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;
70 Cards in this Set
- Front
- Back
what is it called when there is bacteria in the blood
|
bacteremia
**the categories of bacteremia depend on the cause, length of time in the blood and the organism itself |
|
how long does the bacteremia last when its caused by...
1. dental abstracton 2. pneumococcal pneumonia 3. gram - sepsis 4. intra-sbd sepsis 5. infective endocarditis 6. catheter indwelling |
1. dental abstracton: spike and drop in hours
2. pneumococcal pneumonia- spikeand drop ~ 6hrs 3. gram - sepsis: rise and fall with amt of bacteria increasing with each rise 4. intra-abd sepsis: 2 small humps 5. infective endocarditis: low steady level 6. catheter indwelling: linear increase |
|
tell me about bacteremia associated with "normal" events. brushing teeth, normal childbirth, endoscopy, pooping, scraped knuckle etc
|
its NOT a disease state but bacterial level in the blood DO rise
**the body quickly kills the bacteria **caused by normal flora -strep viridans of oral cavity |
|
what is the classification of bacteremia of strep viridans from the oral cavity after brushing teeth
|
NORMAL! its transient and NOT a disease, some bacteria is in blood but the body quickly clears it
|
|
how do you dx an intermittent/recurrent bacteremia
|
when there is a focal infection like abcess or UTI it can leak into the blood
several cultures needed to get the dx and also monitor they tend to increase and clear out and then come back (intra abd sepsis, gram - sepsis) |
|
whats an example of continuous bacteremia
|
endocarditis
catheter indwelling |
|
if you have bacteremia but DONT have an infection with that same bacteria somewhere else in your body is it primary or secondary. give example
|
primary obviously
**bacteria from IV or arterial line **caused by normal flora on skin |
|
what is secondary bacteremia, what are some examples
|
its when to have bacteremia as a result of a bacterial process somewhere else on your person
ex GI/Skin lesion, abcess, hematogenous spread to kidney lots of times |
|
what are some risk factors for bacteremia
|
1. catheters, IV
2. sirgery 3. respiratory infection 4. underlying disease 5. old, young |
|
what are the 2 most common organisms of bacteremis
|
1. staph
2. gram neg bacilli recently there has been an increase in S epidermidis and corynebacterium |
|
if your pt is immunocomprimised and was just recently treated with AB and now has bateremia, what is the likely pathogen
|
something unusual like bacteroides, or another anaerobe
**commonly there is an intra-abd or pelvic focus |
|
what are some unusual pathogens that cause bacteremia, where do you find the focus, who gets them
|
bacteroides, anaerobes
((intra abd, pelvic **seen in pts who just took AB and immunosuppressed |
|
how do you dx bacteremia if you suspect it? whats the problem with this
|
culture the blood!!! blood is sterile so ALL are considered GUILTY until proven innocent- recall there can be transient bacteremias w/normal flora from brushing teeth or what not.
**if you see bacteria in the blood culture the pathogen is GUILTY, but keep in mind there are several transient bacteremias, may need to time your cultures |
|
ok so you think your pt has bacteremia so you culture them and it shows + for one of the following
1. s epidermidis 2. dipeheroids 3. proprionobacteria transient normal flora or bectermia |
skin contaminants UNLESS
>5 CFU or repeat cultures are + then you are thinking IE or catheter based bactermia |
|
what are the 3 organisms that are considered normal flora unless there are >5 CFU or repeat cultures are +, then its NOT just skin contamination but IE or catheter bactermia
|
1. s epidermidis
3. diptheroides 3. proprioobacteria |
|
whats teh tx for bacteremia
|
culture for sensitivities and gram stain
use what works! emperic therapy is initial based on gram stain and adujust after you get sensitivities back |
|
what is SIRS
|
systemic inflammatory response system
**dysregulated host inflammatroy response pt has: fever, tachycardia, tachypnea, leukophilia |
|
what is it called when you have a dysregulated inflammatory response and so get fever, tachycardia, tachypnea, or leukophilia
|
SIRS- systemic, inflammatory response syndrome
|
|
what are some microbeless triggers for SIRS (systemic inflammatory response syndrome)
|
AI
pancreatitis vasculitis burns surgery |
|
whats sepsis
|
its SIRS that is caused by pathogen as ID by culture
**severity based on organ dysfx and hemodynamic compromise |
|
ok so you have SIRS (lots of inflamm --> fever, increased HR, RR, WBC) and you cultured something and ID the pathogen, what is it now called
|
sepsis
|
|
sepsis is defines as
|
SIRS (the dysregulated inflammatory response- fever, increased HR, RR, WBC) due to a culture proven pathogen
**classified based on degree of organ dys and hemodynamic comprimise |
|
describe some findings in SEVERE sepsis
|
1 sign or hypoperfusion or dysfx.
ex molted skin cap refil >3 sec urine output <0.5 ml/kg/hr lactate >2mmol/L abrupt change in metal status abnormal EEG low platelets DIC ARDS |
|
if you have sepsis + one of the following what is the classificaition of sepsis
molted skin long cap refil low urine output high lactate change in mental status (abrupt) |
its SEVERE, these are all signs of hypoperfusion or dysfx
can also be EEG changes, platelets, DIC, ARDS, |
|
ok so if severe sepsis is classified by hypoperfusion or dysfx what defines septic SHOCK
|
low MAP (2/3 DP + 1/3 SP) <60 DESPITE fluid resusitation
need drugs to maintain BP despite adequate fluids |
|
ok so your pt is in sepsis adn you think they just went into septic shock, what happend
|
1. MAP decreased despite fluids (hypotensive)
2. need BP drugs to maintain BP despite fluids |
|
whats MODS
|
multi organ dysfunction
altered organ fx in acutely ill pts, homeostsis is NOT maintained w/o intervention primary: direct insult caused organ damage secondary: due to consequence of host response |
|
if you have altered organ fx such that homeostasis is NOT maintained whats the classification
|
MODS- multi organ dysfx
can be 1 or 2 |
|
what is...
1. bactermia 2. SIRS 3. severe sepsis 3. Septic shock 4. Mods |
1. bactermia: bug in blood
2. SIRS: immune dysreg bc of bug in blood, fever, increase HR, RR, WBC 3. Severe sepsis: sepsis and sign of hypoperfusion or dysfx 3. Septic shock: hypotensive despite fluids 4. Mods: homeostasis NOT maintained |
|
what are the 3 main tx goals of septic shock
|
1. resucutate from sepsis: correct hypoperfision, hypoxia, hypotension,
2. ID source of ifection adn TREAT! 3. maintain organ fx |
|
restore perfusion
kill the bug maintain organs this is tx protocol for what |
septic shock
|
|
is the problem with IE (infective endocarditis) ...
intra or extra cardiac valves? |
intra
valves are insufficient so lead to CHF, myocardial abcess |
|
if you have intraceable CHF and cardiac abcess alon gwith infective emboli othe rplaces in the body what might be the underlying cause`
|
IE
**wides range of sx- sterile/infected emboli, immunological complezes |
|
what can cause IE
|
1. IVDA
2. invasive vascular procedures can be healthcare related, prosthetic valve related, native valve endocarditis ... |
|
can IE result form 1 or 2 bactermia
|
OH ya!
|
|
who gets IE more often
|
men, old
|
|
what are some risk factors for IE
|
1. rheumatic fever
2. calcification, aortic stenosis 3. congenital heart disease 4. MVP 5. prosthetic valves RESIDUAL DAMAGE FROM PREVIOUS IE |
|
what are the 3 ways IE is categorized
|
1. tempo of clinical illness
2. site of infection 3. etiology |
|
what ist eh most significan risk for getting IE
|
residual valvular damage from previous IE
rheumatic fever, aortic stenosis, congenital heart disease like bicuspid aortic valve, MVP, prosthetic valve |
|
acute IE
clinical.. complications.. cause... |
1. abrupt onset, ALWAYS fever,
2. complications in a week- dyspnea, fatigue, CHF, CNS sx 3. Staph aireus |
|
if you have s aureus IE causing fever, dyspnea, fatigue, CHF, adn CNS disease is the onset acute or subacute
|
acute
develops abruptly |
|
whats subacute (chronic) IE like
clinical complications cause |
1. fever. onset to dx ~ 6 weeks
2. anorexia, weight loss, flu like sx, RUQ pain, vomit, distress after eating. 3. strep viridans |
|
IE and
1. s aureus 2. strep viridans |
1. acute
2. subacute (chronic) |
|
how is IE classified
|
microbe
type and site of valve presisposing condition a hemolytic strep, native valve endocarditis CA-s sureus, tricuspid valve, IVDA s epidermidis, prosthetic valve arotic valve IE |
|
is native valve IE common
|
oh ya
|
|
do streptococci cause IE
tell me about strep bovis gram catalase AG |
ya
small, gram +, CATALASE -, non hemolytic, group D AG, coccus |
|
what are the HACEK organisms that cause IE
|
1. haemophilus arphrophilus
2. actinobacillus actinomyvetemcomitans 3. Cardiobacterium hominis 4. Eikenella corrodens 5. Kingella kingae **all are aerobic bacilli normal flora of upper respiratory tract and oropharynx *cause subacute IE complications include massive emboli, and CHF |
|
what are some clinical features of IE
|
fever
petechiae subungual hemorrhage osler nodules janeway lesion roth spots can have CNS diesase also |
|
if you have a fever, subungual hemorrhage, petechiae, osler nodules, roth spots and janeway lesions whats the deal
|
IE
|
|
what are signs of R heart diease
what are signs of L heart disease w/IE |
R: pulm infarcts
L: systemic emboli |
|
how do vegetations occur in IE
|
1. heart endo damage
2. pressure grad against valves 3. fibrin platelet deposition 3. bacteria --> colonized fibrin deposition 4. more thrombus deposits 5. vegetation that increases in size and breaks away |
|
what are the 2 stages of vegetation formation
|
1. NON bacterial thrombotic vegetation (aggregation of platelets and fibrin- caused by TRAUMA, defective valves, endo changes relation to renal failure, stress, malnutrition, neoplasia)
2. Bacteremia: bug adheres to damaged area and begins to replicate and more aggregation |
|
what is the non infectious stage of vegetation formation caused by
|
fibrin and platelets deposit bc of.
1. trauma: iv, catheter etc 2. valve defects: 3. changes in endo bc of: stress, renal failure, malnutrition, neoplaisa |
|
tell me about the second stage of vegetation formation
|
its when you get bacteria in it! the bacteria can replicate and more fibrin/platelets are laid down
can get to be cm large! can break off and cause septic emboli and get into circulation. immune complexese are everywhere now! |
|
what are Janeway lesions
|
1. flat painless, red/blue, macules/nocules
-result of septic emboli from L sided IE. found on palms and soles! seen in Acute IE |
|
what are hte leions on the palms and soles seen in IE called
|
janeway lesions
*8the are flat, painless, and red/blue, |
|
what is a sunungual lesion
|
splinter petechiae, linear hemorrhage in nail beds. seen in IE- along wi/osler nodules, jane way lesion, roth spots
|
|
whats a flea bitten kidney
|
its result of the circulating immune complexes in IE.
bleeding into glomerular spaves appears as petechiae glomerulonephritis |
|
vegestions in IE can cause...
1. microemboli 2. immune complexes 3. continuous bacteremia what are some examples in each |
1. Microemboli- janeway lesion, splinter (subungual) hemorrhage,
Immune complex: flea bitten kidney, glomerulonephritis, oslers nodules, roth spots |
|
what are oslers nodules
|
PAINFUL (janeway is emboli and not painful) node bc of IMMUNE cOMPLEX
intradermal transient nodule seen in fingers and toes. small. |
|
what are roth spots
|
result of IE, immune complex
White area in retina, lymphocytes, edema, hemorrhage |
|
if you have IE do you have continuous or transient bacteremia
|
continuous
|
|
with IE we knoe sx include>
janeway, osler, roth, subungual. what are some others |
petechia,
finger clubbing gangrene 2 to embolization bacteremia stroke fever |
|
what is the duke criteria for IE
|
the new dx
2 major 1 major + 3 minor 5 minor (pathogens hard to culture, little vegetation) MAJOR: + blood culture, evidence of endocardial involvement MINOR: predisposition, fever, vascular phanomenon, immunological phenomenon, microbial evidence, ECG |
|
what are the major and minor criteria for IE
|
Major
+ blood culture evidence of endocardial damage Minor: predisposition, fever, vascular, immunologica, microbial, ECG **need for dx 1. 2 major 2. 1 major and 2 monor 3. 5 minor |
|
whats the tx for IE
|
get C and Sensitivity
HIGH dose AB. bacteriCIDAL conc. for like 4-6 weeks. monotor w/culture |
|
is IE easy to treat
|
nope
decreased metabolic state of bacteria, need a CIDAL AB, tx so long you can get resistance to enterococci and staphylococci |
|
bc IE is so hard to treat w/AB what are other approaches to tx
|
surgery to remove vegetation
**previous IE is HUGE risk factor for another infection |
|
w ehave heard of ppl w/MVP getting prophylactiv AB before dental procedures to prevent IE, is this still done
|
ya. if you have fake valve, previous IE, congenital heart disease, etc
they are prophylaxed for invasive things like: gingival manipulation, periapical tooth, or perforation of oral mucosa NOT: lidocaine injections, x rays, removal of dentures adn things, orthodontics |
|
w/the new guidlines do you prophylax ppl w/Gi/GU procedures
|
nope
|