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)
Hepcidin
released by liver, binds ferroportin on intestinal mucosal cells and macrophages-increased in cases of inflammation: increased hepcidin–>decrease release of iron from macrophages*this is what happens in anemia of chronic disease: decreased iron, decreased TIBC, increased ferritin
Which antibody is found in secretions (tears, saliva, mucus) and breast milk (“colustrum”)?
IgA
Causes of metabolic acidosis with a high anion gap?
MUDPILES!-Methanol (formic acid)-Uremia-DKA-Paraldehyde or Phenformin-Iron tablets or INH (Isoniazid)-Lactic acidosis, hypoxia-Ethylene glycol (oxalic acid)-Salicylates (ie aspirin)
-caine=
NAME?
What does Secretin do?
Stimulates pancreatic HCO3- secretion, decreased gastric acid secretion, increased bile secretion–> it’s “nature’s antacid” –> neutralizes gastric acid in duodenum to allow pancreatic enzymes to function
Murphy’s sign
–>positive in cholecystitis; good way to dx pain in the RUQ–>positive: when deeply palpate, pt has inspiratory arrest b/c such deep pain
4 main functions of T3:
4 B’s:1) Brain maturation (CNS maturation)2) Bone growth (synergistic with GH)3) Beta-adrenergic effects (Beta-1 receptors in heart–> increased CO, HR, SV, contractility)4) increased BMR (via Na/K-ATPase activity –> so increased O2 consumption, RR, body temp)Also: increased glycogenolysis, gluconeogenesis, lipolysis
How to reduce bias:
1) Blind studies 2) Placebos3) Crossover studies (ie each subject is at some point on placebo and some point on drug; so each subject acts as own control to limit confounding bias)4) Randomizaton to limit selection bias and confounding bias
4th-6th branchial arch derivatives:
Neck and Voice box!4th arch –> muscles include cricothyroid muscle; nerve: superior laryngeal branch of CN X6th arch –> all intrinsic muscles of larynx EXCEPT cricothyroid; nerve: recurrent laryngeal branch (CN X)
decreased iron + decreased TIBC + increased ferritin
anemia of chronic disease (inflammation–> increased hepcidin –> decreased release of iron from macrophages
Which antibody is a monomer in circulation, but a dimer when secreted?
IgA
Causes of normal anion gap metabolic acidosis?
NAME?
-operidol=
butyrophenone (neuroleptic) (ie haloperidol)
Somatostatin:-where is it secreted from?-what does it do?
-secreted from D cells in pancreas (islets) and GI mucosa-inhibits:–>decreased gastric acid and pepsinogen secretion–>decreased pancreatic and intestinal secretions–>decreased gallbladder contraction (so, if lots of somatostatin, may get biliary stones
Pain on deep palpation, causing inspiratory arrest
Positive Murphy’s sign–> positive in cholecystitis; way to dx RUQ pain
TBG:-what is it?-how is it affected in hepatic failure? pregnancy? OCP use?
thyroxine-binding globulin –> binds most T3/T4 in blood–>only free hormone is active-reduced in hepatic failure-increased in pregnancy and OCP use (increased estrogen–>increased TBG)
At what age does the moro reflex disappear?
between birth and 3 mos
1st branchial pouch derivatives:
middle ear cavity, eustachian tube, mastoid air cells
Cause of hereditary spherocytosis?
-extravascular intrinsic hemolytic normocytic anemia-caused by defect in proteins interacting with RBC membrane skeleton and plasma membrane (ankyrin, band 3, protein 4.2, spectrin)-premature removal of RBCs by spleen –> splenomegaly, aplastic crisis; ev
Which antibody is produced in primary/immediate response to an antigen?
IgM
Causes of Respiratory alkalosis:
-Hyperventilation (early high-altitude exposure)-Initially after aspirin ingestion (then becomes anion-gap metabolic acidosis)
-azine =
phenothiazine (neuroleptic, antiemetic) (ie chlorpromazine)
What is used more rapidly: oral glucose load or equivalent given by IV?
oral glucose is used more rapidly, d/t GIP = Gastric Inhibitory Peptide = Glucose-dependent insulinotropic peptide
3 causes of gallstones:
-elevated cholesterol and/or bilirubin-decreased bile salts-gallbladder stasis–>all of these can cause stones
TSI
thyroid-stimulating-immunoglobulin–>acts like TSH to stimulate follicular cells in Grave’s disease
when does a child begin to have stranger anxiety?separation anxiety?
stranger anxiety: 7-9 mosseparation anxiety: 12-15 mos
2nd branchial pouch derivatives
Palatine tonsil
Labs for PNH (paroxysmal nocturnal hemoglobinuria)?
increased urine hemosiderin
Which antibody can exist as a pentamer (as well as a monomer)?
IgM
Causes of metabolic alkalosis with compensation (Hypoventilation):
-Diuretics-Vomiting-Antacids-Hyperaldosteronsim (increases H+ secretion)***These are all cases where get rid of acid!
-barbital =
barbiturate (ie phenobarbital)
VIP = Vasoactive Intestinal Peptide:-secreted from?-actions?
source: Parasympathetic ganglia in sphincters, gallbladder, small intestineactions:-increases intestinal water and electrolytes secretion-increases relaxation of intestinal smooth muscle and sphincters
Most common cause of cholecystitis (inflammation of gallbladder)?
Gallstones–>have positive Murphy’s sign!
anti-thyroid peroxidase antibodies
Hashimoto’s
when does a child begin to climb stairs?
12-24 months
3rd branchial pouch derivatives:
dorsal wings –> inferior parathyroidsventral wings –> thymus
complication of PNH?
thrombosis
Which antibody mediates immediate/type I hypersensitivity reactions through release of histamine?
IgE
Causes of Respiratory Acidosis:
*any time can’t get rid of CO2!-airway obstruction-acute lung disease-chronic lung disease-opiods, narcotics, sedatives-weakened respiratory muscles
-zolam =
benzodiazepine (ie alprazolam)
VIPoma:-origin-symptoms?
non-alpha, non-beta pancreatic islet cell tumor-may be associated with MEN I -secretes VIP-symptoms:–>tons of watery diarrhea (b/c VIP stimulates intestinal water and electrolyte secretion) –> so, as a result also have: dehydration, hypokalemia, etc…
Ascending cholangitis =
inflammation of bile duct; usually d/t obstruction of duct by gallstones
Wolff-Chaikoff effect:
transient decrease in T3/T4 due to ingestion of iodide, which inhibits thyroid peroxidase, and therefore organification –> hypothyroidism symptoms
block stacking milestones in child development?
-stacks 3 blocks at 1 year-stacks 6 blocks at 2 years
4th branchial pouch derivatives:
superior parathyroids
Treatment for sickle cell anemia?
-Hydroxyurea –> increases HbF-Bone marrow transplant = ultimately
Which antibody mediates immunity to worms by activating eosinophils?
IgE
How to calculate anion gap:
Anion gap = Na - (Cl + HCO3) = Na - Cl - HCO3
-azepam =
benzodiazepine (ie diazepam)
Endocrine tumor that leads to lots of watery diarrhea?
VIPoma (pancreatic tumor, secretes tons of VIP)
What is acute pancreatitis?
NAME?
Cushing’s syndrome
increased cortisol; causes vary
when can a child begin feeding self with a fork and spoon?
24-26 months
Most common ectopic thyroid tissue site?
Tongue
Coomb’s positive anemia?
autoimmune hemolytic anemia (ie warm agglutinin or cold agglutinin anemias)
which antibody is in lowest concentration in serum?
IgE
3 types of RTA (Renal Tubular Acidosis)
Type 1 = “distal”: defect in CT’s ability to excrete H+ (so increased urinary pH)-associated with hypokalemia and risk for calcium kidney stonesType 2 = “proximal”: defect in PT HCO3 reabsorption-associated with hypokalemia and hypophosphatemic rickets*Type 3 = “hyperkalemic”: Hypoaldosteronism or lack of Ct response to aldosterone-associated with hyperkalemia and can’t excrete ammonium in PT-decreased urinary pH d/t decreased buffering capacity
-etine =
SSRI (ie fluoxetine)
Action = binds vitamin B12 to allow uptake of B12 in terminal ileum?
Intrinsic Factor
Causes of Acute Pancreatitis:
“GET SMASHED”–>Gallstones and Ethanol = Most common causese-Gallstones-Ethanol-Trauma-Steroids-Mumps-Autoimmune disease-Scorpion sting-Hypercalcemia/Hypertriglyceridemia-ERCP (Endoscopic Retrograde Cholangiopancreatography = endoscopic technique to dx/treat problems of pancreatic or biliary ducts; but, main risk of it = acute pancreatitis) -Drugs (ie sultas, HIV drugs…)
1 cause of Cushing’s syndrome?
Exogenous/Iatrogenic steroids–> increased cortisol–> decreased ACTH and decreased CRH
when may a child kick a ball?
24-36 months
Foramen cecum
normal remnant of thyroglossal duct
microangiopathic anemia
-see schistocytes-RBCs damaged when passing through obstructed or narrowed vessel lumina-see in: DIC, TTP-HUS, SLE, malignant HTN; prosthetic valves, aortic stenosis…
Which blood types of mothers may lead to erythroblastosis fetalis and hemolytic disease of newborn?
Type O mothers; because in type O mothers, antibodies are mostly IgG, so can cross placenta and cause fetal hemolysis.But, maternal blood types A and B: anti-A and anti-B antibodies are IgM, so can’t cross placenta…
RBC casts
Glomerulonephritis-Also: ischemia, malignant HTN
-ipramine =
TCA (ie imipramine)
Which substances are secreted by Parietal Cells of stomach?
NAME?
1 cause of chronic pancreatitis?-other main cause?
1 = alcoholismother main cause = smoking
Endogenous causes of Cushing’s syndrome: (and ACTH levels)
1) Cushing’s disease –> pituitary adenoma –> increased ACTH secretion2) Ectopic ACTH: nonpituitary tissue making ACTH (have very high ACTH; ie from Small cell lung cancer, bronchial carcinoids)3) Adrenal: adenoma, carcinoma, nodular adrenal hyperplasia –> decreased ACTH (very low/undetectable)
toilet training age?
24-36 months (pee at three!)
Failure of fusion of the maxillary and medial nasal processes
Cleft lip
rate limiter of heme synthesis?
ALA synthase (delta-aminolevulinic acid synthase)
3 complement pathways:
1) Classic: IgG or IgM mediated; form antigen-antibody complexes2) Alternative: stimulated by spontaneous and microbe surface molecules3) Lectin: mannose
WBC casts
NAME?
-triptyline =
TCA (ie amitriptyline)
Gastrinoma
gastrin-secreting tumor; get constant high levels of acid secretions and ulcers
labs in acute pancreatitis:
-elevated amylase and lipase (lipase = more specific)
Dexamethasone test
test to determine cause of Cushing’s syndrome
tricycle riding age?
3 years (3-cycle at 3!)
Failure of fusion of the lateral palatine processes, the nasal septum, and/or the median palatine processes
Cleft palate
effect of heme on ALA synthase activity
low heme–> increased ALA synthaselots of heme–>decreased ALA synthase
Which 2 complement factors are involved in anaphylaxis?
C3a and C5a
“muddy brown”/Granular casts
Acute tubular necrosis
-olol =
beta-antagonist (ie propranolol)
Secreted by chief cells of stomach
Pepsin
steatorrhea, fat-soluble vitamin deficiency, diabetes
pancreatic insufficiency; may be a result of chronic pancreatitis (which is usually d/t alcoholism or smoking)
Which cause of Cushing’s syndrome is affected by Dexamethasone?
ACTH-Pituitary tumor –> get decreased cortisol levels when give a high dose of dexamethasone
gender identity development age?
24-36 months
Which artery supplies the foregut? midgut? hindgut?
Celiac Artery –> foregutSMA –> midgutIMA –> hindgut
Rate limiter of heme synthesis
ALA synthase (requires B6!)
Which 2 complement factors are involved in opsonization of bacteria?
C3b and IgG
Waxy casts
advanced/chronic renal disease
-terol =
beta2-agonist (ie albuterol)
Action of pepsin?
protein digestion
CA-19-9
specific tumor marker for Pancreatic adenocarcinoma
Causes of primary hyperaldosteronism?-results?-treatment?
Caused by adrenal hyperplasia or aldosterone-secreting adrenal adenoma (Conn’s syndrome)*Effects:-hypertension-hypokalemia-LOW plasma renin-metabolic alkalosis *Trtmnt:-surgery to remove tumor-K-sparing diuretic –> aldosterone antagonist
buttons and zippers, brushes teeth, hops on 1 foot, makes stick figure drawings?
4 years old
Foregut =
pharynx to duodenum; supplied by celiac artery
tea-colored urine + blistering cutaneous photosensitivity?
-Porphyria cutanea tarda (most common porphyria)-d/t deficiency of Uroporphyrinogen Decarboxylase (needed for heme synthesis); get accumulation of Uroporphyrin (hence the tea-colored urine)
What complement complex stimulates cytolysis by MAC?
C5b-9
Hyaline casts
nonspecific
-zosin =
alpha 1-antagonist (ie prazosin)
what activates pepsinogen–>pepsin?
Acid (H+)
CEA
less specific tumor marker for pancreatic adenocarcinoma
Causes of secondary hyperaldosteronism?-results?
–> have an overactive RAAS system, because the kidney “thinks” that there’s a low intravascular volume*Causes:-renal artery stenosis-chronic renal failure-CHF-Cirrhosis-Nephrotic syndrome–> cirrhosis and nephrotic syndrome are low protein states –> so,
imaginary friends age?
4 years old
Midgut =
duodeum to transverse colon (splenic flexure/watershed area); supplied by SMA
painful abdomen + red-wine colored urine + polyneuropathy + psych disturbances; precipitated by drugs:
Acute Intermittent Porphyria -d/t deficiency of Porphobilinogen Deaminase (aka uroporphyrinogen-I-synthase)-accumulate Porphobilinogen, ALA, and uroporphyrin (in urine)
Hereditary angioedema: have increased bradykinin (so increased vasodilation and vascular permeability), episodes of painless, non-pitting, well-circumscribed edema
C1 esterase inhibitor deficiency (C1 esterase inhibitor prevents complement activation on self cells; but, in this case, it is deficient)
What does the presence of casts in urine indicate?
–>casts indicate that hematuria/pyuria is of renal originso, with bladder cancer, kidney stones –> have hematuria, but no castswith acute cystitis –> have pyuria (WBCs), but no casts
-oxin =
cardiac glycoside (inotropic agent) (ie digoxin)
Which cells secrete HCO3-?
-mucosal cells (in stomach, duodenum, salivary glands, pancreas)-Brunner’s glands (in submucosa of duodenum)
painless jaundice in male >50 years old?
consider Pancreatic adenocarcinoma
primary vs secondary vs tertiary adrenal insufficiency:
-primary –> level of adrenal gland-secondary –> level of pituitary (ie no ACTH)-tertiary –> d/t abrupt withdrawal of GCs (still have aldosterone, so no hyperkalemia)primary–> have hyperpigmentation and hyperkalemiasecondary –> no hyperpigmentat
copies line or circle drawings - development age?
3 years old
Hindgut =
distal transverse colon (splenic flexure/watershed area) to rectum; supplied by IMA
Treatment for Acute Intermittent Porphyria?
-Glucose and Heme –> inhibit ALA synthase
recurrent pyogenic sinus and respiratory tract infections (esp S. pneum and H. infl), and increased susceptibility to type III hypersensitivity rxns (esp glomerulonephritis)
C3 complement deficiency
Nephritis vs Nephrotic syndromes:
Nephritic–> Inflammatory; hematuria and RBC casts in urine–>have azotemia (increased BUN and increased Creatinine), oliguria, HTN (d/t salt retention), and mild proteinuria ( Proteinuria (>3.5g/day), frothy urine, hyperlipidemia, fatty casts, edema–>associatd with thromboemolism and increased risk of infection (b/c loss of immunglobulins) **lose charge barrier (fused basement membrane) of glomerular filtration barrier in nephrotic syndrome
-pril =
ACE-inhibitor (ie captopril)
How do NSAIDs lead to acidic damage in stomach?
-Prostaglandins generate mucus that covers that covers the gastric epithelium–>NSAIDs–>decrease PGs–> decrease mucus –> decrease HCO3- –> increased susceptibility to acidic damage in stomach
1 risk factor for Pancreatic Adenocarcinoma?-other risk factors?
1 = Smoking (but, not alcoholism)*other risk factors:-chronic pancreatitis (which is usually caused by alcoholism or smoking… kind of contradicts the not alcoholism thing…)-Jewish and African American males- >50 years old-Diabetes-Genetics
Acute primary adrenal insufficiency:
Caused by Waterhouse-Friderichsen syndrome –> adrenal hemorrhage associated with N. meningitidis septicemia, DIC, petechial rash, endotoxic shock
Changes in the elderly: (sex, sleep, suicide, vision, hearing, immune, bladder, renal, pulmonary, GI, muscle mass, fat)
1) Sex: (note: sex interest does not change)-Men–> slower erection/ejaculation, longer refractory period -Women –> vaginal shortening,thinning, dryness2) Sleep: -decreased REM, slow-wave sleep (stages 3 and 4)-increased latency and awakenings (takes longer to reach REM sleep)3) increased suicide rate (males 65-74 yo have highest suicide rate in US)4) decreased vision, hearing, immune response, bladder control5) decreased renal, pulmonary, GI function6) decreased muscle mass, increased fat*Note: 5 and 6 affect drug dosage and metabolism; for this reason, start SLOW and LOW when giving drugs to elderly!
Gastroschisis
extrusion of abdominal contents through abdominal folds; not covered by peritoneum (increased AFP in amniotic fluid)
Defect in factors I, II, V, VII, X –>?
increased PT (extrinsic pathway defect)
Recurrent Neisseria bacteremia (N. gonococcal and N. meningococcal)
C5-C9 complement deficiency
Lumpy bumby appearance of glomeruli on LM?
Acute PSGN
-afil =
erectile dysfunction (ie sildenafil)
Which glands secrete saliva? What stimulates saliva secretion (PSNS, SNS?)? When is saliva hypotonic/isotonic?
-secreted from parotid, submandibular, sublingual glands-stimulated by Sympathetic AND Parasympathetic activity-Normally is hypotonic, but is more isotonic with higher flow rates, b/c less time for absorption***Sympathetic stimulation–> thicker secretion
Courvoiseier’s sign:
-obstructive jaundice with palpable gallbladder–>pruritus, dark urine, pale stools (all signs of obstructive jaundice…) –>see with pancreatic adenocarcinoma
increased urinary VMA
VMA= breakdown product of norepinephrine*increased in pheochromocytoma–>also have increased plasma catecholamines
Normal bereavement vs Pathologic grief
Normal bereavement: shock, denial, guilt, somatic symptoms; can last up to 2 months; may experience illusionsPathologic grief: excessively intense grief, grief that lasts >2 months; or grief that is delayed, inhibited or denied. May have depressive symptoms, delusions, hallucinations.
Omphalocele
persistence of herniation of abdominal contents into umbilical cord; covered by peritoneum (Increased AFP in amniotic fluid)
Defect in all factors EXCEPT VII and XIII?
increased PTT
DAF (decay accelerating factor) deficiency may cause?
DAF is a complement inhibitor, meant to prevent complement activate on self-cells. If deficient, may lead to Paroxysmal Nocturnal Hemoglobinuria and to complement-mediated lysis of RBCs
child with peripheral and periorbital edema, dark urine, elevated anti-ASO, elevated anti-DNAse B, decreased C3 and total complement levels
Acute PSGN
-tropin =
pituitary hormone (ie somatotropin)
How does Gastrin stimulate acid secretion in stomach?
G cells in antrum of stomach are stimulated by vagus nerve (via GRP transmitter)–> release Gastrin into circulation –> Gastrin stimulates ECL (EnteroChromaffin-Like) cells to release Histamine –> Histamine induces Parietal cells to secrete HCl
Trousseau’s syndrome:
-migratory thrombophlebitis–> redness and tenderness on palpation of extremities–>see with pancreatic adenocarcinoma
Symptoms of pheochromocytoma:
6 P’s:-Pressure –> elevated BP-Pain –> headache-Perspiration-Palpitatons –> tachycardia-Pallor-Panic attacks**symptoms occur in “spells” - relapse and remit
Physiologic effects of stress:
stress induces production of: -free fatty acids-17-OH corticosteroids (increased corticosteroids –> immunosuppression)-lipids-cholesterol-catecholamines-also, affects: water absorption (have decreased water absorption), muscular tonicity, gastrocolic reflex, and mucosal circulation
infant with cyanosis, choking/vomiting with feeding, air bubble in stomach on CXR, polyhydramnios (in utero), can’t pass NG tube into stomach, pneumonitis
Tracheoesophageal fistula (polyhydramnios, b/c fetus can’t swallow amniotic fluid, b/c blind esophagus, etc…)
Defects in platelet plug formation?
increased BT (bleeding time)
pro-inflammatory cytokines?anti-inflammatory cytokines?
IL-1 and IL-6 –> pro-inflammatoryIL-10 and TGF-Beta –> anti-inflammatory
supepithelial humps on EM
Acute PSGN
-tidine =
H2-antagonist (ie cimetidine)
Affects of atropine on GI secretions?
Atropine = anti-cholinergic–> blocks vagal stimulation of parietal cells (use ACh as transmitter)–> BUT, no effect on G cell stimulation by vagal cells, because G cells use a different transmitter, GRP (not ACh) –> so, Gastrin can still stimulate parietal cells to secrete Intrinsic Facor and (via enterochromaffin-like cells and histamine) to secrete HCl
Presentation of pancreatic adenocarcinoma:
-abdominal pain that radiates to back-weight loss-redness and tenderness on palpation of extremities (migratory thromboephlebitis = Trousseau’s sign)-Obstructive jaundice and palpable gallbladder –> pruritus, dark urine, pale stools (=Courvoiseier’s sign
Treatment for Pheochromocytoma?
NAME?
How to calculate BMI?What BMI range = overweight?
BMI = weight in kg/(height in meters)^2Overweight: 25.0-29.9 Obese: >30morbidly obese: >40
infant about 2 weeks old with: palpable “olive” mass in epigastric region and non-bilious projectile vomiting
Congenital pyloric stenosis (most common condition requiring surgery during first month of life)
Bernard-Soulier disease:-defect-labs (BT =bleeding time; PC=platelet count)
defect in Gp1b–> so vWF can’t bind platelets for platelet plug formationincreased BTdecreased PC
functions IL-1 through IL-5
“Hot T-Bone stEAk”IL-1: Hot –> pyrogen, fever, acute inflammationIL-2: T –> stimulates growth of helper and cytotoxic T-cells (note: lots of immunosuppressants block IL-2)IL-3: B–> stimulates Bone marrow stem cells (functions like GM-CSF = granulocyte macrophage colony stimulating factor)IL-4:E –>stimulates class-switching to IgE and IgG. Also: induces differentiation into Th2 cells, and promotes growth of B cellsIL-5: A –> stimulates class-switching to IgA and stimulates eosinophil production (it’s the mucus-producing IL!); also: promotes differentiation of B cells.
Wegener’s vs Goodpasture
both cause Crescentic/RPGN–>Goodpastures only affects lung and kidneys (hematuria + hemoptysis)–>Wegener’s: c-ANCA; and can also affect upper airways, so may present with sinusitis, nasal perforation, as well as hematuria, hemoptysis
-dronate =
bisphosphonate (for osteoporosis) (ie alendronate)
How do prostaglandins protect the stomach?
-decrease acid secretion (Gi–>decreased cAMP–>decreased proton pumping)-increase mucus and HCO3- production
Asterixis:
See in:-liver cell failure-Wilson’s disease
elevated urinary HVA (homovanillic acid)
Neuroblastoma (=most common adrenal medulla tumor in kids)–>HVA=breakdown product of domapine
Drugs, Diseases, and Psychological issues that may lead to sexual dysfunction:
Drugs: antihypertensives, esp Beta-blockers; neuroleptics; SSRIs; ethanolDieases: depression, diabetes, atherosclerosis (because decreased blood flow to area), hyperprolactinemia, low testosteronePsychological: Performance anxiety
What germ layer does the pancreas arise from?
Endodermal
Glanzmann’s thrombasthenia:-defect?-BT/PC?
-defect in GpIIb/IIIa –> platelets can’t link to eachother, so no platelet aggregation for platelet plug formation-increased BT-no effect on PC
Which cytokines are secreted by macrophages?
IL-1, IL-6, IL-8, IL-12, TNF-gamma
subendothelial and maybe intramembranous IgG-based immune complexes, often with C3 deposition seen on EM
Diffuse Proliferative GN
-sartan =
Ang II-receptor-antagonist (ie losartan, valsartan)
3 factors that stimulate G-cells to make Gastrin?
NAME?
Drugs that end in “-dine”
H2 blockers: Cimetadine, Ranitidine, Famotidine, Nizatidine–> take H2 blockers before you “dine”
T3 uptake in hypothyroidism? hyperthyroidism?
NAME?
only serotonin-releasing neurons in CNS?
Raphe nucleus
Ventral pancreatic bud becomes? Dorsal pancreatic bud becomes?
Ventral pancreatic bud –> pancreatic head, uncinate process, and main pancreatic ductDorsal pancreatic bud –> becomes everything else
ITP = Idiopathic Thrombocytopenic Purpura:-defect?-labs?
-defect:have anti-GpIIb/IIIa antibodies–> antibodies bind platelets –> complex gets consumed by splenic macrophages-increased BT-decreased PC-also have increased megakaryocytes (trying to make more platelets!)
Which cytokines are secreted by all T-cells? by Th1 only? by Th2 only?
all T-cells secrete IL-3Th1 secrete: IL-2, IFN-gamma*Th2 secrete: IL-4, IL-5, IL-10
wire looping of capillaries on LM
Diffues Proliferative GN–>see in SLE or MPGN (Membranoproliferative GN)
-chol =
cholinergic/muscarinic agonist (ie bethanechol, carbachol)
What may cause hypertrophy of Brunner’s glands?
Peptic ulcer disease (b/c lots of acid to deal with)–>Brunner’s glands are located in duodenal submucosa; function = secrete alkaline mucus to neutralize acid contents entering duodenum from stomach
Ranitidine
H2 blocker
antimicrosomal, anti-thyroglobulin antibodies
Hashimoto’s
Which stage of sleep do we spend most of the time in?
Stage 2
Annular pancreas
Ventral pancreatic bud abnormally encircles 2nd part of duodenum; forms ring of pancreatic tissue that may cause duodenal narrowing
TTP = Thrombotic Thrombocytopenic Purpura-defect?-labs?
deficiency of vWF metallprotease –> decreased degradation of vWF multimers: so: increased vWF multimers–> increased platelet aggregation and thrombosis–> decreased platelet survival-increased BT-decreased PC-schistocytes-increased LDH
Which cytokine is the major chemotactic factor for neutrophils?
IL-8 (“clean up on aisle 8!” –> neutrophils come clear infections!)
most common cause of death in SLE?
-Diffuse Proliferative GN (associated with anti-dsDNA marker)–> can present as nephrotic and nephritic syndrome concurrently
-curium or -curonium =
paralytic drugs (non-depolarizing NM-blocking drugs; reversed with neostigmine) (ie atracurium, vecuronium)
Trypsinogen:-secreted by?-converted to trypsin by?-action?
-secreted by pancreas-enterokinase/enteropeptidase converts trypsinogen–>trypsin-converts other proenzymes/zymogens and more trypsinogen to active form-trypsin (and other zymogens)–> involved in protein digestion
Cimetidine
H2 blocker–>inhibits cytochrome P450!–>also: -gynecomastia, impotence, decreased libido in males (anti-androgen effects)-can cross BBB (headaches, dizziness, confusion)-can cross placenta
Hurthle cells
enlarged epithelial cells with excessive eosinophilic granular cytoplasm; found in Hashimoto’s
EEG waveform patterns during each sleep stage:
“at night, BATS Drink Blood”awake (eyes open) –> Beta waves (highest frequency, lowest amplitude)awake (eyes closed) –> Alpha waves stage 1 –> Theta wavesstage 2 –> Sleep spindles and K complexesstage 3 –> Delta waves (lowest frequency, highest amplitude)REM –> Beta waves
Potter’s syndrome:
bilateral renal agenesis –> oligohydramnios –> limb deformities, facial deformities, pulmonary hyperplasia *caused by malformation of ureteric bud
Affect of aspirin on BT/PC?
increased BTno effect on PC(like Glanzmann’s)
Interferons alpha, beta, and gamma functions:
-all activate NK cells and kills virus-infected cells-alpha and beta –> inhibit viral protein synthesis-gamma –> stimulate MHC I and II expression and antigen presentation in all cells
Nephritis + IgA immune complexes in mesangium + URI or acute gastroenteritis
Berger’s disease = IgA nephropathy–>related to Henoch-Schonlein disease (vasculitis, also have IgA immune complexes)
-stigmine =
anti-cholinesterase (ie neostigmine, physostigmine, pyridostigmine)
alpha-amylase
secreted by pancreas-digests starch***also have amylase in saliva, which digests starch in saliva
Famotidine
H2 blocker
What cancer is increased risk in Hashimoto’s?
non-Hodgkin’s lymphoma
During which sleep stage does one have sleep spindles and K complexes on EEG?
Stage 2 sleep
Horseshoe kidney
Fusion of inferior poles of both kidneys; get trapped under INFERIOR MESENTERIC ARTERY and thus remain low in the abdomenkidneys function normallyassoc. with Turner’s syndrome
All platelet disorders effects on BT/PC?
-all increase BT-all decrease PC, except Glanzmann’s
All T-cells express:
-TCR (binds antigen-MHC complex)-CD3-CD28 (binds B7 on APC)Th cells –> CD4 alsocytotoxic T-cells –> CD8
Nephritis with mutation in type IV collagen –> split Basement membrane, X-linked
Alport syndrome = “can’t see, can’t pee, can’t hear”–>have nerve disorders, ocular disorders, deafness
-mustine =
nitrosureas (cross BBB, used to treat brain cancers)
Lipase
secreted by pancreas-digests fat
Nizatidine
H2 blocker
pot-bellied, pale, puffy-faced child with protruding umbilicus and protuberant tongue:
Cretinism –> d/t severe fetal hypothyroism-endemic in areas lacking dietary iodine-sporadic d/t defect in T4 formation or developmental failure in thyroid formation
What is the key to initiating sleep?
Serotonergic predominance of the raphe nucleus
Mesonephric duct develops into:
Mesonephric duct = Wolffian duct (development is stimulated by androgen secretion from Leydig cells)*Develops into male internal structures (except prostate!): “SEED”-Seminal vesicles-Epididymis-Ejaculatory duct-Ductus deferens
most common inherited bleeding disorder?
von Willebrand’s disease
CD19, CD20, CD21 –> all present on what cell type?
B-cells
most common glomerular disease in HIV pts?
Focal Segmental Glomerulosclerosis
-statins =
HMG-coA reductase inhibitors (ie atorvastatin)
salivary amylase vs pancreatic amylase:
*both digest starch-salivary: hydrolyzes alpha-1,4-linkages to form disaccharides-pancreatic: hydrolyzes starch to oligosaccharides and disaccharides
Drugs that can cause gynecomastia? (random, not necessarily GI)
“Some Drugs Create Awesome Knockers”-Spirinolactone-Digitalis-Cimetidine-Alcohol-Ketoconazole
Very tender thyroid, following a flulike illness; self-limited hypothyroidism
Subacute thyroiditis = de Quervain’s–>have increased ESR, jaw pain, tender thyroid… may look hyperthyroid early in course
What drug can be used to treat enuresis (bed-wetting) and why?
Imipramine, because it decreases stage 3 sleep (when bed-wetting occurs)
Paramesonephric duct develops into:
Paramesonephric duct = Mullerian duct; develops into female internal structures: -Fallopian tube-Uterus-upper 1/3rd of vagina (Lower 2/3rds of vagina develop from urogenital sinus)
PC, BT, PT, PTT findings in von Willebrand’s disease?
NAME?
CD14, CD16, and CD40 are present on what cell type?
Macrophages
Most common cause of adult nephrotic syndrome?
Membranous GN
-glitazones =
increase target cell response to insulin (ie rosiglitazone, pioglitazone)
D-Xylose absorption test
Test to distinguish GI mucosal damage from other causes of malabsorption–>D-xylose is normally easily absorbed by intestines; if problem with intestinal absorption, get low levels of D-xylose in urine and blood
Mechanism of H2 blockers?
-reversibly block Histamine (released from ECL cells, after stimulation by Gastrin) from binding to the H2 receptor on gastric parietal cells–>get decreased cAMP, meaning no stimulation of the ATP-ase –> decreased H+ secretion from parietal cells into g
rock-hard, painless goiter
Riedel’s thyroiditis –> type of hypothyroidism-thyroid replaced by fibrous tissue-histology: fibrosis, macrophages, eosinophils infiltrate in thyroid
During what sleep stage does teeth grinding (bruxism) occur?
Stage 2 (deeper sleep, when have sleep spindles and K complexes on EEG)
Cause of bicornuate uterus?
Incomplete fusion of paramesonephric ducts
-treatment for von-Willebrand’s disease?
DDAVP = Desmopressin (releases vWF stored in endothelium)
CD16, CD56 are present on what cell type?
NK cells (CD16 is also on macrophages; but CD56 is a unique marker for NK cells)
Spike and dome appearance on EM with subepithelial deposits
Membranous GN
-bendazoles=
anti-parasitic (esp anti-helminthic)
SGTL1 = Sodium-Glucose-Co-Transporter:
Na-dependent transporter; absorbs Glucose and Galactose in enterocytes
What are more potent drugs: H2 blockers or PPIs?
PPIs are more potent than H2 blockers; so, use H2 blockers for less severe cases; PPIs for more severe*note: H2 blockers are reversible; PPIs are irreversible
pretibial myxedema
Grave’s disease
During what sleep stages may one experience sleepwalking, night terrors, or bed-wetting?
Stage 3 sleep (deepest, non-REM sleep; slow-wave sleep; have delta waves on EEG)
Female equivalent of glans penis?
glans clitoris
PC, BT, PT, PTT findings in DIC?-other lab findings?
-decreased PC-increased BT-increased PT-increased PTT-also: schistocytes, increased D-dimers (fibrin split products), decreased fibrinogen, decreased factors V and VIII)
How do superantigens work?
Superantigens (like from S. aureus, and Group A Strep) –> cross-link the TCR on T-helper cells to the MHC class II on APCs: So, get uncoordinated release of IFN-gamma from Th1 cells; IFN-gamma stimulates macrophages, so get release of IL-1, IL_6, and TNF-alpha from macrophages
Foot process effacement on EM
Minimal Change Disease
-dipine =
Ca-channel blockers (specifically dihyropyridine CCB’s) (ie nifedipine, amlodipine)
GLUT-5
absorbs Fructose (by facilitated diffusion) into enterocytes
drugs ending in “-prazole”
PPIs (proton pump inhibitors)-Omeprazole-Lansoprazole-Pantroprazole-Esomeprazole
Thyroid storm:-what is it?-treatment?
-stress-induced catecholamine surge leading to death by arrhythmia–> complication of Grave’s and other hyperthyroid syndromes–>treat with Beta-blockers (Propranolol)
During what sleep stage does one experience: dreaming, loss of motor tone, memory processing, erections, increased brain oxygen use?
REM sleep; Beta waves on EEG
female equivalent of corpus cavernosum and spongiosum?
vestibular bulbs
Causes of DIC?
“STOP Making New Thrombi”-Sepsis-Trauma-Obstetric complications-acute Pancreatitis-Malignancy-Nephrotic syndrome-Transfusion
How do endotoxins/lipopolysaccharides work?
ie in gram (-) bacteria –> stimulate macrophages directly (Th cells not involved, unlike with superantigens) by binding to CD14 receptor –> release of acute phase cytokines (IL-1, IL-6, TNF-alpha)
Treatment for Minimal Change Disease?
Corticosteroids
-prost =
prostaglandin analogues (treat glaucoma) (ie unoprostone)
GLUT-2
Transports all monosaccharides (Glucose, Galactose, Lactose) from intestines into blood
Omeprazole
PPI
Focal patches of hyperfunctioning follicular thyroid cells; cells work independently of TSH d/t a mutation in TSH receptor–>elevated T3 and T4 = hyperthyroid
Toxic multonodular goiter
Alcohol, Benzos, and Barbiturates do what to sleep stages?
Reduced REM and delta (stage 3) sleep
female equivalent of bulbourethral glands?
greater vestibular glands (of Bartholin)
Factor V Leiden
most common cause of inherited hypercoagulability-production of mutant factor V, that can’t be degraded by protein C
After exposure to which diseases/microbes should a person be given preformed/passive antibodies?
“To Be Healed Rapidly”-Tetanus toxin-Botulinum toxin-Hepatitis B-Rabies virus(also: should give RSV abs to premature babies born during winter months)
Selectively lose albumin, but not globulins:
Minimal Change Disease
-mab =
monoclonal antibody (ie infliximab, daclizumab)
Where in GIT is Iron absorbed?
Duodenum
Lansoprazole
PPI
Jod-Basedow phenomenon
Classic example: pt receives radio-contrast dye with iodine and becomes hyperthyroid from it–>thyrotoxicosis if a pt with iodine defiency goiter is made iodine replete
What drug may be useful to treat night terrors and sleepwalking and why?
Benzos; because decrease stage 3 sleep, during which sleepwalking and night-terrors occur
female equivalent of prostate gland?
Urethral and paraurethral glands (of Skene)
Cryoprecipitate
contains fibrinogen, factor, VIII, factor XIII-used to treat coagulation factor deficiencies (if deficient in fibrinogen or factor VIII)
What kind of immune response is induced by live attenuated vaccines? inactivated or killed vaccines?
-live attenuated –> cellular response-inactivated or killed –>humoral imunnity (weaker response; usually need booster shots)
What conditions are associated with nephrotic syndrome caused by Amyloidosis (have amyloid deposits in mesangium)?
Associated w/chronic conditions:-multiple myeloma-TB-Rheumatoid arthritis
alpha 1 blockage leads to?alpha 2 blockage leads to?
alpha1-blockage –> vasodilationalpha2-blockage –> vasoconstriction
Where in GIT is folate absorbed?
Jejunum
1st line treatment for Zollinger-Ellison syndrome?
Proton Pump Inhibitors
Papillary thyroid carcinoma
-most common and excellent prognosis-Orphan Annie nuclei = “ground glass” nuclei -psammoma bodies (whorled, look like a rose!)-increased risk with childhood radiation
What is the principal neurotransmitter in REM sleep?
Acetylcholine
female equivalent of of ventral shaft of penis (penile urethra)?
labia minora
CD30+ and CD15+ cells of B-cell origin?
Reed-Sternberg cells
4 types of hypersensitivity reactions (briefly)
“ACID” (types 1-3 = antibody-mediated) Type 1 - Anaphylactic and AtopicType 2 - CytotoxicType 3 - Immune complexType 4 - Delayed (cell-mediatedd)
Tram-track appearance on LM with GBM splitting
Type I Membranoproliferative GN
phenoxybenzamine:-type of drug?-application?-toxicity?
-nonselective alpha-blocker (irreversible/non-competitive)-used for pheochromocytoma (use phenoxybenzamine before removing tumor)-toxicity: orthostatic hypotension, reflex tachycardia
Where in GIT is Vitamin B12 absorbed?
Terminal ileum, along with bile acids; requires intrinsic factor (from parietal cells)!
Mechanism of PPIs?
Irreversibly inhibit Proton Pump (H/K-ATPase) in parietal cells (so, can’t excrete H+ into gastric lumen from parietal cells)
thyroid cancer with psammoma bodies and orphan annie nuclei?
Papillary thyroid carcinoma
How does NE affect REM sleep?
NE reduces REM sleep
female equivalent of scrotum?
labia majora
Most common Hodgkin’s lymphoma? Prognosis?
-Nodular Sclerosing-Excelent prognosis (b/c Lymphocytes»>R-S cells)-see collagen banding in lymph node-mostly young adults
What type of hypersensitivity reaction is this: anaphlaxic (“wheal and flare”), atopic; free-antigen cross-links IgE on pre-sensitized mast cells and basophils –> release of histamine, etc. How quickly does this reaction develop?
Type I –> happens very rapidly after antigen exposure to pre-formed antibody
Glomerulonephritis associated with HBV, HCV
Type I Membranoproliferative GN
Phentolamine:-type of drug-application?
-nonselective alpha-blocker (reversible/competitive)-give to patients on MAO-inhibitors who eat tyramine-containing foods
Peyer’s patches:-where?-function?
-located in ileum-Peyer’s patches = lymphoid tissue in lamina propria and submucosa of small intestine-function:–>contain M-cells that take up antigen–>B-cells stimulated in germinal centers of Peyer’s patches differentiate into IgA-secreting plasma cel
Bismuth
-treatment of ulcers and traveler’s diarrhea-mechanism: binds to ulcer base, providing physical protection; thus allowing HCO3- secretion to reestablish pH gradient in mucus layer
thryoid cancer associated with childhood irradiaton?
Papillary thryoid carcinoma
How often does REM sleep occur?
Every 90 minutes; increased duration as go through the night
Female and Male remnants of Gubernaculum?
Female: ovarian ligament + round ligament of uterusMale: fibrous tissue that anchors testes within scrotum
t(8;14) c-myc gene
Burkitt’s lymphoma (non-Hodgkin lymphoma; neoplasm of mature B cells)
Hypersensitivity type: IgM, IgG bind fixed antigen on an “enemy” self cell –> lysis by complement or phagocytosis = cytotoxic
type II
“dense deposits” on EM
Type II Membranoproliferative GN
prazosin, terazosin, doxazosin:-types of drugs?-applications?-toxicity?
-alpha-1-selective-blockers-used for hypertension, urinary retention in BPH-toxicities: orthostatic hypotension with first dose; dizziness, headache (should give pts first dose before bed, while lying down)
Lymphoid tissue of the GIT?
Peyer’s patches-located in ileum-B-cells in germinal centers of Peyer’s patches differentiate into IgA-secreting plasma cells –> IgA lives in lamina propria and protects gut from pathogens!
Sucralfate
Same mechanism as bismuth; treatment of ulcers and traveler’s diarrhea–>bind to ulcers, providing physical protection; allows HCO3- secretion to reestablish pH gradient in mucus layer-Requires an acidic environment to polymerize; WONT WORK IF TAKING ANTACIDS CONCURRENTLY!
Medullary thryoid carcinoma:
-from parafollicular “C” cells of thryoid-produces calcitonin-assoc with MEN 2A and 2B-sheets of cells in ayloid stroma
Pulse, BP, eye activity, and penile/clitoral tumescence (swollen-ness) during REM sleep:
-increased and variable pulse and BP-extraocular movements during REM sleep d/t PPRF activity (REM = Rapid eye movements; mediated by PPRF)-Penile/Clitoral tumescence”REM sleep is like sex: increased pulse, penile/clitoral tumescence, decreases with age)
Female and Male remnants of Processus vaginalis?
Female: ObliteratedMale: forms the tunica vaginalis
Most common adult non-Hodgkin lymphoma?
Diffuse large B-cell lymphoma –>20% of cases are in kids though
Hypersensitivity type: Immune complex (antigen-antibody) activates complement–> neutrophils –> release lysosomal enzymes
type III
Pathology behind Diabetic Glomerulonephropathy:
Non-enzymatic glycosylation of GBM –> increased permeability and thickeningAlso: nonenzymatic glycosylation of efferent arterioles –> increased GFR –> mesangial expansion ***see GBM thickening on LM! and mesangial expansion..
mirtazapine:-type of drug-application-toxicity
NAME?
specialized M-cells that take up antigen in GIT?
-in Peyer’s patches –> the lymphoid tissue of GIT!
Misoprostol:-mechanism-clinical uses-side effect-contraindications
Prostaglandin analogMechanism: binds receptor on parietal cell –> stimulates Gi –> decreased cAMP –> decreased stimulation of Proton Pump –> decreased acid production/secretion into gastric lumen Clinical uses:-Prevent NSAID-induced peptic ulcers (b/c NSAIDs decrease prostaglandins)-Treatment of PDA-Induce laborSide effect:-Diarrhea*Conraindication:-Pregnant women/women of child-bearing age (b/c induces labor)
Renal stones + Bone loss + GI upset/ulcers + psychiatric disorders
Primary hyperparathyroidism–> elevated PTH d/t adenoma, usually-Hypercalcemia-Hypophosphatemia-elevated PTH-elevated ALP-elevated cAMP in urine-may be asymptomatic or have weakness and constipation*initiating problem in primary hyper-PTH = elevated PTH
Why is REM sleep also called “paradoxical sleep” or “desynchronized sleep”?
Because it has the same EEG pattern as wakefulness (Beta waves)
t(11;14); affects cyclin D regulatory gene
Mantle Cell Lymphoma-affects older males; poor prognosis
What type of hypersensitivity reaction is serum sickness?
type III: serum sickness–>antibodies to foreign proteins form over about 5 days –> form immune complexes –> deposit in membranes –> fix complement –> tissue damage
Kimmelstein-Wilson lesion:
NAME?
List the B1-selective antagonists (A BEAM):
Acebutolol (partial agonist)BetaxololEsmolol (short-acting)AtenololMetoprolol
IgA in GIT comes from?
Peyer’s patches: have B-cells in germinal centers of Peyer’s patches (lymphoid tissue) that differentiate into IgA-secreting plasma cells–>IgA protects the gut from pathogens!
Octreotide:-mechanism-clinical uses
Somatostatin analog*Somatostatin/Octreotide –> Gi –> blocks/decrease cAMP –> blocks Proton Pump –> decreased acid secretion into gastric lumen *Uses:-secretory diarrhea-acute variceal bleeds-acromegaly (inhibits GH)-VIPoma (pancreatic islet cell tumor that secretes lots of Vasoactive Intestinal Polypeptide, causing lots of diarrhea)-Carcinoid tumors
bone pain and bone spaces filled with brown fibrous tissue
osteitis fibrosa cystica
What mediates the rapid eye movements of REM sleep?
PPRF (paramedian pontine reticular formation/conjugate gaze center)
t(14;18) bcl-2 overexpression
-Follicular Lymphoma-affects adults-indolent course, but difficult to cure-bcl-2 inhibits apoptosis (normally; it’s a proto-oncogene)
fever, urticaria, arthralgias, proteinuria, lymphadenopathy 5-10 days after antigen exposure?
serum sickness (type III hypersensitivity)
Most common type of kidney stones?
Calcium (Calcium oxalate, Calcium phosphate, or both)
List the nonselective Beta-antagonists (Please Try Not being Picky)
PropranololTimololNadololPindolol
Only way body can excrete cholesterol?
Bile
Treatment of VIPoma?
Octreotide
Cause of and Findings in Secondary Hyperparathyroidism:
-usually d/t chronic renal disease. Why?–>renal disease –> can’t convert vitamin D to active form –> decreased Ca absorption in gut –> increased PTH –> increased bone resorption –> increased phosphate and increased ALP from bone resorption –> but,
How do sleep patterns change in depressed patients?
-decreased slow-wave sleep (stage 3)-decreased REM latency (so, get to REM quicker!)-increased REM early in sleep cycle-increased total REM sleep-repeated nighttime awakenings-early-morning awakenings
Lymphoma caused by HTLV-1?
Adult T-cell lymphoma–>adults present with cutaneous lesions–>aggressive
Arthrus reaction
Type III hypersensitivity reaction-test by immunofluorescent staining-intradermal injection of antigen induces antibodies–>form antigen-antibody complexes in the skin –> edema, necrosis, activation of complement*ex = swelling and inflammation following tetanus vaccine.
Calcium kidney stones: -ph they precipitate at?-x-ray appearance?-what conditions may cause them?
-most common type of kidney stones; may be calcium oxalate or calcium phosphate or both-precipitate at neutral or decreased pH-radiopaque on x-ray-conditions that cause hypercalcemia (like cancer, elevated PTH) can lead to hypercalciuria and stones-may ge
List the partial beta-agonists (PAPA):
PindololAcebutolol
How is copper excreted from the body?
Bile; can’t excrete it in Wilson’s disease though…
Treatment of Carcinoid Syndrome?
Octreotide
tap facial nerve –> get contraction of facial muscles
Chovstek’s sign –> sign of hypocalcemia-get with hypoparathyroidism
Hypnagogic vs Hypnopompic hallucinations?
Hypnagogoic = just before sleepHypnopompic = just before awakening*pts wtih narcolepsy may have these hallucinations
Mycosis fungoides/Sezary syndrome
-mature T-cell lymphoma; adults present with cutaneous lesions-indolent
Type IV hypersensitivity? How long does it take?
-Delayed/T-cell-mediated –> sensitized T-cells encounter antigen–> release lymphokines –> macrophage activation…-takes about 48 hours*4 T’s:-T-lymphocytes-Transplant rejections-TB skin tests-Touching (contact dermatitis)
Vitamin C abuse may lead to what type of kidney stones?
Calcium oxalate crystals
Nonselective alpha and beta -antagonists:
CarvelidolLabetalol
3 functions of Bile:
1) Digest and absorb lipids and fat-soluble vitamins2) Excrete cholesterol3) Anti-microbial activity (by disrupting membranes)
Diphenoxylate
opiate-anti-diarrheal drug;–>binds to Mu opiate receptors in GI tract and slows motility
BP cuff causes carpal spasm
Trousseau’s sign –> sign of hypocalcemia; see with hypoparathyroidism
Naroclepsy:-what is it?-main presentation?-treatment?
NAME?
Bence-Jones protein
Multiple Myeloma-Ig light chains in urine (don’t see on urinalysis though)
Direct and Indirect Coombs’ test –> tests for what kind of hypersensitivity rxn?
Type II = antibody-mediated
Ethylene glycol (anti-freeze) may lead to what kind of kidney stones?
Calcium-oxalate kidney stones
Clinical applications of beta-blockers:
-hypertension (decrease CO, decrease renin secrtion - by beta-receptor blockade on JGA cells)-angina pectoris (decrease HR and contractility, so have decreased O2 consumption of myocardium)-MI (metoprolol and carvedilol –> decrease mortality from MIs)-SV
Pale/Clay-colored stools?
NAME?
Side effects of Antacids?
-all can cause hypokalemia (b/c block H/K-ATPase)-Can chelate and decrease effectiveness of other drugs
Hypocalcemia (pee out calcium) + shortened 4th/5th digits + short stature
Pseudohypoparathyroidism = Albright’s hereditary osteodystrophy–>autosomal dominant–>kidney is unresponsive to PTH at renal tubule; so have high PTH, but pee out calcium (clinically looks like PTH is low)
Cataplexy
NAME?
Rouleaux formation
Multiple Myeloma
List 8 disorders/situations with type IV hypersensitivity:
-diabetes - type I-multiple sclerosis-contact dermatitis-PPD-Hashimoto’s thyroiditis-Graft-vs-Host disease-Granulomatous inflammation-Guillain-Barre syndrome
Staghorn calculi
Get these with ammonium-magnesium-phosphate kidney stones (caused by infection with urease-positive bugs…)
Toxicity of Beta-blockers
-impotence!-exacerbates asthma-CV adverse effects (bradycardia, AV block, CHF)-CNS adverse effects (sedation, sleep alterations)-use caustiously with diabetics! (b/c B-blockers block sympathetically-mediated symptoms of hypoglycemia; so, patient won’t be
Cholestyramine
-Bile Acid Resin –> a lipid-lowering agent–>interferes with ability to reabsorb Urobilinogen–> so, more is excreted in stool or kidney; the liver then must use cholesterol to make more…
Side effects of Aluminum Hydroxide (antacid) overuse?
VALUE!
Cabergoline
Dopamine agonist-can be used to treat pituitary adenomas (Bromocriptine is also a dopamine agonist; can be used to treat pit adenoma)
What controls the circadian rhythm?
SCN (suprachiasmatic nucleus) of the hypothalamus drives the circadian rhythm; controls ACTH, prolactin, melatonin, nocturnal NE releaseRetina stimulates SCN –> NE release –> Pineal gland –> MelatoninSo, SCN is regulated by the environment (light); so retina stimulates SCN
most common primary tumor arising within bone in elderly?
Multiple Myeloma
List 7 disorders/situations with type III hypersensitivity
-Serum sickness-Arthus reaction-Post-Strep GN-SLE-Rheumatoid arthritis-Polyarteritis nodosum-Hypersensitivity pneumonitis (ie Farmer’s lung)
Ammonium-Magnesium-Phosphate kidney stones:-ph precipitate at?-X-ray appearance?-Caused by?
NAME?
Bethanechol applications
Bethanecol = direct cholinomimetic-used for postoperative and neurogenic ileus and urinary retention (activates Bowel and Bladder)
Colestipol
Bile-acid resin (like Cholestyramine; lipid-lowering agent)
Side effects of Magnesium Hydroxide (antacid) overuse:
“Must Go to the bathroom” = diarrhea-hypokalemia and decrease efficacy of other drugs (all antacids)-others
Octreotide
=Somatostatin–>used to treat acromegaly (following pit adenoma resection) b/c inhibits GH–>also can treat carcinoid, gastrinoma, glucagonoma
Kubler-Ross Grief Stages
(may not occur in this order)1) Denial2) Anger3) Bargaining4) Grieving5) Acceptance
CRAB symptoms of Multiple Myeloma:
NAME?
List examples of type II hypersensitivity disorders/reactions
-Anemias (hemolytic anemia, pernicious anemia)-erythroblastosis fetalis (Rh incompatibility)-acute hemolytic transfusion rxns-idiopathic thrombocytopenic purpura-rheumatic fever-Goodpasture’s syndrome-Bullous pemphigoid, Pemphigus vulgaris-Grave’s disease
Uric acid kidney stones:-precipitates at what pH?-x-ray appearance?-associated with?
-low pH-radio-lucent-assoc with hyperuricemia (ie gout); also diseases with high cell turnover, like leukemia
Carbachol applications
carbachol = direct cholinomimetic-used for glaucoma, pupillary contraction, relief of intraocular pressure
Colesevelam
-Bile-acid resin (like cholestyramine; lipid-lowering agent)
Side effects of Calcium carbonate (antacid = TUMS!)
-Hypercalcemia-may cause rebound increase in acid!-hypokalemia and decrease efficacy of other drugs (all antacids)
How to dx acromegaly?
elevated serum IGF-1-also failure to suppress serum GH following oral glucose tolerance test
Down syndrome pts: increased risk of which cancers?
NAME?
What type of hypersensitivty reaction is Goodpastures? PSGN?
Goodpastures–> type 2PSGN–> type 3
Cystine kidney stones:-precipitate at what pH?-x-ray appearance?-causes?-treatment?
NAME?
Pilocarpine applications
-pilocarpine = direct cholinomimetic-used to stimulate sweat, tears, saliva (“cry, spit, sweat on your pillow”)
Urobilin
breakdown product of bilirubin, excreted in urine; gives urine it’s color
Magnesium hydroxide
-osmotic laxative-also an antacid (with side effect of diarrhea!)
Central vs Nephrogenic DI
Central –> lack ADHNephrogenic –>lack renal response to ADH
stains TRAP positive (tartrate-resistant acid phosphatase)
Hairy cell leukemia-mature B-cell tumor in elderly; cells have filamentous, hairlike projections
what type of hypersensitivity rxn is Grave’s disease? Hashimoto’s?
Graves–>type 2Hashimoto’s –> type 4
What causes hydronephrosis?
Results for complete or partial obstruction of urinary tract
Which cholinomimetics are resistant to AChE?
Bethanechol, Pilocarpine
Stercobilin
breakdown product of bilirubin, excreted in feces; gives color of stool (without it, have pale/clay-colored stool)
Magnesium citrate
osmotic laxative
Demeclocycline
ADH antagonist –> can lead to nephrogenic DI-Lithium can also cause nephrogenic DI!
Age group affected by ALL?
<15 years old-most responsive to therapy-may spread to CNS and testes-t(12;21) = better prognosis
ANA (anti-nuclear antibodies)
-SLE-nonspecific (Sjogren’s, scleroderma, polymyositis, dermatomyositis, rheumatoid arthritis,juvenile arthritis, MCTD)
polygonal clear cells on histology
Renal cell carcinoma–>cells are filled with lipids and carbohydrates
Methacholine applications?
methacholine = direct cholinomimetic-used as a challenge test to diagnose asthma
Urobilinogen
-breakdown product of conjugated/direct bilirubin, after gut bacteria alter it in the gut; has 3 possible fates:1) excreted in feces as Stercobilin (about 80% of it)2) excreted in urine as Urobilin (very little of it –> about 2%)3) reabsorbed by liver vi
Polyethylene glycol
Osmotic laxative
Desmopressin
=synthetic ADH–> can distinguish b/w central and nephrogenic DI
Hallmark of Acute Leukemias?
-lots of blast cells (>20% blasts)-rapid onset and progression
anti-dsDNA, anti-Smith
SLE (anti-dsDNA=specific for renal disease)
2 main sites of metastasis of renal cell carcinoma?
lung and bone
Neostigmine applications?
neostigmine - anticholinesterase (indirect cholinomimetic)-used for postoperative and neurogenic ileus and urinary retention, myasthenia gravis, reversal of NM jxn blockade-increases endogenous ACh; does not penetrate the CNS
Biggest risk factor for a malignant salivary gland tumor?
Smoking
Infliximab clinical uses?
-monoclonal anti-TNF antibody*Uses:-Crohn’s disease-Rheaumatoid arthritis
Treatment for nephrogenic DI:
-Hydrochlorothiazide –> concentrates urine-Indomethacin –> decreased RBF-Amiloride –> for lithium-induced nephrogenic DI (it’s a K-sparing diuretic)
Auer rods
AML = t(15;17)-responds to vitamin A
anti-IgG antibodies
=Rheumatoid facor = IgM antibodies that attack IgG –> Rheumatoid arthritis
Most common renal malignancy of childhood?
Wilm’s tumor = Nephroblastoma–>2-4 yo
Pyridostigmine applications?
pyridostigmine = anticholinesterase (indirect cholinomimetic)-used for myasthenia gravis (gets RID of MG)-does not penterate CNS-increases endogenous ACh
most common location of benign salivary gland tumor?
Parotid gland
Sulfasalazine:-mechanism?-clinical uses?
=combo of Sulfapyridine (antibacterial) + 5-ASA (aminosalicylic acid = anti-inflammatory)–>activated by colonic bacteria (so, only effective in distal ileum and colon)*clinical uses:-Ulcerative Colitis (always)-Crohn’s (but, only acts in distal ileum and
Demeclocycline
treatment for SIADH
Which leukemia can be treated with Vitamin A?
AML -t(15;17)-auer rods
antimitochondrial antibodies
primary biliary cirrhosis
huge, palpable flank mass and/or hematuria in child 2-4 yo?
Wilm’s tumor = Nephroblastoma
Edrophonium applications
endrophonium = anticholinesterase (indirect cholinomimetic)-used to diagnose myasthenia gravis-increases endogenous Ach
Pleomorphic salivary gland adenoma:
NAME?
Odansetron:-mechanism-clinical uses-side effects
=anti-serotonin and anti-emeticClinical uses:-pts undergoing chemo, to combat nausea/vominiting-pregnant women with morning sicknessside effects:-headache (think opposite of triptans, which are serotonin-agonists; relieve headaches)-constipation (think
Causes of SIADH:
1) Ectopic ADH (ie small cell lung cancer)2) CNS disorders/head trauma3) Pulmonary disease4) Drugs –> ie cyclophosphamide ***SIADH = Syndrome of Inappropriate ADH secretion
t(9,22), bcr-abl
Philadelphia chromosome-CML-30-60 yrs old-more mature cells (<5% blasts); insidious onset-resonds to imatinib = bcr-abl tyrosine kinase inhibitor
anti-desmoglein antibodies
pemphigus vulgaris
WAGR complex:
-Wilm’s tumor-Aniridia (no iris)-Genitourinary malformation-mental-motor Retardationd/t deletion on chromosome 11often obese too
Physostigmine applications
physostigmine = anticholinesterase (indirect cholinomimetic)-used to treat glaucoma and atropine overdose (“phyxes” atropine OD)-crosses the BBB!-increases endogenous Ach
Warthin’s tumor
-benign salivary gland tumor; trapped in a lymph node, surrounded by lymph tissue
Metoclopramide:-mechanism-uses-toxicity/side-effects-contraindications
=D2-receptor antagonist (Dopamine-blocker) uses:-diabetic and post-surgery gastroparesis (delayed gastric emptying)Toxicities/Side effects:-may lower seizure threshold -parkinsonian symptoms (b/c block dopamine)-diarrhea, etc…*Contraindications:-Parki
Empty sella syndrome
unexplained atrophy of pituitary –> get hypopituitarism–>common in obese women
Imatinib
treatment for CML-inhibits bcr-abl tyrosine kinase
anti-microsomal, anti-thyroglobulin antibodies
Hashimoto’s thyroidits
Squamous cell cancer of the bladder associated with?
Schistosomiasis
Echothiophate applications
echothiphate = anticholinesterase (indirect cholinomimetic)-used to treat glaucoma-increases endogenous Ach
Mucooepidermoid carcinoma
NAME?
4 Drugs that may lower seizure threshold? (random, not specific to GI)
1) Metoclopramide (treats gastroparesis)2) Buproprion (anti-depressant w/out sexual side effects; increased seizures, especially pts with bulemia or anorexia)3) Tramadol (used to treat chronic pain; weak opiod-agonist; inhibits serotonin and NE reuptake, but not used to treat depression)4) Enflurane (inhaled anesthetic)
Fatigue + failure to lactate post-partum?
–>Sheehan’s syndrome = postpartum hypopituitarism–>Cause: increased size of ant pituitary during pregnancy, without increased blood supply; so, have increased risk of pituitary infarction. If have lots of bleeding/hemorrhage during delivery or post-part
Teardrop cell
Myelofibrosis–>fibrosis of bone marrow (–>bone marrow is crying because it’s fibrosed :(
anti-Jo-1 antibodies
polymyositis, dermatomyositis
Painless hematuria, no casts:
Bladder cancer –> Transitional cell carcinoma
Donepezil applications
donepezil = anticholinesterase (indirect cholinomimetic)-used to treat Alzheimer’s disease-increases endogenous Ach!
loss of Myenteric/Auerbach’s plexus?
Achalasia –>can’t relax Lower Esophageal Sphincter–>get esophageal aperistalsis–>progressive dysphagia of solids and liquids (vs obstruction, which is dysphagia to solids only)–>increased risk of esophageal carcinoma
Causes of small and large vessel disease in chronic diabetes:
-NON-enzymatic glycosylation –> glucose gets tacked on to thins
JAK2 mutations: positive/negative?Philadelphia chromosome?-polycythemia vera-essential thromboyctopenia-myelofibrosis-CML
JAK2:-positive in polycythemia vera, essential thrombocytosis, myelofibrosis-negative in CMLPhiladelphia:-only positive in CML
anti-SS-A antibodies
=anti-Ro antibodies –> Sjogrens
most common tumor of urinary tract system?
Transitional cell cancer (can occur in renal calyces, pelvis, ureters, bladder…)
pKa = acid dissociation constant = ?
pKa = pH at which amount of the non-protonated form = the amount of the protonated form
Bird’s beak on barium swallow
Achalasia (esophageal aperistalsis; can’t relax LES d/t loss of Myenteric/Auerbach’s plexus)
Kimmelstein-Wilson nodules
–>diabetes
thombolytics mechanism? (streptokinase, urokinase, tPA, APSAC)
aid conversion of plasminogen–>plasmin, which cleaves thrombin and fibrin clots
anti-SS-B antibodies
=anti-La –> Sjogrens
Problems associated with Transitional Cell Carcinoma?
Pee SAC:-Phenacetin (analgesic; acetaminophen=phenacetin derivative)-Smoking-Aniline dyes-Cyclophosphamide (alkylating agent, used to treat cancers/immunosuppressant)
if pH < pKa…
acidic environment; have more of the protonated form (so, basic drugs get trapped)
2 conditions that may lead to secondary achalasia?
-Chaga’s disease (mega-esophagus)-CREST scleroderma (Esophageal dysmotility)
What causes cataracts in chronic diabetes?
NAME?
Affect of aspirin on BT, PT, PTT
increased BT-no effect on PT, PTT
anti-U1-RNP (ribonucleoprotein)
mixed connective tissue disease
Histology of Acute vs Chronic Pyelonephritis?
-Acute –> neutrophil infiltration ito renal interstitium-Chronic –> lymphocytic invasion with fibrosis
if pH > pKa…
basic environment; have more of the nonprotonated form (acidic drugs get trapped)
increased risk of what cancer with Achalasia?
–> esophageal carcinoma
What causes retinopathy and glaucoma in chronic diabetes?
NAME?
Ticlopidine toxicity?
-Neutropenia (should monitor CBC during first few months of trtmt)(Ticlopidine = ADP-receptor blocker, so inhibits platelt aggregation; like Clopidogrel)
anti-smooth muscle antibodies
autoimmune hepatitis
Thyroidization of kidney (eosinophilic casts in tubules)
Chronic pyelonephritis
Treat acidic drug OD (ie slicylates) with?
NaHCO3 (traps the acidic drug in the basic urine)
progressive dysphagia of solids AND liquids, vs just solids vs progressive dysphagia first of solids THEN of liquids?
*solids + liquids–> Achalasia only solids–> obstructionsolids, then liquids–> esophageal cancer
HLA’s associated with DM I?
NAME?
Drug side effect = tinnitus?
Aspirin!
anti-glutamate decarboxylase antibodies
type 1 diabetes
fever + rash + hematuria + flank tenderness 1-2 weeks after taking certain drugs
Drug-induced / Acute Interstitial Nephritis
Treat basic drug OD (ie amphetamines) with?
NH4Cl (ammonium chloride; traps basic drug in the acidic urine)
Painless bleeding in lower 1/3rd of esophagus?
Esophageal varices–>associated with portal HTN
Histology of DM I vs DM II?
DM I –> Islet leukocytic infiltrate (leukocytes!)DM II –> Islet amyloid deposit (amyloid!)
Raloxifene vs Tamoxifen: Which is better for osteoporosis prevention?
-both are SERMs–>antagonists in breast (treat breast cancer)–>agonists in bone (bone-building)-Tamoxifen may increase risk of endometrial carcinoma, b/c it’s a partial endometrial agonist-Raloxifene is an endometrial antagonist, so no increased risk of
anti-TSH receptor antibodies
Grave’s
What causes Acute Interstitial Nephritis?
DRUGS!:-NSAIDs-diuretics-penicillins-sulfonamides-rifampinget interstitial renal inflammation, pyuria, azotemia, 1-2 weeks after taking meds*also: fever, rash, hematuria, flank pain
What class of drugs can cause excess parasympathetic activity (ie DUMBBELSS symptoms)?
Cholinomimetic agents
Dysphagia + Glossitis (swollen, smooth tongue) + Iron-deficiency anemia
Plummer-Vinson syndrome–>Dysphagia is d/t esophageal webs = thin membrane-like protrusion into esophagus–>associated with increased risk of Squamous Cell Carcinoma of Esophagus
Kussmaul respirations
rapid/deep breathing; DKA (try to exhale CO2 to fix acidosis)
anti-Ach receptor antibodies
Myasthenia gravis
Most common cause of acute renal failure in hospital?
Acute tubular necrosis–>can be reversible, but fatal if left untreated
What drug regenerates AchE after organophosphate poisoning?
Pralidoxime (regenerates active AchE) (also, give atropine to treat symptoms!)
Boerhaave syndrome:
-TRANSMURAL esophageal rupture d/t violent vomiting–> vs Mallory-Weiss which is just lacerations at the G-E jxn
labs in DKA
-hyperglycemia-elevated H+ = decreased pH-decreased HCO3 (anion gap met acidosis)-ketonemia-Hyperkalemia (though depleted intracellar K+; decreased insulin shifts K+ outside cells) -Hyponatremia-Leukoctyosis
p-ANCA antibodies
Vasculitides: -microscopic polyangitis-churg-strauss syndrome
3 stages of Acute Tubelar Necrosis:
1) Inciting event(ie renal ischemia from shock, sepsis, or crush injury like myoglobinuria)2) Maintenance phase –> oliguric; 1-3 weeks; risk of hyperkalemia; have muddy brown casts3) Recovery –> polyuric, risk of hypokalemia; get decreased levels of BUN and serum creatinine
What are the symptoms of inhibiting parasympathetic activity?
(ie atropine side effects)Hot as a hareDry as a boneRed as a beetBlind as a batMad as a hatterBloated as a toad
Esophageal pathology associated with lye ingestion and acid reflux?
Esophageal strictures
Treatment of DKA?
NAME?
Boys with recurrent bacterial infections after 6 months, B-cell deficient, and deficient in all classes of Ig’s. What’s the condition and what gene is defective?
Bruton’s agammaglobulinemia; defect in BTK, a tyrosine kinase gene. can form pro-B cells, but not beyond that. X-linked recessive, so increased in males
Definition of Acute Renal Failure = Acute Kidney Injury:
–>abrupt decline in renal function with elevated Creatinine and elevated BUN (so, Azotemia) over several days
In what populations is atropine contraindicated?
-Glaucoma (because don’t want to dilate eyes)-BPH or any urinary retention-GI obstruction (ie ileus)-Dementia or Elderly (because can cause delirium)-Infant with fever (because can cause hyperthermia)-
Barrett’s esophagus: what sort of metaplasia occurs? increased risk of what kind of cancer?
Glandular metaplasia: squamous epithelium of distal esophagus is replaced with columnar/intestinal epithelium-d/t chronic GERD-assoc w/increased risk of Adenocarcinoma of esophagus-also associated with esophagitis and esophageal ulcers
most common tumor of appendix?
-Carcinoid tumor!
Defect in BTK gene
BTK = a tyrosine kinase gene –> defect = Bruton’s agammaglobulinemia
Pre-Renal Azotemia: Acute Renal Failure
–> not enough blood to kidney: so decreased RBF (ie hypotension) –> decreased GFR-Na, H20, and urea are retained by the kidney (not excreted in urine) to conserve volume-So: get elevated BUN/Creatinine ratio
List 4 classes of drugs with anti-cholinergic side effects:
1) First generation H1-Blockers (diphenhydramine, doxylamine, chlorpheniramine)2) Traditional neuroleptics3) TCAs4) Amantadine
What type of esophageal cancer is most common worlwide? in US?
NAME?
recurrent diarrhea + cutaneous flushing + asthmatic wheezing + right-sided valvular disease + elevated 5-HIAA in urine?
Carcinoid syndrome (5-HIAA = serotonin metabolite)
Defect that causes hyper-IgM syndrome?
defective CD40L on helper T-cells–> can’t class switch
Intrinsic Renal: Acute Renal Failure
usually d/t acute tubular necrosis or ischemia/toxins–>have necrosis or something that obstructs the tubule, so get fluid backflow across the necrotic tubule –> decreases GFR-Also: BUN reabsorption impaired –> decreased BUN/Creatinine ratio
List 4 treatment options for Myasthenia Gravis:
1) Anti-cholinesterases (indirect cholinergic agonists)2) Corticosteroids (because MG = autoimmune disease)3) Thymectomy (often curative)4) Plasmapheresis
*What part of esophagus is affected in each of these cancers?-What risk factors cause Squamous Cell Carcinoma?-What risk factors associated with Adenocarcinoma?
Squamous Cell: upper 2/3-smoking-alcohol-achalasia-esophageal webs (ie Plummer-Vinson syndrome)Adenocarcinoma: lower 1/3-Barret’s esophagus-Esophagitis-Diverticula (like Zenker’s)
Treatment for serotonin syndrome?
Octreotide = somatostatin analogue
anaphylaxis on exposure to blood products with IgA; and: sinus and lung infections, milk allergies, and diarrhea…
Selective Ig deficiency, usually to IgA -caused by a defect in isotype switching to a specific class
Postrenal: Acute Renal Failure
–>d/t outflow obstruction (ie stones, BPH, neoplasia, congenital anomalies)–>only have bilateral obstruction with postrenal…
What are the 5 classes of drugs used to treat glaucoma?
1) alpha-agonists2) beta-blockers3) Diuretics (Carbanic anhydrase inhibtors and mannitol)4) cholinomimetics5) prostaglandins
Whipple’s disease:
-Tropheryma whippelii infection (gram +)-PAS + foamy macrophages in intestinal lamina propria-mostly older men-CAN:–>cardiac symptoms–>Arthralgias–>Neurologic symptoms***Also, classic malabsorption symptoms: diarrhea, steatorrhea, weight loss, weakness
When may carcinoid syndrome be subclinical?
if limited to GI tract - only –> because serotonin undergoes first-pass metabolism in liver
normal # of B cells, but decreased plasma cells, decreased Immunoglobulin…
Defect in B-cell maturation –> CVID = common variable immunodeficiency
2 most common causes of chronic renal failure?
NAME?
P-450 Inducers
Barb Steals Phen-phen and Refuses Greasy Carbs Chronically:BarbituratesSt. John’s wortPhenytoinRifampinGriseofulvinCarbamazepineChronic alcohol use
Which part of intestine is affected in Celiac sprue?
NAME?
Rule of 1/3rds in Carcinoid syndrome:
-1/3 metastasize-1/3 present with 2nd malignancy-1/3 multiple
22q11 deletion
90% of pts with DiGeorge syndrome (thymic aplasia) –> failure to develop 3rd and 4th pharyngeal pouches (so, no thymus)
Renal Osteodystrophy:
get this with chronic renal failurefailure of vitamin D hydroxylation –> Calcium wasting and Phosphate retention –> secondary hyperparathyroidism*causes subperiosteal thinning of bones
P-450 inhibitors
Q-MAGIC RACKS:QuinidineMacrolidesAmiodaroneGrapefruit juiceIsoniazidCimetidineRitonavirAcute alcohol abuseCiprofloxacinKetoconazoleSulfonamides
What part of intestine is affected in lactase deficiency?
only tips of intestinal villi (b/c that’s where lactase is located)–>so, get normal look villi
Carcinoid tumors are derived from what kind of cells?
NAME?
absent thymic shadow
NAME?
Autosomal dominant mutation in PKD1 or PKD2 gene?
ADPKD
acetaminophen antidote? (toxic dose = 4 g/day = 8 extra-strength tablets)
N-acetylcysteine (replenishes glutathione)
fat accumulation in enterocytes + malabsorption in childhood + neurologic manifestations?
Abeta-lipoproteinemia–>have decreased synthesis of apo-B –> can’t generate chylomicrons –> decreased secretion of cholesterol and VLDL into bloodstream –> so, fat accumulates in enterocytes***this is a malabsorption syndrome-treat with vitamin E supplementation (helps body produce some apoproteins)
Zollinger-Ellison syndrome
tumor in pancreas or duodenum that secretes gastrin –> so, get hypersecretion of acid in stomach and rugal thickening-get recurrent ulcers!-may be assoc with MEN I (pancreatic endocrine tumors…)
tetany, recurrent viral infections, congenital heart and great vessel/aortic arch defects, cleft palate, mandible deformities…
DiGeorge syndrome = thymic aplasia: no thymus or parathyroids, so: deficient T-cells, PTH, Calcium-absent thymic shadow on CXR
What conditions are associated with ADPKD?
NAME?
salicylates (ie aspirin) antidote?
NaHCO3 (alkalinizes urine)Dialysis
Causes of pancreatic insufficiency? What must be supplemented?
Causes:-cystic fibrosis-obstructing cancer-chronic pancreatitisget malabsorption of fat and fat-soluble vitamins (A, D, E, K)get increased fat in stool*treat by pancreatic enzyme replacement, limit fat intake, and supplement A, D, E, K.
Which thyroid cancer is associated with amiloid deposition?
medullary thyroid carcinoma (MEN 2A and 2B)
Disseminated mycobacterial infections, decreased levels of IFN-gamma
IL-12 receptor deficiency –> so decreased Th1 response –> decreased IFN-gamma secretion
bilaterally enlarged kidneys + oligohydramnios + small/absent bladder in-utero (by US)?
–>ARPKD
amphetamines antidote
NH4Cl (acidifies urine)
List the Malabsorption syndromes:
“These Will Cause Devastating Absorption Problems”-Tropical sprue-Whipple’s disease-Celiac sprue-Disaccharidase deficiency (like lactose intolerance)-Abetalipoproteinemia-Pancreatic insufficiency
Clinical uses for Insulin:
-Type 1 DM-Type 2 DM, once necessary-life-threatening hyperkalemia (b/c insulin shifts potassium INTO cells, so can cause HYPOkalemia) -stress-induced hyperglycemia
Job’s syndrome
=Hyper-IgE syndrome-Th cells don’t produce IFN-gamma –> neutrophils can’t respond to chemotactic stimuli-increased levels of IgE-presentation = FATED:–coarse Facies–non-inflamed staph Abscesses–retained primary Teeth–increased IgE–Dermatological pro
Thin, nonenhancing, cortical, fluid filled cysts in kidney?
Benign simple cysts; incidental finding in elderly***don’t confuse these with medullary cystic disease –> medullary cysts, fibrosis, progressive renal insufficiency, can’t concentrate urine, small kidney –> poor prognosis!
anti-acetylcholinesterase and organophosphates antidote?
Atropine + Pralidoxime
Blunting of villi + Crypt hyperplasia in small intestines?
Celiac sprue
Sulfonylureas mechanism of action:
Sulfonylureas:1st gen:-Tolbutamide-Chlorpropamide2nd gen:-Glyburide-Glimepiride-Glipizide*Mechanism:-Close K+ channels in Beta-cells of pancreas (which is what glucose usually does: glucose–>increased ATP–>closes K+ channels–>depolarizes cell allowing for Calcium influx into cell–>release of insulin into blood) –>SO: stimulates release of endogenous insulin (so, must have some functional Beta cells left to work; so, can only be used in DMII, not in DMI)
Abscesses + still have primary teeth + eczema + high levels of IgE
think Job’s syndrome = Hyper-IgE syndrome
Osmotic diuretic
Mannitol –>increased tubular fluid osmolarity, so helps excrete free H2O)
antimuscarinic, anticholinergic agents (ie atropine) antidote?
physostigmine salicylate
Curling’s ulcer
Burning of the esophagus –> can lead to sloughing of gasric mucosa and Acute Erosive Gastritis
Glyburide
2nd generation sulfonylurea–>stimulates release of endogenous insulin
Recurrent infections, Chronic diarrhea, FTT; have NK cells, but no B or T cells
SCIDVariable causes:-defective IL-2 receptor (most common, X-linked)-Adenosine Deaminase deficiency-failture to synthesize MHC II antigens
Diuretic with Pulmonary edema side effect?
Mannitol
beta-blockers antidote?
(same as verapamil antidote!) = glucagon, calcium, atropine (all increase HR)
Cushing’s ulcer
Brain injury that can lead to Acute Erosive Gastritis:brain injury–> increased vagal stimulation –> increased ACh –> increased H+ production –> Gastritis
Clinical use of Glyburide?
–>Diabetes Type II-stimulates endogenous release of insulin from Beta cells, so must still have some functional islet cells; therefore, it’s useless in type I
Most common cause of SCID?
-defective IL-2 receptor (X-linked)
Diuretic used to treat altitude sickness?
Acetazolamide–>Carbonic anhydrase inhibitor –> helps get rid of HCO3–>can also be used for glaucoma–>may cause hyperchloremic metabolic acidosis….
Iron antidote
deferoxamine
Main causes of Acute Erosive Gastritis:
Acute Erosive Gastritis = disrupton of mucosal barrier –> inflammationMain causes:-Alcoholics-Pts taking daily NSAIDs (ie Rheumatoid Arthritis pts)-Curling’s ulcer = burning esophagus-Cushing’s ulcer = brain injury resulting in increased vagal stimulation-Stress
Side effects of Glyburide?
Hypoglycemia
Cerebellar deficits + spider angiomas + IgA deficiency (so increased risk of sinopulmonary infections)
=Triad of symptoms in Ataxia-telangiectasia:-cerebellar deficits =ataxia-spider angiomas = telangiectasia-IgA deficiency –>d/t defects in ATM (Ataxia Telangiectasia Mutated) gene, which codes for DNA repair mechansims –> so, also hypersensitive to x-ray
Diuretics used to treat Glaucoma?
-Acetazolamide –> for long-term treatment-Mannitol –> for emergencies
lead antidote
CaEDTA (in adults)Dimercaprolsuccimer (in kids)penicillamine
Autoimmune disorder with:-autoantibodies to parietal cells-pernicious anemia (b/c no parietal cells, so no IF, so no B12)-Achlorydia (b/c no acid from parietal cells)
Chronic/Non-erosive gastritis of the Fundus/Body = Type A
Side effects of 1st generation sulfonylureas?
1st gen sulfonylureas = Tolbutamide, Chlorpropramide–>Disulfiram-like effects (so, not used much)*Remember: Disulfiram = Antabuse –> get hangover-like effects
In which immune deficiency are patients hypersensitive to X-ray radiation (b/c it causes chromosomal breaks)?
Ataxia-Telangiectasia –> mutation in ATM gene, which codes for DNA repair enzymes
Diuretic of choice to treat edematous states (ie CHF, cirrhosis, nephrotic syndrome, pulmonary edema…)?
Furosemide (loop diuretic)
mercury, arsenic, gold antidote
-dimercaprol (BAL) (dimes = money = gold; merc = mercury!)-succimer
Cause of chronic/non-erosive gastritis to the fundus/body of the stomach
Autoimmune disorder with: -autoantibodies to parietal cells-pernicious anemia-achlorydia
Side effects of 2nd generation sulfonylureas?
2nd gen sulfonylureas = Glyburide, Glimepiride, Glipizide (all the “G—ides”!) Hypoglycemia
Thrombocytopenic purpura, recurrent pyogenic Infections, Eczema; Low IgM
Triad of symptoms in Wiskott-Aldrich syndome –> “TIE” = Thrombocytopenic purpura, Infections, Eczema-X-linked recessive-get progressive deletion of B and T cells-decreased IgM; increased IgE and IgA
Side effects of Furosemide?
“OH DANG”-Ototoxicity-Hypokalemia-Dehydration-Allergy (sulfa)-Nephritis (Acute Interstitial Nephritis)-Gout
copper, arsenic, gold antidote
penicillamine (copper pennies!)
Cause of chronic/non-erosive gastritis affecting the antrum of the stomach?
H. pylori-this is the most common type of chronic gastritis-increased risk of MALT lymphoma
1st line drug for DM II?
Metformin
Defect in LFA-1 integrin/CD18 protein; poor wound healing – no pus formation, delayed separation of umbilicus
Leukocyte adhesion deficiency (type 1)–>defect in LFA-1 integrin (CD18) protein on phagocytes
NSAIDs inhibit the effect of which type of diuretic? Why?
NSAIDs inhibit Furosemide–>Furosemide/Loop diuretics stimulate Prostaglandin release; so, if give NSAIDs + loop diuretics together –> get decreased diuretic response
cyanide antidote
(may get cyanide poisoning from nitroprusside, used for malignant HTN; also, from house fires – see CN toxicity along with CO poisoning)-nitrite-hydroxocobalamin-thiosulfate
What part of the stomach does H. pylori affect?
Antrum
Metformin mechanism?
unknown exactly; but: -decreases gluconeogenesis in liver (so, decreased glucose!)-increased glycolysis (use that glucose up!)-increase peripheral glucose uptake by whatever insulin that is (so, increased insulin sensitivity)so, overall: decreases glucose in blood!can use in pts without any islet cell function
recurrent infections with staph and strep, partial albinism, peripheral neuropathy/neuro defects; defect in LYST gene
Chediak-HIgashi syndrome:-autosomal recessive-defect in LYST: lysosomal trafficking regulator gene-microtubule dysfunction in phagosome-lysosome fusion-see abnormal giant lysosomal inclusions on LM of peripheral smear
Drugs that are both Ototoxic and Nephrotoxic?
-Aminoglycosides-Loop diuretics (Furosemide)-Cisplatin and Carboplatin (anti-cancer drugs)-Vancomycin
Carbon monoxide antidote
100% O2Hyperbaric O2
Disease in which rugae of stomach look like brain gyrae?
Menetrier’s disease–>gastric hypertrophy-protein loss-parietal cell atrophy-increased mucous cells-precancerous–>rugae are so hypertrophied that look like brain gyri!
Mechanism of Exogenous Insulin?
Binds insulin receptor (Tyrosine Kinase activity)
absent respiratory burst in neutrophils, increased susceptibility to catalase positive organisms (ie S. aureus, E. coli, Aspergillus, Serratia, Nocardia…); negative nitroblue tetrazolium dye reduction test
Chronic granulomatous disease
Ethacrynic acid
Loop diuretic, works the same way as Furosemide. But, not a sulfonamide (unlike furosemide)–>give to pts with sulfa allergy
opioids antidote
naloxone/naltrexone
Main type of stomach cancer?
Adenocarcinoma (almost always)
Which diabetes drug is contraindicated in pts with renal failure?
Metformin–>b/c if renal failure: get reduced clearance of metformin and lactate (which builds up d/t the inhibition of gluconeogenesis, b/c lactate is a substrate for gluconeogenesis); so, increased risk of lactic acidosis
vascular fibroid necrosis, neutrophil infiltration, and infarction of graft within minutes after a transplant:-what type of hypersensitivity reaction is this?
Hyperacute transplant rejection: antibody-mediated (type II hypersensitivity) d/t prefored anti-donor antibodies in the recipient
K+ sparing diuretics:
“K+ STAES”-Spironolactone-Triamterene-Amiloride-Eplerenone
benzodiazepines antidote
flumazenil
Acanthosis nigricans
seen in hyperinsulinemia and in visceral malignancies; often seen in gastric adenocarcinoma
Worst side effect of Metformin?
Lactic acidosis (rare; but its most grave side effect) –> this is why Metformin is contraindicated in pts with kidney failure; b/c decreased clearance of metformin and lactate, and thus increased risk of lactic acidosis
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate, weeks after a transplant:-is this reversible?
Acute transplant rejection-cell-mediated: Cytoplasmic T-cells reacting against foreign MHCs-can reverse with immunosuppressants
Which diuretics lead to increased urinary K+ (decreased blood K+)?
–>all, EXCEPT for K+sparing
TCAs antidote
NaHCO3 (plasma alkalinization)
Virchow’s node:
metastasis from stomach to left supraclavicular node
Biguanides
=diabetes drug class –> only drug in it is Metformin!
obliterative vascular fibrosis; fibrosis of graft tissue and blood vessels, months to years after a transplant:-is this reversible?
Chronic transplant rejection-cytoplasmic T-cells see non-self-MHC I as self-MHC I presenting a non-self antigen–> get T-cell and antibody-mediated vascular damage-irreversible
Which diuretics may lead to decrease pH –> acidemia?
–>Carbonic anhydrase inhibitors–>K+ sparing diuretics
Heparin antidote
protamine (H+ = Proton-amine!)
Krukenberg’s tumor:
bilateral metastasis from stomach to ovaries–>see lots of mucus and signet ring cells in ovaries
Glitazones = Thiazolidinediones:-mechanism?
Includes: Pioglitazone, RosiglitazoneMechanism:-increased insulin sensitivity in peripheral tissues; by binding to PPAR-gamma-nuclear transcription regulator (in adipose tissue and skeletal muscle)
Maculopapular rash, jaundice, hepatosplenomegaly, diarrhea at variable point after a transplant:-what’s the pathogenesis?-what types of transplants is this most common in?
-Graft-vs-Host disease-usually follows a bone marrow or liver transplant (b/c they’re organs rich in lymphocytes)-Pathogenesis: grafted immunocompetent T-cells proliferate in the irradiated immunocompromised host/pt –> graft cells reject cells with “fore
Which diuretics may lead to increase pH –> alkalemia?
–>Loop diuretics–>Thiazides
Warfarin antidote
vitamin Kfresh frozen plasma
Sister Mary Joseph’s nodule:
metastasis from stomach adenocarcinoma to subcutaneous periumbilical area
4 main side effects of Glitazones? (KNOW!)
1) Weight gain2) Edema3) Hepatotoxicity 4) Heart failure (may exacerbate CHF)
Which immunosuppressant drug is a precursor of 6-mercaptopurine?
Azathioprine
Why should ACE-inhibitors NOT be given to pts with renal artery stenosis?
–>pts with renal artery stenosis depend on EA constriction to maintain renal perfusion; but, ACE inhibitors cause EA dilation –> decreased GFR, decreased FF–>so, ACE inhibitors can cause acute renal failure or complicate an existing renal disease in pt
tPA, streptokinase, urokinase antidote?
Aminocaproic acid
signet ring cells
cells seen in diffuse stomach cancer–>filled with mucin; nucleus is pushed to periphery–>see in stomach; also see if metastasis from stomach to ovaries (Krukenber’s tumor)
Acarbose:-class?-mechanism?-side effects?
alpha-glucosidase inhibitor(diabetes drug) –>not used muchmechanism:–>inhibits intestinal brush border alpha-glucosidases –> so, get delayed sugar hydrolysis and glucose absorption –> thus, decreased postprandial hyperglycemiaside effects:-GI disturbances
Mannitol diuresis may prevent nephrotoxicity caused by what immunosuppressant drug?
Cyclosporine
theophylline antidote
Beta-blocker(theophylline is an option for COPD pts; it has a low TI with cardio-toxicity; so, give beta-blockers for the cardio-toxic effects)
Linitis Plastica
Stomach adenocarcinoma; stomach looks like a leather bottle –> thickened and leathery
Miglitol:-class-mechanism-side effects
-alpha-glucosidase inhibitor (diabetes drug) (same class as Acarbose) –>not used much *mechanism:–>inhibits intestinal brush border alpha-glucosidases –> so, get delayed sugar hydrolysis and glucose absorption –> thus, decreased postprandial hyperglyc
Which immunosuppressant drug is a monoclonal antibody that binds to CD3 on T-cells?
Muromonab-CD3 (OKT3)
Verapamil antidote
same as beta-blocker antidote! = glucagon, calcium, atropine (all increase HR)
Pain is increased with eating? decreased with eating?
Increased with eating –> gastric peptic ulcerDecreased with eating –> duodenal peptic ulcer (b/c have bicarb secretion, which soothes ulcer)
Pramlintide:-class of drug-mechanism-side effects?
-Mimetic (diabetes drug)*mechanism: decreases glucagon (hormone secreted by pancreas, raises blood glucose; opposite of insulin) *side effects: hypoglycemia, nausea, diarrhea
Which immunosuppressant drug is a monoclonal antibody that binds IL-2 receptor on activated T-cells?
Daclizumab
Digitalis antidote
-Normalize K+ and Mg2+-lidocaine (if there’s tachyarrhythmia) -anti-dig fab fragments (if there’s arrhythmia)-atropine (if there’s bradycardia)
Role of H. pylori in gastric and duodenal peptic ulcers?
gastric ulcers–> H. pylori in 70% of casesduodenal ulcers–> H. pylori in about 100% of cases
Exenatide:-class of drug?-source of this drug?-mechanism?-side effects?
GLP-1 analog (Glucagon-Like Peptide)mechanism: increase insulin, decrease glucagon releasesource = Gila monster saliva! (sort of; it’s a synthetic version of a protein derived from Gila monster) *Side effects: -Pancreatitis-Nausea -Vomiting
Which immunosuppressant drug inhibits IMP (inosine monophosphate dehydrogenase)?
Mycophenolate
methemoglobin antidote
-methylene blue-vitamin C
Is there an increased risk of cancer with Peptic Ulcer disease?
Trick question:If gastric ulcer –> increased risk of carcinomaIf duodenal ulcer –> NO increased risk of carcinoma
Which diabetes drugs may cause Hypoglycemia?
-Insulin-Pramlintide (mimetic agent) -2nd generation sulfonylureas (glyburide, glimepiride, glipizide)
Which immunosuppressant drug inhibits calcineurin–>loss of IL-2 production –> blockage of T-cell differentiation and activation?
Cyclosporine
methanol, ethylene glycol (anti-freeze) antidote
-Fomepizole = 1st choice! (inhibits alcohol dehydrogenase)-2nd choices = ethanol, dialysis
Recurrent ulcers despite treatment?
Check gastrin levels; may be Zollinger-Ellison syndrome
Which diabetes drug may cause pancreatitis?
Exenatide (GLP-1 analog)
Which immunosuppressive drug binds FK-binding protein–> get loss of IL-2 production?
Tacrolimus
Part of Intestines affected in Crohn’s?
Any part of GIT can be affected; but, usually involves terminal ileum and colon; have skip lesions–>rectal sparing!
Which diabetes drugs may cause disulfiram-like reactions?
1st gen sulfonylureas (tolbutamide, chlorpropamide)
Which immunosuppressive drug inhibits mTOR (mammalian target of rapamycin)–> inhibits T-cell production?
Sirolimus (rapamycin)
Part of intestines affected in ulcerative colitis?
NAME?
Which diabetes drug may cause lactic acidosis?
–>Metformin (therefore contraindicated in renal failure pts)
Which immunosuppressive drug is metabolized by xanthine oxidase, so allopurinol increases its toxicity?
Azathioprine
How much of intestinal wall is affected in Crohn’s? in Ulcerative colitis?
Crohn’s–> transmuralUlcerative Colitis–> only mucosal and submucosal
Which diabetes drug may exacerbate CHF?
Glitazones
Clinical use of Filgrastim and Sargramostim?
–>recombinant cytokines, used to treat post-chemo patients for recovery of bone marrow-Filgrastim =granulocyte-colony-stimulating factor-Sargramostim =granulocty-macrophage colony stimulating factor
Creeping fat
Crohn’s
Which diabetes drugs may cause hepatotoxicity?
Glitazones
Clinical use for recombinant erythropoietin?
Anemias, especially:-renal failure –> because EPO comes from kidneys-pts undergoing chemo
Cobblestone mucosa
Crohn’s
Which diabetes drugs may cause weight gain and edema?
Glitazones
clinical use for recombinant alpha-interferon?
-Hepatitis B and C-Kaposi’s sarcoma-Leukemias-Malignant melanoma
“string sign” on barium swallow
Crohn’s
Propylthiouracil:-clinical use?-mechanism?-Toxicities?
Treatment for Hyperthyroidism (can be given to pregnant women with hyperthyroidism too) Mechanism:-Blocks Peroxidase, so inhibits organification of iodide and coupling of thyroid hormone -Also: blocks 5’-deiodinase –> decreased peripheral conversion of T4–>T3**Overall: decreased Thyroid hormone*Toxicities:-Agruanulocytosis (rare)-Aplastic anemia-skin rash-Hepatotoxicity
clinical use for recombinant Beta-interferon?
Multiple sclerosis
“lead pipe” appearance of intestines on imaging?
Ulcerative Colitis (d/t loss of haustra)
5’-Deiodinase
Enzyme that converts T4 to T3 in peripheral tissue*Propylthiouracil inhibits 5’-deiodinase (so, inhibits peripheral conversion to T3) and also inhibits peroxidase
clinical use for recombinant gamma-interferon?
Chronic granulomatous disease
IBD with: Noncaseating granulomas and Th1 mediated lymphoid aggegates on microscopy:
Crohn’s disease(no granulomas in UC; also UC is Th2-mediated)
Methimazole:-clinical use?-mechanism?-toxicities?
-treatment for hyperthyroidism*Mechanism: -blocks peroxidase –> so, inhibits organification of iodide and coupling of thyroid hormone synthesis *toxicities:-agranulocytosis (rare)-aplastic anemia-skin rash-may be teratogenic (don’t give to pregnant women
Infliximab: target? uses?
anti-TNF-alpha-used to treat: Crohn’s disease, Rheumatoid arthritis, Psoriatic Arthritis, Ankylosing spondylitis
IBD that has a higher association with colorectal cancer?
Ulcerative Colitis(Crohn’s also is associated with it; but higher risk with UC)
Levothyroxine:-clinical use?-mechanism?
treatment for Hypothyroidism and MyxedemaMechanism = Thyroxine (T4) replacement
Adalimumab: target? uses?
anti-TNF-alpha-used to treat: Crohn’s disease, Rheumatoid arthritis, Psoriatic arthritis
Treatment for Crohn’s?
NAME?
Triiodothyronine:-clinical use?-mechanism?
treatment for hypothyroidism and myxedemamechanism = thryoxine (T4) replacement
Abciximab: target? uses?
targets Glycoprotein IIb/IIIa-clinical uses: prevent cardiac ischemia in unstable angina, and in pts treated with percutaenous coronary intervention
Treatment for Ulcerative Colitis?
NAME?
Clinical uses of GH?
NAME?
Herceptin = Trastuzumab: target? clinical use?
NAME?
STD that is commonly mistaken for IBD?
L1,L2, L3 subtypes of Chlamydia –> cause Lymphogranuloma venereum
Clinical uses of Octreotide (Somatostatin)
NAME?
Rituximab: target? uses?
-targets CD20 (so, B-cells!)-used to treat B cell-non Hodgkin’s lymphoma
Dx criteria for IBS?
Recurrent abdominal pain + at least 2 of:-pain improves with defecation-change in stool frequency-change in appearance of stool
Clinical uses of Oxytocin?
NAME?
Omalizumab: target? uses?
NAME?
McBurney’s point:
1/3 distance from ASIS to umbilicus (or 2/3 distance from umbilicus to ASIS!)–>pain is localized here in appendicitis
clinical use of Desmopressin/ADH?
NAME?
Risk/Complication of appendicitis?
Perforation–> get peritonitis
Domeclocyline:-mechanism?-clinical use?-Toxicities?
-ADH antagonist (it’s a member of the Tetracycline family)-Treatment of SIADH (syndrome of inappropraite ADH secretion)*Toxicites:-Nephrogenic DI-photosensitivity-abnormalities of bone and teeth (like tetracycline!) -
“true” vs “false” diverticulum?
true: all 3 gut wall layers involved (ie Meckel’s)false: only mucosa and submucosa outpouch
Triamcinolone (what class of drug is it?)
a glucocorticoid
Most common site of diverticula?
Sigmoid colon
Beclomethasone (what class of drug is it?)
a glucocorticoid
Most common cause of severe left lower quadrant pain?
Diverticulitis (inflammation of diverticula)
Glucorticoids:-mechanism?-clinical uses?-toxicities?
Prednisone, Hydrocortisone, Triamcinolone, Dexamethasone, BeclomethasoneMechanism:-decrease production of leukotrienes and prostaglandins, by inhibiting phospholipase A2 and expression of COX-2Uses:-anti-inflmmatory-Addison’s disease (chronic primary adrenal insufficiency: defiency of cortisol and aldosterone) -immune suppression-asthma-inject directly into keloidsToxicities:-iatrogenic Cushing’s syndrome-tertiary adrenal insufficiency (when drug is stopped after chronic use) -also: psychosis, insomnia, gluacoma, acne
Treatment for diverticulitis?
Antibiotics
left lower quadrant pain + bright red rectal bleeding?
Diverticulitis
stinky breath (halitosis) + dysphagia + esophageal obstruction?
Zenker’s diverticulum = “false” diverticulum at junction of pharynx and esophagus–>have stinky breath d/t trapped food!
Cause of Meckel’s diverticulum?
Persistent vitelline duct or yolk sac
Most common congenital anomaly of GI tract?
Meckel’s diverticulum
Pertechnetate study
Dx for Meckel’s diverticulum
The five 2’s of Meckel’s diverticulum?
-2 inches long-2 ft from ileocecal valve-2% of popl-usually presents during first 2 years of life-may have 2 types of epithelia (gastric/pancreatic)
currant jelly stools?
Intussusception
Where does intussusception commonly occur?
commonly at ileocecal junction
What age group does volvolus usually affect? Where does volvulus usually occur?
-usually in elderly-may occur at cecum and sigmoid colon (b/c have redundant mesentery)
Congenital megacolon d/t failure of neural crest migration?
Hirschsprung’s disease-lack of ganglion cells/enteric nervous plexuses (Auerbach’s and Messner’s) in segment of intestines
What part of GIT is usually affected in Hirschsprung’s?
Involves rectum
Failure to pass meconium?
-Hirschsprung’s-Cystic Fibrosis
Increased risk of Hirschsprung in people with what other syndrome?
Down syndrome
4 GI conditions associated with Down syndrome:
NAME?
Bilous vomiting in baby + “double bubble” (proximal stomach distention)
Duodenal atresia = blind duodenum–>associated with Down syndrome
Necrotizing enterocolitis: most common in what pt popl?
-preemie infants (b/c decreased immunity)
Pain after eating in elderly + weight loss (but, not a gastric ulcer…)
ischemic colitis–>usually occurs at splenic flexure (watershed area) and distal colon
Sawtooth appearance of masses in gut lumen?
Colonic polyps
Area often involved in colonic polyps?
NAME?
90% of colonic polyps are not malignant; which types are most likely to be malignant?
NAME?
multiple non-malignant hamartomas throughout GIT + hyperpigmented mouth, lips, hands, genitalia (so, hyperpigmented mucosal surfaces) + increased risk of Colorectal cancer?
Peutz-Jeghers syndrome–>autosomal dominant
autosomal dominant mutation of APC gene on chromosome 5q?
FAP = Familial Adenomatous Polyposis–>100% of pts progress to colorectal cancer
Lynch syndrome/HNPCC (Hereditary NonPolyposis Colorectal Cancer)
–>autosomal dominant mutation of DNA mismatch repair genes–> 80% of pts progress to Colorectal Cancer –> always involves proximal colon
FAP + osseous and soft tissue tumors + retinal hypertrophy?
Gardner’s syndrome
FAP + malignant CNS tumor?
Turcot’s syndrome
“apple core” lesion on barium enema?
colorectal cancer
CEA tumor marker
colorectal cancer
Iron deficiency anemia in older males or post-menopausal females?
Suspect colorectal cancer
Most common sites of carcinoid tumors?
NAME?
Bronchospasm + Flushing + Diarrhea + Right-sided heart lesion
Serotonin Syndrome (carcinoid tumor that secretes serotonin)
Why is carcinoid syndrome only a “syndrome” once it metastasizes out of GI system?
–> b/c just tumor alone = carcinoid tumor, not syndrome–> if tumor is in the GI, it may secrete serotonin, but don’t see any of the symptoms, b/c the liver metabolizes serotonin–>once it metastasizes, usually to liver, then start seen symptoms associat
form of bilirubin in bloodstream?
unconjugated bilirubin-albumin complex = indirect (water-insoluble) bilirubin
form of bilirubin in liver?
conjugated/direct (water-soluble) bilirubin
form of bilirubin in stool?
stercobilin
form of bilirubin in urine?
urobilin
uridine glucuronyl transferase = UDP glucuronyl transferase
enzyme, converts indirect bilirubin to direct bilirubin in liver
Effects of Portal Hypertension
-Esophageal varices –> Hematemesis-Melena -Splenomegaly-Caput medusae, ascites-Hemorrhoids-Portal hypertensive gastropathy
Effects of liver cell failure:
-Coma–> hepatic encephalopathy; from release of ammonia and other toxic metabolites from liver-Scleral icterus-musty smelling breath-gynecomastia-jaundice-testicular atrophy-asterixis (hand flap)-bleeding tendency (from decreased prothrombin and clotting
liver enzymes (AST, ALT) in alcoholic vs viral hepatitis?
alcoholic hepatitis: AST>ALTviral hepatitis: ALT>AST
Lactulose
-Osmotic laxative-Also: Treatment for hepatic encephalopathy (in liver failure) –> b/c gut bacteria break it down, promoting nitrogen excretion as NH4+
