Week 1 Flashcards

1
Q

aa’s & monosaccharides are absorbed in

A

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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2
Q

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

A

the ileum

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3
Q

All blood leaving the small intestine is directed thru the

A

portal vein to the liver

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4
Q

Metabolic vasodilators

A

CO2, H+, K+, adenosine

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5
Q

Chylomicrons

A

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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6
Q

Mesenteric Ischemia

A

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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7
Q

Secretory diarrhea

A

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

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8
Q

GI Smooth Muscle – Contractile Characteristics

A

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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9
Q

GI Smooth Muscle – Excitation‐Contraction Coupling

A

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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10
Q

Migrating Motor Complex

A

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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11
Q

Submucosal nerve plexus

A

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

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12
Q

Myenteric nerve plexus

A

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

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13
Q

Afferent Sensory Neurons

A

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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14
Q

Efferent Motorneurons

A

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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15
Q

Neural Reflexes influencing GI Function

A

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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16
Q

Extrinsic Autonomic Nervous System

A

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

17
Q

Parasympathetic …

 Sympathetic…

A

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

18
Q

In general:
Parasympathetic …
 Sympathetic…

A

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

19
Q

Vago‐vagal Reflex

A

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:

20
Q

Acetylcholine

A

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

21
Q

Gastrin releasing peptide

A

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

22
Q

Substance P

A

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

23
Q

Vasoactive Intestinal Peptide

A

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

24
Q

Nitric Oxide

A

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

25
Q

Hormone:Cholecystokinin CCK

Cell:

Cell detects:

Hormone release stimulates secretion of:

A

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

26
Q

Hormone: Gastrin

Cell:

Cell detects:

Hormone release stimulates secretion of:

A

Hormone:
Gastrin

Cell:
G cell (stomach antrum)

Cell detects:
Amino acids
Pepsinogen

Hormone release stimulates secretion of:
H+ (from parietal cells)

27
Q

Hormone:
Secretin

Cell:

Cell detects:

Hormone release stimulates secretion of:

A

Hormone:
Secretin

Cell:
S cells (D/J)

Cell detects:
Acid

Hormone release stimulates secretion of:
Pancreatic juice (bicarbonate)
28
Q

Hormone:
Gastric Inhibitory Peptide or Glucose‐Dependent Insulinotropic Peptide (GIP)

Cell:

Cell detects:

Hormone release stimulates secretion of:

A

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

29
Q

Hormone:
Motilin

Cell:

Cell detects:

Hormone release stimulates secretion of:

A

Hormone:
Motilin

Cell:
Endocrine cells

Cell detects:
Fasting state (released cyclically thoughout)

Hormone release stimulates secretion of:
Initiates Migrating Motor Complex

30
Q

Paracrine Regulators

A

further modulate the response

 Histamine (ECL cells) and somatostatin (D cells) = paracrine regulators

31
Q

Borborygmi

A

rumbling noise created by movement of gas in bowels

32
Q

Sympathetic

A

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)

33
Q

Parasympathetic

A

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

34
Q

Esophagus innervation

A

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