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Pharmacology drew > winter 1 > Flashcards

winter 1 Flashcards

1
Q

Acetazolamide

A

Carbonic Anhydrase inhibitor,

  • sulfonamide derivative, organic acid secretion system in proximal tubule, T1/2=6-9 hours
  • primary act in PROXIMAL TUBULE, to inhibit NaHCO3 reabsorption, by stopping Na-H exchange
  • increase excretion of NA and HCO3 without Cl- therefore a mild HyperCL and metabolic acidosis
  • limited diuretic effects because of enhanced Na abs in remaining tube segments as NaCl
  • useful in treating glaucoma,resp alkalosis and cerebral edema of mountain sickness, epilepsy, urine alkalization, and correct metabolic alkalosis by causeing an acidosis
  • TOX-hyper CL metabolic acidosis, urin alkanization –> kidney stones, hypo K, sulfonamide hypersensativity,
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2
Q

Carbonic anhydrase inhibitors

A

Acetazolamide

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3
Q

osmotic diuretics

A

Mannitol(IV) (Osmitrol)

prefered over urea because less irritation and less venous thrombosis

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4
Q

Mannitol (IV Osmitrol)

A

Osmotic diuretic

  • given IV and remains in the extracellular space
  • rapidly filtered by glomeruli and no tube secretion with minimal tubular reabsorption, T1/2= 100 min
  • increases osmotic pressure of tubule–> decreased abs of h20 and solutes in segments permeable to h20
  • oosmotic diuretics increase secretion of all electrolytes
  • uses:oliguric acute renal failure,reduce intraocular and intracranial pressure, urinary excretion of toxins/overdose/prevent renal tox, peripheral edemas
  • tox-pulm edema in pts w/ pulm congestion, contraindicate in renal desease, contra in cranial bleeding
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5
Q

Loop diuretics

A

Furosemide (Lasix)- sulfonamide derivative
Ethacrynic Acid (Edecrine)- phenoxyacetic acid derivative
inhibitors of apical Na-K-Cl symport

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6
Q

Furosemide

A

Loop diuretic T1/2 =1.5 HR

  • bound to plasma proteins-> little filtration, excreted by organic acid secretion mechanism in prox tubule
  • excreted unchanged 65%, metabolized 35%
  • max effect -oral admin at 1-2 hr, IV 20-60 min
  • act in THICK ASCENDING LIMB to block Na-K-Cl symporter on luminal membrane
  • enhance excretion of Na, K, Cl, H, Ca, Mg, NH4, PO4
  • increase renal blood flow and systemic venous capacitance –> decrease LV filling pressure
  • use: CHF, Pulm edema, HTN( thiazides are prefered), HyperCa(by decreasing the driving force of Ca) edema of nephrotic syndrome and cirrhosis
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7
Q

Loop diuretic tox and contraindications

A

-hypotension, hypovoluemia,hyponatremia
hypoCL metabolic acidosis
-hypoK–> cramps and Cardiac arrhythmas
-gout- due to decreased excretion of uric acid from increased competition for organic acid secretory mechanism
-ototox- more common with Ethacrynic Acid
sulfonamide hypersensitivity( not Ethacrynic Acid)
metabolic side effects

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8
Q

Ethacrynic Acid (Edecrine)

A

Loop diuretic T1/2 =1.5 HR

  • bound to plasma proteins-> little filtration, excreted by organic acid secretion mechanism in prox tubule
  • act in THICK ASCENDING LIMB to block Na-K-Cl symporter on luminal membrane
  • enhance excretion of Na, K, Cl, H, Ca, Mg, NH4, PO4
  • increase renal blood flow and systemic venous capacitance –> decrease LV filling pressure
  • use: CHF, Pulm edema, HTN( thiazides are prefered), HyperCa(by decreasing the driving force of Ca) edema of nephrotic syndrome and cirrhosis
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9
Q

Thiazide diuretics

A

inhibitors of apical Na-Cl transport in distal convoluted tubule,
recommended at the initial therapy for chronic primary HTN
hydrochlorothiazide (microzide)
chlorothiazide (Diuril)
chlorthalidone (Thalitone)
indapamide (Lozol)

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10
Q

Thiazide diuretics pharmicokinetics and dynamics

A

-sulfonamide group
-secreted by the organic acid secretion mechanism in the proximal tubule, filtered also
-inhibit Na-CL symporter inapical membrane of early distal convoluted tubule promoting NaCl excretion and water diuresis
-diuretic action independent of Acid base balance
increase excretion of Na, Cl, K, H, decrease Ca excretion

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11
Q

Thiazide diuretics uses and toxicities

A

USES- mild to moderate edema of CHF, HTN(diminished when GFR is below 30-40 ml/min, indapamide may still work at GFR this low)
-prevent osteoporosis and Ca nephrolithiasis
-paradoxic antidiuretic effect in nephrogenic DI
-Ascities (first treat with spironolactone to prevent hypo K)
TOX-hypo K and metabolic ALKALOSIS, GOUT(acid selection system competition)
contraindicated in sulfonamide hypersensativities–> SJS
hyper glycemia
- thiazides ^ LDL, total cholesterol and triglycerides
- indapamide does not so used in pts with ^ LDL( may also have direct affect on vascular smooth muscle via Ca channel blockade

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12
Q

K sparing diuretics

A 
Inhibitors of renal Na channels
-triamterene
-amiloride 
aldosterone receptor blockers
-spironolactone
-eplerenone
-drospirenone
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13
Q

triamterene

A

k sparing diuretic

  • secreted in prox tubule by organic base secretory system
  • t1/2= 4 hours, metabolized in liver to active metabolite 4-hydroxyttriamterene
  • block apical Na channels and spare K by decreasing basal Na/K ATPase and by reduced electrochemical gradient
  • not powerful so used in combination w/other diuretics and counterbalance K wasting of loop and thiazides
  • Liddle syndrome(pseudohyperaldosteronism)
  • TOX- hyperK-> arrhythmia, not administered with spironolactone, caution with RAAS blockers, cause kidney stones
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14
Q

amiloride

A

k sparing diuretic

  • secreted in prox tubule by organic base secretory system
  • t1/2= 21 hours, excreted unchanged by kidney
  • block apical Na channels and spare K by decreasing basal Na/K ATPase and by reduced electrochemical gradient
  • not powerful so used in combination w/other diuretics and counterbalance K wasting of loop and thiazides
  • Liddle syndrome(pseudohyperaldosteronism)
  • TOX- hyperK-> arrhythmia, not administered with spironolactone, caution with RAAS blockers, cause kidney stones
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15
Q

spironolactone

A

aldosterone receptor blocker
used in combination with loop diuretics and thiazides to prevent K wasting
treat hyperaldosteronism
-TOX- hyperK-> arrhythmia, antiandrogeneffects,

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16
Q

desmopressin acetate

A

antidiuretic drug
similar to arginine vasopressin
increases h20 abs in the collecting duct system
has a greater antidiuretic effect than vasopressin but less cardiovascular vaspressor activity
uses: nocturnal enuresis
tox: water intoxication

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17
Q

indapamide

A

Thiazide diuretics

  • thiazides ^ LDL, total cholesterol and triglycerides
  • indapamide does not so used in pts with ^ LDL( may also have direct affect on vascular smooth muscle via Ca channel blockade
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18
Q

Reserpine

A

Peripherally acting Sympathetic neuronal blocker

  • decreases the availability of NE to its receptor by inhibiting NE and DA storage in vesicles, thus less released with each nerve impulse
  • reduces BP via decreased CO and peripheral resistence
  • irreversible effects, thus lower BP may last after drug is stopped
  • SE: sedation and mental depression, may ppt migraines
  • se: nasal congestion, postural hypoTN, bradycardia, fluid retention
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19
Q

methyl dopa

A

centrally acting adrenergic neuronal inhibitor
converted to alpha-methylNE thats acts as an a2 agonist in central vasomotor centers to dampen simp outflow leading to decreased renin, decreased HR and CO(or not)
- MOST IMPORTANT decreased arterial peripherial presure
-SE:peripheral fluid retention, centrally mediated dry mouth, certain autoimmune disorders, hemolytic anemia, abnormal liver function, PARKINSONIAN SIGNS
-rarely used now but MAJOR CURRENT USE IS IN PREGNANCY B/C NO HARM TO FETUS

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20
Q

clonidine

A

centrally acting adrenergic neuronal inhibitor
not a prodrug
similar action to methyl dopa as a a2 agonist to dampen simp outflow leading to decreased renin, decreased HR and CO
-MOST IMPORTANT decreased arterial peripherial pressure
lower doses than methyldopa, in patch form
-no autoimmune SE, rebound HTN, LOCAL SKIN run from patch
-treatment of: adhd, meno hot flash, stress disorder, nicotine and ethos withdrawal

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21
Q

PrazoSin

A

Prototype selective a1 blocker- competitive
-long term treatment of mild to moderate HTN, decreased BP by decreasing TPR
-Relax smooth muscle of bladder neck, relieve urinary obstruction
-MUST BE TAKEN AT LEAST 3X DAY,slowly increase dose
raynauds treatment
SE:First dose phenomenon orthostatic HypoTN, Na H20 retention, reflex tachycardia, not as much as non selective

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22
Q

DoxazoSin

A

newer selective a1 blocker than prazosin
use and side effect just life Prasozin, but with longer half lives(dose 1x/day) so better long term control of HTN and BPH, slowly increase dose
Relax smooth muscle of bladder neck, relieve urinary obstruction
raynauds treatment
SE:First dose phenomenon orthostatic HypoTN, Na H20 retention, reflex tachycardia, not as much as non selective

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23
Q

TerazoSin

A

newer selective a1 blocker than prazosin
use and side effect just life Prasozin, but with longer half lives(dose 1x/day) so better long term control of HTN and BPH, slowly increase dose
Relax smooth muscle of bladder neck, relieve urinary obstruction
raynauds treatment
SE:First dose phenomenon orthostatic HypoTN, Na H20 retention, reflex tachycardia, not as much as non selective

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24
Q

Acebutolol

A

B1 selective blocker
Partial Agonist (ISA)
Membrane stabilizing
low lipid solubility ?

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25
Q

Atenolol

A

B1 selective blocker
Not Partial agonist
Not membrane stabilizing
low Lipid soluble

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26
Q

Esmolol

A

B1 selective blocker
Not partial Agonist
Not Membrane stabilizing
Low Lipid Soluble
rapid action, rapid broken down by plasma esterase’s
reserved fro treatment of HTN emergencies

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27
Q

Metoprolol

A

B1 Selective blocker
Not partial Agonist
Membrane Stabilizing ?
Moderate Lipid Soluble

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28
Q

Nadolol

A 
B1 and B2 blocker
Not partial agonist
no membrane stabilize
Low Lipid solubility
longest activity
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29
Q

Pindolol

A 
B1 and B2 selective blocker
Partial Agonist (ISA), Membrane stabilizer ?
 ISA doesn't affect B2 mediated inhibition, actually enhances the relax adding to anti HTN effect
Moderate Lipid soluble
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30
Q

Propranolol

A

B1 and B2 selective blocker
no partial agonist
Membrane stabilize
High Lipid soluble

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31
Q

Timolol

A 
B1 and B2 selective blocker
no partial agonist
no membrane stabilize
Moderate lipid solubility
used in glaucoma treatment
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32
Q

Labetalol

A

both adrenergic alpha 1 and Beta 1 and B2 blocking(ISA AT B2)

  • BP falls due to DECREASE PERIPHERAL RESISTANCE (due to alpha block and B2 partial sim and decreased renin release) and some decrease CO
  • Use: orally for severe primary HTN, IV for HTN emergency
  • SE: alpha blockade-> postural dizziness which beta block cannot correct, beta blockade-> brady cardia, A-V block at high dose
33
Q

nebivolol

A

selective B1 blocker and NO releaser from vascular endothelium

  • decreased NO degradation
  • BP is dropped due to decreased TPR
  • use-HTN pts with decreased endothelial cell function, mild to mod primary HTN
  • SE: similar to B blockers with less rebound HTN with cessation
34
Q

Selective arteriolar vasodialators

A

hydralazine
minoxidil
decrease BP by decreasing TPR thru direct dilating arterioles( not arteries or veins)

35
Q

hydralazine

A

-Selective arteriolar vasodialators-decrease BP by decreasing TPR thru direct dilating arterioles( not arteries or veins)
-works by releasing NO from endothelium
-high first pass effect with rapid acetylators
-alone- increase hydrostatic pressure in capillaries leading to edema and retention of H2O and Na in the Kidney, also Symp and renal compensation-> massive catecholamine and renin release
SE: tachycardia, edema, and loss of affect, lupus like reaction
-use - effective as “third drug” to diuretics and B blockers

36
Q

minoxidil

A

-Selective arteriolar vasodialators-decrease BP by decreasing TPR thru direct dilating arterioles( not arteries or veins)
-via an active metabolite to open ATP SENSATIVE K CHANNELS in smooth muscle
-alone- increase hydrostatic pressure in capillaries leading to edema and retention of H2O and Na in the Kidney, also Symp and renal compensation-> massive catecholamine and renin release
SE: tachycardia, edema, and loss of affect, hair growth
-use - effective as “third drug” to diuretics and B blockers

37
Q

Ca channel blockers

A

Verampamil- heart specific
DIltiazem- heart specfic
Nifedipine “..DIPINE”- act in arterial tissue
Felodipine
Amlodipine
-most inactivated by liver and all dipines except amlodipine are interfered with by grapefruit juice
-all except first 2 all are dihydropyridines

38
Q

Ace inhibitors

A

”..PRIL”
Captopril
enalapril- prodrug activated to enalaprilat
lisinipril
fosinipril- prodrug, good when used in renal insufficiency pt
quinapril-prodrug
ramipril-prodrug

39
Q

ARBs

Angiotensin II receptor blockers

A

Losartan
Valsartan
Candesartan-prodrug converted in GI tract

40
Q

Renin Inhibitors

A

Aliskiren

inhibits conversion of angiotensinogen to angiotensin 1

41
Q

Nitroglycerin

A

antianginal agent

  • decreases peripheral resistance and thus preload( low doses and Afterload(higher doses)
  • decreases O2 demand of cardiac cells by decreasing cell tension
42
Q

Isosorbide dinitrate

A

antianginal agent

  • decreases peripheral resistance and thus preload( low doses and Afterload(higher doses)
  • decreases O2 demand of cardiac cells by decreasing cell tension
43
Q

ranolazine

A

anti anginal drug
-proposed MOA - shifting of energy production in heart from fatty acids to sugars to reduce O2 demand
- or inhibits late Na channel to reduce calcium overload and reduce O2 demand
-usually used in combo to treat chronic stable angina
SE: dizzy, headache, nausea,constipation, can prolong cardiac QT interval, verapamil can increase affact by increasing abs, diltiazem interferes with its metabolism

44
Q

Ezetimibe

A

Cholesterol abs inhibitor

  • inhibits cholesterol Abs in brush border of small intestine by inhibiting specific protein mediated transport system
  • effect is to decrease LDL in circulation
  • used alone or in combo with statins to treat High LDL type hyperlipidemias
  • enterohepatic recirculation of active metabolite
  • fibrates enhance and BA binding resins decrease availability
  • may raise HDL, unsure effect on VLDL
  • SE: diarrhea, higher risk of increased liver enzymes when used with statins
45
Q

Bile acid binding resins drugs

A

cholestyramine
colestipol
colesevelam

46
Q

cholestyramine

A

Bile acid binding resin
-in intestine exchange Cl- for Bile acids and sequester them from reabs
-overall effect is decreased LDL by Liver taking up more to have cholesterol to synthesize bile acids
-initially increases VLDL( don’t use in high VLDL pts) and may increase HDL
-USE: high LDL hyperlipidemia ,
SE: no systemic toxiciticy, resins can sequester other drugs and nutrients in GI tract and should be taken at separate times, interfere w/ fat soluble vitamins/iron abs

47
Q

colestipol

A

Bile acid binding resin
-in intestine exchange Cl- for Bile acids and sequester them from reabs
-overall effect is decreased LDL by Liver taking up more to have cholesterol to synthesize bile acids
-initially increases VLDL( don’t use in high VLDL pts) and may increase HDL
-USE: high LDL hyperlipidemia ,
SE: no systemic toxiciticy, resins can sequester other drugs and nutrients in GI tract and should be taken at separate times, interfere w/ fat soluble vitamins/iron abs

48
Q

colesevelam

A

Bile acid binding resin
-in intestine exchange Cl- for Bile acids and sequester them from reabs
-overall effect is decreased LDL by Liver taking up more to have cholesterol to synthesize bile acids
-initially increases VLDL( don’t use in high VLDL pts) and may increase HDL
-USE: high LDL hyperlipidemia ,
SE: no systemic toxiciticy, resins can sequester other drugs and nutrients in GI tract and should be taken at separate times, interfere w/ fat soluble vitamins/iron abs

49
Q

Statins

A

HMB CoA reductase inhibitors mainly in the liver-> overall reduction in circulation endogenous cholesterol
-increased LDL receptors in liver and peripheral tissue to decrease LDL in blood
-Most powerful LDL lowering agent(IDL and VLDL also reduced)
- no reduced HDL, slightly increase
SE-increased serum aminotransferase, myopathy can lead to rhabdo ( must monitor creatine kinase levels)
-contraindicate- liver disease and pregnancy and lactation

50
Q

Gemfibrozil

fenofibrate

A

fabric acid analogues
increased clearance of VLDL via increased lipoprotein lipase activity, via increased PPAR-a activity
fenofibrate-increases hepatic LDL R->decreases LDL
both-better at decreasing VLDL and thus triglycerides
-USE- primary high VLDL, secondary hyper lipid due to apolipoprotein E deficit
feno is a prodrug
SE- B: gallstone, GI upset, gemfibrozil- myopathy with statin

51
Q

Phenobarbital

A

first anti seizure drug, barbiturate

  • USE: mono therapy for tonic-clonic seizures and partial seizures, IV for status epilepticus
  • MOA- potentiate of synaptic inhibition via GABAa receptor
  • 40-60% bound, 25% unchanged excrete in urine, rest CYP2C9
  • SE-sedation in adults, irritability in children, induction of CYP3A4 resulting in increased metabolism of oral contraceptives
52
Q

Phenytoin

A

Anti seizure medication
Use-monotherapy for generalized tonic clonic and partial seizures, IV fosphenytoin is prodrug for status epilepticus
-MOA-prolonged rate of recovery of VG Na channels from inactivation
-90% bound in plasma, t1/2 increase with drug concentration, 95% metabolism in liver CYP2C9/10/19
SE: liver enzyme are saturable so other drug interactions ex warfarin
-induction of CYP3A4- ^ drug metabolism(Oral contraceptiv), gingival hyperplasia and SJS

53
Q

Carbamazepine

A

anti seizure drug
USE: mono therapy general tonic clonic and partial seizure
-MOA-prolonged rate of recovery of VG Na channels from inactivation
-metabolized to 10,11 epoxide( just as active), induces own metabolism, 3 wk after initial dose, phenobarbital, phenytoin, valproic acid increase its metabolism
-SE-ACUTE: stupor, coma, hyperirritability, chronic: drowsy, vertigo, ataxia,induction of CYP3A4- ^ drug metabolism(Oral contraceptive)

54
Q

Oxycarbazine

A

anti seizure drug, structurally similar to carbamazepine
USE: monotherapy(4-16yo)/adjunctive therapy for partial seizures
-MOA-prolonged rate of recovery of VG Na channels from inactivation
-is a prodrug and converted to active drug in liver, inactivated by glucuronide conjugation and eliminated by renal, DOES NOT AUTOINDUCE LIKE carbamazepine
-SE- dizzy, nausea, ataxia,induction of CYP3A4- ^ drug metabolism(Oral contraceptive) less than carbamazepine

55
Q

Ethosuximide

A

anti seisure med
USE- mono therapy for partial seizures
MOA- inhibition of T-type Ca channels
-not bound, few interaction, 25% excreted in urine
SE- nausea, vomiting, anorexia, CNS-drowsy, lethargy, euphoria, SJS, aplastic anemia

56
Q

Valproic acid

A

anti seizure drug
Use- mono therapy, absence, myoclonic, partial, tonic clonic seizures, BROAD SPEC AED
MOA- inhibition of T-type Ca channels(main), prolonged rate of recovery of VG Na channels from inactivation, increase GABA synthesis(in vitro)
90% bound, t1/2=15 hours(decreased with other drugs
SE- many- inhibits CYP2C9 so increased concentration of drugs metabolized here, displaces bound phenytoin and lowers IQ in exposed fetuses

57
Q

Gabapentin

A

newer anti seizure drug
adjunctive treatment for partial w/w/o secondary generalzed, main used for neuropathic pain
MOA- unknown
-renal clearance must be determined before giving, excreted unchanged
SE- faigue, ataxia,
Pregambalin- GABA bound to isobutane, anti partial seizure, used in fibromyalgia

58
Q

Lamotrigine

A

newer anti seizure drug BROAD SPEC AED
USE-monotherapy/adjunct for partial, generalized tonic clonic, LGS
MOA-prolonged rate of recovery of VG Na channels from inactivation, inhibit Ca to lesser extent
- t1/2=24-35 hr, other drugs reduce t1/2 to 15hr, reduces valproate
SE-dizzy, ataxia, blurred vision, nausea, SJS when used with other drugs

59
Q

Topiramate

A

newer anti seizure drug BROAD SPEC AED
USE-monotherapy/adjunct for partial, generalized tonic clonic, LGS
MOA- inhibit Na channels and AMPA-kainate receptors, enhance GABA Receptor
little bound 10-20 % and 80% excreted in urine
SE-ataxia, fatigue, weight loss, sleepy, reduces plasma level of oral contraceptives and estradiol

60
Q

Levetiracetam

A

Use – Adjunctive treatment for partial- and tonic/clonic seizures in adults and myoclonic seizures in children; IV preparation for status epilepticus
2. Mechanism of Action – unknown; may prevent presynaptic glutamate release
3. Pharmacokinetics –65% excreted unchanged in urine, no liver enzyme induction, highest safety margin in animal studies, rapid dose titration making this drug useful for adjunctive therapy. FDA approved 3-D “printed” pill in
2015.
4. Side effects – somnolence, dizziness, asthenia , no drug-drug interactions

61
Q

Isolated Familial hyperchylomicronemias

A

↑↑ chylomicron (↑↑ TG)

62
Q

Isolated Familial hypercholesterolemias

A

↑↑ LDL
(↑↑ cholesterol)
BABR

63
Q

Mixed Familial hyperlipoproteinemias

A

↑↑ VLDL, ↑↑ LDL * (↑↑ TG ,↑↑ cholesterol)

64
Q

Familial dysbetalipoproteinemias

A

↑IDL,↑LDL
(↑ TG, ↑ cholesterol)
BABR

65
Q

Isolated Familial hypertriglyceridemias

A

↑↑ VLDL

↑↑ TG, ↑ or normal cholesterol

66
Q

Mixed Familial hypertriglyceridemias

A

↑↑ chylomicron, ↑↑ VLDL (↑↑ TG, ↑ or normal cholesterol)

67
Q

prodrug statins

A

lovastatin
simvastatin
require activation in the liver before active
HMG CoA reductase inhibitors
SE-increased serum aminotransferase, myopathy can lead to rhabdo ( must monitor creatine kinase levels)
-contraindicate- liver disease and pregnancy and lactation

68
Q

active as ingested statins

A

pravastatin
atorvastatin
rosuvastatin
-HMG CoA reductase inhibitors
SE-increased serum aminotransferase, myopathy can lead to rhabdo ( must monitor creatine kinase levels)
-contraindicate- liver disease and pregnancy and lactation

69
Q

Niacin

A

inhibits intracellular lypolysis in fat cells by inhibiting Hormone sensitive lipase

  • reduced VLDLs by depleting the liver of Fatty acids needed to make triglycerides
  • lower VLDL -> lower IDL and LDL in plasma
  • increases extract lipoprotein lipase to further reduce VLDL
  • decreases lipoprotien(a)(major component of LDL) and INCREASES HDL VIA DECREASE CLEARANCE OF HDL APOLIPOPROTEIN A-1
  • use- all primary type hyperlipidemias, HDL deficiency
  • short duration, metabolized to inactive vitamin nicotimamide
70
Q

niacin SE

A

flushing itching or burning feeling of skin
PG mediated and relieved by taking aspirin 30 min before taking drug
some hypoTN in those on antiHTN drugs
- increase liver enzyme
-mild hyper glycemia and glucose intolerance in diabetics
-GI disturbance and peptic ulcers
-nonspecific renal affects- elevated uric acid

71
Q

Omega 3 Acid ethyl esters

A

inhibit synthesis of triglycerides in liver ->decreased VLDL
MOA-1. increased B oxidation of eFFA 2. deceased delivery of EFFA to liver 3. decreased synthesis of eFFA 4. decreased synthesis triglyceride synthesizing enzyme
slightly increased HDL, NO AFFECT ON LDL
USE: combination with statins to treat high LDL and VLDL w/o increased risk of myopathy as with vibrate combination

72
Q

Mipomersen

A

decreases VLDL and LDL by inhibiting formation of apolipoprotein B in GI and liver
oligoneucleotide type inhibitor
-USE- combination w/ others to treat HOMOZYGOUS familial hypercholemia
-given SUB Q
SE-serious liver toxicity

73
Q

Lomitapide

A

decreases VLDL and LDL by inhibiting formation of apolipoprotein B in GI and liver
microsomal triglyceride transfer protein(MTP) type inhibitor
-USE- combination w/ others to treat HOMOZYGOUS familial hypercholemia
- oral med
SE-serious liver toxicity

74
Q

Alirocumab

A

monoclonal antibody that thru PCSK9 decreases LDL R degradation and increases recirculation to liver cell surface to decrease LDL

  • USE-statin intolerant patients, pts with athelerosclerosis who need additional lowering of LDL that other drugs cannot achieve
  • SUB Q injection
  • SE- nonspecific GI, metabolic and neurocognitive rxns
75
Q

Evolocumab

A

monoclonal antibody that thru PCSK9 decreases LDL R degradation and increases recirculation to liver cell surface to decrease LDL

  • USE-statin intolerant patients, pts with athelerosclerosis who need additional lowering of LDL that other drugs cannot achieve
  • SUB Q injection
  • SE- nonspecific GI, metabolic and neurocognitive rxns
76
Q

rapid acting insulins

A
  • regular insulin- only IV usable form of the drug
  • Insulin aspartate- B28 proline replaced with aspartate
  • insulin glulisine- B3 arg replaced with Lys and B29 lysine replaced with glutamic acid
  • insulin lispro- reversed Pro-Lys at B28-29
77
Q

intermediate actin insulin

A

NPH insulin
insulin suspended in zinc and protamine to prolong action
variable length of action based on abs

78
Q

long acting insulin preps

A
  • insulin glargine- Asp at A21 replaced by glycine and 2 Arg added to C terminus
  • insulin detemir- Threonine at B30 omitted and a C14 fatty acid chain is added at B29, binding to albumin in serum and self association
79
Q

Metformin

A

Biguanide- first line Diabetic drug for Type 2
-MOA prevents hyperglycemia but no hypoglycemia thru reduction in hepatic gluconeogenesis thru activation of AMPK in hepatocytes
- not bound and t1/2 =3hr, excreted unchanged in urine
-SE- Gi discomfort, Lactic acidosis( rare but serious)
contraindicated- EtOHism, renal insuffiency, hepatic disease, hypoxic pulmonary disease

Pharmacology drew (9 decks)

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