16/17: Diabetes - Dodge Flashcards

(45 cards)

1
Q

how many ppl have diabetes?

A

1/11

increased in native americans, hispanics, and lower education

increased in the south

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

insulin is created in…

A

beta islet cells of pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

insulin binding to cell receptors –>

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

common theme between dif. DM types

A

dysregulation of the insulin/glucose interplay leading to hyperglycemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

typeII DM

A

insulin resistance

95% of adult DM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

IDDM

A

insulin dependent diabetes mellitus

insulin is being used to treat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

genetic component of DM type I

A

HLA DR3/DR4 gene

twin studies 50%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

diabetic ketoacidosis –>

A

type I DM

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

which type of DM has a higher genetic component?

A

type II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

drugs/medications that may cause diabetes

A
  • thiazides
  • pentamidine
  • protease inhibitors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

prediabetes and diabetes fasting plasma glucose

A

100-125

>126

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

glucose tolerance test prediabetes; diabetes

A

140-199

>200

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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?

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

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
intervention with A1c less than or equal to 7.5%
lifestyle and dietary changes
26
weight loss is _______ important than certain combinations of nutrients
more
27
MOA metformin
decreases hepatic gluconeogenesis and glycogenolysis with increase in peripheral insulin sensitivity and glucose uptake
28
severe side effect metformin
lactic acidosis
29
contraindications for metformin
- renal/hepatic impairment CR>1.5 in men or 1.5 in women | - no preggers
30
what may predispose ppl to lactic acidosis?
CHF with hypoperfusion or chronic hypoxemia
31
start dosing for metformin
500 mg once or twice daily with meals if tolerate meds, double dose to 1000 mg twice daily
32
other oral therapies
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
which med can actually decrease the microvascular complications of diabetes?
sulfonylureas
34
similar to sulfonylureas, stimulate beta cells
glitinides shorter half-life, dosed with meals
35
prevent absorption of simple sugars by decreasing carbohydrate breakdown
alpha-glucosidase inhibitors (acarbose)
36
increased incretin leads to increased insulin secretion
DPP4 inhibitors (sitagliptin)
37
increase insulin and decrease glucagon, increase satiety
GLP-1 receptor antagonist no hypoglycemia, causes weight loss
38
block glucose resporption in kidney
sodium-glucose co-transporter 2 inhibitors | canagliflozin
39
*most effective medication to lower A1c
insulin therapy
40
insulin starting dose
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
initial goal of insulin therapy =
obtain fasting glucose levels less than 130 mg/dL
42
glycemic treatment goals
less than 7% A1C fasting glucose 70-130 peak glucose less tahn 180
43
3 annual screens for DM complications
- spot urine ablumin to creatinine ratio (want less than 30) - foot exam with monofilament testing - dilated eye exam by opthalmologist for diabetic retinopathy
44
main mechanism for chronic complication of diabetes
increased intracellular glucose leads to formation of advanced glycosylation end products AGEs --> accelerate atherscleoris, promote glomerular dysfunction, reduce NO synthesis, endothelila dysfunction
45
can only have macular edema when...
non proliferative retinopathy present