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37 Cards in this Set

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Determinants of BP
Diameter of Arterioles
Heart Rate (B1 Adrenergic Receptors)
Force of Ventricular Contraction (B1 Adrenergic Receptors)
Blood Volume (Renin-Angiotensin System)
Baroreceptors
Detect stretch in carotid sinus-->relay info to vasomotor center
Renin-Angiotensin System
Drop in BP detected by baroreceptors, renin is released from juxtaglomerular cells-->convert Agtensin to Agtensin I. Agtensin I converted to Agtensin II in lungs. Agtensin II directs vasoconstriction & aldosterone synthesis in adrenal cortex
Antihypertensive Agents
Diuretics
Direct Vasodilators
Sympatholytic Agents
Angiotensin Related Agents
Combo Therapy (Most Common)
Diuretics
Increase in the volume of the urine
Increase in renal sodium excretion
Mechanism of action: Thiazides
Inhibit sodium reabsorption at distal tubule
Mechanism of action: High Efficacy Loop Diuretics
Work at Loop of Henle
Inhibit sodium reabsorption from Loop of Henle
Increased Na+ in collecting duct results in increased K+ eliminated -->hypokalemia
Mechanism of action: Potassium Sparing Agents
Work at Collecting Duct
Promotes increase in K+ reabsorption -->potassium sparing
Spironolactone
Potassium Sparing Drug
Reduced expression of the basolateral Na+/K+ ATPase
Triamterine
Potassium Sparing Drug
Blockers of Na+ channels on the apical membrane-->prevents reabsorption of Na+ and excretion of K+
Determinants of BP
Diameter of Arterioles
Heart Rate (B1 Adrenergic Receptors)
Force of Ventricular Contraction (B1 Adrenergic Receptors)
Blood Volume (Renin-Angiotensin System)
Baroreceptors
Detect stretch in carotid sinus-->relay info to vasomotor center
Renin-Angiotensin System
Drop in BP detected by baroreceptors, renin is released from juxtaglomerular cells-->convert Agtensin to Agtensin I. Agtensin I converted to Agtensin II in lungs. Agtensin II directs vasoconstriction & aldosterone synthesis in adrenal cortex
Antihypertensive Agents
Diuretics
Direct Vasodilators
Sympatholytic Agents
Angiotensin Related Agents
Combo Therapy (Most Common)
Diuretics
Increase in the volume of the urine
Increase in renal sodium excretion
Mechanism of action: Thiazides
Inhibit sodium reabsorption at distal tubule
Mechanism of action: High Efficacy Loop Diuretics
Work at Loop of Henle
Inhibit sodium reabsorption from Loop of Henle
Increased Na+ in collecting duct results in increased K+ eliminated -->hypokalemia
Mechanism of action: Potassium Sparing Agents
Work at Collecting Duct
Promotes increase in K+ reabsorption -->potassium sparing
Spironolactone
Potassium Sparing Drug
Reduced expression of the basolateral Na+/K+ ATPase
Triamterine
Potassium Sparing Drug
Blockers of Na+ channels on the apical membrane-->prevents reabsorption of Na+ and excretion of K+
Direct Acting Sympatholytic Agents
Receptor Antagonists
Beta-Blockers
A1 Adrenergic Recepor Antagonists
Indirect Acting Sympatholytic Agents
Interfere with sympathetic neurotransmission
CNS-Acting (Clonidine)
Catecholamine Release Inhibitors (Reserpine)
A1 Adrenergic Receptor Antagonist
Direct Acting Sympatholytic Agent
Vasodilation-->decrease in BP
B1 Adrenergic Receptor Antagonist
Direct Acting Sympatholytic Agent
Descrease contractility in heart-->decrease in BP
Indirect Sympatholytic Agent
Reserpine - Inhibits release of catecholamines from sympathetic nerves
CNS Acting Sympatholytic Agents
Clonidine
Tricks A2 receptors into thinking there are high enough levels of catecholamines around-->inhibits production of more
Sympatholytic Vasodilators
Block sympathetic NS induced constriction of arterial smooth muscle
-A1 adrenergic receptor antagonists
Direct Vasodilators
Directly dilate arterial smooth muscle without inhibiting sympathetic NS
Oral Hypertension Drug
Hydralazine - Opens potassium channels
Calcium Channel Blockers - Block voltage dependent Ca+ channels on vascular smooth muscle
Minoxidil - Reserved for severe hypertension
Parenteral Drug Vasodilators
Used for emergency hypertensive situations
-Too efficacious for outpatient use & too many side effects
Side Effects of Vasodilators
Postural Hypotension
Flushing, Sweating
Headache
-Reflex Responses
Reflex Tachycardia (rational for co-administration with beta blockers)
Reflex Fluid Retention( rational for co-administration with diuretic)
VASODILATORS ARE GENERALLY GIVEN WITH A BETA BLOCKER/DIURETIC TO PREVENT REFLEX RESPONSES
Indirect effects of vasodilators
Reflex increase in HR, Reflex increase in Na+ reabsorption-->increased blood volume/edema
ACE Inhibitors
Angiotensin Converting Enzyme Inhibitors
-Inhibits conversion of Agtensin to Agtensin II-->results in reduced BP
CAPTOPRIL
*all ACE inhibitors end in '-pril'
Mechanism of action for Angiontensin Receptor Antagonists
Inhibits binding of Agtensin II to its receptor-->results in reduced BP
Side Effects of ACE Inhibitors
Dry cough (accumulation of bradykinin)
Change in taste
Edema
Hyperkalemia
Angiotensin Receptor Blockers (ARBs)
Comeptitive Antagonists at AT1 angiotensin receptors
Selective: no effects on bradykinin metabolism (no dry cough)
Complete: blockade of all angiotensin II effects
LOSARTAN
*all ARBs end in '-artan'
First Choice Drugs
Most people: Thiazide Diuretics
Diabetics: ACE Inhibitors
CHD: Beta Blockers