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Diabetes Flashcards

1
Q

Diabetes (definition)

A
  • A chronic disorder characterized by insulin deficiency and glucagon excess

Results in:

  1. Hyperglycemia due to decreased glucose uptake
  2. Increased protein catabolism
  3. Increased lipolysis

Increased risk of:

  1. Opthalmic disease
  2. Renal disease
  3. Neurologic disease
  4. Atherosclerotic vascular disease
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2
Q

Chronic Complications of Diabetes

A
  1. Macrovascular
    » Coronary artery disease
    » Cerebrovascular disease
    » Peripheral artery disease
  2. Microvascular
    » Retinopathy
    » Nephropathy
    » Neuropathy
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3
Q

Diabetes Mellitus Type 1

  • aka Insulin-dependent diabetes
  • aka juvenile onset diabetes

** DO NOT USE AGE AS A DIFFERENTIAL DIAGNOSTIC CRITERIA

A
  • Due autoimmune destruction of Beta cells, resulting in complete (or nearly complete) insulin deficiency
  • age of onset: < 30
  • no association with obesity
  • clinical presentation: acute or subacute
  • Ketosis is common
  • weak genetic predisposition
  • assoc w/ HLA-DR3 and 4
  • “Honeymoon Period”: at time of presentation, patient may still make insulin for
    a number of years

Histology:
- Leukocytic infiltrate in Islets
- Depletion of Beta-cells only; other islet
cells normal
- Years later, no inflammation (“insulitis”) seen

Treatment: Intensive insulin therapy

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4
Q

Diabetes Mellitus Type 2

  • aka non-insulin-dependent diabetes
  • aka adult onset diabetes
A

» Due to combination of insulin resistance
and progressive pancreatic beta cell failure/insulin deficiency
- age of onset: > 40
- Associated with obesity
- Clinical presentation: acute, progressive, or asymptomatic
- Ketosis is rare
- strong genetic predisposition
- no association with HLA system
- Histology: Amyloid (AIAPP) deposit in Islets

Treatment:

  • Diet and exercise
  • Oral agents
  • Insulin
  • Injected non-insulin agents
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5
Q

Gestational Diabetes

A

» Mild hyperglycemia in pregnancy, possibly due to poor insulin receptor function
• Develops in 3rd trimester
• Asymptomatic, diagnosed by OGTT with
specific criteria

May have negative impact on the fetus:

  • Macrosomia: large infant size; can lead to birth trauma
  • hypoglycemia
  • hyperbilirubinemia
  • hypocalcemia
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6
Q

Pancreatic Destruction

A
  • conditions where all pancreatic cells are destroyed (not just Beta cells as in Type 1)
  • e.g., » Chronic pancreatitis, hemochromatosis
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7
Q

Acquired severe insulin resistance

A

» Increases in Glucocorticoid: Cushing syndrome, acromegaly, glucagonoma, pheochromocytoma
» Anti-insulin receptor blocking antibody
» Drugs: glucocorticoids

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8
Q

Genetic defects in insulin action

A

» Insulin receptor mutations

» Lipoatrophic diabetes

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9
Q

Maturity onset diabetes of the young

MODY

A

» Autosomal dominant syndromes due to
single gene mutations affecting beta cell
function

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10
Q

Progressive development of Type 1 Diabetes

A
  1. Genetic predisposition
  2. Triggering event
  3. Active autoimmunity: You need to destroy 80-90% of islets until you see actual changes in glucose intolerance
  4. Progressive loss of glucose-stimulated
    insulin secretion
  5. Overt diabetes
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11
Q

Possible Environmental triggers for Type 1 Diabetes

A 
• Viral
» Rubella
» Coxsackie B4 or B5
» Cytomegalovirus
» Echovirus
• Dietary
» Infant bovine milk consumption
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12
Q

Major Antigens in Type 1 Diabetes

A
  • Glutamic acid decarboxylase (GAD-65)
  • Protein tyrosine phosphatase 2 (IA-2)
  • Insulin
  • Zinc transporter 8 (ZnT8, Slc30A8)
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13
Q

Insulin Resistance

A

Definition: Impaired cellular responses to
the physiological effects of insulin, i.e., decreased glucose uptake by muscle in response to insulin.
• A core defect in type 2 diabetes (92%)
• If pancreatic beta cell function is normal,
insulin resistance may be associated with
hyperinsulinism rather than hyperglycemia

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14
Q

Progression of Type 2 Diabetes

A
  • Genetics & Evironment: initial defect is insulin resistance
  • compensation with increased pancreatic beta cell activity and hyperinsulinemia
  • progressive impairment in beta cell function
  • impaired glucose tolerance
  • frank type 2 diabetes
  • uncontrolled hyperglycemia
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15
Q

Potential causes of Beta cell failure in Type 2 Diabetes

A 
• Genetic factors
• Reduced Beta-cell mass
   » Apoptosis
   » Reduced proliferation
   » Amyloid deposition
• Beta-cell exhaustion
• Glucotoxicity
• Lipotoxicity
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16
Q

Allele associated with loss of insulin secretion over time

A

TCF7L2 T allele

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17
Q

What type of fat topography is more associated with insulin resistance?

A
  • Apple (vs. pear) shaped

- High amount of VISCERAL INTRA-ABDOMINAL fat

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18
Q

Diagnostic Criteria for Diabetes

A

Meet one of the following:

  1. Fasting plasma glucose >126 mg/dl
  2. HbA1C > 6.5%
  3. Random plasma glucose > 200 mg/dl,
    together with symptoms of
    hyperglycemia (polyuria, polydipsia,
    weight loss, blurred vision, etc.)
  4. 2 hour plasma glucose >200 during 75 g
    OGTT (Oral Glucose Tolerance Test)
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19
Q

Prediabetes

A
  1. Impaired Fasting Glucose: Between 100 and 125 mg/dl

2. Intermediate postprandial glucose levels (Impaired Glucose Tolerance) between 140-200 mg/dl

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20
Q

Risk Factors for Type 2 Diabetes

A
  • Family history of diabetes (1st degree relatives)
  • Obesity
  • Sedentary lifestyle
  • Ethnic background (African American or Hispanic)
  • Previously identified IGT or IFG (“Pre-diabetes”)
  • History of gestational diabetes
  • Polycystic ovary syndrome (PCOS)
  • Dyslipidemia (increased Triglyceride, low HDL, small LDL particle size)
  • Hypertension
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21
Q

Clinical Presentation of Type 2 Diabetes

A 
• Symptomatic hyperglycemia: poly’s,
rapid weight loss, blurred vision (changed water content of lens)
• Asymptomatic screening
• Recurrent infections: UTI, cellulitis,
vaginal yeast
• Complications
   » Atherosclerotic vascular disease
   » Microvascular
   » Neuropathy
22
Q

CLINICAL PRESENTATIONS OF HYPERGLYCEMIA

A
  • Polyuria: very high glucose levels will result in osmotic diuresis
  • Polydipsia
  • Dehydration
  • Weight loss
  • Fatigue
  • Blurred vision
  • Infection: Skin, urinary tract, vaginal yeast infection
23
Q

Diabetic Ketoacidosis: Definition and Mech

A
  • Complication of diabetes (usually type 1), resulting from increased insulin demand during increased stress (e.g., infection)
  • insulin is inadequate to allow cells to use glucose, forcing metabolism of fatty acids for energy

Mech: Excess fat breakdown and increased ketogenesis from FFAs –> made into ketone bodies (Beta-hydroxybutryate > acetoacetate)

Hormonal:
» Absolute insulin deficiency
» Increased glucagon

Adipose tissue:
» Increased lipolysis: increased FFA to liver

Liver:
» Increased Beta-oxidation of FFA to Acetyl-CoA
» Increased ketone formation (acetoacetate,
Beta-hydroxybutyrate, acetone)
» Increased gluconeogenesis (and
glycogenolysis)

24
Q

Clinical Presentation of Diabetic Ketoacidosis

A

• Hyperglycemia
- Signs of dehydration: due to osmotic diuresis
» Tachycardia, hypotension, poor skin turgor, etc
• Kussmaul breathing: form of hyperventilation, with very deep in-and-out breathing to get rid of excess CO2
• “Fruity” breath odor
• Impaired consciousness
• Abdominal pain
• Nausea and vomiting

Labs:

  • Increased plasma FFAs
  • Increased plasma and urine ketones
  • anion-gap metabolic acidosis
  • hypokalemia
25
``` HYPERGLYCEMIC HYPEROSMOLAR NONKETOTIC SYNDROME (HONS) ``` aka Hyperosmotic Coma
- When insulin is present but is inadequate for demand, glucose increases without development of ketoacidosis • Differentiated from DKA by: » Occurs in type 2 diabetes » Ketone production absent » Higher plasma glucose » Greater increased serum osmolarity • Water loss is greater in HONS than in DKA. Coma and death in HONS is associated with increased plasma osmolarity • Major risk factor for HONS is inability to maintain adequate hydration. For example, an elderly impaired patient
26
Basal/Bolus Insulin Concept for Intensive Insulin Therapy
Basal Insulin: » Suppresses glucose production between meals and overnight » Nearly constant levels » 50% of daily needs Bolus Insulin (mealtime or prandial) » Limits hyperglycemia after meals » Immediate rise and sharp peak at 1 hour » 10% to 20% of daily requirement at each meal
27
Acute Metabolic Complications of Diabetes
1. Hypoglycemic Coma: from too much insulin 2. Hyperosmolar Hyperglycemic Syndrome (HHS /HHNK) 3. Diabetic Ketoacidosis
28
Chronic Diabetic Complications
1. Microvascular Complications: hyperglycemia is causative - Retinopathy: cause of blindness - Nephropathy: leading cause of end stage renal disease 2. Diabetic Neuropathy: leading cause of non-traumatic lower extremity amputations 3. Macrovascular Complications: Hyperglycemia is a causative risk factor - Coronary artery disease - Peripheral vascular disease
29
Non-Proliferative Diabetic Retinopathy
- EARLY change in diabetes - ASYMPTOMATIC Clinical findings: - Mild: Microaneurysms (weakened areas of blebs and balloons) in the choroid (not the vitreous) - Moderate/severe: - Microaneurysms - Dot-blot hemorrhages - Hard exudates - Soft exudates (cotton wool spots)
30
Proliferative Diabetic Retinopathy
- LATER change in diabetes, progressing from non-prliferative retinopathy Clinical findings: - VEGF increases, causing neovascularization - Intravitreous hemorrhage - Cotton wool spots from exudates Symptoms: - Can be asymptomatic - Rreduced vision or floaters - Sudden loss of vision
31
Treatments for Retinopathy
1. Laser photocoagulation. 2. Intra-occular injection of anti-inflammatory agents. - corticosteroids - Bevacizumab (Avastin): anti-VEGF antibody 3. Surgery: Vitrectomy
32
Diabetic Nephropathy
HALLMARK: KIMMELSTEIN-WILSON NODULES (due to glomerulosclerosis) - Testing: Microalbumin in the urine (MICROALBUMINURIA in stage 2) - Goal: Catch before any rise in creatinine (indicates kidney failure; occurs during Stage 4-5 diabetes) - Quantification: Microalbumin to Creatinine ratio (24 hour collection) Stages: 1. Elevated glomerular filtration rate (GFR). 2. GFR elevated or falls to normal; Microalbuminuria develops (screen all patients yearly). 3. Clinical albuminuria (urine "dipstick positive). Hypertension develops (if not preexisting). 4. BUN and creatinine begin to rise; GFR decreases about 10% annually. 5. (end-stage renal disease, ESRD)— GFR has fallen to approximately <10 mL/min; Dialysis and/or kidney transplantation is needed - Almost all macro-proteinuric patients develop end stage renal disease or die prematurely of cardiovascular disease
33
Prevention of Diabetic Nephropathy
1. Optimal Glycemic control 2. Hypertension control <130/80 - Especially ACE inhibitors (ACE-I) and angiotensin receptor blocking agents (ARB) 3. Protein Restriction
34
Diabetic Peripheral Neuropathy | Symmetrical Polyneuropathy
- most common diabetic neuropathy - Pain, burning, paresthesia, hyperesthesia, allodynia - Numbness, heaviness, feels like a brick - Loss of proprioception - Unsteady gait - Stocking-Glove distribution - Longest nerves affected first
35
Charcot's Arthropathy
- Complication of peripheral neuropathy, where there is progressive degeneration of a weight bearing joint, a process marked by bony destruction, bone resorption, and eventual deformity
36
Pathophysiology of Diabetic Foot Ulceration
1. Neuropathy - Increased risk of traumatic damage - Foot deformity: abnormal pressure distribution and callus formation 2. Peripheral vascular disease - Poor tissue oxygenation 3. Hyperglycemia - Poor wound healing - Immune dysfunction
37
Autonomic Neuropathies
Gastrointestinal - Constipation and/or Diarrhea - Gastroparesis: Early satiety; Nausea and Vomiting; Unintentional weight loss Cardiovascular - Resting tachycardia - Orthostatic hypotension Genitourinary - Urinary hesitancy - Urinary incontinence (overflow incontinence) - Neurogenic bladder - Erectile dysfunction Other: Anhydrosis, gustatory sweating, abnormal pupillary reflexes
38
Mononeuropathy
- Asymmetrical - Onset often painful - Often reversible Mononeuropathy sites - Cranial nerves - Truncal radiculopathies - Femoral neuropathy
39
How does elevated blood sugar/hyperglycemia cause cellular damage?
1. Oxidative Stress: overloading mitochondria 2. Activation of Intracellular Second Messenger Pathways: PKC Activation (Protein Kinase C), which increases activity of various growth factors 3. Disruption of Intracellular Energy Balance: The Polyol Pathway: causes osmotic stress, possibly leading to cataracts 4. AGE (Advanced Glycation End-products) Prevention: maintain tight glycemic control (60-100 mg/dL) Often damage tissues with GLUT2 (high capacity, low affinity) or GLUT3 (high affinity) transporters - GLUT2: pancreatic beta cells, kidney, liver, small intestine - GLUT3: neurons and placenta
40
Glycosylation vs. Advanced Glycation End-products
Glycosylation - a nonenzymatic reversible process, e.g., HbA1c AGE: Formation of irreversible oxidative cross-links
41
True or False: Type 2 diabetes is as strong a risk factor for MI as having had a previous MI
True
42
Metabolic Syndrome
- constellation of findings that predicts Coronary artery disease in diabetes 3 or more of the following: 1. Waistline Circumference: ≥ 35 inches for women or ≥ 40 inches for men. 2. High Triglyceride Level: ≥ 150 mg/dL (or being on medicine to treat high triglycerides). 3. Low HDL Cholesterol Level: < 50 mg/dL for women and < 40 mg/dL for men (or being on medicine to treat low HDL cholesterol). 4. High Blood Pressure: ≥ 130/85 mmHg (or being on medicine to treat high blood pressure). 5. High Fasting Blood Sugar: ≥ 100 mg/dL (or being on medicine to treat high blood sugar)
43
Glycosylated Hemoglobin
- “Gold Standard” test of diabetes control | - Gives an index of control over the preceding 3 months (reflecting the 120 day average lifespan of an erythrocyte).
44
Reducing CV Risk in Patients With Diabetes
1. Reduce HTN: BP 40 mg/dl 5. Give aspirin: 75-325 mg/d ASA (age >40) 6. Smoking cessation
45
Acanthosis Nigricans
Darkening of the skin due to Insulin resistance/hyperinsulinemia - indicates risk of pre-diabetes/diabetes
46
Glucose Measurement
- Typically uses Glucose Oxidase by fingerstick - Results can be affected by oxygen content and vitamin C - Results often inaccurate in critically ill patients
47
Oral Glucose Tolerance Test
- - Administration of a large amount of glucose tests β-cells' ability to increase insulin production - The test is not often used to diagnose diabetes, except during pregnancy, because it is less reproducible than fasting glucose or hemoglobin A1c
48
Central Diabetes Insipidus
- ADH deficiency, due to hypothalamic or posterior pituitary pathology - results in loss of free water Clinical features: - polyuria and polydipsia - Hypernatremia and high serum osmolality - Low urin osmolality Water deprivation test: fails to increase urine osmolality Treatment: DESMOPRESSIN (ADH analog)
49
Nephrogenic Diabetes Insipidus
- impaired renal response to ADH - due to inherited mutations or drugs (lithium, demeclocycline) - clinical features similar to central diabtes insipidus, but NO RESPONSE to Desmopressin
50
Sorbitol
- In some cells (brain, lens, nerve), glucose can accumulate in cells in the absence of insulin. - Glucose can be metabolized by aldose reductase, producing sorbitol. - Sorbitol accumulation affects cell signaling and electrolyte pumps. - This pathway has been suspected of causing peripheral neuropathy and may contribute to retinal aneurysm formation

Endocrinology (11 decks)

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