Thyroid Monitoring and Amiodarone Use: What Patients Need to Know

Amiodarone is a medication used to treat heart rhythm disorders, but it can also cause thyroid dysfunction. Patients on this drug should have their thyroid function regularly monitored, with a baseline check and another three months after starting the medication. Patients with a history of hypothyroidism can still use amiodarone, but with more stringent monitoring. Those with thyroid autoantibodies are at increased risk of drug-induced hyperthyroidism. If thyroid function becomes deranged, amiodarone may need to be discontinued or thyroxine supplements dose-adjusted. Regular thyroid monitoring is crucial for patients on amiodarone.

The risk of osteoporosis increases with over-replacement of thyroxine. Elevated T4 and suppressed TSH levels in blood tests indicate over-replacement with levothyroxine, which can cause confusion in biochemistry abnormalities, although this is more commonly observed in hypothyroidism. Constipation is a symptom of hypothyroidism, not over-replacement with levothyroxine. Muscle weakness and reduced reflexes are also associated with hypothyroidism, not hyperthyroidism. Over-replacement with thyroxine would result in weight loss rather than weight gain.

Managing Hypothyroidism: Dosage, Goals, and Side-Effects

Hypothyroidism is a condition where the thyroid gland doesn’t produce enough thyroid hormone. The management of hypothyroidism involves the use of levothyroxine, a synthetic form of thyroid hormone. The initial starting dose of levothyroxine should be lower in elderly patients and those with ischaemic heart disease. For patients with cardiac disease, severe hypothyroidism, or patients over 50 years, the initial starting dose should be 25mcg od with dose slowly titrated. Other patients should be started on a dose of 50-100 mcg od. After a change in thyroxine dose, thyroid function tests should be checked after 8-12 weeks. The therapeutic goal is to achieve a ‘normalisation’ of the thyroid stimulating hormone (TSH) level, with a TSH value of 0.5-2.5 mU/l being the preferred range.

Women with established hypothyroidism who become pregnant should have their dose increased ‘by at least 25-50 micrograms levothyroxine’* due to the increased demands of pregnancy. The TSH should be monitored carefully, aiming for a low-normal value. There is no evidence to support combination therapy with levothyroxine and liothyronine.

Levothyroxine therapy may cause side-effects such as hyperthyroidism due to over-treatment, reduced bone mineral density, worsening of angina, and atrial fibrillation. Interactions with iron and calcium carbonate may reduce the absorption of levothyroxine, so they should be given at least 4 hours apart.

In summary, the management of hypothyroidism involves careful dosage adjustment, regular monitoring of thyroid function tests, and aiming for a TSH value in the normal range. Women who become pregnant should have their dose increased, and combination therapy with levothyroxine and liothyronine is not recommended. Patients should also be aware of potential side-effects and interactions with other medications.

*source: NICE Clinical Knowledge Summaries

Understanding Hypogonadism: Interpreting Testosterone Results and Treatment Considerations

Hypogonadism, or low testosterone, can present with a variety of symptoms including low libido, erectile dysfunction, and loss of early morning erections. When low testosterone is detected, further testing with follicle-stimulating hormone (FSH), luteinising hormone (LH), and prolactin measurements can help distinguish primary from secondary hypogonadism.

There are several factors that can contribute to reversible hypogonadism, including concurrent illness, certain medications, and lifestyle factors such as excessive alcohol consumption and stress. However, it is important to note that hypogonadism should be treated with testosterone replacement therapy, regardless of age, but only after confirming the diagnosis with repeat testing.

It is also important to consider age-related declines in testosterone levels, which typically occur after the age of 30. However, this decline may be a result of deteriorating general health rather than the cause. Therefore, it is crucial to interpret testosterone results in the context of the patient’s symptoms and overall health status.

In cases where hypogonadism is suspected, referral to an endocrinologist may be necessary if there are suggestive clinical symptoms and chronic androgen deficiency. However, it is important to note that testosterone replacement therapy should not be initiated solely based on age or a single low testosterone result.

For black patients with type 2 diabetes and hypertension, the recommended first-line treatment is an angiotensin II receptor blocker, specifically losartan. This is based on evidence that ACE inhibitors, such as ramipril, may be less effective in patients of African or African-Caribbean ethnicity. For non-diabetic patients of this ethnicity, a calcium channel blocker like amlodipine is recommended. If blood pressure remains uncontrolled, a thiazide-like diuretic such as indapamide may be added as a second or third line of treatment. While lifestyle changes are important, this patient’s stage 2 hypertension and diabetes put him at high risk for complications, making prompt and effective treatment essential.

NICE has updated its guidance on the management of type 2 diabetes mellitus (T2DM) in 2022 to reflect advances in drug therapy and improved evidence regarding newer therapies such as SGLT-2 inhibitors. For the average patient taking metformin for T2DM, lifestyle changes and titrating up metformin to aim for a HbA1c of 48 mmol/mol (6.5%) is recommended. A second drug should only be added if the HbA1c rises to 58 mmol/mol (7.5%). Dietary advice includes encouraging high fiber, low glycemic index sources of carbohydrates, controlling intake of saturated fats and trans fatty acids, and initial target weight loss of 5-10% in overweight individuals.

Individual HbA1c targets should be agreed upon with patients to encourage motivation, and HbA1c should be checked every 3-6 months until stable, then 6 monthly. Targets should be relaxed on a case-by-case basis, with particular consideration for older or frail adults with type 2 diabetes. Metformin remains the first-line drug of choice, and SGLT-2 inhibitors should be given in addition to metformin if the patient has a high risk of developing cardiovascular disease (CVD), established CVD, or chronic heart failure. If metformin is contraindicated, SGLT-2 monotherapy or a DPP-4 inhibitor, pioglitazone, or sulfonylurea may be used.

Further drug therapy options depend on individual clinical circumstances and patient preference. Dual therapy options include adding a DPP-4 inhibitor, pioglitazone, sulfonylurea, or SGLT-2 inhibitor (if NICE criteria are met). If a patient doesn’t achieve control on dual therapy, triple therapy options include adding a sulfonylurea or GLP-1 mimetic. GLP-1 mimetics should only be added to insulin under specialist care. Blood pressure targets are the same as for patients without type 2 diabetes, and ACE inhibitors or ARBs are first-line for hypertension. Antiplatelets should not be offered unless a patient has existing cardiovascular disease, and only patients with a 10-year cardiovascular risk > 10% should be offered a statin.

Diagnosis of Diabetes Mellitus

Diabetes mellitus can be diagnosed based on symptoms and a random glucose level above 11.1 mmol/L or a fasting plasma glucose level above 7 mmol/L. Another option is the two-hour oral glucose tolerance test. Impaired glucose tolerance may be indicated by a post-OGTT plasma glucose level between 7.7 and 11.1 or a fasting plasma glucose level between 6.1 and 7.

For certain groups, an HbA1c level of 48 mmol/mol (6.5%) is recommended as the cut-off point for diagnosing diabetes. However, it is important to note that a value below 48 mmol/mol (6.5%) doesn’t necessarily exclude a diabetes diagnosis using glucose tests. It is crucial to familiarize oneself with the exceptions to these guidelines.

Overall, the diagnosis of diabetes mellitus requires careful consideration of various factors and tests to ensure accurate identification and appropriate treatment.

Placing any object in the mouth of an unconscious patient can be risky as they may not be adequately safeguarding their airway.

In cases of heparin overdose, protamine sulfate is administered.

Insulin therapy can have side-effects that patients should be aware of. One of the most common side-effects is hypoglycaemia, which can cause sweating, anxiety, blurred vision, confusion, and aggression. Patients should be taught to recognize these symptoms and take 10-20g of a short-acting carbohydrate, such as a glass of Lucozade or non-diet drink, three or more glucose tablets, or glucose gel. It is also important for every person treated with insulin to have a glucagon kit for emergencies where the patient is not able to orally ingest a short-acting carbohydrate. Patients who have frequent hypoglycaemic episodes may develop reduced awareness, and beta-blockers can further reduce hypoglycaemic awareness.

Another potential side-effect of insulin therapy is lipodystrophy, which typically presents as atrophy or lumps of subcutaneous fat. This can be prevented by rotating the injection site, as using the same site repeatedly can cause erratic insulin absorption. It is important for patients to be aware of these potential side-effects and to discuss any concerns with their healthcare provider. By monitoring their blood sugar levels and following their treatment plan, patients can manage the risks associated with insulin therapy and maintain good health.

For the management of hot flashes in men undergoing hormonal treatment for prostate cancer, NICE suggests the use of cyproterone acetate, while the use of other medications is not recommended.

Prostate cancer management varies depending on the stage of the disease and the patient’s life expectancy and preferences. For localized prostate cancer (T1/T2), treatment options include active monitoring, watchful waiting, radical prostatectomy, and radiotherapy (external beam and brachytherapy). For localized advanced prostate cancer (T3/T4), options include hormonal therapy, radical prostatectomy, and radiotherapy. Patients may develop proctitis and are at increased risk of bladder, colon, and rectal cancer following radiotherapy for prostate cancer.

In cases of metastatic prostate cancer, reducing androgen levels is a key aim of treatment. A combination of approaches is often used, including anti-androgen therapy, synthetic GnRH agonist or antagonists, bicalutamide, cyproterone acetate, abiraterone, and bilateral orchidectomy. GnRH agonists, such as Goserelin (Zoladex), initially cause a rise in testosterone levels before falling to castration levels. To prevent a rise in testosterone, anti-androgens are often used to cover the initial therapy. GnRH antagonists, such as degarelix, are being evaluated to suppress testosterone while avoiding the flare phenomenon. Chemotherapy with docetaxel is also an option for the treatment of hormone-relapsed metastatic prostate cancer in patients who have no or mild symptoms after androgen deprivation therapy has failed, and before chemotherapy is indicated.

The patient exhibits hypothyroidism, indicated by low free T4 and elevated TSH levels. Considering her age, it is recommended to gradually introduce levothyroxine at a starting dose of 25mcg once daily.

Managing Hypothyroidism: Dosage, Goals, and Side-Effects

Hypothyroidism is a condition where the thyroid gland doesn’t produce enough thyroid hormone. The management of hypothyroidism involves the use of levothyroxine, a synthetic form of thyroid hormone. The initial starting dose of levothyroxine should be lower in elderly patients and those with ischaemic heart disease. For patients with cardiac disease, severe hypothyroidism, or patients over 50 years, the initial starting dose should be 25mcg od with dose slowly titrated. Other patients should be started on a dose of 50-100 mcg od. After a change in thyroxine dose, thyroid function tests should be checked after 8-12 weeks. The therapeutic goal is to achieve a ‘normalisation’ of the thyroid stimulating hormone (TSH) level, with a TSH value of 0.5-2.5 mU/l being the preferred range.

Women with established hypothyroidism who become pregnant should have their dose increased ‘by at least 25-50 micrograms levothyroxine’* due to the increased demands of pregnancy. The TSH should be monitored carefully, aiming for a low-normal value. There is no evidence to support combination therapy with levothyroxine and liothyronine.

Levothyroxine therapy may cause side-effects such as hyperthyroidism due to over-treatment, reduced bone mineral density, worsening of angina, and atrial fibrillation. Interactions with iron and calcium carbonate may reduce the absorption of levothyroxine, so they should be given at least 4 hours apart.

In summary, the management of hypothyroidism involves careful dosage adjustment, regular monitoring of thyroid function tests, and aiming for a TSH value in the normal range. Women who become pregnant should have their dose increased, and combination therapy with levothyroxine and liothyronine is not recommended. Patients should also be aware of potential side-effects and interactions with other medications.

*source: NICE Clinical Knowledge Summaries

Thyroid Hormone Therapy and Monitoring

Thyroxine is an effective treatment for hypothyroidism as it helps to suppress the high levels of thyroid-stimulating hormone (TSH) in the body. The best way to monitor the effectiveness of this treatment is by measuring TSH levels and aiming to bring them into the normal range. In addition to TSH, other tests such as triiodothyronine, free thyroxine (T4), thyroid peroxidase antibody, and protein-bound iodine levels may be used in the initial investigation and diagnosis of thyroid disorders. Proper monitoring and management of thyroid hormone therapy can help improve symptoms and prevent complications.

Treatment Options for Type 2 Diabetes

Type 2 diabetes is a chronic condition that requires careful management to prevent complications. Metformin is the preferred first-line treatment as it increases insulin sensitivity. However, caution should be taken when prescribing metformin to patients with renal impairment. If metformin is not suitable, other options include dipeptidylpeptidase-4 inhibitors, pioglitazone, and sulfonylureas. Pioglitazone can be used as a second-line treatment or in combination with metformin. Acarbose is a weak hypoglycemic agent and is only used in combination with other agents. Sulfonylureas may be considered as first-line therapy in symptomatic patients, but should be prescribed with caution in obese individuals. Insulin may be necessary if oral therapies fail to adequately control HbA1C levels. It is important to consider contraindications and potential side effects when selecting a treatment option.

Treatment Options for Hyponatraemia

Hyponatraemia is a condition where the concentration of sodium in the blood is lower than normal. There are various treatment options available for this condition, depending on the severity and underlying cause.

Restriction of water intake is a common treatment for hyponatraemia caused by the syndrome of inappropriate antidiuretic hormone secretion (SIADH). In this condition, the release of antidiuretic hormone (ADH) is not inhibited by a reduction in plasma osmolality, leading to excessive water retention. Fluid restriction, usually limiting fluids to 500 ml/day below the average daily urine volume, can help normalise blood osmolality.

Intravenous infusion of hypertonic saline is an emergency treatment for acute symptomatic hyponatraemia. Hypertonic saline (3%) is given via continuous infusion to rapidly increase the concentration of sodium in the blood.

Intravenous infusion of isotonic saline is not the first-line treatment for hyponatraemia. It may be used in some cases, but hypertonic saline is preferred for acute symptomatic hyponatraemia.

Oral demeclocycline is a pharmacological intervention reserved for refractory cases of hyponatraemia. It is a tetracycline derivative that decreases urine concentration even in the presence of high plasma ADH levels. However, it can be nephrotoxic.

Oral furosemide is another treatment option that may be used to decrease the reabsorption of water. However, it is not a first-line treatment and should be used with caution to avoid correcting water imbalances too rapidly.

In conclusion, the treatment options for hyponatraemia depend on the underlying cause and severity of the condition. Fluid restriction, intravenous infusion of hypertonic saline, and pharmacological interventions may be used in different situations to help normalise blood sodium levels.

Hypoglycaemic unawareness, where a person with diabetes is unable to recognize the symptoms of low blood sugar, is a reason why they should not drive according to the Driver and Vehicle Licensing Agency (DVLA). To be considered fit to drive, a person with diabetes must have experienced no more than one episode of severe hypoglycaemia in the past year and be aware of the symptoms. Symptoms of mild hypoglycaemia include hunger, anxiety, irritability, palpitations, sweating, and tingling lips. As blood glucose levels drop further, symptoms may progress to weakness, lethargy, impaired vision, confusion, and irrational behavior. Severe hypoglycaemia can result in seizures and loss of consciousness, and between 4 and 10% of deaths in people with Type 1 Diabetes Mellitus are due to hypoglycaemia. Recurrent exposure to hypoglycaemia can lead to a loss of early warning symptoms, making it more difficult for a person to recognize when their blood sugar is low. While most patients with impaired awareness of hypoglycaemia can recognize their symptoms and correct the hypoglycaemia with a small amount of fast-acting carbohydrate taken by mouth, severe hypoglycaemia occurs when patients require treatment by another person because they are incapable of self-management.

Exclusion of agranulocytosis is necessary when using carbimazole.

Carbimazole is a medication used to treat thyrotoxicosis, a condition where the thyroid gland produces too much thyroid hormone. It is usually given in high doses for six weeks until the patient’s thyroid hormone levels become normal, after which the dosage is reduced. The drug works by blocking thyroid peroxidase, an enzyme that is responsible for coupling and iodinating the tyrosine residues on thyroglobulin, which ultimately leads to a reduction in thyroid hormone production. In contrast, propylthiouracil has a dual mechanism of action, inhibiting both thyroid peroxidase and 5′-deiodinase, which reduces the peripheral conversion of T4 to T3.

However, carbimazole is not without its adverse effects. One of the most serious side effects is agranulocytosis, a condition where the body’s white blood cell count drops significantly, making the patient more susceptible to infections. Additionally, carbimazole can cross the placenta and affect the developing fetus, although it may be used in low doses during pregnancy under close medical supervision. Overall, carbimazole is an effective medication for managing thyrotoxicosis, but its potential side effects should be carefully monitored.

Testing for Reduced Serum Testosterone

Patients who exhibit symptoms of reduced serum testosterone should undergo a repeat test, preferably in the morning, along with FSH, LH, and prolactin. This helps determine which part of the hypothalamic-pituitary-gonadal axis is affected. It is crucial to take action as the patient may have an underlying endocrinological cause. If the repeat test shows abnormal results, referral to a secondary care physician is necessary. The physician may then consider treatments such as testogel or nebido.

In summary, testing for reduced serum testosterone is essential in diagnosing and treating patients with symptoms of low testosterone levels. A repeat test, along with other hormone tests, can help identify the root cause of the problem and guide appropriate treatment.

The most effective way to diagnose Addison’s disease is through the short synacthen test. If a patient presents with lethargy, hyponatraemia, and hyperkalaemia, it is highly indicative of Addison’s disease. While the patient’s thyroxine level is slightly low, it is unlikely to be the cause of the hyperkalaemia. It is possible that the patient also has hypothyroidism, but this would not fully explain their symptoms.

Investigating Addison’s Disease: ACTH Stimulation Test and Serum Cortisol Levels

When investigating a patient suspected of having Addison’s disease, the most definitive test is the ACTH stimulation test, also known as the short Synacthen test. This involves measuring plasma cortisol levels before and 30 minutes after administering Synacthen 250ug IM. Adrenal autoantibodies, such as anti-21-hydroxylase, may also be detected.

However, if an ACTH stimulation test is not readily available, a 9 am serum cortisol level can be useful. A level of over 500 nmol/l makes Addison’s disease very unlikely, while a level below 100 nmol/l is definitely abnormal. If the level falls between 100-500 nmol/l, an ACTH stimulation test should be performed.

It is important to note that around one-third of undiagnosed patients with Addison’s disease may also have associated electrolyte abnormalities, such as hyperkalaemia, hyponatraemia, hypoglycaemia, and metabolic acidosis. Therefore, it is crucial to investigate these levels as well to ensure a proper diagnosis and treatment plan.

Understanding Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH)

SIADH is a condition where the release of antidiuretic hormone (ADH) from the posterior pituitary is not inhibited by a reduction in plasma osmolality on drinking water, causing water retention and extracellular fluid volume expansion without oedema or hypertension. This condition is commonly associated with small-cell lung cancer. Hyponatraemia and concentrated urine are the main laboratory findings, and severe cases may present with symptoms of cerebral oedema. Addison’s disease, diuretics, psychogenic polydipsia, and vomiting are not likely causes of hyponatraemia, although they may contribute to it in certain cases.

Causes of hyperprolactinaemia and galactorrhoea: differential diagnosis

Hyperprolactinaemia and galactorrhoea are two related conditions that can have various underlying causes. One common cause is a prolactin-secreting pituitary tumour, which can be either a microadenoma (more common) or a macroadenoma (less common). Another possible cause is the use of certain drugs, such as dopamine receptor antagonists and some antidepressants. Hyperthyroidism is not a likely cause, but hypothyroidism can sometimes lead to hyperprolactinaemia. Finally, while hepatic impairment can cause hyperprolactinaemia, it is not a frequent finding in patients with liver cirrhosis. Therefore, a careful differential diagnosis is needed to identify the specific cause of hyperprolactinaemia and galactorrhoea in each patient.

DVLA Guidelines for Diabetic Drivers

Drivers with diabetes do not need to inform the DVLA if their condition is managed by tablets or diet and they are free of complications such as visual impairment or hypoglycaemic attacks. However, if they are taking tablets that can induce hypoglycaemia, such as sulphonylureas, they must inform the DVLA. Additionally, if they have experienced more than one episode of severe hypoglycaemia within the last 12 months or are at high risk of developing it, they must also inform the DVLA.

In January 2016, the DVLA updated their guidelines, which may be reflected in AKT exam questions. It is important for drivers with diabetes to familiarize themselves with any additions or amendments. One of the changes made was to revise the wording for Group 1 drivers who are managed by tablets that carry a risk of inducing hypoglycaemia, including sulphonylureas and glinides.

It is important to note that drivers who are treated with insulin must inform the DVLA by law. Some people with diabetes may develop associated problems that could affect their ability to drive safely, and it is important to follow the guidelines to ensure the safety of both the driver and others on the road.

Types of Diabetes

There are two major types of diabetes: type 1 and type 2. Type 1 diabetes is characterized by a deficiency of insulin and typically affects children. Patients with type 1 diabetes are thin, lose weight, and are treated with insulin. On the other hand, type 2 diabetes affects an older age group and is associated with weight gain (obesity). It is usually treated with diet and/or drugs. Although not inherited in any mendelian fashion, type 2 diabetes has a familial occurrence due to the body type of the family. Iatrogenic diabetes is caused by medical treatments, while mitochondrial diabetes is a very rare form of diabetes resulting from damage to mitochondrial DNA. Finally, secondary diabetes occurs as a consequence of another disease.

It is important to differentiate between the types of diabetes as this guides treatment. Patients with type 1 diabetes require insulin, while those with type 2 diabetes may initially be treated with diet and/or drugs but may eventually require insulin. Understanding the cause of diabetes is also important in determining the appropriate treatment.

Effects of Cholesterol-Lowering Medications on Glucose Control

The mechanism by which nicotinic acid affects glucose levels is not fully understood, but it may increase blood glucose in some patients by stimulating hepatic glucose output or blocking glucose uptake by skeletal muscle. However, for most patients with diabetes, nicotinic acid has minimal effect. A meta-analysis in 2011 suggested an increased risk of inducing diabetes in patients treated with intensive statin therapy, but this did not examine whether statins worsened glucose control in established diabetics. Cholestyramine may interact with oral hypoglycemics, but it doesn’t typically worsen diabetic control and may even improve it. Fenofibrate and ezetimibe have not been shown to worsen diabetic control. Overall, the effects of cholesterol-lowering medications on glucose control vary and should be monitored closely in patients with diabetes.

Patients taking canagliflozin should have their legs and feet closely monitored for ulcers or infection due to the possible increased risk of amputation. It is important for these patients to attend regular foot checks and practice good foot care. Eye screening, influenza vaccination, and shingles vaccination are not affected by SGLT2 inhibitors and should be attended as normal.

Understanding SGLT-2 Inhibitors

SGLT-2 inhibitors are medications that work by blocking the reabsorption of glucose in the kidneys, leading to increased excretion of glucose in the urine. This mechanism of action helps to lower blood sugar levels in patients with type 2 diabetes mellitus. Examples of SGLT-2 inhibitors include canagliflozin, dapagliflozin, and empagliflozin.

However, it is important to note that SGLT-2 inhibitors can also have adverse effects. Patients taking these medications may be at increased risk for urinary and genital infections due to the increased glucose in the urine. Fournier’s gangrene, a rare but serious bacterial infection of the genital area, has also been reported. Additionally, there is a risk of normoglycemic ketoacidosis, a condition where the body produces high levels of ketones even when blood sugar levels are normal. Finally, patients taking SGLT-2 inhibitors may be at increased risk for lower-limb amputations, so it is important to closely monitor the feet.

Despite these potential risks, SGLT-2 inhibitors can also have benefits. Patients taking these medications often experience weight loss, which can be beneficial for those with type 2 diabetes mellitus. Overall, it is important for patients to discuss the potential risks and benefits of SGLT-2 inhibitors with their healthcare provider before starting treatment.

Cortisol Levels and Cushing Syndrome: Diagnostic Tests and Circadian Rhythms

Plasma cortisol levels in normal individuals follow a circadian rhythm, with the highest levels in the morning and the lowest levels at night. However, in patients with Cushing syndrome, this rhythm is disrupted, and late-night cortisol levels do not fall as they should. This alteration in cortisol secretion can be used to diagnose Cushing syndrome, with an elevated serum cortisol at 2400 h being an early indicator.

The 0900 h cortisol level is not a reliable indicator of Cushing syndrome, as it may still be within the normal range. Instead, a low-dose dexamethasone suppression test is used, where a failure to suppress cortisol suggests Cushing syndrome.

A 24-hour urine collection with cortisol level analysis is a better test for Cushing syndrome than serum cortisol, with two or more samples showing cortisol excretion more than three times the upper limit of normal being a confident diagnosis.

Late-night cortisol samples should be taken between 2300 h and 0100 h, while melatonin, which regulates sleep and wakefulness, follows a reverse circadian rhythm, with levels highest during periods of sleep. Synthetic melatonin is commonly used to alleviate jet lag.

Diagnosis of Primary Hypoadrenalism: A Case Study

A woman presents with a marked postural drop in blood pressure, increased pigmentation, and low cortisol levels, indicating primary hypoadrenalism as the most likely diagnosis. The high adrenocorticotropic hormone (ACTH) level causes pigmentation, and autoimmune destruction of the adrenal glands is responsible for 80% of cases. Hyponatremia and hyperkalemia are common in established cases. The National Institute for Health and Care Excellence recommends hospital admission for serum cortisol levels below 100 nmol/l and referral to an endocrinologist for levels between 100 and 500 nmol/l. Hypovolemia, HIV, hypothyroidism, and psychiatric symptoms are unlikely causes based on the case history.

In the case of a child weighing 25kg or less experiencing hypoglycaemia, glucagon 500 mcg should be given via IM if oral treatment is not possible or ineffective. Hypoglycaemia is clinically defined as a blood glucose level below 3.5 mmol/L, which is the case for this child. Despite the mother’s attempts at oral treatment, the child has not improved, making it necessary to administer glucagon to prevent further deterioration. Once the child is stable, it is advisable to contact the paediatric team for further evaluation and management.

Understanding Hypoglycaemia: Causes, Features, and Management

Hypoglycaemia is a condition characterized by low blood sugar levels, which can lead to a range of symptoms and complications. There are several possible causes of hypoglycaemia, including insulinoma, liver failure, Addison’s disease, and alcohol consumption. The physiological response to hypoglycaemia involves hormonal and sympathoadrenal responses, which can result in autonomic and neuroglycopenic symptoms. While blood glucose levels and symptom severity are not always correlated, common symptoms of hypoglycaemia include sweating, shaking, hunger, anxiety, nausea, weakness, vision changes, confusion, and dizziness. In severe cases, hypoglycaemia can lead to convulsions or coma.

Managing hypoglycaemia depends on the severity of the symptoms and the setting in which it occurs. In the community, individuals with diabetes who inject insulin may be advised to consume oral glucose or a quick-acting carbohydrate such as GlucoGel or Dextrogel. A ‘HypoKit’ containing glucagon may also be prescribed for home use. In a hospital setting, treatment may involve administering a quick-acting carbohydrate or subcutaneous/intramuscular injection of glucagon for unconscious or unable to swallow patients. Alternatively, intravenous glucose solution may be given through a large vein.

Overall, understanding the causes, features, and management of hypoglycaemia is crucial for individuals with diabetes or other conditions that increase the risk of low blood sugar levels. Prompt and appropriate treatment can help prevent complications and improve outcomes.

Correct Management of Type 2 Diabetes and Cardiovascular Disease: Common Misconceptions

There are several misconceptions regarding the management of type 2 diabetes and cardiovascular disease that need to be addressed. One common misconception is that statins should only be started if a formal risk assessment is conducted. However, the National Institute for Health and Care Excellence recommends that statin treatment with atorvastatin 80 mg should always be started for secondary prevention of cardiovascular disease, unless contraindicated.

Another misconception is that blood pressure should be 150/80 mmHg or less. The target for blood pressure in type 2 diabetes is actually 140/90 mmHg, and following a myocardial infarction, it may be prudent to aim even lower.

It is also incorrect to assume that insulin should be started for all patients with type 2 diabetes and cardiovascular disease. Insulin should only be used if clinically indicated due to poor diabetic control.

Contrary to popular belief, the usual cardiac rehabilitation program is not contraindicated for patients with type 2 diabetes and cardiovascular disease. All patients should be given advice about and offered a cardiac rehabilitation program with an exercise component.

Finally, the use of angiotensin-converting-enzyme (ACE) inhibition is not contraindicated in the first six weeks after a myocardial infarction. In fact, people who have had a myocardial infarction with or without diabetes should normally be discharged from the hospital with ACE inhibitor treatment, provided there are no contraindications.

In summary, it is important to dispel these common misconceptions and ensure that patients with type 2 diabetes and cardiovascular disease receive appropriate and evidence-based management.

Diagnosing Chest Tightness and Palpitations in Primary Care

Symptoms of chest tightness and palpitations are common in primary care, but diagnosing the underlying cause can be challenging. Episodic symptoms often require catching the symptoms during an attack to make an accurate diagnosis. Patients may describe a previous attack, but positive examination findings are often lacking when they are asymptomatic. Therefore, history is crucial, and patients should seek review when experiencing symptoms.

In this case, the patient presented with high blood pressure, tachycardia, and glycosuria during an attack. The episodic nature of the symptoms suggested panic attacks, phaeochromocytoma, or a paroxysmal tachyarrhythmia such as Wolff-Parkinson-White (WPW) syndrome. However, WPW typically causes paroxysmal supraventricular tachycardia and would not cause glycosuria. Panic attacks would not cause glycosuria, and the severity of the hypertension would go against this diagnosis. Phaeochromocytoma unifies the history and clinical features and is the underlying disorder.

Phaeochromocytoma is a rare tumour that produces catecholamines and causes episodes of hypertension, chest tightness, sweating, tremor, and flushing. Glycosuria occurs in approximately 30% of patients during an attack. Diagnosis is made by a 24-hour urine collection for metanephrines, and surgical removal is the treatment of choice.

Based on the presence of thyrotoxic symptoms, goitre, and anti-thyroid peroxidase antibodies, the likely diagnosis is

Graves’ Disease: Common Features and Unique Signs

Graves’ disease is the most frequent cause of thyrotoxicosis, which is commonly observed in women aged 30-50 years. The condition presents typical features of thyrotoxicosis, such as weight loss, palpitations, and heat intolerance. However, Graves’ disease also displays specific signs that are not present in other causes of thyrotoxicosis. These include eye signs, such as exophthalmos and ophthalmoplegia, as well as pretibial myxoedema and thyroid acropachy. The latter is a triad of digital clubbing, soft tissue swelling of the hands and feet, and periosteal new bone formation.

Graves’ disease is characterized by the presence of autoantibodies, including TSH receptor stimulating antibodies in 90% of patients and anti-thyroid peroxidase antibodies in 75% of patients. Thyroid scintigraphy reveals a diffuse, homogenous, and increased uptake of radioactive iodine. These features help distinguish Graves’ disease from other causes of thyrotoxicosis and aid in its diagnosis.

Thyroid eye disease is often linked to hyperthyroidism from Graves’ disease, but it can also occur in euthyroid or hypothyroid patients. The severity of the eye disease is not necessarily related to the level of thyrotoxicosis.

Thyroid eye disease is a condition that affects a significant proportion of patients with Graves’ disease. It is believed to be caused by an autoimmune response against an autoantigen, possibly the TSH receptor, which leads to inflammation behind the eyes. This inflammation causes the deposition of glycosaminoglycan and collagen in the muscles, resulting in symptoms such as exophthalmos, conjunctival oedema, optic disc swelling, and ophthalmoplegia. In severe cases, patients may be unable to close their eyelids, leading to sore, dry eyes and a risk of exposure keratopathy.

Prevention of thyroid eye disease is important, and smoking is the most significant modifiable risk factor. Radioiodine treatment may also increase the risk of developing or worsening eye disease, but prednisolone may help reduce this risk. Management of established thyroid eye disease may involve topical lubricants to prevent corneal inflammation, steroids, radiotherapy, or surgery.

Patients with established thyroid eye disease should be monitored closely for any signs of deterioration, such as unexplained changes in vision, corneal opacity, or disc swelling. Urgent review by an ophthalmologist is necessary in these cases to prevent further complications. Overall, thyroid eye disease is a complex condition that requires careful management and monitoring to ensure the best possible outcomes for patients.

When a patient has consistently high prolactin levels without a clear cause, it may be due to a prolactinoma, a type of pituitary tumor. In the case of a microprolactinoma, the prolactin levels may be between 1000-5000 mIU/l, but the patient’s hormone profile and visual fields are normal. Hyperprolactinemia can inhibit the release of gonadotropin-releasing hormone, leading to symptoms such as infertility and decreased libido. Treatment options include surgery or medication with dopamine agonists. Macroprolactinoma, acromegaly, and hypothyroidism are unlikely causes in this case. Psychogenic impotence doesn’t explain the elevated prolactin levels.

Contraindications to Metformin Use

Metformin is a commonly prescribed medication for the treatment of type 2 diabetes. However, there are certain situations where its use is contraindicated. Ketoacidosis, use of iodine-containing contrast media, and use of general anesthesia are all contraindications to metformin use. Additionally, patients with renal impairment are at an increased risk of lactic acidosis and should have their dose reviewed if their estimated glomerular filtration rate (eGFR) is less than 45. Metformin should be avoided if the eGFR is less than 30 and should be withdrawn or treatment interrupted in patients at risk of tissue hypoxia or sudden deterioration in renal function. These patients include those with shock, sepsis, acute heart failure, respiratory failure, and those who have recently had a myocardial infarction. In the case of a patient with a renal calculus and significantly impaired renal function, metformin should be withheld.