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4TH YEAR - CPTP > Week 4 - Diabetes & Lipid Disorders > Flashcards

Week 4 - Diabetes & Lipid Disorders Flashcards

1
Q

What are the effects of insulin on the Liver?

A

o Promotes Glycogen synthesis and storage
o Promotes synthesis of protein, triglycerides, VLDL
o Promotes glycolysis
o Inhibits gluconeogenesis, glycogenolysis, ketogenesis, lipolysis

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2
Q

What are the effects of insulin on muscle?

A

o Promotes protein synthesis – amino acid transport, ribosomal protein synthesis
o Promotes Glycogen synthesis – stimulates Glycogen synthetase and inhibits phosphorylase
o Increased Glucose entry into muscle cells

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3
Q

What are the effects of insulin on addipose tissue?

A

o Triglyceride storage – increased Lipoprotein Lipase (LPL) activity to hydrolyse triglycerides from lipoproteins
o Increased glucose entry – increased availability of glycerol phosphate as substrate for esterification of free fatty acids (FFA) into triglycerides
o Inhibits intracellular lipoprotein lipase

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4
Q

What is the pathogenesis of type 1 DM?

A

Genetic susceptibility & environmental factors
Autoimmune destruction of pancreatic beta-cells&raquo_space;> Insulin deficiency
• Hyperglycaemia
• Ketonaemia - acidic

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5
Q

What is the general management of type 1 DM?

A

Insulin replacement

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6
Q

What is the mechanism of disease in type II DM?

A

Insulin resistance at muscle, liver and in adipose tissue

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7
Q

What is the rough management in type II DM?

A
  • Lifestyle changes
  • Glucose-lowering agents
  • Dietary control - (Reduce calorie load which will Reduce obesity & Reduce insulin resistance)
  • Increase physical exercise
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8
Q

What is the first line drug treatment in Type II DM?

A

Metformin - Biguanide

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9
Q

What type of drug is metformin?

A

Biguanide

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10
Q

What is the mechanism of action of metformin (biguanide)?

A

Inhibits hepatic gluconeogenesis

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11
Q

What are the advantages of metformin (biguanide)?

A

Weight neutral/Weight loss

Low cost & Long track record

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12
Q

What are the disadvantages of metformin (biguanide)?

A

GI adverse effects
• Nausea, Loose stool & Flatulence
Lactic acidosis
• Mainly in patients with → Renal impairment, Heart failure or Liver disease

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13
Q

Name 2 sulponylureas…

A

Gliclazide, Glimepiride, Tolbutamide

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14
Q

What is the mechanism of action of sulponylureas?

A

Increase insulin secretion
• Bind to SU receptor on beta cell
• Open K+ channel & depolarize cell membrane
• Increase insulin release

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15
Q

What are the advantages of sulponylureas?

A

o Works quickly, is Low cost & long track record

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16
Q

What are the disadvantages of sulponylureas?

A

o Hypoglycaemia (tell DVLA) & Weight gain

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17
Q

Name a thiazolidinedione (TZDs)….

A

Pioglitazone

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18
Q

What is the mechanism of action of (TZDs)?

A

o Enhance lipogenesis
o Decrease lipolysis
o Decrease plasma FFAs → PPAR g agonists

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19
Q

What are the advantages of (TZDs)?

A

‘Insulin sensitisers’

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20
Q

What are the disadvantages of (TZDs)?

A

o Fluid retention
o Weight gain
o Increased peripheral fracture rate
o Bladder cancer?

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21
Q

Name a SGLT2 (sodium glucose transporter 2 inhibitor)…

A

Empagliflozin, Dapagliflozin, Canagliflozin

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22
Q

What is the mechanism of action of SGLT2?

A

Prevent renal glucose reabsorption (piss out calories and glucose)
• Inhibit SGLT2 in proximal tubule

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23
Q

What are the advantages of SGLT2?

A

Weight loss

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24
Q

What are the disadvantages of SGLT2?

A

o Increases chances of urinary tract infections and thrush
o Uncertain long term effects
o High cost

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25
Q

What are incretins and where are they made?

A

Hormones secreted by intestinal endocrine cells in response to nutrient intake
• Glucagon-like peptide I (GLP-1) → 30 amino-acid peptide
• Gastric inhibitory peptide (GIP)
• Source → L cells of the gut

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26
Q

What is the action of incretins?

A
  • Glucose homeostasis

* Multiple levels

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27
Q

What is GLP-1 - how does it work around the body?

include all targets - Brain, beta cells, alpha cells, stomach and liver

A

o Brain → Promotes satiety & reduces appetite
o Beta Cells → Enhances glucose-dependent insulin secretion
o Alpha Cells → Suppresses them to reduce glucagon production
o Stomach → Slows rate of gastric emptying
o Liver → reduces hepatic glucose output

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28
Q

What are the limitations of GLP-1 as a therapeutic agent?

A

DPP-IV (Dipeptidyl peptidase IV) cleaves GLP-I at c-terminus

Therefore GLP-I has a short half life ~ 1-2 mins
o Therefore it would require a continuous infusion unless we blocked DPP-IV (the enzyme that is breaking it down)

29
Q

What is the mechanism of action of DPP-IV inhibitors?

A

Inhibit DPP-IV and therefore prolong half-life of GLP-I

30
Q

What are the advantages of DPP-IV inhibitors?

A

o Oral
o No hypoglycaemia
o Well tolerated
o Some licensed at low GFR (in patients with renal impairment)

31
Q

What are the disadvantages of DPP-IV inhibitors?

A

Long term effects uncertain and it is expensive

GLP-1 Mimics

32
Q

What is the mechanism of action of GLP-1 mimics?

A

Resistant to DPP-IV therefore has a half life of hours not minutes
o Enhanced incretin effects

33
Q

What are the advantages of GLP-1 mimics?

A

No hypoglycaemia

Weight loss

34
Q

What are the disadvantages of GLP-1 mimics?

A

o Sc. Injection – similar to an insulin pen
o Adverse effects → nausea & vomiting
o Long term effects unknown
o Expensive

35
Q

What are the three main categories of insulin?

A

Mealtime insulins
Basal insulins
Insulin mixes

36
Q

What is the optimal insulin regimen?

A

Basal - Bolus therapy

37
Q

Give an example of a rapid-acting and a long-acting insulin analogues…

A

Rapid-acting → Novorapid or Humalog

Long-acting → Glargine or Detemir

38
Q

What are the advantages of Insulin analogues?

A

o reduced nocturnal hypo

o reduced fasting glucose (pre-breakfast)

39
Q

What are the disadvantages of Insulin analogues?

A

o ‘active’ self-management

o high cost

40
Q

What is the principle of Continuous Subcutaneous Insulin Infusion (CSII) – “Insulin pump”?

A

Constant infusion rapid-acting analogue
• Smaller sc. volume
• More predictable absorption
Basal rate + meal-time boluses

41
Q

What are the advantages of Continuous Subcutaneous Insulin Infusion (CSII) – “Insulin pump”?

A

o Less hypoglycaemia
o Less glucose variability
o HbA1c reduction
o Flexibility for the patient

42
Q

What are the disadvantages of Continuous Subcutaneous Insulin Infusion (CSII) – “Insulin pump”?

A

o DKA risk

o High cost – few thousand/pump

43
Q

What is the stepwise approach to treating a type 2 diabetic?

A
  • Step 1 → lifestyle measures only
  • Monotherapy → add metformin
  • Dual therapy →add sulphonylurea
  • Triple therapy →add on agent (PPARg, GLP-I enhancer or SGLT2 inhibitor)
  • Insulin (if not already used)
44
Q

What is the direct mechanism of action of Statins?

A

Decreasing cholesterol biosynthesis
• By inhibiting…. HMG-CoA Reductase

Increasing uptake of cholesterol from the circulation into the liver

45
Q

What is the possible indirect mechanism of action of Statins?

A
  • Improved endothelial function
  • Reduced inflammation
  • Plaque stabilisation
  • Inhibition of thrombus formation
46
Q

What are the most potent statins?

A

Atorvastatin and Rosuvastatin

47
Q

What are the side effects of statins?

A

Hepatic – deranged LFTs, Liver injury

Myalgia and Myositis – elevated CK (Creatine Kinase) levels
• “Minor” side effects: skin rash, GI upset, sleep disturbance, aches and pains
• Very small increased risk of diabetes in non-diabetic population
• Peripheral Neuropathy

48
Q

What are possible drug interactions of statins?

A

Statins metabolised by Hepatic Cytochrome P450 (CYP3A4)

CYP3A4 inhibitors include…
• Ciclosporin, Clarithromycin, Erythromycin, Diltiazem, Verapamil, Amlodipine, Amiodarone, Ketoconazole, HIV protease inhibitors, Grapefruit juice!

Risk of increased plasma concentrations of statins causing myopathy and/or rhabdomyolysis

49
Q

Name 3 other classes of lipid lowering drugs

A

Fibric Acid Derivatives – “Fibrates”
Ezetimibe
PCSK9 inhibitors

50
Q

Which enzyme do statins inhibit?

A

HMG-CoA Reductase

51
Q

How do you calculate anion gap?

A

Anion gap= Unmeasured cations – Unmeasured anions

Na + K - (HCO3 - + Cl-)

52
Q

What is the mneumonic for metabolic acidosis (high anion gap?

A

MUDPILES

53
Q

What are the causes of metabolic acidosis + mneumonic?

A
  • M: methanol, metformin
  • U: uremia
  • D: DKA
  • P: paraldehyde, paracetamol,phenformin
  • I : Iron, Isoniazid
  • L: lactic acidosis
  • E: ethanol, ethylene glycol
  • S: salicylate
54
Q

What are the parameters for a diagnosis of DKA?

A

Ketonaemia ≥3 mmol/L or Significant ketonuria (>2+ on urine dipstick)

Blood glucose >11 mmol/L or Known diabetes mellitus

Bicarbonate (HCO3-) < 15 mmol/L and/or venous pH < 7.3

55
Q

Why do you need to monitor potassium?

A

Hypokalaemia and hyperkalaemia are life-threatening conditions and are common in DKA.
Serum potassium is often high on admission (although total body potassium is low) but falls precipitously upon treatment with insulin.
Regular monitoring is mandatory

May need to replace with potassium infusion

56
Q

How should you prescribe insulin in DKA?

A

Insulin IV infusion (6 units/hour)

57
Q

What cautions do you need to take when replacing a patients IV insulin back to their usual regime?

A

Very very short half life of IV insulin and normal insulin takes a while to kick in.

Give fast-acting insulin s/c with a meal and discontinue insulin infusion 30 minutes later
o Then start on Basal-bolus

58
Q

What signs would point towards a severe DKA?

A

The presence of one or more of the following may indicate severe DKA
o Blood ketones > 6 mmol/L
o Bicarbonate level < 5 mmol/L
o Venous/arterial pH < 7.1
o Hypokalaemia on admission (< 3.5 mmol/L)
o GCS < 12 or abnormal AVPU scale
o Oxygen saturation < 92% on air (assuming normal baseline respiratory function)
o Systolic BP < 90 mmHg
o Pulse >100 or <60 bpm
o Anion gap > 16 [Anion Gap = (Na+ + K+) –(Cl- + HCO3-) ]

59
Q

What do you need to monitor in a DKA patient?

A
  • Hourly capillary blood glucose
  • Hourly capillary ketone measurement if available
  • Venous bicarbonate and potassium at 60 minutes, 2 hours and 2 hourly thereafter
  • 4 hourly plasma electrolytes
60
Q

What are your treatment aims in the first 6 hours in a DKA patient?

A

o Clear the blood of ketones and suppress ketogenesis
o Achieve a rate of fall of ketones of at least 0.5 mmol/L/hr
o In the absence of ketone measurement, bicarbonate should rise by 3 mmol/L/hr and blood glucose should fall by 3 mmol/L/hr
o Maintain serum potassium in normal range
o Avoid hypoglycaemia

61
Q

What parameter defines a resolution in DKA?

A

Resolution is defined as blood ketones < 0.3 mmol/L, venous pH > 7.3

62
Q

How do you avoid making a patient hypoglycaemic whilst treating DKA?

A

Replace 0.9% saline with glucose-insulin infusion

63
Q

What action is appropriate if a patient is having a severe hypoglycaemic attack?

A

Dextrose infusion or glucagon

  • Glucagon 1 mg IM
  • Recheck BM in 10 minutes
  • If BM<4.0, Repeat glucose bolus
  • If BM>4.0, give long-acting oral CHO when patient recovered.
64
Q

If diabetic patients are trying to get pregnant what advise should you give?

A

Folic acid supplementation – HIGH DOSE

5 mg pre-conception until 12 weeks post-conception

65
Q

What advice do you give during pregnancy?

A 
Monitor BMs pre-meal (target 4 -5.9) and 1-hour post-meal (target < 7.8) and at night.
Monitor ketones in urine or blood
Counsel about hypoglycaemia
o	Reduced hypoglycaemia awareness
o	Increased CHO requirements
Provide partner with glucagon
66
Q

What is the appropriate treatment During Labour or Caesarean Section?

A
  • GKI (glucose-potassium-insulin) infusion to maintain glucose 4 -7
  • Monitor BM every 30min - 1hour.
67
Q

What is the appropriate action post partum?

A
  • Following pIacental delivery,maternal insulin sensitivity improves.
  • Monitor BMs
  • May need to reduce insulin infusion rate by up to 50% post partum.
  • When converting back to s/c insulin, most need roughly pre-pregnancy dose of insulin
68
Q

If a patient is on a statin and gets community acquired pneumonia what treatment should you use for the pneumonia?
What other considerations should you take?

A

Treat with amoxicillin and clarithromycin (same as all patients)

Stop statin - P450 interaction

69
Q

What enzyme do statins inhibit?

A

HMG-CoA Reductase

4TH YEAR - CPTP (19 decks)

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