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568 Cards in this Set
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- 3rd side (hint)
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What is sensitivity?
|
probabilty that a test detects a disease when disease is present. TP/(TP+FN)
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behavioral science
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What is specificity?
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probability that a disease non-disease when disease is absent. TN/(TN+FP)
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behavioral science
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100% sensitivity means what?
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low false negative rate, good for screening disease with low prevelance
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behavioral science
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100% specificity means what?
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low flase positive rate, good for confirmatory test after a positive screening test.
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behavioral science
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What is case-control study? what does it measure?
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compares group of people with a disease to a group without the disease. Measures odds ratio.
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behavioral science
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What is a cohort study?What does it measure?
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compares a group with an exposure or risk to a group without it. Measures relative risk.
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behavioral science
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What is a cross-sectional study? what does it measure?
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collects data from a group to assess frequency of a disease in a population. Measures prevalence.
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behavioral science
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What is the difference between a double and triple blinded study?
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double = patients and doctors don't know, triple = even researchers analyzing data don't know
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behavioral science
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what does a phase I trial do?
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small number of healthy people, assess safety,toxicity, and pharmokinetics
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behavioral science
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what does a phase II trial do?
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small number of people with the disease studied; assess efficacy, dosing, and adverse effects
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behavioral science
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what do phase III trials do?
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large, randomly assigned groups. compares standard of care to new treatment.
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behavioral science
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what do phase IV trials do?
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postmarketing surviellance, looks for longterm adverse events.
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behavioral science
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What is positive predictive value? (PPV)
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proportion of positive tests that are a true positive. TP/(TP+FP)
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behavioral science
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What is negative predicitive value?
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proportion of negative tests that are a true negative. TN/(FN+TN)
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behavioral science
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contrast prevalence to incidence
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incidence = new cases, prevalence = all currents cases
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behavioral science
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What is an odds ratio?
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used in case-control studies. odds that a group with a disease was exposed to a risk.
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behavioral science
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What is relative risk?
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used in cohort studies. risk of developing a disease if exposed to a risk.
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behavioral science
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what is attrutitable risk?
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proportion of disease occurences cause by an exposure.
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behavioral science
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what is absolute risk reduction (ARR)?
|
absolute reduction in risk between treatment group and a control group.
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behavioral science
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How is number needed to treat calculated?
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number of patients needed to treat for 1 patient to get a benefit. 1/ARR
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behavioral science
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How is number to harm calculared?
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number of patients needed tobe exposed to a risk in order to get it. 1/attributable risk.
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behavioral science
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constract precision vs. accuracy.
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reproducability vs trueness of result
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behavioral science
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What does random error cause?
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reduces precision of a test
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behavioral science
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How do you decrese standard deviation?
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by increasing precision.
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behavioral science
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What does systematic error cause?
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reduces accuracy in a test.
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behavioral science
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What is selection bias?
|
nonrandom assignment to a group.
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behavioral science
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what is recall bias?
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knowledge of presence of a disease alters recall of subjects; common in retrospective.
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behavioral science
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what is sampling bias
|
subjects are not representative of the general population - is a selection bias
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behavioral science
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what is late-look bias?
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information gathered at inapporiate time
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behavioral science
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what is procedure bias?
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subjects in different groups are not treated the same
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behavioral science
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what is confounding bias?
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occurs when a factor is related to both exposure and outcome
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behavioral science
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what is lead-time bias?
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early detection confused with increased survival.
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behavioral science
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what is observer-expectancy effect?
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when researchers belief in the efficacy of a treatment alters treatment changes
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behavioral science
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what is hawthorne effect?
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group being studied changes behavior because they know they are being studied.
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behavioral science
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5 ways bias can be reduced:
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1.blind studies. 2.placebo groups. 3.crossover studies. 4.randomization limits selection and confounding bias 5. matching to reduce confoudning bias.
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behavioral science
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what is postive skew
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mound to the left, tail to the right mean>median>mode.
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behavioral science
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What is negative skew?
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mound to the right, tail to the left. mean<median<mode.
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behavioral science
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What is type I error?
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stating there is an effect when there isn't one
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behavioral science
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What is type II error?
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stating there is not an effect when one does exist (to fail to reject the null hypothesis)
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behavioral science
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What is statistical power and how do you increase it?
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probability of rejecting null hypothesis when it is false. increases with: larger sample size, large expected effect size, increased precision of measurement.
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behavioral science
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What is a confidence interval?
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range of values in which a specificed probability of means would expected to fall.
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behavioral science
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when to use t-test?
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comparing difference of means in 2 groups.
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behavioral science
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when to use ANOVA
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check differences of means in 3 or more groups.
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behavioral science
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When to use Chi-square test?
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check differences in 2 of more percentages or proportions, NOT MEANS.
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behavioral science
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what is pearson's correlation coefficient?
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r is between -1 and +1. closer to 1 the stronger the linear correlation between 2 variables.
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behavioral science
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compare primary, secondary, and tertiary prevention.
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PDR Prevent(vaccines), Detect(pap smear), Reduce disability(chemotherapy)
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behavioral science
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Medicare and medicaid are for what groups?
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medicarE = elderly, medicaiD = destitute.
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behavioral science
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What is apgar score?
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done at 1min and 5min. appearance, pulse, grimace, activity, respiration. >7 is good, <4 means resuscitate!
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behavioral science
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What is a low birth weight?
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<2500g. increased risk or SIDS and increased overall mortality.
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behavioral science
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Give developmental milestones birth-3mo(motor,social,verbal)
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rooting reflex,head up,moro reflex gone;smile;orient to voice.
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behavioral science
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Give developmental milestones b7-9mo(motor,social,verbal)
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sits alone,crawl,transfer toys in hand;stranger anxiety;responds to name, instructions,peekaboo.
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behavioral science
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Give developmental milestones 12-15mo(motor,social,verbal)
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climb stairs, stack blocks by agex3 blocks;rapprochment of mom;200 words and 2 word phrases by 2
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behavioral science
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Give developmental milestones 24-36mo(motor,social,verbal)
|
feeds self,kick ball;core gender identity,parallel play;pee at age 3
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behavioral science
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Give developmental milestones 3yr(motor,social,verbal)
|
ride tricycle,copy circle;spends part of a day away from mom;900 words and complete sentences
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behavioral science
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Give developmental milestones 4yr(motor,social,verbal)
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uses zippers,grooms self,can hop on 1 foot;imaginary friend,cooperative play;can tell detailed story
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behavioral science
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what is rooting reflex
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turn head to stimulus and make sucking face for nipple
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behavioral science
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what is moro reflex
|
kid startled by being dropped
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behavioral science
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what is babinski sign
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tickle foot, toe goes up. not normal after age 2
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behavioral science
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give BMI formula
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weight in kg/(height in meters)^2
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behavioral science
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when does grief become patholgoic
|
after 1 year.
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behavioral science
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What is orotic aciduria(physiology,findings,tx)
|
inability to convert orotic acid to UMP due to defect in UMP synthetase; increased orotic acid in urine,megaloblastic anemia that isn't improved by B12, failure to thrive,no hyperammonemia;oral uridine administration.
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biochem
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What is adenosine deaminase deficiency(give physiology)
|
Excess ATP and dATP via inhibition of ribonucleotide reductase->prevents dna synthesis and decrease lymphocyte count causing SCID.
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biochem
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What is Lesch-Nyan syndrome(physiology,findings)
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defective purine salvage pathway due to absence of HGPRT; excess uric acid leads to retardation,self-mutilation,hyperuricemia,gout,choresoathetosis.
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biochem
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Mutation in ataxia telangiestica
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nonhomologous end joining, which repairs dsDNA breaks.
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biochem
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mutaiton in xeroderma pigmentosum
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nucleotide excision repair, which releases damaged bases
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biochem
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What cell types are permanent
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neurons, skeletal and cardiac muscle, RBCs
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biochem
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what cells types are stable(quiescent)
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hepatocytes,lymphocytes
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biochem
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what cell types are labile?
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bone marrow, gut epithelium,skin,hair follicles,germ cells
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biochem
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I-cell disease(physiology,findings)
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inclusion cell disease, failure of addition of mannose-6-phosphate to lysosome proteins which leads to lysosomal storage disease(proteins never added to lysosome);coarse face,clouded cornea,high plasma levels of lysosomal enzymes.
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biochem
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Chediak-Higashi syndrome(physiology,findings)
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mutation in lysosomal trafficking regulator gene (LYST), microtubule sorting does not occur;recurrent pyogenic infections,partial albinism,peripheral neuropathy.
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biochem
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vimentin stains:
|
connective tissue
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biochem
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desmin stains:
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muscle
|
biochem
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cytokeratin stains:
|
epithelial cells
|
biochem
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GFAP stains
|
neuroglia
|
biochem
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neurofilaments stain
|
neurons
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biochem
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type I collagen(found in,defective in:)
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bone,skin,tendon,dentin,cornea,late wound repair;defective in osteogenesis imperfecta.
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biochem
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type II collagen(found in)
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Cartilage(hyaline),vitreous body,nucleus pulposus)
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biochem
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type III collagen(found in, defective in)
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reticuin,skin,blood vessels,uterus,granulation tissue,fetal tissue;Ehler's danlos
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biochem
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Type IV collagen(found in, defective in)
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basement membrance and basal lamina;alport sydrome
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biochem
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Marfans syndrome is a defect of:
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Fibrillin(found in elastin)
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biochem
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Prader-Willi syndrome(genetics,findings)
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paternal allele on chromosome 15 is not expressed;mental retardation,hyperphagia,obesity,hypogonadism,hypotonia
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biochem
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Angelman's syndrome(genetics,findings)
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Inactivation of mother's allele on chromosome 15; mental retardation,seizures,ataxia,inappropriate laughter
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biochem
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Achondroplasia(dominance,physiology,findings)
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Autosomal dominant. defect in fibroblast growth factor(FGF)receptor 3.;Dwarfism,short limbs,larger head but normal trunk.assoc with advanced paternal age.
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biochem
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Autosomal-dominant polycycstic kidney disease(ADPKD)(dominance,physiology,findings)
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Autosomal dominant;mutation in PKD1, chromosome 16;bilat. massively enlarged kidneys, multiple huge cysts. assoc w/polycystic liver dx,berry anerusyms,mitral valve prolapse.
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biochem
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what diseases are associated with ADPKD?
|
polycystic liver disease, berry aneurysms, mitral valve prolapse.
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biochem
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Familial adenomatous polyposis(dominance,physiology,findings)
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autosomal dominant;mutation on APC gene. chromosome 5;colon covered in polyps after puberty.
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biochem
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Hereditary hemorrhagic telangiectasia(osler-weber-rendu syndrome)(dominance,physiology,findings)
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autosomal dominant;inherited disorder of blood vessels;telangiectasia, recurrent epistaxis, AVMS, skin discolorations.
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biochem
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Hereditary spherocytosis(dominance,physiology,findings)
|
autosomal dominance;spheroids due to spectrin or ankyrin defects;hemolytic anemia, increased MCHC, need spleenectomy to cure.
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biochem
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Huntington's disease(dominance,physiology,findings)
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autosomal dominant;CAG trinucleotide repeat gene on chromosome 4;depression,caudate nucleus atrophy,chorioform movements,decreased levels of GABA and Ach in the brain.
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biochem
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Neurofibromatosis type 1(von recklinghausen disease)(dominance,physiology,findings)
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autosomal dominant;mutation in long arm of chromosome 17;cafe-au-lait spots,neural tumors,lisch nodules, optic gliomas.
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biochem
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neurofibromatosis type 2(dominance,physiology,findings)
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autosomal domaint;NF2 gene on chromosome 22;bilateral acoustic schwannomas, juvenile cataracts
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biochem
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Tuberous sclerosis(dominance,findings)
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autosomal dominant;facial lesions,hypopigmented ash leaf spots,cotical and retinal hamartomas,seizures,cardiac rhabdomyomas,increased incidence of astrocytomas.
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biochem
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von Hippel-Lindau(dominance,physiology,findings)
|
autosomal dominant;deletion of VHL gene(a suppressor) on chromosome 3 which results in constitutive expression of HIF and increased angiogenic factos;hemangioblastomas,bilateral multiple renal cell carcinomas.
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biochem
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|
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Cystic fibrosis(dominance,physiology,findings)
|
autosomal-recessive;defect in CFTR on chromosome 7. CFTR is a calcium channel;meconium ileus in newborns,bronchiectasis,pancreatic insufficiency,nasal polyps,intertility in males due to missing vas deferns.
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biochem
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what lab is diagnostic for cystic fibrosis?
|
increased calcium concentration in sweat (calcium channel can't resorb in skin. Note: in lungs this channel is supposed to EXCRETE calcium).
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biochem
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Fragile-X syndrome(dominance,physiology,findings)
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X-linked;defect in methylation of FMRI gene,is a CGG trinucleotide repeat;mental retardation,macroorchidism,long face and jaw,everted ears,autism, mitral valve prolapse.
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biochem
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Duchenne's dystrophy(dominance,physiology,findings)
|
X-linked frameshift;deletion of dystrophin gene leads to accelerated muscle breakdown;pseudohypertophy of calf,pelvic and girdle muscle weakness at first,onset before 5, use gowers manuever.
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biochem
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Why do mutaitons in dystrophin gene occur so often?
|
longest gene in the human genome, anchors muscle fibers.
|
biochem
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What are the pregancy quad screen results for down syndrome?
|
decrease a-fetoprotein,estirol. increased B-HcG, inhibin A.
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biochem
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What are the pregancy quad screen results for edwards syndrome?
|
decreased: a-fetoprotein,BHcg, estriol. normal: inhibin A.
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biochem
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What are the pregnancy quad screens for Patau's syndrome?
|
decreased: B-HcG, PAPPa and increased:Nuchal translucency.
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biochem
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Cri-du-chat syndrome(dominance,physiology,findings)
|
congenital microdeletion of short arm of chromosome 5;microcephaly,mental retardation,mewing sounds,epicanthal folds,VSD.
|
biochem
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|
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Williams syndrome(dominance,physiology,findings)
|
congenital microdeletion of long arm of chromosome 7,region deleted contains elastin gene;elfin facies,intellectual disability,extreme friendliness.
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biochem
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What are the fat soluble vitamins?
|
ADEK. dependent on ileum and pancreas, tend to accumulate in fat more.
|
biochem
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vitamin A(function, defiency,excess)
|
visual pigments(retinal),essential for epithielial ceel differentiation,prevents squamous metaplasia, used in measles and AML type M3 tx; night blindness, dry skin;arthralgias,fatigue,alopecia,teratogenic!
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biochem
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Vitamin B1(thiamin)(function, defiency)
|
thiamine pyrophosphotase part of: pyruvate DH,A-ketoglutartate DH,trasketolase,branched-amino acid DH; defiency causes wernicke-korsakoff, berberi, low ATP.
|
biochem
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|
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Wernicke-Korsakoff syndrome(cause, findings)
|
B1(thiamin) defienceincy;confusion, opthalmoplegia,ataxia,confabulation,permanent memory loss,damage to medial dorsal nucleus of thalamus, mammary bodies.
|
biochem
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|
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Dry beriberi(cause, findings)
|
low B1(thiamin); polyneuritis, symmetrical muscle wasting
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biochem
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Wet beriberi(cause,findings)
|
high output cardiac failure(dilated cardiomyopathy), edema.
|
biochem
|
|
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vitamen B2(riboflavin)(function, defiency)
|
cofactor in ox/redux reactions, make FAD and FMN; Cheilosis(inflammation and scaling of lips, corner of mouth), corneal vascularization (2C's of B2)
|
biochem
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|
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vitamin B3(niacin)(function, defiency,excess)
|
made from tryptophan, makes NAD. synthesis requires B6!;Glossitis,pellagra(diarrhea,dementia,dermatitis); excess = facial flushing.
|
biochem
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|
|
vitamin B3 deficiency can be caused by what primary things?
|
1. hartnup disease (decreased tryptophan absorption) 2.Malignant carcinoid syndrome(increased tryptophan metabolism) 3. INH (decrease B6). All lead to pellagra.
|
biochem
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|
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Vitamin B5(pantothenate)(function, defiency)
|
Essential part of CoA and fatty acid synthase; dermatitis,enteritis,alopecia,adrenal insufficiency.
|
biochem
|
|
|
vitamin B6(pyridoxine)(function, defiency)
|
converted to pyridoxal phosphate which transaminates ALT and AST,synthesizes heme,niacin,histamine,serotonin,epinephrine,norepi, GABA.;convulsions,hyperirratability,peripheral neuropathy,sideroblastic anemia due to increased heme production.
|
biochem
|
|
|
Vitamin B7(biotin)(function, defiency)
|
cofactor for carboxylation enyzmes(pyruvate carboxylase,acetyl-Coa carboxylase,Propionyl-CoA carboxylase.;very rare, dermatitis,alopecia,enterisis. can be caused by antibiotic use or raw egg overconsumption.
|
biochem
|
|
|
Vitamin B9(folic acid)(function, defiency)
|
converted to tetrahydrofolate, makes nitrogenous bases for RNA and DNA; small pool in liver, macrocytic,megaloblastic anemia, common in alcoholism and pregnancy.
|
biochem
|
|
|
vitamin B12(cobalamin)(function, defiency)
|
cofactor for homocysteine methytransferase and methylmalonyl-CoA mutase, very large reserve pool in liver that takes years to use; macrocytic,megalobastic anemia, hypersegmented PMNs,neurologic symptons.
|
biochem
|
|
|
What are the two vitamin defiency causes of macrocytic,megalolastic anemia? Differences?
|
B9(folic acid) -> no neurologic symptoms. most common type, very small reserve pool. common in pregnancy and alcoholism. B12(cobalamin)has neuro symptoms. HUGE reserve pool in liver.
|
biochem
|
|
|
Vitamin C(function, defiency,excess)
|
facilitates Fe absorption, needed to make collagen, also needed to convert dopamine to NE; scurvy-swollen gums,brusing,hemearthrosis,weak immune system;nausea,vomitting,sleep problems, increased risk of iron toxicity.
|
biochem
|
|
|
Vitamin D(function, defiency,excess)
|
increased intestinal absorption of calcium and phosphate, increased bone minerlization; Rickets in kids, osteomalacia in adults, hypocalcemic tetany; hypercalcemia,hypercalciuria,loss of appetite, seen in sarcoidosis.
|
biochem
|
|
|
Vitamin E(function, defiency,excess)
|
antioxidant, protects erthrocytes and membranes from free radical damage; increased fragility of erythrocytes, posterior column and spinocerebellar tract demyelination.
|
biochem
|
|
|
Vitmain K(function, defiency,excess)
|
Catalyzes gamma-carboxylation of glutamic acid residues on clotting factors. needed for 2,7,9,10,C and S.; neonatal hemorrhage but normal bleeding time, need to give injection to newborns.
|
biochem
|
|
|
Zinc(function, defiency)
|
essential for 100+ enzymes;delayed wound healing,decreased adult hair,dysgeudia, anosmia.
|
biochem
|
|
|
Nitric oxide is made from what amino acid?
|
arginine
|
biochem
|
|
|
Urea is made from what amino acids?
|
arginine and aspartate
|
biochem
|
|
|
Heme is made from what amino acid?
|
glycine and succinyl CoA
|
biochem
|
|
|
Creatine is made from what amino acid?
|
glycine + arginine + SAM
|
biochem
|
|
|
GABA is made from what amino acid?
|
glutamate
|
biochem
|
|
|
glutathione is made from what amino acid?
|
glutamate
|
biochem
|
|
|
pyrimidines are made from what amino acids?
|
glutamate and aspartate
|
biochem
|
|
|
purines are made from what amino acids?
|
glutamate + aspartate + glycine
|
biochem
|
|
|
histamine is made from what amino acid?
|
histidine
|
biochem
|
|
|
describe dopamine synthesis by reactants
|
phenylalanine->tyrosine->DOPA->dopamine
|
biochem
|
|
|
describe melatonin synthesis by reactants
|
tryptophan->serotonin->melatonin
|
biochem
|
|
|
niacin is made from what amino acid?
|
tryptophan
|
biochem
|
|
|
thyroxine and melanin are made from what amino acid?
|
tyrosine
|
biochem
|
|
|
what test can be done to diagnose chronic granulamtous disease?
|
blue pigment DOESN'T form after adding nitroblue tetrazolium to patient's neutrophils. Does form = no disease.
|
biochem
|
|
|
Coldaggulintins are seen in what organism. They are responsible for what?
|
M. Pneumoniae. They lyse red blood cells leading to anemia.
|
micro
|
|
|
What are the trinucleotide repeats in Fragile X syndrome?
|
CGG
|
biochem
|
|
|
What are the trinucleotide repeats in Friedreich's Ataxia?
|
GAA
|
biochem
|
|
|
what are the trinucleotide repeats in huntington's disease?
|
CAG
|
biochem
|
|
|
What are the trinucleotide repeats in myotonic dystrophy?
|
CTG
|
biochem
|
|
|
What is the most common leathal,genetic disease in white populations?
|
cystic fibrosis
|
biochem
|
|
|
What are the two 22q11 deletion syndromes?
|
1. DiGeorge - thymic, parathyroid, and cardiac defects. 2. Velocardiofacial syndrome - palate,facial, and cardiac defects.
|
biochem
|
|
|
Pyruvate dehydrogenase complex deficiency(physioogy, findings, treatment)
|
X-linked mutation in gene for E1-a-subunit of pyruvate DH, causes backup of pyruvate and alanine, resulting in lactic acidosis; neurologic defects in infant;give Lysine and leucine because they are ketogenically metabolized.
|
biochem
|
|
|
Essential fructosuria(physiology,findings)
|
defect in fructosuria, autosomal recessive;fructose is high in blood and urine but is a benign disease/
|
biochem
|
|
|
fructose intolerance(physiology, findings, treatment)
|
autsomal recessive problem in Aldolase B, F-1-P accumulates, causing decrease in phosphate and then a decrease in glyconeolysis and gluconeogenesis; hypoglycemia, jaundice, cirrhosis; decrease intake of fructose and sucrose.
|
biochem
|
|
|
Galastose deficiency(physiology,treatment)
|
problem in galactokinse, galactitol accumulates if galactose present in diet. autsomal recessive;galactose in blood and urine, infantile cataracts,very mild disease.
|
biochem
|
|
|
Classic galactosemia(physiology, findings, treatment)
|
absense of galactose-1-phosphate uridyltransferase, autsomal recessive, accumulation of toxic galactitol; failure thrive, hepatomegaly, infantile cataracts, mental retardation; exclude galactose and lactose from diet.
|
biochem
|
|
|
Which tissues are at risk for sorbitol damage? how does this damage occur?
|
schweann cells, retina, kidnets. They contain low levels of sorbitol dehydrogenase. sorbitol is osmotically active, causing swelling and damage.
|
biochem
|
|
|
ornithine transcarboxylase deficiency(physiology, findings)
|
x-linked recessive, can't eliminate ammonia. Excess caramoyl phosphate is converted into orotic acid; increased orotic acid in blood and urine, decreased BUN, ammonia overdose.
|
biochem
|
|
|
Phenylketonura(physiology, findings, treatment)
|
Due to decrease in phenylalanine hydroxylase or tetrahydrobiopterin, making tyrosine essential; increased PKU in urine, mental retardation, musty body odor, growth retardation; screen 2-3 days AFTER birth(mom hides condition), decrease phentlyalanine intake and increase tyrosine intake.
|
biochem
|
|
|
Alkaptonuria(symptoms,findings)
|
problem in homogentistic acid oxidase in the tyrosine degrdation pathway, autosomal recessive; dark connective tissue, brown pigmented sclera, urine turns black in air, homogenistic acid eats cartilage -> artraglia.
|
biochem
|
|
|
Albinism(physiology, findings)
|
deficient tyrosinase or defective tyrosinase transporter, can result from lack of neural crest cell migration; lack of tyrosine->lack of melain->no skin color, increased skin cancer common.
|
biochem
|
|
|
Homocystinuria(physiology,findings)
|
3 forms:cystathione synthetase deficiency or decreased affinity for cystathionine synthase for pyridoxial phosphate or homocysteine methyltransferase, all lead to excess homocysteine; increased homocysteine in urine, mental retardation, osteoporosis, tall stature, lens subluxation and atherosclerosis.
|
biochem
|
|
|
Cystinuria(physiology, symptom, treatment)
|
defect in transporter in renal PCT for cysteine, ornithine, lysine, and arginine; excess cysteine in urine causes hexagonal crystals and renal staghorn crystals; good hydration and alkalinize urine.
|
biochem
|
|
|
Maple syrup urine disease(physiology, findings)
|
blocked degradation of Ile, Leu, Val due to decreased a-ketoacid DH; increased ketoacids in blood, causes CNS defects, mental retardation, death.
|
biochem
|
|
|
Hartnup disease (physiology, findings)
|
autosomal-recessive disease, defective neutral amino acid transporter in renal + intestinal cells; causes tryptophan excretion and decreased absorption in gut, leading to pellagra.
|
biochem
|
|
|
What are the two types of emphysema?
|
1. centriacinar - associated with smoking. 2. panacinar - associated with A1-antitypsin deficiency.
|
pulmonary
|
|
|
Why do people with emphysema exhale through pursed lips?
|
increased in airway pressure prevents airways from premature collapse.
|
pulmonary
|
|
|
What disease is associated with curschman's spirals and leyden crystals?
|
asthma. spirals = epitheium forms mucus plugs. leyden crystals = eosinophil breakdown.
|
pulmonary
|
|
|
inhale to exhale ratio changes how in asthma?
|
decreased I/E ratio
|
pulmonary
|
|
|
Antracosis, silicosis, and asbestosis all increase risk for what other diseases?
|
cor pulmonale and Caplan's syndrome
|
pulmonary
|
|
|
Calcified pleural plaques are pathonomic for what? Are they precancerous?
|
Asbestos exposure. Are NOT precancerous.
|
pulmonary
|
|
|
What lechitin:sphingomyelin ratio is predictive of neonatal respiratory distress?
|
1.5 or below. 2.0 or above is normal.
|
pulmonary
|
|
|
neonatal therapuetic oxygen can result in what negative outcomes?
|
1. retinopathy of prematurity. 2. bronchopumonary dysplasia.
|
pulmonary
|
|
|
What are th risk factors for neonatal respiratory distress?
|
1. prematurity 2.maternal diabetes(elevated fetal insulin) 3. cesarean birth (less fetal glucocorticoids)
|
pulmonary
|
|
|
What is the treatment for neonatal respirtatory distress syndrome?
|
maternal steriods before birth, artificial surfactant after birth.
|
pulmonary
|
|
|
the initial damage to lung sin ARDS is due to what?
|
1. neutrophillic substances toxic to lungs 2. coagulation cascade 3. oxygen-derived free radicals
|
pulmonary
|
|
|
Obstructive lung disease has a FEV1/FVC of what?
|
UNDER 80!
|
pulmonary
|
|
|
Restrictive lung diseases has an FEV1/FVC of what
|
80 or above BUT both FEV1 and FVC decrease about equally.
|
pulmonary
|
|
|
How does sleep apnea relate to RBC formation?
|
hypoxic intervals -> increased EPO release -> increased erthryopoesis.
|
pulmonary
|
|
|
contrast tension pneumothorax to spontaneous pneumothorax.
|
tension: check valce forms, air can enter but it can't leave thus overinflation. spontaneous: bleb in pleura pops, making the lung collapse on itself and become smaller.
|
pulmonary
|
|
|
What cancer is the leading cause of cancer death?
|
lung
|
pulmonary
|
|
|
what are lung metastases sites?
|
adrenals, bone, liver.
|
pulmonary
|
|
|
what the the classic lung cancer complications?
|
(SPHERE) Superior vena cava syndrome, pancoast tumor, horner syndrome, endocrine, recurrent laryngeal symptoms(hoarse), effusions (pleural or pericardial)
|
pulmonary
|
|
|
Which lung cancers are peripheral? which are central?
|
peripheral - adenocarcinoma, large cell. central - squamous cell, small cell. mesothelioma - pleural.
|
pulmonary
|
|
|
Psammoma bodies are found in what pathology?
|
(PSaMMoma) Papillary carcinoma of the thyroid, serous cysadenocarcinoma of the ovary, meningioma, mesothelioma.
|
path
|
|
|
what organisms cause lobar pneumonia?
|
S. Pneumoniae, klebsiella.
|
pulmonary
|
|
|
what organisms cause interstitial pneumonia?
|
atypical organisms. Viruses(influenza, RSV, adenocarcinoma), Mycoplasma, Legionella, Chlamydia.
|
pulmonary
|
|
|
Hypersensitivity pneumonitis is caused by what type of hypersensitivty reaction?
|
Mixed III/IV. Often seen in farmers and bird owners.
|
pulmonary
|
|
|
Allergic rhinitis is due to what type of hypersensitivity reaction?
|
type I: inflammatory infiltrate with esosinohils.
|
pulmonary
|
|
|
What is the triad of aspirin-intolerant asthma?
|
asthma, aspirin-induced bronchospams,nasal polyps.
|
pulmonary
|
|
|
must suspect what disease in a child with nasal polyps?
|
cystic fibrosis
|
pulmonary
|
|
|
angiofibroma(presentation,age group)
|
benign tumor of nasal mucosa, composed of blood vessels and fibrous tissue. Presents in young males with recurring epistaxis.
|
pulmonary
|
|
|
Nasopharyngeal carcinoma(presents, pathology)
|
associated with EBV. biopsy will reveal pleomorphic keratin filled cells, like a poorly differentiated squamous cell carcinoma. Often presents with lymph node enlargement.
|
pulmonary
|
|
|
What are the risk factors for laryngeal carcinoma?
|
alcohol use and tobacco use.
|
pulmonary
|
|
|
what organims cause bronchopneumonia?
|
S. aureus, HiB, pseudomonas, Moraxella.
|
pulmonary
|
|
|
How does TLC change in obstructive lung disease?
|
increased due to lung trapping
|
pulmonary
|
|
|
Panacinar emphysema is most severe in what lobes? What about centroacinar?
|
Centri - smoking, upper lobes where smoke goes! Pan - A1-antitrypin, worse in lower lobes.
|
pulmonary
|
|
|
A1-antitrypsin deficiency is associated with damage to what two organs?
|
lungs and liver.
|
pulmonary
|
|
|
Allergic bronchopulmonary aspergilliosis(pathophys, associations)
|
is a hypersensitivity reaction to aspergillus. occurs in people with asthma or cystic fibrosis.
|
pulmonary
|
|
|
honey comb lung pathology is associated with what?
|
idopathic pulmonary fibrosis, usually end-stage.
|
pulmonary
|
|
|
hyaline membranes in the lungs are associated with what?
|
acute respiratory distress syndrome
|
pulmonary
|
|
|
what levels increase as surfact is produced in the neonate?
|
lecithin(phospatidylcholine) increase, spingomyelin levels stay constant.
|
pulmonary
|
|
|
hypoxemia in the neonate increases risks of devleoping what?
|
1. patent ductus arteriosus 2. necrotizing enterocolitis.
|
pulmonary
|
|
|
diaphram is inervated by what cervical levels?
|
C345, keeps the diaphram alive!
|
pulmonary
|
|
|
What are the muscles of inspiration during exercise?
|
external intercostals, Scalene, sternomastocleiod
|
pulmonary
|
|
|
what are the muscles of expiration during exercise?
|
rectus abdomins, int + ext obliques, internal intercostals
|
pulmonary
|
|
|
What causes right shift on the oxygen-hemoglobin binding curve?
|
CBEAT - CO2, BPG, Exercise, Acid/Altitude, temperature
|
pulmonary
|
|
|
What gases are perfusion limited?
|
O2(in normal lungs), CO2, N20
|
pulmonary
|
|
|
what gases are diffusion limited?
|
CO, O2(in empysema, interstial fibrosis, etc)
|
pulmonary
|
|
|
Carbon dioxide is transported to the lung in mostly what form?
|
bicarbonate
|
pulmonary
|
|
|
How does glucose and amino acid clearance change in normal pregnancy?
|
reduced reabsorption leads to glycosuria and aminoaciduria.
|
renal
|
|
|
What causes increased anion gap in metabolic acidosis?
|
(MUDPILES) MeOH, uremia, DKA, propylene glycol, iron tablets or INH, lactic acidosis, ethylene glycol, salycylates.
|
renal
|
|
|
what causes normal anion gap metabolic acidosis?
|
(HARD-ASS) hyperalimentation, addisons, renal tubular acidosis, diarrhea, acetazolamide, spironolactone, saline infusion.
|
renal
|
|
|
what causes respiratory acidosis?
|
opiods, obstruction, chronic lung disease.
|
renal
|
|
|
what causes metabolic alkalosis?
|
loop diuretics, vomitting, antacid use, hyperaldosternoism
|
renal
|
|
|
granular, muddy brown casts are associated with what?
|
Acute tubular necrosis
|
renal
|
|
|
hyaline casts are associated with what?
|
nonspecific, can be normal.
|
renal
|
|
|
List 4 things found in nephrotic syndrome.
|
1. proteinura (>3.5g/d), hyperlipidemia, fatty casts, edema.
|
renal
|
|
|
list associations with nephritic syndrome
|
hematuria, RBC casts, azotemia, hypertension, proteinuria (<3.5 g/d)
|
renal
|
|
|
What is the most common type of kidney stone?
|
calcium
|
renal
|
|
|
Renal cell carcinoma mets to where?
|
invades renal vein -> IVC -> blood. goes to lung and bone.
|
renal
|
|
|
What is the most common renal cancer of childhod?
|
Wilm's tumor.
|
renal
|
|
|
What are the risk factors for transitional cell carcinoma?
|
Pee SAC: phenacetin, smoking, aniline dye, cyclophosamide.
|
renal
|
|
|
What is the most common cause of intrinsic renal failure?
|
Acute tubular necrosis.
|
renal
|
|
|
What are the 3 stages of acute tubular necrosis?
|
1. inciting event 2. maintenance phase - oliguric, last 1-3 week, risk of hyperkalemia 3. recovery phase - polyuric, BUN and serum creatinine fall, risk of hypokalemia
|
renal
|
|
|
Acute tubular necrosis is associated with what?
|
shock, sepsis, myoglobinuria, toxins
|
renal
|
|
|
What is renal papillary necrosis associated with?
|
DM, acute pyelonephritis, phenacetin use, sickle cell anemia or trait
|
renal
|
|
|
Can postrenal azotemia occur unilaterally?
|
No. Must be bilateral.
|
renal
|
|
|
What are the 2 forms of renal failure?
|
1. acute tubular necrosis 2. chronic ->DM or hypertension
|
renal
|
|
|
ADPKD is associated with?
|
berry aneurysms, mitral valve prolapse, benign hepatic cysts
|
renal
|
|
|
What are the toxicities of ACE inhibitors
|
CATCHH- cough, angioedma, teratogen (fetal renal malformation), creatinine increase (decreased GFR), hyperkalemia, hypotension.
|
renal
|
|
|
side-effects of lithium
|
LMNOP: lithium side effects: movement, nephrogenic diabetes insipidus, hypOthyroidism, pregnancy issues
|
renal
|
|
|
What is classical conditioning?
|
Learning in which a natural response is elicted by a learned stimulus (think pavlov's dog)
|
psych
|
|
|
what is operant conditioning?
|
learning in which a particular action is elicted because it generates a reward.
|
psych
|
|
|
What is excition (psych)
|
discontinuation of reinforcement (+ or -) eventually eliminates the behavior
|
psych
|
|
|
What is transference?
|
patient projects feelings about another person onto the doctor (sees doc as parent)
|
psych
|
|
|
what is countertransferance?
|
doctor projects feelings about important person unto patient
|
psych
|
|
|
What are ego defenses?
|
Unconscious mental processes used to resolve conflict and prevent undesireable feelings
|
psych
|
|
|
What is dissociation?
|
temporary, drastic changes in personality, memory, behavior, etc to avoid emotional distress
|
psych
|
|
|
compare displacement to projection
|
displacement = avoided ideas or feelings are transferred to some neutral person or object. projection = an unacceptable impulse is attributed to an external source.
|
psych
|
|
|
compare fixation to regression
|
fixation = remain at some childish level. regression = turning back to a past maturational level.
|
psych
|
|
|
what is identification (psych)
|
modeling behavior after a more powerful person
|
psych
|
|
|
what is isolation of an affect?
|
seperation of feelings from an event (describe a murder in cold detail)
|
psych
|
|
|
what is rationalization?
|
proclaiming logical reasons for actions actually performed for other reaons to avoid self-blame
|
psych
|
|
|
compare reaction formation to sublimination
|
reaction formation = a warded off idea or feeling is replaced by the opposite response (homophobic is gay). sublimation = replace an unacceptable wish with one that doesn't conflict with morals.
|
psych
|
|
|
What are the mature defenses?
|
Mature people wear a SASH Sublimation, suppression, humor, altruism.
|
psych
|
|
|
What are effects of infant deprivation?
|
4W's: weak, wordless, wanting, wary.
|
psych
|
|
|
Infant deprivation can be irreverisble after how long?
|
6 months
|
psych
|
|
|
Who is usually the abuser in child abuse?
|
male caregiver
|
psych
|
|
|
How often does ADHD continue into adulthood?
|
50% of the time.
|
psych
|
|
|
What physical change is ADHD associated with?
|
decreased frontal lobe volume.
|
psych
|
|
|
What is conduct disorder?
|
a childhood disorder where there is constant behavior violating the basic rights of others, often becomes antisocial personality disorder.
|
psych
|
|
|
what is oppositional defiant disorder?
|
a childhood disorder with a pattern of defiant behavior towards authority figures in the absence of abuse of sociatal norms.
|
psych
|
|
|
When does tourette's onset? how long does it need to persist before dx? what is it associated with?
|
before 18, it must persist for greater than 1 year. associated with OCD.
|
psych
|
|
|
when does seperation anxiety disorder onset?
|
onsets between 7-9.
|
psych
|
|
|
what is the largest difference between austism and asperger's disease?
|
autism: speech disoder, often below average intelligence aspergers: no language disorder, often normal intelligence.
|
psych
|
|
|
what is Rett's disorder?
|
x-linked disorder seen exclusively in girls, males die in utero. loss of development, loss of verbal abilities, mental retardation, ataxia.
|
psych
|
|
|
what is childhood disintegrative disorder?
|
onset of 304 years, marked regression after at least 2 years of normal development. loss of speech, social skills, bowels, etc, more common in boys.
|
psych
|
|
|
neurotransmitter change in anxiety:
|
increase NE. decreased GABA, 5-HT.
|
psych
|
|
|
neurotransmitter change in depression:
|
decreased ne, 5-ht,dopamine
|
psych
|
|
|
neurotransmitter change in alzheimer's:
|
decreased ach
|
psych
|
|
|
neurotransmitter change in huntington's disease
|
decreased gaba and ach, increased dopamine
|
psych
|
|
|
neurotransmitter change in schizophrenia
|
increased dopamine
|
psych
|
|
|
neurotransmitter change in parkinson's disease
|
decreased: dopamine, increased: 5-ht, ACh
|
psych
|
|
|
order of loss of orientation:
|
1st - time, 2nd - place, 3rd - person.
|
psych
|
|
|
what is a hallucination?
|
perceptions in the absence of external stimuli.
|
psych
|
|
|
what is a delusions
|
false beliefs despite facts to contray
|
psych
|
|
|
what is disorganized speech?
|
words slung together through loose associations
|
psych
|
|
|
visual hallucinations are likely:
|
from a medical illness, i.e. drug intoxication
|
psych
|
|
|
auditory hallucinations are likely:
|
psychiatric
|
psych
|
|
|
olfactory hallucinations are likely:
|
part of epilepsy, seizure and brain tumors
|
psych
|
|
|
tactile hallucinations are likely:
|
common in alcohol withdrawl or cocaine abuse
|
psych
|
|
|
when do hypnagogic hallucinations occur?
|
while GOing to sleep
|
psych
|
|
|
when do hypnopompic hallucinations occur?
|
while pompously awakening
|
psych
|
|
|
How long must psychosis last before schizophrenia can be diagnosed?
|
6 mo.
|
psych
|
|
|
Diagnosis of schizophrenia requires 2 of the following:
|
(+)= symp: delusions, hallucinations, disorganized speech, disorganized or catanoic behavior. - symp: flat affect, social withdraw, lack of motivation, lack of speech
|
psych
|
|
|
What are the 5 subtypes of schizophrenia?
|
1. paranoid (delusions) 2. disroganized (speech) 3. catatonic (automatisms) 4. undifferentiated (elements of all types) 5. residual
|
psych
|
|
|
Patients with schizophrenia are at increased risk for:
|
suicide
|
psych
|
|
|
does schizophrenia present earlier in males or females?
|
Males (teens). Females present in late 20's to 30's.
|
psych
|
|
|
What is a brief psychotic disorder?
|
under 1 mo, usually stress related
|
psych
|
|
|
What is schizophreniform disorder?
|
lasts 1-6 mo
|
psych
|
|
|
What is schizoaffective disorder?
|
atleast 2 weeks of of stable mood with psychotic symptoms plus depressive manic or both
|
psych
|
|
|
What is a delusional disorder?
|
fixed, persistent, nonbizarre belief system lasting over 1 mo.
|
psych
|
|
|
What is a shared psychotic disorder?
|
(also called folie a deux) development of delusions in a person in a close relationship with someone who has a delusion disorder. resolves upon seperation.
|
psych
|
|
|
What is dissociative identity disorder?
|
presence of 2 or more personalities. more common in women w/hx of sexual abuse
|
psych
|
|
|
What is depersonalization disorder?
|
persistent feelings of detachment from one's body or situation
|
psych
|
|
|
What is a dissociative fugue?
|
abrupt change in location causes inabilty to recall past and to general confusion. not related to drugs or a medical condition.
|
psych
|
|
|
Diagnosis of a manic episode requires atleast three of the following:
|
Must last 1 week or more. (DIG FAST) 1. distracted 2. Irresponsibility 3.Grandiosity 4. Flight of ideas 5. Agitation 6. less need for sleep 7. talkative
|
psych
|
|
|
What is a hypomanic episode?
|
less severe manic episode. no psychotic featues.
|
psych
|
|
|
How is bipolar disorder?
|
must have atleast 1 manic episode and 1 hypomanic episode
|
psych
|
|
|
What is a cyclothymic disorder?
|
dysthymia and hypomania, mild form of bipolar lasting at least 2 years.
|
psych
|
|
|
What is major depressive disorder? how do you diagnosis it?
|
self-limited disorder with depressive episodes alsting 6-12 mo. Must have 5 of the following symptoms for 2 or more weeks. (SIG E CAPS) Sleep disturbance, loss on interest, guilt, loss of energy and concentration, appetite change, psychomotor retardation, suicidal ideation.
|
psych
|
|
|
What is dysthymia?
|
mild form of depression lasting at least 2 years
|
psych
|
|
|
Who has a higher lifetime incidence of major depressive episode, male or females?
|
females (25%) to males (12%)
|
psych
|
|
|
What is the most common type of depression?
|
atypical depression.
|
psych
|
|
|
What are the 3 postpartum modd disturbances? treament for each.
|
1. the blues - 50% get, resolves in 10-14 days, no drugs. 2. depression 10% get, lasts 2 weeks to a year, give antidepressants. 3. psychosis .1%, get delusions. lasts 4-6weeks. antipsychotics
|
psych
|
|
|
When is electroconvulsive therapy used? side effects of treatment?
|
It is used in major depressive disorder that is refractory to treatment. sldo in immediate treatment of suicidality. side effects are amenesia lasting 6 mo.
|
psych
|
|
|
What are the risk factors for suicide?
|
SAD PERSONS: Sex(male), Age(teenage or elderly) Depression, Previous attempt, ethanol or drug use, loss of Rational thinking, sickness (a medical illness), organized plan, no spouse, social support lacking.
|
psych
|
|
|
who attempts suicide more often? who succeds more often?
|
women attempt more, males succed more often.
|
psych
|
|
|
How is panic disorder diagnosed?
|
must have 4 of the following : PANICS- Palpations, paresthisias, Abdominal distress, nausea, intense fear of dying, lIghtheadedness, ches pains, chills, choking, sweating, shaking, SOB.
|
psych
|
|
|
What is the difference between acute stress disorder and PTSD?
|
PTSD lasts atleast 1 month, acute stress disorder lasts 2 days to 1 month.
|
psych
|
|
|
What is the different between GAD and adjustment disorder?
|
GAD is anxiety for atleast 6 mo, adjustment disorder lasts under 6 months.
|
psych
|
|
|
What are somatoform disorders?
|
disorders with physical symptoms that have no physical cause but are not being intentionally faked.
|
psych
|
|
|
What is conversion disorder?
|
actue loss of sensory or motor functions following an acute stressor
|
psych
|
|
|
what is body dysmorphic disorder?
|
Preoccupation with minor deficiets in body, constantly seeking cosmetic changes.
|
psych
|
|
|
What is the difference between malingering and a factitous disorder?
|
malingering = secondary gain, i.e. getting days off work or a pension. factitous disorder = gets medical attention from a madeup illnes.
|
psych
|
|
|
What are the cluster A personality disorders?
|
Paranoid = distrust, schzoid = social withdrawl and likes it, schizotypal = magical thinking.
|
psych
|
|
|
What are the cluster B personality disorders?
|
Antisocial = disregard for others rights, boderline = impulsive, unstable relationships, histrionic = excessive emotions, narcissistic = gradiosis, sense of entitlement.
|
psych
|
|
|
what are the cluster C personality disorders?
|
Avoidant= feels inadequate, fear of rejection. Obsessive-compulsive = perfectionism, dependent = submissive and clingy.
|
psych
|
|
|
what are the stages of overcoming substance addiction?
|
1. precontemplation. 2. contemplation 3. preparation 4. action 5. maintenance 6. relapse
|
psych
|
|
|
What are mallory-weiss tears?
|
lacerations at the gastroesophageal junction from excessive vomitting, often painful in contrast to espophageal varices.
|
psych
|
|
|
What is neuroleptic malignant syndrome? What is the treatment?
|
rigidity, myoglobinuria, autonomic instability. seen with antipsychotics overdose. treatment: dantrolene and bromocriptine (d2 agonist)
|
psych
|
|
|
What is tardive dyskinesa? Is it reversible?
|
sterotypical oral-facial movements, from long term antipsychotic use. often NOT reversible.
|
psych
|
|
|
What is serotonin syndrome? what is the treatment?
|
occurs with any drug that increases serotonin (MAO inhibitor, SNRI, TCA) hyperthermia, confusion, myoclonus, cardio collapse, flushing. tx: cyproheptadine (5ht antagonist)
|
psych
|
|
|
What is the most common site of obstructive in the fetus?
|
ureteropelvic junction. Failure to canalize -> block.
|
renal
|
|
|
What does the mesonephros become?
|
male genital system
|
renal
|
|
|
What are the causes of potter sydrome?
|
1. AEPKD 2. bilat renal aplasia 3. posterior urethral valve.
|
renal
|
|
|
How does horseshoe kidney form? what is it associated with?
|
inferior poles of kidnet fuse. turner syndrome
|
renal
|
|
|
Plasma volume is measured with what? What about ECF volume?
|
ECF - inulin. plasma - radiolabeled albumin.
|
renal
|
|
|
Why is inulin used to estimate GFR?
|
it is freely filtered but is it not secreted or reabsorbed.
|
renal
|
|
|
why is PAH used to estimate ERPF?
|
all PAH entering the kidney is excreted. It is borth freely filtered and actively excreted.
|
renal
|
|
|
What is the formula for filtration fraction?
|
FF = GFR/RPF.
|
renal
|
|
|
what affect do prostaglandins have on the afferent arteriole?
|
dilates it, so RPF and GFR both increase, keeping FF the same.
|
renal
|
|
|
what affect does angiotension II have on the efferent arteriole?
|
constricts it, so RPF decreased and GFR increased making FF jump drastically.
|
renal
|
|
|
At what plasma glucose are all glucose transports saturated in the kidney?
|
360 mg/dL
|
renal
|
|
|
ADH primarily regulates what?
|
low blood volume but it secondarily regulates osmolarity.
|
renal
|
|
|
aldosterone primarily regulates what?
|
blod volume
|
renal
|
|
|
What affect to B-blocks have at the juxtatomegular apparatus?
|
they inhibit b-receptors, and thus DECREASE renin release thus DECREASING bloodpressure!
|
renal
|
|
|
What are the endocrine functions of the kidney?
|
1. erythropoietin 2. PT converts 25-OH vit d to 1,23-OH vit d 3. JG make renin 4. prostaglandins dilate affterent arteriole
|
renal
|
|
|
What causes K shift OUT of cells?
|
(DO Insulin LAB) Digitalis, hyperOsmolarity, Insulin deficiency, lysis of cells, acidosis, B0adrenergix antagonist
|
renal
|
|
|
Describe high vs low Ca serum concentration
|
low: tetany, seizure high: stones, bones, groans, psychyiatric overtones.
|
renal
|
|
|
describe low vs high K serum concentration findings
|
low: U wave on ECG, flat T wave, muscle weakness. High: wide QRS, peaked T wave, muscle weakness
|
renal
|
|
|
describe low vs high Mg serum concentration findings
|
low: tetany, arrhythmias.high: decreased DTR, lethargy, bradycardia, hypotension, cardiac arrest, hypocalcemia
|
renal
|
|
|
describe low vs high PO4 serum concentration findings
|
low:bone loss, osteomalacia. high: renal stones, hypocalcemia.
|
renal
|
|
|
compare K changes in types 1, 2, and 4 RTA
|
1+2: hypokalemia. 4: hyperkalemia.
|
renal
|
|
|
What do muddy brown, granular casts indicate?
|
acute tubular necrosis
|
renal
|
|
|
does painless hematuria, no casts indicate a renal or bladder source?
|
bladder.
|
renal
|
|
|
are WBC casts indicative of pyelonephritis or cystitis?
|
casts = also renal origin
|
renal
|
|
|
What are hylaine casts specific for?
|
nothing, are often nornmal
|
renal
|
|
|
What are fatty casts specific for?
|
Nephrotic syndrome
|
renal
|
|
|
Focal segmental glomeruosclerosis is associated with what?
|
HIV infection, heroin use, obesity, interferon treatment
|
renal
|
|
|
What are kimmel-wilson lesions specific for?
|
they are eosinohilic, nodular glomerulosclerosis found in diabetic glomerulonephropathy
|
renal
|
|
|
Renal cell carcinoma originates from what cells?
|
proximal tubule cells.
|
renal
|
|
|
RCC can cause testicular varoceole on only which side?
|
the LEFT. left testicular vein dumps into the left renal vein. on the right, the testicular vein goes right into the IVC.
|
renal
|
|
|
What is the WAGR complex?
|
Wilms tumors, aniridia (no iris), genituurniary malformations, and mental retardation
|
renal
|
|
|
What is the most common childhood renal malignancy?
|
wilms tumor
|
renal
|
|
|
Transitional cell carcinoma of the GU system is associated with what?
|
Pee SAC: phenacetin, smoking, aniline dye, cyclophosamide.
|
renal
|
|
|
In what phase does death usually occur during acute tubular necrosis?
|
the maintenance phase, during oliguria
|
renal
|
|
|
Renal papillary necrosis is associasted with:
|
1. DM 2. acute pyelonephritis 3. chronic phenacetin use 4. sickle cell anemia and trait
|
renal
|
|
|
why is bun creatine serum ratio useful?
|
BUN is usually resorbed but creatine is not. decreased ratio ->renal failure
|
renal
|
|
|
uremia causes:
|
Nausea, pericarditis, asterixis(flapping of wrist), encephalopathy, platlet dysfunction
|
renal
|
|
|
ADPKD is associated with?
|
PKD1 and PKD2 mutaitons
|
renal
|
|
|
Where is most common ectopic thyroid site? why?
|
tongue, foramen cecum connects tongue to pyrimidal lobe of thyroid
|
endocrine
|
|
|
Contrast physical exam of persistent thyroglossal duct cyst to a branchial cleft cyst.
|
thyroglossal = midline, moves with swallowing. Brahcial = lateral, doesn't move with swallowing.
|
endocrine
|
|
|
What chemical determines fetal lung maturation and surfactant production?
|
cortisol
|
endocrine
|
|
|
What is the most common tumor of adults and children in the adrenal medulla? how do they relate to hypertension?
|
adult = pheochromocytoma. kids = neuroblastoma. pheo = episodic hypertension, neuroblastoma doesn't cause this.
|
endocrine
|
|
|
what is is the posterior pituitary derived from? what about the anterior?
|
postier = neuroectoderm. anterior = oral ectoderm (rathke's pouch).
|
endocrine
|
|
|
What do alpha, beta, and gamma cells secrete in the pancreas?
|
alpha - glucagon. beta - insulin. gamma - somatostatin.
|
endocrine
|
|
|
what cell types are insulin independent?
|
(BRICKL) brain, renal, intenstine, cornea, kidney, liver
|
endocrine
|
|
|
describe function of GLUT1, GLUT2 and GLUT4:
|
1: insulin dependent - RBC, brain. 2: bidirectiona: B islet, liver, kidney, small intestine. 4= insulin dependent. adipose tissue, skeletal muscle.
|
endocrine
|
|
|
What causes increased insulin release in normal physiology?
|
hyperglycemia, GH, b2 agonists.
|
endocrine
|
|
|
whar causes decreased insulin release in normal physiology?
|
hypoglycemia, somatostatin, A2 agonists
|
endocrine
|
|
|
Why do RBCs always depend on glucose?
|
they have no mitochondria, thay can't do aerobic metabolism
|
endocrine
|
|
|
How does prolactin inhibit spermatogenesis and ovulation?
|
it inibits GnRH release.
|
endocrine
|
|
|
What is the function of cortisol?
|
(BBIIG) maintain Blood pressue, decease Bone formation, anti-Inflammatory, increase Insulin resistance, increased Gluconeogenesis.
|
endocrine
|
|
|
What is the source of PTH?
|
Chief cells in the parathyroid.
|
endocrine
|
|
|
Where does vitamin D3 come from? What about D2?
|
D3 = sun exposure. D2 = ingested via plants.
|
endocrine
|
|
|
Where is calcitonin made?
|
parafollicular C cells of thyriod.
|
endocrine
|
|
|
What are the 4 functions of T3?
|
(4 b's) brain maturation, bone growth, beta-adrenergic effects, basal metabolic rate
|
endocrine
|
|
|
in men, increased SHBG leads to what?
|
less free testosterone ->gynecomastia
|
endocrine
|
|
|
in women, decreased SHBG leads to what?
|
more free testosterone ->hirsutism
|
endocrine
|
|
|
Where is most t3 formed?
|
AT the target tissue.
|
endocrine
|
|
|
What is the wolf-chaikoff effect?
|
excress iodine temporarily inhibits thyroid peroxidase -> decreased iodine organification ->decreased T3/T4.
|
endocrine
|
|
|
What converts t4 to T3?
|
5'-deiodinase
|
endocrine
|
|
|
What enzyme is responsible for oxidation and organification of iodide aswell as formation of MIT and DIT?
|
peroxidase
|
endocrine
|
|
|
What is a difference in the mechanism of PTU and methimazole?
|
PTU disables peroxidase AND 5'-deiodinase. Methimazole only inhibits peroxidase.
|
endocrine
|
|
|
What is waterhouse friderichsen syndrome?
|
primary adrenal insufficiency due to adrenal hemorrhafge associated with N. Meningitidis septicemia, DIC, and endotoxic shock.
|
endocrine
|
|
|
what are the signs of episodic hyperadrenergic symptoms associated with pheochromocytoma?
|
5P's: Pressure (bp increased), Pain (headache), perspiration, palpitaitons, pallow.
|
endocrine
|
|
|
Why must alpha blockers be given BEFORE b-blockers before pheochromocytoma surgery?
|
pheochromo makes epi and nor-epi (alpha and beta agonists). Blocking only beta will cause unchallenged stimulation of a recepors, causing hypertensive crisis. Block A first to control the a receptors and then block b.
|
endocrine
|
|
|
What is jod-basedow phenomenon?
|
thryotoxicosis when a person with iodine deficency goiter is made iodine replete.
|
endocrine
|
|
|
lymphoma is associated with what thyroid condition?
|
hashimoto's thyroiditis.
|
endocrine
|
|
|
What is psuedohypoparathyroidism? findings?
|
also called Albright's hereditary osteodystrophy. kidnet doesn't respond to PTH. findings: hypocalcemia, short 4/5th digits, short stature.
|
endocrine
|
|
|
compare treatment for nephrogenic diabetes insipidus and central DI.
|
central - give desmopression (ADH analong). for nephrogenic, ADH won't cause a response. instead, give HCTZ, indomethacin or amiloride.
|
endocrine
|
|
|
What is sheehan's sydrome?
|
inschemic infarct of pituitary following pospartum bleeding.
|
endocrine
|
|
|
insulsin is ALWAYS required in what types of diabetes?
|
type 1. type 2 might not need.
|
endocrine
|
|
|
Why does carcinoid syndrome NOT occur if the tumor is limited to the GI tract?
|
5-ht undergoes first pass elimination in the liver
|
endocrine
|
|
|
What is th rule of 1/3 with carcinoid tumors?
|
1/3 metastasize, 1/3 present with a secondary malignancy, 1/3 are at multiple sites.
|
endocrine
|
|
|
What is the pathology seen with Zollinger-ellison syndrome?
|
gsstrin increased causes rugal thickening due to acid hypersecretion.
|
endocrine
|
|
|
What is the treatment stratergy in type 1 DM?
|
low sugar diet and required insulin replacement.
|
endocrine
|
|
|
What is the treatment stratergy in type 2 DM?
|
dietary modification and exercise first, then medicaitons after that. insulin not always required.
|
endocrine
|
|
|
Renal amyloidosis will be positive for what test?
|
the light microscopy - congo red stain shows apple-green birefringece under polarized light.
|
endocrine
|
|
|
What are the derivatives of the: foregut, midget, and hindgut?
|
forgut - pharynx to duodenum. midgut - doudenum to transverse colon. hindgut - distal transverse colon to rectum.
|
GI
|
|
|
abdominal wall, rostral fold closure failure results in:
|
sternal defects
|
GI
|
|
|
abdominal wall, lateral fold closure failure results in:
|
omphalocele, gastrochisis
|
GI
|
|
|
abdominal wall,caudal fold closure failure results in:
|
bladder exostrophy
|
GI
|
|
|
What is the difference in pathology between duodeinal atresia and jejunal, ileal, or colonic atresia?
|
Duodenal - failure to recanalize (like in down syndrome). others: due to a vascular accident (apple peel atresia).
|
GI
|
|
|
Give difference between gastroschisis and omphalocele.
|
gastro - abdominal contents NOT covered by peritoneum. omphalocele - contents ARE covered by peritoneum.
|
GI
|
|
|
Congenital pyloric stenosis occurs most often in who?
|
firstborn males.
|
GI
|
|
|
What is an annular pancreas? what are the bed sequalue of one?
|
ventral pancreatic bud abnormally encircles 2nd part of duodenum. Causes duodenal narrowing.
|
GI
|
|
|
What causes pancreas divisum?
|
ventral and doral pancreatic buds do not fuse.
|
GI
|
|
|
What sturcture does the spleen rise from? What about the pancreas?
|
spleen = mesodermal. pancreas = foregut.
|
GI
|
|
|
What structures are contained in the retroperitoneum?
|
GI structures without and mesentery and non-GI stuff. (SAD PUCKER) Suprarenal gland (adrenal), Aorta and IVC, Duodenum(2nd+3rd), pancreae (except tail), ureters, colon(desc and ascend), kidneys, esophagus, rectum.
|
GI
|
|
|
What are the layers of the gut wall?
|
in to out (MSMS) mucosa, submucosa, muscularis externa, serosa.
|
GI
|
|
|
Describe difference between an ulcer and an erosion in the digestive tract.
|
errosion = mucosal layer only. ulcer = submucosa muscular layer.
|
GI
|
|
|
Where are meissner's and auerbach's plexuses located?
|
meissner = submucosa layer. auerbach = muscularis.
|
GI
|
|
|
What are the frequencies of basal rhythm in the: stomach, duodenum, ileum?
|
stomach = 3 wave/min. Duodenum = 12w/m. Ileum = 8-9 w/m.
|
GI
|
|
|
What causes superior mesenteric artery syndrome?
|
3rd part of duodenum is trapped between the SMA and the aorta, restricting it's lumen.
|
GI
|
|
|
What is a surgerical treatment for protal hypertension?
|
TIPS (transjugular intrahepatic portosystemic shunt) which connects portal vein to hepatic vein.
|
GI
|
|
|
What the pectinate line?
|
line in the anus where endoderm meets the ectoderm.
|
GI
|
|
|
What are the 3 liver zones? which is affected by viruses? which is sensitive to toxic injury?
|
1. periportal. sensitive to viral hepatitis. 2. intermediate 3. pericentral sensitive to toxins and alcoholic hepatitis.
|
GI
|
|
|
What must a gallstone reach to block both bile and pancrastic ducts.
|
The ampulla of vater.
|
GI
|
|
|
Tumors in what part of the pancreas are most likely to obstruct the common bile duct?
|
the head of pancreas.
|
GI
|
|
|
Describe the organization of the femoral vessels.
|
(if you go lateral to medical you hit your NAVEL) Femoral Nerve, Femoral Artery, Femoral Vein, empty space, Lymphatics.
|
GI
|
|
|
What is contained in the femoral triange? what are the borders?
|
femoral artery, vein, nerve. Borders are inguinal ligmant, sartoris muscle and adductor longus muscle.
|
GI
|
|
|
What runs in the femoral sheath? what important structute does not?
|
femoral artery, vein,and deep inguinal lymph nodes do. Femoral NERVE does not!!!
|
GI
|
|
|
What is hasselbach's triangle? What type of hernia goes through it?
|
inferior epigrastric vessel, lateral border of rectus abdominis, inguinal ligament. DIRECT comes through it!
|
GI
|
|
|
Can atropine block parietal cells? what aout G cells?
|
Parietal = yes, they work through Ach. G cells = NO. they are signled by GRP.
|
GI
|
|
|
What are brunner's glands? what are their purpose? when do they hypertrophy?
|
located in duodenum. Secrete alkaline mucus. they hypertrophy in peptic ulcer disease.
|
GI
|
|
|
Where is iron absorbed?
|
absorbed as Fe2+ in the duodenum.
|
GI
|
|
|
Where is folate absorbed?
|
absorbed in the jejunum.
|
GI
|
|
|
Where is B12 and bile acid absorbed?
|
in the terminal iluem.
|
GI
|
|
|
What is the rate limiting step in cholesterol synthesis?
|
Cholesterol 7alpha-hydroxylase.
|
GI
|
|
|
What are the funcitons of bile:
|
1. helps absorb fat. 2. cholesterol excretion. 3. antimicrobial activity via membrane disruption.
|
GI
|
|
|
What is the bodies only way of eliminating cholesterol?
|
Via bile salts.
|
GI
|
|
|
What are the differences between direct and indirect billirubin?
|
direct - conjugated with glucuronic acid, water soluble. indirect - unconjugated, water insoluble.
|
GI.
|
|
|
What causes GERD?
|
decrease in lower esphogeal sphincter tone.
|
GI
|
|
|
What are the 3 organisms that cause esophagitis? describe gross path.
|
Candida - white pseudomembrane. HSV-1: punched out ulcers. CMV: linear ulcers.
|
GI
|
|
|
What is boerhaave syndrome?
|
transmural esophageal rupture due to violent retching.
|
GI
|
|
|
what is plummer-vinson syndrome?
|
triad of: dysphagia due to esophageal webs, glossitis, iron defiency anemia.
|
GI
|
|
|
Where are squamous cell esophageal cancers found? what about adenocarcinoma?
|
squamous - upper 2/3. adenocarinoma - lower 1/3.
|
GI.
|
|
|
pancreatic insufficiency leads to malabsportion of what vitamins?
|
ADEK
|
GI
|
|
|
Celiac sprue is related to what HLA?
|
HLA-DQ2, HLA-DQ8, and nothern european descent.
|
GI
|
|
|
What antibodes are found in celiac sprue? Which is used for screening?
|
1. anti-endomysial. 2. anti-tissue transglutaminase. 3. anti-gliadin. Tissue transglutaminase is use for screening.
|
GI
|
|
|
What is curler's ucler?
|
acute gastritis causes by decreased plasma volume yielded burns and then sloughing of gastric mucosa.
|
GI
|
|
|
What is cushing's ulcer?
|
acutue gastritis caused by increased vagal stimulation from brain injury, leading to increased Ach and then increased H+ production.
|
GI
|
|
|
What is the difference between type A and type B gastritis? which is most common?
|
A: antibodies to partietal cells causes pernicious anemia and achlorhydia. In fundus/body/ B: H. Pylori infection. in anturm, most common.
|
GI
|
|
|
Which stomach cancer is associated with H. Pylori?
|
associated: intestinal and MALT lymphoma. not associated: diffuse.
|
GI
|
|
|
What causes appendicits?
|
adult: obstruction by fecalith. kids: lymphoid hyperplasia.
|
GI
|
|
|
What are the five 2's of Meckel's diverticulum?
|
2 inches long, within 2 inches of ileocecal valve, 2% of population, first 2 years of life,2 types of epithelia (gastric +pancreatic)
|
GI
|
|
|
Ishcemic coloitis most commonly occurs where?
|
splenic flexure and distal colon.
|
GI
|
|
|
What is familial adenomatous polyposis?
|
autosomal dominat APC mutation on 5q. 2 hit hypothesis. 100% get colorectal cancer, always involves rectum.
|
GI
|
|
|
What is Gardner's syndrome?
|
Familial adenomatous popylposis + osseous and soft tissue tumors + hypertrophy of retinal pigment epithelium.
|
GI
|
|
|
What is Turcot's syndrome?
|
familal adenomatous syndrome + malignant CNS tumors.
|
GI
|
|
|
what is hereditary nonpolyposis colorectal caner (or lynch) syndrome?
|
autosomal dominant mutation in DNA-mismatch repair genes. 80% get colorectal cancer. proximal colon always involved.
|
GI
|
|
|
What are the risk factors for colorectal cancer?
|
1. IBD 2. Smoking 3. villous adenomas 4. juvenile polyposis sydrome 4. peutz-jeghers syndrome.
|
GI
|
|
|
What is the order of pathogenesis of colorectal cancer?
|
AK-53. loss of APC gene, K-ras mutation, loss of p53.
|
GI
|
|
|
What are the most common site of carcinoid tumors?
|
1. appendix 2. ileum 3. rectum.
|
GI
|
|
|
What are the aminotransferase (AST and ALT) markers for?
|
Viral hep (ALT>AST) and alcoholic hepatitis (AST>ALT).
|
GI
|
|
|
What is alkaline phosphastase a marker for?
|
obstructive liver disease (HCC), bone disase, bile duct disease.
|
GI
|
|
|
what is gamma-glutamyl transpeptidase a marker for?
|
increaed in liver + biliary disease, not bone.
|
GI
|
|
|
what is amylase a marker for?
|
mumps and acute pancreatitis
|
GI
|
|
|
what is lipase a marker for?
|
acutepancreatitis.
|
GI
|
|
|
What is ceruloplasmin a maker for?
|
it is decreased in wilson's disease.
|
GI
|
|
|
Aspirin is avoided in kids EXCEPT when?
|
always avoided EXCEPT in kawasaki's disease.
|
GI
|
|
|
Is hepatic steatosis reversible?
|
it can be
|
GI
|
|
|
What is associated with hepatocellular carcinoma?
|
Hepatitis B+C, wilson's disease, hemochromatosis, a1-antitrypsin deficiency, alcoholic cirrhosis, and alfatoxin.
|
GI
|
|
|
What lab is increased specific to HCC?
|
alpha-fetoprotein.
|
GI
|
|
|
What is a cavernous hemangioma? what is contraindicated in it?
|
benign liver tumor in people over 30. do NOT biopsy due to bleeding risk!
|
GI
|
|
|
What is a hepatic adenoma?
|
benign liver tumor, related of OCP or steriod use. can regress spontaneously.
|
GI
|
|
|
what is a angiosarcoma?
|
malignant tumor of liver endothelial cells, associated with PVC and arsenix.
|
GI
|
|
|
What is the classic triad of hemochromatosis?
|
1. micronodular cirrhosis 2. DM 3. skin pigmentation. (all add up to bronze diabetes).
|
GI
|
|
|
What genes are associated with hemochromatosis?
|
c282Y or H63D mutation in HFE gene. Associated with HLA-A3.
|
GI
|
|
|
What are the causes of acute pancreatitis?
|
(GET SMASHED) gallstones, ethanol, trauma, steroids, mumps, autoimmune, scorpion sting, hypercalcemia/hypertriglycemia, ERCP, drugs(sulfa)
|
GI
|
|
|
What lab has the highest specificity for acute pancreastitis?
|
lipase.
|
GI
|
|
|
What causes a pancreatic psuedocyst? why is it dangerous?
|
causes by acute pancreatitis. lined by granulation tissue which makes it tend to rupture and causes huge hemorrhage.
|
GI
|
|
|
What are the major causes of chronic pancreatitis?
|
idiopathic and alcohol abuse.
|
GI
|
|
|
What are the risk factors for pancreatic adenocarcinoma?
|
tobacco use, chronic pancreatitis, age over 50, jewis or african american.
|
GI
|
|
|
What is Trousseau's syndrome?
|
a migratory thromophlebitis that causes redness and tenderness on extrememities - seen in pancreatic adenocarcinoma.
|
GI
|
|
|
What are the casues of eosinophilla?
|
(NAACP) Neoplastic, asthma, allergic, collagen vacular disease, parasites.
|
heme/onc
|
|
|
What is anisocytosis?
|
varying size RBC
|
heme/onc
|
|
|
what is poikilocytosis?
|
varying shaped RBC
|
heme/onc
|
|
|
What are platelt's derived from?
|
megakaryocyte
|
heme/onc
|
|
|
what are in alpha granules and dense granules in platlets?
|
alpha - vWF and fibrinogen. dense - ADP, calcium.
|
heme/onc
|
|
|
platlet dysfunction results in:
|
petechiae
|
heme/onc
|
|
|
What is the vWF receptor? what about fibrinogen?
|
VWF - GpIb. fibrinogen - GpIIb/IIIa.
|
heme/onc
|
|
|
What is a normal WBC differential?
|
Neutrophil (54-62%), Lymphocytes (25-33%), monocytes(3-7%), Eosinophils (1-3%), basophils (0.-0.75%)
|
heme/onc
|
|
|
What is contained in neutrophil granules?
|
alkaline phosphotase, collagenase, lysozyme, lactoferrin.
|
heme/onc
|
|
|
What do azurophilic (lysozyme) granules contain?
|
acid phosphotase, peroxidase, B-glucuronidase.
|
heme/onc
|
|
|
What is CD14 a cell maker for?
|
Macrophage.
|
heme/onc
|
|
|
Macrophages differentiate from what other cell?
|
monocyte.
|
heme/onc
|
|
|
What do eosinophils produce that limits mast cell degranulation?
|
histaminase and arylsulfatase
|
heme/onc
|
|
|
What do basohil granules contain?
|
heparin, histamine, leukotrienes.
|
heme/onc
|
|
|
What is the universal donor of plasma, the universal donor to RBCs and universal recipient of plasma?
|
donor of RBC = O type, donor of plasma = AB type. reciepent of plasma = O type.
|
heme/onc
|
|
|
What DECREASES ESR?
|
polycthemia, sickle cell anemia, CHF, microcytosis, hypofibrinogenemia.
|
heme/onc
|
|
|
Basophillic stippling of RBC's is seen in what diseases?
|
Thalasemia, Anemia of chronic disease, Pb poisoning.
|
heme/onc
|
|
|
What dieases cause target cell RBC's?
|
HbC disease, asplenia, liver disease, thalassemia.
|
heme/onc
|
|
|
Which coronary arteries supplies the cardiac papillary muscles?
|
Anterior = LAD. Posterior = RCA.
|
cardio
|
|
|
What can cause a U wave on EKG?
|
bradycardia or hypokalemia
|
cardio
|
|
|
What infections are associated with Reiter's arthritis?
|
chlamydia, N. gonhorreae, salmonella, shigella, yersinia, campylobacter, and ureaplasma.
|
micro
|
|
|
What causes basophillic stippling in RBCs?
|
(TAL) thakassemia, anemia of chronix disease, lead poisoning.
|
heme/onc
|
|
|
what causes an elliptocyte RBC?
|
hereditary elliptocytosis.
|
heme/onc
|
|
|
what causes a macro-ovalocyte?
|
megaloblastic anemia or marrow failure.
|
heme/onc
|
|
|
what causes ringed sideroblasts?
|
excess iron in RBC mitochondria.
|
heme/onc
|
|
|
what causes schistocytes and helmet cells?
|
DIC, TTP/HUS, traumatic hemolysis.
|
heme/onc
|
|
|
what causes spherocytes?
|
hereditary spherocytosis, autoimmune hemolysis
|
heme/onc
|
|
|
what causes teardrop RBCs?
|
bone marrow infiltration
|
heme/onc
|
|
|
what causes target cell RBCs?
|
(HALT) HbC disease, Asplenia, liver disease, Thalassemia.
|
heme/onc
|
|
|
What causes heinz bodies?
|
oxidation of hemoglobin sulfhydryl groups causes denaturation of heme and precipitation. eventually leads to bite cells. Seen in G6PD.
|
heme/onc
|
|
|
What causes howell-jolly bodies?
|
basophillic nuclear remnants in RBCs. normally removed in the spleen so they are seen in aslpenia or naphthalene ingestion (mothballs)
|
heme/onc
|
|
|
What are the iron labs in iron deficiency anemia?
|
decreased serumiron, increased TIBC, decreased ferritin, decreased % transferrin saturation.
|
heme/onc
|
|
|
What are the iron labs in chronic disease?
|
decreased serum iron, decreased TIBC, increased ferritin, NC in %transferrin.
|
heme/onc
|
|
|
what are the iron labs in hemochromatosis?
|
increased: serum iron, %transferrin, and ferritin. decreased: transferrin.
|
heme/onc
|
|
|
what are the iron labs in pregancy/ OCP use?
|
increased transferrin making %transferrin decrease.
|
heme/onc
|
|
|
What are the cis/trans deletions in alpha-thallessemia?
|
cis - common in asians, trans - common in africans
|
heme/onc
|
|
|
How does lead poisoning decrease heme synthesis?
|
lead inhibits ferrochetalase and ALA dehydratase, decreasing heme synthesis. also inhibits rRNA deg, causing basophillic stippling.
|
heme/onc
|
|
|
What are the signs of lead poisining?
|
(LEAD) Lead lines on gingivae (burton's lines) and metaphysis of long bones, Encephalopathy and erthryocyte basophilling stippling, abdominal colic and sideroblastic anemia, drops in wrist and foot.
|
heme/onc
|
|
|
What are the hereditary and reversible causes of sideroblastic anemia?
|
hereditary: x-linked defect in gamma-ALA synthase. Reversible: EtOH, lead, INH.
|
heme/onc
|
|
|
What is the treatment for sideroblastic anemia?
|
B6, pyroxidine which is a cofactor for gamma -ala synthase.
|
heme/onc
|
|
|
Describe difference in labs between folate defiecency and B12 deficiency.
|
folate: high homocysteine but normal methymalonic acid. b12: both are high.
|
heme/onc
|
|
|
What is the difference between the PT and PTT test?
|
PT: tests extrinic + common pathway: (only factors I, II, V, VII, X). PTT: intrinic + common: (all factors except VII and XIII)
|
heme/onc
|
|
|
What induces ectoderm to differentiate into neuroectoderm?
|
notochord underneath the ectoderm
|
neuro
|
|
|
What does neural plate give rise to?
|
neural tube and neural crest cells.
|
neuro
|
|
|
What do the alar and basal plate become in CNS development?
|
Alar(dorsal) - sensory. Basal(ventral)-motor
|
neuro
|
|
|
What is the embyronic structure that failes to fuse that causes neural tube defects?
|
neuropores fail to fuse in week 4.
|
neuro
|
|
|
After an aminotic or materal serum a-fetoprotein is detected, what is the confirmatory for neural tube defects?
|
increased AchE in aminotic fluid.
|
neuro
|
|
|
Describe difference in spina bifida occuta, meningocele, and meningomyelocele.
|
spina bifida occulta - failure of spine canal to close, dura intact, no herniation. can see tuff of hair above it. Meningocele - meninges but NOT spinal cord herniates. Meningomyelocele - spinal cord and meninges herniate.
|
neuro
|
|
|
What is anencephaly in utero associated with?
|
1. polyhydramnios ->no swallowing center, fluid not decreased. 2. maternal DM, type 1.
|
neuro
|
|
|
What is holoprosencepahaly?
|
failure of light and right cerebral hemispheres to seperate.
|
neuro
|
|
|
What is a chiari II(arnold-chiari) malformation?
|
cerebellar herniation through foramen magnum with aqueductal stenosis and thus hydrocephalus. usually paralysed beneath defect.
|
neuro
|
|
|
what is a dandy-walker malformation?
|
agenesis of cerebellar vermis with enlargement of 4th ventricle -> associated with hydrocephalus and spina bifida.
|
neuro
|
|
|
What is a chiari I malformation associated with?
|
syringomyelia, usually c8-t1.
|
neuro
|
|
|
What embryologicaly structute do microglia come from?
|
are Marcophages, come from Mesoderm!
|
neuro
|
|
|
What is nissl substance?
|
RER, found only in cell bodies and dendrites. NOT found in axons!
|
neuro
|
|
|
each oligodendrocyte myelinates how many axons? how about schwann cells?
|
oligo = multiple. schawnn = one.
|
neuro
|
|
|
what cells are destroyed in mulitiple sclerosis?
|
oligodendrocytes.
|
neuro
|
|
|
What cells are destroyed in Gullain-Barre syndrome?
|
schwann cells
|
neuro
|
|
|
Describe 3 layers of peripheral nerve.
|
endoneurium - on single nerve, inflammed in gullian-barre. peri - permeability barrier around fasicle, much rejoin in reattachment. epi - aroud entire nerve, has blood and connective tissue.
|
neuro
|
|
|
What is the limbic system responsible for?
|
5 F's: feeding, fleeing, fighting, feeling, sex.
|
neuro
|
|
|
lateral cerebellar injury causes: medial causes:
|
lateral: injured movement in extremeties, wil fall TOWARD injured side. medial: balance, truncal coordination.
|
neuro
|
|
|
What are the 2 major pathology changes in parkinsons?
|
1. lewy bodies (alpha-synuclein inclusions) and loss of dopaminergic neurons (depigmentaiton) in substantia nigra pars compacta.
|
neuro
|
|
|
Compare damage ro paramedian pontine reticular formation to frontal eye fields.
|
PPRF = eyes look AWAY from lesion. frontal eye field = eyes look TOWARD lesion.
|
neuro
|
|
|
Damage to hippocampus results in?
|
inability to make new memories, antereograde amnesia.
|
neuro
|
|
|
what are the signs of central pontine myelinolysis?
|
acute paralysis, dysarthria, dysphagia, diplopia, LOC. Can cause locked in syndrome!
|
neuro
|
|
|
What is Kluver-blucy syndrome and what is it associated with?
|
damage to bilateral amygdala. results in hyperorality, hypersexuality, disinhibition. associated with HSV-1.
|
neuro
|
|
|
What parts of brain are more vulnerable to hypoxia?
|
Hippocampus, neocortex, cerebellum, watershed areas.
|
neuro
|
|
|
Give time course of irreversible neuronal damage.
|
(12-48h) red neuron. (24-72h) necrosis +PMN. (3-5d)marcopahges. (1-2w)gliosis+vascularization. (>2w) glial scar.
|
neuro
|
|
|
What vein can infect spread from the face to the brain?
|
superior opthalamic vein->cavernous sinus
|
neuro
|
|
|
Primitive lesions reemerge after what kind of lesion?
|
damage to frontal lobe.
|
neuro
|
|
|
What is medial medullary syndrome?
|
caused by paramedian branchs of ASA and vertebral arteries ->contra hemiparesis of body, contra decreased in body proprioception, ipsil hypoglossal dysfunction.
|
neuro
|
|
|
Nucleus ambigous lesions are specific to what artery?
|
PICA
|
neuro
|
|
|
Where are most Charcot-bouchard microaneurysms?
|
usually in small vessels, like basal ganglia or thalamus
|
neuro
|
|
|
differntiate lower motor neuron injuries from upper.
|
lower - less muscle mass, less tone, less reflexes, downgoing toes,flaccid paralysis. upper - increaed tone, DTR, + babinski, spastic paralysis.
|
neuro
|
|
|
Poliomyeltis and Wednig-horrman disease specifically destroys:
|
anterior horns, leading to LMN destruction.
|
neuro
|
|
|
How does b12 degerneration differ from tabes dorsalis?
|
Tabes->dorsal column destruction only. b12->dorsal column AND lateral corticospinal AND spinocerebellar. b12 has more movement ataxia.
|
neuro
|
|
|
What is werdnig-hoffman disease:
|
congenital degeneration of anterior horns->LMN damage. causes floppy baby with hypotonia and tongue fasiculations, who dies by 7 months.
|
neuro
|
|
|
Where does spinal cord damate have to occur to cause Horner's syndrome?
|
above T1.
|
neuro
|
|
|
compare superior colliculi to inferior culliculi.
|
superior = conjugate gaze center, inferior = auditory. (eyes are above the ears)
|
neuro
|
|
|
What is perinaud syndrome?
|
Paralysis of conjugate gaze due to a lesion in the superior colliculi.
|
neuro
|
|
|
What is the only cranial nerve WITHOUT thalamic relay to the cortex?
|
1, olfactory
|
neuro
|
|
|
What does nucleus Solitarius control?
|
visceral Sensory information (taste, baroreceptor, gut distension) from CN VII, IX, X.
|
neuro
|
|
|
What does nucleus aMbiguous control?
|
Motor innervation of pharynx, larynx, upper esophagus (swallowing, palate elevation) CN IX, X
|
neuro
|
|
|
What does dorsal motor nucleus control?
|
sends autonomic fibers to heart, lungs, GI. CN X.
|
neuro
|
|
|
How do you tell if a facial nerve palsy is UMN or LMN damage?
|
forehead spared? yes = UMN damage. Bilateral UMN innervation to each LMN. LMN damage = forehead NOT spared.
|
neuro
|
|
|
What is cavernous sinus syndrome?
|
mass effects in the CS, ophthalmoplegia and decreased corneal + maxiliiary sensation with NORMAL vision.
|
neuro
|
|
|
What nerves lay in the cavenrous sinus?
|
III, IV, V1, V2, VI and postganglionic sympathetics.
|
neuro
|
|
|
HPV proteins E6 and E7 have what functions?
|
E6= p53, E7=Rb.
|
Neuro
|
|
|
Koiliocytes are associated with what infection?
|
HPV
|
neuro
|
|
|
How does C-peptide relate to insulin?
|
C-peptide is made when proinsulin is cleaved into insulin. This means the insulin comes from in the body and is no the result of insulin medication overdose.
|
endocrine
|
|
|
Delirum tremens usually occurs how often after the patients last drink of alcohol? How is it treated?
|
2-5 days. with benzodiazepenes to stop seizures.
|
psych
|
|
|
During what stage of infenction can pertussis infection be treated with antibiotics?
|
1st 1-2 weeks, during the flu like stage. during the paroxysmal stage when coughing is bad antibiotics will not help.
|
micro
|
|
|
In CN V3 motor injury, what is the physical defect?
|
jaw deviates TOWARDS the injury due to unopposed opposite ptergoid muscle.
|
neuro
|
|
|
In a CN x lesion, what is the motor deficit in the mouth?
|
uvula deviates AWAY from the lesion, weak side collapses and points uvula away.
|
neuro
|
|
|
What is the motor deficit in CN XI lesions?
|
weakness in turning head to contralateral side and shoulder droop on ipsilateral side.
|
neuro
|
|
|
What is the motor deficit in CN XII lesions?
|
tongue deviates TOWARD side of the lesion due to weak tongue muscles on affected side.
|
neuro
|
|
|
Compare Rhine and weber test for conductive and sensineural hearing loss
|
conductive: abnormal rhine (bone>air), weber localizes to affected ear. sensineural: normal rhine (air>bone), weber localizes to unaffecred ear.
|
neuro
|
|
|
What produces aqueous humor? what collects it?
|
produces it:Cilliary epithelim (B agonist control). collects it: canal of schlemm.
|
neuro
|
|
|
What is closed/narrow angle glaucoma? what are the two types?
|
Lens pushes the iris into the canal of schlemm/trabecular meshwork. this prevents flow of aqueous humor -> IOP goes up.types: Chronic (asymptomatic, peripheral vision loss and optic n. damage) and acute (emergency! painful, sudden vision loss, rock hard eye.)
|
neuro
|
|
|
What drug should NEVER be given in acute closed angle glaucoma? why?
|
Epinephrine, it stimulates myradiasis which worsens the block.
|
neuro
|
|
|
People with CN IV injury have trouble doing what specific action?
|
Going down stairs. They cannot look down while eyes look towards nose.
|
neuro
|
|
|
Cranial nerve III carries what two types of components?
|
motor ->ocular muscles. Parasympathetic ->are first affected by compression. deficit->blown pupil.
|
neuro
|
|
|
Retinal detachment is associated with:
|
1. high myopia 2. seeing floaters and flashes
|
neuro
|
|
|
What is age related macular degenation?
|
degeneration of macula->central blindness. dry degeneration->slow, prevent with multivitamins. wet->fast, due to chorodial neovascularization. prevent with anti-VEGF.
|
neuro
|
|
|
What are the alzheimiers onset/protection genes?
|
early onset = APP(Ch 21), presenilin-1(Ch 14). late onset = ApoE4(Ch 19). protective = ApoE2(19).
|
neuro
|
|
|
What is Charcot's triad of MS?
|
(SIN) scanning speech, Intention tremor(+incontience + internuclear opthalmoplegia), Nstagmus
|
neuro
|
|
|
What is the pathophysiology of neurodegernation in Krabbe's disease?
|
buildup of galactocerebroside destroy's myelin sheath.
|
neuro
|
