Diabetes Flashcards

1
Q

What is Diabetes Insipidus?

A

DI is an uncommon disorder characterized by an increase in thirst and the passage of large quantities of urine of low specific gravity. Serum osmolality is 285-295.

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2
Q

What causes DI?

A

It is caused by a deficiency of vasopressin or resistance to vasopressin (ADH).

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3
Q

What are the main types of DI?

A

Hypothalamic (Central)- inability to produce or secrete vasopressin (levels will be low)

Nephrogenic (Secondary)- kidney unable to respond to vasopressin (levels are high)

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4
Q

What are the characteristics of primary central DI?

A

Commonly occurs after head trauma or brain surgery

Responds to desmopressin

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5
Q

What are the characteristics of secondary nephrogenic DI?

A

Associated with chronic renal failure, lithium toxicity, hypercalcemia and hypokalemia

abnormal receptors in the kidney

no response to desmopressin

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6
Q

What are the clinical features of DI?

A

Polydipsia, polyuria and diluted urine

Craving of ice water

Serum osmolality is high; urine osmolality is low.

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7
Q

What complicates or aggravates DI?

A

DI is aggravated by administration of high dose corticosteroids, which increases renal free water clearance.

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8
Q

What are the expected laboratory findings in a patient with DI?

A

Evaluation should include an accurate 24 hour urine collection for volume and creatinine. A urine of < 2L/24 hrs (in the absence of hypernatremia) essentially rules out DI.

MRI should be done to evaluate for a thickened pituitary stalk or mass lesions.

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9
Q

How do we diagnose DI?

A

Diagnosis of DI requires clinical judgement, no single diagnostic laboratory test.

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10
Q

How do we distinguish central from secondary DI?

A

A supervised vasopressin challenge test may distinguish central from nephrogenic DI.

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11
Q

How do we treat DI?

A

Mild cases of DI require no treatment other than adequate fluid intake.

Desmopressin acetate is the treatment of choice for central DI.

Central and nephrogenic DI respond partially to hyrdochlorothiazide with potassium supplementation.

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12
Q

What is diabetes mellitus?

A

DM describes a group of disorders characterized by disordered metabolism and inappropriate hyperglycemia. This may be due to deficiencies in insulin secretion, inadequate response to insulin, or both.

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13
Q

What are the most common types of diabetes?

A

Most patients with diabetes have type 1 (90%)

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14
Q

Type 1 DM is characterized by…

A

early onset, autoimmune phenomenon, insulinopenia, or absence of insulin and risk of DKA. It has an association with HLA DR3-DQ2 and DR4 genes.

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15
Q

Type 2 DM is characterized by…

A

late onset and associated with overweight or obesity, positive family history, and associated hyperinsulinemia.

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16
Q

What is prediabetes?

A

A blood glucose level above normal but with out meeting the criteria for diagnosis of DM.

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17
Q

What is metabolic syndrome?

A

Also known as “syndrome X” and “insulin resistant syndrome.” It is a constellation of findings that predisposes to DM, CAD and strokes.

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18
Q

What are the criteria for metabolic syndrome?

A
  1. HDL less than 40 in males, 50 in females
  2. BP > 135/85
  3. TG > 150
  4. Fasting blood sugar 100-125 (impaired fasting glucose)
  5. Two hour glucose tolerance test of 140-199
  6. Waist size of 35 in females and 40 in males
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19
Q

What is the most common complication of DM?

A

Neuropathy is the most common complication of DM. Has characteristic peripheral symmetric poly neruopathy (stocking and glove)

20
Q

What are other complications of DM?

A

Diabetic retinopathy (leading cause of blindness in people over 60).
Diabetic nephropathy (causes half of ESRD).
Peripheral vascular disease
Large vessel atherosclerosis and stroke.
Candidal infections

21
Q

What is Type 1 diabetes?

A

Occurs most often in young people of normal or low weight. There is little or no endogenous insulin secretion. Plasma glucagon is elevated. Pancreatic beta cells fail to respond to stimuli and undergo autoimmune destruction.

Most type 1 DM is an autoimmune disease (90%) with antibodies to insulin.

22
Q

What are the clinical features of T1DM?

A

The most common findings include polydipsia, polyuria, nocturia, and rapid weight loss despite normal increased appetite associated with a random plasma glucose > 200. Blurred vision is common.

23
Q

If untreated what can T1DM result in?

A

DKA, leading to anorexia, N/V, dehydration, stupor and ultimately a coma.

24
Q

How is T1Dm diagnosed?

A

A random plasma glucose of more than 200 with classic symptoms or fasting levels of 126 or greater on more than one occasion is diagnostic. Confirmed with glucose tolerance testing.

25
Q

How is T1DM treated?

A

Diet is central to management. 1 unit of short or rapidly acting insulin for each 10-15 g of ingested carbohydrate in addition to basal insulin needs is recommended.

Insulin may be delivered by subcutaneous injection, injector pens or insulin pump.

26
Q

T/F: Human insulin causes markedly less antibody response than animal insulin and is available in regular or neutral protamine Hagedorn (NPH) formulations.

A

True

27
Q

What does insulin do?

A

Insulins role is to take sugar from the blood and carry it into cells where it can be used to provide energy for the body to work.

28
Q

What happens as your blood glucose rises?

A

Your pancreas secretes insulin

29
Q

What are the characteristics of diabetic retinopathy?

A

non-proliferative: aneurysm, hard-exudate, hemorrhage

proliferative: neovascularization

both have cotton wool spots.

30
Q

What is HbA1c?

A

Hgb is a protein that makes RBCs red. When Hgb picks up glucose from the blood stream, the Hgb becomes glycosylated. Glycosylated Hgb is HbA1c. The HbA1c test measures the percentage of HbA1c in the blood. A number that corresponds to the average blood glucose for the previous three months.

31
Q

What is the A1c goal?

A

<6.5 or 7%

32
Q

What is Type 2 Diabetes?

A

The basic pathophysiology is 2 fold: Insulin levels are high enough to suppress ketoacidosis. Insulin resistance to B-cell produced insulin and relative insulin deficiency, especially with disease progression. Resistance is increased with aging, sedentary lifestyle, and abdominovisceral obesity.

33
Q

What are the characteristics of T2DM?

A

obeisty, Polyuria, polydipsia, candidal vaginitis

ketonuria and weight loss are rare

34
Q

If untreated T2DM can develop into what?

A

hyperosmolar nonketonic states

35
Q

How is T2DM diagnosed?

A

Random glucose greater than 200

36
Q

How is T2DM treated?

A

Exercise and diet.

Metformin , which reduces hepatic glucose production, is the most common first line agent. It promotes weight loss and lowers TGs.

37
Q

What treatment option results in weight loss and lowers blood glucose by slowing gastric emptying, stimulating pancreatic insulin response to glucose and reducing glucagon release after meals?

A

Glucagon like peptide 1 (GLP-1)

38
Q

What treatment option is contraindicated in patients with CHF and liver disease and causes weight gain?

A

Thiazolidinediones, work on adipose tissue (increase insulin sensitivity, increase lipid storage)

39
Q

What treatment option delays the absorption of dietary carbohydrate by blocking the intestineal alpha glucosidase enzyme thereby decreasing postprandial glucose levels?

A

alpha glucosidase inhibitors

40
Q

Which treatment option is typically avoided and results in weight gain and increased risk of hypoglycemia?

A

Sulfonylureas

41
Q

What are the acceptable blood glucose levels for T2DM?

A

70-130 before meals and 180 or less at 1 hr, and less than 150 at 2 hrs post prandially.

42
Q

What are the side effects of metformin?

A

GI upset

43
Q

T/F: The higher the fasting glucose the greater the glucose reduction by Metformin

A

True

44
Q

What is hypoglycemia?

A

Symptoms begin at plasma glucose levels of 60; cognitive impairment begins at 50.

postprandial hypoglycemia is acute and presents with sweating, palpitations, anxiety and tremulousness.

45
Q

What is the Whipple triad?

A

consists of a history of hypoglycemic symptoms, a fasting blood glucose of 45 or less and immediate recovery on administration of glucose.