. Decreased elasticity and compliance of arteries due to accumulation of calcium and collagen and degradation of elastin.
2. Stiffened vessels = increased systolic pressure
3. Defective sodium storage leads to excessive retention

Question 21

Drugs that cause HTN

Answer 21

Cold cures/nasal decongestions
OCP
Steroids
EPO
Ciclosporin A
Liquorice

Question 22

Vicious cycle of RAS and HTN

Answer 22

Positive feedback – vicious circle develops as body thinks ischemia / low perfusion disease needs correcting by increasing BP but really this just aggravates the problem

Question 23

Secondary HTN: Dx
Conns
Apparent mineralocorticoid excess
Liddles syndrome
Gitelman syndrome
Bartters syndrome
Cushings
Phaeochromocytoma

Answer 23

Conns: Benign aldosterone adenoma. K is low but not on diuretic. Increased plasma aldosterone-renin ratio (renin suppresed). Adrenal vein sampling if unsure. CT/MRI then surgery.

AME: Mutation in 11β-hydroxysteroid dehydrogenase which converts cortisol into inert cortisone (liquorice mimics). Thus overload of cortisol. Aldosterone and renin will be normal/low. Urinary cortisol/cortisone ratio is diagnostic. Spironolactone

Liddles: ENaC mutation = open all the time = Na overload. Low K thus metabolic alkalosis. Low renin and aldosterone. Dx with genetic test. Amiloride - K sparing diuretic.

Gitelman: Thiazide (hence G+T) sensitive NaCl is broken so cannot reabsorb Na thus RAS activated =H and K excreted in exchange for Na = alkalosis + hypokalemia. Calcium usually HIGH with thiazides

Barrters: Loop diuretic (B+L) is NaKCl is broken thus cannot reabsorb Na or K = RAS > alkalosis + hypokalemia

Cushings:

1. Urinary cortisol
2. Midnight cortisol serum
3. ACTH + dexamethasone test (should reduce ACTH)
   i. If high dose suppresses then = cushings disease (high ACTH) + exogenous steroids (low ACTH)
   ii. If high dose doesnt suppress then = adrenal (ACTH low) + ectopic ACTH (high ACTH)

Phaeochromocytoma: Asociated with MEN2. HTN, sweating, headache, labile BP
High urine catecholamines and plasma metanephrines

Question 24

Cushings algorithm

Answer 24

There are 4 causes of Cushing’s syndrome: exogenous steroids, adrenal adenoma, ectopic ACTH and a pituitary adenoma.

Only the latter 2 give a high ACTH and only ectopic production does not fall on a high-dose
suppression test.

Question 25

For secondary causes of HTN whats the algorithm

Answer 25

1. Renin must be low 2. Aldosterone high = Conns 3. Aldosterone also low then check cortisol, if high = AME

Question 26

HTN complications + Sx

Answer 26

Acclerates any vascular pthology if systolic >200 = malignant HTN = Headache, visual impairement, cardiac failure, neurological signs, incerased ICP

Question 27

HTN Dx | Stages, 140 (135), 160 (150), 180

Answer 27

Measure BP minimum 2 times. If >140/90 offer ABPM to confirm If <180 consider starting treatment immediately Whilst waiting to confirm investigate end organ damage: • Urine dip – blood/protein • Blood – glucose, electrolytes, creatinine, eGFR, cholesterol • Fundoscopy – hypertensive retinopathy • ECG Stage 1 = >140/90 or average of >135/85 Stage 2 = >160/100 or average of >150/95 Stage 3 = >180 or diastolic >110`

Question 28

Cholesterol metabolism

Answer 28

1. Food is converted into chylomicrons which is then absorbed into tissues, chylomicron remnants are cleared by ApoE 2. Chylomicrons are alternatively transported by VLDL to tissues 3. Lipoprotein lipase converts VLDL into IDL 4. Hepatic lipase converts IDL into LDL, cleared by ApoB, or turn into foam cells - BAD 5. HDL mops up cholesterol

Question 29

Name 5 common causes of secondary hyperlipidemia

Answer 29

``` Renal CKD Hypothyroidism Nephrotic syndrome - if low albumin then liver produces more proteins and lipoproteins Cholestasis DM ``` Atypical antipsychotics, corticosteroids, ciclosporin, beta blockers, retinoids, oral estrogens, anti-retroviral drugs

Question 30

Familial hypercholesterolaemia Mechanism Sx Dx Chloe tends to family at LDL

Answer 30

Mutation to LDLR receptor prevents breakdown of LDL Tendon Xanthomas Raised LDL 1. Total cholesterol >7.5 OR LDL >4.9 AND Tendon xanthomas 2. DNA evidence of LDLR, ApoB100 or PCSK9 mutation Recessive/homozygous version is more severe

Question 31

Remnant hyperlipidaemia Mechanism Sx Dx ApE remains palm but erupts if point

Answer 31

Mutation in ApoE prevents clearance of chylomicron remnants Striate palmar xanthomas (palm creases) Eruptive xanthomas on pointy body High Cholesterol + TGs ApoE phenotyping

Question 32

Familial hypertriglyceridaemia Mechanism Sx Dx Very lazy (VL) Tina layers fat on TiGer causing eruptive spleen

Answer 32

Excess VLDL production Lipidaemia retinalis Eruptive xanthomas on soft body Pancreatitis + hepatosplenamegaly High TGs + fat layer on top of blood sample

Question 33

Familial combined hyperlipidaemia Mechanism Sx Dx Mild Mixxy has yellow eye bags

Answer 33

MOST COMMON! Overproduction of VLDL (TG) and ApoB (LDL) Xanthelesma + strong FH Mild mix of high cholesterol + TG

Question 34

Reasons for raised creatinine kinase

Answer 34

``` Muscular dystrophy MI Rhabdomyolysis Renal disease bodybuilders Statins ```

Question 35

HF and HTN drug treatment

Answer 35

ABDD ACEi + B blocker > Diuretics > Digoxin <55 = ACEi > CB > digoxin > b blocker >55 or black = CCB

Question 36

Difference between cardiac and vasovagal syncope

Answer 36

Vasovagal has prodrome | Carrdiac has no prodrome but will have pre-exisitng condition/FH

Question 37

``` Long GT syndromes 1 swimmer, 2 alarm clocks, 3 sleep Types Sx Dx Mx ```

Answer 37

Type1: Delay of K out of myocyte = prolonged repolarisation = prolonged QT SWIMMING IN COLD WATER Type2: Delay of K out of myocyte = prolonged repolarisation = prolonged QT STARTLED BY ALARM CLOCK Type3: Too many Na ions allowed into cells = prolonged QT SLEEP Ventricular tachy, torsades de pointes > palpitations, fainting and sudden death ECG - Monomorphic VT ICD + b blockers in LQTS 1&2 NOT type 3!

Question 38

ECG findings 1. Wolf-Parkinson-White syndrome 2. Brugada syndrome (decreased Na influx) 3. CPVT: Catecholaminergic polymorphic ventricular tachycardia 4. Arrhythmogenic Right Ventricular Dysplasia

Answer 38

1. Delta wave - slurred upstroke to QRS complex - DELTA WOLF 2. Tombstoning ST elevation + RBBB (sodium channel) 3. Induced by adrenaline, stress, pain - VF + VT during exercise (calcium channel) 4. Prolonged S wave upstroke + Epsilon wave

Question 39

Drugs that can prolong QT interval

Answer 39

Amiodarone Macrolide ABx Tamoxifen

Question 40

Cardiomyopathy and ECG

Answer 40

Arrhythmogenic Right Ventricular Dysplasia Prolonged S wave upstroke + Epsilon wave Cardiomyopathies typically show monomorphic VT AND VF

Question 41

Which drug to always avoid in ACS?

Answer 41

Aspirin

Question 42

Maths | Sens, spec, ppv, npv, liklihood, NNT

Answer 42

Nah?