GI and Liver Flashcards
Gastrin
stimulates gastric acid, blood flow
Cholecystokinin (CCK)
Contraction of gallbladder and secretion of pancreatic enzymes
Secretin
inhibits gastric acid secretion; stimulates secretion of water from the pancreas
Ghrelin
peptide hormone stimulates food intake and digestive function (appetite)
Digestion and Absorption
Requires hydrolysis, enzyme cleavage, fat emulsification
Absorption: moving nutrients from external intestinal lumen to internal environment.
Clinical Manifestations of GI Dysfunction
Anorexia: lack of appetite Vomiting (emesis) Constipation Diarrhea Abdominal Pain GI Bleeding Melena in Lower GI (bloody/dark stool)
GERD
Reflux of gastric contents into esophagus as a result of
Reduction in lower esophageal sphincter tone
Delayed gastric emptying
Increase gastric acid secretion
Irritation of esophageal mucosa
S/S of GERD
Pyrosis (heartburn) cardinal symptom Belching Atypical Symptoms Esophageal pain referred to the neck, mid-back, upper abdomen Chest pain Chronic cough, wheezing, Hoarseness Chronic sore throat, dysphagia
GERD Risk Factors
Factors which reduce LES tone Aging Obesity Pregnancy (hormones_ High fat meals
Peptic Ulcer Disease
A group of ulcerative disorders that occur in areas of the upper gastrointestinal tract that are exposed to acid-pepsin secretions
Erosion of the gastric membrane
Gastric ulcers
Duodenal ulcers
Stress ulcers- Curling’s ulcer stimulates acid production in stomach
Duodenal ulcers are more popular then gastric
PUD Risk Factors
Helicobacter pylori (H-Pylori) infection
90-95% of patients with duodenal ulcers
60-70% of patients with gastric ulcers
NSAIDs
Aspirin: blocks prostaglandins in stomach, this takes away from the stomach’s mucus lining
PUD S/S
Burning, gnawing, cramp-like
Frequently when stomach empty
Midline epigastric, near xiphoid…may radiate to back or right shoulder
Relieved by foods or antacids
Periodicity: daily for weeks, then remits until next occurrence
PUD Complications
Bleeding Hematemesis (blood) Coffee ground emesis Hematochezia (blood stool) Melena (foul/dark bloody stool) Occult bleeding
Gastric Outlet Obstruction
Caused by edema, spasm, scar tissue
Perforation
Peritonitis: inflammation from bacteria throughout GI
Inflammatory Bowel Disease (IBD)
Idiopathic chronic disorders of the GI tract distinguished by the recurrent inflammatory involvement of intestinal segments.
Two main types: Crohn’s disease Ulcerative colitis (UC)
Crohn’s Disease
Granulomatous inflammatory lesions of the GI tract.
Peak age of onset 20-30’s (Crohn’s), and 30’s (UC)
Family history
Genetic predisposition – triggered by dietary antigen or microbial agent
Location: Mouth to anus. Mostly small intestine & proximal colon. Smoker’s and Jews are mostly affected
Pattern: “Cobblestone” inflammatory appearance of submucosal layer Skip lesions (healthy mucosa) if multiple
Manifestations
Intermittent diarrhea, steatorrhea, colicky pain (cramping), weight loss, F/E imbalances, nutritional deficiencies, malaise, low-grade fever.
Complications: anal & perianal fistulas, abscesses, intestinal obstruction
Diagnosis for Crohn’s Disease
Sigmoidoscopy & Colonoscopy with biopsy: inflammation; biopsy often reveals granulomatous inflammation
X-rays
CT scan
Sedimentation rate: elevated shows inflammation
Complete Blood Count: possible anemia
Electrolytes: imbalances (Potassium)
Treatment for Crohn’s Disease
Gastroenterologist referral Corticosteroids Immunosuppressants Antibiotics- Metronidazole (Flagyl) Nutritious diet; residue free/bulk free to allow bowel rest
Ulcerative Colitis
Inflammatory condition confined to the mucosal layer of the rectum and colon
Starts in rectum and spreads proximally through colon
Confluent inflammatory pattern (no “skip” lesions)
Lead to pinpoint mucosal hemorrhages; may develop into crypt abscesses; may become necrotic & ulcerate
Pseudopolyps of mucosal layer (obstruction of bowels)
Manifestations
Bloody diarrhea, nocturnal diarrhea, mild abdominal cramping
Complications: Colon cancer risk; toxic megacolon in severe fulminant type
Ulcerative Colitis Diagnosis and Treatment
Diagnosis: History & Physical/Colonoscopy
Treatment: Diet modifications, Fiber reduces diarrhea
Avoid caffeine, lactose, spicy, and gas-producing foods
Corticosteroids, Immunosuppressants, Surgery
DIVERTICULAR DISEASE
Diverticulum/Diverticula – saclike protrusions of the mucous membrane that herniates outward through muscular layer. (outpouches or outpocketings)
Diverticulosis – the presence of diverticula
Diverticulitis – diverticula become inflamed and may perforate (undigested food, fecal matter, and bacteria become trapped forming fecalith: stone of feces)
Diverticular Disease Risk Factors
Increases dramatically with age More common in North America, Australia, and Europe Affects men and women equally Risk Factors Low fiber diet ↓strength of colon musculature ↓physical activity (strengthens ALL muscles!) Poor bowel habits
ACUTE DIVERTICULITIS
LLQ ABDOMINAL PAIN (93-100%) Tender palpable mass in Left Lower Quadrant Fever Mild to moderate leukocytosis Nausea, vomiting, and anorexia Constipation/Diarrhea
APPENDICITIS
Inflammation of the vermiform appendix
Can lead to gangrene and perforation (peritonitis)
Cause: Intraluminal obstruction w/ fecalith
Signs and Symptoms
Initially: vague epigastric or periumbilical pain
Nausea, vomiting, anorexia
Follow onset of pain
RLQ McBurney’s point rebound tenderness
75% have leukocytosis 10-18,000/mm3
Fever
Psoas sign: extend leg/check for pain by stretching muscle
Obturator test: rotating ankle, leg for pain
DIAGNOSIS/TREATMENT for Appendicitis
Emergency Department History & Physical CT scan** (or U/S) Appendectomy (surgical) IV Antibiotics Complications Peritonitis Abscess formation Septicemia
Intestinal Obstruction
Mechanical vs. Paralytic
Mechanical (feces, stricture, edema):
Hernias, adhesions, strictures, tumors, foreign bodies, intussusception (part of bowel breaks off), volvulus (twisting of bowel)
Severe colicky pain (cramping)
Borborygmy (bowel sounds rapidly present)
Paralytic (failure of motility from NS innervation):
“adynamic”: not moving
Neurogenic or muscular impairment of peristalsis
Paralytic ileus
Absent bowel signs
S/S:
Abdominal distention, pain, constipation, vomiting, Fluid & Electrolyte disturbances.
COLORECTAL CANCER
Uncontrolled growth of malignant cells in the large intestine
Risk Factors - >40-50 age, polyps, family history, DM, Tobacco, diets rich in fats and red meats, ethnicity
S/S – Change in bowel habits, occult blood, bloating, anorexia
Pain/weight loss is a LATE sign!
Diagnosis – Colonoscopy, CoreoEmbryonic Antigen
Treatment – Surgery, chemo, radiation
Screening recommendations: every 2 years for polyps, colonoscopy every 10 years
Peritonitis
Inflammatory response of the peritoneal membrane
Causes:
Bacterial or chemical irritation
Perforated ulcers, diverticulum, appendix
Gangrenous bowel or gallbladder
S/S of Peritonitis
Pain & tenderness Rigid/board-like, distended, guarded abdomen Shallow respirations Nausea/Vomiting Fluid losses; Dehydration Fever ↑WBC count Tachycardia Hypotension
Complications: Paralytic ileus, Hypovolemia, Sepsis
Shock
VIRAL HEPATITIS
Viral infection affecting the liver
Five viral causative agents: A,B,C,D,E
Hepatitis B, C, and D can cause chronic infections
Risk Factors: HAV & HEV Transmitted via fecal-oral route Travel to endemic areas Ingestion of contaminated food, water, milk, or shellfish IgM anti-HAV, IgG anti-HAV Hep A vaccine available
Heptatitis B and C RISK FACTORS
HBV, HCV –blood/body fluids Shared needles Multiple sexual partners Tattoo recipients; body piercings Health care workers Can cause chronic hepatitis & cirrhosis All adolescents are considered high-risk for HBV Risk for hepatocellular CA w/ HCV HBV vaccine available
SIGNS AND SYMPTOMS of Hep B and C
Many are asymptomatic
Nausea, vomiting, anorexia, RUQ abdominal pain, liver enlargement
Malaise, fever
Sclera become yellow (icteric)
Jaundice, dark urine, clay-colored stools
Elevated ALT, AST, bilirubin levels
DIAGNOSIS for Hep B and C
Liver function tests
ALT, AST – hepatic injury
ALT – Think Hepatitis B
AST – Alcohol, Statins, Tylenol
PT/albumin (low) – measure synthetic activity of liver. Long time to clot
Increased Bilirubin – measure of excretory function of liver
CIRRHOSIS
End stage chronic liver disease Irreversible inflammatory disease Disrupts liver structure and function Inflammation causes structural fibrotic changes Disruption of blood flow…portal HTN Obstruction of biliary system…jaundice
S/S of Cirrhosis
Most common: Weight loss (masked by ascites fluid), Weakness, Anorexia, Ascites, Diarrhea, Jaundice Abdominal pain (epigastric or RUQ) If portal HTN & liver failure: esophageal varices, bleeding, encephalopathy (confusion and ammonia in blood), splenomegaly.
The Fate of Bilirubin
The liver converts bilirubin into conjugated bilirubin
Bilirubin passes on to the intestine
Bacteria convert it to urobilinogen
Some is lost in feces
Most is reabsorbed into the blood via portal circulation
Returned to the liver to be reused
Filtered out by the kidneys urine
Why would a man with liver failure develop jaundice?
Bilirubin elevation
Liver Failure Leads To…
Hematologic disorders: Anemia, thrombocytopenia (low platelet), coagulation defects, leukopenia (WBC)
Metabolic disorders: Fluid retention, hypokalemia, disordered sexual functions
Skin disorders: Jaundice, red palms, spider nevi (spider veins)
Hepatorenal syndrome: Azotemia, increased plasma creatinine, oliguria
Hepatic encephalopathy: Asterixis, confusion, coma, convulsions
Ammonia not converted to urea
Disorders of the Gallbladder
Cholelithiasis (gallstones) Cholesterol, calcium salts, or mixed Acute and chronic cholecystitis Inflammation caused by chemical irritation due to concentrated bile. Can result in ischemia from mucosal swelling Choledocholithiasis Stones in the common bile duct Cholangitis Inflammation of the common bile duct
Cholecystitis
Gall bladder disease
Acute – Complete or partial obstruction of the cystic or common bile ducts.
Inflammation caused by chemical irritation from the concentrated bile, mucosal swelling and ischemia.
Bacterial infection
Mucosal necrosis gangrene perforation
Risk Factors
The Five F’s: Females, Fat, Fair-skinned, Family history, 40’s
SIGNS AND SYMPTOMS of Cholecystitis
RUQ pain that radiates to the tip of the right scapula
Murphy’s sign: palpating (pain), can’t take a breath
Excessive belching
Flatus
Nausea and vomiting
Low-grade fever
Elevated WBC count
Worsening symptoms after ingesting fried foods.
Exocrine Pancreas
Acini produce: Inactive digestive enzymes Trypsin inactivator These are sent to the duodenum In the duodenum, the digestive enzymes are activated
Biliary Reflux
- Gallbladder contracts
- Bile is sent down common bile duct
- Blockage forms in ampulla of Vater: bile cannot enter duodenum
- Bile goes up pancreatic duct
- Bile in pancreas disrupts tissues; digestive enzymes activated
ACUTE PANCREATITIS
Rapidly developing, potentially fatal, inflammatory disease of the pancreas
Escape of pancreatic enzymes cause autodigestion of the pancreas and fat necrosis
Causes:
Gall stones/Alcohol/GI surgery
Autodigestion of the Pancreas
Activated enzymes begin to digest the pancreas cells
Severe pain results
Inflammation produces large volumes of serous exudate hypovolemia
Elevated enzymes (amylase, lipase) appear in the blood
Areas of dead cells undergo fat necrosis
Calcium from the blood deposits in them
Hypocalcemia
Acute Pancreatitis S/S
Severe abrupt abdominal pain that may radiate to the back.
Pain worse in supine position
N/V
Hyperglycemia
Hypotension & tachycardia
Fever
Elevated pancreatic enzymes – Amylase, Lipase,
Tx – aggressive hydration, antibiotics, NPO, NGT, pain management, surgery. Grey Turner’s Sign: blood in pancreas, by back. Cullen’s sign: bruising near ubilical area
Chronic Pancreatitis and Pancreatic Cancer
Have signs and symptoms similar to acute pancreatitis
MOST common cause: ETOH (alcohol)
Permanent destruction of exocrine function and later stages also endocrine fxn destruction
Often have:
Digestive problems because of inability to deliver enzymes to the duodenum
Glucose control problems because of damage to islets of Langerhans
Signs of biliary obstruction because of underlying bile tract disorders or duct compression by tumors
