GI Flashcards
(46 cards)
Alcoholic cirrhosis
Symptoms- fatty infiltration will have none, with alcoholic steatoheoatitis- fatigue, weight loss, anorexia, severe nausea fever abdominal pain jaundice worsen with cirrhosis
Patho- fatty deposits within liver increased lipogenesis cholesterol synthesis, decrease fatty acid oxidation by hepatocytes in ability of liberty detox by alcohol formation of acetlyhyde, protein, synthesis, exporter proteins from the liver, along with minerals and vitamins, triggers malnutrition
Nonalcoholic fatty liver cirrhosis
Cause include diabetes, obese, insulin resistance
Symptoms, most common liver disease, United States usually asymptomatic
Path
Patho-infiltration of hepatocytes fat triglycerides some develop Nash
Primary biliary cirrhosis
Auto immune rare
Patho- destruction of bile, ducts in liver
Symptoms include jaundice itching, right upper quadrant pain low-grade fever
Secondary biliary cirrhosis
Due to prolonged partial or complete obstruction of the common bile duct
Patho- Gallstones, tumors, fibrotic structures, chronic pancreatitis
Symptoms include jaundice itching, right upper quadrant pain low-grade fever
Liver injury
Etiology includes drugs, alcohol virus, illness, or idiopathic
Symptoms depends on severity of damage
Path physiology compromise of liver parenchyma
Acute liver failure
Etiology rare in the United States most common is Tylenol overdose
Symptoms occur 6 to 8 weeks after a viral hepatitis or metabolic liver disorder or 5 to 8 weeks after Tylenol overdose causes, anorexia, vomiting, abdominal pain jaundice, ascites, GI bleed, hepatic encephalopathy, elevated liver function, test, direct, and indirect bilirubin, increase prothrombin time and ammonia levels
Patho- severe impairment of liver cells in the setting of no pre-existing liver disease or cirrhosis
Chronic liver injury
Etiology, hepatitis C alcohol, alcohol related Nash hepatitis B
Symptoms develop over years depends on cause as progresses causes jaundice portal, hypertension Ascites, encephalopathy, G.I varices, bleeding, portopulmonary syndrome, individuals are an increased risk for infection due to immune compromise
Patho- cirrhosis causes irreversible inflammatory fibrosis of liver replacement of normal tissue with scar tissue overtime
Jaundice
Hyperbilirubinemia, greater than 2.5 to 3, Patho- obstructive extra common biliary duct or inter hepatic obstruction (disturbances in hepatocyte obstruction obstruction of bile canaliculi) may because by excessive hemolysis
In newborns, impaired bilirubin, uptake and conjugation
Symptoms include yellow or green pigmentation of skin dark urine light colored stools if complete obstruction of bile, fevers, chills, pain if infection, or inflammation itching with the accumulation of Bilirubin on skin
Portal hypertensive
Abnormal increase greater than 3 millimeters and mercury in portal system obstruction or flow impedes through any component portal system or vena cava intrahepatic vascular remodeling with shunts, thrombosis, inflammation of biliary, cirrhosis, viral
hepatitis, schistosomiasis
Post hepatic from hepatic vein thrombosis causes hepatic emesis from bleeding esophageal varices
Hepatic encephalopathy
Impaired behavior, cognitive and motor function, biochemical alterations that affect neurotransmission and brain function, liver dysfunction, collateral, liver circulation, shunts, blood around liver, not allowing for detoxification causes confusion, personality changes, irritability, inhibition altered, mental status, abnormal EEG increase in liver function, test, and ammonia level
Ascites
Accumulation of fluid and peritoneal cavity reducing fluid available for normal physiology
Patho- portal, hypertension, spleen, vasodilation decrease synthesis of albumin by liver, sphlacnic artery vasa, dilation, and renal, water and sodium retention, capillary, hydrostatic, pressure exceeds, capillary, oncotic pressure water pushes to peritoneal space
Cleft lip or palate
Risk factors include environmental such as tobacco smoke, alcohol medication, vitamin deficiency, maternal obesity
Etiology- genetics environmental
Symptoms include feeding issues, swallowing, and speech, difficulty middle ear infections
Patho- in complete fusion of nasomedial and intramedullary process
Physiologic neonatal jaundice
Risk factors include frequent occurrence, poor, caloric, intake, breast-feeding problems, dehydration, hemic, disease, metabolic or endocrine disease, anatomical, liver abnormalities, or infection
Etiology serum bilirubin greater than 2 mg/dl
Symptoms jaundice and Icterus
Pathologic neonatal jaundice
Risk factors include severe illness, TSB level above 5 mg/dl, mothers with preeclampsia, hypertension, diabetes, or vaginal bleeding blood type incompatibility heal disease over 25 years old male children delayed meconium stool, G6PD deficiency, birth trauma
Etiology- serum bilirubin greater than 5 mg/dl
Symptoms- jaundice light colored stool dark urine weight loss persist 1 to 2 weeks if full term 2 to 4 weeks of pre-term
Patho- increased bilirubin production, impaired hepatic, uptake, or excretion of unconjugated bilirubin, delayed maturation of liver bilirubin conjugating mechanisms
Osmotic diarrhea
MOA- magnesium citrate lactulose or MiraLAX other causes include tube, feeds dumping syndrome, pancreatic bile, salt, deficiency, malabsorption, small intestine, bacteria, overgrowth, or celiac disease
Patho- non absorbable substances in intestines pulls water by osmosis into the intestine, causing large volume diarrhea
Secretory diarrhea
Etiology- large volume diarrhea is due to infection like rotavirus endotoxin from c. Diff, ecoli. Cholera, antibiotics in the elderly.
Small volume diarrhea- IBS, crohns, UC, colitis, fecal impact
Patho- excessive mucosal secretion of chloride or bicarbonate secretion of decreased sodium absorption, infection
Motility diarrhea
Due to intestinal shortening, neuropathy, hyperthyroidism laxative abuse
Patho-negative effect on fluid electrolyte acid base balance
Common complications associated with diarrhea
Malabsorption fluid and electrolyte balance acid basin, balance, dehydration, weight loss, fatty stools, and bloating infections usually last less than two weeks associated with fever and cramping bloody stools are usually due to inflammatory disease or dysentery
Bowel obstruction
Etiology- small bowel obstruction is the most common due to adhesions, tumors Crohn’s disease or hernias
Large bowel obstruction usually rare means cancer or diverticulitis
Symptoms in small bowel obstruction-distention colicky pain, nausea vomiting comes in waves with peristalsis may be severe or constant with distention if ischemic pain develops are more intense as it worsens causes fever, leukocytosis extension, rebound tenderness, hypotension, necrosis, perforation, and peritonitis
Large obstruction symptoms -hypogastric pain abdominal descension, vague to excruciating pain, depending on his ischemia and peritonitis
Patho- relates to the location of obstruction and presence of severity of ischemia or torsion intussusception, herniation complete or incomplete obstruction within or outside, intrinsic or extrinsic cause, intestinal wall, simple, strangulated, clothes, loop, mechanical or functional surgical pathophysiology is not well understood
Appendicitis
Etiology- unknown, possibly obstruction of the lumen with stool, tumors or foreign bodies with consequential bacteria infection
Symptoms include left lower quadrant, pain, umbilical, pain, gastric pain, nausea, vomiting, diarrhea, anorexia settles in right lower quadrant, perforation peritonitis abscess
Patho- inflammation of the vermiform appendix, most common surgical urgency of the abdomen and 10 to 19-year-olds obstruction does not allow drainage and increases intraluminal pressure, mucosal blood supply decreases and appendix becomes hypoxic
Pyloric stenosis
Risk factors include congenital or acquired if acquired may be caused by peptic ulcer disease or cancer near the pylorus do ulcers are more likely to cause of obstruction of the pyloris than gastric ulcers
Patho- our blocking of the pylorus, the opening between the stomach and the duodenum
Symptoms can be vague, epigastric fullness, worse after eating and end of day nausea epigastric pain as disease progresses may become anorexic with weight loss, succession splash (vomiting is cardinal symptom) vomiting of undigested food without bile causes dehydration, low potassium low chloride metabolic alkalosis in frequent stools
Cholelithiasis
Etiology- obesity woman OCP, native Americans, low HDL high triglycerides, rapid weight loss
Three types is cholesterol being 90%
Two is black, which is 2% usually hyperbilirubinemia, brown pigment Asian descent (intraductal stasis, colonization of bile with bacteria) three is stones made a bile, cholesterol, or bilirubin
Symptoms- difference between cholelithiasis and cholecystitis-cystitis is inflammation of the gallbladder generally due to cholelithiasis, can have lithiasis and be asymptomatic
Patho- “super saturated” cholesterol forms crystals that aggregate with mucin, matrix within gallbladder that lodges in the cyst or common duct stones more likely secondary to hyperbilirubin Billary secretions hemolytic disease
Ulcerative colitis
Etiology- uncertain can be dietary or immune
Symptoms can be relapsing and remitting effect the colon especially the rectum happens in 20 to 40-year-olds less common smokers continuous lesions limited to mucosa, bloody mucousy diarrhea, urgent to urgency to defecate increase risk of obstruction and colon cancer
Patho- uncertain multiple theories, including immune (IgG, plasma cells, cytokines present) most common rectum and sigmoid: in the mucosal wall
Nutritional implications, severe disease may cause dehydration, weight loss, low potassium, low, albumin, extreme malnutrition
Crohn’s disease
Etiology family, history, smoking, urban residency age less than 40 years old Jewish descendants, genetic mutations in TLR, aggressive response to normal bacteria flora
Symptoms can be relapsing or remitting effects ileoceccal region, small intestine: bloody mucousy, diarrhea associated with vitamin and nutrition deficits increase risk of abscesses perforation, malabsorption, malnutrition obstruction fistula, perforations increase risk of colon cancer
Patho- skip lesions, ulcers transmural- can affect any part of the G.I. track from mouth to anus, fat wrapping wall, thickening, fissure, cobblestone, mucosa, overreaction, normal flora
Nutritional implications deficiency and vitamin B 12 vitamin D, folic and albumin
