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;
146 Cards in this Set
- Front
- Back
What is endocarditis?
|
inflamm of heart valves or endocardium almost always from infectious etiology
|
|
where is endocarditis likely to occur?
|
at area of turbulence, such as congenital heart lesions
at site of high P gradients across small orifices the vegetations are downstream on low P side of gradient |
|
pathgenesis of infective endocarditis?
|
microthrombi inplants in area of endocardial irregulartiy --> small sterile vegetation, which provides focus for bacterial seeding during transient bacteremia
|
|
Which organisms are most likely to adhere to sterile vegetations?
|
some strep viridans species (produce extracellular dextran which promotes adherence to platelet fibrin aggregates)
|
|
what are the organisms that can cause infective endocarditis?
|
strep viridans
staph aureus (coagulase + and -) enterococci group D strep (esp S. bovis) gram - rods (uncommon) fungi (candida and aspergillus) negative blood cultures |
|
Which organism is the most common cause of subacute bacterial endo?
acute endo? endo on prosthetic valve? |
strep viridans
s. aureus (coagulase +) s. aureus (coagulase -) |
|
Which bacteria is commonly found in older men with endocarditis?
|
enterococci (from GU obstruction)
|
|
which bacteria is the marker organism for colon and other GI malig?
|
S. bovis (group D strep)
|
|
Which heart valves are commonly involved in SBE? acute?
|
M > A > T > P
A, and T (but variable) |
|
Which type of endocarditis (acute or SBE) has emboli?
Neurologic findings? |
acute
subacute |
|
what are some of the features of atypical presentation of endocarditis?
|
probs 2/2 embolism
renal failure (immune complex glomerulonephritis or renal infarction) CHF subarachnoid hemorrhage meningitis (2/2 bacterial seeding) brain abscess or epidural abscess |
|
lab findings in endocarditis? (indicate which are acute and subacute)
Anemia? WBC? ESR? Hematuria? RF? |
anemia (more common in SBE, normochromic, normocytic)
high WBC in acute ESR is hihg in SBE microscopic hematuria (SBE) RF (SBE) |
|
How can endocarditis be detected?
|
echocardiogram
TEE (transesophageal echo... detects vegetation in up to 90%) |
|
how should treatment be initiated in acute endocarditis?
SBE? |
start AB after obtaining 2-3 blood cultures
SBE is less urgent, wait for cultures to become + before starting tx |
|
what is the route of administration of AB in endocard?
|
parenteral
|
|
how long shoul dtx be given for AB for endocarditis?
|
4-6 wks
SBE can be tx for 2 wks if organism is susceptable to penicillin |
|
how is endocard therapy monitored?
|
serum bactericidal test (Schlicter test)
measures killing of pts organism based on leel of AB in pts blood |
|
how is the Schlicter test performed? what is its utility?
|
dilute serum in serial fashion
greatest dilution that kills patient's bug = end point it can predict bacteriologic but not clinical outcome |
|
indications for surgical intervention of endocarditis?
|
progressive heart failure
valve dysfxn (perf cusp) inability to control infecion multiple or large emboli fungal endocarditis (there are no cidal antifungal agents) |
|
what is meant by "culture negative" endocarditis?
|
not detectable by conventional blood cultures, or can be noninfectious
|
|
how should culture negative endocarditis be tx?
|
don't tx empirically w/o ID consult
consider pts other illness |
|
which organisms are "culture negative" in endo?
|
coxiella burnetti
legionella |
|
what does a recurrence of fever indicate in endocard?
|
not d/t infection, can be from drugs
thrombophlebitis emboli |
|
what is myocarditis?
|
inflamm process of cardiac muslce that may occur from organisms or the toxins they produce
|
|
si/sx of myocarditis?
|
many pts asymptomatic
can have arrhythmias, ekg abnormalities chf fever/chest discomfort elevated pulse, weak and thready poor quality heart sounds |
|
organisms that can --> myocard?
|
s. aureus
meningococci B. burgdorferi post-strep diphtheria rickettsia (RMSF) histoplasmosis coccidiomycosis toxoplasmosis Chagas disease (trypanosoma cruzi) |
|
what viruses are most common for causing myocard?
|
coxsackie A and B
echovirus |
|
definition of pericarditis?
|
inflamm dz of pericardium that can be acute or chronic
|
|
pathogenesis of pericarditis?
|
hematogenous seedin gduring bacteremia or fungemia
direct extension from contiguous focus of infection immune mech |
|
viruses associated with pericarditis?
|
coxsackie B (most common)
ECHo mumps flu coxsackie A adenovirus herpes |
|
which BACTERIA are associated with pericarditis?
|
s.aureus
trep pneumococci M. tuberculosis (2%, and esp in younger pts) |
|
which fungi --> pericard?
|
all
|
|
which parasites --> pericard?
|
toxoplasma
entameba histolytica (extension from amebic liver abscess) |
|
ekg seen in pericarditis?
|
diffuse ST elevations
|
|
what is the best way to detect pericardial effusion?
|
echocardiogram
|
|
what use is CXR in pericarditis?
|
may show enlarged cardiac silhouette if effusion is large
|
|
management of bacterial, fungal or parasitic pericarditis? (how to dx?)
|
get pericardial fluid for definitive dx (pericardiocentesis or open surgical procedure)
|
|
what causes constrictive percarditis?
management? |
late complication d/t scarring and shrinking pericardium
surgery |
|
Definition of nosocomial FUO?
|
>38.3 C on several occassions
infection not present or incubating on admission evaluation for 3 days cultures for 2 days if no dx, the FUO |
|
HIV associated FUO?
|
>38.3 C on several occassions
+ HIV serology Fever >4 weeks as outpt or 3 days in hospitalized pt |
|
Definition of Neutropenic FUO?
|
>38.3 C on several occassions
Neutrophil count <500 or 1000 and dropping Evaluation for 3 days - cultures for 2 days |
|
Which is the only type of fever that is treated empirically?
|
Neutropenic FUO because it can be deadly and is an EMERGENCY
all others... don't treat empircally b/c it can cause confusion |
|
What is the fractional breakdown of FUO?
|
1/3 malignant
1/3 infectiion 1/3 collagen vascular dz/vasculitis |
|
What is the most common ccause of a prolonged fever?
|
that they don't really have a fever at all... their body temp is just set higher than most
|
|
What is the least common cause of prolonged fever?
|
familial mediterranean fever
|
|
What are dry eyes associated with?
|
RA
Sjogren's SLE |
|
What is conjunctivitis associated with?
|
Cat Scratch
SLE |
|
What are conjunctival petechiae associated with?
|
Endocarditis
sepsis |
|
What is conjunctival suffusion associated with?
|
Leptospirosis
|
|
What are Roth spots associated with?
|
endocarditis
|
|
what are subconjunctival hemorrhages associated with?
|
infectious endocarditis
trichonosis |
|
what is uveitis associated with?
|
TB
Still's Sarcoid SLE |
|
What are Roth spots?
|
hemorrhagic lesions in fundus
|
|
What are WBC scans and what are they used for?
|
Remove pts WBC, tag them with radio isotopes and see where it goes... does it go to an abscess???
|
|
What does an increased alk. phos point to?
|
some sort of bone or liver dz
|
|
How to dx FUO?
|
Fever chart
If persists for 3 weeks, than FUO D/c all nonessential meds, if it resolves = drug fever, if persists for >3 days, continue w/u do abdominal CT and WBC scan; if no focus, is infectious endocarditis suspected? If no, do venous doppler If -, is status deteriorating? If not, just follow pt, if yes, do liver bx and laparotomy |
|
What is sepsis?
|
Clinical evidence of infection and systemic response to the infection
|
|
What is Systemic Inflammatory Response Syndrome (SIRS)?
|
2+ of the following:
fever HR > 90 bpm RR > 20/min WBC > 12,000 |
|
What does + blood culture indicate?
|
indx of failure of host defenses to contain infection at primary focus
index of failure of dr to remove, drain, or otherwise tx infection |
|
What is the indirect way taht bugs enter bloodstream?
What is the direct way? |
through lymphatics
IV catheters, prosthetics, self injection (IV drug users) |
|
When is clearing of organisms impaired?
|
if infection is overwhelming or if it has an intravascular foci
|
|
how do crticosteroids affect clearing of microorganisms?
|
don't affect clearing from blood, but they enhance the entry of organisms from tissue into blood b/c they suppress phagocytic cells at primary site of infection
|
|
Which cells are most important in clearing infection?
|
fixed macrophages in liver and spleen
|
|
Is unimicrobial or polymicrobial bacteremia more common?
|
unimicrobial
|
|
who commonly gets polymicrobial bacteremia?
|
pts with intraabdominal infections and/or bowel obstruction and non-hematologic malignancies
|
|
Which bacteremia very commonly causes a transient pattern?
|
Acute bacterial meningitis
|
|
What can cause continuous bacteremia?
|
infective endocarditis, or some other endovascular infection
suppurative thrombophlebitis infected aneurysm early typhoid fever or brucellosis |
|
What is the main source of bacteremia/fungemia?
|
IV catheter
|
|
What are hte 2 most common organisms of bacteremia/fungemia?
|
Staph
E coli |
|
Which organisms if found in blood are likely just contaminants?
|
coagulase - staph
strep viridans enterococci |
|
How much blood should be drawn to culture for bacteremia? Why?
|
20-30 ml for adults
The more blood you draw the more likely you are to get bacteria in the sample 1-5 ml in an infant |
|
How to make a lab dx of bacteremia and fungemia?
|
2 blood cutlures (2 separate venipunctures)
A single culture will only detect 80-90% of episodes A single culture that grows common skin flora is uninterpretable clinically |
|
How should you culture for FUO?
|
2 blood cultures, if - after 48 hrs, repeat 2x more
|
|
How should cultures be given if endocarditis is suspected?
|
if acute, 3 BC over 1 hr, then start tx
If subacute, 3 BC of 24 hr, if - after 48 hrs, repeat 2x |
|
What % die from bacteremia?
|
17.5%
|
|
What are some of the risk factors for death in bacteremia/fungemia?
|
>70 yo
Fungi or enteric GNR (not E. coli) Source in lungs, bowel or unknown malignancy, AIDS, renal failure Hypotension No fever Prescribing inappropriate antibiotics |
|
Clinical syndrome of shock?
|
hypotension (systolic BP <80-90)
tachycardia weak, thready pulse cool, clammy skin peripheral cyanosis altered respiration (hyperventilation early, followed by hypoventilation) change in mental status oliguria |
|
What are some of the mediators of septic shock?
|
IL-1
TNF-alpha |
|
What are some of the endotoxins involved in septic shock?
|
most are from GNR, so LPS/lipoprotein outer membrane
Lipid A is very active In animal models, endotoxin alone can ==> manifestations of septic shock |
|
What do endotoxins do?
|
activate complement cascade
activates coagulation --> DIC activates fibrinoloysis --> DIC activates kinin system --> hypotension |
|
pathophysiology of septic shock?
|
nidus of infections (caused by endogenous toxins or by activating endogenous mediators) --> activates various cytokines --> effects on myocardium itself (depression or dilatation) or effects on vasculature with both vasodiliatation and vasoconstriction --> maldistribution of blood flow
|
|
what is the prognosis of someone in septic shock?
|
50% recover
50% have multi organ failure and die |
|
what are some of the skin manifestations seen in septic shock?
|
intense vasoconstriction in extremities which can lead to acrocyanosis --> gangrene
esp with gram(-)rods: can get these raised necrotic looking lesions called ecthymic gangronosum - Some will go on to develop a diffuse white out of the lung called ARDS |
|
What is Activated protein C? Side effects?
When should it be used? |
antithrobotic, antiinflamatory and fibrinolytic activity; bleeding = major side effect
Only works if used EARLY! |
|
What are the tx options in septic shock?
|
Supportive
IV ABs |
|
What are the criteria for acute meningitis?
Chronic meningitis? Recurrent meningitis? |
Onset w/i hrs-days, <4 wks duration, bacterial (septic) or aseptic
4+ wks duration Multiple acute episodes w/i <4 wks |
|
What is acute meningitis?
|
inflammation of the meninges
infecction of subarachnoid space exudate over spinal cord and brain CSF w inflammatory changes |
|
Roles of CSF?
|
maintains constant IC pressure
protects against sudden pressure changes possesses antibacterial properties |
|
How do pathogens enter CSF?
|
paracellular passage
transcellular transport invasionw/i WBCs during diapedesis |
|
What are the most common organisms for acute bacterial meningitis?
|
Strep pneumoniae
N. meningitidis Listeria monocytogenes H. influenza B Group B strep gram - enterics Anthrax |
|
which organism is the primary pathogen in acute meningitis in adults?
in children? neonates? |
Strep pneumoniae
N. meningitidis (also associated with outbreaks and increased incidence of infection in household contacts) Broup B beta hemolytic strep |
|
which form of menignitis has a vaccine against it?
|
H. influenza B
|
|
When is the most common time of the year to get meningitis (and for which organism)?
|
Strep pneumonia (winter)
N. meningitidis (spring and winter peak, but year-round) |
|
Which meningiits organism has the highest mortality rate?
|
Strep pnuemonia (30%)
|
|
What is the most common way that acute bacterial meningitis spreads w/i body?
|
hematogenous
direct spread/extension less common (usually post-surgical or cranial injury, 2/2 congenital malformation, and est neighboring infection) |
|
what is the portal of entry for acute bacterial meningitis? wHY?
|
nasopharynx from bacteria in URT
Nasopharyngial mucosal epithelium provides local immunity and is the attachment site for bacteria |
|
How does N. menigitidis breach host defenses?
How do encapsulated organisms do it? |
makes IgA protease and escapes phagocytosis by capsular polysaccharide
inhbiit neutrophil phagocytosis and complement mediated killing |
|
What are hte host defense mech against menigitis?
|
complement
phagocytosis alternative complement pathway (merely the presence of the microbe activates complement) opsonization |
|
describe how the CNS gets infected in acute bacterial meningitis?
|
replication of organism in subepithelial tissue
hematogenous spread to CNS seeding of meninges by organism via choroid plexus penetration of BBB development of inflammatory response (--> brain edema and increased intracranial pressure/brain ischemia) |
|
What is the time frame of stage 1 of neutrophil migration into CSF?
when does it occur? |
1-2 hrs
cytokine release w/i CSF in response to bacterial replication or lysis --> enhanced binding of neutrophils and enodthelial cells |
|
What is stage 2 of neutrophil migration into CSF?
|
cytokine stimulation --> IL8 release by vascular endothelium --> neutrophil diapedesis and entry into CSF
|
|
What is stage 3 of neutrophil migration into CSF?
|
CSF cytokines activate neutrophils --> degranulation --> release of vasoactive lipid autacoids and toxic O2 metabolites --> impairment of BBB with leakage of albumin into CSF --> increasd perm of BBB --> brain edema
|
|
What are the different types of brain edema?
|
Vasogenic edema (disruption of BBB and leakage of capillary vessels)
Cytotoxic edema (increased intracellular fluid from cell injury) Interstitial edema (purulent exudate in arachnoid space interferes with reabsorption of CSF and obstruction of flow, with mov't of fluid from ventricular system to parenchyma) |
|
What bacterial products --> bacterial meningitis?
|
endotoxins
teichoic acid peptidoglycans |
|
what are the cellular mediators in acute bacterial meningitis?
|
TNF
IL1,6,8 Arachidonic acid PAF interferons |
|
What causes the decreased cerebral perfusion?
|
WBC get activated, which --> endothelial injury --> coag cascade activation --> thrombosis --> decreased cerebral blood flow
|
|
What are the pathologic features of acute bacterial meningitis?
|
purulent exuddate over brain, spinal cord and in ventricles
spinal root/nerve inflammation hydrocephalus (arachnoid thickening at base of brain) thrombosis/occlusion of cerebral vessels Subdural effusions |
|
What are the clinical features of acute bacterial meningitis?
|
life threatening emergency
acute and fulminant presentation fever, neck stiff, abnormal consciousness N/V/anorexia Brudzinski and Kernig sign photophobia, lethargy bulging frontanelle (in infants) and headache in adults |
|
What is Brudzinski sign?
Kernig sign? |
flex neck will arch their leg (spinal cord extends all the way to the back and its very stiff so it can bend the knee)
flex hip and knee and you will see the neck flex |
|
what are some of the more serious late complications of acute bacterial meningitis?
|
coma
ataxia seizures focal neurologic signs CN palsies papilledema is unusual |
|
what is papilledema? why is it rare?
|
bulging of optic disc
occurs when a pt is about to herniate, so not an acute sign |
|
what are some features that would suggest N. meningitidis?
Strep pneumonia? |
petechiae, non blanching, red, flat
respiratory infections (ear/sinus) |
|
clinical presentation of neonates with acute bacterial meningitis?
|
non-specific findings
poor feeding increased sleeping decreased urine output irritability vomiting diarrhea |
|
Normal CSF:
# cells/mm3 type of cells Glu Protein Pressure |
0-5
n/a 50-75 15-45 70-180 |
|
Bacterial meningitis CSF:
# cells/mm3 type of cells Glu Protein Pressure stain cytology |
>1000
segs low high high + + |
|
TB meningitis CSF?
# cells/mm3 type of cells Glu Protein Pressure stain cytology |
<500
mono low (20-40) hihg >150 nl/hihg AFB + AFB + |
|
fungal meningitis
# cells/mm3 type of cells Glu Protein Pressure stain cytology |
<500
mono low (20-40) high nl/high + india ink + |
|
Viral meningitis CSF:
# cells/mm3 type of cells Glu Protein Pressure stain cytology |
<1000
mono nml nml/high nml none +/- |
|
what is nml CSF blood glucose in relation to blood glucose?
|
2/3 of blood glucose, any less is a problem
|
|
what happens if the lumbar puncture is traumatic (hits a BV)?
|
can cause increased CSF protein (falsely)
|
|
what population normally has a high CSF protein?
|
neonates
|
|
Where else should be cultured?
|
petechial scrapings (if N. meningitidis)
tympanocentisis in otitis media (strep. pyogenes) sinuses |
|
what is the most important thing to keep in mind with treatment of bacterial meningitis?
|
must achieve bactericidal concentrations of AB in CSF
|
|
What should be used to treat an unknown cause of bacterial meningitis?
|
Vanco + 3rd generation cephalosporin for broad spectrum coverage (get more specific later)
|
|
other than with meds, how should a pt with meningitis be treated?
|
24 hr isolation in first 24 hrs of AB tx (for HiB and N. meningitidis)
steroids given before abx to reduce deafness from Hib Supportive care Tx of other infection sites and predisposing condition |
|
What is the mortality of bacterial meningitis in adults? infants?
|
30%
infants are higher |
|
Which is the most common permanent sequelae of acute bacterial meningitis in children?
|
deafness
|
|
Which organisms for bacterial meningitis have vaccines?
|
Hib
N. meningitidis Strep pneumoniae |
|
When are the vaccines given for Hib?
What is used for post-exposure proph? |
2 months
rifampin (given to members in household under 5 yo) |
|
What is the postexposure proph for N. meningitidis?
|
rifampin or ciprofoxdacin or ceftriaxone
given to household and close contacts, sometimes given to index case |
|
Who gets vaccinated against N. meningitidis?
|
military recruits
immunocompromised travellers to some areas college freshman |
|
Who gets vaccinated against Strep pneumonia?
|
Infants, starting at 2 months
|
|
Which bacterial meningitides have post-exposure proph?
Which don't? |
Hib
N. meningitidis Strep pneumonia Gram - bacilli |
|
Which organism for bacterial meningitis has no immunization?
|
Gram - bacilli
|
|
What is the leading cause of aseptic meningitis?
What are others viruses associated with aseptic meningitis? |
Enterovirus (echo and coxsackie B)
Herpesviruses Arbovirus (insect vector) Mumps HIV LCV (rare, from rodent exposure) |
|
when does LCV normally occur?
|
winter and fall
|
|
what are the bacterial causes fo aseptic meningitis?
|
partially treated bacterial infection
M. tubuerculosis Bartonella Brain abscess Parameningeal focus |
|
Non viruses/bacteria --> aseptic meningitis?
|
rickettsiae
spirochetes mycoplasma protozoa nematode fungi |
|
pathophysiology of viral meningitis?
|
mucosal colonization
escapes host defences, and disseminates and invade CNS |
|
how does viral meningitis spread?
|
Hematogenous spread after replication at specific site s
CNS invasion of BBB and indirect invasion via peripheral or CN (polio or HSV) |
|
What happens after the body is seeded with virus in meningitis?
|
inflammatory response --> alteration ofo BBB (--> introduction of serum proteins and local Ig synthesis)
Eradication of infection requires intact host immune response and T cell function |
|
Clinical features of viral meningitis?
|
presents with fever, ha, stiff neck
Changes in mental status suggest concurrrent encephalitis URI sx myalgias, arthralgias rashes |
|
which virus has a severe and fatal meningitis?
Which is mild and insidious? Which has association with myalgias/arthralgias? which has rashes? |
HSV
Non-polio enteroviruses LCV, leptospirosis mumps, enterovirus, HSV, EBV, leptospirosis |
|
what is arbovirus?
|
ARthropod BOrne vector
|
|
Treatment for viral meningitis?
|
symptomatic tx
antivirals not indicated EXCEPT for HSV IVIG for immunocompromised Treat children with acetominophen (not aspirin --> Reye's) to control fever |
|
Prevention of viral meningitis?
|
MMR prevents mumps as cause of meningitis
|