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Midterm > Physiology [GIT] > Flashcards

Physiology [GIT] Flashcards

1
Q

Who secretes the secritin and its site?

A

Apud cells, in the mucosa of deudenum and upper part of small intestine

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2
Q

Whats the mechanism of secritin secretion?

A

Due to the decrease of ph of fluid bathing the upper part of small intestine below 4.5
-due to the propulsion of acid chyme from pylorus to the deudenum

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3
Q

Whats the action of secritin?

A
  • stimulates the pancreatic juice secretion from the duck larg in volume and electrolytes Hco3
  • inhibit gastric acid secretion
  • augment CCk for secretion of pancreatic digestive enzymes from the acinus of pancreas
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4
Q

Why does the secritin stimulates the pancreatic juice secretion?

A

Increase ph To make the deudenum suitable for the work of pancreatic digestive enzymes

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5
Q

What inhibits the secritin and what does it cause due to?

A
  • nocotin in tobacco

- lead to drop of ph then ulceration

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6
Q

What secrete the GIP (gastrin inhibitory peptide) and where?

A

Special Apud cells in the upper part of small intestine

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7
Q

Whats the mechanism of GIP secretion and its function?

A
  • released due to presence of fat and glucose in the lumin of deudenum
  • inhibit gastric acid secretion in the stomach
  • stimulates insulin secretion
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8
Q

Side release of VIP(vasoactive intestinal peptide)? And mechanism of secretion?

A
  • By apud cell in mucosa of small intestine

- presence of digestion products in the lumin of small intestine

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9
Q

Functions of (vip)vaso active intestinal peptide?

A
  • increase intestinal secretion of water and electrolytes
  • vasodilation of intestinal vessels
  • relaxation of smooth muscle in GIT
  • stimulates secretion of bicarbonate from pancreatic duct
  • inhibit gastric secretion
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10
Q

Whats the site of release of motilin?by what? Mechanism of secretion?

A
  • by apud cells inth mucosa of upper part of small intestine
  • due to presence of digestion products in the lumin of small intestine
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11
Q

Whats the function of motilin?

A
  • stimulates antral and duednal motility

- contraction of LES

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12
Q

What releases the somatostatin?mechanism?

A

By D cells in Git And D cells of pancreas

-stimulated by Hcl in the lumin

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13
Q

Whats the functions of somatostatin?

A
  • inhibit acid secretion

- inhibits gastrin GIP VIP secritin motilin

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14
Q

Where is the chewing nuclei is located?

A

Controled by nuclei in the brainstem

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15
Q

Who’s responsible for the mastication(chewing)?

A
  • Incisors for cutting and molars for grinding

- masticatory muscles(5th cranial nerve) close the mouth with force of 25kg on the incisors and 90kg on molars

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16
Q

How is the mastication process is done?

A

-through mastication reflex(stretch reflex) entering the bolus of food into the mouth leads to stretch of the mastication muscles then leads to stretch reflex with causes the muscles to contract again and close the mouth then relaxe after that till the bolus stretch the muscles again

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17
Q

The swallowing (deglutation) devided into?

A
  • oral stage voluntary
  • pharyngeal stage involuntary
  • esophageal stage involuntary
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18
Q

How is the oral voluntary stage is happening?

A

-Voluntary squeeze the food with ur tongue against the hard palate into the pharynx

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19
Q

How is the pharyngeal stage of swallowing happens?

A

-entering the food to the pharynx stimulates the receptors around its opening which send impulses to brainstem then comes back with pharyngeal peristalsis starts from its superior part and becomes rapid peristalsis in the middle and lower part of the pharyngeal muscles

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20
Q

How to protect the airways during the pharyngeal stage of swallowing?

A
  • the soft palate goes upward to close the posterior nares
  • larynx vocal cord are approximated and the larynx pulled upward by nech muscles then the epiglottis swings back to close the opening of larynx so the food dont go to the trachea
  • relaxation of upper esophageal sphincter (pharngeosophgeal) to pass the food from pharynx to the esophagus
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21
Q

Deglutation or swallowing center is in?

A

Lower bone, medulla

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22
Q

The pharyngeal stage of swallowing reflex initiated by?

A

Entering the food to the pharynx voluntary which elicit pharyngeal reflex

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23
Q

Where the respiratory center resides? And its inhibited by? For how long?

A

Inthe medulla,

  • by swallowing (pharyngeal stage)
  • for 1-2 seconds
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24
Q

The duration of pharyngeal stage of swallowing?

A

1-2 seconds

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25
Q

When does the pharyngeal stage of swallowing inhibit respiratory center?

A

At any time if there was a swallowing happening

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26
Q

What are the two waves in the esophagus?

A
  • primary peristalsis wave which a continuation of pharyngeal peristalsis from the pharynx to the stomach
  • secondary peristalsis wave
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27
Q

How much does it take for the primary wave of esophagus to reach from pharynx to the stomach?

A

8-10seconds

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28
Q

Whats the secondary peristalsis wave of esophagus?where it comes from?when it ends?

A

The wave that takes the remaining food in the esophagus and push it to the stomach

  • from distenationof esophagus due to the remaining food
  • untill all of the food is pushed to the stomach
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29
Q

The secondary peristalsis wave of esophagus initiated by?

A

Partially by enteric NS of esophagus and partially by reflexes transmitted through affernt vegus that goes to the medulla then comes back with effernt vegus

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30
Q

What forms the LES

A
  • smooth muscle of esophagus at the junction with stomach (intrinsic sphincter)
  • fiber crural of diaphragm
  • skeletal muscle (extrinsic sphincter)
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31
Q

Whats the function of LES?

A
  • allow the orderly flow of food to the stomach

- prevent the backflow of gastric content to the esophagus

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32
Q

What prevents the gastric fluid from regrugating even during the increase of intragastric pressure?

A

Flap valve that close to esophgastric junction

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33
Q

Whats the difference between LES and upper , middle portion of the esophagus?

A
  • Les is tonically contracted

- upper, lower relaxed completely

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34
Q

When the LES is not tonically contracted?

A

-in the reciptice relaxtion , when the peristalsis wave reache it to empty into the stomach

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35
Q

TONES OF LES under the neural control?

A
  • AC released by the vagus to contract the LES

- NO,VIP released by interneurons that innervated by other vegus nerves to relax the LES

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36
Q

LES between meals?

A

Tonically contracted to prevent the reflex from the stomach

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37
Q

Abnormalities of the LES?

A
  • Decrease innormal tone will allow gastric regurgitation and ulcer and strictures of the esophagus, eosphagitis
  • Achalasia the LES is not completely relaxed
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38
Q

The Achalasia leads to? Caused by?treated by?

A
  • accumulation of food till the esophagus is dilated
  • defect in myenteric plexus of the esophagus
  • defect inNO,VIP
  • treated by Esophageal muscle incision or inject botolinium toxin in the LES to inhibit the acitylecholine
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39
Q

Whats the function of gallbladder?

A
  • storage of bile
  • concentration of bile
  • prevent increase in intrabiliary pressure
  • acidification of bile
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40
Q

Whats the function of gallbladder?

A
  • storage of bile
  • concentration of bile
  • prevent increase in intrabiliary pressure
  • acidification of bile
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41
Q

How the gallbladder concentrate the bile?

What happens to the rest of the gallbladder content?

A

By absorption of Na by active transport in gallbladder mucosa followed passively Cl,bicarbonate,water
—————————————-
Increase in licithin,cholesterol,bilirubin,bile salts

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42
Q

How the intrabilliary pressure effects bile flow?

A

Increase in this pressure stops the secretion of bile

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43
Q

How is the acidification of bile in gallbladder happen?

And why?

A

By absorption of Hco3 of hepatic liver
—————-
To keep a solution of bilirubin,cholesterol,bile salts,lacithin not precipitated

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44
Q

Whats the Hco3 content in hepatic bile and gallbladder?

A

In hepatic bile:23

In gallbladder:10

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45
Q

The maximum volume of gallbladder?

And it can store?

A

20-60ml
———-
500ml(24h secretion)

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46
Q

Whats the contraction of the gallbladder called?

Who’s responsible for it?

A

Cholagugues

  • cck the major one for the contraction of gallbladder and relaxation of oddi sphincter
  • vegal stimulation is less strong contraction of gallbladder and relaxation of oddi sphincter
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47
Q

Whats the cholelithsias?

A

Presence of gallstones

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48
Q

What are the types of gallstones?

A
  • cholesterol stones(radiolucent)

- calcium stones(radiopaque)

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49
Q

What are the types of gallstones?

A
  • cholesterol stones(radiolucent)

- calcium stones(radiopaque)

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50
Q

How the cholesterol stones is formed?

A

Cholesterol is insoluble in water it needs bile salts and licithin to keep it in bile solution so it form the micelle if the colestrol level exceeded or ultered than the micelle components it starts to crystallize
(Rafiolucent)

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51
Q

Whats the effect of cholecystectomy?

A

Removal of gallbladder
—————————-
It starts emptying slow but continuously direct to
the intestine for sufficient nutrition-avoid fat meals

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52
Q

Secretion of the intestine are?

A
  • mucos
  • alkaline fluid
  • enzymes
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53
Q

Whats the component for the intestinal mucus?

Its fumction?

A 
Mucin
———————
-protect the wall of intestine 
-lubricant to the chyme 
-bind to bacteria and immunoglobulins
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54
Q

Who secret mucus in the intestine?

A
  • surface epithelium cells
  • goblet cells
  • brunners glands in the deudenum
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55
Q

The brunner glands secrete mucus in the intestine in response to?

A
  • chemical and physical irritation of mucosa
  • cholingergic stimulation (vagus)
  • Git hormones(secritin)
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56
Q

What inhibit mucus secretion in intestine?

What does it cause?

A

Sympathetic

-no protection to the walls og intestine so it leads to ulcer in 50% of cases

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57
Q

Who secret the alkaline fluid in the intestine? Its daily formation rate?
Composition of the fluid? Its ph? Who takes it?

A

Crypts cells-bicarbonate and NaCl-ph(7.5-8)
Slightly alkaline-absorped by the villi(isoosmotic)
—————-
1800ml

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58
Q

Whats the purpose of alkaline secretion in the intestine?

A

To be absorbed by the villi and create a medium for digestion inside of it

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59
Q

Where the enzymes of the intestine reside?

and where are the secreted?

A

Brush border of epithelium covering the villi
—————-
Not into the intestine

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60
Q

Whats the enzymes of the intestine?

A
  • peptidase: cut the peptides into A.A
  • enzymes for disaccharide to monosaccharides: sucarose- maltas-isomaltas-lactase
  • lipase for fat to glysrol and fatty acids
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61
Q

The regulation of intestinal secretion due to?

A
  • Local nervous reflex: the major and it caused by destination of Intestine by chyme (the greater the destination the greater the secretion)
  • hormonal: secritin and CCK increase intestinal secretion
  • vip also released by nerve endings leads to increase water and electrolytes in the intestine
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62
Q

What are the normal and abnormal movements of the intestine?

A 
Normal-
Segmentation mixing movement 
Peristalsis movement 
Migrating motor complex MMC
Abnormal-
Dynamic (paralytic)ilues
Peristalsis rush
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63
Q

Whats the rate of segregation movement of the intestine and its function?
Initiated by? Controled by? And effected by?

A

Caused by destination of intestine wall by the chyme

  • separated into segments each one contract and relax
  • function to mix the food
  • at a rate of 12contraction/min in intestine and 8-9time in terminal illium
  • controlled by BER
  • effected by the activity of enteric NS so the atropin inhibit the enteric NS lead to slowen the movement
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64
Q

The maximum frequency of segregation movement is in ?

A

Deudenum and proximal jejunum

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65
Q

Function of peristalsis movement of the intestine?

Where it happens? And its velocity?

A

Propulsion of cyme to ileocecal valve

  • in all the intestine fast in proximal intestine and slow at the terminal intestine
  • moves the chyme in rate of 1cm/min
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66
Q

How much time the chyme required to reach from pylorus to the ileocecal valve?

A

3-5houres

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67
Q

When the MMC of the intestine happens? And its function? What is it formed of?
When its stop?how much it takes to reach its way?

A
  • in between meals
  • take the indigested substance and the remaining of small intestine and takes it to the colon so the bacteria not grow and multiply
  • 2h to reach the colon
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68
Q

What inhibit and enhance the intestinal motility?

A

Enhance:CCk, gastrin, seritonin,insulin
Inhibit:secritin,glucagon

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69
Q

Whats the peristaltic rush? Its function?

What initiates it?

A
  • very powerful and fast peristaltic waves
  • fast for carrying of the irritation and excessive chyme into the colon to relieve the intestine
  • initiated partially by extrinsic Ns in brainstem then comes back to the gut or enhanced direct by myentric plexus
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70
Q

Function of eleocecal valve?and what the thickned part of the ilum forms?

A

Prevent movement of fecal from colon back to the small intestine
—————
Eleocecal sphincter that mildly contricted for emptying from ilum to cecum

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71
Q

When the paralytic ileus occurs ?and why?

What does it cause

A

-Occure in abdominal operation , inhibit peristalsis and intestinal motility due to trauma to the intestine or irritation in peritonum leads to norepinephrine discharge by splanchic nerve
——————————-
No propulsion to colon or absorption leads to irregularities and destination of the the intestine due to gases and fluid

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72
Q

The bilirubin is end product of?

And where do we get it’s soure from?

A

Hemoglobin catabolism

-breaking the old RBCs

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73
Q

Whats the catabolism of hemoglobin?

A

Globin:amino acids
Heme: F+ , 4pyrol rings > biliverden > bilirubin
⬆️
Transferred on transferrin in the blood to synthesis
New hemoglobin

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74
Q

The F+ from hemoglobin metabolism is transferred in blood by? And whats its purpose?

A
  • on trasferrin

- synthesis new hemoglobin

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75
Q

The bilirubin released in blood called?

A

Free bilirubin or unconjigated or indirect

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76
Q

Whats the bilirubin bind to in plasma and why? Where it takes it?

A
  • to albumin
  • so it doesn’t get excreted in urin
  • to the liver for its disassociation
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77
Q

When the the bilirubin reaches the liver its first encounter with?

A

Cytoplasmic protien

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78
Q

Whats the bilirubin conjugated with ? And where?

The enzyme? End product?

A
  • With glucuroneic acid
  • in the liver
  • glucournyle transferade
  • bilirubin diglucorunide
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79
Q

Whats the property of the bilirubin before and after conjugation?

A

Before: lipid soluble
After:water soluble

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80
Q

Bilirubin after its conjugation its excreted to? By?

A

Bile canaliculi

Active transport

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81
Q

The total plasma bilirubin normally includes?

A

Free bilirubin plus small amount of conjugated bilirubin

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82
Q

The small amount of conjugated bilirubin escapes to the blood how its excreted?

A

In urin

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83
Q

What happens to the bilirubin after it gets to intestine?

A
  • Most of glucorunide transfers by bacteria into urobilinogen 50% that reabsorped by hepatogastic circulation
  • the other 50% of urobilinogen turns into stercobilinogen that goes to stool
  • 5% of urobilinogen excreted by the kindney in urin
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84
Q

What gives the urobilinogen its properties and whats its properties?why?

A

Highly soluble
By bacteria
To be reabsorped in the enterohepatic circulation

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85
Q

The urobilinogen in urin oxide ……. To give?

A

Outside the body

Urobilins

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86
Q

Where is the glucuronide is deconjugated? And why?

A

In the intestine

To be absorbed to the enterohepatic circulation

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87
Q

Whats jaundice (ictrus)? And it’s general cause?

A

Yellow tint to the skin sklera and mucous membrane

-increase in free and conjugated bilirubin

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88
Q

Whats the normal value for bilirubin?

At what level its called jaundice?

A
  1. 5mg to 2mg %

- Above 2

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89
Q

When jaundice due to theses process the free bilirubin rises?

A
  • increase production of bilirubin (hemolytic anemia)
  • disturb in hepatic uptake of free bilirubin
  • disturb in cytoplasmic enzyme(intercellular binding protein) and conjugation
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90
Q

The glucuronyle transferase enzyme found in?

A

Smooth ER

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91
Q

How much bilirubin excreted in urin?

A

5%

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92
Q

When jaundice due to one of these processes it rises the conjugated bilirubin?

A
  • intra and extra hepatic bile duct obstruction

- disturb in excretion of conjugated bilirubin into bile canaliculi

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93
Q

Jaundice classified into?

A

Hemolytic jaundice
Hepatocellular jaundice
Obstruction (cholestatic) jaundice

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94
Q

Hemolytic jaundice cause by? Its effect on plasma bilirubin concentration?

A

Increase in bilirubin production by excessive breaking of RBC so the hepatic cell cant secrete and conjugate rapidly
-rises the free bilirubin in the blood(indirect von den bergh)

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95
Q

Whats the effect of hemolytic jaundice on the intestine?

A

The bile conjugate a lot of bilirubin so it’s secreted to the intestine and increase it turning into urobilinogen then to stercobilinogen to the feces(dark stool)

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96
Q

Hemolysis of RBCs can be due to?

A
  • hemolytic anemia: heridatory spherocytosis- sickle cell anemia-thalassemia- erythroblastosis fetalis
  • blood transfusion- malaria-reaction to some drugs as an autoimmune
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97
Q

The liver excretion in the hemolytic jaundice is?

A

Normal

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98
Q

Hepatocelluar jaundice caused by?its effect on the plasma bilirubin concentration?

A

Inability of hepatocytes to excretion or conjugation all bile pigments
-increase both direct and indirect bilirubins(free and conjugated)

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99
Q

Whats the effect of hepatocellular jaundice on intestine?

A

Reduce the bilirubin diglocurnide excretion in the intestine lead to reduce of urobilinogen and stercobilinogen in feces, and urobilinogen in urin

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100
Q

Hepatocellular jaundice occures due to?

A

Viral hepatitis, chemicals chloroform carbon tetrachlorid, arsinic , mercury,
-drugs as tetracyciine, chloramphnicol

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101
Q

What causes the obstructing jaundice (cholistatic)? An its effect on the plasma bilirubin concentration?

A

The bilirubin is conjugated in the live but it cant pass to the intestine due to an obstruction
- the conjugate bilirubin goes back to the blood directly through live sinasoids or indirect through bile duct and lymphtics(direct bilirubin)

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102
Q

Whats the effect of obstruction jaundice on the intestine?

A

No conjugated bilirubin pass to the intestine so no urobilinogen and stercobilinogen (gives pale stole)
-dark urin due to the conjugated bilirubin in the blood(direct von den betgh reaction)

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103
Q

Whats the intrahepatic and extra hepatic causes of obstruction jaundice?

A

Intra: viral hepatitis, liver cirrhosis
Extra: gallstones,carcinoma, strictures

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104
Q

How the obstruction jaundice effect the bile salts?

A

The bile salts and pigments are in the same sac so releasing them must be together
-obstruction leads to no absorption of fat(statoreah) and leading to puritits and bradycardia

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105
Q

How the obstruction jaundice effect the cholesterol?

A

-Increase cholesterol levels(hypercholestrolemia)
- increase level of alkaline phospatase enzyme
These two substances are normally excreted by bile

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106
Q

The general parasympathetic supply of GiT is due to? And ends on?
Its effect onthe GIT in general?

A

Pregangelionic fibers of vagus, sacral nerves

  • ends on the cholenerguc nerve cells of intrinsic Nerve system
  • increase the activity of intrinsic nerve system
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107
Q

The general sympathetic supply of git due to? And end on? Whats its transmitter?
Where it secret the transmitter?

A

-Postganglionic from T5-L2
-End on postgang cholinergic nerouns of intrinsic n or directly on the smooth muscles
-secrete norepinephrine to inhibit acitylecholine
-it inhibit the git activity (inhibit smooth muscles)
——————————-
On the cholinergic neurons of intrinsic nerve system

108
Q

Types of movements in GIT?

A

Propulsive (peristalsis)

Mixing

109
Q

In peristalsis movement the reflex initiated by?

And where the contraction and relaxation happens?

A
  • Distination of the wall from the content of lumin

- contacted behind the stimuli and relaxed infront of the stimuli (receptive relaxation)

110
Q

The propulsion of food in git trackts is at rate?

A

2-25cm/second

111
Q

Where the propulsion movement accours in git?

A

All git from pharynx to the rectum

112
Q

The peristalsis can’t occur in absence of?

So its called?

A

Myenteric plexus

-Myenteric reflex

113
Q

The occurrence of peristalsis is due to?

Increased and decreased by?

A
  • occur independent

- by autonomic ns

114
Q

The local stretch in peristalsis leads to release?

And what casues the relaxation and contraction?

A
  • seritonin
  • stimulates the sensory neurons that stimulate the cholingerig neurons of myentric plexus that pass retrograde stimulates neurons that release AC and substance p to contract the gut
  • same at the contraction except ot stimulates the anterograde neurons which stimulates neurons that release No,Vip,Atp and gives relaxing ahead of the stimuli
115
Q

Whats the true hormones of Git?

A

Hormones that passes to portal venous blood to the heart then come back to git through atrial blood to do its effect on muscle or glands secretion

116
Q

The gastrin family includes?

A

Gastrin, CCK

117
Q

Secretin family includes?

A

Secritin, glucagon ,vip,gip,mitolin,somatostatin,glicentin(gli)

118
Q

What secrete Gastrin and where?

A

G cells, in the antrum and deudenum

119
Q

Mechanism of secretion of gastrin?

A
  • increase ph above 2 after meal intake
  • chemical stimuli soup extract and peptons(protein products for digestion in stomach
  • distinction of pyloric antrum
  • vegus(gastrin releasing peptide)
120
Q

What stimulates the G cells of the gastrin the most?

A

Phenylalanine, tryptophan

121
Q

Inhibition of gastrin secretion?

A 
Luminal
-acces of acids in antrum
-somatostatin
Blood born
-secretin, Gip
122
Q

Action of gastrin?

A
  • stimulates secretion of acid and pepsin
  • trophic (growth of mucosa)function of stomach small intestine and colon
  • stimulates gastric motility
  • stimulates insulin secretion after a meal
123
Q

Cck secretion where? And by what?

Mechanism of secretion?

A
  • by apud cells in upper part of small intestine

- presence of peptide amino acids fatty acids and bile salts s

124
Q

Action of CCK?

A
  • stimulates pancreatic juice from the acinus secretion small in volum rich in enzymes
  • augment secretin functionto produce of alkaline pancreatic juice from the duct
  • trophic for pancreas
  • inhibit gastric empty
  • contraction of the wall of bile
  • enhance the motility of small intestine and colon
125
Q

Whats the functional unit of the liver?

A

Hepatic lobule centered around central vein
-Blood of portal vein pass in the hepatic sinasoids
Then to the central vein then to venaceva
-this sinasoids have kupfer cells in the pores of sinasoids + the sinasoids made of endothelial cells

126
Q

Whats the function of the liver?

A

….

127
Q

How much blood does the liver stores?

A

200-400ml

128
Q

What does the kuppfer cells kill specifically?

A

Colon bacilli+90% of bacteria in venous blood

129
Q

What are the drugs that are excreted by the liver?hormones?

A

Penicillin ereythromyocin sulfonamide

-thyroxine ,steroid , Ca

130
Q

Why the bile is important?And what secretes it and where?

A

-For the fat digestion and absorption (mainly)
Excretion of water sulouble billirubin ,cholesterol
-by hepatocytes then goes to bile duct that opento the deudenum

131
Q

Whats the bile salts?

A

K-Na bile acids conjugation with glysin and tourin(from cystien)

132
Q

Whats the bile acids made of?

A

Cholesterol

133
Q

What are the types of bile acids?

A

Primers:cholicacids and chenodeaoxycholic acid

  • conjugate with glysin and tourin to form torinocholic , glysinocholic acids that form K,Na salts alkaline hepatic bile
  • secondary turned by the bacteria in the colon into deoxycholic(cholic acid),lithocholic(chenodaoxycholic)
134
Q

How much bile acids descend to the colon and its name?

A
  • 10-15%

- deaxycholic, lithocholic

135
Q

Where the conjugation of bile acids with glysin and tourin accours?

A

In the liver

136
Q

Whats the function of bile salts?

A
  • decrease surface tention of fats (phospholipids And monogylisrides) emulsification
  • bile salts are amphipathic with hydrophlic part (hydroxyle and carboxyle groubs and peptide bond) and hydrophobic part
  • form a cylindrical shape called micelle
  • inside the micelle theres lipids and cholesterol the micelle takes it to the brush boreder of the intestine (unstirred surface) tobe absorped passively by microvilli
137
Q

Whats the name of the complex formed by the bile salts?

A

Bile acids-lipid water sulouble complex

138
Q

Whats the level at which the micelle is formed? And what is it?

A

Abve whats Called the critical micelle concentration

-its where the bile salts gathered in a solution to form micelle

139
Q

What happens to the bile salts of micelle when all the content of it is absorbes ? And when all the fat in the in the intestine absorbed?

A
  • freed and goes back to the chyme for a reuse
  • freed and goes back to the liver to be re excreted to the bile duct (goes back by the enterohepatic circulation) by active transport
140
Q

Normally all the ingested fat is absorbed except?

A

The one made by the intestinal flora

141
Q

Whats the enterohepatic circulation?

A

Recirculating bile salts from intestine to liver and from liver to intestine and so on

142
Q

How much of bile salts is absorbed in enterohepatic circulation?and whats lost?

A

90-95%

5-10 in colon the deoxycholic is completely absorbed while only 1%of lithocholic is absorbed and the rest is excreted

143
Q

What type of carriers used in the enterohepatic circulation?

A
  • Bile salts-Na secondary active countertransport in luminal boredr
  • Na-k atpas in the basolateral
144
Q

Wheres the site of absorption of bile salts?and some times absorbed by?

A

Terminal illum

-nonionic diffusion

145
Q

How much bile salts the liver synthesis per day?

A

0.2-0.3 g

146
Q

The total pool of the bile salt in liver is ?

A

3.5g

147
Q

How much the bile salts 3.5 g are recycled? Per meal and per day?

A 
Per meal 2
Per day(6-8)
148
Q

Whats the choliritics? And choligogs?

A

Substances that increase the bile salts production
-vagus,secritin,also the bilesalts themselves
Substances that constric the bile to secrete
-CCK

149
Q

Whats the effect of secritin on the bile salts production?and where it works?

A

Increase water and Hco3 content of bile

-in bile duct and ductules

150
Q

Prevention of enterohepatic circulation or exclude bile salts from the intestine or decrease portion of small intestine leads to?

A

Steatorrhea 50% of fats in the stool

151
Q

Steatorrhea leads to malnutrition of ?

A

Fat soluble vitamins (A D E K)

152
Q

Pancreatic enzymes increased by?

A

Vegus stimulation

153
Q

The pancreatic enzymes works in….. medium?

A

Neutral to alkaline medium

154
Q

Hydrochloritic is?

A

Secretin, increase bile salts production by capious secretion rich in water

155
Q

The vagus choliritic function is due to?

A

AC

156
Q

Saliva is secreted by three main glands

A

Parotid,submandibular,sublingual,buccal glands

157
Q

How much saliva is secreted per day

A

1500ml

158
Q

What does saliva contains

A

Enzymes as (ptyaline,mucin) electrolytes as Na,k,Hco3,Cl

159
Q

The ph of saliva during resting state is?

A

7.0

160
Q

Each salivary glands formed of…..

A

Accini and duct

161
Q

Who secrete the primary secretion in the salivary glands

A

Acinus

162
Q

What are the type of cells in salivary accinus?and thier secretion

A
  • Serous: watery and contain ptyline apla amylase

- muscou: viscous and contain mucin

163
Q

What type of secretion does the salivary glands have?

A

Parotid:serous (25%) of saliva
Sublingual:mucosa (5%) of saliva
Sub mandibluar: mixed(70%)
Buccal only mucus

164
Q

Whats the first stage of salivary secretion?

A

Acinus secreting the primary secretion

165
Q

Where the does the salivary secretion gets modified?

A

In the duct

166
Q

Whats the substances are pumped actuvly or passively in the salivary secretion mechanism?

A

Na active reabsorption
K active secretion
Cl passively reabsorped
Hco3 active secretion

167
Q

Which part of the salivary gland is impermeable to water and why?

A

The dun so that the salivary secretion goes to the oral cavity as hypotonic solution

168
Q

In the first stage of salivary secretion the solute have

A

No difference from the extracellar fluid

169
Q

Under the resting condition the Na and Cl in saliva are while the Hco3 and K

A

Less, higher than the plasma

170
Q

During the maximal salivation (parasympathetic)

A

The Na and Cl,Hco3 are the same in the plasma

While the K is not increasing

171
Q

What reduces the ductal modification in the salivary secretion

A

The rapid flow in short time

172
Q

Whats the function of saliva?

A

Protect oral mucosa
Protect the teeths
Digestion
Swallowing and wetting

173
Q

How does saliva protect oral mucosa?

A 
1-cooling hot food
2-neutralize the acids by buffer to keep mouth ph 7/neutralize gastric acids and heartburn in abnormal regrugation of gastric acids
3-wash away pathogens 
4-laysosomes attack the bacterial wall
5-lactofeerin as bacteriostatic
6-IgmA to destroy bacteria
174
Q

How does saliva protect the teeths?

A

Its ph is 7 at this ph it’s saturated with Ca so the teeth Ca is not lost

  • floride protect the enamel added to water then excreted in saliva
  • proline rich protiens protect ename and bind toxic tennis
175
Q

The absence of saliva called? And it causes?

A

Xerostomia ,dry mucosa and ulceration and infection and increase dental caries

176
Q

How saliva help with digetion?

A

It has ptyaline alpha amaylase digstive enzyme which turn starch to alpha dixtrens and maltirios and maltose

177
Q

Where is the alpha amaylse enzyme is activated and deactivated?

A

Works in the mouth then deactivated in low ph of stomach then reactivates in the small intestine due to high ph

178
Q

How is saliva helps with taste?

A

It act as a solvent for molecules that activate the taste receptors

179
Q

How saliva helps with swallowing?

A

It has mucin(glycoproteins) facilitate the swallowing by lubricating food

180
Q

How saliva helps with the speech?

A

It moist the mouth for the tongue and lips movement

181
Q

The salivation mechanism under what control

A

The autonomic control only

182
Q

The parasympathetic stimulation for salivary secretion with what fibers? And sympathetic too?

A

Para:cholinergic
Sym:adrenegic

183
Q

The parasympathetic stimulation for sublingual and sub mandibluar is due to?

A
  • From the superior salivary nucleus in medulla
  • runs in chordatympani of facial nerve
  • relay in submandibular ganglion
  • the the post synaptic supply the glands
184
Q

Parasympathetic stimulation of parotid glands is due to?

A
  • from inferior salivary nucleus in medulla
  • run in glossopharyngeal nerve
  • relay in otic gangelion
  • post synaptic supply the gland
185
Q

What parasympathetic stimulation do to salivary glands?

A
  • Increase watery secretion rich in electrolytes

- vasodilation of the gland due to Vip

186
Q

Whats the VIP function in the salivary secretion?

A

Comes with acitylecholine and blocked by atropin vasodilation of salivary gland

187
Q

The sympathetic stimulation of the salivary glands is due to?

A

1st and 2nd thoracic segments in spinal cord from lateral horn cells and relay in the superior cervical plexus the post gangelionic supply the glands

188
Q

Where the post synaptic neurons of sympathetic stimulation of salivary glands end?

A

On the blood vessels’s wall of the glands

189
Q

What the sympathetic stimulation do to the salivary secretion ?

A

Vasoconstriction and secretion small amount of saliva rich in organic content

190
Q

How does salivating accours in response to reflex in the stomach and upper intestine?

A

Introduce an irritating food will increase salivation so we can swallow it and it reaches the stomach and dilute it or neutralize it

191
Q

In the conditioned reflex of salivation the impulses comes from where?

A

From cerebral cortex to the salivary nuclei

192
Q

How does the conditioned reflex for salivation works?

A

The appetite center in hypothalamus recieves signals from smell and taste areas in cerebral cortex which stimulates the salivary nuclei to increase salivary secretion

193
Q

Where the appetite center resides?

A

In hypothalamus or amygdala

194
Q

What constitutes the muscles around sphincters?

A

The inner circular layer

195
Q

The muscle fibers of smooth muscles connected by?

A

Gam junction

196
Q

What happens if one muscle layer in GIT is stimulated ?

A

Stimulate the other two because they are connected

197
Q

Git electric activity have two types of waves?

A
  • slow wave

- spikes

198
Q

Whats is the BER (slow wave)

A

Changes in the RMP

199
Q

What the rate of slow waves happening?

A

3 times in the stomach

12 time in the duednum

200
Q

Whats the importance of BER (slow waves)

A

Initiation for spike potential

201
Q

Whats the importance of BER (slow waves)

A

Initiation for spike potential

202
Q

Who makes the BER(slow waves) {pump}

A

Cyclic activation and deactivation of Na-K pump

203
Q

When the spike potential happens?

A

At depolarization of membrane at -40mv

204
Q

The normal resting membrane potential in smooth muscle is?

A

-50 and -60mv

205
Q

What causes the depo and depolarization of spike potential?

A

Repo:k enflux
Depo: Ca influx

206
Q

The spike potential is followed by….

A

Contraction

207
Q

How the Ca participate in smooth mucle contaction

A

Act through calmodulin protien that activates myosin filaments then create attraction force with actine

208
Q

What is the intrinsic innervation of GIT?and thier location

A
  • Myenteric plexus(auerbach): between circular and longitudinal muscle layer
  • submucosal(messiener):between the circular muscle layer and mucosa
209
Q

What the plexus in intrinsic nervous system in git transmitters

A

No,acitylecholine,GABa,seritonin,polypeptides

210
Q

How much the stomach secrete gastric secretions? And whats its content?

A
  1. 5L/day
    - electrolytes:H Na K Cl
    - enzymes:lipase gelatenase pepsin
    - water
    - mucus
    - intrinsic factor for b12 absorption
211
Q

Who’s responsible for the acid secretion process?and why?

A

Pareital cells , its an active process needs energy from the many mitochondria in the pareital cells

212
Q

What are the carriers used in the acid secretion and thier sites?

A
  • H-k atpas (proton pump) inthe luminal or apical surakarta
  • Hco3 and Cl exchange
  • Na-K at the basolateral mem
213
Q

From where we get the Co2 in the acid secretion process?

A

From the metabolism in the cell or from the blood

214
Q

What are the steps of acid secretion process?

A
  • co2 combine with h2o under the Carbonic anhydras to form carbonic acid then disconnect to form Hco3 and H
  • the hco3 pumped to the bllod in exchange for Cl
  • cl transported to the lumin
  • apical H-katpas transport H out of the cell and the K into the cell again thier concentration with energy
  • Na-k pump inthe basolateral pumps 3Na to the blood and 2 k to the cell
  • k is passively goes to the lumin
  • osmosis helps the water to go to the lumin to form iso osmotic Hcl
215
Q

Whats the Alkaline tide?

A

Increase in ph of blood during forming the Hcl inthe stomach lumin and Hco3 increase in the venous blood

216
Q

What are the stimuli of HCL secretion ?

A
  • Histamine by H2 receptors that increase untracellar Camp
  • acitylecholine on m3 muscarinic receptors that increase Ca inside the cell
  • Gastrin act directly on the pareital cells by increasing Ca or stimulation of histamin secretion from Enterochromaffin like cells ECL cells
217
Q

The mechanism of action inHCl stimuli?

A

2ndmessengers trasfere the K-H atpas from itracelluar visicles to the plasma membrane

218
Q

Whats the function of HCL?

A
  • Sterilization of food
  • dissolving the food into chyme
  • absorption of iron and Ca
  • activate the pipsin
  • keep an optimal ph for the pepsin to work
  • stimulate bile flow
219
Q

The mucosal barrier in the stomach formed from?

A

Glycoproteins called musins

220
Q

The mucosal barrier of stomach formed by?

A

Insoulble mucus

  • the mucosal cells membrane is impermeable to H and their is active transport of it outside the cell and Na to the interstium
  • prostaglandins which stimulate mucus and HCO3 and inhibit acid secretion and increase mucosal blood flow
221
Q

What does the Prostaglandins do the the mucosal barrier?

A

stimulate mucus and HCO3 secretion and inhibit gastric secretion and increase mucosal blood flow

222
Q

What disrupts the mucosal barrier in the stomach?

A

Ethanol , vinegar, bile salts , corticosteroids, aspirin, and non steriodal anti inflammatory drugs

223
Q

What inhibits the Prostaglandins synthesis?

A

Asprin non steroidal anti inflammatory drugs

224
Q

Whats the motor function of the stomch?

A

Storage
Mixing and partial digestion
Empty the chym into the deudenum

225
Q

Whats is the physiological division of the stomach and its character and function?

A
  • proximal motor unit (body fundus) thin wall store the food(receptive relation)
  • distal motor unti (pylorus antrum) thick wall mix the food and peristalsis
226
Q

The volume of empty stomach?and it can accommodate?

A

50ml

-1-1.5L

227
Q

Who’s responsible for the receptive relaxation in the stomach and how is the reflex initiated?

A

Initiated by relaxing of the stomach when food inters it by vegal stimulation (gastric distension
-also trigerd by pharynx and esophageal movement during swallowing

228
Q

Who’s responsible for mixing and propulsion of food in the stomach? Whith what?

A
  • Distal motor unit

- BER

229
Q

Where does the BER initiated in the stomach and whithinvthe range of?and increases by?

A

Greater curveture of stomach

  • 3-5 per min
  • vegal stimulation and gastrin from 3 to 5
230
Q

The pressure of the empty stomach is equal to?

A

Inta abdominal pressure even in the distinasion phase

231
Q

What hormones prevent the regurgitation ?by?

A

CCk and secretin by closing the pyloric sphencter

232
Q

The regulation of gastric evacuation is due to?

A

-Gastric factor
Distination of stomach throgh the long and short vego vegal reflex and gastrin increase pyloric pumping force and emptying
-intestinal
Nervous (enterogasrric reflex)
Increase acidity - distination in deudnum - irritation
Hypertoncity - present of fats and proteins
Hormonal:
Fats in deudenum releases Gip and CCK and secretin which close te pyloric sphincter
-consistency of foot
-external effects (pain inhibit gastric motility- depression inhibit or increase gastric motility)

233
Q

The feeding center is in? And inhibited by?when its active?

A

Hypothalamus

  • sateity center
  • always active unless it inhibited bu satiety center
234
Q

How the hunger pains results?

A

In hypoglycemia increas the activity of feeding center sends impulses to limbic cortex to give hunger sensation and impulses to dorsal vagus nucleus in medulla to cause hunger contractions

235
Q

Where is the vomiting center located?

Near to?

A

In the midulla near to respiratory center

236
Q

What causes the vomiting?and the wave it uses?

A 
Reflex:
-mechanic stimulation of the back of the tongue
-obstruction in the intestine and irritation 
-irritating gastric mucosa
——————
-reverse peristalsis
Central
-drugs as apomorphin
-hypoxia and acidosis
-motion sickness
237
Q

What preceded the vomiting ? And whats the mechanism?

A

Salivation-tachycardia-sweating

-deep inspirasion and contacts the abdominal muscles to increase abdominal pressure and squeeze the vomit out

238
Q

Protection of airways inthe vomiting is due to?

What happens to the GIt during vomiting?

A 
Elevation of soft palate to close nasal cavity 
Closer of epiglottis and apnea
-relaxing of stomach wall
- relax LES
-contraction of pyloric sphincter
239
Q

During vomiting the loss of HCL and water causes

A

Metabolic alkalosis

240
Q

What part of stomach is completely abolished by vagectomy

A

Proximal motor unit(receptive relaxation)

241
Q

What portion of pancreas produce pancreatic juice?

A

Exocrine part

242
Q

Whats the zymogen and how they released in pancreas?

A
  • Vesicles that have proteolytic enzymed

- exocytosis

243
Q

How much pancreatic juice and its composition?ph?

A
  • 1500ml per day
  • water and rich in Hco3
  • alkaline
244
Q

The value of Hco3 in pancreatic juice to the plasma is?

A

24 mEq/L in plasma

113 in the juice

245
Q

The intestinal content by the time it reaches the deudenum its ph?

A

6.0-7

It’s rarely alkaline mostly neutral

246
Q

What are the proteolytic enzymes of the pancreas?

A

Trypsin,chymotrypsin,carboxypeptidas,ribonuclease,deoxyribonuclease

247
Q

What the endopeptidas and exopeptidas of pancreas and their function?

A

-Endo:trypsin,chymotrypsin
Partial digestion of protien by cutting peptide boned and form peptides variable in sized
-exo: carboxypeptidas
Act in the end of protien peptide at the catboxyle end of amino acid

248
Q

What activates the proteolytic enzymes of pancreas?and what increases it?

A

When the pancreatic juice released in deudenum the trypsinnogen converted to trypsin by enterokinase(enteropeptidas) then trypsin avtivates the rest and its own self

249
Q

Decrease of enterokinase in pancreas causes?

A

Protien malnutrition

250
Q

What are the pancreatic enzymes for carbohydrates and thier function?

A

-pancreatic alpha amylase turns starch and glycogen and carbohydrates except cellslous into dextrins maltos and maltrios

251
Q

What are the pancreatic enzymes for the fat digestion?

A
  • Lipase digest fat into fatty acids and monogelysrides
  • cholesterol esterhydralaze digest cholesterol esters
  • phosolipase A2 splits fatty acids and lysophospholipids from phospholipds
252
Q

Whats the purpose of trypsin inhibitor?

A

To prevent the activation of trypsin in the anicus and duct and secretory cells otherwise it will ingest it

253
Q

When the pancreatic enzymes leaked into the circulation and how is it measured?

A
  • In acute pancreatitis

- by measuring the levels of amylase and lipase in plasma

254
Q

What are the pumpes used in Hco3 secretion in pancreatic juice ?

A
  • Luminal boreder:HCo3 and Na secondary co active transport

- basolateral border: exchange of Na into the cell and H into the blood

255
Q

What are the steps of Hco3 secretion in pancreas?

A

-Co2 combined with water under infeluence of CA
Forms carbonic acid then splits into H ,Hco3
-hco3 pumped to the lumen with Na
-h pumped to the blood in exchange with Na
-water goes with Na to the lumen of the duct by osmosis so it forms isoosmotic bicarbonate solution

256
Q

Whats the acid tide and when it happens?and its neuralized by?

A

Decrease in ph in the pancreas venous drainage by entry of H
-by alkaline tide from gastric venous blood

257
Q

The regulation of pancreatic secretion by ? And mainly?

A
  • Nervous

- hormonal (mainly)

258
Q

Whats the nervous regulation of the pancreatic secretion?

A

During the cephalic phase of gatric secretion the parasympathetic vegal fibers act on acinus cells and released Acitylecholine which secrete small amount of pancreatic juice rich in enzymes
-Acitylecholine acts by activating phospho lipase C

259
Q

Whats the hormonal regulation of pancreatic secretion?

A

-secretin: act on pancreatic duct and secret capious alkaline fluid rich in Hco3 poor in enzymes
-when the food enter the deudenum it stimulat secretin release then goes to the blood to act on the duct to neutralize the chyme and provide ph
For pancreatic enzymes (act by increasing Camp)
-cck: released by presence of fat and proteins in deudenum then goes to the blood and act on the acinus to release pancreatic juice rich in enzymes (act by activating Phospholipase C)

260
Q

What causes the peptic ulcer?

A 
1-disrup the gastric mucosal barrier
-Alcohol 
-asprin nonsteroudal anti inflammatory 
-helicabecter pylori bacteria infection 
2-excess secretion of HCL 
Zollinger ellison symdrom release too much gastrin which causes prolonged HCL secretion
261
Q

Treatment of ulcer?

A

-inhibit acid secretion
Block h2 histamin receptors by cimitedib
Block of H - k atpase by omeprazole
-eradicate the helicabecter pylori by antibiotc
-stop usage of aspirin
-surgical removal of gastrin secreting tumor

262
Q

The secretion of intrinsic factor and its importance?

A
  • By oxyntic cells(pareital) with HCl
  • For B12 vitamin absorption in the ilum
  • Destruction of pareital cells causes pernicious animia
263
Q

Who secret pepsinogen and activates it? And its function?and deactivated by?

A

Secreted by chief cells
Activated by Hcl at Ph2
Partial digestion of protien
Deactivated by alkaline in deudenum

264
Q

What types of mucos in stomach?

A
  • Soluble: by mucos neck cells of gastric glands by vegal stimulation to lubricate the chyme
  • insoluble by epithelial surface cells and it creates in body funcus and pyloric and esophageal junctions 1.5mm thickness
265
Q

What are the phases of gastric secretion?

A

1-Cephalic phase nervous only 1/3
•Entery of food create conditioned and unconditioned reflex that stimulate the dorsal nuclei which increases the HCL,mucos, pepsinogen,gastrin
•signals comes from apitite center in amygdala of hypothalamus
•gastric secretion increased by: vegus directly on pareital cells and gastrin by gastrin releasing peptide
2-gastric stimulatory phase N&H 2/3
•Long vego vegal refelex
•enteric nervous system
•gastrin release
3-intestinal inhibitory phase N&H
•arival of food to the deudenum depressing gastric secretion by enterogastric reflex+ hormones like Cck gib vip secretin

266
Q

Mechanism of inhibition of gastric secretion?

A
  • Drop of ph brlow 2 in pylori region hcl inhibt it own self
  • increase acidity in deudenum or distination in it
  • presence of fats and proteins to release the hormones cck gib vip
  • emotional depression impulses from cerebral cortex inhibit the dorsal nucei of vegus
  • somatostatin act as paracrine

Midterm (5 decks)

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