Physiology 2.5.14 GI Vomit and Defecation Flashcards

1
Q

Net aboral movements of contents (how uch enteres and leaves)

A

500-600cc enter/day

150 cc leave

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2
Q

Waht are the muscular layers of the large intestine

A

Inner circular laer with outer longitudinal layer

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3
Q

how are outer longtifuindal layers arranged

A

as three bands caleld taeniea coli

They run to rectum

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4
Q

Longitudinal layers from rectum to anus?

Internal anal sphinter!

A

it is continous

Circular muscle thickens at anal canal to beocme the internal anal sphincber

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5
Q

External anal sphcinter

A

Overlapping and goign distal to internal anal sphincter are layer sof striated msucle which make up external anal sphincter

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6
Q

Haustra

A

cotractions of circular muscle divide colon into segments called haustra

Reform elsewhere on colon (haustrations)

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7
Q

PS innervation of 1st half of colon

A

by vagus

Sympathetic from SUPERIOR MESENTERIC GANGLION

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8
Q

PS innervatio nof caudal half of colon

A

Pelvic nerve PS pereganglioinc fiber

Sympathetic from INFERIOR MESENTERIC GANGLION

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9
Q

Innervation of rectum and anal canal

A

Sympathetic fibers form Hypogastric Plexus

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10
Q

INnervation of external anal sphincter

A

Somatic fibers of Pudendal Nerves

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11
Q

What are examples of Osmotic mechanisms of diarrhea

A
Lactose intolerance
sea water
MgSO4
Steratorrhea
Post-prandial dumping syndrome
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12
Q

What are secretory causes of diarrhea

A

Bacterial toxin
Cholear (cAMP mediated Cl- secretino)
Enteropathic E. coli (Increase intracellular concentration)

Gastrinoma

VIPoma

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13
Q

What are malabsorptive cuases of Diarreha

A

Bile acid malabosrption

Gluten enteropahty (Celiac Disease)

Cholelithiasis (gall stones)

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14
Q

exudative causes of diarreha

A

invasive organisms
Salmonella, amoeba histolytica, with inflammation and blood loss
Influenzea, Crohn’s Disease (ileitis)
Ulcerative colitis

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15
Q

Excess motor activity cuases of diarreha

A

Irritable Bowel
bacterial action on unabsorbed long-chain FA
Stress

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16
Q

Results of Chroniic Diarrhea (6)

A
  1. Dehydration
  2. Hypokalemia
  3. Acidosis (loss of HCO3-)
  4. Loss of water soluble vitabmins
  5. Possible loss of Ca2+
    6 Possible loss of fat soluble vitamins
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17
Q

What is Hirschprung’s Disease/Megacolon, denervation

A

Severe constipation is seen in concentinal megacolon

Absencse of ENS in teh internal anal sphcinger and often rectum

Denervated are has increased tone
NO PROPULSIVE ACTIVITY

Colon proximal to diseased area becomes grossly distended

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18
Q

What is Irritable colon syndeome,

A

Increased/decreased signmoidal segmentation

Common in audlts

Abdominal pain is couple with either constipation or dirrhea

Stress produces increased sigmoidal segmentation and constipation in some people

Others, decreased sigmoidal segmenation and diarrhea

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19
Q

How does stress induce irritable colon syndrome

A

Stress produces increased sigmoidal segmentation and constipation in some people, in others, decreased sigmoidal segmentation and dirrhea

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20
Q

What is the mechanism of Diverticula?

A

in older adults, outpoucing of the mucosa thorugh the uscular wall fo teh colon can develop. These are called diverticular and may be due to chornic high intraluminal pressure

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21
Q

What are the phases of vomiting

A
  1. Nausea
  2. Sympathetic discharge
  3. Unuusal motility
  4. Retching
  5. Stop respriation (valsalva aneuoer with Explusion/emesis)
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22
Q

What is the driving force for expulsion

A

Contraction fo the abdominal wall and diaphragm skeletal muscles

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23
Q

What are possible complications of vomiting/emesis (4)

A
  1. Aspiration
  2. Dehydration/Electrolycte Imbalance (hypokalemic alkalosis(
  3. Mallory-Weiss tear (bleeding)
    4Dental Enamel Erosion
24
Q

What are the sites of stimulus origin (4)

A

Chemoreceptor Triger Zone (CTZ)

2 Vestibular system

  1. Irritation of Pharynx
  2. Irritation of GI Tract
25
Q

CTZ - location

what stimulates it

A

Floor of 4th ventricle, area postreme= circumventricular organ outside the BBB

Stimulated by BB chemicals

What kind of receptors present at CTZ

26
Q

What receptors are in CTZ

A
  1. Dopamine, D2
  2. Serotonin 5-HT3 R
  3. R for opioids, Ach,
  4. and, in hte ifnal common pathway to vomiting center, Substance P receptors
27
Q

Irritation of pharynx. how?

A

Gag reflex

28
Q

Irritation of GI tract

A

In enteric plexus and up Vagus N

Chemotehrapy, radiation, distention of acute infectious gastroenteritis vis 5HT3 receptors

29
Q

Mechanics of retching

A
  1. Duodenal contents are forced into stomach by spasm of duodenum.

Antrum is also in spasm ,but the body of the stomach and LES are relaxed

inspiration against a partially closed glottis loweres intrathoracic pressure, and contraction of abdominal muscles raises intra-abodminal pressure

Pressure gradient from abdomen to thorax foreces contents of body of stomach into esopahgus

Hypopharyngeal spcinceter remains closd, and secondary peristaltic waves in esophagus force its conents back onto stomach

Cycle repeated

30
Q

What parts f GI is in spasm during retching? HOw does this affect intra-abdominal pressure

A

Antrum and duodenum in spasm

Leads to high intraabdominal pressure

31
Q

What parts of GI are relaxed

A

Body of stoach and LES relaxed

Low intrathoracic pressure

32
Q

Is the hypoharygeanl sphicner open or closed?

A

closed! , and seconary peristatlitl waves in esopaghus force conents back into stomach

33
Q

What is the mechanics of vomiting

A

Vomiting buidls on a developed retch

Antrum and duodenum in spasm, but body of stomach and lower esophageal sphincter are relaxed

Strong contractions of abdominal muscles force the contents fo the stoamch into the esophagus and through the relaxed hypopharyngeal sphincter

Strong expiration with a closed glottis raises intrathoracic pressure, and exerts pressure on esopahgus

Events occur sequentially, first in abdomen, then in thorax

There may be reverse peristaliss in teha ngrum of the stomahc, but there is no rverse peristaliss int eh body of stomach of esophagus both of which are relaxed

34
Q

If vomiting somatic or autonomic

A

highly integrated chilefly somatic act

35
Q

Describe vomiting innercation

A

Visceral motor activity prepares GI tract for efficent expulsion of vomitus

THe expulsvive force is supplied by skeletal muscles whent eh diaphragm contracts sharply (descends); similar conraciton of abdominal musculature takes place

36
Q

What can activate central or peripheral receptors

A

Motion sickeness
Increased intracranila P
Mental/higher CNS centers

37
Q

What activates CTZ: floor of IV ventricle (area postrema0) cia

A

vestibular app, blood borne, emetics, CuSO4, digitalis, apomorphine and irradiation

38
Q

What GI receptors activate vomiting center

A

Back of throat, increased stomach or duodenal pressure or certain cemciasl in duodenum (ipecac or CuSO4)

39
Q

Categories that cause vomiting (6)

A
GI
Sensory system and brain
Metabolic Disturbances
Pregnancy
Drug Reactions
Illenss
40
Q

wha a GI problems that can lead to vomiting

A

irritation fo GI tract
gastritis (viruses), gastroeneritis

Pyloric stenosis–> Proejctile vomiting

Bowel obstruction, distension, overreating (acute abodmoen, peritonitis, ileus)

Food alelrgeies, cholycysttit, pancreatitis, appendicitis, hepatities
Food poising
Lactose intolerance

41
Q

Sensory system in brain

A
Movements in motion sickeess 
Menier's syndome
Concussion
Cerebral heorrhage
migrain
brain bumors (can lead to chemoR imbalance, benig interacranial hypertension and hydrocephalus
42
Q

Metabolic disorders that lead to vomiging

A
Hypercalemia
Uremia
Adrenal insufficienly
Hypoglycemia
Hyperglycermia
43
Q

Pregnancy leads to vomiting

A

Hyperemesis: mornign sickness

44
Q

Drug reactions to vomigitn

A

alochol
opioids
slective serotonin reupatek inhibitors
chemotheryapy drugs

45
Q

What are exampels of emetics

A

ipecaa
salt water
mustart water morphine
digitalis glycosides

46
Q

What are antiematices

A

Inhibit R
Anticholinergics, anitihistamines
Domaine
serotnone antagonista sn acannabinoids

Pt may need IV fluids

47
Q

What is the resting pressure of ileocecal sphincter

A

20-40 mm HG exists

48
Q

What does distension of ileum lead to for pshcincters

A

Distension of ileum leads to spchinceter realxation for flow of contents from ileum to oon

49
Q

What happesn when distension in colon

A

Contraction fo sphcinger to prevent passage from colon to eleum

50
Q

What happens to internal and external sphcincer when incras in rectom

A

Decrease in P in internal sphincter

Increase in P in external anal Wsphcincter

51
Q

What is mechanism of defecation (6)

A
  1. Adequate stimulus is increased tension in teh rectal wall
  2. Peristalsis and straightening of sigmoid colon plus rectal contraction
  3. Relaxation of internal anal sphincter (PS via sacral cord) as rectal conraction reaches it
  4. Descending colon contractions
  5. VOLUNTARY increase in intrathoracic and intraabdominal pressure
  6. Voluntary realxaion of external anal schincer, a striagted muscle (DEFECATION)
52
Q

what is mass movement

A

strong peristaltil movement originating as high as transverse colon

pushes colonic contents downard with sigmoid conents forced into rectum

53
Q

What happnes when ther eis stretch and tension in walls of rectum

A

activate stretch receptors

afferents form receptors go to defecation center in SACRAL CORD to initiate defecation

SM internal anal spchinceter realxes nd sk musle external spchincter contracts

54
Q

Are efferent pathways for defecationPS or Symp

A

purealy PS

55
Q

Voluntary inhiition of defecation

A

produces song contractions of striated muscles of pelvic diapghragm and exrnal anal sphincter

Motiliy of entire colon is dperessed

56
Q

What happens when feces remains in rectum for a long time

A

rectu relaxes which decreases wall tension thereby removing stimulus and urge to defecate

rectum conetents evacuated backward, with retropulsion into sigmoid colon which as a lower level of motor activity