GI Flashcards
(23 cards)
What is cleft lip/palate
* CM
congenetal malformations of lip or the upper roof of the mouth (split or opening)
CM: Cleft lip can be unilateral or bilateral. nasal and maxillary and upper lip fuse. cleft palate is failure of the hard and soft palate from fusing during development. covered by mouth lining so its hard to see palate deformity
infant high risk of aspiration
cleft lip surgical repair before 3 months. palate is recommended by 18 months of age
Esophageal Atresia
* CM
malformation of esophagus. esophagus can be cut off split into two, may involve the trachea
CM: if it involved the tracheoesophageal fistula (TEF) then baby may choke while feeding, driiling, difficulty breathing. If no TEF then they have “scaphoid” sunken shaped abdomen because no gas, no food or liquids are goign to stomach.
babies
Pyloric stenosis patho
* risk
* CM
aka infantile hypertrophic pyloric stenosis. pyloric sphincter (end of stomach) muscle fibers become thick and stiff so stomach cant empty contents into small intestine.
- risk: lack of neuronal nitric oxide synthase -> failure of smooth muscle relaxation. Gastric hyperacidity. family hx. Use of macrolides (erythryomycin) and given to baby directly or lactation or in utero.
CM: palpated hard, olive-shaped mas sin abdomen (RUQ), projectile vomiting after feeding, hematemesis. failure to gain weight, WAVELIKE stomach contractions. hyperbilirubinemia associated with this.
most cases occur at 3 wks of life.
Color of emesis and their meaning
* red
* brown, granular
* yellow
* deep brown color
red: hematemesis, upper GI bleeding, gastric ulcers or esophageal varices
brown and granular: blood is partially digested in stomach
yellow/green: bile
deep brown: content from lower intestine, possible fecal
Hiatal hernia 3 types & patho
risks
CM
section of the stomach protrudes through opening in the diaphragm aka hiatus.
type I - sliding hiatal hernia; 95% cases, gastroesophageal junction is above diaphrahgm but stomach is still aligned and stomach fundus still below GE junction
type II- GE junction is below diaphragm but the fundus herniates through
Type III- both GE and fundus herniating. and if large enough other organs can go through
risks: age, smoking,
CM: inflammation of esphagus or stomach due to reflux, heartburn, freq belching, chest pain, dysphagia. can worsen when lying down, bending over, cough, or large meals. maybe palpable abdominal mass, can be visualized when coughing or retching.
fundus is the dome shape of upper stomach (upper archway)
small hiatals are usualy asymptomatic. Large causes chym to reflux, risk of ulcer development. can develop a hernia sac which risks ulcers, strangulation of sac -> ischemia, perforation, bleeding, obstruction.
GERD patho
* risk
* CM
abnormalities of LES; LES relaxation, decreased pressure, or GE disruption with hiatal hernia or obesity. chyme (acid,pepsin) periodically backs up from stomach into esophagus
risk: LES abnormalities, pyloric stricture, gastroparesis, pressure changes from obesity, pregnany, or intra-abdominal pressure (bending over etc.). smoking, alcohol, meds can affect LES.
foods that affect - chocolate, caffeine, carbonated bev, citrus, tomatoes, spicy or fatty foods
CM: heartburn (early), epigastric or retrosternal pain (usually after meal), regurgitation. nausea, laryngitis, pharyngitis. Hypersalivate
risk for Barett esophagus (metaplastic columnar epithelium)
Gastritis patho (acute vs chronic)
* CM
inflammation of stomach lining. Acute is caused by infection or autoimmune; usually due to helicobactor pylori. Chronic gastritis is associated with presence of lymphocytes, plasma cells, and macrophages. Acute is mostly neutrophil infiltration.
CM: N/v, epigastric pain, anorexia, hematesis and melena (dark stool) indicates ulceration and bleeding. Acute GI bleed can occur. Chronic increases risk of ulcers, gastric cancer, anemia, hemorrhage
severe stress dye ti nahir syrgerym traumatic injury, burns, or severe infections
Chronic gastritis type A and B affects where
* initial and final phases
type A: less common, affects fundus and the body of the stomach while sparing the antrum (lower part of stomach above the pyloric s.) Autoimmune process, risk of cancer development.
Type B: usually result of H. pylori infection, the stomach antrum is also infected this time. it embeds itself in mucus layer, activates toxins and enzymes that cause inflammation.
initially chronic gastritis is superficial then it extends deeper in mucosa and the gastric glands are affected. final phase is gastric atrophy, glandullar structures are lost.
Peptic Ulcers patho
* duodenal ulcers
* gastric ulcers
* stress ulcers
* Zollinger-Ellison Syndrome
Peptic ulcers disease refers to stomach or duodenal lesions. Risk from GERD, family hx.
- duodenal: 80% of cases, occurs with or without H.pylori. the bacteria releases gastric urease -> turns urea into ammonia and CO2 -> ammonia negates stomach acid protects the bacteria. infection with duodenal ulcers causes reduced bicarb secretion -> lower pH -> gastric metaplasia.
- gastric ulcers: associated with NSAID use, more deadly but less common. increases with aging, H. pylori can play a part. higher risk of gastric cancer.
- stress ulcers: Curling ulcers burn injuries. Cushing ulcers head injuries. develop due to tissue ischemia, acidosis, and decreased GI motility. Hemorrhage is the first sign of stress ulcer.
- Zollinger -Ellison Syndrome: caused by duodenal or pancreatic neuroendocrine tumors that secrete gastrin. same CM as ulcers. diarrhea due to reabsorption inhibition, digestive enzymes are inactivated.
gastric ulcer in antrum increase gastric acid. in body lower gastric acid.
Peptic Ulcer disease CM
GI hemorrhage, obstruction, perforation and other GERD like symptoms
what is cholelithiasis?
3 types?
which is more common?
stones (calculi) inside gallbladder. Risk factors age, obesity, diet, rapid weight loss (bariatric surgery), pregnancy.
type 1 - cholesterol; most common, cause obstruction pain, jaundice. associated with femal hormones.
type 2 - bilirubin (pigmented); usually small, multiple, black stones. More common in asians or in people w/ chronic diseases that cause hemolysis (sickle cell anemia)
mixed - usually found in large numbers, bilirubin (byproduct of blood being digested) is surrounded by cholesterol and calcium
biliary colic pain RUQ pain, epigastric, radiate to back or right shoulder. n/v, usually after a fatty meal.
what is acute cholecystitis
gallbladder inflammation due to cystic duct obstruction. manifestations are the same is biliary colic. BUT pain is more prolonged, steady, severe + fever and leukocytosis.
if gallstones are in the common bile duct what is it called
choledocholithiasis -> acute cholangitis (stasis and infection in the biliary tract) Charcot triad = fever, jaundice, and abdominal pain
high liver enzymes and pacreatic enzymes (it could clog the pancreatic duct)
Patho of Hepatitis
* CM
inflammation of liver caused by infections (viral usually); alcohol, medications (tylenol), antiseizure agents, antibx.
prodromal : 2 weeks after exposure to virus (incubation per.); abd pain, n/v, malaise, anorexia, fever, headache
Icteric phase: 1-2 weeks after prodromal phase, lasts up to 6 wks. jaundice, pruritis, dark tea-colored urine (bilirubinuria) or clay-colored stools (lack of bilirubin), hepatomegaly, RUQ pain
Recovery phase: resolution of jaundice 6-8 wks after exposure, elarged liver for as long as 3 months
Hepatitis A
* mode of transmission
* source
* jaundice?
* Acute vs Chronic
Mode of Transmission:
🦠 Fecal-oral (contaminated food/water, poor hygiene)
sexual contact
Source of Virus:
🍽️ Feces
Key Notes:
Acute only (no chronic form)
Vaccine available
Common in developing countries
Jaundice more common in adults than children
Hepatitis B
* mode of transmission
* source
* jaundice?
* Acute vs chronic
Mode of Transmission:
💉 Blood, 💋 sexual contact, 👶 perinatal (mother to baby)
Source of Virus:
🩸 Blood, semen, vaginal fluids
Key Notes:
Can be acute or chronic
Vaccine available
Risk of cirrhosis 40% & liver cancer
Jaundice is occasional
Hepatitis Type C
* mode of transmission
* source
* jaundice?
* Acute vs Chronic
Mode of Transmission:
💉 Blood (IV drug use, transfusions before 1992)
sexual contact
Source of Virus:
🩸 Blood
Key Notes:
Often becomes chronic 80%
No vaccine
Leading cause of liver transplants
Jaundice uncommon
Hepatitis Type D
* mode of transmission
* source
* jaundice?
* Acute vs Chronic
Mode of Transmission:
💉 Blood, 💋 sexual, 👶 perinatal
(Requires HBV to infect!)
Source of Virus:
🩸 Blood, body fluids
Key Notes:
Only occurs with Hep B (coinfection or superinfection)
Makes HBV infection worse
only chronic with superinfection
jaundice is common
Hepatitis Type E
* mode of transmission
* source
* jaundice?
* Acute vs Chronic
Mode of Transmission:
🦠 Fecal-oral (contaminated water)
fecal-oral/ blood
perinatal
Source of Virus:
🍽️ Feces
Key Notes:
Similar to HAV
Dangerous in pregnant women (↑ mortality)
No vaccine in most countries
rarely chronic unless immunocompromised
Jaundice is common
What is cirrhosis? patho?
risks
CM
chronic, progressive irreversible damage to the liver.
risks: hepatitis, alcoholic liver disease, fatty liver, hemochromatosis, hepatic venous obstruction, etc.
patho: liver fibrosis severity and progression depends on underlying cause. the extracellular matrix of the liver is degraded by protease. when attempting to repair itself regenerative nodules/scar tissue can obstruct liver blood flow or bile flow.
CM: anorexia, weight loss. Portal hypertension (pressure increase in hepatic artery and portal vein) bc of nodules or fibrosis. portal htn -> risk of varicosities in esophagus (varices), stomach, rectum (hemorrhoids) -> acute bleeding. Ascites.
spleen stomach and pancrease use the same vein so they can enlarge as well. hypersplenism = neutropenia
Hepatorenal syndrome
Hepatic encephalopathy
Spontaneous bacterial peritonitis
Hepatopulmonary syndrome
h.renal syndrome: kidney function decline. increase urine due excessive bile bc fat cannot be properly digested = dark urine. splanchnic artery dilation -> less blood circulation to kidneys-> renal failure.
encephalopathy: liver cannot detox blood -> increase ammonia -> neuro impairment. confused, lethargy, hand tremors.
SBP: usually e. coli, compromised immune defense, bacterial overgrowth. bacterial foes from intestins to mesenteric lymph then into ascitic fluid -> bacteremia.
Hepatopulmonary: increase portal pressure -> pulmonary artery vasoconstriction. Hypoxemia.
Nonalcoholic Fatty Liver Disease patho
CM
fat accumulates in the liver cells.
patho: low LDL production, fat isn’t digested, inflammation is caused by lipid peroxidativedamage cell membranes -> stellate cells are stimulated -> fibrosis.
CM: usually asymptomatic, but if symptomatic -> fatigue, malaise, anorexia, nausea, RUQ pain. Hepatomegaly, splenomegaly, portal htn, cirrhosis
