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Summer FDTN Exam 2 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What is diabetes characterized by

A

hyperglycemia and varying degrees of insulin deficiency and resistance

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2
Q

What is impaired glucose tolerance

A

blood glucose varies between normal and overt DM (140-199) seen during an OGTT

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3
Q

What is impaired fasting glucose

A

FPG of 100-125

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4
Q

What is prediabetes

A

Increased risk for diabetes

Must have impaired GT, impaired FG, or A1C 5.7-6.4%

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5
Q

Who has the highest rates of diabetes Type 2

A

American indian/alaska native

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6
Q

What are RF for T2DM

A 
genetics, FHx
BMI, waist circumference 
lifestyle 
age 45+ 
Obesity (childhood weight) 
Physical inactivity 
smoking, diet, meds
Pre-DM, gestational DM
Dyslipidemia 
CVD (HF, MI, HTN) 
PCOS 
Metabolic syndrome 
Hyperuricemia (gout)
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7
Q

A few drugs that can impair glucose tolerance are

A

Fluoroquinolones
Thiazides
Systemis glucocorticoids
Oral contraceptives

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8
Q

What is Metabolic syndrome

A 
3+ of the following: 
1. Abd obesity (waist >40 in men, >35 in women) 
2. TG 150+ 
Low HDL (<40 men, <50 women) 
BP >130/85
FPG >100
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9
Q

Some poor outcomes associated with metabolic syndrome are

A

Risk of T2DM, CVD (assess 10 year risk)

higher incidence with age, if overweight or obese

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10
Q

Management goals for metabolic syndrome are

A

treat underlying cause and CVD RF

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11
Q

How do you manage metabolic syndrome

A
  • Lifestyle mod: Mediterranean, DASH, low glycemic index, high fiber
  • 7-10% reduction in body weight in 1 year
  • Increase physical activity to 150 min/wk
  • Reduce other RF (stop smoking, Tx HTN, lower cholesterol, glycemic control if w/ DM)
  • Metformin (often given to prevent DM)
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12
Q

What are the ways you get blood glucose

A

Diet (goes thru portal vein to liver)
Gluconeogenesis (AA + propionate= glucose)
Glycogenolysis of liver glycogen

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13
Q

What is glucose homeostasis

A

Hepatic glucose production is balanced with peripheral glucose uptake

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14
Q

Where is insulin made and what does it do

A

Hyperglycemia stimulates insulin production by beta cells in islets of Langerhans in the pancreas
Insulin causes glucose transport into adipose tissue

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15
Q

Where is glucagon made and what does it do

A

Hypoglycemia stimulates glucagon production in alpha cells of pancreatic islets
Glucagon causes glycogenolysis and gluconeogenesis

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16
Q

What regulates insulin secretion

A

glucose (mainly)

AA, ketones, various nutrients, GI peptides, and neurotransmitters

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17
Q

What is incretin

A

Enzymes released from neuroendocrine cells after a meal

Amplifies glucose stimulated insulin secretion and suppresses glucagon

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18
Q

What is the most potent incretin

A

GLP-1 (glucagon like peptide)

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19
Q

What happens during a fasting state

A

Low insulin, high glucagon
+gluconeogenesis, glycogenolysis
-glucose uptake in muscle/fat

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20
Q

What happens in post-prandial state

A

high insulin, low glucagon

+carb storage, fat/protein synthesis, skeletal muscle uptake

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21
Q

What is the pathophysiology behind diabetes

A

In insulin resistance, beta cells compensate by increasing insulin
In Impaired GT, beta cells can no longer sustain hyperinsulin state
In overt diabetes, beta cells fail and
you have fasting hyperglycemia
*Post-prandial state labs in a fasting state

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22
Q

What happens during insulin resistance

A

Decreased insulin effectiveness on target tissues (muscle, liver, fat), but Increased circulating insulin normalizes plasma glucose
Impairs glucose utilization= increased hepatic output
Affected by substances secreted by adipocytes (leptin, adiponectin, TNF-alpha, resistin)

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23
Q

What happens during impaired insulin secretion

A

Initially, increases response to insulin resistance. But then, Beta cells fail causing chronic hyperglycemia
High FFA and fat worsen islet fxn; low GLP-1 further reduces insulin secretion

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24
Q

What happens during excessive hepatic glucose production

A

insulin resistance in liver= failure of gluconeogenesis suppression= hyperglycemia and decreased glycogen storage in liver in post-prandial state

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25
Q

What happens during abnormal fat metabolism

A 
insulin resistance causes increased lipolysis and FFA flux from adipocytes= increased VLDL and TG synthesis in liver 
Lipid storage (steatosis) leads to NAFLD and dyslipidemia
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26
Q

How does T2DM usually present

A

Asymptomatic! Hyperglycemia on routine labs

if severeL Polyuria, polydipsia, nocturia, blurred vision, weight loss

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27
Q

Who does the ADA say needs to be screened for T2DM

A

adults BMI 25+ andother RF, screen q 3 years
Everyone 45+: screen q3 years
Pre-diabetic: screen annually
Women with GDM: screen q3 years

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28
Q

Who does USPSTF say needs to be screened for T2DM

A

adults 40-70 overweight or obese: screen with CV risk assessment q3 years

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29
Q

What is your diagnostic criteria for T2DM

A

Sx + random blood glucose 200+
ASx + FPG 126+, OGTT 200+, A1c 6.5%+
-Must repeat on a different day

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30
Q

How do you repeat DM testing

A

1 abn: need 2 readings showing abnormal

2+ abn: make Dx that day

31
Q

*What are normal values

A

FPG <100

OGTT 2 hr: <140

32
Q

What is Glycated Hgb (A1c)

A

3 month average of glucose levels, mainly the last month
Convenient for patient (no fasting, any time of day)
BUT- can be affected by hemoglobinopathy and CKD

33
Q

How is A1c affected by RBC turnover

A

low cell turnover: falsely high levels
-also in iron, B12, or folate deficiency
high cell turnover: falsely low levels
-also in hemolytic anemia, EPO use

34
Q

What should be part of your T2DM evaluation

A 
nutrition, weight, physical activity 
CV risk 
DM related complications 
hypoglycemic episodes 
Labs: A1c, fasting lipids, liver enzymes, urine albumin, SrCr
35
Q

T2DM follow up care should include

A 
Med compliance 
Med intolerance/ADE 
Self management behaviors 
nutrition 
psychosocial health 
need for referrals
36
Q

How do you manage T2DM

A 
glycemic control (pharm or non-pharm) 
Monitor/prevent complications (micro/macro vascular) 
Pt Ed (ntr, hypoglycemia, CV risk, vision, kidneys) 
Health maintenance
37
Q

For T2DM, how often do we measure glycemic control

A

Controlled: 2x year

Uncontrolled/med change: q3 months

38
Q

What are target A1c goals in T2DM

A

individualized, but for MOST < 7.0%
More stringent goal: < 6.5%
Less stringent goal: < 8.0% (Hx severe hypoglycemia, limited life expectancy, elderly, comorbidities)

39
Q

When assessing how stringent to be on A1c goal, what should you consider

A 
Risk of hypoglycemia 
disease duration 
life expectancy 
comorbidities 
existing vascular complications 
attitude and expected Tx efforts 
resources and support system
40
Q

Is self monitoring necessary in T2DM

A

more frequently done in T1DM, BUT
should monitor several times/week when titrating meds
more frequent if w/ illness or change in diet/exercise
measure in AM or before dinner

41
Q

Non-pharm therapy includes

A

diet
exercise
weight reduction
physiologic interventions

42
Q

Goals for medical nutrition therapy if overweight are

A

lower kcal intake
increase physical activity
promote weight loss (correct insulin resistance

43
Q

Goals for medical nutrition therapy is NOT overweight are

A

weight management
consistent day-to-day CHO intake
nutritional content of meals

44
Q

Pharmacologic glycemic control goals are

A

Increase insulin availability
Improve insulin sensitivity
Delay delivery and absorption of CHO from GI
Increase urine glucose excretion

45
Q

When should you start pharm therapy for glycemic control

A

Early! you get improved glycemic control over time, and decreased long term complications
If A1c >7.5% start Rx
If A1z <7.5 % AND highly motivated, trial 3-6 mo. lifestyle modification

46
Q

Initial therapy for most T2DM patients is

A

Metformin!

Only start insulin if pt has a severely high A1c, is unmotivated, and not likely to make a lifestyle change

47
Q

What are complications of T2DM

A

Microvasc: retinopathy, nephropathy, neuropathy
Macro: atherosclerosis (MI, CVA)

48
Q

What is diabetic retinopathy

A

MCC of blindness in adults 20-74
Retinal injury and ischemia 2/2 vascular changes from hyperglycemia
-Macular edema, hemorrhage from new vessels, retinal detachment, neovascular glaucoma
ASYMPTOMATIC until late stages
Can be prevented with glycemic and BP control

49
Q

PE findings in NON-proliferative diabetic retinopathy are

A 
cotton woll spots 
hard exudates 
microaneurysms 
occluded vessels 
dilated, tortuour vessels 
visual loss 2/2 macular edema
50
Q

PE findings in proliferative diabetic retinopathy are

A 
Neovascularization 
pre-retinal and vitreous hemorrhage 
fibrosis 
retinal detachment 
visual loss 2/2 bleeding, retinal detachment, macular ischemia
51
Q

How often do you screen for diabetic retinopathy

A

T2: at time of diagnosis, dilated and comprehensive eye exam by ophthalmologist
T1: w/in 5 years
Repeat annually

52
Q

How do you treat diabetic retinopathy

A

laser therapy
IV ranibizumab injection (anti vascular growth)
Vitrectomy

53
Q

What is diabetic nephropathy

A

leading cause of ESRD

Can be prevented by optimizing BP and glucose control

54
Q

How do you screen for diabetic nephropathy

A 
Urine albumin and eGFR 
T2: at time of diagnosis 
T1: w/in 5 years 
Screen all pts with comorbid HTN 
Repeat annually
55
Q

Diagnostic criteria for diabetic nephropathy

A

Microalbuminuria (30-300) or Macroalbuminuria (>300)

Must have 2-3 abn specimens over 3-6 months (bc a lot of things cause increased albumin

56
Q

How do you treat diabetic nephropathy

A

ACE or ARB (if mild UACR; 30-299) (strong recc. if UACR 300+ or GFR <60)
Protein intake
Refer for renal replacement Tx in GFR <30 (stage 4-5)

57
Q

How does GFR correlate to stages of CKD

A

1: 90+
2: 60-89
3: 30-59
4: 15-29
5: <15

58
Q

Complications of diabetic nephropathy are

A 
high BP 
volume overload 
electrolyte abn
metabolic acidosis 
anemia 
metabolic bone disease
59
Q

MC complications of diabetic neuropathy are

A

Foot ulcers
amputation
*Can prevent by optimizing glucose control

60
Q

RF for ulcers or amputations are

A 
poor glycemic control 
peripheral neuropathy 
smoking 
foot deformities 
callous/corn 
PAD 
Hx foot ulcer 
amputation 
visual impairment 
DKD (esp on dialysis)
61
Q

How do you screen for diabetic neuropathy

A 
Annual history + temp or pinprick sensation + vibratory sensation 
annual monofilament testing 
visually inspect feet at every visit 
T2: at time of diagnosis 
T1: w/in 5 years
62
Q

How do you treat diabetic neuropathy

A

Pregabalin or Duloxetine

Foot care education (well fitting shoes, white socks, caution w/ hot water, LOOK!)

63
Q

What does a comprehensive yearly foot evaluation include

A

skin inspection
assess foot deformities
neuro assessment (monofilament, pin prick, temp)
vascular assessment

64
Q

When would you consider ABI or vascular referral

A

If pt has claudication or decreased/absent pedal pulses

*Podiatry referral if smoker or Hx of LE complications

65
Q

How do you preform the monofilament test

A

place device perpindicular to skin and press until it bends
hold for 1 second and release
Preform while pt eyes closed!

66
Q

All patients with DM should be assessed for

A

CV RF

67
Q

Goal BP for diabetic patients is

A

<140/90

anti-HTN Tx reduces ASCVD events, HF, and microvascular complications

68
Q

How do you decide therapy based on BP level

A

If 140/90 to 160/100: One agent + lifestyle modifications
(if albuminuria, ACE or ARB- if not, ACE, ARB, CCB, or diuretic)
If >160/100: two agents + lifestyle mod (if albuminuria, ACE or ARB + CCB or diuretic- if not, ACE or ARB, CCB, or diuretic)

69
Q

What are statin recommendations for diabetics based on age

A

<40 w/ ASCVD: high dose statin
40+ y/o w/ ASCVD: high dose statin
40+ y/o w/o ASCVD: moderate statin
(if w/ ASCVD, can consider adding ezetimibe of PCSK9 inhibitor if LAL if sill >70 on high dose statin)

70
Q

Antiplatelet recommendation for diabetics (ranked A and B)

A

A: ASA as secondary prevention if w/ DM andHx of ASCVD
A: ASA (75-162) as primary prevention of with T1/T2DM and high CV risk
A: ASA + P2Y12 inhibitor for 1 year after ACS
B: ASA + P2Y12 inhibitor >1 year after ACS
B: Use Clopidogrel if w/ ASCVD but allergic to aspirin

71
Q

What are screening recommendations for CHD

A

A: If ASx, routine screening not recommended
E: may investigate for CAD if w/ atypical cardiac Sx, S/Sx of associated vascular disease, or Q waves on ECG

72
Q

Treatment recommendations for CHD are

A

A: If w/ ASCVD, ACE or ARB
A: T2DM w/ ASCVD, start on anti-hyperglycemic Tx with lifestyle management and metformin
B: if Hx MI, give BB for at least 2 years s/p event
B: T2DM w/ stable CHF, use metformin if GFR >30
B: do not give Metformin to T2DM if unstable or hospitalized with CHF
C: T2DM w/ ASCVD, consider adding canagliflozin after metformin and lifestyle mod

73
Q

Common DM comorbidities are

A 
T1DM 
cancer 
dementia
fatty liver disease 
pancreatitis 
fractures 
hearing impairment 
HIV 
low testosterone in men 
OSA 
periodontal disease 
psychosocial disorder
74
Q

Routine health maintenance includes

A 
Yearly flu vaccine 
Pneumococcal vaccine 
HBV if 19-59 
Updated tetanus + diphtheria 
reproductive counseling 
indicated screenings

Summer FDTN Exam 2 (11 decks)

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