Non-Narcotic Analgesics I
WOTF is NOT a shared side effect of NSAIDs? Inhibition of COX 2 in gastric epithelial cells depresses mucosal cytoprotective PGI2 and PGE2 Bronchial asthma Increased reabsoprtion of K+ Inhibition of action of ADH Promote retention of salt and water by inhibiting reabsorption of chloride
A
What effect might Indomethacin have on Lithium dosing? Increase BA Decrease excretion Decrease BA A and B B and C
A and B
WOTF irreversibly inhibits COX activity? Naproxen ASA Celecoxib Acetaminophen Sulindac
ASA
T/F: The late phase of thermoregulatory response is mediated by ceramide release in neurons of the pre-optic area of the hypothalamus
False; initial phase
T/F: One dangerous side effect of NSAIDs is that they can shorten the gestation period
False; lengthen
T/F: NSAIDS decrease body temperature in the case of fever or overexertion
False; only fever
T/F: Most NSAids are competitive, irreversible, active site inhibitors of COX enzymes
False; reversible
WOTF can activate nociceptors? SATA Heat Acids Pressure Seizures
Heat,acid, pressure
Temperature regulation is present in which part of the brain?
Hypothalamus
WOTF is an immunologic mediator of inflammation IL-8 ICAM-1 C5a LTB4 Histamine
IL-8
In regards to fever pathophysiology, PGE2 triggers the brain to elevate body temperature by: SATA Increasing heat generation Decreasing heat generation Decreasing heat loss Increasing heat loss Stopping heat generation
Increasing heat generation, decreasing heat loss
WOTF drugs is an acetic acid derivative? SATA Acetylsalicylic acid Ketoprofen Indomethacin Aspirin Sulindac
Indomethacin and sulindac ASA and Aspirin are the same, both are salicylates Profens are propionic acid derivatives
WOTF are included in the inflammatory process? SATA Transient local vasoconstriction and decreased capillary permeability Infiltration of leukocytes and phagocytic cells Tissue degeneration and fibrosis Necrosis and peeling Pain
Infiltration of the cells and tissue degeneration and fibrosis. Supposed to be transient local VASODILATION and INCREASED capillary permeability.
_____ forms leukotrienes and lipoxins
Lipoxygenase
WOTF reduce the threshold of the stimulation of nociceptors leading to peripheral sensitization? SATA PGE2 PGD2 PGI2 PGF2-alpha PGE1
PGE2, PGI2
WOTF is NOT a result of autoimmune targeting of normal joint proteins? Release of cytokines Release of TNF Release of growth factors Release of PGF2 alpha Release of interleukins
PGF2 alpha All the others induce COX2 expression
WOTF is NOT a traditional NSAID category? Salicylates Propionic acid derivatives Acetic acid derivatives Sulfonamide derivatives Fenamate derivatives
Sulfonamide
T/F: COX-2 increases PGE2 biosynthesis which stimulates pain pathways
True
T/F: Chronic uses of high doses of NSAIDs can lead to renal failure
True
T/F: NSAIDs can promote hyperkalemia through inhibition of prostaglandin induced renin.
True
T/F: Oxygen radicals and nitric oxide serve as mediators of the inflammatory process
True
T/F: Traditional NSAIDs inhibit both COX 1 and 2
True
T/F: bradykinin is a chemical mediator of inflammation
True
WOTF inflammatory mediators increase the sensitivity of nociceptors and potentiate pain perception? SATA Bradykinin Hydrogen ions serotonin leukotrienes prostaglandins
all
WOTF are chemical mediators of inflammation? SATA histamine 5HT prostaglandins Leutrotrienes DA
all but DA
WOTF may cause fever? SATA Infection Inflammation Headache Graft rejection Malignancy
all but headache
WOTF are Non-Narcotic analgesics? SATA Lidocaine Naproxen Tylenol Ergot Alkaloids Sumatriptan
all but lidocaine
Eicosanoids are derived from ____
arachidonic acid
Chronic, systemic, autoimmune and inflammatory disease that primarily affects joints (also affects skin, lungs, muscle and CVS)
arthritis
WOTF is a selective COX2 inhibitor? Celecoxib Piroxicam Naproxen Meloxicam Ibuprofen
celecoxib
WOTF NSAIDs can cause stroke and MI? Ketoprofen Naproxen Celecoxib Acetominophen Motrin
celecoxib is cox 2 selective nsaid
_____ forms epoxyeicosatetranoic acids
cytochrome P450 epoxygenase
T/F: Neuropeptides such as substance P and calcitonin gene-related peptide may be involved in the inhibition of pain.
false; generation of pain
T/F: Use of NSAIDs in early pregnancy can increase the risk of postpartum hermorrage
false; late
Primary afferent fibers that sense pain:
nociceptors
Arachidonic acid is released from phospholipid membrane by _______
phospholipase A2
WOTF is a chemotactic mediator of inflammation? Bradykinin IL-1 TNF ICAM-1 PAF
platelet activating factor
WOTF is NOT a shared use of NSAIDs? Analgesic Closing patent ductus arteriosus in neonates Skin graft rejection Antipyretics Cardio-protection
skin graft
T/F: COX 1 is a constitutive enzyme involved in physiologic activities such as vascular homeostasis, maintenace of renal and GI blood flow
true
T/F: NSAIDs can caused inhibition of PG-induced inhibition of gastric acid secretion
true
T/F: a shared side effect of NSAIDs is vasomotor rhinitis
true
T/F: Normal use of NSAIDs have no effect on renal function OR blood pressure in normal human subjects
true lol
In rheumatoid arthritis, __-LOX derived leukotrienes activate the surrounding endothelium to recruit inflammatory cells 1 LOX 3 LOX 5 LOX 15 LOX B and C
5 LOX
SATA: Inflammaroty response can be caused by: Infectious agents Noxious chemicals Thermal or physical trauma Antigen-antibody interactions Ischemia
All
WOTF Drugs will interact with NSAIDs? SATA Warfarin Sulfonylurea hypoglycemics methotrexate Lithium Lisinopril
All
WOTF prostaglandins contribute to central sensitization? PGE2 PGD2 PGI2 PGF2-alpha PGE1
All but PGE1, idk what it even does
Which of the following are clinical sides of inflammation? SATA Calor Dolor Rubor Tumor Stupor
All but stupor
WOTF are pharmacological actions of NSAIDS? SATA Decrease in the release of vasodilator PGE2 and PGI2 means increase in vasodilation and indirectly less edema Inhibition of the migration of leukocytes and macrophages into inflammation sites Stabilization of lysosomal membranes Effective against pain of moderate to high intensity Analgesic effect when inflammation has caused peripheral and/or central sensitization of pain perception
B, C, E
________ forms prostaglandins and thromboxanes, as well as prostacyclin
Cyclooxygenase
WOTF processes is indicated in the late phase thermoregulatory response? SATA Mediated by induction of COX-2 and formation of PGE2 PGE2 acts on EP receptors on thermosensitive neurons which triggers the hypothalmus to elevate body temperature Ceramide release in neurons of the pre-optic area of the hypothalamus Mediated by induction of COX-1 and formation of PGE2 PGE2 acts on EP receptors on thermosensitive neurons which triggers the prefrontal cortex to elevate body temperature
First two
macrophages release collagenase and proteases while _____activity leads to the formation of the immune complex
lymphocyte
