<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Phobia and can you explain it in depth? [/INST] A phobia is an anxiety disorder defined by a persistent and excessive fear of an object or situation. Phobias typically result in a rapid onset of fear and are usually present for more than six months. Those affected go to great lengths to avoid the situation or object, to a degree greater than the actual danger posed. If the object or situation cannot be avoided, they experience significant distress. Other symptoms can include fainting, which may occur in blood or injury phobia, and panic attacks, often found in agoraphobia. Around 75% of those with phobias have multiple phobias.Phobias can be divided into specific phobias, social anxiety disorder, and agoraphobia. Specific phobias are further divided to include certain animals, natural environment, blood or injury, and particular situations. The most common are fear of spiders, fear of snakes, and fear of heights. Specific phobias may be caused by a negative experience with the object or situation in early childhood. Social phobia is when a person fears a situation due to worries about others judging them. Agoraphobia is a fear of a situation due to perceived difficulty or inability to escape.It is recommended that specific phobias be treated with exposure therapy, in which the person is introduced to the situation or object in question until the fear resolves. Medications are not helpful for specific phobias. Social phobia and agoraphobia may be treated with counseling, medications, or a combination of both. Medications used include antidepressants, benzodiazepines, or beta-blockers.Specific phobias affect about 6–8% of people in the Western world and 2–4% in Asia, Africa, and Latin America in a given year. Social phobia affects about 7% of people in the United States and 0.5–2.5% of people in the rest of the world. Agoraphobia affects about 1.7% of people. Women are affected by phobias about twice as often as men. The typical onset of a phobia is around 10–17, and rates are lower with increasing age. Those with phobias are more likely to attempt suicide.

Classification
Fear is an emotional response to a current perceived danger. This differs from anxiety which is a response in preparation of a future threat. Fear and anxiety often can overlap but this distinction can help identify subtle differences between disorders, as well as differentiate between a response that would be expected given a persons developmental stage and culture.

ICD-11
The International Classification of Diseases (11th version: ICD-11) is a globally used diagnostic tool for epidemiology, health management and clinical purposes maintained by the World Health Organization (WHO). The ICD classifies phobic disorders under the category of mental, behavioural or neurodevelopmental disorders. The ICD-10 differentiates between Phobic anxiety disorders, such as Agoraphobia, and Other anxiety disorders, such as Generalized anxiety disorder. The ICD-11 merges both groups together as Anxiety or fear-related disorders.

DSM-V
Most phobias are classified into three categories. According to the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-V), such phobias are considered subtypes of anxiety disorder. The categories are:

Specific phobias: Fear of particular objects or situations that results in anxiety and avoidance. May lead to panic attacks if exposed to feared stimulus or in anticipation of encounter. A specific phobia may be further subdivided into five categories: animal, natural environment, situational, blood-injection-injury, and other.
Agoraphobia: a generalized fear of leaving home or a small familiar safe area and of possible panic attacks that might follow. Various specific phobias may also cause it, such as fear of open spaces, social embarrassment (social agoraphobia), fear of contamination (fear of germs, possibly complicated by obsessive–compulsive disorder) or PTSD (post-traumatic stress disorder) related to a trauma that occurred outdoors.
Social anxiety disorder (SAD), also known as social phobia, is when the situation is feared out of a worrying about others judging them. Performance only is a subtype of social anxiety disorder Phobias vary in severity among individuals. Some individuals can avoid the subject and experience relatively mild anxiety over that fear. Others experience full-fledged panic attacks with all the associated impairing symptoms. Most individuals understand that their fear is irrational but cannot override their panic response. These individuals often report dizziness, loss of bladder or bowel control, tachypnea, feelings of pain, and shortness of breath.

Causes
There are multiple theories about how phobias develop and likely occur due to a combination of environmental and genetic factors. The degree to whether environment or genetic influences have a more significant role varies by condition, with social anxiety disorder and agoraphobia having around a 50% heritability rate.

Environmental
Rachman proposed three pathways for the development of phobias: direct or classical conditioning (exposure to phobic stimulus), vicarious acquisition (seeing others experience phobic stimulus), and informational/instructional acquisition (learning about phobic stimulus from others).

Classical conditioning
Much of the progress in understanding the acquisition of fear responses in phobias can be attributed to classical conditioning (Pavlovian model). When an aversive stimulus and a neutral one are paired together, for instance, when an electric shock is given in a specific room, the subject can start to fear not only the shock but the room as well. In behavioral terms, the room is a conditioned stimulus (CS). When paired with an aversive unconditioned stimulus (UCS) (the shock), it creates a conditioned response (CR) (fear for the room) (CS+UCS=CR). For example, in case of the fear of heights (acrophobia), the CS is heights. Such as a balcony on the top floors of a high rise building. The UCS can originate from an aversive or traumatizing event in the persons life, such as almost falling from a great height. The original fear of nearly falling is associated with being high, leading to a fear of heights. In other words, the CS (heights) associated with the aversive UCS (almost falling) leads to the CR (fear).
Though historically influential in the theory of fear acquisition, this direct conditioning model is not the only proposed way to acquire a phobia. This theory in fact has limitations as not everyone that has experienced a traumatic event develops a phobia and vice versa.

Vicarious conditioning
Vicarious fear acquisition is learning to fear something, not by a subjects own experience of fear, but by watching others, oftentimes a parent (observational learning). For instance, when a child sees a parent reacting fearfully to an animal, the child can also become afraid of the animal. Through observational learning, humans can  learn to fear potentially dangerous objects—a reaction observed in other primates. A study on non-human primates, showed that the primates learned to fear snakes at a fast rate after watching parents fearful reactions. An increase in fearful behaviours was observed as the non-human primates observed their parents fearful reactions. Although observational learning has proven effective in creating reactions of fear and phobias, it has also been shown that by physically experiencing an event, increases the chance of fearful and phobic behaviours. In some cases, physically experiencing an event may increase the fear and phobia more than observing a fearful reaction of another human or non-human primate.

Informational/Instructional acquisition
Informational/instructional fear acquisition is learning to fear something by getting information. For instance, fearing electrical wire after hearing that touching it causes an electric shock.A conditioned fear response to an object or situation is not always a phobia. There must also be symptoms of impairment and avoidance. Impairment is defined as an inability to complete routine tasks, whether occupational, academic, or social.  For example, an occupational impairment can result from acrophobia, from not taking a job solely because of its location on the top floor of a building, or socially not participating in an event at a theme park. The avoidance aspect is defined as behaviour that results in the omission of an aversive event that would otherwise occur, intending to prevent anxiety.

Genetic
With the completion of the Human Genome Project in 2003, much research has been completed looking at specific genes that may cause or contribute to medical conditions. Candidate genes were the focus of most of these studies until the past decade, when the cost and ability to perform genome-wide analyses became more available. The GLRB gene was identified as a possible target for agoraphobia. An area still in development is reviewing epigenetic components or the interaction of the environment on genes through methylation. A number of genes are being examined through this epigenetic lens which may be linked with social anxiety disorder, including MAOA, CRHR1, and OXTR. Each phobia related disorder has some degree of genetic susceptibility. Those with specific phobias are more likely to have first degree relatives with the same specific phobia. Similarly, social anxiety disorder is found two to six times more frequently in those with first degree relatives that have it versus those that do not. Agoraphobia is believed to have the strongest genetic association.

Mechanism
Limbic system
Beneath the lateral fissure in the cerebral cortex, the insula, or insular cortex, of the brain has been identified as part of the limbic system, along with the cingulated gyrus, hippocampus, corpus callosum, and other nearby cortices. This system has been found to play a role in emotion processing, and the insula, in particular, may contribute to maintaining autonomic functions. Studies by Critchley et al. indicate the insula as being involved in the experience of emotion by detecting and interpreting threatening stimuli. Similar studies monitoring insula activity have shown a correlation between increased insular activation and anxiety.In the frontal lobes, other cortices involved with phobia and fear are the anterior cingulate cortex and the medial prefrontal cortex. In the processing of emotional stimuli, studies on phobic reactions to facial expressions have indicated that these areas are involved in the processing and responding to negative stimuli. The ventromedial prefrontal cortex has been said to influence the amygdala by monitoring its reaction to emotional stimuli or even fearful memories. Most specifically, the medial prefrontal cortex is active during the extinction of fear and is responsible for long-term extinction. Stimulation of this area decreases conditioned fear responses, so its role may be in inhibiting the amygdala and its reaction to fearful stimuli.The hippocampus is a horseshoe-shaped structure that plays an essential part in the brains limbic system. This is because it forms memories and connects them with emotions and the senses. When dealing with fear, the hippocampus receives impulses from the amygdala that allow it to connect the fear with a certain sense, such as a smell or sound.

Amygdala
The amygdala is an almond-shaped mass of nuclei located deep in the brains medial temporal lobe. It processes the events associated with fear and is linked to social phobia and other anxiety disorders. The amygdalas ability to respond to fearful stimuli occurs through fear conditioning. Like classical conditioning, the amygdala learns to associate a conditioned stimulus with a negative or avoidant stimulus, creating a conditioned fear response often seen in phobic individuals. The amygdala is responsible for recognizing certain stimuli or cues as dangerous and plays a role in the storage of threatening stimuli to memory. The basolateral nuclei (or basolateral amygdala) and the hippocampus interact with the amygdala in-memory storage. This connection suggests why memories are often remembered more vividly if they have emotional significance.In addition to memory, the amygdala also triggers the secretion of hormones that affect fear and aggression. When the fear or aggression response is initiated, the amygdala releases hormones into the body to put the human body into an "alert" state, which prepares the individual to move, run, fight, etc. This defensive "alert" state and response are known as the fight-or-flight response.However, inside the brain, this stress response can be observed in the hypothalamic-pituitary-adrenal axis (HPA). This circuit incorporates the process of receiving stimuli, interpreting them, and releasing certain hormones into the bloodstream. The parvocellular neurosecretory neurons of the hypothalamus release corticotropin-releasing hormone (CRH), which is sent to the anterior pituitary. Here the pituitary releases adrenocorticotropic hormone (ACTH), which ultimately stimulates the release of cortisol. In relation to anxiety, the amygdala activates this circuit, while the hippocampus is responsible for suppressing it. Glucocorticoid receptors in the hippocampus monitor the amount of cortisol in the system and through negative feedback can tell the hypothalamus to stop releasing CRH.Studies on mice engineered to have high concentrations of CRH showed higher levels of anxiety, while those engineered to have no or low amounts of CRH receptors were less anxious. In people with phobias, therefore, high amounts of cortisol may be present, or there may be low levels of glucocorticoid receptors or even serotonin (5-HT).

Disruption by damage
For the areas in the brain involved in emotion—most specifically fear— the processing and response to emotional stimuli can be altered when one of these regions is damaged. Damage to the cortical areas involved in the limbic system, such as the cingulate cortex or frontal lobes, has resulted in extreme emotion changes. Other types of damage include Klüver–Bucy syndrome and Urbach–Wiethe disease. In Klüver–Bucy syndrome, a temporal lobectomy, or removal of the temporal lobes, results in changes involving fear and aggression. Specifically, the removal of these lobes results in decreased fear, confirming its role in fear recognition and response. Damage to both side (Bilateral damage) of the medial temporal lobes is known as Urbach–Wiethe disease. It presents with similar symptoms of decreased fear and aggression but with the addition of the inability to recognize emotional expressions, especially angry or fearful faces.The amygdalas role in learned fear includes interactions with other brain regions in the neural circuit of fear. While damage in the amygdala can inhibit its ability to recognize fearful stimuli, other areas such as the ventromedial prefrontal cortex and the basolateral nuclei of the amygdala can affect the regions ability to not only become conditioned to fearful stimuli but to extinguish them eventually. Through receiving stimulus info, the basolateral nuclei undergo synaptic changes that allow the amygdala to develop a conditioned response to fearful stimuli. Damage to this area, therefore, have been shown to disrupt the acquisition of learned responses to fear. Likewise, damage in the ventromedial prefrontal cortex (the area responsible for monitoring the amygdala) has been shown to slow down the speed of extinguishing a learned fear response and how effective the extinction is. This suggests there is a pathway or circuit among the amygdala and nearby cortical areas that process emotional stimuli and influence emotional expression, all of which can be disrupted when damage occurs.

Diagnosis
It is recommended that the terms distress and impairment take into account the context of the persons environment during diagnosis. The DSM-IV-TR states that if a feared stimulus, whether it be an object or a situation, is absent entirely in an environment, a diagnosis cannot be made. An example of this situation would be an individual who has a fear of mice but lives in an area without mice. Even though the concept of mice causes marked distress and impairment within the individual, because the individual does not usually encounter mice, no actual distress or impairment is ever experienced. It is recommended that proximity to, and ability to escape from, the stimulus also be considered. As the phobic person approaches a feared stimulus, anxiety levels increase, and the degree to which the person perceives they might escape from the stimulus affects the intensity of fear in instances such as riding an elevator (e.g. anxiety increases at the midway point between floors and decreases when the floor is reached and the doors open). The DSM-V has been updated to reflect that an individual may have changed their daily activities around the feared stimulus in such a way that they may avoid it altogether. The person may still meet criteria for the diagnosis if they continue to avoid or refuse to participate in activities they would involve possible exposure to the phobic stimulus.

Specific phobias
A specific phobia is a marked and persistent fear of an object or situation. Specific phobias may also include fear of losing control, panicking, and fainting from an encounter with the phobia. Specific phobias are defined concerning objects or situations, whereas social phobias emphasize social fear and the evaluations that might accompany them.
The DSM breaks specific phobias into five subtypes: animal, natural environment, blood-injection-injury, situational and other. In children, blood-injection-injury phobia, animal phobias, and natural environment phobias usually develop between the ages of 7 and 9 reflective of normal development. Additionally, specific phobias are most prevalent in children between the ages 10 and 13. Situational phobias are typically found in older children and adults.

Treatments
There are various methods used to treat phobias. These methods include systematic desensitization, progressive relaxation, virtual reality, modeling, medication, and hypnotherapy. Over the past several decades, psychologists and other researchers have developed effective behavioral, pharmacological, and technological interventions for the treatment of phobia.

Therapy
Cognitive behavioral therapy (CBT) can be beneficial by allowing the person to challenge dysfunctional thoughts or beliefs by being mindful of their feelings to recognize that their fear is irrational. CBT may occur in a group setting. Gradual desensitization treatment and CBT are often successful, provided the person is willing to endure some discomfort. In one clinical trial, 90% of people no longer had a phobic reaction after successful CBT treatment.Evidence supports that eye movement desensitization and reprocessing (EMDR) is effective in treating some phobias. Its effectiveness in treating complex or trauma-related phobias has not been empirically established. Primarily used to treat post-traumatic stress disorder, EMDR has been demonstrated to ease phobia symptoms following a specific trauma, such as a fear of dogs following a dog bite.

Systematic desensitization
Systematic desensitization is a process in which people seeking help slowly become accustomed to their phobia, and ultimately overcome it. Traditional systematic desensitization involves a person being exposed to the object they are afraid of over time so that the fear and discomfort do not become overwhelming. This controlled exposure to the anxiety-provoking stimulus is key to the effectiveness of exposure therapy in the treatment of specific phobias. It has been shown that humor is an excellent alternative when traditional systematic desensitization is ineffective. Humor systematic desensitization involves a series of treatment activities that elicit humor with the feared object. Previously learned progressive muscle relaxation procedures can be used as the activities become more difficult. Progressive muscle relaxation helps people relax before and during exposure to the feared stimulus.
Virtual reality therapy is another technique that helps phobic people confront a feared object. It uses virtual reality to generate scenes that may not have been possible or ethical in the physical world. It is equally as effective as traditional exposure therapy and offers additional advantages. These include controlling the scenes and having the phobic person endure more exposure than they might handle in reality.

Medications
Medications are a treatment option often utilized in combination with CBT or if CBT was not tolerated or effective. Medications can help regulate apprehension and fear of a particular fearful object or situation. There are various medication options available for both social anxiety disorder and agoraphobia. The use of medications for specific phobias, besides the limited role of benzodiazepines, do not currently have established guidelines due to minimal supporting evidence.

Antidepressants
Antidepressant medications such as selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs), or monoamine oxidase inhibitors (MAOIs) may be helpful in some cases. SSRIs / SNRIs act on serotonin, a neurotransmitter in the brain. Because of serotonins positive impacts mood, an antidepressant may be offered and prescribed as a treatment option. For social anxiety, the SSRIs sertraline, paroxetine, fluvoxamine, and the SNRI venlafaxine have FDA approval. Similar medications may be offered for agoraphobia.

Benzodiazepines
Sedatives such as benzodiazepines (clonazepam, alprazolam) are another therapeutic option, which can help people relax by reducing the amount of anxiety they feel. Benzodiazepines may be useful in the acute treatment of severe symptoms, but the risk-benefit ratio usually goes against their long-term use in phobic disorders. This class of medication has recently been shown as effective if used with negative behaviours such as excessive alcohol use. Despite this positive finding, benzodiazepines are used with caution due to side effects and risk of developing dependence or withdrawal symptoms. In specific phobia for example if the phobic stimulus is one that is not regularly encountered such as flying a short course may be provided.

Beta-blockers
Beta blockers (propranolol) are another therapeutic option, particularly for those with the performance only subtype of social anxiety disorder. They may stop the stimulating effects of adrenaline, such as sweating, increased heart rate, elevated blood pressure, tremors, and the feeling of a pounding heart. By taking beta-blockers before a phobic event, these symptoms are decreased, making the event less frightening. Beta-blockers are not effective for generalized social anxiety disorder.

Hypnotherapy
Hypnotherapy can be used alone and in conjunction with systematic desensitization to treat phobias. Through hypnotherapy, the underlying cause of the phobia may be uncovered. The phobia may be caused by a past event that the person does not remember, a phenomenon known as repression. The mind represses traumatic memories from the conscious mind until the person is ready to deal with them.
Hypnotherapy may also eliminate the conditioned responses that occur during different situations. People are first placed into a hypnotic trance, an extremely relaxed state in which the unconscious can be retrieved. This state makes people more open to suggestion, which helps bring about desired change. Consciously addressing old memories helps individuals understand the event and see it less threateningly.

Prognosis
Outcomes vary widely among the phobic anxiety disorders. There is a possibility that remission occurs without intervention but relapses are common. Response to treatment as well as remission and relapse rates are impacted by the severity of an individuals disorder as well as how long they have been experiencing symptoms. For example, in social anxiety disorder (social phobia) a majority of individuals will experience remission within the first couple of years of symptom onset without specific treatment. On the other hand, in Agoraphobia as few as 10% of individuals are seen to reach complete remission without treatment. A study looking at the 2 year remission rates for anxiety disorders found that those with multiple anxieties were less likely to experience remission.

Specific phobia
The majority of those that develop a specific phobia first experience symptoms in childhood. Often individuals will experience symptoms periodically with periods of remission before complete remission occurs. However, specific phobias that continue into adulthood are likely to experience a more chronic course. Specific phobias in older adults has been linked with a decrease in quality of life. Those with specific phobias are at an increased risk of suicide. Greater impairment is found in those that have multiple phobias. Response to treatment is relatively high but many do not seek treatment due to lack of access, ability to avoid phobia, or unwilling to face feared object for repeated CBT sessions.

Comorbidities
Many of those with a phobia often have more than one phobia. There are also a number of psychological and physiological disorders that tend to occur or coexist at higher rates among this population. As with all anxiety disorders the most common psychiatric condition to occur with a phobia is major depressive disorder. Additionally bipolar disorder, substance dependence disorder, obsessive-compulsive disorder, and post traumatic stress disorder have also been found to occur in those with phobias at higher rates.

Epidemiology
Phobias are a common form of anxiety disorder, and distributions are heterogeneous by age and gender. An American study by the National Institute of Mental Health (NIMH) found that between 8.7 percent and 18.1 percent of Americans have phobias, making it the most common mental illness among women in all age groups and the second most common illness among men older than 25. Between 4 percent and 10 percent of all children experience specific phobias during their lives, and social phobias occur in one percent to three percent of children.A Swedish study found that females have a higher number of cases per year than males (26.5 percent for females and 12.4 percent for males). Among adults, 21.2 percent of women and 10.9 percent of men have a single specific phobia, while multiple phobias occur in 5.4 percent of females and 1.5 percent of males. Women are nearly four times as likely as men to have a fear of animals (12.1 percent in women and 3.3 percent in men) — a higher dimorphic than with all specific or generalized phobias or social phobias. Social phobias are more common in girls than boys, while situational phobia occurs in 17.4 percent of women and 8.5 percent of men.

Society and culture
Terminology
The word phobia comes from the Greek: φόβος (phóbos), meaning "aversion", "fear" or "morbid fear". The regular system for naming specific phobias uses prefixes based on a Greek word for the object of the fear, plus the suffix -phobia. Benjamin Rushs 1786 satyrical text, On the different Species of Phobia, established the terms dictionary sense of specific morbid fears. However, many phobias are irregularly named with Latin prefixes, such as apiphobia instead of melissaphobia (fear of bees) or aviphobia instead of ornithophobia (fear of birds). Creating these terms is something of a word game. Such fears are psychological rather than physiological in origin, and few of these terms are found in medical literature. In ancient Greek mythology Phobos was the twin brother of Deimos (terror).
The word phobia may also refer to conditions other than true phobias. For example, the term hydrophobia is an old name for rabies, since an aversion to water is one of that diseases symptoms. A specific phobia to water is called aquaphobia instead. A hydrophobe is a chemical compound that repels water. Similarly, photophobia usually refers to a physical complaint (aversion to light due to inflamed eyes or excessively dilated pupils), rather than an irrational fear of light.

Non-medical, deterrent and political use
Several terms with the suffix -phobia are used non-clinically to imply irrational fear or hatred. Examples include:

Chemophobia – Irrational fear or hatred of chemistry and synthetic chemicals.
Xenophobia – Irrational fear or hatred of strangers or the unknown, sometimes used to describe nationalistic political beliefs and movements.
Homophobia – Irrational fear or hatred of homosexuality or people who identify or perceived as being lesbian, gay, bisexual or transgender (LGBT).
Islamophobia – Irrational fear or hatred of Islam
Hinduphobia – Irrational fear or hatred of Hinduism or Sanatan Dharma
Biphobia – Irrational fear or hatred of bisexual people
Transphobia – Irrational fear or hatred of transgender peopleUsually, these kinds of "phobias" are described as fear, dislike, disapproval, prejudice, hatred, discrimination, or hostility towards the object of the "phobia" </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Gonorrhea and can you explain it in depth? [/INST] Gonorrhea, colloquially known as the clap, is a sexually transmitted infection (STI) caused by the bacterium Neisseria gonorrhoeae. Infection may involve the genitals, mouth, or rectum. Infected men may experience pain or burning with urination, discharge from the penis, or testicular pain. Infected women may experience burning with urination, vaginal discharge, vaginal bleeding between periods, or pelvic pain. Complications in women include pelvic inflammatory disease and in men include inflammation of the epididymis. Many of those infected, however, have no symptoms. If untreated, gonorrhea can spread to joints or heart valves.Gonorrhea is spread through sexual contact with an infected person. This includes oral, anal, and vaginal sex. It can also spread from a mother to a child during birth. Diagnosis is by testing the urine, urethra in males, or cervix in females. Testing all women who are sexually active and less than 25 years of age each year as well as those with new sexual partners is recommended; the same recommendation applies in men who have sex with men (MSM).Gonorrhea can be prevented with the use of condoms, having sex with only one person who is uninfected, and by not having sex. Treatment is usually with ceftriaxone by injection and azithromycin by mouth. Resistance has developed to many previously used antibiotics and higher doses of ceftriaxone are occasionally required. Retesting is recommended three months after treatment. Sexual partners from the last two months should also be treated.Gonorrhea affects about 0.8% of women and 0.6% of men. An estimated 33 to 106 million new cases occur each year, out of the 498 million new cases of curable STI – which also includes syphilis, chlamydia, and trichomoniasis. Infections in women most commonly occur when they are young adults. In 2015, it caused about 700 deaths. Descriptions of the disease date back to before the Common Era within the Old Testament. The current name was first used by the Greek physician Galen before 200 AD who referred to it as "an unwanted discharge of semen".

Signs and symptoms
Gonorrhea infections of mucosal membranes can cause swelling, itching, pain, and the formation of pus. The time from exposure to symptoms is usually between two and 14 days, with most symptoms appearing between four and six days after infection, if they appear at all.  Both men and women with infections of the throat may experience a sore throat, though such infection does not produce symptoms in 90% of cases. Other symptoms may include swollen lymph nodes around the neck. Either sex can become infected in the eyes or rectum if these tissues are exposed to the bacterium.

Women
Half of women with gonorrhea are asymptomatic but the other half experience vaginal discharge, lower abdominal pain, or pain with sexual intercourse associated with inflammation of the uterine cervix. Common medical complications of untreated gonorrhea in women include pelvic inflammatory disease which can cause scars to the fallopian tubes and result in later ectopic pregnancy among those women who become pregnant.

Men
Most infected men with symptoms have inflammation of the penile urethra associated with a burning sensation during urination and discharge from the penis. In men, discharge with or without burning occurs in half of all cases and is the most common symptom of the infection. This pain is caused by a narrowing and stiffening of the urethral lumen. The most common medical complication of gonorrhea in men is inflammation of the epididymis. Gonorrhea is also associated with increased risk of prostate cancer.

Infants
If not treated, gonococcal ophthalmia neonatorum will develop in 28% of infants born to women with gonorrhea.

Spread
If left untreated, gonorrhea can spread from the original site of infection and infect and damage the joints, skin, and other organs. Indications of this can include fever, skin rashes, sores, and joint pain and swelling. In advanced cases, gonorrhea may cause a general feeling of tiredness similar to other infections. It is also possible for an individual to have an allergic reaction to the bacteria, in which case any appearing symptoms will be greatly intensified. Very rarely it may settle in the heart, causing endocarditis, or in the spinal column, causing meningitis. Both are more likely among individuals with suppressed immune systems, however.

Cause
Gonorrhea is caused by the bacterium Neisseria gonorrhoeae. Previous infection does not confer immunity – a person who has been infected can become infected again by exposure to someone who is infected. Infected persons may be able to infect others repeatedly without having any signs or symptoms of their own.

Spread
The infection is usually spread from one person to another through vaginal, oral, or anal sex. Men have a 20% risk of getting the infection from a single act of vaginal intercourse with an infected woman. The risk for men who have sex with men (MSM) is higher. Insertive MSM may get a penile infection from anal intercourse, while receptive MSM may get anorectal gonorrhea. Women have a 60–80% risk of getting the infection from a single act of vaginal intercourse with an infected man.A mother may transmit gonorrhea to her newborn during childbirth; when affecting the infants eyes, it is referred to as ophthalmia neonatorum. It may be able to spread through the objects contaminated with body fluid from an infected person. The bacteria typically does not survive long outside the body, typically dying within minutes to hours.

Risk factors
It is discovered that sexually active women younger than 25 and men who have sex with men are at increased risk of getting gonorrhea.Other risk factors include:

Having a new sex partner
Having a sex partner who has other partners
Having more than one sex partner
Having had gonorrhea or another sexually transmitted infection

Complications
Medically it has been said that Untreated gonorrhea can lead to major complications, such as:

Infertility in women. Gonorrhea can spread into the uterus and fallopian tubes, causing pelvic inflammatory disease (PID). PID can result in scarring of the tubes, greater risk of pregnancy complications and infertility. PID requires immediate treatment.
Infertility in men. Gonorrhea can cause a small, coiled tube in the rear portion of the testicles where the sperm ducts are located (epididymis) to become inflamed (epididymitis). Untreated epididymitis can lead to infertility.
Infection that spreads to the joints and other areas of the body. The bacterium that causes gonorrhea can spread through the bloodstream and infect other parts of the body, including the joints. Fever, rash, skin sores, joint pain, swelling and stiffness are possible results.
Increased risk of HIV/AIDS. Having gonorrhea increases the susceptibility to infection with human immunodeficiency virus (HIV), the virus that leads to AIDS. People who have both gonorrhea and HIV (untreated by anti-retroviral therapy) are able to pass both diseases more readily to their partners.
Complications in babies. Babies who contract gonorrhea from their mothers during birth can develop blindness, sores on the scalp and infections.

Diagnosis
Traditionally, gonorrhea was diagnosed with Gram stain and culture; however, newer polymerase chain reaction (PCR)-based testing methods are becoming more common. In those failing initial treatment, culture should be done to determine sensitivity to antibiotics.Tests that use PCR (aka nucleic acid amplification) to identify genes unique to N. gonorrhoeae are recommended for screening and diagnosis of gonorrhea infection. These PCR-based tests require a sample of urine, urethral swabs, or cervical/vaginal swabs. Culture (growing colonies of bacteria in order to isolate and identify them) and Gram-stain (staining of bacterial cell walls to reveal morphology) can also be used to detect the presence of N. gonorrhoeae in all specimen types except urine.If Gram-negative, oxidase-positive diplococci are visualized on direct Gram stain of urethral pus (male genital infection), no further testing is needed to establish the diagnosis of gonorrhea infection. However, in the case of female infection direct Gram stain of cervical swabs is not useful because the N. gonorrhoeae organisms are less concentrated in these samples. The chances of false positives are increased as Gram-negative diplococci native to the normal vaginal flora cannot be distinguished from N. gonorrhoeae. Thus, cervical swabs must be cultured under the conditions described above. If oxidase positive, Gram-negative diplococci are isolated from a culture of a cervical/vaginal swab specimen, then the diagnosis is made. Culture is especially useful for diagnosis of infections of the throat, rectum, eyes, blood, or joints—areas where PCR-based tests are not well established in all labs. Culture is also useful for antimicrobial sensitivity testing, treatment failure, and epidemiological purposes (outbreaks, surveillance).In patients who may have disseminated gonococcal infection (DGI), all possible mucosal sites should be cultured (e.g., pharynx, cervix, urethra, rectum). Three sets of blood cultures should also be obtained. Synovial fluid should be collected in cases of septic arthritis.All people testing positive for gonorrhea should be tested for other sexually transmitted diseases such as chlamydia, syphilis, and human immunodeficiency virus. Studies have found co-infection with chlamydia ranging from 46 to 54% in young people with gonorrhea. Among persons in the United States between 14 and 39 years of age, 46% of people with gonorrheal infection also have chlamydial infection. For this reason, gonorrhea and chlamydia testing are often combined. People diagnosed with gonorrhea infection have a fivefold increase risk of HIV transmission. Additionally, infected persons who are HIV positive are more likely to shed and transmit HIV to uninfected partners during an episode of gonorrhea.

Screening
The United States Preventive Services Task Force (USPSTF) recommends screening for gonorrhea in women at increased risk of infection, which includes all sexually active women younger than 25 years. Extragenital gonorrhea and chlamydia are highest in men who have sex with men (MSM). Additionally, the USPSTF also recommends routine screening in people who have previously tested positive for gonorrhea or have multiple sexual partners and individuals who use condoms inconsistently, provide sexual favors for money, or have sex while under the influence of alcohol or drugs.Screening for gonorrhea in women who are (or intend to become) pregnant, and who are found to be at high risk for sexually transmitted diseases, is recommended as part of prenatal care in the United States.

Prevention
As with most sexually transmitted diseases, the risk of infection can be reduced significantly by the correct use of condoms, not having sex, or can be removed almost entirely by limiting sexual activities to a mutually monogamous relationship with an uninfected person.Those previously infected are encouraged to return for follow up care to make sure that the infection has been eliminated. In addition to the use of phone contact, the use of email and text messaging have been found to improve the re-testing for infection.Newborn babies coming through the birth canal are given erythromycin ointment in the eyes to prevent blindness from infection. The underlying gonorrhea should be treated; if this is done then usually a good prognosis will follow.

Treatment
Antibiotics
Antibiotics are used to treat gonorrhea infections. As of 2016, both ceftriaxone by injection and azithromycin by mouth are most effective. However, due to increasing rates of antibiotic resistance, local susceptibility patterns must be taken into account when deciding on treatment. Ertapenem is a potential effective alternative treatment for ceftriaxone-resistant gonorrhea.Adults may have eyes infected with gonorrhoea and require proper personal hygiene and medications. Addition of topical antibiotics have not been shown to improve cure rates compared to oral antibiotics alone in treatment of eye infected gonorrhea. For newborns, erythromycin ointment is recommended as a preventative measure for gonococcal infant conjunctivitis.Infections of the throat can be especially problematic, as antibiotics have difficulty becoming sufficiently concentrated there to destroy the bacteria. This is amplified by the fact that pharyngeal gonorrhoea is mostly asymptomatic, and gonococci and commensal Neisseria species can coexist for long time periods in the pharynx and share anti-microbial resistance genes. Accordingly, an enhanced focus on early detection (i.e., screening of high-risk populations, such as men who have sex with men, PCR testing should be considered) and appropriate treatment of pharyngeal gonorrhoea is important.

Sexual partners
It is recommended that sexual partners be tested and potentially treated. One option for treating sexual partners of people infected is patient-delivered partner therapy (PDPT), which involves providing prescriptions or medications to the person to take to his/her partner without the health care providers first examining him/her.The United States Centers for Disease Control and Prevention (CDC) currently recommend that individuals who have been diagnosed and treated for gonorrhea avoid sexual contact with others until at least one week past the final day of treatment in order to prevent the spread of the bacterium.

Antibiotic resistance
Many antibiotics that were once effective including penicillin, tetracycline, and fluoroquinolones are no longer recommended because of high rates of resistance. Resistance to cefixime has reached a level such that it is no longer recommended as a first-line agent in the United States, and if it is used a person should be tested again after a week to determine whether the infection still persists. Public health officials are concerned that an emerging pattern of resistance may predict a global epidemic. In 2016, the WHO published new guidelines for treatment, stating "There is an urgent need to update treatment recommendations for gonococcal infections to respond to changing antimicrobial resistance (AMR) patterns of N. gonorrhoeae. High-level resistance to previously recommended quinolones is widespread and decreased susceptibility to the extended-spectrum (third-generation) cephalosporins, another recommended first-line treatment in the 2003 guidelines, is increasing and several countries have reported treatment failures."

Prognosis
Gonorrhea if left untreated may last for weeks or months with higher risks of complications. One of the complications of gonorrhea is systemic dissemination resulting in skin pustules or petechia, septic arthritis, meningitis, or endocarditis. This occurs in between 0.6 and 3% of infected women and 0.4 and 0.7% of infected men.In men, inflammation of the epididymis, prostate gland, and urethra can result from untreated gonorrhea. In women, the most common result of untreated gonorrhea is pelvic inflammatory disease. Other complications include inflammation of the tissue surrounding the liver, a rare complication associated with Fitz-Hugh–Curtis syndrome; septic arthritis in the fingers, wrists, toes, and ankles; septic abortion; chorioamnionitis during pregnancy; neonatal or adult blindness from conjunctivitis; and infertility. Men who have had a gonorrhea infection have an increased risk of getting prostate cancer.

Epidemiology
About 88 million cases of gonorrhea occur each year, out of the 448 million new cases of curable STI each year – that also includes syphilis, chlamydia and trichomoniasis. The prevalence was highest in the African region, the Americas, and Western Pacific, and lowest in Europe. In 2013, it caused about 3,200 deaths, up from 2,300 in 1990.In the United Kingdom, 196 per 100,000 males 20 to 24 years old and 133 per 100,000 females 16 to 19 years old were diagnosed in 2005. In 2013, the CDC estimated that more than 820,000 people in the United States get a new gonorrheal infection each year. Fewer than half of these infections are reported to CDC. In 2011, 321,849 cases of gonorrhea were reported to the CDC. After the implementation of a national gonorrhea control program in the mid-1970s, the national gonorrhea rate declined from 1975 to 1997. After a small increase in 1998, the gonorrhea rate has decreased slightly since 1999. In 2004, the rate of reported gonorrheal infections was 113. 5 per 100,000 persons.In the US, it is the second-most-common bacterial sexually transmitted infections; chlamydia remains first. According to the CDC African Americans are most affected by gonorrhea, accounting for 69% of all gonorrhea cases in 2010.The World Health Organization warned in 2017 of the spread of untreatable strains of gonorrhea, following analysis of at least three cases in Japan, France and Spain, which survived all antibiotic treatment.

History
Some scholars translate the biblical terms zav (for a male) and zavah (for a female) as gonorrhea.It has been suggested that mercury was used as a treatment for gonorrhea. Surgeons tools on board the recovered English warship the Mary Rose included a syringe that, according to some, was used to inject the mercury via the urinary meatus into crewmen with gonorrhea. The name "the clap", in reference to the disease, is recorded as early as the sixteenth century, referring to a medieval red-light district in Paris, Les Clapiers. Translating to "The rabbit holes", it was so named for the small huts in which prostitutes worked.In 1854, Dr. Wilhelm Gollmann addressed gonorrhea in his book, Homeopathic Guide to all Diseases Urinary and Sexual Organs. He noted that the disease was common in prostitutes and homosexuals in large cities. Gollmann recommended the following as cures: aconite to cure "shooting pains with soreness and inflammation;" mercury "for stitching pain with purulent discharge;" nux vomica and sulphur "when the symptoms are complicated with hemorrhoids and stricture of the rectum. Other remedies include argentum, aurum (gold), belladonna, calcarea, ignatia, phosphorus, and sepia.Silver nitrate was one of the widely used drugs in the 19th century. However, it became replaced by Protargol. Arthur Eichengrün invented this type of colloidal silver, which was marketed by Bayer from 1897 onward. The silver-based treatment was used until the first antibiotics came into use in the 1940s.The exact time of onset of gonorrhea as prevalent disease or epidemic cannot be accurately determined from the historical record. One of the first reliable notations occurs in the Acts of the (English) Parliament. In 1161, this body passed a law to reduce the spread of "... the perilous infirmity of burning". The symptoms described are consistent with, but not diagnostic of, gonorrhea. A similar decree was passed by Louis IX in France in 1256, replacing regulation with banishment. Similar symptoms were noted at the siege of Acre by Crusaders.
Coincidental to, or dependent on, the appearance of a gonorrhea epidemic, several changes occurred in European medieval society </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Wolff–Parkinson–White syndrome and can you explain it in depth? [/INST] Wolff–Parkinson–White syndrome (WPWS) is a disorder due to a specific type of problem with the electrical system of the heart. About 60% of people with the electrical problem developed symptoms, which may include an abnormally fast heartbeat, palpitations, shortness of breath, lightheadedness, or syncope. Rarely, cardiac arrest may occur. The most common type of irregular heartbeat that occurs is known as paroxysmal supraventricular tachycardia.The cause of WPW is typically unknown and is likely due to a combination of chance and genetic factors. A small number of cases are due to a mutation of the PRKAG2 gene which may be inherited from a persons parents in an autosomal dominant fashion. The underlying mechanism involves an accessory electrical conduction pathway between the atria and the ventricles. It is associated with other conditions such as Ebstein anomaly and hypokalemic periodic paralysis. The diagnosis of WPW occurs with a combination of palpitations and when an electrocardiogram (ECG) show a short PR interval and a delta wave. It is a type of pre-excitation syndrome.WPW syndrome may be monitored or treated with either medications or an ablation (destroying the tissues) such as with radiofrequency catheter ablation. It affects between 0.1 and 0.3% in the population. The risk of death in those without symptoms is about 0.5% per year in children and 0.1% per year in adults. In some cases, non-invasive monitoring may help to more carefully risk stratify patients into a lower risk category.  In those without symptoms ongoing observation may be reasonable.  In those with WPW complicated by atrial fibrillation, cardioversion or the medication procainamide may be used. The condition is named after Louis Wolff, John Parkinson, and Paul Dudley White who described the ECG findings in 1930.

Signs and symptoms
People with WPW are usually asymptomatic when not having a fast heart rate.  However, individuals may experience palpitations, dizziness, shortness of breath, or infrequently syncope (fainting or near fainting) during episodes of supraventricular tachycardia.  WPW is also associated with a very small risk of sudden death due to more dangerous heart rhythm disturbances.

Pathophysiology
Electrical activity in the normal human heart begins when a cardiac action potential arises in the sinoatrial (SA) node, which is located in the right atrium. From there, the electrical stimulus is transmitted via internodal pathways to the atrioventricular (AV) node. After a brief delay at the AV node, the stimulus travels through the bundle of His to the left and right bundle branches and then to the Purkinje fibers and the endocardium at the apex of the heart, then finally to the ventricular myocardium.The AV node serves an important function as a "gatekeeper", limiting the electrical activity that reaches the ventricles. In situations where the atria generate excessively rapid electrical activity (such as atrial fibrillation or atrial flutter), the AV node limits the number of signals conducted to the ventricles. For example, if the atria are electrically activated at 300 beats per minute, half those electrical impulses may be blocked by the AV node, so that the ventricles are stimulated at only 150 beats per minute – resulting in a pulse of 150 beats per minute. Another important property of the AV node is that it slows down individual electrical impulses. This is manifested on the electrocardiogram as the PR interval (the time from electrical activation of the atria to electrical activation of the ventricles), which is usually shortened to less than 120 milliseconds in duration.Individuals with WPW have an accessory pathway that communicates between the atria and the ventricles, in addition to the AV node. This accessory pathway is known as the bundle of Kent. This accessory pathway does not share the rate-slowing properties of the AV node and may conduct electrical activity at a significantly higher rate than the AV node. For instance, in the example above, if an individual had an atrial rate of 300 beats per minute, the accessory bundle may conduct all the electrical impulses from the atria to the ventricles, causing the ventricles to contract at 300 beats per minute. Extremely rapid heart rates such as this may result in hemodynamic instability or cardiogenic shock. In some cases, the combination of an accessory pathway and abnormal heart rhythms can trigger ventricular fibrillation, a leading cause of sudden cardiac death.WPW may be associated with PRKAG2, a protein kinase enzyme encoded by the PRKAG2 gene.

Bundle of Kent
The bundle of Kent is an abnormal extra or accessory conduction pathway between the atria and ventricles that is present in a small percentage (between 0.1 and 0.3%) of the general population. This pathway may communicate between the left atrium and the left ventricle, in which case it is termed a "type A pre-excitation", or between the right atrium and the right ventricle, in which case it is termed a "type B pre-excitation" in old, currently abandoned classification. Problems arise when this pathway creates an electrical circuit that bypasses the AV node. The AV node is capable of slowing the rate of conduction of electrical impulses to the ventricles, whereas the bundle of Kent lacks this capability. When an aberrant electrical connection is made via the bundle of Kent, tachydysrhythmias may therefore result.

Diagnosis
WPW is commonly diagnosed on the basis of the electrocardiogram in an asymptomatic individual. In this case, it is manifested as a delta wave, which is a slurred upstroke in the QRS complex that is associated with a short PR interval. The short PR interval and slurring of the QRS complex are reflective of the impulse making it to the ventricles early (via the accessory pathway) without the usual delay experienced in the AV node.If a person with WPW experiences episodes of atrial fibrillation, the ECG shows a rapid polymorphic wide-complex tachycardia (without torsades de pointes). This combination of atrial fibrillation and WPW is considered dangerous, and most antiarrhythmic drugs are contraindicated.When an individual is in normal sinus rhythm, the ECG characteristics of WPW are a short PR interval (less than 120 milliseconds in duration), widened QRS complex (greater than 120 milliseconds in duration) with slurred upstroke of the QRS complex, and secondary repolarization changes (reflected in ST segment-T wave changes).In individuals with WPW, electrical activity that is initiated in the SA node travels through the accessory pathway, as well as through the AV node to activate the ventricles via both pathways. Since the accessory pathway does not have the impulse slowing properties of the AV node, the electrical impulse first activates the ventricles via the accessory pathway, and immediately afterwards via the AV node. This gives the short PR interval and slurred upstroke of the QRS complex known as the delta wave.In case of type A pre-excitation (left atrioventricular connections), a positive R wave is seen in V1 ("positive delta") on the precordial leads of the electrocardiogram, while in type B pre-excitation (right atrioventricular connections), a predominantly negative delta wave is seen in lead V1 ("negative delta").People with WPW may have more than one accessory pathway – in some cases, as many as eight abnormal pathways have been found. This has been seen in individuals with Ebsteins anomaly.Wolff–Parkinson–White syndrome is sometimes associated with Lebers hereditary optic neuropathy, a form of mitochondrial disease.

Risk stratification
WPW carries a small risk of sudden death, presumably due to rapidly conducted atrial fibrillation causing ventricular fibrillation.  While the overall risk is approximately 2.4 per 1000 person years, the risk in an individual is dependent on the properties of the accessory pathway causing pre-excitation.A higher risk accessory pathway may be suggested by a history of syncope, but risk stratification is best performed by assessing how frequently a pathway can conduct impulse to the ventricles, usually via programmed electrical stimulation (PES) in the cardiac electrophysiology laboratory. This is an invasive but generally low-risk procedure during which the atria are stimulated to try to induce tachycardia. If a tachycardia involving the accessory pathway can be triggered, the cardiologist can then assess how rapidly the accessory pathway is able to conduct. The faster it can conduct, the higher the likelihood the accessory pathway can conduct fast enough to trigger a lethal tachycardia.High-risk features that may be present during PES include an effective refractory period of the accessory pathway less than 250 ms, multiple pathways, septal location of pathway, and inducibility of supraventricular tachycardia (AVRT, atrial fibrillation). Individuals with any of these high-risk features are generally considered at increased risk for SCD or symptomatic tachycardia, and should be treated accordingly (i.e.: catheter ablation).It is unclear whether invasive risk stratification (with PES) is necessary in the asymptomatic individual. While some groups advocate PES for risk stratification in all individuals under 35 years old, others only offer it to individuals who have history suggestive of a tachydysrhythmia, since the incidence of sudden cardiac death is so low (less than 0.6% in some reports).Other methods of risk stratification include observing the ventricular rate during spontaneous atrial fibrillation on a 12-lead ECG.  RR intervals of less than 250 ms suggest a higher risk pathway.  During exercise testing, abrupt loss of pre-excitation as heart rate increases also suggest a lower risk pathway. However, this approach is hampered by the normal improvement in AV node conduction during exercise which can also mask pre-excitation despite ongoing conduction down the accessory pathway.

Treatment
According to the ACLS protocol, people with WPW who are experiencing rapid abnormal heart rhythms (tachydysrhythmias) may require synchronized electrical cardioversion if they are demonstrating severe signs or symptoms (for example, low blood pressure or lethargy with altered mental status). If they are relatively stable, medication may be used.

Medications
WPW pattern with hemodynamically stability and orthodromic AVRT leading to a regular narrow complex tachycardia may be managed similarly to other regular narrow complex supraventricular tachycardias: first with vagal maneuvers followed by a trial of adenosine (first-line therapy). The 2015 ACC/AHA/HRS guidelines recommend beta-blockers or calcium channel blockers as second-line agents, electric cardioversion is reserved for refractory arrhythmias. However, if there is any doubt about the diagnosis of orthodromic AVRT or if aberrant conduction leading to a wide complex QRS is observed, it may be prudent to manage as undifferentiated wide complex tachycardia. People with atrial fibrillation and rapid ventricular response may be treated with amiodarone or procainamide to stabilize their heart rate. Procainamide and cardioversion are accepted treatments for conversion of tachycardia found with WPW. Amiodarone in atrial fibrillation with WPW, is linked to ventricular fibrillation, and thus may be worse than procainamide.AV node blockers should be avoided in atrial fibrillation and atrial flutter with WPW or history of it; this includes adenosine, diltiazem, verapamil, other calcium channel blockers, and beta blockers </s>


<s> [INST] <<SYS>> You are a responsible assistant committed to providing accurate and helpful responses. Avoid sharing harmful or biased content. Clarify any unclear or incorrect questions rather than providing false or misleading information. <</SYS>> What is Ventricular septal defect and can you explain it in depth? [/INST] A ventricular septal defect (VSD) is a defect in the ventricular septum, the wall dividing the left and right ventricles of the heart. The extent of the opening may vary from pin size to complete absence of the ventricular septum, creating one common ventricle. The ventricular septum consists of an inferior muscular and superior membranous portion and is extensively innervated with conducting cardiomyocytes.
The membranous portion, which is close to the atrioventricular node, is most commonly affected in adults and older children in the United States. It is also the type that will most commonly require surgical intervention, comprising over 80% of cases.Membranous ventricular septal defects are more common than muscular ventricular septal defects, and are the most common congenital cardiac anomaly.

Signs and symptoms
Ventricular septal defect is usually symptomless at birth. It usually manifests a few weeks after birth.VSD is an acyanotic congenital heart defect, aka a left-to-right shunt, so there are no signs of cyanosis in the early stage. However, uncorrected VSD can increase pulmonary resistance leading to the reversal of the shunt and corresponding cyanosis.
Pansystolic (Holosystolic) murmur along lower left sternal border (depending upon the size of the defect) +/- palpable thrill (palpable turbulence of blood flow). Heart sounds are normal. Larger VSDs may cause a parasternal heave, a displaced apex beat (the palpable heartbeat moves laterally over time, as the heart enlarges). An infant with a large VSD will fail to thrive and become sweaty and tachypnoeic (breathe faster) with feeds.The restrictive ventricular septal defects (smaller defects) are associated with a louder murmur and more palpable thrill (grade IV murmur). Larger defects may eventually be associated with pulmonary hypertension due to the increased blood flow. Over time this may lead to an Eisenmengers syndrome the original VSD operating with a left-to-right shunt, now becomes a right-to-left shunt because of the increased pressures in the pulmonary vascular bed.

Cause
Congenital VSDs are frequently associated with other congenital conditions, such as Down syndrome.A VSD can also form a few days after a myocardial infarction (heart attack) due to mechanical tearing of the septal wall, before scar tissue forms, when macrophages start remodeling the dead heart tissue.
A congenital VSD can result from a disturbance in the morphogenesis of the heart in its embryonic stages. In the fifth week of gestation, the heart undergoes multiple processes of septation and forming a dextral loop. Interfering with the latter leads to insufficient leftward movement of the ventricular outflow tract over the atrioventricular canal, which in turn can result in a VSD or, in the most extreme cases, a double outlet right ventricle with one.A ventricular septal defect arises when the superior part of the interventricular septum, which separates the right and left ventricles of the heart, fails to fully develop. The right ventricle pumps blood to the lungs to get oxygen, while the left ventricle pumps blood to the rest of the body to provide oxygen to tissues. A ventricular septal defect results in the mixing of oxygen-rich blood with oxygen-poor blood, increasing strain on the heart and lungs.

Pathophysiology
During ventricular contraction, or systole, some of the blood from the left ventricle leaks into the right ventricle, passes through the lungs and reenters the left ventricle via the pulmonary veins and left atrium.  This has two net effects.  First, the circuitous refluxing of blood causes volume overload on the left ventricle.  Second, because the left ventricle normally has a much higher systolic pressure (~120 mmHg) than the right ventricle (~20 mmHg), the leakage of blood into the right ventricle therefore elevates right ventricular pressure and volume, causing pulmonary hypertension with its associated symptoms.
In serious cases, the pulmonary arterial pressure can reach levels that equal the systemic pressure. This reverses the left to right shunt, so that blood then flows from the right ventricle into the left ventricle, resulting in cyanosis, as blood is by-passing the lungs for oxygenation.This effect is more noticeable in patients with larger defects, who may present with breathlessness, poor feeding and failure to thrive in infancy. Patients with smaller defects may be asymptomatic. Four different septal defects exist, with perimembranous most common, outlet, atrioventricular, and muscular less commonly.

Diagnosis
A VSD can be detected by cardiac auscultation.  Classically, a VSD causes a pathognomonic holo- or pansystolic murmur.  Auscultation is generally considered sufficient for detecting a significant VSD. The murmur depends on the abnormal flow of blood from the left ventricle, through the VSD, to the right ventricle.  If there is not much difference in pressure between the left and right ventricles, then the flow of blood through the VSD will not be very great and the VSD may be silent.  This situation occurs a) in the fetus (when the right and left ventricular pressures are essentially equal), b) for a short time after birth (before the right ventricular pressure has decreased), and c) as a late complication of unrepaired VSD.  Confirmation of cardiac auscultation can be obtained by non-invasive cardiac ultrasound (echocardiography).  To more accurately measure ventricular pressures, cardiac catheterization, can be performed.

Classification
Although there are several classifications for VSD, the most accepted and unified classification is that of Congenital Heart Surgery Nomenclature and Database Project.
The classification is based on the location of the VSD on the right ventricular surface of the inter ventricular septum and is as follows:

Multiple
Type 1
Type 1 is sub aortic

Type 2
Type 2 also known as perimembranous, paramembranous, conoventricular, membranous septal defect, and subaortic.
Most common variety found in 70%

Type 3
Type 3 also known as inlet (or AV canal type).

Commonly associated with atrioventricular septal defect, found in about 5%

Type 4
Type 4 also known as muscular (trabecular)

Located in the muscular septum, found in 20%. Can be sub classified again based on the location into anterior, apical, posterior and mid

Type: Gerbode
Type: Gerbode also known as left ventricular to right atrial communication

Due to absence of Atrioventricular septum.

Treatment
Most cases do not need treatment and heal during the first years of life. Treatment is either conservative or surgical.  Smaller congenital VSDs often close on their own, as the heart grows, and in such cases may be treated conservatively.
Some cases may necessitate surgical intervention, i.e. with the following indications:

Failure of congestive cardiac failure to respond to medications
VSD with pulmonic stenosis
Large VSD with pulmonary hypertension
VSD with aortic regurgitationFor the surgical procedure, a heart-lung machine is required and a median sternotomy is performed.  Percutaneous endovascular procedures are less invasive and can be done on a beating heart, but are only suitable for certain patients.  Repair of most VSDs is complicated by the fact that the conducting system of the heart is in the immediate vicinity.
Ventricular septum defect in infants is initially treated medically with cardiac glycosides (e.g., digoxin 10-20 μg/kg per day), loop diuretics (e.g., furosemide 1–3 mg/kg per day) and ACE inhibitors (e.g., captopril 0.5–2 mg/kg per day).

Transcatheter closure
A device, known as the Amplatzer muscular VSD occluder, may be used to close certain VSDs. It was initially approved in 2009. It appears to work well and be safe. The cost is also lower than having open heart surgery. The device is placed through a small incision in the groin.The Amplatzer septal occluder was shown to have full closure of the ventricular defect within the 24 hours of placement.  It has a low risk of embolism after implantation.  Some tricuspid valve regurgitation was shown after the procedure that could possibly be due from the right ventricular disc.  There have been some reports that the Amplatzer septal occluder may cause life-threatening erosion of the tissue inside the heart. This occurs in one percent of people implanted with the device and requires immediate open-heart surgery.  This erosion occurs due to improper sizing of the device resulting with it being too large for the defect, causing rubbing of the septal tissue and erosion.

Surgery
Surgical closure of a Perimembranous VSD is performed on cardiopulmonary bypass with ischemic arrest </s>