Author Archives: Alila Medical Media

Hypokalemia: Causes, Symptoms, Effects on the Heart, Pathophysiology, with Animation

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Hypokalemia refers to abnormally low levels of potassium in the blood.

In normal circumstances, more than 90% of the total body potassium is INTRA-cellular; the remaining is in the EXTRA-cellular fluid and blood plasma. The ratio of intracellular to extracellular potassium is important for generation of action potentials and is essential for normal functions of neurons, skeletal muscles and cardiac muscles. This is why potassium levels in the blood are strictly regulated within a narrow range between 3.5 and 5mmol/L. As the normal daily dietary intake of potassium varies widely and can be as much as 100mmol a day, the body must quickly and precisely react to keep blood potassium levels within the normal limits. This is achieved by 2 mechanisms:
– Excretion of potassium through the kidneys and intestines; with the kidneys playing a predominant role.
– Shifting of potassium from the extracellular fluid into the cells by the sodium/potassium pump. The pump is mainly regulated by hormones such as insulin and catecholamines.

Hypokalemia is defined as a serum potassium concentration LOWER than 3.5 mmol/L. Hypokalemia may result from INCREASED excretion, inadequate intake or shift of potassium from the extracellular fluid into the cells. Poor intake or intracellular shift ALONE rarely causes the disease, but may be a contributing factor. Most commonly, hypokalemia is caused by excessive loss of potassium in the urine, from the GI tract, or skin. The cause is usually apparent by the patient’s history of predisposing diseases or medication. Urine potassium levels are measured to differentiate between RENAL and NON-renal causes. Depending on the level of severity, symptoms may include muscle weakness, cramping, tremor, intestinal obstruction, hypotension, respiratory depression and abnormal heart rhythms.

As potassium levels decrease in the extracellular space, the MAGNITUDE of the potassium gradient across the cell membrane is INCREASED, causing HYPER-polarization. This moves the membrane voltage FURTHER from the threshold, and a GREATER than normal stimulus is required to generate an action potential. The result is a REDUCED excitability or responsiveness of the neurons and muscles. In the heart, however, HYPER-excitability is observed. This is because hyperpolarization ENHANCES the “FUNNY” currents in cardiac pacemaker cells, resulting in a FASTER phase-4 depolarization and thus a FASTER heart rate. The effect is greatest in Purkinje fibers as these are more sensitive to potassium levels, as compared to the SA node. Increased automaticity of Purkinje fibers may lead to the development of one or more ECTOPIC pacemaker sites in the ventricles, causing ventricular premature beats, tachycardia and fibrillation.

Reduced extracellular potassium, paradoxically, also inhibits the activity of some potassium channels, SLOWING down potassium EFflux during RE-polarization and thus DELAYS ventricular repolarization. As hypokalemia becomes more severe, especially in patients with other heart conditions, the inward current may exceed the outward current, resulting in EARLY afterdepolarization and consequently extra heartbeats. Prolonged repolarization may also promote re-entrant arrhythmias.

Early ECG changes in hypokalemia are mainly due to delayed ventricular repolarization. These include flattening or inversion of T wave, increasingly prominent U wave, ST-segment depression, and prolonged QU interval.

Hypokalemia-induced arrhythmias require immediate potassium replacement. Oral administration is safer but may not be effective in severe cases. If potassium infusion is indicated, continuous cardiac monitoring and hourly serum potassium determinations must be performed to avoid hyperkalemia complications. In the long-term, the underlying causes must be addressed.

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Hyperkalemia: Causes, Effects on the Heart, Pathophysiology, Treatment, with Animation.

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Hyperkalemia refers to abnormally high levels of potassium in the blood. In normal circumstances, more than 90% of the total body potassium is INTRAcellular; the remaining is in the EXTRAcellular fluid and blood plasma. The ratio of INTRAcellular to EXTRAcellular potassium is important for generation of action potentials and is essential for normal functions of neurons, skeletal muscles and cardiac muscles. This is why potassium levels in the blood are strictly regulated within a narrow range between 3.5 and 5mmol/L. As the normal daily dietary intake of potassium varies widely and can be as much as 100mmol a day, the body must quickly and precisely react to keep blood potassium levels within the normal limits. This is achieved by 2 mechanisms:
– Excretion of potassium through the kidneys and intestines; with the kidneys playing a predominant role.
– Shifting of potassium from the extracellular fluid into the cells by the sodium/potassium pump. The pump is mainly regulated by hormones such as insulin and catecholamines.

Hyperkalemia is defined as a serum potassium concentration HIGHER than 5mmol/L. Hyperkalemia may result from decreased excretion, excessive intake, or shift of potassium from INSIDE the cells to EXTRA-cellular space. Usually, a combination of factors is responsible. The most common scenario is a RENAL INsufficiency combined with excessive potassium supplements OR administration of certain drugs. Impaired kidney function is most prominent; excessive intake or extracellular shift is rarely the only cause.
Mild hyperkalemia is often without symptoms, although some patients may develop muscle weakness. Slow or chronic increase in potassium levels is less dangerous, as the kidneys eventually adapt by excreting more potassium. Sudden onset and rapid progression of hyperkalemia, on the other hand, can be fatal. Primary cause of mortality is the effect of potassium on cardiac functions. As potassium levels INcrease in the EXTRAcellular space, the MAGNITUDE of potassium gradient across the cell membrane is REDUCED, and so is the ABSOLUTE value of the resting membrane potential. Membrane voltage becomes less negative, moving closer to the threshold potential, making it EASIER to initiate an action potential. The effect this has on excitability of myocytes, however, is complex. While initial changes seem to increase myocyte excitability; further rise of potassium has the OPPOSITE effect. This is because the value of membrane potential at the onset of an action potential DETERMINES the number of voltage-gated sodium channels activated during depolarization. As this value becomes less negative in hyperkalemia, the number of available sodium channels DEcreases, resulting in a SLOWER influx of sodium and subsequently SLOWER impulse conduction.
In experimental models, ECG changes produced by hyperkalemia follow a typical pattern that correlates with serum potassium levels: peaked T-wave, P wave widens and flattens, PR interval lengthens, QRS complex widens and eventually blends with T-wave. In practice, however, this pattern is present only in a fraction of hyperkalemia patients and does NOT always correlate with potassium levels. This makes diagnosis on the basis of ECG alone very difficult. Given the dangerous nature of acute hyperkalemia, it must be suspected in any patient having new bradycardia or conduction block, especially in those with renal problems.
Severe hyperkalemia is treated in 3 steps:
– Calcium infusion is given to rapidly REVERSE conduction abnormalities. Calcium antagonizes the effect of potassium at the cellular level, stabilizing membrane potential. However, it does not remove potassium, and should not be used in the case of digoxin toxicity.
– Insulin is administered to stimulate the sodium/potassium pump, promoting INTRA-cellular shift of potassium.
– Hemodialysis is performed to remove potassium from the body.
Longer term treatment for hyperkalemia without conduction problems consists of reducing intake and increasing excretion.

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Effect of Alcohol on the Brain, with Animation.

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Alcohol, or more specifically, ethanol, affects brain functions in several ways. Alcohol is generally known as a DEPRESSANT of the central nervous system; it INHIBITS brain activities, causing a range of physiological effects such as impaired body movements and slurred speech. The pleasurable feeling associated with drinking, on the other hand, is linked to alcohol-induced dopamine release in the brain’s reward pathway. Alcohol also increases levels of brain serotonin, a neurotransmitter implicated in mood regulation.
The brain is a complex network of billions of neurons. Neurons can be excitatory or inhibitory. Excitatory neurons stimulate others to respond and transmit electrical messages, while inhibitory neurons SUPPRESS responsiveness, preventing excessive firing. Responsiveness or excitability of a neuron is determined by the value of electrical voltage across its membrane. Basically, a neuron is MORE responsive when it has more POSITIVE charges inside; and is LESS responsive when it becomes more NEGATIVE.
A balance between excitation and inhibition is essential for normal brain functions. Short-term alcohol consumption DISRUPTS this balance, INCREASING INHIBITORY and DECREASING EXCITATORY functions. Specifically, alcohol inhibits responsiveness of neurons via its interaction with the GABA system. GABA is a major INHIBITORY neurotransmitter. Upon binding, it triggers GABA receptors, ligand-gated chloride channels, to open and allow chloride ions to flow into the neuron, making it more NEGATIVE and LESS likely to respond to new stimuli. Alcohol is known to POTENTIATE GABA receptors, keeping the channels open for a longer time and thus exaggerating this inhibitory effect. GABA receptors are also the target of certain anesthetic drugs. This explains the SEDATIVE effect of alcohol.
At the same time, alcohol also inhibits the glutamate system, a major excitatory circuit of the brain. Glutamate receptors, another type of ion channel, upon binding by glutamate, open to allow POSITIVELY-charged ions into the cell, making it more POSITIVE and MORE likely to generate electrical signals. Alcohol binding REDUCES channel permeability, LOWERING cation influx, thereby INHIBITING neuron responsiveness. GABA ACTIVATION and glutamate INHIBITION together bring DOWN brain activities. Depending on the concentration of ethanol in the blood, alcohol’s depressant effect can range from slight drowsiness to blackout, or even respiratory failure and death.
Chronic, or long-term consumption of alcohol, however, produces an OPPOSITE effect on the brain. This is because SUSTAINED inhibition caused by PROLONGED alcohol exposure eventually ACTIVATES the brain’s ADAPTATION response. In attempts to restore the equilibrium, the brain DECREASES GABA inhibitory and INCREASES glutamate excitatory functions to compensate for the alcohol’s effect. As the balance tilts toward EXCITATION, more and more alcohol is needed to achieve the same inhibitory effect. This leads to overdrinking and eventually addiction. If alcohol consumption is ABRUPTLY reduced or discontinued at this point, an ill-feeling known as WITHDRAWAL syndrome may follow. This is because the brain is now HYPER-excitable if NOT balanced by the inhibitory effect of alcohol. Alcohol withdrawal syndrome is characterized by tremors, seizures, hallucinations, agitation and confusion. Excess calcium produced by overactive glutamate receptors during withdrawal is toxic and may cause brain damage. Withdrawal-related anxiety also contributes to alcohol-seeking behavior and CONTINUED alcohol abuse.

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Cardiac Action Potential, with Animation.

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The heart is essentially a muscle that contracts and pumps blood. It consists of specialized muscle cells called cardiac myocytes. The contraction of these cells is initiated by electrical impulses, known as action potentials. Unlike skeletal muscles, which have to be stimulated by the nervous system, the heart generates its OWN electrical stimulation. In fact, a heart can keep on beating even when taken out of the body. The nervous system can make the heartbeats go faster or slower, but cannot generate them. The impulses start from a small group of myocytes called the PACEMAKER cells, which constitute the cardiac conduction system. These are modified myocytes that lose the ability to contract and become specialized for initiating and conducting action potentials. The SA node is the primary pacemaker of the heart. It initiates all heartbeats and controls heart rate. If the SA node is damaged, other parts of the conduction system may take over this role. The cells of the SA node fire SPONTANEOUSLY, generating action potentials that spread though the contractile myocytes of the atria. The myocytes are connected by gap junctions, which form channels that allow ions to flow from one cell to another. This enables electrical coupling of neighboring cells. An action potential in one cell triggers another action potential in its neighbor and the signals propagate rapidly. The impulses reach the AV node, slow down a little to allow the atria to contract, then follow the conduction pathway  and spread though the ventricular myocytes. Action potential generation and conduction are essential for all myocytes to act in synchrony.

Pacemaker cells and contractile myocytes exhibit different forms of action potentials.

Cells are polarized, meaning there is an electrical voltage across the cell membrane. In a resting cell, the membrane voltage, known as the RESTING membrane potential, is usually negative. This means the cell is more NEGATIVE on the INSIDE. At this resting state, there are concentration gradients of several ions across the cell membrane: more sodium and calcium OUTSIDE the cell, and more potassium INSIDE the cell. These gradients are maintained by several pumps that bring sodium and calcium OUT, and potassium IN. An action potential is essentially a brief REVERSAL of electric polarity of the cell membrane and is produced by VOLTAGE-gated ion channels. These channels are passageways for ions in and out of the cell, and as their names suggest, are regulated by membrane voltage. They open at some values of membrane potential and close at others.

When membrane voltage INCREASES and becomes LESS negative, the cell is LESS polarized, and is said to be DE-polarized. Reversely, when membrane potential becomes MORE negative, the cell is RE-polarized. For an action potential to be generated, the membrane voltage must DE-polarize to a critical value called the THRESHOLD.

The pacemaker cells of the SA node SPONTANEOUSLY fire about 80 action potentials per minute, each of which sets off a heartbeat, resulting in an average heart rate of 80 beats per minute. Pacemaker cells do NOT have a TRUE RESTING potential. The voltage starts at about -60mV and SPONTANEOUSLY moves upward until it reaches the threshold of -40mV. This is due to action of so-called “FUNNY” currents present ONLY in pacemaker cells. Funny channels open when membrane voltage becomes lower than     -40mV and allow slow influx of sodium. The resulting DE-polarization is known as “pacemaker potential”. At threshold, calcium channels open, calcium ions flow into the cell further DE-polarizing the membrane. This results in the rising phase of the action potential. At the peak of depolarization, potassium channels open, calcium channels inactivate, potassium ions leave the cell and the voltage returns to -60mV. This corresponds to the falling phase of the action potential. The original ionic gradients are restored thanks to several ionic pumps, and the cycle starts over.

Electrical impulses from the SA node spread through the conduction system and to the contractile myocytes. These myocytes have a different set of ion channels. In addition, their sarcoplasmic reticulum, the SR, stores a large amount of calcium. They also contain myofibrils. The contractile cells have a stable resting potential of -90mV and depolarize ONLY when stimulated, usually by a neighboring myocyte. When a cell is DE-polarized, it has more sodium and calcium inside the cell. These positive ions leak through the gap junctions to the adjacent cell and bring the membrane voltage of this cell up to the threshold of -70mV. At threshold, FAST sodium channels open creating a rapid sodium influx and a sharp rise in voltage. This is the depolarizing phase. L-type, or SLOW, calcium channels also open at -40mV, causing a slow but steady influx. As the action potential nears its peak, sodium channels close quickly, voltage-gated potassium channels open and these result in a small decrease in membrane potential, known as EARLY RE-polarization phase. The calcium channels, however, remain open and the potassium efflux is eventually balanced by the calcium influx. This keeps the membrane potential relatively stable for about 200 msec resulting in the PLATEAU phase, characteristic of cardiac action potentials. Calcium is crucial in coupling electrical excitation to physical muscle contraction. The influx of calcium from the extracellular fluid, however, is NOT enough to induce contraction. Instead, it triggers a MUCH greater calcium release from the SR, in a process known as “calcium-induced calcium release”. Calcium THEN sets off muscle contraction by the same “sliding filament mechanism” described for skeletal muscle. The contraction starts about half way through the plateau phase and lasts till the end of this phase.

As calcium channels slowly close, potassium efflux predominates and membrane voltage returns to its resting value. Calcium is actively transported out of the cell and also back to the SR. The sodium/potassium pump then restores the ionic balance across the membrane.

Because of the plateau phase, cardiac muscle stays contracted longer than skeletal muscle. This is necessary for expulsion of blood from the heart chambers. The absolute refractory period is also much longer – 250 msec compared to 1 msec in skeletal muscle. This long refractory period is to make sure the muscle has relaxed before it can respond to a new stimulus and is essential in preventing summation and tetanus, which would stop the heart from beating.

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Anesthesia, with Animation

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Anesthesia is the use of drugs to prevent or reduce pain during a medical procedure. There are two major classes of drugs:
– Local anesthetics: these drugs block transmission of pain signals from peripheral nerve endings to the central nervous system. And
– General anesthetics: these act on the central nervous system itself to induce unconsciousness and total lack of sensation.
There are 3 major categories of anesthesia procedures:
– Local anesthesia: a local anesthetic is administered directly to the site of procedure to numb a small area such as a tooth during a dental manipulation.
– Regional anesthesia: a local anesthetic is injected near a cluster of nerve roots to prevent pain sensation from the area innervated by those nerves. Epidural given to women in labor is an example of this type.
– General anesthesia: general anesthetics are used to suppress the entire central nervous system, resulting in loss of consciousness. A cocktail of several drugs are inhaled, given intravenously, or both. This type is used for major surgical procedures.
Apart from pain management, general anesthesia has some other goals: prevent formation of new memories, relax muscles, and suppress autonomic response to surgical injuries which could otherwise be extreme and harmful. General anesthetics are commonly used in combination with other drugs to achieve these end points.
An example of general anesthetic drug is Propofol. The exact mechanism of action of Propofol remains unclear, but it is thought to inhibit responsiveness of neurons via its binding to GABA receptor. GABA is a major inhibitory neurotransmitter in the central nervous system. Upon binding, it triggers GABA receptor – a ligand-gated chloride channel – to open and allow chloride ions flow into the neuron, making the cell hyperpolarized and less likely to fire. In other words, GABA makes the brain cells less responsive to new stimuli. Propofol binding has been proposed to potentiate GABA receptor, keeping the channel open for longer time and thus exaggerating this inhibition effect.
It is believed, however, that under anesthesia the brain does not simply shut down. Instead, the connections between different parts of the brain are lost. Using various brain imaging techniques it’s been shown that an anesthetized brain is still reactive to stimuli such as light and sounds, but somehow this sensory information is not processed resulting in no further consequences. A variety of anesthetic drugs are available, each of which may have different target molecules in the brain. However, if used at a high enough dosage, they can all cause unconsciousness. This is probably because consciousness is the result of a complex network of various brain functions, disruption of any of which could result in network dysfunction.
Emerging from unconscious state is not simply the result of drugs wearing off. As the connections between parts of the brain were lost, the brain has to somehow find the way to connect them back upon awakening. This usually happens in a certain order: the most basic and essential functions, such as respiratory and digestive reflexes, come back first, more complex brain functions return after. This may explains why older patients and people with pre-existing neurological conditions may take longer to recover all cognitive brain functions. The risk and extent of postoperative delirium – a state of mental confusion after surgery – are also higher in these patients.
The right dose of overall anesthesia is critical. It is usually calculated based on patient’s weight, age and medical history. Past or current uses of recreational drugs also have to be taken into account. Too much anesthesia results in a too deep state of unconsciousness, and consequently greater risks of postoperative complications and long-term cognitive dysfunction. On the other hand, a too low dose may cause the patient to wake up during the surgery, a phenomenon known as anesthesia awareness, which might be a traumatic experience to some patients.

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Eye Floaters and Flashes, with Animation.

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From the patient’s point of view, floaters are objects that drift around in the field of vision. They may look like blobs, little worms or cobwebs that move with the eye’s movement. They seem impossible to focus on and are most visible when looking against a bright plain background such as a blue sky or a blank computer screen. Floaters are in fact particles suspended inside the vitreous body – the gel-like structure that fills the space between the lens and the retina. What we see, however, are not the floaters themselves, but the shadows they cast on the retina. The closer they are to the retina, the larger and clearer they appear in the field of vision.

Commonly, floaters develop as part of normal aging. With age, the gel-like vitreous body undergoes syneresis – a process in which water is separated from solid components, creating pockets of fluid that are perceived by the patient as blobs or little worms. The major structural protein of the vitreous – collagen fibrils – become denatured, clump together and can be seen as floating strings or cobwebs. The fluid pockets may collapse, causing the vitreous to shrink and pull away from the retina. This pulling exerts mechanical stimulations on the retina, producing “flashes of light” or photopsias in peripheral vision. Eventually, the vitreous is separated from the retina. This is known as posterior vitreous detachment or PVD. PVD is very common but is generally benign and does not require treatment. The floaters may be a nuisance to vision, but in most people, the brain will eventually learn to ignore them. Complications may happen, however, in a small number of cases. As the vitreous detaches, it may pull the retina with it, resulting in a retinal tear. Fluid from the vitreous may then sip through the tear and cause the retina to separate from the underlying tissue. This is known as retinal detachment and is a sight-threatening condition. Worrying signs to watch out for include:

  • A sudden increase in number of new floaters, especially tiny ones as these may represent pigments or blood cells released from the damaged retina or blood vessels.
  • A shade or curtain of vision – a sign of loss of vision from the detached part of the retina.

People with high degree of myopia are at higher risks of having PVD. The longer shape of the eyeball in myopia increases the likelihood of PVD and also the risk of retinal complications. This is because the retina is stretched over a larger surface and becomes thinner and more vulnerable to tears.

Other risk factors for PVD include intraocular inflammation, trauma, previous eye surgery, diabetes and family history.

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QRS Transitional Zone and R Wave Progression Explained, with Animation.

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The chest leads look at the heart in a horizontal plane. V1 represents the rightmost view, and V6 – the leftmost. The QRS complex represents depolarization of the ventricles which starts with the interventricular septum. In normal conduction, depolarization of the septum is initiated from the left bundle going to the right, TOWARD V1 and AWAY from V6. This results in a small positive deflection in V1 and a negative deflection in V6. The signals then move both directions to the two ventricles, but as the left ventricle is usually much larger, the NET movement is to the left, AWAY from V1, TOWARD V6. This corresponds to a negative wave in V1 and a positive wave in V6. Thus, the QRS complex starts as predominantly negative in V1, and ends as predominantly positive in V6. Somewhere in between, usually from V3 to V4, it is isoelectric, with equal positive and negative deflections. This is known as the transitional zone. In addition, there is a gradual increase in amplitude of R wave from V1 to V5. This is known as R wave progression.

The normal transitional zone is between V3 and V4. When transition happens at or before V2, it is referred to as early transition, rightward shift, or counter-clockwise rotation. This is because these ECG patterns would have been generated if the heart had rotated counter-clockwise around the longitudinal axis. Reversely, when the transition occurs after V4, it is referred to as late transition, leftward shift, or clockwise rotation. These shifts may or may not be signs of heart diseases. In many cases, these are simply artefacts, resulting from incorrect placement of the chest electrodes – too low or too high. In other cases, they are due to normal anatomical variations of the heart’s shape and orientation. Clockwise rotation is more commonly associated with cardiovascular diseases while counter-clockwise rotation is more common in healthy individuals.

Some clinical causes of clockwise rotation include:

  • Physical rotation of the heart in conditions such as chronic obstructive pulmonary disease
  • Conduction problems due to anterior myocardial infarction
  • Heart chambers dilatation (Dilated cardiomyopathy)

Some clinical causes of counter-clockwise rotation include:

  • Conduction problems due to posterior myocardial infarction
  • Electrical shift to the right in conditions such as right ventricular hypertrophy

When the transitional zone is absent, or is not clear, it is usually clinical. In this case it may be helpful to look at R wave progression.

Non-progression or poor progression of R wave – R wave stays low and S wave remains deep throughout all chest leads. This is an extreme case of clockwise rotation and is suggestive of extensive anterior myocardial infarction.

Reverse progression of R wave – tall R wave in V1, tallest in V1 or V2 – is usually seen in right ventricular hypertrophy. Increased muscle mass in the right ventricle results in net electrical movement towards the right chest leads.

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Fibrilación Auricular e Ictus, con Animación.

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La fibrilación auricular es la arritmia cardíaca más común. En un corazón sano, el nodo sinoatrial o nódulo SA inicia todos los impulsos eléctricos en las aurículas. En la fibrilación auricular, los impulsos eléctricos se inician al azar en muchos otros sitios llamados sitios ectópicos, dentro y alrededor de las aurículas, comúnmente cerca de las raíces de las venas pulmonares. Estas señales eléctricas caóticas desincronizadas, hacen que las aurículas tiemblen o fibrilen en lugar de contraerse.
Aunque la frecuencia auricular durante la fibrilación auricular puede ser extremadamente alta, la mayor parte de los impulsos eléctricos no pasan por el nódulo auriculoventricular – nodo AV – a los ventrículos. Esto es debido a las propiedades refractarias de las células del nodo AV. Aquellas que vienen a través del mismo son irregulares. La frecuencia ventricular o la frecuencia cardíaca es, por lo tanto irregular y pueden variar desde lenta – menos de 60 – a rápida -más de 100 – latidos por minuto.
En el ECG, la fibrilación auricular se caracteriza por la ausencia de ondas P y complejos QRS estrechos e irregulares. Recordatorio: la onda P representa la actividad eléctrica del nodo SA que es ahora oscurecida por las actividades de varios sitios ectópicos. La línea de base puede aparecer ondulada o totalmente plana en función del número de sitios ectópicos en las aurículas. En general, un mayor número de sitios ectópicos resulta en una línea de base plana.
A medida que las aurículas no funcionan correctamente, el corazón bombea menos sangre, y puede provocar una insuficiencia cardíaca. La complicación más común de la fibrilación auricular, sin embargo, es la formación de coágulos de sangre en las aurículas. A medida que las aurículas no se vacían por completo en los ventrículos, la sangre puede estancarse dentro de las aurículas y puede formar coágulos de sangre. Estos coágulos pueden entonces pasar al torrente sanguíneo, atascarse en las arterias pequeñas y bloquearlas. Así que cuando un coágulo de sangre bloquea una arteria en el cerebro, puede provocar un ictus, o infarto cerebral.

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Formation of Urine – Nephron Function, with Animation.

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The kidneys filter blood plasma, removing metabolic wastes, toxins from the body and excrete them in the form of urine. During this process, they also maintain constant volume and composition of the blood, or homeostasis.
Blood enters the kidney via the renal artery, which divides to smaller arteries and finally arterioles. The arterioles get into contact with functional units of the kidney called nephrons. This is where blood filtration and urine formation take place. The filtered blood is then collected in to a series of larger veins and exits the kidney through the renal vein. The urine is collected in collecting ducts and leaves the kidney via the ureters.
Each kidney contains over a million nephrons. A nephron consists of 2 major parts: a capsule known as glomerular capsule, or Bowman’s capsule; and a long renal tubule. Renal tubules of several nephrons connect to a common collecting duct.
There are 3 steps in the formation of urine:
– glomerular filtration takes place in the Bowman’s capsule
– tubular re-absorption and secretion occur in the renal tubule
– water conservation happens in the collecting duct
Blood enters the Bowman’s capsule via the afferent arteriole, passes through a ball of capillaries called the glomerulus, and leaves via the efferent arteriole. The afferent arteriole is significantly larger than the efferent arteriole, creating a blood flow with a large inlet and small outlet. As a result, the blood hydrostatic pressure in these capillaries is much higher than normal. Hydrostatic and osmotic pressures drive water and solutes from blood plasma through a filtration membrane into the capsular space of nephron. The filtration membrane acts like a sieve allowing only small molecules to pass through. These include water, inorganic ions, glucose, amino acids and various metabolic wastes such as urea and creatinine. This fluid is called glomerular filtrate. The amount of filtrate produced per minute is called glomerular filtration rate, or GFR. The GFR is kept at a stable value by several feedback mechanisms within the kidneys. This is known as renal autoregulation. The GFR is also under sympathetic and hormonal control. GFR control is generally achieved by constriction or dilation of the afferent arteriole, which causes the glomerular blood pressure to fall or rise, respectively.
In a healthy person, the total filtrate volume amounts between 150 and 180 litters a day. However, only about 1% of this is excreted as urine, the rest 99% is re-absorbed back to the blood as the filtrate flows through the long renal tubule. This is possible because the efferent arteriole, after exiting the Bowman’s capsule, branches out to form a network of capillaries, known as peri-tubular capillaries, which surround the renal tubule.
The first part of the renal tubule – the proximal convoluted tubule, re-absorbs about two thirds of the filtrate. In this process, water and solutes are driven through the epithelial cells that line the tubule into the extracellular space. They are then taken up by the peritubular capillaries. Sodium re-absorption is most important, as it creates osmotic pressure that drives water and electrical gradient that drives negatively charged ions. Sodium level inside the epithelial cells is kept low thanks to the sodium-potassium pumps that constantly pump sodium ions out into the extracellular space. This creates a concentration gradient that favors sodium diffusion from tubular fluid into the cells. Sodium is absorbed by symport proteins that also bind glucose and some other solutes. Nearly all glucose and amino acids are re-absorbed back to the blood at this stage. About half of nitrogenous wastes also re-absorbs back to the bloodstream. The kidneys reduce the blood levels of metabolic wastes to a safe amount, but do not completely eliminate them. Some of the re-absorption also occurs by the paracellular route through tight junctions between the epithelial cells.
At the same time, tubular secretion, where additional wastes, drugs and other solutes leave the bloodstream to join the tubular fluid, also takes place.
The processes of re-absorption and secretion continue in the nephron loop – the loop of Henle, and the distal convoluted tubule. However, these parts of the tubule also have some other important functions.
The main function of the loop of Henle is to create and maintain an osmolarity gradient in the medulla that enables the collecting ducts to concentrate urine at a later stage. The ascending limb of the loop actively pumps sodium out making the medulla “salty”. The descending limp of the loop is permeable to water but much less to sodium. As the water exits the tubule by osmosis, the filtrate gets more and more concentrated as it reaches the bottom. The ascending limb, on the other hand, is permeable to ions but not water. As a result, the filtrate loses sodium as it goes up and becomes more diluted at the top of the loop. The medulla is in equilibrium with the loop and hence has the same salinity gradient – saltier at the bottom.
Re-absorption and secretion in the distal convoluted tubule are under control of various hormones. This is how the kidney respond to the body’s needs and adjust the composition of urine accordingly.
The collecting duct receives tubular fluid from several nephrons. The main function of the collecting duct is to concentrate urine and therefore conserve water. This is made possible by the osmolarity gradient generated by the loop of Henle. As it gets saltier deep in the medulla, the filtrate loses more and more water as it flows down the collecting duct. The collecting duct is also under hormonal control so it can adjust the amount of re-absorbed water accordingly to the body’s state of hydration. For example, when the body is dehydrated, more water is re-absorbed back to the blood and the small volume of excreted urine is more concentrated.

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Ectopic Pregnancy, with Animation

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An ectopic pregnancy is a pregnancy that occurs outside the uterus. Normally, fertilization takes place in the widest section of the fallopian tube. The fertilized egg then travels toward the uterus where it is to be implanted. Ectopic pregnancy happens when the egg gets stuck on its way and starts to develop inside the tube. This is known as tubal pregnancy. Implantation may also occur in the cervix, ovaries and abdominal cavity but tubal pregnancy is by far the most common. With extremely rare exceptions, the fetus cannot survive outside the uterus. Without treatment, the growing tissue may rupture, resulting in destruction of the surrounding maternal structures and a massive blood loss that could be life-threatening.

Signs and Symptoms 

An ectopic pregnancy may have no signs, or may feel like a normal pregnancy at first, with positive pregnancy test result for hCG. First clinical symptoms usually appear after 4 weeks from the last normal menstrual period and may include abdominal pain, vaginal bleeding, or both. There may also be shoulder pain. If the fallopian tube ruptures, heavy bleeding, fainting and shock can be expected. This is a medical emergency and requires immediate attention.

Causes

Tubal pregnancy occurs because of problems in transportation of the fertilized egg through the tube. Fallopian tubes are lined with hair-like structures called cilia that help to move the egg through. It is believed that a reduction in number of cilia may slow down the transport and lead to tubal pregnancies. Cilia degeneration can happen as a result of tubal tissue scarring or as an effect of certain chemicals or drugs.

Risks factors include:

-Inflammation of fallopian tubes – salpingitis; or infection of pelvic organs – pelvic inflammatory disease. These infections are commonly caused by gonorrhea or chlamydia.
-Use of an intrauterine device as a contraceptive method
-Tubal or intrauterine surgeries such as tubal ligation, tubal reversal and dilation & curettage
-Previous ectopic pregnancy
-Abnormal fallopian tubes due to birth defects
-Smoking
-Exposure to certain fertility drugs
-Daughters of mothers who have taken the synthetic estrogen diethylstilbestrol during pregnancy

Diagnosis is often based on blood tests for hCG and a transvaginal ultrasound.
If the ectopic pregnancy is detected early, methotrexate may be injected to dissolve the pregnancy tissue. In other cases, a keyhole surgery may be performed. If the fallopian tube has ruptured, an emergency open surgery is required. The ruptured tube is usually removed. After treatment the hCG levels are monitored to ensure that the entire ectopic tissue has been taken out. An hCG level that remains high would require further treatment.

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