10.4 - Pathological Conditions of GI Accessory Organs Flashcards

1
Q

Cause and Pathophysiology of Appendicitis?

A

Cause:
Obstruction of appendiceal lumen by:
- fecaliths (hardened stool)
- lymphoid hyperplasia (children/young adults)
- tumors or foreign bodies

Pathophysiology:
- Obstruction of appendiceal lumen = ↑ intraluminal pressure = impaired venous outflow = ischemia & bacterial overgrowth = necrosis = perforation (bc necrotic tissue is impaired) = peritonitis (leakage of non-sterile tissue in peritoneum )

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2
Q

Structural Changes and Clinical Significance of Appendicitis?

A

Structural Changes
- Edema & inflammation of appendix
- Necrosis & rupture of appendix = abscess formation or diffuse peritonitis

Clinical Significance:
Symptoms
- Periumbilical pain migrating to RLQ (McBurney’s point)
- nausea
- vomiting
-fever
- leukocytosis

Complications
- Rupture
- abscess
- peritonitis & sepsis

Management
- Surgical removal (appendectomy)
- Antibiotics

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3
Q

Cause and Pathophysiology of Gallstone (Cholelithiasis)

A

Cause
1) Cholesterol stones
-n Supersaturation of bile with cholesterol, stasis, & crystallization

2) Pigment stones
- Chronic hemolysis (e.g., sickle cell disease) or infection

3) Risk factors
- Obesity, rapid weight loss, pregnancy, female sex (estrogen-related), and genetic predisposition

Pathophysiology
- Imbalance in the composition of bile (cholesterol, bile salts, and lecithin) = precipitation of cholesterol or bilirubin

  • Stasis of bile in the gallbladder promotes stone formation
  • Obstruct the bile duct or cystic duct = cholecystitis
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4
Q

Structural Changes and Clinical Signs of Gall Stones

A

Structural Changes
- Formation of solid deposits (stones) in gallbladder or bile ducts = chronic irritation of gallbladder wall = thickening or calcification (porcelain gallbladder)

Clinical Significance
S&S
- Asymptomatic; Symptomatic = biliary colic (RUQ pain after fatty meals), nausea, and vomiting

Complications
- Cholecystitis, choledocholithiasis (common bile duct stones)
- pancreatitis
- cholangitis (swelling of bile duct system itself)

Management
- Symptomatic = cholecystectomy (surgical removal of gallbladder)

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5
Q

Cause of Cholescystitis

A

1) Gallstones (Calculous Cholecystitis)
- Majority of cases (~90%)
- Gallstones obstruct cystic duct = bile stasis & inflammation

2) Acalculous Cholecystitis
- Occurs in critically ill patients (i.e., sepsis or trauma
- Results from bile stasis, ischemia, & infection without gallstones

3) Other Causes
- Infections (e.g., Salmonella
- CMV in immunocompromised patients)
- Tumors obstructing bile flow

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6
Q

Pathophysiology of Cholecystitis

A

1) Obstruction
- Gallstone obstruction at cystic duct = stasis of bile = bile concentration = irritation of gallbladder lining

2) Inflammation
- Release of pro-inflammatory mediators (e.g., prostaglandins) = edema & mucosal damage
- Secondary bacterial infections (e.g., E. coli, Klebsiella)

3) Ischemia
- Prolonged inflammation = impaired blood flow = tissue ischemia = necrosis = gangrene

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7
Q

Structural Changes of Cholecystitis

A

1) Acute Cholecystitis
- Gallbladder wall thickening
- Mucosal damage with possible ulceration
- Pericholecystic fluid & abscess formation (severe cases)

2) Chronic Cholecystitis:
- Gallbladder wall fibrosis & calcification (“porcelain gallbladder”)
↓ gallbladder motility

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8
Q

Clinical Signs of Cholecystitis

A

Symptoms
- RUQ pain
- radiating right shoulder (referred pain: bc source of pain also causes nerve irritation)
- Fever
- nausea
- vomiting
- leukocytosis
- Positive Murphy’s sign (pain on deep palpation during inspiration)

Complications
- Empyema = Accumulation of pus in gallbladder
- Perforation = Rupture of the gallbladder = peritonitis
- Choledocholithiasis = gallstone obstruction of bile duct
Cholangitis = Bile duct infection
- Chronic inflammation  ↑ risk of gallbladder cancer

Management
1) Supportive care
- IV fluids, antibiotics, pain medications (analgesics)

2) Surgical Intervention
- Cholecystectomy
- Laparoscopic (far more common) or open surgery

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9
Q

Causes and Pathology of Pancreatitis

A

Cause
- Acute = gallstones or alcohol use (most common), hypertriglyceridemia, trauma, infections, & drugs

  • Chronic = chronic alcohol use, genetic predisposition (CFTR mutations), or recurrent acute pancreatitis

Pathophysiology
- Premature activation of pancreatic enzymes (e.g., trypsin) = auto digestion of pancreas = inflammation & necrosis follow

  • Chronic pancreatitis = fibrosis & loss of exocrine/endocrine functions of the pancreas
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10
Q

Structural Changes and Clinical Significance of Pancreatitis

A

Structural Changes
1) Acute
- Edema, necrosis, hemorrhage, pseudocysts formation

2) Chronic
- Fibrosis, calcifications, dilated pancreatic ducts, loss of acinar & islet cells.

Clinical Significance
1) Acute symptoms
- Severe epigastric pain radiating to the back, nausea, & vomiting

2) Chronic symptoms
- Epigastric pain, malabsorption
- steatorrhea (fatty stools bc of issue of releasing pancreatic enzymes to support digestion)
- diabetes mellitus (bc of role pancreas plays in endocrine function)

3) Complications
- Pseudocysts, necrosis, infection, organ failure, & pancreatic cancer

4) Management
- Supportive care (IV fluids, analgesics)
- treat underlying cause (e.g., gallstone removal)

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11
Q

Causes and Pathophysiology of Pancreatic Cancer

A

Cause
1) Risk factors
- Smoking, chronic pancreatitis, family history, BRCA mutations, and diabetes mellitus
- Most are adenocarcinomas of pancreatic duct

Pathophysiology
- Oncogenic mutations (e.g., KRAS) =dysregulated cell proliferation = tumor growth disrupts pancreatic & adjacent organ functions = metastasis occurs early due to rich vascular and lymphatic supply

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12
Q

Structural Changes and Clinical Signs of Pancreatic Cancer

A

Structural Changes
- Tumor in the pancreatic head obstructing the bile duct = jaundice
- Fibrotic and infiltrative lesions spread locally & metastasize to distant organs (e.g., liver, lungs)

Clinical Significance
1) Symptoms
- Late presentation with vague symptoms
- Epigastric pain, weight loss, jaundice (duct obstruction), & new-onset diabetes

2) Prognosis
- Poor (advanced stage diagnosis)

3) Management
- Surgery (e.g., Whipple procedure) if localized
- Chemotherapy & palliative care

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