Term
| what is the main way to distinguish between diabetes mellitus and insipidus |
|
Definition
| melllitus has glucose in the urine |
|
|
Term
| why is the glucose in the urine in diabetes |
|
Definition
| glucose in the blood exceeds capacity for reahsption so it is excreted in the urine |
|
|
Term
| what is the cause of type I diabetes (3) |
|
Definition
| B cells cant make enough insulin, destoried B cells dont respond to glucose, B cell lesions and necrosis |
|
|
Term
| what are 5 signs of type I diabetes |
|
Definition
polydipsia
polyphagia
polyuria
ketoacidosis
hyperglycemia |
|
|
Term
| describe the typical type I diabetes patient |
|
Definition
onset in childhood
looks undernourished |
|
|
Term
| does diabetes have a genetic predisposition |
|
Definition
| type II more than type I. but yes |
|
|
Term
| what is the treatment for type I diabetes |
|
Definition
|
|
Term
| describe the typical type II diabetes patient |
|
Definition
|
|
Term
| what is the cause of type II diabetes |
|
Definition
insulin resistant and inabilit to make enough insulin
can progress to be like type I |
|
|
Term
| what is the treatment for type II diabetes |
|
Definition
weight reduction, exercise, dietary modification
oral hypoglycemics
last resort: exogenous insulin |
|
|
Term
| what are 6 complications of diabetes |
|
Definition
hyperglycemia
increased BP
neuropathy
proteinuria
cardiovascular disease (more type II)
diabetic retinopathy
diabetic neuropathy |
|
|
Term
| what is the treatment for neuropathy and proteinuria |
|
Definition
|
|
Term
| what is the treatment for diabetic cardiovascular disease |
|
Definition
| statins lower lipid and cholesterol, stop smoking |
|
|
Term
| what is the treatment for diabetic neuropathy |
|
Definition
| foot care, ulcer care, erythromycin for vagus neuropathy causing GI immotility |
|
|
Term
| what are the two types of diabetes insipidus, what causes each |
|
Definition
central: deficiency in ADH
nephrogenic: lack of response to ADH |
|
|
Term
| how can you distinguish between central and nephrogenic diabetes insipidus |
|
Definition
| demopressin replaces ADH so if urine production decreases they have central |
|
|
Term
| how does diabetes insipidus cause disease (no matter which type) |
|
Definition
| causes lack of reabsorption of water in the CD |
|
|
Term
|
Definition
| B cells of islets of langerhans |
|
|
Term
| what are normal fasting insulin levels |
|
Definition
|
|
Term
| what occurs in fasting metabolism |
|
Definition
adipose releases FA which is processed in liver to glucose
pancreas releases glucagon which signals to the liver to make glucose
glucose is first used in the brain then other major organs |
|
|
Term
| what are normal prandial insulin levels |
|
Definition
|
|
Term
| what occurs in prandial metabolism |
|
Definition
carbs are ingested and turned into glucose which is ingested and distributed to the organs
pancreas releases insulin which tells the liver, muscle, and adipose to store glucose |
|
|
Term
| how does glucose get into the cell |
|
Definition
insulin turns on GLUT facilitated diffusion transporters which activate TK which intrinsically phosphorlyates various substrates
insulin stimulates translocation of GLUT4 transporters to the membrane allowing for glucose to get into the cell |
|
|
Term
| how are B cells activated to release insuln |
|
Definition
glucose comes through GLUT2 receptors and glucokinase phosphorlyates it so it can stay in the cell.
G6P is shuttled to ATP production which increases ATP in relation to ADP
ratio switches on K channel and cell moves from basal state (hyperpolarized and inhibited) to depolarized
this causes Ca cannels to open and Ca moves in stimulating release of insulin |
|
|
Term
|
Definition
| single chain precursor called preproinsuln (A and B chains connected by C peptide) is cleaved in ER to proinsulin, processed in golgi to insulin, and released with C peptide |
|
|
Term
| what is the clinical significance of C peptide |
|
Definition
| helps determine if insulin levels are due to edogenous (no C) or endogenous (has C) insulin |
|
|
Term
| what is the best determinant of insulin levels, why |
|
Definition
| HBA1C because it shows BG over several months |
|
|
Term
| what is the cycle of insulin |
|
Definition
| increases after a meal and is at low basal levels between meals |
|
|
Term
|
Definition
| B cells of islets of langerhans |
|
|
Term
| what are normal fasting insulin levels |
|
Definition
|
|
Term
| what occurs in fasting metabolism |
|
Definition
adipose releases FA which is processed in liver to glucose
pancreas releases glucagon which signals to the liver to make glucose
glucose is first used in the brain then other major organs |
|
|
Term
| what are normal prandial insulin levels |
|
Definition
|
|
Term
| what occurs in prandial metabolism |
|
Definition
carbs are ingested and turned into glucose which is ingested and distributed to the organs
pancreas releases insulin which tells the liver, muscle, and adipose to store glucose |
|
|
Term
| how does glucose get into the cell |
|
Definition
insulin turns on GLUT facilitated diffusion transporters which activate TK which intrinsically phosphorlyates various substrates
insulin stimulates translocation of GLUT4 transporters to the membrane allowing for glucose to get into the cell |
|
|
Term
| how are B cells activated to release insuln |
|
Definition
glucose comes through GLUT2 receptors and glucokinase phosphorlyates it so it can stay in the cell.
G6P is shuttled to ATP production which increases ATP in relation to ADP
ratio switches on K channel and cell moves from basal state (hyperpolarized and inhibited) to depolarized
this causes Ca cannels to open and Ca moves in stimulating release of insulin |
|
|
Term
|
Definition
| single chain precursor called preproinsuln (A and B chains connected by C peptide) is cleaved in ER to proinsulin, processed in golgi to insulin, and released with C peptide |
|
|
Term
| what is the clinical significance of C peptide |
|
Definition
| helps determine if insulin levels are due to edogenous (no C) or endogenous (has C) insulin |
|
|
Term
| what is the best determinant of insulin levels, why |
|
Definition
| HBA1C because it shows BG over several months |
|
|
Term
| what is the cycle of insulin |
|
Definition
| increases after a meal and is at low basal levels between meals |
|
|
Term
| what are the short acting insulins (4) |
|
Definition
insulin lispro
insulin aspart
insulin glulisine
insulin regular |
|
|
Term
| what are the long acting insulins (2) |
|
Definition
insulin glargine
insulin detemir |
|
|
Term
| what are the insulin AA combinations (3) |
|
Definition
lispro + protamine
asprt + protamine
NPH + R |
|
|
Term
| what insulins have the best HBA1C control |
|
Definition
|
|
Term
| what are the side effects of all insulin medications (2) |
|
Definition
hypooglycemia
lipodystrophy |
|
|
Term
| what are the ratings of the hypoglycemic effects of the different types of insulin |
|
Definition
short acting has most
long acting is second
no peak insulin has no effect |
|
|
Term
| what are three sources of insulin, which is used today |
|
Definition
beef - outdated
pork - outdated
E. coli produces human insulin |
|
|
Term
| how is insulin administered (2) |
|
Definition
subcutaneous
IV (emergency) |
|
|
Term
| which type of insulin is the most rapidly absorbed |
|
Definition
|
|
Term
| how well is insulin absorbed |
|
Definition
depends on prep
human is absorbed the best and most quickly |
|
|
Term
| where is insulin metabolized and by what |
|
Definition
| metabolized to be inactive in liver and kidney by insulinase |
|
|
Term
| how long does it take for short acting insulin to kick in, how long does it last |
|
Definition
onset <15 min
duration 3-6 hours |
|
|
Term
| why is long acting insulin long acting, what is the duration |
|
Definition
NPH (insulin isophane suspension complexed with zinc) allows slow release
12-18h |
|
|
Term
| which insulin has slow release and rapid onset, how does it work |
|
Definition
insulin combined with AA
onset <10min because insulin dosent stick together due to AA substitution and is more free for use |
|
|
Term
| how long does no peak insulin last |
|
Definition
| 24 hours of consistant plasma levels |
|
|
Term
| how is a pregnant woman with diabetes treated |
|
Definition
|
|
Term
| how do insulin pumps work |
|
Definition
| uses short acting insulin on continous infusion to provide steady basal insulin level and bolus injections depending on size and time of meal |
|
|
Term
|
Definition
emergency, when someone needs insulin fast
ketoacidosis |
|
|
Term
| what is a non-intensive diabetes treatment |
|
Definition
| NPH with lispro at breakfast and dinner |
|
|
Term
| what are the two most populat insulin redigmen, which is bettwe |
|
Definition
glargine x2 and lispro x4
or
insulin pump
best one depends on pt |
|
|
Term
| what is the general pathway in diabetes treatment |
|
Definition
diet and exercise (if type II)
check liver function - if abnormal use insulin
check kidney function (Cr)- if not abnormal use metformin
if still hyperglycemic- try sulfonylurea
if still hypoglycemic- try combo meal time + basal medication)
if still hyperglycemic- use insulin |
|
|
Term
| what drug is contraindicated with oral hypoglycemics |
|
Definition
|
|
Term
| what drugs antagonize insulin or oral hypoglycemics (4) |
|
Definition
corticosteroids, estrogen, thyroid hormones
thiazides |
|
|
Term
| what are the 4 sulfonylureases |
|
Definition
gen 1: chlorpropamide
gen 2: glipizide, glyburide, glomepiride |
|
|
Term
| what are the two thiazolidiendiones |
|
Definition
pioglitazone
rosiglitazone |
|
|
Term
| what are the two aa derivatives |
|
Definition
|
|
Term
| what are the two a-glycosidase inhibitors |
|
Definition
|
|
Term
|
Definition
|
|
Term
| what drugs mimic incretin (2) |
|
Definition
|
|
Term
| what drugs inhibit DPP-4 (3) |
|
Definition
stilagliptin
saxagliptin
linagliptin |
|
|
Term
| what drug is synthetic amylin hormone |
|
Definition
|
|
Term
| what drig is a SGLT2 inhibitor |
|
Definition
|
|
Term
| what is used as a anti-hypoglycemic (2) |
|
Definition
glucagon
glucose tablets
glucose source - grape juice |
|
|
Term
| what are the 5 categories of oral hypoglycemics |
|
Definition
sulfonylureases
thiazolidiendiones
AA derivatives
a-glucosidase inhibitors
biguanides |
|
|
Term
|
Definition
bind and block K channel on B cells depolarizing, opening Ca channel letting it in and causing insulin release
reduce glucagon (indurect due to insulin decrease)
increase insulin blocking (maybe increasing receptors) |
|
|
Term
| MOA thiazolidiendiones (3) |
|
Definition
increase sensitivity to insulin in tissues
decrease hepatic glucose output
use PPARy in adipose to increase insulin receptors |
|
|
Term
|
Definition
|
|
Term
| a-glucosidase inhibitor MOA |
|
Definition
inhibit enzyme in SI brush border decreasing sugar absorption
prevents post-prandial rise in glucose |
|
|
Term
|
Definition
inhibits gluconeogenesis
stimulates glucolysis
increases glucose uptake in tissues |
|
|
Term
| exenatide and liraglutide MOA |
|
Definition
mimics incretins
incretins are released from intestines in response to food and increase insulin secretion |
|
|
Term
| sitagliptin, saxagliptin, linagliptin MOA |
|
Definition
| inhibit dipeptitdyl peptidase 4 (DPP-4) so incretin cannot be degradedand insulin increases |
|
|
Term
|
Definition
synthetic amylin hormone
normally made in pancreas after meal to slow rate of food absorption in intestines and reduce appetite |
|
|
Term
|
Definition
| blocks Na/glucose cotransporter 2 in PCT preventing reabsorption |
|
|
Term
|
Definition
| stops active hypoglycemia |
|
|
Term
| side effects sulfonylureases (4) |
|
Definition
all cause hypoglycemia
mostly 1st gen causes: hyponatremia, disulfram, hypotension (so basically don't use in old people) |
|
|
Term
| thiazolidiendione side effects (2) |
|
Definition
hypoglycemia
MI and other cardio events - dont use with CHF pt (especially rosiglitazone) |
|
|
Term
| AA derivative side effects |
|
Definition
|
|
Term
| a-glucosidase inhibitor side effects (3) |
|
Definition
flatulence
diarrhea
abdominal cramps
NO hypoglycemia |
|
|
Term
|
Definition
lactic acidosis in pt with renal or heart failure
NO hypoglycemia |
|
|
Term
| exenatide, liraglutide side effects (5) |
|
Definition
liragltide; weight loss
hyoiglycemia: low risk
nausea, vomiting, diarrhea |
|
|
Term
| sitagliptin, saxagliptin, linagliptin side effects (2) |
|
Definition
|
|
Term
| pramlintide side effects (3) |
|
Definition
weight loss
nausea
hypoglycemia |
|
|
Term
| SGLT2 inhibitor side effects (3) |
|
Definition
increased K
female GU infections |
|
|
Term
| how is glucagon administered |
|
Definition
|
|
Term
| how is canaglifolozin administered |
|
Definition
| oral once a day before first meal |
|
|
Term
| how is pramlintide administered |
|
Definition
|
|
Term
| how is sitagliptin, saxagliptin, linagliptin administered |
|
Definition
|
|
Term
| how is exenatide, liraglutide administered |
|
Definition
|
|
Term
| what is sitagliptin, saxagliptin, linagliptin used for |
|
Definition
| type II diabetes - need functioning B cells |
|
|
Term
| what is exenatide, liraglutide used for |
|
Definition
| type II diabetes - need functioning B cells |
|
|
Term
| what is pramlintide used for |
|
Definition
| adjunct to insulin in type I or II diabetes (lower insulin though) |
|
|
Term
| where is metformin metabolized and excreted |
|
Definition
not metabolized
excreted in urine |
|
|
Term
| what plasma protein is metformin bound to |
|
Definition
|
|
Term
| which oral hypoglycemic has the shortest half life |
|
Definition
|
|
Term
| how are thiazolidiendiones used |
|
Definition
| with insulin or in another combo (not enough alone) |
|
|
Term
| where are sulgonylureases metabolized and excreted |
|
Definition
|
|
Term
| which drug should you never use in pregnant diabetic patients, why |
|
Definition
thiazolidiendiones
can cross placenta and deplete fetal pancreas of insuln |
|
|
