Hypertension Flashcards

1
Q

Name 4 examples of ACE-inhibitors.

A
-Prils!
Captopril
Enalapril
Lisinopril
Ramipril
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2
Q

MOA ACE-inhibitors (5)

A

Inhibit angiotensin converting enzyme (prod by lungs), causing:
• Inhibit ANGIOTENSIN 2 - vasoconstrictor and growth promoter by stim adrenals
• increase BRADYKININ: vasodilator (release NO and prostacyclin)
• reduce ALDOSTERONE secretion: reduced Na and H20 retention
• reduce activity of sympathetic nervous system: A2 usually promote release noradrenaline, inhibit NA reuptake
• also improve ß receptor density, variation HR, baroreceptor functions, autonomic function

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3
Q

Indications ACE-I (3)

A
  • Hypertension!
  • Heart failure (LV dysfunction, slow progress) first line!
  • Renal dysfunction ( esp diabetics ) .
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4
Q

Contraindications ACE-I (3)

A

Pregnancy
Renovascular disease
Aortic stenosis

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5
Q

Adverse effects ACE-I (6)

A
  • First dose hypotension (so give at night before bed)
  • Dry cough (bradykinin)
  • Functional renal failure (in bilat renal a stenosis, foetus with oligohydramnios)
  • Hyperkalemia (reduced aldosterone)
  • Rare: urticaria, angioedema (esp afro-caribbean)
  • Dizzy, headache, diarrhea, muscle cramps
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6
Q

Drug interactions ACE-I (3)

A
  • K sparing diuretics, K supplements (hyperk )
  • NSAIDs (hypotension and hyperk )
  • Loop and thiazide diuretics indicated! (diuretics increase renin which would normally decrease efficacy but ACE-I interrupt loop to make diuretics more effective-beneficial!)
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7
Q

Calcium channel blockers 3 types or classes and example of each

A
  • Phenilakylamines: verapamil! Rate-limiting.
  • Benzothiazepines: diltiazem
  • dihydropyridines: nifedipine! (Short acting 1st gen), felodipine (long-acting 2nd gen), amlodipine! (3rd gen), nimlodipine
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8
Q

MOA CCBS (4)

A

Dihydropyridines: block L-type calcium channels in vascular cells (control contractile state of actomyosin), therefore reduce calcium influx → vasodilatation reduce peripheral vascular BP, lower arterial BP

Rate limiting or phenylalkalines: block channels in vascular AND heart - reduce cardiac contractility, reduced myocardial oxygen consumption, decreased HR and as above. High doses may affect AVN conduction.

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9
Q

Which population does CCBS work best for for HT??

A

Black patients -more effective than ACE-I or ARBS

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10
Q

Indications CCBs (4)

A
  • Treat and prophylax angina (esp dihydropyridines;benzothiazepines)
  • And HT (long acting dihydropyridines eg felodipine , amlodipine;and nifedipine)
  • Supraventricular arrhythmia (verapamil and diltiazem )
  • Raynaud syndrome (nifedipine)
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11
Q

Contraindications calcium channel blockers (3)

A
  • Cardiogenic shock
  • Dihydropyridines: advanced aortic stenosis
  • Verapamil and diltiazem: severe heart failure (negative inotropic action) ß blockers (R AV block and impaired cardiac output), severe bradycardia
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12
Q

Adverse effects dihydropyridines (4)

A

(CCBS: nifedipine, amlodipine, felodipine)
• Headache and flushing (vasodilation)!
• Ankle swelling (increased pedal capillary pressure)!
• reflex tachycardia (activation baroreceptors and SNS )
• hypotension, rash, dizzy, possible risk GIT bleed elderly, exacerbate HF

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13
Q

Adverse effects benzothiazepines and phenylalkylamines (3)

A

(Ccbs: diltiazem and verapamil)
• heart block (negative inotrope)
• constipation (relax smooth muscle)
• hypotension, rash, bradycardia, CCF

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14
Q

Drug interactions CCBS

A

Dihydropyridines and B blockers favourable in moderate-severe HT uncomplicated by HF

IV verapamil and beta blockers: potentially fatal in treatment tachy-arrythmias

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15
Q

3 types diuretics used in HT

A

Thiazides (preferred - most relevant)
Loop diuretics
K-sparing diuretics

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16
Q

Thiazides diuretics MOA (2)

A
  • Act on cortical nephron to inhibit reabsorption Na and Cl in early distal convoluted tubule resulting in natriuresis
  • activate atp-regulated potassium channels in resistance arterioles, causing hyperpolarisation. This inhibits calcium influx into vascular smooth muscle cells with consequent VASODILATION and reduced peripheral vascular resistance.
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17
Q

Examples thiazides diuretics (2)

A

Hydrochlorothiazide
Bendroflumethiazide
(-Thiazide)

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18
Q

Indications thiazides diuretics in HT

A

Stage 1 where CCBS contraindicated

Severe hypertension in combination

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19
Q

Indications thiazides - like diuretics in HT

A

Same as thiazides, but preferred

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20
Q

Examples thiazide-like diuretics (2)

A

Chlortalidone

Indapamide

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21
Q

Adverse effects thiazides diuretics (3)

A
  • impotence (increased plasma renin)
  • electrolyte changes: hypo-everything. Hypo Na, K, mg
  • metabolic changes: hyper- everything. Hyper uricemia, glycemia, calcemia, cholesterolemia
22
Q

ß blockers - 2 types and examples

A

(-olol)

• Cardio-selective (B1 receptors): atenolol! Bisoprolol, metoprolol
• Non-selective (B 1 and 2): Propanolol!
Vasodilating: carvedilol

23
Q

MOA B blockers (6)

A
Decrease heart rate!
Decrease systolic BP!
Decrease cardiac contractile activity
Decrease myocardial oxygen demand
Reduce renin secretion
Reduce sympathetic
Acutely increase peripheral resistance!
24
Q

Indications ß blockers (6)

A
  • Angina
  • Post MI
  • Arrhythmia
  • HT 4th line and with associated IHD
  • Stabilise pts with dissecting aortic aneurysms (IV)
  • Thyrotoxicosis, glaucoma, anxiety
  • CHRONIC Hf from LV systolic dysfunction first line! With an ace-i: bisoprolol, metoprolol, carvedilol
25
Q

Contraindications B blockers ( 5 )

A
  • Asthma (nonselective -propanolol) and COPD
  • IDDM
  • Av block
  • Peripheral vascular disease
  • Bradycardia, hypotension
  • nstemi pts at risk of developing cardiac shock (early mortality)
  • pts with symptoms related to coronary vasospam or cocaine use (worsen spasms )
26
Q

Adverse effects B blockers (9)

A
  • Bronchospasm!
  • Increase peripheral vascular resistance /vasoconstriction in acute dose
  • Heart block
  • Bradycardia
  • Intolerance: fatigue, cold extremities, depression!
  • Hypoglycemia, reduced glucose tolerance in diabetes!
  • Heart failure (negative inotrope)
  • Metabolic: increase tg, fall HDL, increase K
  • Hypotension, dizzy
27
Q

Drug interactions ß blockers (4)

A
  • Pharmacokinetic: reduce hepatic blood flow so inhibit drug metabolism of verapamil and lignocaine
  • Cimetidine cause accumulation propanalol
  • Pharmacodynamic: verapamil and lignocaine exaggerate negative inotrope and Av nodal effects
  • Insulin and oral hypoglycemics exaggerate hypoglycemia
28
Q

Which drugs are used for HT in pregnancy? (2)

A

1st line: alpha - methyldopa (alpha 2 agonist)

Severe HT: hydralazine

29
Q

Name 2 examples of alpha 1 antagonists

A

Prazosin

Doxazosin

30
Q

When should statins be prescribed to hypertensive patients without hypercholesterolaemia?

A

Hypertension and 3 other risk factors for cardiovascular disease

31
Q

Name 3 types ARBs

A
  • Sartan!
    • losartan
    • valsartan
    • olmesartan
32
Q

Moa arb?

A

Angiotensin 2 receptor blockers, causing vasodilation and ultimate reduction in peripheral resistance.

33
Q

ARBs AE?

A

angioedema in some

Much less side effects than ace-i so good alternative of side effects

34
Q

Drug interaction ARBs?

A

Don’t give with ace-i

35
Q

Name 5 drug interactions with thiazide diuretics

A
  • Corticosteroids, amphotericin b:hypokalaemia
  • NSAIDs: reduce efficacy by inhibit PGE and prostacyclin synthesis causing Na and water retention
  • lithium: toxicity- more absorption from pct
  • digoxin: toxicity hypoka hypomg
  • CCB: decreased efficacy
36
Q

Where on the nephron does thiazide diuretics work on?

A

Distal convoluted tubule

37
Q

Name 2 aldosterone antagonists

A

• Spironolactone
• eplerenone
Aka potassium sparing diuretic

38
Q

Moa aldosterone antagonist type potassium sparing diuretics?

A

Competitive antagonist at aldosterone r, therefore reduce Na reabsorption and so K and H secretion.

39
Q

Name indications spironolactone

A

Aldosterone and agonist type K sparing diuretic
• ht not as first line, thiazide-like preferred. Useful in CHF
• hyperaldosteronism primary (Conn syndrome) or secondary (CHF, liver disease and cirrhosis, nephrotic syndrome)

40
Q

Name 2 drug interactions with potassium sparing diuretics

A
  • Digoxin: interfere with secretion - toxicity

* ace-i: increase risk hyperkalaemia

41
Q

Name 2 adverse effects with potassium sparing diuretics

A
  • Gynaecomastia

* menstrual irregularities

42
Q

Indications alpha 1 blockers

A
  • Ht especially poorly controlled on 3 or 4 drugs and CHF
  • prostate hyperplasia
  • coronary artery disease
43
Q

Moa alpha 1 blockers (2)

A
  • Inhibit alpha 1 adrenoreceptor mediated vasoconstriction, thus reducing peripheral resistance and venous pressure
  • lower plasma LDL, VLDL and triglycerides, increase HDL
44
Q

Excretion of beta blockers?

A

Polar drugs so excreted unchanged by kidneys

Accumulate in renal failure, esp atenolol

45
Q

Name 3 centrally acting alpha blockers

A
  • Reserpine
  • methyldopa
  • moxonidine
46
Q

Which hypertensive agent used in pregnancy? (2)

A

Methyldopa

Hydralazine if severe

47
Q

What is minoxidil and what used for?

A
  • K channel activator

* severe, resistant ht

48
Q

What is nitroprusside and what used for?

A
  • Break down NO vasodilator

* malignant ht infusion

49
Q

Name the 3 B blockers with proven benefit in chronic Hf

A
  • Carvedilol
  • bisoprolol
  • metoprolol
50
Q

Treatment of choice hypertension <55 age?

A

Ace-i/arb

51
Q

Treatment of choice hypertension with diabetes?

A

Ace-i/ arb

52
Q

Treatment of choice hypertension > 55 age?

A

CCB/ thiazide like diuretic