Inhibitors of stomach action
CCK, Secretion, GIV/VIP
amylase AKA
Ptyalin
Carbohydrates
30-40% digested by the time it leaves the stomach-when chewing food, amylase is mixed w/ food and starts digesting carbs - increased HCL content in stomach breaks down salivary amylase
Protein
pepsin a peptic enzyme is most active in an acidic environment, that is why the parietal cells secrete HCI-collagen is digested by pepsin, which allows digestion of proteins- pepsin provides 10-20% of protein digestion, allows pancreatic secretions to digest remainder more easily
Fats
up to 10% of triglycerides are digested in the mouth by lingual lipase from saliva - fat clumps together in aqueous medium
stomach
little absorption takes place here- only alcohol and some drugs are at small quantities
gastritis
acute mucosal inflammation with hemorrhaging
hemorrhaging
vascular damage involved
acute gastritis risk factors
-NSAIDs (excessive use) - decreases protective mucosal lining -excessive alcohol consumption -smoking-chemo drugs: attacks highly prolific cells ex. epithelial cells - bacterial/ viral infections -stress"acute" = "all of a sudden" and short duration
acute gastritis S&S
abdominal pain, nausea, vomiting, indigestion, bloating, belching- w/ erosive gastritis- often asymptomatic
Emesis
vomiting
dyspepsia
indigestion
Chronic atrophic gastritis
chronic inflammation leading to mucosal atrophy and intestinal metaplasia -> cancer
Chronic atrophic gastritis causes
-chronic infection by H-pyloric -autoimmune associated with pernicious anemia-toxic exposures alcohol, smoke- postsurgical -motor and mechanical, including obstructions -miscellaneous
H-pyloric
bacteria -major factor in peptic ulcers
pernicious anemia
Vitamin B12 deficiency (deadly)
achlorhydria
lack of HCL secretion by parietal cells
achlorhydria leads to
-poor absorption of Fe, iron def anemia- poor absorption of Fe Ca2+, osteoporosis - more susceptible to GI infections -reduced secretions of duodenal hormones
pernicious anemia
lack of intrinsic factor. cannot absorb B12 causing macrocytic anemia
Peptic Ulcers
-a breach in the mucosa of the tract that extends through the muscularis mucosa or deeper- can occur anywhere in alimentary tract but are more prevalent in duodenum and stomach - are chronic, often solitary, 2-4 cm, and assocaited to areas with aggressive action of acid/peptic jucies
Peptic Ulcers S&S
abdominal pain, bloating, heartburn, nausea, vomiting sever- vomiting blood, melena cases
NSAIDS
Inhibit COX-1+2 enzymes and reduce prostaglandins. prostaglandins stimulate mucus and bicarbonate secretion, providing protection against mucus damage
Zollinger-Ellison syndrome
-Gastrinoma-Hypergastrinemia-these ulcers are unresponsive to treatments of normal peptic ulcers
Peptic Ulcers risk factors
H pylori infectionsNSAIDAsprinCigarettesalcoholgastric hyperacidityduodenal- gastricreflux
Gastrinoma
gastrin produced by tumors
Zollinger-Ellison syndrome S&S
diarrhea and peptic ulcer S&S
Zollinger-Ellison syndrome treatment
H+/K+ ATPase inhibitors and excision of tumor-slow parietal cell function and production of HCL
Peutz-Jeghers Hamartomatous polyps
-polyps involving the mucosal epithelium, lamina propria, and muscularis mucosa of the alimentary tract- brown or grey spots of lips, gums, oral mucosa- can be singular or multiple - have a increased risk of developing cancer from damage and repair to polyp repeatedly - DO NOT go away- rare autosomal disease (genetic condition) detected around age 10
Hamartomatous
tissue is same as tissue around it -benign
gastric carcinoma
-very common tumor in the world -often late stage diagnosis- early stages are often asymptomatic
gastric carcinomarisk factors
-infection of H. pylori -diet high in nitrites derived from nitrates (preserved food)-smoked or salted food, pickled veggies, chili peppers-lack of fresh fruit and veggies-low socioeconomic status -cigarette smoking -chronic gastritis -partial gastrectomy-gastric adenomas-barretts esophagus slight increase risk with blood group A-family history
Nitrosamines
-proteins are acted upon bacteria to form amines-nitrites (in veggies) + amines at high temp cooking form nitrosamines which are highly carcinogenic -cook at lower temp and longer time is OK- reduce consumption of foods with nitrates and nitrites (smoked)-buy uncured bacon
small intestine
digestion is completed and virtually all absoprtion occurs - 20 feet long in s cadaver, 8-13 ft in living person3 divisions 1) duodenum (10 in retroperitoneal)2) jejunum (8ft)3) ileum (12 ft)
duodenum
bile duct and pancreatic duct empty into duodenum via hepatopancreatic ampulla- ampulla opens into the major duodenal papilla
hepatopancreatic ampulla AKA
Ampulla of Vater
Ampulla is controlled by
Sphincter of Oddi
illeum
connects to the cecum at the ileocecal valve
Mesentery proper
suspends jejunum and ileum in the abdominal cavity
cecum
pouch at the beginning of the large intestine
plicae circularis
are folds (1cm deep) of the mucosa and submucosa
Villi
fingerlike projections of the mucosa, looks like velvet- lined with absorptive columnar cells which have microvilli on top (brush border) which have enzymes that complete digestion of carbs and protein -goblet cells, enteroendocine cells, and T cells called intraepithelial lymphocytes are also on villi - inside villi core there is a dense capillary bed and a lymph capillary
capillary bed
for absoprtion
lymph capillary
lacteal
Crypts of Lieberkuhn
pits between the villi -lined with immature columnar cells that secret intestinal juice -crypts decrease in # along the tube but globet cells increase in #
Paneth
cells at pit secrete lysozyme (antibacterial)
Peyer's Patches (lymphoid follicles)
in submucosa that are aggregated and increase in abundance toward the end of the small intestine - part of the immune system
Brunner's Glands
Only in the submucosa of duodenum - produce alkaline mucus (bicarbonate rich) that neutralizes acidic chyme - protects small intestine from ulcers
Ileocecal valve
prevent the backflow from the cecum -once past this valve chyme become Feces