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ZCP302 > Hypertension > Flashcards

Hypertension Flashcards

1
Q

Define Hypertension

A

Increased blood pressure of greater than 140/90mmHg. BP = Cardiac Output × Peripheral Vascular Resistance.

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2
Q

What is meant by systolic and diastolic blood pressure?

A

Systolic is the peak pressure in the arteries during ventricular contraction.
Diastolic is the pressure in the arteries when the chambers are filling.

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3
Q

What is the difference between hypertensive emergency and urgency?

A

Hypertensive urgency is a BP of 180/120 without progressing end-organ damage.
Hypertensive emergency is a BP of 180/120 with acute end-organ damage.

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4
Q

What is Renin?

A

It is an enzyme stored in the juxtaglomerular cells in renal afferent arterioles. Renin is released by decreased renal blood flow or low salt delivered to the TAL and catecholamines.

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5
Q

What are some effects of angiotensin II effects?

A

Cause vasoconstriction. Increase PVR.
Stimulate NA and Adrenaline from the adrenal cortex. Stimulates vasopressin.
Stimulates aldosterone synthesis. This increases sodium and water reabsorption from the kidney. Increases plasma volume and PVR.

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6
Q

What is a natriuretic hormone and what is its function?

A

Atrial natriuretic peptide. It increases GFR, inhibits sodium and H2O reabsorption. Functional antagonist of RAAS. Also causes smooth muscle cell relaxation and increased endothelial permeability.

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7
Q

What are the neuronal regulations of BP?

A

Stimulation of post-synaptic Rs - alpha 1 Rs on arterioles and venules cause vasoconstriction. Beta 1 Rs in the heart - increase HR and force of contraction.
B2 Rs in arteries and veins - vasodilation.
Stimulation of pre-synaptic Rs -
A2 Rs - inhibition of NA release. B2 Rs - facilitate NA release.
Baroreceptors, found in the carotid arteries and aortic arch. An increase in BP increases the firing of baroreceptors. Decreases heart rate, vasoconstriction and sympathetic outflow.

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8
Q

What are vascular endothelial mechanisms?

A

Arterial pressure is determined by vascular radius and compliance (measure of the blood vessel to stretch). Essential hypertension occurs when there is a deficiency in the synthesis of vasoactive substances.

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9
Q

What is the MoA of Thiazide diuretics and its indications?

A

Inhibit reasborption of Na and Cl by inhibiting the transporter on the luminal membrane of the DCT. Used for hypertension (first-line) in black patients and oedema.

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10
Q

What are some side effects of thiazides?

A

Hypokalaemia, Hypercalcaemia and C/I in Gout and severe hepatic and renal failure.

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11
Q

List 4 drug interactions of thiazides.

A

Lithium, NSAIDs, Digoxin and Beta blockers and antidiabetic drugs.

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12
Q

What is the MoA of Loop diuretics

A

Inhibit reabsorption of Na and Cl by competing with CL ions for binding to Na/K2Cl cotransporter on the atypical membrane in the TAL of Henle.

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13
Q

What are some pharmacokinetics of loop diuretics?

A

Rapidly absorbed. Onset of action, within 20-60 mins. Secretion due to high PPB. Hepatic metabolism.

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14
Q

What are some indications of K sparing diuretics?

A

Spironolactone, eplerenone and amiloride is for resistant hypertension, primary hyperaldosteronism and Oedema.

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15
Q

What is the MoA of ACEIs?

A

They inhibit ACE, which inhibits the conversion of angiotensin I to angiotensin II. Decreases vasoconstriction and aldosterone release. This will also reduce the breakdown of bradykinin leading to vasodilation leading to decreasing PVR.

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16
Q

What are C/Is of ACEIs?

A

Pregnancy, history of angio-oedema, hyperkalaemia, renal artery stenosis.

17
Q

What are some side effects of ACEIs?

A

Persistant dry cough caused by inhibition of bradykinin breakdown. Angio-oedema. Hyperkalaemia.

18
Q

List 4 Drug interactions of ACEIs and ARBs.

A

Diuretics, ARBs, K sparing agents, ARBs, digoxin and lithium.

19
Q

What are some cautions with ARBs?

A

Dizziness, skin rash, headaches, GI disturbances, Fatigue but lower incidence of cough and angio-oedema.

20
Q

What is the MoA of peripheral a1 R antagonists.

A

They block a1 Rs, which prevents vasoconstriction. This decreases PVR which decreases BP.

21
Q

What are some adverse effects of peripheral a1 blockers?

A

Dizziness, headaches, orthostatic hypotension, priapism and CNS effects (vivid dreams, depression).

22
Q

What is the MoA of Methyldopa?

A

Its an analogue of of L-DOPA. Its converted to a-methylnorepinephrine which leads to SNS stimulation and its more selective for a2 than a1. Central a2 stimulation leads to antihypertensive effect.

23
Q

What are some pharmacokinetics of methyldopa?

A

50% oral dose absorbed. Crosses BBB. Extensive hepatic metabolism. 70% renal elimination.

24
Q

List the locations of beta-1 and beta-2 receptors.

A

B1 - cardiac myocytes, JGM complex and Lipocytes.
B2 - Bronchiole smooth muscle, skeletal muscle, pancreas and liver, peripheral blood vessell

25
Q

What is the MoA of beta blockers?

A

Cardiac effects: Negative inotropic and chronotropic effect. Also reduces firing of nodes.
Renal effects: reduced renin release, which inhibits RAAS.

26
Q

What are some adverse effects of beta blockers?

A

Bradycardia, heart block, exercise intolerance, bronchospasm, diabetogenic, mask symptoms of hypoglycaemia, dyslipidaemias. CNS effects (drowsiness, mental depression).

27
Q

What are 4 drug interactions of beta blockers?

A

Insulin and oral antidiabetic drugs, cholestyramine, pheytoin, NSAIDs, Lidocaine.

28
Q

How do we discontinue beta-blockers?

A

Taper slowly over 1-2 weeks because abrupt discontinuation leads to withdrawal. Up-regulation of Beta-Rs, which increases sensitivity to agonists.

29
Q

What do vasodilators do to lower blood pressure?

A

They relax smooth muscles of blood vessels and cause vasodilation, which decreases PVR and decreases arterial BP. This however causes a compensatory response triggered by RAAS and baroreceptors reflexes.

30
Q

What is the MoA of CCBs?

A

They inhibit L-type voltage-gated calcium channels at the alpha subunit. This reduces Ca from the sarcoplasmic reticulum. In vascular SM this reduces the contractility of the muscles leading to vasodilation. It also reduces contractility of cardiac muscles.

31
Q

What are some indications of CCBs?

A

Dihydropyridine derivatives
Hypertension - not short-acting nifedipine.
Stable angina
Cerebrovascular events - nimodipine.

32
Q

Give 5 common adverse effects of CCBs

A

Headaches, N & V, Dizziness, Fatigue, Constipation, Flushing.

33
Q

What are some cautions of CCBs?

A

HF, Aortic stenosis, Renal and Hepatic impairment.

ZCP302 (7 decks)

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