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

Although Ca2+entry during the action potential (AP) is essential for contraction, it only accounts for about 25% of the rise in intracellular Ca2+. The rest is released from Ca2+stores in the sarcoplasmic reticulum (SR). In relaxation, about 80% of Ca2+is rapidly pumped back into the SR (sequestered) by Ca2+ATPase pumps. The Ca2+that entered the cell during the AP is transported out of the cell primarily by the Na+/Ca2+exchanger in the membrane. When more action potentials occur per unit time, more Ca2+enters the cell during the AP plateau, more Ca2+is stored in the SR, more Ca2+is released from the SR and thus more Ca2+is left inside the cell and greater tension is produced during contraction. Increased heart rate increases the force of contraction in a stepwise fashion as intracellular [Ca2+] increases cumulatively over several beats; this is the Treppe effect. Cardiac glycosides such as digoxin have a positive inotropic effect.

During the AP plateau, Ca2+enters the cell and activates Ca2+sensitive Ca2+release channels in the sarcoplasmic reticulum allowing stored Ca2+to flood into the cytosol; this is called Ca2+-induced Ca2+release. In relaxation, about 80% of Ca2+is rapidly pumped back into the SR (sequestered) by Ca2+ATPase pumps. The Ca2+that entered the cell during the AP is transported out of the cell primarily by the Na+/Ca2+exchanger in the membrane which pumps one Ca2+ion out in exchange for three Na+ions in, using the Na+electrochemical gradient as an energy source. Increased heart rate increases the force of contraction in a stepwise fashion as intracellular [Ca2+] increases cumulatively over several beats; this is the Treppe effect. Factors that affect intracellular [Ca2+] and hence cardiac contractility are called inotropes.

Phagocytosis is largely responsible for depletion of cells coated with antibodies. Cells opsonized by IgG antibodies are recognized by phagocyte Fc receptors, which are specific for the Fc portions of some IgG subclasses. In addition, when IgM or IgG antibodies are deposited on the surfaces of cells, they may activate the complement system by the classical pathway. Complement activation generates by-products, mainly C3b and C4b, which are deposited on the surfaces of the cells and recognized by phagocytes that express receptors for these proteins. The net result is phagocytosis of the opsonized cells and their destruction.

Cushing’s syndrome is a group of symptoms and signs brought on by long-term exposure to high amounts of endogenous or exogenous glucocorticoids. Cushing’s syndrome affects about 10-15 persons per million, and it is more common in those who have had a history of obesity, hypertension, or diabetes.

Cushing’s syndrome has a wide range of clinical manifestations that are dependent on the degree of cortisol overproduction. The appearance might be vague and the diagnosis difficult to detect when cortisol levels are just somewhat elevated. On the other hand, in long-term cases of severely increased cortisol levels, the presentation might be colourful and the diagnosis simple.

Cushing’s syndrome has the following clinical features:
Obesity and weight growth in the true sense
Supraclavicular fat pads are fat pads that are located above the clavicle.
Buffalo hump
Fullness and plethora of the face (‘moon facies’)
Muscle atrophy and weakening at the proximal level
Diabetes mellitus, also known as impaired glucose tolerance
Hypertension
Skin thinning and bruising
Depression
Hirsutism
Acne
Osteoporosis
Amenorrhoea or oligomenorrhoea

Cortisol levels fluctuate throughout the day, with the greatest levels occurring around 0900 hours and the lowest occurring at 2400 hrs during sleep. The diurnal swing of cortisol levels is lost in Cushing’s syndrome, and levels are greater during the whole 24-hour period. In the morning, levels may be normal, but they may be high at night-time, when they are generally repressed. As a result, random cortisol testing is not an effective screening technique and is not advised.

The following are the two most common first-line screening tests:
Cortisol levels in the urine are measured every 24 hours.
A diagnosis of Cushing’s syndrome can be made if more than two collections measure cortisol excretion more than three times the upper limit of normal.
Physical stress (e.g., excessive exercise, trauma), mental stress (e.g., sadness), alcohol or drug misuse, complex diabetes, and pregnancy can all cause false positives.
Renal dysfunction, inadequate collection, and cyclical Cushing’s disease can all cause false negatives.
The overnight low-dose dexamethasone suppression test (LDDST) involves giving 1 mg of dexamethasone at 11 p.m. and measuring blood cortisol levels at 8 a.m. the next day.
Cushing’s syndrome is diagnosed when cortisol is not suppressed to less than 50 nmol/L.
It might be difficult to tell the difference between mild Cushing’s disease and normal cortisol production.
False positives can occur as a result of depression, severe systemic sickness, renal failure, prolonged alcohol misuse, old age, and the use of hepatic enzyme-inducing medicines, among other things.
False negatives are extremely uncommon in Cushing’s disease patients.

A characteristic biochemical picture might also be helpful in confirming the diagnosis of Cushing’s syndrome. The following are the primary characteristics:
Hypokalaemia
Alkalosis metabolique

Following neuronal injury, as seen in traumatic brain injury, the axon undergoes anterograde degeneration. Degradation starts from the cell body (proximally) and progresses distally. The axon becomes fragmented and degenerates.

The brain shows no reactive changes to injury is incorrect. Following major injury such as stroke, the brain undergoes a process of liquefactive degeneration, which leaves cystic spaces within the brain.

Axonal regeneration does not occur to any significant extent within the central nervous system unlike what is seen in the peripheral nervous system.

Astrocytes undergo reactive gliosis, leaving behind a firm translucent tissue around sites of damage.

Conjunctivitis occurring in the first 28 days of life (Ophthalmia neonatorum) is most commonly caused by Chlamydia trachomatis in the UK.

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

Immunodeficiency is present in all patients with chronic lymphocytic leukaemia (CLL), though it is often mild and not clinically significant. Infections are the leading cause of death in 25-50 percent of CLL patients, with respiratory tract, skin, and urinary tract infections being the most common.

Hypogammaglobulinemia is the most common cause of immunodeficiency in CLL patients, accounting for about 85 percent of all cases.

In foreign body aspiration, the foreign body is more likely to enter the right main bronchus because it is shorter, wider and more vertical than the left main bronchus. In a patient who is standing or sitting, the foreign body tends to become lodged in the posterobasal segment of the inferior lobe of the right lung.

The beta-adrenoceptors in the heart, peripheral vasculature, bronchi, pancreas, and liver are blocked by beta-adrenoceptor blocking drugs (beta blockers).

Beta blockers come in a wide range of strengths, with the choice largely determined by the disease being treated and the patient’s unique circumstances. The intrinsic sympathomimetic activity, lipid solubility, duration of action, and cardioselectivity of beta blockers all differ.

Some beta blockers are lipid (lipophilic) soluble, while others are water soluble (hydrophilic). Drugs that are more lipid-soluble are absorbed faster from the gut, undergo more first-pass metabolism, and are eliminated faster. They’re also more likely to get into the brain and cause central effects like insomnia and nightmares. Propranolol, pindolol, labetalol, and metoprolol are examples of lipid-soluble beta blockers. Beta blockers that are water-soluble are less likely to enter the brain and are more resistant to first-pass metabolism. They are excreted by the kidneys, and in renal impairment, dosage reduction is frequently required. Atenolol, nadolol, celiprolol, and sotalol are examples of water-soluble beta blockers.

Depression of the mandible is generated by the digastric, geniohyoid, mylohyoid and lateral pterygoid muscles on both side, assisted by gravity. The lateral pterygoid muscles are also involved as this movement also involves protraction of the mandible. The masseter muscle is a powerful elevator of the mandible.

Overdosing on calcium-channel blockers should always be taken seriously and regarded as potentially fatal. Verapamil and diltiazem are the two most lethal calcium channel blockers in overdose. These work by binding the alpha-1 subunit of L-type calcium channels, preventing calcium from entering the cell. In cardiac myocytes, vascular smooth muscle cells, and islet beta-cells, these channels play an important role.

>10 tablets of verapamil (160 mg or 240 mg immediate or sustained-release capsules) or diltiazem can cause serious toxicity (180 mg, 240 mg or 360 mg immediate or sustained-release capsules)

In children, 1-2 tablets of verapamil or diltiazem (immediate or sustained-release)

Symptoms usually appear within 1-2 hours of ingestion with standard preparations. However, with slow-release preparations, significant toxicity may take 12-16 hours to manifest, with peak effects occurring after 24 hours.

The following are the main clinical features of calcium-channel blocker overdose:
Nausea and vomiting
Hypotension
Bradycardia and first-degree heart block
Myocardial ischaemia and stroke
Renal failure
Pulmonary oedema
Hyperglycaemia

The following are some of the most important bedside investigations to conduct:
Blood glucose
ECG
Arterial blood gas
Other investigations that can be helpful include
Urea & electrolytes
Chest X-ray (pulmonary oedema)
Echocardiography

The obturator nerve is a sensory and motor nerve that emerges from the lumbar plexus and innervates the thigh.

This nerve supplies motor innervation to the medial compartment of the thigh, making it necessary for thigh adduction.

Primary wound healing, or healing by first intention, occurs within hours of repairing a full-thickness surgical incision. This surgical insult results in the mortality of a minimal number of cellular constituents. Healing by first intention can occur when the wound edges are opposed, the wound is clean and uninfected and there is minimal loss of cells and tissue i.e. surgical incision wound. The wound margins are joined by fibrin deposition, which is subsequently replaced by collagen and covered by epidermal growth.

Historically, MRSA has been treated successfully with outpatient oral sulphonamides, clindamycin, rifampin, doxycycline, or a combination of these agents. With the development of increasing drug resistance of MRSA to these traditional antimicrobials, there has been a search for more effective antibiotics. One recent study demonstrated that vancomycin, linezolid, and quinupristin-dalfopristin were the most effective antibiotics against multiple strains of MRSA.

Proton pump inhibitors (PPIs) have a variety of side effects, including:
Vomiting and nausea
Pain in the abdomen
Flatulence
Diarrhoea
Constipation
Headache

PPIs have been linked to a significant increase in the risk of focal tachyarrhythmias (link is external).
Low serum magnesium and sodium levels have been linked to long-term use of PPIs, according to the US Food and Drug Administration (link is external).

Long-term PPI use has also been linked to an increased risk of fracture, according to epidemiological evidence (link is external). Observational studies have discovered a slight link between hip, wrist, and spine fractures. However, there is no link between the two and an increased risk of pelvic fracture. For this reason, the MHRA recommends that patients at risk of osteoporosis who take PPIs maintain an adequate calcium and vitamin D intake.

Plasmodium falciparum induces the expression of red cell protein, making cerebral malaria more severe. Bacteria may invade a host passively through micro traumata or macro traumata in the skin or mucosa. On the other hand, bacteria that invade
through intact mucosa first, adhere to this anatomical barrier, then actively
breach it.

Alteplase is a recombinant tissue-type plasminogen activator (tPA), a naturally occurring fibrin-specific enzyme that has selectivity for activation of fibrin-bound plasminogen. It has a short half-life of 3 – 4  minutes and must be given by continuous intravenous infusion but is not associated with antigenic or hypotensive effects, and can be used in patients when recent streptococcal infections or recent use of streptokinase contraindicates the use of streptokinase.

Pectoralis major is a thick, fan-shaped muscle situated in the chest. It makes up the bulk of the chest musculature in the male and lies underneath the breast in the female. It overlies the thinner pectoralis minor muscle.
Superficial muscles of the chest and arm showing pectoralis major (from Gray’s Anatomy)
Pectoralis major has two heads; the clavicular head and the sternocostal head. The clavicular head originates from the anterior border and medial half of the clavicle. The sternocostal head originates from the anterior surface of the sternum, the superior six costal cartilages and the aponeurosis of the external oblique muscle. It inserts into the lateral lip of the bicipital groove of the humerus.
Pectoralis major receives dual innervation from the medial pectoral nerve and the lateral pectoral nerve.
Its main actions are as follows:
Flexes humerus (clavicular head)
Extends humerus (sternocostal head)
Adducts and medially rotates the humerus
Draws scapula anteriorly and inferiorly

Hutchinson sign relates to involvement of the tip of the nose from facial herpes zoster. It implies involvement of the external nasal branch of the nasociliary nerve which is a branch of the ophthalmic division of the trigeminal nerve.

The nasociliary branch of the trigeminal nerve innervates the apex and lateral aspect of the nose, as well as the cornea. Therefore, lesions on the side or tip of the nose should raise suspicion of ocular involvement.

In non-shockable (PEA/asystole) cardiac arrests, adrenaline should be given as soon as circulatory access is gained. The dose is 1 mg via IV or IO (10 mL of 1:10,000 or 1 mL of 1:1000).

Once chest compressions have been resumed after the third shock in a shockable (Vf/pVT) cardiac arrest, adrenaline should be administered. The dosage is one milligram (10 mL of 1:10,000 or 1 mL of 1:1000)

It should be given every 3-5 minutes after that (i.e. alternate loops) and without interrupting chest compressions.
Systemic vasoconstriction is caused by the alpha-adrenergic effects of adrenaline, which raises coronary and cerebral perfusion pressures.

Adrenaline’s beta-adrenergic effects are inotropic (increased myocardial contractility) and chronotropic (increased heart rate), and they can increase coronary and cerebral blood flow. However, concomitant increases in myocardial oxygen consumption and ectopic ventricular arrhythmias (especially in the absence of acidaemia), transient hypoxemia due to pulmonary arteriovenous shunting, impaired microcirculation, and increased post-cardiac arrest myocardial dysfunction may offset these benefits.

Although there is no evidence of long-term benefit from its use in cardiac arrest, the improved short-term survival reported in some studies justifies its use.

Heparin is a polymer of glycosaminoglycan. It occurs naturally and is found in mast cells. Clinically, it is used in two forms:
1. Unfractionated: widely varying polymer chain lengths
2. Low molecular weight: Smaller polymers only

Heparin works by binding to and activating the enzyme inhibitor antithrombin III. Antithrombin III inactivates thrombin (factor IIa) by forming a 1:1 complex with thrombin. The heparin-antithrombin III complex also inhibits factor Xa and some other proteases involved with clotting. The heparin-ATIII complex can also inactivate IX, XI, XII, and plasmin.

Heparin is not thrombolytic or fibrinolytic. It prevents the progression of existing clots by inhibiting further clotting. The lysis of existing clots relies on endogenous thrombolytics.

Heparin is used for:
1. Prevention and treatment of venous thromboembolism
2. Treatment of disseminated intravascular coagulation
3. Treatment of fat embolism
4. Priming of haemodialysis and cardiopulmonary bypass machines

There is no evidence that heparin is superior to low-molecular-weight heparins in preventing mortality from thrombosis.

Vitamin K is used to reverse the effects of warfarin but not heparin. For heparin, protamine sulphate is used to counteract its effects.

Short vessels called arteriovenous anastomoses (AVAs) link tiny arteries and veins. They have a large lumen diameter. The strong and muscular walls allow AVAs to completely clog the vascular lumen, preventing blood flow from artery to vein (acting like a sphincter). When the AVAs open, they create a low-resistance connection between arteries and veins, allowing blood to flow into the limbs’ superficial venous plexuses. There is no diffusion of solutes or fluid into the interstitium due to their strong muscle walls.

AVAs are densely innervated by adrenergic fibres from the hypothalamic temperature-regulation centre. High sympathetic output occurs at normal core temperatures, inducing vasoconstriction of the AVAs and blood flow through the capillary networks and deep plexuses. When the temperature rises, sympathetic output decreases, producing AVA vasodilation and blood shunting from the artery to the superficial venous plexus. Heat is lost to the environment as hot blood rushes near to the skin’s surface.
AVAs are a specialized anatomical adaptation that can only be found in large quantities in the fingers, palms, soles, lips, and pinna of the ear.

A thyroid function test is used in the diagnosis of hyperthyroidism.
Serum TSH should be the first-line investigation for patients with suspected hyperthyroidism as it has the highest sensitivity and specificity for hyperthyroidism.

A normal TSH level almost always excludes the diagnosis, though there are rare exceptions to this.

Antithyroglobulin antibodies are commonly present in Graves’ disease, but the test has a sensitivity of 98% and specificity of 99, and is not widely available.

Radioactive iodine uptake scan using iodine-123 – shows low uptake in thyroiditis but high in Graves’ disease and toxic multinodular goitre. It is however, not first-line investigation in this case

Thyroid ultrasound scan – is a cost-effective and safe alternative to the radioactive iodine uptake scan.

Metformin is a biguanide used as the first-line to treat type 2 diabetes mellitus. It has a good reputation as it has an extremely low risk of causing hypoglycaemia compared to the other agents for diabetes. It does not affect the insulin secreted by the pancreas or increase insulin levels. Toxicity with metformin can, however, cause lactic acidosis with associated hypoglycaemia.

The Kiesselbach plexus is a vascular network formed by five arteries that supply oxygenated blood to the nasal septum, which refers to the wall separating the right and left sides of the nose. The five arteries that form the Kiesselbach plexus: the sphenopalatine artery, which branches from the maxillary artery originating behind the jawbone; the anterior ethmoidal artery, which branches from the ophthalmic artery behind the eye; the posterior ethmoidal artery, which also branches from the ophthalmic artery; the septal branch of the superior labial artery, which is a branch of the facial artery supplying blood to all of the superficial features of the face; and finally, the greater palatine artery, which is a terminal branch of the maxillary artery.

The RAS pathway begins with renin cleaving its substrate, angiotensinogen (AGT), to produce the inactive peptide, angiotensin I, which is then converted to angiotensin II by endothelial angiotensin-converting enzyme (ACE). ACE activation of angiotensin II occurs most extensively in the lung. Angiotensin II mediates vasoconstriction as well as aldosterone release from the adrenal gland, resulting in sodium retention and increased blood pressure.

Plasmodium falciparum malaria is transmitted by female of the Anopheles genus of mosquito. The Aedes genus is responsible for transmitting diseases such as dengue fever and yellow fever.
Plasmodium falciparumis found globally but is mainly found in sub-Saharan Africa.
The incubation period of Plasmodium falciparum malaria is 7-14 days.
Sporozoites invade hepatocytes. Within the hepatocyte asexual reproduction occurs producing merozoites, which are released into the blood stream and invade the red blood cells of the host.
Artesunate is the drug treatment of choice for Plasmodium falciparum malaria. Quinine can still be used where artesunate is not available. Often combination therapy with drugs such as doxycycline or fansidar is also required.
The classic symptom of malaria is the malarial paroxysm, a cyclical occurrence of a cold phase, where the patient experiences intense chills, a hot stage, where the patient feels extremely hot and finally a sweating stage, where the fever declines and the patient sweats profusely. There may also, however, be a continuous fever.

Benign enlargement of the prostate is common in men older than 50 years. The cause is possibly an imbalance in the hormonal control of the gland. The median lobe of the gland enlarges upward and encroaches within the sphincter vesicae, located at the neck of the bladder. The leakage of urine into the prostatic urethra causes an intense reflex desire to micturate. The enlargement of the median and lateral lobes of the gland produces elongation and lateral compression and distortion of the urethra so that the patient experiences difficulty in passing urine and the stream is weak. Back-pressure effects on the ureters and both kidneys are a common complication. The enlargement of the uvula vesicae (owing to the enlarged median lobe) results in the formation of a pouch of stagnant urine behind the urethral orifice within the bladder. The stagnant urine frequently becomes infected, and the inflamed bladder (cystitis) adds to the patient’s symptoms.

In all operations on the prostate, the surgeon regards the prostatic venous plexus with respect. The veins have thin walls, are valveless, and are drained by several large trunks directly into the internal iliac veins. Damage to these veins can result in a severe haemorrhage.