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1
Q

CYP450 inducers

A 
Chronic alcoholics
St. John's Wart (STeal)
Phenobarbitol and Phenytoin (PHEN-PHEN)
Nevirapine (NEVeR)
Rifampin (Refuse)
Grisofulvin (GReasy)
Carbamazepine (CARBs)
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2
Q

CYP450 inhibitors

A 
Acute Alcohol Abuse
Ritonavir
Amiodarone
Cimetidine
Ketoconazole
Sulfonamides
INH
Grapefruit Juice
Quinidine
Macrolides - erythromycin

(AAA RACKS IN GQ Magazine)

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3
Q

Sulfa drugs

A 
Sulfonamide antibiotics
Sulfonylureas
Probenecid
Furosemide
Acetazolamide
Celecoxib
Thiazides
Sulfasalazine
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4
Q

MTX, Nitrofurantoin, Carmistine, Bleomycin, Busulfan, Amiodarone

A

Pulmonary Fibrosis

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5
Q

AD

A

Marfans
Huntington
Acute intermittent porphyrias
Familial hypercholesterolemia

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6
Q

AR

A 
Tay Sachs (hexosaminidase A)
Cystic Fibrosis
Sickle Cell
PKU
Wilson Dz (ATP 7B)
Classic Galactosemia
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7
Q

X-linked Recessive

A 
G6PD
DMD
Lesch-Nyhan
Hemophilia A/B
Red-Green
Menke
Ornithene Transcarbamolase Def
SCID
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8
Q

Mitochondrial

A

MERRF (Myoclonic Epilepsy with Ragged Red Fibers)
MELAS (Mitochondiral Encephalopathy, LActic ACidosis, Stroke-like episodes)
Leber Hereditary Optic Neuropathy

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9
Q

X-linked Dominant

A

Fragile X

Hypophosphatemic Rickets

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10
Q

Anthrax exotoxin - bug and MOA (2)

A

Bacillus anthracis

  • Edema factor (converts ATP to cAMP) - causes edema and phagocyte dysfunction
  • Lethal factor - Zn-depenent protase - cuases apoptosis and mutisystem physiologic disruption
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11
Q

Bordetella pertussis - two toxins and MOA of each

A
  1. PErtussis toxin - disnhibits AC through Gi ADP-ribosylation, inc cAMP - causes edema adn phagocytic dysfunction
  2. AC-toxin - fxns as AC, increasing cAMP levels - causes edema and phagocytic dysfunction
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12
Q

Clostridium botulinum - toxin and MOA

A

Botulinum toxin, blocks presynaptic release of ACh at NMJ, resulting in flaccid paralysis.

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13
Q

Clostridium difficile - two toxins and MOA

A
  1. Toxin A - recrutis, activates neutrophils leading to cytokine release resulting in mucosal inflammation, fluid loss, diarrhea
  2. Toxin B - Induces actin depolymerization, leading to mucosal cell death, bowel wall necrosis and psudomembrane formation
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14
Q

Shigella dysenteruae - toxin and MOA

A

Shiga toxin - halts protein syntehsis by disabling 60s ribosomal subunit, leading to intestinal epithelial cell death and diarrhea

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15
Q

Streptococcus pyogenes - two toxins and MOA

A
  1. Pyrogenic exotoxin - acts as superantigen, inducing shock and fever, assocaited with scarlet fever and streptococcal TSS
  2. Streptolysin O and S - damages erythrocyte membranes, causing beta-hemolysis
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16
Q

Common antibiotic resistance mechanisms to penicillins

A

Beta lactamase, Extended spectrum Beta Lactamase
Mutated Penicillin Binding Protein
Mutated porin protien

17
Q

Common antibiotic resistance mechanisms to vancomycin

A

mutated peptidoglycan cell wall (VRE- vanc resistant enterococcus)
imparied influx/increased efflux

18
Q

Common antibiotic resistance mechanisms to quinolones

A

mutated DNA gyrase

impaired influx/increased efflux

19
Q

Common antibiotic resistance mechanisms to aminoglycosides

A

aminoglycoside-modifying enzymes
mutated ribosomal subunit protein
mutated porin protein

*Pseudomonas

20
Q

Common antibiotic resistance mechanisms to tetracyclines

A

impaired influx/increased efflux

inactive enzyme

21
Q

Common antibiotic resistance mechanisms to rifamycins

A

mutated RNA polymerase

22
Q

Class three antiarrhythmics (K-blockers)

A

sotalol, dofetilide, amiodarone

23
Q

Class four antiarrhythmis (L-type Ca-CB)

A

verapamil, diltizem

24
Q

drug that interacts with A1 receptor on cardiac cells, activating K-channels and increasing potassium conductance, causing membrane potential to remain negative for a longer period - resulting in slowing of sinus rate and increased AV nodal conduction delay

A

adenosine

25
Q

Drug that inhibits Na/K/ATPase pump on myocardial cells, resutling in increased intracellular Na, leading to rise in intracellular calcium facilitate dby Na-Ca exchanger.

A

Digoxin

26
Q

What type of drug increases refractory period of AV node and slows rate of discharge of sinus or ectopic peacemakers?

A

Esmolol - Beta clocker (calss two antiarrhythmics)

27
Q

Where do thiazide diuretics work?

A

at distal tubule, increasing Cl and Na reabsorption

28
Q

Best drug for decreasing TG

A

fibrates

29
Q

best drug for decreasing LDL

A

statins

30
Q

drug that decreases LDL, but may increase TG

A

resins (bile acid sequesteration blockers)

31
Q

Highest increase in HDL

A

niacin

32
Q

DoC for a person who develops sustained tonic-clonic seizures without gain of consciousness between episodes.

A

This is status epilepticus - give IV benzo to increase frequency of GABA-A receptor activation to increase Chloride channel opening to increase post-synaptic Cl influx.

33
Q

MOA of amphotericin toxicities

A

binds slightly to cholesterol in cell membranes

34
Q

The most potent diuretic, used to quickly tx acute decompensated HF. Where does it act?

A

Loops. Act on the thick ascending loop Na/K/2Cl. (furosemide)

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