3.1 Hypertension And Heart Failure Flashcards

(42 cards)

1
Q

How do you calculate mean arterial pressure?.

A

CO x TPR.

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

What is resistance to flow inversely proportional to?

A

Inversely proportional to the radius (to the 4th power)

So, Vacoconstiction = increased peripheral resistance = increased BP

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

What can hyperinsulinemia and hyperglycaemia lead to?

A

Endothelial dysfunction and reactive oxygen species, decreased NO

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

Why do you need to treat Hypertension?

A

Precursor to cardiovascular disease

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

Define hypertension

A

An elevation in blood pressure that is associated with an increase in risk of some harm

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

What are some causes of hypertension?

A

White coat/clinic
Isolated systolic/diastolic (only one is raised)
Prehypertensive
Secondary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How do you diagnose and treat hypertension?

A
  • screening sessions
  • increase public awareness of risk factors
  • reliable diagnoses based on clinical guidelines
  • promote appropriate lifestyle changes to limit risk
  • regulate monitoring and refinement of medication.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the clinical methods of diagnoses of hypertension?

A

Measure BP with patient sat relaxed with a supported arm

Measurements in both arms should be similar, within 20mmHg

Severe = medical emergency, send to A&E

Patient management follows diagnoses

Cardiovascular risk and wend organ damage should be assessed whilst waiting for HT conformation

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

Normal BP?

A

<120/80 mmHg

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

Stage 1 hypertension measuring ?

A

140/90 mmHg or higher

Home - 135/80 mmHg

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

Stage 2 hypertension BP?

A

160/100 mmHg or higher

Home 150/95

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

Severe hypertension bp?

A

SYSTOLIC IS 180 mmHg or higher or diastolic is 110 mmHg or higher

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

What is prehypertension?

A

Elevated BP below stage 1 diagnoses with no end organ damage that can be treated in the first instance with lifestyle changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What can lifestyle changes can treat elevated bp in prehypertension?

A

Regular exercise
Modified health/balanced diet
Reduction in stress and increased relaxation
Limited/reduced alcohol intake
Discourage excessive caffeine consumption
Smoking cessation
Reduction in dietary sodium

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

What are some primary HT therapeutic agents?

A

ACE inhibitors
Angiotensin receptor blockers
Calcium channel blockers
Diuretics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Where does ACE and Ang 2 act?

A

Luminal surface of capillary endothelial cells, predominantly in the lungs

Catalysts conversion of Ang 1 to And 2 which is a vasoconstrictor

Ang 2 acts through AT1 and AT2 receptors

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

Name 4 ACE inhibitors.

A

Captopril
Enalapril
Lisinopril
Ramipril

18
Q

Why do ace inhibitors cause a dry cough?

A

ACE substrate = bradykinin

If ACE is inhibited, get a build up of bradykinin = dry cough

19
Q

What side affects are associated with ACE inhibitors?

A

Dry cough
Angioedema
Renal failure
Hyperkalaemia

20
Q

How do angiotensin 2 receptor blockers work?

A

Block AT1 receptors which carry out majority of angiotensin 2 functions (unlike AT2 receptor)

Directly targeting AT1 receptors means they’re more effective at inhibiting Ang 2 mediated vasoconstriction

21
Q

What side effects do you get with ang 2 receptor antagonists?

A

Renal failure and hyperkalaemia

No dry cough as no effect on bradykinin

22
Q

Name 4 ang 2 receptor antagonists

A

Losartan
Candesartan
Eprosartan
Irbesartan

23
Q

What do calcium channel blockers target?

A

Calcium inhibiated smooth muscle contraction

There are three classes that interact with different sites on a1 subunit of VOCC selectivity for vascular smooth muscle cells or myocardium

24
Q

What are the three classes of calcium channel blockers?

A
  • Dihydropyridine

Non dihydropyridine
- Phenylalkamines and benzothiazapines

25
How do dihydropyridine CCB work and what are their properties?
More selective for peripheral vasculature, show little chronological or inotropic effect - first line CBB for HT - good oral absorption - protein bound - metabolised by liver
26
Name an example of a dihydropyridine CBB and name its adverse effects.
Amolodipine is an example Adverse effects - sympathetic NS activation = tachycardia (rare) - palpitation - flushing/sweating/throbbing headache - oedema
27
What is the mode of phenylalkylamines CBB?
Depresses SA node and slows AV conduction, negative inotropy Prolongs the AP and effective refractory period Impede ca transport across myocardial and vascular smooth muscle cell membrane
28
Give an example of a phenylalkylamine and give it’s adverse effects
Verapamil Effects include - constipation - bradycardia - negative inotrope = can worsen heart failure, especially with a beta blocker
29
What are the properties of benzothiazapines CBB ?
Impede ca transport across ca and smooth muscle cell membrane Prolong AP
30
Name a benzothiazapines CCB and give its adverse effects
Diltiazem Effects - risk of bradycardia - negative inotropic effect less than verapamil = can worsen heart failure
31
What are some adverse effects of thiazides? Name an example
Example = bendroflumethiazide Effects - hypokalaemia - increased urea and Uris acid levels - impaired glucose tolerance especially with beta blockers - cholesterol and triglycerides levels increase - activates RAAS
32
Why is there no point in giving ARBs to a low renin patient?
Low activity in RAAS system anyway so no point in targeting it for treatment.
33
In pregnancy or a hypertensive emergency, what centrally acting drugs would you use?
Labetalol reduced sympathetic outflow
34
What is spironolactone?
Mineralocorticoid/ aldosterone receptor antagonists
35
What is amiloride?
A K+ sparing diuretic acting on distal tubule
36
What is the effect of alpha adrenoreceptors blocking agents? Name an example.
Doxazosin is an example They antagonise the contractile effects of noradrenaline on vascular smooth muscle Reduced peripheral vascular resistance Benign effect on plasma lipids/glucose Safe in renal disease Adverse effects - postural hypotension - headache and fatigue - oedema
37
What is the effect of beta adrenoreceptors blockers? Name an example
Bisoprolol is an example Decreased sympathetic tone by blocking Nad and reducing myocardial contraction = decreased CO = decreased renin secretion
38
What are the adverse effects of beta adrenoreceptors blockers?
Adverse effects - bronchoconstriction so don’t give in asthma, COPD and 2nd/3rd degree heart block - mask tachycardia = sign of insulin induced hyperglycaemia = caution in diabeties - lethargy and impaired concentration - reduced excersise tolerance - bradycardia - raynauds E.g bisoprolol
39
What are the aims of heart failure treatment?
Manage symptoms Increase exercise tolerance Decreased mortality Address arrhythmia NB: furosemide is typically used in most patients for symptoms but has little impact on survival
40
How can ace inhibitors and ARBs treat heart failure?
In LV dysfunction Low initial dose reduces risk of sudden rapid fall in BP, especially in patients already taking diuretics If ACE inhibitors not tolerated, use ARB as alternative If not working can use both together Make sure you monitor renal function
41
Why may a patient be given spironolactone with a ACE inhibitor or diuretic?
It maximises their effects. NB: spironolactone is a aldosterone/mineralocorticoid receptor antagonist
42
What is the role of B adrenoreceptors antagonists?
Recommended for all patients with stable clinical heart failure Introduced once ACE inhibitor or ARB therapy is initiated Blunts sympathetic influences especially on HR = slower HR = longer diastolic filling period = better filling = more output May stabilise electrical conduction reducing arrhythmia May also blunt circulating RAAS by working on renin but probably minor since already on ACE Low initial dose which may cause transient worsening of symptoms