Pathology VII Flashcards
How is hypopituitarism treated?
Substitution therapy- corticosteroids, thyroxine, sex steroids, human growth hormone (p.301)
Outline the acute manifestations of diabetes mellitus.
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)
What are the common presenting symptoms of DM Type I?
Polydipsia, polyuria, polyphagia, weight loss (p.302)
What is the difference between a presenting acute diabetic emergency in a patient with DM Type I vs DM Type II?
Type I- DKA; Type II- Hyperosmolar coma (p.302)
What endocrine hormones are secreted in excess in patients with diabetes mellitus?
Unopposed secretion of GH and epinephrine often exascerbate hyperglycemia (p.302)
What are the four types of chronic damage seen in patients with diabetes mellitus?
Nonenzymatic glycolysation- small vessel disease, large vessel atherosclerosis; osmotic damage- neuropathy, cataracts (p.302)
What are the two classes of chronic damage seen in patients with diabetes mellitus.
Nonenzymatic glycolysation; osmotic damage (p.302)
Describe the manifestations of chronic diabetes mellitus that are associated with nonenzymatic glycosylation causing small vessel disease.
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).
What eye symptoms are associated with Diabetes mellitus?
Retinopathy (hemorrhage, exudates, microaneurysma, vessel proliferation), glaucoma (p.302)
What nephrologic symptoms are associated with Diabetes mellitus?
Nepropathy- nodular sclerosis, progressive proteinuria, chronic renal failure, arteriosclerosis leading to hypertension, Kimmelsteil-Wilson nodules (p.302)
What renal finding is characteristic of Diabetes mellitus on pathology?
Kimmelsteil- Wilson nodules (p.302)
Describe the manifestations of chronic diabetes mellitus that are associated with nonenzymatic glycosylation causing large vessel atherosclerosis.
CAD, peripheral vascular occlusive disease, and gangrene (limb loss, cerebrovascular disease) (p.302)
Describe the manifestations of chronic diabetes mellitus that are associated with Osmotic damage.
Neuropathy (motor, sensory, and autonomic degeneration), cataracts (p.302)
What causes osmotic damage in patients with diabetes mellitus?
Sorbitol accumulation in organs with aldose reductase (p.302)
Name three tests that are helpful in diagnosis of diabetes mellitus.
Fasting serum glucose, oral glucose tolerance test, HbA1c (p.302)
What does HbA1c measure?
Average blood glucose over the prior 3 months (p.302)
What is the difference in pathology that distinguishes DM Type I from DM Type II?
Type I- autoimmune destruction of pancreatic B-cells; Type II- increased resistance to insulin with progressive pancreatic B-cell failure (p.303)
What is the genetic predisposition of DM Type I?
Relatively weak genetic disposition (about 50% concordance in identical twins); polygenic (p.303)
What is the genetic predisposition of DM Type II?
Relatively strong genetic disposition (90% concordance in identical twins), polygenic (p.303)
Is there an HLA system association in DM Type I?
Yes- HLA-DR3 and HLA-DR4 (p.303)
Is there an HLA system association in DM Type II?
No (p.303)
What is the difference in histology in DM Type I vs DM Type II?
DM type I: islet leukocytic infiltrate (with decreased number of beta cells); Type II: islet amyloid (AIAPP) deposit (p.303)
What causes DKA?
Usually caused by increased insullin requirements due to increased stress (e.g. infection) (p.303)
What is the pathophysiology associated with DKA?
Excess fat breakdown and increased ketogenesis from increased free fatty acids are made into ketone bodies (p.303)
