A posterior wall MI occurs when posterior myocardial tissue (now termed inferobasilar), usually supplied by the posterior descending artery — a branch of the right coronary artery in 80% of individuals — acutely loses blood supply due to intracoronary thrombosis in that vessel. This frequently coincides with an inferior wall MI due to the shared blood supply.

The ECG findings of an acute posterior wall MI include the following:

1. ST segment depression (not elevation) in the septal and anterior precordial leads (V1-V4). This occurs because these ECG leads will see the MI backwards; the leads are placed anteriorly, but the myocardial injury is posterior.
2. A R/S wave ratio greater than 1 in leads V1 or V2.
3. ST elevation in the posterior leads of a posterior ECG (leads V7-V9). Suspicion for a posterior MI must remain high, especially if inferior ST segment elevation is also present.
4. ST segment elevation in the inferior leads (II, III and aVF) if an inferior MI is also present.

The following ECG leads determine the location and vessels involved in myocardial infarction:

ECG Leads Location Vessel involved
V1-V2 Septal wall Left anterior descending
V3-V4 Anterior wall Left anterior descending
V5-V6 Lateral wall Left circumflex artery
II, III, aVF Inferior wall Right coronary artery (80%) or Left circumflex artery (20%)
I, aVL High lateral wall Left circumflex artery
V1, V4R Right ventricle Right coronary artery
V7-V9 Posterior wall Right coronary artery

Flexor carpi ulnaris is a fusiform muscle located in the anterior compartment of the forearm. It belongs to the superficial flexors of the forearm, along with pronator teres, palmaris longus, flexor digitorum superficialis and flexor carpi radialis. Flexor carpi ulnaris is the most medial of the superficial flexors.

Innervation of the flexor carpi ulnaris muscle is from the brachial plexus via the ulnar nerve (C7-T1).

Flexor carpi ulnaris receives its arterial blood supply via three different routes. Proximally, a branch of the posterior ulnar recurrent artery supplies the muscle as it passes between the humeral and ulnar heads. Branches of the ulnar artery supply the middle and distal parts of the muscle, with an accessory supply also present distally via the inferior ulnar collateral artery.

Due to its position and direction in the forearm, flexor carpi ulnaris can move the hand sideways as well as flexing it. Contracting with flexor carpi radialis and palmaris longus, flexor carpi ulnaris produces flexion of the hand at the wrist joint. However, when it contracts alongside the extensor carpi ulnaris muscle in the posterior compartment, their counteracting forces produce adduction of the hand at the wrist, otherwise known as ulnar deviation or ulnar flexion

Juxtaglomerular cells synthesise renin. These cells are specialised smooth muscle cells that are located in the walls of the afferent arterioles, and there are some in the efferent arterioles.

Codeine phosphate is a weak opioid and can be used for the relief of mild to moderate pain where other painkillers such as paracetamol or ibuprofen have proved ineffective.Codeine is metabolised to morphine which is responsible for its therapeutic effects. Codeine 240 mg is approximately equivalent to 30 mg of morphine. The capacity to metabolise codeine can vary considerably between individuals; there is a marked increase in morphine toxicity in people who are ultra rapid metabolisers, and reduced therapeutic effect in poor codeine metabolisers. Codeine is contraindicated in patients of any age who are known to be ultra-rapid metabolisers of codeine (CYP2D6 ultra-rapid metabolisers).Codeine is also contraindicated in children under 12, and in children of any age who undergo the removal of tonsils or adenoids for the treatment of obstructive sleep apnoea due to reports of morphine toxicity.

Hypothyroidism is diagnosed using the results of thyroid function tests (TFTs).

In the early stages of the disease, the earliest biochemical change noticed is a rise in thyroid-stimulating hormone (TSH) levels. Free triiodothyronine (T3) and thyroxine (T4) levels are usually normal.

In primary hypothyroidism, the serum TSH level is usually greater than 10 mU/L, and free T4 levels are below the reference range.

Subclinical hypothyroidism is diagnosed when the serum TSH level is above the reference range, and the free T4 levels are within the reference range. The test should, however, be repeated after 3-6 months to exclude transient causes of raised TSH.

In summary, how to interpret TFTs in cases of suspected hypothyroidism is shown below:

Subclinical hypothyroidism
TSH is raised
Free T4 is normal
Free T3 is normal

Primary hypothyroidism
TSH is raised
Free T4 is lowered
Free T3 is lowered or normal

Secondary hypothyroidism
TSH is lowered or normal
Free T4 is lowered
Free T3 is lowered or normal

Dynamic compression occurs because as the expiratory muscles contract during forced expiration, all the structures within the lungs, including the airways, are compressed by the positive intrapleural pressure. Consequently the smaller airways collapse before the alveoli empty completely and some air remains within the lungs (the residual volume). Physiologically this is important as a completely deflated lung with collapsed alveoli requires significantly more energy to inflate. Dynamic compression does not occur in normal expiration because the intrapleural pressure is negative throughout the whole cycle.

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

Meckel’s diverticulum has certain classic characteristics.
1. It lies on the antimesenteric border of the middle-to-distal ileum
2. It is approximately 2 feet proximal to the ileocaecal junction
3. It appears as a blind-ended tubular outpouching of bowel
4. It is about 2 inches long,
5. It occurs in about 2% of the population,
6. It may contain two types of ectopic tissue (gastric and pancreatic).
7. The diverticulum is supplied by the superior mesenteric artery.
8. Proximal to the major duodenal papilla the duodenum is supplied by the gastroduodenal artery (branch of the coeliac trunk)
9. Distal to the major duodenal papilla it is supplied by the inferior pancreaticoduodenal artery (branch of superior mesenteric artery).
10. The arterial supply to the jejunoileum is from the superior mesenteric artery.

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.

Insulin has a number of effects on glucose metabolism, including:
Inhibition of glycogenolysis and gluconeogenesis
Increased glucose transport into fat and muscle
Increased glycolysis in fat and muscle
Stimulation of glycogen synthesis
By inhibiting gluconeogenesis, insulin maintains the availability of amino acids as substrates for protein synthesis. Thus, insulin supports protein synthesis through direct and indirect mechanisms.

Laboratory results often show that:
PFA-100 test results are abnormal.
Low levels of factor VIII (if a factor VIII/VWF binding assay is conducted)
APTT is Prolonged (or normal)
PT is normal
VWF values are low.
Defective Platelet aggregation
The platelet count is normal.

Angiotensin-converting enzyme (ACE) inhibitors are the most common cause of drug-induced angioedema in the United Kingdom and the United States, owing to their widespread use.

Angioedema is caused by ACE inhibitors in 0.1 to 0.7 percent of patients, with data indicating a persistent and relatively constant risk year after year. People of African descent have a five-fold higher chance of contracting the disease.

Swelling of the lips, tongue, or face is the most common symptom, but another symptom is episodic abdominal pain due to intestinal angioedema. Itching and urticaria are noticeably absent.

The mechanism appears to be activated complement or other pro-inflammatory cytokines like prostaglandins and histamine, which cause rapid vasodilation and oedema.

Other medications that are less frequently linked to angioedema include:
Angiotensin-receptor blockers (ARBs)
Nonsteroidal anti-inflammatory drugs (NSAIDs)
Bupropion (e.g. Zyban and Wellbutrin)
Beta-lactam antibiotics
Statins
Proton pump inhibitors

The majority of these reactions are minor and can be treated by stopping the drug and prescribing antihistamines.

Elderly patients and children are more susceptible to side effects. Antihistamines are competitive inhibitors at the H1-receptor. The newer antihistamines e.g. cetirizine cause less sedation and psychomotor impairment than the older antihistamines because they are much less lipid soluble and penetrate the blood brain barrier only to a slight extent. Antihistamines are used as a second line adjunct to adrenaline in anaphylaxis.

Fick’s law tells us that the rate of diffusion of a gas increases:
the larger the surface area involved in gas exchange
the greater the partial pressure gradient across the membrane
the thinner the membrane
the more soluble the gas in the membrane
the lower the molecular weight of the gas

To avoid the spread of infection, infected patients should be isolated. All lesions should be crusted over before children return to nursery or school, even if the standard exclusion time is 5 days.

In order for primary active transport to pump ions against their electrochemical gradient, chemical energy is used in the form of ATP. This is facilitated by the Na+/K+-ATPase antiporter pump, which uses metabolic energy to move 3 Na+ions out of the cell for every 2 K+ions that come in, against their respective electrochemical gradients. As a result, the cell the maintains a high intracellular concentration of K+ions and a low concentration of Na+ions.

Bartter’s syndrome is an autosomal recessive renal tubular disorder characterized by hypokalaemia, hypochloraemia, metabolic alkalosis, and hyperreninemia with normal blood pressure. The underlying kidney abnormality results in excessive urinary losses of sodium, chloride, and potassium.

Bartter’s syndrome does not cause an elevated potassium level, but instead causes a decrease in its concentration (hypokalaemia). The other choices are causes of hyperkalaemia or elevated potassium levels.

Renal failure, Addison’s disease (adrenal insufficiency), congenital adrenal hyperplasia, renal tubular acidosis (type 4), rhabdomyolysis, burns and trauma, tumour syndrome, and acidosis are non-drug causes of hyperkalaemia. On the other hand, drugs that can cause hyperkalaemia include ACE inhibitors, angiotensin receptor blockers, NSAIDs, beta-blockers, digoxin, and suxamethonium.

Autosomal dominant polycystic kidney disease (ADPKD) presents with abdominal or loin discomfort due to the increasing size of the kidneys, acute loin pain with or without haematuria, hypertension, and male infertility. It is the most common cause of serious renal disease and the most common inherited cause of renal failure in adults.

Alport syndrome has hearing loss and eye abnormalities in addition to symptoms of kidney disease.

Renal cell carcinoma presents with additional features of unexplained weight loss, loss of appetite, fever of unknown origin and anaemia.

Most vasoconstrictors bind to G-protein coupled receptors. These mediate elevation in intracellular [Ca2+] which leads to vascular smooth muscle contraction. Important vasoconstrictors include noradrenaline, endothelin-1 and angiotensin II.

Increased intracellular Ca2+ is as a result of the release of Ca2+from the sarcoplasmic reticulum and depolarisation and entry of Ca2+via L-type voltage-gated Ca2+channels. Most types of vascular smooth muscle do not generate action potentials – instead, the depolarisation is graded, which allows graded entry of Ca2+.
sequestration by the sarcoplasmic reticulum Ca2+ATPase, removal from the cell by a plasma membrane Ca2+ATPase and Na+/Ca2+exchange decreases intracellular Ca2+, resulting in vasodilation. Relaxation is a result of most endogenous vasodilators when there is an increase in cyclic guanosine monophosphate (cGMP) like nitric oxide) or cyclic adenosine monophosphate (cAMP) like prostacyclin and beta-adrenergic receptor agonists. These activate protein kinases causing substrate level phosphorylation.
Clinically effective vasodilators are L-type Ca2+channel blocker drugs.

When you take too much aspirin, you have a mix of respiratory alkalosis and metabolic acidosis. Respiratory centre stimulation produces hyperventilation and respiratory alkalosis in the early phases. The direct acid actions of aspirin tend to create a higher anion gap metabolic acidosis in the latter phases.
Below summarizes some of the most common reasons of acid-base abnormalities:

Respiratory alkalosis:
– Hyperventilation (e.g. anxiety, pain, fever)
– Pulmonary embolism
– Pneumothorax
– CNS disorders (e.g. CVA, SAH, encephalitis)
– High altitude
– Pregnancy
– Early stages of aspirin overdose

Respiratory acidosis:
– COPD
– Life-threatening asthma
– Pulmonary oedema
– Respiratory depression (e.g. opiates, benzodiazepines)
– Neuromuscular disease (e.g. Guillain-Barré syndrome, muscular dystrophy
– Incorrect ventilator settings (hypoventilation)
– Obesity

Metabolic alkalosis:
– Vomiting
– Cardiac arrest
– Multi-organ failure
– Cystic fibrosis
– Potassium depletion (e.g. diuretic usage)
– Cushing’s syndrome
– Conn’s syndrome

Metabolic acidosis (with raised anion gap):
– Lactic acidosis (e.g. hypoxaemia, shock, sepsis, infarction)
– Ketoacidosis (e.g. diabetes, starvation, alcohol excess)
– Renal failure
– Poisoning (e.g. late stages of aspirin overdose, methanol, ethylene glycol)

Metabolic acidosis (with normal anion gap):
– Renal tubular acidosis
– Diarrhoea
– Ammonium chloride ingestion
– Adrenal insufficiency

Heart Sound – Phase of Cardiac Cycle – Mechanical Event:
First heart sound – Start of systole – Caused by closure of the atrioventricular (mitral & tricuspid) valves
Second heart sound – End of systole – Caused by closure of the semilunar (aortic and pulmonary) valves
Third heart sound – Early diastole – Caused by rapid flow of blood from the atria into the ventricles during the ventricular filling phase
Fourth heart sound – Late diastole – Caused by filling of an abnormally stiff ventricle in atrial systole

The following are the NICE guidelines on the management of bacterial conjunctivitis:
– Infective conjunctivitis is a self-limiting illness that usually settles without treatment within 1-2 weeks. If symptoms persist for longer than two weeks they should return for review.
– Seek medical attention urgently if marked eye pain or photophobia, loss of visual acuity, or marked redness of the eye develop.
– Remove contact lenses, if worn, until all symptoms and signs of infection have completely resolved and any treatment has been completed for 24 hours.
– Lubricant eye drops may reduce eye discomfort; these are available over the counter, as well as on prescription.
– Clean away infected secretions from eyelids and lashes with cotton wool soaked in water.
– Wash hands regularly, particularly after touching the eyes.
– Avoid sharing pillows and towels.
– It is not necessary to exclude a child from school or childcare if they have infective conjunctivitis, as mild infectious illnesses should not interrupt school attendance. An exception would be if there is an outbreak of infective conjunctivitis, when advice should be sought from the Health Protection Agency by the school.
– Adults who work in close contact with others, or with vulnerable patients, should avoid such contact until the discharge has settled.

The following structures are the layers of the anterior abdominal wall from the most superficial to the deepest layer:

Skin
Fatty layer of the superficial fascia (Camper’s fascia)
Membranous layer of the superficial fascia (Scarpa’s fascia)
Aponeurosis of the external and internal oblique muscles
Rectus abdominis muscle
Aponeurosis of the internal oblique and transversus abdominis
Fascia transversalis
Extraperitoneal fat
Parietal peritoneum

Parkinson’s disease (PD) is one of the most common neurologic disorders, affecting approximately 1% of individuals older than 60 years and causing progressive disability that can be slowed but not halted, by treatment. The 2 major neuropathologic findings in Parkinson’s disease are loss of pigmented dopaminergic neurons of the substantia nigra pars compacta and the presence of Lewy bodies and Lewy neurites. See the images below.

Naloxone is a short-acting, specific antagonist of mu(μ)-opioid receptors. It is used to reverse the effects of opioid toxicity.

It can be given by a continuous infusion if repeated doses are required and the infusion rate is adjusted according to the vital signs. Initially, the infusion rate can be set at 60% of the initial resuscitative IV dose per hour.

Naloxone has a shorter duration of action (6-24 hours) than most opioids and so close monitoring according to the respiratory rate and depth of coma and repeated injections are necessary. When repeated doses are needed in opioid addicts, naloxone administration may precipitate a withdrawal syndrome with abdominal cramps, nausea and diarrhoea, but these usually settle within 2 hours.

An initial dose of 0.4 to 2 mg can be given intravenously and can be repeated at 2 to 3-minute intervals to a maximum of 10mg.

If the intravenous route is inaccessible, naloxone can be administered via an IO line, subcutaneously (SQ), IM, or via the intranasal (IN) route.

Escherichia coli O157 is a serotype of Escherichia coli.
The Escherichia coliO157 strain is ‘enterohaemorrhagic’ and causes severe forms of acute haemorrhagic diarrhoea. It can also cause non-haemorrhagic diarrhoea.

Incubation period of Escherichia coli O157 is usually 3-4 days and bloody diarrhoea usually begins on the 3rd or 4th day of the infection.

Infections with Escherichia coliO157 are more common during the warmer months than in winter.

Haemolytic uraemic syndrome develops in approximately 6% of patients. It is commonly seen in children and in the elderly.

Escherichia coli O157 can also cause:
Haemorrhagic colitis
Haemolytic uraemic syndrome
Thrombotic thrombocytopenic purpura but not immune thrombocytopenic purpura.

The reduced indirect inguinal hernia can be controlled by pressure over the internal ring; a direct inguinal hernia cannot.

An indirect inguinal hernia can be reduced superiorly then superolaterally, while a direct inguinal hernia can be reduced superiorly then posteriorly.

An indirect inguinal hernia takes time to reach full size, but a direct inguinal hernia appears immediately upon standing.

Indirect inguinal hernias are seen as elliptical swelling, while direct inguinal hernias appear as symmetric, circular swelling.

Diagnosis of tapeworm is by direct visualisation of characteristic eggs in stool. Humans may be infected by pork or beef tapeworm. Treatment is with praziquantel or niclosamide. Specialist advice should be sought for the management of neurocysticercosis.Iron-deficiency anaemia is typically seen in hookworm infection. Threadworms migrate from the intestine at night to lay eggs on the perianal skin. Mebendazole is first line treatment for threadworms.

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

The volume of air that remains in the lungs after a single breath is known as functional residual capacity (FRC). It is calculated by combining the expiratory reserve volume and residual volume.