Keystone #3

Treatment of Breast Cancer

*Breast* Partial mastectomy (lumpecomy) Mastectomy -Simple -Skin-sparing - Total skin sparing LCIS = No ink on margin DCIS = 2 mm margin (higher rate of recurrence) *Nodes* Inject dye around tumor and wait for it to be taken up by nodes and excise 2 to check for cancer *Adjuvant Therapy* Chemotherapy (Anthracycline +Taxane, anti-HER therapy) Endocrine therapy (Selective estrogen Reuptake modulator, Aromatase inhibitor) Radiation: -Whole breast radiation -Partial breast radiation -Intraoperative radiation - Radiation done for breast concerveing surgery, high risk or tumor >5 CM w/ LN involvement

Post-operative Recovery and Outcomes

*Post OP* Care plans Care coordination Enhanced recovery after surgery Rounding* *Outcomes* Quality and value Patient reported outcomes including quality of life complications/adverse events Morbidity and mortality conference*

Work-up of Testicular Mass

*Testing* Alpha-fetoprotein: produced by yolk sac tumors and embryonal cancers (which are NSGCT) - Never elevated in seminoma - If elevated in seminoma, have pathology recheck the specimen and treat NSGCT Human chorionic gonadotropin (hCG) - can be elevated in seminoma, as 15% of seminoma have syncytitrophoblasts - Also produced by choriocarcinoma Lactic acid dehydrogenate (LDH) - Reflects tumor burden Also get BC for anemia, creatinine to look for renal failure (and going to get a CT with contrast), and LFTs *Imaging* Scrotal US - Confirm that the mass is testicular and solid (no one goes to OR w/o US) - Confirm intra-testicular vs extra0testicular mass - May id mass amenable to partial orchietomy, used in very select cases CT of abdomen and pelvis - Done before orchietomy to evaluate for retroperitoneal LN/ distant mets - CXR to evaluate pulmonary mets

Palliative Care options

- First decide if cancer is curable or treatable - Then decide if a non-curative surgery is needed - Cytorecuctive therapy - Maetastecomy - palliative therapy - Hospice

Variceal Hemorrhage

80% of cases of upper GI bleed in cirrhotics Important causes of morbidity and mortality Hemodynamic resuscitation (Large bore IVs, blood products) Consider intubation Call GI Begin octreotide drip antibiotic prophylaxis

Gastroesophageal Reflux Disease (GERD)

3-4% of population but only a few ppl will get mucosal injury Pathology: Incompetent antireflux barrier (relaxation of LES transiently, altered anatomy (hiatal hernia) or decreased LES pressure (scleroderma)); Aggressive reflux , reduced clearance of acid from esophagus (Sjogren's or reduced motility), or increase abdominal pressure (pregnancy) Symptoms: heartburn, regurgitation, water brash (mouth fills with saliva/sour taste), dysphagia (inflammation or stricture), hoarseness, globus sensation (lump in throat), chronic cough, asthma, Odynophagia (indicates ulcer) DX: therapeutic trial with acid suppressing meds - run tests only if atypical symptoms, chronic or refractory symptoms, or warning symptoms (dysphagia, bleeding, weight loss) -> endoscopy to look for inflammation or amulatory pH probe to try an correlate symptoms to increase in esophageal pH Complications: Ulcer, stricture, Barrett's esophagus (squamous epithelium replaced by columnar epithelium which can be complicated by dysplasia and then adenocarcinoma) Treatment: Lifestyle mods (elevated head of bed, avoid fatty foods, chocolate, peppermint, alcohol, weight loss, avoid late meals), meds (PPI, H2 blocker, antacids), Surgery (fundoplication - reinforce LES)

Diarrhea Definition Chronic

Change in bowel habits from baseline Chronic > 4 weeks (osmotic, secretory, maldigestive/malabsorptive, inflammatory, functional)

Acute Diarrhea

< 2 weeks (infections, medications) Risk factors: - Travelers (e colie and campylobacter) - Outdoors (Giardia and cryptosporidium - Cruise ship (norovirus) - Contaminated foods (staph aureus, salmonella, e coli, bacillus cereus) - daycare (rotavirus and adenovirus) - Nosocomial (c difficile) - Drugs that increase risk = Abx, NSAIDS, metformin, beta blockers, SSRIs, PPI, misoprostol Usually self limiting *nonenterotoxigenic* - short duration, symptomatic therapy (hydration) *Enterotoxigenic* - longer duration, fever, low vol, bloody stools, >48hrs, severe pain, elderly, immunocompromised. Symptomatic therapy and stool studies and empiric or specific Abx

DDx of "Extreme" hepatocellular injury pattern

Acute viral hepatitis hepatic ischemia DILI (acetaminophen) Toxin (mushroom poisoning)

Ascites

Always tap ascites Reasons to tap: - new onset to confirm etiology - rule out infection if signs are present (fever, abdominal pain, leukocytosis) - Any evidence of deterioration (most cases of SBP do not present with "peritonitis" - rule applies to all pts with decompensated cirrhosis) - relief of symptoms due to tense ascites Coagulopathy is NOT a contraindication to paracentesis - complication rate is 1% but coagulopathy is present in 70% of pts - no objectively determined threshold for plts or clotting parameters beyond which to tap - no role for FFP or platelets FIRST TAP: - SAAG (serum ascites-albumin gradient) - cell count with differential FOLLOWING TAPS or if you suspect infection: - Cell count with differential - Ascitic fluid culture In absence of other evidence of liver disease: - Cytology, AFB culture, etc SAAG > 1.1 = portal hypertension Management: Na restriction (2g/day), spironolactone and furosemide. Avoid IV diuretics b/c can make renal fxn worse. Fluid restriction not needed if serum Na > 120 Avoid use of NSAIDs in pts with cirrhosis - adverse renal effects on top of bleeding risks (you can give acetaminophen but less than 2g/day)

Treatments directed at abdominal pain

Antispasmodics - used to treat abdominal pain and spasms in all IBS subtypes Peppermint oil also has antispasmodic affects Tricyclic antidepressant agents appear effective in treating IBS symptoms

Liver Tests

Ast/Alt = hepatocellular injury Alcoholic liver disease = AST> 2x ALT Alkaline phosphatatse = cholestasis (can elevate from extra-hepatic places so look for increase in GGT or 5'nucleotidase to confrim source is the liver ALT more specific for liver; AST can come from muscles, RBCs, etc)

Tagged RBC ("bleeding") Scan

Autologus RBCs labelled with Tehnetium-99m Tagged RBCs reinfused and imaging performed can be re-imaged every few hrs if needed can be helpful for evaluating intermittent bleeding, esp if bleeding persists/recurs after negative endoscopic evaluation requires active bleed of .1-.5 ml/min localization of actual bleeding site ccan be trick though

Genetic testing for breast cancer

BRACA 1/2 vs Multigene panel - minority have BRACA mutuation, but increases lifetime risk by alot when you have it Impacts patient and family and also impacts treatment options

Pathology Role in Cancer

Best available assessment of disease biology - Diagnosis - Grade - Stage - Margin status Decisions on adjuvant therapy or clinical trials come from this. *TUMOR BOARDS*

Chemotherapy Side Effects Bleomycin Etopside Cisplatin Ifosfamide

Bleomycin (anti-tumor antibiotics - damages DNA by generating free radicals) - *Pulmonary fibrosis* - Reduciton of FiO2 - Avoid fluid overload Etopside (Topoisomerase II Inhibitor) - Renal insufficiency (mild), myelosuppression, alopecia, secondary leukemia (dose dependent) Cisplatin (platinum coordination complex) - Renal insufficiency, N/V, Neuropathy, 35% ototoxicity Ifosfamide (nitrogen mustard alkylating agent) - Hemorrhagic cystitis (mesna is prophylaxis)

Purpose of cancer screening

Catch the cancer before it becomes symptomatic (Clinical pattern recognition vs incidental presentation) Distinguish between screening and diagnostic testing Watch out for alarm symptoms and make sure to follow up on the tests you order! Diagnosis actually comes from procedure/biopsy and the imaging to see if it's primary or metastatic disease Inform the pt about the dx in person; but make sure they know there is an abnormal result asap

Gastroparesis

Causes: Diabetic gastropathy, nerve damage, post-viral gastroenteritis, scleroderma symptoms: postprandial bloating, early satiety, delayed vomiting of partially digested contents, refractory gastroesophageal reflux Dx: succussion splash, UGI showing dilated stomach, scintography for rate of gastric emptying Treatment: Improve underlying condition, promotility agents (metoclopramide, erythromycin), placement of PEG/PEJ tubes

Inflammatory Diarrhea

Chornic Signs: *Pain*, *Blood*, weight loss, urgency, tenesmus, fever Examples: Celiac, IBS (Crohns or UC), microscopic colitis, NSAID enteritis Tests: Stool leukocytes (Fecal wbcs, lactoferrin or caprotectin), fecal occult blood test, serum tissue transglutaminase IgA or total IgA, upper endoscopy with biopsy of small intestines, colonoscopy

Malabsorption and Maldigestion

Chronic Due to loss of digestive enzymes, membrane transporters or mucosal epithelium Signs: Resolves with fasting, *Weight loss*, steatorrhea Examples: Pancreatic exocrine insufficiency, small intentional bacterial overgrowth, bariatric surgery, IBS, cystic fibrosis, PPI Risk factors: alcoholism, celiac disease, cystic fibrosis, chornic infections Tests: Duodenal biopsies and tissue transglutaminase IgA (rule out Crohn's and Celiac), quantitative fecal fat > 7g gat/d, breath testing, pancreatic calcifications

Secretory Diarrhea

Chronic Excessive secretion or poor absorption of electrolytes Signs: Watery, large volumes, NO blood, *Nocturnal* diarrhea, *continues with fasting*, recurrent dehydration Causes: Toxins, inflammation, meds, *neuroendocrine tumors*, bile acids, villous adenoma Dx: id past medical hx, id physcial findings, Text: Fecal Na and K < 50 and *NO* osmotic gap

Osmotic Diarrhea

Chronic Substance in intestine lumen that draws out and holds H2O Signs: Watery, NO blood, Resolves with fasting, bloating, NO weight loss Causes: magnesium, Carbohydrate malabsorption (lactose intolerant, fructose overload, lactulose or sorbitol - cant absorb period, other disease that cause malabsorption of carbs - bacytieral overgrowth, celiac disease, crohn's disease, etc.) Test: Calculate stool osmotic gap: 290 - 2(Na+K)... >125 = osmotic diarrhea. Low Stool pH in carb malabsorption

Mechanism of FGID

Combination of Gut, CNS, hypothalamic pituitary adrenal axis, sympathetic and parasympathetic NS, enteric NS, and vagus nerve Altered brain gut communication can cause distrubed gut function, sensation, and CNS function Some people think the gut microbiota has some role in causing FGID There are alot of mediators of gut function but *SEROTONIN* affects all three areas: Motility, visceral sensation, and secretion (95% of all serotonin is involved in GI tract - most of which is found in enterochromaffin cells where it plays a critical role in peristalsis What it all boils down to is dysmotility and altered sensation (either hypersensitivity or hyposensitivity) FGID also causes: Hypersensitivity from increased vigilance, to visceral stimuli, visceral hyperalgesia (stress causes increased CRF release which causes hypersensitivity in the colon), autonomic hyperacitivity (sweating, anxiety, fear dry mouth, lightheadedness), and healthcare-seaking behavior

Treatment of GI bleeding

DEPENDS ON SOURCE OF BLEED! Acid suppression (PPI); IV octreotide for acute variceal bleeding endoscopic hemostasis: placement of hemoclips, cauterixation, treatment of superficial mucosal lesions with laser or argon plasma coagulator, injection of epinephrine, ligation or gluining of varicies IR: angiography with embolization of bleeding vessel, TIPS for refratory variceal bleeding Surgery: reserved for failure of nonsurgical Rx for ulcer bleeding, for example USE endoscopy for UGI bleed, but probably don't use colonoscopy for LGI bleed (bowel prep needed) - Resuscitation and stabilization should be priorities prior to either though. If pt is bleeding massively and can't be stabalized, forgo the endoscopy and consider alternatives

Dysphagia Odynophagia Pyrosis Regurgitation Acalasia Dyspepsia Gastroparesis

Difficulty swallowing pain with swallowing retrosternal burn effortless return of esophageal or gastric contents to the pharynx failure to relax the LES Disturbed digestion - blanket term Delayed gastric emptying

Functional GI Disorders (FGID)

Disorders of gut-brain interaction characterized by Rome criteria Can occur anywhere along GI tract from esophagus to anus (IBS is the major one) and can have symptoms outside GI Classified by GI symptoms related to any combination of the following: - Motility disturbance - Visceral hypersensitivity - Altered mucosal and immune fxn - Altered gut microbiota - altered CNS processing Hard to distinguish what symptoms are caused by what in patients with both IBS and IBD Chronic GI: Symptoms must be present for at least 6 months, present within the last 3 months, and occur on average at least once per day FGID can be broken down into 6 categories: - IBS - Functional constipation - Functional diarrhea - Functional abdominal bloating/distention - Opioid-induced constipation (OIC) - Unspecified FBD Found in western word caucasian young females with hx of anxiety, depression or abuse (sexual, physical, psychological)

DCIS

Ductal Carcinoma In-Situ Non-invasive breast cancer Non-obligate precursor to invasive cancer Gade: low, intermediate, high 14-53% progress to invasive cancer over 10 years *Atypical Ductal Hyperplasia* if less than 2mm of it - Benign lesion but causes 2-6 fold increase risk

Spontaneous Bacterial Peritonitis (SBP)

Dx: >250 PMNs/mm3 in ascitic fluid is presumptive evidence of SBP cultures are negative 50% of the time Treat with *Cefotaxime* 5-7 days and IV albumin on day 1 and 3 to help prevent renal dysfuction - Prophylactic Abx given to cirrhotic pts who present with GI bleed

Head and Neck cancers

Dysphagia from tumor and from therapy - often requires PEG (percutaneous Endoscopy Gastrostomy) for nutritional support - post therapy fibrosis adn decreased secretions Therapy: Radiation and surgery Providers: ENT, Rad onc, PEG from GI, Radiology, or surgery

Risk Factors for Breast Cacner

Early menarche + Later childbirth (length of this gap is important) Family history

Alternative meds

Fecal transplant Herbal therapies complementary therapies acupuncture Cognitive behavior therapy (control pain)

Zollinger-Ellison Syndrome

Gastrin-producing neuroendocrine tumor 90% located in the gastric triangle (around the head of the pancreas - duodenal intestine) elevated blood gastrin levels which stimulates gastric acid production increasing basal acid output which causes ulcers and diarrhea. Other causes of high gastrin levels are more common: PPI use, Atrophic gastritis, or renal failure

Occult GI Bleeding

Hidden or secret bleed - not visible to pt or physician manifested by Fe deficiency or positive fecal occult blood tests - typical of early colon cancers

DDx of hyperbilirubinemia w/o cholestasis

Hyperbilirubinemia of sepsis - direct bilirubin, minimal elevation in alk phos, ALT, AST Gilbert's syndrome - unconjugated (indirect) hyperbilirubinemia Hemolysis - same as gilbert's but with signs of hemolysis on peripheral smear, increased LDH, decreased haptoglobin

Functional Diarrhea

IBS - distrubed intestinal and colonic motor and sensroy respose Signs: Alternating constipation and diarrhea, and pain which is relieved by defication Red flags: nocturnal, volume depletion, malnutrition, blood in stool, acute onset, >40 yo, male

Achalasia

Lack of relaxation of LES during swallowing Degeneration of myenteric (Auerbach) plexus Middle aged males and females Dysphagia for SOLIDS and LIQUIDS Slowly progressive etiology - mostly idiopathic or p[seudoalchalasia due to malignant tumor, paraneoplastic, chagas disease Increase risk to develope esophageal cancer (SCC) can cause pulmonary problems due to chronic aspiration Dx: Barium study to see dilate esophagus, impaired emptying, and distal tapering, or use manometry or EGD Treatment: Ballon dilation, surgical myotomy, or endoscopic injection of botulinum toxin

Odynophagia

Less common than dysphagia. 2 main causes: - Infectious esophagitis (herpes, CMV, etc) - usually immunocompromised - Pill esophagitis - doxycycline, tetracycline, alendronate, asa, nsaids, potassium chloride, direct caustic effect, stand and drink water while taking pill

Causes of Massive lower GI Bleed

Less common: IBD, Colon cancer, hemorrhoids More common: Ischemia, AVMs, Diverticular bleeds

Risk Reduction for breast cancer

Lifestyle: wight loss, exercise, alcohol, breast feed Medical: Risk reducing meds (40% reduction) Surgical: Prophylactic mastectomies (95% reduction)

LCIS

Lobular Carcinoma In-Situ 1-2% develope invasive cancer per year (lifetime risk 30-40%) Often multifocal Pleomorphic LCIS is considered different (more aggressive) *Atypical Lobular Hyperplasia* - if you have less than 2 mm of it. Benign lesion but increase risk 2-6 fold

Patterns of Spread for Testicular Tumor

Local: -Uncommon to have extension to scrotal wall or up the spermatic cord. Tunica albuginea as a barrier to local growth - Iatrogenic (induced by physician) scrotal violation may result in inguinal mets (thus the incision for a radical orchiectomy is inguinal) Regional: - predictable lymphatic spread to the *retroperitoneal* LN - Right testis - landing zone is interaortocaval area - Left testis - landing zone is para-aortic area - Right to left cross-over mets are common, but left to right are not Metastatic: - Choriocarcinoma: unusual as more hematogenous rather than lymph and thus can have early mets, especially to lung - Advanced disease: Can have visceral mets to the lung, liver, brain, bone, and lupraclavicular nodes - Half of NSGCT present with mets

IBS - D Meds

Loperamide - improved stool consistency, pain, urgency, and subjective overall response, in other studies increased nightly pain Bile Acids Probiotics Rifaximin - nonabsorbable antibiotic, for the treatment of IBS-D (550 mg 3 times daily in patients with nonconstipated IBS resulted in significantly more patients reporting adequate relief of global IBS symptoms and bloating) Eluxadoline - m-receptor agonist/dopioid receptor antagonist that has been developed as a treatment for patients with IBS-D

Treatment of NSGCT

Low Stage - Stage 1: RPLND vs Chemo vs surveillance - 75% of stage 1 are cured by orchiectomy alone - T2 (invades tunica vaginalis), presence of lymphovascular invasion, and >40% embryonal component are predictive of microscopic mets *NEVER USE RADIATION* - Patients with persistently elevated tumor markers after orcheitomy should be treated with hemo as that is a marker of distant disease - compliance is critical for pts on surveillance plan High Stage: - Chemo -Post-chemo residual masses treated with RPLND: 40% fibrosis, 40% teratoma, 20% viable tumor - Teratoma = non-responsive to chemo - Salvage chemo for pts that do not normalize markers after chemo - 70% of pts with high grade are cured

Epidemiology of Bladder Cancer and Risk Factors

Male:Female = 4:1 Median age 72yo Low death rate leads to a lot of pts on surveillance - high cost per cancer patinet - lifetime cost per patient = $180,000 (a lot of CTs needed) Risk Factors: - Smoking, incrases hazard ratio by 3 or 4, especially if >40 pack years. Quitting reduces risk, but never down to the non-smoker level - Enviornmental/Occupational: truck drivers, hair-dressers, dry cleaners, dental technicians, plumbers - Pelvic radiation - Cyclophosphamide: 4-9 fold increased risk - Chronic cystitis: indwelling catheters - Schistosomiasis exposure (parasite that causes swimmers itch , katayama fever, or a chronic version in the GI or G *No common familial syndromes*

Hepatic Encephalopathy

May be precipitated by bleeding, infection, dehydration, electrolyte abnormalities, narcotics or benzodizepines Clinical diagnosis, usually based on presence of signs of advanced liver disease, asterixis and hyperreflexia Elevated blood ammonia levels not required to make Dx Treatment: Id and correct precipitating cause, lactulose orally or per enema, Rifaximin, NO role for protein restriction

Choriocarcinoma

May hemorrhage paradoxically, may present with small testicular mass and distant mets Exception to normal stepwise spread to LN - pure chorio -> mets chorio by hematogenous spread, not lymphatic

Evaluation of surgical risk

Medical comorbidity and performance status are important This is why pts must be cleared before surgery and optimized - comorbidities looked at and consulted with proper physicians AHA has guidelines but also use *INDICATIONS CONFERENCE*

Who gets cancer?

Modifiable risks: *Tobacco* use and *obesity* are the 2 biggest risk factors! Non-Modifiable: Genetics

Surveillance and Recurrence

Monitor for: - Local recurrence - Distant disease - Complications of treatment NED = no evidence of disease (use this instead of "cured") Recurrence and decisions about *Salvage* therapy

Teratoma

More than 1 germ cell layer - Cartilage, bone, intestinal, pancreatic, liver, muscle, neural, connective tissue Teratoma is *not* chemosensitve - Retroperitoneal teratoma is poor prognosis

Symptoms of Testicular Cancer

Most common is painless enlargement of testis - 98-99% are unilateral - Acute pain/swelling seen in 10% only (due to intratesticular hemorrhage) Typical delay in presentation is 3-6 month. may be mis diagnosed initially (frequently as epididymitis) 10% are detected on routine physical exam (importance of self exam) Metastatic symptoms in 10% (abdominal pain, back pain, cough, hemoptysis, dyspnea, anorexia, nausea/vomiting, bone pain, neck mass, neurologic, lower extremity edema, gynecomastia) *Part of your physical exam for a young man for almost anything should be a scrotal exam* Mass will be ROCK HARD Hydrocele may be present and can make dx harder

Epidemiology of Testicular Cancer and Risk Factors

Most common solid tumor in men 20-34 2-3 new cases / 100,000 men annually in US 90=95% are from *Germ Cell Tumors* - Seminoma - Nonseminoma (NSGCT) = Teratoma, embryonal, choriocarcinoma, or yolk sac - "S TECY" Remainder are from supporting cells - Leydig cells - Sertoli cells - Gonadoblastoma Risk factors: - Cryptorchidism (undescended testis) = 3-14x the risk. Pre-pubertal orchiopexy (placing the testy in scrotum) decreases the risk

Yolk Sac

Most common testis tumor of *Children*

MELD score

Used to prioritize pts for liver transplant Considers INR, Creatinine, and Bilirubin

Esophageal dysphagia

Onset after several seconds location: suprasternal notch or substernally (location of sticking does not predict lvl of the lesion) Symptoms: worse with solid foods -> mechanical obstruction; same w/ solids or liquids -> motility disorder Causes: Esophagitis (peptic, infectious, radiation, corrosive, eosinophilic esophagitis), mechanical obstruction (cancer, stricture (peptic, radiation, corrosive ingestion), webs, rings, foreign body) motility (achalasia, scleroderma) Dx: upper endoscopy, barium radiography, esophageal manometry

Indications for Endoscopy

Other tests inconclusive Evaluate for inflammatory or infectious causes If considering celiac disease If > 50 yo or FH of CRC

Obscure GI Bleeding

Overt or occult bleeding that persists or recurs after initial negative endoscopic/colonoscopic evaluation usual approach is to confirm negative endoscopies, then focus on potential small bowel source - video capsule endoscopy, deep enteroscopy, angiography, CT enterography vs empiric Fe replacement

Approach to chronic diarrhea patient

PMH: meds, diabetes, radiation, pancreatitc, scleroderma FH: celiac, IBD, autoimmune Exam: Volume depletion, cachexia, edema, rash, thyroid mass, lymphadenopathy, fistula, abdominal tenderness, anal function Tests: WBC, PLT, ESR, CR, Hgb, Albumin, Electrolytes, Eosinophilia, tTG IgA, total IgA, TSH, FT4, Chromagranin A (neuroendocrine tumor) Stool testing: Giardia, crypto antigen, ova, parasite, c diff, hemoccult, calprotecting, quantative fecal fat, ph, ion gap,

IBS - C Meds

Polyethylene gylcerol improved freq, consistency, and straining, but not bloating or pain Lubiprostone- a luminally acting prostone that selectively activates type 2 chloride channels Linaclotide - a 14-amino acid peptide that acts as a guanylate cyclase C agonist. Improves abdominal symptoms and bowel symptoms

Esophageal Cancer

Progressive dysphagia, vomiting, fatigue, anemia, weight loss initial test often endoscopy with biopsies staging with CT/PET, EUS (need all 3) If curative intent: rarely only endoscopic therapy (very early stage), Surgery (esophagectomy with gastric pull-up) w or w/o chemo and radiation, neogastric tube for nutritional support if need be If metastatic spread, then palliative therapy only: esophageal stent, tumor debulking, PEG tube, chemo and radiation to shrink tumor Esophageal stent: improves dysphagia (not perfect, so still some limitations of intake). Complications: pain, GERD, Disloaction if tumor shrinks, perforation, bleeding, airway compromise - better for middle and lower tumors!

Colorectal Screening

Purpose to ID cancer at earlier stage when it asymptomatic and then remove percancerous polyps Non-invasive: fecal occult blood testing (FOBT) and stool DNA (sDNA) Invasive: Flexible sigmoidoscopy, colonoscopy, barium enema (DCBE), Ct colonography Only endosopies have ability to remove precancerous polyps WHEN TO SCREEN? -Starting at age 50 (for average risk) - Age 40 or 10 yrs younger than first degree relative w/ CRC - 8 years aver dx with ulerative colitis - if UC and Primary sclerosing cholangitis (PSC) then start when dx made\ - FAP (familial adenomatous polyposis) start at age 10 - 100% chance of cancer so prophylactic colectomy - HNPCC (Lynch syndrome) start at age 20 or 10yrs younger than relative dx

Treatment of Testicular cancer

Radical inguinal orchiectomy +/- testicular prosthesis (NEVER PERFORM A TESTICULAR MASS BIOPSY) After orchietomy: - Surveillance - Chemo - Radiation - Surgery (RPLND) Mortality = <5%

RPLND

Retroperitoneal LN Dissection Diagnostic and therapeutic Morbidity 5-25% - Pneumonitis, chylous ascites, ileus, lymphocele, ejaculation issues, infertility Modified RPLND When suspicious LN found, complete bilateral RPLND

IBS

Rome IV diagnostic criteria Symptoms: recurrent abdominal pain on average of 1 day per week for last 3 months with 2 of the following: related to dedication, associated with change of stool frequency, associated with change in stool form (1-2 or 6-7 or both are abnormal) Chronicity: Chriteria fulfilled for the last 3 months with symptoms onset at least 6 months prior to dx IBS - D accompanied by diarrhea (6-7 <25% of time) IBS - C accompanied by constipation (1-2 <25% of time) IBS - M includes both diarrhea and constipation IBS - Unclassified are pts who have IBS but don't fall into one of the 3 categories More prevalent than asthma or htn in US IBS has a high societal burden with a high cost of healthcare utilization, unnecessary interventions, and missed days of work ($10 billion direct, $20 billion indirect cost) Patient burden is huge and causes loss of work and social isolation (worse quality of life than DM or GERD) DX: history is important. Full GI ROS, identify severity.effects and chronicity of complaints, identify psychosocial stressors. Red flags: weight loss, hematochezia, melena, nocturnal symptomos, family hx of IBD or colorectal cancer, age of onset > 50, malnutrition, skin rashes, inflammatory arthropathy, abdominal mass. Diagnostic testing should be limited unless alarm symptoms or for an evalutation for culprit organic disease. There are alot of things that mimic FGID/IBS Pts will have hyperanelgesia around their GI Treatment: Biopsychosocial model Goals: Global relief of symptoms including impact on pts overall well-being and individual symptom relief including abdominal pain, bloating, and altered bowel habits. Patient education and establishing a relationship with the physician is important. Treatment should be based on symptoms but *FIBER* is a cornerstone in management - certain forms of fiber can exacerbate the condition so stick with soluble psyllium/ispaghula husk and not insoluble bran fiber. *Diet restrictions can help* - gluten restrictions can help even if pt doesnt habve celiac disease, FODMAP (foods that produce gas) restrictions helps

Meckel's Diverticulum

SMALL BOWEL BLEED Most common anomaly of GI tract (occurs in 2% but asymptomatic in most) - located in distal ileum Results from failure of the omphalomesenteric duct to undergo involution during development True diverticulum containing heterotopic mucosa, most commonly gastric mucosa Bleeding occurs due to ulceration w/in the diverticulum or from adjaccent mucosa due to ectopic acid production - most common in kids Can also cause obstruction (intussusception, volvulus) or diverticulitis DX: will see a concentration of gastric mucosa in LRQ on special contrast CT Treatment by resection

Prognosis of cancer

STAGING! TNM vs Local/Regional/Metastatic Use imaging to stage Helps determine if tumor is resectable vs boarderline-resectable vs unresectable Helps decide if treatment is curative or palliative

Fe deficiency in adults

Should be assumed due to occult blood loss until proven otherwise should always be evaluated, not simply rx'd with supplemental Fe Lab features: Decreased saturation of transferrin with Fe (represents decrease in Fe and compensatory increase in transferrin lvls), decreased ferritin, w/ or w/o microcytic anemia

Staging of Testicular Cancer

Stage I: Testis Stage II: Retroperitoneal LN Stage III: mets/visceral disease

Treatment of Seminoma

Stage related Treat with radiation and save chemo for Salvage therapy Stage I = 95% cure rate Stage IIA = 92-94% 5-yr survival RPLND is not used for Seminoma as tumor is very sticky; there is a role of surgery for post-chemo RPLND but very technically challenging and typically mass removal rather than full template RPLND Radiation for stage 1: - Ipsilateral pelvis and para-aortic regions - 26 gy used - toxicities include infertility despite shielding or PUD or mild pancreatitis - Therapy induced second malignancies have not been reported with <40 gy High stage (>IIA): - Cisplatin- based chemo (*B*leomycin, *E*toposide, Cis*p*latin = BEP) - worry about fibrosis with Bleo - 90% have complete response and 90% of residual masses are fibrosis - surgical excision for prost-chemotherapy residual masses is difficult and rarely needed

Organic disease vs Functional disorder

Structural change to tissue or organ - peptic ulcer disease, celiac disease, pancreatitis vs Conditions in which the pt has a variable combination of symptoms w/o any readily identifiable structural or biochemical abnormality

Colorectal Cancer

Symptoms: Blood in stool, change in bowel pattern, abd pain, frequently asymptomatic until more advanced Evaluation: Colonoscopy with biopsies, universal testing for HNPCC (DNA MMR IHC vs MSI), CT CEA; Also EUS or MRI if rectal cancer Management: Curative intent (can include some stage IV pts) - surgery +/- chemo (and xrt if rectal) - palliative (chemo and xrt if rectal, diverting ostomy vs stent if obstructing, pain management for late ds (if use narcotics don't forget bowel regimen to prevent constipation/obstruction) Surveillance: CT, CEA, Colonoscopy Genetic evaluation? Family counseling for increased risk and more aggressive screening

Eosinophilic Esophagitis

Symptoms: Dysphagia, food impaction, associated with allergic rhinitis, asthma, and food allergies Endoscopy: Trachealization, furrows, strictures, diffuse narrowing, eosinophilic abscesses Histology: Abundant eosinophils (overlaps with GERD) Treatment: PPI< topical steroids, elimination diet

Pancreatic Cancer

Symptoms: Jaundice (obstructive), malabsorption, pruritis, abdominal pain Evaluation: Tissue acquistion (EUS, ERCP with brushing, CT guided bx, metastatic bx), staging with CT, EUS, CA 19-9 Treatment: If curative intent - surgery +/- chemo, if palliative, biliary stent celiac plexus ablation, pain management (can be challenging) Surveillance: CT

Angiography

Useful to both ID and treat (embolize) sites of bleeding Procedure of choice in hemodynamically unstable ptss ID of bleeding site requires acctive bleeding of at least .5-1 ml/min Does not require bowel prep Risk: contrast allergies, contrast-induced AKI, bleeding from puncture site, bowel ischemia

Peptic Ulcer Disease (PUD)

Symptoms: Stomach pain REDUCED by food or antiacids (burning, gnawing, hunger pain, worse at night or in between meals, relief more common with duodenal ulcer, acute severe pain -> perforation), nausea/vomiting, hematemesis/melena (bleeding ulcer), commonly asymptomatic until catastrophic (NSAID induced, or in the elderly) Causes: NSAIDS, Heliobacter pylori, hypersecretory states (Zollinger-Ellison syndrome), or severe physiological stress (cushing') H Pylori - motile gram neg spiral shaped bacteria - fecal oral or contaminated water supplies - most infections are asymptomatic - lives in gastric mucus layer (non-invasive) and disrupts this layer making host susceptible to damage - makes urease to buffer acid - some strains express CagA which allows bacteria to cause more tissue inflammation - 90% of PUD patients are infected - combining HP plus NSAIDS = 60 fold increase in PUD - eradication of HP reduces ulcer risk 90% - Can cause gastric adenocarcinoma or MALT lymphoma (about 80% regress w/ HP eradication) - dx by urease breath test, stool Ag, serology (IgG to HP - still positive years after eradication), or gastric biopsy - all tests except serology can be falsely positive w/ recetn or ongoing abx and/or PPI use - Treatment: Abx resistance is common so tripple therapy (PPI + 2 abx for 2 weeks - clathromycin plus ampicillin or metronidazole) then confirm with breath test or stool Ag NSAIDS - 25% of chronic NSAID users develop ulcers - 4% of 2 week users - risk factors: age, smoking, hx of pud, HP, high dose - directly damages epithelial cells with is the basis for the enteric coating, inhibits Cox-1 which prevents local production of prostaglandins (pgs are protective factors for intestinal mucosa), risk lower if only using a Cox-2 inhibitor, taking a PPI or misoprostol (pg E1 analog) can be protetive

Embryonal

Tendency to invade tunica and cord structures ITn 40-60% of NSGCT >40% embryonal is a risk factor for nodal disease

Physical findings in chronic liver disease/cirrhosis

Terry's (white) nails Dupuytren's contracture palmar erythema spider angiomata gynecomastia Decompenstaion leads to ascites, variceal bleeding, hepatic encephalopathy

DDx of Testicular Swelling

Testicular torsion Epididymitis/epididymal-orchitis Hydrocele spermatocele hematocele varicocele Typically get a US for pt with scrotal swelling to verify no non-palpable mass Consider testicular cancer as the cause of abdominal pain in a young man

Iberogast

The herbal combination preparation STW 5 (Iberogast®, Steigerwald Arzneimittelwerk GmbH, Darmstadt, Germany) has been comprehensively studied for the treatment of functional gastrointestinal disorders of the upper and lower abdomen. STW 5 contains alcoholic extracts of Iberis amara totalis recens, Angelicae radix, Cardui mariae fructus, Chelidonii herba, Liquiritiae radix, Matricariae flos, Melissae folium, Carvi fructus and Menthae piperitae folium and has been used for the therapy of functional gastrointestinal disorders for five decades.

Surgical prinicples

Think fast, move slow, use both hands, and avoid wasted motion Negative margins and resect lymphnodes when needed leads to lower recurence

Treatment of Chronic Diarrhea

Treat undelying condition Bulk stool with fiber (psyllium, Calcium polycarbophil) Decrease peristalsis/motility (opiates - codeine, diphenoxylate, loperamide) Decrease secretion (octreotide) Bind bile salts (Cholestyramine)

Treatment of cancer Neoadjuvant Adjuvant Salavage

Treatment is a *Sequence* Radiation and surgery are local therapies Chemo is systemic therapy Use NCCN (National Comprehensive Ccancer Network) guidelines to make decisions or a *Multidisciplinary tumor board* Neoadjuvant = Before Adjuvant = After (base on pathology) Salvage = Later (delayed based on recurrence) There is a role for clinical trials and CER (comparative effectiveness research )

Seminoma

Typical = 85% of cases - Radiation sensitive - Syncytiotrophoblasts in 10-15% (produce Beta hCG) - PURE seminomas never make Alpha Fetoprotien (fetal form of albumin) - Occasionally can have met of NSGCT (<10%) Anaplastic (5-10% - Greater met potential (25-29%) - Present in 30% who die of seminoma Spermatocytic (2-12% - Older pts (>50yo) - Favorable prognosis *makes HCG only. If you see AFP, treat as non-seminoma testicular cancer*

Aortoenteric Fistula

UPPER GI BLEED Secondary AEF follows aortic aneurysm repair is most common as apposed to primary AEF - perigraft infection causes fistula (can occur at any time after repair) CT: ectopic gas, focal bowel wall thickening, breach of the aortic wall, extravasation of contrast into bowel lumen "Herald Bleed" - self-limiting bleed that presages exsanguinating hemorrhage if the AEF is not fixed in a timely fassion

Hematemesis Coffee ground emesis Melena Hematochezia

Vomit containing obvious blood (profuse bleed) Vomit containing dark, altered blood (slow bleed) Black tarry sticky stool (slow bleed or UGI) Stools containing obvious blood (profuse bleed or LGI)

DDx of "mild" hepatocellular Injury pattern

chronic viral hepatitis NAFLD Autoimmune hepatitis Drug-induced liver injury congestive hepatopathy Wilson's disease Alpha 1 antitrypsin deficiency

IBgard

delivers microspheres of ultra-purified peppermint oil quickly and reliably where they are needed most, in the small intestine. 40% reduction in IBS symptoms

Oropharyngeal dysphagia

location of symptoms above suprasternal notch Immediate onset of symptoms manifestation: difficulty initiating swallowing, cough, choking, drooling, nasal regurgitation - often worse with liquids Causes: poor dentition, reduced saliva (Sjorgren's, anticholinergics, antihistamines), neuromuscular disorders (myasthenia gravis, neuropathies, stroke parkinsons, botulism), structural lesions (tumor, zenker diverticulum) Dx: Videofluoroscopy, varium radiography, nasopharyngeal laryngoscopy

DDX of cholestatic injury pattern

primary biliary cholangitis primary sclerosisng cholangitis DILI biliary obstruction infiltrative process (TB, amylodosis, lymphoma, diffuse metastatic dz)

Diverticulitis

protrusion of mucosa and submucosa through weak spots in circular muscle (where vasa recta penetrate to inner layers) - if causes vessel erosion, then you get bleeding into the gut lumen