Class 9: GI Flashcards
1
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Slide 6
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2
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Gastritis
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-Acute or chronic inflammation of the stomach
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Q
Acute gastritis
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-d/t local irritants
-Symptomatic or asymptomatic
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Q
Etiology of chronic gastritis
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-H. pylori is most common
-Autoimmune & multifocal is least common but increases the risk of carcinoma
-Chemical from reflux of duodenal contents, pancreatic secretions, bile
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Chronic gastritis can lead to…
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Atrophy of the epithelium of the stomach
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Pathophysiology of gastritis
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-Occurs as a result of the breakdown of the normal gastric mucosal barrier
-Hydrochloric acid backflows into the mucosa
-Edema & disruption of capillary walls with loss of plasma into the gastric lumen… possible hemorrhage
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Q
Clinical manifestations of gastritis
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-Anorexia, N/V, epigastric pain, feeling of fullness
-Hemorrhage with ETOH
-Self limiting, lasting from a few hours to days with complete healing
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Clinical manifestations of chronic gastritis
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-Patients lose intrinsic factor leading to cobalamin deficiency; changes in RBC production; anemia and neurological complications
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Intrinsic factor
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A substance secreted by gastric mucosa that is essential for absorption of cobalamin (vitamin B12)
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Etiology of gastritis + drugs
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-ASA, corticosteroids & NSAIDS
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Etiology of gastritis + diet
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Alcohol & spicy/irritating foods
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Etiology of gastritis + microorganisms
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-H. pylori, salmonella & staphylococcus organisms
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Etiology of gastritis + environmental factors
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-Radiation & smoking
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Etiology of gastritis + pathophysiological conditions
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-Burns, hiatal hernia, physiological stress, reflux, renal failure (uraemia), sepsis & shock
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Etiology of gastritis + other factors
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-Endoscopic procedures, nasogastric suction & psychological stress
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Q
Gastritis is that…
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Gut feeling you get when you stay up all night & do not eat
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Diet considerations in gastritis
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Stomach lining needs to be coated, if they cannot eat then TF is initiated
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GERD pathophysiology
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Backflow regulated by the stomach sphincter; transient relaxation is common after meals (especially with fatty foods)
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Most common clinical manifestation of GERD
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Epigastric pain or heartburn, belching & chest pain
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Other manifestations of GERD
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-Respiratory symptoms: Wheezing, coughing, and dyspnea
-Otolaryngologic symptoms: Hoarseness, sore/lump in throat and choking
21
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Differentiating between GERD & MI
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-Give a pink lady (antacid)
-Trops
22
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GERD assessment + neuro
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Dysphagia & pain
23
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GERD assessment + CV
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Chest pain, tachycardia & aBP
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GERD assessment + resp
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Sore/lump in throat, hoarseness of cords, wheezing, coughing, dyspnea, crackles if aspiration pneumonia has occurred
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GERD assessment + GI
Nutritional status, odynophagia (painful swallowing), heartburn, N/V & weight loss
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Food..
Makes GERD feel better if pt is sitting up
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Complication of GERD
Barret esophagus-scarring, edema & spasms (strictures)
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PUD
-Group of disorders resulting from exposure of upper GI acid-pepsin secretions. Mostly duodenal and gastric; (duodenal much more common)
-Men 55-70 most commonly affected
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Etiology of PUD
H. Pylori & NSAIDs
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Pathophysiology of PUD
-Only develops in the presence of an acidity
-Mucosa barrier becomes impaired, and backflow of acid lead to PUD
-Affects all layers of mucosa and eventually penetrates through
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Manifestations of PUD
-Pain usually on empty stomach; relieved by food or antacids
-Burning or cramping
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Complications of PUD
Hemorrhage, gastric outlet obstruction (from edema, spasm or contraction of scar tissue), and perforation (which can lead to peritonitis)
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In a true ulcer...`
A GI bleed develops
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Gastric ulcers often leads to...
Duodenal ulcers
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GERD leads to...
Duodenal ulcers
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Ulcers can...
Develop into shock
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Slide 18
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GI bleed indications
Site of bleeding is indicated by colour and texture: bright red to tarry black (melena)
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Upper GI bleeds..
Often coffee-ground material (partially digested) or bright red
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Bright red vs dark red blood
Brighter red means bleeding closer to the source; darker means further from source (e.g. source is duodenum, which is high up, blood in stools will be dark; hemorrhoids often produce bright red blood)
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Considerations when determining if it is an upper or lower GI bleed
May be hard to pinpoint source such as with hypermotility. Blood may be bright red even if source is high in GI tract
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GI bleeds are...
An emergency
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Slide 21
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Slide 22
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Urine output
-0.5-1cc/kg/hr
-If pt is not voiding it will lead to ketoacidosis
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Obstruction/ileus
-Any condition that prevents normal flow of chime through intestine
-Loss of intestinal motility in the absence of an ileus
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Classification of an obstruction/ileus
Simple or functional
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Primary causes of small bowel obstructions
-Adhesions * (most common for adults)
-Hernia
-Tumors
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Primary causes of large bowel obstructions
-Malignancy
-Volvulus (twisting, torsion)
-Strictures related to diverticulitis
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Paralytic ileus is caused by...
-Narcotics, sedation, anesthetics, & giving a lot of food or liquids too quickly
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Functional obstructions
Paralytic ileus & constipation
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Intussusception is...
Most common in kids
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Slide 24
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Slide 25
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Manifestations of intestinal obstructions
-May be sudden and dramatic symptoms of pain (intermittent), vomiting, distention, borborygmus (rumbling bowel sounds)**, peristaltic rushes, restlessness and awareness of peristaltic movements
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Tx of intestinal obstructions
Tx is based on the cause, it may respond to decompression but may require surgery
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Stomach & intestinal dysfunction key assessment points
-aBowel sounds, N/V, anorexia, distention & aLab values
-GI pain
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Intestinal dysfunction GI pain
-Usually sharp or burning
-May be steady or intermittent
-May be referred
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Slide 29
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Slide 30
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Hepatitis A pathophysiology
-Widespread inflammation of the liver tissue
-Liver damage is mediated by cytotoxic cytokines and natural killer cells that cause lysis of infected hepatocytes
-Damage results from liver necrosis
-Inflammation of periportal areas interrupts flow of bile
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Transmission of hepatitis A
-Transmitted through feces (fecal-oral route; contaminated water and food; blood)
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Incubation period of hepatitis A
2-7 weeks
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Manifestations of hepatits A
-Fatigue, fever, N/V, hepatomegaly, jaundice, dark urine, anorexia, rash
-Usually a mild disease
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Hepatitis A...
Interrupts flow of bile out of the liver
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Fulminant viral hepatitis
-Results in severe impairment or necrosis of the liver cells commonly caused by tyelenol OD
-May occur with hepatitis B or C virus
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Fulminant viral hepatitis pathophysiology
-Edematous hepatocytes and patchy areas of necrosis and inflammatory cell infiltrates and disrupts the parenchyma
-Acute liver failure develops within 6-8 weeks after initial symptoms of hepatitis
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Manifestations of fulminant viral hepatitis
Anorexia, vomiting, abdominal pain, progressive jaundice, followed by ascites and GI bleed
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Jaundice
-May occur as a result of liver dysfunction
-Results from 1. Extrahepatic (post-hepatic) obstruction to bile flow, 2. Intrahepatic obstruction, 3. Prehepatic excessive production of unconjugated bilirubin
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Pathophysiology of jaundice
Conjugated bilirubin cannot flow out of the liver because of obstruction or inflammation of the bile ducts stools become light or clay coloured
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Jaundice can lead to...
-Pruritis which occurs d/t bile salts accumulating under the skin
-Dark brown/reddish urine
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Slide 34
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Portal HTN pathophysiology + intrahepatic
Results from vascular remodelling with intrahepatic shunts, thrombosis, inflammation or fibrosis such as in cirrhosis of the liver, viral hepatitis, or schistosomiasis (parasitic infection)
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Portal HTN pathophysiology + posthepatic
Causes occur from hepatic vein thrombosis or cardiac disorders that impair the pumping ability of the right side of the heart (RV HF); blood backs up and there is increased pressure in the portal system
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Portal HTN pathophysiology + prehepatic
Causes occur with narrowing of the hepatic portal vein
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Longterm complications of portal HTN
Varices, splenomegaly, hepatopulmonary syndrome and portopulmonary hypertension
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Manifestations of portal HTN
Most common clinical manifestation is vomiting of blood from bleeding esophageal varices, then slow, chronic bleeding from varices causes anemia or melena
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Prehepatic, intrahepatic, & posthepatic are...
All right sided heart issues
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Progression of portal HTN
-Backup leads to varices, ascites and right sided HF
-Varices can result in profound bleed: Melena, frank red blood & vomiting
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Tx of portal HTN
-Rapid treatment needed: Volume replacement, drugs, endoscopy, balloon tamponade & surgery (portacaval shunt)
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Non-alcoholic fatty liver disease (NAFLD) & non-alcoholic steatohepatitis (NASH)
These present as cirrhosis but are in the absence of ETOH
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Slide 37
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Cirrhosis of the liver pathophysiology
-Irreversible inflammatory, fibrotic liver disease
-Occurs d/t a disorganized regenerative process
-Overgrowth of new & fibrous tissue distorts the structure, resulting in lobules of irregular size and shape impeding blood flow
-Leads to poor cellular nutrition, and hypoxia causing inadequate flow and scar tissue decreasing the function of the liver
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Manifestations of liver cirrhosis + labs
-Abnormal AST, ALT, GGT, & Alk Phos
-Normal blood values; albumin, bilirubin (initially low but then increase), PTT
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Initial manifestations of liver cirrhosis
Abdominal pain, fatigue, slight weight loss, and enlargement of the liver & spleen
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Manifestations as liver cirrhosis progresses
Jaundice, skin lesions, peripheral neuropathy, portal HTN, esophageal and gastric varices, edema, ascites, hepatic encephalopathy & hepatorenal syndrome
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Liver failure leads to...
Kidney failure
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Ascites
-Sodium, water and protein accumulate in peritoneal cavity due to pressure changes in lymphatic system capillaries. -Oncotic and osmotic pressures rise
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Tx of ascites
-May require paracentesis as abdominal pressures increase
-Sodium restriction & diuretics
-Colloids to increase oncotic pressure
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Ascites decrease...
Alveoli expansion
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Slide 42
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Ascites is the most...
Common complication of cirrhosis but can also occur with right sided HF, abdominal malignancies, nephrotic syndrome & malnutrition
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Pathophysiology of ascites
Contributing factors include: Portal HTN, decreased synthesis of albumin by the liver, splanchnic arterial vasodilation, and renal sodium and water retention
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Ascites may cause
Bacterial peritonitis (fever, chills, abdominal pain, decreased bowel sounds, and cloudy ascitic fluid)
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Slide 44
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Hepatic encephalopathy is AKA
Portosystemic encephalopathy
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Pathophysiology of hepatic encephalopathy
-Complex neurologic syndrome characterized by impaired cognitive function, asterixis, and EEG changes
-Increased amounts of Ammonia and GABA (inhibitory transmitter) may contribute to reduced LOC
-May develop rapidly and become an EMERGENCY situation quickly
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Manifestations of hepatic encephalopathy
aGait & personality, memory loss, irritability, lethargy and sleep disturbances
-Symptoms can progress to confusion, flapping tremor of the hands, stupor, convulsions and coma
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Tx of hepatic encephalopathy
& when you weren't looking, I added some lactulose
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Liver dysfunction can lead to...
Hepatic encephalopathy
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Gallbladder structure
Saclike organ
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Function of the gallbladder
-Store and concentrate bile between meals
-Aids in digestion of fats
-Bile is released in response to food
-Conditions slowing or obstructing flow of bile out of the gallbladder lead to gallbladder disease
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About bile
Bile is an alkaline, bitter tasting, yellowish green fluid that contains bile salts, cholesterol, bilirubin, electrolytes, and water
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Pathophysiology of gallbladder cholelithiasis (gallstones)
-Gallstones are formed from impaired metabolism of cholesterol, bilirubin and bile salts
-Form when there is decreased motility and biliary stasis
-Stones may lay dormant and silent until they become lodged in the cystic or common duct, causing pain when the gallbladder contracts
105
Types of gallstones
Cholesterol (most common), pigmented (black-hard, brown-soft) and mixed
106
Manifestations of gallbladder cholelithiasis
-Often asymptomatic
-Epigastric and RUQ pain and intolerance to fatty foods are cardinal manifestations
-Heartburn, flatulence, epigastric discomfort, pruritus, jaundice and food intolerances to fats and cabbage
-Biliary colic (pain) occurs 30 min to several hours after eating a fatty meal
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Pathophysiology of gallbladder cholecystitis
-Caused by the lodging of a gallstone in the cystic duct causing distention & inflammation
-Colic pain but decreased blood flow can result in ischemia, necrosis, and perforation of the gallbladder
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Manifestations of gallbladder cholecystitis
-Fever, leukocytosis, rebound tenderness and guarding
-Serum bilirubin and alkaline phosphatase (ALP) may be elevated
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Slide 52
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Diagnostic tests associated with gallbladder disorder
-Endoscopic Retrograde Cholangiopancreatography (ERCP)
-Radiographic and endoscopic; diagnosis & treatment
-X-rays, ultrasound, CT, scintigraphy (nuclear scanning)
