Diabetes Flashcards
What is T1DM?
When the pancreas can no longer produce insulin
Pathophysiology of T1DM
-what happens
-what gene
Autoimmune B cell destruction -> no insulin produced, and insulin is needed for glucose uptake into cells
Glucose stays in blood -> hyperglycaemia
Associated with HLA genes (DR3DQ2, DR4DQ8)
If both parents have HLA gene, what is the risk of the child getting T1DM?
What does this show?
30% risk
Only 5% acc get the condition -> strong environmental contribution
What are the environmental factors influencing T1DM?
Maternal -> gestational infections
Viral infections -> coxackie b4
Early exposure to cows milk
Vitamin D deficiency
Pollution
How does T1DM present?
(Usually acute onset)-
Hyperglycaemia symptoms:
Polydipsia
Polyuria
Weight loss
Thrush due to mellitus
Weakness, fatigue
Blurred vision
Recurrent Infections
Often kids come in in DKA which is how they’re diagnosed
Normal blood glucose levels
4.4-6.1mmol/L
What BG level is diagnostic of diabetes
Fasting 7mmol/L or higher
Random 11.1mmol/L or higher
HbA1c 48mmol/L is diagnostic of diabetes
How is T1DM diagnosed?
Classic symptoms
Blood glucose levels and HbA1c
Autoantibodies -> IAA, GAD, ICA
C-peptide -> little or none
Urinalysis -> for ketones
What are the components of managing T1DM
Basal-bolus regime:
Long acting insulin injected once a day
Short acting insulin injected 30mins before meals
carbohydrate intake monitoring
BG and ketone monitoring
complication awareness and management
Can give metformin as well as insulin in high BMI
Education is important
Goal is avoid hypo, prevent hyper
Annual review assessment:
Weight, BP, HbA1c, retinal screening, foot risk assessment
What are some treatment options for those with severe and poorly managed T1DM?
pancreatic islet transplantation-
Harvested from cadavers, injected into portal vein where they seed themselves in liver
whole pancreas transplant
Often done in those with end stage kidney disease
What are the complications of T1DM?
Hypoglycaemia
Hypergylcaemia
artery disease 2ndary to hyper
Diabetic foot
Stroke
Hypertension
Retinopathy
Kidney disease
UTIs and fungal infections
What is DKA?
What is its pathophysiology
When glycogen stores are exhausted and there is low glucose, fatty acids are converted to ketones which can be used as fuel
Usually kidneys buffer ketones so blood doesn’t become acidotic
In T1DM, insulin deficiency prompts body to inc fat metabolism, increasing ketone production
DKA= when ketone levels exceed body capacity to excrete them
What are the key features of DKA?
ketoacidosis- blood becomes acidic
dehydration- effect of polyuria
potassium imbalance- serum is normal-high but total body is low, as none is drawn into cells
When starting treatment with insulin there is a risk of developing hypokalaemia
How does DKA present?
Nausea and vomiting
Acetone smell to breath
Dehydration
Confusion + altered consciousness
Raised anion gap
Kussmauls respiration- deep rapid breathing pattern (associated with severe metabolic acidosis)
How is DKA diagnosed and treated?
Diagnosis needs all 3 of:
Hyperglycaemia
Ketosis (blood ketones 3+)
Acidosis (blood pH below 7.3)
Management plan with FIG-PICK-
Fluids- IV 0.9% NaCl
Insulin- IV 0.1units/kg/hour
Glucose- monitor
Also:
Potassium- infusion
Infection- may be underlying cause
Chart fluid balance
Ketones- monitor
What is a complication of DKA in children?
Cerebral oedema
Can cause brain cells to shrink and become dehydrated
Rapid treatment of dehydration and hyperglycaemia can cause sudden shift of water into cells, causing oedema (brain swelling)
What is HHS?
Hyperosmolar Hyperglycaemic State
Water loss and hyperglycaemia, but with absence of ketones
(More common in type 2)
How does HHS present?
How is HHS treated?
Extreme hyperglycaemia
Hyperosmolarity
Weight loss
Tachycardia
Hypotension
Confusion or coma
IV fluids and careful monitoring
What causes HHS, and who gets it?
Common in older people
Precipitated by;
-meds like thiazide diuretics and steroids
-Infection
-trauma that has compromised water intake
-other endocrine conditions that can affect insulin
-non compliance
What is T2DM?
Insulin resistance x impaired insulin production
Explain the pathophysiology and risk factors of T2DM
Repeat glucose exposure builds resistance -> more insulin needed for glucose uptake into cells
Pancreatic B cells may become fatigued over time with repeat exposure to glucose, and both of these factors leads to chronic hyperglycaemia (which also damages B cells)
Risk factors:
Genetics (Fhx), age, ethnicity
Obesity, sedentary lifestyle, high carb/sugar diet
What are the other hormonal changes in T2DM
Incretin effect decreased
Gucagon secretion increased
Common presentation of T2DM
Combination of risk factors and the following symptoms: (gradual onset)
-tiredness
-polyuria and polydypsia
-blurred vision
-unintentional weight loss
-infection eg thrush
-slow wound healing
-glucosuria
-acanthosis nigricans (dark velvety thickening of the skin, associated with insulin resistance)
What are the key HbA1c values in T2DM?
42-48 is pre diabetic (can be reversed)
48 is diagnostic of diabetes
53 is reasonable target in a diagnosed patient
