anatomy, physiology & pathophysiology- conversion...
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CLINICAL UPDATECLINICAL UPDATEGASTROENTEROLOGY
NURSING
Joe Garzia StafraceCertified Gastroenterology Nurse (Ch. US)
Anatomy, Physiology & Anatomy, Physiology &
Pathophysiology Pathophysiology ––
EsophagusEsophagusJGS
Gastrointestinal3
Anatomy and Physiology Anatomy and Physiology -- EsophagusEsophagus
� A hollow, muscular tube app 1O” x 1”.
� Conveyer; 3rd organ;
� Posterior to trachea and larynx.
� 3 Layers –
� UES and LES
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MotilityMotility
� At rest, both UES and LES are closed
� Peristalsis
� 3 to 5 cm /sec
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Pathophysiology Pathophysiology -- VaricesVarices
� Esophageal Varices
Related to Portal Hypertension,
alcoholic cirrhosis, cirrhosis.
Varices may be asymptomatic with a high risk for rupture. Graded I to IV.
Rx – Injection, EVL, IV vasopressin, balloon tamponade, PS Shunt.
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PathophysiologyPathophysiology –– EsophagealEsophageal TumorsTumors
� Squamous Cell Carcinoma, Barrett’s, Adenocarcinoma.
� Chronic Irritation of the esophageal mucosa [caustic ingestion, chronic and persistent reflux, excessive smoking or drinking)
Prime Ind. – Dysphagia and Odynophagia, anorexia, weight loss, anemia, hoarseness.
OGD – Brushings and Biopsy
Survival rate only 3%.
Rx –Stenting, Palliative, Surgery.
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Pathophysiology Pathophysiology -- OtherOther
� Diverticula – Zenker’s, Traction, Epiphrenic, Intramural.
� Strictures – caustic, Candidiasis, Reflux.
� Rings and Webs – thin, circumferential mucosal shelves
� Foreign bodies
� Infectious diseases
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Pathophysiology Pathophysiology -- OtherOther
� Mallory-Weiss tears – Rx conservative
� Motility Disorders :–1. Achalasia – defective peristalsis and ↑ LES pressure =
dysphagia to solids and liquids, regurgitation, and weight loss. Rx – Pneumatic dilatation, Botox, Hellers, Nitrates.
2. DES – unknown cause. Dysphagia to solids and liquids (very H&C). Rx – long term anticholinergics, nitrates.
3. Nutcracker Esophagus – Rx as DES
� Caustic – Accidental and Suicidal ingestion of ↑ acid or alkaline.
Rx – acid (large volumes of milk and water)
� Congenital defects – atresia, fistula.
� Fistulas in adults – Cancer, benign inflammatory process or trauma. Chronic cough, fever, recurrent pulmonary infections, dysphagia. Rx – stenting, surgery.
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Anatomy, Physiology & Anatomy, Physiology &
Pathophysiology Pathophysiology ––
StomachStomach� Joe Garzia Stafrace CGN
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Anatomy and Physiology Anatomy and Physiology -- StomachStomach� J-Shaped, distensible, below diaphragm
� 10-12” Long x 4- 6” Wide
� Maintains relatively low levels of microbes
� Digests food and prepares nutrients for absorption
� Serves as a reservoir
� Mixes and delivers chyme to SI for
further digestion and absorption
� Originates signals for hunger
or satiety.
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Pathophysiology Pathophysiology -- UlcersUlcers� When the normal balance between factors that
promote mucosal injury (e.g., gastric acid, pepsin, bile acids) and those that protect the mucosa(e.g., an intact epithelium, mucus) is upset, ulcers or inflammation may arise.
� Mechanical – Chemical – Infectious – Ischemic
Pyloric Sphincter
pressure -Reflux
NSAIDs, Alcohol
Atrophy
H.pylori
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Pathophysiology Pathophysiology –– Ulcers Ulcers -- RxRx� PPI - decrease gastric acid by inhibiting the enzyme
responsible for completing the final step of acid secretion.
� H2 Blockers – reduce the amount of acid produced by the stomach and blocking H2 acid prod.
� Sucralfate – protects the site of disrupted mucosa by forming a protective gel layer.
� Antacids – neutralize pH, strengthen the gastric mucosal barrier, tones the LES.
{antacids should be taken 1 to 3 hours after meals and before sleep}
� Surgical Options -
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Pathophysiology Pathophysiology –– Helicobacter pyloriHelicobacter pylori� Transmission via fecal-oral or oral-oral pathways
� Linked to gastritis, gastric and duodenal ulcers and cancer
� Investigate – serology, breath, tissue
� Rx – PPI + Metro +Tetra/Amox
Gastric Cancer
� Hereditary, Type A Blood, lower socioeconomic
� Incidence increases with age, +HP, high starch, nitrates, pickled vegetables, salted fish and meat
Anatomy, Physiology & Anatomy, Physiology &
Pathophysiology Pathophysiology ––
Small IntestineSmall IntestineJoe Garzia Stafrace CGN
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Pathophysiology Pathophysiology –– Small IntestineSmall IntestinePathologic conditions of the small intestine can affect
absorption of nutrients in the affected area.
Duodenal Ulcer
Disease
Parasitic
Infestations
Bacterial and
Viral Infections
Crohn’s Disease
Meckel’s
diverticulum
Vitamin B12
deficiency
Small Bowel
TumorsCeliac Disease
Short Bowel
Syndrome
Whipple’s
disease
Lactose
Intolerance
Hirschsprung’s
disease
Appendicitis Intussusception
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Anatomy, Physiology & Anatomy, Physiology &
PathophysiologyPathophysiology ––
Large Intestine (Colon)Large Intestine (Colon)� Joe Garzia Stafrace CGN
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Anatomy Anatomy –– Large IntestineLarge Intestine� 4 to 5 feet long and
approximately 2” in diameter.
� 4 layers form the lining:-Serosa, Muscularis, Submucosa, Mucosa. The
rectum does not have the serosalayer.
� Secretes h2o, mucous, pot. and bicarbonate.
� Absorption – Receives 1-2Lts but retains 150-200mls. Sod, Chl, Water are absorbed (asc)
� Sterocobilin
� Protein metabolism; Bacteria; Toxins
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PathophysiologyPathophysiology–– LargeLarge IntestineIntestine� Polyps – Sesile, Pedunculated,
� Juvenile, Familial polyposis coli- highly potentially cancerous
Gardner’s Syndrome Peutz-Jeghers SyndromePolyps are alsoPresent in Skull,Mandible andLong Bones.
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PathophysiologyPathophysiology–– Large IntestineLarge Intestine
Angiodysplasia
OWR or HHT
Colitis – IBD Ischemic, Radiation,
Necrotizing, UC,
Crohn’s,
Pseudomembraneous
Ulcerative
Colitis
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PathophysiologyPathophysiology–– Large IntestineLarge Intestine
� Ulcerative Colitis1. Affects mucosa & sub-
mucosa.2. Pain crampy, lower abdo,
relieved by bowel movement
3. Bloody stools4. No abdominal mass5. Continuous from rectum
Colon6. Fever, dehydration 7. Affects only and anemia in
severe cases8. Extraintestinal symptoms
– arthritis, conjunctivitis, pseudopolyps, rectal prolapse, hemorrhoids, anal fissures,, erythemanodosum, renal.
� Crohn’s Disease1. A transmural disease
(granulomas)2. Pain constant, not relieved by
bowel movement3. Not grossly bloody4. Abdominal mass (RIF)5. May be discontinuous (skip
areas)6. May affect any part of the GI
Tract7. Stricture and Fistula
formation are common8. Edema, mucosal ulceration
(cobblestone appearance), fissures, abscesses, granulomas, growth failure, malnutrition and weight loss
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PathophysiologyPathophysiology–– Large IntestineLarge Intestine� IBS IBS IBS IBS –––– ‘‘‘‘The money spinnerThe money spinnerThe money spinnerThe money spinner’’’’---- 25 to 50% of visits to GI 25 to 50% of visits to GI 25 to 50% of visits to GI 25 to 50% of visits to GI
Specialists are IBS related problems.Specialists are IBS related problems.Specialists are IBS related problems.Specialists are IBS related problems.
an an an an exageratedexageratedexageratedexagerated motility response to environmental stressmotility response to environmental stressmotility response to environmental stressmotility response to environmental stress
A motility disorder without evidence of anatomical abnormality or organic illness. Symptoms vary in pattern and intensity. Not related to other diseases.
Rx – Sympathetic reassurance that organic causes have been ruled out. A high-fiber diet. Anticholinergic agents. Psychological support.
� Parasitic InfestationsParasitic InfestationsParasitic InfestationsParasitic Infestations
� DiverticularDiverticularDiverticularDiverticular DiseaseDiseaseDiseaseDisease
DiverticulosisDiverticulitis
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PathophysiologyPathophysiology–– Large IntestineLarge Intestine
� MELANOSIS COLI
� Intestinal Obstruction – Congenital or Acquired
� Neurogenic Obstruction
� Vascular Obstruction
� Anorectal Disorders
Hemmohoids, Fecal Impaction, Encopresis, AnorectalAbscess, Anorectal Fistula, Anal Fissure, Rectal Prolapse.
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PathophysiologyPathophysiology–– Large IntestineLarge IntestineColon Cancer – The Increased Risk Group
Risk category Age to Begin Recommendation Comments
People with a small, single adenoma
3-6 years after initial polypectomy
Colonoscopy N- screen as per average risk
Large (1cm+) adenoma, multiple, high-grade dysplasia / villous
Within 3 years after initial polypectomy
Colonoscopy N- repeat in 3 years
N- screen as per average risk
Personal history of CRC
Within 1 year after cancer resection
Colonoscopy N-repeat in 3 years
N-repeat in 5 years
Either CRC or adenomatous polyps
In any 1st degree relative before age 60, or in 2+ 1st degr
Relatives at any age
Age 40, or 10 years prior the youngest case in the immediate family
Colonoscopy Every 5 – 10 years. CRC in 2nd or 3rd
degree relatives less
ACS: NCS; ACG; SGA;WHO;ICS
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The Horror Show
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What goes in must come outWhat goes in must come out
ANAL PROBLEMS
Perianal haematoma
ANAL FISSURE
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THE BILIARY SYSTEMTHE BILIARY SYSTEM� ANATOMY
Gallbladder, Hepatic, Cystic, and Common Bile ducts
3” x 1” and capable of holding 50mls of bile
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THE BILIARY SYSTEMTHE BILIARY SYSTEM
� Physiology - GBTo Collect, Concentrate, and Store bile.
Bile is an alkaline, greenish-yellow fluid continuously secreted by the liver. 97% water; bile slats; fatty acids; lipids, mainly cholesterol and lecithin; electrolytes; bilirubin; other organic substances.
Functions of Bile:- emulsification of undigested fats; absorption of fat-soluble vitamins; activation of intestinal and pancreatic enzymes; bilirubin, sex, thyroid, adrenal hormones, and cholesterol elimination;
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THE BILIARY SYSTEMTHE BILIARY SYSTEM
� PathophysiologyIncreases with age. 4Fs x 6.
Cholelithiasis – 5th leading cause of Hospitalization and accounts to 90% of all biliary diseases. ¾ are Cholesterol.
Choledocholithiasis – 40% are Pigment stones. Symptoms include colic, Obstructive jaundice with pruritis.
Acalculous Cholecystitis – related to typhoid, shigellosis; viral gastroenteritis; pneumonia.
Cholangitis – a rare bacterial infection {E.coli and Klebsiella} of the bile duct with poor prognosis – a Med & Surg emerg.
Cholecystitis – Acute or Chronic inflammation of the GB.
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E.R.C.P. E.R.C.P.
((EndoscopicRetroCholangioPancreographyEndoscopicRetroCholangioPancreography))
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