pharmacology Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

Enzyme kinetics:

  1. Michaelis-Menten kinetics
  2. Lineweaver-Burk plot
  3. Enzyme inhibition
A
  1. Michaelis-Menten kinetics
    - Km is inversely related to the affinity of the enzyme for its substrate.
    - Vmax is directly proportional to the enzyme concentration
    - most enzyme reactions follow a hyperbole curve (follow Michaelis-Menten kinetics). However, enzymatic rnxs that follow cooperative kinetics (hemoglobin) have sigmoid curve.
  2. Lineweaver-Burk plot
    - inc y-intercept, dec Vmax
    - the further to the right the x-intercept, the greater the Km, and lower the affinity
  3. Enzyme inhibition
    - competitive inhbitors cross each other competitively, whereas noncompetitive inhibitors do not
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pharmacokinetics:

  1. Bioavailability (F)
  2. Volume of distribution (Vd)
A
  1. Bioavailability (F)
    - fraction of administered drug that reaches systemic circulation unchanged
    - for an IV dose F=100%
    - orally, F typically <100% to incomplete absorption and first pass metabolism
  2. Volume of distribution (Vd)
    - theoretical fluid volume required to maintain the total absorbed drug amount at the plasma concentration
    - Vd of plasma protein-bound drugs can be altered by liver and kidney disease (dec protein binding, inc Vd)
    - Vd=amount of drug in body/plasma drug concentration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Volume of distribution (Vd): distribution, drug types

  1. low (4-8L)
  2. Medium
  3. High
A

Vd, distribution, drug types

  1. Low (4-8L)bloodlarge/charged molecules; plasma protein bound
  2. mediumECFsmall hydrophilic molecules
  3. Highall tissuessmall lipophilic molecules, especially if bound to tissue protein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Pharmacokinetics:

  1. Half-life (t1/2)
  2. Clearance (CL)
A

1.Half-life (t1/2)
-The time required to change the amount of drug in body by ½ during elimination (or constant infusion).
-property of first-order elimination.
-A drug infused at a constant rate takes 4-5 half lives to reach steady state
T1/2=0.7 x Vd/CL

2.Clearance (CL)
-relates the rate of elimination to the plasma concentration
-clearance may be impaired with defects in cardiac, hepatic, or renal function
CL=rate of elimination of drug/plasma drug concentration/plasma drug concentration=Vd x Ke (elimination constant)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Dosage calculations

A

-loading dose=Cp x Vd/F
-maintenance dose=Cp x CL/F
Cp=target plasma concentration
-in renal or liver dz, maintenance does dec and loading dose is unchanged
-time to steady state depends primarily on t1/2 and is independent of dosing frequency or size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Elimination of drugs:

  1. zero-order elimination
  2. first-order elimination
A
  1. zero-order elimination
    - rate elimination is constant regardless of Cp (ie. Constant amount of drug elimination per unit time)
    - Cp dec linearly with time
    - examples of drugs: Phenytoin, Ethanol, Aspirin (at high or toxic concentration)
    - capacity-limited elimination
    * **PEA (a pea is round, shaped all the 0 like in zero-order
  2. first-order elimination
    - rate of elimination is directly proportional to the drug concentration (ie. Constant fraction of drug eliminated per unit time)
    - Cp dec exponentially with time
    - flow dependent elimination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Urine pH and drug elimination:

  1. Weak acids
  2. weak bases
A

-ionized species are trapped in urine and cleared quickly. Neutral forms can be reabsorbed

1.Weak acid- ex: phenobarbital, methotrexate, aspirin. Trapped in basic environments. Treat overdose with bicarbonate
RCOOH (lipid soluble)  [RCOO- + H+] (trapped)

2.Weak bases- ex: amphetamines. Trapped in acidic environments. Treat overdose with ammonium chloride
RNH3 (trapped)  [RNH2 + H+] (lipid soluble)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Drug metabolism

  1. Phase I
  2. Phase II
A
  1. Phase I
    - reduction, oxidation, hydrolysis with cytochrome P-450 usually yield slightly polar water soluble metabolites (often still active)
    - geriatric pts lose phase I first
  2. Phase II
    - conjugation (Glucuronidation, Acetylation, Sulfation) usually yields very polar, inactive metabolites (renally excreted)
    - Geriatric pts have GAS (phase II). Pts who are slow acetylation have greater side effects from certain drugs because of the dec rate of metabolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Efficacy vs. potency

A
  1. Efficacy -maximal effect a drug can produce. High efficacy drug classes are analgesic (pain) medications, antibiotics, antihistamines, decongestants. Partial agonists have less efficacy than full agonists
  2. potency- amount of drug needed for given effect. Inc potency, inc affinity for receptor. High potent drug classes include chemotherapeautic (cancer) drugs, antihypertensive (blood pressure) drugs, and antilipid (cholesterol) drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Receptor Binding:

  1. competitive antagonist
  2. Noncompetitive antagonist
  3. Partial agonist
A
  1. competitive antagonistshifts curve to rightdec potency, no change in efficacy. Can be overcome by increasing the concentration of agonist substrate. Ex: Diazepam + flumazenil on GABA receptor
  2. Noncompetitive antagonistshifts curve downdec efficacy. Cannot be overcome by increasing agonist substrate concentration. Ex: NE + phenooxybenzamine on alpha-receptors
  3. Partial agonist acts at same site as full agonist, but with reduced maximal effect dec efficacy. Potency is a different variable and can be inc or dec. Ex:morphine (full agonist) + buprenorphine (partial agonist) at opioid micro-receptor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Therapeutic index

A
  • Measurement of drug safety
  • LD50/ED50= median lethal dose/median effective dose
  • TITLE: Therapeutuc Index= LD50/ED50
  • safer drugs have higher TI values.
  • ex: of drugs with low TI values include digoxin, lithium, theophylline, and warfarin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Therapeutic window

A

Meaure of clinical drug safety. Range of minimum effective dose to minimum toxic dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Central & peripheral nervous system

1.para/sympathetic & somatic systems and their effects on organs system

A

1.parasympathtic:
-cardiac and smooth muscles,
-gland cells
Nerve terminals

  1. sympathetic
    - sweat glands
    - cardiac and smooth muscle
    - gland cells
    - nerve termainals
    - renal vasculature
    - smooth muscle
  2. somatic
    - skeletal muscle
  • *note: that the adrenal meduall and asweat flands are part of the sympathetic nervous systentbut are innervated by cholinergic fibers
  • botulinum toxix prevents release of neurotransmitter at all cholinergic terminals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

ACh receptors

A
  • Nicotinic ACh receptors are ligand-gated Na+/K+ channels; N(N) [found in automatic ganglia] and N(M) [found in neuromuscular junction) subtypes
  • muscarinic ACh receptors are G-protein-coupled receptors that act through 2nd messengers
  • 5 subtypes: M1, M2, M3, M4, M5
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

G-protein-linked 2nd messengers: sympathetic:

  1. receptors (4)
  2. G-protein class
  3. major functions
A
  1. alpha1–>q–>inc vascular smooth muscle contraction, inc pupillary dilator muscle contraction (mydriasis), inc intestinal and bladder sphincter muscle contraction
  2. alpha2–>i–>dec sympathetic outflow, dec insulin release dec lipolysis, inc platelet aggregation
  3. beta1–>s–>inc heart rate, inc contractility, inc renin release, inc lipolysis
  4. beta2–>s–>vasodialtion, bronchodilation, inc heart rate, inc contractility, inc lipolysis, inc insulin release, dec uterine tone (tocolysis), ciliary muscle relaxation, inc aqueous humor production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

G-protein-linked 2nd messengers: parasymathetic

  1. receptors (3)
  2. G-protein class
  3. major functions
A
  1. M1–>q–>CNS, enteric nervous system
  2. M2–>i–>dec heart rate and contractility of atria

3.M3–>q–>inc exocrine gland secretion (eg. lacrimal, gastric acid), inc gut peristalsis, inc bladder contraction, bronchoconstriction, inc pupillary sphincter muscle contraction (miosis), ciliary muscle contraction (accommodation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

G-protein-linked 2nd messengers: Dopamine

  1. receptors (2)
  2. G-protein class
  3. major functions
A
  1. D1–>s–>relaxes renal vascular smooth muscle

2. D2–>i–>modulates transmitter release, especially in brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

G-protein-linked 2nd messengers: Histamine

  1. receptors (2)
  2. G-protein class
  3. major functions
A
  1. H1–>q–>inc nasal and bronchial mucus production, contraction of bronchioles, pruritus, pain
  2. H2–>s–>inc gastric acid secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

G-protein-linked 2nd messengers: Vasopressin

  1. receptors (2)
  2. G-protein class
  3. major functions
A
  1. V1–>q–>inc vascular smooth muscle contraction

2. V2–>s–>inc H2O permeability and reabsorption in the collecting tubules of the kidney (V2 is found in the 2 kidneys)

20
Q

Chollinomimetic agents: direct agonists

  • clinical applications–>action
    1. Bethanechol
    2. Carbachol
    3. Pilocarpine
    4. Methacholine
A
  1. Bethanechol
    - posoperative ileus, neurogenic ileus, and urinary retention
    - activates bowel, and bladder smooth muscle; resistant to AChE.
    - “Bethany, call (bethanechol) me, maybe, if you want to activate your bowels and bladder.”
  2. Carbachol
    - glaucoma, pupillary contraction, and relief of intraocular pressure
    - carbon copy of acetylcholine
  3. Pilocarpine
    - potent stimulator of sweat, tears, and saliva. Open angle and closed-angle glaucoma
    - contracts ciliary muscle of eye (open-angle glaucoma), pupillary sphincter (closed-angle glaucoma); resistant to AChE.
    - “you cry, drool, and sweat on your pillow.”
  4. Methacholine
    - challenge test for dx of asthma
    - stimulates muscarinic receptors in airway when inhaled
21
Q

Chollinomimetic agents: indirect agonists (anticholinesterases)

  • clinical applications–>action
    1. neostigmine
    2. pyridostigmine
    3. edrophonium
    4. physostigmine
    5. donepezil
A
  1. neostigmine
    - postoperative and neurogenic ileus and urinary retention, myasthenia gravis, reversal of neuromuscular junction bloackade (postoperative)
    - inc endogenous ACh
    - Neo CNS= No CNS penetration
  2. pyridostigmine
    - myasthenia gravis (long acting); does not penetrate CNS
    - inc endogenous ACh; inc strength. Pyridostigmine gets rid of myasthenia gravis
  3. edrophonium
    - diagnosis of myasthenia gravis (extremely short acting)
    - inc endogenous ACh
  4. physostigmine
    - anticholingeric toxicity (crosses blood-brain barrier–>CNS)
    - inc endogenous ACh. Physostigmine “phyxes” atropine overdose
  5. donepezil
    - alzheimer’s disease
    - -inc endogenous ACh

Note:with all cholinomimetic agents, watch for exacerbation of COPD, asthma, peptic ulcers when giving to susceptible patients

22
Q

cholinesterase inhibitor poisoning

A
  • often due to organophosphates, such as parathion, that irreversibly inhibit ACheE
  • causes Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal muscle and CNS, Lacrimation, Sweating, Salivation

-antidote–atropine + pralidoxime (regenerates active AChE)

  • DUMBBELSS
  • organophosphates are components of insecticides; poisoning usually seen in farmers
23
Q

muscarinic antagonists: organ systems & applications

  1. atropine, homatropine, tropicamide
  2. benztropine
  3. scopolamine
  4. ipratropium, tiotropium
  5. oxybutynin
  6. glycopyrrolate
A
  1. atropine, homatropine, tropicamide
    - eye
    - produce mydriasis and cycloplegia
  2. benztropine
    - CNS
    - parkinson’s dz–Park my benz
  3. scopolamine
    - CNS
    - motion sickness
  4. ipratropium, tiotropium
    - respiratory
    - COPD, asthma, “I pray I can breathe soon.”
  5. oxybutynin
    - genitourinary
    - reduce urgency in mild cystitis and reduce bladder spasms
  6. glycopyrrolate
    - gastrointestinal, respiratory
    - parenteral: preoperative use to reduce airway secretions
    - oral: drooling, peptic ulcer
24
Q

Atropine effects on organ system & toxicity

  1. eye
  2. airway
  3. stomach
  4. gut
  5. bladder
  6. toxicity
  7. side effects
A

-muscarinic antagonist. used to treat bradycardia and for ophthalmic applications
1.eye
-inc pupil dilation, cycloplegia
-blocks DUMBBeLSS. skeletal muscle and CNS excitation mediated by nicotinic receptors.
2.airway
-dec secretions
3.stomach
-dec acid secretion
4.gut
-dec motility
5.bladder
-dec urgency in cystitis
6.toxicity
-inc body temperature (due to dec sweating); rapid pulse; dry mouth; dry flushed skin; cycloplegia; constipation; disorientation
-can cause acute angle-closure glaucoma in elderly (due to mydriasis), urinary retention in men with prostatic hyperplasia, and hyperthermia in infants
7.side effects
-hot as a hare
-dry as a bone
-red as a beet
-blind as a bat
-mad as a hatter
Jimson weed (Datura)–>gardener’s pupil (mydriasis due to plant alkaloids)

25
Q

Direct Sympathomimetics:alpha 1+2, beta 1+2, dopamine, applications

  1. epinephrine
  2. norepinephrine
  3. isoproterenol
  4. dopamine
  5. dobutamine
  6. phenylephrine
  7. albuterol, salmeterol, terbutaline
  8. ritodrine
A
  1. epinephrine
    - alpha 1 +++
    - alpha 2 +++
    - beta 1 ++++
    - beta 2 ++++
    - dopamine 0
    - applications: anaphylaxis, glaucoma (open angle), asthma, hypotension
  2. norepinephrine
    - alpha 1 ++++
    - alpha 2 ++++
    - beta 1 ++
    - beta 2 0
    - dopamine 0
    - applications: hypotension (but dec renal perfusion)
  3. isoproterenol
    - alpha 1 0
    - alpha 2 0
    - beta 1 ++++
    - beta 2 ++++
    - dopamine 0
    - applications: torsade de pointes (tachycardia decreases QT interval), bradyarrhythmias (but can worsen ischemia)
  4. dopamine
    - alpha 1 +++ high dose
    - alpha 2 +++ high dose
    - beta 1 +++ med dose
    - beta 2 ++ medium dose
    - dopamine +++ low dose
    - applications
  5. dobutamine
    - alpha 1 +
    - alpha 2 +
    - beta 1 ++++
    - beta 2 +
    - dopamine 0
    - applications: heart failure, cardiac stress testing; inotropic and chronotropic
  6. phenylephrine
    - alpha 1 +++
    - alpha 2 ++
    - beta 1 0
    - beta 2 0
    - dopamine 0
    - applications: hypotension (vasoconstrictor), ocular procedures (mydriatic), rhinitis (decongestant)
  7. albuterol, salmeterol, terbutaline
    - alpha 1 0
    - alpha 2 0
    - beta 1 ++
    - beta 2 ++++
    - dopamine 0
    - applications: metaproterenol and albuterol for acute asthma; salmeterol for long term asthma or COPD control; terbutaline to reduce premature uterine contractions
  8. Ritodrine
    - alpha 1 0
    - alpha 2 0
    - beta 1 0
    - beta 2 ++++
    - dopamine 0
    - applications: reduces premature uterine contractions
26
Q

Indirect Sympathomimetics: description & applications

  1. amphetamine
  2. ephedrine
  3. cocaine
A
  1. amphetamine
    - indirect general agonist, releases stored catecholamines
    - applications: narcolepsy, obesity, attention deficit disorder
  2. ephedrine
    - indirect general agonist, releases stored catecholamines
    - applications: nasal decongestion, urinary incontinence, hypotension
  3. cocaine
    - indirect general agonist, reuptake inhibitor
    - applications: causes vasoconstriction and local anesthesia; never give beta-blockers if cocaine intoxication is suspected (can lead to unopposed alpha 1 activation and extreme hypertension)
27
Q

norepinenephrine vs. isoproterenol

A
  • norepinenephrine causes an increase in systolic and diastolic pressures as a result of alpha 1 mediated vasoconstriction–>inc mean arterial pressure–>bradycardia
  • however, isoproterenol has littler alpha effect but causes beta 2 mediated vasodilation, resulting in dec mean arterial pressure and inc heart rate through beta 1 and reflex activity
28
Q

Sympathoplegics: clonidine, alpha-methyldopa

A
  • centrally acting alpha 2 agonists, dec central sympathetic outflow
  • applications: hypertension, especially with renal dz (no dec in blood flow to kidney)
29
Q
alpha-blockers:applications &amp; toxicity
nonselective 
1.phenoxybenzamine (irreversible)
2.Phentolamine (reversible)
alpha1 selective (-osin ending)
1.prazosin, terazosin, doxazosin, tamsulosin
alpha2 selective
1.mirtazapine
A

nonselective

  1. phenoxybenzamine (irreversible)
    - pheochromocytoma (use phenoxybenzamine before removing tumor, since high levels of released catecholamines will not be able to overcome bloackage)
    - orthostatic hypotension, reflex tachycardia
  2. Phentolamine (reversible)
    - give to patients on MAO inhibitors who eat tyramine-containing foods

alpha1 selective (-osin ending)

  1. prazosin, terazosin, doxazosin, tamsulosin
    - hypertension, urinary retention in BPH
    - 1st dose orthostatic hypotension, dizziness, HA

alpha2 selective

  1. mirtazapine
    - depression
    - sedation, inc serum cholesterol, inc appetite
30
Q

Beta blockers

  1. applications (6)
  2. effects
  3. toxicity
  4. selectivity
A
  1. angina pectoris–>dec HR and contractility, resulting in dec O2 consumption
  2. MI–>beta blockers dec mortality
  3. SVT (metoprolol, esmolol)–> dec AV conduction velocity (class II antiarrhythmic)
  4. Hypertension–>dec cardiac output, dec renin secretion (due to beta-receptor blockade on JGA cells)
  5. CHF–>slows progression of chronic failure
  6. Glaucoma (timolol)–>dec secretion of aqueous humor

toxicity: impotence, exacerbation of asthma, cardiovascular adverse effects (bradycardia, AV block, CHF), CNS adverse effects (seizures, sedation, sleep alterations); use with caution in diabetics

Selectivity: beta1 selective antagonists (b1>b2)–acebutolol (partial agonist), betaxolol, esmolol (short acting), atenolol, metoprolol
***A BEAM of beta1 blockers. advantageous in pts with comorbid pulmonary dz.

nonselective antagonist (b1=b2)--propranolol, timolol, nadolol, pindolol
**please try not Being picky

nonselective (vasodilatory) alpha and beta antagonists–carvedilol, labetalol

partial beta-agonists–pindolol, acebutolol
**PAPA

31
Q

Specific antidotes for toxins

  1. acetaminophen
  2. salicylates
  3. amphetamines (basic)
  4. acetylcholinesterase inhibitors, organophosphates
  5. antimuscarinic, anticholinergic agents
  6. beta-blockers
  7. digitalis
  8. iron
  9. lead
  10. mercury, arsenic, gold
  11. copper, arsenic, gold
  12. cyanide
  13. methemoglobin
  14. carbon monoxide
  15. methanol, ethylene glycol (antifreeze)
  16. opioids
  17. benzodiazepines
  18. TCAs
  19. Heparin
  20. Warfarin
  21. tPA, streptokinase, urokinase
  22. Theophylline
A
  1. N-acetylcysteine (replenished glutathione)
  2. NaHCO3 (alkalinize urine), dialysis
  3. NH4Cl (acidify urine)
  4. atropine, pralidoxime
  5. physostigmine salicylate, control hyperthermia
  6. glucagon
  7. normalize K+, Lidocaine, Anti-dig Fab fragments, Mg2+ (KLAM)
  8. Deferoxamine, deferasirox
  9. CaEDTA, dimercaprol, succimer, penicillamine
  10. Dimercaprol (BAL), succimer
  11. penicillamine
  12. nitrite + thiosulfate, hydroxocobalamin
  13. methylene blue, vit C
  14. 100% O2, hyperbaric O2
  15. fomepizole>ethanol, dialysis
  16. naloxone/naltrexone
  17. flumazenil
  18. NaHCO3 (plasma alkalinization)
  19. Protamine
  20. Vit K, fresh frozen plasma
  21. aminocaproic acid
  22. beta blocker
32
Q

Drug reactions: cardiovascular effect & agents

  1. coronary vasospasm
  2. cutaneous flushing
  3. dilated cardiomyopathy
  4. torsades de pointes
A
  1. cocaine, sumatriptan, ergot alkaloids
  2. vancomycin, adenosine, niacin, Ca2+ channel blockers VANC
  3. doxorubicin (Adriamycin), daunorubicin
  4. class III (sotalol) and class IA (quinidine) antiarrhythmics
33
Q

Drug reactions: hematologic effect & agents

  1. agranulocytosis
  2. aplastic anemia
  3. direct Coombs-positive hemolytic anemia
  4. Gray baby syndrome
  5. hemolysis in G6PD-deficient patients
  6. megaloblastic anemia
  7. thrombotic complications
A
  1. clozapine, carbamazepine, colchicine, propylthiouracil, methimazole, dapsone
    - agranulocytosis could certatinly cause pretty major damage
  2. chloramphenicol, benzene, NSAIDs, propylthiouracil, methimazole
  3. methyldopa, penicillin
  4. chloramphenicol
  5. isoniazid (INH), sulfonamides, primaquine, aspirin, ibuprofen, nitrofurantoin
    - hemolysis IS PAIN
  6. phenytoin, methotrexate, sulfa drugs
    - having a blast with PMS
  7. OCPs (estrogens)
34
Q

drug reactions: respiratory effect & agents

  1. cough
  2. pulmonary fibrosis
A
  1. ACE inhibitors
    - ARBs like losartan–no cough
  2. BLeomycin, amiodarone, busulfan
    - its hard to BLAB when you have pulmonary fibrosis
35
Q

drug reactions: GI effect & agents

  1. acute cholestatic hepatitis, jaundice
  2. focal to massive hepatic necrosis
  3. hepatitis
  4. pseudomembranous colitis
A
  1. erythromycin
  2. Halothane, Amanita phalloides, Valproic acid, Acetaminophen
    - “Liver HAVAc”,
  3. INH
  4. Clindamycin, Ampicillin
36
Q

drug reactions: Reproductive/endrocrine effects & agents

  1. adrenocortical insufficiency
  2. gynecomastia
  3. hot flashes
  4. hyperglycemia
  5. hypothyroidism
A
  1. glucocorticoid withdrawl (HPA suppression)
  2. Spironolactone, Digitalis, Cimetidine, chronic alcohol use, estrogens, Ketoconazole
    - “some drugs create awkward knockers.”
  3. tamoxifen, clomiphene
  4. niacin, tacrolimus, protease inhibitors, HCTZ, corticosteroids
  5. lithium, amiodarone, sulfonamides
37
Q

drug reactions: musculoskeletal/connective tissue effects & agents

  1. fat redistrubution
  2. gingival hyperplasia
  3. gout
  4. myopathies
  5. osteoporosis
  6. photosensitivity
  7. Rash (Stevens-Johnson syndrome)
  8. SLE-like syndrome
  9. Teeth (kids)
  10. Tendonitis, tendon rupture, and cartilage damage
A
  1. glucocorticoids, protease inhibitors
  2. phenytoin, verapamil
  3. furosemide, thiazides, niacin, cyclosporine
  4. fibrates, niacin, colchicine, hydroxychloroquine, interferon-alpha, penicillamine, statins, glucocorticoids
    - “fish N chips give you myopathies”
  5. corticosteroids, heparin
  6. sulfonamides, amiodarone, tetracycline
    - “SAT for a photo”
  7. penicillin, ethosuximide, carbamazepine, sulfa drugs, lamotrigine, allopurinol, phenytoin, phenobarbital
    - “bad rash after a PEC SLAPP
  8. hydralazine, INH, Procrainamide, Phenytoin
    - “it’s not HIPP to have lupus.”
  9. tetracyclines
  10. fluoroquinolones
38
Q

drug reactions: Renal/GU effects & agents

  1. diabetes insipidus
  2. Fanconi’s syndrome
  3. hemorrhagic cystitis
  4. interstitial nephritis
  5. SIADH
A
  1. lithium, demeclocycline
  2. expired tetracycline
  3. cyclophosphamide, ifosfamide (prevent by coadministering with mesna)
  4. methicillin, NSAIDs, furosemide
  5. carbamazepine, cyclophosphamide
39
Q

drug reactions: neurologic effects & agents

  1. Cinchonism
  2. Parkinson-like syndrome
  3. seizures
  4. Tardive dyskinesia
A
  1. quinidine, quinine
  2. antipsychotics, reserpine, metoclopramide
  3. isoniazid, bupropion, imipenem/cilastatin, tramadol, enflurane, metoclopramide
    - “with seizuresm I bite my tongue.”
  4. antipyschotics
40
Q

drug reactions: multiorgan effects & agents

  1. antimuscarinic
  2. disulfiram-like reaction
  3. nephrotoxicity/ototoxicity
A
  1. atropine, TCAs, H1-blockers, neuroleptics
  2. metronidazole, certain cephalosporins, procarbazine, 1st generation sulfonylureas
  3. aminoglycosides, vancomycin, loop diuretics, cisplatin
41
Q

P-450 interactions: inducers & inhibitors

A
Inducers:
1.modafinil
2.barbiturates
3.St.John's wart
4.Phenytoin
5.Rifampin
6.Griseofulvin
7.carbamazepine
8.chronic alcohol use
"momma barb steals phen-phen and refuses greasy carbs chronically."
Inhibitors:
1.macrolides
2.amiodarone
3.grapefruit juice
4.isoniazid
5.cimetidine
6.ritonavir
7.acute alcohol abuse
8.ciprofloxacin
9.ketoconazole
10.sulfonamides
11.gemfibrozil
12.quinidine
"magic racks in GQ"
42
Q

sulfa drugs

A

-probenecid
-furosemide
-acetazolamide
-celecoxib
-thiazides
-sulfonamide antibiotics
-sulfasalazine
-sulfonylureas
Popular FACTSSS
-pts with sulfa allergies may develop fever, urinary tract infection, pruritic rash, Stevens-Johnson syndrome, hemolytic anemia, thrombocytopenia, agranulocytosis, and urticaria (hives).
-symptoms range from mild to life-threatening

43
Q
drug names: ending, category, example
Antimicrobial:
1.--azole
2.--cillin
3.--cycline
4.--navir
A
  1. antifungal–>ketoconazole
  2. penicillin–>methicillin
  3. antibiotic, protein synthesis inhibitor–>tetracycline
  4. protease inhibitor–>saquinavir
44
Q
drug names: ending, category, example
CNS:
1.--triptan
2.--ane
3.--caine
4.--operidol
5.--azine
6.--barbital
7.--zolam
8.--azepam
9.--etine
10.--ipramine
11.--triptyline
A
  1. 5-HT 1B/1D agonists (migrane)–>sumatriptan
  2. inhalational general anesthetic–>halothane
  3. local anesthetic–>lidocaine
  4. butyrophenone (neuroleptic)–>haloperidol
  5. phenothiazine (neuroleptic, antiemetic)–>chlorpromazine
  6. barbiturate–>phenobarbital
  7. benzodiazepine–>alprazolam
  8. benzodiazepine–>diazepam
  9. SSRI–>fluoxetine
  10. TCA–>imipramine
  11. TCA–>amitriptyline
45
Q
drug names: ending, category, example
Autonomic:
1.--olol
2.--terol
3.--zosin
A
  1. beta-antagonist–>propanolol
  2. beta2-agonist–>albuterol
  3. alpha1-antagonist—>prazosin
46
Q
drug names: ending, category, example
cardiovascular:
1.--oxin
2.--pril
3.--afil
A
  1. cardiac glycoside (inotropic agent)–>digoxin
  2. ACE inhibitor–>captopril
  3. Erectile dysfunction–>sildenafil
47
Q

drug names: ending, category, example
other:
1.–tropin
2.–tidine

A
  1. pituitary hormone–>somatotropin

2. H2 antagonist–>cimetidine