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Pathophysiology > GI Path (Part I and II) > Flashcards

GI Path (Part I and II) Flashcards

Contains both Part I and II. Happy studying!

1
Q

What is the esophagus?

A

Hollow, distensible muscular tube that extends from the epiglottis to the gastroesophageal junction.

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2
Q

Through which arteries are blood supplied to the esophagus?

A
  1. Cervical - inferior thyroid artery
  2. Thoracic - bronchial arteries and aorta
  3. Abdominal - left gastric and inferior phrenic arteries
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3
Q

What are the common causes of esophageal stenosis?

A
  1. GERD (chronic)
  2. Irradiation
  3. Ingestion of caustic agents
  4. Other severe injury
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4
Q

What is the timeline of dysphagia associated with esophageal stenosis?

A

Progressive

Difficulty eating solids followed by difficulty drinking liquids.

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5
Q

What are differences between primary and secondary esophageal dysmotility in regards to mechanism of disease?

A

1° - Achalasia, congenital esophageal dysfunction

2° - Secondary to stroke, myastenia gravis, ALS, polio.

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6
Q

What are the characteristics of the achalasia triad?

A
  1. Incomplete relaxation of lower esophageal sphincter
  2. Increased tone of lower esophageal sphincter
  3. Esophageal aperistalsis (lack of peristalsis)
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7
Q

What are the findings of esophageal varices? Identify the most significant risk!

A

Anatomical findings:
Tortuous dilated veins w/i submucosa of distal esophagus and proximal stomach.
(Overlying mucosa may be ulcerated and necrotic.)

Risk:
Rupture –> massive, fatal bleeding

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8
Q

What are the morphologic findings, cause and clinical presentation of Mallory-Weiss tears?

A

Morphologic findings:
Esophageal lacerations at the gastroesophageal junction.

Cause:
Severe retching or vomiting
(alcoholism, bulimia, pregnancy, food poisoning)

Clinical presentation:
Hematemesis, retching, abdominal pain, hx of severe vomiting, melenic stools

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9
Q

What are the common causes of esophagitis?

A
  1. Irritants (alcohol, acid/alkalis, hot fluids, smoking)
  2. Medications
  3. Iatrogenic (chemotherapy, radiation, GVHD)
  4. Infections (HSV, cytomegalovirus, candida)
  5. Immune-mediated (eosinophilic)
  6. Reflux (of gastric contents)
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10
Q

What is the mechanism, clinical features and complications of reflux esophagitis (GERD)?

A

Mechanism:
Reflux of gastric contents into lower esophagus causing mucosal injury

Clinical features:
+40-year-olds, heartburn, dysphagia, sour-taste

Complications:
Esophageal ulceration, hematemesis, melena, stricture development, Barrett esophagus

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11
Q

What is the epidemiology and clinical features of Barrett esophagus?

A

Epidemiology:
White males > 40 y/o

Clinical features:
Prompted by GERD symptoms but requires endoscopy and biopsy

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12
Q

What is the relationship between GERD, Barrett esophagus and esophageal adenocarcinoma?

A

Barrett esophagus:

  • complication of GERD
  • metaplasia of esophageal squamous mucosa
  • increase risk of esophageal adenocarcinoma
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13
Q

What are the two forms of esophageal cancer?

A
  1. Adenocarcinoma

2. Squamous cell carcinoma

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14
Q

Compare the 2 forms of esophageal cancer in regards to:

1) precursor lesion
2) common anatomical location
3) epidemiology

A

Precursor lesion

1) Adeno: Barrett esophagus, flat, raised lesions in intact mucosa that can become exophytic nodules
1) SCC: gray-white, plaque-like mucosal thickening

Common anatomical location

2) Adeno: distal 3rd of esophagus
2) SCC: middle 3rd of esophagus

Epidemiology

3) Adeno: white males > females
3) SCC: adult male > 45 y/o, male > female, blacks > whites

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15
Q

What is the anatomy and physiology of the stomach?

A

1) Cardia:
- mucin-secreting foveolar cells

2) Fundus :
- HCl and intrinsic factor-producing parietal cells
- pepsinogen-producing chief cells

3) Antrum
- gastrin-releasing G-cells
- parietal cells stimulation by gastrin

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16
Q

What is the definition of gastritis v. gastropathy?

A

Gastritis:
- inflammation (neutrophils), irritation or erosion of lining of the stomach

Gastropathy:
- cell injury and regeneration is present but inflammatory cells are rare or absent

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17
Q

What are the common causative factors for gastritis v. gastropathy?

A

Gastritis:

  • H. pylori
  • NSAIDs

Gastropathy:

  • NSAIDs
  • Alcohol
  • Bile
  • Stress-induced injury
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18
Q

What is the disease mechanism for gastritis v. gastropathy?

A

Both results from the destruction of protective and defensive forces of the stomach.

(mucus secretion, bicarbonate secretion, mucosal blood flow, epithelial regeneration, prostaglandin synthesis)

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19
Q

What is the underlying mechanism of chronic gastritis and autoimmune gastritis?

A

Chronic gastritis:
H. pylori in gastric mucous create imbalance in defence and bacterial damage.
(flagella, urease, adhesions, toxins)

Autoimmune gastritis:
Immune-mediated loss of parietal cells and reduction in acid and intrinsic factor secretion
(low acid, low intrinsic factor, low serum pepsinogen)

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20
Q

What is epidemiology of chronic gastritis and autoimmune gastritis?

A

Chronic gastritis:
US - poverty, crowding, limited education, poor sanitation, birth outside US, rural

Autoimmune gastritis:
Patients with autoimmune disease, thyroiditis, DM, graves

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21
Q

What are the location of chronic gastritis and autoimmune gastritis and their clinical sequelae?

A

Chronic gastritis:

  • Antrum
  • peptic ulcer, adenocarcinoma, lymphoma

Autoimmune gastritis:

  • Body
  • atrophy, pernicious anemia, adenocarcinoma, carcinoid tumor
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22
Q

Describe the following for peptic ulcers:

  • risk factors
  • causative agents
  • anatomical locations
  • clinical features
A

Risk factors:
NSAID, smoking, corticosteroids use, previous hx of ulcers, cirrhosis, COPD, renal failure, hyperparathyroidsim

Causative agents:
Gastric acid, H. pylori, NSAID, imbalance of mucosal defenses

Anatomical location:
Gastric antrum and first portion of duodenum, esophagus 2° to GERD

Clinical features:
Recurring lesions, burning and aching pain 1-3 hours post-eating and at night, N/V, bloating, belching, relieved by alkali or food

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23
Q

Describe the following for gastric adenocarcinoma:

  • epidemiology
  • infectious risk factors
  • clinical features
A

Most common stomach malignancy.

Epidemiology:
Low socioeconomics, mucosal atrophy, intestinal metaplasia, gastrectomies, male >55 y/o, males > females

Infectious risks:
H. pylori and EBV

Clinical features:
Early - dyspepsia, dysphagia, nausea
Late - weight loss, anorexia, altered bowel habits, anemia, hemorrhage

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24
Q

What is the anatomy and physiology of the small and large bowel?

A 
Small:
Duodenum (25cm)
- mixing of food with bile and enzymes
Jejunum (2.5cm)
- absorb carbs and proteins, nutrients
Ileum (3.5cm)
- absorb Vit B12

Large:
Absorbs water and electrolytes and vitamins (K, B12, thiamine, riboflavin)

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25
Q

What are the blood supply to the small and large intestines?

A

Superior mesenteric arteries
- small intestine to the middle third of transverse colon

Inferior mesenteric arteries
- last third of transverse colon to sigmoid colon

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26
Q

What are the common causes and clinical features of bowel obstruction?

A

Causes:
- hernias, intestinal adhesions, intussusception, volvulus, tumors, infarctions

Clinical features:
abdominal pain, distention, vomiting, constipation

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27
Q

Describe how the extent of intestinal damage is dictated by the mechanism of obstruction of blood flow in ischemic disease.

A

Ischemic damage to the bowel can range from
- mucosal
infarction (no deeper than the muscularis
mucosa)
- mural infarction of mucosa and submucosa
- transmural infarction involving all three layers of the wall.

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28
Q

What are some factors that determine the severity of ischemic bowel disease (IBD)?

A

Severity of vascular compromise, time frame during which it develops and vessels affected are major variables that determines of IBD.

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29
Q

What are the two phases of injury in ischemic bowel disease?

A
  1. Initial hypoxic injury when epithelial cells are relatively resistant to transient hypoxia.
  2. Reperfusion injury is initiated by restoration of blood supply (can involve free radicals, neutrophil infiltration, and inflammatory mediators)
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30
Q

What are the aspects of intestinal vascular anatomy that contribute to the distribution of ischemic disease?

A
  1. Watershed zones: refers to intestinal segments at the end of their respective arterial supplies.
  2. Patterns of intestinal microvessels: run alongside glands, crypt, surface and hairpin turn into postcapillary venules (leaves epithelium vulnerable to ischemic injury)
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31
Q

Describe the typical patient with ischemic bowel disease including signs and symptoms?

A

Patient:
Older adult with coexisting cardiac or vascular disease

Signs/Symptoms:
sudden, severe abdominal pain, N/V, bloody diarrhea, melena.
could lead to shock, vascular collapse, blood loss

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32
Q

What are hemorrhoids and the risk factors for their development?

A

Hemorrhoids = dilated anal and perianal collateral vessels that connect the portal and caval venous systems to relieve elevated venous pressure within hemorrhoid plexus.

Risk factors:
- constipation, straining (increase abdominal and venous return), venous stasis of pregnancy, portal hypertension

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33
Q

Distinguish between internal and external lesions of hemorrhoids.

A

Internal:
- within distal rectum

External:
- located below anorectal line

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34
Q

Define diarrhea and dysentery.

A

Diarrhea:
increase in stool mass, frequency and fluidity

Dysentery:

  • painful
  • bloody
  • small-volume
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35
Q

What are the four subtypes of diarrhea?

A

(S.O.M.E.)

  1. Secretory - persists during fasting, isotonic stool
  2. Osmotic - less intense w/ fasting, osmotic forces exerted by unabsorbed solutes (lactase deficiency)
  3. Malabsorptive - relieved by fasting, inadequate nutrient absorption (steatorrhea)
  4. Exudative - persists during fasting, inflammatory disease w/ purulent and bloody stools
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36
Q

What are the characteristics, hallmark findings and causes of malabsorptive diarrhea?

A

Characteristics:
- weight loss, anorexia, abdominal distention, borborygmi, muscle wasting

Findings:
- steatorrhea, excessive fecal fat, bulky/frothy/greasy/yellow/ clay-colored stool

Causes:
- inadequate nutrient absorption, pancreatic insufficiency, celiac disease, Crohn’s disease

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37
Q

What is the pathogenesis of celiac disease? What is the morphologic findings and associations with other diseases (malignancy)?

A

Pathogenesis:
- intestinal immune reaction to gluten, it’s breakdown and presentation to T-cells that recruit cytokines leading to damage

Other diseases:

  • enteropathy-associated T-cell lymphoma
  • small-intestinal adenocarcinoma
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38
Q

What is the underlying defect in lactase deficiency and the common signs/symptoms?

A

Underlying defect:
Mutations in the gene encoding lactase (congenital) or downregulation of lactase gene (acquired).

Signs/Symptoms:
Osmotic diarrhea with watery, frothy stool and abdominal distention.

39
Q

What is the difference between diverticulosis and diverticulitis?

A

Diverticulosis:
- multiple acquired pseudodiverticula outpouching of the colonic mucosa and submucosa.

Diverticulitis:
- inflammatory changes of diverticula because of obstruction with stasis contents.

Diverticulosis becomes diverticulitis when diverticula are inflamed.

40
Q

For diverticulosis and diverticulitis, what is the:

  • epidemiology
  • pathogenesis
  • clinical features?
A

Epidemiology:

  • 50% western adult > 60 y/o
  • rare in developing countries and individuals younger than 30 y/o

Pathogenesis:
- diverticula develop when intraluminal pressure is elevated in sigmoid colon

Clinical features:
- mostly asymptomatic but also cramping, abdominal discomfort, constipation, diarrhea

41
Q

(1 of 3)

Compare and contrast ulcerative colitis (UC) and Crohn disease (CD) including:

  1. affected layer of bowel wall
  2. distribution of lesions
  3. epidemiology
  4. pathogenesis
A
  1. Affected layer:
    UC - mucosa, submucosa
    CD - transmural
  2. Distribution of lesions
    UC - diffuse (colon and rectum)
    CD - skip lesions (ileum, colon, and rectum)
  3. Epidemiology
    Both - in adolescents and young adults, common in whites, 3-5x in eastern European
  4. Pathogenesis:
    Both - alterations in host interactions with intestinal microbiota, intestinal epithelia dysfunction, aberrant mucosal immune responses, altered gut microbiome
42
Q

(2 of 3)

Compare and contrast Crohn disease (CD) and ulcerative colitis (UC) including:

  1. macroscopic findings
  2. intestinal complications
A
  1. Macroscopic findings
  2. Intestinal findings

CD: strictures, thick bowel wall, moderate pseudopolyps, deep ulcers, marked lymphoid reaction, firbrosis, serosistis, granulomas, fistulas/sinuses

UC: thin bowel wall, marked pseudopolyps, superficial ulcers, mild fibrosis

43
Q

(3 of 3)

Compare and contrast Crohn disease (CD) and ulcerative colitis (UC) including:
7. malignant potential

A
  1. Malignant potential:
    CD - only with colonic involvement
    UC - YES
44
Q

What are HAMARTOMATOUS polyps and it’s malignancy predisposition?

A

Disorganized and tumor-like polyps due to genetics or acquired syndromes (Peutz-Jeghers Syndrome).

Increases risk for malignancy.

45
Q

What are HYPERPLASTIC polyps and it’s malignancy predisposition?

A

Epithelial proliferations resulting from incomplete epithelial turnover and a “pileup” of goblet cells.

No malignant potentials.

46
Q

What are ADENOMATOUS polyps and it’s malignancy predisposition?

A

Benign neoplastic polyps from epithelial dysplasia.

Increase risk with increase size.

47
Q

(1 of 2)

Describe the following for colorectal cancer:

  1. epidemiology
  2. dietary influences/factors
  3. prognostic indicators
A
  1. Epidemiology
    - peaks at 60-70 y/o
    - males > females
    - prevalent developing countries
  2. Dietary influences/factors:
    - low intake of fiber
    - high intake of carbs and fat
  3. Prognostic indicators
    - depth of invasion
    - presence of lymph node metastases
48
Q

(2 of 2)

Describe the following for colorectal cancer:
4. clinical characteristics

A
  1. Clinical characteristics:
    - proximal colon = polypoid exophytic masses along wall of cecum and ascending colon; rare obstruction
    - distal colon = annular lesions into “napkin rings” constrictions, sometimes obstructive
    - cecal/right-sided = fatigue and weakness, Fe-deficiency anemia
    - Left sided = occult bleeding, changes in bowel habits, cramping, LLQ discomfort
49
Q

Where does colorectal carcinoma commonly metastasize to?

A

Liver is most common.
Lymph nodes (complicates survival)
Lungs and others (limit survival; 15%)

50
Q

What is the pathogenesis and common clinical features of acute appendicitis?

A

Pathogenesis:

  • increased intraluminal pressure that compromises venous outflow
  • associated with obstruction (fecalith) leading to injury or stasis of luminal contents
  • inflammatory response

Clinical features:

  • preumblical pain to RLQ (Mcburney’s Sign = deep tenderness between umbilicus and right anterior superior iliac spine)
  • N/V, low grade fever and elevated WBC
  • or none of these
51
Q

What are the functions of the liver?

A
  1. Carbohydrate, amino acid and lipid metabolism
  2. Waste product removal
  3. Vitamin and mineral storage
  4. Drug inactivation
  5. Phagocytosis and antigen presentation
  6. Synthesis of plasma proteins
  7. Removal of circulating hormones, antibodies and toxins
  8. Synthesis and secretion of bile
52
Q

What is the hepatic portal and systemic circulation to the liver?

A

Capillaries of digestive organs ends in the liver sinusoids. Hepatic portal vein receives blood from superior/inferior mesenteric, splenic, gastric and cystic veins.

53
Q

What is reversible and irreversible hepatocyte injury and their repair mechanism?

A

Reversible:
- show hepatocytes may show cholestasis (fat/bilirubin accumulation)

Irreversible:
- hepatocyte necrosis or apoptosis

Repair:

  • regeneration of lost hepatocytes
  • scar formation in chronic injury
  • stellate cell converted to fibrogenic myofibroblast (scar)
54
Q

Describe the mechanism of liver regeneration.

A

Mitotic replication of hepatocytes adjacent to those that have died. Stem cell proliferation and differentiation contributes to parenchymal restoration creating ductular reactions.

55
Q

What is acute liver failure and its potential outcomes?

A

Liver disease that produces hepatic encephalopathy w/i 6 months of initial diagnosis. Shrinkage of the liver due to loss of parenchyma.

Outcomes:
- jaundice, hepatic encephalopathy, coagulopathy, portal hypertension, hepatorenal syndrome

56
Q

What is cirrhosis and its morphologic features?

A

Diffuse transformation of the liver into regenerative parenchymal nodules surrounded by fibrous bands. (associated with chronic liver disease)

57
Q

What is the viral genome of Hepatitis A through E?

A

A: ssRNA

B: partially dsDNA

C: ssRNA

D: circular defective ssRNA

E: ssRNA

58
Q

What is the route of transmission of Hepatitis A through E?

A

A: fecal-oral (contaminated food/water)

B: parenteral, sexual contact, perinatal

C: parental, intranasal cocaine use

D: parental

E: fecal-oral

59
Q

What is the frequency of chronic liver disease from Hepatitis A through E?

A

A: Never

B: 5-10%

C: >80%

D: 10% (coinfection w/ HBV) 90-100% (superinfection w/ chronic HBV)

E: Immunocompromised only

60
Q

Are there any risks to hepatocellular carcinoma of Hepatitis A through E?

A

Only Hepatitis C.

61
Q

What is epidemiology of autoimmune hepatitis?

A

Higher in Caucasians but other groups are susceptible. Associated with other autoimmune diseases, autoantibodies and therapeutic response to immunosuppression.

62
Q

Distinguish between Type I and Type II autoimmune hepatitis with respect to pathogenesis.

A

Type I:
- classic, presence of anti-nuclear, anti-smooth muscle actin, anti-mitochondrial and anti-soluble liver antigen

Type II:

  • seen in children and teenagers
  • anti-liver kidney microsome-1 antibodies and anti-liver cytosol-1 antibodies
63
Q

What is the morphologic findings and pattern of injury in acetaminophen-induced hepatic injury?

A

Pattern:
Hepatocellular necrosis beginning in the centrilobar hepatocytes and extending to entire lobules

Morphology:
Massive necrosis

64
Q

What are the three (3) liver alterations of fatty liver disease and their morphologic changes?

A
  1. Steatosis - increase lipid droplets w/i cells and can displace nucleus
  2. Hepatitis - hepatocytes balloon and necrotize becoming Mallory-Denk bodies surrounded by neutrophils
  3. Fibrosis - liver fibrosis can become brown and shrunken
65
Q

Describe the pathogenesis of alcoholic liver disease and the acceleration of the process.

A
  1. Acetaldehyde
    - peroxidation of lipids and acetaldehyde formation affect cytoskeleton and membrane function
  2. Alcohol
    - affects mitochondrial function and membrane fluidity
  3. Reactive oxygen species
    - damage membranes and proteins, infiltrate hepatocyte necrosis

Acceleration:
Concurrent viral hepatitis (HCV)

66
Q

What is NAFLD and NASH?

A

Non-alcoholic fatty liver disease (NAFLD)
- fatty liver in non-alcoholics

Non-alcoholic steatohepatitis (NASH)
- generalized and overt clinical features of liver injury

67
Q

What are the medical conditions or diagnoses associated with NAFLD?

A
  • steatosis, steatohepatitis and cirrhosis but less prominent
  • associated with insulin resistance and metabolic syndrome
  • obesity (BMI >30 in whites and >25 asians)
  • dyslipidemia
  • hypertension
68
Q

What is the pathogenesis of NASH and NAFLD?

A
  1. obesity and insulin resistance leads to excessive intrahepatic lipids
  2. increases sensitivity to cytokines, activating inflammasomes
  3. lipid metabolism are toxic due to ROS production, ER stress and mitochondrial dysfunction
  4. insults triggers stellate cell activation, collagen deposition and hepatic fibrosis
69
Q

What is the genetic mutation, pathogenesis, and morphologic features of HEMOCHROMATOSIS?

A 
Genetic mutation:
- HFE gene encoding an HLA class I-like molecule, results in lower hepcidin volume or function

Pathogenesis:
- decreased hepcidin volume and function leads to excessive iron which is toxic to host

Morphologic features:
- hemosiderin deposits organs and joints as well as cirrhosis and pancreatic fibrosis.

70
Q

What is the genetic mutation, pathogenesis, and morphologic features of WILSON DISEASE?

A

Genetic mutation:
- impaired ATP7B gene resulting in impaired excretion of copper into bile and incorporation of copper into ceruloplasmin (autosomal recessive)

Pathogenesis:

  • free copper (Cu) accumulate in liver and produces ROS by Fenton reaction
  • in circulation, ROS causes red cell hemolysis and allow Cu deposition in other tissues

Morphologic features:

  • chronic hepatitis and cirrhosis
  • eye lesions called Kayser-Fleischer rings
71
Q

What is the genetic mutation, pathogenesis, and morphologic features of ALPHA-1 ANTITRYPSIN DEFICIENCY?

A

Genetic mutation:
- PiZ; PiZZ homozygotes produced 10% of normal alpha-1-AT (autosomal recessive)

Pathogenesis:

  • PiZ protein misfolds and aggregates (glutamine-lysine sub)
  • stresses ER and stimulates apoptosis

Morphologic features:
- presence of round-oval cytoplasmic globular inclusions in hepatocytes that is PAS-positive and diastase resistant.

72
Q

Describe the metabolism of bilirubin.

A

Metabolism:

  1. heme –> biliverdin (via heme oxygenase)
  2. biliverdin –> bilirubin (via biliverdin reductase)
  3. albumin binds bilirubin and transport to liver
  4. bilirubin conjugated with glucuronic acid (via UDP-glucuronyltransferase) in ER
  5. bilirubin glucuronides excreted into bile and deconjugated in gut lumen into urobilinogens
  6. urobilinogens are excreted in feces, reabsorbed in ileum and colon, returned to liver and re-excreted in bile or urine
73
Q

Describe bile formation.

A

Bile acids are catabolic products of cholesterol that are conjugated with taurine or glycine into bile salts.

74
Q

What is the relationship of jaundice to serum bilirubin level?

A

Jaundice evident when serum bilirubin level rises above 2-2.5 mg/dL.

75
Q

Distinguish between conjugated and unconjugated hyperbilirubinemia by mechanism.

A

Conjugated hyperbilirubinemia:

  • water-soluble, non-toxic, loosely bound to albumin
  • excreted in urine

Unconjugated:

  • insoluble, toxic, tightly bound to albumin
  • diffuses into tissues, severe in hemolytic disease
76
Q

What are the common causes of conjugated and unconjugated hyperbilirubinemia?

A

Conjugated:

  • decreased hepatocellular excretion
  • impaired bile flow

Unconjugated:

  • excess production bilirubin
  • reduced hepatic uptake
  • impaired bilirubin conjugation
77
Q

Define cholestasis and distinguish between extra- and intrahepatic causes.

A

Cholestasis: condition caused by obstruction of bile channels or by defects in hepatocyte bile secretion

Extrahepatic:
gallstones, malignancy, postsurgical strictures

Intrahepatic:
diseases of intrahepatic biliary tree or hepatocellular secretory failure

78
Q

Describe complication of ascending cholangitis and the outcome of cholestasis if left untreated.

A

Cholangitis: bacterial infection of biliary tree

Complications:

  • duct obstruction
  • severe; purulent bile fills bile ducts causing sepsis

Outcome:
- inflammation, periportal fibrosis, obstructive biliary cirrhosis.

79
Q

Compare and contrast
PRIMARY BILIARY CHOLANGITIS with
PRIMARY SCLEROSING CHOLANGITIS.

A

1° Biliary:
- progressive, inflammatory, often granulomatous, destruction of small-medium intrahepatic bile ducts.
- often occurs in middle-age women
- associated with anti-mitochondrial
antibodies (AMA)
- Sjögren syndrome and Hashimoto thyroiditis.

1° Sclerosing
- progressive inflammatory and sclerosing destruction of
intrahepatic and extrahepatic bile ducts of all sizes.
- diagnosis by imaging of the biliary tree.
- often occurs in younger men
- association with
IBD, particularly ulcerative colitis.

80
Q

What are the causes and the clinical consequences of hepatic circulatory disorders, including portal hypertension?

A
  1. Impaired blood inflow
    - portal vein obstruction, intrahepatic/extrahepatic thrombosis
    = esophageal varices, splenomegaly, intestinal congestion
  2. Impaired intrahepatic blood flow
    - cirrhosis, sinusoid occlusion
    = ascites, esophageal varices, hepatomegaly, elevated aminotransferases
  3. Hepatic vein outflow obstruction
    - hepatic vein thrombosis, sinusoid obstructive syndrome
    = ascites, hepatomegaly, abdominal pain, jaundice, elevated aminotransferases
81
Q

What is the most common neoplasm of the liver and the most common primary sites of the originating tumor?

A

Metastatic carcinoma is the most common neoplasm and commonly originates in the hepatocytes (some bile ducts).

82
Q

What are the etiologic agents and pathogenesis of hepatocellular carcinoma (HCC)?

A 
Etiologic agents:
Viral infections (Hep B and C) and toxins (aflatoxins, alcohol).

Pathogenesis:
Chronic liver disease, beta-catenin mutations, TP53 inactivation.

83
Q

Describe the following for cholelithiasis (gallstones):

  • pathogenesis
  • prevalence
  • risk factors
A

Pathogenesis:
- cholesterol exceed solubilizing capacity of bile and crystallizes out of solution

Prevalence:

  • obese patients
  • 80% in Western countries

Risk factors:

  • age, female, oral contraceptives, weight loss, gallbladder stasis, dyslipidemia (cholesterol)
  • Asians, rural, hemolysis, biliary infection, GI disorders (pigment)
84
Q

What are the mechanism of disease and relationship to cholithiasis for:

  • acute calculous
  • acalculus
  • chronic cholecystitis
A

Acute calculous:

  • chemical irritation and inflammation of the gallbladder wall due to obstruction of bile outflow
  • 90% for gallstones

Acalculous:
- in ill patients, arises from major surgery, severe trauma, severe burns, sepsis, dehydration, gallbladder
stasis, sludging, vascular compromise, and
bacterial contamination
- 5-12% for gallstones

Chronic cholecystitis:
- repeated bouts
of acute cholecystitis, but can develop
without any history of acute attacks
- always associated with gallstones
85
Q

What are the risk factors for carcinoma of the gallbladder?

A
  • more common in women
  • ages > 70
  • cholethiasis
  • bile acids
  • primary sclerosing cholangitis
86
Q

Understand the anatomy and physiology of the pancreas.

A
  • retroperitoneal organ
  • endocrine = islets of langerhans (insulin, glucagon, somatostatin)
  • exocrine = acinar cells, ducts (synthesize enzymes, bicarbonates, mucins)
87
Q

What are the most common etiologies of acute pancreatitis?

A

Metabolic
- alcoholism, hypercalcemia, hyperlipoproteinemia, drugs

Genetic
- mutations in the cationic trypsinogen (PRSS1) and trypsin inhibitor (SPINK1)

Mechanical
- trauma, perioperative injury, iatrogenic injury, dye injection, gallstones

Vascular:
- shock, atheroembolism, polyatertis nodosa

Infectious:
- mumps, coxsackievirus

88
Q

What are the five basic alterations in acute pancreatitis?

A
  1. microvascular leakage –> edema
  2. necrosis of fat by lipases
  3. acute inflammatory reaction
  4. proteolytic destruction of pancreatic parenchyma
  5. destruction of blood vessels leading to interstitial hemorrhage
89
Q

What are the common clinical features of the acute pancreatitis?

A
  • abdominal pain
  • elevated lipase and amylase
  • absent bowel sounds
90
Q

Describe the following for CHRONIC PANCREATITIS:

  • etiologies
  • clinical features
A

Etiologies:
- alcohol abuse, duct obstruction, tropical, hereditary, CFTR mutations, autoimmune

Clinical features:
- bouts of jaundice, vague indigestion, persistent abdominal/back pain

91
Q

Describe the following for CHRONIC PANCREATITIS:- pathogenesis

A
  • Ductal obstruction by concretions
  • Toxic-metabolites (lipid accumulations, acinar cell loss, parenchymal fibrosis
  • Oxidative stress (membrane damage, inflammatory cell recruitments, fusion of lysosomes and zymogen granules leading to acinar cell necrosis, inflammation and fibrosis)
  • Inappropriate activation of pancreatic enzymes
92
Q

What is the epidemiology of pancreatic carcinoma (infiltrating ductal adenocarcinoma)?

A

Third leading cause of cancer deaths in US. Highest mortality rate. 5-year survival rate is 8%.

93
Q

What are the common clinical features of pancreatic carcinoma (infiltrating ductal adenocarcinoma) and why jaundice may occur?

A

Weight loss, anorexia, generalized malaise and weakness. New onset diabetes.

Obstructive jaundice occurs due to carcinoma in the head of the pancreas blocking the bile/pancreatic duct preventing bile drainage.

94
Q

What is the prognosis of pancreatic carcinoma (infiltrating ductal adenocarcinoma)?

A

Poor prognosis.

Pathophysiology (9 decks)

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