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PHY 503 > TBL 3 > Flashcards

TBL 3 Flashcards

1
Q

Chemical digestion

Fats

A

LIPIDS:
Triglycerides are absoped as FATTY ACIDS & MONOGLYCERIDES

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2
Q

Chemical Digestion

Protiens

A
  • AMINO ACIDS:
    absorped as small peptides and amino acids
  • AA uptake in sodium coupled transporters
  • peptides absorped faster than AA and require PepT1(ogliopeptides)
  • Pepsin activated at low pH levels 1.8-3.0..irreversible inactivated at 7.2
  • Bicarb layer protects mucous lining
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3
Q

Chemical Digestion

Carbohydrates

A

STARCHES absorped as MONOSACCHARIDES

A-amalyse enzyme starts in mouth..digest starches

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4
Q

Enzyme Release

Salivary Glands

A

Amylase break down starches
Lipase break down triglycerides

Carbs (Starches) are the only macronutrient that digest in the mouth

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5
Q

Enzyme Release

Stomach

A

Pepsin breaks down protiens
Lipase breaks down triglycerides

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6
Q

Enzyme Release

Pancreas

ACTIVE ENZYMES

A

a-amylase & lipase

starches and triglycerides

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7
Q

Enzyme Release

Intestines

A

Enterokinase (activate trypsin)
Diasaccharides (complex sugars)
Dipeptides (peptides)

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8
Q

Trypsin

A

A protease that ACTIVATES SECRETED XYMOGENS (Lysine & Argenine)
Breaks down peptides to ogliopeptides

Chymotrypsin cleaves to trypsin

Released in pancreas

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9
Q

Goblet Cells

A

Secrete mucus, deuodnum to ileum

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10
Q

Stem Cells

A

Repairs cell complex when old cells die

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11
Q

Endocrines

A

Hormones released in the blood

Gastrin is an example

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12
Q

Paracrines

A

Act on neighboring cells in the same tissue

Somatostatin and histamine are examples

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13
Q

Neurocrines

A

Neurotransmitters

That thanksgiving smell makes you hungry!

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14
Q

Hormone

Secretin

A
  1. Released from S-CELLS in DUODENUM
  2. INHIBITS GASTRIC ACID RELEASE
  3. STIMULATE PEPSIN & HCO3- SECRETION

The duodenum pH IS <4.5

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15
Q

Hormone

Gastrin

A
  1. Secrete gastric acid & growth of mucosa, duodenum, and colon
  2. Antrum and Duodenum
  3. Little (17AA): secrete from G Cells
  4. Big (34AA): secrete from duodenal
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16
Q

Gastrinoma

A
  • Causes hypergastrinemia
  • Increase parietal cell mass & acid secretion (low pH)
  • peptic ulcer
  • Decrease bile & lipase (causing diarrhea, steatorrhea, hypokalemia)
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17
Q

Hypokalemia

A

Less K+ in the blood due to loss of K+ from diarrhea, vomiting, etc.

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18
Q

Zollinger Ellison Syndrome

A

Gastrin levels increase after injecting secretin due to failure of inhibiting gastrin release

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19
Q

Hormone

CCK

A
  1. In the DUODENUM & JEJUNUM
  2. Release bile into duodenal
  3. Empty gallbladder
  4. Inhibits gastric emptying
  5. Fatty acids, peptieds, and AA stimulate release

Your stomach wont deliver any more food until the batch is digested, this is what it means for gastric emptying to be paused

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20
Q

Hormone

GLIP

Secretin family

A
  1. STIMULATES insulin release
  2. INHIBITS gastric acid secretion
  3. Oral glucose, only released when injested…meaning when there is a presence of food in the intestines that needs to be digested
21
Q

Hormone

Motilin

A

Stimulates upper GI motility during fasting periods

Released from M-CELLS

22
Q

Hormones

Somatostatin

In D cells of the corpus

A

1.Inhibits PARIETAL CELL acid secretion (decreasing acid release)
2.STIMULATED by ACID
3.INHIBITED by ACh D-Cells

Paracrine

Inhibits histamine and gastrin release

23
Q

Hormones

Histamine

Paracrine

A

Released from ECL cells w/ gastrin & ACh
1. Stimulates acid secretion
2. H2 receptors block acid secretion
3. Hypergastrinemia Acid supression so gastrin remains high

CIMETIDINE & RATITIDINE

24
Q

VIP

A
  • Relaxes the smooth muscle in the gut
  • Stimulate fluid secretion and electrolytes
25
Q

GRP/ Bombesin

A

Increase gastric release

26
Q

Enkephalins

A

Increase smooth muscle tone
* Stifness decreases GI motility

27
Q

Myenteric A. Plexux

A

Located in the proximal esophagus to anus

28
Q

Submucosal Meissner Plexus

A

Large Intestines Only
* Sensory, local secretion & absorption, and contraction

Nerve plexus

29
Q

Ascending cholinergic

A

Ms contraction promels intraluminal distally towards anus
* ACh for contraction
* Peptide YY is located in colon, senses fat and protiesn, slows intestinal emptying (inhibit motility for more nutrient absorption)

30
Q

IPAN

A

Inintiate peristalsis and dynamic contraction

31
Q

Mast Cells

A
  1. Monitor sensory input from lumen
  2. Respond to foreign antigers chemically (histamine)
  3. Increase gut motility to rid foreign antigers
  4. TnFa can be released immediately
32
Q

Peristalsis

A
  1. __
  2. I. contraction ahead of bolus
  3. continued contraction before bolus
  4. force bolus foward
33
Q

Dysphagia

A
  1. Anestesia: aspiration of stomach contents
  2. Stroke: damage cranial nerves and leads to aspiration
  3. MS Diseases: Polio, Myestenia Gravis, Botulism

Swallowing disorders

34
Q

Gastroenphageal Reflux Disease

A

In the lower esophageal spincter
1. Backwash of acid, pepsin, & bile into esophagus
2. Barret esophagus: tissue replaced by goblet cells, increase cancer risk

35
Q

Gastric Motility

A
  1. Caudad Area: mix food with gastric juice
  2. nitric oxide relaxes orad area (upper stomach)
36
Q

What happens during increased gastric emptying?

A
  1. INCREASED orad tone & DECREASED pylorus tone
  2. force contraction
  3. Empty intestines
37
Q

Acinar cells

A

Secrete Cl- and enzymes
Isotonic
1. Na/K pump moves Na+ basolaterally inward
2. Na/K/Cl cotransporter bring cl- into cell
3. Rise in K+
4. Cl- secretes into lumen
5. Na+ driven into lumen

CCK & ACh increase acinar secretion of Na& Cl

38
Q

Duct cells

A

Secrete bicarb and K+
High mitochondria
pH < 7.4

Secretin

Ouabaine BLOCKS HCO3-
Atrophine BLOCKS ACh and Ca2+

39
Q

Pancreatitis

A

Decrease HCO3-
Leads to dehydration and oily stool (steatorrhea)
Alcohol & Cystic Fibrosis
Failure of the pancreas

40
Q

Stomach

A
  • Functions for food storage and protien digestion
  • Cardia – Located near the gastroesophageal junction, devoid of acid-secreting cells.
    Body (Corpus) – The largest portion, where acid-secreting cells are located.
    Antrum – The distal region that leads to the pylorus, involved in secreting regulatory hormones.
  • Gastric (oxyntic) glands: Secrete digestive substances like acid and pepsinogen.
    Pyloric glands: Primarily secrete regulatory hormones, including gastrin and somatostatin.
  • Superficial epithelial cells and mucous neck cells secrete bicarbonate and mucus, forming an alkaline barrier.
    Parietal cells secrete acid and intrinsic factor, crucial for vitamin B12 absorption.
    Chief cells secrete pepsinogen, which is activated by the acidic environment to break down proteins.
    Endocrine cells release regulatory hormones (gastrin, somatostatin) that help manage digestion.

Cardia, Fundus, Antrum, Cells

41
Q

What is Hirschsprung disease and how is it treated?

A
  • mutations in multiple genes (e.g., endothelin-B receptor) leading to the failure of neural crest cells to migrate caudally
  • Constipation Megacolon Narrowed colon segment (usually in the rectum)
  • Absence of ganglion cells in the submucosal (Meissner’s) and myenteric (Auerbach’s) plexuses.
  • Surgical removal of the aganglionic segment of the colon to restore normal function.
42
Q

What systems are involved in neuroendocrine control of pancreatic secretion?

A

Parasympathetic nervous system: Main regulator during fasting (phase 3)
Cholecystokinin (CCK): Stimulates enzyme secretion during the fed state.
Adrenergic pathways: Can suppress fasting secretion through α-adrenergic tone.

43
Q

What is the relationship between migrating motor complexes (MMCs) and pancreatic secretion?

A

Phase I: Quiescent motility, minimal pancreatic secretion.
Phase II: Increased motility, increased secretion.
Phase III: Maximal motility and peak secretion.
Phase IV: Secretion declines after phase III

44
Q

Telenzepine (M1 antagonist)

A

reduce pancreatic enzyme secretion by more than 85% during phases II and III.

45
Q

What is nonpropulsive segmentation in the colon?

A

Nonpropulsive segmentation is driven by slow-wave activity, resulting in circular muscle contractions that churn the colonic contents.
This movement pushes material toward the cecum (orad direction).
Haustra (the typical segmented appearance) are formed during this process, giving the colon its segmented look.
The primary function is mixing, and it helps with fluid and electrolyte absorption.
Material stays in the proximal large intestine for longer periods during this phase.

46
Q

What is mass peristalsis, and when does it occur?

A

Mass peristalsis is a strong, propulsive contraction that moves colonic contents distally (20 cm or more).
It occurs 1-3 times a day, often triggered by eating.
During mass peristalsis, haustra disappear as the contents are propelled forward, and they reappear afterward.
Mass peristalsis is the primary form of propulsive motility in the colon.

47
Q

What motor activity occurs in the distal colon?

A

n the distal colon, the primary motor activity is nonpropulsive segmentation through annular or segmental contractions.
This is where the final desiccation (water absorption) of colonic contents occurs.
The contents are stored in the distal colon until an occasional mass peristalsis moves them into the rectum.

48
Q

How does the rectum fill, and what role does mass peristalsis play?

A

The rectum remains nearly empty due to nonpropulsive segmentation until mass peristalsis occurs in the distal colon.
Mass peristalsis propels contents into the rectum, triggering rectal filling.
This process facilitates the storage and eventual evacuation of fecal material.

PHY 503 (1 decks)

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