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128 Cards in this Set

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Abdominal Hernias
=hernias are protrusions of peritoneum through an opening --> usually at sites of weakness
Diaphragmatic Hernia
=Abdominal structures enter the thorax --> most commonly a HIATAL HERNIA in which the stomach herniates UPWARD through the esophageal hiatus of the diaphragm

**May occur in infants as a result of defective development of the PLEUROPERITONEAL MEMBRANE
Indirect Inguinal Hernia
**An INdirect hernia goes through the INternal (=deep) inguinal ring + external (=superficial) inguinal ring and INto the scrotum

**Enters the internal inguinal ring LATERAL to the inferior epigastric artery

**Occur in INfants due to failure of the PROCESSUS VAGINALIS to close

**Much more common in MALES.
Direct Inguinal Hernia
=protrudes through the inguinal (=Hesselbach's) triangle

**Bulges directly through the abdominal wall MEDIAL to hte inferior epigastric artery and goes through the EXTERNAL (=superficial) inguinal ring ONLY

**Usually occurs in OLDER men
What makes up Hesselbach's Triangle?
1) Inferior epigastric artery

2) Lateral border of the rectus abdominis

3) Inguinal ligament
MD's don't LIe!
M-edial to the inferior epigastric artery = D-irect hernia

L-ateral to inferior epigastric artery = I-ndirect hernia
What is Achalasia?
=failure of relaxation of lower esophageal sphincter due to LOSS of myenteric (=Auerbach's plexus)

**Secondary achalasia may arise from CHAGA'S DISEASE
Findings:
**Causes PROGRESSIVE DYSPHAGIA

=Barium swallow does DILATED esophagus w/ an area of distal stenosis
=BIRD'S BEAK ON BARIUM SWALLOW

**Associated w/ an increased risk of esophageal carcinoma.
What is Meckel's Diverticulum?
**Most common congenital anomaly of the GI tract:

=persistence of the vitelline duct or yolk stalk

=may contain ectopic acid-secreting gastric mucosa and/or pancreatic tissue
Manifestations:
=bleeding
=intussusception (telescoping)
=volvulus (twisting of intestine causes obstruction + possible vascular compromise)
=obstruction near the terminal ileum
The Rule of 2's:
=2 inches long
=2 feet from the ileoceccal valve
=2% of the population
=Commonly presents in first 2 years of life
=May have 2 types of epithelia
NOW...Meckel's Diverticulum is NOT the same as an omphalomesenteric cyst =
=cystic dilation of the vitelline duct
Enzyme markers of GI pathology
I will give you the enzyme, you tell me its major diagnostic use.
Aminotransferases (AST + ALT)
- Viral Hepatitis (ALT > AST)

- Alcoholic Hepatitis (AST > ALT)

- Myocardial infarction (AST only)
GGT
(=gamma-glutamyl transpeptidase)
=various liver diseases
Alkaline Phosphatase
=Obstructive liver disease (=i.e. hepatocellular carcinoma)

=Bone disease
Amylase
=Acute pancreatitis

=Mumps
Lipase
=Acute pancreatitis
Ceruloplasmin
DECREASED indicates Wilson's Disease

COLOR PLATE 51
What is Barrett's Esophagus?
=Glandular (columnar epithelial) metaplasia --> replacement of NONKERATINIZED SQUAMOUS epithelium w/ gastric COLUMNAR epithelium in the distal esophagus
What causes Barrett's Esophagus?
Chronic acid reflux
What is the result of Barrett's esophagus?
Possible ADENOCARCINOMA

BARRett's =
Becomes Adenocarcinoma, Results from Reflux
What are the risk factors for esophageal cancer?
ABCDEEF.

**Most esophageal cancer is SQUAMOUS CELL CARCINOMA
=Barrett's leads to adenocarcinoma

1) Alcohol
2) Barrett's Esophagus
3) Cigarettes
4) Diverticuli
=i.e. Zenker's diverticulum
5) Esophageal web
=i.e. Plummer-Vinson
6) Esophagitis
=due to reflux, irritants, infection
7) Familial
What the hell is Plummer-Vinson Syndrome?
1) Atrophic glossitis
2) Esophageal Webs
3) Anemia
What is congenital pyloric stenosis?
=hypertrophy of the pylorus causes obstruction

**Palpable "olive" mass in the epigastric region + nonbilious PROJECTILE vomiting at ~2 weeks of age

=occurs 1/600 live births --> usually 1st-born MALES

=treatment: surgical incision
Symptoms of Malabsorption Syndromes:
=diarrhea
=steatorrhea
=weight loss
=weakness
Celiac Sprue
=autoantibodies to GLUTEN (=gliadin) in wheat and other grains

**PROXIMAL SMALL BOWEL only.
Tropical Sprue
=probably INFECTIOUS + responds to antibiotics

**Can affect ENTIRE small bowel
Whipple's Disease
=infection w/ Tropheryma whippelii

**KEY:
=you will see PAS-POSITIVE MACROPHAGES in the intestinal lamina propria + mesenteric nodes
Disaccharidase Deficiency
Most common is LACTASE DEFICIENCY --> milk intolerance
Pancreatic Insufficiency
=due to CF or chronic pancreatitis

**Causes malabsorption of protein, fat, and vitamines ADEK

recall = fat soluble vitamins --> ADEK
Gastritis
=can be ACUTE or CHRONIC
What is ACUTE Gastritis?
=also called "EROSIVE" gastritis

=disruption of the mucosal barrier --> inflammation
Causes of acute gastritis:
1) Stress

2) NSAIDs

3) Alcohol

4) Uricemia

5) Burns (=Curling's ulcer)

6) Brain injury (=Cushing's ulcer)
What is Curling's Ulcer?
=acute ulcer (called stress ulcers) of the duodenum resulting as a complication of SEVERE BURNS --> i.e. reduced plasma volume leads to a sloughing of the gastric mucosa

**A similar situation occurs in Cushing's Ulcers when there is INCREASED ICP.
CHRONIC Gastritis
=nonerosive

Type A = FUNDAL
=Autoimmune disorder characterized by Autoantibodies to PARIETAL cells, pernicious anemia, and achlorhydra (=absence of gastric acid)
=think, the 4 A's!

Type B = ANTRAL
=caused by. H. pylori infection (a BUG)

**BOTH carry increased risk of gastric carcinoma.
Peptic Ulcer Disease
**Think either GASTRIC ulcers or DUODENAL ulcers
What causes GASTRIC ULCERS?
=due to DECREASED mucosal protection against gastric acid

**H.pylori infection in 70%
=chronic NSAID use also implicated
Symptoms:
Pain GREATER w/ meals + weight loss
What causes Duodenal Ulcers?
=due to INCREASED gastric acid secretion OR decreased mucosal protection

**Almost 100% have H.pylori infection
Symptoms:
=hypertrophy of Brunner's glands

=Pain DECREASES w/ meals + weight GAIN
Appearance of Ulcers
=have clean "punched-out" margins UNLIKE the raised/irregular margins of carcinoma
Potential complications of these ulcers:
=bleeding
=penetration
=perforation
=obstruction

**NOT intrisically precancerous.
How would you treat H. pylori infection?
TRIPLE THERAPY

1) Metronidazole
2) Bismuth salicylate
3) Either amoxicillin OR tetracycline
4) w/ or w/o a PPI

note: incidence of peptic ulcer disease is 2X as great in SMOKERS
Stomach Cancer
=Almost always ADENOCARCINOMA

**early aggressive local spread and node/LIVER metastasis

**Termed "Linitis Plastica" when it's diffusely infiltrative = thickened, rigid appearance
What is associated w/ stomach cancer?
1) Dietary nitrosamines

2) Achlorhydria

3) Chronic gastritis
What is Virchow's node?
=involvement of the supraclavicular node by metastasis from the stomach
What is Krukenberg's tumor?
=bilateral metastasis to the ovaries

**Abundant mucus, "SIGNET-RING" cells
Inflammatory Bowel Disease
**Let's contrast Crohn's Disease w/ Ulcerative Colitis.
Possible Etiology.
C = Infectious

UC = Autoimmune
Location.
Crohn's:
=may involve any portion of the GI tract--usually the terminal ileum and colon
=SKIP LESIONS
=RECTAL SPARING

UC:
=Colitis --> COLON inflammation
=CONTINUOUS lesions
=ALWAYS w/ RECAL INVOLVEMENT
Gross Morphology.
C:
=TRANSMURAL inflammation
=COBBLESTONE mucosa
=Creeping fat
=Bowel-wall thickening --> "string sign" on barrium swallow X-ray
=Linear ulcers + fissures and fistulas

UC:
=Mucosal and submucosal inflammation ONLY
=Friable mucosal pseudopolyps w/ freely hanging mesentary
Microscopic morphology.
C:
=Noncaseating granulomas
=Lymphoid aggregates

UC:
=Crypt abscesses and ulcers
=Bleeding
=NO granulomas
Complications.
C:
=Strictures and fistulas
=Perianal disease
=Malabsorption
=Nutritional depletion

UC:
=Severe stenosis
=TOXIC MEGACOLON
=COLORECTAL CARCINOMA
Extraintestinal manifestations.
C:
=Migratory polyarthritis
=Erythema nodosum
=Ankylosing spondylitis
=Uveitis
=Immunologic disorders

UC:
=Pyoderma gangrenosum
=Primary sclerosing cholangitis

Images 114 + 115.
Appendicitis
=affects all age groups --> most common indication for emergent abdominal surgery in children

**Inital diffuse periumbilical pain --> localized pain at McBurney's point (+nausea and fever)

**May perforate --> peritonitis
Differntial for Appendicitis:
**Diverticulitis
=elderly

**Ectopic pregnancy
=use B-hCG to rule out
Diverticulum
=blind pouch leading off the alimentary tract (=lined by mucosa, muscularis, and serosa) --> communicates w/ the lumen of the gut

**Most often occur in the SIGMOID COLON and are ACQUIRED
What is the difference between a "True" diverticulum and a "False" diverticulum?
TRUE
=all 3 gut layers outpouch

FALSE (=pseudodiverticulum)
=only mucosa and submucosa outpouch --> i.e. lack or have an attenuated muscularis externa
=occur especially where VASA RECTA perforate the muscularis externa
What is Diverticulosis?
=MANY diverticula
=Really common --> 50% of patients > 60 y.o.

=caused by an increased intraluminal pressure and focal weakness in the colonic wall

**Most frequently involves the SIGMOID COLON.
Risk Factors + Symptoms of Diverticulosis
**Associated w/ LOW-FIBER diets

Symptoms:
=Usually asymptommatic
=Can be associated w/ vague discomfort and/or recal bleeding
Diverticulitis
=Inflammation of diverticula causing LLQ pain

**May lead to:
=perforation
=peritonitis
=abscess formation
=bowel stenosis

COLOR IMAGE 31
What is intussusception?
="telescoping" of 1 bowel segment into distal segment --> can compromise blood supply

**Often due to intraluminal mass

COLOR IMAGE 34
What is volvulus?
=twisting of a portion of the bowel around its mesentery --> can lead to obstruction and infection

**may occur at the sigmoid colon where there is redundant mesentery
What is Hirschsprung's disease?
**Congenital megacolon
=characterized by LACK of enteric nervous plexus (=Auerbach's and Meissner's plexuses) in segment on intestinal biopsy

**Due to failure of neural crest cell migration
=SO, you have this dilated portion of the colon PROXIMAL to the aganglionic segment --> resulting in a "transition zone"
Presentation of Hirschsprung's Disease
Chronic constipation early in life

**Increased risk w/ Down Syndrome
What are the risk factors for colorectal cancer?
**3rd most common cancer!

1) Colorectal villous adenomas
2) Chronic inflammatory bowel disease
=esp. UC
3) High fat, low fiber diets
4) Increasing age
5) Familial adenomatous polyposis (FAP)
6) Hereditary nonpolyposis colorectal cancer (HNPCC)
7) DCC gene deletion
8) Personal and family history of colon cancer

**Peutz-Jeghers--a benign polyposis syndrome--is NOT a risk factor!
Which patients should be screened for colorectal cancer?
= patients >50 y.o. should be screened w/ stool occult blood test + colonoscopy
Laboratory/Imaging findings in colorectal cancer.
=Visualized on barium swallow X-ray as "apple core" lesion

=CEA --> nonspecific tumor marker
Cirrhosis and Portal Hypertension
"Cirrho" (=greek) --> means tawny yellow = i.e. the color of the diseased liver
What is cirrhosis?
=replacement of liver tissue by diffuse fibrosis + regenerative nodules --> leads loss of normal architecture + progressive loss of liver function

**Depending on the size of the nodules, there are 3 macroscopic types:
1) Micronodular
2) Macronodular
3) Mixed
Micronodular
=nodules < 3 mm + of uniform size

**Due to METABOLIC insult:
=alcohol
=hemochromatosis
=Wilson's disease
Macronodular
=nodules > 3mm --> varied size

**Usually due to significant liver injury leading to hepatic necrosis:
=post-infectious--usually hepatitis C
=drug-induced hepatitis

**Macronodular has increased risk of hepatocellular carcinoma
Effects of Liver Cell Failure
1) Coma
2) Scleral icterus
3) Fetor hepaticus
=breath smells like freshly opened corpse
4) Spider nevi
5) Gynecomastia
6) Jaundice
7) Loss of "sexual" hair
8) Liver "flap" = ASTERIXIS
=course hand tremor --> signals impending coma
9) Bleeding tendency
=decreased prothrombin + clotting factors
10) Anemia
11) Ankle edema
Cirrhosis can lead to portal HTN.
Cirrhosis = most common cause of portal HTN in US

**In less developed countries = schistosomiasis
Effects of Portal Hypertension
1) Esophageal varices
=can lead to Hematemesis

2) Melena
=due to either varices OR a peptic ulcer

3) Splenomegaly

4) Caput medusae

5) Ascites

6) Hemorrhoids
What is the surgical treatment of portal HTN?
=do a PORTACAVAL SHUNT between the splenic vein (=part of the portal system) + the left renal vein

**May relieve portal HTN + associated varices, etc.

COLOR IMAGE 29
What are the characteristic histological features of Alcoholic Hepatitis?
1) Swollen + necrotic hepatocytes
2) Neutrophil infiltration
3) MALLORY BODIES
=intracytoplasmic eosinophilic inclusions
4) Fatty change
5) Sclerosis around the central vein
Lab Values in Alcoholic Hepatitis.
AST > ALT = ALCOHOLIC hepatitis

**Usually the AST (SGOT) to ALT (SGPT) ratio is > 1.5

ALT > AST = VIRAL hepatitis
What is Budd Chiari Syndrome?
=Occlusion of the IVC or hepatic veins w/ centrilobular congestion + necrosis --> leading to congestive liver disease
What is congestive liver disease?
=Hepatomegaly
=Ascites
=Abdominal pain
=Eventual liver failure
What is associated w/ Budd-Chiari Syndrome?
- Polycythemia vera
- Pregnancy
- Hepatocellular carcinoma
What is Wilson's Disease?
**AUTOSOMAL-RECESSIVE

=Inadequate hepatic COPPER excretion + failure of copper to enter circulation as ceruloplasmin

=Leads to copper accumulation --> especially in the liver, brain, cornea, kidneys + joints

**ALSO known as HEPATOLENTICULAR DEGENERATION
What are the symptoms that characterize Wilson's disease?
**ABCD**

1) Asterixis

2) Basal ganglia degeneration
=Parkinsonian symptoms

3) The C's:
=Ceruloplasmin DECREASED
=Cirrhosis
=Corneal deposits --> Kayser-Fleischer rings
=Copper accumulation
=Carcinoma--hepatocellular
=Choreiform movements

4) Dementia
How would you treat Wilson's disease?
Penicillamine.
What is hemochromatosis?
=Hemosiderosis --> the deposition of hemosiderin (iron)

=Hemochromatosis is the DISEASE caused by this iron deposition

**Can be PRIMARY (=autosomal recessive) OR SECONDARY (=due to chronic transfusion therapy)
What are the classic symtpoms?
CLASSIC TRIAD

1) Micronodular cirrhosis
2) Pancreatic fibrosis
3) Skin pigmentation = "BRONZE" diabetes
What are the results/manifestations of hemochromatosis?
1) CHF
2) Increased risk of hepatocellular carcinoma
What lab results would you expect?
=INCREASED ferritin

=INCREASED iron

=DECREASED TIBC --> INCREASED transferrin saturation

**Total body iron may reach 50g! This is enough to set off metal detectors at airports!
Treatment
-Repeated phlebotomy
-Deferoxamine

COLOR IMAGE 26
What is jaundice?
**Normally liver cells convert unconjugated (INDIRECT) bilirubin --> conjugated (DIRECT) bilirubin

**DIRECT bilirubin is WATER-SOLUBLE and can be excreted into urine AND by the liver into bile to be converted by gut bacteria to urobilinogen (=some of which is reabsorbed)

**recall: some urobilinogen is ALSO formed directly from heme metabolism
Hereditary Hyperbilirubinemias
1) Gilbert's Syndrome

2) Crigler-Najjar Syndrome

3) Dubin-Johnson Syndrome
Gilbert's Syndrome
**Essentially ASYMPTOMATIC w/ no clinical consequeneces

**Associated w/ STRESS.

=Unconjugated bilirubin IS elevated w/o overt hemolysis
=MILDLY decreased UDP-glucuronyl transferase
Crigler-Najjar Syndrome, Type I
**ABSENT UDP-glucuronyl transferase
=prevents early in life
=patients die w/i a few years

**Type I is a very severe disease--but type II is less severe and responds to phenobarbital.
Findings in Crigler-Najjar Syndrome
1) Jaundice

2) Kernicterus
=bilirubin deposition in the brain

3) Increased unconjugated bilirubin
Dubin-Johnson Syndrome
**Benign**
=Conjugated hyperbilirubinemia due to DEFECTIVE liver excretion

**GROSSLY BLACK LIVER**
Rotor's Syndrome
=Similar to Dubin-Johnson Syndrome but EVEN MILDER --> does NOT cause black liver
Quick Review of Bilirubin Synthesis
-Hb via heme oxygenase --> Biliverdin
-Biliverdin via biliverdin reductase --> BILIRUBIN

NOW, this unconjugated (NONPOLAR) bilirubin is transported in plasma tightly bound to ALBUMIN

**After bilirubin enters the hepatocyte it is CONJUGATED.
=usually into bilirubin diglucocoronide by UDP-glucuronyl transferase

**This conjugation allows easy excretion into BILE
What happens after it is excreted into bile?
**Bilirubin is incorporated into mixed micelles and excreted into the DUODENUM --> small intestine

=NOW, most bile salts are reabsorbed actively in the terminal ileum --> "enterohepatic circulation" and will enter the portal system to go back to the liver
=BUT some will escape reabsorption and go into the colon where they will be degraded into urobilinogens + urobilin --> give stool its characteristic BROWN COLOR
What is primary sclerosing cholangitis?
**Can be BOTH intra- and extra-hepatic

**Inflammation + fibrosis of bile ducts --> alternating strictures + dilation w/ "beading" on ERCP

ERCP = endoscopic retrograde cholangiopancreatography
What can primary sclerosing cholangitis be associated with?
=Ulcerative colitis

**Can lead to SECONDARY BILIARY CIRRHOSIS
Symptoms in Cholangitis
***CHARCOT'S TRIAD:***

1) Jaundice
2) Fever
3) RUQ pain
What is biliary cirrhosis?
**Can be PRIMARY or SECONDARY
PRIMARY Biliary Cirrhosis
**Intrahepatic, AUTOIMMUNE disorder

Symptoms:
=Severe obstructive jaundice
=Steatorrhea
=Pruritus
=Hypercholestrolemia (=xanthoma)

Labs:
1) INCREASED alkaline phosphatase
2) INCREASED serum mitochondrial antibodies
SECONDARY Biliary Cirrhosis
**Due to EXTRA-hepatic biliary obstruction

**INCREASED pressure in intrahepatic ducts --> injury/fibrosis

**Often complicated by:
=ascending cholangitis (bacterial infection)
=bile stasis
="bile lakes"

Labs:
1) INCREASED alkaline phosphatase
2) INCREASED conjugated bilirubin
Risk factors for Hepatocellular Carcinoma
**Also called "hepatoma"
**Most common PRIMARY malignant tumor of the liver in adults

-Hepatitis B + C
-Wilson's disease
-Hemochromatosis
-alpha1-antitrypsin deficiency
-alcoholic cirrhosis
-carcinogens (=i.e. aflatoxin B1 found in rice in asian countries)

**note: concurrent infection w/ HBV AND aflatoxin B1 = greatly increases risk of hepatocellular carcinoma
How does hepatocellular carcinoma present?
1) Tender hepatomegaly
2) Ascites
3) Polycythemia (=i.e. hypoxia)
4) Hypoglycemia (=i.e. can't undergo gluconeogenesis)
How does hepatocellular carcinoma spread?
=like renal cell carcinoma--spreads hematagenously
Lab Studies
=Elevated alpha-fetoprotein

**Be careful because it could lead to Budd-Chiari Syndrome!
Reye's Syndrome
RARE
=often fatal childhood hepatoencephalopathy

**Associated w/:
1) VIRAL infection
=VZV
=Influenza B
2) Salicylates
=NEVER give aspirin to a kiddo
=use acetaminophen w/ caution
Findings in Reye's Syndrome
1) Fatty liver (=microvesicular fatty change)
2) Hypoglycemia
3) Coma
What causes Gallsones?
=form when solubilizing bile acids + lecithin are OVERWHELMED by increased cholesterol and/or bilirubin
What are the risk factors for Gallstones?
**The 4 F's!**

1) FEMALE
2) FAT
3) FERTILE
4) FORTY
What are the different types of stones?
1) Cholesterol Stones
2) Mixed Stones
3) Pigment stones
Cholesterol Stones
=Radiolucent w/ 10-20% opaque due to calcifications

**Associated with:
1) Obesity
2) Crohn's disease
3) Cystic fibrosis
4) Advanced age
5) Clofibrate
6) Estrogens
7) Multiparity
8) Rapid weight loss
9) Native American origin
Mixed Stones
=Radiolucent
=Have BOTH cholesterol AND pigment components

**MOST COMMON TYPE**
Pigment Stones
=Radiopaque

**Seen in patients with:
1) Chronic RBC hemolysis
2) Alcoholic cirrhosis
3) Advanced age
4) Biliary infection
How do you diagnose/treat gallstones?
ULTRASOUND

Treat w/ cholecystectomy.
What causes Acute Pancreatitis?
Caused by activation of pancreatic enzymes --> leads to AUTODIGESTION

**Causes = GET SMASHeD!!
1) Gallstones
2) Ethanol
3) Trauma
4) Steroids
5) Mumps
6) Autoimmune disease
7) Scorpion sting
8) Hypercalcemia/ Hyperlipidemia
9) Drugs--i.e. sulfa drugs
Clinical Presentation
1) Epigastric abdominal pain RADIATING TO THE BACK

2) Anorexia

3) Nausea
Labs
1) Elevated amylase

2) Elevated lipase
=MORE SPECIFIC!
What can acute pancreatitis lead to?
- DIC
- ARDS
- Diffuse fat necrosis
- Hypocalcemia
- Pseudocyst formation
- Hemorrhage
- Infection
Chronic pancreatitis
1) Chronic calcifying pancreatitis
=associated w/ alcoholism

COLOR IMAGE 135

2) Chronic obstructive pancreatitis
=strongly associated w/ GALLSTONES
What drug can cause a FATAL pancreatitis?
Didanosine (dddI)
=reverse transcriptase inhibitor
Overview of Pancreatic Adenocarcinoma
**Prognosis averages 6 months or LESS--very aggressive
=usually has already metastasized at presentation

**Tumors most common in pancreatic head (=obstructive jaundice)
How does pancreatic adenocarcinoma present?
1) Abdominal pain radiating to the back
2) Weight loss
=due to malabsorption + anorexia
3) Migratory thrombophlebitis
=Trousseau's Syndrome
4) Obstructive Jaundice w/ Palpable Gallbladder
="Courvoisier's Sign"

COLOR IMAGE 134
What is Courvoisier's Sign?
=States that in the presence of a PALPABLE GALLBLADDER, jaundice is unlikely to be caused by gallstones

**i.e. gallstones are formed over a long extended period of time --> gallbladder is more likely to be fibrotic and shrunken
Review: What is Trousseau's Syndrome?
=some malignancies--especially adenocarcinoma of the pancreas and lung are associated w/ HYPERCOAGULABILITY

SO, blood may spontaneously form clots in the portal vessels, deep veins of the extremities, or superficial veins all around the body

**when different clots form in superficial veins all around the body = migratory thrombophlebitis --> can signal malignancy