Diabetes part 1 - waldron Flashcards

1
Q

what does anaerobic breakdown by glycolysis yield

A

8-10 ATP

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2
Q

what does aerobic respiration by Krebs cycle yield

A

25 ATP

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3
Q

what are the main subtypes of Diabetes

A

Type 1 (T1DM) and Type 2 (T2DM)

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4
Q

what populations do we typically see T1DM in

A

children or adolescents

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5
Q

what population do we typically see T2DM in

A

affects more middle-age and older adults with prolonged hyperglycemia due to poor lifestyle and diet

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6
Q

what secretes insulin

A

pancreas

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7
Q

where are the islets of langerhans

A

in the pancrease

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8
Q

what are the two subclasses of endocrine cells

A

alpha cells: glucagon secreting
beta cells: insulin producing

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9
Q

what is the etiology of T1DM

A

characterized by destruction of pancreatic beta cells, usu caused by autoimmune process
result: absolute destruction of beta cells and absent/extremely low insulin levels

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10
Q

what is the etiology of T2DM

A

insidious onset of imbalance btwn insulin levels and insulin sensitivity, causing functional deficit of insulin
insulin resistance is multifactorial but commonly develops from obesity and aging

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11
Q

what type of DM have more complex interplay between genetics and lifestyle

A

T2DM

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12
Q

what does polymorphisms influence the risk for

A

T1DM

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13
Q

What is MODY

A

mature onset diabetes of young
non-insulin dependent diabetes diagnosed at young age (usu. < 25)
autosomal dominant transmission, does not involve autoantibodies as in T1DM
genetics unclear

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14
Q

what is diabetes during pregnancy

A

gestational diabetes

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15
Q

what are endocrinopatheis

A

acromegaly, cushings syndrome, glauconoma, hyperthyroidism, hyperaldosteronism, somatostatinomas: all associated with glucose intolerance and DM

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16
Q

what ethnic groups have the most prevalence of diabetes

A

native american
non-hispanic black
hispanic

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17
Q

what is the epidemiology of T1DM

A

peaks 4-6yo and 10-14 yo
F > M with aging (not as much in children)

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18
Q

what is the epidemiology of T2DM

A

onset usually later in life (adolescent obesity causing increase in younger people)
2-6x more prevalent in african american, native american, etc

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19
Q

what can hyperglycemia alone impair

A

pancreatic beta-cell function and contributes to impaired insulin secretion

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20
Q

what serum glucose levels are likely to cause symptoms of polyuria and polydipsia

A

> 250 mg/dL

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21
Q

what is insulin resistance

A

excess fatty acids and pro-inflammatory cytokines lead to impaired glucose transport and increased fat breakdown
inadequate production of insulin to compensate for their insulin resistance

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22
Q

what does chronic hyperglycemia cause

A

non-enzymatic glycation of proteins and lipids measurable via glycated hemoglobin (HbA1c)

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23
Q

what does glycation lead to

A

microvascular damage in retina, kidney and peripheral nerves; higher glucose levels hasten process

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24
Q

what does the damage from glycation lead to

A

classic diabetic complications: diabetic retinopathy, nephropathy and neuropathy (preventable blindness, dialysis and amputation)

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25
Q

what are the typical presentation of diabetes

A

polyuria, polydipsia and weight loss (catabolism)

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26
Q

what is seen on PE with hyperglycemia

A

fatigue, poor skin turgor, distinctive fruity odor on their breath (ketosis): if DKA Kussmaul respirations, N/V

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27
Q

what will be seen on fundoscopic exam with DM

A

macular hemorrhages or exudates; neovascularization

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28
Q

What is the presentation of T2DM

A

overweight/obese with signs of insulin resistance
acanthosis nigricans, blurry vision, frequent yeast/fungal infections, numbness/neuropathic pain

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29
Q

what is the presentation of hyperglycemia

A

dry mouth
increase thirst
blurred vision
weakness
AH
frequent urination

30
Q

how do you diagnose DM

A

fasting plasma glucose (FPG) levels
HbA1c (glycosylated Hb)
OGTT (oral glucose tolerance testing)
Urine “spilling”

31
Q

what is a HbA1c for T2DM

A

> 6.5%

32
Q

what is the diagnostic criteria per the ADA

A

one of the following:
fasting plasma glucose (FPG) > 126mg/dL
random glucose > 200 mg/dL with symptoms of hyperglycemia
2-hr plasma glucose > 200 mg/mL during 75g OGTT

33
Q

with is the OGTT

A

oral glucose tolerance testing
2 hour after ingesting of concentrated glucose solution
more sensitive for diagnosing DM and impaired gluocse tolerance but less convenient and reporducible than FPG
rare as routine testing except for gestational diabetes and research
*best test

34
Q

what is the BG to make the A1c of 7

A

155BG

35
Q

what is the diagnostic criteria for pre-diabetes

A

one of the following:
FBG >100-125 mg/dL
2-hr OGTT plasma glucose of 140-199 mg/dL
HbA1c 5.7-6.4%

36
Q

what tests are useful in the management of chronic (already diagnosed) DM

A

home glucose testing
HbA1c
urine albumin
serum lipid monitoring

37
Q

what other test is strongly recommended for chronic DM management

A

monitor thyroid status annually via TSH (higher associated incidence of hypothyroidism)

38
Q

what is a normal PPG level

A

<139

39
Q

what is a normal HbA1c

A

< 5.6%

40
Q

what level is a a random plasma glucose considered diabetes

A

> 200

41
Q

what is a normal FPG

A

<99

42
Q

what is always the first step in DM treatment

A

diet (carbs and caloric restriction) and exercise ( more than 150min weekly)

43
Q

What is SDOH

A

social determinants of health
access to healthy food, housing, social support, ability to afford meds, etc. need to be considered
barriers to care need to be addressed/remove if any treatment is to be effective

44
Q

what are key patient characteristics that need to be assessed with glycemic management

A

current lifestyle
comorbidities
clinical characteristics (age, HbA1c, weight, etc)
issues such as motivation and depression
cultural and socio-economic context

45
Q

what are treatment complication of DM

A

hypoglycemia
too much insulin or medicine / too much exercise / NOT eating an anticipated scheduled meal

46
Q

what is the BG for hypoglycemia

A

< 50 mg/dL

47
Q

what are the signs/symptoms of hypoglycemia

A

sleepiness, sweating, pallor, lack or coordination, irritability, hunger

48
Q

what is the treatment for hypoglycemia

A

glucose
tabs, icing, candy vs IM injection/IV if unable to protect airway

49
Q

what are the microvascular disease complications of DM

A

retinopathy
nephropathy
neuropathy
also - impaired skin healing

50
Q

what is the treatment for diabetic retinopathy

A

intensive glycemic and blood pressure control
advanced: retinal laser photocoagulation, vitrectomy, vascular endothelial growth factor (VEGF) inhibitors etc.

51
Q

what is the leading cause of chronic kidney disease in the US

A

diabetic nephropathy

52
Q

what is diabetic nephropathy

A

thickening of glomerular basement membrane, mesangial expansion and glomerular sclerosis; causes glomerular hypertension and progressive decline in GFR
systemic HTN may accelerate progression

53
Q

how do you diagnose diabetic nephropathy

A

urinary albumin

54
Q

when is a urine dipstick positive

A

only if protein excretion > 300-500mg/day

55
Q

what is the treatment of diabetic nephropathy

A

intensive glycemic and blood pressure control
ACE or ARB: renal protecting, treat HTN and prevent progression of renal disease
consider nephrology consult/co-management

56
Q

how often is urinary albumin level monitored

A

minimally annually

57
Q

what is diabetic neuropathy

A

result of nerve ischemia: direct effect of hyperglycemia, intracellular metabolic changes that impair nerve function

58
Q

what are the different types of diabetic neuropathy

A

symmetric polyneuropathy (small and large-fiber variants)
autonomic neuropathy
radiculopathy
cranial neuropathy
mononeuropathy

59
Q

what is systemic polyneuropathy

A

most common - affects distal feet and hands (stocking-glove distribution)
paresthesia, dysesthesia, painless loss of touch, vibration, proprioception or temp

60
Q

what is the presentation of small-fiber symmetric polyneuropathy

A

pain, numbness, loss of temperature sensation with preserved vibration and position sense

61
Q

what is the presentation of large-fiber symmetric polyneuropathy

A

muscle weakness, loss of vibration and position sense, lack of DTRs; atrophy of intrinsic muscles of feet (foot drop common)

62
Q

what are signs of autonomic neuropathy

A

orthostatic hypotension
exercise intolerance
resting tachy
dysphagia
N/V due to gastroparesis
constipation and diarrhea etc

63
Q

what are radiculopathies

A

most common proximal L2-L4 nerve roots; pain, weakness, atrophy of LEs (diabetic amyotrophy)
proximal T4-T12 nerve roots, causes abdominal pain (thoracic polyradiculopathy)

64
Q

what are cranial neuropatheis

A

dipolpia, ptosis, an isocoria

65
Q

what are mononeuropathies

A

finger weakness/numbness (median nerve) or foot drop (peroneal nerve) - prone to nerve compressive d/o - CTS
can occur at several places simultaneously

66
Q

how are DM complications managed

A

glycemic control
regular foot care
management for pain

67
Q

what are macrovascular disease associated with DM

A

atherosclerosis of large vessels; hyperinsulinemia, dyslipidemias, hyperglycemia
angina pectoris/MI
TIA/stroke
peripheral arterial disease

68
Q

what is the treatment of macrovascular disease

A

intensive control of atherosclerotic risk factors; multifactorial
normalization of PG, lipids, GP
smoking cessation
ACEi (arb) - renal and cardiovascular management

69
Q

what are diabetic cardiomyopathies

A

atherosclerosis, HTN esp with LVH, microvascular disease, endothelial and autonomic dysfunction, obesity, metabolic disturbances

70
Q

what are infective complications of DM

A

prone to bacterial and fungal infections; AE of hyperglycemia on granulocyte and T-cell function
increased susceptibility to fungal infection
bacterial foot infections (increased osteomyelitis); exacerbated by LE vascular insufficiency, neuropathy

71
Q

What is NAFLD

A

non-alcoholic fatty liver disease
increasingly common in T2DM
mainstay of treatment is diet, exercise and weight loss

72
Q

what are routine screenings for DM

A

foot exam (minimally annually)
retinal exam (annually - min every 2 years)
HbA1c: based on control and disease severity
spot or 24-hr urine (annually with serum creatinine)
cardiac (min annual EKG and lipids, BP every visit)