Hyperkalaemia causes a rapid reduction in resting membrane potential leading to increased cardiac depolarisation and muscle excitability. This in turn results in ECG changes which can rapidly progress to ventricular fibrillation or asystole. Very distinctive ECG changes that progressively change as the K+level increases:
K+>5.5 mmol/l – peaked T waves (usually earliest sign of hyperkalaemia), repolarisation abnormalities
K+>6.5 mmol/l – P waves widen and flatten, PR segment lengthens, P waves eventually disappear
K+>7.0 mmol/l – Prolonged QRS interval and bizarre QRS morphology, conduction blocks (bundle branch blocks, fascicular blocks), sinus bradycardia or slow AF, development of a sine wave appearance (a pre-terminal rhythm)
K+>9.0 mmol/l – Cardiac arrest due to asystole, VF or PEA with a bizarre, wide complex rhythm.

Antibodies:
Neutralise toxins and prevent attachment of pathogens
Target, opsonise or agglutinate (clump together) antigens for phagocytosis
Activate the complement cascade (leading to lysis or opsonisation of the pathogen)
Act as antigen receptors on B lymphocytes
Activate antibody-dependent cell-mediated cytotoxicity by natural killer (NK) cells or T cytotoxic cells
Provide mucosal immunity (IgA-mediated)
Stimulate degranulation of mast cells (IgE and IgG mediated)
Provide passive immunity to the newborn (through transplacental passage of IgG and secretion of IgA in breast milk)

Thumb abduction is mediated by the abductor pollicis longus and brevis, which are innervated by the radial and median nerves, respectively.

Cardiac myocytes contract by excitation-contraction coupling, just like skeletal myocytes. Heart myocytes, on the other hand, utilise a calcium-induced calcium release mechanism that is unique to cardiac muscle (CICR). The influx of calcium ions (Ca2+) into the cell causes a ‘calcium spark,’ which causes more ions to be released into the cytoplasm.

An influx of sodium ions induces an initial depolarisation, much as it does in skeletal muscle; however, in cardiac muscle, the inflow of Ca2+ sustains the depolarisation, allowing it to remain longer. Due to potassium ion (K+) inflow, CICR causes a plateau phase in which the cells remain depolarized for a short time before repolarizing. Skeletal muscle, on the other hand, repolarizes almost instantly.

The release of Ca2+ from the sarcoplasmic reticulum is required for calcium-induced calcium release (CICR). This is mostly accomplished by ryanodine receptors (RyR) on the sarcoplasmic reticulum membrane; Ca2+ binds to RyR, causing additional Ca2+ to be released.

Meta-analysis is a quantitative, formal, epidemiological study design used to systematically assess previous research studies to derive conclusions about that body of research. Outcomes from a meta-analysis may include a more precise estimate of the effect of treatment or risk factor for disease, or other outcomes, than any individual study contributing to the pooled analysis. The examination of variability or heterogeneity in study results is also a critical outcome.
The benefits of meta-analysis include a consolidated and quantitative review of a large, and often complex, sometimes apparently conflicting, body of literature. The specification of the outcome and hypotheses that are tested is critical to the conduct of meta-analyses, as is a sensitive literature search.

Important medical questions are typically studied more than once, often by different research teams in different locations. In many instances, the results of these multiple small studies of an issue are diverse and conflicting, which makes the clinical decision-making difficult. The need to arrive at decisions affecting clinical practise fostered the momentum toward evidence-based medicine. Evidence-based medicine may be defined as the systematic, quantitative, preferentially experimental approach to obtaining and using medical information. Therefore, meta-analysis, a statistical procedure that integrates the results of several independent studies, plays a central role in evidence-based medicine.

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 nerve

2. Optic nerve (II)
Manifested by visual field defects, pupillary abnormalities, optic neuritis, optic atrophy, papilledema

3. 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 muscles

12.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.

Damage to the deep fibular nerve results in loss of dorsiflexion of the ankle, with resultant foot drop with high-stepping gait, loss of toe extension, weakness of foot inversion and loss of sensation over the webspace between the 1st and 2nd toes.

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.

Pronator quadratus is a small, square-shaped muscle that lies in the anterior compartment of the forearm. It arises from the distal fourth of the anterior surface of the ulna and inserts into the distal fourth of the anterior surface of the radius.
Pronator quadratus is innervated by the anterior interosseous nerve. It receives its blood supply from the anterior interosseous artery, which is a branch of the common interosseous artery, which in turn is a branch of the ulnar artery.
The main action of pronator quadratus is to assist pronator teres with pronation of the forearm. The deep fibres bind the radius and ulna together.
The pronator quadratus muscle highlighted in blue (adapted from Gray’s Anatomy)

Calcium-channel blockers, also known as calcium antagonists, stop calcium from entering cells through the L-type calcium channel. This causes vascular smooth muscle in vessel walls to relax, resulting in a decrease in peripheral vascular resistance.
They can be used for a variety of things, including:
Hypertension
Angina
Atrial fibrillation
Migraine

Calcium-channel blockers can be divided into two categories: dihydropyridines and non-dihydropyridines. The basic chemical structure of these two classes differs, as does their relative selectivity for cardiac versus vascular L-type calcium channels.

Dihydropyridines have a high vascular selectivity and lower systemic vascular resistance and blood pressure. As a result, they’re frequently used to treat hypertension. Modified release formulations are also used to treat angina, but their powerful systemic vasodilator and pressure-lowering effects can cause reflex cardiac stimulation, resulting in increased inotropy and tachycardia, which can counteract the beneficial effects of reduced afterload on myocardial oxygen demand.

The suffix -dpine distinguishes dihydropyridines from other pyridines. Examples of dihydropyridines that are commonly prescribed include:
Amlodipine
Felodipine
Nifedipine
Nimodipine

The phenylalkylamine class and the benzothiazepine class are two subgroups of non-dihydropyridines.

Phenylalkylamines are less effective as systemic vasodilators because they are relatively selective for the myocardium. This group of drugs lowers myocardial oxygen demand and reverses coronary vasospasm, making them useful in the treatment of angina. They are also occasionally used to treat arrhythmias. A phenylalkylamine calcium-channel blocker like verapamil is an example.

In terms of selectivity for vascular calcium channels, benzothiazepines fall somewhere between dihydropyridines and phenylalkylamines. They can lower arterial pressure without producing the same level of reflex cardiac stimulation as dihydropyridines because they have both cardiac depressant and vasodilator effects. Diltiazem is the only benzothiazepine currently in clinical use.