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Endocrinology - Chapters > Chapter 69 - Diabetes Mellitus > Flashcards

Chapter 69 - Diabetes Mellitus Flashcards

0
Q

What is the general pathophysiology behind Type 2 diabetes?

A

Glucose intolerance due to

  1. lesions - blunted Beta cell response to glucose
  2. defect at the insulin receptor
  3. defect in hepatic uptake of glucose that contributes to glucose intolerance
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1
Q

What is the general pathophysiology mechanism behind Type 1 diabetes?

A

destruction of Beta Cells in the islets of Langerhans

-Beta cells secrete insulin

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2
Q

Which type of diabetes is the most common?

A

type 2

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3
Q

Testing for diabetes type 2 should be considered in all patients _____ years old, and if normal, should be repeated at _____ intervals.

A

greater than or equal to 45 years old

should be repeated ever 3 years

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4
Q

T2DM : Testing should be considered at a younger age (

A

overweight BMI = greater than 25

normal BMI = 18.5 - 24.9

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5
Q

T2DM: What kind of lifestyle would cause a person to be tested at a younger age?

A

sedentary

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6
Q

T2DM : If a person has _____ relatives with diabetes the patient will need to be screened for diabetes at a younger age.

A

first degree relatives

i.e. parent or sibling, 45%-80% in T2DM, 5% in T1DM; equates to a 40% risk

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7
Q

T2DM: Which populations need to be screened for diabetes at a younger age?

A

African American, Latino, Hispanic American, Native American, Asian American, Pacific Islander)

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8
Q

T2DM: IF a patient has delivered a baby weighing over _________, have experienced unexplained perinatal death, or have been diagnosed with gestational diabetes they need to be screened for diabetes at a younger age.

A

9 pounds, 4kg

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9
Q

T2DM: T/F If a patient is hypertensive (greater than or equal to 140/90 mmHg) they should be tested for diabetes at a younger age.

A

true

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10
Q

T2DM: a patient with a HDL cholesterol level ____ and/or a triglyceride level ______ should be tested for diabetes at a younger age (<30 years).

A

HDL - greater than or equal to 35 mg/dL

triglyceride - greater than or equal to 250 mg/dL

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11
Q

T2DM: T/F Patients who have had on previous testing, impaired glucose tolerance or impaired fasting glucose should be tested at a younger age.

A

true

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12
Q

T2DM: What is impaired glucose tolerance?

A

plasma glucose greater than or equal to 140 mg/dL but less than 200 mg/dL

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13
Q

T2DM: What is impaired fasting glucose?

A

plasma glucose 100-125 mg/dL

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14
Q

T2DM: T/F Patients who have other clinical conditions associated with insulin resistance (PCOS, acanthosis nigricans (60-90% in T2DM) should be tested at an earlier age and more frequently for diabetes. Patients with a history of vascular disease, particularly cardiovascular and cerebrovascular disease should also be tested at an earlier age and more frequently.

A

true

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15
Q

T1DM commonly presents with classic acute symptoms of hyperglycemia, what are they?

A

polydipsia, polyuria, weight loss, and less frequently, polyphagia, blurred vision, pruritis, 25% for the first time in diabetic ketoacidosis (DKA).

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16
Q

In patients with _____, the disease is often present for many years (average 4 to 7 years) before diagnosis, and as many as 50% have an established cardiovascular complication at the time of diagnosis.

A

T2DM

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17
Q

_______ may be associated with impairment of growth, susceptibility of infections (balanitis, vaginitis), and slow wound healing.

A

Chronic hyperglycemia

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18
Q

What is the standard diagnostic test for diabetes?

A

OGTT

Oral glucose tolerance test

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19
Q

Measurement of ______ is a useful tool for monitoring glycemic control and for making therapeutic decisions, but is not recommended for diagnostic purposes.

A

Glycosylated hemoglobin (HbA ic)

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20
Q

Is OGTT still used for diagnosis for gestational diabetes?

*OGTT = Oral glucose tolerance test

A

yes

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21
Q

People who have blood glucose levels greater than normal but less than those diagnostic for diabetes, a state referred to as ______. These people are generally euglycemic and have abnormal glucose responses only when challenged with an OGTT.

A

pre-diabetes

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22
Q

Pre-diabetes patients, depending on the diagnostic test, this group or metabolic stage is referred to as having either _____ or ______.

A

impaired fasting glucose (IFG)

impaired glucose tolerance (IGT)

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23
Q

Obese patients younger than 60 years and at very high risk for T2DM may benefit from the addition of _____.

A

metformin

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24
Q

What is normal fasting plasma glucose level?
What is imparied fasting plasma glucose level?
What is fasting plasma glucose level that is diagnostic of DM?

A

normal: 100 and 126

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25
Q

What is the normal glucose level at 2 hour postload?
What is the impaired glucose tolerance at 2 hour postload?
What is 2 hour post load level diagnostic for DM?

A

normal: 140 and 200

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26
Q

What are the 3 autoantibody markers measured for screening for T1DM?

A

antibodies to islet cells, insulin, glutamic acid decarboxylase, and tyrosine phosphatase

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27
Q

Should you routinely screen healthy children and those at high risk for T1DM?

A

NO!!! NEITHER should be routinely screened
**From book: Several reasons mitigate against the routine screening of both healthy children in the general population and those at high risk for developing T1DM (siblings of patients with T1DM); these include lack of established cut off values for immune markers, lack of consensus regarding effective therapy for patients with positive test results, and lack of cost effectiveness.

28
Q

T/F Screening of certain HIGH RISK populations for T2DM is considered cost-effective.

A

TRUE

high risk populations = African American, Latino, Hispanic American, Native AMerican, Asian American, Pacific Islander

29
Q

_________ = the presence of glucose intolerance that develops during pregnancy and usually returns to normal after delivery.

A

Gestational Diabetes Mellitus (GDM)

30
Q

Screening for Gestational Diabetes Mellitus is routinely performed between ___ and ___ weeks of gestation in women older than ____ and in younger women who fulfill one or more criteria. What are the criteria?

A
  • between 24 and 28 weeks in women older than 25 years old
  • younger women who fulfill one or more of the following criteria
  • -overweight
  • -sedentary lifestyle
  • -1st degree relative with diabetes
  • -member of a high risk population
  • -HDL 250
31
Q

T/F Women at high risk (obese, personal historl of GDM, glycosuria, first degree relative with diabetes) should be screened at thir initial obstetric or prenatal visit.

A

true

32
Q

What does a positive screening test (plasma glucose > 140 mg/dL 1 hour after a 50-g glucose challenge administered to a nonfasting patient) dictates the need for what diagnostic test?

A

Diagnostic testing with a 3 hour, 100 gram OGTT performed in a fasting state (>8 hours without caloric intake).

34
Q

T1 vs. T2

previous terminology- describe each

A 
T1 = insulin dependent diabetes mellitus, type 1, juvenile onset diabetes
T2 = non-insulin dependent mellitus, type 2, adult onset diabetes
35
Q

T1 & T2

age of onset?

A

T1 = usually 40 years, but increasingly at younger ages due to obesity

36
Q

T1 vs T2

Genetic prediposition?

A 
T1 = moderate; environmental factors required for expression; 35% - 50% concordance in monozygotic twins; several candidate genes proposed
T2 = Strong; 60% - 90% concordance in monozygotic twins; many candidate genes proposed; some genes identified in maturity-onset diabetes of the young
37
Q

T1 vs T2

Human leukocyte antigen association?

A

Type 1 = Linkage to DQA and DQB, influenced by DRB3 and DRB4 (DR2 protective)
Type 2 = none known

38
Q

T1 vs T2

other associations?

A 
T1 = Autoimmune; Graves' disease, Hashimoto thyroiditis, vitiligo, addisons disease, pernicious anemia
T2 = heterogenous group, ongoing subclassification based on identification of specific pathogenic processes and genetic defects
39
Q

T1 vs T2

Findings at diagnosis?

A 
T1 = 85% - 90% of patients have one and usually more autoantibodies to ICA512, IA-2, IA-2Beta, GAD65, IAA
T2 = possibly complications (micro & macrovascular) caused by significant hyperglycemia in the preceding asymptomatic period
40
Q

T1 vs T2

Endogenous insulin levels?

A 
T1 = low or absent
T2 = usually present (relative deficiency), early hyperinsulinemia
41
Q

T1 vs T2

insulin resistance

A 
T1 = only with hyperglycemia
T2 = mostly present
42
Q

T1 vs T2

Prolonged fast?

A 
T1 = hyperglycemia, ketoacidosis
T2 = Euglycemia
43
Q

T1 vs T2

stress, withdrawl of insulin?

A 
T1 = Ketoacidosis
T2 = Nonketotic hyperglycemia, occasionally ketoacidosis
44
Q

_____ = autoimmune destruction of the pancreatic islet Beta cells with absolute loss of insulin secretion. The disease has strong human leukocyte antigen (HLA) associations and numerous antibody markers of immune destruction.

A

type 1 DM

45
Q

______ and _____ are inherited genes present in 90% or more of patients with T1DM compared to less than 50% of the general population.

A

HLA-DR3 & HLA-DR4

46
Q

After diagnosis of Type 1 diabetes and the institution of insulin therapy, patients usually have some degree of recovery of Beta cell function to the extent that exogenous insulin requirements drop to extremely low levels. This period is called _______.

A

honeymoon period

47
Q

The honeymoon period in Type 1 diabetes usually lasts for a couple of months but may be as long as a year. Patients should continue insulin administration throughout this time, even at low doses. Beta cell insulin secretion eventually fails completely, and at this point, patients become ______, with _____ developing in the absence of insulin replacement.

A 
insulin dependent
DKA develops (Diabetic Ketoacidosis)
48
Q
  1. insulin resistance
  2. Beta cell dysfunction
  3. dysregulated hepatic glucose production (HGP)
  4. Abnormal intestinal glucose absorption
  5. obesity
    * These five main elements characterize _____.
A

Type 2 diabetes

49
Q

_______ results from defective intracellular signaling following binding of insulin to its receptor

A

insulin resistance

50
Q

Insulin resistance in what?

A

decreased intracellular glucose transporter activity

51
Q

In the _______ phase of Type 2 Diabetes, the pancreatic Beta cells compensate for a genetically predetermined peripheral (skeletal muscle, adipose tissue, and liver) INSULIN RESISTANCE by producing more insulin (HYPERINSULINEMIA) to maintain euglycemia.

A

Preclinical phase

52
Q

T2DM:
With time, the Beta cells gradually fail to compensate for the progressive increase in insulin resistance (IGT or IGF, 40% reduction of Beta cell mass) and eventually hyperglycemia manifest as _________ (80-90% reduction of Beta Cell Mass).

A

diabetes mellitus

53
Q

T2DM:
Classically, early loss of the first phase of glucose stimulated insulin secretion occurs (___ minutes), with subsequent gradual loss of the second phase (starting ____ minutes after glucose stimulus and peaking at ____ minutes).

A

10 minutes

30 min - 60 min

54
Q

T2DM:
other features of _______ =
1. dysrhythmic pulsatile insulin secretion
2. defective glucose potentiation of nonglucose insulin secretagogues (the incretins: glucose-dependent insulinotropic polypeptide [GIP] & glucagon-like peptide-1 [GLP-1])
3. Increased proinsulin-to-insulin ratio (from defective protease activity)
4. accumulation of islet amyloid poplypeptide
5. increased glucoagon secretions from islet alpha cells
6. glucotoxicity

A

BETA CELL DYSFUNCTIONS!!!!!!!!!!

55
Q

_____ refers to the effect of chronic hyperglycemia in DECREASING INSULIN SECRETION (through impaired Beta Cell sensitivity) and DECREASING INSULIN ACTIVITY (by increasing insulin resistance and insulin receptor tyrosine kinase activity).
** This is a function of the DURATION & MAGNITUDE of the hyperglycemia and contributes to the progressive worsening of hyperglycemia.

A

Glucotoxicity

56
Q

__________ = exacerbate hyperglycemia through increased oxidation in skeletal muscle and liver, where they decrease glucose utilization and increase gluconeogenesis.

A

Free Fatty Acids

57
Q

_____ = the result of unrestrained adipose tissue lipolysis in the relative absence of insulin, also have a toxic effect on Beta cells

A

Elevated FFA levels

*lipotoxicity

58
Q

In obesity, the increase in FFA’s released from visceral fat stimulate increased hepatic synthesis of _______ and may impair first pass hepatic metabolism of insulin, contributing to _____.

A

triglycerides; hyperinsulinemia

59
Q

Before the appearance of fasting hyperglycemia (elevated FPG), in the later stages of compensatory hyperinsulinemia, it is possible to demonstrate _________, that is not clinically evident.
-FPG = fasting plasma glucose

A
  • Abnormal Postprandial Glucose (PPG) metabolism, IGT

- IGT = impaired glucose tolerance

60
Q

T2DM:
The relative contributions of insulin resistance and insulin secretory defect to the pathogenesis in individual patients vary, with ______ playing a dominant role in most patients who are obese and _____ being more important in those of normal weight.

A

obese pts = insulin resistance

normal weight pts = failure of insulin secretion

61
Q

T2DM:
______ = results from inadequate suppression of hepatic gluconeogenesis, the result of hepatic insulin resistance, exacerbated by waning insulin secretion from failing Beta cells. Postprandial is markedly increased, with a variable increase in basal rate. Within the diabetic liver, ______ & ______ also occur.

A
  • Excessive HGP (hepatic glucose production)

- Glycogen synthesis & Increased fat synthesis also occurs w/in diabetic liver

62
Q

T2DM:
T/F Hyperglycemia, with or without autonomic nerve involvement, may contribute to **gastric dysmotility (symptomatic or not) and **alterations in the rate and timing of absorption (usually increased), with consequent exacerbation of hyperglycemia, resulting in a vicious cycle.

A

true

63
Q

T2DM:
*____ is the precursor of the extensive vasculopathy seen in patients with diabetes. FFAs that are increased in T2DM acutely impair *this as well as RAISE BLOOD PRESSURE.

A

Endothelial dysfunction

64
Q

T2DM:
Endothelial dysfunction:
____ improves endothelium dependent vasodilation.

A

Insulin

65
Q

T2DM:
Endothelial dysfunction:
What is the effect of insulin resistance and hyperinsulinemia?

A
  • well insulin improves endothelial vasodilatation, but with insulin resistance and hyperinsulinemia =
    1. impairment of vascular nitric oxide production
    2. insulin-induced vasodilation occur, WITH PROLIFERATION of VASCULAR SMOOTH MUSCLE CELLS
66
Q

T2DM:
Endothelial Dysfunction:
Several markers of _________ , (including interleukin-6 [IL-6), C-reactive protein, and TNF-alpha) have been demonstrated in people with IGT.
IGT= impaired glucose tolerance

A

acute inflammation

67
Q

T2DM:
Endothelial dysfunction:
What is low-grade chronic inflammation in this group of patients associated with?

A

insulin resistance through interference with insulin signal transduction

68
Q

T2DM:
What are the other endocrine associations in pt’s with T2DM?
hint: adrenal gland & male hormone

A

Subclinical Hypercortisolism

Lowered Levels of Testosterone in males

Endocrinology - Chapters (20 decks)

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