Neutropenia is defined as a total neutrophil count of < 2.0 x 109/l.
It can be caused by:
Viral infections
Collagen disease e.g. SLE and RA
Chemotherapy and radiotherapy
Hypersplenism
Marrow infiltration
Vitamin and folate deficiency
Drug reactions
Drugs that cause neutropenia include flecainide, phenytoin, carbimazole, indomethacin and co-trimoxazole.

The administration of oxygen to a patient before intubation is called pre-oxygenation and it helps extend the ‘safe apnoea time’.

The Functional residual capacity (FRC) is the volume of gas that remains in the lungs after normal tidal expiration. It is the most important store of oxygen in the body. The aim of pre-oxygenation is to replace the nitrogen in the FRC with oxygen.

Apnoea can be tolerated for longer periods before critical hypoxia develops if the FRC is large. Patients with reduced FRC reach critical hypoxia more rapidly.

ACTH secretion is stimulated by corticotropin-releasing hormone (CRH) from the hypothalamus.

Klebsiella spp. are facultatively anaerobic Gram-negative rods, found in the normal intestinal and respiratory flora. These organisms are usually opportunistic pathogens that cause nosocomial infections, most commonly pneumonia and UTI.

The parietal cells operate in close association with another type of cell called enterochromaffin-like cells (ECL cells), the primary function of which is to secrete histamine. The ECL cells lie in the deep recesses of the oxyntic glands and therefore release histamine indirect contact with the parietal cells of the glands.

CD8+ T-cells (Cytotoxic T cells)
Recognise antigen only in association with HLA Class I molecules (found on all nucleated cells; present endogenous antigens such as those found in cells infected by viruses or intracellular bacteria.)
Comprise about 25% of peripheral T-cells
Responsible for cytotoxic killing of target cells

The common peroneal nerve often referred to as the common fibular nerve, is a major nerve that innervates the lower extremity. It is one of the two major branches off the sciatic nerve and receives fibres from the posterior divisions of L4 through S2 nerve roots. The common peroneal nerve separates from the sciatic nerve in the distal posterior thigh proximal to the popliteal fossa. After branching off of the sciatic nerve, it continues down the thigh, running posteroinferior to the biceps femoris muscle, and crosses laterally to the head of the lateral gastrocnemius muscle through the posterior intermuscular septum. The nerve then curves around the fibular neck before dividing into two branches, the superficial peroneal nerve (SPN) and the deep peroneal nerve (DPN). The common peroneal nerve does not have any motor innervation before dividing; however, it provides sensory innervation to the lateral leg via the lateral sural nerve.

The superficial peroneal nerve innervates the lateral compartment of the leg, and the deep peroneal nerve innervates the anterior compartment of the leg and the dorsum of the foot. These two nerves are essential in the eversion of the foot and dorsiflexion of the foot, respectively. The superficial and deep peroneal nerves provide both motor and sensory innervation.

The most common presentation with common peroneal nerve injury or palsy is acute foot drop, although symptoms may be progressive and can include sensory loss or pain. Weakness in foot eversion may occur if the superficial peroneal nerve component is involved.

Atropine 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 atropine 500 mcg IV:
Shock
Syncope
Myocardial ischemia
Insufficiency of the heart

If this does not work, give additional 500 mcg doses at 3-5 minute intervals until a maximum dose of 3 mg is reached. The heart rate can be slowed paradoxically if the dose is higher than 3 mg.

The ALS bradycardia algorithm also suggests the following interim measures:
Transcutaneous pacing
Isoprenaline infusion 5 mcg/min
Adrenaline infusion 2-10 mcg/minutes
Alternative drugs (aminophylline, dopamine, glucagon, glycopyrrolate)

In order for primary active transport to pump ions against their electrochemical gradient, chemical energy is used in the form of ATP. The Na+/K+-ATPase antiporter pump uses metabolic energy to move 3 Na+ions out of the cell for every 2 K+ions in, against their respective electrochemical gradients. As a result, the cell the maintains a high intracellular concentration of K+ions and a low concentration of Na+ions.

Clearance of a substance can provide an accurate estimate of the glomerular filtration rate (GFR) provided that the substance is:freely filterednot reabsorbed in the nephronnot secreted in the nephronnot synthesised or metabolised by the kidney

Angina pectoris is the most common symptom of ischemic heart disease and presents with chest pain relieved by rest and nitro-glycerine.

Nitrates are the first-line treatment to relieve chest pain caused by angina. The commonly used nitrates are:
1. Nitro-glycerine (NTG) – angina pectoris (treatment/prophylaxis), acute coronary syndrome, heart failure, hypertension
2. Isosorbide mononitrate (ISMN) – chronic angina pectoris (treatment)
3. Isosorbide dinitrate (ISDN) – angina pectoris (treatment/prophylaxis)

The nitrate drugs cause vasodilation via the action of nitric oxide.

The contraindications to the use of nitrate are the following:
1. Allergy to nitrates
2. Concomitant use of phosphodiesterases (PDE) inhibitors such as tadalafil and sildenafil
3. Right ventricular infarction
4. Hypertrophic cardiomyopathy
5. Cardiac tamponade
6. Constrictive pericarditis
7. Hypotensive conditions
8. Hypovolaemia
9. Marked anaemia
10. Mitral stenosis
11. Raised intracranial pressure due to cerebral haemorrhage or head trauma
12. Toxic pulmonary oedema

At rest, saliva is predominantly produced by the submandibular gland (65%) but when stimulated, the parotid glands produce a higher proportion of the total saliva production (50%) than at rest. Saliva is alkaline and hypotonic to plasma. The predominant digestive enzymes in saliva are alpha-amylase and lingual lipase; lingual lipase is not functionally very important, but alpha-amylase is important for the initiation of starch digestion. Saliva production is decreased by inhibition of the parasympathetic nervous system e.g. by sleep, dehydration, anticholinergic drugs and fear.

Atrial natriuretic peptide (ANP) is released from cardiac atrial muscle cells in response to atrial stretch caused by an increase in intravascular fluid volume and is also produced in collecting duct cells.
Atrial natriuretic peptide acts to inhibit sodium reabsorption in the distal nephron.

Glucagon is a peptide hormone that is produced and secreted by alpha cells of the islets of Langerhans, which are located in the endocrine portion of the pancreas. The main physiological role of glucagon is to stimulate hepatic glucose output, thereby leading to increases in glycaemia. It provides the major counter-regulatory mechanism to insulin in maintaining glucose homeostasis.
Hypoglycaemia is the principal stimulus for the secretion of glucagon but may also be used as an antidote in beta-blocker overdose and in anaphylaxis in patients on beta-blockers that fail to respond to adrenaline.
Glucagon then causes:
Glycogenolysis
Gluconeogenesis
Lipolysis in adipose tissue
The secretion of glucagon is also stimulated by:
Adrenaline
Cholecystokinin
Arginine
Alanine
Acetylcholine
The secretion of glucagon is inhibited by:
Insulin
Somatostatin
Increased free fatty acids
Increased urea production

Glycolysis is the metabolic pathway that converts glucose into pyruvate. The free energy released by this process is used to form ATP and NADH. Glycolysis is inhibited by glucagon, and glycolysis and gluconeogenesis are reciprocally regulated so that when one cell pathway is activated, the other is inactive and vice versa.

Glucagon has a minor effect of enhancing lipolysis in adipose tissue. Lipolysis is the breakdown of lipids and involves the hydrolysis of triglycerides into glycerol and free fatty acids. It makes fatty acids available for oxidation.

The glenohumeral joint possesses the capability of allowing an extreme range of motion in multiple planes.

Flexion – Defined as bringing the upper limb anterior in the sagittal plane. The usual range of motion is 180 degrees. The main flexors of the shoulder are the anterior deltoid, coracobrachialis, and pectoralis major. Biceps brachii also weakly assists in this action.

Extension—Defined as bringing the upper limb posterior in a sagittal plane. The normal range of motion is 45 to 60 degrees. The main extensors of the shoulder are the posterior deltoid, latissimus dorsi, and teres major.

Internal rotation—Defined as rotation toward the midline along a vertical axis. The normal range of motion is 70 to 90 degrees. The internal rotation muscles are the subscapularis, pectoralis major, latissimus dorsi, teres major, and the anterior aspect of the deltoid.

External rotation – Defined as rotation away from the midline along a vertical axis. The normal range of motion is 90 degrees. Primarily infraspinatus and teres minor are responsible for the motion.

Adduction – Defined as bringing the upper limb towards the midline in the coronal plane. Pectoralis major, latissimus dorsi, and teres major are the muscles primarily responsible for shoulder adduction.

Abduction – Defined as bringing the upper limb away from the midline in the coronal plane. The normal range of motion is 150 degrees. Due to the ability to differentiate several pathologies by the range of motion of the glenohumeral joint in this plane of motion, it is essential to understand how different muscles contribute to this action.

Myeloma laboratory findings include:
– The presence of a paraprotein in serum or urine (the paraprotein is IgG in 60 percent of cases, IgA in 20 percent, and light chain only in almost all the rest),
– Increased serum immunoglobulin-free light chain proteins generated by plasma cells but not coupled with heavy chains 
– Reduced IgG, IgA, and IgM levels in the blood (immune paresis)
– Anaemia, whether normochromic, normocytic, or macrocytic. 
– On a blood film, a Rouleaux formation has been marked.
– In advanced illness, neutropenia and thrombocytopenia are common.
– ESR is high.
– Plasma cells in the bone marrow are overabundant, typically in aberrant forms. – Hypercalcemia
– Creatinine levels are high.
– Serum albumin levels are low in advanced illness.
60 percent of patients have osteolytic lesions, osteoporosis, or pathological fractures.

The quadriceps femoris muscle translates to “four-headed muscle” from Latin. It bears this name because it consists of four individual muscles; rectus femoris, vastus medialis, vastus lateralis, and vastus intermedius. Out of all four muscles, only the rectus femoris crosses both the hip and knee joints. The others cross only the knee joint. These muscles differ in their origin, but share a common quadriceps femoris tendon which inserts into the patella. The function of the quadriceps femoris muscle is to extend the leg at the knee joint and to flex the thigh at the hip joint.

Cates Plot, since 1999, has been used to create visual representations to communicate the risks and benefits of treatments. The essence of Cates Plot is the use of 4 face categories to visually indicate the following:

People not affected by a treatment (green faces for those with a good outcome and red for those with a bad outcome)
People for which treatment changes their category from a bad outcome to a good outcome (yellow faces)
People for which treatment causes an adverse event and changes their category from a good outcome to a bad outcome (crossed out green faces)

A lesion at the optic chiasm will result in a bitemporal hemianopia.
A lesion of the optic nerve will result in ipsilateral monocular visual loss.
A lesion of the optic tract will result in a contralateral homonymous hemianopia.

Theophylline and Ethylenediamine are combined in a 2:1 ratio to form Aminophylline. Its solubility is improved by the addition of Ethylenediamine. It has a lower potency and a shorter duration of action than Theophylline.
It is used to treat the following conditions:
Heart failure
It is used to treat the following conditions:
COPD
Bradycardias

Aminophylline has the following properties:
Phosphodiesterase inhibitor that increases intracellular cAMP and relaxes smooth muscle in the bronchial airways and pulmonary blood vessels.
Mast cell stabilization is achieved by using a non-selective adenosine receptor antagonist.
It has slight positive inotropic and chronotropic effects, increasing cardiac output and decreasing systemic vascular resistance, lowering arterial blood pressure. It has been used historically in the treatment of refractory heart failure and is indicated by the current ALS guidelines as a substitute treatment for bradycardia.

The daily oral dose for adults is 900 mg, divided into 2-3 doses. For severe asthma or COPD, a loading dosage of 5 mg/kg over 10-20 minutes is given, followed by a continuous infusion of 0.5 mg/kg/hour. The therapeutic range is small (10-20 microgram/ml), hence assessments of aminophylline plasma concentrations are useful during long-term treatment.

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.

There are three types of muscle:
Skeletal muscle
Cardiac muscle
Smooth muscle

Individual 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.

Weber syndrome is a midbrain stroke characterized by crossed hemiplegia along with oculomotor nerve deficits and it occurs with the occlusion of the median and/or paramedian perforating branches of the basilar artery.

Typical clinical findings include ipsilateral CN III palsy, ptosis, and mydriasis (such as damage to parasympathetic fibres of CN III) with contralateral hemiplegia.

Acromioclavicular joint injuries account for more than forty percent of all shoulder injuries. Mild injuries are not associated with any significant morbidity, but severe injuries can lead to significant loss of strength and function of the shoulder. Acromioclavicular injuries may be associated with a fractured clavicle, impingement syndromes, and more rarely neurovascular insults.

The AC joint is a diarthrodial joint defined by the lateral process of the clavicle articulating with the acromion process as it projects anteriorly off the scapula. The joint is primarily stabilized by the acromioclavicular ligament, which is composed of an anterior, posterior, inferior, and superior component. Of note, the superior portion of the AC ligament is the most important component for the stability of the AC joint. Supporting structures include two coracoclavicular ligaments (trapezoid and conoid ligaments), which provide vertical stability, as well as the coracoacromial ligament.

Patients with an AC joint injury typically present with anterosuperior shoulder pain and will describe a mechanism of injury of blunt trauma to the abducted shoulder or landing on an outstretched arm, suggestive of this type of injury. They may describe pain radiating to the neck or shoulder, which is often worse with movement or when they try to sleep on the affected shoulder. On examination, the clinician may observe swelling, bruising, or a deformity of the AC joint, depending on the degree of injury. The patient will be tender at that location. They may have a restriction in the active and passive range of motion secondary to pain. Piano key sign may be seen, with an elevation of the clavicle that rebounds after inferior compression.

Standard X-rays are adequate to make a diagnosis of acromioclavicular joint injury and should be used to evaluate for other causes of traumatic shoulder pain.

Mitochondrial diseases are a group of disorders caused by dysfunctional mitochondria. Most cases are maternally inherited, as we inherit our mitochondrial DNA from our mothers only, although mutations in nuclear DNA cause some cases.

Examples of Mitochondrial Diseases include:
1. Mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes (MELAS)
2. Mitochondrial epilepsy with ragged red fibres (MERRF)
3. Leber’s hereditary optic neuropathy (LHON)
4. Diabetes mellitus and deafness (DAD)
5. Neuropathy, ataxia, retinitis pigmentosa, and ptosis (NARP)
6. Leigh syndrome (subacute sclerosing encephalopathy).

Red-green colour blindness and G6PD deficiency have an X-linked recessive pattern of inheritance.

Tay-Sachs Disease and spinal muscular atrophy have an autosomal recessive pattern of inheritance.

The purine nucleoside adenosine is used to diagnose and treat paroxysmal supraventricular tachycardia. Adenosine works by stimulating A1-adenosine receptors and opening potassium channels that are sensitive to acetylcholine. This causes the atrioventricular (AV) node’s cell membrane to become hyperpolarized, slowing conduction by inhibiting calcium channels.
Patients who have had a heart transplant are extremely sensitive to the effects of adenosine and should start with a lower dose of 3 mg, then 6 mg, and finally 12 mg.

Dipyridamole potentiates the effects of adenosine, so it should be used with caution in patients who are taking it.

The use of adenosine is contraindicated in the following situations:
Asthma
COPD (chronic obstructive pulmonary disease)
Decompensated heart failure 
Long QT syndrome
AV block in the second or third degree
Sinusitis is a condition in which the sinuses become (unless pacemaker fitted)
Hypotension that is severe

Second line drugs to reduce the severity and duration of anaphylactic symptoms are intravenous or intramuscular chlorpheniramine and hydrocortisone. The recommended dose is 10 mg chlorpheniramine and 200 mg hydrocortisone in adults.

Healthcare-associated bacteraemia is most commonly caused by intravenous access. Any intravenous device that is left in place for a long time increases the risk of infection. It allows bacteria like Staphylococcus aureus and Staphylococcus epidermidis to enter the body.

High-dose inhaled short-acting beta2-agonists are the first line treatment for acute asthma(salbutamol or terbutaline). Oxygen should only been given to hypoxaemic patients (to maintain oxygen saturations of 94 – 98%). A pressurised metered dose inhaler with spacer device is preferred in patients with moderate to severe asthma (4 puffs initially, followed by 2 puffs every 2 minutes according to response, up to 10 puffs, whole process repeated every 10 – 20 minutes if necessary). The oxygen-driven nebuliser route is recommended for patients with life-threatening features or poorly responsive severe asthma (salbutamol 5 mg at 15 – 30 minute intervals). Continuous nebulisation should be considered in patients with severe acute asthma that is poorly responsive to initial bolus dose (salbutamol at 5 – 10 mg/hour) The intravenous route should be reserved for those in whom inhaled therapy cannot be used reliably.

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.

Patellar dislocation is a disabling musculoskeletal disorder which predominantly affects younger people who are engaged in multidirectional physically active pursuits. Conservative (non-operative) treatment is the treatment of choice for FTPD (first time patellar dislocation). Quadriceps strengthening exercises are considered one of the principal management aims for people following FTPD. A United Kingdom (UK) survey of physiotherapy practice has shown that quadriceps strengthening and specific-vastus medialis obliquus (VMO) or distal vastus medialis (VM) muscle strengthening or recruitment exercises were two of the most frequently used interventions for this population. Specific VM exercises are favoured in some quarters based on the assumption that the VM has an important role in preventing excessive lateral patellar translation.

The endocervix is the most common site of Neisseria gonorrhoeae infection in women. Symptoms of infection, when present, include dysuria, cervical discharge, and lower abdominal pain. However, 50% of cases in women may be asymptomatic leading to complications such as pelvic inflammatory disease (PID), which may cause sterility, ectopic pregnancy, or perihepatitis.

PID is also known as Fitz-Hugh-Curtis syndrome is defined as an inflammation of the upper genital tract due to an infection in women. The disease affects the uterus, fallopian tubes, and ovaries. It is typically an ascending infection, spreading from the lower genital tract.

The recommended intramuscular or oral regimens for PID are as follows:

Ceftriaxone at 500 mg IM in a single dose (for persons weighing ≥150 kg, administer 1 g of ceftriaxone); plus doxycycline at 100 mg PO BID for 14 days with metronidazole at 500 mg PO BID for 14 days.

Only about 2% of asthma attacks requires intubation and most severe cases are managed with non-invasive ventilation techniques.

Though life-saving in the crashing asthmatic, intubation in asthmatic patients is associated with significant morbidity and mortality and is risky. Indications for intubation in asthmatic patients include:
Severe hypoxia
Altered mental state
Respiratory or cardiac arrest
Failure to respond to medications

Ketamine (1-2 mg/kg) is the preferred induction agent. It has bronchodilatory properties and does not cause hypotension.

Propofol poses a risk of hypotension but can also be used.

Dietary fat is chiefly composed of triglycerides. In the duodenum fat is emulsified by bile acids, a process where larger lipid droplets are broken down into much smaller droplets providing a greater surface area for enzymatic digestion. Once inside the epithelial cell, lipid is taken into the smooth endoplasmic reticulum where much of it is re esterified. Dietary and synthesised lipids are then incorporated into chylomicrons in the Golgi body, which are exocytosed from the basolateral membrane to enter lacteals. Chylomicrons consist mainly of triglyceride with small amounts of cholesterol and cholesteryl esters in the centre with a phospholipid coat studded with apolipoproteins. Fat-soluble are absorbed into enterocytes from micelles by simple diffusion together with the products of fat digestion.

Dopamine is a catecholamine that occurs naturally and is used to treat low cardiac output, septic shock, and renal failure. It is both adrenaline and noradrenaline’s immediate precursor.

Dopamine acts on D1 and D2 dopamine receptors in the renal, mesenteric, and coronary beds at low doses (1-5 g/kg/min). Dopamine causes a significant decrease in renal vascular resistance and an increase in renal blood flow at these doses. Within this dose range, it is also involved in central modulation of behaviour and movement.

Dopamine stimulates beta- and alpha-adrenergic receptors directly and indirectly at higher doses. Beta-stimulation predominates at a rate of 5-10 g/kg/min, resulting in a positive inotropic effect that increases cardiac output and coronary blood flow. Alpha-stimulation predominates at infusion rates greater than 15 g/kg/min, resulting in peripheral vasoconstriction and an increase in venous return and systolic blood pressure.

Below is a summary of the mechanisms and effects of various inotropic agents:
Inotrope
Mechanism
Effects
Adrenaline (epinephrine)
Beta-1 and -2 agonist at increasing doses;
Alpha-agonist at high doses
Increased cardiac output;
Vasoconstriction at higher doses
Noradrenaline (norepinephrine)
Mainly alpha-agonist;
Beta-1 and -2 agonist at increasing doses
Vasoconstriction;
Some increased cardiac output
Dopamine
Dopamine agonist at low doses;
Beta-1 and -2 agonist at increasing doses;
Alpha-agonist at high doses
Increased cardiac output;
Vasoconstriction at higher doses
Dobutamine
Mainly beta-1 agonist
Increased cardiac output

Because the middles of the shafts of the ribs are lower than either the anterior or posterior end, elevation of the ribs also moves the middles of the shafts laterally. This ‘bucket handle’ upwards and lateral movement increases the lateral dimensions of the thorax.

Inguinal hernias can present with an array of different symptoms. Most patients present with a bulge in the groin area, or pain in the groin. Some will describe the pain or bulge that gets worse with physical activity or coughing. Symptoms may include a burning or pinching sensation in the groin. These sensations can radiate into the scrotum or down the leg. It is important to perform a thorough physical and history to rule out other causes of groin pain. At times an inguinal hernia can present with severe pain or obstructive symptoms caused by incarceration or strangulation of the hernia sac contents. A proper physical exam is essential in the diagnosis of an inguinal hernia. Physical examination is the best way to diagnose a hernia. The exam is best performed with the patient standing. Visual inspection of the inguinal area is conducted first to rule out obvious bulges or asymmetry in groin or scrotum. Next, the examiner palpates over the groin and scrotum to detect the presence of a hernia. The palpation of the inguinal canal is completed last. The examiner palpates through the scrotum and towards the external inguinal ring. The patient is then instructed to cough or perform a Valsalva manoeuvre. If a hernia is present, the examiner will be able to palpate a bulge that moves in and out as the patient increases intra abdominal pressure through coughing or Valsalva.

Groin hernias are categorized into 2 main categories: inguinal and femoral.

Inguinal hernias are further subdivided into direct and indirect. An indirect hernia occurs when abdominal contents protrude through the internal inguinal ring and into the inguinal canal. This occurs lateral to the inferior epigastric vessels. The hernia contents may extend into the scrotum, and can be reduced superiorly then superolaterally. A direct inguinal hernia is protrusion of abdominal contents through the transversalis fascia within Hesselbach’s triangle. The borders of Hesselbach’s triangle are the inferior epigastric vessels superolaterally, the rectus sheath medially, and inguinal ligament inferiorly.

A femoral hernia is a protrusion into the femoral ring. The borders of the femoral ring are the femoral vein laterally, Cooper’s ligament posteriorly, the iliopubic tract/inguinal ligament anteriorly and lacunar ligament medially.

Opponens digiti minimi (ODM) is an intrinsic muscle of the hand. It’s a triangular muscle that extends between the hamate bone (carpal bone) and the 5th metacarpal bone. It forms the hypothenar muscle group together with the abductor digiti minimi and flexor digiti minimi brevis, based on the medial side of the palm (hypothenar eminence). These muscles act together in moving the little finger. The opponens digiti minimi is responsible for flexion, lateral rotation and opposition of the little finger.
Its origin is the hook of hamate and flexor retinaculum. It inserts into the medial border of 5th metacarpal bone. It is innervated by the deep branch of the ulnar nerve, which stems from the brachial plexus (C8, T1 spinal nerves).
Its blood supply is by the deep palmar branch of ulnar artery and deep palmar arch, which is the terminal branch of the radial artery.

Cushing’s syndrome is a group of symptoms and signs brought on by long-term exposure to high amounts of endogenous or exogenous glucocorticoids.

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.

Because cortisol enhances the vasoconstrictive impact of endogenous adrenaline, patients with Cushing’s syndrome are usually hypertensive.

Hyperglycaemia (due to insulin resistance) rather than hypoglycaemia is a common symptom.
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 throughout the 24-hour period. In the morning, levels may be normal, but they may be high at night-time, when they are generally repressed.

A dexamethasone suppression test or a 24-hour urine free cortisol collection can both be used to establish the existence of Cushing’s syndrome.

Elevation of the eyeball is produced by the superior rectus and the inferior oblique muscles.

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.

A history of stroke and poor nutritional status points towards a nutritional deficiency as the most likely cause of her symptoms. The examination would differentiate between Vitamin B12 and Folic acid deficiency as in the former. The patient has a beefy red tongue and symptoms indicating peripheral nervous system involvement or subacute combined spinal cord degeneration. The patient may also have a lemon-yellow skin colour, loss of proprioception and vibratory sense and oral ulceration.

Investigations in B12 deficiency can reveal the following:
1. Macrocytic anaemia
2. Neutropoenia
3. Thrombocytopaenia
4. Blood film: anisocytosis, poikilocytosis
5. Low serum B12
6. Raised serum bilirubin (haemolysis)
7. Intrinsic factor antibodies
8. Positive Schilling test

Medial medullary syndrome is a form of stroke that affects the medial medulla of the brain. It is caused by a lesion in the medial part of the medulla, which is due to an infraction of vertebral arteries and/or paramedian branches of the anterior spinal artery.

It is characterized by contralateral paralysis of the upper and lower limb of the body, a contralateral decrease in proprioception, vibration, and/or fine touch sensation, paresthesias or less commonly dysesthesias in the contralateral trunk and lower limb, and loss of position and vibration sense with proprioceptive dysfunction. Ipsilateral deviation of the tongue due to ipsilateral hypoglossal nerve damage can also be seen.

A risk ratio of 1 indicates no difference in risk between groups.If the risk ratio of an event is > 1, the rate of that event is increased in the exposed group compared to the control group.If the risk ratio is < 1, the rate of that event is reduced in the exposed group compared to the control group.

Warfarin is teratogenic and can cause a host of abnormalities in the growing foetus. These include hypoplasia of the nasal bridge, stippling of the epiphyses, multiple ophthalmic complications, growth retardation, pectus carinatum, atrial septal defect, ventriculomegaly and a patent ductus arteriosus.

The following drugs have been linked to impaired glucose tolerance:
Thiazide diuretics, e.g. Bendroflumethiazide
Loop diuretics, e.g. furosemide
Steroids, e.g. prednisolone
Beta-blockers, e.g. atenolol

Flecainide inhibits the transmembrane influx of extracellular Na+ ions via fast channels on cardiac tissues resulting in a decrease in rate of depolarisation of the action potential, prolonging the PR and QRS intervals. At high concentrations, it exerts inhibitory effects on slow Ca2+ channels, accompanied by moderate negative inotropic effect.

A way to help remember the structures transected by the transverse thoracic plane is CLAPTRAP:
C: cardiac plexus
L: ligamentum arteriosum
A: aortic arch (inner concavity)
P: pulmonary trunk
T: tracheal bifurcation (carina)
R: right-to-left movement of the thoracic duct (posterior to the oesophagus)
A: azygos vein drains into superior vena cava
P: pre-vertebral fascia and pre-tracheal fascia end

Beta-blockers may reduce the response to adrenaline in the treatment of anaphylactic reactions.

Noncardioselective beta-blockers in particular can antagonize the broncho dilating and cardio stimulatory effects of adrenaline by blocking beta-2 adrenergic receptors in the smooth muscles of the bronchial tree and in the heart muscles.

Approximately one-third of patients who suffer DVT or PE have an identifiable heritable risk factor, although additional risk factors are usually present when they develop the thrombosis. The history of a spontaneous DVT in a close relative increases an individual’s risk of DVT even if no known genetic predisposition can be identified.