Lecture 26: Treatment of Diabetes 1 Flashcards Preview

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Flashcards in Lecture 26: Treatment of Diabetes 1 Deck (31)
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1
Q

define diabetes

A

metabolic disorder of multiple aetiology characterised by:

  • chronic hyperglycaemia
  • disturbances of carb, fat and protein metabolism
  • defects in insulin secretion, insulin action or both
2
Q

what 3 things would you look out for in a young patient suspected of diabetes (Type 1)

A
  • polyuria
  • polydipsia
  • polyphagia
3
Q

give the two main classifications of diabetes and describe them

A

Type 1

  • insulin dependent
  • pancreatic B cells destroyed so no insulin made

Type 2

  • insulin resistant
  • insulin stops working at target tissues ( muscle)
4
Q

explain how a T2D patient might become insulin dependent

A
  • insulin resistant
  • pancreatic B cells produces excess insulin to try and overcome this
  • B cells become exhausted and die
5
Q

what molecule is measured when trying to measure insulin levels in plasma

A

C peptide

6
Q

what are the types of diabetic complications that can occur

A
  • microvascular e.g. retinopathy, nephropathy
  • macrovascular e.g. atherosclerosis
  • neuropathy
7
Q

outline the differences between T1D and T2D

A

T1D:

  • childhood/teen onset
  • freq. malnourished
  • 10-20% prevalence
  • moderate genetic predisposition (epigenetic)
  • B cell/insulin defect

T2D

  • middle age onset
  • freq. obese
  • 80-90% prevalence
  • very strong genetic predisposition
  • insulin resistance or insulin insufficiency
8
Q

how are insulin levels measured

A

C peptide ELISA

9
Q

why is C peptide measured (not just insulin) to determine insulin levels in blood

A
  • might measure inactive forms of insulin

- active form only consists of A chain and B chain

10
Q

what stimulates insulin secretion

A
  • metabolic signals e.g. blood glucose

- vagal stimulation

11
Q

describe B cells release of insulin in phases

A
  • biphasic pulsatile release into portal vein –> significant amount removed by first pass through liver
  • rapid 1st phase triggered by ^ glucose levels
  • slow sustained 2nd phase of newly formed vesicles triggered independently of glucose
  • half life is 5-6mins
12
Q

what would be seen in insulin secretion phases for T2D

A

no/insufficient 2nd phase

13
Q

how is insulin released from B cells

A
  • glucose enters B cells via GLUT 2
  • glucose metabolism initiated by glucokinase (phosphorylation - liver and B cells only)
  • ^ ATP and dec. in ADP
  • alters/closes K-ATP channels
  • B cell depolarises –> activation of voltage dependent Ca2+ influx
  • ^ of intracellular Ca2+ triggers insulin secretion
14
Q

how does insulin stimulate glucose uptake

A
  • insuline binds to tyrosine kinase receptors
  • signalling pathway stimulated
  • triggers glucose uptake by GLUT 4 in liver muscle and fat cells
15
Q

describe the metabolic effects of insulin on liver

A
  • anabolic
  • ^ glycolysis
  • ^ glycogen synthesis
  • dec. gluconeogenesis
  • dec. glycogenolysis
16
Q

describe effect of insulin on skeletal muscle

A
  • ^ GLUT4 translocation
  • ^ glycogen synthesis
  • ^ glycolysis
  • ^ a.a. uptake and prot synthesis
17
Q

describe effect of insulin on fat cells

A
  • ^ GLUT4 translocation
  • ^ glycerol
  • -> ^ synthesis of fatty acids and triglycerides
  • -> inhibits lipolytic actions of adrenaline, GH and glucagon
18
Q

outline some medical indications for insulin

A
  • needed for Px w/ T1D
  • emergency treatment of ketoacidosis
  • improves control of diabetes in T2D and for intercurrent events e.g. surgery or infection
  • during pregnancy
  • emergency treatment of hyperkalaemia
19
Q

how is insulin that is used for therapy treatments retrieved from

A

made as recombinant human protein in bacteria

20
Q

why is oral administration of insulin not successful

A
  • insulin is a peptide

- degraded by GIT

21
Q

how is insulin most commonly administered

A

Subcutaneously

22
Q

what effect does having different formulations of insulin have

A

rate of absorption delayed by ^ particle size

23
Q

what are the 3 insulin formulations and how do they differ

A

short acting (pen)

  • onset 30min
  • short duration

intermediate acting

  • 16-35hr onset
  • longer half life
  • insulin coupled w/ zinc

long acting

  • > 35hr onset
  • coupled w/ zinc
24
Q

what is insulin glargine (Lantus) and why is it good

A
  • modified insulin
  • long acting
  • provides constant basal insulin supply
  • prolonged absorption from site of injection
  • reduces risk of night time hypoglycaemia
25
Q

what is the best therapy for T1D

A

mixture of short and medium lasting insulin injected before meals

  • new strategy incl. long lasting insulin delivered by pump w/ short acting taken before meals
26
Q

list some factors affecting subcutaneous absorption of insulin after self administration

A
  • site of injection
  • exercise = blood flow at site
  • depth of injection
  • conc. and dose of insulin
  • insulin degrading activity in subcutaneous tissue
27
Q

give some side effects of insulin therapy

A
  • hypoglycaemia –> coma –> brain damage
    (reversible with glucagon or sweet drinks)
  • allergic reactions
  • lipodystrophy
  • lipohypertrophy
28
Q

how can insulin affect serum K+ levels

A
  • stimulates K+ uptake into cells via activation of Na/K ATPase pump
  • IV insulin can lead to dangerous reduction in serum K+
  • diabetic ketoacidosis
29
Q

explain how ketoacidosis occurs

A
  • T1D Px doesn’t take insulin
  • body shifts to start breaking down fat as source of energy
  • prod. ketones and acids which lower blood pH
30
Q

give some signs of diabetic ketoacidosis

A
  • thirsty
  • dehydrated
  • fruity smelling breath
  • ^ blood glucose
  • drowsiness
  • ^ HR
  • vomiting
  • weight loss
  • frequent urination
31
Q

treatment for DKA

A

give saline and IV insulin

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