Pharmacology Flashcards
what is the mechanism of Acetaminophen toxicity in the liver?
Specifically, acetaminophen is converted by CYP450 enzymes into NAPQI, which results in severe liver damage when accumulated in excess.
Acetaminophen is not a CYP inhibitor or inducer
sx: N/V, abdominal pain –> later on at higher doses, can cause hepaticc necrosis/juandice +/-encephalopathy, nephrotoxicity
antidote: NAC and activated charcoal
which diabetes drug can cause vitamin B12 deficiency if taken a long time
metformin (decreases absorption of)
Glucocorticoids MOA
steroid binding to intracellular glucocorticoid receptors followed by translocation to the nucleus where it inactivates NF-κB –>:
- reduction in the transcription of proinflammatory mediators such as COX-2 , NOS, and inflammatory cytokines (IL-1 thru IL-6, IL-8, IL-10, IL-13, GM-CSF, TNF-α, Interferon-γ)
- upregulation in the synthesis of annexin A1, which inhibits phospholipase A2 and neutrophil penetration through endothelium of blood vessels
Omalizumab MOA
Omalizumab binds mostly unbound serum IgE and blocks binding of IgE to the Fc portion of mast cells, preventing degranulation
T/F: M3 muscarine antagonists are not recommended in uncontrolled narrow-angle glaucoma.
true (tiotropium, atropine, scopalamine)
cocaine MOA
blocking reuptake of the neurotransmitters norepinephrine, dopamine, and serotonin.
What drugs are indicated for patient with acute gout attack
NSAID
Colchicine
corticosteroids/glucocorticoids (injection preferred)
^after NSAID failure
what drugs are indicated for preventative/chronic management of gout
- Xanthine oxidase inhibitors
- allupurinol, febuxostat
- probenecid
^reduce the urice acid level in the body
MOA of colchicine
microtubule inhibition by binding to tubulin –> white blood cell migration and phagocytosis is inhibited
colchicine adverse effects
GI:
N/V/D –> d/t loss of GI epithelium turnover which promotes BM
abdominal pain
what are the xanthine inhibitors
- allopurinol –> competitive inhibitor (mn: PURE competition)
- febuxostat –> non-competitive inhibitor
side effects of allopurinol
for this reason, many patients don’t tolerate it well. febuxostat is used as a second line of tx for patients who don’t tolerate allopurinol
MOA of allopurinol and febuxostat
Can we give patients aspirin for pain control of gout attack?
NO, not at normal dosages
it is dose dependent, see image
what co-administration needs to be given with the XO inhibitors
cochicine because the changing ration of uric acid in the blood due to the XO inhibitors can cause acute gout attacks which colchicine will supress
What DMARD is this based on the MOA shown
what’s its indication
leflunamide
what DMARD acts by inhibiting calcineurin?
what’s its indication
cyclosporin
probenecid side effects and administration precautions
Give with colchicine if acute setting
don’t use if renal problems
increased risk for developing uric acid kidney stones d/t increased secretion
Adverse Effects: GI irritation, rash, aplastic anemia; don’t give if pt has sulfa allergey
MOA of probenicid
whats its indication
blocks reabsorption of uric acid in proximal tubule –> increased excretion
indicated for gout
what is the indication for prescribing leflunamide
RA, if the patient fails Methotrexate
GAS (strep. pyogenes) virulence factors
- bacterial capsule is responsible for evasion of phagocytosis.
- protein F is required for adherence to the host cell
- Streptokinase lysis clots and helps invasion into tissues.
- C-5 peptidase lyses complement complexes evading the complement component of the immune system
- Streptococcal pyogenic exotoxin is responsible for generating fever and immunomodulation
indication and MOA of cyclophosphamide
indication: RA
MOA:
Staining features/virulence factors of Staphylococcus aureus
- gram positive
- beta hemolytic
- coagulase positive (differentiates s. aureus and s. epidermidis)
- catalase positive –> converts H2O2 to water and oxygen (differentiates it from strep)
- ferments mannitol
- contains alpha toxin and beta toxin
^pretty much all positives (mn: Aureas does All the Areas)
*** the other key thing that differentiates it from strep is that it is arranged in clusters rather than chains
what is the basic differentiating factor between staph aureus and strep pyogenes ( in terms of structure)
Food poisoning due to staphylococcal enterotoxin is characterized
by a short incubation period ___-___ hours
1-8 hours
True/False:
Coagulase-positive staphylococci are considered
pathogenic for humans
TRUE
treatment for penicillin G- resistant S. aureus
Penicillin G-resistant S. aureus strains from clinical
infections always produce penicillinase. They
constitute >95% of S. aureus isolates in communities in
the United States.
• They are often susceptible to β-lactamase-resistant
penicillins, cephalosporins, or vancomycin.
• Vancomycin-resistant strains are rare.
sulfa drug rxn
what are the 5 types of typhus infections and what was their causative agent
- Rocky Mountain spotted fever –> tickborne,
- scrub typhus, –> mite-borne
- rickettetsialpox, –> mite-borne
- endemic typhus, spread by a body louse
- murine endemic typhus spread by a flea.
Answer: DHFR and DHPS
what is the abx treatment for rickettsiae infection causing typhus?
tetracycline/docycycline
are are the two most likely late sequelae of streptococcal pyogenes infections
- rheumatic fever
- glomerular nephritis
Patient with anal itching presents. no other symptoms. microscopu of a the area shows this. What’s the diagnosis?
enterobius (pinworm) which is in the nematode family
which organism is most usually responsible for toxic shock syndrome
Staph
the ___________ lab test differentiates between staph aureus from non pathogenic staphylococci
Coagulase test
What drugs are indicated for patient with acute gout attack
NSAID
Colchicine
corticosteroids/glucocorticoids (injection preferred)
^after NSAID failure
what drugs are indicated for preventative/chronic management of gout
- Xanthine oxidase inhibitors
- allupurinol, febuxostat
- probenecid
^reduce the urice acid level in the body
MOA of colchicine
microtubule inhibition by binding to tubulin –> white blood cell migration and phagocytosis is inhibited
colchicine adverse effects
GI:
N/V/D –> d/t loss of GI epithelium turnover which promotes BM
abdominal pain
what are the xanthine inhibitors
- allopurinol –> competitive inhibitor (mn: PURE competition)
- febuxostat –> non-competitive inhibitor
side effects of allopurinol
for this reason, many patients don’t tolerate it well. febuxostat is used as a second line of tx for patients who don’t tolerate allopurinol
MOA of allopurinol and febuxostat
Can we give patients aspirin for pain control of gout attack?
NO, not at normal dosages
it is dose dependent, see image
what co-administration needs to be given with the XO inhibitors
cochicine because the changing ration of uric acid in the blood due to the XO inhibitors can cause acute gout attacks which colchicine will supress
What DMARD is this based on the MOA shown
what’s its indication
leflunamide
what are the best NSAIDs for gout?
sulindac, naproxen, indomethacin
what DMARD acts by inhibiting calcineurin?
what’s its indication
cyclosporin
probenecid side effects and administration precautions
Give with colchicine if acute setting
don’t use if renal problems
increased risk for developing uric acid kidney stones d/t increased secretion
Adverse Effects: GI irritation, rash, aplastic anemia; don’t give if pt has sulfa allergey
MOA of probenicid
whats its indication
blocks reabsorption of uric acid in proximal tubule –> increased excretion
indicated for gout
what is the indication for prescribing leflunamide
RA, if the patient fails Methotrexate
GAS (strep. pyogenes) virulence factors
- bacterial capsule is responsible for evasion of phagocytosis.
- protein F is required for adherence to the host cell
- Streptokinase lysis clots and helps invasion into tissues.
- C-5 peptidase lyses complement complexes evading the complement component of the immune system
- Streptococcal pyogenic exotoxin is responsible for generating fever and immunomodulation
indication and MOA of cyclophosphamide
indication: RA
MOA:
Staining features/virulence factors of Staphylococcus aureus
- gram positive
- beta hemolytic
- coagulase positive (differentiates s. aureus and s. epidermidis)
- catalase positive –> converts H2O2 to water and oxygen (differentiates it from strep)
- ferments mannitol
- contains alpha toxin and beta toxin
^pretty much all positives (mn: Aureas does All the Areas)
*** the other key thing that differentiates it from strep is that it is arranged in clusters rather than chains
what is the basic differentiating factor between staph aureus and strep pyogenes ( in terms of structure)
Food poisoning due to staphylococcal enterotoxin is characterized
by a short incubation period ___-___ hours
1-8 hours
True/False:
Coagulase-positive staphylococci are considered
pathogenic for humans
TRUE
treatment for penicillin G- resistant S. aureus
Penicillin G-resistant S. aureus strains from clinical
infections always produce penicillinase. They
constitute >95% of S. aureus isolates in communities in
the United States.
• They are often susceptible to β-lactamase-resistant
penicillins, cephalosporins, or vancomycin.
• Vancomycin-resistant strains are rare.
what are the 5 types of typhus infections and what was their causative agent
- Rocky Mountain spotted fever –> tickborne,
- scrub typhus, –> mite-borne
- rickettetsialpox, –> mite-borne
- endemic typhus, spread by a body louse
- murine endemic typhus spread by a flea.
Answer: DHFR and DHPS
what is the abx treatment for rickettsiae infection causing typhus?
tetracycline/docycycline
are are the two most likely late sequelae of streptococcal pyogenes infections
- rheumatic fever
- glomerular nephritis
Patient with anal itching presents. no other symptoms. microscopu of a the area shows this. What’s the diagnosis?
enterobius (pinworm) which is in the nematode family
which organism is most usually responsible for toxic shock syndrome
Staph
the ___________ lab test differentiates between staph aureus from non pathogenic staphylococci
Coagulase test
what rare but strange MSK side effect can occur with taking fluoroquinalones
achilles tendon tear/rupture or swelling
what is an MAO
Monoamine oxidase
MAOI = drug that inhibites monoamine oxidase
*assoc with serotonin syndrome
T/F: metronidazole only works on anaerobes
TRUE
esp c diff, b frag, H pylori
what drug to use to treat necrotizing fascitis
clindamycin (with penicillin G)
ketoconazole
an antigunal medication
MOA: blocks ergosterol synthesis by inhibiting 17,20 lyase
AE: decrease in testosterone (p/w gynecomastia in men)
off label use: Cushing’s syndrome (b/c it also blocks upstream enzymes req. for cortisol synth.)
what are pediculocides
drugs that kill pediculus humanus (lice) of the head (capitis) and body (corporis)
what is ascaris
giant intestinal roundworm
causes intestinal pain, constipation (high pitched bowel sounds)
tx: mebendazole
mebendazole - what is it used to treat?
intestinal nematodes and tapeworms
what drugs are used to treat tapeworms
niclosamid, praziquantel, albendazole (or mebendazole)
praziquantel treats _______and _________
tapeworms (cestodes) and flukes (trematodes)
how does niclosamide work?
transport chain uncoupler
how does ivermectin work?
Glu Cl- channel agonistm
ivermectin treats
threadworm, dog heartowrm, wuchereria (elephantiasis), lice
limitation of treatment of lice with benzyl alcohol?
it only kills adult lice
what is “rid” OTC shampoo?
contain pyrethrins (from chrysanthemom flower), which kill lice via Na+ channel blockers
which drugs kill lice eggs and adults?
malathion
spinosad
what toxicities/AEs are associated with Quinidine (class 1A antiarrhythmic)
- cinchonism: a syndrome of tinnitus, headache and dizziness
- thrombocytopenia
- QT prolongation (torsades, syncope)
what toxicities/AEs are associated with procainamide (class 1A antiarrhythmic)
- (chronic use) drug-induced lupus (sx arthralgia, arthritis, pleuritis, pericarditis, parenchymal pulmonary disease)
- QT prolongation (torsades, syncope)
what toxicities/AEs are associated with disopyramide
- acute heart failure (cannot be used in patients with impaired systolic function.)
- anticholinergic side effect sx: dry eyes, dry mouth, urinary retention
- QT prolongation (torsades, syncope)
what toxicities/AEs are associated with lidocaine
neurological side effects: tremor, convulsions (seizure), paresthesias
which drugs are high risk for causing DILE
There are four main drugs that are known for causing drug-induced lupus:
- hydralazine
- isonazid (INH)
- procainamide
- phenytoin/penicillamine
What are the class 1A antiarrhythmics
Quinidine (prom queen)
Procainamide (prom king)
disopyramide (disappear)
tx of choice for Wolff parkinson-white syndrome
procainamide
avoid class 1A antiarrhythmics (Quinidine (prom queen)
Procainamide (prom king)
disopyramide (disappear)) if a patient has _________
heart failure (b/c negative inotropy can lead to heart failure) ESPECIALLY disopyramide
the class IB antiarrhythmics are
mexiletine (mexican flag)
lidocaine (lied to me)
which class of antiarrhythmics is best for heart damaged by ischemia?
class 1B (mexiletine and lidocaine)
what toxicities/AEs are associated with mexilitine
N/V
what are the class 1C antiarrhythmics
flecainide (flakes)
propafenone (purple phone)
indications for using class 1C antiarrhythmic drugs?
Ventricular tachycardia
other arrhythmias that are refractory to other tx (b/c it is most likely to cause an arrhythmia)
what toxicities/AEs are associated with propafenone?
metallic taste (fenny taste)
Beta-1 receptors are predominantly found in
the heart, the kidney, and fat cells.
when are beta blockers contraindicated?
- when pt taking Ca2+ channel blockers (risk of AV block)
- pheochromocytoma
- cocaine toxicity
-bradycardia (non physiologic)
what is an off-label use for propanalol
Propranolol has the best CNS penetration among all beta blockers and is thus used as an anxiolytic (reduces sympathetic sx of anxiety)
another use is as a local anesthetic
which of the Class II (K blockers) antiarrhythmics is indicated for life threatening V Tach
amiodarone
what toxicities/AEs are associated with dronedarone?
GI disturbances (mn: you get motion sickness flying on a drone)
what toxicities/AEs are associated with class IV antiarrhythmics (verapamil and diltiazem)
hyperprolactinemia, flushing, bradycardia, constipation
more serious: heart block and SA node depression*
therefore, contraindicated in pts with bradycardia and heart failure
dangerous drug interaction with class IV antiarrhythmics (verapamil and diltiazem)
don’t give with beta blockers –> decreases conduction velocity
what toxicities/AEs are associated with adenosine (Misc antiarrhythmic)
flushing, bronchoconstriction, dyspnea, chest pain, hypotension
Digoxin MOA
mimics effect of vagal nerve innervation:
- decreases AV node firing (via inhibiting the sodium/potassium-ATPase in cardiac myocytes. This inhibition increases the intracellular sodium content –> The increase in intracellular Na+ decreases the activity of the Na+/Ca2+ exchanger, which results in an increase in the intracellular Ca2+ concentration –> increase in cardiac contractility)
BUT, it’s a positive inotrope (increased contractility, so that the heart can pump more blood with fewer contractions)
*obviously these effects are complimentary, but it can seem counterintuitive because positive inotropy is also an effect of the sympathetic nervous system via beta 1 rec activation
ind/for HFrEF (adjunct) and A-fib
does not provide mortality benefit
what toxicities/AEs are associated with digoxin
+N/V/D + confusion, tachyarrhythmias (+/- AV block), and visual changes (particularly “Halo-ing” and yellowing appearance of visual objects (“xanthopsia”)), hyperkalemia (a/w pooer prognosis) and hyponatremia (d/t direct inh. of na/k pump)
Digoxin is renally cleared and has a narrow therapeutic window, so toxicity frequently results from alterations in kidney function.
antidote: magnesium, digoxin specific immune fabs
which class IV antiarrhythmic can be used to treat HTN
diltiazem
what side effects are common to all Class IV antiarrhythmics (Ca channel blockers)
constipation, hyperprolactinemia, heart block, bradycardia
what are the calcium channel blockers
Dihydropyridines (selective for Ca2+ channels on vascular smooth muscle so they treat HTN)
Amlodipine
Nicardipine
Nifedipine
Non-dihydropyridines (selective for heart tissue so they treat arrhythmias)
verapamil
diltiazem
what are the indications for Ca channel blockers (by type)
dihydropyridines (-dipine): HTN (main indication), angina, Raynaud’s phenomenon, cerebral vasospasms after subarachnoid hemorrhage
non-dihydropyridines (verapamil and diltiazem): tachyarrhythmias, angina, HTN (diltiazem only)
what side effects are common to all dihydropyridines (-dipine)
reflex tachycardia, vasodilation, gingival hyperplasia
what are the sx of alcohol withdrawal
anxiety, tremors, diaphoresis, and possibly seizures
what is Lactulose and what is it indicated for
a synthetic disaccharide laxative → decreases absorption of ammonia in the bowel: lactulose is converted to lactic acid by intestinal flora → acidification in the gut leads to conversion of ammonia (NH3) to ammonium (NH4+) → ammonium is excreted in the feces → decreased blood ammonia concentration
used for hepatic encaphlopathy
1st line tx for status epilepticus
IV benzodiazapines
MOA: enhance effects of GABA at GABA-A rec –> increased Cl influx –> no AP
prophylaxis for recurrence of status epilepticus
phenytoin
MOA: blocks presynaptic voltage gated Na channels
Black box warning: Hypotension and cardiac arrhythmias with rapid infusion
n/b it’s a P450 inducer
a pt develops elevated serum creatinine or even acute renal failure following initiation of ACE inhibitor for HTN. What’s the pathogenesis of this?
ACE inhibitors lower angiotensin II levels, causing systemic vasodilation and reduced blood pressure. However, they also cause efferent arteriolar dilation and lower intraglomerular pressure, preventing the kidney from maintaining GFR in the setting of reduced renal perfusion. Many patients experience up to a 30% increase in serum creatinine within 2-5 days of starting ACE inhibitors. Patients with bilateral RAS (who are heavily dependent on angiotensin II to maintain GFR) can experience a precipitous fall in GFR and develop acute renal failure.
n/b: This affect does not occur in the affarent arterioles because there are sufficient local vasodilators (PGs and NO) to counteract the effects of ang II
a pt develops hyperkalemia following initiation of ACE inhibitor for HTN. What’s the pathogenesis of this?
ACE inhibitors decrease ang II –> ang II not available to stimulate secretion of aldosterone from adrenal gland –> decreased aldosterone –> decreased expression of Na/K ATPase –> decreased Na reabsorption and K secretion in the distal and collecting tubules
*to remember the direction that Na and K are flowing, remember that in the Na/K ATPase, K is entering the cell, and Na is leaving the cell. The side of the cell where the blood vessel runs, is by default “outside” as in the rest of the body, rather than the side with the lumen (in the kidneys).
what drugs are a/w acute tubular necrosis?
aminoglycosides, vancomycin, antiretrovirals, foscarnet, cisplatin, ethylene glycol
other things (not drugs): lead, radiocontrast agents, myoglobinuria from rhabdomyolysis, and hemoglobinuria
statin MOA
inhibition of the rate limiting step in cholesterol synthesis (HMG-CoA reductase)
in utero lithium exposure (tx for bipolar disorder) can cause what defect
Ebstein’s anomaly in infants. Ebstein’s anomaly is characterized by apical displacement of the tricuspid valve leaflets, decreased volume of the right ventricle, and atrialization of the right ventricle.
how does cabergoline affect pituitary adenoma?
Prolactin levels typically fall significantly within the first 2-3 weeks of therapy with a corresponding improvement in hypogonadal symptoms. Although decreased tumor size may not be visible on imaging for several weeks, mass-effect symptoms (eg, visual field defects) usually start to improve much sooner, often within the first several days of treatment with eventual normalization in many cases.
What are the non-sedating antihistamines and how do they work?
- cetirizine (mn: setirizine is second generation)
- Loratadine
- fexofenadine
- desloratadine
called 2nd generation antihistamines, they are non sedating because they are are hydrophilic and have poor penetration of the blood-brain barrier (BBB).
what is the MOA of orListat (weight loss drug)
inhibits resorption of fats in the du-O-denum by c-O-valently binding lipases
mn: starts with an O for duodenum and covalent binding, has an L for loss of weight
What does a benzodiazapine overdose look like and what is the antidote?
The presence of sedation with normal vital signs and an unremarkable physical examination is most consistent with benzodiazepine overdose.
Flumazenil functions as a competitive antagonist at the benzodiazepine binding site and may be used as an antidote to reverse benzodiazepine sedation related to overdose or procedural sedation.
**by contrast, and opioid overdose would present with resporatory depression (At least)
antidote to anticholinergic toxicity?
physostigmine (acetylcholinesterase inhibitor)
antidote to antipsychotic medication overdose
diphenhydramine
anatidote to serotonin syndrome
cyproheptadine
antidote to cocaine overdose
benzodiazapines (bind to GABA-a receptor, enhancing transmission)
antidote to cholinergic crisis
atropine then pralidoxime
Atropine binds to and inhibit muscarinic acetylcholine receptors,
how is metformin metabolized
renally
Management of gastroesophageal reflux disease includes lifestyle and dietary modifications (eg, weight loss, tobacco avoidance) and medications such as
proton pump inhibitors (PPIs) (eg, pantoprazole, omeprazole) or histamine 2 receptor antagonists (eg, famotidine). PPIs irreversibly inhibit the H+/K+ ATPase on parietal cells, which decreases gastric acid secretion.
what are the kidney acting drugs and where do they act?
COLT PAw Mn for the diuretics in order of where they operate
- Carbonic anhydride inhibitors: pct
- Osmotic diuretics: pct (eg mannitol) ..indicated for acute high ICP
- Loop diuretics : ascending limb of loop of Henley . E.g furosemide.. prevents sodium potassium chloride reuptake
- Thiazide diuretics: dct (acting on na/cl cotransporters) ..best for HTN and elderly e.g. Chlorothiazide. Chlorthalidone. Hydrochlorothiazide
- Potassium sparing diuretics: cd
- Aldosterone receptor blockers (a type of k sparing): CD e.g. Spironolactone
- ENaC channel inhibitors → decrease sodium reabsorption: amiloride, triamterene
mech. of extrapyramidal sx in haloperidol toxicity
Blockade of central dopamine D2 receptors in the brain leads to the extrapyramidal symptoms
PSEUDOPARKINSONISM · AKATHISIA · DYSTONIC REACTIONS · TARDIVE DYSKINESIA.
organophosphate toxicity p/w
can cause bronchorrhea/bronchospasm and bradycardia, clinical features are dominated by other findings of cholinergic excess (eg, salivation/drooling, lacrimation, diaphoresis); pupils are also usually constricted.
heparin acts on which anticoagulation protein
antithrombin III. binds to/increases activity of it
Hirudin
Lepirudin
Bivalirudin
Desirudin
Argatroban
dabigatran
what are these drugs?
direct thrombin inhibitors
indications: HIT (alternative to heparin), coronary syndromes, AFIB
warfarin MOA
Vit K antagonist via epoxide reductase inhibition
which medications interfere with folate metabolism and are therefore a/w neural tube defects
Valproic acid
Phenytoin
TMP
Sulfonamides
methotrexate
what are the drug induced causes of restrictive lung disease
mn: BB AMMo
- Bleomycin
- Busulfan
- AMiodarone
- MethOtrexate
what are the aromatase inhibitors
aromatase converts testosterone to estradiol
they are anastrazole, letrozole, exemestane
tx for hepatic encephalopathy
lactulose (ist line) : lactulose (gets converted to lactic acid –> acidifcation of gut causing conversion of ammonia into excretable form)
rifaximin (add on drug): oral abx that decreases ammonia producing intestinal bacteria
what is atropine used for
It’s a muscarinic antagonist, so it’s used to
- reverse excessive muscarinic activation (e.g. antidote for organophosphate poisoning)
- bradycardic arrest
- to dilate the pupil (but on the flipside can cause acute closed angle glaucoma in older adults)
cocaine moa
Cocaine is an indirect sympathomimetic that acts to inhibit the reuptake of as norepinephrine, dopamine, and serotonin from the neuronal synapse
PCP Moa
Phencyclidine (PCP) acts as an N-methyl-D-aspartate receptor antagonist.
Nitroprusside
what is it?
what is it used for?
a vasodilator used to treat cardiogenic shock and would worsen the blood pressure in distributive shock
It is metabolized into nitric oxide (NO), which is a potent vasodilator in the smooth muscle of the vasculature that acts by increasing cyclic guanosine monophosphate (cGMP
AE: metabolite of nitroprusside, thiocyanate, can build up and cause toxicity, which presents as nausea and vomiting.
what is the pressor of choice in pts with septic shock with acidosis.
vasopressin (ADH) works well in acidic environments
Etanercept
what is it
what is it for?
Etanercept inhibits tumor-necrosis factor (TNF) activity by competitively binding to TNF and preventing it from interacting with cell surface receptors. It is an anti-inflammatory agent used for the treatment of rheumatoid arthritis, psoriasis, and psoriatic arthritis.
Benzodiazepines moa
Benzodiazepines act by binding to the benzodiazepine binding site of GABA a receptors, which allosterically modulates the binding of GABA, resulting in an increased frequency of chloride ion channel opening
which lipid lowering agent is most effective at reducing cardiovascular events
statins
HMG CoA reductase inhibitor
indications for Niacin (Vit B3) over fibrates or statins?
Niacin (vitamin B3) given in pharmacologic doses is the most effective agent for raising HDL levels, but does not reduce the risk of cardiovascular events and is associated with adverse effects (eg, flushing, hyperglycemia). It is primarily used for patients who have failed other lipid-lowering drugs.
Fibrates activate peroxisomal proliferator-activated receptor alpha, a transcription factor that increases lipoprotein lipase activity. Fibrates decrease triglyceride levels and raise HDL levels. However, fibrates are inferior to statins for reducing cardiovascular events and are primarily used to prevent pancreatitis in patients with very high triglyceride levels.
hydroxyurea MOA
inhibits ribonucleotide reductase and therefore inhibits cell division during S phase
Ind/for
- acute and chronic myelogenous leukemia
- primary myelofibrosis
- sickle cell dz (first line)
AE: megaloblastic anemia
what is the antidote to metoprolol toxicity (pt on metoprolol with syncopal episode)
glucagon because it activates beta receptors
The treatment of choice for pulmonary sarcoidosis is________
oral glucocorticoid therapy.
what ligands signal via JAK-STAT pathway (non rec. tyrosine kinase) (mn: JAcK the PIGGl_ET_)
Prolactin, Interleukins and IFN, GH, G-CSF, EPO, TPO
which ligands (other than the adrenergic ones) signal via the Gq –> PLC —> PKC pathway? (mn: Q magazine –> Tough, Angsty Guys take Oxy and get Gas
TRH, Ang II, GnRH, oxytocin, gastrin
T/F: desmopressin (ADH analog) and vasopressin act at the same receptor
FALSE
Unlike vasopressin (natural ADH), desmopressin has a negligible impact on the V1 receptor (Ie it’s selective for the kidney with V2 rec) and does not use the PLC pathway to exert its effect.
MOA for dihydropyridine vs non-dihydropyridines
Nondihydropyridine CCBs exert their primary action by blocking the L-type calcium channels, thereby decreasing phase 0 depolarization and conduction velocity in the sinoatrial and AV nodes.
tx for giardia
metronidazole
indications for octreotide
A synthetic drug that mimics the action of somatostatin and is used in treating acromegaly, carcinoid tumors, vasoactive intestinal peptide tumors, pancreatitis, and gastrointestinal bleeding
TMP-SMX MOA
Both of these antibiotics inhibit the folate synthesis pathway. In the folate synthesis pathway, pteridine and para-aminobenzoic acid are incorporated into folic acid. Also inhibition of dihydrofolate reductase
They block these steps
ind/for: (mn)
- Toxoplasmosis prophylaxis
- m
- Pneumocystis jirovecii pneumonia
- Shigella
- Salmonella
- m
- urinary tract(traX) infections
AE: megaloblastic anemia, agranulocytosis, leukopenia
what comprises the “triple therapy” indicated for H. Pylori
- PPIs
- Clarithromycin
- amoxicillin/metronidazole
what differentiates DILE from SLE
DILE can manifest with various features that are also seen in idiopathic SLE (e.g., fever, arthritis, malar rash, serositis) but typically does not affect the CNS or kidneys, unlike SLE.
“Assuming the drug follows first-order kinetics, approximately how long will it take for drug Y to reach steady state?”
how do you solve this
- first, you need the principle that in First-order kinetics, a drug infused at a constant rate takes 4–5 half-lives to reach steady state
- then you need to calculate the half-life (image)
- then multiply the half life value times 4
If you’re given the half life, then just multiply that times 4-5
what is the equation for Filtration fraction
FF=GFR/RPF
RPF=RBF(1-HCT)
trastuzumab, panitumumab, erlotinib, pan and imatinib are what types of targeted immunotherapy drugs and what are their indications
they all target tyrosine kinase receptor
Trastuzumab is ind/for HER2+ breast and gastric cancer
panitumumab ind/for metastatic colorectal cancer,
Imatinib is ind/for CML and kit-positive gastrointestinal stromal tumors
erlotinib is HER1/EGFR inhibitor ind/for non–small cell lung cancer and pancreatic cancer. (Not all non–small cell lung cancers respond to erlotinib. If the tumor has a K-Ras mutation or EML4-ALK translocation, another drug should be used.)
what type of targeted immunotherapy drug is bortezomib and what’s it’s indication
inhibits a proteasome that degrades IκB (IκB downreguates NF-kB entry into cell) –> inhibit degredation of inhibitor of NF-kB = more inhibition of NF-kB
ind/for multiple myeloma and mantle cell lymphoma
what type of targeted immunotherapy drug is rituximab and what’s it’s indication
acts on CD20 recs on B cells, making them more susceptible to attack by the immune system
ind/for non-hodgkins lymphoma, CLL, ITP, TTP, AIHA, RA, MS
what type of targeted immunotherapy drug is bevacizumab and what’s it’s indication
VEGF inhibitor (inhibits blood supply to cancer cells)
ind/fo non–small cell lung cancer; glioblastoma; and cancers of the colon, cervix, ovaries, and breast. It is also used to treat noncancerous disorders such as diabetic retinopathy and macular degeneration.
erlotinib AE
adverse effects include diarrhea, an acne-like rash, anorexia, and fatigue. The degree of rash often correlates with drug efficacy. Rarer, but more serious, adverse effects are interstitial lung disease and hepatic failure.
imatinib AE
Adverse effects include GI distress, edema, and hepatotoxicity.
panitumumab AE
Adverse effects include rash and dermatologic toxicity, severe infusion reactions, pulmonary fibrosis, and electrolyte abnormalities.
trastuzumab AE
Like most monoclonal antibodies, trastuzumab can lead to fever, chills, nausea, dyspnea, and rashes. The biggest concern in terms of toxicity is congestive heart failure.
What adverse effects are expected to be see (in common) during targeted therapy with crizotinib, erlotinib, panitumumab, and trastuzumab ?
What adverse effects are expected to be see during targeted crizotinib, erlotinib, panitumumab, and trastuzumab therapy?
Adverse effects of rituximab
Adverse effects of rituximab are fewer than those associated with many other chemotherapeutic agents. The most common are weakness, nausea, diarrhea, edema, and increased infections.
bevacizumab AE
Adverse effects include hypertension, fatigue, nausea, headache, arthralgia, and nosebleeds.
what kind of targeted immunotherapy is denosumab and what’s its indication
a monoclonal antibody against RANK-L, which, in turn, is an activator of NF-κB.
Loop diuretics AE
(furosemide, torsemide, bumetanide)
- sensorineural hearing loss, tinnitus, vertigo
- hypokalemia, hypocalcemia
mn: I will be FUROus if you don’t keep me in the loop
“You bet (bu-met anide)”
and “Torso before thighs”
thiazide diuretic AE
hyponatremia, hypomagnesemia, hypercalcemia
what are the ototoxic drugs
aminoglycosides, salicylates, cisplatin, loop diuretics
ACE inhibitor AE
Side effects include Cough, Angioedema, Teratogenesis (neonatal renal failure), elevated Creatinine, (decreased GFR), Hyperkalemia (from reduced aldosterone) and Hypotension
mn: Captopril’s CATCHH
*use caution in pts with bilateral renal artery stnosis
In the kidney, angiotensin II preferentially constricts the efferent arteriole, which increases glomerular filtration. Blockade of this response is accomplished by what drug classes
by ACE inhibitors (eg, ramipril) or angiotensin II receptor blockers (eg, losartan, valsartan) causes the filtration pressure to fall, leading to a reduced GFR
argatroban, bivalirudin, and dabigatran are all what type of drugs
Direct thrombin (IIa) inhibitors
hemophilia A 1st line treatment
Factor 8 replacement
Ticagrelor MOA and indication
Ticagrelor binds the adenosine diphosphate (ADP) P2Y12 receptor on platelets, blocks ADP-mediated activation of the glycoprotein IIb/IIIa receptor complex –> prevents platelet aggregation by blocking.
ind/for: acute coronary syndrome and in patients undergoing percutaneous coronary intervention.
Microangiopathic hemolytic anemia is an AE of what drugs
cancer chemotherapy drugs (eg, cisplatin, cyclophosphamide).
what is DRESS syndrome
Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is a type 4 HSR that typically occurs 2-8 weeks after exposure to high-risk drugs
mn: I spilled ALL the CARBs with that Phenny, LAMe Sulfur smell (on my dress) –> allopurinol, carbamazipine, phenytoin, lamotrigine, Sulfonamide abx (TMP-SMX)
+dapsone, minocycline, vancomycin
sx: high fever with generalized, high surface area rash + end organ damage, generalized lymphadenopathy (+eosinophilia on CBC)
what sleep aid drug can be given to elderly
Ramelteon, a melatonin agonist, has a lower side-effect burden than other sedative-hypnotic agents and is effective in reducing time to sleep onset in the elderly.
Benzodiazepines, antihistamines, and sedating antidepressants should be avoided in the treatment of insomnia in elderly patients due to their adverse effects.
which antidepressant can cause priapism
trazadone
tx for pinworms
albendazole, mebendazole, pyrantal pamoate
doxorubicin toxicity
DILATED cardiomyopathy
methotrexate AE
hepatitis, pulmonary fibrosis, bone marrow suppression
what drugs are valsartan and losartan
Ang 2 rec blockers
mn: -artan = A R Ten-uate (ang 2 rec attenuation)
(block ang II rec type 1)
effects: decrease vasoconstricion and secretion of aldosterone
AE: angioedema, hyperkalemia, decreased GFR, hypotension, teratogen
what is aliskiren
direct renin inhibitor –> decreased conversion of angiotensinogen to angiotensin I –> less vasoconstriction and decreased secretion of aldosterone
mn aLESkiREN: LESS RENin with aliskiren.
AE of ACE inhibitors
(ACE inhibitor)
mn: CAPTOPRIL:
- Cough, Angioedema,
- Pemphigus vulgaris,
- Teratogenicity,
- hypOtension,
- high Potassium,
- Renal failure,
- Increased creatinine,
- Low GFR.
what drugs are captopril and lisinopril
ACE inhibitors
what drug is indapamide
thiazide diuretic
along with chlorthalidone and hydrochlorothiazide
MOA
what drug is succinylcholine?
depolarizing neuromuscular blocking drug (The only one)
MOA: agonist at nicotinic (type m) rec agonist –> prolonged depolarization/inability to contract the muscle
Ind/for: surgery or mechanical ventilation
what drug is used before general anesthesia to decrease salivary and bronchial secretions (helps maintain airway patency) and prevent myocardial depression (minimizes risk of hypotension)
atropine, a muscarinic acetylcholine rec antagonist
In myasthenia gravis
patients are VERY sensitive to __________ and VERY insensitive to ____________
^both NMJ blockers
VERY sensitive vecuronium and
insenstitive to succinylcholine, respectively
because in MG, there’s antibodies against the AcH receptors, which causes downregulation of the number of these receptors
antidote to heparin overdose
protamine sulfate
which thyroid drug has 2 MOAs
Propylthyiouracil
- blocks peripheral conversion of T4 to T3
- inhibits thyroid peroxidase (does iodine organification and coupling of iodotyrosines)
by contrast, methimazole only does the latter.
n.b Beta blockers are also able to block T4 –> T3 conversion
MOA of choelstyramine
bile acid sequestrant
dronedarone, amiodarone, sotolol, ibutilide, dofetilide
^these belong to what drug class
class III antiarrhythmics: K+ channel blockers
*but dronedarone and amiodarone share the same MOA as all the other classes
AE of amiodarone
what drugs are Spironolactone, Triamterene, Eplerenone, and Amiloride
K-sparing diuretics
the ones ending in -one are aldosterone rec blockers (in late DCT and CD)
triamterene and amiloride are ENaC blockers
mn: To remember that Spironolactone, Triamterene, Eplerenone, and Amiloride are K+-sparing, think of STEAK!
what kind of drug is amlodipine and what are the other drugs in its class
dihydropyridine CCBs (ind/for htn b/c they act at L type Ca channels on vascular smooth muscle AND ind/for arrhythmia beause they also act at those same channels, decreasing phase 0 depolarization and conduction velocity in the sinoatrial and AV nodes.)
mn: -di-p-ine (di (hydro)- p (yrid) - ine
the others are:
Nicardipine
Nifedipine
what drug is bicalutamide
it goes with flutamide (anti-androgen)
MOA: competitive inh. at androgen receptor
ind/for coadministration with GnRH to avoid temporary overstimulation of androgen rec prior to downregulation of the receptors
mn: don’t BICker over a FLUTe
what drug is abiraterone
17α-hydroxylase/17,20-lyase inhibitor
metformin MOA and AE
inhibiting mitochondrial glycerol-3-phosphate dehydrogenase, which reduces availability of gluconeogenesis substrates (eg, glycerol, lactate)
.Metformin also upregulates AMP-activated protein kinase, which inhibits lipogenesis and subsequently lowers circulating lipid levels.
AE: B12 def (chronic administration), lactic acidosis (d/t increase lactate production as a result of inhibited gluconeogenesis), and diarrhea.
Contraindicated in pts with renal insufficiency b/c it is renally excreted
Acute Angle closure gloucoma can be precipitated by what medications
topical and systemic medications that cause pupillary dilation, such as alpha-adrenergic agonists (eg, naphazoline) and drugs with strong anticholinergic effects (eg, tricyclic antidepressants, antihistamines). Acute blockage results in a rapid rise in intraocular pressure that typically causes severe eye pain, conjunctival injection, and corneal edema (haziness). If not corrected, the elevated pressure can damage the optic nerve and cause permanent vision impairment.
what drugs are Terazosin, doxazosin, prazosin, and tamsulosin
selective alpha 1 adrenergic antagonists ind/for BPH and (last line) for HTN
amphotericin B toxicity
The most dangerous adverse effect of amphotericin B is its nephrotoxicity; this is due to both a decrease in glomerular filtration rate and direct toxic effects on the tubular epithelium. Nephrotoxicity can lead to anemia (decreased erythropoietin production) and electrolyte abnormalities. Hypokalemia and (less often) hypomagnesemia are common due to an increase in the membrane permeability of the distal tubule. Hypokalemia can cause weakness and arrhythmias. ECG findings in hypokalemia include T wave flattening, ST-segment depression, prominent U waves, and premature atrial and ventricular contractions. Profound hypokalemia can cause ventricular tachycardia or fibrillation
which lipid lowering drug can cause gallstones
fibrates
which diuretic can cause senorineural hearing loss
furosemide
indications fro Carbonic anhydrase inhibitors such as acetazolamide
- narrow angle glaucoma,
- pseudotumor cerebri /idiopathic Intracranial HTN
- metabolic alkalosis or resp alkalosis as in altitude sickness
- cystinuria (cysteine kidney stone prevention) –> alkalinzation of the filtrate/urine makes cystine more soluble
aspirin should be avoided in yound children d/t risk of Reye syndrome EXCEPT for in what condition
Kawasaki disease (medium vessel vasculitis)
to avoid coronary artery aneurysm
Reye syndrome p/w: N/V/D, hepatomegaly, AMS and lethargy
lithium AE and Toxicity
mn: L(hi)THIUM
Low (or High) Thyroid
Heart (Ebstein anomaly)
Insipidus – nephrogenic diabetes Insipidus (ADH resistance in the renal collecting ducts) snd CKD
Unwanted movements (tremor)
Thiazides, ACE inhibitors, NSAIDs, and other drugs affecting clearance are implicated in lithium toxicity.
manifestation of frank TOXICITY:
- N/V
- slurred speach
- seizures
- hyperreflexia
- ataxia
treat with hydration with isotonic sodium chloride
dextromorphan MOA and AE
NMDA glutamate rec. antagonist
abuse potential –> antidote = naloxone
AE.: serotonin syndrome if used with other serotinergic drugs
what drugs are cetirizine, loratadine, fexofenadine, and desloratadine
2nd gen antihistamine (don’t cross CNS, so less sedating)
AE of acetazolamide (carbonic anhydrase inhibitor)
proximal renal tubular acidosis (type 2RTA)
paresthesias
NH3 toxicity
hypokalemia
calcium phosphate stones
Mixed metabolic acidosis and respiratory alkalosis can be seen in __________toxicity, as the acidic metabolites trigger the brain to hyperventilate and eliminate excess acid in the form of CO2.
aspirin
N-acetyltransferase polymorphism affects metabolism of which drugs
isoniazid, sulfasalazide, hydralazine
N-acetyltransferase polymorphism refers to the fact that there’s a natural variance in the expression of N-acetyltrasferease in the liver which is responsible for metabolizing these ^ drugs
carbamazepine AE
- SJS and DRESS syndrome
- drug induced SIADH
- Aplastic anemia and agranulocytosis
- CYP induction
what drugs can cause anticholinergic toxicity
- atropine, scopolamine (motion sickness med)
- antihistamines
- TCAs
sx with mn: red as a beet, dry as a bone, hot as a haire, blind as a bad, mad as a hatter, full as a flask
antidote: physostigmine (AChE inhibitor)
acetaminophen MOA
what acid base abnormality is found in salicylate poisoning
early poisoning sx: salicylates directly stiulate respiratory center, –> hyperventilation and respiratory alkalosis
late sx: salicylates disrupt Ox Phos –> body switches to anaerobic metabolism –> lactic acidosis
other sx unrelated to acid base abnormalities: N/V, headache, tinnitus, fever, AMS
antidote: activated charcoal and sodium bicarb (alkalization of urine promotes salicylate excretion)
severe TCA overdose Tox symptoms
mn: 3 C’s for tri-Cy-Cli-Cs
- convulsions
- cardiotox (QT prolong, arythmias)
- coma or obtundedness
+hyperpyrexia (temp >106 F)
tx: charcoal and supportive care (+ECG monitoring) + sodium bicarb to prevent arrhythmias
n. b that these are the sx of severe overdose. anticholinergic sx can also occur at lower doses
beta blockers toxicity
HEART
- bradycardia
- AV block
- acute heart failure
LUNGS
- dyspnea, bronchospasm
METABOLIC
- hypoglycemia + hypoglycemia unawareness
- dislipidemia
CNS (severe)
- sedation
- seizures
neostigmine moa and indication
inhibit the degradation of acetylcholine (AChE inhibitor)
reversal agent for -curium agents (as used to induce paralysis during procedures)
Which abx are a/w ototoxicity?
The macrolides and vancomycin
macrolides: every cop is an ass face
erythro-
clarithro-
azyithro-
fidazomicin
main AE of Fluoroquinolones
diarrhea, rash, headache, dizziness
dofetilide and ibutilide are what kind of drugs
class III antiaryhthmics (K+ channel blockers)
along with dronedarone, amiodarone, and sotolol, but these 2 are selective for K channels
tx for Congenital Toxoplasmosis.
Pyrimethamine, Sulfadiazine, and Leucovorin
Organisms Typically not covered by 1st–4th generation cephalosporins are
LAME: Listeria, Atypicals (Chlamydia,Mycoplasma), MRSA, and Enterococci.
Patients with gonococcal urethritis who have coinfection with C trachomatis or uncertain C trachomatis status (as in this patient whose NAAT results are pending) require what abx regimen
a third-generation cephalosporin (eg, ceftriaxone) and a tetracycline (eg, doxycycline) to cover gonococcus and possible C trachomatis coinfection. Patients with gonococcal urethritis who have negative C trachomatis NAAT should be treated with third-generation cephalosporin (eg, ceftriaxone) alone
drug of choice for slowing the progression of or preventing diabetic nephropathy
The main therapies used to prevent diabetic nephropathy are ACE inhibitors or AT receptor blockers (ARBs). These antihypertensive drugs act by reducing AT II levels, thus reducing intraglomerular pressure by preferentially dilating the efferent arteriole.
ACE inhibitors protect the kidney in early diabetic nephropathy by reducing the high glomerular pressures (hyperfiltration) seen in early stages of disease.
milrinone MOA
By blocking PDE-3, milrinone increases the amount of cAMP available inside myocardial cells and the smooth muscle cells of the peripheral vasculature. In myocardial cells, increased cAMP leads to increased cardiac contractility. In vascular smooth muscle cells, increased cAMP leads to smooth muscle relaxation because the normal effect of cAMP is to reduce the activity of myosin light chain kinase. Therefore increased cAMP secondary to milrinone leads to decreased peripheral vascular resistance.
which steroid drug has predominately mineralcorticoid (aldosterone) effect
fludrocortisone, which is why it’s used to treat primary adrenal insufficiency
which abx is assoc with “red man” syndrome (RMS),
“red man” syndrome (RMS), a non-allergic drug reaction that occurs when vancomycin is infused too rapidly.
RMS arises due to the direct activation of mast cells by vancomycin, which results in the release of vasoactive mediators (eg, histamine).
tx for Raynaud phenomenon
CCBs
MOA of botulinum toxin
Botulinum toxin prevents vesicular fusion by cleaving a component of the soluble N-ethylmaleimide-sensitive factor attachment protein receptor complex
TCAs MOA
TCAs inhibit the reuptake of serotonin and norepinephrine (but their chief AE is d/t anticholinergic activity rather than serotonin syndrome) and block H1 receptors, α1-adrenergic receptors, and muscarinic receptors.
what drug is amoxapine
TCA
along with:
Amitriptyline, nortriptyline,
imipramine, desipramine, clomipramine,
doxepin
Diphenoxylate and loperamide are what kind of meds
both opiate-based medications designed to inhibit peristalsis in the gastrointestinal tract
Treatments for hepatic encephalopathy
include lactulose (increases conversion of ammonia to ammonium) and rifaximin (decreases intraluminal ammonia production).
tx for Wilson’s dz
ammonium tetrathiomolybdate: facilitates urinary excretion of copper
penicillamine: copper chelating agent
trientine: copper chelating agent
zinc: competes with copper for absorbtion in the gut via the same transporter
management of esophageal varices
Acute management of variceal hemorrhage requires rapid lowering of portal pressure. Somatostatin and octreotide (a long-acting somatostatin analog) inhibit the release of hormones that induce splanchnic vasodilation, indirectly causing splanchnic vasoconstriction and reduced portal blood flow.
what’s the MOA of canagliflozin and dapagliflozin
for this reason, check creatinine before rx
what drugs are hydroxyzine, promethazine, chlorpheniramine, diphenhydramine
n.b. first-generation antihistamines are lipophilic and easily cross the blood-brain barrier, where they may cause significant sedation and cognitive dysfunction. First-generation antihistamines are considered potentially inappropriate medications for elderly patients, especially those with pre-existing cognitive or functional impairment.
first-generation antihistamines
what drugs are loratadine, cetirizine
Newer-generation antihistamines
do not have the same degree of antimuscarinic, antiserotonergic, or anti-alpha adrenergic properties and their side effects are minimal. Moreover, second-generation antihistamines are less lipophilic, do not readily cross the blood-brain barrier, and are usually nonsedating.
what drugs are canagliflozin, dapagliflozin and empaglioflozin
SGLT-2 inhibitors (PCT of kidney) –> increase glucose excretion by blocking the reabsorption cotransporter –> used for diabetes
a/w UTIs and yeast infections, polyuria, weight loss, dehydration,
contraindications: CKD, Urinary tract anomalies
mn: the sugar FLOZ (flows) out
which antithyroid medication, methimazole or PTU, is preferred in the 1st trimester
Methimazole is preferred for most non pregnant patients due to the hepatotoxicity of PTU. However, methimazole has potential teratogenic effects, so PTU is preferred in the first trimester of pregnancy.
mn: P = primary/first , T=trimester, U= use
what is the EXACT MOA of apixaban
Direct factor Xa inhibitors (eg, apixaban) are often used for stroke prevention in atrial fibrillation as they are administered orally and do not require monitoring of drug levels (unlike warfarin). This class of medications blocks the active site of factor Xa, which prevents it from converting prothrombin to thrombin. Direct factor Xa inhibitors are denoted by names that end in “Xa-ban.”
NOT conversion of X to Xa!!!
what drugs are argatroban, bivalirudin, and dabigatran
direct thrombin inhibitors
What drug to use to lower BP without worsening ECG abnormalities
dihydropyridine CCBs
Nifedipine, amlodipine, felodipine (because they predominately act on blood vessels, not the heart)
dapsone MOA, AE, and indications
inhibits bacterial synthesis of dihydrofolic acid, via competition with para-aminobenzoate for the active site of dihydropteroate synthase, thereby inhibiting nucleic acid synthesis.
DRESS, hemolytic anemia, methemoglobinemia (contraindicated in G6PD deficiency)
ind/for dermatitis herpetiformis, leprosy, malaria, pneumocystitis jiroveci prophylaxis
prophylactic tx to prevent pneumocystitis pneumonia (for immunocompromised)
TMP/SMX
Atovaquone and dapsone are alternative agents used to in patients with trimethoprim-sulfamethoxazole allergy.
1st line tx for PTSD
SSRIs or SNRIs
what class of drugs are exenatide, liraglutide
GLP-1 agonists (for diabetes control) –> increases insulin release
AE: pancreatitis, weight loss
which drug class can cause transient bluish discoloration to vision
PDE-5 inhibitors (sildenafil, tadalafil, avanafil, verdenafil)
(b/c PDE5 inhibitors can also inhibit PDE6 in the retina, which is involved in color vision)
can also cause sudden monocular vision loss, affarent pupillary defect, and opticn disc edema (less common)
what drugs are used as prophylaxis against catecholamine surge following adrenalectomy
phenoxybenzamine (alpha blocker) then beta blocker (but not beta blocker first)
which drugs can cause interstitial lung disease
amiodarone, methotrexate, bleomycin
which drugs can cause SIADH
most common drugs include
carbamazepine,
oxcarbazepine,
chlorpropamide,
cyclophosphamide,
selective serotonin reuptake inhibitors (SSRI)
