Type 1 Diabetes Flashcards Preview

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Flashcards in Type 1 Diabetes Deck (63)
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1
Q

When glucose stimulates insulin secretion, you get regulated secretion of insulin in the form of _____

A

insulin and c peptide (96%) and proinsulin/intermediates (4%)

2
Q

Insulin secretory vesicles

A

10k granules/beta cell

3
Q

Secretory granules contain insulin and ____

A

zinc, proinsulin, proteolytic enzymes, iapp (islet amyloid polypeptide)

4
Q

Glucose is taken up by the beta cell via ___

A

Glut2

5
Q

Rate limiting step of glucose in beta cell

A

glucokinase

6
Q

Insulin vesicle release are dependent on the contribution of ____ form voltage gated channels.

A

Calcium

7
Q

______ is used diagnosticlaly to determine if someone is secreting insulin

A

c-peptide release

8
Q

Insulin release in beta cell

A

glucose –> glut 2–> glycolysis –>atp/adp ratio increase –> atp sensitive potassium channel –> voltage gated ca channel –> calcium –> vesicle release

9
Q

Stimulators of insulin secretion

A

nutrient load, vagus nerve (inhibited by sympathetics, cephalic phase sight/smell of food, gut hormons (GLP1/GIP)

10
Q

Inhibitors of insulin secretion

A

starvation/hypoglycemia, glucagon, epinephrine, growth hormone, cortisol

11
Q

The major regulator of insulin secretion is ___

A

glucose

12
Q

If secretory stimulus persists, a ___ response follows which involves active synthesis of insulin in the beta cells

A

second/delayed

13
Q

sulfonylureas stimulate/inhibit insulin secretion

A

stimulate

14
Q

Insulin is a ____ hormone

A

anabolic

15
Q

Principal metabolic function of insulin

A

increase rate of glucose transport into select cells in body

16
Q

Type 1 diabetes subtypes

A

1a = autoimmune, 1b = non-autoimmune

17
Q

Most T1D are auto/non auto immune

A

autoimmune

18
Q

Gestational diabetes is a precursor of ____

A

t2d

19
Q

LADA

A

latent auto-immune diabetes of adulthood –> adult age at diagnosis, initially appears as nonobese t2d –> initially controlled with meal planning with or without oral pills –> low c peptide concentration and antibody psotiive

20
Q

monogenic diabetes

A

characterized by pancreatic beta cell dysfunction –> autosomal dominant

21
Q

T1D or T2D? absolute insulin deficiency

A

t1d

22
Q

T1D or T2D? abrupt onset

A

t1d

23
Q

T1D or T2D? life long insulin injection

A

t1d

24
Q

T1D or T2D? propensity for development of dka

A

t1d

25
Q

T1D or T2D? predominant under 30 yrs old

A

t1d

26
Q

T1D or T2D? insulin resistance with relative insulin deficiency

A

t2d

27
Q

T1D or T2D? gradual onset of hyperglycemia with decline of beta cell function

A

t2d –> initially silent

28
Q

T1D or T2D? oral treatment

A

t2d

29
Q

T1D or T2D? hhnk

A

t2d –> hyperosmolar hyperglycemic non-ketosis

30
Q

T1D or T2D? dka

A

either

31
Q

T1D or T2D? family history rare

A

t1d

32
Q

T1D or T2D? family history common

A

t2d

33
Q

T1D or T2D? first functional bnormality is decrease in insulin secretion

A

t1d

34
Q

T1D or T2D? first functional abnormality is decreased insulin secretion and decreased response to insulin

A

t2d

35
Q

T1D or T2D? insulinitis

A

t1d

36
Q

T1D or T2D? amyloid deposition, fibrosis, beta cell mass reduction

A

t2d

37
Q

T1D or T2D? absence of beta cells, increase in alpha and gamma cells

A

t1d

38
Q

Dx of t2d

A

diabetes symptoms + glucose >200 or fasting glucose >126 or 2 hour glucose ogtt >200, a1c > 6.5

39
Q

HbA1c

A

non enzymatic glycosylation of hemoglobin AA residues – accumulates over 2-3 lifespan of rbc’s

40
Q

T/F HbA1c can be used for dx

A

T

41
Q

highest risk ethnicity for t1d

A

n europe

42
Q

peak ages for onset of t1d

A

5-7rs and onset of puberty

43
Q

T/F t1d onset is more common in winter

A

T

44
Q

Risk factor for t1d or not? viral infection

A

yes

45
Q

Risk factor for t1d or not? immunization

A

yes

46
Q

Risk factor for t1d or not? cows milk

A

yes

47
Q

Risk factor for t1d or not? high socioeconomic status

A

yes

48
Q

Risk factor for t1d or not? obesity

A

yes

49
Q

Risk factor for t1d or not? d deficiency

A

yes

50
Q

Risk factor for t1d or not? low birthweight

A

no

51
Q

Ab measured during preclinical t1d

A

islent cell antibodies, insulin autoantibodies, antibodies to glutamic acid decarboxylase (GAD), antibodies to tyrosine phosphatase like proteins such as insulinoma associated protein (IA2)

52
Q

The ____ has been identified as a candidate t1d autoantigen since 60-80% have autoantibodies to it.

A

ZnT8 cation efflux zinc transporter

53
Q

Pathogenesis of t1d

A

chronic auto-immune insulitis –> high risk MHC class II genes encoding HLADQ induce presentation of peptides form islet autoantigens to CD4 and CD8 –> destruction of beta cells –> cellular infiltrate –> destruction of beta cells but not alpha or gamma cells

54
Q

T/F there is often a concurrence of other auto-immunities with t1d

A

T

55
Q

Tx of T1d

A

insulin replacement, education, adjust doses according to cho intake, exercise, blood glucose profile, test glucose levels, screen for complications

56
Q

The ______ approach involves basal insulin to meet the insulin requirement to suppress hepatic glucose production between meals and bolus insulin to meet the insulin requirement after eating.

A

basal-bolus approach

57
Q

Dx? Low blood pressure, high heart rate, plasma glucose 550, urine ketones +

A

type 1d + dka

58
Q

DKA

A

no insulin –> starvation –>

  1. liver production of glucose –> glucosuria –> polyuria –> dehydration
  2. muscle –. increase plasma glucose and muscle wasting –> weight loss
  3. adipose –> increase plasma FFA –> increase plasma Beta hydroxybutyrate and acetoacetate –>acidosis
59
Q

Acute problems with DKA

A

hyperosmolar dehydration and acidosis

60
Q

DKA tx adverse events

A

cerebral edema, hypokalemia

61
Q

Tx of DKA

A

insulin + fluid/electrolyte

62
Q

hypoglycemia

A

most common in t1d from overdose of insulin

63
Q

relative hypoglycemia

A

patients with chronically high glucose suddenly have a reduction to normal or less high glucose