Endocrinology Flashcards
How does T1DM commonly present?
What are the investigations for diagnosis?
Presents in 25-50% of cases with DKA. The rest will present with the triad of polyuria, polydipsia and weight loss.
Should diagnose with a single random glucose BM of >11mM (or after OGTT) or fasting >7mM if symptomatic.
Asymptomatic must have the above criteria on two separate occasions.
Test for associated autoimmune thyroid disease.
Test for associated coeliac disease
Test baseline FBC, glucose and U+Es
How is T1DM managed?
Need to have well controlled glucose levels.
Insulin regime-
Long acting insulin taken at night (Lantus)- this is the basal dose.
Short acting insulin taken 30 mins before a meal (Actrapid)- this is the bolus dose
Insulin pump-
This is much more accurate and controlled levels of insulin, less injections and more flexible with eating. However need to have the pump attached at all times, small risk of infection, risk of pump becoming occluded. Need to change cannula site every 2-3 days to avoid lipodystrophy and allow effective uptake.
Two types:
Patch- As a patch, once the patch is finished it can be removed- insulin release via a separate controller.
Tethered- The control (with the insulin) is worn around the belt area with a tube attached to the injection site.
What are the short term complications of T1DM?
Hypoglycaemia-
Taking too much insulin, poor consumption of carbohydrates or poor processing of carbohydrates i.e. vomiting, diarrhoea, sepsis, malnourishment etc.
Most patients will feel a hypo coming on i.e. dizziness, pallor, sweating, hunger, tremor, irritability etc. This can become more severe leading to unconsciousness, coma and even death.
Manage by giving fast acting glucose (Lucozade) and slow acting for when the fast actin wears off (biscuits). If patient can’t tolerate oral or is unconscious- give IM glucagon injection and IV dextrose infusion.
Other causes of hypos- Glycogen Strorage Disease, Hypothyroidism, liver cirrhosis, alcoholism etc.
Hyperglycaemia-
Will need adjustment of their insulin regime. I.e patients will know 1 unit of insulin reduces their BG by 4mM and so can alter their units based on their intake to avoid hyperglycaemia.
What are the long term complications of T1DM? (RECAP)
Macrovascular: Coronary artery disease Diabetic foot disease HTN Stroke
Microvascular-
Retinopathy
Peripheral neuropathy
Nephropathy
Infections: UTI Skin infections Candida (thrush) Pneumonia
What are the main factors of DKA?
Ketosis-
Reduced production of insulin/reduced intake of insulin means cells can’t take up glucose and so uses the glycogen stores. Once the glycogen stores have been exhausted ketones are produced. Bicarbonate is increased to buffer the pH, but ketones will use this up too and so develop a ketoacidosis. Since oral intake will remain and the glucose is not being processed- will develop a hyperglycaemia.
Dehydration-
Hyperglycaemia means the kidney is overloaded with glucose and so excretes this out. The glucose draws out water with it leading to dehydration. Hence develop polydipsia.
Hypokalaemia-
Usually insulin draws K+ into the cells. No insulin means K+ remains outside of cells, kidneys excrete K+ out of the body but since no stores in the body- total body hypokalaemia which can lead to arrhythmias.
How does DKA present?
How is DKA diagnosed?
Presentation- Polydipsia Polyuria Weight loss Vomiting Sepsis/other potential triggers Altered consciousness Acetone breath Dehydration symptoms and hypotension
Diagnosis-
BM >11mM
Serum ketones> 3mM
Acidosis ph<7.3
How is DKA managed?
Need to reverse the ketosis/hyperglycaemia, hypokalaemia and dehydration:
(1) Slow fluid infusion (over 48hrs)
(2) Fixed rate insulin infusion.
Ensure not to give fluid to fast to avoid cerebral oedema. In dehydration fluid moves from the intracellular compartment to extracellular, therefore fluid moves out of the brain which can lead to cell atrophy and death. Once fluid is introduced, it moves quickly back into the intracellular compartment of the brain leading to cerebral oedema. Should therefore monitor GCS freuqntl and be cautious of headaches, bradycardia, altered consciousness etc- Manage with slowing down IV fluids, IV mannitol and Iv hypertonic saline.
Avoid bolus fluids unless requiring resuscitation
Treat triggers i.e. Abx for sepsis
Prevent hypoglycaemias- once BG drops <14mM treat with Iv insulin
Add K+ and monitor
Monitor pH, glucose and ketones
What is adrenal insufficiency?
This refers to the reduction in steroids- steroids are essential for living therefore insufficiency is life-threatening unless replaced.
Primary- (aka Addison’s disease)
Adrenal glands affected, can be due to damage, but more commonly congenital underdevelopment (hypoplasia). Therefore get reduced cortisol and aldosterone.
Secondary-
Pituitary gland affected i.e. post surgery, infection, radiotherapy, ischaemia. This causes a reduced ACTH and so reduced cortisol.
Tertary-
Hypothalamus affected i.e. stopping steroids drastically after long term use (>3wks). This causes a reduced CRH and so reduced cortisol.
How does adrenal insufficiency present in babies?
How does it present in children?
Babies- Poor feeding Failure to thrive Vomiting Lethargy Jaundice Hypoglycaemia
Children- Nausea and vomiting Abdominal pain Muscle weakness/cramps Weight loss/poor weight gain Reduced appetite Failure to develop Brown pigmentation
How is adrenal insufficiency invesitgated?
Glucose- Hypoglycaemia
U+Es- Hyponatremia, hyperkalaemia
Also check cortisol, renin, aldosterone and ACTH.
Primary- Low cortisol, low aldosterone, high ACTH, high renin
Secondary- Low cortisol, low ACTH, normal aldosterone, normal renin
Short Syncathen test can be conducted. Measure baseline cortisol first thing in the morning and give syncathen (ACTH). Measure cortisol again at 30 mins then 60 mins. If cortisol ahs not increased to double the baseline = primary adrenal insufficiency.
How is adrenal insufficiency managed?
What are the sick day rules?
Steroid treatment.
Hydrocortisone replaces cortisol.
Fludrocortisone replaces aldosterone.
Since steroids are needed for survival patients need a steroid card and ID tag.
Should not miss doses and increase with sickness.
Need monitoring in clinic for- growth and development, U+Es, glucose, bone profile, Vitamin D and BP.
Sick day- (i.e. fever, D+V etc) Refer to sick day rules plan: Increase steroids Increase carbohydrate intake If D/V then take steroids IM, need hospital admittance for IV steroids.
What is Addisonian/adrenal crisis?
How is it managed?
Absence of steroids has lead to life threatening situation.
Can occur as first presentation of Addison’s disease OR person with established Addison’s is suffering for trauma/infection OR patient on long term steroids has abruptly stopped their steroids.
Presentation: Reduced consciousness Hypotension Hypoglycaemia HypoNa and HyperK+
Investigations should not be made, concentrate on management.
Management: IV hydrocortisone IV fluids Intensive monitoring including electrolyte and fluid balance Correction of hypoglycaemia.
What is congenital adrenal hyperplasia?
How does it present?
How is it managed?
Autosomal recessive disease where there is a deficiency of 21-hydroxylase enzyme.
Progesterone is usually converted into cortisol and aldosterone (dependent on 21-hydroxylase) and also into testosterone (independent of 21-hydroxylase). Therefore deficiency of 21-hydroxylase means more progesterone is converted into testosterone.
Presentation-
Severe cases-
Females can have ambiguous genitalia.
At birth baby will have hypoglycaemia, hyponatraemia and hyperkalaemia, leading to poor feeding, vomiting, dehydration, arrhythmias.
Mild cases will present in later childhood or at puberty:
Females- taller for age, facial hair, absent period, deep voice, early puberty.
Males- taller for age, deep voice, large penis, small testicles, early puberty.
Management-
Hydrocortisone
Fludrocortisone
Females with ambiguous genitalia can have corrective surgery.
Why do patients with congenital hyperplasia have hyperpigmented skin?
Have less cortisol therefore body produces ACTH.
ACTH produces melanocyte stimulating hormone as a by product.
Leads to hyperpigmentation.
What is growth hormone deficiency?
How does it present?
Reduced production of GH. Can be due to underdeveloped pituitary gland, genetic mutation of the GH or GHRH gene, or seocndary to pituitary damage i.e. infection, trauma or surgery. Can occur alongside other pituitary hormone deficiencies i.e. LH/FSH, thryid hormone and adrenal hormones in hypopituitarism.
Important for growth of organs, bones and height.
Presentation:
Neonates/at birth:
Micropenis
Severe jaundice
Hypoglycaemia
Older infants/children: Poor/halted growth after the age of 2-3yrs old Slow development of movement/strength Delayed puberty Short stature
