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five cardinal signs of inflammation
rubor (redness)
calor (heat)
dolor (pain)
tumor (swelling)
functio laesa (loss of function)
acute inflammation
caused by bacterial infections and trauma
start with physical assessment!
rice - rest, ice, compress, elevation
heat 24-48 hrs post-injury
three phases of acute inflammation
vascular
cellular
opsonization
stage 1 - vascular phase
small moment of vasoconstriction
rapid vasodilation of arterioles and venules = redness + pain
fluid into tissues = swelling, pain, and tissue damage
increasing blood viscosity → increases clotting = stops bleeding
neutrophils
first responders
phagocytosis
treats bacterial infections
eosinophils
treats allergic and parasitic infections
weak phagocyte
controls inflammatory response
basophils and mast cells
responds to allergic reactions where IgE antibody is present
releases histamine
monocytes/macrophages
helps with chronic inflammation → longer lasting than neutrophils
phagocytosis
regeneration of tissues through vasoactive mediators (ex. prostaglandins, cytokines, gf)
stage 2 - cellular phase
wbc moves from tissues to site of injury
margination: tumbling of wbc
adhesion: sticking of wbc to wall of injury site
transmigration: movement of wbc to isf
stage 3 - opsonization
inflammation + phagocytosis
chronic inflammation
caused by: viral infections and autoimmune disorders
symptoms: tissue destruction, scarring, diminished mobility, loss of function
local inflammation
cardinal signs and exudate
types of exudate
serous (watery)
hemorrhagic (bloody)
purulent (pus)
fibrinous and membranous (sticky meshwork)
systemic inflammation
fever or hypothermia
tachycardia/pnea
leukocytosis
malaise + nausea
anorexia
left shift = high release of immature wbc from bone marrow
pus
wbcs
tissue debris
proteins
abscess
localized area of inflammation with pus contained within neutrophil
ulceration
epithelial layer becomes necrotic
cox-1
physiologic prostaglandins
protects stomach lining = decreases gastric acid + increases mucus
platelet aggregation
renal perfusion
relaxes smooth muscle = vasodilation and bronchodilation
cox-2
physiological prostaglandins
vasodilation and inflammation
edema and pain
leukocytosis → releases inflammatory cytokines
non-selectives nsaids
inhibit cox-1 and cox-2
decreases inflammatory prostaglandins = lowers pain and inflammation
stops stomach lining protection
lowers renal perfusion (kidney issues)
selective nsaids
inhibits cox-2
lowers inflammation
viruses
smallest pathogen
cannot replicate outside the host
some remain latent until triggered by stress/hormone changes (ex. herpes and cold sores)
fungal infections
found everywhere
opportunistic: causes illness when host is compromised
antibiotic resistance
genetic mutation
modification of target molecule
high efflux of antibiotic
antibiotic resistance caused by
treat the bug with the right drug
maintain adequate blood levels
trough: lowest concentration of antibiotic in blood
check before next dose
peak: highest concentration of antibiotic in blood
check after dosage
antibiotic resistance tips
finish antibiotics
draw blood culture before antibiotics
assess for suprainfection, toxicity, hypersensitivity reactions
take oral antibiotics on empty stomach and do not co-administer with other meds
adverse reactions of antibiotics
superinfection: new infection caused by resistant organism which can kill good bacteria
steven johnson syndrome: life threatening skin reaction thru blisters and sloughed skin
red man syndrome: antibiotic given too quickly → flushing, pain, redness at insertion site (slow down infusion!)
antimicrobial stewardship
using antibiotics correctly and only when needed
ex. pt asks for antibiotics for viral cold
you do not give bc antibiotics are only for bacterial infections
sirs
systemic inflammatory response syndrome
temp can be too high or too low
wbc can be too high or too low
high hr + rr
sepsis
sirs and infection
two or more sirs symptoms
confirmed or suspected infection
severe sepsis
end organ damage and high serum lactate levels
septic shock
end organ damage and high serum lactate levels
main one - hypotension
why is urine output important in sepsis?
decreased urine output can indicate poor renal perfusion
first priorities when a patient is severely deteriorating from sepsis
abc’s
a - hi-flow supplement
b - ventilation
c - 30 ml/kg of crystalloids
but if patient is unresponsive cab
what should happen before starting broad-spectrum antimicrobial therapy when possible?
obtain cultures first
major nursing priority in sepsis
maintain oxygenation and adequate tissue perfusion
older adult considerations for sepsis
uti is more common
check for cognitive and behavioral changes
do not rely on the presence of fever to indicate infection in older adults
what medications may be needed if hypotension persists despite fluid resuscitation?
vasopressin - norepinephrine or dopamine
disseminated infection
infection that spreads beyond the original site
hai
health associated infection
clabsi - central line-associated bloodstream infection
cauti - catheter associated urinary infection
surgical site infections
ventilator-associated events
common pathogens associated with hais
mrsa and c. diff
sources of infection
endogenous - from self
exogenous - from outside
latrogenic - from procedure
nosocomial - from hospital post leaving (24-48 hrs)
what is the most important basic intervention for preventing infection transmission?
hand hygiene
three transmission-based precautions
airborne
contact
droplet
airborne precautions
for small droplets in the air
ex. tb, rubeola (measles) and varicella (chicken pox)
ppe, mask, gloves
contact precautions
through direct and indirect contact
ex. hep-A, herpes, mrsa, and vre
droplet precautions
no gloves needed
ex. influenza, pertussis, bacterial, meningitis, mumps, pneumonia
what virus causes covid-19?
sars-cov-2: single stranded rna corona
comes from nasal, bronchial epithelial cells, pneumocytes
droplets and close face-to-face transmission
can covid be transmitted before symptoms appear?
yes
what test is used to detect sars-cov-2 rna?
pcr
what is a major priority when caring for a patient with severe covid?
supporting oxygenation and respiratory function
what respiratory support may be needed for severe covid?
oxygen through a nasal cannula and, if necessary, invasive mechanical ventilation
lower uti
bacterial infection of the lower urinary tract
bacteria colonize the urethra into the bladder
symptoms - nocturia, suprapubic pain, and bladder spasms
cystitis
inflammation/infection of the bladder
urethritis
inflammation/infection of the urethra
can be associated with stis
most common cause of uti
e. coli
gram-negative enteric bacteria
major risk factor for a catheter-associated uti
indwelling urinary catheter
what urine findings can occur with a uti?
cloudy or foul-smelling urine and hematuria
what can flank or lower back pain suggest?
urinary tract involvement beyond simple bladder irritation, especially if infection is progressing upward
what diagnostic test is commonly used to evaluate a uti?
urinalysis
what should patients generally be encouraged to do during a uti?
drink more and pee more
what should patients avoid while experiencing uti symptoms?
caffeine
coffee, tea
alcohol
citrus
what is phenazopyridine used for?
temporary burning relief
used for 1-2 days
how often should a patient empty the bladder?
every 4 hours while awake
before and after intercourse
what intervention first?
physical assessment
culture and sensitivity
broad spectrum antibiotics until results showing specific antibiotics
what happens as the cd4 count decreases?
immune function becomes impaired and the risk of opportunistic infections increases
hiv stages
acute infection
asymptomatic infection
symptomatic infection/aids progression (200 cells/µl)
what can acute hiv infection look like?
flu-like symptoms occurring about 2–4 weeks after infection
what are examples of manifestations associated with hiv/aids?
oral candidiasis and kaposi sarcoma lesions
what is art?
antiretroviral therapy
decrease viral load, maintain/increase cd4 count, prevent hiv-related symptoms
what does viral load tell you?
amount of hiv circulating in the blood
older adult considerations for hiv
adults are more likely to be infected and die at age 65
intention healings
primary intention - wound healing through sutures
secondary intention - wound left open bc edges cannot be brought tg
tertiary - wound is intentionally left open for a few days to clear out any infection or dirt, and is then surgically closed later
wound healing stages
inflammatory phase
immediate
hemostasis + scab forms
proliferative phase
2-3 days post-injury lasts 3 weeks
fibroblasts = making new tissue
remodeling
3 weeks - 6 months post-injury
remodels scar
development of immune response
develops for fetuses at 5-6 weeks
secondary lymphoid organs developed at birth
IgA and IgM reach adult levels at age 1
elderly immune system
slow ability to adapt to environmental stress
decrease of thymus gland
t cells
transmission of aids
sex
blood to blood contact
perinatally - mother to infant
innate vs adaptive
innate - phagocytes
adaptive - lymphocytes
cells that recognize and respond to foreign antigens (ex. disease)
humoral immunity
medicated by molecules in blood
b lymphocytes (bone marrow)
defense against extracellular microbes
cell-mediated immunity
mediate by specific t lymphocytes
made in thymus
defense against intracellular microbes ex. viruses