B8 W4 Flashcards
What are the tissues of pancreas?
Exocrine
Intercalated ducts
Function to secrete bicarbonate and reduce acidity of chyme
Cholecystokinin
Secreted by duodenal cells and pancreatic I cells. Stimulates release of bile and pancreatic lipase and protease
Nerve for parasympathetic control of bicarbonate secretion
Vagus nerve
What is required to give free flow for bicarbonate and enzymes to the intestines
Water- lack of this leads to auto digestion of pancreatic tissue
Which pancreatic cells secrete somatostatin?
Delta cells
Where is preproinsulin cleaved to form proinsulin?
Rough endoplasmic reticulum
Organelle where proinsulin matures into active insulin
Golgi body by action of endopeptidases which release central c-peptide fragment
Insulin effect on hepatocytes
Glycogenolysis, gluconeogenesis, ketogenesis, proteolysis, lipolysis
Insulin effect on skeletal muscle cells
Glucose uptake, glycogenesis, amino acid transport, protein synthesis, K+ accumulation
What does insulin binding to skeletal muscle decreased?
Glycogen phosphorylate, proteolysis
Insulin effect on adipose tissue?
Glucose uptake, protein synthesis, lipogenesis, amino acid transport, K+accumulation
How does insulin affect lipolysis and proteolysis?
Decreases
What are the effects of insulin?
Anabolic
Where is GLP-1, 2 and 3 produced?
L cells
Effects of glucagon
Catabolic
What do delta cells porduce?
Found in the pancreas and produce somatostatin to inhibit glucagon and insulin release
Howis incretin affected in type 2 diabetes?
Diminshed
Neonatal diabetes of young
Not related to autoimmne disease, it is a genetic mutation
Genetic associations of type 1 diabetes
MHC complex, and immunoregulatory genes
Severe insulin deficinecy
Increases glucagon levels and growth hromone and cortisol secretion. Increases hepatic glucose production and causes hyperglycaemia, elecrolyte depletion and dehydration
How does acidosis affect blood vessels?
Vasodilation
LADA
rapid onset and progression to insulin dependency. Lacks ketoacidosis symtpoms. Elevated pancreatic autoantiboides and risk factors for metabolic syndrome.
What is the effect of increased ketone bodies?
Osmootic diuresis, vomiting and acidosis
Claudication
Cramping due to blocking of blood vessels
Pre-proliferative retinopathy
Severe damage of retina vessels, leading to blood leakage
Proliferative retinopathy
Scar tissue forms
Diabetes insipidus
Not caused by glucose intake-related to nephrogenic dysfnction or neurological
Neurological diabetes insipidus
Related to ADH deficiency
PPAR gamma agonist
Thiazolidinediones
PPAR alpha
Nuclear receptor for insulin sensitisation- found in liver, heart, skeletal muscle and vascular wall
PPAR gamma
Nuclear receptor for insulin sensitisationn- found in pancreatic beta cells, adipose tissue, skeletal muscle, vascular endothelium
Which cells produce GLP-1
L cells
K cells
Produce GIP
Long acting glp-1
Exenatide
GLP 1
Increases insulin secretion, delays gastric emptying and reduces gastric volume. Reduce HBA1c and reduce weight. Causes GI disturbance and pancreatitis.
Gliptins
DPP-4 inhibitors- weight nuetral and are injectable. Cause mild GI symtposm, increase respiratory infection.
Familial renal glucosuria
Caused by mutation in SGLT 2 transporter
Giflozins
SGLT2 inhibiots