Scenario 1: Gout
A 68-year-old obese male presents to the clinic with a 3-day history of fever with chills, and Lt. great toe pain that has gotten progressively worse. Patient states this is the first time that this has happened, and nothing has made it better and walking on his right foot makes it worse. He has tried acetaminophen, but it did not help. He took several ibuprofen tablets last night which did give him a bit of relief.
HPI: hypertension treated with Lisinopril/HCTZ .
SH: Denies smoking. Drinking: “a fair amount of red wine” every week. General appearance: Ill appearing male who sits with his right foot elevated.
PE: remarkable for a temp of 100.2, pulse 106, respirations 20 and BP 158/92. Right great toe (first metatarsal phalangeal [MTP]) noticeably swollen and red. Unable to palpate to assess range of motion due to extreme pain. CBC and Complete metabolic profile revealed WBC 15,000 mm3 and uric acid 9.0 mg/dl.
Diagnoses the patient with acute gout.
Question:
Explain the pathophysiology of gout.
Hyperuricemia, the condition that causes gout, is the body’s inflammatory reaction to an excess of uric acid in the blood. When uric acid levels in the blood rise over around 6.8 mg/dl, Request Unlock a crystallized, insoluble precipitate is formed and deposited into connective tissue all throughout the body. Purine metabolism and renal function are connected to how the body responds to uric acid buildup. Overproduction of uric acid, a byproduct of purine nucleotide breakdown, is thought to contribute to the high purine synthesis rates seen in gout patients. His gout results from his age, his gender, and the fact that he consumes a decent quantity of red wine each week. Gout was diagnosed based on his VS and examination of his great toe and his blood uric acid level of 9.0mg/dl.
Scenario 1: Gout
A 68-year-old obese male presents to the clinic with a 3-day history of fever with chills, and Lt. great toe pain that has gotten progressively worse. Patient states this is the first time that this has happened, and nothing has made it better and walking on his right foot makes it worse. He has tried acetaminophen, but it did not help. He took several ibuprofen tablets last night which did give him a bit of relief.
HPI: hypertension treated with Lisinopril/HCTZ .
SH: Denies smoking. Drinking: “a fair amount of red wine” every week. General appearance: Ill appearing male who sits with his right foot elevated.
PE: remarkable for a temp of 100.2, pulse 106, respirations 20 and BP 158/92. Right great toe (first metatarsal phalangeal [MTP]) noticeably swollen and red. Unable to palpate to assess range of motion due to extreme pain. CBC and Complete metabolic profile revealed WBC 15,000 mm3 and uric acid 9.0 mg/dl.
Diagnoses the patient with acute gout.
Question:
Explain why a patient with gout is more likely to develop renal calculi.
Renal stones occur much more often in those who have primary gout. Urate excretion by the kidneys is hindered in persons with Request Unlock primary gout, even though the kidneys eliminate most of the uric acid in the body. Acute nephropathy may be caused by monosodium urate crystals that deposit within the renal tubules and the slow rate at which the kidneys excrete urate in people with primary gout, a metabolic disorder. Renal stones may develop in the renal tubules, pelvis, or ureters, leading to blockage and potentially life-threatening acute renal failure.
Scenario 2: Osteoporosis
A 78-year-old female was out walking her small dog when her dog suddenly tried to chase a rabbit and made her fall. She attempted to try and break her fall by putting her hand out and she landed on her outstretched hand. She immediately felt severe pain in her right wrist and noticed her wrist looked deformed. Her neighbor saw the fall and brought the woman to the local ER for evaluation. Radiographs revealed a Colles’ fracture (distal radius with dorsal displacement of fragments) as well as radiographic evidence of osteoporosis. A closed reduction of the fracture was successful, and she was placed in a posterior splint with ace bandage wrap and instructed to see an orthopedist for follow up.
Question:
Discuss what is osteoporosis and how does it develop pathologically?
In humans, osteoporosis affects more bones than any other illness. Fractures are likely due to inadequate bone minerals, lower bone strength, and compromised structure. Three basic types of bone cells contribute to bone development, maintenance, and breakdown. In ideal conditions, osteoblasts—immature bone cells—allow the bone Request Unlock to develop and be laid down. Osteocytes are the cells that continually renew bone as part of the body’s natural regenerative process. The osteoblasts make bone regrowth possible thanks to the osteoclasts’ removal of old bone cells. Bone resorption is the job of cells called osteoclasts. As we age, we lose bone far more than we gain it. Around the time we hit 30, we’ve reached our maximal bone mass or bone density. Primary and secondary osteoporosis are the two forms of the disease. The most prevalent kind of osteoporosis, primary osteoporosis, is a hormone-mediated form in which falling estrogen or testosterone levels speed up bone loss. Osteoporosis in women is a progressive disease that starts before menopause and progresses more quickly in the early years following. Furthermore, white people are disproportionately affected by this condition.
Scenario 3: Rheumatoid Arthritis
A 48-year-old woman presents with a five-month history of generalized joint pain, stiffness, and swelling, especially in her hands. She states that these symptoms have made it difficult to grasp objects and has made caring for her grandchildren problematic. She admits to increased fatigue, but she thought it was due to her stressful job.
FH: Grandmothers had “crippling” arthritis.
PE: remarkable for bilateral ulnar deviation of her hands as well as soft, boggy proximal interphalangeal joints. The metatarsals of both of her feet also exhibited swelling and warmth.
Diagnosis: rheumatoid arthritis.
Question:
The pt. had various symptoms, explain how these factors are associated with RA and what is the difference between RA and OA?
Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease that may affect many body parts, mainly the Request Unlock joints. Antibodies against self-antigens and inflammatory cytokines, particularly pro-inflammatory CD4+ T cells, mediate symptoms. TNF and Interleukin-1 encourage synovial cells to release protease that destroys hyaline cartilage, and many inflammatory cells are implicated. Joint swelling and bone or tissue fusion are symptoms of rheumatoid arthritis. The most prevalent sites of joint damage are fingers, toes, wrists, elbows, ankles, and knees. The patient’s feet and hands are both affected by RA. RA, an inflammatory disease, destroys joint tissue, whereas bone is lost due to osteoarthritis. Osteoarthritis (OA) is articular cartilage degeneration in a specific body area. An earlier injury or infection may have damaged the normal cartilage, resulting in secondary OA. The prevalence of primary OA increases dramatically beyond age 65, and there is a clear association between obesity and the development of OA. Osteoarthritis (OA) as a noninflammatory disease process
Scenario5: Multiple Sclerosis (MS)
A 28-year-old obese, female presents today with complaints for several weeks of vision problems (blurry) and difficulty with concentration and focusing. She is an administrative para-legal for a law firm and notes her symptoms have become worse over the course of the addition of more attorneys and demands for work. Today, she noticed that her symptoms were worse and were accompanied by some fine tremors in her hands. She has been having difficulty concentrating and has difficulty voiding. She went to the optometrist who recommended reading glasses with small prism to correct double vision. She admits to some weakness as well. No other complaints of fevers, chills, URI or UTI
PMH: non-contributory
PE: CN-IV palsy. The fundoscopic exam reveals edema of right optic nerve causing optic neuritis. Positive nystagmus on positional maneuvers. There are left visual field deficits. There was short term memory loss with listing of familiar objects.
DIAGNOSIS: multiple sclerosis (MS).
Question:
Describe what is MS and how did it cause the above patient’s symptoms?
Degeneration of central nervous system (CNS) myelin, scarring, and axonal loss characterize Multiple Sclerosis (MS), a chronic inflammatory illness. MS is triggered by Request Unlock an autoimmune reaction to self or microbial antigens in those genetically predisposed to the disease. Her first symptoms of multiple sclerosis, such as a sudden decline in her eyesight, are typical of an acute neurological event. Diffuse central nervous system involvement may manifest via various symptoms, including paresthesia’s affecting the face, trunk, or limbs, weakness, vision abnormalities, and urinary difficulties. Regular exercise, quitting smoking, and avoiding overwork, excessive weariness, and heat exposure are all recommended for MS management.