Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Unit 10 Gastrointestinal Pathophysiology > Disorders of Motility > Flashcards

Disorders of Motility Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pyloric (gastric outlet) obstruction

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Pyloric (gastric outlet) obstruction: Clinical Manifestations

A

Clinical manifestations

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Simple obstruction vs. Functional obstruction

A

*Simple obstruction
Presence of a lesion

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Large Bowel Obstruction

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Gastriris: clinical manifestation

A

Vague abdominal discomfort, epigastric tenderness, and bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Chronic Antral Gastritis

A

Nonimmune
Type B
Associated with H. pylori and NSAIDs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Alkaline Reflux Gastritis

A

Stomach inflammation caused by reflux of bile and alkaline pancreatic secretions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Alkaline Reflux Treatment

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Peptic Ulcer Disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Peptic Ulcer: Risk Factors

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Duodenal Ulcers- developmental factors

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Duodenal Ulcers- clinical manifestations

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Duodenal ulcers- treatment

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Gastric Ulcer

A

*tends to develop in the astral region of stomach, adjacent to the acid-secreting mucosa of the body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Gastric Ulcer- Pathophysiology

A

Frequent cause: H. pylori
Primary defect: Increased mucosal permeability to hydrogen ions
Gastric secretion: Normal or less than normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Gastric Ulcer- clinical manifestation & treatment

A 
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..)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Ulcerative Colitis

A
  • chronic inflammatory disease that causes ulceration of the colonic mucosa.
  • sigmoid colon and rectum
  • common in those 20-40 years of age, Jewish descent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Ulcerative colitis- pathophysiology & suggested causes

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Ulcerative Colitis- clinical manifestation

A

Diarrhea (10 to 20 bowel movements per day), bloody stools, cramps
Remission and exacerbations

36
Q

ulcerative colitis treatment

A

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
Q

Chrohn Disease

A

-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
Q

Crohn Disease strong association to

A

Nucleotide-binding oligomerization domains (CARD15/NOD2) gene mutations

39
Q

Crohn Disease clinical manifestations

A

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
Q

Crohn Disease treatment

A

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
Q

Celiac Disease

A

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.

42
Q

Diverticula (disease of the colon)

A

Herniation of mucosa through the muscle layers of the colon wall

43
Q

Diverticulosis

A

Asymptomatic diverticular disease

44
Q

DivertiCULITIS

A

*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.

45
Q

Diverticulosis, Diverticula/ Diverticulitis Clinical manifestations.

A

Low cramping abdominal pain, diarrhea, constipation, distension, flatulence
Diverticulitis: Fever, leukocytosis

46
Q

Diverticulosis, Diverticula/ Diverticulitis : Treatment

A

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
Q

Appendicitis

A

Inflammation of the vermiform appendix
Possible causes
Obstruction, ischemia, increased intraluminal pressure, infection, ulceration

48
Q

Appendicitis: clinical manifestation & treatment

A 
Clinical manifestations
Epigastric and right lower quadrant pain, rebound tenderness
Nausea, vomiting, fever, leukocytosis
Complications: Perforation, peritonitis
Treatment
Antibiotics and appendectomy
49
Q

Portal Hypertension

A

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
Q

Portal Hypertension: Causes

A

Causes

  • Prehepatic
  • Intrahepatic
  • Posthepatic
  • Can cause fatal consequences
51
Q

Portal Hypertension: Consequences in Varices & Splenomegaly

A 
*Varices:
Distended, tortuous, collateral veins
Lower esophagus, stomach, rectum
If rupture: Life threatening
*Splenomegaly:
Enlargement of the spleen
Thrombocytopenia: Increased risk for bleeding
52
Q

Portal Hypertension: consequences in Hepatopulmonary syndrome

A

Respiratory complications with pulmonary hypertension
Intrapulmonary vasodilation
Intrapulmonary shunting and hypoxia
Portopulmonary hypertension (pulmonary vasoconstriction and vascular remodeling)

53
Q

Portal Hypertension: clinical manifestations

A

vomiting blood; ascites (accumulation of fluid in the peritoneal cavity)

54
Q

Portal Hypertension treatment

A

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
Q

Ascites- define, clinical manifestations, evaluation

A

**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
Q

Ascites Treatment

A
  • 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
57
Q

Ascites Treatment cont’d

A
  • 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
Q

Jaundice (called icterus)

A

Yellow or greenish pigmentation of the skin caused by hyperbilirubinemia (total plasma bilirubin concentrations >2.5 to 3 mg/dl)

59
Q

Jaundice clinical manifestation

A

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
Q

Jaundice causes?

A
  • 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)
61
Q

Jaundice treatment

A

Correct the cause: Jaundice is only a sign of an underlying disorder.

62
Q

Viral Hepatitis

A
  • 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
63
Q

Chronic active hepatitis

A

Occurs with hepatitis B and hepatitis C with a predisposition to cirrhosis and hepatocellular carcinoma.

64
Q

Fulminant Hepatitis

A
  • Is a complication of hepatitis B (with or without hepatitis D infection) or hepatitis C.
  • Causes widespread hepatic necrosis.
  • Is often fatal.
65
Q

Viral Hepatitis: Incubation Phase

A

Varies, depending on the virus.

66
Q

Viral Hepatitis: Prodromal phase w clinical manifestation

A

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
Q

Viral Hepatitis: Icteric Phase w clinical manifestation

A

Is the actual phase of illness.

Clinical manifestations: Jaundice and hyperbilirubinemia; fatigue and abdominal pain

68
Q

Viral Hepatitis: Recovery phase

A

Begins with the resolution of jaundice.
Symptoms resolve after several weeks.
Chronic or chronic active hepatitis may develop.

69
Q

Viral Hepatitis Treatment

A
  • 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
70
Q

Hepatitis A

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

71
Q

Hepatitis A Prevention

A

Handwashing
Administration of immunoglobulin before exposure or early in the incubation period
Administration of vaccines

72
Q

Hepatitis B

A

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
Q

Hepatitis B cont’d

A
  • Hepatitis B vaccine prevents the transmission & development of hepatitis B
  • Hepatitis B immunoglobulin provides postexposure prophylaxis against hepatitis B
74
Q

Hepatitis C

A
  • 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
Q

Hepatitis D

A

Dependent on hepatitis B for replication

Treatment: Pegylated interferon alph

76
Q

Hepatitis E

A

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
Q

Cirrhosis

A
  • irreversible inflammatory fibrotic disease that disrupts liver function and even liver structure.
  • most common cause alcohol abuse & viral hepatitis
78
Q

Cirrhosis cont’d

A
  • 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.
79
Q

Alcoholic Liver disease

A

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
Q

Steatosis (alcoholic fatty liver)

A

Is the mildest form of alcoholic liver disease

Is reversible if drinking is stopped.

81
Q

Alcoholic hepatitis (steatohepatitis)

A

Is characterized by inflammation.

Degeneration and necrosis of the hepatocytes occur.

82
Q

Alcoholic cirrhosis (fibrosis)

A

Toxic effects of alcohol metabolism on the liver, immunologic alterations, oxidative stress from lipid peroxidation, and malnutrition occur.

83
Q

Alcoholic Liver Disease clinical manifestations

A

Nausea, anorexia, fever, abdominal pain, and jaundice

84
Q

Cirrhosis Treatment

A

Cessation of alcohol
Rest, a nutritious diet
Corticosteroids, antioxidants, drugs that slow fibrosis
Management of complications: Ascites, gastrointestinal bleeding, infection, and encephalopathy

85
Q

Nonalcoholic fatty liver disease

A

Is the infiltration of hepatocytes with fat that occurs in the absence of alcohol intake.
Is associated with obesity.

86
Q

Biliary (bile canaliculi)

A

*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
Q

Primary sclerosis cholangitis

A

Chronic inflammatory fibrotic disease of the medium- and large-sized bile ducts outside of the liver

Unit 10 Gastrointestinal Pathophysiology (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions