Unit 5 Digestive System Flashcards

1
Q

What are the various types of liver cancer and their risk factors?

A

1) Hepatocellular carcinoma
* Arises from the liver cells
2) Cholangiocarcinoma
* A primary cancer of bile duct cells

Risk factors:

  • Hep B and C
  • Alcoholic cirrhosis
  • Aflatoxin
  • Drinking water contaminated with arsenic
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2
Q

What is cirrohosis and what are its implications for the body?

A
  • Fibrosis replacement of hepatic tissue
  • Loss of liver function

Manifestations

  • Hepatomegaly
  • Jaundice
  • Abdominal pain
  • Portal hypertension
    • Ascites
    • Esophageal varices
    • Splenomegaly

http://postimg.org/image/y5he6d4ej/

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3
Q

What is portal hypertension and how does it contribute to liver failure?

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4
Q

What is hepatisis?

A

A medical condition defined by the inflammation of the liver and characterized by the presence of inflammatory cells in the tissue of the organ.

The condition can be self-limiting (healing on its own) or can progress to fibrosis (scarring) and cirrhosis.
Hepatitis may occur with limited or no symptoms, but often leads to jaundice, anorexia (poor appetite) and malaise.

Hepatitis is acute when it lasts less than six months and chronic when it persists longer.

A group of viruses known as the hepatitis viruses cause most cases of hepatitis worldwide, but hepatitis can also be caused by toxic substances (notably alcohol, certain medications, some industrial organic solvents and plants), other infections and autoimmune diseases.

Causes:

Viral Hepatitis (A, B, C)
Autoimmune hepatitis
Alcohol-induced liver diseases

  • Metabolic end products – liver cells injury

Outcomes: Cirrhosis, portal hypertension and liver failure

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5
Q

What are the categories of jaundice? How do they differ from each other?

A

Prehepatic

  • Major cause is excessive hemolysis of red blood cells
  • Unconjugated bilirubin

Intrahepatic

  • Caused by disorders that directly affect the ability of the liver to remove bilirubin from the blood or conjugate it so it can be eliminated in the bile
  • Conjugated bilirubin

Posthepatic

  • Occurs when bile flow is obstructed between the liver and the intestine
  • Conjugated bilirubin
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6
Q

Describe how the liver normally breakdown down bilirubin? Explain the pathogenesis of jaundice.

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7
Q

What is intestinal malabsorption and what are its causes/manifestations?

A

Failure to transport dietary constituents from the lumen of the intestine to the extracellular fluid

Causes:

  • Celiac disease
  • Inflammatory reaction
  • Neoplasm
  • Colorectal cancer

Symptoms:

  • Diarrhea
  • Steatorrhea
  • Flatulence
  • Bloating
  • Abdominal pain
  • Cramps
  • Weight loss and abdominal distention
  • Weakness, muscle wasting
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8
Q

What is colorectal cancer. Describe its etiology, CMs and prognosis.

A
  • 90% are older than 50 years of age
  • family history of cancer, polyposis of the colon, environment, diet, ulcerative colitis
  • early symptom – occult blood in stools, change in bowel habits, sense of urgency or incomplete emptying

Clinical Manifestations (http://postimg.org/image/yeht3vrb5/)

http://postimg.org/image/nwtgqsbab/

Tumors of the right side: Polypoid mass

Tumors of the left side: Ulcerating – napkin ring lesion

Sigmoid colon and rectum: Malignant ulcers

Early symptom is bleeding, followed by change in bowel habits

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9
Q

What are preventation measures for colorectal cancer?

A
  • Diet
  • All men and women after 40 years of age – DRE annually
  • After 50 years of age – stool for occult blood and proctosigmoidoscopy every 3 to 5 years
    • recommended by the American Cancer Society
  • Polypectomy
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10
Q

What is IBS and what are the general etiology of an IBD?

A

IBS

  • Persistent or recurrent symptoms of abdominal pain
  • Altered bowel function
  • Varying complaints of flatulence, bloating
  • Anxiety or depression

IBD

chronic inflammation of the mucosa of the small and large colon

Etiology/risk factors
? genetic predisposition
? autoimmune – abnormal T cell reactions

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11
Q

Compare Chrohn’s Disease with Ulcerative Colitis.

A

Table comparing CM and Pathological Features

http://postimg.org/image/kclk6blyb/

Picture of CD and UC

http://postimg.org/image/6msbkrur5/

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12
Q

Compare the pathological features of UC and CD for fun again!

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13
Q

What are the Extra-intestinal/systemic manifestations of UC and CD?

A

Eyes
Skin and mucosa
Bones and joints
Liver and gall bladder
Alterations in coagulation

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14
Q

Which are diseases of the sm and lg instestine?

A

Irritable bowel syndrome
Inflammatory bowel disease
Cancer of the colon and rectum
Mal-absorption syndrome

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15
Q

What is stomach cancer and what are its risk factors and clinical manifestations?

A

adenocarcinoma

  • uncommon under age 40
  • mean age at diagnosis is 63 years

3 types

  • polypoid (fungating mass)
  • ulcerating mass
  • diffusely spreading (linitis plastica) – rigid atonic stomach

Risk Factors

  • Genetic predisposition
  • Carcinogenic factors in the diet
  • Autoimmune gastritis
  • Gastric adenomas or polyps

Manifestations:

  • asymptomatic until the disease is advanced
  • non specific symptoms
  • dyspepsia
  • anorexia
  • vague pain
  • weight loss
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16
Q

Where in the stomach do most cancers occur?

17
Q

What is peptic ulcer disease?

A
  • a group of disorders
  • is a break in the protective mucosal lining of the gastrointestinal tract caused by the action of acid and pepsin
  • most common forms are Gastric Ulcer and Duodenal Ulcers
    • a chronic health problem
    • remissions and exacerbations
    • many different types, duration and locations
    • duodenal ulcers – more common
  • Disruption of the gastric mucosa is caused by imbalance between mucosa barrier and irritation (aggressive) forces
18
Q

Describe the mucosal barrier of the stomach.

A

1) thick mucus layer
2) cells are tight: back diffused H+ are actively extruded by ionic barrier mechanism
3) regenerative capacity of epithelial cells
4) control action by the small intestine
5) prostaglandins - secreted by gastric mucosal cells (inhibts acid production by the stomach)
6) mucosal blood flow

19
Q

What are two major causes of gastric irritation?

A

Nonsteroidal anti-inflammatory drugs (NSAIDs)/Aspirin/Alcohol

  • Irritate the gastric mucosa and inhibit prostaglandin synthesis

Infection with H. pylori

  • Thrives in acid environment of the stomach
  • Disrupts the mucosal barrier that protects the stomach from harmful effects of its digestive enzymes
20
Q

Describe the pathogenesis of a peptic ulcer in terms of agressive forces and defensive forces of the stomach.

A

Imbalance of defensive and aggressing forces

Defensive Forces (aggressive forces)

  • Secretion of a surface mucus layer by epithelial cells (Acid secretion)
  • Secretion of bicarbonate into the mucus layer (Peptic activity derived from pepsinogen)
  • Protection against diffusion of H+ into the mucosa (H pylori infection)
  • Regenerative capacity of mucosal epithelial cells (NSAIDS/aspirin/alcohol)
  • Mucosal elaboration of prostaglandins having “cytoprotective” activity (Impaired inhibition of stimulatory mechanism such as gastrin release)
21
Q

What are the clinical manifestations of peptic ulcers?

A

BOTH DU and GU

  • pain and discomfort
  • between meals and midnight
  • periodicity with intervals of weeks and months

DU

  • Incidence-more common
  • Age – younger
  • Pathogenesis – increased HCL
  • Clinical manifestations – longer remission than relapse
  • Pain – antacid
  • Pain – food
  • No risk of gastric cancer

GU

  • Less common
  • Older – 55-65
  • Normal acid – associated with chronic gastritis
  • More episodes of relapse
  • Pain – antacid
  • Food-pain
  • High risk of gastric cancer
22
Q

What are the complications of a peptic ulcer?

A
  • Bleeding
  • Perforation
  • Penetration
  • Obstruction
  • Malignant change (gastric ulcer)

http://postimg.org/image/gcty5xchd/

23
Q

What are the major types of chronic gastritis?

A

Helicobacter pylori gastritis

  • Most common cause of chronic gastritis
  • Faeco-oral transmission (contaminated foods), sharing utensils

Autoimmune and multifocal gastritis

  • Less than 10% of chronic gastritis
  • Gastric atrophy – intrinsic factor deficiency

Chemical gastropathy

  • Alkaline reflux from the duodenum
  • Bile reflux
24
Q

What are two classes of gastritis?

A

Acute gastritis
Transient inflammation of the gastric mucosa
Most commonly associated with local irritants such as bacterial endotoxins, alcohol, and aspirin

Chronic gastritis
Characterized by the absence of grossly visible erosions and the presence of chronic inflammatory changes
Leads eventually to atrophy of the glandular epithelium of the stomach