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176 Cards in this Set

  • Front
  • Back
most enzymatic reactions follow a hyperbolic curve i.e. they follow:
Michaelis-Menten kinetics

**Velocity over [Substrate]**
enzymatic reactions that exhibit a sigmoid curve indicate ________________ kinetics
*cooperative* kinetics

- e.g. hemoglobin curve
MM kinetics players:

[S] =
concentration of the Substrate
MM kinetics players:

Km =

(formula)
[S] at 1/2 Vmax
Km is inversely related to:
the affinity of the enzyme for its substrate

- the larger the Km, the less affinity an enzyme has for a substrate
Vmax is DIRECTLY proportional to:
[E],

the enzyme concentration

- the larger the [E], the higher the Vmax
Lineweaver-Burk plot: increasing the y-intercept =>
DECreasing the Vmax
L-B plot: the further the x-intercept is to the right, the greater:
the Km,

and the LOWER the affinity
pharmacokinetics =
the effects of the body on the drug
**pharmacokinetics ~~ ADME, which stands for:**
Absorption

Distribution

Metabolism

Excretion
pharmacodynamics =
effects of the drug on the body

- includes r' binding, efficacy, potency, SE's/toxicity
bioavailability (F) =
*fraction* of administered drug that reaches systemic circulation unchanged
**for an IV dose, F =

(bioavailability)
100%

- duh
orally, F is typically <100%, due to:

(2)
incomplete absorption,

FPE
Volume of Distribution (Vd) =
theoretical volume occupied by the total absorbed drug amount at the plasma concentration
formula for Vd:
Vd = amount of drug in the body /
plasma drug concentration
the apparent Vd of plasma protein-bound drugs can be altered by liver and kidney dz, e.g.
decreased protein binding => increased Vd

also, drugs may distribute in more than one compartment
LOW Vd ~~
plasma protein-bound drugs

- found in blood
medium Vd ~~
ECF
HIGH Vd ~~
ALL tissues, including fat
a drug infused at a constant rate takes _____________________ to reach steady state
**4-5 half lives**
it takes _____ half-lives to reach ___% of the steady-state level
3.3 half-lives to reach 90% of the steady-state level
Clearance (Cl) =
**volume of plasma** cleared of drug per unit time
Clearance may be impaired with defects in:

(3)
1. cardiac,

2. hepatic,

or

3. renal function
in renal or hepatic dz, maintenance dose ______________ and loading dose ________________
decreases;

loading dose is usually unchanged
**time to steady state depends on half-life and is INDEPENDENT of:**

(2)
dose OR dosing frequency
Cp =
*target* plasma conc. at steady state
zero-order elimination means:
rate of elimination is CONSTANT, regardless of Cp

- that is, **a constant AMOUNT of drug is eliminated per unit time**

=> Cp decreases *linearly* with time
zero-order elimination is _____________- _____________ elimination
capacity-limited elimination
3 best examples of drugs that show zero-order elimination:

PEA
Phenytoin

Ethanol

Aspirin

(all at high or toxic concentrations)

*PEA is round like a Zero*
first-order elimination means rate of elimination is:
proportional to the drug concentration

- i.e. **a constant FRACTION of drug is eliminated per unit time**

- that's why t1/2 is a first-order property

=> Cp decreases *exponentially* with time
first-order elimination is ________ - _______________ elimination
flow-dependent elimination
what kind of mlcls are **trapped** in urine and cleared quickly?
*ionized* mlcls

- but neutral mlcls can be reabsorbed
weak acids are trapped in:
basic environments

- treat acid OD with bicarb
3 examples of weak acid drugs:
1. Phenobarbitol

2. MTX

3. Aspirin
weak bases (like amphetamines) are trapped in acidic environments; treat OD with:
ammonium chloride

NH4Cl
Phase I drug metabolism =

(3 means, 1 effect)
1. reduction

2. oxidation

3. hydrolysis with cytochrome P450

=> slightly-polar, water-soluble metabolites which are often still active
Phase II metabolism =
conjugation

=>=> VERY polar, INactive metabolites, which are renally excreted
**conjugation (i.e. Phase II) has 3 forms:**
Glucuronidation

Acetylation

Sulfation

(GAS)
geriatric patients lose ________ ___ first
Phase I first;

- therefore, geriatric pts have GAS
(conjugation/Phase II)
pts who are slow acetylators have greater SE's from certain drugs b/c of:
rate of decrease in metabolism
efficacy =
max effect that a drug can produce
high-efficacy drug classes include:

(4)
1. analgesics

2. antibiotics

3. antiHISTamines

4. decongestants
partial agonists have less __________ than full agonists
efficacy

- the maximum effect that they are capable of producing is lower than that of the full agonists
potency =
*amount* of drug *needed* for a given effect
increased potency ~~
**increased affinity for the r'**
examples of highly-potent drug classes:

(3)
1. chemo

2. anti-HTN

3. statins
2 effects of competitive antagonists on efficacy and potency:
1. NO change in efficacy

2. dec. potency (shift curve right)
both noncompetitive antagonists and irreversible antagonists shift the curve:
DOWN

=> *DEC efficacy*
partial agonists like Buprenorphine decrease:
efficacy

- duh
therapeutic index = m. of drug safety;

formula =
TD50 / ED50
TD50 =

ED50 =
median toxic dose

median effective dose
therapeutic window = m. of:
clinical drug's effectiveness for a pt

- define better check
safer drugs have higher:
T. index values
4 examples of HIGH (bad) T Index drugs:
1. Digoxin

2. Li2+

3. Theophylline

4. warfarin
which 2 components of the sympathetic NS are innervated by the parasympathetic NS?
1. adrenal medulla

2. sweat glands
botulinum toxin prevents release of NT at:
ALL cholinergic terminals
Nicotinic r's are ligand-gated ________ channels
Na+/K+
2 types of Nicotinic chans, and their locations:
1. Nn
(autonomic ganglia)

2. Nm
(NMJ's)
3 features of Muscarinic ACH r's:
1. G-prot-coupled r's

2. act through 2nd messengers

3. five subtypes
4 kinds of sympathetic r's and their G-prot. class:
a1 (q class)

a2 (i class)

B1 (s)

B2 (s)

QISS class
3 functions of a1 r's:
1. vasoconstriction

2. contract pupillary dilator muscle
=> dilation [mydriasis]

3. contraction of intestinal and bladder sphincter muscles
4 functions of a2 r's:
1. dec. sympathetic outflow

2. dec. insulin release

3. dec. lipolysis

4. inc. plat. agg.
4 functions of B1 r's:
1. inc. HR

2. inc. contractility

3. inc. renin release

4. inc. lipolysis
9 functions of B2 r's:
1. vasodilation

2. bronchodilation
(that's why you use B2 agonists to tx asthma)

3. inc. HR

4. inc. contractility

5. inc. lipolysis

6. inc. insulin release

7. dec. uterine tone

8. relax ciliary muscles (=> dilation/mydriasis)

9. inc. aqueous humor production
G-prot. class of M1, M2, and M3 r's, respectively:
M1 = q class

M2 = i class

M3 = q class
M1 r's are found in:

(2)
1. CNS,

2. enteric NS
2 functions of M2:
1. dec. AV node conduction => dec. HR

2. dec. contractility of *atria*
2 functions of M3:
1. inc. exocrine gland secretion
(lacrimal, salivary, gastric acid)

2. inc. gut peristalsis

3. inc. bladder contraction

4. bronchoconstriction

5. inc. pupillary sphincter muscle contraction
(=> miosis)

6. ciliary muscle contraction
(=> accomodation)
G-prot. class of D1 and D2 r's, respectively:
D1 = s

D2 = i
function of D1:
relaxes renal vascular SM
function of D2 r's:
modulate transmitter release, esp. in brain
G-prot. class of Histamine 1 and H2 r's:
H1 = q

H2 = s
5 functions of H1 r's:
1. inc. nasal and bronchial mucus production

2. inc. vascular permeability

3. bronchoconstriction (via mast cells)

4. pruritus

5. pain
1 function of H2 r's =
inc. gastric secretion
G-prot. class of Vasopressin1 and V2 r's:
V1 = q

V2 = s
functions of V1 r's:

(2)
general vasoconstriction,

release of PG's
=> renal vasodilation
function of V2 r's =
inc. H2O permeability and reabsorption in the collecting tubules of the kidney

(via ADH)
release of NOR from a sympathetic nerve ending is modulated by:

(3)
1. NOR itself
(acting on presynaptic a2-r's)

2. A2

3. other substances
MG used to be diagnosed with Edrophonium; now it's diagnosed with:
anti-ACH r' AB test
with ALL cholinergic agents, watch for exacerbation of:

(3)
1. COPD

2. asthma

3. peptic ulcers
what enzyme makes ACH?
choline acetyltransferase
cholinesterase poisoning often occurs via:
organophosphates/pesticides

which **IRREVERSIBLY** inhibit ACHE
symps of irreversible ACHE inhibition =

DUMBBELSS
1. diarrhea

2. urination

3. miosis
(excessive constriction)

4. Bronchospasm

5. Bradycardia

6. Excitation (of skel. muscle, CNS)

7. Lacrimation

8. Sweating

9. Salivation
antidote to organophosphates =
Atropine (competitive inhibitor of oP's ) + Pralidoxime (regenerates ACHE if given early)
Atropine is a muscarinic antagonist used for:

(2)
1. bradycardia

2. ophthalmic applications
Atropine in the eye:

(2)
1. mydriasis
(dilation of pupil)

2. cycloplegia
(paralysis of the ciliary muscle of the eye)
Atropine in the airway:
decreases secretions
Atropine in the stomach:
decreases acid secretions
Atropine in the gut:
decreased motility
Atropine in the bladder:
**dec. urgency** in cystitis
Atropine stops DUMBBELSS, except for:
***E, Excitation of skeletal muscle and CNS, which is mediated by Nicotinic r's***
7 SE's of Atropine:
1. hot as a hare
(due to decreased sweating; HR increases too)

2. tachycardia

3. red as a beet

4. dry as a bone
(skin, mouth)

5. blind as a bat
(mydriasis)

6. can't pop a squat
(constipation, urinary retention)

7. mad as a hatter
disorientation
Atropine can also cause:

(3)
1. acute/closed-angle glaucoma in the elderly, due to mydriasis

2. urinary retention in men with BPH

3. hyperthermia in infants
Jimson wee (datura) => gardener's pupil, which is:
mydriasis due to plant alkaloids
NEVER give _______________ if cocaine intoxication is suspected;
B-blockers

- can lead to unopposed a1 activation and extreme HTN
NOR vs. Isoproterenol

NOR causes increase in systolic and diastolic BP's as a result of a1-mediated vasoconstriction, =>
inc. MAP => bradycardia

- Isoproterenol, however, has little alpha effect but causes *B2-*mediated vasodilation, resulting in DEC. MAP, and INC. HR through B1 and reflex activity
SE's of B-blockers:

(5)
1. impotence

2. adverse CV effects
(brady, AV block, CHF)

3. adverse CNS effects
(sez's, sedation, sleep alterations)

4. dyslipidemia
(Metoprolol only)

5. exacerbations in asthma/COPD
never give B-blockers to:
cocaine users,

due to risk of unopposed alpha-adrenergic r' agonist activity
in diabetics, benefits of B-blockers:
outweigh the potential risk of masking hypoglycemia;

USE in diabetics
B1-selective properties B-blockers:

(5)

A BEAM
1. Acebutolol

2. Betaxolol

3. Esmolol

4. Atenolol

5. Metoprolol
which 2 B-blockers are partial agonists?

(activate B1 and B2)
1. Acebutolol
(B1>B2)

2. Pindolol
(B1=B2)
3 nonselective B-blockers

(i.e. B1 = B2):

Try Nonselective Pills
1. Timolol

2. Nadolol

3. Propranolol
2 non-selective ALPHA and B-antagonists:
1. Carvedilol

2. Labetalol
what does Nebivolol do?
combines cardiac-selective B1-blocking with

stimulation of B3 r's,

which activate NO synthase in the vasculature
what is the antidote for Acetaminophen?
N-acetylcysteine

(replenishes glutathione)
what is the antidote for ACHE inhibitors and organophosphates?

(2)
Atropine followed by Pra-li-doxime (which DOES undo E of skel. musc. and CNS, unlike Atropine)
what is the antidote for basic amphetamines?
NH4Cl

(which acidifies urine, thereby trapping the basic amphetamines and excreting them)
what is the antidote for anti-muscarinic and anticholinergic agents?

(2)
Physostigmine (ACHE inhibitor = pro-ACH),

control hyperthermia
what is the antidote for Benzo's?
Flumazenil
what is the antidote for B-blockers?
Glucagon
what is the antidote for Carbon Monoxide?

(2)
100% O2,

hyperbaric O2

(^at a pressure greater than nl)
what is the antidote for copper/arsenic/gold?
Penicillamine
what is the antidote for cyanide?

(3)
Nitrite,

Thiosulfate,

hydroxo-cobalamin
what is the antidote for Digitalis?
anti-digoxin Fab AB's
what is the antidote for Heparin?
Protamine

(reverses heparin effects)
what is the antidote for Iron?

(2)
DeFEroxamine, deFErasirox
what is the antidote for Lead?

(4)
1. EDTA

2. Dimercaprol

3. Succimer

4. Penicillamine
what is the antidote for Mercury?

(2)
Dimercaprol (BAL),
Succimer

(Penicillamine for Lead, Arsenic, Copper, Gold)
- you would not use Penicillamine for Mercury;

(Dimercaprol for Lead, Arsenic, Gold, Mercury)
- you would not use Dimercaprol for Copper
what is the antidote for methanol or ethylene glycol (antifreeze)?

(first-line, second-line)
Fomepizole

- second choice = ethanol, dialysis
what is the antidote for Methemoglobin?

(2)
Methylene blue,

Vit. C
what is the antidote for opioids?
Naloxone
what is the antidote for Salicylates?

(2)
HCO3 (bicarb - aspirin is an acid),

dialysis
what is the antidote for TCA's?
NaHCO3
(alkalizes plasma, adds Na+ for heart)
Aminocaproic acid is the antidote for:

(3)
1. tPA

2. streptokinase

or

3. urokinase
what is the antidote for Warfarin/Coumadin?

(2)
FFP if active bleeding/need immediate;

Vit. K (slower)
coronary vasospasm occurs with:

(3)
1. cocaine

2. Sumatriptan

3. ergot alkaloids
drugs that cause cutaneous flushing:
VANC



1. Vancomycin

2. Adenosine

3. Niacin
(B3)

4. Ca2+-blockers
drugs that cause DCM:
"-rubicins"
Some Risky Meds Can Prolong QT
Sotalol

Reserpine
(anti-HTN)

Macrolides

Chloroquine
(a quinidine anti-malarial)

Protease inhibitors

Quinidine

Thiazides
hot flashes:

(2)
1. Tamoxifen

2. Clomiphene
(hypothal. EST r' antagonist that stimulates ovulation)
HYPERglycemia:
Taking Pills Necessitates Having Blood Checked




1. Tacrolimus
(immuno-suppressant folowing transplant)

2. Protease inhibitors
(-navirs)

3. Niacin
(B3)

4. HCTZ

5. B-blockers

6. Corticosteroids
hypothyroidism:

(3)
1. Li2+

2. Amiodarone

3. Sulfonamides
(antib's)
as a prokinetic, what does Erythromycin cause?

(2)
acute cholestatic hepatitis and jaundice
diarrhea:
Might Excite Colon On Accident


1. Metformin

2. Erythromycin

3. Colchicine
(relieves pain in gout)

4. Orlistat
(lipase inhibitor)

5. Acarbose
focal-to-massive hepatic necrosis:
liver HAVAc



1. Halothane
(volatile anesthetic)

2. Amanita phalloides (death cap mushroom)

3. Valproic acid

4. Acetaminophen
TB drug that causes hepatitis:
INH

(Injures Neurons and Hepatocytes)
pancreatitis:
Drugs Causing A Violent Abd. Distress




1. Didanosine
(ddI)

2. Corticosteroids

3. Alcohol

4. Valproic acid

5. Azathioprine
(imm-suppressant for transplants)

6. Diuretics (Furosemide, HCTZ)
Pseudomembranous colitis:

(3)
1. Clindamycin

2. Ampicillin

3. Cephalosporins

(antibiotics predispose to superinfection with R C. diff)
agranulocytosis (killing granulocytes):
Drugs CCCrush Myeloblasts and Promyelocytes


1. Dapsone
(leprosy)

2. Clozapine

3. CBZ

4. Colchicine

5. Methimazole

6. PTU
aplastic anemia:
Can't Make New Blood Cells Properly



1. CBZ

2. Methimazole

3. NSAIDs

4. Benzene

5. Chloramphenicol

6. PTU
Direct Coombs-positive HmA:

(2)
1. Methyldopa

2. Penicillin
drug that can cause gray Baby Syndrome:
chloramphenicol
**hemolysis in G6PD**:
D PAINS


1. Dapsone
(leprosy antib')

2. Primaquine
(for malaria)

3. Aspirin and NSAIDs

4. INH

5. Nitrofurantoin
(UTI antib')

6. Sulfonamides
megaloblastic anemia:

(3)
1. Phenytoin

2. MTX

3. Sulfa drugs
thrombocytopenia:

(2)
1. Heparin

2. Cimetidine
(H2-blocker for PUD)
class of hematologic drugs that can cause thrombotic complications:
OCP's
cinchonism:
(temporary deafness, ringing in ears, HA, rash)

(2)
1. Quinidine

2. Quinine
Parkinson-like syndrome:
*ARM*


1. high-potency typical Antipsychotics

2. Reserpine
(treats HTN by preventing DOPA leaving (VMAT))

3. Metoclopramide (via D2 block)
(antiemetic, pro-gastrokinetic)
sez's:
I BITE 'M


1. INH

2. Bupropion

3. Imipenem/cilastatin

4. Tramadol
(centrally-acting opioid)

5. Enflurane
(volatile liquid anesthetic)

6. Metoclopramide
tardive dyskinesia:

(2)
1. typical antipsychotics (high-potency)

2. Metoclopramide
(anti-emetic, pro-gastrokinetic)
diabetes insipidus:

(2)
1. Li2+

2. Demeclocycline
(tetracycline antib')
Fanconi syndrome:

(1)
expired tetracycline
hemorrhagic cystitis:

(2)
1. Cyclophosphamide
(treats leukemia and lymphoma)

2. Ifosfamide
(alkylating agent for CA)

- prevent by co-administering with mesna
interstitial nephritis:

(3)
1. PCN's

2. NSAID's

3. Furosemide
SIADH:

(3)
1. CBZ

2. Cyclophosphamide

3. SSRI's
fat redistribution/central obesity/peripheral wasting:
fat PiG


1. Protease inhibitors

2. Glucocorticoids
gingival hyperplasia:
PVC-N



1. Phenytoin

2. Verapamil
(Ca2+ antagonist)

3. Cyclosporine
(immunosuppressive)

4. Nifedipine
(Ca2+ antagonist)
hyperuricemia (gout):
Painful, Tophi, and Feet Need Care



1. Pyrazinamide

2. Thiazide diuretics

3. Furosemide

4. Niacin
(B3)

5. Cyclosporine
myopathy:

(8)
1. fibrates
(treat hyperTG)

2. Niacin

3. Colchicine
(for pain in gout)

4. Hydroxychloroquine
(anti-inflammatory)

5. INF-a

6. Penicillamine
(chelator)

7. statins

8. glucocorticoids
osteoporosis:

(2)
1. corticosteroids

2. heparin
photosensitivity:
only *SAT Q* mins in the sun


1. Sulfonamides

2. Amiodarone

3. Tetracyclines

4. Q's
global rash (SJS):
AASP


1. AED's (Ethosuximide, CBZ, Lamotrigine, Phenytoin, Phenobarbital)

2. Allopurinol

3. Sulfa drugs

4. Penicillin
5 causes of DILE:
1. Hydralazine

2. Procainamide

3. INH


(not as bad)
4. Minocycline
5. Quinidine
teeth discoloration:

(1)
tetracyclines
tendonitis, tendon rupture, and cartilage damage:

(1 class)
FQ's
dry cough:

(1 class)
ACEI's
pulmonary fibrosis:

BAM-B had pulm. fibrosis
1. Bleomycin
(antib', Hodgkins)

2. Amiodarone

3. MTX

4. Busulfan
(anti-neoplastic)
4 with antimuscarinic effect:
1. Atropine

2. TCA's

3. H1-blockers

4. low-potency antipsychotics (C, T)
Disulfiram-like rxn to alcohol:

(intense nausea, flushing, as if on Disulfiram as an alcoholic)

(5)
1. Metronidazole

2. certain cephalosporins

3. Griseofulvin

4. Procarbazine
(anti-neoplastic)

5. 1st-gen sulfonylureas
nephrotoxicity AND ototoxicity:
VALC

1. Vancomycin

2. Aminoglycosides

3. loop diuretics

4. Cisplatin
(chemo)
8 inducers of cytochrome P-450:
1. chronic alcohol use

2. Modafinil

3. Phenytoin

4. Phenobarbital

5. Nevirapine

6. Rifampin

7. Griseofulvin

8. CBZ
8 substrates of cytochrome P-450:

Always, Always, Always, Always Think When Starting Others
1. AED's

2. antidepressants

3. antipsychotics

4. anesthetics

5. Theophylline

6. Warfarin

7. Statins

8. OCP's
12 inhibitors of P-450:

A cute Gentleman Cipped Iced Grapefruit juice Quickly And Kept Munching on Soft Cinnamon Rolls
1. acute alcohol use

2. Gemfibrozil

3. Ciprofloxacin

4. Isoniazid

5. grapefruit juice

6. Quinidine

7. Amiodarone

8. Ketoconazole

9. Macrolides

10. Sulfonamides

11. Cimetidine

12. Ritonavir
8 Sulfa drugs:
Popular FACTSSS


1. Probenecid
(excretion of uric acid)

2. Furosemide

3. Acetazolamide
(carbonic anhydrase inhibitor)

4. Celecoxib
(cox-2 inhibitor)

5. Thiazides

6. Sulfonamide antibiotics

7. Sulfasalazine

8. Sulfonylureas
(anti-diabetic)
pts with sulfa allergies may develop:

(7 symps)
1. fever

2. UTI

3. SJS

4. HmA

5. thrombocytopenia

6. agranulocytosis

7. urticaria (hives)

- symps range from mild to life-threatening