Clinmed: Gastroenterology

Front 1

What are the 4 quadrants of the abdomen?

Back 1

1. RUQ (right upper quadrant)
2. RLQ (right lower quadrant)
3. LUQ (left upper quadrant)
4. LLQ (left lower quadrant)

Front 2

What is the equipment needed for the abdominal exam?

Back 2

stethoscope
ruler
measuring tape
pen
gloves, lubricating gel for rectal

Hint 2

Mosbys p532

Front 3

What are 3 surface landmarks of the abdomen?

Back 3

1. umbilicus
2. anterior superior iliac spine
3. inguinal ligament

Front 4

What structures are found in the RUQ?

Back 4

liver
gallbladder
head of pancreas
pylorus of stomach
duodenum
hepatic flexure of colon
portion of ascending and transverse colon
RT adrenal gland
upper portion of RT kidney

Hint 4

Mosbys p534

Front 5

What structures are found in the RLQ?

Back 5

cecum
appendix
portion of ascending colon
lower portion of RT kidney
RT ureter
RT spermatic cord
RT fallopian tube and ovary
bladder if distended
uterus if distended

Hint 5

Mosbys p534

Front 6

What structures are found in the LUQ?

Back 6

left lobe of liver
spleen
body of pancreas
fundus and body of stomach
splenic flexure of colon
portion of transverse and descending colon
LT adrenal gland
upper portion of LT kidney

Hint 6

Mosbys p534

Front 7

What structures are found in the LLQ?

Back 7

portion of descending colon
sigmoid colon
lower portion of LT kidney
LT ureter
LT spermatic cord
LT fallopian tube and ovary
bladder if distended
uterus if distended

Hint 7

Mosbys p534

Front 8

What structures are found in the RT hypochondriac region?

Back 8

portion of liver
gallbaldder
portion of duodenum
hepatic flexure of colon
RT adrenal gland
portion of RT kidney

Hint 8

Mosbys p534

Front 9

What structures are found in the epigastric region?

Back 9

portion of liver
head and body of pancreas
portion of duodenum
pylorus of stomach

Hint 9

Mosbys p534

Front 10

What structures are found in the LT hypochondriac region?

Back 10

portion of liver
spleen
tail of pancreas
fundus and body of stomach
splenic flexure of colon
LT adrenal gland
portion of LT kidney

Hint 10

Mosbys p534

Front 11

What structures are found in the RT lumbar region?

Back 11

portion of duodenum and jejunum
ascending colon
portion of RT kidney

Hint 11

Mosbys p534

Front 12

What structures are found in the umbilical region?

Back 12

portion of duodenum, jejunum and ileum
omentum
mesentary

Hint 12

Mosbys p534

Front 13

What structures are found in the LT lumbar region?

Back 13

portion of jejunum and ileum
desending colon
portion of LT kidney

Hint 13

Mosbys p534

Front 14

What structures are found in the RT inguinal region?

Back 14

portion of ileum
cecum
appendix
LT ureter
LT spermatic cord
LT fallopian tube and ovary

Hint 14

Mosbys p534

Front 15

What structures are found in the hypogastric region?

Back 15

portion of ileum
bladder
uterus (in pregnancy)

Hint 15

Mosbys p534

Front 16

What structures are found in the LT inguinal region?

Back 16

sigmoid colon
LT ureter
LT spermatic cord
LT fallopian tube and ovary

Hint 16

Mosbys p534

Front 17

What is diastasis recti and what causes it?

Back 17

separation of rectus abdominis muscles; often caused by obesity or pregnancy (but of little clinical significance)

Hint 17

Mosbys p536

Front 18

How long must you listen to bowel sounds to determine their absence?

Back 18

5 min

Hint 18

Mosbys p536

Front 19

Is bright red stool indicative of an upper or lower GI bleed?

Back 19

usually lower GI bleed
(though can also occur in massive upper GI bleed)

Front 20

Is black tarry stool indicative of an upper or lower GI bleed?

Back 20

upper GI bleed

Front 21

What are the most common causes of hematochezia in adults?

Back 21

hemorrhoids
diverticulitis
colon cancer

Front 22

If you give a patient a narcotic for abdominal pain, will it obscure the correct diagnosis or delay appropriate treatment?

Back 22

NO!

Hint 22

Cope p5

Front 23

What is an intussusception?

Back 23

medical condition where one part of the intestine invaginates into another part of the intestine; can result in obstruction

Front 24

What is dyspepsia?

Back 24

acute, chronic, or recurrent discomfort or pain in upper abdomen
epigastric pain or burning

Hint 24

Current p502

Front 25

Where does upper GI become lower GI?

Back 25

ligament of Treitz
located at duodeno-jejunal junction
connects duodenum to diaphragm

Hint 25

http://tiny.cc/ligamentoftreitz

Front 26

Define transaminitis.

Back 26

elevated transaminases:
1. ALT (alanine transaminase)
2. AST (aspartate transaminase)

Front 27

What do elevated ALT and AST indicate?

Back 27

possible liver damage

Front 28

What AST and ALT levels indicate alcoholic liver disease?

Back 28

AST levels that are 2-3x ALT levels

Front 29

What AST and ALT levels indicate ischemic hepatitis?

Back 29

>1000

Front 30

What are the risk factors for colorectal cancer?

Back 30

1. >50y/o
2. poor diet (high in red meat, low in fiber)
3. lack of exercise
4. smoking
5. alcohol
6. obesity
7. PMH of colorectal cancer, intestinal polyps, chronic inflammatory bowel disease (Crohn's disease, ulcerative colitis), Gardner syndrome, breast cancer, endometrial cancer, ovarian cancer
8. FH of colon cancer, familial adenomatous polyposis (FAP), familial hereditary nonpolyposis colorectal cancer (HNPCC), Gardner syndrome
9. Ashkenazi Jewish descent

Hint 30

Mosbys p531

Front 31

What is Cullen's sign and what may it indicate?

Back 31

periumbilical ecchymosis; may indicate acute pancreatitis or hemoperitoneum (2° to blunt abdominal trauma, ruptured AAA or ruptured ectopic pregnancy)

Hint 31

Mosbys p557

Front 32

Pain the RUQ may indicate?

Back 32

hepatomegaly
hepatitis
cholecystitis
duodenal ulcer
pneumonia

Hint 32

Mosbys p551

Front 33

Pain in the RLQ may indicate?

Back 33

Meckel's diverticulitis
regional ileitis
perforated cecum
appendicitis
ovarian cyst
salpingitis
ruptured ectopic pregnancy
renal/ureteral stone
strangulated hernia

Hint 33

Mosbys p551

Front 34

What is Meckel's diverticulum?

Back 34

congenital bulge in distal ileum

Front 35

Pain in the LUQ may indicate?

Back 35

gastric ulcer
splenomegaly
ruptured spleen
perforated colon
aortic aneurysm
pneumonia

Hint 35

Mosbys 551

Front 36

Pain in the LLQ may indicate?

Back 36

regional ileitis
sigmoid diverticulitis
ulcerative colitis
perforated colon
renal/ureteral stone
ovarian cyst
salpingintis
ruptured ectopic pregnancy
strangulated hernia

Hint 36

Mosbys 551

Front 37

Periumbilical pain may indicate?

Back 37

acute pancreatitis
early appendicitis
diverticulitis
intestinal obstruction
aortic aneurysm
mesenteric thrombosis

Hint 37

Mosbys p551

Front 38

What sounds are expected when percussing the abdomen?

Back 38

tympany over stomach and intestines
dullness over organs

Hint 38

Mosbys p537

Front 39

What is Grey Turner's sign and what may it indicate?

Back 39

flank ecchymosis; may indicate acute pancreatitis or hemoperitoneum (2° to blunt abdominal trauma, ruptured AAA, ruptured ectopic pregnancy, or coagulopathy)

Hint 39

Mosbys p557

Front 40

Where is McBurney's point located?

Back 40

two-thirds the distance from the umbilicus to the ASIS

Front 41

What is McBurney's sign and what may it indicate?

Back 41

reboud tenderness and sharp pain when McBurney's point palpated; may indicate appendicitis

Hint 41

Mosbys p557

Front 42

What is Murphy's sign and what may it indicate?

Back 42

abrupt cessation of inspiration on palpation of gallbladder; may indicate cholecystitis

Hint 42

Mosbys p557

Front 43

What is the ddx for generalized abdominal distension?

Back 43

obesity
enlarged organs
gas
fluid

Hint 43

Mosbys

Front 44

What is the ddx for abdominal distension in RLQ/LLQ?

Back 44

distended bladder
pregnancy
ovarian tumor
uterine fibroids (benign tumors)

Hint 44

Mosbys

Front 45

What is the ddx for abdominal distension in RUQ/LUQ?

Back 45

gastric dilation
pancreatic cyst
carcinoma

Hint 45

Mosbys

Front 46

What is the ddx for assymetric abdominal distension?

Back 46

enlarged organ
bowel obstruction
hernia
cyst
tumor

Hint 46

Mosbys

Front 47

What is the difference between a reducable and non-reducable hernia?

Back 47

contents can be pushed back in if reducible
contents can't be pushed back in if non-reducable

Hint 47

Mosbys

Front 48

What is the definition of a strangulated hernia?

Back 48

non-reducible hernia + blood supply to contents obstructed

Hint 48

Mosbys

Front 49

Limited abdominal movement may indicate?

Back 49

peritonitis

Hint 49

Mosbys

Front 50

When evaluating abdominal movement, visible peristalis may indicate?

Back 50

bowel obstruction

Hint 50

Mosbys

Front 51

When evaluating abdominal movement, marked pulsation may indicate?

Back 51

AAA

Hint 51

Mosbys

Front 52

What is borborygmi?

Back 52

stomach growling

Front 53

What are the characteristics of normal bowel sounds?

Back 53

generalized irregular clicks and gurgles
5-35 per minute

Hint 53

Mosbys

Front 54

Increased bowel sounds may indicate?

Back 54

borborygmi
gastroenteritis
early abdominal obstruction

Hint 54

Mosbys

Front 55

Decreased bowel sounds may indicate?

Back 55

peritonitis
paralytic ileus

Hint 55

Mosbys

Front 56

High-pitched, tinkling abdominal sounds may indicate?

Back 56

intestinal air or fluid under pressure (ex: early abdominal obstruction)

Hint 56

Mosbys

Front 57

What are evaluating during abdominal inspection?

Back 57

color (bruising, jaundice)
venous pattern
lesions/masses (striae, scarring)
contour (flat, rounded, scaphoid)
symmetry (distension, bulges)
surface movement

Hint 57

Mosbys

Front 58

What is normal liver span?

Back 58

6-12 cm
if >12 cm, may indicate hepatomegaly
if <6 cm, may indicate liver atrophy

Hint 58

Mosbys

Front 59

When might liver span be overestimated?

Back 59

upper border obscured by pleural effusion or consolidation

Hint 59

Mosbys

Front 60

Where is lower liver border normally?

Back 60

at/slighly below costal margin

Hint 60

Mosbys

Front 61

Where is upper liver border normally?

Back 61

between 5th and 7th ICS

Hint 61

Mosbys

Front 62

What is the most common cause of peptic ulcer disease?

Back 62

h. pylori

Front 63

What is a hiatal hernia?

Back 63

herniation of upper part of stomach into thorax through weakness or tear in diaphragm

Front 64

What is SAAG and when would you order it?

Back 64

serum ascites albumin gradient; to determine if ascites is transudate (portal HTN) or exudate

Hint 64

Current

Front 65

How is SAAG calculated?

Back 65

SAAG = serum ALB - ascitic fluid ALB

Front 66

How is SAAG interpreted?

Back 66

portal HTN if >1.1 g/dL
condition unrelated to portal HTN if <1.1 g/dL

Front 67

Where does bile drain?

Back 67

gallbladder for storage or duodenum

Hint 67

Interpreting Laboratory Data p236

Front 68

What foods should be eaten for diarrhea?

Back 68

bananas

Front 69

What foods prevent or treat constipation?

Back 69

increase fluids (water, fruit juice)
increase fiber (fruit, prunes, apricots, vegetables, beans)
increase bran (bran cereals, bran muffins, shredded wheat, whole wheat bread)
decrease milk, bananas, cheese and yogurt

Front 70

How does hepatic dysfunction affect lab results?

Back 70

reduced clotting factor production
increased PT
increased PTT

Hint 70

Interpreting Laboratory Data p11

Front 71

What drugs are hepatotoxic?

Back 71

rifampin
isoniazid

Hint 71

Interpreting Laboratory Data p39

Front 72

How do hepatotoxic drugs affect lab results?

Back 72

↑ ALT
↑ AST

Hint 72

Interpreting Laboratory Data p39

Front 73

What is pyloric stenosis?

Back 73

postnatal muscular hypertrophy of the pyloris causing stenosis

Front 74

PYLORIC STENOSIS:

Back 74

ETIOLOGY:
postnatal muscular hypertrophy of the pylorus with progressive gastric outlet obstruction
cause unknown
1-8:1000 births, 4:1 male predominance, 13% positive FH

CLINICAL PRESENTATION:
postprandial projectile non-bilious blood-streaked vomiting, usually starts between 2-4 weeks (but may start at birth to 12 weeks)
increased hunger, avid nursing
fretfulness, constipation, weight loss, dehydration, apathy
postprandial abdominal distention
visible gastric peristalsis from left to right
palpable RUQ oval mass 5-15 mm, especially after vomiting
hypochloremic alkalosis
upper GI contrast radiograph or abdominal US

MANAGEMENT:
1. correct dehydration and electrolyte imbalances
2. Ramstedt pyloromyotomy → incision down to mucosa along pyloric length

COMPLICATIONS:
none

PREVENTION:
none

Front 75

What is intussusception?

Back 75

invagination of intestine into another part of intestine causing obstruction

Front 76

INTUSSUSCEPTION:

Back 76

ETIOLOGY:
most common cause of intestinal obstruction in children <2y/o
3:1 female predominance
85% idiopathic
other causes include small bowel polyp, Meckel diverticulum, omphalomesenteric remnant, duplication, Henoch-Schönlein purpura, lymphoma, lipoma, parasites, foreign bodies, viral enteritis with hypertrophy of Peyer patches, celiac disease, CF
lymphoma most common cause if >6y/o
usually occurs at ileocecal valve

CLINICAL PRESENTATION:
recurrent paroxysms of abdominal pain with screaming and drawing up of knees
vomiting, diarrhea
bloody mucoid stool within 12 hours
lethargic between paroxysms
+/- fever
abdominal distention and tenderness
sausage-shaped mass in epigastric region
symptoms can persist for days if incomplete obstruction or spontaneous resolution

MANAGEMENT:
barium enema (contraindicated if signs of strangulated bowel, perforation, toxicity) or air enema for diagnosis and reduction
surgery if extremely ill, perforation, or enema reduction unsuccessful

COMPLICATIONS:
incarceration, necrosis
intestinal perforation, peritonitis, hemorrhage

PREVENTION:

Front 77

Define melena.

Back 77

black tarry stools due to presence of blood exposed to gastric acid

Front 78

Define hematochezia.

Back 78

bright red stools due to presence of blood

Front 79

Define hematemesis.

Back 79

vomiting blood

Front 80

Define singultus.

Back 80

hiccups

Front 81

Define eructation.

Back 81

belching

Front 82

Define tenesmus.

Back 82

feeling of incomplete defecation

Front 83

*Define icterus.

Back 83

AKA jaundice → yellow pigmentation of skin and mucous membranes due to accumulation of bilirubin in tissues

Front 84

Define aerophagia.

Back 84

air swallowing

Front 85

Define odynophagia.

Back 85

painful swallowing

Front 86

Define dysphagia.

Back 86

difficulty or painful swallowing

Front 87

Define flatulence.

Back 87

gas

Front 88

Define heartburn.

Back 88

substernal burning often radiating to neck

Front 89

What disorder is characterized by heartburn?

Back 89

GERD

Front 90

List types of dysphagia.

Back 90

oropharyngeal
esophageal

Front 91

What is the generic name for Advil?

Back 91

ibuprofen

Front 92

Describe the biliary system.

Back 92

Front 93

What is the approach to the patient with dysphagia?

Back 93

1. distinguish between oral, pharyngeal, or esophageal dysphagia
2. upper endoscopy
3.

ORAL DYSPHAGIA:
1. difficulty in transferring food from oropharnyx to upper esophagus
2. symptoms include drooling, spillage from mouth, inability to chew or initiate swallowing, dry mouth

PHARYNGEAL DYSPHAGIA:
1. difficulty in transferring food to upper esophagus
2. symptoms include immediate sense of bolus catching in neck, need to swallow repeatedly to clear bolus, coughin or choking during meals, neurological symptoms (dysphonia, dysarthria)

ESOPHAGEAL DYSPHAGIA:
1. impaired transport of bolus through esophagus
2. may be caused by obstruction of esophagus or impaired motility
3. if obstruction → usually occurs with solids, predictable, recurrent
4. if motility disorder → occurs with solids and liquids, unpredictable, episodic

Front 94

Define dysarthria.

Back 94

impaired ability to articulate words
manifests as slurred speech

Front 95

Define dysphonia.

Back 95

impaired ability to produce vocal sounds

Front 96

What is the ddx for dysphagia?

Back 96

OROPHARYNGEAL:
Neurologic disorders
Brainstem cerebrovascular accident, mass lesion
Amyotrophic lateral sclerosis, multiple sclerosis, pseudobulbar palsy, post-polio syndrome, Guillain-Barré syndrome
Parkinson disease, Huntington disease, dementia
Tardive dyskinesia
Muscular and rheumatologic disorders
Myopathies, polymyositis
Oculopharyngeal dystrophy
Sjögren syndrome
Metabolic disorders
Thyrotoxicosis, amyloidosis, Cushing disease, Wilson disease
Medication side effects: anticholinergics, phenothiazines
Infectious disease
Polio, diphtheria, botulism, Lyme disease, syphilis, mucositis (Candida, herpes)
Structural disorders
Zenker diverticulum
Cervical osteophytes, cricopharyngeal bar, proximal esophageal webs
Oropharyngeal tumors
Postsurgical or radiation changes
Pill-induced injury
Motility disorders
Upper esophageal sphincter dysfunction


ESOPHAGEAL:
1. Mechanical obstruction Mechanical obstruction Solid foods worse than liquids
Schatzki ring Intermittent dysphagia; not progressive
Peptic stricture Chronic heartburn; progressive dysphagia
Esophageal cancer Progressive dysphagia; age over 50 years
Eosinophilic esophagitis Young adults; small-caliber lumen, proximal stricture, corrugated rings, or white papules
Motility disorder Solid and liquid foods
Achalasia Progressive dysphagia
Diffuse esophageal spasm Intermittent; not progressive; may have chest pain
Scleroderma Chronic heartburn; Raynaud phenomenon

Front 97

What is upper endoscopy?

Back 97

endoscope inserted into mouth and extended to esophagus, stomach, and duodenum
allows for visualization, foreign object removal, stricture dilation, bleeding cauterization, biopsy

Front 98

What are the indications for upper endoscopy?

Back 98

GERD
peristent nausea and vomiting
unexplained upper abdominal pain
foreign body removal
dysphagia
monitor disease progession or treatment
unclear findings on abdominal x-ray, CT, or MRI
upper GI bleed

Front 99

What and where is virchow's node?

Back 99

lymph node in left supraclavicular fossa
takes supply from abdominal cavity
enlargment is strong indicator of abdominal cancer

Front 100

What is the difference between dyspepsia and heartburn?

Back 100

dyspepsia → epigastric pain or burning
heartburn → retrosternal burning often radiating to neck

Front 101

What is another name for heartburn?

Back 101

pyrosis

Front 102

What is GERD?

Back 102

esophageal disorder characterized by reflux of stomach contents into esophagus

Front 103

What is the etiology of GERD?

Back 103

impaired lower esophageal sphincter function

worsened by hiatial hernia, diminished peristalsis (scleroderma), diminished salivation (sjogren's, anticholinergics, oral radiation), impaired gastric emptying

affects 20% of adults

Front 104

What is the clinical presentation of GERD?

Back 104

heartburn → substernal burning, 30-60 minutes following meals or upon bending/reclining, relief with antacids or baking soda
regurgitation
dysphagia
atypical manifestations include sore throat, chronic cough, non-cardiac chest pain, asthma, chronic laryngitis

physical exam normal!!!

Front 105

What are the complications of GERD?

Back 105

reflux esophagitis (1/3 of patients)
Barrett's esophagus

Front 106

What is Barrett's esophagus?

Back 106

complication of GERD where squamous epithelium of esophagus is replaced by metaplastic columnar epithelium containing columnar and goblet cells

Front 107

What is the etiology of Barrett's esophagus?

Back 107

chronic GERD (occurs in <10% of GERD patients)

Front 108

What is the diagnostic workup of Barrett's esophagus?

Back 108

endoscopy → orange gastric type epithelium that extends from stomach to distal esophagus in tongue-like or circumferential fashion
biopsy

Front 109

What is the clinical presentation of Barrett's esophagus?

Back 109

chronic GERD → heartburn, regurgitation

Front 110

What is the management of Barrett's esophagus?

Back 110

1. long-term PPI → 1-2x daily
2. monitor with endoscopy every 3 years

Front 111

What are the complications and prognosis of Barrett's esophagus?

Back 111

esophageal adenocarcinoma
though number of patients who progress to adenocarcinoma is small if treat with PPIs and surveillance

Front 112

What is Mallory-Weiss Syndrome?

Back 112

mucosal tear at gastro-esophageal junction

Front 113

What is the etiology of Mallory-Weiss Syndrome?

Back 113

sudden increase in trans-abdominal pressure → lifting, stretching, vomiting, retching, straining

Front 114

What is the clinical presentation of Mallory-Weiss Syndrome?

Back 114

history of vomiting, retching, straining
self-limited hematemesis
+/- melena

Front 115

What is the diagnostic workup of Mallory-Weiss Syndrome?

Back 115

upper endoscopy → 0.5-4cm linear mucosal tear in gastroesophageal junction or in gastric mucosa

Front 116

What is the management of Mallory-Weiss Syndrome?

Back 116

1. bleeding often self-limiting and no therapy required
2. if bleeding continues → endoscopic hemostatic therapy → can inject epinephrine, compress artery with endoclip, or cauterize
3. if endoscopic therapy fails → angiographic arterial embolization or surgery
4. fluid replacement and blood transfusions as needed

Front 117

What are the risk factors for Mallory-Weiss Syndrome?

Back 117

alcoholism

Front 118

What are the complications of Mallory-Weiss Syndrome?

Back 118

35% complicated with peptic ulcer disease, erosive gastritis, AV malformations, esophageal varices

higher risk of continued bleeding if portal HTN

Front 119

What are esophageal varices?

Back 119

dilated submucosal veins in the esophagus

Front 120

What is the etiology of esophageal varices?

Back 120

secondary to portal HTN

causes of portal HTN include cirrhosis

Front 121

What are the risk factors of esophageal varices?

Back 121

alcoholism

Front 122

What is the clinical presentation of esophageal varices?

Back 122

upper GI bleed (33%)
hypovolemia (manifests with postural vital signs or shock)

*varices do not cause dysphagia or dyspepsia

Front 123

What is the diagnostic workup of esophageal varices?

Back 123

upper endoscopy

Front 124

What is the management of esophageal varices?

Back 124

HOSPITALIZATION:
1. bleeding often self-limited (50%) but can be life-threatening
2. rapid fluid replacement and blood transfusions
3. if platelet count <50,000/mcL or INR >2.0 → platelets or FFP
4. prophylactic antibiotics
5. vasoactive drugs to reduce portal HTN
6. if abnormal PT → subcutaneous vitamin K
7. endoscopy
-active bleeding requires intubation
-banding or sclerotherapy
-banding is first-line
-banding must be repeated every 1-3 weeks until obliterated
-sclerotherapy often done when active bleeding present, then banding done after
8. if bleeding not controlled by above → consider balloon tube tamponade, portal decompression, shunt
9. prevention of rebleeding → B-blocker, liver transplant

Front 125

What is the prognosis of esophageal varices?

Back 125

if no treatment → 60% chance of recurrent bleeding within 6 weeks

risk of bleeding increases if:
-large size (>5cm)
-endoscopy reveals red whale markings
-severe liver disease
-active alcoholism

advanced liver disease has poor outcome

Front 126

What are the complications of esophageal varices?

Back 126

rebleeding

Front 127

What is the most common cause of portal HTN?

Back 127

cirrhosis

Front 128

What is the prevention of esophageal varices?

Back 128

if cirrhosis → endoscopy → B-blocker and/or band ligation depending on results

Front 129

What is Zenker's diverticula?

Back 129

protrusion of pharyngeal mucosa that occurs at the pharyngeal esophageal junction between the inferior pharngeal constrictor and cricopharyngeus

Front 130

What is the etiology of Zenker's diverticula?

Back 130

loss of elasticity of upper esophageal sphincter → restricted opening during swallowing

Front 131

What is the clinical presentation of Zenker's diverticula?

Back 131

insidious onset over years

intially:
vague oropharyngeal dysphagia
throat discomfort
coughing

as diverticuum enlarges and retains food:
haliotosis
regurgitation
throat gurgling
nocturnal choking
neck protrusion

Front 132

What is the diagnostic workup of Zenker's diverticula?

Back 132

barium swallow

Front 133

What is the management of Zenker's diverticula?

Back 133

1. if small + asymptomatic → observation
2. if symptomatic → esophageal myotomy +/- surgical diverticulectomy

Front 134

What are the complications of Zenker's diverticula?

Back 134

aspiration pneumonia
bronchiectasis
lung abscess

Front 135

Back 135

Zenker's diverticulum

Front 136

What is Schatzke's ring?

Back 136

smooth, thin (<4mm), circumferential mucosal structure in distal esophagus at squamocolumnar junction

Front 137

What is the etiology of Schatzke's ring?

Back 137

associated with GERD, hiatal hernia

Front 138

What is the clinical presentation of Schatzke's ring?

Back 138

dysphagia → occurs with solid food (think steak), intermittent, not progressive
may pass after drinking fluids or regurgitation

Front 139

What is the diagnostic workup of Schatzke's ring?

Back 139

barium swallow

Front 140

What is the management of Schatzke's ring?

Back 140

1. bougie dilator or endoscopic surgical incision of ring
2. if repeated dilation required or heartburn → PPI

Front 141

What is achalasia?

Back 141

disorder of esophagus characterized by non-peristaltic esophageal contractions and impaired relaxation of lower esophageal spincter

Front 142

What is the etiology of achalasia?

Back 142

cause unusually unknown

associated with degeneration of postganglionic inhibitory neurons in myenteric plexus that release nitric oxide and VIP

causes include genetics, Trypanosoma cruzi (organism that causes Chagas disease), carcinoma, and possibly viral or autoimmune

rare
most common in 25-50y/o

Front 143

What is the clinical presentation of achalasia?

Back 143

dysphagia → esophageal, localized to lower chest, both food and liquids, worsens with hurried eating or emotional stress, slowly progressive
common complaints → taking longer to eat, having to drink lots of fluids to clear food, having to stand up and arch back or strain to clear food
regurgitation → food non-digested, non-acidic, non-bilious, white and foamy, make wake up at night coughing or choking
history of pneumonia
mild weight loss

Front 144

What is the diagnostic workup for achalasia?

Back 144

barium swallow → dilation and "bird-beaking" (smooth symmetrical narrowing) of distal esophagus, no peristaltic activity, poor esophageal emptying

esophageal manometry → no peristalsis + incomplete relaxation of lower esophageal sphincter on swallowing

Front 145

What is the management of achalasia?

Back 145

surgical myotomy
pneumonic dilation
botulin injections
for symptoms → sublingual nitrogen, CCBs, phophodiesterase inhibitors, anticholinergics

Front 146

What are the complications and pronosis of achalasia?

Back 146

severe weight loss if untreated
respiratory complications like stridor
post-botulin injections → recurrence
post-myotomy → GERD, strictures, Barrett's esophagus

Front 147

What is the prevention for Barrett's esophagus?

Back 147

manage GERD appropriately

Front 148

Back 148

Barrett's esophagus

Front 149

Back 149

bird-beaking of achalasia

Front 150

Back 150

esophageal varices

Front 151

Back 151

candidal esophagitis

Front 152

Back 152

schatzke's ring

Front 153

Back 153

mallory-weiss tear

Front 154

What is the diagnostic workup of GERD?

Back 154

labs normal
initial endoscopy not indicated if typical symptoms suggestive of non-complicated GERD

Front 155

What is the management of GERD?

Back 155

1. if typical symptoms → empiric therapy with PPI (omeprazole 20mg PO daily) 30 min before breakfast x 4-8 weeks
2. if alarm features (dysphagia, odynophagia, weight loss, iron deficiency anemia) or non-responsive to PPI → upper endoscopy with biopsy
3. appropriate counseling

Front 156

What is the patient education and prevention of GERD?

Back 156

1. avoid coffee, alcohol, citrus fruit, tomatoes, spicy foods, fatty foods, chocolate, peppermint
2. stop smoking
3. eat smaller meals
4. avoid lying down within 3 hours of eating
5. elevate head of bed 6 inches
6. take antacids before meals or to relieve symptoms → quick onset, provide relief for <2 hours
7. take OTC H2-receptor antagonists before meals or to relieve symptoms → slow onset (30 minutes), provide relief for 8 hours

Front 157

What is dyspepsia?

Back 157

1. acute, chronic or recurrent discomfort or pain in the epigastric region
2. epigastric pain or burning, early satiety or postprandial fullness

Front 158

What is the etiology of dyspepsia?

Back 158

eating fatty foods, eating too quickly, overeating, eating during stressful situations
excessive coffee or alcohol consumption
lactose intolerance
medications → iron, aspirin, NSAIDs, opioids, antibiotics (metronidazole, macrolides), antihypertensives (ACE inhibitors, ARBs), cholesterol-lowering agents (niacin, fibrates), digoxin, DM (metformin), corticosteroids, estrogen, SSRIs, serotonin-norepinephrine reuptake inhibitors, cholinesterase inhibitors, parkinson drugs
pregnancy
functional dyspepsia
GERD
peptic ulcer disease
diabetic gastroparesis
malabsorption conditions
parasitic infection (Giardia, Strongyloides)
pancreatic carcinoma
chronic pancreatitis
MI
paraesophageal hernia
gastric volvulus
intra-abdominal malignancy
CKD
DM
thyroid disease

occurs in 25% of adult population
accounts for 3% of office visitis

Front 159

What are the risk factors for dyspepsia?

Back 159

anxiety, depression, martial problems, employment problems, physical abuse, sexual abuse, history of psychotropic meds

Front 160

What is the clinical presentation of dyspepsia?

Back 160

epigastric pain or burning
early satiety
postprandial fullness
nausea and vomiting
bloating

Front 161

What is the diagnostic workup of dyspepsia?

Back 161

1. H. pylori testing
2. CBC, LYTES, Ca2+, HFP, thyroid function tests if >50y/o
2. endoscopy or abdominal imaging if >55y/o, constant or severe pain, weight loss, dysphagia, persistent vomiting, hematemesis, melena, anemia

Front 162

What is the management of dyspepsia?

Back 162

1. identify and discontinue offending agents (coffee, alcohol, medications)
2. H. pylori testing → urea breath test, IgG serology or fecal antigen
3. if H. pylori negative → trial empiric PPI x 4 weeks +/- antibiotics
4. if H. pylori positive → antibiotics +/- PPI
5. endoscopy indicated if failure to respond to empiric therapy or relapse
6. if endoscopy normal → diagnose as functional dyspepsia
7. if endoscopy abnormal → treat underlying disorder
8. alternatives include peppermint, caraway, psychotherapy, hypnotherapy

Front 163

What is the patient education for dyspepsia?

Back 163

1. reduce or discontinue drinking coffee and alcohol
2. if postprandial symptoms → eat small low-fat meals
3. keep food diary → food intake and symptoms

Front 164

What is the prevention of dyspepsia?

Back 164

avoid precipitating factors

Front 165

If H. pylori test negative and patient not taking NSAIDs, peptic ulcer disease can be excluded, true or false?

Back 165

true

Front 166

What is a hiatal hernia?

Back 166

herniation of part of stomach into thoracic cavity through esophageal hiatus in diaphragm

types include sliding, paraesphageal, and mixed

Front 167

What is the etiology of a hiatal hernia?

Back 167

cause unknown

associated with aging, obesity, smoking

may be congenital

very common
usually seen in >50y/o

Front 168

What is the clinical presentation of a hiatal hernia?

Back 168

asymptomatic
worsening of GERD

Front 169

What is the management of a hiatal hernia?

Back 169

1. appropriate GERD management
2. if paraesophageal hernia or non-responsive to GERD management → surgery

Front 170

What are the complications of a hiatal hernia?

Back 170

if paraesophageal hernia:
ulceration → bleeding → iron deficiency anemia
incarceration
strangulation

Front 171

What are the risk factors of hiatal hernia?

Back 171

aging, obesity, smoking

Front 172

What is the diagnostic workup of a hiatal hernia?

Back 172

upper endoscopy best for sliding hiatal hernia
barium swallow best for paraesophageal hernia

Front 173

What is erosive/hemorrhagic gastritis?

Back 173

damage to stomach lining without inflammation

Front 174

What is the etiology of erosive/hemorrhagic gastritis?

Back 174

alcoholism
NSAIDS
portal HTN
stress associated with severe illness
less common → caustic ingestion, radiation

Front 175

What are the risk factors for erosive/hemorrhagic gastritis?

Back 175

if stress associated →
trauma, liver failure, kidney disease, CNS injury, multi-organ failure, burns, coagulopathy, sepsis, shock, mechanical ventilation

Front 176

What is the clinical presentation of erosive/hemorrhagic gastritis?

Back 176

often asymptomatic
epigastric pain
nausea and vomiting
anorexia
upper GI bleed → hematemesis (coffee grounds), melena, bloody aspirate from NG suction

Front 177

What is the diagnostic workup of erosive/hemorrhagic gastritis?

Back 177

upper endoscopy → subepithelial petechiae, erosions, hemorrhages → vary in size, superificial, focal or diffuse

labs nonspecific → possible anemia

Front 178

What diseases comprise inflammatory bowel disease?

Back 178

ulcerative colitis
Crohn's disease
toxic megacolon

Front 179

What is ulcerative colitis?

Back 179

chronic recurrent inflammatory bowel disease characterized by diffuse mucosal inflammation of the rectum and colon

Front 180

What is Crohn's disease?

Back 180

chronic recurrent inflammatory bowel disease characterized by patchy transmural inflammation of any segment of the GI tract from mouth to anus

Front 181

What part of the GI tract is affected by ulcerative colitis?

Back 181

occurs at rectum and extends proximally to colon

Front 182

What part of the GI tract is affected by Crohn's disease?

Back 182

occurs in patches anywhere from mouth to anus

Front 183

List the extra-intestinal manifestations of ulcerative colitis and Crohn's disease.

Back 183

erythema nodosum
pyoderma gangrenosum
episcleritis or uveitis
oral ulcers
hepatitis
sclerosing cholangitis
arthritis → oligoarticular or polyarticular, peripheral, non-deforming
spondilitis or sacroiliitis
thromboembolism

Hint 183

Current ch15

Front 184

What is erythema nodosum?

Back 184

inflammatory disorder characterized by red indurated tender subcutaneous nodules

Front 185

Where does erythema nodosum most commonly present?

Back 185

shins

Front 186

Back 186

erythema nodosum

Front 187

Back 187

pyoderma gangrenosum

Front 188

What is diverticulosis?

Back 188

GI condition characterized by outpocketings in colon

Front 189

What is the etiology of diverticulosis?

Back 189

usually caused by long-standing fiber deficiency

other causes include inherent weakness in colonic wall or connective tissue disease (scleroderma, Marfan syndrome, Ehlers-Danlos syndrome)

possible hereditary factors

Front 190

What is the incidence of duverticulosis for <40y/o, 60/yo and 80y/o?

Back 190

<40y/o → <5%
60y/o → 30%
80y/o → >50%

Front 191

What is the clinical presentation of diverticulosis?

Back 191

usually asymptomatic and discovered incidentally via colonoscopy or barium enema
may have abdominal pain, chronic constipation, or fluctuating bowel habits
physical exam usually normal
may have LLQ tenderness with palpable thickened sigmoid and descending colon

Front 192

What is imaging modality is most sensitive for detecting diverticulosis?

Back 192

barium enema

Front 193

What is the diagnostic workup of diverticulosis?

Back 193

barium enema most sensitive for detecting diverticulosis
screening labs normal
imaging not indicated for diagnosis

Front 194

What is the management of diverticulosis?

Back 194

1. high-fiber diet → fruits, vegetables, and whole-grains
2. fiber supplements → bran powder, pysllium, or methylcellulose

Front 195

What are the complications of diverticulosis?

Back 195

lower GI bleeding
diverticulitis

Front 196

What is the patient education for diverticulosis?

Back 196

1. recommended daily fiber intake:
-38g for men <50y/o
-30g for men >50y/o
-25g for women <50y/o
-21g for women >50y/o
2. increase fiber intake by eating more fruits, vegetables and whole-grains
3. increase fiber intake slowly to prevent gas, cramping, and bloating
4. drink plenty of fluids
5. exercise regularly

Front 197

What is the prevention for diverticulosis?

Back 197

eat fiber!

Front 198

What part of the GI tract does diverticulosis affect?

Back 198

nearly always affects sigmoid and descending colon
15% affects proximal colon

Front 199

What are the USPSTF and American Cancer Society's screening recommendations for colorectal neoplasms?

Back 199

USPSTF:
1. recommends screening for colorectal cancer via fecal occult blood, sigmoidoscopy, or colonoscopy from 50-75y/o
2. recommendes against screening from 76-85y/o unless specific circumstance
3. recommends against screening >85y/o

ACS:
Beginning at age 50:
Tests that find polyps and cancer
•Flexible sigmoidoscopy every 5 years*
or
•Colonoscopy every 10 years or
•Double-contrast barium enema every 5 years*
or
•CT colonography (virtual colonoscopy) every 5 years*

Tests that primarily find cancer
•Yearly fecal occult blood test (gFOBT)**
or
•Yearly fecal immunochemical test (FIT) every year**
or
•Stool DNA test (sDNA), interval uncertain**

if test positive → do colonoscopy
for fecal occult blood tests → do series of 3

Front 200

What is pruritus ani?

Back 200

itching of the anogenital area

Front 201

What is the etiology of pruritus ani?

Back 201

contact dermatitis (soaps, colognes, douches, contraceptives, scented toilet paper)
irritating secretions (diarrhea, vaginal discharge, trichomoniasis)
infectious disorders (candidiasis, dermatophytosis, erythrasma, pinworms)
dermatologic disorders (intertrigo, seborrheic dermatitis , psoriasis, lichen simplex chronicus, lichen sclerosus)
hemorrhoids
nerve impingement of lumbosacral spine
SCC of anus
paget disease

Front 202

What is the clinical presentation of pruritus ani?

Back 202

anal pruritus
+/- erythema, fissuring, maceration, lichenification, excoriations

Front 203

What is the diagnostic workup of pruritus ani?

Back 203

wet mount → trichimoniasis, yeast
stool → pinworms
wood lamp → coral red fluorescence with erythrasma
spinal radiograph → spinal disease

Front 204

What is the management and appropriate referral of pruritus ani?

Back 204

pramoxine cream or lotion
hydrocortisone-pramoxine cream, lotion or ointment
capsaicin
balneol perianal cleansing lotion
tucks premoistened pads, ointment or cream

apply after a bowel movement

no referral

Front 205

What are the complications and prognosis of pruritus ani?

Back 205

often persistent or recurrent

Front 206

What is the patient education of pruritus ani?

Back 206

practice proper anal hygiene
change underwear daily

Front 207

What is proctitis?

Back 207

inflammation of anal and rectal mucosa

Front 208

What is the etiology of proctitis?

Back 208

INFECTIOUS:
usually STI via anal intercourse → gonorrhea, chlamydia, syphilis, HSV, condylomata acuminata

NON-INFECTIOUS:
fissures, fistulas, abscesses, ulcerative colitis, Crohn's disease, colorectal cancer

Front 209

What is the clinical presentation of proctitis?

Back 209

anorectal discomfort
tenesmus
constipation
mucus or bloody discharge
other symptoms dependent on etiology

Front 210

What is the diagnostic workup of proctitis?

Back 210

dependent on suspected etiology
GCCHDNA
RPR
HSV culture
biopsy for warts

Front 211

What is the management, appropriate referral, and patient education for proctitis?

Back 211

dependent on underlying cause
gonorrhea → ceftriaxone
chlamydia → doxycycline
syphilis → benzanthine penicillin
HSV → acyclovir
condylomata acuminata → cryosurgery, excision, etc.

Front 212

What are the complications and prognosis of proctitis?

Back 212

if untreated → abscesses, strictures, fistulas

Front 213

What is rectal prolapse?

Back 213

protrusion through the anus of some or all layers of the rectum

Front 214

What is the etiology of rectal prolapse?

Back 214

mucosal prolapse (common):
hemorrhoids

full prolapse (uncommon):
chronic constipation + weakened pelvic support (especially elderly, paraplegic, psychotic)
trauma
surgery

Front 215

What is the clinical presentation of rectal prolapse?

Back 215

rectal prolapse
intially reduces spontaneously after defecation
over time becomes chronically prolapsed
mucous discharge
bleeding
anal sphincter weakness
incontinence

Front 216

What is the diagnostic workup of rectal prolapse?

Back 216

none

Front 217

What is the management, appropriate referral, and patient education of rectal prolapse?

Back 217

1. manual reduction
2. rectal exam to confirm complete reduction
3. apply lubricant and gauze tape over anal opening for several hours following reduction
4. refer for colonoscopy or surgical consult
5. prevent constipation
6. if severe, cannot be reduced, recurs after reduction, suspected ischemia or necrosis → emergency surgical consult and hospitalization

Front 218

What are the complications and prognosis of rectal prolapse?

Back 218

superficial ulceration
venous engorgement
thrombosis
rectal incarceration, strangulation, ischemia and necrosis

Front 219

What is a perirectal abscess?

Back 219

abscess near rectal wall
may be ischiorectal, intersphincteric, or supralevator

Front 220

What is the etiology of perirectal abscess?

Back 220

blocked gland
infected fissure
STI
Crohn's disease (36%)
DM
leukemia
malignancy

Front 221

What is the clinical presentation of a perirectal abscess?

Back 221

pain
fever
mucous or bloody discharge with bowel movement
fluctuant mass palpable along rectal wall

Front 222

What is the diagnostic workup of a perirectal abscess?

Back 222

none

Front 223

What is the management, appropriate referral, and patient education of a perirectal abscess?

Back 223

1. if uncomplicated → I&D under local anesthesia
2. if complicated → surgical consult
3. consider admitting if ill-appearing, febrile, elderly, obese, debilitated
4. FU d/t high incidence of fistula

Front 224

What are the complications and prognosis of a perirectal abscess?

Back 224

sepsis
high incidence of fistula

Front 225

What is an anal fissure?

Back 225

linear or rocket-shaped anal ulcers <5mm in length

Front 226

What is the etiology of anal fissures?

Back 226

trauma during defecation → straining, constipation

if off midline → suspect Crohn's disease, TB, syphilis, HIV, anal carcinoma

Front 227

What is the clinical presentation of anal fissures?

Back 227

severe tearing pain during defecation → throbbing discomfort → constipation due to fear of recurrent pain
mild hematochezia → blood on stool or toilet paper
anal fissure → looks like crack in epithelium

Front 228

What is the diagnostic workup of anal fissures?

Back 228

none

Front 229

What is the management, appropriate referral, and patient education of anal fissures?

Back 229

topical anesthetics → EMLA cream
sitz baths
treat constipation → fiber supplements

Front 230

What are the complications and prognosis of anal fissures?

Back 230

chronic anal fissures
fibrosis
skin tags

healing occurs within 2 months
recurrence occurs in 40%

Front 231

What are hemorrhoids?

Back 231

dilated veins in lower rectum or anus

Front 232

What is the etiology of hemorrhoids?

Back 232

straining, constipation, low fiber diet, obesity, pregnancy, prolonged sitting, ulcerative colitis, Crohn's disease

Front 233

What is the clinical presentation of hemorrhoids?

Back 233

discomfort
hematochezia
protrusion

internal:
normally painless (above dentate line → not innervated by cutaneous nerves)
but can cause irritation and pruritus if prolapse
mucus discharge
bleeding

external hemorrhoids:
visible

Front 234

What is the diagnostic workup of hemorrhoids?

Back 234

positive fecal occult blood
anoscopy for internal hemorrhoids
hematocrit if excessive bleeding or anemia suspected

Front 235

What is the management, referral, and patient education of hemorrhoids?

Back 235

1. treat constipation → high fiber diet, increase fluid intake with meals, bran fiber, commercial bulk laxatives
2. if refractory to above treatment → injection sclerotherapy, rubber band ligation, or application of electrocoagulation
3. if severe bleeding → surgical excision
4. refer if conservative treatment fails or surgery required

Front 236

What are the complications and prognosis of hemorrhoids?

Back 236

internal hemorrhoids may become strangulated
external hemorrhoids may become thrombosed

recurrence common unless diet altered

Front 237

What is the difference between internal and external hemorrhoids?

Back 237

internal hemorrhoids occur above dentate/pectinate line while external hemorrhoids occur below it

Front 238

What are the 4 stages of internal hemorrhoids?

Back 238

•Stage I - Internal hemorrhoids that bleed
•Stage II – Internal hemorrhoids that cause bleeding and prolapse with straining but return to their resting point by themselves
•Stage III - Internal hemorrhoids that bleed and prolapse with straining and require manual effort for replacement into the anal canal
•Stage IV - Internal hemorrhoids that do not return into the anal canal and are therefore constantly outside

Front 239

Back 239

thrombosed external hemorrhoids

Front 240

What is hepatitis A?

Back 240

acute infectious disease of the liver

Front 241

hepatitis A ETIOLOGY

Back 241

hepatitis A virus (RNA virus)
route of transmission = fecal/oral
risk factors = undercooked shellfish, crowding, poor sanitation, IV drugs

Front 242

hepatitis A CLINICAL PRESENTATION

Back 242

30 day incubation
more severe in adults than children
abrupt or insidious onset
prodrome → fatigue, nausea,
vomiting, diarrhea or constipation, anorexia, upper respiratory symptoms, myalgia, arthralgia, aversion to smoking
low-grade fever
jaundice
RUQ or epigastric pain → mild, constant, worse with exertion or jarring
hepatomegaly and tenderness
splenomegaly
enlarged cervical and epitrochlear lymph nodes

Front 243

hepatitis A DIAGNOSTIC WORKUP

Back 243

WBC → normal to low
markedly elevated AST/ALT
proteinuria
bilirubinuria
elevated AST/ALT → elevated BILI and ALK PHOS
positive IgM and IgG

Front 244

hepatitis A PREVENTION

Back 244

hepatitis A vaccine
hand washing

Front 245

hepatitis A COMPLICATIONS

Back 245

acute cholecystitis
if concomitant hepC → fulminant hepatitis

Front 246

hepatitis A PROGNOSIS

Back 246

subsides in 2-3 weeks
complete recovery in 3 months
may persist for 1 year
does not cause chronic hepatitis

Front 247

hepatitis A MANAGEMENT

Back 247

symptomatic:
bed rest if symptoms marked
IV 10% glucose if vomiting marked
meals as tolerated
avoid alcohol, exercise, hepatotoxic drugs

HOSPITALIZATION:
1. encephalopathy
2. INR >1.6
3. unable to maintain hydration

Front 248

What is the etiology of spontaneous bacterial peritoninitis?

Back 248

absence of apparent intra-abdominal infection

cirrhosis complicated by ascites (20-30%)

gram-negative (klebsiella, E coli)
gram-positive (strep pneumo, viridans strep, enterococci)
NO anaerobic bacteria

Front 249

What is the clinical presentation of spontaneous bacterial peritonitis?

Back 249

history of chronic liver disease and ascites
fever
abdominal pain
signs of chronic liver disease
change in mental status
sudden worsening of renal function

Front 250

What is the diagnostic workup of spontaneous bacterial peritonitis?

Back 250

paracentesis → ascitic fluid
cell count w/ diff → PMN >250 cells/mcL diagnostic
BC

Front 251

What is the management, referral, and patient education for spontaneous bacterial peritonitis?

Back 251

1. antibiotics if PMN >250 → 3rd generation cephalosporin → cephtriaxone
2. repeat paracentesis after 48 hours → adjust antibiotics if PMN not decreased
3. IV albumin if at risk for kidney injury
4. prevention → ciprofloxacin daily x 1 year

Front 252

What are the complications and prognosis of spontaneous bacterial peritonitis?

Back 252

recurrence within 1 year (70%)

kidney injury (40%) → major cause of death

30% mortality (<10% if treated early)

Front 253

Define ascites.

Back 253

pathological accumulation of fluid in peritoneal cavity

Front 254

What is alcoholic hepatitis?

Back 254

acute or chronic inflammation and parenchymal necrosis of the liver due to excessive alcohol intake

Front 255

What is the etiology of alcoholic hepatitis?

Back 255

excessive alcohol intake
>80g/day for men

Front 256

What is the clinical presentation of alcohol hepatitis?

Back 256

history of >50g alcohol daily x 10 years
recent history of heavy drinking
fever
nausea
anorexia
jaundice
RUQ pain
hepatomegaly and tenderness
possible splenomegaly or ascites
may be asymptomatic or progress to cirrhosis

Front 257

What is the diagnostic workup of alcohol hepatitis?

Back 257

elevated AST → rarely above 300 units/L
AST 2x > ALT
elevated ALK PHOS → rarely 3x above normal
elevated bilirubin

leukocytopenia or leukocytosis
folate deficiency anemia
hypoalbuminemia
prolonged PT

Front 258

What is the management, patient education, and referral for alcoholic hepatitis?

Back 258

1. d/c alcohol
2. treat deficiencies if present


HOSPITALIZATION:
1. inability to maintain hydration
2. total bilirubin >10mg/dL
3. INR >1.6
4. hepatic encephalopathy

Front 259

What are the complications and prognosis of alcoholic hepatitis?

Back 259

reversible but most common cause of cirrhosis

Front 260

What is the prevention of alcoholic hepatitis?

Back 260

avoid alcohol

Front 261

Excessive alcohol can result in?

Back 261

alcoholic hepatitis
fatty liver
cirrhosis

Front 262

What are the most common causes of cirrhosis?

Back 262

1. alcoholism
2. hepC

Front 263

What is fatty liver?

Back 263

abnormal accumulation of triglycerides in hepatic cells

Front 264

What is the etiology of fatty liver?

Back 264

alcoholic fatty liver → excessive alcohol intake

non-alcoholic fatty liver:
obesity
obstructive sleep apnea
hypertriglyceridemia
endocrinopathies → DM, Cushing's syndrome, polycystic ovary syndrome, hypopituitarism
medications → corticosteroids, TPN
poisons
starvation and refeeding syndrome

risk increased if psoriasis

Front 265

What is the clinical presentation of fatty liver?

Back 265

often asymptomatic
mild RUQ pain
hepatomegaly

Front 266

What is the diagnostic workup of fatty liver?

Back 266

mildly elevated AST/ALT
mildly elevated ALK PHOS
AST/ALT ratio >1.0 in non-alcohlic fatty liver
liver biopsy → steatosis

Front 267

What is the management, patient education, and referral for fatty liver?

Back 267

1. treat underlying cause
2. dietary fat restriction
3. exercise
4. weight loss

Front 268

What is metabolic syndrome?

Back 268

obesity
HTN
hypertriglyceridemia
DM

Front 269

*What does the AST/ALT ratio tell you?

Back 269

think alcoholic hepatitis if >2.0
think viral hepatitis if <1.0

Front 270

What is hemocromatosis?

Back 270

autosomal recessive disease characterized by increased iron absorption and subsequent iron overload

Front 271

What is the etiology of hemochromatosis?

Back 271

autosomal recessive genetic disorder → increased iron absorption in duodenum → accumulation of iron (hemosiderin) in pituitary, heart, liver, pancreas, kidneys, adrenals, testes

rarely recognized until 5th decade

Front 272

What is the clinical presentation of hemochromatosis?

Back 272

usually asymptomatic
FH or abnormal iron studies
onset >50y/o
fatigue, arthralgias
skin pigmentation, cardiomegaly, hepatomegaly, cirrhosis, DM, impotence, arthritis

Front 273

What is the management, patient education, and referral for hemochromatosis?

Back 273

1. avoid dietary iron (red meat), raw shellfish, alcohol, iron supplement, vitamin C
2. therapeutic phlebotomy → 1-2 units weekly
3. liver biopsy to determine if cirrhosis present
4. genetic testing for 1st-degree relatives
5. monitor hct and iron studies

Front 274

What are the complications and prognosis for hemochromatosis?

Back 274

CHF
hepatic insufficiency
pancreatic insufficiency
hypogonadism

Front 275

What is the diagnostic workup of hemochromatosis?

Back 275

elevated IRON, TIBC, and FERR
mildly elevated AST and ALK PHOS

Front 276

What is Wilson's disease?

Back 276

autosomal recessive disorder characterized by abnormal copper accumulation

Front 277

What is the etiology of Wilson's disease?

Back 277

autosomal recessive genetic disorder → excessiveabsorption of copper in small intestine → decreased secretion of copper by liver → accumulation of copper in liver, brain, kidney, and cornea

usually presents <40y/o

Front 278

What is the clinical presentation of Wilson's disease?

Back 278

consider if:
adolescent with hepatitis, splenomegaly, coombs-negative hemolytic anemia, portal HTN, neurological or psychological abnormalities, chronic or fulminant hepatitis

Front 279

What is the diagnostic workup of Wilson's disease?

Back 279

↓ serum ceruloplasmin
↑ urinary copper

Front 280

What is the management of Wilson's disease?

Back 280

1. restrict dietary copper (mushrooms, organs, shellfish, nuts, chocolate)
2. oral penicillamine
3. refer all patients

Front 281

Back 281

Kaiser-Fleischer brownish ring at rim of cornea → Wilson's disease

Front 282

What is Budd-Chiari syndrome?

Back 282

hepatic vein obstruction

Front 283

What is the etiology of Budd-Chiari syndrome?

Back 283

hereditary or acquired hypercoagulable state → polycythemia vera, myeloproliferative disease, FVL, protein S or C deficiency,

Front 284

What is the clinical presentation of Budd-Chiari syndrome?

Back 284

may be fulminant, acute, subacute, or chronic (usually subacute)
jaundice
RUQ pain, hepatomegaly, tenderness
splenomegaly
ascites

Front 285

What is the diagnostic workup of Budd-Chiari syndrome?

Back 285

imaging → occlusion/absence of flow in hepatic vein(s) or inferior vena cava

Front 286

What are the complications of Budd-Chiari syndrome?

Back 286

hepatocellular carcinoma

Front 287

What is the clinical presentation of cirrhosis?

Back 287

Front 288

What is cholelithiasis?

Back 288

gallstones

may be cholesterol or calcium bilirubinate (<20%)

Front 289

What is the etiology of cholelithiasis?

Back 289

affect women > men
highest rates if >60y/o, Mexican American, Native American

Front 290

What are the risk factors of cholelithiasis?

Back 290

>60y/o
Mexican American
Native American
obesity, especially women
rapid weight loss
DM
cirrhosis, HepC in men
hypertriglyceridemia
drugs
Crohn's
prolonged fasting
hormone replacement therapy

Front 291

What is the clinical presentation of cholelithiasis?

Back 291

often asymptomatic and discovered incidentally
epigastric or RUQ pain → severe pain, radiation to RT scapula, episodic

Front 292

What is the diagnostic workup of cholelithiasis?

Back 292

ultrasound

Front 293

What is the management of cholelithiasis?

Back 293

1. if asymptomatic + no indications for cholecystectomy → lifestyle modifications
2. if asymptomatic + >3cm, Native American, bariatric surgery candidate, heart transplant candidate → cholecystectomy
3. if symptomatic → cholecystectomy
4. if cholecystectomy refused → oral cheno- and ursodeoxycholic acids x 2 years to dissolve stones

Front 294

What are the complications and prognosis of cholelithiasis?

Back 294

gallstone ileus

recurrence common in cholecystectomy not performed or ursodeoxycholic acids discontinued

Front 295

What is the prevention of cholelithiasis?

Back 295

low-carb diet
physical activity
caffeine (women)
magnesium and unsaturated fats (men)
aspirin, NSAIDs
cholecystectomy

Front 296

What is cholecystitis?

Back 296

inflammation of the gallbladder

Front 297

What is the etiology of acute cholecystitis?

Back 297

gallstones (90%) → gallstone obstructs cystic duct → inflammation of gallbladder

suspect acalculous cholecystitis if RUQ pain following surgery or in critically ill + no oral intake for prolonged period

infection in AIDs patient

Front 298

What are the risk factors of acute cholecystitis?

Back 298

gallstones
AIDs
surgery or critically ill + no oral intake for prolonged period

Front 299

What is the clinical presentation of acute cholecystitis?

Back 299

RUQ or epigastric pain → steady, severe, precipitated by large fatty meal, lasting 12-18 hours
fever
nausea and vomiting
Murphy sign
rebound tenderness
palpable gallbladder

Front 300

What is the diagnostic workup of acute cholecystitis?

Back 300

CBC → leukocytosis
abdominal x-ray → radiopaque gallstones (15%)
RUQ ultrasound → gallbladder wall thickening, pericholecystic fluid, sonographic murphy sign
HIDA scan → obstructed cystic duct

Front 301

What is the management of acute cholecystitis?

Back 301

HOSPITALIZATION:
1. IV antibiotics
2. analgesics
3. NPO
4. cholecystectomy
5.

Front 302

What are the complications and prognosis of cholecystitis?

Back 302

chronic cholecystitis
gangrene of gallbladder

Front 303

What is the patient education and prevention of cholecystitis?

Back 303

cholecystectomy

Front 304

HIDA scan only reliable if bilirubin ...

Back 304

<5 mg/dL

Front 305

Chronic Cholecystitis

Back 305

caused by recurrent acute cholecystitis or chronic irritation of gallbaldder by stones
treat with cholecystectomy
complications include pancreatitis, gallbladder carcinoma

Front 306

What is choledocolithiasis?

Back 306

gallstone in common bile duct

Front 307

What is the etiology of choledocolithiasis?

Back 307

gallstones (15%) → obstruction of common bile duct → biliary pain and jaundice

Front 308

What is the clinical presentation of choledocolithiasis?

Back 308

history of biliary pain or jaundice
RUQ or epigastric pain → sudden onset, severe, radiation to RT scapula
fever
nausea & vomiting
jaundice
RUQ tenderness
hepatomegaly

Front 309

What is the diagnostic workup of choledocolithiasis?

Back 309

increased AST/ALT
increased serum bilirubin
bilirubinuria
ERCP or PCT

Front 310

What is the management of choledocolithiasis?

Back 310

HOSPITALIZATION:
1. assess liver function → correct prolonged PT with IV vitamin K → ERCP → endoscopic sphincterotomy → stone extraction → cholecystectomy

Front 311

What are the complications and prognosis of choledocolithiasis?

Back 311

pancreatitis
if obstruction >30 days → cirrhosis → hepatic failure with portal HTN

Front 312

What is the patient education and prevention of choledocolithiasis?

Back 312

cholecystectomy

Front 313

What is Charcot triad?

Back 313

classic presentation of cholangitis → biliary pain + fever + jaundice

Front 314

What is cholangitis?

Back 314

infection of the common bile duct

Front 315

What is the etiology of cholangitis?

Back 315

choledocolithiasis

Front 316

What is the clinical presentation of cholangitis?

Back 316

Charcot triad → biliary pain + fever + jaundice

Front 317

What are the diagnostic criteria for cholangitis?

Back 317

Charcot triad (biliary pain + fever + jaundice)
or
2 elements of the Charcot triad + lab evidence of inflammation (elevated WBC, elevated CRP), elevated liver function tests, and evidence of biliary dilation or obstruction

Front 318

What is the management of cholangitis?

Back 318

HOSPITALIZATION:
same as choledocolithiasis + IV antibiotics

Front 319

What is primary sclerosing cholangitis?

Back 319

diffuse inflammation of the biliary tract leading to fibrosis and strictures

Front 320

primary sclerosing cholangitis ETIOLOGY

Back 320

associated with ulcerative colitis, less with Crohn's
rare
men 20-50y/o

Front 321

primary sclerosing cholangitis RISK FACTORS

Back 321

ulcerative colitis
Crohn's disease
FH

smoking = decreased risk

Front 322

primary sclerosing cholangitis CLINICAL PRESENTATION

Back 322

progressive jaundice
fatigue, pruritus, indigestion, anorexia
symptoms of cholestasis

Front 323

primary sclerosing cholangitis DIAGNOSTIC WORKUP

Back 323

elevated ALK PHOS
magnetic resonance cholangiography → segmental fibrosis of bile ducts with saccular dilations between strictures

Front 324

primary sclerosing cholangitis MANAGEMENT

Back 324

antibiotics for cholangitis
balloon dilation
stenting

cancer surveillance

liver transplant

Front 325

primary sclerosing cholangitis COMPLICATIONS
PROGNOSIS

Back 325

osteoporosis
malabsorption of fat-soluble vitamins
gallstones etc.

cholangiocarcinoma (20%) → CA 19-9 + RUQ US annually for serveillance

colorectal cancer if ulcerative colitis → annual colonoscopy

12-17 year survival rate

Front 326

What is pancreatitis?

Back 326

inflammation of the pancreas

Front 327

acute pancreatitis ETIOLOGY

Back 327

MOST COMMON:
biliary tract disease
alcoholism

LESS COMMON:
idiopathic
genetics
abdominal trauma
infection
hypercalcemia
hypertriglyercidemia
chylomicronemia
vasculitis
neoplasma (rare)
drugs
peritoneal dialysis

Front 328

acute pancreatitis RISK FACTORS

Back 328

smoking increases risk of alcoholic and idiopathic causes
older age
obesity

Front 329

acute pancreatitis CLINICAL PRESENTATION

Back 329

epigastric pain → abrupt onset, steady, severe, boring, deep, radiation to back, history of episodes, associated with heavy meal or alcohol intake, better by sitting and leaning forward, worse by walking or lying down
fever
weakness
sweating
nausea and vomiting
hypotension
tachycardia
pallor, cool clammy skin, mild jaundice
abdominal distension and tenderness, guarding, rigidity, rebound

Front 330

acute pancreatitis DIAGNOSTIC WORKUP

Back 330

elevated amylase and lipase 3x above normal within 24 hours
lipase more accurate than amylase
lipase remains elevated longer than amylase
leukocytosis etc
abdominal radiographs → possible gallstone, sentinal loop, cutoff sign,

Front 331

What are the ranson criteria for acute pancreatitis?

Back 331

3 or more of the following predicts severe course complicated by pancreatic necrosis:
>55y/o
WBC >16,000/mcL
glucose >200 mg/dL
LD >350 units/L
AST >250 units/L

Worsening prognosis if develop any of the following in the first 48 hours:
Hct decreases >10%
calcium <8 mg/dL
BUN increase >5%
arterial PO2 <60 mmHg
base deficit >4 mEq/L
fluid sequestration >6 L

mortality rates based on number of above criteria present:
0-2 = 1%
3-4 = 16%
5-6 = 40%
7-8 = 100%

Front 332

What is the clinical significance of the ranson criteria?

Back 332

predicts prognosis and mortality rate of pancreatitis

Front 333

What is pancreatitis?

Back 333

inflammation of the pancreas

Front 334

acute pancreatitis ETIOLOGY

Back 334

MOST COMMON:
biliary tract disease
alcoholism

LESS COMMON:
idiopathic
genetics
abdominal trauma
infection
hypercalcemia
hypertriglyercidemia
chylomicronemia
vasculitis
neoplasma (rare)
drugs
peritoneal dialysis

Front 335

acute pancreatitis RISK FACTORS

Back 335

smoking increases risk of alcoholic and idiopathic causes
older age
obesity

Front 336

acute pancreatitis CLINICAL PRESENTATION

Back 336

epigastric pain → abrupt onset, steady, severe, boring, deep, radiation to back, history of episodes, associated with heavy meal or alcohol intake, better by sitting and leaning forward, worse by walking or lying down
fever
weakness
sweating
nausea and vomiting
hypotension
tachycardia
pallor, cool clammy skin, mild jaundice
abdominal distension and tenderness, guarding, rigidity, rebound

Front 337

acute pancreatitis DIAGNOSTIC WORKUP

Back 337

elevated amylase and lipase 3x above normal within 24 hours
lipase more accurate than amylase
lipase remains elevated longer than amylase
leukocytosis etc
abdominal radiographs → possible gallstone, sentinal loop, cutoff sign,

Front 338

What are the ranson criteria for acute pancreatitis?

Back 338

3 or more of the following predicts severe course complicated by pancreatic necrosis:
>55y/o
WBC >16,000/mcL
glucose >200 mg/dL
LD >350 units/L
AST >250 units/L

Worsening prognosis if develop any of the following in the first 48 hours:
Hct decreases >10%
calcium <8 mg/dL
BUN increase >5%
arterial PO2 <60 mmHg
base deficit >4 mEq/L
fluid sequestration >6 L

mortality rates based on number of above criteria present:
0-2 = 1%
3-4 = 16%
5-6 = 40%
7-8 = 100%

Front 339

What is the clinical significance of the ranson criteria?

Back 339

predicts prognosis and mortality rate of pancreatitis

Front 340

What is hemolytic uremic syndrome (HUS)?

Back 340

disorder characterized by thrombocytopenia, microangiopathic hemolytic anemia, and renal failure

Front 341

What is the etiology of HUS?

Back 341

associated with E. coli 0157:H7 → produces shiga-like toxin → damages endothelial cells → causing thrombus formation → platelet aggregation → thrombocytosis + microangiopathic hemolytic anemia; commonly affects children

Front 342

What is the clinical presentation of HUS?

Back 342

influenza-like or GI prodrome
bloody diarrhea
hematuria
oliguria
actue renal failure (because kidneys require high volume of blood flow)

Front 343

What is the diagnostic work-up of HUS?

Back 343

CBC → anemia, thrombocytopenia
RETIC → high
blood smear → schistocytes
indirect BILI → high
LD → high
CREAT → high
PT → normal
PTT → normal
bleeding time → prolonged
E. coli O157:H7 → positive

Front 344

What are the complications of HUS?

Back 344

permanent kidney damage
death

Front 345

What is the managment of HUS?

Back 345

1. hospitalize → observe
2. supportive care
3. dialysis if necessary
4. antibiotics and platelet transfusions contraindicated

Front 346

What are the 4 types of diarrhea?

Back 346

secretory
osmotic
exudative
altered intestinal transit time

Front 347

What is the duration for acute and chronic diarrhea?

Back 347

acute <2 weeks
chronic >2 weeks

Front 348

Define diarrhea.

Back 348

increased number of bowel movements (>3 per day) or liquidity of feces

Front 349

What is the etiology of acute diarrhea?

Back 349

NON-INFLAMMATORY:
viruses → norovirus, rotavirus (schools, nursing homes, cruiseships)
protozoa → giardia lamblia, cryptosporidium, cyclospora
non-invasive bacteria:
-preformed enterotoxin → s. aureus, b. cereus, c. perfringens
-enterotoxin production → v. cholerae, ETEC

INFLAMMATORY:
viral → CMV
protozoa → entamoeba histolytica
invasive bacteria → shigella, campylobacter jejuni, salmonella, EIEC, yersinia, listeria, gonorrhea, chlamydia
toxin-producing bacteria → CDIF (recent antibiotics), vibrio parahaemolyticus

can also be caused by drugs

Front 350

What is the clinical presentation of acute diarrhea?

Back 350

<2 weeks in duration

NON-INFLAMMATORY:
diarrhea typically mild, large volume
stool → watery, non-bloody
nausea and vomiting
periumbilical cramps and bloating

INFLAMMATORY:
fever
diarrhea typically small volume (<1L/day)
stool → bloody, pus
LLQ cramps, urgency, tenesmus

Front 351

What is the diagnostic workup of acute diarrhea?

Back 351

NON-INFLAMMATORY:
none unless severe or persists >7 days
negative fecal leukocytes

INFLAMMATORY:
positive fecal leukocytes or lactoferrin
stool culture
O&P
E coli 0157:H7
CDIF if risk factors

Front 352

What is the management, referral, and patient education for acute diarrhea?

Back 352

NON-INFLAMMATORY:
1. self-limited within 5 days
2. rehydration therapy → 1 liter water, 1 tbsp sugar, 1 tsp salt
3. antidiarrheals → loperamide
4. peptol-bismol → traveler's diarrhea, viral enteritis
5. if persists >7 days → order fecal leukocytes or lactoferrin, stool culture, O&P

INFLAMMATORY:
1. do not treat with antidiarrheals
2. antibiotic treatment depends on underlying cause
-if empiric → consider if bloody stool, severe fever, tenesmus, fecal lactoferrin (but not due to E coli)
-if specific → shigellosis, cholera, extraintestinal salmonellosis, traveler's diarrhea, C difficile infection, giardiasis, and amebiasis

HOSPITALIZATION:
severe dehydration
severe or worsening bloody diarrhea
severe or wrosening diarrhea in >70y/o or immunocompromised
severe abdominal pain
severe infection (high fever, rash, leukocytosis) or sepsis

Front 353

What are the complications and prognosis of acute diarrhea?

Back 353

severe dehydration → hypokalemia, metabolic acidosis
toxic colitis
sepsis

Front 354

Bacteria of >14 days in duration can be caused by bacteria, true or false?

Back 354

false except for CDIF

Front 355

What is the non-pharmacologic management of diarrhea?

Back 355

1. adequate oral fluids with carbs and lytes (oral rehydration solution → 1L water, 1 tbsp sugar, 1 tsp salt)
2. drink tea or flat carbonated beverages
3. eat soft easily digested foods (bananas, applesauce, soup, crackers, toast, rice)
3. avoid fiber, fats, milk products, caffeine, alcohol

Front 356

List malabsorption disorders.

Back 356

Whipple's disease
short bowel syndrome
celiac sprue

Front 357

What is Whipple's disease?

Back 357

rare multisystemic malabsorption disorder caused by bacteria Tropheryma whippelii

Front 358

What is the etiology of Whipple's disease?

Back 358

bacteria Tropheryma whippelii
source of infection unknown

commonly affects men 40-70y/o

Front 359

What is the clinical presentation of Whipple's disease?

Back 359

arthralgias → migratory, non-deforming, typically first symptom
intermittent low-grade fever
abdominal pain
distension
flatulence
chronic diarrhea
steatorrhea (excess fat in stool)
malabsorption
weight loss
lymphadenopathy
hyperpigmentation of sun-exposed areas
peripheral edema

Front 360

What is the diagnostic workup of Whipple's disease?

Back 360

possible abnormalities include:
iron deficiency anemia
B12/folate deficiency anemia
decreased calcium, magnesium, cholesterol, vitamin A, vitamin D
hypoalbuminemia
increased fecal fat
endoscopy → biopsy of duodenum → periodic acid-Schiff (PAS)-positive macrophages with characteristic bacillus
confirm by PCR

Front 361

What is the management, referral, and patient education for Whipple's disease?

Back 361

1. antibiotics → TMP-SMX x 1 year
2. if severely ill → IV ceftriaxone x 2 weeks, then TMP-SMX x 1 year
3. repeat duodenal biopsy at 6 and 12 months

Front 362

What are the complications and prognosis of Whipple's disease?

Back 362

CHF
valvular regurgitation (heart murmur)
CNS involvement (lethargy, dementia, myoclonus, seizures, coma

recovery in 1-3 months
relapse in 33% when d/c treatment

Front 363

What is celiac disease?

Back 363

permanent dietary disorder caused by immunlogic response to gluten

Front 364

What is the etiology of celiac disease?

Back 364

autoimmune → immunologic response to gluten → diffuse damage to proximal small intestinal mucosa → malabsorption

1:100 whites

Front 365

What is the clinical presentation of celiac disease?

Back 365

symptoms often present for 10 years before diagnosis
weakness
abdominal distention
chronic diarrhea
steatorrhea
weight loss
muscle wasting
growth retardation
atypically fatigue, depression, short stature, delayed puberty, amenorrhea, infertility, dermatitis herpetiformis (pruritic papulovesicles over the extensor surfaces of the extremities and over the trunk, scalp, and neck)

Front 366

What is the diagnostic workup of celiac disease?

Back 366

SCREENING:
positive IgA endomysial antibody test
positive IgA tTG antibody test

CONFIRMATION:
endoscopy → distal duodenum or proximal jejunum mucosal biopsy


increased fecal fat



possible abnormalities include:
iron, B12, and folate deficiency
hypocalcemia
mild increased AST/ALT
elevated alk phos
hypoalbuminemia
decreased vitamin A or D
prolonged PT

Front 367

What is the management, referral, and patient education of celiac disease?

Back 367

1. gluten-free diet → avoid wheat, rye, barley
2. avoid dairy until GI symptoms improve (often lactose intolerant)
3. avoid dietary supplements initially
4. bone scan to assess for osteoporosis → calcium, vitamin D and bisphosphonate if positive
5. monitor IgA endomysial antibody and IgA tTG antibody → negative after 6-12 months of gluten-free diet
6. dietician/support groups

Front 368

What are the complications and prognosis of celiac disease?

Back 368

COMPLICATIONS:
associated autoimmune disorders
refractory to gluten-free diet


PROGNOSIS:
excellent
improvement within few weeks if strict gluten-free diet

Front 369

What is gluten?

Back 369

storage protein found in certain grains (wheat, rhy, barley)

Front 370

What is short bowel syndrome?

Back 370

disorder of malabsorption due to removal of segment of small intestine

Front 371

What is the etiology of short bowel syndrome?

Back 371

surgical resection of small intestine

d/t Crohn's disease, trauma, volvulus, mesenteric infarction, tumor, radiation enteritis

Front 372

What is the clinical presentation of short bowel syndrome?

Back 372

symptoms dependent on site and length of resection

terminal ileum → malabsorption of bile salts, vitamin B12, fat-soluble vitamins

extensive small bowel → diarrhea, weight loss,

Front 373

What is the diagnostic workup of short bowel syndrome?

Back 373

vitamin deficiencies
increased fecal fat

Front 374

What is the management of short bowel syndrome?

Back 374

dependent on location and severity of resection:
low-fat diet
vitamin B12 IM injections
bile salt binding resins
vitamins
antidiarrheals
PPIs
parenteral nutrition

Front 375

What is the management of laxative abuse syndrome?

Back 375

refer to mental health professional, dietician, and support groups

Front 376

What is the prophylaxis and treatment for traveler's diarrhea?

Back 376

PROPHYLAXIS:
1. not recommended unless comorbidities → heart disease in elderly, IBD, IBS, DM, HIV, immunosuppressant therapy
2. daily ciprofloxacin
3. start upon arrival and continue 1-2 days after leaving
4. not recommended if travel >3 weeks

TREATMENT:
1. usually self-limited occuring within 1 week of travel
2. supply traveler in case significant diarrhea develops
3. loperamide → 4mg loading dose then 2mg after each loose stool up to 16mg/day (only if no fever or bloody stool)
4. single oral dose of ciprofloxacin
5. oral rehydration solution

Front 377

What is the etiology of traveler's diarrhea?

Back 377

bacteria (80%)
most common → ETEC, shigella, campylobacter jejuni
less common → Aeromonas, Salmonella, noncholera vibriones, E histolytica, G lamblia
sometimes caused by virus (rotavirus, adenovirus)
associated with change in climate, living conditions/sanitation, food/drink, bowel flora

Front 378

What is a fecal impaction?

Back 378

large mass of dry hard stool in the rectum due to chronic constipation

Front 379

What is the etiology of fecal impaction?

Back 379

chronic constipation d/t:
colon neurogenic disorders
spinal cord disorders
severe psychiatric disease
prolonged bed rest
medications (opioids)

Front 380

What is the clinical presentation of fecal impaction?

Back 380

decreased appetitie
nausea and vomiting
abdominal pain and distention
paradoxical diarrhea (fluids leak around impaction)
firm feces palpable on DRE

Front 381

What is the management of fecal impaction?

Back 381

enemas (saline, mineral oil, diatrizoate)
digital disruption
prevent constipation (stool softeners, regular bowel movements)

Front 382

What is the clinical presentation of acute upper GI bleed?

Back 382

hematemesis → bright red or brown "coffee grounds"
melena (usually)
hematochezia (if massive bleed)

Front 383

What is the etiology of acute upper GI bleed?

Back 383

peptic ulcer disease (80%)
cirrhosis → portal HTN → esophageal varices, gastric or duodenal varices, portal HTN gastropathy (10-20%)
mallory-weiss tear (5-10%)
vascular anomalies (7%)
gastric neoplasms (1%)
erosive gastritis
erosive esophagitis

Front 384

Why should you be wary when ordering a hct if suspect active bleeding?

Back 384

poor early indicator of bleed (just because normal does not mean that there is no blood loss)
takes 24-72 hours to normalize

Front 385

What is the management of upper GI bleed?

Back 385

1. 80% self-limited
2. assess hemodynamic status → BP, HR
3. IV fluids
4. labs → CBC, CREAT, liver enzymes, PT/INR, type&screen
5. packed RBCs, platelets, and FFP as needed
6. NG tube
7. endoscopy

Front 386

What is the anatomical distinction between upper and lower GI bleed?

Back 386

ligament of Treitz

Front 387

What is the clinical presentation of active lower GI bleed?

Back 387

maroon stool = small intestine or RT colon
hematochezia
-bright red streaking = anorectal
-bright red large = colon
*but remember 10% are d/t massive upper GI bleed

Front 388

What is the etiology of active lower GI bleed?

Back 388

if <50y/o:
infectious colitis
anorectal disease → hemorrhoids (10%), rectal ulcers (9%)
IBD

if >50y/o:
diverticulosis (50%)
malignancy (7%)
vascular ectasias (3%)
ischemia

20% idiopathic

Front 389

What is the management of active lower GI bleed?

Back 389

1. initial management same as upper GI bleed
2. NG aspiration to exclude upper GI source
3. if <45y/o + small volume bleed → anoscopy or sigmoidoscopy
4. if large bleed → colonoscopy
5. nuclear bleeding scan and angiography

Front 390

What is an occult GI bleed?

Back 390

bleeding unapparent to patient

Front 391

What is the etiology of occult GI bleed?

Back 391

35-55% upper GI bleed
15-30% colon

1. neoplasm
2. vascular abnormalities
3. acid-peptic lesions → esophagitis, peptic ulcer disease, hiatal hernia erosions
4. infections → TB, hookworm
5. medications → aspirin, NSAIDs
6. IBD

Front 392

How is an occult GI bleed detected?

Back 392

fecal occult blood (FOBT, FIT)
iron deficiency anemia in absence of visible blood loss

Front 393

What is the management of occult GI bleed?

Back 393

1. if asymptomatic + routine colorectal cancer screening → colonoscopy
2. if symptomatic → upper endoscopy + colonoscopy
3. if <60y/o + still unexplained despite above → further eval of small intestine
4. if >60y/o + still unexplained → empiric trial of iron supplementation → further eval if refractory
5. d/c antiplatelet agents

Front 394

What is the pathophysiology of Gilbert's syndrome?

Back 394

familial form of unconjugated hyperbilirubinemia

decreased activity of uridine diphosphate-glucuronyl transferase (which normally conjugates bilirubin) → unconjugated hyperbilirubinemia

Front 395

What is the clinical presentation of Gilbert's syndrome?

Back 395

usually asymptomatic
mild jaundice if fasting, exertion, stress, infection
unconjugated hyperbilirubinemia
normal LFTs

Front 396

What is the pathophysiology of hemolysis?

Back 396

increased destruction of RBCs → increase in unconjugated bilirubin → unconjucated hyperbilirubinemia

Front 397

What is the ddx for indirect hyperbilirubinemia?

Back 397

indirect = unconjugated

1. physiologic → neonatal jaundice
2. increased production → hemolytic disorders → sickle cell anemia, G6PD deficiency, hematomas, drug rxn (probenecid, rifampin), transfusion rxn
3. impaired uptake → CHF, drugs, contrast
4. impaired conjugation → Gilbert's syndrome, Crigler-Najjar syndrome

Front 398

What is the ddx for direct hyperbilirubinemia?

Back 398

direct = conjugated

1. hepatocellular disease → hepatitis, hemochromatosis, Wilson's disease, acute fatty liver of pregnancy, hepatotoxicity
2. biliary obstruction → choledocolithiasis, cholangitis, primary biliary cirrhosis, pancreatitis
3. congenital disorders → Dubin-Johnson syndrome, Rotor's syndrome

Front 399

What is the pathophysiology of jaundice in biliary obstruction?

Back 399

biliary obstruction → impaired flow of bile into intestine → bile contains conjugated bilirubin → conjugated hyperbilirubinemia

Front 400

What is the pathophysiology of jaundice in hepatocellular disease?

Back 400

hepatocellular disease → impaired secretion of conjugated bilirubin into bile → conjugated hyperbilirubinemia

Front 401

List categories of tests to think about when evaluating the liver.

Back 401

1. synthetic liver function
2. excretory liver function and cholestasis
3. hepatocellular injury
4. detoxifying liver function and serum ammonia
5. specific diseases

Front 402

What is included in an LFT panel?

Back 402

ALT
AST
bilirubin
alkaline phosphatase
albumin

Front 403

What does AST stand for?

Back 403

aspartate aminotransferase

Front 404

What does ALT stand for?

Back 404

alanine aminotransferase

Front 405

What liver tests are used to evaluate plasma protein synthesis?

Back 405

albumin
prealbumin
PT/INR (clotting proteins)

Front 406

What liver tests are used to evaluate hepatocellular injury?

Back 406

AST
ALT

Front 407

What liver test is used to evaluate detoxification?

Back 407

ammonia

Front 408

What liver tests are used to evaluate cholestasis?

Back 408

bilirubin
alkaline phosphatase

Front 409

What is albumin?

Back 409

major plasma protein

Front 410

What are the functions of albumin?

Back 410

maintain oncotic pressure
bind and transport anions, FAs, hormones, and drugs

Front 411

Why are serum album levels often normal in acute viral hepatitis or drug-related hepatotoxicity?

Back 411

serum albumin half-life = 20 days
complete cessation of albumin synthesis results in only 25% decrease in serum concentration after 8 days
thus serum albumin concentrations are slow to fall following injury

Front 412

Why are the indications for ordering albumin?

Back 412

measure of protein synthetic function

Front 413

What is the normal range of albumin?

Back 413

3.5-5.5 grams/dL

Front 414

What is the significance of a decreased albumin level?

Back 414

LIVER DYSFUNCTION:
viral hepatitis
hepatic cirrhosis
toxin ingestion

NON-LIVER:
malnutrition
malabsorption
protein loss from gut (nephrotic syndrome)
protein loss from kidney (protein-losing enteropathy)
protein loss from skin (burns)
inflammation (negative acute phase reactant)
volume overload (IV fluids)

Front 415

What does it mean that albumin is a negative acute phase reactant?

Back 415

in setting of inflammation, liver produces less albumin

Front 416

When does hypoalbuminemia produce symptoms?

Back 416

not until albumin really low (<2-2.5g/dL)

Front 417

What are the symptoms of hypoalbuminemia?

Back 417

peripheral edema
pulmonary edema
ascites

Front 418

What is the significance of hyperalbuminemia?

Back 418

anabolic steroids

FALSELY ELEVATED:
marked dehydration
ampicillin
heparin

Front 419

What is the normal range for prealbumin?

Back 419

19.5-35.8 mg/dL

Front 420

What are the indications for ordering a prealbumin?

Back 420

evaluation of protein nutrition
especially to monitor IV or tube feeding

Front 421

Compare albumin and prealbumin.

Back 421

both synthesized by liver
both bind and transport solutes

prealbumin → short half life (2 days), levels respond quickly to disease, high % of tryptophan and amino acids
albumin → long half life (20 days), levels respond slowly to disease

Front 422

What is string sign?

Back 422

1. radiographic sign seen on contrast GI studies
2. indicates narrowing of bowel loop (potentially dispensible or permanently narrowed)
3. usually seen in terminal ileum in Crohn's disease where bowel loop irritability → severe spasm → may lead to fibrosis and permanent narrowing
4. may also be caused by carcinoid, hypertrophic pyloric sphincter

Front 423

Back 423

string sign

Front 424

What is an apple core lesion?

Back 424

1. radiographic sign seen on barium enema
2. usually occur in sigmoid colon, sometimes esophagus
3. appears when mass encircles and narrows a tubular structure of the body
4. often caused by adenocarcinoma or lymphoma

Front 425

Back 425

apple core lesion

Front 426

Back 426

subdiaphragmatic free air

Front 427

What is subdiaphragmatic free air?

Back 427

1. radiograph sign seen on abdominal x-ray
2. air beneath diaphragm
3. indicates pneumoperitoneum
4. caused by perforation → most often peptic ulcer perforation

Front 428

What is a sentinal loop?

Back 428

1. radiographic sign seen on abdominal x-ray
2. isolated distended loop of bowel near site of inflammation/injury
3. body attempts to localize inflammation → distension caused by local paralysis and accumulation of gas

Front 429

What is the most common cause of string sign?

Back 429

Crohn's disease

Front 430

What is the normal range for total bilirubin?

Back 430

0.3-1.0 mg/dL

Front 431

What is the normal range for indirect (unconjugated) bilirubin?

Back 431

0.2-0.7 mg/dL

Front 432

What is the norma range for direct (conjugated) bilirubin?

Back 432

0.1-0.3 mg/dL

Front 433

Describe bilirubin metabolism.

Back 433

RBC breakdown in spleen → unconjugated bilirubin released, bound to albumin, and transported to liver → unconjugated bilirubin converted to conjugated bilirubin → conjugated bilirubin secreted into bile and excreted in feces

Front 434

At what total bilirubin concentration does jaundice develop?

Back 434

2-4 mg/dL

*normal 0.3-1.0 mg/dL

Front 435

What does the MELD score stand for?

Back 435

model for end-stage liver disease score

Front 436

What does the MELD score consist of and what is its clinical usefulness?

Back 436

Criteria include:
1. serum total bilirubin mg/dL
2. serum creatinine mg/dL
3. INR

Clinical usefulness:
1. to determine liver transplant allocation in U.S.
2. to predict mortality in cirrhotic patients undergoing non-transplant surgical procedures
-mortality increases 1% for each MELD point up to 20 and 2% for every MELD point over 20

Front 437

Back 437

colon cut-off sign

Front 438

Back 438

string of pearls sign (small bowel obstruction)

Front 439

What are the causes of false positive and negative of fecal occult blood?

Back 439

false positive: aspirin, NSAIDs, fish, poultry, red meat, turnips, horseradish

false negative: vitamin C

Front 440

What is psyllium?

Back 440

AKA metamucil
bulk-forming laxative used to treat constipation

Front 441

What is methycellulose?

Back 441

used to treat constipation

Front 442

When should diarrhea NOT be treated with antidiarrheals?

Back 442

bloody stool
high fever
systemic toxicity
d/c if worsening diarrhea

okay if mild to moderate diarrhea with none of the above

Front 443

What is the clinical presentation of laxative abuse syndrome?

Back 443

dehydration
electrolyte imbalance
prolonged use causes constipation
laxative dependency → larger doses of laxative needed to produce same effect on colon
intestinal paralysis, colonic infection, IBS, colon cancer, liver damage
bloody stool → anemia
if recovering → water retention, edema, weight gain

Front 444

Antibiotics are not recommended in diarrhea caused by?

Back 444

salmonella
campylobacter
E coli O157:H7
Yersinia
Aeromonas

Front 445

Why is ipecac no longer used to induce vomiting?

Back 445

only causes partial evacuation
delays or prevents use of activated charcoal
increases risk of pulmonary aspiration
increases risk of toxic effects on heart

Front 446

List type of drugs used to treat diarrhea.

Back 446

antiperistaltic agents
absorbents
bismith subsalicylate
polycarbophil
bile acid sequestrants

Front 447

bismuth subalicylate (AKA pepto-bismol)

Back 447

antidiarrheal

MOA:

INDICATIONS:
symptomatic treatment of mild nonspecific diarrhea
adjunct for traveler's diarrhea
adjunct for H pylori

CONTRAINDICATIONS:
children recovering from viral illness due to risk of Reye's syndrome
breast feeding

ADVERSE EFFECTS:
black tongue
black stool

DRUG INTERACTIONS

DOSING:

PATIENT EDUCATION:

Front 448

List antiperistaltic agents.

Back 448

loperamide
diphenoxylate
paregoric

Front 449

loperamide

Back 449

antiperistaltic agent

MOA:
acts on opioid receptor to inhibit peristalsis and prolong transit time

INDICATIONS:
chronic diarrhea associated wtih IBD
acute nonspecific diarrhea
traveler's diarrhea

CONTRAINDICATIONS:
children <2
breast feeding
abdominal pain w/out diarrhea
bloody diarrhea
diarrhea with high fever
acute dysentary
bacterial enterocolitis
pseudomembranous colitis
acute ulcerative colitis


ADVERSE EFFECTS:
constipation
nausea
abdominal cramps
dizziness

DRUG INTERACTIONS

DOSING:

PATIENT EDUCATION:

Front 450

List categories of drugs used to treat constipation.

Back 450

bulk forming agents
surfactants/stool softeners
lubricants
osmotic agents
stimulants
enemas
sugar alcohol/synthetic sugar

Front 451

Castor oil should be avoided in what patient population?

Back 451

pregnant women → may stimulate contractions

Front 452

List bulk forming agents.

Back 452

psyllium
methylcellulose
polycarbophil

Front 453

Polycarbophil can be used to treat diarrhea and constipation, true or false?

Back 453

true

Front 454

psyllium

Back 454

Bulk-producing laxative
antidiarrheal
MOA:
Soluble fiber
Absorbs water in intestine to form viscous liquid which promotes peristalsis and reduces transit time
INDICATIONS:
Dietary fiber supplement
Treatment of constipation lasting <1 week

CONTRAINDICATIONS:
Nausea, vomiting, abdominal pain
Fecal impaction, GI obstruction
Use caution in elderly, swallowing disorders, esophageal disorders

ADVERSE EFFECTS:
Abdominal cramps, constipation, diarrhea, esophageal or bowel obstruction

DRUG INTERACTIONS
None

DOSING:

PATIENT EDUCATION:
Take with 8oz water to prevent choking

Front 455

What type of drug is docusate?

Back 455

stool softener

Front 456

dronabinol (THC)

Back 456

marijuana derivative

antiemetic
appetite stimulant

INDICATIONS:
chemotherapy-related nausea and vomiting
AIDs-related anorexia

CONTRAINDICATIONS:
hypersensitivity
history of schizophrenia, mania, depression
caution if elderly, hepatic disease, seizures, history of substance abuse

ADVERSE EFFECTS:
sedation, dysphoria, vertigo, disorientation, vertigo

PATIENT EDUCATION:
use caution when performing taks that require mental alertness
potential for abuse
may cause withdrawl with abrupt discontinuation
psychiatric monitoring

Front 457

metoclopramide

Back 457

INDICATIONS:
symptomatic treatment of GERD or diabetic gastric stasis

MOA:
blocks dopamine receptors in CNS
blocks seratonin receptors
enhances response to Ach in upper GI tract → enhanced motility and accelerated gastric emptying

ADVERSE EFFECTS:
extrapyrimidal symptoms → restlessness,

Front 458

What causes pruritus in patients with liver disease?

Back 458

deposition of bile acids in skin

Front 459

Why does bile acid malabsorption manifest as chronic diarrhea?

Back 459

larger amounts of bile acids than normal enter colon, stimulating water secretion and intestinal motility, causing symptoms of chronic diarrhea

Front 460

What occurs first, jaundice or conjuctival icterus?

Back 460

conjunctival icterus

Front 461

Where does colon cancer most commonly metastasize to?

Back 461

liver

Front 462

Most colon cancers arise from?

Back 462

adenomas

Front 463

Which has a greater risk of malignancy, tubular adenomas or villous adenomas?

Back 463

villous adenomas

Front 464

What are the risk factors for colon cancer?

Back 464

>50y/o
hx of adenomatous poyps - villous > tubular
hx of IBD - ulcerative colitis > Crohn's disease
positive FH - first-degree relatives