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.
Px with DM2 that takes gliclazide (sulfonylurea) that is programmed for an endoscopy. What is the most appropriate advice regarding his diabetic management?
Remember sulfonylureas are associated with hypoglycemia in the fasted state. An endoscopy is a minor procedure, so sulfonylureas should ne omitted on the day of the procedure until the px can eat and drink again.
DM perioperative management
Sulfonylureas (glibenclamide and gliclazide) Only omit the day of the surgery and restart once eating and drinking
Metformin (including Glucophage SR) Take as normal Unless surgery with contrast dye, needs to be stopped 2 days before. Can be restarted 2 days after contrast dye.
Pioglitazone Take as normal
DPP IV inhibitor (gliptins) Take as normal
Long acting GLP-1 analogue (exenatide) take as normal.
REMEMBER glycemia should be checked regularly before, during and after surgery. If at any point glucose level >11mmol/L consider starting an insulin infusion IV.
Hypercalcaemia aetiology
Primary hyperparathyroidism> main cause of hypercalcaemia but mainly mild = asymptomatic pxs.
Malignancy > Multiple myeloma, production of PTH like molecule (by Squamous cell carcinoma of the lung) this is a common cause that requires hospital admission
Familial hypocalciuric hypercalcaemia
Immobilization
Sarcoidosis
Remember moans, groans, stones and bones (Lethargy, confusion, depression AND constipation AND kidney stones/ nephrolithiasis AND only in hyperparathyroidism bone pain AND short QT
Hypercalcamia management
The initial management of severe hypercalcaemia is rehydration (typically 3-4L/day). Increasing circulating volume helps to increase the urinary output of calcium
Following rehydration bisphosphonates may be administered IV
Calcitonin> fewer side effects than bisphosphonates but less effective in reducing hypercalcaemia.
Steroids > If sarcoidosis
Cinacalcet hydrochloride is a calcimimetic agent that effectively reduces parathyroid levels in px with secondary hyperparathyroidism.
Haemodialysis or peritoneal dialysis may be relevant in patients with severe hypercalcaemia secondary to renal failure.
Furosemide has limited role > It is occasionally used where there is fluid overload but it does not reduce serum calcium.
DM2 diagnosis symptomatic vs asymptomatic
If symptomatic random glucose >11.1mmol/L or fasting >7mmol/L
If asymptomatic 2 fasting venous plasma glucose samples in the abnormal range are recommended for the Dx (>7mmol/L)
Oral glucose tolerance test is no longer recommended
DKA precipitating factors and Dx
Infection Missed insulin dose Cardiovascular disease (stroke or MI)
Dx: capillary blood glucose >11mmol/L or known DM
Capillary ketones > 3mmol/L or urine ketones ++ or more
Blood gas > pH less than 7.3 and/or bicarbonate less than 15mmol/L
DKA management
ABC! Pxs may have lost up to 5 liters!
If SBP <90mmHg then 1L of saline 0.9% in 10-15 mins
If SBP >90mmHg then 1L of saline 0.9% over 1 hour
Following saline infusion then insulin therapy is added (>1 hour after IV saline has started, if added earlier then ↑ risk of cerebral oeadema)
If plasma glucose <12mmol/L then replace normal saline with dextrose 5% to prevent over-rapid correction of blood glucose and hypoglycaemia
Hypokalaemia may need to be corrected with KCl (40mmol/L KCl can be added after the 1st L of fluid is administered if K is 3.5-5.5mmol)
REMEMBER
0.9% saline FIRST
Followed by insulin and KCl
If glucose falls <14mmol/L commence dextrose 10% ALONGSIDE saline
How can someone differentiate between Cushing’s disease and Ectopic ACTH-producing tumours?
Remember
24h urinary free cortisol as outpatient screening tool
Overnight dexamethasone suppression test to diagnose Cushing’s syndrome
ACTH levels differentiate between ACTH dependent aetiologies and independent. (small cell lung cancer and Cushing’s disease vs. Adrenal adenoma/carcinoma)
***High dose dexamethasone suppression test is used to differentiate between Cushing’s disease and Ectopic ACTH-producing tumours
A pituitary adenoma is semi-autonomous so a low-dose dexamethasone test will not suppress it but a high dose will. (bilateral adrenal hyperplasia= hyperactivity of BOTH adrenals)
An ectopic ACTH producing tumour will not respond as it is fully autonomous (unilateral adrenal hyperplasia)
What is the most likely visual abnormality associated with pituitary tumour?
Bitemporal hemianopia by tumour pressing optic chiasma.
Hyperprolactinaemia patophysiology
An excess of prolactin secretion, may cause syndrome of gallactorrhoea-amenorrhoea.
The amenorrhoea is caused by inhibition of hypothalamic release of luteinizing hormone releasing hormone (LHRH) with a decrease in LH and follicle-stimulating hormone (FSH) secretion.
Prolactin inhibits the LH surge that causes ovulation.
Gynecomastia and especially galactorrhoea in men is rare.
Hyperprolactinaemia causes
Physiologic (pregnancy, nipple stimulation/suckling, stress)
Pituitary tumours (prolactinomas)
Hypothalamic diseases > mass compressing like craniopharyngioma and meningioma
Hyperprolactinaemia as a result of decreased inhibitory action of dopamine (antipsychotic drugs like Haloperidol; clozapine and olanzapine also cause hyperprolactinaemia but not on standard doses)
Hypothyroidism> thyrotropin-releasing hormone (TRH) increases prolactin
Clinical features of hyperprolactinaemia
Galactorrhoea usually in women
(men and premenopausal women rarely get galactorrhoea)
Menstrual abnormalities (amenorrhoea or oligomenorrhoea)
Disturbed gonadal function in men (erectile disfunction, decreased libido, gynecomastia in men, reduced fertility)
Mass effects> headaches and visual field defects (uni or bitemporal defects, bitemporal is more common)
Hypotuitarism
Dx of hyperprolactinaemia
Always exclude pregnancy, lactation, hypothyroidism and medications before starting work-up
Serum prolactin < 2,000mU/L is suggestive of a tumour (microprolactinoma or non-functioning macroadenoma)
> 4,000mU/L is diagnostic of macroprolactinoma
Imaging MRI
Thyroid lump work-up
Ultrasound as they are extremely sensitive for thyroid nodules.
Followed by Fine-needle aspiration cytology (FNAC)
Then Radionuclide imaging and MRI if thyroid carcinoma.
Most appropriate in lumps >2cm FNAC
initial= ultrasound
38YO female stopped taking combined oral contraceptive pills 6 months ago, she has been amenorrhoeic since then. She does not take any regular medications. Her pregnancy test is negative. She does not suffer from any headaches or visual changes. BMI 24.
FSH 25IU/L (normal Luteal 2-8, Ovulation 5-25, postmenopause >25)
LH 16 IU/L (normal luteal 3-16, ovulation 16-84, postmenopause 17-75UI/L)
Prolactin 540mU/L (normal <440mU/L or <25ng/mL)
LFT, RFT and TFT are normal.
Dx?
Post pill amenorrhoea
It is a biochemical result of a normal (or low normal) FSH and LH and a normal to mildly raised prolactin.
Here FSH and LH are normal (FSH upper limit)
The distractor is premature ovarian failure. FSH would normally be >25IU/L.
2 values of >25UI/L 4 weeks apart are required for the diagnosis (Guidelines of the ESHRE 2015)
Hypothalamic amenorrhoea can be considered but the BMI would be below 17kg/m2.
(The results would be low GnRH, FSH, LH and oestrogen levels)
Safety issues of biguanides and sulphonylureas
Biguanides No risk of hypoglycemia Weight loss Cardiovascular benefits If eGFR < reduce dose If eGFR <30 discontinue
Sulphonylureas
Risk of hypoglycemia
Weight gain
If renal impairment ↑ risk of hypoglycemia
Safety issues of Gliptins DPP4 inhibitors and pioglitazones
DPP4
Rare hypoglycemia
Neutral weight
Risk of pancreatitis and HF
Pioglitazones Rare hypoglycemia Weight gain Bladder cancer concerns (contraindicated, asses risk for bladder cancer) Contraindicated in HF Fractures in women
Safety issues of repaglinide and SGLT-2 inhibitors (gliflozins)
Repaglinide
Risk of hypoglycemia
Weight gain
Avoid in liver disease
SGLT-2
Rare hypoglycemia
Weight loss
Life threatening DKA at only moderately raised blood sugars (<14mmol/L)
GLP-1 agonists incretin mimetics safety issues
Rare hypoglycemia
Weight loss
Concerns about breast cancer
NICE has strict criteria for the use of GLP-1 agonist (enormous cost)
DM2 medications that may cause weight loss
Biguanides (metformin)
SGLT-2 (gliflozins)
GLP-1 agonists (incretin mimetics)
DM2 medications that cause weight gain
Sulphonylureas (glyclazide)
Pioglitazone
Repaglinide
DM2 medications that cause hypoglycemia
Sulphonylureas (metformin)
Repaglinide
Rare DPP4i (gliptins) Pioglitazone SGLT-2i (gliflozins) GLP-1 agonist (incretin mimetics)
DM2 medication contraindicated in HF
Pioglitazone
DPP4i (gliptins)
Metformin has cardiovascular benefits
What should be done with metformin with a px with eGFR of 42?
Reduce dose!
If eGFR <30 then discontinue.
DM2 medications contraindicated in obese with low eGFR and HF
Biguanides (metformin) because of eGFR below 30
Sulfonylurea because of weight gain and increased risk of hypoglycemia secondary to renal impairment
SGLT-2i because of renal impairment
Pioglitazone because of weight gain and HF
DM2 medications that can be used in eGFR <30 RIP Repaglinide Inagliptin (Lina but with lower L) Pioglitazone
In this case the best medication would be insulin.
Hypertension associated with hypokalaemia, refractory hypertension (3 or more drugs), and hypertension before 40YO.
With or without
hypokalaemia, metabolic alkalosis, normal sodium or upper limit, weakness, headaches and lethargy.
Conn’s syndrome!
(Hypernatraemia, hypertension and hypokalaemia)
Tx with aldosterone antagonists (spironolactone) prior to adrenalectomy.
Different from Addison’s
Drop in aldosterone > drop in sodium > drop in BP (postural)
Drop in weight
Drop in energy
Only K is raised.
Hypothalamic amenorrhoea
Due to chronic illness like being significantly underweight (anorexia nervosa).
Low gonadotropins and low oestradiol with clinical picture of excessive exercise, low weight or stress.
Subacute thyroiditis best medication.
De Quervain’s thyroiditis
Propranolol.
They refer hyperthyroidism symptoms and high T4 and low TSH is seen. ***A decrease in radionuclide uptake is seen in subacute thyroiditis.
It is viral in origin and may have a recent upper respiratory tract infection. (This can be omitted in stems)
Tx aims to relieve symptoms> propranolol to reduce HR and palpitations.
Carbimazole and propylthiouracil are not indicated as subacute thyroiditis is transient.
Osteomalacia common causes and clinical features.
Normal bony tissue but decreased mineral content
Rickets the epiphysis has not fused (in younger people)
Vit D deficiency (malabsorption, lack of sunlight, diet)
Renal failure
Drug induced (anticonvulsants)
Features Bone pain Fractures Muscle tenderness Proximal myopathy.
Slight increase in ALP (in Vit D deficiency osteomalacia)
Subclinical hypothyroidism management
TSH high with T4 normal.
Must be repeated at 3 months.
If asymptomatic just reassure.
If symptomatic consider levothyroxine and TFT should be checked every 2 to 3 years.
Features of congenital hypothyroidism.
Hoarseness of voice Large fontanelles Macroglosia Jaundice Umbilical hernia Poor feeding.
In the UK congenital hypothyroidism is picked up on screening (heel prick test). If congenital hypothyroidism is picked then further tests are done and levothyroxine is started.
Osteoporosis treatment.
Biphosphonates (alendronate or risedronate as 1st line)
Calcium supplements are only considered if the calcium intake is inadequate (<700mg/day SIGN and <1000mg/day NICE)
Hormone replacement therapy (HRT) should not be considered as 1st line management due to its adverse effects (breast cancer, venous thromboembolism, coronary disease and stroke)
Raloxifene is a selective oestrogen receptor modulator (SERM) and may be considered as an alternative treatment option for the secondary prevention of osteoporotic fractures in post-menopausal women.
*Most of our Ca is in our bone. Biphosphonate will bind to the surfaces of the bones and slow down the bone reabsorption action of the osteoclasts.
T-score in normal, osteopenia and osteoporosis.
≥-1.0 = normal
- 1.0 to -2.5 = osteopenia
- 2.5 or lower = osteoporosis.
28YO woman with palpitations and tremors of the hands. These started a month ago. She delivered her first child vaginally 3 months ago and is still breastfeeding. TSH 0.2 (0.5-5.7mU/L), free thyroxine (T4) 48 (9-18mmol/L), free triiodothyronine (T3) 15 (3.5-6.5mmol/L) and tests positive for thyroid peroxidase antibodies and she has a normal ESR.
What is the most appropriate action?
Give propranolol.
Classic example of postpartum thyroiditis in the hyperthyroid phase.
2 phases
Hyperthyroid first 4 months
Hypothyroidism 4 to 6 months later.
It usually resolves spontaneously within a year from delivery.
Tx is symptomatic.
Levothyroxine if in hypothyroidism symptoms present.
Shock (confusion, postural hypotension, tachycardia and oliguria)
Abdominal pain (may be severe enough to mimic acute abdomen)
Hypoglycemia
Are signs and symptoms of…?
Addisonian crisis due to low cortisol levels.
Tx
IV fluids if shocked
IV hidrocortisone 100mg followed by 8 hourly doses
Calcium gluconate/chloride if hyperkalaemia
Fluids and steroids resolve hyponatraemia
Hypoglycemia treated with IV glucose infusion
If it improves in 72 hours then switch to oral steroids.
If adrenal pathology is identified then fludrocortisone may be indicated.
Hashimoto’s thyroiditis clinical features
Symptoms of hypothyroidism
Tiredness
Dry skin
Cold intolerance
AND
The thyroid gland may be enlarged.
Low T4 level and high TSH
Associated with autoimmune conditions like Addison’s, DM, and pernicious anaemia.
A px with history of Addison’s presents with suspected COVID-19, all vitals normal except 38.5C
What should be done with his/her medications?
Double the dose of hydrocortisone.
Not just in COVID-19, any infection.
Pxs with Addison’s are unable to produce sufficient endogenous steroids so hydrocortisone or prednisolone need to be doubled during these sick days.
If she presented with signs of Addisonian crisis then call an ambulance and hydrocortisone IM.
Nodule within thyroid gland or diffuse thyroid swelling
Cervical lymphadenopathy or supraclavicular
Unexplained hoarseness or voice change
Enlarging painless thyroid mass over weeks.
Usually with normal thyroid function test
Thyroid cancer!
Thyroid adenoma
Benign tumour
“Cold” (not producing thyroid hormones)
Rarely “hot” (produces thyroid hormones = hyperthyroidism)
Non toxic (simple) goitre
vs.
Toxic multinodular goitre
Non-toxic
Non-functioning nodules
TF test is normal
Toxic Multinodular goitre
Diffuse swelling of the thyroid gland
Functioning nodules
TSH low and T3, T4 high
Hyperthyroidism
Goitre
Upper eyelid retraction, lid lag, exophthalmos
TSH low
T3 and T4 high
Thyroid autoantibodies (anti-thyroid peroxidase, anti-thyroglobulin antibodies and TSH-receptor antibodies) may be seen
Radioactive iodine uptake test is increased
Grave’s disease!
Hasimoto’s vs De Quervain’s thyroiditis
Hashimoto’s
Hypothyroidism
Usually middle aged women
Thyroid gland may enlarge rapidly (painless goitre)
TSH high
T3 and T4 low
Thyroid autoantibodies (anti-thyroid peroxidase and anti-thyroglobulin antibodies) may be seen.
De Quervain's Neck pain Fever Lethargy soon after viral illness TSH low T3 and T4 high Radioactive iodine uptake test is decreased
When to make a C-peptide test and why?
C-peptide is released at the same time as insulin, for every insulin molecule there is a molecule of C-peptide.
If no insulin is produced then there won’t be C-peptide.
If C-peptide is detected (high levels) and the px has hyperglycemia then DM2 is more likely (as insulin is being produced but there is no response)
Differentiates DM1 from DM2
***Not accurate in LADA (Latent autoimmune diabetes of the adult, DM1 in <50 years)
Difference between Osteoporosis, Paget’s and Osteomalacia with serum calcium, phosphate and alkaline phosphate.
Osteoporosis ALL normal
Paget’s only alkaline phosphatase high.
Calcium and phosphate normal
Osteomalacia
Low calcium and phosphate
Alkaline phosphatase high.
Grave’s disease treatment for a woman that wants to become pregnant.
Propylthiouracil alone
Even though carbamizole is better, only PTU is considered for pre conception women.
Treatment can have a 12 to 18 month duration, remission is seen in 50% of cases.
Carbimazole has been associated with aplasia cutis and omphalocele
New guidelines suggest PTU pre conception and during 1st trimester and at the beginning of the 2nd trimester change to carbimazole (reduces risk of hepatotoxicity with PTU)
98% cure rate is seen with surgery but medication may be attempted 1st
29YO male with a swollen, painful right wrist joints. He gives a hx of noticing change in shoe size, constipation, feeling cold and needing more warm clothes to keep him warm. His skin is found to be dry and his right wrist is erythematous and tender to touch. What is the single most likely diagnosis?
Pseudogout.
Recognize hypothyroidism signs.
The change in show size can be due to myxoedema.
Pseudogout can be precipitated by hypothyroidism.
Most affected joint = knee
Other joints commonly affected> wrist, shoulder, and ankle.
Positive birefringent crystals in synovial fluid elevation are pathognomonic of acute pseudogout.
Acromegaly investigations
Initial test > insulin like growth factor
(used as screening test and occasionally used to monitor disease)
Most definitive test> Oral glucose tolerance (OGTT) with serial growth hormone measurements.
In normal pxs, GH is usually suppressed with glucose.
In acromegaly, there is no suppression of GH with glucose.
GH levels are not recommended as they tend to vary during the day and are therefore unreliable.
Summary of DM2 medications safety issues.
Remember
With bad kidneys dont give MS (metformin and sulphonylureas)
Heart has 4 chambers so dont use DPP4i (gliptins)
Pie comes with the die (pioglitazone has risk of bladder Ca and HF)
SPR cause weight gain (sulpho, pioglitazone and repaglinide)
The rest causes weight loss except DPP4i (gliptins) which have no effect.
SPR without the P have risk of hypoglycemia (Sulpho and repaglinide)
