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Gastrointestinal System - Coggle Diagram
Gastrointestinal System
Pathology
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Resources:
- Webpath - Dr. puru recommendation
Pancreas
Acute Pancreatitis
Chronic Pancreatitis
Chronic Pancreatitis
Chronic pancreatitis is the irreversible inflammation of the pancreas leading to fibrosis of the pancreas' parenchymaEtiology
- :first_place_medal:Chronic Alchohol Use :champagne::first_place_medal:
- Middle age men :man::skin-tone-4:
- Long standing duct obstruction
- pseudocysts,calculi,trauma,neoplasms, pancreas divisum
- Tropical pancreatitis
- Africa,Asia tropical – malnutrition
- Hereditary pancreatitis
- PRSS1,SPINK1 gene
- Cystic fibrosis
Pathogenesis
- Initial Aggressors act on pancreas
- Toxic metabolites
- the metabolites of alcohol can result in acinar destruction and fibrosis
- Oxidative stress
- alcohol can induce membrane lipid oxidation,chemokines,fusion of lysosomes and zymogen granules
- Ductal obstruction
- protein plugs, calculi, calcify
- Chronic Inflammation occurs
- Parenhymal Fibrosis
- TGFB & PDGF induces fibrosis
- most prominent thing found in ultrasound
- Reduce number and size of acini
- Infiltrates of lymphocytes
Signs and Symptoms
Less severe than acute pancreatitis
- Sometimes Asymptomatic
- epigastric pain radiating to back
- weight loss
- Pancreatic insuffiency (endocrine & exocrine)
- diabetes mellitus
- fat malabsorption: fat in stools
Aggrevating factors of symptoms
- alcohol consumption
- heavy meals
- pancreas works extra hard
- Drugs
- opiates (morphine, heroine, codenine)
- drugs that increase sphincter tone of Oddi
Investigations and Lab Results
- Ultrasound and CT scan shows Pancreas having calcium fat depositis
- 72 hour stool collection (gold standard according to osmosis)
Management
Summary
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Acute Pancreatitis
Acute pancreatitis is the reversible inflammation of the pancreas, but it is more severe than chronicEtiology
I GET SMASHED
- Idiopathic
- :first_place_medal:Gallstones (Female) :first_place_medal:
- gallstones trapped in duct causes pressure build up and damage to acinar cells and leakage of digestive enzymes
- :first_place_medal:Ethanol/Alcohol (Male) :first_place_medal:
- Trauma (knife wound)
- Mumps
- Autoimmune Condition
- Hypertriglyceremia and Hypercalcemia
- Hypertriglyceridemia
- chylomicrons stuck in capillaries make them ischemic
- improves with fasting
- Hypercalcemia
- calcium deposits in pancreas activates trypsin
- Genetics (usually Kids)
- Activation Cationic trypsinogen (PRSS1) gene
- trypsin gets activated early and cause autodigestion of pancreatic tissue
- Deactivation of trypsin inhibitor (SPINK) gene
- Endocscopic Retrograde CholangeaoPancreatography (ERGP)
- technique used to treat biliary and pancreatic diseases
- Drugs
Physiology
- Pancreatic enzymes gets secreted into duct as zymogen granules
- Only in duodenum does the digestive enzymes get activated via trypsin
- Trypsinogen gets converted to trypsin in duodenum
- Trypsin gets deactivated quickly with Trypsin inhibitor (SPINK gene)
- trypsin has a short half life
- once trypsin gets removed the enzymes deactivates as a method of regulation
Pathogenesis Generalized
- Early conversion of Trypsinogen to trypsin before reaching duodenum
- Digestive Enzymes activated
- Autodigestion of pancreatic tissues
- Adipose tissue digestion --> Fat necrosis
- Triggering of nerves stimulating pain --> epigastric pain radiating to back
- Digestive enzymes leak into blood vessels
- Protein digestion --> Blood vessel necrosis --> haemorrhage (bleeding) and ecchymosis of abdomen
Diagram Sums it up very well
Osmosis Review
Pathogenesis of Gallstones
- symptoms can include mild jaundice
Pathogenesis of Heriditary Pancreatitis
- Activation of cationic trypsinogen, PRSS1 mutation which creates long lasting trypsin
- Prevents the deactivation of trypsin
- Activation of digestive enzymes --> pancreatitis
Signs and Symptoms
- Epigastric pain sometimes radiating to the back :star:
- improves as you lean forward (prayer sign)
- Cullen Sign / Grey Turner Sign
- Ecchymosis in abdominal area
- increase serum lipase and amylase
- Nausea
- Vomitting for several hours
- mild jaundice
- fatty stools
eg

Severe Cases
- decreased bowel sounds
- hypovolumic shock
- due to leakage of fluid into interstitial space
- leads to DIC bc activation of clotting factors
Complications
- Pseudocyst
- common complication
- false cyst (true one is always lined w epithelium)
- Hypovolemic shock
- leakage of fluid into interstitial space
- death due to DIC bc activation of clotting factors
- Gram -ve infection (in 40%-60% patients)
Laboratory Findings
- Serum Amylase increased in 24 hours
- Serum Lipase increased in 72-96 hours
- Glycosuria (in 10% of patients)
- Hypocalcemia
- this occurs when theres fat necrosis
- calcium saponification occurs whereby fatty acid binds with calcium to form calcium soaps
- Ultrasound
Management
- Resting the pancreas
- no food taken orally, just parietal nutrtion
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Summary
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Physiology
Mouth
Esophagus
Stomach
Stomach Overview
Functions of the Stomach
- absorption of water, alcohol, vitamin B12, iron
- digestion of fat and protein
- motility: segmentation and peristalsis
Gastric Secretions
Classified by: Mechanism
- Exocrine: secrete to duct :door:
- HCl :lemon:
- (+) acidity
- parietal cell
- Mucous :sneezing_face:
- secreted by more cardiac and pylorus than oxytonic/gastric glands
- neutralize acidity (protective)
- mucous neck cell
- Intrinsic Factor (IF) :pill:
- B12 absorption
- Parietal cell
- Pepsin + Lipase :scissors:
- Paracrine: secrete to neighbor :house_buildings:
- Histamine
- Somatostatin
- (-) acidity (protective)
- D cell
- Endocrine: secrete to blood :syringe: secreted more by gastric glands than cardiac/pylorus glands
- Gastrin
- hormone that stimulates more secretion of acid
- G cell (neuroendocrine cell)
- Ghrelin
Cells of Gastric Gland
- Mucous Neck Cell
- produces mucous to protect stomach epithelium
- Parietal Cell :ribbon: :heartpulse: :lemon:
- Produces HCl
- Produces Intrinsic Factor (IF)
- stains P for Pink (eosinophillic)
- Chief Cell :male-police-officer::skin-tone-3: :scissors:
- Produces Pepsinogen
- Produces gastric Lipase
- Neuroendocrine Cell
- Different types which produces hormones
- eg: G cell produces Gastrin
- Stem Cell
- can change into any cell of gastric gland
Protective Defenses of Stomach
- Mucous
- Bicarbonate and
- Stomach Epithelial Regeneration Rate
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Peristalsis

(toothpaste analogy)
- Inner Circular: Segmentation (squeeze)
- Outer Longitudinal: Push
Oesophageal Phase of Deglutition
- relaxation of UES
- relaxation of LES via release of NO and vasoactive intestinal peptide (VIP) which is a inhibitory neurotransmitter that causes relaxation
Achalasia: dysphagia due to incomplete relaxation of LES due to defective NO and VIP release
on the other hand..
GERD: acid reflux due to incomplete closure of LES caused by decrease neural activity in area
Ingestion: Saliva
Composition of Saliva:
- serous solution mostly H2O
- alkaline
- salts
- enzymes: amylase, lipase,
- antimicrobial properties: IgA
Function of Saliva:
- protection from microbes
- lubrication
- speech, deglutition (swallow), taste
- digestion
- salivary amylase
- lingual lipase
Mechanism of Salivary Secretion
- saliva begins as isotonic solution gets excreted by acinar cells
- myoepithelial cells contracts and secretes isotonic saliva into striated duct
- NaCl gets reabsorbed from saliva by duct cells (in exchange of K+) making it hypotonic
Regulation of Saliva Secretion
- stimulates: PSNS
- suppresses: SNS
- aldosterone reuptakes more salt making saliva more hypotonic
Deglutition
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Buccal, Pharyngeal, Esophageal

once food touches pharynx process becomes involuntarynerves involved:
- afferent: glossopharyngeal nerves
- efferent: 5th, 9th, 10th, 12th cranial nerves
theres so many nerves bc there are so many protective reflexes involved
Buccal Phase
saliva needed to allow lubrication of foodPharyngeal Phase
Protective Reflexes of Deglutition:

pic for reference
- Elevation of soft palate
- prevent food from going into nasal cavity
- closing of epiglottis and vocal cords
- prevents food from entering trachea
- inhibition of breathing
- prevent food from entering trachea
Oesophageal Phase
- relaxation of UES
- relaxation of LES via release of NO and vasoactive intestinal peptide (VIP) which is a inhibitory neurotransmitter that causes relaxation
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Drugs
Metronidazole
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