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.

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.

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

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.

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.

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.

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.

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. 

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.

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.

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.

(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.

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.