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DEMS Unit 2 > Type 1 Diabeetus > Flashcards

Type 1 Diabeetus Flashcards

1
Q

Pre-diabeetus

A
  • High glucose that causes macrovascular disease (heart attacks, stroke, etc)
  • Fasting: 100-126 mg/dL (5 mmolar)
  • OGTT: 140-200 mg/dL
  • HbA1c: 5.7-6.4%

10% per year progress to diabeetus

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2
Q

Normal blood glucose levels

A
  • Fasting: 100

- OGTT:

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3
Q

Types of diabeetus

A
  1. T1D
  2. T2D
  3. Gestational DM - diagnosed based upon effects on the baby (have a big baby = more C-sections, shoulder dislocations, etc)
  4. Pancreatic DM
  5. Monogenic DM
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4
Q

T1D patient

A
  • Peeing every 1 to 2 hours
  • Fruity breath (ER for DKA)
  • More realistic scale is between 70-180 mg/dL for ppl with T1D
  • Night time blood sugar mid 100s (140-150) to not have Sx
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5
Q

Monitoring blood sugar

A
  • continuous monitor

- test strips from fingerprick

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6
Q

How to handle patients with DM

A
  • Manage expectations
  • Disease of education (what do you like to do? Adjust accordingly)
  • Low is worse than high, but don’t stay too high too long
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7
Q

What % of beta cells left when clinical onset of T1D?

A

10-20% of beta cells left

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8
Q

T1D

A
  • common and increasing T cell mediated autoimmune disease
  • assoc. with other autoimmune diseases
  • predictable based upon autoantibodies to islets
  • environmental determinants unknown
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9
Q

Incidence and prevalence of T1D

A
  • General population 1:300 T1D by age 20
  • 1st degree relative 1:20
  • High genetic risk (HLA genes) 1:15
  • Genes and FDR 1:4 or 1:2
  • Monozygotic twins 1:3 to 1:1

If care for 2000 peds patients, 3-6 will have diabetes

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10
Q

What are the highest odds ratios for developing T1D?

A
  • HLA genes
  • Insulin genes

(Note that some HLA genes are protective, and increased insulin expression in thymus is protective)

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11
Q

Linkage allele

A

Things that always go together (like DQ and DR in the HLA)

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12
Q

Classes of HLA

A

Class I
Class II
Class III

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13
Q

Markers of immune system response to beta-cell & markers of metabolic changes

A

Immune system:
- islet autoantibodies - insulin, IA-2, GAD65,
ZnT8
- T Cell response

Metabolic changes:

  • IV tolerance test
  • OGTT
  • Mixed tolerance test
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14
Q

Structure of insulin release

A
  1. Beta cell sense glucose
  2. Release insulin (hexamer around a zinc)
  3. Islet antigen 2 potentiates release
    T-cells can target anything in this pathway
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15
Q

DAISY study

A
  • Approximately age 8: GAD, ICA512 and mIAA become positive (develop antibodies) and 5 years later kid has diabetes
  • The more antibodies you had, the more likely to develop diabetes
  • If have 2 or more islet autoantibodies, you will 100% develop diabetes when followed long enough
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16
Q

Pancreatic pathology

A
  • not well biopsied
    1. Not everything is abnormal, patchy and spread out
    2. Can have functioning islets next to atrophied islets w/o beta cells
17
Q

Potential environmental triggers of T1D

A
  1. Infections - it is not due to immunization
  2. Diet
  3. Weight
  4. Hygiene hypothesis
18
Q

Accelerator hypothesis

A
  • The increase in T1D incidence has occurred parallel to the increase in obesity
  • Hypothesis: obesity causes beta-cell stress and results in exposure of beta-cell antigens to immune system (not the case)
19
Q

Hygiene Hypothesis

A
  • Hypothesis: lack of immune stimulation at a young age suppresses natural immune system development leading to more allergies & autoimmune disorders
  • We are too clean!
20
Q

LADA or Type 1.5 diabetes

A

Can have autoimmune component and can have insulin resistance, so it is a combo of the two main types of DM.

12% of T2D had autoantibodies at the time of diagnosis

Definition:

  • Age 30-70 at time of diagnosis
  • At least 6 mo. of non-insulin required therapy
  • Presence of diabetes associated autoantibodies
21
Q

Tx of T1D

A
  1. Decreased glucose transport into cells via GLUT4
  2. Increased glucose production
    - Glycogen
    - Gluconeogenesis
  3. Increased activity of hormone sensitive lipase
    - mobilization of FFA
    - B-hydroxybuterate and acetoacetate
22
Q

Primary Prevention (genetically at risk)

A

Goal: prevent development of antibodies and DM
Interventions must be very safe and minimal risk because kids are so young

  • having hydrolyzed formula did not change whether or not you developed autoantibodies
23
Q

Secondary prevention

A

Goal: stop progression to clinical disease (past just a genetic risk)

  • Parenteral insulin given: does not delay development of T1D
  • Oral insulin because gut is lymphoid organ: may reduce if you have autoAbs
24
Q

How does oral tolerance work?

A

Get more Tregs

25
Q

Tertiary therapy

A

Goal: Control clinical condition

  • intensive vs. conventional therapy on B-cell function: makes a big difference because you preserve beta cell function for longer. Less progression to retinopathy
  • anti-CD3 to kill T-cells; no significant infections. Did not meet primary end points, but if used in children or early on in diagnosis, then you seem to do better. Used in prevention (so people that don’t yet have diabetes can have benefit)
  • Abatacept: selectively modulates co-stimulatory molecule via CD86:26 pathway

VERY good thing to make some of your own insulin

26
Q

What are thresholds for diagnosing diabeetus

A
  • Increased glucose to the point that it causes microvascular disease
  • Fasting glucose > 126 mg/dL
  • Oral glucose load test (OGTT) 75g, 2 hrs later > 200 mg/dL
  • Random blood sugar and symptoms > 200 mg/dL
  • HbA1C > 6.5%

DEMS Unit 2 (19 decks)

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