Both the medial and lateral pterygoids are innervated by the mandibular division of the trigeminal nerve.

Angiotensin II acts to:Stimulate release of aldosterone from the zona glomerulosa of the adrenal cortex (which in turn acts to increase sodium reabsorption)Cause systemic vasoconstrictionCause vasoconstriction of the renal arterioles (predominant efferent effect thus intraglomerular pressure is stable or increased, thereby tending to maintain or even raise the GFR)Directly increase Na+reabsorption from the proximal tubule (by activating Na+/H+antiporters)Stimulate synthesis and release of ADH from the hypothalamus and posterior pituitary respectivelyStimulate the sensation of thirstPotentiate sympathetic activity (positive feedback)Inhibit renin production by granular cells (negative feedback)

Measles belongs to the paramyxoviridae group of viruses. The incubation period is 7-18 days (average 10) and it is spread by airborne or droplet transmission. The classical presentation is of a high fever with coryzal symptoms and photophobia with conjunctivitis often being present. The rash that is associated is a widespread erythematous maculopapular rash. Koplik spots are pathognomonic for measles, and are the presence of white lesions on the buccal mucosa.Differential diagnoses would include:RubellaRoseola infantum (exanthem subitom)Scarlet feverKawasaki diseaseErythema infectiosum (5thdisease)EnterovirusInfectious mononucleosisDiagnosis can be confirmed by the following means:Salivary swab for measles specific IgMSerum sample for measles specific IgMSalivary swab for RNA detectionPossible complications include:Otitis mediaFebrile convulsionsPneumoniaBronchiectasisDiarrhoeaMeningitisEncephalitisImmunosuppressionSubacute sclerosing panencephalitisDeath

Etomidate causes the least cardiovascular depression of the intravenous induction agents, with only a small reduction in the cardiac output and blood pressure. In the past, etomidate was widely used to induce anaesthesia in the shocked, elderly or cardiovascularly unstable patient. However, more recently it has become less popular as a single induction dose blocks the normal stress-induced increase in adrenal cortisol production for 4 – 8 hours, and up to 24 hours in elderly and debilitated patients. Although no increase in mortality has been identified following a single dose during induction of anaesthesia, the use of etomidate has declined due to a perceived potential morbidity.

Clinical features of DKA: Symptoms: Polyuria, polydipsia, thirst, lethargy, weight loss, nausea, vomiting, anorexia, abdominal pain, dehydration, headache, altered mental stateSigns: Dry mucous membranes, ketotic breath, tachycardia, hypotension, Kussmaul breathing, focal signs of precipitant e.g. infection

CD4+ T-cells (Helper T cells)Recognise antigen only in association with HLA class II molecules (found on antigen presenting cells (APCs) e.g. dendritic cells, B-cells; present exogenous antigens that have been phagocytosed/endocytosed into intracellular vesicles)Form most of the circulating T-cell population (about 75%)Secrete cytokines (e.g. IFN-gamma) which are required for recruitment and activation of other immune cells such as macrophages, T cytotoxic cells and NK cells and for the activation of and production of immunoglobulin from B-cells

Angiotensin II increases Na+reabsorption from the proximal tubule (by activating Na+/H+antiporters).

Penicillin penetration into the cerebrospinal fluid is generally poor. However, when the meninges are inflamed, as in meningitis, penetration of penicillin is increased. Benzylpenicillin should be given before transfer to hospital if meningococcal disease (meningitis with non-blanching rash or meningococcal septicaemia) is suspected, once this does not delay transfer. Benzylpenicillin is no longer the drug of first choice for pneumococcal meningitis.

On standing from a prone position, gravity causes blood to pool in veins in the legs. Central venous pressure (CVP) falls, causing a fall in stroke volume and cardiac output (due to Starling’s law) and thus a fall in blood pressure. Normally this fall in BP is rapidly corrected by the baroreceptor reflex which causes venoconstriction (partially restoring CVP), and an increase in heart rate and contractility, so restoring cardiac output and blood pressure. Impaired autonomic nervous activity in the elderly accounts for the greater likelihood of postural hypotension. Any symptoms of dizziness, blurred vision or syncope is due to a transient fall in cerebral perfusion that occurs before cardiac output and mean arterial pressure (MAP) can be corrected.

The majority of extensor carpi radialis longus originates from the lateral supracondylar ridge of humerus (distal third) and anterior aspect of the lateral intermuscular septum of the arm. A small portion of its fibres originate from the common extensor tendon attached to the lateral epicondyle of humerus. The fibres unite into a muscle belly which extends approximately to the middle of the forearm. The muscle belly is then replaced by a flat tendon that travels distally along the lateral surface of the radius, together with the tendon of extensor carpi radialis brevis. Both tendons course towards the radial styloid process, deep to the tendons of abductor pollicis longus and extensor pollicis brevis muscles. Proximal to the wrist, the tendons of extensor carpi radialis longus and brevis pass behind the radial styloid process within a common synovial sheath and continue along the radial groove deep to the extensor retinaculum of the wrist. At this level, the tendon of extensor carpi radialis longus is crossed by the tendon of extensor pollicis longus, after which it inserts on the posterior aspect of the base of the second metacarpal bone. Some tendon slips can insert into the first and third metacarpal bones.Extensor carpi radialis longus receives innervation from the radial nerve, with contributions mainly from spinal nerves C5-C8. The radial nerve is a branch of the brachial plexus.Extensor carpi radialis longus receives blood supply mainly from the radial artery. It directly supplies the distal part of the muscle, while the rest of the muscle receives blood from one of its radial recurrent branches. The brachial artery also supplies a small portion of the muscle via the radial collateral artery.Extensor carpi radialis longus primarily acts on the wrist joint to produce two major actions: (1) wrist extension by working synergistically with extensor carpi radialis brevis and extensor carpi ulnaris, and (2) hand abduction (radial deviation), with the help of flexor carpi radialis.

Thoracotomy describes an incision made in the chest wall to access the contents of the thoracic cavity. Thoracotomies typically can be divided into two categories; anterolateral thoracotomies and posterolateral thoracotomies. These can be further subdivided into supra-mammary and infra-mammary and, of course, further divided into the right or left chest. Each type of incision has its utility given certain circumstances.A scalpel is used to sharply divide the skin along the inframammary crease overlying the fifth rib. Electrocautery is then used to divide the pectoralis major muscle and serratus anterior muscle. Visualization of the proper operative field can be achieved with the division and retraction of the latissimus dorsi. Either the fourth or fifth intercostal space is then entered after the division of intercostal muscles above the rib to ensure the preservation of the neurovascular bundle. Once the patient is properly secured to the operating table, the ipsilateral arm is raised and positioned anteriorly and cephalad to rest above the head. The incision is started along the inframammary crease and extended posterolaterally below the tip of the scapula. It is then extended superiorly between the spine and the edge of the scapula, a short distance. The trapezius muscle and the subcutaneous tissues are divided with electrocautery. The serratus anterior and latissimus dorsi muscles are identified and can be retracted. The intercostal muscles are then divided along the superior border of the ribs, and the thoracic cavity is accessed.

Hypokalaemia can occur with both thiazide and loop diuretics. The risk of hypokalaemia depends on the duration of action as well as the potency and is thus greater with thiazides than with an equipotent dose of a loop diuretic. Hypokalaemia is dangerous in severe cardiovascular disease and in patients also being treated with cardiac glycosides. Often the use of potassium-sparing diuretics avoids the need to take potassium supplements. In hepatic failure, hypokalaemia caused by diuretics can precipitate encephalopathy, particularly in alcoholic cirrhosis.

In pregnancy and postpartum, lithium is an effective treatment for relapse prevention in bipolar disorder. However, lithium has also been associated with risks during pregnancy for both the mother and the unborn child. Recent large studies have confirmed the association between first-trimester lithium exposure and an increased risk of congenital malformations.Lithium levels need to be monitored more frequently throughout pregnancy and the postnatal period. If given in the 1st-trimester, lithium is associated with a risk of fetal cardiac malformations, such as Ebstein’s anomaly. If given in the 2nd and 3rd-trimesters, there is a risk of the following:1. hypotonia2. lethargy3. feeding problems4. hypothyroidism5. goitre6. nephrogenic diabetes insipidus in the neonate

The following are the lesions of the cranial nerves:1. Olfactory nerve (I)Reduced taste and smell, but not to ammonia which stimulates the pain fibres carried in the trigeminal nerve2. Optic nerve (II)Manifested by visual field defects, pupillary abnormalities, optic neuritis, optic atrophy, papilledema3. Oculomotor nerve (III)A fixed, dilated pupil which doesn’t accommodate, ptosis, complete internal ophthalmoplegia (masked by ptosis), unopposed lateral rectus causes outward deviation of the eye. If the ocular sympathetic fibres are also affected behind the orbit, the pupil will be fixed but not dilated.4. Trochlear nerve (IV)Diplopia due to weakness of downward and inward eye movement. The most common cause of a pure vertical diplopia. The patient tends to compensate by tilting the head away from the affected side.5. Trigeminal nerve (V)Reduced sensation or dysesthesia over the affected area. Weakness of jaw clenching and side-to-side movement. If there is a lower motor neuron (LMN) lesion, the jaw deviates to the weak side when the mouth is opened. There may be fasciculation of temporalis and masseter.6. Abducens nerve (VI)Inability to look laterally. The eye is deviated medially because of unopposed action of the medial rectus muscle.7. Facial nerve (VII)Facial weakness. In an LMN lesion the forehead is paralysed – the final common pathway to the muscles is destroyed; whereas the upper facial muscles are partially spared in an upper motor neurone (UMN) lesion because of alternative pathways in the brainstem. There appear to be different pathways for voluntary and emotional movement. CVAs usually weaken voluntary movement, often sparing involuntary movements (e.g., spontaneous smiling). The much rarer selective loss of emotional movement is called mimic paralysis and is usually due to a frontal or thalamic lesion.8. Vestibulocochlear nerve (VIII)Unilateral sensorineural deafness, tinnitus. Slow-growing lesions seldom present with vestibular symptoms as compensation has time to occur.9. Glossopharyngeal nerve (IX)Unilateral lesions do not cause any deficit because of bilateral corticobulbar connections. Bilateral lesions result in pseudobulbar palsy. These nerves are closely interlinked.10. Vagus nerve (X)Palatal weakness can cause ‘nasal speech’ and nasal regurgitation of food. The palate moves asymmetrically when the patient says ‘ahh’. Recurrent nerve palsy results in hoarseness, loss of volume and ‘bovine cough’.11. Accessory nerve (XI)Weakness and wasting of sternocleidomastoid and trapezius muscles12.Hypoglossal nerve (XII)An LMN lesion produces wasting of the ipsilateral side of the tongue, with fasciculation; and on attempted protrusion the tongue deviates towards the affected side, but the tongue deviates away from the side of a central lesion.

A L’Abbé plot is a scatter plot with the risk in the control group on the x-axis and the risk in the experimental group on the y-axis. It can be used to evaluate heterogeneity in meta-analysis. Furthermore, this plot can aid to choose a summary measure (odds ratio, risk ratio, risk difference) that will result in more consistent results.

The only medication that does not commonly cause tremors is carbamazepine.The other drugs present with the following types of tremors as a side effect to their usage:1. Sodium valproate – Postural tremor is most common, but a resting tremor can also occur. Approximately 25% of patients taking sodium valproate are found to develop a tremor within 12 months of starting therapy.2. Lithium – fine hand tremor is very commonly seen and reported in as many as 50% of patients during the first week of therapy. The tremor tends to reduce with time and is only present in around 5% of patients taking the medication two years or longer.3. Atypical antipsychotics, such as olanzapine and quetiapine – tremor and limb shakiness.

Newborn babies have a higher concentration of red blood cells with shorter lifespan leading to higher bilirubin levels than in adults. This condition is short-lived and harmless but with potential serious causes that need to be assessed for if present. The most obvious physical sign of jaundice is a yellow discolouration of the sclera, skin and mucous membranes. At a bilirubin level of 35 μmol/L or higher, the eye is affected. The bilirubin level will need to be higher than 255 μmol/L for the feet and extremities to be affected.

Chronic kidney disease (CKD) is a disorder in which kidney function gradually deteriorates over time. It’s fairly prevalent, and it typically remains unnoticed for years, with only advanced stages of the disease being recognized. There is evidence that medication can slow or stop the progression of CKD, as well as lessen or prevent consequences and the risk of cardiovascular disease (CVD).CKD is defined as kidney damage (albuminuria) and/or impaired renal function (GFR 60 ml/minute per 1.73 m2) for three months or longer, regardless of clinical diagnosis.A prolonged decline in GFR of 25% or more with a change in GFR category within 12 months, or a sustained drop in GFR of 15 ml/minute/1.73 m² per year, is considered accelerated CKD progression.End-stage renal disease (ESRD) is defined as severe irreversible kidney impairment with a GFR of less than 15 ml/minute per 1.73 m² and a GFR of less than 15 ml/minute per 1.73 m².

At muscarinic receptors, atropine blocks the action of the parasympathetic neurotransmitter acetylcholine. As a result, it inhibits the vagus nerve’s effects on both the SA and AV nodes, increasing sinus automaticity and facilitating AV node conduction.At muscarinic receptors, atropine blocks the action of the parasympathetic neurotransmitter acetylcholine. As a result, it inhibits the vagus nerve’s effects on both the SA and AV nodes, increasing sinus automaticity and facilitating AV node conduction.The most common cause of asystole during cardiac arrest is primary myocardial pathology, not excessive vagal tone, and there is no evidence that atropine is helpful in the treatment of asystole or PEA. As a result, it is no longer included in the ALS algorithm’s non-shockable section. Atropine is most commonly used in the peri-arrest period. It is used to treat bradycardia (sinus, atrial, or nodal) or AV block when the patient’s haemodynamic condition is compromised by the bradycardia.If any of the following adverse features are present, the ALS bradycardia algorithm recommends a dose of 500 mcg IV:ShockSyncopeMyocardial ischaemiaHeart failureAtropine is also used for the following purposes:Topically as a cycloplegic and mydriatic to the eyesTo cut down on secretions (e.g. in anaesthesia)Organophosphate poisoning is treated withAtropine’s side effects are dose-dependent and include:Mouth is parchedVomiting and nauseaVision is hazyRetention of urineTachyarrhythmiasIt can also cause severe confusion and hallucinations in patients, especially the elderly.

Discrete data is quantitative data that can only take whole numerical values e.g. number of children, number of days missed from work.

5, 10, 15 /20, 25, 30 /35, 40, 45 /50, 60, 70Sample size (n) = 12Median = [(n+1)/2]th value = (12+1)/2 = 6.5 = halfway between 6th and 7th value = (30 +35)/2 = 32.5The lower (first) quartile = halfway between 15 and 20 = 17.5The upper (third) quartile = halfway between 45 and 50 = 47.5The interquartile range is the difference between the upper quartile and lower quartile = 47.5 – 17.5 = 30

Chlorphenamine is a competitive inhibitor at the H1-receptor (an antihistamine).

Angiotensin-converting enzyme (ACE) inhibitors prevent angiotensin I from being converted to angiotensin II. Angiotensin II has a variety of effects:Sympathetic activity has increased.Vasoconstriction in the arteriesSecretion of VasopressinSecretion of aldosteroneThe increase in systemic blood pressure is caused by arteriolar vasoconstriction. Vasopressin stimulates water reabsorption in the kidneys as well as the thirst sensation. In the distal convoluted tubules and collecting ducts, aldosterone causes the reabsorption of sodium and water from the urine in exchange for potassium secretion. As a result, ACE inhibitors lower systemic blood pressure while also causing hyperkalaemia.Angiotensin-converting enzyme inhibitors (ACE inhibitors) are used in a variety of clinical settings, including heart failure. According to a meta-analysis, ACE inhibitors reduce death, MI, and overall admission in patients with heart failure by 28%.ACE inhibitors are also used in the following clinical settings:HypertensionChronic kidney diseaseDiabetic nephropathy Following a myocardial infarctionIn the presence of renal artery stenosis, ACE inhibitors are contraindicated because they can cause or exacerbate renal failure.The most common side effect of ACE inhibitors is a dry cough caused by increased bradykinin production. There is, however, no known link to fibrosis of the lungs.

Fluid filtration out of the capillaries is usually slightly greater than fluid absorption into the capillaries. About 8 L of fluid per day is filtered by the microcirculation and returns to the circulation by the lymphatic system. Lymphatic capillaries drain into collecting lymphatics, then into larger lymphatic vessels. Both of these containing smooth muscle and unidirectional valves. From this point, lymph is propelled by smooth muscle constriction and vessel compression by body movements into afferent lymphatics. It then goes to the lymph nodes where phagocytes remove bacteria and foreign materials. It is here that most fluid is reabsorbed by capillaries, and the remainder returns to the subclavian veins via efferent lymphatics and the thoracic duct. The lymphatic system has a major role to play in the body’s immune defence and also has a very important role in the absorption and transportation of fats.

The two heads of the flexor pollicis brevis usually differ in their innervation. The superficial head of flexor pollicis muscle receives nervous supply from the recurrent branch of the median nerve, whereas the deep head receives innervation from the deep branch of the ulnar nerve, derived from spinal roots C8 and T1.

Facial nerve palsy can result in inability to close the eye due to paralysis of the orbicularis oculi muscle. Elevation of the eyelid in eye opening is a function of the levator palpebrae superioris muscle and the superior tarsal muscle, innervated by the oculomotor nerve and the sympathetic chain respectively.

There are three types of muscle:Skeletal muscleCardiac muscleSmooth muscleIndividual muscle is enveloped in a layer of dense irregular connective tissue called the epimysium. The epimysium protects the muscles from friction against bones and other muscles.Skeletal muscle is composed of muscle fibres, referred to as myofibers which is ensheathed by a wispy layer of areolar connective tissue called the endomysium. The endomysium is the smallest and deepest component of muscle connective tissue. Myofibers grouped together in bundles form fascicles, or fasciculi. These are surrounded by a type of connective tissue called the perimysium.Beneath the endomysium lies the sarcolemma, an elastic sheath with infoldings that invaginate the interior of the myofibers, particularly at the motor endplate of the neuromuscular junction.

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.Iatrogenic corticosteroid injection is the most prevalent cause of Cushing’s syndrome. Cushing’s illness is the second most prevalent cause of Cushing’s syndrome. Cushing’s disease is distinct from Cushing’s syndrome in that it refers to a single cause of the illness, a pituitary adenoma that secretes high quantities of ACTH, which raises cortisol levels.Cushing’s syndrome has several endogenous sources, including:Cushing’s disease is caused by a pituitary adenoma.Adrenal adenoma Ectopic corticotropin syndrome, e.g. small cell cancer of the lungAdrenal carcinoma is a cancer of the adrenal gland.Hyperplasia of the adrenal glands

The most common type of adult leukaemia is chronic lymphocytic leukaemia (CLL). It develops as a result of relatively mature lymphocytes clonally proliferating. The B-cell lineage accounts for approximately 95% of cases. CLL is primarily a disease of adult men, with men over the age of 50 accounting for more than 75% of CLL patients.It is the most indolent form of chronic leukaemia, and it is frequently discovered by chance when blood counts are taken for other reasons, such as ‘well man’ screening tests. The patient may develop lymphadenopathy, hepatosplenomegaly, anaemia, and infections as the disease progresses.The following are examples of CLL laboratory findings:Clonal B cell lymphocytosis (diagnosed at greater than 5 x 109/l, but can reach 300 x 109/l)In advanced disease, normocytic, normochromic anaemia is present.Patients with autoimmune-related haemolytic anaemias have a positive direct antiglobulin test (DAT).Although bone marrow aspiration is not always required, it can aid in the diagnosis of CLL. If there has been rapid lymph node enlargement, a lymph node biopsy is required to rule out Richter’s syndrome. This is the transition from low-grade lymphoma to high-grade lymphoma, which is characterised by fever, weight loss, and pain.Although there is no cure for CLL, it can be managed with chemotherapy regimens that help patients live longer. Early treatment has no benefit, and the standard treatment for early disease is to watch and wait, with examinations and blood counts every 3 to 12 months. Chemotherapy is usually reserved for patients who have a disease that is active and causing symptoms.The following is the overall prognosis for CLL:1/3 will not require treatment and will live a long time.1/3 will go through an indolent phase before the disease progresses.1/3 of patients will have an aggressive disease that requires immediate treatment.

Graves disease is the most common cause of hyperthyroidism. It is an autoimmune disease in which autoantibodies against TSH receptors are produced. These antibodies bind to and stimulate these TSH receptors leading to an excess production of thyroid hormones. Therefore, the signs and symptoms of Graves disease are the same as those of hyperthyroidism, reflecting the actions of increased circulating levels of thyroid hormones: increased heat production, weight loss, increased 02 consumption and cardiac output and exophthalmos (bulging eyes, not drooping eyelids). TSH levels will be decreased (not increased) as a result of the negative feedback effect of increased T3 levels on the anterior pituitary.