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Endocrine > Diabetes Mellitus > Flashcards

Diabetes Mellitus Flashcards

1
Q

Insulin is the primary _____ hormone of the body

A

anabolic

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2
Q

What processes does insulin regulate?

A

carbohydrate utilization/ storage
protein synthesis
lipogenesis

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3
Q

What hormones are counter-regulatory to insulin?

A

epinephrine
cortisol
growth hormone

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4
Q

Describe the regulation of glucose release from pancreatic beta cells

A
  • glucose is transported into the beta cell, enters glycolysis and generates ATP.
  • increased ATP closes an ATP-sensitive membrane potassium channel
  • K channel closure depolarizes the cell, which then opens voltage-dependent calcium channels and triggers insulin secretion.
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5
Q

Insulin response to a constant glucose simulus is _______

A

biphasic:

early peak and more prolonged second phase

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6
Q

What are initiators of insulin release?

A

glucose
some amino acids
sulfonylureas- stimulate closer of K channel

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7
Q

What are inhibitors of insulin release?

A

somatostatin
epinephrine
K channel openers ex diazoxide

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8
Q

What cell types do NOT have insulin receptors

A

kidney, nerve, retina

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9
Q

What are the four categories of DM?

A

type 1- autoimmune
type 2- metabolic syndrome
“other”
gestational

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10
Q

Diabetes mellitus is defined by the degree of _________

A

hyperglycemia

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11
Q

What kinds of deficits can cause “other” DM?

A 
defects in insulin action
defects in B cell function (MODYs)
drugs
infections- CMV, rubella
endocrinopathies
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12
Q

What are the diagnostic criteria for DM?

A
  • A1c > 6.5%
  • FPG > 125
  • two hour plasma glucose >200 for OGTT
  • any random plasma glucose >200 in symptomatic patient
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13
Q

What are the parameters for impaired fasting glucose (IFG)?

A

fasting glucose above 100 but below 126

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14
Q

What are the parameters for impaired glucose tolerance (IGT)?

A

plasma glucose between 140 and 200 two hours into OGTT

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15
Q

People with _____ are at increased risk for developing frank diabetes

A

pre-diabetes

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16
Q

People with _____ are at increased risk for developing frank diabetes

A

pre-diabetes

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17
Q

In type 1 diabetes, autoimmune destruction of B cells leads to:

A

absolute insulin deficiency

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18
Q

What HLA haplotypes are associated with type 1 diabetes?

A

DR3, DR4, DQ8

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19
Q

What antibodies can be found in type 1 diabetes?

A

insulin autoantibodies, islet cell antibodies, and anti-glutamic acid decarboxylase (GAD) antibodies

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20
Q

80-90% of beta cells are destroyed before ______ develops in type 1 diabetes

A

hyperglycemia

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21
Q

What is the renal threshold for glycosuria?

A

200

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22
Q

Describe effects of absolute insulin deficiency in type 1 diabetes

A

protein degradation, lipolysis, and inability to maintain body tissue, resulting in weight loss
osmotic diuresis

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23
Q

Type 1 diabetes symptoms are usually present for _____ before diagnosis

A

days- few weeks

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24
Q

What are the two major physiologic abnormalities in type 2 diabetes?

A

insulin resistance

impaired insulin secretion

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25
Q

The pathophysiological manifestations of type 2 diabetes occur at the level of the ____ and ________

A

liver and peripheral tissues- adipose and muscle

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26
Q

What is the major cause of fasting hyperglycemia in people with type 2 diabetes?

A

insulin resistance causes increased hepatic glucose production via gluconeogenesis and glycogenolysis

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27
Q

As type 2 diabetes progresses, in addition to insulin resistance, there is a ____ in insulin secretion

A

decrease

28
Q

Describe the patterns of insulin secretion in type 2 diabetes?

A

secretory defect in response to glucose- no first phase peak, prolonged second phase secretion
normal response to other stimuli ex arginine

29
Q

Insulin resistance is usually present for years before ________ develops

A

hyperglycemia

30
Q

Describe the presentation of type 2 diabetes

A
  • less acute/ dramatic than type 1
  • weight gain
  • less notable polyuria and polydipsia
31
Q

Who should be screened regularly for diabetes?

A

people over 45 yrs old

people with BMI>25 and other risk factors

32
Q

Who should be screened regularly for diabetes?

A

people over 45 yrs old

people with BMI>25 and other risk factors

33
Q

About 65% of people with DM2 die from ______ disease

A

cardiovascular

34
Q

What are risk factors for gestational diabetes?

A

obesity
family history of Dm2
previous history of GDM
age >40

35
Q

What is the acute complication of type 1 diabetes?

A

DKA

36
Q

DKA is caused by a profound lack of ____ and increased counter-regulatory hormones

A

insulin

37
Q

What are the symptoms of DKA

A 
dehydration and electrolyte imbalances due to osmotic diuresis 
hyperglycemia
acidosis
ketosis
glycogen depletion
abdominal pain, NV
lethargy, fatigue
acetone breath
38
Q

Describe the “vicious cycle” seen in DKA

A

volume contraction causes a decreased

GFR–> causes less glucose excretion–> more hypertonicity, volume losses, and further declining GFR

39
Q

What is the effect of DKA on potassium?

A

acidosis causes shift out of cell
serum levels can look normal even with total body potassium depletion
–> must include potassium in treatment of DKA

40
Q

What measures are necessary to manage the low bicarbonate levels in DKA?

A

None, should resolve when acidosis is treated

41
Q

What are Kussmaul respirations?

A

deep fast breathing, compensation for metabolic acidosis

42
Q

What is the most lethal complication of DKA?

A

cerebral edema

43
Q

How is hyeprosmolar nonketotic syndrome different from DKA?

A

seen in DM2

no acidosis or ketosis

44
Q

Why does ketosis not develop in HNKS?

A

type 2 diabetics have enough insulin to suppress ketone formation

45
Q

Why does ketosis not develop in HNKS?

A

type 2 diabetics have enough insulin to suppress ketone formation
no Kussmaul respirations, less pronounced GI symptoms

46
Q

What drugs are associated with the onset of HNKS

A

diuretics, esp K depleting
niacin
new anti psychotics
glucocorticoids

47
Q

What are the two categories of symptoms caused by hypoglycemia?

A
  1. adrenergic: weakness, sweating, tachycardia, palpitations, tremor, nervousness, irritability
    earlier signs
  2. neuroglycopenic: hypothermia, confusion, seizure, coma. later signs- hypoglycemic unawareness.
48
Q

What can predispose to hypoglycemia?

A 
excess insulin
exercise
missed meal/ snack
low A1c
diabetic gastroparesis
alcohol
impaired renal clearance of insulin
sulfonylureas
49
Q

What can predispose to hypoglycemia?

A 
excess insulin
exercise
missed meal/ snack
low A1c
diabetic gastroparesis
alcohol
impaired renal clearance of insulin
sulfonylureas
50
Q

Constrast the Somogyi effect vs the Dawn phenomenon

A

Somogyi: fasting hyperglycemia that occurs as a rebound response from an overnight low (triggering a counter-regulatory response).
Treatment – decrease PM insulin dose

Dawn: fasting hyperglycemia due to the normal peaking of counter-regulatory hormones in the AM (e.g. cortisol)
Treatment – increase PM insulin dose

51
Q

What are the chronic complications of DM?

A

microvascular and macrovascular problems

52
Q

Describe the stages of diabetic retinopathy

A

 Stage 1: non-proliferative retinopathy, characterized by microaneurysms, hard exudates, and dot and blot hemorrhages.
 Stage 2: pre-proliferative retinopathy characterized by cotton wool spots and intra-retinal microaneuryms (IRMA).
 Stage 3: proliferative retinopathy, characterized by neovascularization, new vessels tend to be weak and can rupture

53
Q

The changes of diabetic retinopathy do not affect vision until there is _____

A

bleeding

54
Q

How can proliferative diabetic retinopathy be treated?

A

laser photcoagulation

55
Q

How can proliferative diabetic retinopathy be treated?

A

laser photcoagulation

56
Q

_______ results from leaking capillaries in the macula and is the leading cause of blindness in DM2

A

macular edema

57
Q

________ is the leading cause of ESRD

A

diabetic nephropathy

58
Q

Describe the histologic changes seen in diabetic nephropathy

A

Basement membrane thickening
Increased glomerular leakage
Loss of glomerular charge selectivity
Reduced size selectivity of the glomerular barrier

59
Q

Early in the course of diabetes, there is _______ in the kidneys

A

hyperfiltration

60
Q

The first clinical evidence of diabetic nephropathy is _______

A

microalbuminuria

61
Q

Development of gross proteinuria is thought to represent ________ damage to the kidneys

A

irreversible

62
Q

After development of gross proteinuria, it is usually about ____ years to the development of ESRD

A

8 years

63
Q

What are the classes of diabetic neuropathy?

A
  • peripheral
  • autonomic: GI, GU, CV
  • acute onset mononeuropathies, radiculopathies
64
Q

What is the presentation of cardiac autonomic neuropathy?

A

resting tachycardia

orthostatic hypotension with supine hypertension

65
Q

What are the macrovascular complications of diabetes?

A

damage to the large blood vessels resulting in coronary artery, cerebrovascular, and peripheral vascular disease.

66
Q

In type 1 DM, ______ is an important determinant of risk of macrovascular complications

A

duration of DM- highest risk after about 25 years

67
Q

What are cause of hypoglycemia in non-diabetic patients?

A
  • excess insulin, ex insulinoma
  • substance other than insulin stimulating insulin receptors, ex IGF-2 in some tumors
  • non-insulin receptor mediated cause, hypoglycemia in the setting of low insulin. ex impaired GNG or glycogenolysis

Endocrine (19 decks)

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