Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI > Physiology > Flashcards

Physiology Flashcards

1
Q

Layers of the GI wall?

A
  • mucosa:
    innermost layer, layer of epithelial cells specialized for absorption and secretion, highly vascularized
  • submucosa: consists of collagen, elastin, glands, and blood vessels
  • circular and longitudinal smooth muscle: provides motility for GI tract
  • Serosa: faces the blood, not found in the esophagus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Fxn of the mouth? Enzymes?

A
  • mostly mechanical digestion: mastication - food is broken down into small particles so food particles can be chemically digested - form a bolus
  • enzymes: lingual amylase and lingual lipase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is involved in swallowing?

A
  • 26 muscles and 5 cranial nerves (5, 7, 9, 10, 12)
  • esophageal: begins with cricopharyngeal relaxation, involuntary
  • permanent spasm ( cramping of muscle, UES will remain closed)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Composition of saliva?

A
  • secreted by serous nad mucous cells
  • 97-99.5% water, slightly acidic
  • lytes
  • salivary amylase and lingual lipase
  • mucin
  • metabolic wastes: urea, uric acid
  • lysozyme, IgA and cyanide compound protect against microorganisms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Fxns of saliva?

A
  • salivary glands produce 1 L/ day of saliva
  • each gland delivers saliva to mouth through a duct
  • initial digestion of starches and lipids by enzymes
  • dilution and buffering of ingested foods
  • lubrication of ingested food to aid its movement
  • many more fxns
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Secretion impt in GI?Produced by?

A
  • addition of fluids, enzymes, lytes, and mucus to lumen of GI tract
  • secretions produced by:
    salivary glands
    gastric mucosal cells (gastric secretion)
    pancreatic exocrine cells (pancreatic secretion)
    liver (bile)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Fxn of stomach, small and large intestine?

A
  • stomach: digestion and break down of food to smaller, absorb-able particles
  • small intestine: absorption of nutrients
  • large intestine: absorption of water
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

parts of the stomach? Specialized for?

A
  • specialized for accumulation of food: capable of expanding, can hold 2-3 L
  • gastric juice converts food into semiliquid (Chyme)
  • 4 parts: cardia, fundus, body and pylorus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Fxns of stomach?

A
  • short term reservoir
  • absorption, digestion and secretion
  • chemical and enzymatic digestion is initiated, particularly of proteins
  • liquefication of food - into chyme
  • slowly released into small intestine for further processing
  • stomach uses pepsin and peptidase (enzymes) to break down proteins
  • acid provides good enviro for enzymes to work in
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

3 phases of digestion?

A
  • cephalic phase: cortex, amygdala, and hypothalamus (through vagus nerve)
  • gastric phase: hydrochloric acid and pepsin
  • intestinal phase: enterogastrone hormones secreted in duodenum and lower GI tract
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Gastric secretion of enzymes?

A
  • gastric mucosal cells secrete gastric juice: HCL and pepsinogen intiate protein digestion, intrinsic factor reqd for absorption of Vit B12. Mucus protects gastric mucosa from HCL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Cell types of gastric mucosa (secretion)?

A
  • body of stomach contains oxyntic glands:
    parietal cells: HCl and intrinsic fator
    chief cells: pepsinogen
  • antrum of stomach contains pyloric glands:
    G cells: Gastrin into circulation,
    mucous neck cells: mucus, HCO3, and pepsinogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Secretion and fxn of gastrin?

A
  • secreted by G cells in stomach in response to eating: stimuli include proteins, dissension of stomach, and vagal stimulation
  • gastrin releasing pepride (GRP): released from vagal nerve endings onto G cells
  • promotes H+ secretion by gastric parietal cells
  • stimulates growth of gastric mucosa
  • other fxns:
    1: pepsinogen release
    2: increase stomach motility
    3: relax pylorix sphincter
    4: contract LES
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Fxn of ACh?

A
  • released from vagus nerve
  • binds to receptors on parietal cells
  • produces H+ secretion by parietal cells
  • atropine blocks muscarinic receptors on parietal cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Fxn of histamine?

A
  • released from mastlike cells in gastric mucosa
  • binds to H2 receptors on parietal cells
  • produces H+ secretion by parietal cells
  • cimetidine blocks H2 receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Peptic ulcer pathogenesis?

A
  • H pylori
  • NSAIDs/ ASA
  • cigarettes, ETOH
  • decreased mucous secretion
  • delayed gastric emptying
  • decreased prostaglandin synthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are segementation contractions?

A
  • circular muscle contracts sending chyme in both directions

- intestine then relaxes allowing chyme to merge back together

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are peristaltic contractions?

A
  • longitudinal muscle contracts propelling chyme along small intestine
  • simultaneously, portion of intestine caudad to bolus relaxes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

UGI bleeding most common causes?

A
  • duodenal ulcer
  • gastric erosion, itis
  • GU
  • varices
  • M-W tear
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Innervation of the GI tract?

A
  • autonomic nervous system has extrinsic and intrinsic component
  • extrinsic: sympathetic and parasympathetic innervation
  • intrinsic: enteric nervous system, contained within wall of GI tract, communicates with extrinsic component
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Where does parasympathetic nerve supply come from?

A
  • nucleus ambiguus and dorsal motor nucleus of vagus nerve

- provides motor innervation to the esophageal muscular coat and secretomotor innervation of glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Where does sympathetic nerve supply come from?

A
  • cervical and thoracic sympathetic chain
  • regulates blood vessel constriction, esophageal sphincters contractions, relaxation of muscular wall and increases in glandular and peristaltic activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Fxn of intrinsic innervation?

A

can direct all fxns of GI in absence of extrinsic innervation

  • controls contractile, secretory, and endocrine fxns of GI tract
  • receives input from:
    1. parasympathetic and sympathetic nervous systems
    2. mechanoreceptors and chemoreceptors in mucosa
  • sends info directly to smooth muscle, secretory, and endocrine cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

4 fxnly diff cell types in stomach glands? What are gastric pits?

A
  • gastic mucosa has numerous openings called gastric pits
  • gastric glands empty into bottom of pits
  • 4 diff celly types compose glands -
    mucous cells
    chief cells
    Tparietal cells
    enteroendocrine cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Steps of cephalic phase?

A
  1. sight and thought of food activate cerebral cortex
  2. stimulation of taste and smell receptors
    - activate hypothalmus and medulla oblongata - send impulse down vagus nerve
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Gastric phase?

A
    1. stomach distension activates stretch receptors = vagovagal reflexes - medulla an dthen vagus nerve and local reflexes
    1. food chemicals (esp peptides and caffeine) and rising pH activate chemoreceptors - activate G cells to release gastrin into blood
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Intestinal phase?

A
    1. presence of low pH, partially digested foods, fats, or hypertonic soln in duodenum when stomach begins to empty - leads to intestinal gastrin release to blood
      (gastrin stimulates gastric emptying)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Small intestine is primary site for?

A
  • digestion and absorption of nutrients

- bile duct and pancreatic duct empty into duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Blood flow into liver?

A
  • largest internal organ
  • receives major blood supply from hepatic portal vein: brings venous blood rich in nutrients from digestive tract
  • high blood flow: 1350 ml/min to liver sinusoids (1050 from portal vein and 300 from hepatic artery) = fxnl and nutritive blood circulation
  • physiologically: low vascular resistance (small difference b/t pressures in portal vein and hepatic vein) - in cirrhosis: vascular resistance increases, and blood flow decreases (leads to portal HTN and ascites)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Sinusoids fxn like?

A
  • blood capillaries
  • hepatocytes are in contact with blood in sinusoids within the liver
  • arranged to form fxn units called lobules
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Hepatic fxn?

A
  1. carb metabolism
  2. lipid metabolism
  3. protein metabolism
  4. removal of drugs and hormones
  5. excretion/secretion of bilirubin
  6. synthesis of bile salts
  7. storage of some compounds
  8. phagocytosis
  9. aids in synthesis of active Vitamin D
  10. urea formation from ammonium
32
Q

Why is hyperglycemia common in pts with cirrhosis after eating a carb rich meal?

A
  • combo of pathological glucose tolerance test, hyperinsulinemia and increase insulin tolerance (liver insufficiency - leads to decrease of glucose utilization - leads to hyperglycemia - leads to hyperinsulinemia - leads to downregulation fo insulin receptors and insulin resistance)
33
Q

Why does hypoglycemia occur in alcohol abusers?

A
  • alcohol suppresses citrate cycle and thereby impairs gluconeogenesis from amino acids
34
Q

Process of carb breakdown?

A
  • carbs - broken down into disaccharides and then into monosaccharides
35
Q

Process of protein breakdown?

A
  • proteins - broken down into peptides and then into AA’s
36
Q

Process of lipid breakdown?

A
  • lipids get broken down into diglycerides and then into monoglycerides and fatty acids
37
Q

How are carbs absorbed?

A
  • monosaccharides (mostly glucose) are absorbed
  • monomers are carrid by transporter molecules across the epithelial cells and into blood capillary present in villus - into portal vein and into liver
38
Q

Fat metabolism?

A
  • oxidation of fatty acids to supply energy for other body fxn
  • synthesis of large quantities of cholesterol (80% of cholesterol synthesized in liver is converted into bile salts), phospholipids, and most lipoproteins
  • inactivation of steroids and their excretion from the body
39
Q

What can hyperammonemia lead to and what are symptoms?

A
  • can lead to hepatic encephalopathy = toxic effect of ammonia in the brain
  • mental changes (disorientation, sleeping disorders, chaotic speech, personality changes)
  • motor changes (increased in muscle reactivity, hyperreflexia, tremor)
40
Q

Bile secretion is necessary for?

A
  • digestion and absorption of liquids in small intestine
  • mix of bile salts, bile pigments, and cholesterol
  • bile salts emulsify lipids to prepare them for digestion
41
Q

steps of bile secretion and recycling?

A
  1. produced and secreted by liver
  2. stored in gallbladder
  3. ejected into small intestine when gallbladder contracts
  4. after lipids absorbed, bile salts are recirculated to liver via enterohepatic circulation:
    absorption of bile salts from ileum into portal circulation, and delivery back to liver
  5. extraction of bile salts from portal blood by hepatocytes
42
Q

How is bilirubin formed and how is it conjugated?

A
  • from hemoglobin
  • Hb is phagocytosed by tissue macrophages int he spleen
  • iron released in bound to transferrin and transported in the blood
  • the remainder of heme group is converted to biliverdin, which is rapidly reduced to bilirubin
  • bilirubin is attached to albumin
  • albumin is removed as unconjugated bili passes through the hepatocyte membrane
  • bili is conjugated with glucoronic acid, sulphate
  • conjugated bili has higher solubility
  • hepatocytes actively transport conjugated bili into bile canaliculi
  • conjugate bili then enters duodenum through sphinter of oddi
43
Q

Role of small intestine in bile metabolism?

What happens to reabsorbed urobilirubin?

A
  • bile and bile salts increase growth of intestinal bacteria
  • in return, intestinal bacteria metabolize conjugated bile into urobilirubin
  • this is highly soluble an dis reabsorbed back into blood
  • 95% of reabsorbed urobilirubin is excreted again by liver into bile
  • 5% is excreted into urine
  • small part excreted into feces
44
Q

When does the sphincter of oddi open?

A
  • within 30 min of food intake, presence of aminoacids and fatty acids in duodenum activates cholecystokinin which causes gallbladder contractions and excretion of bile
  • 50-1000 ml of bile is produced daily
  • bile is concentrated in gallbladder
45
Q

Detectable jaundice - at what total plasma bili?

Causes?

A
  • detectable when above 2 mg/dL (will see in sclera)

causes:

  • excess production of bili (hemolytic anemia)
  • decreased uptake of bili into hepatic cells
  • disturbed intracellular protein binding or conjugation
  • disturbed secretion of conjugated bili into bile canaliculi
  • intrahepatic or extrahepatic bile duct obstruction
46
Q

What causes obstructive jaundice?

A
  • bile is prevented from flowing out of biliary duct
  • occurs if gall stones or tumors block the duct
  • conjugated bili builds up in biliary duct, pressure within biliary duct increases
  • conjugated bili is returned to blood, either by rupture of bile canaliculi or via lymphatic drainage of liver
  • conj. bili in blood is good dx test for obstructive jaundice
  • unconjugated levels with be either normal or decreased
47
Q

Fxn of gallbladder?

A
  • stores bile (50 ml)
48
Q

Other impt fxns of liver?

A
  • formation and secretion of bile
  • detoxificaiton of various substances: metabolic products of intestinal microbes, exogenous toxins (alcohol, meds, poisons), hormones
  • synthesis of plasma proteins: albumin, clotting factors
    coag: synth. of coag factors
  • blood reservoir: filtration, storage of blood
  • immunity: kupffer cells = macrophages
  • vitamins: metabolism and storage of vitamins A, D, B12
  • relation to blood formation: storage of vitamin B12, metabolism of Fe and its storage as ferritin, production of erythropoiein
49
Q

Cirrhosis leads to what?

A
  • 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 diseases such as varices and ascites
50
Q

How is relfux of pancreatic duct prevented?

A
  • ductal pressure is 15-30 mm Hg vs 7-17 in CBD thus preventing reflux an damage
51
Q

Main pancreatic duct?

A
  • duct of wirsung, runs the entire length of the pancreas

- joins CBD at ampulla of Vater

52
Q

Innervation of pancreas?

A
  • sympathetic fibers from splanchnic nerves
  • parasympathetic fibers from vagus
  • parasympathetic fibers stim both exocrine and endocrine secretion
  • sympathetic fibers have inhibitory effect
  • rich afferent sensory fiber network
  • ganglionectomy or celiac ganglion blockade interrupt somatic fibers (pancreatic pain)
53
Q

Fxn of acinar cells of pancreas?

A
  • Exocrine: secretes essential digestive enzymes through pancreatic duct into duodenum
54
Q

Endocrine cells of pancreas?

A
  • islets of langerhans
  • 4 major cell types:
    alpha cells: glucagon
    beta cells: insulin
    delta cells: somatostatin
    F cells: pancreatic polypeptide (secretes insulin and glucagon into blood stream)
55
Q

Physiology of exocrine pancreas?

A
  • 500-800 ml pancreatic fluid secreted/day
  • alkaline pH results from secreted bicarb which neutralizes gastric acid and regulate pH of the intestine
  • enzymes digest carbs, proteins, and fats
56
Q

What hormones stimulate and inhibit bicarb secretion?

A
  • major stimulants: secretin, cholecystokinin, gastrin, acetylcholine
  • major inhibitors: atropine, somatostatin, pancreatic polypeptide and glucagon
  • secretin: released from duodenal mucoas in response to duodenal luminal pH of less than 3
57
Q

Only digestive enzyme secreted by pancreas in its active form?

A
  • amylase
  • fxns optimally at pH of 7
  • hydrolyzes starch and glycogen to glucose, maltose, maltotriose, and dextrines
58
Q

Lipase fxns optimally at what pH? fxn?

A
  • at pH of 7-9

- emulsify and hydrolyze fat in presence of bile salts

59
Q

Most impt stimulant of acinar cells?

A
  • CCK

- secretion of CCK in presence of amino acids and fatty acids in intestinal lumen

60
Q

Major stimulant of ductal cells?

A
  • aqueous secretion of HCO3
  • secretin
  • secreted in response to H+ in intestine
61
Q

Most impt adipose secretions?

A
  • resistin
  • adiponectin
  • leptin
62
Q

How does obesity lead to hyperglycemia?

A
  • increased adiposity leads to decreased adiponection which leads to:
  • IRS-1 and decreased glucose uptake
  • decrease in fatty acid oxidation and decreased FFA clearance
  • increase in gluconeogenesis
63
Q

Why is the 3rd portion of the duodenum the most vulnerable to traumatic rupture?

A
  • because it is the most fixed portion of the duodenum
64
Q

Fxn of GI peptides?

A
  • includes hormones, neurocrines, and paracrines

regulate fxns of GI tract:

  • contraction and relaxation of smooth muscle wall and sphincters
  • secretion of enzymes for digestion
  • secretion of fluids and electrolytes
  • regulate secretion of other GI peptides
65
Q

Fxns of the small intestine?

A

electrolyte absorption:

  • mostly along length of small intestine
  • Fe and Ca2+ absorption
  • Na+ coupled with absorption of glucose and amino acids
  • ionic iron stored in mucosal cells with ferritin
  • K+ diffuses in respones to osmotic gradients
  • Ca2+ absorption reg by vit D and PTH

water absorption:
95% absorbed in small intestine by osmosis, water uptake coupled with solute uptake

66
Q

What increases the small intestine’ absorptive surface area?

A
  • intestinal lining
  • villi: finger like projections of mucosa
  • microvilli: tiny projections on luminal membrane of each intestinal cell
  • gives apical region striated appearance called brush border
67
Q

Process of carbohydrate absorption?

A
  • monosaccharides glucose and galactose are absorbed via cotransport with Na ions, all monosaccharides enter capillary blood in villi and are transported to liver via the hepatic portal vein
  • occurs in small intestine (brush border)
68
Q

Process of protein absorption?

A
  • through pepsin (stomach), pancreatic enzymes and brush border of small intestine
  • amino acids are absorbed via cotransport with Na, enter capillary blood in villi and are transported to liver via hepatic portal vein
69
Q

Process of fat absorption?

A
  • emulsified by detergent action of bile salts ducted in from the liver and pancreatic lipase in small intestine
  • digestion by pancreatic enzyme lipase yields free fatty acids and monoglycerides. These then often assoc with bile salts to form micelles which ferry tehm to intestinal mucosa
  • fatty acids and monoglycerides leave micelles and diffuse into epithelial cells, there they are recombined and packaged with other fatty substances and proteins to form chylomicrons
  • chylomicrons are extruded from epithelial cells by exocytosis. Chylomicrons enter lacteals and are carried away from the intestine in the lymph
70
Q

Fxns of the large intestine?

A
  • reabsorb water and compact material into feces
  • absorb vitamins produced by bacteria
  • store fecal matter prior to defecation
71
Q

Physiology of diff colon regions?

A
  1. ascending colon: specialized for processing chyme delivered from terminal ileum
  2. transverse colon: specialized for storage and dehydration of feces and is primary site for removal of water and electrolytes and storage of feces
  3. descending colon: conduit b/t transverse and sigmoid colon
  4. rectosigmoid region, anal canal, and pelvic floor musculature maintains fecal continence - sigmoid and rectum are reservoirs with capacity up to 500 mL
72
Q

Fxn of colon?

A
  • proximal half of colon is concerned with absorption and distal half fxns in storage
  • transit of small labeled markers through large intestine occurs in 36-48 hrs
  • movement of colon acccomplished by haustrations (mixing movements) and mass movements (propulsive movements)
73
Q

What may trigger mass movements?

A
  • increased delivery of ileal chyme into ascending colon following a meal (gastrocolic reflex)
  • irritants: castor oil, threatening agents such as parasites and enterotoxins can initiate mass movement
  • starts in middle of transverse colon and is preceded by relaxation of circular muscle and downstream disappearance of haustral contractions
74
Q

Reabsorption in large intestine includes?

A
  • water
  • vitamins: K, biotin, B5
  • organic wastes: urobilongens and sterobilinogens
  • bile salts
  • toxins
  • no villi
  • mucosa contains numerous tubular glands called crypts (responsible for mucus secretion)
75
Q

Major fxn of the rectum?

A
  • last portion of digestive tract
  • terminates at the anal canal
  • 15 cm
  • storage is the major fxn
76
Q

How does sensory innervation maintain continence of the bowel?

A
  • mechanoreceptors in rectum detect distension and supply ENS
  • anal canal in region of skin is innervated by somatosensory nerves that transmit signals to CNS
  • this region has sensory receptors of pain, temp, and touch
  • contraction of internal anal sphincter and puborectalis msucle blocks the psasage of feces and maintains continence
77
Q

Process of BM through anus?

A
  • rectum fills with feces leads to increasing pressure
  • contractions of abdominal and pelvic floor muscles create intra-abdominal pressure which:
  • increases intra-rectal pressure
  • sphincters relaxes
  • then feces enter the canal
  • peristaltic waves push feces out of the rectum
  • relaxation of internal and external anal sphincters allows the feces to exit from the anus
  • levatori ani muscles pull anus up over exiting feces (physiologic valve)

GI (21 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions