Endo 15: Type I Diabetes Mellitus Flashcards
What acts as a marker for insulin function?
- C PEPTIDE
- -> it is linked to insulin production
What causes T1DM ?
- destruction of Beta cells
Autoimmune destruction of islet cells
What is a histological feature of T1DM?
- there is a lot of lymphocyte infiltration of the beta cells
- -> which destroys B-cells
- -> so they can no longer release insulin
What is the importance of the autoimmune basis of T1DM?
- increased prevalence of other autoimmune disease
- risk of autoimmunity in relatives
- more complete destruction of B-cells
- autoantibodies can be useful clinically
- immune modulation offers possibility of novel treatments
What are 2 most significant marker for clinically defining someone who might have T1DM?
- Islet cell antibodies (ICA)
- Glutamic Acid Decarboxylase antibodies (GADA) –> neurotransmitter
others:
- insulin antibodies (IAA)
What are some symptoms of T1DM?
Symptoms:
- polyuria
- nocturia
- polydipsia
- blurred vision
- weight loss
- fatigue
- thrush (due to increased risk of infections)
What are signs of T1DM?
Signs:
- dehydration
- cachexia
- hyperventilation (may have metabolic acidosis)
- smell of ketones
- glycosuria
- ketonuria
What is the effect of Insulin on:
HGO:
Glucose uptake:
Proteolyic breakdown:
Glycerol release from fatty tissue:
HGO: decrease
Glucose uptake: increase
Proteolyic breakdown: decrease
Glycerol release from fatty tissue: decrease
Describe the mechanism of diabetic ketoacidosis in T1DM
- glucose = isn’t taken up into cells + utilized
so most energy = from fatty acids - if you have insulin deficiency, fatty acids come out of adipocytes –> into circulation (instead of glycerol)
- then fatty acids go to the liver
- and is converted to ketones
- there is no insulin to inhibit this process
- -> so you get ore ketone bodies produced by the liver
What are main aims of treatment of T1DM?
- reduce early mortality
- avoid acute metabolic decompensation
- identify requirement for exogenous insulin
- prevent longterm complications such as retinopathy, neuropathy, nephropathy etc.
note: increase in ketone = insulin DEFICIENCY
-
How would you control diet in T1DM?
- reduce fat
- reduce refined carbohydrate
- increase complex carbs
- increase soluble fibre
What are some treatments for T1DM?
with meals:
- short acting insulin
- human insulin
- insulin analogues e.g lispro, aspart etc
background insulin:
- long acting
- non-C bounds to zinc or protamine
- insulin analogues e.g glargine, determir, degludec
note: type + dose = dependent on how much patient eats in each meal and when they eat.
How do insulin pump act as a method of treatment for T1DM?
what are disadvantages of it?
- provides continuous insulin delivery
- has preprogrammed basal rates + bolus for meals
DSADV:
- doesn’t measure glucose
- no completion of feedback loop
How do islet cell transplants act as a method of treatment for T1DM?
what are disadvantages of it?
- islet cells = harvested/isolated/injected into liver
DSADV:
- risk of rejection
- long waiting list
note: transplant if there is severe hypoglycemia + can’t be controlled by insulin pump
How do capillary monitoring act as a method of treatment for T1DM?
what are disadvantages of it?
- prick finger tips
- capillary glucose levels
- -> reflects venous blood glucose
- patients can titrate insulin dose according to reading
Long term blood glucose control is monitored by measuring:
HbA1c
- HbA1c red cells react with glucose
- high HbA1c = high glucose level in blood
- lower HbA1c = lower risk of microvascular complication
note: not that useful in those with renal failure/ Hb Opathy
What are the major acute complications associated with T1DM? (rapid decompensation)
- hyperglycemia
- metabolic acidosis
Why would hyperglycemia occur in T1DM?
- reduced glucose utilisation in tissues –> causes increased hepatic glucose production
Why would metabolic acidosis occur in T1DM?
- increased ketone body production in liver
- causes increase in circulating acetoacetate + hydroxybutyrate
- causes osmotic dehydration _ poor tissue perfusion
Define hypoglycemia
+
severe hypoglycemia
hypoglycemia = condition when the plasma glucose level = < 3.6 mmol/L
severe hypoglycemia = hypo requiring help of another person to treat
what are some Hypoglycemia symptoms + signs?
Increased autonomic activation:
- palpitations
- tremor
- sweating
- cold extremities
- anxiety
Impaired CNS function:
- drowsiness
- confusion
- coma
How would you treat hypoglycemia orally?
- feed patient glucose as solution/ tablets
- give complex CHO
How would you treat hypoglycemia parenterally?
if consciousness = impaired:
- give IV dextrose
- 1mg Glucagon IM
