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Endocrine System > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Insulin synthesis

A

Pre-proinsulin –> proinsulin –> insulin + cleaved C peptide

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2
Q

C peptide

A

Good indicator of Beta islets cell function. Lasts longer than insulin

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3
Q

Insulin

A

Glycogenesis

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4
Q

Glucagon

A

Glycogenolysis

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5
Q

T1DM

A

Autoimmune Beta cell destruction causing an absolute insulin deficiency - little/no insulin being produced. Therefore, increased glucose in the blood and less glucose bing stored and/or used in the organs

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6
Q

T1DM is associated with HLA-DR3 T/F

A

T1DM is associated with Human leukocyte antigen DR3 or 4. (HLA-DR3/4)

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7
Q

T1DM definition

A

A metabolic disorder characterised by high glucose levels due to absolute insulin deficiency.

  • 10-20% of all diabetes
    most common under age of 20yrs
    peak incidence at 10-14yrs

Personal/family history of autoimmune disease e.g. Hashimoto’s - increases risk

Accute manifestation = DKA.

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8
Q

T1DM Symptoms

A 
polyuria 
polydipsia 
polyphagia 
weight loss 
fatigue 
poor wound healing
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9
Q

T1DM Management

A

Insulin

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10
Q

What would you expect to see with T1DM on investigation?

A

Low C-peptide (tested in patients with atypical features)

High blood sugar

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11
Q

Investigations

A
  • Random blood glucose: >11mmol/l with clinical features –> same day referral
  • Fasting blood glucose ≥ 7.0mmol/L is typical
  • OGTT >11 mmol/l two hours after a 75g oral glucose load
  • HbA1c: >48 mmol/l suggests hyperglycaemia over 3 months. use for monitoring

NB: HBa1C is inaccurate in children, haemolytic anaemia and pregnancy

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12
Q

What investigations could you consider in T1DM

A
  • C-peptide: if atypical features are present e.g. age > 50, BMI >25kg/m2
  • Autoantibodies: if atypical features are present, e.g. anti-glutamic acid decarboxylase
  • VBG: If concerned about DKA
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13
Q

First line management of T1DM

A

Basal bolus regime

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14
Q

Management

A

Urgent referral to daibetes specialist

Lifestyle

  • diet high in fibre and low in fat, sugar and sal
  • educate regarding carb counting, allows insulin dose to be matched to intake

Insulin therapy

  • Basal bolus: 1st line, long acting regularly (basal) with rapid acting insulin before meals (bolus)
  • basal - Levemir (detemir) given twice daily. Lantus (glargine) one daiy is an alternative
  • bolus insulin lispro (humalog), insulin aspart (novorapid)

Mixed insulin regime - mixed insulin comprises a short acting and long acting insulin, BD.
- used when unable to tolerate basal-bolus regime

Continuous insulin infusion: Disabling hypoglycaemia or persistent hyperglycaemia (HbA1c >69mmol/mol)

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15
Q

Monitoring

A

Glucose
- HbA1c: measured every 3-6 months with a target of ≤48 mol/mol
- Selft monitoring: check blood at least 4 times a day with the following targets
on waking: 5-7mmol/L
before meals and other times 4-7mmol/L

Retinopathy
- Immediate ophthalmoogy referral upon diagnosis and annually thereafter
arrange urgent review thereafter if:
- acute reduction in acuity
- pre proliferative or proliferative retinopathy
- diabetic maculopathy

Diabetic foot
- Should be assess at least annually; refer urgently to foot protection service if at risk (e.g. ulceration)

Diabetic nephropathy
- Annual measurement of eGFR and urinary albumin:creatinine ratio

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16
Q

Complications

A

Macrovascular
- IHD, PVD, Stroke

microvascular
- Diabetic nephropathy
neuropathy and retinopathy

17
Q

DKA

A
  • Metabolic state as a complication of T1DM (predominantly)
  • Medical emergency: dehydration and electrolyte imbalance
  • Triad: hyperglycaemia, acidosis and ketonaemia
  • Mortality rate <1% in UK
  • May be a first presentation of T1DM
  • Often a precipitating factor: infection, trauma, surgery, corticosteroid use
18
Q

Increased lipolysis is a feature of DKA - T/f

A

Increased lipolysis is a feature of DKA. as Fats used as the alternative fuel, fats are broken down and transported to the liver. The liver then converts this into ketone bodies and these are used by cells for energy. However this increases the acidity of your blood and acetone which give the sweet smelling breath.

19
Q

How does DKA lead to acidosis?

A

net reduction of insulin -reduced glucose entry into cells –> metabolism of lipids as an alternative energy sours
–> increase FFA to liver increased ketogenesis –> acidosis

20
Q

Kussmal breathing

A

Deep breathing due to metabolic acidosis

21
Q

Kussmal breathing

A

Deep breathing due to metabolic acidosis

Increased acidity of blood–> Reduced CO2 –> reduced acidity

22
Q

Why replace potassium in patients with DKA?

A

When you are acidityc lots of H+ irons in blood. They move into your cells, and potassium moves out into the blood (via the transporter). This contributes to hyperkalaemia. This can be worsened for your Na+/K+ atpase so this can also worsen your hyperkalaemia. Despite all this there is total body potassium loss as the potassium in your blood is being excreted out into your urine. Therefore serum potassium levels in DKA doesnt reflect your total body potassium. this is why you replace K+ in people with DKA as they are overall losing K+

23
Q

Clinical features of DKA

A 
Abdo pain 
N+V 
Polyuria and polydipsia 
weight loss 
inability to tolerate oral fluids 
lethargy and confusion
24
Q

Signs of DKA

A
  • Fruity pear drop smell
  • Dehydration
  • mild: only just detectable
  • moderate: dry skin and mucus membranes; reduced skin turgor
  • shock: tachycardia, hypotension, drowsiness, reduced urine output
  • Kussmal breathing
25
Q

investigations of DKA

A

Bedside:

  • urine dip: glycosuria and ketonuria
  • Bedside ketone and capillary glucose

Bloods:

  • ABG/VBG: quickest way to ascertain pH and HCO2 levels
  • U&E: electrolyte derangement and AKI due to dehydration
  • FBC and CRP: raised inflammatory markers may suggest underlying infection as a percipitant
  • Infection screen: if an infection is the suspected trigger
26
Q

Diagnostic criteria of DKA

A

Triad: Hyperglycaemia, acidosis, ketonaemia

  • Glucose > 11mmol/L or known DM
  • HCO3 <15 mmol/L and/or venous pH <7.30
  • Ketonaemia (≥3mmonl/l( or 2+ ketonuria

NB: can have DKA in children and young people with normal blood glucose. Also low ketone levels does not exclude DKA

27
Q

First line treatment of DKA with a SBP above 90 in adults

A

1L of normal saline over 1 hour

Then 1L Normal saline with KCL over the next 2, 2, 4, 4, the 6 hours.

Insulin - fixed rate insulin infusion
Give anticoags and closely monitor

28
Q

First line treatment of DKA with a SBP below 90

A

1L of normal saline over 15mins

- call for senior help

29
Q

Complications of DKA

A

Hypokalaemia and Hyper
- potentially life-threatening
Hyperkal - extracellular shift of K+ due to acidosis
hypo- due to correction of acidosis

Hypoglycaemia

  • due to rapid correction of ketoacidosis
  • may get rebound ketosis

Cerebral oedema

  • more common in children (70-80% of diabetes-related deaths)
  • Likely to be iatrogenic.
  • DKA = Hypervolaemic Hypoglycaemic state - drop in serum osmolality, if drops too quick you can get cerebral oedema.
30
Q

T1DM and Lorry Drivers

A
  • Need to monitor blood sugars atleast twice daily
  • need to check 2 hours before starting their drive
  • Need to monitor every 2 hours.
31
Q

DKA

A

Triad:

  • Acidaemia (pH < 7.3)
  • Hyperglycaemia
  • Ketones

An alternative metabolic pathway which occurs when the body requires energy but the body does not have enough insulin to turn sugar (carbohydrates) into energy

Ketones are produced when the liver metabolises fatty acids. They are then released into the blood stream which if excessively released can turn the blood acidotic having global negative impact.

32
Q

DKA presentation

A

Presentation:

  • General drowsiness
  • Vomiting
  • Dehydration
  • In severe cases they could feel SOB with a tachypnoea in their bodies attempt to “blow off” CO2 to try and compensate for the metabolic acidosis.

Treatment: FLUIDS, actarapid 50U and 50ml 0.9% saline mix infused at 0.1units/kg/hr. Potassium replacement. Glucose infusion once BM <14mmol

Continue fixed rate insulin until ketones <0.3mmon/l, venous pH >7.3 and Bicarb >18mmol/L

  • Always continue the long acting insulins even on a sliding scale/fixed rate infusion.
33
Q

HHS

A

Typically those with T2DM are at risk of this

  • It is a complication where high blood sugar (>35) results in high osmolality without significant ketoacidoses
  • symptoms include marked dehydration, weakness, leg cramps, vision problems, and an altered level of consciousness
  • Acidosis is ABSENT as no switch to ketone metabolism
  • Osmolality >340mosmol/kg
  • Treatment: FLUIDS! Only give insulin if levels are not falling by 5mmol/L/hour, replace potassium, give DVT prophylaxis if no contraindication.
  • Keep blood glucose at least 10-15mmol for the first 24 hours to avoid cerebral oedema
34
Q

Hyperglycaemia

A
  • High blood sugars
  • If you ever see high BM don’t forget to check ketones and pH also!
  • Treatment: Fast acting insulin such as actarapid or novorapid
35
Q

Hypoglycaemia

A
  • Blood sugars <4
  • Symptoms: Drowsy, confused, coma
  • Treatment:
  • oral sugar (gluco-gel/lucozade)
  • Glucagon (however, if they dont have a good store of sugar within cells or you have maximised the glucagon receptors then this wont necessarily work)
  • Glucose/Dextrose infusion

Endocrine System (10 decks)

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