Endocrinology Flashcards
Electrolyte abnormality in alcoholics.
Remember there are 2 hypos associated with alcoholism.
Hypoglycemia and hypokalaemia.
Vomiting → loss of K in the vomitus AND loss of hydrochloridric acid → metabolic alkalosis → activation of RAAS mechanism → loss of K in urine.
Many patients with K deficiency are also magnesium deficient.
A 34 YO female with milk discharge, she is nulliparous and has not had any menstruation in the last 6 months.
What hormone is affected?
Hyperprolactinaemia causes a syndrome of galactorrhoea and amenorrhoea.
Laboratory finding that leads to diabetes insipidus diagnosis.
After giving vasopressin there will be an increase in urine osmolality = Central Diabetes Insipidus.
If no changes after vasopressin = Nephrogenic Diabetes Insipidus.
Female with hx of breast cancer, depression (takes fluoxetine), drowsiness and excessive thirst.
Hypercalcemia!
Drowsiness and increased thirst with Hx of breast cancer should spark hypercalcemia as a differential.
Breast cancer usually causes bone metastases, this causes hypercalcemia.
Increased thirst is a feature of hypercalcemia NOT hyponatremia.
Also, depression worsens with hypercalcemia.
46 yo female, lives in UK, complains of weight gain, constipation and sensitivity to cold. She has a pulse of 50, regular.
Hypothyroidism.
Most common cause → nutritional deficiency
*But on developed countries like UK it is AUTOIMMUNE.
Addison’s disease clinical features
In developed countries it is autoimmune
Rest of the world → tuberculosis
(Other causes include metastasis, CMV and adrenal hemorrhage)
Associated with DM, thyroid disorders and vitiligo.
Acutely it presents as an Addisonian crisis.
Chronically pxs present with insidious and mild symptoms like
- Fatigue and weakness
- Salt cravings (primary insufficiency)
- Hyperpigmentation (primary insufficiency)
- Postural hypotension
- Abdominal pain, nausea, vomiting, anorexia and weight loss.
- Syncope and dizziness
- Personality changes, irritability and confusion.
Addison’s disease investigations.
Electrolytes?
How is the test done?
How do I exclude Addison’s disease in that test?
Plasma renin and aldosterone will be increased or decreased?
Will I find antibodies?
Should I do another test if there are no antibodies?
Low 9am cortisol
Hyponatremia and hyperkalaemia
ACTH stimulation test (Synacthen test)
→ IM ACTH administered and cortisol levels measured after.
Cortisol of >550 nmol/L excludes Addison’s disease.
ACTH ↑
↑ Plasma renin and ↓ plasma aldosterone.
21 hydroxylase adrenal antibodies.
CT abdomen if antibodies are negative.
What endocrinological disease should I suspect in a patient with Meningitis?
SIADH (syndrome of inappropriate antidiuretic hormone secretion)
Results in euvolaemic hyponatraemia.
Hypernatremia is often seen in Diabetes Insipidus which is not the case.
A man with prostate cancer has confusion, thirst, lower back pain and abdominal pain. What is the most likely diagnosis?
What would be the most likely finding in the ECG?
What is the single most appropriate investigation?
Hypercalcemia
Shortening of QT interval
The most appropriate investigation would be a serum calcium.
There are no symptoms of tingling or numbness in the legs so there is no rush to perform a MRI to investigate malignant spinal cord compression.
Hypercalcemia clinical features
Decreased mental activity like lethargy, confusion and depression (groans)
Decreased bowel activity = constipation (moans)
Polyuria and polydipsia caused by nephrogenic diabetes insipidus. Calcium precipitates in the kidney resulting in kidney stones an nephrolitiasis. (stones)
Bone pain is only seen when it is hyperparathyroidism which is causing hypercalcaemia (bones)
short QT
Causes of Cushing syndrome (2 groups)
ACTH (adrenocorticotropic hormone) dependent disease
Excessive ACTH from pituitary (Cushing’s disease)
Ectopic ACTH producing tumours like small cell lung cancer and carcinoid tumours.
Non ACTH dependent
Adrenal adenomas
Adrenal carcinomas
Excess glucocorticoid administration (main cause)
Clinical features of Cushing’s syndrome
Round face Acne and hirsutism Weight gain (truncal obesity, buffalo lump) Skin may look thin and fragile Purple striae on abdomen, breasts, thighs, axilae Proximal muscle weakens Depression and insomnia Growth arrest in children.
Cushing’s syndrome outpatient tests
24 hour urinary free cortisol (as outpatient screening tool)
Overnight dexamethasone suppression test
Administration of 1mg dexamethasone midnight followed by serum cortisol measurement at 9am
Cortisol <50nmol/L makes Cushing’s unlikely (best to establish Cushing’s syndrome diagnosis)
Cushing’s syndrome inpatient tests
ACTH levels (once the diagnosis of Cushing’s syndrome is confirmed. It differentiates between ACTH dependent and independent aetiologies.)
High-dose dexamethasone suppression test: Differentiates between a pituitary adenoma and an ectopic source. The output of a pituitary adenoma will suppress with high-dose dexamethasone (cortisol suppressed). The output of an ectopic source will not suppress (cortisol not suppressed)
ECG changes in hyperkalaemia
Tall-tented T waves
Small P waves
Widened QRS leading to a sinusoidal pattern and asystole.
Severity of hyperkalaemia
Mild 5.5 to 5.9 mmol/L
Modertae 6.0 to 6.4 mmol/L
Severe ≥6.5 mmol/L
Causes of hyperkalaemia
Acute renal failure
Potassium-sparing diuretics, ACEi, ARB, spironolactone
Metabolic acidosis
Addison’s
Management of hyperkalaemia
Stop drugs that cause hyperkalaemia
ECG changes > IV calcium (chloride or gluconate)
Used to stabilise cardiac membrane
ECG changes are more accurate than plasma K levels
If severe hyperkalaemia and short-term shift in K extracellular to intracellular fluid compartment is needed > Insulin and dextrose infusion.
REMEMBER ≥ 6.5 use Calcium gluconate
6.0 to 6.4 AND ECG changes USE calcium gluconate
Diabetes insipidus main forms and clinical features.
Cranial DI: decreased secretion of ADH reduces the ability to concentrate urine and so causes polyuria and polydipsia.
Nephrogenic DI: decreased ability to concentrate urine because resistance to ADH in the kidney
Marked polyuria (sometimes more than 3L a day)
Polydipsia and chronic thirst
Nocturia
Most appropriate initial test for a suspected diabetes insipidus
Urine osmolality
If the osmolality is >800mOsm/kg then we proceed further by getting plasma osmolality and performing a fluid deprivation test.
The fluid deprivation test is to differentiate between central or nephrogenic diabetes insipidus.
Difference in fluid deprivation test between central DI and nephrogenic DI
Central DI the urine volume decreases and urine osmolality increases after administering desmopressin.
Nephrogenic DI: there is no change after administering desmopressin
Central DI after fluid deprivation <300
after desmopressin >800
Nephrogenic DI after fluid deprivation <300
After desmopressin <300
Primary hypothyroidism causes
Autoimmune hypothyroidism (Hashimoto’s)
Iatrogenic: radioiodine tx, surgery, radiotherapy to the neck
Drugs: amiodarone, contrast media, iodides, lithium and antithyroid medication
Congenital defects (absence of thyroid gland)
Secondary hypothyroidism causes
Isolated TSH deficiency
Hypopituitarism: neoplasm, infiltrative, infection and radiotherapy
Hypothalamic disorders: neoplasms and trauma
Hypothyroidism signs and symptoms
Tiredness, lethargy, intolerance to cold
Dry skin and hair loss
Slowing of intellectual activity (poor memory and difficulty concentrating)
Constipation
Decreased appetite with weight gain
Menorrhagia and later oligomenorrhoea or amenorrhoea.
Dry coarse skin, hair loss and cold peripheries.
Puffy face, hands and feet (myxoedema)
Bradycardia
(In autoimmune hypothyroidism, pxs may have features of other autoimmune diseases like vitiligo, pernicious anaemia, Addison’s and DM)
TSH and free T4 in Graves’ disease and Subacute thyroiditis (De Quervain’s thyroiditis)
TSH is low
Free T4 is high
In Grave’s radioactive iodine uptake test is increased
In De Quervain’s radioactive iodine uptake test is decreased (usually followed by URTI)
TSH levels and free T4 in Primary Secondary Sick euthyroid syndrome Subclinical hypothyroidism Poor compliance with thyroxine medication.
Primary TSH high and free T4 low
Secondary TSH low and Free T4 low
Sick euthyroid syndrome TSH low and Free T4 low
Subclinical hypothyroidism TSH high free T4 normal
Poor compliance with thyroxine medication TSH high and free T4 normal.
23 YO female with lethargy, dry skin on her legs. TSH 9.8 mU/L (0.5-5.7mU/L) and free thyroxine (T4) 11pmol/L (9-18)
The test is repeated 3 months later. TSH 8.8 and T4 15. She has no goitre palpable on examination, and she is trying to conceive.
What would be the most appropriate next step?
Consider starting levothyroxine.
She has subclinical hypothyroidism. (High TSH and low T4)
She is symptomatic, below 65 and is trying to conceive so she would benefit from levothyroxine.
(If >65YO no tx required, tx may cause AFib)
It is managed in primary care.
T3 level is no required unless T4 levels are abnormal.
Best test and management for phaeochromocytoma
24 hour urinary collection of metanephrines (S95% vs 86% of catecholamines)
Surgical resection with BP stabilization Alpha blocker (phenoxybenzamine) 7-10 days BEFORE surgery to allow for expansion of blood volume.
Beta blocker (propranolol) after alpha blocker.
If done incorrectly unopposed alpha stimulation can precipitate a hypertensive crisis
Hyperthyroidism clinical features
Hyperactivity, irritability Insomnia Heat intolerance Sweating Palpitations Fatigue Weight loss Increased appetite Pruritus Increase stool frequency Oligomenorrhoea or amenorrhoea Sinus tachycardia, AFib Fine tremor
Thyroid storm and clinical features
An acute and exaggerated presentation of hyperthyroidism most commonly precipitated by treatment with radioiodine, thyroid surgery, myocardial infarction and infection.
Classic features of hyperthyroidism Altered mental status Elevated temperature Tachycardia AFib Diarrhoea and vomiting Other features include acute abdomen and heart failure
Investigation and treatment of thyroid storm
TSH, free T3 and T4 Uptake scan (Tc-99m) aids confirmation
Tx: ALWAYS ABC first
Seek help from endocrinology team
3 domains of tx:
1. Counteracting the peripheral effects of thyroid hormone.
Beta blockade > propranolol if no contraindication
Once adequately beta blocked > Digoxin to control the heart rate
- Inhibiting thyroid hormone synthesis
Antithyroid drugs > Propylthiouracil (PTU is preferred over carbimazole in emergencies as it prevents peripheral T4 to T3 conversion. Carbimazole works by reducing the production of T3 and T4 which has a slower clinical effect)
Lugol’s iodine following PTU (Lugol’s will prevent the release of hormone)
Prevent peripheral conversion of T4 to T3 > hydrocortisone/dexamethasone
- Tx systemic complications
If the cause is infection > IV co-amoxiclav
Elevated temperature > Paracetamol
The dose of antithyroid drugs can be adjusted in 5 days. Stop propranolol and iodine in 10 days. In dire circumstances, thyroidectomy may be indicated if there is no improvement in 24 hours.
