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Gastrointestinal > UWorld 2 > Flashcards

UWorld 2 Flashcards

1
Q

Which bilirubin is conjugated?

A

Direct

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2
Q

Evaluation of elevated alk phos

A

Indicates cholestasis. All patients (with or without hyperbillirubinemia) should be worked up with US to assess for intrahepatic or extrehepatic causes of biliary obstruction

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3
Q

postcholecystectomy syndrome

A

Persistant abdominal pain or dyspepsia (nausea) that occurs either postop (early) or months to years (late) after the procedure.

PCS can be due to biliary (retained common bile duct or cystic duct stone, biliary dyskinesia) or extra-biliary (pancreatitis, peptic ulcer disease, coronary artery disease) causes

Patients usually notice same pain they had before surgery, new pain just after surgery or the same pain that never went away.

Lab can show high alk phos, mildly abnormal LFTs and dilated common bile duct on abdominal US. These findings suggest common bile duct stones or biliary sphincter of Oddi dysfunction. Next step is endoscopic US, ERCP or MRCP for final dx and guiding therapy. Tx is aimed at causative factor

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4
Q

Pancreatitis and pleural effusion

A

Usually L side

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5
Q

Clinical features of acute diverticulitis

A

Clinical presentation

1) Abdominal pain (usually LLQ)
2) Fever, nausea and vomiting
3) Ileus (peritoneal irritation)

Diagnosis
1) Abdominal CT (oral and IV contrast)

Management

1) Bowel rest
2) Antibiotics (cipro, metronidazole)

Complications
1) Abscess, obstruction, fistula, perforation

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6
Q

Findings suggestive of diverticulitis

A

Diverticulitis is inflammation due to microperforation of a diverticulum. Chronic constipation and a low fiber/high fat diet are risk factors for diverticular disease

Some patients can present with urinary urgency or frequency due to bladder irritation from inflamed sigmoid colon.

Findings - pericolic fat, presence of diverticula, bowel wall thickening, soft tissue masses (phlegmons), pericolic fluid collections suggesting abscess

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7
Q

UC

A

Symptoms

1) Blood diarrhea
2) Weight loss, fever

Endoscopic findings

1) Erythema, friable mucosa
2) Psuedopolyps
3) Involvement of rectosigmoid
4) Continuous colonic involvement (no skip lesions)

Bx

1) Mucosal and submucosal inflammation (NOT transmural)
2) Crypt abscesses

Complications

1) Toxic megacolon
2) PSC (elevated alk phos in patient with UC should raise suspicion)
3) Colorectal cancer (requires screening)
4) Erythema nodosum, pyoderma gangrenosum
5) Spondyloarthritis
6) Uveitis

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8
Q

Perianal fistula - UC or Crohn?

A

Crohn

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9
Q

IBD and melanoma

A

Higher risk of melanoma

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10
Q

Features of Carcinoid Syndrome

A

Clinical

1) Skin - episodic flushing, telangiectasias, cyanosis
2) GI - diarrhea, cramping
3) Cardiac - valvular lesions (right more than left)
4) Pulm - Bronchospasm
5) Miscellaneous - niacin deficiency (dermatitis, diarrhea and dementia)

Dx

1) Elevated 24h urinary excretion of 5-HIAA
2) CT/MRI of abdomen of pelvis to localize tumor
3) OctreoScan to detect mets
4) Echo (if symptoms of carcinoid heart disease are present)

Tx

1) Octreotide for symptomatic patients and prior to surgery/anesthesia
2) Surgery for liver mets

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11
Q

Clinical features of IBS

A

Roma Diagnostic Criteria - Recurrent abdominal pain/discomfort at least 3 days per month for the past 3 months and at least 2 of the following:

1) Symptom improvement with bowel movement
2) Change in frequency of stool
3) Change in form of stool

Warning signs/symptoms - signs/symptoms suggesting etiologies other than IBS

1) Rectal bleeding
2) Nocturnal (awakens from or prevents sleep) or worsening abdominal pain
3) Weight loss
4) Abnormal labs (anemia and lyte disorders)

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12
Q

3 Ds of niacin deficiency

A

Dermatitis, Diarrhea and Dementia

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13
Q

Workup of IBS

A

IBS criteria without warning signs and no FHx of IBD or CRC doesnt require much workup. A colonoscopy would show normal colonic mucosa.

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14
Q

Chronic epigastric pain that suddenly worsens and becomes diffuse with a pneumoperitoneum

A

Concerning for likely perforated peptic ulcer disease

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15
Q

Common causes of ascites

A

Extraperitoneal causes

1) Cirrhosis (80% of USA cases) - alcoholic liver disease and hep C are most common causes of cirrhosis
2) Acute liver failure
3) Alcoholic hepatitis
4) Budd-Chiari
5) Heart failure
6) Hypoalbuminemia
7) Malnutrition
8) Nephrotic syndrome

Peritoneal causes

1) Malignancy (ovarian, pancreatic)
2) Infection (TB, fungal)

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16
Q

What should all patients with new-onset ascites receive?

A

Paracentesis to determine the cause

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17
Q

Clinical features of esophageal perforation

A

Etiology

1) Spontaneous rupture (Boerhaave)
2) Instrumentation (endoscopy)
3) Esophagitis (infectious/pills/caustic)
4) Esophageal ulcer

Clinical

1) Chest and abdominal pain, systemic findings (fever)
2) SubQ emphysema in the neck
3) Hamman sign (crunching sound on chest auscultation)

Dx

1) CXR or CT - Wide mediastinum, pneumomediastinum, pneumothorax, air around paraspinal muscles, pleural effusion (late)
2) CT - Esophageal wall thickening, mediastinal air fluid level
3) Water soluble contrast esophagogram - look at perforation site. If nondiagnostic, do barium (more inflammatory but more sensitive)

Management

1) ABx and supportive care for all patients
2) Surgical repair for significant leakage with systemic inflammatory response
* **Primary closure if perf is confirmed to avoid mediastinitis

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18
Q

Inflammatory diarrhea

A

Typical cause is idiopathic IBD.

Infectious causes are less likely if chronic (more than 4w)

Look for weight loss, anemia, elevated ESR and reactive thrombocytosis. Positive FOBT. Acute phase reactants in blood. Blood/leukocyte positive stool.

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19
Q

Secretory diarrhea

A

Usually from some medication use or hormonal disturbances

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20
Q

Osmotic diarrhea

A

Caused by ingestion of osmotically active, poorly absorbable substances. Lactose intolerance is a classic example

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21
Q

Motor diarrhea

A

Hyperthyroidism

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22
Q

All patients with chronic liver disease should receive what?

A

Vaccines against Hep A and Hep B

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23
Q

GI granulomas can be found in what conditions?

A

Crohn**, GI TB infection, sarcoidosis, Yersinia infection

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24
Q

Alarm symptoms regarding GERD

A

1) Melena
2) Persistent vomiting
3) Hematemesis
4) Weight loss
5) Anemia
6) Dysphagia/odynophagia

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25
Q

Lynch Syndrome

A

Hereditary NonPolyposis Colorectal cancer

Amsterdam Criteria 1:

1) At least 3 relatives with CRC, one of whom must be a first degree relative of the other two
2) Involvement of 2 or more generations
3) At least one case diagnosed before age 50
4) Familial adenomatous polyposis has been excluded

2 subgroups

1) Hereditary site specific colon cancer (Lynch 1)
2) Cancer family syndrome (Lynch 2) - really associated with more extracolonic tumors like endometrial* carcinoma, which develops in 43% of females in affected families.

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26
Q

Duodenal ulcer

A

Epigastric pain and intermittent melena. Pain is worse on empty stomach (due to unopposed gastric acid emptying into duodenum) and improves with food (due to alkaline fluid secretion into duodenum) - this is opposite of gastric ulcer pattern

Majority of DUs are caused by either H Pylori or NSAIDs. If there is no history of NSAID use look for H Pylori. Can be confirmed by endoscopic bx or urea breath test. Management of DU due to H Pylori:

1) Antisecretory therapy - preferably PPI AND
2) ABx eradication - amoxicillin plus clarithromycin

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27
Q

Dubin Johnson

A

Predominantly conjugated chronic hyperbilirubinemia that is NOT associated with hemolysis

Benign. More in Sephardic jews but can be in anyone.

Clinically, icterus is evident, though the physical exam is typically otherwise normal. Most patients are asymptomatic with some complaining of nonspecific issues (fatigue, ab pain, weakness). Icterus may be so mild as to only become evident in the context of a trigger such as illness, pregnancy, or OCP use

Routine labs are unremarkable, including CBC and LFTs. Bilirubin usually ranges 2-5 but can be normal or very high (20-25).

Urinary coproporphyrin studies. People with DJS have 80% Copro I whereas normal people have majority Copro III.

Grossly, liver is black. Histo it’s normal though, though dense pigment composed of epinephrine metabolites in lysosomes can be seen.

“That DJ has got some dark ass beats”

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28
Q

Dx of DJS

A

Conjugated hyperbilirubinemia with a direct bilirubin fraction of at least 50% and an otherwise normal liver function panel must be present.

Confirmation can be obtained by evaluating urinary coproporphyrin for unusually high Copro I

No tx required and prognosis is great

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29
Q

Rotor Syndrome

A

Benign condition in which there is a defect of hepatic storage of conjugated bilirubin, resulting in its leakage into the plasma

Chronic and mild hyperbilirubinemia of both conjugated and unconjugated forms then develops, without any sign of hemolysis

Liver function tests are normal. Pigmented granules are not seen in hepatocytes

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30
Q

Gilbert’s Syndrome

A

Occurs in patients with no apparent liver disease who have mild unconjugated hyperbilirubinemia thought to be provoked by one of the classic triggers (fasting, stress, illness)

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31
Q

Crigler-Najjar

A

Type 1 is more severe and often results in permanent neurologic impairment or death.

Very rare, autosomal recessive. Significant unconjugated hyperbilirubinemia.

Phototherapy or plasmapharesis are usually helpful in short term, but liver transplant is only curative option

32
Q

Red flags when evaluating minimal BRBPR

A

1) Change in bowel habits
2) Abdominal pain
3) Weight loss
4) Fe deficiency anemia
5) FHx of CRC

33
Q

Diverticulosis

A

Associated with chronic constipation. Usually ASx but potential complications include hemorrhage and diverticulitis.

Risk of complications is lower with high intake of fruit and vegetable fiber and higher with heavy meat consumption, aspirin, or NSAID use, obesity, and possibly smoking

34
Q

Young patient with chronic diarrhea, abdominal pain and weight loss

A

Always suspect Crohn Disease

35
Q

Most common causes of acute pancreatitis

A

1) Alcohol
2) Gallstone
3) Hypertriglyceridemia
4) Meds (Azathioprine, valproic acid, thiazides)
5) Infections (CMV)
6) Recent ERCP
7) Trauma

36
Q

How high do triglycerides need to be in order for it to be a legit cause of acute pancreatitis?

A

Over 1000. Look for eruptive xanthomas (yellow-red papules on arms and shoulders). These are due to subQ fat deposition and are associated with hypertriglyceridemia.

This high of a level though usually is due to familial hyperTG. So look for a younger patient or FHx of an early cardiac death.

Get a fasting lipid profile to check out this cause of pancreatitis.

37
Q

When should ERCP be considered in acute pancreatitis?

A

For biliary pancreatitis. These patients may have normal US. They usually have ALT above 150.

Also consider ERCP if patient has had more than 1 episode of acute pancreatitis of unknown cause

38
Q

Cancer risk in patient with FAP

A

100% without elective proctocolectomy

39
Q

Etiology of Acute Liver Failure

A

1) Viral hepatitis (HSV, CMV, Hep A, B, D, E)
2) Drug tox - acetaminophen OD and idiosyncratic
3) Ischemia - shock liver, Budd Chiari
4) Autoimmune hepatitis
5) Wilson Disease
6) Malignant infiltration

40
Q

Clinical pres for acute liver failure

A

1) Generalized symptoms (fatigue, lethargy, anorexia, nausea)
2) RUQ abdominal pain
3) Pruritus and jaundice due to hyperbilirubinemia
4) Renal insufficiency
5) Thrombocytopenia
6) Hypoglycemia

41
Q

Diagnostic requirements for acute liver failure

A

1) Severe acute liver injury (ALT and AST often above 1000) - often 10x normal
2) Signs of hepatic encephalopathy (confusion, asterixis)
3) Synthetic liver dysfunction (INR at least 1.5)

42
Q

Single most prognostic indicator in acute liver failure

A

PT

Patients who improve typically have decreasing transaminases, bilirubin and PT/INR

BUT, patients with rapidly worsening ALF can also have decreasing transaminases but with WORSENING PT/INR

Worsening PT/INR and bilirubin suggest worsening synthetic function.

43
Q

ALF definition

A

Acute onset of severe liver injury with encephalopathy and impaired synthetic function in a patient without cirrhosis or underlying liver disease

44
Q

Cirrhosis and binding proteins

A

Decreased synthesis of serum binding proteins for triiodothyronine (T3) and thyroxine (T4) such as thyroxine binding globulin, albumin and lipoproteins.

This lowers the TOTAL T3 and T4. Free T3 and T4 is usually unchanged as nearly all T3 and T4 is bound to the serum binding proteins.

45
Q

Adrenal insufficiency men vs women

A

May present with fatigue, weakness, anorexia and weight loss.

Androgen production occurs in adrenal glands in women. who can develop decreased axillary and pubic hair and loss of libido

Men lack these findings bc androgen production is in the testes.

46
Q

When do symptoms of duodenal ulcer classically occur?

A

Absence of food buffer (2-5h after meals, on an empty stomach or at night)

47
Q

PUD is one of the most common causes of what?

A

Melena (upper GI bleed above ligament of Treitz)

48
Q

Hepatorenal syndrome

A

One of the most dangerous complications of end stage liver disease. Occurs in up to 10% of patients with cirrhosis.

Characterized by decreased glomerular filtration in absence of shock, proteinuria, or other clear cause of renal dysfunction, and a failure to respond to a 1.5L normal saline bolus

Thought to be from renal vasoconstriction in response to decreased total renal blood flow and vasodilatory substance synthesis.

Type 1 - rapidly progressive. Most patients die within 10w without treatment

Type 2 - More slow. Average survival 3-6 months.

Most common causes of death are infection and hemorrhage.

No med is consistently helpful. Mortality for these patients placed on dialysis is very high. Liver transplant is only intervention with established benefit.

Kidneys of HRS patients are essentially normal on bx and renal function improves with liver transplant.

49
Q

Patient has features of cholestasis (impaired biliary flow) like fatigue, pruritus, and elevated alk phos. RUQ US shows evidence for intrahepatic cholestasis. Now what?

A

RUQ US helps distinguish intrahepatic (no biliary tract dilation) from extrahepatic (biliary tract dilation like due to gallstones) cholestasis.

If US suggests intrahepatic process the next step is to get serum anti-mitochondrial antibody titers which have high sensitivity for primary biliary cholangitis/cirrhosis (same thing, new name)

50
Q

PBC

A

chronic liver disease characterized by autoimmune destruction of the intrahepatic bile ducts with resulting cholestasis.

presents most commonly in middle aged women and is insidious in onset.

As disease progresses, jaundice, hepatomegaly, high alk phos, steatorrhea, and portal HTN may develop. Additional complications can include severe hyperlipidemia (with xanthelasma) and metabolic bone disease.

PBC is often associated with other autoimmune diseases like thyroid diseases.

51
Q

Autoimmune hepatitis antibody involved

A

Associated with elevated titers of ANA and anti-smooth muscle antibodies.

Characterized by fluctuating hepatocellular injury (elevated transaminases) rather than cholestasis

First line treatment is steroids

52
Q

Drugs associated with pancreatitis

A

Drug induced pancreatitis makes up 5% of acute pancreatitis.

1) Anti-seizure drugs (Valproic acid)
2) Drugs for IBD (sulfasalazine, 5-ASA)
3) Immunosuppressive agents (Azathioprine)
4) HIV related meds (didanosine, pentamidine)
5) ABx (metronidazole, tetracycline)
6) Diuretics (Furosemide, thiazides)

53
Q

Drug induced pancreatitis presentation

A

Usually mild. N/V, and abd pain radiating to back. Labs show elevated serum amylase and lipase. CT shows swelling of the pancreas with prominent peripancreatic fluid and fat stranding.

Supportive treatment with fluids and lyte replacement is recommended.

54
Q

Treatment for acute cholecystitis

A

Supportive care (nothing by mouth, IV ABx, analgesics)

Lap Chole is recommended shortly after hospitalization and should be performed immediately in cases of perforation or gangrene.

55
Q

HBsAg

A

The first serologic marker detected in the serum after inoculation.

It precedes the onset of clinical symptoms and elevation of serum aminotransferases.

Also remains detectable during entire symptomatic phase of acute hep B and suggests infectivity

56
Q

Anti-HBs

A

Appears in serum after either successful HBV vaccination or clearance of HBsAg, and remains detectable for life in most patients.

Indicates non-infectivity and immunity. However, there is a time lag btw the disappearance of HBsAg and the appearance of anti-HBs called the window period.

57
Q

HBcAg

A

This marker is not detectable in serum as it is normally sequestered within the HBsAg coat

58
Q

Anti-HBc

A

IgM appears shortly after the emergence of HBsAg and may be the only diagnostic marker for acute HBV infection during the window period.

IgG remains detectable during recovery from acute HBV infection or progression to chronic infection

59
Q

HBeAg

A

This antigen is detectable shortly after the appearance of HBsAg and indicates active viral replication/infectivity.

It is associated with presence of HBV DNA. HBeAg tends to disappear shortly after the aminotransferase levels peak and before HBsAg is eliminated. It is followed by appearance of anti-HBe

60
Q

Anti-HBe

A

Marker suggests cessation of active viral replication and low infectivity

61
Q

Early phase of Acute HBV

A

1) HBsAg positive
2) HBeAg positive
3) IgM anti-HBc positive
4) HBV DNA really positive

62
Q

Window phase of Acute HBV

A

1) IgM anti-HBc positive

2) HBV DNA positive

63
Q

Recovery phase of Acute HBV

A

1) IgG anti-HBc positive
2) Anti-HBs positive
3) Anti-HBe positive
4) HBV DNA likely positive

64
Q

Chronic HBV carrier

A

1) HBsAg positive

2) IgG Anti-HBc positive

65
Q

Acute flare of chronic HBV

A

1) HBsAg positive
2) HBeAg likely positive
3) IgM Anti-HBc positive
4) IgG Anti-HBc positive
5) HBV DNA positive

Only scenario where both IgM and IgG for HBc are positive

66
Q

Vaccinated for HBV

A

Anti-HBs positive

67
Q

Immune due to natural HBV infection

A

1) IgG anti-HBc positive

2) Anti-HBs positive

68
Q

Positive urine bilirubin assay

A

Reflects buildup of conjugated bilirubin

Note: Positive urine urobilinogen assay reflects buildup of unconjugated bilirubin (hemolysis for example)

69
Q

Why does too much conjugated bilirubin cause a positive urine bilirubin assay?

A

Conjugated bili (loosely bound to albumin - unconjugated is tightly bound) is water soluble so it can be excreted in urine. Normally bili doesnt make it to the urine though bc the intestines usually degrades it all.

If there is hepatic dysfunction though, or biliary obstruction or a defect in hepatic bilirubin secretion there is plasma buildup of conjugated bilirubin which leaks into the urine, making it dark and causing a positive urine bilirubin assay

70
Q

Pancreatic adenocarcinoma

A

Risk factors

1) Smoking
2) Hereditary pancreatitis
3) Nonhereditary chronic pancreatitis
4) Obesity and lack of physical activity

Clinical presentation

1) Systemic symptoms (weight loss, anorexia)
2) Abdominal pain/back pain (80%)
3) Jaundice (56%)
4) Recent onset atypical diabetes mellitus
5) Unexplained migratory superficial thrombophlebitis*
6) Hepatomegaly and ascites with mets

Labs

1) Cholestasis (increased alk phos and direct bilirubin)
2) Increased CA 19-9 (not as screening tho)
3) Abdominal US (if jaundice) or CT (if no jaundice)

71
Q

Cancers of head vs tail of pancreas

A

1) Cancers of the head of the pancreas (60-70%) typically present with jaundice (common bile duct obstruction, elevated alk phos and bilirubin) and steatorrhea (pancreatic exocrine insufficiency or pancreatic duct blockage). In patients with these findings, US is preferred for detecting pancreatic head tumors excluding other potential causes of biliary obstruction (choledocholithiasis)
2) Cancers in the body and tail usually do not present with obstructive jaundice. Abdominal CT scan is preferred (more sensitive and specific) and helps exclude other conditions. US is less sensitive for visualizing the pancreatic body and tail due to overlaying bowel gas and for detecting smaller tumors (less than 3cm)

72
Q

Patients with upper GI bleeding and depressed level of consciousness should receive what treatment?

A

Intubate! protect airway as part of initial stabilization and resuscitation.

73
Q

Dx of lactose intolerance

A

1) Positive hydrogen breath test - rise in measured breath H after ingestion of lactose, thus indicating bacterial carb metabolism
2) Positive stool test for reducing substances
3) Low stool pH - due to fermentation products
4) Increased stool osmotic gap

No steatorrhea

74
Q

Lactose intolerance and calculating the stool osmotic gap

A

Osmotic gap is 290 - 2(stool Na plus stool K).

Greater than 50 in all forms of osmotic diarrhea, including lactose intolerance

75
Q

Acalculous cholecystitis

A

Acute inflammation of gallbladder without gallstones most commonly seen in hospitalized and severely ill patients

Risk factors

1) Severe trauma, extensive burns, recent surgery (cardiopulmonary, aortic, abdominal)
2) Prolonged fasting or TPN
3) Critical illness (sepsis, ICU, mechanical vent)

Clinical presentation

1) Unexplained fever, vague/RUQ ab discomfort, leukocytosis
2) Possible jaundice, RUQ mass, abnormal LFTs

Dx

1) Ab US (preferred)
2) Cholescintigraphy (HIDA) or abdominal CT if US is not diagnostic

76
Q

RUQ pain following serious serious

A

Keep acalculous cholecystitis in mind.

Gastrointestinal (4 decks)

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