Endo 3 Flashcards
Is diabetes a symptom or disease?
- both
- symptom: large amount of urine produced (polyuria)
- disease occurs becuase of hyperglycemia or not enough ADH both of which are characterized by polyuria
- most common endocrine dysfunction!
What is diabetes mellitus?
- “lots of sweet urine”
- sometimes called sugar diabetes
- lots of sugar in the urine (these glucose should be taken back into the blood to be used but it is instead getting out in the urine)
- lots of urine because the glucose will pull water with it into the urine by osmosis
What is diabetes insipidus?
- “tasteless urine”
- disease of where there is a lack thereof or a lack of responsiveness to ADH
- ADH works to concentrate the urine (diuresis is peeing, ADH keeps you from making a lot of urine)
What is the common cause for diabetes insipidus?
- decrease or blockade of the secretion of ADH which is called central diabetes insipidus because it happens in the CNS
- may be due to trauma to the stalk connecting the pituitary to the hypothalamus (infundibulum)
- pituitary tumours or surgery on the tumours as well as infection of pituitary and hypothalamus can lead to damage
What is the treatment for diabetes insipidus?
- without ADH water is not as well reabsorbed resulting in increased urine flow
- ADH nasal spray
What is the uncommon cause of diabetes insipidus? How is it treated?
- nephrogenic DI
- kidney becomes insensitive to the ADH
- damage is often secondary to drug use (lithium, demeclocycline, amphotericin B)
- treatment is to consume adequate amounts of fluid to avoid dehydration and alterations in electrolyte levels (try to also give them ADH and electrolytes)
Describe normal regulation of blood glucose levels
- normal BG level is 4.5mmol/L
- BG rises (stimulus)
- pancreas is detector and control centre
- response and release: insulin
- insulin causes effectors to take up glucose
How is ADH stimulated?
- high blood osmotic pressure (such as when you are dehydrated) stimulates neurosecretory cells in the supraoptic nucleus of hypothalamus to release ADH in the posterior pituitary
- ADH leaves the pituitary and travels to kidney where it causes the kidney to reabsorb water from the filtrate while also increasing blood pressure and inhibiting sweating
Describe the blood supply to the pancreas
- pancreas sits near abdominal aorta
- splenic artery provides blood to pancreas (these create anastomosis with some vessels off of the inferior mesenteric artery)
- pancreaticoduodenal comes off common hepatic
- superior mesenteric artery
- head of pancreas gets blood from celiac which gives off common hepatic and superior mesenteric then creates an anastomosis
What is the function of the exocrine acinus?
- 99% of pancreas volume consists of this which secrete 1.2-1.5L of bicarbonate fluid per day
- contains digestive enzymes and bicarbonate that buffer the gastric juice
What makes up the endocrine part of the pancreas?
- islet of Langerhans
- beta cells: secrete insulin when blood glucose is high and when there is parasympathetic stimulation
- alpha cells: secrete glucagon when blood glucose is low but also when there is sympathetic stimulation- glucagon leads to glucose production in the liver (a bit larger than beta cells and stain darker)
What is insulin? What do the effectors do under the influence of insulin?
- polypeptide released by beta cells of pancreas
- water soluble and has cell surface receptor with intrinsic tyrosine kinase activity
- accelerate facilitated diffusion of glucose into the cells (glucose brings water so cells will fill with water), speed conversion of glucose into glycogen (glycogen doesn’t exert much osmotic pressure), speed synthesis of fatty acids, speed synthesis of proteins from amino acids, slow glycogen breakdown into glucose (glycogenolysis)
- all of these lower blood glucose and ultimately inhibit insulin release
What are the 2 types of diabetes mellitus?
-in both types, BG stays high (hyperglycemia) after meals, sugar is spilled into urine (glycosuria), and lots of urine is produced (polyuria)
Insulin dependent diabetes mellitus (IDDM) or Type 1: Inadequate insulin production- beta cells in pancreas don’t produce insulin at all or enough. Treated with insulin injection which decrease blood sugar. Usually occurs in young adults so called juvenile onset diabetes. Beta cells are ruined by some sort of autoimmune response.
Noninsulin dependent diabetes mellitus (NDDM) or Type 2: Inadequate response to insulin- resistant to the effects of insulin. Disease is associated with adulthood and is called adult-onset diabetes. Increases in body weight are important correlate in T2D and certain cultural groups are at risk suggesting genetic factors. T2D can also be treated with insulin but diet/exercise and antihyperglycemics (like metformin) are used. T2D is showing up in juvenile population because of childhood obesity increases (26% children aged 2-17 in Canada are overweight/obese, 60% adults are overweight and 23% are obese).
What is the effect of a lack of insulin?
- cells starve to death and begin to burn fat in large quantities
- burning of fat leads to production of poorly metabolized fragments of fat called ketone bodies
- ketone bodies contain odorous molecules such as acetone so breath smells fruity, ketone bodies are also acidic so body’s pH falls- ketoacidosis
- fat begins to deposit on BV walls (retinas can become damaged and gangrene can occur in hands and feet); atherosclerosis, amputation
- loses weight and is constantly hungry
- person begins to starve to death
- insulin dependence occurs only in very severe T2D since most T2D have high adiposity
How do diabetic foot ulcers develop?
- large amounts of lipid in the bloodstream and other problems caused by hyperglycemia lead to damage to the arterial walls and poor circulation
- areas which are predisposed to poor circulation and have friction will tend to ulcerate and may become infected
What were the results of the glucose screening programs for moms?
- hard to tell the two curves apart between normal and GDM
- altered glucose response is normal part of pregnancy that helps fetal growth
- mother’s normal response to glucose in the 3rd trimester looks a lot like T2D
- women who screen positive are likely to develop T2D later in life so perhaps GDM is the unmasking of latent T2D
- screening doesn’t seem to make any difference in outcomes of pregnancies
- perhaps GDM isn’t a disease at all
- women with T1D and T2D still need to be followed carefully
