The lymphatics from the anus, skin of the perineum and the scrotum end in the superficial inguinal nodes. In case of a malignant growth of the anus, the superficial inguinal lymph nodes would most likely be enlarge.

Nephrotic syndrome is a syndrome comprising of signs of nephrosis, including proteinuria, hypoalbuminemia, and oedema. It is a component of glomerulonephritis, in which different degrees of proteinuria occur. Essentially, loss of protein through the kidneys leads to low protein levels in the blood , which causes water to be drawn into soft tissues (oedema). Severe hypoalbuminemia can also cause a variety of secondary problems, such as water in the abdominal cavity (ascites), around the heart or lung (pericardial effusion, pleural effusion), high cholesterol, loss of molecules regulating coagulation (hence increased risk of thrombosis). The most common sign is excess fluid in the body due to the serum hypoalbuminemia. Lower serum oncotic pressure causes fluid to accumulate in the interstitial tissues. Sodium and water retention aggravates the oedema.

Head and neck cancer is a group of cancers that starts within the mouth, nose, throat, larynx, sinuses, or salivary glands. The TNM staging system used for head and neck cancers is a clinical staging system that allows physicians to compare results across patients, assess prognosis, and design appropriate treatment regimens. The staging is as follows; Primary tumour (T): Tis: pre-invasive cancer (carcinoma in situ), T0: no evidence of primary tumour, T1: tumour 2 cm or less in its greatest dimension, T2: tumour more than 2 cm but not more than 4 cm, T3: tumour larger than 4 cm, T4: tumour with extension to bone, muscle, skin, antrum, neck, etc and TX: minimum requirements to assess primary tumour cannot be met. Regional lymph node involvement (N): N0: no evidence of regional lymph node involvement, N1: evidence of involvement of movable homolateral regional lymph nodes, N2: evidence of involvement of movable contralateral or bilateral regional lymph nodes, N3: evidence of involvement of fixed regional lymph nodes and NX: Minimum requirements to assess the regional nodes cannot be met. Distant metastases (M): M0: no evidence of distant metastases, M1: evidence of distant metastases and MX: minimum requirements to assess the presence of distant metastases cannot be met. Staging: Stage I: T1 N0 M0, Stage II: T2 N0 M0, Stage III: T2NOMO and T3N1MO, Stage IV: T4N1M0, any TN2M0, any TN3M0, any T and any NM1. The depth of infiltration is predictive of the prognosis. With increasing depth of invasion of the primary tumour, the risk of nodal metastasis increases and survival decreases. The patient in this scenario therefore has a T2 tumour.

The efferent lymphatics from the anal canal proceed to the internal iliac lymph nodes. This would most likely form the site of enlargement in the lymphatics.

The Fick’s principle states that the uptake of a substance by an organ equals the arteriovenous difference of the substance multiplied by the blood flowing through the organ. We can thus calculate the pulmonary blood flow with pulmonary arterial (i.e., mixed venous) oxygen content, aortic oxygen content and oxygen uptake. The pulmonary blood flow, systemic blood flow and cardiac output can be considered the same assuming there are no intracardiac shunts. Thus, we can calculate the cardiac output. Cardiac output = oxygen uptake/(aortic − mixed venous oxygen content) = 200 ml/min/(15 ml O2/100 ml − 10 ml O2/100 ml) = 200 ml/min/(5 ml O2/100 ml) = 200 ml/min/0.05 = 4000 ml/min.

It is crucial to remember to use pulmonary arterial oxygen content and not peripheral vein oxygen content, when calculating the cardiac output by Fick’s method.

Stage IIIA breast cancer is T0–2 N2 M0 or T3 N1-2 M0 disease. It describes invasive breast cancer in which either: the tumour is smaller than 5 cm in diameter and has spread to 4 to 9 axillary lymph nodes; or it is found through imaging studies or clinical exam to have spread to internal mammary nodes (near the breastbone found during imaging tests or a physical exam); or the tumour is larger than 5 cm and has spread to 1 to 9 axillary nodes, or to internal mammary nodes. In this stage, the cancer has not metastasized (spread to distant sites).

Beta-thalassaemia is due to decreased production of β-polypeptide chains, with an autosomal inheritance pattern. Carrier patients (heterozygotes) are asymptomatic and have mild to moderate microcytic anaemia. This is known as thalassaemia minor. Homozygotes (β-thalassaemia major, or Cooley’s anaemia) develop severe anaemia and marrow hyperactivity. The disease presents at 1-2 years of age with severe anaemia and transfusional and absorptive iron overload. Patients also present with jaundice, leg ulcers, massive splenomegaly and cholelithiasis. The disease can also lead to splenic sequestration leading to faster destruction of transfused red blood cells. Increased marrow activity causes thickening of cranial bones. Involvement of long bones is also seen, which can cause pathological fractures and growth impairment. There is iron deposition in various organs, which can lead to heart failure or hepatic failure (leading to cirrhosis). Thalassaemias are suspected in presence of family history, or signs suggesting microcytic haemolytic anaemia. Further test and quantitative haemoglobin studies are useful. In beta-thalassaemia, there is an increase in serum bilirubin, iron and ferritin levels. There is severe anaemia, often with haemoglobin < 6 g/dl. There is an elevated red blood cell count, which are microcytic. Peripheral blood smear is diagnostic with nucleated erythroblasts, target cells, small pale red blood cells, and punctate basophilia.

There are two stages to determine the blood group, known as ABO typing. The first stage is called forward typing. In this method, RBCs are mixed with two separate solutions of type A or type B antibodies to see if they agglutinate. If this blood clumps, this indicates the presence of antigens within the blood sample. For example, a sample of type B blood will clump when tested with type A antibodies as it contains type B antigens. Group B – has only the B antigen on red cells (and A antibody in the plasma)

Group B – has only the B antigen on red cells (and A antibody in the plasma)

Group AB – has both A and B antigens on red cells (but neither A nor B antibody in the plasma)

Group O – has neither A nor B antigens on red cells (but both A and B antibody are in the plasma). Many people also have a Rh factor on the red blood cell’s surface. This is also an antigen and those who have it are called Rh+. Those who have not are called Rh–. A person with Rh– blood does not have Rh antibodies naturally in the blood plasma (as one can have A or B antibodies, for instance) but they can develop Rh antibodies in the blood plasma if they receive blood from a person with Rh+ blood, whose Rh antigens can trigger the production of Rh antibodies. A person with Rh+ blood can receive blood from a person with Rh– blood without any problems. The patient’s blood group is B positive as he has antigen B, antibody A and Rh antigens.

The glossopharyngeal nerve, known as the ninth cranial nerve (CN IX), is a mixed nerve that carries afferent sensory and efferent motor information. The glossopharyngeal nerve has five distinct general functions:

– The branchial motor (special visceral efferent), supplies the stylopharyngeus muscle.

– The visceral motor (general visceral efferent), provides parasympathetic innervation of the parotid gland via the otic ganglion.

– The visceral sensory (general visceral afferent), carries visceral sensory information from the carotid sinus and carotid body.

– The general sensory (general somatic afferent), provides general sensory information from the inner surface of the tympanic membrane, upper pharynx (GVA), and the posterior one-third of the tongue.

– The visceral afferent (special visceral afferent), provides taste sensation from the posterior one-third of the tongue, including the circumvallate papillae.

Excess of circulating free thyroid hormones (thyroxine and/or triiodothyronine) leads to hyperthyroidism. Common causes include Graves’ disease, toxic thyroid adenoma and toxic multinodular goitre. Grave’s disease is the most common cause and is responsible for 70-80% cases of hyperthyroidism. Other causes include excess intake of thyroid hormone, amiodarone-related. It is important that hyperthyroidism is not confused with hyperthyroxinaemia (high levels of thyroid hormone in blood), which includes causes like thyroiditis. Both the conditions lead to thyrotoxicosis (symptoms due to hyperthyroxinemia). Symptoms include weight loss associated with increased appetite, anxiety, weakness, heat intolerance, depression, increased sweating, dyspnoea, loss of libido, diarrhoea, palpitations and occasionally arrhythmias. If there is an acute increase in metabolic rate, the condition is known as ‘thyroid storm’. Elderly sometimes present only with fatigue and weight loss and this is called apathetic hyperthyroidism. Neurological symptoms are also seen in hyperthyroidism and these are tremor, chorea, myopathy and periodic paralysis. One of the most serious complications of hyperthyroidism is stroke of cardioembolic origin due to coexisting atrial fibrillation.