Diabetes Mellitus Flashcards

1
Q

what is DM?

A

a group of disorders characterized by the presence of HYPERGLYCEMIA that results from defects in SECRETION OF INSULIN OR ACTION OF INSULIN OR BOTH

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2
Q

what can DM result in?

A

blindness
renal failure
CVD
stroke…

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3
Q

what are the types of DM?

A

type I - insulin dependent
type II - non insulin dependent
gestational diabetes
secondary diabetes

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4
Q

what is type I DM due to?

A

autoimmune destruction of beta cells of islet of pancreas - marked reduction in insulin secretion

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5
Q

what is type II DM due to?

A

obesity (syndrome x/metabolic syndrome/insulin resistance syndrome)

target tissues do NOT response to circulating insulin - insulin resistant! and there is a decrease in insulin secretion over time = beta cell fatigue! (so insulin levels can be high, normal, low depending on stage of the disease)

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6
Q

what is the most common cause of insulin resistance in obesity?

A
  • decreased number of insulin receptors

- postreceptor failure to activate tyrosine kinase

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7
Q

what may insulin resistance in obese people also be due to…?

A
  • reduced adiponectin
  • increase leptin (leptin resistance)
  • increase free FA
  • omentin
  • reduced glucagon like peptide (GLP-1)
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8
Q

what is omen tin?

A

protein expressed and secreted from visceral but not subcutaneous adipose tissue

plasma levels of omen tin-1 are higher in people with higher WHR

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9
Q

what is GLP-1?

A

an incretin that increases insulin secretion

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10
Q

what are the presenting features of DM?

A
  • polydipsia
  • polyphagia
  • dehydration
  • decreased immunity
  • polyuria
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11
Q

what is the classical triad of DM? more common with type I DM

A

polyuria
polydipsia
polyphagia

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12
Q

why may weight loss be observed in patients with type 1?

A

accelerated lipolysis and muscle proteolysis

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13
Q

what type of metabolism does DM affect?

A

protein,carb,fat

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14
Q

why is there hyperglycemia with DM?

A
increase gluconeogenesis in liver
\+PEPCK
\+pyruvate carboxylase
\+ F 1,6 BP
\+ G-6-P

decreased number of GLUT 4 in peripheral tissues

both because of decreased number of insulin receptors/post receptor defects

also… decreased secretion of insulin from pancreas

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15
Q

what is inhibited with low insulin and high glucagon?

A

glycolysis

glycogenesis

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16
Q

where is glucose completely reabsorbed?

A

renal tubule

17
Q

why is there polyuria in DM?

A

with hyperglycemia - lots of glucose is filtered that may exceed the capacity of the tubule so now glucose is osmotically active and drags water along with it - they both leave in urine!

18
Q

what are the acute complications of DM?

A

ketoacidosis - type I
hyperosmolar non-ketotic coma - type II
hypoglycemia in DM on treatment

19
Q

what are the chronic complications of DM?

A

microvascular

macrovascular

20
Q

what are microsvascular complication of DM?

A
  • neuropathy
  • nephropathy
  • retinophathy

occurs in tissues that do not require insulin for glucose entry - retina, nervous tissue, lens

21
Q

how can hyperglycemia result in tissue damage?

A

sorbitol formation - vision changes

22
Q

what contributes to nephropathy?

A

non-enzymatic glycation of proteins in the BM of kidney

AGEs (advanced glycation end products)

23
Q

what is the earliest sign of renal involvement in a diabetic?

A

increased loss of albumin in urine (microalbuminuria)

24
Q

what are macrovascular complications of DM?

A

atherosclerotic changes
hypertriacylglyceridemia - due to decreased action of LPL
AGEs - glycation of LDL

25
Q

what are lab tests that diagnose DM?

A

fasting BG > 126
random BG > 200
OGTT

26
Q

define pre-diabetics?

A

fasting BG of 100-125 - IFG

or

2 hour post oral glucose TT GL 140-200 –IGT

comonly associated with insulin resistance / obesity

advice dietary mod. + exercise

27
Q

what is sulonylurea?

A

increases insulin secretion from pancreas

28
Q

what is metformin?

A

decreases glucose output of liver, increases glucose utilization by muscle - improves insulin resistance