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pharmacology 2 > insulin 1 > Flashcards

insulin 1 Flashcards

1
Q

why is it necessary to control blood glucose

A

glucose is an obligatory energy source of the brain
food supply is intermittent
a variable metabolic demand

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2
Q

islets of langerhans are located

A

in the endocrine pancreas

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3
Q

beta cells

A

insulin producing

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4
Q

alpha cells

A

produce glucagon

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5
Q

D cells

A

produce somatostatin

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6
Q

adrenaline made in

A

adrenal medulla

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7
Q

glucocorticoids made in

A

adrenal cortex

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8
Q

growth hormone made in

A

pituitary

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9
Q

the only hormone that decreases blood glucose

A

insulin

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10
Q

hormones that raise blood glucose

A

glucagon, adrenalin, glucocorticoids, growth hormone

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11
Q

insulin stored in

A

beta cell granules

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12
Q

insulin stored as

A

pro-insulin

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13
Q

when insulin is cleaved

A

undergoes proteolytic cleavage
protease removes C peptide
mature insulin is the alpha and beta chain

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14
Q

stimulants for release of insulin

A

hyperglycaemia
amino acids and FAs
peptide gut hormones - incretins (GLP1 glucagon like peptide 1, GIP and others)

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15
Q

incretins

A

peptide gut hormones
GLP1, GIP
released from the gut, not triggered when glucose is give IV

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16
Q

3 metabolic targets of insulin

A

CHO
Fat
Protein

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17
Q

CHO metabolism in the liver being acted on by insulin

A

decrease gluconeogenesis
decrease glucogenolysis
increase glycolysis
increase glycogenesis

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18
Q

insulin action on fat metabolism

A

increase lipogenesis

decrease lipolysis

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19
Q

insulin action on protein metabolism

A

decrease protein breakdown
increase amino acid uptake
increase protein synthesis

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20
Q

insulin action on CHO

A

increase glucose uptake

increase glycolysis

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21
Q

insulin effects on adipose tissue

A

increase fat storage
increase TGs and FAs
reduce fat breakdown

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22
Q

insulin receptor

A 
receptor tyrosine kinase 
insulin binds insulin receptor 
dimerisation and autophosphorylation
phosphorylates IRS1,2,3,4
(insulin receptor substrate)
activates PI3K/Akt pathway which activates GLUT4 transporter which brings glucose into the cells
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23
Q

GLUT4

A

glucose transporter which brings glucose into the cell

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24
Q

glycogen synthase

A

activated by insulin

produces glycogen from glucose

25
Q

PI3K/Akt pathway

A
  • GLUT4
  • glycogen synthase
  • cell growth
26
Q

diabetes is

A

chronic metabolic disorders characterised by hyperglycaemia

27
Q

diabetes is caused by

A

relative or absolute insulin deficiency

28
Q

diabetes presents with

A 
polyuria - due to glycosuria 
polydipsia - thirst 
polyphagia - hunger 
weight loss - catabolism 
tiredness/confusion/irritability 
poor wound healing and infections - candidiasis
29
Q

diagnosing hyperglycaemia

A

fasting blood glucose > 7mmol/L
2h after meal (OGTT)>11.1
casual blood test >11.1

30
Q

pre diabetic state

A

FBG 5.6-6.9

impaired OGTT - 7.8-11.0

31
Q

glycated haemoglobin

A

covalent modification of haemoglobin
random event where heamoglobin is covalently modified with a haemoglobin
increased event with raised blood glucose
long term measure of blood glucose control as opposed to a snapshot
<6% normal
6-6.4% pre diabetes
>6.5% diabetes
<7% good control
>8% poor control

32
Q

TYPE 1 DM

A

absolute insulin deficiency
auto immune destruction of beta cells
usually juvenile onset
not associated with obesity

33
Q

type 2 diabetes

A

most cases of adult cases
relative insulin deficiency
peripheral resistance to normal insulin levels
subsequent progressive decreased in beta cell function
many become insulin dependant over time
strongly associated with obesity

34
Q

genetic of DM

A

both types are caused by a mix of genetic and environmental factors
but the genetic causes differ

35
Q

diabetes rates

A 
rising globally 
population growth 
population aging 
increasing age specific rates of diabetes due to obesity 
higher in men
36
Q

acute complications of diabetes

A

diabetic ketoacidosis - insufficient or absent insulin in IDDM, fats are used for energy they produce acetyl CoA, ketones which are strong acids - osmotic pull leads to low pH and dehydration
life threatening hyperosmolar state

37
Q

treatment of acute diabetic ketaacidosis

A

check potassium
if less than 5, they need potassium
delay insulin if less than 3.3
then give insulin

38
Q

causes of acute diabetic ketaacidosis

A

poor therapeutic adherence
new diagnosis
infection

39
Q

complications of chronic diabetess

A

vascular disease
microvascular - increases CVS risk, hypertensive, heart attack, stroke
75% diabetes death due to cardiovascular event
microvascular - diabetic retinopathy, increases vascular permeability and neovacularisation, new blood vessels prone to bleeding causing haemorrhages and lipid exudates

40
Q

blindness in diabetes

A

commonest cause of working age blindness - diabetic retinopathy
cataracts, blindness

41
Q

kidney chronic complications in diabetes

A

diabetic nephropathy
glomerular disease
decreased GFR and albuminuria

may go on to need dialysis and renal transplant

42
Q

diabetic foot

A

common and costly
ulcers, gangrene, amputation
increase risk of amputation risk

43
Q

cause of diabetic foot

A

neuropathy - loss of feeling
motor neuropathy - foot dephormaties

lead to neuropathic ulcers

PVD - ischaemic ulcers in peripheral vascular disease
immunosuppression leading to infections

44
Q

autonomic neuropathy

A

CVS - postural hypotension, arrythmias, sudden death

erectile dysfunction, abnormal sweating, gut motility problems

45
Q

treating type 1 diabetes

A

insulin discovered 1921
recombinant human insulin introduced in the 80s
aim of therapy - maintain normoglycemia to prevent complications

46
Q

treatment of type 1 diabetes

A

recapitulate physiological pattern of pancreatic insulin secretion

47
Q

administration of insulin

A

peptide - destroyed in the gut
administered subcutaneously, or IV in emergency
injection sites must be rotated to prevent scarring which reduces scarring which may affect absorbtion

48
Q

pharmacokinetics of insulin

A

absorption affected by formulation, blood flow, scars
short lived effects - short half life
enzymatically inactivated in cells after uptake

49
Q

types of insulin

A 
ultra rapid acting 
short acting 
intermediate acting 
long acting 
mixtures
50
Q

regular/neutral insulin

A

short acting
30-60 minutes
1-2 hour peak

51
Q

ultra rapid acting

A

aspart, lispro, glulisine
15 minute onset
30-60 minute peak

52
Q

long acting insulin

A 
glargine 
determir
degludec
1-2 onset 
flat peak
53
Q

mimicking normal insulin levels

A
  • constant basal insulin production and post prandial insulin surges
    basal bolus injection - long acting insulin at bedtime
    prandial rapid acting insulin - bolus
    4 or more injections per day
    superior control, especially analogues
54
Q

insulin pump

A

basal infusion and patient activated bolus

55
Q

intensive insulin therapy

A

decreased complication rates

reduced injury to GFR and eye disease

56
Q

intensive insulin therapy problems

A

increase in hypoglycaemic events, especially with multiple injections
fear of hypoglycaemia
lack of hypoglycaemia awareness in autonomic neuropathy patients

57
Q

artificial pancreas system

A

closed loop system
continuous glucose monitoring
delivery of insulin and glucose
decrease in hypo and hyperglycaemia

58
Q

adjunct T1D therapies

A

therapeutic adherence for intensive insulin therapy is poor
sotagliflozin - SGLT1/2 inhibitor
decrease glucose absorption in the gut, decrease renal glucose absorption
decrease in hypoglycaemia and creates weightloss
increase in diabetic ketoacidosis events

59
Q

side effects of inulin ttherapy

A

hypoglycaemia - increased with intensive insulin therapy - IM/IV glucagon
weight gain
injection site problem - scarring, lipohypertrophy, lipoatrophy leads to poor absorption

pharmacology 2 (19 decks)

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