Author Archives: Alila Medical Media

Antihistamines Pharmacology, with Animation

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Antihistamines are medications that counteract the action of histamine. Histamine is most notoriously known as a mediator of allergic reactions, but it’s also involved in important physiological processes such as immune response, gastric acid secretion, sleep and wake cycle, cognitive ability and food intake.
Histamine is synthesized from the amino acid histidine. It is present in all tissues but most abundant in the skin, lungs and gastrointestinal tract. Most of histamine in tissues is stored as granules inside mast cells. In the brain, histamine also functions as a neurotransmitter. It is found in histaminergic neurons of the hypothalamus, whose axons project throughout the brain.
Histamine exerts its action by binding to histamine receptors, H-receptors, all of which are G-protein- coupled. There are four H-receptors, with different tissue expression patterns and functions. Both H1 and H4 are involved in allergic inflammation, but only H1-antihistamines are currently available for allergy treatment. The major function of H2-receptor is to stimulate gastric acid secretion, so H2-antihistamines are used to treat gastric acid disorders such as gastric reflux and peptic ulcers.
The term “antihistamine” generally refers to allergy-treating H1-antihistamines.
Most allergies occur upon a repeated exposure to an allergen. Mast cells that were previously sensitized to the allergen are activated, releasing histamine and other inflammatory chemicals. Histamine causes dilation and increased permeability of blood vessels, stimulation of sensory nerves, contraction of smooth muscle; and is responsible for most allergic symptoms, ranging from watery eyes, runny nose, sneezing, itching; to swelling, hives, and difficulty breathing due to bronchospasm. When released systemically, histamine can cause extensive vasodilation and bronchoconstriction which may lead to life-threatening anaphylaxis.
Most H1-antihistamines are not similar to histamine in structure and do not compete with it for binding to H1-receptor. Instead, they bind to a different site on the receptor and stabilize it in its inactive state. The first-generation H1-antihistamines derive from the same chemical class as muscarinic, adrenergic and serotonin antagonists, so they also have anti-cholinergic, anti-adrenergic, and anti-serotonin effects. More importantly, they can cross the blood-brain barrier and interfere with histamine functions in the brain, causing drowsiness, cognitive impairment and increased appetite. Some of these drugs are actually used for their sedative side effect, as sleeping aid medications.
Second-generation antihistamines are less able to cross the blood-brain barrier, and are therefore minimally or non-sedating. They are also highly selective for H1-receptor and have no anti-cholinergic effects.

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Antihypertensive Medications, with Animation

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Hypertension is most commonly associated with an increase in vascular resistance caused by narrower or stiffer blood vessels; but other mechanisms, including increased cardiac output, large blood volume, or excess venous return, are possible. These factors are the targets of antihypertensive agents, which can be grouped into several categories:
– Diuretics, which promote sodium and water excretion by the kidneys and thereby decrease blood volume.
– Medications that inhibit the sympathetic nervous system or the renin-angiotensin system.
– And vasodilators, which dilate blood vessels, and thereby decrease vascular resistance.
Of the three classes of diuretics used for treating hypertension, thiazides are the most commonly prescribed. Thiazides act on the distal tubule of nephrons, which reabsorbs only a small portion of the sodium load, so their diuretic effect is less powerful than that of loop diuretics, which act on the thick ascending limb of the loop of Henle. However, thiazides also have a vasodilation effect by an unknown mechanism. The two classes produce similar side effects, but the side effects are more severe with loop diuretics.
Potassium-sparing diuretics act mainly in the collecting duct and have only a mild diuretic effect, but they can compensate for the potassium loss induced by other diuretics, and are therefore commonly used in conjunction with thiazide or loop diuretics.
Sympathetic inhibitors, or sympatholytics, act on adrenergic receptors to block sympathetic activity. There are beta-blockers, alpha-blockers, mixed alpha and beta-blockers, and central sympatholytics.
Beta blockers are typical first-line treatment for hypertension. They reduce heart rate and cardiac contractility and thus decrease cardiac output.
Alpha-1 blockers are effective in reducing sympathetic vasoconstriction, but their action can lead to an excessive baroreceptor-mediated reflex that increases heart rate and produces tachycardia.
Non-selective adrenergic antagonists block both alpha and beta receptors. By inhibiting beta receptors in the heart, they are able to lower blood pressure without inducing reflex tachycardia.
Central sympatholytics stimulate alpha-2 receptors in the brainstem to reduce sympathetic tone. They reduce heart rate, contractility and vasoconstriction, but may also cause sedation.
Renin-angiotensin system blockers include ACE inhibitors and angiotensin receptor blockers.
ACE inhibitors are commonly used as first-line treatment for hypertension. They block the conversion of angiotensin-I to angiotensin-II, which in turn leads to a reduction in aldosterone. Their action reduces systemic vasoconstriction and increases sodium and water excretion by the kidneys.
Angiotensin receptor blockers inhibit the effects of angiotensin-II. Their indications are similar to those of ACE inhibitors.
Vasodilators include calcium channel blockers, direct arterial vasodilators and nitrodilators.
Calcium channel blockers inhibit L-type calcium channels that are responsible for smooth muscle contraction, cardiac myocyte contraction, and action potential generation in cardiac nodal tissue.
The dihydropyridine class acts on peripheral blood vessels. They are powerful vasodilators but their action can lead to reflex tachycardia and increased cardiac contractility.
Non-dihydropyridine agents, on the other hand, primarily act to decrease heart rate, contractility and cardiac conduction speed; and are less effective on peripheral vessels. By having cardiac depressant effect, they can reduce blood pressure without producing reflex cardiac stimulation. However, they should not be used for patients with systolic heart failure.
The mechanisms of direct arterial vasodilators are not entirely clear. They can cause reflex tachycardia and are only used for short-term treatment of refractory hypertension.
Nitrodilators act by releasing nitric oxide, a powerful vasodilator. They are administered intravenously to manage hypertensive crises and to control blood pressure during surgery.

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Adrenergic Receptors and Drugs, with Animation

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Adrenergic drugs are medications that stimulate or inhibit adrenergic receptors. Adrenergic receptors mediate the action of noradrenaline, also known as norepinephrine; and adrenaline, also known as epinephrine. Adrenergic neurotransmission is responsible for the body’s sympathetic response – the “fight or flight” state – which dilates pupils, increases heart rate and respiratory rate, diverts blood flow to the muscles, inhibits activities that are not essential in emergency, and releases stored energy. Adrenergic receptors are also active in the central nervous system, in processes such as memory and alertness.
There are several types of adrenergic receptors, all of which are G-protein coupled, but they differ in several aspects:
– They couple with different G-proteins, leading to different downstream signalings, and hence different cellular responses.
– They differ in sensitivity to different drugs.
– While several receptors may coexist in the same tissue, there is usually one that predominates and is mainly responsible for the tissue’s adrenergic response. For example: alpha-1 receptor predominates in peripheral vascular smooth muscle – its activation induces vasoconstriction; beta-1 is prominent in the heart – it increases heart rate and cardiac contractility when activated; beta-2 activation results in bronchodilation in the lungs; and alpha-2 reduces sympathetic outflow in the brainstem. Alpha-2 can also act at the pre-synaptic neuron, where it inhibits neurotransmitter release, as a feedback mechanism.
Most adrenergic drugs act directly at the receptors, only a few act indirectly by promoting neurotransmitter release, or by preventing its degradation.
Non-specific drugs are those that can bind to several receptors. Non-specific agonists include epinephrine, norepinephrine and dopamine. Their relative activity via different receptors depends on the dose administered. For example, epinephrine has a greater affinity for beta receptors in small doses, but can bind to alpha receptors equally well at higher doses. At low levels, epinephrine preferentially binds to vascular beta-2-receptor and causes vasodilation. As the concentration of epinephrine increases, lower affinity alpha-receptors begin to bind epinephrine, producing vasoconstriction. Because there are more alpha-receptors than beta-receptors in peripheral blood vessels, alpha-mediated vasoconstriction eventually overrides beta-mediated vasodilation. Thus, at higher pharmacologic doses, epinephrine induces vasoconstriction via alpha receptors; increases heart rate, cardiac contractility via beta-1 receptor; and dilates bronchi via beta-2 receptor. Epinephrine is the treatment of choice for cardiac arrest, anaphylaxis, and severe croup.
Specific drugs target only a certain type of receptor:
– Alpha-1 specific agonists induce smooth muscle contraction and are used as vasopressors for treatment of shock, hypotension; as nasal decongestants; or to dilate pupils.
Alpha-1 antagonists, on the other hand, are used to treat hypertension, and to relax smooth muscle within the prostate for treatment of benign prostatic hyperplasia.
– Alpha-2 agonists act on alpha-2 receptors in the brainstem to reduce sympathetic tone, and are used to treat hypertension. Stimulation of peripheral alpha-2 receptors may initially cause vasoconstriction, but it is quickly overridden by the central effect.
– Beta-1 agonists increase heart rate and contractility, and are indicated for treatment of cardiogenic shock and heart failure.
– Beta-2 agonists relax smooth muscles. They are used to dilate bronchi, for treatment of asthma, obstructive pulmonary disease, and anaphylaxis. Some are used to relax uterine smooth muscle to delay preterm birth.
Beta antagonists, or beta blockers, are used for the treatment of hypertension, ischemic heart disease, obstructive cardiomyopathy, and arrhythmias.

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Cholinergic Drugs – Pharmacology, with Animation

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Acetylcholine is a major neurotransmitter of the nervous system. It is released by motor neurons at neuromuscular junctions to stimulate skeletal muscle contraction. Acetylcholine is also the primary neurotransmitter of the parasympathetic nervous system responsible for the body’s “rest and digest” state. It slows heartbeats, slows respiratory rate, contracts smooth muscles of the gastrointestinal tract and urinary bladder, stimulates various secretions, and constricts pupils. Acetylcholine is also active in several brain regions associated with cognition and movement.
A neuron that uses mainly acetylcholine as neurotransmitter is called a cholinergic neuron.
Acetylcholine is an ester of choline. It is synthesized and stored in the nerve terminal. When a cholinergic neuron is stimulated, acetylcholine is released into the synaptic cleft where it binds to its receptor on the postsynaptic cell, triggering cellular response. Acetylcholine is rapidly cleared from the synapse by the enzyme acetylcholinesterase, which binds to acetylcholine and hydrolyzes it into choline and acetate. The enzyme molecule quickly recycles itself each time, ready for another round of reaction.
There are 2 main types of acetylcholine receptors: muscarinic and nicotinic, each type has several subtypes, or classes. Each receptor class is specific to certain synapses or tissues.
Cholinergic agonists are drugs that mimic or enhance the action of acetylcholine, while cholinergic antagonists are those that inhibit its action. Because action of acetylcholine is widespread, cholinergic drugs may produce lots of side effects when administered systemically. Drugs that target a particular receptor class are more specific and are therefore preferred.
Cholinergic agonists can be direct-acting or indirect-acting:
Direct-acting agonists mimic acetylcholine, they bind to acetylcholine receptor and activate downstream signaling. They are not easily metabolized by acetylcholinesterase and therefore last longer at the synapse. Examples are drugs used as eye drops to constrict pupil and reduce intraocular pressure for treatment of glaucoma. Some agents are used to increase smooth muscle tone in urinary bladder and gastrointestinal tract, or to stimulate saliva secretion to treat dry mouth.
Indirect agonists act by inhibiting the enzyme acetylcholinesterase, thereby increasing the concentration of acetylcholine available at the synapse.
Reversible inhibitors form a transient, reversible complex with the enzyme. They slow down the recycling of the enzyme, making it less available for breaking down acetylcholine. Some of these drugs are used to treat myasthenia gravis, or to reverse the effects of anesthesia. Others are given to boost cholinergic activities in Alzheimer’s brain to compensate for the loss of functioning neurons.
Irreversible cholinesterase inhibitors bind to the enzyme in an irreversible manner and permanently inactivate it. These drugs are very toxic, they are used as insecticides and “nerve gases”.
Cholinergic antagonists inhibit acetylcholine action by several mechanisms:
Botulinum toxin, Botox, is a bacterial toxin. It blocks acetylcholine release by inhibiting exocytosis. Botox is used to treat localized muscle spasms, movement disorders and strabismus. It is given by direct injection into the affected muscle.
Nicotinic antagonists compete with acetylcholine for binding to nicotinic receptor. They are most commonly used to relax skeletal muscles during surgery.
Muscarinic antagonists compete with acetylcholine for binding to muscarinic receptor. They are used to treat bradycardia, diarrhea and bladder spasms, dilate bronchi, reduce secretions, and dilate pupils. Some are used as sedatives and to counteract cholinesterase inhibitors.

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Inotropes, Mechanisms of Action, with Animation

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Mechanisms of action of positive inotropes: calcitropes (catecholamines, phosphodiesterase-3 inhibitors, digoxin), Levosimendan and Omecamtiv mecarbil
Inotropes are medicines that alter the force of contraction of the heart. By definition, there are positive inotropes that strengthen cardiac contraction, and negative inotropes that weaken it. However, when not specified otherwise, the term “inotrope” usually refers to positive inotropes, which are the topic of this video. Negative inotropes, such as beta blockers and calcium channel blockers, significantly overlap with antiarrhythmic agents, and are covered in another video.
Inotropes are used in conditions where there is a sudden low cardiac output, such as acute heart failure or cardiogenic shock. Cardiac output is the product of stroke volume – the amount of blood pumped in one heartbeat, and heart rate – the number of beats in one minute. More forceful contractions induced by inotropes pump more blood out of the heart, increasing stroke volume. Many inotropes also accelerate heart rate, which contributes to increased cardiac output.
Cardiac muscle contractions are triggered by a surge in intracellular calcium concentration. When cardiac muscle cells are stimulated by action potentials, calcium channels open, allowing calcium to rush in. This calcium influx activates ryanodine receptor on the membrane of the sarcoplasmic reticulum, the SR, causing more calcium release from the SR, in a process known as “calcium-induced calcium release”. Calcium then binds to troponin units on actin myofilaments and sets off muscle contraction by the sliding filament mechanism.
Most inotropes act by raising the levels of intracellular calcium; they can also be called calcitropes.
Many calcitropes operate via the catecholamine pathway. They bind to beta-adrenergic receptor, activating a signaling cascade that leads to production of cyclic-AMP, cAMP, a second messenger. cAMP promotes phosphorylation and hence activation of both L-type calcium channel that allows calcium influx from the extracellular fluid, and ryanodine receptor that mediates calcium release from the SR. The result is an increase in intracellular calcium that drives a stronger contraction. Most catecholamines have a short half-life and are given by continuous infusion.
Some other agents are inhibitors of the enzyme phosphodiesterase-3, PDE3. Because PDE3 breaks down cAMP, inhibition of PDE3 results in accumulation of cAMP and subsequent increase in intracellular calcium.
Digoxin, a widely used inotrope, acts by inhibiting the sodium-potassium pump, causing intracellular sodium concentration to rise. This then leads to higher levels of intracellular calcium via the action of sodium-calcium exchanger.
The problem with most calcitropes is that they increase contractility at the expense of cellular energy, meaning the heart muscle requires more oxygen to operate. This may lead to adverse effects including higher mortality. Other strategies have been explored to design inotropes that can boost cardiac output without increasing myocardial oxygen demand.
Levosimendan is a calcium sensitizing drug. It enhances troponin C sensitivity to intracellular calcium, thereby increasing the force of contraction without consuming more cellular energy.
Omecamtiv mecarbil, OM, is a new drug that is still under investigation. OM increases the efficiency of heart muscle contraction. It binds to cardiac myosin, stabilizing myosin-actin connection. This increases the number of myosin heads bound to actin, producing more force during cardiac contraction.

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Anatomy and Physiology of the Skin, with Animation

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The skin covers the body and protects it from the external environment. It also prevents water loss, provides sensory function, plays a role in body temperature regulation, and is the site of vitamin D synthesis.
The skin is composed of 2 layers: the outer epidermis and the deeper dermis. The dermis is connected to underlying structures via a subcutaneous tissue, the hypodermis, which is not technically considered part of the skin.
The epidermis provides barrier and protection, it consists mainly of the protein keratin, a tough and water-insoluble structural protein.
The dermis constitutes the bulk of the skin, it provides support and flexibility. The dermis consists mainly of collagen, and to a lesser extent, elastin fibers. Loss of collagen and elastin, such as with aging, causes the skin to slack. The boundary surface between the epidermis and dermis is not flat but wavy, meaning the 2 tissues interlock, strengthening their connection. With age, this boundary flattens and the skin becomes more fragile. The dermis is well vascularized and contains sensory nerves, hair follicles, sebaceous glands and sweat glands. It has 2 zones: the upper papillary dermis with loose connective tissue, and the lower reticular dermis with denser connective tissue. The dermis houses immune cells and allows inflammatory response to activate upon exposure to invading organisms.
The hypodermis is composed of loose connective and adipose tissues. This is where most of the body fat is stored. The hypodermis provides thermal insulation, padding and serves as the body main energy storage.
The thickness and proportion of the epidermis and dermis vary greatly depending on their location on the body, but the skin is classified as thick or thin based on the thickness of the epidermis alone. Thick skin is found only in areas where there is a lot of abrasion: palms, soles, digits; and has 5 epidermal layers. Thin skin is everywhere else and has 4 epidermal layers.
Most cells of the epidermis are keratin-producing cells, or keratinocytes. New cells are constantly produced by mitotic cell division in the basal layer. They then move towards the skin surface as they age and differentiate, changing shape, from cuboidal to flat. The distinct epidermal layers represent different stages of keratinocyte differentiation, from their birth to their death.
The spinous layer is characterized by presence of abundant desmosomes which connect keratin filaments of adjacent cells, anchoring them together, providing resistance to physical stress.
The granular layer is loaded with keratohyalin granules. These granules release several substances that cross-link keratin filaments, converting them into an impermeable keratin matrix. This process is known as cornification or keratinization, the result of which is the most superficial layer, the cornified layer, about 30 cells thick. These fully keratinized dead cells form the skin barrier. They are shed periodically from the surface as new cells are moving up. The entire epidermis is replaced every 30 to 40 days. The renewal process becomes slower with age but faster in injured skin, when cell proliferation is accelerated for wound healing.
The epidermis also contains immune cells, touch sensory cells and melanocytes. Melanocytes produce the pigment melanin and transfer it to keratinocytes. The amount of melanin produced is the major determinant of skin color. Melanin synthesis is stimulated by UV light and is thought to be a protective mechanism against UV radiation damage.

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Antiviral Drugs, with Animation

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Antiviral drugs are medications used to treat viral infections. Because viruses replicate entirely inside host cells using the host’s machinery, it is difficult to develop drugs that affect viruses without also harming the host. Antiviral drugs do not inactivate or kill viruses, they merely inhibit viral reproduction by interfering with a certain stage of the virus life cycle.
A virus is composed of a genome, DNA or RNA, wrapped inside a protective protein coat, called a capsid. Most animal viruses also have an additional lipid membrane, called an envelope, with protein spikes that serve to attach to host cells.
A viral life cycle typically consists of the following steps:
– attachment to host cell receptor, followed by viral entry: via endocytosis, membrane fusion, or both.
– release of viral genome, also known as uncoating,
– replication of viral genome,
– synthesis and processing of viral proteins, assembly of viral components into new viruses,
– and release of new viruses from host cell.
Antiviral strategies aim to block viral reproduction at any of these stages.
To prevent viral attachment, a drug can either bind to host cell receptor/coreceptor, or to the viral spike protein. Examples are HIV drugs – CCR5-antagonists. They bind to CCR5 coreceptor, masking its binding site for HIV.
For enveloped viruses, one strategy is to prevent fusion of viral and host cell membrane. An agent can bind directly to the viral protein that is responsible for fusion, or disrupt the condition that is required for fusion.
Several drugs have been developed to inhibit the uncoating of influenza A virus – they impair the function of the protein responsible for viral genome release from endosomes.
Viruses that use reverse transcriptase for replication are usually targeted for this enzyme. Because the process of reverse transcription, converting RNA to DNA, occurs only in these viruses and not human cells, drugs targeting reverse transcriptase are generally safe for humans. Most of these agents are nucleoside or nucleotide analogs. They compete with regular nucleotides, insert themselves into the growing chain of DNA, and stop the process prematurely. There are also non-nucleoside reverse transcriptase inhibitors, which bind non-competitively to the reverse transcriptase, impairing its function. The 2 classes of inhibitors are usually combined for maximum effects.
Retroviruses, such as HIV, use viral enzyme integrase to insert their genome into host cell DNA, a critical step for viral reproduction. Drugs that inhibit integrase have been developed to treat HIV and other retroviruses.
Viruses with large DNA genomes usually encode their own DNA polymerase for DNA replication. Viral DNA polymerases are the target of many currently available antiviral drugs. Most of these drugs are nucleoside analogs, they incorporate into the growing DNA and cause premature termination of viral DNA synthesis.
Another approach is to inhibit viral protein synthesis by antisense mechanism. Antisense antiviral drugs are short synthetic nucleic acid strands that are complementary to part of an essential viral mRNA. They bind specifically to the viral mRNA, effectively preventing it from being translated into protein.
Some viruses require activity of a specific protease to cleave precursor viral proteins into functional components for viral assembly. Several drugs have been developed to target this protease in HIV.
Influenza virus requires action of viral enzyme neuraminidase to release new viruses from host cell. Blocking neuraminidase is an effective way to treat influenza.

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Overview of The Musculoskeletal System

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The musculoskeletal system provides mechanical support for the body, protects internal organs and permits movement. It is composed of bones, cartilage, skeletal muscles, joints, and connective tissues such as tendons and ligaments. Bones also serve as the body’s main mineral reservoir, they store calcium and phosphate and release them according to the body’s needs. Red bone marrow is the body’s production center for blood cells.
The central nervous system controls body movements by stimulating skeletal muscles to contract. Contraction of skeletal muscles moves bones, which act as levers. Bones articulate with each other through joints. Cartilage provides padding for the ends of bones within joints. Muscles are connected to bones by tendons, while bones are held together by ligaments.
Bones are classified according to their shapes and corresponding functions: long bones are responsible for most body movements; short bones provide some limited motion; while flat bones and irregular bones are mainly protective and supportive.
The bone tissue, or osseous tissue, is composed of bone cells and a characteristic extracellular matrix. Bone matrix is made of an organic component, mainly collagen, and an inorganic component of minerals, mainly calcium. Collagen gives bones flexibility while calcium provides stiffness. Without calcium, bones would be soft and bend easily. On the other hand, without collagen, bones would be brittle like chalk.
Bones renew and remodel throughout a person’s life in a process known as bone remodeling, which constantly removes old bone tissue and adds new bone tissue. Bone remodeling serves to re-shape bones to adjust to changing mechanical needs and to repair everyday micro-damages as well as fractures following injuries. This process also underlies the mechanism by which the constant levels of plasma calcium and phosphate are maintained. Bone remodeling is performed by 2 types of cells: osteoclasts, which dissolve bone matrix, and osteoblasts, which deposit new matrix around themselves to form new bone tissue. Bone remodeling is under control of complex signaling pathways. Major regulators include parathyroid hormone, vitamin D, growth hormones, glucocorticoids, thyroid hormones, estrogen and testosterone.
The most common bone disease is osteoporosis, or porous bone, in which bones lose mass and weaken, increasing risks of fractures. Osteoporosis is commonly due to old age and some other unavoidable factors, but can also develop from, or worsen by hormone imbalances, deficiencies in calcium, vitamin D or proteins, and sedentary lifestyles.
The most common and also most movable type of joint is synovial joint. The bones of a synovial joint are separated by a cavity containing synovial fluid, which serves as lubricant. Together, the fluid and the cartilage that lines the bone surfaces make the movements at synovial joints almost friction-free. There are also small fibrous sacs containing synovial fluid, called bursae, located between muscles, or between a tendon and a bone. Bursae cushion muscle movements and help tendons slide smoothly over the joints.
The most common disease of joints is arthritis. There are 2 main types of arthritis:
– Osteoarthritis, also called degenerative joint disease, is the “wear and tear” condition of the joint, commonly due to old age. Osteoarthritis is characterized by loss of cartilage, bone spurring and no major inflammation.
– Rheumatoid arthritis is a result of joint inflammation, with immune cells and inflammatory chemicals causing damage to the joint. It’s not clear how rheumatoid arthritis starts but genetic predisposition together with infection of the joint are likely to be among the causes.
Muscular tissue consists of specialized elongated muscle cells, called muscle fibers, which are bundled into fascicles. Muscle fibers, fascicles and whole muscles are wrapped in layers of connective tissue, which provides support and protection. These connective tissue coverings are continuous with the tendon that connects to a nearby bone. Fascicle arrangement determines the strength of a muscle and the direction it pulls. Most common muscle disorders are caused by injury or overuse, and include sprains, strains, cramps, and tendinitis.

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Current status of possible treatments for COVID-19, with Animation, updated May 1, 2020

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Convalescent plasma, Remdesivir, Chloroquine and hydroxychloroquine: mechanisms of action, current status, effectiveness and side effects.
At this time, no specific drugs or therapies have been proven effective for prevention or treatment of COVID-19. Current disease management is supportive care, including supplemental oxygen and mechanical ventilator when indicated.
However, several possible treatment options are under intensive investigations:
Convalescent plasma: when someone is infected with SARS-CoV-2, the coronavirus that causes COVID-19, their immune system produces antibodies to fight the virus. People with healthy immune systems produce enough antibodies to fight the disease and recover, while those with compromised immune systems may struggle. Antibodies from blood plasma of recovered patients can be given to people with active illness to help neutralize the virus. This approach has been used in the past for some other diseases, with varying success. Studies are underway to determine its effectiveness in COVID-19, and if convalescent plasma is best used to prevent infections in high-risk individuals; to prevent mild infections from becoming severe; or to improve recovery in severely ill patients. The FDA has allowed emergency use of convalescent plasma in patients with serious or immediately life-threatening COVID-19 infections. While the treatment concept is simple, the process involves multiple steps, from selecting donors, to collecting, processing blood and safety screening. On average, plasma from one donor is only enough to treat 1 to 3 patients. For these reasons, convalescent plasma is considered a temporary solution while antiviral drugs and vaccines are developed.
Remdesivir is an antiviral drug originally created by Gilead Sciences to fight Ebola virus, but it was proved effective in treating SARS and MERS coronaviruses in laboratory and animal research. Recent studies show that Remdesivir inhibits SARS-CoV-2 infections in cultured cells, and efficiently prevents COVID-19 disease progression in monkeys. Remdesivir is an adenosine nucleotide analogue. During viral RNA synthesis, it incorporates into the nascent RNA and causes premature termination, thus interrupting viral RNA production. There are currently 6 ongoing clinical studies, some of which are large-scale phase 3 trials; and initial results are encouraging. However, as an experimental drug, Remdesivir is not expected to be available in large amounts very soon.
Chloroquine and its derivative hydroxychloroquine had recently made headlines thanks to early reports from China and France about its effectiveness in treating severely ill COVID-19 patients. Having been used to treat malaria and some autoimmune diseases, these drugs are readily available. In laboratory studies, the drugs have been shown to block entry of the virus by interfering with host cell receptor. In addition, they also inhibit virus/host cell fusion, preventing the release of viral nucleocapsid. However, more recent human studies suggest that these drugs may produce serious side effects that can be fatal. Specifically, they may cause QT interval prolongation, an abnormal heart rhythm that can quickly develop into lethal rhythms of ventricular tachycardia and fibrillation. The FDA now recommends against taking chloroquine or hydroxychloroquine for COVID-19 infections unless they are prescribed in hospitals under close supervision, or as part of a clinical trial.

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Antibiotic Resistance, with Animation

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Bacterial infections are treated with antibiotics. Antibiotic resistance occurs when an infection responds poorly to an antibiotic that once could treat it successfully. It’s the bacteria that have become resistant to the antibiotic, not the patient. This happens because the bacteria acquire a mutation – a change in their DNA – that gives them a new protein as a tool to fight the antibiotic. There are many mechanisms by which this tool may work. It can:

– prevent the antibiotic from entering the bacterial cell;

– pump the antibiotic out of the cell;

– destroy the antibiotic by enzymatic reaction;

– modify the antibiotic’s target so it no longer binds to the drug;

– or give the cell a way to bypass the antibiotic’s target, making the drug irrelevant.

Mutations in bacterial genome occur all the time, spontaneously, but only the ones that confer a certain advantage would persist to the next generation. Let’s consider a situation when a new mutation emerges and makes the bacteria resistant to a certain antibiotic. In the absence of the antibiotic, such mutation offers no advantage, and because mutations usually come with slower growth, the mutation would be diluted and eventually disappear in the following generations. On the other hand, in the presence of the antibiotic, only bacteria that carry such mutation would survive and they would soon take over the whole bacterial population. The use of antibiotic is therefore the factor that drives the selection of antibiotic-resistant organisms.

Mutations that confer antibiotic resistance can be transmitted not only vertically, from parent cells to offspring, but also horizontally, from one bacterial cell to another, using mobile genetic elements such as plasmids or bacteriophages. This means a bacterial strain can share their antibiotic resistance with other bacterial strains and even with distantly related bacterial species. Horizontal transfer is a major mechanism underlying the spread of antibiotic resistance among bacterial species. These antibiotic-resistant bacteria can infect humans, animals and spread between them through food and the environment.

Antibiotic resistance is one of the biggest global health concerns. Infections by antibiotic-resistant bacteria are much harder, sometimes impossible, to treat. Some bacteria, called superbugs, are resistant to most of the common antibiotics, and are especially difficult to kill. Treatments for infections caused by such bacteria are costly and toxic to the patients.

While the emergence of antibiotic resistance is inevitable, the process is greatly accelerated by misuse and overuse of antibiotics. To help control spread of antibiotic resistance, antibiotics must be taken correctly, only when prescribed by a healthcare professional, who should do so only when antibiotics are needed, according to current guidelines. Antibiotics should not be used to promote growth or prevent diseases in healthy animals. Measures that help prevent infections also help reduce antibiotic overuse.

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