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Pathophys 2 > Diabetes > Flashcards

Diabetes Flashcards

1
Q

First phase insulin release: When does it occur?

A

During the “cephalic phase” - within first ten minutes of eating

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2
Q

What is normal blood glucose?

What does blood glucose need to be to spill into the urine?

A

100 = normal

300 = into urine

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3
Q

Four characteristics of Type 1 Diabetes

A
  • 10% of all diabetes patients
  • Usually autoimmune disorder
  • Affects production of insulin: Absolute insulin deficiency due to Beta-cell destruction
  • Idiopathic
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4
Q

2 characteristics of type 2 diabetes

A
  • Insulin resistance with relative insulin deficiency

* Accounts for almost 90% of diabetic patients

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5
Q

Syndromes that can create hyperglycemia: Mimic DM (7)

A
  • Maturity-onset Diabetes of the young: MODY
  • Exocrine Pancreatic Defects
  • Endocrinopathies
  • Infections
  • Drugs
  • Genetic Syndromes
  • Gestational Diabetes
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6
Q

What is MODY? + 3 characteristics

A

Maturity Onset Diabetes of the Young:

o Group of disorders
o Represent genetic defects in beta cell function: Variety of mutations that produce defects in insulin production
o Manifest like a more mild version of Type 1 DM

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7
Q

4 exocrine pancreatic defects that can mimic Type I Diabetes

A

o Chronic pancreatitis
o Pancreatectomy
o Neoplasia
o Cystic Fibrosis

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8
Q

3 endocrinopathies that can mimic DM, and the hormone that causes elevated blood glucose

A

o Acromegaly
o Cushing Syndrome
o Hyperthyroidism

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9
Q

3 Infections implicated in triggering Type 1 diabetes

A

o Cytomegalovirus
o Coxackie Virus B (Hand, Foot, Mouth)
o Mumps

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10
Q

6 Drugs – when taken, elevate blood glucose, cause temporary hyperglycemia

A 
o	Glucocorticoids
o	Thyroid hormone
o	Alpha-interferon
o	Beta-adrenergic agonists
o	Protease inhibitors
o	Thiazides
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11
Q

Why do beta adrenergic agonists elevate blood glucose?

A

Any sympathetic stimulation elevates blood glucose

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12
Q

3 Genetic Syndromes associated with diabetes

A

o Down’s Syndrome
o Turner Syndrome
o Kleinfelter Syndrome

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13
Q

Gestational Diabetes: 4 characteristics

A

o Temporary Diabetic State
o 3% of pregnancies in US
o Type 2 Diabetic Disorder
o These patients are more likely to develop Type 2 diabetes later in life

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14
Q

When is the most common clinical manifestation of Type I Diabetes?

A

Teenage years

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15
Q

Two pre-diabetic conditions of Type II Diabetes

A
  • Impaired glucose tolerance (IGT)

* Impaired fasting glucose (IFG)

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16
Q

3 Diabetic Screening Tools

A
  • Fasting Plasma Glucose (FPG)
  • HbA1C
  • Oral Glucose Tolerence Test (OGTT)
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17
Q

Fasting Plasma Glucose: Numbers for…
• Normal fasting glucose
• Impaired Fasting Glucose
• Diabetes Mellitus

A

• Normal fasting glucose 126mg/dL

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18
Q

What is HbA1C? What is the time frame it measures?

A

Represents the percentage of Glucose attached to Hemoglobin. “Glycocylated Hemoglobin.” Reflects longer time scale, but heavily weighted to the last 2-3 weeks.

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19
Q

HbA1C: Numbers
• Normal
• Impaired Glucose Tolerance
• DM

A

• Normal: 6.5

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20
Q

Oral Glucose Tolerance Test: What does it do? What are you looking for?

A

• Challenges your body in terms of how it handles glucose: Looking for a spike followed by a return to fasting state

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21
Q

To what patient should you give the OGTT? To what patient should you NOT give the OGTT?

A
  • Given to pregnant women at 26 weeks

- NOT given to someone with a FBG of > 130. REALLY dangerous!

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22
Q

DM Type 1: When do classic clinical manifestations occur?

A

At >90% Beta cell destruction

Diabetic Ketoacidosis occurs

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23
Q

What are the two mechanisms for beta cell destruction in Type 1 Diabetes?

A
  • T-cell mediated immune attack against poorly defined beta-cell antigens
  • Cytokine-induced beta cell damage
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24
Q

3 mechanisms of cytokine-induced beta cell damage

A
  • IFN-gamma
  • TNF-alpha
  • Interluken-1 induced apoptosis
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25
Q

Auto-antibodies against islet cells or insulin:
• Detected in ____% of patients
• Usually accompanied by …

A

70-80%

Usually accompanied by by auto-antibodies against beta-cell antigens

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26
Q

A mutation in what gene causes suseptability to DM1?

A

MHC II Locus of the Genome

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27
Q

A mutation in the MHC II locus in the genome causes what?

A

Susceptibility to DM 1
o Presence / mutation of certain MHC II Alleles
o Affects T Cell antigen presentation

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28
Q

What occurs with a non-MHC genetic predisposition to diabetes? (2)

A

o Tandem repeat polymorphs of insulin gene

o Affects negative selection of insulin-reactive T-cells

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29
Q

What environmental factors predispose a person to DM1?

A

Infection (mumps, rubella) – doesn’t cause the problem, but triggers the autoimmunity that is already there

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30
Q

What is the most powerful risk factor for Type 2 Diabetes?

A

OBESITY

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31
Q

What body type is considered a risk factor for diabetes?

A

Apple shape; waist-to-hip ratio of >1

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32
Q

Concordance rates of DM2:
• Between identical twins:
• Between 1st degree relatives:
• General population:

A
  • Between identical twins: 50-90%
  • Between 1st degree relatives: 20-40%
  • General population: 5-7%
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33
Q

Two metabolic characteristics of DM2:

A
  • 1) PRIMARY EVENT: Decreased sensitivity to insulin by peripheral tissue (insulin resistance)
  • Source of injury, beta cells burn out. Result:

• 2) SECONDARY EVENT: Beta-cell dysfunction manifested as inadequate insulin secretion relative to insulin resistance and hyperglycemia

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34
Q

Insulin resistance can clinically precede DM by _____ years

A

10-20

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35
Q

Abnormalities in individuals with insulin resistance (4)

A
  • Down-regulation of insulin receptors
  • Decreased insulin receptor-initiated kinase activity
  • Reduced levels of insulin receptor signaling intermediates (PI-33K and MAPK)
  • Impaired docking and fusion of GLUT4-containing vesicles with the plasma membrane
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36
Q

3 stages of beta cell dysfunction

A
  • Hyperinsulinemic State
  • Early Beta-Cell failure
  • Late beta cell failure
37
Q

When does a hyperinsulenemic state occur?

A

During early insulin resistance, insulin secretion is higher at every level of plasma glucose.

Can maintain normal levels for years, but beta cells start to burn out.

38
Q

• Early Beta-Cell failure manifests subtly as: (3)

A
  • Loss of normal pulsatile / oscilating pattern of insulin secretion
  • Loss of the “rapid phase” of insulin secretion triggered by elevation of plasma glucose
  • Eventually, secretory defects effect all phases of insulin release, even though some basal secretion persists
39
Q

• Late Beta-cell failure (can) manifest as: (4)

A
  • Decreased beta-cell mass
  • Islet cell degeneration
  • Amyloid islet deposition
  • Absolute insulin deficiency may appear (looking more like Type 1)
40
Q

Why are obesity and DM2 linked? (3)

A

1) Elevated circulating Free Fatty Acids (FFAs)
2) Adipocyte hypertrophy stimulates release of cytokines that attract macrophages
3) Chronic inflammation causes increased lipolysis in adipose tissue, which elevates circulating FFAs

41
Q

Free Fatty Acids cause:

… esp:

A

Insulin resistance in fat, skeletal muscle and liver cells

.. especially TNF-alpha

42
Q

Macrophages in adipose: Lean v Obese people

A

o Adipocytes in lean people contain 5-10% macrophages

o Adipocytes in obese people contain 50% macrophages

43
Q

Leptin

  • Where does it act?
  • What does it induce?
  • When does it change?
A

o Acts primarily in the brain at feeding centers in the hypothalamus

o Induces satiety: Helps regulate appetite and feeding relative to energy stores

o Individuals within a normal range of BMI: Lectin levels will increase with higher body fat percentage

44
Q

What are the two adipokines?

A
  • Adiponectin: Insulin sensitization

* Resistin: Insulin resistance

45
Q

What is the role of adiponectin?

  • What releases it?
  • When?
A

Increases insulin sensitivity

  • Released by adipose tissue
  • During Times of plenty
46
Q

What is the role of resistin?

  • What releases it?
  • When?
A

Decreases insulin sensitivity / increases insulin resistance

  • Released by adipose tissue during lean times of the year
  • Tends to decrease insulin sensitivity
47
Q

Define gestational diabetes

A

Any degree of gluocse intolerence with onset or first recognition during pregnancy.

48
Q

Gestational diabetes complicates about ____% of all pregnancies

A

2.6% of pregnancies

49
Q

Early pregnancy metabolism (3)

A
  • Body goes into fat storage mode
  • Body increases insulin sensitivity
  • Mom’s blood insulin is normal
50
Q

Late pregnancy metabolism

A
  • HPL (Human Placental Lactogen) kicks in and cuases mom to be insulin resistant
  • Gives baby an opportunity to siphon mom’s blood glucose
  • Mom’s blood insulin rises
51
Q

What happens physiologically during gestational diabetes?

A

Mom’s pancreas cannot create enough insulin to compensate for the insulin resistance

52
Q

Effect of hyperglycemia on a fetus (2). When do most problems occur?

A
  • Congenital heart abnormalities
  • Increased growth → Vulnerability to ischemia –> Can lead to still birth ☹

• Most problems during 1st trimester

53
Q

Typical onset of Gestational Diabetes

A

24-28 weeks

54
Q

Classic manifestations of DM (in order)

A 
o	Hyperglycemia
o	Glucosuria (once blood glucose is higher than renal threshold)
o	Polyuria (due to osmotic diuresis, which traps water)
o	Polydipsia (because of dehydration due to polyuria)
55
Q

List four acute complications of DM. When does each occur?

A

o Hypoglycemia: Complication of DM treatment (insulin, oral diabetic drugs)

o Hyperglycemic (hyperosmolar) coma: DM2 more likely

o Diabetic Ketoacidosis: complication of DM1

o Hyperosmolar hyperglycemic nonketotic syndrome: HHNK, DM2. Wild hyperglycemia, polyuria, polydipsia, but no DKA.

56
Q

What contributes to hyperglycemia (3)?

A

o Obvious mechanism: Food consumed. Insulin deficiency or resistance means glucose is trapped in the blood.

o Because the liver is not receiving any glucose, it thinks that it is in a fasting state. (Breaks glycogen stores, performs gluconeogenesis → more gluc into bloodstream, thereby WORSENING hyperglycemia)

o Even though person may be obese and eating, they often have highly stimulated appetites, because metabolic tissue can’t access blood glucose.

57
Q

What number indicates hypoglycemia in adults v children?

A

o Adults: Hypoglycemia when < about 70

o Children: Hypoglycemia when < 50 or 60

58
Q

Define hypglycemia

A

o Def: A drop in blood glucose below what is normal for age / sex

59
Q

What is the most common acute complication of Type 1 Diabetes?

A

Hypoglycemia

60
Q

Two causes of hypoglycemia

A
  • Metformin or other oral drugs

- Took too much insulin for food consumption (miscalculation(

61
Q

Two autonomic symptoms of hypoglycemia

A
  • Adrenergic: Tremors / shakiness, anxiety, palpitations / tachycardia
  • Cholinergic: Sweating, hunger
62
Q

Two neurologic symptoms of hypoglycemia

A
  • Weak / fatigued / drowsy, headache, behavior change, confusion
  • Diplopia, difficulty speaking – can almost seem drunk. Seizures, coma
63
Q

Role of SNS in hypoglycemia

A

Activation of SNS helps make you aware of need for glucose, also enables body to start gluconeogenesis, glucogenelysis, etc.

64
Q

What happens with hypoglycemic desensitization (3)

A

o Repeated episodes can cause hypoglycemia unawareness: Loss of autonomic / neurologic cues & loss of SNS stimulation
o The better a person is at controlling glucose, the more likely you are to get to this.
o Counterregulatory mechanisms also become impaired:

65
Q

Review Glucose Counter Regulation chart on page 10

A

ok!

66
Q

What is the cause of diabetic ketoacidosis?

A

Develops when there is an absolute deficiency of insulin or an increase in a counter-regulatory hormone like catecholamines or glucagon

67
Q

Risk factors for DKA

A

ANY KIND OF STRESS: Infection, trauma, surgery, MI, increased psychological stress

68
Q

Why is it rare to see DKA with Type II DM?

A

o Because any amount of insulin in the bloodstream helps maintain fat stores.

69
Q

What does absence of insulin stimulate?

A

Absence of insulin stimulates elevated fat breakdown → Ketones → Metabolic acidosis

70
Q

Clinical manifestations of DKA (9)

A
  • Kussmaul respirations
  • Postural dizziness
  • CNS depression – stuporous state
  • Ketonuria
  • Nausea
  • Abdominal pain
  • Dehydration (Thirst / polyuri)
  • Hypertensive
  • Tachycardic
71
Q

What are Kussmaul respirations?

A

(hyperventilation in an attempt to compensate)

72
Q

3 components you’ll see in the labs of a DKA patient

A
  • Ketones in urine and plasma
  • Acidity of 7.3 or less
  • High potassium levels
73
Q

Why would you see a lot of potassium in a DKA patient’s labs? What is happening?

A
  • Potassium shifts out of cells (especially vulnerable to acidosis)
  • Insulin brings potassium into cells
  • Patient is actually hypokalemic! They are peeing off potassium
74
Q

When do you see HHNK?

A

Usually Type 2

75
Q

Define HHNK

A

o A constellation of s&s that reflect a hyperglycemic and Non-Ketotic state
o Insulin levels are high enough to suppress lipolysis, but not high enough to facilitate glucose entry into skeletal muscles and fat tissue.

76
Q

What does HHNK stand for?

A

Hyperosmolar Hyperglycemic Nonketotic Syndrome

77
Q

Four clinical manifestations of HHNK

A
  • Hyperglycemia
  • Glucosuria
  • Polyuria
  • Polydipsia
78
Q

Tissue that is especially vulnerable to uncontrolled diabetes (2). Why?

A
  • Vasculature
  • Neural

• Why? These cells cannot regulate the amount of glucose that enters… it simply diffuses in. Therefore, the cellular levels of glucose become really high → Altered cellular metabolism.

79
Q

Three categories of DM complications

A
  • Macrovascular Disease
  • Microvascular Disease (capillaries)
  • Neuropathy
80
Q

3 manifestations of macrovascular disease in DM

A
  • Coronary Artery Disease ATHEROSCLEROSIS
  • Cerebrovascular Disease STROKE
  • Peripheral Vascular Disease PERIPHERAL ARTERIAL DISEASE (Poor circulation to legs)
81
Q

2 Manifestations of Microvascular disease

A
  • Diabetic Nephropathy

* Diabetic Retinopathy

82
Q

What does diabetic nephropathy cause?

A

o Cause of about 1/3 of all renal failure

83
Q

Pathophysiology of diabetic nephropathy

A

o Glomerular basement membrane starts to thicken
→ sclerosis (scarring) of glomerular capillaries
→ Compensatory hypertrophy, hyperfiltration of other nephrons (which have trouble keeping up)
→ Cascades toward renal failure

84
Q

Two phases of diabetic retinopathy

A
  • Non proliferative phase

* Proliferative phase

85
Q

Clinical manifestations of diabetic retinopathy: Non-proliferative phase

A

• Edema, exudate, capillaries start getting damaged – vision is not really impaired unless it’s affecting the macula

86
Q

Clinical manifestations of diabetic retinopathy: Proliferative phase

A

• Retina becomes hypoxic
• Angiogenesis (new capillaries form to compensate for ischemia) – can pull on retina, cause it to detach
o Impairs vision

87
Q

Two types of diabetic neuropathy

A
  • Sensory Neuropathy

* Autonomic Neuropathy

88
Q

Characteristics of Sensory Neuropathy (5)

A

o Tends to happen earlier
o Most notable in the extremities – esp lower limbs
o Usually bilateral, very symmetrical

o Characterized as:
• A dulled perception of vibration, temp
• Allodinia: Enhanced sensitivity to light touch (felt as excruciating pain) occurs sometimes

89
Q

Characteristics of Autonomic Neuropathy (2 characteristics, 3 clinical manifestations)

A

o Occurs with long-standing diabetes
o Autonomic nerves, reflexes, fucntions are dulled

o Can cause…
• GI issues: N/V, Loss of appetite, bowel / bladder dysfunction
• Erectile dysfunction
• Orthostatic hypotension: Dulling of the barrow reflex, “autonomic dysreflexia”

Pathophys 2 (9 decks)

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