First Pass Miss Flashcards

Question

What lab tests are helpful in determining the etiology of the ascites fluid?

Answer 1

1. Protein content 2. WBC's and type - monocytes elevated in TB, PMNs in bacterial peritonitis 3. Malignant cells - diagnostic of cancer 4. Amylase - elevated in pancreatitis - > pancreatitis is a cause of ascites because malnutrition leads to decreased protein and hence oncotic pressure 5. Gram stain and culture - diagnostic of infection

Answer 2

Protein content: High in chronic infection and tumor (exudate) Low in portal hypertension - transudate If serum minus ascities albumin is greater than 1.1 g/dL -> portal HTN is very likely

Answer 3

1. Spontaneous bacterial peritonitis 2. Umbilical hernia with rupture -> Flood syndrome! 3. Can lead to pleural effusions and generally diaphragm harder to move -> breathing difficulties 4. Drug dilution due to increased volume of distribution

Answer 4

Type 1 - rapid development of kidney failure in less than two weeks, worst prognosis Type 2 - Slower onset -> diuretic resistant or unresponsive ascites Patients will have oliguria but no ultrasound or urine sediment signs of ATN Must rule out pre-renal azotemia by trying volume expansion with saline to see if kidney function improves

Answer 5

``` Peritoneal infections, i.e. TB Cancer - primary or metastatic to peritoneum Nephrotic syndrome Pancreatitis CHF, constrictive pericarditis ```

Answer 6

Swollen and necrotic hepatocytes with a NEUTROPHILIC inflammatory infiltrate. Mallory-Denk bodies -> alcoholic hyaline - eosinophilic cytoplasmic inclusions which are inclusions of damage keratin filaments Can be some centrilobular fibrosis

Answer 7

Mild to moderate increase in serum transaminases, especially AST > ALT. "Make a toAST with alcohol" Elevated bilirubin, alkphos, **GGT** with cholestasis, and mild leukocytosis due to neutrophils

Answer 8

Bronze diabetes Liver - micronodular cirrhosis and HCC Pancreas - diabetes mellitus Myocardium - restrictive -> dilated cardiomyopathy Joint synovial tissue - arthropathy Pituitary - hypogonadism Skin - increased melanin in epidermis, increased hemosiderin in dermis

Answer 9

Defective transport of copper in liver -> decreased incorporation of copper into ceruloplasmin -> decreased excretion of excess copper into bile -> toxic copper accumulation

Answer 10

Liver - fat and glycogen accumulation -> hepatitis -> cirrhosis CNS - neuronal injury -> neurologic and psychiatric manifestations. Basal ganglia involvement: Temors, rigidity, dysarthria Elsewhere: depression, anxiety, psychosis

Answer 11

Probably an autoimmune disease characterized by progressive T-cell mediated destruction of small to medium sized intrahepatic ducts As it is autoimmune, it is classically seen in middle-aged women with other autoimmune disorders (i.e. Sjogren's, RA, Hashimoto) Pathognomonic is florid duct lesion: giant cell neck to ducts -> starts as granulomatous inflammation in portal tract and worsens to biliary cirrhosis

Answer 12

Cholestatic lab profile (increased alk phos, GGT, cholesterol, conjugated bilirubin) Increased IgM levels -> antimitochondrial antibodies and lipoprotein X (type of LDL only seen in bile diseases)

Answer 13

Ursodeoxycholic acid -> protects against bad bile acids, and symptomatic treatment of complications (i.e. vitamin D, cholestyramine, portal HTN treatments like octeotide)

Answer 14

Progressive destruction of large intrahepatic and extrahepatic bile ducts Found mostly in middle-aged men, strongly associated with ulcerative colitis, p-ANCA+ Complications: Gallbladder cancer, cholangiocarcinoma, biliary cirrhosis

Answer 15

Think sclerosing + targetting bile ducts Alternating areas of stricture (concentric, "onion-skin" fibrosis around ducts) and dilatation "beads". Basically strictures of fibrosis that look like hyperplastic arteriolosclerosis of ducts, and dilations that are like "beads" - seen on barium study via ERCP

Answer 16

Acute hepatitis - phenytoin Chronic hepatitis - alpha-methyldopa, nitrofurantoin Cholestasis - estrogens Cholestasis/hepatitis - amox/clav, chlorpromazine Macrovesicular fatty liver - corticosteroids Microvesicular fatty liver - tetracycline overdose Dose-related cirrhosis - methotrexate, need multiple liver biopsies Granulomatous - allopurinol

Answer 17

Hepatic veno-occlusive disease | -> a cause of intrahepatic portal HTN

Answer 18

Phase I - toxic Phase II - safe N-acetylcysteine works to replenish intracellular glutathione stores involved in dealing with toxic NAPQI accumultation. These are also depleted in alcoholism and malnutrition

Answer 19

Unpredictable, idiosyncratic -> occurs rarely for any drug, includes herbals - > long latent period (sensitization?) for several weeks before reaction - > rechallenge with same drug will lead to rapid reaction - > associated with fever, rash, eosinophilia (suggesting hypersensitivity) -> drug acts as a hapten for immunologic response, or produces toxic metabolites

Answer 20

Acute hepatitis with delayed onset May cause DRESS syndrome though: Drug Reaction with Eosinophilia and Systemic Symptoms -> fever, rash, eosinophilia, lymphadenopathy -> mechanism unclear

Answer 21

Generally causes hepatitis in children, or immunosuppressed adults. Anicteric hepatitis with no chronic phase propensity, may be lethal in immunosuppressed

Answer 22

HSV -> seen by inclusion bodies on light microscope Treatment is acyclovir or vidarabine

Answer 23

No -> chronic carrier state can be though. Drugs: Think NRTI wielding mace and lamb (lamivudine), as well as IFN-alpha antenna Most commonly used are entecavir and tenofovir, suppressing virus

Answer 24

Fecal-oral, especially from contaminated water RNA hepevirus Unique - only human hepatitis virus with an animal reservoir (swine)

Answer 25

Men who have sex with men (trauma during sex), people born in areas with high rates of chronic HBV (especially Asia), and those with multiple sex partners

Answer 26

Bile duct hamartoma - caused by persistence of embryonic bile duct structures -> presence of multiple with intervening connective tissue may look like metastatic adenocarcinoma, need to differentiate based on lack of cellular atypia

Answer 27

Occurs in young adults, especially with oral contraceptives in women, or anabolic steroids in men Usually found as an incidental finding -> looks like an oncocytoma of kidney, with a central scar and radiating bands of fibrous tissue

Answer 28

Central scar, with abnormally large arterial branches accompanied by bile ductular proliferation (which don't drain anything) and chronic inflammation, with no well defined portal triads Hyperplasia grows between radial spokes of fibrosis There are no clinical sequellae -> just need to differentiate between important masses Proliferations occur due to alterations in blood flow leading to increased oxygenation by hepatic artery and thus release of growth factors causing reactive hyperplasia

Answer 29

Gross - diffuse, pale, fine nodularity of the liver Microscopic - Regenerative nodules WITHOUT fibrosis (check trichrome stain), often with obliterated portal vein branches Lack of fibrosis will help differentiate from cirrhosis Arise in individuals with a predisposition for decreased blood flow to liver: i.e. hematologic / neoplastic disorders. Possible consequence: may develop portal HTN

Answer 30

Frequently subcapsular - most common benign liver tumor Large, thin-walled, blood-filled spaces lined by normal-appearing endothelial cells, separated by scarce fibrous connective tissue

Answer 31

Hepatocellular adenoma Present in young women on oral contraceptives. May cause an acute abdomen due to rupture and intraperitoneal hemorrhage Subcapsular, green, well-circumscribed, but more likely to bleed than cavernous hemangioma

Answer 32

Sheets and cords of relatively normal-looking hepatocytes, containing glycogen or triglycerides (functioning properly) but with NO portal tracts and scattered arteries and veins which are prone to hemorrhage.

Answer 33

Spread from colon, pancreas, lung (hepatic artery), breast (after lung) Early - elevated Alk Phos (indicates metastasis to liver) and LDH (nonspecific for cell death) Late - increased serum bilirubin and transaminases - due to necrosis of hepatocytes from ischemia and blockage of bile drainage = HEPATOMEGALY

Answer 34

1. Asymptomatic HBV carrier state 2. Cirrhosis (repeated cycles of necrosis and regeneration is progressively mutagenic) - most common in US 3. Exposure to aflatoxin - > stored grains and peanuts from Aspergillus flavus, induces p53 mutations

Answer 35

Portal vein -> portal hypertension Hepatic vein -> Budd-Chiari syndrome, can even extend to right atrium thru IVC

Answer 36

Sudden liver enlargement (hepatomegaly), pain, and ascites - due to acute hepatic venous occlusion Centrilobular congestion and necrosis can be seen

Answer 37

highly variable. May be trabeculated or pseudoacinar if more well differentiated. Can be told apart from benign by presence of prominent nucleoli, eosinophilic cytoplasm, and lack of simple hepatocellular cords (tend to grow in clusters / acini) Will cause elevated alpha-fetoprotein (fetal albumin)

Answer 38

Hepatocellular carcinoma, fibrolamellar variant Prognosis is good because it is well circumscribed and individuals often have no underlying liver disease (can resect just fine) - > well-differentiated tumor cells in abundant fibrous stroma and parallel lamellae of collagen - > appears grossly like oncocytoma

Answer 39

Carcinoma of the bile duct epithelium (intrahepatic or extrahepatic) Risk factors: often absent, but include primary sclerosing cholangitis, congenital biliary tract abnormalites leading to stasis, Thorotrast exposure, and Clonorchis sinesis (liver fluke) -> looks like regular desmoplastic adenocarcinoma, very poor prognosis if intrahepatic (detected late)

Answer 40

Grossly - Large, hemorrhagic, necrotic nodular mass Microscopically - small, round, blue-cell tumor with evidence of epithelial (embryonal to fetal hepatocellular) differentiation +/- mesenchymal differentiation (may even have random bone deposits) Expresses alpha-fetoprotein -Aggressive but treatable malignancy of children

Answer 41

Bacteria in the gut deconjugate it to urobilinogen. Urobilinogen can be excreted in stool after being made into stercobilin -> gives the stool its brown color. Some urobilinogen is reabsorbed -> can be excreted again in bile, or transported to kidneys where it is oxidized to urobilin -> gives the urine its yellow color.

Answer 42

Phrygian cap -> fundus (body, as opposed to neck and cystic duct) of the gallbladder folded inward

Answer 43

Cholesterolosis - aggregates of foamy macrophages within the subepithelium of gallbladder (looks a bit like Whipple's disease, but in gallbladder). Grossly -> little yellow deposits within the mucosa. Increased bile cholesterol increases cholesterol absorption by gallbladder mucosa -> accumulate in subepithelium

Answer 44

1. Chronic hemolysis -> increased biliary excretion of conjugated bilirubin, and a small percentage always becomes UNconjugated - > forms black stones which conjugate with Ca+2 and are radioopaque 2. Biliary tract infections -> microbial deconjugation of bile acids - >forms brown stones which are soft and soap and radiotranslucent 3. Gallbladder hypomotility -> thickens bile

Answer 45

Female Fat Fertile (pregnant) Forty + Native American -> cholesterol stones

Answer 46

1. *Acute cholecystitis 2. Hydrops of gallbladder due to chronic obstruction - gallbladder filled with mucin 3. Choledocholithiasis -Obstruction of the common bile duct 4. Chronic cholecystitis 5. Gallstone ileus 6. Carcinoma of the gallbladder

Answer 47

Calculous cholecystitis - obstruction of neck of gallbladder via a stone = retention of bile, gallbladder distention, and vascular compression in the wall (venous congestion, causing hemorrhagic infarct overtime) Acalculous happens in critically ill patients with hypoperfusion or hypomotility

Answer 48

Chronic cholelithiasis and bacterial contamination Chronic inflammation - lymphocytes, macrophages, plasma cells, and fibrosis Rokitansky-Aschoff sinuses - mucosal diverticula seen in gallbladder wall due to contraction against thick gallbladder wall -> Porcelain gallbladder is most well-recognized variant

Answer 49

A type of carcinoma of the extrahepatic bile ducts, which is located at the origin of the common hepatic duct (before it merges with cystic duct) Risk factors for all adenocarcinomas of extrahepatic bile ducts: Older males, biliary tract infections, PSC, choledochal cysts

Answer 50

Cephalic phase - Vagus nerve - acetylcholine Gastric phase - Duct cells are stimulated by -> secretin, produced by S cells in duodenum Intestinal phase - Acinar cells are stimulated by -> cholecystokinin, released by I cells, "I like fat"

Answer 51

Ventral bud - forms off of the hepatic diverticulum (off the biliary tree endoderm which will induce formation of liver) -> will form the caudal portion of the head of the pancreas as well as the uncinate process Dorsal bud - comes off of duodenum dorsally - forms the rostral portion of head of pancreas plus body and tail

Answer 52

I GET SMASHED Idiopathic, Ischemia **Gallstones **Ethanol Trauma - i.e. MVA in children, stabbings ``` Steroids Mumps infection Autoimmune disease Scorpion stings Hypercalcemia / hypertriglyceridemia (>1000 mg/dL) ERCP - to clear stone Drugs ```

Answer 53

Acute abdominal pain, often radiating to the back - > made better by leaning forward to take pancreas off retroperitoneum - >orthostatic changes due to volume depletion - > worsened by food Increased serum amylase or lipase (more specific marker)

Answer 54

DIC - circulating amylase and lipase damage endothelium ARDS - damage to pulmonary membranes Shock - bleeding and loss of edema fluid -> progress to renal failure Metabolic effects -> lactic acidosis, hyperglycemia, hypoalbuminemia, hypocalcemia Extrapancreatic fat necrosis - circulating lipases

Answer 55

ADPKD, von Hippel-Lindau | -> cysts are lined with epithelium (vs pseudocysts)

Answer 56

Ductal cells of pancreas (acinar is insanely rare) -> especially in head, where there are many ducts -> differentiated from chronic pancreatitis by loss of normal lobular architecture in adenocarcinoma

Answer 57

-> happens in black male diabetic smokers with chronic pancreatitis Microscopic - loss of normal lobular architecture with haphazard, irregularly glandular structure, desmoplasia, and **perineural invasion** -> can be painful

Answer 58

Migratory thrombophlebitis - redness and tenderness on palpation of extremities -> thrombosis of arms and legs due to hypercoagulability. The adenocarcinoma produces a procoagulant (probs mucin)

Answer 59

Mild = interstitial damage, with absence of organ failure or necrosis Moderately severe = local complications and may have transient organ failure for <48 hours Severe = necrotizing - persistent organ failure + local complications, high mortality, especially if infected

Answer 60

Mutation in trypsin making it resistant to lysis Autosomal dominant -> cumulative risk of pancreatic cancer is 40% (very high)

Answer 61

Early phase - within 1 week, systemic inflammatory response syndrome +/- organ failure Late phase - after 1 week, characterized by local complications

Answer 62

Grey Turner's sign - flank discoloration -> secondary to retroperitoneal hemorrhage Cullen's sign - periumbilical discoloration Paralytic ileus (absent ball sounds) Pleural effusions, ascites, jaundice

Answer 63

Present of at least 2/3 of the following: 1. Acute epigastric pain radiating to the back 2. Amylase and lipase levels elevated >3x ULN 3. Characteristic imaging findings

Answer 64

Cause is an infection, usually by E.coli, Klebsiella, or Enterococcus Treatment - broad spectrum antibiotics until aspiration biopsy tells you sensitivities. Surgical debridement after infection clears.

Answer 65

Treat if they are symptomatic -> can treat endoscopically (via ERCP or across stomach), percutaneously under CT guidance, or surgically These are local fluid collections which may cause severe pain, obstruction, bleeding, infection, leakage / rupture

Answer 66

Oral pancreatic enzyme replacement therapy (when 90% of function is lost) -> improves maldigestion of fat, and gives negative feedback for CCK release Analgesia, with denervation of the pancreas and Whipple procedure of needed.

Answer 67

1. New onset diabetes - in the absence of pancreatitis or past history, especially late in life 2. Depression - new onset depression with unclear reasoning, common in pancreatic cancer Courvoisier sign - palpable, non-tender gallbladder in presence of obstructive jaundice

Answer 68

Severe, constant RUQ pain which may radiate to the shoulder Positive Murphy's sign (inspiratory arrest on RUQ palpation)

Answer 69

Upper 1/3 - Superior vena cava via inferior thyroid veins LN: deep cervical nodes Middle 1/3 - azygous system LN: mediastinal Lower 1/3 - portal system via left gastric vein (coronary vein), which forms an anastamosis with the azygous system LN: celiac and gastric nodes

Answer 70

Transfer - Bolus propulsion into posterior pharynx and proximal esophagus, past the UES -> failure = transfer dysphagia = oropharyngeal dysphagia Transport - Peristalsis propels food through esophagus into stomach (includes LES)

Answer 71

Transport dysphagia Occurs because LES fails to fully relax after swallow - > esophageal contractions are often uncoordinated or absent as well, leading to absent persitalsis - > preferential loss of inhibitory neurotransmitters (NO/VIP) from Auerbach's plexus - > high LES pressure on esophageal manometry - > bird beak sign on X-ray

Answer 72

Achalasia caused by carcinomas of the proximal stomach -> may infiltrate Auerbach plexus by mass effect or cause ganglionic destruction by paraneoplastic secretion -> EGD is needed to make this diagnosis in the presence of achalasia

Answer 73

Disorder of esophageal motility where peristalsis is replaced by a series of repetitive, non-propulsive, high amplitude contractions (vs nutcracker esophagus where they are propulsive) Major difference from achalasia: Peristalsis and LES function are preserved. They are really opposite ends of the spectrum. - > causes dysphagia and chest pain - > precipitated by emotional stress or after drinking very hot or cold liquids Corkscrew appearance on esophageal manometry

Answer 74

Smooth muscle (distal 1/2) infiltration and atrophy from collagen deposition - > Decreased LES pressure (always open) - > minimal or aperistalsis (dysmotility) - > early: aperistalsis and GERD - > late: esophagitis and strictures

Answer 75

Depending on the cause. I.e. treatment of neuromyopathies like dermatomyositis or MG (immunosuppressants or anti-Ach-E) Treatment of UES dysfunction via myotomy (incision of sphincter muscle) or Botulinum toxin (botox) for cricopharyngeal achalasia Altering food consistency if post-stroke / postsurgical

Answer 76

Nitrates, calcium channel blockers, tricyclics r/o cardiac disease first before starting all these cardiac-active drugs

Answer 77

Mucosal herniation (pseudodiverticulum since not the whole wall) caused by high intraluminal pressures 1. Zenker diverticulum - most common 2. Epiphrenic diverticulum - > in association with achalasia or hiatal hernia

Answer 78

A mid-esophageal diverticulum caused by something pulling on the esophagus Commonly due to malignancy or TB with scarring

Answer 79

Webs - Idiopathic, partially circumferential membranous thickenings in upper esophagus, cause intermittent obstruction and dysphagia -> middle-aged women, in association with GVHD, GERD, and blistering skin diseases Rings - idiopathic, same as webs just slightly thicker and extend for the entire circumference

Answer 80

A ring - found proximal to GE junction, covered with squamous epithelium B ring / Schatzki ring - occurs AT GE junction, often superiorly covered with squamous epithelium and inferiorly covered with glandular epithelium. Happens in association with hiatal hernia

Answer 81

1. Mallory-Weiss syndrome - partial-thickness longitudinal mucosal lacerations at GE junction 2. Boerhaave syndrome - transmural, distal rupture due to violent wretching -> can cause mediastinitis and subcutaneous emphysema (due to air in mediastinum) and is a surgical emergency

Answer 82

Generally immunocompromised individuals 1. Candida - white pseudomembranes 2. HSV-1 - punched out ulcers 3. CMV - linear ulcers from base of esophagus wall thickness

Answer 83

Grossly - Mild hyperemia, can't tell much Microscopically - Intraepithelial eosinophils (first infiltrate seen in GI inflammation), later neutrophils, and bazal zone hyperplasia with elongation of lamina propria papillae Same risk factors as hiatal herna: increased intraabdominal pressure or decreased LES tone

Answer 84

Squamous cell carcinoma, arises usually mid-esophagus but can be anywhere RF: alcohol and tobacco smoking**, hot liquids and achalasia (irritation), caustic strictures with repeated injuries, Plummer-Vinson, etc

Answer 85

Pleomorphic adenoma - benign mixed tumor Arises from intercalated ductal reserve cells or myoepithelial cells Makes sense because the tumor is actually heterogenous Epitheloid component and mesenchymal / stromal component which can be very diverse

Answer 86

Papillary Cystadenoma Lymphomatosum Always arises in the parotid gland in male smokers

Answer 87

Adenoid cystic carcinoma Prognosis is poor because of common recurrence and VERY late metastases. 15 year survival is significantly worse than 5 year survival. anastomosing cords around cystic spaces containing homogenous, hyaline material -> looks like thyroidization with desmoplasia outside

Answer 88

Acute or chronic inflammation of the salivary gland Parotid glands - often viral infection like mumps or HIV Bacteria - i.e. Staph aureus, can cause or complicate it by filling it with pus Autoimmune disorders like Sjogren's syndrome may cause it

Answer 89

Spreads much easier from stomach than colon because the lamina propria of the stomach DOES contain lymphatic tissue -> can metastasize with this little invasion of mucosa

Answer 90

Stimulated by increased acid or loss of vagal stimulation Released by D cells of pancreas and stomach / duodenum, as well as hypothalamus -> widespread inhibitory action on release of hormones, including gastrin and histamine

Answer 91

1. Advanced age - decreased mucus production 2. NSAIDS - loss of PGE2, which is needed to maintain blood flow to mucosa, and maintain production of HCO3- / mucin 3. Uremia - acidosis will allow less bicarbonate to be excreted 4. Low O2 -> shock, high altitudes, severe burns

Answer 92

1. NSAIDs 2. Intracranial trauma - stimulation of vagal nerve increases gastric acid secretion - > Cushing ulcer 3. Major physiologic stress - shock, sepsis, burns (Curling ulcer) leads to decreased perfusion of mucosa (decrease nutrients) and systemic acidosis (Decrease bicarbonate excretion)

Answer 93

Grossly - Erythematous, rough-appearing gastric mucosa with active inflammation. Mucosal atrophy and intestinal G-cell metaplasia and hyperplasia is also present Microscopically - acute on chronic inflammation (neutrophils + chronic inflammatory infiltrate) + presence of spiral-shaped bacteria in superficial mucus

Answer 94

Loss of self-tolerance of CD4+ T cells to gastric parietal cells - > stimulation of autoantibodies to parietal cells or intrinsic factor - > chronic inflammation and destruction of gastric body and fundus by CD8 activation Inflammation found deep in mucosa rather than near surface (i.e. H. pylori gastritis)

Answer 95

Increased production of TGF-alpha leads to diffuse hyperplasia of mucous glandular epithelium in body and fundus, with atrophy of parietal and chief cells -> thick rugae -> protein-losing enteropathy and premalignant

Answer 96

Fundic Gland Polyp - associated with proton pump inhibitor use Inflammatory / hyperplastic are most common

Answer 97

Intestinal-type - Chronic atrophic gastritis of both types (causes intestinal metaplasia), dietary nitrosamines, gastric adenoma, smoking Diffuse-type - risk factors unknown (thus increasing in prevalence)

Answer 98

Signet-Ring Cell Adenocarcinoma Associated with loss of E-cadherin Microscopically - mucin-filled cells with peripheral nuclei, widespread over stomach. Infiltrating singly or in small nests (glandular differentiation with intracellular mucin) -> induces linitis plastica or "leather bottle" from invasion of stomach wall

Answer 99

Acanthosis nigricans - axillary browning Leser-Trelat sign - multiple keratoses appearing all over body

Answer 100

1. Sister Mary Joseph nodule - periumbilical nodular metastasis 2. Krukenberg tumor - bilateral metastases to ovaries, with abundant mucus secretion. Only signet-ring cell type.

Answer 101

EGD - allows direct visualization of the mucosa for ulcers / erosions as well as direct biopsy -> this also allows for direct testing of H. pylori Young patients with positive H. pylori serology and no "alarm" symptoms may be treated empirically Older patients with "alarm" symptoms need biopsy to rule out gastric cancer Alarm symptoms include: weight loss / anorexia, NV with coffee ground emesis, melena, anemia

Answer 102

Vagotomy - sometimes with antrectomy Subtotal gastrectomy - remove acid producing organ Usually done when complications of PUD are arising, but you should rule out gastrinoma first

Answer 103

Recurrent ulcers in duodenum / jejunum, with abdominal pain and diarrhea (from malabsorption because pancreatic enzymes don't work at low pH) -> failure to lower gastrin levels when IV secretin is given

Answer 104

High risk - indomethacin, ketoroLAC (mainly used as analgesic per sketchy), aspirin, piroxicam (think of the sox cam in sketchy) Low risk: Ibuprofen, diclofenac, naproxen, meloxicam (more COX-2 per sketchy, thus less side effects), especially celecoxib

Answer 105

1. Age > 60 years 2. Prevent healing - Concurrent use of corticosteroids / anticoagulants 3. Use of several or high dose NSAIDs

Answer 106

PPI + bismuth + tetracycline + metronidazole Must be used if patient has a penicillin allergy or there has been past macrolide use

Answer 107

Undergoes extensive crosslinking in ulcer base if the environment is acidic Concern - contains aluminum hydroxide -> special care for patients who may have aluminum overload, i.e. renal failure

Answer 108

PPI infusion, and octreotide Mechanism - octreotide reduces portal pressures by inhibiting glucagon-mediated splanchnic vasodilation Also need 72 hours of PPIs to prevent rebleeding in non-variceal GI bleeds

Answer 109

2 inches long, 2 feet from ileocecal valve, in 2% of the population, occurring in first 2 years of life, contains 2 types of epithelia (gastric / pancreatic) Most common congenital anomaly of the GI tract

Answer 110

``` Pertechnetate scan (Actively uptaken and secreted by mucosal epithelial cells of gastric tissue) -> remember this can cause bleeding ``` -> also intussusception, volvulus, obstruction

Answer 111

Villous atrophy / blunting with crypt hyperplasia for regeneration, and chronic inflammation surrounding Worst in proximal small intestine Hypersensitivity to gliadin associated with anti-endomysial Abs, anti-deamidated gliadin, and anti-tissue transglutaminase (IgA/IgG) associated with dermatitis herpetiformis T cell lymphoma and small intestinal adenocarcinoma

Answer 112

Numerous, distended foamy macrophages in lamina propria as well as mesenteric lymph nodes which stain PAS+. They can only be seen by EM since they are so small -> intracellular gram + systemic infection seen in older men -> Whipped cream CAN C: cardiac symptoms A: arthralgias N: neurologic symptoms

Answer 113

Secondary reperfusion injury -> due to oxygen-derived free radicals Splenic flexure is most vulnerable - watershed area between SMA / IMA

Answer 114

Ileum (remember this is the only common primary malignancy of small bowel, per pathoma), appendix, rectum Grossly - yellow-to-white mass with variable degree of wall inflammation and fibrosis which may lead to kinking Microscopic - Small round cells with salt and pepper chromatin and high vascularization Small bowel - may cause obstruction due to prominent desmoplasia, and can metastasize Appendix / rectal - Usually found incidentally, almost never metastasize if makes it to liver - carcinoid syndrome: wheezing, flushing, diarrhea, right-sided valvular heart disease, precipitated by emotional stress

Answer 115

B cell lymphomas MALT lymphoma - marginal zone (MAnTLe doesn't go with MALT) lymphoma associated with chronic gastritis due to H. pylori

Answer 116

Burkitt lymphoma - sporadic form seen here in the U.S. t(8;14) which happens independent of EBV Mediterranean lymphoma - aggressive B cell lymphoma in children / young adults which is cured with antibiotics

Answer 117

Gastrointestinal stromal tumor - tyrosine kinase mutations, specifically c-KIT -> treated well with imatinib - looks very similar to leiomyosarcoma (grows outward and will not cause symptoms unless obstructing lumen)

Answer 118

Rapid - Sudan stain to see qualitative amount of fat in stool 72-hour fecal fat collection - monitor fat intake for 72 hours and measure fat concentration in stool (collect in a coffee jar). if <94% of fat has been absorbed, that's abnormal

Answer 119

Give patient PABA linked to bentiramide -> if chymotrypsin is present, PABA will be reabsorbed. PABA will show up in urine if pancreas is functioning properly. Problem - test can also be positive if small bowel absorption is diminished (no PABA reabsorbed)

Answer 120

Give patient D-xylose, which is passively absorbed in small intestine. Normal test is about 25% of given xylose showing up in the urine. Causes for decreased blood or urine levels of xylose include: 1. Decreased small bowel absorptive capacity (i.e. Celiac's) 2. Bacterial overgrowth -> before it reaches the small bowel Passively reabsorbed so not affected by pancreatic insufficiency

Answer 121

Hydrogen breath test -Give lactose. A greater than 20 PPM rise over several hours in breath hydrogen is noted if you have lactose deficiency. This is because lactose hits your colonic bacteria who ferment it. baseline is given via lactulose which is always fermented if there is some question of the result

Answer 122

Small bowel CT enterography or X-ray Small bowel enteroscopy and biopsy (this must be done if past 1st section of small bowel, which is farthest an EGD can be advanced) Wireless capsule endoscopy (swallow a camera pill)

Answer 123

Fat malabsorption - due to deconjugation of bile salts Direct damage to mucosal epithelium Iron deficiency SCFA production and carbohydrate fermation in colon -> diarrhea, gas, cramping

Answer 124

Preganglionic nerve fiber hypertrophy can be seen which stains very intensely for acetylcholinesterase -> much easier than simply saying that ganglion cells are absent, because it could just be your sample or cut

Answer 125

atypical p-ANCA - more typical of ulcerative colitis -> smoking is protective anti-Saccharomyces cervisiae antibodies - more typical of Crohn disease -> smoking predisposes

Answer 126

Transmural fibrosis and chronic inflammation, sometimes with noncaseating granulomas which would be pathognomonic Inflammation will be patchy even on a microscopic level. Ulcers will progress from superficial to deep and narrow.

Answer 127

"string sign" due to thickening of smooth muscle and fibrotic strictures -> most common in terminal ileum

Answer 128

Active - superficial, broad-based ulcerations and hemorrhage with intervening inflammatory pseudopolyps Pseudopolyp - what remains of the mucosa level which as not ulcerated Loss of haustra on imaging - "lead pipe" appearance on barium enema

Answer 129

Toxic megacolon - knockout of submucosal plexus by inflammatory mediators leads to stasis and functional obstruction of bowel -> expansion of bowel with risk of perforation / rupture This is also called fulminant colitis

Answer 130

Outpouchings of the mucosa / submucosa of the colon through the muscularis propria at points where the vasa recta enter (false diverticula) Appear commonly in the sigmoid colon (where the water has been mostly reabsorbed so poop takes more force to propel)

Answer 131

Disruption of intestinal peristalsis (i.e. Hirschsprung) Risk factors: recent abdominal surgery, opiates, hypokalemia, sepsis

Answer 132

Formation of adhesions - abnormal fibrous bands between tissues, especially in Crohn's disease or following surgery

Answer 133

Erythema nodosum - red markings due to fat inflammation on extensor surfaces of skin, common on shins Pyoderma gangrenosum - ulcerating lesion with heaped up edges Eyes - Uveitis, iritis, episcleritis Peripheral arthritis - occurs only during exacerbations Central arthritis - sacroilitis / ankylosing spondylitis, not associated with IBD activity

Answer 134

1. Extent of colonic involvement 2. Duration of disease 3. Age at symptom onset 4. Primary sclerosing cholangiitis - associated, and an indepedent risk factor Colonoscopy with multiple biopsies every 2 years after 8-10 years with disease, with colectomy for at least low-grade dysplasia

Answer 135

Problem of disordered motility and/or nociception - > multifactorial, and often associated with altered microbiome following infectious enteritis. - > Psychosocial factors also play a role

Answer 136

Severe acute - Oral prednisone with 5-ASA + IV steroids if extremely severe Maintenance - immunomodulator therapy -Guidelines stay start immunomodulators for maintenance therapy of right-sided colitis

Answer 137

Cushing syndrome Adrenal insufficiency - negative feedback causes atrophy Hyperglycemia / diabetes - insulin resistance and increased gluconeogenesis Psychosis - insomnia first Cataracts Hypokalemia - via mineralocorticoid effects Osteoporosis with avascular necrosis of femoral head - broken chairleg Skin thinning / bruising with streaks from capillary atrophy

Answer 138

Typically used in acute episodes only, try to avoid maintenance treatment with it, although about 1/3 of patients are steroid-dependent Moderate disease -> oral budesonide which is not absorbed, stays in GI tract Severe disease - IV steroids i.e. methylprednisolone / hydrocortisone Steroids can also be used to treat chemotherapy-induced nausea: dexamethasone

Answer 139

Anti-alpha4-integrins - used for WBC adhesion Vedolizumab - think "Vital"-zumab treatment of choice because it doesn't cross BBB like Natalizumab which is used in the treatment of multiple sclerosis (increased risk of PML)

Answer 140

Hyoscyamine, dicyclomine - > antimuscarinic medications which predominately block Ach release in smooth muscle GI tract - > side effects include dry mouth, dry skin, and urinary retention

Answer 141

Used for treatment of IBS-D, it is a 5HT3 antagonist (similar to zofran) which is specific to causing constipation in the gut by slowing movement

Answer 142

Senna - slow-acting, weak - think of the senna suntan lotion stimulating that man's belly in sketchy Bisacodyl - very strong These both stimulate the enteric nervous system directly and produce strong but brief peristaltic movements

Answer 143

Autosomal dominant disorder GI tract: Large, pedunculated, hamartomatous polyps Major characteristic difference: Large bundles of smooth muscle within the polyps in PJS They are NOT premalignant, although PJS is associated with increased risk of cancer - > associated with melanotic macules of lips, face, hands, and feet - > increased risk of breast and GI cancers

Answer 144

Tubular - Usually asymptomatic, but some occult bleeding is possible Villous - rectal bleeding is common. Cells are also so dysplastic that they release alot of protein -> hypoproteinemia due to protein-losing enteropathy. Can also secrete Cl- causing metabolic alkalosis -> hypokalemia

Answer 145

Gardner syndrome Also associated with soft tissue tumors: fibromatosis of retroperitoneum (fibroblast proliferation), and dental abnormalities

Answer 146

1. 2-hits to APC 2. KRAS mutations - Ras becomes GTPase-activating protein (GAP) resistant 3. Loss of TGF-beta signalling (important inhibitor of epithelial proliferation) 4. TP53 knockout - DNA repair checkpoint is lost 5. Additional mutations and acquisition of telomerase

Answer 147

``` 0 = CIS before invasion thru muscularis mucosa (no lymphatics in mucosa) 1 = no deeper than muscularis propria 2 = Through muscularis propria 3 = lymph node metastases 4 = distant metastases (most commonly liver, then elsewhere) ```

Answer 148

Flexible sigmoidoscopy - if adenoma is found. Also, if FOBT is +, need colonoscopy CT colonography - polyp >6mm is found Note: >1cm on colonoscopy with biopsy is considered to have malignant potential

Answer 149

EGD beginning at age 10 for intestinal hamartomas Colonoscopies every 3 years beginning at age 25 looking for CRC Breast surveillance starting at age 25 - breast cancer Abdominal / pelvic exams with PAPs starting at age 25 -ovarian and testicular cancer

Answer 150

Neoadjuvant - surgery with PRE-operative chemo -> Stage II (no lymph node involvement) Adjuvant - surgery with POST-operative chemo -> used when lymph node involvement is seen (Stage III)

Answer 151

Invades thru M cells then lives intracellularly in macrophages and reticuloendothelial system, including liver and spleen. Virulence factor includes a Type III secretion system from a Salmonella pathogenicity island which translocates proteins from its intracellular vacuole into the macrophage cytoplasm, preventing maturation of mature phagolysosome.

Answer 152

Early constipation or diarrhea for 1-2 weeks (BEFORE fever) Flu-like symptoms begin by end of first week Second week - high fever, often with loss of diarrhea, and appearance of rose spots, hepatosplenomegaly, and relative bradycardia 3rd-4th week: Systemic complications -> hematogenous spread of bacteria just about anywhere

Answer 153

Nontyphoidal - Neutrophil inflammation and gastroenteritis -antibiotics NOT indicated Typhoid - monocytic inflammation and significantly less diarrhea -ceftriaxone or fluoroquinolones

Answer 154

1. Cholera 2. VIPoma - stimulates enterocytes to secrete 3. Celiac sprue - crypt hyperplasia with increased secretion Fasting will not help the active secretion. However, fasting would help conditions of decreased absorption (i.e. other mechanism of Celiac sprue, lactose malabsorption)

Answer 155

VIP - as in VIPoma PGE - as in colitis (produced in inflammation) Gastrin - as in Gastrinoma Serotonin - as in carcinoid syndrome (ondansetron blocks and causes constipation)

Answer 156

Colon: Bile acid malabsorption (direct secretagogues), fatty acid malabsorption (fatty acids interact with gut bacteria to increased net secretion), colitis (increased PGE)

Answer 157

Whenever there is a partial iliectomy (<100 cm lost) -> enough of bile salts are reabsorbed for liver to make enough daily, so you don't have malabsorption, but many bile salts reach colon and act as secretagogues on colonic epithelium Treatment: Cholestyramine - bile salt binding resin >100cm is steatorrhea, and u got worse issues on your hands (Adding cholestyramine would make it worse) -> decrease fat take, use Medium chain FA, supplement FADEK, give oral calcium to bind fatty acids

Answer 158

Less than 1/3 of small bowel left (<200 cm) Symptoms of extreme malabsorption and thus increased diarrhea: - steatorrhea - fluid / electrolyte imbalances - malnutrition - increased gastrin to compensate with further diarrhea - > PPIs to deal with gastrin and antibiotics to prevent bacterial overgrowth - > vein and liver disease can be caused by parenteral nutrition - > consider small bowel + liver transplant if needed

Answer 159

Sympathetic denervation of the smooth muscle in the IAS leads to required voluntary contraction by EAS striated muscle to maintain continence - > causes problems at night where you shit yourself because you aren't awake to think about your need to contract EAS - > decreased resting IAS tone on manometry studies Bezoar - vegetables in stomach which can't be moved -> scleroderma is a worse version of this

Answer 160

Increased parasympathetic tone relative to sympathetic -> increased secretions Stasis of gut - bacterial overgrowth, bile acid deconjugation, fat malabsorption -> further diarrhea Diabetes causes non-alcoholic fatty liver disease

Answer 161

Constipation or diarrhea Calcium stimulates gastrin -> Hypergastrinemia -> peptic ulcer disease + diarrhea Calcium stimulates pancreas -> pancreatitis Note: ZE syndrome (gastrinoma) associated with parathyroid adenoma

Answer 162

Angiodyplasias Pancreatitis Ascites Duodenal polyps with hypertrophy of brunner's glands

Answer 163

Bleeding, diarrhea, malabsorption, protein-losing enteropathy In liver: "vanishing bile duct" syndrome -> cholestasis / jaundice

Answer 164

1. Dubin-Johnson syndrome (NOT SJS lul) 2. Rotor syndrome Will not have symptoms of cholestasis since the problem is only with excretion of bilirubin and not any of the other components of bile.