ANALGESICS - INTRO
88 important questions on ANALGESICS - INTRO
What is recommended for mild nociceptive pain according to the WHO Pain Ladder?
Non opioids such as Paracetamol and NSAIDs are recommended for mild nociceptive pain according to the WHO Pain Ladder.
What is the mechanism of action for opioids in pain management?
Opioids inhibit neurotransmitter release, leading to no pain sensation. They suppress nociceptors. Examples include morphine, tramadol, pethidine, and codeine.
Which medications are suggested for moderate nociceptive pain?
Weak opioids such as codeine and tramadol are suggested for moderate nociceptive pain according to the WHO Pain Ladder.
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What does the WHO Pain Ladder recommend for severe nociceptive pain?
Strong opioids such as Perthidine and morphine, which can also be combined with NSAIDs, are recommended for severe nociceptive pain.
What is the role of COX-1 in the body?
COX-1 is constitutive, present normally in tissues regulating its physiological functions. It is responsible for forming protective PGs in the GIT and Kidney.
Name some NSAIDs used in drug management of pain.
NSAIDs used in pain management include ibuprofen, diclofenac, acetaclofenac, and meloxicam.
How is COX-2 different from COX-1?
COX-2 is inducible and formed during inflammation, unlike COX-1, which is constitutive and present normally in tissues regulating physiological functions.
Can adjuvants be used in the WHO Pain Ladder for nociceptive pain?
Adjuvants may be added where necessary in the WHO Pain Ladder for managing nociceptive pain.
What are adjuvants in the context of pain management, and give examples?
Adjuvants in pain management include carbamazepine and amitriptyline, which suppress transmission of neuronal impulses.
What are Non-Steroidal Anti-inflammatory Drugs (NSAIDs) and their effects?
NSAIDs (COX 1 & 2 Inhibitors) are agents with Anti-inflammatory, Analgesic, and Antipyretic effects. Examples include:
- Aspirin
- Ibuprofen
- Mefenamic Acid
- Diclofenac
What are the two main classifications of analgesics?
Analgesics are classified into:
- Non opioids Analgesics
- Used in mild & moderate pain
- NSAIDS, Paracetamol
- Opioids/Narcotic Analgesics
- Used in Moderate & Severe Pain
- Natural: Morphine/Codeine
- Synthetic Opioids
Where is COX-3 found and what is its significance?
COX-3 is found in the CNS. Paracetamol inhibits COX-3 in the CNS, hence it has no anti-inflammatory effects.
What is the role of Paracetamol in prostaglandin synthesis inhibition?
Paracetamol (COX-3 Inhibitor in CNS) is an Analgesic-Antipyretic with no anti-inflammatory action.
What are adjuvants in the context of analgesics?
Adjuvants include:
- Amitriptyline
- Pregabalin
- Prednisolone
What is the effect of NSAIDs on COX enzymes?
NSAIDs inhibit COX1 and COX2, thus stopping pain generation. Meloxicam is an NSAID that selectively inhibits COX-2, safer to use in PUD than non-selective NSAIDs.
What happens when nociceptors are activated due to nerve injury?
When nociceptors are activated due to injury to nerves, they release glutamate and neuropeptides from sensory terminals, which activates neurons.
Why is Meloxicam considered safer for use in PUD compared to other NSAIDs?
Meloxicam is an NSAID that selectively inhibits COX-2, making it safer to use in PUD than non-selective NSAIDs, which inhibit both COX1 and COX2.
What substances are released in response to tissue injury?
In response to tissue injury, the following substances are released:
- Bradykinin
- 5-HT
- Prostaglandin
- K⁺
- Histamine
- CGRP
- Substance P
What role do mast cells play in tissue injury?
Mast cells release histamine in response to tissue injury. This contributes to the inflammatory response and is part of the body's mechanism to address the injury.
What do bradykinin and prostaglandins do in response to tissue injury?
Bradykinin and prostaglandins sensitize or activate nociceptors, which in turn releases substance P and calcitonin gene-related peptide (CGRP).
How does substance P affect mast cells?
Substance P acts on mast cells to cause degranulation and the release of histamine which activates nociceptors.
What role do prostaglandins play in acute asthma?
Prostaglandins play a role in acute asthma by mediating inflammation. The process involves phospholipids converting to arachidonic acid via phospholipase A2, then to PGs/THXA2 via COX enzyme.
How do CGRP and Substance P interact with neurons during tissue injury?
CGRP and Substance P are released and interact with dorsal root ganglion neurons, transmitting signals to the spinal cord as part of the pain response mechanism.
What is the effect of substance P on plasma?
Substance P causes plasma extravasation.
What are the effects of PGE₂ and PGI₂ in inflammation?
- Vasodilation
- Increased vascular permeability
- Increased cytokine release
- Increased leukocyte migration
- Pain
What is the pathway of signal transmission from a lesion to the spinal cord?
The pathway involves the release of substances like CGRP and Substance P, which interact with dorsal root ganglion neurons, transmitting signals to the spinal cord.
How does aspirin affect the lipoxygenase pathway in asthma?
Aspirin stimulates the lipoxygenase (LOX) pathway involving leukotrienes that stimulate an acute attack of asthma, hence it is contraindicated in asthma.
What does COX-2 inhibition result in?
- Anti-inflammatory effects
- Analgesic effects
What is the role of leukotrienes in asthma?
Leukotrienes play a major role in the pathogenesis of asthma attack. They are produced from arachidonic acid via the LOX enzyme and cause airway muscle tightening and fluid production.
What are the functions of Thromboxane A2 (TBX2)?
- Potent vasoconstrictor
- Stimulate platelet aggregation
What role does CGRP play in blood vessels?
CGRP dilates blood vessels resulting in oedema and causes additional release of bradykinin.
Describe the process involving phospholipids in the LOX pathway.
In the LOX pathway, phospholipids are converted to arachidonic acid by phospholipase A2, then to leukotrienes by the LOX enzyme. This pathway is a major source of pro-inflammatory leukotrienes.
What are the functions of Prostaglandins PGI2 and PGE2?
- Potent vasodilator
- Inhibit platelet aggregation
How is serotonin (5-HT) involved in nociceptor activation?
Serotonin (5-HT) is released from platelets and activates nociceptors.
What are the effects of LTC₄ and LTD₄ in the lungs/asthma?
- Bronchoconstriction
- Mucus secretion
- Edema
- Eosinophil migration
What is the role of PGE1 in the GIT?
PGE1 is responsible for secretion of mucus in the stomach and reduces HCl production.
What is the significance of the LOX pathway in allergies?
The LOX pathway is the major source of pro-inflammatory leukotrienes (LTs), which play a key role in allergies by causing airway muscle tightening and excess mucus and fluid (edema) production.
How does PGI2 affect blood vessels?
PGI2 is responsible for endothelial relaxation resulting in vasodilation.
How do LOX inhibition and LT receptor antagonism affect the lungs?
- Decrease bronchoconstriction
- Anti-inflammatory effects
What happens to phospholipids released after cell injury?
Phospholipids released after cell injury are converted to Arachidonic acid by an enzyme called Phospholipase A2 by steroids.
What is the function of PGE2/PGE1 in the uterus?
PGE2/PGE1 (Misoprostol) induce contractions (induce labor).
What is the role of Prednisolone in prostaglandin synthesis?
Prednisolone (steroid) inhibits Phospholipase A2 enzymes, hence inhibition of prostaglandin synthesis.
Why is Aspirin contraindicated in Asthma?
Aspirin stimulates the LOX pathway is the major source of pro-inflammatory leukotrienes (LTs), which play a key role in allergies by causing airway muscle tightening and excess mucus and fluid (edema) production.
What is the role of COX-1 and COX-2 inhibition in the CNS?
- Antipyretic effects
- Analgesic effects
What enzyme converts phospholipids into arachidonic acid in the mechanism of analgesic?
Phospholipase A2 is the enzyme that converts phospholipids into arachidonic acid in the mechanism of analgesic.
What effect do PGE2 and PGI2 have on the kidneys?
PGE2 and PGI2 cause vasodilation leading to increase in renal blood flow and glomerular filtration rate.
Which drugs inhibit the enzyme cyclo-oxygenase in the analgesic mechanism?
NSAIDS (Aspirin) inhibit the enzyme cyclo-oxygenase (COX1, COX2) in the analgesic mechanism.
Elaborate the role of low dose Aspirin in Pre-eclampsia/CHF/HBP/Angina.
Condition Role of Low-Dose Aspirin
- Pre-eclampsia - Prevention (High Risk) - Modifies certain prostaglandin effects, reduces microthrombosis.
- HBP (Pregnancy) - Prevents Superimposed PE - Affects platelet aggregation and vascular inflammation.
- Angina - Preventive/Anti-thrombotic - Inhibits platelet aggregation, prevents clot formation.
- CHF - Secondary prevention - Manages underlying coronary disease/ischemia.
What are autacoids that mainly cause or sensitize pain, and how are they inhibited?
Histamine and prostaglandins are autacoids that mainly cause/sensitize pain. They are inhibited by antagonists. Autacoids antagonists include antihistamines and NSAIDs.
What does the Cyclo-oxygenase (COX) enzyme catalyze?
Cyclo-oxygenase (COX) enzyme catalyzes the conversion of Arachidonic acid to Endoperoxides.
What induces COX-2 expression?
- Immune responses to injury or infection
Compare and elaborate why misoprostol (PG1) is used to induce labor as well as for management of PUD in terms of the mechanism of Action.
it can both protect the stomach lining (anti-secretory) and induce smooth muscle contractions (uterotonic)
What are some consequences of prolonged NSAID use on kidneys?
Prolonged use of NSAIDs causes damage to the kidneys by reducing blood flow to the kidneys.
What is the role of H1 receptor antagonists in blocking pain?
H1 receptors antagonists inhibit histamine, hence blocking allergic reactions. Examples include chlorpheniramine, diphenhydramine, promethazine, and mepyramine.
How many types of cyclo-oxygenase enzymes are there?
There are three types of cyclo-oxygenase enzymes: COX-1, COX-2, and COX-3.
What role does paracetamol play in the analgesic mechanism?
Paracetamol acts on COX 3 in the analgesic mechanism, affecting the conversion of arachidonic acid to endoperoxides.
What is the role of PGD2?
PGD2 has other functions e.g. neuro functions, pain, Temperature regulation, release of hormones, mainly produced by mast cells, lymphocytes.
What do COX-1, COX-2, and COX-3 convert Arachidonic acid into?
COX-1, COX-2, 3 converts Arachidonic acid to prostaglandins (biosynthesis of prostaglandins and Thromboxane-A2).
What happens when cell membranes break down in relation to autacoids?
When cell membranes break down, they expose chemical substances that stimulate reactions with enzymes. This results in the synthesis of autacoids, which are mediators of pain, inflammation, and allergies.
What are the products formed from endoperoxides in the analgesic mechanism?
Endoperoxides are converted into prostacyclins (PGI2), PGF, PGE2, PGD2, and thromboxane A2 (TBX2) in the analgesic mechanism.
How do NSAIDs function in the mechanism of blocking pain?
NSAIDs (Non-Steroidal Ant-inflammatory Drugs) inhibit prostaglandins, which are autacoids that engineer inflammation and pain.
How do analgesics function to relieve pain?
Analgesics relieve pain by inhibiting autacoids.
What induces the release of autacoids?
The release of autacoids is induced by:
- Chemical irritant
- UV light
- Trauma
- Immune irritants
- Bacterial toxins
What is the effect of glucocorticoids like prednisolone in the analgesic mechanism?
Glucocorticoids (Prednisolone) inhibit phospholipase A2, reducing the conversion of phospholipids to arachidonic acid in the analgesic mechanism.
What is the function of PGE2 (dinoprostone)?
PGE2 (dinoprostone) acts on the uterus and induces labour.
Which substances are derived from arachidonic acid in the analgesic mechanism?
Arachidonic acid is converted into endoperoxides, which then form prostacyclins (PGI2), PGF, PGE2, PGD2, and thromboxane A2 (TBX2).
What is the role of PGF 2a?
PGF 2a (prostanod) induces labour.
What are examples of biogenic amines in autacoids?
Examples of biogenic amines in autacoids include Histamine and Serotonin (5 HT).
What are prostonoids and what do NSAIDs target?
- Prostonoids include prostaglandins, thromboxanes, and prostacyclines.
- NSAIDs target prostonoids.
What is the function of PGI2/PG I 2 (prostacyclin)?
PGI2/PG I 2 (prostacyclin) is responsible for endothelium vasodilation.
What mainly triggers pain, fever, and inflammation?
Pain, fever, and inflammation are mainly triggered by autacoids. Autacoids are biological chemical substances produced by a wide variety of cells in the body that mediate pain.
What is the note regarding the ratio of TBX2 and PGs?
The ratio of TBX2 and PGs have effects if they are not balanced (if one is inhibited the other gets activated).
Where are prostonoids present and what do they offer?
- Prostonoids are present in the GIT, respiratory, reproductive, urinary, cardiovascular system.
- They offer possibilities for treatment within different body systems.
What are examples of polypeptides in autacoids?
Examples of polypeptides in autacoids are Angiotensin and Kinins (Bradykinin and Kallikidin).
What are the types of endogenous chemical substances the body uses to communicate?
The body communicates using:
- Neurotransmitters (nerve action) e.g. Acetylcholine, Serotonin
- Hormones (endocrine, systemic action)
- Autacoids are mediators of pain (local action at the site of injury e.g. histamine, serotonin, Bradykinin, prostaglandins)
How do autacoids act in the body?
They act with intense biological activity similar to hormones except they act locally near their site of synthesis and release with a brief duration.
What is acute pain and how is it characterized?
Acute pain typically has a sudden onset and recedes during the healing process. It can be considered as "good pain" as it serves an important protective mechanism.
How do drugs interact with the body's endogenous molecules?
Drugs mimic the body’s endogenous molecules and may work as agonist or antagonist to correct or alter the normal physiology of the body.
What is the primary effect of autacoids?
The effects of autacoids are primarily local, not systemic, and are referred to as local hormones.
How is chronic pain described and what are its characteristics?
Chronic pain can be considered "bad pain" because it persists long after recovery from an injury. It is often refractory to common analgesic agents (Opiates and NSAIDS) and can result from nerve injury (neuropathic pain).
How is pain frequently classified?
Pain is frequently classified as:
- Physiologic or acute pain (useful pain, acts as a warning when in contact with a stimulus e.g. inflammatory pain).
- Pathologic or chronic pain (caused by disease e.g. neuralgia; neuropathic pain due to nerve damage by a disease conditions such as Shingles/Herpes Zoster, diabetes).
What is neurogenic/neuropathic pain?
Neurogenic/neuropathic pain results from direct stimulation of nervous tissue of the peripheral or CNS. It is generally felt as burning or tingling sensation and often occurring in an area of sensory loss.
Where is localized pain felt?
Localized pain is felt at the site of injury.
How does visceral pain occur and where is it often referred?
Visceral pain results from the activation of nociceptors of internal organs, e.g., thoracic, pelvic, or abdominal viscera. It is felt as a poorly localized aching or cramping sensation and often referred to cutaneous sites as referred pain.
How can injury be caused according to the nociceptors information?
The injury may be from physical stimuli such as mechanical, thermal, or electrical stimuli, or from chemical stimuli such as the presence of a toxin or excess of a non-toxic substance.
Where are most nociceptors located?
Most nociceptors are either in the skin (cutaneous nociceptors) or the walls of viscera (visceral nociceptors).
What characterizes referred pain?
Referred pain is felt in a part other than that in which the cause that produced it is situated (e.g., angina pectoris).
What is the significance of pain as described?
Pain serves as a protective mechanism by inducing the sufferer to remove or withdraw from the source of pain. It is sensitized by pain receptors, known as nociceptors.
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