2024-02-25T22:24:53+03:00[Europe/Moscow] en true <p>Cells are found throughout sinusoids and conduct phagocytosis of bacteria translocating from the gut</p>, <p>The liver's immune system</p>, <p>Responsible for control of ferroportin, vulnerable to excessive cytokine production. This is why inflammatory disease can cause chronic inflammatory anemia</p>, <p>Mechanism that allows for release of iron from cells</p>, <p>Circulates to the parietal cells in the body of the stomach to stimulate gastric acid secretion</p>, <p>Secreted by small intestine cells, signals presence of fat digestion products. Circulates to the gall bladder to stimulate contraction and bile secretion</p>, <p>Secreted from cells in the ileum, circulate to the stomach to decrease stomach motility and to the pancreas to promote insulin secretion</p>, <p>The nervous system of the gut, rich in opioid peptides and their receptors</p>, <p>Gut's amine secretors</p>, <p>Amines secreted by EC cells</p>, <p>Gastric acid producers</p>, <p>Purpose of low stomach pH (as low as 2)</p>, <p>Presence of food in the stomach stimulated gastrin (stimulates gastric acid production and stimulates histamine secretion). Acidification of the stomach lumen inhibits gastrin-secreting cells</p>, <p>Stomach protections from gastric acid</p>, <p>Why do NSAIDs have the potential to damage to GI track?</p>, <p>Risk factors for peptic ulcers</p>, <p>Why does smoking increase risk of peptic ulcers?</p>, <p>Risk factors for pancreatitis</p>, <p>Functions potentially impacted by pancreatitis</p>, <p>End products of digestion</p>, <p>Types of diarrhea</p>, <p>Common immune-based gut disorder</p>, <p>MoA in Celiac Disease</p>, <p>Risk factor for Inflammatory Bowel Diseases</p>, <p>Two common inflammatory bowel diseases</p>, <p>Symptoms of inflammatory bowel diseases</p>, <p>Symptoms that can distinguish Chron's from UC</p>, <p>Pathology of IBS</p>, <p>Most efficient IBS treatment</p>, <p>Inheriting the autosomal dominant mutation for this increases your risk of multiple forms of cancer (stomach, hepatobiliary, small intestine, renal pelvis, ureter and endometrial/ovarian (in females)) and is the only way for you to get non-polyposis colorectal cancer.</p>, <p>Common microbial causes for pediatric gastroenteritis</p>, <p>Differentiating between Infantile Gastroesophageal Reflux (GER) and Infant and pediatric Gastroesophageal Reflux Disease (GERD)</p>, <p>This disease is cause by lack of innervation by enteric nerves and typically requires surgical resection. Typical manifestation is failure to produce a bowel movement after birth</p>, <p>Gerontologic GI considerations</p>, <p>Blood flow and the liver</p>, <p>Physiologic considerations with the liver</p>, <p>The liver and <span class="tt-bg-red">bilirubin metabolism</span></p>, <p>Two outcomes during <span class="tt-bg-red">first pass drug metabolism</span></p>, <p>Adjustment of drug dosing in liver disease</p>, <p>Mediators of liver metabolism</p>, <p>Roles of liver in metabolism</p>, <p>Additional features of the liver</p>, <p>Most specific liver marker, biproduct of liver cell necrosis</p>, <p>Considerations in Acute liver disease</p>, <p>Disease that presents with blockage of bile flow</p>, <p>Symptoms of acute cholestasis</p>, <p>General term for liver inflammation</p>, <p>Considerations with different types of viral hepatisis</p>, <p>Hereditary disease whose pathology is the inverse of the pathology of chronic inflammatory anemia (too much hepcidin activity)</p>, <p>Management of nonalcoholic fatty liver disease in children</p>, <p>Gerontologic considerations for the liver</p>, <p>Hepatitis A incubation period</p>, <p>Viral infection that can lead to hepatocellular carcinoma</p> flashcards

Module 7- GI and Liver

Advanced pathophysiology- Ch. 13 & Ch. 14

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  • Cells are found throughout sinusoids and conduct phagocytosis of bacteria translocating from the gut

    Kupffer Cells

  • The liver's immune system

    Reticuloendothelial system

  • Responsible for control of ferroportin, vulnerable to excessive cytokine production. This is why inflammatory disease can cause chronic inflammatory anemia

    Hepcidin

  • Mechanism that allows for release of iron from cells

    Ferroportin

  • Circulates to the parietal cells in the body of the stomach to stimulate gastric acid secretion

    Gastrin

  • Secreted by small intestine cells, signals presence of fat digestion products. Circulates to the gall bladder to stimulate contraction and bile secretion

    Cholecystokinin (CCK)

  • Secreted from cells in the ileum, circulate to the stomach to decrease stomach motility and to the pancreas to promote insulin secretion

    Glucagon-like peptide 1 (GLP-1)

  • The nervous system of the gut, rich in opioid peptides and their receptors

    Enteric nervous system

  • Gut's amine secretors

    enterochromaffin (EC) cells

  • Amines secreted by EC cells

    Stomach: Histamine (stimulates gastric acid secretion) Small Intestine: Serotonin (increases gastric motility)

  • Gastric acid producers

    Parietal cells

  • Purpose of low stomach pH (as low as 2)

    killing ingested bacteria and activating proteolytic enzyme pepsin

  • Presence of food in the stomach stimulated gastrin (stimulates gastric acid production and stimulates histamine secretion). Acidification of the stomach lumen inhibits gastrin-secreting cells

    Gastric phase

  • Stomach protections from gastric acid

    Mucous neck cells-secrete bicarbonate-rich mucus Prostaglandins-protective (reduce acid secretion, increase mucus secretion, increase mucosal blood flow)

  • Why do NSAIDs have the potential to damage to GI track?

    They inhibit prostaglandin production, thus increasing the risk of acid damage

  • Risk factors for peptic ulcers

    hyperacidity, smoking, reflux of small intestine bile acids or digestive enzymes in to stomach, NSAIDs

  • Why does smoking increase risk of peptic ulcers?

    Decreases gastric mucosal blood flow (increased opportunity for damage and slower healing)

  • Risk factors for pancreatitis

    Alcohol use, gallstones and drug reactions

  • Functions potentially impacted by pancreatitis

    Bicarbonate and insulin production

  • End products of digestion

    Starches, proteins, triglycerides, phospholipids, cholesterol esters

  • Types of diarrhea

    1. secretory (cholera) 2.malabsorptive (celiac) 3.inflammatory (IBS) 4.osmotic (lactose intolerance)

  • Common immune-based gut disorder

    Celiac disease

  • MoA in Celiac Disease

    Basically, pathologic immune activation (lymphocytes, dendritic cells, and cytokine milieu). Basically a hypersensitivity reaction to gluten

  • Risk factor for Inflammatory Bowel Diseases

    Family history and diagnosis of another autoimmune disease

  • Two common inflammatory bowel diseases

    Chron's disease and ulcerative colitis

  • Symptoms of inflammatory bowel diseases

    abdominal pain, frequent diarrhea, rectal bleeding, anemia

  • Symptoms that can distinguish Chron's from UC

    Chron's: relapsing/remitting abd pain, skip legions (especially in the ileum) fistulas UC: More blood loss

  • Pathology of IBS

    We don't know

  • Most efficient IBS treatment

    Pattern tracking and avoiding triggers

  • Inheriting the autosomal dominant mutation for this increases your risk of multiple forms of cancer (stomach, hepatobiliary, small intestine, renal pelvis, ureter and endometrial/ovarian (in females)) and is the only way for you to get non-polyposis colorectal cancer.

    Lynch syndrome

  • Common microbial causes for pediatric gastroenteritis

    Viral: Rotavirus (preventable by vaccination) and norovirus Parasitic: Giardia or Cryptosporidium

  • Differentiating between Infantile Gastroesophageal Reflux (GER) and Infant and pediatric Gastroesophageal Reflux Disease (GERD)

    GER: Presents in the infant period and typically resolves by 12 months, painless

    GERD: Can present at any time, pain, recurrent vomiting, dysphagia, and food refusal

  • This disease is cause by lack of innervation by enteric nerves and typically requires surgical resection. Typical manifestation is failure to produce a bowel movement after birth

    Hirschsprung disease

  • Gerontologic GI considerations

    Higher incidence of GI symptoms, problems with mouth, teeth and decreasing muscle and sphincter tone increase risk for aspiration, d/t anatomy diverticular disease is more common

  • Blood flow and the liver

    High rate of blood flow. About 20-25% of cardiac output. Two main blood sources are the portal vein (deoxygenated, about 75-80% of hepatic bf) and the hepatic artery (source of oxygenated blood)

  • Physiologic considerations with the liver

    1. large role in metabolism 2. produces bile (needed for fat digestion/absorption) 3. Protein synthesis (most plasma proteins) 4. Biotransformation of bilirubin 5. Drug metabolism 6. production of clotting factors 7. Vulnerable to infection (hepatitis) and damage

  • The liver and bilirubin metabolism

    The heme created by the breakdown of RBCs is converted to bilirubin. Bilirubin attaches to albumin (indirect bilirubin) for transport. Indirect bilirubin cannot be excreted by the body, so liver cells convert it to direct bilirubin by conjugating it to glucuronic acid. Direct bilirubin can travel freely in the blood and is secreted into bile (and bile is secreted into the intestines and excreted as stool). Bilirubin gives bile and stool it's color.

  • Two outcomes during first pass drug metabolism

    1. Inactivated by the liver: dosage must reflect this 2.Prodrugs- activated by liver metabolism

  • Adjustment of drug dosing in liver disease

    Hepatic dosing- (depending on first pass drug metabolism liver disease could result in a medication not being effective or OD at a normal dose)

  • Mediators of liver metabolism

    Insulin and glucagon

  • Roles of liver in metabolism

    Excess glucose stored as glycogen or synthesized into triglycerides (which can be packaged as VLDL), can also produce glucose from glycogen during fasting, also synthesizes cholesterol

  • Additional features of the liver

    1. Vitamin and mineral storage (vitamins A, E and B12), also iron storage as ferritin, synthesis of transferrin (iron-binding and regulating) and hepcidin 2. Regenerative capacity (complete restoration of function after mild-moderate liver damage and ability to use living donors)

  • Most specific liver marker, biproduct of liver cell necrosis

    Alanine aminotransferase (ALT)

  • Considerations in Acute liver disease

    1. >50% of cases are caused by drug-induced liver injury 2. Prodrome symptoms (fatigue and nausea) which can resolve spontaneously 3. Appearance of jaundice indicates more severe insult

  • Disease that presents with blockage of bile flow

    Acute cholestasis

  • Symptoms of acute cholestasis

    Jaundice (hyperbilirubinemia), elevated GGT, ALP, increased circulating bile salts (itching (pruritis) indicate cutaneous deposition of bile salts), pale stools, and dark urine.

  • General term for liver inflammation

    Hepatitis

  • Considerations with different types of viral hepatisis

    Hep A: Oral-fecal transmission Hep B: no cure, only prevention by vaccine Hep C: often asymptomatic. Now curable with an expensive medication

  • Hereditary disease whose pathology is the inverse of the pathology of chronic inflammatory anemia (too much hepcidin activity)

    Hereditary hemochromatosis

  • Management of nonalcoholic fatty liver disease in children

    Similar to adults- weight reduction (through lifestyle changes or medical management)

  • Gerontologic considerations for the liver

    1. Decreased bf and liver mass 2. high rates of polypharmacy (often multiple providers) 3. Increased incidence of autoimmune damage (autoimmune hepatitis and primary biliary cholangitis)

  • Hepatitis A incubation period

    about 4 weeks

  • Viral infection that can lead to hepatocellular carcinoma

    Hepatitis C