Urinary tract infections (UTIs) are common in adults and can affect different parts of the urinary tract. Lower UTIs are more common and can be managed with antibiotics. For non-pregnant women, local antibiotic guidelines should be followed, and a urine culture should be sent if they are aged over 65 years or have visible or non-visible haematuria. Trimethoprim or nitrofurantoin for three days are recommended by NICE Clinical Knowledge Summaries. Pregnant women with symptoms should have a urine culture sent, and first-line treatment is nitrofurantoin, while amoxicillin or cefalexin can be used as second-line treatment. Asymptomatic bacteriuria in pregnant women should also be treated with antibiotics. Men with UTIs should be offered antibiotics for seven days, and a urine culture should be sent before starting treatment. Catheterised patients should not be treated for asymptomatic bacteria, but if they are symptomatic, a seven-day course of antibiotics should be given, and the catheter should be removed or changed if it has been in place for more than seven days. For patients with signs of acute pyelonephritis, hospital admission should be considered, and local antibiotic guidelines should be followed. The BNF recommends a broad-spectrum cephalosporin or a quinolone for 10-14 days for non-pregnant women.

The patient’s symptoms were indicative of a psychiatric condition associated with somatic symptom disorders, rather than a manifestation of hypochondria or cancer.

Unexplained Symptoms in Psychiatry

In psychiatry, there are several terms used to describe patients who present with physical or psychological symptoms for which no organic cause can be found. Somatisation disorder is characterized by the presence of multiple physical symptoms that persist for at least two years, and the patient refuses to accept reassurance or negative test results. Illness anxiety disorder, also known as hypochondriasis, involves a persistent belief in the presence of an underlying serious disease, such as cancer, despite negative test results. Conversion disorder typically involves the loss of motor or sensory function, and the patient does not consciously feign the symptoms or seek material gain. Dissociative disorder involves the process of separating off certain memories from normal consciousness, and may present with psychiatric symptoms such as amnesia, fugue, or stupor. Factitious disorder, also known as Munchausen’s syndrome, involves the intentional production of physical or psychological symptoms, while malingering refers to the fraudulent simulation or exaggeration of symptoms for financial or other gain. These terms help clinicians to better understand and diagnose patients with unexplained symptoms.

The Process of Energy Production from Glucose in the Human Body

The breakdown of fuel molecules, particularly glucose, is a crucial process in the human body. While fat and protein can also be used for fuel, glucose has the simplest method of metabolism. For this process to occur, nutrients from the diet must be absorbed and distributed to individual cells. Most cells in the body have the necessary machinery for producing ATP from glucose.

The process of producing energy from glucose involves three main steps. First, glycolysis occurs, where the 6-carbon glucose molecule is split into two 3-carbon particles. Next, the Kreb cycle, also known as the tricarboxylic acid cycle, modifies 3-carbon containing acids in a series of steps to produce NADH. Finally, the electron transfer chain takes place inside mitochondria, where the NADH generated during the Kreb cycle is used to produce energy in the form of ATP through a series of redox reactions.

In summary, the process of energy production from glucose is a fundamental process in the human body. It involves the breakdown of glucose into smaller particles, modification of these particles to produce NADH, and the use of NADH to produce ATP through a series of redox reactions.

Functions of the Liver in Regulating Blood Composition

The liver plays a crucial role in regulating the composition of blood to maintain appropriate levels of solutes, toxins, and drugs. It achieves this through various metabolic reactions, including removing excess solutes, synthesizing deficient solutes, and storing solutes for later use. One of the liver’s essential functions is to maintain blood glucose levels by storing excess glucose as glycogen after a meal and releasing it back into the bloodstream as glucose during fasting. Additionally, the liver can produce glucose through gluconeogenesis using other substances such as fat, protein, or other sugars.

The liver also processes nitrogenous waste from protein catabolism by converting ammonium from amino acids to urea, which is less toxic and can be excreted by the kidneys. Another critical function of the liver is producing bilirubin from haem in red blood cells, which is then processed to make bile exclusively in the liver. The liver also produces various plasma proteins, including albumin, hormones, cytokines, and C-reactive protein, but not immunoglobulins, which are made by plasma cells. Overall, the liver’s functions are vital in maintaining the body’s homeostasis and ensuring proper blood composition.

Based on her symptoms, positive Schirmer’s test, and family history of autoimmune conditions, it can be concluded that she is suffering from Sjogren’s syndrome. This condition is linked to various other medical conditions, most of which are autoimmune or rheumatic disorders, including coeliac disease, fibromyalgia, lupus, multiple sclerosis, spondyloarthropathy, and certain types of cancer like non-Hodgkin lymphoma. However, there is no known association between Sjogren’s syndrome and atrial fibrillation, hyperparathyroidism, Conn’s syndrome, or osteoarthritis.

Understanding Sjogren’s Syndrome

Sjogren’s syndrome is a medical condition that affects the exocrine glands, leading to dry mucosal surfaces. It can either be primary or secondary to other connective tissue disorders, such as rheumatoid arthritis. The condition is more common in females, with a ratio of 9:1. Patients with Sjogren’s syndrome have a higher risk of developing lymphoid malignancy, which is 40-60 times more likely than the general population.

The symptoms of Sjogren’s syndrome include dry eyes, dry mouth, vaginal dryness, arthralgia, Raynaud’s, myalgia, sensory polyneuropathy, recurrent episodes of parotitis, and subclinical renal tubular acidosis. To diagnose the condition, doctors may perform a Schirmer’s test to measure tear formation, as well as check for the presence of rheumatoid factor, ANA, anti-Ro (SSA) antibodies, and anti-La (SSB) antibodies.

Management of Sjogren’s syndrome involves the use of artificial saliva and tears, as well as medications like pilocarpine to stimulate saliva production. It is important for patients with Sjogren’s syndrome to receive regular medical care and monitoring to manage their symptoms and reduce the risk of complications.

Ziehl-Neelsen stain is used for mycobacteria, not Gram staining. Van Gieson and Masson trichrome are for connective tissues, while Von Kossa identifies tissue mineralisation.

Understanding Tuberculosis: The Pathophysiology and Risk Factors

Tuberculosis is a bacterial infection caused by Mycobacterium tuberculosis. The pathophysiology of tuberculosis involves the migration of macrophages to regional lymph nodes, forming a Ghon complex. This complex leads to the formation of a granuloma, which is a collection of epithelioid histiocytes with caseous necrosis in the center. The inflammatory response is mediated by a type 4 hypersensitivity reaction. While healthy individuals can contain the disease, immunocompromised individuals are at risk of developing disseminated (miliary) TB.

Several risk factors increase the likelihood of developing tuberculosis. These include having lived in Asia, Latin America, Eastern Europe, or Africa for years, exposure to an infectious TB case, and being infected with HIV. Immunocompromised individuals, such as diabetics, patients on immunosuppressive therapy, malnourished individuals, or those with haematological malignancies, are also at risk. Additionally, silicosis and apical fibrosis increase the likelihood of developing tuberculosis. Understanding the pathophysiology and risk factors of tuberculosis is crucial in preventing and treating this infectious disease.

The correct diagnosis for this patient is Klumpke paralysis, which is often caused by shoulder dystocia during birth or traction injuries. The patient presents with a claw-like deformity in their hand, indicating damage to the C8 and T1 branches of the brachial plexus. This condition is also associated with Horner’s syndrome, which the patient is experiencing.

Bell’s palsy, C8 radiculopathy, and Erb-Duchenne paralysis are all incorrect diagnoses for this patient. Bell’s palsy only affects the facial nerve and would not cause the other symptoms seen in this patient. C8 radiculopathy would not result in the claw-like deformity or T1 dermatome involvement. Erb-Duchenne paralysis affects a different part of the brachial plexus and presents differently from this patient’s symptoms.

Horner’s syndrome is a condition characterized by several features, including a small pupil (miosis), drooping of the upper eyelid (ptosis), a sunken eye (enophthalmos), and loss of sweating on one side of the face (anhidrosis). The cause of Horner’s syndrome can be determined by examining additional symptoms. For example, congenital Horner’s syndrome may be identified by a difference in iris color (heterochromia), while anhidrosis may be present in central or preganglionic lesions. Pharmacologic tests, such as the use of apraclonidine drops, can also be helpful in confirming the diagnosis and identifying the location of the lesion. Central lesions may be caused by conditions such as stroke or multiple sclerosis, while postganglionic lesions may be due to factors like carotid artery dissection or cluster headaches. It is important to note that the appearance of enophthalmos in Horner’s syndrome is actually due to a narrow palpebral aperture rather than true enophthalmos.

The thoracoacromial artery originates from the axillary artery’s second part. It is a broad, brief trunk that penetrates the clavipectoral fascia and terminates by dividing into four branches, located deep to pectoralis major.

The Thoracoacromial Artery and its Branches

The thoracoacromial artery is a short trunk that originates from the axillary artery and is usually covered by the upper edge of the Pectoralis minor. It projects forward to the upper border of the Pectoralis minor and pierces the coracoclavicular fascia, dividing into four branches: pectoral, acromial, clavicular, and deltoid.

The pectoral branch descends between the two Pectoral muscles and supplies them and the breast, anastomosing with the intercostal branches of the internal thoracic artery and the lateral thoracic artery. The acromial branch runs laterally over the coracoid process and under the Deltoid, giving branches to it before piercing the muscle and ending on the acromion in an arterial network formed by branches from the suprascapular, thoracoacromial, and posterior humeral circumflex arteries. The clavicular branch runs upwards and medially to the sternoclavicular joint, supplying this articulation and the Subclavius. The deltoid branch arises with the acromial branch, crosses over the Pectoralis minor, and passes in the same groove as the cephalic vein, giving branches to both the Pectoralis major and Deltoid muscles.

The antecubital fossa is where the brachial artery and median nerve are located in close proximity. Surgeons typically access the brachial artery in this area for embolectomy procedures. However, care must be taken to avoid damaging the median nerve when applying vascular clamps to the artery.

Anatomy of the Brachial Artery

The brachial artery is a continuation of the axillary artery and runs from the lower border of teres major to the cubital fossa where it divides into the radial and ulnar arteries. It is located in the upper arm and has various relations with surrounding structures. Posteriorly, it is related to the long head of triceps with the radial nerve and profunda vessels in between. Anteriorly, it is overlapped by the medial border of biceps. The median nerve crosses the artery in the middle of the arm. In the cubital fossa, the brachial artery is separated from the median cubital vein by the bicipital aponeurosis. The basilic vein is in contact with the most proximal aspect of the cubital fossa and lies medially. Understanding the anatomy of the brachial artery is important for medical professionals when performing procedures such as blood pressure measurement or arterial line placement.

The medial longitudinal fasciculus is located in the midbrain and pons and is responsible for conjugate gaze. Lesions in this area can cause internuclear ophthalmoplegia, which affects adduction but not convergence. A 3rd nerve palsy affects multiple muscles and can involve the pupil, while abducens nerve lesions affect abduction. Lesions in the midbrain and superior pons contain the centres of vision.

Understanding Internuclear Ophthalmoplegia

Internuclear ophthalmoplegia is a condition that affects the horizontal movement of the eyes. It is caused by a lesion in the medial longitudinal fasciculus (MLF), which is responsible for interconnecting the IIIrd, IVth, and VIth cranial nuclei. This area is located in the paramedian region of the midbrain and pons. The main feature of this condition is impaired adduction of the eye on the same side as the lesion, along with horizontal nystagmus of the abducting eye on the opposite side.

The most common causes of internuclear ophthalmoplegia are multiple sclerosis and vascular disease. It is important to note that this condition can also be a sign of other underlying neurological disorders.

Carpal Tunnel Syndrome and Median Nerve Innervation

Carpal tunnel syndrome is a condition that can cause weakness in the abductor pollicis brevis muscle, which is innervated by the median nerve. This muscle, along with the opponens pollicis, is controlled by the median nerve. The flexor pollicis brevis muscle may also be innervated by either the median or ulnar nerve. In this case, the symptoms suggest carpal tunnel syndrome, which is often associated with acromegaly. Early intervention is crucial in treating carpal tunnel syndrome, as permanent nerve damage can occur if decompression is delayed.

Prognostic Factors in Acute Myeloid Leukemia

Acute myeloid leukemia (AML) is a type of cancer that affects the blood and bone marrow. The APML subtype of AML has a higher five-year survival rate of 70% compared to the average rate of 25%. However, it is a medical emergency upon presentation due to the risk of coagulopathy, tumor lysis, and life-threatening infections. Urgent treatment with ATRA chemotherapy is necessary. Younger patients tend to have a better prognosis and can tolerate intensive chemotherapy better. Certain cytogenetic changes, such as t(15;17) in APML and t(8;21) and inv(16), are associated with a favorable prognosis. However, complex cytogenetics are not. A performance status of 3, which indicates that an individual spends more than 50% of the day in bed, is not ideal for intensive chemotherapy. AML that arises from a pre-existing condition, such as a myeloproliferative neoplasm, has a worse prognosis than AML that arises de novo.

Overall, the prognostic factors in AML is crucial for determining the appropriate treatment plan and predicting outcomes.

The rectum can produce potassium-rich secretions, which is why resins are given to treat hyperkalemia and why patients with villous adenoma of the rectum may experience hypokalemia.

Potassium Secretions in the GI Tract

Potassium is secreted in various parts of the gastrointestinal (GI) tract. The salivary glands can secrete up to 60mmol/L of potassium, while the stomach secretes only 10 mmol/L. The bile, pancreas, and small bowel also secrete potassium, with average figures of 5 mmol/L, 4-5 mmol/L, and 10 mmol/L, respectively. The rectum has the highest potassium secretion, with an average of 30 mmol/L. However, the exact composition of potassium secretions varies depending on factors such as disease, serum aldosterone levels, and serum pH.

It is important to note that gastric potassium secretions are low, and hypokalaemia (low potassium levels) may occur in vomiting. However, this is usually due to renal wasting of potassium rather than potassium loss in vomit. Understanding the different levels of potassium secretion in the GI tract can be helpful in diagnosing and treating potassium-related disorders.

Understanding Parathyroid Hormone and Its Effects

Parathyroid hormone is a hormone produced by the chief cells of the parathyroid glands. Its main function is to increase the concentration of calcium in the blood by stimulating the PTH receptors in the kidney and bone. This hormone has a short half-life of only 4 minutes.

The effects of parathyroid hormone are mainly seen in the bone, kidney, and intestine. In the bone, PTH binds to osteoblasts, which then signal to osteoclasts to resorb bone and release calcium. In the kidney, PTH promotes the active reabsorption of calcium and magnesium from the distal convoluted tubule, while decreasing the reabsorption of phosphate. In the intestine, PTH indirectly increases calcium absorption by increasing the activation of vitamin D, which in turn increases calcium absorption.

Overall, understanding the role of parathyroid hormone is important in maintaining proper calcium levels in the body. Any imbalances in PTH secretion can lead to various disorders such as hyperparathyroidism or hypoparathyroidism.

The Transpyloric Plane and its Anatomical Landmarks

The transpyloric plane is an imaginary horizontal line that passes through the body of the first lumbar vertebrae (L1) and the pylorus of the stomach. It is an important anatomical landmark used in clinical practice to locate various organs and structures in the abdomen.

Some of the structures that lie on the transpyloric plane include the left and right kidney hilum (with the left one being at the same level as L1), the fundus of the gallbladder, the neck of the pancreas, the duodenojejunal flexure, the superior mesenteric artery, and the portal vein. The left and right colic flexure, the root of the transverse mesocolon, and the second part of the duodenum also lie on this plane.

In addition, the upper part of the conus medullaris (the tapered end of the spinal cord) and the spleen are also located on the transpyloric plane. Knowing the location of these structures is important for various medical procedures, such as abdominal surgeries and diagnostic imaging.

Overall, the transpyloric plane serves as a useful reference point for clinicians to locate important anatomical structures in the abdomen.

Gynaecomastia can be caused by testicular cancer, specifically seminoma that secretes beta-HCG. This hormone acts as a tumour marker for testicular germ cell cancer and increases oestrogen levels, leading to an imbalance of oestrogen to androgen ratio. This imbalance promotes the growth of breast tissue, resulting in gynaecomastia.

Alpha-fetoprotein is another tumour marker for testicular cancer, but it does not affect oestrogen levels or breast glandular tissue. It is important to note that gynaecomastia is a separate condition from metastatic testicular cancer in the breast.

Testicular involution, or shrinkage of the testes, is not a common symptom of testicular cancer. Instead, patients typically present with a painless swelling or nodule in the testis.

Elevated testosterone levels are not associated with testicular cancer, as they would prevent the growth of breast tissue and gynaecomastia.

Understanding Gynaecomastia: Causes and Drug Triggers

Gynaecomastia is a condition characterized by the abnormal growth of breast tissue in males, often caused by an increased ratio of oestrogen to androgen. It is important to distinguish the causes of gynaecomastia from those of galactorrhoea, which is caused by the actions of prolactin on breast tissue.

Physiological changes during puberty can lead to gynaecomastia, but it can also be caused by syndromes with androgen deficiency such as Kallmann and Klinefelter’s, testicular failure due to mumps, liver disease, testicular cancer, and hyperthyroidism. Additionally, haemodialysis and ectopic tumour secretion can also trigger gynaecomastia.

Drug-induced gynaecomastia is also a common cause, with spironolactone being the most frequent trigger. Other drugs that can cause gynaecomastia include cimetidine, digoxin, cannabis, finasteride, GnRH agonists like goserelin and buserelin, oestrogens, and anabolic steroids. However, it is important to note that very rare drug causes of gynaecomastia include tricyclics, isoniazid, calcium channel blockers, heroin, busulfan, and methyldopa.

In summary, understanding the causes and drug triggers of gynaecomastia is crucial in diagnosing and treating this condition.

The trachea divides into two branches at the fifth thoracic vertebrae, or sometimes the sixth in individuals who are tall.

Anatomy of the Trachea

The trachea, also known as the windpipe, is a tube-like structure that extends from the C6 vertebrae to the upper border of the T5 vertebrae where it bifurcates into the left and right bronchi. It is supplied by the inferior thyroid arteries and the thyroid venous plexus, and innervated by branches of the vagus, sympathetic, and recurrent nerves.

In the neck, the trachea is anterior to the isthmus of the thyroid gland, inferior thyroid veins, and anastomosing branches between the anterior jugular veins. It is also surrounded by the sternothyroid, sternohyoid, and cervical fascia. Posteriorly, it is related to the esophagus, while laterally, it is in close proximity to the common carotid arteries, right and left lobes of the thyroid gland, inferior thyroid arteries, and recurrent laryngeal nerves.

In the thorax, the trachea is anterior to the manubrium, the remains of the thymus, the aortic arch, left common carotid arteries, and the deep cardiac plexus. Laterally, it is related to the pleura and right vagus on the right side, and the left recurrent nerve, aortic arch, and left common carotid and subclavian arteries on the left side.

Overall, understanding the anatomy of the trachea is important for various medical procedures and interventions, such as intubation and tracheostomy.

The inferior mesenteric artery is responsible for supplying blood to the hindgut, which includes the distal third of the colon and the rectum superior to the pectinate line. In this case, the patient’s sudden onset of severe abdominal pain and history of atrial fibrillation suggest acute mesenteric ischemia, with the affected artery being the inferior mesenteric artery. Therefore, if a thrombus were to block this artery, the distal third of the colon and superior rectum would experience ischaemic changes. It is important to note that the ascending colon, caecum, ileum, appendix, greater omentum, and stomach are supplied by different arteries and would not be affected by a thrombus in the inferior mesenteric artery.

The Inferior Mesenteric Artery: Supplying the Hindgut

The inferior mesenteric artery (IMA) is responsible for supplying the embryonic hindgut with blood. It originates just above the aortic bifurcation, at the level of L3, and passes across the front of the aorta before settling on its left side. At the point where the left common iliac artery is located, the IMA becomes the superior rectal artery.

The hindgut, which includes the distal third of the colon and the rectum above the pectinate line, is supplied by the IMA. The left colic artery is one of the branches that emerges from the IMA near its origin. Up to three sigmoid arteries may also exit the IMA to supply the sigmoid colon further down the line.

Overall, the IMA plays a crucial role in ensuring that the hindgut receives the blood supply it needs to function properly. Its branches help to ensure that the colon and rectum are well-nourished and able to carry out their important digestive functions.

Even if there are nerve lesions located proximally, complete loss of triceps muscle function may not occur as the axillary nerve can innervate the long head of the triceps muscle.

The Radial Nerve: Anatomy, Innervation, and Patterns of Damage

The radial nerve is a continuation of the posterior cord of the brachial plexus, with root values ranging from C5 to T1. It travels through the axilla, posterior to the axillary artery, and enters the arm between the brachial artery and the long head of triceps. From there, it spirals around the posterior surface of the humerus in the groove for the radial nerve before piercing the intermuscular septum and descending in front of the lateral epicondyle. At the lateral epicondyle, it divides into a superficial and deep terminal branch, with the deep branch crossing the supinator to become the posterior interosseous nerve.

The radial nerve innervates several muscles, including triceps, anconeus, brachioradialis, and extensor carpi radialis. The posterior interosseous branch innervates supinator, extensor carpi ulnaris, extensor digitorum, and other muscles. Denervation of these muscles can lead to weakness or paralysis, with effects ranging from minor effects on shoulder stability to loss of elbow extension and weakening of supination of prone hand and elbow flexion in mid prone position.

Damage to the radial nerve can result in wrist drop and sensory loss to a small area between the dorsal aspect of the 1st and 2nd metacarpals. Axillary damage can also cause paralysis of triceps. Understanding the anatomy, innervation, and patterns of damage of the radial nerve is important for diagnosing and treating conditions that affect this nerve.

The most likely mode of transmission for measles is through aerosols. The woman’s symptoms and subsequent rash near the hairline indicate a measles infection, which is highly contagious and can be spread through the air when an infected person coughs or sneezes. While contaminated surfaces may also transmit the virus, it is not the primary mode of transmission. Measles is not transmitted through the faecal-oral route or intravenously, as it is found in the nose and throat of an infected person and not in their faeces or blood.

Measles: A Highly Infectious Disease

Measles is a viral infection caused by an RNA paramyxovirus. It is one of the most infectious viruses known and is spread through aerosol transmission. The incubation period is 10-14 days, and the virus is infective from the prodromal phase until four days after the rash starts. Measles is now rare in developed countries due to immunization programs, but outbreaks can occur when vaccination rates drop.

The prodromal phase of measles is characterized by irritability, conjunctivitis, fever, and Koplik spots. These white spots on the buccal mucosa typically develop before the rash. The rash starts behind the ears and then spreads to the whole body, becoming a discrete maculopapular rash that may become blotchy and confluent. Desquamation may occur after a week, typically sparing the palms and soles. Diarrhea occurs in around 10% of patients.

Measles is mainly managed through supportive care, and admission may be considered for immunosuppressed or pregnant patients. It is a notifiable disease, and public health should be informed. Complications of measles include otitis media, pneumonia, encephalitis, subacute sclerosing panencephalitis, febrile convulsions, keratoconjunctivitis, corneal ulceration, diarrhea, increased incidence of appendicitis, and myocarditis.

If an unvaccinated child comes into contact with measles, MMR should be offered within 72 hours. Vaccine-induced measles antibody develops more rapidly than that following natural infection.

The muscles located in the deep posterior compartment are:

Muscular Compartments of the Lower Limb

The lower limb is composed of different muscular compartments that perform various actions. The anterior compartment includes the tibialis anterior, extensor digitorum longus, peroneus tertius, and extensor hallucis longus muscles. These muscles are innervated by the deep peroneal nerve and are responsible for dorsiflexing the ankle joint, inverting and evert the foot, and extending the toes.

The peroneal compartment, on the other hand, consists of the peroneus longus and peroneus brevis muscles, which are innervated by the superficial peroneal nerve. These muscles are responsible for eversion of the foot and plantar flexion of the ankle joint.

The superficial posterior compartment includes the gastrocnemius and soleus muscles, which are innervated by the tibial nerve. These muscles are responsible for plantar flexion of the foot and may also flex the knee.

Lastly, the deep posterior compartment includes the flexor digitorum longus, flexor hallucis longus, and tibialis posterior muscles, which are innervated by the tibial nerve. These muscles are responsible for flexing the toes, flexing the great toe, and plantar flexion and inversion of the foot, respectively.

Understanding the muscular compartments of the lower limb is important in diagnosing and treating injuries and conditions that affect these muscles. Proper identification and management of these conditions can help improve mobility and function of the lower limb.

Hyperprolactinaemia, which is characterized by high levels of prolactin, is a common side effect of certain atypical antipsychotics like risperidone. This medication can cause galactorrhoea, which is the abnormal secretion of milk due to the development of breast tissue and mammary glands.

Different antipsychotics have their own unique side effect profiles, and the most likely culprits of hyperprolactinaemia are haloperidol (a conventional antipsychotic) and risperidone (an atypical antipsychotic). While it is uncommon for most atypical antipsychotics to cause galactorrhoea, risperidone is an exception.

Other antipsychotics like clozapine are associated with agranulocytosis and myocarditis, while olanzapine is linked to dyslipidaemia, diabetes mellitus, and weight gain.

Atypical antipsychotics are now recommended as the first-line treatment for patients with schizophrenia, as per the 2005 NICE guidelines. These agents have a significant advantage over traditional antipsychotics in that they cause fewer extrapyramidal side-effects. However, atypical antipsychotics can still cause adverse effects such as weight gain, hyperprolactinaemia, and clozapine-associated agranulocytosis. Elderly patients who take antipsychotics are at an increased risk of stroke and venous thromboembolism, according to the Medicines and Healthcare products Regulatory Agency.

Clozapine is one of the first atypical antipsychotics to be developed, but it carries a significant risk of agranulocytosis. Therefore, full blood count monitoring is essential during treatment. Clozapine should only be used in patients who are resistant to other antipsychotic medication. The BNF recommends introducing clozapine if schizophrenia is not controlled despite the sequential use of two or more antipsychotic drugs, one of which should be a second-generation antipsychotic drug, each for at least 6-8 weeks. Clozapine can cause adverse effects such as reduced seizure threshold, constipation, myocarditis, and hypersalivation. Dose adjustment of clozapine may be necessary if smoking is started or stopped during treatment.

The Golgi apparatus is responsible for adding mannose-6-phosphate to proteins, which facilitates their transport to lysosomes.

Functions of Cell Organelles

The functions of major cell organelles can be summarized in a table. The rough endoplasmic reticulum (RER) is responsible for the translation and folding of new proteins, as well as the manufacture of lysosomal enzymes. It is also the site of N-linked glycosylation. Cells such as pancreatic cells, goblet cells, and plasma cells have extensive RER. On the other hand, the smooth endoplasmic reticulum (SER) is involved in steroid and lipid synthesis. Cells of the adrenal cortex, hepatocytes, and reproductive organs have extensive SER.

The Golgi apparatus modifies, sorts, and packages molecules that are destined for cell secretion. The addition of mannose-6-phosphate to proteins designates transport to lysosome. The mitochondrion is responsible for aerobic respiration and contains mitochondrial genome as circular DNA. The nucleus is involved in DNA maintenance, RNA transcription, and RNA splicing, which removes the non-coding sequences of genes (introns) from pre-mRNA and joins the protein-coding sequences (exons).

The lysosome is responsible for the breakdown of large molecules such as proteins and polysaccharides. The nucleolus produces ribosomes, while the ribosome translates RNA into proteins. The peroxisome is involved in the catabolism of very long chain fatty acids and amino acids, resulting in the formation of hydrogen peroxide. Lastly, the proteasome, along with the lysosome pathway, is involved in the degradation of protein molecules that have been tagged with ubiquitin.

The facial nerve innervates the posterior belly of digastric, while the mylohoid nerve innervates the anterior belly.

The Anterior Triangle of the Neck: Boundaries and Contents

The anterior triangle of the neck is a region that is bounded by the anterior border of the sternocleidomastoid muscle, the lower border of the mandible, and the anterior midline. It is further divided into three sub-triangles by the digastric muscle and the omohyoid muscle. The muscular triangle contains the neck strap muscles, while the carotid triangle contains the carotid sheath, which houses the common carotid artery, the vagus nerve, and the internal jugular vein. The submandibular triangle, located below the digastric muscle, contains the submandibular gland, submandibular nodes, facial vessels, hypoglossal nerve, and other structures.

The digastric muscle, which separates the submandibular triangle from the muscular triangle, is innervated by two different nerves. The anterior belly of the digastric muscle is supplied by the mylohyoid nerve, while the posterior belly is supplied by the facial nerve.

Overall, the anterior triangle of the neck is an important anatomical region that contains many vital structures, including blood vessels, nerves, and glands. Understanding the boundaries and contents of this region is essential for medical professionals who work in this area.

Hypogammaglobulinaemia, which is characterized by low antibody levels, can lead to recurrent bacterial infections. One possible cause of this condition is diabetic nephropathy, which results in the loss of proteins in the kidney. Therefore, the patient’s susceptibility to bacterial infections may be due to her low antibody levels caused by the loss of proteins in her kidneys. Other conditions or drugs are unlikely to explain her low antibodies or increased susceptibility to bacterial infections.

Causes of Secondary Immunodeficiency

Secondary immunodeficiency refers to a weakened immune system that is caused by factors outside of genetics. There are various causes of secondary immunodeficiency, including hypogammaglobulinaemia, nephrotic syndrome, protein-losing enteropathy, chronic lymphocytic leukemia (CLL), severe malnutrition, and certain drugs such as gold, penicillamine, and phenytoin.

Hypogammaglobulinaemia is a condition where the body produces low levels of immunoglobulins, which are antibodies that help fight infections. Nephrotic syndrome and protein-losing enteropathy are conditions that cause excessive loss of protein from the body, leading to a weakened immune system. CLL is a type of cancer that affects the white blood cells, which are responsible for fighting infections. Severe malnutrition can also lead to a weakened immune system as the body lacks the necessary nutrients to support immune function.

In addition, certain drugs such as ciclosporin and cyclophosphamide can also cause T-cell deficiency, which weakens the immune system. AIDS is another example of a T-cell deficiency caused by the human immunodeficiency virus (HIV).

It is important to identify and address the underlying cause of secondary immunodeficiency to prevent further complications and improve overall health.

Common Tumours in Children Under 1 Year Old

Embryonal ‘-blastoma’ tumours are frequently found in children under 1 year old. These tumours include retinoblastoma, neuroblastoma, nephroblastoma, medulloblastoma, and hepatoblastoma. Among these, neuroblastoma is the most common and typically affects infants under 1 year old. It originates from neural crest cells in the adrenal medulla and often presents as a large abdominal mass in an otherwise healthy child.

Acute lymphoblastic leukaemia (ALL) is the most common cancer in children overall, but it is less common in infants under 1 year old. Unfortunately, the prognosis for those who develop ALL before their first birthday is poorer. Astrocytomas, the most common type of CNS tumour, tend to affect slightly older children.

Retinoblastomas are embryonal tumours of the retina, with half being spontaneous and the other half being familial due to an inherited mutation in the pRB tumour suppressor gene. Wilms’ tumour, also known as nephroblastoma, is another embryonal tumour that affects the kidneys and may present as an abdominal mass in infants.

In summary, embryonal ‘-blastoma’ tumours are common in children under 1 year old, with neuroblastoma being the most prevalent. Other tumours, such as ALL and astrocytomas, tend to affect slightly older children. Early detection and treatment are crucial for improving outcomes in these young patients.

Metastatic ovarian cancer can be detected in the para-aortic lymph nodes as the ovaries drain to this lymphatic group. This is different from other pelvic organs, which usually drain to the internal and external iliac lymph nodes. The external iliac lymph nodes do not drain the ovary, while the internal iliac lymph nodes do not drain the ovary but drain other pelvic viscera. The deep inguinal lymph nodes drain the clitoris and glans penis, while the superficial inguinal lymph nodes drain the anal canal (below pectinate line), skin below the umbilicus, scrotum, and vulva, but are not significant in the lymphatic drainage of the ovary.

Lymphatic Drainage of Female Reproductive Organs

The lymphatic drainage of the female reproductive organs is a complex system that involves multiple nodal stations. The ovaries drain to the para-aortic lymphatics via the gonadal vessels. The uterine fundus has a lymphatic drainage that runs with the ovarian vessels and may thus drain to the para-aortic nodes. Some drainage may also pass along the round ligament to the inguinal nodes. The body of the uterus drains through lymphatics contained within the broad ligament to the iliac lymph nodes. The cervix drains into three potential nodal stations; laterally through the broad ligament to the external iliac nodes, along the lymphatics of the uterosacral fold to the presacral nodes and posterolaterally along lymphatics lying alongside the uterine vessels to the internal iliac nodes. Understanding the lymphatic drainage of the female reproductive organs is important for the diagnosis and treatment of gynecological cancers.

Down’s syndrome is not caused by genetic imprinting, which involves the expression of genes based on parental origin and is seen in certain inherited disorders like Prader-Willi syndrome and Angelman syndrome. Instead, Down’s syndrome is a rare chromosomal abnormality.

Down’s Syndrome: Epidemiology and Genetics

Down’s syndrome is a genetic disorder that is caused by the presence of an extra copy of chromosome 21. The risk of having a child with Down’s syndrome increases with maternal age, with a 1 in 1,500 chance at age 20 and a 1 in 50 or greater chance at age 45. This can be remembered by dividing the denominator by 3 for every extra 5 years of age starting at 1/1,000 at age 30.

There are three main types of Down’s syndrome: nondisjunction, Robertsonian translocation, and mosaicism. Nondisjunction accounts for 94% of cases and occurs when the chromosomes fail to separate properly during cell division. Robertsonian translocation, which usually involves chromosome 14, accounts for 5% of cases and occurs when a piece of chromosome 21 attaches to another chromosome. Mosaicism, which accounts for 1% of cases, occurs when there are two genetically different populations of cells in the body.

The risk of recurrence for Down’s syndrome varies depending on the type of genetic abnormality. If the trisomy 21 is a result of nondisjunction, the chance of having another child with Down’s syndrome is approximately 1 in 100 if the mother is less than 35 years old. If the trisomy 21 is a result of Robertsonian translocation, the risk is much higher, with a 10-15% chance if the mother is a carrier and a 2.5% chance if the father is a carrier.

The risk of ventricular arrhythmias is increased when amiodarone and erythromycin are used together due to their ability to prolong the QT interval. Manufacturers advise against using multiple drugs that prolong QT interval to avoid this risk. WPW syndrome is a congenital condition that involves abnormal conductive cardiac tissue and can lead to reentrant tachycardia circuit in association with SVT. Amiodarone can cause a slate-grey appearance of the skin, while drugs like rifampicin can cause orange discoloration of body fluids. COPD is associated with multifocal atrial tachycardia.

Amiodarone is a medication used to treat various types of abnormal heart rhythms. It works by blocking potassium channels, which prolongs the action potential and helps to regulate the heartbeat. However, it also has other effects, such as blocking sodium channels. Amiodarone has a very long half-life, which means that loading doses are often necessary. It should ideally be given into central veins to avoid thrombophlebitis. Amiodarone can cause proarrhythmic effects due to lengthening of the QT interval and can interact with other drugs commonly used at the same time. Long-term use of amiodarone can lead to various adverse effects, including thyroid dysfunction, corneal deposits, pulmonary fibrosis/pneumonitis, liver fibrosis/hepatitis, peripheral neuropathy, myopathy, photosensitivity, a ‘slate-grey’ appearance, thrombophlebitis, injection site reactions, and bradycardia. Patients taking amiodarone should be monitored regularly with tests such as TFT, LFT, U&E, and CXR.

Polyposis syndromes are a group of genetic disorders that cause the development of multiple polyps in the colon and other parts of the gastrointestinal tract. These polyps can increase the risk of developing cancer, and therefore, early detection and management are crucial. There are several types of polyposis syndromes, each with its own genetic defect, features, and associated disorders.

Familial adenomatous polyposis (FAP) is caused by a mutation in the APC gene and is characterized by the development of over 100 colonic adenomas, with a 100% risk of cancer. Screening and management involve regular colonoscopies and resectional surgery if polyps are found. FAP is also associated with gastric and duodenal polyps and abdominal desmoid tumors.

MYH-associated polyposis is caused by a biallelic mutation of the MYH gene and is associated with multiple colonic polyps and an increased risk of right-sided cancers. Attenuated phenotype can be managed with regular colonoscopies, while resection and ileoanal pouch reconstruction are recommended for those with multiple polyps.

Peutz-Jeghers syndrome is caused by a mutation in the STK11 gene and is characterized by multiple benign intestinal hamartomas, episodic obstruction, and an increased risk of GI cancers. Screening involves annual examinations and pan-intestinal endoscopy every 2-3 years.

Cowden disease is caused by a mutation in the PTEN gene and is characterized by macrocephaly, multiple intestinal hamartomas, and an increased risk of cancer at any site. Targeted individualized screening is recommended, with extra surveillance for breast, thyroid, and uterine cancers.

HNPCC (Lynch syndrome) is caused by germline mutations of DNA mismatch repair genes and is associated with an increased risk of colorectal, endometrial, and gastric cancers. Colonoscopies every 1-2 years from age 25 and consideration of prophylactic surgery are recommended, along with extra colonic surveillance.