First Aid - Pharmacology

Front 1

Enzyme Kinetics - explain Km

Back 1

Km reflects the affinity of the enzyme for its substrate. It is the point on the substrate concentration vs. velocity graph where the substrate concentration leads to a reaction rate that is 1/2 of Vmax.

Km = [s] at 1/2 Vmax

Front 2

Enzyme Kinetics - explain Vmax

Back 2

Vmax is directly proportional to the enzyme concentration. It is the maximum reaction rate that can be achieved, after which point increasing the substrate concentration will not increase the rate. Thus, the enzymes are completely saturated with substrate.

Front 3

Enzyme Kinetics - explain the inverse graph and how to interpret Km and Vmax

Back 3

If you plot 1/[s] vs. 1/[v] the curve becomes linear. The y-intercept is 1/Vmax and the x-intercept is 1/-Km. If the x intercept moves to the right, Km is increased and thus affinity is lower. If the y intercept moves up, Vmax goes down.

The slope of this line is Km/Vmax.

Front 4

Enzyme Kinetics - explain the effects of competitive and non-competitive inhibitors on the inverse line (1/[s] vs. 1/v)

Back 4

A non-competitive inhibitor will decrease Vmax but the binding affinity remains unchanged (Km does not change). Therefore you see the line rotate counter-clockwise, with a higher y-intercept but the same x-intercept.

A competitive inhibitor does not effect Vmax but it increases Km (lower binding affinity). Therefore, the x-intercept shifts to the right and the y-intercept remains unchanged. Thus the line has a steeper slope (see picture).

Front 5

Enzyme Kinetics - explain the differences between competitive and non-competitive inhibitors

Back 5

Competitive inhibitors -
Resemble substrate.
Overcome by increased [s]
Bind the active site
No effect on Vmax.
Increases Km
Decreases potency.

Noncompetitive inhibitors -
Does not resemble substrate
Not overcome by increased [s]
Does not bind the active site
Decreases Vmax
No effect on Km
Decreases efficacy.

Front 6

Pharmacokinetics - Volume of Distribution (Vd)

Back 6

Relates the amount of drug in the body to the plasma concentration. Vd of plasma protein-bound drugs can be altered by liver and kidney disease (decreased protein binding, increased Vd).

Vd = (amount of drug in the body) / (plasma drug concentration)

Drugs with:
Low Vd (4-8 L) distribute in blood; are large or charged molecules.
Medium Vd distribute in extracellular space or body water; are small hydrophilic molecules that do not bind plasma proteins.
High Vd (> body weight) distribute into all tissues; are small, lipophilic molecules that bind strongly to extravascular proteins.

Front 7

Pharmacokinetics - Clearance (CL)

Back 7

Relates the rate of elimination to the plasma concentration.
CL = (rate of elimination of drug) / (plasma drug concentration)
= Vd x Ke (elimination constant)

Front 8

Pharmacokinetics - Half-life (t1/2)

Back 8

The time required to change the amount of drug in the body by 1/2 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

# half lives / concentration
1 / 50%
2 / 75%
3 / 87.5%
4 / 93.75%

Front 9

Pharmacokinetics - Bioavailability (F)

Back 9

Fraction of administered drug that reaches circulation.
IV: F = 100%
Orally: F = % that survives first pass in liver or gut

Front 10

Dosage calculations - Loading dose? Maintenance dose?

Back 10

Loading dose = Cp x Vd/F
- If you have a large volume of distribution, the loading dose needs to be higher
- If you have a small bioavailability, the loading dose needs to be higher

Maintenance dose = Cp x CL/F
- If the clearance rate is high, you needa high maintenance dose.

Cp = target plasma concentration

In renal or liver disease, maintenance dose decreases and loading dose is unchanged. Frequency of dosing is not affected by time to steady state but is affected by t1/2.

Front 11

Elimination of drugs - Zero-order elimination

Back 11

Rate of elimination is constant regardless of Cp (i.e., constant AMOUNT of drug is eliminated per unit time). Cp decreases linearly with time. Examples of drugs - Phenytoin, Ethanol, and Aspirin (at high or toxic concentrations).

Front 12

How to remember some examples of drugs that are zero-order elimination?

Back 12

PEA - a pea is round, shaped like the "O" in zero-order
Phenytoin
Ethanol
Aspirin (at high or toxic concentrations)

Front 13

Elimination of drugs - First-order elimination

Back 13

Rate of elimination is proportional to the drug concentration (i.e., constant FRACTION of drug eliminated per unit time). Cp decreases exponentially with time.

Front 14

Urine pH and drug elimination - basics

Back 14

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

Front 15

Urine pH and drug elimination - Weak acids

Back 15

Examples: phenobarbital, methotrexate, aspirin. Trapped in basic environments. Treat overdose with bicarbonate.

RCOOH <===> RCOO- + H+
(lipid soluble) (trapped)

Front 16

Urine pH and drug elimination - Weak bases

Back 16

Examples: amphetamines. Trapped in acidic environments. Treat overdose with ammonium chloride.
RNH3+ <======> RNH2 + H+
(trapped) (lipid soluble)

Front 17

Phase I vs. phase II metabolism

Back 17

Phase I - (reduction, oxidation, hydrolysis) usually yields slightly polar, water-soluble metabolites (often still active) - cytochrome P-450

Phase II - (Glucuronidation, Acetylation, Sulfation) usually yields very polar, inactive metabolites - Conjugation

Geriatric patients lose phase I first.

Patients who are slow acetylators have greater side effects from certain drugs because of decreased rate of metabolism.

Front 18

How to remember which phase of metabolism geriatric patients still have?

Back 18

Geriatric patients have GAS (phase II).

Front 19

Efficacy vs. Potency

Back 19

Efficacy - maximal effect a drug can produce. High-efficacy drug classes are analgesic (pain) medications, antibiotics, antihistamines, and decongestants.

Potency - amount of drug needed for a given effect. Increased potency, increased affinity for receptor. Highly potent drug classes include chemotherapeutic (cancer) drugs, antihypertensive (blood pressure) drugs, and antilipid (cholesterol) drugs.

Front 20

Pharmacodynamics - Competitive antagonists

Back 20

Shift dose vs. % of maximum effect curve to right --> decreased potency, no change in efficacy.

Example - Diazepam + flumazenil on GABA receptor

Front 21

Pharmacodynamics - Noncompetitive antagonists

Back 21

Shifts curve down --> decreased efficacy.
Example - NE + phenoxybenzamine on alpha-receptors

Front 22

Pharmacodynamics - Partial agonists

Back 22

Acts at same site as full agonist, but with reduced maximal effect --> decreased efficacy.
Potency is a different variable and can be increased or decreased.

Examples - Morphine + buprenorphine at opioid mu receptor.

Front 23

Therapeutic Index

Back 23

Measurement of drug safety.

LD50 (median lethal dose)
------------------------------------
ED50 (median effective dose)

Safer drugs have higher TI values.

Front 24

How to remember the numerator and denominator for therapeutic index?

Back 24

TILE
TI = LD50 / ED50

Front 25

Central and peripheral nervous system - pharmacology details?

Back 25

Parasympathetic - Preganglionic ACh (N), postganglionic ACh (M) - Cardiac and smooth muscle, gland cells, nerve terminals

Sympathetic - preganglionic ACh (N), postganglionic varies

Sweat glands - Postsynaptic ACh (M)
Most sympathetic - Postsynaptic NE (alpha, beta) - cardiac and smooth muscle, gland cells, nerve terminals

Renal vascular smooth muscle - D (D1)

Adrenal medulla - Presynaptic is ACh (N), postsynaptic is endocrine (secretes NE, Epi)

Somatic - ACh (N) - skeletal muscle

Note that adrenal medulla and sweat glands are part of the sympathetic NS but are innervated by cholinergic fibers. Botulinum toxin prevents release of neurotransmitter at all cholinergic terminals.

Front 26

ACh receptors - details?

Back 26

Nicotinic ACh receptors are ligand-gated Na+/K+ channels; N(n) (found in autonomic 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

Front 27

G-protein-linked second messengers - alpha 1 - G-protein class? Major functions?

Back 27

Gq

Increases vascular smooth muscle contraction, increases pupillary dilator muscle contraction (mydriasis), increases intestinal and bladder sphincter muscle contraction.

Front 28

G-protein-linked second messengers - alpha 2 - G-protein class? Major functions?

Back 28

Gi

Decreases sympathetic outflow, decreases insulin release.

Front 29

G-protein-linked second messengers - Beta 1 - G-protein class? Major functions?

Back 29

Gs

Increased heart rate, increased contractility, increased renin release, increased lipolysis.

Front 30

G-protein-linked second messengers - Beta 2 - G-protein class? Major functions?

Back 30

Gs

Vasodilation, bronchodilation, increased heart rate, increased contractility, increased lipolysis, increased insulin release, decreased uterine tone.

Front 31

G-protein-linked second messengers - M1 - G-protein class? Major functions?

Back 31

Gq

CNS, enteric nervous system

Front 32

G-protein-linked second messengers - M2 - G-protein class? Major functions?

Back 32

Gi

Decreases heart rate and contractility of atria

Front 33

G-protein-linked second messengers - M3 - G-protein class? Major functions?

Back 33

Gq

Increased exocrine gland secretions (e.g., sweat, gastric acid), increased gut peristalsis, increased bladder contraction, bronchoconstriction, increased pupillary sphincter muscle contraction (miosis), ciliary muscle contraction (accomodation)

Front 34

G-protein-linked second messengers - D1 - G-protein class? Major functions?

Back 34

Gs

Relaxes renal vascular smooth muscle.

Front 35

G-protein-linked second messengers - D2 - G-protein class? Major functions?

Back 35

Gi

Modulates transmitter release, especially in brain.

Front 36

G-protein-linked second messengers - H1 - G-protein class? Major functions?

Back 36

Gq

Increases nasal and bronchial mucus production, contraction of bronchioles, pruritis, and pain

Front 37

G-protein-linked second messengers - H2 - G-protein class? Major functions?

Back 37

Gs

Increases gastric acid secretion.

Front 38

G-protein-linked second messengers - V1 - G-protein class? Major functions?

Back 38

Gq

Increased vascular smooth muscle contraction

Front 39

G-protein-linked second messengers - V2 - G-protein class? Major functions?

Back 39

Increased H2O permeability and reabsorption in the collecting tubules of the kidney (V2 is found in the 2 kidneys).

Front 40

How can you remember the G-protein class of the various ANS and other receptors?

Back 40

Kiss (qiss) and kick (qiq) til you're sick (siq) of sex (sqs).

Alpha 1 - q
Alpha 2 - i
Beta 1 - s
Beta 2 -s
M1 - q
M2 - i
M3 - q
D1 - s
D2 - i
H1 - q
H2 - s
V1 - q
V2 - s

Front 41

Explain the pathway for Gq, Gi, and Gs.

Back 41

Gq - receptor is activated by ligand, then Gq activates phospholipase C. This cleaves lipids to create PIP2. PIP2 splits into DAG and IP3. DAG --> protein kinase C, IP3 -> increases [Ca2+]in.

Gs: Receptor is activated by ligand, Gs activates adenylyl cyclase --> ATP is converted to cAMP --> activates protein kinase A --> increases [Ca2+]in (heart) and activates Myosin light-chain kinase (smooth muscle0

Gi - inhibits adenylyl cyclase --> decreases [Ca2+] in (heart) and deactivates MLCK (smooth muscle)

Front 42

Explain the cholinergic nerve terminal.

Back 42

Choline is transported into the cell (blocked by hemicholinium). Choline + acetyl-CoA (catalyzed by Choline Acetyltransferase) is converted to Acetylcholine. ACh is then transported into vesicles (blocked by vesamicol). Vesicles are then released by exocytosis (activated by Ca2+, inhibited by botulinum).

ACh binds to cholinoceptors on the postsynaptic membrane. ACh is degraded by Acetylcholinesterase to Choline + Acetate.

Front 43

Explain the noradrenergic nerve terminal.

Back 43

Tyrosine is transported into cells. It is converted first to DOPA (inhibited by metyrosine). DOPA is then converted to Dopamine. Dopamine is transported into vesicles (blocked by reserpine) where it is converted to norepinephrine. Norepinephrine is released by exocytosis (activated by Ca2+, inhibited by Guanethidine), activated by amphetamine).

NE acts on adrenoceptors (alpha or beta) and then diffuses out of the cleft, or is brought back by reuptake transport molecules (blocked by cocaine, TCAs, and amphetamine).

Front 44

Explain negative feedback at the NE nerve terminal.

Back 44

NE diffuses back and hits alpha2 receptors which inhibit further exocytotic release of NE molecules. Angiotensin II receptors, when activated, promote exocytosis of NE. M2 receptors, when activated, also act to prevent NE release.

Front 45

Cholinomimetic agents - Bethanechol - Clinical uses? Action?

Back 45

Uses: Postoperative and neurogenic ileus and retention

Action:
Activates Bowel and Bladder smooth muscle; resistant to AChE.

Front 46

How to remember action of bethanechol?

Back 46

"Bethany, call (bethanechol) me if you want to activate your Bowels and Bladder."

Front 47

Cholinomimetic agents - Carbachol - Clinical uses? Action?

Back 47

Uses: Glaucoma, pupillary contraction, and relief of intraocular pressure

Action: CARBon copy of acetylcholine

Front 48

Cholinomimetic agents - Pilocarpine - Clinical uses? Action?

Back 48

Clinical uses: Potent stimulator of sweat, tears, saliva

Action: Contracts ciliary muscle of eye (open angel), pupillary sphincter (narrow angle); resistant to AChE.

Front 49

How to remember actions of pilocarpine?

Back 49

You cry, drool, and swaet on your PILOw.

Front 50

Cholinomimetic agents - Methacholine - Clinical uses? Action?

Back 50

Uses: Challenge test for diagnosis of asthma.

Action: Stimulates muscarinic receptors in airway when inhaled.

Front 51

Cholinomimetic agents - Neostigmine - Clinical uses? Action?

Back 51

Uses: Postoperative and neurogenic ileus and urinary retention, myasthenia gravis, reversal of neuromuscular junction blockade (postoperative)

Action: Increases endogenous ACh; no CNS penetration.

Front 52

How to remember the details of neostigmine?

Back 52

NEO CNS = NO CNS penetration.

Front 53

Cholinomimetic agents - Pyridostigmine - Clinical uses? Action?

Back 53

Uses: Myasthenia gravis (long acting); does not penetrate CNS.

Action: Increases endogenous ACh; increases strength

Front 54

How to remember details of pyridostigmine?

Back 54

pyRIDostigmine gets RID of myasthenia gravis

Front 55

Cholinomimetic agents - Edrophonium - clinical uses? Action?

Back 55

Uses: Diagnosis of myasthenia gravis (extremely short acting)

Action: Increases endogenous ACh.

Front 56

Cholinomimetic agents - Physostigmine - clinical uses? action?

Back 56

Uses: Glaucoma (crosses blood-brain barrier --> CNS) and atropine overdose

Action: Increases endogenous ACh.

Front 57

How to remember details of physostigmine?

Back 57

PHYsostigmine PHYxes atropine overdose.

Front 58

Cholinomimetic agents - Echothiophate - Clinical uses? Action?

Back 58

Uses: Glaucoma

Action: Increases endogenous ACh.

Front 59

Cholinomimetic agents - Donepezil - Clinical uses? Action?

Back 59

Uses: Alzheimer's disease

Action: Increases endogenous ACh.

Front 60

What do you need to watch out for with all cholinomimetic agents?

Back 60

Exacerbation of COPD, asthma, and peptic ulcers when giving to susceptible patients.

Front 61

Cholinesterase inhibitor poisoning - details?

Back 61

Often due to organophosphates, such as parathion, that irreversibly inhibit AChE.

Causes Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeletal muscle and CNS< Lacrimation, Sweating, and Salivation.

Antidote - atropine + pralidoxime (regenerates active AChE)

Organophosphates are components of insecticides; poisoning usually seen in farmers.

Front 62

How to remember effects of cholinesterase inhibitor poisoning?

Back 62

DUMBBELSS

Diarrhea
Urination
Miosis
Bronchospasm
Bradycardia
Excitation of smooth muscle and CNS
Lacrimation
Sweating
Salivation

Front 63

Muscarinic antagonists - Atropine, homatropine, tropicamide - Organ System? Application?

Back 63

Eye - produces mydriasis and cycloplegia

Front 64

Muscarinic antagonists - Benztropine - Organ system? Application?

Back 64

CNS - Parkinson's disease

Front 65

How to remember details of benztropine?

Back 65

PARK my BENZ - treats parkinson's disease

Front 66

Muscarinic antagonists - Scopalamine - organ system? Application?

Back 66

CNS - motion sickness

Front 67

Muscarinic antagonists - Ipratropium - Organ system? Application?

Back 67

Respiratory - Asthma, COPD

Front 68

Muscarinic antagonists - Oxybutynin, glycopyrrolate - Organ system? Application?

Back 68

Genitourinary - Reduce urgency in mild cystitis and reduce bladder spasms

Front 69

Muscarinic antagonists - Methscopolamine, pirenzepine, propantheline - Organ system? Application?

Back 69

Gastrointestinal - Peptic ulcer treatment

Front 70

Atropine - effects on Eye? Airway? Stomach? Gut? Bladder? Toxicity?

Back 70

Muscarinic antagonist. Used to treat bradycardia and for opthalmic applications.

Eye - Increased pupil dilation, cycloplegia
Airway - Decreased secretions
Stomach - Decreased acid secretions.
Gut - Decreased motility
Bladder - decreased urgency in cystitis

Blocks DUMBBELSS

Toxicity - Increased body temperature (due to decreased sweating); rapid pulse; dry mouth; dry, flushed skin; cycloplegia; constipation; disorientation.
Can cause acute angle-closure glaucoma in elderly, urinary retention in men with prostatic hyperplasia, and hyperthermia in infants.

Front 71

how to remember side effects of atropine?

Back 71

Hot as a hare
Dry as a bone
Red as a beet
Blind as a bat
Mad as a hatter

Front 72

Sympathomimetics - Epinephrine - Which receptors? Applications?

Back 72

alpha 1 - strong
alpha 2 - strong
beta 1 - strong
beta 2 - medium
Dopamine 1 - no effect

Used for anaphylaxis, glaucoma (open angle), asthma, hypotension

Front 73

Sympathomimetics - Norepinephrine - Which receptors? Applications?

Back 73

alpha 1 - strong
alpha 2 - strong
beta 1 - medium
beta 2 - no effect
Dopamine - no effect

Used for hypotension (but decreases renal perfusion)

Front 74

Sympathomimetics - Isoproterenol - Which receptors? Applications?

Back 74

Alpha 1 - no effect
alpha 2 - no effect
Beta 1 - strong
Beta 2 - strong
Dopamine - no effect

Used for AV block (rarely used)

Front 75

Sympathomimetics - Dopamine - Which receptors? Applications?

Back 75

Alpha 1 - strong (high dose)
alpha 2 - strong (high dose)
beta 1 - strong (medium dose)
beta 2 - medium (medium dose)
dopamine 1 receptor - weak agonist (low dose)

Used for shock (renal perfusion), heart failure; inotropic and chronotropic; D1 > Beta > alpha

Front 76

Sympathomimetics - Dobutamine - Which receptors? Applications?

Back 76

alpha 1 - weak
alpha 2 - weak
beta 1 - strong
beta 2 - weak
dopamine - no effect

Used for heart failure, cardiac stress testing; inotropic, but not chronotropic.

Front 77

Sympathomimetics - Phenylephrine - which receptors? applications?

Back 77

alpha 1 - strong
alpha 2 - medium
beta 1 - no effect
beta 2 - no effect
dopamine - no effect

Used for pupillary dilation, vasoconstriction, nasal decongestion.

Front 78

Sympathomimetics - Metaprotereonol, albuterol, salmeterol, terbutaline - Which receptors? Applications?

Back 78

alpha 1 - no effect
alpha 2 - no effect
beta 1 - medium
beta 2 - strong
dopamine - no effect

MAST: Metaproterenol and Albuterol for acute asthma; salmeterol for long-term treatment; Terbutaline to reduce premature uterine contractions

Front 79

Sympathomimetics - Ritodrine - Which receptors? Applications?

Back 79

alpha 1 - no effect
alpha 2 - no effect
beta 1 - no effect
Beta 2 - strong
dopamine - no effect

Used to reduce premature uterine contractions.

Front 80

Indirect Sympathomimetics - Amphetamine - Action? Application?

Back 80

Indirect general agonist, releases stored catecholamines.

Used to treat narcolepsy, obesity, attention deficit disorder.

Front 81

Indirect Sympathomimetics - Ephedrine - Action? Application?

Back 81

Indirect general agonist, releases stored catecholamines.

Nasal decongestion, urinary incontinence, hypotension.

Front 82

Indirect Sympathomimetics - Cocaine - Action? Application?

Back 82

Indirect general agonist, uptake inhibitor.

Causes vasoconstriction and local anesthesia.

Front 83

Describe how norepinephrine effects SBP, DBP, and HR.

Back 83

NE has alpha > beta effects.

Increased SBP due to increased contractility (Beta 1). Increased DBP due to increased TPR (alpha 1). Decreased HR due to reflex bradycardia.

Front 84

Describe how isoproterenol effects SBP, DBP, and HR.

Back 84

Isoproteronol is beta effects only.
Increased SBP due to increased contractility (but then reduces due to Beta 2 response and reflex sympathetic outflow from hypotension). Decreased DBP due to vasodilation. Increased HR due to Beta 1 agonism.

Front 85

Sympathoplegics - Clonidine, alph-methyldopa - action? application?

Back 85

Centrally acting alpha-2-agnonist --> decreased central adrenergic outflow.

Treats hypertension, especially with renal disease (no decrease in blood flow to kidney).

Front 86

Alpha-blockers - Phenoxybenzamine - Application? Toxicity?

Back 86

Nonselective, irreversible alpha blocker

Pheochromocytoma (use phenoxybenzamine before removing tumor, since high levels of released catecholamines will not be able to overcome blockage).

Toxicity: Orthostatic hypotension, reflex tachycardia.

Front 87

Alpha-blockers - Phentolamine - Application? Toxicity?

Back 87

Nonselective, reversible alpha blocker

Give to patients on MAO inhibitors who eat tyramine-containing foods (It is thought that tyramine displaces norepinephrine from vesicles, causing huge release of NE --> hypertensive crisis).

Front 88

Alpha-blockers - Prazosin, terazosin, doxazosin - Application? Toxicity?

Back 88

Selective alpha1 blockers

Used for hypertension, urinary retention in BPH.

Toxicity: 1st-dose orthostatic hypotension, dizziness, headache

Front 89

Alpha-blockers - Mirtazapine - Application? Toxicity?

Back 89

Treats depression with insomnia.

Toxicity: Sedation (has H1 agonist properties), increased serum cholesterol,, increased appetite.

Front 90

Describe the effects of epinephrine injection in terms of the effects of epinephrine without alpha blockade and after alpha blockade.

Back 90

Before alpha blockade, epinephrine causes increase in SBP due to Beta-1 agonism and increase in DBP due to alpha-1 agonism.

After alpha blockade, you only have Beta activity and so their is a net depressor effect.

Front 91

Describe the effects of phenylephrine injection in terms of the effects of phenylephrine without alpha blockade and after alpha blockade.

Back 91

Before alpha blockade, you have a net pressor effect (stronger than epinephrine because ONLY alpha agonist).

After alpha blockade, you have no response to the phenylephrine injection.

Front 92

Beta-blockers - give examples

Back 92

anything ending in -lol

Acebutolol, betaxolol, esmolol, atenolol, metoprolol, propranolol, timolol, pindolol, labetalol

Front 93

Beta-blockers - Effect on hypertension

Back 93

Decreased cardiac output, decreased renin secretion (due to beta-receptor blockade on JGA cells)

Front 94

Beta-blockers - Effect on Angina Pectoris

Back 94

Decreased heart rate and contractility --> decreased O2 consumption

Front 95

Beta-blockers - Effect on MI

Back 95

Beta-blockers decrease mortality

Front 96

Beta-blockers - effect on SVT

Back 96

Propranolol, esmolol
Decrease AV conduction velocity (class II antiarrhythmic)

Front 97

Beta-blocker effects on CHF

Back 97

Slows progression of chronic failure

Front 98

Beta-blocker effects on Glaucoma

Back 98

Timolol
Decreases secretion of aqueous humor.

Front 99

Beta-blocker - toxicities

Back 99

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

Front 100

Beta-blocker - Beta1 selective antagonists (Beta1 > Beta2)

Back 100

Acebutolol (partial agonist), Betaxolol, Esmolol (short acting), Atenolol, Metoprolol

A BEAM of beta1-blockers. Advantageous in patients with comorbid pulmonary disease.

Front 101

Beta-blocker - Nonselective antagonists (Beta1 = Beta2)

Back 101

Propranolol, Timolol, Nadolol, and Pindolol

Please Try Not Being (beta) Picky

Front 102

Beta blockers - Nonselective (vasodilatory) alpha- and beta-antagonists

Back 102

Carvedilol, labetalol

Front 103

Beta-blockers - Partial Beta-agonists

Back 103

Pindolol, Acebutolol

(PAPA)

Front 104

Specific Antidotes - Acetaminophen

Back 104

N-acetylcysteine (replenishes glutathione)

Front 105

Specific Antidotes - Salicylates

Back 105

NaHCO3 (alkalinize urine), dialysis

Front 106

Specific Antidotes - Amphetamines (basic)

Back 106

NH4Cl (acidify urine)

Front 107

Specific Antidotes - Acetylcholinesterase inhibitors, organophosphates

Back 107

Atropine, pralidoxime

Front 108

Specific Antidotes - Antimuscarinic, anticholinergic agents

Back 108

Physostigmine salicylate

Front 109

Specific Antidotes - Beta-blockers

Back 109

Glucagon

Front 110

Specific Antidotes - Digitalis

Back 110

Stop dig; normalize K+, Lidocaine, Anti-dig Fab fragments, Mg2+ (KLAM)

Front 111

Specific Antidotes - Iron

Back 111

Deferoxamine

Front 112

Specific Antidotes - Lead

Back 112

CaEDTA, dimercaprol, succimer penicillamine

Front 113

Specific Antidotes - Mercury, arsenic, gold

Back 113

Dimercaprol (BAL), succimer

Front 114

Specific Antidotes - Copper, Arsenic, Gold

Back 114

Penicillamine

Front 115

Specific Antidotes - Cyanide

Back 115

Nitrite, Hydroxocobalamin, Thiosulfate

Front 116

Specific Antidotes - Methemoglobin

Back 116

Methylene blue, vitamin C

Front 117

Specific Antidotes - Carbon monoxide

Back 117

100% O2, hyperbaric O2

Front 118

Specific Antidotes - Methanol, ethylene glycol (antifreeze)

Back 118

Fomepizole > ethanol, dialysis

Front 119

Specific Antidotes - Opioids

Back 119

Naloxone/naltrexone

Front 120

Specific Antidotes - Benzodiazepines

Back 120

Flumazenil

Front 121

Specific Antidotes - TCAs

Back 121

NaHCO3 (plasma alkalinization)

Front 122

Specific Antidotes - Heparin

Back 122

Protamine

Front 123

Specific Antidotes - Warfarin

Back 123

Vitamin K, fresh frozen plasma

Front 124

Specific Antidotes - tPA, streptokinase, urokinase

Back 124

Aminocaproic acid

Front 125

Specific Antidotes - Theophylline

Back 125

Beta-blocker

Front 126

Drug reactions - Coronary vasospasm

Back 126

Cocaine, sumatriptan

Front 127

Drug reactions - Cutaneous flushing

Back 127

VANC: Vancomycin, Adenosine, Niacin, Ca2+ channel blockers

Front 128

Drug reactions - Dilated cardiomyopathy

Back 128

Doxorubicin (adriamycin), daunorubicin

Front 129

Drug reactions - Torsades de pointes

Back 129

Class III (sotalol), class IA (quinidine) antiarrhythmics

Front 130

Drug reactions - Agranulocytosis

Back 130

Clozapine, Carbamezapine, Colchicine, Propylthiouracil, Methimazole, Dapsone

Front 131

How to remember drugs that cause agranulocytosis?

Back 131

Agranulocytosis Could Certainly Cause Pretty Major Damage

Clozapine, Carbamezapine, Colchicine, Propylthiouracil, Methimazole, Dapsone

Front 132

Drug reactions - Aplastic anemia

Back 132

Chloramphenicol, benzene, NSAIDs, propylthiouracil, methimazole

Front 133

Drug reactions -
Direct Coombs-positive hemolytic anemia

Back 133

Methyldopa

Front 134

Drug reactions -
Gray baby syndrome

Back 134

Chloramphenicol

Front 135

Drug reactions -
Hemolysis in G6PD-deficient patients

Back 135

Isoniazid (INH), Sulfonamides, Primaquine, Aspirin, Ibuprofen, Nitrofurantoin

Front 136

How to remember drugs that cause hemolysis in G6PD-deficient patients?

Back 136

hemolysis IS PAIN

Isoniazid (INH), Sulfonamides, Primaquine, Aspirin, Ibuprofen, Nitrofurantoin

Front 137

Drug reactions - Megaloblastic anemia

Back 137

Phenytoin, Methotrexate, Sulfa drugs

Front 138

How to remember drugs that cause megaloblastic anemia?

Back 138

having a blast with PMS

Phenytoin, Methotrexate, Sulfa drugs

Front 139

Drug reactions - Thrombotic complications

Back 139

OCPs (e.g., estrogens and progestins)

Front 140

Drug reactions - Cough

Back 140

ACE inhibitors (note: ARBs like losartan -- no cough)

Front 141

Drug reactions - Pulmonary fibrosis

Back 141

Bleomycin
Amiodarone
Busulfan

Front 142

How to remember drugs that cause pulmonary fibrosis?

Back 142

it's hard to BLAB when you have pulmonary fibrosis
Bleomycin
Amiodarone
Busulfan

Front 143

Drug reactions - Acute cholestatic hepatitis

Back 143

Macrolides

Front 144

Drug reactions - Focal to massive hepatic necrosis

Back 144

Halothane, Acetaminophen, Valproic acid, Amanita phalloides (liver HAVAc)

Front 145

How to remember drugs that cause focal to massive hepatic necrosis?

Back 145

Liver HAVAc
Halothane
Acetaminophen
Valproic acid
Amanita phalloides

Front 146

Drug reactions - Hepatitis

Back 146

INH

Front 147

Drug reactions - Pseudomembranous colitis

Back 147

Clindamycin, Ampicillin

Front 148

Drug reactions - adrenocortical insufficiency

Back 148

Glucocorticoid withdrawal (HPA suppression)

Front 149

Drug reactions - Gynecomastia

Back 149

Spironolactone, Digitalis, Cimetidine, chronic Alcohol use, estrogens, Ketoconazole

Front 150

How to remember drugs that cause gynecomastia?

Back 150

Some Drugs Create Awesome Knockers
Spironolactone
Digitalis
Cimetidine
chronic Alcohol use
Ketoconazole

Front 151

Drug reactions - Hot flashes

Back 151

Tamoxifen, clomiphene (both are SERMs)

Front 152

Drug reactions - Hypothyroidism

Back 152

Lithium, amiodarone, sulfonamides

Front 153

Drug reactions - Hyperglycemia

Back 153

Niacin, tacrolimus, protease inhibitors

Front 154

Drug reactions - fat redistribution

Back 154

Glucocorticoids, protease inhibitors

Front 155

Drug reactions - Gingival hyperplasia

Back 155

Phenytoin, verapamil

Front 156

Drug reactions - Gout

Back 156

Furosemide, Thiazides, Niacin, Cyclosporin, Pyrazinamide

Front 157

Drug reactions - Myopathies

Back 157

Fibrates
Niacin
Colchicine
Hydroxychloroquine
Interferon alpha
Penicillamine
Statins
Glucocorticoids

Front 158

How to remember drugs that cause myopathies?

Back 158

Fish N CHIPS Give you myopathies

Fibrates
Niacin
Colchicine
Hydroxychloroquine
Interferon alpha
Penicillamine
Statins
Glucocorticoids

Front 159

Drug reactions - osteoporosis

Back 159

Corticosteroids, heparin

Front 160

Drug reactions - Photosensitivity

Back 160

Sulfonamides
Amiodarone
Tetracyclines

Front 161

How to remember drugs that cause photosensitivity?

Back 161

i SAT for a photo

Sulfonamides
Amiodarone
Tetracyclines

Front 162

Drug reactions - Rash (Stevens-Johnson syndrome)

Back 162

Penicillin, Ethosuximide, Carbamazepine, Sulfa drugs, Lamotrigine, Allopurinol, Phenytoin, Phenobarbital

Front 163

How to remember drugs that cause rash (stevens-johnson syndrome)?

Back 163

I got a rash after a PEC SLAPP

Penicillin
Ethosuximide
Carbamazepine
Sulfa drugs
Lamotrigine
Allopurinol
Phenytoin
Phenobarbital

Front 164

Drug reactions - SLE-like syndrome

Back 164

Hydralazine
Isoniazid
Procainamide
Phenytoin

Front 165

How to remember drugs that cause lupus-like syndrome?

Back 165

its not HIPP to have lupus

Hydralazine
INH
Phenytoin
Procainamide

Front 166

Drug reaction - Tendonitis, tendon rupture, and cartilage damage (kids)

Back 166

Fluoroquinolones

Front 167

Drug reaction - diabetes insipidus

Back 167

Lithium, demeclocycline

Front 168

Drug reaction - Fanconi's syndrome

Back 168

Expired tetracycline

Front 169

Drug reaction - Interstitial nephritis

Back 169

Methicillin, NSAIDs, furosemide

Front 170

Drug reaction - Hemorrhagic cystitis

Back 170

Cyclophosphamide, ifosfamide (prevent by coadministering with mesna)

Front 171

Drug reaction - SIADH

Back 171

Carbamazepine, cyclophosphamide

Front 172

Drug reaction - cinchonism

Back 172

Quinidine, quinine

Cinchonism means overdose on quinine derivatives

Front 173

Drug reaction - Parkinson-like syndrome

Back 173

Antipsychotics, reserpine, metoclopramide

Front 174

Drug reaction - seizures

Back 174

Bupropion, imipenem/cilastatin, isoniazid

Front 175

Drug reaction - Tardive dyskinesia

Back 175

Antipsychotics

Front 176

Drug reaction - Antimuscarinic

Back 176

Atropine, TCAs, H1 blockers, neuroleptics, digoxin

Front 177

Drug reaction - Disulfiram-like reaction

Back 177

Metronidazole, certain cephalosporins, procarbazine, 1st-generation sulfonylureas

Front 178

Drug reaction - Nephrotoxicity/ototoxicity

Back 178

Aminoglycosides, vancomycin, loop diuretics, cisplatin

Front 179

P-450 Interactions - inducers (+)

Back 179

Quinidine
Barbiturates
St. John's Wort
Phenytoin
Rifampin
Griseofulvan
Carbamazepine
Chronic alcohol use

Front 180

How to remember CYP450 inducers?

Back 180

Queen Barb Steals Phen-phen and Refuses Greasy Carbs Chronically

Quinidine
Barbiturates
St. John's Wort
Phenytoin
Rifampin
Griseofulvan
Carbamazepine
Chronic alcohol use

Front 181

P-450 interactions - Inhibitors (-)

Back 181

Macrolides
Amiodarone
Grapefruit juice
Isoniazid
Cimetidine
Ritonavir
Acute alcohol abuse
Ciprofloxacin
Ketoconazole
Sulfonamides

Front 182

How to remember CYP450 inhibitors?

Back 182

MAGIC RACKS

Macrolides
Amiodraone
Grapefruit Juice
Isoniazid
Cimetidine
Ritonavir
Acute alcohol abuse
Ciprofloxacin
Ketoconazole
Sulfonamides

Front 183

Sulfa drugs - details?

Back 183

Probenecid, Furosemide, Acetazolamide, Celecoxib, Thiazides, Sulfonamide antibiotics, Sulfasalazine, Sulfonylureas (Popular FACTSSS)

Patients with sulfa allergies may develop fever, UTI, pruritic rash, Stevens-Johnson syndrome, Hemolytic anemia, thrombocytopenia, agranulocytosis, and urticaria (hives). Symptoms range from mild to life-threatening.

Front 184

How to remember the sulfa drugs?

Back 184

Popular FACTSSS

Probenacid
Acetazolamide
Celecoxib
Thiazides
Sulfonamide antibiotics
Sulfasalazine
Sulfonylureas

Front 185

Drug name - Category? Example?
-azole

Back 185

Antifungal
Ketoconazole

Front 186

Drug name - Category? Example?
-cillin

Back 186

Penicillin

Methicillin

Front 187

Drug name - Category? Example?
-cycline

Back 187

Antibiotic, protein synthesis inhibitor

Tetracycline

Front 188

Drug name - Category? Example?
-navir

Back 188

Protease inhibitor

Darunivir

Front 189

Drug name - Category? Example?
-triptan

Back 189

5-HT(1b/1d) agonists (migraine)

Sumatriptan

Front 190

Drug name - Category? Example?
-ane

Back 190

Inhalation general anesthetic
Halothane

Front 191

Drug name - Category? Example?
-caine

Back 191

Local anesthetic.
Lidocaine

Front 192

Drug name - Category? Example?
-operidol

Back 192

Butyrophenone (neuroleptic)

Haloperidol

Front 193

Drug name - Category? Example?
-azine

Back 193

Phenothiazine (neuroleptic, antiemetic)
Chlorpromazine

Front 194

Drug name - Category? Example?
-barbital

Back 194

Barbiturate.
Phenobarbital

Front 195

Drug name - Category? Example?
-zolam

Back 195

Benzodiazepine
Alprazolam

Front 196

Drug name - Category? Example?
-azepam

Back 196

Benzodiazepine.
Diazepam

Front 197

Drug name - Category? Example?
-etine

Back 197

SSRI
Fluoxetine

Front 198

Drug name - Category? Example?
-ipramine

Back 198

TCA
Imipramine

Front 199

Drug name - Category? Example?
-triptyline

Back 199

TCA
Amitriptyline

Front 200

Drug name - Category? Example?
-olol

Back 200

Beta antagonist
Propranolol

Front 201

Drug name - Category? Example?
-terol

Back 201

Beta-2 agonist
Albuterol

Front 202

Drug name - Category? Example?
-zosin

Back 202

alpha1-antagonist
Prazosin

Front 203

Drug name - Category? Example?
-oxin

Back 203

Cardiac glycoside (inotropic agent)
Digoxin

Front 204

Drug name - Category? Example?
-pril

Back 204

ACE inhibitor
Captopril

Front 205

Drug name - Category? Example?
-afil

Back 205

Erectile dysfunction
Sildenafil

Front 206

Drug name - Category? Example?
-tropin

Back 206

Pituitary hormone
Somatotropin

Front 207

Drug name - Category? Example?
-tidine

Back 207

H2 antagonist
Cimetidine

Front 208

Which lipid lowering medication class causes hypertriglyceridemia as a side-effect?

Back 208

Bile acid-binding resins (cholestyramine, etc). Because the enterohepatic circulation is inhibited, de novo bile acid synthesis is upregulated roughly 10-fold. This causes increased hepatic production of VLDL and triglycerides as a side effect.

Front 209

How is lactase deficiency similar to the mechanism of polyethylene glycol laxative?

Back 209

Both cause osmotic diarrhea

Front 210

What is the mechanism by which ACE-inhibitors can cause angioedema?

Back 210

ACE breaks down bradykinin, when ACE inhibitors are used, they can cause dangerous accumulation of bradykinin which is a potent vasodilator and can cause significant angioedema when at high levels

Front 211

What is the main way that nitroglycerine works to treat angina pectoris?

Back 211

Venodilation --> venous pooling and decreased Left heart preload --> decreased oxygen demand

NOT aterial dilation (does have this effect at high levels but this woudl cause reduced coronary perfusion)

Front 212

How does Ziduvodine work?

Back 212

It ends cDNA chain elongation by preventing the 3' --> 5' phosphodiester bond formation.

It has an azido group in the place of the 3' OH group found on normal thymidine molecules

Front 213

A patient experiences sexual side effects associated with SSRI therapy. WHat alternate antidepressant is a good fit?

Back 213

Bupropion - does not have sexual side effects (thought to be because it works on NE and not really on Serotonin)

Front 214

What portion of the EKG is changed with beta blockers?

Back 214

PR interval elongation (slows AV conduction)

Front 215

Of spironolactone and furosemide, which has been shown to improve survival in patients with CHF?

Back 215

Spironolactone - NOT by its diuretic effect, but by its blockage of aldosterone

Aldosterone has neurohormonal effects on the heart that induce further remodeling and fibrosis.

Furosemide has been shown to significantly improve symptoms, but has NOT been shown to improve overall survival.

Front 216

What pharmacokinetic property of methadone makes it a good substitute for patients with heroine addiction?

Back 216

long half-life --> chronic suppression of withdrawal symptoms

Front 217

Thiopental is used for anesthesia induction because of what property?

Back 217

It rapidly accumulates in the brain within 1 minute, but then its plasma and brain concentrations drop rapidly as it redistributes into skeletal muscle and adipose tissue where it accumulates.

This makes it a perfect induction agent because the patient is rendered unconscious from the drug very rapidly, but then the drug quickly leaves the CNS>

Front 218

What is the first line drug for trigeminal neuralgia, and how does it work?

Back 218

Carbamazepine - inhibits neuronal high-frequency firing by reducing the ability of sodium channels to recover from inactivation

Front 219

What property of lidocaine and other class IB antiarrhythmics makes them good for arrhythmias following an ischemic event?

Back 219

They are use-dependent - they do not bind avidly to resting sodium channels. Therefore, they are particualrly useful in binding and inhibiting ectopic pacemakers, which are constitutively activated.

Front 220

What woudl propranolol's effect on renin secretion be?

Back 220

By blocking Beta1 receptors on JGA cells, renin secretion is inhibited.

Front 221

What would propranolol's effect on bradykinin be?

Back 221

Beta blockers have no effect on ACE levels, so bradykinin would be unaffected.