Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

First AId 2CK > Gastrointerology > Flashcards

Gastrointerology Flashcards

1
Q

Spontaneous Bacterial Peritonitis

A
  • infection without perforation of the bowel
  • E.coli is most common organism
  • Anaerobes rarelt causes
  • Pneumococcus (respiratory pathogen) associated with SBP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Best initial test for SBP

A
  • Cell count with more than 250 neutrophils
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Dx options for SBP

A
  • Gram stain is almost always negative

- Fluid cx is best test but is usually never a

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Treatment of spontaneous bacterial peritonitis

A
  • ceftoxamine or ceftriaxone

-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pt has low albumin. Prophylaxis for SPBP

A
  • Prophylactic norfloxacin or trimethoprim/sulfamethoxazole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Dysphagia

A

difficulty swallowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Odynophagia

A

pain with swallowing due to abnormalities in orpharynx or esophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Oropharyngeal dysphagia

A
  • usually involves aspiration of food into the lungs

liquids more than solids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Causes of oropharyngeal dysphagia

A
  • Neuro disease (e.g. stroke)
  • Myasthania gravia
  • Prolonged intubuation
  • Zenker’s diverticulum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Obstructive causes of esophageal dysphagia

A

Difficulty swallowing solids more than liquids

  • Strictures
  • Schatzki rings
  • Esophageal webs
  • Esophageal carcinoa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Motility disorder causes of esophageal dysphagia

A
  • Achalasia
  • Scleroderma
  • Esophageal spasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Dx of oropharyngeal dysphagia

A

Video fluorosopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Dx of esophageal dysphagia

A

Barrium swallow (aka esophagram) followed by endoscopy, manometry and/or pH monitoring

  • if obstructive causes suspected, proceed directly to endoscopy w/ biopsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Causes of infectious esophagitis

A
  • Candida albicans
  • HSV
  • CMV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Candida albicans esophagitis

A
  • cause of 90% of esophagitis in AIDS patients
  • oral thrush CAN be present but not always
  • upper endoscopy shows yellow white plaques ADHERENT to mucosa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Tx of Candida albicans esophagitis

A

Nystatin oral suspension or Fluconazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

HSV esophagitis

A
  • oral ulcers found on exam
  • upper endoscopy shows small, deep ulderations, multinucleated giant cells w/ intranuclear inclusions on biopsy + Tzanck smear
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Tx of HSV esophagiti

A

Acyclovir IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

CMV esophagitis

A
  • associated with retinitis and colitis esp in AIDS patients
  • on endoscopy, large, superficial ulcerations
  • Intranuclear and intracytoplasmic inclusions on biopsy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Tx of CMV esophagitis

A

Gancyclovir IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Esophageal webs associated with which syndrome?

A

Plummer Vinson syndrome

  • esophageal webs
  • glossitis
  • iron deficiency anemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Musculature of esophagus

A
  • Upper 1/3 is skeletal
  • Middle is mixed skeletal and smooth muscle
  • Lower 1/3 is smooth muscle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Esophageal Spasm

A
  • motility disorder in which normal peristalsis is periodically intermittent by high amplitude nonperistaltic contractions
  • aka nutcracker esopagus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Hx and PE: esophageal spasm

A
  • sudden onset of chest pain not related to exertion
  • can be precipitated by drinking hot or cold liquids
  • relieved by nitroglycerin
  • EKG and stress test will be normal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Dx of esophageal spasm

A

Barrium swallow shows corkcrew shaped esophagus

- Manometry shows high-amplitude simultaneous contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Tx of esophageal spasm

A

Nitrates
Calcium channel blockers for symptomatic relief
Esophageal myometry for severe incapacitating symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Achalasia

A

impaired relaxation of lower esophageal sphincter

  • loss of peristalsis in distal 2/3 of esophagus
  • due to generation of neurons in myenteric (Auerbach’s) plexus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Achalasia: Hx and PE

A
  • often in young patient < 50
  • progressive dysphagia to BOTH solids and liquids at same time
  • no association w/ tobacco or alcohol use
  • regurgitation of undigested food
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Achalasia: Dx

A
  • Barium swallow shows “bird’s beak” tapering of distal esophagus
  • Manometry shows increased LES resting pressure, incomplete LES relaxation upon swallowing, and decreased peristalsis
  • CXR shows widening of esophagus
  • Upper endoscopy shows normal mucosa to r/o malignancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Tx of Achalasia

A
  • Nitrates, CCBs
  • pneumatic dilitation
  • botulinium toxin injection
  • surgical resectioning or myometry
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Zenker’s diverticulum

A

cervical outpouching of cricopharyngeal muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Hx and PE; Zenker’s diverticulum

A
  • presents with chest pain, dysphagia, halitosis, regurgitation of undigested food
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Dx of Zenker’s diverticulum

A

Barium swallow will show outpouchings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Tx of Zenker’s diverticulum

A

IF symptomatic, treat w/ surgical resection of diverticulum

For Zenker’s diverticulum, myotomy of cricopharygeus is required to relieve high pressure zone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Schatzki ring

A
  • peptic stricture or scarring/tightening of distal esophagus
  • associated with acid reflux and hiatal hernia
  • associated with intermittent dysphagia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Dx and Tx of Schatzki ring

A
  • seen on Barium swallow

- treated with pneumatic dilitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Scleroderma

A

presents with symptoms of reflux and have clear hx of scleroderma or progressive systemic sclerosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Dx of scleroderma

A

Manometry shows decreased LES pressure from inability to close LES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Mgmt of GI associated scleroderma

A

PPIs to manage reflux symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Mallory Weiss tears

A
  • NONPENETRATING tear of only mucosa
  • presents with upper GI bleeding after severe vomiting or retching
  • repeated retching followed by bright red blood or black stool
  • no dysphagia is presents
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Tx of Mallory Weiss tears

A

Often M-W tears resolve spontaneously

- severe cases managed with epinepherine or electrocautery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Boerhaave syndrome

A

full thickness esophageal rupture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Manometry is diagnostic criteria for which 3 GI disease

A
  • Achalasia
  • Esophageal spasm
  • Scleroderma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Most common esophageal cancer worldwide

A

Squamous cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Most prevalent esophageal cancer in Western World

A

Adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Risk factors for SCC

A

Alcohol and tobacco

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Risk factors for Adenocarcinoma

A

Barrett’s esophagus (columnar metaplasia of distal esophagus 2/2 to chronic GERD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Esophageal Cancer: Hx and PE

A
  • patients > 50 y/o
  • dysphagia first for SOLIDS the progressive dysphagia for liquids
  • more than 5 - 10 years of GERD symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Best initial test for esophageal cancer

A

Barium study

- will show narrowing of esophagus with irregular border protruding into lumen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Confirmation of esophageal cancer

A

Endoscopy with biopsy can only confirmcancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Tx for Esophageal Cancer

A
  1. No resection = no cure
  2. Chemotherapy and radiation used in addition to surgical resection
  3. Stent placment for lesions that can’t be resected surgically
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

GERD

A

inappropriate relaxation of LES sphincter that allow reflux of gastric contents
- can be due to incompetent LES, gastroparesis, or hiatal hernia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

GERD symptoms can be worsened by…

A 
Nicotine
Alcohol
Caffeine
Chocolate
Peppermint
Late night meals
Obesity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Hx and PE: GERD

A
    • patients present w/ heartburn that occurs 30 - 90 minutes after meal, worsens with reclining and improves with antacids
    • sour taste, sore throat, hoarseness, or cough
  • PE exam is usually normal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Dx of GERD

A

Primarily clinical diagnosis
empiric trial of lifestyle mods and treatment if attempted first
- if empiric tx fails then EGD w/ biopsy is indicated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Indications for EGD in setting of GERD

A
  • Signs of obstruction
  • Weight losss
  • Anemia or heme-positive stools
  • More than 5 - 10 years of symptoms to exclude Barrett sesophagus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Tx of GERD

A

Lifestyle modifications
- Avoid alcohol, caffeine, chocolate, late time snacks
- pharm meds
-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Pharm tx in mild GERD

A

Antacids or H2 blockers (e.g. ranitidine_

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Pharm tx in persistent GERD

A

PPIs (omeprazole, lansoprazole)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Surgical tx of GERD

A
  • when medical treatment is not working

- Nissen fundoplications: wrapping the stomach around LES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Complications of GERD

A
  • Erosive esophagitis
  • Esophageal peptic stricture (Schatzki rigns)
  • Aspiration pneumonia
  • Upper GI bleeding
  • Barrett’s esophagus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Barrett’s esophagus

A
  • histological changes in lower esophagus (columnar metaplasia)
  • needs at least 5 years of reflux to develop
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Dx of Barrett’s esophagus

A

EGD with biopsy

- has great risk of turning into adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Hiatal hernia

A
  • herniation of stomach into the ches through the diaphragm
65
Q

Sliding hiatal hernia

A

GE junction and portion of stomach are displaced ABOVE diaphragm

66
Q

Paraesophageal hiatal hernia

A

GE junction remains below diaphragm while fundus herniates into thorax

67
Q

Hiatal hernia: PE and Hx

A

May be asymptomatic

- patients with sliding hiatal hernias may present with GERD

68
Q

Hiatal hernia: Dx

A

incidental finding on CXR

- diagnosed with Barium study or EGD

69
Q

Tx of sliding hernia

A

Medical therapy and lifestyle modifications to decrease GERD symptoms

70
Q

Tx of paraeophageal hernia

A

Surgical gastropexy (attachment of stomach to rectus sheath and closure of hiatrus) is recommended to prevent gastric volvulus

71
Q

Acute gastritis

A

rapidly developing, superficial lesions that often due to NSAID use, alcohol, H. pylori, infxn and stress from severe illness

72
Q

Type A gastritis

A
  • subset of chronic gastritis (10%)
  • occurs in fundus and due to AUTOANTIBODIES TO PARIETAL CELLS
  • causes pernicious anemia and associated w/ other autoimmuen disorders
  • increased risk of gastric cancers
73
Q

Type B gastritis

A
  • subset of chronic gastritis (90%)
  • occurs in antrum and may be caused NSAIDS or H. pylori infection
  • often asymptomatic but associated with inc risk of PUD and gastric cancer
74
Q

Gastritis: HE and PE

A
  • can be asymptomatic

- can present with GI bleeding w/o pain

75
Q

Dx of Gastritis

A
  • UPPER ENDOSCOPY to evaluate GI mucosa
76
Q

H. pylori infection diagnosis

A
  • EGD with biopsy
  • Urease breath tests
  • serum IgG antibodies (show hx of exposure but no current infxn)
  • H. pylori stool antigen
77
Q

Treatment of gastritis

A
  • Decrease intake of exacerbating agents
  • Triple therapy (amoxicillin, clarithromycin, omepraxole)
  • give prophylactic PPIs for stress ulcers
78
Q

Curling ulcers

A
  • stress ulcers associated with burns
79
Q

Cushing ulcers

A
  • stress ulcers associated with traumatic brain injury
80
Q

Krukenberg tumor

A

gastric cancer that metastasizes to ovary

81
Q

Gastric cancer

A

malignant tumor with poor prognois

  • seen in Korea and Japan
  • most are adenocarcinomas with two morphologies: intestinal type and diffiuse type
82
Q

Intestinal gastric cancer

A

differentiated cancer that originates from intestinal metaplasia of gastric mucosal cells

  • diet hih in nitrites and salt
  • diet low in antioxidants
  • H. pylori colonization
  • chronic gastritis
83
Q

Diffuse gastric cancer

A
  • undifferentiated cancer not associated w/ H. pylori or chronic gastritis
  • unknown risk facors
  • “signet ring cells on biopsy”
84
Q

MALT (mucosa-associated lymphoid tissue) lymphoma

A
  • rare gastric tumor that presents in patients with H. pylori infection
  • only malignancy that can be cured with abx
  • treat with triple therapy (amoxicillin, clarithromycin, and omeprazole)
85
Q

Gastric Cancer: Hx and PE

A
  • early stages are usually asymptomatic, but may be associated with indigestion and loss of appetite
  • late stage disease presents with abdominal pain, weight loss, and upper GI bleeding
86
Q

Dx of Gastric Cancer

A

Upper endoscopy with biopsy

87
Q

Tx of Gastric Cancer

A 
If detected early, treatment is surgical resection
Late stage (most patients), usually incurable
88
Q

Peptic Ulcer Disease

A
  • result from damage to gastric or duodenal mucosa caused by impaired mucosal defense or increase in acidic gastric contents
89
Q

Most causative agent of PUD

A

H. pylori - responsible for 90% of duodenal ulcers and 70% of gastric ulcers

90
Q

Other causes of PUD

A
  • Corticosteroid use
  • NSAIDS
  • Alcohol
  • Tobacco
91
Q

PUD: Hx and PE

A

presents with chronic or periodic dull, burning epigastric pain that is related to meals and can radiate to back

  • may complain of nausea, hematemesis or bloody stools
  • exam may be normal but epigastric tenderness and positive guiaic stools
  • acute perforation presents with rigid abdomen, rebound tenderness
92
Q

Gastric ulcers vs. Duodenal ulcers Hx

A

Gastric ulcers have “GREATER” pain with eating

Duodenal ulcers have “DECREASED” pain with eating

93
Q

Diagnostic test for PUD

A

Upper endoscopy is most accurate test to confirm and rule out bleeding

94
Q

Diagnosis of PUD

A
  • rule out performations
  • upper endoscopy
  • H. pylori testing
  • in recurrent cases, check serum gastrin to r/o Zollinger- Ellison syndrome
95
Q

Perforations in Gastric Ulcers

A

Abdominal X-ray shows free air under the diaphragm

96
Q

Perforations in Duodenal Ulcers

A

CT scan with contrast shows air in the retroperitoneal space.
- Order CBC to detect GI bleeding

97
Q

Upper GI Bleeding: Hx and PE

A
  • Hematemesis (“coffee-ground emesis”)
  • Melena > Hematachezia
  • Hypovolemia (e.g. tachycardia, lightheadedness, hypotension)
98
Q

Upper GI Bleeding: Dx

A

NG tube and lavage

If stable, endoscopy

99
Q

Upper GI Bleeding: Etiology

A

PUD (** most important**)
Esophagitis/gastritis
Mallory Weiss Tear
Esophageal varices

100
Q

Upper GI Bleeding: Initial Management

A 
Protect airway (intubation may be needed)
Stabilize patient w/ IV fluids and packed red blood cells

** hematocrit may be normal in early acute blood loss**

101
Q

Upper GI bleeding: long-term management

A

Endoscopy followed by therapy directed at the underlying cause

102
Q

Lower GI Bleeding

A

Hematochezia > melena, but can be either

103
Q

Lower GI Bleeding: Dx

A
  • Rule out upper GI bleding with NG lavage if brisk
  • Anoscopy/sigmoidoscopy for patients < 45 y/o with small volume bleeding
  • Colonoscopy if stable; arteriography or exploratory laparotomy if stable
104
Q

Lower GI Bleeding: Etiologies

A 
Diverticulosis (60%) ****
Angiodysplasia
IBD
Hemorrhoids/fissures
Neoplasm
AVM
105
Q

Lower GI Bleeding: Initial Management

A 
Protect airway (intubation may be neede)
Stabilize pt with IV fluids and packed RBCs
106
Q

Lower GI Bleeding: Long-term management

A

Depends on the underlying etiology
Endoscopic therapy (e.g. epinepherine injection)
Intra-arterial vasopressin infusion or embolization or surgery for diverticular disease

107
Q

Most common cause of upper GI bleeding

A

PUD

108
Q

Most common cause of lower GI bleeding

A

Diverticulosis

109
Q

Common features seen in variceal bleeding

A
  • Vomiting +/- black stool
  • Spider angiomata and caput medusa
  • Splenomegaly
  • Palmar erythema
  • Asterixis
110
Q

Treatment of Variceal Bleeding

A
  1. Fluid replacement w/ high volumes
  2. PRBCs if Hct < 30
  3. Fresh frozen plasma if PT or INR is elevated
  4. Platelets if below < 50K
  5. Octreotide for variceal bleeding
  6. Endoscopy to determine diagnosis and administer some treatment
  7. IV PPI for upper GI bleeding
  8. Surgery if med treatment is refractory
111
Q

Management of variceal bleeding in addition to fluids, blood, platelets, plasma

A
  1. Octreotide to reduce portal pressure
  2. Banding to obliterate esophageal varices
  3. TIPS to decrease portal pressure in those not controlled by octreotide and banding
  4. Propranolol to prevent subsequent episodes of bleeding
  5. Abx to prevent SBP with ascites
112
Q

Mesenteric Ischemia

A
  • insufficient blood supply to small intestine resulting in ischemia and potentially necrosis
113
Q

Two most common causes of mesenteric ischemia

A
  1. Acute arterial occlusion from thrombosis

2. Embolism

114
Q

Risk factors for acute arterial occlusion induced mesenteric ischemia

A

Atherosclerosis

- commonly occurs in SMA

115
Q

Risk factors for embolism

A

Atrial fibrillation and stasis from reduced ejection fraction

116
Q

Mesenteric Ischemia: Hx and PE

A

severe abdominal pain out of proportion to exam

  • patient has prior episodes of abdominal pain after eating (intestinal angina)
  • other symptoms include nausea, vomiting, diarrhea, and bloody stools
  • abdominal exam unremarakable until late in disease
117
Q

Mesenteric ischemia: Dx

A
  • MESENTERIC ANGIOGRAPHY
  • Labs show leukocytosis, metabolic acidosis (with increased lactase, amylase, LDH, CK
  • AXR shows bowel wall edema (“thumbprinting”) and air wihin bowel
118
Q

Mesenteric ischemia

A
  • Volume resuscitation, broad spectrum abx

- For acute arterial thrombosis or emboli, treat with anticoagulation and either laparotomy or angioplasty

119
Q

Cirrhosis

A

fibrosis and nodular regeneration resulting from chronic livery injury (intrahepatic or extrahepatic)

120
Q

Intrahepatic causes of cirrhosis

A
  • All causes of chronic hepatitis
121
Q

Extrahepatic causes of cirrhosis

A
  • Biliary tract disease (primary biliary cirrhosis, primary sclerosing angitis)
  • Posthepatic causes (including right sided HF, constrictive endocarditis, Budd-Chiari syndrome)
122
Q

Cirrhosis: Hx and PE

A
  • presents with JAUNDICE, ASCITES, SPONTANEOUS BACTERIAL PERITONITIS, HERPATIC ENCEPHALOPATHY (asterixis, AMS), GASTROESOPHAGEAL VARICES, coagulopathy, and renal dysfunction
  • exam reveals large palpaple or firm liver or signs of portal hypertension and liver failure
123
Q

Spontaneous bacterial peritonitis

A

diagnosed as > 250 PMNs/ml in the ascitic fluid

124
Q

Effects of portal hypertension

A
  • Esophageal varices –> hematemesis
  • Peptic ulcer –> melena
  • Splenomegaly
  • Caput medusa
  • Hemorrhoids
125
Q

Effects of liver cell failure

A
  • Coma
  • Scleral icterus
  • Fetor hepaticus (breath smells like open corpse)
  • Spider nevi
  • Gynecomastia
  • Jaundice
  • Loss of sexual hair
  • Liver “flap” - asterixis
  • Bleeding tendency (decreased prothrombin)
  • Anemia
  • Testicular atrophy
  • Ankle edema
126
Q

Diagnosis of cirrhosis

A
  • Liver biopsy shows bridging fibrosis and nodular regeneration
  • labs show decreased albumin, increased INR/PT and increased bilirubin
  • if ascites is present, etiology determined by SAAG (serum- ascites albumin gradient)
127
Q

SAAG

A

serum albumin - ascites albumin

128
Q

SAAG > 1.1

A

Related to portal hypertension

  • Presinusoidal: splenic or portal vein thrombosis
  • Sinusoidal: cirrhosis
  • Postsinusoidal: right heart failure, constrictive pericarditis, Budd-Chiari
129
Q

SAAG < 1.1

A

Not related to portal hypertension

  • Nephrotic syndrome
  • TB
  • Malignancy with peritoneal carcinomatosis (e.g. ovarian cancer)
130
Q

36 y/o F with PMH of hypercholesteremia and type 2 DM presents with intermittent dull RUQ discomfort. Pt doesn’t drink alcohol. PE is unremarkable. Labs show elevated AST and ALT but otherwise normal. Hepatitis serologies are negative. Likely diagnosis?

A

Nonalcoholic fatty liver disease

  • condition associated with insulin resistance and metabolic syndrome
  • in earliest stage, can be reversed with weight loss and fat-restricted diet
  • in later stages, irreversible and can lead to nonalcoholic steatohepatitis and cirrhosis
131
Q

Complications of cirrhosis

A
  • Ascites
  • Spontaneous bacterial peritonitis
  • Hepatorenal syndrome
  • Hepatic encephalopathy
  • Esophageal varices
  • Coagulopathy
132
Q

Ascites: Mechanism

A
  • Increased portal hypertension results in transudative effusion
  • Portal exam reveals abdominal distention, fluid wave, and shifting dullness for percussion
133
Q

Ascites: Management

A

Sodium restriction and diuretics (furosemide and spironolactone); large-volume paracentesis
- Treat underlying liver disease

134
Q

Spontaneous bacterial peritonitis: Mechanism

A
  • presents with fever, abdominal pain, chills, nausea, and vomiting
  • diagnostic paracentesis shows > 250 PMNs/ml and positive gram stain
135
Q

SBP: Management

A

IV antibiotics (3rd generation cephalosporin)
IV albumin
Prophylaxis with fluoroquinolone to prevent recurrence

136
Q

Hepatorenal syndrome

A

acute prerenal failure in setting of advanced cirrhosis
Diagnosis of exclusion
Urinary sodium < 10 mEq/L

137
Q

Hepatorenal syndrome management

A

Difficult to treat
Often requires dialysis
Only cure is liver transplantation

138
Q

Hepatic encephalopathy

A

decreased clearance of ammonia

often precipitated by dehydration, infection, electrolyte abnormalities, and GI bleeding

139
Q

Hepatic encephalopathy management

A

Protein restriction, lactulose and/or rifaximin

Correct underlying triggers (e.g. replete potassium)

140
Q

Esophageal varices

A

portal hypertension leads to increased flow through portosystemic anastamoses

141
Q

Esophageal varices management

A

Endoscopic surveillance in all patients with cirrhosis

  • medical prophylaxis with B-blockers to prevent bleeding
  • for acute bleeding, endoscopy with band ligation or sclerotherapy is needed
142
Q

Coagulopathy

A

impaired synthesis of all clotting factors except Factor VIII

143
Q

Coagulopathy management

A

For acute bleeding, administer fresh frozen plasma

Vitamin K will not correct coagulopathy

144
Q

Primary Biliary Cirrhosis

A

autoimmune disorder characterized by destruction of intrahepatic bile ducts
- seen in middle aged women with autoimmune conditions

145
Q

Primary Billiary Cirrhosis: Hx and PE

A

presents with progressive jaundice, pruritis, and fat-soluble vitamin deficienies (A,D,E, K)

146
Q

Primary Biliary Cirrhosis: Dx

A

Lab findings include increased alk phosphatase, increased bilirubin,
positive antimitochondrial antibody
increased cholesterol

147
Q

Tx of Primary Biliary Cirrhosis

A

Ursodeoxycholic acid (slows progression of disease)
Cholestyramine for pruritis
Liver transplantation

148
Q

Hepatocellular Carcinoma

A

in US, primary risk factor are

  • CIRRHOSIS from alcohol
  • CHRONIC HEPATITIS
  • AFLATOXINS (in various food sources)
  • HBV infections
149
Q

Hepatocellular Carcinoma: Hx and PE

A
  • presents with RUQ tenderness, abdominal distention, and signs of chronic liver disease (jaundice, easy bruisability, and coagulopathy)
  • exam shows enlarged liver
150
Q

Hepatocellular Carcinoma: Dx

A

Ultrasound or CT
abnormal LFTs
significantly elevated alpha-fetoprotein levels

151
Q

Hepatocellular Carcinoma: Surgical Tx

A

Surgical: partial hepatectomy for single lesions < 5cm with no cirrhosis; orthotopic liver transplant for cirrhotic patients

152
Q

Hepatocellular Carcinoma: Nonsurgical Tx

A

Copyright (c) USMLEWorld, LLC., Please do not save, print, cut, copy or paste anything while a test is active.

153
Q

Hemochromatosis

A

state of Fe overload in which hemosiderin accumulates in liver, pancreas (islet cells), heart, adrenals, testes, and pituitary

154
Q

Primary hemachromatosis

A

autosomal recessive disease characterized by mutations in HFE chene that results in excessive absorption of dietary Fe

155
Q

Secondary hemachromatosis

A

Occurs in patients receiving chronic transfusions therapy (alpha thalassemia)

156
Q

Hemachromatosis: Hx and PE

A

presents with abdominal pain, DIABETES MELLITUS, ARTHROPATHY OF MCP joints, HEART FAILURE, or cirrhosis

  • exam shows bronze pigmentation, cardiac dysfunction (CHF), hepatomegaly, and testicular atrophy. labs show DM
  • hemachromatosis doesn’t affect lung, kidney, eye
157
Q

Hemachromatosis: Diagnosis

A
  • increased serum Fe, percent Fe saturation, and ferritin with decreased transferrin
  • transferrin > 45% is highly suggestive of Fe overload
  • perform liver biopsy, MRI, and HFE
158
Q

Hemachromatosis: Tx

A
  • WEEKLY PHLEBOTOMY to normalize serum Fe levels, then maintain phlebotomy every 2-4 months
  • DEFEROXAMINE can be used for maintenance therapy
159
Q

Hemachromatosis: Complications

A
  • CIRRHOSIS
  • HEPATOCELLULAR CARCINOMA
  • Restrictive cardiomyopathy
  • Arrhythmias
  • DM
  • Impotence

First AId 2CK (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions