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4TH YEAR - CSIM2 > Vascular Medicine (week 7) > Flashcards

Vascular Medicine (week 7) Flashcards

1
Q

What is the definition of atherosclerosis?

A

A disease of the arteries characterized by the deposition of fatty material on their inner walls.

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2
Q

Presentation of atherosclerosis depends largely on which arteries are affected. How will it manifest in the coronary arteries?

A

Angina
MI
Microvascular disease

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3
Q

Presentation of atherosclerosis depends largely on which arteries are affected. How will it manifest in the carotid arteries?

A

Stroke

TIA (via thrombus)

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4
Q

Presentation of atherosclerosis depends largely on which arteries are affected. How will it manifest in the peripheral arteries?

A

Exertional leg pain (claudication)

Critical limb ishaemia

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5
Q

Presentation of atherosclerosis depends largely on which arteries are affected. How will it manifest in the Renal arteries?

A

CKD

Reno-vascular HTN

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6
Q

Why does atherosclerosis increase risk of ACS, stroke and critical limb ischaemia?

A

Presence of endothelial dysfunction after established atherosclerosis; this leads to Vasoconstriction and decreased perfusion ischaemia but also an increased risk of plaques rupturing and forming a thrombus.
In combination these increase the risk of ACS, STROKE & CRITICAL LIMB ISCHAEMIA

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7
Q

What are the symptoms of peripheral arterial disease?

A

Most cases are asymptomatic.
In symptomatic patients:
- Most have atypical exertional leg pain.
- 10-30% present with classic intermittent claudication.
- Rest pain or ischaemic ulcers are signs of critical limb ishaemia.

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8
Q

What are the signs of peripheral arterial disease?

A

The 6 Ps

Pain, Pallor, Pulselessness, Poikilothermia (“coldness”), Paralysis, Paresthesia

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9
Q

How do we diagnose peripheral arterial disease? What are the parameters?

A

Ankle-brachial index (ABI).
ABI is the ratio of ankle SBP to brachial SBP
(measured at the ankle by Doppler USS)

  • Ankle-Brachial Index Severity
  • > 1.30 Noncompressible
  • 0.91-1.30 Normal
  • 0.71-0.90 Mild
  • 0.41-0.70 Moderate
  • 0-0.40 Severe
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10
Q

When do you usually get symptoms of atherosclerosis in coronary artery disease?

A

Atherosclerosis is usually asymptomatic until vessels narrow severely or are totally blocked.

This is usually down to an ACUTE event - like a THROMBUS (ruptured plaque)

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11
Q

What is the most common precipitating event to cause symptoms in patients with coronary artery disease?

A

ACUTE event - like a THROMBUS (ruptured plaque)

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12
Q

What are the most common symptoms of coronary artery disease?

A
  • Chest pain
  • Dyspnoea
  • Palpitations
  • Syncope
  • Fatigue
  • Peripheral oedema – this will happen if there is left ventricular damage due to MI and then develop heart failure.
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13
Q

How do we categorise CV risk factors (give 3 examples or each)?

A

Modifiable
• Smoking
• Hyperlipidemia – higher LDLs = higher risk.
• Hypertension – single biggest risk factor for having a recurrent stroke having had a single TIA.
• Diabetes Mellitus
Fixed
• Older age
• Male Sex
• FHx – especially stuff like familial hypercholesterolaemia – 50% chance if FHx positive.
• 1st degree relative who develops CVD at an early age (male below 55yrs, women below 65yrs)
• Ethnicity – Indian subcontinent at higher risk.
• Previous CVD

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14
Q

What is the single biggest risk factor for having a recurrent stroke having had a single TIA?

A

Hypertension

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15
Q

What is the metabolic syndrome?

A

Insulin resistance, associated with a cluster of risk factors
o Insulin resistance and hyper-insulinaemia
o Central obesity
o Hypertension
o Dyslipidaemia (Increased Triglycerides, decreased HDL-Cholesterol)
o Impaired glucose tolerance

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16
Q

What is angina?

A

A pain or discomfort in the chest or adjacent areas (caused by insufficient blood flow to the heart muscle)

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17
Q

What is the typical type of pain associated with angina?

A

Angina pains are typically central crushing chest pains and patients can describe it as having a heavy weight in the middle of your chest.

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18
Q

What is the typical location of pain associated with angina?

A
  • Usually retrosternal, but radiation to the neck, jaw, epigastrium, or arms is not uncommon
    • Pain above the mandible, below the epigastrium, or localized to a small area over the left lateral chest wall is rarely angina
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19
Q

What is the typical duration of pain associated with angina?

A
  • Typically minutes in duration

- Fleeting discomfort or a dull ache lasting for hours is rarely angina

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20
Q

What are the common precipitating factors of angina?

A

Exertion – most important factor to consider.

Others = Emotion, Eating, Extreme weather

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21
Q

What is the difference between stable and unstable angina?

A

Unstable Angina = Angina pains which are rapidly worsening (on minimal/no exertion), or not relieved by rest.
Stable is relieved by rest

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22
Q

What are the non-organic differentials of chest pain?

A

Anxiety (very big one, especially if you start to hyperventilate) If they haven’t got angina this is one of your next big differentials.

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23
Q

What are the pulmonary differentials of chest pain? How do you differentiate?

A
  • PE – sudden, sharp and severe
  • Pleurisy – Inflammation of pleura, varies with respiration.
  • Pneumothorax
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24
Q

What are the MSK differentials of chest pain? How do you differentiate?

A

Chostochondritis (sternal pain) or trauma

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25
Q

What are the GI differentials of chest pain? How do you differentiate?

A

Ulcer/reflux (worse after eating),
Gallstones,
Pancreatitis - back pain

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26
Q

What are the cardiac differentials of chest pain? How do you differentiate?

A
  • Angina – shorter duration
  • MI – Symptoms that are lasting longer than 15 mins, nausea, pale, etc.
  • Pericarditis – Pain that varies with respiration and position (worse if you sit up)
  • Aortic Dissection – tearing feeling, radiates to back.
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27
Q

What are the 2 categories that ACS is split into (from ECG)?

Give examples of each

A

No ST Elevation

a. NSTEMI
b. Unstable Angina – troponin is not elevated (this means no myocardial damage has been done)

ST Elevation

a. NQMI (non- Q wave MI) likely to have T wave changes
b. QwMI (Q wave MI) this implies the whole thickness of the myocardium had been infarcted to cause the Q-wave

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28
Q

Why do we split ACS into STEMI and NSTEMI?

A

We split NSTEMI and STEMI because treatment is so different.
o STEMI – straight to cath lab and get coronary arteries opened up
o NSTEMI – there is no evidence that acute management will make a significant difference to the long-term prognosis.

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29
Q

How does thrombus characteristics effect the presentation of an ACS?

A

o If the artery occludes completely, will lead to an MI (likely STEMI).
o If artery is sub-occlusive or occludes and then reopens, you will get unstable angina/NSTEMI

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30
Q

What is the ECG change that caries the highest 6 month mortality?
o T-wave inversion
o ST elevation
o ST depression

A

ACS mortality at 6 months (%)
o T-wave inversion – 3.4%
o ST elevation – 6.8%
o ST depression – 8.9%

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31
Q

What are the 3 factors that contribute to the diagnosis of ACS? (need 2 to diagnose ACS)

A 
Chest Pain (clinical manifestation)
o	ECG changes consistent with ischaemia or necrosis. (perform immediately)
o	Elevation of cardiac markers
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32
Q

What is the classical clinical presentation of ACS?

A
  • Chest pain associated with MI lasting longer than 20 minutes and not relieved by rest or nitroglycerin (GTN).
    • May be accompanied by dyspnoea, nausea, vomiting, fatigue, diaphoresis, and palpitations
Atypical presentations (more common in diabetics/elderly)
•	Breathlessness, tachycardia, N&V, sweating and clamminess
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33
Q

When should you take the ECG of a patient with suspected ACS?

A
  • Perform immediately
    • If ECG is normal or non diagnostic in a patient with continuing symptoms repeat after 30mins
    • If symptoms resolve repeat ECG after 2 hours – changes can occur late
    • Repeat ECG if pain persists
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34
Q

Which factors of the ECG at the time of chest pain dictate risk of death or MI at 30 days?
• ST depression 10%
• T-wave inversion 5%
• No ECG changes 1-2%

A

The risk of death or MI at 30 days is strongly related to the ECG at the time of chest pain
• ST depression 10%
• T-wave inversion 5%
• No ECG changes 1-2%

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35
Q

Name 3 cardiac markers…

A

cardiac-specific troponins
creatine kinase (serum CK and CK-MB)
myoglobin

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36
Q

Which leads correlate to the Anterior/Septal region of the heart? Which artery is likely to be occluded?

A

V1, V2, V3 & V4

LAD

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37
Q

Which leads correlate to the Inferior region of the heart? Which artery is likely to be occluded?

A

II, III, aVF

RCA (&/or LCx)

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38
Q

Which leads correlate to the Lateral region of the heart? Which artery is likely to be occluded?

A

I, aVL, V5, V6

LCx or Diagonal of LAD

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39
Q

What does ST depression on an ECG suggest?

A

Ischaemia

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40
Q

What does T wave inversion on an ECG suggest?

A

Past MI/Ischaemic event

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41
Q

When is Troponin detectable, when do you measure it? When does it peak?

A

Detectable very early, within 3 hours.

Current ESC recommendations are to measure troponin on admission and 6-9 hours later,

Peaks at about 18 hours.

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42
Q

Apart from MI, when else can troponin be elevated?

A

PE, sepsis, AF, LVF and post-op

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43
Q

What Troponin measurements are required for a diagnosis of acute MI?

A

Current ESC recommendations are to measure troponin on admission and 6-9 hours later, a troponin result >99th centile (TnT > 14) and a rise or fall of >20% on the second sample required for diagnosis of AMI.

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44
Q

What score is used to stratify risk of ACS?

A

GRACE score

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45
Q

What does the GRACE score measure?

A

Gives you risk of death and death + MI, in hospital and after 6 months

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46
Q

What are the therapeutic goals of ACS treatments?

A

Reduce myocardial ischaemia
Control of symptoms
Prevention of MI and death

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47
Q

What categories of medications are used in the treatment of ACS?

A

o Anti-ischaemic agents
o Anti-platelet agents
o Anti-thrombin agents (Fibrinolytics)
o Coronary revascularisation

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48
Q

What are the drug therapies in NSTE-ACS?

A 
o	Aspirin
o	Clopidogrel / Ticagrelor
o	Fondaparinux
o	GPIIb/IIIa receptor antagonists (high risk pts only)
o	Beta blockers
o	Nitrates (if ongoing pain/LVD)
o	Statins (very good acutely and long term.)
o	ACE inhibitors
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49
Q

What is a common side effect of ACEi?

A

Dry cough

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50
Q

What is the post hospital discharge care in ACS?

A 
o	A	Antiplatelets and ACE-I
o	B	Beta blockers and Blood Pressure
o	C	Cholesterol and Cigarettes
o	D	Diet and Diabetes
o	E	Education and Exercise
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51
Q

What is the most significant modifiable risk factor in CV and renal disease?

A

HTN

Risk of cardiovascular disease doubles for every 20/10 mmHg increase in BP

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52
Q

What is the most common cause of HTN?

A

Essential HTN (80% of cases)

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53
Q

What is the single highest stroke risk factor after a single TIA?

A

HTN

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54
Q

What are the renal causes of HTN?

A
  • Glomerulonephritis
  • Polycystic kidneys (autosomal dominant inheritance)
  • Diabetes
  • Reno vascular disease
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55
Q

What are the endocrine causes of HTN?

A

Steroid excess

hyperaldosteronism (Conn’s)

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56
Q

Which drugs can commonly cause HTN?

A
  • Sympathomimetic amines (cold and flu remedies)
  • Amphetamines - increase HR and BP
  • Cocaine
  • Oestrogens (e.g. OCP)
  • Cyclosporin
  • Erythropoetin
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57
Q

What vascular disease’s commonly cause HTN?

A
  • Renal artery stenosis
  • Fibromuscular disease in younger women – stent will cure
  • Atheroma in middle age older smokers
  • Coarctation
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58
Q

What are the two main pathophysiological drivers of HTN?

A

o Reduced elasticity and compliance of large arteries
- Part of normal ageing but accelerated in HTN due to accumulation of arterial calcium and collagen + degradation of elastin
- Stiffened conduit vessels increase rate of return of reflected pressure waves raising peak systolic pressure
o Defective sodium storage leading to retention
- HTN often a failure to deal with excess Na

59
Q

What is Liddle’s syndrome?

A

A channelopathy involving increased activity of the epithelial sodium channel (ENaC) which causes the kidneys to excrete potassium but retain too much sodium and water, leading to hypertension

60
Q

Which hormones can cause secondary endocrine hypertension? What is the name of the condition for each hormone?

A
  • Catecholamine excess → Phaeochromocytoma (tumour anywhere along the sympathetic chain that produces catecholamine)
  • Glucocorticoid excess → Cushings syndrome (ACTH producing)
  • Hyperaldosteronism –>Conn’s syndrome
  • Growth hormone excess → acromegaly
61
Q

What is the typical biochemistry of Conn’s Syndrome?

A
  • Normal sodium
  • Low K (esp patients that aren’t on a diuretic, very suspicious)
  • Low renin
  • High aldosterone
62
Q

What is commonly found on CT/MRI in Conn’s Syndrome?

A

Adrenal benign adenoma

63
Q

What are the three main causes of cushings syndrome? Which is the most common?

A

• Iatrogenic e.g steroids for asthma, IBD etc
(Most common)
• Cushing’s disease → Pituitary dependent ACTH
• Adrenal cortisol → Cancers

64
Q

How does cushings syndrome cause HTN?

A

Excess cortisol binds to aldosterone receptor activating RAS

65
Q

What are the characteristic symptoms of Phaeochromocytoma?

A
  • Hypertension
  • Postural hypotension
  • Headache
  • Labile BP

(many asymptomatic)

66
Q

What inherited disorder is associated with Phaeochromocytoma?

A

MEN 2 (AD inheritance)

67
Q

What are the clinical features of Liddle Syndrome?

A

o Hypokalaemia
o Metabolic alkalosis
o High bicarbonate
o Low PRA & aldosterone

68
Q

What is the treatment for Liddle Syndrome?

A

Amiloride

69
Q

How does liddle cause HTN?

A

Na channel held open, absorb more and more sodium, increase water retention and increases BP.

70
Q

What tests would you do to diagnose Conn’s?

A

Test Renin - Low

Test Aldosterone - High = ? primary hyperaldosteronism

71
Q

What tests would you do to diagnose Liddle’s?

A

Test Renin - Low
Test Aldosterone - Low
Test Cortisol/Cortisone - Normal
Test DOC (DeOxyCortisol) - Low = ? Liddle syndrome (genetic test to confirm)

72
Q

What is the staging of HTN?

A

o Stage 1 hypertension:
• Clinic blood pressure (BP) is 140/90 mmHg or higher and
• ABPM (ambulatory BP) or HBPM average is 135/85 mmHg or higher

o Stage 2 hypertension:
• Clinic BP 160/100 mmHg is or higher and
• ABPM or HBPM daytime average is 150/95 mmHg
or higher

o Severe hypertension:
• Clinic BP is 180 mmHg or higher or
• Clinic diastolic BP is 110 mmHg or higher

73
Q

What actions are indicated if you discover HTN in a patient?

A

o Stage 1 hypertension:
Ok to monitor lifestyle modification arrange 24 hour monitor

o Stage 2 hypertension:
Lifestyle modification
Fairly urgent 24 hour monitor.
Treat if BP remains high in clinic or on 24 hour BP

o Severe hypertension:
Treat immediately may be an emergency

74
Q

What is the cardiovascular risk score?

A

Q-risk 2

75
Q

What is the definition of white coat HTN?

A

o Definition = Blood pressure >149/90 mmHg when measured in office
o Normal daytime ambulatory pressure <135/85 mmHg

76
Q

What should we offer to all patients with HTN?

To assess CV risk and end organ damage

A

o Test urine for presence of protein
o Take blood to measure glucose, electrolytes, creatinine, estimated glomerular filtration rate and cholesterol
o Examine fundi for hypertensive retinopathy
o 12-lead ECG

77
Q

What imaging should be done in patients with suspected acute stroke? Why is it useful?

A

CT preferably within 1 hour
• Will often be normal before 12 hours
• Will reliably exclude ICH (ICH are big white blobs)

(Beyond 2-3 weeks will not differentiate between haemorrhage and infarction)

78
Q

What are the early signs of infarct on CT?

A

o Loss of grey/white matter differentiation
o Loss of insular ribbon on insular cortex
o Loss of definition of lentiform nucleus

79
Q

What is the benefit of MRI DWI (Diffusion weighted Imaging)?

A

Allows you to see the development of ischaemia in real time. Acute lesion is bright white (infracting as we speak)

80
Q

What is the relationship between increased plasma cholesterol and risk of CHD?

A

Exponential relationship

Higher cholesterol = higher risk

81
Q

What is the role of macrophages in the pathophysiology of atherosclerotic plaque formation?

A
  • Macrophages try to mop up any cholesterol in sub-endothelial space.
    • If there is more cholesterol in there than the macrophages can safely dispose of then they get transferred into foam cells.
    • Once they die, foam cells become the basis of the atherosclerotic plaque.
82
Q

What are the possible symptoms of dyslipidaemia disorders?

A

Thirst/polyuria
Muscle and joint pains
Dyspnoea
Angina or claudication

83
Q

Which clinical examinations are very important to undertake?

A

o BMI & waist circumference
o Proteinurea - Cholesterol up as albumin goes down.
o Inspect for stigmata of hyperlipidaemia
• Eyes – eyelids, cornea, retina
• Achilles & digital extensor tendons
• Knees, elbows, palms and flexors
o CV examination – Heart sounds, pulses, bruits
o BP

84
Q

What is proteinurea a sign of?

A

Sign of kidney dysfunction or nephrotic syndrome (massive protein loss) → body reacts by massively increase in protein release by the liver, including apoprotein Beta (which carries cholesterol) this massive increases cholesterol levels.
• Cholesterol up as albumin goes down

85
Q

What are possible stigmata of hyperlipidaemia?

A
  • Eyes – eyelids, cornea, retina
  • Achilles & digital extensor tendons
  • Knees, elbows, palms and flexors
86
Q

What are the basic serum lipid measurements? What are their uses?

A

o Total Cholesterol
→ includes both atherogenic (LDL-C, IDL-C and VLDL-C) and anti-atherogenic fractions (HDL-C).
o HDL-Cholesterol
→ anti-atherogenic fraction, essential for risk assessment
o Triglycerides
→ not considered directly atherogenic but is a risk modifier, a component of the “Metabolic syndrome”, sentinel marker of secondary hyperlipidaemias and risk factor for pancreatitis,.
• 12h fasting triglycerides <4.5 required for calculation of LDL-C.

87
Q

What are the 2 calculated lipid variables?

A 
o	LDL-Cholesterol → Considered the most important class of atherogenic lipoproteins
o	Non-HDL-C → Total atherogenic lipoproteins, alternative to LDL-C which can be used when TG are elevated or patient is non-fasting
88
Q

How do you calculate LDL-Cholesterol?

A

LDL-C = TC – (HDL-C + TG/2.2) TG = triglycerides

89
Q

How do you measure non-HDL-C?

A

Non-HDL-C = TC – HDL-C

90
Q

What are the uses and limitations of LDL-C and non-HDL-C?

A
  • LDL-C is important for diagnosis of Familial Hypercholesterolaemia
  • Non-HDL-C is preferred for assessment of response to treatment
  • Both LDL-C and Non-HDL-C can be used as treatment targets.
    • BUT Calculation of LDL-C assumes a constant Cholesterol /TG ratio in VLDL, which requires fasting to ensure absence of postprandial lipoproteins, including chylomicrons and chylomicron remnants

• Fasting only matters if you are trying to accurately measure LDL. Non HDL-C doesn’t require fasting.

91
Q

What are the 3 main apolipoproteins that we measure?

A

o Apolipoprotein A1 (ALRIGHT)
o Apolipoprotein B (BAD)
o Lipoprotein (a)

92
Q

What is the significance of the 3 apolipoproteins we measure?

A

Apolipoprotein A1 (ALRIGHT)
• The major structural and functional apolipoprotein of the non-atherogenic HDL particles, each of which may contain multiple copies, ApoA1 concentrations correlate with HDL-C.
Apolipoprotein B (BAD)
• Each of the atherogenic lipoproteins LDL, IDL and VLDL contains one copy of apolipoprotein B100
• Chylomicrons (CM), CM Remnants contain apolipoprotein B48 (truncated form)
Lipoprotein (a)
• A highly atherogenic modified form of LDL with the polymorphic plasminogen-like apolipoprotein(a) covalently linked to apolipoprotein B100

93
Q

What can we use apolipoproteins for?

A

Apolipoprotein can be used to assess risk and as treatment targets

94
Q

Name some common secondary dyslipidaemia’s

A

These are distinctly separate conditions that can cause an increase in cholesterol and LDL concentration (can also be caused by drugs) & includes:
• DM, Obesity, untreated hypothyroidism, alcohol excess, CKD, nephrotic syndrome, gout

95
Q

Exclusion of secondary dyslipidaemia is a key investigation. Which tests should you undertake and for what causes?

A

o Renal profile - (Na+,K+,Creatinine, eGFR) → to Exclude Renal Failure
o Liver profile - (TProt, Alb, ALP, ALT, GGT) → Cholestasis, M protein
o Thyroid profile - (TSH, FT4) → Hypothyroidism
o Glucose (Fasting) or HbA1c → Diabetes
o Dipstick urinalysis - (protein) → Nephrotic Syndrome

96
Q

What is the mechanism for familial hypercholesterolaemia?

A

Reduction in receptor mediated clearance of LDL. Due to mutation of LDLR, APOB or PCSK9 gene

97
Q

What is the prevalence of familial hypercholesterolaemia?

A

Prevalence → 1 in 250

98
Q

What is the lipid profile of familial hypercholesterolaemia?

A
  • Elevated LDL-cholesterol,
  • TC 9-12mmol/L.
  • Low normal fasting triglycerides
99
Q

What is the inheritance of familial hypercholesterolaemia?

A

o Inheritance → Autosomal co-dominant

100
Q

What are the physical signs in familial hypercholesterolaemia?

A
  • Tendon Xanthomas
    • Corneal arcus,
      Also planar digital and natal cleft cutaneous xanthomas, aortic stenosis
101
Q

What is the CHD risk for familial hypercholesterolaemia?

A

CHD risk → Very high (symptomatic in 50% of males by age 50, 50% of females by age 60)

102
Q

What is the prevalence of Familial Combined Hyperlipidaemia (FCH)?

A

1 in 100

103
Q

What is the lipid profile of Familial Combined Hyperlipidaemia (FCH)?

A
  • Elevated LDL-cholesterol and/or triglyceride
  • TC 6.5-10mmol/L, TG 2.3 – 6.0, can be higher
  • Frequent low HDL-Cholesterol
  • Non-HDL-cholesterol/ApoB ratio <5
  • VLDL-Cholesterol/Total TG Ratio <0.69
104
Q

What is the mechanism for Familial Combined Hyperlipidaemia (FCH)?

A

Overproduction of VLDL and apolipoprotein B. Genetic cause unknown, probably multigenic

105
Q

What are the physical signs in Familial Combined Hyperlipidaemia (FCH)?

A

Non-specific, xanthelasma

106
Q

What is the CHD risk for Familial Combined Hyperlipidaemia (FCH)?

A

CHD risk → High

107
Q

What is the mechanism for Familial Hypertriglyceridaemia?

A

milder forms probably multigenic

More severe forms often monogenic e.g. lipoprotein lipase or apoCII deficiency

108
Q

What is the prevalence of Familial Hypertriglyceridaemia?

A

Prevalence → 1 in 300, severe form rarer

109
Q

What is the lipid profile of Familial Hypertriglyceridaemia?

A
  • Elevated triglyceride, TG 2.3 –10.0 in mild/moderate, in severe TG >10mmol/L, can be >100mmol/L
  • Usuallly normal apolipoprotein B (<1.3 g/L)
  • Small, dense LDL (“pattern B” on gradient gel)
  • Low HDL-cholesterol frequent (except xs alcohol)
110
Q

What is the inheritance of Familial Hypertriglyceridaemia?

A

Mild forms overlap with FCH

Severe forms usually autosomal recessive

111
Q

What are the physical signs in Familial Hypertriglyceridaemia?

A

Eruptive xanthomas

Lipaemia retinalis in severe

112
Q

What is the CHD risk for Familial Hypertriglyceridaemia?

A

CHD risk → variable, severe forms prone to pancreatitis, metabolic syndrome, diabetes mellitus

113
Q

What is the best tool for calculating CVD risk?

what risk does it calculate and what is the threshold for treatment?

A

Q-Risk 2 is the best CVD Risk Assessment tool

  • Risk is 10 year risk of MI or Stroke
  • 10% is threshold for Cholesterol lowering meds (statin)
114
Q

When can you not use Q-Risk 2?

A

Q risk 2 is not used in people who are already high risk, e.g.:
o Due to familial/inherited dyslipidaemias
o People with pre-existing CVD
o CKD with eGFR < 60
o Type I DM
o People aged 85 or older who are at increased risk of CVD because of age alone, particularly those who smoke or have raised blood pressure

115
Q

When is a cardiac death classified as sudden?

A

Within 1 Hour of the onset of cardiac symptoms

116
Q

What is the commonest cause of syncope in hypertrophic cardiomyopathy patients?

A

Vasovagal Syndrome (a simple faint is always more common, no matter what underlying condition they have)

117
Q

What is the commonest cause of sudden death is the UK?

A

Coronary artery disease (furred up and blocked arteries around the heart)

118
Q

What are the RED FLAG symptoms for collapse?

A

o Often rapid recovery
o Seizure activity may occur in all forms of cardiac syncope as well as epilepsy
o Any pre-existing cardiac history
o Any malignant sounding family history

119
Q

What could a black out with swimming, exercise or with ‘startle reflex‘ be a symptom of?

A

Could be LQTS

120
Q

What could a black out with pain, stress, adrenaline (could be a temper tantrum) be a sign of?

A

CPVT (Catecholaminergic polymorphic ventricular tachycardia) in children/teens (or vasovagal)

121
Q

What is CPVT?

A

Catecholaminergic polymorphic ventricular tachycardia
= a condition characterized by an abnormal heart rhythm (arrhythmia).
As the heart rate increases in response to physical activity or emotional stress, it can trigger an abnormally fast and irregular heartbeat called ventricular tachycardia.

122
Q

What is a Q wave on ECG a sign of?

A

Silent infarct

123
Q

What is a delta wave on ECG a sign of?

A

WPW syndrome.
Slurred upstroke in the QRS complex associated with a shortened PR interval.
Accessory pathway, a piece of tissue that bridges the gap between atria and ventricles, forming an abnormal conduction pathway.

124
Q

What is a Bifascicular block?

A

Specific ECG pattern

Bifasicular block = RBBB and left axis deviation (sign of wear and tear).

125
Q

What is a Trifascicular block?

A

Specific ECG pattern

Trifasicular block = 1st degree heart block (prolonged PR), RBBB & left axis deviation

126
Q

What ECG signs would be evident in a patient with Long QT syndrome?

A

Can causes a notched T wave and a prolonged QT interval.

127
Q

What ECG signs would be evident in a patient with Brugada syndrome?

A

Tends to cause young men to die in the night.

ST elevation and RBBB.

128
Q

What is the pathophysiology of brugada syndrome?

A

Sodium channel genetic abnormality

Southeast Asian populations

129
Q

How do channelopathies cause cardiac arrest?

What arrhythmia will this typically cause?

A
  • The balance of ions moving in and out of myocytes is disordered
    • Regional differences across the whole of the myocardium mean cells are firing & resetting at slightly different times

…tends to cause polymorphic VT (torsades de pointes – VT in a wave form ~~~~) or VF

130
Q

How do cardiomyopathies cause cardiac arrest?

A
  • Hypertrophic cardiomyopathy (HCM)(muscle bound) alters the ‘grain’ of the myocardium.
    Like rocks in a river, ‘turbulence’ can occur with regional differences

In ARVC (Arrhythmogenic right ventricular cardiomyopathy) clusters of fat and fibrous tissue get deposited 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

131
Q

What is the most common cause of cardiac sudden death?

A

MI

132
Q

What syndrome typically causes a monomorphic VT?

A

Short QT syndrome

133
Q

Which channels are affected in most Long QT syndromes?

A

Potassium channels most commonly

Can also involve sodium or calcium channels

134
Q

What arrhythmias are commonly caused in cardiomyopathies?

A

Tend to cause a mix of monomorphic VT and VF

135
Q

When is the maximum sensitivity for cardiac markers?

A

12-24 hours after onset of symptoms

136
Q

What are the preffered cardiac markers?

A

Cardiac Troponins (cTnT and cTnI)

137
Q

When should you measure a patients CArdiac markers?

A

Current ESC recommendations are to measure troponin on admission and 6-9 hours later.

138
Q

What cardiac marker test results are required for a diagnosis of acute MI?

A

A troponin result >99th centile (TnT > 14) and a rise or fall of >20% on the second sample required for diagnosis of AMI.

139
Q

What are the signs of Ischaemia (on investigation)?

A
  • ECG changes indicative of new ischaemia (new ST-T changes or new left bundle branch block [LBBB]);
  • Development of pathological Q waves in the ECG;
  • Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality.
140
Q

What are the options for Risk Factor Reduction Post MI?

A 
Cholesterol
BP 
Smoking – stop
Diet
Drugs
•	Aspirin
•	Beta-blockers
•	Statins
•	ACE inhibitors
141
Q

Should you use NSAIDS in patients with a previous MI?

A

No, NSAIDs increase the risk of death and/or recurrent MI in patients that have had a previous MI.

142
Q

What is the definition of ‘NNT’ (numbers needed to treat)?

A

The NNT is the number of patients you need to treat to prevent one additional bad outcome (death, stroke, etc.).

143
Q

How do you calculate NNT?

A

NNT is the inverse of the ARR, i.e. NNT = 1/ARR

ARR = CER (Control Event Rate) - EER (Experimental Event Rate).

Example: if a drug reduces the risk of a bad outcome from 50% to 40%, the ARR = 0.5 - 0.4 = 0.1.

Therefore, the NNT = 1/ARR = 10.

4TH YEAR - CSIM2 (20 decks)

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