Hypertension Flashcards

1
Q

What is the resting BP in hypertension?

A

SBP > 140mmHg

DBP > 90mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Organs that will be damaged by hypertension

A

heart, brain, retina, kidney, dissecting aortic aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Tissues damaged due to artherosclerosis

A

Coronary, cerebral vessels, carotids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What two broad changes occur in the cardiovascular system in response to hypertension?

A

Cardiac and vascular hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Lifestyle changes to treat hypertension?

A

regular exercise, reduced dietary salt, decreased alcohol, lower weight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Groups of commonly used antihypertensive drugs

A
angiotensin converting enzyme inhibitors and angiotensin antagonists
beta blockers
calcium channel blockers
diuretics (thiazides, loops, K+ sparing)
extras
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where does angiotensinogen come from?

A

liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what converts angiotensinogen into angiotensin I?

A

renin from juxta-glomerular cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what converts angiotensin I to angiotensin II?

A

ACE (lungs and elsewhere)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does angiotensin II cause?

A

vasoconstriction (has direct effect on lumen diameter), aldosterone output, sodium and water retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what converts bradykinin to inactive products?

A

ACE (lungs and elsewhere)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

where are angiotensin I and II found?

A

in the bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What do ACE inhibitors do? -opril, -april

A
  • prevent angiotensin II formation and inhibit bradykinin breakdown, resulting in lower peripheral resistance and sodium and water excretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the indications for use of ACE inhibitors?

A

hypertension, heart failure, preserve renal function in diabetes (diabetic nephropathy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

contraindications for ACE inhibitors?

A
  • less effective in patients of African origin
  • renal failure if there is also renal artery stenosis
  • avoid in pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Common side effects of ACE inhibitors?

A

cough (from high bradykinin), headache, marked hypotension (start with low dose), hyperkalaemia (beware of K+ supplements or K+ sparing diuretics)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

infrequent side effects of ACE inhibitors?

A

rash/itch, taste disturbances, angioedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Example of ACE inhibitor?

A

perindopril

19
Q

Example of an angiotensin receptor blocker (ARBs)?

- sartans

A

irbesartan

20
Q

What do ARBs do?

A

are angiotensin I receptor antagonists: inhibit angiotensin -induced vasoconstriction and aldosterone output; effect is reduced total peripheral resistance and increased Na+ and water excretion *no dry cough as seen in ACE inhibitors

21
Q

What are the indications for use of ARBs?

A

hypertension, heart failure, diabetic nephropathy, for patients intolerant to ACE inhibitors e.g. cough

22
Q

adverse effects of ARBs?

A

hypotension (less than ACE inhibitors), hyperkalaemia, avoid in pregnancy, beware of renal artery stenosis

23
Q

What do calcium channel blockers do?

A

block L-type (voltage operated) calcium channels, reduces Ca2+ entry into the vascular/cardiac cells *not skeletal muscle, therefore there is a reduction in intracellular calcium = vasodilation and reduced cardiac contractility and reduced atrioventricular conduction

24
Q

2 examples of calcium channel antagonists? Key difference between the two?

A

verapamil - reduces venous pressure (preload), has stronger effects on the heart
and amlodipine - reduces arteriolar pressure (afterload), stronger effects on HR (up), BP (down) and TPR (down)

25
Q

what are indications for calcium channel blockers/antagonists?

A

hypertensions, angina, tachydysrhythmias (TDRs)

26
Q

What are contraindications for calcium channel blockers?

A

heart failure or beta-blockers (with verapamil)

27
Q

Side effects of calcium channel blockers

A
  • cardiac depression (both rate and force reduced), bradycardia (therefore contraindicated in heart failure)
  • flushing, oedema, dizziness, headache
  • constipation, nausea
28
Q

what do diuretics do?

A
  • increase water and sodium excretion from the kidney
  • reduce circulating blood volume in hypertension; there is an initial drop in CO and; in longer term CO and TPR return to normal levels
29
Q

What do thiazides e.g. hydrochlorothiazide and indapamide act on?

A

distal tubule

30
Q

Example of a diuretic?

A

frusemide, more potent than thiazides, used in acute scenarios

31
Q

What do loop diuretics such as frusemide act on?

A

loop of Henle

32
Q

Uses of thiazides such as hydrochlorothiazide and frusemide?

A
  • mild to moderate hypertension

- oedema due to: 1)congestive heart failure (+/- hypertension), 2) +/- pulmonary congestion and renal or liver disease

33
Q

Side effects of thiazides generally?

A

rash, hypokalaemia, hyperuricaemia, glucose intolerance, hyperchlesterolaemia

34
Q

Side effects of loop diuretics?

A
  • hypovolaemia: dizziness, weakness, nausea, cramps, hypotension
  • hearing loss
  • increased magnesium, calcium excretion
35
Q

What is an important drug interaction with the use of diuretics?

A

Digoxin - toxicity is greatly increased

also consider K+ supplementation or combination with K+ sparing diuretics

36
Q

What do beta-adrenoceptor antagonists do - what are their effects?

A

decrease sympathetic input to the heart (therefore reduced CO and HR - and TPR to a lesser extent), inhibit renin release by decreasing Ang II levels, reduce sympathetic outflow from CNS if lipid soluble

37
Q

2 examples of beta-adrenoceptor antagonists and their selectivities?

A

Propranolol - non selective beta 1 and 2 antagonist

Atenolol - beta 1 selective antagonism

38
Q

Clinical uses for beta adrenoceptor antagonists?

A

angina, post myocardial infarct, hypertension, dysrhythmias, clinically stable heart failure

39
Q

Factors to consider when choosing a hypertensive

A
  • patient’s CV risk profile
  • presence of target organ damage, renal disease, diabetes
  • presence of coexisting conditions which may favour/limit use of particular classes (diabetes, respiratory)
  • individual patient variability to different classes
  • adverse effects
  • interactions with other co-prescribed drugs
  • cost, compliance
40
Q

Most effective combination for hypertension?

A

ACE inhibitor or ARB

+ calcium channel blocker

41
Q

Other effective combination therapies?

A
  • ACE inhibitor/ARB + thiazide diuretic esp. in heart failure or post stroke (low dose thiazide diuretic for people aged 65+)
  • ACE inhibitor/ARB + beta-blocker esp. post MI or heart failure
  • beta-blocker + dihydropyridine calcium channel blocker esp. coronary heart disease
  • thiazide diuretic + Ca2+ channel blocker
  • thiazide diuretic + beta-blocker *not recommended in people with glucose intolerance, metabolic syndrome or established diabetes
42
Q

In newly diagnosed hypertension, is it best to start with mono or combination therapy?

A

One drug to start, then 2 then 3. If after 3, target BP is still not reached, then refer to a specialist.

43
Q

Dangerous combinations to avoid

A
  • ACE inhibitor/ARB antagonist + K+-sparing diuretic (risk of hyperkalaemia)
  • verapamil + beta-blocker (risk of heart block)
  • ACE inhibitor + Ang II receptor antagonist (increases risk of hypertensive symptoms, syncope and renal dysfunction)