Fibroblasts migrate to the wound (about 2 – 5 days after wounding), proliferate and secrete extracellular matrix comprising mainly collagen (type III) and fibronectin to plug the gap.

Macrolide antibiotics (e.g. clarithromycin and erythromycin) are cytochrome P450 enzyme inhibitors. They increase blood levels of theophylline leading to hypokalaemia, and potentially increasing the risk of Torsades de pointes when they are prescribed together.

Co-prescription with theophylline should be avoided.

Factors that enhance theophylline clearance include cigarette smoking, carbamazepine, phenobarbital, phenytoin, primidone, and rifampin.
Medications that inhibit clearance include ethanol, ciprofloxacin, erythromycin, verapamil, propranolol, ticlopidine, tacrine, allopurinol, and cimetidine.

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.

Conjugate eye deviation towards the side of the lesion is seen in damage to the frontal eye field of the frontal lobe. Homonymous hemianopia is typically a result of damage to the occipital lobe (or of the optic radiation passing through the parietal and temporal lobes). Auditory agnosia may been seen in a lesion of the temporal lobe. Hemispatial neglect may be seen in a lesion of the parietal lobe. Receptive dysphasia is seen in damage to Wernicke’s area, in the temporal lobe.

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.

The NICE guidelines for pregnant women with lower UTIs are:
1. Prescribe an antibiotic immediately, taking into account the previous urine culture and susceptibility results or avoiding past antibiotics that may have caused resistance
2. Obtain a midstream urine sample before starting antibiotics and send for urine culture and susceptibility
– Review the choice of antibiotic when the results are available
– change the antibiotic according to susceptibility results if the bacteria are resistant, using a narrow-spectrum antibiotic wherever possible

The first choice of antibiotics for pregnant women aged 12 years and over is:
1. Nitrofurantoin
100 mg modified-release PO BD for 3 days – if eGFR >45 ml/minute

The second-choice (no improvement in lower UTI symptoms on first-choice for at least 48 hours, or when first-choice is not suitable) are:
1. Amoxicillin
500 mg PO TDS for seven days (ONLY if culture results available and susceptible)
2. Cefalexin
500 mg BD for seven days
Alternative second-choices – consult local microbiologist, choose antibiotics based on culture and sensitivity results

Because the anatomical position of the penis is erect, the paired corpora cavernosa are defined as dorsal in the body of the penis and the single corpus spongiosum as ventral. The nerves and vessels lie superficial to the corpus cavernosum. The urethra lies within the corpus spongiosum.

Atropine 500 mcg IV bolus should be administered if there are any adverse features or risk of asystole. If the reaction is not adequate, repeat the steps every 3 to 5 minutes up to a maximum dose of 3 mg. In the case of acute myocardial ischemia or myocardial infarction, atropine should be taken with caution since the increased heart rate may aggravate the ischemia or increase the size of the infarct.

Acute inflammation is defined as inflammation occurring within minutes to hours in response to an injury lasting for less than two weeks.

Acute inflammation
Rapid onset (minutes to hours)
Quick resolution (usually days)

Chronic inflammation
May last weeks, months, or years

There are five cardinal signs of inflammation:
1) Pain
2) Redness
3) Warmth
4) Oedema
5) Loss of function

During acute inflammation, neutrophils are activated and attracted to the site of inflammation in response to various interleukins and cytokines. This process takes place via the following mechanism:
1) Margination
Neutrophils flow nearer the vessel wall rather than in the axial stream, which is referred to as margination
2) Rolling along the surface of vascular endothelium
3) Adhesion to the endothelium by interaction with adhesion molecules (ICAMS and VCAMS)
4) Diapedesis is the movement of neutrophils from the endothelial cells into the interstitial space by squeezing through the gaps between adjacent endothelial cells

Bradykinin and histamine are both responsible for vasodilation which causes oedema and decreases intravascular osmotic pressure.

Neutrophils dominate early (<2 days)
– Many in the bloodstream
– Attach firmly to adhesion molecules
– Apoptosis after 24-48hrs
Monocytes/macrophages dominate late (>2 days)
– Live longer
– Replicate in tissues

Parasympathetic preganglionic neurones originate in the brainstem from which they run in cranial nerves III, VII, IX and X and also from the second and third sacral segments of the spinal cord. Parasympathetic preganglionic neurones release acetylcholine into the synapse, which acts on cholinergic nicotinic receptors on the postganglionic fibre. Parasympathetic peripheral ganglia are generally found close to or within their target, whereas sympathetic peripheral ganglia are located largely in two sympathetic chains on either side of the vertebral column (paravertebral ganglia), or in diffuse prevertebral ganglia of the visceral plexuses of the abdomen and pelvis. Parasympathetic postganglionic neurones release acetylcholine, which acts on cholinergic muscarinic receptors.

Concomitant treatment with NSAIDs increases the risk of renal damage, and with potassium-sparing diuretics (or potassium-containing salt substitutes) increases the risk of hyperkalaemia. Hyperkalaemia and other side effects of ACE inhibitors are more common in the elderly and in those with impaired renal function and the dose may need to be reduced.

Autoregulation is the ability to maintain a constant blood flow despite variations in blood pressure (between 50 – 170 mmHg). It is particularly important in the brain, kidney and heart. There are two main methods contributing to autoregulation:
The myogenic mechanism involves arterial constriction in response to stretching of the vessel wall, probably due to activation of smooth muscle stretch-activated Ca2+channels and Ca2+entry. A reduction in pressure and stretch closes these channels, causing vasodilation.
The second mechanism of autoregulation is due to locally produced vasodilating factors; an increase in blood flow dilutes these factors causing vasoconstriction, whereas decreased blood flow has the opposite effect.

An exudate is an inflammatory fluid emanating from the intravascular space due to changes in the permeability of the surrounding microcirculation.

Some common causes of exudates are: pneumonia, empyema, lung cancer, breast cancer, cancer of the pleura, SLE, rheumatoid arthritis, pericarditis, subphrenic abscess, chylothorax.

Myxoedema, nephrotic syndrome, congestive cardiac failure, and liver cirrhosis all cause TRANSUDATE.

Raised platelet levels have emerged as a cancer risk marker, according to a large population-based study published in 2017(link is external). According to the study, 12 percent of men and 6% of women with thrombocytosis were diagnosed with cancer within a year. These figures increased to 18% in men and 10% in women if a second platelet count was taken within 6 months of the first and showed an increased or stable elevated platelet count.

The researchers discovered that thrombocytosis linked to cancer is most common in colorectal and lung cancers, and it is linked to a worse prognosis. Furthermore, one-third of the cancer patients in the study had no other symptoms that would have prompted an immediate cancer referral.

The exact mechanism by which these cancers cause thrombocytosis is unknown, but one theory proposes the existence of pathogenic feedback loops between malignant cells and platelets, with a reciprocal interaction between tumour growth and metastasis, as well as thrombocytosis and platelet activation. Another hypothesis is that thrombocytosis occurs independently of cancer but aids in its spread and progression.

The findings show that routinely testing for thrombocytosis could cut the time it takes to diagnose colorectal and lung cancer by at least two months. In the UK, this could result in around 5500 earlier cancer diagnoses per year.

Because the positive predictive value of thrombocytosis in middle age for cancer (10%) is higher than the positive predictive value for a woman in her 50s presenting with a new breast lump (8.5%), this is clearly an important research paper that should be used to adjust future clinical practise. The current NICE guidelines predate these new research findings, so we’ll have to wait and see how they affect cancer referral guidelines in the UK.

Because there are so many possible cancers associated with thrombocytosis, the treating clinician should take a thorough history and perform a thorough clinical examination if a patient is diagnosed with it. Further investigation and the most appropriate referral route should be aided by this information.

It’s worth noting that the patients in the study had their blood tests done for a medical reason rather than as a random screening test.

If there are no other symptoms to guide investigation and referral (one-third of the patients in the study had no other symptoms), keep in mind that the two most common cancers encountered were colorectal and lung cancer, so a chest X-ray and a faecal immunochemical test (FIT) for faecal blood may be reasonable initial investigations.

The palmaris longus is a small, fusiform-shaped muscle located on the anterior forearm of the human upper extremity. The palmaris longus muscle is commonly present but may be absent in a small percentage of the population, ranging from 2.5% to 26% of individuals, depending on the studied population.

The palmaris longus belongs to the anterior forearm flexor group in the human upper extremity. The muscle attaches proximally to the medial humeral epicondyle and distally to the palmar aponeurosis and flexor retinaculum. The blood supply to the palmaris longus muscle is via the ulnar artery, a branch of the brachial artery in the human upper extremity.

The palmaris longus muscle receives its innervation via branches of the median nerve containing nerve roots C5-T1. Median nerve injury at or above the elbow joint (including brachial plexus and nerve root injury) can lead to deficits in the palmaris longus and other forearm flexor muscles, leading to weakened elbow flexion, wrist flexion, radial deviation, finger flexion, thumb opposition, flexion, and abduction, in addition to the loss of sensory function in the distribution of the median nerve.

The only mechanism by which insulin facilitates uptake of glucose into cells is by facilitated diffusion through a family of hexose transporters.

The major transporter used for glucose uptake is GLUT4. GLUT4 is made available in the plasma membrane by the action of insulin.
When insulin concentrations are low, GLUT4 transporters are present in cytoplasmic vesicles, where they are cannot be used for transporting glucose.

Angina pectoris is the most common symptom of ischemic heart disease and presents with chest pain relieved by rest and nitro-glycerine.

Nitrates are the first-line treatment to relieve chest pain caused by angina. The commonly used nitrates are:
1. Glyceryl trinitrate
2. Isosorbide dinitrate

Side effects to nitrate therapy are common especially
The most common side effects are:
1. Headaches
2. Feeling dizzy, weak, or tired
3. Nausea
4. Flushing

The serious but less likely to occur side effects are:
1. Methemoglobinemia (rare)
2. Syncope
3. Prolonged bleeding time
4. Exfoliative dermatitis
5. Unstable angina
6. Rebound hypertension
7. Thrombocytopenia

Dry eyes, bradycardia, and metabolic acidosis have not been reported.

Neisseria gonorrhoeae is primarily spread by sexual contact or through transmission during childbirth. It causes gonorrhoea which is a purulent infection of the mucous membrane surfaces.

Lactic acidosis is a common finding in critically ill patients and commonly associated with other serious underlying pathologies. It occurs when pH is <7.35 and lactate is >5 mmol/L. Anion gap is increased in lactic acidosis.

Acquired lactic acidosis is classified into two subtypes:
Type A: lactic acidosis due to tissue hypoxia and
Type B: due to non-hypoxic processes affecting the production and elimination of lactate

Some causes of type A and type B lactic acidosis include:
Type A lactic acidosis
Left ventricular failure
Severe anaemia
Shock (including septic shock)
Asphyxia
Cardiac arrest
CO poisoning
Respiratory failure
Severe asthma and COPD

Type B lactic acidosis:
Regional hypoperfusion
Renal failure
Liver failure
Sepsis (non-hypoxic sepsis)
Thiamine deficiency
Alcoholic ketoacidosis
Diabetic ketoacidosis
Cyanide poisoning
Methanol poisoning
Biguanide poisoning

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.

Factors that elevate intracellular Ca2+ increase nitric oxide (NO) production by the endothelium included local mediators such as histamine and serotonin, bradykinin, and some neurotransmitters like substance P. NO production is also stimulated by increased flow (shear stress) and additionally activates prostacyclin synthesis. As a result of basal production of NO, there is continuous modulation of vascular resistance and as a result, there is increased production of nitric oxide acts which causes vasodilation. Platelet activation and thrombosis are inhibited by nitric oxide.

A lesion of the visual cortex will result in a contralateral homonymous hemianopia with macular sparing.

Serum concentrations of the p24 antigen are usually high in the first few weeks after human immunodeficiency virus (HIV) infection and testing for p24 antigen is therefore a useful way of diagnosing very early infection. P24 is the viral protein that makes up most of the core of the HIV.

ELISA and other antibody tests, though a very sensitive way of detecting the presence of HIV, cannot be used in the early stages of the disease. This is because of the window period of 6-12 weeks before antibodies are produced. These tests will be negative during a seroconversion illness.

The ‘rapid HIV test’ is an HIV antibody test. It will also be negative during the ‘window period’ since it takes time for antibodies to be produced. It is called the ‘rapid test’ as it can detect antibodies in blood or saliva much quicker than the other antibody tests and results are often back within 20 minutes.

CD4 and CD8 counts are usually normal in the early stages of the HIV infection and cannot be used in this case.

Anterior cord syndrome is an incomplete cord syndrome that predominantly affects the anterior 2/3 of the spinal cord, characteristically resulting in motor paralysis below the level of the lesion as well as the loss of pain and temperature at and below the level of the lesion. The patient presentation typically includes these two findings; however, there is variability depending on the portion of the spinal cord affected. Other findings include back pain, or autonomic dysfunction such as hypotension, neurogenic bowel or bladder, and sexual dysfunction. The severity of motor dysfunction can vary, typically resulting in paraplegia or quadriplegia.

Proprioception, vibratory sense, two-point discrimination, and fine touch are not affected in anterior cord syndrome. These sensations are under the control of the dorsal column of the spinal cord, which is supplied by two posterior spinal arteries running in the posterior lateral sulci.

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.

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.

Most NSAIDs act as non-selective inhibitors of the enzyme cyclo-oxygenase (COX). They inhibit both COX-1 and COX-2 isoenzymes.

Only about 60% of patients will respond to any given NSAID.

It can take 21 days of treatment for a clinically appreciable reduction in inflammation to be apparent. If no improvement is seen after 21 days, the NSAID should be changed.

The use of NSAIDs in the 3rd trimester of pregnancy is associated with the following risks: delayed onset of labour, premature closure of ductus arteriosus and foetal kernicterus.

Side effects are lowest in Ibuprofen and highest in indomethacin. so side effects are more commonly seen with indomethacin than naproxen.

The NICE guidelines for women with lower UTIs who are not pregnant are:
1. Consider prescribing a different antibiotic if symptoms do not improve within 48 hours or worsen at any time
2. If the urine culture and susceptibility test results are available, review the choice of antibiotic according to the results and change the antibiotic accordingly if symptoms are not improving or bacteria is resistant to the prescribed antibiotic

The first choice of antibiotics for non-pregnant women aged 16 years and over is:
1. Nitrofurantoin
100 mg modified-release PO BD for 3 days – if eGFR >45 ml/minute
2. Trimethoprim
200 mg PO BD for three days

The second-choice (no improvement in lower UTI symptoms on first-choice for at least 48 hours, or when first-choice is not suitable) are:
1. Nitrofurantoin
100 mg modified-release PO BD for three days – if eGFR >45 ml/minute
2. Pivmecillinam
400 mg PO initial dose, then 200 mg PO TDS for three days
3. Fosfomycin 3 g single sachet dose

The NICE guidelines do NOT recommend isolating a patient with viral conjunctivitis from others or skipping school or work. The disease is contagious, but the spread of the disease can be controlled by maintaining good hygiene practices such as:
1. frequent hand washing
2. use of separate flannels and towels
3. Avoid close contact with others

Antibiotic prescriptions are not part of the NICE guidelines for viral conjunctivitis as they will not affect the course of the disease. Most cases of viral conjunctivitis are self-limiting and resolve within one to two weeks.

The NICE guidelines recommend that symptoms may be eased with self-care measures such as:
1. Bathing/cleaning the eyelids with cotton wool soaked in sterile saline or boiled and cooled water to remove any discharge
2. Cool compresses applied gently around the eye area
3. Use of lubricating drops or artificial tears

Phenoxymethylpenicillin (penicillin V) is less active than benzylpenicillin but both have similar antibacterial spectrum. Because penicillin V is gastric-acid stable, it is suitable for oral administration, but should not be used for serious infections as absorption can be unpredictable and plasma concentrations can be variable.
Its uses are:
1. mainly for respiratory tract infections in children
2. for streptococcal tonsillitis
3. for continuing treatment after one or more injections of benzylpenicillin when clinical response has begun.
4. for prophylaxis against streptococcal infections following rheumatic fever and against pneumococcal infections following splenectomy or in sickle-cell disease.

It should not be used for meningococcal or gonococcal infections.

Mannitol is the most widely used osmotic diuretic that is most commonly used to reduce cerebral oedema and intracranial pressure.
Mannitol has four FDA approved uses clinically:
1. Reduction of intracranial pressure and brain mass
2. reduce intraocular pressure if this is not achievable by other means
3. promote diuresis for acute renal failure to prevent or treat the oliguric phase before irreversible damage
4. promote diuresis to promote the excretion of toxic substances, materials, and metabolites

It can be used in rhabdomyolysis-induced renal failure, especially in crush injuries. Mannitol reduces osmotic swelling and oedema in the injured muscle cells and helps restore skeletal muscle function.

It is a low molecular weight compound and can be freely filtered at the glomerulus and not reabsorbed. This way 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).

Mannitol causes an expansion of the extracellular fluid space, which may worsen congestive cardiac failure. Contraindications to the use of mannitol include:

1. Anuria due to renal disease
2. Acute intracranial bleeding (except during craniotomy)
3. Severe cardiac failure
4. Severe dehydration
5. Severe pulmonary oedema or congestion
6. Known hypersensitivity to mannitol

Rodents and domestic animals are the primary reservoirs for the Leptospira spp, although other animals, including cows, horses, mongooses, and frogs, can also harbour the leptospires. Humans may be directly infected from animal urine or indirectly by contact with soil or water that is contaminated with urine from infected animals. Infected humans can shed leptospires in urine for up to 11 months, infected cows for 3.5 months, infected dogs for 4 years, and infected rodents possibly for their entire lifetime.

The organisms enter the host through mucous membranes or abraded skin. The incubation period ranges from 5 to 14 days.

Enterochromaffin-like cells (ECL cells) are a type of neuroendocrine cell located beneath the epithelium in the stomach glands. They’re most typically located near the parietal cells of the stomach. The ECL cells’ primary role is to produce histamine, which stimulates the formation of stomach acid by the parietal cells.

The table below summarizes the many cell types found in the stomach, as well as the substances secreted by each cell type and the function of the secretion:

Cell type/ Substance secreted/ Function of secretion
Parietal cells/ Hydrochloric acid/ Kills microbes and activates pepsinogen
Parietal cells/ Intrinsic factor/Binds to vitamin B12 and facilitates its absorption
Chief cells/ Pepsinogen/ Protein digestion
Chief cells/ Gastric lipase/ Fat digestion
G-cells/ Gastrin/ Stimulates gastric acid secretion
Enterochromaffin-like cells (ECL cells) /Histamine/ Stimulates gastric acid secretion
Mucous-neck cells/ Mucous and bicarbonate/ Protects stomach epithelium from acid
D-cells/ Somatostatin/ Inhibits gastric acid secretion

The following drugs have been linked to impaired glucose tolerance:
Thiazide diuretics, e.g. Bendroflumethiazide
Loop diuretics, e.g. furosemide
Steroids, e.g. prednisolone
Beta-blockers, e.g. atenolol

Fick’s law tells us that the rate of diffusion of a gas increases:
the larger the surface area involved in gas exchange
the greater the partial pressure gradient across the membrane
the thinner the membrane
the more soluble the gas in the membrane
the lower the molecular weight of the gas

Bupivacaine has a longer duration of action than the other local anaesthetics, up to 8 hours when used for nerve blocks. It has a slow onset, taking up to 30 minutes for full effect. It is often used in lumbar epidural blockade and is particularly suitable for continuous epidural analgesia in labour, or for postoperative pain relief. It is the principal drug used for spinal anaesthesia.

The I-cells in the duodenum generate and release cholecystokinin (CCK), a peptide hormone. It has a crucial role in the digestion process as a hormonal regulator.

CCK cells are concentrated in the proximal small intestine, and when food is consumed, the hormone is produced into the bloodstream. The presence of partly digested lipids and proteins in the duodenum is one of the most powerful stimulus for CCK synthesis.

CCK’s key physiological effects include:

Encourages the pancreas to release digesting enzymes into the small intestine.
Stimulates gallbladder contraction and sphincter of Oddi relaxation, resulting in bile delivery into the duodenum.
Gastric emptying is inhibited, and gastric acid output is reduced.
Satiety induction is a process that involves inducing a feeling of fullness.

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:
Tremor
Agitation
Sweating
Insomnia
Headache
Increased body temperature
Increased blood pressure
Diarrhoea and vomiting
Less common clinical features associated with levothyroxine overdose include:
Seizures
Acute psychosis
Thyroid storm
Tachycardia
Arrhythmias
Coma

The 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.

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.

The musculocutaneous nerve is relatively protected in the axilla, hence injury to it is uncommon. A stab wound in the axilla is the most prevalent source of damage. Because of the activities of the pectoralis major and deltoid, the brachioradialis, and the supinator muscles, arm flexion and forearm flexion and supination are diminished but not completely lost. Over the lateral part of the forearm, there is a lack of sensation.

Glucagon is a peptide hormone that is produced and secreted by alpha cells of the islets of Langerhans, which are located in the endocrine portion of the pancreas. The main physiological role of glucagon is to stimulate hepatic glucose output, thereby leading to increases in glycaemia. It provides the major counter-regulatory mechanism to insulin in maintaining glucose homeostasis.
Hypoglycaemia is the principal stimulus for the secretion of glucagon but may also be used as an antidote in beta-blocker overdose and in anaphylaxis in patients on beta-blockers that fail to respond to adrenaline.
Glucagon then causes:
Glycogenolysis
Gluconeogenesis
Lipolysis in adipose tissue
The secretion of glucagon is also stimulated by:
Adrenaline
Cholecystokinin
Arginine
Alanine
Acetylcholine
The secretion of glucagon is inhibited by:
Insulin
Somatostatin
Increased free fatty acids
Increased urea production

Glycolysis is the metabolic pathway that converts glucose into pyruvate. The free energy released by this process is used to form ATP and NADH. Glycolysis is inhibited by glucagon, and glycolysis and gluconeogenesis are reciprocally regulated so that when one cell pathway is activated, the other is inactive and vice versa.

Glucagon has a minor effect of enhancing lipolysis in adipose tissue. Lipolysis is the breakdown of lipids and involves the hydrolysis of triglycerides into glycerol and free fatty acids. It makes fatty acids available for oxidation.

Because digoxin has a narrow therapeutic index, it can cause toxicity both during long-term therapy and after an overdose. Even when the serum digoxin concentration is within the therapeutic range, it can happen.

Acute digoxin toxicity usually manifests itself within 2-4 hours of an overdose, with serum levels peaking around 6 hours after ingestion and life-threatening cardiovascular complications following 8-12 hours.

Chronic digoxin toxicity is most common in the elderly or those with impaired renal function, and it is often caused by a coexisting illness. The clinical signs and symptoms usually appear gradually over days to weeks.

The following are characteristics of digoxin toxicity:
Nausea and vomiting
Diarrhoea
Abdominal pain
Confusion
Tachyarrhythmias or bradyarrhythmias
Xanthopsia (yellow-green vision)
Hyperkalaemia (early sign of significant toxicity)

Some precipitating factors are as follows:
Elderly patients
Renal failure
Myocardial ischaemia
Hypokalaemia
Hypomagnesaemia
Hypercalcaemia
Hypernatraemia
Acidosis
Hypothyroidism
Spironolactone
Amiodarone
Quinidine
Verapamil
Diltiazem

Inflammation can be divided intoacute inflammation, which occurs over seconds, minutes, hours, and days, andchronic inflammation, which occurs over longer periods.
Acute inflammationcommences within seconds or minutes following the injury of tissues. There are numerous potential stimuli for an acute inflammatory response including infections (bacterial, viral, fungal, parasitic), tissue necrosis, foreign bodies, and Immune reactions (hypersensitivity reactions). The chief cell type of acute inflammation is the neutrophil.
There are three main processesthat occur in the acute inflammatory response:
Increased blood flow
Increased capillary permeability
Neutrophil migration
1. Increased blood flow:
Vasoactive mediators are released, such as nitric oxide, histamine, bradykinins, and prostaglandin E2. These mediators cause vasodilatation and increased blood flow to the area (causing redness and heat).
2. Increased capillary permeability:
The vasoactive mediators also cause increased capillary permeability by causing endothelial cell contraction that widens the intercellular gaps of venules. This allows an outpouring of protein-rich fluid (exudate) into the extracellular tissues that results in a reduction of intravascular osmotic pressure and an increase in extravascular/interstitial pressure. The increased interstitial osmotic pressure leads to oedema.
3. Neutrophil migration:
Neutrophils leave the vasculature through the following sequence of events:
Margination and rolling: neutrophils flow nearer the vessel wall, rather than in the axial stream, which is referred to as margination. Following margination the neutrophils begin rolling along the surface of the vascular endothelium.
Activation and adhesion: then as a result of interaction with endothelial cell adhesion molecules (CAMs) that is mediated by selectins, the neutrophils are activated and adhere to the endothelium.
Transmigration: once bound to the endothelium, neutrophils squeeze through gaps between adjacent endothelial cells into the interstitial fluid, in a process calleddiapedesis.

Treatment should be commenced with antibiotics immediately before laboratory confirmation due to the potentially life-threatening nature of the disease.

In a hospital setting, 2g of IV ceftriaxone (80 mg/kg for a child) or IV cefotaxime (2 g adult; 80 mg/kg child) are the drugs of choice.
In the prehospital setting, IM benzylpenicillin can be given as an alternative.

Glucagon is a peptide hormone that is produced and secreted by alpha cells of the islets of Langerhans, which are located in the endocrine portion of the pancreas. The main physiological role of glucagon is to stimulate hepatic glucose output, thereby leading to increases in glycaemia. It provides the major counter-regulatory mechanism to insulin in maintaining glucose homeostasis.
Hypoglycaemia is the principal stimulus for the secretion of glucagon but may also be used as an antidote in beta-blocker overdose and in anaphylaxis in patients on beta-blockers that fail to respond to adrenaline.
Glucagon then causes:
Glycogenolysis
Gluconeogenesis
Lipolysis in adipose tissue
The secretion of glucagon is also stimulated by:
Adrenaline
Cholecystokinin
Arginine
Alanine
Acetylcholine
The secretion of glucagon is inhibited by:
Insulin
Somatostatin
Increased free fatty acids
Increased urea production

Glycolysis is the metabolic pathway that converts glucose into pyruvate. The free energy released by this process is used to form ATP and NADH. Glycolysis is inhibited by glucagon, and glycolysis and gluconeogenesis are reciprocally regulated so that when one cell pathway is activated, the other is inactive and vice versa.

Glucagon has a minor effect of enhancing lipolysis in adipose tissue. Lipolysis is the breakdown of lipids and involves the hydrolysis of triglycerides into glycerol and free fatty acids. It makes fatty acids available for oxidation.

Meckel’s diverticulum has certain classic characteristics.
1. It lies on the antimesenteric border of the middle-to-distal ileum
2. It is approximately 2 feet proximal to the ileocaecal junction
3. It appears as a blind-ended tubular outpouching of bowel
4. It is about 2 inches long,
5. It occurs in about 2% of the population,
6. It may contain two types of ectopic tissue (gastric and pancreatic).
7. The diverticulum is supplied by the superior mesenteric artery.
8. Proximal to the major duodenal papilla the duodenum is supplied by the gastroduodenal artery (branch of the coeliac trunk)
9. Distal to the major duodenal papilla it is supplied by the inferior pancreaticoduodenal artery (branch of superior mesenteric artery).
10. The arterial supply to the jejunoileum is from the superior mesenteric artery.

Pathogenicity is the ability to cause disease.

Lymphatic vessels from the pharynx and palate drain into the deep cervical lymph nodes.

ADH release is inhibited by low plasma osmolality, alcohol, caffeine, glucocorticoids and atrial natriuretic peptide (ANP).

ADH release is stimulated primarily by raised plasma osmolality detected by osmoreceptors in the anterior hypothalamus. Other factors that increase ADH release include: extracellular fluid volume depletion, angiotensin II, nausea, pain, stress, exercise, emotion, hypoglycaemia.

Cephalosporins of the first generation  include cephalexin, cefradine, and cefadroxil. Urinary tract infections, respiratory tract infections, otitis media, and skin and soft-tissue infections are all treated with them.

Second-generation cephalosporins include cefuroxime, cefaclor, and cefoxitin. These cephalosporins are less vulnerable to beta-lactamase inactivation than the ‘first-generation’ cephalosporins. As a result, they’re effective against germs that are resistant to other antibiotics, and they’re especially effective against Haemophilus influenzae.

Cephalosporins of the third generation include cefotaxime, ceftazidime, and ceftriaxone. They are more effective against Gram-negative bacteria than second generation’ cephalosporins. They are, however, less effective against Gram-positive bacteria such Staphylococcus aureus than second-generation cephalosporins.