UWorld 1 Flashcards
Dysphagia, coughing, regurgitation, halitosis and a neck mass
Zenker
Zenker (pharyngoesophageal) diverticulum
Clinical
1) Usually at least 60 years old
2) More common in males
3) Dysphagia
4) Halitosis
5) Regurgitation and aspiration
6) Variable neck mass
Dx
1) Barium esophagram
2) Esophageal manometry
Management
1) Open/endoscopic surgery
2) Cricopharyngeal myotomy
Potential complications - tracheal compression, ulceration with bleeding, regurgitation, pulmonary aspiration
What is thought to cause ZD?
Upper esophageal sphincter dysfunction and esophageal dysmotility
It’s above the upper esophageal sphincter. Caused by posterior herniation btw fibers of the cricopharyngeal muscle.
Precipitating factors for hepatic encephalopathy
1) Drugs (sedatives, narcotics)
2) Hypovolemia (diarrhea, vomiting, diuretics, high volume paracentesis)
3) Excessive nitrogen load (GI bleeding, constipation, high protein diet)
4) HypoK and metabolic alkalosis
5) Hypoxia and hypoglycemia
6) Infection (pneumonia, UTI, spontaneous bacterial peritonitis)
7) Portosystemic shunting (surgical shunts)
Clinical presentation of hepatic encephalopathy
Stage 1
1) Hypersomnia, insomnia, or inverted sleep cycle
2) Slightly impaired cognition
3) Mild confusion
4) Tremor, possible asterixis
Stage 2
1) Lethargy with slow response to stimuli
2) Moderate confusion
3) Difficulty with writing, slurred speech
Stage 3
1) Marked confusion
2) Sleeping but arousable
Stage 4 - stupor or coma
What test can help support a clinical suspicion of hepatic encephalopathy?
Ammonia level, thought it is fairly nonspecific and may be elevated in ASx patients
When should you give ABx ppx in a patient with GI bleed?
Cirrhotics - decreases infectious complications, recurrent bleeding and mortality
Somatostatin analogs
Octreotide. Inhibits the release of vasodilator hormones, which leads indirectly to splanchnic vasoconstriction and decreased portal flow.
Hemoglobin goal in a variceal bleed
Keep above 9. Get serial blood counts.
Platelet transfusion below 50k.
Common complications of an esophageal variceal bleed
Coagulopathy, anemia, thrombocytopenia
Clinical features of chronic Hep C
Clinical
1) Can be asymptomatic or develop fatigue (most common)***
2) Serum LFTS can be elevated or normal (up to a third of patients)
3) Can progress to cirrhosis in up to 20% of cases
4) Increased risk of HCC
Extrahepatic manifestations
1) Heme - Essential mixed cryoglobulinemia
2) Renal - Membranoproliferative glomerulonephritis
3) Skin - porphyria cutanea tarda, lichen planus
4) Endocrine - Increased risk of diabetes
Intermittent elevations of transaminases with fragile skin, photsensitivity, and vesicles /erosions on dorsum of the hands.
Hep C with porphyria cutanea tarda (all patients with PCT should be screened for Hep C)
Essential mixed cryoglobulinemia
Half of Hep C patients have cryoglobulinemia
Due to circulating immune complexes that deposit in small to medium vessels and may be associated with low serum complement levels. Patients can develop palpable purpura, arthralgias, renal complications (usually membranoproliferative glomerulonephritis)
Pathophys of hepatic encephalopathy
CNS complication of cirrhosis due to liver’s inability to convert ammonia to urea
Tx of hepatic encephalopathy
Involves supportive care, treating the underlying precipitant, and lowering the serum ammonia.
Nonabsorbable disaccharides (lactulose, lacitol) are preffered for lowering serum ammonia.
Colonic bacteria metabolize lactulose to short chain fatty acids (lactic acid, acetic acid). This acidifies the colon to stimulate conversion of the absorbable ammonia to the nonabsorbable ammonium (an ammonia trap) and also causes a catharsis
ABx (rifaximin) can decrease the number of ammonia-producing bacteria in the colon. They are usually added to lactulose if patient does not improve within 48h
Catharsis using any laxative may help as well.
Spontaneous Bacterial Peritonitis
Clinical
1) Temp of at least 37.8C (100F) - patients with cirrhosis are usually relatively hypothermic so any temp of 100 should be investigated
2) Abdominal pain/tenderness
3) AMS (abnormal connect-the numbers test - Reitan trail test)
4) Hypotension, hypothermia, paralytic ileus (dilated loops of bowel on XR) with severe infection
Diagnosis from ascitic fluid
1) PMNs of at least 250
2) Positive culture, often gram negative organisms (E Coli, Kleb)
3) Protein less than 1
4) SAAG of at least 1.1
Tx
1) Embiric ABx - third generation cephalosporins (cefotaxime)
2) Fluoroquins for SBP ppx
What exactly IS spontaneous bacterial peritonitis?
Ascitic fluid infection without an obvious intraabdominal surgical etiology
Most likely due to either intestinal bacterial translocation directly into the ascitic fluid or hematogenous spread to the liver and ascitic fluid (due to other bacterial infections)
Major risk factors for pancreatic cancer
Hereditary
1) First degree relative with pancreatic cancer
2) Hereditary pancreatitis
3) Germline mutations (BRCA1, BRCA2, Peutz-Jeghers Syndrome)
Environmental
1) Cigarette smoking (most significant)
2) Obesity, low physical activity
3) Nonhereditary chronic pancreatitis
Long standing diabetes is also a risk factor
Common causes of steatorrhea
Pancreatic insufficiency
1) Chronic pancreatitis due to alcohol abuse, cystic fibrosis, or autoimmune/hereditary pancreatitis
2) Pancreatic cancer
Bile salt related
1) Small bowel Crohn’s
2) Bacterial overgrowth
3) Primary biliary cirrhosis
4) Primary sclerosing cholangitis
5) Surgical resection of ileum (at least 60-100cm)
Impaired intestinal surface epithelium
1) Celiac disease
2) AIDS enteropathy
3) Giardiasis
Other rare causes
1) Whipple Disease
2) ZE Syndrome
3) Medication - induced
Presentation of steatorrhea
Patients typically develop loose, greasy, malodorous stools that float in the toilet (occasionally with oil droplets) and are difficult to flush
Other symptoms include abdominal distension and borborygmi
Nutritional deficiencies (fat soluble vitamins, vitamin B12) may occur and lead to clinical symptoms and weight loss despite a good appetite
Confirmed by fecal fat tests (Sudan stain on spot stool specimen or 72h collection).
Very basic chronic pancreatitis presentation
Long term alcohol use can cause it. Progressive inflammation results in permanent damage to endocrine AND exocrine pancreas. After 90% functional loss, patients develop fat and protein malabsorption
They typically develop postprandial epigastric pain (15-30 minutes after a meal) that is intermittent early in the disease and becomes persistent with disease progression
Primary sclerosing cholangitis
Clinical
1) Fatigue and pruritus
2) Majority of patients asymptomatic at time of dx
3) About 90% of patients have underlying IBD, mainly UC
Lab/imaging
1) Cholestatic liver function test pattern (serum aminotransferases usually less than 300)
2) Multifocal stricturing/dilation of intrahepatic and/or extrahepatic bile ducts on cholangiography
Liver bx
1) Fibrous obliteration of small bile ducts with concentric replacement by connective tissue in an “onion skin” pattern
Complications
1) Intrahepatic and/or extrahepatic biliary stricture
2) Cholangitis and cholelithiasis (cholesterol and/or pigment stones)
3) Cholangiocarcinoma (10-15% lifetime risk)
4) Cholestasis (low fat soluble vitamins, osteoporosis)
5) Colon cancer
Dx of PSC
US is usually nondiagnostic. Cholangiogram (either endoscopic retrograde or magnetic resonance) usually confirms the dx by showing multifocal narrowing with intrahepatic and extrahepatic duct dilation (beading)
Liver bx can determine stage and prognosis. Usually shows onion skin pattern.
Prognosis of PSC
It’s a progressive condition. Disease course includes cholestatic complications (fatigue, pruritus, steatorrhea, fat soluble vitamin deficiencies, metabolic bone disease) and hepatic failure
Patients who do not get a liver transplant have a mean survival of 12 years after dx.
Cirrhosis, neuropsych symptoms, and brownish/gray-green rings in eye in young adult. What disease? Background info.
Hepatolenticular Degeneration (WIlson Disease)
Kayser-Fleisher Rings are the eye rings - granular copper deposits in cornea
Rare, autosomal recessive disease most often identified in younger people ages 5-40.
The genetic mutations involved hinder Cu metabolism by reducing the formation and secretion of ceruloplasmin and by decreasing the secretion of Cu into the biliary system.
Cu is pro-oxidant, and as it accumulates in greater quantities within the liver, it causes damage to hepatic tissue through the generation of free radicals. Eventually, Cu leaks from injured hepatocytes into the blood to be deposited in various tissues, including the basal ganglia (hepatolenticular degeneration) and cornea
Presentation and dx of Wilson Disease
ASx liver function abnormalities, chronic hepatitis, fulminant hepatitis, portal HTN, or macronodular cirrhosis.
Neuropsych - Parkinson-like tremor, rigidity, ataxia, slurred speech, drooling, personality changes, depression, paranoia, catatonia.
Wilson’s is also associated with Fanconi Anemia, hemolytic anemia, and neuropathy
Gold standard for dx is Liver Bx that shows hepatic copper greater than 250 dry weight.
More commonly, dx is confirmed by low serum ceruloplasmin (particularly less than 20) in conjunction with increased urinary copper excretion or Kayser-Fleishcer rings
Tx of Wilson’s Disease
Must be adhered to for the patient’s lifetime and focuses on removing accumulated copper in the tissues and preventing re-accumulation
First line meds - copper chelators like D-penicillamine or trientine
Oral Zinc is also recommended as it prevents copper absorption
Liver transplant may be only option of those with fulminant hepatitis or decompensated liver disease that does not respond to pharm
Ascites fluid characteristics
Color
1) Bloody - trauma, malignancy, TB (rarely)
2) Milky - Chylous, pancreatic
3) Turbid - Possible infection
4) Straw color - likely more benign causes
Neutrophils
1) Less than 250 - no peritonitis
2) 250 and up - Peritonitis (secondary or spontaneous bacterial)
Total protein
1) 2.5 and up (high protein ascites) - CHF, constrictive pancreatitis, peritoneal carcinomatosis, TB, Budd-Chiari Syndrome, Fungal (coccidiomycosis)
2) Less than 2.5 - Cirrhosis, nephrotic syndrome
SAAG
1) 1.1 and up (indicates portal HTN) - cardiac ascites, cirrhosis, Budd-Chiari
2) Less than 1.1 (absence of portal HTN) - TB, peritoneal carcinomatosis, pancreatic ascites, nephrotic syndrome
SAAG
Serum-to-Ascites Albumin Gradient. Subtract the peritoneal albumin from the serum albumin
Above 1.1 - possible portal HTN etiology, therefore the ascites may be due to increased hydrostatic pressure within hepatic capillary beds
Less than 1.1 - Increased capillary permeability (eg malignant ascites, pancreatitis, nephrotic, TB)
Crohn’s vs UC - granulomas
Crohn’s
Features of malabsorption in celiac disease
1) General - Bulky, foul smelling, floating stools
2) Fat and protein - Loss of muscle mass, loss of subq fat, fatigue
3) Iron - Pallor (anemia), fatigue
4) Calcium and Vit D - Bone pain (osteomalacia), fracture (osteoporosis)
5) Vit K - Easy bruising
6) Vit A - Hyperkeratosis
Dx of Celiac
IgA anti-tissue transglutaminase and IgA anti-endomysial antibodies
BUT, many patients with bx-confirmed (villous atrophy) disease will have negative antibody results since IgA deficiency is fairly common in Celiac
If suspicious for Celiac is high but IgA serology is negative, measure total IgA (or get IgG based serology)
Collagenous Colitis
Uncommon disorder producing chronic watery diarrhea. Colon is frequently involved, but colonoscopy shows normal mucosa.
Bx shows mucosal subepithelial collagen deposition
ZE Syndrome
Epi
1) Age 20-50
2) 80% Sporadic/20% MEN1
Clinical
1) Multiple and refractory peptic ulcers
2) Ulcers distal to duodenum
3) Chronic diarrhea
Dx
1) Markedly elevated serum gastrin (more than 1000) in the presence of normal gastric acid (pH less than 4)
Workup
1) Endoscopy
2) CT/MRI and somatostatin receptor scintigraphy for tumor localization
Diagnosis of ZES
Gastrinoma is usually in pancreas or duodenum
Dx is suggested by marked elevation in serum gastrin (above 1000) in presence of acidic gastric pH (less than 4).
Endoscopy reveals ulcers usually (90%) and sometimes will ID a primary duodenal gastronoma
CT, MRI and somatostatin receptor scintigraphy can be used to ID pancreatic tumors and metastatic disease
If gastrinoma is confirmed, patients should be screened for MEN with assays for PTH, ionized Ca, and Prolactin
Compensated vs uncompensated cirrhosis
Patients with compensated cirrhosis typically are either ASx or complain of vague symptoms (anorexia, weakness, fatigue)
Those with decompensated cirrhosis may present with jaundice, pruritus, upper GI bleeding, abdominal distention due to ascites, or confusion due to hepatic encephalopathy
Major cause of morbidity and mortality in cirrhosis
Esophageal varices. They can occur in half of patients.
Gold standard for diagnosis of cirrhosis
Liver biopsy, though clinical impression and history is usually enough
ASx patient with elevated Alk Phos with normal hepatic enzymes, normal RUQ US, and positive anti-mitochondrial antibody assay
Early Primary biliary cholangitis (formerly primary biliary cirrhosis)
Chronic, progressive liver disease characterized by cholestasis with autoimmune destruction of intrahepatic bile ducts
Most common in middle aged women and has insidious onset. Pruritus and fatigue are usually first symptoms.
As it progresses, jaundice, steatorrhea, HSM, eyelid xanthelasma, portal HTN, and osteopenia may develop
Drug of choice - ursodeoxycholic acid. Less effective in advanced disease that may require liver transplant.
Ursodeoxycholic acid
used in a number of cholestatic disorders. It is a hydrophilic bile acid that decreases biliary injury by the more hydrophobic endogenous bile acids.
Also increases biliary secretion and may have additional anti-inflammatory effects. It delays progression in PBC and may improve symptoms and possibly survival.
Start it in PBC as soon as dx is made, even if patient is asymptomatic
Liver transplant is definitive treatment but only indicated in those with severe liver damage or cirrhosis
Solid liver masses
Focal nodular hyperplasia
1) Associated with anomalous arteries
2) Arterial flow and central scar on imaging
Hepatic adenoma
1) Women on long term OCPs
2) Possible hemorrhage or malignant transformation
Regenerative nodules
1) Acute or chronic liver injury (cirrhosis)
HCC
1) Systemic symptoms
2) Chronic hepatitis or cirrhosis
3) Elevated AFP
Liver mets
1) Single/multiple lesions
2) Known extrahepatic malignancy
Dx of hepatic adenoma
It’s benign!
US shows well-demarcated, hyperechoic lesions
Contrast CT can show early peripheral enhancement.
Needle bx is not recommended for suspected hepatic adenoma due to risk of bleeding. Surgical excision is preferred.
Long term complications are progressive growth, rupture, and malignant transformation
HCC (brief)
Characterized by rapidly enlarging liver mass, often with satellite lesions. It usually occurs in patients with cirrhosis or chronic hepatitis (esp B)
Hydatid cyst
Caused by echinococcus tapeworm. In USA, most cases are seen in immigrants, although occasional cases may be seen in individuals from the southwest who have been exposed to sheep and dogs
It causes cystic not solid liver lesions
Nonalcoholic fatty liver disease
Definition
1) Hepatic steatosis on imaging or biopsy
2) Exclusion of significant alcohol use
3) Exclusion of other causes of fatty liver
Clinical
1) Mostly ASx
2) Metabolic Syndrome
3) With or without steatohepatitis (AST/ALT less than 1)
4) Hyperechoic texture on US
Tx
1) Diet and exercise
2) Consider bariatric surgery if BMI is at least 35
Typical patient with NAFLD
Middle aged, obese, with features of the metabolic syndrome
Histology of NAFLD
Can range from bland steatosis to inflammation and necrosis (steatohepatitis) to fibrosis and cirrhosis
Can resemble alcohol-induced fatty liver (macrovesicular fat deposition, peripheral displacement of nuclei) but occurs in patients with minimal or no alcohol history
pathophys of NAFLD
Can be due to increased transport of free fatty acids from adipose tissue to the liver, decreased oxidation of FFA in the liver, or decreased clearance of FFA from the liver (due to decreased VLDL production)
Frequently related to peripheral insulin resistance leading to increased peripheral lipolysis, triglyceride synthesis, and hepatic uptake of fatty acids
Hepatic FFA increases oxidative stress and production of proinflammatory cytokines (tumor necrosis factory alpha)
Acute erosive gastritis
Characterized by the development of severe hemorrhagic erosive lesions after exposure to gastric mucosa to various injurious agents or after a substantial reduction in blood flow
Aspirin decreases the protective prostaglandin production. In addition, aspirin and alcohol cause direct mucosal injury
Acute mucosal injury decreases the normal protective barriers (decreased levels of secreted mucins and bicarb and decreased integrity of the epithelium), thus permitting acid and other luminal substances (proteases and bile acids) to penetrate into the lamina propria, thereby causing additional injury to vasculature and subsequent hemorrhage.
Patients may manifest with hematemesis and abdominal pain
***NSAIDs and aspirin cause acute erosive gastritis and upper GI bleeding. Alcohol can make it worse. It is NOT the platelet dysfunction that NSAIDs cause. It is direct injury.
Etiologies of acute pancreatitis
1) Chronic alcohol use
2) Gallstones
3) Hyperlipidemia (types 1, 4, and 5)
4) Drugs (didanosine, azathioprine, valproic acid)
5) Infections (CMV, Legionella, Aspergillus)
6) Trauma
7) Iatrogenic (post-ERCP)
Clinical presentation of acute pancreatitis
Diagnosis requires 2 of the following
1) Acute epigastric abd pain often radiating to the back
2) Increased amylase, lipase (more than 3 times normal limit)
3) Abdominal imaging showing focal or diffuse pancreatic enlargement with heterogeneous enhancement with IV contrast (CT) or diffusely enlarged and hypoechoic pancreas (US)
Other findings
1) n/v, leukocytosis
2) Severe disease with possible abdominal tenderness, fever, tachypnea, hypoxemia and hypotension
3) ALT level above 150 - biliary pancreatitis
Complications of acute pancreatitis
1) Pleural effusion
2) Ileus
3) Pancreatic pseudocyst/abscess/necrosis
4) ARDS
Pathophys of acute pancreatitis
Early in pancreatitis, the pancreas synthesizes digestive enzymes but cannot secrete them. These enzymes leak out of the acinar cells into the systemic circulation.
Amylase rises within 6-12h of symptom onset and may remain elevated for 3-5 days.
Lipase rises within 4-8h of symptom onset but remains elevated longer than amylase (8-14d)
As a result, lipase is more useful and sensitive than amylase for dx (esp in alcoholics and patients presenting later in disease course)
When is imaging needed for acute pancreatitis
If diagnosis is unclear, or patient does not improve with conservative management (to ID infection or necrosis)
Once diagnosis is made, US can be done to find cause (gallstones)
Early ERCP for suspected biliary pancreatitis may decrease morbidity and mortality.
ERCP is also useful for evaluating patients with recurrent pancreatitis or draining pancreatic pseudocysts
Lab values consistent with Fe deficiency anemia
Low serum Fe and ferritin with high TIBC
New Fe def anemia in elderly patient
Should be considered to be from GI blood loss (polyps, cancer, angiodysplasia) until proven otherwise
A positive FOBT without lab values is enough to guide management to colonoscopy and endoscopy
A negative FOBT is not enough to rule out occult GI bleed.
Elderly patients with IDA should get colonoscopy and endoscopy despite a single negative FOBT, esp if no other obvious source of chronic blood loss is identified.
Isotope-labeled erythrocytes scintigraphy
Radioisotope scan that is useful in determining the source of active bleeding but not diagnostic in absence of active bleed
Typically used in acute (NOT chronic) GI blood loss when source of bleeding remains unidentified on colonoscopy and endoscopy
Clinical clues for common etiologies of cirrhosis (11)
More common
1) Chronic hepatitis B or C infections - IV drug use, blood transfusions, multiple sexual contacts
2) Alcoholic liver disease - excessive alcohol intake
3) Nonalcoholic fatty liver disease - Diabetes, obesity and/or metabolic syndrome
4) Hemochromatosis - FHx of cirrhosis; history of diabetes, bronze skin, high transferrin saturation
Less common
1) Autoimmune - FHx of cirrhosis, history of other coexisting autoimmune disorders (thyroiditis), anti-smooth muscle/liver kidney microsomal type 1 antibodies
2) PBC - more common in women, fatigue, pruritus, elevated alk phos, positive antimitochondrial antibody
3) PSC - Associated with IBD
4) Alpha 1 antitrypsin deficiency - coexisting lung involvement. FHx of cirrhosis
5) Cardiac cirrhosis - coexisting R-sided HF
6) Meds - Methotrexate, isoniazid
7) Wilson Disease - FHx of cirrhosis at young age, KF rings in eyes
Most likely cause of cirrhosis
Alcohol or hepatitis or NAFLD. Pick one of these 3 if the question is about “most likely” in USA
Mallory-Weiss tear
Etiology
1) Sudden increase in abdominal pressure (forceful retching, blunt abdominal trauma)
2) Mucosal tear in esophagus or stomach (submucosal arterial or venous plexus bleeding)
3) Risk - hiatal hernia, alcoholism***
Clinical
1) Vomiting, retching
2) Hematemesis
3) Epigastric pain
Dx
1) Longitudinal laceration on endoscopy near GEJ
Tx
1) Most heal spontaneously
2) Endoscopy therapy for persistent bleeding (electrocoagulation or local injection of epinephrine)
Toxic megacolon
Typically presents with total or segmental nonobstructive colonic dilation, severe bloody diarrhea and systemic findings (fever, tachy)
IBD patients are at the highest risk of developing it early in the disease, within 3 years of dx.
Other causes of toxic megacolon:
1) Ischemic colitis
2) Volvulus
3) Diverticulitis
4) Infections (C Dif)
5) Obstructive colon cancer (less common)
Dx is confirmed on plain abdominal XR and at least of the following:
1) Fever above 38C
2) Pulse over 120
3) WBC over 10,500
4) Anemia
May also see volume depletion, AMS, hypotension, lyte issues. Plain XR shows dilated Right or Transverse Colon (greater than 6cm), possible multiple air-fluid levels, and thick haustral markings that do not extend across the entire lumen
Tx - it’s an emergency! Can cause perforation. Give IV fluids, broad spectrum ABX, NG decompression, and bowel rest.
IV steroids are preferred for treating IBD-induced toxic megacolon
Emergency surgery (subtotal colectomy with end ileostomy as procedure of choice) may be needed if it does not resolve
D-xylose
monosccharide that can be absorbed in the proximal small intestine WITHOUT degradation by pancreatic or brush border enzymes
It is then excreted in the urine.
In the D-xylose test, patient is given an oral dose with subsequent assay of urine and venous blood.
Patients with proximal intestine mucosal disease (Celiac) cannot absorb D-xylose in the intestine, and urinary and venous D-xylose levels will be low. Fecal levels will be high.
Patients with malabsorption due to enzyme deficiencies (chronic pancreatitis) will have normal absorption of D-xylose.
False positive D-xylose test
False positive is decreased urinary excretion of xylose even though they have normal mucosal absorption.
Can be seen in patients with delayed gastric emptying or impaired glomerular filtration.
Small intestinal bacterial overgrowth (SIBO)
Characterized by alterations in the flora of the SI, usually due to abnormal intestinal anatomy or motility,
A false positive D-xylose test can be seen in SIBO due to bacterial fermentation of the ingested d-xylose dose before it can be absorbed.
Treatment with Rifaximin will improve this condition (if D-xylose is still positive on rifaximin, the prob is most likely Celiac)
Intestinal lactase deficiency
Causes diarrhea, abdominal pain, and flatulence after consuming milk or milk-containing products. Normal D-xylose.
Gallbladder stasis
Presence of proteins and fatty acids in the duodenum acts as a stimulus for release of CCK, which in turn stimulates the contraction of the gallbladder. In patients on TPN or prolonged fasting, the normal stimulus for CCK release and GB contraction is absent.
This leads to biliary stasis and promotes the formation of bile sludge and gallstones.
Small bowel (ileal) resection (or Crohn’s) also contributes to formation of gallstones via DECREASED enterohepatic circulation of bile acids that results in altered hepatic bile composition, which becomes supersaturated with cholesterol and promotes gallstone formation
Mechanism for gallstone formation during pregnancy and in women on OCPs
Estrogen-induced increase in cholesterol secretion.
Estrogen causes an increase in cholesterol secretion and progesterone causes a reduction in bile acid secretion, causing increased cholesterol saturation of bile.
Progesterone also slows GB emptying and facilitates formation of cholesterol gallstones.
Diffuse esophageal spasm
Pathophys - Uncoordinated, simultaneous contractions of esophageal body
Symptoms - intermittent Chest pain, dysphagia for solids and liquids
Dx - Esophagram shows “corkscrew pattern.” Manometry - intermittent peristalsis, multiple simultaneous contractions
Tx - CCBs. Alternative is nitrates or TCAs
Endoscopy is often normal.
Prinzmetal angina
Angina due to coronary artery spasm. Typical symptoms include episodic chest pain at rest. Patients may have normal ECG findings btw attacks, with variable ST abnormalities during acute events.
Dysphagia rules this out.
Globus sensation
Functional disorder of esophagus characterized by sensation of foreign body in throat. Often worse when swallowing saliva and is frequently associated with anxiety.
Pain, dysphagia, dysphonia or systemic symptoms are NOT TYPICAL and would suggest something else.
Shock Liver (Ischemic hepatic injury)
Occurs in setting of hypotension (septic shock, heart failure) and manifests as acute, massive increases in AST and ALT with milder associated increases in total bili and alk phos.
In patients who survive the inciting condition, liver enzymes typically return to normal within a few weeks.
Look for a patient who comes in in shock and develops massive liver enzyme elevations like a day later.
Unexplained leukocytosis in hospitalized patient
Should raise suspicion for C dif, even without diarrhea
Risk factors for C Diff
Recent hospitalization, advanced age, antibiotic use (fluoroquinolones, penicillins, cephalosporins, clindamycin)
Asymptomatic funguria
Common in patients with longstanding indwelling urinary catheters
Actual symptomatic fungal UTIs are rare. In cases of uncomplicated symptomatic fungal UTIs, antifungals arent needed.
Treatment of patient with suspected C Dif colitis
empiric metronidazole while awaiting stool studies
Most frequent sources for liver mets
GI malignancies like colorectal or pancreatic cancers since venous drainage is through the portal system directly to liver
Lung, breast, skin also spread to liver often.
Liver is common site for mets bc of its dual blood supply (systemic and portal) and hepatic sinusoidal fenestrations allow for easier met deposition
Management of hepatic encephalopathy
1) Supportive care (volume repletion [albumin] if needed, restraints if agitated, correct lytes)
2) Adequate nutrition without protein-restricted diet unless patient is unable to tolerate protein intake
3) Treat precipitating cause (GI bleed, hypovolemia, infection, lyte abnormalities)
4) Lower serum ammonia.
4a) Lactulose orally or enema if unable to take oral
4b) Rifaximin orally if no improvement in 48h with lactulose or unable to take lactulose
HE and K - whats the connection?
Hypokalemia increases renal ammonia production. Metabolic alkalosis (from intravascular volume depletion, poor oral intake) stimulates conversion of ammonium (can’t cross BBB) to ammonia (can cross BBB).
This is why patients with HE and hypoK require intravascular volume repletion (albumin) and K repletion.
Disaccharides (lactulose or lacitol) convert ammonia to ammonium (ammonia trap).
Burning, localized pain and regional hyperesthesia/allodynia in context of recent cancer treatment
Shingles - consider it when patients have regional pain and no conclusive evidence of disease in the local internal organs
Shingles
Can occur at any age. Most common after age 50. Risk goes up with age.
Frequently triggered by severe physical stress (cancer tx) or immunosuppressed states, but many cases are spontaneous
Reactivation of varicella zoster in DRG where it was dormant since last chickenpox infection
Pain may precede rash by several days
Post-herpetic neuralgia
Patients may develop persistent hypersensitivity of afferent pain fibers after shingles infection.
Tx of shingles
Antivirals (acyclovir, valacyclovir, famciclovir) in first few days of outbreak can shorten the duration of symptoms and decrease the risk of post-herpetic neuralgia
MEN syndromes
Type 1
1) Primary hyperparathyroidism (more than 90%)
2) Enteropancreatic tumors (60-70%)
3) Pituitary tumors (10-20%)
Type 2A
1) MTC (More than 90%)
2) Pheochromocytoma (40-50%)
3) Parathyroid hyperplasia (10-20%)
Type 2B
1) MTC
2) Pheo
3) Other - mucosal and intestinal neuromas, marfanoid habitus
Signs of liver mets
Abdominal pain, microcytic anemia, positive FOBT, and hepatomegaly with a hard edge
Moderate abnormalities in LFTs (high alk phos with mild elevations in AST and ALT) - this makes a liver injury less likely (more likely to be infiltrative or cholestatic in the case described)
Pleural effusion on Left (hepatic hydrothorax from cirrhosis is on the right usually)
Alcoholic cirrhosis on PE and Labs
Liver is often shrunken and edge is not palpable. AST usually greater than ALT by factor of 1.5-2
Underlying causes of oropharyngeal dysphasia
Presents with difficulty initiating swallowing due to inability to properly transfer food from mouth to pharynx
Etiologies include stroke, advanced dementia, oropharyngeal malignancy, neuromuscular disorders (MG)
Complications of oropharyngeal dysphagia
Coughing, choking, nasal regurgitation on swallowing.
Aspiration pneumonia and weight loss** (look for recurrent RLL pneumonias)
Initial evaluation in patient with oropharyngeal dysphagia
Videofluoroscopic modified barium swallow
Colon cancer screening in high risk patients
FHx of adenomatous polyps or CRC - 1st degree relative at age younger than 60
1) Colonoscopy at age 40 OR 10 years before the age of dx in the relative (whichever comes first)
2) Repeat every 3-5y
IBD - UC or Crohn
1) Begin 8 years post diagnosis (12-15 years if disease only in L colon)
2) Colonoscopy with biopsies every 1-2 years
Familial adenomatous polyposis
1) Begin at age 10-12
2) Colonoscopy every year
Hereditary nonpolyposis CRC (Lynch Syndrome)
1) Begin at age 20-25
2) Colonoscopy every 1-2 years
Management of gallstones
Gallstones without symptoms - No tx needed in most patients (only 20% of ASx gallstones will develop symptoms within 15y) - exception is patients at higher risk of developing gallbladder cancer (like if they have a porcelain gallbladder)
Gallstones with typical biliary colic symptoms - elective lap chole, possible ursodeoxycholic acid in poor surgical candidates
Complicated gallstone disease (acute cholecystitis, choledocholithiasis, gallstone pancreatitis) - chole within 72h
Overview of chronic pancreatitis
Etiology
1) ***Alcohol use (even prolonged use of socially acceptable amounts)
2) Cystic fibrosis (common in kids)
3) Ductal obstruction (malignancy, stones)
4) Autoimmune
Clinical presentation
1) Chronic epigastric pain with intermittent pain-free intervals
2) Malabsorption - steatorrhea, weight loss (from reduced exocrine function like less amylase, protease, lipase)
3) Diabetes mellitus
Lab results/imaging
1) Amylase/lipase can be normal and nondiagnositc
2) CT scan or MRCP can show calcifications, dilated ducts and enlarged pancreas
Tx
1) Pain management
2) Alcohol and smoking cessation
3) Frequent, small meals
4) Pancreatic enzyme supplements
What marker is elevated in pancreatic cancer?
CA 19-9
Chronic mesenteric ischemia
Can present with dull abdominal pain (usually after eating) and unintentional weight loss due to avoidance of food.
Mood cases due to atherosclerosis
Dx with mesenteric angiogram
Achalasia vs pseudoachalasia
Patient presents with dysphagia to solids and liquids and a dilated esophagus with smooth tapering of distal esophagus. Primary achalasia is loss of peristalsis in distal esophagus with lack of LES relaxation. Pseudo is due to esophageal cancer (narrowing of distal esophagus NOT due to denervation)
So what clues point you to pseudo?
1) Tobacco and alcohol use are major risk factors for esophageal cancer
2) Significant weight loss
3) rapid symptom onset (less than 6 months)
4) Presentation at age greater than 60
Moral of the story: In all patients with suspected achalasia, get an endoscopy to rule out malignancy
In primary achalasia, it is usually easy to pass scope through LES and scope will show normal mucosa and dilated esophagus
If endoscopy shows malignancy, do CT for staging
Tx for achalasia
Low surgical risk - Lap myotomy, pneumatic balloon dilatation
High surgical risk - BoTox, nitrates, CCBs
ONLY consider treatment after malignancy is excluded by endoscopy
Esophageal cancer
Subtypes
1) Adeno - distal esophagus, arises from Barret esophagus
2) SCC - anywhere in esophagus
Risk
1) Acid reflux, obesity, also smoking (adeno)
2) Smoking, alcohol, caustic injury (SCC)
Symptoms
1) CP
2) Weight loss
3) Dysphagia (solids)
Dx
1) Endoscopy with bx
2) CT (PET/CT) for staging
Dx of esophageal cancer
Young, low risk patients with undetermined esophageal symptoms may start with Barium esophagram
Those over 55 OR who have alarm symptoms (weight loss, gross or occult bleeding, early satiety) will usually go straight to endoscopy
