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GS Pharmacology > Antihypertensives > Flashcards

Antihypertensives Flashcards

1
Q

Secondary hypertension

A

disorder in which a known primary pathology can directly or indirectly result in hypertension

possible pathologies:

  • aldosteronism
  • pheocromocytoma
  • glomerulonephritis
  • toxemia of pregnancy
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2
Q

Aldosteronism

A

“tumor of the adrenal cortex” that causes the body to make too much aldosterone, which regulates sodium and potassium

causes high bp thru sodium retention which causes water retention and thus increases blood volume increases the bp

also causes loss of potassium, can lead to hypokalemia

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3
Q

Pheocromocytoma

A

“tumor of the adrenal medulla”

  • very rare
  • causes high bp & high heart rate
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4
Q

Glomerulonephritis

A

inflammation of glomeruli of kidneys

  • can be primary or secondary
  • normal glomeruli filter electrolytes and fluid from blood into urine
  • thus high bp is cause by positive feedback loop of electrolyte and fluid retention, increasing the blood volume
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5
Q

Toxemia of Pregnancy

A
  • increased blood pressure due to fluid retention of pregnancy
  • can lead to pre-eclampsia then eclampsia
  • other symptoms are proteinuria and hyperreflexia
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6
Q

Idiopathic Hypertension

A

primary hypertension

  • hypertension with no other known primary pathology
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7
Q

Hypertension Guidelines

A
  • Normal
    • SBP<120
    • DBP<80
  • Prehypertension
    • SBP: 120-139
    • DBP: 80-89
  • Hypertension stage 1
    • SBP: 140-159
    • DBP: 90-99
  • Hypertension stage 2
    • SBP >160
    • DBP >100
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8
Q

Classes of Antihypertensives (6)

A
  1. Diuretics
  2. Alter Sympathetic Nervous System
    1. Beta-blockers
    2. Alpha-blockers
    3. Central sympatholytics
  3. Vasodialators
  4. Angiotensin II inhibitors
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9
Q

Mean Arterial BP

A

= cariac output x total peripheral resistence

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10
Q

Cardiac Output

A

= Stroke volume x heart volume

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11
Q

Stoke volume

A

function of contractile strength of heart muscle

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12
Q

Sympathetic BP Reflexes

A

If BP goes down:

  • increase resisteance
  • increase heart rate
  • reabsorb salt and water
  • plasma renin is stimulated to reabsorb salt and water
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13
Q

Diuretics

A

decreases extracellular volume-> reduced vascular resistance-> initial decrease of cardiac output then return to normal

  • thiazides
  • potassium sparing diuretic
    • amiloride
    • spironolactone
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14
Q

Thiazides

A
  • effective long term monotherapy or in con junction w/ drug from another class
  • if alone, potassium sparing diuretic should be considered
  • doses: 12.mg-25mg/day
  • good for:
    • elderly with low renin levels and no signs of renal insufficiency
  • bad for:
    • diabetics
    • patients w/ left ventricular hypertrophy
  • Toxicity/ adverse effects:
    • hypokalemia (low K+)
    • hyperlipoproteinemia (high cholesterol)
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15
Q

Beta-blockers

A
  • blocks beta receptors
  • blocking of beta 1 receptors leads to vasodilation
  • blocking of beta 2 receptors inhibits vasodilation
    • beta 2 receptors are found in peripherial vessels and brochi of lungs
  • also antagonizes renin release from kidneys caused by sympathetic nervous system
  • does not cause hypotension in patients with normal blood pressure
  • can be SELECTIVE
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16
Q

Propranolol

A
  • non-selective beta-blocker
  • initially causes slower heart rate, cardiac output, and increased peripherial cascular resistance
  • peripheral vascular resitance returns to normal or lower than pretreatment levels
  • inihibits renin release by catecholamines
  • high lipid solubility -> can cross blood brain barrier
  • Good:
    • low incidence of GI disturbances
    • doesn’t cause postural hypotension, reflex tachycardia, or salt or water retention
    • post MI patients
    • young (<50) patient who also have rapid heart rate
    • for those with mild hypertension & high plasma renin
  • Bad:
    • less effective than diurectic if used alone
    • can increase triglycerides & HDLs
    • can cause bradycardia
    • diabetics
    • because of beta 2 blockage-> very bad for asthma & PVD (peripherial vascular disease) patients
17
Q

Metropolol & Atenolol

A
  • aka Lopressor & Tenormin
  • beta 1 receptor selective
    • beta 2 is blocked but to much lesser extent as in propranolol
  • Good:
    • patients w/ asthma, diabetes, & PVD
18
Q

Nadolol & Carteolol

A
  • aka Corgard & Catrol
  • non-selective beta-blockers
  • very long half-life-> can be given once daily
19
Q

Pindolol, Acebutolol, & Penbutolol

A
  • aka Visken, Sectral, & Levatol
  • beta-blockers w/ intrinsic sympathomimetic activity
  • Good:
    • lowers blood pressure by decreasing peripherial vascular resistance
    • doesn’t increase serum triglycerides or HDLs
    • patients w/ cardiac failure or PVD
  • Bad:
    • depresses cardiac output and heart rate less than other beta-blockers
20
Q

alpha adrenoreceptor blockers

A
  1. Names: Prazosin (Minipress)- alpha 1 specific
  2. Uses: HTN, especially those with high cholesterol & prostatism
  3. Mechanism: reduces arterial pressure by dilating resistance & capacitance vessels
  4. Contraindications: nm
  5. Adeverse Effects:
    • positional hypotension with first dose
    • salt & h2o retention
    • causes positive test for antinuclear factor in blood serum
  6. Other:
    • pressure reduced more in upright than supine position
    • more effective with diuretic and/or beta blocker
      *
21
Q

alpha-methyldopa

A
  1. Other name/class: Aldomet/ central acting sympatholytics
  2. Uses: HTN wioth pre-eclampsia or moderate HTN in combo w/ diuretic
  3. Mechanism:
    • activation of alpha 2 receptors
    • reduces release of presynaptic norepi
    • decreases peripheral resistance w/o affecting hr or cardiac output
  4. Contraindications: nm
  5. Adverse Effects:
    • sedation
    • mental lassitude
    • impaired mental concentration
  6. Other: half-life of 2hr, but max effect can last up to 24 hrs
22
Q

Clonidine

A
  1. Other name/class: Catapres/ central acting sympatholytic
  2. Uses: HTN w/ thiazide diuretic
  3. Mechanism:
    • activation of alpha 2 receptors
    • decreases sympathetic tone
    • increases parasympathetic tone
    • decreases heart rate & relaxes capacitance vessels
    • decreases cardiac ouput
  4. Contraindications: nm
  5. Adverse Effects:
    • dry mouth
    • sedation
    • withdrawl can cause life threatening HTN event
  6. Other:
    • tricyclic antidepressants may block antiHTN effect
    • reduces supine bp more, but rarely causes positional hypotension
    • half-life of 8-12hrs
      *
23
Q

Hydralazine

A
  1. Other name/class: apresoline/ vasodilator
  2. Uses: HTN
  3. Mechanism:
    • unclear, maybe NO release from endothelium &/or hyperpolarization of smooth muscle
    • direct relaxation of arteriolar smooth muscle
  4. Contraindications:
  5. Adverse Effects:
    • positional hypotension
  6. Other:

GS Pharmacology (4 decks)

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