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Endocrinology > Pathology VII > Flashcards

Pathology VII Flashcards

1
Q

How is hypopituitarism treated?

A

Substitution therapy- corticosteroids, thyroxine, sex steroids, human growth hormone (p.301)

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2
Q

Outline the acute manifestations of diabetes mellitus.

A

Insulin deficiency (and glucagon excess) cause decreased glucose uptake, increased protein catabolism, and increased lipolysis. This causes hyperglycemia, glycosuria, osmotic diuresis, and electrolyte depletion; increased plasma amino acids, nitrogen loss in urine; increased plasma FFAs, ketogenesis, ketonuria, and ketonemia. This causes dehydration and acidosis and can ultimately cause coma/ death if untreated (p.302)

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3
Q

What are the common presenting symptoms of DM Type I?

A

Polydipsia, polyuria, polyphagia, weight loss (p.302)

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4
Q

What is the difference between a presenting acute diabetic emergency in a patient with DM Type I vs DM Type II?

A

Type I- DKA; Type II- Hyperosmolar coma (p.302)

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5
Q

What endocrine hormones are secreted in excess in patients with diabetes mellitus?

A

Unopposed secretion of GH and epinephrine often exascerbate hyperglycemia (p.302)

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6
Q

What are the four types of chronic damage seen in patients with diabetes mellitus?

A

Nonenzymatic glycolysation- small vessel disease, large vessel atherosclerosis; osmotic damage- neuropathy, cataracts (p.302)

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7
Q

What are the two classes of chronic damage seen in patients with diabetes mellitus.

A

Nonenzymatic glycolysation; osmotic damage (p.302)

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8
Q

Describe the manifestations of chronic diabetes mellitus that are associated with nonenzymatic glycosylation causing small vessel disease.

A

Diffuse thickening of the basement membrane causes retinopathy (hemorrhage, exudates, microaneurysma, vessel proliferation), glaucoma, nephropathy (nodular sclerosis, progressive proteinuria, chronic renal failure, arteriosclerosis leading to hypertension, Kimmelstiel-Wilson nodules).

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9
Q

What eye symptoms are associated with Diabetes mellitus?

A

Retinopathy (hemorrhage, exudates, microaneurysma, vessel proliferation), glaucoma (p.302)

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10
Q

What nephrologic symptoms are associated with Diabetes mellitus?

A

Nepropathy- nodular sclerosis, progressive proteinuria, chronic renal failure, arteriosclerosis leading to hypertension, Kimmelsteil-Wilson nodules (p.302)

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11
Q

What renal finding is characteristic of Diabetes mellitus on pathology?

A

Kimmelsteil- Wilson nodules (p.302)

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12
Q

Describe the manifestations of chronic diabetes mellitus that are associated with nonenzymatic glycosylation causing large vessel atherosclerosis.

A

CAD, peripheral vascular occlusive disease, and gangrene (limb loss, cerebrovascular disease) (p.302)

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13
Q

Describe the manifestations of chronic diabetes mellitus that are associated with Osmotic damage.

A

Neuropathy (motor, sensory, and autonomic degeneration), cataracts (p.302)

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14
Q

What causes osmotic damage in patients with diabetes mellitus?

A

Sorbitol accumulation in organs with aldose reductase (p.302)

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15
Q

Name three tests that are helpful in diagnosis of diabetes mellitus.

A

Fasting serum glucose, oral glucose tolerance test, HbA1c (p.302)

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16
Q

What does HbA1c measure?

A

Average blood glucose over the prior 3 months (p.302)

17
Q

What is the difference in pathology that distinguishes DM Type I from DM Type II?

A

Type I- autoimmune destruction of pancreatic B-cells; Type II- increased resistance to insulin with progressive pancreatic B-cell failure (p.303)

18
Q

What is the genetic predisposition of DM Type I?

A

Relatively weak genetic disposition (about 50% concordance in identical twins); polygenic (p.303)

19
Q

What is the genetic predisposition of DM Type II?

A

Relatively strong genetic disposition (90% concordance in identical twins), polygenic (p.303)

20
Q

Is there an HLA system association in DM Type I?

A

Yes- HLA-DR3 and HLA-DR4 (p.303)

21
Q

Is there an HLA system association in DM Type II?

A

No (p.303)

22
Q

What is the difference in histology in DM Type I vs DM Type II?

A

DM type I: islet leukocytic infiltrate (with decreased number of beta cells); Type II: islet amyloid (AIAPP) deposit (p.303)

23
Q

What causes DKA?

A

Usually caused by increased insullin requirements due to increased stress (e.g. infection) (p.303)

24
Q

What is the pathophysiology associated with DKA?

A

Excess fat breakdown and increased ketogenesis from increased free fatty acids are made into ketone bodies (p.303)

25
Q

What type of ketone bodies predominates in DKA?

A

B-hydroxybutryate > acetoacetate (p.303)

26
Q

What are the symptoms of DKA?

A

Kussmaul respirations, nausea/vomiting, abdominal pain, psychosis/ delirium, dehydration, fruity breath odor (p.303)

Endocrinology (26 decks)

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