T1DM Flashcards
main characteristic of T1DM?
difference to T2DM?
complete lack of insulin
whilst T2DM is the relative lack of insulin and insensitivity
how can T1DM unusually end up presenting in later life?
as Latent Autoimmune Diabetes in Adults (LADA)
is DKA a feature of T1DM?
yes
it is not a significant feature of T2DM as there is enough insulin present to suppress ketoacidosis
How can monogenic diabetes present itself?
Type 1 or Type 2
e.g. MODY
what can also cause a diabetes presentation?
pancreatic damage e.g. due to alcohol
which type has more of a genetic role in its development?
T2DM
T1 is usually autoimmune
why is beta cell failure in T2 relative?
insulin is produced by not enough to stimulate the insulin receptors
what mediates autoimmune destruction of beta cells?
multiple relapse-remitting processes include different antibodies destroying the cells in phases
what is the honeymoon phase in autoimmune destruction of beta cells
last phase where beta cells are in non-hyperglycaemia response with just enough insulin
what happens to cause a breach in autoimmunity control?
Tregs normally keep check on effector T cells that are destructive
the Tregs are eventually overcome and complete destruction of beta cells takes place
what increases the risk of autoimmune diabetes
a background of autoimmune disorders increases the prevalence of other autoimmune disorders
a risk in relatives
test for auto-antibodies
which alleles pose a significantly increased risk of T1?
HLA-DR alleles specifically DR3 and DR4 have significant risk
possible environmental triggers of T1?
autumn/winter months see more T1DM diagnoses due to possible infection cause
what are the markers of T1DM?
o Islet cell antibodies.
o Insulin antibodies.
o Glutamic acid decarboxylase (GADA- created GABA neurotransmitter)
o Insulinoma-associated-2 autoantibodies receptor like family.
what are the symptoms of T1DM?
Polyuria
nocturia.
Polydipsia.
Blurring of vision.
Thrush- yeast infection
Weight loss.
Fatigue.
what are the signs of T1DM?
Dehydration. Cachexia – muscle wasting/weakness. Hyperventilation – Kussmahl breathing Ketone smell. Glycosuria and Ketonuria.
what is the function of insulin
release post-prandial to increase the absorption of glucose
- inhibits glycerol leaving adipocytes (therefore no gluconeogenesis)
what is the result of a lack of insulin on adipocytes?
FFAs are released and turned into ketone bodies inside the liver
these KBs are taken up by muscles and the brain
causes ketonuria
what are the aims of treatment for T1?
- reduce early mortality
- avoid acute metabolic decompensation
- prevent long term complications (retinopathy, nephropathy, vasc disease)
how is life preserved in T1?
using exogenous insulin
what dietary changes need to be made?
- reduce calories of fat and refined carbs
- increase calories of complex carbs and increase soluble fibre
- distribute food evenly throughout the day, regular meals and snacks
what must be taken into consideration when giving insulin?
people have a basal level of insulin so treatment must retain this
when must insulin be given?
- meals: short acting insulin, human or analogue (lispro, Aspart, Glulisine)
- background: long-acting, non-c bound to zinc/protamine or analogue (Glargine, Determir , Degludec)
alternative treatment option
- insulin pumps: gives continuous delivery, pre-programmed basal and bolus rates but does not measure glucose feedback
- islet cells transplants: donor donates pancreas islet cells inserted into diabetic’s liver portal vessels to release insulin ; patient on immunosuppressants; treatment reserved for those with erratic control of diabetes
how can treatment be monitored?
- capillary monitoring: either via a continuous monitor attached to the belly or through finger pricks. Allows adjustment of insulin dose.
- HbA1c red cells monitoring: glucose binds to RBCs irreversibly so can give a long-term view of glucose control. Can allow you to monitor blood glucose over a 3-month long period (life of a RBC).
what is a low Hb1AC associated with?
Lowering HbA1C is associated with a lower risk of microvascular complications.
acute complications of T1?
- metabolic acidosis (ketoacidosis)
- hyperglycaemia
what causes the acute complication: metabolic acidosis?
due to circulating acetoacetate/hydroxybutyrate (ketone bodies) and osmotic dehydration and poor tissue perfusion.
[Diabetic ketoacidosis CAN occur in T2DM and new onset diabetes BUT it is most common in T1DM]
what essentially causes hyperglycaemia (high glucose in the blood)? pathophysiology
- reduced uptake of glucose
- reduced tissue glucose utilisation
- increased HGO.
- In treating hyperglycaemia, patients MAY become hypoglycaemic.
what may be a consequence of treating diabetes?
hypoglycaemia (<3.6mmol/L)
- most mental processes inhibited at <3
- coma at <2 with long term effects on brain
- severe hypoglycaemia contribute to arrhythmia and sudden death
- recurrent hypos–> loss of warning to body
who are affected by hypos?
o Low quality glycaemic control patients.
o More common in patients with low HbA1C.
when can hypos strike?
o Anytime but often a clear pattern (i.e. pre-lunch hypos).
o Nocturnal which are common but not often recognised by the patient.
what are the triggers of hypos?
o New exercise.
o Missed meals.
o Inadequate snacks and alcohol.
o Bad insulin regime.
symptoms and signs of hypoglycaemia
<3.6 mmol/L
- increased autonomic activation (palpitations, sweating, tremor)
- impaired CNS functions
increased autonomic activation due to hypoglycaemia
o Palpitations. o Tremor. o Sweating. o Pallor/cold extremities. o Anxiety.
hypoglycaemia increases the release of catecholamines in order to increase glucose production and decrease glucose utilisation in order for the brain to have sufficient glucose. There is increased adrenergic activity.
what are the impaired CNS function symptoms due to hypoglycaemia?
o Drowsiness, confusion and altered behaviour.
o Coma.
treatment of hypoglycaemia due to diabetes treatment
- oral feed glucose (tablets or solution) and complex carbs
- parenteral if unconscious
(IV dextrose, 1mg glucagon IM)
how is DKA precipitated?
o New diagnosis of T1DM.
o Not taking insulin.
o Intercurrent stress (e.g. pneumonia).
o Fasting and not taking enough insulin.
what are the main 4 causes of DKA?
- fasting
- insulin def
- stress hormones
- dehydration
how is metabolic acidosis caused?
due to ketones (these are slightly acidic)
- produced as a result of fatty acid breakdown (lipolysis)
- reduction in bicarbonate production decreases blood pH
leads to
- Kussmahls respiration to blow off CO2
- hyperventilation
- vomiting
- abdominal pain
- fruity smell in breath
- ketonuria
urinary losses in DKA
water lost in urine so Na+ is lost
K+ is also lost but even though acidosis shows high K+to compensate for the acidosis, total body K+ is low
clinical features of DKA
o Polyuria & polydipsia due to diuresis.
o Dehydration.
due to drop in blood pH: o Hyperventilation. o Abdominal pain and vomiting. o Coma. o Glycosuria and Ketonuria.
investigations for DKA
o Capillary and plasma glucose. o Creatinine, K+, Na+. o FBC. o Arterial blood gas. o Amylase. o ECG, CXR, septic screen.
what are the treatments for DKA?
[FIPBO]
1) Fluids: H2O as normal saline 2) Insulin: dependent on blood glucose levels In second phase DKA, give 5% dextrose. 3) Potassium: usually found intracellular 4) Bicarbonate (increase pH) 5) Other: Cardiac monitor, catheterise, antibiotics, NG tube, heparin, arterial line or central line
why does blood pH drop?
ketone bodies are slightly acidic
causes hyperventilation/Kussmahls in order to remove CO2
