Drugs for Hypertension Flashcards

1
Q

what is primary “essential” hypertension?

A
  • no known cause, represents 90-95% of cases

- genetic predisposition, dietary salt intake, adrenergic tone

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2
Q

what is secondary hypertension?

A
  • known cause; represents 5-10% of cases

- ex. adrenal cortical tumours, drugs

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3
Q

what are the physiological effects of hypertension?

A
  • prolonged force on vessels thickens muscles in the arterial system
  • heart constantly works harder to expel blood against a greater force, increasing the workload of the heart
  • increase force damages inner lining of arteries (susceptible to atherosclerosis and to narrowing of vessel lumen)
  • tiny vessels are damaged and destroyed leading to losses in vision, kidney function and cerebral function
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4
Q

what is hypertension a risk factor for?

A
  • CVA, CAD, CHF, cardiac death, renal failure, peripheral vascular disease, and dementia
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5
Q

what parameters control BP?

A
  • BP=CO X peripheral resistance
  • CO: product of heart rate and amount of blood that is ejected with each beat (stroke volume)
  • peripheral resistance: arteries possess smooth muscle in the media that responds to alpha 1 receptors. when stimulated they produce contraction of the smooth muscle layer and increase lumen of the vessel increasing peripheral resistance
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6
Q

what is the compensatory action by kidneys to regulate blood pressure?

A
  • engages kidneys to increase urine output, reducing blood volume and stroke volume decreasing blood pressure
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7
Q

what is the compensatory action of the cardiovascular system to regulate blood pressure?

A
  • decreases in heart rate cause decrease in cardiac output, which decreases blood pressure; also causing vasodilation in periphery
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8
Q

what are some lifestyle modifications with hypertension?

A
  • reduce sodium intake
  • healthy diet
  • low risk alcohol consumption
  • regular physical activity
  • maintenance of ideal body weight
  • smoking cessation
  • stress management
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9
Q

why should beta blockers not be used as a mono therapy for hypertension in those 60+?

A
  • do not help to decrease the risk for myocardial infarction or stroke
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10
Q

what is the mechanism of action of thiazide and thiazide- like diuretics?

A
  • first line therapy for management of hypertension
  • reduces stroke volume by blocking sodium/chloride transporter in the distal tubule facilitating the excretion of electrolytes
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11
Q

what are some caution precautions when using thiazide diuretics?

A
  • severe renal disease, diabetes, GOUT, liver disease, hyperlipidemia
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12
Q

when are thiazide diuretics contraindicated?

A
  • pregnancy
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13
Q

when should thiazide diuretics be administered?

A
  • during the day to prevent nocturia
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14
Q

what are some adverse effects of thiazide diuretics?

A
  • GI upset, orthostatic hypotension, hyperglycaemia, fluid and electrolyte imbalance
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15
Q

what are some drug to drug interactions with thiazide diuretics?

A
  • lithium, NSAIDs, anti diabetic drugs
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16
Q

what is important to monitor with thiazide diuretics?

A
  • sodium and potassium levels, kidney function and blood pressure within 4-6 weeks of starting therapy
  • dizziness and lightheadedness
17
Q

what is the mechanism of action of angiotensin converting enzyme (ACE inhibitors)?

A
  • decreases peripheral resistance and decrease blood volume
  • blocks conversion of angiotensin I to angiotensin II
  • increase production of vasodilatory kinins
  • inhibits aldosterone secretion
18
Q

when are ACE inhibitors contraindicated?

A
  • in pregnancy, use caution with potassium-sparing supplements and diuretics
  • decreased antihypertensive activity with NSAIDS
19
Q

what are some adverse effects with ACE inhibitors?

A
  • may induce dry cough
  • hyperkalemia
  • GI irritation and constipation
  • sudden drop in BP (first dose phenomenon)
  • allergic reaction of the lips, mouth, and throat occurring during first month of administration
20
Q

what is the mechanism of action of angiotensin II receptor blockers?

A
  • decrease peripheral resistance and decreases blood volume
  • block angiotensin II receptors in arteriolar smooth muscle and in adrenal cortex
  • inhibit the release of aldosterone
  • no effect on bradykinin
21
Q

what type of patients are prescribed angiotensin II receptor blockers?

A
  • people who cannot tolerate adverse effects of ACE inhibitor drugs
22
Q

what are the common adverse effects and drug to drug interactions with angiotensin II receptor blockers?

A
  • similar to ACE inhibitors
23
Q

what is the mechanism of action for calcium channel blockers?

A
  • block calcium ion channels
  • relax vascular smooth muscle, decreasing peripheral resistance
  • slow heart rate , reducing cardiac output and cardiac workload
24
Q

when should you be cautious administering calcium channel blockers?

A
  • in those with liver and kidney impairment
25
Q

what are some adverse effects of calcium channel blockers?

A
  • dizziness
  • light-headed
  • fatigue
  • flushing
  • nausea
26
Q

what should be avoided when taking calcium channel blockers?

A
  • avoid grapefruit juice, increases serum CCB levels
27
Q

what part of the autonomic nervous system increases heart rate and smooth muscle constriction of arterial walls?

A
  • sympathetic division
28
Q

what is the mechanism of action of alpha and beta adrenergic receptors?

A
  • block adrenergic effects on arterioles
  • block action of NE and E on cardiac muscle reducing speed and force of contraction
  • decrease renin secretion by the kidneys, reducing the production of angiotensin I and decreasing TPR
29
Q

when are beta blockers most effective?

A
  • in patients under the age of 60 with concomitant cardiovascular conditions
  • previous history of MI and/or angina
30
Q

what would be some patient precautions when taking beta adrenergic antagonists?

A
  • diabetes, depression, asthma, COPD

- reduction in heart rate may cause fatigue and activity intolerance