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Endocrinology > Diabetes > Flashcards

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
Q 
HYPERGLYCEMIC HYPEROSMOLAR
NONKETOTIC SYNDROME (HONS)

aka Hyperosmotic Coma

A
  • 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
Q

Basal/Bolus Insulin Concept for Intensive Insulin Therapy

A

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
Q

Acute Metabolic Complications of Diabetes

A
  1. Hypoglycemic Coma: from too much insulin
  2. Hyperosmolar Hyperglycemic Syndrome (HHS /HHNK)
  3. Diabetic Ketoacidosis
28
Q

Chronic Diabetic Complications

A
  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
Q

Non-Proliferative Diabetic Retinopathy

A
  • 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
Q

Proliferative Diabetic Retinopathy

A
  • 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
Q

Treatments for Retinopathy

A
  1. Laser photocoagulation.
  2. Intra-occular injection of anti-inflammatory agents.
    - corticosteroids
    - Bevacizumab (Avastin): anti-VEGF antibody
  3. Surgery: Vitrectomy
32
Q

Diabetic Nephropathy

A

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
Q

Prevention of Diabetic Nephropathy

A
  1. Optimal Glycemic control
  2. Hypertension control <130/80
    - Especially ACE inhibitors (ACE-I) and angiotensin receptor blocking agents (ARB)
  3. Protein Restriction
34
Q

Diabetic Peripheral Neuropathy

Symmetrical Polyneuropathy

A
  • 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
Q

Charcot’s Arthropathy

A
  • 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
Q

Pathophysiology of Diabetic Foot Ulceration

A
  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
Q

Autonomic Neuropathies

A

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
Q

Mononeuropathy

A
  • Asymmetrical
  • Onset often painful
  • Often reversible

Mononeuropathy sites

  • Cranial nerves
  • Truncal radiculopathies
  • Femoral neuropathy
39
Q

How does elevated blood sugar/hyperglycemia cause cellular damage?

A
  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
Q

Glycosylation vs. Advanced Glycation End-products

A

Glycosylation - a nonenzymatic reversible process, e.g., HbA1c

AGE: Formation of irreversible oxidative cross-links

41
Q

True or False: Type 2 diabetes is as strong a risk factor for MI as having had a previous MI

A

True

42
Q

Metabolic Syndrome

A
  • 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
Q

Glycosylated Hemoglobin

A
  • “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
Q

Reducing CV Risk in Patients With Diabetes

A
  1. Reduce HTN: BP 40 mg/dl
  2. Give aspirin: 75-325 mg/d ASA (age >40)
  3. Smoking cessation
45
Q

Acanthosis Nigricans

A

Darkening of the skin due to Insulin resistance/hyperinsulinemia
- indicates risk of pre-diabetes/diabetes

46
Q

Glucose Measurement

A
  • Typically uses Glucose Oxidase by fingerstick
  • Results can be affected by oxygen content and vitamin C
  • Results often inaccurate in critically ill
    patients
47
Q

Oral Glucose Tolerance Test

A
    • 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
Q

Central Diabetes Insipidus

A
  • 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
Q

Nephrogenic Diabetes Insipidus

A
  • 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
Q

Sorbitol

A
  • 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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