Everything Flashcards
GGT (gamma-glutamyl transpeptidase)
serum marker for liver disease; elevated with heavy alcohol consumption
sensitivity =
NAME?
Defective sonic hedgehog gene?
-gene is involved in patterning along anterior-posterior axis-defect assoc with holoprosencephaly (forebrain fails to develop into 2 hemispheres; have 1 central eye…)
ErythrocytosisAnisocytosisPoikilocytosisReticulocyte
NAME?
site of B cell localization and proliferation in lymph nodes?
Follicle - in outer cortex
Which kidney is usually taken during liver donor transplantation and why?
Left Kidney; because it has a longer renal vein
List the 4 most important pharmacokinetics equations: (Vd, Cl, LD, MD)
1) Vd = (amount of drug given)/([drug] in plasma)2) Cl = (Vd X 0.7)/t1/23) LD = Css X Vd4) MD = Css X Cl
Retroperitoneal structures:
“SAD PUCKER”-Suprarenal (adrenal) gland-Aorta and IVC-Duodenum (2nd, 3rd, and 4th parts)-Pancreas (except tail)-Ureters-Colon (descending and ascending)-Kidneys-Esophagus (lower 2/3)-Rectum (upper 2/3)
decreased ceruloplasmin?
Wilson’s disease
Wheezing (asthma symptoms) + diarrhea + facial flushing + mass lesion in appendix area: Diagnosis? Treatment?
Carcinoid syndrome–> ultimate treatment = surgery–> symptomatic treatment = Octreotide (long-acting somatostatin analog)
specificity =
NAME?
Defect in FGF gene?
-involved in lengthening of limbs-defect –> Achondroplasia
Spectrin
supplies the biconcavity/flexibility of RBCs
Which part of lymph node houses T cells?
Paracortex - area of cortex between follicles and medulla-becomes enlarged during extreme immune responses-not well developed in DiGeorge syndrome pts (b/c no T cells…)
Where is the macula densa located?
Distal convoluted tubule
competitive vs noncompetitive inhibitors:1) Resemble substrate?2) Overcome by increased [S]?3) Bind active site?4) Effect on Vmax?5) Effect on Km?6) Pharmacodynamics: effect on potency? efficacy?
Competitive inhibitors:1) Yes2) Yes3) Yes4) Vmax does not change5) Km increases6) decreased potency (increased Km, decreased potency); no effect on efficacyNoncompetitive inhibitors:1) No2) No3) No4) Vmax decreases5) Km does not change6) decreased efficacy (decreased Vmax, decreased efficacy); no effect on potentcy
GI ligament that is a derivative of the fetal umbilical vein? what structure does it contain? what does it connect?
Falciform ligament-contains the ligamentum teres-derivative of the fetal umbilical vein-connects liver to anterior abdominal wall
elevated amylase?
-acute pancreatitis-also elevated in MUMPS!
Most common adrenal medulla tumor in adults? kids?
adults–> pheochromocytoma (causes HTN)kids–> neuroblastoma (does not cause HTN)
Positive Predictive Value = PPV =
= TP/(TP + FP)PPV = proportion of test results that are true positiveif increased prevalence, then increased PPV
Hox genes: -what do they code for? if defective?
-code for DNA-binding transcription factors; involved in segmental organization of embryo in a cranio-caudal direction-Hox mutations–> appendages in wrong locations (ie extra fused digit between 3rd and 4th fingers)
1/3 of platelets are stored in?
Spleen (lifespan = 8-10 days)
lymph node drainage from upper limb, lateral breast?
Axillary lymph nodes
Where are JG cells located?
Afferent arteriole
Zero-order elimination
rate of elimination of drug is constant, regardless of the plasma concentration; Cp decreases linearly with time.Examples = PEA: Phenytoin, Ethanol, Aspirin
GI ligament that contains the portal triad (hepatic artery, portal vein, common bile duct)?
Hepatoduodenal ligament
elevated lipase?
acute pancreatitis
Aldosterone is secreted from?
zona glomerulosa of adrenal cortex–> “salt”–> stimulated by Renin-angiotensin
Negative Predictive Value = NPV =
NAME?
When is embryo most susceptible to teratogens?
between 3-8 weeks, embryonically (so, 5-10 weeks of pregnancy) = “embryonic period” (b/c this is when organogenesis occurs)note: before week 3: all-or-none (miscarriage or nothing)after week 8: growth and function are affected
Causes of polycythemia/erythrocytosis?
-Any time have increased EPO (hypoxia, renal cell carcinoma, HCC, pheochromocytoma, hemangioblastoma)-Down’s babies at birth-Polycythemia vera –> have increased RBCs, but normal EPO
lymph node drainage from stomach
celiac nodes
ureterovesicular junction
narrowest part of the ureter; common site for stones to get stuck
First-order elimination
Rate of elimination is proportional to drug concentration (a constant fraction of the drug is eliminated per unit time); the plasma concentration decreases exponentially with time.
Which GI ligament may be compressed to control bleeding by placing fingers in the omental foramen?
Hepatoduodenal ligamentf
elevated Alkaline Phosphatase?
non-specific:-obstructive liver disease (hepatocellular carcinoma)-bone disease-bile duct diseaseif elevated ALP, can then check GGT. If elevated GGT, then know it’s d/t liver disease
Cortisol (and some sex hormones) secreted from?
zona fasciculata of adrenal cortex–> “sugar”–> stimulated by ACTH, hypothalamic CRH
Point prevalence =
NAME?
What week, embryologically, does the heart begin to beat?
week 4
Barr bodies
=inactivated X in neutrophils–>seen in all women + KF men
lymph node drainage from duodenum and jejunum
superior mesenteric node
nephrocalcinosis
calcification of the medullary periods; assoc w/hyperparathyroidism
Phase I vs Phase 2 metabolism:Which phase do geriatric patients lose first?
Phase I: -reduction, oxydation, hydrolysis-usually yields slightly polar, water-soluble metabolites (often still active)-cytochrome P-450Phase II:-GAS: Glucuronidation, Acetylation, Sulfation-usually yields very polar, inactive metabolites (renally excreted)*Geriatric patients lose phase 1 first
Frequency of waves/peristalsis in stomach? duodenum? ileum?
stomach–> 3 waves/minduodenum–> 12 waves/minileum–> 8-9 waves/min
What is Reye’s syndrome? What are the signs/symptoms?
=Childhood Hepatoencephalopathy:–>mitochondrial abnormalities–>fatty liver (microvesicular fatty change)–>hypoglycemia–>vomiting–>hepatomegaly–>comaMechanism: aspirin metabolites decrease Beta-oxidation by reversible inhibition of mitochondrial enzy
Androgens (sex hormones) are secreted from?
zona reticularis of adrenal cortex–> “sex”–> stimulated by ACTH, hypothalamic CRH
Prevalence =
NAME?
When is it “embryo”? “fetus”?
-“embryo”–> weeks 3-8-“fetus”–> at week 8, on
When do you see hypersegmented polymorphic neutrophils?
NAME?
lymph node drainage from sigmoid colon
colic –> inferior mesenteric node
passage of ureters in relation to the uterine artery and ductus deferens?
ureters pass under uterine artery and under ductus deferens (retroperitoneal) –>”water passes under the bridge”-water=ureters-bridge=uterine arteries and ductus deferens
Efficacy vs Potency
Efficacy: -proportional to Vmax (increase Vmax, increase efficacy)-maximal effect a drug can produce-high efficacy drugs: analgesics, antibiotics, antihistamines, decongestantsPotency:-inversely proportional to Km (increase Km, decrease potency)-amount of drug needed for a given effect-increased potency, increased affinity for receptor-highly potent drugs: chemo drugs, anti-hypertensive drugs, antilipid drugs
Meissner’s plexus:-where’s it located?-other name?-what’s its function?
-located in Submucosa -“submucosal plexus”-controls secretory activity; secretes mucus (so is near the lumen…)
One disease when children should be treated with aspirin?
Kawasaki’s (to prevent coronary artery thrombosis)
Catecholamines are secreted from?
chromaffin cells of adrenal medulla (neural crest derivative!)–>stimulated by preganglionic sympathetic fibers
Incidence =
NAME?
When does hCG secretion begin?
within 1 week after fertilization
Neutrophil chemotactic factors?
-Leukotriene B4-IL-8-C5a
lymph node drainage from rectum?
internal iliac node
60-40-20 rule (of total body weight):
60% = total body water40% = ICF20% = ECF
Pharmacodynamics: Effects of adding competitive antagonists, noncompetitive antagonists, and partial agonists to an agonist on pharmacodynamic curves:
1) Competitive antagonist + agonist –> shift curve to the right = decreased potency (increased Km); no change on efficacy2) Noncompetitive antagonist plus agonist: shift curve down = decreased efficacy (decreased Vmax); no effect on potency3) Partial agonist: acts at the same site as a full agonist, but with reduced maximal effect. Get decreased efficacy (decreased Vmax); potency is variable, can be either increased or decreased.
Auerbach’s plexus:-where’s it located?-other name?-what’s its function?
-located in Musculara externa (really, between muscularis externa inner circular and outer longitudinal layers) -“Myenteric plexus”-controls muscle contractions; coordinates motility along entire gut wall
Best indicators of Liver function and progrnosis?
Prothrombin time and Serum albumin*hypoalbuminemia + elevated PT = POOR prognosis.
Adrenal gland drainage: Left adrenal? Right adrenal?
Left adrenal –> L adrenal vein –> L renal vein –> IVCRight adrenal –> R adrenal vein –> IVC(same as left and right gonadal veins!)
Odds Ratio = OR =
=(a/b)/(c/d) = ad/bc*use OR for case-control studies
What week does the neural tube close?
Neural tube formed by neuroectoderm and closes by week 4 (this is why MUST already be taking folic acid prior to pregnancy, b/c spinal development occurs within the first 4 weeks!)
CD14 = cell marker for?
Macrophages
lymph node drainage from anal canal?
superficial inguinal node
How to measure plasma volume?
radiolabeled albumin
Therapeutic Index: What is it? What’s the equation? Is it safer to have a higher or lower TI?*Examples of drugs with low TI?
TI = measurement of drug safetyTI = LD50/ED50 = median lethal dose/median effective dose(“TILE”)Safer drugs have higher TI valuesExamples of drugs with low TI (must monitor these patients!):-Phenobarbital-Lithium-Digoxin-Coumadin/Warfarin
Roles of the mucosa of the GI tract?
mucosa = innermost layer of gut wall*has 3 parts, each with a role:-epithelium–> absorption-lamina propria–> support-muscularis mucosa–> motility
3 stages of alcoholic liver injury:-Reversible?
1) Hepatic steatosis–> Macrovesicular steatosis/fatty change associated with moderate alcohol intake–>REVERSIBLE with alcohol cessation2) Alcoholic hepatitis:–>from sustained, long-term alcohol intake–>swollen and necrotic hepatocytes; neutrophil infiltration–>Mallory bodies (intracytoplasmic eosinophilic inclusions)3) Alcoholic cirrhosis:–>shrunken liver with “hobnail” appearance–>sclerosis around central vein–>looks like chronic liver disease: hypoalbuminemia, jaundice…–>IRREVERSIBLE
neurohypophysis (post pit) is derived from? adenohypophysis (ant pit)?
-neurohypophysis = neuroectoderm derivative-adenohypophysis = surface ectoderm derivative (from Rathke’s pouch)!
Relative Risk = RR=
= [a/(a+b)]/[c/(c+d)]*use RR for cohort studies
Adenohypophysis arises from which embryologic derivative/germ layer?
Adenohypophysis = Ant pituitary; arises from Rathke’s pouch, from Surface Ectoderm
Causes of Eosinophilia?
*DNA-CAAPA:-Drugs-Neoplastic-Asthma (and Churg-Strauss)-Collagen Vascular diseases-Allergic processes-Addison’s (adrenal insufficiency)-Parasites (invasive)-Acute Interstitial Nephritis
lymph node drainage from testes
superficial and deep plexuses –> para-aortic nodes = retroperitoneal nodes
how to measure extracellular volume?
Inulin
Nicotinic vs Muscarinic ACh receptors
Nicotininc ACh receptors = Na+/K+ channelsMuscarinic ACh receptors = G-protein-coupled receptors, act through 2nd messengers; 5 subtypes = M1, M2, M3, M4, M5
cell type in esophagus?
stratified squamous epithelium
Hepatic steatosis:
-macrovesicular fatty change of liver; see hepatocytes filled with lipid droplets-Reversible effect of moderate alcohol intake; can reverse by stopping to drink alcohol***can also get fatty liver from certain HIV drugs; metabolic syndrome; etc…
Rathke’s pouch gives rise to?
Adenohypophysis (ant pit)!–> Rathke’s pouch = oral ectoderm
Attributable Risk =
= [a/(a+b)] - [c/(c+d)]*AR is the proportion of disease occurences attributable to exposure to a risk factor
Neurohypophysis arises from which embryologic germ layer/derivative?
Neuroectoderm
Phagocytes:-in brain-in tissue-in liver-in joints
NAME?
lymph node drainage from thigh (superficial)
superficial inguinal nodes
Glomerular Filtration barrier is composed of: -Fenestrated Capillary Endothelium-Fused basement membrane -Epithelial layerWhat is each one’s role?Composition?What is lost in nephrotic syndrome? What’s the result?What is lost in Minimal Change disease?
Fenestrated Capillary Endothelium:-Size barrierFused basement membrane:-negative Charge barrier-has heparin sulfate-lose charge barrier in neprhotic syndrome; get: albuminuria, hypoproteinemia, generalized edema, hyperlipidemia*Epithelial layer:-consists of podocyte foot processes-lose podocytes in MCD
Gq:-what receptors stimulate it?-what are its effects?
-Stimulated by alpha 1, M1, M3, H1, V1-stimulates phospholipase C, which stimulates lipid conversion to PIP2, which stimulates increased diacylglycerol and increased inositol triphosphate. –> increased DAG leads to increased protein kinase C–> increased
cell type in stomach?
gastric glands
Mallory bodies
intracytoplasmic eosinophilic inclusions within hepatocytes; see in alcoholic hepatitis
hormones secreted from posterior pituitary?
NAME?
Absolute Risk Reduction
the reduction in risk associated with a treatment as compared to a placebo
Neural Crest derivatives:
-ANS-dorsal root ganglia-cranial nerves-celiac ganglion-melanocytes-chromaffin cells of adrenal medulla-parafollicular (C) cells of thyroid-Schwann cells-pia and arachnoid-bones of skull-odontoblasts (teeth–>crest toothpaste!)-aorticopulmonary septum (sp
Mast cells vs Basophils?
Both are similar, mediate allergic rxn-Basophils in Blood-Mast cells in tissue-mast cells are involved in type 1 hypersensitivity rxns
lymph node drainage from lateral side of dorsum of foot
popliteal nodes
What substances can be used to measure GFR?
-Inulin or Creatinine Clearance.Inulin is freely filtered, but is neither reabsorbed nor secreted.BUT: Creatinine clearance slightly overestimates GFR, b/c creatinine is moderately secreted by renal tubules
Gs:-what receptors stimulate it?-what are its effects?
-stimulated by: B1, B2, D1, H2, V2-stimulates adenylyl cyclases –> increases cAMP –> increases protein kinase A –> increased intracellular Calcium *lots of bacterial toxins use this mechanism!
where in GIT are Brunner’s glands?
Duodenum–>submucosal glands that produce alkaline-rich/bicarb secretion
7 diseases associated with increased risk of hepatocellular carcinoma:
-Hepatitis B-Hepatitis C-Hemochromatosis-Carcinogens (specifically Alfatoxin from Aspergillus)-Alcoholic cirrhosis-alpha-1-antitrypsin deficiency-Wilson’s disease
hormones from anterior pituitary?-which are acidophils?-basophils?
“FLAT PiG”-FSH-LH-ACTH-TSH-Prolactin-GHAcidophils: GH, ProlactinBasophils = “B-FLAT” = FSH, LH, ACTH, TSH
Number needed to treat = NNT =
= 1/absolute risk reduction = 1/[a/(a+b)]
Which germ layer does the spleen arise from?
Mesoderm
Langerhans cells
NAME?
lymph node drainage of prostate
internal iliac nodes
What substance can be used to meausre the ERPF (Effective Renal Plasma Flow)?
-PAH clearance; b/c all PAH entering kidney is secreted
Gi:-what receptors stimulate it?-what are its effects?
-stimulated by: alpha 2, M2, D2-inhibits adenylyl cyclase (so decreased cAMP and decreased protein kinase A)…
Where in GIT are Crypts of Lieberkuhn?
Duodenum, Jejunum, Ileum, and Colon
cancer associatd with elevated alpha-fetoprotein?
Hepatocellular carcinoma
alpha- vs beta-subunit of pituitary hormones:
-alpha = common to TSH, LH, FSH, hCG-beta = determines hormone specificity; different in all of them!
Number needed to harm = NNH =
NAME?
Nucleus pulposus is derived from?
Notochord; Notochord induces ectoderm to differentiate into neuroectoderm and form the neural plate; neural plate gives rise to neural tube and neural crest cells; notochord becomes the nucleus pulposus of the intervertebral disk in adults
Main inducers of primary antibody response?
Dendritic cells = professional APCs
right lymphatic duct vs thoracic duct drains?
right lymphatic ducts drains: right arm and right half of headthoracic duct drains: everything else
ERPF vs true RPF?
ERPF underestimates true RPF by about 10%
alpha 1 receptor:-which G-protein class?-Major functions?
GqFunctions:-increase vascular smooth muscle contraction (increase BP)-mydriasis-increase intestinal and bladder sphincter muscle contraction
Where in GIT are villi and microvilli?
Small intestine; not Colon (makes sense, b/c villi are there to increase absorptive surface)
Common benign liver tumor in 30-50 year olds?
-Cavernous Hemangioma–>DON’T biopsy it! b/c may lead to hemorrhage
Hormones produced by alpha, beta, and delta cells of Islets of Langerhans in pancreas?
alpha cells –> glucagon (peripheral)beta cells –> insulin (central)delta cells –> somatostatin (interspersed)note: somatostatin is also produced by delta cells in gastric mucosa and throughout gutinsulin inhibits glucagon release by alpha cells!
Precision, Accuracy, Reliability, Validity, Random error, Systemic error
Precision = ReliabilityAccuracy = ValidityRandom error - reduces precision in a testSystemic error - reduces accuracy in a test
Agenesis vs Hypoplasia vs Aplasia
Agenesis: No primordial tissue, so no organHypoplasia: Primordial tissue present, but incomplete organ developmentAplasia: Primordial tissue present, but no organ
clock-face chromatin
Plasma cells (B cells differentiate into plasma cells; plasma cells produce lots of antibody specific to a particular antigen)
Where are B cells found in the spleen?
Follicles within white pulp of spleen
RBF =?
RBF = RPF/(1-Hct)
alpha 2 receptor:-G-protein class?-major functions?
GiMajor functions:-decrease sympathetic outflow (decrease NE secretion)-decrease insulin release-decrease BP (vasodilation)-increase glucagon secretion from alpha cells in pancreas
Where in GIT are goblet cells?
Ileum–> has most goblet cells in the small intestine; but, also found in other parts of small intestine: as go along the small intestine, # of goblet cells increases
Nutmeg liver
Backup of blood into liver; d/t right heart failure and Budd-Chiari syndrome–>if it persists, may result in cardiac cirrhosis
Does insulin cross the placenta?
nope!
Standard error of the mean = SEM =
=σ/sqrt of nused in Normal/Guassian/Bell-Shaped curves (where mean = mode = median)where: σ = standard deviationsqrt of n = square root of sample size*note: SEM decreases as n (sample size) increases
Malformation vs Deformation
Malformation: Intrinsic disruption (like a teratogen); occurs during embryonic period (3-8 weeks)Deformation: extrinsic disruption; occurs after embryonic period (after week 8)
plasma cell neoplasm?
Multiple Myeloma –> make a whole bunch of one particular type of B cell, all making one type of antibody (so see monoclonal antibody spike)
Where are T cells found in spleen?
PALS = periarterial lymphatic sheath within white pulp of spleen
Normal Filtration Fraction =?
20%
Beta 1 receptor:-G-protein class?-Major functions?
GsFunctions:-increase HR-increase contractility-increase renin release-increase lipolysis
Where in GIT are Peyer’s patches?
only in Ileum
Condition that looks similar to Right Heart Failure (Hepatomegaly, etc) BUT, absence of jugular venous distension:
Budd-Chiari syndrome
Effects on insulin release of:-GH-somatostatin-Beta-agonists-alpha-agonists
GH–>increase insulinSomatostatin–>decreases insulinBeta-agonists–>stimulate insulinAlpha-agonists–>inhibit insulin
In a normal/gaussian/bell-curve (where mean=median=mode), what percent of the population is 1 σ (standard deviation) to either side of mean? 2σ to either side of mean? 3σ on either side of mean?What percent of the population correlates wtih a σ = 1.645 on either side of the mean?
1σ on either side of mean = 68% of popl2σ = 95%3σ = 100% (99.7%)1.645σ = 90% of popl
teratogenic effect of aminoglycosides?
CN VIII toxicity (hearing problems)
CD3
on ALL T-cells –>Th also have CD4–>Cytotoxic also have CD8
immunlogic results of/response to splenic dysfunction?
splenic dysfunction: decreased IgM–>decreased complement activation –> decreased C3b opsonization –> increased susceptibility to encapsulated organisms (SSHiNK: Salmonella, S. pneum, H. influenza, N. meningitidis, K. pneumonia)
Effect of prostaglandings on kidney:Effect of NSAIDs on kidney?
Prostaglandins dilate afferent arteriole –> so, get:-increased RPF-increased GFR-constant FF*NSAIDs–>inhibit PGs –> get constriction of Afferent Arteriole:-decreased RPF-decreased GFR-constant FF
Beta 2 receptor:-G-protein class?-Major functions?
GsFunctions:-vasodilation-bronchodilation-increase HR (compensatory to increase BP)-increase contractility-increase lipolysis-increase insulin release-decrease uterine tone
Where does celiac trunk come off the abdominal aorta?
T12
Budd-Chiari syndrome:
-Occlusion of IVC or hepatic veins –> leads to congestive liver disease (hepatomegaly, ascites, abdominal pain, eventually liver failure)–>may have varices and visible abdominal/back veins–>Looks kind of similar to Right heart failure, BUT absence of J
Cell types that don’t need insulin for glucose uptake?
“BRICK L”-Brain-RBCs-Intestine-Cornea-Kidney-Liver
relationship of mean, median,mode in a positively-skewed statistical distribution?
positive skew: asymmetry with tail on the right mean > median > mode
teratogenic effect of DES (diethylstilbestrol), a synthetic estrogen
Vaginal clear cell adenocarcinoma (in female fetuses, when older)
anti-AB antibodies (Ig type?)
-IgM –> don’t cross placenta
Howell-Jolly bodies, Target cells, and thrombocytosis
Post-splenectomy
Effect of Angiotensin II on kidneys?
Acts on Efferent Arteriole; constricts EA:-decreased RPF-increased GFR-increased FF
M1 receptor:-G protein?-Functions?
GqFunctions:-CNS, enteric nervous system
Where does the SMA come off the abdominal aorta?
L1
Liver cirrhosis + Panacinar Emphysema?
alpha-1-antitrypsin deficiency –>this is a CODOMINANT trait
GLUT-1
-RBCs-Brain*tissues with GLUT-1 receptors take up glucose regardless of insulin levels
relationship of mean, median,mode in a negatively skewed statistical distribution
negative skew - asymmetry with tail on leftmean < median < mode
Ebstein’s anomaly (enlarged Right atrium; small Right ventricle) - assoc with which teratogen?
Lithium
anti-Rh antibodies (Ig type?)
=IgG –> can cross placenta and cause hemolytic disease of newborn (erythroblastosis fetalis) if fetus is Rh+
Thymus is derived from what branchial pouch?
3rd branchial pouch
Effect of ACE-inhibitors on kidneys?
ACE-inhibitors–> inhibit Ang II –> dilate Efferent Arteriole:-increased RPF-decreased GFR-decreased FF*so, may have increased Creatinine levels in blood (b/c decreased GFR, and Creatinine clearance is a measure of GRF, so decreased Creatinine clearance –> more Creatinine in blood)
M2 receptor:-G-protein?-Functions?
GiFunctions:-decreased HR and contractility of atria
Where do the renal arteries come off the abdominal aorta?
L1
PAS-positive globules in liver?
alpha-1-antitrypsin deficiency
GLUT-2
NAME?
Null hypothesis = H0 =
hypothesis of no difference; there’s no association between disease and the risk factor in the population
Neural tube defects –> caused by which teratogens?
-Folate antagonists-Carbamazepine-Valproate (Valproate and Carbamazepine decrease folate absorption; so, if pts are taking these drugs during pregnancy, then must take extra folate)
Blood type A (example)
NAME?
Where in thymus does positive selection occur? Negative selection?
positive –> corexnegative –> medulla/corticomedullary jxn
What is Creatinine in urine a measurement of?
Glomerular Filtration Rate
M3 receptor: -G-protein?-Functions?
GqFunctions:-increase exocrine gland secretions (ie sweat, gastric acid)-increase gut peristalsis-increase bladder contraction-bronchoconstriction-increase miosis-accommodation (ciliary muscle contraction)
Where does the inferior mesenteric artery come off the abdominal aorta?
L3
Cause of physiologic jaundice in neonates? Treatment?
Immature UDP-glucuronyl transferase at birth (physiologic): can’t convert unconjugated bilirubin to conjugated in liver –> get unconjugated/indirect hyperbilirubinemia –> Jaundice*Treat with phototherapy: converts unconjugated bilirubin to a water-soluble form, so it can be renally excreted! COOL!
GLUT-4
*Requires insulin to be activated!-Adipose tissue-Skeletal muscle
Alternative hypothesis = H1
hypothesis that there is some difference; there is some association between the disease and the risk factor in the population
infant with flat nasal bridge, “railroad track” ears, thin upper limb, small palpebral fissures, epicanthal folds, upturned nose, smooth philtrum (space from nose to upper lip)… may be caused by which teratogen?
Alcohol (Fetal Alcohol Syndrome)
erythroplastosis fetalis-cause?-symptoms?-hypersensitivity type?-how to prevent?
-type 2 hypersensitivity rxn-cause: Rh- mother exposed to Rh+ fetal blood during delivery; makes anti-Rh IgG –> can cross placenta in subsequent pregancies, causing hemolytic disease of newborn in next fetus who is Rh+-Symptoms in infant: hepatosplenomeg
beta-2-microglobulin is found on which class of MHC molecule?
MHC I: has a heavy chain and a beta-2-microglobulin chain
Where in kidney is glucose normally reabsorbed?
Proximal tubule by Na+/glucose cotransport
D1 receptor:-G-protein?-Functions?
GsFunctions:-relaxes renal vascular smooth muscle
What level is the bifurcation of the abdominal aorta?
L4
What is jaundice? What are the 3 causes/types of pathologic jaundice (not counting physiologic neonatal jaundice)?
Jaundice = yellowing of skin and/or sclerae d/t elevated bilirubin*Causes:-Hepatocellular injury-Obstruction to bile flow-Hemolysis
Anabolic effects of insulin (X6)
1) increases glucose transport into adipose and skeletal muscle2) increases glycogen synthesis and storage3) increases TG synthesis and storage4) increases Na retention in kidneys5) increases protein synthesis in muscles6) increases cellular uptake of K and AAs
type 1/alpha error = false positive error
stating there is an effect or difference when none exists; accepting H1 (rejecting H0) when H0 is really true*ie convicting an innocent man
Which fetal structure secretes hCG?
Syncytiotrophoblast (outer layer of chorionic villi)
Deficiency of Factor VIII?
Hemophilia A(“Aight”)
Which HLA genes code for MHC I? MHC 2?
MHC I: HLA-A, HLA-B, HLA-CMHC II: HLA-DR, HLA-DP, HLA-DQ
At what plasma glucose levels does glucosuria begin (threshold)?At what glucose levels is Tm (all transporters fully saturated)?
-see glucosuria at plasma glucose levels of 160-200-all transporters are fully saturated (Tm) at plasma glucose levels = 350 mg/dL
D2 receptor:-G protein?-Functions?
GiFunctions:-modulates transmitter release, especially in brain
Muscle types composing the Esophagus:
upper 3rd–> striated muscle (voluntary)middle 3rd–> striated + smooth muscle*lower 3rd–> smooth muscle (involuntary)
Jaundice, elevated bilirubin in response to fasting, stress, exercise?
–> Gilbert’s syndrome–> have mildly decreased UDP-glucuronyl transferase (so decreased conversion of indirect to direct bilirubin) or decreased bilirubin intake–>mild disease; quite common, but most pts don’t even know they have it–>when flares: have
Glucagon:-secreted by?-secreted in response to?-inhibited by?-effects?
-secreted by alpha cells of islets of pancreas-secreted in response to hypoglycemia-inhibited by: insulin, hyperglycemia, somatostatin-effects:–>glycogenolysis, gluconeogenesis–>lipolysis and ketone production–>increases glucose production/release so i
p value
p = probablity of making a type 1 (alpha) error ps not actually there)
Decidua basalis
maternal component of the placenta; derived from the endometrium; if absent, get placenta accreta (placenta attaches to myometrium instead of to endometrium; so, no separation of placenta after birth; get massive bleeding after delivery)
Deficiency of Factor IX?
Hemophilia B (“Benine”)
which cell types express MHC I? MHC II?
MHC I –> expressed on almost all nucleated cells (not expressed on RBCs)MHC II: expressed only on APCs
Hartnups disease:
deficiency of neutral amino acid (tryptophan) transporter in proximal tubule; so, can’t reabsorb tryptophan-results in pellagra (niacin/B3 deficiency; b/c B3 is derived from Tryptophan)
H1 receptor:-G protein?-Functions?
GqFunctions:-increase nasal and bronchial mucus production-bronchiole contraction-pruritus-pain
Artery that supplies the Foregut? Innervation of the foregut?
NAME?
pathologic jaundice early in life + kernicterus (bilirubin deposition in brain) + elevated unconjugated bilirubin
Crigler-Najjar Syndrome Type 1–>absent UDP-glucuronyl transferase (so can’t convert indirect to direct bilirubin) –> get elevated indirect/unconjugated bilirubin
Bromocriptin
dopamine agonist–>inhibits prolactin secretion; so, can be used to treat prolactinomas
Type 2/Beta error = False negative error
stating there is not an effect or difference when one exists; not rejecting H0 when it actually is false (so choosing H0 when H1 is true) *ie setting a guilty man free
How many umbilical artery/ies? Vein/s?
2 umbilical arteries1 umbilical vein*both are derived from the allantois
Vitamin K deficiency?
decreased synthesis of “diSCo 1972”-proteins C and S-Factors X, IX, VII, II (10, 9, 7, 2)*Vitamin K normally catalyzes carboxylation of glutamic acid residues on proteins involved with blood clotting
HLA-A3
Hemochromatosis
Where in nephron is glucose, AAs, and most of bicarbonate, Na, Cl, and water reabsorbed?
Early proximal tubule
H2 receptor:-G protein?-Functions?
GsFunctions:-increase gastric acid secretion
Artery and Nerve that supply the Midgut?
NAME?
Treatment for Crigler-Najjar syndrome type 1?
-phototherapy (makes Unconjugated bilirubin water-soluble, so can excrete in urine)-Plasmapheresis (get rid of excess unconjugated bilirubin)–>Crigler Najjar type 1 is fatal within a few years
Drug types that stimulate prolactin secretion?
NAME?
Beta
probability of making a type 2 (beta) error
Urachal duct: what is it? what’s it formed from? what if duct fails to obliterate?
During 3rd week: yolk sac forms allantois, which extends into urogenital sinus; allantois becomes urachus, which is a duct between bladder and yolk sac (so, connects fetal bladder to maternal system)*If urachus does not obliterate after birth:-patent urachus –> urine discharge from umbilicus-vesicourachal diverticulum –> outpouching of bladder; asymptomatic
Vitamin K antagonist?
Warfarin–>acts by inhibiting Epoxide Reductase (vitamin K–>activated vitamin K)
HLA-B27
PAIR: -Psoriasis-Ankylosing spondylitis-Inflammatory bowel disease-Reiter’s syndrome
Where in kidney is there “isotonic absorption”?
Early proximal tubule
V1 receptor:-G protein?-Functions?
GqFunctions:-increase vascular SM contraction
Artery and Nerve that supply the hindgut?
NAME?
Crigler-Najjar type 2: -what is it?-treatment?
milder form of Crigler-Najjar type 1; have decreased amount of UDP-glucuronyl transferase (not absent, as in type 1)–>can treat with phenobarbital (increases synthesis of liver enzymes, including UDP glucuronyl transferase)
Why is a side effect of anti-psychotic drugs galactorrhea?
-anti-psychotics are dopamine antagonists-dopamine inhibits prolactin; if decrease dopamine, then increase prolactin-prolactin stimulate milk production!
Power =
= 1 - Betaprobability of rejecting H0 when it is in fact false or likelihood of finding a difference when one in fact existsif increase sample size, then increase power (power in #s!)
urine discharge from umbilicus in neonate: what’s the cause/abnormality?
NAME?
Antithrombin inhibits?
Antithrombin inhibits:-thrombin-factors VIIa, IXa, Xa, XIa, XIIa
HLA-B8
Graves disease
Which part of nephron generates and secretes ammonia?
Early proximal tubule
V2 receptor:-G protein?-Functions?
GsFunctions:-increase H20 permeability and reabsorption in the collecting tubules of the kidney(“V2 is found in the 2 kidneys”)
Watershed area of the GIT?
=> splenic flexure-supplied by the terminal branches of the IMA and SMA, so most sensitive to hypoxia
Phenobarbital
Treatment for Crigler-Najjar type 2 (and can be used for symptomatic Gilbert’s)–>increases synthesis of liver enzymes –> so, increases synthesis of UDP-glucuronyl transferase
Prolactin functions:
-stimulates milk production in breast-inhibits GnRH –> so decreases LH and FSH –> so inhibits ovulation in females, spermatogenesis in males
Meta analysis
pools data/results from several similar studies to reach an overall conclusion; increases power
Vitelline duct: What is it? Abnormalities associated with it?
-Vitelline duct = omphalomesenteric duct –> connects yolk sac to midgut lumen–> obliterated at 7th week*Abnormalities:-Vitelline fistula = failure of duct to close; get meconium discharge from umbilicus-Meckel’s diverticulum = partial closure of duct, m
Drug that activates antithrombin?
Heparin
HLA-DR2
-Multiple sclerosis-Hay fever-SLE-Goodpasture’s
Which part of the nephron is the most hypertonic/concentrated urine?
Thin descending limb of loop of Henle–>impermeable to sodium; passively reabsorbs water b/c sodium can’t get in, so the medulla is hypertonic –> water leaves nephron into medulla, making urine more concentrated.
What class of drugs are these:Bethanochol, Carbachol, Pilocarpine, Methacholine?
Cholinomimetic agents: Direct agonists
What structures make up the foregut? midgut? hindgut?
foregut: stomach to proximal duodenum; also: liver, gallbladder, pancreas, spleenmidgut: Distal duodenum to proximal 2/3 of transverse colon*hindgut: distal 1/3 or transverse colon to upper part of rectum; inludes splenic flexure (watershed area)
Conjugated Hyperbilirubinemia + Black liver on gross examination–>otherwise benign
=Dubin-Johnson syndrome–>defective liver excretion of bilirubin; so get elevated conjugated bilirubin in blood
Somatotropin = Growth Hormone:-stimulated by?-inhibited by?-when is their increased secretion?
NAME?
Confidence Interval = CI =
Range from [mean - Z(SEM)] to [mean + Z(SEM)]example, for a 95% CI: = mean +/- 1.96 X SEM = mean +/- 1.96 X (σ/sqrt n)if 95% CI for a mean difference between 2 variable includes 0, then there’s no significan different and H0 is not rejected*if 95% CI for odds ratio or relative risk includes 1, H0 is not rejected
meconium discharge from umbilicus: what abnormality caused this?
Vitelline fistula (failure of the vitalline/omphalomesenteric duct to close)
Coagulase
Produced by S. aureus–>can convert fibrinogen–>fibrin
HLA-DR3
Diabetes type I
Which part of nephron is impermeable to water?
Thick ascending limb of loop of Henle
What class of drugs are these:Neostigmine, Pyridostigmine, Edrophonium, Physostigmine, Echothiophate, Donepezil
Cholinomimetic agents: Indirect agonists = anti-cholinesterases
Portal triad:
NAME?
Rotor’s syndrome:
mild disorder, similar to Dubin-Johnson syndrome (but less severe); have defective liver excretion of bilirubin, so mildly elevated conjugated bilirubin in blood; unlike Dubin-Johnson syndrome, does not cause black liver
17-alpha-hydroxylase deficiency:-what’s increased/decreased?-symptoms
-increased MCs (aldosterone)-decreased GCs (cortisol) and androgens-symptoms:–>Hypertension–>Hypokalemia —>XY: decreased DHT –> pseudohermaphroditism (looks female, but no internal reproductive structures b/c of mullerian inhibiting factor)–>XX: loo
CI 90%, Z = ?CI 95%, Z = ?CI 99%, Z = ?
CI 90%, Z = 1.645CI 95%, Z = 1.96CI 99%, Z = 2.58*95% CI, corresponds to p=0.05
Meckel’s diverticulum cause?
Due to partial closure of the Vitelline duct (instead of full closure)
tPA, Streptokinase, Urokinase:
All facilitate: plasminogen–> plasmin(so, stimulate breakdown of clots!)
HLA-DR4
NAME?
Which part of nephron is the “diluting segment”, where urine has the lowest osmolality?
Early distal convoluted tubule
What class of drugs are these:Atropine, homatropine, tropicamide, benztropine, scopolamine, ipratropium, oxybutynin, glycopyrrolate, methscopolamine, pirenzepine, propantheline
muscarinic antagonists = cholinergic antagonists
Branches of celiac trunk?
celiac trunk comes off abdominal aorta at T12branches:-common hepatic artery-splenic artery-left gastric artery–> these branches make up the main blood supply of the stomach!
Disease d/t problem with bilirubin uptake into liver?
-Gilbert’s–>elevated unconjugated bilirubinemia
phenotypic female who lacks internal reproductive structures; has HTN and hypokalemia
17-alpha-hydroxylase deficiency–>XY pseudohermaphrodite, but decreased DHT; no internal organs b/c of MIF
t-test vs ANOVA vs chi^2
t-test –> checks difference between means of 2 groupsANOVA –> checks difference between means of 3 or more groupschi-square test –> checks the difference between 2 or more percentages or proportions of categorical outcomes (not of mean values)
Truncus Arteriosus: What does it give rise to?Pathologies associated with abnormal formation?
Gives rise to ascending aorta and pulmonary trunk:-Have neural crest migration –> truncal and bulbar ridges that spiral and fuse to form the aorticopulmonary septum –> ascending aorta and pulmonary trunkPathologies:-Transposition of great vessels (failure to spiral)-TOF (skewed AP septum development)-Persistent TA (from partial AP septum development)
vWF receptor on platelets? Fibrinogen receptor on platelets?
-vWF –> GpIb-Fibrinogen –> GpIIb/IIIa***vWF and Fibrinogen are both inside platelets
HLA-DR5
-Pernicious anemia –> B12 deficiency-Hashimoto’s thyroiditis
Where are Na, K, and Cl actively reabsorbed and Mg and Ca indirectly reabsorbed?
Thick ascending limb of loop of Henle (this is the part that is also impermeable to H20; so, have reabsorption of electrons + water cannot leave (nor enter) –> so this portion of the loop makes the urine less concentrated as it ascends; eventually, it has the lowest osmolality at the early distal convoluted tubule)
List the direct agonists/cholinomimetic agents (X4):
NAME?
Which arteries supply the lesser curvature of the stomach? greater curvature?
lesser curvature –> L and R gastric arteries (L gastric comes off the Celiac trunk; the two gastrics anastamose)Greater curvature: L and R gastro-omental arteries (also anastomose with each other)
Diseases d/t problem with bilirubin conjugation
-Gilbert’s-Crigler-Najjar types 1 and 2-physiologic neonatal jaundice–>elevated unconjugated bilirubinemia
phenotypic female with normal internal sex organs, but lacks secondary sex characteristics; has HTN and hypokalemia
-XX with 17-alpha-hydroxylase deficiency
correlation coefficient = r:
r is always between -1 and 1; the closer the absolute value of r is to 1, the stronger the correlation between the 2 variables*usually report r^2 = coefficient of determination
Bulbus cordis gives rise to:
Right Ventricle and smooth parts (outflow tract) of LV and RV
ESR in pregnancy?
increased
HLA-DR7
steroid-responsive nephrotic syndrome
Where in nephron does PTH act?
Early proximal tubule: PTH inhibits Na/P cotransport –> get increased phosphate excretionEarly distal convulted tubule: increased Ca/Na exchange –> get increased Ca reabsorption
List the indirect agonists/cholinomimetic agents = anticholinesterases (X6)
NAME?
3 Portosystemic shunts (alleviate portal hypertension)
1) Esophageal varices –> anastomosis at the esophagus2) Caput medusae –> anastomosis at the umbilicus3) Internal hemorrhoids –> anastomosis at the rectum
Diseases d/t problem with bilirubin excretion from liver?
-Dubin-Johnson-Rotor’s–>elevated direct/conjugated bilirubinemia
21-hydroxylase deficiency:-what’s increased/decreased?-symptoms?
-increased androgens-decreased MCs (aldosterone) and GCs (cortisol)-symptoms:–>masculinization (female pseudohermaphrodite)–>hypOtension–>hyperkalemia–>increased renin activity***this is the most common form of congenital adrenal hyperplasia
Medicare vs Medicaid:
Medicare: pts > 65 years old ( e for elderly), <65 with certain disabilities, and pts with ESRDMedicaid: federal and state healt assistance for people with very low income (d for destitute)
Left horn of sinus venosus gives rise to:
coronary sinus
Decreased ESR:
NAME?
only lymphocyte member of innate immune system?
natural killer cells
Where in nephron does Angiotensin II act?
Early proximal tubule –> AT II stimulates Na/H exchange –> increased Na and water reabsorption
List the muscarinic antagonists;
NAME?
type of hemorrhoids and cancers seen above and below the pectinate line:
above pectinate line:-internal hemorrhoids (not painful)-adenocarcinomabelow pectinate line:-external hemorrhoids (painful)-squamous cell carcinoma (main risk factor for squamous cell carcinoma here = HPV 16,18,31)
Penicillamine
Treatment for Wilson’s disease
11-beta-hydroxylase deficiency: -what’s increased/decreased?-symptoms?
-increased: Androgens and 11-Deoxycorticosterone (not aldosterone though)-decreased: GCs (cortisol) and Aldosterone-symptoms:–>Hypertension (d/t 11-deoxycorticosterone)–>Masculinization
core ethical principles: autonomy, beneficence, nonmaleficence, justice
autonomy - must respect patients as individuals and honor their preferences in medical carebeneficence - physicians must act in patients’ best interest; may conflict with autonomy. if pt can make an informed decision, then pt ultimatley has right to decidenonmaleficence - “do no harm”; but, if benefits of an intervention outweigh risks, pt may make informed decision to proceed (ie with surgeries, meds…)justice - treat persons fairly
Right horn of sinus venosus gives rise to:
smooth part of right atrium
Spur cell (Acanthocyte)
Liver disease, Abetalipoproteinemia –>irregularly spiked RBCs
What CD-?’s are expressed on NK cells?
NAME?
ADH vs Aldosterone:
ADH primarily regulates osmolarity; but, also responds to low blood volume, when necessary (b/c low volume takes precedence over osmolarity)Aldosterone primarily regulates blood volume
Cholinesterase inhibitor poisoning symptoms (ie excess parasympathetic activity): Antidote to anti-AchE poisoning?
NAME?
Pathway of bile: from production to secretion into duodenum:
Bile made in liver –> R and L hepatic ducts –> Common hepatic duct –> some into common bile duct, some into cystic duct –> from cystic duct, stored in gallbladder, then released back into cystic duct when needed, into common bile duct –> common bile duct meets pancreatic duct at Ampulla of Vater –> bile released via Sphincter of Oddi into Ampulla of Vater in duodenum!
Kayser-Fleischer ring
yellow-green-golden brown corneal ring seen in Wilson’s disease
Finasteride
-inhibits 5-alpha-reductase–>so: decreased DHT–>used to treat male baldness! and BPH
Exceptions to informed consent:
1) Pt lacks decision-making capacity or is legally incompetent (ie minors)2) Implied consent in an emergency3) Therapeutic privilege - withholding information when disclosure would severely harm pt or undermind informed decision-making capacity4) Waiver - pt waives right of informed consent
Right common cardinal vein and right anterior cardinal vein give rise to:
SVC
basophilic stippling
TAIL:-Thalassemias-Anemia of chronic disease-Iron deficiency-LEAD poisoning!–>have denatured RNA within RBCs
Which cytokines activate natural killer cells?
IL-12IFN-alphaIFN-beta
Juxtaglomerular Apparatus:
-JG cells in AA-Macula densa = Na sensor –> in distal convoluted tuule*JGA defends GFR via the RAAS system: JG cells secrete renin in response to low renal BP, low Na delivery to distal tubule, and increased sympathetic tone (beta-1 receptors)
What’s parathion?
Parathion = insecticide = organophosphate; causes cholinesterase-inhibitor poisoning (DUMBBELSS)
Lodging of a gallstone where may lead to obstruction of both bile and pancreatic ducts?
if gallstone is lodged in Ampulla of Vater
decreased levels of ceruloplasmin?
seen in Wilson’s disease–>ceruloplasmin=major copper-carrying protein in blood
Functions of Cortisol (X5):
“BBIIG”1) Blood pressure maintenance (stimulates alpha-1 receptors on arterioles)2) decreased Bone formation (side effect = osteoporosis)3) anti-Inflammatory/Immunosuppressive4) increases Insulin resistance (diabetogenic)5) increases Gluconeogenesis, lipolysis, proteolysis
Minors: Exceptions for when parental consent is NOT required:
NAME?
Where does fetal erythropoiesis occur at different stages?
“Young Liver Synthesizes Blood”Yolk sac –> 3-8 weeksLiver –> 6-30 weeksSpleen –> 9-28 weeksBone marrow –> 28 weeks onward
type of anemia caused by folate or B12 deficiency?
Macrocytic, Megaloblastic anemia
which cytokine induces Th2 formation? which cytokines are secreted by Th2 and what are their actions?
IL-12 induces Th2Th2 makes:-IL-4 –> stimulates B-cells-IL-5 –> stimulates B-cells-IL-10 –> inhibits Th-1 cells and macrophages
Which cells secrete renin?
JG cells (in Afferent Arteriole)
When do you give atropine + pralidoxime?
Give as an antidote to organophosphate poisoning/ Cholinesterase-inhibitor poisoning
What sort of tumor may obstruct the common bile duct?
Tumors of head of pancreas –> can compress ampulla, like a gallstone, thus obstructing common bile duct
Signs/symptoms of Wilson’s disease: “CCCCCopper is Hella BADDD”
-decreased Ceruloplasmin-Corneal deposits = Kayser-Fleischer rings-Cirrhosis-Copper accumulation (in liver, brain, cornea, kidneys, joints, etc)-hepatocellular Carcinoma (increased risk)-Hemolytic anemia-Basal ganglia degeneration (specifically, degenerat
source of PTH?
NAME?
Advance directives:-Oral-Living will-Durable power of attorney
oral advance directive - use incapacitated pt’s prior oral statements as a guide; more valide if pt was informed, directive was specific, pt made a choice; decision was repeated over time to multiple peopleliving will = written advance directive - written by pt ahead of time, in case he/she become incapacitated and cannot communicate*durable power of attorney - pt designates a surrogate to make medical decisions in case he/she loses decision-making capacity; surrogate retains power unless revoked by a patient; more flexible than a living will
Which fetal shunt is patent in about 20-30% of normal adults?
Patent Forament Ovale (kept closed b/c LA pressure > RA pressure)
iron deficiency anemia + esophageal web + atrophic glossitis?
Plummer-Vinson syndrome
which cytokine induces Th1 formation? which cytokines are secreted by Th1 and what are their actions? Which cytokine inhibits Th1?
IL-4 induces Th1Th1 secretes:-IL-2 –> stimulates T-cells-IFN-gamma –> stimulates macrophages*IL-10 (secreted by Th2 cells) inhibit Th1 cells
How may NSAIDs cause acute renal failure?
NSAIDs inhibit the renal production of prostaglandins, which normally keep the afferent arterioles vasodilated and maintain GFR-NSAIDS–>constrict AA–>decrease both RPF and GFR
Atropine:-class of drug?-clinical uses?-effects on eyes, airway, stomach, gi, bladder?-toxicity?
atropine = muscarinic antagonistused to treat bradycardia and for ophthalmic applicationseffects: blocks DUMBBELSS!-Eye–> increases mydriasis, cycloplegia-Airway–>decreases secretions-stomach –> decreases acid secretions-GI –> decreases motility-bladder –> decreases urgency in cystitis*Toxicity: Hot as a hare, Dry as a bone, Red as a beet, Blind as a bat, Mad as a hatter, Bloated as a toad:-increased body temp, decreased sweating-rapid pulse-dry mouth; dry/flushed skin-cycloplegia (blurry, near vision)-constipation (and urinary retention in men with prostatic hyperplasia)-disorientation-acute angle-closure glaucoma in elderly-hyperthermia in infants
Lateral to Medial organization of the Femoral Region:
Lateral: “NAVeL” :Medial-Nerve-Artery-Vein-Lymphatics
What part of brain is degenerated in Wilson’s disease?
Basal ganglia, specifically Putamen, degeneration–>get Parkinsonian symptoms
PTH functions/effects (X4):
1) increases bone resorption–>increases Ca and P2) increases kidney reabsorption of Ca (in distal convoluted tubule)3) decreases kidney reabsorption of phosphate4) increases vitamin D (calcitriol) production by stimulating kidney 1-alpha-hydroxylasestimulates osteoclasts (and thus bone resorption) by increasing production of M-CSF and RANK-L in osteoblasts, which stimulates osteoclastslow serum Phosphorous stimulates vitamin D conversion to active form –> vitamin D stimulates phosphate release from bone and increases phosphate reabsorption (though PTH causes decreased phosphate reabsorption)
Can a pt’s family require a doctor to withhold information from the pt?
No.
Ductus Venosus
shunts blood from umbilical vein to IVC (bypasses hepatic circulation)
“crew cut” on skull x-ray?
Bone Marrow expansion –> see in beta-thal major-thalassemias-Sickle cell disease
What are the antigen presenting cells?
NAME?
4 endocrine functions of the kidneys:
1) Erythropoietin production2) 1,25-(OH)2-vitamin D production –> in proximal tubule; convert vit D to active formNote: vitamin D–> increases Ca and P absorption in intestinesnote: PTH acs directly on the kidney to reabsorb P, but not reabsorb P*note: PTH also stimulates formation of active Vitamin D, which increases absorption of both Ca and P in intestines! 3) Renin –> beta-1 effect4) Prostaglandins –> vasodilates AA to increase GFR
What sympathomimetic should be used to treat:-anaphylactic shock?-cardiogenic shock?-septic shock?
NAME?
Femoral triangle: -formed by?-contains?
formed by:-inguinal ligament-sartorius muscle-adductor longus musclecontains:-femoral nerve, artery, vein (lateral–>medial)
micronodular Cirrhosis + Diabetes + skin pigmentation?
Hemochromatosis = “Bronze” diabetes
what stimulates PTH secretion?
NAME?
Priority of surrogates, if a patient becomes incompetent, but did not prepare an advance directive:
spouse > adult children > parents > siblings > other relatives
Foramen Ovale
shunts blood entering RA from IVC into LA so that it can be pumped out through the aorta to the head and body
chipmunk facies
beta-thal major
What are the 2 signals needed for Helper T-cell activation?
signal 1: foreign antigen, after being phagocytosed by APC, is presented on MHC II of APC and is recognized by TCR on the Th cellsignal 2 = “co-stimulatory signal”: interaction between B7 (on APC) and CD28 (on Th cell)
Hormones that act on the kidney:
1) ANP2) PTH3) AT II4) Aldosterone5) ADH
Epinephrine:-type of drug-what receptors does it act on?-clinical applications
-direct sympathomimetic-acts on alpha 1, alpha 2, beta 1, beta 2-use for anaphylaxis, open angle glaucoma, asthma, hypotension (anaphylactic shock)
What does the femoral sheath contain?
NAME?
Deferoxamine
Treatment for hereditary Hemochromatosis–>also do repeated phlebotomy
vitamin D3 vs D2?
D3–> from sunD2–> from plants*both are converted to 25-OH vitamin D in liver and to 1,25-(OH)2 vitamin D (active form) in kidney
Exceptions to confidentiality:
-potential harm to others is serious-likelihood of harm to self is great-no alternative means exist to warn or to protect those at risk-physicians can take steps to prevent harm:1) reportable disease - physicians my have to warn public officials and ident
Ductus Arteriosus
connects pulmonary artery to aortic arch; blood from LV can bypass pulmonary circulation
Ringed sideroblasts
sideroblastic anemia = defect in heme synthesis (x-linked defect in ALA synthase gene) -treat with B6 (Pyridoxine)
2 signals needed for cytotoxic T-cell activation?
signal 1: viral or self proteins are presented on MHC I and recognized by TCR on cytotoxic T-cellsignal 2: IL-2 from Th1 cell activates cytotoxic T-cell to kill the virus-infected cell
ANP = Atrial Natriuretic Peptide
NAME?
norepinephrine:-type of drug-what receptors does it act on?-applications
-direct sympathomimetic-acts on alpha 1, alpha 2, beta 1-use for hypotension (septic shock)
Sliding vs Paraesophageal Hiatal Hernias:
*Both are types of diaphragmatic hernias, which occur at the gastro-esophageal jxn; stomach herniates upward through the esophageal hiatus of the diaphragm.-sliding hiatal hernia: GE jxn is displaced; have an “hourglass stomach”-paraesophageal hernia: GE jxn is normal; cardia of stomach moves into the thorax
Causes of hemochromatosis?
-herditary (autosomal recessive)-secondary to repeated blood transfusions (ie in Beta-thalassemia major)
Conversion of vitamin D to active form:-enzyme?-what stimulates enzyme?-where does it happen?
1-alpha-hydroxylase-PTH stimulates enzyme-in kidney
What are considered “reportable diseases” (which may be exceptions to confidentiality)
1) STDs: AIDS, gonorrhea, syphilis (sometimes chlamydia, depends on state)2) Hepatitis3) Child immunization infections: MMR and chickenpox4) Food poisoning: shigella, salmonella 5) TB
Fossa Ovalis
Foramen Ovale, after it closes (upon baby’s first breaths)
Lead poisoning symptoms: LEEAADDS
-Lead lines on gingivae (Burton’s lines) and on epiphyses of long bones on x-ray-Encephalopathy-Erythrocyte basophilic stippling-Abdominal colic-Anemia (sideroblastic anemia)-Drops (wrist and foot drop)-Dimercaprol and EDTA = treatment-Succimer = treatmen
2 signals needed for B-cell activation and class-switching?
First, helper T-cells are activated LOOK UP IN IMMUNO BOOK!
PTH:
-secreted in response to low plasma Ca, high plasma P, or low plasma vitamin D-causes: increased Ca reabsorption in DCT, decreased P reabsorption in PCT, and increased vit D productionAlso causes: increased Ca and P absorption from gut (b/c of effects of
isoproterenol:-type of drug-what receptors does it act on?-applications
-direct sympathomimetic-acts equally on beta 1 and beta 2 receptors-used for AV block
“hourglass stomach”
sliding hiatal hernia
lab findings in Hemochromatosis: ferritin, iron, TIBC, transferring?
-elevated ferritin (stores iron within cells)-elevated iron-decreased TIBC (indirect measure of transferrin, which transports iron in blood)-elevated transferritin saturation (serum Fe/TIBC)
functions of vitamin D (X2):
NAME?
What do you do if a 17 year old girl is pregnant and requests an abortion?
many states require parental notification or consent for minors for an abortion; UNLESS SHE IS AT MEDICAL RISK, do not advise a patient to have an abortion regardless of her age or the condition of the fetus
What happens when infant takes a breath at birth?
Breath–> decreased resistance in pulmonary vaculature –> pressure in LA > pressure in RA; foramen ovale closes –> increased O2 leads to decreased PG’s –> closure of ductus arteriosus
Dimercaprol
treatment for lead poisoning (also EDTA)
Th1 cells:-regulate:-secrete which cytokines?-activate what?-inhibited by?
-regulate cell-mediated response-secrete Th1 cytokines: IL-2, IFN-gamma-activate macrophages and CD8+ T-cells-inhibited by IL-10 (from Th2 cell)
AT II = Angiotensin II
-Causes EA constriction –> decreased RPF, increased GFR and increased FF; also get compensatory Na reabsorption in proximal and distal nephron (b/c goal is to increase BP!)
dopamine:-type of drug-what receptors does it act on?-applications
-direct sympathomimetic-acts on all receptors, but its effects vary by dose:low dose –> acts on D1medium dose –> acts on B1 > B2*high dose –> acts on alpha 1 and alpha 2-used for shock (increases renal perfusion), heart failure
What kind of inguinal hernia occurs in infants?
INdirect inguinal hernia in INfants–>goes through the INternal/deep inguinal ring, external/superficial inguinal ring, and into the scrotum (Basically, follows the path of the testes)–>occurs in infants d/t failure of processus vaginalis to close–> Covered by all 3 layers of spermatic fascia
Which HLA is associated with hemochromatosis?
HLA-A3
why is their increases vitamin D and hypercalcemia in sarcoidosis?
-b/c granulomas –> macrophages generate vitamin D (active form)
what to do if a patient is suicidal?
assess the seriousness of the threat; if serious, suggest that the patient voluntarily remain in the hospital; a patient can be hospitalized involuntarily if he/she refuses.
How does deoxygenated blood in fetus go back to mother’s circulation?
After circulating, blood goes through internal iliac arteries to Umbilical arteries —> mother!
Succimer
=treatment for kids with lead poisoning (“SUCks to be a kid with lead poisoning”)
Th2 cells:-regulate?-secrete which cytokines?-another action they do?-inhibited by?
-regulate humoral response-secrete Th2 cytokines: IL-4, IL-5, IL-6, IL-10-help B-cells make antibody (IgE> IgG)-inhibited by IFN-gamma (from Th1 cell)
Aldosterone:
NAME?
dobutamine:-type of drug-what receptors does it act on?-applications
-direct sympathomimetic-acts on Beta 1 mostly (also, slightly on alpha 1, alpha 2, beta 2)-used for heart failure, cardiac stress testing, cardiogenic shock
What type of inguinal hernia passes through the inguinal/Hesselbach’s triangle?
Direct inguinal hernia–> only covered by external spermatic fascia (unlike indirect, which is covered by all 3 layers)–>usually in older men
Complications/Results of Hemochromatosis:
NAME?
Source of Calcitonin?
Parafollicular (C) cells of thyroid (neural crest derivative!)
Apgar score
= assessment of newborn health via a 10-point scale; evaluated at 1 minute and 5 minutes post-birthbased on:-Appearance-Pulse-Grimace-Activity-Respiration> or = to 7 - good4-6 - assist and stimulate<4 at later time points, then risk that child will
Amniotic fluid findings in neural tube defects
increased alpha-fetoprotein and increased Acetylcholinesterase (AChE)
Hypersegmented neutrophils + glossitis +increased homocysteine and:-normal methylmalonic acid?-increased methylmalonic acid?
-if normal methylmalonic acid: Folate deficiency -if increased methylmalonic acid: B12 deficiency***both cause megaloblastic macrocytic anemia (so have impaired DNA synthesis and ineffective erythropoiesis = pancytopenia)
How do natural killer cells induce apoptosis?
use perforin and granzymes to induce apoptosis
ADH/Vasopressin
-secreted in response to elevated plasma osmolarity and decreased blood volume-causes increased # of water channels and increased water reabsorption
phenylephrine:-type of drug-what receptors does it act on?-applications
-direct sympathomimetic-acts on alpha 1 mostly (and a little on alpha 2)-used for pupillary dilation, vasoconstriction, nasal decongestion; good for stopping epistaxis
Hernia that’s most common in women?
Femoral hernia
Cause of primary biliary cirrhosis?
–>Autoimmune reaction: get lymphocytic infiltrate and granulomas–>mostly seen in middle-aged women–>anti-mitochondrial antibodies
Medullary thyroid carcinoma:
abnormal growth of C-cells (doesn’t really affect Calcium metabolism though; despite that Calcitonin is released from C cells)
Definition of low birth weight?
<2500 gassociated with increased physical and emotional problemscaused by prematurity or intrauterine growth retardation*complications: infections, RDS, necrotizing enterocolitis (if feed neonate with formula too soon), intraventricular hemorrhage, and persistent fetal circulation (PDA, PFO…)
Anencephaly: Findings in amniotic fluid?
-malformation of anterior end of neural tube –> no brain-increased alpha-fetoprotein in amniotic fluid + polyhydramnios (b/c no swallowing center in brain)
Megaloblastic anemia that’s not correctable by vitamin B12 or Folate?
–> Orotic Aciduria
How do cytotoxic T-cells induce apoptosis?
release cytotoxic granules containing preformed proteins: -perforin (delievers granules into target cell)-granzyme (activates apoptosis inside target cell)-granulysin (antimicrobial, induces apoptosis)
6 situations that shift K+ out of cells –> causing HYPERkalemia:
NAME?
Metaproterenol, Albuterol, Salmeterol, Terbutaline:-types of drugs?-what receptors do they act on?-Applications
-direct sympathomimetics-B2-agonists (also act very slightly on B1)-Metaproterenol and Albuterol –> used for acute asthma-Salmeterol –> for long-term treatment of asthma-Terbutaline –> to reduce premature uterine contractions
Hernia that’s a leading cause of bowel incarceration/obstruction?
Femoral Hernia
Elevated anti-mitochondrial antibodies?
Primary biliary cirrhosis
hormones that use cAMP signaling pathways:
“FLAT CHAMP + GCG” (all the ant pit hormones, except prolactin and GH)-FSH-LH-ACTH-TSH-CRH-hCG-ADH (V2 receptor)-MSH (melanocyte stimulating hormone)-PTH-GHRH-Calcitonin-Glucagon
Berkson’s bias
a type of selection bias; studies on hospitalized patients
Holoprosencephaly: What is it? What conditions are associated with?
no separation of hemispheres, so may get one central eye (cyclopia), etc…-Associated with: Patau’s syndrome (trisomy 13), severe fetal alcohol syndrome, cleft lip/palate, abnormal sonic hedgehog gene
Pancytopenia =
NAME?
Natural Killer vs Cytotoxic T-cells
Both induce apoptosis of virally-infected or tumor cellsNK cells –> Recognize ABSENCE of MHC-1 on target cell surfaceCytotoxic T-cells –> have CD8, which BINDS to MHC-1 on virus-infected cells
4 situations that shift K+ into cells –> causing HYPOkalemia:
NAME?
Ritodrine:-type of drug-what receptors does it act on?-applications
-direct sympathomimetic-acts on B2 receptors ONLY!-used to reduce premature uterine contractions
Hesselbach’s triangle:-borders?-what type of hernia goes through it?
Borders:-inguinal ligament-inferior epigastric artery-lateral border of rectus abdominisDirect inguinal hernias (older men) go through Hesselbach’s triangle
Causes and pathophysiology of Secondary Biliary Cirrhosis?
–>Extrahepatic biliary obstruction (like a gallstone, biliary stricture, carcinoma of head of pancreas, chronic pancreatitis) –> so, get increased pressure in intrahepatic ducts –> injury and fibrosis –> bile stasis
hormones that use cGMP signaling pathway:
*Vasodilators:-ANP-NO
selection bias
nonrandom assignment to study group (ie berkson’s bias; loss to follow-up)
Chiari II
cerebellar tonsillar herniation through foramen magnus with aqueductal stenosis and hydrocephaly; often presents with syringomyelia
Fanconi’s anemia
DNA repair defect –> get aplastic anemia(NOT the same as Fanconi’s syndrome = proximal tubule reabsorption defect in kidneys!)
What part of the antibody is recognizes antigens?
the antigen binding fragment on the Fab part of the antibody; the VL and VH (variable light and variable heavy) chains recognize antigens.
Too rapid correction of Hyponatremia?
get Central Pontine Myelinosis (irreversible; acute paralysis, dysarthria, dysphagia, diplopia, loss of consciousness)
List 3 indirect sympathomimetics:-What are their actions?-What are their clinical applications?
1) Amphetamines:-indirect general sympathetic agonist; release stored catecholamines-used for narcolepsy, obesity, ADD2) Ephedrine:-indirect general sympathetic agonist-release stored catecholamines-used for nasal decongestion, urinary incontinence, hypotension3) cocaine:-indirect general sympathetic agonist; uptake inhibitor-causes vasoconstriction and local anesthesia
G cells (antrum of stomach) secrete?
Gastrin (“pro-gastric”)
“onion skin” bile duct fibrosis?
Primary Sclerosing Cholangitis (a biliary tract disease)
hormones that use IP3 signaling pathway:
“GOAT + HAG” (post pit hormones!)-GnRH-Oxytocin-ADH (V1 receptor)-TRH-Histamine (H1)-Angiotensin II-Gastrin
recall bias
knowledge of presence of disorder alters recall by subjects
Dandy Walker
Large posterior fossa, absent cerebellar vermis with cystic enlargement of 4th ventricle; may lead to hydrocephalus and spina bifida
Why anemia in kidney disease?
decreased EPO –> decreased hematopoiesis
Which part of the antibody fixes complement?
Complement binding is at CH2 of the Fc part of the antibody (of IgG and IgM only)
U waves on ECG, flattened T waves, arrhythmias and paralysis?
low serum K+
clonidine and alpha-meythldopa:-type of drugs?-act on what type of receptor?-applications?
NAME?
I cells (duodenum, jejunum) secrete?
CCK (“pro-duodenum”, “anti-gastric”–> CCK stimulates pancreatic secretions)
Presentation and Labs in Biliary Tract Diseases (Primary and Secondary Biliary Cirrhosis, Primary Sclerosing Cholangitis):
Presentation:-Pruritis-Jaundice-Dark urine (b/c elevated urobilinogen in urine)-Pale stools (b/c bile not making it into stools)-HepatosplenomegalyLabs:-Conjugated/Direct Hyperbilirubinemia-elevated cholesterol-elevated ALP
hormones that use cytosolic steroid receptors:
“VET CAP” (adrenal hormones + vitamin D!)-Vitamin D-Estrogen-Testosterone-Cortisol-Aldosterone-Progesterone
sampling bias
subjects are not representative relative to general population; so, results are not generalizable
Syringomyelia
-enlargement of central canal of spinal cord; usually at C8-T1*loss of pain and temperature sensation in upper extremities with preservation of touch sensation *associated with Chiari II malformation
Aplastic anemia
NAME?
Which part of antibody do macrophages bind to?
Fc fragment, below the complement binding area
Peaked T waves, wide QRS, arrhythmias:
high serum K+
-azole =
anti-fungal (ie ketoconazole)
S cells (duodenum) secrete?
Secretin (“pro-HCO3”, “nature’s antacid”)
Pruritus in a middle-aged woman + elevated conjugated bilirubinemia?
–>Consider primary biliary cirrhosis–>may also consider primary sclerosing cholangitis
hormones that use nuclear steroid receptors:
-Thyroid hormones –> T3, T4
late-look bias
information gathered at an inappropriate time; a type of recall bias-ie using a suvery to study a fatal disease (b/c only pts still alive can answer the survey…)
Aortic Arch Derivatives:
1st aortic arch –> Maxillary artery (branch of external carotid)2nd aortic arch –> Stapedial artery and Hyoid artery3rd aortic arch –> common carotid artery and proximal part of the internal carotid artery4th aortic arch –> on left: aortic arch; on right: proximal part of right subclavian artery*6th aortic arch –> proximal part of pulmonary arteries and (on left only) ductus arteriosus
Hemolytic anemia in a newborn?
Pyruvate kinase deficiency –> decreased ATP –> rigid RBCs
Which part of the antibody determines the isotype (ie IgG, IgM, IgD, IgE, IgA)? idiotype (ie unique antigen-binding pocket)?
Isotype –> determined by the FcIdiotype –> determined by Fab
effects of low serum Ca?
NAME?
-cillin =
penicillin (ie methicillin)
D cells (pancreatic islets, GI mucosa) secrete?
Somatostatin (inhibits everything!)
Complication of Secondary Biliary Cirrhosis?
Ascending cholangitis = infection of biliary tree (makes sense, b/c have an obstruction of bile flow; bile stasis; etc…)
hormones that use intrinsic tyrosine kinase (MAP kinase pathway) signaling pathway:
*growth factors:-insulin-IGF-1-FGF (fibroblast growth factor)-PDGF (platelet-derived growth factor)
procedure bias
subjects in different groups are not treated the same - ie pay more attention to treatment group, stimulating greater compliance
Derivative of 1st branchial cleft
1st cleft –> external auditory meatus
HbC defect
Glutamic acid-to-lysine mutation *pts with HbSC (1 of each mutant gene) have milder disease than HbSS pts (full sickle cell)
opsonization vs neutralization vs complement activation:
opsonization - antibody promotes phagocytosisneutralization - antibody prevents bacteral adherencecomplement activation - antibody activates complement, enhancing opsoninzation and lysis
effects of high serum Ca?
“stones, bones, groans, moans”-delirium-renal stone-abdominal pain
-cycline =
antibiotic, protein synthesis inhibitor (ie tetracycline)
Which hormone is increased in Zollinger-Ellison syndrome?
Gastrin
What condition is Primary Sclerosing Cholangitis associated with?
Ulcerative Cholitis-primary sclerosing cholangitis can also lead to secondary biliary cirrhosis
hormones that use receptor-associated tyrosine kinase (JAK/STAT pathway) signaling pathway:
-Prolactin-GH-cytokines (IL-2, IL-6, IL-8…)
confoundibg bias
occurs with 2 closely associated factors; the effect of 1 factor distorts or confuses the effect of the other
Branchial Cleft Cysts vs. Thyroglossal Duct Cysts
Branchial Cleft cysts –> within lateral neck; doesn’t move with swallowing; d/t persistent cervical sinus Thyroglossal duct cyst –> in midline of neck; moves with swallowing
older pt, unexplaned anemia:
must rule out colon cancer
Main antibody in secondary/delayed response to an antigen, and most abundant antibody in blood?
IgG (t1/2 of IgG = 21 days; one reason it’s most abundant!)
effects of low serum Phosphate?
bone loss and osteomalacia
-navir =
protease inhibitor (HIV trtmt) (ie saquinavir)
Which GI hormone is stimulated by Phenylalanine and Tryptophan?
Gastrin
Biliary tract disease with Hypergammaglobulinemia (IgM)?
–>Primary sclerosing cholangitis
Which is the active form of hormones: bound or unbound?
-unbound –> free hormone = active hormone
lead-time bias
early detection confused with increased survival; seen with imporved screening (the natural history of the disease is not changed; but, early detection makes it seem as though survival has increased)
1st branchial arch derivatives:
Ms and Ts!Cartilage: Meckel’s; Mandible, Malleus, Mandibular ligamentMuscles of Mastication: Temporalis, Masseter, lateral and Medial pterygoids, Mylohyoid, Tensor Tympani, Tensor veli palatini, ant Two-Thirds of TongueNerves: CN V2 and V3 (Mandibular and Maxillary of Trigeminal)
reversible etiologies of sideroblastic anemia?
NAME?
Which antibodies can fix complement?
IgM and IgG
effectsof high serum Phosphate?
renal stones, metastatic calcifications
-triptan =
5-HT1B/1D-agonists (for migraines) (ie sumatriptan)
What AAs may stimulate gastrin release?
Phenylalanine and Tryptophan
5 main risk factors for gallstones/cholelithiasis:
5 F’s:-Female-Forty-Fat-Fertile (multiparity)-Feathers (Native Americans)
SHBG (sex hormone-binding globulin):-what happens if increased in men?-if decreased in women?-during pregnancy?
-if increased in men–> decreased free testosterone –> gynecomastia-if decreased in women–> increased free testosterone–> hirsutism*have increased SHBG levels during pregnancy
Pygmalion effect
when a researcher’s belief in the efficacy of a treatment changes the outcome of that treatment
2nd branchial arch derivatives:
S’s!Cartilage: Stapes, Styloid process, Stylohyoid ligament, etcMuscles: Stapedius, Styloyoid, etcNerve: CN VII (Seven! for Smiles!)
what vitamin should be supplemented in vegans/vegetarians?
B12 (may get deficiency –> megaloblastic anemia)
Which antibody can cross the placenta?
IgG
Compensatory response to respiratory acidosis or alkalosis?
–> kidneys!if respi acidosis –> kidneys increase renal HCO3 reabsorptionif respi alkalosis –> kidneys decrease renal HCO3 reabsorption–> these compensatory mechanisms take time, are delayed! (unlike compensation of metabolic acidosis/alkalosis, whic
-ane=
inhalational general anesthetic (ie halothane)
What does CCK cause?
Stimulates pancreatic secretion, gallbladder contraction, and gastric emptying
Charcot’s triad of cholangitis (infection of biliary tree/common bile duct):
1) Jaundice2) Fever3) RUQ pain
Source of T3 vs T4?
T4 is from follicles of thyroidT3 is formed from T4 conversion in blood
Hawthorne effect
when a group being studied changes its behavior owing to the knowledge being studied
3rd branchial arch derivatives:
Pharyngeal! Cartilage: greater horn of hyoidMuscle: stylo-pharyngeusNerve: glossopharyngeal (CN IX)
