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Physiology And Pharmacology > GI Tract > Flashcards

GI Tract Flashcards

1
Q

Role of cholecystokinin

A

Gallbladder contraction Relaxation of sphincter of oddi

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2
Q

Pathway of bile from liver to duodenum

A

Liver to right and left hepatic ducts to common bile duct

cystic duct into gall bladder then to common bile duct joined by pancreatic duct and into duodenum via ampulla and sphincter of oddi

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3
Q

How bile is concentrated in gall bladder

A

Cl and sodium are pumped out in exchange of bicarbonate and water follows by osmosis

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4
Q

Intestinal lipid absorption

A

Before this, triacylglycerides are deesterified by lipase enzymes that separate the glycerol back bone from the hydrocarbon chains, forming glycerol and fatty acids (soluble).

  1. Long chain fatty acids converted back to triglycerides (reesterificatiom) in SER of intestinal endothelium, fat droplets form
  2. Apoproteins from RER go to SER and form chylomicrons and lipoproteins
  3. Chylomicrons migrate to membrane via vesicles, exocytose and go into lymphatic capillaries (lacteals)
  4. Short and medium chain fatty acids and glycerol go straight into cell and into bloodstream because water soluble
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5
Q

Function of bile

A

Allows for breakdown of fatty droplets, increasing surface area for lipases to react with. Bile salts also form vescicles around fats until they are absorbed

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6
Q

What lipases do

A

Breakdown TAG into glycerol group and fatty acids

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7
Q

Role of liver in bile formation

A

Conjugation of unconjugated bilirubin

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8
Q

Transport of bilirubin in plasma and liver

A
  1. Bilirubin from breakdown of erythrocytes travels in blood to liver bound to albumin
  2. In liver, it is conjugated and excreted into bile
  3. In ilium, bilirubin is converted to urobilinogen, then stirocobulin which is the excreted
  4. Part of the urobilinogen goes to the kidneys where it gives urine its yellow color.
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9
Q

causes of Gallstones

A

Too much absorption of water from bile Too much absorption of bile Too much cholesterol in bile Inflammation of epithelium

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10
Q

Simulation of salivation. Parasympathetic and sympathetic, receptors and effects on secretion

A

Parasympathetic NS activate parotid and submandibular glands. Vasodilation. Causes profuse secretion of watery saliva with low organic material. Muscarinic receptors

Sympathetic stimulation of B adrenergic receptors via chorda lingual nerve. Vasoconstriction. Causes low amount of salivary secretion with high organic material

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11
Q

Functions of saliva

A

Digestive, protective, lubrication, speech

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12
Q

Salivary glands

A

Parotid gland

Submandibular gland

Sublingual gland

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13
Q

Primary secretion of saliva

A

In acinar cells concentration of ions isotonic to plasma Secretes proteins

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14
Q

Secondary secretion of saliva

A

in duct cells

Modified concentrations of ions

Na and cl reabsorbed, K and bicarbonate added

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15
Q

Effect of atropine

A

Lowers salivary secretion by blocking muscarinic receptors

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16
Q

Cephalon phase of acid secretion

A

Before and during food being eaten. Initiated via sight or smell, from brain to cells via parasympathetic vagus nerve

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17
Q

Gastric phase of acid secretion

How food stimulates it and what chemicals are involved

A

Phase of when food has been injested. Stimulates by stretching the stomach and raising stomach pH 3 chemicals stimulate HCl and intrinsic factor secretion: 1. Acetylcholine 2. Gastrin 3. Histamine

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18
Q

Intestinal phase of acid secretion

A

Initial stimulation of stomach by the arrival of chyme causing stretch of duodenum. Soon after, enterogastric reflex starts causing inhibition of parasympathetic stimulation and regulation via enteric nervous system CCK released

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19
Q

Retropropulsion

A

Bonus sent back to proximal stomach by contraction of pyloric sphincter

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20
Q

Intrinsic factor

A

Glycoproteins produced by parietal cells that combines with B12 to aid absorption in the ileum

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21
Q

Stomach layers

A

Mucosa

Muscularis mucosa

Submucosa: connective tissue containing vessels

Muscularis: 3 layers of muscle

Serosa: outermost thin connective tissue

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22
Q

Zollinger-Ellison syndrome

A

Cindition where rumors form in pancreas of duodenum that produce large amounts of Gastrin that through the circulation cause increased stomach acid secretion

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23
Q

How mucus and bicarbonate secretion create mucosal barrier

A

Bicarbonate is released by surface mucous cells and acts as a buffer by binding to H

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24
Q

Mechanism of secretion of HCl (endocrine and neurocine activation)

A

G cells, detect food and produce Gastrin in the bloodstream or ACh sends signal via muscarinic receptor.

Gastrin binds to CCK-2 receptors on ECL cells causing them to produce and release histamine.

Histamine binds to H2 receptors on parietal cells and

Parietal cells produce HCl

25
Q

Somatostatin function

A

Acid activated D cells which produce somatostatin. Somatostatin inhibits the production of acid

Quicker and better relief than Histamine inhibitors

26
Q

Omeprazol mechanism of action

A

Inhibits H+/K+ ATPase in parietal cells so no HCl secretion

27
Q

Activation of g cells

A

Acetylcholine

Gastrin Releasing Peptide, peptides and amino acids

28
Q

Composition of pancreatic juice

A

High in bicarbonate (HCO3) to neutralize gastric acid

Proteolytic enzymes (proteins)

Amylase (starch)

Lipase (neutral fats)

29
Q

How secretin and CCK are released and what they activate in the body (2 each)

A

Proteins and fats cause release of CCK, which stimulates secretion of proenzymes (pancreas) and bile (gall bladder)

Low pH causes release of secretioe, which stimulates bicarbonate rich secretion (pancratic juice in pancreas) and the production of bile (liver)

30
Q

Pacemaker cells in GI tract

A

Interstitial cells of Cajal

31
Q

Mechanism that allows for reduced atp usage in smooth muscle

A

Latch bridge mechanism

32
Q

Segmentation

A

The contraction of smooth muscle in small and large intestine, causing the segmentation and separation of food in both directions, allowing for greater mixing.

33
Q

Effect of following on motility

Vagal stimulation

CCK

GIP

Secretin

Sympathetic

Parasympathetic

A

Vagal: increase

CCK: decrease

gIP: decrease

Secretin: decrease

Parasympathetic: both

Sympathetic: inhibits

34
Q

Secretin 3 effects (stomach, liver, pancreas)

A

Stimulates bicarbonate secretion by pancreas

Inhibits stomach activity

Stimulates bile production in liver

35
Q

CCK effects (stomach, gall bladder, pancreas)

A

Stimulates gallbladder contraction

Inhibits stomach activity

stimulates enzyme rich secretions in pancreas

36
Q

Plexuses of enteric nervous system

A

Myenteric and submucosal plexuses

37
Q

Entry and exit of monosaccharides in epithelial cells

A

In (galactose and glucose) glucose sodium symporter (SGLT1)(Fructose) glut 5 transporter

Out: glut2 facilitated diffusion

38
Q

Enzyme responsible for protein breakdown

A

Breakdown of polypeptide: pepsin (stomach)

Breakdown of tri and dipeptides: proteolytic enzymes like trypsin and chymotrypsin (pancreas)

39
Q

Absorption of peptides and amino acids (type of channels)

A

Peptides: H symporter (9pepT1)

Amino acids: sodium symporter

Peptides get transformed to Amino acids by peptidases and out by channel

40
Q

Hartnup disease (digestive deficiency) and inheritance pattern.

A

Autosomal recessive

Reduced absorption of neutral amino acids (e.g. phenylalanine)

41
Q

Cystinuria inheritance pattern and what it is

A

Reduced absorption of free L-arginine. Autosomal recessive.

42
Q

Absorption of vitamin A, E, K

A

A: absorbed in chylomicrons and VLDL, bought to liver

E: Absorbed in chylomicros and VLDL, in the form of alpha and gamma tocopherol. Brought to liver. Alpha form becomes part of hepatically derived VLDL, beta is excreted.

K: Produced by intestinal bacteria and similar to A&E.

43
Q

Vitamin B12 (cobalamine) absorption in the body

A
  1. goes into stomach where it binds to haptocorrin
  2. travels to duodenum where proteases from pancrease causes detachement of haptocorrin
  3. binds with IF in jejunum
  4. gets absorbed in terminal illeum
44
Q

Calcium absorption

A

Vitamin D aids in calcium absorption by causing expression of calcium channel and production of calbindin which aids in absorption

45
Q

Canniculi in parietal cells: what they are and their functions

A

Infoldings on the membrane of parietal cells. Serve to increase surface area.

46
Q

4 molecules that regulate parietal cell secretionsand where they come from

A

Acetylcholine (comes from post ganglionic neurons)

Histamine (comes from mast-like cells of oxyntic mucosa nexxt to parietal cells)

Gastrin (released from G cells of antral mucosa and release into bloodstream)

Somatostatin comes from D-cells which detect acid and inhibit action of the other

47
Q

Jaundice -> what it is, when it becomes pathological

A

Excessive billirubin in bile (normal values are 3-10 mg/ml. pathologic is over 18mg/ml)

48
Q

Activation of bile production by nerve stimulation and secretion of secretin and CCK

A

Nerve impulse initiates bile production.

Acydic chyme in duodenum stimulates secretin secretion into blood.

Fatty acids and AA cause secretion of CCK into blood.

CCK causes gallbladder contraction and secretin causes production of HCO3 rich bile.

49
Q

VLDL

IDL

LDL

HDL

Pathway from VLDL to LDL and role of HDL

From liver to liver

A

VLDL: Package of TAG, cholesterol and apoproteins by the liver. Goes to tissues for distribution.

IDL: produced when VLDL distributes most of it’s TAG, so mostly has cholesterol.

LDL: produced from IDL and only has cholesterol. Distributes it to tissues

HDL: produced by the liver and send empty in the circulation to get any excess cholesterol.

LDL and HDL go back to liver after circulating and depending on chelesterol needs, either get excreted or recirculated.

50
Q

Bile flow is dependent/ independent of liver blood flow past a certain PO2

As blood pressure increases, billiary blood flow ____

A

Bile flow is independent of liver blood flow past a certain PO2

As blood pressure increases, billiary blood flow does not change

51
Q

4 main secretions of the stomach (3 for digestion, 1 for protections)

A

Digestive: HCL, intrinsic factor and pepsin

Protective: mucous

52
Q

Organization of the pancreas cells (Pancreatic duct epithelial cells and acinar cells)

A

Epithelial cells: produce the fluid and bicarbonate rich fluid (stimulated by secretin)

Acinar Cells: produce the proenzymes (stimulated by CCK)

53
Q

What happens to chylomicrons after they have entered lacteals (veins, tissues, liver, new packaging, vein)

A

From the lacteals, they drain in the subcalvian and go through the circulation.

If a muscle cell or other needs them as they pass, enxymes called lipoprotein lipases can break them down into fatty acid and glycerol and take them in for use.

Whatever remains by the time it gets to the liver is called chylomicron remnant. This is taken in by the liver and packaged into VLDL, which can be sent to adipocytes, muscle cells…

54
Q

Parasympathetic and sympathetic neural control of the stomach -> associated neurotransmitters

Parasympathetic (inhibitory and exitatory)
Sympathetic (inhibitory)

A

Parasympathetic inhibitory: VIP (vasoactive intestinal peptide), ADP

Parasympathetic exitatory: acetylcholine

Sympathetic inhibitory: noradrenaline

55
Q

Gastric contractile activity

A

Peristaltic wave towards pylorus every 3 minutes, interstitial cells of cajal. Vigorous mixing occurs at pylorus, a lot gets sent back (retropropulsion).

56
Q

Motilin effects

A

Increases gastric motility

Increases intestinal motility

57
Q

Organization of a villi

A
58
Q

Enzyme responsible for digestion of and products:

Starch

Maltose

Sucrose

Lactose

A

Starch: alha amylase (glucose and maltose)

Maltose: maltase (glucose)

sucrose: sucrase (fructose and glucose)
lactose: lactase (glucose and galactose)

59
Q

What is released by chief cells in the stomach

A

Pepsinogen that gets activated to pepsin

Physiology And Pharmacology (5 decks)

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