Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
116 Cards in this Set
- Front
- Back
TB meds - 1st line
|
isoniazid
rifampin pyrazinamide ethambutol previously also streptomycin |
|
AE of izoniazid (INH)
|
peripheral neuropathies, so can give with vitamin B (pyridoxine)
|
|
what determines most whether a course of tb therapy has been completed
|
doses taken, not length of time
|
|
what med can be used as prophylaxis for TB
-and what to monitor monthly |
INH isoniazid for 6 to 12 months. monitor BUN , liver enzymes, and creatinine levels monthly
|
|
classes of TB range from
|
class 0 to class 5
-no exposure to infection to -suspected disease; diagnosis pending |
|
preferred treatment for LATENT infections
|
9 months of INH or 4 months of RIF
(the 2 months RIF plus PZA is no longer reccommended bc of liver injury) |
|
clinical manifestations of TB
|
persistent low-grade fever
anorexia weight loss night sweats fatigue cough sputum production non-resolving bronchopneumonia (dyspnea, hemoptyosis, productive cough) |
|
assessment of resp fn of TB patients may show
|
-breath sounds diminished bronchial sounds, crackles
-fremitus -egophony -dullness on percussion |
|
TB medication instructions to patient
|
on empty stomach or at least 1 hour before meals, although frequently results in GI upset
- |
|
isoniazid education
|
-avoid tyramine and histamine, (would result in decreased anti-TB effectiveness as well as HA flushing hypotension, lightneadedness, palpitations, diaphoresis)
-avoid alcohol (would increase risk hepatitis) -pyridoxine as prophylaxis for SE neuritis |
|
rifampin education
|
can increase metabolism of beta blockers, oral anticoagulants, digoxin, qunidine, corticosteroids, hypoglycemic agents, oral contraceptives, theophylline, verapmil
-may discolor urine and contact lenses |
|
general SE of anti-TB meds
|
hepatitis, neurologic changes (hearing loss, neuritis), and rash
|
|
what to monitor to detect changes in liver and kidney fn in TB patients taking meds
|
liver enzymes, BUN and creatinine levels
|
|
what to monitor to eval anti-TB treatment effectivness
|
sputum culture
|
|
miliary TB
|
spread or dissemination of TB to non-pulmonary sites. the result of invasion of the bloodstream by the tubercle bacillus (Ghon tubercle)
|
|
where can TB spread to
|
lungs, spleen, liver, kidneys, meninges, and other organs
|
|
meningitis is...
|
an inflammation of the pia mater, the arachnoid, and the CCF-filled subarachnoid space
|
|
septic meningitis is bacterial and the 3 most causative organisms are...
|
-streptococcus pneumoniae (pneumococcal meningitis)
-Neisseria meningitidis (college - meningococcal meningitis) -Haemophilus influenzae (most predominant in 3mo to 3yrs but is decreasing) |
|
risk factors for bacterial meningitis
|
-winter and early spring
-tobacco use and viral URI (increase amt of droplet production) -otitis media and mastoiditis (bacteria can cross the epithelial membrane and enter the subarachnoid space) -immunosuppressed people |
|
transmission of meningitis
|
-through bloodstream as a consequence of other infections
-direct spread after traumatic injury to invasive procedures -N. meningitidis is concentrated in the nasopharynx and is transmitted yb secretion or aerosol contamination |
|
CSF studies of bacterial meningitis demonstrate
|
decreased glucose
increased protein levels increased WBC count increased CSF pressure |
|
complications of meningitis
|
visual impairment, deafness, seizures, paralysis, hydrocephalus, septic shock
|
|
frequent initial symptoms of meningitis
|
headache and fever
|
|
clinical manifestations of meningitis in adults including the 4 classic signs
|
#1 - nuchal rigidity
#2 - positive Brudzinski's sign #3 - positive Kernig's sign #4 - photophobia -headache and fever that usually remains high -rash in 50% pt with N. meningitidis (petechial with purpuric lesions to large areas of ecchymosis) -disorientation and memory impairment -w progression - lethargy, coma -w S. pneumonae - 30% with seizures -increased ICP 2 to accumulation of purulent exudate - |
|
Kernig's sign of meningitis
|
When the patient is lying with the thign flexed on the abdomen, the leg cannot be completely extended
|
|
Brudzinski's sign of meningitis
|
When the patient's neck of flexed, flexion of the knees and hips is produced; when the lower extremity of one side is passively flexed, a similar movement is seen in the opposite extremity.
-more sensitive indicator than Kernig's sign of meningitis |
|
initial signs of increased ICP
|
decreased LOC and focal motor deficits
|
|
in 10% of patients with meningococcal meningitis, an acute fulminant infection occurs, producing signs of....
|
overwhelming septicemia: an abrupt onset of high fever, extensive purpuric lesions over the face and extremities, shock, and signs of DIC. death may occur within a few hours
|
|
are vaccines available for meningitis?
|
yes
|
|
meds for meningitis prophylaxis if you come in contact with it or live in the same HH
|
#1 - rifampin (Rifadin) within 24 hours
-or Cipro and Rocephin |
|
medical treatment of meningitis (meds and such)
|
-high dose IV antibiotics
---penicillin and chloramphenicol to cross BBB, then something more specific to culture -IV dexamethasone (Decadron) - corticosteroid -IV fluids for dehydration and shock -anticonvulsants - Dilantin, phenobarbital - for seizures |
|
nursing interventions for meningitis
|
admin fluids, antibiotics, corticosteroids, and anticonvulsants
-airborne precaution until 24 hours after initiation of Abx -oral and nasal discharge is infectious -continuous neuro status and VS -pulse ox and ABG values to quickly ID need for resp support if increasing ICP compromises the brainstem - w possibly mech ventilation -reduce body temp as quickly as possible -protect from injury 2 seizures -watch for SIADH |
|
when a patient is on corticosteroids, closely monitor...
|
blood glucose and serum potassium levels
|
|
clinical manifestations of meningitis in a child, with the most common first symptom
|
#1 generalized seizure
-abrupt onset fever, chills, HA, irritability, agitation, photophobia, positive Brudzinki's and Kernig's signs, resists ANY flexion of the neck |
|
opisthotonos def
|
head is drawn into extreme over extension and the child will resist ANY flexion of the neck. occurs in meningitis
|
|
clinical manifestations in infants and young children of meningitis
|
poor feeding and sucking, vomiting, irritability, high pitched cry, generalized seizures, bulging fontanelles, ?nucchal rigidity
|
|
clinical manifestation of meningitis in a neonate
|
difficult to diagnose and can be deadly, so if fever assume meningitis
-fever, weak and sucking sucking, poor muscle tone, poor cry, seizures, irregular respirations, bulging fontanelle |
|
HSV-1 viral encephalitis cause
|
by following a retrograde intraneoronal path the brain, may also be caused by a reactivated latent virus
|
|
HSV-1 encephalitis causes...
|
inflammation and hemorrhagic necrosis of the temporal lobe
|
|
initial symptoms of HSV-1 encephalitis
|
fever, headache, confusion
-also FOCAL neurologic symptoms that reflects the area of cerebral inflammation and necrosis |
|
diagnosis of HSV-1 encephalitis
|
-MRI - edema in temporal lobe
-EEG - high voltage spikes from temporal lobe -lumbar puncture - high opening pressure and low glucose and high protein levels -viral cultures are almost always NEGATIVE |
|
medical treatment of HSV-1 encephalitis
|
-acyclovir (Zovirax) - early administration. tx for 3 weeks to prevent relapse. slow IV admin over 1 hours to prevent crystallization of the med in the urine. dose decreased if renal insufficiency
|
|
AE of acyclovir (Zovirax) therapy
|
renal toxicity, so monitor labs and urinary output
|
|
arthropod-borne virus encephalitis
|
most common is West Nile and then St. Louis
|
|
patho of arthropod-borne virus encephalitis
|
viral replication occurs at the site of the mosquito bite. immune response attempts to control viral replication. if inadequate, viremia will ensue. virus gains access to the CNS, resulting in encephalitis. spreads from neuron to neuron. meningeal exudates compound the clinical presentation by irritating the meniges and increasing ICP
|
|
clinical manifestations of West Nile virus encephalitis
|
-only 1 in 150 develop severe illness including encephalitis
-begins with early flu-like sypmtoms, but specific neurologic manifestations depend on the viral type -a macuopapular or morbilliform rash on the neck, trunk, arms and legs -flaccid paralysis -can result in Parkinsonia-like moviements, reflecting inflammation of the basal ganglia -seizure are a poor prognostic indicator but are more common in St. Louis type |
|
diagnosis of West Nile virus
and incubation period |
MRI - inflammation in the periventriular area
CSF eval - IgM antibodies to West Nile Virus -bc viremia is brief, serum cultures are not useful -3 to 14 days |
|
in general, what do PCRs show?
|
viral DNA
|
|
medical management of arthropod borne encephalitis
|
no specific medication
-control seizures and increased ICP |
|
standard antifungal for C. neoformans
|
amphotericin B
|
|
common Adverse rxns to amphotericin B
|
fever, chills, body aches, hypotension - can give Benadryl and Tylenol 30 min before to prevent these flu-like SE
-renal insufficiency is a serious reaction |
|
SE of fluconzole
|
N/V, transient increase in liver enzymes
|
|
food born organisms that can enter the bloodstream, causing bacteremia, and disseminate to other organisms
|
E.Coli
Salmonell Shigella |
|
if initial smear results reveal ________, antibiotic therapy is instituted
|
gram-negative organisms
|
|
salmonellosis - causative organism?
|
salmonella species, especially Enteritidis salmonella,
these are gram negative bacilli |
|
salmonella species are found in
|
-50% commercailly available chicken products
-eggs -raw milk -occasionally beef |
|
about 40% of deaths caused by Salonella occur in
|
nursing home residents
|
|
clinical manifestation of Salmonella infection
|
-? asymptomatic carrier state, gastroenteritis, or systemic infection
-diarrhea with gastroenteritis is common -less common is bacteremia and disseminated disase accompanied by diarrhea |
|
transmission of Salmonella species
|
-foods (chicken, eggs, raw milk, occasionally beef)
-infected person (stool, bedpans, other objects, hands) |
|
treatment of Salmonella infection
|
-if only gastroenteritis - usually not treated because antiobiotic use may increase the period of time that the patient carries the bacteria while not improving the clinical outcome
-if systemic - antimicrobial therapy |
|
onset of Salmonella infection
|
8-48 hours after ingestion
|
|
giardia lamblia - causative organism?
|
protozoal parasite Giardia lamblia
|
|
transmission of giardia lamblia
|
food or drink that is contaminated with viable cysts of the organism Giardia lamblia,
-often when traveling to endemic areas or by drinking contaminated water from mountain streams in the US -also close contact, like day care settings -also possible is sexual contact transmission |
|
clinical manifestations of Giardia lamblia
|
-often infection goes unnoticed
-more easily recognized in children -in extreme cases - --abdominal pain --chronic diarrhea (usually containing mucus and fat, but not blood) --exam of stool reveals the trophozoite or cyst stages of the parasitic life cycle |
|
treatment of Giardia lamblia
|
metronidazole (Flagyl) is common, but success rates inconsistent
|
|
education of Giardia lamblia
|
-easily transmitted in family or group settings
-personal hygiene measuress -caution in travel or camp settings where water is not treated |
|
Shigella infection / shigellosis / bacillary dysentary - causative organism?
|
Shigella species, a gram-negative organism
|
|
what does the Shigella species do?
|
invades the lumen of the intestine and causes disease and severe watery (possibly bloody ) diarrhea
|
|
Shigella is aka
|
bacillary dysentary
|
|
onset of shigella infection
|
12-48 hours after ingestion
|
|
transmission of shigella infection
|
through the fecal-oral route, with easy transmission from one person to another
|
|
shigella exhibits...
|
high levels of virulence - infection with a very small number or organisms can cause disease
|
|
repeat of shigella transmission
|
fecal oral route
-easy transmission -high levels of virulence (small number of organism can cause disease) -occurs easily with improper hygiene so affects children more |
|
shigella in the very young can be complicated by ...
|
pulmonary or neurologic symptoms
|
|
treatment of shigella
|
antimicrobial therapy administered early.
-then more specific therapy when final microbiologic testing reveals the organism's sensitivity |
|
what is the most common aerobic organism colonizing the large bowel?
|
E. coli
|
|
patho of E.coli
|
certain strains of E. coli with increased virulence have been responsible for significant outbreaks of diarrheal disease in recent years. called enterotoxigenic E. coli (ETEC) because of production of enterotoxins
|
|
enterotoxigenic E. coli strains .. clincial manifesations..
|
cholera-like disease
-rapid, severe dehydration and increased risk for death |
|
transmission of E. coli
|
ingestion of undercooked beef. lives in the intestines of cattle and can be introduced into meat at the time of slaughter
|
|
measures to control nausea
|
-antiemetic
-if mild - take sips of weak tea, carbonated drinks, or tap water -after N/V subsides, clear liquids for 12 to 24 hours, and the diet is gradually progressed to a low-residue, bland diet |
|
what is the most dangerous form of food poisoning?
|
botulism caused by C. botulinum,
|
|
botulism - causative organism
|
clostridum botulinum
|
|
what does C. botulinum do in the body
|
blocks Ach-containing vesicles from fusing with the terminal membranes of the motor-neuron end-plate, resulting in a flaccid paralysis
1. release of neurotoxin 2. bilateral cranial nerve involvement 3. respiratotry impairment |
|
onset of botulism
|
12-48 hours
|
|
transmission of botulism
|
direct contact
-not contagious through P2P contact |
|
precautions necessary with botulism patient
|
standard precautions
|
|
Gi manifestations of botulism
|
-abdominal cramps
-nausea -vomiting -?diarrhea |
|
if inhaled, manifestations of botulism
|
-fever
-symmetric descending flaccid paralysis with multiple cranial nerve palsies -classic - diplopia, dysphagia, dry mouth, lack of fever, alert mental status -possible? - ptosis of the eyelids, blurred vision, enlarged sluggish pupils, dysarthria, dysphonia |
|
treatment of botulism
|
trivalent equine antitoxxin to minimize subsequent nerve damage. 2% rate of anaphylaxis to this so have benadryl and epinephrine on hand
|
|
Legionnaire's disease def
|
a multisystem illness that usually includes pneumonia
|
|
Legionnaire's disease - causative organism?
|
Legionella pneumophilia
|
|
transmission of Legionnaire's disease
|
-aerosolized route from an environmental source to a person's respiratory tract
-NOT from person to person soil and stagnant water (small streams, hot tubs, fountains), in air conditioning, respiratory therapy equipment -more common in hospitals due to immunosuppressed patients and complex plumbing systems |
|
mortality rate Legionnaire's disease
|
12%
|
|
risk factors Legionnaire's disease
|
-immunosuppression
-older age -diabetes -alcohol abuse -smoking -other pulmonary disease |
|
clinical manifestations of Legionnaire's disease
|
-early - malaise, myalgias, HA, dry cough
-increasing pulmonary symptoms - including productive cough, dyspnea and chest pain -usually febrile up to 103 F -diarrhea and other GI symptomes -if severe - multiorgan involvement and failure -culture of lung tissue to detect antigen or antibody |
|
incubation period Legionnaire's disease
|
2-10 days
|
|
most frequently used test for Legionnaire's disease
|
urinary antigen, but detects only one subgroup of the several species, so use multiple tests
|
|
medical treatment of Legionnaire's disease
|
#1azithromycin (Zithromax)
-erythromycin -clarithromycin -levofloxacin -IV fluids -isolation not required, no P2P transmission |
|
leprosy is aka
|
Hansen's disease
|
|
leprosy - causative organism?
|
mycobacterium leprae
|
|
transmission of leprasy
|
skin to skin
skin to mucous membranes |
|
patho of leprasy
|
gets into body and attacks the skin and peripheral nerves. 3 kinds of lesions may form
|
|
3 kinds of lesions of leprosy
|
tuberculoid lesions
lepromatous lesions borderline lesions |
|
tuberculoid lesions are..
|
colorless or slightly reddish brown
-loss of sensation usually in area around lesion |
|
lepromatous lesions
|
grow all over the body, are easily infected, led to deep ulcers and scars
-may lead to amputation bc of decreaed perfusion and necrosis |
|
borderline lesions
|
cross between tuberculoid and lepromatous lesions
|
|
medical treatment of leprosy
|
dapsone w rifampin
or other anti-TB drugs to decrease risk of resistant strains |
|
when are leprosy patients no longer contagious?
|
when they start abx
|
|
rabies definition
|
infection of nervous system by virus that is fatal
|
|
transmission of rabies
|
saliva of infected mammal through bite or skin abrasion, usually from wild or nocturnal animals
-bats are a big problem |
|
incubation of rabies
|
1-3 months, if bitten, NEED vaccinations shots
|
|
if rabies symptoms appear,
|
it will be fatal
|
|
clinical manifestations of rabies
|
-will be fatal
-period of general malaise, sore throat, -followed by excitement, maniacal behavior, hypersensitivity, and attempt to swallow lead to spasms, which leads to drooling (hydrophobic phase) |
|
2 immunizations to get if bitten for rabies prophylaxis
|
-passive immunization-human rabies immune globulin (HRIG)
-active immunization-human diploid cell rabies vaccine (HDCV) |
|
human rabies immune globulin (HRIG)
|
ASAP after exposure
-short -term passive immunity -1 shot dose |
|
human diploid cell rabies vaccine (HDRV)
|
-dose 1 at same time as HRIG
-followed by 4 more injections at days 3, 7, 14, and 21 |