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Pharm I > test 6 > Flashcards

test 6 Flashcards

1
Q

What is Hypertension

A

•A sustained systolic blood pressure of greater than 140 mmHg or a sustained diastolic pressure of greater than 90 mmHg

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2
Q

Prehypertension

A

• 120-139/80-89 mmHg

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3
Q

Stage I hypertension

A

• 140-159/90-99 mmHg

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4
Q

Stage II hypertension

A

• ≥ 160/ ≥ 100 mmHg

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5
Q

Primary (Essential) HTN

A
  • No identifiable cause
  • Most common form
  • 90%
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6
Q

Secondary HTN

A
  • Caused by a specific disease process

* Valve disease, coarctation of aorta, pregnancy

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7
Q

Diagnosis of HTN

A
  • Repeated, reproducible measurements of elevated blood pressure
    * At least three pressure readings over several weeks
    * Evidence of organ damage
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8
Q

Risk Factors for HTN

A
  • Advance age
  • Diabetes
  • Obesity
  • Family history
  • Stress
  • Smoking
  • Poor diet (high fat and sodium)
  • Lack of physical activity
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9
Q

Complications of HTN

A
  • Stroke
  • Ischemic heart disease
  • LV hypertrophy
  • Aortic aneurysm
  • Arrhythmias
  • End organ damage
    * Kidneys, eyes
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10
Q

most antihypertensives work by

A
  1. Reducing cardiac output and/or (HR and contractility)
  2. Decreasing peripheral resistance (vascular tone)
    BP = CO X PVR
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11
Q

4 anitomical sites that control BP

A

1) arteries
2) veins
3) heart
4) kidneys
- all controlled by CNS (sympathetic nerves)

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12
Q

Cardiac output and peripheral vascular resistance are controlled by two overlapping control mechanism

A
  1. Baroreceptor reflexes

2. Renin-angiotensin-aldosterone system

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13
Q

Baroreceptors and the Sympathetic Nervous System

A

•Responsible for the rapid, moment to-moment
adjustments in blood pressure
•Located in the aortic arch and carotid sinuses

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14
Q

Renin-angiotensin-aldosterone System

A

• Baroreceptors respond to reduced arterial pressure by releasing renin
• Renin converts angiotensinogen -> angiotensin I
• Angiotensin I -> angiotensin II by Angiotensin-converting enzyme (ACE)
• Angiotensin II is a potent vasoconstrictor
• Angiotensin II decreases glomerular filtration and increases aldosterone secretion
• Aldosterone increases renal sodium and water reabsorption
-kidneys handle the long term control of BP by controlling the blood volume

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15
Q

More than likely to treat HTN

A

•Frequently more than one category of drug therapy is used to treat HTN to minimize side-effects (combination therapy)

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16
Q

Antihypertensive Drugs

A
  • Angiotensin II receptor blockers
  • Renin inhibitors
  • ACE inhibitors
  • Diuretics
  • β-blockers
  • Calcium channel blockers
  • α-blockers
  • Others
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17
Q

Current recommendations are to initiate

therapy with

A
  • Thiazide diuretic
  • ACE inhibitor
  • Angiotensin receptor blocker (ARB)
  • Calcium channel blocker
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18
Q

Diuretics

A
  • Lower BP by depleting the body of sodium and water, therefore, reducing blood volume
  • Safe
  • Inexpensive
  • Often the first-line drug of choice
  • Often used in combination therapy
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19
Q

how does Thiazide Diuretics work

A

•Inhibit the Na+/Cl cotransporter in the distal tubule
•Increase sodium and water excretion causing a decrease in extracellular volume
-decrease cardiac output => decreasing BP
-decrease in PVR

20
Q

Thiazide Diuretics

A
  • Useful in combination therapy with:
    * β-blockers, ACE inhibitors, ARBs, potassium sparing diuretics
  • Not effective in patients with inadequate kidney function because drug needs to be excreted in the tubular lumen where the transporter exists
  • Can induce hypokalemia, hyperuricemia, hyperglycemia
  • Not recommended during pregnancy
21
Q

How do Loop Diuretics work

A

•Inhibit the Na+/K+/2Cl- cotransporter in the ascending limb
•Blocks Na+, K+, and 2Cl reabsorption in the kidneys
•Cause decreased renal vascular resistance
•Cause increased renal blood flow
-increases excretion of Na, K, and Cl

22
Q

Loop Diuretics

A
  • Acts promptly
  • Works well in patients with poor renal function
  • Can cause hypokalemia
23
Q

Potassium-sparing Diuretics

A
  • Aldosterone receptor antagonist
    * Causes more sodium and water to pass into the collecting duct
  • Reduces potassium loss in the urine
  • Used in combination with loop and thiazide diuretics to reduce potassium loss
24
Q

β-blockers

A

•Block β1 and/or β2 receptors
•Decrease sympathetic outflow from CNS
•Decease CO
• HR and contractility
•Inhibit release of renin from kidneys -> decreases anigotensin II => decrease in PVR => decreased BP
-decrease in angiotensin II => decrease in adosterone => decrease in Na and water reabsorption => decreased CBV => decreased CO => decreased BP
-decrease in BP

25
Q

β-blockers Adverse Effects

A
  • Bradycardia
  • Hypotension
  • Fatigue
  • Insomnia
  • Sexual dysfunction
  • Altered lipid pane
    * Decrease HDL
    * Increase triglycerides
26
Q

β-blockers that can be given through IV

A

• Esmolol, metoprolol, and propranolol

27
Q

Stop using β-blockers?

A
  • Abrupt withdrawal may induce
  • Angina
  • MI
  • Death
  • Must be tapered over a few weeks
28
Q

how do ACE Inhibitors work

A
  • Block the angiotensin converting enzyme (ACE)
  • Prevents pulmonary and renal endothelium from converting angiotensin I into angiotensin II (potent vasoconstrictor)
  • Decrease angiotensin II levels in the blood
  • Vasodilation of arterioles and veins
  • Increase bradykinin levels
  • Reduce secretion of aldosterone
    * Resulting in decrease sodium and water retention
29
Q

angiotensin converting enzyme (ACE) and bradykinin

A
  • ACE is responsible for the breakdown of bradykinin
  • Bradykinin Increases production of nitric oxide and prostacyclin by blood vessels
    * Potent vasodilators
30
Q

ACE Inhibitors: Therapeutic Uses

A
  • Course of action in patients with diabetic nephropathy (diabetic kidney disease)
    * Slows progression
    * Decreases albuminuria
  • Standard of care following MI
31
Q

Chronic treatment of ACE Inhibitors achieves

A
  • Sustained blood pressure reduction
  • Regression of LV hypertrophy
  • Prevention of ventricular remodeling after MI
32
Q

ACE Inhibitors: Adverse Effects

A
  • Dry cough (number one cause of being taken off drug)
  • Rash
  • Fever
  • Altered taste
  • Hypotension
  • Hyperkalemia
  • Fetal malformations
33
Q

how do angiotensin II receptor blockers (ARBs) work

A
  • Block angiotensin II receptors
    * Decreasing activation by angiotensin II
  • Produce arteriolar and venous dilation
  • Block aldosterone secretion
    * Lowering BP and decreasing sodium and water retention
  • Does not increase bradykinin levels
34
Q

angiotensin II receptor blockers (ARBs) course of action in patients with

A
  • Diabetes Mellitus (DM)
  • Heart failure (HF)
  • Chronic kidney disease
35
Q

angiotensin II receptor blockers (ARBs) Adverse effects

A
  • Similar to ACE inhibitors
    * Less risk of cough
  • Should not be combined with ACE inhibitors
    * Similar mechanism and adverse effects
  • Teratogenic (Don’t take while pregnant)
36
Q

How do Renin Inhibitors work

A
  • Directly inhibits renin
    * Decreases sodium and water retention
  • As effective as ARBs, ACE inhibitors, and thiazides
  • Should not be combined with ACE inhibitor or ARB
  • Can cause diarrhea and cough
  • Contraindicated during pregnancy
37
Q

how do Calcium Channel Blockers work

A
  • Prevents inward movement of calcium into heart cells and smooth muscle of the coronary and peripheral arteriolar vasculature
  • Causes smooth muscle relaxation
  • Dilates mainly arterioles
  • Can be used as initial therapy or add-on therapy
38
Q

what do α1-blockers do

A
  • Selectively block the α1 -receptors in arterioles and venules
  • Decrease PVR and BP by causing relaxation of both arterial and venous smooth muscle
  • Cause reflex tachycardia and postural hypotension
  • Cause salt and water retention
    * Used with diuretic
  • Not used as initial treatment for HTN
39
Q

α/β-blockers

A

•Labetalol and carvedilol
•Block α1, β1, and β2
receptors
• PVR and BP (block α1)
•Carvedilol is mainly used to treat heart failure
•Labetalol used to treat gestational hypertension

40
Q

Clonidine (CATAPRESS)

A
  • α2 agonist
  • Decreases sympathetic outflow from CNS
    * PVR and BP
  • Causes relaxation of venules
41
Q

Clonidine: Side Effects

A
  • Dry mouth
  • Sedation
  • Constipation
  • Rebound HTN following abrupt withdrawal
42
Q

Methyldopa (ALDOMET)

A
  • α2 agonist
  • Similar to clonidine
  • Decreases sympathetic outflow from CNS
  • Used to treat HTN during pregnancy
43
Q

how does hydralazine work

A
  • Causes reflex stimulation of heart
    * Increased contractility, HR, and oxygen consumption
    * Causes angina, MI, or heart failure
  • Increases renin causing sodium and water retention
  • Used in conjunction with a β-blocker and diuretic to reduce side effects
  • Can be used during pregnancy
  • Can cause lupus-like syndrome at high doses
44
Q

Minoxidil: Side Effects (vasodilator)

A
  • Severe tachycardia
    * Dose-dependent
  • Palpitations
  • Angina
  • Headache
  • Sweating
  • Hypertrichosis
    * Excessive hair growth
  • Co-administered with β-blocker and diuretic
45
Q

Nitroprusside: Side Effects

A
  • Accumulation of cyanide (cyanide poisoning)
    * Use is limited to 3 days or less
  • Arrhythmias
  • Excessive hypotension
46
Q

Treatment of HTN on Pump

A
  • Flow
  • Anesthetic depth
  • Drugs

Pharm I (15 decks)

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