Gentamicin, an aminoglycoside antibiotic, acts by binding to the 30S subunit of the bacterial ribosome inhibiting the binding of aminoacyl-tRNA, and thus prevents initiation of protein synthesis.

Two of its most notable side effects are reversible nephrotoxicity(caused by the inhibition of protein synthesis in renal cells, which causes acute tubular necrosis) and hearing loss (caused by damage to the vestibular apparatus of the inner ear).

Both side effects are dose-related and occur commonly in the elderly.

A median nerve block is a simple, safe, and effective method of obtaining anaesthesia to the palmar aspect of the thumb, index finger, middle finger, radial portion of the palm and ring finger. The median nerve lies deep to the flexor retinaculum and about one centimetre under the skin of the volar wrist.
The palmaris longus tendon lies superficial to the retinaculum and is absent in up to 20% of patients.
The median nerve is located slightly lateral (radial) to the palmaris longus tendon and medial (ulnar) to the flexor carpi radialis tendon.

The procedure is as follows:
– Check sensation and motor function of the median nerve. Wear gloves and use appropriate barrier precautions.
– Locate the flexor carpi radialis and palmaris longus tendons, which become prominent when the patient flexes the wrist against resistance. The palmaris longus tendon is usually the more prominent of the two tendons.
– Needle-entry site: The needle will be inserted adjacent to the radial (lateral) border of the palmaris longus tendon just proximal to the proximal wrist crease. If the palmaris longus tendon is absent, the needle-entry site is about 1 cm ulnar to the flexor carpi radialis tendon.
– Cleanse the site with antiseptic solution. Place a skin wheal of anaesthetic, if one is being used, at the needle-entry site.
– Insert the needle perpendicularly through the skin and advance it slowly until a slight pop is felt as the needle penetrates the flexor retinaculum. When paraesthesia in the distribution of the median nerve confirms proper needle placement, withdraw the needle 1 to 2 mm.
– Aspirate to exclude intravascular placement and then slowly (i.e., over 30 to 60 seconds) inject about 3 mL of anaesthetic. If the patient does not feel paraesthesia, redirect the needle in an ulnar direction, under the palmaris longus tendon. If paraesthesia is still not felt, slowly inject 3 to 5 mL of anaesthetic in the proximity of the nerve 1 cm deep to the tendon.
– Allow about 5 to 10 minutes for the anaesthetic to take effect.

Lithium is the drug of choice for bipolar disorders but is commonly associated with side effects and toxicity.

Fine hand tremor is very commonly seen and reported in as many as 50% of patients during the first week of therapy with Lithium. The tremor tends to reduce with time and is only present in around 5% of patients taking the medication two years or longer. Lithium tremors are more common with older age, presumably due to the additive effects of age-related essential tremors.

Option The normal therapeutic range is 2.0-2.5 mmol/l: Lithium should be carefully monitored as it has a very low therapeutic index. The normal therapeutic range is 0.4-0.8 mmol/l. Levels should be checked one week after starting therapy and one week after every change in dosage. (Option Levels should be checked one month after starting therapy)

Option It can induce hyperthyroidism: Lithium has a known effect on thyroid function. Lithium decreases the production of T4 and T3 and commonly causes hypothyroidism. More rarely, lithium causes hyperthyroidism due to thyroiditis.

Option It can induce diabetes mellitus: Lithium can induce nephrogenic diabetes insipidus but not diabetes mellitus.

Avulsion fractures of the fibular head are rare and are so-called the arcuate signal. The “arcuate signal” is used to describe an avulsed bone fragment related to the insertion site of the tendon of the biceps femoris associated with the arcuate complex, which consists of the fabellofibular, popliteofibular, and arcuate ligaments. Such lesions are typically observed in direct trauma to the knee with excessive varus and internal rotation forces or indirect trauma with the same direction of the force.

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
Of the muscles listed in the options, only the anterior scalene is situated within the posterior triangle of the neck.

Bordetella pertussis is a Gram negative coccobacillus that causes whooping cough. B. pertussis is spread via the respiratory droplet route and expresses fimbriae that aid their adhesion to the ciliated epithelium of the upper respiratory tract, and produce a number of exotoxins, causing the characteristic thickened bronchial secretions, paralysis of cilia and lymphocytosis.

Glanzmann’s thromboasthenia is a rare platelet disorder in which platelets contain defective or low levels of glycoprotein IIb/IIIa.

Acetaminophen is an acetanilide derivative and is a widely used non-prescription analgesic and antipyretic medication for mild-to-moderate pain and fever.

The route of elimination: Paracetamol is metabolised extensively in the liver and excreted in the urine mainly as inactive glucuronide and sulfate conjugates, <5% is excreted as free (unconjugated) acetaminophen, and >90% of the dose administered is excreted within 24 hours.

It is thought to work by selectively inhibiting COX-1 receptors in the brain and spinal cord: It is categorized by the FDA as an NSAID as it is believed to selectively inhibit cyclo-oxygenase 3 (COX-3) receptors in the brain and spinal cord.

COX-3 is a unique variant of the more known COX-1 and COX-2. It is responsible for the production of prostaglandins in central areas, which sensitizes free nerve endings to the chemical mediators of pain. Therefore, by selectively inhibiting COX-3, paracetamol effectively reduces pain sensation by increasing the pain threshold.

Toxicity is primarily due to glutathione production: Acetaminophen metabolism by the CYP2E1 pathway releases a toxic metabolite known as N-acetyl-p-benzoquinoneimine (NAPQI). NAPQI primarily contributes to the toxic effects of acetaminophen. NAPQI is an intermediate metabolite that is further metabolized by fast conjugation with glutathione. The conjugated metabolite is then excreted in the urine as mercapturic acid. High doses of acetaminophen (overdoses) can lead to hepatic necrosis due to depleting glutathione and high binding levels of reactive metabolite (NAPQI) to important parts of liver cells.

Acetaminophen can be administered orally, rectally, or intravenously. It is predominantly metabolized in the liver, and the elimination half-life is 1-3 hours after a therapeutic dose. But maybe greater than 12 hours after an overdose.

It is primarily metabolized via the cytochrome p450 enzyme system: It is predominantly metabolized in the liver by three main metabolic pathways:
1. Glucuronidation (45-55%)
2. Sulphate conjugation (30-35%)
3. N-hydroxylation via the hepatic cytochrome p450 enzyme system (10-15%)

The risk of mortality in the control group (usual therapy) minus the risk of death in the treatment group equals the absolute risk reduction (ARR) of treatment.
30/1000 minus 10/1000 = 20/1000 = 0.02

NNT = 1/ARR = 1/0.02 = 50
As a result, 50 people would need to be treated in order to prevent one additional fatality, and 500 people would need to be treated in order to avoid 10 additional deaths.

ADH, or antidiuretic hormone, is a hormone that regulates water and electrolyte balance. It is released in response to a variety of events, the most important of which are higher plasma osmolality or lower blood pressure. ADH increases plasma volume and blood pressure via acting on the kidneys and peripheral vasculature.

It causes vasoconstriction by binding to peripheral V1 Receptors on vascular smooth muscle via the IP3 signal transduction and Rho-kinase pathways. The systemic vascular resistance and arterial pressure rise as a result. High levels of ADH appear to be required for this to have a major impact on arterial pressure, such as in hypovolaemic shock.

Because the anatomical position of the penis is erect, the paired corpora cavernosa are defined as dorsal in the body of the penis and the single corpus spongiosum as ventral. The nerves and vessels lie superficial to the corpus cavernosum. The urethra lies within the corpus spongiosum.

Listeria monocytogenes is a gram-positive bacteria that does not produce spores.

Staphylococcus aureus is a gram-positive bacteria, while Candida albicans is a gram-positive yeast with a single bud.

Among the choices, gram-negative bacteria include only Klebsiella pneumoniae and Pseudomonas aeruginosa.

Pseudomonas aeruginosa is an oxidase-positive bacterium, while Klebsiella pneumoniae is an oxidase-negative bacterium.

P. aeruginosa can cause urinary tract infections (UTIs) and is spread through poor hygiene or contaminated medical equipment or devices, such as catheters that haven’t been fully sterilized.

Nitric oxide (NO) production by the endothelium is increased by factors that elevate intracellular Ca2+, including local mediators such as bradykinin, histamine and serotonin, and some neurotransmitters (e.g. substance P). Increased flow (shear stress) also stimulates NO production and additionally activates prostacyclin synthesis. The basal production of NO continuously modulates vascular resistance; increased production of nitric oxide acts to cause vasodilation. Nitric oxide also inhibits platelet activation and thrombosis.

ADH binds V2 receptors on renal principal cells in the late distal tubule and collecting ducts, raising cAMP levels and causing intracellular vesicles to fuse with the apical membrane. In their membrane these vesicles have water channels called aquaporins, which increase the water permeability allowing greater water reabsorption and concentration of urine. ADH also binds to V1 receptor receptors on vascular smooth muscle, causing vasoconstriction and enhancing the effect of aldosterone on sodium reabsorption in the distal tubule. ADH release is stimulated primarily by raised plasma osmolality detected by osmoreceptors in the anterior hypothalamus. Other factors that increase ADH release include: extracellular fluid volume depletion, angiotensin II, nausea, pain, stress, exercise, emotion, hypoglycaemia. ADH release is inhibited by low plasma osmolality, alcohol, caffeine, glucocorticoids and atrial natriuretic peptide (ANP). ADH deficiency (or an inadequate response to ADH) results in diabetes insipidus. Excess levels of ADH results in syndrome of inappropriate ADH secretion (SIADH).

A median nerve injury affecting the extrinsic and intrinsic muscles of the hand will present with:

Loss of sensation to the lateral palm and the lateral three and a half fingers.

Weakness of flexion at the metacarpophalangeal joints of the index and middle finger. This is because of paralysis of the lateral two lumbricals.

Weakness of flexion of the proximal interphalangeal joints of all four fingers due to paralysis of the flexor digitorum superficialis

Weakness of flexion at the distal interphalangeal joints of the index and middle finger following paralysis of the lateral half of the flexor digitorum profundus.
Weakness of thumb flexion, abduction and opposition due to paralysis of the flexor pollicis longus and thenar muscles

Ipratropium bromide is an antimuscarinic drug used in the management of acute asthma and COPD. It can provide short-term relief in chronic asthma, but short-acting β2agonists act more quickly and are preferred.

The BTS guidelines recommend that nebulised ipratropium bromide (0.5 mg 4-6 hourly) can be added to β2agonist treatment for patients with acute severe or life-threatening asthma or those with a poor initial response to β2 agonist therapy.
The aerosol inhalation of ipratropium can be used for short-term relief in mild chronic obstructive pulmonary disease in patients who are not already using a long-acting antimuscarinic drug (e.g. tiotropium).

Its maximum effect occurs 30-60 minutes after use; its duration of action is 3-6 hours, and bronchodilation can usually be maintained with treatment three times per day.
The commonest side effect of ipratropium bromide is dry mouth. It can also trigger acute closed-angle glaucoma in susceptible patients. Tremor is commonly seen with β2agonists but not with antimuscarinics. Ipratropium bromide should be used with caution in: Men with prostatic hyperplasia and bladder-outflow obstruction (worsened urinary retention has been reported in elderly men), People with chronic kidney disease (CKD) stages 3 and above (because of the risk of drug toxicity), People with angle-closure glaucoma (nebulised mist of antimuscarinic drugs can precipitate or worsen acute angle-closure glaucoma)

Mucus contains chemicals such as alpha-1-antitrypsin, lysozyme, and IgA that protect the airway from pathogens and damaging proteases released from dead bacteria and immune cells. Early-onset emphysema results from a genetic deficit of alpha-1-antitrypsin, which is caused by unregulated protease activity in the lungs, which results in the degradation of elastin in the alveoli.

Mannitol is an osmotic diuretic that stops the absorption of water throughout the tubule, thus increasing the osmolality of both glomerular and tubular fluid. It is used to:
1. decrease intraocular pressure in glaucoma
2. decrease intracerebral pressure
3. oliguria.

Furosemide is a loop diuretic that inhibits the Na/K/2Cl transported in the ascending limb of the Loop of Henle.

Bendroflumethiazide is a thiazide diuretic which inhibits the Na/Cl transporter.

Spironolactone is a potassium-sparing diuretic that acts as an aldosterone receptor antagonist.

Acetazolamide is a carbonic anhydrase inhibitor.

An action potential is a self-propagating response, successive depolarisation moving along each segment of an unmyelinated nerve until it reaches the end. It is all-or-nothing and does not decrease in size. Conduction in myelinated fibres is much faster, up to 50 times that of the fastest unmyelinated nerve. Myelinated fibres are insulated except at areas devoid of myelin called nodes of Ranvier. The depolarisation jumps from one node of Ranvier to another by a process called saltatory conduction. Saltatory conduction not only increases the velocity of impulse transmission but also conserves energy for the axon because depolarisation only occurs at the nodes and not along the whole length of the nerve fibre. Larger diameter myelinated nerve fibres conduct nerve impulses faster than small unmyelinated nerve fibres.

HBsAg is the serological hallmark of HBV infection. After an acute exposure to HBV, HBsAg appears in serum within 1 to 10 weeks. Persistence of this marker for more than 6 months implies chronic HBV infection.

Anti-HBs is known as a neutralizing antibody, and confers long-term immunity. In patients with acquired immunity through vaccination, anti-HBs is the only serological marker detected in serum.

HBcAg is an intracellular presence in infected hepatocyte, thus it is not identified in the serum. During acute infection, anti-HBc IgM and IgG emerges 1–2 weeks after the presence of HBsAg along with raised serum aminotransferase and symptoms. After 6 months of acute infection, anti-HBc IgM wears off. Anti-HBc IgG continues to detect in both patients with resolved HBV infection and chronic hepatitis B.

Hepatitis D virus, also known as the delta hepatitis virus, is a defective ssRNA virus that requires HBV for replication. The infection can occur in one of two clinical forms, co-infection or superinfection. In a co-infection, the patient is simultaneously infected with HBV and HDV. In a superinfection, an HDV infection develops in a patient with a chronic HBV infection.

Serum concentrations of the p24 antigen are usually high in the first few weeks after human immunodeficiency virus (HIV) infection and testing for p24 antigen is therefore a useful way of diagnosing very early infection. P24 is the viral protein that makes up most of the core of the HIV.

ELISA and other antibody tests, though a very sensitive way of detecting the presence of HIV, cannot be used in the early stages of the disease. This is because of the window period of 6-12 weeks before antibodies are produced. These tests will be negative during a seroconversion illness.

The ‘rapid HIV test’ is an HIV antibody test. It will also be negative during the ‘window period’ since it takes time for antibodies to be produced. It is called the ‘rapid test’ as it can detect antibodies in blood or saliva much quicker than the other antibody tests and results are often back within 20 minutes.

CD4 and CD8 counts are usually normal in the early stages of the HIV infection and cannot be used in this case.

Somatostatin-producing cells present in the pyloric antrum, duodenum, and pancreatic islets are known as D-cells or delta-cells. Somatostatin inhibits gastric acid secretion by acting directly on acid-producing parietal cells in the stomach via a G-protein coupled receptor.

Somatostatin affects hormones in the following ways:
Inhibits the anterior pituitary’s secretion of growth hormone.
Inhibits the anterior pituitary’s secretion of thyroid-stimulating hormone.

The secretion of various gastrointestinal hormones is inhibited (including gastrin, CCK, secretin, motilin, VIP and GIP)

Reduces the rate at which the stomach empties.
Inhibits the release of insulin and glucagon from the pancreas.

The pancreas’ exocrine secretory activity is inhibited.
Somatostatin can also slow the digestive process by suppressing the production of hormones such gastrin, secretin, and histamine, which reduces gastric acid secretion.

A somatostatinoma is a cancerous tumour of the endocrine pancreas’ D-cells, which make somatostatin. Somatostatin inhibits pancreatic and gastrointestinal hormones when levels are high. The following clinical characteristics are related with somatostatinomas:

Insulin secretion blockage causes diabetes mellitus.
Gallstones by inhibition of CCK and secretin Steatorrhoea via inhibition of CCK and secretin

Hypochlorhydria is caused by the suppression of gastrin, a hormone that increases gastric acid output regularly.

Compliance changes at different lung volumes. Initially at lower lung volumes the compliance of the lung is poor and greater pressure change is required to cause a change in volume. This occurs if the lungs become collapsed for a period of time. At functional residual capacity (FRC) compliance is optimal since the elastic recoil of the lung tending towards collapse is balanced by the tendency of the chest wall to spring outwards. At higher lung volumes the compliance of the lung again becomes less as the lung becomes stiffer. At all volumes, the base of the lung has a greater compliance than the apex. Patients with emphysema have increased compliance. Compliance is affected by a person’s age, sex and height.

Functional hyposplenism is characterised by the blood film findings of Howell-Jolly bodies or siderotic granules on iron staining. The most frequent cause is surgical removal of the spleen e.g. after traumatic rupture, but hyposplenism can also occur in sickle cell anaemia, gluten-induced enteropathy, amyloidosis and other conditions.

Fibrinolytic drugs act as thrombolytics by activating plasminogen to form plasmin, which degrades fibrin and so breaks up thrombi.

A scatterplot is a useful summary of a set of bivariate data (two variables), usually drawn before working out a linear correlation coefficient or fitting a regression line. It gives a good visual picture of the relationship between the two variables, and aids the interpretation of the correlation coefficient or regression model. Each unit contributes one point to the scatterplot, on which points are plotted but not joined. The resulting pattern indicates the type and strength of the relationship between the two variables.

Iliacus is innervated by the femoral nerve.

Propofol is a short-acting anaesthetic that is thought to work by potentiating GABA and glycine. It induces anterograde amnesia and anaesthetic effects and is used to induce anaesthesia, outpatient surgeries and preoperative sedation. The dose for induction of anaesthesia is 1.5-2.5mg/kg. The dose for maintenance of anaesthesia is 4-12 mg/kg/hour. Following intravenous injection, propofol acts within 30 seconds and its duration of action is 5-10 minutes.

Propofol produces a 15-25% decrease in blood pressure and systemic vascular resistance without a compensatory increase in heart rate. It is negatively inotropic and decreases cardiac output by approximately 20%.

The main side effects of propofol are:
Pain on injection (in up to 30%)
Hypotension
Transient apnoea
Hyperventilation
Coughing and hiccough
Headache
Thrombosis and phlebitis

Since the introduction of the HIB vaccine, most cases of acute epiglottitis are now caused by Streptococcus spp. The condition is now rare in children.

The mean incubation period for P. falciparum is 12 days.

WHO World Malaria Report 2019 states that an estimated 228 million cases of malaria occurred worldwide in 2018, and reports steadily decreasing the number of cases since 2010. In 2018, nineteen sub-Saharan African countries and India carried approximately 85% of the global malaria burden. The most prevalent and pathogenic malaria parasite, most commonly associated with severe illness and death, especially in the WHO African region, accounting for 99.7% malaria cases, is P. falciparum.

The vector for Plasmodium spp. is a female Anopheles mosquito that inoculates sporozoites contained in her salivary glands into the puncture wound when feeding. Sporozoites enter peripheral bloodstream and are uptake by hepatocytes, where they undergo an asexual pre-erythrocytic liver-stage as liver schizonts lasting up to 2 weeks before the onset of the blood stage.

Intravenous or intramuscular artesunate is the first-line treatment in all patients worldwide and should be used for at least 24 hours and until the oral medication is tolerated.