Physiology Block 3 Week 13 01 Overview of GI Physiology Flashcards
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 Pylorus 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
Mucosa:
- Epithelium
- 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
Absorption
Secretion
Blood Flow
Invaginations
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
- COLON ONLY
- 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
Resting:
Baseline slow waves do not cause contraction (except STOMACH)
Slow waves are not action potentials
Spikes:
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
- Norepinephrine
- 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
Ganglions:
- Celiac
- Superior Mesenteric
- Inferior Mesenteric
Autonomic Nervous System: Parasympathetic
Rest and Digest
Cranial Division via Cranial Nerve X (Vagus Nerve) Innervates: -Esophagus -Stomach -Pancreas -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
- Acetylcholine
- 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
Ileus
Decreased small bowel activity–No mixing in the small intestine
Many causes:
- post-op
- Narcotics
- 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
Secretin
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
Countercurrent
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:
- wheat
- barley
- rye
- 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
Cirrhosis
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
