Lidocaine is a tertiary amine that is primarily used as a local anaesthetic but can also be used intravenously in the treatment of ventricular dysrhythmias.
Lidocaine works as a local anaesthetic by diffusing in its uncharged base form through neural sheaths and the axonal membrane to the internal surface of the cell membrane sodium channels. Here it alters signal conduction by blocking the fast voltage-gated sodium channels. With sufficient blockage, the membrane of the postsynaptic neuron will not depolarise and will be unable to transmit an action potential, thereby preventing the transmission of pain signals.
Each 1 ml of plain 1% lidocaine solution contains 10 mg of lidocaine hydrochloride. The maximum safe dose of plain lidocaine is 3 mg/kg. When administered with adrenaline 1:200,000, the maximum safe dose is 7 mg/kg. Because of the risk of vasoconstriction and tissue necrosis, lidocaine should not be used in combination with adrenaline in extremities such as fingers, toes, and the nose.
The half-life of lidocaine is 1.5-2 hours. Its onset of action is rapid within a few minutes, and it has a duration of action of 30-60 minutes when used alone. Its duration of action is prolonged by co-administration with adrenaline (about 90 minutes).
Lidocaine tends to cause vasodilatation when used locally. This is believed to be due mainly to the inhibition of action potentials via sodium channel blocking in vasoconstrictor sympathetic nerves.

Passive inspiration is produced by contraction of the diaphragm (depressing the diaphragm) and the external intercostal muscles (elevating the ribs). In inspiration, elevation of the sternal ends of the ribs (‘pump handle’ movement), elevation of the lateral shafts of the ribs (‘bucket handle’ movement) and depression of the diaphragm result in expansion of the thorax in an anteroposterior, transverse and vertical direction respectively. This results in an increased intrathoracic volume and decreased intrathoracic pressure and thus air is drawn into the lungs.

Penicillins and the other ß-lactam antibiotics are bactericidal. They produce their antimicrobial action by preventing cross-linkage between the linear peptidoglycan polymer chains that make up the bacterial cell wall. They, therefore, inhibit cell wall synthesis.
The integrity of the ß-lactam ring is essential for antimicrobial activity. Many bacteria (including most Staphylococci) are resistant to benzylpenicillin and phenoxymethylpenicillin because they produce enzymes (penicillinases, ß-lactamases) that open the ß-lactam ring.

Propofol has some antiemetic properties. It’s for this reason that it’s used to treat postoperative nausea and vomiting. Propofol is mostly processed in the liver, with the kidneys excreting just around 1% of it unaltered. Propofol, unlike thiopental, does not produce tissue necrosis when it is extravasated. Propofol lowers intracranial pressure via lowering brain metabolic rate and cerebral blood flow. Propofol is thought to be safe for people with bronchial asthma and chronic obstructive pulmonary disease.

About 25% of filtered sodium is reabsorbed in the the loop of Henle.

Transfusion-associated circulatory overload (TACO) presents as acute or worsening respiratory distress within 6 hours of transfusion of a large volume of blood. It is common in patients with diminished cardiac reserve or chronic anaemia. Elderly patients, infants and severely anaemic patients are particularly susceptible. Typical clinical features of TACO include: Acute respiratory distress, Tachycardia, Hypertension, Acute/worsening pulmonary oedema on chest X-ray. The BNP is usually raised to at least 1.5 times the pre-transfusion baseline.

Febrile transfusion reaction presents with a 1 degree rise in temperature from baseline during transfusion. Patient may have chills and malaise. It is the most common transfusion reaction (1 in 8 transfusions) and is usually caused by cytokines released from leukocytes in transfused red cell or platelet components.

TRALI (Transfusion Related Acute Lung Injury) is a clinical syndrome with abrupt onset of non-cardiogenic pulmonary oedema within 6 hours of transfusion not explained by another risk factor. Associated with the presence of antibodies in the donor blood to recipient leukocyte antigens. patients present with dyspnoea, hypertension, hypotension, acute leukopenia.

Graft versus host disease(GVHD) is an immune mediated condition that arises from a complex interaction between donor and recipients adaptive immunity. It presents as dermatitis, hepatitis and enteritis developing within 100 days after stem cell or bone marrow transplant.

Acute haemolytic reaction aka immediate haemolytic transfusion reaction presents with fever, chills, pain at transfusion site, nausea, vomiting, dark urine and feeling of ‘impending doom’. Often, it occurs due to ABO incompatibility.

Phyllocontin continus contains aminophylline (a mixture of theophylline and ethylenediamine), a bronchodilator used in the management of COPD and asthma.
This patient is exhibiting symptoms of theophylline toxicity, which may have been triggered by the prescription of the antibiotic. Quinolone antibiotics, such as ciprofloxacin and levofloxacin, and macrolide antibiotics, such as erythromycin, increase the plasma concentration of theophyllines and can lead to toxicity.
The drugs that commonly affect the half-life and the plasma concentration of theophylline are summarised in the table below:
Drugs increasing plasma concentration of theophylline
Drugs decreasing plasma concentration of theophylline
Calcium channel blockers, e.g. Verapamil
Cimetidine
Fluconazole
Macrolides, e.g. erythromycin
Quinolones, e.g. ciprofloxacin
Methotrexate
Barbiturates
Carbamazepine
Phenobarbitol
Phenytoin (and fosphenytoin)
Rifampicin
St. John’s wort

Aerosols are airborne particles less than 5 µm in size containing infective organisms.

They usually cause infection of both the upper and/or lower respiratory tract.

The organisms can remain suspended in the air for long periods and also survive outside the body.

They can be transmitted through the ventilation systems and can spread over great distances.

Some examples of organisms transmitted by the aerosol route include: Varicella zoster virus, Mycobacterium tuberculosis and measles virus

The stages of wound healing are: haemostasis, inflammatory, proliferative and remodelling (maturation) phases in that order. The first stage in the healing process of a laceration is haemostasis. Haemostasis is the process of the wound being closed by clotting.

The inflammatory phase occurs just after and up to 48 hours after injury– Blood vessels dilate to allow white blood cells, antibodies, growth factors, enzymes and nutrients to reach the wounded area leading to the characteristic signs of inflammation seen.

Epithelialisation and angiogenesis are not phases of wound healing but occur during the proliferative phase. This ia after haemolysis and inflammation phases have occurred.

The maturation phase is the final phase and occurs when the wound has closed. It involves remodelling of collagen from type III to type I. Apoptosis remove unwanted cells, cellular activity reduces and the number of blood vessels in the wounded area regresses and decreases. This can continues for up to 1 year after injury.

Cardiovascular effects such as flushing, tachycardia, hypotension and bronchospasm are associated with significant histamine release; histamine release can be minimised by administering slowly or in divided doses over at least 1 minute. Atracurium undergoes non-enzymatic metabolism which is independent of liver and kidney function, thus allowing its use in patients with hepatic or renal impairment. Atracurium has no sedative or analgesic effects. All non-depolarising drugs should be used with care in patients suspected to be suffering with myasthenia gravis or myasthenic syndrome, as patients with these conditions are extremely sensitive to their effects and may require a reduction in dose.