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41 Cards in this Set
- Front
- Back
GI tract cellular components
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Smooth muscle
Epithelium Neurons Bacteria Immune cells Blood vessels |
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Basic processes of the GI tract:
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Ingestion
Digestion, secretion and absorption Motility |
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A few cell types accomplish all intestinal functions:
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Muscle cells
Neurons Epithelial cells Immune cells Interstitial cells of Cajal, myofibroblasts, glia, stem cells |
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GI Muscle cells
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Contraction - Propulsion
Two types of muscle cells in the intestine A. Skeletal muscle - esophagus B. Smooth muscle – BVs, CM, LM and MM Small mononucleated cells form muscle layers Distinct from skeletal muscle - graded response to excitatory and inhibitory inputs (neural, chemical, mechanical) Tone: maintained contractile state of cell Active relaxation (VIP, NO) |
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GI Neurons
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Peripheral Nervous System
Somatic sensory Afferent - sensory signals from intestine Autonomic Nervous System Parasympathetic Sympathetic Enteric Nervous System autonomous within intestinal wall |
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enteric nervous system
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organized into ganglia.
Regulation of motility, blood flow and secretion - absorption. Complex, integrated sensory and motor pathways. But not pain. |
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GI pain
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Pain is a key symptom of intestinal pathology.
Contrast the normal with painful/inflamed states: Lack of sensation of intestinal activity Minimal knowledge of events Visceral/intestinal/gastric pain Severe, poorly localized Crampy, alternating OR unremitting |
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GI Epithelial cells
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An epithelial mucosa constitutes the physical barrier between the lumen and the body.
Functions include secretion, absorption, lubrication, protection. |
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mucosa
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The epithelial cell is the principal cell of the mucosa
Dynamic – constantly growing*, hence dividing and maturing; dying Functional - secretory/absorptive *Target in chemotherapy, radiation enteritis Intestinal mucosa - simple columnar epithelium |
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GI immune cells
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The largest component of the immune system
The lumen – the outside is inside Challenges include: Antigens, bacteria, physical damage Immune cells are resident in the mucosa Eosinophils, neutrophils, monocytes/macrophages, T cells, mast cells |
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liver functions
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Metabolism
Detoxification Glycogen storage Bile production |
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Gall bladder
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Muscular sack
Stores and concentrates bile Releases bile into duodenum in response to a meal. Cholecystokinin from enteroendocrine cells. |
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Pancreas islets
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Hormone production and secretion (endocrine pancreas)
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pancreas acini
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Digestive enzyme production and secretion (exocrine pancreas)
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Motility
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the appropriate and timely passage of ingested material along the intestinal tract
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Sphincters create functional compartments
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regulated via neuronal input and smooth muscle contraction
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GI innervation
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Intrinsic (enteric) innervation regulates function
Extrinsic innervation modulates, conveys information to the CNS |
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Achalasia symptoms
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– dysphagia, regurgitation, chest pain
Lack of esophageal peristalsis Incomplete relaxation of LES, LES hypertrophy Increased resting tone of LES |
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LES
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lower esophogeal sphincter
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peristaltic reflex
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oral-contraction
anal-relaxation |
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layering of GI tract
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longitudinal muscle
myenteric plexus circular muscle submucosal plexus mucosa |
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Gastro-esophageal reflux disease
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Exposure of esophagus to gastric juice (heart burn)
Transient(sudden) LES relaxations Loss of LES tone Impaired esophageal clearance of stomach contents Treatment: PPI, antacids, H2 receptor antagonists |
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Regions of the stomach
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Gastroparesis
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Delayed gastric emptying
Nausea, vomiting, bloating, early satiety, pain Idiopathic, diabetes vagus nerve is damaged and the muscles of the stomach and intestines do not work normally |
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Mechanisms of gastroparesis
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Autonomic (parasympathetic and enteric) neuropathy – impaired relaxation of pyloric sphincter
Antral hypomotility – interstitial cells of Cajal Gastric hypersensitivity- early satiety, pain and nausea |
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stimuli for emesis
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distention, irritation of GI tract
drugs, motion and intracranial pressure, strong noxious perceptions |
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emesis risk for health
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- aspiration(foreign materials - lungs), electrolyte imbalance
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emesis process
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Glottis closes
LES relaxes Reverse peristaltic waves Abdominal muscles contract |
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achalasia etiology
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is unknown but suspected to involve loss of inhibitory muscle motor neurons (NO and VIP)
Treatment – Heller myotomy(cut muscle), Botulinum toxin, dilation |
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IBS
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Characterized by chronic abdominal pain and altered bowel habits in the absence of any organic cause
3:1 female Pain relieved by defecation Duration of months Altered motility patterns Enhanced gastro-colic reflex Alternating symptoms |
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Post-infectious IBS
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Subset of IBS patients suffer severe gastroenteritis prior to symptom onset.
Walkerton, ON. Previous immune stimulation resets the balance of neural signalling in the gut |
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Treatment of IBS
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Dietary adjustment- fibre supplement
Serotonin signaling Very high placebo response – role of the CNS in regulating symptoms |
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Mechanical Obstruction of the Intestine
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Obstruction
Mechanical Developmental Inflammatory – eg stricture (IBD) Tumour Adhesions Inappropriate connection of adjacent intestinal segments (eg, splenic flexure of colon to mid-jejunum), or intestine-other organ (colon-bladder) |
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Strangulation
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Associated with herniation of the abdominal muscle
inguinal hernia Entrapment and constriction of the intestine causes obstruction, ischemia and occasionally gangrene |
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Hirschprung’s disease
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Non-propulsive region causing functional obstruction in infant
distended colon upstream of band of constriction, risk of toxicity Histological Diagnosis absence of enteric ganglia – no enteric neurons in constricted segment Surgical excision and anastomosis (different connection). Stem cells |
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Difference between CD-UC
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IBD
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Crohn’s disease (CD) and ulcerative colitis (UC)
Pain, bleeding, diarrhea, fever Impaired growth, anemia, weight loss Cause is unknown Genetic susceptibility Possible environmental factors IBD likely arises from exposure of a genetically susceptible individual to an environmental trigger. prevelance increases far equator developed nations mostly |
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CD location
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anywhere from mouth to anus
ileum most common, Crohn’s colitis is possible typically terminal ileum |
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CD characteristics
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Skip lesions in ileum
Cobblestoning of normal mucosa with surrounding fissured, inflamed tissue Stricturing disease - surgical resection due to redundancy of ileum disease may recur |
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CD nutrients
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can lead to “short gut” syndrome.
Basic absorption of nutrients requires adequate small intestinal length (=area) B12 absorption unique to ileum |
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CD immunology
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CD4 IFN-y, TNF bad
CD4 IL10, TGFB good |