Diabetes Flashcards

1
Q

What is the pancreas and what does it secrete?

A

-is an endocrine and exocrine gland
-secretes several enzymes into duodenum for digestion (exocrine)
-secretes insulin when glucose increases, glucagon when glucose decreases (endocrine)

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2
Q

Which pancreatic cells secrete insulin and glucagon?

A

-alpha = glucagon
-beta = insulin

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3
Q

What is the islet of Langerhans in the pancreas?

A

group of cells that secrete hormones into blood (endocrine)

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4
Q

What is the pathway when blood glucose is high?

A

high blood glucose -> beta cells in the pancreas release insulin -> liver produces glycogen and cells take up glucose -> blood glucose decreases and no stimulus to release insulin

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5
Q

What is the pathway if the blood glucose is low?

A

low blood glucose -> alpha cells in the pancreas release glucagon -> liver breaks down glycogen -> blood glucose rises and no stimulus to release glucagon

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6
Q

What is glucose homeostasis?

A

-the reciprocally regulated pathways of glycolysis and gluconeogenesis
- When blood sugar rises, liver combats
-when blood sugar decreases, the liver combats
-keeps the blood sugar relatively steady (90mg/100mL)

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7
Q

What is type 1 diabetes?

A

-develops suddenly and in young people
-no functional beta cells from autoimmune destruction by T-cells
-does not secrete insulin
-causes episodic hyperglycemia
-10% of primary cases

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8
Q

What is type 2 diabetes?

A

-occurs in older people
-insulin resistance or deficiency in secretion
-insulin levels are normal or elevated because the body compensates because they are not responding
-also causes hyperglycemia
-90% of primary cases

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9
Q

What is diabetes mellitus?

A

-a group of metabolic diseases-caused by elevated glucose levels

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10
Q

What is primary diabetes mellitus?

A

-95% of cases
-type 1 and type 2

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11
Q

What is secondary diabetes mellitus?

A

-5% of cases
-as a result of a disease or medication
caused by:
-endocrine diseases
-chronic pancreatitis
-cushing’s syndrome

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12
Q

How is type 1 diabetes controlled?

A

-insulin injections
-prevents hyperglycemia and ketoacidosis
-mimic basal and reactive insulin secretions to respond to glucose levels

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13
Q

How is type 2 diabetes controlled?

A

-diet change and exercise
-block liver glucose production
-maintain glucose levels
-prevent long-term complications

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14
Q

What factors can lead to type 2 diabetes?

A

-genetics
-aging
-peripheral insulin resistance
-diet

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15
Q

What organs can sense insulin?

A

-liver
-muscle
-adipose tissue

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16
Q

What do the insulin-sensing organs do when they are resistant to insulin?

A

-pancreas -> beta cell disfunction
-liver -> increased glucose output (no insulin to stop it)
-muscle -> decrease in glucose uptake
-adipose tissue -> exaggerated lipolysis

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17
Q

List some signs/symptoms of hyperglycemia

A

-fasting glucose of >6.5 mmol/L
-polyuria (increased pee)
-polydipsia (thirst)
-glucosuria (peeing glucose)
-weight change
-fatigue

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18
Q

What are the long-term complications of hyperglycemia?

A

-hypertension
-glaucoma
-hemorrhage
-gangrene
-infections -> amputations
-peripheral neuropathy
-pyelonephritis

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19
Q

What are the two groups of long-term diabetes complications?

A

-macrovascular: Complications of large and medium-sized vessels ex. stroke, coronary heart disease
-microvascular: complications of small vessels ex. retinopathy, neuropathy

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20
Q

What occurs with neuropathy complications?

A

loss of automatic and peripheral neural function
-injuries
-gangrene
-amputations

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21
Q

What occurs with retinopathy complications?

A

-failing eyesight
-blindness
-glaucoma

22
Q

what is nephropathy?

A

-chronic kidney disease
-renal disease
-microalbuminuria

23
Q

What is cerebrovascular disease?

A

-stroke
-ischaemic attacks

24
Q

What occurs with coronary heart disease?

A

-angina
-hypertension
-heart failure

25
Q

What is insulin?

A

-peptide hormone
-precursor -> proteolytic cleavage -> dipeptide and protein C
-beta cell secretes both insulin and pro-insulin
-biggest anabolic enzyme in the body

26
Q

What are the levels of pro-insulin in a type 2 diabetic and how is it measured?

A

-high levels
-easier to measure levels of protein C to estimate insulin levels
-each have antibodies

27
Q

What regulates insulin release?

A
  1. glucose, AA, FA, ketones -> stim release
  2. glucagon and somatostatin -> inhibit release
  3. a-adrenergic stim -> inhibits release
  4. b-adrenergic stim -> promotes release
  5. elevated intracellular Ca -> promotes release
28
Q

What are the difference glut receptors?

A

-glut 1 in brain is insulin insensitive
-muscle = glut 4 = insulin sensitive
-beta cell = glut 2

29
Q

What is the pathway of insulin release?

A

-glut 2 takes up glucose -> respiration -> ATP produced -> ATP:ADP increases -> closes K channel -> Ca channel opens -> Ca enters -> pushes out insulin

30
Q

What is the difference between oral and IV glucose?

A

-oral glucose: more insulin secretion
-IV: less insulin secretion
-why?: oral elicits gut hormones which augment the insulin response

31
Q

Where is insulin catabolized?

A

-by kidney
-by insulinase

32
Q

What does an influx of calcium do to insulin?

A

-ca influx = pulsatile secretion of insulin
-activation of transcription factors for insulin

33
Q

What was the first insulin from and what is it now?

A

-beef or pork insulin
-now usually human insulin = fewer allergies, less resistance

34
Q

Which insulin form is rapid and which is prolonged?

A

-rapid: humalog
-prolonged: lantus

35
Q

How do insulin preparations vary?

A

-onset of action
-time to peak
-duration
-route of admin

36
Q

What are the different ways insulin can be administered?

A

-SC
-Insulin pump
-powder inhaler
-IV

37
Q

he will ask to name each of the types, two of each, don’t need to know rest

A
38
Q

What are the names of the Rapid-acting analogs? Clear or cloudy?

A

-Humalog (lispro)
-Novorapid (aspart)

-both are clear

39
Q

What are the names of the regular/fast-acting analogs? Clear or cloudy?

A

-Humulin-R
-Novolin GE toronto

-clear

40
Q

What are the names of the intermediate-acting analogs? Clear or cloudy?

A

-Humulin N & L
-Novolin GE NPH

-cloudy

41
Q

What are the names of the long-acting analogs?

A

-Humulin-U

-cloudy

42
Q

What are the names of the extended-acting analogs?

A

-Lantus (glargine)

-clear

43
Q

What are the names of the premixed insulin?

A

-Humalog Mix25
-Novolin GE 10/90

-cloudy

44
Q

What does the proportions on premixed insulin mean?

A

-ex. Novolin GE 20/80
-% rapid or fast / % intermediate

45
Q

What makes the insulin types cloudy?

A

-additives
-zinc analogs
-makes it long-acting

46
Q

What is the structure of human insulin?

A

-51AA
-two chains connected by 2 disulfide bridges

47
Q

What is the half-life of human insulin and what is it degraded by?

A

-5-10 min
-deg. by glutathione-insulin transhydrogenase (insulinase)

48
Q

What is the structural difference between human, bovine, and pork insulin?

A

-human: 51 AA
-bovine: differs in 3 AAs from human
-pork: differs in 1 AA from human

49
Q

What are the effects of rapid insulin?

A

-incr. GLC tranport, AA, K+ into insulin sensitive cells

50
Q

What are the effects of intermediate insulin?

A

-stim. protein synth
-Inhibit protein breakdown
-activate glycogen synthase
-inhibit gluconeogenic enzymes

51
Q

What are the effects of delayed insulin?

A

-incr. mRNA for lipogenic enzymes = lipogenesis

52
Q
A