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Pharmacology > Hypertension(Katzung) 1st part lang > Flashcards

Hypertension(Katzung) 1st part lang Flashcards

1
Q

Bp of 120-135/80-89

A

Prehypertension

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2
Q

Bp of >140/90

A

Hypertension

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3
Q

140-159/90-99

A

Stage 1

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4
Q

> 160/100

A

Stage 2

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5
Q

Starting at what bp pressure does cardiovascular disease risk doubles with each increment of 20/10 mmhg

A

115/75

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6
Q

Patients in whom no specific cause of hypertension can be found

A

Essential/ primary hypertension

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7
Q

Causes o lf hypertension that are amendable to surgical treatment

A 
Renal artery constriction
Coarction of aorta
Pheochromocytoma
Cushing's
Primary aldosteronism
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8
Q

Functional variations of the genes of these proteins can cause essential hypertension

A

Angiotensinogen
ACE
B2 adrenoreceptor
A adducin

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9
Q

Formula for BP

A

BP=CO*PVR

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10
Q

Anotomic sites for control of BP

A

Resistance arterioles
Capacitance venules
Pump output of the heart
Kidney volume

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11
Q

Responsible for rapid moment to moment adjustments in bp

A

Baroreflexes

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12
Q

Sympathetic activation of batoreceptor reflex acts through

A

Arterioles
Heart
Capacitance vessels

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13
Q

Decresed pressure in the renal arterioles and decreased sympathetic neural activity through via b adrenoreceptors causes the kidney to release….

A

Renin

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14
Q

Causes direct constriction of resistance vessels. Stimulation of aldosterone synthesis in the adrenal cortex which causes increase renal sodium absorption and intravascular volume

A

Angiotensin 2

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15
Q

Released from the posterion pituitary gland which regulates water reabsorption by the kidneys

A

Vasopressin

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16
Q

Reduces peripheral vascular resistance. Inhibits cardiac function and increases venous pooling.

A

Sympathoplegic agents

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17
Q

Maximal lowering of bp of less than 10 mmhg bust is useful in the long term reduction of renal disease in diabetic persons and reduction of heart failure

A

ACE inhibitors

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18
Q

Reduce mortality after MI and particularly indicated in patients with an infarct and hypertension

A

B blockers

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19
Q

Contribute to vascular resistance by increasing vessel stiffness and neural activity

A

Sodium

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20
Q

Effective in lowering bp by 10-15 mmhg and adequate for treatment of mild to moderate hypertension. In severe hypertension, theses drugs are used in combination with sympathoplegic and vasodilator drugs to control tendency towards Na retention

A

Diuretics

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21
Q

Diminished by sympathoplegic and vasodilator drugs thus vasculature behaves like a inflexible tube

A

Vascular responsiveness

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22
Q

Necessary for severe hypertension when multiple drugs with Na retaining properties are used; renal insufficiency when gfr is less than 30-40 ml/ minute; and cardiac failure and cirrosis in which Na retention is marked

A

Furosemide ir other powerful diuretics(acts at the loop of henle)

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23
Q

Most common adverse effect of diuretics(except for K sparing diuretics)

A

K depletion

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24
Q

Hazardous in patients taking digitalis, in those with chronic arrhythmias and in those with MI or left ventricular dysfunction

A

Hypokalemia

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25
Q

Causes magnesium depletion, impair glucose tolerance and increase serum lipid concentrations. Also increase uric acid concentration and may precipitate gout

26
Q

A steroid associated with gynecomastia

A

Spironolactone

27
Q

May produce hyperkalemia in patients with renal insufficiency and those taking ACE inhibitors, angiotensin receptor blockers and spironolactone.

A

K sparing diuretics

28
Q

May cause sedation, mental depression, distirbance in sleep and nightmares

A

Sympathoplegic drugs that act on CNS

29
Q

Causes effects similar to those of surgical sympathectomy including inhibition of ejaculation and hypotension that is increased by upright posture and after exercise

A

Sympatheplegic drugs that reduce release of epinephrine

30
Q

Effective in lowering bp in patients resistant to antihypertensive drugs

A

Renal sympathetic denervation

31
Q

Sympathoplegic agents are most effective in patients when used with these drugs

32
Q

With the exception of clonidine, these drugs are rarely used today

A

Centrally acting sympathoplegic drugs

33
Q

Antihypertensive action is modulated by stimulation of central a-adrenoreceptors.

A

Methyldopa(a-methlynorepinephrine, and a-methyldopamine)

34
Q

Antihypertensive action was discovered when it was tested as a nasal decongestant

35
Q

Hypotensive effect is excerted at the a-adrenoreceptors of the medulla. Reduces sympathetic and increases parasympathetic tone producing low bp and bradycardia. It also decreases circulating catecholamine levels.

36
Q

Binds to nonadrenoreceptor site imidazoline which also mediate antihypertensive effects

37
Q

Reduce norepinephrine release and may act on postsynaptic a2 adrenoreceptors to inhibit activity of appropriate neurons

A

Clonidine and methyldopa

38
Q

Primarily used for hypertension during pregnancy. Reduce bp chiefly by reducing vascular resistance with variable reduction in hr and cardiac output. One potential advantage of this drug is reduction in vascular resitance

A

Methyldopa

39
Q

Enters the brain via aromatic amino acid transporter and effects can persist for 24 hours

A

Methyldopa

40
Q

Most common side effect of methyldopa particularly at the onset of therapy

41
Q

Long term therapy causes mental lassitude and impaired mental concentration

A

Methyldopa

42
Q

Use of this drig can cause lactation both in men and women due to increased prolactin levels

A

Methyldopa

43
Q

Can develop a positive Coombs test and is rarely associated with hemolytic anemia, hepatitis and drug fever.

A

Methyldopa

44
Q

Bp lowering effects of clonidine are due to

A

Reduction of cardiac output due to decreased hr.
Relaxation of capacitance vessels.
Reduction of peripheral vascular resistance

45
Q

Reduces bp in the supine position and only rarely causes postural hypotension

A

Methyldopa and clonidine

46
Q

Severe hypertension can complicate a massive oversdose

47
Q

Lipid soluble and rapidly enters the brain from the circulation. Anti hypertensive effect is related to blood concentration and must be given twice a day. Increasing the dose of this drug is more effective but also more toxic. A transdermal prep is available

48
Q

Common side effects od clonidine therapy

A

Sedation and dry mouth

49
Q

Not given in patients who are at risk for mental depression. Concominant administration with tricyclic may block effects of this drug.

50
Q

Withdrawal use of this drug can cause life threatening hypertensive crisis mediated by increased sympathetic nervous activity.

51
Q

Treatment for hypertensive crisis cause by clonidine withdrawal

A

Reinstitution of clonidine

A and B adrenoreceptor blocking agents

52
Q

Can produce profound sympathoplegia and pharmacologic sympathectomy including marked postural hypotension, diarrhea, impaired ejaculation. It is also too polar to enter the CNS

A

Guanethidine

53
Q

Replaces norepinephrine at nerve endings. Drugs that block catecholamine uptake including cocaine, amphetamine, tricyclic antidepressants, phenothiazines and phenoxybenzamine block its effects.

A

Guanethidine

54
Q

Halflife of 5 days

A

Guanethidine

55
Q

Can produce hypertension in patients taking guanethidine

A

Sympathomimetic agents

56
Q

Can produce hypertensive crisis by releasing catecholamines in patients with pheochromocytoma

A

Guanethidine

57
Q

Attenuates antihypertensive effect of guanethidine and can cause severe hypertension.

A

Tricyclic antidepressants

58
Q

Interferes with vesicular membrane associated transporter(VMAT) resulting in depletion of norepinephrine, dopamine, and serotonin in both PNS and CNS. Chromafgin granules of the adrenal medulla are also depleted by the use of this drug.

59
Q

Readily enters the brain and depletion of cerebral amines causes sedation, mental depression, and parkonsinism symptoms

60
Q

Effects of reserpine for treatment of mild hypertension

A

Decreased CO and PVR

61
Q

Most of the unwanted effects of reserpine result from the actions of what body parts

A

GI and Brain

Pharmacology (7 decks)

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