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296 Cards in this Set
- Front
- Back
general pathophysiology of burn injuries
|
thermal insult -> vascular damage (release of vasoactive substances)
*subsequent inflammatory rxn, release of inflamm. mediators *increased vascular permeability, third spacing of fluids |
|
three features seen grossly in burn injury?
|
1. zone of coagulation (center of injury, non-viable tissue)
2. zone of stasis (marked inflammation, border zone of viability and vascular integrity) 3. zone of hyperemia (viable tissue surrounding injury) |
|
describe 1st - 4th degree burns
|
1. 1st degree - pain, erythema, reddening of skin surface
2. 2nd - pain, skin blisters 3. 3rd - destruction and ulceration of skin, may be white, leathery, often no pain in center 4. deep injury to SQ tissue |
|
what is the continuum of heat injury?
|
heat cramps -> heat exhaustion -> heat stroke
|
|
medications that predispose to heat injury?
|
B-Blockers
anticholinergics lithium diuretics TCAs antihistamine |
|
why are antipyretics NOT indicated in heat stroke?
|
increased temp. is not due to hypothalamic dysfunction
|
|
manifestations of heat stroke in:
1. muscles 2. kidneys 3. coagulation ability 4. pulmonary 5. hepatic |
1. rhabdomyolysis, elevated CPK
2. insufficiency, acute renal failure 3. DIC, hemorrhage 4. tachypnea, pulmonary edema, ARDS 5. elevated AST, ALT |
|
treatment of heat stroke?
|
*rapid cooling (ice packs in groin, axillae, neck - NOT on limbs)
*rehydration *O2 |
|
4 degrees of frostbite?
|
1st - edema, erythema, decreased sensation
2nd - clear blister formation 3rd - necrosis of skin, blood filled blisters 4th - skin and soft tissue gangrene |
|
treatment for frostbite?
|
*rewarming ASAP
*elevation to reduce edema *protect with sterile dressings, silver sulfadiazine ointment *oral and topical corticosteroids to decrease release of inflammatory mediators |
|
definition of hypothermia?
|
body temp <95 deg. F
(body heat loss exceeds production) |
|
mild hypothermia is defined as?
|
body core T 33-35 deg. C
|
|
s/s seen in mild hypothermia?
|
*cold, shivering
*peripheral vasoconstriction *lethargy, confusion, impairment of judgement *decreased fine motor skills |
|
moderate hypothermia is defined as?
|
body core T 28-32 deg. C
|
|
s/s of moderate hypothermia?
|
*increasing CNS depression, stupor
*cardiorespiratory depression (hypotension, bradycardia, bradypnea) *peripheral vasoconstriction *risk of atrial & ventricular arrythmias |
|
severe hypothermia is defined as?
|
core body T <29 deg.C
|
|
s/s of severe hypothermia?
|
*loss of thermoregulatory control
*rigidity *apnea *pulselessness *unresponsive, fixed pupils *arreflexia |
|
treatment of hypothermia?
|
rapid rewarming
bretylium for arrythmias |
|
describe the ECG changes seen in severe hypothermia
|
Osborne waves (J waves)
|
|
what is the difference between an:
1. exogenous infection 2. endogenous infection 3. toxin-induced skin disease |
1. MC - cuts, bites, skin disease, burns
2. skin manifestations of an underlying disease process. (systemic infections, underlying tissue) 3. toxin produced at a different site |
|
what are some environmental factors that increase the chance of exogenous infection?
|
moisture
trauma introduction of foreign body pressure (ie. bedsore) compromised blood supply (PVD, DM) |
|
what is folliculitis?
|
infection of hair follicles
|
|
where on the body is folliculitis MC seen?
|
areas of friction and sweat gland activity
|
|
MCC of folliculitis?
|
Staph aureus
|
|
which bacteria causes "hot-tub" folliculitis?
|
P. aeruginosa
|
|
which bacteria is a major skin anaerobe that contributes to acne?
|
Propionibacterium acnes
|
|
what is furuncle?
|
BOIL - small abscess in the region of a hair follicle
|
|
MCC of furuncles?
|
Staph aureus
|
|
what leads to recurrent furunculosis?
|
repeated self-inoculation
|
|
a confluence of multiple furuncles becomes a ?
|
carbuncle
|
|
treatment for furuncles and folliculitis
|
most are self-resolving
(furuncles may require drainage) |
|
treatment for chronic furunculitis?
|
bacitracin, neomycin cream
|
|
treatment for carbuncles?
|
surgical drainage, Abx. tx (cloxacillin, flucloxacillin)
|
|
what class of exogenous infections do the following belong to: impetigo, erysipelas, cellulitis?
|
spreading infections
|
|
four exotoxins of Staph aureus?
|
1. alpha toxin
2. exfoliatin 3. PTSAgs (pyrogenic toxin superantigens) 4. TSST-1 (toxic shock syndrome toxin) |
|
which exotoxin is found in almost all S. aureus?
|
alpha toxin
|
|
function of alpha toxin of S. aureus?
|
forms pores in lipid bilayer
(causing cell lysis, death, tissue necrosis) |
|
function of exfoliatin toxin of S. aureus?
|
cleaves desmoglien, separates skin layers
|
|
which Staph exotoxin is produced by a bacteriophage?
|
exfoliatin
|
|
two exotoxins found in Streptococcus pyogenes?
|
M protein
SPEs (streptococcal pyrogenic antigens) |
|
which strep exotoxin is present on all strep?
|
M protein (surface protein)
|
|
significance of M protein as an exotoxin for strep?
|
can determine the sequelae fo a strep infection (ie. nephrotogenicity)
|
|
how many different SPE toxins are there?
|
9
|
|
SPE types A and B are associated with?
|
toxic shock
|
|
SPE type C is associated with?
|
scarlet fever
|
|
what is the difference between impetigo, erysipelas, and cellulitis?
|
impetigo - confined to epidermis
erysipelas - involved dermal lymphatics cellulitis - major focus is SQ fat layer |
|
in general, which is the more aggressively spreading bacteria when it comes to skin infections: staph or strep?
|
strep
(opposite of endocarditis) |
|
two MC organisms found in impetigo?
|
staph
strep |
|
what is the characteristic clinical appearance of impetigo?
|
honey colored crust
|
|
in impetigo - what is significant about the exudates and crust?
|
contain infectious bacteria (if the crust is not removed, new lesions form about the periphery)
|
|
possible complication of impetigo caused by group A strep?
|
poststreptococcal glomerulonephritis
|
|
treatment of impetigo?
|
penicillin
bacitracin or mupirocin to limit spread (treatment may not prevent glomerulonephritis) |
|
strains of S. aureus with the group II bacteriophage may cause what skin infection?
|
bullous impetigo
|
|
function of group II bacteriophage in S. aureus?
|
encodes for exfoliatin toxin (this cleaves desmoglein in epidermis, results in superficial flaccid bullae that are easily ruptured)
|
|
treatment for bullous impetigo?
|
anti-staph antibodies
|
|
MCC of erysipelas?
|
Strep
(pyogenes, occasionally group B, C or D) |
|
erysipelas are MC in which age group?
|
elderly
|
|
describe an erysipela
|
abrupt onset
fiery red swelling of face or extremities well defined margins rapid progression intense pain |
|
erysipelas can progress to?
|
lymphadenitis
septicemia local skin necrosis |
|
treatment for erysipelas?
|
penicillin
erythromycin |
|
describe the borders of cellulitis compared to the borders of erysipelas
|
cellulitis - borders blend with surrounding tissues
erysipelas - distinct borders |
|
describe the clinical presentation of cellulitis
|
localized pain
erythema swelling heat can spread rapidly |
|
what may cellulitis be accompanied by?
|
lymphangitis and inflammation of draining lymph nodes
|
|
two MCC of cellulitis?
|
Staph aureus
Strep pyogenes |
|
which is worse - staph or strep cellulitis?
|
strep
(more rapidly spreading, diffuse, frequently associated with lymphangitis and fever) |
|
recurrent strep cellulitis is due to what strains?
|
group A, C or G strep PLUS skin lesions
|
|
when is recurrent staph cellulitis seen?
|
in immunocompromised or chronic nasal carriers
|
|
what bacteria commonly causes cellulitis in DM and PCD?
|
Strep agalactiae
|
|
what bacteria commonly causes periorbital cellulitis in children?
|
Haemophilus influenza type b
(spread from sinusitis, otitis media, epiglottitis) |
|
what bacteria, commonly found in aquatiums, causes cellulitis?
|
Mycobacterium marinarum
|
|
when is pseudomonas cellulitis MC seen?
|
hospitalized and immunocompromised hosts
|
|
treatment of cellulitis?
|
erythromycin
|
|
MC wound pathogen in clean surgical wounds?
|
Staph aureus
|
|
pathogen found in cat bite wounds?
|
Pasteurella multocida
|
|
MC pathogen in burn wounds?
|
Pseudomonas aerunginosa
|
|
MC pathogen in puncture wounds?
|
Clostridium tetani
|
|
MC pathogen in traumatic wounds?
|
Clostridium perfringens
|
|
describe the shape and gram staining of Pasteurella multocida
|
gram negative rod
|
|
what is characteristic about the staining of Pasteurella multoceda?
|
bipolar staining
|
|
biochemical characteristics of Multocida pasteurella?
|
nonmotile
catalase + oxidase + facultative anaerobe |
|
where is Pasteurella multocida commonly found?
|
normal flora in respiratory and GI tracts of animals and birds
|
|
two virulence factors posessed by Pasteurella multoceda?
|
capsule (antiphagocytic)
endotoxin |
|
complications of a Pasteurella multoceda infection?
|
*osteomyelitis
*septicemia, meningitis |
|
treatment for a Pasteurella multoceda infection?
|
penicillin or tetracycline
*unless* cat bite -> then treat with ampicillin and don't suture! |
|
25% of burns result in?
|
pseudomonal infection
(can lead to septicemia with >50% mortality) |
|
regarding pseudomonas:
1. gram stain, structure 2. oxidase 3. fermenting or non-fermenting? 4. aerobe or anaerobe? |
1. gram - rod
2. oxidase + 3. non-fermenting 4. primarily aerobe |
|
what is significant about the nutrient requirements of Pseudomonas aeruginosa?
|
not many nutrients required, can grow in distilled water and many other environments
|
|
significance of the water soluble pigments produced by pseudomonas?
|
*can flouresce under UV light
*green pus typical *fruity odor |
|
function of the following virulence factors posessed by pseudomonas?
1. pili 2. flagella 3. capsule |
1. attachment
2. dissemination 3. antiphagocytic |
|
function of the following exotoxins produced by pseudomonas aeruginosa?
1. elastase 2. alkaline phosphatase 3. phopholipase C 4. heat stabile phospholipase |
1. tissue damage
2. proteolysis, tissue damage 3. tissue damage 4. tissue damage |
|
treatment of burns infected with pseudomonas aeruginosa?
|
*topical application of antibacterial agents (ie. silver nitrate)
*surgical debridement |
|
best antibiotic combination to treat pseudomonas?
|
ALWAYS TEST SENSITIVITY 1ST
-aminoglycoside + extended spectrum penicillin |
|
describe clostridium in the following context:
1. gram stain, shape 2. aerobe or anaerobe 3. spore or no spore? |
1. gram + rod
2. strict anaerobe 3. spore forming |
|
MC species in clostridium cellulitis?
|
C. perfringens
|
|
what causes the crepitus felt in clostridial cellulitis?
|
gas found in skin
|
|
treatment of clostridial cellulitis?
|
debridement
penicillin |
|
what is the difference between type I and II necrotizing fasciitis?
|
type I - seen in pts following a surgical procedure, with DM or severe PVD (caused by mixed aerobic and anaerobic bacteria)
type II - formerly streptococcal gangrene, caused by group A strep. |
|
bacterial causes of synergistic necrotizing fasciitis?
|
combination of gram - rods and strict anaerobes (ie. Bacteroides or Clostridia)
|
|
where is necrotizing fasciitis commonly seen?
|
on or about feet
(rapid extension along fascia in to leg) |
|
treatment for necrotizing fasciitis type I?
|
ampicillin PLUS clindamycin PLUS FQ
|
|
four types of "endogenous" skin infections?
|
abscesses
necrosis rashes noninfectious lesion |
|
MCC of abscesses?
|
intravascular infx (esp. staph aureus)
|
|
two manifestations of necrosis?
|
purpura fulminans
ecthyma gangrenosum |
|
what is purpura fulminans?
|
skin manifestations of DIC
|
|
when is erythmea gangrenosusm commonly seen?
|
in immunocompromised
usually with P. aeruginosa |
|
what type of rash would be seen in meningiococcemia?
|
hemorrhagic rash
|
|
what type of rash is seen in typhoid fever, rocky mountain spotted fever?
|
macular rash
|
|
scarlet fever is caused by?
|
group A strep exotoxin
|
|
scalded skin syndrome and TSS are caused by what bacteria?
|
Staph
|
|
SSSS is most commonly seen in which age group?
|
children <5yr (including neonates)
|
|
SSSS is caused by what in particular?
|
Staph aureus group II
*toxin - exfoliatin |
|
TSS is caused by what in particular?
|
toxic shock sydrome toxin (TSST) - present in 5-25% of S. aureus
|
|
can Strep cause a toxic shock syndrome?
|
yes
strep can produce pyrogenic exotoxins that cause streptococcal toxic shock syndrome (STSS) |
|
skin manifestations of TSS?
|
diffuse red rash
*lasts 1-2 wks, then see peeling of skin |
|
other clinical s/s of TSS?
|
*redness of eyes, mouth, throat
*confusion, seizures, H/A *myalgias *hypotension *organ failure |
|
mortality rate of TSS?
|
30-60%
|
|
treatment of TSS?
|
fluid replacement
general supportive care clindamycin gamma globulin |
|
define:
1. autograft 2. syngeneic graft |
1. from one part of an individual to another part of the same individual
2. between genetically identical individuals of the same species |
|
define:
1. allogeneic graft (allograft) 2. xenogeneic graft (xenograft) |
1. between genetically disparate individuals of the same species
2. between individuals of different species |
|
most grafts are of what type?
|
allografts
|
|
what are the two ways in which recipient T cells can be activated against graft antigens?
|
1. direct recognition (some transplants)
2. indirect recognition (all transplants) |
|
describe indirect recognition of graft antigens
|
host APCs activate host T cells using host MHC molecules
|
|
describe direct recognition of graft antigens
|
donor APCs activate host T cells in host lymph node using donor MHC molecules
(donor MUST have same MHC molecules as host in order for this to occur) |
|
compate the rejection time of a primary allograft vs a secondary (repeated) allograft
|
primary - longer time to rejection
secondary - shorter time until rejection due to immunological memory |
|
initial graft rejections are usually due to what immune response?
|
T cell activity
(NOT antibodies) |
|
in relation to major and minor histocompatibility genes, discuss the:
location |
major - MHC I and II
minor - all chromosomes |
|
in relation to major and minor histocompatibility genes, discuss the:
# of loci |
major: 5-10
minor: 100+ |
|
in relation to major and minor histocompatibility genes, discuss the:
rejection speed |
major - rapid
minor - variable |
|
in relation to major and minor histocompatibility genes, discuss the:
generation of Ab |
major - lots of Ab generated
minor - few if any made |
|
in relation to major and minor histocompatibility genes, discuss the:
polymorphism |
major - high (lots of variety)
minor - low |
|
in relation to major and minor histocompatibility genes, discuss the:
function |
major - Ag presentation
minor - ? |
|
in relation to major and minor histocompatibility genes, discuss the: tolerization by the host immune system
|
major - difficult
minor - easier |
|
what is the "law of transplantation"
|
a recipient MAY reject a graft if that graft expresses histocompatibility genes (antigens) not
expressed by host genes [recipient may reject a graft if it is foreign] |
|
what happens to a graft that is taken from a homozygote and given to a heterozygote?
|
acceptance
|
|
what heppens to a graft that is taken from a heterozygote and goven to a homozygote?
|
rejection
|
|
what are the 3 patterns of rejection?
|
1. chronic rejection
2. acute rejection 3. hyperacute rejection |
|
T cells mediate what kinds of rejection?
|
chronic and acute rejection
|
|
how long for graft destruction in chronic rejection?
|
weeks -> months -> years
|
|
how long for graft destruction in acute rejection?
|
10-14 days
|
|
what is the hyperacute rejection mediated by?
|
Ab
(Abs are usually against MHC class I) |
|
two situations in which hyperacute rejection occurs?
|
1. recipient is repeatedly exposed to graft antigens
2. naturally occuring Ab exists |
|
how fast is the graft destroyed in a hyperacute rejection?
|
within a few days
|
|
why is there little cellular infiltrate seen in a hyperacute rejection compared to the other rejection types?
|
no time for vasculature to get established - therefore no way for inflammatory cells to get there
(other graft types have time for vasculature to get established) |
|
incompatibilities with minor histocompatiblity genes generally results in what type of rejection?
|
chronic
|
|
incompatibilities with major histocompatiblity genes generally results in what type of rejection?
|
acute
|
|
which type of organ transplant is hyperacute rejection commonly seen in?
|
renal
|
|
what are some factors affecting graft rejection?
|
1. presensitixation
2. degree of genetic mismatch 3. lymphatic drainage 4. tissue typ einvolved 5. graft size 6. immune response genes |
|
describe lymphatic drainage issues in relation to graft rejection
|
decrease lymphatic drainage, increase chance of survival (less way for APCs and T cells to drain to lymph nodes)
|
|
describe graft size in relation for graft rejection
|
increased graft size sometimes increases survivability "overwhelmed immune system"
|
|
what is significant about liver transplants and rejection?
|
liver transplants seen to be viable across genetic barriers (HLA mismatch)
(many surgeons believe that HLA matching has no relevance to survival of liver transplants) |
|
what is a unique type of rejection seen in bone marrow transplants?
|
graft-vs-host (GVH)
|
|
how can acute GVH be prevented?
|
deplete marrow of mature T cells before transplanting
|
|
does MHC matching need to be performed for bone marrow transplants?
|
yes - some needs to be done
(necessary for positive and negative selection to operate) |
|
why do T cells not respond well to xenografts?
|
MHC I and II molecules on those cells re too different to fil well with host TCRs
|
|
3 mechanisms of hyperacute rejection seen in xenografts?
|
1. pre-existing antibodies to carbohydrate structures
2. compliment 3. MK cell mediated killing of donor cells lacking appropriate MHC I molecules |
|
what happens when pig cells are transfected with human DAF, CD59 genes, etc?
|
pig cells are now able to INACTIVATE HUMAN COMPLIMENT components binding to their surface
|
|
what happens when pig cells are transfected with human MHC I genes?
|
pig cells now have MHC I molecules to bind inhibitory receptors on human NK cells and prevent attack
|
|
how can a general immune deficiency be induced in order to minimize/prevent reaction to a graft?
|
1. radiation
2. Ab against T cell markers 3. drugs cytotoxic for rapidly dividing cells 4. drugs with narrow specificity for proliferating T cells (cyclosporin) |
|
Cutaneous manifestations of:
1. papillomavirus 2. parvovirus B19 3. herpesviruses - HSV and VZV 4. herpesviruses - EBV and HHV-6 5. herpesviruses - CMV 6. smallpox |
1. papules
2. macules, papules 3. vesicles 4. macules 5. macules, papules 6. vesicles, pustules |
|
cutaneous manifestations of
1. coxsackie 2. measles 3. rubella |
1. vesicles
2. macules, papules 3. macules |
|
following the primary infection - where does VZV establish latent infection?
|
dorsal root ganglia
-or- extramedullary cranial nerve ganglia |
|
in what type of patients does VZV cause serious morbidity and mortality?
|
immunosuppressed patients
|
|
recurrent VZV disease is called?
|
Zoster or shingles
|
|
most cases of VZV occur in what population?
|
children <15yrs
|
|
seasonality to VZV?
|
winter and early spring
|
|
incidence of Zoster in pts that have had varicella?
|
20%
|
|
reactivation of VZV is associated with what conditions?
|
aging
immunosuppression |
|
seasonality for zoster?
|
NONE
|
|
manifestations of zoster in the immunocompromised?
|
may disseminate
(causing skin lesions, CNS, pulmonary, hepatic involvement) |
|
transmission of VZV?
|
Aerosolized droplets
Direct contact *very contagious* |
|
describe the pathogenesis of a primary VZV infection
|
* virus spreads to lymphatics, then to blood
*viremia causes seeding of liver and spleen *secondary viremia occurs about 14 days post infection - manifests as infection of skin and mucosal surfaces |
|
describe Ig levels after a VZV infection
|
IgM and IgA decrease after 1yr
IgG declines but persists at a low level |
|
what type of immunity plays a role in host defense against recurrent VZV infection?
|
cellular immunity
CTLs NK cells ADCC |
|
paitents that are deficient in cell mediated immunity are at risk of?
|
severe disease caused by VZV
|
|
incubation period of VZV?
|
14-17 days
(shorter in immunocompromised pts) |
|
in which patient group are prodromal symptoms of VZV absent?
|
young children
|
|
prodromal symptoms seen in older pts?
|
fever (1-6 days)
H/A backache sore throat |
|
describe the appearance and character of the varicella rash
|
crops of vesicles appear every 2-4 days
*rash appears on trunk first, then spreads to limbs |
|
in what stage of the rash is moderate to severe pruritis present?
|
vesicular stage
|
|
evolution of the vesicles in a chickenpox rash
|
1. thin walled vessicle with clear fluid ->
2. vesicle becomes cloudy and depressed in center with irregular border -> 3. crust forms in center and eventually replaces remaining portion of vesicle at periphery |
|
when is the vesicle no longer infectious?
|
when it crusts
|
|
describe the skin lesions seen in shingles
|
*crops of varicella like lesions
*involves a single dermatome *pain, parasthesias *never cross midline |
|
MC reactivation of VZV occurs at which spinal levels?
|
trunk (T3-L2)
|
|
DDx of zoster that involves trigeminal nerve?
|
HSV
|
|
MC complication of VZV in children?
|
bacterial infection
|
|
other complications of VZV?
|
encephalitis
hepatitis pneumonia |
|
when is hemorrhagic chickenpox seen?
|
immunocompromised pts
(50% mortality rate) |
|
a bacterial infection of chickenpox can result in?
|
bullous impetigo
|
|
treatment of VZv if needed?
|
acyclovir
sorivudine famcyclovir valacyclovir foscarnet |
|
what type of VZV vaccine is available?
|
live, attenuated
(doesn't prevent shingles) |
|
what can be given to provide passive immunization to chickenpox?
|
VZIG
(varicella zoster immunoglobulin) *effective when administered up to 3 days after exposure |
|
major use for VZIG?
|
immunocompromised children
newborn infants whose mothers have active varicella at the time of delivery |
|
HHV-6 causes what childhood disease?
|
roseola infantum (exanthema subitum - "sudden rash")
|
|
characterize the onset of roseola infantum?
|
fever as high as 105
lasts 3-4 days |
|
in roseola infantum - what occurs after the rash?
|
lymphadenopathy
(fever is prodromal) |
|
where does HHV-6 primarily infect and replicate?
|
CD4+ T cells
|
|
describe the rash and prognosis of roseola infantum (exanthema subitum)
|
faint macular rash
mild self-limiting disease |
|
hand-foot-and mout disease (HFMD) is primarily caused by?
|
coxsackie viruses A9, A16
enterovirus 71 |
|
what is the classic sign of HFMD?
|
exanthema on buccal mucosa
(also found on dorsum of hands and margin of heels) |
|
HFMD primarily occurs in which population?
|
children <4 yrs of age
|
|
herpangina is primarily caused by?
|
coxsackie A viruses
|
|
describe the s/s of herpangina
|
abrupt onset
fever, sore throat, excessive salivation *grouped, grey vesicles in mouth |
|
course of herpangina?
|
*self limiting*
fever lasts 1-4 days disease lasts 4-5 days |
|
how many serotypes of measles are there?
|
one
(reason for effectiveness of vaccine) |
|
function of H and F protien located on viral envleope of the measles virus?
|
H protien - promotes attachment to cell receptors
F protien - promotes viral-cell and cell-cell fusion |
|
transmission of measles?
|
respiratory droplets
-or- direct contact with nasal or throat secretions |
|
how long after the rash appears is transmission of measles possible?
|
4-5 days
|
|
what is a characteristic histologic feature of measles infection?
|
multinucleated giant cells
(with eosinophilic and intranuclear inclusion bodies) |
|
how does measles cause immunosuppression?
|
*infects lymphocytes, monocytes, macrophages
*inhibits lymphocyte proliferation |
|
how long can clinically significant immunosuppression last post-infection?
|
up to 1 yr
|
|
how long do antibodies to measles persist?
|
for life
|
|
what immune response is responsible for most symptoms seen in measles?
|
cellular immune response
|
|
how does measles differ in a CMI deficient patient?
|
no rash
|
|
describe the prodromal phase of measles. when does it begin?
|
*low grade fever, malaise
*coryza, sore throat, H/A *conjunctivitis *sneezing and cough begins 8-12 days after infection |
|
what are Koplicks spots and when do they appear in relation to the measles rash?
|
red patches with central white specks that appear on buccal mucosa 2-3 days prior to onset of measles rash
|
|
describe the rash seen in measles. where does it begin and spread?
|
maculopapular
begins at hairline - rapidly progresses to the face, neck trunck and extremities |
|
complications fo a measles infection?
|
inner ear infx
bronchopneumonia acute postinfectious encephalitis |
|
death in a measles infection in children <2yrs is MC due to what complication?
|
pneumonia
|
|
treatment for measles?
|
supportive
(no antivirals) |
|
what type of vaccine is the measles?
|
live, attenuated
|
|
measles vaccine is contraindicated in?
|
pregnancy
allergy to eggs, neomycin comprised immunity |
|
what is unique about the replication of the smallpox virus?
|
replicates entirely in the cytoplasm of the cell
(large dsDNA genome, doesn't need nucleus to replicate) |
|
transmission of smallpox?
|
respiratory route
|
|
what is characteristic about the smallpox lesions?
|
*all lesions are in the same stage of development
*centrifugal (distal) rash distribution *lesions on palms and soles (firm, round, deep seated pustules) |
|
describe the prodrome seen in smallpox
|
fever >101
prostration, H/A, backache, chills, vomiting, abd. pain |
|
where do the first lesions in smallpox appear?
|
oral mucosa, face or forearms
|
|
the other diseases caused by poxviruses?
|
1. molluscum contagiosum
2. ORF 3. cowpox |
|
what is the signifance of cowpox in relation to smallpox?
|
provides immunity to smallpox
|
|
does pseudocowpox provide immunity to smallpox?
|
NO
|
|
most vaccine responses are due to which immune response (innate or adaptive)
|
adaptive
(specificity, memory) |
|
what are the three pathogen repication sites in the body (therefore the 3 points of focus for the immune response)?
|
1. vesicular
2. cystosolic 3. extracellular |
|
where do most pathogenic bacteria replicate?
|
vesicles
|
|
where do most viruses live?
|
cytosol
|
|
which type of immune response activates macrophages to kill intravesicular pathogens?
|
Th1 response
|
|
whic type if immune response activates B cells to make antibodies and occurs extracellularly?
|
Th2
|
|
influenza vaccine has been "associated with"?
|
Guillan Barre syndrome
|
|
HBV vaccine has been "associated with"
|
MS
|
|
MMR vaccine has been "associated with"
|
autism
IBS |
|
aluminum containing vaccines have been "associated with"?
|
MMF
(macrophagic myofaciitis) |
|
what is a first generation vaccine?
|
live or attenuated
dead or inactivated |
|
what is a second generation vaccine?
|
recombinant
extracts (proteins, peptides) conjugated |
|
what is a third generation vaccine?
|
DNA
(currently in clinical trials) |
|
2 risks of an attenuated vaccine?
|
1. necessary epitopes not present
2. wild-type reversion |
|
give an example of a dead or inactivated vaccine
|
IPV
|
|
give an example of an extract vaccine
|
diptheria and tetanus toxins
|
|
give an example of a conjugated vaccine
|
Hib
(direceted against Haemophilus protein, LPS protein used for immunogenesis) |
|
what is a conjugated vaccine?
|
desired pathogenic epitope is combined with an immune stimulatory molecule (ie. LPS)
|
|
DNA vaccines are currently experimental for?
|
pathogens
allergies cancer autoimmunity |
|
how is an adjuvant useful in enhancing the efficacy of a vaccine?
|
enhances the immunogenicity by acting on APCs
|
|
risks of using an adjuvant in a vaccine?
|
induction of inflammatory diseases (SLE, MS)
|
|
examples of adjuvants?
|
pertussis toxin (DPT)
emulsification in oil aluminum salts |
|
what is an ISCOM?
|
immune stimulatory complex
very effective with peptide vaccines |
|
what are some general reasons to delay or avoid vaccination
|
1. serious allergic rxn (ie. anaphylaxis) after a previous vaccine dose
2. serious allergic rxn to a vaccine component 3. moderate to severe disease with or w/o fever (mild colds etc. should not prevent immunization unless in the immunocompromised) |
|
what is the only vaccine that is recommended to be given before the age of 2 months if the mother has the disease?
|
Hep B
|
|
describe diptheria
|
serious disease that produces a toxin which can cause heart and nerve problems
|
|
DTaP stands for?
|
diptheria
tetanus acellular pertussis |
|
DTaP provides:
1. lifelong immunity to? 2. immunity requiring a booster every 10 yrs. to? |
1. pertussis
2. diptheria, tetanus |
|
specific DTP risk?
|
anaphylaxis
|
|
when is it contraindicated to give Hib and DTap together?
|
in first immunization (reduces Hib-specific immune response)
*can combine in later immunizations* |
|
what is the polio vaccine of choice in the US?
|
IPV
(inactivated poliovirus vaccine) |
|
when should IPV not be given?
|
if severely alelrgic to neopmycin or streptomycin
|
|
reason we vaccinate for mumps?
|
major cause of deafness
paralysis, seixures testicular swelling (past puberty) miscarriage if infected in pregnancy |
|
specif MMR risks?
|
anaphylaxis
encephalomyelitis, thrombocytopenia (very rare) |
|
when should the MMR be avoided?
|
severe egg or neomycin allergies
gammaglobulin w/i last 3 mo immunosuppressive tx (steroids) |
|
risks specific to varicella vaccine?
|
encephalomyelitis (very rare)
|
|
varicella vaccine should be avoided in?
|
severe egg or neomycin allergies
gammaglobulin w/i last 3 mo immunosuppressive tx |
|
who should recieve the influenza virus vaccine?
|
*women pregnant during influenza season
*residents of nursing homes/long care facilities *children aged 6mo-18yr on chronic ASA *healthcare workers *out of home caregivers and household contacts of children <6mo |
|
why is it recommended that healthy children between 6 and 23 months be immunized against influenza?
|
*hopitalization rates for this age group are high
*mortality rate from influenza is high in this age group |
|
immunization with the rotavirus vaccine is currently not recommended. why?
|
associated w/ intussusception
|
|
two forms of pneumococcal vaccines?
|
PCV (pneumococcal conjugate)
PPV (pneumococcal polysaccharide) |
|
when is PCV recommended?
|
healthy infants
unhealthy children >2yrs |
|
when is PPV recommended?
|
everyone else
(does not induce immune response in children younger than 2yrs) |
|
when is the meningococcal conjugate vaccine (MCV4) recommended?
|
all by high school entry
*prevents bacterial meningitis |
|
what is the principle behind a vaccine for a malignancy?
|
induce an immune response specific for tumor cells
|
|
what is the principle behind a vaccine against autoimmune diseases?
|
induce tolerance against known pathogenic autoantigens
(promising for DM and MS) |
|
besides allergies, when is MMR contraindicated?
|
pregnancy
immunodeficiency or malignancy (ok in HIV) |
|
besides allergies, when is varicella vaccine contraindicated?
|
pregnancy
immunodeficiency or malignancy (not ok in HIV) |
|
define shock
|
the inadequate delivery of oxygen and nutrients necessary for normal tissue and cellular function
|
|
6 types of shock?
|
hypovolemic
cardiogenic neurogenic septic obstructive psychogenic |
|
describe the following in class I hypovolemic shock:
1. blood loss 2. BP 3. pulse pressure 4. urine output |
1. up to 750 mL (15%)
2. normal 3. normal or increased 4. normal |
|
describe the following in class II hypovolemic shock:
1. blood loss 2. BP 3. pulse pressure 4. urine output |
1. 750-1500 mL (15-30%)
2. normal 3. decreased 4. decreased |
|
describe the following in class III hypovolemic shock:
1. blood loss 2. BP 3. pulse pressure 4. urine output |
1. 1500-2000 mL (30-40%)
2. decreased 3. decreased 4. markedly decreased |
|
describe the following in class IV hypovolemic shock:
1. blood loss 2. BP 3. pulse pressure 4. urine output |
1. >2000 mL (>40%)
2. decreased 3. decreased 4. decreased |
|
causes of cardiogenic shock?
|
*cardiac pump failure*
massive MI blunt cardiac injury cardiac tamponade air embolus |
|
what causes neurogenic shock?
|
loss of vasomotor tone - results is diminished tissue perfusion (relative hypovolemia)
|
|
treatment for neurogenic shock?
|
IV fluids
vasopressors (DA, dobutamine) |
|
treatment for septic shock?
|
IV fluids
Abx vasopressors Activated protein C (inhibits cytokines) |
|
examples of causes of obstructive shock?
|
tension pneumothorax
cardiac tamponade |
|
treatment for obstructive shock?
|
treat the underlying problem
|
|
describe the trimodal distribution seen in shock
|
most shock pts die within the first hour
*then see a second wave at 2 hrs *then see a third wave at 2-4 wks (due to sepsis, multi-system organ failure) |
|
what are the 2 determinants of CaCO2 (arterial oxygen content)?
|
Hgb
O2 sat |
|
what is the formula for delivery of oxygen?
|
DO = CO x CaCO2
CaCO2 = 4/3 Hgb x SaO2 |
|
through which can you push fluids faster: one central line or two large bore peripheral IVs?
|
two large bore peripheral IVs
|
|
how much fluids need to be administered for 1 L of blood loss?
|
3-4 L
(leaks into interstitial and extracellular compartments) |
|
what is the Parkland formula for fluid resuscitation in burns?
|
IVF = 4 ml/kg x TBSA
*50% infused over first 8hrs, rest over second 16 hrs (2nd and 3rd degree burns only) |
|
what are the 3 phases of fluid resuscitation?
|
1. resuscitaton
2. maintenance 3. diuresis (urine output is good indicator of recovery) |