Addison’s disease occurs when the adrenal glands do not produce enough steroid hormones. This includes glucocorticoids, mineralocorticoids, and sex steroids. The most common cause is autoimmune adrenalitis, which accounts for about 70-80% of cases. It is more prevalent in women and typically occurs between the ages of 30 and 50.

The clinical symptoms of Addison’s disease include weakness, lethargy, low blood pressure (especially when standing up), nausea, vomiting, weight loss, reduced hair in the armpits and pubic area, depression, and hyperpigmentation (darkening of the skin in certain areas like the palms, mouth, and exposed skin).

Biochemically, Addison’s disease is characterized by increased levels of ACTH (a hormone that tries to stimulate the adrenal glands), low sodium levels, high potassium levels, high calcium levels, low blood sugar, and metabolic acidosis.

People with Addison’s disease have a higher risk of developing type 1 diabetes, Hashimoto’s thyroiditis, Grave’s disease, premature ovarian failure, pernicious anemia, vitiligo, and alopecia.

Management of Addison’s disease should be overseen by an Endocrinologist. Treatment typically involves taking hydrocortisone, fludrocortisone, and dehydroepiandrosterone. Some patients may also need thyroxine if there is hypothalamic-pituitary disease present. Treatment is lifelong, and patients should carry a steroid card and a MedicAlert bracelet in case of an Addisonian crisis.

In order to achieve satisfactory bronchodilation, most individuals require a plasma theophylline concentration of 10-20 mg/litre (55-110 micromol/litre). However, it is possible for a lower concentration to still be effective. Adverse effects can occur within the range of 10-20 mg/litre, and their frequency and severity increase when concentrations exceed 20 mg/litre.

To measure plasma theophylline concentration, a blood sample should be taken five days after starting oral treatment and at least three days after any dose adjustment. For modified-release preparations, the blood sample should typically be taken 4-6 hours after an oral dose (specific sampling times may vary, so it is advisable to consult local guidelines). If aminophylline is administered intravenously, a blood sample should be taken 4-6 hours after initiating treatment.

This presentation strongly suggests a diagnosis of whooping cough, which is an infection of the upper respiratory tract caused by the bacteria Bordetella pertussis. The disease is highly contagious and is transmitted through respiratory droplets. The incubation period is typically 7-21 days, and it is estimated that about 90% of close household contacts will become infected.

The clinical course of whooping cough can be divided into two stages. The first stage, known as the catarrhal stage, is similar to a mild respiratory infection with symptoms such as low-grade fever and a runny nose. A cough may be present, but it is usually mild compared to the second stage. This phase typically lasts about a week.

The second stage, called the paroxysmal stage, is characterized by the development of a distinctive cough. The coughing occurs in spasms, often preceded by an inspiratory whoop sound. These spasms are followed by a series of rapid, hacking coughs. Patients may experience vomiting and may develop subconjunctival hemorrhages and petechiae. Between spasms, patients generally feel well and there are usually no abnormal chest findings. This stage can last up to 3 months, with a gradual recovery over this period. The later stages of this phase are sometimes referred to as the convalescent stage.

Complications of whooping cough can include secondary pneumonia, rib fractures, pneumothorax, hernias, syncopal episodes, encephalopathy, and seizures.

Public Health England (PHE) provides recommendations for testing for whooping cough based on the age of the patient, time since onset of illness, and severity of presentation. For infants under 12 months of age, hospitalised patients should undergo PCR testing, while non-hospitalised patients within two weeks of onset should be tested using culture of a nasopharyngeal swab or aspirate. Non-hospitalised patients presenting over two weeks after onset should be investigated with serology for anti-pertussis toxin IgG antibody levels.

For children over 12 months of age and adults, patients within two weeks of onset should be tested using culture of a nasopharyngeal swab or aspirate. Patients aged 5 to 16 who have not received the vaccine within the last year and present over two weeks after onset should have oral fluid testing for anti-pertussis toxin IgG antibody levels.

Aminoglycosides have the ability to pass through the placenta and can lead to damage to the 8th cranial nerve in the fetus, resulting in permanent bilateral deafness.

ACE inhibitors, such as ramipril, can cause hypoperfusion, renal failure, and the oligohydramnios sequence if given in the 2nd and 3rd trimesters.

Aminoglycosides, like gentamicin, can cause ototoxicity and deafness in the fetus.

High doses of aspirin can lead to 1st trimester abortions, delayed onset labor, premature closure of the fetal ductus arteriosus, and fetal kernicterus. However, low doses (e.g. 75 mg) do not pose significant risks.

Benzodiazepines, including diazepam, when administered late in pregnancy, can result in respiratory depression and a neonatal withdrawal syndrome.

Calcium-channel blockers, if given in the 1st trimester, can cause phalangeal abnormalities. If given in the 2nd and 3rd trimesters, they can lead to fetal growth retardation.

Carbamazepine can cause hemorrhagic disease of the newborn and neural tube defects.

Chloramphenicol is associated with grey baby syndrome.

Corticosteroids, if given in the 1st trimester, may cause orofacial clefts.

Danazol, if given in the 1st trimester, can cause masculinization of the female fetuses genitals.

Finasteride should not be handled by pregnant women as crushed or broken tablets can be absorbed through the skin and affect male sex organ development.

Haloperidol, if given in the 1st trimester, may cause limb malformations. If given in the 3rd trimester, there is an increased risk of extrapyramidal symptoms in the neonate.

Heparin can lead to maternal bleeding and thrombocytopenia.

Isoniazid can cause maternal liver damage and neuropathy and seizures in the neonate.

Isotretinoin carries a high risk of teratogenicity, including multiple congenital malformations, spontaneous abortion, and intellectual disability.

Lithium, if given in the 1st trimester, poses a risk of fetal cardiac malformations.

Glanzmann’s thrombasthenia is an uncommon condition affecting platelets, where they have a deficiency or abnormality in glycoprotein IIb/IIIa. This disorder leads to platelet dysfunction and can result in various complications.

Conn’s syndrome, also known as primary hyperaldosteronism, is often characterized by hypertension along with hypokalaemia and hypernatraemia. On the other hand, Addison’s disease typically leads to hypotension, hyponatremia, and hyperkalaemia. Hyponatraemia is commonly associated with pituitary adenoma, while acute renal failure (ARF) is characterized by elevated levels of urea and creatinine, and hyperkalaemia is frequently observed in ARF.

Further Reading:

Hyperaldosteronism is a condition characterized by excessive production of aldosterone by the adrenal glands. It can be classified into primary and secondary hyperaldosteronism. Primary hyperaldosteronism, also known as Conn’s syndrome, is typically caused by adrenal hyperplasia or adrenal tumors. Secondary hyperaldosteronism, on the other hand, is a result of high renin levels in response to reduced blood flow across the juxtaglomerular apparatus.

Aldosterone is the main mineralocorticoid steroid hormone produced by the adrenal cortex. It acts on the distal renal tubule and collecting duct of the nephron, promoting the reabsorption of sodium ions and water while secreting potassium ions.

The causes of hyperaldosteronism vary depending on whether it is primary or secondary. Primary hyperaldosteronism can be caused by adrenal adenoma, adrenal hyperplasia, adrenal carcinoma, or familial hyperaldosteronism. Secondary hyperaldosteronism can be caused by renal artery stenosis, reninoma, renal tubular acidosis, nutcracker syndrome, ectopic tumors, massive ascites, left ventricular failure, or cor pulmonale.

Clinical features of hyperaldosteronism include hypertension, hypokalemia, metabolic alkalosis, hypernatremia, polyuria, polydipsia, headaches, lethargy, muscle weakness and spasms, and numbness. It is estimated that hyperaldosteronism is present in 5-10% of patients with hypertension, and hypertension in primary hyperaldosteronism is often resistant to drug treatment.

Diagnosis of hyperaldosteronism involves various investigations, including U&Es to assess electrolyte disturbances, aldosterone-to-renin plasma ratio (ARR) as the gold standard diagnostic test, ECG to detect arrhythmia, CT/MRI scans to locate adenoma, fludrocortisone suppression test or oral salt testing to confirm primary hyperaldosteronism, genetic testing to identify familial hyperaldosteronism, and adrenal venous sampling to determine lateralization prior to surgery.

Treatment of primary hyperaldosteronism typically involves surgical adrenalectomy for patients with unilateral primary aldosteronism. Diet modification with sodium restriction and potassium supplementation may also be recommended.

Fluoroquinolones are a rare but acknowledged cause of tendinopathy and spontaneous tendon rupture. It is estimated that tendon disorders related to fluoroquinolones occur in approximately 15 to 20 out of every 100,000 patients. These issues are most commonly observed in individuals who are over the age of 60.

The Achilles tendon is the most frequently affected, although cases involving other tendons such as the quadriceps, peroneus brevis, extensor pollicis longus, the long head of biceps brachii, and rotator cuff tendons have also been reported. The exact underlying mechanism is not fully understood, but it is believed that fluoroquinolone drugs may hinder collagen function and/or disrupt blood supply to the tendon.

There are other risk factors associated with spontaneous tendon rupture, including corticosteroid therapy, hypercholesterolemia, gout, rheumatoid arthritis, long-term dialysis, and renal transplantation.

This patient is highly likely to have developed a tubo-ovarian abscess (TOA), which is a complication of pelvic inflammatory disease. TOA occurs when a pocket of pus forms in the fallopian tube and/or ovary. If the abscess ruptures, it can lead to sepsis and become life-threatening.

The initial imaging modality of choice is transabdominal and endovaginal ultrasound. This imaging technique often reveals multilocular complex retro-uterine/adnexal masses with debris, septations, and irregular thick walls. These masses can be present on both sides.

Urgent hospital admission is necessary, and the usual management involves draining the abscess and administering intravenous antibiotics. The abscess drainage can be guided by ultrasound or CT scanning.

In some cases, laparotomy or laparoscopy may be required to drain the abscess.

Every year in the UK, 5,000 individuals lose their lives to suicide. Shockingly, only 25% of these individuals were known to receive specialized mental health services. The demographic with the highest suicide rates is men aged between 30 and 60, but there is a concerning increase in rates among teenagers aged 15 to 19.

It is crucial for doctors to be able to identify and provide support to patients who suffer from severe depression or other mental health issues, as they are at a higher risk of suicide. Certain factors significantly increase the risk of suicide, including a history of self-harm, previous mental illness, being male, experiencing severe depression, and substance abuse. It is important to note that combinations of these risk factors are more significant than individual factors alone.

Despite the belief that hospital admission provides a safe environment, the risk of suicide remains high for inpatients. Additionally, the risk remains elevated in the months following discharge from the hospital.

On the other hand, there are protective factors that decrease the likelihood of suicide. These include having dependent children, having family members who would be deeply affected by the loss, and having religious beliefs.

Haemothorax often leads to reduced or absent air entry, a dull percussion sound, and decreased fremitus on the affected side. Commonly observed symptoms in patients with haemothorax include decreased or absent air entry, a dull percussion note when the affected side is tapped, reduced fremitus on the affected side, and in cases of massive haemothorax, tracheal deviation away from the affected side. Other signs that may be present include a rapid heart rate (tachycardia), rapid breathing (tachypnoea), low blood pressure (hypotension), and signs of shock.

Further Reading:

Haemothorax is the accumulation of blood in the pleural cavity of the chest, usually resulting from chest trauma. It can be difficult to differentiate from other causes of pleural effusion on a chest X-ray. Massive haemothorax refers to a large volume of blood in the pleural space, which can impair physiological function by causing blood loss, reducing lung volume for gas exchange, and compressing thoracic structures such as the heart and IVC.

The management of haemothorax involves replacing lost blood volume and decompressing the chest. This is done through supplemental oxygen, IV access and cross-matching blood, IV fluid therapy, and the insertion of a chest tube. The chest tube is connected to an underwater seal and helps drain the fluid, pus, air, or blood from the pleural space. In cases where there is prompt drainage of a large amount of blood, ongoing significant blood loss, or the need for blood transfusion, thoracotomy and ligation of bleeding thoracic vessels may be necessary. It is important to have two IV accesses prior to inserting the chest drain to prevent a drop in blood pressure.

In summary, haemothorax is the accumulation of blood in the pleural cavity due to chest trauma. Managing haemothorax involves replacing lost blood volume and decompressing the chest through various interventions, including the insertion of a chest tube. Prompt intervention may be required in cases of significant blood loss or ongoing need for blood transfusion.