Overdosing on calcium-channel blockers should always be taken seriously and regarded as potentially fatal. Verapamil and diltiazem are the two most lethal calcium channel blockers in overdose. These work by binding the alpha-1 subunit of L-type calcium channels, preventing calcium from entering the cell. In cardiac myocytes, vascular smooth muscle cells, and islet beta-cells, these channels play an important role.The standard ABC approach should be used to resuscitate all patients as needed. If life-threatening toxicity is expected, intubation and ventilation should be considered early on. If hypotension and shock are developing, early invasive blood pressure monitoring is recommended.The primary goal of specific treatments is to support the cardiovascular system. These are some of them:1. Fluid resuscitation: Give up to 20 mL of crystalloid per kilogramme of body weight.2. Calcium supplementationThis can be a good way to raise blood pressure and heart rate temporarily.via central venous access: 10% calcium gluconate 60 mL IV (0.6-1.0 mL/kg in children) or 10% calcium chloride 20 mL IV (0.2 mL/kg in children)Boluses can be given up to three times in a row.To keep serum calcium >2.0 mEq/L, consider a calcium infusion.3. Atropine: 0.6 mg every 2 minutes up to 1.8 mg is an option, but it is often ineffective.4. HIET (high-dose insulin-euglycemic therapy):The role of HIET in the step-by-step management of cardiovascular toxicity has changed.5. Vasoactive infusions:This was once thought to be a last-ditch measure, but it is now widely recommended that it be used sooner rather than later.Insulin with a short half-life 50 mL of 50 percent glucose IV bolus plus 1 U/kg bolus (unless marked hyperglycaemia present)Short-acting insulin/dextrose infusions should be continued.Glucose should be checked every 20 minutes for the first hour, then hourly after that.Regularly check potassium levels and replace if they fall below 2.5 mmol/L.Titrate catecholamines to effect (inotropy and chronotropy); options include dopamine, adrenaline, and/or noradrenaline infusions.6. Sodium bicarbonate: Use 50-100 mEq sodium bicarbonate (0.5-1.0 mEq/kg in children) in cases where a severe metabolic acidosis develops.7. Cardiac pacing: It can be difficult to achieve electrical capture, and it may not improve overall perfusion.Bypass AV blockade with ventricular pacing, which is usually done at a rate of less than 60 beats per minute.8. Intralipid transportCalcium channel blockers are lipid-soluble agents, so they should be used in refractory cases.

Lymphatic drainage of the thyroid gland involves the lower deep cervical, prelaryngeal, pretracheal, and paratracheal nodes. The paratracheal and lower deep cervical nodes, specifically, receive lymphatic drainage from the isthmus and the inferior lateral lobes. The superior portions of the thyroid gland drain into the superior pretracheal and cervical nodes.

ADH, or antidiuretic hormone, is a hormone that regulates water and electrolyte balance. It is released in response to a variety of events, the most important of which are higher plasma osmolality or lower blood pressure. ADH increases plasma volume and blood pressure via acting on the kidneys and peripheral vasculature.It causes vasoconstriction by binding to peripheral V1 Receptors on vascular smooth muscle via the IP3 signal transduction and Rho-kinase pathways. The systemic vascular resistance and arterial pressure rise as a result. High levels of ADH appear to be required for this to have a major impact on arterial pressure, such as in hypovolaemic shock.

A lower target of 88 – 92% oxygen saturation is indicated for patients at risk of hypercapnic respiratory failure e.g. patients with COPD. Until blood gases can be measured, initial oxygen should be given using a controlled concentration of 28% or less, titrated towards the SpO2 of 88 – 92%. The aim is to provide the patient with enough oxygen to achieve an acceptable arterial oxygen tension without worsening carbon dioxide retention and respiratory acidosis.

A pathogen is an organism that is capable of causing disease.

Meckel’s diverticulum has certain classic characteristics.1. It lies on the antimesenteric border of the middle-to-distal ileum2. It is approximately 2 feet proximal to the ileocaecal junction3. It appears as a blind-ended tubular outpouching of bowel4. 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.

Polydipsia is the feeling of extreme thirstiness. It is often linked to polyuria, which is a urinary condition that causes a person to urinate excessively. The cycle of these two processes makes the body feel a constant need to replace the fluids lost in urination. In healthy adults, a 3 liter urinary output per day is considered normal. A person with polyuria can urinate up to 15 liters of urine per day. Both of these conditions are classic signs of diabetes. The other options are also types of diabetes, except for psychogenic polydipsia (PPD), which is the excessive volitional water intake seen in patients with severe mental illness or developmental disability. However, given the patient’s previous head injury, the most likely diagnosis is cranial diabetes insipidus. By definition, cranial diabetes insipidus is caused by damage to the hypothalamus or pituitary gland after an infection, operation, brain tumor, or head injury. And the patient’s history confirms this diagnosis. To define the other choices, nephrogenic diabetes insipidus happens when the structures in the kidneys are damaged and results in an inability to properly respond to antidiuretic hormone. Kidney damage can be caused by an inherited (genetic) disorder or a chronic kidney disorder. As with cranial diabetes insipidus, nephrogenic diabetes insipidus can also cause an elevated urine output. Diabetes mellitus is classified into two types, and the main difference between them is that type 1 diabetes is a genetic disorder, and type 2 diabetes is diet-related and develops over time. Type 1 diabetes is also known as insulin-dependent diabetes, in which the pancreas produces little or no insulin. Type 2 diabetes is termed insulin resistance, as cells don’t respond customarily to insulin.

Cysts are resistant forms and are responsible for transmission of giardiasis. Both cysts and trophozoites can be found in the faeces (diagnostic stages). The cysts are hardy and can survive several months in cold water. Infection occurs by the ingestion of cysts in contaminated water, food, or by the faecal-oral route (hands or fomites). In the small intestine, excystation releases trophozoites (each cyst produces two trophozoites).Trophozoites multiply by longitudinal binary fission, remaining in the lumen of the proximal small bowel where they can be free or attached to the mucosa by a ventral sucking disk.Encystation occurs as the parasites transit toward the colon. The cyst is the stage found most commonly in non diarrheal faeces.Because the cysts are infectious when passed in the stool or shortly afterward, person-to-person transmission is possible. While animals are infected with Giardia, their importance as a reservoir is unclear.

Flexor digiti minimi brevis muscle is located on the ulnar side of the palm, lying on the radial border of the abductor digiti minimi. Together with the abductor digiti minimi and opponens digiti minimi muscles, it forms the hypothenar eminence. The muscle is situated inferior and lateral to adductor digiti minimi muscle and superior and medial to opponens digiti minimi muscle. The proximal parts of flexor digiti minimi brevis and abductor digiti minimi muscles form a gap through which deep branches of the ulnar artery and ulnar nerve pass.

Carbohydrates are the main energy source of most diets. They provide 17 kJ (4 kcal) of energy per gram. Most dietary carbohydrate is in the form of polysaccharides. The principal ingested polysaccharides are starch which is derived from plant sources and glycogen which is derived from animal sources. Dietary fibre consists of indigestible carbohydrate (found in plant foods) such as cellulose, lignin and pectin.

The liver produces bile on a constant basis, which is then stored and concentrated in the gallbladder. In a 24-hour period, around 400 to 800 mL of bile is generated.Bile is involved in the following processes:Fats are broken down into fatty acids.Waste products are eliminated.Cholesterol homeostasis is the balance of cholesterol in the body.The enteric hormones cholecystokinin and secretin are primarily responsible for bile secretion. When chyme from an unprocessed meal enters the small intestine, they are released, and they play the following function in bile secretion and flow:Cholecystokinin promotes gallbladder and common bile duct contractions, allowing bile to reach the intestine.Secretin enhances the secretion of bicarbonate and water by biliary duct cells, increasing the amount of bile and its flow into the gut.Bile acids have a hydrophobic and hydrophilic area, making them amphipathic. Bile acids’ amphipathic nature allows them to perform the following crucial functions:Emulsification of lipid aggregates increases the surface area of fat and makes it easier for lipases to digest it.Lipid solubilization and transport: solubilizes lipids by creating micelles, which are lipid clumps that float in water.

In infants and young children, lymphocytosis often occurs in response to infections that would normally produce a neutrophil reaction in adults.Lymphocytosis occurs in:1. Viral infections (e.g. infectious mononucleosis, HIV, rubella, mumps, viral hepatitis, cytomegalovirus, herpes simplex or zoster)2. Bacterial infections (e.g. pertussis, tuberculosis, toxoplasmosis, syphilis)3. Chronic lymphoid leukaemias4. Acute lymphoblastic leukaemias5. Non-Hodgkin lymphoma6. Thyrotoxicosis

Gallbladder inflammation can cause pain in the right upper quadrant and right shoulder, which is caused by irritation of the diaphragmatic peritoneum. Pain from areas supplied by the phrenic nerve is often referred to other somatic regions served by spinal nerves C3-C5.

Escherichia coli is a Gram-negative bacilli that is an important member of the intestinal flora. It is the most common cause of UTI in adults (about 70 – 95% of cases), followed by Staphylococcus saprophyticus (about 5 – 10% of cases), and an important cause of neonatal meningitis. E. coli O157 strain is implicated in the development of dysentery associated with haemolytic uraemic syndrome characterised by haemolytic anaemia, thrombocytopenia and acute renal failure.

A range of one SD above and below the mean (+/- 1 SD) includes 68.2% of the sample values.A range of two SD above and below the mean (+/- 2 SD) includes 95.4% of the sample values.A range of three SD above and below the mean (+/- 3 SD) includes 99.7% of the sample values.

Clinical features of DKA: Symptoms: Polyuria, polydipsia, thirst, lethargy, weight loss, nausea, vomiting, anorexia, abdominal pain, dehydration, headache, altered mental stateSigns: Dry mucous membranes, ketotic breath, tachycardia, hypotension, Kussmaul breathing, focal signs of precipitant e.g. infection

FUSEDCARS can be used to remember some of the causes of a normal anion gap acidosis:Fistula (pancreaticoduodenal)Ureteroenteric conduitSaline administrationEndocrine (hyperparathyroidism)DiarrhoeaCarbonic anhydrase inhibitors (e.g. acetazolamide)Ammonium chlorideRenal tubular acidosisSpironolactone

Insulin is produced by beta cells, located centrally within the islets of Langerhans, in the endocrine tissues of the pancreas. Insulin is a polypeptide hormone consisting of two short chains (A and B) linked by disulphide bonds. Proinsulin is synthesised as a single-chain peptide. Within storage granules, a connecting peptide (C peptide) is removed by proteases to yield insulin. Insulin release is stimulated initially during eating by the parasympathetic nervous system and gut hormones such as secretin, but most output is driven by the rise in plasma glucose concentration that occurs after a meal. The effects of insulin are mediated by the receptor tyrosine kinase.

Ludwig’s angina is life-threatening cellulitis of the soft tissue involving the floor of the mouth and neck. It involves three compartments of the floor of the mouth: the sublingual, submental, and submandibular.Ludwig’s angina usually originates as a dental infection of the second or third mandibular molars. The infection begins in the subgingival pocket and spreads to the musculature of the floor of the mouth. It progresses below the mylohyoid line, indicating that it has moved to the sublingual space. As the roots of the second and third mandibular molars lie below this line, infection of these teeth will predispose to Ludwig’s angina. The infection spreads lingually rather than buccally because the lingual aspect of the tooth socket is thinner. It initially spreads to the sublingual space and progresses to the submandibular space.The disease is usually polymicrobial, involving oral flora, both aerobes, and anaerobes. The most common organisms are Staphylococcus, Streptococcus, Peptostreptococcus, Fusobacterium, Bacteroides, and Actinomyces.

Free movement of the tendons in the carpal tunnel is facilitated by synovial sheaths, which surround the tendons. All of the tendons of the FDP and FDS are contained within a single synovial sheath with a separate sheath enclosing the tendon of the FPL.

When autonomic reflexes are impaired or intravascular volume is markedly depleted, a significant reduction in blood pressure occurs upon standing, a phenomenon termed Postural Hypotension (orthostatic hypotension). Orthostatic hypotension can cause dizziness, syncope, and even angina or stroke. When autonomic reflexes are impaired, blood pressure falls progressively after standing because the gravitational pooling of blood in the legs cannot be compensated by sympathetic vasoconstriction.

All lymphatics from the tongue ultimately drain into the deep cervical chain of nodes along the internal jugular vein, particularly the jugulo-omohyoid lymph node.

Extensor digitorum is a long muscle located in the posterior compartment of the forearm. Together with the extensor carpi ulnaris and extensor digiti minimi, extensor carpi radialis longus and brevis as well as the brachioradialis, it belongs to the group of superficial extensors of the forearm. These muscles can be easily palpated in the lateral aspect of the posterior forearm, especially during the extension of hand when they are contracted.Extensor digitorum runs from the lateral epicondyle of humerus to the medial four phalanges of the hand. In this way, it generates the pull for the extension of the four medial fingers in their metacarpophalangeal and both interphalangeal joints. Extensor digitorum also participates in the extension of the wrist.Extensor digitorum is innervated by posterior interosseous nerve which is a continuation of a deep branch of radial nerve (root value C7 and C8).Extensor digitorum is vascularized by the branches of three different arteries: (1) posterior interosseous artery, (2) radial recurrent artery, and (3) anterior interosseous artery. Anterior and posterior interosseous arteries are the branches of the common interosseous artery that arises from the ulnar artery. The radial recurrent artery is a branch of the radial artery.

Distribution of data is usually unimodal (one peak) but may be bimodal (two peaks) or uniform (no peaks, each value equally likely). The normal distribution is a symmetrical bell-shaped curve. The mean, median, and mode of a normal distribution are equal. In a positive skew, the right tail is longer and the mass of distribution is concentrated on the left; mean > median > mode. In a negative skew, the left tail is longer and the mass of distribution is concentrated on the right; mean < median < mode.

Heroin is injected into the veins and is the most commonly abused drug. Acute intoxication with opioid overuse is the most common cause of death by drug overdose. The clinical features of opioid overdose are:1. Decreased respiratory rate2. Reduced conscious level or coma3. Decreased bowel sounds4. Miotic (constricted) pupils5. Cyanosis6. Hypotension7. Seizures8. Non-cardiogenic pulmonary oedema (with IV heroin usage)The main cause of death secondary to opioid overdose is respiratory depression, which usually occurs within 1 hour of the overdose. Vomiting is also common, and aspiration can occur.Naloxone is a short-acting, specific antagonist of mu(μ)-opioid receptors. It is used to reverse the effects of opioid toxicity. It can be given by a continuous infusion if repeated doses are required and the infusion rate is adjusted according to the vital signs. Initially, the infusion rate can be set at 60% of the initial resuscitative IV dose per hour.Naloxone has a shorter duration of action (6-24 hours) than most opioids, and so close monitoring according to the respiratory rate and depth of coma with repeated injections is necessary. When repeated doses are needed in opioid addicts, naloxone administration may precipitate a withdrawal syndrome with abdominal cramps, nausea and diarrhoea, but these usually settle within 2 hours.An initial dose of 0.4 to 2 mg can be given intravenously and can be repeated at 2 to 3-minute intervals to a maximum of 10mg. If the intravenous route is inaccessible, naloxone can be administered via an IO line, subcutaneously (SQ), IM, or via the intranasal (IN) route.

Flecainide is an antiarrhythmic drug of class Ic that works by blocking the Nav1.5 sodium channel in the heart, prolonging the cardiac action potential and slowing cardiac impulse conduction. It has a significant impact on accessory pathway conduction, particularly retrograde conduction, and significantly reduces ventricular ectopic foci.Many different arrhythmias can be treated with flecainide, including:Pre-excitation syndromes (e.g. Wolff-Parkinson-White)Acute atrial arrhythmiasVentricular arrhythmiasChronic neuropathic painThe use of flecainide is contraindicated in the following situations:Abnormal left ventricular functionAtrial conduction defects (unless pacing rescue available)Bundle branch block (unless pacing rescue available)Distal block (unless pacing rescue available)Haemodynamically significant valvular heart diseaseHeart failureHistory of myocardial infarctionLong-standing atrial fibrillation where conversion to sinus rhythm not attemptedSecond-degree or greater AV block (unless pacing rescue available)Sinus node dysfunction (unless pacing rescue available)Flecainide should only be used in people who don’t have a structural heart problem. The CAST trial found a significant increase in sudden cardiac death and all-cause mortality in patients with an ejection fraction of less than 40% after a myocardial infarction, where it tended to be pro-arrhythmic.Anti-arrhythmic drugs have a limited and ineffective role in the treatment of atrial flutter. It’s important to keep in mind that flecainide shouldn’t be used by itself to treat atrial flutter. When used alone, there is a risk of inducing 1:1 atrioventricular conduction, which results in an increase in ventricular rate that is paradoxical. As a result, it should be used in conjunction with a beta-blocker or a calcium channel blocker with a rate-limiting effect.

Digoxin is excreted through the kidneys, and impaired renal function can lead to elevated digoxin levels and toxicity.The patient’s digoxin dose should be reduced in this case, and their digoxin level and electrolytes should be closely monitored.

Antidiuretic hormone induces the kidneys to release less water, resulting in reduced urine production. In the case of dehydration, ADH levels rise, resulting in a considerable decrease in urine output as well as an increase in plasma protein, blood Hct, and serum osmolality.

Abciximab (ReoPro) is a glycoprotein IIb/IIIa receptor antagonist that is a chimeric monoclonal antibody. It is primarily used during and after coronary artery procedures such as angioplasty to inhibit platelet aggregation.The use of abciximab is contraindicated in the following situations:Internal bleeding is present.Within the last two months, you’ve had major surgery, intracranial surgery, or trauma.Stroke in the previous two yearsIntracranial tumourAneurysm or arteriovenous malformationHaemorrhagic diathesis is a type of haemorrhagic diathesis.VasculitisRetinopathy caused by hypertension

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.