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Physiology 2 Flashcards

1
Q

The GI Tract is all smooth muscle except?

A

upper 1/3 of esophagus and anal sphincter (striated)

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2
Q

Types of Smooth Muscle Contraction?

A
  1. Phasic - parastalic

2. Tonic - can last hours

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3
Q

Chewing does?

A
  1. breaks down food particles
  2. mixes food with saliva
  3. increase surface are to digest better
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4
Q

Functions of stomach?

A
  1. storage-most in orad area
  2. break down food particles in small cubic sizes
  3. gastric emptying
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5
Q

GERD

A
  • acid reflux
  • heartburn
  • hiatal hernia, pregnancy, failure of secondary peristalsis
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6
Q

Oxyntic Cells

A

Parietal Cells, in body of stomach, weak motility

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7
Q

Pyloric

A

antrum, very strong contractions, muscle is thicker in this area

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8
Q

accommodation

A

relaxation

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9
Q

Cells of Caja

A

-slow waves always present from these intestinal cells
“gastric pacemaker”
3-5 depolarizations/min

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10
Q

Vagal Stimulation effect on slow waves

A

-increase height of waves (so increase frequency of contraction)

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11
Q

What empties fastest in the stomach?

A

-isotonic water (everything becomes isotonic when it goes in duodenum)

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12
Q

CCK effect on emptying?

A

inhibits

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13
Q

Effect of acid on peristalsis?

A

decrease from neural reflex

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14
Q

Failure of Gastric Emptying

A
  • fullness, loss of appetite, nausea
  • obstruction-ulcer, nausea
  • vagotomy
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15
Q

Increased Gastric Emptying

A
  • inadequate regulation

- diarrhea, duodenal ulcer

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16
Q

Reason for irregular contractions in small intestine?

A
  1. mixing
  2. digesting
  3. absorption
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17
Q

Peristalsis

A

propulsion, moves food only 4-5cm at a time, short

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18
Q

Migrating Motor Complex

A
  • “housekeeper” reflex
  • goes away when you start to eat
  • # of contractions per minute except areas of extreme contractility (90min) b/c of motiline (creates wave beginning in stomach)
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19
Q

Small Intestine Motility

A

-must have spikes to have contraction

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20
Q

Teniae Coli

A

-longitudinal muscle

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21
Q

Haustra

A

-segmentation in colon, can disappear and reappear in different areas

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22
Q

Achalsia

A

food stuck in esophagus

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23
Q

rectosphinteric reflex

A

when rectum is distended, it will contract external sphincter
absent in paraphalgicts (rectal sphincter causes defication)
voluntary rexed for deification

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24
Q

Salivary Secretion Components

A
  1. alpha amylase - pH 7, lingual lipase (acidic), solubilization (to taste food)
  2. lubrication - needed for speech
  3. protective function - allows drinking hot, dilute noxious substances, dec. cavities, sec. F, Ca, P, lysosomes to wash particles from teeth
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25
Q

Salivary Glands`

A
  1. Parotid - watery 25-40% of output
  2. Submaxilary - watery and mucus
  3. Submandibular
    - recieve lots of blood flow, CN nerves VII & IX both sympathetic and parasympathetic
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26
Q

Acinar cells

A

secretion goes unchanged in intercalated duct, then modified: abs NaCl, sec. K+ and bicarb in striated duct

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27
Q

Xerostamia

A

-absence of saliva

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28
Q

Ion concentration with flow rate

A
  • hypotonic at all rates
  • high K+ concentration all the time
  • Na+ concentration low at low rates
  • bicarb high at high rates
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29
Q

Changes in concentration as saliva moves from acinus to duct opening?

A
  • Na+ decreases, K+ increases (secreted into duct)

- more happens the longer it stays in the gland

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30
Q

Kallikrein

A

salivary glands secrete it into the blood stream, acts on plasma proteins to cause secretion of Bradykinin to increase blood flow

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31
Q

What happens if you denervate salivary glands

A

they shrink

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32
Q

What 5 things does the stomach secrete?

A
  1. Hydrogen Ion
  2. Pepsinogens
  3. Mucus
  4. Intrinsic Factor
  5. Water
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33
Q

Hydrogen Ion’s Job in Stomach?

A
  • activates conversion of pepsinogen into pepsin
  • kills bacteria
  • digests protein

***absence increases infection for small bowel

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34
Q

Pepsinogen’s Job in Stomach?

A

-pepsin digests protein by cleaving interior peptide bonds

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35
Q

Mucus’ Job in Stomach?

A
  • lubricates food

- protects lining of stomach

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36
Q

Intrinsic Factor’s Job in Stomach?

A
  • lubricates food

- protects lining of stomach

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37
Q

Water’s Job in Stomach?

A
  • dissolves and dilutes ingested material

- secretes 1.5L per day

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38
Q

How long can the liver’s stores of Vit B12 last?

A

5 years

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39
Q

What does the oxyntic gland mucosa secrete?

A

HCl

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40
Q

What does the pyloric mucosa release?

A

gastrin

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41
Q

What do mucus neck cells secrete?

A

mucus with vagal stimulation

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42
Q

What happens if you block carbanic anhydrase?

A

decrease acid secretion

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43
Q

How is H+ ion secreted?

A

down electrical gradient
against concentration gradient
into mucosa

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44
Q

What disrupts the cell membrane and cause the separation of charges across the mucosa to decrease pd?

A

aspirin and alcohol

45
Q

What keeps acid from hurting stomach?

A

gastric mucosal barrier

46
Q

Concentration of ions in gastric juice depending on the rate of secretion?

A
  • Cl is constant
  • H+ increases with increasing secretion
  • Na+ decreases with increasing secretion
  • K+ increases with increasing secretion
47
Q

Electrolytes with chronic vomiting

A

hypokalemia, low Na+, loose H+

metabolic alkalosis

48
Q

Chronic Diarrhea

A

metabolic acidosis

49
Q

Non-oxyntic Fluids

A
  • low volume with no acid production
  • electrolytes like conc. in plasma
  • produced continually at low rates, overwhelmed when secretion is stimulated from parietal cells
50
Q

Increase in Oxyntic fluid due to?

A

acid stimulation

51
Q

What are the 3 major stimulants of gastric acid secretion?

A

-gastrin: travels through circulation
-histamine: released from intracromlin like cells
stimulates acid secretion
-G cell
-Neuron

parital cell has all 3 receptors

gastrin + histamine decarboxylase activity (increased response)

52
Q

Bile acid secretion

A
  • independent of serum gastrin
  • middle of the night
  • peak is unrelated to plasmic gastrin levels
53
Q

“fasting output”

A

-10% of max output of stomach

54
Q

How much output does acid secretion peak at?

A

30mEq/hr

55
Q

Cephalic Phase

A
  • chew up food, then spit it out: 30% response of acid secretion (better the food, more acid)
  • mechanisms are all in the head
56
Q

What happens in the absence of gastrin?

A

vagus stimulates acid secretion

  1. direct stimulation of parietal cell via Ach
  2. release of gastrin via GRP
57
Q

What part of food stimulates gastrin release?

A

protein (AA and peptides), lasts 1.5hr, 50-60% of acid secretion

58
Q

What does distention do?

A
  1. parietal cells to secrete (short intermediate reflux) - local
  2. long-vaso-vagal reflux, stimulate gastric cells to release gastrin (GRP)
59
Q

Mechanisms Regulating Gastrin Release

A

Vagus Nerve
-Ach at nicotenic receptor
-GR4 cell inhibits somatostatin release
Distention

60
Q

Summary of all Mechanisms Stimulating Gastric Acid Secretion

A
  • Cephalic: chewing, swallowing, smell, taste
  • Gastric: distention, digested protein
  • Intestinal: digested protein
61
Q

Direct Inhibiters of Gastrin Release

A
  1. somatostatin
  2. secretin
  3. GIP
62
Q

pH and volume in response to a meal

A

meal: pH increases to 5-6 b/c of protein buffers

volume increase: stomach begins to secrete

63
Q

Regulation of Pepsin Secretion

A
  • Ach stimulates pepsin secretion from cell
  • H+ turns pepsinogen to pepsin
  • pH of 4 or less, automatic conversion
  • vagus nerve stimulates pepsin secretion
64
Q

Effect of smoking on pancreatic secretions?

A

decreases them

65
Q

How much does pancreas secrete per day?

A

1-2L

66
Q

What is secreted from pancreatic duct cells?

A

water and bicarb

67
Q

Acinus

A

in pancreas

-blind system “grapes”, elaborate enzymatic components

68
Q

Ductal cells % of pancreas?

A

4%

69
Q

Acinus cells % of pancreas?

A

80%

70
Q

Absence of pancreatic secretion causes?

A

malabsorption, especially protein & fat

71
Q

CCK with Pancreas?

A

major secretion regulator, triggers vago-vagal signals

-use ACh as receptor, we don’t have CCK-1 receptors

72
Q

Duct Cell in Pancreas

A

Cations: Na+ (water follows in aquaporin 1)
transport mechanisms are proteins
-Na+/K+ATPase
secondary transport: Na+ in/ H+ out of cell
-passive conductance: Cl- in cell more to lumen (abnormal in cystic fibrosis)

73
Q

Electrolytes in Pancreatic Secretion and Changes with Flow?

A

K+ & Na+ is constant: similar to plasma conc.
Low flow: dec. HCO3- inc. Cl-
High flow: inc. HCO3- dec. Cl-

74
Q

Anion concentration in High Pancreatic Secretion Rates?

A
  • Na+Cl- low secretion rates
  • Na+HCO3- high secretion rates
  • the slower the secretion the longer the exchanges (so more Cl-) can occur
75
Q

The steps of pancreatic enzyme secretion?

A
  1. RER- proteins are secreted, move to smooth golgi, then condensing vacuoles (proenzymes)
  2. In zymogen granules, fuze with luminal membrane
    - from condensing vacuole step on, need energy
76
Q

What determines the types of enzymes found in pancreatic secretion?

A

what you eat
carbs-amylase
protein-trypsin

77
Q

What protects the pancreas from the enzymes?

A
  1. Enzymes in membranes
  2. Enzymes are “pro” inactive form
  3. Trypsin responsible for activation of other enzymes
  4. Cell is antitrypsin
  5. Trypsin is autocatalytic
78
Q

Pancreatic secretion after a meal?

A
  • increase in protein
  • acid secretion
  • increase bicarb and volume
79
Q

What stimulates pancreatic secretion?

A

vagus, from cephalic phase
-conditional stimuli, smell, taste, chewing, swallowing, hypoglycemia

  • strong aciner cell stimulation
  • weak duct cell stimulation
80
Q

Secretin Release (pancreas)

A

-measure bicarb secretion
-threshold for release is 4.5 pH
-cells don’t respond to decreasing pH past 3
-if inc. volume, get higher rates of secretion
(when fat, protein, H+ enter duodenum, H+ acts on S cells to make secretin duct & aciner, also CCK cause ACh to release on duct cells)

81
Q

Phe + Secretin

A 
potent release of CCK
the 2 combine have a huge response
1. conserves hormones 
2. if needed lots of hormones, it would have other effects
POTENTIATION
82
Q

Pancreatitis

A
  • decreased volume and bicarbonate
  • may impair digestion
  • 10% hereditary (gets rid of protective mechanisms)
83
Q

Kwashiorkor

A
  • a pancreatic insufficiency
  • malnutrition
  • decreased volume, bicarb, enzymes
  • steatorrhea
84
Q

Cystic Fibrosis

A
  • no Cl- conductance in apical membrane
  • mucus secretion
  • decreased volume, bicarb, enzymes
  • steatorrhea
85
Q

Bile acids

A
  • synthesized from cholesterol

- secreted by hepatocytes into ducts

86
Q

Secretin Stimulates what into the Bile Ducts?

A
  • HCO3-
  • Na+
  • H2O
87
Q

Spincter of Oddi at rest?

A

-closed, so bile flows into gallbladder

88
Q

CCK stimulates ACh to do what to gallbladder and sphincter of Oddi?

A
  1. gallbladder contractions

2. relaxes sphincter of Oddi

89
Q

% of bile acid reabsorbed due to passive diffusion?

A

40%

90
Q

Amount of bile salts in the pool?

A

2.5g

91
Q

% of bile acids actively reabsorbed in the ileum?

A

55%

92
Q

% of bile acids lost in stool?

A

5%

93
Q

4 Important Bile Acids?

A 
Primary: synthesized by liver 
1) Cholic Acid
2) Chenodeoxycolic 
Secondary
3) Deoxycholic Acid
4) Lithocholic Acid
94
Q

While have bile salt instead of bile acids?

A

Bile acids have pKa~7, the live conjugates them to amino acids (bile salts)

  1. glycine pKa~3.7
  2. taurine pKa~1.5
95
Q

Micelle Formation

A

Polar Part: nucleus, hydroxyl group, ionized acidic group
Hydrophobic Part: hydrocarbon steroid body
-it solublizes products of fat digestion

96
Q

Biliary Histology

A

-stuff is extracted from portal vein, secreted into bile duct, flow of bile is countercurrent from flow of blood (dec. conc. gradient)

97
Q

How much bile aids secreted per day?

A

30g

98
Q

Max synthesis of bile acids per day?

A

3-5g

99
Q

Enterohepatic Circulation

A

bile acids actively transported into bile, stored in gallbladder, secreted in duodenum

  • dehydroxylate bile salts
  • if you inhibit 7 hydroxylase enzyme, stops production
100
Q

Bile acids reabsorbed in blood

A
  • continuous process
  • secretion of bile acids osmotically drives electrolytes H20
  • cholesterol and phospholipids still depend on bile acids
101
Q

Bilirubin

A
  • produced by metabolism of broken RBC
    1. formation of Fe, chelated & disposed of
    2. green-biliredin, yellow bilirubin (bound to plasma albumen in blood)
  • active process that excretes bilirubin from intestine (not very effective)
102
Q

Bilirubin Glucuronide

A

water soluble

bacteria converts it to bilirubin

103
Q

Stirkobiligin

A

makes poop brown (pigment)

104
Q

Secretion of Water & Electrolytes

A
  • osmotically drive secretion of H2O & electrolytes
  • liver ducts secretin inc. Na+ bicarb and H2O
  • Interdigestive phase: sphincter of Oddi, filling pressure of 10-20mmHg holds 20-50mL of bile
105
Q

CCK on Gallbladder Function

A
  • acts through vagal stimulation

- ACh causes contraction of gall bladder and relaxes sphincter of Oddi

106
Q

Micellar Solution

A
  • isotonic

- all cations are osmotically inactive by being bound to bile acids

107
Q

Cholesterol Stones

A
  • all bile produced is supersaturated with cholesterol - 50% normal
  • bile acid pool reduced 50%
  • crystal formation
108
Q

Pigment Stones

A

10-20%
-bile saturated with unconjugated bilirubin
-high beta glucuronidase: causes it
-gall bladder wall damaged by bacteria - E. coli
surface is damaged, physical or bacteria

GI (19 decks)

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