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Pharmacology drew > Winter 2 > Flashcards

Winter 2 Flashcards

1
Q

Sulfonylureas drugs

A

-Glyburude, glipizide, glimepiride

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2
Q

hydralazine

A
  • Selective arteriolar vasodialators
  • decrease BP by decreasing TPR thru direct dilating arterioles( not arteries or veins)
  • PRIMARY AFTERLOAD REDUCTION IN CHF -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

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3
Q

Lidocaine

A

Class 1B anti arrhythmic drugs

  • Rapidly interact with Phase 0 Na channels, shortens phase 3( decreasing AP duration and ERP due to inhibition of late Na channels open in the plateau -USE- emergent treatment of Vent arrhythmias during MI/ ischemia
  • suppress vent arhtyhm via decrese slope of phase 4 and increase threshold, abolish reentry arrhythmias, stop TdP b/c down APD
  • IV only -SE-drowsyness , slurred speech, confusion, arrhythmias in presence of Hyper K
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4
Q

fifth generation Cephalosporins

A

Ceftaroline-Parenteral

  • increased binding to PBP 2a–> used to treat MRSA
  • CAP- s. pneumo, S aureus(metacillin resistant only), h flu, kleb pneumo, e coli
  • Acute skin infections- MRSA
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5
Q

Exenatide

A

GLP-1 agonist BID sub Q injection b4 meals

  • rapidly absorbed after injection and peak action in 2 hours, little metabolism and excrete via kidney Bind to GLP-1 R in pancreatinc B cells and increase insulin synthesis and secretion in glucose dependent manner
  • delay gastric emptying and decrease apatite - decrease the release of post prandial glucagon( mech unknown)
  • antagonize glucagon and increase affect of insulin
  • SE- GI disturbance, nausea at start of therapy, weight loss, hypo glycemic when combined w. sulfonylurea, pancreatitis( rare but serious), delay in gastric empty can alter other drugs

contra- pancreatitis history,

USE- mono or combination therapy for DM2

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6
Q

Procainamide

A

Class 1A anti arrhythmic drugs -blocks Na channels to decrease slope of phase 0 and blocks K channels(metabolite) to prolonge Action potential duration and Effective refractory period

  • USA IV only, acetylated in the liver to NAPA->K channel effects, NAPA eliminated via kidney
  • SE-lupus syndrome, confusion (CNS effect), GI intolerance, less a block/atropine effect, V arrhythmias but less TdP than quinidine
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7
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 NEW- -SE-GI disturbance, increase triglycerides, contra- hypertriglyceridemia, pancreatitis history, esophageal/ GI disorders, - treat DM2, taken BID

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8
Q

Amylin Analogues

A

Pramlitide

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9
Q

Cefixime

A

third generation Cephalosporins, oral 2nd line N gonorrhea

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10
Q

thiazolidinediones drugs

A

pioglitazone rosiglitazone

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11
Q

excretion of penicillins

A

10% Glomerular filtration, 90% tubular secretion - dose modification for renal function -exception: Naficillin- biliary excretion, oxacillin and dicoxacillin by both renal and biliary( no dose adjustment for renal function w/ these drugs)

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12
Q

carvedilol

A

antioxidant, alpha blocker and B blocker

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13
Q

Treatment go Digitalis toxicity

A

-discontine or reduce dose -discontinue or reduce diuretics of K gets too low( many pts have high RAAS-> decreased K and that ^ neg effects of digoxin) -above don’t work then administer KCl - administer Digoxin Abs in life threatening tox or sever HYPER K due to masive inhibition of Na/K ATPase - Lidocaine and propanolol- rapidly counteract dig toxicity arrhythmia

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14
Q

MOA of penicillins

A
  • inhibition of cell wall synthesis -B lactam ABx inhibit the transpeptidase enzyme and the production of a highly cross linked peptidoglycan cell wall - only effect actively dividing cells that are producing cell walls - binding to penicillin binding proteins -activation of cell wall autolytic enzymes, autolysin - use in combinatinon with aminoglycosides
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15
Q

nesiritide

A

vasodialator and diuretic only given IV

decreases arterial and venous smooth muscle tone via increaseing [cGMP]i

-diuretic action from its natural ability to act as a natriuretic peptide

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16
Q

Glyburide

A

Sulfonylureas insulin secretagogues -require functioning Beta cells–> only intreating early Type 2 diabetes, T1/2=10 hrs -Bind to K ATP channel on B cells and inhibit their activity causing depolarization-> influx of calcium-> insulin release -highly bound, metabolized in liver and secreted in urine -SE- HYpoglycemia, Weight gain, sulfur allergy -contra- hepatic impairment, renal insufficiency, pregnant and brest feeding -clinical use- type 2DM, BID, lose efficacy as B cell function decreases, and can be combined w/ metformin and thiazolidinediones

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17
Q

Antipseudomonal Penicillins

A

Ticarcillin + Clavulanate potassium

Piperacillin + Tazobactam

tilcarcillin- used in pseudoonas and mixed anaerobic aerobic infections caused by bacteroides(metronidazole prefered)

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18
Q

Penicillin V

A

more stable under acidic conditions therefore better GI absorption - less active than PenicillinG- only used for moderate infections

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19
Q

Nitroglycerin

A

antianginal agent

  • PRIAMARY PREOAD REDUCTION IN CHF
  • decreases peripheral resistance and thus preload( low doses and Afterload(higher doses)
  • decreases O2 demand of cardiac cells by decreasing cell tension
  • long term therapy an lead to tolerance
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20
Q

AceButolol

A

Class II anti arrhythmia drugs

  • B adrenergic blocker
  • B1 selective blocker, reduces risk of bronchospasm -Partial Agonist (ISA)

diminish phase 4 depolarization, depressing automaticity, especially in nodal tissues

  • treat arrhythms cause by too much symp activity
  • careful in use w/ Ca channel blockers b/c together can too much depress normal cardiac function
  • Membrane stabilizing
  • low lipid solubility ?
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21
Q

Ceftriaxone

A

third generation Cephalosporins,

  • Parenteral first line N gonnorrhoeae
  • neuro complication from lyme disease
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22
Q

macrolides

A

Erythromycin, and semisynthetic derivatives clarithromycin, azithromycin

  • broken down by acid, poor abs with food, esters of the base made to increase Abs
  • wide distribution except to CNS, can cross placenta and in breast milk, avoid use in liver disease

MOA- bacteriostatic by reversible binding to the 50S subunit to inhibit protein synthesis, similar binding site to chloramphenicol-> they have antagonistic effects on eachother

-resistance- breakdown by bacterial esterases, MODIFICATION OF THE 50S BINDING SITE or methylase enzyme that binds to prevent drug from binding

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23
Q

DPP-4 inhibitors

A

sitagliptin

  • DPP-4 is an enzyme that degrades incretin hormones, taken 1x/day
  • increase the circulating levels of GLP-1 and GIP thus increasing post prandial insulin and decreased glucagon level
  • other drugs- saxagliptin, linagliptin, alogliptin
  • high oral availability, inhibit DPP-4 for 12 hours -saxagliptin is a prodrug

SE- increased rate of infection, headache, hypoglycemia when given with other drugs, pancreatitis, hypersensitivity rxn

use-mono/combination therapy for DM2

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24
Q

Piperacillin + Tazobactam

A

Ureidopenicillins, Antipseudomonal Penicillins

  • piperacillin is B lactamase sensative and tazobactam is given with it to stop this
  • broader spectrum of action than carbenicillin and ticarcillin, esp in G- aerobic bacilli and mixed infections
  • Use- CAP, HAP w/ fluoroquinolone, septicemia from G- bac, UTI in hospitilized(w/aminogylcoside), OB infections, intraabdominal infections,
  • less sodium than ticarcillin –> better for CHF pts, less prolonging of bleeding time
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25
Q

Digoxin use and toxicities

A
  • slow oral route for non emergent cases, fast IV for emergent cases
  • can be anti arrhythmic, protect vent rate in Afib and flutter - given w/ loading dose first of just maintenance doses( this way safer) TOX-LOW MARGIN OF SAFTY

GI- anorexia, nausea, vomiting, dhrea

CV-every known type of arrthymia( V fib and Vtach are most serious)

CNS- mental disoreintations( digitalis dilerium)

Vision- blurred , white border/halos on objects

  • sudden increase in plasma Ca can induce arrthymia in these patients
  • use with k wasting drugs will ^ risk of neg side effects(K is an antidote for dig tox)
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26
Q

Bromocriptine

A

dopamine agonist

MOA- increase insulin sensativity

reset circadian rhythm to help with insulin resistance

met by the liver, wuick release, first pass met

SE-hypoTN, faint, dizzy, hypo glycemia when w/ sulfonureas

-USE- DM2 adjunct/monotherapy

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27
Q

Class II anti arrhythmia drugs

A

Propanolol Acebutolol Esmolol

diminish phase 4 depolarization, depressing automaticity, especially in nodal tissues

  • treat arrhythms cause by too much symp activity
  • careful in use w/ Ca channel blockers b/c together can too much depress normal cardiac function
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28
Q

Class III anti arrhythmia drugs

A

Amiodarone

Dofetilide

  • inhibit the outflowing K channel and prolong the repolarization, causing longer APD and ERP,
  • no affect on other AP phases
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29
Q

Imipenem + Cilastatin

A

Carbapenems, B Lactam Abx

  • not orally absorbed, broken down in kidney by dehydropeptidase so cilastatin is added to inhibit this
  • renal excretion and dose adjustment for renal impairment, resistant to breakdown by most B lactamases
  • inhibits >90% of clinically important bacteria, ^ permeability in G-, resistant to B lactamase, ^ affinity for PBP
  • use only in the worst infections in hospitals, ex: Pseudmonas resistant to all others ( combo w/ aminoglycoside)
  • causes induction of B Lactamases to decrease effectivity of other B Lactam ABx,
  • tox-can cause seizures, NV, allergic rxn -finish this
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30
Q

Digoxin Immune Fab

A

antigen binding fragments that bind digoxin and the resulting Fab-Fragment-Dititalis complex is excreted int the urine -used in Digoxin toxicity

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31
Q

Bacterial resistance to penicillins

A
  • structural differences in PBPs -inibality of penicillin to penetrate to site of action, ex G+ have action near surface where G- have to diffuse thru outermembrane thru morons and many penicillins cannot, eflux pumps ex:pseudomonas lacks high permeability porins, p. aeruginosa, e. coli, N. gonorrhea have active eflux pumps
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32
Q

Cephalosporin MOA

A

interfere w/ bacterial cell wall synthesis- B lactam ring - split B lactam ring destroy activity

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33
Q

Digoxin

A

Digitalis glycoside -increase myocardial contraction and decrease heart rate

  • MOA- ^ contractility- inhibits surface bound Na/K ATPase -> increasing intracell Na-> reversal of Na/Ca symporter-> increased [Ca]i and increased force of contraction b/c of Ca
  • inotropic effects- ^ CO(quickly), diuresis (eventually and not direct effect), some SNS reversal
  • MOA- decreased HR-VAGAL and EXTRAVAGAL( at dangerous high doses)
  • interactions- phenylbutazone, phenobarbital and phenytoin, Quinidine, antacids, sulfasalazine, bile acid binding resins
  • renal diseaseand hypothyroidism ^ t1/2
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34
Q

Cefoxitin

A

second generation Cephalosporins - activity against B. fragilis

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35
Q

Dofetilide

A

Class III anti arrhythmia drugs

  • inhibit the outflowing K channel and prolong the repolarization, causing longer APD and ERP, pure class 3
  • USE-SV arrhythmias, corrected via suppress reentry phenomena, very good for A FIB
  • iv and oral
  • TOX- ventriculat TdP especially in high IV doses
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36
Q

repaglinide

A

Meglitinides, insulin secretagogues, REPAGLINIDE, nateglinide MOA-require functioning Beta cells–> only intreating early Type 2 diabetes, -Bind to K ATP channel on B cells and inhibit their activity causing depolarization-> influx of calcium-> insulin release - quickly absorbed, highly bound, met in liver -Hypoglycemia( less frequent w/ nateglinide) -contra- hepatic impairment, renal insufficiency USE- DM type 2, quicker acting so more preprandial dosing, can be used in sulfer allergies, mono therapy or w/ metformin

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37
Q

thiazolidinediones

A

increase insulin sensitivity in target tissues -PPARgamma agonists - increased sensitivity to insulin stimulate uptake of glossy and fatty acids, alters adipokine production - increased sensitivity in liver and muscle too -long term lower Triglyceride and slight increase HDL and LDL -highly bound, long t1/2 and met in liver -SE-weight gain and edema(most important) osteoporosis and fracture in women, increased risk of CHF, contra- preg, hepatic inpairment( freq LFT needed), heart failure

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38
Q

third generation Cephalosporins

A

Ceftriaxone -Parenteral (longest t.5=8hrs) biliary secretion-> no dose adjust in renal DS

Cefixime- oral

Cefotaxime-Parenteral

Ceftazidime -Parenteral, good 4 pseudomonas

more G- than 2nd gen- B lactamase resistant lessG+ than 1st gen -useful- G- rods resistant to other ceph, pen and aminoglycosides ABx

-DONT USE w/ enterobacter( makes Chromosoaml B lactamase) - CNS for meningitis- empirical for sepsis

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39
Q

Class 1 anti arrhythmic drugs

A

1A- Quinidine and Procainamide 1B- Lidocaine( Xylocaine) 1C- Flecainide -block mainly Na channels - Quinidine and active metabolite of procainamide also blocks K channels - Use dependent- preferentially block channels in tissues that are abnormally firing high rate - inhibit Na channels in phase 4 and 0 to slow rate of rise of phase 0(1C>1A>1B) - increase the threshold for excitability

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40
Q

Canagliflozin

A

SLGT2 inhibitors -inhibits glucose reabs in the proximal tubule -> decrease blood glucose and increase Glucose in urine - High oral availability, peak at 1-2 hours T1/2=10-13 -SE- Genital mycotic infections, UTI, diuretic effect, CANAgliflozin increases serum digoxin, dapagliflozin increased risk of bladder cancer contra- sever renal impairment USE- mono and adjunct therapy for Dm2, 1x/day before first meal

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41
Q

penicillinase resistant penicillins

A

methicillin naficillin(IVprefered) oxacillin

IV usage for serious systemic Staph infections

  • relatively resistant to B-lactamases b/c of bulkier side chains -naficillin is most resistant

naficillin-biliary excretion, oxacillin- biliary and renal, no dose adjustment in renal disease

  • these are less active than Penicillin G, use dropped sue to MRSA
  • USES- G+ cocci B lacatamase producers-S aureus,( skin infecions, osteomyolitis, acute endocarditis
  • not effective to G- aerobes(e coli, kleb, enterbacter)
  • methicillin- type 4 interstitial nephritis- use vanco to treat MRSA in hospital
42
Q

Esmolol

A

Class II anti arrhythmia drugs -B 1 adrenergic blocker Not partial Agonist Not Membrane stabilizing Low Lipid Soluble rapid action, rapid broken down by plasma esterase’s - acute arrhythmias during surgeries

43
Q

Magnesium

A

treatment of TdP, unknown MOA

44
Q

GLP-1 agonist

A

Exenatide( short acting) liraglutide(longer acting abiglutide( longer acting) -incretins are GI hormones secreted after a meal that augment insulin release from B cells -GLP-1 is an incretin, GLP-1 agonists are used to treat DM 2 Bind to GLP-1 R in pancreatinc B cells and increase insulin synthesis and secretion in glucose dependent manner - delay gastric emptying and decrease apatite - decrease the release of post prandial glucagon( mech unknown)

45
Q

ARBs, Angiotensin II receptor blockers

A

Losartan Valsartan Candesartan-prodrug converted in GI tract provide better treatment of CHF b/c they also block the locally produced AII in the heart and reduce the Hypertrophy from the AII

46
Q

Ceftazidime

A

third generation Cephalosporins -Parenteral Pseudomonal coverage

47
Q

Diltiazem

A

Class IV anti arrhythmia drugs, Ca channel blocker - deceases L type Ca channels activity to decrease the slope of phase 0 and 4- slowing conduct velocity and automaticity -mainly in the AV node, increase APD and ERP -USE- better at rhythms that must pass the AV node, SVT>VT, yet good at stopping DADs, reentry SVT and protecting normal Vent rate during aFIB and flutter -IF GIVEN IV MAY MAKE ARRHYTHMIAS WORSE WHEN WPW W/ A FIB -iv and oral, met in liver( careful w/ liver disfunction) -TOX- decreased normal sinus rate and AV conduction, negative intrepid effect, avoid combo w/ B Blockers

48
Q

Cefuroxime oral Cefuroxime IV

A

second generation Cephalosporins -sinusitis, otitis media bugs(S. pnumo, Hflu, moraxella, s. pyogenes) -useful in CAP- H Flu, S. pneumo, K pneumo)

49
Q

thiazolidinediones uses

A

treatment of DM type 2 taken once a day -Nuclear receptor agonist so they take time before you se any affect, 1-3 months -monotherapy or conjunction w/ metformin, sulfonylureas, or insulin

50
Q

Ace inhibitors drugs

A

”..PRIL”

Captopril

enalapril- prodrug activated to enalaprilat

lisinipril

fosinipril- prodrug, good when used in renal insufficiency pt

quinapril-prodrug

ramipril-prodrug

51
Q

amoxcillin

A

extended spectrum penicillins better oral absorption\

  • food doesn’t interfere with abs -suseptible to B-lactamase enzymes produced by G+and G- BUGs so paired with B lactamase inhibitors- clavulanate+ amoxcillin=augmentin
  • HELPSS ME spectrum of action
  • amox causes less diarrhea than ampicillin, decrease effectiveness w/ real contraceptive
  • amox and ampicillin can cause non allergic skin rash-1-28 days later
52
Q

cefazolin

A

first generation Cephalosporins-parenteral

  • drug of choice for pre surgery prophylaxis
  • alternate for staph and strep in pts w/penicillin allergy
  • sensative to B lactamase
53
Q

bisprolol

A

B blocker

54
Q

Glucagon

A

emergency treatment of severe hypoglycemia via sim of breakdown of hepatic glycogen stores

  • treatment of overdose of B-adrenoreceptor blocker
  • binds G protein coupled Receptors-> stim adenylate cyclase–> increased cAMP
  • stim gluconeogenesis and ketogenesis

SE- transient NV, intropic effect–> transient tachycardia and HTN

55
Q

toxic effects of tetracyclines

A
  • GI side effects-NV
  • superinfections- via disrupting normal flora from candidia or drug resistant BActeria, ex: C dif
  • bones and teeth- binds to calcium and complex deposited in teeth and bone-> yellow teeth and bone deformity, dont use in preg and children under 8
  • renal tubular acidosis and damage
  • light sensativity
56
Q

Cefprozi

A

second generation -sinusitis, otitis media bugs(S. pnumo, Hflu, moraxella, s. pyogenes)

57
Q

NITROPRUSSIDE

A

antianginal agent only given IV

  • PRIAMARY PREOAD and afterload REDUCTION IN CHF
  • decreases peripheral resistance and thus preload( low doses and Afterload(higher doses)
  • decreases O2 demand of cardiac cells by decreasing cell tension
58
Q

ACE inhibitors actions

A

inhibits ACE-> decreased AII in the blood and a reduced vaso constrict effect and reduced aldosterone-> decreased preload and afterload

  • ^CO and decreased pulm and peripheral congestion
  • SE- nonproductive cough
  • too much reduction in arterial BP may occur when in combination use with other antihypertensives or diuretics
  • reduce AII production in the heart that contributes to hypertrophy in CHF
59
Q

dopamine

A

B1 adrenergic agonist -endogenous catecholamine only given IV for severe, refractory CHF -causes increased cardiac output mainly by increased ventricular B1 R action ( positive intrepid effect, increases HR and O2 demand more than dobutamine -low to intermediate dose can increase renal Blood flow -> increased Na and H20 excretion -tolerance can develop - out of favor b/c of side effects( tach, ^ O2 demand and arrhythmia)

60
Q

clarithromycin

azithromycin

telithromycin

A

macrolide antibiotics that bind to and inhibit the 50S subunit in bacterial, different side groups give each different activity

-be sure to look this stuff up dummy

61
Q

Meglitinides

A

insulin secretagogues, REPAGLINIDE, nateglinide MOA-require functioning Beta cells–> only intreating early Type 2 diabetes,

  • Bind to K ATP channel on B cells and inhibit their activity causing depolarization-> influx of calcium-> insulin release
  • quickly absorbed, highly bound, met in liver -Hypoglycemia( less frequent w/ nateglinide)
  • contra- hepatic impairment, renal insufficiency USE- DM type 2, quicker acting so more preprandial dosing can be used in sulfer allergies, mono therapy or w/ metformin
62
Q

Amiodarone

A

Class III anti arrhythmia drugs

  • inhibit the outflowing K channel and prolong the repolarization, causing longer APD and ERP does show some class 1, 2 and 4 activity, can cause TdP SE
  • decrease conduct velocity via decreased cell-cell coupling
  • USE-severe and refractory SVT and VT, also decreases amount of time ICD must fire, LIMITED by toxicities
  • IV and incomplete oral ABS, concentrated in tissues w/ long half life( weeks), long time to make effect, similar structure to thyroxine
  • TOX- interstitial pulm fibrosis, dizzy, hyper or hypothyroid, blue skin discoloration(I in skin), TdP
63
Q

Cefaclor

A

second generation Cephalosporins

  • sinusitis, otitis media bugs(S. pnumo, Hflu, moraxella, s. pyogenes)
  • B lactamase sensative
64
Q

rosiglitazone

A

increase insulin sensitivity in target tissues -PPARgamma agonists - increased sensitivity to insulin stimulate uptake of glossy and fatty acids, alters adipokine production - increased sensitivity in liver and muscle too -long term lower Triglyceride and slight increase HDL and LDL -highly bound, long t1/2 and met in liver -SE-weight gain and edema(most important) osteoporosis and fracture in women, increased risk of CHF, contra- preg, hepatic inpairment( freq LFT needed), heart failure -treatment of DM type 2 -taken once a day -Nuclear receptor agonist so they take time before you se any affect, 1-3 months -monotherapy or conjunction w/ metformin, sulfonylureas, or insulin

65
Q

isosorbide dinitrate

A

antianginal agent

  • PRIAMARY PREOAD REDUCTION IN CHF
  • decreases peripheral resistance and thus preload( low doses and Afterload(higher doses)
  • decreases O2 demand of cardiac cells by decreasing cell tension
  • long term therapy an lead to tolerance
66
Q

Penicillin G Benzathine

A
  • provide slow release from the injection area allowing low persistent concentration of the drugs
  • IM in gluteus maximus -1.2 mil units = 26 day activity
  • has local anesthetic efffecs
  • Strep pharengitis, prophylaxis for Reumatic fever, syphillis -
67
Q

SLGT2 inhibitors

A

Canagliflozin and other ..”gliflozin -inhibits glucose reabs in the proximal tubule -> decrease blood glucose and increase Glucose in urine - High oral availability, peak at 1-2 hours T1/2=10-13 -SE- Genital mycotic infections, UTI, diuretic effect, CANAgliflozin increases serum digoxin, dapagliflozin increased risk of bladder cancer contra- sever renal impairment USE- mono and adjunct therapy for Dm2, 1x/day before first meal

68
Q

Inamrinone

A

Phosphodiesterase inhibitor

  • non-glycoside , non- catecholamine positive intrepid drug, a bipyrine
  • USE- IV only for treatment of severe refractory CHF or after tolerance to other B agonists develops
  • MOA-Phosphodiesterase inihibitor-> increased cAMP->increased free Ca availability for contractual proteins in systole
  • also improves relaxation via more Ca uptake during diastole - little tolerance develops peripheral vasodilator actions
  • tox-THROMBOCYTOPENIA, increased O2 demand( can be fatal in ischemic heart disease
69
Q

cephalexin

A

first generation Cephalosporins- oral -for UTI, minor staph, minor polymicrob lesion

70
Q

Dobutamine

A

B1 adrenergic agonist -synthetic catecholamine only given IV for severe, refractory CHF -causes increased cardiac output mainly by increased ventricular B1 R action ( positive intropic effect -SE- can cause some tach and increase cardiac O2 demand and arrhythmia ( not as much as other B agonists) - tolerance can develop to to down reg of B1 Receptors

71
Q

Augmentin

A

Amoxcillin plus clavulanic acid

USE- Resp tract infections- otitis media and sinusitis, UTI-e coli, klebsiella, enterobacter, skin/skin structures- human and animal bites, gonorrhea

72
Q

Flecainide

A

Class 1C anti arrhythmic drugs

  • interacts more slowly w/ phase 0 Na channels more than other class 1 drugs
  • marked depression of phase 0 slope in Na dependent myocardial fibers
  • inhibits some K channels and also blocks late opening Na channel-> no net effect on action potential duration or ERP
  • increases threshold for phase 0
  • USE- reserved for severe arrthymia resistant to other drugs -well absorbed, minimal biotransformation
  • SE-negative intrepid effects aggravate CHF,, dizzy nausea, headache, blurry vision, aggravate arrhythmias/ induce Vtach aggravated by hyper K
73
Q

Penicillin G Procaine

A
  • provide slow release from the injection area allowing low persistent concentration of the drugs
  • IM in gluteus maximus -600,000 units = several day activity
  • has local anesthetic efffecs S. pyogenes (GAS)
  • SE- bad taste, dizzy palpation, auditory/visual disturbance
74
Q

metoprolol

A

B blocker

75
Q

Tolvaptan

A

Vasopressin antagonist V-2 receptor antagonist for oral treatment of hyponatremia from increased vasopressin activity

  • no reduction in mortality in CHF pt
  • useful intreating SIADH
76
Q

tetracycline

A

broad spectrum bacteriostatic agent to inhibit protein synthesis by binding to the 30S subunit of ribosomes, and blocking amino acyl T-RNA to Bind and add AA

  • excreted via renal filter(10-50%), in bile
  • resistance- increased efflux pumps, Tet(AE) conver resistance to G- to tetra, doxy and minocycline, production of protein to prevent binding to 30S tet(M) ,enzymatic inactivation
  • USE-not 1st choice for G+, G- aerobes, or anaerobes
  • drugs of choice for- spirochetes(Lyme Ds), clamidia, Rickettsiae(RMSF)(DOXY), Mycoplasm pneumo, brucella, H pylori, peridontitis
77
Q

Ticarcillin + Clavulanate potassium

A

carboxypenicillin -Antipseudomonal Penicillins

  • ticarcillin is B-lastamase sensative so adm w/ clavulanate K
  • better anti pseudomonal than older drugs, extended spectrum for infection by G- aerobic rods, and mixed aerobic/anaerobic infections
  • tox-excess Na in dosage forms, can prolong bleeding time
78
Q

first generation Cephalosporins

A

cefazolin- parenteral

cephalexin-oral

poor entry to CNS- not 4 meningitis

  • good for G+ and modest for some G-, -G+ except MRSA and S. epidermis,enterococci, PECK(G- enterics), oral cavity anaerobs( except b fragilis)
  • cefazolin drug of choice for pre surgery prophylaxis
  • alternate for staph and strep in pts w/penicillin allergy oral form–for UTI, minor staph, minor polymicrob lesion,
  • B lactamase sensative
79
Q

sitagliptin

A

DPP-4 inhibitors, prodrug metabolize by CYP3A4/5 -DPP-4 is an enzyme that degrades incretin hormones, taken 1x/day -increase the circulating levels of GLP-1 and GIP thus increasing post prandial insulin and decreased glucagon level -other drugs- saxagliptin, linagliptin, alogliptin -high oral availability, inhibit DPP-4 for 12 hours -saxagliptin is a prodrug SE- increased rate of infection, headache, hypoglycemia when given with other drugs, pancreatitis, hypersensitivity run - reduce dose with CYP3A4/5 inhibitors use-mono/combination therapy for DM2

80
Q

Adenosine

A

class IV anti arrhythmia drug

  • decreases conduct velocity and decreases abnormal impulse formation in the AV node via inhibit Ca influx by activating ACh sensitive phase 4 K current( cause hyper polarization) prolongues AV node refractory period
  • USE_ drug of choice for PSVT of AV and WPW origin
  • low TOX,- apprehension, fear of doom, sob , flushing, and chest pain - 15s duration of action
81
Q

Pramlitide

A

Amylin Analogue -MOA- acts in hindbrain to suppress glucagon, delay gastric emptying, and promote satiety - SUB Q injection, not high bound and excrete in kidney SE- hypoglycemia, Nausea, weight loss contra- gastroparesis or GI motility disorders -USE- treatment of DM 1 and 2 as an adjunct to insulin, preprandial injection separate from insulin, mealtime glucose can be reduced by 50 %

82
Q

fourth generation Cephalosporins

A

Cefepime-Parenteral

extend spectrum conpaired to third gen -Plasmid and chromosomal B lactamamse resistant

–UTI, skin/soft tissue, pneumo, complicated intra AB

  • treat G- bugs resistant to 3rd gen- pseudomonas/ some enterobacteriaceae
  • use-more useful in enterobacter, Penicillin resistant Strep
  • penetrates CNS well to treat meningitis
83
Q

Aztreonam

A

monobactam b/c only has monocyclic bantam ring

  • highly resistant to B lactase produced by G- bac, poor orally, parenteral, excrete renally, t.5=1-2hr
  • only effective against G- rods,
  • use- in G- infections w/ pt w/ history of B lactam sensitivity, if G+ also present another ABX NEEDS TO BE ADDED
  • renal excretion and dose adjustment for renal impairment
84
Q

Quinidine

A

Class 1A anti arrhythmic drugs

  • blocks Na channels to decrease slope of phase 0 and blocks K channels to prolonge Action potential duration and Effective refractory period
  • USE-limited by side effects, maintain normal rhythm after A fib(Less now in USA), V fib of brugada syndrome, A fib of pts w/short QT
  • IV and oral forms
  • SE-other arrhythmias TdP due to prolonged QT, nausea vomit, Dhrea, alpha blocking action and atropine like effect -> decreased BP and ^ sinus rate, ^ digoxin levels
85
Q

milrinone

A

Phosphodiesterase inhibitor

  • non-glycoside , non- catecholamine positive intrepid drug, a bipyrine
  • USE- IV only for treatment of severe refractory CHF or after tolerance to other B agonists develops
  • MOA-Phosphodiesterase inihibitor-> increased cAMP->increased free Ca availability for contractual proteins in systole - also improves relaxation via more Ca uptake during diastole
  • little tolerance develops peripheral vasodilator actions
  • tox-increased O2 demand( can be fatal in ischemic heart disease
86
Q

Penicillin G

A

natural penicillin, oral arm only 33% absorbed gastric acid destroys this and food interferes w/ abs, K and Na salts of Penicillin G given for parenteral use

  • adm w/ aminoglycosides to enhance effect, probenecid increases plasma levels
  • effective for G+ and G- aerobic cocci, most sprocetes, some G+ aerobic and anaerobic bacilli non resistent Staph and strep
  • sensative staph and strep, pneumococal pneumo( use macrolide until sensative test), pneumococal meningitis, strep thraot, spirochete - syphillis, actinomyces israelii

add more drugs from p13

87
Q

Verampamil

A

Class IV anti arrhythmia drugs, Ca channel blocker - deceases L type Ca channels activity to decrease the slope of phase 0 and 4- slowing conduct velocity and automaticity

  • mainly in the AV node, increase APD and ERP
  • USE- better at rhythms that must pass the AV node, SVT>VT, yet good at stopping DADs, reentry SVT and protecting normal Vent rate during aFIB and flutter
  • IF GIVEN IV MAY MAKE ARRHYTHMIAS WORSE WHEN WPW W/ A FIB
  • iv and oral, met in liver( careful w/ liver disfunction)
  • TOX- decreased normal sinus rate and AV conduction, negative intrepid effect, avoid combo w/ B Blockers
88
Q

Liraglutide

A

GLP-1 agonist once per day sub Q -slowly absorbed after injection and peak action in 8-12 hours after injection, highly bound to plasma proteins -Bind to GLP-1 R in pancreatinc B cells and increase insulin synthesis and secretion in glucose dependent manner - delay gastric emptying and decrease apatite - decrease the release of post prandial glucagon( mech unknown) -antagonize glucagon and increase affect of insulin -SE- GI disturbance, nausea at start of therapy, weight loss, hypo glycemic when combined w. sulfonylurea, pancreatitis( rare but serious), delay in gastric empty can alter other drugs contra- pancreatitis history, black box warning for pts w/ history of medullary cancer, caused thyroid cancer in rodents USE- mono or combination therapy for DM2

89
Q

Conivaptan

A

Vasopressin antagonist V-1a and V-2 receptor antagonist for IV treatment of hyponatremia from increased vasopressin activity

  • no reduction in mortality in CHF pt
  • useful intreating SIADH
90
Q

pioglitazone

A

increase insulin sensitivity in target tissues -PPARgamma agonists - increased sensitivity to insulin stimulate uptake of glossy and fatty acids, alters adipokine production - increased sensitivity in liver and muscle too -long term lower Triglyceride and slight increase HDL and LDL -highly bound, long t1/2 and met in liver -SE-weight gain and edema(most important) osteoporosis and fracture in women, increased risk of CHF, contra- preg, hepatic inpairment( freq LFT needed), heart failure -treatment of DM type 2 -taken once a day -Nuclear receptor agonist so they take time before you se any affect, 1-3 months -monotherapy or conjunction w/ metformin, sulfonylureas, or insulin

91
Q

Sulfonylureas

A

insulin secretagogues -Glyburude, glipizide, glimepiride -require functioning Beta cells–> only intreating early Type 2 diabetes -Bind to K ATP channel on B cells and inhibit their activity causing depolarization-> influx of calcium-> insulin release -highly bound, metabolized in liver and secreted in urine -SE- HYpoglycemia, Weight gain, sulfur allergy -contra- hepatic impairment, renal insufficiency, pregnant and brest feeding -clinical use- type 2DM, BID, lose efficacy as B cell function decreases, and can be combined w/ metformin and thiazolidinediones

92
Q

propanolol

A

Class II anti arrhythmia drugs

-B1 and B2 selective blocker good to reduce incidence of adrenergically driven arrhythmic death after MI

diminish phase 4 depolarization, depressing automaticity, especially in nodal tissues

  • treat arrhythms cause by too much symp activity
  • careful in use w/ Ca channel blockers b/c together can too much depress normal cardiac function

_membrane stabilizing property can inhibit some arrhythmias but at higher doses therefor risk of side effects

  • no partial agonist
  • Membrane stabilize
  • High Lipid soluble
93
Q

Tigecycline

A

derative of minocycline

  • Parenteral adm, T1/2 of 36 hours, eliminated via non renal mech-> no dose adjust in renal disease
  • binds to 30S subunit to inhibit bacterial protein production, but not pumped out by Tet(AE) or Tet(K)-> useful in tetracycline resistant bacteria( except proteus and pseudomonas), not inhibited by TET(M) protein( prevents binding to 30s of other tetras
  • USE-against MRSA, B lactamase producing G- and Acinetobcater, used in skin/skin structure and abdominal infections
94
Q

Cefotaxime

A

third generation Cephalosporins-Parenteral

95
Q

extended spectrum penicillins

A

Ampicillin amoxicillin, great er action on G- than pen G

  • suseptible to B-lactamase enzymes produced by G+and G- BUGs so paired with B lactamase inhibitors- clavulanate
  • greater activity to non B-lactamase producing G+ and G- bugb/c they better penetrate the membrane
  • HELPSS ME spectrum of action
  • same tox as Penicillin G
  • amox causes less diarrhea than ampicillin, decrease effectiveness w/ oral contraceptives
96
Q

second generation Cephalosporins

A

Cefaclor oral-more type 3 hypersense- serum sickness, good sinusitis/OM

Cefoxitin -parenteral

Cefuroxime oral

Cefuroxime IV- cvr s. pneumom and sinusitis/otitis media

Cefprozi oral

poor entry to CNS( except cefuroxime),not 4 meningitis, some treat b fragilis

  • less G+ activity but more G- than 1st gen-(h flu Moraxella)
  • No pseudomonas activity, DONT USE w/ enterobacter( makes Chromosoaml B lactamase)
97
Q

Adverse effects of penicillins

A
  • hypersensitivity rxn, .7-8%, 2nd only to blood products to allergic rxns in hospital patients
  • major allergic determinants are breakdown products ex: Benzylpenicilloyl
  • minor determinants: penicillinitself and other breakdown products
  • Anti Penicillin ABs are present in most persons, adults more suseptible than children
  • oral adm is less sensitizing than parenteral, topical is worst - cross sensitizing and cross allergic, direct proportion to the duration of treatment and total doses received

type2-cytotoxin( hemolytic anemia), type 3( IC mediated, type4 CMI- delayed( methicillin most common- allergic interstitial nephritis- T4)

98
Q

type 1 Hypersensitivity to penacillins

A
  • most common, IgE mediated, release of histamine from mast cells, 1 -72 hours post adm, skin testing most useful
  • Skin reactions ‐ Rash, Angioedema (swelling of lips, tongue, face), urticaria, pruritis
  • GI Manifestations – Nausea, abdominal pain, vomiting, and diarrhea
  • Respiratory tract involvement – dyspnea or wheezing
  • Cardiovascular manifestations – hypotension, tachycardia, and arrythmias
  • Fatality is usually due to laryngeal edema or cardiovascular collapse
99
Q

Acarbose

A

alpha glucosidase inhibitor -competitive inhibitor of enteric a-glucosidase( enzyme that breaks down complex carbs and oligosaccharides) -delay post prandial abs of gluscose -attenuates plasma glucose increases post prandial-> insulin sparing effect -SE- GI disturbance(fart, drhea, ab pain) -contra- IBS, any condition worsened by gas - USE- type 2 DM, prior to each meal, mono therapy or with other meddler insulin -in mild to mod hypoglycemia pts should be given dextrose not sucrose

100
Q

Class IV anti arrhythmia drugs

A

Verapamil

Diltiazem

block Votage sensative L type Ca channels

decrease inward current carried by calcium

Pharmacology drew (9 decks)

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