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Clin Med Exam 3 > Type 2 DM > Flashcards

Type 2 DM Flashcards

1
Q

what components result in hyperglycemia? (HINT: 3)

A

insulin resistance, impaired insulin secretion, increased glucose production

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2
Q

what is Type 2 DM associated with?

A

obesity

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3
Q

what is more common, T1DM or T2DM?

A

T2DM

>90% of all diabetics have T2DM

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4
Q

circulating endogenous insulin is sufficient to prevent what?

A

ketoacidosis

but it’s inadequate to prevent hyperglycemia

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5
Q

what is the genetic influence for T2DM?

A

Strong genetic influences

-Concordance amongst monozygotic twins over 40 is 70%

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6
Q

what is the most important environmental factor causing insulin resistance?

A

OBESITY

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7
Q

what is T2DM the leading cause of in the US?

A
  • end-stage renal disease
  • Non-traumatic lower extremity amputations
  • Adult blindness
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8
Q

pathophysiology of T2DM?

A
  • Dysregulation or deficiency on release of insulin by beta cells
  • Inadequate or defective insulin receptors
  • Production of inactive insulin or insulin that is destroyed before it can carry out its function
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9
Q

what will the pathophysiology of T2DM result in?

A

Inability to transport glucose into fat and muscle cells

-This starves the body cells and causes the breakdown of fat and protein

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10
Q

what factors, that you need one of are used to diagnosis diabetes? (HINT: 4)

A

one of the following:
-Fasting plasma glucose ≥ 126 mg/dL

  • Random blood glucose >200mg/dL
  • Hemoglobin A1c > 6.5%
  • Two hour plasma glucose >200 mg/dL during an oral glucose tolerance test

(Screening tests should be repeated prior to making diagnosis)

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11
Q

abnormal glucose homeostasis (pre diabetes) factors?

A
  • fasting plasma glucose 100-125
  • plasma glucose levels 140-199 following a glucose tolerance test
  • A1c of 5.7-6.4%
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12
Q

if you have abnormal glucose homeostasis (pre diabetes), what are you at increased risk of getting?

A

increase risk of progression to T2DM and increased risk of CV disease
(if have diabetes, your risk for an MI is equivalent for someone who has already had an MI)

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13
Q

how do you do a oral glucose tolerance test?

A

-Eat balanced diet (with at least 150 g carbs) for 3 days prior to test
-Fasting blood glucose measured upon arrival
-Drink 75-100g of glucose
-Blood glucose is measured at timed intervals
(1 hr after, 2 hrs after, maybe 3 hrs after)

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14
Q

what is the normal blood glucose at 1hr?

A

<180

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15
Q

what is the normal bg at 2hrs?

A

<140

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16
Q

at what bg is pre-diabetes diagnosed?

A

Pre-diabetes is diagnosed if BG at 140-199 after 2 hours

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17
Q

at what bg is diabetes diagnosed?

A

BG >200

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18
Q

risk factors for T2DM?

A
  • 1st degree relative with T2DM
  • overweight/obesity (BMI >25)
  • physical inactivity
  • NA & AA
  • previous impaired fasting glucose, impaired glucose tolerance, or HgbA1c
  • hx of gestational diabetes or baby >9lbs
  • polycystic ovarian syndrome
  • HbA1c 5.7-6.4% (pre-diabetes)
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19
Q

at what age are all individuals screened for T2DM?

A

All individuals ≥45 years

-If normal, then every 3 years thereafter

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20
Q

when would you screen earlier than 45 y/o for T2DM?

A

earlier (<30 years) in:

  • BMI ≥25 or central obesity
  • habitually sedentary
  • 1st degree relative w/DM
  • NA or AA
  • baby >9lbs
  • HTN (>140/90)
  • HDL <35 or TG >250
  • hx of prediabetes
  • hx of CVD
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21
Q

what’s the difference with clinical presentation upon diagnosis b/w T1DM and T2DM?

A

T1DM present with DKa

T2DM usually don’t have symptoms and dx is often incidental

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22
Q

most common clinical presentation of T2DM?

A

-most are overweight or obese (but may have weight loss b/c of fat breaking down in hyperglycemic state)

polyuria, polydipsia, polyphasic, weight loss, fatigue, weakness

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23
Q

neuropathic complications at time of presentation for T2DM?

A

peripheral neuropathy & gastroparesis

24
Q

CV complications at the time of presentations for T2DM?

A

MI

25
Q

what kind of skin infections do T2DM get?

A

chronic skin infections - esp fungal

26
Q

physical exam findings for T2DM?

A
  • central obesity
  • eye hemorrhages, exudates, neovascularization
  • acanthosis ingrains (dark discoloration of skin)
  • candida infections
  • decr sensation
  • loss of deep tendon reflexes in ankle
  • muscle atrophy
  • feet ulcers
27
Q

what is acanthosis nigrans?

A

possible physical exam finding for T2DM

  • dark discoloration of skin
  • hyperketatotic
  • defect in insulin receptor gene
  • extreme insulin resistance
28
Q

when have decreased sensation, what is it to?

A
  • light touch
  • temperature
  • proprioception
29
Q

why is it common for diabetics to get foot ulcers?

A

Have poor circulation in feet because of CV complications -> if accidentally injure feet and get a little cut, won’t feel it because of peripheral neuropathy -> won’t heal because of poor circulation -> may end in amputation

30
Q

treatment goals of T2DM?

A
  • education and nutrition counseling
  • weight loss
  • glucose control
  • avoid drugs that exacerbate diabetes
31
Q

CV risk factor management for T2DM?

A
  • smoking cessation
  • aspirin
  • BP control
  • management of dyslipidemia
  • diet
  • exercise
32
Q

routine health maintenance of T2DM?

A
  • monitor A1c every 3 months
  • check urine microalbumin yearly (look for kidney disease)
  • podiatry referral for annual routine foot care
  • ophthalmology referral for annual routine eye care
  • self-monitoring of glucose levels with glucometer
33
Q

how much of an A1c drop is associated with improved outcomes from microvascular complications?

A

Every 1% drop in A1c is associated with improved outcomes from microvascular complications
-No clear benefit for macrovascular complications

34
Q

what is the number 1 nonpharmacologic therapy for T2DM?

A

weight reduction

35
Q

what is the alternate 1st line therapy for people that can’t tolerate metformin?

A

sulfonylurea

  • stimulates secretion from pancreatic beta cells
  • often added in combo with metformin
36
Q

what can metformin cause besides diarrhea?

A 
lactic acidosis (rare)
-impaires lactate uptake by liver (avoid in liver failure and renal impairment)
37
Q

metabolism and excretion of sulfonylureas?

A

Glyburide

  • metabolized by liver
  • excreted 50% by kidneys & 50% by liver

Glipizide

  • metabolized by liver
  • excreted by kidneys

Glimepiride

  • metabolized by liver
  • excreted by kidneys
38
Q

C/I’s for SU’s

A
  • hepatic insufficiency
  • renal insufficiency

(both have increased risk of hypoglycemia)

39
Q

metabolism and excretion of glinides?

A

Repaglinide

  • hepatically metabolized
  • 90% excreted in feces

Nateglinide

  • hepatically metabolized
  • renal excretion of active metabolites
40
Q

C/I with glinides

A

care with nateglinide in renal dysfunction

41
Q

metabolism and excretion of alpha-glucosidase inhibitors?

A

Acarbose
-excreted 50% in feces (unabsorbed) and 50% in urine

Miglitol
-excreted unchanged by kidneys

42
Q

C/I for alpha-glucosidase inhibitors?

A

careful in kidney insufficiency

43
Q

TZD MOA

A
  • sensitive peripheral tissues to insulin
  • low risk of hypoglycemia
  • monotherapy or in combo with SUs, Metformin, or insulin
44
Q

BBW for GLP-1 agonists?

A

causes medullary thyroid cancer in mice

  • hasn’t happened in humans yet
  • C/I if personal or family hx of THYROID CANCER
45
Q

when do you consider using DPP-4 inhibitors?

A

consider for mono therapy in patients who can’t take metformin, SUs, or TZDs
(pts with CKD or at particularly high risk of hypoglycemia)

-can be considered as an add-on drug for other patients

46
Q

why aren’t DPP-4 inhibitors used much?

A

Not used much due to modest glucose lowering effect, expense, and limited clinical experience

47
Q

when do you switch a pt to insulin in terms of their A1c?

A

if A1c >8.5%

48
Q

when do you add insulin?

A

if goal A1c not met on 2 oral agents -> add insulin

-alternatively add GLP-1 agonist

49
Q

what does better, insulin combo with oral or D/C oral and just do insulin?

A

insulin combo wth oral

50
Q

what is hyperglycemic hyperosmolar state (non-ketonic, HNNK)?

A

Hyperglycemic condition resulting in hypovolemia and electrolyte abnormalities

  • Don’t develop anion gap like they do in DKA -> not likely to become acidotic
  • This is the DKA version for T2DM
  • Won’t get ketones in blood, will get them in urine
51
Q

precipitating factors of hyperglycemic hyperosmolar state (non-ketonic, HNNK)?

A

Major illness:
-MI, CVA, Sepsis, Pancreatitis

Drugs that effect carb metabolism:
-Steroids, Thiazides, Atypical antipsychotics

Compliance issues

52
Q

clinical presentation of hyperglycemic hyperosmolar state (non-ketonic, HNNK)?

A

Sx’s develop insidiously:

  • Polyuria
  • Polydipsia
  • Weight loss
  • Lethargy
  • Decreased skin turgor
  • Dry mucous membranes
  • Tachycardia
  • Hypotension
53
Q

Lab abnormalities of hyperglycemic hyperosmolar state (non-ketonic, HNNK)?

A

-marked hyperglycemia (BS>1000)
-Hyperosmolality
-Pre-renal azotemia (volume depletion)
-absence of severe ketosis
-Low potassium, magnesium, and phosphate levels
(major electrolyte problems which can lead to arrhythmias)

54
Q

what is the critical 1st step to treating hyperglycemic hyperosmolar state (non-ketonic, HNNK)?

A

IV FLUIDS

55
Q

what is the treatment of hyperglycemic hyperosmolar state (non-ketonic, HNNK)?

A

IV FLUIDS (#1)
IV insulin
Electrolyte monitoring and replevin (K, Mg, Phosphate)

56
Q

Long term complications of T2DM?

microvascular

A

Retinopathy
-Leading cause of blindness in the US

Nephropathy
-Can progress to ESRD requiring hemodialysis

Neuropathy

  • Pain and numbness of lower extremities
  • Gastroparesis

Clin Med Exam 3 (6 decks)

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