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Phisiology Hope > Gastro > Flashcards

Gastro Flashcards

1
Q

THE ALIMENTARY TRACT: GI segments

A
  • Mouth
  • Pharynx
  • Esophagus
  • Stomach
  • Small Intestine
  • Large Intestine
  • Sphincters between segments
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2
Q

THE ALIMENTARY TRACT: Accessory organs

A
  • Liver
  • Gall bladder
  • Pancreas
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3
Q

Functions of the Alimentary Tract

A

Provides the body with a continual supply of water, electrolytes, vitamins, and nutrients, by:

  • Movement of food
  • Secretion of digestive juices and digestion of the food
  • Absorption of water, nutrients and digestive products
  • Circulation of blood to carry away the absorbed substances
  • Local, nervous, and hormonal control
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4
Q

Each part of the Alimentary Tract is adapted to its specific functions:

A
  • Simple passage of food (esophagus)
  • Temporary storage of food (stomach)
  • digestion and absorption (small intestine)
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5
Q

LAYERS

A
  • Serosa
  • Longitudinal Muscle Layer
  • Circular Muscle Layer
  • Submucosa
  • Mucosa
    The motor functions of the gut are performed by the different
    layers of smooth muscle.
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6
Q

Gastrointestinal smooth muscle function as a syncytium

A

• Within each bundle, muscle fibers are electrically connected with one another through gap junctions → low-resistance movement of ions
• Electrical signals that initiate contractions → travel readily
from one fiber to the next within each bundle but more
rapidly along the length of the bundle than sideways.
• Each bundle is partly separated from the next by loose connective tissue, but the muscle bundles fuse with one another at many points

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7
Q

Gastrointestinal smooth muscle function as a syncytium 2

A

• Each muscle layer represents a branching latticework of
smooth muscle bundles.
• Each muscle layer functions as a syncytium → when an action potential is elicited anywhere within the muscle mass, it generally travels in all directions in the muscle.

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8
Q

Electrical Activity of GI Smooth Muscle

A 
Electrical Activity of GI Smooth Muscle
• Excited by almost continual slow, intrinsic electrical activity
along the membranes of the muscle fibers
• SLOW WAVES
• SPIKE POTENTIALS
• TONIC CONTRACTIONS
- Exhibited by some GI Smooth Muscles
- No slow waves
- Last minutes to hours
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9
Q
  • NOT true action potentials; slow, undulating changes in the RMP
  • Slowest: Stomach- Fastest: Small intestines
  • Sodium entry
  • Pacemaker: Interstial cells of Cajal
A

SLOW WAVES

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10
Q
  • True action potentials
  • Threshold: -40mV
  • Sodium and calcium entry
A

SPIKE POTENTIALS

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11
Q
  • Exhibited by some GI Smooth Muscles
  • Not associated with the basic electrical rhythm of slow waves but often lasts several minutes to hours
  • often increases or decreases in intensity but continues
A

TONIC CONTRACTIONS

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12
Q

Factors that depolarized the membrane (less negative; more excitable)

A
  1. stretching of muscle
  2. stimulation of acetylcholine released from the parasympathetic nerves
  3. stimulation by several specific GI hormones
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13
Q

Factors that make the membrane hyperpolarized (more negative; less excitable)

A
  1. stimulation of norepinephrine/epinephrine

2. stimulation of the sympathetic nerve (secrete norepinephrine at their endings)

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14
Q

MECHANISMS FOR TONIC CONTRACTIONS:

A

• Continuous Repetitive Spike Potentials → the greater the
frequency, the greater the degree of contraction
• Hormones → continuous partial depolarization of the smooth
muscle membrane without causing action potentials
• Continuous entry of Calcium (unclear mechanism)

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15
Q
  • Local, independent neural control of the GI tract → especially important in controlling gastrointestinal movements and secretion.
  • Can function independently of these extrinsic nerves
  • But stimulation by the parasympathetic and sympathetic systems can greatly enhance or inhibit gastrointestinal functions
A

ENTERIC NERVOUS SYSTEM

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16
Q

NEURAL CONTROL OF GI TRACT

A

• Intrinsic Control - Enteric nervous system

  • Myenteric (Auerbach’s) plexus
  • Submucosal (Meissner’s) plexus

• Extrinsic Control - Autonomic nervous system

  • Parasympathetic – mainly stimulates ACh
  • Sympathetic – mainly inhibits NE
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17
Q
  • an outer plexus lying between Inner Circular and Outer
    Longitudinal layers
  • GI Movements
  • Mainly excitatory except for Pyloric Sphincter and Ileocecal Valve, where relaxation occurs
A

MYENTERIC (AUERBACH’S) PLEXUS

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18
Q
  • Submucosa
  • GI secretions, absorption, contraction of submucosal
    muscle
A

SUBMUCOSAL (MEISSNER’S) PLEXUS

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19
Q

• Consists mostly of a linear chain of many interconnecting
neurons that extends the entire length of the GI tract.
• Concerned mainly with controlling muscle activity along the length of the gut, because:
- It extends all the way along the intestinal wall
- It lies between the longitudinal and circular layers of intestinal smooth muscle.

A

MYENTERIC PLEXUS

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20
Q

• Not entirely excitatory, some of its neurons are inhibitory
• Fiber endings secrete an inhibitory transmitter, possibly
VASOACTIVE INTESTINAL POLYPEPTIDE or some other inhibitory peptide.
• Inhibitory signals affect intestinal sphincters impeding
movement of food along the GI tract:
- Pyloric sphincter – emptying of the stomach into the duodenum
- Sphincter of the ileocecal valve – emptying from the SI
into the cecum

A

MYENTERIC PLEXUS

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21
Q

Principal effects of Myenteric Plexus when stimulated:

A
  • ↑ tonic contraction, or “tone,” of the gut wall
  • ↑ intensity of the rhythmical contractions
  • ↑ rate of the rhythm of contraction
  • ↑ velocity of conduction of excitatory waves along the gut wall → more rapid movement of peristaltic waves
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22
Q
  • Mainly concerned with controlling function within the inner wall of each minute segment of the intestine.
  • Control local intestinal secretion, local absorption, and local contraction of the submucosal muscle that causes various degrees of infolding of the gastrointestinal mucosa.
A

SUBMUCOSAL PLEXUS

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23
Q

ENTERIC NEUROTRANSMITTERS

A
  • Acetylcholine – most often excitatory

* Norepinephrine/Epinephrine – most often inhibitory

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24
Q
  • Parasympathetic stimulation increases activity of the ENS

* Sympathetic stimulation usually inhibits GIT activity

A

AUTONOMIC CONTROL OF GIT

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25
Q

• Cranial parasympathetic nerve fibers are almost entirely in the VAGUS NERVE
- Esophagus, stomach, and pancreas; somewhat less to
the intestines down through the first half of the large
intestine
• Sacral parasympathetics (S2, S3, S4) pass through the PELVIC NERVES to the distal half of the large intestine and all the way to the anus.
- Sigmoidal, rectal, and anal
- Fibers function especially to execute the defecation
• Postganglionic neurons located mainly in the myenteric and submucosal plexuses

A

PARASYMPATHETIC CONTROL

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26
Q

• Sympathetic fibers to the GIT are from T5-L2
• Most of the preganglionic fibers that innervate the gut enter the sympathetic chains that lie lateral to the spinal column, and many of these fibers then pass on through the
chains to outlying ganglia such as to the celiac ganglion and various mesenteric ganglia
• Most of the postganglionic sympathetic neuron bodies are in these ganglia, and postganglionic fibers then spread through postganglionic sympathetic nerves to all parts of the gut.
• Nerve endings secrete mainly norepinephrine but also small amounts of epinephrine.

A

SYMPATHETIC CONTROL

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27
Q

Inhibits GIT activity causing many effects opposite to those of the parasympathetic system. it exert its effects in two ways:

A
  1. To a slight extent by direct effect of secreted norepinephrine to inhibit intestinal tract smooth muscle (except the mucosal muscle, which it excites)
  2. To a major extent by an inhibitory effect of norepinephrine on the neurons of the entire enteric nervous system.
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28
Q

• Many afferent sensory nerve fibers innervate the gut.
• Some of them have cell bodies in the ENS itself and in the
DRG of the spinal cord.
• Sensory stimuli:
- Irritation of the gut mucosa
- Excessive distention of the gut
- Presence of specific chemical substances
• Signals transmitted can cause excitation or, under other
conditions, inhibition of intestinal movements or intestinal
secretion

A

AFFERENT SENSORY INFORMATION FROM THE GUT

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29
Q

TYPES OF GASTROINTESTINAL REFLEXES

A
  1. Reflexes that are integrated entirely within the gut wall ENS
  2. Reflexes from the gut to the pre vertebral sympathetic ganglia and then back to the GIT
    e. g. Gastrocolic, Enterogastric, Colonoileal Reflexes
  3. Reflexes from the gut to the spinal cord or brain stem and then back to the GIT
    - E.g. defecation reflexes
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30
Q

Reflex from stomach to cause colon evacuation

A

gastrocolic reflex

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31
Q

Reflex from colon and small intestine to inhibit gastric motility and secretion

A

enterogastric reflex

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32
Q

Reflex rom the colon to inhibit emptying of ileal contents into the colon

A

colonoileal reflex

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33
Q

TYPES OF GI TRACT MOVEMENTS

A
  • Propulsive movements: cause food to move forward along the tract at an appropriate rate to accommodate digestion and absorption
  • Mixing movements: keep the intestinal contents thoroughly mixed at all times
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34
Q

• Peristalsis: the basic propulsive movement of the gastrointestinal tract
• A contractile ring appears around the gut and then moves
forward; Any material in front of the contractile ring is moved forward
• Inherent property of many syncytial smooth muscle tubes
• Stimulation at any point in the gut can cause a contractile
ring to appear in the circular muscle, and this ring then
spreads along the gut tube.
• Other stimuli: chemical or physical irritation; parasympathetic signals

A

PROPULSIVE MOVEMENTS

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35
Q
  • usual stimulus for intestinal peristalsis
  • If a large amount of food collects at any point in the gut, stretching of the gut wall stimulates the ENS to contract the gut wall 2 to 3 cm behind this point, and a contractile ring appears that initiates a peristaltic movement.
A

Gut distention

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36
Q

Effectual peristalsis requires an active myenteric plexus

A

• Peristalsis occurs only weakly or not at all in any portion of
the GIT that has congenital absence of the myenteric plexus
• Depressed or completely blocked in the entire gut when
treated with atropine → paralysis of cholinergic nerve endings of the myenteric plexus.

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37
Q

• Myenteric reflex or peristaltic reflex
- Distention → GI segment excitation → peristalsis: starting
from orad going to anal direction → pushing the intestinal
contents in the anal direction
- Gut sometimes relaxes several cm downstream toward
the anus (receptive relaxation) ➔ allowing food to be
propelled more easily toward the anus than toward the
mouth.
- Complex pattern does not occur in the absence of the
myenteric plexus

• Peristaltic reflex + anal direction of movement of the peristalsis

A

THE LAW OF THE GUT

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38
Q

• Differ in different parts of the GIT
• In some areas, the peristaltic contractions themselves cause most of the this
• At other times, local intermittent constrictive contractions occur every few centimeters in the gut wall.
- These constrictions usually last only 5 to 30 seconds; then new constrictions occur at other points in the gut, thus “chopping” and “shearing” the contents first here and then there.

A

MIXING MOVEMENTS

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39
Q
  • Requires active myenteric plexus
  • Stimulus: Distention, irritation, parasympathetics
  • Myenteric Reflex/Peristaltic Reflex: Muscles upstream
    will exhibit contraction while muscles downstream will
    exhibit “receptive relaxation”
  • LAW OF THE GUT: Myenteric Reflex + Anal Direction of
    Peristalsis
A

Propulsive Movements/Peristalsis

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40
Q
  • Local intermittent constrictive contractions every few centimeters
  • Chopping and shearing of food
A

Mixing Movements

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41
Q

SPLANCHNIC CIRCULATION

A
  • Blood from the gut, spleen and pancreas will go immediately to the liver via the PORTAL VEIN and leave via the HEPATIC VEIN into the SVC
  • WATER-SOLUBLE NUTRIENTS - goes to the portal vein and liver
  • FATS -not carried in the portal blood; goes to the lacteals and thoracic duct
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42
Q

• The time that food remains in each part of the GIT is critical for optimal processing and absorption of nutrients.
• Appropriate mixing must be provided.
• Nervous and hormonal mechanisms control the timing → optimal timing
- Because the requirements for mixing and propulsion are
quite different at each stage of processing

A

PROPULSION OF FOOD IN THE GI TRACT

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43
Q

HUNGER VS APPETITE

A
  • Hunger - Intrinsic desire for food; Principal determinant of the amount of food that a person ingests
  • Appetite - Principal determinant of the type of food that a person preferentially seeks
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44
Q 
- Teeth designed for chewing
Anterior teeth (incisors) → cutting
Posterior teeth (molars) → grinding
  • Mostly due to the CHEWING REFLEX
    »Bolus of food in the mouth → inhibition of CN V → relaxation of jaw muscles → rebound contraction
    »Automatically raises the jaw to cause closure of the
    teeth, also compresses the bolus
    »Chewing increases surface area of food
A

MASTICATION

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45
Q

Purpose of Chewing

A

o Breaks cells - breaks apart indigestible cellulose
o Increases surface area - decreases particle size
o Mixes food with saliva
o Begins digestion of starches (α-amylase, lingual lipase)
o Lubricates food for swallowing

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46
Q
  • Complicated mechanism
  • Pharynx subserves respiration and swallowing
  • Pharynx is converted for only a few seconds at a time
    into a tract for propulsion of food.
A

SWALLOWING (DEGLUTITION)

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47
Q

Swallowing can be divided into:

A
  1. Voluntary Stage - initiates the swallowing process
  2. Pharyngeal Stage - involuntary and constitutes passage of food through the pharynx into the esophagus
    - Trachea Closed
    - UES Relaxes
    - Peristalsis Occurs
  3. Esophageal Stage - involuntary; transport food from pharynx to stomach
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48
Q

Esophageal Stage (2 Types of Peristalsis)

A

o Primary Peristalsis continuation of the peristaltic
wave: pharynx → esophagus
o Secondary Peristalsis: due to distention of the
esophagus itself by the retained food

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49
Q

(NERVOUS CONTROL OF SWALLOWING)

  • Sensory input from pharnyx and esophagus
  • Coordinates activity from vagal nuclei with other centers
    (e. g., inhibits respiratory center)
A

Swallowing Center - medulla

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50
Q

(NERVOUS CONTROL OF SWALLOWING)

  • Food in pharynx → afferent sensory input via vagus/glossopharyngeal N. → swallowing center → brain stem nuclei → efferent input to pharynx
A

Pharyngeal Phase

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51
Q

(NERVOUS CONTROL OF SWALLOWING)

  1. Primary peristalsis
    - Continuation of pharyngeal peristalsis
    - Coordinated by swallowing center
    - Cannot occur after vagotomy (striated muscle)
  2. Secondary peristalsis
    - Stretch related afferent sensory input to ENS and
    swallowing center are both involved
    - Can occur after vagotomy (SM)
A

Esophageal Phase

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52
Q

INGESTION OF FOOD

A

RECEPTIVE RELAXATION OF THE STOMACH

  • Precedes peristaltic wave in the esophagus
  • Accommodates incoming food

LOWER ESOPHAGEAL SPHINCTER

  • Tonically Contracted (30mmHg)
  • Prevents Reflux (along with valve-like mechanism of the esophagus)
  • Exhibits receptive relaxation to food also
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53
Q

MOTOR FUNCTIONS OF THE STOMACH

A
  1. STORAGE OF FOOD - Up to 1.5 L
  2. MIXING OF FOOD WITH GASTRIC SECRETIONS
    - Formation of Chyme
    - Retropulsion also seen
    - Hunger contractions cause Hunger Pangs, especially in young healthy people
  3. SLOW EMPTYING OF CHYME
    - Intense antral peristaltic contractions against the pylorus
    promote gastric emptying
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54
Q
  • Allows water easily
  • does NOT allow food until chyme becomes almost
    fluid-like
A

PYLORIC SPHINCTER

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55
Q

GASTRIC EMPTYING (Promoters and Inhibitors)

A

Promoters: Gastrin, stomach wall stretch(minor only)

Inhibitors: CCK, Enterogastric nervous feedback reflexes,
secretin and GIP

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56
Q

Small intestinal motility contributes to digestion and absorption by:

A
  1. Mixing chyme - with digestive enzymes and other secretions
  2. Circulation of chyme - to achieve optimal exposure to
    mucosa
  3. Propulsion of chyme - in an aboral direction
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57
Q

Two types of movements in small intestine following a meal

A
  1. Peristalsis - a propulsive movement; recall “Law of
    Gut.” → 3-5 hours for food to go from pylorus to ileocecal
    valve
  2. Segmentation: a mixing movement
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58
Q

• Purpose: housekeeping function
- Sweeps undigested residue toward colon to maintain low
bacterial counts in upper intestine.
• Most coordinated, rapid peristalsis
• Occurs between meals
• Characteristics
- Periods of intense peristaltic contractions
- Takes ~90 min to go from stomach to colon
- Mediated by motilin and ENS

A

MIGRATING MOTILITY COMPLEXES (MMC)

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59
Q

• Functions as a valve and a sphincter
• Valvular function
- prevents backflow into small intestine mechanically
• Sphincter function
- regulates movement of ileal contents into large intestine
- ENS and extrinsic nerves

A

ILEOCECAL JUNCTION

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60
Q

• Functions of large intestine smooth muscle:
- Mixes chyme: enhances fluid / electrolyte absorption
(haustral contractions)
- Propels fecal material (mass movements)
• Very sluggish movement - 8-15 hours from ileocecal valve to the colon
• Chyme becomes Feces
• Proximal Half: Absorption of water
• Distal Half: Storage of feces

A

MOTILITY OF THE LARGE INTESTINES

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61
Q
  • Purpose - Mixing movements facilitate fluid and electrolyte absorption (minimal propulsion)
  • Structural and functional basis
  • They appear and disappear every 30-60s
  • Require contraction of longitudinal and circular SM
  • Circular SM is concentrated in some areas
A

HAUSTRAL CONTRACTIONS

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62
Q

• Propulsive movements that occur from cecum to sigmoid
colon
• Initiated by Gastrocolic Reflex, Duodenocolic Reflex and irritation in the colon
• Stimulates desire for defecation - Prevented by Internal Anal Sphincter and External Anal Sphincter

A

MASS MOVEMENTS

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63
Q

(CONTROL OF DEFECATION)

  • Mediated entirely by ENS is initiated when feces enters
    rectum via mass movements
  • Rectal distention initiates afferent signals that spread through myenteric plexus to descending and sigmoid colon, and rectum.
  • Causes contractions that force feces toward anus.
A

Intrinsic reflex

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64
Q

Internal anal sphincter relaxes and if external anal sphincter is voluntarily relaxed, __ occurs.

A

defecation

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65
Q

(CONTROL OF DEFECATION)

  • Parasympathetic cord reflex greatly intensifies intrinsic reflex (but is not different qualitatively)
  • Rectal distention also initiates cord reflex. Afferent signals go to sacral cord and then back to descending and
    sigmoid colon, and rectum by way of parasympathetic fibers in pelvic nerves.
  • Sensory and motor fibers for defecation reflex.: S2, S3, S4
  • Intact when spinal cord is injured at higher levels.
A

Spinal cord reflex

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66
Q

(CONTROL OF DEFECATION)

  • Afferent signals entering spinal cord initiate other effects
    that require intact spinal cord.
    o Deep breath, closure of glottis, and increased abdominal
    pressure (valsalva maneuver)
    o All work to move fecal contents downward
  • Spinal transection or injury can make defecation a difficult
    process
    o Cord defecation reflex can be excited (either digitally
    or with enema)
A

Involvement of higher centers

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67
Q

Reflex where there is stretch bowel, proximal contraction, distal relaxation.

A

Peristaltic Reflex

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68
Q

Reflex from duodenum to regulate gastric emptying

A

Enterogastric Reflex

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69
Q

(Reflex)

gastric distention relaxesileocecal sphincter

A

Gastroileal Reflex (gastroenteric)

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70
Q

overdistention or injury of bowel segment causes entire bowel to relax.

A

Intestino-intestinal Reflex

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71
Q

distention of stomach/duodenum initiates mass movements.

A

Gastro- and Duodenocolic Reflexes

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72
Q

rectal distention initiates defecation

A

Defecation Reflex (rectosphincteric)

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73
Q

Stimuli for: Protein, Distention, Nerve (Acid inhibit release)
Site of Secretion: G cells of the antrum, duodenum, and jejunum
Actions: Stimulates GASTRIC ACID SECRETION AND MUCOSAL GROWTH.

A

Gastrin

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74
Q

Stimuli for secretion: Protien, Fat, Acids
Site of Secretion: I cells of the duodenum, jejunum, and ileum
Actions:
- Stimulates pancreatic enzyme secretion, pancreatic bicarbonate secretion, gallbladder contraction, growth of exocrine pancreas
- Inhibits gastric emptying and appetite to prevent overeating

A

Cholecystokinin

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75
Q

Stimuli for secretion: Acid, Fat
Site of Secretion:S cells of the duodenum, jejunum, and ileum
Actions:
- Stimulates Pepsin secretion, Pancreatic bicarbonate secretion, Biliary bicarbonate secretion and Growth of exocrine pancreas
- Inhibits Gastric Acid secretion

A

Secretin

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76
Q

Stimuli for secretion: Protein, Fat, Carbohydrate
Site of Secretion: K cells of the duodenum and jejunum
Actions:
- Stimulate Insulin release
- Inhibits Gastric acid secretion
*slows the emptying of gastric contents into the duodenum when user intestine is overloaded with food products

A

Gastric inhibitory peptide (GIP) or Glucose-dependent insulinotropic peptide

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77
Q

Stimuli for secretion: Fat, Acid, Neve
Site of Secretion: M cells of the duodenum and jejunum
Actions: Stimulates Gastric motility and Intestinal motility

A

Motilin

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78
Q

Motilin is released cyclically and stimulates waves of gastrointestinal motility called __ that move through the stomach and small intestine every 90 minutes in a fasted person.

A

interdigestive myoelectric complexes

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79
Q

Throughout the gastrointestinal tract, secretory glands subserve two primary functions:

A
  1. digestive enzymes are secreted in most areas of the alimentary tract, from the mouth to the distal end of the
    ileum
  2. mucous glands, from the mouth to the anus, provide mucus for lubrication and protection of all parts of the alimentary tract.
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80
Q

Anatomical Types of Glands

A

Single secretory cells - goblet cells
Pits – Crypts of Lieberkuhn
Tubular glands – oxyntic gland
Complex glands – salivary gland and pancreas

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81
Q

(stimulation of GIT)

Trophic stimulation – contact with food increases mucus secretion and juices

A

Local stimulation

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82
Q

Stimulation of enteric nervous system:

A

(1) tactile stimulation
(2) chemical irritation
(3) distention of gut wall

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83
Q

Autonomic stimulation of GIT: Parasympathetic

A

stimulates secretion via CN IX (glossopharyngeal) and CN X (vagus) (salivary, esophageal, gastric, pancreas, Brunner’s glands in the duodenum

pelvic parasympathetic nerves (distal portion of the large intestines)

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84
Q

Autonomic stimulation of GIT: Sympathetic

A

dual effect; sympa alone slightly increases secretion, superimposed on parasympathetic stimulation, decreases secretion (primarily via reduction of blood supply of glands)

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85
Q

Stimulation of GIT: Hormonal

A

GI hormones – polypeptides or polypeptide derivatives

Significant in the release of gastric and pancreatic secretion

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86
Q

Source: Gastric antrum (G cells)
Stimulus for secretion: Oligopeptides
Pathway of action: Endocrine
Targets: ECL cells and parietal cells of the gastric corpus
Effects: Stimulation of parietal cells to secrete H+ and ECL cells to secrete histamine

A

Gastrin

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87
Q

Source: Duodenum (I cells)
Stimulus for secretion: Fatty acids, hydrolyzed protein
Pathway of action: Paracrine, endocrine
Targets: Vagal afferent terminals, pancreatic acinar cells
Effects: Inhibition of gastric emptying and H+ secretion; stimulation of pancreatic enzyme secretion, gallbladder contraction, inhibition of food intake

A

Cholecystokinin

88
Q

Source: Duodenum (S cells)
Stimulus for secretion: Protons
Pathway of action: Paracrine, endocrine
Targets: Vagal afferent terminals, pancreatic duct cell
Effect: Stimulation of pancreatic ductile secretion (H2O and HCO3-)

A

Secretin

89
Q 
Source: Intestine (K cells)
Stimulus for secretion: Fatty acids, glucose
Pathway of action: Endocrine
Targets: Beta cells of the pancreas
Effect: Stimulation of insulin secretion
A

Glucoinsulinotropic peptide (GIP)

90
Q

Source: Intestine (L cells)
Stimulus for secretion: Fatty acids, glucose, hydrolyzed protein
Pathway of action: Endocrine, paracrine
Targets: Neurons, smooth muscle
Effects: Inhibition of gastric emptying, pancreatic secretion, gastric acid secretion, intestinal motility, food intake

A

Peptide YY (PYY)

91
Q

Source: Intestine (L cells)
Stimulus for secretion: Fatty acids, glucose, hydrolyzed protein
Pathway of action: Endocrine, paracrine
Targets: Neurons, epithelial cells
Effects: Glucose homeostasis, epithelial cell proliferation

A

Proglucagon-derived peptides 1/2 (GLP-1/2)

92
Q

Basic Mechanism of Secretion

A
  • Secretion of Organic Substances
  • Water and Electrolyte Secretion
    »Some electrolytes are actively secreted, some are passively secreted along an electrochemical gradient
    »Water follows by osmosis
    »Needed to “wash away” the organic substances through the secretory border of the cells
93
Q
  • Lubricant and protectant
  • Composed of water, electrolytes, glycoproteins
  • Secreted along the entire GIT
A

Mucus

94
Q

Functions of Mucus

A

(1) Adhere tightly to food or other particles and to spread as a thin film over the surfaces
(2) Sufficient body that it coats the wall of the gut and prevents actual contact of most food particles with the mucosa
(3) Low resistance for slippage, so the particles can slide along the epithelium with great ease
(4) Causes fecal particles to adhere to one another
(5) Strongly resistant to digestion by the gastrointestinal enzymes
(6) Buffering and neutralizing capacity: glycoproteins, bicarbonate ions

95
Q

Salivary Glands

A

Major: Parotid, submandibular and sublingual glands

Minor: Buccal glands

96
Q

Location: Anterior to ear
Type of gland: Compound tubuloalveolar gland
Type of secretion: Serous

A

Parotid

97
Q

Location: Infero-lateral area of oral cavity
Type of gland: Compound tubuloalveolar gland
Type of secretion: Mixed

A

Submandibular

98
Q

Location: Floor of oral cavity
Type of gland: Compound tubuloalveolar gland
Type of secretion: Mucous

A

Sublingual

99
Q

Saliva Composition and pH

A 
Composition:
Water
Electrolytes: Na, Cl, K, HCO3, Ca, Mg
Protein: Enzymes: Ptyalin (salivary amylase);Lingual Lipase; Lysozymes;
Mucin; Growth factors

pH: 6-7

100
Q

Functions of Saliva

A
  • Oral hygiene and protection of oral mucosa
  • Lubrication of food
  • Initial digestion of protein and fat
  • Facilitation of taste
  • Mucosal growth
101
Q
  • Flow of saliva washes away bacteria and food particles
  • Anti-bacterial factors
    Thiocyanate ions
    Lysozymes – directly kill bacteria, helps thiocyanate ions enter bacteria, digest food particles
  • Immunoglobulins (IgA)
A

Functions of Saliva as Oral Hygiene

102
Q

Saliva contains two major types of protein secretion:

A

(1) a serous secretion that contains ptyalin (an α-
amylase) , which is an enzyme for digesting starches

(2) mucus secretion that contains mucin for
lubricating and for surface protective purposes

103
Q

Nervous Regulation of Salivary Secretions: PARASYMPATHETIC STIMULATION

A
  • Salivatory nuclei (Superior and Inferior) in the junction of the medulla and pons
  • Taste and tactile stimuli (sour, smooth)
  • Appetite center (increases salivation in response to smell, taste or thought of food)
  • Reflexes from the stomach or small intestine (irritating food, nausea - to dilute or neutralize irritating substance)
104
Q

Nervous Regulation of Salivary Secretions: SYMPATHETIC STIMULATION

A
  • Can slightly increase salivation
  • The sympathetic nerves originate from the superior cervical ganglia and travel along the surfaces of the blood vessel walls to the salivary glands.
105
Q

Secondary Regulation of Salivary Secretions

A
  • Dependent blood supply to the glands
  • The parasympathetic nerve signals that induce copious salivation also moderately dilate the blood vessels.
  • In addition, salivation itself directly dilates the blood vessels, thus providing increased salivatory gland nutrition as needed by the secreting cells.
  • Part of this additional vasodilator effect is caused by KALLIKREIN secreted by the activated salivary cells, which in turn acts as an enzyme to split one of the blood proteins, an alpha2-globulin, to form BRADYKININ, a strong vasodilator
106
Q

ESOPHAGUS: Types of glands

A
  1. Simple mucous glands – throughout the body of the esophagus
  2. Compound mucous glands- at gastric end and to a lesser extent in the initial portion of the esophagus
107
Q

Functions of Mucus in the Esophagus

A
  1. Provide lubrication for swallowing

2. Protection from excoriation by food and from digestion by acid from the stomach during reflux

108
Q

Parts of the Stomach

A

Gastric glands – body and fundus (80%); secrete HCL, pepsinogen, intrinsic factor and mucus

Pyloric glands – antral portion (20%); secrete mainly MUCUS

109
Q

Cell Types and Substance secreted

A
  1. Mucous neck cells - secrete mainly MUCUS and also BICARBONATE
  2. Parietal/Oxyntic Cells - secrete HCL and INTRINSIC FACTOR
  3. Peptic/Chief Cells - secrete large quantities of PEPSINOGEN
  4. Enterochromaffin-like cell - secrete HISTAMINE (stimulates acid)
  5. D cells - secrete SOMATOSTATIN (inhibit acid)
  6. G cells - secrete GASTRIN (stimulates acid)
110
Q

Gastric Juice: Composition and pH

A 
Composition:
Hydrochloric acid
Pepsinogen
Intrinsic factor
Mucus
Gastrin

pH – 0.08 (1-2)

111
Q

Phases of Gastric Secretion

A
  1. Cephalic
  2. Gastric
  3. Intestinal
112
Q

(Phases of Gastric Secretion)

  • Sight, smell, thought, or taste of food
  • The greater the appetite, the more intense is the stimulation
  • Originates in the cerebral cortex and in the appetite centers of the amygdala and hypothalamus -> dorsal motor nuclei of the vagi -> vagus nerves to the stomach
  • 30 % of the gastric secretion
A

Cephalic Phase

113
Q

(Phases of Gastric Secretion)

  • Long vagovagal reflexes from the stomach to the brain and back to the stomach
  • Local enteric reflexes
  • Gastrin mechanism
  • All of these cause secretion of gastric juice during several hours while food remains in the stomach
  • 60 % of the total gastric secretion
A

Gastric Phase

114
Q

(Phases of Gastric Secretion)

  • Food in the upper portion of the small intestine, particularly in the duodenum cause stomach secretion of small amounts of gastric juice
  • Due to gastrin secreted by duodenal mucosa
  • 10 % of the acid response to a meal
A

Intestinal Phase

115
Q

Regulation of pepsinogen secretion by the peptic cells in the oxyntic glands occurs in response to two main types of signals:

A

(1) stimulation of the peptic cells by acetylcholine released from the vagus nerves or from the gastric enteric nervous plexus
(2) stimulation of peptic cell secretion in response to acid in the stomach.

116
Q

Inhibition of Gastric Secretion

A
  1. The presence of food in the small intestine initiates a reverse enterogastric reflex
  2. The presence of acid, fat, protein breakdown products, hyperosmotic or hypo-osmotic fluids, or any irritating factor in the upper small intestine
117
Q

Production of HCl

A
  1. K+ ions diffuse passively from the parietal cell into the lumen
  2. An active transport pump brings K+ ions back into the parietal cell, simultaneously secreting H+ from the cell to the lumen.
  3. Cl- ions diffuse passively from the cell to the lumen, and their negative charges balance the positive charges of the secreted H+
  4. An exchanger on the opposite face of the parietal cell balances this loss of Cl- by importing Cl- from the blood in exchange for bicarbonate ions (HCO3-)
  5. Within the cell, water reacts with CO2 to form carbonate (H2CO3), which dissociates into H+ and HCO3
118
Q
  • slightl to moderate effects in inhibiting gastric secretion
A

GIP, Vasoactive intestinal polypeptide, somatostatin

119
Q
  • lies parallel to and beneath the stomach

- is a large compound gland with most of its internal structure similar to that of the salivary glands

A

Pancreas

120
Q

__ are secreted by pancreatic acini, and large volumes of sodium bicarbonate solution are secreted by the small ductules and larger ducts leading from the acini.

A

pancreatic digestive enzymes

121
Q

Pancreatic Juice

A
  • HCO3
  • Enzymes – in the form of zymogens or inactive enzymes
  • Water
122
Q

Phases of Pancreatic Secretion

A
  1. Cephalic Phase
  2. Gastric Phase
  3. Intestinal Phase
123
Q

(Phases of Pancreatic Secretion)

  • Acetylcholine release by the vagal nerve endings in the pancreas
  • Causes moderate amounts of enzymes to be secreted into the pancreatic acini (20% of the total secretion of pancreatic enzymes after a meal)
A

Cephalic Phase

124
Q

(Phases of Pancreatic Secretion)

  • Nervous stimulation of enzyme secretion continues
  • Accounts for another 5 to 10 % of pancreatic enzymes secreted after a meal
A

Gastric phase

125
Q

(Phases of Pancreatic Secretion)

  • After chyme leaves the stomach and enters the small intestine, pancreatic secretion becomes copious, mainly in response to the hormone secretin
A

Intestinal Phase

126
Q

Control of Pancreatic Secretions

A
  • Acetylcholine, which is released from the parasympathetic vagus nerve endings and from other cholinergic nerves in the enteric nervous system
  • Cholecystokinin, which is secreted by the duodenal and upper jejunal mucosa when food enters the small intestine
  • Secretin, which is also secreted by the duodenal and jejunal mucosa when highly acidic food enters the small intestine
127
Q

PROTEIN: Pancreatic Enzymes and products

A

Trypsin - Peptides
Chymotrypsin - Peptides
Carboxypolypeptidase - Free amino acids

128
Q

CARBOHYDRATES: Pancreatic Enzymes and products

A

Pancreatic amylase -> Mostly disaccharides and a few trisaccharides

129
Q

FATS: Pancreatic Enzymes and products

A

Pancreatic Lipase - Hydrolyzing neutral fat into fatty acids and monoglycerides
Cholesterol esterase - Hydrolysis of cholesterol esters
Phospholipase - Splits fatty acids from phospholipids

130
Q
  • prevents activation of trypsin both inside the secretory
    cells and in the acini and ducts of the pancreas
  • prevents activation of the others as wel
A

Trypsin Inhibitor

131
Q

Secretion of bicarbonate ions

A
  • HCO3 actively transported out
  • Na leaks out
  • Water follows by osmosis
132
Q

Functions of Bile

A
  1. Role in fat digestion and absorption
  2. Means for excretion of several important waste products from the blood.
    - bilirubin, an end product of hemoglobin destruction
    excesses of cholesterol
133
Q

Bile acids in the bile do two things in Fat digestion and absorption

A
  1. Help to emulsify the large fat particles of the food into many minute particles
  2. Aid in absorption of the digested fat end products through the intestinal mucosal membrane
134
Q

Bile is secreted in two stages by the liver:

A

(1) The initial portion is secreted by the principal functional
cells of the liver, the hepatocytes; this initial secretion contains large amounts of BILE ACIDS, CHOLESTEROL,
AND OTHER ORGANIC CONSTITUENTS. It is secreted into minute bile canaliculi that originate between the
hepatic cells.
(2) second portion of liver secretion is added to the initial bile. This additional secretion is a WATERY SOLUTION OF SODIUM AND BICARBONATE IONS secreted by secretory epithelial cells that line the ductules and ducts

135
Q

Regulation of Bile Secretion by Secretin

A
  • Adds a second portion of liver secretion in its course through the bile ducts
  • Watery solution of sodium and bicarbonate ions secreted by secretory epithelial cells that line the ductules and ducts
  • Can increase the total quantity of bile by as much as an additional 100 percent
136
Q
  • most potent stimulus for causing gall bladder contraction
A

Cholecystokinin

137
Q

Storage and Concentration of Bile

A
  • Maximal volume: 30-60 ml
  • Can store up to 12 hours worth of bile (450ml)
  • Via active transport of Na
  • Followed by secondary absorption of Cl, water and other contents
  • Usual concentration is 5-fold
  • Maximal concentration is 20-fold
138
Q

Enterohepatic Circulation of Bile Salts

A

About 94 percent of the bile salts are reabsorbed into the blood from the small intestine

  • about one half of this by DIFFUSION THROUGH the mucosa in the early portions of the small intestine
  • remainder half by an ACTIVE TRANSPORT process through the intestinal mucosa in the distal ileum.
139
Q
  • strong stimulating effect of bile acids to cause bile secretion
  • also stimulate pancreatic secretion
A

Secretin

140
Q
  • Compound mucous glands located in the wall of the first few centimeters of the duodenum between pylorus and papilla of vater
  • Inhibited by sympathetic stimulation
A

Brunner’s Glands

141
Q

Brunner’s Glands secrete large amounts of alkaline mucus in response to

A

(1) tactile or irritating stimuli on the duodenal mucosa
(2) vagal stimulation
(3) gastrointestinal hormones, especially secretin.

142
Q
  • Located over the entire surface of the small intestine

Epithelium:
Goblet cells – secrete mucus
Enterocytes – in crypts, secrete water and electrolytes ; on the villi, reabsorb water and electrolytes ; absorb nutrients

A

Crypts of Lieberkuhn

143
Q

Digestive Enzymes in the Small Intestine

A

(1) several peptidases for splitting small peptides into amino acids
(2) four enzymes-sucrase, maltase, isomaltase, and lactase-for splitting disaccharides into monosaccharides
(3) small amounts of intestinal lipase for splitting neutral fats into glycerol and fatty acids

144
Q

Enterocyte Secretion

A
  • Average 1800mL/day
  • pH 7.5-8
  • Provides a watery vehicle for the absorption of substances from chyme
  • Two active secretory processes:
    1. Active secretion of Cl
    2. Active secretion of HCO3
145
Q

Components of Enteric Juice

A
  • Mucus
  • Water
  • Electrolytes
146
Q

Regulation of Enteric Juice Secretion

A
  • Local enteric nervous reflexes, especially reflexes initiated by tactile or irritative stimuli from the chyme in the intestines
147
Q

Colonic Secretions

A
  • Also produced by crypts similar to that of the small intestines
  • No digestive enzymes; contains NO VILLI
  • Principal secretion is mucus by mucous cells
  • The amount of fluid within the large intestines is determined by the balance between secretion and absorption for fecal formation
148
Q

Regulation of Colonic Secretions

A
  • Direct, tactile stimulation of the epithelial cells lining the large intestine
  • Local nervous reflexes to the mucous cells in the crypts of Lieberkühn
  • Stimulation of the pelvic nerves from the spinal cord, which carry parasympathetic innervation to the distal one half to two thirds of the large intestine, also can cause marked increase in mucus secretion
149
Q

General Principles of Digestion

A
  • Chemical vs. Mechanical Digestion
  • Mainly by hydrolysis (reverse of formation of complex molecules)
  • Partial chemical digestion – mouth, stomach
  • Complete chemical digestion – small intestines (Luminal enzymes; Brush border enzymes)
150
Q

Brush Border Enzymes

A

Peptidases – oligopeptides to free amino acids
Disaccharidases – di- to monosaccharides (Sucrase; Maltase; Isomaltase; Lactase)
Intestinal Lipase – neutral fats into glycerol and free fatty acids

151
Q

Enzymes for Carbohydrate digestion

A

Ptyalin or Salivary Amylase – oral cavity
Pancreatic Amylase – small intestine
Brush border enzymes – small intestine

152
Q

Brush Border Carbohydrate Hydrolases (enzyme and products)

A

Sucrase: Glucose, fructose
Isomaltase: Glucose
Glucoamylase: Glucose
Lactase: Glucose, galactose

153
Q

Hydrolysis of Fats

A

Fat in the diet: Triglycerides
Enzyme: Pancreatic Lipases
Products: Glycerol and free fatty acids

154
Q

Hydrolysis of Proteins

A

Enzymes: Trypsin, chymotrypsin, carboxypeptidase
Products: Free amino acids

155
Q
  • the important peptic enzyme of the stomach
  • is most active at a pH of 2.0 to 3.0 and is inactive at a pH above about 5.0.
  • for this enzyme to cause digestion of protein, the stomach
    juices must be acidic
A

Pepsin

156
Q
  • is converted into elastase, which then digests elastin fibers that partially hold meats together.
A

Proelastase

157
Q

Sites of absorption

A

Stomach – alcohol and drugs (aspirin); very minimal
Small intestines – nutrients
Large intestines – water and electrolytes

158
Q

The __ is a poor absorptive area of the gastrointestinal tract because it lacks the typical villus type of absorptive membrane, and also because the junctions between the epithelial cells are tight junctions.

A

stomach

159
Q
  • increase the surface area of the absorptive mucosa about threefold; well developed in the duodenum and jejunum
A

valvulae conniventes (folds of Kerckring)

160
Q
  • lie so close to one another in the upper small intestine that they touch in most areas
  • presence of it on the mucosal surface enhances the total absorptive area another 10-fold
A

villi

161
Q

Absorption of Water

A
  • Transported entirely by diffusion or osmosis
  • Lumen to enterocyte (villus) to plasma
  • Opposite direction in diarrhea when hyperosmotic solutions are discharged from the stomach into the duodenum
162
Q

Absorption of Sodium

A

Primary: Active transport via NA+/K+ PUMPS at the basolateral membrane of the epithelial cells; powers and provides the electrochemical gradient needed for the secondary active absorption of glucose and amino acids

Secondary: Sodium channels and co-transport proteins (glucose, amino acids and Na+/H+ exchanger); drag of Cl ions

163
Q

Absorption of Chloride

A
  • Mainly by diffusion; follows electrochemical gradient produced by Na transport
  • Via chloride-bicarbonate exchangers in the brush border (ileum)
  • Exits through Chloride channels on the basolateral membrane
164
Q

Absorption of Bicarbonate

A
  • Via Active Absorption of Bicarbonate Ions
  • In the lumen of the small intestines
  • HCO3- + H+ → H2CO3 → CO2 + H2O
  • CO2 eventually absorbed in the blood and eliminated via the lungs
165
Q

Absorption of Calcium, Iron, Potassium, Magnesium , Phosphate

A
  • Actively absorbed depending on the needs of the body

- Monovalent ions more readily absorbed than bivalent ions

166
Q

Absorption of Carbohydrates

A
  • Absorbed mainly as glucose (80%)

- Galactose and fructose (20%)

167
Q

Absorption of Other Monosaccharides

A

GLUCOSE: via secondary active transport with sodium (SGLT1) from the lumen going inside the epithelial cell; via facilitated diffusion through the basolateral membrane and into the paracellular space (GLUT2)

GALACTOSE: Exactly the same as glucose

FRUCTOSE: Via facilitated diffusion only (GLUT5); phosphorylated and transported as glucose across the basolateral membrane (GLUT2); rate of transport is half that of glucose and galactose

168
Q

Absorption of Proteins

A
  • Absorbed as free amino acids, dipeptides and tripeptides
  • Mostly via SECONDARY ACTIVE TRANSPORT WITH SODIUM
  • Some via FACILITATED DIFFUSION through specific transport proteins
  • PepT1 is a transporter of oligopeptides; symporter with H+
169
Q

Absorption of Fats

A
  • Absorbed mainly as monoglycerides and free fatty acids
  • Transported mainly by diffusion via micelles
  • Enter the cell’s smooth ER and synthesized as triglycerides (TGs)
  • The new TGs enter the lacteal as chylomicrons
  • Some short- and medium- chain fatty acids are absorbed directly into the portal blood.
170
Q

Functions of Bile Salts

A

Primary: Help in the absorption of fatty acids, monoglycerides, cholesterol and other lipids from the intestinal tract

Secondary: Detergent/emulsifying action on the fat particles in the food -> decreases the surface tension of the particles and allows agitation in the intestinal tract to break the fat globules into minute sizes

171
Q

Absorption in the colon:

A

Absorbing colon = proximal half

Storage colon = distal half

172
Q

Absorption in the colon: Formation of Feces

A

Volume of chyme entering the large intestines: 1500mL
Volume of water excreted in feces: 100mL
Concentration of ions excreted in feces: 1-5mEqs/L ( Na, Cl)
Maximum absorptive capacity of large intestines: 5-8L/day

173
Q

Absorption of Ions in the Colon

A

In the colon, Na+ and Cl- ions are actively absorbed.

174
Q

Three driving forces for osmotic movement of water (fluid absorption) in the large intestines:

A
  1. Electroneutral NaCl absorption stimulated by various growth factors
  2. Absorption of short-chain fatty acids (acetate, butyrate, propionate) via sodium-monocarboxylate transporters (SMCTs)
  3. Absorption of Na+ via Na channel ENaC
175
Q
  • Capable of digesting small amounts of cellulose

- Produce vitamin K, vitamin B12, thiamine, riboflavin, and various gases

A

Colonic Microflora

176
Q

Where is the swallowing center found?

A

Medulla

177
Q

What happens to the soft palate and uvula during swallowing?

A

Rises up to close posterior nares

178
Q

What happens to the glottis during swallowing?

A

Closes to prevent aspiration

179
Q

Paralysis of Swallowing: CAUSES

A
  • Damaged CN V, IX, X
  • Damaged swallowing center (Encephalitis, Poliomyelitis)
  • Paralyzed swallowing muscles (Muscle Dystrophy, MG, Botulism)
  • Deep anesthesia ->may lead to aspiration
180
Q

4 Basic Layers of the GI Tract?

A

Mucosa
Submucosa
Muscularis
Serosa

181
Q

Differentiate between Myenteric vs Submucosal Plexus

A

Myenteric: Auerbach’s Plexus, for motility, between inner circular and outer longitudinal muscle layers
Submucosal: Meissner’s Plexus, for secretion, at the Submucosal layer

182
Q
  • Damage to the Myenteric plexus of the lower 2/3 of the esophagus
  • Lost of receptive relaxation
  • May lead to Megaesophagus -> infection -> ulceration -> rupture -> death
  • Dx: Bird’s Beak Appearance
  • Tx: Heller’s Myotomy with fundoplication
A

Achalasia

183
Q
  • Inflammation of the stomach lining
  • Range from superficial to severe excoriation (ulcers)
  • Certain Substances may damage gastric barrier (mucosa + tight junctions between cells), e.g. Aspirin, NSAIDs, Alcohol, Smoking
A

Gastritis

184
Q

Types of Gastritis

A

Type A Gastritis: Autoimmune
Achlorhydia
Pernicious Anemia

Type B Gastritis: Bacteria-associated (H. pylori)

185
Q

Differentiate Brunner’s Gland from Peyer’s Patches

A

Brunner’s Gland: submucosa of the duodenum, secretes bicarbonate (alkaline)

Peyer’s Patches: lamina propia of the mucosa of the ileum, secretes IgA

186
Q

Source: S Cells, Duodenum
Stimulus: Acid entering duodenum
Stomach motility and secretion: Inhibits
Pancreas: stimulates Fluid Secretion (HCO3-)

A

Secretin

187
Q

Source: I Cells, Duodenum
Stimulus: Fat and amino acids entering duodenum
Stomach Motility and Secretion: Inhibits Emptying
Pancreas: Stimulates enzyme secretion
Gallbladder: GB contraction and Sphincter of Oddi relaxation

A

CholeCystoKinin (CCK)

188
Q

Source: G Cells, Stomach Antrum,
Stimulus: Stomach distention, GRP; stomach acid inhibits
Stomach Motility and Secretion: Stimulates

A

Gastrin

189
Q

Source: K Cells, Duodenum
Stimulus: Fat, CHO, amino acids
Stomach Motility and Secretion: Inhibits (only above normal physiologic levels)

A

Glucose-dependent Insulinotropic Peptide

190
Q

Source: Upper duodenum
Stimulus: Fasting
Stomach Motility and Secretion: Stimulates

A

Motilin

191
Q
  • Excoriated mucosa of the stomach and intestines

- Imbalance between gastric acid-pepsin secretion and protective mechanisms of stomach and intestines

A

Peptic Ulcer Disease (PUD)

192
Q

Protective Mechanisms in GIT to prevent Peptic Ulcer Disease

A
  • Gastric barrier
  • Alkaline secretions in the duodenum by pancreatic juice and Brunner’s Glands
  • Feedback mechanism for gastric acid secretion
  • Secretin secretion
193
Q
  • is a common accompaniment of gastric atrophy and achlorhydria. Normal gastric secretions contain a glycoprotein called intrinsic factor, secreted by the same parietal cells that secrete hydrochloric acid.
  • In the absence of intrinsic factor, only about 1/50 of the vitamin B12 is absorbed. And, without intrinsic factor, an adequate amount of vitamin B12 is not made available from the foods to cause young, newly forming red blood cells to mature in the bone marrow. The result is __.
A

Pernicious anemia

194
Q

What are the two divisions of the pancreas?

A

Exocrine Pancreas: Proteases, Amylases, Lipases, Bicarbonate

Endocrine Pancreas: Insulin, Glucagon, Somatostatin

195
Q

Pancreatic juice will eventually drain into which structure?

A

Ampulla of Vater

196
Q
  • Inflammation of the pancreas
  • Maybe acute or chronic
  • Other causes: trauma, scorpion bites, etc.
  • Amount of trypsinogen overwhelms trypsin levels, activating other proteases in a vicious cycle (autodigestion)
  • Serum amylase, lipase levels increase
  • SSx: epigatric pain radiating to the back, Cullen’s Sign, Grey-Turner’s Sign
  • Tx: Meperidine, Supportive
A

Pancreatitis

197
Q

The most common cause of pancreatitis is __, and the second most common cause is __

A

drinking excess alcohol; blockage of the papilla of Vater by a gallstone

198
Q

In what forms are carbohydrates, proteins and fat absorbed?

A

Monosaccharides, amino acids/di or tri-peptides, micelles

199
Q

Several diseases can cause decreased absorption by the mucosa; they are often classified together under the general term __

A

sprue

200
Q
  • Due to deficient Lactase especially in adult Asians (Due to non-milk drinking habits of adult Asians)
  • Decreased Lactase ->bdecreased breakdown of Lactose by small intestines -> Lactose metabolized by intestinal bacteria -> Acids released as metabolic waste products by bacteria -> osmotic diarrhea
A

Lactose Intolerance

201
Q
  • Susceptibility to Gluten (found in wheat and rye)
  • Causes blunting of microvilli of villi -> malabsorption of nutrients
  • Tx: remove gluten from diet
A

Non-Tropical (Gluten Enteropathy/Celiac Sprue)

202
Q
  • Due to unknown infectious agent
  • Found in the Tropics
  • Also with blunted microvilli
  • Tx: antibiotics (e.g. Doxycycline)
A

Tropical Sprue

203
Q

Signs and Symptoms of Sprue

A

Steatorrhea (non-absorption of fats)
Wasting (decreased carbohydrates, proteins)
Inadequate blood coagulation (decreased Vit K)
Megaloblastic anemia (decreased Vit B12 and folic Acid)

204
Q

Differentiate Bolus, Chyme and Feces

A

Bolus: from mouth to stomach
Chyme: in the small intestines
Feces: in the large intestines

205
Q

Main site for the absorption of carbohydrates, proteins and fats?

A

Jejunum

206
Q

Main site for absorption of water?

A

Jejunum

207
Q
  • Slow movement of feces in the large intestines
  • it is often associated with large quantities of dry, hard feces in the descending colon that accumulate because of overabsorption of fluid.
  • Infants rarely affected (but must learn to control defecation)
A

Constipation

208
Q
  • One of the many causes of constipation
  • Basically Achalasia of the Large Intestines
  • Can lead to Megacolon
A

Hirschprung Disease

209
Q
  • Rapid movement of feces in large intestines
  • Many types (e.g. infectious, osmotic, psychogenic)
  • Infectious diarrhea: helps clear GI tract of offending agent
  • Cholera: can lead to severe dehydration and death
A

Diarrhea

210
Q
  • means inflammation usually caused either by a virus or by bacteria in the intestinal tract. In usual infectious diarrhea, the infection is most extensive in the large intestine and the distal end of the ileum.
  • Everywhere the infection is present, the mucosa becomes irritated and its rate of secretion becomes greatly enhanced. In addition, motility of the intestinal wall usually increases manifold.
A

Enteritis

211
Q
  • diarrhea that accompanies periods of nervous tension, such as during examination time or when a soldier is about to go into battle
  • is caused by excessive stimulation of the parasympathetic nervous system, which greatly excites both (1) motility and (2) excess secretion of mucus in the distal colon.
A

psychogenic emotional diarrhea

212
Q
  • is a disease in which extensive areas of the walls of the large intestine become inflamed and ulcerated
  • The motility of the ulcerated colon is often so great that mass movements occur much of the day rather than for the usual 10 to 30 minutes
  • Also, the colon’s secretions are greatly enhanced
  • > repeated diarrheal bowel movements.
A

Ulcerative colitis

213
Q
  • upper gastrointestinal tract rids itself of its contents when almost any part of the upper tract becomes excessively irritated, overdistended, or even overexcitable.
  • Excessive distention or irritation of the duodenum provides an especially strong stimulus for __
  • Preceded by nausea and anti-peristalsis
  • Can also happen when Chemoreceptor Trigger Zone (floor of 4th ventricle) is stimulated
  • Stimulated by morphine, digitalis, motion sickness
A

Vomiting

214
Q

GI Obstruction: SSx depends on site of obstruction

A

Pylorus: vomiting of gastric contents, metabolic alkalosis

Small intestines: severe dehydration, possibly no acid-base abnormality (equal acids and antiacids vomited)

Large intestines: feces accumulation, no vomiting at the start, may lead to rupture

215
Q
  • GI Gases
  • Derived from
    Swallowed air (nitrogen, oxygen)
    Gut bacteria (methane, carbon dioxide, hydrogen)
    Diffusion of gases from blood to GI tract
  • Certain food increase __ from anus
    beans, cabbage, onion, cauliflower, corn, and certain irritant foods such as vinegar
    Reason: may serve as suitable medium for bacteria
A

Flatus

Phisiology Hope (7 decks)

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