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GIGU Exam 1 > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

Type 1: Age of Onset

A

Peak in early childhood and adolescence

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2
Q

Type 2: Age at Onset

A

Post-pubertal

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3
Q

Type 1: Ketosis at Onset

A

Common

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4
Q

Type 2: Ketosis at Onset

A

Uncommon

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5
Q

Type 1: Family Hx

A

5-10%

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6
Q

Type 2: Family Hx

A

> 50%

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7
Q

Type 1: Pathophysiology

A

Autoimmune disease

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8
Q

Type 2: Pathophysiology

A

Insulin resistance

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9
Q

Type 1: Associated Conditions

A
  • Autoimmune thyroid disease
  • Celiac disease
  • Addison’s disease
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10
Q

Type 2: Associated Conditions

A
  • Obesity
  • Lipid abnormalities
  • PCOS
  • NAFLD
  • Sedentary/inactive
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11
Q

Type 1: Blood Glucose

A

Overtly elevated

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12
Q

Type 2: Blood Glucose

A

Mild to moderate elevation

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13
Q

Type 1: Insulin

A

Absent

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14
Q

Type 2: Insulin

A

Elevated until later in progression

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15
Q

Type 1: C-Peptide

A

Absent

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16
Q

Type 2: C-Peptide

A

Elevated until later in progression

17
Q

Obesity’s Role in Development of T2DM

A
  • Adipose tissue is inflamed and recruits M1 macrophages –> adipose tissue releases more inflamatory markers –> disruption of adipokines –> release of FAs
  • Associated with IL-6 and other pro-inflammatory markers (TNF alpha, IFN gamma, CRP)
18
Q

T2DM stems from an initial ___ ____

A

Insulin resistance

19
Q

Incretin Effect is abolished in:

A

T2DM
- Release of GI peptides is lost and thus insulin release is primarily due to glucose alone

20
Q

Timeline of Insulin Resistance Progressing to T2DM

A

(1) Peripheral systemic insulin resistance
(2) Reactive hyperinsulinemia – postprandial glucose levels are not normal but more insulin is required to do the job (reactive hyperinsulinemia)
(3) Postprandial hyperglycemia
(4) Disrupted response to oral glucose tolerance test
(5) Blunted incretin release
(6) Chronic elevated insulin levels
(7) Mild to moderate chronically elevated glucose levels
(8) Frank hyperglycemia

Timeline of development can be 5-30 years

21
Q

Pre-Diabetes

A

Timeline: -10 years to 0 years (time of Dx)
- Gradual decrease in beta cell function
- Gradual increase in insulin resistance
- Sharp increase in insulin secretion that starts to decrease when near time of dx
- Increasing postprandial glucose levels
- Increasing fasting glucose

22
Q

T1DM: Patient Characteristics

A
  • Skinny
  • Polydipsia
  • Polyuria
  • High blood glucose levels
  • DKA
23
Q

Type 1 DM

A
  • Disease of inadequate insulin secretion
  • T-cell mediated destruction of beta cells, often from autoimmune disease (no insulin or C-Peptide produced)
  • Increased blood glucose, FAs, ketoacids, AAs, increased conversion of FA to Ketoacids
24
Q

Decreased utilization of Ketoacids results in:

A

Diabetic Ketoacidosis (DKA)

25
Q

T1DM: Osmotic Diuresis / Glucosuria

A
  • Increased blood glucose increases filtered load of glucose, exceeds reabsorptive capacity of proximal tubule
  • Water and electrolyte reabsorption also blunted
  • Polyuria and thirst (polydipsia)
26
Q

T1DM: Hyperkalemia (Shift of K+ out of Cells)

A
  • Intracellular concentration of K+ is low
  • Lack of insulin effect on Na/K ATPase
  • Plasma levels may be normal, total K+ is usually low due to polyuria and dehydration
27
Q

Development of T1DM: HLA Class II Alleles

A
  • DQ2/DQ8 found in more than 90% of individuals
  • Heterogenous genotypes DR3/DR4 are most common in children diagnosed prior to age 5
  • HLA Class II that lack Asp57 of the beta chain a
28
Q

Purpose of Insulin Injections

A
  • Goal is to recreate normal physiology (basal and bolus insulin)
  • Timing insulin dose to meal consumption helps mimic physiological response
29
Q

T1DM: Environmental Causes

A
  • Obesity
  • Viral infections
  • Too few childhood infections dampening the effectiveness of the immune system
  • Wheat gluten
  • Vitamin D deficiency
  • Early exposure to cows milk
30
Q

Complications from DM:

A
  • Increased risk of CVD and ischemic vascular disease
  • Increased risk of non-fatty liver disease (NFLD)
  • Steatohepatitis
  • Increased risk of kidney failure
  • Risk of blindness
  • Skin ulcers and amputations
  • Reduced wound healing

GIGU Exam 1 (14 decks)

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