CV Flashcards

Question

Apoprotein function

Answer 1

crucial for regulating interactions of lipoproteins with metabolizing enzymes and cellular receptors

Answer 2

- HDL transfers its ApoE and ApoCII (mature CM) - LPL activated by ApoCII, cleaving TG - glycerol goes to liver, FAs enter cells for storage or energy - CM now CM remnants - CM remnants taken up by liver (mediated by receptor that recognizes ApoE) - CM remnants degraded, resulting in release of amino acids, fatty acids, and cholesterol

Answer 3

Add fatty acids to free cholesterol to make CE (ACAT in enterocytes, LCAT in HDL)

Answer 4

- G3-P is the starting material for TG synthesis in adipose and liver - G3-P can be made from DHAP (liver and adipose) or glycerol (liver)

Answer 5

- LPL is low (since insulin isn't there to stimulate it) | - Increased TG levels in blood since they're not getting cleaved in CM

Answer 6

- VLDL mature when they receive ApoE and ApoCII from HDL - VLDL TG are cleaved by LPL to provide fatty acids for use or storage - VLDL become IDL as their TG are removed - Some IDL are taken up by the liver in a receptor mediated process (mainly LDL receptor mediated) - The remaining IDL become LDL when they lose additional TG and return ApoE and ApoCII to HDL - VLDL /IDL/LDL can also transfer some of their TG to HDL in exchange for CE - Some LDL travel to peripheral tissues where they are taken up to provide cholesterol for things such as membrane and steroid synthesis - The remaining LDL are taken up by the liver - Excess LDL may be oxidized and taken up by arterial wall macrophages (initiate atherosclerosis) - LDL can also become Lp(a) when apo(a) forms a covalent bond with ApoB100. Lp(a) are also taken up by macrophages thus promoting atherosclerosis

Answer 7

Hepatic lipase

Answer 8

cholesterol ester transfer protein

Answer 9

Liver; circulates in plasma bound to HDL; transfers CE to ApoB100 containing lipoproteins and TG to HDL

Answer 10

-IDL and LDL can enter cells through the LDL receptor, the LDL receptor-related protein (LRP) and scavenger (SR family) receptors but the high affinity LDL receptor is considered to be the cholesterol “gatekeeper” in the liver -Oxidized LDL are recognized by scavenger receptors which are highly expressed on macrophages -Endocytosis occurs upon binding and lipoprotein contents are degraded as described for chylomicrons -Free cholesterol suppresses expression of the LDL receptor but not the LRP or scavenger receptors Because of this, you can get a lot of lipid accumulating in macrophages -Proprotein convertase subtilisin kexin type 9 (PCSK9) binds to the LDL-R and promotes its degradation within the liver

Answer 11

ATP binding cassette family

Answer 12

- HDL contribute ApoCII and ApoE to chylomicrons and VLDL - They also pick up more cholesterol from cells as they circulate – including from arterial wall macrophages. The cholesterol is esterified by LCAT - HDL donate CE to VLDL/IDL/LDL in exchange for TRG in the process catalyzed by CETP as described earlier - They can also be taken up by the liver through scavenger receptors - The net result is delivery of peripheral cholesterol back to the liver on IDL/LDL and HDL.

Answer 13

Hormone sensitive lipase

Answer 14

Heart, kidneys; Galphas, cAMP; increase CO, renin release

Answer 15

airway, blood vessels; Galphas, cAMP; smooth muscle relaxation, vasodilation

Answer 16

blood vessels; Galphaq, PLC; vasoconstriction

Answer 17

presynaptic neurons; Galphai, cAMP; inhibit NE or ACh release

Answer 18

heart; Galphai, cAMP; decrease HR

Answer 19

airway, endothelial cells; Galphaq, PLC; smooth muscle constriction, vasodilation

Answer 20

Alpha 2; inhibitory

Answer 21

Beta 2; excitatory

Answer 22

Decrease cAMP>>decrease PKA>>dephosphorylation | Open K channels>>hyperpolarization>>less firing

Answer 23

Activate PLC>>increase DAG>>increase PKC>>increase phosphorylation>>increase altering activity of enzymes and receptors Activate PLC>>increase IP3>>increase Ca>>increase Ca/calmodulin>>increase NO synthesis>>vasodilation

Answer 24

Adenylyl cyclase on>>increase cAMP>>increase PKA>>increase Ca>>increase contractility

Answer 25

Adenylyl cyclase on>>increase cAMP>>(-) myosin light chain kinase>>decrease phosphorylation of smooth muscle myosin>>vasodilation

Answer 26

Activate PLC>>increase DAG>>increase PKC>> increase phosphorylation>>increase altering activity of enzymes and receptors Activate PLC>>increase IP3>>increase calcium>>increase Ca/calmodulin>>increase myosin kinase

Answer 27

Inactivate adenylyl cyclase>>decrease cAMP>>(+) myosin light chain kinase>> increase phosphorylation of smooth muscle myosin>>vasoconstriction

Answer 28

Calcifications in muscular artery walls, typically involves internal elastic lamina, age >50 years, lumen unaffected, usually not clinically significant

Answer 29

Small arteries and arterioles, may cause downstream ischemia, hypertension

Answer 30

Homogenous, pink hyaline thickening with associated luminal narrowing

Answer 31

Increased smooth muscle cell matrix synthesis in response to hemodynamic stress Leakage of plasma protein across injured endothelial cells

Answer 32

- Concentric, laminated (onion-skin) thickening of the walls with luminal narrowing - associated with severe hypertension

Answer 33

Genetic abnormalities, family history, increasing age, male

Answer 34

Hyperlipidemia, hypertension, cigarettes, diabetes, inflammation

Answer 35

Family history/genetics

Answer 36

Hypertension

Answer 37

Diabetes, hypothyroidism

Answer 38

C-reactive protein

Answer 39

Chronic inflammatory and healing response of arterial wall to endothelial injury; progression occurs through endothelial cells, smooth muscle cells, lipoproteins, monocyte-derived macrophages, T lymphocytes

Answer 40

1. endothelial injury and dysfunction 2. Accumulation of lipoproteins (mainly LDL) in vessel wall 3. monocyte adhesion to endothelium 4. platelet adhesion 5. factor release from platelets, macrophages, and vascular walls 6. smooth muscle proliferation, ECM production, recruitment of T cells 7. lipid accumulation

Answer 41

Causes increased vascular permeability, leukocyte adhesion, and thrombosis

Answer 42

Migrate into intima, transform into macrophages and foam cells

Answer 43

Induces smooth muscle cell recruitment

Answer 44

- Hemodynamic disturbances - Plaques tend to occur at sites of altered flow - ostia of exiting vessels, branches, posterior aorta - Hypercholesterolemia

Answer 45

- Lipoproteins accumulate within the intima - Aggregate or are oxidized by free radicals - Modified LDL cannot be completely degraded - Accumulates in macrophages, results in foam cells

Answer 46

- Toxic to endothelial cells, smooth muscle cells and macrophages - Stimulates release of cytokines, growth factors and chemokines that further recruit and activate macrophages – vicious cycle

Answer 47

- Inflammation - Infection - Smooth muscle proliferation and matrix synthesis

Answer 48

- Possibly triggered by accumulation of cholesterol crystals and free fatty acids in macrophages - Inflammasome activation, produce pro-inflammatory cytokine IL-1 - Cytokines and chemokines recruit and activate more inflammatory cells - Chronic inflammatory reaction in vessel wall activates endothelial and smooth muscle cells, contributes to atherosclerosis

Answer 49

- Convert a fatty streak into a mature atheroma, contribute to growth of atherosclerotic lesions - More inflammation may breakdown the ECM → unstable plaque

Answer 50

Flat yellow spots that may join to form streaks

Answer 51

Lipid-filled foamy macrophages

Answer 52

No; only when they develop into plaques

Answer 53

- White-yellow and encroach on the lumen - Red-brown if superimposed thrombus over ulcerated plaques - Patchy, rarely circumferential - Varying sizes and stages of development is normal

Answer 54

Likely because of hemodynamics

Answer 55

- Lower abdominal aorta - Coronary arteries - Popliteal arteries - Internal carotid arteries - Circle of Willis

Answer 56

- Three components: - Smooth muscle cells, macrophages, and T-cells - Extracellular matrix, including collagen, elastic fibers and proteoglycans - Intracellular and extracellular lipids - Typically fibrous cap of smooth muscle and dense collagen - Shoulder area with macrophages, T cells and smooth muscle - Deep is a necrotic core, with lipid (cholesterol and cholesterol esters), foam cells, fibrin, thrombus, debris - Neovascularization at periphery

Answer 57

Large elastic (aorta, carotid, iliac) and large and medium-sized muscular (coronary, popliteal) arteries

Answer 58

- Acute occlusion - Chronic narrowing of the vessel lumen - Aneurysm formation - Embolism

Answer 59

Stenosis that causes ischemia; generally 70% in coronaries

Answer 60

- Can result in exertional chest pain (stable angina) - Sudden cardiac death - Chronic ischemic heart disease

Answer 61

- Mesenteric occlusion and bowel ischemia - Ischemic encephalopathy - Intermittent claudication

Answer 62

- Rupture/fissuring – exposes thrombogenic plaque constituents - Erosion/ulceration – exposes thrombogenic subendothelial basement membrane to blood - Hemorrhage into the atheroma – expands its volume

Answer 63

- Intrinsic factors – plaque structure and composition - “Vulnerable” plaques – thin fibrous caps, large lipid cores, greater inflammation - Extrinsic factors - adrenergic stimulation - emotional distress

Answer 64

- Atheroembolism - Rupture can discharge necrotic debris into the bloodstream, producing microemboli - Aneurysm formation - Pressure or ischemic atrophy of the underlying media, with loss of elastic tissue, causes weakness and potential rupture

Answer 65

- Adrenergic agonists - Platelet contents - Endothelial cell dysfunction - Mediators from vascular cells

Answer 66

- Begins early in life – possibly in fetal life or shortly after birth - Typical atherosclerotic lesion forms over 20-30 years – initially clinically insignificant - Exception – homozygous familial hypercholesterolemia

Answer 67

- Initiation and formation - Adaptation - Clinical

Answer 68

TG>>>phospholipid>CE>FC/protein

Answer 69

TG>CE/phospholipid>protein>FC

Answer 70

CE>phospholipid/protein>TG/FC

Answer 71

protein>phospholipid>CE>TG/FC

Answer 72

- Due to a mutation in the gene encoding LDL receptor - Results in loss of feedback control, with elevated levels of cholesterol - Cannot bind or clear LDL from circulation - Also have increased LDL synthesis - Autosomal dominant, one of the most frequently occurring Mendelian disorders - Over 900 mutations have been identified - Familial hypercholesterolemia is present in 3-6% of survivors of MI

Answer 73

- Apolipoprotein E is present on chylomicrons, chylomicron remnants, VLDL and IDL - Binds to LDL receptor, helps clear these from circulation - Three common electrophoretic isoforms – E3 (most common), E4, and E2 - Different phenotypes have variability in metabolism - approximately 20% of variation in serum cholesterol is attributed to this polymorphism

Answer 74

- LDL-like particle, glycoprotein apo (a) is linked to apoB-100 by a disulfide bond - Function and atherogenic properties are not well understood, but - High levels are associated with increased risk of atherosclerosis - Levels are heritable - Levels are not altered by most cholesterol lowering drugs

Answer 75

- 1/500 - 50% of normal high-affinity LDLR - 2-3x cholesterol elevation; LDL-C>220 - tendinous xanthomas, premature atherosclerosis

Answer 76

- 1/1 mil - 5-6x cholesterol elevation; LDL-C>400 - skin xanthomas, atherosclerosis, MIs before 20 - if untreated, premature death secondary to MI

Answer 77

ApoE2 (E2/E2); has much lower affinity for LDLR so lipoproteins accumulate in blood

Answer 78

- Typically will give values for total cholesterol (TC), HDL cholesterol (HDL-C), LDL cholesterol (LDL-C), triglycerides (TG) - Usually directly measures TC, HDL-C, and TG

Answer 79

Friedewald formula; LDL-C = TG - HDL-C - VLDL-C

Answer 80

- All TG is carried by VLDL – no chylomicrons present - Explains, for the most part, why fasting specimen is recommended for LDL-C value - TG/cholesterol ratio is invariant – changes as TG level increases - Explains, for the most part, why it is not accurate with high TG levels (generally about 400 mg/dL)

Answer 81

deficiency of oxygen

Answer 82

- Most common type of cell injury in clinical medicine - Results from hypoxia due to reduced blood flow - Compromises delivery of substrates for glycolysis – get compromised aerobic and anaerobic metabolism - Causes more rapid tissue injury than hypoxia alone

Answer 83

- Ischemic necrosis caused by occlusion of either the arterial supply or venous drainage - Coagulative necrosis develops distal to it

Answer 84

- Imbalance between supply (perfusion) and demand (for oxygenated blood) - Also reduces availability of nutrients and removal of metabolic wastes - Ischemia is less well tolerated than just hypoxia, such as with anemia, lung disease, etc - Vast majority (>90%) of cases due to reduced flow from atherosclerotic coronary arteries - IHD frequently called coronary artery disease (CAD) - Typically a long period (decades) of silent progression before onset of symptoms – due to atherosclerosis

Answer 85

- Emboli, myocardial vessel inflammation, or vascular spasm | - Increased demand may make some occlusion symptomatic – tachycardia, hypoxemia, systemic hypotension

Answer 86

- Angina pectoris (“chest pain”) - Ischemia is not severe enough to cause infarction, but symptoms portend infarction risk - Myocardial Infarction - Ischemia causes frank cardiac necrosis - Chronic ischemic heart disease with heart failure - Sudden Cardiac Death

Answer 87

- Paroxysmal and usually recurrent attacks of substernal or precordial chest discomfort - Caused by transient myocardial ischemia that is insufficient to induce myocyte necrosis - Three overlapping patterns - Some are silent (no symptoms), particularly in geriatric population and those with diabetic neuropathy

Answer 88

- Most common form, caused by imbalance between coronary perfusion relative to myocardial demand - May be secondary to physical activity, emotional excitement, or psychological stress - Typically described as a deep, poorly localized pressure, squeezing or burning sensation; unusually as pain - Usually relieved with rest or drugs such as vasodilators or calcium channel blockers

Answer 89

- Uncommon form of episodic ischemia, caused by coronary artery spasm - May have underlying atherosclerosis, but unrelated to activity - Generally responds to vasodilators

Answer 90

- Pattern of increasingly frequent, prolonged (> 20 min), or severe angina or chest discomfort described as frank pain - Precipitated by progressively lower levels of activity or at rest - Typically caused by disruption of an atherosclerotic plaque with partial thrombosis, and possibly embolization and/or vasospasm - Approximately half have evidence of myocardial necrosis - MI may be imminent

Answer 91

- present on the postsynaptic membrane of the effector organs - Coupled with Gq and initiates reactions through activation of phospholipase C >>↑IP3 >>↑Ca2+>> Contraction

Answer 92

- present on presynaptic nerve endings, β cell of pancreas, on vascular smooth muscle - Coupled with Gi and inhibits AC and decreases cAMP signaling

Answer 93

Aorta, coronary a. - vasoconstriction

Answer 94

inhibitory receptor of SNS; brain - modulate dopamine transmission

Answer 95

Only when agonists are given locally or in high oral doses

Answer 96

- Heart - Kidney (juxtaglomerular cells) - Presynaptic adrenergic/cholinergic nerve terminals - Adipose tissue

Answer 97

- Vascular smooth muscle (arterioles; EXCEPT skin and cerebral) - Bronchiole smooth muscle - Liver

Answer 98

1: increases contractility and stimulation of SA node>>increase CO 2: decrease TPR by vasodilation

Answer 99

Phenylephrine - 1 | Clonidine - 2

Answer 100

Dobutamine - 1 Albuterol - 2 Isoproterenol - non Dopamine - non

Answer 101

Epi NE Ephedrine Pseudoephedrine

Answer 102

Amphetamine | Cocaine

Answer 103

Phenoxybenzamine | Phentolamine

Answer 104

Prazosin - 1 Terazosin - 1 Doxazosin - 1

Answer 105

``` Acebutolol Esmolol Metoprolol Pindolol Propranolol Carvedilol ```

Answer 106

- Synthetic drug favors α1 over α2 - Marked vasoconstriction - Increases peripheral arterial resistance and decreases venous capacitance - Clinical usage: - Nasal congestion - Hypotension/shock - Causes mydriasis

Answer 107

- Treatment systemic hypertension (2nd line therapy) - Decreases HR and reduces TPR >>decreased CO - Will see a brief RISE in BP followed by prolonged hypotension when given parenterally - Reduces arterial pressure, decreases RENAL vascular resistance and maintains renal blood flow - Very lipid soluble (enters CNS) - Well absorbed orally & widely distributed - Targets cardiac centers in CNS - Typical administration: oral or transdermal - α2:α1 specificity ratio is 200:1

Answer 108

- Beta 1 - now known to have actions at alphas - clinical usage - heart failure>>severe cardiac decompensation - cardiac stress testing

Answer 109

- Beta 2 - relaxes bronchial smooth muscle with little effect on HR - Clinical usage - bronchospasm and COPD

Answer 110

- Positive chronotropic and inotropic actions >> increasing cardiac output (β1) - Potent vasodilator (β2) - Fall in diastolic blood pressure; systolic remains same or rises slightly - Lowers peripheral mean arterial pressure - Clinical - mild or transient episodes of heart block that don't require shock or pacemaker therapy

Answer 111

- Low doses activate D1 in renal and vascular beds >> local vasodilatation, renal blood flow and glomerular filtration >> diuresis - Mid doses activate cardiac β1-receptors (direct and indirect) >> increased heart rate, cardiac contractility and stroke volume >> increased CO - Higher doses activate systemic α-receptors >> vasoconstriction >> increased systemic resistance - May mimic actions of epinephrine - Clinical Usage: Adjunct in the treatment of shock that persists after adequate fluid volume replacement - MI, open heart surgery, renal failure, cardiac decompensation

Answer 112

- Potent cardiac stimulant and vasoconstrictor - Leads to increased SV, HR, and CO - β1-receptors induce positive inotropic and chronotropic actions - Acts directly on myocardium and SA node - α1-receptors cause vasoconstriction in vascular beds >> predominates at high doses - Activates β2-receptors in skeletal muscle blood vessels and liver >> dilation - Vasculature β2-receptors are more sensitive than α –receptors >> can decrease diastolic pressure

Answer 113

ACLS (asystole or pulseless arrest), bradycardia, acute bronchospasm, local vasoconstriction (surgery), anaphylaxis

Answer 114

-Less effective that epi @ alpha receptors -Little beta 2 effect -CV effects: increase TPR, diastolic, and systolic BP (baroreceptor reflex reduces HR) Clinical: shock or severe hypotension

Answer 115

- High oral bioavailability and long duration of action (hours) - Releases tissue stores of NE >> a & b-adrenergic stimulation - Activation of β receptors (early asthma treatment) - Causes mild stimulation of CNS/improves athletic performance

Answer 116

- Used to treat nasal, sinus, and Eustachian tube congestion - Stimulates a-adrenergic receptors of respiratory mucosa causing vasoconstriction - Stimulates b-adrenergic receptors causing bronchial relaxation, increased heart rate and contractility - Precursor to methamphetamine >> ↓OTC availability

Answer 117

- Acts as both an norepinephrine transporter (NET) substrate and a reuptake blocker, eliciting reverse transport and blocking normal uptake, thereby increasing NE levels in and beyond the synaptic cleft - CNS >> stimulant >> Narcolepsy, ADHD - Periphery >> ↓reuptake of NE and release of stored catecholamines

Answer 118

- Blocks the norepinephrine transporter (NET) - Required for cellular uptake of norepinephrine - Norepinephrine accumulates in the synaptic cleft to stimulate a & b adrenoceptors

Answer 119

- Examples: Cocaine, amphetamines, etc. - Mental status: hyperalert, agitation, hallucinations, paranoia - Pupils: mydriasis - Vital signs: tachycardia, hypertension, hyperthermia, widened pulse pressure, tachypnea, hyperpnea - Other manifestations: diaphoresis, tremors, hyperreflexia, seizures

Answer 120

Phenoxybenzamine

Answer 121

- Slightly more selective to α1 - Noncompetitive - May also block the reuptake of norepinephrine - Absorbed well after oral administration but bioavailability is low - Can enter CNS - Attenuates vasoconstriction and reduces BP

Answer 122

- Competitive block at α1 and α2 | - Effects similar to phenoxybenzamine

Answer 123

- Pheochromocytoma - tumor of adrenal medulla or sympathetic ganglia - tumor secretes catecholamines (NE, epi) - can add beta antagonist after the fact to have unopposed alpha vasoconstriction first

Answer 124

- Primary hypertension - Lower peripheral vascular resistance - BPH - helps with urinary continence by relaxing smooth muscle in bladder neck, prostate capsule, and prostatic urethra

Answer 125

- orthostatic hypotension - dizziness, headache - miosis - nasal congestion - urination

Answer 126

DIMINISHES

Answer 127

- Well absorbed PO - t1/2 - 3-10 hours (EXCEPT esmolol ~10-20 minutes) - typically metabolized in liver (poor metabolizers have higher plasma concentrations)

Answer 128

- Prototypical β-blocking drug - Undergoes extensive first-pass metabolism - Bioavailability is low - Amount reaching circulation varies among individuals - Very lipid soluble; crosses BBB - Also formulated as sustained release

Answer 129

- β1-selective (modest) - Safer for patients who experience bronchoconstriction after propranolol - Undergoes CYP2D6 metabolism - Poor metabolizers exhibit 3x-10x higher plasma concentrations after administration of metoprolol than extensive metabolizers - Available in sustained release tablets

Answer 130

- Ultra-short acting β1-adrenergic antagonist - Gets metabolized by esterases in red blood cells - Peak effect occurs within 6-10 min - Block lasts ~20 min post-infusion - CV Clinical usage: supraventricular arrhythmias, arrhythmias associated with thyrotoxicosis, and perioperative hypertension

Answer 131

- Partial β-agonists with intrinsic sympathetic activity (ISA) - Pindolol is a non-selective β-blocker - Acebutolol β1-blocker - Exhibit low level agonist activity while acting as a receptor site antagonist - CV Clinical usage: hypertension and angina - Good for patients that exhibit bradycardia - ISA activity prevents severe bradycardia from occurring

Answer 132

- β-blockers with ISA cause mild peripheral vasodilation without reducing cardiac output (e.g., pindolol, acebutolol) - They act as partial agonists - Interact with β receptors to cause measurable agonist response while blocking the greater agonist effects of endogenous catecholamines at the same time - Provide low-grade β stimulation at rest but act as typical β blockers when sympathetic activity is high - β-blockers without ISA lower blood pressure by decreasing cardiac output and inhibiting renin release and central sympathetic outflow - ISA’s are beneficial for bradyarrhythmias or peripheral vascular disease, but can potentially be used for hypertension

Answer 133

- Non-selective β-adrenergic receptor antagonist & α1-receptor antagonist - Stronger ability to antagonize catecholamines at β-receptor - Antioxidant properties - Contributes to clinical benefit in chronic heart failure - Racemic mixture with stereoselective metabolism: (R)-carvedilol

Answer 134

- Hypertension: β-adrenergic receptor antagonists with clinical indication - Heart failure: following MI, long-term use improves symptoms, reduces hospitalization, and enhances survival - Ischemic Heart Disease: reduce anginal episodes and improve exercise tolerance - Cardiac arrhythmias: supraventricular and ventricular show benefit after treatment with β receptor antagonists - Hyperthyroidism symptoms with propranolol

Answer 135

- Depresses myocardial contractility and excitability - Heart failure >> Causes cardiac decompensation - Severe hypotension - Bradycardia - AV block - Fatigue/exercise intolerance - Erectile dysfunction

Answer 136

- Generally avoided in patients with: - Asthma - Nodal dysfunction (sinoatrial or atrioventricular) - In combination with other drugs that inhibit AV conduction (EX: verapamil) - Diabetes (better treated with ACE inhibitors) - β-adrenergic receptor blockers WITHOUT ISA: - Increase triglycerides in plasma (EX: propranolol) - Lower HDL cholesterol - β-adrenergic receptor blockers WITH ISA have little effect on blood lipids - SHOULD NEVER BE ABRUPTLY STOPPED (taper 2 wks) - To avoid acute tachycardia, hypertension, and/or ischemia

Answer 137

-Bradycardia, hypotension most common

Answer 138

Drugs: lovastatin, pravastatin, simvastatin, fluvastatin, atorvastatin, rosuvastatin, pitavastatin MOA: block HMG-CoA reductase to increase LDLR expression Lipid profile: Lower LDL, some TG, increase HDL some Clinical: Adverse effects: elevated serum aminotransferase activity, myalgia, myositis/myopathy, rhabdomyolysis, increased risk of diabetes Contraindications: liver disease, pregnant, breast-feeding, or women who will become pregnant, children Route:

Answer 139

Drugs: colestipol, cholestyramine, colesevelam MOA: bind to bile acids to prevent their reabsorption>>increase excretion of bile>>increase liver bile acid synthesis>>greater demand for liver cholesterol Lipid profile: decrease LDL some Clinical: Adverse effects: constipation, bloating, steatorrhea, impaired absorption of ADEK, impaired absorption of certain drugs Contraindications: homozygous LDLR deficiency, diverticulitis Route: drink mix, tablet, suspension

Answer 140

Drug: ezetimibe MOA: blocks NPC1L1 to inhibit cholesterol absorption>>more LDLR by liver Lipid profile: lower LDL some Clinical: homozygous FH with statin Adverse effects: myopathy when taken with statin Contraindications: Route:

Answer 141

Drug: Niacin MOA: inhibit DGAT and to prevent VLDL secretion; inhibit hormone sensitive lipase Lipid profile: increase HDL Clinical: FH not achieving target LDL reduction with other drugs, may be useful in Lp(a) Adverse effects: flushing, nausea and abdominal discomfort, elevated aminotransferase levels, acanthosis nigricans, hyperglycemia, hyperuricemia, macular edema Contraindications: peptic ulcer, liver disease Route:

Answer 142

Drugs: gemfibrozil, fenofibrate MOA: peroxisome proliferator activated receptor alpha agonists>>upregulate LPL, ApoA1, ApoA2 and down-regulate ApoCIII; stimulate beta-oxidation Lipid profile: decrease TG Clinical: hypertriglyceridemia Adverse effects: GI, myopathy, high levels of aminotransferases, decreased WBC or hematocrit, rhabdo, cholesterol gallstones Contraindications: hepatic or renal dysfunction, biliary disease; drug interactions: potentiate anticoagulants, myopathy with statin Route:

Answer 143

``` Drugs: lovaza, epanova MOA: Lipid profile: lower TG some Clinical: hypertriglyceridemia Adverse effects: belching, taste alteration, vomiting, constipation, pruritis, rash, increased aminotransferases, increased LDL, prolongation of bleeding, hypersensitivity Contraindications: fish allergy Route: ```

Answer 144

Drugs: alirocumab, evolocumab MOA: bind PCSK9 and prevent it from binding LDLR (prevents lysosomal degradation) allows more LDLR on surface of liver so more LDL into hepatocytes Lipid profile: lower LDL Clinical: FH or clinical atherosclerotic disease Adverse effects: hypersensitivity, injection site reaction Contraindications: Route: injection

Answer 145

MOA: antisense oligonucleotide binds to Apo100 mRNA, prevents ApoB100 synthesis Lipid profile: LDL Clinical: homozygous familial hypercholesterolemia Adverse effects: injection site reaction, flu-like symptoms, hepatotoxicity Contraindications: Route: injection

Answer 146

MOA: MTTP inhibitor>>decreased CM and VLDL synthesis Lipid profile: LDL Clinical: homozygous familial hypercholesterolemia Adverse effects: GI disturbances, hepatotoxicity, embryotoxicity Contraindications: Route:

CV Flashcards

(170 cards)