Airflow obstruction according to the latest NICE guidelines, is defined as:

Mild airflow obstruction = an FEV 1 of >80% in the presence of symptoms

Moderate airflow obstruction = FEV 1 of 50-79%

Severe airflow obstruction = FEV 1 of 30-49%

Very severe airflow obstruction = FEV1<30%.

A daily calcium intake of 1,000 to 1,300 mg is advised for adults. Women have a slightly higher calcium need than men and are at a higher risk of developing osteoporosis as they age.

Calcium-rich foods include the following:
Milk, cheese, and butter as dairy products.
Broccoli, spinach, and green beans as green veggies.
Bread, rice, and cereals as whole grain foods.
Sardines, salmon, and other bony fish
Eggs
Nuts
The following foods have the least calcium:
Carrot
Fruits such as kiwis, raspberries, oranges, and papaya
Chicken and pork in meats.

1: 1000 Adrenaline solution dosage for children above the age of 12 and adults, including pregnant women (over 50 kg) is 0.50 mL, which is equivalent to 500 mcg of adrenaline.

B-cells (20% of lymphocytes) mature in the bone marrow and circulate in the peripheral blood until they undergo recognition of antigen. B-cell immunoglobulin molecules synthesised in the cell are exported and bound to the surface membrane to become the B-cell receptor (BCR) which can recognise and bind to a specific antigen (either free or presented by APCs). The BCR is also important for antigen internalisation, processing and presentation to T helper cells. Most antibody responses require help from antigen-specific T helper cells (although some antigens such as polysaccharide can lead to T-cell independent B-cell antibody production). When the B-cell is activated, the receptor itself is secreted as free soluble immunoglobulin and the B-cell matures into a memory B-cell or a plasma cell (a B-cell in its high-rate immunoglobulin secreting state). Plasma cells are non-motile and are found predominantly in the bone marrow or spleen. Most plasma cells are short-lived (1 – 2 weeks) but some may survive much longer. A proportion of B-cells persist as memory cells, whose increased number and rapid response underlies the augmented secondary response of the adaptive immune system.

In its typical anatomical orientation, the heart has 5 surfaces formed by different internal divisions of the heart:

Anterior (or sternocostal) – Right ventricle
Posterior (or base) – Left atrium
Inferior (or diaphragmatic) – Left and right ventricles
Right pulmonary – Right atrium
Left pulmonary – Left ventricle

The silhouette sign of Felson is with respect to the right middle lobe. The right heart border should have a distinct appearance due to the right atrium abutting aerated right middle lobe. The consolidation in the right middle lobe has resulted in loss of this silhouette.

The female Anopheles mosquito is the vector for Plasmodium falciparum transmission. Treponema pallidum is transmitted through sexual transmission or direct skin contact. Clostridium perfringens is spread by direct skin contact or through oral-faecal route. The oral-faecal pathway is how Vibrio cholerae spreads. Mycoplasma tuberculosis is spread via the airborne route.

Acetazolamide is a non-competitive, reversible inhibitor of carbonic anhydrase found in the cytosol of cells and on the brush border of the proximal convoluted tubule. Bicarbonate and hydrogen ions are converted to carbonic acid by carbonic anhydrase, which then converts carbonic acid to carbon dioxide and water. As a result, acetazolamide reduces the availability of hydrogen ions, causing sodium and bicarbonate ions to accumulate in the renal tubule, resulting in diuresis.
The mechanism of action of the various types of diuretics is summarised below:

1) Loop diuretics, e.g. furosemide, bumetanide
Act on the Na.K.2Cl co-transporters in the ascending loop of Henlé to inhibit sodium, chloride and potassium reabsorption.

2) Thiazide diuretics, e.g. Bendroflumethiazide, hydrochlorothiazide
Act on the Na.Cl co-transporter in the distal convoluted tubule to inhibit sodium and chloride reabsorption.

3) Osmotic diuretics, e.g. mannitol
Increases the osmolality of the glomerular filtrate and tubular fluid, increasing urinary volume by an osmotic effect.

4) Aldosterone antagonists, e.g. spironolactone
Acts in the distal convoluted tubule as a competitive aldosterone antagonist resulting in inhibition of sodium reabsorption and increasing potassium reabsorption.

5) Carbonic anhydrase inhibitors, e.g. acetazolamide
Inhibit the enzyme carbonic anhydrase preventing the conversion of bicarbonate and hydrogen ions into carbonic acid.

The adrenal glands produce too little steroid hormones, which causes Addison’s disease. The production of glucocorticoids, mineralocorticoids, and sex steroids are all altered. The most prevalent cause is autoimmune adrenalitis, which accounts for 70-80 percent of cases.

It affects more women than males and occurs most frequently between the ages of 30 and 50.

The following are some of the clinical signs and symptoms of Addison’s disease:

Weakness and sluggishness
Hypotension is a condition in which the blood pressure (notably orthostatic hypotension)
Vomiting and nausea
Loss of weight
Axillary and pubic hair loss
Depression
Hyperpigmentation is a condition in which a person’s (palmar creases, buccal mucosa and exposed areas more commonly affected)
The following are the classic biochemical hallmarks of Addison’s disease:
Hyponatraemia
Hyperkalaemia
Hypercalcaemia
Hypoglycaemia
Acidosis metabolica
When ACTH levels are combined with cortisol levels, it is possible to distinguish between primary and secondary adrenal insufficiency:
In primary insufficiency, levels rise.
In secondary insufficiency, levels are low or low normal.

The maximum daily dose of paracetamol in an adult is 4 grams. Doses greater than this can lead to hepatotoxicity and, less frequently, acute kidney injury. Early symptoms of paracetamol toxicity include nausea, vomiting, and abdominal pain, and usually settle within 24 hours. Symptoms of liver damage include right subcostal pain and tenderness, and this peaks 3 to 4 days after paracetamol ingestion. Other signs of hepatic toxicity include encephalopathy, bleeding, hypoglycaemia, and cerebral oedema.

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)

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

Amoxicillin and Ampicillin are more hydrophilic (broad-spectrum) penicillins than benzylpenicillin and phenoxymethylpenicillin. Because they may penetrate through gaps in the outer phospholipid membrane, they are effective against Gram-negative bacteria. Amoxicillin and Ampicillin are resistant to penicillinase-producing microbes.

Community-acquired pneumonia, otitis media, sinusitis, oral infections, and urinary tract infections are among the most prevalent conditions for which they are prescribed. The normal adult oral dose of Amoxicillin is 500 mg three times/day, which can be increased to 1 g three times/day if necessary. Ampicillin is given to adults in doses of 0.5-1 g every 6 hours.

Ketamine is the only anaesthetic agent available that has analgesic, hypnotic, and amnesic properties. When used correctly it is a very useful and versatile drug.
Ketamine acts by non-competitive antagonism of the NMDA receptor Ca2+ channel pore and also inhibits NMDA receptor activity by interaction with the phencyclidine binding site.
Ketamine can be used intravenously and intramuscularly. The intramuscular dose is 10 mg/kg, and when used by this route, it acts within 2-8 minutes and has a duration of action of 10-20 minutes. The intravenous dose is 1.5-2 mg/kg administered over a period of 60 seconds. When used intravenously, it acts within 30 seconds and has a duration of action of 5-10 minutes. Ketamine is also effective when administered orally, rectally, and nasally.
Ketamine causes tachycardia, an increase in blood pressure, central venous pressure, and cardiac output, secondary to an increase in sympathetic tone. Baroreceptor function is well maintained, and arrhythmias are uncommon.
The main disadvantage to the use of ketamine is the high incidence of hallucinations, nightmares, and other transient psychotic effects. These can be reduced by the co-administration of a benzodiazepine, such as diazepam or midazolam.
The main side effects of ketamine are:
Nausea and vomiting
Hypertension
Nystagmus
Diplopia
Rash

Primary hyperaldosteronism occurs when there are excessive levels of aldosterone independent of the renin-angiotensin axis. Secondary hyperaldosteronism occurs due to high renin levels.
The causes of primary hyperaldosteronism include:
Adrenal adenoma (Conn’s syndrome) – the most common cause of hyperaldosteronism (,80% of all cases). These are usually unilateral and solitary and are more common in women.
Adrenal hyperplasia – this accounts for ,15% of all cases. Usually, bilateral adrenal hyperplasia (BAH) but can be unilateral rarely. More common in men than women.
Adrenal cancer – a rare diagnosis but essential not to miss
Familial aldosteronism – a rare group of inherited conditions affecting the adrenal glands
The causes of secondary hyperaldosteronism include:
Drugs – diuretics
Obstructive renal artery disease – renal artery stenosis and atheroma
Renal vasoconstriction – occurs in accelerated hypertension
Oedematous disorders – heart failure, cirrhosis and nephrotic syndrome
Patients are often asymptomatic. When clinical features are present, the classically described presentation of hyperaldosteronism is with:
Hypertension
Hypokalaemia
Metabolic alkalosis
Sodium levels can be normal or slightly raised
Other, less common, clinical features include:
Lethargy
Headaches
Muscle weakness (from persistent hypokalaemia)
Polyuria and polydipsia
Intermittent paraesthesia
Tetany and paralysis (rare)
Often the earliest sign of hyperaldosteronism is from aberrant urea and electrolytes showing hypokalaemia and mild hypernatraemia. If the patient is taking diuretics, and the diagnosis is suspected, these should be repeated after the patient has taken off diuretics.
If the diagnosis is suspected, plasma renin and aldosterone levels should be checked. Low renin and high aldosterone levels (with a raised aldosterone: renin ratio) is suggestive of primary aldosteronism.
If the renin: aldosterone ratio is high, then the effect of posture on renin, aldosterone and cortisol can be investigated to provide further information about the underlying cause of primary hyperaldosteronism. Levels should be measured lying at 9 am and standing at noon:
If aldosterone and cortisol levels fall on standing, this is suggestive of an ACTH dependent cause, e.g. adrenal adenoma (Conn’s syndrome)
If aldosterone levels rise and cortisol levels fall on standing, this is suggestive of an angiotensin-II dependent cause, e.g. BAH
Other investigations that can help to distinguish between an adrenal adenoma and adrenal hyperplasia include:
CT scan
MRI scan
Selective adrenal venous sampling

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.

Abductor digiti minimi is a short intrinsic muscle of the hand. It belongs to the group of muscles collectively called hypothenar muscles due to their acting on the 5th finger. Besides abductor digiti minimi, other hypothenar muscles include flexor digiti minimi brevis and opponens digiti minimi.

The main function of abductor digiti minimi involves abduction of the 5th finger, as well as flexion of its proximal phalanx. Along with other hypothenar muscles, this muscle forms the hypothenar eminence on the medial side of the palm.

Like other hypothenar muscles, abductor digiti minimi receives nervous supply from the deep branch of the ulnar nerve, derived from root values C8 and T1.

Abductor digiti minimi receives arterial blood supply from the palmar branch of ulnar artery, palmar digital artery, as well as branches of the ulnar side of the superficial palmar arch. The venous blood from the muscle is drained via the venous networks of the palm into the deep veins of the arm (vv. ulnares).

Hypoglycaemia is defined as plasma glucose of less than 4 mmol/L.

Diverticulitis refers to inflammation and infection associated with a diverticulum and is estimated to occur in 10% to 25% of people with diverticulosis. Peridiverticular and pericolic infection results from a perforation (either macroscopic or microscopic) of a diverticulum, which leads to contamination, inflammation, and infection. The spectrum of disease ranges from mild, uncomplicated diverticulitis that can be treated in the outpatient setting, to free perforation and diffuse peritonitis that requires emergency laparotomy. Most patients present with left sided abdominal pain, with or without fever, and leucocytosis. The most common location for diverticulitis is the sigmoid colon.

A lesion of the parietal optic radiation will result in a contralateral homonymous inferior quadrantanopia.
A lesion of the temporal optic radiation will result in a contralateral homonymous superior quadrantanopia.

Benign enlargement of the prostate is common in men older than 50 years. The cause is possibly an imbalance in the hormonal control of the gland. The median lobe of the gland enlarges upward and encroaches within the sphincter vesicae, located at the neck of the bladder. The leakage of urine into the prostatic urethra causes an intense reflex desire to micturate. The enlargement of the median and lateral lobes of the gland produces elongation and lateral compression and distortion of the urethra so that the patient experiences difficulty in passing urine and the stream is weak. Back-pressure effects on the ureters and both kidneys are a common complication. The enlargement of the uvula vesicae (owing to the enlarged median lobe) results in the formation of a pouch of stagnant urine behind the urethral orifice within the bladder. The stagnant urine frequently becomes infected, and the inflamed bladder (cystitis) adds to the patient’s symptoms.

In all operations on the prostate, the surgeon regards the prostatic venous plexus with respect. The veins have thin walls, are valveless, and are drained by several large trunks directly into the internal iliac veins. Damage to these veins can result in a severe haemorrhage.