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PharmOrgans Flashcards

1
Q

CCB MOA and toxicity

A

-blocks voltage depedent L type calcium channels of cardiac and smooth muscle,thereby reducing muscle contractility
-verapamil, diltiazem (heart) > amlodipine, nifedipine (periph)
arteries affected more than veins

Tox: cardiac depression, AVblock, PERIPHERAL EDEMA,FLUSHING, dizziness, constipation, reflex tachycardia,

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2
Q

Hydralazine MOA use, toxicity

A

increased cGMP,causing smooth muscle relaxation. Vasodilates arterioles more than veins, decreased afterload

Severe HTN, CHF, first line for pregnany with methyldopa

Tox: compensatory tachycardia, FLUID RETENTION, LUPUS LIKE syndrome

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3
Q

Malignant HTN tx

A

nitroprusside, nicardipine, labtolol

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4
Q

Nitropruusside MOA/Tox

A

increases cGMP which increases NO, but can cause cyanide toxicity (dilates arteries and vens),

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5
Q

HTN drugs used in pregnancy

A

Hydralazine, methyldopa, labetalol, Nifedipine and CCB “HTN moms like Nifedipine”

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6
Q

Drugs cauing SLE like sx

A

Sulfonamides, hydralazine, isoniazid, procainamide, phenytoin

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7
Q

nitroglycerin, isosorbide, dinitrate MOA,use, tox

A

vasodilates by releasing NO in smooth muscle, causing increased cGMP and smooth muscle relaxation, dilates veins&raquo_space; arteries, causing decreased preload

Use: angina, pulm edema

Tox: reflex tachy, hypoTN, flushing, heaedache

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8
Q

HMG-CoA reductase:

  • Effect on LDL, HDL, TG
  • MOA
  • SE/Tox
A

decrease LDL XXX
increase HDL X
decrease TG X
MOA: inhibits HmG CoA to mevalonate

SE: hepatotoxicity,rhabdomyolysis
Check LFTs, CPKs

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9
Q

Niacin (VitB3)

  • Effect on LDL, HDL, TG
  • MOA
  • SE/Tox
A

Decrease LDL XX
increased HDL XX
decrease TG X

Inhibits lipolysis in adipose tissue, reduces hepatic VLDL secretion

SE: red flushed face,rash, itching (can decrease overtime or with aspirin use)
hyperglycemia,hyperuricemia

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10
Q

Bile acid resins (cholestyramine, colestipol)

  • Effect on LDL, HDL, TG
  • MOA
  • SE/Tox
A

Decreases LDL XX
Increases HDL ~X
Increases TG ~X
Prevents intestinal RAB of BA, liver must use cholesterol to make more

Tox: pts hate it,it tastes bad, GI discomfort, Cholesterol gallstones

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11
Q

Cholesteral absorbtion blockers (ezetimibe)

  • Effect on LDL, HDL, TG
  • MOA
  • SE/Tox
A

LDL decreased XX
No HDL change
No TG change

Pevent cholesterol RAB at small intestine at brush border
rarely, rising LFTs and diarrhea

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12
Q

Fibrates

  • Effect on LDL, HDL, TG
  • MOA
  • SE/Tox
A

Decrease LDL X
Increase HDL X
Decrease TG XXX

Upregulate LPL, causing increased TG clearance

Mypsitis, hepatotoxic, cholesterol gallstones

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13
Q

Cardiac glycosides:

MOA/Use/Toxicity

A

MOA: inhibits Na/K ATPase, leading to indirect inhibtion of Na/Ca exchanger, causing positive inotropy

Use fo CHF (increased contractility), atrial fibrillation (decreased condction at AV node and depresion of SA node)

Tox: cholinergic - nausea, vomitting, diarrhea, blurry YELLOW vision
EKG Changes: increased PR interval, decreased QT interval, T wave inversion, AV block, arrhthmia
can cause hyperkalemia

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14
Q

Mg2+ use

A

antiarrythmic - Use for Torsades de pointes and for digoxin toxicity

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15
Q

adenoseone use

A

antiarryhthmic which causes increased K efflux, causing hyperpolarization, so no depolarizations allowed

Drug of choice for dx/abolishing SVT

Tox: flushing, hypotension, chest pain

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16
Q

Antiarryhthmics - Class 1 MOA

A

Local anesthetic,slow or block conduction, increases effective refractory potential decreaes slope of phase 0, increases thresold for firing in abnormal pacemaker cells

HyperK causes increased toxicity for all class I drugs

Think: Double Quarter Pounder, Mayo Lettuce Tomato, Fries Please

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17
Q

Class IA:

Drugs, MOA,Tox

A

quinidine, procainamide,disopyramide
-increases AP duration, increases ERP, increases QT interval

Tox: Qunidine (cinchonism)
procainamide (reversible SLE like syndrome)
disopyramide (heart failure)

thrombocyotopenia, torsades de pointes

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18
Q

Class IB: Drugs, MOA,Tox

A

Lidocaine, mexiletine, tocainde
Decreases AP duration, preferentially affect ischemic or depolarized purkine/ventricular tissue
Useful in acute ventricular arrhyhtmias, esecially post MI

Tox: local anestheticcardiovascular depression

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19
Q

Class 1C: Drugs, MOA,Tox

A

flecainde, propafenone

MOA: used for ventricular tachcardias that rogress to VF and intractable SVT. Used only as last resort

Tox: proarrythmogenic,especially post mI (CONTRAINDICATED)
Prolons refractory period in AV node

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20
Q

Mechanism of action in anti arrythmics and affeceted phase?

A

1: Na blockers - affect p0
2: beta blockers - affect p4
3: potassium blockers - affect p3
4: CCB - affect p0

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21
Q 
Aniarrhythmics class II 
Drugs, MOA, tox
A

Metoprolol, propanolol, esmolol, atenolol, timolol
Decrease SA and AV node by decreasing cAMP, decrease Ca currents, decreases slope 4

Tox: impotence,exacerbate asthma, may mask hypoglycemia, can exercbate vasospasm in prinzmetal angina

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22
Q

Antiarryhtmics class III

A

amiodarone, Ibutilide, Dofetilide, Sotalol
K channel blockers
Increase AP duration, increase ERP, increased QT interval
Tox:
-sotalol causes torsades de pointes
-Amiodarone: Pulm fibrosis, hepatotoxic,hypo and hyperthyroidism, corneal deposits, photodermatitis, skin deposits

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23
Q

Amiodarone toxicity

A

-Amiodarone: Pulm fibrosis, hepatotoxic,hypo and hyperthyroidism, corneal deposits, photodermatitis, skin deposits

Check LFT,TFT,and PFTs for pts on this

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24
Q

Class 4 Antiarrythmics

Drugs,MOA, tox

A

Verapamil,diltiazem
MOA:decreases conduction velocity, increases ERP, increases PR interval
Constpation, flushing, edema, torades de pointes

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25
Q

Propylthiouracil,methimazole MOA,Use, Toxicity

A

MOA: block peroxidase, thereby inhibiting organification of iodide and coupling of thyroide hormone synthesis. Also decreases periph converion of T4 to T3

Use: hyperthyroidism

Tox: skin rash, AGRANULOCYTOSIS,aplastic anema, hepatotoxicity

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26
Q

Levothyroxine, triiodothyronine MOA,Use, Toxicity

A

thyroxine replacement,which is used for hypothyroidism

tox: tachycardia,heat intolerance, tremors, arryhtmias

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27
Q

GH use?

A

GH deficiency, Turner syndrome

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28
Q

Somatostatin/Octreotride use?

A

Acromegaly,carcinoid, gastrinoma, glucagonoma (esophaeal varices)

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29
Q

Oxytocin

A

Stimulates labor,uterine contractions, milk let down, controls uterine hemorrhage

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30
Q

ADH/desmopressin use?

A

Central DI

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31
Q

Demeclocycline MOA, Use, Toxicity

A

ADH antagonist
use: SIADH
Nephrogenic DI, photosensitvity, abnl bones and teeth

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32
Q

Glucocoticoids

MOA, Use, Toxicity

A

MOA: Decrease production of leukotrienes and prostaglandins by inhibting prohpholipase A2 and expression of Cox2

use: addisons, inflammation, immune suppression, asthma

SE: Iatrogenic Cushing’s disease - buffalo hump, moon facies, truncal obesity, muscle wasting, thin skin, easy bruiseability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes

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33
Q

H2 blockers (cimetidine, ranitidine, famotidine, nizatidine) MOA, Use, Toxicity

A

MOA: reversible block of histamine H2 receptors, causing decreased H+ production by parietal cells

Use: PUD, gastritis, GERD

Tox: Cimetidine inhibits P450, also has anti androgenic effects, can cross BBB (cause confusion,dizziness,and headaches). Cimetidine/ranitidine cause decreased Creatinine excretion by kidneys, thrombocytopenia

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34
Q

PPI (omeprazole, lansoprazole, esomeprazole, pantoprazole,dexlansoprazole)
MOA, Use, Toxicity

A

MOA: Inhibits H/K ATPase i stomach parietal cells
Use: PUD,gastritis, GERD, ZE syndrome, erosive esophagitis
Tox: increased risk for Cdiff infection, pneumonia, hip fractures, decreased serum Mg2+ after chronic use

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35
Q

Bismuth/Sucralfate MOA, Use, Toxicity

A

Binds to ulcer abse, providing protection and allowing HCO3- secretion to restablish pH gradient in mucous layer

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36
Q

Misoprostal MOA, Use, Toxicity

A

MOA: PGE1 analog,increases proxn and secretion of gastric mucous barrier, decreases acid production
Use: prevention of NSAID induced PUD, maintenance of PDA
tox: diarrhea (CONTRAINDICATED IN PREGNANT, causes abortion)

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37
Q

Octreotride MOA, Use, Toxicity

A

Somatostatin analog, used for acue variceal bleeds, VIPoma, carcinoid tumors, acromegaly

Tox: nausea, cramps, steatorrhea

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38
Q

Antacid toxicty for AlOH3, MgOH2, and CaCO3

A

AlOH3: Constipation and hypophosphotemia, prox muscle weakness, seizures, osteodystrophy

MgOH2: Diarrhea, hyporeflexia,hypoTN, cardiac arrest

CaCO3: hypercalcemia, rebound acid secretion

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39
Q

Osmotic laxatives (Magnesium hydroxide, magnesium citrate, polethylene glycol, lactulose) MOA, Use, Toxicity

A

Provide osmotic to draw water out

Use:consntipation (lactulose also for hepatic encephalopathy)

Tox: diarrhea, dehydration

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40
Q

Infliximab MOA, Use, Toxicity

A

Monoclonal Ab to TNFa

used for Chrohns disease, UC, RA

Tox: inffxn (latent TB), fever,hypoTN

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41
Q

Sulfasalazine MOA, Use, Toxicity

A

MOA: combo of antibacterial and anti inflammatory thats activated by gut bacteria

Use; CD, UC (IBD)

Tox: maliase, nausea, oligospermia, sulfonamide toxicity

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42
Q

Odansetron MOA, Use, Toxicity

A

5HT3 antagonist, central anti emetic (okay in pregnancy)
Used for psot op and chemo pts
Headahce, constipation SE

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43
Q

Metroclopramide MOA, Use, Toxicity

A

D2 receptor antagonist, causing increased resting tone, contractility, LES tone, and motility in GI.
use: Diabetic and post surg gastroparesis, antiemetic

Tox: parkinsonian effects,restlessness,drowsiness,fatigue, depression, nauesa, diarrhea

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44
Q

Promotility agents (Bethanechol, neostigmine, macrolides, metoclopramide)

MOA for each?

A

Cholingeric agent: bethanechol, neostigmine
Macrolides (eryhtromycin): increases 5HT
Metoclopramide: decreases dopamine

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45
Q

Heparin MOA, Indications, Toxicity

A

MOA: Cofactor for activation of antithrombin, causes decreased thrombin, decreased factor Xa, short half life

Use: iemdaite anticoag for PE, ACS, MI, DVT, used during pregnancy (safe in pregnancy). Follow PTT

Tox: bleeding, thrombocytopenia (HIT), osteoporsis, drug drug interactions

Note: MWH heparins (enoxaparin, dalteparin) act more on factor Xa and have better bioavailability and 2-4 times longer half life, can be administered subQ without lab monitoring.

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46
Q

What is HIT and what is its tx

A

Development of IgG ab against heparin bound to Platelet Factor 4 - these Ab-heparin-PF4 complexes activate platelets, causing thrombosis and thrombocytopenia

Bivalirudin, lepirudin

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47
Q

Lepirudin, bivalirduin?

A

Derivatives of hirudin, inhibit thrommbin (hence same job as antithrobin), used as alternative to heparin for pts with HIT

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48
Q

Warfarin MOA, Indications, Toxicity

A

MOA: intereferes with synthesis and gamma carboxyltion of Vit K dependent clotting factors II, VII, IX, X and proteins C and S. Does so by inhibiting Vit K epoxide reductase so vit K cannot activate the clotting factors

Metabolized by P450
increased PT/INR

Use: chronic anticoagulation, DVT, PE, Afib)
CONTRAINDICATED IN PREGNANCY

Tox: Bleeding, teratogenic, skin/tissue necrosis, drug-drug interactions

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49
Q

Direct Throbin inhibitors?

A

Argotraban, Dabigatran

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50
Q

ThrombolyticsMOA, Indications, Toxicity (tPA/alteplase, streptokinase)

A

MOA: Aid in conversion of plasminogen to plasmin, which cleaves thrombin and fibrin clots. Increases PT, PTT, but no change in platelets.

Use: early MI, early ischemic stroke, PE

Tox: Bleeding, many contraindications eg pts with active bleeding,intracranial bleeding, surgery, etc…

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51
Q

Aspirin MOA, Indications, Toxicity

A

MOA: Irreversibly inhibits COX1 and COX2 by covalent acetylation. Platelets cannot synthesize newenzymes so effects last until platelets die. Decreased conversion of arachidonic acids to TXA2, increased bleeding time. No change in PT or PTT

Use; Antipyretic, analgesic, anti inflammatory, anti platelet

Tox: Tinnitus (CNVIII), gastic ulceration, ARF< interstinal nepgritis, Respiratory alkalosis, Reye’s syndrome

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52
Q

ADP receptor inhibitor (clopidogrel, ticagrelor) MOA, Indications, Toxicity

A

inhibit platelet aggreagation by irrversibly blocking ADP receptors, inhibit fibrinogen binding, prevenging Gp2B3A from binding fibrinogen

Use; ACS, stening, decrease thrombotic stroke

Tox: none really

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53
Q

Cilastazol, dipyridamole MOA, Indications, Toxicity

A

Phosphodiesterase III inhibitor, increases cAMP in platelets, thus inhibiting platelet aggregation, vasodilators

Use: intermittent claudication, coronary vasodilation, prevent stroke/TIA, angina ppx

Tox: Nausea, headache, facial flushing, hypoTn, abdominal pain

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54
Q

GpIIbIIIa inhibitors (Abciximabb, tirofiban, eptifibatide)

A

Bind to Gp2b3a receptor on activatedplatelets, preventing aggregation.

Use: ACS

Tox: Bleeding, thrombocytopenia

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55
Q

Direct Xa inhibitors are?

A

Rivoroxaban, Apixaban

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56
Q

LMWH (Enoxaparan, Dalteparin)

A

Stimulate antithrombin to inactivate Xa, long t/12, subQ injection

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57
Q 
Cancer drugs that work on:
G1 Phase
S Phase
G2 Phase
M phase
A

G1: none
S phase: antimetabolites, etoposide
G2: etoposide, bleomycin
M: vinca alkaloids, taxols

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58
Q

Common SE of cancer drugs, and why?

A

Diarrhea, hair loss, BM supppression –> because these cells are usuaslly rapidly dividing as well and hence are affected

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59
Q

Methotrexate MOA, Indications, Toxicity

A

Folic acid analog that inhibits dihydrofolate reductase –> decrease dTMP –> ddecreased DNA and protein synthesis
ANTIMETABOLITE

Use: leukemia, lymphomas, sarcomas, RA, psoriasis abortion, ectoic pregnancy

Tox: Myelosuppresion (reversible with leucovorin [folinic acid]). Macrovseciular fatty change in liver
Fibrotic lung dz
teratogenic

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60
Q

5-fluorouracil MOA, Indications, Toxicity

A

Pyrimidine analog bioactivated to 5F-dUMP which complexes folic acid –> inibits thymidylate synthase -> causes decreased dTMP –> decreased DNA
ANTIMETABOLITE

USed: Colon cancers, basl carcinomas, pancreatic cancers, ACTINIC KERATOSIS AS TOPICAL USE

Tox: myelosuppresion which is not reversible with leucovorin. OD can be treated with thymidine, uridine
Photosensitivity

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61
Q

Cytarabine MOA, Indications, Toxicity

A

Decreasedpyrimidine analog, which inhibits DNA polyermase

Leukemia/lymphomas

Tox: leukopenia,thrombocytopenia,megalobalstic anemiea

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62
Q

Azathioprine/6-MP MOA, Indications, Toxicity

A

Purine analog –> decreass de no purine synthesis
activated by HGPRT
Works on PRPP amidotransferase

Use: leukemia

Tox: Bone marrow, Gi, liver

Metabolized by xanthine oxidase and thus increased toxicity with allopurinol

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63
Q

Dactinomycin MOA, Indications, Toxicity

A

Intercalates in DNA

WIlms tumor, Eewings Sarcoma, Rhabdosarcoma (PEDIATRIC TUMORS)

Tox: myelosuppression

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64
Q

Doxorubin, daunorubicin MOA, Indications, Toxicity

A

generates free radicals which damage DNA and noncovalently intercaltes in DNA, reaking up DNA
-used for solid tumors, leukemias, and lymphomas

Tox: cardiotoxicity (dilated cardiomyopathy), myelosuppresion, alopecia

Dexrazoxane (used to prevent cardiotox)

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65
Q

Bleomycin MOA, Indications, Toxicity

A

induces free radical formation, which causes breaks in DNA

use in testicular cancer, hodkins lymphoma

PUlm fibrosis, skin changes

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66
Q

Cyclophosphamide, ifosfamide MOA, Indications, Toxicity

A

Covaentlyl X link DNA at guanine. Requires activation by liver

Tox: myelosuppression, HEMORRHAGIC cystitis, partially prevented with mesna, increased risk of TRANSITIONAL CELL CARCINOMA

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67
Q

Nitrosoureas (nitrogen mustards) - carmustine, lomustine, semustine MOA, Indications, Toxicity

A

requrie biactivation, cross blood brain barrier –> CNS

Glioblastoma multiforme, CNS tumors

Cns tox (diziness, ataxia possible)

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68
Q

Busulfan MOA, Indications, Toxicity

A

Alkylates DNA

CML

Tox: Pulm fibrosis,hyperpigmentation

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69
Q

Vincristine/Vinblastine MOA/Tox

A

Alkaloids that bind to tubulin in M phase and block polymerization of microtubules so mitotic spindle cannot form

Tox: vincristine: neurotoxicity (peripheral neuropathy,areflexia)
vinblastine: MYELOSUPPRESSIOn

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70
Q

Paclitaxel, taxols MOA/Tox

A

hyperstabilize polymerized microtubules in M phase so mitotic spindles cannot break down (anaphase cannot occur)

Used in ovarian and brreast carcinomas

Tox: myelosuppression and hypersensitivity

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71
Q

Cistplatin, carboplatin, oxaloplatin MOA/Use/Tox

A

Cross link DNA
Testicular, bladder, ovary, and lung carcinoma
Nephrotoxic,acoustic nerve damage,
Prevent nephrotoxicity with amifostine and chloride diuresis

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72
Q

Etoposide,teniposide MOA/Use/Tox

A

Inhibits topoisomerase II –> causeded DNA degradation
used: SCLC, prostate Ca, testocular cancer

Tox: GI irritation, alopecia, bone marrow suppression

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73
Q

Hydroxyurea MOA/Use/Tox

A

Inhibits ribonucleotide rectuase –> decrease DNA synthesis

Use: melanoma, CML, sickle cell disease

BM suppresison, GI irritability

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74
Q

Predisone, prednisolone MOA/Use/Tox

A

May trigger apoptosis

Tox: cushing like symptoms, immunosuppresion, glaucoma, cataracts, acne, osteoporosis, htn, peptic ulcer disease, hyperglycemia, psychosis

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75
Q

Tamoxifen/Raloxifene MOA/Use/Tox

A

SERMS 0 receptor antagonist in breast and agonists in bone. Blocks binding of estrogen to estrogen receptors.

Used for estrogen + breast cancer tx and prevention. Alsoused to prevent osteoporsis (raloxifene)

Tox:
Tamoxifen: partial endometrial agonist, increases risk fo endometrail cancer
Raloxifene: no endometrail agonist component, no risk

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76
Q

Trastuzumab (Herceptin) MOA/Use/Tox

A

Mab against HER-2, a tyrosne kinase

Her2 positive breast cancer

Cardiotoxic

77
Q

Imatinib (gleevec) MOA/Use/Tox

A

brc-abl tyrosine kinase inhibitor

Use: CML, GI stromal tumors, ~ALL, ~AML

Tox: fluid retention

78
Q

Rituximab MOA/Use/Tox

A

Mab against CD20

Use: NHlLymphoma, RA

79
Q

NSAIDs MOA/Use/Tox(Ibuprofen, naproxen, ketorolac, indomethacin)

A

Reversibly inhibit COX1/COX2, blocks prostaglandin synthesis

Antipyretic, analgesic, anti inflamamtory

Tox: interstitial nephritis, gastric ulcer, renal ischemia

80
Q

Cox-2 inhibitor (celecoxib) MOA/Use/Tox

A

Reversibly inhibit COX2 found in inflammatory cells and vascular endothelum, which is used for inflammatory and pain, and spares COX-1 which is usually used to maintain the gastric mucosa. Spares platelet fxn as TXA prodx is dependent on Coxx 1

Use: RA, OA, in pts with ulcers and gastrititis

Tox: risk of thrombosis, sulfa allergy

81
Q

Acetaminphen MOA/Use/Tox

A

Reversibly inhibits cyclooxygenase, mostly in CNS, inactivatedperipherally.

Antipyretic, analgestic,but NOT ANTI INFLAMMATORY. No anti platelet effects. used for children with viral infxn

Tox: OD causes hepatic necrosis

82
Q

Bisphosphonates MOA/Use/Tox

A

Pyrophosphate analogs, binds hydroxyappatite in bone, inhibits osteoclast activity.

Use: osteoporsis, hypercalcemia, paget’s disease of bone

Tox: Corrosive esophagitis, jaw osteonecrosis

83
Q

Allopurinol MOA/Use/Tox

A

Inhibit Xanthine oxidase, decreases conversion of xanthine to uric acid.

use: Gout, leukemia, lymphoma
Dont give with salicylates.

84
Q

Febuxostat MOA

A

inhibits xanthine oxidase

85
Q

Probenicid MOA

A

Inhibits RAB of uric acid in PCT (also inhibits secretion of PCN)

86
Q

Colchicine MOA and SE

A

Binds and stabilizes ubulin to inhibit polymerization, impaires leukocyte chemotaxis and degradutulation

Tox: GI side effects (diarrhea)

87
Q

Acute gout drugs

A

NSAIDS (naproxen, indomethacin)

GLucocorticoids

88
Q

Etanercept MOA use, tox

A

fusion protein that is a TNFa receptor DECOY

Use: RA, Psoriasis, AS

Tox: CAN CAUSE REACTIVATION OF TB, immunosuppressd via preventing activation of macrophages

89
Q

Infliximan, adalimumab MOA/Use/Tox

A

Anti TNFa mab

CD, RA,AS,Psoriasis

Tox: reactivate TB

90
Q

Glaucoma drugs MOA

A

decrease IOP via decreased amount of aqueous humor (inhibit synthesis/secretion or increase drainage)

91
Q

Glaucoma alpha agonists and MOA

A

epinephrine, brimonine: decrease aqueous humor syntehsis

92
Q

Glaucoma drugs Beta blockers

A

Timolol, betaxolol, carteolol

Decrease aqueous humor synthesis

93
Q

Glaucoma drug diuretic

A

Acetazolamide

Decreases aqwous humor synthesis via inhibition of carbonic anhydrase

94
Q

Glaucoma cholinergic meds

A

Pilocarpine, carbachol (direct) and physostigmine (indirect): creases outflow of aqueous humor via contx of ciliary muscle and opening of trabecular meshwork

95
Q

Glaucoma prostagladin drug

A

Latanoprost, increases outflow of aqueous humor

96
Q

Opiod Analgesics: MOA, use,tox

A

Morphine, fentanyl,codeine, heroin,methadone, meperidine, dextrometorphan

MOA: Opoid receptor agonists (mu = morphine, delta, kappa) to modulate synaptic transmission. open K+ channels, close Ca2+ channels –> decrease synaptic transmission Inhibits release of ACh, NE, 5HT, glutamate, substance P

Use: pain, cough suppression, diarrhea (loperamide, diphenoxylate), acute Pulm edema

Tox: additiction, resp depression, constpation, miosis, CNS depression

No tolerance to miosis or constipation but does develop to the pain effects

97
Q

Opioid overdose treatment?

A

Naloxone, naltrexone (opioid receptor antagonist)

98
Q

Tramadol MOA/Use/Tox

A

Weak opioid agonist, also inhibits 5HT and NE reuptake
use: chronic pain

tox: similar to opioids, decreases seizure threshold

99
Q

Phenytoin MOA/Use/Tox

A

Increase Na channel inactivation, inhibition of glutamate release fro presynaptic neurons

Use: Tonic clonic seizures

Toxx: GINGIVAL HYPERPLASIA, hirsutism, SJS, Drug induced lupus, induces P450, megaloblastic anemia, osteopenia, peripheral neuropathy

100
Q

Carbamazepine MOA/Use/Tox

A

increases Na channel inactivation

Use: Simple partial, complexpartial, and generalized tonic clonic seizures , trigeminal neuralgia

Tox: hepatotoxic, Stvens Jonhson syndrome , agranulocytosis, induces P450, SIADH

101
Q

Lamotrigine: MOA/Use/Tox

A

Blocks voltage gated Na channel inactivation

Use: partial seizures

102
Q

Gabapentin MOA

A

Designed as GABA analog but primarily inhibits high voltage activated Ca channels,

Use: periph neuropathy, postherpatic neuralgia, migraines, partial and generalized seizures

103
Q

Valproic acid MOA/Use/Tox

A

Increases Na channel ainactivation, increases GABA concentration

Use: tonic clonic first line, myoclonic seizures

Tox: spna bifida, hepatotoxic, CONTRAINDICAED IN PREGNANCY

104
Q

Ethosuximide MOA/Use/Tox

A

blocks thalamic T type Ca channels, 1st line for absence seizures

tox: SJS, fatigue, GI heaedache

105
Q

teratogenic epilepsy drugs are…

A

Phenytoin, carbamazepine, valproic acid

106
Q

Drugs that cause SJS

A

Ethosuximide, lamotrigine, carbamazepine, phenytoine, phenobarbital

Sulfonamides, penicillins, allopurinol

107
Q

barbiturates MOA/Use/Tox

A

Facilitate GABA action by increases DURATION of Cl opening

Sedative for anciety,seizures, insomnia, etc..

Tox: cardiorespiratory depression (can be fatal), induces P450

108
Q

BZD MOA/Use/Tox

A

Facilitate GABA action by increasing FREQUENCY of Cl channel opening.

Tox: dependence,CNS depression

109
Q

Inhaled anesthetic effects/toxicity

A

Halothane, isoflurane, sevoflurane, nitrous oxide
Myocardial depression, respiratory depression, nausea, increased cerebral blood flow

tox HEPATOXIC (halothane), nephrotoxic (methyoxyflurane), malignant hyperthermia

110
Q

Ketamine MOA

A

PCP analog that acts as dissociative anesthetic. Blocks NMDA receptors. Cause disorientation, hallucination,and bad dreams

111
Q

Propofol MOA

A

Used for ICu sediation, rapid anesthetic induction. Potentiates GABA

112
Q

Local Anesthetics MOA/Use/Tox
Esters: procaine, cocaine, tetracaine
Amides: lidocaine, mepivacaine,bupivicaine

A

MOA: block Na channels by binding to receptor on inner portion of channel. most effective in rapidly firing neurons.

Decreased fxn in decreased pH (like abscess)

Tox: CNS exciation, HTN

bupivicaine: cardiovascular toxicity
cocaine: arrhythmias

113
Q

Succinylcholine MOA, Tox

A

Depolarizing neuromuscular argent, ACh receptor agonist, produces sustained depolarization and prevents muscle contraction.
Used: muscle paralysis during surgery

Tox: hypercalcemia, hyperkalemia, Malignant hyperthermia (tx with dantrolene)

114
Q

Rocoronium,tobocuranine, mivacirium….

A

Nondepolarizing neuromusclar blocking drugs, competitive antagonists, comete with Ach for receptors

reversal of blockade with neostigmine, edrophonium, other cholinesterase inhibitors

115
Q

Dantrole MOA/USe

A

Prevents Ca release from sarcoplasmic reticulum

Use: treat malignant hyperthermia and neuroleptic malignant syndrome

116
Q

Parkinson Drugs

A

BALSA

Bromocriptine, Amantidine, L dopa/Carbidopa, Selegiline, Antimuscarincs (eg Benztropine)

117
Q

Bromocriptine, pramipexole, ropinrole

A

Dopamine agonists (eg used in parkinsons)

118
Q

Amantadine MOA/USE

A

increases dopamine release

parkinson’s disease

119
Q

L dopa/carbidopa MOA/USe/Tox

A

Dopaminergic agent (converted to dopamine in CNS)

Use in Parkinsons

Tox: arrhythias from increased periph formation of catecholamines. Can lead to dyskinesia after chronic use

120
Q

Selegiline MOA/Use

A

Selective MA type B inhibtior, helpes prevent L dopa degradation (thus making Dopamine more available)

Use: PD

121
Q

Memantine MOA/Use/Tox

A

NMDA receptor antagonist, helps prevent excitotoxicity

Use: Alzheimers disease

Tox: dizziness, confusion,hallucinations

122
Q

Donepzil, rivastigmine, galantine MOA/Use/Tox

A

Acetylcholinesterase inhibitor

Alzheimers

Nausea/dizziness/insomnia

123
Q

Huntingtons drugs

A

Tetrabanazine,reserpine (inhibit VMAT, limit dopamine release)

Haloperidol (dopamine receptor antagonist)

124
Q

Sumatriptan MOA/Use/Tox

A

5HT1b1d agonist, inhibits trigeminal nerve activation

use: acute migraine, cluster headaches
tox: coronary vasospasm, CI in prinzmetal/pts with CAD

125
Q

Treatment for alcohol withdrawal

A

BZD

126
Q

Anxiety tx

A

SSRI, SNRI, Buspirone

127
Q

ADHD treatment

A

Methylphenidate, amphettamines

128
Q

Bipolar disorder

A

Mood stabiizers(lithium, Valproic acid, carbamazepine) , atypical antipsychotics

129
Q

Bulimia tx

A

SSRI

130
Q

Depression tx

A

SSRIs, SNRIs, TCAs,buspirone, mirtazapine (esp if they have insomnia)

131
Q

OCD tx

A

SSRIs, clomipramine

132
Q

Panic disorder

A

SSRIs, venlafaxine, BZD

133
Q

PTDS

A

SSRIs

134
Q

Schizophrenia

A

Antipsychotics

135
Q

Social Phobias

A

SSRIs

136
Q

Tourettes syndrome

A

Antipsychotics (haloperidol, risperdal)

137
Q

CNS stimulants: drugs, MOA, use

A

methylphenidate, dextroamphetatmine, methamphetamine

MOA increases catecholamines at the synaptic cleft, especialyl NE and dopamine.

use: ADHD, narcolepsy, apeptite control

138
Q

Typical Antipsychotics MOA, use, toxicity

A

Haloperidol, trifluperazine, flupheanzine, thioridazine, chlorpromazine (haloperidol + azines)

All typical antipsychotics block Dopamine D2 receptors (increase cAMP)

Use: schizophrenia (for + sx), psychosis, mania, tourette’s syndrom

Tox: slow to remove from body since high lipid solublility, EPS, hyperprolactinoma (from dopamine antagonist), antimuscarinic (dry mouth, constiation), alpha 1 antagonist (hypotension), histamine antagonist (sedation)

Major Tox: NEUROLEPTIC MALIGNANT SYNDROME (rigidity, myoglobinuria, autonomic instability, hyperpyrexia)

TARDIVE DYSKINESIA, NMS especially with haloperidol

139
Q

High and low potency antipsychotics and SE

A 
High: Trifluoperazine, flupheanazine, haloperidol
Neurologic SE (EPS) are more common

Low: Chlorpromazine,thioridazine - alpha, muscarnicc, histamine side effects
SE: corneal depostis

140
Q

NMS Sx and tx

A

rigidity, myoglobinuria, autonomic instability, hyperpyrexia

FEVER = Fever, enceophlopathy, vitals unstable, elevated enzymes, rigid muscles

Tx: dantrolene, D2 agonists (bromocriptine)

141
Q

Evolution of EPS side effects Ias sen in antipsychotics/neruoleptics)

A

4 hr:acute dystonia

4d: akathisisa
4w: bradykiniesiea
4m: tardive dyskinesiea

142
Q

Atipical antipsychotics MOA, use, toxicity

A

MOA: varied effect on 5HT, dopamine, alpha, and histamine receptors

Clozapine, Olanzapine, quetiapine, risperidone, aripiprazole, ziprasidone

Use: Schizophrenia, positive and negative sx, BPD, OCD< anxiety disorder, depression, mania

Tox: fewer EPS and anticholiernic se than traditional antipsychotics.

Olanzapine/clozapine may cause significant weight gain

Clozapine: AGRANULOCYTOSIS
Ziprasidone: increased QT interval

143
Q

Lithium MOA, use, toxicity

A

MOA: not established
USe: mood stabilizer for BPD, acute manic events, and SIADH

Tox: tremor, sedation, edema, heart block, HYPOTHYROIDISM, polyuria, teratogenic (ebsteins abnormality), nephrogenic diabetes insipidus

Excreted momstly by kidneys

144
Q

Busprione MOA, use, toxicity

A

MOA: stimulates 5HT1a receptors
use: GAD, doesnt cause sedation, addiction or tolerance, takes 1-2 weeks for effect.

145
Q

SSRI MOA, use, toxicity

A

Fluoxetine, paroxteine, sertraline, citalopram

MOA: seratonin specific reuptake inhibitor
Use: Depression, GAD, Panic disorder, OCD, bulimia, socal phobias, PTSD

Tox: GI distress, decreased sexual dysfunction,

seratonin syndrome if combined with other pro seratoningergic drug (MAO, SNRI, TCA) - HYPERTHERMIA, CONFUSION, MYOCLONUS, Cardiovascular collapse, flushing, diarrhea

146
Q

Treatment for seratonin syndrome?

A

Crpoheptadine

147
Q

SNRIsMOA, use, toxicity

A

Venlafaxine, duloxetine

MOA: inhibit Seratonin and NE reuptake

use: Depression. ~GAD.panic attacks for velafaxine
Duloxetine also used for pts with diabetic peripheral nueorpathy

tox: increased BP, stimulant effects

148
Q

TCAs MOA, use, toxicity

A

Amitryptiline, nortriptyline, imipramine, desipramine, clomipramine, doxepin

MOA:Block reuptake of NE and seratonin
Use: major depression, OCD (clomipramine), fibromyalgia

Tox: Tri-Cs - convulsion, coma, cardiotoxicity (arryhtmias) , also respiratory depression,confusion, and hallucinations in elderly due to antcholernigc SE
sedation, alpha 1 blocking effects including hypotension, anticholnergic SE (tachycardia, dry mouth, urinary retention)

Tx: NaHCO3 for cardiovascular toxicity

149
Q

MOA inhibitors: MOA, use, toxicity

A

tranylcyproamine, phenelzine, Isocarboxazid, elegiline

MOA:: nonselective MAO inhibition, increase levels of amine neurotransmitters (NE, 5HT,dopamine)

Use: atypical depression, anxiety

Tox: Hypertensive crisis (especially with tyramine ingestion) .
Contraindicated with SSRI, TCA, StJohns wort, meperidine, and dextrometoprhan (to avoid Seratonin syndrome)

150
Q

Buproprion MOA, use, toxicity

A

Increases Ne and dopamine, unsure how

used for depression and smoking cessation

tox: timulant side effects, seizure in bulimic pts, no sexual side effects

151
Q

Mirtazaine MOA, use, toxicity

A

alpha 2 antagonist (increases release of NE and 5HT and 5HT3 receptor antagonist)

Use: depression, insomnia

Tox: Sedation, increased appetite, weight gain, dry mouth

152
Q

TrazadoneMOA, use, toxicity

A

MOA: inhibits seratonin reuptake

Use: insomnia mostly

Tox: PRIAPISM, postural hypotension

153
Q

Mannitol MOA, use, toxicity

A

MOA: osmotic diuretic, increases tublar flow osmolarity, increases urine flow, decreased intracranial and intraocular ppressure

Use: drug OD, elevated intracranial/intraocular pressure
Acute glaucoma, shock

Tox: Pulm edema,dehydration.

Contraindicated in CHF

154
Q

Acetazolamide MOA, use, toxicity

A

MOA: Carbonic anhydrase inhibitor,which limits NaHCO3 diuresis and reduction in total body HCO3

use: diuresis, glaucoma (decreases prdxn of aqueous humor), **MAINE USE ** –> urinary alkalinzation, metabolic alkalosis, alitutude sickness (to excrete HCO3), pseudotomor cerebri
tox: hyperchoremic metabolic acidosis, sulfa allergy

155
Q

Loop Diuretics MOA, use, toxicity

A

MOA: sulofamide loop diuretic, inhibits cotransport of Na, K, 2 Cl- of thick ascending limb of loop of Henele. Causes body to lose Ca2+. Prevents urine concentration.

use: CHF, cirrhosis,nephrotic state,hypercalcemia,~HTN

Tox: Ototoxivity, hypokalemia, dehydration, allergy, nephritis, Gout (OH DANG)

156
Q

Thiazides MOA, use, toxicity

A

chlorthalidone, HCTZ, chlorothiazide

MOA: inhibit NaCl RAB in early dtal tubule, reduces dilating capacity. retains Ca2+ within the body by reducing Ca2+ secretion

Use: HTN, CHF, hypercalcuria, nephrogenic DI

Tox: hyperglycemia, hyperlipidemia, hyperuricemia, hypercalcemia (hyper GLUC)

157
Q

K sparing diuretics MOA, use, toxicity

A

Spironolactone, triamterne, eplerenone, amiloride

S and E: competitive aldosterone receptor antagonists in collecing tuule
T and A: block Na channels in the CCT

Use: hyperaldosternemia, K+ depletion, CHF

Tox: Hyperkalemia, antiandrogen/progesteronic effects with spironolactone (gynecomastica,menstrual irregularies)

158
Q

Aliskinen

A

Renin inhibitor, only used in HTN, it is teratogenic

159
Q

ARB: MOA, use, toxicity

A

Inhibits AII receptors
blocks stimulation of aldosterone
blocks vasoconstriction

no cough, ~angioedemea

160
Q

ACE inhibitors MOA, use, toxicity

A

Captoppril,lisinopril, enalapril
MOA: inhibits ACE conversion ofAI to AII –> decreases GFR by preventing constrictoin of efferent arterioles. Levels of renin increase. Also, inhibiting ACE also prevents inactivation of bradykinin, a vasodilator.

prevents left heart modeling in HTN,CHF,and postMI pts.

Tox: CATCHH
Cough, angioedema,teratogen, creatinine increase (decrease GFR), hyperkalemia, hypotension

161
Q

Leuprolide: MOA, use, toxicity

A

GnRH analog with agonist properties if used pulsatile, but antagonist if used continuously (downregulates GnrH receptors in pituitary)

use: infertility (pulsatile),psotate cancer (continuous), uterine fibroids, precocious puerty (continuous)

162
Q

Testosterone, methyltestosterone MOA, use, toxicity

A

MOA:: agonist at androgen receptors

Use: Treats hypogonadism, promotes development of secondary sex characteristics, stimulation of anabolism to promote recovery afterburn or innjury.

Tox: causes masculinization in females, gonadal atrophy in males, premature closure of epiphyseal plates,increase LDL, decrease HDL

163
Q

Finasteride MOA, use, toxicity

A

5a reductase inhibitor,which inhibits conversion of testoserone to DHT (more potenet form). Useful in PH and hair growth.

164
Q

Flutamide: MOA, use, toxicity

A

Nonsteroidal competitive inhibitor of androgens at testosterone receptor, used in prostate carcnoma

165
Q

Estrogens MOA, use, toxicity

A

bind estrogen receptors

use: hypogonadism in females or ovarian failure, menstrual abnormalities, HRT in postmenopasaul women
tox: increased risk of endometrial cancer, clear cell adenocarcnoma of vagina in females exposed to DES

increased risk of thrombi

CONTRAINDICATIONS: ER positive breast cancer, history of DVTs

166
Q

Clomiphene

A

SERM: partialagonist at estrogen receptor in hypothalamus, prevents normal feedback inhibiton and increases release of LH and FSH from pituiarty, which stimulates ovulation.

Use: infertility,PCOS

SE: hot flashes, ovarian enlargement, visual disturbances, multiple pregnancies

167
Q

Tamoxifen

A

Antagonist on breast tissue, used to treat and prevent recurrent ER positive beast cancer

168
Q

Raloxifene

A

Agonist on bone, reduces resoprtion on bone

169
Q

Hormone Replacement Therapy

A

Used for relief or prevention of menopausal symptoms and osteoporisis (decreases osteoclast activity)

Upposed estrogen therapy can increased risk for endometrial cancer so progesterone is added too

170
Q

Aramotase inhibitors

A

Anastrozole, exemestane

used in post menopausal women with breast cancer

171
Q

Progestins use/MOA

A

MOA: binds progesterone receptors, reduces growth and vascularization of endometrium

Used in OCPs and in treatment of endometrial cancer and abnormal uterine bleeding

172
Q

Mifepristone MOA, use, toxicity

A

MOA: competitive inhibitor of progestins at progesterone receptor

use: terminate pregnancy
tox: heavy bleeding, GI effects, abnd pain

173
Q

OCPs (dual hormone)

A

Estrogen and progestins inhibit LH and FSH, and ths prevent estrogen surge,which means no LH surge, which means no ovulation

Progestins: cause thickening of cervical mucus, thereby limiting sperm etnry. Progestins also inhibit endometrial proliferation, decreasing chance of implantation

Contraindicated in smkers > 35 years old (CVD rsk), and datients with history of thromboembolism, stroke

174
Q

Terbutaline

A

B2 agonist that relaxes the uteris, reduces premature contractions

175
Q

Tamulosin

A

alpha 1 antagonist used to treat BPH by inhibiting smooth muscle contraction of prostate

176
Q

Sildenafil, vardenefil MOA, use, toxicity

A

Use: inhibits phsphodiesterase 5, causing increased cGM, smooth muscle relaxation in penis, increases blood flow

Use: ED

Tox: HA, flushing, impaired BLUE GREEN color vision, hypotension

177
Q

Danazol: MOA, use, toxicity

A

Synthetic androgen that acts as a partial agonist at androgen receptors

Use: endometriosis

tox: weight gain, edema, acne, hirsuitism, masculinzation, hepatotoxicity

178
Q

Asthma drugs include..

A

Beta 2 agonists, methylxanthines,muscarinic antagonists, corticosteroids, antileukotrienes, omalizumab

179
Q

Muscarininc antagonists

A

Ipra and tiotroprium - competitive block of muscarinic receptors, preventing bronchoconstriction. also used for COPD.

180
Q

Steroids in asthma use

A

Beclomethasone, fluticasone: inhibit synthesis of cytokines, inactivate NFkB, the txn factor taht induces prxn of TNFa and other inflammatory agents. 1st line agent ofr chronic asthma

181
Q

zileuton

A

Antileukotriene - 5 lipoxygenase pathway inhibitor, blocks conversion of arachnidodic acids to leukotrienes

182
Q

Montelukas, zafirlukast

A

antileukotrienes - blocks leukotriene receptors, especially good for aspirin induced asthama. Blocks LTAD4

183
Q

Omalizumab MOA

A

monoclonal anti-IgE Ab that binds to serum IgE. used in severe asthma cases

184
Q

Guaifenesin

A

Expectorant - loosens sputum,thins respiratory secretion, doesnt spress cough reflex

185
Q

N-Acetylcysteine (other than OD)

A

mucolytic that can loosen mucous plugs in CF patients
can also prevent contrast induced nepropathy

also used for acetaminphen OD

186
Q

Bosentan

A

Used to treat pulmonary arterial hypertension - antagonizes endothelin 1 receptors, decreases pulm vascular resistance

187
Q

Dextromethophan

A

Antitussive (antagonizes NMDA glutamate receptors) - synthetic morphine analog

Naloxone can be given for overdose

188
Q

Pseudophedrine, phenylephrine MOA, use, toxicity

A

Sympathomimetic alpha agonistic nasal decongestants

reduces hyperemia, edema, and congestion, open obstructed eustachian tubes. Pseudophedrine can also be used as a stimulant

tox: HTN, and can cause CNS stimulation, anxiety. Must be careful for medication overdose, causing decreased effects (tachyphylaxis)

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