Factors that increase glucagon secretion:
↓ Blood glucose
↑ Amino acids
Cholecystokinin
Catecholamines
Acetylcholine

Factors that decrease glucagon secretion:
↑ Blood glucose
Insulin
Somatostatin
Fatty acids, ketoacids

Chlamydia psittaci is a microorganism that is commonly found in birds.

These bacteria can infect people and cause psittacosis. Psittacosis is an infectious disease that may cause high fever and pneumonia associated with headaches, altered mental state, and hepatosplenomegaly.

The mean incubation period for P. falciparum is 12 days.

WHO World Malaria Report 2019 states that an estimated 228 million cases of malaria occurred worldwide in 2018, and reports steadily decreasing the number of cases since 2010. In 2018, nineteen sub-Saharan African countries and India carried approximately 85% of the global malaria burden. The most prevalent and pathogenic malaria parasite, most commonly associated with severe illness and death, especially in the WHO African region, accounting for 99.7% malaria cases, is P. falciparum.

The vector for Plasmodium spp. is a female Anopheles mosquito that inoculates sporozoites contained in her salivary glands into the puncture wound when feeding. Sporozoites enter peripheral bloodstream and are uptake by hepatocytes, where they undergo an asexual pre-erythrocytic liver-stage as liver schizonts lasting up to 2 weeks before the onset of the blood stage.

Intravenous or intramuscular artesunate is the first-line treatment in all patients worldwide and should be used for at least 24 hours and until the oral medication is tolerated.

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.

Post-streptococcal glomerulonephritis is a postinfectious immune-mediated reaction secondary to infection with Streptococcus pyogenes. It typically occurs 2 weeks or more after acute/initial infection, and presents with haematuria, reduced urine output, peripheral oedema, proteinuria, and hypertension. Permanent kidney damage is rare.

Angiotensin-converting enzyme inhibitors (ACE inhibitors) e.g. captopril inhibit the conversion of angiotensin I to angiotensin II, and thus have a vasodilatory effect, lowering both arterial and venous resistance. The cardiac output increases and, because the renovascular resistance falls, there is an increase in renal blood flow. This latter effect, together with reduced aldosterone release, increases Na+ and H2O excretion, contracting the blood volume and reducing venous return to the heart.

CD4+ T-cells (Helper T cells)Recognise antigen only in association with HLA class II molecules (found on antigen presenting cells (APCs) e.g. dendritic cells, B-cells; present exogenous antigens that have been phagocytosed/endocytosed into intracellular vesicles)Form most of the circulating T-cell population (about 75%)Secrete cytokines (e.g. IFN-gamma) which are required for recruitment and activation of other immune cells such as macrophages, T cytotoxic cells and NK cells and for the activation of and production of immunoglobulin from B-cells

Insulin has a number of effects on glucose metabolism, including:
Inhibition of glycogenolysis and gluconeogenesis
Increased glucose transport into fat and muscle
Increased glycolysis in fat and muscle
Stimulation of glycogen synthesis
By inhibiting gluconeogenesis, insulin maintains the availability of amino acids as substrates for protein synthesis. Thus, insulin supports protein synthesis through direct and indirect mechanisms.

Aplastic anaemia is a life-threatening failure of haemopoiesis characterised by pancytopenia and hypocellular bone marrow. It is rare and patients present with features of recurrent infections secondary to (leukocytopenia), increased bleeding tendency (secondary to thrombocytopenia) and anaemia. In aplastic anaemia, there is damage to the bone marrow and the haematopoietic stems cells leading to pancytopenia.

The anterior triangle is the triangular area of the neck found anteriorly to the sternocleidomastoid muscle. It is formed by the anterior border of sternocleidomastoid laterally, the median line of the neck medially and by the inferior border of the mandible superiorly. The apex of the anterior triangle extends towards the manubrium sterni. The anterior triangle contains:
Muscles: thyrohyoid, sternothyroid, sternohyoid muscles
Organs: thyroid gland, parathyroid glands, larynx, trachea, esophagus, submandibular gland, caudal part of the parotid gland
Arteries: superior and inferior thyroid, common carotid, external carotid, internal carotid artery (and sinus), facial, submental, lingual arteries
Veins: anterior jugular veins, internal jugular, common facial, lingual, superior thyroid, middle thyroid veins, facial vein, submental vein, lingual veins
Nerves: vagus nerve (CN X), hypoglossal nerve (CN XII), part of sympathetic trunk, mylohyoid nerve

The posterior triangle is a triangular area found posteriorly to the sternocleidomastoid muscle. It has three borders; anterior, posterior and inferior borders. The anterior border is the posterior margin of the sternocleidomastoid muscle. The posterior border is the anterior margin of the trapezius muscle, while the inferior border is the middle one-third of the clavicle. The investing layer of deep cervical fascia and integument forms the roof of the space, while the floor is covered with the prevertebral fascia along with levator scapulae, splenius capitis and the scalene muscles. The inferior belly of omohyoid subdivides the posterior triangle into a small supraclavicular, and a large occipital, triangle.
Contents:
Vessels: the third part of the subclavian artery, suprascapular and transverse cervical branches of the thyrocervical trunk, external jugular vein, lymph nodes
Nerves: accessory nerve (CN XI), the trunks of the brachial plexus, fibers of the cervical plexus

Extravasation of thiopental during injection can lead to tissue damage. Accidental intra-arterial injection causes vasospasm and may lead to thrombosis and tissue necrosis. Other side effects include involuntary muscle movements on induction, cough and laryngospasm, arrhythmias, hypotension, headache and hypersensitivity reactions. Thiopental sodium has anticonvulsant properties and does not cause seizures.

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.

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

Hutchinson sign relates to involvement of the tip of the nose from facial herpes zoster. It implies involvement of the external nasal branch of the nasociliary nerve which is a branch of the ophthalmic division of the trigeminal nerve.

The nasociliary branch of the trigeminal nerve innervates the apex and lateral aspect of the nose, as well as the cornea. Therefore, lesions on the side or tip of the nose should raise suspicion of ocular involvement.

The biceps brachii muscle is one of the chief muscles of the arm. The origin at the scapula and the insertion into the radius of the biceps brachii means it can act on both the shoulder joint and the elbow joint, which is why this muscle participates in a few movements of the arm. It derives its name from its two heads which merge in one unique distal body, defining the unusual structure of the muscle.

The biceps brachii muscle is supplied by the musculocutaneous nerve (C5-C6), a branch of the brachial plexus.

Arterial supply to the biceps brachii muscle varies considerably, coming from up to eight vessels originating from the brachial artery in the middle third of the arm.

In the shoulder joint both muscle heads partially enforce opposite movements. The long head pulls the arm away from the trunk (abduction) and turns it inwards (inward rotation) whereas the short head pulls the arm back towards the trunk (adduction). When both heads contract simultaneously it leads to an arm bend (flexion). In the elbow joint the muscle bends the forearm (flexion) and rotates it outwards (supination). The supination is most powerful in a flexed elbow. In addition to the movement functions, the biceps has the important task to support the humeral head within the shoulder joint. Its antagonist is the triceps brachii in the posterior compartment of the arm.

Tombstoning ST elevation myocardial infarction can be described as a STEMI characterized by tombstoning ST-segment elevation. This myocardial infarction is associated with extensive myocardial damage, reduced left ventricle function, serious hospital complications and poor prognosis. Tombstoning ECG pattern is a notion beyond morphological difference and is associated with more serious clinical results.

Studies have shown that tombstoning is more commonly found in anterior than non-anterior STEMI, thus, higher rates of left anterior descending artery disease are observed in patients with tombstoning pattern.

The following ECG leads determine the location and vessels involved in myocardial infarction:

ECG Leads Location Vessel involved
V1-V2 Septal wall Left anterior descending
V3-V4 Anterior wall Left anterior descending
V5-V6 Lateral wall Left circumflex artery
II, III, aVF Inferior wall Right coronary artery (80%) or Left circumflex artery (20%)
I, aVL High lateral wall Left circumflex artery
V1, V4R Right ventricle Right coronary artery
V7-V9 Posterior wall Right coronary artery

Lithium is the drug of choice for bipolar disorders but is commonly associated with side effects and toxicity.

Fine hand tremor is very commonly seen and reported in as many as 50% of patients during the first week of therapy with Lithium. The tremor tends to reduce with time and is only present in around 5% of patients taking the medication two years or longer. Lithium tremors are more common with older age, presumably due to the additive effects of age-related essential tremors.

Option The normal therapeutic range is 2.0-2.5 mmol/l: Lithium should be carefully monitored as it has a very low therapeutic index. The normal therapeutic range is 0.4-0.8 mmol/l. Levels should be checked one week after starting therapy and one week after every change in dosage. (Option Levels should be checked one month after starting therapy)

Option It can induce hyperthyroidism: Lithium has a known effect on thyroid function. Lithium decreases the production of T4 and T3 and commonly causes hypothyroidism. More rarely, lithium causes hyperthyroidism due to thyroiditis.

Option It can induce diabetes mellitus: Lithium can induce nephrogenic diabetes insipidus but not diabetes mellitus.

The beta-adrenoceptors in the heart, peripheral vasculature, bronchi, pancreas, and liver are blocked by beta-adrenoceptor blocking drugs (beta blockers).

Beta blockers come in a wide range of strengths, with the choice largely determined by the disease being treated and the patient’s unique circumstances. The intrinsic sympathomimetic activity, lipid solubility, duration of action, and cardioselectivity of beta blockers all differ.

Some beta blockers are lipid (lipophilic) soluble, while others are water soluble (hydrophilic). Drugs that are more lipid-soluble are absorbed faster from the gut, undergo more first-pass metabolism, and are eliminated faster. They’re also more likely to get into the brain and cause central effects like insomnia and nightmares. Propranolol, pindolol, labetalol, and metoprolol are examples of lipid-soluble beta blockers. Beta blockers that are water-soluble are less likely to enter the brain and are more resistant to first-pass metabolism. They are excreted by the kidneys, and in renal impairment, dosage reduction is frequently required. Atenolol, nadolol, celiprolol, and sotalol are examples of water-soluble beta blockers.

A low pH in the stomach inhibits gastrin secretion, therefore when the stomach is empty or when acid has been secreted for some time after food has entered it, there is inhibition of acid secretion. However, when food first enters the stomach, the pH rises, and this leads to release of the inhibition and causes a maximum secretion of gastrin. Thus gastric acid secretion is self-regulating.

Haemostasis is your body’s defence against an injury that causes bleeding. It stops bleeding in three main steps:

1) Primary haemostasis – formation of a weak platelet plug
– The primary reaction of the body is to cause local vasoconstriction at the site of injury and decrease blood flow to the affected area
– the release of cytokines and inflammatory markers lead to adhesion of platelets and aggregation at the site of injury forming a platelet plug
– the injured vessel wall has exposed subendothelial collagen that releases von Willebrand factor

Any damage to the vessel wall causes the release of the Von Willebrand factor, which is necessary for platelet adhesion. Tissue Thromboplastin is also released, which activates the coagulation pathway, a component of secondary haemostasis. The coagulation cascade ultimately results in the conversion of fibrinogen to fibrin.

2) Secondary haemostasis
3) Fibrinolysis

Fibrin (factor Ia) is a long, thin protein with branches produced at the end of the coagulation cascade when fibrinogen (factor I) is converted to fibrin, which stabilizes the blood clot.

Anti-nuclear antibodies(ANAs) also referred to as anti-nuclear factors (ANFs) are autoantibodies that bind to contents of the cell nucleus. They can be of any immunoglobulin class.

CREST syndrome is usually associated with anti-centromere antibodies.

ELISA testing is cheaper but not the most accurate means of testing for ANAs. Indirect immunofluorescence testing is the most reliable.

Nucleolar staining is suggestive of scleroderma, while homogenous staining is suggestive of lupus.

Anti-dsDNA antibodies are found in 80 – 90% of patients with SLE

The anterior triangle is the triangular area of the neck found anteriorly to the sternocleidomastoid muscle. It is formed by the anterior border of sternocleidomastoid laterally, the median line of the neck medially and by the inferior border of the mandible superiorly. The apex of the anterior triangle extends towards the manubrium sterni. The anterior triangle contains:
Muscles: thyrohyoid, sternothyroid, sternohyoid muscles
Organs: thyroid gland, parathyroid glands, larynx, trachea, esophagus, submandibular gland, caudal part of the parotid gland
Arteries: superior and inferior thyroid, common carotid, external carotid, internal carotid artery (and sinus), facial, submental, lingual arteries
Veins: anterior jugular veins, internal jugular, common facial, lingual, superior thyroid, middle thyroid veins, facial vein, submental vein, lingual veins
Nerves: vagus nerve (CN X), hypoglossal nerve (CN XII), part of sympathetic trunk, mylohyoid nerve

The posterior triangle is a triangular area found posteriorly to the sternocleidomastoid muscle. It has three borders; anterior, posterior and inferior borders. The anterior border is the posterior margin of the sternocleidomastoid muscle. The posterior border is the anterior margin of the trapezius muscle, while the inferior border is the middle one-third of the clavicle. The investing layer of deep cervical fascia and integument forms the roof of the space, while the floor is covered with the prevertebral fascia along with levator scapulae, splenius capitis and the scalene muscles. The inferior belly of omohyoid subdivides the posterior triangle into a small supraclavicular, and a large occipital, triangle.
Contents:
Vessels: the third part of the subclavian artery, suprascapular and transverse cervical branches of the thyrocervical trunk, external jugular vein, lymph nodes
Nerves: accessory nerve (CN XI), the trunks of the brachial plexus, fibers of the cervical plexus

Klebsiella is a type of bacteria commonly found in nature. In humans, the bacteria are often present in parts of the digestive tract and respiratory flora, where they do not generally cause problems. They are anaerobic Gram-negative rods. They are usually opportunistic pathogens which cause nosocomial infections, the most common ones being pneumonia and UTI.

Peripheral nerves are nerves that lie outside the brain and spinal cord. Peripheral nerves readily regenerate, while central nervous system axonal injury does not spontaneously regenerate.
If there is damage to the axons of peripheral nerves, the nerves will regenerate at a slow rate of 1 mm per day. The slow regeneration process may lead to muscle atrophy before regeneration is complete.

Each peripheral nerve has a single cell body that supplies nutrients to the growing nerve fibre. The cell body does not undergo mitosis; only the axon is regenerated.

Schwann cells of the peripheral nervous system provide support for this process, while the analogous oligodendrocytes of the central nervous system do not. Schwann cells themselves do not cause regeneration. Schwann cells provide myelin for myelinated fibres and surround non-myelinated fibres with their cytoplasm.

If an axon is completely severed, as in the case of amputation, the axonal fibres regenerating from the cell body may never find their original route back to the muscle. Instead, they may form a traumatic neuroma, a painful collection of nerve fibres and myelin.

Theophylline and Ethylenediamine are combined in a 2:1 ratio to form Aminophylline. Its solubility is improved by the addition of Ethylenediamine. It has a lower potency and a shorter duration of action than Theophylline.
It is used to treat the following conditions:
Heart failure
It is used to treat the following conditions:
COPD
Bradycardias

Aminophylline has the following properties:
Phosphodiesterase inhibitor that increases intracellular cAMP and relaxes smooth muscle in the bronchial airways and pulmonary blood vessels.
Mast cell stabilization is achieved by using a non-selective adenosine receptor antagonist.
It has slight positive inotropic and chronotropic effects, increasing cardiac output and decreasing systemic vascular resistance, lowering arterial blood pressure. It has been used historically in the treatment of refractory heart failure and is indicated by the current ALS guidelines as a substitute treatment for bradycardia.

The daily oral dose for adults is 900 mg, divided into 2-3 doses. For severe asthma or COPD, a loading dosage of 5 mg/kg over 10-20 minutes is given, followed by a continuous infusion of 0.5 mg/kg/hour. The therapeutic range is small (10-20 microgram/ml), hence assessments of aminophylline plasma concentrations are useful during long-term treatment.

Majority of carbohydrates are broken down into monosaccharides (glucose, fructose galactose) and are absorbed by the small intestine. Enzymes released from the brush border break down carbohydrate. Some carbohydrates, such as cellulose, are not digested at all, despite being made of multiple glucose units. This is because the cellulose is made out of beta-glucose that makes the inter-monosaccharide bindings different from the ones present in starch, which consists of alpha-glucose. Humans lack the enzyme for splitting the beta-glucose-bond.

The principal brush border enzymes are dextranase and glucoamylase. Other brush border enzymes are maltase, sucrase, and lactase.

Pancreatic amylase breaks down some carbohydrates (notably starch) into oligosaccharides. Dextranase and glucoamylase, then further break down oligosaccharides.

Trypsin aids in digestion of protein.

Chymotrypsin is a proteolytic enzyme that digests protein

Carboxypeptidase hydrolyses the first peptide or amide bond at the carboxyl or C-terminal end of proteins and peptides

A papule is a solid, well circumscribed, skin elevation measuring less than 0.5 cm in diameter.

A nodule is a solid, well circumscribed, raised area that lies in or under the skin and measures greater than 0.5 cm in diameter. They are usually painless.

A bulla is a visible collection of clear fluid measuring greater than 0.5 cm in diameter.

A furuncle, or boil, is a pyogenic infection of the hair follicle commonly caused by infection with Staphylococcus aureus.

A pustule is a small visible skin elevation containing an accumulation of pus.

Exocrine pancreatic secretion is controlled by:
Parasympathetic stimulation which enhances secretion of both the enzyme and aqueous components
Sympathetic stimulation which inhibits pancreatic secretion
Secretin which stimulates secretion of the alkaline-rich fluid from ductal cells
Cholecystokinin which stimulates secretion of the enzyme-rich fluid from acinar cells
Somatostatin which inhibits secretion from both acinar and ductal cells
Gastrin which stimulates pancreatic acinar cells to secrete digestive enzymes

Anti-cyclic citrullinated peptide (anti-CCP) is an antibody present in 60-80% of rheumatoid arthritis patients. It is measured by enzyme-linked immunosorbent assay (ELISA). It may be present years before the onset of the disease and is associated with a more severe disease course.

While most patients with anti-CCP antibodies are also positive for rheumatoid factor (RF), RF antibody is not specific for rheumatoid arthritis as it can occur in patients with other conditions such as infections and other autoimmune conditions.

ESR, antinuclear antibodies(ANA) and Synovial fluid examination are not specific for rheumatoid arthritis.

Neutrophils are the most abundant peripheral blood leucocyte, comprising about 50 – 70% of circulating white cells. Neutrophils have a characteristic dense nucleus consisting of between two and five lobes, and a pale cytoplasm with an irregular outline containing many fine pink-blue or grey-blue granules. The granules are divided into primary, which appear at the promyelocyte stage, and secondary, which appear at the myelocyte stage and predominate in the mature nucleus. Both types of granule are lysosomal in origin; the primary contains myeloperoxidase and other acid hydrolases; the secondary contains lactoferrin, lysozyme and other enzymes. The lifespan of neutrophils in the blood is only 6 – 10 hours. In response to tissue damage, cytokines and complement proteins, neutrophils migrate from the bloodstream to the site of insult within minutes, where they destroy pathogens by phagocytosis.