Gi Physiology And Biochemistry (L09, L11, L14, L18, L21)

Front 1

functions of colon 3

Back 1

Storage, concentration of undigested material
Electrolyte & water transport
Propulsion of content

Front 2

regulation of reflexes of GI tract mechanism 3

Back 2

1. Neural regulation
a. Short neural reflex
b. Long neural reflex
2. Chemical regulation
 Endocrine
 Paracrine

Front 3

difference between the short and long neural reflexes 2

Back 3

1. Short reflexes (from GI receptors through enteric nerve plexuses to effector cells)
2. Long reflexes (from GI receptors to CNS by afferent nerves & back to enteric nerve plexuses and effector cells by way of ANS)
(Parasympathetic: excitatory; Sympathetic: inhibitory)

Front 4

list the major GI hormones and paracrines 5+2

Back 4

Major GI hormones - Gastrin, cholecytokinin, secretin, GIP, motilin
Paracrines - Histamine, Somatostatin

Front 5

what is the function of D cell and G cell and ECL cell

Back 5

enterochromaffin-like (ECL) cells – histamine
D-Cells – somatostatin
G-cells – gastrin

Front 6

gastric juice components

Back 6

NaCl KCl and HCl

Front 7

mechanism of HCl secretion 2+2

Back 7

breakdown of water to form H+ and excrete to lumen by H+/K+ antitransport (requice ATP).
there is K+ pump outflux for replacing K+
bicarbonate is produced and excrete into Blood via bicarbonate/Cl- antitransport
CFTR Cl - channel: Cl - outflux for recycling

CFTR = Cystic fibrosis transmembrane conductance regulator

Front 8

regulation of HCl secretion

Back 8

1. gastrin - by G cell (hormonal)
functions: promote ECL cells secretion (no. and size) and act on the CCK-beta receptor to activate increase Ca level
2. ECL cell secrete histamine (paracrine)- histamine act one he H2 receptor to activate adenylate cyclase to form cAMP
3. neural control: Ach act on muscarinic receptor => IP3 to increase Ca level; also increase gastrin and histamine
4. somatostatin : inhibition of HCl secretion

Front 9

stimulation and inhibition of HCl secretion three phases and their specific action 3+3

Back 9

1. cephalic phase (chewing, sight) promote the Ach released by vagus nerve
2. gastric phase
2.1 distension of stomach - vasovagal reflex
2.2 proteins product in stomach - gastrin secretion
3. intestinal phase - distension, acidity, nutrients conc. => inhibition by decrease secretin and release somatostatin.
distension of duodenum =>vagovagal reflex

Enterogastrone (CCK and secretin) - secreted by intestines.

Front 10

regulation of secretion of pepsinogen (from chief cell)

Back 10

simulation:
neural: ACh from vagus & enteric nerve plexuses;
high acidity: acid in stomach through local nerve reflex

inhibition
excess acidity (ph <3) => increase somatostatin => decease acid & gastrin secretion

Front 11

mucous and bicarbonate functions and production sites 2

Back 11

produced in mucous neck cell and columnar epithelial cells -
a physical and alkaline barrier to protect against pepsin and acid.
almost neutral at the base

Front 12

drugs/factors that inhibit mucous and bicarbonate secretion 2

Back 12

adrenergic agonist => decrease carbonate
NSAID => decrease bicarbonate and mucus secretion
predispose to ulcer and gastritis

Front 13

intrinsic factor production site and functions

Back 13

produced in parietal cells - intrinsic factor is important for the absorption of vit B12.

Front 14

consequence of insufficient / no Vit B12

Back 14

1. megaloblastic anemia - inhibit DNA syn, growth of cell without cell division
2. pernicious anemia - due to autoimmune destruction of parietal cells => no intrinsic factor => NO RBC maturation

Front 15

carbohydrate digestion
different sites, their enzymes, and reaction involved
4 sites,

Back 15

mouth cavity:
salivary amylase: starch → α-dextrins
endoglucosidase, cleave α-1,4 glycosidic bonds
optimal pH ~ 6-7.9, maintained by bicarbonate ion in saliva

Duodenum pancreatic amylase
starch, α-dextrins → disaccharide
DO NOT cleave α-1,6 glycosidic bonds

Small Intestinal brush border
maltase, isomaltase, lactase, sucrase

Fermentation in colon
when high amylase, less well hydragrated dietary fibres and undigested sugars
fermentation by colonic bacteria: saccharides → gases, FA, lactate

Front 16

pathology of carbohydrate digestion 3
and clinical presentation 3

Back 16

primary deficiency of carbohydrase
- low synthesis rates / mutated genes → deficiency
secondary to malabsorption
- accumulation of undigested saccharide in large bowl
secondary to intestinal injury
- brush border epithelium damage

clinical presentation
1. copious flatus and hyperactive bowel sounds (gas)
2. explosive diarrhea (partially digested saccharides, retain of water, osmotic effect => water retention
3. abdomen distention and cramps (water and gas)

Front 17

protein digestion sites and reactions
three phrases

Back 17

gastric
pepsin secretion excite CCK and secretin => intestinal and pancreatic secretion of trypsin and inhibit HCl production
protein → polypeptides

pancreatic
enteropeptidase: trypsinogen → trypsin
- chymotrypsinogen → chymotrypsin
- proelastase → elastase
- procarboxypeptidase → carboxypeptidase

small intestinal brush border
- aminopeptidases
- intracellular peptidases (Dipeptidase, Tripeptidase, endopeptidase)
- peptides → a.a.

Front 18

Pancreatitis pathology 2pts

Back 18

inflam. of the pancreas due to activation of pancreatic enzymes (esp. trypsin)

within the pancreas → autodigestion

- usually involve malfunction in genes coding for trypsin inhibitor / regulator (eg. SPINK1, CTRC)

Front 19

lipid digestion phrases and reactions involve

Back 19

1. lingual and gastric lipase for short chain FA
2. Duodenum
2.1 bile salts - emulsification
2.2 pancreatic lipase: TG/DG → FA + 2-MG
inhibited by bile salts
colipase: bind FA and lipase tgt; overcome the bile salts
2.3 lipid esterase: vit A esterase, chol. esterase (need bile salts)
2.4 phospholipase A2 (need bile salts)

Front 20

Regulation of pancreatic exocrine secretion 3

Back 20

1. Cephalic phase (minor)
sight, smell, taste, chewing of food → ACh release by vagus nerve

2. Gastric phase (negligible)
- nervous stimulation

3. Intestinal phase (major) (hormonal and neural)
3.1 acid chyme → S-cells → secretin
secretion of large amount of water & bicarbonate

3.2 partially digested protein & fat → I-cells → CCK
secretion of pancreatic enzymes

3.3 CCK also stimulates the contraction of gallbladder
relaxation of sphincter of Oddi

3.4 vagus nerve - ACh as neurotransmitter
to promote acinar cells secretion

Front 21

content of bile 6

Back 21

water + electrolytes + organic compounds (bile acids, chol, phospholipids, bilirubin)

Front 22

synthesis of bile salt 4

Back 22

1. syn. by hepatocytes from chol.
2. primary bile acid (major): cholic acid, chenodeoxycholic acid
3. secondary bile acid (intestinal bacteria): deoxycholic acid, lithocholic acid

conjugated bile acid (=bile salt): glycine & taurine – conjugation  of  1°  &  2°  bile  acids

Front 23

secretion of bile salts 4

Back 23

First stage: Hepatocytes secrete fluid rich in bile salts, chol and other organic
compounds → canaliculi → bile duct

Second stage: Ductal epithelial cells add water and bicarbonate (← secretin)

Storage & conc: Bile enters gall bladder between meals → concentrated by reabsorption of water & electrolytes

Release: During meals → CCK → gall bladder contracts and release bile
(CCK under neural and hormonal control)

Front 24

digestive Functions of biliary secretion 3

another biliary secretion function 1

Back 24

bile acid: aid fat digestion & absorption, promote absorption of fat-soluble Vit

bicarbonate: neutralizes acid chyme

excretory function (bile pigments, excess chol, drugs)

Front 25

movement of food during swallowing (3 phrases)

Back 25

1. Oral phase: Voluntary transfer of food or drink to pharynx by tongue
2. Pharyngeal Phase: Elevation of soft palate to prevent food from entering nasal cavity; larynx raised; glottis closed; respiration inhibited;
Epiglottis cover glottis to prevent food from entering trachea (aspiration)
3. Esophageal phase: relaxation of upper esophageal sphincter; closure of sphincter after passage of food; glottis opens; breathing resumes;
peristaltic waves move food down esophagus towards stomach; relaxation of lower esophageal sphincter; receptive relaxation of stomach; then closure of lower esophageal sphincter.

Front 26

movement of food through esophagus

Back 26

from higher intraluminal pressure to lower pressure

Front 27

swallowing reflex

Back 27

afferent and efferent nerve supply
control swallowing center

Front 28

assistance in movement of food through esophagus 4

Back 28

primary peristaltic contractions
secondary peristaltic contractions
Upper sphincter
lower sphincter

Front 29

causes of dysphagia 4

Back 29

1. Painful disease of mouth & pharynx
e.g. Stomatitis, ulcers
2. Paralysis of mechanisms of swallowing
(Neural causes e.g. damage of swallowing centre e.g.
poliomyelities; damage in nerves involved in swallowing;
Neuromuscular transmission e.g. myasthenia gravis;
Muscular e.g. muscle dystrophy;
Motility e.g. achalasia)
3. External compression on esophagus
e.g. goitre, enlarged lymph nodes
4. Intrinsic disease of esophagus
e.g. stricture, cancer of esophagus

Front 30

Motor Functions of Stomach 3 functions in fed state

Back 30

1. storage of food - receptive relaxation
mediated by vagovagal reflex and coordinated by swallowing centre
2. mixing and grinding contractions mix ingested food with gastric juice, digestion and solubilize food substances, reduce particle size
3. controlled emptying: optimal time for intestinal digestion and absorption

Front 31

mixing two types

Back 31

slow waves:
regular depolarization => 3-5 waves per minute => weak contraction => weak mixing effect

contraction in natrum: retropulsion
=> propel the chyme back
break down and mix food

Front 32

coordination / control of gastric emptying

reason
structure
mechanism
control

Back 32

structure: phyloric sphincter
emptying process: antral peristaltic contraction

Regulation by both neural & hormonal:
- weak gastric factors promote emptying (stretch teh wall)
- duodenal factors inhibit emptying (distension of duodenum & presence of hypertonic solutions, low pH, fatty acids or monoglycerides in the duodenum)
- hormonal factors include:
secretin, CCK, GIP, gastrin

reason? Rate of gastric emptying is regulated to ensure that gastric contents are not emptied into the duodenum at a rate faster than the small intestine can neutralize gastric acid and process the chyme

Front 33

function of stomach in fasted state

Back 33

hunger contractions to increase drive to acquire food
MMC migrating myoelectric complex) => clear of any debris

Front 34

vomiting reflex neural pathway 4

Back 34

 Emetic stimuli

 Afferent pathway:vagal and sympathetic
chemoreceptor trigger zone: flood of 4th ventricle near area postrema
(no blood brain barrier here, triggering drugs: morphine and apomorphine esp after general anesthesia)

 Vomiting centre
in medulla, near tractus solitarius at level of dorsal motor nucleus of the vagus nerve

 Efferent pathway: V, VII, IX, X, XII to upper GIT and spinal nerve to diaphragm and abdominal mus

Front 35

what are the stimuli for vomiting 5

Back 35

-irritation of GI mucosa
-tactile stimuli (gag reflex) CNX
-activation of chemoreceptor @ postrema which is outside BBB, sensitive to toxin
- rotating movement of head (motion sickness) by vestibular system (CN VIII vestibulocochlear nerve)
- high brain centers: psychiatric disorders and stress

Front 36

complications of vomiting 4

Back 36

dehydration
electrolyte imbalance - hypochloremic metabolic alkalosis & hypokalemia
acid base imbalance
aspiration and pneumonia

Front 37

two mixing of small intestine

Back 37

1. peristaltic contractions
progressive contractions of curcularr smoooth muscle => long transit time
2. Mixing (segmentation) contractions
by slow depolarization, back and forth, help mix te content (reflex: gastroileal reflex, intestino-intestinal reflex)

Front 38

motility of large intestine (control)

Back 38

inactive in most of the time
segmentation contraction of circular mus, longitudinal mus strips => form haustrations

mass movement (perisatltic wave)
Distension of rectum => rectosphincter reflex
initiation of mass movement: gastrocolic & duodenal reflex

Front 39

Dysphagia
causes 4 x 2

Back 39

Painful disease of mouth & pharynx
Paralysis of swallowing mechanisms
External compression on esophagus
Intrinsic disease of esophagus