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CPT QUIZ > 3.1) Hypertension > Flashcards

3.1) Hypertension Flashcards

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1
Q
  1. What is blood pressure? Is this uniform throughout the body?
A

BP is the driving force to perfuse organs with blood (force per unit area acting on vessels)
It is NOT uniform— differs based on position, time and activities

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2
Q

What is the equation for mean arterial pressure?

A

Mean arterial pressure= cardiac output x total peripheral resistance

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3
Q

Which systems are responsible for blood pressure regulation?

A

Autonomic sympathetic activity and Renin-angiotensin-aldosterone system

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4
Q

Which endogenous chemicals can be released to modify BP?

A

Autacoids— bradykinin and nitric oxide—- act on vascular smooth muscle to cause vasodilation.

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5
Q

What is the relationship between radius, smooth muscle tone and peripheral resistance?

A

Radius decreases cause resistance increase.
Smooth muscle tone changes total peripheral resistance.

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6
Q

How does an increased peripheral resistance impact on BP?

A

Increased peripheral resistance increases BP

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7
Q

What is hypertension?

A

High blood pressure
Above 135 ambulatory
Above 140 in clinic

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8
Q

What is the importance of reducing BP?

A

A reduction in both SBP and DBP reduces cardiovascular disease risk.

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9
Q

What are some of the different types of hypertension?

A

Essential/primary/idiopathic- no known cause
Secondary- as a result of other pathology
Pre-hypertension- state preceding hypertension (where prophylaxis is helpful)
Isolated diastolic/systolic hypertension
White coat/clinical hypertension- anxiety of attending practice increases BP

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10
Q

How is hypertension staged?

A

Desired= 120/80mmHg

Stage 1= ranging clinic pressure 140/90- 159/99mmHg
Stage 2= clinic pressure of 160/100 mmHg or higher but less than 180/120mmHg
Stage 3 (severe)= clinical systolic BP of 180 or higher

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11
Q

What is prehypertension?
How is this treated?

A

Between 120/80 and 140/90 mmHg
Treated with promotion of regular exercise, modifications to diet, reduction of stress, reduced alcohol intake, discouraging excessive caffeine, reduction of dietary sodium

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12
Q

Which agents can be used to treat primary hypertension?

A

Angiotensin converting enzyme inhibitors (ACEi)
Angiotensin receptor (AT1) blockers (ARBs)
Calcium channel blockers (CCBs)
Diuretics- thiazide and thiazide-like

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13
Q

How does the RAAS system increase BP?

A
  • decrease in renal perfusion detected by macula densa cells of DCT, stimulates release of renin from granular cells.
  • renin cleaves angiotensinogen to angiotensin I
  • angiotensin I to lungs acted on by ACE to form angiotensin II
    -angiotensin II has actions on: increases sympathetic activity, increases tubular reabsorption of sodium and electrolytes in nephron (absorbs water also- increasing plasma volume), stimulates adrenal cortex to increase aldosterone release (increases expression eNac to reabsorb more), arteriolar vasoconstriction.
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14
Q

How do ACEi have an anti-hypertensive effect?

A

Limit the conversion of angiotensin I to angiotensin II. Therefore, reduced amounts of angiotensin II to have hypertensive effects.

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15
Q

Why might ARBs be more effective at controlling hypertension than ACEi?

A

Angiotensin II can also be produced from angiotensin I independently of ACE via action of chymases. Thus this form of angiotensin II will not be prevented from acting in the case of ACEi.

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16
Q

Give examples of ACEi

A

Lisinopril
Ramipril

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17
Q

What are some of the side effects of ACEi agents?

A

Hypotension
Dry cough— due to potential ion of bradykinin
Hyperkalaemia— lower aldosterone, increases K+
Cause or worsen renal failure
Angioedema

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18
Q

Contraindications of ACEi?

A

Renal artery stenosis
Acute kidney injury
Pregnancy
Chronic kidney disease
Idiopathic angioedema

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19
Q

Interactions with ACEi may include?

A

Hyperkalaemia causing drugs (potentiates)
NSAIDs- disruption to renal function
Other antihypertensive agents— hypotension

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20
Q

ARBs target which receptor?

A

AT1 receptor

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21
Q

What are examples of ARBs?

A

Candesartan
Losartan

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22
Q

Do ARBs have an effect on bradykinin?

A

No—- less likely to have a dry cough or angioedema

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23
Q

What are the possible side effects of ARBs?

A

Hypotension
Hyperkalaemia- low aldosterone, increases K+
Cause or worsen renal failure

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24
Q

What are some of the contraindications of ARBs?

A

Renal artery stenosis
AKD
Pregnancy
CKD

25
Q

Interactions between ARBs and other drugs?

A

Hyperkalaemia causing drugs
NSAIDs- affect renal function
Other antihypertensive agents

26
Q

What are the 3 classes of CCBs?
What do they all interact with?

A

Dihydropyridines
Non-dihydropyridines- phenylalkylamines and benzothiazepines

All interact with different sites on alpha 1 subunits of voltage gated calcium channels.
Have different selectivity for vascular smooth muscle or myocardium

27
Q

Which agents fall into the dihydropyridine class?
What tissue are these selective for?

A

Amlodipine
Nifedipine
Nimodipine

Selective for peripheral vasculature

28
Q

What is special about amlodipine in relation to other dihydropyridines?

A

Has a longer half life

29
Q

Which of the dihydropyridines is selective for cerebral vasculature?

A

Nimodipine

Useful in ischaemic effects of subarachnoid haemorrhage

30
Q

Side effects of dihydropyridines include?

A

Ankle swelling
Flushing
Headaches (vasodilation in the cerebral vasculature)
Palpitations (compensatory tachycardia)

31
Q

Contraindications of D-CCBs?

A

Unstable angina
Severe aortic stenosis

32
Q

What is a possible DDI of D-CCBs?

A

Amlodipine and simvastatin
—-causes increased effect of statin

33
Q

Phenylalkylamines have what mechanism of action?

A

Class IV anti-arrhythmic agents- prolongs the action potential to have a negative inotropic and chronotropic effect

34
Q

Which drug is an example of a phenylalkylamine?

A

Verapamil

35
Q

Side effects of Non-dihydropyridine calcium channel blockers include?

A

Constipation
Bradycardia
Heart block
Cardiac failure

36
Q

Contraindications of ND-CCBs include?

A

Poor left ventricular function (caution)
AV nodal conduction delay

37
Q

Interactions with ND-CCBs may include?

A

Beta blockers
Other anti hypertensive and anti-arrhythmic agents

38
Q

Diltiazem is an example of which class of agent?

A

Benzothiazepine
Non-dihydropyridine calcium channel blocker

39
Q

What is the mechanism of action of the azide and thiazide- like diuretics?

A

Inhibit the Na+/Cl- co-transporter in the distal convoluted tubule, reduces sodium and water reabsorption

40
Q

Give examples of thiazide agents

A

Bendroflumethiazide
Indapamide

41
Q

What are some of the side effects of diuretic use?

A

Hypokalaemia
Hyponatraemia
Hyperuricaemia (gout)
Arrhythmia
Increased plasma glucose
Increases cholesterol and triglyceride plasma levels

42
Q

What are some of the contraindications to thiazide diuretics?

A

Patients already experiencing hypokalaemia, hyponatraemia and gout

43
Q

What are some of the DDIs associated with thiazide diuretics?

A

NSAIDs
Hypokalaemia causing drugs ie loop diuretics (electrolyte monitoring required)

44
Q

Which treatments are firstline for individuals aged 55 or less no Afro-Caribbean heritage?
Which other demographic also?

A

ACEi/ARBs

Type 2 diabetes mellitus

45
Q

What if firstline for patients aged 55 or over or with an Afro-Caribbean heritage?

A

CCBs

46
Q

Second line management?

A

T2DM/under 55= add CCB or thiazide like diuretic
Without T2DM/Afro-Caribbean= add ACEi/ARB or thiazide like diuretic

47
Q

Third line management?

A

ACEi or ARB + CCB + thiazide like diuretic

48
Q

What is resistant hypertension?

A

Hypertension that persists after step 3 of management.
Need to consider patient adherence or secondary cause for hypertension that could control BP once managed

49
Q

What does Step 4 of management involve?

A

Spironolactone (if patients K+ normal)
- could cause hyperkalaemia, gynaecomastia
Contraindicated in situations potassium is high or Addisons
Instead use alpha and beta blockers or centrally acting drugs ie labetalol to reduce sympathetic outflow

50
Q

Give examples of beta blockers

A

Labetalol
Bisoprolol
Metoprolol

51
Q

How do beta blockers work?

A

Decease sympathetic tone by blocking noradrenaline binding and reducing myocardial contraction (reducing CO)

52
Q

What are some of the side effects of beta blockers?

A

Brconshospasm
Heart block
Raynaud’s
Lethargy
Impotence

53
Q

In what circumstances may beta blockers be contraindicated?

A

Asthma (beta 2 antagonists), haemodynamic instability, hepatic failure

54
Q

What are some of the DDI that may occur with beta blockers?

A

ND-CCBs- verapamil and diltiazem can cause asystole

55
Q

Doxasozin is a drug within which class?

A

Alpha adrenoceptor blocker (antagonist)

56
Q

Which receptors are specifically targeted by alpha blockers?
How does this achieve changes to BP?

A

Alpha 1 receptors
Reduce peripheral vascular resistance- act on alpha 1 receptors in smooth vascular muscle.

57
Q

What are some of the side effects of alpha blockers?

A

Postural hypotension
Dizziness
Syncope
Headache
Fatigue

58
Q

In which circumstances are alpha blockers contraindicated?

A

Postural hypotension

59
Q

Indicate some of the DDIs associated with alpha blockers

A

D-CCBs- increased risk of oedema

CPT QUIZ (19 decks)

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