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PHARMACOLOGY > Hypertension and Anti-hypertensive Agents > Flashcards

Hypertension and Anti-hypertensive Agents Flashcards

1
Q

what is hypertension

A

high blood pressure
>140 systolic
>90 diastolic

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2
Q

what is arterial blood pressure

A
  1. proportional to the product of cardiac output (CO) + total peripheral resistance (TPR)
    - CO: product of heart rate and efficiency
    - TPR: elastic resistance of vessels + degree of vascular sm contraction
  2. blood pressure can be reduced by:
    - reducing CO
    - total blood volume
    - increasing blood vessel diameter
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3
Q

effects of sympathetic and parasympathetic activity on cardiac tissue

A
  1. heart rate:
    - increased by symp NS
    - decreased by para NS = dominant
  2. contractile force:
    - increased by symp NS = dominant
    - decreased by para NS
  3. symp NS increases contraction of vascular sm
  4. symp NS increases renin release from kidneys
    = sodium + water retention
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4
Q

what are short term changes in blood pressure carried out by

A

baroreceptor reflex

stretch sensitive receptors imbedded in walls of carotid sinus/aortic arch => info about state of arterial contraction/relaxation -> delivered to medulla by afferent neurons

medulla send out stimulatory signals to activate symp/para NS => changes in HR/BP

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5
Q

how to baroreceptors respond to increased BP

A

baroreceptors activity increases
sympathetic activity decreases
parasympathetic activity increases

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6
Q

how to baroreceptors respond to decreased BP

A

baroreceptors activity decreases
sympathetic activity increases
parasympathetic activity decreases

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7
Q

what are other BP regulators

A
  1. angiotensin II
  2. vasopressin
  3. prostaglandins
  4. endothelins
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8
Q

angiotensin II

A

increases sympathetic response
decreases parasympathetic response
increases H20 retention
acts directly on vascular sm = vasoconstriction

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9
Q

vasopressin

A

antidiuretic hormone

increases water retention

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10
Q

prostaglandins

A

vasoconstrictive/dilative eicosanoids

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11
Q

endothelins

A

vasoconstrictive/dilative

paracrine: made in endothelial cells - act on vascular sm

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12
Q

renin-angiotensin system

A
  1. renin is secreted by granular cells ling kidney arterioles in response to:
    - Na+ loss
    - decreased BP
    - sympathetic activity on kidneys
    - B agonists
    - PGI2
  2. renin converts angiotensinogen > angiotensin I
  3. angiotensin-converting enzyme (ACE) converts
    angiotensin I > angiotensin II
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13
Q

functions of angiotensin II

A
  1. increases vasopressin = fluid retention from kidney
  2. stimulates thirst
  3. potent vasoconstrictor
  4. acts on CNS - stimulate increased sympathetic outflow (NE)
  5. promotes Na+ retention by increasing aldosterone secretion

= INCREASE BLOOD PRESSURE

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14
Q

primary hypertension

A

due to dysfunction of blood pressure regulation mechanisms

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15
Q

secondary hypertension

A

due to diseases that inhibit the flexibility of peripheral blood vessels (diabetes, atherosclerosis) //
affect coronary output (coronary artery disease/congestive heart failure)

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16
Q

diseases aggravated by high BP

A 
atherosclerosis
congestive heart failure
stroke
renal disease
retinal detachment
Alzheimer's
17
Q

nonpharmacological treatment of high BP

A 
weight reduction
exercise
quit smoking
reduce alcohol 
reduce sodium intake
reduce saturated fat intake
relaxation techniques
18
Q

drugs used to treat hypertension

A
  1. diuretics (increase urine)
  2. B-blockers (decrease BP/HR/E)
  3. a1 antagonists
  4. a2 partial agonists
  5. calcium channel blockers
  6. potassium channel activators
  7. ACE inhibitors
  8. angiotensin receptor antagonists
19
Q

what is the site of diuretic drug action

A

nephron

20
Q

symport

A

coupled transport of 2 or more substance across a membrane in same direction

21
Q

antiport

A

2 or more substances exchanged in opposite directions

22
Q

loop diuretics

A

inhibit Na+/K+/2Cl- symport by blocking reabsorption of Na+/K+/2Cl-
= flow of water blood to the lumen of Loop of Henle

used to treat hypertension associated with acute pulmonary edema and congestive heart disease

side effects: K+ and Mg2+ loss, uric acid retention

23
Q

thiazide diuretics

A

inhibit Na+Cl- symport in endothelial cells that line distal convoluted tubule

  • same effect as loop diuretics = LESS POTENT
    (less absorption of compounds in DCT - treat less severe hypertension)

side effects: K+ and Mg2+ loss, uric acid retention, hyperglycemia, erectile dysfunction

24
Q

what does K+ loss lead to

A

cardiac arrhythmias - block repolarisation phase of cardiac contraction

25
Q

interactions of diuretics with other drugs

A

diuretics cause decreased lithium excretion via kidneys

diuretics increase risk of cardiac glycoside-induced arrhythmias (digoxin)

diuretics = less effective when taken with NSAIDs (aspirin)

26
Q

B-blockers

A

reduction in cardiac output = competitive antagonism of B1 adrenergic receptors
reduction in renin release from kidneys
act on CNS - reduce sympathetic outflow

PROPANOLOL (nonspecific - acts on B1/2 = block relaxation)

Side effects: can worsen asthma/cause heart failure with congestive heart disease patients

27
Q

a1 antagonists

A

block vasoconstrictive actions of a1 receptors in vascular sm

DOXAZOSIN

Side effects: first dose effect hypotension /impotence

28
Q

a2 agonists

A

bind to a2 inhibitory autoreceptors in sympathetic neurons and medulla

CLONIDINE

Side effects: orthostatic hypotension, rebound hypertension

29
Q

calcium channel blockers

A

block L-type Ca2+ channels in arterial sm = preventing vasoconstirction

VERAPAMIL

Side effects: cardiodepression/AV node block
potential for many drug-drug interactions - ability to block p-glycoprotein efflux pump

30
Q

potassium channel activator

A

sm relaxation = open K+ ATP channels in vascular sm,
hyperpolarisation
inhibits calcium entry
stimulates renin release

MINOXIDIL = decrease BP

Side effects:
stimulates hair growth
cause fluid retention (coadministered with a loop diuretic)
reflex tachycardia

31
Q

ACE inhibitors

A

bind to active site of ACE
reversible inhibition of angiotensin II converting enzyme
best in patients with high levels of renin

CAPTOPRIL

Side effects: persistent cough, angioedema, teratogenic

toxic drug interactions: increased risk of sudden death when combined with cotrimoxazole = hyperkalemia (K+ loss)

32
Q

angiotensin II receptors antagonists

A

blocks binding of angiotensin II to AT1 angiotensin receptors (competitive)

LOSARTAN

Side effects: hypotension, headaches, GI upset - no cough = stronger than ACE inhibitors

33
Q

why are most anti-hypertensive drugs used in combination with other bp lowering drugs

A

reduces dose needed to achieve desired BP
allower lower value to be reach as opposed to single drug
side effects reduced
typical combination: diuretic + antihypertensive

34
Q

pulmonary hypertension

A

elevated BP in pulmonary arteries (lungs 02 -> heart )

: pulmonary embolism, COPD, sleep apnea, heart defects, sickle cell anemia, cirrhosis of liver, AIDS

treatment: diuretics, cardiac glycosides calcium channel blockers

EPOPROSTENOL, AMBRISENTAN, SILDENAFIL

35
Q

EPROPROSTENOL

A

prostacyclin: synthetic PGI2

binds to IP receptor = lowers cAMP formation + PKA activation
PKA phosphorylates myosin light chain kinase

= inhibits sm contraction => vasodilation
lowers cytoplasmic Ca2+
blocks release of ET-1

36
Q

AMBRISENTAN

A

competitive antagonist of endothelin- ET-1a/b receptors
main target: ET-1a R in sm = vasocontriction visa IP3=mediated Ca2+ release

= teratogens

37
Q

SILDENAFIL

A

phosphodiesterase V inhibitor
phosphodiesterase V converts cGMP > GMP
cGMP + NO activate a K+ channel in vascular sm

38
Q

peripheral vascular disease

A

caused by atherosclerotic plaques

treatment:

antiplatelet drugs: ASPIRIN / CLOPIDOGREL

cholesterol-lowering drugs: STATINS

ACE inhibitors: CAPTOPRIL

PHARMACOLOGY (24 decks)

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