kania pt 0 Flashcards

1
Q

hyperglycemia

A

results from defects in insulin secretion, resistance to insulin action, or both

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

autoimmune destruction of beta cells

A

leads to insulin deficiency and/or resistance to insulin

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

effects of long-term hyperglycemia

A

leads to organ damage in eyes, kidneys, nerves, heart, and blood vessels

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

signs and symptoms of hyperglycemia

A

relate to alterations in carbohydrates, fat, and protein metabolism

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

function of insulin and counterregulatory hormones

A

regulation of carbohydrate and fatty acid metabolism

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

organs involvement in glucose homeostasis

A

brain –> insulin dependent
fat/muscle tissue –> insulin dependent
liver –> plasma glucose levels with increased production; production decreases with rise of insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

increase in insulin means

A

decrease glucose production by liver
decreased glycogenolysis and gluconeogenesis
stimulate tissue glucose uptake
suppress FFA release from fat cells

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

egregious eleven (ominous octet)

A

1) beta cells may be destroyed or simply quit working (leads to decrease insulin)
2) decreased incretin effect
3) dysfunction of a cell leads to increase glucagon levels
4) adipose insulin resistance leads to increased lipolysis
5) muscle insulin resistance leads to decrease peripheral muscle uptake (not using glucose adequately)
6) liver insulin resistance leads to increase glucose production (cannot recognize glucagon)
7) changes of hormones in the brain –> increased appetite, decreased morning dopamine surge, increased sympathetic tone
8) different gut bacteria can modify blood glucose levels and may decrease GLP-1 levels
9) beta cell destruction via autoimmune reactions or increased inflammation
10) quick stomaching empty –> increased glucose absorption
11) up regulation of SGLT2 –> increased glucose reabsorption in kidney

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

why do many older adults not get diagnosed with T2DM despite having clinical presentation?

A

common symptoms (polyuria, nocturia, etc) are associated with old age
pt just assume that is the cause not T2DM

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

metabolic syndrome

A

HTN
obesity
dyslipidemia (high TG and low HDL)

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

drugs that increase hepatic glucose output

A

glucocorticoids
sympathomimetics
niacin (with higher doses only)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

drugs that decrease insulin secretion

A

phenytoin
beta blockers
calcium channel blockers (can lead to proteinuria)
immunosuppressants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

B-block usage

A

able to use, but consider the indication and if its necessary
caution use in brittle diabetics especially with ultra short-acting agents
can mask the signs and sx of acute hypoglycemia

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

A1C criteria for diabetics

A

greater or equal to 6.5%
patients with high red blood cell turnover (like in sickle cell anemia or pregnancy) do not have to have this for diangosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

treatment for IFG, IGT, or increased risk for diabetes

A

need monitoring
consider pre diabetic drug therapy, but definitely lifestyle changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

normal levels

A

under 100 mg/dL (FBG)
under 5.7% (A1C)
under 140 mg/dL (2hr OGTT)
under 200 mg/dL (random glucose)

17
Q

T2DM prevention

A

weight loss of 7% percent
increase exercise to 150min/week of moderate activity
initation of metformin in some patients (be careful of B12 levels, always administer with food)
monitor patients annually
utilize self-management programs and tech tool to support and maintain lifestyle mods

18
Q

goals of therapy

A

keep patient asymptomatic (but not too low when it comes to the polys)
prevent long-term complications
maintain patients near eyglycemia
achieve and maintain an appropriate body weight (maybe 10-15 lbs)
maintain normal growth and development in children
enhance patient education and self-reliance in management
eliminate or minimize all cardiovascular risk factors

19
Q

components of therapy

A

meals
monitoring
movement
medication
(must take all 4 into consider, cannot evaluate one without the other)

20
Q

general approach

A

educate the patient and family about the disease and treatment
set realistic goals
formulate a plan for achieving glycemic control
obtain agreement with the pt regarding goals and treatment and provide supportive follow-up

21
Q

monitor carbohydrate intake parameters

A

45gm per meal for women
60gm per meal for men

22
Q

key patient education factors

A

continuous
disease state
drug therapy (adverse effects, how to take, etc)

23
Q

prevention and treatment of complications

A

foot care
annual eye exam
dental care every 6 months
diabetic kidney disease –> annual microalbuminuria screening
CV –> control lipids and BP; quit smoking