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VTT Pharm-5
Pain and Inflammation
| Question | Answer |
|---|---|
| What are the two ways patients respond to pain? | Physiological - increased heart rate, blood pressure, temperature, respiratory rate Behavioral - Sensitive to touch, aggression, vocalization, avoiding using affected area, decreased activity, decreased grooming |
| What are nociceptors | Pain receptors |
| What is Visceral Pain? | Pain that arises from the organs. Deep in the body cavity. |
| What is Somatic pain? | Pain that arises from the musculoskeletal system. More superficial in location. |
| What is neuropathic pain | Can arise due to injury to the PNS or CNS. Described in humans as “burning” or “shooting” |
| What is pathological pain? | Pain that serves no purpose |
| What is preemptive pain control and what are the benefits? | Intervention before tissue damage occurs. It’s easier to control pain before the body is aware of it. Wind-up pain is behind the rationale that pain control is enhanced with preemptive intervention. |
| What is multimodal analgesia? | Using more than one class of drugs to control pain. They intervene at different sites within the pain pathways. |
| What are prostaglandins? | They are chemicals that affect several body functions. Prostaglandins formed by COX-1 are involved in the regulation homeostatic functions throughout the body. Prostaglandins formed by COX-2 initiate inflammation and pain. |
| What are histamines? | Chemical involved with allergic responses in the body. Drugs that cause a histamine release can induce vasodilation and activate the vomiting reflex. |
| What are they 4 steps of the pain pathway? | Transduction, transmission, modulation, and perception |
| What is transduction (pain pathway)? | Pain sensation is transformed into electrical signals by nociceptors. We can block transduction by giving local Ax before the tissue damage starts. We cannot block it after damage has already occurred. |
| What is transmission (pain pathway)? | The pain signals are sent to the spinal cord. Local Ax also blocks transmission. Example: ring block |
| What is modulation (pain pathway)? | Pain signals are modulated (suppressed or amplified) by the spinal cord and sent to the brain. Epidurals (spinal blocks) stop the spine from sending any pain signals to the brain. |
| What is perception (pain pathway)? | The brain recognizes the pain and the patient perceives the pain. Opioids work by blocking the perception of pain |
| What is wind-up pain? | When the spinal cords are overloaded with pain signals, they amplify everything and send it to the brain to deal with. |
| What does Lipooxygenase do? | It breaks down arachidonic acid into leukotrienes |
| What do leukotrienes do? | They call white blood cells to the injured area and promotes cleanup and healing. These are good! |
| What does Cyclooxygenase do? | They break down arachidonic acid into prostaglandins. COX-1 are involved in the regulation homeostatic functions throughout the body like renal perfusion and promoting formation of GI mucosa. Prostaglandins formed by COX-2 initiate inflammation and pain. |
| How to corticosteroids work? | They block the formation of arachindonic acid. They work earlier in the inflammatory pathway than NSAIDs do, and so are more effective anti-inflammatory agents. |
| How do NSAIDs work? | They inhibit cyclooxygenase from creating prostaglandins. They work later in the inflammatory pathway than corticosteroids. Selective COX-2 inhibitors are supposed to have less adverse side effects than non-selective inhibitors. |
| Can we give both steriods and NSAIDs to a patient? | No! This creates major GI issues and liver/kidney damage. |
| Why are cats more sensitive to NSAIDs? | They are not as good at metabolizing NSAIDs as humans or cats. There are only two FDA approved NSAIDs for cats (meloxicam and robenacoxib) and none are approved for long-term use. |
| What are some adverse side effects of Glucocorticoids? | Very slow healing, immunosuppression, Cushing's disease (hyperadrenocorticism), PUPD, muscle wasting |
| What happens if Glucocorticoids are suddenly stopped? | Addison's disease (hypoadrenocorticism), BP drops, death in severe cases |
| What are the opioid receptors? | Mu, Kappa, Sigma, Delta |
| What are opioid agonists? | Drugs that bind with opioid receptor sites and produce opioid effects including analgesia and sedation. All agonists are schedule II controlled substances. Examples: Morphine, Oxymorphone, Hydromorphone, Methadone, Fentanyl |
| What are some adverse effects of opioids? | Side effects include bradycardia, respiratory depression, excitement, panting, vomiting, and constipation |
| What are Opioid Agonists-Antagonists? | They bind with kappa receptors but antagonize mu receptors. We can use these to reverse the adverse effects of a pure mu drug, while still keeping some pain relief. Examples: Butorphanol, Pentazocine (CIV) |
| What are Opioid Partial Agonists? | They bind with the mu receptors but only partially activate them. Buprenorphine is the primary drug in this category and has a longer duration of action than morphine. |
| What are Opioid antagonists? | They bind (high affinity) to receptors but induces no intrinsic activity. By doing so, it blocks other things from binding to it. Naloxone is an example of an opioid antagonist. |
| Where in the body can you find opioid receptors? | You can find opioid receptors in the CNS (brain, spine) and in the GI Tract, Urinary Tract, smooth muscle |
| What is morphine? | Pure agonist opioid (CII). |
| What is oxymorphone? | Pure agonist (CII) More potent than morphine and has less side effects (less histamine release), but very expensive! |
| What is hydromorphone? | Pure agonist (CII ) More potent that morphine, less sedation, less histamine release (less side effects). Less expensive than oxymorphone |
| What is methadone? | A pure opioid agonist and NMDA antagonist (CII) Similar effects to oxy and hydromorphone. Least likely of all of them to cause vomiting. |
| What is fentanyl? | Pure opioid agonist (CII) Great analgesia, very short duration of action (20 - 30min). For this reason, CRI and TD patch is common |
| What is buprenorphine? | A partial opioid agonist (CIII). Effective for mild to moderate pain. Can be used to reverse effects of pure agonists while maintaining some analgesia. In high doses, respiratory depression is hard to reverse. |
| What is butorphanol? | An opioid agonist-antagonist (Kappa-mu) - CIV For mild to moderate pain. Can be used to reverse adverse effects of pure agonists while maintaining analgesia Partially toxic to spinal cord, so no epidurals. |
| What is tramadol? | Mu agonist, SNRI (CIV) Effective for mild pain. Makes for a good adjunct analgesia but not great on its own. Naloxone only partially reverses effects of tramadol |
| What is codeine? | Opioid agonist (CII) Effective for mild pain, oral form only Cats are sensitive to codeine |
| Why is it recommended to take NSAIDs with food? | NSAIDs can inhibit the "good" prostaglandins from doing their job. Eating food triggers the body to activate processes like increasing GI mucus production which can help combat it. |
| What are some examples of Non-selective NSAIDs? | salicyclic acid (aspirin), diclofenac, phenylbutazone, flunixin meglumine |
| What are some examples of selective COX-2 NSAIDs? | meloxicam, carprofen, deracoxib, firocoxib, robenacoxib, Galliprant |
| What are some examples of glucocorticoids? | prednisone, prednisolone, dexamethasone, hydrocortisone |
| What is a free radical scavenger? | Free radicals are unstable molecules that are generated by white blood cells. Free radical scavengers get rid of the free radicals in the body |
| What are monoclonal antibody drugs? | Great for osteoarthritis in dogs and cats, very expensive. Examples: bedinvetmab (dogs), frunevetmab (cats) |
Created by:
grace3050
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