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Endocrinology > Clinical Approach to Diabetes and Hypoglycemia > Flashcards

Clinical Approach to Diabetes and Hypoglycemia Flashcards

1
Q

In what area of the U.S. is DM most prevalent?

A
  • deep southeast
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2
Q

What is Latent Autoimmune Adult Diabetes (LADA)?

A
  • diabetics who do not fit type 1 or 2 categories
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3
Q

Is the onset of T1DM abrupt?

A

YES

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4
Q

Is the onset of T2DM abrupt?

A

NO

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5
Q

What is double diabetes?

A
  • pt has T1DM with a family hx of T2DM
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6
Q

What is impaired glucose tolerance (pre-diabetes)?

A
  • risk of developing DM.
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7
Q

How many adults in the U.S. have pre-diabetes (risk of developing T2DM)?

A
  • 78 million
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8
Q

How many adults in the U.S. have T2DM?

A
  • 29 million and growing
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9
Q

Do whites or black have a higher risk of developing T2DM?

A
  • blacks
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10
Q

What is the fastest growing minority group in the U.S. for T2DM?

A
  • hispanic americans
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11
Q

What are some environmental (acquired factors) that can lead to T1DM?

A
  • viral infections
  • nutrition
  • chemical agents
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12
Q

How is insulin secreted in non-diabetics?

A
  • in 2 phases
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13
Q
  • how is insulin secreted in pts with T2DM?
A
  • loss of phase 1 secretion

* so we want to try to promote phase 1 secretion when treating.

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14
Q

What is Hgb A1c?

A
  • 3 month average of plasma glucose attached to valine on B-chain of hemoglobin A; benchmark for assessment of glycemic control (we want it to be less than 7% in T2DM).
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15
Q

To what does a reduction in HbA1c correlate in T2DM?

A
  • reduction in risk for microvascular complications: retinopathy, nephropathy, and neuropathy.
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16
Q

How do steroids impact diabetics?

A
  • increase hepatic gluconeogenesis, glycogenolysis, and antagonist peripheral insulin response, decreasing glucose uptake.
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17
Q

What is the first line treatment for T2DM?

A
  • metformin
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18
Q

What is the most common ADR of metformin?

A
  • lactic acidosis
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19
Q

What agents can we use when we need supplementation with metformin?

A
  • sulfonylureas (glipizide..)= cheapest.
  • incretins (GLP agonists or DPP-4 inhibitors)= well tolerated and oral.
  • SGLT-2 inhibitors= increase glycosuria.
  • amylin
  • insulin
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20
Q

What are the 3 rapid-acting mealtime insulins?

A
  1. aspart
  2. lispro
  3. glulisine
21
Q

What are the long-acting (24 hour) peakless insulins?

A
  • glargine

- detimir

22
Q

What are insulin pumps?

A
  • senses sugar and injects insulin as needed
23
Q

What are the complications of T2DM?

A
  • MICROvascular= retinopathy, neuropathy, nephropathy

- MACROvascular= MI, stroke, peripheral vascular disease

24
Q

If we reduce HbA1c by just 1%, by what percent will microvascular complications be reduced?

A
  • 35%
25
Q

What may you see in the rare case of autonomic neuropathy associated with T2DM?

A
  • GI dysfunciton
  • orthostatic hypotension
  • cardiorespiratory arrest
  • bladder dysfunciton
  • impotence
26
Q

What is the number one cause of end-stage renal disease?

A
  • T2DM
27
Q

Does diabetic neuropathy tend to affect the lower or upper extremities first?

A
  • lower (symmetrical)
28
Q

Can diabetics present with atypical symptoms of MI?

A
  • YES. They may not present with chest pain.
29
Q

Can pts with DM have postgustotory sweating?

A
  • YES
30
Q

What are the nonparmacologic therapies for T2DM?

A
  • diet (restricting refined carbs)
  • exercise
  • vitamins
31
Q

What are the 2 endocrine emergencies?

A
  1. DKA= hyperglycemia, acidosis, and ketosis

2. hyperosmolar nonketoitic coma

32
Q

What causes the mortality in DKA?

A
  • acidosis and dehydration
33
Q

How do you treat DKA?

A
  • fluids (normal saline) and insulin
34
Q

How do you treat hyperosmolar nonketotic coma?

A
  • fluids
35
Q

What is hypoglycemia?

A
  • neuroglycopenic and/or neurogenic symptoms
  • low plasma glucose (less than 70 mg/dL
  • symptom relief after administration of carbohydrates
36
Q

What are the symptoms of hypoglycemia?

A
  • neurogenic (autonomic)= trembling, palpitations, sweating, anxiety, hunger, nausea, tingling.
  • neurglycopenic= confusion, weakness, drowsiness, vision changes, difficulty speaking, headache, dizziness.
37
Q

Who is at risk to develop hypoglycemia?

A

those with:

  • autonomic neuropathy
  • DM with a beta blocker
  • deficiencies in counter-regulatory hormones
38
Q

What is reactive hypoglycemia?

A
  • post-prandial symptoms, which are usually ADRENERGIC responses.
39
Q

How do we treat reactive hypoglycemia?

A
  • frequent small meals
  • propantheline bromide or calcium channel blockers
  • acarbose (delays carbohydrate absorption)
40
Q

What is alimentary hypoglycemia?

A
  • occurs following GI surgery or vagotomy.

- a short-circuited GI tract results in increased carbohydrate absorption.

41
Q

How do you resolve alimentary hypoglycemia quickly?

A
  • feeding
42
Q

What is fasting hypoglycemia?

A
  • wake up with a glucose less than 70.
  • neuroglycopenic symptoms including stroke may occur.
  • more serious implications than reactive hypoglycemia.
43
Q

Are most islet cell tumors malignant or benign?

A
  • benign
44
Q

What is factitious hypoglycemia?

A
  • hypoglycemia that doesn’t make sense. Typically in patients with access to insulin or sulfonylureas, making themselves hypoglycemic.
  • will see low c-peptide levels, bc it is being taken exogenously.
45
Q

What is the most common cause of drug induced hypoglycemia?

A
  • alcohol= reduces gluconeogenesis acutely.
46
Q

Can renal disease cause hypoglycemia?

A
  • YES bc the kidneys are necessary for insulin clearance.
47
Q

What does the workup involve for hypoglycemia?

A
  • exclude drug induced
  • pre-existing hepatic or renal disease
  • pituitary or adrenal disease
  • retroperitoneal tumor
  • carbohydrate or meal induced
48
Q

How do you treat hypoglycemia?

A
  • glucose
  • glucagon
  • terbutaline (B2 agonist)
  • somatostain analogue= reduces insulin.

Endocrinology (18 decks)

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