| Course | HS200 Diseases of the Human Body |
|---|---|
| Unit | Unit 10 |
| Paper type | Pathophysiology case report |
| Length | About 1,100 words, 6 pages double-spaced |
| Format | APA 7 student paper |
| School | Purdue University Global |
| Program | BS in Health Science |
| Updated | October 2026 |
Free sample paper for HS200 Unit 10
A New Headache, a Tired Jaw and a Threat to Sight: A Unit 10 Pathophysiology Case Report on Giant Cell Arteritis
[Student Name]
Purdue University Global
HS200: Diseases of the Human Body
Unit 10 Pathophysiology Case Report
[Instructor Name]
[Date]
The patient is composite; the review, guideline and textbook cited are real, and treatment is described at the level of mechanism.
Presentation
A composite 72-year-old retired machinist visits his primary care clinic with a headache over his right temple that began three weeks ago. He has never had headaches before. His scalp is tender when he combs his hair. His jaw aches after a few minutes of chewing and eases when he stops. He has lost weight without trying, feels tired and has had low fevers. Yesterday, the vision in his right eye dimmed for about a minute and then returned. He also reports stiffness in his shoulders and hips in the morning. On examination, the artery at his right temple is thickened, tender and has a weak pulse. Blood tests show a high erythrocyte sedimentation rate and C-reactive protein, both markers of inflammation, and mild anemia.
Cause
Giant cell arteritis is an inflammation of large and medium-sized arteries, especially the branches of the carotid artery that supply the head, and sometimes the aorta. It occurs almost only in people over 50, most often in their seventies, and affects women more often than men, with the highest rates reported in people of northern European ancestry. The cause is not fully known. Aging of the artery wall and changes in the immune system are thought to set the stage, with an unknown trigger starting an immune attack on the artery wall (Salvarani et al., 2008).
Mechanism
The inflammation begins in the outer layer of the artery, where immune cells called dendritic cells are activated. They recruit T lymphocytes and macrophages into the wall. Some macrophages fuse into large cells with many nuclei, the giant cells that give the disease its name. These cells release chemicals that damage the artery's elastic layer and stimulate the inner lining to thicken. As the lining thickens, the channel inside the artery narrows, reducing blood flow to the tissues it supplies. Meanwhile, inflammatory signals, especially interleukin-6, circulate in the blood and act on the liver and brain, producing the body-wide effects (Rogers, 2023).
Linking Each Finding to the Mechanism
1. New temporal headache and scalp tenderness. The inflamed temporal artery and scalp arteries are painful, and their walls are swollen and tender.
2. Pain in the jaw while chewing, called jaw claudication. Chewing muscles need more blood when working. Narrowed arteries cannot deliver it, so the muscles ache with use and recover with rest, just as leg muscles do in narrowed leg arteries.
3. Brief vision loss. The arteries supplying the optic nerve are narrowed. A brief drop in flow dims vision; if flow stops, the optic nerve can be permanently damaged within hours, causing blindness.
4. Thickened, tender artery with a weak pulse. The swollen wall can be felt, and the narrowed channel weakens the pulse.
5. Fever, weight loss and tiredness. Circulating inflammatory signals act on the brain's temperature center and change metabolism.
6. High sedimentation rate and C-reactive protein. The liver responds to interleukin-6 by producing inflammatory proteins, raising these markers.
7. Anemia. Long-lasting inflammation reduces the body's use of iron for red cell production.
8. Shoulder and hip stiffness. A large share of patients also develop polymyalgia rheumatica, an inflammatory condition causing morning stiffness in these areas, and the two are thought to share a mechanism.
Every finding in this case, from the tired jaw to the dimming eye, is a symptom of an artery wall that is inflamed and a channel that is narrowing.
Why a New Headache in an Older Adult Matters
A first-ever headache pattern after age 50 deserves attention on its own, because the common headaches of younger adults, such as migraine and tension headaches, usually begin earlier in life. In this case, the headache's location over the temple, the scalp tenderness and the jaw pain point toward the arteries, while the fever, weight loss and raised inflammatory markers point toward a body-wide inflammatory process. Other causes considered in older adults include bleeding inside the skull, a tumor, an infection and glaucoma that closes the eye's drainage angle suddenly. The combination of findings here fits giant cell arteritis far better than any of these, but the reasoning shows why the case could not be treated as an ordinary headache.
Diagnosis
Diagnosis combines the clinical picture, inflammatory markers and evidence of artery inflammation from a biopsy of the temporal artery or from ultrasound or other imaging of the arteries. Because the disease affects arteries in patches, a biopsy can miss inflamed segments.
Management at the Level of Mechanism
Because vision loss can be sudden and permanent, treatment is started promptly when the diagnosis is strongly suspected, often before biopsy results are available. High-dose glucocorticoids suppress the immune activity in the artery wall and reduce the inflammatory signals; when vision is threatened, they may be given intravenously. Guidelines also describe tocilizumab, a drug that blocks interleukin-6 signaling, as a treatment that can help control the disease and reduce long-term steroid exposure (Maz et al., 2021). Treatment continues for many months, tapered slowly, and patients are monitored for relapse and for steroid side effects such as bone loss and high blood sugar.
Outcome in the Case
He is started on high-dose steroids the same day and referred urgently to rheumatology and ophthalmology. His headache improves within days, his jaw no longer aches when he eats, and his vision does not dim again. An ultrasound of his temporal arteries shows inflammation, supporting the diagnosis. He is started on a bone-protecting medicine and calcium with vitamin D because of the long steroid course, and his blood sugar is checked regularly.
Summary
Giant cell arteritis shows the course's central idea in one disease: an immune response directed at the body's own tissue produces local damage, narrowing the arteries and threatening the organs they supply, and body-wide signals produce fever, fatigue and abnormal blood tests. Understanding the mechanism explains why the disease is treated as an emergency when vision is involved. It also gathers concepts from across the course: inflammation and immunity from the second unit, the difference between local signs and body-wide symptoms, the distinction between tests that confirm inflammation and tests that locate it, and the way a narrowed vessel produces pain with demand, the same principle that explains angina in the heart and cramping in the legs.
References
Maz, M., Chung, S. A., Abril, A., Langford, C. A., Gorelik, M., Guyatt, G., Archer, A. M., Conn, D. L., Full, K. A., Grayson, P. C., Ibarra, M. F., Imundo, L. F., Kim, S., Merkel, P. A., Rhee, R. L., Seo, P., Stone, J. H., Sule, S., Sundel, R. P., ... Mustafa, R. A. (2021). 2021 American College of Rheumatology/Vasculitis Foundation guideline for the management of giant cell arteritis and Takayasu arteritis. Arthritis Care & Research, 73(8), 1071-1087. https://doi.org/10.1002/acr.24632
Rogers, J. L. (Ed.). (2023). McCance & Huether's pathophysiology: The biologic basis for disease in adults and children (9th ed.). Elsevier.
Salvarani, C., Cantini, F., & Hunder, G. G. (2008). Polymyalgia rheumatica and giant-cell arteritis. The Lancet, 372(9634), 234-245. https://doi.org/10.1016/S0140-6736(08)61077-6
What the HS200 Unit 10 assignment asks for
To close the course, students write a case report bringing together cause, mechanism, presentation, diagnosis and management for one condition. Reports of five to eight pages are common. Instructors expect each finding in the case to be traced to a step in the mechanism, with diagnosis and treatment explained by what they reveal or change in that mechanism. Many prompts allow conditions with partly unknown causes, provided the report says what is and is not known. Medications should be named by class and the step each acts on, without detailed dosing. Current guidelines and reviews, cited with year, are expected.
Inside the HS200 Unit 10 example
The report presents the history and examination, then explains the cause as partly unknown, with age and immune changes setting the stage. A mechanism section moves from activated cells in the artery wall to giant cells, a thickening lining and circulating inflammatory signals. Eight numbered findings are each linked to the mechanism, and the highlighted sentence ties them together. A section explains why a first headache after 50 must be taken seriously and which other causes were considered. Diagnosis, management by mechanism with guideline support, the patient's outcome and a summary linking the case to the whole course follow. Every numbered finding uses plain words first, then the technical term, so a nonclinical reader can follow.
Where the points sit in the HS200 Unit 10 rubric
Case reports in this course are typically graded on completeness of the causal chain, accuracy of the mechanism, how well each finding is linked to it, the explanation of diagnosis and management and use of sources. The link between findings and mechanism is where most marks sit, since the course exists to build that skill. Completeness rewards covering cause through outcome. Management earns credit when treatment is tied to the step it targets. Sources should be current and cited with year. Clear organization, plain explanations of technical terms and a summary connecting the case to course concepts complete the score. Reports that name what remains uncertain about the cause are often credited for accuracy.
Common HS200 Unit 10 mistakes, and how to avoid them
A frequent weakness is a case report that describes the disease from a textbook and mentions the patient only at the start. Another is listing findings without explaining how each arises. Some students give detailed drug doses, which is outside the scope of this course. Others claim a known cause for a condition whose cause is uncertain. Leaving out why the case is urgent misses its most important clinical point. If your final case concerns a different condition, perhaps a thyroid storm or a kidney disease, send the case details, and we will build a report that links every finding to the mechanism. Dropping the patient from the middle sections, so the report reads like a textbook chapter, is another common problem.
Get an HS200 Unit 10 example written to your instructions
Tell us which condition the Unit 10 case uses, or whether a choice is allowed, and attach the final prompt and rubric along with any earlier HS200 work worth building on. Within 24-48h the report is back, organized under the prompt's own headings. A first custom sample is free, with a composite patient at its center. The paper above is an original model document written by our desk, not a submitted student paper and not an official Purdue University Global document.
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HS200 Unit 10 questions, answered
Can the final case report reuse a condition from an earlier unit?
Some sections allow it and some require a new condition, so the prompt decides. Where reuse is allowed, it can deepen earlier work, but the final report needs more than a stitched-together version of previous papers. The mechanism and management sections in particular should go further than any earlier assignment did, since the final unit is graded as synthesis.
How much should the report say about medications?
Enough to name each class and the step in the mechanism it acts on. HS200 is not a pharmacology course, so doses and schedules are unnecessary and can distract. A sentence explaining that levodopa replaces a missing precursor earns more than a paragraph listing brand names, because it shows the treatment was understood through the disease.
What if the prompt assigns a condition with an unknown cause?
Say what is known and what is not, and cite the uncertainty. Many chronic conditions have contributing factors rather than a single cause, and a report that presents those factors by strength of evidence is more accurate than one choosing a cause for neatness. The mechanism section can still be detailed, since how damage produces signs is often better understood than why it begins.
Where can I find a free HS200 Unit 10 sample paper?
The complete Unit 10 case report on giant cell arteritis is on this page, linking every finding in a 72-year-old to inflamed artery walls.
Why is giant cell arteritis treated as an emergency?
Narrowed arteries can cut off blood to the optic nerve, causing permanent blindness within hours, so steroids are started as soon as the diagnosis is strongly suspected.