N368 test 2 drugs for lipid disorders and HTN Flashcards
dyslipidemia
in presynaptic nerve terminal from choline andacetyl coenzyme A
pannel for lipid disorder
total cholesterol, triglyceride, HDL, LDL
Therapeutic Prevention of CVD
start pharmacotherapy for lipid control and lifestyle medication
three different lipids
triglycerides = 90% of fat in body 3 fatty acids + 1 glycerol, phospholipids = essential in building the bilayer phospholipid membrane, and steroids = hormones, cholesterol
cholesterol important for
Vitamin D production, Bile acids, cortisol, estrogen, testosterone.
Lipoproteins
carriers of lipid of molecules
HDL
High Density Lipoprotein
LDL
Low Density Lipoprotein - carriers cholesterol; transfers cholesterol from liver to tissues and organs; known as bad cholesterol because too much can accumulate in the vessels causing atherosclerosis. Lowering LDL can decrease risk for CVD
VLDL
Very Low Density Lipoprotein: is a major carrier for triglycerides = so if high you can say high triglycerides
HDL
Opposite to LDL; good cholesterol; assists in transportation of cholesterol away from body tissues and back to liver; good cholesterol.
lifestyle changes for lipid disorder
monitor blood-lipid levels; maintain weight, exercise; reduce dietary saturated fat and cholesterol; incr soluble fiber diet, reduce or cease tobacco and alcohol
pharmacotherapies for lipid disorders
statins - try to inhibit the prod of cholesterol
Bile-acid-binding resins - try to use up cholesterol to form bile which is excreted.
fibric acid derivatives
Nicotinic acid
cholesterol absorption
major side effect of statins
muscle or joint pain; must monitor liver enzymes every 6 months
bile-acid resin
bind with bile-acids in small intestines
*prototype drug cholestyramine
bile-acid resin major adverse effect
GI tract, gas,
nicotinic acid
decrease adipose tissue lipolysis which in turn reduces circulating free fatty acids; resulting reduction in VLDL and increase HDL
fibric-acid agents
mechanism unknown
prototype gemfibrozil
tx: severe hypertriglyceridemia
fibric-acid agents adverse effects
GI distress, watch for bleeding with clients on anticoagulants
Do not use with Bile acid binding resins, which interrupt the absorption of this lipid disorder controlling drug
Cholesterol Absorption Inhibitor
Adverse effects of nicotinic acid
_Adverse effects: cutaneous flushing with pruritis, hot flushes, nausea, excess gas, liver toxicity
Prototype drug for nicotinic acid
Prototype drug: niacin
Mechanism of action of nicotinic acid and primary use
_Mechanism of action: to decrease VLDL levels
Primary use: to reduce triglycerides; increase HDL levels
Prehypertension requires what therapy
lifestyle modifications: diet, exercise, stop smoking, reduce cholesterol, lower sodium intake
hypertension stage 1 requires what therapy
anti-HTN mediction: thiazide diuretic
HTN stage 2 requires what therapy
two ant-HTN drugs
secondary HTN
chronic renal disease, cushing’s syndrome, clampsia (r/t pregnancy) - siezures, strokes, or blinding may result if not treated; drug use can cause HTN too.
essential HTN
SNS hyperactivity
Renin-Angiotensin System hyperactivity
Increase cellular sodium/calcium level
untreated HTN can lead to?
CVD, hemorrhagic stroke, kidney failures, visual impairment because high vascular pressure behind eye
mechanisms controlling blood pressure
blood volumes (ADH & Aldosterone), peripheral resistance from diameter of arterioles (sns activity, RAS, increase in blood viscosity), cardiac output (stroke volume, HR)
Cholesterol Absorption Inhibitor prototype drug
ezetimibe (Vytorin)
primary use of cholesterol absorption inhibitors
modest reduction in LDL (20%)
adverse effects of cholesterol absorption inhibitor
no significant adverse effects
fibrinic-acid agents mechanism
_Mechanism of action: unknown
polycythemia
too many RBCs; continual production of RBCs
prototype for Bile-Acid Resins
Prototype drug: cholestyramine (Questran)
mechanism for Bile-Acid Resins
Mechanism: bind with bile acids (containing cholesterol) in small intestine, forming insoluble complexes that are excreted in feces.
Cardiac Output formula
Stroke Volume x Heart Rate
Primary use of Statins
Primary use: Reduces serum-lipid levels (esp. decrease in cholesterol level)
Statin mechanism of action
Mechanism of action: inhibits HMG-CoA reductase _ inhibit synthesis of cholesterol
Prototype Drug for Statins
Prototype drug: atorvastatin (Lipitor)
Major Adverse effect of Nicotinic Acid = Niacin
_Adverse effects: cutaneous flushing with pruritis
Beta 1 agonists do what to HR
increase heart rate
how many SNS receptors for NE
alpha 1 - arterioles = vasoconstriction - TX = shock
alpha 2 - arterioles = vasodilation - TX = HTN
Beta 1 - Heart = Increase HR - TX cardiac arrest
Beta 2 - Bronchi = bronchodilation - TX = asthma
Greater resistance in the arteries yields higher?
BP
brain center for regulating BP
medulla oblongata
Baroreceptors and Chemoreceptors in carotid arteries
baroreceptors = pressure chemoreceptors = levels of O2 and CO2 or pH
ADH does what to BP
BP by raising systemic blood volumes
Aldosterone does what to BP
increases the reabsorption of water and sodium and therefore increases bp
Epinephrine and norepinephrine do what to BP
increase BP
Non-pharmacologic Management of BP
_Losing weight
_Limiting foods high in fat and sodium
_Limiting use of tobacco and alcohol
_Beginning an exercise program
Pharmacotherapy of HTN:
Primary Antihypertensive Agents
_Diuretics _Angiotensin-converting enzyme (ACE) inhibitors _Angiotensin II receptor blockers (ARB) _Beta-adrenergic antagonists (BB) _Calcium channel blockers (CCB)
Secondary Antihypertensive
Agents
_Alpha1-adrenergic antagonist
_Alpha2-adrenergic agonists
_Direct-acting vasodilators
Beta Blocker
reduce HR and contractility therefore lower cardiac output and BP goes down
ACE inhibitor
blocking angiotensin II which is a vasoconstrictor, so reduces blood pressure, and block aldosterone which can result in HYPOKYLEMIA - so must monitor for this.
Angiotensin Receptor Blockers
prevent angiotensin II from reaching its receptors, causing vasodilation.
Calcium Channel Blockers
Block Calcium ion channels in arterials, smooth muscles causing vasodilation
alpha 1 blocker
inhibit sympathetic activation in arterioles; can result in orthostatic hypotension as adverse effect
alpha 2 agonist
directly causes vasodilation
Primary HTN: Diuretics
Mechanism of Action: by increasing urine output & decrease fluid volume
Thiazide Diuretics
Chlorothiazide (Diuril) and hydrochlorothiazide (HydroDiuril).
primary HTN: Diuretics loop diuretics
_Loop diuretics
_Bumetanide (Bumex)
_Furosemide (Lasix)*
can cause HYPOKYLEMIA
primary diurectics: potassium-sparing
_Potassium-sparing diuretics
_Spironolactone (Aldactone)*
can cause HYPERKYLEMIA
BB mechanism blcok
beta1 and beta 2 adrenergic
Adverse effects of Beta Blockers
bronchoconstriction, sedation
Mechanism of action of calcium channel blcokers
reduce BP by blocking calcium ion channels in arterial smooth muscle, causing vasodilation
contraindication for calcium channel blocker
CHF or other cardiac problem
nonselective calcium channel blockers
Non-selective drugs- affecting both heart and vessels
_Verapamil (Calan, Isoptin, Covera)*
_Diltiazem (Cardizem, Tiazac)*
adverse effects of calcium channel blocking
dizziness, headache, flushing, constipation; can cause CHF (especially with non-selective CCB) **
ACEI Adverse effect
persistent cough and hypotension
if PT gets cough or hypotension you switch them to
ARB - Affecting Renin-Angiotensin System2: ARB
can cause hypotension but not the dry cough associated with ACEI
Secondary HTN drug: Clonidine is what class
alpha-2 agonist; major side effect DIZZINESS
If protein in urine means
means kidney impairment because destruction of the kidney tissues, something that must be monitored with drugs with HTN
furosemide (Lasix) is what
Primary HTN: Diuretic for treatment of HTN
