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a&P & patho finals > gi tract > Flashcards

gi tract Flashcards

1
Q

4 major functions…

A

motility, secretion, digestion, absorption

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2
Q

length of the digestive tract:

A

8-10 m

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3
Q

most of the absorption occurss in the_____ ______

A

small intestine

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4
Q

absorption in sm intestines depends on

A

transport proteins, secondary MonoSS, AA, Purines/pyrimides, surface area, bile emulsifiers, chylomicrons support of lipids

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5
Q

motility

A

muscle movements that support digestive activities

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6
Q

peristalisis

A

wave motions in the sm intestine that allow food movment to the next segement

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7
Q

migrating myoelectric complex:

A

current that depolarizes smooth muscle cells

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8
Q

segementations:

A

process that occurs in the small in testine that breaks down food bolus into much smaller particles

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9
Q

endocrine hormones

A

gastrin, gherlin, cholecystokinin

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10
Q

exocrine:

A

enzmyes, bile, gastric juices, pancreatic juces (bicarb, bile salts from gallbladder

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11
Q

cephalic phase

A

smells food sitms the stomach to produce gastric juices

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12
Q

gastric phase

A

Proteins: AA in stomach stims the receptors to further promote local secretion of gastrin, gastric juces/motility enteric nervous system

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13
Q

interstitial phase

A

as chyme reaches sm intestine chem receptors stim SI to release hormones that decrease stomach stomach motility+

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14
Q

protiens involved in digestion

A

trypsin, chymotrypsin, brush border peptidases

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15
Q

carbs involved in digestion

A

poly ss, bursh border ss

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16
Q

nucleic acids involved in digestion

A

nucleases, bursh boarder

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17
Q

lipids

A

bile/salts/lecithin, brush border

18
Q

how can lipids be broken down?

A

simple diffusion, exocrine enterokinase will convert typsinogen into tyrpsin ( active form), endocrine: cholecystokinin ( decreases gastric juces & promotes breakdown), secretin: occurs when Hcl & lipids enter the duodenum–> decreases gastric juices

19
Q

potential pacemaker of bowels…..

A

segmentation

20
Q

accessory organs

A

liver (bile salts), pancreas(exocine: pancreatic jucies secreted through the pancreatic duct–> common bile duct–> secretes in the duodenum via sphincter of Oddi, endocrine: primary secretion are insulin & glucagon

21
Q

pancreatic secretions:

A

HCO3—+ph in duodenum (secretion stimmed by secretin)
Trypsinogen
Chymotrypsin
Amylase
Lipase
nuclease(secretion stim by cholecystokinin (CCK)

22
Q

Hiatal hernia

A

When part of the stomach passes through the diaphragm into the chest cavity
Pregnancy, hort esophagus, weak diaphragm
Patho:
Sliding→ esophagus & stomach move together
Paraesophageal ( rolling)- fundus moves through the diaphragm( can become tangled)–> ischemic
Clinical manifestations:
Heartburn, reflux of stomach contents into esophagus, worse when supine, bending over, coughing→ dysphagia
Tx: surgical repair; eat many small meals- do not lie down after eating

23
Q

GERD- gastroesophageal reflux disease

A

tomach contents irritate lining of esophagus causing I/N/F→ scarring→stenosis
Clinical manifestations: heartburn 30-60 mins after eating

24
Q

pepic ulcers is mainly cuased by…manifestations….

A

H pylori infection, characterized by Pain 2-3 hours after meal/ when lying down and relieved by eating food, heartburn, N/V, weight changes, risk of iron deficiency, occult blood in stool

25
Q

gastritis

A

inflammation of stomach
acute ( spicy food),chronic (alcohol abuse), gastoenteritis ( infection of the stomach)- staph

26
Q

gallstones (cholelithiasis)

A

too much cholsterol/billirubin
common in females, + cholesterol diets, multipar—> inflammation, jaundice, pancreatitis, colicky RUQ pain (reffered)

27
Q

what causes jaundice?

A

too much conjugated/unconjugated billirubin
( unconjugated= difficult to clear/conjugated–> cuaes puritis)

28
Q

hepatitis

A

can be viral/toxic–> can cause necrosis and scarring of the liver,

pre-icteric:jaundice/fatigue, Nausea, headache, RUQ pain, eleated liver enxymes

Icteric: Intrahepatic jaundice→ CM of jaundice
Bilirubin may be conjugated→ dark urine, pruritus, enlarged & tender liver, trouble making bile→ light coloured stool

post-icteric: recovery ( 16 weeks)

29
Q

cirrohsis

A

diffus fibrosis of liver/los of organization
1) fatt liver ( alchoholism)
2) alcohol hepatitis: chronic inflammation–> necrosis of hepatocytes
3)end stage–> failure

30
Q

loss of hepatocyte function causes ….

A
  • Impaired metabolism of macromolecules, drugs
    Impaired digestion/absorption of lipids
    Prolonged clotting times
    Decreased conjugation of bilirubin
31
Q

loss of bile causes…

A
  • impaired digestion/absorption of lipids, post-hepatic jaundice if the bile ducts= compressed by scarring
    Portal HTN: splenomegaly, esophageal varices, ++ pressure in the mesenteric GI vessels, ascites
32
Q

acute pancreatitis

A

ob of the duct (alc abuse)

33
Q

chronic pancreatitis

A

chronic inflammtion—. necrosis/fibrosis/alt hormone secretion

34
Q

cIBD/CHronhs disease

A

inflammation & excessive release of cytokines—> lesions of the mucosa in the SI

35
Q

ulcerative colitis

A

Inflammation of excessive release of cytokines stress, inflammation in rectum, moves proximally, deeper lesion—> submucosa

36
Q

appendicitis

A

bacteria reproduce causing inflammation, swelling & compression of BV→ ischemia→ necrosis of walls-peritonitis
Manifestations: periumbilical pain, severe LRQ pain n/v, bursts can go away and be more diffuse, hypotension/tachycardia, systemic signs of inflammation

37
Q

Peritonitis:

A

chemical causes ex: pancreatitis
bacterial: burst appendix
Patho:
Bowel inflammation__> ++ permeability allowing bacteria to leave the GI tract and infect the peritoneum
Exudate secreted by the peritoneum to seal fluids, bacteria→ formation of abscess
Abdominal distention→ contraction of abdominal muscles
Fluid in the peritoneal space

38
Q

peritonitis manifestations

A

Sudden-diffuse pain that’s exacerbated when moving
N/V from p, irritation of intestines
Trouble breathing
Hypovolemia ( shocky)- pallor, dry, tachycardia hypotension
Abdo distention/rigidity
No bowel sounds→ secondary functional ob→ paralytic ileus

39
Q

intestinal ob

A

Mechanical or functional
Patho: mechanical
Stretch of smooth muscle before ob→ cells of S.M contract increasing p in veins→ edema
Excess of fluids leads to emesis—> imbalances
Loss of motility, -bowel sounds
Inflammation due to bacterial overgrowth—> peritonitis→sepsis
Patho:functional
Same as mechanical though no reflex of the S.M

40
Q

intestinal ob manifestations:

A

SI
Severe colicky pain during s.m contraction w sounds, paralytic ileus ( no sounds), V of materials before the ob & may include bile ( poop), anxiety, diaphoresis, tachycardia, hypovolemia/dehydration—> shock
LG
slowly/milder CM, mild pain, C/A, when abdo→distended=more p

a&P & patho finals (7 decks)

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