GI Reading Flashcards
Life-threatening, acute inflammation and infection of visceral/parietal peritoneum and endothelial lining of abdominal cavity
Results in vascular dilation and increased capillary permeability
Results from perforation or external penetrating wound, gangrenous gallbladder/bowel segment, bowel obstruction, ascending infection through genital tract, invasive tumors, leakage/contamination during surgery, infection by skin pathogens when undergoing CAPD
When diagnosis and treatment delayed dilation cont - cont shunt fluid and get third spacing
Result in sig decrease circ volume, hypovolemic shock, AKI, impaired fluid and electrolyte balance
Peristalsis slows/stops, lumen bowel becomes distended with gas and fluid
Bacteria causing this can result in septic shock
Resp probs - increased abdominal pressure
Pain
Peritonitis
Acute inflammation of the veriform appendix that occurs most often among young adults
RLQ pain
When lumen obstructed, leading to infection as bacteria invade the wall of the appendix
The initial obstruction is usually the result of fecaliths composed of Ca phosphate-rich mucus and inorganic salts
When lumen blocked, mucosa secrets fluid increasing internal pressure and restricting blood flow which results in pain; if process occurs slow - abscess may develop; if quickly = may cause peritonitis
All comps of peritonitis are serious - gangrene and sepsis within 24-36 hr; perforation may develop within 24 hours but risk rises rapidly after 48 hrs
Appendicitis
Extensive, irreversible scarring of liver usually caused by chronic rxn to hepatic inflammation and necrosis - directly impairs cellular regulation; typ develops slowly and has progressive, prolonged, destructive course result in ESLD
Widespread fibrotic/scarred bands CT change liver’s A&P
Inflammation caused by toxins/disease resulting in extensive degeneration and destruction of hepatocytes (liver cells)
As develops, tissue more nodular thus blocking bile ducts and norm blood flow resulting in compression
Early: enlarged and firm; as becomes harder, less liver func, decreases in size
Elevated serum liver enzymes
Portal HTN
Ascites and gastroesophageal varices
Splenomegaly
Biliary obstruction
Hepatic encephalopathy
Hepatorenal syndrome
Hepatopulmonary syndrome
Cirrhosis
Widespread inflammation and infection of liver cells
Viral - acute/chronic - most common; A-E
Less common - caused by chems, drugs, herbs
With inflammation - exposure to drugs and chems
Secondary infection
Causative agent - enlarged and congested with inflammatory cells, lymphocytes, fluid resulting in RUQ pain and discomfort
Livers lobular pattern distorted and cellular regulation compromised resulting in widespread inflammation, necrosis, and hepatocellular regeneration - increasing pressure within portal circ, interferes with blood flow into hepatic nodules
Edema of liver’s bile channels = jaundice
Hepatitis
ESLD/acute liver failure - not responded to conventional medical/surgical intervention
Causes: cirrhosis (most common), chronic hep B/C, bile duct disease, autoimmune liver disease, alcoholic liver disease, fatty liver disease
Liver transplantation
Inflammation of gallbladder affects many adults - very commonly affluient countriesl most pts have acutel affects nutrition
Acute
Chronic
Cholecystitis
Calculus - chem irritation and inflammation from gallstones obstruct cystic duct, gallbladder neck or common bile duct
Acalculous - inflammation without gallstones - associated with biliary stasis caused by any condition that affects regular filling/emptying of gallbladder
Acute Cholecystitis
Repeated episodes of cystic duct obstruction
Calculi almost always present
Young, thin women (esp athletic ones)
Chronic Cholecystitis
Serious and sometimes life-threatening inflammation of pancreas
Caused by premature activation of excessive pancreatic enzymes that destroy ductal tissue and pancreatic cells resulting in autodigestion and fibrosis of pancreas
Severity depends on extent of inflammation and tissue damage
release pancreatic enzymes may contripute to ductal rupture; increased pressure present
Autodigestion of pancreas
Have: lipolysis, proteolysis, necrosis of blood vessels, inflammation
Pancreatic abscesess can form in inflammatory stages - must be drained to prevent sepsis
Acute pancreatitis
Progressive, destructive disease of pancreas with remission and exacerbations
Inflammation and fibrosis of tissue contribute to pancreatic insufficiency and diminished func of organ
Alcoholism main factor
Early on: pancreatic secretions plug ducts and flow juices - duct changes further one and ulcerates
Inflammatory process causes fibrosis resulting in hard and firm organ as a result of cell atrophy and pancreatic insufficiency
From: inflammation, spasm, obstruction sphincter of Oddi (gallstones)
Lesions cause obstruction and backlow secretions
Steatorrhea
Loss endocrine func = DM
Pulm comps: pleuritic pain, pleural effusions, pulmonary infiltrates, palomary ascites may decrease diaphgramatic excursion and lung expansion resulting in impaired ventilation
Ill pation: ARDS may develop
Chronic pancreatitis
Primary = adenocarcimoas - rapid growing and spread to surrounding organs via extension or invasion into lymphatic or vascular sys
Jaundice, head - poorly defined margins, body and tail large - palpable on tinier indiv
VTE common comp
Necrotic products of pancreatic tumor - believed have thromboplastic properties causing hypercoaguable state
Risk factors
Key features
Pancreatic cancer
DM
Chronic pancreatitis
Cirrhosis
High intake red meat - esp processed meat
Long-term exposure to chems: gas and pesticides
Obesity
Older age
Male gender
Cig smoking
Fam hx
Genetic mutations (p16/BRCA2)
Risk factors - Pancreatic cancer
Jaundice
Icterus
Clay-colored (light) stools
Dark urine
Abdominal pain, usually vague, dull, nonspecific that radiates to the back
Weight loss
Anorexia
N&V
Glucose intolerance
Splenomegaly
Flatulence
GI bleeding
New-onset DM
Ascites (abd fluid)
leg/calf pain (from thrombophlebitis)
Weakness and fatigue
Key features - Pancreatic cancer
