Fa - Pharm 5

Front 1

Cladribine =

Back 1

adenosine analog R to degradation by adenosine deaminase

=> adenosine toxicity kills HCL cells

Front 2

MTX = folic acid analog that binds:

Back 2

DHFR

Front 3

5-FU =

Back 3

pyrimidine analog that inhibits thymidylate synthesis

=> inhibits DNA synth

Front 4

Leucovorin = N-formyl-THF = Folinic Acid;

=>

(2)

Back 4

1. "rescue" from MTX toxicity
(inhibits MTX)

or

2. potentiation of 5-FU

Front 5

Enoxaparin =

Back 5

LMW heparin (binds and activates ATIII)

=> inactivation of 10a

- less effective than unfractioned heparin

Front 6

main SE of Vincristine =

(vinca alkaloid)

Back 6

neurotoxicity

(due to failure of MT polym in axons)

Front 7

ultimately, Aminocaproic acid inhibits:

Back 7

fibrinolysis

- so does Tranexamic acid

Front 8

**what does desmopressin do in the blood?

(NOT at the tubules)

Back 8

***releases Factor 8 and vWF from the endothelium

(tx for vWD)

Front 9

what are Gardos channel blockers?

Back 9

meds that block the efflux of K+ and water from the cell, preventing dehydration and subsequent polymerization of HbS

= tx for SCA

Front 10

4 opioids:

Back 10

1. Meperidine

2. Diphenoxylate

3. Dextromethorphan

4. Loperamide

Front 11

example of a nonselective MAOI:

Back 11

Phenelzine

Front 12

“-dipines” =

Back 12

dihydropyridine Ca2+-chan blockers

Front 13

non-dihydropyridine blockers =

(2)

Back 13

1. Verapamil

2. Diltiazem

Front 14

SER Syndrome:

Sinners Sell Drugs That Make Me Trip

Back 14

St. John's Wort

SSRI's

Dextromethorphan

TCA's

MAOI's

Meperidine

Triptans
(anti-migraine)

Front 15

8 features of SER Syndrome:

Back 15

1. confusion

2. agitation

3. tremor

4. tachycardia

5. HTN

6. clonus

7. hyperthermia

8. diaphoresis

Front 16

SER Syndrome is treated with:

Back 16

Cyproheptadine

- anti-H with anti-SER properties

Front 17

Abciximab =

Back 17

GP2b3a r' blocker

- mimics Glanzman (deficiency in GP2b3a)

Front 18

Fondaparinux =

Back 18

Factor 10a inhibitor

Front 19

Unfractioned heparin binds:

Back 19

BOTH ATIII and thrombin

=> inactivation of BOTH Factor 10a AND thrombin

= more effective than LMW heparin (like Enoxaparin)

Front 20

Trastuzumab =

Back 20

AB against ERB-B2 (HER2/neu)

Front 21

major SE of ganciclovir =

Back 21

neutropenia,

ESP. when given with Zidovudine

Front 22

most prominent SE of Cisplatin =

Back 22

nephrotoxicity

- prevented with Amifostine (f.r. hunter) and hydration

Front 23

Ticlopidine =

Back 23

inhibitor of plat. ADP release (like Clopidogrel)

=> plats aren't activated to express GP2b/3a

Front 24

serious SE of Ticlopidine =

Back 24

neutropenia

=> fever and mouth ulcers

Front 25

another name for TNF-a =

Back 25

cachectin

- released by mP's and neoplasms

~~ systemic inflammation

- cachexia and septic shock at high concentrations

Front 26

Rituximab =

Back 26

anti-CD20 agent

Front 27

vinca alkaloids act at the:

Back 27

M phase

- prevent division

Front 28

Argatroban =

Back 28

DIRECT thrombin inhibitor => anticoagulation

Front 29

what does Sucralfate do?

Back 29

coats ulcer base, like Bismuth

Front 30

what do vinca alkaloids do?

Back 30

bind B tubulin, preventing MT polymerization

=> MT's destroyed

Front 31

mech. of Colchicine:

Back 31

binds tubulin => prevents MT polym.

Front 32

1st-gen/typical antipsychotics are either low-potency or high; respective SE's =

Back 32

non-neurologic if low-potency
(sedation, anti-cholinergic, orthostatic hypotension)

neurologic if high-potency
(EPS, which includes rigidity)

Front 33

2 low-potency neuroleptics:

(first-gen antipsychotics)

Back 33

1. Chlorpromazine

2. Thioridazine

Front 34

2 high-potency neuroleptics:

Back 34

1. Haloperidol

2. Fluphenazine

Front 35

main SE of Lamotrigine =

Back 35

skin rash

- pot. fatal in children

Front 36

**improvement in strength of MG pt following Edrophonium admin. means:

Back 36

they are being under-treated

=> **inc. dose of [Neostigmine]

Front 37

remember that Edrophonium is a:

Back 37

rapidly-reversible ACHE inhibitor

=> inc. ACH concentration

Front 38

Ca2+ chan. blockers like Nimodipine can be used to prevent:

Back 38

vasospasm following subarachnoid hemorrhage (SAH)

Front 39

specific mech. of Morphine:

Back 39

acts via G/2nd messengers to INCREASE K+ efflux

=> cells hyperpolarized

=> no pain transmission

Front 40

Modafinil =

Back 40

non-amph. for NARCOLEPSY

Front 41

Timolol and other B-blockers in the eye:

Back 41

decrease production of aqueous humor [by ciliary epithelium]

- treat glaucoma

Front 42

drug-induced Parkinsonism is the result of blocking:

Back 42

D2

- neuroleptics, anti-emetics

Front 43

drug-induced Parkinsonism is treated with:

Back 43

Benztropine or Amantadine

- L-dopa and DOPA agonists can't be used - will ppt psychosis

Front 44

most effective way to reduce blood Li2+ =

Back 44

hemodialysis

Front 45

Li2+ is excreted:

Back 45

by the kidneys

- acts JUST LIKE Na+

=> anything that damages kidneys OR causes an increase in PCT Na+ reabsorption will cause Li2+ toxicity

Front 46

3 classes of drugs that inc. Na+ reabsorption at the PCT:

Back 46

1. NSAIDs

2. Thiazide diuretics

3. ACEI's

Front 47

"-capones" =

Back 47

COMT inhibitors

=> prevent peripheral conversion of L-dopa

=> inc. L-dopa into brain

Front 48

big difference b/w Entacapone and Tolcapone:

Back 48

Tolcapone blocks peripheral AND central conversion of L-dopa, and has an inc. risk for hepatotoxicity

Front 49

Carbidopa =

Back 49

DOPA decarboxylase inhibitor,
which prevents peripheral shunting of DOPA/L-dopa

(like "-capones" / COMT inhibitors

Front 50

caveat with prescribing COMT inhibitors:

Back 50

**useless** by themselves

Front 51

"-gelines" =

Back 51

MAOI's

Front 52

Atropine does not fix muscular or CNS excitation in cholinergic syndrome, but _____________ does

Back 52

Pralidoxime

Front 53

Ceftriaxone does not cover Listeria, so you need to add:

Back 53

Ampicllin

- Ampicillin = d.o.c. for Listeria

Front 54

B6 increases:

Back 54

peripheral metabolism of L-dopa

=> Parkinson symps return

Front 55

main problem with Cimetidine (H2-blocker) =

Back 55

gynecomastia

Front 56

"blood/gas partition coefficient" =

Back 56

solubility in the blood

Front 57

**highly-soluble inhaled anesthetic =>

Back 57

higher solubility in the blood

=> slower equilibrium with the brain

=> longer onset

Front 58

an inhaled anesthetic with low blood solubility =>

Back 58

QUICK onset of action

(reaches brain faster)

Front 59

the lower the MAC,

Back 59

the more potent the inhaled anesthetic

(MAC = conc. that renders 50% unresponsive to painful stimuli)

Front 60

what's one way to decrease tolerance to Morphine?

Back 60

give a Glutamate (NMDA channel) inhibitor,

like Ketamine

Front 61

higher peripheral (lipid) solubility means:

Back 61

**more anesthetic is extracted from the blood**

=> need GREATER concentration in order to reach brain and be effective

Front 62

***both blood solubility AND tissue solubility are BARRIERS to reaching the brain***

Back 62

the higher blood and lipid solubility are, the LONGER the anesthetic will take to work, and the MORE anesthetic you need

Front 63

TCA's have a __________________ effect on the CV system

Back 63

Quinidine-like

- prolong QT, arrhythmias

- by blocking fast Na+ channels

Front 64

TCA toxicity is treated with:

Back 64

NS and HCO3

- increases Na+, to offset inhibition of Na+ chans by TCA (with subsequent cardiac issues)

Front 65

sexual SE's are common to:

Back 65

SSRI's

- use Bupropion instead

Front 66

almost all volatile anesthetics increase:

Back 66

cerebral blood flow

=> inc. ICP

- in all other major organs, blood flow and thus organ function is DEcreased

Front 67

Phenytoin toxicity:

(3)

Back 67

1. gingival hyperplasia
(via inc. PDGF)

2. ataxia
(cerebellum)

3. nystagmus
(vestibular syst)

Front 68

4 effects of Benzo's:

Back 68

1. hypnotic

2. anxiolytic

3. anti-convulsant

4. muscle relaxant

Front 69

mech. of Benzo's:

Back 69

increase Cl- channel opening

=> enhance GABA

Front 70

2 symps of opioid use to which tolerance does NOT occur:

Back 70

1. constipation

2. miosis

- take daily laxatives

Front 71

4 mechanisms of TCA's:

Back 71

1. NOR and SER reuptake inhibitors

2. Muscarinic r' antagonists

3. α1 blockers

4. H1 blockers

Front 72

2 high-potency antipsychotics:

Back 72

1. Haloperidol

2. Fluphenazine

Front 73

Taxanes bind B tubulin and:

Back 73

STABILIZE MT's

=> can't depolym => arrest

Front 74

2 low-potency antipsychotics:

Back 74

1. Chlorpromazine

2. Thioridazine

Front 75

Mirtazapine = tetracycline; mech:

(3)

Back 75

1. blocks a2
=> NOR and SER release into terminal

2. 5HT2 antagonist

3. 5HT3 antagonist

Front 76

chronic topical corticosteroid administration =>

Back 76

atrophy of dermis, drying/cracking of skin, tightening, telangiectasias, and ecchymoses

Front 77

nucleotide =

Back 77

P'd nucleoside

Front 78

nucleoside antivirals must be:

Back 78

P'd into nucleotides in order to function

Front 79

***what is the mechanism of the cyclovirs?

Back 79

they are *viral-kinase-dependent nucleosides*

- get P'd in order to become nucleotides, => effects

- nucleotides like Cidofovir and Tenofovir, and nucleosides ZDZ and Lamivudine, get phosphorylated by the HOST cell kinase

Front 80

what do all P'd nucleotide analogs eventually do?

(2)

Back 80

1. inhibit DNAP

2. cause chain termination

Front 81

Probenecid and Sulfinpyrazone are:

Back 81

uricosuric agents, which help excrete uric acid

- NOT used in pts with renal issues, for fear of nephrolithiasis

- Allopurinol CAN be used despite renal issues

Front 82

chronic use of steroids =>

Back 82

osteoporosis,

among other things

Front 83

"-dronates" =

Back 83

Bisphosphonates,

pyrophosphate analogs
(component of hydroxyapatite)

Front 84

PROG is required for endometrial cells to:

Back 84

grow, differentiate into decidual cells that can accommodate pregnancy, and stabilize

- withdrawal of PROG will result in apoptosis, => bleeding

Front 85

TNF-a ~~

Back 85

systemic inflammatory response
(IL-1, IL-6 as well)

- cachexia and septic shock at high concentrations

Front 86

6 absolute contraindications to OCP's:

Back 86

1. Hx of thromboembolic event or stroke

2. >35 and smoke heavily

3. hyperTG

4. decompensated or acute liver dz
(impaired metabolism)

5. preg

6. Hx of EST-dependent tumor

Front 87

what is the standard prescription for gonococcal urethritis?

Back 87

ceftriaxone for N. gonorrhea,

Z-pak for [probably concomitant] Chlamydia

Front 88

B-lactam antib's can often cause:

Back 88

acute interstitial nephritis

- duh: Penicillin is a B-lactam

Front 89

Azathioprine =

Back 89

**prodrug of 6MP**

- inhibits de novo synthesis of Purines
(pure As Gold)

Front 90

Pyridoxine = B6 =

Back 90

nec. cofactor in any transamination (AA becomes a-keto or vice versa)

- eaten up by INH

Front 91

Rasburicase =

Back 91

uric acid excreter, like Allopurinol

- couple of steps further downstream

Front 92

what do topoisomerases do?

Back 92

relieve the strain of supercoiling

Front 93

Arachidonic Acid is a:

Back 93

PUFA

Front 94

B-blockers __________ EF

Back 94

INCREASE it

- via dec. AF

Front 95

mech, and indication of Chlorpromazine:

Back 95

D2 r' inhibitor,

antiemetic

Front 96

"-mustins" and Streptozocin are:

Back 96

alkylating agents used against brain tumors

Front 97

1st-line tx for Toxoplasmosis gondii =

Back 97

Pyrimethamine and Sulfadiazine

Front 98

6 atypical antipsychotics:

Back 98

1. Olanzapine

2. Clozapine

3. Quetiapine

4. Risperidone

5. Aripiprazole

6. Ziprasidone

Front 99

mechanism of typical antipsychotics/neuroleptics:

Back 99

block D2