168-169 DM Flashcards Preview

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Flashcards in 168-169 DM Deck (32):
1

DM dx

>126 fasting
>200 PG
(impaired >100-125, 140-200)

2

Hb A1C

attachment of glucose to hemoglobin

RBC last ~120 days so good marker

3

type I DM cause

autoimmune destruction of B cells in pancreas

dep of exogenous insulin

ketosis under basal conditions

4

type 2 DM causes

insulin resistance w/ decreased insulin release

5

type I DM - age and presentation

10-14 years usually

polyuria, weight loss, fatigue

6

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

7

DM 1 - islet specific autoantibodies

islet cell abs (ICA)
Glutamic acid decarboxylase abs (GADA)
insulinoma associated 2 abs (IA2A)
insulin abs (IAA)
ZnT8 abs

8

at what point does DM 1 present?

late in course of disease - need a large amount of destruction of B cells

9

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

10

Rx for diabetic ketoacdisosis

immediate - IV insulin, fluid, electrolytes

after recovery - restore nitrogen and electrolytes

11

IM vs IV insulin

IV insulin is fast acting, IM takes hours to take affect --> insulin will correct low pH on its own usually

12

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

13

DM2 - insulin? ketoacidosis? appearance? dx age?

not completely dep on exogenous insulin --> not prone to ketoacidosis

usually obese --> increases insulin resistance

dx > 40 usually

14

what causes hyperglycemia in DM2

insulin resistance (decreased GLUT4 uptake) + impaired insulin secretion (increases glucose production by liver) --> hyperglycemia

15

B cells response to insulin resistance?

obese people get hyperglycemia --> relative insulin deficiency beceause can't secret enough insulin to lower glucose levels

16

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

17

insulin - rapid

rapid acting - lispro, aspart, glulisine
onset in 15-30 min, peak 30-2 hrs, duration 3 hrs``

18

insulin - short acting

short acting - regular
onset 30min-1hr, peak 2-5 hrs, duration 5-8 hrs

19

insulin - intermidiate

intermediate - NPH
onset 1-2 hrs, peak 4-8 hrs, duration 14-18 hrs

20

insulin - long acting

long acting - glargine, detemir
onset 1-2 hrs, no peak, duration ~20 hrs

21

DM2 Rx

Treatment strategy for type 2 DM—dietary modification and exercise for weight loss; oral
hypoglycemics and insulin replacement.

22

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

23

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).

24

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.

25

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.

26

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.

27

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

28

Amylin analogs

pramlintide

decreases glucaon

Rx- DM1, DM2

SE- hypoglycemia, nausea, diarrhea

29

DM2 first drug to use?

metformin
then add on drugs with different types of mechanisms

insulin tends to be last drug

30

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)

neuropathy

31

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
degeneration)

Cataracts

32

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