Week 1 Flashcards by Adam strohschein

aa’s & monosaccharides are absorbed in

duodenum & jejunum thru secondary active transport

 Na/K ATPases keep Na levels within enterocytes low; coupled transport w/Na often drives uptake of nutrients

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Cobalamin (B12) & bile salts/acids are absorbed in

the ileum

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All blood leaving the small intestine is directed thru the

portal vein to the liver

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Metabolic vasodilators

CO2, H+, K+, adenosine

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Chylomicrons

are too large to pass through capillary cells so lipids are absorbed through lacteals (lymphatics)
which empty into the bloodstream via the thoracic duct

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Mesenteric Ischemia

Causes:
 Occlusive mechanisms including thrombi (mesenteric infarction)
 Non‐occlusive mechanisms: prolonged reflex vasoconstriction (due to hypovolemia, heart
failure) or abnormal levels of circulating vasoconstrictors (e.g, epinephrine, angiotensin II)
o Effects:
 Postprandial Pain, Sitophobia
 Necrosis of the tips of the villi
 Loss of barrier function of the wall of the gutuptake of vasodilator toxins (endotoxin) from
the gutresults in Septic Shock

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Secretory diarrhea

Infection leads to excess secretion of chloride (occurring in the crypts) drawing water into lumen

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GI Smooth Muscle – Contractile Characteristics

o Rhythmic “phasic” (seconds) contractions and long “tonic” contractions (minutes to hours).
o Basal resting tension or “tone” is maintained without elevation in intracellular Ca++ and without
energy expenditure. (Ex: sphincters are tonically contracted; don’t use energy, just general tone) o GI smooth muscle has a remarkable ability to shorten (e.g., to 50% of resting length!!!)
o Can initiate depolarization in response to stretch leading to contraction.

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GI Smooth Muscle – Excitation‐Contraction Coupling

o Slow wave electrical activity (3‐12/min, 5‐15 mV) initiated by interstitial cells of Cajal are phasic and propagated over a few centimeters to neighboring cells
o Slow waves generated by increase in Ca followed by repol. by K+ channels o Amplitude, but not frequency, of slow waves can be altered by signals
releasing calcium from internal stores or opening Ca++ channels on plasma
membrane
o Muscle contraction accompanies action potential.

o Excitation‐contraction coupling initiated by increases in intracellular calcium ion concentration
 Binding of ACh to muscarinic Rincreased influx of Ca into cellactivation of calmodulin‐
dependent myosin light chain kinasephosphorylation of myosinincreased myosin ATPase activity & binding of myosin to actincontractiondephosphorylation of myosin by myosin light chain phosphataserelaxation or sustained contraction due to the latch bridge & other mechanisms

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Migrating Motor Complex

relaxation of sphincters (fully opens all sphincters) and contractions in stomach
and small intestine occurring during fasting (interdigestive) controlled by hormone motilinrepeated giant
waves that sweep from stomach to large intestine to empty everythingwhy gum doesn’t stay for 7 years

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Submucosal nerve plexus

within small and large intestine, sensory and blood flow; Meissner’s

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Myenteric nerve plexus

bw circular & longitudinal muscle layer from esophagus to internal anus; Auerbach’s

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Afferent Sensory Neurons

o Excited by fast distension of the gut wall or chemical signals from the lumen of the gut transmitted to sensory neurons.
o Many of the sensory neurons are stimulated by serotonin (5‐HT) released from mucosal enterochromaffin cells (ECL)
 Sensory neurons respond w/ a few AP’s followed by hyperpolarization (adaptation)
o Transfer information about gut environment to interneurons in myenteric plexus which relay signals
up and down the gut.

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Efferent Motorneurons

o found primarily in the myenteric plexus
o usually unipolar in structure
o excited by fast EPSPsrespond with sustained trains of action potentials
o carry “efferent” information to GI smooth muscle, vascular smooth muscle, GI exocrine secretory
cells and GI endocrine secretory cells
o excitatory fibers release acetylcholine, neurokinin A and substance P
o inhibitory fibers release vasoactive intestinal peptide (VIP) and nitric oxide (NO) on smooth muscle
cellsrelaxation

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Neural Reflexes influencing GI Function

o “Short” = involve only nerves of the enteric plexes; occur right in your GI wall
o “Long” = both CNS and ANS are involved

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Extrinsic Autonomic Nervous System

o Afferent information leaving GI tract is carried by autonomic nerves
o Parasympathetic: mostly cholinergic of vagus nerve; stimulates activity of the enteric plexuses,
increases GI motility and secretory activity.
o Sympathetic: mostly adrenergic, generally inhibits activity of the enteric plexuses, decreases GI
motility, contracts GI sphincters, constricts GI microvasculature

Parasympathetic …

 Sympathetic…

Parasympathetic increases activity: cholinergic, vagus“rest and digest”
 Sympathetic stimulation decreases activity: noradrenaline, dopamine, neuropeptide Y

In general:
Parasympathetic …
 Sympathetic…

Parasympathetic increases activity: cholinergic, vagus“rest and digest”
 Sympathetic stimulation decreases activity: noradrenaline, dopamine, neuropeptide Y

Vago‐vagal Reflex

o Vagal afferent info is transmitted to autonomic centers in the medulla
o Vagal efferents coordinate excitatory (ACh) & inhibitory (NO) activity within the Enteric Nervous System to mediate peristalsis:

Acetylcholine

primary excitatory transmitter from sensory cells
& from motoneurons to muscle, epithelium, secretory cells and at
interneuronal junctions increase intracellular Ca++

Gastrin releasing peptide

released from vagal nerve endings to stimulate G cell secretion of gastrin.

Substance P

(tachykinin) ‐ an excitatory transmitter generally co‐released with acetylcholine.

Vasoactive Intestinal Peptide

(VIP) – Promotes motility
 Relaxes smooth muscle in esophagus and stomach (“inhibitory”)
 Stimulates fluid secretion and promotes dilation of the GI vasculature increase cAMP

Nitric Oxide

(NO) ‐ an inhibitory transmitter co‐released with VIP from inhibitory motoneurons,
hydrophobic‐ intracellular targets.

Hormone:Cholecystokinin CCK Cell: Cell detects: Hormone release stimulates secretion of:

Hormone: Cholecystokinin CCK ``` Cell: I cells (D/J) ``` Cell detects: Fat Amino acids Hormone release stimulates secretion of: Pancreatic enzymes Bile salts for fat uptake

Hormone: Gastrin Cell: Cell detects: Hormone release stimulates secretion of:

Hormone: Gastrin ``` Cell: G cell (stomach antrum) ``` Cell detects: Amino acids Pepsinogen Hormone release stimulates secretion of: H+ (from parietal cells)

Hormone: Secretin Cell: Cell detects: Hormone release stimulates secretion of:

Hormone: Secretin ``` Cell: S cells (D/J) ``` Cell detects: Acid ``` Hormone release stimulates secretion of: Pancreatic juice (bicarbonate) ```

Hormone: Gastric Inhibitory Peptide or Glucose‐Dependent Insulinotropic Peptide (GIP) Cell: Cell detects: Hormone release stimulates secretion of:

Hormone: Gastric Inhibitory Peptide or Glucose‐Dependent Insulinotropic Peptide (GIP) ``` Cell: K cells (D/J) ``` Cell detects: Carbohydrates Fat Hormone release stimulates secretion of: Inhibits gastric acid secretion Stimulates insulin release from pancreas

Hormone: Motilin Cell: Cell detects: Hormone release stimulates secretion of:

Hormone: Motilin Cell: Endocrine cells ``` Cell detects: Fasting state (released cyclically thoughout) ``` Hormone release stimulates secretion of: Initiates Migrating Motor Complex

Paracrine Regulators

further modulate the response |  Histamine (ECL cells) and somatostatin (D cells) = paracrine regulators

Borborygmi

rumbling noise created by movement of gas in bowels

Sympathetic

associated with T1‐L2 spinal cord segments = Fight or Flight  Function: inhibit peristalsis and vasoconstrict  Preganglionic: cell bodies lie in thoracolumbar lateral horn; relatively short  Single sympathetic preganglionic axon has many collateral branchesmay synapse with ≥ 20 postganglionic neuronssynapse with several visceral effectors  Terminate in paravertebral or prevertebral ganglia; ACh is neurotransmitter  Postganglionic: highly branched; long; release NE as neurotransmitter (except for sweat glands)

Parasympathetic

associated with brain stem (cranial nerves) and spinal cord segments S2‐S4 = Rest, Read, and Digest  Function: stimulate peristalsis, relax sphincters, stimulate glandular secretion  Preganglionic: fibers originate in cranial and sacral regions; relatively long; use ACh  Postganglionic: short; release ACh

Esophagus innervation

fibromuscular tube extending from cricoid cartilage to stomach (11th thoracic vertebra) o Upper 1/3: parasympathetics from recurrent laryngeal nerve o Esophageal plexus: below bifurcation of trachea  Parasympathetics: from vagus (CN X) – supply smooth muscle and glands  Post‐ganglionic sympathetics: from ~T1‐4 – directly or via cardiac or pulmonary plexuses innervate vascular smooth muscle  Vagus provides VA from esophagus; thoracic splanchnic branches carry visceral pain from esophagus