Bordetella pertussis is a Gram negative coccobacillus that causes whooping cough. B. pertussis is spread via the respiratory droplet route and expresses fimbriae that aid their adhesion to the ciliated epithelium of the upper respiratory tract, and produce a number of exotoxins, causing the characteristic thickened bronchial secretions, paralysis of cilia and lymphocytosis.

Helicobacter pylori is a ubiquitous organism that is present in about 50% of the global population. Chronic infection with H pylori causes atrophic and even metaplastic changes in the stomach, and it has a known association with peptic ulcer disease. The most common route of H pylori infection is either oral-to-oral or faecal-to-oral contact.

Bartter’s syndrome is an autosomal recessive renal tubular disorder characterized by hypokalaemia, hypochloraemia, metabolic alkalosis, and hyperreninemia with normal blood pressure. The underlying kidney abnormality results in excessive urinary losses of sodium, chloride, and potassium. Bartter’s syndrome does not cause an elevated potassium level, but instead causes a decrease in its concentration (hypokalaemia). The other choices are causes of hyperkalaemia or elevated potassium levels. Renal failure, Addison’s disease (adrenal insufficiency), congenital adrenal hyperplasia, renal tubular acidosis (type 4), rhabdomyolysis, burns and trauma, tumour syndrome, and acidosis are non-drug causes of hyperkalaemia. On the other hand, drugs that can cause hyperkalaemia include ACE inhibitors, angiotensin receptor blockers, NSAIDs, beta-blockers, digoxin, and suxamethonium.

Innate, or non-specific, immunity is the immune system we are born with.There are three aspects of innate immunity:1. Anatomical barriers, such as:The cough reflexEnzymes in tears and skin oilsMucus – which traps bacteria and small particlesSkinStomach acid2. Humoral barriers, such as:The complement systemInterleukin-13. Cellular barriers, such as:NeutrophilsMacrophagesDendritic cellsNatural killer cellsAntibody production is part of the specific, or inducible immune response. T-lymphocytesare responsible for the cell mediated immune response which is part of specific, or inducible immunity.

Extensor pollicis brevis is a short and slender muscle located in the posterior compartment of the forearm, extending from the posterior surface of radius to the proximal phalanx of thumb. It is one of the deep extensors of the forearm, together with supinator, abductor pollicis longus, extensor pollicis longus and extensor indicis muscles.Extensor pollicis brevis is a deep extensor of the thumb that lies deep to extensor digitorum muscle. It sits directly medial to abductor pollicis longus and posterolateral to extensor pollicis longus muscle. Just above the wrist, extensor pollicis brevis obliquely crosses the tendons of extensor carpi radialis brevis and extensor carpi radialis longus muscles.Extensor pollicis brevis is innervated by posterior interosseous nerve which is a continuation of a deep branch of radial nerve (root value C7 and C8).Extensor pollicis brevis receives its blood supply by posterior interosseous artery and perforating branches from the anterior interosseous artery, which are the branches of common interosseous artery. The common interosseous artery arises immediately below the tuberosity of radius from the ulnar artery.Together with extensor pollicis longus, extensor pollicis brevis is in charge of extension of the thumb in the first metacarpophalangeal joint. It also extends the thumb in the carpometacarpal joint of the thumb. This movement is important in the anatomy of the grip, as it enables letting go of an object. As it crosses the wrist, extensor pollicis brevis also participates in the extension and abduction of this joint.

Signs and symptoms of Sickle cell disease(SCD):Acute and chronic pain: The most common clinical manifestation of SCD is vaso-occlusive crisis; pain crises are the most distinguishing clinical feature of SCDBone pain: Often seen in long bones of extremities, primarily due to bone marrow infarctionAnaemia: Universally present, chronic, and haemolytic in natureAplastic crisis: Serious complication due to infection with parvovirus B19 (B19V)Splenic sequestration: Characterized by the onset of life-threatening anaemia with rapid enlargement of the spleen and high reticulocyte countInfection: Organisms that pose the greatest danger include encapsulated respiratory bacteria, particularly Streptococcus pneumoniae; adult infections are predominantly with gram-negative organisms, especially SalmonellaGrowth retardation, delayed sexual maturation, being underweightHand-foot syndrome: This is a dactylitis presenting as bilateral painful and swollen hands and/or feet in childrenAcute chest syndrome: Young children present with chest pain, fever, cough, tachypnoea, leucocytosis, and pulmonary infiltrates in the upper lobes; adults are usually afebrile, dyspnoeic with severe chest pain, with multilobar/lower lobe diseasePulmonary hypertension: Increasingly recognized as a serious complication of SCDAvascular necrosis of the femoral or humeral head: Due to vascular occlusionCentral nervous system (CNS) involvement: Most severe manifestation is strokeOphthalmologic involvement: Ptosis, retinal vascular changes, proliferative retinitisCardiac involvement: Dilation of both ventricles and the left atriumGastrointestinal involvement: Cholelithiasis is common in children; liver may become involvedGenitourinary involvement: Kidneys lose concentrating capacity; priapism is a well-recognized complication of SCDDermatologic involvement: Leg ulcers are a chronic painful problem

Heparin-induced thrombocytopenia (HIT) is a prothrombotic disorder caused by antibodies that recognize complexes of platelet factor 4 (PF4) and heparin. HIT is frequently considered in the differential diagnosis of thrombocytopenia occurring in patients on heparin therapy. HIT is a challenging diagnosis because of routine heparin use in hospitalized patients, the common occurrence of thrombocytopenia. The process of heparin dependent IgG antibodies binding to heparin/platelet factor 4 complexes activates platelets and produces a hypercoagulable state. This syndrome typically develops 5-10 days (range 4-15 days) after heparin is commenced. It can occur with unfractionated heparin, low molecular weight heparin, or, rarely, fondaparinux. The diagnosis of HIT requires the combination of a compatible clinical picture and laboratory confirmation of the presence of heparin dependent platelet activating HIT antibodies. Discontinuation of heparin alone or initiation of a vitamin K antagonist alone like warfarin, is not sufficient to stop the development of thrombosis in patients with acute HIT. If there is moderate clinical suspicion for HIT, all sources of heparin must be discontinued and there must be consideration of anticoagulant treatment with a non-heparin drug.

Sensory innervation to the external ear is supplied by both cranial and spinal nerves. Branches of the trigeminal, facial, and vagus nerves (CN V, VII, X) are the cranial nerve components, while the lesser occipital (C2, C3) and greater auricular (C2, C3) nerves are the spinal nerve components involved. The lateral surface of the tympanic membrane, the external auditory canal, and the external acoustic meatus are all innervated by nervus intermedius (a branch of CN VII), the auriculotemporal nerve (CN V3), and the auricular branch of the vagus nerve. The concha receives split innervation from nervus intermedius, the auricular branch of the vagus nerve, and the greater auricular (spinal) nerve. Beyond the concha, the anteromedial and anterosuperior parts of the pinna are innervated by the auriculotemporal nerve, and a portion of the lateral helix by the lesser occipital nerve. The greater auricular nerve provides innervation to the area of the pinna inferolateral to the lobule.

Paracetamol is a non-opioid analgesic, similar in efficacy to aspirin, with antipyretic properties but no anti-inflammatory properties. It is well absorbed orally and does not cause gastric irritation. Paracetamol is a suitable first-line choice for most people with mild-to-moderate pain, and for combination therapy.

Insulin is an anabolic hormone. Its actions can be broadly divided into:Lipid metabolismProtein metabolism andCarbohydrate metabolismFor lipid metabolism, insulin:Stimulates lipogenesisInhibits lipolysis by lipaseFor carbohydrate metabolism, insulin:Decreases gluconeogenesisStimulates glycolysisPromotes glucose uptake in muscle and adipose tissuePromotes glycogen storageIncreases glycogenesisDecreases glycogenolysisProtein metabolism:Stimulates protein synthesisAccelerates net formation of proteinStimulates amino acid uptakeInhibits protein degradationInhibits amino acid conversion to glucose

Gastrin is a peptide hormone that aids in gastric motility by stimulating the generation of gastric acid by the parietal cells of the stomach. G-cells in the stomach’s pyloric antrum, the duodenum, and the pancreas release it.The following stimuli cause the release of gastrin:Stimulation of the vagus nerveHypercalcaemiastomach bloatingProteins that have been partially digested, particularly amino acids.The presence of acid and somatostatin inhibits the release of gastrin.Gastrin’s main actions are as follows:Gastric parietal cells are stimulated to release hydrochloric acid.ECL cells are stimulated to produce histamine.Gastric parietal cell maturation and fundal growth stimulationCauses the secretion of pepsinogen by the gastric chief cells.Improves antral muscle mobility stimulates gastric contractionsIncreases gastric emptying rate and stimulates pancreatic secretionGallbladder emptying is induced.

Severe hyperkalaemia can result in a heart attack or a life-threatening arrhythmia. T waves become narrow-based, pointed, and tall if hyperkalaemia is not treated. The QRS complex widens and eventually merges with the T wave, resulting in a classic sine-wave electrocardiogram. Ventricular fibrillation and asystole are likely to follow.

Activated vitamin D acts to:GUT:increase calcium and phosphate absorption in the small intestine (the main action)KIDNEYS:increase renal calcium reabsorption (in the distal tubule via activation of a basolateral Ca2+ATPase pump), increase renal phosphate reabsorption, inhibit 1-alpha-hydroxylase activity in the kidneys (negative feedback)PARATHYROID GLANDS:inhibit PTH secretion from the parathyroid glands

In non-shockable (PEA/asystole) cardiac arrests, adrenaline should be given as soon as circulatory access is gained. The dose is 1 mg via IV or IO (10 mL of 1:10,000 or 1 mL of 1:1000).Once chest compressions have been resumed after the third shock in a shockable (Vf/pVT) cardiac arrest, adrenaline should be administered. The dosage is one milligram (10 mL of 1:10,000 or 1 mL of 1:1000)It should be given every 3-5 minutes after that (i.e. alternate loops) and without interrupting chest compressions.Systemic vasoconstriction is caused by the alpha-adrenergic effects of adrenaline, which raises coronary and cerebral perfusion pressures.Adrenaline’s beta-adrenergic effects are inotropic (increased myocardial contractility) and chronotropic (increased heart rate), and they can increase coronary and cerebral blood flow. However, concomitant increases in myocardial oxygen consumption and ectopic ventricular arrhythmias (especially in the absence of acidaemia), transient hypoxemia due to pulmonary arteriovenous shunting, impaired microcirculation, and increased post-cardiac arrest myocardial dysfunction may offset these benefits.Although there is no evidence of long-term benefit from its use in cardiac arrest, the improved short-term survival reported in some studies justifies its use.

The brachialis muscle is a prime flexor of the forearm at the elbow joint. It is fusiform in shape and located in the anterior (flexor) compartment of the arm, deep to the biceps brachii. The brachialis is a broad muscle, with its broadest part located in the middle rather than at either of its extremities. It is sometimes divided into two parts, and may fuse with the fibres of the biceps brachii, coracobrachialis, or pronator teres muscles. It also functions to form part of the floor of the cubital fossa.The brachialis is primarily supplied by the musculocutaneous nerve (C5, C6). In addition, a small lateral portion of the muscle is innervated by the radial nerve (C7).

Erythropoietin is a glycoprotein hormone that regulates the formation of red blood cells (red cell production). It is mostly produced by interstitial fibroblasts in the kidney, which are located near the PCT. It is also produced in the liver’s perisinusoidal cells, however this is more common during the foetal and perinatal periods.The kidneys produce and secrete erythropoietin in response to hypoxia. On red blood cells, erythropoietin has two main effects:- It encourages stem cells in the bone marrow to produce more red blood cells.- It protects red blood cell progenitors and precursors from apoptosis by targeting them in the bone marrow.As a result of the increased red cell mass, the oxygen-carrying capacity and oxygen delivery increase.

Flumazenil is a benzodiazepine antagonist that can be helpful in some overdose situations. It works quickly (in less than a minute), but the effects are fleeting, lasting less than an hour. The dose is 200 micrograms every 1-2 minutes with a maximum dose of 3 milligrams per hour.Flumazenil should be avoided by patients who are addicted to benzodiazepines or who take tricyclic antidepressants because it can cause withdrawal symptoms. It can cause seizures or cardiac arrest in these situations.

External (lateral) rotation at the hip joint is produced by the gluteus maximus together with a group of 6 small muscles (lateral rotators): piriformis, obturator internus, superior and inferior gemelli, quadratus femoris and obturator externus.

Peroneus brevis is innervated by the superficial peroneal nerve.Peroneus longus is innervated by the superficial peroneal nerve.Peroneus tertius is innervated by the deep peroneal nerve.

Oedema is defined as a palpable swelling produced by the expansion of the interstitial fluid volume. A variety of clinical conditions are associated with the development of oedema, including heart failure, cirrhosis, and nephrotic syndrome. The development of oedema requires an alteration in capillary dynamics in a direction that favours an increase in net filtration and also inadequate removal of the additional filtered fluid by lymphatic drainage. Oedema may form in response to an elevation in capillary hydraulic pressure (which increases the delta hydraulic pressure) or increased capillary permeability, or it can be due to disruption of the endothelial glycocalyx, decreased interstitial compliance, a lower plasma oncotic pressure (which reduces the delta oncotic pressure), or a combination of these changes. Oedema can also be induced by lymphatic obstruction since the fluid that is normally filtered is not returned to the systemic circulation.

A refractory period follows each action potential. The absolute refractory time and the relative refractory period are two divisions of refractory periods. Because the sodium channels seal after an AP, they enter an inactive state during which they cannot be reopened regardless of membrane potential, this time occurs.The sodium channels slowly come out of inactivation during the relative refractory period that follows. During this time, a stronger stimulus than that required to initiate an action potential can excite the cell. The strength of the stimulus required early in the relative refractory period is relatively high, and it steadily decreases as more sodium channels recover from the inactivation of the refractory period.Nodes of Ranvier are periodic holes in a myelinate axon when there is no myelin and the axonal membrane is exposed. There are no gated ion channels in the portion of the axon covered by the myelin sheath, but there is a high density of ion channels in the Nodes of Ranvier. Action potentials can only occur at the nodes as a result of this.

Impetigo is a highly contagious infection of the superficial epidermis that most commonly affects young children but can occur in any age group. In children it is the most common bacterial skin infection and it is the third most common skin disease overall, behind dermatitis and viral warts.The commonest causative organism is Staphylococcus aureus. Streptococcus pyogenesis the second commonest and causes fewer cases, either alone or in combination withS. aureus.The streptococcal form tends to be commoner in warmer, more humid climates. (Hirschmann JV. Impetigo: etiology and therapy. Curr Clin Top Infect Dis. 2002;22:42–51.)Impetigo is most commonly spread by direct person-to-person contact, and can spread rapidly through families and school classes. It can also, less commonly, be spread by indirect contact.There are two main forms of impetigo:Non-bullous impetigo – lesions usually start as tiny pustules or vesicles that evolve rapidly into honey-crusted plaques that tend to be under 2 cm in diameter. These can be itchy but are rarely painful.Bullous impetigo – lesions have a thin roof and tend to rupture spontaneously. This type is more likely to be painful and may be associated with systemic upset.

The release of cytokines from Reed-Sternberg cells can cause fever in patients with Hodgkin lymphoma, which increases and decreases in a cyclical pattern of 1 to 2 weeks. This is called Pel-Ebstein or Ebstein-Cardarelli fever, specifically seen in Hodgkin lymphoma. The fever is always high grade and can reach 40 degrees or higher.Cyclical fever in other conditions is common but is not termed as Pel-Ebstein fever. This term is reserved only with Hodgkin lymphoma.

Absolute risk reduction (ARR) is computed as the difference between the absolute risk in the control group (ARC) and the absolute risk in the treatment group (ART).ARR = ARC-ARTARR = (25/500) – (10/500)ARR = 0.03

Preload refers to the initial stretching of the cardiac myocytes before contraction. It is therefore related to muscle sarcomere length. The sarcomere length cannot be determined in the intact heart, and so, other indices of preload are used, like ventricular end-diastolic volume or pressure. The end-diastolic pressure and volume of the ventricles increase when venous return to the heart is increased, and this stretches the sarcomeres, which increase their preload.

At the neuromuscular junction, acetylcholine is released from the prejunctional membrane which acts on cholinergic nicotinic receptors on the postjunctional membrane.

Pronator teres syndrome (PTS) is caused by a compression of the median nerve (MN) by the pronator teres (PT) muscle in the forearm. The median nerve, C6 and C7, innervates the pronator teres.

Gluteus minimus is innervated by the superior gluteal nerve.Gluteus medius is innervated by the superior gluteal nerve.Gluteus maximus is innervated by the inferior gluteal nerve.

An overdose of levothyroxine can happen by accident or on purpose. Intentional overdosing is sometimes done to lose weight, but it can also happen in patients who are suicidal. The development of thyrotoxicosis, which can lead to excited sympathetic activity and high metabolism syndrome, is the main source of concern. The time between ingestion and the emergence of clinical features associated with an overdose is often quite long.After a levothyroxine overdose, the majority of patients are asymptomatic. Symptoms and signs are usually only seen in patients who have taken more than 10 mg of levothyroxine in total.The following are the most commonly seen clinical features in patients developing clinical features:TremorAgitationSweatingInsomniaHeadacheIncreased body temperatureIncreased blood pressureDiarrhoea and vomitingLess common clinical features associated with levothyroxine overdose include:SeizuresAcute psychosisThyroid stormTachycardiaArrhythmiasComaThe continued absorption of the ingested levothyroxine causes a progressive rise in both total serum T4 and total serum T3 levels in the first 24 hours after an overdose. However, in some cases, the biochemical picture is completely normal. Thyroid function tests are not always recommended after a thyroxine overdose. Although elevated thyroxine levels are common, they have little clinical significance and have no impact on treatment. Following a levothyroxine overdose, the following biochemical features are common:T4 and T3 levels in the blood are elevated.Free T4 and Free T3 levels are higher.TSH levels in the blood are low.If the patient is cooperative and more than 10 mg of levothyroxine has been consumed, activated charcoal can be given (i.e., likely to become symptomatic)Within an hour of ingestion, the patient presents.The treatment is mostly supportive and aimed at managing the sympathomimetic symptoms that come with levothyroxine overdose. If beta blockers aren’t an option, try propranolol 10-40 mg PO 6 hours or diltiazem 60-180 mg 8 hours.

Thyroid hormones have multiple physiological effects on the body. These include:1. Heat production (thermogenesis)2. Increased basal metabolic rate3. Metabolic effects: (a) Increase in protein turnover (both synthesis and degradation are increased, although overall effect is catabolic)(b) Increase in lipolysis(c)Increase in glycogenolysis and gluconeogenesis4. Enhanced catecholamine effect – Increase in heart rate, stroke volume and thus cardiac output5. Important role in growth and development