Graves’ Disease

Student’s Name

Institutional Affiliation Rasmussen University

Essentials of Pathophysiology, NUR2063

Prof Kendra Nielson

15/10/2022

I interviewed my 40-year-old neighbor for this project, who has been treated for

hyperthyroidism caused by Graves' illness. She enthusiastically agreed to take part, and here is

how it went down:

The affected person's interview:

INTERVIEWER: Which immune system disorder do you have?

INTERVIEWEE: I was diagnosed with hyperthyroidism due to Graves' disease.

INTERVIEWER: How long have you had this disorder?

INTERVIEWEE: I have had this condition for nearly ten years.

INTERVIEWER: How has this disorder changed your life (home and work)?

INTERVIEWEE: I live a disciplined life following treatment. Eat on time, eat

appropriately, and practice yoga regularly. Try to sleep for seven to eight hours. Please continue

to give my all at work. My diet has to be modified. I must prepare my meals and fill my plate

with things that will not exacerbate my Graves' disease symptoms. To feel my best, I take a

variety of treatments, including medicines and radioactive iodine, as part of my Graves' disease

treatment plan.

INTERVIEWER: Are you able to carry out daily activities independently?

company offers me both remote and office hours, which allows me to alter my schedule

accordingly.

INTERVIEWER: What therapies are you using to manage this disorder?

INTERVIEWEE: My family physician diagnosed Graves' disease and started me on

antithyroid medication. I had a thyroidectomy five years ago because I had a huge goiter

compressing adjacent structures, including the trachea, and making breathing difficult.

INTERVIEWER: What, if any, side effects does the treatment have?

INTERVIEWEE: I experienced a skin rash and vasculitis in the early stages of starting

the medicine. Some of the medications I take are teratogenic, and I was cautioned not to become

pregnant. If I were to consider getting pregnant, I was told to adjust my medication first.

INTERVIEWER: Has this disorder changed your body?

INTERVIEWEE: I have an increased hunger yet have lost weight. I have more bowel

movements. My skin is warm and wet, and my hair is fine and brittle. I have lid retraction, which

makes me appear "wide-eyed," as if I were "frozen in panic." I also have muscle weakness,

particularly in my thighs and upper arms.

INTERVIEWER: Does this disorder have any emotional effects on you?

INTERVIEWEE: I have anxiety, irritability, mood changes, and difficulties sleeping. I

sometimes feel like I have drunk too much coffee. This has had a significant influence on my

life. However, my medicine has helped alleviate my symptoms.

INTERVIEWER: Have alternative therapies, such as Eastern medicine (acupuncture,

herbal treatment, yoga), been tried or recommended

alternative methods should supplement rather than replace current treatment procedures.

However, regular yoga practice is required.

Graves’ disease

Introduction

Graves' disease, first identified by Irish surgeon Robert James Graves, is an autoimmune

disorder in which the immune system produces antibodies that activate and target the thyroid

gland, resulting in hyperthyroidism due to excess thyroid hormone synthesis. The CINAHL

Nursing Guide defines Grave's Disease. "Graves' disease (GD) is an autoimmune disease

characterized by hyperthyroidism (i.e., excessive thyroid hormone synthesis) caused by the

activity of autoantibodies directed against thyroid antigens" (Boling & Karakashian, 2018).

Pathophysiology

Typically, the hypothalamus, located near the base of the brain, detects low thyroid

hormone levels in the blood and releases thyrotropin-releasing hormone into the hypophyseal

portal system, a network of capillaries that connects the hypothalamus to the anterior pituitary.

The anterior pituitary gland then secretes thyroid-stimulating hormone (TSH), also known as

thyrotropin. TSH stimulates the thyroid gland, which is located in the neck and resembles two

thumbs hooked together in the shape of a "V." Thousands of follicles, or little spheres lined with

follicular cells, make up the thyroid gland.

Thyroglobulin, a protein found in follicles, is converted by follicular cells into two

iodine-containing hormones, triiodothyronine or T3 and thyroxine or T4. These hormones enter

the bloodstream after being released from the thyroid gland and bind to circulating plasma
proteins. Only a tiny quantity of T3 and T4 move unbound in circulation, yet these two hormones

are recognized by practically every cell in the body. Once within the cell, T4 is mainly

transformed into T3 and can start working. T3 accelerates the basal metabolic rate. T3 boosts

cardiac output, induces bone resorption (thinning of the bones), and activates the sympathetic

nervous system, which is responsible for our 'fight-or-flight' reaction.

The cause of Graves' disease, like many autoimmune diseases, is unknown, but it is more

common in those with a positive family history. It is caused by environmental factors like stress,

smoking, illness, iodine exposure, and postpartum, as well as by immunological reconstitution

after highly active antiretroviral therapy (HAART) (Pokhrel & Bhusal, 2018). For some reason,

B cells in Grave's disease begin to create a variety of antibodies against thyroid proteins. The

most prevalent antibody is thyroid-stimulating immunoglobulin, which binds to the TSH receptor

on thyroid cells, simulating TSH and activating thyroid cells to release more T3 and T4.

However, thyroid-stimulating immunoglobulins can have a direct effect on specific tissues.

Thyroid hypertrophy, defined as growth in the interstitium of the tissue, and hyperplasia, defined

as an increase in the number of follicular cells, cause the thyroid to enlarge. As the follicle cells

cluster together, they alter their shape, becoming taller than a healthy thyroid.

Second, in response to the thyroid-stimulating antibody, follicular cells begin to express

proteins on their surface that attract neighboring T cells. Circulating T lymphocytes link to

follicular cells and penetrate the thyroid tissue's interstitium or the area between follicular cells.

(Pokhrel & Bhusal, 2018)

Third, thyroid-stimulating antibodies stimulate fibroblasts in the tissue around the eyes

and skin, causing them to multiply and produce extracellular matrix proteins called

glycosaminoglycans, which accumulate in the tissues over time. (Pokhrel & Bhusal, 2018)
Signs and symptoms/ Clinical presentation

Graves' disease symptoms include hyperthyroidism, ophthalmopathy, and dermopathy.

The majority of Graves' disease patients exhibit characteristic hyperthyroidism signs and

symptoms. It is unusual for Graves' disease to appear with only Graves' ophthalmopathy and

dermopathy. Thyroid-stimulating immunoglobulins target and activate the TSH receptor,

resulting in goiter - an enlarged thyroid - due to the gland's hypertrophy and hyperplasia; weight

loss despite an increase in appetite due to the higher basal metabolic rate; heat intolerance

because the body produces more heat; and rapid heart rate, sweating, hyperactivity, anxiety, and

insomnia due to thyroid hormones' effect on the sympathetic nervous system.

Graves’ ophthalmopathy is caused by an accumulation of glycosaminoglycans around the

eyes. The ophthalmopathy causes exophthalmos or outward bulging of the eyeball; weakens the

muscles that control eye and upper eyelid movements, and can damage the cornea over time

because exophthalmos can dry out the eyes and raise the risk of corneal ulcers. Pretibial

myxedema, produced by glycosaminoglycan accumulation, can cause non-pitting edema

(swelling) and skin thickening, most commonly above the shins (Davies et al., 2020).

Thyroid storm, a potentially fatal complication of hyperthyroidism in which the body

enters a state of severe hypermetabolism, can occur when someone with hyperthyroidism

discontinues therapy, acquires an infection, or undergoes surgery. Heat intolerance becomes a

severe fever, and a fast heart rate becomes cardiac arrhythmia. Individuals with Graves' disease

are also more likely to develop rheumatoid arthritis, diabetes mellitus type 1, myasthenia gravis,

and potentially celiac disease.

Diagnosis
A detailed history and physical examination are required to diagnose Graves' disease. A

positive family history of Graves' disease, orbitopathy (exophthalmos is quite specific for

Graves' disease), diffusely enlarged thyroid with or without bruit, and pretibial myxedema

should all be included in the history (Boling & Karakashian, 2018). Thyroid function testing can

also be used. TSH, T3, and T4 levels in the blood are measured. If TSH is suppressed, Free T4

(FT4) and Free T3 must be ordered (FT3). If free hormone tests are not accessible, total T4

(Thyroxine) and total T3 (Triiodothyronine) can be ordered. TSH suppression, elevated FT4 or

FT3 levels, or both, confirms hyperthyroidism. Only TSH is reduced in subclinical

hyperthyroidism, whereas FT4 and FT3 levels are normal. Thyroid-stimulating antibodies will be

measured to ensure Graves' disease is the cause of hyperthyroidism. Finally, if Graves’ diagnosis

is ambiguous or if there appears to be another cause of hyperthyroidism, radioiodine scans and

iodine uptake studies might aid in the diagnosis (Boling & Karakashian, 2018).

Treatment

Graves' disease is generally treated with medicine, such as beta-blockers to relieve the

immediate symptoms of hyperthyroidism and anti-thyroid medications to limit thyroid hormone

production and release. Thionamides, such as methimazole, propyl-tio-uracil, or PTU, should be

used to begin treatment. Thionamides block the enzyme thyroid peroxidase inside thyroid cells,

inhibiting thyroid hormone synthesis. Radioiodine therapy, followed by replacement hormone

therapy, can partially or fully damage thyroid function. Surgery removes the thyroid when a huge

goiter compresses surrounding tissues. Graves' ophthalmopathy frequently necessitates different

treatments, such as steroids, radiation therapy, and surgery. (Davies et al., 2020).
References

Pokhrel, B., & Bhusal, K. (2018). Graves’ disease.

Boling, B. R. D. C.-C., & Karakashian, A. R. B. (2018). Graves’ Disease: Diagnosis and

Treatment. CINAHL Nursing Guide

Davies, T. F., Andersen, S., Latif, R., Nagayama, Y., Barbesino, G., Brito, M., ... & Kahaly, G. J.

(2020). Graves’ disease. Nature reviews Disease primers, 6(1), 1-23.