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Flashcards in 168-169 DM Deck (32):

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).



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.


Glitazones/ thiazolidinediones:

Pioglitazone, Rosiglitazone

increases insulin sensitivity in peripheral tissue. Binds to PPAR-g nuclear transcription regulator.

Used as monotherapy in type 2 DM or combined with above agents.

Weight gain, edema. Hepatotoxicity, heart failure.


GLP-1 analogs (GLP-1 has a very short half life naturally)

Exenatide, Liraglutide

increases insulin, decreases glucagon release.

Rx - Type 2 DM.

Nausea, vomiting; pancreatitis.


DPP-4 inhibitors

Linagliptin, Saxagliptin, Sitagliptin

inhibits peptidase that breaks down GLP-1 --> increases insulin, decreases glucagon release

Rx- DM2

SE - mild urinary or respiratory infections


Amylin analogs


decreases glucaon

Rx- DM1, DM2

SE- hypoglycemia, nausea, diarrhea


DM2 first drug to use?

then add on drugs with different types of mechanisms

insulin tends to be last drug


diabetic microvacular damage occurs where?

increased AGE, PKC, hexosamine --> Small vessel disease (diffuse thickening
of basement membrane)

retinopathy (hemorrhage, exudates, microaneurysms, vessel proliferation)

nephropathy (nodular sclerosis, progressive proteinuria, chronic renal failure, arteriosclerosis leading to hypertension, Kimmelstiel-Wilson nodules)



osmotic damage with hyperglycemia?

Osmotic damage (sorbitol accumulation in organs with aldose reductase due to loss of NADPH from high glucose):

Neuropathy (motor, sensory, and autonomic



DM macrovessel damage?

Large vessel atherosclerosis, CAD, peripheral vascular occlusive disease, and gangrene --> limb loss, cerebrovascular disease

most people die from ischemic heart disease, by far