endocrinology Flashcards
What is Addisons disease ?
autoimmune destruction of the adrenal gland
results in reduced cortisol and aldosterone being produced.
Features of Addisons disease?
lethargy
weakness
anorexia
N&V
Weight loss
Salt craving
Hyperpigmentation
Vitiligo
Loss of pubic hair in woman
Hypotension
Hypoglycaemia
Hyponatraemia and hyperkalaemia
Crisis - collapse, shock, pyrexia
Causes of hypoadrenalism
primary causes
Autoimmune
Infections 0 adrenal desctruction can be caused by infection such as TB , fungal infections and HIV
Genetics - mutations in genes like CYP21A2 and AIRE (APS-1)
Metastatic infiltration - such as lung or breast Ca
Adrenal heamorrhage - Trauma, anticoagulation, and sepsis can lead to adrenal haemorrhage, resulting in acute adrenal insufficiency.
Secondary causes
pituitary disorders (e.g. tumours, irradiation, infiltration)
Exogenous glucocorticoid therapy- supresses the hypothalamic pituitary axis
Addisons disease management?
Give a glucocorticoid and a mineralocorticoid
This usually means that patients take a combination of:
hydrocortisone: usually given in 2 or 3 divided doses. Patients typically require 20-30 mg per day, with the majority given in the first half of the day
fludrocortisone
patient education with Addisons?
emphasise the importance of not missing glucocorticoid doses
consider MedicAlert bracelets and steroid cards
patients should be provided with hydrocortisone for injection with needles and syringes to treat an adrenal crisis
discuss how to adjust the glucocorticoid dose during an intercurrent illness (see below)
Management of Addisons with intercurrent illness?
in simple terms the glucocorticoid dose should be doubled, with the fludrocortisone dose staying the same
Adrenal Crisis?
Adrenal crisis: An acute life-threatening condition characterized by severe hypotension, hypoglycemia, and altered mental status. Immediate treatment with intravenous hydrocortisone, fluids, and electrolyte correction is crucial.
Differentials for Addison’s disease?
Adrenal Insufficiency Secondary to Pituitary Disease
Adrenal Tuberculosis
Sepsis
Management of adrenal crisis
IV or IM hydrocortisone immediately
Patients should go to hospital immediately
1L of NaCl over 30 minutes
Monitor BP, HR, electrolyte and glucose status
IV hydrocortisone - infusion or QDS until patient is haemodynamically stable
Offer at least 40 mg oral hydrocortisone daily in 2 to 4 divided doses or at least 10 mg oral prednisolone daily in 1 to 2 divided doses until any underlying cause has resolved and the person is clinically stable.
ECG findings in hyperkalaemia?
ypical ECG findings include peaked T waves, flattened P waves, prolonged PR interval, widened QRS complex and sine wave pattern in severe cases
causes of hyperkalaemia ?
AKI
CKS
Addisons
Congenital adrenal hyperplasia
potassium sparing duretics
ACEi
Acidosis
Tumour Lysis syndrome
Rhabdo
what is considered hypoglycaemia?
BM < 3.3
causes of hypoglycaemia?
Diabetes (excess insulin, sulfonylureas) more likely to occur in diabetes who have a viral illness, have drunk alcohol or exercised more than usual, or just changed dose of a new medication
Non-diabetic causes
indomethacin, pentamidine, quinine, sulfonamide, IGF-1 and lithium.
Alcohol consumption
This is due to its inhibitory effect on gluconeogenesis and glycogenolysis.
Rarer causes:
hypopituitarism and Addisons disease
Insulinoma
what is the normal response when blood glucose drops?
The initial response to declining blood glucose involves the autonomic nervous system and counter-regulatory hormones. As glucose levels drop, the pancreas reduces insulin secretion, which normally facilitates cellular uptake of glucose. Concurrently, there is an increase in glucagon release from pancreatic alpha cells. Glucagon promotes glycogenolysis and gluconeogenesis in the liver, elevating plasma glucose concentrations.
Adrenaline (epinephrine) is also released from the adrenal medulla, stimulating hepatic glycogenolysis and inhibiting insulin release further. This hormone additionally activates lipolysis in adipose tissue, providing free fatty acids as an alternative energy source for peripheral tissues, thereby sparing glucose for cerebral use.
Cortisol and growth hormone are secreted in response to prolonged hypoglycaemia. Cortisol enhances gluconeogenesis and decreases peripheral utilisation of glucose by antagonising insulin action at target tissues. Growth hormone similarly supports gluconeogenesis while promoting lipolysis.
why do patients get symptoms when they are hypoglycaemic?
The symptoms of hypoglycaemia can be attributed to neuroglycopenia and autonomic activation. Neuroglycopenic symptoms arise due to insufficient glucose supply to the brain, manifesting as confusion, altered consciousness, seizures or even coma if untreated. Autonomic symptoms such as tremors, palpitations and sweating are mediated by adrenaline release.
what is Hypoglycaemia-Related Autonomic Failure (HAAF)
The development of HAAF further exacerbates the risk of hypoglycaemic episodes. This syndrome is characterised by both a diminished autonomic response to hypoglycaemia and a reduction in symptomatic awareness of low blood glucose levels.
Repeated episodes of hypoglycaemia can lead to this phenomenon, creating a vicious cycle. With reduced autonomic responses, the body’s ability to counteract falling glucose levels is further compromised. Meanwhile, decreased symptomatic awareness may delay the recognition and treatment of hypoglycaemic events.
Clinical features of hypoglycaemia?
Autonomic symptoms
- sweating
- tachycardia
- pallor
- tremors
- Hunger
Neuroglycopenic symptoms
- cognitive impairment
- dizziness and weakness
- vision changes
- moods changes
- seizure
Fatigue, nausea and abdominal discomfort, parenthesis
diagnosis for hypoglycaemia ?
Whipple’s triad aids the diagnosis of hypoglycaemia. It consists of symptoms or signs of hypoglycaemia, low blood glucose, and the resolution of symptoms with the correction of blood glucose.
further tests to diagnose the cause of hypoglycaemia?
Serum insulin: elevated in insulinoma.
Serum C-peptide: elevated in insulinoma or sulfonylurea use.
Serum cortisol: reduced in adrenal insufficiency or hypopituitarism.
48 to 72-hour fast with serial blood glucose, serum proinsulin, C-peptide and insulin levels: the gold standard investigation for insulinoma.
TSH, U&E, LFTs: abnormalities help identify secondary causes of hypoglycaemia such as hypothyroidism, chronic liver disease or kidney disease.
Management of Hypoglycaemia?
In the community
oral glucose - liquid or sugar lumps
Glucogel or dextrogel
Hospital setting
If alert - the same as above
SC or IM glucagon
20% glucose may be given through a large vein
complications of hypoglycaemia?
Short term
Neuroglycopenic complications include coma and seizures. These can lead to permanent neurological sequelae and should be managed in an intensive care setting.
Long term
Recurrent episodes of hypoglycaemia lead to ‘hypoglycaemic unawareness’ where patients do not develop autonomic symptoms of low blood glucose. This is more frequent in type II diabetes and increases the chance of neuroglycopenic complications of hypoglycaemia.
100mls of 20% glucose or 150mls of 10% glucose
If no IV access
1mg of glucagon IM
Symptoms of hypercalcaemia?
polyuria, polydipsia, constipation, nausea, fatigue and cognitive impairment
muscle and bone pain
Investigations for hypercalcaemia?
calcium profile
PTH
vitamin D
causes of hypercalcaemia?
primary hyperparathyroidism
Malignancy (lung and breast Ca, multiple myeloma)
Bony mets
Graves disease
Sarcoidosis
Addisons disease
Management of hypercalcaemia?
Immediate stabilisation
Rehydration
Inhibition of bone resorption - bisphosphanates can e used to inhibit osteoclast activity and reduce serum calcium levels
If hypercalcaemia is due to granulomatous diseases or lymphomas, corticosteroids may be administered to reduce calcium levels.
In severe cases. -dialysis
Treat underlying cause
what is primary hyperparathyroidism?
What are the symptoms
What would be seen on investigations?
Most cases due to solitary adenoma (80%), multifocal disease occurs in 10-15% and parathyroid carcinoma in 1% or less
Symptoms
May be asymptomatic if mild
Recurrent abdominal pain (pancreatitis, renal colic)
Changes to emotional or cognitive state
Hormone profile
PTH (Elevated)
Ca2+ (Elevated)
Phosphate (Low)
Urine calcium : creatinine clearance ratio > 0.01
what is secondary hyperparathyroidism?
What are the symptoms
What would be seen on investigations?
Parathyroid gland hyperplasia occurs as a result of low calcium, almost always in a setting of chronic renal failure
Clinical features
May have few symptoms
Eventually may develop bone disease, osteitis fibrosa cystica and soft tissue calcifications
Hormone profile
PTH (Elevated)
Ca2+ (Low or normal)
Phosphate (Elevated)
Vitamin D levels (Low)
what is tertiary hyperparathyroidism?
What are the symptoms
What would be seen on investigations?
Occurs as a result of ongoing hyperplasia of the parathyroid glands after correction of underlying renal disorder, hyperplasia of all 4 glands is usually the cause
Features
Metastatic calcification
Bone pain and / or fracture
Nephrolithiasis
Pancreatitis
Hormone profile
Ca2+ (Normal or high)
PTH (Elevated)
Phosphate levels (Decreased or Normal)
Vitamin D (Normal or decreased)
Alkaline phosphatase (Elevated)
