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Bmsc 208 > GI 7 > Flashcards

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

A

M cells

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
Q

During feeding state and 3-6 hours following what state is body in

A

Anabolism
Body will store nutrients

26
Q

During fasting state body is in

A

Catabolism
High levels of breakdown

27
Q

What is the hunger center

A

LH- Lateral hypothalamus

28
Q

Communication between 2 areas for satiety

A

ARC - Arcuate nucleus
PVN- paraventricular nucleus

29
Q

What in medulla plays role in appetite and satiety

A

NTS- nucleus tractus solitarii

30
Q

What maintains body weight at a relatively stable value

A

Behavioural mechanisms

31
Q

Theories of long term regulation of feeding behaviour

A
  1. Glucostatic theory
  2. Lipostatic theory
32
Q

Glucostatic theory

A

Glucose metabolism in the hypothalamus regulates food intake (proved to be short term)

33
Q

Lipostatic theory

A

Signals from the bodies fat stores regulate food intake (long term regulator)

34
Q

If weight is lost during starvation

A

Weight is rapidly gained when food is freely available

35
Q

What is ob/ob gene

A

Encodes a protein that tell brain fat reserves are normal

36
Q

What was ob/ob mouse

A

Obese

37
Q

Leptin

A

Released from adipocytes and regulates body mass by acting on neurons of hypothalamus that decrease appetite and increase energy expenditure

38
Q

In most obese individuals what does leptin do

A

Brain doesnt respond to it

39
Q

Elevated leptin

A

Decrease energy intake
Increase energy output

40
Q

What does leptin act on

A

Arcuate nucleus

41
Q

Response to elevated leptin

A
  1. Inhibition of lateral feeding center
  2. Activation of paraventricular nucleus (PVN)
42
Q

What are 2 responses of activation of PVN from increased leptin

A

Humoral response
Visceromotor response

43
Q

Humoral response

A

Increase TSH, ACTH from pituitary
- increased metabolic rate throughout body

44
Q

Visceromotor response

A

Increased sympathetic output
- increase body temp to increase metabolism

45
Q

What do anorectic peptide do when increased leptin

A

Reduce food intake

46
Q

Response to decreased leptin

A
  1. Reduced activation of a-MSH and CART neurons
  2. Activation of NPY and AgRP containing neurons
47
Q

Reduced activation of a-MSH and CART neurons

A

Reduced activation of PVN (decreased TSH and ACTH)
- Decreased metabolic rate
Activation of parasympathetic output

48
Q

Activation of NPY and AgRP containing neurons

A

-stimulation of feeding center
- further inhibition PVN

49
Q

Orexigenic peptides

A

From NPY/AgRP neurons of Arcuate nucleus
- facilitate eating

50
Q

When is aMSH/CART neuron activity high

A

High leptin level

51
Q

Why did leptin supplementation fail to treat obesity

A

Have to have OB/OB mutation (rare)

Bmsc 208 (33 decks)

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