Testes are retroperitoneal organs and its lymphatic drainage is to the lumbar and para-aortic nodes along the lumbar vertebrae.

The scrotum is the one which drains into the nearby superficial inguinal nodes.

The glans penis and clitoris drains into the deep inguinal lymph nodes.

In experimental studies, the researcher introduces an intervention and studies the effect. The study subjects are allocated into different groups by the investigator through the use of randomisation. Randomisation serves to remove any potential bias.

A cohort study is a form of longitudinal, observational study that follows a group of patients (the cohort) over a period of time to monitor the effects of exposure to a proposed aetiological factor upon them.

A case-control study is a type observational study. Here, patients who have developed a disease are identified and compared on the basis of proposed causative factors that occurred in the past, to a control group.

Clinical trials are experimental studies. Examples include: double blind, single blind, and unblinded studies(both patient and researcher are aware of the treatment they receive)

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.

Synthesis of platelets occurs in the bone marrow by fragmentation of megakaryocytes cytoplasm, derived from the common myeloid progenitor cell. The average time for differentiation of the human stem cell to the production of platelets is about 10 days. The major regulator of platelet formation is thrombopoietin and 95% of this is produced by the liver. Normal platelet count is 150 – 450 x 109/L and the normal lifespan of a platelet is about 10 days. Usually about one-third of the marrow output of platelets may be trapped at any one time in the normal spleen.

Cortisol is a steroid hormone produced in the zona fasciculata of the adrenal cortex. It is released in response to stress and low blood glucose concentrations.
Cortisol acts to: raise plasma glucose by stimulating glycolysis and gluconeogenesis in the liver and inhibiting peripheral glucose uptake into storage tissues, increase protein breakdown in skeletal muscle, skin and bone to release amino acids, increase lipolysis from adipose tissues to release fatty acidsand at higher levels and mimic the actions of aldosterone on the kidney to retain Na+ and water and lose K+ ionssuppress the action of immune cells

Sickling of red blood cells can lead to several different clinical syndromes. If the sickling occurs in the corpora cavernosa, it can lead to a sustained, painful erection of the penis, referred to as priapism. One of the complications is long-term impotence. It is important to seek a urological opinion immediately in this case, but in the interim, treat with perineal ice packs and walk up and down the stairs.

Intrinsic factor is essential for the absorption of the small amounts of vitamin B12 normally present in the diet from the terminal ileum. The parietal cells of the stomach produce intrinsic factor, and following a gastrectomy, the absorption of vitamin B12 will be markedly reduced, and a deficiency state will exist.

Helicobacter pylori is a curved, non-spore forming, Gram-negative bacteria that is primarily linked to gastric infections. Once acquired, it colonizes the stomach for a long time and can cause a low-grade inflammatory process, producing a chronic superficial gastritis.

H. pylori can be recovered from gastric biopsy materials. Samples must be transported quickly to the laboratory.
Helicobacter infections usually are identified by nonculture methods. H. pylori can be presumptively identified in a gastric biopsy specimen by testing for the presence of a rapid urease reaction.

Serologic testing is an important screening method for the diagnosis of H. pylori infection. It can also be diagnosed by faecal antigen detection, microscopic examination of stained gastric tissue, and DNA amplification tests.

Legionella pneumophilais a Gram negative bacterium that is found in natural water supplies and in the soil, transmitted predominantly via inhalation of aerosols generated from contaminated water (direct person-to-person spread of infected patients does not occur). It is the cause of Legionnaires’ disease. Outbreaks of Legionnaires’ disease have been linked to poorly maintained air conditioning systems, whirlpool spas and hot tubs.

The clinical features of the pneumonic form of Legionnaires’ disease include:
Mild flu-like prodrome for 1-3 days
Cough (usually non-productive and occurs in approximately 90%)
Pleuritic chest pain
Haemoptysis
Headache
Nausea, vomiting and diarrhoea
Anorexia
Legionella pneumophilainfections can be successfully treated with macrolide antibiotics, such as erythromycin, or quinolones, such as ciprofloxacin. Tetracyclines, such as doxycycline, can also be used.
The syndrome of inappropriate antidiuretic hormone secretion (SIADH) can occur with Legionnaires’ disease and will result in hyponatraemia as is seen in this case.
Legionella pneumophilainfections are resistant to amoxicillin but can be successfully treated with macrolide antibiotics, such as erythromycin, or quinolones, such as ciprofloxacin. Tetracyclines, such as doxycycline, can also be used. The majority of cases of Legionnaires’ disease are caused by Legionella pneumophila, however many other species of Legionella have been identified.
Legionella longbeachae is another less commonly encountered species that has also been implicated in outbreaks. It is predominantly found in soil and potting compost, and has caused outbreaks of Pontiac fever, the non-respiratory and less severe variant of Legionnaires’ disease.

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

Herpes simplex virus is the most common cause of infective encephalitis and has a predilection for the temporal lobes. Herpes simplex is transmitted through direct contact. It invades skin locally producing skin vesicles by its cytolytic activity.

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.

Causes of neutropaenia:
Drug-induced (e.g. chemotherapy, chloramphenicol, co-trimoxazole, phenytoin, carbamazepine, carbimazole, furosemide, chloroquine, clozapine, some DMARDs)
Benign (racial or familial)
Cyclical
Immune (e.g. SLE, Felty’s syndrome, hypersensitivity and anaphylaxis)
Leukaemia
Infections (e.g. HIV, hepatitis, fulminant bacterial infection)
General Pancytopaenia
Hypersplenism, aplastic anaemia, malignant infiltration of bone marrow, megaloblastic anaemia, chemotherapy, myelodysplasia

An action potential is a self-propagating response, successive depolarisation moving along each segment of an unmyelinated nerve until it reaches the end. It is all-or-nothing and does not decrease in size. Conduction in myelinated fibres is much faster, up to 50 times that of the fastest unmyelinated nerve. Myelinated fibres are insulated except at areas devoid of myelin called nodes of Ranvier. The depolarisation jumps from one node of Ranvier to another by a process called saltatory conduction. Saltatory conduction not only increases the velocity of impulse transmission but also conserves energy for the axon because depolarisation only occurs at the nodes and not along the whole length of the nerve fibre. Larger diameter myelinated nerve fibres conduct nerve impulses faster than small unmyelinated nerve fibres.

Monocytes spend only a short time in the marrow and, after circulating for 20-40 hours, leave the blood to enter the tissues where they become macrophages. Macrophages form the reticuloendothelial system in the liver, spleen and lymph nodes. The lifespan of macrophages may be as long as several months or even years. In tissues the macrophages become self-replicating without replenishment from the blood. They assume specific functions in different tissues e.g. dendritic cells which are involved in antigen presentation to T-cells. Macrophages may be activated by cytokines such as IFN-gamma, contact with complement or direct contact with the target cell through leucocyte adhesion molecules.

Chronic hepatitis and carrier state does not occur in hepatitis A infection and complete immunity is attained after infection.

In atrial flutter, ventricular rate control is usually used as a stopgap measure until sinus rhythm can be restored. A beta-blocker (such as bisoprolol), diltiazem, or verapamil can be used to lower the heart rate.

Electrical cardioversion, pharmacological cardioversion, or catheter ablation can all be used to restore sinus rhythm. Cardioversion should not be attempted until the patient has been fully anticoagulated for at least three weeks if the duration of atrial flutter is unknown or has lasted for more than 48 hours. Emergency electrical cardioversion is the treatment of choice when there is an acute presentation with haemodynamic compromise. For the treatment of recurrent atrial flutter, catheter ablation is preferred.

One of the results of Klebsiella pneumoniae is pneumonia that is usually a very severe infection. It is characterised by thick, bloody sputum (red currant jelly sputum), and is associated with complications like lung abscess, cavitation, necrosis, empyema and pleural effusions.

Mannitol is an osmotic diuretic that can be used to treat cerebral oedema and raised intraocular pressure. Mannitol is a low molecular weight compound and is, therefore, freely filtered at the glomerulus and is not reabsorbed. It, therefore, increases the osmolality of the glomerular filtrate and tubular fluid, increasing urinary volume by an osmotic effect. It also does not cross the blood-brain-barrier (BBB).

Infection of the genital mucosa by Neisseria gonorrhoeae involves attachment to and invasion of epithelial cells. Initial adherence of gonococci to columnar epithelial cells is mediated by type IV pili assembled from pilin subunit PilE proteins and pilus tip-associated PilC proteins, it then invades the epithelial layer, triggering a local acute inflammatory response.