The pectoralis major is the superior most and largest muscle of the anterior chest wall. It is a thick, fan-shaped muscle that lies underneath the breast tissue and forms the anterior wall of the axilla.

Its origin lies anterior surface of the medial half of the clavicle, the anterior surface of the sternum, the first 7 costal cartilages, the sternal end of the sixth rib, and the aponeurosis of the external oblique of the anterior abdominal wall.
The insertion of the pectoralis major is at the lateral lip of the intertubercular sulcus of the humerus. There are 2 heads of the pectoralis major, the clavicular and the sternocostal, which reference their area of origin.
The function of the pectoralis major is 3-fold and dependent on which heads of muscles are involved:
– Flexion, adduction and medial rotation of the arm at the glenohumeral joint
– Clavicular head causes flexion of the extended arm
– Sternoclavicular head causes extension of the flexed arm

Arterial supply of the pectoralis major, the pectoral artery, arises from the second branch of the axillary artery, the thoracoacromial trunk.

The 2 heads of the pectoralis major have different nervous supplies. The clavicular head derives its nerve supply from the lateral pectoral nerve. The medial pectoral nerve innervates the sternocostal head. The lateral pectoral nerve arises directly from the lateral cord of the brachial plexus, and the medial pectoral nerve arises from the medial cord.

Granulomatous inflammation is a distinctive pattern of chronic inflammation that is encountered in a limited number of infectious and some non-infectious conditions. Briefly, a granuloma is a cellular attempt to contain an offending agent that is difficult to eradicate. In this attempt, there is often strong activation of T lymphocytes leading to macrophage activation, which can cause injury to normal tissues. IL-1 is important in initiating granuloma formation, IL-2 can cause them to enlarge and TNF-α maintains them.

In February 2016 the Society of Critical Care Medicine published a JAMA article reformatting the definitions of sepsis in an attempt to overcome the shortcomings of the old definitions.
The main changes are a new definition of sepsis, the replacement of the SIRS criteria with the quick Sepsis-related Organ Failure Assessment (qSOFA), and the complete removal of “severe sepsis” as an entity.
The new definition of sepsis is that it is “life-threatening organ dysfunction caused by a dysregulated host response to infection.”
Septic shock is “a subset of sepsis in which underlying circulatory and cellular metabolism abnormalities are profound enough to increase mortality.”
In essence this means that septic shock is sepsis plus the following, despite adequate fluid resuscitation:
Vasopressors required to maintain a MAP > 65 mmHg
Serum lactate > 2 mmol/l
The qSOFA score is a bedside prompt designed to identify patients with suspected infection who are at greater risk for a poor outcome outside of the intensive care unit. It uses the following three criteria:
Hypotension (SBP < 100 mmHg)
Tachypnoea (RR > 22)
Altered mental status (GCS < 15)
The presence of 2 or more of the qSOFA criteria near the onset of infection is associated with greater risk of death or a prolonged intensive care unit stay.

Codeine phosphate is a mild opiate that can be used to treat mild to moderate pain when other pain relievers like paracetamol or ibuprofen have failed. It can also be used to treat diarrhoea and coughs that are dry or painful.

The use of all opioids is contraindicated for the following reasons:
Respiratory depression (acute)
Patients who are comatose
Head injury (opioid analgesics impair pupillary responses, which are crucial for neurological evaluation)
Intracranial pressure has risen (opioid analgesics interfere with pupillary responses vital for neurological assessment)
There’s a chance you’ll get paralytic ileus.

The use of codeine phosphate is contraindicated in the following situations:
Because of the significant risk of respiratory side effects in children under the age of 12, it is not recommended for children under the age of 12.

Patients of any age who have been identified as ultra-rapid codeine metabolizers (CYP2D6 ultra-rapid metabolizers)

Because codeine can pass through breast milk to the baby and because mothers’ ability to metabolise codeine varies greatly, it is especially dangerous in breastfeeding mothers.

If other painkillers, such as paracetamol or ibuprofen, fail to relieve acute moderate pain in children over the age of 12, codeine should be used. In children with obstructive sleep apnoea who received codeine after tonsillectomy or adenoidectomy, a significant risk of serious and life-threatening adverse reactions has been identified.

During quiet respiration, the approximate position of the right oblique fissure can be marked by a line on the thoracic wall that begins at the spinous process of vertebra T4, crosses the fifth intercostal space laterally and then follows the contour of rib 6 anteriorly.

Hyoscine butylbromide is an antispasmodic drug that blocks muscarinic receptors and reduces intestinal motility. It is used for gastrointestinal and genitourinary smooth muscle spasms and symptomatic relief of IBS.

It has the following contraindications:
1. Closed-angle glaucoma
2. Gastrointestinal obstruction
3. Intestinal atony
4. Paralytic ileus
5. Toxic megacolon
6. Severe ulcerative colitis
7. Significant bladder outflow obstruction
8. Urinary retention
9. Myasthenia gravis

Use cautiously in the following conditions:
1. Acute myocardial infarction (in adults)
2. Arrhythmias (may be worsened)
3. Autonomic neuropathy
4. Hypertension
5. Cardiac insufficiency (due to association with tachycardia)
6. Congestive cardiac failure (maybe worsened)
7. Cardiac surgery (due to association with tachycardia)
8. Gastro-oesophageal reflux disease
9. Ulcerative colitis
10. Prostatic hyperplasia
11. Use in children (increased risk of side effects)

Eversion of the foot is primarily produced by the fibularis longus and fibularis brevis, both innervated by the superficial fibular nerve. The fibularis tertius, innervated by the deep fibular nerve, also assists in this action.

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

The NICE guidelines do NOT recommend isolating a patient with viral conjunctivitis from others or skipping school or work. The disease is contagious, but the spread of the disease can be controlled by maintaining good hygiene practices such as:
1. frequent hand washing
2. use of separate flannels and towels
3. Avoid close contact with others

Antibiotic prescriptions are not part of the NICE guidelines for viral conjunctivitis as they will not affect the course of the disease. Most cases of viral conjunctivitis are self-limiting and resolve within one to two weeks.

The NICE guidelines recommend that symptoms may be eased with self-care measures such as:
1. Bathing/cleaning the eyelids with cotton wool soaked in sterile saline or boiled and cooled water to remove any discharge
2. Cool compresses applied gently around the eye area
3. Use of lubricating drops or artificial tears

Categorical data or data that is ordered is Ordinal data e.g. disease staging system, pain scoring system.

Disease staging system is the correct answer

The FDA categorizes Paracetamol as an NSAID (nonsteroidal anti-inflammatory drug) as it is believed to selectively inhibit cyclo-oxygenase 3 (COX-3) receptors in the brain and spinal cord.

COX-3 is a unique variant of the more known COX-1 and COX-2. It is responsible for the production of prostaglandins in central areas, which sensitizes free nerve endings to the chemical mediators of pain. Therefore, by selectively inhibiting COX-3, paracetamol effectively reduces pain sensation by increasing the pain threshold.
Acetaminophen does not inhibit cyclooxygenase in peripheral tissues and, therefore, has no peripheral anti-inflammatory effects.
The antipyretic actions of acetaminophen are likely attributed to direct action on heat-regulating centres in the brain, resulting in peripheral vasodilation, sweating, and loss of body heat.

CSF fills the ventricular system, a series of interconnected spaces within the brain, and the subarachnoid space directly surrounding the brain. The intraventricular CSF reflects the composition of the brain’s extracellular space via free exchange across the ependyma, and the brain “floats” in the subarachnoid CSF to minimize the effect of external mechanical forces. The volume of CSF within the cerebral ventricles is approximately 30 mL, and that in the subarachnoid space is about 125 mL. Because about 0.35 mL of CSF is produced each minute, CSF is turned over more than three times daily. Approximately 500 mL of CSF is produced per day, at a rate of about 25 mL per hour.

CSF is a filtrate of capillary blood formed largely by the choroid plexuses, which comprise pia mater, invaginating capillaries, and ependymal cells specialized for transport. The choroid plexuses are located in the lateral, third, and fourth ventricles. The lateral ventricles are situated within the two cerebral hemispheres. They each connect with the third ventricle through one of the interventricular foramina (of Monro). The third ventricle lies in the midline between the diencephalon on the two sides. The cerebral aqueduct (of Sylvius) traverses the midbrain and connects the third ventricle with the fourth ventricle. The fourth ventricle is a space defined by the pons and medulla below and the cerebellum above. The central canal of the spinal cord continues caudally from the fourth ventricle, although in adult humans the canal is not fully patent and continues to close with age.

Infectious mononucleosis is caused by Epstein-Barr virus (EBV). The incubation period for EBV varies from 2 weeks to 2 months.

The usual incubation period for rubella is 14 days; with a range of 12 to 23 days.

Gonorrhoea has a short incubation period of approximately 2 to 7 days.

The mumps virus can be isolated from infected saliva and swabs rubbed over the Stensen’s duct from 9 days before onset of symptoms until 8 days after parotitis appears.

Scarlet fever, which appears within 1 to 2 days after bacterial infection, is characterized by a diffuse red rash that appears on the upper chest and spreads to the trunk and extremities. The rash disappears over the next 5 to
7 days and is followed by desquamation.

Adenosine is usually the treatment of choice for terminating paroxysmal supraventricular tachycardia including those associated with accessory conduction pathways e.g. Wolff-Parkinson-White syndrome.

Cardiac muscle is striated, and the sarcomere is the contractile unit, similar to skeletal muscle. Contracture is mediated by the interaction of calcium, troponins, and myofilaments, much as it occurs in skeletal muscle. Cardiac muscle, on the other hand, differs from skeletal muscle in a number of ways.

In contrast to skeletal muscle cells, cardiac myocytes have a nucleus in the middle of the cell and sometimes two nuclei. The cells are striated because the thick and thin filaments are arranged in an orderly fashion, although the arrangement is less well-organized than in skeletal muscle.

Intercalated discs, which work similarly to the Z band in skeletal muscle in defining where one cardiac muscle cell joins the next, are a very significant component of cardiac muscle.

Adherens junctions and desmosomes, which are specialized structures that hold the cardiac myocytes together, are formed by the transverse sections. The lateral sections produce gap junctions, which join the cytoplasm of two cells directly, allowing for rapid action potential conduction. These critical properties allow the heart to contract in a coordinated manner, allowing for more efficient blood pumping.

Cardiac myocytes have the ability to create their own action potentials, which is referred to as myogenic’. They can depolarize spontaneously to initiate a cardiac action potential. Pacemaker cells, as well as the sino-atrial (SA) and atrioventricular (AV) nodes, control this.

The Purkinje cells and the cells of the bundle of His are likewise capable of spontaneous depolarization. While the bundle of His is made up of specialized myocytes, it’s vital to remember that Purkinje cells are not myocytes and have distinct characteristics. They are larger than myocytes, with fewer filaments and more gap junctions than myocytes. They conduct action potentials more quickly, allowing the ventricles to contract synchronously.
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.

A granuloma is a collection of five or more epithelioid macrophages, with or without attendant lymphocytes and fibroblasts; epithelioid macrophages are altered macrophages which have turned themselves over to becoming giant phagocytosing and killing machines, they often fuse to become multinucleate (Langhans) giant cells.

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.

Hand-foot syndrome in children is typically the first symptom of the disease, produced by infarction of the metaphysis of small bones. The disease is inherited as an autosomal recessive trait. By adulthood, the spleen has usually infarcted. Infection with the B19 parvovirus is usually followed by an aplastic crisis. Thrombocytopenia is caused by splenic sequestration.

Although Ca2+entry during the action potential (AP) is essential for contraction, it only accounts for about 25% of the rise in intracellular Ca2+. The rest is released from Ca2+stores in the sarcoplasmic reticulum (SR). In relaxation, about 80% of Ca2+is rapidly pumped back into the SR (sequestered) by Ca2+ATPase pumps. The Ca2+that entered the cell during the AP is transported out of the cell primarily by the Na+/Ca2+exchanger in the membrane. When more action potentials occur per unit time, more Ca2+enters the cell during the AP plateau, more Ca2+is stored in the SR, more Ca2+is released from the SR and thus more Ca2+is left inside the cell and greater tension is produced during contraction. Increased heart rate increases the force of contraction in a stepwise fashion as intracellular [Ca2+] increases cumulatively over several beats; this is the Treppe effect. Cardiac glycosides such as digoxin have a positive inotropic effect.

The ventilation/perfusion ratio (V/Q ratio) is a ratio used to assess the efficiency and adequacy of the matching ventilation and perfusion.

A pulmonary artery carries deoxygenated blood from the right side of the heart to the lungs. When a large pulmonary embolus completed blocked a pulmonary artery the alveoli were ventilated but not perfused at all, then the V/Q ratio would be infinity.

Long-term administration of oxygen, usually at least 15 hours daily, improves survival in COPD patients who have severe hypoxaemia.

Long-term oxygen therapy should be considered in:

A non-smoker with COPD and a PaO2<7.3 kPa when stable

A non-smoker with COPD and PaO27.3–8 kPa when stable and with secondary polycythaemia, peripheral oedema, or evidence of pulmonary hypertension

Severe chronic asthma with PaO2<7.3 kPa or persistent disabling breathlessness

A patient with Interstitial lung disease with PaO2<8 kPa and in patients with PaO2>8 kPa with disabling dyspnoea

A patient with cystic fibrosis when PaO2<7.3 kPa or if PaO27.3–8 kPa in the presence of secondary polycythaemia, nocturnal hypoxaemia, pulmonary hypertension, or peripheral oedema

Pulmonary hypertension, without parenchymal lung involvement when PaO2<8 kPa

Neuromuscular or skeletal disorders, after specialist assessment

Obstructive sleep apnoea despite continuous positive airways pressure therapy, after specialist assessment

Pulmonary malignancy or other terminal disease with disabling dyspnoea

Heart failure with daytime PaO2<7.3 kPa when breathing air or with nocturnal hypoxaemia

Hepatitis B vaccine should be stored at 35°-46° F (2°-8° C) and should not be frozen.

There is no association between hepatitis B vaccination and Guillain-Barre syndrome. Infection with the bacterium Campylobacter jejuni is one of the most common risk factors for GBS. People can also develop GBS after having the flu or other infections (such as cytomegalovirus and Epstein Barr virus).

Hepatitis B vaccine is prepared from initial concentration of surface antigen.

To ensure adequate immunity, anti-HBs (HBsAb) titres may be checked 4-8 weeks following the last shot of the hepatitis B vaccine series.

Raised platelet levels have emerged as a cancer risk marker, according to a large population-based study published in 2017(link is external). According to the study, 12 percent of men and 6% of women with thrombocytosis were diagnosed with cancer within a year. These figures increased to 18% in men and 10% in women if a second platelet count was taken within 6 months of the first and showed an increased or stable elevated platelet count.

The researchers discovered that thrombocytosis linked to cancer is most common in colorectal and lung cancers, and it is linked to a worse prognosis. Furthermore, one-third of the cancer patients in the study had no other symptoms that would have prompted an immediate cancer referral.

The exact mechanism by which these cancers cause thrombocytosis is unknown, but one theory proposes the existence of pathogenic feedback loops between malignant cells and platelets, with a reciprocal interaction between tumour growth and metastasis, as well as thrombocytosis and platelet activation. Another hypothesis is that thrombocytosis occurs independently of cancer but aids in its spread and progression.

The findings show that routinely testing for thrombocytosis could cut the time it takes to diagnose colorectal and lung cancer by at least two months. In the UK, this could result in around 5500 earlier cancer diagnoses per year.

Because the positive predictive value of thrombocytosis in middle age for cancer (10%) is higher than the positive predictive value for a woman in her 50s presenting with a new breast lump (8.5%), this is clearly an important research paper that should be used to adjust future clinical practise. The current NICE guidelines predate these new research findings, so we’ll have to wait and see how they affect cancer referral guidelines in the UK.

Because there are so many possible cancers associated with thrombocytosis, the treating clinician should take a thorough history and perform a thorough clinical examination if a patient is diagnosed with it. Further investigation and the most appropriate referral route should be aided by this information.

It’s worth noting that the patients in the study had their blood tests done for a medical reason rather than as a random screening test.

If there are no other symptoms to guide investigation and referral (one-third of the patients in the study had no other symptoms), keep in mind that the two most common cancers encountered were colorectal and lung cancer, so a chest X-ray and a faecal immunochemical test (FIT) for faecal blood may be reasonable initial investigations.

Gas gangrene usually occurs within 3 days of injury, and is characterised by pain, rapidly spreading oedema, myositis, necrosis, palpable crepitus and systemic toxicity. Diagnosis is clinical and laboratory confirmation should not delay urgent surgical intervention. Hyperbaric oxygen therapy can be considered in addition to surgery and antibiotic therapy, to stop toxin production and inhibit bacteria from replicating and spreading (as Clostridium spp. are obligate anaerobes).

Compressive causes of CN III palsy cause early pupillary dilatation because the parasympathetic fibres run peripherally in the nerve and are easily compressed. In diabetes mellitus the lesions are ischaemic rather than compressive and therefore typically affect the central fibres resulting in pupillary sparing.

The use of a beta-blocker at the same time increases the risk of myocardial depression, but it is not a contraindication.
The use of adenosine is contraindicated in the following situations:
Asthma
COPD (chronic obstructive pulmonary disease)
Decompensated heart failure 
Long QT syndrome
AV block in the second or third degree
Sinusitis is a condition in which the sinuses become (unless pacemaker fitted)
Hypotension that is severe

Serum concentrations of the p24 antigen are usually high in the first few weeks after human immunodeficiency virus (HIV) infection and testing for p24 antigen is therefore a useful way of diagnosing very early infection. P24 is the viral protein that makes up most of the core of the HIV.

ELISA and other antibody tests, though a very sensitive way of detecting the presence of HIV, cannot be used in the early stages of the disease. This is because of the window period of 6-12 weeks before antibodies are produced. These tests will be negative during a seroconversion illness.

The ‘rapid HIV test’ is an HIV antibody test. It will also be negative during the ‘window period’ since it takes time for antibodies to be produced. It is called the ‘rapid test’ as it can detect antibodies in blood or saliva much quicker than the other antibody tests and results are often back within 20 minutes.

CD4 and CD8 counts are usually normal in the early stages of the HIV infection and cannot be used in this case.

Clostridium difficile, a Gram-positive, anaerobic, spore forming bacteria is present in the gut of approximately 3% of healthy adults (2012 UK HPA estimates). Following use of broad spectrum antibiotics, which alter normal gut flora, Clostridium difficile associated diarrhoea (CDAD) occurs.

About 80% of Clostridium difficile infections are seen in people over the age of 65 and its main clinical features are:
Abdominal cramps, severe bloody and/or watery diarrhoea, offensive smelling diarrhoea, and fever.

Hartmann’s pouch is a diverticulum that can occur at the neck of the gallbladder. It is one of the rarest congenital anomalies of the gallbladder. Hartmann’s gallbladder pouch is a frequent but inconsistent feature of normal and pathologic human gallbladders. It is caused by adhesions between the cystic duct and the neck of the gallbladder. As a result, it is classified as a morphologic rather than an anatomic entity.

There is a significant association between the presence of Hartmann’s pouch and gallbladder stones. It is the most common location for gallstones to become lodged and cause cholestasis.

The most common cause of upper gastrointestinal bleeding is peptic ulcer disease, particularly gastric and duodenal ulcers. Duodenal ulcers are most commonly associated with bleeding compared with gastric ulcers. Posterior duodenal ulcers are considered to be the most likely to cause severe bleeding because of its proximity to the branches of the gastroduodenal artery (GDA).