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pharmacology 2 > insulin 1 > Flashcards

insulin 1 Flashcards

(59 cards)

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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

Study These Flashcards
A

activated by insulin

produces glycogen from glucose

25
PI3K/Akt pathway
- GLUT4 - glycogen synthase - cell growth
26
diabetes is
chronic metabolic disorders characterised by hyperglycaemia
27
diabetes is caused by
relative or absolute insulin deficiency
28
diabetes presents with
``` polyuria - due to glycosuria polydipsia - thirst polyphagia - hunger weight loss - catabolism tiredness/confusion/irritability poor wound healing and infections - candidiasis ```
29
diagnosing hyperglycaemia
fasting blood glucose > 7mmol/L 2h after meal (OGTT)>11.1 casual blood test >11.1
30
pre diabetic state
FBG 5.6-6.9 | impaired OGTT - 7.8-11.0
31
glycated haemoglobin
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
TYPE 1 DM
absolute insulin deficiency auto immune destruction of beta cells usually juvenile onset not associated with obesity
33
type 2 diabetes
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
genetic of DM
both types are caused by a mix of genetic and environmental factors but the genetic causes differ
35
diabetes rates
``` rising globally population growth population aging increasing age specific rates of diabetes due to obesity higher in men ```
36
acute complications of diabetes
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
treatment of acute diabetic ketaacidosis
check potassium if less than 5, they need potassium delay insulin if less than 3.3 then give insulin
38
causes of acute diabetic ketaacidosis
poor therapeutic adherence new diagnosis infection
39
complications of chronic diabetess
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
blindness in diabetes
commonest cause of working age blindness - diabetic retinopathy cataracts, blindness
41
kidney chronic complications in diabetes
diabetic nephropathy glomerular disease decreased GFR and albuminuria may go on to need dialysis and renal transplant
42
diabetic foot
common and costly ulcers, gangrene, amputation increase risk of amputation risk
43
cause of diabetic foot
neuropathy - loss of feeling motor neuropathy - foot dephormaties lead to neuropathic ulcers PVD - ischaemic ulcers in peripheral vascular disease immunosuppression leading to infections
44
autonomic neuropathy
CVS - postural hypotension, arrythmias, sudden death | erectile dysfunction, abnormal sweating, gut motility problems
45
treating type 1 diabetes
insulin discovered 1921 recombinant human insulin introduced in the 80s aim of therapy - maintain normoglycemia to prevent complications
46
treatment of type 1 diabetes
recapitulate physiological pattern of pancreatic insulin secretion
47
administration of insulin
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
pharmacokinetics of insulin
absorption affected by formulation, blood flow, scars short lived effects - short half life enzymatically inactivated in cells after uptake
49
types of insulin
``` ultra rapid acting short acting intermediate acting long acting mixtures ```
50
regular/neutral insulin
short acting 30-60 minutes 1-2 hour peak
51
ultra rapid acting
aspart, lispro, glulisine 15 minute onset 30-60 minute peak
52
long acting insulin
``` glargine determir degludec 1-2 onset flat peak ```
53
mimicking normal insulin levels
- 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
insulin pump
basal infusion and patient activated bolus
55
intensive insulin therapy
decreased complication rates | reduced injury to GFR and eye disease
56
intensive insulin therapy problems
increase in hypoglycaemic events, especially with multiple injections fear of hypoglycaemia lack of hypoglycaemia awareness in autonomic neuropathy patients
57
artificial pancreas system
closed loop system continuous glucose monitoring delivery of insulin and glucose decrease in hypo and hyperglycaemia
58
adjunct T1D therapies
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
side effects of inulin ttherapy
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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