Exam Flashcards
(44 cards)
Paresthesia
Any abnormal sensations: burning, tingling, aching, cold sensation,
Dysesthesia
Painful paresthesia
Allodynia
Pain caused by a non-painful stimulus
Hyperalgesia
Hypersensitivity to the pain stimulus, causing more pain then it should
4 phases of nociception
Transduction- transmitting action potential
Transmission- stimuli passing to brain
Perception- processing or experiencing the pain
Modulation- how each person uniquely copes with pain
Strong opioid agonists
Morphine
Fentanyl
Meperidine
Methadone
Hydromorphone
Moderate to strong opioid agonists
Codeine
Oxycodone
Hydrocodone
Tapentadol
Morphine
Mechanism of action: endogenous opioid at the mu receptors
Can cause drowsiness, reduction in anxiety
Nursing considerations of morphine
Resp depression
Orthostatic hypotension
Cough suppression
Emesis- nausea
Birth defects
Meperidine function
Strong opioid
It is not preferred anymore because of the short half-life, lots of drug interactions
Methadone
Strong opioid
Pain and treat opioid addiction
-increased QT prolongation
-very long acting- up to 72 hours
Codeine function
Less harmful effects to strong opioids but doesn’t cause as much effects
Can combine with acetaminophen
-cough suppressant
Pentazocine
Agonist antagonist med- mu antagonist, kappa agonist
Not as much risk for abuse because less affect and less consequences
Increases cardiac output- avoid in MI patients
Tapentadol
Moderate to strong opioid
Blocks reuptake of norepinephrine a little bit so there is less constipation than other opioids
How do opioids affect mu and kappa receptors
Activate mu and kappa receptors
Buprenorphine
Partial mu agonist and kappa antagonist
Used for opioid use disorder
Prolongs QT interval
Tramadol- more important
Analog of codeine
Weak agonist activity at mu receptors
Side effect of seizures
-hard to wean- 5mg tapering opposed to morphine tapering at 0.5 intervals
Acetaminophen
Non opioid
Works at liver level so can’t have alcohol with
NSAIDS
Non steroid anti inflammatory
Can’t use with kidney issues
Polyphagia
Excessive hunger- high glucose but body not able to take that glucose for energy
Polydipsia
Excessive thirst- such high glucose in blood so water is pulled from cells stimulating thirst
DKA
Diabetic ketoacidosis
Primarily in T1D but can be T2 in extreme stress
Develops over hours to days
Presence of ketones in urine and blood
Polyuria, polydipsia, dehydration
Later manifestations severe hypotension
Kaussmaul’s respirations and fruity odour on breath
Electrolyte imbalances- hyponatremia and hypokalemia