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Biology 2401 > DIG PATHO > Flashcards

DIG PATHO Flashcards

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1
Q
  1. What does GERD stand for?
A

Gastroesophageal reflux disease

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2
Q
  1. Describe the development of GERD, its most frequent clinical manifestation and in what the long-term inflammation involved in GERD can result.
A

Return of stomach contents in esophagus (because of relaxation of the lower esophageal sphincter) can occur spontaneously, the gastric contents are usually neutralized and cleared within minutes

Heartburn

Lead to fibrosis and precancerous lesions

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3
Q
  1. Define dyspepsia and gastroparesis.
A

Painful digestion with possible feelings of bloating, nausea and heartburn

Slowing of movement of food from the stomach

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4
Q
  1. Be familiar with factors that increase the likelihood of GERD.
A

Infancy – positional and reduced sphincter tone

Increased intra-abdominal pressure (obesity, pregnancy)

Smoking

Certain foods relax LES (fat, coffee, alcohol)

Lupus

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5
Q
  1. What is a peptic ulcer?
A

Is a break in the protective mucosal lining of the lower esophagus, stomach or duodenum

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6
Q
  1. Define melena and hematemesis (know that these can be complications of peptic ulcer disease).
A

Hematemesis: vomiting of blood, either bright red or “coffee ground” appearing (slightly digested blood)

Melena: black foul smelling stools from digestion of blood

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7
Q
  1. Describe three other complications of peptic ulcer disease (other than melena and hematemesis).
A

Perforation (ulcer erodes through wall and contents enter peritoneal cavity)

Penetration (same, but erosion is into another organ (liver))

Gastric/duodenal outlet obstruction (from edema or scarring)

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8
Q
  1. Identify and describe the pathophysiology behind the effects of the two high risk factors for the development of peptic ulcers.
A

Helicobacter pylori: passes through the mucus layer that protects the stomach: Stomach acid keeps mucin lining of epithelial cell layer in a spongy gel-like state. This consistency is impermeable to H. pylori however the bacterium releases urease which neutralizes the stomach acid causing the mucin to liquefy, and the bacterium can now penetrate it and reach epithelial cells inducing inflammation

NSAIDS interfere with prostaglandin synthesis: This blocks production of mucus and bicarbonate, and increases acid production, making the stomach vulnerable to injury from acid and enzymes

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9
Q
  1. What are two similarities between duodenal ulcers and gastric ulcers?
A

Caused by H. pylori and NSAIDS

Clinical manifestations include intermittent pain in epigastric region

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10
Q
  1. What are three differences between duodenal ulcers and gastric ulcers? (include the pattern of pain)
A

Gastric ulcers: 25% as common as duodenal ulcers, Tend to develop in order people (55-65), Frequently occurs immediately after eating, Gastric tend to be chronic, Hard to treat

Duodenal ulcers:
Occur with greater frequency than other types, Tend to develop in younger people (commonly in males), Pain begins 2-3 hours after eating, Have periods of remission Can be relieved by ingestion of food

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11
Q
  1. What are the main treatments for peptic ulcers?
A

Eradicate H. pylori with antibiotics

Reduce acidity (antiacids, proton pump inhibitors, histamine 2 receptor)

Minimally invasive surgical resection if ulcers are bleeding or have perforated the GI wall

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12
Q
  1. What are the two diseases that make up inflammatory bowel disease?
A

Ulcerative colitis & Crohn’s disease

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13
Q
  1. Describe and differentiate between these two diseases, including: a. Typical age range affected b. Regions of the bowel affected and the nature of the inflammatory process c. The appearance of the inflamed tissues d. Risk factors e. Clinical manifestations f. Possible complications
A

Ulcerative colitis: 20-40 & Crohn’s: 20-30

Ulcerative: colonic mucosa, most commonly in the rectum and sigmoid colon & Crohn’s: both large and small intestine

Crohns: inflammation of entire width (serous to mucosa) skip lesions & Ulcerative: inflammation of mucosa, continuous

Ulcerative: age, family history & Crohns: family history

Crohns: Most common symptom is diarrhea (not as commonly bloody as with UC) (with tenesmus), accompanied by weight loss and abdominal pain (usually in lower right quadrant & Ulcerative: c inflammatory disease that causes ulceration of the colonic mucosa, most commonly in the rectum and sigmoid colon. Usually beginning in the rectum, the ulceration spreads in a continuous manner. Condition can be sporadic in time

Crohns: fistula, strictures, perianal abscesses & ulcerative: cancer

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14
Q
  1. What is toxic megacolon?
A

An abrupt increase in diameter of colon (within one to a few days) that could rupture

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15
Q
  1. What is celiac disease?
A

Malabsorptive disease where the mucosa fails to absorb digested nutrients

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16
Q
  1. Describe the development of celiac disease.
A

T-cell mediated autoimmune disorder: persons with the disease show an intense immune reaction to gluten (gliadin), the protein components of cereal grains. The inflammation brought on by the immune reaction damages small intestinal villous epithelium, interfering with absorption of macro and micronutrients

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17
Q
  1. Describe the clinical manifestations of celiac disease and the consequences of malabsorption of nutrients in childhood and adulthood.
A

End result is loss of ability of intestine to absorb nutrients, Childhood, this produces a failure to thrive, Abdominal pain, Diarrhea with fatty stools

Malabsorption:

osteoporosis, seizures/tetany, from lack of calcium

Anemia from lack of iron

Short stature, when it develops in childhood, from general malnutrition

Pregnancy: miscarriage, neural tube defects (due to lack of folic acid, and other nutrients)

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18
Q
  1. Define portal hypertension and its cause.
A

Abnormally high blood pressure in the hepatic portal venous system

Caused by disorders that obstruct blood flow through the portal venous system or vena cava, including thrombosis of hepatic veins, severe right-sided heart failure, alcoholic cirrhosis

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19
Q
  1. Define ascites and describe two causes for ascites.
A

Accumulation of fluid in the peritoneal cavity

Caused by portal hypertension, can also be caused by decrease in serum protein production by the liver, which lowers osmotic pressure of capillaries resulting in more retention of fluid in the tissues, which then seeps into peritoneal cavity

20
Q
  1. How can ascites be treated? What could happen if fluid is removed too quickly?
A

Treatment can include paracentesis (drainage of abdominal cavity, using a needle) to remove fluid and relieve breathing, but this must be done with caution (to avoid hypotension and shock), and ascites will re-occur if liver problem isn’t fixed

21
Q
  1. Describe the development of varices associated with the portal system, and name the most common clinical manifestation.
A

There are veins that drain from the esophagus into the hepatic portal vein, and also veins that drain from the esophagus into the inferior vena cava

If pressure in the portal system becomes greater than normal, there will be an increased resistance for the blood to flow from the esophagus into portal system

Collateral veins (portosystemic shunts) will develop between the 2 sets of veins in the esophagus, and blood will back up from the portal system through the esophageal veins and into the inferior vena cava

This results in blood tending to bypass the liver

The collateral veins that develop cannot withstand the pressure of the blood coming through the portal system

They swell and distend, becoming esophageal varices

Manifestation: vomiting of blood from hemorrhaging esophageal varices

22
Q
  1. Where are two other places where collateral shunts can occur due to portal hypertension? Name the varices that result.
A

Between veins on the abdominal wall (varices called caput medusae) & veins in the wall of the rectum (hemorrhoids)

23
Q
  1. Describe the development of hepatic encephalopathy and its clinical manifestations.
A

Decrease in liver function, and collateral vessels that shunt blood past the liver, allow toxins to remain in bloodstream and reach the brain (most hazardous is ammonia, which the liver should be converting to urea)

Neurotransmission is affected

Display personality changes, loss of memory, confusion, flapping of hands, worsening to coma

24
Q
  1. Define asterixis.
A

Uncontrollable flapping of the hands

25
Q
  1. Define icterus and describe two causes of icterus that are related to diseases of gastrointestinal organs.
A

RBC are broken down in the spleen & liver. One of the breakdown products of RBC is bilirubin, which the liver can further process & excrete in the bile (when some of this bile is processed by bacteria in the intestine, it changes colour & results in brown coloured feces)

Malfunctioning of the liver & obstructions of the common bile duct with the result that the liver cannot excrete processed bilirubin

26
Q
  1. Why may the feces be light in colour (“clay coloured”) and the urine dark in colour with jaundice?
A

Excess bilirubin in the blood can be then passed into urine via kidney, resulting in a darker colour of the urine

27
Q
  1. Where does jaundice often occur first?
A

Skin and sclera

28
Q
  1. Describe why splenomegaly may occur with liver disorders and how blood cell numbers can be affected.
A

Spleen enlarges due to portal hypertension (hypertension in portal vein causes back-up of blood into the splenic vein)

Formed elements take longer to filter through the enlarged spleen, leading to increased rate of removal

Result = anemia, thrombocytopenia, leukopenia

29
Q
  1. Define acute hepatitis and outline some of its common causes and diagnostic features.
A

Acute inflammation sometimes leading to destruction of hepatocytes and replacement with scar tissue

Drugs, toxins, autoimmune responses. Cause is viral: hepatitis B & hepatitis C

Jaundice, due to obstruction of bile secretion, detection of liver enzymes and metabolites in blood (liver function tests)

30
Q
  1. Name the viral strains involved in hepatitis.
A

A (infectious hepatitis, passed through fecal/oral route), B (serum hepatitis), C, D, & E

31
Q
  1. Name and describe the stages of disease of a typical acute viral hepatitis infection.
A

Prodromal phase = viral inflammatory effects: begins 2 weeks after exposure and ends with jaundice. Marked by fatigue, vomiting, headache, cough, low-grade fever. Disease very infectious during this stage

Icteric phase = effects of liver damage: begins after prodromal, lasts 2-6 weeks. Jaundice, dark urine, clay-coloured stools, liver is enlarged and tender – palpation causes pain

Convalescent phase = healing and repair: begins with resolution of jaundice and most symptoms, about 6-8 weeks after exposure, but liver remains large and tender. Liver returns to normal function 2-12 weeks after onset of jaundice

32
Q
  1. Define and describe chronic hepatitis, name causative organisms and possible resulting diseases.
A

Liver enzymes remain abnormal, and viral antigen persists, for longer than 6 months

Virus (usually HCV, can be HBV/HDV) persists in hepatocytes, producing a prolonged immune response, extending liver damage

Risk factor for cirrhosis and liver cancer

33
Q
  1. Describe the damage to the liver caused by acute hepatitis.
A

If intrahepatic ducts are damaged, obstruction and jaundice can occur. Damage is more extensive with HBV and HCV

34
Q
  1. How is the type of virus determined for a case of hepatitis?
A

– Determinative test for specific type of hepatitis is based on antibody assay.

35
Q
  1. What disorders can result from cirrhosis?
A

Hepatomegaly, splenomegaly, ascites, portal hypertension, hepatic encephalopathy and esophageal varices

36
Q
  1. Describe two types of alterations that occur in the liver during the development of cirrhosis
A

Liver metabolism is altered, and liver structure is altered by blockage of channels necessary for liver function

37
Q
  1. What is the “treatment” for cirrhosis? (Why is treatment in quotation marks?)
A

No specific treatment – rest, vitamin supplements, good nutrition, management of complications, possible liver transplant

38
Q
  1. Define liver failure.
A

Inability of the liver to perform its normal synthetic and metabolic function as part of normal physiology. Most severe clinical consequence of liver disease – can result from acute or chronic diseases

39
Q
  1. Name and describe the clinical manifestations of liver failure.
A

Fetor hepaticus – chronic musty odor of breath

Anemia, thrombocytopenia, leukopenia

Loss of clotting factors (made by liver) lead to purpura (purple discolouration 5-10mm), petechiae (< 5mm), spider angioma (appearance of radiating blood vessels on skin surface), epistaxis (nose bleeds)

Hemolysis, caused by changes in the RBC membrane lipids

Hepatorenal syndrome – kidney failure (oliguria) generally due to decreased blood volume brought about through bleeding, loss of fluid, vasodilation resulting from liver failure

Hepatic encephalopathy

40
Q
A
41
Q
  1. Define cholelithiasis and cholecystitis
A

Cholelithiasis: formation of gallstones. If these obstruct the outlet to the gallbladder, can cause cholecystitis (inflammation of the gallbladder)

42
Q
  1. From what are most gallstones formed, and what conditions lead to their formation?
A

80% formed from cholesterol

Abnormalities in the composition of bile (e.g. more cholesterol excreted into bile), stasis of bile (gallbladder obstruction), inflammation of the gallbladder (causes excessive absorption of water and bile salts)

43
Q
A
44
Q
  1. Define: fetor hepaticus, purpura, petechiae, spider angioma, and epistaxis.
A

Fetor hepaticus – chronic musty odor of breath

when small blood vessels burst, causing blood to pool just under the skin.

pinpoint, round spots that appear on the skin as a result of bleeding

vascular lesions, The lesion contains a central, red spot and reddish extensions which radiate outward like a spider’s web.

nose bleed

45
Q
  1. Define acute pancreatitis and describe its characteristic manifestations, underlying pathophysiology, and to what disease it can lead.
A

A reversible inflammatory process caused by premature activation of pancreatic enzymes

Characteristic feature is ongoing abdominal pain, aggravated by eating

Outflow of pancreatic digestive enzymes is obstructed (by gallstones in the common bile duct), causing accumulation of pancreatic secretions, resulting in pathologic activation of enzymes within the pancreas. This results in autodigestion, leading to vascular damage, necrosis, edema, inflammation

Can develop into “severe-acute” form, which involves release of inflammatory cytokines into the bloodstream, which causes systemic effects which can lead to renal failure, respiratory distress syndrome

46
Q
  1. Define chronic pancreatitis and be familiar with characteristic manifestations. Identify the most common cause and for what condition chronic pancreatitis is a risk factor.
A

Prolonged, progressive and irreversible destruction of the exocrine and then endocrine pancreas

Manifestations relate to loss of pancreatic function, and the outcomes of chronic inflammatory processes:

Malabsorption, weight loss, diabetes mellitus

Release of inflammatory cytokines into the bloodstream -> systemic effects, anorexia, nausea & vomiting

Risk factor for pancreatic cancer

Most common cause is chronic alcohol abuse (exact pathogenesis not well understood)

Biology 2401 (30 decks)

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