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AC1 > Week 1 > Flashcards

Week 1 Flashcards

1
Q

What is essential or primary hypertension?

A

Do not know the underlying cause but know how to treat it

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2
Q

What is secondary hypertension?

A

Due to an underlying cause. More cases of secondary hypertension than primary.

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3
Q

What is pseudo-resistant hypertension?

A

Apparent resistance to treatment, may reside in some artefacts

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4
Q

What is resistant or refractory hypertension?

A

Does not respond to any know drug therapies or treatments

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5
Q

What is isolated systolic hypertension?

A

Common in older people, due to very stiff larger arteries

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6
Q

What is stage 1 Essential/Primary hypertension?

A

Under 140/90 mmHg

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7
Q

What is stage 2 Essential/Primary hypertension?

A

140/90 to 179/119 mmHg

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8
Q

What is severe Essential/Primary Hypertension?

A

180/120 mmHg or more

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9
Q

What does a lack of nocturnal dip if someone has high BP mean?

A

Greater risk of developing CV events compared to dippers

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10
Q

What are some causes of secondary hypertension?

A
  • Primary hyperaldosteronism (Conn’s syndrome)
  • Renovascular disease
  • Obstructive sleep apnoea
  • Chronic Kidney Disease
  • Phaeochromocytoma
  • Aortic coarctation
  • Cushing’s disease
  • Hyperparathyroidism
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11
Q

What is phaeochromocytoma?

A

Endocrine tumour which develops in medulla or adrenal glands

Symptoms:

  • Severe hypertension (intermittently)
  • Hot flushes
  • Palpitations
  • Sweating attacks
  • Chest pain
  • Headache
  • Blurred vision
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12
Q

What are some causes of pseudo-resistant hypertension?

A
  • White-coat hypertension
  • Inaccurate measurement (eg. cuff size - a small cuff on a large arm will over-read the BP and overestimate the hypertension)
  • Poor adherence to treatment
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13
Q

Define resistant hypertension

A

Defined when a patient’s BP is not controlled to recommended BP goals ie. <140/90 mmHg, despite treatment with an appropriate combination of three drug therapies ie. A+C+D, prescribed at their maximum recommended and/or tolerated doses.

Not synonymous with uncontrolled BP

Most resistant hypertension is due to systolic hypertension.

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14
Q

What are some characteristics of resistant hypertension?

A
  • Older age (especially >75 years)
  • High baseline BP
  • Chronicity of uncontrolled hypertension
  • Target organ damage (LVH and/or CKD)
  • DIabetes
  • Obesity
  • Atherosclerotic vascular disease
  • Aortic stiffening
  • Women
  • Black African origin
  • Excessive dietary sodium and alcohol consumption
  • Drugs
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15
Q

How is blood pressure related to cardiac output and systemic vascular resistance?

A

BP is proportional to CO x SVR

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16
Q

What are some classes of drugs to treat hypertension?

A 
Diuretics
Beta-blockers
Calcium channel blockers
ACEi, ARBs, Direct renin inhibitors
Alpha-blockers
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17
Q

How do thiazide diuretics work?

A

Act on distal convoluted tubule.
Inhibit Na+/Cl- co-transport from lumen.
Increase sodium and water excretion.
Increase potassium loss.

Vasodilate by potassium channel activation.
Prevent heart attacks and strokes.
Adverse effects: high uric acid and gout; low potassium and low sodium; raised glucose and cholesterol.

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18
Q

How do potassium-sparing diuretics work?

A

Aldosterone antagonist (spironolactone, eplerenone)

eNAC blocker (amiloride)

  • Weak agents
  • Useful in combination with other drugs
  • Useful against aldosterone excess

Side effects:

  • High serum potassium and low sodium
  • Gynaecomastia (spironolactone)
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19
Q

What are some examples of calcium channel blockers and what do they do?

A

Verapamil, Diltiazem, Dihydropyridine (eg. nifedipine, amlodipine)

They are arterial dilators

20
Q

What is the target BP for patients over 80yo?

A

Clinic BP <150/90

21
Q

What BP drug would you first prescribe for someone over 55 without T2DM?

A

CCB

22
Q

What BP drug would you first prescribe for someone of Black-African descent without T2DM?

A

CCB

23
Q

What BP drug would you first prescribe to someone with T2DM?

A

ACEi or ARB

24
Q

What BP drug would you first prescribe to someone under 55 who is not of Black-African origin and does not have T2DM?

A

ACEi or ARB

25
Q

What are some long term consequences of uncontrolled high blood pressure?

A
  • Myocardial infarction; arrhythmias; atrial fibrillation; heart failure; cardiomyopathy
  • Stroke (ischaemic, haemorrhagic)
  • Kidney failure
  • Retinopathy
  • Peripheral vascular disease
26
Q

Define heart failure?

A

Clinical definition:
Heart failure is defined, clinically, as a syndrome in which patients have typical symptoms (eg. breathlessness, ankle swelling and fatigue) and signs (eg. elevated jugular venous pressure, pulmonary crackles and displaced apex beat) resulting from abnormality of cardiac structure or function

Pathophysiological definition:
Heart failure can be defined as an abnormality of cardiac structure or function leading to failure of the heart to deliver oxygen at a rate commensurate with the requirements of the metabolising tissues

27
Q

What is hypertensive nephrosclerosis?

A

Hypertensive nephrosclerosis is a blood pressure-related pathologic process marked by a progressive decline in renal function.

28
Q

What is hypertensive retinopathy?

A

Spectrum of microvascular signs in the retina pathophysiologically related to elevated blood pressure

29
Q

What is peripheral vascular disease?

A
  • Circulation disorder that causes the blood vessels outside of your heart and brain to narrow or block. Due to severe atherosclerotic plaques with reduced blood flow.
  • Smoking by far the strongest risk factor.
  • Medical: quit smoking, lower BP and lipids, control diabetes, give anti-platelets
  • Surgery: angioplasty or bypass graft
30
Q

What are the differences between the population strategy and high risk strategy for disease prevention?

A

Population strategy:

  • It attempts to control determinants of incidence rather than cases
  • It is population based
  • It is more radical
  • It is more permanent

High risk strategy:

  • Extension of traditional clinical approach
  • It does not produce lasting population changes
  • It needs to be repeated from generation to generation
31
Q

How do you calculate heart rate?

A

300 divided by the number of large squares between 2 QRS complexes

32
Q

What is a normal PR interval?

A

0.12 - 0.2 seconds (3-5 small squares)

33
Q

What is a normal QRS interval?

A

<0.12 seconds (<3 small squares)

34
Q

Define cardiac arrhythmia

A

Any variation from the normal rhythm or rate of heart beat

OR

A disturbance in the electrical activity of the heart due to a disorder of impulse formation and/or impulse conduction, which may be paroxysmal or continuous

35
Q

What factors can enhance automaticity?

A

Catecholamine excess
Ischaemia
Abnormal pH
Electrolyte abnormalities

36
Q

What are the prerequisites for ‘classic’ re-entry to occur?

A

Prerequisites for ‘classic’ re-entry to occur are:

  • At least two conduction pathways between atria and ventricles (normal AV node pathway plus ‘accessory’ pathway) OR the presence of a barrier along the conduction pathway
  • Unidirectional block in one of the pathways
  • Conduction must be slow enough (and/or refractory period short enough) to prevent the depolarisation wave encountering refractory tissue within the circuit
37
Q

What are the cardiac causes for arrhythmias?

A
  • Altered impulse formation

- Altered impulse conduction

38
Q

What are the different types of AV conduction disturbance?

A

Atrioventricular (AV) conduction disturbance (also called heart blocks or AV blocks)

  • 1st degree (delayed conduction)
  • 2nd degree (intermittent conduction)
    Mobitz type 1 (Wenckebach)
    Mobitz type 2
  • Complete / 3rd degree (complete conduction block)
39
Q

What should you consider if you see persistent unexplained tachycardia?

A

Pulmonary embolism

40
Q

What are causes of Cardiac Arrhythmias?

A
  • Cardiac ischaemia
  • Excessive discharge or sensitivity to autonomic transmitters
  • Exposure to toxic substances
  • Unknown aetiology
41
Q

How do cardiac glycosides work?

A

Increased force of contraction and blocks AV node

  • Usually digoxin
  • Inhibits the Na+/K+ ATPase pump
  • Increased intracellular Na+
  • Ca2+ exchanged for Na+ passively
  • Via Ca2+/Na+ exchangers that rely on Na+ concentration gradient
  • Thus cytoplasmic Ca2+ increased as less extruded
  • Increases vagal drive, slows the heart rate down
42
Q

What is the MoA of Class I anti-arrhythmics?

A

Na+ channel blocker

43
Q

What is the MoA of Class II anti-arrhythmics?

A

Beta-blockers

44
Q

What is the MoA of Class III anti-arrhythmics?

A

K+ channel blocker

Delay repolarisation

45
Q

What is the MoA of Class IV anti-arrhythmics?

A

Ca2+ channel blocker

Reduces amplitude and shortens Phase 2

AC1 (9 decks)

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