Platelets are the first cells to be attracted to the wound site due to the release of the Von Willebrand factor from the damaged endothelium. Platelets, in turn, release cytokines such as platelet-derived growth factor, which will attract other inflammatory cells to the wound site.

The maximum flow rate generated during a forceful exhalation, after maximal inspiration is the peak expiratory flow rate (PEFR).PEFR is dependent upon initial lung volume. It is, therefore, dependant on patient’s age, sex and height.PEFR is dependent on voluntary effort and muscular strength of the patient.PEFR is decreased with increasing airway resistance, e.g. in asthma, and it correlates well with the forced expiratory volume in one second (FEV1) value measured in spirometry. This correlation decreases in patients with asthma as airflow decreases.

Somatostatin-producing cells present in the pyloric antrum, duodenum, and pancreatic islets are known as D-cells or delta-cells. Somatostatin inhibits gastric acid secretion by acting directly on acid-producing parietal cells in the stomach via a G-protein coupled receptor.Somatostatin affects hormones in the following ways:Inhibits the anterior pituitary’s secretion of growth hormone.Inhibits the anterior pituitary’s secretion of thyroid-stimulating hormone.The secretion of various gastrointestinal hormones is inhibited (including gastrin, CCK, secretin, motilin, VIP and GIP) Reduces the rate at which the stomach empties.Inhibits the release of insulin and glucagon from the pancreas.The pancreas’ exocrine secretory activity is inhibited.Somatostatin can also slow the digestive process by suppressing the production of hormones such gastrin, secretin, and histamine, which reduces gastric acid secretion.A somatostatinoma is a cancerous tumour of the endocrine pancreas’ D-cells, which make somatostatin. Somatostatin inhibits pancreatic and gastrointestinal hormones when levels are high. The following clinical characteristics are related with somatostatinomas:Insulin secretion blockage causes diabetes mellitus.Gallstones by inhibition of CCK and secretin Steatorrhoea via inhibition of CCK and secretinHypochlorhydria is caused by the suppression of gastrin, a hormone that increases gastric acid output regularly.

The most frequent cause of red eye is conjunctivitis. It is caused by inflammation of the conjunctiva which can be infective or allergic and accounts for about 35% of all eye problems presenting to general practice.Viral conjunctivitis is commonly caused by adenoviruses and it is the most common infectious conjunctivitis.The common bacterial causes of conjunctivitis are Haemophilus influenzae, Streptococcus pneumoniae, and Staphylococcus aureus.The clinical features of infective conjunctivitis include:Acute onset of conjunctival erythemaFeeling ‘grittiness’, ‘foreign body’ or ‘burning’ sensation in the eye.Watering and discharge which may cause transient blurring of visionThe discharge for viral conjunctivitis is less than that of bacterial conjunctivitis and usually watery.

Plasma potassium greater than 5.5 mmol/L is hyperkalaemia or elevated plasma potassium level. Among the causes of hyperkalaemia include congenital adrenal hyperplasia. Congenital adrenal hyperplasia is a general term referring to autosomal recessive disorders involving a deficiency of an enzyme needed in cortisol and/or aldosterone synthesis. The level of cortisol and/or aldosterone deficiency affects the clinical manifestations of congenital adrenal hyperplasia. When it involves hypoaldosteronism, it can result in hyponatremia and hyperkalaemia. While hypercortisolism can cause hypoglycaemia.The other causes of hyperkalaemia may include renal failure, excess potassium supplementation, Addison’s disease (adrenal insufficiency), renal tubular acidosis (type 4), rhabdomyolysis, burns, trauma, Tumour lysis syndrome, acidosis, and medications such as ACE inhibitors, angiotensin receptor blockers, NSAIDs, beta-blockers, digoxin, and suxamethonium. Bartter’s syndrome is characterized by hypokalaemic alkalosis with normal to low blood pressure. Type 1 and 2 renal tubular acidosis both cause hypokalaemia. Gitelman’s syndrome is a defect of the distal convoluted tubule of the kidney. It causes metabolic alkalosis with hypokalaemia and hypomagnesemia. And excessive liquorice ingestion causes hypermineralocorticoidism and hypokalaemia as well. Thus, among the choices, only congenital adrenal hyperplasia can cause hyperkalaemia.

Treatment for oral candidiasis is with nystatin mouthwash. In unresponsive cases, oral fluconazole is used

Diabetes insipidus is the inability to produce concentrated urine. It is characterised by the presence of excessive thirst, polyuria and polydipsia. There are two distinct types of diabetes insipidus:Cranial (central) diabetes insipidus and;Nephrogenic diabetes insipidusCranial diabetes insipidus is caused by a deficiency of vasopressin (anti-diuretic hormone). Patients with cranial diabetes insipidus can have a urine output as high as 10-15 litres per 24 hours, but adequate fluid intake allows most patients to maintain normonatraemia. 30% of cases are idiopathic, and a further 30% are secondary to head injuries. Other causes include neurosurgery, brain tumours, meningitis, granulomatous disease (e.g. sarcoidosis) and drugs, such as naloxone and phenytoin. A very rare inherited form also exists that is associated with diabetes mellitus, optic atrophy, nerve deafness and bladder atonia.Nephrogenic diabetes insipidus is caused by renal resistance to the action of vasopressin. As with cranial diabetes insipidus, urine output is markedly elevated. Serum sodium levels can be maintained by secondary polydipsia or can be elevated. Causes of nephrogenic diabetes insipidus include chronic renal disease, metabolic disorders (e.g. hypercalcaemia and hypokalaemia) and drugs, including long-term lithium usage and demeclocycline.In view of the history of long-term lithium use, in this case, nephrogenic diabetes insipidus is the most likely diagnosis.

Bumetanide is 40 times more powerful than furosemide, and one milligram is roughly equivalent to 40 milligrams of furosemide. This patient is currently taking 80 mg of furosemide and should be switched to a 2 mg bumetanide once daily.

Mannitol is the most widely used osmotic diuretic that is most commonly used to reduce cerebral oedema and intracranial pressure. It is recommended to use mannitol for the reduction of CSF pressure/cerebral oedema in a dose of 0.25-2 g/kg as an intravenous infusion over 30-60 minutes. This can be repeated 1-2 times after 4-8 hours if needed.Mannitol has several contraindications and some of them are listed below:1. Anuria due to renal disease2. Acute intracranial bleeding (except during craniotomy)3. Severe cardiac failure4. Severe dehydration5. Severe pulmonary oedema or congestion6. Known hypersensitivity to mannitol

At rest the right dome of the diaphragm lies slightly higher than the left; this is thought to be due to the position of the liver. In normal expiration, the normal upper limits of the superior margins are the fifth rib for the right dome, the fifth intercostal space for the left dome and the xiphoid process for the central tendon.

Acute lymphoblastic leukaemia (ALL) is caused by an accumulation of lymphoblasts in the bone marrow and is the most common malignancy of childhood. The incidence of ALL is highest at 3 – 7 years, with 75% of cases occurring before the age of 6. 85% of cases are of B-cell lineage. Haematological investigations reveal a normochromic normocytic anaemia with thrombocytopenia in most cases. The total white cell count may be decreased, normal or increased. The blood film typically shows a variable number of blast cells. The bone marrow is hypercellular with >20% blast cells.

Contractility of myocardial cells depends on the intracellular [Ca2+], which is regulated by Ca2+entry across the cell membrane during the plateau of the action potential and by Ca2+uptake into and release from the sarcoplasmic reticulum (SR).

In the United Kingdom, antibiotic resistance is becoming a significant factor in the treatment of urinary tract infections and pyelonephritis. E. coli (the main causative organism of both urinary tract infections and acute pyelonephritis) resistance to the following antibiotics in laboratory-processed urine specimens is:30.3 percent trimethoprim (varies by area from 27.1 to 33.4 percent )19.8 percent co-amoxiclav (varies by area from 10.8 to 30.7 percent )Ciprofloxacin (Cipro): 10.6% (varies by area from 7.8 to 13.7 percent )Cefalexin has a concentration of 9.9%. (varies by area from 8.1 to 11.4 percent )

All older antihistamines such as chlorphenamine cause sedation. The newer antihistamines e.g. cetirizine cause less sedation and psychomotor impairment than the older antihistamines because they are much less lipid soluble and penetrate the blood brain barrier only to a slight extent.

Hepatitis B surface antigen (HBsAg) is a protein on the surface of the hepatitis B virus, that is the first serologic marker to appear in a new acute infection.It can be detected as early as 1 week and as late as 9 weeks. It can be detected in high levels in serum during acute or chronic hepatitis B virus infection. The presence of HBsAg indicates that the person is infectious. The body normally produces antibodies to HBsAg as part of the normal immune response to infection. HBsAg is the antigen used to make hepatitis B vaccine.Hepatitis B surface antibody (anti-HBs) indicates recovery and immunity from the hepatitis B virus infection. Anti-HBs also develops in a person who has been successfully vaccinated against hepatitis B.Total hepatitis B core antibody (anti-HBc): Appears at the onset of symptoms in acute hepatitis B and persists for life. The presence of anti-HBc indicates previous or ongoing infection with hepatitis B virus in an undefined time frame. It is not present following hepatitis B vaccination.IgM antibody to hepatitis B core antigen (IgM anti-HBc) indicates recent infection with hepatitis B virus (<6 months). Its presence indicates acute infection.The following table summarises the presence of hepatitis B markers according to each situation:Susceptible to infection:HBsAg = NegativeAnti-HBc = NegativeAnti-HBs = NegativeImmune due to natural infection:HBsAg = NegativeAnti-HBc = PositiveAnti-HBs = PositiveImmune due to vaccination:HBsAg = NegativeAnti-HBc = NegativeAnti-HBs = PositiveAcute infection:HBsAg = PositiveAnti-HBc = PositiveAnti-HBs = NegativeIgM anti-HBc = PositiveChronic infection:HBsAg = PositiveAnti-HBc = PositiveAnti-HBs = NegativeIgM anti-HBc = Negative

First line treatment of threadworms is with mebendazole, with treatment of the whole family, and a repeat treatment after 2 weeks. Threadworms live in the large bowel, but direct multiplication of worms does not occur here. Threadworms most commonly infect children, and may be symptomatic or cause pruritus ani.

Dynamic compression occurs because as the expiratory muscles contract during forced expiration, all the structures within the lungs, including the airways, are compressed by the positive intrapleural pressure. Consequently the smaller airways collapse before the alveoli empty completely and some air remains within the lungs (the residual volume). Physiologically this is important as a completely deflated lung with collapsed alveoli requires significantly more energy to inflate. Dynamic compression does not occur in normal expiration because the intrapleural pressure is negative throughout the whole cycle.

CLL (chronic lymphocytic leukaemia) is the most common type of chronic lymphoid leukaemia, with a peak incidence between the ages of 60 and 80. It is the most common type of leukaemia in Europe and the United States, but it is less common elsewhere. The CLL tumour cell is a mature B-cell with low immunoglobulin surface expression (IgM or IgD). The average age at diagnosis is 72 years, with only 15% of cases occurring before the age of 50. The male-to-female ratio is about 2:1. Over 80% of cases are identified by the results of a routine blood test, which is usually performed for another reason. Lymphocytic anaemia, thrombocytopenia, and normochromic normocytic anaemia are common laboratory findings. Aspiration of bone marrow reveals up to 95% lymphocytic replacement of normal marrow elements.

Because the middles of the shafts of the ribs are lower than either the anterior or posterior end, elevation of the ribs also moves the middles of the shafts laterally. This ‘bucket handle’ upwards and lateral movement increases the lateral dimensions of the thorax.

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 sluggishnessHypotension is a condition in which the blood pressure (notably orthostatic hypotension)Vomiting and nauseaLoss of weightAxillary and pubic hair lossDepressionHyperpigmentation 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:HyponatraemiaHyperkalaemiaHypercalcaemiaHypoglycaemiaAcidosis metabolicaWhen 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.

An antidote for digoxin overdose is digoxin-specific antibody (Digifab). It’s a lyophilized preparation of digoxin-immune ovine Fab immunoglobulin fragments that’s sterile, purified, and lyophilized. These fragments were extracted from the blood of healthy sheep that had been immunised with a digoxin derivative called digoxin-dicarboxymethoxylamine (DDMA), a digoxin analogue that contains the functionally important cyclopentaperhydrophenanthrene:lactone ring moiety coupled to keyhole limpet hemocyanin (KLH).Digifab has a higher affinity for digoxin than digoxin does for its sodium pump receptor, which is thought to be the site of its therapeutic and toxic effects. When given to a patient who is intoxicated, Digifab binds to digoxin molecules, lowering free digoxin levels and shifting the equilibrium away from binding to receptors, reducing cardio-toxic effects. The kidney and reticuloendothelial system then clear the Fab-digoxin complexes.The following summarises the indications for Digifab in acute and chronic digoxin toxicity:Acute digoxin toxicityChronic digoxin toxicityCardiac arrestLife-threatening arrhythmiaPotassium level > 5 mmol/l>10 mg digoxin ingested (adult)>4 mg digoxin ingested (child)Digoxin level > 12 ng/mlCardiac arrestLife-threatening arrhythmiaSignificant gastrointestinal symptomsSymptoms of digoxin toxicity

Of the filtered sodium, about 65% is reabsorbed in the proximal tubule.

Factors causing bronchoconstriction:Via muscarinic receptorsParasympathetic stimulationStimulation of irritant receptorsInflammatory mediators e.g. histamine, prostaglandins, leukotrienesBeta-blockers

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.

Starling’s equation for fluid filtration describes fluid flow at the capillary bed.Filtration forces (capillary hydrostatic pressure and interstitial oncotic pressure) stimulate fluid movement out of the capillary, while resorption forces promote fluid movement into the capillary (interstitial hydrostatic pressure and plasma oncotic pressure). Although the forces fluctuate along the length of the capillary bed, overall filtration is achieved.At the capillary bed, there is fluid movement.The reflection coefficient (σ), the surface area accessible (S), and the hydraulic conductance of the wall (Lp) are frequently used to account for the endothelium’s semi-permeability, yielding:Volume / min = LpS [(Pc- Pi) –  σ(πp– πi)]Volume /min = (Pc-Pi) – (πp–πi) describes the fluid circulation at the capillaries.Where:Pc= capillary hydrostatic pressurePi= interstitial hydrostatic pressureπp= plasma oncotic pressureπi= interstitial oncotic pressure

Blood transfusion can be a life-saving treatment with significant clinical benefits, but it also comes with a number of risks and potential complications, including:Immunological side effectsErrors in administration (episodes of ‘wrong blood’)Viruses and Infections (bacterial, viral, possibly prion)ImmunodilutionA culture of better safety procedures as well as steps to reduce the use of transfusion has emerged as a result of growing awareness of avoidable risk and improved reporting systems. Transfusion errors, on the other hand, continue to occur, and some serious adverse reactions go unreported.Transfusion-associated graft-vs-host disease (TA-GVHD) is a rare blood transfusion complication that causes fever, rash, and diarrhoea 1-4 weeks after the transfusion. Pancytopenia and liver function abnormalities are common laboratory findings.TA-GVHD, unlike GVHD following allogeneic marrow transplantation, causes profound marrow aplasia with a mortality rate of >90%. Survival is uncommon, with death occurring within 1-3 weeks of the onset of symptoms.Because of immunodeficiency, severe immunosuppression, or shared HLA antigens, viable T lymphocytes in blood components are transfused, engraft, and react against the recipient’s tissues, and the recipient is unable to reject the donor lymphocytes.The following is a list of the most common transfusion reactions and complications:1) Reaction to a febrile transfusionThe temperature rises by one degree from the baseline. Chills and malaise are also possible symptoms.The most common response (1 in 8 transfusions).Cytokines from leukocytes in transfused red cell or platelet components are usually to blame.Only supportive. The use of paracetamol is beneficial.2) Acute haemolytic reaction is a type of haemolytic reaction that occurs when theFever, chills, pain at the transfusion site, nausea, vomiting, and dark urine are all symptoms of a transfusion reaction.Early on, many people report a sense of ‘impending doom.’The most serious reaction. ABO incompatibility is frequently caused by a clerical error.STOP THE TRANSFUSION OF INFORMATION. IV fluids should be given. It’s possible that diuretics will be required.3) Haemolytic reaction that is delayedIt usually happens 4 to 8 days after a blood transfusion.Fever, anaemia, jaundice, and haemoglobinuria are all symptoms that the patient has.Positive Coombs test for direct antiglobulin.Because of the low titre antibody, it is difficult to detect in a cross-match, and it is unable to cause lysis at the time of transfusion.The majority of delayed haemolytic reactions are harmless and do not require treatment.Anaemia and renal function should be monitored and treated as needed.4) Reaction to allergensForeign plasma proteins are usually to blame, but anti-IgA could also be to blame.Urticaria, pruritus, and hives are typical allergic reactions. It’s possible that it’s linked to laryngeal oedema or bronchospasm.Anaphylaxis is a rare occurrence.Antihistamines can be used to treat allergic reactions symptomatically. It is not necessary to stop transfusions.If the patient develops anaphylaxis, the transfusion should be stopped and the patient should be given adrenaline and treated according to the ALS protocol.5) TRALI (Transfusion Related Acute Lung Injury)Within 6 hours of transfusion, there was a sudden onset of non-cardiogenic pulmonary oedema.It’s linked to the presence of antibodies to recipient leukocyte antigens in the donor blood.The most common cause of death from transfusion reactions is this.STOP THE TRANSFUSION OF INFORMATION. Oxygen should be given to the patient. Around 75% of patients will require aggressive respiratory support.The use of diuretics should be avoided.6) TACO (Transfusion Associated Circulatory Overload)Acute or worsening respiratory distress within 6 hours of a large blood transfusion. Fluid overload and pulmonary and peripheral oedema can be seen. Rapid blood pressure rises are common. BNP is usually 1.5 times higher than it was before the transfusion. It is most common in the elderly and those who have chronic anaemia.Blood transfusions should be given slowly, over the course of 3-4 hours.

In the absence of any contra-indications, high-dose NSAIDs are the first-line treatment for acute gout. Naproxen 750 mg as a stat dose followed by 250 mg TDS is a commonly used and effective regime.Aspirin should not be used in gout as it reduces the urinary clearance of urate and interferes with the action of uricosuric agents. Naproxen, Diclofenac or Indomethacin are more appropriate choices.Allopurinol is used prophylactically, preventing future attacks by reducing serum uric acid levels. It should not be started in the acute phase as it increases the severity and duration of symptoms.Colchicine acts on the neutrophils, binding to tubulin to prevent neutrophil migration into the joint. It is as effective as NSAIDs in relieving acute attacks. It also has a role in prophylactic treatment if Allopurinol is not tolerated.NSAIDs are contra-indicated in heart failure as they can cause fluid retention and congestive cardiac failure. Colchicine is the preferred treatment in patients with heart failure or those who are intolerant of NSAIDs.

Parathyroid hormone (PTH) is a peptide hormone synthesised by the chief cells of the parathyroid glands, located immediately behind the thyroid gland. PTH is primarily released in response to decreasing plasma [Ca2+] concentration. PTH acts to increase plasma calcium levels and decrease plasma phosphate levels.Parathyroid hormone (PTH) acts to increase calcium reabsorption in the distal tubule of the nephron (by activating Ca2+entry channels in the apical membrane and the Ca2+ATPase pump in the basolateral membrane) and increase phosphate excretion by inhibiting reabsorption in the proximal tubule of the nephron.

The first place that haematopoiesis occurs in the foetus is in the yolk sac. Later on, it occurs in the liver and spleen, which are the major hematopoietic organs from about 6 weeks until 6 – 7 months gestation. At this point, the bone marrow becomes the most important site. Haemopoiesis is restricted to the bone marrow in normal childhood and adult life.

The gluteal muscles are a group of muscles that make up the buttock area. These muscles include: gluteus maximus, gluteus medius. and gluteus minimus.The gluteus maximus is the most superficial as well as largest of the three muscles and makes up most of the shape and form of the buttock and hip area. It is a thick, fleshy muscle with a quadrangular shape. It is a large muscle and plays a prominent role in the maintenance of keeping the upper body erect.The innervation of the gluteus maximus muscle is from the inferior gluteal nerve.