GIT Flashcards
Layers
Mucosa (simple columnar epithelium)
Sub mucosa (CT)
Muscularis (smooth muscle)
Enteric plexus (nerves)
Serosa/ peritoneum (epithelium)
4 cells in mucosa of stomach
Parietal»_space; HCl +intrinsic factor for B12 absorption
Chief» pepsinogen, peptic
Mucous» alkaline protective mucus
G cells» gastrin- somatostatin -histamine-serotonin
Hcl and i trinsic factor
Parietal/ oxyntic
Food enter lumen (first step)
CO2 enter parietal cell
Combines with H2O in presence of carbonic anhydrase enzyme forming
Carbonic acid
Which dissociates into
Bicarbonate ion and proton
Second step of HCl secretion
Proton pumped out into lumen and bicarbonate pumped out into interstitial space by bicarbonate chloride anti portal
Cl- gets into parietal cell and gets out by chloride channel meeting the proton in the lumen
Combines and forms HCl
Activation of pepsinogen
Chief cells secrete pepsinogen which is inactive
When it meets HCl in lumen it becomes pepsin that digests proteins
Proteins digested into…
Protease
Peptones
HCl is only present when ..
Food is in lumen
T/f HCl is formed inside parietal cells
False outside in lumen to prevent damage
Gastric juice pH and components
1-3.5
Salts /enzymes/HCl/ mucus/ H2O
Inflammation in stomach lining
Gastritis
Symptoms of gastritis
Heartburn
Upper abdominal pain
Nausea
Gastritis causes
Infection with helicobacter pylori, an acid loving bacteria in stomach
Non steroidal anti inflammatory drugs
Auto immune
Radiation
NSAIDs
Non steroidal anti inflammatory drugs
Acute gastritis signs
Mucosal and sub mucosal lymphocytes infiltrated with pockets of polymorph nuclear cells (neutrophils)
Edema water + vaculated epithelium+ lymphocytes
Mild mucosal defects
Inflammation types and differences
Acute» short term/ immense pain treated/healing after
Chronic»long term/active inflammation damage and healing within
Cell in chronic
Lymphocyte+ monocyte+ giant multinucleated cell
Cells in acute
Neutrophils
Complex reaction to deal with offensive agent to neutralise its effects, minimise spread and erdicate
Inflammation
Acute suppurative inflammation
Components
Cause
Example
Pus» living and dead bacteria+ toxins+ liquified necrotic tissue+ leucocytes+ pus cells+ macrophages+ RBCs
Pyogenic microorganisms» staphylococus aureus
Appendicitis
Chronic non specific cholecystitis
Gall bladder
Partially ulcerated mucosa
Fibrosis of wall
Endarteritis obliterans.
Diffuse chronic inflammatory cellular infiltrate ( lymphocytes- plasma- macrophages)
Shortest VS largest part of small intestine
Duodenum
Ileum(peyers patches/ lymph nodules)
Mucosa of small intestine
Digest and absorb
Microvilli and villi
Goblet cells to produce mucus
Intestinal glands(crypts od lieberkuhn) mucosa at villi base
Brunner glands
Duodenal glands mucous at sub mucosa
Gall bladder duct
Cystic
Liver duct
Hepatic
Bile duct?
Cystic+ hepatic
Common hepatic duct?
Right+ left
Pancreas duct
Pancreatic
Hepatopancreatic
Bile+ pancreatic
Liver function
Bile production to emulsify fats
Detoxification hepatocytes convert ammonia to urea
Phagocytosis kupffer cells
Synthesis albumin heparin globulins
Liver stages
Fatty»steatohepatitis»cirrhosis
Black eye
Fatigue
Inflammation under eye
The cycle of blood to liver
In» hepatic artery (O2 rich)
Hepatic portal vein(nutrient rich small intestine)
Out» hepatic vein
Hepatic duct(bile)
Gall baldder
Stores bile
Too much bile= too much cholesterol= stones
Stones block cystic duct, hepatic comma inability to detoxify
Pancreas
Mixed
Endocrine(islands of langerhans)
Exocrine(pancreatic acini, grape like shape)
Acini forms… Separated by …
Lobules
Septa
Large intestine
No microvilli
Crypts glands
Function of large intestine
Converting chyme to feces
18-24 h movement
1500ml» 150ml excreted feces
Reabsorbs and secretes mucus
Feces contain
Water
Epithelial tissue
Cellulose
Mucus function
Bacterial action
Protection(parasympathetic stimulation , increased goblet cell secretion)
Gases from legumes and artificial sugars to sorbitol
Produces vitamin K
