GI Flashcards
0
Q
What are stellate cells?
A
Ito cells Reside w/in Space of Disse Store lipid and vitam A Produce reticular fibers Cirrhosis: multiply and produce large amounts of ECM
1
Q
What activities are carried out in Zone 1 vs Zone 3 of hepatic lopules?
A
Zone 1: adjacent to triad, O2 rich. gluconeogenesis, B-oxidation, AA metabolism, formation of urea
Zone 3: adjacent to central vein, O2 poor. P450 reactions, lipid synthesis, glycolysis
2
Q
3 classifications of liver disease
A
- Hepatocellular: acute, fulminant, chronic
- Cholestatic: intrahepatic, extrahepatic
- Cirrhosis
3
Q
What viruses are associated with hepatocellular injury?
A
Hepatotropic: Hepatitis A,B,C,D,E
Systemic: EBV, CMV, HSV, enterovirus
4
Q
What are microscopic features of acute hepatitis?
A
lobular disarray - disruption of architecture
ballooning degeneration
apoptotic bodies (Councilman bodies)
inflammatory infiltrates, activated Kupffer cells
regeneration (with resolution)
5
Q
What is fulminant hepatitis?
A
Rare variant of acute hepatitis. Rapid onset of liver failure over period of days - weeks.
Heralded by AMS and coagulopathy
6
Q
Causes of fulminant hepatitis
A
Drugs (acetaminophen overdose, antimycobacterial (rifampin, isoniazid), antidepressants (MAOi), halothane, mushroom poisoning) Virus (HAV, HBV + HDV) Autoimmune Ischemia Metabolic
7
Q
What is chronic hepatitis?
A
Evidence of ongoing liver injury for >6mos
May be viral (HBV, HDV, HCV), autoimmune or metabolic
8
Q
What is the predominant microscopic feature of chronic hepatitis?
A
inflammatory infiltrate surrounding portal tracts
fibrosis
9
Q
What is “bridging” necrosis?
A
Seen in chronic hepatitis
fibrosis / necrosis stretching between portal tracts or from portal tract to central vein
10
Q
What are microscopic indicators of HBV, HCV, and autoimmune hepatitis?
A
HBV: ground-glass cytoplasm
HCV: microvessicular fatty change and portal tract lymphoid aggregates
autoimmune: plasma cell infiltrates of portal triad
11
Q
What is choledocholithiasis?
A
gall stones w/in the common bile duct
12
Q
What are the characteristic lab findings assoc. with cholestasis?
A
Elevated alkaline phosphatase
elevated gamma-glutamyl transferase (GGT)
elevated 5’ nucleotidase
13
Q
What hepatic condition presents with the highest aminotrasnferase elevations?
A
ALT/AST elevation hallmark of hepatocellular necrosis: Acute Hepatitis 10-30x Biliary obstruction 1-5x Cirrhosis 1-3x Hepatic metastases 1-2x
14
Q
What defines acute liver failure?
A
Rapid onset of hepatic dysfunction with no underlying liver disease progressing to encephalopathy w/in 8-12 weeks
15
Q
What are symptoms of acute liver failure?
A
Mental status changes Jaundice, dark urine, light stool Seizure Hypoglycemia Coagulopathy Hepatorenal syndrome
16
Q
How is cholestasis diagnosed?
A
Elevated alkaline phosphatase Elevated GGT, 5' nucleosidase Hypercholesterolemia Hyperbilirubinemia (conjugated) Prolonged prothrombin time (Vit K deficiency) Anti-mitochondrial Ab (primary)
Imaging
Liver biopsy
17
Q
What are the physical signs of portal hypertension?
A
- Ascites
- Splenomegaly
- Abdominal vasculature accentuation
18
Q
3 classifications of portal HTN
A
Pre hepatic
Intrahepetic
Post hepatic
19
Q
What does TIPS stand for?
A
Transjugular Intrahepatic Portosystemic Shunt
Performed by interventional radiologist - treatment for portal HTN
20
Q
How do acute and chronic hepatic encephalopathy differ?
A
Acute: Type A: assoc. w/ acute disease. Delirium and convulsions progressing to coma. BBB and cerebral edema are common.
Chronic: Types B and C: chronic disease: pathogenesis unclear. Asterixis, Hyperreflexia, Mental disturbances, EEG changes
Production of toxic substances by gut bacteria implicated
21
Q
What is therapy for chronic hepatic encephalitis?
A
Treat precipitating factor
Lactulose
Abx: Rifaximin, neomycin
Liver transplant
22
Q
What does protein content of ascites fluid indicate?
A
Etiology of ascites
Serum albumin - ascites albumin
if > 1.1, portal HTN likely
Elevated ascites albumin: tumor or chronic infection
23
Q
What are complications of ascites
A
Spontaneous Bacterial Peritonitis - esp. low protein fluid
Flood’s syndrome: ruptured umbilical hernia
Plural effusion
Drug dilution in “3rd space”
24
What is hepatorenal syndrome?
```
Renal failure w/ accompanying advanced severe liver disease
No ATN (tubules intact - low urine Na+), but severe oliguria
```
25
How is hepatorenal syndrome diagnosed and treated?
Diagnosis: rule out pre-renal azotemia via trial of fluid expansion
Treatment: Often liver transplant. Dialysis.
26
Primary cause of unconjugated bilirubinemia
Hemolytic jaundice: production of bilirubin in excess of liver's ability to process it.
27
What are the 2 leading causes for liver transplant?
```
Hep C (45%)
Alcoholic cirrhosis (15%)
```
28
At what pressure within the hepatic portal vein is variceal bleeding likely?
>12mmHg
29
5 factors that contribute to chronic ascites
1. Portal HTN -> systemic vasodilation, decreased effective bv, SNS activation
2. RAAS activation -> increased Na+
3. ADH -> increased H2O
4. Increased transsinusoidal filtration
5. hypoalbuminemia -> decreased osm
30
What microscopic feature is associated with alcoholic hepatitis?
Mallory bodies or alcoholic hyalin: eosinophilic cytoplasmic inclusions
31
What are transaminase levels in alcoholic hepatitis?
Mild to moderate increase with AST > ALT
| vs. viral where ALT > AST
32
Is alcoholic cirrhosis micro or macronodular?
typically micro
33
In what setting does Non-alcoholic Fatty Liver Disease typically present?
Obesity and Insulin resistance.
34
4 metabolic liver diseases
Non-alcoholic fatty liver disease
Hemochromatosis
a1 antitrypsin deficiency
Wilson's disease
35
What mutation is often seen in hemochromatosis?
```
HFE gene (6p) mutation
Autosomal Recessive
```
36
What organs are affected by hemochromatosis?
Liver - micronodular cirrhosis, hepatocellular carcinoma
Myocardium - dysfunction
Pancreas - fibrosis, cell loss -> diabetes mellitus
Joints - synovial tissue damage -> arthropathy
Endocrine glands - hypopituitarism -> hypogonadism
37
What is another name for Wilson disease?
Hepatolenticular degeneration
| Lenticular = putamen and caudate = basal ganglia
38
What is Wilson's disease?
Autosomal recessive defect in copper ATPase
| defective transport in liver -> decreased incorporation into ceruloplasmin and decreased excretion in bile
39
Symptoms of Wilson's disease
Hepatitis / cirrhosis
CNS injury (tremor, rigidity, dysarthria, depression, anxiety, psychosis)
Kaiser-Fleischer rings, sunflower cataracts
Hemolytic episodes
40
What gene is involved in a1-antitrypsin deficiency?
SERPINA-1
Autosomal codominant
chromosome 16: Pi locus: normal = MM, severe = ZZ
41
who should be screened for a1-antitrypsin deficiency?
All people w/ COPD, unexplained liver disease, and 1st degree family members of probands
42
How does a1-antitrypsin deficiency disease cause liver damage?
Accumulation of misfolded, polymerized a1-AT proteins in hepatocyte ER
43
Manifestations of a1-AT deficiency
```
Panlobular emphysema (esp. basilar)
Hepatitis (neonatal hepatitis), cholestatic jaundice, cirrhosis, hepatocellular carcinoma
Eosinophilic inclusion bodies in hepatocytes
```
44
Pathology of primary biliary cirrhosis
Autoimmune, Tcell mediated destruction of small - medium bile ducts
Granulomatous destruction of bile ducts w/ chronic inflammatory infiltrate
45
Lab findings in Primary Biliary Cirrhosis
elevated hepatic alkaline phosphatase, GGT, cholesterol, conjugated bilirubin
elevated IgM, antimitochondrial Ab and lipoprotein X
46
What is treatment for PBC?
Urodeoxycholic Acid
Symptomatic treatment (pruritis, osteoporosis, portal HTN)
Liver transplant
47
What is Primary Sclerosing Cholangitis?
progressive destruction of large intra and extrahepatic bile ducts
autoimmune, ANCA assoc., close assoc. with ulcerative colitis
Mostly men <40
Produces alternating stricture and dilation in ducts
48
What are complications of Primary Sclerosing Colangitis?
Progressive biliary obstruction and portal fibrosis
Biliary cirrhosis
Increased risk of cholangeosarcoma
49
What is DILI?
Drug Induced Liver Injury
| Most common reason for FDA removal of approved drugs
50
What part of the liver is initially affected by acetaminophen toxicity?
Zone 3 (P450 activity)
51
2 ways in which ETOH contribute to acetaminophen toxicity
Induction of P450 pathway
| Depletion of GSH stores
52
First line treatment for acetaminophen OD?
N-acetylcysteine
53
Describe unpredictable / idiosyncratic DILI
Usually latent "sensitization" period before symptoms, more rapid on re-challenge
Associated fever, rash, eosinophilia
54
2 theories to explain unpredictable DILI
1. Hypersensitivity: drug + carrier = macromolecule = neo-antigen -> Immune response -> hepatotoxicity
2. Metabolic + genetic: drug + genetics -> novel metabolite -> liver injury
55
What drugs are associated w/ cholestasis?
Phenothiazines (Chlorpromazine)
Oral Contraceptives (estrogens)
Erythromycin Estolate
Amoxicillin / Clavulanate (augmentin)
56
What effect does Chlorpromazine (thorazine) have on the liver?
Assoc. with cholestasis + inflammation via unknown mechanism
3-5 weeks after initiation of therapy
Resolves w/ discontinuation
PBC-like
57
What effect does Methotrexate have on the liver?
Fatty change related to cumulative dose
Toxicity lower in RA, higher in psoriasis
Liver biopsy in follow up
58
Name some drugs assoc. w/ chronic hepatitis
```
Acetaminophen
Amiodarone
Aspirin
Dantrolene
Ethanol
Isoniazid
a-methyldopa
Vit-a
nitrofurantoin
```
59
Name some drugs associated with granuloma formation
```
Allopurinol
Hydralazine
Penicillin
Quinidine
Sulfonamides, sulfonylureas
a-methyldopa
```
60
3 drugs associated with "predictable" hepatotoxicity
Acetaminophen
CCl4
Amanita Phalloides
61
What is the cause of dental carries?
Dissolution of inorganic component of tooth by organic acids via microbial metabolism of carbohydrates
62
What microbes are primarily involved in the formation of dental carries?
S. mutans - crown
| Lactobacillus - root
63
What is oral tori?
bony overgrowth of palate or lingual side of mandible.
| No need for removal unless impedence of function or speech
64
What causes amalgam tattooing?
insoluble silver salt (from silver amalgam filling) deposited in collagen fibers of lamina propria
65
What are Fordyce Spots?
Occurrences of sebaceous glands in oral cavity
not apparent in children, activated at puberty
No clinical significance, found in 82% of population
66
Epulis fissuratum
"denture injury tumor" due to mechanical irritation of ill-fitting denture
Usually no pain or tenderness unless infection is involved
67
Papillomatosis
found on soft tissue of vault of hard palate
| numerous papillary projections due to mechanical irritation and ill-fitting denture, food debris
68
Is oral papilloma cancerous?
NO - benign w/ stratified squamous epithelium
69
What is an aphthous ulcer?
Canker sore
Recurrent, superficial ulcer of non-keratinized epithelium
Persist 8-14 days
Causes: psychic, autoimmune, microbial, traumatic endocrine, hereditary
Treatment: tetracycline mouthwash, kenalog in orabase, analgesics
70
What is treatment for oral herpes?
Acyclovir ointment
| Systemic acyclovir for immunocompromised patients.
71
What oral ulcers should be considered for biopsy?
Highly suspicious, slow healing ulcers in patients who are poor historians.
72
What is Moniliasis? Culture? treatment?
Oral thrush - Candida albicans
Culture: Sabouraud's agar
Treatment: Nystatin, Ketoconazole, Fluconazole, saline baking soda rinse
73
Oral manifestation of Addison's disease and treatment
Hyperpigmented spots due to pituitary stimulation of melanotrophic activity
treated w/ corticosteroids
74
What are oral manifestations of leukemia?
gingival hyperplasia, gingivitis, hemorrhage, petechia, mucosal ulceration
75
What is Paget's disease, oral manifestations, treatment
Abnormal bone resorption and deposition
Oral: enlargement of maxilla / mandible, spacing of teeth
Treatment: NSAID, ASA, calcitoinin, diphosphonates, mithramycin
76
Oral presentation of Lichen Planus
Pruritic, Purple, Polygonal, Planar, Papules and Plaques
Oral: Wickham Striae: white, lace-like patterns on top of papules
may be erosive - low, but increased risk for malignancy
Yeast infection common
Treat with corticosteroids
77
Oral manifestations of HIV / AIDS
Hairy leukoplakia
Candidiasis
Herpes outbreaks
Kaposi's sarcoma - most frequent malignancy of AIDS
78
What is the organism involved in cat scratch disease?
Bartonella henselae
| Children w/ cervical lymphadenopathy referred for dental exam to exclude oral infection
79
In VZV outbreak, when should anti-virals be started?
w/in 72 hours of onset
80
What is leukoplakia?
white patch or plaque on oral mucosa that does not scrape off and cannot be otherwise classified.
Homogenous or Erythroleukoplakia (4-5x increased risk of malignant transformation)
81
Infrequent agents of viral hepatitis
CMV: children, anicteric, no chronicity. May be lethal in immunocompromised
EBV: self-limited mono. 40% have elevated transaminase. no chronicity
HSV: immunocompromised, high mortality. Liver biopsy shows viral inclusion bodies
82
HBV genome
incomplete dsDNA
83
HAV genome
ssRNA
84
How is HAV transmitted?
fecal-oral route - contaminated food and water
85
How is Hep A diagnosed?
IgM antibody: current infection
| IgG antibody: previous infection
86
HAV therapy
Supportive
| Infection spontaneously clears - no carrier state
87
How does Hep B result in death?
Cirrhosis w/ liver failure
| Hepatocellular carcinoma
88
What is vertical transmission?
Mother to child
89
What is the gold standard for diagnosis of HBV?
Serum HBV DNA by PCR
90
If acute HBV infection is suspected, what test should be ordered to confirm?
IgM anti-HBVc
91
What marker is seen in patients immunized against HBV?
IgG anti-HBs
92
What is the earliest detectable Ab in HBV infection?
IgM anti-HBs
93
What does the presence of anti-HBcAg indicate?
Exposure to virus. will be positive for life.
94
What ethnicity has the highest rate of HBV carriage in USA?
Asian
95
Most commonly used HBV medications
entecavir (guanosine analog)
tenofovir (adenosine analog)
both inhibit HBV RT
96
Post-exposure treatment for HBV
HB immunoglobin
| HB vaccine
97
By age, what % of HBV infected patients will become chronic carriers?
Infant: 90%
1-5 yrs: 30%
Adult: 5-8%
98
What does HDV require for replication?
HBsAg
99
Which has a worse prognosis HBV + HDV co-infection of superinfection
superinfection: 90% develop chronic liver disease, 80% cirrhosis w/in 5 years
co-infection: 2% develop chronic disease. Co-infection is typically self-limited and resembles acute Hep B
100
What is treatment of HDV?
HBV treatment!
101
In HCV infection, what is assumed with symptoms of chronic liver disease?
End Stage Liver Disease has occurred.
Acute Hepatitis rare, usually asymptomatic until late in course
102
What is Von Meyenberg Complex?
Bile duct hamartomas - non neoplastic - persistence of embryonic structure
Collection of small, irregular bile ducts in fibrous tissue
Multiple small, pale spots on liver
103
3 non-neoplastic tumors of liver
1. Von Meyenberg Complex
2. Nodular Hyperplasia (oral contraceptives, anabolic steroids)
3. Nodular Regenerative Hyperplasia: regenerative nodules w/o fibrosis
104
Complication of Nodular regenerative hyperplasia of liver
Portal HTN
105
What is the most common benign hepatic tumor?
Cavernous hemangioma
106
What is hepatic cell adenoma associated with? appearance?
Young women taking contraceptives (long-term)
| Solitary, well circumscribed, soft green mass lacking portal tracts
107
Complication of hepatic adenoma?
Hemorrhage - acute onset of RUQ pain
108
What is the risk of malignant transformation in hepatic adenoma?
Very small risk
| B-catenin gene: elevated risk if present
109
Malignancies that most frequently metastasize to the liver
Lung, GI (colon), pancreas, breast
110
What lab abnormalities are found in tumors that have metastasized to the liver?
early: alkaline phosphatase and lactate dehydrogenase
Late: serum bilirubin and ALT / AST levels
111
3 major risk factors for hepatocellular carcinoma
HBV carrier state (incorporation into cellular DNA -> oncogene activation and HBV X-protein expression)
Cirrhosis (repetitive regenerative cycles -> mutations (RAS, p53, etc))
Exposure to aflatoxin (p53 mutation)
112
What is Budd-Chiari?
Occlusion of IVC or hepatic veins w/ centrilobular congestion and necrosis
Sudden liver enlargement, pain, and ascites
May occur w/ hepatocellular carcinoma
113
What lab abnormalities may be seen in hepatocellular carcinoma?
a-fetoprotein: neither sensitive nor specific
ALP and LD elevation
Late: bilirubin and ALT/AST elevation
114
What is an important variant of hepatocellular carcinoma?
Fibrolamellar variant
young adults, no predisposing factors, otherwise normal liver
well differentiated tumor cells in dense fibrous stroma w/ parallel collagen lamellae
Good prognosis
115
Risk factors for cholangiocarcinoma
Primary sclerosing cholangitis
Congenital biliary tract structural abnormalities
Thorotrast exposure
Chronic parasitic biliary tract infection (Opisthorchis sinensis)
116
What is angiosarcoma?
Endothelial tumor - hemorrhagic nodules and blood filled cysts
In liver associated with vinyl chloride, thorotrast, arsenic exposure
117
What is hepatoblastoma?
tumor of young children
large, soft, hemorrhagic, necrotic mass
microscopic: small, round blue cells. epithelial mesenchymal differentiation
118
What marker is elevated in hepatoblastoma?
a-fetoprotein
119
2 functions of bile
absorption of fat via formation of micelles
| rid body of cholesterol via bile salts and bilirubin
120
What is a choledocal cyst?
Dilation or outpouching of common bile duct
121
2 causes of biliary atresia
1. Hypoplasia or aplasia (rare)
| 2. Idiopathic neonatal bile duct destruction (several weeks after birth)
122
What is the most common type of gallstone in US?
Cholesterol
123
How are cholesterol gallstones formed?
supersaturation of bile with cholesterol + bile stasis -> crystal nucleation
124
Risk factors for cholesterol gallstones
Due to excess cholesterol secretion (+/- decreased bile salt secretion)
- Estrogens (contraceptive use)
- Age
- Obesity / rapid weight loss
- Inherited metabolic disorders
125
How do cholesterol gallstones appear on xray?
radiolucent
126
2 types of pigment gallstones and causes.
1. black stones: chronic hemolysis. Unconjugated bilirubin precipitates with Ca++
2. brown stones: assoc. with biliary tract infections (Flukes)
127
2 causes of acute cholecystitis
1. calculus: stone obstructs neck of gallbladder or cystic duct -> distention and vascular compression
2. acalculus: critically ill patients - biliary sludge obstructs cystic duct -> poor biliary perfusion, possibility of infection
128
What is seen on CBC in acute cholecystitis?
elevated WBC, esp. neutrophils
129
What are Rokitansky-Aschoff sinuses?
Feature of chronic cholecystitis
| mucosal diverticula w/in gallbladder wall
130
What is a significant risk factor for cancer of the gallbladder?
Porcelain gallbladder : dystrophic calcification
131
Prognosis for carcinoma of the gallbladder?
very poor - diagnosis frequently incidental
Frequent local invasion of liver, and adjacent viscera
Metastasis to lymph nodes, peritoneum, lungs
132
What is a Klatskin tumor?
tumor at origin of common bile duct- slowly progressive
| Subtype of carcinoma of extrahepatic bile duct
133
3 regulators of pancreatic exocrine function
Vagus nerve
CCK: HCO3- secretion
Secretin: zymogen secretion
134
How is trypsin activated?
Trypsin (from pancreas) activated by enterokinase on brush border of duodenum
135
Systemic and local complications of acute pancreatitis
Systemic:
- DIC
- ARDS
- ARF (shock -> ATN -> ARF)
- metabolic hypocalcemia, hypoalbuminemia, hyperglycemia, acidosis)
Local:
-pseudocyst, abscess, biliary / duodenal obstruction
136
What defines chronic pancreatitis and what are symptoms?
Frequently relapsing inflammation -> progressive pancreatic injury
Usually alcohol related
May be CF, obstruction, idiopathic
Symptoms: pain, loss of function (malabsorption, DM), biliary / duodenal obstruction
137
Differentiate true pancreatic cysts from pseudocysts
true cysts: lined with epithelium, associated with ADPKD, VHL
pseudocysts: complications of pancreatitis - no epithelial lining
138
What are risk factors for pancreatic adenocarcinoma?
Smoker, male, black, Native American, high fat diet, nitrosamine exposure, diabetes mellitus
139
What part of the pancreas is most frequently involved in adenocarcinoma?
Head > body > tail
140
How does pancreatic cancer usually spread?
```
Local:
Head: duodenum, common bile duct
Body and Tail: vertebrae, retroperitoneal and abdominal organs
Metastasis:
lymph nodes, liver
```
141
What causes hereditary pancreatitis?
Autosomal Dominant
Mutation of trypsinogen on chromosome 7
Trypsin is resistant to lysis -> prolonged activity
142
What are lab findings in acute pancreatitis?
```
Lipase and amylase 3x normal (lipase more specific for pancreas)
AST 2x (gallstone)
```
143
What imaging studies are preferred in diagnosis of acute pancreatitis?
Initial: ultrasound
Prognosis: CT - specific and indicates extent of necrosis -> complication / mortality risk
144
According to Ranson's criteria, what features on admission are suggestive of gallstone pancreatitis?
Age >70
WBC/mm^3 >18,000
Glucose (blood) >220
LDH >400
145
What organisms are most frequently involved in necrotizing pancreatisis?
E. coli
Klebsiella
Enterococcus
146
How is infected pancreatic necrosis treated?
surgical debridement
| Abx use is controversial
147
Should pancreatic pseudocysts be treated?
Only if symptomatic
148
What is a Bentiromide test?
Test of pancreatic function. Oral dose given (Bentiromide has PABA linked) chymotrypsin cleaves, frees PABA for absorption and renal excretion.
Low PABA in urine indicates decreased pancreatic function
149
How is a secretin stimulation test performed?
IV secretin given
Tube placed in pancreatic duct, timed periodic collections measuring for HCO3- levels: low indicates chronic pancreatitis
Cumbersome, unpleasant, rarely done
150
What is the role of the Schilling test in pancreatitis diagnosis / treatment?
Pancreatitis -> reduced absorption of fat soluble vitamins (B)
Schilling test will be abnormal
Administration of pancreatic enzymes will normalize Schilling test, suggesting chronic pancreatitis
151
At what point in pancreatic disease is steatorrhea usually apparent? How is it treated?
90% loss of lipase activity
Supplement pancreatic enzymes w/ 30,000 IU lipase activity at each meal
Acid suppression and low-fat diet
152
Pancreatic adenocarcinoma 5 year survival rate
<5%
153
What are some indications for cholecystectomy?
Symptomatic gallstones, hemolytic anemia, gastric bypass, porcelain bladder, gallbladder adenoma >1-2cm
154
What is a drug that can be used to treat cholesterol gallstones
Ursodeoxycholic acid
Inhibits HMG coA reductase -> reduced cholesterol production
Reduces hepatic cholesterol secretion in bile
155
What is cholangitis?
Infection of the common bile duct
Usually gram neg organisms. can spread to liver and blood.
Charcot's triad: pain, fever, jaundice
156
3 risk factors for carcinoma of the extrahepatic biliary ducts
In Asia: parasites - Chloronorchis sinensis, infections, IBD, sclerosing cholangitis
157
What is sudan black staining used for?
Sudan black stain of stool: shows excess fat in stool (steatorrhea) chronic pancreatitis
158
Describe venous drainage of esophagus
Upper 1/3: SVC
Mid 1/3: Azygos
Lower 1/3: Hepatic portal vein via L. gastric (coronary) vein
159
What is the muscular distribution of the esophagus?
Upper 1/3: Skeletal
Mid 1/3: Mixed
Lower 1/3: Smooth
160
What are Auerbach and Meisner's plexuses?
Auerbach: peristalsis
Meisner: sensory
161
What is EGD used for?
Esophagogastroduodenoscopy: used to visualized epithelium of esophagus, stomach, duodenum. Allows biopsy capability.
162
3 components of swallowing (esophageal phase
Primary: swallow-initiated
Secondary: stretch-initiated
Tertiary: uncoordinated, non-propulsive
163
What factors can trigger diffuse esophageal spasm?
Stress, very hot or very cold liquids
164
What happens with the lower esophageal sphincter in Diffuse Esophageal Spasm?
Normal function is preserved.
165
How does scleroderma affect the esophagus?
Collagen deposition in smooth muscle -> aperistalsis in distal esophagus
Incompetent LES
166
How are strictures and obstructive ring lesions of the esophagus usually treated?
Dilation - usually balloon or bougie
| Surgery - uncommon
167
What are possible pharmacological treatments for GERD
```
Acid suppressors (H2RA, PPI, antacid)
Prokinetics (metoclopramide, domperidone, cisapride)
```
168
Where are Meissner and Auerbach plexuses located in esophagus?
Meissner: within the submucosa
Auerbach: between layers of muscularis propria
169
What are pulsion diverticula and 2 examples
Outpouchings of esophagus due to high pressure
1. Zenker: hypopharynx: between inferior pharyngeal constrictor and cricopharyngeus
2. Epiphrenic: just above LES: associated w/ motility disorders (achalasia, hiatal hernia)
170
What causes an esophageal traction diverticulum?
Continuous external traction - mediastinal inflammation / fibrosis
Located mid-esophagus
171
Who is most at risk for esophageal webs?
Middle aged women
172
Plummer-Vinson
Esophageal webs, iron-deficiency anemia, glossitis, cheilosis, koilonchia (spoon nails)
Increased risk for pharyngeal and esophageal carcinoma
173
2 examples of esophageal rings
A ring: proximal to GE junction
B ring: located at squamo-columnar GE junction. Almost always associated w/ hiatal hernia
174
2 subtypes of hiatal hernias
1. Sliding: GE junction and portion of stomach slide through esophageal hiatus
2. Paraesophageal: "rolling" portion of fundus prolapses into thorax adjacent to esophagus. GE junction stays in abdomen.
175
2 esophageal lacerations
1. Mallory-Weiss: after prolonged vomiting / retching as w/ ETOH intox. superficial longitudinal tears at GE junction
2. Boerhaave: distal esophageal rupture -> mediastinitis - catastrophic event
176
3 types of esophagitis
1. Iatrogenic: (radiation, GVHD)
2. Infectious: immunocompromise: candida, HSV
3. Reflux: GERD
177
Complications of Barret's Esophagus
Epithelial dysplasia
| Adenocarcinoma
178
How many layers of muscle surround the stomach?
3 layers of smooth muscle: innermost oblique, inner circular, outer longitudinal
Note: Auerbach's plexus between circular and longitudinal
179
3 etiologies of gastric ulceration
1. NSAID use
2. Intracranial trauma: vagal stimulus -> increased gastric H+ secretion
3. Physiologic stress (shock, sepsis, burns): decreased perfusion of gastric mucosa, systemic acidosis (-> decreased HCO3-)
180
What are Cushing and Curling ulcers?
Cushing: gastric ulceration due to intracranial injury
Curling: gastric ulceration assoc. with burns
181
What is the most common cause of chronic gastritis?
H. pylori infection (90% of cases)
182
H.pylori virulence factors
flagella
urease (urea -> NH3 -> neutralization of acid)
Lewis antigens: allow adherence to gastric foveolar epithelium
toxins
183
3 diagnostic tests for H.pylori
1. H. pylori fecal Ag test
2. Carbon labeled Urea breath test (detects exhaled labeled CO2)
3. H. pylori serology: not helpful for post-treatment follow up
184
What happens in autoimmune gastritis?
Uncommon
CD4+ cells lose tolerance for parietal cell antigens -> anti parietal cell and anti-IF antibodies
Hyperplasia of G cells -> increased gastrin production
B12 deficiency
185
How is the spinal cord affected by autoimmune gastritis?
B12 deficiency -> demyelination of neurons
| Posterior and lateral columns most effected -> loss of position and vibratory sensation (leg > arms) w/ sensory ataxia
186
What are the most common locations for gastric ulcers
proximal duodenum > antrum > elsewhere
187
Clinical presentation of gastric ulcer
Recurrent epigastric pain - worse at night and few hours post-meal
-relieved w/ food and alkalai
188
Describe Menetrier disease
Excessive productin of TNF-a -> hyperplasia of foveolar mucous epithelium and atrophy of parietal and chief cells
Protein loss
increased risk of gastric adenocarcinoma
189
What is Zollinger-Ellison Syndrome?
Gastrin secreting tumor -> intractible peptic ulcer disease and mucosal hyperplasia (esp. parietal cells)
190
How is peptic ulcer disease diagnosed?
History and physical
EGD
Upper GI series (75% sensitivity)
191
What patients can be tested and treated for H. pylori w/o undergoing endoscopy?
Patient <45 w/ ulcer symptoms and no alarm signs or complications
192
What NSAIDS are "high risk" for Ulcer development?
Indomethacin
Ketorolac
Piroxicam
193
Who is a candidate for co-administration of NSAID and acid suppressive agent?
Patient requiring chronic NSAID use and having at least 1 risk factor for development of gastric ulcer (>60 yoa, multiple NSAID, corticosteroid or anticoagulant use, Hx of PUD or GI complications)
194
2 prokinetic agents that can be used to treat gastroparesis
1. Dopamine antagonist: DA has anti-motility action on GI
| 2. 5-HT agonist: Serotonin stimulates motility
195
What is the preferred drug for hospitalized patients w/ gastroparesis?
Eythromycin: motilin receptor agonist
196
What is the MOA of Metoclopramide?
D2 antagonist
5-HT4 agonist
Accelerates gastric emptying in treatment of gastroparesis
197
What is the treatment of choice for variceal bleeding?
Endoscopic sclerotherapy
| Endoscopic ligation is also acceptable
198
In a patient with an active GI bleed, when should PPI be given?
Post-endoscopy. No value to Pre-endoscopy admin.
199
Drugs used to treat ulcerative colitis
5-aminosalicylates: oral - active management, maintain remission
rectal - most effective for patients w/ proctitis
corticosteroids: suppress migration of PMNs. Used for management of acute / extensive disease.
Immunomodulators (6MP, Azathioprine): if corticosteroid unresponsive
200
What receptors are found in high density in the emesis center of the medulla?
5-HT3
M1
H1
201
Treatment for hypertrophic pyloric stenosis
pyloromyotomy
202
What is Meckel diverticulum? complication?
Failure of embryonic vitelline duct to involute
| Often contains heterotropic foci (gastric mucosa) -> gastric acid production -> GI bleeding, pain, perforation
203
What serology can be used to diagnose Celiac Disease?
Anti-gliadin Ab
| Anti-tissue transglutaminase Ab
204
What is the dermatologic presentation of celiac sprue? Cause?
Dermatitis Herpetiformis: Pruritic vessicles that form on back and extensor surfaces of extremities
Caused by anti-gliadin IgA
205
What is Abetalipoproteinemia?
Autosomal recessive
Deficient apoprotein B -> defective lipid transport -> lipid accumulation in enterocytes
Vacuolization of enterocytes, acanthocytes
206
Is celiac sprue associates w/ malignancy risk?
Yes
Non-Hodgkin's Lymphoma
Sm. intestinal adenocarcinoma
Sq. cell carcinoma of esophagus
207
What is Whipple Disease?
bacterial infection affecting middle-aged white men
Tropheryma whippelli
PAS+ macrophages (foamy) fill lamina propria of sm. intestine
also affects joints, brain, heart valves
-> chronic malabsorption, arthropathy, lymphadenopathy, hyperpigmentation, psychiatric complaints, cardiac dysfunction
208
Where are GI carcinoid tumors usually found?
Appendix, ileum, rectum
209
Where do MALT lymphomas generally develop? What is a common associated disorder?
stomach > sm. intestine > colon
Very often associated w/ H. pylori infection
210
What are important factors that go with Burkitt's Lymphoma?
| genetics, infections
c-myc gene translocation (t[8;14])
latent EBV infection
HIV associated
211
What is GIST and what is it associated with (origin, genetics)?
Gastrointestinal stromal tumor - from interstitial cells of Cajal
Varying malignant potential
mutations: c-KIT, PDGFRA: tyrosine kinase receptors
212
How does steatorrhea -> renal stones?
Malabsorbed FAs bind Ca++ which would normally bind oxalate in the colon
Oxalate is then available for colonic reabsorption -> renal oxalate stones
213
How does smoking effect the risk of developing either of the 2 forms of IBD?
Crohn's: current and former smokers - increased risk of developing
Ulcerative Colitis: former and non-smokers have increased risk
214
What serum markers are found in Crohn's and UC?
Ulcerative Colitis: p-ANCA (60-80%)
| Crohn's: ASCA: (70%)
215
What is recommended for colon cancer surveillance in UC and Crohn's?
Colonoscopy every 2 years w/ multiple biopsy after 8-10 yrs. of diagnosis
216
What are some causes of sm. bowel obstruction?
```
#1: adhesions from prior surgery
Other: hernia, crohn's, volvulus, neoplasm, foreign body
```
217
What is open loop vs. closed loop bowel obstruction?
Open loop: Intestinal flow blocked, but decompression possible via vomiting
Closed loop: Inflow and outflow blocked -> gas and secretion accumulation w/ no means of decompression
218
what is obstipation?
inability to pass flatus or feces
| sign of obstruction along w/ pain, vomiting and distension
219
What organisms tend to flourish in sm. bowel obstrution?
E.coli
Klebsiella
S.faecalis
Normally sm. intestine is nearly sterile
220
Outline treatment for intestinal obstruction
IV fluids (NaCl, lactated ringer's) - monitor electrolytes
Add KCl if needed after adequate urine formed
NG tube - decompression, avoid aspiration of stomach contents
Imaging - monitor - surgery if no resolution
221
What cancers are associated with Peutz-Jeghers?
colon, pancreas, breast, testicular, ovarian, cervical
222
What ovarian cells do LH and FSH work on respectively and what is the effect?
Rising FSH (folicular phase) induces increase in LH receptors in Theca
LH works on Theca cells -> androgen production (Prog, Androstenedione, T) Theca lacks aromatase
FSH works on granulosa cells -> Estradiol from androgens Granulosa cells lack 17a-hydroxylase
223
What causes the LH surge and what is its effect?
increasing estradiol levels -> pos. feedback @ hypothalamus -> LH surge -> ovulation
**Ovulation 36 hrs. after surge**
224
What genes are involved in migration of GnRH secreting neurons? What is the route of migration?
Genes: Kal-1 (encodes for Anosmin), Kal-2, Prox-2
Migration from olfactory placode to Arcuate Nucleus of medial basal hypothalamus
225
Primary amenorrhea
Absence of menses by 16 regardless of growth / pubertal dev
-or-
Absence of menses by 13 w/o dev. of 2ndary sex characteristics
226
Secondary amenorrhea
lack of menses for 3 cycles
227
What is idiopathic hypogonadotrophic hypogonadism? subtype?
Functional congenital absence of GnRH secretion
Kallman: defective migration of GnRH cells and formation of olfactory bulb: IHH + anosmia and other defects
228
What is the cause of Functional Hypothalamic Amenorrhea? How is it diagnosed?
No pathologic disease found
Eating disorders, weight loss, exercise, stress
Low leptin levels believed to be involved - neg. impact on GnRH secretion
Diagnosis: Estrogen <50pg/mL; no withdrawal bleeding on Progesterone challenge
229
Female Athletic Triad
Disordered eating
Menstrual dysfunction
Osteoporosis
230
What are treatments for hyperprolactinemia?
DA agonists: bromocriptine, cabergoline
| Surgery if adenoma
231
What is the most common cause of gonadal dysgenesis in women?
Turner syndrome (X0)
Accelerated postnatal follicular atresia -> primary amenorrhea
High LH and FSH, but low estrogen
232
With what disease is Premature Ovarian Failure associated?
Fragile X Syndrome: CGG repeat amplification (usually >500)
| Also: autoimmune oophoritis (polyglandular autoimmune disease)
233
Describe the pathogenesis of Polycystic Ovary Syndrome
Elevated LH production -> excess androgen production by theca cells
Depressed FSH production -> low estrogen level, depressed follicle maturation
Insulin intolerance contributes to androgen production by theca cells
Obesity -> increased adipose -> aromatization of androgen -> estrone -> promotes high LH, low FSH
234
Rotterdam criteria for PCOD
2+ of the following:
1) Menstrual irregularity (amen or oligo (<9/yr))
2) Hyperandrogenism / -emia
3) 12+ follicles 2-9mm / ovary
**Other causes of hyperandrogen ruled out**
