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

6.1- Hypertension and Heart Failure Flashcards

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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
Describe the effect of CCB's on vessels?
Vasodilates peripheral, coronary and pulmonary arteries NO significant effect on veins Short acting dihydropyridines --> baroreflex mediated tachycardia
26
How do thiazide diuretics work?
reduce distal sodium tubular reabsorption sustained action blood pressure reduction
27
How do thiazides reduce blood pressure?
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
Name 5 side effects of bendroflumethiazide
``` HYPOKALAEMIA Increased uric acid and urea acid levels Impaired glucose tolerance Cholesterol and TG levels increased Activates RAAS ```
29
Describe treatment for HTN under 55 yrs?
``` ACE inhibitor or ARB then A+CCB then A+ CCB+diuretic ```
30
Describe HTN treatment if over 55 yrs and black
C then C+A or D A+C+D
31
How would you treat resistant hypertension?
A+C+D | consider spironolactone or an alpha or beta blocker
32
What is a hypertensive emergency vs urgency?
Urgency>180/120 | Emergency> 200/130
33
What complications arise from malignant hypertension?
Pulmonary oedema Renal failure Aortic dissection Papilloedema
34
How does NO cause rapid vasodilation?
causes rapid vasodilation-->decreased preload--> reduces EDV--> reduces SV--> Reduces BP
35
How is rapid reduction in BP achieved?
IV THERAPIES | for GTN/ Sodium nitroprusside
36
How does Sodium Nitroprusside work for malignant HTN?
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
What is dangerous about Sodium Nitroprusside?
it gets broken to CYANIDE; therefore caution in liver disease but renal excretion Avoid prolonged use >72 hours
38
How does GTN treat malignant HTN?
Glceryl Trinitrate Exogenous source of NO More powerful venous vasodilator than arterial iV use with powerful rapid onset and offset
39
What are some side effects of GTN?
Headache Hypotension TACHYPHYLAXIS
40
What is tachyphylaxis and where is it seen?
seen as a side effect of GTN Reduced efficacy due to tolerance after approx 48 hours
41
Name 3 generals symptoms of HEART failure
breathlessness ankle swelling fatigue
42
Give 5 investigative signs of HF
``` Cardiomegaly Third heart sound Cardiac murmurs ECHO abnormalities RAISED NT-proBNP ```
43
Give 4 causes of LHF
mitral and aortic valve stenosis Coronary Heart Disease (CHD) Hypertension (HTN) Cardiomyopathy
44
Give 3 causes of RHF
Intrinsic; RV infarction Volume overload ( shunts; VSD or ASD/ pulmonary and tricuspid regurg) Increased afterload
45
Give 4 causes of increased afterload in RHF
Left heart failure Pulmonary Embolus (PE) Chronic lung disease Cor pulmonale
46
What type of heart failure is worse, systolic or diastolic?
DIASTOLIC; preserved ejection fraction i.e. less volume pumped out per contraction problem filling the heart
47
What are the 3 main principles for treating HF?
1) Treat signs and symptoms, improve QOL 2) Prevent hospital admissions 3) Reduce mortality
48
What is the main drug of choice for heart failure?
DIURETICS | loop diuretics mainly; for patient comfort ie reduce symptoms like oedema
49
Which 2 loop diuretics are mainly used in HF?
Furosemide Bumetanide; alternative to furosemide 40 mg Furosemide= 1 mg po bumetanide
50
Describe 5 ADR's of loop diuretics
``` hyponatraemia hypokalaemia postural hypotension syncope hyperuricaemia/gout ```
51
How is SYSTOLIC HF treated?
RAAS antagonists; ie ACE inhibitors, ARB's and aldosterone antagonists Beta-blockers
52
What is the significance of ABBAA
ACE inhibitor Beta blocker Aldosterone antagonist
53
In systolic HF, why do you need further therapy of an aldosterone antagonist in addition to an ARB or ACE inhibitor?
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
How do aldosterone antagonists work and give 2 examples
block endothelial dysfunction and myocardial fibrosis that result from aldosterone escape therefore no coronary events mild diuretic effect e.g. Spironolactone, Eplerenone
55
How do beta blockers reduce myocardial oxygen demand?
1) Reduce heart rate and negative inotropic effect via Beta1 adrenorceptor to reduce CO 2) Reduce BP--> less afterload on heart
56
Give 4 physiological effects of Beta blockers
Reduce HR and negative inotropic effect to reduce CO Reduce BP--> decreased afterload Reduce mobilisation of glycogen Negate unwanted effects of catecholamines
57
Name 3 BNP recommended beta blockers
BISOPROLOL; high beta1 selectivity CARVEDILOL NEBIVOLOL; B1 selective at low doses also NO potentiating--> also a vasodilator
58
How do Beta blockers aid HF?
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
What is IVABRADINE?
If (funny current) channel inhibitor at the SAN reduces heart rate ie slower upstroke of SAN potential
60
What is VASARTAN?
ARB/ Neprilysin inhibitor | NEPRILYSIN degrades BNP and bradykinin, both vasodilators
61
How to manage disease modifying therapies?
Titrate up to max possible doses ( start low) | Monitor HR, renal function and BP when uptitrating
62
Benefits of disease modifying therapies?
Improve symptoms and QOL Improve ventricular function Reduce hospital admission and death

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