Nurs 605 Module 3 Flashcards
What is impetigo?
skin infection caused by staph aureus
usually persisting skin infection that worsens
What are the clinical manifestations of impetigo?
manifested by honey coloured, crusted lesions, can be bullous or non bullous
What is the first line treatment for impetigo?
Mupirocin 2% apply to affected areas TID x 7 days
Fucidin 2% apply to affected areas TID-QID x 7 days
What is the second line treatment for impetigo?
no reaction to topical agents
cloxacillin 500mg PO QID x 7 days
cephalexin 500mg PO QID x 7 days
Your patient presents with impetigo and has a beta lactam allergy. Topical treatments have not worked; what would be your choice of systemic antibiotic?
Erythromycin 500mg QID x 7 days or
Clindamycin 300mg TID PO x 7 days
What is folliculitis?
inflammation of the hair follicle
What are the clinical manifestations of folliculitis?
redness, tenderness to the hair follicle, can progress to a furuncle (large boil)
What is the first line treatment for folliculitis?
hot compresses and antiseptic cleanser/antibacterial ointment
What is the second line treatment for folliculitis?
if no success with compresses
Mupirocin 2% apply topically TID x 7 days or
Fucidin 2% apply topically TID x 7 days
What is the treatment for herpes simplex?
valcyclovir 1000mg PO BID x 7-10 days or acyclovir 400mg PO TID x 7-10 days
What is the treatment for herpes zoster?
valcyclovir 1000mg PO BOD x 7-10 days
acyclovir 400mg PO TID x 7-10 days
Describe the patho of Alzheimer’s disease (AD)
dementia without a neurological atencedant event such as stroke or brain trauma loss of localized neurons to the hippocampus and frontal cortex=loss of memory amyloid plaques (excess protein deposits) and neurofibillary tangles (phospholated form of proteins) are noted to the AD brain
What are the pharmacological options for Alzheimer’s disease and how do they work? What are the adverse effects?
anticholinesterase inhibtors and NDMA antagonists work to restore cholinergic functions
there is no neurodegerative aspects of these medications
memantine, tacrine, galantamine, donepezil are all meds of these classes
adverse effects: cholinergic effects; nausea, diarrhea, dry mouth abdominal pain, hepatotoxicity
Describe the patho of Parkinson’s disease (PD)
progressive neurological changes that primarily concern dopamine neurotransmitter
dopamine basal ganglia undergo changes that cause misfiring of muscarinic receptors
manifestations of PD including bradykinesia (loss of control of voluntary movement), PD gait, tremors, and muscle rigidity or stiffness
What are the pharmaceutical options of PD? How do they work? What are the adverse side effects
levodopa is the primary PD medication, used in conjuction with a decarboxylased inhibitor
works to decrease the deficiency of dopamine and block the firing of muscarinic receptors
adverse effects: long term- rapid fluctuating clinical states, dyskinesia -involuntary movements
acute side effects: nausea/anorexia; postural hypotension; changes in mental states ie) hallucinations
Describe “red flag” headaches that require urgent referral or work up
age <3-5 years
acute or new onset of headache
very pain, worse in their life-thunderclap headache, pressures
neurological changes-seizures
valsalva effect-headache worsesn with cough or sneezing
What are the pharmacological options to manage headaches
NSAIDs - ibuprofen, naproxen ASA acetaminophen opiods -codeine or tramadol ergot alkaloids (DEH) triptans-sumatriptan etc.
What is medication overuse headache? What is the solution?
MOH, secondary diagnosis to migraines rebound headaches when medications are not taken occurs with >15 uses of analgesics increasing frequency of headches decreased analgesic effectiveness sedation/drowsiness other CNS effects solution is to stop offending medication try DEH if not tried amytriptyline for preventative measures
Describe the pharmacology of phenytoin and its adverse effects
inhibits sodium and calcium channels acts on glutamate neurotransmitter used a preventative AED zero order kinetic drug increased concentrations can cause toxicity
primary adverse effect is gingival hyperplasia (overgrowth of the gums)
those on phenytoin should get dental exams q3 months
Describe the pharmacology of carbamezepine and its adverse effects
inhibits glutamate neurotransmitter
stops sodium and calcium channels from opening
increased risk of SJS and toxic epidermal necrolysis
teratogenic
sedating, ataxia
Describe the pharmacology of valproic acid and its adverse effects
acts on GABA neurotransmitter
assists in closing the sodium and calcium channels
hepatotoxicity
teratogenic, try to avoid in pregnant women
Describe the pharmacology of lamotrigine and its adverse effects
acts on glutamate neurotransmitter
inihibits sodium and calcium channels
SJS
sedation, ataxia
rash
Describe the pharmacology of diazepam and its adverse effects
benzodiazepine
used in acute seizure activity or status epilepticus
acts on GABA
sedating, abrupt discontinuation can cause withdrawl seizures
What is Steven Johnson’s Syndrome?
Type 4 mediated hypersensitivity
occurs with AEDs and other drugs
carbamezapine and phenytoin can cause this
starts off with flu like symptoms
involves 10% of body surface
painful, blister like rashese that break and create raw skin
What anti-epileptic drugs would you choose for someone who has grand mal seizures?
phenytoin, carbamenzapine, lamotrigine, valproic acid
What anti epileptic drugs would you choose for someone who has absence seizures?
valproic acid, diazepam
What are the reproductive risks for women taking AEDs?
some drugs are tetragenic, can cause neural tube defects
pregnant women must be taking 1-4mg of folic acid daily alongside their AED before pregnancy and after
valproic acid and carbamezapine are at greatest risk of neural tube defects
AEDs can reduce COC efficacy
backup methods such as condoms are advised
IUDs are a good option
What are the conditions for stopping AEDs?
no seizures in 2-5 years normal IQ normal neurological exam single type of seizure normal EEG taper over 3 months
Describe the pharmacokinetics of phenytoin. Why is it important to monitor trough levels of phenytoin in the clinical setting?
phenytoin is a zero order kinetic meaning changes in concentration of the drug does not effect its clearance
there is high risk of toxicity of phenytoin as it can accumulate in plasma
important to monitor trough levels in order to adjust phenytoin accordingly
