Kaplan Notes

Neuro-Anatomy Spinal cord Funiculus: white matter that may contain tracts; tract: collection of fibers w/same origin Conus medullaris: end of SC (contains S3-S5) and ends at L2 vertebra Cauda equine: dorsal & ventral roots of lumbar, sacral & coccy spinal nerves Cervical enlargement (lg ventral horn): C5-T1 b/c of motor to upper limb (~L2-S3) Lower motor neuron: voluntary and reflex of skeletal (deep tendon or myotatic reflex) afferent limb of latter is 1a sensory neuron and afferent limb is LMN Knee: tests quads; ankle: gastrocnemius; forearm: brachioradialis UMN have a net inhibitory effect on muscle stretch reflexes why lesion = hyperrefl. Motor neuron: precentral gyrus in cortex posterior limb of internal capsule midbrain (crus cerebri) pons base pyramids (medulla) pyramidal decussation lateral corticospinal tracts ventral horn (synapse) Romberg sign: means smthg wrong in dorsal columns (i.e. tabes dorsalis in syph); with eyes open and positive for swaying means its a cerebellar problem Lateral horn: T1-L2 has pre-ganglionic sympathetics The cell body of upper motor neurons is in the primary motor cortex (precentral gyrus) Brainstem Superior colliculi: conjugate gaze; inferior colliculi: auditory before goes to thal and cortex Just below the colliculus (dorsal view/back view): CN IV 3 pairs of cerebellar peduncles = contain axons of the UMNs of the CS tracts & corticobulbar tract CN 6, 7, 8 exit at the ponto-medullary junction; while 5 is more in pons Spinal accessory nerve originates from the spinal cord thru the foramen magna, NOT brainstem Optic N: retinal ganglion cells axons (the 2nd neuron) coalesce and form the CNII myelinated by oligodendrocytes thus the only CN affected by central demyelinating dz: MS [other myelinated by schwamm cells] CNIII: is the only controller of eye adduction thru the medial rectus but also thru SR & IR Pupillary light reflex: When light comes in thru CNII via retinal ganglion cells projects to pretectal nucleus (midbrain) projects bilaterally to both Edinger-Westphal nuclei (CNIII, preganglionic parasympathetic) ciliary ganglion (postganglionic parasym) sp. CNV: if pain + temp only lost in jaw, probably lesion in pons/medulla/cervical spinal cord b/c the spinal trigeminal nucleus extends down to that point; whereas the tracts carrying motor and proprioception stay in the midbrain near CNV, and do not extend down that point all of these lost would indicate a lesion in the brainstem CNVII: the upper half of face is innervated bilaterally, while the lower half of the phase is innervated unilaterally, and from the UMN (corticobulbar lesion) of the contralateral side of the cortex (the ipsa side just innervates the forehead and orbicularis oculi) Facial nerve lesion (LMN): complete ipsa facial weakness UMN lesion in cortex/corticobulbar lesion: contralateral lower face weakness CNIX: only motor is to stylophayngeus determine integrity by gag reflex CNX: innervates all musc of palate except for tensor palati (V), and all for phaynx for swallowing except for stylopharyngeus (IX), all the larynx LESION: nasal speech, regurgitation, dysphagia, palate droop, uvula devitates away from lesion (opposite of tongue [due to genioglossus muscle] & jaw upon protrusion [due to lateral pterygoid musc.]] deviate towards), horseness/fixed vocal cord, loss of motor to gag reflex XI: lesion shows difficulty combing hair b/c of trapezius innervation in order to upwardly rotate the scapula during abduction) Upper medulla: OLIVE! Cerebellum Vermal lesions: ataxic gait, trouble maintaining posture Romberg: sway with eyes open and closed; vs dorsal column lesion: Romberg shows swaying with eyes closed ONLY Fall TOWARD lesion b/c of crossing on way to cortex, and then crossing back Thiamine def w/alcohol: also influces purkinje cells in vermis Hemisphere lesion: distal musculature intention tremor (vs. PD); also get dysmetria (tested: finger-to-nose test); dysdiadochokinesia: cant perform alternating mvmt like pronation and supination of forearm at a fast pace; scanning dysarthria words divided into individual syllabus disrupting s peech melody; conjugate gaze drifting off target & nystagmus w/fast component TOWARD lesion (vs. AWAY from lesion in vestibular nuc. Dz) MS: scanning speech, intention tremor, nystagmus Upper limb Supinators: supinator (radial N.) & biceps brachi (musculocutaneous N.) Radial N lesion: [prox] wrist drop, loss of other extensors inc finger extension, weakened supination, sensory loss of posterior forearm & hand [distal at midshaft of humerus] wrist drop but no loss of elbow extension like above; weakened supination & sense loss [distal at radial head fracture or dislocation] weakness of digit extension, weakened supinator, sense loss on posterior forearm & hand Abdominal anatomy: Extraperitoneal layer: is where testis comes form Meckels/vit/ophthm duct: fuses around 8-10wks Respiratory diverticulum comes off of the gut-tube Gastchitis: failure of closure abdominal folds Ventral mesentery leads to: lesser omentum, visceral peritoneum of liver, falcifiform ligament Lesser omentum: hepatogastral ligament and hepatoduodenal ligament (contains portal triad w/biliary duct that empties into 2nd part of duodenum) Spleen: splenorenal ligament is btwn spleen & dorsal ab wall & contains the splenal A from the aorta (remember embryo picture) Secondary retroperitoneal: was intraperitoneal & became retro after gut tube rotated Secondary must always be in front of primarily retroperitoneal organs 6th wk: intestinal loop migrates out and grows w/the SMA peritoneal organs drain into the portal sys [&secondary retroP: duo, panc, asc/desc colon, upper rectum]; primarily retroperitoneal drain into the IVC [kidney, adrenal, ureter, aorta, IVC, lower rectum, anal canal] Kidney Anatomy Sites of stone obstruction: uretopelvic junction, pelvic brim/external&internal iliac A bifurcation, vesicouretal junction (MC b/c smallest) Ureter: on surface of psoas major while it travels done Lowest part of peritoneal cavity: recto-uterine pouch (where fluid accumulates) posterior fornix (cervix area) right next to pouch of douglas can penetrate into here into P. cavity Looking at CTs of abdomen: Veterbral marker with IVC just in front to left and abdominal aorta just in front to right; portal V. is always going to be anterior to the IVC! Kidney is surrounded by fat so see black arnd kidney and can better identify Adrenal: triangle and anteromedial to kidney, also surr by FAT and separate from kidney by FAT Psoas right next to vertebrae w/ureter anterior to it as dot!; distinguish from kid b/c NO FAT L4 catched the upper part of the ileum M. part of iliac crests; also see aorta bifurcation and still IVC to the left

Goljan Study Guide Take 2Cell Injury & Inflmm Hypoxemia: dec pO2; any time you have inc in pCO2, pO2 must go down Hypoxemia can cause hypoxia; hypoxemia is caused by perfusion, ventilation, diffusion defects Hypoxia: besides hypoxemia, can also have anemia (norm saturation too), CO (headache first sign), methemoglobinemia (chocolate colored bl, from nitrates, from dapsone (a sulfa drug), Bactrim); cytochrome oxidase inhibition (from CO & CN), uncoupling agents Leads to lactic acidosis b/c relying on anaerobic glycolysis for ATPs leads to coagulation necrosis = denatures the enzymes from the lactic acidosis All ATPase pumps ruined cell swells due to Na influx Ca: activates phospholipases, and enzy in nucleus (chromatin disappears), affects mito, ALL due to SERCA loss (hyperCa can activate enzymes in acute panc!); cell mem damage is worst! Free rads: radiation creates hydroxyl free radicals; also creates double stranded breaks in DNA; how Fe causes damage in liver and heart (free radical); acetaminophen free rads (NAPQI) PMNs are involved in liq necrosis; the exception is in the brain Strep has hyaluronidases which break down GAGs allowing infection to spread = cellulitis Blue stain in histology: CALCIUM like in pancreatitis Immune complex damage: HOW? Activates alternative compl sys: C5a = PMN chemotactic Rheumatic fever valve veggies: sterile, fibrin-like material = fibrinoid necrosis Fibrinoid necrosis: necrosis of immunological disease; RA nodule: fibrinoid necrosis Yellow fever: hits zone II of liver Alcoholics: excess NADH: driving pyruvate into lactate and taking P away from gluconeogenesis (fasting hypoG) & NADH favors the formation of beta-hydroxybuteric acid (low N = acetoacetic acid) Glycerol-3-phosphate shuttle for NADH also for backbone of TGs = fatty liver (VLDL) Types of Calcification: dystrophic (damaged tissue calcification w/normal serum Ca) & metastatic (calcification due to high serum Ca or high Phos since P drive Ca into tissues) Alcoholic body: Mallory bodies = ubiquinated keratin (intermediate filaments) Only G1 and G0 phases can be altered in length. Metaplasia of eso: from sq glandular w/goblet cells Histamine: redness, warmth, tumor; dolor: from bradykinin (& PGE2), brady also makes edema Myeloperoxidase: inside the lysosome of the monocytes (not macs) and PMN G6PD def: infection sets it off b/c the respiratory burst requires NADPH (NADPH oxidase) C3a, C5a: anaphylaxis, stimulate mast cells, inc vessel permability & inflmm Post MI w/PMNs: increased PMN count b/c epi & cortisol released w/demarginates them CD10: the calla Ag in ALL (B cell); CD45 on all leukocytes Fibronectin: key in wound healing Granuloma: type IV HPY, pink w/giant cells, macs process Ag and present it to helper T cell (MHCII) helper Ts release IFN-gamma triggers mac to kill the organisms; pink cells are epitheloid activated macrophages they die in style after by fusing together and forming multi-cellular giant cells; IL-12 key in helping helper Ts act as memory cells and is released from macs Older ppl & +PPD: dont respond as well; same with AIDS patients (dont have granulomas either) ESR: IgM causes the RBCs to clump along w/fibrinogen; why cold agglutination in occurs (RBCs norm negatively charged to keep them from sticking to one another); cryoglobulins can also do this Acute appendicitis: leukocytosis, left shift, & toxic granulation (more azurophilic granules = lysosomes w/myeloperoxidase); left shift: bands and/or metamyelocyte or myelocyte Fluids & Dynamics Pitting edema: have edema from lymphatic block, from exudate and transudate, and trasudate is really the only one that pits Lymphatic block & Chlamydia: AKA lymphogranuloma venereum, it is a primary infection of the lymphatics! Thats why you get scaring ulcers w/scar tissue that blocks lymph = lymphedema of scrotum; also primary PAINLESS ulcer w/LAD, rectal disease w/BRBPR; scarring also leads to rectal strictures, anogenital fistulas Calculating serum vs. urine osmolality: serum: double serum Na and add 10; urine osmolality: Dr. Roses way: take the last 2 #s of specific gravity and multiply by 30 Hyperglycemia in diabetic: dilutional hypoNa b/c glucose brings H20 OUT and hypertonicity Urea doesnt control H20 mvmt b/c its permeable to cell membrane Isotonic loss: hemorrhage, diarrhea; isotonic gain: isotonic saline Hypertonic loss: diuretic (leads to hypoNa, H20 moves into the ICF compartment) SIADH: usu a serum Na ovarian > cervical (b/c we screen for it) MC gyn killer: ovarian > cervical > endometrial MC benign tumor in women: leiomyoma; MC skin CA that invades but doesnt mets: BCC MC benign tumor in males: lipoma Adrenal adenoma: if secreting cortisol, causes atrophy of the fasiculata & reticularis but NOT glomerulosa; if conns, then there wld be atrophy of the glomerulosa Vascular malignancy: can see wibble palad bodies (contain vWF), meaning endothelial origin Mechanism of retinoic acid for APL Tx: matures the blasts so malig cell benign cell Smoking causes CA via: polycyclic hydrocarbons; causes lung, sq of mouth, larynx, lung, panc adeno, bladder transitional (papillary tumor) HPV: sq CA of cervix, vagina, vulva and anus E6 knocks off p53 (17) and E7 knocks Rb (13) Arsenic: sq cell of skin, angiosarcoma of liver MC CA associated w/radiation: leukemia MC of that associated w/radiation is CML; also see papillary carcinoma of the thyroid RB: inherited = JUST NEED ONE MUTANT MCC white reflex is congential cataracts; steroids predispose to cataracts (Cushings syndrome) Host defense: most key is cytotoxic CD8 T cells; also NKs (INF-gamma helps enhance both of these in tackling sq CA) = kill via apoptosis (= no inflmm) Cachexia: caused by TNF-alpha, its irreversible Associations w/disseminated CAs: hyercoag (trousseaus sign), thrombocytosis (also caused by splenectomy, Fe-def, TB) usually a missed CRC (thrombocytosis) MCC fever in malignancy: GN infection E.coli from cath, pseudo from respirator MC collagen vascular dz associated w/CA: dermatomyositis a/w leukemias, lymphoma & lung CA Marantic endocarditis: sterile vegetation on mitral valve & a/w mucus-producing CA i.e. CRC these veggies can also mets HCC paraneo: makes EPO and Insulin-like factor polycythemia and hypoglycemia RCC: makes EPO & PTrP Yolk-sac tumors: high AFP, aka endodermal sinus tumor Anti-CEA + CEA Ag: in CRC, can deposit in glomerulus = diffuse membranous glomerulonephritis Medullary Carcinoma of thyroid: hypoCa, Cushings, amyloid w/calcitonin Hematology Cardiology S3 always means volume overloaded and is the result of turbulence when the blood flows into ventricle S4 is always the atrial kick hitting resistance i.e. hypertrophy, compliance issue** TR: pansystolic, S3 & S4, left parasternal border, inc intensity on inspiration (like all R heart sounds), neck vein accentuation, infective endocarditis from IVDA AR: S3&4 sounds, volume overloaded, bounding pulses, dripping blood onto anterior leaflet (one side of outflow tracts of aorta) = Austin Flint murmur LHF: heart failure cells on cytology = alveolar macrophages phagocytose RBCs hemosiderin TX HF: right or left = restrict salt and water; ACE-I dec afterload AND preload via angioII and aldosterone, respectively; research shows increased longevity: spironolactone + ACE-I Hi output heart failure: Endotoxic shock, graves, AV fistulas, pagets, thiamine deficiency Shock: Vasodilation from inc C3a, C5a, NO inc venous return hi output fail B1 def: run out of ATP sm musc reacts by vasodilating b/c cant contract see above Graves: inc beta Rs on heart AV fistula: returns faster to the heart; test by pressing on proximal portion of fistula and heart rate decreases = Brenhams sign Fetal Circulation: syncytiotrophoblast layer of chorionic villus cytotrophoblast layer myxomatous stroma fetal bl vessel in villus umbilical vein O2 saturation arterial: 95%; O2 saturation returning venous; 75% PDA: pink top, blue bottom all blood that bypasses lungs dumps distal to subclavian A. thru patent PDA and steps-down blood going to lower extremities **congenital rubella** RL shunts: increased risk for septic emboli from infective endocarditis, inf endo in general, polycythemia Transposition of great vessels: incompatible unless PDA, VSD, ASD Pre-ductal and post-ductal coarctation: pre is congenital (Turners) & post develops Post: cause of HTN, high renin, claudication in lower extremities, higher BP in upper>lower, use of collateral circulation: 1)superficial epigastric A with internal mammary A feel pulsation where indirect inguinal hernia would be 2)intercostals rib notching on CXR Berry aneurysms too from no internal elastic lamina & no sm musc (subarachnoid hemorrhage) Sudden cardiac death: severe coronary a. dz, high risk smokers, no heart pathology changes, no coronary thrombosis v-fib MCCD Chronic ischemic heart dz: little infarcts, EF 0.2 vs 0.66, fibrous tissue heart failure MCCD Reperfusion injury: injured tissue encounters O2 O2 free rads Ca comes in injured myos die LAD MI: anterior 2/3s IV septum (where most conduction bundles located) complete heart block, anterior heart, part of SA node RCA MI: entire posterior heart, entire RV, post 1/3 IV septum SA node: 50% from LAD, 50% from RCA AV node: 95% from RCA If AV node blocked: sinus bradycardia Can lead to atypical chest pain i.e. GERD symptoms w/epigastric pain Can lead to papillary musc rupture: the only two muscles are the posteromedial pap and posteromedio papillary musc. Mural thrombosis: a mixed clot, meaning plates and coagulation factors on top Fibrinous pericarditis post-MI: chest pain relieved when leaning forward, 3 part rub 1st wk: not autoimmune, transmural infarction and inc vessel permability 6 wks: Dresslers syndrome with Systemic Sx Constrictive pericarditis: cardial knock Pericardial effusion: kussmauls and pulsus paradoxus (frequently the 2 go together) + distant sounds MC due to pericarditis (from Coxsackie) Ventricular Aneurysm: MCCD is heart failure NOT rupture MI enzymes: CK-MB: starts in 6 hrs, peaks in 24hrs, disappears post 3d; if present = re-infarction Troponin I: earlier start at 4hrs, peaks at 24h, lasts 7d MVP: myxomatous degeneration with GAG, Dermatan sulfate in excess Jones criteria for acute rheumatic fever: joint pain and swelling, dyspnea, rales in lung, pansystolic murmur in apex (MR), S3 & S4, erythema marginatum, subQ nodules that = RA nodules on extensors, Syndhams chorea ***only a few things that cause polyarthritis in children: juvenile RA, henock-scholein purpura, rubella, acute rheumatic fever*** Marfans MCCD: MVP and conduction deficits NOT a AD Infective endocarditis: MCC: viridans, 2MCC: staph; if UC/colon CA: strep bovis (group D) MC valve: mitral>aorta; MC in IVDA: T>Aorta Pathophys: NOT emboli, but immune complex vasculitis (type III HPY) roth spots (look just like koplick spots), splinter hemorrhages, Oslers nodes, janeway lesions, glomeruloneph, etc. Congestive cardiomyopathies: commonly drug-induced i.e. doxirubucin Coxsackie virus: MCC myocarditis & pericarditis, viral meningitis, hand foot mouth dx, herpangina any heart biop w/lymphocytes probably coxsackie-caused myocarditis Respiratory SVC Syndrome vs. Pancoast tumor: SVC in from a mediatinal mass b/c the lung tumor affects the SVC near the heart *ant. Med. Sx: headaches, JVD, facial plethora, red face Pancoast is from a sulcus lung tumor at the top of the lungs near the brachial plexus *in the posterior mediastinum Sx: pain due to brachial plexus in the C8, T1, T2 nerve distribution, problems with veins/arteries toosee next point, horners, brachial plex = absent reflex, atrophy hand [#1943] brachiocephalic obstruction thru apical tumor, this vein is the union of the internal jugular & subclavian (the external jugular drains into the subclavian); BC vein also drains right lymphatic duct (drains right upper ext, right face & neck, right hemithorax, right UQ in ab); Sx: right sided face and arm swelling w/engorged subQ veins An A-a gradient: tells you theres a problem in the lungs; a normal gradient says theres a problem outside the lungs causing hypoxemia i.e. resp center depression, obesity, ALS Laryngeal CA: synergy btween smoking and alcohol (a sq cell carcinoma) Inc in surfactant in fetus: glucocorticoids, thyroxine, prolactin; insulin decreases it (gest. Diabetes issue) 3 main causes RDS in neonate: prematurity, diabetes, C section Often leads to PDA since the baby is hypoxemic Macrosomia in gest diabetes mechanism: insulin made by baby stimulates synthesis of TG and deposition of fat + inc AA uptake by muscles (~GH) = inc in adipose and muscle mass Hyaline membranes come from: degeneration of type II pneumocytes, leakage of fibrinogen, all these congeal to form membrane; remember type II is the repair cell and makes surfactant ARDS vs RDS (neonate): not the lack of surfactant, but lung collapse due to neutrophils and inflmm. MCC ARDS: septic shock; MCC DIC: septic shock ex: septic shock ARDS on 2nd d DIC 3rd PMNs role: put holes thru the pulm capillaries as they enter lungs (leaky capillary syndrome) protein and fibrinogen spills in hyaline membranes massive pulm shunting Pneumonia: In the community, typical is strep pneumo and atypical is mycoplasma, 2nd: chlamydia pneumo In the hospital (nosocomial): E coli, pseudomonas, staph aurus Lung findings: decreased percussion (dull), inc TVF, egophony, pectoriloquy Pleural effusion: only thing is decreased percussion (dull) Rhinovirus: MCC of cold; acid labile (destroyed in stomach) (viral pnemo) RSV: MCC bronchiolitis, small airway dz (viral pneumo) Chlamydia trachomatis: 1 wk post birth, wheezing, pnemo, inc AP diameter, tympanic percussion sounds, no fever, crusty eyes bilaterally, staccato coughs (bac. Pneumo) Klebsiella: alcoholics, high spiking fever, cough of mucoid sputum (the capsule of kleb is thick); lives in upper lobes and can cavitate just like TB Sq cell carcinoma of lung can also cavitate in upper lobes Legionella: atypical cough that is not productive, water mists, hyponatremia due to interstitial nephritis from the bacteria knocks off JG cells no renin no also salt wasting in urine; Tx: erythromycin Bactrim: for PCP (3g, pneumonia, pulm infarction (fibrin & protein leaks)GI Herpes esophagitis: in HIV patients; Candida esophagitis: HIV-defining (not in mouth); cryptosporidium parvi: MCC diarr in HIV, partially acid-fast (t-cell btwn 75-50) EBV: Tx acyclovir Exudative tonsillitis: 30% GABHS, 70% virus adeno, EBV **most pus on tonsils is viral Group A strep, 3wks later rheumatic fever; culture: nothing (its not infective endocarditis) MCC sq dysplasia & CA: smoking, synergy w/alcohol Veracious carcinoma: chewing tabacco, HPV Addisons dz: very first place seen hyperpigmentation is Buccal mucosa Peutz-Jeghers: blotchy hyperpigmentation, hamaratomatous polyps in SI (not sigmoid), they are non-neoplastic and wont become CA MC salivary gland tumor: pleomorphic adenoma, mixed tumor (w/2 diff tissues of same cell layer), MC in parotid Mumps: inc amylase, no infertility if orchitis b/c unilateral; also oophoeritis in females Dysphagia w/solids not liquids: obstruction esophageal web in Plummer Vinson, eso CA Dysphagia w/solids AND liquids: peristalsis, upper 1/3: striated musc so myasthenia gravis; lower 1/3: smooth musc so scleroderma or achalasia Chagas dz: myocardidis, CHF, congestive cardiomyopathy, Romanas sign: swelling around eye Left gastric vein: esophageal varices, azygous vein drains into it, and it drains into portal vein Diverticulosis: MCC of hematochezia; 2nd MCC: angiodysplasia: wall stress greater where diameter greater in cecum telangiectasias angiodysplasia rupture w/hematochezia Meckels: also bleeds, melana though, RLQ pain, also hematemesis Congenital Pyloric Stenosis: 3wks, vomit non-billous Downs w/duo atresia: at birth, vomit billous, no mvmt so air trapped: double bubble sign = air trapped in stomach & in prox duodenum Stomach: Pernicious anemia: hits body and fundus (auto-AB) H. pylori: pylorus and antrum CA: lesser curvature of pylorus & antrum (where H. pylori) Melena: acid converts Hb hematin (black) Perforated Duodenal ulcer: stressful job, epigastric pain radiates to L shoulder = air under diaphragm Adenocarcinoma of stomach leads to krukenberg tumor: hematogenous spread Japan: smoked products leads to gastric CA; also HTLV-1; China: nasopharyngeal carcinoma Left supraclavicular node: virchows, gastric CA mets; R-SCV node: lung CA MAI: more common than TB in HIV pts, acid fast positive, helperT50yo, FAP, Gardners, Turcot; **not: P-j, hyperplastic polyps, juv polyps MCC appendicitis in kids: measles OR adenovirus (lymphoid tissue in appendix hyperplasia obstruction); MCC adults: fecalith ~to acute cholecystitis: blockage ischemia (but stone w/GB, not fecalith)Hepatobiliary & Pancreas Primarily unconj bili: hemolytic anemias, spherocytosis, SCDz, ABO hemolytic dz of the newborn, Rh hemolytic dz of the newborn, physiologic jaundice of the newborn (when the cant conjugate it) 20-50% direct: hepatitis doesnt take up unconj and spills out conjugated >50% direct: obstruction intrahepatic or extrahepatic Sx: dark urine and pale stools Dark urine not due to the normal urobillinogen that colors stool and urine when bile is broken down by bacteria; due to conj bilirubin Sx: high cholesterol, pruritis from bile salts in skin, hi alk phos, hi GGT (obs.) Liver Enzymes: AST/ALT: Indices of liver necrosis (hepatitis), ALT is more specific b/c found in liver, AST in musc, RBCs and liver; in viral hepatitis, ALT>AST b/c more liver specific AST>ALT in alco cirrhosis, fatty change, alc hepatitis b/c of MITOCHONDRIA specificity of AST Alk phos and GGT hi in obstruction (also >50% direct bili); GGT is more liver specific GGT: also up in alcoholism b/c in SER reved up in alcoholism **PT & albumin are the BEST measures of liver damage severity PBC: anti-mitochondrial ABs ~ to Hashimotos: anti-microsomal ABs HCC markers: AFP, alpha-1 antitrypsin (elevated in CA); CEA is a marker for Px Hepatitis (viral): C&D: The only ones that dont offer protective ABs i.e. if you have antiD-IgG, ACTIVE dz HAV, HBV, HEV offer protective ABs A&E: parentally A: no chronic carrier state (only acute); A also often in Daycare centers (vaccines!); jails! E: only chronic carrier if pregnant chronic liver dz B: IVDA, accidental needle stick; C: post transfusion hepatitis Window: only core AB IgM Entamoeba histolytica: amoeba that phagocytosis RBCs Sheeper Herders Dz: from gonococcus vermicularis, dog is definitive host b/c has adults that are having sex (dog ate sheep meat w/larva); owner is the intermediate host b/c has eggs that form larvae: Dz: cysts if ruptured = anaphylactic shock T. solium (pig tapeworm): person who eats pig meat with larva is definitive host then makes food and gets eggs in salad then person who eats eggs gets larva = intermediate host Dz: cystocercosis larva migrate and form cysts lined by calcium brain = seizures Nutmeg liver: MCC is RHF; also thrombus in hepatic vein MCC: polycythemia vera; 2nd MCC: OCPs Mallory bodies: ubiquinated keratin microfilaments; seen in alc cirrhosis Ito cells: normally store vitA, but in alcoholics, acetaldehyde (toxin in alcoholics) stimulates Ito cell to make fibrous tissue and collagen. Cholangiocarcinoma: connected to UC and PSC (MCC of PSC is UC); in 3rd wrld countries: Clonorchis sinesis (Chinese liver fluke) PBC: woman, 40-50yo, jaundice only until late, autoimmune granulomatous destruction of bile ducts in portal triad. Drugs and liver: OCPs and anabolic steroids: intrahepatic cholestasis (ex: weight-lifter has jaundice with no viral titers, hi alk phos and GGT (both mean obstruction)) Pregnancy: intrahepatic cholestasis from estrogen OCPs & anabolic steroids: predispose to benign liver tumor: hepatic adenoma that ruptures intraperitoneal hemorrhage Hemochromatosis: damage isnt due to Fe but to the hydroxyl free radicals produced by Fe Fe also goes to: pancreas, skin (bronze diabetes w/both), polyarthritis when in joints, pituitary (hypopituitarism), restrictive cardiomyopathy Tx: phlebotomy *hemosiderosis: acquired Fe overload from alcohol Wilsons Dz: low total Cu 95% of Cu bound to ceruloplasm = total Cu; in Wilsons, low ceruloplasm so low total Cu, but high free Cu (more unbound). Lenticular nuc deposits: = putamen and globus palidus Complication of alcoholic-induced ascites: spontaneous peritonitis usually due to E. coli Child w/nephrotic syndrome-induced ascites due to strep pneumoniae HCC almost always develops in the background of cirrhosis MCC: pigment cirrhosis from hemochromatosis, then hep B & C Makes: EPO (polycythemia) & IL-GF (hypoglycemia) Common: to find blood in a tap of the ascites fluid Bile stones: too much cholesterol (fibrates) or too little bile salts (as in cirrhosis, obstruction, cholestyramine, Crohns) Dx: US; for anything related to the pancreas: CT (because GI obstructs on US) Cystic Fibrosis: problem with CFTR at the golgi apparatus where it was suppose to be modified; when missing CFTR, Na+ is reabs OUT of the secretion in airway and Cl- cannot be pumped out = dry!Renal Penetrance: present in AD conditions, example of 100% penetrance is APC; incomplete penetrance is marfans where someone can have gene but has no phenotype whatsoever. ADPKD: more prone to get berry aneurysms (and also charcot-bouchard microaneurysms thru HTN), MVP, diverticulosis (MCC hematochezia) itis means immune complex for kidney disorders i.e. IgA glomerulonephritis, diffuse membranous glomerulonephritis, post-strep glom-nephritis Nephritic: will not have pitting edema b/c not enough protein lost; dec filtration and filtration of Na HTN; classically: hematuria, RBC casts, oliguria, dysmorphic RBCs, HTN, mild/moderate proteinuria Nephrotic: fatty casts are pathonognomic (from cholesterol in the urine) Lipoid/MCD: Hx of URI in child Tx: corticosteroids Diffuse membranous: caused by many things like drugs, CA, infections NSAIDs, hepB, captopril, malaria, syphilis, colon CA (immune complex is anti-CEA Abs); MC adults Membranoproliferative: I hepC; II autoAB against C3 (low complement C3) Tram-tracks: due to mesangial cell going btwn BM and endothelial cell Focal segmental glomerulosclerosis: IVDAs and AIDs PGE2: works at the afferent arteriole of the glomerulus; PGI2 in the rest of the blood vessels Nephrotoxic ATN If drugs, involves the PT MC: AGs, 2MC: intravenous pyelograms (elderly) Chronic pyelonephritis: blunted calyces under cortical scar Analgesic nephropathy: acetaminophen (makes free radicals that damage tubular cells of medulla) & aspirin (blocks PGE2, so AGII takes over, contricts and less blood flow to peritubular capillaries that comes from the EA and are around the cortical tubules and renal medulla) = ring sign on peylogram bc renal papilla are gone; similar patho w/diabetic nephropathy and sickle dz & trait Nephrosclerosis: outside of kidney has cobblestone/bumpy appearance; underlying hyaline arteriolosclerosis dec bl flow tubular atrophy fibrosis of glomeruli (HTN, diabetes) Flee-bitten kidney: malignant HTN hyperplastic arteriolosclerosis; the fleas are BV rupture leading to petechial cortex Multiple pale infarcts: embolizations to kid causing coagulative necrosis (i.e. atrial fib) Renal adenocarcinoma is MC kidney mass (PT); wilms is MC child (also PT, malignant, primitive) MCC RCC: smoking; make EPO and PTHrP (hypercalcemia) WAGR: chrom 11, wilms, aniridia, hemihypertrophy, GU malform, mental retard Cystitis: PMNs, RBCs & bacteria; dipstick + for RBCs, leukocyte esterase measures enzymes in leukocytes, most pathogens are nitrate reducers so dip measures nitrites that pathogen did nitrate nitrite Chlamydia = sterile pyuria: dysuria, inc freq, PMNs, RBCs, no bacteria, + leukocyte esterase TB: also sterile pyuria; kidney MC organ that military TB goes too Ureaplasma: also sterile pyuriaGYN MC CA of the penis: squamous, more common in uncircumscribed but also in poor hygiene smegma is carcinogenic Testes descent: MIF 1st half, test and DHT 2nd half; seminoma: risk if not descended by 2yo even in good testicle; increased bHCG Seminoma: MC testicular tumor Parallels dysgerminoma in females, esp Turners must surgically remove ovaries MC testicular in kids: yolk sac tumor; AFP Most severe: choriocarcinoma; bHCG Ex: male w/SOB (mets to lungs) and gynecomastia (bHCG is like LH and makes boobs) Epididymitis: 35yo is pseudomonas Torsion: absent cremasteric reflex, goes back up into inguinal canal b/c ascends; painful! DHT: in embryogenesis fuses labia (scrotum), penis, throws in prostate (why we use finesteride) BPH: periurethral portion; Prostate CA: periphery of prostate gland (rectal exam w/hardness) Virulization: hirstuism + male secondary sex characteristics (i.e. acne, deeper voice), clitoromegaly (pathognomonic) Most testosterone in women: ovary; DHEA: adrenal; so if hirsutism in woman, can have ovarian origin if testosterone high, or adrenal origin if adrenal high PCOS: hirsutism due to ovarian origin (therefore high testosterone) LH in theca cell makes 17keto-steroids DHEA and androstenedione testosterone Test granulosa cell FSH stimulates aromatase estradiol In PCOS: LH inc DHEA, androstendione and testosterone Obesity: inc estrone from aromatized androstenedione and estradiol from testosterone endometrial hyperplasia Inc estrogens suppress FSH, encourage LH OCPs: progestin blocks the LH Cysts: FSH constantly suppressed so follicle degenerates = cyst Anovulatory bleeding: MCC abnormal bleeding in