GI

Question 1

Alcoholic cirrhosis

Answer 1

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

Question 2

Nonalcoholic fatty liver cirrhosis

Answer 2

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

Question 3

Primary biliary cirrhosis

Answer 3

Auto immune rare
Patho- destruction of bile, ducts in liver
Symptoms include jaundice itching, right upper quadrant pain low-grade fever

Question 4

Secondary biliary cirrhosis

Answer 4

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

Question 5

Liver injury

Answer 5

Etiology includes drugs, alcohol virus, illness, or idiopathic
Symptoms depends on severity of damage
Path physiology compromise of liver parenchyma

Question 6

Acute liver failure

Answer 6

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

Question 7

Chronic liver injury

Answer 7

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

Question 8

Jaundice

Answer 8

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

Question 9

Portal hypertensive

Answer 9

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

Question 10

Hepatic encephalopathy

Answer 10

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

Question 11

Ascites

Answer 11

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

Question 12

Cleft lip or palate

Answer 12

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

Question 13

Physiologic neonatal jaundice

Answer 13

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

Question 14

Pathologic neonatal jaundice

Answer 14

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

Question 15

Osmotic diarrhea

Answer 15

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

Question 16

Secretory diarrhea

Answer 16

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

Question 17

Motility diarrhea

Answer 17

Due to intestinal shortening, neuropathy, hyperthyroidism laxative abuse
Patho-negative effect on fluid electrolyte acid base balance

Question 18

Common complications associated with diarrhea

Answer 18

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

Question 19

Bowel obstruction

Answer 19

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

Question 20

Appendicitis

Answer 20

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

Question 21

Pyloric stenosis

Answer 21

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

Question 22

Cholelithiasis

Answer 22

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

Question 23

Ulcerative colitis

Answer 23

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

Question 24

Crohn’s disease

Answer 24

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

Question 25

Irritable bowel syndrome

Answer 25

Etiology- functional disorder no specific altered structure or biochemical process, visceral, hypersensitivity or hyperalgesia, abnormal G.I. permeability motility secretion sensitivity post inflammatory dysbiosis, psychosocial factors
Symptoms can be mild to debilitating, lower, abdominal pain, discomfort, bloating, fecal urgency, incomplete, evacuation, nausea, diarrhea, constipation, that can be prominent or mixed
Patho- several hypothesis include visceral, hypersensitivity, abnormal, G.I. motility and or secretion food, allergy or intolerance or psychosocial
Nutritional implications usually none
Usually much less severe disorder, characterized by abdominal pain, constipation, diarrhea, or combination maybe some inflammation associated very minimal non-destructive cause

Question 26

Diverticulosis/diverticulitis

Answer 26

Etiology- age genetics obesity, lack of exercise medication, including NSAIDs altered biome abnormal colonic peristalsis, inflammatory bowel disease, allergies, psychosocial
Symptoms include left lower quadrant, pain, and western countries , right lower quadrant pain in Asian countries also have diarrhea constipation distention flatulence if diverticula are inflamed, can cause fever, leukocytosis, and tenderness
Patho- mucosa herniate through smooth muscle layer of colon wall flame infect abscess hernia obstruct rupture caused tinnitus left colon most common site, more common and elders, usually in the sigmoid

Question 27

Gastric ulcers

Answer 27

Etiology- h pylori infection, age 55 to 65 usually caused by NSA reflux, pancreatic enzyme, reflux, damage cells
Symptoms- gastrinoma (tumor or several tumors, pancreatic or duo derma) increased gastrin, increased gastric acid (zollinger Ellison syndrome) 90% if patients will have stomach/duodenal, 25% genetic disorders, multiple endocrine neoplasia type 1, also causes tumors in pituitary and parathyroid gland, 75% spontaneous occurrence. Pain, Antiacid, cause relief, can cause Melena, hematemesis, coffee ground, complications-bleeding, perforation, lumen contents- peritonitis, possible pain is worse with eating, immediate onset more acid more pains
,

Question 28

Duodenal ulcers

Answer 28

Most frequent and younger patients duodenal (HCl plus pepsin)
Pain, food relief, pain recurs when stomach empties

Question 29

Stress related musical disease

Answer 29

Cushing ulcer versus curlings
Cushing- increased ICP triggers vagus nerve (parasympathetic) increased gastric acid
Curlings- decreased plasma volume, blood flow redistribution, ischemic cell necrosis, gastric mucosa breakdown
Extreme physical stress-critically ill patients (vent dependent, trauma, burns, TBI)

Question 30

Upper GIB

Answer 30

Etiology- esophagus, stomach duodenum, esophageal varices, gastric varices, Mallory Weiss tear, tear in esogastric junction, CA, angiodysplasia, PUD, severe retching, hemorrhoids
Sometimes include acute bleeding, may result in hypovolemic shock if rapid
Hematemesis- vomit either bright red or dark grainy blood with coffee, ground appearance maybe old blood not acute, melena-black sticky tarry stool

Question 31

Lower GIB

Answer 31

Small intestine colon rectum caused by polyps, inflammatory bile disease, diverticulitis, cancer, vascular ectasias, hemorrhoids
Occult- trace amounts in normal appearance, stool or gastric secretions detectable only with a guaiac test, associated with iron deficiency, usually associated with concerns for cancer
Hematochezia- red blood from rectum clinically blood loss 1000 thousand milliliters or more will have symptoms of hypovolemic shock

Question 32

Peptic ulcer disease

Answer 32

Broad descriptive category, break-in, or ulceration and lower portion of esophagus, stomach or duodenum 10 to 15% of population have peptic ulcer disease may be higher underlying tissue exposed to acid auto digestion may erode through exposed vessels
Risk factors- h pylori, alcohol, smoking, increased age, obesity, cirrhosis, genetics, COPD, cirrhosis, and NSAIDS-suppress prostaglandin synthesis, decreased bicarbonate production, decreased mucin, which results in decreased mucus, high HCl, production

Question 33

Upper gastrointestinal organs

Answer 33

Parotid submandibular salivary sublingual salivary glands
Tongue faring, larynx, trachea, esophagus, stomach, and small intestine, then includes a duodenum, the jejunum and the ileum

Question 34

Lower gastrointestinal organs

Answer 34

Large intestine includes vermiform appendix, cecum, ileum, ascending colon, hepatic flexure, transverse colon, splenic flexure, descending colon, sigmoid colon, anal canal rectum

Question 35

Ancillary organs

Answer 35

Liver gallbladder, pancreas

Question 36

Three muscle valve system

Answer 36

Lower esophageal sphincter (LES)
Pyloric sphincter
Ileocecal sphincter

Question 37

GI circulation A&P

Answer 37

General GI blood flow: celiac, superior, inferior mesenteric arteries
-celiac-stomach and proximal intestine (duodenum)
-superior mesenteric-remaining small intestine and proximal colon
-inferior mesenteric-distal colon, vasa recta-branches over the musculature of stomach, small intestine, and colon-penetrated muscularis and forms arterial plexus within submucosa, small vein draining- parallel arterial circulation and delivery blood to portal vein (splenic drains stomach, superior mesmeric drains upper intestine, inferior mesenteric drains to distal colon, all drain to portal vein and the liver and then back to heart)

Question 38

Hepatic blood flow

Answer 38

Hepatic portal vein-splenic vein (inferior splenic vein drains here) and superior mesenteric vein, deoxygenated from here, deliver 800-1200 ml/min to liver, 70-75% of blood received by liver
Hepatic vein to inferior vena cava, to heart to abdominal aorta, to hepatic artery (from celiac artery-oxygenated) 400-500 ml/min, approximately 25% of total cardiac output

Question 39

Hepatitis A

Answer 39

Spread by fecal, oral, parenteral, sexual
Incubation is 30 days
Test include anti-HAV antibodies
If a patient is hepatitis A IgM (-), IgG (+), they are immune due to prior infection and cleared or vaccination
If a patient is IgM(-) and IgG (-) they have never been exposed and are not vaccinated

Question 40

Hepatitis B

Answer 40

Spread sexual, parenteral
Incubation 60 to 180 days
Test- HBsAg, antiHBs, HBeAg, antiHB3, antiHbc, IgM, IgG, HBV DNA
If patient is HB ag surface (-) and HB ab (+) resolved infection
If patient is HB ag surface (-), HBA core (-), and HB ab surface (+) -immune by vaccination
If Hb ag surface (+), Hb IgG(+), Hb ab surface (-)- active infection

Question 41

Hepatitis C

Answer 41

Parenteral
Incubation 35 to 72 days
Tests- anti HCV antibodies
If patient is anti HCV IgG(+) and HCV PCR (+) current infection

Question 42

Hepatitis D

Answer 42

Fecal oral, parenteral, sexual
Incubation 30-180 days (depends on Heb B incubation)
Test- anti HDV, and HDV (RNA)

Question 43

Hepatitis E

Answer 43

Fecal oral
Incubation 15-60 days
Test-anti HEV IgG, and HEV RNA

Question 44

Hepatitis phases

Answer 44

-Prodromal about two weeks after infection symptoms include fatigue, anorexia, malaise, nausea, vomiting, headache, hyperalgia, cough, low-grade fever, very infectious
-icteric phase- when the two weeks post prodromal last 2 to 6 weeks symptoms include jaundice dark urine Clay colored stool and large liver, tender to percussion and palpation fatigue abdominal pain, hepatitis B D and C if not jaundice may not be diagnosed and become critically, ill and unaware
-recovery phase-resolution of jaundice in about 68 weeks after exposure liver remains in large and tender liver function test return to normal to 12 weeks after onset of jaundice
-Chronic phase liver function test remain abnormal. These individuals are at a higher risk for cirrhosis and primary hepatic, cellular carcinoma they are carriers and can infect others.

Question 45

Pancreatitis

Answer 45

Etiology- obstruction of pancreatic enzyme outflow of either the bile or pancreatic duct usually by a gallstone secondary cause may be direct cellular injury by alcohol, drugs or viral infection symptoms if acute epigastric or mid abdominal constant pain raging from mild abdominal discomfort to severe capacitating pain may radiate to back nausea, vomiting, or caused by paralytic,l obstruction of pancreatic enzyme outflow of either the bile or pancreatic duct usually by a gallstone secondary cause may be direct cellular injury by alcohol, drugs or viral infection symptoms, if acute epigastric or mid abdominal constant pain range from mild abdominal discomfort to severe and capacitating pain may radiate to back nausea, vomiting, or caused by paralytic ileum, caused by either pancreatitis or peritonitis Joness may occur secondary to an obstructed, bile duct or edema induct
Patho- uncertain reflux, bile acids into pancreatic duct from gallstone obstruction ethanol metabolize within the pancreas, create inter, cellular injury, calcium overload, alterations in shack, proteins, mitochondrial, and Evert reticular injury primary pathophysiology appears to be calcium overload, which results in trypsin activation, causing auto digestion of the pancreas overtime and low calcium as a mesenteric fat is digested by pancreatic enzymes can cause hypoparathyroidism low magnesium if severe can result in SIRS RECURRENT PANCREATIC, FIBROSIS, AND LEAD TO CHRONIC PANCREATITIS
Chronic is due to alcohol use caused by chronic exacerbation of acute pancreatitis, maybe idiopathic or caused by gallstones smoking high triglycerides pancreatic tissue is replaced by fiber tissue pseudo structures calcifications
Lab markers for amylase and lipase

Question 46

G.I. changes associated with aging

Answer 46

May begin at age 50 with tooth loss, osteoporosis, oral cavity, gum, loss changes in the gums
Taste buds decline in salivary secretions decrease decrease ability to taste
Decrease motility changes in upper esophageal, sphincter, and esophagus that can cause dysphasia or Gerd
Decreased stomach lining capacity to resist damage increases
Small intestine, decrease lactose levels, overgrowth bacteria causes lactose intolerance, pain, and bloating
Decrease absorption of some nutrients villa become shorter , deficiency in a vitamin B 12 iron and calcium
Decrease motility of large intestine and rectum can cause constipation
Rate of liver regeneration decreases hepatic, blood flow, enzymatic activity causes, decreased drug metabolism, different efficacy of meds detoxification decreases, but liver function test from main normal
Pancreatic fibrosis fatty deposits, atrophy, beta cells decrease in number and function
Changes in neural hormone control
Anorexia multifactoral as above increase risk of mortality