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Endocrine - DVR > 168-169 DM > Flashcards

168-169 DM Flashcards

1
Q

DM dx

A

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

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2
Q

Hb A1C

A

attachment of glucose to hemoglobin

RBC last ~120 days so good marker

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3
Q

type I DM cause

A

autoimmune destruction of B cells in pancreas

dep of exogenous insulin

ketosis under basal conditions

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4
Q

type 2 DM causes

A

insulin resistance w/ decreased insulin release

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5
Q

type I DM - age and presentation

A

10-14 years usually

polyuria, weight loss, fatigue

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6
Q

type I DM - HLA, what causes disease, markers?

A

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

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7
Q

DM 1 - islet specific autoantibodies

A 
islet cell abs (ICA)
Glutamic acid decarboxylase abs (GADA)
insulinoma associated 2 abs (IA2A)
insulin abs (IAA)
ZnT8 abs
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8
Q

at what point does DM 1 present?

A

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

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9
Q

lack of insulin affect

A

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

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10
Q

Rx for diabetic ketoacdisosis

A

immediate - IV insulin, fluid, electrolytes

after recovery - restore nitrogen and electrolytes

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11
Q

IM vs IV insulin

A

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

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12
Q

electrolytes with diabetic keptacidosis

A

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

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13
Q

DM2 - insulin? ketoacidosis? appearance? dx age?

A

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

usually obese –> increases insulin resistance

dx > 40 usually

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14
Q

what causes hyperglycemia in DM2

A

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

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15
Q

B cells response to insulin resistance?

A

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

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16
Q

Rx DM1

A

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
Q

insulin - rapid

A

rapid acting - lispro, aspart, glulisine

onset in 15-30 min, peak 30-2 hrs, duration 3 hrs``

18
Q

insulin - short acting

A

short acting - regular

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

19
Q

insulin - intermidiate

A

intermediate - NPH

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

20
Q

insulin - long acting

A

long acting - glargine, detemir

onset 1-2 hrs, no peak, duration ~20 hrs

21
Q

DM2 Rx

A

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

22
Q

DM2 sulfonylureas

A

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
Q

DM2 metformin -mechanism, use, side effects

A

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
Q

a-glucosidase

A

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
Q

Glitazones/ thiazolidinediones:

A

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
Q

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

A

Exenatide, Liraglutide

increases insulin, decreases glucagon release.

Rx - Type 2 DM.

Nausea, vomiting; pancreatitis.

27
Q

DPP-4 inhibitors

A

Linagliptin, Saxagliptin, Sitagliptin

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

Rx- DM2

SE - mild urinary or respiratory infections

28
Q

Amylin analogs

A

pramlintide

decreases glucaon

Rx- DM1, DM2

SE- hypoglycemia, nausea, diarrhea

29
Q

DM2 first drug to use?

A

metformin
then add on drugs with different types of mechanisms

insulin tends to be last drug

30
Q

diabetic microvacular damage occurs where?

A

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
Q

osmotic damage with hyperglycemia?

A

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
Q

DM macrovessel damage?

A

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

most people die from ischemic heart disease, by far

Endocrine - DVR (22 decks)

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