168-169 DM Flashcards
DM dx
> 126 fasting
200 PG
(impaired >100-125, 140-200)
Hb A1C
attachment of glucose to hemoglobin
RBC last ~120 days so good marker
type I DM cause
autoimmune destruction of B cells in pancreas
dep of exogenous insulin
ketosis under basal conditions
type 2 DM causes
insulin resistance w/ decreased insulin release
type I DM - age and presentation
10-14 years usually
polyuria, weight loss, fatigue
type I DM - HLA, what causes disease, markers?
DR3 and DR4
protection with DR2, DR5, DQB1
T-cell mediated disease (b cell antigens to lymph node and activate T cells)
abs present, but not cause –> dx and predicts disease though before
DM 1 - islet specific autoantibodies
islet cell abs (ICA) Glutamic acid decarboxylase abs (GADA) insulinoma associated 2 abs (IA2A) insulin abs (IAA) ZnT8 abs
at what point does DM 1 present?
late in course of disease - need a large amount of destruction of B cells
lack of insulin affect
liver releases glucose from glycogen and amino acids from muscle AND fat broken down in glycerol and FFA (glycerol –> G6P, FFA –> acetyl CoA –> acetoacetyl CoA –> ketones –> lower pH)
glucose is lost in urine because GLUT4 isn’t inserted into muscle and fat membranes –> polyuria and polydipsia
Rx for diabetic ketoacdisosis
immediate - IV insulin, fluid, electrolytes
after recovery - restore nitrogen and electrolytes
IM vs IV insulin
IV insulin is fast acting, IM takes hours to take affect –> insulin will correct low pH on its own usually
electrolytes with diabetic keptacidosis
potassium - most inside cells; acidosis causes K to leave cell in exchange for H+ coming in - tries to dry pH down
lose K in urine
as acidosis is corrected, K falls rapdily as it goes back into cell
need to add K quickly in Rx
DM2 - insulin? ketoacidosis? appearance? dx age?
not completely dep on exogenous insulin –> not prone to ketoacidosis
usually obese –> increases insulin resistance
dx > 40 usually
what causes hyperglycemia in DM2
insulin resistance (decreased GLUT4 uptake) + impaired insulin secretion (increases glucose production by liver) –> hyperglycemia
B cells response to insulin resistance?
obese people get hyperglycemia –> relative insulin deficiency beceause can’t secret enough insulin to lower glucose levels
Rx DM1
exogenous insulin - combine different types to achieve normal insulin profile
rapid acting - lispro, aspart, glulisine
onset in 15-30 min, peak 30-2 hrs, duration 3 hrs
short acting - regular
onset 30min-1hr, peak 2-5 hrs, duration 5-8 hrs
intermediate - NPH
onset 1-2 hrs, peak 4-8 hrs, duration 14-18 hrs
long acting - glargine, detemir
onset 1-2 hrs, no peak, duration ~20 hrs
insulin - rapid
rapid acting - lispro, aspart, glulisine
onset in 15-30 min, peak 30-2 hrs, duration 3 hrs``
insulin - short acting
short acting - regular
onset 30min-1hr, peak 2-5 hrs, duration 5-8 hrs
insulin - intermidiate
intermediate - NPH
onset 1-2 hrs, peak 4-8 hrs, duration 14-18 hrs
insulin - long acting
long acting - glargine, detemir
onset 1-2 hrs, no peak, duration ~20 hrs
DM2 Rx
Treatment strategy for type 2 DM—dietary modification and exercise for weight loss; oral
hypoglycemics and insulin replacement.
DM2 sulfonylureas
oral therapy
stimulate insulin secretion (only good for DM2)
Close K+ channel in B-cell membrane, so cell depolarizes –> triggering of insulin release via Ca2+ influx.
side effects - hypoglycemia, weight gain
First generation: Tolbutamide, Chlorpropamide
Second generation: Glyburide, Glimepiride, Glipizide
DM2 metformin -mechanism, use, side effects
decreases liver glucose output
Exact mechanism is unknown. decreases gluconeogenesis, increases glycolysis, increases peripheral glucose uptake (insulin sensitivity).
Rx - Oral. First-line therapy in type 2 DM.
Can be used in patients without islet function.
side effects - GI upset; most serious adverse effect is lactic acidosis (thus contraindicated in renal failure).
a-glucosidase
Acarbose, Miglitol
Inhibit intestinal brush-border a-glucosidases.
Delayed sugar hydrolysis and glucose absorption –> decreased postprandial hyperglycemia.
Used as monotherapy in type 2 DM or in combination with above agents.
GI disturbances.
