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ENDOCRINE > A. DIABETES > Flashcards

A. DIABETES Flashcards

1
Q

what is diabetes mellitus

A

chronic metabolic disorder characertised by hyperglycaemia

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2
Q

what is type 1 DM characterised by

A

insulin deficiency so patients inject insulin as they can’t make insulin (5-15%)

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3
Q

what is type 2 DM characterised by

A

impaired β-cell function or loss of insulin sensitivity (insulin resistance)
(85-95%)
normally older people

complex:
- impaired insulin signalling pathways which decrease target-cell inflammation
- nutrient oversupply, cellular stress and inflammation causing molecular changes in cells

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4
Q

what are the 3 main consequences of hyperglycaemia

A
  1. glucosuria (glycosuria)
  2. polyuria (due to osmotic diuresis)
  3. polydipsia
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5
Q

what are other consequences of hyperglycaemia

A
  • increased urinogenital infections eg: thrush, UTIs due to glucose in urine which is a nice culture of pathogens
  • blurred vision/vision disturbance due to altered refractive index of lens
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6
Q

what normally happens with normal glucose plasma concentration

A

glucose gets filtered into ultra filtrate in kidney and gets reabsorbed back into blood so hardly any glucose in urine

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7
Q

what happens when glucose plasma concentration is greater than 8.9-10.6mmol/L

A
  • glucose levels in the filtrate is very high
  • exceeds renal reabsorptive capacity as there is limited reabsorptive capacity
  • excess stays in filtrate and appears in urine
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8
Q

what does glucosuria cause

A
  • an increase in urinary osmotic pressure so water stays in filtrate and urine
  • leads to a decrease in renal water reabsorption

= OSMOTIC DIURESIS
osmotic pressure increased in urine leading to excessive production of urine

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9
Q

what does polyuria cause

A

dehydration and hence thirst

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10
Q

how is thirst activated

A

there is a fall in blood volume and an increase in plasma osmolarity which activates osmoreceptors in hypothalamus

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11
Q

what are metabolic consequences of impaired glucose utilisation

A
  • lethargy, weakness
  • weight loss (T1DM)
  • ketoacidosis (T1DM)
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12
Q

what are microvascular (affecting capillaries) long-term complications of DM

A
  • nephropathy
  • neuropathy
  • retinopathy

likely with increased duration of chronic hyperglycaemia/DM

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13
Q

what are macrovascular (affecting medium-large arteries) long-term complications of DM

A
  • ischaemic heart disease
  • stroke
  • peripheral vascular disease
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14
Q

what are normal plasma glucose levels

A
  • fasting <7.0 mmol/L (for 8 hours)
  • random <11.1mmol/L
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15
Q

what are normal HbA1c levels

A

20–42 mmol/mol (4.0 - 6.0%)

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16
Q

what is HbA1c test

A

measures glycated or glycosylated haemoglobin - indicator of glycaemic control during previous 2-3 months (lifespan of RBC)

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17
Q

diagnosis of DM with signs/symptoms

A

1 of:
- fasting ≥ 7.0 mmol/L
- random ≥ 11.1 mmol/L
- HbA1c ≥ 48mmol/mol (or 6.5%)

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18
Q

diagnosis of diabetes in asymptomatic patient

A

2 abnormal test results on different days

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19
Q

what is type 1 diabetes

A
  • autoimmune
  • progressive destruction of islet β-cells by autoantibodies
  • onset <40 years
  • rapid onset as pathophysiological changes occur much earlier
  • need to lose 90% of β-cells to show signs and symptoms
  • no secondary complications at diagnosis
  • under or normal weight
  • tendency to ketosis
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20
Q

what causes type 1 DM

A

susceptibility genes and environmental triggers like viruses and toxins which which switch the genetically pre-disposed individual to having autoimmune disease

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21
Q

what is ketogenesis

A

synthesis of ketone bodies by liver from fatty acid breakdown products (C fragments)

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22
Q

example of the breakdown products (ketone bodies) of the fatty acids

A

2x acetyl CoA which forms acetoacetate by oxidative phosphorylation or tricarboxylic acid cycle (generate ATP in glucose metabolism)
-β-hydroxybutyrate & acetone formed

we normally have a small amount in the blood

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23
Q

how does insulin and glucagon affect ketogenesis

A

inhibited by insulin
stimulated by glucagon

24
Q

what happens in starvation and T1DM regarding ketogenesis

A

Catabolism
- we start to break down fats (energy reserve) as we don’t have insulin action - ketosis/ketoacidosis
- hence we make more ketone bodies which causes metabolic acidosis (decrease in blood pH)
- as we have more acidic ketone bodies (acetoacetate and β-hydroxybutyrate)

25
Q

treatment of T1DM

A
  • insulin
  • regular exercise
  • healthy diet
26
Q

T2DM

A
  • onset >40 years
  • gradual onset
  • secondary complications present in 25% patients at time of diagnosis due to being hyperglycaemic for a while
  • usually overweight
  • > 25 years (black, S.Asian) risk is 2-4x greater due to greater risk of developing central adiposity/obesity
  • risk is 2-6x greater if have family history of DM
  • no ketones in urine
27
Q

what causes type 2 DM

A

susceptibility genes and environmental triggers like reduced physical activity and increased calorie consumption

28
Q

treatment of T2DM

A
  • diet 10-20% then
  • drugs (80-90%, 20% insulin) as diabetes advances and β-cells have insufficient activity
29
Q

secondary causes of DM (ie not caused by gland/hormone directly) - endocrine

A
  • Cushing’s: excess of cortisol
  • Acromegaly: excess of growth hormone
  • Phaeochromocytoma: excess of adrenaline

These hormones increase blood glucose

30
Q

secondary causes of DM (ie not caused by gland/hormone directly) - pancreatic disease

A
  • chronic pancreatitis
  • surgery
  • cystic fibrosis
  • tumour

impairs function of pancreas so insufficient islets of Langerhans and hence a decrease in insulin secretion

31
Q

secondary causes of DM (ie not caused by gland/hormone directly) - genetic disorders

A
  • down’s syndrome
  • prader-Willi syndrome

impairs function of pancreas so insufficient islets of Langerhans and hence a decrease in insulin secretion

32
Q

secondary causes of DM (ie not caused by gland/hormone directly) - drug induced

A
  • steroids
  • beta-blockers
  • diuretics

disturb lipid and glucose metabolism leading to precipitation/worsening of diabetes

33
Q

what are the aims of management of DM

A
  • alleviate symptoms
  • minimise risk of long-term, secondary complication
34
Q

non-pharmacological treatment for DM

A
  • healthy diet (weight loss?)
  • exercise (improve insulin sensitivity and weight loss to reduce CV risk)
  • smoking cessation to decrease CV risk
35
Q

when is insulin used

A

type 1 and type 2
inadequate control with drugs or pregnancy

36
Q

insulin injection sites (sc)

A
  • upper outer arms
  • lower abdomen
  • upper outer thighs
  • buttocks
37
Q

why do you need to rotate injection site

A

to avoid lipodystrophy to limit erratic drug absorption

(lipoatrophy - fat shrinkage and lipohypertrophy - fat enlargement)

38
Q

when are insulin pumps used

A

T1DM
- continuous subcutaneous insulin infusion
- continuous basal dose with patient-activated bolus doses at meal times

39
Q

when are insulin injections used

A
  • for fine control in serious illness
  • in diabetic ketoacidosis
  • in surgery (peri-operative)

short-acting soluble insulin for urgent treatment

40
Q

cell replacement therapy for type 1 diabetics

A
  • islet transplantation (β-cells) so don’t need insulin
  • some require 2 transplants
  • require immunosuppression to prevent rejection as autoantibodies may start to destroy transplant β-cells
41
Q

artificial pancreas for type 1 diabetics

A
  • continuous glucose monitoring system with a insulin pump (hybrid closed system)
42
Q

what is the first stage of management of type 2 diabetes

A

diet/lifestyle interventions trialled for 3 months

  • healthy cardio protective diet
  • weight loss if overweight
  • moderation of alcohol
  • smoking cessation
43
Q

what is first line treatment for T2DM

A

metformin (caution in renal impairment as affects excretion) or
DPP-4 inhibitor (gliptins ie - sitagliptin)
Pioglitazone (eg - thiazolidinedione)
Sulphonylurea (eg - glicazide, tolbutamide)
SGLT2 inhibitor (dapagliflozin)
GLP-1 analogue/incretin mimetic (exenatide, liraglutide)

44
Q

what is first line treatment for T2DM if have CHF/CVD/QRISK3 ≥10%

A

metformin + SGLT2 inhibitor (CV and renal benefits)

45
Q

how does metformin (biguanide) work

A

MOA not clear, activate AMP kinase which is involved in metabolic activity?
- reduces gluconeogenesis
- increases liver sensitivity by decreasing storage of lipid in liver
- increases glucose uptake/utilisation in skeletal muscle

46
Q

how do sulphonylureas work

A
  • stimulate insulin release by blocking islet β-cell ATP-sensitive K channel so there is increased exocytosis
47
Q

how does pioglitazone work

A

PPARᵧ (peroxisome proliferator activated receptor-gamma) agonist ‘insulin sensitiser’
- improves glucose uptake/utilisation (skeletal muscle, liver, adipose) and lipid metabolism (liver, adipose)

48
Q

what do incretins do (GLP-1, GIP)

A

islet β-cells
- stimulate glucose-induced insulin release

islet α-cells
- inhibit glucagon release

therefore lower blood glucose

also:
- reduce gastric emptying as increase transit time of food in gut and hence a rapid rise of blood glucose with carbs is slowed
- promote satiety
- reduce hepatic glucose production (gluconogenesis)

49
Q

what happens to incretin effects on insulin release in T2DM

A

decreased

50
Q

what does DDP-4 (dipeptidyl peptidase-4) do

A

breaks down incretins

51
Q

what can GLP-1 analogues be used for

A

weight loss medications

52
Q

what is SGLT2 responsible for

A

reabsorption of glucose from ultrafilitrate

53
Q

how do SGLT2 inhibitors work (sodium-glucose co-transporter 2)

A
  • inhibit SGLT2 in renal PCT to inhibit renal glucose reabsorption and increase urinary glucose excretion to get a a decrease in blood glucose
  • CV and renal benefits in CHF and CKD (unlikely to be released to improvement in glycaemic control)
54
Q

side effects of SGLT2

A

polyuria
polydipsia
xerostomia (dry mouth)

55
Q

what if first line/other drugs don’t work

A

dual therapy or triple therapy if have CHF/CVD/QRISK3 ≥10%

start insulin with/without other drugs then may need to intensify regime or add drugs due to loss of insulin secretory capacity

56
Q

bariatric surgery for DM

A
  • BMI ≥ 35, expedited assessment for metabolic surgery
  • BMI ≥ 30 (failed to lose weight and failed drug intervention), consider metabolic surgery
    (ethnicity prone to central adiposity, BMI ≥ 27.5)
57
Q

very low calorie diets for DM (on NHS)

A
  • 800 calories per day
  • rapid weight loss and reduced CV risk
  • can reverse diabetes for at least 2 years
  • careful management required

ENDOCRINE (17 decks)

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