Term
What do the following pharmacological terms indicate about a drug?
1) Km
2) Vmax |
|
Definition
1) Affinity of enzyme for substrate
- Low Km binds tightly
- Km is the same as the [S] at 1/2 Vmax
2) Directly proportional to enzyme concentration
- Increase y-intercept on enzyme kinetic curve, decrease Vmax |
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Term
What are the effects of competitive vs. non-competitive inhibitors in terms of the following.
1) Resemble substrate
2) Overcome by increase [S]
3) Bind active site
4) Effect on Vmax
5) Effect on Km
6) Pharmacodynamics |
|
Definition
1) Competitive (Y) Non-competitive (N)
2) Competitive (Y) Non-competitive (N)
3) Competitive (Y) Non-competitive (N)
4) Competitive (N) Non-competitive (decrease)
5) Competitive (increase) Non-competitive (N)
6) Competitive (decrease potency)
Noncompetitive (decrease efficacy) |
|
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Term
What is the "Volume of distribution" of a drug?
Which drugs have large vs. small Vd? |
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Definition
1) Relates the amount of drug in the body to the plasma concentration.
Vd= amount of drug in body/[D]plasma
Vd of plasma protein-bound drugs can be altered by liver and kidney disease (decrease protein binding, increased Vd)
2)
- Low Vd= blood distribution (large or charged)
- Mid Vd= distribute in extracellular space or body water (small hydrophilic molecules that do not bind plasma proteins)
- High Vd (>body weight) distribute into all tissues (small lipophilic molecules that bind strongly to extra-vascular proteins) |
|
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Term
| How is a drug's "clearance" determined? How does this relate to volume of distribution? |
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Definition
CL=(Rate of elimination of drug/plasma drug concentration)
= Vd x Ke
Drugs with higher volumes of distribution (i.e small lipophillic drugs that bind extravascular proteins) and have higher rates of clearance. |
|
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Term
| How is t 1/2 calculated and what does it mean? How does it relate to volume of distribution and to clearance? |
|
Definition
The time it takes for 1/2 amount of drug in body to be eliminated (1st order kinetics)
t1/2= (0.7)X Vd/CL
Drugs infuse dat constant rate take 4-5 half lives to reach steady state
Higher Vd has higher half life
Higher clearance has lower half life |
|
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Term
| What does an oral bioavailability of 50% mean? |
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Definition
| 50% of drug administered actually reaches circulation (vs. 100% in IV administration) |
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Term
| What are "loading" and "maintenance" doses and how are they calculated? |
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Definition
Give a loading dose (depends on VOD) to get the drug to desired level and then a maintenance (depends on clearance) dose to keep it there.
Time to steady state depends on half life and NOT on frequency or size of dose.
Cp= target plasma concentration
F= bioavailability
LD= Cp X (Vd/F)
MD= Cp X (CL/F) |
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Term
| What do it mean for a drug to exhibit "zero-order" kinetics and which drugs do so? |
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Definition
Rate of elimination is constant regardless of Cp (constant "amount" of drug eliminated per unit time), so Cp decreases linearly with time
PEA (round like "0")
- Phenytoin
- Ethanol
- Aspirin |
|
|
Term
| What do it mean for a drug to exhibit "first-order" kinetics? |
|
Definition
Rate of elimination is proportion to drug concentration (constant "Fraction" of drug eliminated per unit time).
- Cp decreases exponentially (vs. zero-order, where it decreases linearly)
- "Drug A is eliminated more slowly as its plasma concentration decreases" |
|
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Term
| What is the relationship between urine pH and drug elimination? |
|
Definition
Ionized species are trapped in urine and cleared quickly, while neutral species can be reabsorbed.
1) Weak acids (phenobarbital, MTX, aspirin)
- Trapped in basic environments (treat overdose with Bicarbonate)
2) Weak bases (Amphetamines)
- Trapped in acidic environments (Treat overdose with ammonium chloride) |
|
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Term
| How might you treat an amphetamine overdose differently from a phenobarbitol overdose? |
|
Definition
1) Trap ionized species with their counter-species.
2) Amphetamines are weak bases, so they will be trapped by acids like Ammonium Chloride
Phenobarbital (as well as aspirin and MTX) are weak acids, which must be trapped by a base (bicarbonate) |
|
|
Term
| What is the difference between phase 1 and phase 2 metabolism of drugs? |
|
Definition
1) Phase 1 (Oxidation, Reduction, Hydrolysis)
- CYP
- Yields slightly polar, water-soluble metabolites (often still active)
2) Phase 2 (Glucuronidation, Acetylation, Sulfation)
- Conjugation
- Yields very polar, inactive metabolites that are Renally excreted |
|
|
Term
| Why might you have to adjust dosing of many drugs when considering Geriatric patient populations? |
|
Definition
They lose Phase 1 (CYP) metabolism and are eft with GAS (phase 2)
- Glucuronidation, Acetylation, Sulfation. |
|
|
Term
| What is the difference between drug efficacy and drug potency? Which are affected by competitive and non-competitive inhibitors, respectively? |
|
Definition
1) Efficacy is maximal effect drug can produce
- Relates to Vmax, which is reduced by non-competitive inhibitors
- High: Analgesics, antibiotics, antihistamines and decongenstants
2) Potency is amount of drug needed for a given effect
- Relates to affinity for receptor (Km)
- Reduced by competitive inhibitors
- Chemotherapy drugs, anti-hypertensives and anti-lipid drugs have high potency |
|
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Term
| Which drug types are highly efficacious? What about potent? |
|
Definition
1) Efficacy (maximal effect drug can produce- Vmax)
- Analgesics, Antibiotics, Anti-histamines, Decongestants
2) Potency (amount of drug required to elicit given response- Km)
- Anti-HTN, Chemotherapy, Anti-lipid (cholesterol) drugs |
|
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Term
A common drug used to treat anxiety is Diazepam. Benzodiazepines can be reduced with flumazenil, which is a competitive antagonist of GABA.
What affect would addition of flumazenil have on a dose response curve for Diazepam? |
|
Definition
Competitive inhibitors incease Km, which decreases potency.
Reduced potency will cause a right-shift, with no effect on Vmax (efficacy). |
|
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Term
Phenoxybenzamine acts as a non-competitive inhibitor of NE on alpha adrenergic receptors.
What affect would addition of phenoxybenzamine have on a dose response curve for NE? |
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Definition
Non-competitive inhibitors reduce efficacy (Vmax), but do not influence affinity (Km), so potency remains unchanged.
% of maximal effect is reduced and curve is shifted down |
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Term
Buprenorphine is a partial agonist at the opioid u receptor (morphine receptor).
What affect would addition of Buprenorphine have on a dose response curve of Morphine? |
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Definition
Partial agonist act the same as full agonists, but with reduced maximal effect, thereby decreasing efficacy (shifting curve down).
Potency (affinity) may be either increased or decreased, and in this case, it would be increased (shifted to left).
"Drug is active at lower concentrations, but cannot achieve maximal effect of morphine" |
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Term
| What does a therapeutic index of 0.8 mean for a drug in terms of safety? |
|
Definition
TI= LD50/ED50, meaning that the dose that causes death in 50% of patients is 80% of the dose that has an effect in 50% of people.
A TI less than 1 means that the drug is very UNSAFE.
The higher a TI, the safer. |
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Term
| Which are the different types of ACh receptors and where are they found? |
|
Definition
1) Nicotinic: ligand-gated Na/K channels
- Nn: Autonomic ganglia
- Nm: NMJ
2) Muscarinic: GPCRs that act through 2nd messengers
Parasympathetic (except in Sweat glands)
- M1 (q)
- M2 (i)
- M3 (q) |
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Term
Through which G-protein class does each of the following sympathetic adrenergic receptors function and what is its effect?
1) Alpha 1
2) Alpha 2
3) Beta 1
4) Beta 2 |
|
Definition
1) Gq (PLC/PIP2/IP3 + DAG)
- Increase vascular smooth muscle contraction
- Pupillary dilator muscle contraction (mydriasis),
- Increased intestinal and bladder sphincter muscle contraction
2) Gi
- Decrease sympathetic outflow
- Decrease insulin release
3) Gs (AC/cAMP/PKA/Ca influx (heart) and MLCK (smooth muscle)
- Increase HR, contractility
- Increase renin release
- Increase lipolysis
4) Gs
- Vasodilation
- Bronchodilation
- Increase HR, contractility and lipolysis (like B1
- Increase insulin release
- Decrease uterine tone |
|
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Term
Through which G-protein class does each of the following parasmypathetic adrenergic receptors function and what is its effect?
1) M1
2) M2
3) M3 |
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Definition
1) Gq
- CNS and enteric nervous system
2) Gi
- Decrease heart rate and contractility
3) Gq
- Increase exocrine gland secretions (sweat, gastric acid)
- Gut peristalsis
- Increase bladder contraction, bronchoconstriction
- Contract pupillary sphincter (Myosis)
- Contract ciliary muscle (Accommodation) |
|
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Term
| What are the sympathetic and parasympathetic receptors that mediate pupillary constriction/dilation? |
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Definition
Both function through Gq, where DAG activates PKC and IP3 increases intracellular calcium
1) Sympathetic= Dilation
- Alpha 1 receptors (Gq)
2) Parasympathetic= Constriction
- M3 receptors (Gq) |
|
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Term
| What are the differential modes of action of D1 and D2 dopamine receptors? |
|
Definition
GPCRs
1) D1: Gs (cAMP)
- Relaxes renal vascular smooth muscle (dobutamine is sometimes used to save kidneys)
2) D2: Gi
- Modulates transmitter release, especially in brain |
|
|
Term
| What are the differential modes of action of H1 and H2 dopamine receptors? |
|
Definition
Histamine receptors are GPCRs
1) H1: Gq
- Increase nasal and bronchial mucus production
- Contraction of bronchioles
- Pruritis
- Pain (via bradykinin)
2) H2: Gs
- Increases gastric acid secretion from parietal cells |
|
|
Term
| What are the differential modes of action of V1 and V2 dopamine receptors? |
|
Definition
| ADH receptors are GPCRs 1) V1: Gq - Increase vascular smooth muscle contraction 2) V2: Gs - Increase water permeability and reabsorption in collecting tubules of kidney (V2 is found in the 2 kidneys) |
|
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Term
| Which GPCRs act via Gq subtypes? How does Gq signaling work? |
|
Definition
"HAVe 1 M&M": H1, alpha1, V1, M1 and M3
1) Gq activates PLC, which cleaves lipids to produce PIP2
2) PIP2 is split into DAG and IP3
3) DAG activates PKC and IP3 increases intracellular calcium |
|
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Term
| Which GPCRs act via Gs subtypes? How does Gs signaling work? |
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Definition
B1, B2, D1, H2, V2
1) Gs activates AC, which increases cAMP
2) cAMP activates PKA, which phosphorylates MLCK (smooth muscle) and increases intracellular Ca2+ (Heart) |
|
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Term
| Which GPCRs act via Gi subtypes? How does Gi signaling work? |
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Definition
"MAD 2's" M2, Alpha 2, D2
1) Gi inhibits AC to decreases production of cAMP
2) Without cAMP, there is no PKA activation, no increase in calcium (heart) and no MLCK phosphorylation (smooth mucle) |
|
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Term
Describe the process of ACh synthesis and how each of the following drugs modulate it.
1) Hicholinium
2) Vesamicol
3) Botulinum |
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Definition
Choline is taken up by nerve terminal and addd to acetyl-CoA (ChAT) to form ACh, which is packaged into secretory granules and released to bind M or N receptors.
**Uptake of choline is rate-limiting step**
1) Inhibits uptake
2) Inhibits vesicular packaging
3) Inhibits vesicle fusion and ACh release |
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Term
Describe the process of NE synthesis and how each of the following drugs modulates it.
1) Metyrosine
2) Reserpine
3) Guanethidine
4) Amphetamine
5) Cocaine, TCAs |
|
Definition
Tyrosine is taken up by nerve terminal and converted to L-DOPA (tyrosine hydroxylase). L-DOPA becomes Dopamine via DOPA decarboxylase. Dopamine is packaged into vesicles and becomes NE via Dopamine beta hydroxylase.
1) Hypertension drug that inhibits tyrosine hydroxylase
2) Anti-psychotic/hypertensive that Inhibits vesicular monoamine transporter (VMAT) that would package dopamine, preventing conversion to NE
3) Guanethidine inhibits NE release by replacing NE in vesicles
4) Amphetamines increase NE release and inhibit reuptake.
5) Cocaine and TCAs block NE reuptake |
|
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Term
| How is NE release modulated by "release-modulating" receptors on the presynaptic nerve terminal? |
|
Definition
1) Receptors for ACh (M2) and NE (alpha 2) reduce release
2) Receptors for AngII (AII) increase release |
|
|
Term
A number of cholinomimetic agents are available. What are the actions and clinical applications of the following?
1) Bethanechol
2) Carbechol
3) Pilocarpine
4) Methacholine |
|
Definition
Are are direct cholinergic agonists.
1) Bethanechol
- Post-operative and neurogenic ileus and urinary
retention
- Activates Bowel and Bladder smooth muscle
- resistant to AChE
2) Carbechol
- Used in glaucoma, pupillary contraction and relief of intra-ocular pressure
3) Pilocarpine
- Contracts ciliary muscle of eye (open angle), pupillary sphincter (narrow angle)
- Potent stimulator of sweat, tears and saliva
4) Methacholine
- Challenge test in asthma diagnosis
- Stimulates M receptors in airway when inhaled |
|
|
Term
A number of cholinomimetic agents are available. What are the actions and clinical applications of the following?
1) Neostigmine
2) Pyridostigmine
3) Edrophonium
4) Physiostigmine
5) Echothiophate
6) Donepezil |
|
Definition
All are indirect agonists (AChE-inihibitors) that increase endogenous ACh levels
1) Neostigmine (NO CNS)
- Post-operative and neurogenic ileus and urinary retention, Myasthenia gravis, reversal of NMG blockage
2) Pyridostigmine (NO CNS)
- Myesthenia gravis (long-acting)
3) Edrophonium
- Diagnosis of myasthenia gravis (short-acting)
4) Physiostigmine
- Glaucoma (crosses BBB)
- Atropine overdose
5) Echotiophate
- Glaucoma
6) Donepezil
- Alzheimer's disease |
|
|
Term
| What drugs are used in the diagnosis and treatment of Myesthenia gravis? |
|
Definition
Autoimmune disease of post-synaptic ACh receptors at NMJ
Indirect cholinomimetic drugs work
1) Diagnose with Edrophonium (short-acting)
2) Treat with Pyridostigmine (long-acting) and/or Neostigmine |
|
|
Term
| What is the general strategy for treating glaucoma and what drugs are available? |
|
Definition
Reduce IOP with direct and indirect cholinergic mimetics
1) Carbachol (direct)
- Pupillary constriction and release of IOP
2) Physostigmine (indirect)
- Crosses BBB and is also used for atropine overdose
3) Echothiophate (indirect) |
|
|
Term
| Which patients should be avoided/monitored closely when prescribing cholinomimetic agents |
|
Definition
Lungs and Gastric are affected
1) COPD/Asthma exacerbation (M3)
2) PUD (may activate M3 receptors) |
|
|
Term
| What drugs are useful in treating post-operative and neurogenic ileus and urinary retention? |
|
Definition
1) Bethanechol (direct cholinomimetic)
2) Neostigmine (AChE-inhibitor) |
|
|
Term
| How do you reverse of NMJ blockage after surgery? How would you treat an atropine overdose? |
|
Definition
1) Neostigmine: AChE inhibitor
2) Physiostigmine (crosses BBB): AChE inhibitor |
|
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Term
What is the pathophysiology underlying organophosphate poisoning and what are the classic symptoms?
How do you treat? |
|
Definition
1) Irreversible AChE inhibitor causing DUMBBELSS
2) Diarrhea, Urination, Miosis, Bronchospasm, Bradycardia, Excitation of skeeletal muscle and CNS, Lacrimation, Sweating and Salivation
3) Give Atropine + Pralidoxine (regenerates active AchE) |
|
|
Term
Which of the following would NOT be caused by organophosphate poisoning?
1) Diarrhea
2) Myosis
3) Dry skin
4) Bradycardia
5) Bronchospasm
6) Urination |
|
Definition
3- ACh excess would cause sweating by binding M3 receptors (Gq)
1) Increased gut peristalsis (M1 and M3)
2) Pupil constriction (M3)
4) Brady cardia (M2- contracitlity and HR decrease)
5) Bronchospasm (M3)
6) Urination (M3)
AChE inhibitor causes DUMBELSS (diarrhea, urination, miosis, bronchospasm, excitation of skeletal muscle and CNS, Lacrimation, Sweating and Salivation |
|
|
Term
How are each of the following Muscarinic antagonists used?
1) Atropine/homatropine
2) Tropicamide
3) Benztropine
4) Scopolamine
5) Ipratroprium
6) Oxybutynin, Glycopyrrolate
7) Methscopolamine, Pirenzepine, Propanethline |
|
Definition
1) Mydriasis and Cycloplegia (eye surgery)
2) Mydriasis and Cycloplegia (eye surgery)
3) Works in CNS for Parkinsons
4) Motion sickness- CNS
5) Asthma, COPD
6) GU (reduce urgency in mild cystitis and reduce spasms)
7) GI (PUD) |
|
|
Term
| Why might you give Oxybutynin or Glycopyrrolate to treat mild cystitis? |
|
Definition
| Anti-muscarinin drugs: Prevent urgency and reduce bladder spasms |
|
|
Term
| Why might you give Methscopolamine, Pirenzepine or Propantheline to treat PUD? |
|
Definition
| Anti-muscariniscs that will prevent gastric acid release in response to M3 activation (CN X to parietal cells) |
|
|
Term
Which of the following would NOT be treated with a muscarinic antagonist?
1) PUD
2) Parkinson's disease
3) COPD
4) Alzheimer's disease
5) Mild cystitis |
|
Definition
| 4- You already have low ACh in nucleus basalis of meynart here. |
|
|
Term
How does atropine act in the following locations?
1) Eye
2) Airway
3) Stomach
4) Gut
5) Bladder |
|
Definition
"Hot as a hare, Dry as a bone, Red as a beet, Blind as a bat, Mad as a hatter"
Muscarinic antagonists used to treat bradycardia and for opthalmic applications.
1) Pupil dilation and cycloplegia (M3)
2) Decreased secretions (M3)
3) Decreased acid secretion (M1)
4) Decreased motility (M3)
5) Decreased urgency in cystitis (M3) |
|
|
Term
| What are the important side effects associated with using a muscarininc antagonist like Atropine? |
|
Definition
"Hot as a hare, Dry as a bone, Red as a beet, Blind as a bat, Mad as a hatter"
1) Increased body temperature (less sweating)
2) Dry mouth
3) Dry flushed skin
4) Cycloplegia- Acute closed angle glaucoma in elderly
5) Constipation
6) Disorientation |
|
|
Term
| Why is atropine particularly dangerous in the elderly, infants, ad men > 50 |
|
Definition
1) Elderly- acute closed angle glaucoma
2) Hyperthermia (less sweating)
3) Urinary retention if they have BPH |
|
|
Term
What are the effects of the following drugs on a1, a2, B1, B2 and D1 receptors?
1) Epinephrine
2) NE
3) Isoproterenol
4) Dopamine
5) Dobutamine
6) Phenylephrine |
|
Definition
1) a1 (+++), a2 (+++), b1 (++++), b2 (++), D1 (0)
- Used for anaphylaxis, glaucoma (open), asthma and hypotension
2) a1 (++++), a2 (++++), b1 (++), b2 (0), D1 (0)
- Hypotension (but decreases renal perfusion)
3) B1 and B2 ONLY (++++)
- AV block (rare)
4) a1 (++++ high dose), a2 (++++ high dose), b1 (++++ medum dose), b2 (++ medium dose), D1 (+ low dose)
- Shock (renal perfusion), heart failure
- Inotropic and chronotropic; D1>b>a
5) a1 (+), a2 (+), b1 (++++), b2 (+), D1 (+)
- Heart failure, cardiac stress testing; inotropic and chronotopric
6) a1 (++++), a2 (++)
- Pupillary dilation (ocular), Vasoconstriciton (hypotension) and Nasal decongestion (Rhinitis) |
|
|
Term
Dopamine is commonly used to preserve renal perfusion in shock and to treat heart failure by increasing HR and contractility.
How does the concentration of administration alter the activity of Dopamine? |
|
Definition
1) Low dose (D1+)
2) Medium dose (B1++++ and B2++)
3) High dose (a1++++ and a2++++) |
|
|
Term
| What is the action of Isoproterenol and what is its major utility? |
|
Definition
| Only activates B1 and B2 (++++) and used in AV block (rare) |
|
|
Term
| Why is NE dangerous to use to treat hypotension? What are other sympathomimetics that might be better options? |
|
Definition
1) NE: a1 (++++), a2 (++++), b1 (++)
- Does not preserve renal perfusion!
2) Dopamine (preserves renal perfusion) or Epinephrine could also be used |
|
|
Term
Which sympathomimetic is used for each of the following?
1) Anaphylaxis and open angle glaucoma
2) AV block
3) Shock
4) Heart failure and cardiac stress testing
5) Pupillary dilation and Nasal decongestion |
|
Definition
1) Epinephrine
- a1/2 (+++), B1 (++++), B2 (++)
2) Isoproterenol
- B1/B2 (++++)
3) Dopamine
- Preserves renal perfusion
4) Doputamine
- B1 (++++) ,a1/a2/b2 (+)
5) Phenylephrine
- a1 (++++), a2 (++) |
|
|
Term
| Which sympathomimetic drugs act preferentially on Beta receptors and exhibit B2>B1? |
|
Definition
MAST (B2 ++++ and B1 ++)
- Metaproterenol and Albuterol for acute asthma
- Salmeterol for long-term asthma treatment
- Tolbutamine to reduce premature uterine contractions
Ritodrine also reduces premature uterine contractions, but has NO B1 effects. |
|
|
Term
Which of the following does NOT function primarilly as a B2 agonist?
1) Albuterol
2) Salmeterol
3) Tulbutamine
4) Doputamine
5) Ritrodrine |
|
Definition
| 4- Dobutamine is used in HF and for cardiac stress testing, hitting B1>>>>B2 |
|
|
Term
How do indirect sympathomimetics like Amphetamines, Ephedrine and Cocaine work?
What are they used for? |
|
Definition
1) Amphetamines- releases stored catecholamines
- Narcolepsy, obesity, ADD
2) Ephedrine- Releases stored catecholamines
- Nasal decongestion, urinary incontinence, hypotension
3) Cocaine- Uptake inhibitor
- Vasoconstriction and local anesthesia |
|
|
Term
| What is the differential effect of NE vs. Isoproterenol on BP and HR? |
|
Definition
1) NE (a>b)-Increases BP, widens PP and decreases HR (reflex bradycardia)
- Get BP up in hypotension
2) Isoproterenol (B >a)- Decreases BP, widens PP and increases HR (reflex tachycardia)
- Get HR up in AV block |
|
|
Term
What kinds of drugs are Clonidine and ALpha-methyldopa?
How are they used? |
|
Definition
1) Sympathoplegics that are centrally acting alpha-2 agonists, decreasing central adrenergic outflow
**Pre-synaptic alpha 2 receptors inhibit release**
2) Used in hypertension, especially with renal disease (no decrease in renal perfusion) |
|
|
Term
| How might you treat hypertension in someone with ESRD? |
|
Definition
| Clonidine or Alpha-methyldopa- centrally acting a-2 agonists that do not reduce renal BF. |
|
|
Term
When surgically removing a pheochromocytoma, what drug might you use to prevent hypertensive crisis?
What side effects would you expect to see? |
|
Definition
Phenoxybenzamine- irreversible, non-selective alpha blocker that is protective in case high levels of catecholamines are released with removal
Side effects include orthostatic hypotension and reflex tachycardia |
|
|
Term
A patient taking a MAO-i goes on a cheese binge and you are terribly worried become of the tyramine.
What do you do? What side effects of this treatment should you look out for? |
|
Definition
Give them Phentolamine, a reversible non-selective alpha blocker
Side effects include orthostatic hypotension and reflex tachycardia |
|
|
Term
| Why might you use drugs like prazosin, terazosin or doxazosin? What side-effects would you be considered about |
|
Definition
The "zosins" are selective a1 blockers that are used to treat
- Hypertension
- Urinary retention in BPH (given with finesteride)
SE include 1st dose orthostatic hypotension, dizziness and headache |
|
|
Term
| What is the clinical use of Mirtazapine and what side effects are expected with its use? |
|
Definition
1) Selective a2 blocker (operates through Gi) that treats depression.
2) Sedation, increased serum cholesterol, increased appetite |
|
|
Term
| How might addition of phentolamine alter BP in a patient who is already taking Epinephrine or Phenylephrine? |
|
Definition
Phentolamine is a reversible non-selective alpha blocker used to treat MAO-i + tryamine toxicity.
1) Epinephrine has both alpha and beta agonist activities, so an alpha blocker would actually reverse the BP changes causing a net "depressor" effect via B2
2) Phenylephrine is a pure alpha agonist (a1 >a2), so alpha blockage would suppress its effects, but not reverse them, since it has no beta action. |
|
|
Term
A patient who is taking a hypertensive medication receives phenoxybenzamine in preparation for removal a pheochromocytoma, but he goes into hypotensive crisis.
What medication might he have been taking? |
|
Definition
Epinephrine.
Since epinephrine has alpha and beta activity, a pure alpha antagonist like phenoxybenzamine would cause unopposed B2 response, with vasodilation and a drop in BP. |
|
|
Term
| There are a wide variety of available beta-blockers. What are their major applications and how do they achieve each? |
|
Definition
HAMS Can Grub
1) Hypertension: Decrease CO and renin secretion (blockage of beta receptors on JGA cells)
2) Angina: Decrease HR and contractility, resulting in decreased O2 consumption
3) MI: Lower mortality
4) SVT (propranolol and esmolol): Decrease AVE conduction velocity (class II anti-arrythmic)
5) CHF: Slows progression of chronic failure
6) Glaucoma: decreased secretion of aqueous humor |
|
|
Term
| What beta blockers are useful in treating SVT? |
|
Definition
| Esmolol (short acting) and Propranolol |
|
|
Term
| What are the major side effects of using a beta blocker to treat hypertension? |
|
Definition
Use with caution in diabetics and those with obstructive lung disease.
1) Impotence
2) Exacerbation of asthma
3) CV effects (Bradycardia and AV block)
4) CNS (Sedation and sleep alteration) |
|
|
Term
| Which beta blockers are "selective" and which are not? Which beta blockers can cause vasodilatory effects? |
|
Definition
1) B1-selective are useful in patients with pulmonary disease
- A BEAM
- Acetbutolol, Betaxolol, Esmolol, Atenolol, Metoprolol
2) Non-selective antagonists
"Please Try Not being Picky"
- Propranolol, Timolol, Nadolol, Pindolol
3) Alpha activity
- Carvedilol, Labetaolol |
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Term
| Which beta blockers are partial agonists?l |
|
Definition
PAPA
Partial beta-Agonists= Pindolol (non-selective and Acetbutolol (B1 selective) |
|
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Term
Which of the following beta blockers is NOT b1-selective?What are the others?
1) Acetbutolol
2) Betaxolol
3) Timolol
4) Esmolol
5) Atenolol
6) Metoprolol |
|
Definition
Timolol
"Please Try Not being Picky"
Propranolol, Timolol, Nadolol, Pindolol |
|
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Term
Which of the following beta blockers is useful in treating patients with COPD?
1) Timolol
2) Propranolol
3) Pindolol
4) Nadalol
5) Betaxolol |
|
Definition
5- It is beta-1-selective
All others are non-selective |
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Term
| What differentiates Carvedilol and Labetalol from Propranolol? |
|
Definition
| Are are non-selective beta blockers, but Carvedilol and Labetalol also hit alpha receptors and can causes vasodilation, while Propranolol will not. |
|
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Term
What is the appropriate antidote for the following toxicities?
1) Amphetamines
2) Organophosphates
3) Anti-muscarinic agents (atropine)
4) Beta blockers
5) Digitalis |
|
Definition
1) Ammonium chloride will acidify urine and cause excretion of basic compound
2) Atropine or Pralidoxime
3) Physiostigmine salicylate (also for Glaucoma)
4) Glucagon
5) Stop dig; normalize K+, Lidocaine, Anti-dig Fab fragments, Mg2+ (KLAM) |
|
|
Term
What is the appropriate antidote for the following toxicities?
1) Acetaminophen
2) Salicylates
3) Iron
4) Lead
5) Mercury, arsenic or gold
6) Copper, arsenic, or gold |
|
Definition
1) N-acetylcystine (replenish GSH)
2) Alkalinize urine with NaHCO3 or Dialysis
3) Deferoxamine
4) CaEDTA, dimercaprol, succimer (kids), penicillamine
5) Dimercaprol (BAL), succimer
6) Penicillamine |
|
|
Term
What is the appropriate antidote for the following toxicities?
1) Cyanide
2) Methemoglobin
3) CO
4) Methanol, ethylene glycol (anti-freeze)
5) Opioids
6) Benzodiazepines |
|
Definition
1) Nitrite, hydroxocobalamin, thiosulfate
2) Methylene blue, vitamin C
3) 100% O2 and hyperbaric O2
4) Fomepizole> ethanol, dialysis
5) Naloxone
6) Flumazenil (competitive GABAR antagonist) |
|
|
Term
What is the appropriate antidote for the following toxicities?
1) TCAs
2) Heparin
3) Warfarin
4) tPA, streptokinase, urokinase
5) Theophylline |
|
Definition
1) NaHCO3 (plasma alkalization, like with aspirin or phenobarbital)
2) Protamine
3) Vitamin K, FFP
4) Aminocaproic acid
5) Beta blocker |
|
|
Term
What is the appropriate antidote for the following toxicities?
1) tPA, streptokinase, urokinase
2) Cyanide
3) Mercury
4) Digitalis
5) Methanol |
|
Definition
1) Aminocaproic acid
2) Nitrite, Hydroxycobalamin, Thiosulfate
3) Dimercaprol, Succimer
4) Stop dig, Manage K+, Lidocaine, Anti-Fab, Mg2+
5) Fomepizole > Alcohol, Dialysis |
|
|
Term
What agents cause the following drug reactions in the CV system?
1) Vasospasm (coronary)
2) Cutaneous flushing
3) Dilated cardiomyopathy
4) Torsades de pointes |
|
Definition
1) Cocaine, sumatriptan
2) VANC, Vancomycin, Adenosine, Niacin, Ca2+- blocker
3) Doxorubicin (Adriamycin), Danorubicin
4) Class III (sotalol), Class IA (quinidine) anti-arrythmics |
|
|
Term
What agents cause the following drug reactions in the Hematologic system?
1) Agranulocytosis
2) Aplastic anemia
3) Direct coomb's positive hemolytic anemia
4) Gray baby |
|
Definition
1) "Agranulocytosis Could Certainly Cause Pretty Major Damage"
- Clozapine, Carbamazepine, Colchicine, Propylthiouracil, Methimazole, Dapsone
2) Chloramphenicol, Benzene, NSAIDS, Propylthioruracil, Methimazole
3) Methyldopa
4) Chloramphenicol |
|
|
Term
What drugs cause the following hematologic abnormalities?
1) Hemolysis in G6PD-deficient patients
2) Megaloblastic anemia
3) Thrombotic complications
4) Aplastic anemia |
|
Definition
1) "hemolysis IS PAIN"
- Isoniazid, Sulfonamides, Primaquine, Aspirin, Ibuprofin, Nitrofurantoin
2) Phenytoin, MTX, Sulfa drugs (having a blast with PMS)
3) OCPs (estrogens and progestins)
4) Chloramphenicol, Benzene, NSAIDS, Propylthiouracil, Methimazole |
|
|
Term
Which of the following DOES NOT cause agranulocytosis?
1) Clozapine
2) Primaquine
3) Carbamazepine
4) Colchicine
5) Propylthiouracil
6) Dapsone |
|
Definition
2) Primaquine causes hemolytic anemia in G6PD deficiency, along with Isoniazid, Sulfonamides, Aspirin, Ibuprofin, Nitrofurantoin.
For Agranulocysosis: "Agranulocytosis Could Certainly Cause Pretty Major Damage"
- Clozapine, Carbamezapine, Colchicine, Propylthiouracil, Methimazole, Dapsone |
|
|
Term
Which of the following does NOT cause cutaneous flushing?
1) Vancomycin
2) Aspirin
3) Niacin
4) Calcium channel blockers
5) Adenosine |
|
Definition
| 2- Aspirin is more likely to cause Hemolytic anemia is G6PD deficiency. |
|
|
Term
|
Definition
| Ace inhibitors (NOT ARBs) |
|
|
Term
| Which drugs cause pulmonary fibrosis? |
|
Definition
BLAB
1) Bleomycin
2) Amiodarone
3) Busulfan |
|
|
Term
| What drug is known to cause acute cholestatic hepatitis? |
|
Definition
| Erythromycin (not other macrolides) |
|
|
Term
| Which drugs can cause focal to massive hepatic necrosis? What about hepatitis? |
|
Definition
1) Hepatic necrosis: HAVAc
- Halothane, Acetaminophen, Valproic acid, Amanita phalloides
2) Hepatitis: INH |
|
|
Term
| Which drugs cause psuedomembranous colitis? |
|
Definition
1) Clindamycin (50S)
2) Ampicillin (aminopenicillin) |
|
|
Term
| Which drugs are known to cause Gynecomastia? |
|
Definition
Some Drugs Create Awesome Knockers
1) Spironolactone
2) Digitalis
3) Cimetidine
4) Alcohol use
5) Ketoconazole |
|
|
Term
Some drugs can mess with the reproductive and endocrine systems. Which drugs cause
1) Adrenocortical insufficiency
2) Hot flashes
3) Hypothyroidism
4) Hyperglycemia? |
|
Definition
1) Glucocorticoid withdrawal (HPA suppression)
2) Tamoxifen and Clomiphene
3) Lithium, Amiodarone (also pulmonary fibrosis), Sulfonamides
4) Niacin, Tacrolimus, Protease inhibitors |
|
|
Term
| Which drugs cause Fat redistribution? |
|
Definition
1) Glucocorticoids
2) Protease inhibitors |
|
|
Term
| Which drugs cause gingival hyperplasia |
|
Definition
1) Phenytoin (also megaloblastic anemia)
2) Verapamil |
|
|
Term
| Gout is treated with Xanthine oxidase inhibitors or Colchicine, but which drugs can actually cause it? |
|
Definition
Those that cause hyepruricemia
1) Furosemide
2) Thiazides
3) Naicin
4) Cyclosporine
5) Pyrazinamide |
|
|
Term
| Which drugs are known to cause myopathies? |
|
Definition
"Fish N CHIPS GIve you myopathies"
1) Fibrates
2) Niacin
3) Colchicine
4) Hydroxychlorquine
5) Interferon alpha
6) Penicillamine
7) Statins
8) Glucocorticoids |
|
|
Term
| Which drugs cause osteoporosis? |
|
Definition
1) Corticosteroids
2) Heparin |
|
|
Term
| Which drugs cause photosensitivity? |
|
Definition
SAT for a photo
1) Sulfonamide
2) Amiodarone
3) Tetracycline |
|
|
Term
| Which drugs cause the characteristic rash in Steven-Johnson's syndrome? |
|
Definition
bad rash after a PEC SLAPP
1) Penicillin
2) Ethosuximide
3) Carbamazepine
4) Sulfa drugs
5) Lamotrigine
6) Allopurinol,
7) Phenytoin
8) Phenobarbitol |
|
|
Term
| Which drugs can create SLE-like symptoms? |
|
Definition
Its not HIPP to have lupus
1) Hydralazine
2) INH
3) Procainamide
4) Phenytoin |
|
|
Term
| Which drugs are not given to kids because of risk of tendonitis and tendon rupture? |
|
Definition
|
|
Term
Which drugs cause the following renal/GU side effects?
1) Diabetes insipidus
2) Fanconi syndrome
3) Interstitial nephritis
4) Hemorrhagic cystitis
5) SIADH |
|
Definition
1) Lithium, Demeclocycline
2) Expired tetracycline
3) Methicillin, NSAIDS, Furosemide
4) Cyclophosphamide, Ifosfamide (prevent with co-administration of Mesna)
5) Carbamezepine, Cyclophosphamide |
|
|
Term
Which drugs can cause the following CNS side effects?
1) Cinchonism (tinnitus and slight deafness)
2) Parkinson-like
3) Seizures
4) Tardive dyskinesia |
|
Definition
1) Quinidine, quinine
2) Anti-psychotics, Reserpine, Metoclopramide
3) Buproprion, Imipenem/cilastatin, INH
4) Anti-psychotics |
|
|
Term
Some drugs can cause multi-oragn dysfunction. Which agents cause the following?
1) Anti-muscarinic
2) Disulfriram-like
3) Nephrotoxicity/Ototoxicity |
|
Definition
1) Atropine, TCAs, H1 blockers, Neuroleptics
2) Metronidazole, Certain Cephalosporins, Procarbazine, 1st generation suflonylureas.
3) Vancomycin, Aminoglycosides, Loop diuretics, Cisplatin |
|
|
Term
| What are the "inducers" of CYP 450 metabolism? |
|
Definition
Barb Steals Phen-phen and Refuses Greasy Carbs Chronically
1) Barbiturates
2) St. john's wart
3) Phenytoin
4) Rifampin
5) Griseofulvin
6) Carbamazepine
7) Chronic alcohol use |
|
|
Term
| What are the "inhibitors" of CYP 450 metabolism? |
|
Definition
MAGIC RACKS (and Quinidine)
1) Macrolides
2) Amiodarone
3) Grapefruit juice
4) INH
5) Cimetidine
6) Ritonavir
7) Acute alcohol abuse
8) Cipro
9) Ketoconazole
10) Sulfonamides |
|
|
Term
| How does acute vs. chronic alcohol use influence CYP metabolism? |
|
Definition
| Acutely, OH- inhibits CYPs, and then chronically it induces them |
|
|
Term
Which of the following does NOT induce CYP 450 metabolism?
1) Barbiturates
2) Carbamazepine
3) Griseosulvin
4) RItonavir
5) Chronic alcohol use |
|
Definition
| 4- Ritonavir inhibits it. |
|
|
Term
Which drug does NOT inhibit CYP metabolism?
1) Macrolides
2) Amiodarone
3) Rifampin
4) Quinidine
5) Cipro
6) Ketoconazole |
|
Definition
|
|
Term
| What are the major sulfa drugs that are available? |
|
Definition
Popular FACTSSS
**May develop fever, UTI, pruritic rash, Stevens-Johnson, Hemolytic anemia, TP, agranulocytosis and urticaria**
1) Probenecid (gout)
2) Furosemide (loop diuretic)
3) Acetazolamide (CA inhibitor)
4) Celecoxib (non-steroidal for pain)
5) Thiazide (diuretic)
6) Sulfmonamide antibiotics
7) Sulfsalazine (cancer)
8) Sulfonylurea (diabetes) |
|
|
Term
Drugs can sometimes be identified by handy endings. What kind of drugs have the following endings?
1) azole
2) cillin
3) cycline
4) navir |
|
Definition
1) Anti-fungal like Ketoconazole
2) Penicillin
3) Antibiotic-protein synthesis inhibitor (Tetracycline)
4) Protease inhibitor (Saquinavir) |
|
|
Term
Drugs can sometimes be identified by handy endings. What kind of drugs have the following endings?
1) triptan
2) ane
3) caine
4) operidol
5) azine |
|
Definition
1) 5-HT1b/1d agonist (migraine like Sumatriptan)
2) Inhalation general anesthetic (Halothane)
3) Local anesthetic (Lidocaine)
4) Butryophenone (neuroleptic like Haloperidol)
5) Phenothiazine (neuroleptic, anti-emetic)- Chlorpromazine |
|
|
Term
Drugs can sometimes be identified by handy endings. What kind of drugs have the following endings?
1) Barbital
2) Zolam
3) Azepam
4) Etine
5) Ipramine
6) Tryptyline |
|
Definition
1) Bartiburate (phenobarbitol)
2) Benzodiazepine (Alprazolam)
3) Benzodiazepine (Diazepam)
4) SSRI (Fluoxetine)
5) TCA (Imipramine)
6) TCA (Amitryptyline) |
|
|
Term
Drugs can sometimes be identified by handy endings. What kind of drugs have the following endings?
1) Olol
2) Terol
3) Zosin
4) Oxin |
|
Definition
1) Beta blocker (Timolol)
2) B2 agonist (Albuterol)
3) Alpha 1 antagonist (Prazosin)
4) Carciac glycoside (inotrope like Digoxin) |
|
|
Term
Drugs can sometimes be identified by handy endings. What kind of drugs have the following endings?
1) Pril
2) Afil
3) Tropin
4) Tidine |
|
Definition
1) ACE inhibitor (Captopril)
2) ED drug (Sildenafil)
3) Pituitary hormone (Somatotropin)
4) H2 antagonist (Cimetidine) |
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