GI pathophysiology Flashcards

1
Q

What are the layers of the GI wall, list them from the innermost to the outermost.

Also, explain a little bit about each one such as:
-what does the layer consist of?

A

Mucosa; epithelial cells specialized for absorption & secretion, highly vascularized.

Submucosa; consists of collagen, elastin, glands, nerves, and blood vessels.

Circular and Longitudinal smooth muscle: provides motility for GI tract

Serosa: faces the blood

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2
Q

Function of the mouth? What enzymes are found here?

A

-Function: mostly mechanical digestion, mastication, bolus formation.

Enzymes:

  • lingual amylase (carbs)
  • lingual lipase (lipids)
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3
Q

Which CN are involved with swallowing?

The esophageal phase of swallowing begins what group of muscles relaxing?

A

CN V, VII, IX, X, XII

Esophageal phase begins with cricopharyngeal relaxation.

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4
Q

What is the composition of saliva?

How much is produced each day?

What are the functions of saliva?

A
  • 97-99.% water
  • lytes; Na+, K+, Cl-, PO4, HCO3
  • salivary amylase & lipase
  • mucin
  • metabolic wastes
  • lysozymes, IgA, and cyanide cmpd protect against microorganisms

1L/day is produced

Function:

  • initial digestion of starches and lipids by salivary enzymes
  • dilution and buffering of ingested foods
  • lubrications of ingested food to aid its movement
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5
Q

What is the function of:

  • stomach
  • small intestine
  • large intestine
A

Stomach: digestion and break down of food to smaller, absorb-able particles(Chyme). Can hold 2-3L. Initial digestion of proteins.

Small intestine: primary site of digestion and absorption of nutrients, bile and pancreatic duct empty into duodenum.

Large intestine: absorption of water

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6
Q

What are the three phases of digestion? What stimulates each of these phases?

A

-cephalic phase:sight, thought, taste, and smell of food activates the cortex, amygdala, hypothalamus, vagus nerve.

Gastric phase: stomach distension activates stretch receptors…medulla..vagus nerve. Food chemicals activate G cells to release gastrin into blood increasing hydrochloric acid and pepsin.

Intestinal Phase: presence of food stimulates enterogastrone hormones (any hormone secreted by the mucosa of the duodenum in the GI tract) secreted in duodenum and lower GI tract.

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7
Q

Describe the chemical digestion of chyme in the duodenum?

A

-acid chyme or fatty protein rich chyme enters the duodenum and causes the duodenal wall to release secretin. Secretin enters the blood stream and causes the pancreas release bicarbonate rich pancreatic juice to neutralize the acidic stomach acids.

If protein rich chyme the duodenum releases CCK which then enters the bloodstream and causes the pancreas to release enzyme rich pancreatic juice.

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8
Q

Gastric Secretion:

  • what type of cells are found in the body and antrum? What is secreted from these?
  • what type of glands are found in the body and antrum?
A

Body: oxyntic glands

  • Parietal cells: HCl and Intrinsic factor
  • Chief cells: pepsinogen

Antrum: pyloric glands

  • G cells: gastrin (directly into circulation)
  • Mucous neck cells: mucus, HCO3, pepsinogen
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9
Q

Function of Gastrin?

A
  • secreted by G cells in response to eating (stimuli: protein, distention of stomach, and vagal nerve stimulation)
  • promotes secretion of H+ by gastric parietal cells
  • pepsinogen release
  • increase stomach motility
  • relax pyloric sphincter
  • control LES
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10
Q

Regulation of HCl from parietal cells?

A

Ach; released from vagus nerve, promotes HCl secretion
–Antagonist: atropine

Histamine: released from mastlike cells in gastric mucosa, stimulates HCl secretion
–antagonist: Cimetidine (inhibits acid production)

Gastrin: released from G cells of stomach, stimulates HCl secretion

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11
Q

What are some causes of peptic ulcers?

A
  • h. pylori
  • NSAID/Aspirin
  • Alcohol
  • psychological stress
  • decreased mucous secretion
  • delayed gastric emptying
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12
Q

Describe Segmentation and peristaltic contractions.

A

-Segmentation: circular muscle contraction sending chyme in both directions. (Mixing)

Peristaltic: longitudinal muscles contract propelling chyme along small intestine

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13
Q

5 MC causes of GI bleeding

A
  • Duodenal ulceration
  • Gastric erosions (gastritis)
  • Gastric ulceration s
  • varices
  • Mallory weiss tear: found int pts with persistent retching and vomiting following an alcoholic binge. Upper GI bleeding 2ndry to longitudinal mucosal lacerations at the Gastroesophageal junction or the gastric cardia)
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14
Q

Digestive Enzymes & their targets

  • Stomach (2)
  • pancreas (5)
  • intestine (3)
A

Stomach:

  • pepsin: proteins
  • lipase: triglycerides

pancreas:
-amylase: starch
-lipase/colipase: triglycerides
-phospholipase: phospholipids
-Trypsin: peptides
-Chymotrypsin: peptides
peptide = broken down protein

Intestine:

  • enterokinase: activates trypsin
  • disaccharidases: complex sugars
  • peptidases: peptides
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15
Q

Innervation of the GI tract:

-what are the two components of the ANS?

A

Extrinsic: Sympathetic and parasympathetic innervation

Intrinsic: aka enteric nervous system (miesseners and myenteric plexuses)

  • contained all within the wall of GI tract.
  • communicates with extrinsic component.
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16
Q

Parasympathetic nerve supply comes from what nerve? Sympathetic?

A

parasympathetic nerve supply comes from the nucleus ambiguus and vagus nerve.

Sympathetic nerve supply comes from the cervical and thoracic sympathetic chains

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17
Q

Can intrinsic innervation direct all functions of the GI in absence of extrinsic innervation?

A

-Yes! controls contractile, secretory, and endocrine functions.

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18
Q

What are gastric pits?

A

openings in the gastric mucosa where gastric glands empty into.

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19
Q

Liver:

  • receives major blood supply from where?
  • describe the difference in pressures between the portal vein and the hepatic vein
  • why is this difference important?
  • describe the effects of cirrhosis on the liver.
A
  • Liver receives major blood supply from the hepatic portal vein, which comes off the celiac axis
  • LOW VASCULAR RESISTANCE. There is a small difference between the pressures in the portal vein and hepatic vein
  • This is important because as vascular resistance increases, blood flow decreases (ex. cirrhosis…portal HTN…ascities)

Effects of cirrhosis
-cirrhosis leads to scar tissue which can obstruct blood and bile flow. obstruction of hepatic venous blood flow can increase pressures within other veins leading to other circulatory dz such as varices and ascites.

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20
Q

What are the sinusoids within the liver?

A

type of blood vessel with fenestrated endothelium that serves as a location for mixing the oxygen rich blood from the hepatic artery and the nutrient rich blood from the portal vein. The hepatocytes are in contact with these sinusoids.

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21
Q

Hepatocytes perform the functions of the liver, what are the functions of the Liver?

A
  • carb metabolism
  • lipid metabolism
  • protein metabolism
  • removal(detoxification) of drugs and hormones
  • excretion/secretion of bilirubin
  • synthesis of bile salts
  • storage of cmpds (glucose)
  • phagocytosis
  • aid in synthesis of Vit D, A, B12
  • urea formation from ammonium*
  • synthesis of plasma proteins (albumin, clotting factors)
  • coagulation (synthesis of coagulation factors)
  • blood resevoir
  • immunity (kuppfer)
22
Q

WHat is the purpose of carb metabolism in the liver?

  • What happens to blood sugar with liver cirrhosis? Alcohol abusers?
A

purpose of carb metabolism in the liver is to have a glucose buffer by storing glycogen. REmoving excess glucose from blood thereby maintaining a normal blood glucose concentration.

Cirrhosis:
-after a carb rich mean they get HYPERGLYCEMIA. Liver isnt sufficient to store the glucose.

Alcohol abusers:
-alcohol suppresses citrate cycle and thereby impaires gluconeuogenesis from amino acids resulting in HYPOGLYCEMIA.

23
Q

Describe the 3 basic steps in food digestion of:

  • carbs
  • proteins
  • lipids
A

Carb…disaccharides…monosaccharaids

Proteins.. peptides…amino acids

Lipids…diglycerides…monoglycerides & fatty acids

24
Q

Describe Lipid metabolism

A

Lipid ingestion…chylomicron formation in the intestine and transported to the liver. Liver converts chylomicron to VLDL and sends to adipose tissue. When departing the adipose tissue VLDL is now converted to LDL. LDL can be found in peripheral blood vessels/organs where it may accumulate and cause plaques. HDL takes up LDL from the periphery and returns it to the liver for further excretion and/or conversion to be recycled.

25
Q

Do we ingest most of our cholesterol?

A

NO, we predominantly synthesize cholesterol in the liver.

26
Q

Metabolism of Protein

A

-amino acids are converted to NH3 (ammonia) and then Urea in the liver. Urea is excreted into the blood stream to be excreted by the kidney.

27
Q

Disorders of Protein metabolism: Describe each.

  • ammonia detoxification disorder
  • hyperammonemia
  • hepatic coma
A

ammonia detoxification disorder= failure of urea formation leading to accumulation of ammonia.

Hyperammonemia = hepatic encephalopathy; mental changes & motor changes (hyperreflexia, tremor)

Hepatic Coma = death.

Ammonia. is. toxic.

28
Q

What does bile do?
What is bile?

Describe Bile secretion and recycling

A

Bile is mixture of water (97%) bile salts, bile pigments, and cholesterol

Bile emulsifies lipids to prepare them for digestion and absorption in the small intestine.

Bile secretion:

  • produced and secreted by the liver. Stored in the gallbladder.
  • ejected into small intestine when gallbladder contracts.

Bile Recycling:
-Bile aids in the breakdown of lipids, after lipids are absorbed, bile salts are re-circulated to liver via enterohepatic circulation (absorption of bile salts from ileum into portal circulation, delivery back to liver) Extraction of bile salts from the portal blood by hepatocytes.

29
Q

Describe the formation, processing, secretion, and excretion of bilirubin..

A

Formation:
Hgb phagocytosed by tissue mfs in the spleen. Iron is released and remainder of heme group is converted to biliverdin which is rapidly reduced to unconjugated bilirubin and bound to albumin and brought to the liver.

Processing:
Once in the liver, albumin unbinds by passing through hepatocyte membrane and conjugates w/ glucoronic acid.

Secretion:
-hepatocytes transport conjugated bili into the bile canaliculi where then it enters the duodenum throught he sphincter of oddi. This bilirubin has high solubility so it is able to be excreted through the urine and feces.

30
Q

What is the role of the small intestine in bile metabolism?

A

-bile and bile salts increase the growth of intestinal bacteria, the bacteria metabolize conjugated bile to urobilinogen which is reabsorbed back into the blood and excreted via the kidneys.

31
Q

Fate of reabsorbed urobilirubin?

A
  • 95% of reabsorbed urobilirubin is excreted again by liver into bile
  • 5% excreted into urine
  • small part excreted into feces
32
Q

the sphincter of oddi opens within how many minutes of food intake? how much bile is produced each day? how much can be stored in the gallbladder at one time?

A

Oddi opens within 30mins

Produce 500-1000ml/day

stores 50-80ml

33
Q

Jaundice:

  • detectable total plasma bilirubin level
  • what are the causes of jaundice pre-liver, within the liver, and post-liver?
A

-detectable total plasma bilirubin is greater than 2mg/dL

Causes:

  • -preliver: excess production of bilirubin (RBC lysis)
  • -WIthin liver: decreased uptake of bilirubing into hepatic cells
  • disturbed intracellular protein binding or conjugation.
  • -Post liver: disturbed secretion of conjugated bilirubin into the bile canaliculi
  • intrahepatic or extraheptaic bile duct obstruction.
34
Q

Obstructive jaundice

  • pathophysiology
  • what type of bilirubin will be elevated? how does it become elevated?
A

pathophys: gall stones or tumors can block the bile duct. CONJUGATED bilirubin builds up in biliary duct increasing pressure within this duct potentially leading to rupture of the bile canaliculi or lymphatic drainage of the liver. In these ways the conjugated bilirubin is returned to the blood.

35
Q

Gallbladder:

  • stores how much bile?
  • what are the ducts?
A

stores 50-80ml of bile

-heptic ducts, cystic duct, both of these come together to form the common duct.

36
Q

Pancreatic duct

  • what is the main duct that runs the entire length of the pancreas?
  • what is the ductal pressure? What is the purpose of this pressure?
A

Main duct that runs the entire length of the pancreas is the Wirsung duct.

Ductal pressure is 15-30mmhg (compared to 7-17mmhg in Common bile duct). The purpose of this is to prevent bile reflux into the pancreas. Bile reflux into the the pancreatic duct induces SEVERE pancreatitis

37
Q

Pancreas innervation

  • which part of the autonomic nervous system stimulates exocrine and endocrine secretion?
  • which nerve fibers are inhibitory of pancreatic secretions?
A

the parasympathetic fibers stimulate exocrine and endocrine secretion.

sympathetic nerve fibers have inhibitory effects.

38
Q

Pancreas:

  • Exocrine; what are the cells, what is their function?
  • endocrine: what are the cells, what do they secrete?
A

Exocrine: 98%

  • acinar cells
  • secretes essential digestive enzymes (CCK) through pancreatic duct into duodenum.

Endocrine: 2%

  • islets of langerhans
  • alpha cells (glucagon)
  • beta cells (insulin)
  • delta cells (somatostatin)
  • F cells (pancreatic polypeptide)
39
Q

BIcarbonate secretion:

  • what stimulates this
  • what inhibits this
A
  • stimulants: secretin, CCK, gastrin, Ach

- inhibitors: atropine, somatostatin, pancreatic polypeptide, and glucagon

40
Q

WHat enzymes are secreted from the exocrine pancreas? what is their function

A

amylase: hydrolyzes starch and glycogen to glucose, maltose, maltotriose, and dextrins
* ONLY enzyme secreted in active form.

lipase: emulsify and hydrolyze fat in presence of bile salts. requires co-lipase.

41
Q

Adipose tissue

-what are the major hormones secreted? What are their effects?

A
  • resistin; shown to cause high levels of LDL …CVD.
  • adiponectin; protein hormone, modulates glucose regulation and FA oxidation
  • leptin: satiety hormone, regulates energy balance by inhibiting hunger.
42
Q

WHat enzymes are produced in the duodenum?

A
  • intestinal gastrin
  • secretin
  • CCK
  • VIP; stimulates buffer secretion; dilates intestinal capillaries, inhibits HCl production, relaxes intestinal smooth muscle

-Motilin: stimulates migrating motility complex

43
Q

Causes of malabsorption of nutrients

A
  • anything that interferes with delivery of bile or pancreatic juice
  • damaged intestinal mucosa
44
Q

Functions of Small intestine?

What features of the small intestine increase absorptive surface?

A

-electrolyte absorption and water absorption (95% is absorbed via osmosis)

Vili; finger like projections of mucosa

Microvilli: tiny projection on luminal membrane of each intestinal cell. Give apical region appearance called “brush border”

45
Q

What is the function of brush border enzymes?

A

help with the final stage of digestion of nucleic acids, carbs, and proteins so that they are able to enter the capillary blood in the villi and are transported to the liver via the hepatic portal vein.

46
Q

functions of the large intestine

A
  • reabsorb water and compact material into feces
  • absorb vitamins produced by bacteria
  • store fecal matter prior to defecation.
  • ascending: processing chyme
  • transverse: storage and dehydration of feces and primary site for removal of water and electorlytes and the storage of feces
    descending: just a conduit..

rectosigmoid, anal canal, and pelvic flood musculature maintains fecal continence

47
Q

Motility of the large intestine:

-how does material move throughout?

A
  • mixing movements (haustrations); contraction of circular muscle.
  • propulsive movements (mass movement); begins in middle of transverse colon. Preceeded by relaxation of circular muscle and the downstream disappearance of haustral contractions.
48
Q

Large intestine

-function

A

Functions: reabsorption

  • water
  • Vit: K, biotin, B5
  • organic wastes; urobilinogens, sterobilinogens
  • bile salts
  • toxins

*NO VILLI!!! only in the small intestine.

49
Q

The rectum

  • length
  • function
  • unique feature
  • what muscles maintain continence?
A

length: 15cm
function: storage

Unique: sensory receptors of pain, temprature, and touch

Internal anal sphincter and puborectalis muscle maintain continence

50
Q

Anus:

-describe the passage of feces.

A

rectum fills with feces increasing pressure

  • contractions of abdominal and pelvic floor muscles create intra-abdominal pressure which increases intra-rectal pressure.
  • sphincters relax and feces enters the anal canal.
  • peristaltic waves push the feces out of the rectum.
  • relaxation of the internal and external anal sphincers allow the feces to exit from the anus.
  • levator ani muscles pull up the anus over the exiting feces.