UWorld 3 Flashcards
Medication-induced esophagitis
1) ABx - tetracyclines
2) Anti-inflammatory agents - Aspirin and many NSAIDs
3) Bisphosphonates - Alendronate, risedronate
4) Others - Potassium chloride, Iron
Pill esophagitis pathophys
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
Pill esophagitis presentation
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
Endoscopy in candida and herpes esophagitis
Candida - white plaques
Herpes - Ulcerating lesions that are vesicles and round/ovoid ulcers
CMV - Large linear ulcers
All of these are in the immunocompromised
Patient with cirrhosis and ascites accompanied by either fever or mental status change.
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.
Secretin stimulation test
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)
Calcium infusion study
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
Upper GI bleed effects on renal function
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
When is Alk Phos high?
Biliary obstruction and skeletal disease with increased osteoblast activity (Paget)
Mild elevations can be seen in IBD or intra-abdominal infections
When is prolonged PT seen?
Warfarin, vit K deficiency, certain hered coagulation disorders, ABx use and liver disease
Urine sodium (or FENa) in a patient who is volume depleted
Low since kidney tries to keep Na to restore circulatory volume.
FENa is high in intrinsic renal disease
Imaging of choice in suspected pancreatitis
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
Stool elastase
Marker for pancreatic exocrine function. Low levels are seen in chronic pancreatitis. Not acute.
Acute cholangitis
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
NSAIDs and anemia
NSAIDs are common cause of Fe deficiency anemia, esp in elderly who may have low grade chronic anemia at baseline
How long does GERD usually take to cause adenocarcinoma?
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.
Esophageal stricture
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).
Episodic painless GI bleeding
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.
Clinical features of colovesical fistula
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
Pellagra
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.
Clinical presentation of severe pancreatitis
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
What is associated with higher risk of severe pancreatitis
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
Complications of severe pancreatitis
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)
What is severe pancreatitis?
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
How drugs/toxins cause liver injury (and which ones)?
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
What kind of liver injury do tetracycline, valproate and antiretrovirals cause?
Fatty liver
Isoniazid, phenytoin, halothane, alpha-methyldopa all cause what kind of drug damage to the liver?
Hepatitis (just like viral hepatitis pattern)
What meds cause cholestasis pattern of liver injury?
Chlorpromazine, nitrofurantoin, erythromycin, anabolic steroids
What meds cause toxic or fulminant liver failure?
CCl4, acetaminophen
What meds cause granulomatous liver injury?
Allopurinol and phenylbutazone
Pancreatic pseudocyst
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)
Diagnostic test of choice for ZD
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
Pleural fluid analysis in Boerhaave
Exudative with low pH and very high amylase (over 2500)
Tx for Boerhaave
Surgery - for thoracic perfs
Conservative (ABx) for cervical perfs
Fictitious diarrhea
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
Clinical features of alcoholic hepatitis
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
History of anticoagulation, symptoms of weakness and dizziness and evidence of anemia and tachycardia
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
pRBC transfusion thresholds
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
FFP
contains all clotting factors and plasma proteins from one unit of blood.
Usually indicated for severe coagulopathy (liver disease, DIC) with active bleeding.
Platelet transfusion threshold
Usually less than 10k. Less than 50k with active bleeding
Whole blood transfusion
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
Whipple’s Disease
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
Evaluating ASx elevation of aminotransferases
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
Where are AST and ALT located?
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.
Patient with small, nonbleeding varices
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
Vanishing Bile Duct Syndrome
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
Treatment of Ascites
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)
Zn deficiency
May result from chronic TPN or malabsoprtion. Symptoms include alopecia, skin lesions, abnormal taste, and impaired wound healing.
Selenium deficiency
Also may result from TPN, malabsorption or malnutrition (nuts, meat, fish).
Most important feature is cardiomyopathy
Small Intestinal Bacterial Overgrowth
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)
Gilbert’s Syndrome
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
MALT lymphoma
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
Chronic mesenteric ischemia
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
Hepatic hydrothorax cause and tx
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
Dyspepsia
Epigastric fullness or discomfort after eating. Often associated with nausea and symptoms of GERD like heartburn
Alarm symptoms with dyspepsia
Weight loss, gross or occult bleeding, anemia, dysphagia, persistent vomiting, or early satiety
Abdominal succussion splash
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
Most common cause of gross lower GI bleeding in adults
Diverticulosis
Alcoholic hepatitis lab markers
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.
Acute pancreatitis from cholesterol emboli
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)
Porcelain gallbladder
Requires chole bc of increased risk of gallblader adenocarcinoma (2-5%).
Calcified rim in GB wall with a central bile filled dark area
Spider angioma and palmar erythema pathogen
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
Caput medusae pathogen
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
Dupuytren contracture pathogen
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
Lower extremity edema pathogen in cirrhosis
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.
Colon cancers and polyps
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
Neutrophilic cryptitis - UC or Crohn’s?
Both. In Crohn’s, it’s transmural though. Remember IBD has bimodal age distribution so old people can get it too.
