GI 7 Flashcards

1
Q

Defecation

A

Two reflexes initiated by distension of the rectum
Short and long reflex

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2
Q

Short reflex of defecation

A

Local peristaltic waves

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3
Q

Long reflex of defecation

A

Relaxation of internal sphincter (smooth muscle)
Contraction of external (skeletal)
More forceful peristaltic contractions form parasympathetic input

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4
Q

What is the defecation reflex completed by

A

Voluntary relaxation of external sphincter (skeletal) and aided by increased abdominal pressure

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5
Q

Diarrhea

A

An increase in frequency, volume, and fluid content of feces due to increased secretion, reduced absorption or increased motility

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6
Q

What is diarrhea induced by

A

Osmotic, secretory, inflammatory or motility

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7
Q

Osmotic diarrhea

A

Excess solute stays within lumen of GI which prevents normal amt of H20 absorption
Water stays and leaves

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8
Q

Inflammatory diarrhea

A

Due to infection
Breaks barrier and causes damage to int preventing proper absorption

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9
Q

What can secretory be caused by

A

Immune cells (flush out GI)
Bacteria

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10
Q

How does cholera cause secretory diarrhea

A

Cholera toxin causes persistent opening of Cl leak channels
Cl draws Na, water into lumen
Creates watery secretion

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11
Q

Use of penicillin based antibiotics can alter

A

Normal bacterial flora
Remaining bacteria have reduced competition for space and nutrients

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12
Q

What does reduced competition of bacteria leave you prone to

A

Infection by C.difficile

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13
Q

What does c. Difficile cause

A

Colitis: watery diarrhea, fever, nausea, abdominal pain

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14
Q

What is cure for C. difficile infection

A

Fecal transplant from healthy individual
Rapid addition of good bacteria

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15
Q

Vomiting

A

Contents of stomach and occasionally small int are forcefully expelled through mouth
- associated with nausea

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16
Q

Vomiting center is where

A

Medulla

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17
Q

Vomiting center in medulla causes 3 responses

A
  1. Retrograde contractions in small int and stomach (towards stomach +lower esophageal)
  2. Contraction of abdominal inspiratory muscles (diaphragm) increases gastric pressure
  3. Relaxation of esophageal sphincters
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18
Q

What is outside BBB and communicated with vomiting center

A

Chemoreceptor trigger zone

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19
Q

Causes of vomiting

A

Abnormal vestibular input (motion sickness, spinning)
Input from sensory receptors in stomach and intestines
Direct input from drugs, toxins in chemoreceptor trigger zone

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20
Q

Where is immune function in GI tract

A

Gut -Associated lymphoid tissue (GALT)
80% of lymphocytes located in gut

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21
Q

What cells play big role in immune responses

22
Q

How do M cells work in immune responses

A

Receptor mediated endocytosis
- transport antigens to macrophages, lymphocytes, and dendritic cells
- release cytokines to attract more immune cells

23
Q

What do cytokines do in gut

A
  • attract more immune cells to attack invaders
  • trigger increased Cl secretion (diarrhea) to flush out pathogens
24
Q

What do we rely on to regulate intake

A

Behavioural mechanisms
Appetite and satiety

25
During feeding state and 3-6 hours following what state is body in
Anabolism Body will store nutrients
26
During fasting state body is in
Catabolism High levels of breakdown
27
What is the hunger center
LH- Lateral hypothalamus
28
Communication between 2 areas for satiety
ARC - Arcuate nucleus PVN- paraventricular nucleus
29
What in medulla plays role in appetite and satiety
NTS- nucleus tractus solitarii
30
What maintains body weight at a relatively stable value
Behavioural mechanisms
31
Theories of long term regulation of feeding behaviour
1. Glucostatic theory 2. Lipostatic theory
32
Glucostatic theory
Glucose metabolism in the hypothalamus regulates food intake (proved to be short term)
33
Lipostatic theory
Signals from the bodies fat stores regulate food intake (long term regulator)
34
If weight is lost during starvation
Weight is rapidly gained when food is freely available
35
What is ob/ob gene
Encodes a protein that tell brain fat reserves are normal
36
What was ob/ob mouse
Obese
37
Leptin
Released from adipocytes and regulates body mass by acting on neurons of hypothalamus that decrease appetite and increase energy expenditure
38
In most obese individuals what does leptin do
Brain doesnt respond to it
39
Elevated leptin
Decrease energy intake Increase energy output
40
What does leptin act on
Arcuate nucleus
41
Response to elevated leptin
1. Inhibition of lateral feeding center 2. Activation of paraventricular nucleus (PVN)
42
What are 2 responses of activation of PVN from increased leptin
Humoral response Visceromotor response
43
Humoral response
Increase TSH, ACTH from pituitary - increased metabolic rate throughout body
44
Visceromotor response
Increased sympathetic output - increase body temp to increase metabolism
45
What do anorectic peptide do when increased leptin
Reduce food intake
46
Response to decreased leptin
1. Reduced activation of a-MSH and CART neurons 2. Activation of NPY and AgRP containing neurons
47
Reduced activation of a-MSH and CART neurons
Reduced activation of PVN (decreased TSH and ACTH) - Decreased metabolic rate Activation of parasympathetic output
48
Activation of NPY and AgRP containing neurons
-stimulation of feeding center - further inhibition PVN
49
Orexigenic peptides
From NPY/AgRP neurons of Arcuate nucleus - facilitate eating
50
When is aMSH/CART neuron activity high
High leptin level
51
Why did leptin supplementation fail to treat obesity
Have to have OB/OB mutation (rare)