Genitourinary Id2final

GENITOURINARY DISEASES I. URINARY TRACT INFECTIONS A. Can present w/ back pain B. Female M/C: UT in close proximity to bacteria from anus 1. Hygiene: Wiping A to P NOT P to A 2. Shorter tract: urethra C. Normal urinary tract is sterile (with chemicals in it) D. M/c bacterial infection in humans (UTI) 1. Upper Respiratory Tract Infections m/c viral infection E. Lower UTI: M/C UTI 1. Urethritis: Chlamydia, Gonorrhea 2. Cystitis: M/C of lower UTI: Infection of urinary bladder: less S & S than Urethritis F. Upper UTI 1. Pyelonephritis: Kidney Infections (Pyelo = pelvis) abscess death/dialysis: night sweats, fever G. PATHOPHYSIOLOGY 1. 100,000/ml is threshold (Bacteria to DX UTI): Some patients are symptomatic with less 2. B/w 10,000 – 100,000 is contaminated 3. Neonates- m/c in boys from anomalies-diverticula=stasis: 30 days old or less 4. Anything that slows down the flow of urine 5. Preschool – m/c in girls from hygiene 6. Adults – m/c in women from hygiene H. Four pathways 1. Ascending form urethra: M/C way 2. Lymphatic spread: 2nd m/c: close by & share drainage 3. Hematogenous spread: Pelvis to vessels 4. Direct extension: Pelvic abscess from ovary or uterus: Frequent emptying decreases UTIs G. Risk Factors: Female 1. Neurologic disease:urinary catheter 2. Diabetes: sugar in urine that bacteria can feed off of and therefore are more prone to UTI’s (Infra somatic cystitis  air in wall of bladder from aerobic bacteria) 3. Renal failure: Prerenal; postrenal - worst stasis 4. Pregnancy: higher risk d/t incomplete emptying or obstructed ureters 5. Pathogens a. E. Coli: M/C b. Proteus Mirabilis: gas producing 6. Defense Mechanisms a. Low pH: 4.8 - 8 b. Normal Micturition: prevents stasis 1. Detrusor mm contracts 2. Trigone muscle relaxes c. High Osmolarity: High chemical content H. LOWER UTI: Presentation inconsistent: 1. Some asymptomatic, some just have urgency, some have extreme pain 2. Urinary frequency 3. Dysuria (pain or burning) 4. Urgency 5. Urge incontinence: leak 6. Suprapubic pain 7. Hematuria a. Gross: Patient will see in toilet b. Microscopic

I. PYELONEPHRITIS: Most cases are retrograde migration of lower UTI: sepsis death 1. Fever of unknown origin 2. CVA pain (costovertebral angle): Murphy’s Punch- m/c in diabetes 3. Radiating pain into groin, Anterior and inner thighs, back 4. Chills, Fever, night sweats 5. Malaise: Fatigue 6. Vomiting – electrolyte imbalance 7. Diarrhea 8. Can be fatal or can cause renal failure 9. CLINICAL TESTING a. Clean catch UA: Wipe w/alcohol pad → start urination → stop → catch mid-steam urine → stop before urination is complete b. Urine Culture & Sensitivity c. CBC: Elevated WBC, Anemia (mild) d. KUB (kidney, ureter, bladder plain film of abdomen) e. Ultrasound f. IVP (Intravenous Pyelogram): Outlines renal substance g. CT scan: For tumors or abscess f. Cystoscopy: for biopsy g. Retrograde pyelography (obstruction): Dye from urethra up and stops where infection is or Check for stones/ chronic UTI 10. Dx by S & S usually J. Non-gonococcal Urethritis (Non-specific Urethritis): most common STD 1. NGU twice as common as gonorrhea 2. Chlamydia is most common bug 3. Often asymptomatic (~25%): easily transmitted 4. Symptoms a. Dysuria b. Whitish discharge c. Meatal edema (edema of urethral meatus) 5. Treatment w/ antibiotics: 25% untreated = asymptomatic K. Gonorrhea: “The Clap” (Test or punishment?): 2nd M/C STD 1. Neisseria Gonorrhoeae 2. Urethra is mc sight of infection 3. Contraction rates (single intercourse) a. 20% for males b. 80% for females 4. Symptoms a. Dysuria b. Urethral discharge c. Urethral itching 5. Treatment w/ antibiotics L. Herpes Simplex: “Cold Sores”= Type I- clear vesicles transudate crusts: contagious after lesion gone 1. HSV II infection affecting ~20% of adults 2. Spread through direct contact 3. Causes blisters/ulcers around genitals 4. May also infect the eye, skin, other organs 5. No cure, only symptom control M. Genital Warts: Immune system suppression of HPV- can reoccur; not painful unless abraided 1. Condylomata acuminata 2. Cause by form of HPV- wart is overproduction of tissue 3. Represents 1/3 of cases of STDs, 20 million people

4. Most people are exposed at some point in life 5. Treat with antiviral creams, cryotherapy, and laser: N. Urolithiasis: Calculus in the urinary tract: AKA – renal colic = crescendo/decrescendo (wave-like) 1. Types of stones a. Calcium (70%): (Gallstones are mostly cholesterol) b. Uric acid (8%): Gout, ureacemia: Sharp,jagged damage pain c. Struvite (15%) d. Cystine(3%): Homocystinuria 2. 250k – 750K /year 3. M:F 4:1 4. Incidence is highest in summer (dehydrate) 5. Signs/symptoms: a. Acute colicky CVA/flank pain b. N/V c. Referred pain to testes/vulva/groin: Ipsilateral d. FCNS suggests infection: Fever, chills, night sweats. Can obstruct stasis infection 6. Diagnostic work-up: a. UA (hematuria- micro/macro) b. Plain film radiography: R/O AAA- m/c, Ca++ lymph nodes- paraspinal= Retroperitoneal c. Renal US (best) d. IVP 7. DDx: a. Pyelonephritis b. Cystitis c. Diverticulitis d. PID 8. Rx a. Increased fluid (for small stones to flush out) intake unless there is obstruction 1. Never push fluid if obstructed- will burst kidney. b. Low calcium diet c. Uretoscopic stone removal d. Extracorporeal shockwave lithotripsy e. 50% pass within 48 hrs: 50% recurrence rate without Rx & diet changes O. Glomerulonephritis: Autoimmune inflammation of glomerulus, progressive to renal failure 1. Synonyms: Post-infectious GN; Acute nephritic syndrome 2. Epidemiology a. 50% affect < 13 y/o b. M/c cause of chronic renal failure (~25%) (2nd DM) c. Post group A beta strep infection m/c d. Collagen vascular dz (SLE especially) e. Idiopathic P. Proteinuria 1. Normal adult excretes ~150 mg/day (0-+2 on dipstick): small chain proteins excreted daily 2. 3.5% prevalence in normal adults 3. Perform 3 separate dip tests: 3 separate specimens, different days? Positive again-follow up if Negative – dx: transient functional proteinuria 4. Causes a. IDDM b. Nephrotic syndrome c. Amyloid d. Lymphoma e. NSAID use f. Orthostatic proteinuria (only when upright): pressure problem

Q. Nephritic Syndrome 1. Secondary to GN (Glomerulonephritis) 2. Signs/symptoms a. Edema (periorbital, scrotal) (d/t hypoproteinemia/proteinuria) b. HTN (damage to kidney and edema- ↑ in total peripheral resistance) c. Hematuria- damaged glomerulus d. Proteinuria- damaged membrane = leaks: +2-+4 on dipstick R. Nephrotic syndrome: forms in basement membrane of glomerulus 1. M/c cause is membranous GN 2. Signs/symptoms a. Peripheral edema (more widespread than nephritic)- dependant edema = pretibial/ankle b. Ascites c. HTN (high blood pressure) d. Pleural effusion & periquadrial effusion e. Hypoalbuminemia (low blood albumin): leaks in to urine f. hyperlipidemia/hypercholesterolemia g. 1/3 of pt has DM, SLE, amyloidosis S. Acute Renal Failure: Sudden decrease in renal fxn: PNS & CNS S&S: major tremors, less blood supply 1. Inability to maintain fluid/electrolyte balance 2. Inability to eliminate wastes: a. Intra-renal failure= damage to kidney: b. Post-renal failure= urine can’t get out- obstruction c. Pre-renal failure = low blood perfusion 3. Signs/symptoms a. N/V: systemic b. Oliguria/anuria: below 100cc/day c. Altered sensation- toxemia 4. Laboratory/ physical findings/ causes a. Elevated BUN/Creatinine-best b. Electrolyte imbalance: low Na+ & K+ c. Anemia, platelet dysfxn: erythropoietin, bleeding 5. Pre-renal failure (m/c cause): low blood supply: a. Inadequate renal perfusion: 1. Hypovolemia- shock 2. CHF: low pressure = low perfusion b. Sepsis: bacterial- 90% mortality 6. Intrinsic renal failure a. Renal dz b. GN, drug toxicity, ATN (acute tubular necrosis) T. Post-renal (AKA: obstructive uropathy – least common) 1. Outlet obstruction 2. BPH (m/c cause) 3. Prostate CA 4. Ureteral stones 5. Bilateral renal vein occlusion- tumor U. Chronic Renal Failure: Progressive decrease in renal fxn: >250,000 dialysis pts/year 1. Signs/symptoms: Pallor, Ecchymosis, Edema, HTN, Depression, Fatigue, N/v, pruritis 2. Etiology: DM (37%)-Pre, HTN (30%)-Pre & intra, GN (12%) - Intrinsic a. Polycystic kidney dz: fatal in newborn: Giant renal cyst b. Drug toxicity c. Obstructive uropathy

d. Renal artery stenosis 3. Laboratory findings a. Elevated BUN/creatinine b. Proteinuria, RBC casts-Pyelonephritis c. Electrolyte imbalances V. Renal Cysts: fluid-filled epithelium-lined cavities: Found on 50% of autopsies 1. Rarely symptomatic 2. Simple cysts are ~70% of all renal masses 3. Polycystic renal dz: a. M/c hereditary dz in the USA b. 50% have renal failure by age 60 c. Repeated UTIs, large kidneys (huge,lobulated), flank pain d. 50% pts also have liver, pancreas cysts-Psuedofibrous,fluid-filled, no epithelia e. Thoraco-lumbar junction anomalies have more renal anomalies: Cardiac- mid & upper W. Renal Cell Carcinoma: Adenocarcinoma-glandular: Malignant transformation of renal tubular cells 1. AKA – hypernephroma: 1:10,000 people/yr (collecting tubules) 2. 50-70 y/o: Male: female 2:1 3. Etiology: Familial, Smoking, Obesity, Diuretics, Tylenol- (cox2 inhibitors also) 4. Signs/symptoms: rapid growth, very vascular a. Hematuria (50-60%)-painless!TQ: Small amount m/c capsule edema b. Abdominal mass (25-45%) c. Anemia (20-40%) d. Flank pain (35-40%) e. HTN (20-40%)- renal artery stenosis f. Wt loss (30-35%): stage 3-4 cancer g. Classic Triad (5-10%): Hematuria, Flank pain, Abdominal mass 5. Treatment: Nephrectomy, Radiotherapy, Chemotherapy (5% response rate): growth rate faster than treatment killing rate. 6. Prognosis: Mets to abd, bone, liver, anywhere blood goes. a. Stage I (asymptomatic) ~90% b. Stage II (asymptomatic) ~75% c. Stage III ~20% d. Stage IV ~5% e. Metastasis: To mesenchymal tissues: 1. Glandular mets to mesenchymal tissue 2. Mesenchymal mets to soft tissue-glandular tissue (sarcoma) 3. Carcinoma mets to bone X. Prostate Diseases: Prostatitis, Benign prostatic hyperplasia, Prostate carcinoma 1. Prostate specific antigen (PSA): Normal 0-4 ng/ml (like ESR, to gauge RX effectiveness) a. Elevated in: BPH, Prostate CA (not 100% accurate), Post-rectal examination, trauma b. Most sensitive for BPH, not for screening cancer 2. Prostatitis: Men over 50: May be aseptic or septic: DRE-in front of rectum, surrounds urethra: “feels” like the tip of the nose- lobulated slightly- midline uncus- if smooth = swollen a. Signs/symptoms 1. Dysuria (burning/pain is deep inside the pelvis) 2. Polyuria: frequency due to pain- not emptying bladder 3. Pelvic/ back pain 4. Urethral discharge (prostatic fluid)- clear to white 5. Fever- low grade, unless infection present b. Dx made by c/s of prostate secretions if infected c. Antibiotics if infectious d. Kiegal exercises: contract/relax- stop stream: helps BPH, sex- maintains erection –more female; less incontinence

e. Proscar- suppresses growth 3. Benign Prostatic Hyperplasia: BPH, Benign overgrowth of the prostate: some cancer risk a. Generally begins in periureteral area b.80% of men by age 80 c. Med/surg intervention in 20% men by age 75 d. TURP is the 10th mc surg in USA (>400k/yr) e.10-30% w/ BPH has an occult CA f. Clinical presentation 1. Enlarged prostate on DRE loss of sulcus 2. Poor correlation b/w size and symptoms: outer vs midline growth 3. Hesitancy 4. Decreased caliber and force of stream 5. Double voiding (go again soon after or start & stop 6. Post-void dribbling 7. Nocturia g. D/Dx: Prostatitis, Prostate CA, Urethral stricture, h. Dx workup: 1. PSA, Protease secreted by epithelial cells, Elevated in ~40% pts w/ BPH 2. UA 3. Ultrasound (to make sure there is no mass hidden in the BPH) i. Treatments: Avoid caffeine, Avoid meds (cold and allergy drugs- antihistamine & MAO inhibitors), Meds, TURP (roto roter), Stents, Laser, Coils j. Prognosis is good (>70%) 4. Prostate Cancer: Has surpassed lung CA as m/c CA in men: 100,000 new cases/yr; 30,000 deaths/yr: Uncommon <50, 80% new cases >65 y/o, Average age at dx is 72 a. Black males (1 in 9) m/c population in world b. Clinical presentation c. Generally asymptomatic (symptoms usually from BPH) d. Bone pain/fx may be initial presentation e. Outflow obstruction: central growth f. Mass on DRE (10% have normal DRE): deep in gland g. D/Dx: BPH, Prostatitis, Prostate stones, h. Diagnosis: Elevated PSA (may be normal in 20%) 1. Elevated acid phos (extracapsular extension) 2. Biopsy i. Treatment (chemo, rad, prostatectomy) j. Px depends on stage (~90% w/ stage I to 10% w/ stage IV) Y. Testicular Torsion: Twisting of spermatic cord: Leads to testicular ischemia infarct: 1:4000 incidence 1. 70% occur b/w 1 – 18 yrs old: can be spontaneous 2. D/dx: Testicular tumors, Epididymitis, Incarcerated hernia, Orchitis, Hydrocele 3. Clinical findings: Sudden hemiscrotal pain (10% are painless), Swelling-unilateral, N/v, Afebrile 30% of pts report previous episode of pain: (a jump up & land hard may fix) Z. Epididymitis: Septic traumatic inflammation of epididymis: >600K visits per year 1. Occurs in sexually active men: 2. D/dx: Orchitis, Testicular torsion, Hydrocele, Varicocele, 3. Agents: N. gonorrheae, C. trachomatis 4. Clinical presentation: Tender scrotal swelling, Erythema, Dysurea, Urethral discharge, Fever 5. Rx: Ice packs w/ scrtal elevation, Analgesics, Antibiotics 6. Px usually self limited AA. Hydrocele: Fluid collection in the scrotal space: If congenital, assoc. w/ inguinal hernia 1. In adults: Infection, Tumor, Trauma 2. Clinical presentation: Scrotal enlargement- unilateral-fluid, Pain/radiating to back 3. Rx none if asymptomaticL you want pain- or may be cancer

BB. Orchitis: Infection of the testicle: Inflammation 1. Usually viral (mumps/coxsackie B virus) 2. Occurs in post-pubertal males 3. Clinical presentation: Testicular pain/swelling, May be bilateral, Inguinal lymphadenopathy 4. History of recent mumps 5. Rx- observation if viral 6. May lead to sterility CC. Testicular Cancer: Three types 1. Seminoma (mc) 2. Teratoma (has all three germ layers so the cell can differentiate into any type of cell in the body) 3. Choriocarcinoma 4. 2-3/100k/yr: M/c in young adults (30-40) 5. Clinical presentation: Scrotal mass, D/n illuminate, Not painful (even less than normal testicle) 6. Pain from mets is more common 7. Workup (70% have elevated hCG/AFP) 8. Rx- surgical resection, chemo, radiation 9. Px → 70 – 85% for early stages DD. Bladder Cancer: Range from low-grade to high-grade 1. Cell types: Transitional cell (93%); Squamous cell (6%); Adenocarcinoma (1%) 2. 54,000 new cases/yr, 12,000 deaths: 4(F)-10(M)% of all cancers: M/c over age 60 3. 25% result from occupational exposure: Dye, Textile, Rubber tire, Petroleum workers 4. 15 – 65% associated w/ smoking 5. Clinical presentation: Gross painless hematuria, Microscopic hematuria, Frequency, urgency 6. Mets pain in distant organ (eg, back pain) 7. Diagnosis: H&P (History and Physical Exam), UA, Cystoscopy, 8. Rx- chemo, radiations, TURP, cystectomy 9. Px- dependent on cell type and grade II. Liver Function A. Anatomy: 4 lobes 1. Right, Left, Caudate, and Quadrate: Weighs ~ 3 lbs B. Blood supply 1. Hepatic artery (oxygenated blood)(20%) 2. Hepatic portal vein (nutrients)(80%) 3. Hepatic veins (drain liver) 4. Holds 1 pints of blood 5. Only organ that can regenerate- 75% damage before failure 6. Over 500 functions: Produces bile, Produces plasma proteins, Produces cholesterol Converts glucose to glycogen, Stores iron, Converts ammonia to urea, Clears drugs, Blood clotting 7. Normal portal venous pressure = 5 – 10 mm Hg C. Hepatitis: Liver inflammation 1. Types a. Viral (A, B, C, D, E, X?) b. Alcoholic hepatitis c. Drug-induced hepatitis d. Toxic hepatitis (carbon tetrachloride, benzene) e. Leptospirosis f. Toxoplasmosis g. EBV, CMV, HIV 2. Hepatitis A: Caused by HAV (Hepatitis A Virus)(RNA virus), Fecal-oral route, close family a. Acute dz that is self-limiting: 9 – 45/100,000/yr b. Institutionalized children: Day care centers: Male homosexuals; Exposure imported apes

Undercooked mussels, clams, oysters c. Highly contagious: Represents 33% of viral hepatitides in USA d. M/c in 2-5 y/o (day care) and age >50 e. Infants may be non-jaundiced; Neonates have subclinical infection f. Incubation 15-45 days g. Rarely causes fulminant hepatitis: Rarely transmitted thru infected blood h. D/Dx: Other hepatitides, Viral illness w/ liver involvement (CMV, EBV), Non-viral hepatitides i. Clinical presentation: Often asymptomatic (25% adults, 90% <2 y/o), Anorexia, Malaise, Hepatomegaly (87%), RUQ tenderness, Splenomegaly rare (9%), Jaundice, Dark urine (bilirubinuria), Fever variable (precedes jaundice) j. Workup: LFTs (Liver function Tests), HAV antibody, ALT/AST (often > 8x normal), Bilirubin (usually 5 – 15x normal), Alk phos (1 – 3x normal), Albumin, prothrombin normal WBC most often normal, Hepatitis A IgM 1. Imaging studies not normally useful 2. No such thing as chronic hepatitis A: Acute dz lasting < 6 wks Rarely prolonged (3-5 months); No carrier state k. Treatment: Avoid hepatically metabolized drugs 1. IV fluid replacement for vomiting (rare) 2. Steroids not normally helpful: Follow-up as outpatient l. Px: <0.1% fatality rate, 60% w/ fulminant recover, Evidence of previous dz in 40% adults 3. Hepatitis B: Acute viral hepatitis (AKA serum hepatitis): Uncommon chronic form (5-10%) a. 4000 – 5000 deaths/yr from chronic HBV: Incubation 30 – 180 days: DNA virus; 200 – 300k new acute cases/yr (300 deaths) b. At risk populations: blood transmission: IV drug users, Homosexual males, Hemodialysis and hemophilic pts, Health care workers, Neonates/infants c. M/c in 20-45 y/o d. D/Dx: Other viral& non-viral hepatitides: Other viral illness w/ liver involvement e. Clinical presentation of acute dz: Most often anicteric (no jaundice) and asymptomatic Anorexia, Malaise, N/v, Serum sickness (hives, rash, arthralgia (painful joints)), Hepatomegaly, splenomegaly (uncommon), Jaundice, bilirubinuria, +/- fever f. Clinical presentation of chronic dz (1-2%): Similar to acute HBV g. Asymptomatic chronic active carrier-Pts has active virus in system- is contagious h. Hepatic decompensation- Dz damages so badly that the liver stops functioning Without liver transplant the pt will die 4. Hepatitis C: Most common infectious type of hepatitis: Viral infection of the liver with HCV a. Non-A, non-B RNA virus: Intermediate incubation (15-150 days) b. Mcc of non-alcoholic liver dz in US (40%) c. Epidemiology: Transfused hemophiliacs, IV drug users, Occupational needle sticks Hemodialysis d. Male = female: 18-39 y/o mc e. Clinical presentation: Gradual symptom onset, Milder that HAV/HBV, RUQ tenderness, Hepatomegaly, Jaundice, Dark urine (bilirubinuria), 1. Many are anicteric (no jaundice) and asymptomatic (75%) f. Immunity after infxn is incomplete g. Fulminant acute dz is rare (0.1%) h. Persistent infection is common (50-70%)- Results in chronic hepatitis i. Cirrhosis develops in 20-50%; Hepatocellular CA develops in 50% j. D/Dx (other inflamm hepatic dzs) k. Diagnostic workup: Acute hepatitis c antibody, LFTs, Biopsy for complications l. Rx: Avoid meds metabolized by liver, Otherwise acute Rx is non-specific m. Follow-up for complications n. Interferon may be helpful in relapses

o. Acute dz lasts <6 wks: No vaccine: Immune globulin injections are not helpful 5. Alcoholic Hepatitis: Most common form of hepatitis: Most common cause of cirrhosis a. S/Sx similar to other hepatitis x flu-like Sx: Hepatomegaly; Splenomegaly more common than viral, Ascites D. Cirrhosis: Risks of Hepatocellular CA 1. Laboratory tests: HBsAg, Elevated ALT/AST, Hyperbilirubinemia, Elevated alk. Phos 2. Treatment: IV fluids for dehydration, Treat for hepatic failure, if present: Avoid hepatically metabolized drugs: Steroids not helpful: Interferon for chronic cases; Liver transplant a. Antiviral agents: Famciclovir, Lamivudine 3. Prevention: Avoid high-risk behaviors, Testing of blood supply, a. Hepatitis B vaccine: High risk groups (90% effective): Childhood vaccination, HBV hyperimmune globulin-Given after needle stick/after birth w/ infected mom Given after sexual exposure 4. Hepatic Cirrhosis: Caused by hepatocellular injury: Results in fibrosis ad nodular regeneration a. Micronodular, macronodular, mixed forms: 9 deaths/100k people/yr in US (11th m/c cause of death) b. Most common causes: Alcoholism, Viral hepatitis (especially HBV and HCV) c. Other causes: Drugs (tylenol), chronic CHF, hemochromatosis, amyloidosis d. Clinical Presentation 1. Early: Weakness, fatigability, disturbed sleep, Muscle cramps, weight loss 2. Advanced: Anorexia, weight loss, N/v, hematemesis (esophageal varicies), Jaundice, Hepatomegaly, Ascites, Amenorrhea (lack of steroids that are usually made in liver that later are used to make the hormones): Impotence in men (lack of steroids that are usually made in liver): Skin lesions, Spider nevi (especially on face), Palmar erythema (alcohol abuse), Glossitis, chelitis, Ecchymosis, CNS damage, Asterixis (intermittent lapse of body position)(pt just falls for no reason), Tremor, Delirium, Dysarthria (slurred speech), Coma e. Laboratory findings: Macrocytic anemia, Abnormal LFTs, Decreased albumin, Leukopenia f. Rx: Avoid hepatotoxic meds; Treat dz that caused cirrhosis, Treat complications (ascites, varicies, CHF) 5. Primary Biliary Cirrhosis: Autoimmune dz: Destruction of intrahepatic bile ducts (in the liver) a. M/c in females (95%): 40-60 y/o age group b. Associated w/ PSS, SLE, Sjogrens Synd, RA, other connective tissue arthropathies c. S/Sx: Fatigue, Pruritis, ~50% are asymptomatic, Hepatosplenomegaly, jaundice later on d. Laboratory tests: Anti-mitochondrial antibodies (98% specific) (AMA); Abnormal LFTs e. Rx: Methotrexate, Cholchicine, Urosidol, Steroids, Liver transplant f. Px: Asymptomatic → 10 –16 yrs: Symptomatic → 7 yrs E. Hepatic Tumors: 1. Benign: Hemangioma, Adenoma 2. Malignant: Hepatocellular Carcinoma, Cholangiocarcinoma, Metastasis (m/c liver malignancy) 3. Hemangioma: M/c primary benign liver tumor; Vascular tumor; Asymptomatic; Found incidental 4. Adenoma: Rare solitary or multiple tumor; Usually asymptomatic 5. Hepatocellular CA: Malignant tumor of hepatocytes; a. Associated with: Chronic liver dz, Cirrhosis, HBV, HCV, Hepatotoxins (ETOH, steroids) b. Clinical presentation: Weight loss, anorexia, Ascites, Hepatomegaly, 33% are asymptomatic c. Diagnostic evaluation: Elevated alpha feto-protein in ~90%; Not used to diagnose only monitor; Elevated LFTs (Liver Function Tests), MRI, US/CT-guided biopsy d.. Treatment: Dependent on size of lesion/mets; Resection; Chemotherapy e.. Px : 20-30% following resection 6. Cholangiocarcinoma: Intrahepatic bile duct malignancy: Rare in US/Europe: More common Asia a. Presents as liver mass: Associated with liver fluke infestation

b. Slow progression to metastasis c. More common in primary biliary cirrhosis F. Cholelithiasis: Gallstones: Affects 20,000,000 Americans 1. Predisposing factors ( 6 F’s → Fair skin, Female, Fat, Forty, Flatulence, Fertile); OCA use, DM 2. ~20% chance of developing biliary colic: Pts are asymptomatic unless passing a stone 3. S/Sx: Colicky RUQ pain; Night pain; Refers to right shoulder; Lasts minutes to hours 4. 75% of stones contain cholesterol 5. Ultrasound is imaging procedure of choice 6. Rx: Cholecystectomy, ESWL, dissolution 7. Px: Good G. Cholecystitis: Acute and chronic forms: 95% associated with gallstones: 1. M/c in same groups as cholelithiasis (6Fs) 2. Clinical presentation: RUQ pain/tenderness; Pain radiating to right shoulder; Murphy's sign; Fever (~33%); Jaundice (25-50%); Fever, chills, n/v 3. Diagnostic workup: US (procedure of choice): MRI/CT to r/o more ominous causes 4. Treatment: Laparoscopic cholecystectomy (lap chole)- The stump that is left will grow and make a small replacement gallbladder Tx cont;s: Open cholecystectomy; Broad-spectrum antibiotics 5. Prognosis: Excellent: 1% complication rate with lap chole H. Cholangitis: Inflammation of bile ducts: Complication of cholelithiasis(~1%) 1. Occurs during 7th decade and older 2. Clinical presentation: Charcot's Triad-Fever/chills,RUQ pain; Jaundice, Bilirubinuria, All S/Sx present in 50-85% of pts 3. Diagnostic workup: US, ERCP (Endoscopic Retrograde CholangioPancratogram)-PRN 4. Treatment: Biliary decompression; ERCP (maybe w/ stent placement), Percutaneous transhepatic biliary drainage, Broad-spectrum antibiotics 5. Prognosis is excellent: Chronic dz associated w/ porcelain GB I. Primary sclerosing cholangitis: Diffuse inflammation leading to stricture- Liver stops= Jaundice, Malaise, Itching, Anorexia 1. M/c in M 20 – 40 J. Gall bladder cancer: Adenocarcinoma m/c 1. Asymptomatic unless dz is advanced: Usually found during surgery for stones, Weight loss, anorexia, Palpable GB, RUQ pain; Associated with stones in 80% 2. Porcelain GB also associated 3. Poor Px K. Acute Pancreatitis: Supposed to be the most painful organ dz in medicine (describe pain as stabbing with a hot knife in stomach or back): Most often secondary to biliary disease 1. Enzymes released into pancreas 2. S/Sx: Severe abdominal/back pain, Fetal position, N/v, Mild jaundice, Shock, Lipase and amylase levels increased, 3. CT/MRI for Dx 4. Treatment: IV hydration; NPO; NG suction (stomach pumped); Pain control; Treat complications 5. Prognosis: 5-10% mortality;Worse in older, sicker patients L. Chronic Pancreatitis: Recurrent Pancreatitis: Classically associated with alcoholics: Male:female 5:1 1. S/Sx: Recurrent epigastric/back pain; Abdominal tenderness/guarding; Weight loss; Foulsmelling stools (chalky white in color and float) 2. Associated with alcoholism/biliary dz 3. Major D/Dx is pancreatic CA 4. KUB may reveal calcifications (looks like rice in mid-abdomen) 5. 50% pts die w/in 10 yrs (malignancy) M. Pancreatic Carcinoma: 1. Adenocarcinoma 2. 2nd m/c tumor of GI system (m/c in colon cancer)

3. M:F 2:1 4. M/c in head of pancreas 5. S/Sx: Jaundice (head of pancreas and not the tail b/c does not obstruct bile duct) a. Abdominal pain b. Weight loss, anorexia, nausea c. Biliary obstruction S/Sx (head tumor) d. CT/MRI are best imaging procedures e. Poor Px from early mets