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Family Medicine EOR > GI-/nutritional 11% > Flashcards

GI-/nutritional 11% Flashcards

1
Q

Tearing rectal pain and bleeding which occurs with or shortly after defecation, bright red blood on toilet paper

A

Anal fissure

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2
Q

Treatment for anal fissure

A

Sitz baths, increase dietary fiber, and water intake, stool softeners or laxatives

Usually heals in 6 weeks

Botulinum toxin A injection (if failed conservative treatment)

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3
Q

What are the 4 cardinal signs of strangulated bowel?

A 
The 4 cardinal signs of strangulated bowel: 
fever, 
tachycardia, 
leukocytosis, and 
localized abdominal tenderness.
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4
Q

Presents with: diffuse abdominal pain, nausea, and several episodes of emesis

He has not had any flatus for at least 2 days

He has a midline abdominal scar and a right subcostal scar

ABD X-ray: air fluid level

A

Small bowel obstruction

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5
Q

Diagnostics of small bowel obstruction

A

Abdominal series

CT Abdominal and pelvis

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6
Q

What is Treatment for SBO?

A

1st
Patients with SBO are often significantly dehydrated. Aggressive fluid resuscitation (with an isotonic intravenous fluid such as normal saline) and electrolyte repletion. + NGT

  1. Complete obstruction: 12-24 hr NPO
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7
Q

SBO with signs of bowel ischemia/peritonitis?

A

SURGICAL EMERGENCY

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8
Q

Gradually increasing abdominal pain with longer intervals between episodes of pain,

abdominal distention, obstipation,

less vomiting (feculent),

more common in the elderly

A

LARGE BOWEL OBSTRUCTION

FEBRILE + TACHYCARDIA –> SHOCK

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9
Q

MCC of large bowel obstruction

A 
CANCER
stricture
hernia
volvulus 
Fecal impaction
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10
Q

KUB shows dilated loops of bowel with air-fluid levels with little or no gas in the colon is what?

A

Large bowel obstruction

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11
Q

Physical exam finding of LBO?

A

Look for vomiting of partially digested food, severe abdominal distensions and high pitched hyperactive bowel sounds progressing to silent bowel sounds.

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12
Q

The initial diagnosis of cholelithiasis is best made with what imaging technique?

A

US

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13
Q

stones in the gallbladder (i.e., gallstones) without inflammation

A

Cholelithiasis

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14
Q

CARDINAL SYMPTOM OF GALLSTONES DUE TO TEMPORARY OBSTRUCTION OF CYSTIC DUCT

A

biliary colic

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15
Q

Complications of cholelithiasis

A

CHOLECYSTITIS : cystic duct obstruction by gallstones

CHOLEDOCOLITHIASIS:
gallstones in the biliary tree – associated with ductal dilation and biliary colic or jaundice. Treat with stone extraction via ERCP

CHOLANGITIS
biliary tract INFECTION secondary to obstruction by gallstones. Diagnose with ERCP

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16
Q 
Abrupt RUQ pain
constant 
slowly resolves 
20min- hrs 
nausea 
precipitated by fatty foods and large meals
A

BIliary colic

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17
Q

Right subscapular pain of biliary colic is known as?

A

BOAS SIGN

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18
Q

As ALK-P is not specific to liver what is it also elevated in?

A

Bone, gut and placenta

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19
Q

ELEVATED ALK-P with GGT

A

Obstruction to bile flow (cholestasis) in any part of biliary tree

IF normal makes cholestasis unlikely

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20
Q

What are some of the causes of DECREASED ALBUMIN

A

1st - Chronic liver disease

    • Nephrotic syndrome
  2. -Malnutrition
    - inflammatory state (Burn, sepsis, trauma)
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21
Q

When is PT prolonged?

A

PT is not prolonged until most of the liver’s synthetic capacity is lost, which corresponds to advanced liver disease.

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22
Q

Asx cholelithiasis aka Biliary colic TX

A

observe

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23
Q

symptomatic patients with cholelithiasis Tx?

A

Cholecystectomy

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24
Q

What does

4Fs represent?

A

Fat, Forty, Female, Fertile

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25
Q

What are Gallstones have been classified into all of the following

A

Cholesterol
Pigment
mixed

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26
Q

Which antibiotic is a major cause of biliary sludge?

A

Ceftriaxone is a major cause of biliary sludge. The mechanism of biliary sludge formation during ceftriaxone therapy appears to be the propensity of ceftriaxone to bind calcium and form insoluble crystals in bile in the gallbladder, resulting in biliary sludge or frank stones

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27
Q

Inflammation of the gallbladder; usually associated with gallstones

RUQ pain after a high-fat meal
Low-grade fever, leukocytosis, JAUNDICE

A

cholecystitis

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28
Q

What is the most specific test for acute cholecystitis?

A

HIDA SCAN

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29
Q

Chronic cholecystitis may lead to

A

porcelain GB (premalignant condition)

Patients with chronic cholecystitis rarely have abnormal laboratory studies

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30
Q

Which of the following signs is associated with acute cholecystitis?

A

Murphy’s sign

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31
Q

Prophylactic cholecystectomy for asymptomatic cholelithiasis is generally

A

not recommended

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32
Q

Ultrasound findings that suggest acute cholecystitis are

A

pericholecystic fluid, gallbladder thickening, and sonographic Murphy sign. CT scan and MRI is more sensitive in diagnosis of choledocholithiasis

The HIDA scan is expensive and reserved for cases in which the ultrasound study or CT scan is nondiagnostic but there is a high suspicion of cholecystitis.

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33
Q

WHAT ARE THE COMPLICATIONS OF GALLSTONES?

A

Acute cholecystitis

Hydrops of gallbladder

Gastric outlet obstruction

Acute biliary pancreatitis

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34
Q

A patient with cirrhosis develops acute hepatic encephalopathy. Initial pharmacologic treatment of this disorder consists of which of the following?

Asterixis (flapping tremor), dysarthria, delirium, coma

A

Lactulose

as it binds to ammonia in GI tract and comes out as diarrhea

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35
Q

What is late sign of hepatic fibrosis?

A

Cirrhosis

Characterized by regenerative nodules surrounded by dense fibrotic tissue
The liver unable to regenerate due to large amounts of scar tissue

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36
Q

most common cause of cirrhosis

A

Chronic hepatitis

Other causes:
Chronic HEP C
ALCOHOL ABUSE

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37
Q

↑ Copper, ↓ Ceruloplasmin + family history

A

Wilsons disease

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38
Q

spider angiomata, palmar erythema, jaundice, scleral icterus, ecchymoses, caput medusae, hyperpigmentation

A

Cirrhosis

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39
Q

α-fetoprotein level at diagnosis to screen for

A

hepatocellular carcinoma

Screen every 6 months with US

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40
Q

why All patients with cirrhosis should undergo esophagogastroduodenoscopy (EGD)

A

to rule out esophageal varices

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41
Q

best follow-up test for HCC if α-fetoprotein elevated and/or liver mass found on ultrasound

A

MRI

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42
Q

Fever and abdominal pain in a patient with cirrhosis think

A

SBP

Dx: with cell count of ascites fluid

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43
Q

triad of abdominal pain, ascites, and hepatomegaly

A

Budd Chiari (hepatic vein thrombosis)

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44
Q

GOLD STANDARD and is often required for definitive diagnosis of cirrhosis

A

Liver Biopsy

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45
Q

Typically AST > ALT. Enzymes normalize as cirrhosis progresses

↑ ALP and ↑ GGT

Anemia from hemolysis, folate deficiency, and splenomegaly

Decreased platelet count from portal hypertension with splenomegaly

Decreased bilirubin conjugation by the liver ⇒ ↑ unconjugated bilirubin ⇒ jaundice

Decreased albumin production by the liver ⇒ hypoalbuminemia

Decreased clotting factor production by the liver ⇒ Prolonged prothrombin (PT),

A

Liver cirrhosis

Ultrasound: helpful to determine liver size and evaluate for hepatocellular carcinoma

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46
Q
  1. Treatment for Cirrhosis?
  2. How to treat autoimmune hepatitis?
  3. how to Tx Wilson’s disease?
  4. How to treat DECOMPENSATION related to cirrhosis?
  5. What is the primary prophylaxis against variceal related hemorrhage?
  6. what is the treatment for encephalopathy?
  7. How to reduce ascites?
  8. Medication to treat pruritus related to uremia or cirrhosis?
A
  1. cirrhosis is irreversible
    - –Stop alcohol
    - –Antiviral treatment for Hepatitis C
    - –For advanced cirrhosis ⇒ liver transplant may be necessary
  2. Corticosteroids for autoimmune hepatitis
  3. Chelation therapy (e.g. penicillamine) for WILSONS Dz
  4. Diuretics, antibiotics, laxatives, enemas, thiamine, steroids, acetylcysteine, pentoxifylline for DECOMPENSATION
  5. Nonselective BB (nadolol and propranolol) for primary prophylaxis against
    - -variceal hemorrhage or ——–esophageal variceal ligation (EVL)
  6. Encephalopathy ⇒ lactulose + neomycin or Rifaximin
  7. ASCITES ⇒
    sodium restriction, paracentesis, spironolactone, lasix
  8. PRURITUS: ⇒ cholestyramine (QUESTRAN)
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47
Q

Polyps in the distal colon are commonly benign if seen in the proximal colon they are more likely

A

CANCEROUS

Villous adenomas have a 30-70% risk of malignant transformation

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48
Q

The most common cause of painless rectal bleeding in the pediatric population

A

polyp

Once identified follow-up colonoscopy in 3-5 years

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49
Q

development of hundreds to thousands of colonic adenomatous polyps

A

Familial adenomatous polyposis (FAP)

Autosomal dominant

Risk of colorectal cancer 100% by 30-40 years of age

The family should undergo yearly sigmoidoscopy beginning at 12 years of age

Prophylactic colectomy recommended

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50
Q

Painless rectal bleeding and a change in bowel habits in a patient 50-80 years of age

A

COLON CANCER

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51
Q

Apple core lesion on barium enema

A

ADENOMA MC

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52
Q

Screening with colonoscopy begins at 50 then every 10 years until

A

75

Fecal occult blood testing – annually after age 50

Flexible sigmoidoscopy – every 5 years with FOB testing

Colonoscopy – every 10 years

CT colonography – every 5 years

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53
Q

More likely to be malignant

A

sessile, > 1 cm, villous

Tumor Marker: CEA

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54
Q

Less likely to be malignant colon cancer

A

Pedunculated, < 1 cm, tubular

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55
Q

Patients who are older than 50 with new-onset constipation should be evaluated for

A

Colon cancer

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56
Q

laxatives? 3

A

Bulk-forming laxatives first line — Bulk-forming laxatives include psyllium seed (eg, Metamucil), methylcellulose (eg, Citrucel), calcium polycarbophil (eg, FiberCon®), and wheat dextrin (eg, Benefiber)

Osmotic laxatives can be used in patients not responding satisfactorily to bulking agents. Start with low-dose polyethylene glycol (PEG) as it has been demonstrated to be efficacious and well-tolerated in older adults.

Stimulant laxatives — Stimulant laxatives affect electrolyte transport across the intestinal mucosa and enhance colonic transport and motility.

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57
Q

The most common cause of acute diarrhea

Hypokalemia and metabolic acidosis

A

Diarrhea breakout in a daycare center: Rotavirus

Diarrhea on a Cruise Ship: Norovirus

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58
Q

Traveler’s diarrhea:

Prophylaxis:

FQ

A

E coli

Occurs in the first 2 weeks of travel, lasts 4 days without treatment
Defined as: 3+ unformed stools in 24 h with at least one of the following: fever, nausea, vomiting, abdominal cramps, tenesmus, bloody stools
Complications: Dehydration (MC), Guillain-Barre, Reiter syndrome

TX: Empiric treatment with ciprofloxacin 500 mg BID × 1-3 d and loperamide (if older than 2 y)

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59
Q

1.Diarrhea after a picnic and egg salad:

2Diarrhea from shellfish

  1. Diarrhea from poultry or pork
  2. Diarrhea in a patient post antibiotics
  3. Diarrhea in poorly canned home foods
A

1.Staph. A

2.Vibrio cholerae
Tx:

  1. Salmonella
    Tx: Ceftriaxone and sometimes a fluoroquinolone or azithromycin
  2. C. diff
  3. C. perfringens
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60
Q

Diarrhea after drinking (not so) fresh mountain stream water

Dx:

Tx:

A

Giardia lamblia - incubates for 1-3 weeks,
causes foul-smelling bulky stool and
wax and wane over weeks before resolving

Dx: stool cyst or trophozoites

Tx: Tinidazole
OR
flagyl

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61
Q

a flu-like bacterial infection characterized by fever, GI symptoms, and headache

Transmitted via the consumption of fecally contaminated food or water
GI symptoms may be marked constipation or “pea soup diarrhea”
Rose spots may be present (2-3 mm papule on trunk usually)
More common in the developing world (usually immigration cases)

A
  • Enteric fever (salmonella typhi):

TX:
Ceftriaxone and sometimes a fluoroquinolone or azithromycin
No treatment except in immunocompromised or enteric fever (S. typhi)

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62
Q

predominantly affects children

and is often spread in areas with crowded conditions (like daycare centers)

Abdominal pain + inflammatory diarrhea (small volume) frequent, mucous and bloody stool,😡
nausea, vomiting (less common), possible fever

A

Shigellosis

Tx: TMP-SMX
Alternative:
Cipro/FQ

Drugs to stop diarrhea (such as diphenoxylate or loperamide) may prolong the infection and should not be used

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63
Q

Consumption of undercooked ground beef Shiga-like toxin

Watery, voluminous, nonbloody diarrhea with nausea and vomiting→ Dysentery (bloody)

No fecal leukocytes

A

Enterohemorrhagic E. coli (EHEC

Antibiotics not recommended, except in severe disease

Complication: Hemolytic uremic syndrome (AKI, thrombocytopenia, hemolytic anemia)

64
Q

Causes a life-threatening, rice water diarrhea

The organism is typically found in seafood - Consumption of contaminated, locally harvested shellfish

A

CHOLERA

Treated with both glucose and Na rich electrolyte fluids
Doxycycline

65
Q

What is the main risk factor for esophagitis?

A

Immunocompromised

66
Q

An endoscopy for presumed esophagitis shows multiple shallow ulcers. What is the most likely diagnosis?

Tx?

A

Herpes simplex virus

Tx: Acyclovir

67
Q

odynophagia (pain while swallowing food or liquids) is the hallmark sign of?

A

INFECTIVE ESOPHAGITIS

This occurs mainly in patients with impaired host defenses. Primary agents include Candida albicans, herpes simplex virus, and cytomegalovirus. Symptoms are odynophagia and chest pain

68
Q

linear yellow-white plaques with odynophagia or pain on swallowing

TX?.

A

Candida

Fluconazole 100mg PO QD

69
Q

large solitary ulcers or erosions on EGD,

TX?

A

Ganciclovir

70
Q

mechanical or functional abnormality of the LES

A

Reflux esophagitis:

71
Q

Patient with asthma symptoms + GERD not responsive to antacids

impaction (food being stuck at the lower end of the esophagus)

barium swallow will show a ribbed esophagus and multiple corrugated rings

TX?

A

Eosinophilic esophagitis

treat by removing foods that incite allergic response, topical steroids via inhaler

72
Q

What medications x2 can cause esophagitis? or gastritis?

A

NSAIDS or bisphosphonates

73
Q

Dysphagia lasting weeks-months after therapy

Radiation exposure of 5000 cGy associated with increased risk for stricture

A

Radiation: radiosensitizing drugs include doxorubicin, bleomycin, cyclophosphamide, cisplatin

74
Q

Ingestion of alkali or acid from attempted suicide

A

Corrosive esophagitis
Tx:
Steroids

75
Q

Dyspepsia (belching, bloating, distension, and heartburn) and abdominal pain are common indicators of gastritis
Three causes:

A

Gastritis: inflammation of the stomach lining

H.pylori

Inflammation: (NSAID and ALCOHOL)
–NSAIDs: cause gastric injury by diminishing local prostaglandin production in the stomach and duodenum

– Alcohol: a leading cause of gastritis

Autoimmune or hypersensitivity

76
Q

Gram-negative spiral-shaped bacillus

A

H. pylori

77
Q

most sensitive and specific for detection of Helicobacter infections?

correct combination for triple therapy ?

A

endoscopic biopsy with histologic examination

In the office setting, stool examination for H. pylori antigen

–C.-A.-P.
Clarithromycin + amoxicillin + PPI

78
Q

disorders is most likely a side effect associated with proton pump inhibitors (PPIs)?

–3
At risk for?

Electrolyte issue and vitamin

Infection

A

Hip fracture
Proton pump inhibitors may promote hypochlorhydria and interfere with absorption of calcium, leading to increased frequency of hip fracture

LOW B-12 and MAg.

pneumonia
(Decreased gastric acid production may also allow for bacterial overgrowth and is associated with increased risk of respiratory infections such as pneumonia. PPIs have also been associated with C.diff associated diarrhea.)

79
Q

Pernicious anemia: + schilling test + ↓ intrinsic factor and parietal cell antibodies

A

PErnicious anemia

80
Q

1st line TX gastritis?

A

stop NSAIDs, empiric therapy with acid suppression 4-8 wk of PPI

If no response, consider upper GI endoscopy with biopsy and ultrasound

81
Q

H.pylori TX?

A

treat with (CAP) – clarithromycin + amoxicillin +/- metronidazole + PPI (i.e. Omeprazole)

Quadruple therapy (PPI, Pepto, and 2 antibiotics) for one week

82
Q

GERD

the test of choice but not necessary for typical uncomplicated cases
Indicated if refractory to treatment or is accompanied by dysphagia, odynophagia, or GI bleeding

gold standard for diagnosis (but usually unnecessary)

A

Endoscopy w/ bx

pH Probe

83
Q

GERD Treatment
Mild
Severe

Complications?

A

Lifestyle:H2 receptor blockers, proton pump inhibitors, diet modification (avoid fatty foods, coffee, alcohol, orange juice, chocolate; avoid large meals before bedtime); sleep with trunk of body elevated; stop smoking

Nissen fundoplication

Barrett’s esophagus

84
Q

What to do if Barrett’s esophagus?

A

Once Barrett’s esophagus has been identified, screening every 3 to 5 years by upper endoscopy is recommended to look for dysplasia or adenocarcinoma.

85
Q

Patients with foul odor of the breath and increasing symptoms think

A

Zenker’s Diverticulum which is an outpouching of hypopharynx resulting in regurgitation of solid foods – needs surgical repair.

86
Q

Melena

A

Upper GI bleed

87
Q

Upper abdominal pain

Worse with meals

Better w/ meals –>

Dx: upper endoscopy

Bx for H.pylori
all ulcers with malignant features should be biopsied

In patients with active bleeding, a negative biopsy result does not exclude H. pylori. get breath test or stool antigen

Tx

A

PUD MC UPper GI bleed cause:

–>gastric ulcer
It is most commonly found at the lesser curvature of the antrum

Duodenal 
Duodenal ulcer (food classically decreases pain think Duodenum = Decreased pain with food)

Treatment for H.Pylori: PPI + Amoxicillin 1g PO BID + Metronidazole or Clarithromycin 500 mg PO BID
Think Baseball “CAP” = Clarithromycin + Amoxicillin + PPI

88
Q

Odynophagia, gastroesophageal reflux, dysphagia

Dx.

A

esophageal ulcer
Esophagitis

endoscopy

89
Q

What is a risk factor for an increased incidence of duodenal and gastric ulcers, as well as a decrease in rate of healing?

A

smoking

90
Q

gastrinoma; tumor of the pancreas that causes the stomach to produce too much gastrin with subsequent acid secretion leading to ulcer formation. Diagnosed with gastrin levels >200 pg/mL)

A

Zollinger - Ellison syndrome

PPI and resect the tumor

91
Q

Emesis, retching, or coughing prior to hematemesis

A

Mallory weiss tear
is a linear mucosal tear in the esophagus at the gastroesophageal junction

MCC alcohol

Dx:upper endoscopy

Tx: self limiting

92
Q

Jaundice, abdominal distention (ascites)

A

Variceal hemorrhage or portal hypertensive gastropathy

93
Q

Dysphagia, early satiety, involuntary weight loss, cachexia

A

Malignancy

H. Pylori is the most important risk factor

Treat with gastrectomy, radiation therapy and chemotherapy

94
Q

Describe the mnemonic WEAPON for gastric cancer

A

WEAPON”: Weight loss, Emesis, Anorexia, Pain/epigastric discomfort, Obstruction, Nausea

95
Q

What are the most common early symptoms? What is the most common symptom?

A

The most common early symptoms are mild epigastric discomfort and indigestion. The most common symptom is weight loss.

96
Q

Which side is the supraclavicular lymph node involvement in gastric cancer?

A

The left side! Virchow’s node (left supraclavicular) is associated often with gastric cancer. The RIGHT supraclavicular node is associated with Hodgkins lymphoma, as the right node drains the mediastinum and it is common for HL to originate in the mediastinum.

97
Q

Metastatic signs include

A

Virchow’s node (Supraclavicular)

Sister Mary Joseph’s node (Umbilical)

98
Q

Hematochezia: bright red blood per rectum (BRBPR)

A

lower GI bleed

Diverticulosis is generally an incidental finding since diverticular bleeding is usually of greater volume. MCC

99
Q

rectal bleeding and abdominal pain

A

Proctitis

100
Q

painless rectal bleeding, no red flag signs

A

Polyp

101
Q

Painless rectal bleeding and a change in bowel habits in a patient 50-80 years of age

A

Colorectal cancer:

102
Q

What is the most common site of an anal fissure?

A

Posterior midline

are believed to result from laceration by a hard or large stool or from frequent loose bowel movements

103
Q

anal fissure tx

accronym
WASH

A

topical vasodilators (nifedipine or nitroglycerin) for one month
W arm sitz baths
A nalgesics: 2% lidocaine jelly
S tool softeners (Colace)
H igh Fiber: the recommended dietary fiber intake is between 20 and 35 grams per day

Second-line therapy

Topical Ca channel blocker

104
Q

treatment option following failure of conservative treatment for anal fissure?

A

Lateral anal sphincterotomy

Cisapride is a prokinetic agent. It’s not used in the treatment of anal fissure.

105
Q

a 67-year-old man with a long history of constipation presents with steady left lower quadrant pain. Physical exam reveals low-grade fever, mid-abdominal distention, and lower left quadrant tenderness. Stool guaiac is negative. An absolute neutrophilic leukocytosis and a shift to the left are noted on the CBC.

A

Diverticulitis

is defined as inflammation of the diverticula caused by obstructing matter

Infection and macroperforation. Presents with constipation. LLQ pain, fever, ↑ WBC, ↑ CRP, and may bleed

106
Q

a 63-year-old male who is being evaluated in the emergency department for an episode of painless bright red blood per rectum for two hours.

A

Diverticulosis will present as

is defined as large outpouchings of the mucosa in the colon

Presents with painless rectal bleeding, particularly in an elderly pa

107
Q

complication of diverticulitis?

A

Fistula
B Colonic stricture
C Abscess

108
Q

Diverticulitis presents commonly as left lower quadrant pain, tenderness, palpable mass, and abdominal distention.

A

CT scan is the best imaging modality during acute episode of diverticulitis

CT will demonstrate fat stranding and bowel wall thickening

Occult blood in the stool and mild to moderate leukocytosis may occur with diverticulitis.

Barium enema and endoscopy are contraindicated during the initial stages of an acute attack because of the risk of free perforation.

109
Q

he most common organisms involved in the development of diverticulitis are

A

E. coli and B. fragili

110
Q

perianal pruritus that is worse at night

Dx:

Tx

A

Pinworm (Enterobius vermicularis):

“scotch tape test’ done in the early morning. Can see the eggs under microscopy

TX with mebendazole

111
Q

GI symptoms and weight loss

Transmission from raw or undercooked meat
Associated with B12 deficiency

Tx

A

TAPEWORM

DX: Tape test for D. latum, stool sample: eggs

TX: Praziquantel

112
Q

cough, weight loss, anemia recent travel

Larvae invade the skin, travel to lung, cough, and swallow, reside in the intestine

EOSINOPHILLIA and ANEMIA

A

HOOKWORM

DX: Stool sample - adult worms
TX: mebendazole

113
Q

pancreatic duct, common bile duct, and bowel obstruction

Most common intestinal helminth worldwide found in contaminated soil

A

ROUND WORM

A high load may cause pancreatic duct, common bile duct, and bowel obstruction
DX: stool sample eggs or adult worms
TX: albendazole

114
Q

Fecal-oral, contaminated water/food, anal-oral
Bloody diarrhea, tenesmus. abdominal pain

Associated with LIVER ABSCESS

A

AMEBIASIS

DX: Stool sample—trophozoites
TX: Iodoquinol or paromomycin and Flagyl for liver abscess

115
Q

also known as snail fever and bilharzia, is a disease caused by parasitic flatworms called

A

Schistosomiasis

Penetration of skin (contaminated freshwater) → enter the bloodstream and migrate to the liver, intestines, and other organs
Symptoms include rash, abdominal pain, diarrhea, bloody stool, or blood in the urine
DX: Eggs in urine or feces

TX: Praziquantel

116
Q

if BRBPR or suspected thrombosis

Varicose veins of anus and rectum
Risk factor: Constipation/straining, pregnancy, portal HTN, obesity, prolonged sitting or standing, anal intercourse

A

ANOSCOPY FOR HEMORRHOIDS

117
Q

lower 1/3 of the anus (below dentate line)

Thrombosed:
Significant pain, and pruritus but no bleeding
Palpable perianal mass with a purplish hue

A

EXTERNAL HEMORRHOID

Treat with excision for thrombosed external hemorrhoids

118
Q

upper 1/3 of the anus

Bright red blood per rectum, pruritus and rectal discomfort

A

INTERNAL

Treatment: Fiber, sitz bath, ice packs, bed rest, stool softeners, topical steroids
Rubber band ligation If protrudes with defecation, enlargement, or intermittent bleeding
Closed hemorrhoidectomy if permanently prolapsed

119
Q

Involves protrusion of the stomach through the diaphragm via the esophageal hiatus
It can cause symptoms of GERD

A

HIATAL HERNIA

DX: barium upper GI series, upper endoscopy
Tx: acid reduction may suffice, although surgical repair can be used for more serious cases (15%)

120
Q

Hematochezia and pus-filled diarrhea, fever, tenesmus (feeling of incomplete defecation) anorexia, weight loss

A

UC

Barium enema: Lead pipe appearance (loss of haustral markings)

121
Q

UC TX?

A

Colectomy is curative

Medications: Prednisone and mesalamine

122
Q 
Mouth to anus
Skip lesions
Transmural thickening
Fistulas common, abscess
Abdominal pain, aphthous ulcers,

Result of barium enema?

A

CHRONS

Barium enema: Cobblestone appearance

123
Q

CHRON’S TX

A

Flares: Prednisone +/- Mesalamine +/-

Maintenance: Mesalamine
Surgery is not curative. Adjacent portion of the bowel is affected post-op

124
Q

abdominal pain and altered bowel function

A

IRRITABLE BS

Comorbid: Depression, anxiety, somatization

125
Q

According to the Rome IV criteria, IBS is defined as

DX of exclusion

All labs normal, no mucosal lesions: CBC, renal panel, FOBT, O&P, sed rate, ± flex sig
Colonoscopy, barium enema, ultrasound, or CT
Endoscopy in patients with persistent symptoms, weight loss/anorexia, bleeding or history of other GI

A

ABD PAIN

at least 1 day per week in the

last 3 months, associated W/ two or more of the following criteria:

  • Related to defecation
  • change in stool frequency
  • change in stool form (appearance)
126
Q

serotonin agonist introduced for the treatment of IBS

A

Tegaserod maleate (Zelnorm)

127
Q

what is converted to unconjugated bilirubin from heme?

Heme is broken down into iron and protoporphyrin

A

iron is recycled

protoporphyrin

128
Q

What makes stool brown and urine yellow?

A

Normal intestinal microflora will act on the bile and convert it to urobilinogen which is oxidized to stercobilin (which makes stool brown) and urobilin (which makes urine yellow)

129
Q

increases the level of UCB which overwhelms the liver’s ability to conjugate UCB. Dark urine and increased risk for pigmented bilirubin gallstones result/.

A

Extravascular hemolysis/ineffective erythropoiesis: –> jaundice

130
Q

what is uridine glucuronyl transferase (UGT)?

A

Albumin transports UCB to the liver for conjugation by uridine glucuronyl transferase (UGT) in hepatocytes

131
Q

mildly low UGT activity which increases UCB. Jaundice occurs during stress like a severe infection. Otherwise, pts are asymptomatic.

A

Gilbert syndrome

132
Q

the absence of UGT which increases UCB causing kernicterus which is usually fatal.

A

Crigler-Najjar syndrome

133
Q

deficiency of bilirubin canaliculi transport protein which increases CB. The liver is pitch-dark.

A

Dubin-Johnson syndrome:Dubin-Johnson syndrome:

134
Q

what is Rotor syndrome?

A

Rotor syndrome is similar to Dubin-Johnson syndrome except that the liver is not dark.

135
Q

obstructive jaundice): associated with gallstones, pancreatic carcinoma, liver fluke, and cholangiocarcinoma. This also increases the CB, and alkaline phosphatase and decreases urine urobilinogen. Dark urine, pale stool, pruritus due to increased bile acids, steatorrhea.

A

Biliary tract obstruction

Predominant alkaline phosphatase elevation —

Elevation of the serum alkaline phosphatase out of proportion to the serum aminotransferases suggests biliary obstruction or intrahepatic cholestasis

136
Q

disrupts both hepatocytes and small bile ductules which increases both CB and UCB.

Dark urine due to elevated urine bilirubin.

A

viral hep

137
Q

Urinary bilirubin indicates that

A

conjugated hyperbilirubinemia present

Abdominal ultrasound (preferred) or CT abdomen Liver biopsy (definitive)

138
Q

Elevated INR — An elevated INR that corrects with vitamin K administration suggests

A

impaired intestinal absorption of fat-soluble vitamins and is compatible with obstructive jaundice

139
Q

the classic triad of pancreatic calcification (plain abdominal x-ray), steatorrhea (high fecal fat), and diabetes mellitus

A

chronic pancreatitis

140
Q

Symptoms: Tea-colored urine, vague abdominal discomfort, nausea, pruritus, pale stool

A

viral hepatitis

141
Q

Acute - fatigue malaise, nausea, vomiting, anorexia, fever and right upper quadrant pain.

Transmission: Fecal-oral
Serum IgM anti-HAV

Vaccine: killed (inactivated) - given in two doses, recommended for travelers.

A

hep A

142
Q 
Acute and Chronic
Transmission: Sexual or sanguineous
Serology:
HBeAg – highly infectious
HBsAg – ongoing infection

Anti-HBc –???

Anti-HBs – immune
Risk of hepatocellular carcinoma

A

HEP B ASSOCIATED WITH HEP D

The vaccine is given to all infants (birth, 1-2 mo, 6-18 mo)

Anti-HBc – had/have infection
IgM – acute
IgG – not acute

143
Q

Transmission: IV drug use is the most common. Also sexual or sanguineous

A

Screen with testing for anti-HCV antibodies
Diagnosis with HCV RNA quantitation

Treatment: antiretrovirals target complex of enzymes needed for HCV RNA synthesis

144
Q

Only occurs when coinfected with Hepatitis B

A

D

145
Q

Liver enzymes: AST:ALT ratio > 2:1

A

Alcoholic Hepatitis

146
Q

Acetaminophen toxicity TX

A

N-Acetylcysteine within 8-10 hrs

147
Q

Risk factors: Obesity, hyperlipidemia, insulin resistance

Liver enzymes: ALT > AST

A

Fatty Liver Disease:

Liver biopsy: Large fat droplets (macrovesicular fatty infiltrates)

148
Q

dilated veins in the distal esophagus or proximal stomach caused by elevated pressure in the portal venous system, typically from cirrhosis

Presents with: hematemesis with coffee ground/ Melena

Initial presentation: tachycardia/hypotension ⇒ may bleed massively but cause no other symptoms

A

Esophageal varices

Varices offer a channel that diverts pressure from the portal circulation. Often found in lower 1/3 of the esophagus and can extend into gastric veins

Dx: EMERGENT EGD after stabilizing patient
diagnostic and therapeutic

Labs: Hgb, Hct and Platelet (usually low in liver patients)

149
Q

Treatment for esophageal varices? Liver related

A

Treatment consists of intravenous octreotide which is a somatostatin analog that decreases portal blood flow
MOA:
Octreotide inhibits the release of glucagon, which is a splanchnic vasodilator.

Antibiotic prophylaxis with IV ciprofloxacin x1 week to lower the risk of a bacterial infection,
and
in severely-ill individuals, IV ceftriaxone is given instead

An upper endoscopy is done within 12 hours of presentation and variceal ligation with elastic bands placed on the varices to stop them from bleeding

150
Q

What is endoscopic sclerotherapy?

A

a sclerosant solution like sodium morrhuate is injected in the varices endoscopically

151
Q

What to do with massive bleed and if endoscopic therapy fails to stop the bleeding in esophageal varices?

A

Balloon tamponade using Blakemore tube
This applies direct pressure which can stop an ongoing bleed. It can be used for about 48 hours

When endoscopic approaches fail, another procedure is a
transjugular intrahepatic portosystemic shunt or TIPS, which creates a path between the portal and systemic circulation in order to lower the portal pressure

152
Q

How to preventrebleeds?

A

Nonselective beta-blockers - propranolol, nadolol (treatment of choice in primary prophylaxis to prevent rebleeds)
Isosorbide: long-acting nitrate

153
Q

What are considered alarm symptoms or features with abdominal pain, IBS?

x5

A

Alarm features include

  • Weight loss
  • Iron deficiency anemia –

-Family history of certain organic GI illnesses (eg, inflammatory bowel disease, celiac sprue, colorectal cancer)

Although rectal bleeding and nocturnal symptoms have also been considered alarm features

They are not specific for organic disease.

154
Q

What is post-parandial urgency with irritable bowel disease?

A

Postprandial urgency is common, as is alternation between constipation and diarrhea.
Symptoms not consistent with IBS should alert the clinician to the possibility of an organic pathology.

Inconsistent symptoms include the following: Onset in middle or older age Acute symptoms (IBS is defined by chronicity) Progressive symptoms 
Nocturnal symptoms 
Anorexia or weight loss 
Fever 
Rectal bleeding 
Painless diarrhea 
Steatorrhea 
Gluten intolerance
155
Q 
Which of the following infections has been associated with an increased prevalence of IBS?
Giardia lamblia
Escherichia coli
Shigella
Salmonella
A

Infection with G lamblia has been shown to lead to an increased prevalence of IBS as well as chronic fatigue syndrome. In a historic cohort study of patients with G lamblia infection as detected by stool cysts, the prevalence of IBS was 46.1% as long as 3 years after exposure, compared with 14% in controls.

Family Medicine EOR (4 decks)

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