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Therapeutics 2 - Exam 2 > diabetes flashcards > Flashcards

diabetes flashcards

1
Q

what are the cardinal signs or “polys” for diabetes? specifically type 1

A

polydipsia (excessive thirst)
polyuria (excessive urination)
polyphagia (constant hunger/big appeptite)

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2
Q

what are the diagnostic criteria for diabetes? A1C, FBG, OGTT, random plasma glucose

A

A1C >6.5
Fasting blood glucose > 126 mg/dL
2hr OGGT >200 mg/dL
random glucose >200 mg/L

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3
Q

What are characteristics of type I diabetes mellitus?

A

complete glucose intolerance
no functioning insulin-secreting pancreatic beta cells
dependent on exogenous insulin; tendency toward ketoacidosis
early age of onset (autoimmune)
family history often negative

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4
Q

What are common autoantibodies found in type I diabetics?

A

ICA- islet cell cytoplasmic autoantibodies
IAA- insulin autoantibodies

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5
Q

What does presence of c-peptide indicate in a diabetic?

A

Indicates that some beta cell mass is left; beta cells are still secreting insulin

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6
Q

At what point does a type I diabetic begin to have abnormal FBG?

A

When >70% of beta cell mass is lost

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7
Q

What autoantigens are most associated with type I diabetes?

A

Islet antigen 2 (IA-2), phogrin (IA-2B), zinc transporter, glutamic acid decarboxylase, voltage gated Ca2+, vesicle-associated membrane protein2 (VAMP- 2)

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8
Q

What are characteristics of non-obese diabetes mellitus?

A

very small percent (10%)
onset around 25; maturity onset diabetes of the young
yes family history
low insulin secretion (insufficient for glycemic control)
includes mutations in specific proteins

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9
Q

What are characteristics of obese diabetes mellitus?

A

largest % of population (80%)
onset usually over 35yo
yes family history
insulin secretion low for body mass
insulin resistance in tissues + decreased BCM

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10
Q

What are consequences of lack of insulin?

A

hyperglycemia (decreased glucose uptake in cells, decreased glycogen synthesis, increased conversion of amino acids to glucose–ketoacidosis)
glucosuria (glucose in the urine)
hyperlipidemia (fatty acid mobilization from fat cells; ketoacidosis)
uninhibited glucagon (increased glucagon levels even with increased blood glucose levels)

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11
Q

What are complications of diabetes?

A

cardiovascular micro and macro angiopathies
Neuropathy
cataracts
nephropathy
susceptibility to infections

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12
Q

Goals of insulin therapy

A

reduce symptoms of diabetes
keep average blood glucose levels below 150mg/dL
prevent/delay onset of complications

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13
Q

What causes diabetic ketoacidosis?

A

uncontrolled oxidation of fatty acids (accumulation of ketone bodies) (byproduct organic acid)

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14
Q

What functional group in glucose makes it reactive?

A

aldehyde

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15
Q

What products can glucose be oxidized into?

A

reactive dicarbonyls
- glyoxal
- methylglyoxal

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16
Q

What is AGE/RAGE

A

AGE – advanced glycation end products
formed by oxidation products of glucose and proteins that bind irreversibly
results in loss of protein function
RAGE – receptor for advanced glycation end products

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17
Q

Where is RAGE located?

A

leukocytes and endothelial cells
cell surface proteins
peptides containing CML and CEL (lysine + glucose products) bind to RAGE and promote inflammation

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18
Q

what happens when rage is bound?

A

inflammation

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19
Q

what is aldose reductase pathway (poly pathway)? where is it located?

A

occurs in nerves; consumes large amounts of NADPH and causes oxidative damage of neurons

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20
Q

what pathway is aldose reductase in?

A

polyol pathway

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21
Q

what is the result of polyol pathway?

A

neuropathy

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22
Q

what/where is hexosamine pathway?

A

F6P accumulates; causes changes in protein function

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23
Q

What is rate-limiting step of glucose utilization?

A

fructose-6-phosphate –-> G3P

24
Q

What happens in the protein kinase C pathway?

A

Buildup of G3P activates protein kinase C inappropriately
protein modification

25
Q

What is the AGE pathway?

A

buildup of G3P (due to oxidative stress)
oxidized glucose (methylglyoxal) reacts with proteins to form AGE
causes loss in protein function and chronic inflammation

26
Q

What is the effect of methylglyoxal on cardiovascular tone?

A

ACh and Nitric Oxide unable to relax smooth muscle
local control of cardiovascular tone lost

27
Q

What kind of receptor is the insulin receptor?

A

receptor tyrosine kinase

28
Q

What is the role of a-subunits in the insulin receptor?

A

represses the catalytic activity of the beta subunit

29
Q

How does insulin binding activate the insulin receptor?

A

relieves the repression of beta subunit catalytic activity by binding

30
Q

What is the role of beta subunits in the insulin receptor?

A

contain tyrosine kinase catalytic domains
autophosphorylate

31
Q

Phosphorylation of what causes a rise in lipogenesis when insulin binds to the insulin receptor?

A

MAPK

32
Q

What causes an increase in glycolysis when insulin binds to the insulin receptor?

A

PI3K

33
Q

What is the effect of insulin binding ?

A

increased lipogenesis
increased glycolysis
increased glycogen synthesis
increased gluconeogenesis

34
Q

What is the impact of insulin on the liver?

A

inhibits glycogenolysis
inhibits ketogenesis
inhibits gluconeogenesis
stimulates glycogen synthesis
stimulates triglyceride synthesis

35
Q

What is the impact of insulin on the skeletal muscle?

A

stimulates glucose transport and amino acid transport

36
Q

What is the impact of insulin on the adipose tissue?

A

stimulates triglyceride storage
stimulates glucose transport

37
Q

Where does glucose get disposed/ used in the fasting state?

A

75% non-insulin dependent: Liver, GI, Brain
25% insulin dependent: skeletal muscle
glucagon is secreted

38
Q

Where does glucose get disposed/used in the fed state?

A

80-85% is insulin depended in skeletal muscle (glut-4 transporters)
4-5% is insulin dependent in adipose tissue
glucagon secretion is inhibited
insulin inhibits release of FFA from adipose tissue

39
Q

How do serum FFA levels impact insulin action/sensitivity?

A

decreased serum FFA enhances insulin action and reduces hepatic glucose production
increased FFA levels may decrease insulin sensitivity

40
Q

Which glucose transporter stimulates secretion of insulin?

A

GLUT2 (located in beta cells; tells beta cells when to secrete insulin)
gets last dibs per km

41
Q

What does glut3 do?

A

located in nervous system; transports glucose to neurons
gets first dibs per km

42
Q

Which glucose transporter is insulin induced?

A

GLUT4!
located on skeletal muscle and adipocytes

43
Q

What do pancreatic alpha cells produce?

A

glucagon

44
Q

What do pancreatic beta cells produce?

A

insulin, amylin

45
Q

what do pancreatic delta cells produce?

A

somatostatin

46
Q

Effect of glucagon?

A

stimulates glycogen breakdown; increases blood glucose

47
Q

Effect of somatostatin?

A

General inhibitor of insulin/glucagon secretion

48
Q

Effect of insulin?

A

Stimulates uptake and utilization of glucose

49
Q

effect of amylin?

A

co-secreted with insulin to slow gastric emptying, decrease food intake, and inhibit glucagon secretion; also reduced blood glucose

50
Q

How is insulin processed?

A

Cleaved to A&B chains and c-peptide by proconvertases; causes oxidative stress if too much insulin is produced; b-cell death

51
Q

What Regular human insulins are available?

A

humulin
novolin

52
Q

What are the ultra rapid-onset, very short acting insulins?

A

Lispro (Humalog)
Aspart (Novolog)
Glulisine (Apidra)

53
Q

What are the rapid onset/ medium- to short acting insulins?

A

Regular (R) human insulin
- Humulin, Novolin

54
Q

What are the intermediate acting insulins?

A

NPH (N)

55
Q

What are the slow-onset, long acting insulins?

A

glargine (Lantus)
detemir (Levemir)
degludec (Tresiba)

Therapeutics 2 - Exam 2 (10 decks)

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