Questions for midterm 3 Flashcards
4 things present in the gastric secretion and where they come from
Mucus (goblet cells)
HCl (parietal cells - same as intrinsic factor)
Pepsin (chief cells)
Gastric lipase (chief cells)
3 ways the gastric epithelium protects itself from stomach acid
Mucus and bicarbonate layer
Tight junctions to prevent the penetration of HCl
Luminal membrane is impermeable to H+ ions
4 mucosal protective mechanisms
Mucus
Bicarbonate
Prostaglandins (mucosal blood flow)
Rapid turnover of mucosa
3 things H pylori secretes that can damage the epithelium
Urease (it neutralizes stomach acid and produces ammonia as a damaging byproduct)
Enzymes
Exotoxins
3 effects of H pylori on the epithelium
Mucosal damage
Inflammation
Mucosal cell death
3 ways H pylori is transmitted
Person to person
Exposure to gastric secretions
Water borne
6 ways to test for H pylori
Endoscopy and a biopsy Culture Breath test Urease test ELISA Rapid test for H pylori
2 ways to treat H pylori
Antibiotics
Proton pump inhibitors
What are 2 helpful actions of prostaglandins
Support platelets (helps the blood clotting function)
Protect the stomach (protects lining from effects of acid)
From COX 1
3 harmful effects of prostaglandins
Inflammation
Pain
Fever
Which COX pathway do you want to inhibit?
COX 2
3 functions of aspirin
Inhibits blood clotting
Prevents stroke
Prevents CV attack
Celecoxib
Selective COX 2 inhibitor
Good because it causes less bleeding and fewer ulcers
4 harmful effects of ASA and non-selective NSAIDS
Disrupt the mucosal barrier
Reduce bicarbonate production
Directly damage the gastric mucosal epithelium
Reduce the production of prostaglandins
Insulin
Released from pancreatic beta cells when there are high levels of glucose in the blood
Acts on the liver, adipose, and muscle to increase glucose uptake and storage, reduce gluconeogenesis, glycogenolysis, and glucose release
Glucagon
Release from pancreatic alpha cells when blood glucose levels are low
Acts on the liver to increase gluconeogenesis, glycogenolysis, and reduce glucose storage
5 hormones from pancreatic islets and the cells they are released from
Insulin (beta) Glucagon (alpha) Somatostatin (delta) Pancreatic polypeptide (PP cells) Ghrelin (epsilon cells)
Why do diabetic patients have increased appetite?
Her body is in starvation mode
No signals from ghrelin and no negative feedback from leptin
But not helping because she cannot use the glucose
Incretins
Hormones from the gut that prepare the beta cell to secrete insulin
Incretin effect in T2D
Lost
GLP-1
From proglucagon, cleaved in intestinal L cells to GLP-1
Secreted from small intestine
Causes proliferation of beta cell and the release of insulin in response to glucose
Suppresses glucagon secretion
Inhibits gastric emptying/secretion/pancreatic secretion
Decreases food intake and body weight
Deficient in T2D
GIP
Secreted from K cells in the first part of the small intestine
Enhances the release of insulin in response to infusions of glucose
No effect on satiety or body weight
Does not inhibit glucagon
Normal levels but decreased responsiveness in T2D
GLP-2 function
Increases the size of the villi
3 functions of GLP-1 in the beta cells
Increases insulin gene transcription
Leads to beta cell proliferation
Decreased beta cell apoptosis
Why was GLP-1 approved to manage diabetes?
Glucose dependent insulin release (no risk for hypoglycemia)
Lowers blood glucose levels in normal people and those with T2D
Can help product enough insulin to overcome the resistance (to a point)
Why is high glucose toxic for the beta cells?
Glucotoxicity
Lipotoxicity
Is GLUT2 or GLUT4 insulin dependent?
GLUT4
Found in the muscle and adipose (need insulin to take glucose into cells)
