Pectoralis major is a thick, fan-shaped muscle situated in the chest. It makes up the bulk of the chest musculature in the male and lies underneath the breast in the female. It overlies the thinner pectoralis minor muscle.
Superficial muscles of the chest and arm showing pectoralis major (from Gray’s Anatomy)
Pectoralis major has two heads; the clavicular head and the sternocostal head. The clavicular head originates from the anterior border and medial half of the clavicle. The sternocostal head originates from the anterior surface of the sternum, the superior six costal cartilages and the aponeurosis of the external oblique muscle. It inserts into the lateral lip of the bicipital groove of the humerus.
Pectoralis major receives dual innervation from the medial pectoral nerve and the lateral pectoral nerve.
Its main actions are as follows:
Flexes humerus (clavicular head)
Extends humerus (sternocostal head)
Adducts and medially rotates the humerus
Draws scapula anteriorly and inferiorly

E.Colistrain 0157 causes enterohaemorrhagic diarrhoea and can be followed by haemolytic uraemic syndrome (renal failure, haemolytic anaemia and thrombocytopenia).

Immunoglobulin A is predominant in saliva.

Coagulative necrosis is the most common form of necrosis characterised by the loss of cell nuclei, but with general preservation of the underlying architecture. Dead tissue is macroscopically pale and firm. This is the classic pattern seen in myocardial infarction.Liquefactive necrosis leads to complete loss of cellular structure and conversion into a soft, semi-solid mass. This is typically seen in the brain following cerebral infarction.Caseous necrosis is most commonly seen in tuberculosis. Histologically, the complete loss of normal tissue architecture is replaced by amorphous, granular and eosinophilic tissue with a variable amount of fat and an appearance reminiscent of cottage cheese.Gangrenous necrosis is necrosis with putrefaction of tissues due to exposure to air (dry gangrene) or infection (wet gangrene).

Adverse effects of loop diuretics include:
Mild gastrointestinal disturbances, pancreatitis and hepatic encephalopathy
Hyperglycaemia
Acute urinary retention
Water and electrolyte imbalance
Hyponatraemia, hypocalcaemia, hypokalaemia, hypomagnesaemia, hypochloraemiaHypotension, hypovolaemia, dehydration, and venous thromboembolism
Metabolic alkalosis
Hyperuricaemia
Blood disorders (bone marrow suppression, thrombocytopenia, and leucopenia)
Visual disturbance, tinnitus and deafness
Hypersensitivity reactions

Examples of type IV reactions includes:
Contact dermatitis
Hashimoto’s thyroiditis
Primary biliary cholangitis
Tuberculin skin test (Mantoux test)
Chronic transplant rejection
Granulomatous inflammation (e.g. sarcoidosis, Crohn’s disease)

Flow through airways is described by Darcy’s law which states that flow is directly proportional to the mouth-alveolar pressure gradient and inversely proportional to airway resistance. Airway resistance is primarily determined by the airway radius according to Poiseuille’s law, and whether the flow is laminar or turbulent. Parasympathetic stimulation causes bronchoconstriction and sympathetic stimulation causes bronchodilation, but mediated by beta2-adrenoceptors. Muscarinic antagonists e.g. ipratropium bromide cause bronchodilation.

Calcium gluconate is given to antagonise cardiac cell membrane excitability to reduce the risk of arrhythmias. It has no effect on serum potassium levels unlike the alternative drugs listed above.

A posterior cerebral stroke will most likely result in a contralateral homonymous hemianopia with macular sparing.

Grey baby syndrome is a rare but causes significant adverse effect caused by the build-up of chloramphenicol in neonates (particularly preterm babies).

The following are the main characteristics of ‘grey baby syndrome’:

Skin that is ashy grey in colour.
Feeding problems
Vomiting
Cyanosis
Hypotension
Hypothermia
Hypotonia
Collapse of the cardiovascular system
Distension of the abdomen
trouble breathing

Damage to the C5 and C6 nerve roots causes Erb’s palsy.

The spinal accessory nerve (CN XI) innervates the trapezius muscle, thus you would not expect this muscle to be impacted.

The trapezius is a muscle that runs from the base of the neck across the shoulders and into the centre of the back.

CML is a myeloproliferative disorder characterised by an abnormal pluripotent haemopoietic stem cell. A cytogenetic abnormality known as the Philadelphia chromosome, which results from a reciprocal translocation between the long arms of chromosomes 9 and 22, causes more than 80% of cases of CML.

CML is a disease that develops slowly over several years. This is known as the ‘chronic stage.’ This stage is usually asymptomatic, and 90 percent of patients are diagnosed at this point, with the disease being discovered frequently as a result of a routine blood test. During this stage, the bone marrow contains less than 10% immature white cells (blasts).

When CML cells expand, symptoms typically begin to appear. The ‘accelerated stage’ is what it’s called. Approximately 10% of people are diagnosed at this point. During this stage, between 10% and 30% of blood cells in the bone marrow are blasts. During this stage, common clinical features include:
Fatigue and exhaustion
Night sweats and fever
Distension of the abdomen
Pain in the left upper quadrant (splenic infarction)
Splenomegaly (commonest examination finding)
Hepatomegaly
Bruising is simple.
Gout is a type of arthritis that affects (rapid cell turnover)
Hyperviscosity is a condition in which the viscosity of (CVA, priapism)
A small percentage of patients experience a ‘blast crisis’ (blast stage). More than 30% of the blood cells in the bone marrow are immature blast cells at this stage. Patients with severe constitutional symptoms (fever, weight loss, bone pain), infections, and bleeding diathesis typically present at this stage.

In CML, laboratory findings include:
White cell count is abnormally high (often greater than 100 x 109/l).
Increased number of immature leukocytes causes a left shift.
Anaemia that is mild to moderately normochromic and normocytic.
Platelets can be low, normal, or elevated, and the Philadelphia chromosome can be found in > 80% of patients.
Serum uric acid and ALP levels are frequently elevated.
Tyrosine kinase inhibitors (TKIs), such as imatinib and dasatinib, are the current mainstay of CML treatment.
Allogenic bone marrow transplantation is now only used in cases where TKIs have failed to work.

The femoral nerve runs down the front of the leg from the pelvis. It gives the front of the thigh and a portion of the lower leg sensation.

Extension of the leg at the knee joint, flexion of the thigh at the hip are produced by muscles that is primarily innervated by the femoral nerve.

Damage to the long thoracic nerve results in weakness/paralysis of the serratus anterior muscle causing difficulty abducting the upper limb above 90 degrees and giving a ‘winged ‘ scapula appearance where the medial border, particularly the inferior angle, of the scapula moves laterally and posteriorly away from the thoracic wall (this becomes more pronounced if the patient presses the upper limb against a wall).

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.

Overdosing on calcium-channel blockers should always be taken seriously and regarded as potentially fatal. Verapamil and diltiazem are the two most lethal calcium channel blockers in overdose. These work by binding the alpha-1 subunit of L-type calcium channels, preventing calcium from entering the cell. In cardiac myocytes, vascular smooth muscle cells, and islet beta-cells, these channels play an important role.

The standard ABC approach should be used to resuscitate all patients as needed. If life-threatening toxicity is expected, intubation and ventilation should be considered early on. If hypotension and shock are developing, early invasive blood pressure monitoring is recommended.

The primary goal of specific treatments is to support the cardiovascular system. These are some of them:

1. Fluid resuscitation: Give up to 20 mL of crystalloid per kilogramme of body weight.

2. Calcium supplementation
This can be a good way to raise blood pressure and heart rate temporarily.
via central venous access: 10% calcium gluconate 60 mL IV (0.6-1.0 mL/kg in children) or 10% calcium chloride 20 mL IV (0.2 mL/kg in children)
Boluses can be given up to three times in a row.
To keep serum calcium >2.0 mEq/L, consider a calcium infusion.

3. Atropine: 0.6 mg every 2 minutes up to 1.8 mg is an option, but it is often ineffective.

4. HIET (high-dose insulin-euglycemic therapy):
The role of HIET in the step-by-step management of cardiovascular toxicity has changed.

5. Vasoactive infusions:
This was once thought to be a last-ditch measure, but it is now widely recommended that it be used sooner rather than later.
Insulin with a short half-life 50 mL of 50 percent glucose IV bolus plus 1 U/kg bolus (unless marked hyperglycaemia present)
Short-acting insulin/dextrose infusions should be continued.
Glucose should be checked every 20 minutes for the first hour, then hourly after that.
Regularly check potassium levels and replace if they fall below 2.5 mmol/L.
Titrate catecholamines to effect (inotropy and chronotropy); options include dopamine, adrenaline, and/or noradrenaline infusions.

6. Sodium bicarbonate: Use 50-100 mEq sodium bicarbonate (0.5-1.0 mEq/kg in children) in cases where a severe metabolic acidosis develops.

7. Cardiac pacing: It can be difficult to achieve electrical capture, and it may not improve overall perfusion.
Bypass AV blockade with ventricular pacing, which is usually done at a rate of less than 60 beats per minute.

8. Intralipid transport
Calcium channel blockers are lipid-soluble agents, so they should be used in refractory cases.

Weber syndrome is a midbrain stroke characterized by crossed hemiplegia along with oculomotor nerve deficits and it occurs with the occlusion of the median and/or paramedian perforating branches of the basilar artery.

Typical clinical findings include ipsilateral CN III palsy, ptosis, and mydriasis (such as damage to parasympathetic fibres of CN III) with contralateral hemiplegia.

Lithium is the drug of choice for recurrent bipolar illness but should be carefully monitored as it has a very low therapeutic index. The normal therapeutic range is 0.4-0.8 mmol/l.

The lower end of the range is usually the target for the elderly and as maintenance therapy. Toxicity is usually seen at levels >1.5 mmol/l. Samples should be taken 12 hours after the dose, and levels should be checked one week after starting therapy and one week after every change in dosage.

In all non-sensitised pregnant women who are RhD-negative, it is recommended that routine antenatal anti-D prophylaxis is offered. Even if there is previous anti-D prophylaxis, use of routine antenatal anti-D prophylaxis should be given for a sensitising event early in the same pregnancy. Postpartum anti-D prophylaxis should also be given even if there has been previous routine antenatal anti-D prophylaxis or antenatal anti-D prophylaxis for a sensitising event in the same pregnancy.

Multiple myeloma is a clonal abnormality affecting plasma cells in which there is an overproduction of functionless immunoglobulins. The most common patient complaint is bone pain, especially in the back and ribs. Anaemia and renal failure are common, along with hypercalcemia. Hypercalcemia may lead to an altered mental status, as in this case.

Chronic lymphocytic leukaemia occurs due to the overproduction of lymphocytes, usually B cells. CLL may present with an asymptomatic elevation of B cells. Patients are generally more than 50 years old and present with non-specific fatigue and weight loss symptoms.

There is no history of alcohol abuse in this case. Furthermore, patients with a history of alcohol abuse may have signs of liver failure, which are not present here.

Metastatic prostate cancer would most often cause lower backache as it metastasises first to the lumbar spine via the vertebral venous plexus.

A patient with Vitamin B12 deficiency would have anaemia, megaloblastic, hypersegmented neutrophils, and signs of peripheral neuropathy.

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.

Even if there is no evidence of infection, prophylactic antibiotics should be administered for all human bite wounds that are less than 72 hours old. The first-line therapy is 7 days of co-amoxiclav. In penicillin-allergic people, metronidazole + doxycycline is an option. Streptococcus spp., Staphylococcus aureus, Haemophilus spp., Eikenella corrodens, Bacteroides spp., and other anaerobes are the most prevalent organisms found in human bites.

A plasma potassium less than 3.5 mmol/L defines hypokalaemia.

Excessive liquorice ingestion causes hypermineralocorticoidism and leads to hypokalaemia.

Gitelman’s syndrome causes metabolic alkalosis with hypokalaemia and hypomagnesaemia. It is an inherited defect of the distal convoluted tubules.

Bartter’s syndrome causes hypokalaemic alkalosis. It is a rare inherited defect in the ascending limb of the loop of Henle.

Type 1 and 2 renal tubular acidosis both cause hypokalaemia

Type 4 renal tubular acidosis causes hyperkalaemia.

Myeloma laboratory findings include:
– The presence of a paraprotein in serum or urine (the paraprotein is IgG in 60 percent of cases, IgA in 20 percent, and light chain only in almost all the rest),
– Increased serum immunoglobulin-free light chain proteins generated by plasma cells but not coupled with heavy chains 
– Reduced IgG, IgA, and IgM levels in the blood (immune paresis)
– Anaemia, whether normochromic, normocytic, or macrocytic. 
– On a blood film, a Rouleaux formation has been marked.
– In advanced illness, neutropenia and thrombocytopenia are common.
– ESR is high.
– Plasma cells in the bone marrow are overabundant, typically in aberrant forms. – Hypercalcemia
– Creatinine levels are high.
– Serum albumin levels are low in advanced illness.
60 percent of patients have osteolytic lesions, osteoporosis, or pathological fractures.

Carbamazepine is a drug of choice for simple and complex focal seizures and is a first-line treatment option for generalised tonic-clonic seizures. It is also used in trigeminal neuralgia and diabetic neuropathy. Carbamazepine may exacerbate tonic, atonic, myoclonic and absence seizures and is therefore not recommended if these seizures are present.

According to a 2018 audit conducted by the Royal College of Emergency Medicine (RCEM), the standard of care for children presenting to EDs with fractured limbs has deteriorated, with most patients waiting longer than ever before for pain relief. More than one-tenth of the children who came in with significant pain from a limb fracture received no pain relief at all.

For all patients, including children, the Agency for Health Care Policy and Research (AHCPR) in the United States recommends using the ABCs of pain management:
A – Ask about pain regularly. Assess pain systematically.
B – Believe the patient and family in their reports of pain and what relieves it.
C – Choose pain control options appropriate for the patient, family, and setting.
D – Deliver interventions in a timely, logical, coordinated fashion.
E – Empower patients and their families. Enable patients to control their course to the greatest extent possible.

The RCEM guidelines recommend assessing a child’s pain within 15 minutes of arrival. This is a fundamental requirement. For the assessment of pain in children, a variety of rating scales are available; which one is used depends on the child’s age and ability to use the scale. These are some of them:
Faces of Wong-Baker Scale for assessing pain
Scale of numerical evaluation
The behavioural scale is a scale that measures how people behave.

The RCEM has provided the following visual guide:
The RCEM has established the following guidelines for when patients in severe pain should receive appropriate analgesia:
100% within 60 minutes of arrival or triage, whichever is earliest
75% within 30 minutes of arrival or triage, whichever is earliest
50% within 20 minutes of arrival or triage, whichever is earliest

Acute haemolytic transfusion reactions present with: Feeling of ‘impending doom’ as the earliest symptom, fever and chills, pain and warmth at transfusion site, nausea and vomiting, back, joint, and chest pain. Transfusion should be stopped immediately and IV fluid (usually normal saline) administered.

Supportive measures and paracetamol can be given since patient has fever but it is not the immediate first step.

Gastrin secretion is inhibited by:
Low gastric pH (negative feedback mechanism)
Somatostatin
Secretin
Gastric inhibitory polypeptide (GIP)
Cholecystokinin

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

Gentamicin is given by injection because it is NOT absorbed orally.

It is excreted in the kidneys by glomerular filtration

Gentamicin is not to be used for the treatment of Neisseria meningitidis, Neisseria gonorrhoea, or Legionella pneumophila.There is a risk of patient going into shock from lipid A endotoxin release.

Two of its most notable side effects are hearing loss reversible nephrotoxicity and which are both dose-related and levels should be monitored in patients.

Pilocytic astrocytoma (PCA), previously known as cystic cerebellar astrocytoma or juvenile pilocytic astrocytoma, was first described in 1931 by Harvey Cushing, based on a case series of cerebellar astrocytomas; though he never used these terms but rather described a spongioblastoma. They are low-grade, and usually well-circumscribed tumours, which tend to occur in young patients. By the World Health Organization (WHO) classification of central nervous system tumours, they are considered grade I gliomas and have a good prognosis.

PCA most commonly occurs in the cerebellum but can also occur in the optic pathway, hypothalamus, and brainstem. They can also occur in the cerebral hemispheres, although this tends to be the case in young adults. Presentation and treatment vary for PCA in other locations. Glial cells include astrocytes, oligodendrocytes, ependymal cells, and microglia. Astrocytic tumours arise from astrocytes and are the most common tumour of glial origin. The WHO 2016 categorized these tumours as either diffuse gliomas or other astrocytic tumours. Diffuse gliomas include grade II and III diffuse astrocytomas, grade IV glioblastoma, and diffuse gliomas of childhood. The other astrocytic tumours group include PCA, pleomorphic xanthoastrocytoma, subependymal giant cell astrocytoma, and anaplastic pleomorphic xanthoastrocytoma.

PCA can present with symptoms secondary to the posterior fossa mass effect. This may include obstructive hydrocephalus, with resultant headache, nausea and vomiting, and papilledema. If hydrocephalus occurs before the fusion of the cranial sutures (<18-months-of-age), then an increase in head circumference will likely occur. Lesions of the cerebellar hemisphere result in peripheral ataxia, dysmetria, intention tremor, nystagmus, and dysarthria. In contrast, lesions of the vermis cause a broad-based gait, truncal ataxia, and titubation. Posterior fossa lesions can also cause cranial nerve palsies. Diplopia may occur due to abducens palsy from the stretching of the nerve. They may also have blurred vision due to papilledema. Seizures are rare with posterior fossa lesions.