16/17: Diabetes - Dodge Flashcards

1
Q

how many ppl have diabetes?

A

1/11

increased in native americans, hispanics, and lower education

increased in the south

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2
Q

what does calcium rushing into the islet cell in response to glucose cause?

A

ca2+ activates insulin gene expression via CREB –> exocytosis of stored insulin

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3
Q

insulin is created in…

A

beta islet cells of pancreas

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4
Q

insulin binding to cell receptors –>

A

glut 4 translocation to the cell membrane –> cell takes in glucose

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5
Q

common theme between dif. DM types

A

dysregulation of the insulin/glucose interplay leading to hyperglycemia

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6
Q

typeII DM

A

insulin resistance

95% of adult DM

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7
Q

type I diabetes is caused by…

A

complete or near complete insulin deficiency usually seen with >70% destruction of beta cells

no insulie

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8
Q

IDDM

A

insulin dependent diabetes mellitus

insulin is being used to treat

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9
Q

genetic component of DM type I

A

HLA DR3/DR4 gene

twin studies 50%

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10
Q

diabetic ketoacidosis –>

A

type I DM

30% children or adolescents diagnosed with type I DM after being treated for DKA

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11
Q

which type of DM has a higher genetic component?

A

type II

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12
Q

MODY

maturity onset diabetes of youth

A
  • early onset of hyperglycemia, beta cell genetic defects
  • appears morel like type 2 DM in a younger person
  • AD, most common monogenetic syndrome associated with DM
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13
Q

LADA latent autoimmune diabetes of adults

A

WILL require treatment with insulin much like type I DM

  • slow destruction of beta islet cells
  • misdiagnosed as type 2
  • tequire insulin due to insulin deficiency from autoimmune islet destruction
  • will have low c peptide
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14
Q

drugs/medications that may cause diabetes

A
  • thiazides
  • pentamidine
  • protease inhibitors
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15
Q

symptoms of DM

A
  • always tired
  • frequent urination
  • wounds willnot heal
  • blurry vision
  • always thirsty
  • vaginal infections
  • numbness or tingling of feet
  • sexual problems
  • always hungry
  • sudden weight loss
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16
Q

diabetes screening guidlines

A

every 3 yrs starting at age 45

if pt overweight with at least one additional risk factor screen earlier

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17
Q

prediabetes and diabetes fasting plasma glucose

A

100-125

>126

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18
Q

glucose tolerance test prediabetes; diabetes

A

140-199

>200

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19
Q

hemoglobin A1c prediabetes

A
  1. 7-6.4%

6. 5% —> diagnostic of diabetes**

20
Q

what hemoglobin A1c level is diagnostic of diabetes?

A

> 6.5%

21
Q

type I DM treatment :

A

require insulin!

  • in basal/bolus (long and short)
  • continuous infusion (short with short)
  • split/mixed
22
Q

does type 2 require insulin?

A

not at first, many will eventually require insulin as the disease progresses

> 10-12% A1c with ketosis and/or weight loss = insulin required; >10-12 alone is strongly recommended

23
Q

standard oral therapy for type II DM

A

metformin

24
Q

when do type II DM need more than one med?

A

greater than 9.0% A1c –> recommend treatment with two oral agents or insulin mono-therapy

25
Q

intervention with A1c less than or equal to 7.5%

A

lifestyle and dietary changes

26
Q

weight loss is _______ important than certain combinations of nutrients

A

more

27
Q

MOA metformin

A

decreases hepatic gluconeogenesis and glycogenolysis with increase in peripheral insulin sensitivity and glucose uptake

28
Q

severe side effect metformin

A

lactic acidosis

29
Q

contraindications for metformin

A
  • renal/hepatic impairment CR>1.5 in men or 1.5 in women

- no preggers

30
Q

what may predispose ppl to lactic acidosis?

A

CHF with hypoperfusion or chronic hypoxemia

31
Q

start dosing for metformin

A

500 mg once or twice daily with meals

if tolerate meds, double dose to 1000 mg twice daily

32
Q

other oral therapies

A

sulfonylureas (stimulate insulin secretion by pancreas beta cells) (weight gain, hypoglycemia, increased CV events) (glyburide, glipizide, glimepiride)

and

Thiazolidinediones (pioglitazone)(increased risk for fluid retention and CHF)(bladder cancer risk)

33
Q

which med can actually decrease the microvascular complications of diabetes?

A

sulfonylureas

34
Q

similar to sulfonylureas, stimulate beta cells

A

glitinides

shorter half-life, dosed with meals

35
Q

prevent absorption of simple sugars by decreasing carbohydrate breakdown

A

alpha-glucosidase inhibitors (acarbose)

36
Q

increased incretin leads to increased insulin secretion

A

DPP4 inhibitors (sitagliptin)

37
Q

increase insulin and decrease glucagon, increase satiety

A

GLP-1 receptor antagonist

no hypoglycemia, causes weight loss

38
Q

block glucose resporption in kidney

A

sodium-glucose co-transporter 2 inhibitors

canagliflozin

39
Q

*most effective medication to lower A1c

A

insulin therapy

40
Q

insulin starting dose

A

0.1-0.2 units/kg initially - 10 units minimum

monitor morning fasting glucose and titrate insulin until goal of 70-130 is met

41
Q

initial goal of insulin therapy =

A

obtain fasting glucose levels less than 130 mg/dL

42
Q

glycemic treatment goals

A

less than 7% A1C

fasting glucose 70-130
peak glucose less tahn 180

43
Q

3 annual screens for DM complications

A
  • spot urine ablumin to creatinine ratio (want less than 30)
  • foot exam with monofilament testing
  • dilated eye exam by opthalmologist for diabetic retinopathy
44
Q

main mechanism for chronic complication of diabetes

A

increased intracellular glucose leads to formation of advanced glycosylation end products AGEs

–> accelerate atherscleoris, promote glomerular dysfunction, reduce NO synthesis, endothelila dysfunction

45
Q

can only have macular edema when…

A

non proliferative retinopathy present