De Quervain’s tenosynovitis is a condition characterized by inflammation of the synovium surrounding a tendon. Specifically, it affects the tendon sheath that encloses two adjacent tendons – the extensor pollicis brevis and abductor pollicis longus – responsible for extending and abducting the thumb. It is important to note that De Quervain’s syndrome only affects these two tendons and not the extensor pollicis longus or any flexors. Additionally, the adductor pollicis muscle is not involved in this condition. Tenderness over the first dorsal compartment is a common sign of De Quervain’s tenosynovitis, as the affected tendons do not travel underneath it.

De Quervain’s Tenosynovitis: Symptoms, Diagnosis, and Treatment

De Quervain’s tenosynovitis is a condition that commonly affects women between the ages of 30 and 50. It occurs when the sheath containing the tendons of the extensor pollicis brevis and abductor pollicis longus becomes inflamed. The condition is characterized by pain on the radial side of the wrist, tenderness over the radial styloid process, and pain when the thumb is abducted against resistance. A positive Finkelstein’s test, in which pain is elicited by ulnar deviation and longitudinal traction of the thumb, is also indicative of the condition.

Treatment for De Quervain’s tenosynovitis typically involves analgesia, steroid injections, and immobilization with a thumb splint (spica). In some cases, surgical intervention may be necessary. With proper diagnosis and treatment, patients can experience relief from the pain and discomfort associated with this condition.

The patient’s symptoms are consistent with acute closed-angle glaucoma, which is an urgent ophthalmological emergency. They are experiencing a headache with unilateral eye pain, reduced vision, visual haloes, a red and congested eye with a cloudy cornea, and a dilated, unresponsive pupil. These symptoms may be triggered by darkness or dilating eye drops. Treatment should involve laying the patient flat to relieve angle pressure, administering pilocarpine eye drops to constrict the pupil, acetazolamide orally to reduce aqueous humour production, and providing analgesia. Referral to secondary care is necessary.

It is important to differentiate this condition from other potential causes of the patient’s symptoms. Central retinal vein occlusion, for example, would cause sudden painless loss of vision and severe retinal haemorrhages on fundoscopy. Migraines typically involve a visual or somatosensory aura followed by a unilateral throbbing headache, nausea, vomiting, and photophobia. Subarachnoid haemorrhages present with a sudden, severe headache, rather than a gradually worsening one accompanied by eye signs. Temporal arteritis may cause pain when chewing, difficulty brushing hair, and thickened temporal arteries visible on examination. However, the presence of a dilated, fixed pupil with conjunctival injection should steer the clinician away from a diagnosis of migraine.

Acute angle closure glaucoma (AACG) is a type of glaucoma where there is a rise in intraocular pressure (IOP) due to a blockage in the outflow of aqueous humor. This condition is more likely to occur in individuals with hypermetropia, pupillary dilation, and lens growth associated with aging. Symptoms of AACG include severe pain, decreased visual acuity, a hard and red eye, haloes around lights, and a semi-dilated non-reacting pupil. AACG is an emergency and requires urgent referral to an ophthalmologist. The initial medical treatment involves a combination of eye drops, such as a direct parasympathomimetic, a beta-blocker, and an alpha-2 agonist, as well as intravenous acetazolamide to reduce aqueous secretions. Definitive management involves laser peripheral iridotomy, which creates a tiny hole in the peripheral iris to allow aqueous humor to flow to the angle.

Enzymes play a crucial role in the breakdown of carbohydrates in the gastrointestinal system. Amylase, which is present in both saliva and pancreatic secretions, is responsible for breaking down starch into sugar. On the other hand, brush border enzymes such as maltase, sucrase, and lactase are involved in the breakdown of specific disaccharides. Maltase cleaves maltose into glucose and glucose, sucrase cleaves sucrose into fructose and glucose, while lactase cleaves lactose into glucose and galactose. These enzymes work together to ensure that carbohydrates are broken down into their simplest form for absorption into the bloodstream.

The larynx is located in the front of the neck, specifically at the level of the vertebrae C3-C6. This area also includes important anatomical landmarks such as the Atlas and Axis vertebrae (C1-C2), the thyroid cartilage (C5), and the pulmonary hilum (T5-T7).

Anatomy of the Larynx

The larynx is located in the front of the neck, between the third and sixth cervical vertebrae. It is made up of several cartilaginous segments, including the paired arytenoid, corniculate, and cuneiform cartilages, as well as the single thyroid, cricoid, and epiglottic cartilages. The cricoid cartilage forms a complete ring. The laryngeal cavity extends from the laryngeal inlet to the inferior border of the cricoid cartilage and is divided into three parts: the laryngeal vestibule, the laryngeal ventricle, and the infraglottic cavity.

The vocal folds, also known as the true vocal cords, control sound production. They consist of the vocal ligament and the vocalis muscle, which is the most medial part of the thyroarytenoid muscle. The glottis is composed of the vocal folds, processes, and rima glottidis, which is the narrowest potential site within the larynx.

The larynx is also home to several muscles, including the posterior cricoarytenoid, lateral cricoarytenoid, thyroarytenoid, transverse and oblique arytenoids, vocalis, and cricothyroid muscles. These muscles are responsible for various actions, such as abducting or adducting the vocal folds and relaxing or tensing the vocal ligament.

The larynx receives its arterial supply from the laryngeal arteries, which are branches of the superior and inferior thyroid arteries. Venous drainage is via the superior and inferior laryngeal veins. Lymphatic drainage varies depending on the location within the larynx, with the vocal cords having no lymphatic drainage and the supraglottic and subglottic parts draining into different lymph nodes.

Overall, understanding the anatomy of the larynx is important for proper diagnosis and treatment of various conditions affecting this structure.

Beta-blockers have an added advantage in treating hypertension as they can suppress the release of renin from the kidneys. This is because the release of renin is partly regulated by β1-adrenoceptors in the kidney, which are inhibited by beta-blockers. By reducing the amount of circulating plasma renin, the levels of angiotensin II and aldosterone decrease, leading to increased renal loss of sodium and water, ultimately lowering arterial pressure.

It is important to note that atenolol does not compete with aldosterone, unlike spironolactone, a potassium-sparing diuretic that does compete with aldosterone for its receptor. Additionally, atenolol does not inhibit the conversion of ATI to ATII, which is achieved by ACE-inhibitors like ramipril.

While both beta-1 and beta-2 receptors are present in the heart, atenolol primarily acts on beta-1 receptors, resulting in negative inotropic, negative chronotropic, and positive lusitropic effects. Lusitropy refers to the relaxation of the heart.

Therefore, the statement that atenolol inhibits the release of renin is correct, and the fifth option is incorrect.

Beta-blockers are a class of drugs that are primarily used to manage cardiovascular disorders. They have a wide range of indications, including angina, post-myocardial infarction, heart failure, arrhythmias, hypertension, thyrotoxicosis, migraine prophylaxis, and anxiety. Beta-blockers were previously avoided in heart failure, but recent evidence suggests that certain beta-blockers can improve both symptoms and mortality. They have also replaced digoxin as the rate-control drug of choice in atrial fibrillation. However, their role in reducing stroke and myocardial infarction has diminished in recent years due to a lack of evidence.

Examples of beta-blockers include atenolol and propranolol, which was one of the first beta-blockers to be developed. Propranolol is lipid-soluble, which means it can cross the blood-brain barrier.

Like all drugs, beta-blockers have side-effects. These can include bronchospasm, cold peripheries, fatigue, sleep disturbances (including nightmares), and erectile dysfunction. There are also some contraindications to using beta-blockers, such as uncontrolled heart failure, asthma, sick sinus syndrome, and concurrent use with verapamil, which can precipitate severe bradycardia.

Tardive dyskinesia is a condition that can occur as a result of long-term use of antipsychotic drugs, which is likely in this patient due to his history of mental illness. It is believed that blocking the dopamine receptor can cause hypersensitivity of the D2 receptor in the nigrostriatal pathway, leading to excessive movements.

It should be noted that antiemetic medications that use dopamine antagonism in the chemoreceptor trigger zone are more likely to cause acute dystonias rather than tardive dyskinesia. Additionally, degeneration of dopaminergic neurons in the substantia nigra is associated with Parkinson’s disease and would not produce these symptoms. Abrupt withdrawal of dopaminergic agents is also not expected to result in tardive dyskinesia. Finally, carbidopa inhibits the conversion of L-DOPA into dopamine and does not cause tardive dyskinesia.

Antipsychotics are a type of medication used to treat schizophrenia, psychosis, mania, and agitation. They are divided into two categories: typical and atypical antipsychotics. The latter were developed to address the extrapyramidal side-effects associated with the first generation of typical antipsychotics. Typical antipsychotics work by blocking dopaminergic transmission in the mesolimbic pathways through dopamine D2 receptor antagonism. However, they are known to cause extrapyramidal side-effects such as Parkinsonism, acute dystonia, akathisia, and tardive dyskinesia. These side-effects can be managed with procyclidine. Other side-effects of typical antipsychotics include antimuscarinic effects, sedation, weight gain, raised prolactin, impaired glucose tolerance, neuroleptic malignant syndrome, reduced seizure threshold, and prolonged QT interval. The Medicines and Healthcare products Regulatory Agency has issued specific warnings when antipsychotics are used in elderly patients due to an increased risk of stroke and venous thromboembolism.

Hyperglycemia is the correct answer. Most patients who take steroids experience an increase in appetite and weight gain, so anorexia or weight loss are not appropriate responses.

Steroid hormones can also affect the aldosterone receptor in the collecting duct, potentially leading to hyponatremia.

Although changes in vision are possible due to steroid-induced cataracts, they are much less common.

High levels of non-endogenous steroids have several risk factors, including hyperglycemia, high blood pressure, obesity (particularly around the waist), muscle wasting, poor wound healing, and mood swings or depression.

Corticosteroids are commonly prescribed medications that can be taken orally or intravenously, or applied topically. They mimic the effects of natural steroids in the body and can be used to replace or supplement them. However, the use of corticosteroids is limited by their numerous side effects, which are more common with prolonged and systemic use. These side effects can affect various systems in the body, including the endocrine, musculoskeletal, gastrointestinal, ophthalmic, and psychiatric systems. Some of the most common side effects include impaired glucose regulation, weight gain, osteoporosis, and increased susceptibility to infections. Patients on long-term corticosteroids should have their doses adjusted during intercurrent illness, and the medication should not be abruptly withdrawn to avoid an Addisonian crisis. Gradual withdrawal is recommended for patients who have received high doses or prolonged treatment.

The prothrombin time (PT) is used to assess the extrinsic pathway of the clotting cascade, while the activated partial thromboplastin time (aPTT) is used to assess the intrinsic pathway. The thrombin time is used to assess fibrin formation. A 50:50 mixing study is used to determine if a prolonged PT or aPTT is due to factor deficiency or a factor inhibitor.

The Coagulation Cascade: Two Pathways to Fibrin Formation

The coagulation cascade is a complex process that leads to the formation of a blood clot. There are two pathways that can lead to fibrin formation: the intrinsic pathway and the extrinsic pathway. The intrinsic pathway involves components that are already present in the blood and has a minor role in clotting. It is initiated by subendothelial damage, such as collagen, which leads to the formation of the primary complex on collagen by high-molecular-weight kininogen (HMWK), prekallikrein, and Factor 12. This complex activates Factor 11, which in turn activates Factor 9. Factor 9, along with its co-factor Factor 8a, forms the tenase complex, which activates Factor 10.

The extrinsic pathway, on the other hand, requires tissue factor released by damaged tissue. This pathway is initiated by tissue damage, which leads to the binding of Factor 7 to tissue factor. This complex activates Factor 9, which works with Factor 8 to activate Factor 10. Both pathways converge at the common pathway, where activated Factor 10 causes the conversion of prothrombin to thrombin. Thrombin hydrolyses fibrinogen peptide bonds to form fibrin and also activates factor 8 to form links between fibrin molecules.

Finally, fibrinolysis occurs, which is the process of clot resorption. Plasminogen is converted to plasmin to facilitate this process. It is important to note that certain factors are involved in both pathways, such as Factor 10, and that some factors are vitamin K dependent, such as Factors 2, 7, 9, and 10. The intrinsic pathway can be assessed by measuring the activated partial thromboplastin time (APTT), while the extrinsic pathway can be assessed by measuring the prothrombin time (PT).

The endocrine system is primarily regulated by the pituitary gland, which is itself controlled by the hypothalamus. The neurohypophysis is influenced by the hypothalamus because its cell bodies are located within the hypothalamus, while the adenohypophysis is regulated by neuroendocrine cells in the hypothalamus that release trophic hormones into the pituitary portal vessels. The pituitary gland subsequently secretes various hormones that impact different parts of the body.

The pituitary gland is a small gland located within the sella turcica in the sphenoid bone of the middle cranial fossa. It weighs approximately 0.5g and is covered by a dural fold. The gland is attached to the hypothalamus by the infundibulum and receives hormonal stimuli from the hypothalamus through the hypothalamo-pituitary portal system. The anterior pituitary, which develops from a depression in the wall of the pharynx known as Rathkes pouch, secretes hormones such as ACTH, TSH, FSH, LH, GH, and prolactin. GH and prolactin are secreted by acidophilic cells, while ACTH, TSH, FSH, and LH are secreted by basophilic cells. On the other hand, the posterior pituitary, which is derived from neuroectoderm, secretes ADH and oxytocin. Both hormones are produced in the hypothalamus before being transported by the hypothalamo-hypophyseal portal system.

Autonomic dysreflexia is a condition that occurs in patients who have suffered a spinal cord injury at or above the T6 spinal level. It is caused by a reflex response triggered by various stimuli, such as faecal impaction or urinary retention, which sends signals through the thoracolumbar outflow. However, due to the spinal cord lesion, the usual parasympathetic response is prevented, leading to an unbalanced physiological response. This response is characterized by extreme hypertension, flushing, and sweating above the level of the cord lesion, as well as agitation. If left untreated, severe consequences such as haemorrhagic stroke can occur. The management of autonomic dysreflexia involves removing or controlling the stimulus and treating any life-threatening hypertension and/or bradycardia.