cholesterol and hypertension Flashcards

1
Q

what does a statin do?

A

decreases production of cholesterol in liver and increases receptors for LDL on liver cells
overall effect = lower LDL, lower triglycerides, higher HDL

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2
Q

most common adverse effect statin

A

myopathy (muscle injury) = muscle aches and weakness

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3
Q

rare but serious side effect of statins?

A

rhabdomyolysis

Muscle lysis with severe muscle pain

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4
Q

are statins safe in pregnancy?

A

No

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5
Q

What does nicotinic acid (Niacin) do?

A

inhibits hepatic secretion of triglycerides

overall effect of lowering LDL, triglycerides, and increasing blood HDL

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6
Q

what are the side effects of niacin?

A
•	Intense facial flushing
•	Hepatotoxicity
•	Hyperglycemia
•	Skin rash
•	Increased uric acid levels
*these limit use in patients
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7
Q

what do bile acid sequestrants do?

A

bind bile acids in the GI, blocking absorption, which increases demand for bile acid production in liver which requires LDL

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8
Q

bile acid sequestrants may decrease absorption of which type of drugs?

A

Thiazide diuretics, digoxin, warfarin, and certain antibiotics
(due to binding of + with - )

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9
Q

what do cholesterol absorption inhibitors do?

A

Inhibit transport protein responsible for absorbing dietary cholesterol

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10
Q

why are cholesterol absorption inhibitors used in combo with statins?

A

because they can produce compensatory increase in hepatic cholesterol synthesis

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11
Q

what do fibric acid derivatives (Fibrates) do?

A

increases synthesis of enzyme that breaks down lipoproteins by binding ppar-alpha
increases HDL, but no effect on LDL

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12
Q

adverse effects of Fibrates?

A

Increased risk for gallstones
Myopathy (if on statins - low dose, and carefully monitor for myopathy)
Hepatotoxicity

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13
Q

what is the site of action for loop diuretics?

A

ascending loop of Henle, sodium & chloride reapsorption

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14
Q

what is the site of action for thiazide diuretics?

A

Distal convoluted tubule, Block sodium & chloride reabsorption

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15
Q

what is the site of action for potassium sparing diuretics?

A

collecting duct, aldosterone receptors

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16
Q

why is there a risk for hypokalemia with loop and thiazide diuretics?

A

because the transporter that is blocked also blocks reabsorption of K+

17
Q

why do potassium-sparing diuretics spare potassium?

A

because blocking of the aldosterone receptor increases potassium retention

18
Q

what is necessary to avoid when on potassium-sparing drugs?

A

ACE inhibitors or renin inhibitors because they also conserve potassium
(RAAS pathway)

19
Q

what is the main adverse effect of potassium-sparing diuretics?

A

hyperkalemia

20
Q

what do beta blockers do?

A

they block beta 1 receptors (cardiac & juxtaglomerular cells)
Cardiac effect = lowered CO (blocked binding of catecholamines)
juxtaglomerular effect = decreased vascoconstriction d/t decreased renin release

21
Q

what’s the difference between 1st and 2nd gen beta blockers?

A

1st gen is non-selective so also blocks beta 2 receptors in lungs which can cause bronchoconstriction (not approp for people with asthma/lung disease)
and inhibits breakdown of glycogen in muscles/liver (not approp for diabetics)

22
Q

what do ACE inhibitors do?

A

inhibits the the enzyme that converts angiotensin I to II = vasodilation
decreases total blood volume = decreased CO
elevated levels of bradykinin = vasodilation

23
Q

what are adverse effects of ACE inhibitors?

A

first dose hypertension - first few doses should be low

hyperkalemia - due to inhibition of RAAS pathway, avoid potassium supplements and potassium-sparing diuretics

24
Q

what are the adverse effects of ACE inhibitors caused by bradykinin?

A

persistent cough
rare but fatal angioedema
drug interaction with NSAIDs - reduces effect of ACE inhibitor

25
Q

what do angiotensin receptor blockers do?

A

block binding of angiotensin II to receptor on arterioles
= vasodilation
and decrease aldosterone release from adrenal cortex
- causing water and sodium excretion

26
Q

what do direct renin inhibitors do?

A

bind renin blocking conversion of angiotensinogen to angiotensin I
which effects RAAS pathway, lowering BP similar to ACEI & ARBs

27
Q

adverse effects of DRIs?

A

hyperkalemia (d/t RAAS pathway) - avoid potassium supplement/potassium-sparing diuretics

28
Q

what do calcium channel blockers do?

A

decrease contraction blocking uptake of calcium into cells

29
Q

what is the difference between dihydropyridine and non-dihydropyridine calcium channel blockers?

A
dihydropyridine = vasodilation, act only on arteries
non-dihydropyridine = act on heart and arteries, so vasodilation AND decrease CO
30
Q

adverse effects of calcium channel blockers?

A
Flushing
Dizziness
Headache
Peripheral edema
Reflex tachycardia (dihydro only)
Rash (dihydro only)
constipation (non-dyhydro)
compromise cardiac function (non-dihydro)
31
Q

what do centrally acting alpha 2 agonists do?

A

bind alpha 2 receptors in brain, decreasing sympathetic flow to heart & vessels (decrease CO and peripheral resistance)

32
Q

adverse effects of centrally acting alpha 2 agonists

A

dizziness, drowsiness, dry mouth (3 Ds)

Rebound hypertension if withdrawn abruptly