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.

Metronidazole and the other 5-nitroimidazole agents inhibit nucleic acid synthesis by forming toxic free radical metabolites in the bacterial cell that damage DNA.

Vancomycin inhibits cell wall peptidoglycan formation by binding the D-Ala-D-Ala portion of cell wall precursors.

Erythromycin inhibits protein synthesis and blocks translocation by binding to the 23S rRNA of the 50S ribosomal subunit.

Chloramphenicol blocks peptidyl transferase at 50S ribosomal subunit.

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

An overview of the different mechanisms of action of the various types of antimicrobial agents is shown below:
1. Inhibition of cell wall synthesis
– Penicillins
– Cephalosporins
– Vancomycin
2. Disruption of cell membrane function
– Polymyxins
– Nystatin
– Amphotericin B
3. Inhibition of protein synthesis
– Macrolides
– Aminoglycosides
– Tetracyclines
– Chloramphenicol
4. Inhibition of nucleic acid synthesis
– Quinolones
– Trimethoprim
– 5-nitroimidazoles
– Rifampicin
5. Anti-metabolic activity
– Sulphonamides
– Isoniazid

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 vasoconstriction
Cause 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 respectively
Stimulate the sensation of thirst
Potentiate sympathetic activity (positive feedback)
Inhibit renin production by granular cells (negative feedback)

Klebsiella is a Gram-negative, rod-shaped, non-motile bacteria. The absence of motility distinguishes Klebsiella spp. from most other members of the family Enterobacteriaceae.

K. pneumoniae is the most commonly isolated species and has the distinct feature of possessing a large polysaccharide capsule. The capsule offers the organism protection against phagocytosis and antimicrobial absorption,
contributing to its virulence.

Colonization of gram-negative bacilli in the respiratory tracts of hospitalized patients, particularly by K. pneumoniae, increases with the length of hospital stay. It is a frequent cause of lower respiratory tract infections among hospitalized patients and in immunocompromised hosts such as newborns,
elderly patients, and seriously ill patients on respirators.

Anaphylaxis can be triggered by any of a very broad range of triggers, but those most commonly identified include food, drugs, latex and venom. Of foods, nuts are the most common cause; muscle relaxants, antibiotics, NSAIDs and aspirin are the most commonly implicated drugs. Food is the commonest trigger in children and drugs the commonest in adults. A significant number of cases are idiopathic. Most reactions occur over several minutes; rarely, reactions may be slower in onset. The speed of onset of the reaction depends on the trigger e.g. intravenous medications will cause a more rapid onset than stings which in turn will cause a more rapid onset than ingestion of food.

A patient suffering from acute ischemic stroke can commonly present with hypertensive emergencies. Thrombolytic therapy is contraindicated in a patient with:
1. Systolic blood pressure greater than 185 mmHg
2. Diastolic blood pressure greater than 110 mmHg

But delaying thrombolytic therapy is associated with increased morbidity in patients with acute ischemic stroke.

Managing high blood pressure in acute ischemic stroke requires a slower and more controlled reduction in BP. In the presence of an ischaemic stroke, rapid reduction of MAP can compromise blood flow, causing further ischemia and worsening of the neurological deficit.

Intravenous labetalol is the agent of choice. The dose is 10 mg IV over 1-2 minutes. This dose can be repeated, or an infusion can be set up that runs at 2-8 mg/minute. Thrombolysis can be performed once the blood pressure is brought down to less than 180/105 mmHg.

A nitrate infusion (for example, Isoket) can be used as an alternative in patients with contraindications to the use of beta-blockers (e.g., asthma, heart block, cardiac failure).

M. tuberculosis is the causative agent of pulmonary tuberculosis (TB). The most commonly used diagnostic test for the diagnosis of pulmonary TB is the direct sputum smear microscopy (DSSM) wherein the presence of acid-fast bacilli (AFB) is tested.

The most common method is the hot method or also known as Ziehl-Neelsen method. This is a staining method special for Mycobacteria species because they are known to be acid-fast which means that they are not easily decolorized by acid alcohol. Once the DSSM tests positive for acid-fast bacilli, this indicates possible infection with tuberculosis. The gold standard for diagnosis is still culture but Mycobacteria species are slow-growers that is why DSSM is considered the best diagnostic method. A positive AFB smear and correlation with symptoms is usually used by physicians to create a final diagnosis of pulmonary tuberculosis.

Eosinophils comprise 1 – 3% of circulating white cells. Eosinophils are similar to neutrophils, except that the cytoplasmic granules are coarser and more deeply red staining, and there are rarely more than three nuclear lobes. They are less motile, but longer lived. They enter inflammatory exudates and have a special role in allergic responses, defence against parasites and removal of fibrin formed during inflammation. Thus they play a role in local immunity and tissue repair.

For hip extension, the gluteus maximus and hamstring muscles work together. To compensate for gluteus maximus weakness, the hamstring frequently acts as the primary hip extensor.

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%)