Endo Flashcards
Which else could cause galactorrhea
Other Causes of Galactorrhoea?
Physiological: Pregnancy, postpartum, nipple stimulation
Drugs: Antipsychotics (e.g. risperidone, haloperidol), antidepressants (SSRIs, TCAs), antiemetics (metoclopramide, domperidone), methyldopa, verapamil, oestrogen, opioids
Endocrine: Hypothyroidism (raised TRH stimulates prolactin), Cushing’s, acromegaly
Pituitary pathology: Prolactinoma, stalk compression, non-functioning adenoma
Renal failure & liver disease (reduced prolactin clearance)
Chest wall injury (e.g., trauma, herpes zoster, surgery affecting afferent sensory pathways)
Prolactinoma levels - mild elevation, moderate elevation, high and very high
- Prolactin Level Thresholds (UK Guidance)
✅ Mild Elevation (500–2000 mU/L) → Consider Non-Tumour Causes
Physiological: Pregnancy, stress, nipple stimulation.
Drugs: Antipsychotics (risperidone), metoclopramide, SSRIs, oestrogens.
Hypothyroidism (Check TSH & T4 – TRH stimulates prolactin release).
Chronic kidney disease & liver disease.
✅ Moderate Elevation (2000–5000 mU/L) → Possible Microprolactinoma
Order MRI pituitary if no other cause is found.
Check for symptoms (menstrual irregularities, galactorrhoea, hypogonadism).
✅ High Elevation (>5000 mU/L) → Likely Macroprolactinoma
MRI Pituitary with contrast to assess tumour size.
Consider visual field testing (compressive symptoms if >10 mm).
💡 Very high prolactin (>10,000 mU/L) strongly suggests a macroprolactinoma rather than medication-induced hyperprolactinaemia.
surgical sieve
When stuck, use the surgical sieve:
Vascular (stroke, infarction)
Infective (TB, syphilis, abscess)
Trauma (head injury, surgery)
Autoimmune (hypophysitis)
Metabolic (chronic liver/kidney disease, hypothyroidism)
Neoplastic (prolactinoma, pituitary adenoma, craniopharyngioma)
Iatrogenic (drugs, radiation, surgery)
Congenital (Kallmann syndrome, genetic mutations)
long term follow up measures for Cushing’s disease (post-transphenoidal resection),
Long-term Follow-up Measures for Cushing’s Disease (Post-Transsphenoidal Resection)
Patients who have undergone transsphenoidal resection for Cushing’s disease require lifelong follow-up to monitor for recurrence and manage complications of prior hypercortisolism.
Follow-up Measures
✅ Endocrine Monitoring:
Serum cortisol and ACTH: Monitor for recurrence (low levels postoperatively suggest remission).
Dexamethasone suppression test or 24-hour urinary free cortisol: To check for residual or recurrent disease.
Morning cortisol (9 AM) or ACTH stimulation test: Assess for adrenal insufficiency due to prolonged suppression of the HPA axis.
✅ Hormonal Replacement (if needed):
Hydrocortisone replacement (if secondary adrenal insufficiency develops post-surgery).
Levothyroxine and sex hormone replacement (if pituitary function is compromised).
✅ Metabolic and Cardiovascular Risk Monitoring:
Blood glucose/HbA1c (increased diabetes risk).
Bone mineral density (DEXA scan) (osteoporosis risk).
Lipid profile, blood pressure (Cushing’s predisposes to CV disease).
✅ Imaging and Surveillance:
Pituitary MRI: If recurrence is suspected.
Periodic visual field testing: If mass effect on optic chiasm was present.
✅ Lifestyle and Patient Education:
Encourage weight control, regular exercise, and calcium/vitamin D supplementation.
Advise on sick day rules if on steroids.
Psychological support for depression or body image issues.
long term complications of Cushing’s disease (Diabetes mellitus & osteoporosis).
Long-term Complications of Cushing’s Disease
Even after successful treatment, long-term complications from previous hypercortisolism persist, requiring ongoing management.
(i) Diabetes Mellitus
Mechanism: Chronic glucocorticoid excess induces insulin resistance and β-cell dysfunction.
✅ Management:
Monitor fasting glucose and HbA1c regularly.
Lifestyle modifications (diet, exercise, weight loss).
Pharmacological treatment if needed (Metformin, insulin if severe).
(ii) Osteoporosis
Mechanism: Excess cortisol increases bone resorption and reduces bone formation.
✅ Management:
DEXA scan at diagnosis and post-treatment.
Calcium (1000-1200 mg/day) & Vitamin D (800 IU/day) supplementation.
Bisphosphonates (e.g., alendronate) if osteoporosis is confirmed.
Weight-bearing exercise to maintain bone strength.
Minimise falls risk (home modifications, balance training).
💡 Exam Tip: If asked about complications of Cushing’s, mention that even after cure, CV risk, osteoporosis, and diabetes need lifelong monitoring.
Sick day rules and important patient advice when on corticosteroid replacement regimen.
Sick Day Rules & Important Patient Advice on Corticosteroid Replacement
Patients on long-term hydrocortisone or other steroid replacement (e.g., after adrenal insufficiency post-Cushing’s or Addison’s disease) must increase their steroid dose during illness to prevent adrenal crisis.
Sick Day Rules:
✅ Mild illness (e.g., fever, flu, vomiting once but tolerating fluids):
Double the usual hydrocortisone dose until recovery (typically 2-3 days).
Maintain adequate fluid and salt intake.
✅ Severe illness (e.g., vomiting multiple times, unable to take tablets, high fever, surgery, trauma, hospital admission):
IM or IV hydrocortisone 100 mg STAT (self-administration or A&E).
Seek urgent medical attention.
✅ If undergoing surgery or major stress:
Hydrocortisone 100 mg IV before surgery, followed by continuous infusion or high-dose oral replacement post-op.
General Advice for Patients:
📌 NEVER stop steroids abruptly – taper if stopping.
📌 Carry a steroid emergency card or medic alert bracelet.
📌 Educate family members on how to give IM hydrocortisone injection.
📌 Always inform doctors, dentists, or paramedics about steroid dependence.
💡 Exam Tip: In a viva, if the examiner asks for important patient advice on steroids, always mention dose adjustment during illness, emergency injection, and medical alert identification.
Graves patient - after examining neck, examiner asks if there is anything you want to ask
Graves’ Disease: What to Ask After Examining the Neck
After examining a patient’s neck (goitre, thyroid bruit, signs of hyperthyroidism), you should ask:
(i) Confirmation Questions
🔹 “Would you like me to examine the eyes and peripheral signs?”
(Graves’ often has exophthalmos, lid lag, dermopathy – examiner may expect this).
🔹 “Would you like me to check for signs of thyroid dermopathy or acropachy?”
(Graves’ can have pretibial myxoedema and thyroid acropachy – rare but pathognomonic).
(ii) Important History Questions to Ask the Patient
🔹 Symptoms of thyroid storm: Palpitations, fever, agitation (to rule out emergency).
🔹 Symptoms of compressive goitre: Difficulty swallowing, hoarseness, stridor (check for tracheal deviation).
🔹 Previous treatments: History of antithyroid drugs, radioactive iodine, surgery.
🔹 Family history of thyroid disease (autoimmune thyroid disease has a genetic link).
🔹 Pregnancy or planning pregnancy? (Radioactive iodine is contraindicated).
💡 Exam Tip: If asked, “What do you want to do next?” after examining a Graves’ patient:
1️⃣ Confirm Graves’ disease (TSH, T3/T4, TRAb).
2️⃣ Assess for complications (eye disease, thyroid storm, cardiac arrhythmias).
3️⃣ Discuss management options (Carbimazole/PTU, radioiodine, surgery).
Graves aetiology
Aetiology (Causes & Risk Factors)
Autoimmune: TSH receptor autoantibodies (TRAb) stimulate thyroid hormone production.
Genetic factors: Associated with HLA-DR3 and CTLA-4 genes.
Environmental factors:
Smoking (increases risk of Graves’ ophthalmopathy).
Stress and emotional triggers.
Postpartum period (immune modulation).
Iodine excess or deficiency (can precipitate disease in susceptible individuals).
Other autoimmune conditions: Type 1 diabetes, rheumatoid arthritis, pernicious anaemia.
Graves ix
Investigations (UK Guidelines – NICE & BTF)
1. Blood Tests
✅ Thyroid Function Tests (TFTs):
↓ TSH (suppressed)
↑ Free T3 (FT3) and/or Free T4 (FT4) (elevated)
✅ Autoantibodies:
TSH receptor antibodies (TRAb) → Positive in >90% of Graves’ cases.
Thyroid peroxidase antibodies (TPO-Ab) → Present in ~70% but non-specific.
✅ Other tests:
Full Blood Count (FBC) – to check for thyroid disease-associated anaemia.
Liver function tests (LFTs) – before starting carbimazole (as it can cause hepatotoxicity).
2. Imaging (If Unclear Diagnosis)
✅ Thyroid uptake scan (Technetium or Radioiodine uptake scan)
Diffusely increased uptake in Graves’ disease.
Helps differentiate from toxic multinodular goitre (TMNG) or thyroiditis.
✅ Orbital MRI/CT – if severe thyroid eye disease (TED).
Graves mx
Management (UK Guidelines – NICE, BTA 2022)
1. Medical Treatment
1st Line: Antithyroid drugs (ATDs)
Carbimazole (1st choice) – Start 10-40 mg OD, then titrate down.
Propylthiouracil (PTU) – Alternative if pregnant (1st trimester) or carbimazole allergy.
Block & Replace Regimen (high-dose carbimazole + levothyroxine) – Sometimes used but not preferred in routine care.
⚠ Monitor TFTs every 4-6 weeks initially, then adjust dose.
⛔ Carbimazole risk: Agranulocytosis (rare) → Warn about sore throat, fever (requires urgent FBC).
- Radioiodine Therapy (Definitive Treatment)
Highly effective and 1st-line if relapse after ATDs or patient prefers definitive treatment.
Contraindications: Pregnancy, breastfeeding, severe active thyroid eye disease (TED).
Can cause hypothyroidism, requiring lifelong levothyroxine replacement. - Surgery (Total Thyroidectomy)
Indications:
Large goitre causing compression.
Persistent hyperthyroidism despite medical therapy.
Severe thyroid eye disease (TED) not responding to other treatments.
Requires lifelong levothyroxine post-thyroidectomy.
Risks: Hypoparathyroidism, recurrent laryngeal nerve injury. - Management of Thyroid Eye Disease (TED)
Smoking cessation (reduces risk & severity).
Mild cases: Lubricating eye drops, selenium supplements.
Moderate-severe cases: Steroids (IV methylprednisolone), orbital radiotherapy, or decompression surgery.
Exam Tips for OSCE/Viva
✅ Always check for eye signs (proptosis, diplopia, lid lag, chemosis) in Graves’ disease.
✅ Ask about smoking (increases risk of TED).
✅ Be aware of Carbimazole risks (agranulocytosis, hepatotoxicity).
✅ Radioiodine contraindications: Pregnancy, breastfeeding, severe eye disease.
✅ Surgical complications: Hypoparathyroidism, recurrent laryngeal nerve injury.
acromegaly patient on steroids - you can ask them one question (NOT why are you on steroids)
What other drugs are you on/? Pt. told me the other drugs she was on – Hydrocortisone, thyroxine etc. So I stated that this would be consistent with a TSS operation where the entire pituitary is taken out.
Graves - aetiology, ix and mx
Investigations (UK Guidelines – NICE & BTF)
1. Blood Tests
✅ Thyroid Function Tests (TFTs):
↓ TSH (suppressed)
↑ Free T3 (FT3) and/or Free T4 (FT4) (elevated)
✅ Autoantibodies:
TSH receptor antibodies (TRAb) → Positive in >90% of Graves’ cases.
Thyroid peroxidase antibodies (TPO-Ab) → Present in ~70% but non-specific.
✅ Other tests:
Full Blood Count (FBC) – to check for thyroid disease-associated anaemia.
Liver function tests (LFTs) – before starting carbimazole (as it can cause hepatotoxicity).
2. Imaging (If Unclear Diagnosis)
✅ Thyroid uptake scan (Technetium or Radioiodine uptake scan)
Diffusely increased uptake in Graves’ disease.
Helps differentiate from toxic multinodular goitre (TMNG) or thyroiditis.
✅ Orbital MRI/CT – if severe thyroid eye disease (TED).
Management (UK Guidelines – NICE, BTA 2022)
1. Medical Treatment
1st Line: Antithyroid drugs (ATDs)
Carbimazole (1st choice) – Start 10-40 mg OD, then titrate down.
Propylthiouracil (PTU) – Alternative if pregnant (1st trimester) or carbimazole allergy.
Block & Replace Regimen (high-dose carbimazole + levothyroxine) – Sometimes used but not preferred in routine care.
⚠ Monitor TFTs every 4-6 weeks initially, then adjust dose.
⛔ Carbimazole risk: Agranulocytosis (rare) → Warn about sore throat, fever (requires urgent FBC).
- Radioiodine Therapy (Definitive Treatment)
Highly effective and 1st-line if relapse after ATDs or patient prefers definitive treatment.
Contraindications: Pregnancy, breastfeeding, severe active thyroid eye disease (TED).
Can cause hypothyroidism, requiring lifelong levothyroxine replacement. - Surgery (Total Thyroidectomy)
Indications:
Large goitre causing compression.
Persistent hyperthyroidism despite medical therapy.
Severe thyroid eye disease (TED) not responding to other treatments.
Requires lifelong levothyroxine post-thyroidectomy.
Risks: Hypoparathyroidism, recurrent laryngeal nerve injury. - Management of Thyroid Eye Disease (TED)
Smoking cessation (reduces risk & severity).
Mild cases: Lubricating eye drops, selenium supplements.
Moderate-severe cases: Steroids (IV methylprednisolone), orbital radiotherapy, or decompression surgery.
Exam Tips for OSCE/Viva
✅ Always check for eye signs (proptosis, diplopia, lid lag, chemosis) in Graves’ disease.
✅ Ask about smoking (increases risk of TED).
✅ Be aware of Carbimazole risks (agranulocytosis, hepatotoxicity).
✅ Radioiodine contraindications: Pregnancy, breastfeeding, severe eye disease.
✅ Surgical complications: Hypoparathyroidism, recurrent laryngeal nerve injury.
Conns ix
Conn’s Syndrome (Primary Hyperaldosteronism) – Investigations
Conn’s syndrome is caused by autonomous aldosterone overproduction, usually due to an aldosterone-producing adrenal adenoma or bilateral adrenal hyperplasia. Investigations aim to confirm hyperaldosteronism, assess its cause, and localise the source.
- Screening Tests (Confirm Hyperaldosteronism)
✅ Plasma Aldosterone-to-Renin Ratio (ARR) [Initial Test]
↑ Aldosterone, ↓ Renin → Suggests primary hyperaldosteronism.
Performed after correcting hypokalaemia & discontinuing interfering medications (e.g., stop ACE inhibitors, ARBs, beta-blockers).
✅ Serum Electrolytes
↓ Potassium (Hypokalaemia) (but may be normal in some cases).
↑ Sodium (Mild Hypernatraemia).
Metabolic alkalosis (due to H+ loss from kidneys).
2. Confirmatory Tests (Prove Aldosterone Autonomy)
If ARR is high, confirm with one of the following:
✅ Saline Suppression Test
IV saline infusion → Normally, aldosterone should suppress.
If aldosterone remains high, this confirms primary hyperaldosteronism.
✅ Fludrocortisone Suppression Test
Administer fludrocortisone → Normally, aldosterone should suppress.
Failure of suppression confirms diagnosis.
✅ Captopril Challenge Test
Captopril (ACE inhibitor) reduces aldosterone in normal individuals.
In Conn’s, aldosterone remains high despite ACE inhibition.
3. Localisation Tests (Differentiate Unilateral vs. Bilateral Disease)
Once primary hyperaldosteronism is confirmed, localisation helps guide treatment.
✅ Adrenal CT Scan
Adrenal adenoma (Conn’s adenoma): Unilateral lesion.
Bilateral adrenal hyperplasia: Normal or both adrenals slightly enlarged.
✅ Adrenal Venous Sampling (AVS) [Gold Standard]
Compares aldosterone levels in both adrenal veins.
Lateralisation → Unilateral adenoma (surgical candidate).
No lateralisation → Bilateral hyperplasia (medical management with spironolactone).
✅ Metomidate PET-CT (if needed)
Special imaging for small aldosterone-secreting tumours.
4. Additional Tests
✅ ECG – Look for U waves, prolonged QT (hypokalaemia effects).
✅ 24-hour Ambulatory Blood Pressure Monitoring – If resistant hypertension.
Key Exam Points:
💡 ARR is the best screening test (high ARR suggests Conn’s).
💡 Saline or fludrocortisone suppression confirms the diagnosis.
💡 Adrenal CT helps but AVS is the gold standard for localisation.
💡 Conn’s = Hypertension + Hypokalaemia (but some have normal K⁺!).
Hypokalaemia signs and symptoms
Neuromuscular Symptoms:
Muscle weakness (mild to severe)
Fatigue or generalized weakness
Muscle cramps and spasms
Paralysis (severe cases)
Hyporeflexia (reduced reflexes)
Cardiovascular Symptoms:
Arrhythmias (e.g., premature ventricular contractions, atrial fibrillation, ventricular tachycardia)
ECG changes:
Flattened T waves
Prominent U waves
ST segment depression
Prolonged QT interval
Hypotension or lightheadedness, especially on standing
Gastrointestinal Symptoms:
Constipation (due to smooth muscle dysfunction)
Nausea or vomiting
Renal Symptoms:
Polyuria (increased urination)
Polydipsia (increased thirst)
Other Symptoms:
Respiratory weakness (severe cases can affect diaphragm function leading to breathing difficulties)
In severe cases, hypokalaemia can lead to life-threatening arrhythmias and respiratory failure, requiring urgent medical attention.
Causes of hypokalaemia
Causes of hypokalaemia can be broadly categorized into decreased intake, increased loss, and shift into cells. Here are the key causes:
- Decreased Potassium Intake:
Inadequate dietary intake (rare, but possible in cases of malnutrition or starvation) - Increased Potassium Loss:
Gastrointestinal loss:
Vomiting (loss of potassium-rich gastric acid)
Diarrhoea (loss of potassium in stool)
Laxative abuse
Renal loss:
Diuretics (especially loop diuretics and thiazides)
Hyperaldosteronism (primary or secondary)
Cushing’s syndrome (excess cortisol)
Renal tubular acidosis (Type 1 and Type 2)
Magnesium deficiency (can exacerbate potassium loss)
Post-renal transplantation (increased renal excretion) - Shift of Potassium into Cells:
Alkalosis (e.g., vomiting or overuse of bicarbonate)
Insulin therapy (especially in diabetic ketoacidosis, where insulin pushes potassium into cells)
Beta-adrenergic agonists (e.g., salbutamol or terbutaline for asthma or COPD)
Refeeding syndrome (in malnourished patients when nutrition is reintroduced too quickly)
Periodic paralysis (e.g., familial hypokalemic periodic paralysis) - Other Causes:
Bartter syndrome and Gitelman syndrome (inherited disorders that cause renal potassium wasting)
Magnesium deficiency (magnesium depletion can impair potassium reabsorption in the kidneys)
Excessive sweating (in hot weather or physical activity)
Alcoholism (due to inadequate intake and associated electrolyte disturbances)
Hypokalaemia often requires a full assessment to determine the underlying cause, as it can have serious consequences, including arrhythmias and muscle weakness.
A well-spoken Caucasian gentleman in his 60s was referred by his GP to the MAU because of hypokalaemia refractory to oral treatment, and difficult to treat hypertension. Six months ago he was routinely followed up at the urology clinic for bladder cancer which was treated with intravesical BCG therapy. At this appointment it was discovered that he had hypokalaemia. Treatment has been going on for 6 months and he has been on oral Sando-K tablets for the whole period. His hypertension has also worsened during this period. He reports excessive daytime sleepiness which affects his daily activities and his work as a photographer.
PMH included well-controlled asthma and migraine, for which he was on salbutamol/Seretide, and amlodipine respectively.
FH: he had no siblings and neither did his parents. His father died of a heart attack at the age of 73.
SH: lives at home with wife and two university-aged children. Finds it difficult to stay up during the day and falls asleep easily. Never smoker and minimal drinker.
What do you think the diagnosis could be?
Conn’s?
A well-spoken Caucasian gentleman in his 60s was referred by his GP to the MAU because of hypokalaemia refractory to oral treatment, and difficult to treat hypertension. Six months ago he was routinely followed up at the urology clinic for bladder cancer which was treated with intravesical BCG therapy. At this appointment it was discovered that he had hypokalaemia. Treatment has been going on for 6 months and he has been on oral Sando-K tablets for the whole period. His hypertension has also worsened during this period. He reports excessive daytime sleepiness which affects his daily activities and his work as a photographer.
PMH included well-controlled asthma and migraine, for which he was on salbutamol/Seretide, and amlodipine respectively.
FH: he had no siblings and neither did his parents. His father died of a heart attack at the age of 73.
SH: lives at home with wife and two university-aged children. Finds it difficult to stay up during the day and falls asleep easily. Never smoker and minimal drinker.
Conn’s - How would you manage this patient?
1️⃣ Initial Assessment and Investigation:
Review of Medications:
Confirm the use of diuretics, salbutamol, or any other drugs that may contribute to hypokalaemia (e.g., beta-agonists can shift potassium into cells).
Review for any new medications that might impact potassium levels or blood pressure.
Electrolyte Assessment:
Measure serum potassium, sodium, renal function (creatinine, eGFR), aldosterone, renin, and plasma cortisol.
Urinary Potassium:
Assess urinary potassium to confirm whether the hypokalaemia is due to renal loss or another mechanism (e.g., potassium shift into cells).
Blood Pressure Monitoring:
Record blood pressure to assess for hypertension and ensure that it is adequately managed.
2️⃣ Addressing Hypokalaemia:
Potassium Repletion:
For severe hypokalaemia (K+ < 2.5 mmol/L), treat with IV potassium replacement (as per local guidelines), initially 20–40 mmol in 500 mL normal saline or 5% dextrose.
Oral potassium can be used for mild hypokalaemia (K+ > 2.5 mmol/L), but it is less effective in cases resistant to treatment.
Monitor potassium regularly (every 2–4 hours during IV administration).
Identify Underlying Cause:
If secondary hyperaldosteronism or primary hyperaldosteronism is suspected, further workup with aldosterone-renin ratio or imaging (CT of the adrenal glands) is warranted.
3️⃣ Management of Hypertension:
BP Control:
Given the difficult-to-treat hypertension, the use of angiotensin-converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), or calcium channel blockers (e.g., amlodipine, which the patient is already on) could be considered.
If primary hyperaldosteronism is confirmed, aldosterone antagonists such as spironolactone should be introduced for better blood pressure and electrolyte control.
Further Investigation of Hypertension:
Investigate for any underlying causes of secondary hypertension (e.g., renal artery stenosis, pheochromocytoma, or hyperaldosteronism). This may involve imaging (CT, MRI, renal duplex ultrasound).
Specialist Referral:
If the cause of hypertension is not well-controlled with initial measures, refer to a hypertension clinic or endocrinologist for further evaluation (e.g., for potential primary aldosteronism).
4️⃣ Management of Sleepiness/Daytime Fatigue:
Daytime Sleepiness:
Since this patient reports significant daytime sleepiness, explore the possibility of sleep apnoea (which can contribute to both daytime fatigue and hypertension). A sleep study would help confirm this diagnosis.
If sleep apnoea is diagnosed, CPAP therapy may be needed to manage the condition, improving sleep quality and possibly impacting hypertension.
5️⃣ Specific Management for Potential Adrenal Insufficiency (if relevant):
If adrenal insufficiency (e.g., post-adrenalectomy or secondary adrenal failure) is suspected:
Hydrocortisone replacement therapy will be necessary to address cortisol deficiency.
If aldosterone deficiency is also present, fludrocortisone should be added to correct sodium and potassium balance.
6️⃣ Specialist Referrals:
Endocrinology: If there is a suspicion of primary hyperaldosteronism, adrenal insufficiency, or other endocrine causes, refer to endocrinology for specialized investigations, such as adrenal vein sampling or CT imaging of the adrenals.
Urology: If related to BCG therapy or past bladder cancer treatments, discuss with urology for follow-up and to rule out any lingering effects from cancer treatment (e.g., immune-mediated electrolyte disturbances).
7️⃣ Hospital Admission:
Hospital Admission Criteria:
Given the refractory hypokalaemia, hypertension, and excessive daytime sleepiness, admission to the medical ward for closer monitoring of electrolytes, blood pressure, and response to potassium supplementation may be required.
If adrenal insufficiency or hyperaldosteronism is suspected, admission may be necessary for more intensive management and investigations.
8️⃣ Discharge and Next Steps:
Follow-up Arrangements:
Arrange for close follow-up to monitor electrolytes, blood pressure, and symptoms (particularly daytime sleepiness).
Provide education on the importance of medication adherence and regular monitoring of potassium levels.
Patient Education:
Explain the potential causes of hypokalaemia and hypertension, and discuss the treatment options based on diagnosis.
Advise the patient to avoid self-medicating with potassium supplements without guidance from a healthcare professional.
Summary:
Main Goals:
Correct hypokalaemia, assess its cause (potential hyperaldosteronism or adrenal insufficiency), and manage hypertension.
Specialist referrals may be needed based on the diagnosis (endocrinology, urology).
Sleep study if daytime fatigue suggests sleep apnoea.
A well-spoken Caucasian gentleman in his 60s was referred by his GP to the MAU because of hypokalaemia refractory to oral treatment, and difficult to treat hypertension. Six months ago he was routinely followed up at the urology clinic for bladder cancer which was treated with intravesical BCG therapy. At this appointment it was discovered that he had hypokalaemia. Treatment has been going on for 6 months and he has been on oral Sando-K tablets for the whole period. His hypertension has also worsened during this period. He reports excessive daytime sleepiness which affects his daily activities and his work as a photographer.
PMH included well-controlled asthma and migraine, for which he was on salbutamol/Seretide, and amlodipine respectively.
FH: he had no siblings and neither did his parents. His father died of a heart attack at the age of 73.
SH: lives at home with wife and two university-aged children. Finds it difficult to stay up during the day and falls asleep easily. Never smoker and minimal drinker.
Do they need to stay in hospital?
Yes, this patient may need to stay in hospital due to refractory hypokalaemia and difficult-to-treat hypertension, which require close monitoring and correction, particularly if there is a suspicion of an underlying endocrine disorder such as hyperaldosteronism or adrenal insufficiency. Admission allows for proper electrolyte monitoring, blood pressure control, and further investigation.
A well-spoken Caucasian gentleman in his 60s was referred by his GP to the MAU because of hypokalaemia refractory to oral treatment, and difficult to treat hypertension. Six months ago he was routinely followed up at the urology clinic for bladder cancer which was treated with intravesical BCG therapy. At this appointment it was discovered that he had hypokalaemia. Treatment has been going on for 6 months and he has been on oral Sando-K tablets for the whole period. His hypertension has also worsened during this period. He reports excessive daytime sleepiness which affects his daily activities and his work as a photographer.
PMH included well-controlled asthma and migraine, for which he was on salbutamol/Seretide, and amlodipine respectively.
FH: he had no siblings and neither did his parents. His father died of a heart attack at the age of 73.
SH: lives at home with wife and two university-aged children. Finds it difficult to stay up during the day and falls asleep easily. Never smoker and minimal drinker.
. Advise patient on next stops
Follow-up with specialists:
Endocrinology: For further investigation into potential causes like hyperaldosteronism or adrenal insufficiency.
Urology: To monitor any long-term effects of BCG therapy for bladder cancer.
Close monitoring of electrolytes: Regular follow-up to monitor potassium levels, renal function, and blood pressure.
Adherence to treatment: Ensure strict adherence to prescribed medications, particularly potassium supplementation and antihypertensive medications.
Lifestyle modifications: Advise on reducing salt intake, maintaining hydration, and avoiding self-medicating with potassium supplements.
Sleep study referral: If daytime sleepiness persists, consider referral for a sleep study to rule out conditions like sleep apnoea.
Return if symptoms worsen: Advise seeking immediate care if symptoms like severe fatigue, dizziness, or worsening hypertension occur.
