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825 > DM Pathophysiology > Flashcards

DM Pathophysiology Flashcards

1
Q

Diabetes

A
  • Chronic, metabolic disorder of fat, carb, and protein metabolism
  • Hyperglycemia arising from defects in insulin secretion, action, or both
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2
Q

Type I DM

A
  • B-cell destruction
  • Absolute insulin deficiency
  • 5-10% of DM cases
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3
Q

Type II DM

A
  • Insulin resistance _ relative insulin deficiency

- 90-95% of all DM cases

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4
Q

DM I Pathophysiology

A

Autoimmune cells
destruction of B-cells

Four Features of Disease Progression:

  1. Pre-clinical period: presence of immune markers
  2. Hyperglycemia after 80-90% of B-cells are destroyed due to deficiency of insulin and amylin
  3. Honeymoon phase - transient remission
  4. Established disease
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5
Q

T1DM Autoimmune Markers

A
  • Type I diabetes: immune mediated in >95% of cases
  • Idiopathic in less than 5%
  • GAD65 (70-90%), IAA, ICA512, ZnT8
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6
Q

Insulin Cleavage

A
  • Synthesized as preproinsulin
  • Cleaved to proinsulin
  • Proinsulin split into insulin and C peptide
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7
Q

T2DM Pathophysiologu

A
  • Progressive, heterogeneous disorder with ongoing B-cell failure
  • Relative insulin deficiency
  • Range from severe insulin resistance, minimal insulin secretory defects, primary defect in insulin secretion
  • Majority of patients have glycemic control that deteriorates with time
  • Metabolic disorder
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8
Q

T2DM Development

A
  • Healthy individuals: insulin secretion by pancreatic islet allows for normal glucose disposal into insulin-sensitive tissues
  • Prediabetes: genetic predisposition, over-nutrition, and physical inactivity reduce the response to insulin-stimulated glucose uptake that is compensated for by increasing insulin production
  • Type 2 DM: insulin secretion no longer compensates for increased peripheral insulin demand
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9
Q

T2DM Progression

A
  • Insulin Resistance
  • Increased insulin production
  • Death/burnout of beta cells
  • Reduced or absent insulin
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10
Q

T2DM: Insulin Resistance

A
  • Body cells become less responsive to the insulin we make

- Usually takes a long time to develop (years to decades)

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11
Q

T2DM Beta Cell Burnout

A
  • By the time of T2DM diagnosis, more than 80% of B-cells may be gone
  • Progression doesn’t always occur
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12
Q

Hyperglycemia - Ominous Octet

A
  1. Decreased insulin secretion
  2. Increased glucagon secretion
  3. Increased HGP
  4. Neurotransmitter dysfunction
  5. Decreased glucose uptake
  6. Increased glucose reabsorption
  7. Increased lipolysis
  8. Decreased incretin effect
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13
Q

Egregious Eleven: B-Cell destruction Effects

A
  1. Pancreatic B-Cells
  2. Incretin Effect
  3. Alpha-cell defect
    4-6. Adipose, Muscle, Liver
  4. Brain
  5. Colon/Biome
  6. Immune Dysregulation/inflammation
  7. Stomach/Small Intestine
  8. Kidneys: SGLT2
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14
Q

Pancreatic B-Cells Dysfunction

A
  • Insulin resistant organs: liver, muscle, adipose tissue (increased lipid exposure can lead to B-cell dysfunction)
  • Other organs: brain, colon, immune system
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15
Q

Incretin Effect

A
  • Resistance to the action of glucose-dependent insulinotrophic polypeptide also called gastric inhibitory polypeptide (GIP)
  • B-cell resistance to the stimulatory effect of GIP on insulin secretion
  • Deficiency of GLP-1: resistance to stimulatory effect of GLP-1 on insulin secretion
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16
Q

Alpha-cell Defect

A

-Increased glucagon

17
Q

Adipose, Muscle Liver

A
  • Insulin promotes fuel storage (anabolism) in these tissues
  • Also prevents the breakdown of release of fuel that have already been stored (catabolism)
  • Insulin resistance and inflammation lead to production/release of FFAs and insulin resistance-provoking proinflammatory cytokines in the adipose cells
18
Q

Brain Effects

A
  • May experience insulin resistance like other organs
  • Increased appetite due to decreased GLP-1/GIP
  • Decreased morning dopamine surge
  • Increased sympathetic tone
19
Q

Colon/Biome

A
  • Gut microbiome role in digestion: strengthens immune system, prevents infection
  • Antibiotic use may increase risk of T2DM: kill “good” bacteria allowing for “bad” bacteria to dominate GI tract, alters nutrient absorption/metabolism
  • Associated insulin resistance
20
Q

Stomach/Small Intestine

A
  • Amylin production decreased as a result of B-cell dysfunction: amylin co-secreted with insulin from B-cell
  • Effects of decreased amylin: accelerated gastric emptying, increased glucose absorption in small intestine, corresponding increases in postprandial glucose levels
21
Q

Kidneys Effects

A
  • As blood glucose increases, the kidney begins to reabsorb the glucose so it will not go into urine
  • Up-regulates SGLT-2 protein in kidney to further hyperglycemia
22
Q

Complexities of Diabetes

A
  • Increased insulin resistance
  • Increased hepatic glucose production
  • B-cell failure or destruction
  • Abnormalities in incretin action
  • Enhanced renal SGLT2 activity
  • Abnormalities of glucagon physiology

825 (27 decks)

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