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Summer FDTN Exam 2 > Diabetes > Flashcards

Diabetes Flashcards

(74 cards)

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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
What happens during abnormal fat metabolism
``` 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 ```
26
How does T2DM usually present
Asymptomatic! Hyperglycemia on routine labs | if severeL Polyuria, polydipsia, nocturia, blurred vision, weight loss
27
Who does the ADA say needs to be screened for T2DM
adults BMI 25+ andother RF, screen q 3 years Everyone 45+: screen q3 years Pre-diabetic: screen annually Women with GDM: screen q3 years
28
Who does USPSTF say needs to be screened for T2DM
adults 40-70 overweight or obese: screen with CV risk assessment q3 years
29
What is your diagnostic criteria for T2DM
Sx + random blood glucose 200+ ASx + FPG 126+, OGTT 200+, A1c 6.5%+ -Must repeat on a different day
30
How do you repeat DM testing
1 abn: need 2 readings showing abnormal | 2+ abn: make Dx that day
31
*What are normal values
FPG <100 | OGTT 2 hr: <140
32
What is Glycated Hgb (A1c)
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
How is A1c affected by RBC turnover
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
What should be part of your T2DM evaluation
``` nutrition, weight, physical activity CV risk DM related complications hypoglycemic episodes Labs: A1c, fasting lipids, liver enzymes, urine albumin, SrCr ```
35
T2DM follow up care should include
``` Med compliance Med intolerance/ADE Self management behaviors nutrition psychosocial health need for referrals ```
36
How do you manage T2DM
``` glycemic control (pharm or non-pharm) Monitor/prevent complications (micro/macro vascular) Pt Ed (ntr, hypoglycemia, CV risk, vision, kidneys) Health maintenance ```
37
For T2DM, how often do we measure glycemic control
Controlled: 2x year | Uncontrolled/med change: q3 months
38
What are target A1c goals in T2DM
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
When assessing how stringent to be on A1c goal, what should you consider
``` Risk of hypoglycemia disease duration life expectancy comorbidities existing vascular complications attitude and expected Tx efforts resources and support system ```
40
Is self monitoring necessary in T2DM
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
Non-pharm therapy includes
diet exercise weight reduction physiologic interventions
42
Goals for medical nutrition therapy if overweight are
lower kcal intake increase physical activity promote weight loss (correct insulin resistance
43
Goals for medical nutrition therapy is NOT overweight are
weight management consistent day-to-day CHO intake nutritional content of meals
44
Pharmacologic glycemic control goals are
Increase insulin availability Improve insulin sensitivity Delay delivery and absorption of CHO from GI Increase urine glucose excretion
45
When should you start pharm therapy for glycemic control
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
Initial therapy for most T2DM patients is
Metformin! | Only start insulin if pt has a severely high A1c, is unmotivated, and not likely to make a lifestyle change
47
What are complications of T2DM
Microvasc: retinopathy, nephropathy, neuropathy Macro: atherosclerosis (MI, CVA)
48
What is diabetic retinopathy
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
PE findings in NON-proliferative diabetic retinopathy are
``` cotton woll spots hard exudates microaneurysms occluded vessels dilated, tortuour vessels visual loss 2/2 macular edema ```
50
PE findings in proliferative diabetic retinopathy are
``` Neovascularization pre-retinal and vitreous hemorrhage fibrosis retinal detachment visual loss 2/2 bleeding, retinal detachment, macular ischemia ```
51
How often do you screen for diabetic retinopathy
T2: at time of diagnosis, dilated and comprehensive eye exam by ophthalmologist T1: w/in 5 years Repeat annually
52
How do you treat diabetic retinopathy
laser therapy IV ranibizumab injection (anti vascular growth) Vitrectomy
53
What is diabetic nephropathy
leading cause of ESRD | Can be prevented by optimizing BP and glucose control
54
How do you screen for diabetic nephropathy
``` Urine albumin and eGFR T2: at time of diagnosis T1: w/in 5 years Screen all pts with comorbid HTN Repeat annually ```
55
Diagnostic criteria for diabetic nephropathy
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
How do you treat diabetic nephropathy
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
How does GFR correlate to stages of CKD
1: 90+ 2: 60-89 3: 30-59 4: 15-29 5: <15
58
Complications of diabetic nephropathy are
``` high BP volume overload electrolyte abn metabolic acidosis anemia metabolic bone disease ```
59
MC complications of diabetic neuropathy are
Foot ulcers amputation *Can prevent by optimizing glucose control
60
RF for ulcers or amputations are
``` poor glycemic control peripheral neuropathy smoking foot deformities callous/corn PAD Hx foot ulcer amputation visual impairment DKD (esp on dialysis) ```
61
How do you screen for diabetic neuropathy
``` 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
How do you treat diabetic neuropathy
Pregabalin or Duloxetine | Foot care education (well fitting shoes, white socks, caution w/ hot water, LOOK!)
63
What does a comprehensive yearly foot evaluation include
skin inspection assess foot deformities neuro assessment (monofilament, pin prick, temp) vascular assessment
64
When would you consider ABI or vascular referral
If pt has claudication or decreased/absent pedal pulses | *Podiatry referral if smoker or Hx of LE complications
65
How do you preform the monofilament test
place device perpindicular to skin and press until it bends hold for 1 second and release Preform while pt eyes closed!
66
All patients with DM should be assessed for
CV RF
67
Goal BP for diabetic patients is
<140/90 | anti-HTN Tx reduces ASCVD events, HF, and microvascular complications
68
How do you decide therapy based on BP level
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
What are statin recommendations for diabetics based on age
<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
Antiplatelet recommendation for diabetics (ranked A and B)
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
What are screening recommendations for CHD
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
Treatment recommendations for CHD are
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
Common DM comorbidities are
``` T1DM cancer dementia fatty liver disease pancreatitis fractures hearing impairment HIV low testosterone in men OSA periodontal disease psychosocial disorder ```
74
Routine health maintenance includes
``` 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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