Week 3- Endocrine Disorders Flashcards
(36 cards)
islets of Langerhans have four types of hormone-secreting cells:
- alpha cells (secrete glucago)
- beta cells (secrete insulin and amylin)
- delta cells (secrete gastrin and somatostatin)
- F (or PP) cells (secrete pancreatic polypeptide that stimulates gastric secretion and antagonizes cholecystokinin)
beta cells of the pancreas synthesize
insulin from the precursor proinsulin
does insulin circulate freely
yes, it is unbound
_______facilitates the rate of glucose uptake into many cells within the body
Insulin
insulin binding cascade
-insulin binds with an enzyme-linked plasma membrane receptor that contains tyrosine kinase on the cytosolic surface
-Insulin binding sends signals to activate glucose transporters (GLUT) for entry of glucose into the cell
glucagon is produced by
alpha cells of pancrease
______ glucose levels cause glucagon release to be inhibited;______ glucose levels and sympathetic stimulation promote glucagon release
High
insulin lowers blood sugar
glucagon raises blood sugar
insulin lowers blood sugar
glucagon raises blood sugar`
stimulates lipolysis, which has a ketogenic effect caused by the metabolism of free fatty acids in the liver
glucagon
result of a loss of beta cells in the pancreatic islets.
type 1 diabetes
autoimmune type 1 diabets
-environmental and genetic factors trigger cell-mediated destruction of pancreatic beta cells
- Autoimmune type 1 diabetes is called type 1A.
non immune type 1 diabets
-less common
-secondary to other diseases (pancreatitis)
t-ype 1B diabetes
-occurs mostly in people of Asian or African descent
type 1 diabetse onset
long preclinical period with gradual destruction of beta cells
With insulin deficiency, lipolysis is enhanced and there is an increase in the amount of nonesterified fatty acids delivered to the liver. The consequence is increased gluconeogenesis contributing to hyperglycemia
With insulin deficiency, lipolysis is enhanced and there is an increase in the amount of nonesterified fatty acids delivered to the liver. The consequence is increased gluconeogenesis contributing to hyperglycemia
-potentially life-threatening sequelae of Type I DM
-caused by increased levels of circulating ketones in the absence of the antilipolytic effect of insulin
diabetic ketoacidosis
diabetic ketoacidosis sxs
unintentional weight loss, vomiting, weakness, and cognition changes. Dehydration and metabolic abnormalities worsen with progressive uncontrolled osmolar stress, which can lead to lethargy, May even cause respiratory failure, coma, and death.
Abdominal pain is also a common complaint in DKA
-breath with sweet fruity odor
are diagnosis for type 1 and type 2 diabetes the same?
yes
-HbA1c, 2 hour OGTT, fasting insulin
type 1 DM treatment
-Avoidance of cow’s milk
-gluten-free diet
-omega-3 fatty acids and vitamin D
-injecting insulin and momnintor blood sugar
insulin resistance and decreased insulin secretion by beta cells
type 2 diabetes
insulin resistance and decreased insulin secretion by beta cells
type 2 diabetes
constellation of disorders (central obesity, dyslipidemia, prehypertension, and an elevated fasting blood glucose level) that together confer a high risk of developing type 2 diabetes and associated cardiovascular complications.
mystabollic syndrome
a suboptimal response of insulin-sensitive tissues (especially liver, muscle, and adipose tissue) to insulin.
insulin resistance
hormones produced in adipose tissue
Adipokines
Adipokines in obese individuals
-increased serum levels of leptin (leptin resistance) and resistin
-decreased levels of adiponectin
