Rapid Review: Lab/Diagnostic Findings and Clinical Presentations; and MISC! Flashcards
Question: Lab/Diagnostic Finding or Clinical Presentation Answer: Diagnosis/Disease associated with finding/presentation
Anticentromere antibodies
Scleroderma (have excessive fibrosis and collagen deposition throughout the body; 2 types. the type associated with anti-centromere antibodies is the Crest type: CREST syndrome = Calcinosis, Raynaud’s phenomenon, Esophageal dysmotility, Sclerodactyly, Telangiectasia)
Antidesmoglein (epithelial) antibodies
Pemphigus vulgaris (blistering)
List the 4 most important pharmacokinetics equations: (Vd, Cl, LD, MD)
1) Vd = (amount of drug given)/([drug] in plasma)2) Cl = (Vd X 0.7)/t1/23) LD = Css X Vd4) MD = Css X Cl
List the 4 most important pharmacokinetics equations: (Vd, Cl, LD, MD)
1) Vd = (amount of drug given)/([drug] in plasma)2) Cl = (Vd X 0.7)/t1/23) LD = Css X Vd4) MD = Css X Cl
Anti-glomerular basement membrane antibodies
Goodpasture’s syndrome (glomerulonephritis and hemoptysis)
competitive vs noncompetitive inhibitors:1) Resemble substrate?2) Overcome by increased [S]?3) Bind active site?4) Effect on Vmax?5) Effect on Km?6) Pharmacodynamics: effect on potency? efficacy?
Competitive inhibitors:1) Yes2) Yes3) Yes4) Vmax does not change5) Km increases6) decreased potency (increased Km, decreased potency); no effect on efficacyNoncompetitive inhibitors:1) No2) No3) No4) Vmax decreases5) Km does not change6) decreased efficacy (decreased Vmax, decreased efficacy); no effect on potentcy
competitive vs noncompetitive inhibitors:1) Resemble substrate?2) Overcome by increased [S]?3) Bind active site?4) Effect on Vmax?5) Effect on Km?6) Pharmacodynamics: effect on potency? efficacy?
Competitive inhibitors:1) Yes2) Yes3) Yes4) Vmax does not change5) Km increases6) decreased potency (increased Km, decreased potency); no effect on efficacyNoncompetitive inhibitors:1) No2) No3) No4) Vmax decreases5) Km does not change6) decreased efficacy (decreased Vmax, decreased efficacy); no effect on potentcy
antihistone antibodies
drug-induced SLE. drugs:
1) hydralazine - treats severe HTN (1st line for HTN in pregnancy, with methyldopa), CHF
2) isoniazid (INH) - treatment and prophylaxis for Mycobacterium tuberculosis
3) phenytoin - anti-epileptic
4) procainamide - anti-arrhythmic
Zero-order elimination
rate of elimination of drug is constant, regardless of the plasma concentration; Cp decreases linearly with time.Examples = PEA: Phenytoin, Ethanol, Aspirin
Zero-order elimination
rate of elimination of drug is constant, regardless of the plasma concentration; Cp decreases linearly with time.Examples = PEA: Phenytoin, Ethanol, Aspirin
Anti-IgG antibodies
Rheumatoid arthritis (systemic inflammation, joint pannus, boutonniere deformity)
First-order elimination
Rate of elimination is proportional to drug concentration (a constant fraction of the drug is eliminated per unit time); the plasma concentration decreases exponentially with time.
First-order elimination
Rate of elimination is proportional to drug concentration (a constant fraction of the drug is eliminated per unit time); the plasma concentration decreases exponentially with time.
antimitochondrial antibodies (AMAs)
Primary biliary cirrhosis (female>male; autoimmune disease of liver - get slow progressive destruction of bile canaliculi, so bile builds up in liver = cholestasis, and damages tissue over time, leading to scarring, fibrosis, cirrhosis; portal hypertension)
Phase I vs Phase 2 metabolism:Which phase do geriatric patients lose first?
Phase I: -reduction, oxydation, hydrolysis-usually yields slightly polar, water-soluble metabolites (often still active)-cytochrome P-450Phase II:-GAS: Glucuronidation, Acetylation, Sulfation-usually yields very polar, inactive metabolites (renally excreted)*Geriatric patients lose phase 1 first
Phase I vs Phase 2 metabolism:Which phase do geriatric patients lose first?
Phase I: -reduction, oxydation, hydrolysis-usually yields slightly polar, water-soluble metabolites (often still active)-cytochrome P-450Phase II:-GAS: Glucuronidation, Acetylation, Sulfation-usually yields very polar, inactive metabolites (renally excreted)*Geriatric patients lose phase 1 first
antineutrophil cytoplasmic antibodies (ANCAs)
vasculitis
1) c-ANCA: Wegener’s granulomatosis (a rapidly progressive (crescentic) glomerulonephritis (RPGN))
2) p-ANCA: microscopic polyangiitis (pauci-immune glomerulonerphritis, RPGN), and Churg-Strauss syndrome (pauci-immune, asthma, sinusitis, palpable purpura, peripheral neuropathy))
* “pauci-immune” = form of vasculitis associated with minimal evidence of hypersensitivity upon immunofluorescence.
Efficacy vs Potency
Efficacy: -proportional to Vmax (increase Vmax, increase efficacy)-maximal effect a drug can produce-high efficacy drugs: analgesics, antibiotics, antihistamines, decongestantsPotency:-inversely proportional to Km (increase Km, decrease potency)-amount of drug needed for a given effect-increased potency, increased affinity for receptor-highly potent drugs: chemo drugs, anti-hypertensive drugs, antilipid drugs
Efficacy vs Potency
Efficacy: -proportional to Vmax (increase Vmax, increase efficacy)-maximal effect a drug can produce-high efficacy drugs: analgesics, antibiotics, antihistamines, decongestantsPotency:-inversely proportional to Km (increase Km, decrease potency)-amount of drug needed for a given effect-increased potency, increased affinity for receptor-highly potent drugs: chemo drugs, anti-hypertensive drugs, antilipid drugs
antinuclear antibodies (ANAs: anti-Smith and anti-dsDNA)
SLE (type III hypersensitivity)
Pharmacodynamics: Effects of adding competitive antagonists, noncompetitive antagonists, and partial agonists to an agonist on pharmacodynamic curves:
1) Competitive antagonist + agonist –> shift curve to the right = decreased potency (increased Km); no change on efficacy2) Noncompetitive antagonist plus agonist: shift curve down = decreased efficacy (decreased Vmax); no effect on potency3) Partial agonist: acts at the same site as a full agonist, but with reduced maximal effect. Get decreased efficacy (decreased Vmax); potency is variable, can be either increased or decreased.
Pharmacodynamics: Effects of adding competitive antagonists, noncompetitive antagonists, and partial agonists to an agonist on pharmacodynamic curves:
1) Competitive antagonist + agonist –> shift curve to the right = decreased potency (increased Km); no change on efficacy2) Noncompetitive antagonist plus agonist: shift curve down = decreased efficacy (decreased Vmax); no effect on potency3) Partial agonist: acts at the same site as a full agonist, but with reduced maximal effect. Get decreased efficacy (decreased Vmax); potency is variable, can be either increased or decreased.
antiplatelet antibodies
ITP (idiopathic thrombocytopenic purpura)
Therapeutic Index: What is it? What’s the equation? Is it safer to have a higher or lower TI?*Examples of drugs with low TI?
TI = measurement of drug safetyTI = LD50/ED50 = median lethal dose/median effective dose(“TILE”)Safer drugs have higher TI valuesExamples of drugs with low TI (must monitor these patients!):-Phenobarbital-Lithium-Digoxin-Coumadin/Warfarin
Therapeutic Index: What is it? What’s the equation? Is it safer to have a higher or lower TI?*Examples of drugs with low TI?
TI = measurement of drug safetyTI = LD50/ED50 = median lethal dose/median effective dose(“TILE”)Safer drugs have higher TI valuesExamples of drugs with low TI (must monitor these patients!):-Phenobarbital-Lithium-Digoxin-Coumadin/Warfarin
anti-topoisomerase antibodies
diffuse systemic scleroderma
Nicotinic vs Muscarinic ACh receptors
Nicotininc ACh receptors = Na+/K+ channelsMuscarinic ACh receptors = G-protein-coupled receptors, act through 2nd messengers; 5 subtypes = M1, M2, M3, M4, M5
Nicotinic vs Muscarinic ACh receptors
Nicotininc ACh receptors = Na+/K+ channelsMuscarinic ACh receptors = G-protein-coupled receptors, act through 2nd messengers; 5 subtypes = M1, M2, M3, M4, M5
anti-transglutamase/anti-gliadin/anti-endomysial antibodies
Celiac disease (diarrhea, distention, weight loss)
Gq:-what receptors stimulate it?-what are its effects?
-Stimulated by alpha 1, M1, M3, H1, V1-stimulates phospholipase C, which stimulates lipid conversion to PIP2, which stimulates increased diacylglycerol and increased inositol triphosphate. –> increased DAG leads to increased protein kinase C–> increased
Gq:-what receptors stimulate it?-what are its effects?
-Stimulated by alpha 1, M1, M3, H1, V1-stimulates phospholipase C, which stimulates lipid conversion to PIP2, which stimulates increased diacylglycerol and increased inositol triphosphate. –> increased DAG leads to increased protein kinase C–> increased
“Apple core” lesion on abdominal x-ray
colorectal cancer (usually left-sided)
Gs:-what receptors stimulate it?-what are its effects?
-stimulated by: B1, B2, D1, H2, V2-stimulates adenylyl cyclases –> increases cAMP –> increases protein kinase A –> increased intracellular Calcium *lots of bacterial toxins use this mechanism!
Gs:-what receptors stimulate it?-what are its effects?
-stimulated by: B1, B2, D1, H2, V2-stimulates adenylyl cyclases –> increases cAMP –> increases protein kinase A –> increased intracellular Calcium *lots of bacterial toxins use this mechanism!
Azurophilic granular needles in leukemic blasts
Auer rods (acute myelogenous leukemia, especially the promyelocytic (M3) type)
Gi:-what receptors stimulate it?-what are its effects?
-stimulated by: alpha 2, M2, D2-inhibits adenylyl cyclase (so decreased cAMP and decreased protein kinase A)…
Gi:-what receptors stimulate it?-what are its effects?
-stimulated by: alpha 2, M2, D2-inhibits adenylyl cyclase (so decreased cAMP and decreased protein kinase A)…
Bacitracin response (what organis are sensitive? resistant?)
Sensitive: Streptococcus pyogenes (group A)
Resistant: Streptococcus agalactiae (group B)
alpha 1 receptor:-which G-protein class?-Major functions?
GqFunctions:-increase vascular smooth muscle contraction (increase BP)-mydriasis-increase intestinal and bladder sphincter muscle contraction
alpha 1 receptor:-which G-protein class?-Major functions?
GqFunctions:-increase vascular smooth muscle contraction (increase BP)-mydriasis-increase intestinal and bladder sphincter muscle contraction
“bamboo spine” on X-ray
Ankylosing spondylitis (chronic inflammatory arthritis: HLA-B27)
alpha 2 receptor:-G-protein class?-major functions?
GiMajor functions:-decrease sympathetic outflow (decrease NE secretion)-decrease insulin release-decrease BP (vasodilation)-increase glucagon secretion from alpha cells in pancreas
alpha 2 receptor:-G-protein class?-major functions?
GiMajor functions:-decrease sympathetic outflow (decrease NE secretion)-decrease insulin release-decrease BP (vasodilation)-increase glucagon secretion from alpha cells in pancreas
Basophilic nuclear remnanats in RBCs
Howell-Jolly bodies (due to splenectomy or nonfunctional spleen)
Beta 1 receptor:-G-protein class?-Major functions?
GsFunctions:-increase HR-increase contractility-increase renin release-increase lipolysis
Beta 1 receptor:-G-protein class?-Major functions?
GsFunctions:-increase HR-increase contractility-increase renin release-increase lipolysis
basophilic stippling of RBCs
lead poisoning or sideroblastic anemia
Beta 2 receptor:-G-protein class?-Major functions?
GsFunctions:-vasodilation-bronchodilation-increase HR (compensatory to increase BP)-increase contractility-increase lipolysis-increase insulin release-decrease uterine tone
Beta 2 receptor:-G-protein class?-Major functions?
GsFunctions:-vasodilation-bronchodilation-increase HR (compensatory to increase BP)-increase contractility-increase lipolysis-increase insulin release-decrease uterine tone
bloody tap on LP
subarachnoid hemorrhage
M1 receptor:-G protein?-Functions?
GqFunctions:-CNS, enteric nervous system
M1 receptor:-G protein?-Functions?
GqFunctions:-CNS, enteric nervous system
“boot-shaped” heart on x-ray
tetralogy of fallot, RVH
M2 receptor:-G-protein?-Functions?
GiFunctions:-decreased HR and contractility of atria
M2 receptor:-G-protein?-Functions?
GiFunctions:-decreased HR and contractility of atria
branching gram + rods with sulfar granules
actinomyces israelii
M3 receptor: -G-protein?-Functions?
GqFunctions:-increase exocrine gland secretions (ie sweat, gastric acid)-increase gut peristalsis-increase bladder contraction-bronchoconstriction-increase miosis-accommodation (ciliary muscle contraction)
M3 receptor: -G-protein?-Functions?
GqFunctions:-increase exocrine gland secretions (ie sweat, gastric acid)-increase gut peristalsis-increase bladder contraction-bronchoconstriction-increase miosis-accommodation (ciliary muscle contraction)
bronchogenic apical lung tumor
pancoast tumor (carcinoma that occurs in apex of lung and may affect cervical sympathetic plexus / compress sympathetic ganglion and cause Horner’s syndrome- ptosis + miosis + anhidrosis)
D1 receptor:-G-protein?-Functions?
GsFunctions:-relaxes renal vascular smooth muscle
D1 receptor:-G-protein?-Functions?
GsFunctions:-relaxes renal vascular smooth muscle
“brown” tumor of bone
Hemorrhage (hemosiderin) causes brown color of osteolytic cysts. Due to:
1) hyperparathyroidism
2) osteitis fibrosa cystica
D2 receptor:-G protein?-Functions?
GiFunctions:-modulates transmitter release, especially in brain
D2 receptor:-G protein?-Functions?
GiFunctions:-modulates transmitter release, especially in brain
cardiomegaly with apical atrophy
Chaga’s disease (trypanosoma cruzi)
H1 receptor:-G protein?-Functions?
GqFunctions:-increase nasal and bronchial mucus production-bronchiole contraction-pruritus-pain
H1 receptor:-G protein?-Functions?
GqFunctions:-increase nasal and bronchial mucus production-bronchiole contraction-pruritus-pain
cellular crescents in Bowman’s capsule
rapidly progressive crescentic glomerulonephritis
H2 receptor:-G protein?-Functions?
GsFunctions:-increase gastric acid secretion
H2 receptor:-G protein?-Functions?
GsFunctions:-increase gastric acid secretion
“chocolate cyst” of ovary
Endometriosis (frequently involves both ovaries)
V1 receptor:-G protein?-Functions?
GqFunctions:-increase vascular SM contraction
V1 receptor:-G protein?-Functions?
GqFunctions:-increase vascular SM contraction
circular grouping of dark tumor cells surrounding pale neurofibrils
Homer Wright rosettes (neuroblastoma, medulloblastoma, retinoblastoma)
V2 receptor:-G protein?-Functions?
GsFunctions:-increase H20 permeability and reabsorption in the collecting tubules of the kidney(“V2 is found in the 2 kidneys”)
V2 receptor:-G protein?-Functions?
GsFunctions:-increase H20 permeability and reabsorption in the collecting tubules of the kidney(“V2 is found in the 2 kidneys”)
collonies of mucoid Pseudomonas in lungs
cystic fibrosis (AR mutation to CFTR resulting in fat-soluble vitamin deficiency and mucous plugs)
What class of drugs are these:Bethanochol, Carbachol, Pilocarpine, Methacholine?
Cholinomimetic agents: Direct agonists
What class of drugs are these:Bethanochol, Carbachol, Pilocarpine, Methacholine?
Cholinomimetic agents: Direct agonists
decreased alpha-fetoprotein in amniotic fluid/maternal serum
down syndrome or other chromosomal abnormality
What class of drugs are these:Neostigmine, Pyridostigmine, Edrophonium, Physostigmine, Echothiophate, Donepezil
Cholinomimetic agents: Indirect agonists = anti-cholinesterases
What class of drugs are these:Neostigmine, Pyridostigmine, Edrophonium, Physostigmine, Echothiophate, Donepezil
Cholinomimetic agents: Indirect agonists = anti-cholinesterases
degeneration of dorsal column nerves
tabes dorsalis (tertiary syphilis)
What class of drugs are these:Atropine, homatropine, tropicamide, benztropine, scopolamine, ipratropium, oxybutynin, glycopyrrolate, methscopolamine, pirenzepine, propantheline
muscarinic antagonists = cholinergic antagonists
What class of drugs are these:Atropine, homatropine, tropicamide, benztropine, scopolamine, ipratropium, oxybutynin, glycopyrrolate, methscopolamine, pirenzepine, propantheline
muscarinic antagonists = cholinergic antagonists
depigmentation of neurons in substantia nigra
parkinson’s disease (basal ganglia disorder: rigid, resting tremor, bradykinesia)
List the direct agonists/cholinomimetic agents (X4):
NAME?
List the direct agonists/cholinomimetic agents (X4):
NAME?
desquamated epithelium casts in sputum
Curschmann’s spirals (bronchial asthma; can result in whorled mucous plugs)
List the indirect agonists/cholinomimetic agents = anticholinesterases (X6)
NAME?
List the indirect agonists/cholinomimetic agents = anticholinesterases (X6)
NAME?
dissarayed granulosa cells in eosinophilic fluid
call-exner bodies (granulosa-theca cell tumor of ovary)
List the muscarinic antagonists;
NAME?
List the muscarinic antagonists;
NAME?
dysplastic squamous cervical cells with nuclear enlargement and hyperchromasia
koilocytes (HPV: predisposes to cervical cancer)
Cholinesterase inhibitor poisoning symptoms (ie excess parasympathetic activity): Antidote to anti-AchE poisoning?
NAME?
Cholinesterase inhibitor poisoning symptoms (ie excess parasympathetic activity): Antidote to anti-AchE poisoning?
NAME?
enlarged cells with intranuclear inclusion bodies
“owl’s eye” appearance of CMV
What’s parathion?
Parathion = insecticide = organophosphate; causes cholinesterase-inhibitor poisoning (DUMBBELSS)
What’s parathion?
Parathion = insecticide = organophosphate; causes cholinesterase-inhibitor poisoning (DUMBBELSS)
enlarged thyroid cells with ground glass nuclei
“orphan annie” eye nuclei (papillary carcinoma of the thyroid)
When do you give atropine + pralidoxime?
Give as an antidote to organophosphate poisoning/ Cholinesterase-inhibitor poisoning
When do you give atropine + pralidoxime?
Give as an antidote to organophosphate poisoning/ Cholinesterase-inhibitor poisoning
eosinophilic cytoplasmic inclusion in liver cell
Mallory bodies (alcoholic liver disease)
Atropine:-class of drug?-clinical uses?-effects on eyes, airway, stomach, gi, bladder?-toxicity?
atropine = muscarinic antagonistused to treat bradycardia and for ophthalmic applicationseffects: blocks DUMBBELSS!-Eye–> increases mydriasis, cycloplegia-Airway–>decreases secretions-stomach –> decreases acid secretions-GI –> decreases motility-bladder –> decreases urgency in cystitis*Toxicity: Hot as a hare, Dry as a bone, Red as a beet, Blind as a bat, Mad as a hatter, Bloated as a toad:-increased body temp, decreased sweating-rapid pulse-dry mouth; dry/flushed skin-cycloplegia (blurry, near vision)-constipation (and urinary retention in men with prostatic hyperplasia)-disorientation-acute angle-closure glaucoma in elderly-hyperthermia in infants
Atropine:-class of drug?-clinical uses?-effects on eyes, airway, stomach, gi, bladder?-toxicity?
atropine = muscarinic antagonistused to treat bradycardia and for ophthalmic applicationseffects: blocks DUMBBELSS!-Eye–> increases mydriasis, cycloplegia-Airway–>decreases secretions-stomach –> decreases acid secretions-GI –> decreases motility-bladder –> decreases urgency in cystitis*Toxicity: Hot as a hare, Dry as a bone, Red as a beet, Blind as a bat, Mad as a hatter, Bloated as a toad:-increased body temp, decreased sweating-rapid pulse-dry mouth; dry/flushed skin-cycloplegia (blurry, near vision)-constipation (and urinary retention in men with prostatic hyperplasia)-disorientation-acute angle-closure glaucoma in elderly-hyperthermia in infants
eosinophilic cytoplasmic inclusion in nerve cell
Lewy body (parkinson’s disease)
What sympathomimetic should be used to treat:-anaphylactic shock?-cardiogenic shock?-septic shock?
NAME?
What sympathomimetic should be used to treat:-anaphylactic shock?-cardiogenic shock?-septic shock?
NAME?
eosinophilic globule in liver
Councilman body (toxic or viral hepatitis, often yellow fever)
Epinephrine:-type of drug-what receptors does it act on?-clinical applications
-direct sympathomimetic-acts on alpha 1, alpha 2, beta 1, beta 2-use for anaphylaxis, open angle glaucoma, asthma, hypotension (anaphylactic shock)
Epinephrine:-type of drug-what receptors does it act on?-clinical applications
-direct sympathomimetic-acts on alpha 1, alpha 2, beta 1, beta 2-use for anaphylaxis, open angle glaucoma, asthma, hypotension (anaphylactic shock)
eosinophilic inclusion bodies in cytoplasm of hippocampal nerve cells
Rabies virus (Lyssavirus)
norepinephrine:-type of drug-what receptors does it act on?-applications
-direct sympathomimetic-acts on alpha 1, alpha 2, beta 1-use for hypotension (septic shock)
norepinephrine:-type of drug-what receptors does it act on?-applications
-direct sympathomimetic-acts on alpha 1, alpha 2, beta 1-use for hypotension (septic shock)
extracellular amyloid deposition in gray matter of brain
senile plaques (Alzheimer’s disease)
isoproterenol:-type of drug-what receptors does it act on?-applications
-direct sympathomimetic-acts equally on beta 1 and beta 2 receptors-used for AV block
isoproterenol:-type of drug-what receptors does it act on?-applications
-direct sympathomimetic-acts equally on beta 1 and beta 2 receptors-used for AV block
Giant B cells with bilobed nuclei with prominent inclusions (“owl’s eye”)
Reed-Sternberg cells (Hodgkin’s lymphoma)
dopamine:-type of drug-what receptors does it act on?-applications
-direct sympathomimetic-acts on all receptors, but its effects vary by dose:low dose –> acts on D1medium dose –> acts on B1 > B2*high dose –> acts on alpha 1 and alpha 2-used for shock (increases renal perfusion), heart failure
dopamine:-type of drug-what receptors does it act on?-applications
-direct sympathomimetic-acts on all receptors, but its effects vary by dose:low dose –> acts on D1medium dose –> acts on B1 > B2*high dose –> acts on alpha 1 and alpha 2-used for shock (increases renal perfusion), heart failure
Glomerulus-like structure surrounding vessel in germ cells
Schiller-Duval bodies (yolk sac tumor)
dobutamine:-type of drug-what receptors does it act on?-applications
-direct sympathomimetic-acts on Beta 1 mostly (also, slightly on alpha 1, alpha 2, beta 2)-used for heart failure, cardiac stress testing, cardiogenic shock
dobutamine:-type of drug-what receptors does it act on?-applications
-direct sympathomimetic-acts on Beta 1 mostly (also, slightly on alpha 1, alpha 2, beta 2)-used for heart failure, cardiac stress testing, cardiogenic shock
“hair-on-end” (crew-cut) appearance on x-ray
Beta-thalassemia, sickle cell anemia (marrow expansion)
phenylephrine:-type of drug-what receptors does it act on?-applications
-direct sympathomimetic-acts on alpha 1 mostly (and a little on alpha 2)-used for pupillary dilation, vasoconstriction, nasal decongestion; good for stopping epistaxis
phenylephrine:-type of drug-what receptors does it act on?-applications
-direct sympathomimetic-acts on alpha 1 mostly (and a little on alpha 2)-used for pupillary dilation, vasoconstriction, nasal decongestion; good for stopping epistaxis
hCG elevated
choriocarcinoma, hydatidiform mole (occurs with and without embryo)
Metaproterenol, Albuterol, Salmeterol, Terbutaline:-types of drugs?-what receptors do they act on?-Applications
-direct sympathomimetics-B2-agonists (also act very slightly on B1)-Metaproterenol and Albuterol –> used for acute asthma-Salmeterol –> for long-term treatment of asthma-Terbutaline –> to reduce premature uterine contractions
Metaproterenol, Albuterol, Salmeterol, Terbutaline:-types of drugs?-what receptors do they act on?-Applications
-direct sympathomimetics-B2-agonists (also act very slightly on B1)-Metaproterenol and Albuterol –> used for acute asthma-Salmeterol –> for long-term treatment of asthma-Terbutaline –> to reduce premature uterine contractions
Heart nodules (granulomatous)
Aschoff bodies (rheumatic fever)
Ritodrine:-type of drug-what receptors does it act on?-applications
-direct sympathomimetic-acts on B2 receptors ONLY!-used to reduce premature uterine contractions
Ritodrine:-type of drug-what receptors does it act on?-applications
-direct sympathomimetic-acts on B2 receptors ONLY!-used to reduce premature uterine contractions
Heterophile antibodies
Infectious mononucleosis (EBV)
List 3 indirect sympathomimetics:-What are their actions?-What are their clinical applications?
1) Amphetamines:-indirect general sympathetic agonist; release stored catecholamines-used for narcolepsy, obesity, ADD2) Ephedrine:-indirect general sympathetic agonist-release stored catecholamines-used for nasal decongestion, urinary incontinence, hypotension3) cocaine:-indirect general sympathetic agonist; uptake inhibitor-causes vasoconstriction and local anesthesia
List 3 indirect sympathomimetics:-What are their actions?-What are their clinical applications?
1) Amphetamines:-indirect general sympathetic agonist; release stored catecholamines-used for narcolepsy, obesity, ADD2) Ephedrine:-indirect general sympathetic agonist-release stored catecholamines-used for nasal decongestion, urinary incontinence, hypotension3) cocaine:-indirect general sympathetic agonist; uptake inhibitor-causes vasoconstriction and local anesthesia
Hexagonal, double-pointed, needle-like crystals in bronchial secretions
Bronchial asthma (Charcot-Leyden crystals: eosinophilic granules)
clonidine and alpha-meythldopa:-type of drugs?-act on what type of receptor?-applications?
NAME?
clonidine and alpha-meythldopa:-type of drugs?-act on what type of receptor?-applications?
NAME?
High level of D-dimers
DVT, pulmonary embolism, DIC
-azole =
anti-fungal (ie ketoconazole)
-azole =
anti-fungal (ie ketoconazole)
Hilar lymphadenopathy, peripheral granulomatous lesion in middle or lower lung lobes (can calcify)
Ghon complex (Primary TB: Mycobacterium bacilli)
-cillin =
penicillin (ie methicillin)
-cillin =
penicillin (ie methicillin)
“Honeycomb lung” on x-ray
Interstitial fibrosis
-cycline =
antibiotic, protein synthesis inhibitor (ie tetracycline)
-cycline =
antibiotic, protein synthesis inhibitor (ie tetracycline)
Hypersegmented neutrophils
Megaloblastic anemia (B12-deficiency: neurologic symptoms; folate deficiency: no neurologic symptoms)
-navir =
protease inhibitor (HIV trtmt) (ie saquinavir)
-navir =
protease inhibitor (HIV trtmt) (ie saquinavir)
hypochromic, microcytic anemia
iron-deficiency anemia, lead poisoning, thalassemia (HbF sometimes present)
-triptan =
5-HT1B/1D-agonists (for migraines) (ie sumatriptan)
-triptan =
5-HT1B/1D-agonists (for migraines) (ie sumatriptan)
increased alpha-fetoprotein in amniotic fluid/maternal serum
dating error, anencephaly, spina bifida (neural tube defects)
-ane=
inhalational general anesthetic (ie halothane)
-ane=
inhalational general anesthetic (ie halothane)
increased uric acid levels
Gout, Lesch-Nyhan syndrome, tumor lysis syndrome, loop and thiazide diuretics
-caine=
NAME?
-caine=
NAME?
intranuclear eosinophilic droplet-like bodies
cowdry type A bodies (HSV or CMV)
-operidol=
butyrophenone (neuroleptic) (ie haloperidol)
-operidol=
butyrophenone (neuroleptic) (ie haloperidol)
iron-containing nodules in alveolar septum
ferruginous bodies (asbestos: increases chance of mesothelioma)
-azine =
phenothiazine (neuroleptic, antiemetic) (ie chlorpromazine)
-azine =
phenothiazine (neuroleptic, antiemetic) (ie chlorpromazine)
large lysosomal vesicles in phagocyte, immunodeficiency
Chediak-Higashi disease (congenital failure of phagolysosome formation)
-barbital =
barbiturate (ie phenobarbital)
-barbital =
barbiturate (ie phenobarbital)
“lead pipe” appearance of colon on x-ray
ulcerative colitis (loss of haustra)
-zolam =
benzodiazepine (ie alprazolam)
-zolam =
benzodiazepine (ie alprazolam)
linear appearance of glomeruli on immunofluorescence
Goodpasture’s syndrome
-azepam =
benzodiazepine (ie diazepam)
-azepam =
benzodiazepine (ie diazepam)
Low serum ceruloplasmin
Wilson’s disease (hepatolenticular degeneration)
-etine =
SSRI (ie fluoxetine)
-etine =
SSRI (ie fluoxetine)
“lumpy-bumpy” appearance of glomeruli on immunofluorescence
post-streptococcal glomerulonephritis (immune complex deposition of IgG and C3b)
-ipramine =
TCA (ie imipramine)
-ipramine =
TCA (ie imipramine)
lytic (“hole-punched”) bone lesions on x-ray
multiple myeloma
-triptyline =
TCA (ie amitriptyline)
-triptyline =
TCA (ie amitriptyline)
mammary gland (“blue-domed”) cyst
fibrocystic change of the breast
-olol =
beta-antagonist (ie propranolol)
-olol =
beta-antagonist (ie propranolol)
monoclomal antibody spike
1) Multiple myeloma (called the M protein; usually IgG or IgA)
2) Monoclonal gammopathy of undetermined significance (MGUS; normal consequence of aging)
3) Waldenstrom’s (M protein=IgM) macroglobulinemia
4) Primary amyloidosis
-terol =
beta2-agonist (ie albuterol)
-terol =
beta2-agonist (ie albuterol)
monoclonal globulin protein in blood/urine
Bence Jones proteins (multiple myeloma [kappa of lambda Ig light chains in urine]), Waldenstrom’s macroglobulinemia (IgM)
-zosin =
alpha 1-antagonist (ie prazosin)
-zosin =
alpha 1-antagonist (ie prazosin)
mucin-filled cell with peripheral nucleus
Signet ring (gastric carcinoma)
-oxin =
cardiac glycoside (inotropic agent) (ie digoxin)
-oxin =
cardiac glycoside (inotropic agent) (ie digoxin)
narrowing of bowel lumen on barium radiograph
“string sign” (Crohn’s disease)
-pril =
ACE-inhibitor (ie captopril)
-pril =
ACE-inhibitor (ie captopril)
needle-shaped, negatively birefringent crystals
Gout (monosodium urate crystals)
-afil =
erectile dysfunction (ie sildenafil)
-afil =
erectile dysfunction (ie sildenafil)
Nodular hyaline deposits in glomeruli
Kimmelstiel-Wilson nodules (diabetic nephropathy)
-tropin =
pituitary hormone (ie somatotropin)
-tropin =
pituitary hormone (ie somatotropin)
Novobiocin response
on the office’s staph retreat, there was NO StRES:
Sensitive: Staphylococcus epidermidis
Resistant: Staphylococcus saprophyticus
-tidine =
H2-antagonist (ie cimetidine)
-tidine =
H2-antagonist (ie cimetidine)
“nutmeg” appearance of liver
chronic passive congestion of liver due to right heart failure
-dronate =
bisphosphonate (for osteoporosis) (ie alendronate)
-dronate =
bisphosphonate (for osteoporosis) (ie alendronate)
“onion-skin” periosteal reaction
“going out for EWINGS and ONION RINGS!”
Ewing’s sarcoma (malignant round-cell tumor)
-sartan =
Ang II-receptor-antagonist (ie losartan, valsartan)
-sartan =
Ang II-receptor-antagonist (ie losartan, valsartan)
Optochin response
OVRPS (overpass):
Sensitive: Strep pneumoniae
Resistant: Viridans streptococcus
-chol =
cholinergic/muscarinic agonist (ie bethanechol, carbachol)
-chol =
cholinergic/muscarinic agonist (ie bethanechol, carbachol)
Periosteum raised from bone, creating triangular area
Codman’s triangel on x-ray (osteosarcoma, Ewing’s sarcoma, pyogenic osteomyelitis)
-curium or -curonium =
paralytic drugs (non-depolarizing NM-blocking drugs; reversed with neostigmine) (ie atracurium, vecuronium)
-curium or -curonium =
paralytic drugs (non-depolarizing NM-blocking drugs; reversed with neostigmine) (ie atracurium, vecuronium)
Podocyte fusion on EM
minimal change disease (child with nephrotic syndrome)
-stigmine =
anti-cholinesterase (ie neostigmine, physostigmine, pyridostigmine)
-stigmine =
anti-cholinesterase (ie neostigmine, physostigmine, pyridostigmine)
polished, “ivory-like” appearance of bone at cartilage erosion
eburnation (osteoarthritis resulting in bony sclerosis)
-mustine =
nitrosureas (cross BBB, used to treat brain cancers)
-mustine =
nitrosureas (cross BBB, used to treat brain cancers)
Protein aggregates in neurons from hyperphosphoylation of protein tau
neurofibillary tangles (Alzheimer’s disease and CJD)
-statins =
HMG-coA reductase inhibitors (ie atorvastatin)
-statins =
HMG-coA reductase inhibitors (ie atorvastatin)
Pseudopalisading tumor cells on brain biopsy
Glioblastoma multiforme
-glitazones =
increase target cell response to insulin (ie rosiglitazone, pioglitazone)
-glitazones =
increase target cell response to insulin (ie rosiglitazone, pioglitazone)
RBC casts in urine
Acute glomerulonephritis
-bendazoles=
anti-parasitic (esp anti-helminthic)
-bendazoles=
anti-parasitic (esp anti-helminthic)
Rectangular, crystal-like, cytoplasmic inclusions in Leydig cells
Reinke crystals (Leydig cell tumor)
-dipine =
Ca-channel blockers (specifically dihyropyridine CCB’s) (ie nifedipine, amlodipine)
-dipine =
Ca-channel blockers (specifically dihyropyridine CCB’s) (ie nifedipine, amlodipine)
Renal epithelial casts in urine
Acute toxic/viral nephrosis
-prost =
prostaglandin analogues (treat glaucoma) (ie unoprostone)
-prost =
prostaglandin analogues (treat glaucoma) (ie unoprostone)
Rhomboid crystals, positively birefringent
pseudogout (calcium pyrophosphate dihydrate)
-mab =
monoclonal antibody (ie infliximab, daclizumab)
-mab =
monoclonal antibody (ie infliximab, daclizumab)
Rib notching
Coarctation of the aorta
alpha 1 blockage leads to?alpha 2 blockage leads to?
alpha1-blockage –> vasodilationalpha2-blockage –> vasoconstriction
alpha 1 blockage leads to?alpha 2 blockage leads to?
alpha1-blockage –> vasodilationalpha2-blockage –> vasoconstriction
Ring-enhancing brain lesions in AIDS
toxoplasma gondii
phenoxybenzamine:-type of drug?-application?-toxicity?
-nonselective alpha-blocker (irreversible/non-competitive)-used for pheochromocytoma (use phenoxybenzamine before removing tumor)-toxicity: orthostatic hypotension, reflex tachycardia
phenoxybenzamine:-type of drug?-application?-toxicity?
-nonselective alpha-blocker (irreversible/non-competitive)-used for pheochromocytoma (use phenoxybenzamine before removing tumor)-toxicity: orthostatic hypotension, reflex tachycardia
Sheets of medium-sized lymphoid cells (“starry sky” appearance on histology)
Burkitt’s lymphoma (t[8:14] c-myc activation, associated with EBV; “black sky” made up of malignant cells)
Phentolamine:-type of drug-application?
-nonselective alpha-blocker (reversible/competitive)-give to patients on MAO-inhibitors who eat tyramine-containing foods
Phentolamine:-type of drug-application?
-nonselective alpha-blocker (reversible/competitive)-give to patients on MAO-inhibitors who eat tyramine-containing foods
silver-staining spherical aggregation of tau proteins in neurons
Pick bodies (Pick’s disease: progressive dementia, changes in personality)
prazosin, terazosin, doxazosin:-types of drugs?-applications?-toxicity?
-alpha-1-selective-blockers-used for hypertension, urinary retention in BPH-toxicities: orthostatic hypotension with first dose; dizziness, headache (should give pts first dose before bed, while lying down)
prazosin, terazosin, doxazosin:-types of drugs?-applications?-toxicity?
-alpha-1-selective-blockers-used for hypertension, urinary retention in BPH-toxicities: orthostatic hypotension with first dose; dizziness, headache (should give pts first dose before bed, while lying down)
“Soap bubble” in femur or tibia on x-ray
Giant cell tumor of bone (generally benign)
mirtazapine:-type of drug-application-toxicity
NAME?
mirtazapine:-type of drug-application-toxicity
NAME?
“Soap bubble” in femur or tibia on x-ray
Giant cell tumor of bone (generally benign)
List the B1-selective antagonists (A BEAM):
Acebutolol (partial agonist)BetaxololEsmolol (short-acting)AtenololMetoprolol
List the B1-selective antagonists (A BEAM):
Acebutolol (partial agonist)BetaxololEsmolol (short-acting)AtenololMetoprolol
“spikes” on basement membrane, “dome-like” subepithelial deposits
Membranous glomerulonephritis (may progress to nephrotic syndrome)
List the nonselective Beta-antagonists (Please Try Not being Picky)
PropranololTimololNadololPindolol
List the nonselective Beta-antagonists (Please Try Not being Picky)
PropranololTimololNadololPindolol
“spikes” on basement membrane, “dome-like” subepithelial deposits
Membranous glomerulonephritis (may progress to nephrotic syndrome)
List the partial beta-agonists (PAPA):
PindololAcebutolol
List the partial beta-agonists (PAPA):
PindololAcebutolol
Stacks of red blood cells
Rouleaux formation (high ESR, multiple myeloma)
Nonselective alpha and beta -antagonists:
CarvelidolLabetalol
Nonselective alpha and beta -antagonists:
CarvelidolLabetalol
Stacks of red blood cells
Rouleaux formation (high ESR, multiple myeloma)
Clinical applications of beta-blockers:
-hypertension (decrease CO, decrease renin secrtion - by beta-receptor blockade on JGA cells)-angina pectoris (decrease HR and contractility, so have decreased O2 consumption of myocardium)-MI (metoprolol and carvedilol –> decrease mortality from MIs)-SV
Clinical applications of beta-blockers:
-hypertension (decrease CO, decrease renin secrtion - by beta-receptor blockade on JGA cells)-angina pectoris (decrease HR and contractility, so have decreased O2 consumption of myocardium)-MI (metoprolol and carvedilol –> decrease mortality from MIs)-SV
stippled vaginal epithelial cells
“clue cells” (Gardnerella vaginalis)
Toxicity of Beta-blockers
-impotence!-exacerbates asthma-CV adverse effects (bradycardia, AV block, CHF)-CNS adverse effects (sedation, sleep alterations)-use caustiously with diabetics! (b/c B-blockers block sympathetically-mediated symptoms of hypoglycemia; so, patient won’t be
Toxicity of Beta-blockers
-impotence!-exacerbates asthma-CV adverse effects (bradycardia, AV block, CHF)-CNS adverse effects (sedation, sleep alterations)-use caustiously with diabetics! (b/c B-blockers block sympathetically-mediated symptoms of hypoglycemia; so, patient won’t be
stippled vaginal epithelial cells
“clue cells” (Gardnerella vaginalis)
Bethanechol applications
Bethanecol = direct cholinomimetic-used for postoperative and neurogenic ileus and urinary retention (activates Bowel and Bladder)
Bethanechol applications
Bethanecol = direct cholinomimetic-used for postoperative and neurogenic ileus and urinary retention (activates Bowel and Bladder)
“tennis-racket”-shaped cytoplasmic organelles (EM) in Langerhans cells
Birbeck granules (histiocytosis X: eosinophilic granuloma)
Carbachol applications
carbachol = direct cholinomimetic-used for glaucoma, pupillary contraction, relief of intraocular pressure
Carbachol applications
carbachol = direct cholinomimetic-used for glaucoma, pupillary contraction, relief of intraocular pressure
“tennis-racket”-shaped cytoplasmic organelles (EM) in Langerhans cells
Birbeck granules (histiocytosis X: eosinophilic granuloma)
Pilocarpine applications
-pilocarpine = direct cholinomimetic-used to stimulate sweat, tears, saliva (“cry, spit, sweat on your pillow”)
Pilocarpine applications
-pilocarpine = direct cholinomimetic-used to stimulate sweat, tears, saliva (“cry, spit, sweat on your pillow”)
thrombi made of white/red layers
Lines of Zahn (arterial thrombus, layers of platelets/RBCs)
Which cholinomimetics are resistant to AChE?
Bethanechol, Pilocarpine
Which cholinomimetics are resistant to AChE?
Bethanechol, Pilocarpine
thrombi made of white/red layers
Lines of Zahn (arterial thrombus, layers of platelets/RBCs)
Methacholine applications?
methacholine = direct cholinomimetic-used as a challenge test to diagnose asthma
Methacholine applications?
methacholine = direct cholinomimetic-used as a challenge test to diagnose asthma
“thumb sign” on lateral x-ray
epiglottitis (Haemophilus influenzae)
Neostigmine applications?
neostigmine - anticholinesterase (indirect cholinomimetic)-used for postoperative and neurogenic ileus and urinary retention, myasthenia gravis, reversal of NM jxn blockade-increases endogenous ACh; does not penetrate the CNS
Neostigmine applications?
neostigmine - anticholinesterase (indirect cholinomimetic)-used for postoperative and neurogenic ileus and urinary retention, myasthenia gravis, reversal of NM jxn blockade-increases endogenous ACh; does not penetrate the CNS
“thumb sign” on lateral x-ray
epiglottitis (Haemophilus influenzae)
Pyridostigmine applications?
pyridostigmine = anticholinesterase (indirect cholinomimetic)-used for myasthenia gravis (gets RID of MG)-does not penterate CNS-increases endogenous ACh
Pyridostigmine applications?
pyridostigmine = anticholinesterase (indirect cholinomimetic)-used for myasthenia gravis (gets RID of MG)-does not penterate CNS-increases endogenous ACh
Thyroid-like appearance of kidney
chronic bacterial pyelonephritis
Edrophonium applications
endrophonium = anticholinesterase (indirect cholinomimetic)-used to diagnose myasthenia gravis-increases endogenous Ach
Edrophonium applications
endrophonium = anticholinesterase (indirect cholinomimetic)-used to diagnose myasthenia gravis-increases endogenous Ach
Thyroid-like appearance of kidney
chronic bacterial pyelonephritis
Physostigmine applications
physostigmine = anticholinesterase (indirect cholinomimetic)-used to treat glaucoma and atropine overdose (“phyxes” atropine OD)-crosses the BBB!-increases endogenous Ach
Physostigmine applications
physostigmine = anticholinesterase (indirect cholinomimetic)-used to treat glaucoma and atropine overdose (“phyxes” atropine OD)-crosses the BBB!-increases endogenous Ach
“tram-track” appearance on LM
membranoproliferative glomerulonephritis
Echothiophate applications
echothiphate = anticholinesterase (indirect cholinomimetic)-used to treat glaucoma-increases endogenous Ach
Echothiophate applications
echothiphate = anticholinesterase (indirect cholinomimetic)-used to treat glaucoma-increases endogenous Ach
“tram-track” appearance on LM
membranoproliferative glomerulonephritis
Donepezil applications
donepezil = anticholinesterase (indirect cholinomimetic)-used to treat Alzheimer’s disease-increases endogenous Ach!
Donepezil applications
donepezil = anticholinesterase (indirect cholinomimetic)-used to treat Alzheimer’s disease-increases endogenous Ach!
triglyceride accumulation in liver cell vacuoles
fatty liver disease (alcoholic or metabolic syndrome)
pKa = acid dissociation constant = ?
pKa = pH at which amount of the non-protonated form = the amount of the protonated form
pKa = acid dissociation constant = ?
pKa = pH at which amount of the non-protonated form = the amount of the protonated form
triglyceride accumulation in liver cell vacuoles
fatty liver disease (alcoholic or metabolic syndrome)
if pH < pKa…
acidic environment; have more of the protonated form (so, basic drugs get trapped)
if pH < pKa…
acidic environment; have more of the protonated form (so, basic drugs get trapped)
WBCs that look “smudged”
CLL (almost always B cell; affects elderly)
if pH > pKa…
basic environment; have more of the nonprotonated form (acidic drugs get trapped)
if pH > pKa…
basic environment; have more of the nonprotonated form (acidic drugs get trapped)
WBCs that look “smudged”
CLL (almost always B cell; affects elderly)
Treat acidic drug OD (ie slicylates) with?
NaHCO3 (traps the acidic drug in the basic urine)
Treat acidic drug OD (ie slicylates) with?
NaHCO3 (traps the acidic drug in the basic urine)
“wire loop” glomerular appearnce on LM
Lupus nerphropathy
Treat basic drug OD (ie amphetamines) with?
NH4Cl (ammonium chloride; traps basic drug in the acidic urine)
Treat basic drug OD (ie amphetamines) with?
NH4Cl (ammonium chloride; traps basic drug in the acidic urine)
“wire loop” glomerular appearnce on LM
Lupus nerphropathy
What class of drugs can cause excess parasympathetic activity (ie DUMBBELSS symptoms)?
Cholinomimetic agents
What class of drugs can cause excess parasympathetic activity (ie DUMBBELSS symptoms)?
Cholinomimetic agents
Yellow CSF
Xanthochromia (previous subarachnoid hemorrhage)
What drug regenerates AchE after organophosphate poisoning?
Pralidoxime (regenerates active AchE) (also, give atropine to treat symptoms!)
What drug regenerates AchE after organophosphate poisoning?
Pralidoxime (regenerates active AchE) (also, give atropine to treat symptoms!)
Yellow CSF
Xanthochromia (previous subarachnoid hemorrhage)
What are the symptoms of inhibiting parasympathetic activity?
(ie atropine side effects)Hot as a hareDry as a boneRed as a beetBlind as a batMad as a hatterBloated as a toad
What are the symptoms of inhibiting parasympathetic activity?
(ie atropine side effects)Hot as a hareDry as a boneRed as a beetBlind as a batMad as a hatterBloated as a toad
Erlenmeyer flask bones on X-ray (bones flare out)
Osteopetrosis (abnormal osteoclasts)
In what populations is atropine contraindicated?
-Glaucoma (because don’t want to dilate eyes)-BPH or any urinary retention-GI obstruction (ie ileus)-Dementia or Elderly (because can cause delirium)-Infant with fever (because can cause hyperthermia)-
In what populations is atropine contraindicated?
-Glaucoma (because don’t want to dilate eyes)-BPH or any urinary retention-GI obstruction (ie ileus)-Dementia or Elderly (because can cause delirium)-Infant with fever (because can cause hyperthermia)-
“double bubble” or “soap bubble” appearance on x-ray
Giant cell tumor (osteoclastoma)
List 4 classes of drugs with anti-cholinergic side effects:
1) First generation H1-Blockers (diphenhydramine, doxylamine, chlorpheniramine)2) Traditional neuroleptics3) TCAs4) Amantadine
List 4 classes of drugs with anti-cholinergic side effects:
1) First generation H1-Blockers (diphenhydramine, doxylamine, chlorpheniramine)2) Traditional neuroleptics3) TCAs4) Amantadine
codman’s triangle or sunburst pattern on x-ray
osteosarcoma (osteogenic sarcoma); pattern is from elevation of periosteum
List 4 treatment options for Myasthenia Gravis:
1) Anti-cholinesterases (indirect cholinergic agonists)2) Corticosteroids (because MG = autoimmune disease)3) Thymectomy (often curative)4) Plasmapheresis
List 4 treatment options for Myasthenia Gravis:
1) Anti-cholinesterases (indirect cholinergic agonists)2) Corticosteroids (because MG = autoimmune disease)3) Thymectomy (often curative)4) Plasmapheresis
Disease associated with HLA-A3
Hemochromatosis
What are the 5 classes of drugs used to treat glaucoma?
1) alpha-agonists2) beta-blockers3) Diuretics (Carbanic anhydrase inhibtors and mannitol)4) cholinomimetics5) prostaglandins
What are the 5 classes of drugs used to treat glaucoma?
1) alpha-agonists2) beta-blockers3) Diuretics (Carbanic anhydrase inhibtors and mannitol)4) cholinomimetics5) prostaglandins
Disease associated with HLA-B27
PAIR: Psoriasis, Ankylosing spondylitis, Inflammatory bowel disease, Reither’s syndrome (Reactive arthritis)
P-450 Inducers
Barb Steals Phen-phen and Refuses Greasy Carbs Chronically:BarbituratesSt. John’s wortPhenytoinRifampinGriseofulvinCarbamazepineChronic alcohol use
P-450 Inducers
Barb Steals Phen-phen and Refuses Greasy Carbs Chronically:BarbituratesSt. John’s wortPhenytoinRifampinGriseofulvinCarbamazepineChronic alcohol use
Disease associated with HLA-B8
Graves’ disease
P-450 inhibitors
Q-MAGIC RACKS:QuinidineMacrolidesAmiodaroneGrapefruit juiceIsoniazidCimetidineRitonavirAcute alcohol abuseCiprofloxacinKetoconazoleSulfonamides
P-450 inhibitors
Q-MAGIC RACKS:QuinidineMacrolidesAmiodaroneGrapefruit juiceIsoniazidCimetidineRitonavirAcute alcohol abuseCiprofloxacinKetoconazoleSulfonamides
Diseases associated with HLA-DR2
Multiple sclerosis, hay fever, SLE, Goodpasture’s
acetaminophen antidote? (toxic dose = 4 g/day = 8 extra-strength tablets)
N-acetylcysteine (replenishes glutathione)
acetaminophen antidote? (toxic dose = 4 g/day = 8 extra-strength tablets)
N-acetylcysteine (replenishes glutathione)
Disease associated with HLA-DR3
Diabetes mellitus type I
salicylates (ie aspirin) antidote?
NaHCO3 (alkalinizes urine)Dialysis
salicylates (ie aspirin) antidote?
NaHCO3 (alkalinizes urine)Dialysis
Diseases associated with HLA-DR4
Rheumatoid arthritis, Diabetes mellitus type I
amphetamines antidote
NH4Cl (acidifies urine)
amphetamines antidote
NH4Cl (acidifies urine)
Disease associated with HLA-DR5
Pernicious anemia –> B12 deficiency,
Hashimoto’s thyroiditis
anti-acetylcholinesterase and organophosphates antidote?
Atropine + Pralidoxime
anti-acetylcholinesterase and organophosphates antidote?
Atropine + Pralidoxime
Disease associated with HLA-DR7
Steroid-responsive nephrotic syndrome
antimuscarinic, anticholinergic agents (ie atropine) antidote?
physostigmine salicylate
antimuscarinic, anticholinergic agents (ie atropine) antidote?
physostigmine salicylate
Abdominal pain, ascites, hepatomegaly
Budd-Chiari syndrome (posthepatic venous thrombosis)
beta-blockers antidote?
(same as verapamil antidote!) = glucagon, calcium, atropine (all increase HR)
beta-blockers antidote?
(same as verapamil antidote!) = glucagon, calcium, atropine (all increase HR)
Achilles tendon xanthoma
familial hypercholesterolemia (decreased LDL receptor signaling)
Iron antidote
deferoxamine
Iron antidote
deferoxamine
Adrenal hemorrhage, hypotension, DIC
Waterhouse-Friderichsen syndrome (meningococcemia)
lead antidote
CaEDTA (in adults)Dimercaprolsuccimer (in kids)penicillamine
lead antidote
CaEDTA (in adults)Dimercaprolsuccimer (in kids)penicillamine
Arachnodactyly (spider-like fingers), lens dislocation, aortic dissection, hyperflexible joints
Marfan’s syndrome (fibrillin defect)
mercury, arsenic, gold antidote
-dimercaprol (BAL) (dimes = money = gold; merc = mercury!)-succimer
mercury, arsenic, gold antidote
-dimercaprol (BAL) (dimes = money = gold; merc = mercury!)-succimer
Athlete with polycythemia
erythropoietin injection
copper, arsenic, gold antidote
penicillamine (copper pennies!)
copper, arsenic, gold antidote
penicillamine (copper pennies!)
back pain, fever, night sweats, weight loss
Pott’s disease (vertebral TB)
cyanide antidote
(may get cyanide poisoning from nitroprusside, used for malignant HTN; also, from house fires – see CN toxicity along with CO poisoning)-nitrite-hydroxocobalamin-thiosulfate
cyanide antidote
(may get cyanide poisoning from nitroprusside, used for malignant HTN; also, from house fires – see CN toxicity along with CO poisoning)-nitrite-hydroxocobalamin-thiosulfate
Bilateral hilar adenopathy, uveitis
Sarcoidosis (non-caseating granulomas)
Carbon monoxide antidote
100% O2Hyperbaric O2
Carbon monoxide antidote
100% O2Hyperbaric O2
blue sclera
osteogenesis imperfecta (collagen defect)
opioids antidote
naloxone/naltrexone
opioids antidote
naloxone/naltrexone
bluish line on gingiva
Burton’s line (lead poisoning)
benzodiazepines antidote
flumazenil
benzodiazepines antidote
flumazenil
Bone pain, bone enlargement, arthritis, increased hat size, fractures
Paget’s disease of bone (increased osteoblastic AND osteoclastic activity)
TCAs antidote
NaHCO3 (plasma alkalinization)
TCAs antidote
NaHCO3 (plasma alkalinization)
bounding pulses, diastolic heart murmur, head bobbing
aortic regurgitation
Heparin antidote
protamine (H+ = Proton-amine!)
Heparin antidote
protamine (H+ = Proton-amine!)
“butterfly” facial rash and Raynaud’s phenomenon in a young female
SLE
Warfarin antidote
vitamin Kfresh frozen plasma
Warfarin antidote
vitamin Kfresh frozen plasma
cafe-au-lait spots, polyostotic fibrous displasia, precocious puberty
McCune-Albright syndrome (mosaic G-protein signaling mutation)
tPA, streptokinase, urokinase antidote?
Aminocaproic acid
tPA, streptokinase, urokinase antidote?
Aminocaproic acid
cafe-au-lait spots, Lisch nodules (iris hamartoma =excess of normal iris tissue)
Neurofibromatosis type I (and pheochromocytoma, optic gliomas) and Neurofibromatosis type II (and bilateral acoustic neuromas)
theophylline antidote
Beta-blocker(theophylline is an option for COPD pts; it has a low TI with cardio-toxicity; so, give beta-blockers for the cardio-toxic effects)
theophylline antidote
Beta-blocker(theophylline is an option for COPD pts; it has a low TI with cardio-toxicity; so, give beta-blockers for the cardio-toxic effects)
calf pseudohypertrophy
muscular dystrophy (most commonly Duchenne’s): X-linked recessive deletion of dystrophin gene
Verapamil antidote
same as beta-blocker antidote! = glucagon, calcium, atropine (all increase HR)
Verapamil antidote
same as beta-blocker antidote! = glucagon, calcium, atropine (all increase HR)
“cherry red spot” on macula
1) Tay-Sachs (ganglioside accumulation)
2) Niemann-Pick (sphingomyelin accumulation)
3) Central retinal artery occlusion
Digitalis antidote
-Normalize K+ and Mg2+-lidocaine (if there’s tachyarrhythmia) -anti-dig fab fragments (if there’s arrhythmia)-atropine (if there’s bradycardia)
Digitalis antidote
-Normalize K+ and Mg2+-lidocaine (if there’s tachyarrhythmia) -anti-dig fab fragments (if there’s arrhythmia)-atropine (if there’s bradycardia)
chest pain on exertion
angina (stable: moderate exertion; unstable: minimal exertion)
methemoglobin antidote
-methylene blue-vitamin C
methemoglobin antidote
-methylene blue-vitamin C
chest pain, pericardial effusion, friction rub, persistent fever following MI
Dressler’s syndrome (autoimmune-mediated post-MI fibrinous pericarditis; 1-12 weeks after acute episode)
methanol, ethylene glycol (anti-freeze) antidote
-Fomepizole = 1st choice! (inhibits alcohol dehydrogenase)-2nd choices = ethanol, dialysis
methanol, ethylene glycol (anti-freeze) antidote
-Fomepizole = 1st choice! (inhibits alcohol dehydrogenase)-2nd choices = ethanol, dialysis
child uses arms to stand up from squat
Gower’s sign (Duchenne muscular dystrophy)
child with fever develops rash on face that spreads to body
“slapped cheeks” (erythema infectiosum/fifth disease: parvo B19)
chorea, dementia, caudate degeneration
Huntington’s disease (autosomal-dominant CAG repeat expansion)
5 C’s of Huntington’s disease?
Chorea Crazy Caudate degeneration CAG repeats Choline (decrease Ach)
chronic exercise intolerance with myalgia, fatigue, painful cramps, myoglobinuria
McArdle’s disease (muscle glycogen phosphorylase deficiency)
Cold intolerance
Hypothyroidism
conjugate lateral gaze palsy, horizontal diplopia
internuclear ophthalmoplegia (damage to MLF; bilateral [multiple sclerosis], unilateral [stroke])
continuous “machinery” heart murmur
PDA (close with indomethacin; open with misoprostol (a PG))
decreased Ach in? increased Ach in?
decreased Ach: Alzheimer’s and Huntington’s
increased Ach: Parkinson’s
cutaneous/dermal edema d/t connective tissue deposition
myxedema (caused by hypthyroidism, Grave’s disease (periorbital) = not a typo! :))
dark purple skin/mouth nodules
Kaposi’s sarcoma (usually AIDS pts; assoc with HHV-8)
Deep, labored breathing/hyperventilation
Kussmaul breathing (diabetic ketoacidosis)
Dermatitis, dementia, diarrhea
Pellagra (niacin [vitamin B3] deficiency)
Dilated cardiomyopathy, edema, polyneuropathy
wet beriberi(thiamine [vitamin B1] deficiency)
dog or cat bite resulting in infection
Pasteurella multocida (cellulitis at inoculation site)
dry eyes, dry mouth, arthritis
Sjogren’s (autoimmune destruction of exocrine glands)
dysphagia (esophageal webs), glossitis, iron deficiency anemia
Plummer-Vinson syndrome (may progress to esophageal squamous cell carcinoma)
elastic skin, hypermobility of joints
Ehler’s-Danlos syndrome (type III collagen defect)
enlarged, hard left supraclavicular node
Virchow’s triad (commonly abdominal metastasis)
Erythroderma, lymphadenopathy, hepatosplenomegaly, atypical T-cells
1) Sezary syndrome (cutaneous T-cell lymphoma)
2) Mycosis fungoides
facial muscle spasm upon tapping
Chvostek’s sign (hypocalcemia)
fat, female, forty, and fertile
acute cholelithiasis (bile duct blockage)
fever, chills, headache, myalgia, following antibiotic treatment for sphyilis
Jarisch-Herxheimer reaction (rapid lysis of spirochetes results in toxin release)
fever, cough, conjunctivitis, coryza (allergy symptoms), diffuse rash
Measles (Morbillivirus)
fever, night sweats, weight loss
1) B symptoms (Lymphoma)
2) TB
fibrous plaques in soft tissue of penis
Peyronie’s disease (connective tissue disorder)
gout, mental retardation, self-mutilation behavior in a boy
Lesch-Nyhan syndrome (HGPRT-deficiency; X-linked recessive)
Green-yellow rings around peripheral cornea
Kayser-Fleischer rings (copper accumulation from Wilson’s disease)
Hamartomatous GI polyps, hyperpigmentaion of mouth/feet/hands
Peutz-Jeghers syndrome (genetic benign polyposis can cause bowel obstruction; increased cancer risk)
hepatosplenomegaly, osteoporosis, neurologic symptoms
Gaucher’s disease (glucocerebrosidase deficiency; “crinkle-tissue paper cytoplasm”)
Hereditary nephritis, sensourineural hearing loss, cataracts
Alport syndrome (mutation in alpha chain of collagen IV; “can’t see, can’t pee, can’t hear)
hypercoagulability (leading to migrating DVTs and vasculitis)
Trousseau’s sign (adenocarcinoma of pancreas of lung)
hyperphagia, hypersexuality, hyperorality, hyperdocility
Kluver-Bucy syndrome (bilateral amygdala lesion)
hyperreflexia, hypertonia, positive Babinski
UMN damage
hypertension, hypokalemia, metabolic alkalosis
Conn’s syndrome (primary hyperaldosteronism)
hyporeflexia, hypotonia, atrophy
LMN damage
hypoxemia, polycythemia, hypercapnia
“blue boater” (chronic bronchitis: hyperplasia of mucous cells)
non-painful, indurated, ulcerated genital lesion
chancre (primary syphilis = treponema pallidum)
painful, indurated, ulcerated genital lesion, with exudate
chancroid (hamophilus ducreyi)
infant with ftt, hepatosplenomegaly, neurodegeneration, cherry red spots on macular disc
Niemann-Pick disease (genetic sphingomyelinase deficiency)
infant with ftt, hypoglycemia, hepatomegaly
Cori’s disease (debranching enzyme deficiency)
infant with microcephaly, rocker-bottom feet, clenched hands, and structural heart defect
Edward’s syndrome (trisomy 18)
Keratin pearls on a skin biopsy
squamous cell carcinoma
large rash with bull’s-eye appearance
erythema chronicum migrans from Ixodes tick bite (Lyme disease: Borrelia)
lucid interval after traumatic brain injury
epidural hematoma (middle meningeal artery rupture)
male child, recurrent infections, no mature B cells
Bruton’s disease (X-linked agammaglobulinemia)
mucosal bleeding and prolonged bleeding time
Glanzmann’s thrombasthenia (defect in platelet aggregation due to lack of GpIIb/IIIa)
multiple colon polyps, osteomas/soft tissue tumors, impacted/supernumerary teeth
Gardner’s syndrome (subtype of FAP)
myopathy (infantile hypertrophic cardiomyopathy), exercise intolerance
Pompe’s disease (lysosomal alpha-1,4-glucosidase deficiency)
necrotizing vasculitis (lungs) and necrotizing glomerulonephritis
1) Wegener’s (c-ANCA)
2) Goodpasture’s syndrome (anti-BM antibodies)
neonate with arm paralysis following difficult birth
Erb-Duchenne’s palsy (superior trunk [C5-C6] brachial plexus injury: “waiter’s tip”)
no lactation postpartum, absent menstruation, cold intolerance
Sheehan’s syndrome (pituitary infarction)
nystagmus, intention tremor, scanning speech, bilateral internuclear ophthalmoplegia
multiple sclerosis
oscillating slow/fast breathing
Cheyne-Stokes respirations (central apnea in CHF or increased intracranial pressure)
painful blue fingers/toes, hemolytic anemia
cold agglutinin disease (autoimmune hemolytic anemia caused by Mycoplasma pneumoniae, infectious mononucleosis)
painful, pale, cold fingers/toes
Raynaud’s syndrome (vasospasm in extremities)
painful, raised red lesions on palms and soles
Osler’s node (infective endocarditis)
painless erythematous lesions on palms and soles
Janeway lesions (infective endocarditis)
painless jaundice
cancer of the pancreatic head obstructing bile duct
palpable purpur on buttocks/legs, joint pain, abdominal pain (child)
Henoch-Schonlein purpura (IgA vasculitis affecting skin and kidneys)
pancreatic (Zollinger-Ellsion syndrome, insulinomas, VIPomas, glucagonomas), pituitary (prolactin or GH), parathyroid tumors
MEN 1 = “Wermer’s syndrome” (autosomal dominant)
pink complexion, dyspnea, hyperventilation
“pink puffer” (emphysema: centroacinar [smoking], panacinar [alpha-1-antitrypsin deficiency])
polyuria, acidosis, growth failure, electroylte imbalances
Fanconi’s syndrome (proximal tubular reabsorption defect)
positive anterior “drawer sign”
ACL (anterior cruciate ligament) injury
ptosis (droopy eyelid), miosis, anhidrosis
Horner’s syndrome (sympathetic chain lesion)
pupil accommodates but doesn’t react
Argyll Robertson pupil (neurosyphilis)
rapidly progressive leg weakness that ascends (following GI/upper respiratory infection)
Guillan-Barre syndrome (autoimmune acute inflammatory demyelinating polyneuropathy)
rash on palms and soles
CARS:
- Coxsackie A
- Rocky mountain spotted fever
- Syphilis (secondary)
Recurrent colds, unusual eczema, high serum IgE
hyper-IgE syndrome = Job’s syndrome (neutrophil chemotaxis abnormality)
red “currant jelly” sputum in alcoholic or diabetic patients
Klebsiella pneumoniae
red, itchy, swollen rash of nipple/areola
Paget’s disease of breast (represents underlying neoplasm)
red urine in the morning, fragile RBCs
paroxysmal nocturnal hemoglobinuria
renal cell carcinoma (bilateral), hemangioblastoma, angiomatosis, pheochromocytoma
von-Hippel-Lindau disease (dominant tumor suppressor gene mutation)
resting tremor, rigidity, akinesia, postural instability
Parkinson’s disease (nigrostriatal dopamine depletion)
retinal hemorrhages with pale centers
Roth’s spots (bacterial endocarditis)
severe jaundice in neonate
Crigler-Najjar syndrome (congenital unconjugated hyperbiliribunemia)
severe RLQ pain with rebound tenderness
McBurney’s sign (appendicitis)
short stature, increased incidence of tumors/leukemia, aplastic anemia
Fanconi’s anemia (genetic loss of DNA crosslink repair; often progresses to AML)
single palm crease
Simian crease (Down’s syndrome)
situs inversus, chronic sinusitis, bronchiectasis, infertility
Kartagener’s syndrome (dynein arm defect affecting cilia)
skin hyperpigmentation
Addison’s disease (primary adrenocortical insufficiency causes increased ACTH and alpha-MSH production)
slow, progressive muscle weakness in boys
Becker’s muscular dystrophy (X-linked missense mutation in dystrophin; less severe than Duchenne’s
small, irregular red spots on buccal/lingual mucosa with blue-white centers
Koplik spots (measles; rubeola virus)
smooth, flat, moist white lesions on genitals
condylomata lata (secondary syphilis)
splinter hemorrhages in fingernails
bacterial endocarditis
“strawberry tongue”
1) Scarlet fever
2) Kawasaki disease
3) Toxic Shock Syndrome
streak ovaries, congenital heart disease, horseshoe kidney, cystic hygroma at birth
Turner syndrome (45XO, short stature, webbed neck, lymphedema)
sudden swollen/painful big toe joint, tophi
gout/podagra (hyperuricemia)
swollen gums, mucous bleeding, poor wound healing, spots on skin
scurvy (vitamin C deficiency: can’t hydroxylate proline/lysine for collagen synthesis)
swollen, hard, painful finger joints
osteoarthritis (osteophytes on PIP [Bouchard’s nodes], DIP [Heberden’s nodes])
systolic ejection murmur (crescendo-decrescendo)
aortic valve stenosis
thyroid and parathyroid tumors (medullary thryoid carcinoma - secretes calcitonin), pheochromocytoma
MEN 2A = Sipple’s syndrome (autosomal dominant “ret” mutation)
Thyroid tumor (medullary thyroid carcinoma - secretes calcitonin), Pheochromocytoma, Ganglioneuromatosis (oral/intestinal - associated with marfanoid habitus)
MEN 2B (autosomal dominant “ret” mutation)
toe extension/fanning upon plantar scrape
Babinski sign (UMN lesion)
unilateral facial drooping involving forehead
Bell’s palsy (LMN CN VII palsy)
urethritis, conjunctivitis, arthritis in a male
reactive arthritis associated with HLA-B27
vascular birthmark (port-wine stain)
hemangioma (benign, but associated with Sturge-Weber syndrome)
vomiting blood following esophagogastric lacerations
Mallory-Weiss syndrome (alcoholic and bulimic patients)
“waxy” casts with very low urine flow
chronic end-stage renal disease
WBC casts in urine
acute pyelonephritis
weight loss, diarrhea, arthritis, fever, adenopathy
Whipple’s disease (Tropheryma whippeli)
“worst headache of my life”
subarachnoid hemorrhage
Ptosis or Diplopia that worsens throughout the day?
Myasthenia gravis
Signs of lead toxicity:
ABCDEFG!
Anemia
Basophilic stippling
Colicky pain
Diarrhea
Encephalopathy
Foot drop
Gums ("lead line")Which coronary artery is most often occluded and what kind of MI does it cause?
coronary artery occlusion most commonly occurs in the LAD (left anterior descending). this causes an anterior wall MI
Cardiac output = ?
CO = SV X HR
Fick Principle:
CO = (rate of O2 consumption)/(arterial O2 content - venous O2 content)
Mean Arterial Pressure = ?
MAP = 2/3(DP) + 1/3(SP) MAP = CO X TPR P = Q X R
- TPR = total peripheral resistance
- P = MAP
- Q=CO
- R = TPR
Pulse pressure = ?
Systolic pressure - Diastolic pressure
pulse pressure is proportional to SV
Stroke Volume = ?
SV = CO/HR = EDV - ESV
What factors affect stroke volume?
List 3 conditions which lead to increased SV:
SV CAP:
-Contractility
-Afterload
-Preload
(increased SV when increased contractility, increased preload, or decreased afterload)
-get increased SV in:
1) anxiety (b/c increased catecholamines)
2) pregnancy (b/c increased blood volume and preload)
3) exercise (b/c increased preload and catecholamines)
List 4 factors that increase contractility (and thus SV too):
1) Catecholamines (via B1 receptors)
2) increased intracellular Calcium
3) decreased extracellular Sodium (and therefore decreased Na+/Ca2+-exchanger –> so increased intracellular calcium)
4) Digitalis (blocks Na+/K+-ATPase leading to decreased Na+/Ca2+-exchanger and increased intracellular calcium)
List five factors that decrease contractility (and thus SV too):
1) Beta-1 Blockade
2) Heart failure
3) Acidosis
4) Hypoxia/Hypercapnea
5) non-dihydropyridine Calcium channel blockers (ie Verapamil and Diltiazem)
List 3 ways to decrease the Oxygen demand in a heart attack (mechanism + types of drugs used to achieve mechanism)?
1) decrease afterload –> give Ace-inhibs or ARBs
2) decrease contractility –> Beta-blockers
3) decrease HR –> Beta-blockers
Ejection Fraction = ?
EF = SV/EDV = (EDV - ESV)/EDV
basically, EF = what heart can pump out/what heart can hold
*normal EF > 55%
Resistance: relationship to length viscosity? radius?
Equation: Resistance = (8nviscosity X length)/(piXr^4)
So:
*Resistance is proportional to length
*Resistance is proportional to viscosity
*Resistance is inversely proportional to radius (specifically, 1 R is inversely proportional to r^4)
3 states in which see increased viscosity:
- Viscosity depends mostly on hematocrit; see increased viscosity in:
1) Polycythemia
2) Hyperproteinemic states (ie multiple myeloma)
3) Hereditary spherocytosis
List the classes of antiarrhythmic drugs
"No Bad Boy Keeps Clean" Class I - Na+ channel blockers; 3 subclasses Class 2 - Beta-Blockers Class 3 - K+ channel blockers Class 4 - Ca2+ channel blockers
List the class I antiarrhythmic drugs:
What is their mechanism?
Na+ channel blockers
3 subclasses: “Double Quarter Pounder - Lettuce, Tomato, Mayo, (Pickles) - Fries, Please”
Class Ia: “Double Quarter Pounder”
Disopyramide
Quinidine
Procainamide
Class Ib: "Lettuce, Tomato, Mayo" Lidocaine Mexiletine Tocainide (Phenytoin)
Class Ic: “Fries, Please”
Flecainide
Propafenone
*Class I anti-arrhythmics decrease the slope of phase 0 depolarization
List the class II antiarrhythmic drugs:
What is their mechanism?
Beta-Blockers
Propranolol Esmolol Metoprolol Atenolol Timolol
*Class II drugs decrease the slope of phase 4; increase the PR interval
List the class III antiarrhythmic drugs:
Mechanism?
K+ channel blockers
“K IS BAD”
Ibutilide Sotalol Bretylium Amiodarone Dofetilide
*act on phase 3; increase AP duration by slowing the efflux of K from the cell; increase QT interval
List the class IV antiarrhythmic drugs:
Mechanism?
Ca2+ channel blockers
Verapamil
Diltiazem
*decrease phase 0, so slow depolarization; increase the effective refractory period; increase the PR interval
Which anti-arrhythmic drugs increase the QT interval?
Class IA (qunidine, procainamide, disopyramide) Class III
Both cause a prolonged AP duration and increase the ERP (effective refractory period)
*Note: a side effect of increased QT interval = torsades de pointes
Which anti-arrhythmic drug causes an increased QT interval but has a low risk of causing torsades de pointes?
Amiodarone
Which anti-arrhythmic drugs decrease the AP duration?
Class IB: Lidocaine, Mexiletine, Tocainide (and Phenytoin)
Which class of anti-arrhythmic drugs are contra-indicated post-MI?
Class IC is CI post-MI (Flecainide, Propafenone)
Which 2 drugs can be used to treat WPW (Wolf-Parkinson-White)?
Procainamide (only indication for this drug; side effect = drug-induced lupus)
Amiodarone
What should be checked before initiating Amiodarone therapy?
Amiodarone = a class III antiarrhythmic
Toxicities include: Pulmonary fibrosis, Hepatotoxicity, Hypothyroidism/Hyperthyroidism (because it is 40% iodine by weight); also: corneal deposits, skin deposits, photosensitivity, neurologic effects, constipation, CV effects….
So, before starting treatment: check PFTs, LFTs, TFTs (pulmonary, liver, and thyroid function tests)
Which anti-arrhythmic drug is 40% iodine by weight?
Amiodarone (a class III antiarrhythmic)
Drug of choice in diagnosing/abolishing SVT (supraventricular tachycardia)?
Adenosine (increases K+ out of cells –> hyperpolarizes the cell and decreases intracellular calcium)
Can block effects of adenosine with THEOPHYLLINE.
Indications for Mg2+ as an anti-arrhythmic?
Torsades de pointes and Digoxin toxicity
Drug class of choice to decrease LDL?
Statins = HMG-CoA reductase inhibitors (lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin)
Side effects of Statins?
Hepatotoxicity (increased LFTs)
Myopathy/Rhabdomyolysis
Drug of choice to increase HDL?
Niacin = Vitamin B3
Which lipid-lowering agent has side effects that include: -red, flushed face -hyperglycemia, -hyperuricemia ?
Niacin (Vitamin B3; lipid lowering agent of choice to increase HDL)
Drug class of choice to decrease triglycerides?
#1 = Fibrates (gemfibrozil, clofibrate, bezafibrate, fenofibrate) #2 = Omega 3 FAs
Which lipid-lowering agents may lead to myositis and hepatotoxicity?
Statins and Fibrates (so don’t use these 2 classes together!)
Digoxin mechanism and clinical use?
- inhibits Na+/K+-ATPase thereby inhibiting Na+/Ca2+-exchanger. This leads to increased intracellular Calcium and increased contractility. So can be used in CHF to increase contractility
- Also stimulates vagus nerve, so stimulates the parasympathetic NS! So, it can be used in atrial fibrillation (because slows the rate of AV node conduction and depresses the SA node)
Digoxin toxicities (KNOW this :))
- cholinergic: nausea, vomiting, diarrhea, blurry yellow vision
- ECG: increased PR, decreased QT, T-wave inversion, arrhythmia, hyperkalemia, bradycardia
- worsened by renal failure (because decreased excretion), hypokalemia, quinidine (decreased digoxin clearance)
Digoxin antidotes:
- normalize K+ and Mg2+
- Lidocaine (if there’s a tachyarrhythmia)
- cardiac pacer
- anti-Dig-Fab fragments (if there’s an arrhythmia)
List 4 drugs that decrease BP (anti-hypertensives…) that are SAFE to use in PREGNANCY:
Hydralazine
Nifedipine
Labetalol
Methyldopa
Anti-hypertensive treatment choice for Essential HTN?
- Diuretics (spec thiazides, ie hydrochlorothiazide)
- ACE-inhibs, ARBs
- CCBs
*Note: only use thiazides in essential HTN pts without CHF or diabetes; if a pt has CHF or diabetes, then ACE-inhibs = #1 choice!
Can also use Beta-Blockers
Anti-hypertensive treatment choice in CHF?
- Loop Diuretics (ie furosemide; because increase Calcium excretion in urine!)
- ACE-inhibs/ARBs
- Beta-blockers in compensated CHF (use cautiously!)
- K-sparing diuretics (ie spironolactone)
anti-hypertensive treatment choices in diabetes pts?
- ACE-inhibs/ARBs
- CCBs
- Diuretics
- Beta-blockers (use cautiously, because may mask symptoms of hypoglycemia!)
- alpha-blockers
Why must one be careful when using Beta-Blockers in a diabetic pt?
beta-blockers may mask the symptoms of hypoglycemia; so, pt may be hypoglycemia, but won’t show normal symptoms… DANGER!
Which CV drug vasodilates arterioles more than veins and reduces afterload?
Hydralazine (used for severe HTN, HTN in pregnancy, CHF)
Calcium Channel Blockers:
- 2 types?
- actions
Dihyropyridines
Non-dihydropiridines
Reduce muscle contractility
*need to add more info here…
CV drug that can cause cyanide toxicity?
Nitroprusside (used to treat malignant hypertension)
CV drug that decrease preload AND afterload?
Nitroprusside (malignant HTN trtmnt)
Nitroglycerin, Isosorbide dinitrate, Isosorbide mononitrate:
- Vasodilators (relase NO in smooth muscle cause increased cGMP and smooth muscle relaxation)
- dilate veins way more than arteries, so get decreased preload
- Uses: angina, pulmonary edema; aphrodisiac and erection enhancer!
- Isosorbide Mononitrate - active metabolite of isosorbide dinitrate; has almost 100% bioavailability
CV drug class that may enhance erections?
Nitrates
Nitrates toxicities
- Reflex tachycardia (side effect of all vasodilators)
- Hypotension
- Cutaneous flushing and throbbing headaches
- “Monday disease” = tolerance development during week, then on weekend lose tolerance, get tachycardia, dizziness, headache on re-exposure.
Drugs with side of effect of coronary vasospasm:
cocaine
sumatriptan
amphetamines
drugs with cutaneous flushing side effect
“VANC”
- vancomycin
- adenosine
- niacin (also nitrates!) (can give aspirin to prevent niacin-induced flushing)
- Ca-channel blockers
drugs with dilated cardiomyopathy side effect
doxorubicin
daunorubicin
(these are both anti-cancer drugs that act by forming free radicals)
drugs with torsades de pointes side effects
- anti-arrhythmics: class IA (ie quinidine) and class III (ie sotalol)
- macrolides
- haloperidol
- risperidone
- chloroquine
- methodone
- HIV-protease inhibitors
- cause torsades by prolonging the QT interval
- *treat torsades with an Mg2+ push
drugs with side effect of agranulocytosis
“Agranulocytosis Could Certainly Cause Pretty Major Damage”
- Clozapine
- Carbamezapine
- Colchicine
- Propylthiouracil (hyperthyroidism trtmt)
- Methimazole (hyperthyroidism trtmt)
- Dapsone
drugs with side effect of aplastic anemia
chloramphenicol benzene NSAIDs propylthiouracil methimazole
drug with reaction of: direct coombs-positive hemolytic anemia
methyldopa (anti-HTN, used to treat HTN in pregnant women)
drug that may cause gray baby syndrome
chloramphenicol
drugs that may cause hemolysis in G6PD-deficient pts
“hemolysis IS PAIN and fava beans….”
- Isoniazid
- Sulfonamides
- Primaquine (malaria)
- Aspirin (only at high doses)
- Ibuprofen
- Nitrofurantoin (antibiotic)
- fava beans!
drugs that may cause megaloblastic anemia
“having a blast with PMS”
- Phenytoin
- Methotrexate
- Sulfa drugs
drugs that may have thrombotic complications
oral contraceptives (estrogens and progesterones)
drugs that may lead to thrombocytopenia:
- heparin
- H2-blockers (ie antacids: cimetidine, ranitidine, famotidine, nizatidine
drugs with side effect of cough
ACE-inhibitors (ARBs do NOT cause cough..)
drugs that may cause pulmonary fibrosis
“BAB”
- bleomycin (anti-cancer drug)
- amiodarone (class III antiarrhythmic)
- busulfan (anti-cancer drug)
drugs with side effect of acute cholestatic hepatitis
erythromycin (a macrolide; not all macrolides cause acute cholestatic hepatitis though)
drugs with side effect of focal to massive hepatic necrosis
HAVA
- Halothane (inhaled anesthetic)
- Acetaminophen
- Valproic acid (anti-epileptic)
- Amanita phalloides (poisonous mushroom)
drug that may cause hepatitis
INH (Isoniazid)
drugs that may cause pseudomembranous colitis (c. diff)
- clindamycin
- ampicillin
drugs that may cause adrenocortical insufficiency (ie tertiary adrenal insufficiency)
rapid glucocorticoid withdrawal (suppresses the HPA)
drugs that may cause gynecomastia
“Some Drugs Create Awesome Knockers”
- Spironolactone
- Digitalis
- Cimetidine
- Alcohol (chronic use)
- Ketoconazole
- also estrogens
drugs that may cause hot flashes
SERM: tamoxifen, clomiphene
drugs that may cause hypothyroidism
- lithium
- amiodarone
- sulfanamides
drugs that may cause hyperglycemia
- niacin
- tacrolimus (immunosuppressive used in transplant pts)
- protease inhibitors
