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Stage 4 > Vascular disease > Flashcards

Vascular disease Flashcards

1
Q

3 stages of Atherosclerosis

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

Vasodilatory factors and vasoconstriction factors

A

Vasodilation: NO, PGI2, COX

Vasoconstriction: ET-1, Angiotensin II, Thromboxane 2

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3
Q

Order of Ix + Mx in carotid artery stenosis

A
  1. Colour duplex ultrasound
  2. CT/MRI angiography
  3. Endarterectomy if over 70% stenosed
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4
Q

Peripheral artery disease
Sx
Ix
Mx

A

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

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5
Q

6P’s of critical limb ischemia

Intermittent claudication vs critical limb ischemia

A

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

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6
Q

Metabolic syndrome

A

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
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7
Q

3 features of typical angina

A
  1. Constricting pain in chest/shoulders/arms/jaw
  2. Comes on with exertion
  3. Relieved with rest or GTN within 5 minutes
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8
Q

First line Ix in suspected ACS

A
  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%
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9
Q

MI = high troponin AND

A

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

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10
Q

Decubitus angina

Prinzmetals angina

A

Decubitus angina = Angina lying down

Prinzmetals angina = vasospasm of coronary artery causing angina like symptoms

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11
Q

Type 1 MI

Type 2 MI

A

Occlusion (complete occlusion = Q wave and ST elevation)

HF or arrhythmias

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12
Q

ACS algorithm

A
  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
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13
Q

Other causes of raised troponin

A 
PE
sepsis
post-op
AF
LVF
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14
Q

MI + ECG leads + Artery

A

II, III, aVF = Inferior = R coronary artery

V1-V4 = Anterior = L anterior descending

I, V5-V6 = Lateral = Circumflex artery

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15
Q

TIMI

GRACE

A

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

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16
Q

ECG changes risk order

A
  1. ST elevation with co-existing depression
  2. ST depression
  3. ST elevation
  4. T wave inversion
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17
Q

MI Mx

A
  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
18
Q

Subsequent MI Mx - A3BCDE

A

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

19
Q

Normal angina Mx

A
  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
20
Q

Hypertension
NICE definition
Pathophysiology (3)

A

> 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
21
Q

Drugs that cause HTN

A 
Cold cures/nasal decongestions
OCP
Steroids
EPO
Ciclosporin A
Liquorice
22
Q

Vicious cycle of RAS and HTN

A

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

23
Q 
Secondary HTN: Dx
Conns
Apparent mineralocorticoid excess
Liddles syndrome
Gitelman syndrome
Bartters syndrome
Cushings
Phaeochromocytoma
A

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

24
Q

Cushings algorithm

A

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.

25
Q

For secondary causes of HTN whats the algorithm

A
  1. Renin must be low
  2. Aldosterone high = Conns
  3. Aldosterone also low then check cortisol, if high = AME
26
Q

HTN complications + Sx

A

Acclerates any vascular pthology

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

27
Q

HTN Dx

Stages, 140 (135), 160 (150), 180

A

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`

28
Q

Cholesterol metabolism

A
  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
29
Q

Name 5 common causes of secondary hyperlipidemia

A 
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

30
Q

Familial hypercholesterolaemia
Mechanism
Sx
Dx

Chloe tends to family at LDL

A

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

31
Q

Remnant hyperlipidaemia
Mechanism
Sx
Dx

ApE remains palm but erupts if point

A

Mutation in ApoE prevents clearance of chylomicron remnants

Striate palmar xanthomas (palm creases)
Eruptive xanthomas on pointy body

High Cholesterol + TGs
ApoE phenotyping

32
Q

Familial hypertriglyceridaemia
Mechanism
Sx
Dx

Very lazy (VL) Tina layers fat on TiGer causing eruptive spleen

A

Excess VLDL production

Lipidaemia retinalis
Eruptive xanthomas on soft body
Pancreatitis + hepatosplenamegaly

High TGs + fat layer on top of blood sample

33
Q

Familial combined hyperlipidaemia
Mechanism
Sx
Dx

Mild Mixxy has yellow eye bags

A

MOST COMMON!
Overproduction of VLDL (TG) and ApoB (LDL)

Xanthelesma + strong FH

Mild mix of high cholesterol + TG

34
Q

Reasons for raised creatinine kinase

A 
Muscular dystrophy
MI
Rhabdomyolysis
Renal disease
bodybuilders
Statins
35
Q

HF and HTN drug treatment

A

ABDD
ACEi + B blocker > Diuretics > Digoxin

<55 = ACEi > CB > digoxin > b blocker
>55 or black = CCB

36
Q

Difference between cardiac and vasovagal syncope

A

Vasovagal has prodrome

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

37
Q 
Long GT syndromes
1 swimmer, 2 alarm clocks, 3 sleep
Types
Sx
Dx
Mx
A

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!

38
Q

ECG findings
1. Wolf-Parkinson-White syndrome

  1. Brugada syndrome (decreased Na influx)
  2. CPVT: Catecholaminergic polymorphic ventricular tachycardia
  3. Arrhythmogenic Right Ventricular Dysplasia
A
  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
39
Q

Drugs that can prolong QT interval

A

Amiodarone
Macrolide ABx
Tamoxifen

40
Q

Cardiomyopathy and ECG

A

Arrhythmogenic Right Ventricular Dysplasia
Prolonged S wave upstroke + Epsilon wave

Cardiomyopathies typically show monomorphic VT AND VF

41
Q

Which drug to always avoid in ACS?

A

Aspirin

42
Q

Maths

Sens, spec, ppv, npv, liklihood, NNT

A

Nah?

Stage 4 (12 decks)

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