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)