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Pharmacology Term 6 > 6.1- Hypertension and Heart Failure > Flashcards

6.1- Hypertension and Heart Failure Flashcards

1
Q

Name 3 mechanisms of physiological control

A

ANS; baroreceptors
RAAS
Vasoactive agents; metabolites, bradykinin, endothelium, nitric oxide

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2
Q

Which 3 diuretics are used in treating hypertension and heart failure

A

Loop diuretics: ___ semides and ___tanides
Thiazides
K+ sparing/ aldosterone antagonists: spironolactone and__renones

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3
Q

Name 5 drugs which treat HTN and heart failure

A 
Diuretics 
ACE inhibitors \_\_\_renones
ARB’s \_\_\_\_ sartans 
CCB’s\_\_\_\_\_dipines ie DIHYDROPYRIDINES
Beta blockers
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4
Q

What is hypertension clinically defined as?

A

140/90 mmHg or above

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5
Q

Distinguish between primary and secondary hypertension

A

Primary hypertension: is WITHOUT a single evident cause

Secondary hypertension: high BP WITH a discrete underlying cause

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6
Q

Give 4 causes of secondary HTN

A

Endocrine:
Cushing’s Syndrome; Adrenocortical Hyperplasia
Phaeochromocytoma
Conn’s Syndrome; Primary Hyperaldosteronism

Mechanical: coarctation of aorta

Renal: glomerulonephritis, renal artery stenosis

Pregnancy: Pre-eclampsia

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7
Q

Classify the 3 stages of hypertension

A

Stage 1: BP> 140/90 mmHg
Stage 2: BP> 160/100 mmHg
Stage 3: BP> 180/120 mmHg

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8
Q

What does the QRISK score do?

A

Estimates a patient’s % chance of having CVD in the next 10 years

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9
Q

What makes up lifestyle therapy for HTN?

A 
Patient education
Maintain normal weight (BMI)
Keep dietary sodium low 
Limit alcohol consumption 
Reduce intake of total and saturated fat
Smoking cessation 
Discourage excessive caffeine consumption
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10
Q

What does ACD stand for?

A

ACE inhibitors/ ARB’s

Calcium channel blockers

Diuretics

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11
Q

What are ACE inhibitors?

A

Competitive inhibitors of ACE

-reduced formation of angiotensin II
- mainly arteriolar vasodilators but some venodilation
- circulating aldosterone is reduced
POTENTIATE the action of BRADYKININ

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12
Q

How often should ACE inhibitors be given and give 2 examples

A

E.g. ramipril, enalapril

Oral, once daily titrate dose

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13
Q

Describe the PK of ACEi’s

A

Variable bioavailability

Enalapril and ramipril are prodrugs metabolised in the liver to ___prilats an active metabolite

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14
Q

Give 4 Main Side effects of ACE inhibitors

A

Dry cough
Angioedema ( common in black pop) ( bc of bradykinin making capillaries leaky)
Renal failure ( including renal artery stenosis)
Hyperkalaemia

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15
Q

When are ACE inhibitors contraindicated?

A

Pregnancy

Renal artery stenosis

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16
Q

Why do you get dry cough when you take ACE inhibitors?

A

Due to lack of bradykinin by ACE enzymes

Therefore unmetabolised bradykinin causes CONSTRICTION of non-vascular smooth muscle in the bronchus—-> leading to cough

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17
Q

What are ARB’s?

A

Angiotensin Receptor Blockers
Bind to angiotensin II type 1 (AT1) receptor
Inhibit vasoconstriction and aldosterone stimulation caused by angiotensin II

E.g. losartan

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18
Q

Describe the PK of ARB’s

A

Oral once daily, titrate dose as required
Low availability, high protein binding
Well tolerated

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19
Q

a) Give 2 side effects of ARB’s

b) Give 2 contraindications of ARB’s

A

a) hyperkalaemia
Renal failure

b) pregnancy
Renal artery stenosis

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20
Q

Name 5 ways in which Angiotensin II increases blood volume and blood volume

A

Arteries (smooth muscle)—>vasoconstriction
Adrenal Cortex; aldosterone release; reabsorption of Na+
SNS; NA release
Brain; stimulates ADH, Vasopressin, thirst
Kidney; Na+ reabsorption in renal tubule
Heart; increases contractility; ventricular hypertrophy

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21
Q

How do calcium channel blockers work?

A

-bind to specific alpha subunit of L-type calcium channel, reducing cellular calcium entry

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22
Q

Name the 3 main groups of CCB’s and which are anti-arrhythmics?

A

1) Dihydropines e.g. Felodipine and Amlodipine

2) Benzothiazepines ( anti-arrhythmic)
3) Phenylalkylamines e..g Verapamil anti-arrhythmic

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23
Q

Describe the PK of CCB’s

A

good oral absorption
protein bound>90%
metabolised by the liver ( many by CYP3A4)

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24
Q

Give 5 adverse effects of CCB’s

A 
SNS activation; tachycardia and palpitations
Flushing, sweating 
Throbbing headache
Oedema
Gingival hyperplasia( rare)
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25
Q

Describe the effect of CCB’s on vessels?

A

Vasodilates peripheral, coronary and pulmonary arteries
NO significant effect on veins
Short acting dihydropyridines –> baroreflex mediated tachycardia

26
Q

How do thiazide diuretics work?

A

reduce distal sodium tubular reabsorption
sustained action
blood pressure reduction

27
Q

How do thiazides reduce blood pressure?

A

act in DCT on Na/Cl transporter
initial blood volume decrease
later; TPR falls
dose-blood pressure response curve flat ie ALL OR NOTHING

28
Q

Name 5 side effects of bendroflumethiazide

A 
HYPOKALAEMIA
Increased uric acid and urea acid levels 
Impaired glucose tolerance 
Cholesterol and TG levels increased 
Activates RAAS
29
Q

Describe treatment for HTN under 55 yrs?

A 
ACE inhibitor or ARB
then 
A+CCB
then 
A+ CCB+diuretic
30
Q

Describe HTN treatment if over 55 yrs and black

A

C
then
C+A or D
A+C+D

31
Q

How would you treat resistant hypertension?

A

A+C+D

consider spironolactone or an alpha or beta blocker

32
Q

What is a hypertensive emergency vs urgency?

A

Urgency>180/120

Emergency> 200/130

33
Q

What complications arise from malignant hypertension?

A

Pulmonary oedema
Renal failure
Aortic dissection
Papilloedema

34
Q

How does NO cause rapid vasodilation?

A

causes rapid vasodilation–>decreased preload–> reduces EDV–> reduces SV–> Reduces BP

35
Q

How is rapid reduction in BP achieved?

A

IV THERAPIES

for GTN/ Sodium nitroprusside

36
Q

How does Sodium Nitroprusside work for malignant HTN?

A

releases NO; a potent vasodilator of arterioles and venules

  • IV use with powerful rapid onset and offset
  • BREAKDOWN to CYANIDE; caution in liver disease, but renal excretion.
37
Q

What is dangerous about Sodium Nitroprusside?

A

it gets broken to CYANIDE; therefore caution in liver disease but renal excretion

Avoid prolonged use >72 hours

38
Q

How does GTN treat malignant HTN?

A

Glceryl Trinitrate
Exogenous source of NO
More powerful venous vasodilator than arterial
iV use with powerful rapid onset and offset

39
Q

What are some side effects of GTN?

A

Headache
Hypotension

TACHYPHYLAXIS

40
Q

What is tachyphylaxis and where is it seen?

A

seen as a side effect of GTN

Reduced efficacy due to tolerance after approx 48 hours

41
Q

Name 3 generals symptoms of HEART failure

A

breathlessness
ankle swelling
fatigue

42
Q

Give 5 investigative signs of HF

A 
Cardiomegaly
Third heart sound 
Cardiac murmurs
ECHO abnormalities
RAISED NT-proBNP
43
Q

Give 4 causes of LHF

A

mitral and aortic valve stenosis
Coronary Heart Disease (CHD)
Hypertension (HTN)
Cardiomyopathy

44
Q

Give 3 causes of RHF

A

Intrinsic; RV infarction

Volume overload ( shunts; VSD or ASD/ pulmonary and tricuspid regurg)

Increased afterload

45
Q

Give 4 causes of increased afterload in RHF

A

Left heart failure
Pulmonary Embolus (PE)
Chronic lung disease
Cor pulmonale

46
Q

What type of heart failure is worse, systolic or diastolic?

A

DIASTOLIC; preserved ejection fraction
i.e. less volume pumped out per contraction
problem filling the heart

47
Q

What are the 3 main principles for treating HF?

A

1) Treat signs and symptoms, improve QOL
2) Prevent hospital admissions
3) Reduce mortality

48
Q

What is the main drug of choice for heart failure?

A

DIURETICS

loop diuretics mainly; for patient comfort ie reduce symptoms like oedema

49
Q

Which 2 loop diuretics are mainly used in HF?

A

Furosemide
Bumetanide; alternative to furosemide
40 mg Furosemide= 1 mg po bumetanide

50
Q

Describe 5 ADR’s of loop diuretics

A 
hyponatraemia 
hypokalaemia
postural hypotension 
syncope 
hyperuricaemia/gout
51
Q

How is SYSTOLIC HF treated?

A

RAAS antagonists; ie ACE inhibitors, ARB’s and aldosterone antagonists

Beta-blockers

52
Q

What is the significance of ABBAA

A

ACE inhibitor
Beta blocker
Aldosterone antagonist

53
Q

In systolic HF, why do you need further therapy of an aldosterone antagonist in addition to an ARB or ACE inhibitor?

A

bc despite use of ARB or ACEi, you get aldosterone escape
there is still some aldosterone that is produced–> this causes endothelial dysfunction+ leads to myocardial fibrosis—> coronary events–> MI

54
Q

How do aldosterone antagonists work and give 2 examples

A

block endothelial dysfunction and myocardial fibrosis that result from aldosterone escape therefore no coronary events
mild diuretic effect

e.g. Spironolactone, Eplerenone

55
Q

How do beta blockers reduce myocardial oxygen demand?

A

1) Reduce heart rate and negative inotropic effect via Beta1 adrenorceptor to reduce CO
2) Reduce BP–> less afterload on heart

56
Q

Give 4 physiological effects of Beta blockers

A

Reduce HR and negative inotropic effect to reduce CO

Reduce BP–> decreased afterload

Reduce mobilisation of glycogen

Negate unwanted effects of catecholamines

57
Q

Name 3 BNP recommended beta blockers

A

BISOPROLOL; high beta1 selectivity

CARVEDILOL

NEBIVOLOL; B1 selective at low doses also NO potentiating–> also a vasodilator

58
Q

How do Beta blockers aid HF?

A

Failing myocardium is dependent on HR so beta blockers aid this
Initiate at low does
Titrate SLOWLY
may have to alter concomitant meds e..g diuretic

59
Q

What is IVABRADINE?

A

If (funny current) channel inhibitor at the SAN
reduces heart rate
ie slower upstroke of SAN potential

60
Q

What is VASARTAN?

A

ARB/ Neprilysin inhibitor

NEPRILYSIN degrades BNP and bradykinin, both vasodilators

61
Q

How to manage disease modifying therapies?

A

Titrate up to max possible doses ( start low)

Monitor HR, renal function and BP when uptitrating

62
Q

Benefits of disease modifying therapies?

A

Improve symptoms and QOL
Improve ventricular function
Reduce hospital admission and death

Pharmacology Term 6 (10 decks)

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