ADVANCED PATHOPHYSIOLOGY MODULE QUESTIONS AND ANSWERS +A GRADE GUARANTEED

QUESTION 1. 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. • Undigested uric acid accumulates w/in lysosomes, damaging lysosomal membrane. Subsequent enzyme leakage results in cell death and tissue injury • Disturbances in maintaining serum urate levels result in hyperuricemia and deposition of sodium urate crystals in the tissues, leading to painful disorders, known as gout • Noninfectious inflammatory joint disease (gout); inflammation is caused by an immune response to the deposition of crystals of monosodium urate in and around the joint. • Gout is an inflammatory response to excessive uric acid in the blood and other body fluids. Elevated levels lead to the formation of monosodium urate (MSU) crystals in and around the joins. When the uric acid concentration is high enough, it crystallizes and forms insoluble precipitates of MSU that are deposited in connective tissues throughout the body. Crystallization in synovial fluid triggers the release of chemokines and interleukins. • Crystallization in synovial fluid causes acute, painful inflammation of the joint. The inflammatory response triggers macrophages. • Prolong accumulation results in joint damage= gouty arthritis • Individuals with gout may have an accelerate rate of purine synthesis accompanied by an overproduction of uric acid, others break down purine nucleotides at an accelerate rate, also resulting in an overproduction of uric acid. • Gout can be caused either by the overproduction or uric acid or the underexcretion of uric acid. The accumulation of uric acid forms monosodium urate crystals found in synovial fluid. The crystals in the synovial fluid cause an inflammatory response, which then causes tissue damage and further inflammation Gout is a noninfectious inflammatory disorder that presents as a response to an excessive amount of uric acid in the body fluids. It is caused by either the overproduction or underexcretion of uric acid. When there is an excess amount of uric acid, it forms monosodium urate crystals which are found in synovial fluid. The presence of these crystals in the synovial fluid of joints creates an inflammatory response. The inflammatory response triggers a release of chemokines, interleukins, and macrophages. This inflammatory response causes symptoms of pain and inflammation of the affected joints. QUESTION 1. 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. • Uric acid is mostly excreted through the kidneys. The overproduction and under secretion of uric acid can reduce the effectiveness of kidneys excreting uric acid. This results in the formation of monosodium urate crystals in the renal tubules, which then results in nephropathy. Renal stones are significantly more prevalent in individuals with gout compared to the general population. These renal calculi are often made of monosodium urate. Individuals with gout are significantly more prone to the formation of renal calculi. The kidneys are affected by gout because the kidneys are responsible for excreting most of the uric acid in the body. An excess amount of uric acid decreases the effectiveness of the kidney’s ability