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GIR Test 1 > B5.001 - Big Case DM2 > Flashcards

B5.001 - Big Case DM2 Flashcards

1
Q

What is acanthosis nigricans

A

a common condition characterized by velvety, hyperpigmented plaques on skin. Esp. neck and axillae

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2
Q

pathophys of acanthosis nigricans

A

insulin resistance and hyperinsulinemia plays a role in the development of acanthosis nirgricans. Elevated levels of insulin may stimulate keratinocyte and dermal fibroblast proliferation via interaction with IGFR1 resulting in the plaque like lesions that typify the disorder

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3
Q

recommendations for diabetes screening

A

beginning at 45 at least every 3 years

screen more frequently if BMI >25 and person has 1 other risk factor

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4
Q

risk factors for diabetes

A 
family Hx (1st degree relative)
High risk race
history of gestational diabetes or delivery of baby >9lb
polycystic ovary syndrome
HTN
HDL <35, TG >250 
Hx of CVD
sedintary
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5
Q

normal HbA1c, IFG or IGT, T2DM

A

normal <5.7
IFG or IGT 5.7-6.4
T2DM >6.5

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6
Q

fasting plasma glucose level
normal
IFG or IGT
T2DM

A

normal <100
IFG or IGT 100-125
T2DM >126

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7
Q

OGTT normal, IFG/IGT, T2Dm

A

normal <140
IFG/IGT 140-199
T2DM >200

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8
Q

what is the best way to prevent progression to T2DM

A

Lifestyle changes

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9
Q

what are the 3 major components of progression to T2DM

A

Impaired incretin action
insulin resistance
relative insulin deficiency

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10
Q

describe the general role of obesity in development of insulin resistance

A

abdominal adipose tissue is more metabolically active than subcutaneous fat
increased release of FFA, TNF-alpha and resistin leading to proinflammatory state and insulin resistance

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11
Q

definition of metabolic syndrome

A 
abdominal obesity, waist circumference >40, women >35
TGs >150
HDL-C <40, <50
blood pressure >135/85
fasting glucose >100
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12
Q

role of beta cells in T2DM

A

reduction in number of Bcells
pancreas cant renew B cells after 30 yo
glucolipotoxicity and amyloid deposition result in B cell apoptosis through oxidative and endoplasmic reticulum stress

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13
Q

describe the role of alpha cells in T2DM

A

abnormal glucagon released by alpha cells
elevated fasting glucose
non suppression after meal ingestion

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14
Q

how does sympathetic and parasympathetic NS control glucose metabolism

A

directly through neuronal input

indirectly through circulation to affect release of insulin and glucagon and production of hepatic glucose

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15
Q

other than SYM and PARA what affects glucose metabolism

A

vagus nerve

hypothalamus

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16
Q

what is C peptide

A

a peptide made along with insulin, more stable than insulin so a better marker for insulin production

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17
Q

what does incretin do

A

a substance that stimulates insulin secretion

released by gut in response to food

18
Q

what are 2 incretins

A

GLP-1

GIP

19
Q

what happens to incretins in T2DM

A

plasma levels of GLP-1 are diminished
the contributes to rise in plasma glucagon secretion and impaired suppression of hepatic glucose production that occurs after a meal
GIP less able to stimulate glucose dependent insulin secretion

20
Q

role of alpha cells in T2DM

A

elevated secretion of glucagon
leads to markedly increased rate of hepatic glucose production
possible liver HS to stimulatory effect of glucagon in hepatic gluconeogenesis

21
Q

role of GLP-1 in liver, brain, pancreas, stomach, beta cell

A

liver - less glucagon = less hepatic glucose output
brain - promotes satiety and reduction of appetite
pancreas - alpha cell decreases post meal glucagon secretion
stomach - slows gastric emptying
beta cell - increases insulin secretion

22
Q

what degrades GLP-1

A

DDP-4

23
Q

what is DDP-4

A

ubiquitous serine protease
high levels in lumen of intestine, liver, lung, kidney
membrane bound and free circulating form
degrades GLP-1, GIP

24
Q

what type of cell expresses DPP-4

A

on surface of T cells, T cell activation and other immunological responses

25
Q

what drug is used for monotherapy in T2DM

A

metformin

26
Q

complications of T2DM

A

hyper/hypoglycemia
macrocirculation- atherosclerosis
microcirculation - basement membrane of small blood vessels and capillaries

27
Q

what does T2DM affect cardiovascularly

A

increased risk of MI, CHF, major source of morbidity

28
Q

describe diabetic nephropathy and how to diagnose

A

glomerulosclerosis

first indicator microalbuminuria

29
Q

diabetic retinopathy

A

progressive irreversible vision loss

pools of blood or hemorrhages on the retina of an eye are visible

30
Q

what is non proliferative v proliferative diabetic retinopathy

A

non proliferative - aneurysm, hard exudate, hemorrhage

proliferative - growth of abnormal blood vessels due to ischemia

31
Q

sensory motor polyneuropathy

A 
aka peripheral neuropathy
primarily lower extremities
decreased deep tendon reflexes
numb feet
decreased proprioception and sensation
unsteady gait
increased risk of foot injury
32
Q

what is autonomic neuropathy

A

can affect almost any system

affects autonomic nervous system

33
Q

treatment for diabetic neuropathy

A

best treatment is prevention with adequate glycemic control

34
Q

how does DM predispose to infection

A

normal inflammatory response is diminished

slower than normal healing

35
Q

describe how DM leads to high risk foot infections

A

neuropathy leads to decreased pain sensation –> dec. pressure sensation–> increased dryness –> increased fissures

36
Q

describe the process of peripheral vascular disease

A

decreased circulation –> decreased WBC –> decreased O2 –> poor wound healing –> decreased antibiotic function –> gangrene

37
Q

screening for retinopathy

A

dilated eye exam
IV fluorescein angiography
optical coherence imaging

38
Q

screening for nephropathy

A

urine micralbumin

39
Q

neuropathy screening

A

monofilament testing

40
Q

screening for dyslipidemia

A

fasting lipid profiles, at least annually

41
Q

3 components for prevention of complications

A
  1. good glycemic control
  2. lower risk of other factors like smoking and activity levels
  3. having routine screening

GIR Test 1 (15 decks)

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