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Questions and Answers
Where are prostanoids primarily discovered?
Where are prostanoids primarily discovered?
- Blood plasma
- Seminal fluid (correct)
- Nervous tissue
- Lymphatic fluid
How do prostanoids function in the body?
How do prostanoids function in the body?
- As neurotransmitters
- As autocrine or paracrine signaling molecules (correct)
- Only as hormones
- Exclusively in immune responses
Which of the following are related compounds to prostanoids?
Which of the following are related compounds to prostanoids?
- Steroids and peptides
- Thromboxanes and leukotrienes (correct)
- Cytokines and interleukins
- Neurotransmitters and enzymes
What is the primary role of the compounds thromboxanes and leukotrienes?
What is the primary role of the compounds thromboxanes and leukotrienes?
Which statement about the signaling roles of prostanoids is true?
Which statement about the signaling roles of prostanoids is true?
What is one effect of increased hepatic production of C-reactive protein on the body?
What is one effect of increased hepatic production of C-reactive protein on the body?
What consequence does increased production of proteolytic enzymes by chondrocytes primarily lead to?
What consequence does increased production of proteolytic enzymes by chondrocytes primarily lead to?
Which of the following is a direct result of increased osteoclast activity?
Which of the following is a direct result of increased osteoclast activity?
How does cartilage degeneration typically affect joint health?
How does cartilage degeneration typically affect joint health?
Increased osteoclast activity primarily leads to which of the following conditions?
Increased osteoclast activity primarily leads to which of the following conditions?
What do NSAIDs primarily inhibit in the context of rheumatoid arthritis (RA)?
What do NSAIDs primarily inhibit in the context of rheumatoid arthritis (RA)?
How do NSAIDs affect fever in the body?
How do NSAIDs affect fever in the body?
What physiological mechanism do NSAIDs use to enhance heat dissipation?
What physiological mechanism do NSAIDs use to enhance heat dissipation?
What is the result of NSAIDs blocking PGE2 during an inflammatory response?
What is the result of NSAIDs blocking PGE2 during an inflammatory response?
What aspect of the inflammatory response is NOT affected by NSAIDs?
What aspect of the inflammatory response is NOT affected by NSAIDs?
What cardiovascular events are associated with NSAIDs, excluding aspirin?
What cardiovascular events are associated with NSAIDs, excluding aspirin?
Which NSAID is least likely to be harmful regarding cardiovascular events?
Which NSAID is least likely to be harmful regarding cardiovascular events?
What is a potential CNS adverse effect of NSAIDs?
What is a potential CNS adverse effect of NSAIDs?
How do NSAIDs affect bronchoconstriction in asthmatic patients?
How do NSAIDs affect bronchoconstriction in asthmatic patients?
What can potentially displace salicylate due to its high protein binding?
What can potentially displace salicylate due to its high protein binding?
What is a symptom of mild salicylate toxicity?
What is a symptom of mild salicylate toxicity?
Which of the following is NOT typically associated with mild salicylate toxicity?
Which of the following is NOT typically associated with mild salicylate toxicity?
During mild salicylate toxicity, which of these symptoms indicates mental confusion?
During mild salicylate toxicity, which of these symptoms indicates mental confusion?
Which group of symptoms corresponds to mild salicylate toxicity?
Which group of symptoms corresponds to mild salicylate toxicity?
What is a common first sign of mild salicylate toxicity?
What is a common first sign of mild salicylate toxicity?
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Study Notes
C-Reactive Protein
- Hepatic production of C-reactive protein is increased.
Proteolytic Enzymes & Cartilage Degeneration
- Chondrocytes produce and release more proteolytic enzymes, which leads to cartilage degeneration.
Osteoclasts & Bone Erosion
- Increased osteoclast activity results in focal bone erosions and osteoporosis.
Prostaglandins & Inflammation
- Prostaglandins were first discovered in seminal fluid.
- They act as autocrine or paracrine signaling molecules.
- Prostaglandin-like compounds include thromboxanes and leukotrienes.
- Prostaglandins in rheumatoid arthritis (RA) suppress inflammation but do not affect disease progression.
- Prostaglandin E2 (PGE2) is involved in fever, as inflammation triggers cytokine release, leading to PGE2 production and subsequently fever.
- Nonsteroidal anti-inflammatory drugs (NSAIDs) block PGE2, increasing heat dissipation through peripheral vasodilation and sweating.
- NSAIDs can decrease normal body temperature.
Aspirin & Cardiovascular Risk
- NSAIDs, excluding aspirin and naproxen, have been linked to an increased risk of cardiovascular events, including myocardial infarction and stroke.
- Naproxen appears to have the lowest risk of cardiovascular harm.
NSAIDs & Bronchoconstriction
- NSAIDs inhibit prostaglandin synthesis, which can shift the balance towards leukotriene synthesis, resulting in bronchoconstriction.
- Caution should be exercised when using NSAIDs in individuals with asthma.
NSAIDs & CNS Effects
- NSAIDs can cause central nervous system (CNS) side effects such as headaches, tinnitus, and dizziness.
Aspirin & Drug Interactions
- Salicylate (the active ingredient in aspirin) is highly protein-bound (80-90%).
- Drugs that are also highly protein-bound may displace salicylate (and vice versa), potentially increasing levels of both drugs.
- Examples of drugs that can interact with aspirin include warfarin, phenytoin, and valproic acid.
Aspirin Toxicity
- Mild aspirin toxicity (salicylism) is characterized by symptoms such as nausea, vomiting, hyperventilation, headache, mental confusion, dizziness, and tinnitus.
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