The anterior triangle is the triangular area of the neck found anteriorly to the sternocleidomastoid muscle. It is formed by the anterior border of sternocleidomastoid laterally, the median line of the neck medially and by the inferior border of the mandible superiorly. The apex of the anterior triangle extends towards the manubrium sterni. The anterior triangle contains:
Muscles: thyrohyoid, sternothyroid, sternohyoid muscles
Organs: thyroid gland, parathyroid glands, larynx, trachea, esophagus, submandibular gland, caudal part of the parotid gland
Arteries: superior and inferior thyroid, common carotid, external carotid, internal carotid artery (and sinus), facial, submental, lingual arteries
Veins: anterior jugular veins, internal jugular, common facial, lingual, superior thyroid, middle thyroid veins, facial vein, submental vein, lingual veins
Nerves: vagus nerve (CN X), hypoglossal nerve (CN XII), part of sympathetic trunk, mylohyoid nerve

The posterior triangle is a triangular area found posteriorly to the sternocleidomastoid muscle. It has three borders; anterior, posterior and inferior borders. The anterior border is the posterior margin of the sternocleidomastoid muscle. The posterior border is the anterior margin of the trapezius muscle, while the inferior border is the middle one-third of the clavicle. The investing layer of deep cervical fascia and integument forms the roof of the space, while the floor is covered with the prevertebral fascia along with levator scapulae, splenius capitis and the scalene muscles. The inferior belly of omohyoid subdivides the posterior triangle into a small supraclavicular, and a large occipital, triangle.
Contents:
Vessels: the third part of the subclavian artery, suprascapular and transverse cervical branches of the thyrocervical trunk, external jugular vein, lymph nodes
Nerves: accessory nerve (CN XI), the trunks of the brachial plexus, fibers of the cervical plexus

An intravenous insulin infusion should be started at a concentration of 1 unit/mL, at a fixed rate of 0.1 units/kg/hour. Established subcutaneous long-acting insulin therapy should be continued concomitantly. Blood ketone and blood glucose concentrations should be checked hourly and the insulin infusion rate adjusted accordingly. Blood ketone concentration should fall by at least 0.5 mmol/litre/hour and blood glucose concentration should fall by at least 3 mmol/litre/hour.

Multiple investigations may be done to establish a diagnosis of active tuberculosis. In this case, sputum for acid-fast bacilli would be the best option as it can be done immediately, give fast results, and promptly initiate treatment. Three-morning sputum samples are collected and tested for acid-fast bacilli using gram staining.

Blood culture would yield results in tuberculous bacteraemia and would be less sensitive than sputum testing.

A chest X-ray would not differentiate active tuberculosis from an old infection in which the Ghon complex has formed, and the body’s immune reaction contains the Mycobacterium tuberculosis bacteria.

Mantoux test shows the presence of antibodies to tuberculosis and may be positive if the patient has had a previous infection or been vaccinated against tuberculosis.

A CT chest would also be unable to differentiate between an active infection and the findings of old tuberculosis infection.

Clostridium spp. are obligatory anaerobic spore-forming Gram-positive bacilli. Toxin production is the main pathogenicity mechanism.

There are 4 classes of haemorrhage. Classification is based on clinical signs and physiological parameters.

In CLASS I:Blood loss (ml) is < or = 750
Blood loss(% blood volume) < or = 15%
Pulse rate (bpm) is <100
Respiratory rate is 14-20
Urine output (ml/hr) is >30
Pulse pressure is normal or increased
Systolic BP is normal
CNS/mental status patient is slightly anxious

In CLASS II:
Blood loss (ml) is 750 – 1500
Blood loss(% blood volume) is 15 – 30%
Pulse rate (bpm) is 100 – 120
Respiratory rate is 20-30
Urine output (ml/hr) is 20-30
Pulse pressure is decreased
Systolic BP is normal
CNS/mental status patient is mildly anxious

In CLASS III:
Blood loss (ml) is 1500 – 2000
Blood loss(% blood volume) is 30- 40%
Pulse rate (bpm) is 120 – 140
Respiratory rate is 30-40
Urine output (ml/hr) is 5-15
Pulse pressure is decreased
Systolic BP is decreased
CNS/mental status patient is anxious, confused

In CLASS IV:
Blood loss (ml) is >2000
Blood loss(% blood volume) is >40%
Pulse rate (bpm) is >140
Respiratory rate is >40
Urine output (ml/hr) is negligible
Pulse pressure is decreased
Systolic BP is decreased
CNS/mental status patient is confused, lethargic

Haemostasis is your body’s defence against an injury that causes bleeding. It stops bleeding in three main steps:

1) Primary haemostasis – formation of a weak platelet plug
– The primary reaction of the body is to cause local vasoconstriction at the site of injury and decrease blood flow to the affected area
– the release of cytokines and inflammatory markers lead to adhesion of platelets and aggregation at the site of injury forming a platelet plug
– the injured vessel wall has exposed subendothelial collagen that releases von Willebrand factor

Any damage to the vessel wall causes the release of the Von Willebrand factor, which is necessary for platelet adhesion. Tissue Thromboplastin is also released, which activates the coagulation pathway, a component of secondary haemostasis. The coagulation cascade ultimately results in the conversion of fibrinogen to fibrin.

2) Secondary haemostasis
3) Fibrinolysis

Fibrin (factor Ia) is a long, thin protein with branches produced at the end of the coagulation cascade when fibrinogen (factor I) is converted to fibrin, which stabilizes the blood clot.

Flexor hallucis longus is innervated by the tibial nerve, composed of spinal roots L4, L5, S1, S2, and S3.

Hyperkalaemia causes a rapid reduction in resting membrane potential leading to increased cardiac depolarisation and muscle excitability. This in turn results in ECG changes which can rapidly progress to ventricular fibrillation or asystole. Very distinctive ECG changes that progressively change as the K+level increases:
K+>5.5 mmol/l – peaked T waves (usually earliest sign of hyperkalaemia), repolarisation abnormalities
K+>6.5 mmol/l – P waves widen and flatten, PR segment lengthens, P waves eventually disappear
K+>7.0 mmol/l – Prolonged QRS interval and bizarre QRS morphology, conduction blocks (bundle branch blocks, fascicular blocks), sinus bradycardia or slow AF, development of a sine wave appearance (a pre-terminal rhythm)
K+>9.0 mmol/l – Cardiac arrest due to asystole, VF or PEA with a bizarre, wide complex rhythm.

Homonymous quadrantanopia is not a disease; it is a clinical finding that points towards a lesion of the optic radiations coursing through the temporal lobe.
Homonymous superior quadrantanopia is caused by damage to the contralateral inferior parts of the posterior visual pathway: the inferior optic radiation (temporal Meyer loop), or the inferior part of the occipital visual cortex below the calcarine fissure.

Benign prostatic hyperplasia (BPH), also known as benign prostatic hypertrophy, is characterized by an enlarged prostate gland.

The prostate is divided into four major lobes. The median lobe is the most commonly affected by benign prostatic enlargement, resulting in urethral obstruction and urine symptoms.