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Unit 10 Gastrointestinal Pathophysiology > Disorders of Motility > Flashcards

Disorders of Motility Flashcards

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1
Q

GERD: Gastroesophageal reflux disease

A

Acid and pepsin refluxes from the stomach into the esophagus, causing esophagitis.
Conditions that increase abdominal pressure can contribute to GERD.
- Vomiting, coughing, lifting, bending, or obesity

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2
Q

GERD: Clinical manifestations & evaluation

A

CM: Heartburn from acid regurgitation, chronic cough, laryngitis
Upper abdominal pain within 1 hour of eating

Evaluation: Biopsy- Dysplatic changes (Barret esophagus)

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3
Q

GERD: treatment

A
  • Proton pump inhibitors: Most effective
  • Histamine type 2 (H2) receptor antagonists, prokinetic agents, and antacids; pain medication
  • Elevate head of the bed 6 inches; reduce weight; stop smoking
  • Surgery: Laparoscopic fundoplication
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4
Q

Hiatal Hernia: Clinical Manifestations

A

-A hiatal hernia is a condition where the top of your stomach bulges through an opening in your diaphragm

Asymptomatic
Heartburn, regurgitation, dysphagia, and epigastric pain

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5
Q

Hiatal Hernia: Treatment

A 
Small, frequent meals; avoidance of recumbent position after eating
Avoidance of abdominal supports and tight clothing; weight control for obese individuals
Antacids to alleviate reflux esophagitis
Contraindicated agents (delay gastric emptying): Drugs that relax the lower esophageal sphincter (anticholinergic, nitrates, calcium channel blockers)
Paraesophageal: Laparoscopic surgery (fundoplication)
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6
Q

Pyloric (gastric outlet) obstruction

A

Blocking or narrowing of the opening between the stomach and duodenum
Acquired or congenital

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7
Q

Pyloric (gastric outlet) obstruction: Clinical Manifestations

A

Clinical manifestations

Epigastric pain and fullness, nausea, succussion splash, vomiting; if prolonged, malnutrition and dehydration

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8
Q

Pyloric obstruction: Treatment

A

Gastric drainage; intravenous (IV) fluid and electrolytes
Proton pump inhibitors or histamine type 2 (H2) receptor antagonists
Surgery or stenting

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9
Q

Intestinal Obstruction and ileus

A

Any condition that prevents the flow of chyme through the intestinal lumen or failure of normal intestinal motility in the absence of an obstructing lesion

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10
Q

Intestinal obstruction and ileus: clinical manifestations

A
  • Small intestine obstruction: Colicky pains caused by intestinal distention, followed by nausea and vomiting
  • Most common: fibrous adhesions

*Large intestine obstruction: Hypogastric pain and abdominal distention

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11
Q

Intestinal obstruction and ileus: treatment

A

Replacement of fluid and electrolytes
Gastric or intestinal suction
Adhesions: Laparoscopic procedures
Strangulation and complete obstruction: Immediate surgical intervention
Colonic pseudo-obstruction: Neostigmine, a parasympathomimetic and colonoscopic decompression

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12
Q

Simple obstruction vs. Functional obstruction

A

*Simple obstruction
Presence of a lesion

*Functional obstruction: Paralytic ileus
Failure of motility, especially after surgery

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13
Q

Large Bowel Obstruction

A

Most common: Colorectal cancer, volvulus (twisting), and strictures related to diverticulitis

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14
Q

Acute colonic pseudo-obstruction (Ogilvie syndrome)

A

Massive dilation of the large bowel; patients who are critically ill and older adults who are immobilized

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15
Q

Gastritis

A

*inflammatory disorder of the gastric mucosa

Acute gastritis: Massive dilation of the large bowel; patients who are critically ill and older adults who are immobilized

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16
Q

Gastriris: clinical manifestation

A

Vague abdominal discomfort, epigastric tenderness, and bleeding

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17
Q

Acute gastritis treatment

A

Healing usually occurs spontaneously within a few days.
Discontinue injurious drugs.
Administer antacids.
Decrease acid secretion with a histamine type 2 (H2) receptor antagonist and proton pump inhibitor.

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18
Q

Chronic Fundal Gastritis

A

Immune
Type A
Associated with autoantibodies to parietal cells and intrinsic factor, resulting in gastric atrophy and pernicious anemia

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19
Q

Chronic Antral Gastritis

A

Nonimmune
Type B
Associated with H. pylori and NSAIDs

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20
Q

Chronic gastritis: clinical manifestations

A

Manifestations do not often correlate with the severity of the disease
Anorexia, fullness, nausea, vomiting, epigastric pain, and gastric bleeding

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21
Q

Chronic gastritis: treatment

A

Smaller meals; soft, bland diet; avoidance of alcohol and NSAIDs
Administration of combination antibiotics
Vitamin B12: For pernicious anemia

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22
Q

Alkaline Reflux Gastritis

A

Stomach inflammation caused by reflux of bile and alkaline pancreatic secretions

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23
Q

Alkaline Reflux Gastritis: Clinical Manifestation

A

Nausea, bilious vomiting (vomiting in which the vomitus contains bile)
Sustained epigastric pain that worsens after eating and is not relieved by antacids

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24
Q

Alkaline Reflux Treatment

A

Avoidance of aspirin and alcohol
Low-fat diet
Possible surgical correction

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25
Peptic Ulcer Disease
Break or ulceration in the protective mucosal lining of the lower esophagus, stomach, or duodenum 1) Acute versus chronic ulcers 2) Superficial (erosions) versus deep
26
Peptic Ulcer: Risk Factors
Genetic predisposition H. pylori infection Habitual use of NSAIDs Excessive use of alcohol, smoking, acute pancreatitis, chronic obstructive pulmonary disease, obesity, cirrhosis, and over 65 years of age
27
Duodenal Ulcers- developmental factors
1) most common of the peptic ulcers 2) Developmental factors Increased numbers of parietal (acid-secreting) cells High gastrin levels Rapid gastric emptying Acid production caused by cigarette smoking
28
Duodenal Ulcers- clinical manifestations
Chronic intermittent pain in the epigastric area. Pain begins 30 minutes to 2 hours after eating when the stomach is empty. Pain is relieved by food
29
Duodenal ulcers- treatment
Antacids: To neutralize gastric contents, elevate pH, inactivate pepsin, and relieve pain Proton pump inhibitors, anticholinergic drugs: To suppress acid secretion Bismuth and combinations of antibiotics, supplemented with vitamin C: To eradicate H. pylori Sucralfate and colloidal bismuth: To coat ulcer Surgical resection **Risk of duodenal ulcer may be reduced with a diet high in Vitamin A and fibre
30
Gastric Ulcer
*tends to develop in the astral region of stomach, adjacent to the acid-secreting mucosa of the body.
31
Gastric Ulcer- Pathophysiology
Frequent cause: H. pylori Primary defect: Increased mucosal permeability to hydrogen ions Gastric secretion: Normal or less than normal
32
Gastric Ulcer- clinical manifestation & treatment
``` Clinical manifestations Pain occurs immediately after eating Tends to be chronic Anorexia, vomiting, and weight loss Treatment Same as the treatment for duodenal ulcers (antacids, proton pump inhibitors..) ```
33
Ulcerative Colitis
* chronic inflammatory disease that causes ulceration of the colonic mucosa. - sigmoid colon and rectum - common in those 20-40 years of age, Jewish descent
34
Ulcerative colitis- pathophysiology & suggested causes
Suggested causes Infectious, immunologic (anticolon antibodies), dietary, genetics Pathophysiology Lesions are continuous with no skipped lesions, are limited to the mucosa, and are not transmural.
35
Ulcerative Colitis- clinical manifestation
Diarrhea (10 to 20 bowel movements per day), bloody stools, cramps Remission and exacerbations
36
ulcerative colitis treatment
Treatment First-line therapy: 5-aminosalicylic acid (mesalazine) Steroids and salicylate Immunosuppressive agents Broad-spectrum antibiotics Surgery: Resection of the colon or a colostomy Increased risk for colon cancer is demonstrated.
37
Chrohn Disease
-Granulomatous colitis, ileocolitis, or regional enteritis -Idiopathic inflammatory disorder; affects any part of the digestive tract, from mouth to anus -Difficult to differentiate from ulcerative colitis Similar risk factors and theories of causation -Causes “skip” lesions -Ulcerations: Longitudinal and transverse inflammatory fissures extend into lymphoid tissue. : Produces a “cobblestone” appearan
38
Crohn Disease strong association to
Nucleotide-binding oligomerization domains (CARD15/NOD2) gene mutations
39
Crohn Disease clinical manifestations
Abdominal pain and diarrhea are the most common signs; more than five stools per day. Anemia may develop as a result of malabsorption of vitamin B12 and folic acid.
40
Crohn Disease treatment
Treatment : Similar to ulcerative colitis Immunomodulatory agents Tumor necrosis factor–alpha (TNF-α) blocking agents: To treat fistulas and maintain remission Surgery: Complication: Short bowel syndrome with malabsorption, diarrhea, and nutritional deficiencies
41
Celiac Disease
a digestive and autoimmune disorder that can damage your small intestine. People with celiac disease might experience symptoms like diarrhea, bloating, gas, anemia and growth issues. Celiac disease can be triggered by a protein called gluten. Gluten is found in grains, like wheat, barley and rye.
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Diverticula (disease of the colon)
Herniation of mucosa through the muscle layers of the colon wall
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Diverticulosis
Asymptomatic diverticular disease
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DivertiCULITIS
*inflammatory stage of diverticulosis Possible causes Associated with those older than 60 years of age, decreased dietary fiber, increased intracolonic pressure, abnormal neuromuscular function, and alterations in intestinal motility.
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Diverticulosis, Diverticula/ Diverticulitis Clinical manifestations.
Low cramping abdominal pain, diarrhea, constipation, distension, flatulence Diverticulitis: Fever, leukocytosis
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Diverticulosis, Diverticula/ Diverticulitis : Treatment
Treatment - Increase of dietary fiber intake to increase stool weight, lower colonic pressures, improve transit times, and relieve symptoms - Uncomplicated diverticular disease: Bowel rest and antibiotic administration - Surgical resection
47
Appendicitis
Inflammation of the vermiform appendix Possible causes Obstruction, ischemia, increased intraluminal pressure, infection, ulceration
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Appendicitis: clinical manifestation & treatment
``` Clinical manifestations Epigastric and right lower quadrant pain, rebound tenderness Nausea, vomiting, fever, leukocytosis Complications: Perforation, peritonitis Treatment Antibiotics and appendectomy ```
49
Portal Hypertension
Abnormally high blood pressure in the portal venous system primarily caused by resistance to portal blood flow Increase to at least 10 mm Hg (normal is 3 mm Hg)
50
Portal Hypertension: Causes
Causes - Prehepatic - Intrahepatic - Posthepatic - Can cause fatal consequences
51
Portal Hypertension: Consequences in Varices & Splenomegaly
``` *Varices: Distended, tortuous, collateral veins Lower esophagus, stomach, rectum If rupture: Life threatening *Splenomegaly: Enlargement of the spleen Thrombocytopenia: Increased risk for bleeding ```
52
Portal Hypertension: consequences in Hepatopulmonary syndrome
Respiratory complications with pulmonary hypertension Intrapulmonary vasodilation Intrapulmonary shunting and hypoxia Portopulmonary hypertension (pulmonary vasoconstriction and vascular remodeling)
53
Portal Hypertension: clinical manifestations
vomiting blood; ascites (accumulation of fluid in the peritoneal cavity)
54
Portal Hypertension treatment
Beta-blockers: To prevent variceal bleeding Bleeding varices Fluid resuscitation Administration of prophylactic antibiotics, vasoactive drugs (nonselective β-receptor antagonists and terlipressin) Endoscopic variceal band ligation, compression of the varices with an inflatable tube or balloon, and injection of a sclerosing agent
55
Ascites- define, clinical manifestations, evaluation
**Accumulation of fluid in the peritoneal cavity **Most common cause: Cirrhosis **Clinical manifestations: Abdominal distention, increased abdominal girth, and weight gain **Evaluation Serum-ascites albumin gradient (SAAG): Most specific diagnostic indicator
56
Ascites Treatment
- Dietary salt restriction - Potassium-sparing diuretics - Strong diuretics, such as furosemide or ethacrynic acid - Vasopressin receptor 2 antagonists: For dilutional hyponatremia - Possible administration of albumin - Monitor serum electrolytes, especially sodium and potassium
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Ascites Treatment cont'd
- Paracentesis: Removal of 1 or 2 L of ascitic fluid and relief of respiratory distress * Removing too much fluid too fast relieves pressure on the blood vessels, causing arteriolar vasodilation and carries the risk of hypotension, shock, or death. * Ascitic fluid reaccumulates in individuals with irreversible disease. * Is likely to cause peritonitis - Transjugular intrahepatic portosystemic shunt or peritoneovenous shunt: For refractory ascites - Liver transplant: Best treatment option
58
Jaundice (called icterus)
Yellow or greenish pigmentation of the skin caused by hyperbilirubinemia (total plasma bilirubin concentrations >2.5 to 3 mg/dl)
59
Jaundice clinical manifestation
Dark urine Clay-colored stools Yellow discoloration possibly occurring first in the sclera of the eye and then progressing to the skin Skin xanthomas (cholesterol deposits) and pruritus
60
Jaundice causes?
- Extrahepatic obstruction to bile flow (gallstones) - Intrahepatic obstruction (hepatocellular disease such as cirrhosis or hepatitis) - Prehepatic obstruction: Excessive production of bilirubin (excessive hemolysis of red blood cells)
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Jaundice treatment
Correct the cause: Jaundice is only a sign of an underlying disorder.
62
Viral Hepatitis
* Systemic viral disease that primarily affects the liver - Hepatitis A: Formally known as infectious hepatitis - Hepatitis B: Formally known as serum hepatitis - Hepatitis C, D, E: Can cause hepatic cell necrosis, Kupffer cell hyperplasia, and infiltration of liver tissue by mononuclear phagocytes * Obstruction of bile flow and impairment of hepatocyte function
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Chronic active hepatitis
Occurs with hepatitis B and hepatitis C with a predisposition to cirrhosis and hepatocellular carcinoma.
64
Fulminant Hepatitis
* Is a complication of hepatitis B (with or without hepatitis D infection) or hepatitis C. * Causes widespread hepatic necrosis. * Is often fatal.
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Viral Hepatitis: Incubation Phase
Varies, depending on the virus.
66
Viral Hepatitis: Prodromal phase w clinical manifestation
Begins approximately 2 weeks after exposure; ends with the appearance of jaundice. Clinical manifestations: Fever, malaise, anorexia, and liver enlargement and tenderness. Is highly transmissible.
67
Viral Hepatitis: Icteric Phase w clinical manifestation
Is the actual phase of illness. | Clinical manifestations: Jaundice and hyperbilirubinemia; fatigue and abdominal pain
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Viral Hepatitis: Recovery phase
Begins with the resolution of jaundice. Symptoms resolve after several weeks. Chronic or chronic active hepatitis may develop.
69
Viral Hepatitis Treatment
- Restrict physical activity as needed. - Maintain a low-fat, high-carbohydrate diet if bile flow is obstructed. - Avoid direct contact with blood or body fluids of individuals with hepatitis B or hepatitis C
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Hepatitis A
Can be found in the feces, bile, and sera of infected individuals. Is usually transmitted by the fecal-oral route Risk Factors: Crowded, unsanitary conditions Food and water contamination
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Hepatitis A Prevention
Handwashing Administration of immunoglobulin before exposure or early in the incubation period Administration of vaccines
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Hepatitis B
Is transmitted through contact with infected blood, body fluids, and contaminated needles. Maternal transmission occurs if the mother is infected during the third trimester.
73
Hepatitis B cont'd
* Hepatitis B vaccine prevents the transmission & development of hepatitis B * Hepatitis B immunoglobulin provides postexposure prophylaxis against hepatitis B
74
Hepatitis C
* responsible for most cases of posttransfusion hepatitis. * Iimplicated in infections related to IV drug use and human immunodeficiency viral (HIV) infection. * Co-infection with hepatitis B is common. * Approximately 80% of those with hepatitis C develop chronic liver disease. * No vaccine is available. * Administer antiviral medications
75
Hepatitis D
Dependent on hepatitis B for replication | Treatment: Pegylated interferon alph
76
Hepatitis E
Fecal-oral transmission Contaminated water or uncooked meat Most common in Asian and African countries Common in developing countries Vaccine in China but not in other countries
77
Cirrhosis
* irreversible inflammatory fibrotic disease that disrupts liver function and even liver structure. * most common cause alcohol abuse & viral hepatitis
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Cirrhosis cont'd
- Hepatic function from nodular and fibrotic tissue synthesis (fibrosis) decreases. - Biliary channels become obstructed and cause portal hypertension. - Because of the hypertension, blood is shunted away from the liver, and hypoxic necrosis develops.
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Alcoholic Liver disease
Oxidation of alcohol, causing damage to hepatocytes **Impairs the hepatocytes’ ability to oxidize fatty acids, synthesize enzymes and proteins, degrade hormones, and clear portal blood of ammonia and toxins
80
Steatosis (alcoholic fatty liver)
Is the mildest form of alcoholic liver disease | Is reversible if drinking is stopped.
81
Alcoholic hepatitis (steatohepatitis)
Is characterized by inflammation. | Degeneration and necrosis of the hepatocytes occur.
82
Alcoholic cirrhosis (fibrosis)
Toxic effects of alcohol metabolism on the liver, immunologic alterations, oxidative stress from lipid peroxidation, and malnutrition occur.
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Alcoholic Liver Disease clinical manifestations
Nausea, anorexia, fever, abdominal pain, and jaundice
84
Cirrhosis Treatment
Cessation of alcohol Rest, a nutritious diet Corticosteroids, antioxidants, drugs that slow fibrosis Management of complications: Ascites, gastrointestinal bleeding, infection, and encephalopathy
85
Nonalcoholic fatty liver disease
Is the infiltration of hepatocytes with fat that occurs in the absence of alcohol intake. Is associated with obesity.
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Biliary (bile canaliculi)
*Cirrhosis begins in bile canaliculi and ducts. 1) Primary biliary cirrhosis (autoimmune): T lymphocyte–mediated and antibody-mediated destruction of the small intrahepatic bile ducts 2) Secondary biliary cirrhosis Obstruction of common bile duct
87
Primary sclerosis cholangitis
Chronic inflammatory fibrotic disease of the medium- and large-sized bile ducts outside of the liver

Unit 10 Gastrointestinal Pathophysiology (3 decks)

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