UWorld 3

Question 1

Medication-induced esophagitis

Answer 1

1) ABx - tetracyclines
2) Anti-inflammatory agents - Aspirin and many NSAIDs
3) Bisphosphonates - Alendronate, risedronate
4) Others - Potassium chloride, Iron

Question 2

Pill esophagitis pathophys

Answer 2

Due to direct effect of certain meds on mucosa. Mucosal injury can be due to acid effect (tetracyclines), osmotic tissue injury (KCl) or disruption of normal gastroesophageal protection (NSAID)

Can be worse in people with coexisting GERD

Question 3

Pill esophagitis presentation

Answer 3

Sudden onset odynophagia and retrosternal pain that can sometimes cause trouble swallowing.

Most common in mid esophagus due to compression by aortic arch or an enlarged left atrium

Dx is usually clinical but can be confirmed on endoscopy, which shows discreet ulcers with relatively normal-appearng surrounding mucosa

Tx is stopping offending agent to prevent future injury

Question 4

Endoscopy in candida and herpes esophagitis

Answer 4

Candida - white plaques

Herpes - Ulcerating lesions that are vesicles and round/ovoid ulcers

CMV - Large linear ulcers

All of these are in the immunocompromised

Question 5

Patient with cirrhosis and ascites accompanied by either fever or mental status change.

Answer 5

Think spontaneous bacterial peritonitis.

Paracentesis is test of choice, with main diagnostic criteria being a positive ascites fluid culture and neutrophil count of at least 250.

Question 6

Secretin stimulation test

Answer 6

Secretin stimulates the release of gastrin by gastrinoma cells.

Normal gastric G cells are inhibited by secretin; therefore, secretin administration should not cause a rise in serum gastrin concentrations in patients with other causes of hypergastrinemia (such as failure of gastric acid secretion - achlorhydria)

Question 7

Calcium infusion study

Answer 7

Usually reserved for patients who have gastric acid hypersecretion and are strongly suspected of having gastrinoma despite a negative secretin test. Calcium infusion can lead to an increase in serum gastrin levels in patients with gastrinoma

Question 8

Upper GI bleed effects on renal function

Answer 8

Patients with upper (not lower) GI bleed often have elevated BUN and elevated BUN/Cr ratio.

Possible causes include increased urea production from intestinal breakdown of hemoglobin and increased urea reabsorption in proximal tubule due to associated hypovolemia

Question 9

When is Alk Phos high?

Answer 9

Biliary obstruction and skeletal disease with increased osteoblast activity (Paget)

Mild elevations can be seen in IBD or intra-abdominal infections

Question 10

When is prolonged PT seen?

Answer 10

Warfarin, vit K deficiency, certain hered coagulation disorders, ABx use and liver disease

Question 11

Urine sodium (or FENa) in a patient who is volume depleted

Answer 11

Low since kidney tries to keep Na to restore circulatory volume.

FENa is high in intrinsic renal disease

Question 12

Imaging of choice in suspected pancreatitis

Answer 12

RUQ US. CT is NOT required to diagnose someone who meets criteria for acute pancreatitis. Plus RUQ US is more sensitive for detecting gallstones.

CT only needed when it’s an atypical presentation or to check for complications like pancreatic hemorrhage or necrosis

Question 13

Stool elastase

Answer 13

Marker for pancreatic exocrine function. Low levels are seen in chronic pancreatitis. Not acute.

Question 14

Acute cholangitis

Answer 14

Charcot triad - Fever, jaundice, RUQ pain. Confusion and hypotension make up Reynolds pentad

Clinical

1) Fever, jaundice, RUQ pain (charcot)
2) Mental status changes, hypotension (Reynolds)
3) Liver failure
4) AKI

Dx

1) Biliary dilation on US or CT (common bile duct)
2) Increased alk phos, GGT, direct bilirubin
3) Leukocytosis, increased CRP

Tx
1) Biliary drainage. ERCP with sphincterotomy or percutaneous transhepatic cholangiography

2) Broad-spectrum ABx - B lactam/B-lactamase inhibitor, third gen cephalosporin with metronidazole

Question 15

NSAIDs and anemia

Answer 15

NSAIDs are common cause of Fe deficiency anemia, esp in elderly who may have low grade chronic anemia at baseline

Question 16

How long does GERD usually take to cause adenocarcinoma?

Answer 16

More than 20 years. So if the question stem sounds sorta like adenocarcinoma but they’ve had GERD for shorter than this think maybe stricture.

Question 17

Esophageal stricture

Answer 17

Chronic GERD with new dysphagia and symmetric lower esophageal narrowing suggests esophageal (peptic) stricture

Longstanding GERD predisposes for Barrett’s and esophageal strictures. Other causes of strictures are radiation, systemic sclerosis, and caustic ingestions

Typically cause slowly progressive dysphagia to solid foods without anorexia or weight loss. As they progress they can actually block reflux leading to improvement in GERD symptoms.

Barium - symmetric, circumferential narrowing

Even so, if you have strictures in setting of Barrett’s, rule out adenocarcinoma via endoscopy which may be diagnostic and therapeutic (dilation is performed if no malignancy is detected).

Question 18

Episodic painless GI bleeding

Answer 18

Suggests angiodysplasia.

Characterized by dilated submucosal veins and AV malformations with increased incidence over age 60. May occur anywhere along GI tract, but most common in R Colon*

More frequently diagnosed in patients with advanced renal disease and vW Disease, possibly due to the bleeding tendency associated with these disorders.

Angiodysplasia may also be more common in patients with aortic stenosis, maybe due to acquired vW factor deficiency (from disruption of the vW multimers as they traverse the turbulent valve space induced by AS)

Angiodysplastic bleeding as been reported to improve after AVR.

Dx usually made via endoscopic studies (upper GI endo, colonoscopy). Not uncommon for angiodysplasia to be missed*** on colonoscopy due to poor bowel prepartion or location behind a haustral fold.

Patients with anemia or gross or occult bleeding can be treated endoscopically usually with cautery. ASx patients don’t require treatment.

Question 19

Clinical features of colovesical fistula

Answer 19

Etiology

1) Diverticular disease (Sigmoid most common)
2) Crohn Disease
3) Malignancy (Colon, bladder, pelvic organs)

Clinical pres

1) Pneumaturia (air in urine)
2) Fecaluria
3) Recurrent UTIs (mixed flora)

Dx

1) Abdominal CT with oral or rectal (not IV) contrast (will see contrast in bladder plus thickened colonic and vesicular walls)
2) Colonoscopy to exclude colonic malignancy

Tx is usually surgical following resolution of infection

Question 20

Pellagra

Answer 20

AKA Niacin deficiency. 3 D’s.

In developing countries, seen in populations that subsist on corn products (niacin is in unabsorbable form in corn).

In developed countries, it is usually seen in patients with impaired nutritional intake (alcoholism, chronic illness).

Pellagra can also be seen in those with carcinoid syndrome (due to depletion of tryptophan - niacin is made from tryptophan) or Hartnup Disease (congeital disorder of tryptophan absorption).

Prolonged isoniazid therapy can interfere with tryptophan metabolism and lead to pellagra too.

Question 21

Clinical presentation of severe pancreatitis

Answer 21

1) Fever, tachy, hypotension
2) Dyspnea, tachypnea and/or basilar crackles
3) Abdominal tenderness and or distension
4) Cullen sign - periumbilical bluish coloration indicating hemoperitoneum
5) Gray-Turner sign - Reddish-brown coloration around flanks indicating retroperitoneal bleed

Question 22

What is associated with higher risk of severe pancreatitis

Answer 22

1) Age over 75
2) Obesity
3) Alcoholism
4) CRP above 150 at 48h after presentation
5) Rising BUN and Cr in first 48h
6) CXR with pulmonary infiltrates or pleural effusion
7) CT/MRCP with pancreatic necrosis and extrapancreatic inflammation

Question 23

Complications of severe pancreatitis

Answer 23

1) Pseudocyst
2) Peripancreatic fluid collection
3) Necrotizing pancreatitis
4) ARDS
5) ARF
6) GI bleeding
7) Hypotensive episodes may incite an underlying MI
8) Pericardial effusion (potential complication of pancreatitis in general)

Question 24

What is severe pancreatitis?

Answer 24

Most patients with acute pancreatitis have mild disease and recover with conservative management (fluids, bowel rest, pain meds) in 3-5d. BUT 15-20% can develop severe acute pancreatitis - defined as pancreatitis with failure of at least 1 organ

Abdominal imaging (CT or MRCP) is indicated for suspected severe pancreatitis to look for pancreatic necrosis and extrapancreatic inflammation, which also indicate severe acute pancreatitis.

Severe pancreatitis causes local release of activated pancreatic enzymes that enter vascular system and increase vascular permeability within and around the pancreas.

This leads to large volumes of fluid migrating from vascular system to the surrounding retroperitoneum. Systemic inflammation also ensues as the inflammatory mediators enter vascular system. Net effect is widespread vasodilation, capillary leak, shock and associated end organ damage. Treatment usually involves supportive care with several liters* of IV fluid to replace lost volume

Question 25

How drugs/toxins cause liver injury (and which ones)?

Answer 25

Typically cause injury due to either:
1) Direct toxic effects - these are dose dependent and have short latent periods. CCl4, Acetaminophen, Tetracycline, substances found in amanitia mushroom

OR

2) Idiosyncratic reactions - not dose dependent and have variable latent periods. Isoniazid, chlorpromazine, halothane, antiretroviral therapy

Also can break down by morphology.

1) Cholestasis - caused by meds like chlorpormazine, nitrofurantoin, erythromycin, anabolic steroids
2) Fatty liver - caused by tetracycline, valproate, anti-retrovirals
3) Hepatitis (Panlobular mononuclear infiltration and hepatic cell necrosis) - halothane, phenytoin, isoniazid, alpha-methyldopa, viral hepatitis
4) Toxic or fulminant liver failure - CCl4, acetaminophen
5) Granulomatous - allopurinol and phenylbutazone

Question 26

What kind of liver injury do tetracycline, valproate and antiretrovirals cause?

Answer 26

Fatty liver

Question 27

Isoniazid, phenytoin, halothane, alpha-methyldopa all cause what kind of drug damage to the liver?

Answer 27

Hepatitis (just like viral hepatitis pattern)

Question 28

What meds cause cholestasis pattern of liver injury?

Answer 28

Chlorpromazine, nitrofurantoin, erythromycin, anabolic steroids

Question 29

What meds cause toxic or fulminant liver failure?

Answer 29

CCl4, acetaminophen

Question 30

What meds cause granulomatous liver injury?

Answer 30

Allopurinol and phenylbutazone

Question 31

Pancreatic pseudocyst

Answer 31

CT shows round, well-circumscribed, encapsulated fluid collection in pancreatic bed. Patient with history of alcohol use and a recent episode of pancreatitis with new progressive abdominal distention, nausea and vomiting.

Usually no necrosis or solid material. Surrounded by thick fibrous capsule. Containing enzyme rich fluid, tissue and debris.

They can leak amylase-rich fluid into circulation and increase serum amylase.

Complications include spontaneous infection, duodenal or biliary obstruction, pseduoaneurysm (due to digestion of adjacent vessels), pancreatic ascites and pleural effusion. Imaging confirms the dx.

In patients with minimal or no symptoms and without complications (pseudoaneurysm), expectant management (symptomatic therapy, nothing by mouth) is preferred initially.

Endoscopic drainage is reserved for those with significant symptoms (abdominal pain, vomiting), infected pseudocyst (plus IV ABx), or evidence of pseudoaneurysm (usually embolized before drainage procedure)

Question 32

Diagnostic test of choice for ZD

Answer 32

Contrast esophagram. Oral contrast in patient with history of aspiration has a risk for pneumonitis, but positioning techniques can help and is still indicated unless patient has severe swallowing difficulty

Question 33

Pleural fluid analysis in Boerhaave

Answer 33

Exudative with low pH and very high amylase (over 2500)

Question 34

Tx for Boerhaave

Answer 34

Surgery - for thoracic perfs

Conservative (ABx) for cervical perfs

Question 35

Fictitious diarrhea

Answer 35

Laxative abuse. Characterized by very frequent, watery, nocturnal diarrhea. Dx can be confirmed with characteristic bx finding of dark brown discoloration of colon with lymph follicles shining through as pale patches (melanosis coli)

10-20 BMs per day.

May also see histo evidence of pigment in the macrophages of lamina propria

Question 36

Clinical features of alcoholic hepatitis

Answer 36

Clinical presentation

1) Jaundice, anorexia, fever
2) RUQ and/or epigastric pain
3) Abdominal distension due to ascites
4) Prox muscle weakness from muscle wasting (if malnourished)
5) Possible hepatic encephalopathy
6) tender hepatomegaly
7) Macrocytic anemia

Lab/Imaging

1) Elevated AST and ALT usually less than 300 though
2) AST to ALT ratio at least 2
3) Elevated GGT, bilirubin, and/or INR
4) leukocytosis, predominantly neutrophils
5) Decreased albumin if malnourished
6) Abdominal imaging may show fatty liver

Question 37

History of anticoagulation, symptoms of weakness and dizziness and evidence of anemia and tachycardia

Answer 37

Should immediately raise concern for internal hemorrhage.

Risk of bleeding on warfarin is highest in patients with diabetes, who are over 60, have HTN, or have alcoholism.

A supratherapeutic INR also increases one’s risk. Just remember that RP hematomas can happen even with normal INR levels though.

Back pain raises flags for RP hematoma. This warrants an abdominal CT. You’ll see a large isodense collection in RP which lies anterior to psoas muscle and displaces the R kidney anteriorly

Question 38

pRBC transfusion thresholds

Answer 38

1) Hgb less than 7 - generally indicated
2) Hgb 7-8 - Cardiac surgery, Onc patients in tx, Heart failure
3) Hgb 8-10 - Symptomatic anemia, ongoing bleeding, acute coronary syndrome, noncardiac surgery
4) Hgb more than 10 - not generally indicated

Question 39

FFP

Answer 39

contains all clotting factors and plasma proteins from one unit of blood.

Usually indicated for severe coagulopathy (liver disease, DIC) with active bleeding.

Question 40

Platelet transfusion threshold

Answer 40

Usually less than 10k. Less than 50k with active bleeding

Question 41

Whole blood transfusion

Answer 41

includes pRBCs in addition to plasma. May be used in patients with severe hemorrhage (major trauma) requiring massive blood transfusions to assist in volume expansion

Question 42

Whipple’s Disease

Answer 42

Rare multisystemic illness. Infectious disease caused by the bacillus Tropheryma whippelii.

Most often seen in white men in fourth to sixth decades of life and often presents with weight loss.

GI symptoms include ab pain, diarrhea, and malabsorption with distension, flatulence, and steatorrhea.

Extraintestinal manifestations include migratory polyarthropathy, chronic cough, myocardial or valvular involvement leading to congestive failure or valvular regurgitation.

Later signs of disease may be characterized by dementia and other CNS findings like supranuclear ophthalmoplegia and myoclonus.

Intermittnt low grade fever, pigmentation and LAD may also be seen. PAS positive material in lamina propria of SI is classical bx finding

Question 43

Evaluating ASx elevation of aminotransferases

Answer 43

1) First step is to take thorough history to rule out more common hepatitis risk factors (alcohol or drug use, travel outside country, blood transfusions, high risk sex practices).
2) Have pt discontinue all alcohol and drug use then repeat liver studies
3) If elevation of LFTs continues over a 6 month period, it is now chronic. Testing for viral hep B and C, hemochromatosis and fatty liver should be done at this time.
4) If these test show nothing then look for muscle disorders (polymyositis) and thyroid disease

Question 44

Where are AST and ALT located?

Answer 44

AST is present and very active in liver, heart, kidney and skeletal muscle

ALT is found mostly in liver and is more specific for hepatocyte injury. “L for Liver”

Both are pretty much found everywhere though. This is just where each is most active.

Question 45

Patient with small, nonbleeding varices

Answer 45

ppx tx with nonselective B blockers (propranolol, nadolol) is recommended to reduce likelihood of variceal hemorrhage. This lowers adrenergic tone in mesenteric arterioles. This causes unopposed alpha mediated vasocontriction and decreased portal venous flow. Actually lowers mortality rate

Endoscopic variceal ligation can be used as alternative primary prevention in patients with contraindications to B blocker therapy

Question 46

Vanishing Bile Duct Syndrome

Answer 46

Look for “liver bx shows markedly decreased quantity of bile ducts.”

Rare disease involving progressive destruction of intrahepatic bile ducts. Histo hallmark is ductopenia.

Primary Biliary Cirrhosis is number one cause of ductopenia in adults.

Other causes:

1) Failing liver transplant
2) Hodgkin’s disease
3) Graft vs host
4) Sarcoid
5) CMV
6) HIV
7) Medication toxicity

Question 47

Treatment of Ascites

Answer 47

Starts with Na and water restriction (2L per day). Diuretic therapy, if needed is usually started with spironolactone.

When max dose of spironolactone fails to improve the patient’s status, giving a loop diuretic (furosemide) is recommended. Aggressive diuresis (more than 1L per day) is not recommended due to the risk of hepato-renal syndrome

Slow tapping of up to 2-4 L of ascitic fluid daily (with/without albumin infusion) is the best next conservative measure. For this, renal function should be frequently monitored. Less aggressive paracentesis is recommended in patients with borderline renal function.

In summary: step wise

1) Sodium and water restriction
2) Spironolactone
3) Loop diuretic (not more than 1L per day of diuresis)
4) Frequent abdominal parecentesis (2-4 L per day, as long as renal function is OK)

Question 48

Zn deficiency

Answer 48

May result from chronic TPN or malabsoprtion. Symptoms include alopecia, skin lesions, abnormal taste, and impaired wound healing.

Question 49

Selenium deficiency

Answer 49

Also may result from TPN, malabsorption or malnutrition (nuts, meat, fish).

Most important feature is cardiomyopathy

Question 50

Small Intestinal Bacterial Overgrowth

Answer 50

Etiology

1) Anatomical abnormalities (strictures, surgery)
2) Motility disorders (diabetes, scleroderma)
3) Other causes (ESRD, AIDS, Cirrhosis, advanced age)

Signs/symptoms
1) Abdominal pain, diarrhea, bloating, excess flatulence, malabsorption, weight loss, anemia, nutritional deficiencies

Dx

1) Endoscopy (gold standard) with jejunal aspirate showing more than 10 to the 5th organisms per mL
2) Glucose breath hydrogen testing

Common organisms

1) Strep
2) Bacteroides
3) Escherichia
4) Lactobacillus

Tx

1) 7-10d course of ABx (rifaximin, amoxicillin-clavulanate)
2) Avoid antimotility agents (narcotics)
3) Dietary changes (high fat, low carb)
4) Trial of promotility agents (metoclopramine)

Question 51

Gilbert’s Syndrome

Answer 51

Familial disorder of bilirubin glucoronidation in which production of UDP glucuronyl transferases is reduced.

Genetic defect mapped to promoter region of UDP gluc transferase gene.

9% of people in western countries are homozygous for this mutation with another 30% heterozygous and asymptomatic.

Clinical:

1) Icterus secondary to a mild, predominantly unconjugated hyperbilirubinemia (normal levels in these patients are less than 3)
2) patients who are symptomatic tend to have nonspecific complaints, including malaise, fatigue, or abdominal discomfort.
3) Certain events, such as hemolysis, fasting or consuming a fat free diet, physical exertion, febrile illness, stress, or fatigue are thought to be triggers for hyperbili in these patients

Dx
1) Suggested in those patients with no apparent liver diseaes who have mild unconjugated hyperbili thought to be provoked by one of the classic triggers.

tx - generally considered unneeded. Mode of inheritance should be discussed with patients as a means of preventing needless tests in similarly affected family

KNOW HOW TO DIFFERENTIATE FROM THE TWO TYPES OF CRIGLER NAJJAR

Question 52

MALT lymphoma

Answer 52

H pylori has big role in pathogenesis of this disease. Low grade versions of this lymphoma will regress with eradication of the H Pylori. ABx therapy is go to tx for MALT lymphoma without metastasis

Chemo typically plays a role in management of patients with MALT lymphoma if eradication of H Pylori fails to regress the lymphoma. Such thereapeutic regimens include CHOP (cyclophosphamide, adriamycin, vincristine, prednisone) or CHOP plus bleomycin

Question 53

Chronic mesenteric ischemia

Answer 53

Etiology - atherosclerosis (smoking, dyslipidemia) of celiac or SMA

Clinical

1) Crampy, postprandial epigastric pain
2) Food aversion and weight loss

Dx

1) Signs of malnutrition, abdominal bruit
2) CT angio (preferred), Doppler US

Management

1) Risk reduction (tobacco reduction), nutritional support
2) Endovascular or open surgical revascularization

Question 54

Hepatic hydrothorax cause and tx

Answer 54

Patients with cirrhosis and portal HTN frequently have abdominal ascites and peripheral edema secondary to low albumin levels and resulting abnormal extracellular fluid volume regulation. A small number may also develop pleural effusions (R side usually) called hepatic hydrothorax.

Generally causes transudative pleural effusions and is much more common on right side. It is thought to happen secondary to small defects in diaphragm which permit abdominal ascites to pass into pleural space

best option for tx is liver transplant.

Primary tx for most patients is therapeutic thoracentesis followed by salt restricted diet and diuretics. For refractory effusions, transjugular intrahepatic portosystemic shunt (TIPS) is indicated

Question 55

Dyspepsia

Answer 55

Epigastric fullness or discomfort after eating. Often associated with nausea and symptoms of GERD like heartburn

Question 56

Alarm symptoms with dyspepsia

Answer 56

Weight loss, gross or occult bleeding, anemia, dysphagia, persistent vomiting, or early satiety

Question 57

Abdominal succussion splash

Answer 57

PE maneuver. Elicited by placing the stethoscope over the upper abdomen and rocking the patient back and forth at the hips.

Retained gastric material more than 3 hours after a meal will generate a splash sound, indicating presence of a hollow viscus filled with fluid and gas.

Test has modest sensitivity and specificity for gastric outlet obstruction but it does suggest need for more definitive evaluations. Initial management of GOO includes NG tubes suctioning to decompress the stomach, IV hydration and endoscopy for definitive diagnosis

Question 58

Most common cause of gross lower GI bleeding in adults

Answer 58

Diverticulosis

Question 59

Alcoholic hepatitis lab markers

Answer 59

1) AST and ALT elevations with AST more than twice as high as ALT. This is due to hepatic deficiency of pyridoxal-5-phosphate, an ALT enzyme cofactor. Both are usually still less than 300 though and almost always less than 500.
2) High GGT, an ezyme present in liver and other cells
3) High Ferritin, an acute phase reactant.

Question 60

Acute pancreatitis from cholesterol emboli

Answer 60

Patients with risk factors for aortic atherosclerosis (hypercholesterolemia, diabetes, peripheral vascular disease) who undergo cardiac cath or a vascular procedure are at higher risk for cholesterol emboli. They can occlude blood vessels and cause:

1) Skin manifestations - livedo reticularis (reticulated, mottled, discolored skin), blue toe syndrome
2) Kidney - AKI
3) GI - Pancreatitis**, mesenteric ischemia

Treat this like other pancreatitis. Most acute pancreatitis attacks self resolve and improve within 4-7 days with conservative management. Patient should receive nothing by mouth except essential meds (antiplatelet therapy to prevent stent thrombosis)

Question 61

Porcelain gallbladder

Answer 61

Requires chole bc of increased risk of gallblader adenocarcinoma (2-5%).

Calcified rim in GB wall with a central bile filled dark area

Question 62

Spider angioma and palmar erythema pathogen

Answer 62

Both arise from hyperestrinism due to impaired hepatic metabolism of circulating estrogens, a process that begins in cytochrome P450 system. Circulating estrogens affect vascular wall dilation.

Other manifestations of hyperestrinism in cirrhosis patients is gynecomastia, testicular atrophy and decreased body hair in males

Question 63

Caput medusae pathogen

Answer 63

From dilation of superficial veins on the abdominal wall due to portal HTN.

Portal HTN is from increased resistance to portal flow at the sinusoids and leads to increased pressure at the portosystemic collateral veins in the anterior abdomen, rectum and distal esophagus.

This then predisposes to esophageal varices, rectal varices and caput. Simialrly, portal HTN causes enlargement of spleen (which drains into portal vein via splenic vein) due to vascular congestion of the red pulp

Question 64

Dupuytren contracture pathogen

Answer 64

Occurs when palmar fascia thickens and shortens, deforming the hand. Usually most notable initially in 4th and 5th digits and occurs due to fibroblast proliferation and collagen deposition, which are likely worsened by oxidative stress from increased free radical production

Question 65

Lower extremity edema pathogen in cirrhosis

Answer 65

Liver is main site of protein synthesis, and cirrhotic liver typically doesnt make enough albumin. Hypoalbuminemia leads to both a decrease in intravascular oncotic pressure and fluid shifts to the extravascular space, predisposing to edema of lower extremities.

Question 66

Colon cancers and polyps

Answer 66

Most colon cancers develop from polyps. The risk factors for a polyp progressing to malignancy are villous adenoma, sessile adenoma and size bigger than 2.5cm. Only adenomatous polyps are clearly premalignant but less than 1% progress to malignancy.

Hyperplastic polyps are non-neoplastic and do not require further workup

Question 67

Neutrophilic cryptitis - UC or Crohn’s?

Answer 67

Both. In Crohn’s, it’s transmural though. Remember IBD has bimodal age distribution so old people can get it too.