Physiology Block 3 Week 13 01 Overview of GI Physiology Flashcards Preview

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Flashcards in Physiology Block 3 Week 13 01 Overview of GI Physiology Deck (46)

Parotid Gland

Largest of the salivary glands


Small intestine relative lengths

Duodenum= 5%
Jejunum= 40%
Ileum= 55%


Sphincters and Valves (Tonic Contraction)

Upper Esophageal Sphincter
Lower Esophageal Sphincter
Sphincter of Oddi
Ileocecal Valve
Internal anal sphincter
External Anal Sphincter--under voluntary control

GI tract tends to move and contract--Phasic
Sphincters remain tight and maintain tone--Tonic


General Organization of the GI Tract

In to Out

-Lamina Propria
-Muscularis Mucosa

Submucosa: Meissner's (Submucosal) Plexus

Muscularis Propria: Auerbach's (Myenteric) Plexus
-Circular Muscle
-Interstitial cells of Cajal
-Longitudinal Muscle

Serosa or Adventitia


Submucosa Functions

Blood Flow


Interstitial cells of Cajal

In muscularis propria between circular muscle and longitudinal muscle

Determines the rate at which things contract (pacemaker)


Inflammatory Bowel Disease

Ulcerative Colitis (UC)
Crohn's Disease (CD)


Ulcerative Colitis

Inflammatory Bowel Disease
-mucosa and submucosa
-continuous starting in rectum
-pain, fevers, blood per rectum, weight loss, increased risk of colon cancer


Crohn's Disease (Colitis)

Inflammatory Bowel Disease
-any portion of GI tract from MOUTH TO ANUS
-all GI tract layers
-may have skip areas
-pain, fevers, weight loss, STRICTURES (narrowing) due to all layers involved, FISTULAS (an abnormal connection between different organs)

**cobblestone like appearance because all layers involved

Enterocutaneous fistula--connection between GI and skin


Muscle Arrangement and Pacemaker cells

Action potential in 1 muscle fiber is easily transmitted to adjacent fibers, allowing multiple fibers to function as a syncytium

Each region of GI tract has underlying electrical activity that determines contraction rates:
-stomach: 3 contractions/min
-duodenum: 12/min
-ileum: 8/min

Interstitial cells of Cajal (pacemaker cells)--determines rate of contraction (between circular and longitudinal cells)


Myenteric (Auerbach's plexus)

Responsible for mixing and propagation functions
Located between longitudinal and circular muslce layers in muscularis propria


Meissner's Plexus (Submucosal plexus)

Responsible for secretion and absorption at the mucosal level
Responsible for blood flow at mucosal and submucosal levels
Influence on neuro-endocrine cells


Membrane potentials in intestinal smooth muscle

Baseline slow waves do not cause contraction (except STOMACH)
Slow waves are not action potentials

Occur on top of slow waves and are what cause PHASIC contractions
Occur only when there is enough depolarization to reach threshold and continues
The more action potentials, the stronger the smooth muscle contraction
CALCIUM influx make contractions last longer than skeletal muscle

Factors that alter resting membrane potential:
Less negative = depolarization
-Stretch (a bolus from eating)
-Acetylcholine (released by parasympathetic NS)
-Parasympathetic NS activity

More negative = hyperpolarization--inhibits activity
-Sympathetic NS activity


Autonomic Nervous System: Sympathetic

Stress, Fight or Flight

When active inhibits GI (slows it down)

Sympathetic nervous causes constriction of blood vessels to GI tract, diverting blood during times of stress

Originates between T5 and L2
Pre-Ganglionic fibers (short) enter sympathetic chain and release Acetylcholine
Post-ganglionic fibers (long) innervate the entire gut and release Norepinephrine

-Superior Mesenteric
-Inferior Mesenteric


Autonomic Nervous System: Parasympathetic

Rest and Digest

Cranial Division via Cranial Nerve X (Vagus Nerve)
-Small Intestine
-Large Proximal Large Intestine
-Sacral division via 2nd, 3rd, 4th sacral segments to pelvic nerves
-Distal Colon: rectum and Anus

Pre-ganglionic fibers (long) END in Enteric NS (Myenteric and Meissner)

Parasympathetic NS increases GI activity and functions


Stimulatory Substances Produced by Myenteric Plexus

Myenteric Plexus = motility

-substance P

Causes constriction to propel food forward


Inhibitory Substances Produced by Myenteric Plexus

Myenteric Plexus = motility

-Vasoactive Intestinal Peptide (VIP)
-Nitric Oxide (NO)

Things distal to bolus relax


Propulsive Movements

Forward movement of a contractile ring around the gut wall

Stimulus is distention of wall
Via ENS myenteric plexus, ring forms and PERISTALTIC movement is initiated
Responses in retrograde direction normally die out rapidly


Mixing Movements

Peristaltic against closed sphincter
Constrictive--attempt to break down to small components for easier absorption



Decreased small bowel activity--No mixing in the small intestine

Many causes:
-electrolyte disorder (K+, Ca2+)
-severe illness

Avoiding post-op ileus:
-get patient out of bed ASAP after surgery
-turn patient every 2 hours
-more pain meds = longer to resolve


GI tract Reflexes

Intra-gut reflexes (ENS) have an effect on contraction and secretion

Gut to pre-vertebral sympathetic ganglia and back to another portion of the gut

Gut to CNS (spine or brain)


Intra-gut reflexes (ENS)

Have effect on contraction, secretion
-duodenal distension slows gastric emptying


Gastro-colic Reflex

Stomach distention causes increased colonic motility


Entero-Gastric Reflex

Duodenal distension inhibits gastric emptying


Colo-Ileal Reflex

Cecal distension slows ileal emptying


Defecatory Reflex

Rectum to spinal cord and back to rectum


Reflex to relives tension on stomach wall

Stomach to brain via vagus n and back to stomach via vagus n

Relieves tension on stomach wall to accommodate more food


Cholecystokinin (CCK)

Released by cells in duodenum and Jejunum in response to fats being present

Causes gallbladder to contract, releasing bile to emulsify fats

Slows down gastric motility so what is present in small intestine can be addressed



Released by duodenum in response to acidic gastric contents being present

Slows down gastric motility so what is present in small intestine can be addressed


Gastric Inhibitory Peptide (GIP)

Released from upper small intestine in response to presence of fatty acids, amino acids, and carbohydrates

Slows down gastric motility so what is present in small intestine can be addressed


Villi Structure

Crypt (below surface)--produces fluids released and then is absorbed by the villus

Villus (apical side of lumen)--absorption of substances once broken down to small substances

Small Intestine: Villi present
Colon: No villi present because not involved in AA, protein, or carbohydrate absorption


Microvasculature of the Villus

80% of the oxygen diffuses form artery to vein

Tip of villus is vulnerable to ischemia


Celiac Sprue

Intolerant to gluten

Damage to villi
Crypts secrete fluids and future villus cells

Diarrhea from malabsorption
Weight loss

Usually of Irish decent

Due to gluten in diet:
-some vitamins and medicines


Splanchnic Circulation

Splenic Vein drains into portal vein

Majority of blood flow into liver is from portal vein
-~25% is from hepatic artery

Portal Vein P > Hepatic Vein P
--pumps venous blood toward heart



Scarring in sinusoids can cause enough Pressure to build up and cause blood to flow around the liver


Budd Chiari

If clot hepatic vein, liver can't drain itself
The pressure backs up and will have congested liver


Splanchnic Venous Flow

Portal vein:
-Superior Mesenteric Vein
-Splenic Vein
-Inferior Mesenteric Vein


Splanchnic Arterial Flow

Celiac Trunk:
Common Hepatic a:
Proper hepatic-->Liver

Celiac Trunk:
Splenic a


GI Blood Flow: Neural Control

Parasympathetic NS increases flow and GLANDULAR ACTIVITY

Sympathetic NS causes VASOCONSTRICTION and decreases flow

*blood shunted away from GI tract in times of heavy exercise, circulatory shock, need to mobilize blood


GI Blood Flow: Local metabolic Control

Increased flow to intestinal wall and villi during absorption
*returns to normal flow between meals


Factors responsible for Increased GI Blood Flow

Dilators: CCK, VIP, Gastrin, Secretin

Kinin release--induce vasodilation

Metabolic need for increased blood flow during times of demand


Which of the following is not true of the myenteric plexus?

A. It is located in the muscularis propria
B. It is responsible for secretion
C. It is responsible for mixing movements
D. It results in 12 contractions per min in the duodenum

B. It is responsible for secretion

This is Meissner's plexus


Which of the following is true regarding the interaction between the autonomic NS and the GI tract?

A. Sympathetic input originates between levels T1-T10
B. Sympathetic activity working in conjunction with the enteric NS increases propagation
C. Parasympathetic input is mostly from CN 9
D. The defecatory reflex involves parasympathetic input from levels S2-S4

D. The defecatory reflex involves parasympathetic input from levels S2-S4


The greatest percentage of blood flow entering the liver is from?

Portal Vein


Which of the following is an inhibitory substance produced by the myenteric plexus?

A. Vasoactive intestinal peptide
B. Acetylcholine
C. Substance P
D. Cholecystokinin

A. Vasoactive intestinal peptide

Nitric Oxide as well


True statements regarding villi are?

A. Countercurrent flow allows oxygen to diffuse from vein to the artery
B. Villi are localized throughout the GI tract but in greatest concentration in the small intestine
C. Villi are only located in the small intestine
D. Celiac sprue results in irreversible villi damage

C. Villi are only located in the small intestine