NUR 250 Patho Exam 1 Exemplars
Acute and Chronic Gastritis Clinical Manifestations - ANS--Most often asymptomatic or
report mild dyspepsia
-Underlying condition may mask symptoms
-Potential symptoms may include abdominal pain or upset, burning sensation in chest or
upper abdomen, feeling of fullness, bloating, belching, and reflux
-More severe symptoms include, nausea, vomiting, GI bleeding, fever, and weight loss
\Acute Gastritis etiology - ANS-- Infection-induced Usually due to H. pylori
-Drug-induced - E.g., NSAIDs, steroids, some chemotherapeutic drugs, alcohol, and iron
supplements
- Ulcerohemorrhagic - Occurs with critical illness; due to physiologic stress and ischemic
changes caused by shock, hypotension, or release of vasoactive substances
\Acute Gastritis Pathogenesis - ANS--Acute imbalance between mucosal injury and repair
mechanisms
-Development of mucosal hyperemia and erosive changes with histologic presence of
inflammation
\Acute Gastritis Treatment - ANS--Elimination of causative agent or exacerbating factors
-Eradication of H. pylori infection if indicated
-Medications to treat dyspepsia (e.g., protein pump inhibitor [PPI] or histamine blocker)
-Surgical intervention for GI bleeding
\acute glomerulonephritis - ANS--Occurs most often in children or young adults
-Common cause: acute infection such as post-streptococcal infection (Group A Beta
Hemolytic Streptococcus) from strep throat or skin infection
-Complications: Minimal change nephropathy, Nephrotic Syndrome
\Alcohol Fatty liver - ANS--mild form of alcoholic liver disease
-Can be caused by small amounts of alcohol, may be asymptomatic and is reversible with
cessation of drinking
\Alcoholic cirrhosis - ANS--caused by toxic effects of alcohol metabolism in the liver,
immunologic alterations, inflammatory cytokines, oxidative stress from lipid peroxidation and
malnutrition
-Alcohol Is transformed to acetaldehyde and excessive amounts significantly alter
hepatocyte function and activate hepatic stellate cells
-Mitochondrial function is impaired, decreasing oxidation of fatty acid
-Fibrosis and scarring alter the structure of the liver and obstruct biliary and vascular
channels
\Alcoholic steatohepatitis - ANS--precursor of cirrhosis characterized by inflammation,
degeneration and necrosis of hepatocytes and infiltration of neutrophils and lymphocytes
-Mechanism of the hepatocyte injury is not clearly understood but immunologic factors,
endotoxins from gut bacteria and inflammatory mediators
\Appendicitis Clinical Manifestations - ANS-Cramping abdominal pain, tenderness with
palpation of the right lower abdominal quadrant, nausea or vomiting, increased white blood
cell count, and low-grade fever
\Appendicitis Etiology - ANS--Not fully understood
-Believed to be due to appendiceal obstruction
, \Appendicitis Pathogenesis - ANS--Obstruction is thought to lead to bacterial overgrowth and
luminal distention
-Increased intraluminal pressure and/or excessive inflammation can inhibit blood flow
causing vascular compromise to the affected tissue
-may become gangrenous and can rupture
\Appendicitis Treatment - ANS-Gold standard - Laparoscopic surgery
\Ascites clinical manifestations - ANS--Increased abdominal girth
-Weight gain
Bulging flanks
-Decreased appetite
-Abdominal discomfort
-Dyspnea
\ascites etiology - ANS--Portal hypertension
-Arterial vasodilation of splanchnic circulation
-Decreased SVR
-Capillary permeability increases
-decreased synthesis of albumin; portal HTN and reduced albumin cause the capillary
hydrostatic pressure to exceed the osmotic pressure - this pushes the fluid into the
peritoneal cavity; peripheral vasodilation decreases effective circulating blood volume,
activating aldosterone and ADH = sodium and water retention
\Ascites evaluation - ANS-paracentesis, biochemical analysis and microscopic exam
\Ascites treatment - ANS-remove 1 or 2L of ascitic fluid, peritneovenous shunt, transjugular
intrahepatic portosystemic shunt o
\Biliary Cirrhosis - ANS--damage and inflammation leading to cirrhosis begin in bile canaliculi
and bile ducts rather than in the hepatocytes
\Cholelithiasis Clinical Manifestations - ANS-often asymptomatic; abdominal pain; jaundice;
heartburn; flatulence; food intolerance
\Cholelithiasis etiology - ANS-1) Cholesterol gallstones form in bile that is supersaturated
with cholesterol produced by the liver
-Usually occurs in the gallbladder
2) Pigmented stones - form from a increased level of unconjugated bilirubin with binds with
calcium
-Associated with chronic liver disease
\Cholelithiasis evaluation - ANS-u/s; CT; oral cholecystogram; IV cholangiography
\Cholelithiasis treatment - ANS--dietary factors may prevent the development of gallstones;
-endoscopic removal of gallstones
\Chronic Active Hepatitis - ANS--Persistence of CMs and liver inflammation after the acute
stages of HBV and HCV
--> Liver functions remain abnormal for longer than 6 months and hepatitis B surface antigen
(HBsAg) remains
--> Extrahepatic manifestation - arthralgias, fatigue, neurologic and renal symptoms
\Chronic gastritis etiology - ANS--Infection-induced - Usually due to H. pylori
-Chemical and caustic agents (e.g., NSAIDs, excessive alcohol ingestion, radiation
exposure)
Autoimmune disease (e.g., Crohn disease, Wegener granulomatosis, and sarcoidosis)
\Chronic Gastritis Pathogenesis - ANS--Begins with superficial gastritis
-Progresses to atrophic gastritis
-Advances to gastric atrophy
Acute and Chronic Gastritis Clinical Manifestations - ANS--Most often asymptomatic or
report mild dyspepsia
-Underlying condition may mask symptoms
-Potential symptoms may include abdominal pain or upset, burning sensation in chest or
upper abdomen, feeling of fullness, bloating, belching, and reflux
-More severe symptoms include, nausea, vomiting, GI bleeding, fever, and weight loss
\Acute Gastritis etiology - ANS-- Infection-induced Usually due to H. pylori
-Drug-induced - E.g., NSAIDs, steroids, some chemotherapeutic drugs, alcohol, and iron
supplements
- Ulcerohemorrhagic - Occurs with critical illness; due to physiologic stress and ischemic
changes caused by shock, hypotension, or release of vasoactive substances
\Acute Gastritis Pathogenesis - ANS--Acute imbalance between mucosal injury and repair
mechanisms
-Development of mucosal hyperemia and erosive changes with histologic presence of
inflammation
\Acute Gastritis Treatment - ANS--Elimination of causative agent or exacerbating factors
-Eradication of H. pylori infection if indicated
-Medications to treat dyspepsia (e.g., protein pump inhibitor [PPI] or histamine blocker)
-Surgical intervention for GI bleeding
\acute glomerulonephritis - ANS--Occurs most often in children or young adults
-Common cause: acute infection such as post-streptococcal infection (Group A Beta
Hemolytic Streptococcus) from strep throat or skin infection
-Complications: Minimal change nephropathy, Nephrotic Syndrome
\Alcohol Fatty liver - ANS--mild form of alcoholic liver disease
-Can be caused by small amounts of alcohol, may be asymptomatic and is reversible with
cessation of drinking
\Alcoholic cirrhosis - ANS--caused by toxic effects of alcohol metabolism in the liver,
immunologic alterations, inflammatory cytokines, oxidative stress from lipid peroxidation and
malnutrition
-Alcohol Is transformed to acetaldehyde and excessive amounts significantly alter
hepatocyte function and activate hepatic stellate cells
-Mitochondrial function is impaired, decreasing oxidation of fatty acid
-Fibrosis and scarring alter the structure of the liver and obstruct biliary and vascular
channels
\Alcoholic steatohepatitis - ANS--precursor of cirrhosis characterized by inflammation,
degeneration and necrosis of hepatocytes and infiltration of neutrophils and lymphocytes
-Mechanism of the hepatocyte injury is not clearly understood but immunologic factors,
endotoxins from gut bacteria and inflammatory mediators
\Appendicitis Clinical Manifestations - ANS-Cramping abdominal pain, tenderness with
palpation of the right lower abdominal quadrant, nausea or vomiting, increased white blood
cell count, and low-grade fever
\Appendicitis Etiology - ANS--Not fully understood
-Believed to be due to appendiceal obstruction
, \Appendicitis Pathogenesis - ANS--Obstruction is thought to lead to bacterial overgrowth and
luminal distention
-Increased intraluminal pressure and/or excessive inflammation can inhibit blood flow
causing vascular compromise to the affected tissue
-may become gangrenous and can rupture
\Appendicitis Treatment - ANS-Gold standard - Laparoscopic surgery
\Ascites clinical manifestations - ANS--Increased abdominal girth
-Weight gain
Bulging flanks
-Decreased appetite
-Abdominal discomfort
-Dyspnea
\ascites etiology - ANS--Portal hypertension
-Arterial vasodilation of splanchnic circulation
-Decreased SVR
-Capillary permeability increases
-decreased synthesis of albumin; portal HTN and reduced albumin cause the capillary
hydrostatic pressure to exceed the osmotic pressure - this pushes the fluid into the
peritoneal cavity; peripheral vasodilation decreases effective circulating blood volume,
activating aldosterone and ADH = sodium and water retention
\Ascites evaluation - ANS-paracentesis, biochemical analysis and microscopic exam
\Ascites treatment - ANS-remove 1 or 2L of ascitic fluid, peritneovenous shunt, transjugular
intrahepatic portosystemic shunt o
\Biliary Cirrhosis - ANS--damage and inflammation leading to cirrhosis begin in bile canaliculi
and bile ducts rather than in the hepatocytes
\Cholelithiasis Clinical Manifestations - ANS-often asymptomatic; abdominal pain; jaundice;
heartburn; flatulence; food intolerance
\Cholelithiasis etiology - ANS-1) Cholesterol gallstones form in bile that is supersaturated
with cholesterol produced by the liver
-Usually occurs in the gallbladder
2) Pigmented stones - form from a increased level of unconjugated bilirubin with binds with
calcium
-Associated with chronic liver disease
\Cholelithiasis evaluation - ANS-u/s; CT; oral cholecystogram; IV cholangiography
\Cholelithiasis treatment - ANS--dietary factors may prevent the development of gallstones;
-endoscopic removal of gallstones
\Chronic Active Hepatitis - ANS--Persistence of CMs and liver inflammation after the acute
stages of HBV and HCV
--> Liver functions remain abnormal for longer than 6 months and hepatitis B surface antigen
(HBsAg) remains
--> Extrahepatic manifestation - arthralgias, fatigue, neurologic and renal symptoms
\Chronic gastritis etiology - ANS--Infection-induced - Usually due to H. pylori
-Chemical and caustic agents (e.g., NSAIDs, excessive alcohol ingestion, radiation
exposure)
Autoimmune disease (e.g., Crohn disease, Wegener granulomatosis, and sarcoidosis)
\Chronic Gastritis Pathogenesis - ANS--Begins with superficial gastritis
-Progresses to atrophic gastritis
-Advances to gastric atrophy
