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Glycopyrrolate, sold under the name Cuvposa, is an inhibitor of cholinergic muscarinic receptors used in various medical settings. Muscarinic receptors are metabotropic acetylcholine receptors found in target tissues and glands regulated by our parasympathetic nervous system—which ultimately regulate our "rest and digest" responses. This drug is commonly used to inhibit salivary and respiratory secretions and prevent reflex bradycardia during surgical procedures. The primary mechanism of action of this drug is the blockage of acetylcholine's effects at the parasympathetic sites in various tissues—including the central nervous system, smooth muscle, and secretory glands. It may be administered intravenously, intramuscularly, orally, topically, or by inhalation. The specific effects are dependent on the administration route (for example, topically for sweat glands vs more systemic if via IV). This links to the current course content as it is used to slow down the parasympathetic nervous system by limiting ACh-dependent responses. Thus, this drug blocks drooling—common response of the parasympathetic NS—by inhibiting the synaptic response between the postganglionic neuron and the target cell(s).

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Movement control is one of the main losses when someone is diagnosed with Parkinson's Disease. This is a neurodegenerative disease that worsens overtime and often contribute to loss of function in the nervous system. Parkinson's is a degeneration of neurons responsible for producing dopamine in the brain. Dopamine is a neurotransmitter that helps with muscle control and movements. Patients who have Parkinson's on a physiological level tend to have an imbalance in their motor areas due to lack of dopamine. This causes tremors, slower movements (bradykinesia) and/or increased muscle stiffness. A person can also experience mood changes, cognitive issues and sleep irregularities on top of motor impairments. This disease relates to our class content because we discussed the process of muscle contractions and how the muscle goes from a contracted state to a relaxed state. Muscle stiffness is a side effect of Parkinson's which means that the muscles remain in a "partially contracted state" which lowers the muscles ability to have smooth movements. Excitatory signals are constantly firing which leads to higher calcium ion levels and more interaction between the myosin and actin.

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Dexmedetomidine is a medication used to sedate patients and manage pain during surgery and certain medical procedures. It works by crossing the blood-brain barrier and binding to alpha-2 adrenergic receptors in the brainstem's preganglionic sympathetic neurons, creating a negative feedback loop by hyperpolarizing the axon terminal and modulating acetylcholine release in a region responsible for wakefulness and arousal. Activation of these receptors inhibits norepinephrine release, leading to reduced sympathetic nervous system activity. As a result, patients experience sedation, analgesia, lower heart rate, and decreased blood pressure.

This drug relates to the course because it directly suppresses the sympathetic nervous system activity by reducing norepinephrine release in the CNS. This causes the parasympathetic nervous system to be in more control, counteracting the normal fight-or-flight response.

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Chronic stress is an extended and constant feeling of pressure or tension that continues over a long period of time. Chronic stress results from an ongoing situation or circumstances, such as high work or school related demands, relationship problems, financial struggles, or health issues. This constant state of stress can wear down the body and mind, affecting both physical and mental health. From the physical aspect, you can find yourself struggling to do a daily task regardless of how big or small it may be. You may experience constant fatigue, muscle tension, heart rate increase and sleep issues. When you're stressed, your body activates the "fight or flight" response which is triggered by the synaptic nervous system. Your body is constantly releasing adrenaline and cortisol hormones which leads to rapid heart rate and high blood pressure. Your heart rate stays higher than it should, never allowing you to reach homeostasis. These hormones also suppress the immune & digestive system’s functioning. Your immune responses are weakened which make the body more susceptible to infections and illnesses. Your digestive systems are much more uncontrolled which can lead to weight gain and lost, as well as indigestion, and irritable bowel syndrome.

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Acebutolol is a medication used to treat high blood pressure. The brand name of Acebutolol in the United States is Sectral. The drug acts as a β1 receptor antagonist. By looking slightly ahead in the lecture slides, I found that  β1 receptors are a part of the sympathetic nervous system. They are found in cardiac muscle and the kidneys. This receptor is largely in charge of increasing heart rate as well as the force of contraction in the heart.  β1 receptors are activated by epinephrine which increases blood pressure and heart rate. As a  β1 receptor antagonist, acebutolol blocks these receptors which stops epinephrine from docking, increasing heart rate and blood pressure. This relates to this course as we are learning about the autonomic nervous system. The sympathetic nervous system which is home to  β1 receptors is a part of the autonomic nervous system. This is the “fight or flight” system which causes many responses in the human body such as an increase in heart rate.

Acebutolol. [accessed 2025 Mar 2]. https://go.drugbank.com/drugs/DB01193.

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Pheochromocytomas are a rare form of tumor that are located within the adrenal medulla (the inner portion) of the adrenal gland. Most pheochromocytomas are benign, however some can be malignant, and while typically located within one adrenal gland, they can be in both. The cells responsible for these tumors are chromaffin cells, which release the hormones adrenaline and noradrenaline. The population most susceptible to developing pheochromocytomas are those between the ages of 30 and 50.  Since these tumors can often go undiagnosed, there are not always “normal” symptoms, however the symptoms that people may have with this tumor are: high blood pressure, an irregular heartbeat, excessive sweating, and headaches. To be diagnosed with a pheochromocytoma one will have to undergo lab testing of their urine and blood as well as have some imaging done.

One form of treatment for these tumors is use of medications such as alpha or beta blockers. This relates to content from the course because each of these drugs work to inhibit the actions and properties of noradrenaline, associated with the sympathetic nervous system, thus allowing for the parasympathetic system to have more control over an individual's blood pressure and regular heart rate and preventing irregular activity.

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Multiple System Atrophy, a rare disease that is neurodegenerative(progresses through life with the death of nerve cells) affects the body’s ability to control automatic functions. For example things like breathing, pumping blood through the heart, and digestion are not efficient, or possible, like they usually are due to damage to the autonomic nervous system, specifically in the basal ganglia, brainstem, and cerebellum. The buildup of the α-synuclein protein causes said damage by killing important nerve cells that are crucial for movement. The protein accumulates abnormally within the glial cells in the brain, forming clumps called glial cytoplasmic inclusions which inhibit the normal function of these cells, leading to damage to the myelin sheath that insulates nerve fibers and ultimately causing neuron death. There is no cure for this and it often ends in fatality, but there are some medications and lifestyle changes that can improve the disease while the patient is alive. One example is Levodopa, a pill that works to travel into the brain and act as a replacement for dopamine, allowing the patient to function and helps to control the parts of the brain that have been compromised.

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Achalasia is a rare esophagus disorder where the lower esophageal sphincter (LES) cannot relax, preventing food and drinks from entering the stomach easily. This happens when the network of nerves in the digestive tract  (controls the movement of the intestines) degenerates, leading to the loss of inhibitory neurons that normally release nitric oxide (NO) and vasoactive intestinal peptide (VIP) to relax the LES. Without these signals, the LES remains overly contracted, and muscle contractions in the esophagus are damaged. Achalasia cannot be cured, however it can be managed with certain drugs and surgery.

Calcium channel blockers like nifedipine and diltiazem help manage achalasia by relaxing the LES. They do this by blocking L-type calcium channels in the smooth muscle, which prevents calcium from entering the cells. Since calcium is needed for muscle contraction, this helps reduce LES pressure, making it easier for food and liquids to pass into the stomach.

This disease connects to what we learned in class about how smooth muscle contraction depends on calcium entering through voltage-gated calcium channels, and the steps of proper muscle relaxation.

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Alacrima is a medical condition characterized by a deficiency or absence of tear production. Alacrima comes traditionally as a symptom of a larger disease. Patients with Alacrima can experience dry eyes, leading to corneal damage and discomfort. Alacrima will also lead to an increased risk of infection due to a lack of moisture.

Alacrima is caused by a dysfunction of the lacrimal glands. This dysfunction comes from the autonomic nervous system, which affects the parasympathetic pathways that stimulate tears. Alacrima is often synonymous with Achalasia-Alacrima-Adrenocorticotropic hormone [ACTH] Insensitivity Syndrome (Tripple A Syndrome) and Riley-Day Syndrome.

Relates to class and the autonomic nervous system because this shows a major deficiency in the PNS. The PNS is not able to send ACh to stimulate tear production. This could be because of nerve degeneration or incomplete innervation.

Treatment often consists of artificial tears, gels, and cyclosporine, which has been found to treat some autoimmune disorders.

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Hyperhidrosis is a condition that causes excessive sweating, or sweating more than normal. The body uses sweating as a negative feedback loop in the body in order to cool itself when the body’s temperature gets too hot. The mechanism of sweating is controlled by the sympathetic nervous system, which mobilizes the body in response to stressful situations. One of the responses of the sympathetic nervous system is producing sweat. People with hyperhidrosis have an oversensitive sympathetic nervous system, which causes the overproduction of sweat. There are two types of hyperhidrosis, primary hyperhidrosis which is genetically inherited, and secondary hyperhidrosis, which is caused by other conditions such as neurologic syndromes.

One medication that is used to treat hyperhidrosis is an oral medication called an ​​anticholinergics. Some examples of this medication are glycopyrrolate, oxybutynin, and benztropine. ​​Anticholinergics relate to this course because it is a competitive antagonist for acetylcholine that binds to M3 muscarinic receptors on eccrine sweat glands that are activated by the sympathetic nervous system and produce sweating. When ​​anticholinergics bind to the receptors, it prevents acetylcholine from binding, which inhibits sweat production.

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Duchenne Muscular Dystrophy (DMD) is a progressive neuromuscular disorder that causes severe muscle weakness and degeneration. It mainly affects boys because of a lack of dystrophin, a protein that helps keep muscle cells stable. Without dystrophin, muscle fibers break down more easily, leading to inflammation, scarring, and eventual muscle loss. Over time, this not only affects movement but also impacts the heart and breathing muscles, which are essential for survival. Aside from its effects on voluntary muscles, DMD also disrupts the autonomic nervous system (ANS), which controls things like heart rate, blood pressure, and breathing. People with DMD often have an imbalance between the sympathetic (fight-or-flight) and parasympathetic (rest-and-digest) nervous systems, particularly when it comes to heart function. Many individuals with DMD have higher resting heart rates and lower heart rate variability, showing that their sympathetic nervous system is overactive. This puts extra strain on the heart and can lead to dilated cardiomyopathy, where the heart becomes weaker and less efficient. Problems with blood vessel regulation can also reduce circulation, making it harder for muscles to get the oxygen and nutrients they need. On the other hand, the parasympathetic nervous system, which normally helps slow the heart rate and recover from stress, is weakened in DMD. This makes patients more prone to irregular heartbeats and reduces their ability to adjust their heart rate and blood pressure to different situations. The combination of an overactive sympathetic system and a weakened parasympathetic system leads to worsening heart problems over time. These autonomic issues also affect breathing, making it harder for patients to control their ventilation as their muscles weaken. DMD connects to ANS physiology because it highlights how important the balance between sympathetic and parasympathetic activity is for maintaining heart and vascular function.

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Guanfacine is a medication that treats high heart rate. Specifically, Guanfacine relaxes blood vessels and decreases heart rate, allowing blood to flow more easily through the body. Guanfacine functions by acting as a ligand for the alpha2 adrenergic receptor, thereby inhibiting the GPCR (G-protein coupling receptor) production of cAMP and norepinephrine release. GPCR receptors are ligand receptors with a seven transmembrane domain and heteromeric G-proteins consisting of three subunits, alpha, beta, and gamma, attached on the intracellular side. Similar to how Acetylcholine binds to the acetylcholine receptor, allowing the receptor to change its shape and function, Guanfacine binds to the alpha2 adrenergic receptor and changes its shape. However, there are many differences in the mechanisms of these reactions. When acetylcholine binds to the acetylcholine ionotropic ligand receptor, it opens the gates allowing Na+ to pass through into the sarcolemma. When guanfacine binds to the alpha2 adrenergic receptor, it stimulates the production of secondary messengers, which further down a pathway. Eventually, both the release of norepinephrine and cAMP-PKA (aka protein kinase A) activation is inhibited. Without PKA, proteins in heart muscles wont be phosphorylated to cause Ca+ influx and therefore a higher heart rate, AND norepinephrine wont be available to stimulate the sympathetic nervous system. Ultimately, the inhibition of cAMP and norepinephrine release stops the sympathetic nervous system from going crazy, and the medicine effectively decreases heart rate.

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Addison’s disease happens when the adrenal glands in our body don’t make enough cortisol and aldosterone which are two hormones that are important in maintain balance in our bodies. Cortisol helps the body handle stress and supports brain function, while aldosterone regulates salt and water levels, which affect blood pressure and muscle contractions.

When cortisol is too low, the nervous system is affected because cortisol helps regulate brain function. People with this disease may feel extreme fatigue, brain fog, and even dizziness because their nervous system isn’t getting the support it needs. Low aldosterone leads to an imbalance in sodium and potassium (which are key for nerve signaling and muscle contractions as we learned in the last unit). Without enough sodium, nerve signals slow down, leading to weakness, muscle cramps, or even severe cases of paralysis.

This connects to what we have learned about neurons and muscle function. The sodium-potassium pump is disrupted in Addison’s disease because of the loss of aldosterone. Without the right balance of these ions, nerves and muscles can’t work properly which is why patients experience weakness and fatigue.

People with Addison’s disease use hormone replacement therapy to restore cortisol and aldosterone levels, helping their nervous system and muscles function normally.

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Crisponi syndrome and cold-induced sweating syndrome (CISS) were originally thought to be two different diseases, but now recognized as the same disease at different stages in life. CISS presents itself in infancy through issues regulating body temperature, unusual facial features (small chin, low-set ears, flared nostrils, a wide space between the nose and mouth), and malformations in feet and hands. Infants with CISS begin to develop high fevers that could lead to seizures and death because of their inability to regulate body temperature. However, if a child survives infancy they are expected to have a normal lifespan but develop cold-induced sweating as they age. The cause behind CISS is due to a mutation in the CRFL1 gene, which produces proteins important for nerve cells that regulate the sweat glands. Before maturation, the sweat glands are innervated by noradrenergic neurons (meaning they use noradrenaline) and then they switch to cholinergic (acetylcholine-releasing) signaling. The signal which tells the neurons to change comes from the CRFL1 complex, and if these genes are mutated, the signal won’t happen and sweating will become an issue for those affected by this mutation.

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Tizanidine is a medication that acts as a muscle relaxant and works by targeting the central nervous system to reduce muscle spasms. It acts on alpha 2 receptors by binding to the receptor as an alpha 2 agonist and prevents the release of Norepinephrine at the axon terminal. The receptors are part of the sympathetic nervous system by regulating the " Flight or fight" response and also play a role in regulating muscle tone. When it inhibits norepinephrine to be released it allows a decrease in the output of the sympathetic neurons in the nervous system, which allows the stimulation of muscle contractions to be reduced. Tizanidine relates to the course material because it shows how drugs can treat conditions by altering the autonomic nervous system. It acts as an alpha 2 agonist, inhibiting the binding of norepinephrine, a drug that triggers the sympathetic nervous system, by binding to the alpha 2 receptor. This controls the sympathetic nervous system response and allows muscle relaxation to happen.

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Metoprolol is a beta-blocker commonly that is used to treat hypertension and other cardiovascular conditions. It selectively blocks beta-1 adrenergic receptors found in the heart. When someone is under normal conditions the activation of these receptors through epinephrine and norepinephrine increases heart rate and contractility leading to higher blood pressure. Metoprolol reduces heart rate by blocking these receptors and this decreases the force of contraction and lowers blood pressure. Metoprolol’s ability to regulate autonomic nervous system activity and maintain cardiovascular homeostasis makes it an important and necessary medication for patients with hypertension and heart disease.

This drug is directly related to class content because it affects the autonomic nervous system in the sympathetic division. The sympathetic nervous system is responsible for the "fight or flight" response which increases cardiovascular output when activated. By inhibiting beta-1 receptors, metoprolol counteracts any extra sympathetic stimulation. This prevents conditions such as hypertension, angina, and arrhythmias. Metoprolol also reduces myocardial oxygen demand, the hearts need for oxygen, by making it useful in managing chronic heart failure and post-myocardial infarction recovery. It slows the heart rate so doctors must be cautious when using it in patients with bradycardia or heart block.

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Tyrosine Hydroxylase Deficiency is a disorder where the body doesn’t produce enough of the enzyme Tyrosine Hydroxylase. This enzyme is vital for the production of Dopamine. This disorder relates to our course because we know how enzymes facilitate molecule interactions and speed up needed chemical reactions. As well, Dopamine is a neurotransmitter that allows it to send necessary signals to the body. It is essential for body movements to be smooth and controlled. Therefore, when there is a lack of dopamine, it can cause muscle stiffness and tremors. Since this disorder is caused by mutations in genes that cause the lack of enzymes, symptoms are found early into childhood. There are three levels of the disorder, depending on the severity. Mild THD is characterized by minor problems with walking, running, etc. Moderate THD also includes minor muscle spasms and abnormal eye movements. Severe forms of THD are apparent in the first six months of life. Children with the disorder meet important milestones like sitting up and walking much later than most. Even so, the disorder can cause severe issues with even learning those milestones.

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Horner's Syndrome is a disruption of innervation around the eye. Horner's Syndrome patients experience three primary symptoms: eyelid drooping, pupil constriction, and reduced perspiration in one side of the face. While this condition can in rare cases present congenitally, it is largely an acquired condition through other sympathetic nerve disruption. Reasons for this condition can be separated into three categories of location sympathetic nerve disruption. First order neurons are neurons within the brain and are disrupted by conditions like Encephalitis or Meningitis. Second order neurons are located around the thorax and are damaged by things like an aneurysm or lymph node enlargement. Third Order Neurons exist around the internal corticoid artery and are effected by things like Giant cell arteritis and cluster headaches. Sympathetic nerve supply to the superior tarsal muscle pulls your eyelid up. When your eye does not get the sympathetic nerve supply it needs to dilate your eyes, parasympathetic nerves are uncontrolled and constrict the pupil. Disruption of sympathetic nerve supply from first and second order neurons can reduce the amount of sweat on one side of the face. Horner's Syndrome demonstrates how the body can be affected when one of the core principles of physiology, cell to cell communication, is disrupted.

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Multiple System Atrophy – Cerebellar Type (MSA-C)

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Multiple System Atrophy – Cerebellar Type (MSA-C)

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Multiple System Atrophy – Cerebellar Type (MSA-C) targets the cerebellum and brainstem while also disrupting the autonomic nervous system which results in movement and balance difficulties as well as impaired regulation of automatic functions such as blood pressure. A buildup of the protein α-synuclein in oligodendrocytes triggers the breakdown of nerve cells. The resulting damage produces cerebellar atrophy which makes balance and coordination hard while also disrupting communication between brain regions by affecting the pons and inferior olives. The disease creates damage to preganglionic neurons which work in both sympathetic and parasympathetic nervous systems resulting in problems with blood pressure regulation as well as bladder control and other involuntary bodily functions. There is no cure available but dopaminergic drugs and autonomic symptom therapies help control certain effects. MSA-C demonstrates motor control and neurophysiology principles and explains autonomic regulation because it reveals cerebellar movement coordination coupled with nervous system management of involuntary functions.

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 Multiple System Atrophy – Cerebellar Type (MSA-C) 

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Midodrine is an oral drug prescribed to patients in order to treat low blood pressure, aka hypotension (<90/60mmHg), which is what causes dizziness and fainting due to the brain not receiving enough blood. Some common causes of hypotension include dehydration, heart conditions such as arrhythmia, or medications that block calcium channels or cause sodium loss. It has minimal activity in the CNS, since it does not cross the blood-brain barrier. The midodrine binds to and activates alpha 1A and 1B (cause muscle contraction and vasoconstriction) receptors to trigger peripheral arterial and venous constriction. This constriction of the veins and arteries increases resistance, which helps to elevate blood pressure without raising your heart rate. Midrodine relates to this course as its primary effects are geared towards stimulating alpha-1 adrenergic receptors found in the walls of your blood vessels in order to cause contraction. This stimulation of nerve endings and contraction of the blood vessels increases blood pressure.

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is this appropriate i don't even know what would be suitable here...

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Priapism is a physiological disorder in which the shaft of the penis remains rigid, but the glans is soft in the absence of sexual stimulation for an extended period of time. It is associated with blood disorders or side effects of various medications such as antidepressant or alpha blockers. Blood becomes trapped in the penis due to continued dilation of the arteries in the penis despite relaxation of the penile smooth muscles. Consequentially, blood cannot drain and fully relax the penis. Looking deeper this is often caused from an excess of neurotransmitters (nitric oxide) between the synapses not being properly drained. This is connected to class material as we understand muscle contraction and relaxation is facilitated through neurotransmitter activity and transport. Though the muscles are relaxed here from nitric oxide, it is key in blood flow which in excess increases the drainage block. The autonomic nervous system is not functioning efficiently here to recognize that nitric oxide needs to be inhibited or degraded between the synapses like it would for Ach.

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Guanethidine is an antihypertensive medication used to combat high blood pressure. It works by interrupting the release or distribution of norepinephrine at the sympathetic neuroeffector junction. It does not interfere with the effector cell or norepinephrine’s interaction with its receptor. Guanethidine is taken up into nerve axon terminals through norepinephrine transporters, and then takes the place of norepinephrine in the transport vesicles. This then leads to the gradual depletion of norepinephrine stores in nerve endings, meaning it decreases its overall release in response to an action potential. This relates to our topics because it shows how without a release of norepinephrine to then bind to its receptors, much like acetylcholine and sodium channels with muscle contractions, there would be a lack of a response in the postsynaptic cell because no action potential would be generated. Guanethidine leads to the relaxation of blood vessels which leads to lower blood pressure.

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A drug called methyldopa is used to treat hypertension or high blood pressure. It works directly on the central nervous system instead of the heart or blood vessels. It transforms into a substance that triggers the brain's alpha-2 receptors. Blood pressure decreases because nerve signals that often cause them to tighten are slowed down because of methyldopa.

(b) What physiological pathway does this medication target, and how does it work in the body?

Methyldopa targets the sympathetic nervous system, which regulates heart rate and blood vessel constriction. The medication is converted into a chemical that inhibits norepinephrine production by stimulating alpha-2 adrenergic receptors in the brainstem. Methyldopa inhibits sympathetic activity, which relaxes blood vessels and lowers blood pressure, whereas norepinephrine typically increases heart rate and pressure. This makes it especially useful for situations where other medications would be unsafe, such as pregnancy-related hypertension.

How does this connect with class?

This ties into our class discussions on how drugs manipulate neurotransmitters to push down HR and hypertension. Methyldopa, by counteracting the sympathetic nervous system, reduces the release of norepinephrine and epinephrine, which typically raise heart rate and blood pressure during stress. I see how hypertension affects the body from EMT work, highlighting the brain's blood pressure regulation using drugs, interesting to see something on the other side of the spectrum.

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Phenylephrine/Sudafed (treats stuffy/runny nose)

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Phenylephrine/Sudafed (treats stuffy/runny nose)

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Phenylephrine, commonly known and sold as Sudafed PE, and pseudoephedrine, sold as Sudafed are both nasal decongestants. Phenylephrine stops congestion by binding to alpha-1 adrenergic receptors, which are proteins responsible for the regulation of heart rate and blood pressure. Once phenylephrine binds to alpha-1 adrenergic receptors, the blood vessels restrict and slow/stop the fluid draining from the blood vessels. The congestion comes from the fluid secreted by the blood vessels into the nasal cavity, but by constricting the blood vessels, the running nose and congestion will stop. Pseudoephedrine work in the same way, but also indirectly increases the release of norepinephrine, which may raise heart rate as a result. This medication can be bought in a pharmacy and can be taken orally as pills, chewable tablets, and liquids. This connects to the course because it directly has an impact on the sympathetic division of the autonomic nervous system. As a response to a virus or pollen, the body uses the parasympathetic system to dilate the blood vessels causing a runny nose through secretion of mucus, and then phenylephrine and pseudoephedrine mimics the sympathetic system by binding to the alpha-1 adrenergic receptors and constricting the blood vessels.

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Orthostatic hypotension is when a person's blood pressure drops significantly when they stand up from a sitting or lying down position.  When you stand up, gravity makes blood pool in your legs and lower body. Normally, the body compensates for this by raising your heart rate by constricting the blood vessels through the autonomic nervous system, to make sure that your brain gets enough blood. With orthostatic hypotension, this process is delayed or insufficient, causing a drop in blood pressure and reduced blood flow to the brain. It is typically managed with lifestyle changes like increased fluid and salt intake, or with medications like Fludrocortisone, which help the body retain salt and water.  This disorder relates to class content because it is a part of the autonomic nervous system, which controls blood pressure. The sympathetic nervous system not being able to constrict the blood vessels efficiently is the main cause of this disorder.

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Familial dysautonomia(FD) is an extremely rare genetic disorder that affects the communication, development, and survival of neurons in the ANS and results in absent or impaired autonomic bodily functions.

Individuals with this disorder tend to suffer from multiple complications from a young age and their average life expectancy is around 30 years. Their symptoms include decreased/loss of pain sensitivity, unstable BP, inability to suck, swallow, produce tears, regulate body temperature, autonomic crises, vomiting episodes, and more. There are currently only ~350 reported cases in the world and it primarily affects Ashkenazi jews.

Unfortunately, there is not a cure for FD- management focuses on symptom relief.

This is caused by a mutation in a gene that inhibits neuronal communication entirely with a reduction of IKAP proteins- which alters and inhibits overall axonal transport.

Familial dysautonomia relates to this class directly because this disorder produces symptoms that affect multiple aspects of the autonomic nervous system due to impaired visceral reflexes. In class we discuss how neurons transmit information and FD inhibits signaling within the neuron regardless of the specific receptor.

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Patients who have Pure Autonomic Failure experience a sudden drop in blood pressure when standing up which results in dizziness and sometimes fainting as a main symptom. Some other symptoms include excessive sweating, difficulty urinating, constipation, erectile dysfunction, and visual disturbances. These symptoms are all because there are issues with the autonomic nervous system regulation, which is responsible for the involuntary bodily functions. There is no cure for the condition but there are medications to help manage the symptoms. Fludrocortisone, Midodrine, and Droxidopa are used to help with the drop in blood pressure. Fludrocortisone is the most common medication and it works with the sodium potassium pump within kidney cells. It forces the reabsorption of sodium ions into the plasma, which then triggers the urinary excretion of potassium ions which ultimately leads to increased sodium retention. The increase in sodium allows for an increase in volume of blood and therefore blood pressure.

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Postprandial Hypotension is a condition that causes a drop in blood pressure, within two hours after a meal which can lead to dizziness or fainting. Typically, after eating, blood is directed to the GI tract to help with digestion and our autonomic nervous system (ANS) makes up for this change by increasing heart rate and vasoconstriction to maintain a stable blood pressure. In individuals with this condition, this response is impaired so this leads to the drop in blood pressure. This condition is often seen in older patients with a decline in the autonomic nervous system or in patients that have had a stroke, accident or other damage to key nerves or blood pressure receptors. A major condition that stimulates the onset of PPH is high blood pressure, which stiffens arteries making them harder to dilate and constrict as needed.

This directly related to the course because it has a major autonomic nervous system component to it, specifically the balance between the sympathetic and parasympathetic NS which is impaired in this condition.

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Clonidine is a drug that is used to treat high blood pressure. It is classified as an antihypertensive. It doesn’t cure hypertension, but it does help to manage it and keep the blood pressure down. It targets alpha receptors and signals the brain to stop vasoconstriction. This system, in turn, reduces blood pressure. It also reduces heart rate. Alpha receptors are neuroreceptors in the brain that respond to norepinephrine and epinephrine. These receptors regulate the sympathetic nervous system. Clonidine is related to this course because it binds to alpha receptors to inhibit the release of the neurotransmitter norepinephrine. When norepinephrine is not inhibited, it stimulates the body’s fight-or-flight system. This causes vasoconstriction when the blood vessels contract. This contraction of the vessels causes hypertension. So, when Clonidine binds to alpha receptors, it stops this release to norepinephrine. This prevents the contraction of the blood vessels which will decrease blood pressure.

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Dopamine beta-hydroxylase (DBH) deficiency is a rare disorder that affects the autonomic nervous system by disrupting the synthesis of norepinephrine and epinephrine. This disorder results from mutations in the DBH gene. The DBH enzyme in this gene is responsible for converting dopamine into norepinephrine in sympathetic neurons and the adrenal medulla. There are a few things wrong at the physiological level. There would be deficient sympathetic nervous system activity. The SNS relies on NE as a primary neurotransmitter. Since NE is missing, sympathetic signaling is severely impaired which can lead to drastic blood pressure drops when standing up (orthostatic hypotension) and difficulty maintaining vascular tone. There can also be excess dopamine accumulation. Without DBH, dopamine is not converted to NE. Instead, it accumulates abnormally in the plasma and cerebrospinal fluid. However, dopamine itself can’t substitute for NE in sympathetic neurons. There can also be impaired stress and exercise response in the person. The fight-or-flight response is compromised because E is missing (E is normally produced by the adrenal glands). Patients experience exercise intolerance, dizziness, and fainting because their body can’t properly adjust heart rate and vascular tone under stress.

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Salbutamol/Ventolin is an inhaled treatment used to treat asthma and COPD - diseases characterized by the hyper contraction of a person's airways leading to blockage and difficulty breathing. These are connected to our class as they are not only treatments specific to the parasympathetic division of the autonomic nervous system, but they are also therapies that target specific cell cascades. Both therapies proceed by the mechanism of binding to beta-2-receptors on the cell membrane of bronchial smooth muscle. Once bound to the receptor, these therapies trigger a cascade that results in increased production of cyclic AMP (adenosine mono phosphate) in the cell. Protein kinase A is activated by this uptake in cyclic AMP which is responsible for phosphorylating contraction-specific proteins in the cell. Phosphorylation of these proteins results in a cellular decrease in calcium which ultimately inhibits MLCK (myosin light chain kinase) which is responsible for muscle contraction. This chain of events effectively causes bronchodilation or relaxation of the smooth muscle in the airways. Because of this, people who experience asthmatic attacks are provided fast relief.