MIX Flashcards
Von Gierke Disease (type I) mutated enzyme
glucose-6-phosphatatse
Pompe disease (type II) mutated enzyme
lysosomal alpha-1,4-glucosidase
Cori Disease (type III) mutated enzyme
debranching enzyme (alpha-1,6-glucosidase)
McArdle disease (type V) mutated enzyme
skeletal muscle glycogen phosphorylase
Fabry disease mutated enzyme
alpha-galactosidease
Gaucher disease mutated enzyme
glucocerebrosidase
Niemann-Pick mutated enzyme
sphingomyelinase
Tay-Sachs mutated enzyme
hexosaminidase A
Krabbe disease mutated enzyme
galactrocerebrosidase
metachromic leukodystrophy mutated enzyme
arylsulfatase A
Hurler syndrome mutated enzyme
alpha-L-iduronidase
Hunter syndrome mutated enzyme
iduronate sulfatase
_1 (alpha1) receptor action
increase vascular smooth muscle contraction, increase pupillary dilator muscle contraction (mydriasis), increase intestinal and bladder sphincter muscle contraction
_2 (alpha2)receptor action
decrease sympathetic outflow, decrease insulin reslease, decrease lipolysis, increase platelet aggregation, decrease aqueous humor production
_1 (beta1) receptor action
increase heart rate, increase contractility, increase renin release, increase lipolysis
_2 (beta2) receptor action
vasodilation, bronchodilation, increase lipolysis, increase insulin release, decrease uterine tone (tocolysis), ciliary muscle relaxation, increase aqueous humor production
M1 receptor action
CNS, enteric nervous system
M2 receptor action
decrease heart rate and contractility of atria
M3 receptor action
increase exocrine gland secretions (lacrimal, salivary, gastric acid), increase peristalsis of gut, increase bladder contraction, bronchoconstriction, increase pupillary sphincter muscle contraction (miosis), ciliary muscle contraction (accomodation)
D1 receptor action
relaxes renal vascular smooth muscle
D2 receptor action
modulates transmitter release, especially in the brain
H1 receptor action
increases nasal and bronchial mucus production, increase vascular permeability, contraction of bronchioles, pruritus, pain
H2 receptor action
increase gastric acid secretion
V1 receptor action
increase vascular smooth muscle contraction
V2 receptor action
increased H2O permeability and reabsorption in collecting tubules of the kidney
bethanechol use
post-op ileus, neurogenic ileus, urinary retention
carbachol use
constricts pupil, relieves intraocular pressure in glaucomoa
methacholine use
challenge test for asthma dx
pilocarpine use
open angle and closed angle glaucoma
donepezil use
alzheimer disease
galantamine use
alzheimer disease
rivastigmine use
alzheimer disease
edrophonium use
historically used to diagnose myasthenia gravis
neostigmine use
post-op ileus, neurogenic ileus, urinary retention, myasthenia gravis, reversal of neuromuscular junction blockade post-op
physostigmine use
used to treat anticholinergic toxicity (ie atropine tox, TCA od); is able to cross BBB
pyridostigmine use
myasthenia gravis
atropine use
eye: mydriasis (pupillary dilation), hard to seeairway: decreased secretionsstomach: decreased acid secretiongut: decreased motilitybladder: decreased urgency
homatropine use
eye: mydriasis (pupillary dilation), hard to see
tropicamide use
eye: mydriasis (pupillary dilation), hard to see
benztropine use
Parkinson disease; acute dystonia
glycopyrrolate use
GI (oral administration): drooling, peptic ulcerrespiratory (parenteral administration): pre-op to reduce secretions
hyoscyamine use
GI: antispasmotic for IBS
dicyclomine use
GI: antispasmotic for IBS
ipatropium use
respiratory: COPD, asthma
tiopropium use
respiratory: COPD, asthma
oxybutynin use
GU: reduce bladder spasm and urge incontinence (overactive bladder)
solifenacin use
GU: reduce bladder spasm and urge incontinence (overactive bladder)
tolterodine use
GU: reduce bladder spasm and urge incontinence (overactive bladder)
scopalamine use
CNS: motion sickness
tetrodotoxin symptoms
nausea, vomiting, paresthesias, weakness, dizziness, loss of reflexes after eating poorly prepared pufferfish
ciguatoxin symptoms
temperature related dysesthesia (Cold feels hot)= specific finding; otherwise looks like cholinergic poisoning (diarrhea, urination, miosis, bradycardia, lacrimation, sweating salivation) after eating reef fish
scombroid poisoning
burning sensation in mouth, flushing of face, erythema, urticaria, pruritus, headache; anaphylaxis-like presentation
albuterol use
acute asthma
salmeterol use
long-term asthma, COPD control
dobutamine use
heart failure (inotropic> chronotropic), cardiac stress testing
dopamine use
unstable bradycardia, HF, shock; inotropic/chronotropic effects predominate at high dosese
epinephrine use
anaphylaxis, asthma, open-angle glaucoma (alpha effects predominate at high doses)
isoproterenol use
electrophysiologic evaluation of tachyarrhythmias
norepinephrine use
hypotension
phenylephrine use
hypotension (vasoconstrictor), dilates pupils, decongestant
amphetamine use
narcolepsy, obesity, ADHD
cocaine use
vasoconstriction, local anesthesia
ephedrine use
nasal decongestant, urinary incontinence, hypotension
clonidine use
hypertensive urgency, ADHD, Tourettes
_-methyldopa use
hypertension in pregnancy
phenoxybenzamine use
used pre-op before pheochromocytoma surgery to prevent catecholamine/hypertensive crisis
phentolamine use
for patients on MAO inhibitors who eat tyramine-containing foods
prazosin use
BPH urinary symptoms; PTSD; hypertension
terazosin use
BPH urinary symptoms; hypertension
doxazosin use
BPH urinary symptoms; hypertension
tamsulosin use
BPH urinary symptoms
mirtazapine use
depresson, increases appetite
metoprolol use
angina pectoris, MI (dec mortaility), SVT, hypertension, HF
esmolol use
angina pectoris, SVT, hypertension, HF
carvedilol use
angina pectoris, MI (dec mortaility), hypertension, HF
timolol use
glaucoma
toxin use
antidote/treatment
acetaminophen antidote
N-acetylcysteine
AchE inhibitors antidote
atropine, pralidoxime
organophosphates antidote
atropine, pralidoxime
amphetamines antidote
NH4Cl
antimuscarinic agents antidote
physostigmine salicylate
anticholinergic agents antidote
physostigmine salicylate
benzodiazepines antidote
flumazenil
beta blockers antidote
glucagon
carbon monoxide antidote
100% O2, hyperbaric O2
copper, arsenic, gold antidote
penicillamine
cyanide antidote
nitrite+ thiosulfate, hydroxocobalamin
digitalis (Digoxin) antidote
anti-dig Fab fragments
heparin antidote
protamine sulfate
iron antidote
deferoxamine, deferasirox
lead antidote
EDTA, dimercaprol, succimer, pencillamine
mercury, arsenic, gold antidote
dimercaprol (BAL), succimer
methanol antidote
fomepizole, ethanol
ethylene glycol antidote
fomepizole, ethanol
methemoglobin antidote
methylene blue, vitamin c
opioids antidote
naloxone, naltrexone
salicylates antidote
sodium bicarb
TCAs antidote
sodium bicarb
tPA, streptokinase, urokinase antidote
aminocaproic acid
warfarin antidote
FFP, vit K
Inspiration does what to flow to the heart
increased venous return to RA
Hand Grip does what to flow to the heart
increases afterload
valsalva (phase II)does what to flow to the heart
decreased preload
standing up does what to flow to the heart
decreased preload
rapid squatting does what to flow to the heart
increased venous return, increased preload
Inspiration changes heart sounds how?
increased intensity of right heart sounds
Hand Grip changes heart sounds how?
increased intensity of MR, AR, VSD murmursdecreased intensity of hypertrophic cardiomyopathy murmur MVP: later onset of click/murmur
valsalva (phase II) changes heart sounds how?
decreased intensity of most murmurs (inc. AS)increased intensity of hypertrophic cardiomyopathy murmurMVP: earlier onset of click/murmur
standing up changes heart sounds how?
decreased intensity of most murmurs (inc. AS)increased intensity of hypertrophic cardiomyopathy murmurMVP: earlier onset of click/murmur
rapid squatting changes heart sounds how?
decreased intensity of hypertrophic cardiomyopathy murmur increased intensity of AS murmurMVP: later onset of click/murmur
Alcohol exposure in utero
VSD, PDA, ASD, TOF
congenital rubella
septal defects, PDA, pulmonary artery stenosis
Down syndrome
AV septal defect (endocardial cushion defect), ASD, VSD
Infant of Diabetic Mother
Transposition of the great vessels
Marfan
MVP, thoracic aortic aneurysm and dissection, aortic regurg
prenatal lithium exposure
Ebstein anomaly (tricuspid valve anomaly)
Turner syndrome
coarctation of the aorta, bicuspid aortic valve
Williams Syndrome
supravalvular aortic stenosis
22q11 (Di George)
truncus arteriosus, TOF
VSD is associated with
alcohol exposure, Down syndrome
PDA is associated with
alcohol exposure, Down syndrome, congenital rubella
TGA is associated with
infants of diabetic mother
truncus arteriosus is associated with
digeorge
coarctation of the aorta is associated with
Turner syndrome
TOF is associated with
alcohol exposure, DiGeorge
ASD is associated with
Down syndrome, alcohol exposure
dihydropyridines except nimodipine
act on vascular smooth musle (vs. non-dihydropyridines which act on heart)
block voltage dependent L-type calcium channels of smooth muscle–> decrease muscle contractility
nimodipine
(dihydropyridine)
acts on vascular smooth musle (vs. non-dihydropyridines which act on heart)
block voltage dependent L-type calcium channels of smooth muscle–> decrease muscle contractility
clevidipine
(dihydropyridine)
acts on vascular smooth musle (vs. non-dihydropyridines which act on heart)
block voltage dependent L-type calcium channels of smooth muscle–> decrease muscle contractility
verapamil
(non-dihydropyridine); class IV antiarrhythmic
acts on heart
block voltage dependent L-type calcium channels of cardiac muscle–> decrease muscle contractility
decrease conduction velocity, increase refractory period, increase PR interval
diltiazem
(non-dihydropyridine); class IV antiarrhythmic
acts on heart
block voltage dependent L-type calcium channels of cardiac muscle–> decrease muscle contractility
decrease conduction velocity, increase refractory period, increase PR interval
hydralazine
increases cGMP–> smooth muscle relaxation; vasodilation of arterioles > veins –> results in reduced afterload
nitroprusside
increases cGMP by directly releasing NO
fenoldopam
dopamine D1 receptor agonist–> coronary, peripheral, renal, splanchnic vasodilation–> decreased BP, increased natriuresis
nitrates (nitroglycerin, isosorbide dinitrate, isosorbide mononitrate)
increase NO in vascular smooth muscle–> increase in cGMP and smooth muscle relaxation (veins»_space; arteries, decreased preload)
lovastatin, simvastatin, etc
HMG-CoA reductase inhibitors
inhibits conversion of HMG-CoA to mevalonate (cholesterol precursor)
DECREASES LDL, some decrease in TG, some increase in HDL
cholestyramine
bile acid resin
prevents intestinal reabsorption of bile acids; liver must use cholesterol to make more
decreases LDL, slight increase in HDL, slight increase in TG (not good)
colestipol
bile acid resin
prevents intestinal reabsorption of bile acids; liver must use cholesterol to make more
decreases LDL, slight increase in HDL, slight increase in TG (not good)
colesevelam
bile acid resin
prevents intestinal reabsorption of bile acids; liver must use cholesterol to make more
decreases LDL, slight increase in HDL, slight increase in TG (not good)
ezetimibe
prevents cholesterol absorption at the small intestine brush border
decreases LDL
gemifibrozil
fibrate
upregulates LPL–> increased triglyceride clearance
activates PPARalpha to induce HDL synthesis
DECREASES TGs, some decrease in LDL, some increase in HDL
clofibrate
fibrate
upregulates LPL–> increased triglyceride clearance
activates PPARalpha to induce HDL synthesis
DECREASES TGs, some decrease in LDL, some increase in HDL
benzafibrate
fibrate
upregulates LPL–> increased triglyceride clearance
activates PPARalpha to induce HDL synthesis
DECREASES TGs, some decrease in LDL, some increase in HDL
fenofibrate
fibrate
upregulates LPL–> increased triglyceride clearance
activates PPARalpha to induce HDL synthesis
DECREASES TGs, some decrease in LDL, some increase in HDL
Niacin (Vit b3)
inhibits lipolysis in adipose tissue; reduces hepatic VLDL synthesis
decreases LDL, increases HDL, slight decrease in TG
digoxin
cardiac glycoside
direct inhibitition of Na/K ATPase –> indirect inhibition of the Na/Ca exchanger–> increased intracellular calcium–> positive inotropy
stimulates vagus nerve–> decreased heart rate
quinidine
sodium channel blockers (class Ia)
slow or block conduction (especially in depolarized cells); decreases slope of phase 0 depolarization
state dependent (selectively depress tissue that is frequently depolarized– eg tachycardia)
increase AP duration, increase effective refractory period in ventricular action, prolong QT interval
procainamide
sodium channel blockers (class Ia)
slow or block conduction (especially in depolarized cells); decreases slope of phase 0 depolarization
state dependent (selectively depress tissue that is frequently depolarized– eg tachycardia)
increase AP duration, increase effective refractory period in ventricular action, prolong QT interval
disopyramide
sodium channel blockers (class Ia)
slow or block conduction (especially in depolarized cells); decreases slope of phase 0 depolarization
state dependent (selectively depress tissue that is frequently depolarized– eg tachycardia)
increase AP duration, increase effective refractory period in ventricular action, prolong QT interval
lidocaine
sodium channel blockers (class Ib)
slow or block conduction (especially in depolarized cells); decreases slope of phase 0 depolarization
state dependent (selectively depress tissue that is frequently depolarized– eg tachycardia)
decreases AP duration, preferentially affects ischemic or depolarized purkinje and ventricular tissue
mexiletine
sodium channel blockers (class Ib)
slow or block conduction (especially in depolarized cells); decreases slope of phase 0 depolarization
state dependent (selectively depress tissue that is frequently depolarized– eg tachycardia)
decreases AP duration, preferentially affects ischemic or depolarized purkinje and ventricular tissue
flecainide
sodium channel blockers (class IC)
slow or block conduction (especially in depolarized cells); decreases slope of phase 0 depolarization
state dependent (selectively depress tissue that is frequently depolarized– eg tachycardia)
significantly prolongs effective refractory period in AV node and accessory bypass tracts; no effect in Purkinje or ventricular tissue; minimal effect on AP duration
propafenone
sodium channel blockers (class IC)
slow or block conduction (especially in depolarized cells); decreases slope of phase 0 depolarization
state dependent (selectively depress tissue that is frequently depolarized– eg tachycardia)
significantly prolongs effective refractory period in AV node and accessory bypass tracts; no effect in Purkinje or ventricular tissue; minimal effect on AP duration
metoprolol
beta blockers (class II)
decrease SA and AV nodal activity by decreasing cAMP and decreasing calcium currents; suppress abnormal pacemakers by decreasing the slope of phase 4
AV node particularly sensitive; increases PR interval
propanolol
beta blockers (class II)
decrease SA and AV nodal activity by decreasing cAMP and decreasing calcium currents; suppress abnormal pacemakers by decreasing the slope of phase 4
AV node particularly sensitive; increases PR interval
esmolol
beta blockers (class II)
decrease SA and AV nodal activity by decreasing cAMP and decreasing calcium currents; suppress abnormal pacemakers by decreasing the slope of phase 4
AV node particularly sensitive; increases PR interval
VERY SHORT ACTING
atenolol
beta blockers (class II)
decrease SA and AV nodal activity by decreasing cAMP and decreasing calcium currents; suppress abnormal pacemakers by decreasing the slope of phase 4
AV node particularly sensitive; increases PR interval
timolol
beta blockers (class II)
decrease SA and AV nodal activity by decreasing cAMP and decreasing calcium currents; suppress abnormal pacemakers by decreasing the slope of phase 4
AV node particularly sensitive; increases PR interval
carvedilol
beta blockers (class II)
decrease SA and AV nodal activity by decreasing cAMP and decreasing calcium currents; suppress abnormal pacemakers by decreasing the slope of phase 4
AV node particularly sensitive; increases PR interval
amiodarone
potassium channel blockers (class III)
increases AP duration, increases refractory period, and increases QT interval
ibutilide
potassium channel blockers (class III)
increases AP duration, increases refractory period, and increases QT interval
dofetilide
potassium channel blockers (class III)
increases AP duration, increases refractory period, and increases QT interval
sotalol
potassium channel blockers (class III)
increases AP duration, increases refractory period, and increases QT interval
adenosine
increased K+ efflux from cells–> hyperpolarizes cell–> decreases calcium influx
dihydropyridines except nimodipine
hypertension, angina (inc. Prinzmetal), Raynaud phenomenon
nimodipine
subarachnoid hemorrhage (prevents cerebral vasospasm)
clevidipine
hypertensive urgency or emergency
verapamil
hypertension, angina, atrial fibrillation/flutter
prevention of nodal arrhythmias (SVT), rate control in a fib
diltiazem
hypertension, angina, atrial fibrillation/flutter
prevention of nodal arrhythmias (SVT), rate control in a fib
hydralazine
severe, acute HTN, heart failure
safe to use in pregnancy
nitroprusside
hypertensive emergency
fenoldopam
hypertensive emergency
nitrates (nitroglycerin, isosorbide dinitrate, isosorbide mononitrate)
angina, acute coronary artery syndrome, pulmonary edema
lovastatin, simvastatin, etc
lipid lowering agent
cholestyramine
lipid lowering agent
colestipol
lipid lowering agent
colesevelam
lipid lowering agent
ezetimibe
lipid lowering agent
gemifibrozil
lipid lowering agent
clofibrate
lipid lowering agent
benzafibrate
lipid lowering agent
fenofibrate
lipid lowering agent
Niacin (Vit b3)
hyperlipidemia
digoxin
heart failure (increased contractility), a fib (decreased conduction at AV note, depression of SA node)
quinidine
atrial and ventricular arrhythmias; reentrant and ectopic SVT and VT
procainamide
atrial and ventricular arrhythmias; reentrant and ectopic SVT and VT
disopyramide
atrial and ventricular arrhythmias; reentrant and ectopic SVT and VT
lidocaine
acute ventricular arrhythmias (especially post-MI), digitalis-induced arrhythmias
mexiletine
acute ventricular arrhythmias (especially post-MI), digitalis-induced arrhythmias
flecainide
SVT (inc. a fib)
propafenone
SVT (inc. a fib)
metoprolol
SVT, ventricular rate control for afib and aflutter
propanolol
SVT, ventricular rate control for afib and aflutter
esmolol
SVT, ventricular rate control for afib and aflutter
atenolol
SVT, ventricular rate control for afib and aflutter
timolol
SVT, ventricular rate control for afib and aflutter
carvedilol
SVT, ventricular rate control for afib and aflutter
amiodarone
a fib, a flutter, ventricular tachycardia
ibutilide
a fib, a flutter
dofetilide
a fib, a flutter
sotalol
a fib, a flutter, ventricular tachycardia
adenosine
diagnosis and stopping SVT
very short acting
magnesium
torsades de points and digoxin toxicity
with which conditions do you have a failure to agglutinate with ristocetin assay?
vWD and Bernard-Soulier syndrome
t(8;14)
Burkitt Lymphoma
t(9;22)
CML
t(11;14)
mantle cell lymphoma
t(14;18)
follicular lymphoma
t(15;17)
M3 type of AML
Medication
Effect on fetus
ACE inhibitors
renal damage
alkylating agents
absence of digits, multiple anomalies
aminoglycosides
CN VIII toxicity (deafness)
carbamazepine
facial dysmorphism, developmental delay, neural tube defects, phalanx/fingernail hypoplasia
Diethylstilbestrol (DES)
vaginal clear cell adenocarcinoma, congenital mullerian anomalies
folate antagonists
neural tube defects
isoretinoin
multiple birth defects
lithium
ebstein anomaly (atrialized RV)
methimazole
aplasia cutis congenita
phenytoin
fetal hydantoin syndrome- cleft palate, cardiac defects, phalanx/fingernail hypoplasia
tetracyclines
discolored teeth
thalidomide
limb defects (flipper limbs)
valproate
inhibition of maternal folate absorption (–> neural tube defects)
warfarin
bone deformities, fetal hemorrhage, abortion, ophthalmologic abnormalities
alcohol
FAS
cocaine
abnormal fetal growth, fetal addiction, placental abruption
smoking
low birth weight, preterm labor, placental problems, IUGR, ADHD
iodine (lack or excess)
congenital goiter or hypothyroidism
maternal diabetes
caudal regression syndrome, congenital heart defects, neural tube defects
vitamin A excess
high risk for SAB and birth defects
x-rays
microcephaly, intellectual disability
vagina
stratified squamous epithelium, non-keratinized
ectocervix
stratified squamous epithelium, non-keratinized
transformation zone
squamocolumnar junction (MC area for cervical cancer)
endocervix
simple columnar epithelium
uterus
simple pseudostratified columnar epithelium; long tubular glands in follicular phase and coiled glands in the luteal phase
fallopian tube
simple columnar epithelium, ciliated; peg cells secrete nutrients
ovary outer surface
simple cuboidal epithelium (aka germinal epithelium)
demeclocycline
ADH antagonist
somatostatin (octreotide)
basically stops the secretion of a bunch of hormones; reduces acid secretion from parietal cells, suppresses release of gastrin and CCK, inhibits release of glucagon
canagliflozin (SGLT-2 inhibitor)
block reabsorption of glucose in the proximal collecting tubule
conivaptan, tolvaptan (ADH antagonist)
blocks action of ADH at the V2 receptor
methimazole
blocks thyroid peroxidase–> inhibits oxidation of iodide and coupling of iodine–> inhibition of thyroid hormone synthesis
propylthiouracil
blocks thyroid peroxidase–> inhibits oxidation of iodide and coupling of iodine–> inhibition of thyroid hormone synthesis
also blocks 5’-deiodase which decreases peripheral conversion of T4 to T3
chlorpropamide (1st gen sulfonylurea)
closes K+ channel in the beta cell–> cell depolarization–> calcium influx–> insulin release
tolbutamide (1st gen sulfonylurea)
closes K+ channel in the beta cell–> cell depolarization–> calcium influx–> insulin release
glimepiride (2nd gen sulfoylurea)
closes K+ channel in the beta cell–> cell depolarization–> calcium influx–> insulin release
glipizide (2nd gen sulfoylurea)
closes K+ channel in the beta cell–> cell depolarization–> calcium influx–> insulin release
glyburide (2nd gen sulfoylurea)
closes K+ channel in the beta cell–> cell depolarization–> calcium influx–> insulin release
pramlintide (amylin analogs)
decreased gastric emptying, decreased glucagon
Metformin (biguanide)
decreases gluconeogenesis, increases glycolysis, increases peripheral glucose uptake (increases insulin sensitivity)
pioglitazone, rosiglitazone (glitazones, thiazolidinediones)
increased insulin sensitivity in peripheral tissue (via binding to PPAR-y which regulates fatty acid storage and glucose metabolism)
exenatide (GLP-1 analog)
increases insulin release and decreases glucagon release
liraglutide (GLP-1 analog)
increases insulin release and decreases glucagon release
linagliptin (DPP-4 inhibitor)
increases insulin release and decreases glucagon release
saxagliptin (DPP-4 inhibitor)
increases insulin release and decreases glucagon release
sitagliptin (DPP-4 inhibitor)
increases insulin release and decreases glucagon release
acarbose (alpha-glucosidase inhibitor)
inhibits intestinal bursh border alpha-glucosidases (which normally breaks down starches into glucose)–> delayed carbohydrate hydrolysis and glucose absorption–> decreased postprandial hyperglycemia
glucocorticoids
interactions with glucocorticoid response elements, inhibition of phospholipase A2, inhibition of transcription factors such as NF-KB
cinacalcet
sensitizes calcium sensing receptor (CaSR) in parathyroid gland to circulating calcium–> decreased PTH release
Microcytic Anemias
Iron deficiency, anemia of chronic disease, thalassemias, lead poisoning, sideroblastic anemia
normocytic, non-hemolytic anemia (nml to low retic count)
anemia of chronic disease, aplastic anemia, chronic kidney disease, early iron deficiency anemia, pure red cell aplasia
normocytic, hemolytic anemia (increased retic count)- INTRINSIC
hereditary spherocytosis, G6PD deficiency, pyruvate kinase deficiency, HbC defect, paroxysmal nocturnal hemoglobinuria, sickle cell anemia
normocytic, hemolytic anemia (increased retic count)- EXTRINSIC
autoimmune, microangiopathic, macroangiopathic, infections
macrocytic, megaloblastic
folate deficiency, B12 deficiency, orotic aciduria
macrocytic, non-megaloblastic
liver disease, alcoholism, reticulocytosis
RBC casts are seen in which 2 conditions?
glomerulonephritis, malignant hypertension
WBC cast are seen in which 3 conditions?
tubulointerstitial inflammation, acute pyelonephritis, transplant rejection
fatty casts (oval fat bodies) are seen in which condition?
nephrotic syndrome
granular (muddy brown) casts are seen in which condition?
acute tubular necrosis
waxy casts are seen in which condition?
end-stage renal disease/ chronich renal failure
hyaline casts are seen in which condition?
nonspecific, can be normal finding, often seen in concentrated urine samples
what casts are found in glomerulonephritis?
RBC casts
what casts are found in malignant hypertension?
RBC casts
what casts are found in tubulointerstitial inflammation?
WBC casts
what casts are found in acute pyelonephritis?
WBC casts
what casts are found in transplant rejection?
WBC casts
what casts are found in nephrotic syndrome?
fatty casts
what casts are found in acute tubular necrosis?
granular, muddy brown casts
what casts are found in ESRD?
waxy casts
arginine
nitric oxide
arginine+ aspartate
urea
glycine+ succinyl coa
heme
glycine + arginine + sam
creatinine
glutamate
gaba
gluatmate
glutathione
glutamate + aspartate
pyrimidines
glutamate + aspartate + glycine
pryimidines
histidine
histamine
phenylalanine
tyrosine (–>DOPA–> DOPAMINE)
tryptophan
serotonin (–> melatonin)
tryptophan
niacin
tyrosine
thyroxine, melanin
acanthocyte (spur cell)
liver disease, abetalipoproteinemia
basophilic stippling
lead disease
degmacyte (bite cell)
G6PD deficiency
elliptocyte
heretidary elliptocytosis
macro-ovalocyte
megaloblastic anemia
ringed sideroblast
sideroblastic anemia (excess iron in mitochondria=pathologic)
shistocyte (helmet cell)
DIC, TTP/HUS, HELLP, mechanical hemolysis
sickle cell
sickle cell anemia
spherocyte
hereditary spherocytosis, drug and infection induced hemolytic anemia
dacrocyte (teardrop cell)
bone marrow infiltration (myelofibrosis)
target cell
HbC disease, asplenia, liver disease, thalassemia (HALT)
heinz bodies
preciptiation of Hb–> leads to bite cells; see in G6PD deficiency and also alpha thalassemia
Howell-Jolly bodies
basophilic nuclear remnants unable to be cleared by spenic macrophages; seen in functional asplenia or asplenia
S-100 is a marker for?
melanoma, langerhans cell histiocytosis (mesodermal origin)
What causes methemoglobin
nitrates, benzocaine
psammoma bodies?
mesothelioma, ovarian serous cystadenocarcinomas, meningiomas, papillary thyroid carcinoma
what cases methemoglobin?
nitrites, benzocaine
what kind of shift does carboxyhemoglobin cause?
LEFT SHIFT! (decreased O2 binding capacity)
what is caplan syndrome
pneumoconiosis w/ intrapulmonary nodules and RA