Features of cell damage that tend to be reversible include: swelling of endoplasmic reticulum and some mitochondrialoss of ribosomescell stress response Features of cell damage that tend to be irreversible include: loss of nucleolus, no ribosomes, swelling of all mitochondria, nuclear condensation, membrane blebs and holes, lysosome rupture, fragmentation of all inner membranes, nuclear breakup

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).

Monocytes account for around 5 to 10% of peripheral white cells. Monocytes in peripheral blood are generally bigger than other leukocytes and feature a large central oval or indented nucleus with clumped chromatin. The abundant cytoplasm staining blue and containing numerous fine vacuoles gives the appearance of ground glass. Cytoplasmic granules are another type of granule. Monocytes evolve from the granulocyte-macrophage progenitor to become monoblasts, promonocytes, monocytes, and tissue macrophages (in increasing order of maturity). Monocytes only stay in the bone marrow for a short time before exiting to circulate in the bloodstream for 20-40 hours before becoming macrophages.

Diphtheria is an infection caused by the bacterium Corynebacterium diphtheriae. Signs and symptoms may vary from mild to severe. They usually start two to five days after exposure. Symptoms often come on fairly gradually, beginning with a sore throat and fever. In severe cases, a grey or white patch develops in the throat. This can block the airway and create a barking cough as in croup. The neck may swell in part due to enlarged lymph nodes.The disease may remain manageable, but in more severe cases, lymph nodes in the neck may swell, and breathing and swallowing are more difficult. People in this stage should seek immediate medical attention, as obstruction in the throat may require intubation or a tracheotomy. Abnormal cardiac rhythms can occur early in the course of the illness or weeks later, and can lead to heart failure. Diphtheria can also cause paralysis in the eye, neck, throat, or respiratory muscles. Patients with severe cases are put in a hospital intensive care unit and given a diphtheria antitoxin (consisting of antibodies isolated from the serum of horses that have been challenged with diphtheria toxin). Since antitoxin does not neutralize toxin that is already bound to tissues, delaying its administration increases risk of death. Therefore, the decision to administer diphtheria antitoxin is based on clinical diagnosis, and should not await laboratory confirmation.Antibiotics are used in patients or carriers to eradicate C. diphtheriae and prevent its transmission to others. The Centres for Disease Control and Prevention recommends either:MetronidazoleErythromycin is given (orally or by injection) for 14 days (40 mg/kg per day with a maximum of 2 g/d), orProcaine penicillin G is given intramuscularly for 14 days (300,000 U/d for patients weighing 10 kg); patients with allergies to penicillin G or erythromycin can use Rifampicin or clindamycin.

Phagocytosis is largely responsible for depletion of cells coated with antibodies. Cells opsonized by IgG antibodies are recognized by phagocyte Fc receptors, which are specific for the Fc portions of some IgG subclasses. In addition, when IgM or IgG antibodies are deposited on the surfaces of cells, they may activate the complement system by the classical pathway. Complement activation generates by-products, mainly C3b and C4b, which are deposited on the surfaces of the cells and recognized by phagocytes that express receptors for these proteins. The net result is phagocytosis of the opsonized cells and their destruction.

Activated leukocytes, adipocytes, and endothelial cells all release interleukin 6 (IL-6), a significant proinflammatory cytokine. The main downstream mediator of the acute phase response is C-reactive protein, which is predominantly produced by IL-6–dependent hepatic biosynthesis.

The major role of chemokines is to act as a chemoattractant to guide the migration of cells like neutrophils to the site of infection.

Histologic findings in EBV infectious mononucleosis: Oropharyngeal epithelium demonstrates an intense lymphoproliferative response in the cells of the oropharynx. The lymph nodes and spleen show lymphocytic infiltration primarily in the periphery of a lymph node. Relative lymphocytosis (≥ 60%) plus atypical lymphocytosis (≥ 10%) are the characteristic findings of Epstein Barr virus (EBV) infectious mononucleosis.

Based on the aforementioned findings in this case, the most likely diagnosis is medullary carcinoma of the thyroid associated with multiple endocrine neoplasia (MEN). Medullary thyroid cancer is a tumour of the parafollicular cells (C cells) of the thyroid and is neural crest in origin. It may be familial and occur as part of the MEN 2A disease spectrum. Less than 10% of thyroid cancers are of this type with patients typically presenting as children or young adults. Diarrhoea occurs in 30% of the cases. In association with MEN syndromes, medullary thyroid cancers are always bilateral and multicentric. Spread may either be lymphatic or haematogenous, and as these tumours are not derived primarily from thyroid cells, they are not responsive to radioiodine. Toxic nodular goitre is very rare. In sporadic medullary carcinoma of the thyroid, patients typically present with a unilateral solitary nodule and it tends to spread early to the lymph nodes in neck.

Inflammation is the immediate response of the body towards infections or irritations. The cardinal signs of inflammation are 1. redness/rubor, 2. tumour/swelling, 3.dolar/pain, 4.calor/heat and organ dysfunction (function laesa). Inflammation has 2 components; vascular and cellular. Blood vessels dilate upstream of the inflamed area leading to the rubor and calor and constrict downstream, increasing pressure and causing fluid to leak out of the capillary, resulting in swelling. The cellular component includes infiltration by neutrophils. Leukocyte arrival and functions include; 1. margination: cells marginated from the centre to the periphery of the vessel, 2. rolling: selectins are upregulated on the vessel walls, 3. adhesion: upregulation of the adhesion molecules ICAM and VCAM on the endothelium interact with integrins on the leukocytes resulting in adhesion, 4. diapedesis and chemotaxis: diapedesis is the transmigration of the leukocyte across the endothelium of the capillary and towards a chemotactic product and 5. phagocytosis: engulfing the offending substance/cell.