UW Deck 2 Flashcards
runs through ventral pons
fibers of CNs 5-8, corticospinal tracts, medial lemniscus, lateral spinalothalamic tract
vagus by the ear
auricular branch: cutaneous sensation of posterior external auditory canal; stimulation of vagal nerve with otoscope speculum –> decrease HR and BP –> vasovagal syncope event
sensation to most of external auditory canal
trigeminal nerve
facial nerve PANS efferent
salivation: submandibular and sublingual
viral myocarditis histology
lymphocyte infiltrate, focal necrosis
heart failure + recent viral infxn
dilated cardiomyopathy due to viral myocarditis (virus damages heart) –> systolic dysfunction
LVH, concentric hypertrophy
diastolic dysfunction –> wall stress –> heart failure/systolic dysfunction
dilated cardiomyopathy
dx of exclusion (pericardial dz, CAD, valvular dz, congenital dz, cardiac rhythm disturbances), systolic dysfunction, decreased stroke volumes, increased end volumes, regurgitation, dilation of all 4 chambers, primary (idiopathic), secondary (exogenous toxic agents)
vasopressin increases reabsorption of
water and urea @ inner medullary collecting duct, V2-receptor mediated
kidney filtration
simple diffusion depending on starling forces; filtration coefficient (kf) depends on area of capillary available for diffusion and permeability of capillary membrane; net filtration pressure (use oncotic and hydrostatic pressure – don’t need coefficient)
calcium handling in kidney
50-60% filtered ca reabsorbed in proximal tubules (paracellular pathway), reabsorption by distal tubule depends on parathyroid hormone
creatinine
freely filtered, secreted a litle by proximal tubules
PAH
freely filtered, entirely secreted by proximal tubules
wolff-parkinson-white
accessory AV conduction pathway: conduction reaches ventricles via accessory pathway slightly faster than AV nodal pathway –> recurrent paroxysmal supraventricular tachycardia, ventricular preexcitation, shortened PR interval, delta wave at start of QRS, widened QRS. Can also set up reentry arrhythmia (down AV node, up accessory pathway, normal QRS)
ST segment
plateau phase
T wave
ventricular repolarization
viral meningitis (vs. bacterial)
lymphocytic predominance, slightly elevated CSF protein, no organism on CSF gram stain and culture, more moderate symptoms (no stupor, coma, severe meningeal irritation)
bacterial meningitis (vs. viral)
high protein, low glucose, neutrophils predominate, really high WBC, often positive CSF culture/gram stain; mental status changes, seizures
meningitis common sx
fever, headache, nuchal rigidity, photophobia, painful extraocular movements
aseptic meningitis bugs
MCC: enterovirus family: coxsachie, poliovirus, echovirus, enterovirus; enterovirus = fecal-oral transmission, don’t cause gastroenteritis
adult bacterial meningitis bugs
- s pneumo, 2. n meningitis
polio virus
fever, malaise, aseptic meningitis –> myalgia, asymmetric paralysis (legs), damages anterior horn LMN –> hyporeflexic
aseptic meningitis via respiratory droplets
varicella, mumps, adenovirus, these 3 can also cause encephalitis
sexually transmitted viruses that can cause aseptic meningitis
HIV and HSV 2 more common than HSV 1, EBV, and CMV
arboviruses that can cause aseptic meningitis
togaviridae, flaviviridae, bunyaviridae; most common in summer and fall when arthropods are most active
meningitis in HIV/AIDS
cryptococcus neoformans
cryptococcal meningitis
headache/fever/lethargy, immune compromised (cancers), low glucose, increased protein, lymphocytes predominate, increased cell count; transparent capsule on india ink stain of CSF (ink stains background, bug stays transparent), thick polysaccharide capsule
listeria meningitis
ampicillin, GP rod, tumbling motility
fungal cell wall
not made of peptidoglycan
increased mixed venous blood oxygen
abnormal hb (binds with greater affinity to oxygen), oxidative metabolism inhibition (cyanide toxicity)
Obstructive lung disease
increase PaCO2
Diffusion problem
calculate A-a gradient; more normal PaCO2 (because it diffuses 20x better than oxygen) decreased PaO2
Perfusion problem
CO2 and O2 do not equilibrate with outside
Calculate A-a gradient
arterial PO2 given by ABG; PAO2 @ sea level (alveolar gas equation) = 150 - (PaCO2/0.8)
normal A-a gradient
10-15 mmhg
normal PAO2 –> normal PaO2
104 mmhg –> 95-100 mmhg (below 95: hypoxemia); drop occurs due to bronchial venous blood
PO2
inspired air: 160 mmhg –> mixes with water in trachea: becomes 150 mmhg –> alveolus: 104 mmhg; venous blood equilibrates with alveoli (40 mmhg –> 104 mmhg) –> drops to 95-100 mmhg because of bronchial venous blood
PCO2
venous blood PCO2: 45 –> alveolar PCO2 = 40 –> trachea CO2: 0 mmHg
venous/alveolar equilibration
NL: full equilibration after passing through 1/3 of capillaries (fast diffusion, perfusion-limited equilibration); if capillary perfusion is poor: slower or incomplete equilibration; tracheal air = alveolar air; venous blood = arterial blood
poor ventilation, what would alveolar gas composition be?
close to venous gas composition
diffusion-limited gas exchange
emphysema, pulmonary fibrosis, exercise (high perfusion)
4 major causes of hypoxemia
right to left shunt (congenital heart diseases); V/Q mismatch (pneumonia, COPD, pulmonary embolism); alveolar hypoventilation (sedative overdose, sleep apnea, myasthenia gravis, high altitude –> low oxygen pressure in alveoli); diffusion problems (alveolar hyaline membrane disease)
cryptococcus neoformans
immunocompromised patients, inhaled –> asx lung infection/pulmonary cryptococcosis (mucicarmine stain lung tissue and bronchoalveolar washings) –> meningitis (india ink CSF); serologic testing (latex agglutination) to detect capsular antigen in CSF
oral thrush
white plaques, associated with immunosuppression, diabetes, antibiotics, steroids\
esophagitis
HIV+ candida infection, odynophagia, dx with endoscopy + bx
renal osteodystrophy
decreased calcitriol (active vitamin D), retention of phosphates (bind Ca –> exacerbates hypocalcemia) –> hyperparathyroidism + more bone turnover (exacerbates hyperphosphatemia)
hypercoagulable state
surgery
marantic endocarditis
disseminated cancer associated with hypercoagulability –> NBTE (non-bacterial thrombotic endocarditis)
non-bacterial thrombotic endocarditis (NBTE)
sterile fibrinous vegetations along edges of valves = thrombus, no inflammation, often due to hypercoagulable state due to underlying disease
trousseau’s sign
tumor-associated procoagulants release –> migratory thrombophlebitis (seen in pts with disseminated cancers)
hypercalcemia in hospitalized pt
hypercalcemia of malignancy, pth-like substance from tumor
extrahepatic biliary atresia
congenital, jaundice, dark urine/light stools, conjugated hyperbilirubinemia, intrahepatic bile ductular proliferation, portral tract edema and fibrosis, parenchymal cholestasis, increased alk phos, ggt
hemolytic disease in Rh+ newborn
jaundice, unconjugated hyperbilirubinemia, hemolytic anemia, + coombs test
gilbert dz
mild unconjugated hyperbilirubinemia during stress
A1AT deficiency, effect on liver
hepatic intracytoplasmic inclusions that are eosinophilic on H&E, strongly PAS positive
physiologic jaundice
goes away after a week
d-isoimmunization
Rh disease
most potent chemotactic eicosanoid
leukotriene B4 (also 5-HETE = leukotriene precursor)
irreversible changes in ASD
chronic pulmonary HTN –> permanent eisenmanger syndrome, pulmonary sclerosis so severe/irreversible that you can’t fix the ASD because the RV won’t be able to pump; atrial and ventricular enlargement can be reversed
long qt syndrome
if pt is otherwise healthy, long qt = congenital issue, predispose to torsades to points –> syncope or death; 2 common congenital disorders related to K+ channel mutation –> delayed rectifying K+ current
jervell and lange-nielsen
autosomal recessive, neurosensory deafness, long qts
romano-ward syndrome
more common than jervell and lange-nielsen, no deafness, long qt
sudden onset syncope
suggests arrhythmia
qt
start of qrs –> up to t wave
mutations that cause dilated cardiomyopathy
mutations that affect cytoskeleton proteins or mitochondrial enzymes
HOCM
syncope upon exertion
sarcoidosis
immune mediated = disordered immune regulation –> intraalveolar and interstitial accumulation of CD4 T cells –> high CD4/CD8 ratio in bronchoalveolar lavage fluid (differentiates sarcoidosis from hypersensitivity pneumonitis or AIDS-related lymphocytic interstitial pneumonitis - have low CD4/CD8 ratios)
high neutrophils in lungs
bacterial PNA, acute toxic injury
high CD8 cells in lungs
lung transplant + chronic rejection
intussusception
impaired venous drainage, necrosis, colicky abdominal pain, current jelly stools = mucus + blood
inferior mesenteric vein
does not course with the inferior mesenteric artery, drains into splenic vein –> portal vein
celiac trunk
supplies foregut except mouth, pharynx, proximal esophagus
internal iliac supplies certain parts of the gut
middle rectal artery, inferior rectal artery (via pudendal)
external iliac supplies
anterior abdominal wall, lower extremities
schwannoma tumor marker
S-100 (both melanomas and schwannomas are S-100 because both are derived from neural crest cells)
schwannoma etiology
can come from any CN (except 2) because they’re all covered by schwann cells, tumors of PNS
schwannoma histology
biphasic pattern (antoni a + b), spindle cells (elongated with regular oval nuclei), highly cellular areas = antoni a, low cellularity = antoni b, antoni a areas may have palisading patterns = picket fence)
mitral stenosis from acute rheumatic fever
takes years or decades to develop, MCC mitral stenosis = chronic rheumatic fever
myocarditis from ARF
can cause dilated cardiomyopathy –> mitral regurgitation
acute rheumatic fever and PSGN
rarely occur together, caused by different strains
ARF, sydenham
CNS involvement
cirrhosis
diffuse hepatic fibrosis, normal lobular architecture –> nodular parenchymal regeneration, micronodular (<3 mm in diameter) or macronodular
Dubin-Johnson
accumulation of course pigmented granules
intrahepatic hydatid cysts + surrounding fibrosis
echinococcus
granulomatous destruction of bile ducts
primary biliary cirrhosis
hereditary pancreatitis
mutated trypsinogen that cannot be inactivated by pancreatic secretory trypsin inhibitor (PSTI) –> premature activation + recurrent acute pancreatitis
gastric adenocarcinoma
associated strongly with h. pylori
liver cirrhosis most commonly associated with
alcoholism, hep b and c
megaloblastic anemia associated with
B12, folate deficiency, methotrexate, phenotoin, some inborn metabolic errors
common colds
coronavirus, rhinovirus, adenovirus
bronchopneumonia
patchy inflammation of a number of lobules
interstitial pneumonia
inflammation confined to alveolar walls
lobar pneumonia
inflammation involves entire lobe; 4 phases: congestion (first 24 hrs: vascular dilatation, alveolar exudate mostly bacteria, red/boggy lung) –> days 2-3: red hepatization: alveolar exudate contains erythrocytes, neutrophils, fibrin, red firm/hepatocyte-like –> days 4-6: gray hepatization: gray/brown firm lobe, RBCs disintegrated, fibrin and neutrophils remain –> resolution: enzymatic digestion of exudate
diastolic depolarization
depolarization of SA, AV node occur during diastole
crohn’s
increased Nf-kb –> increased cytokines and inflammation, but persistence of microbes –> chronic inflammation
inflammatory bowel disease
multigenic, possibly involves HLA, NOD2 (intracellular microbe receptor –> triggers Nfkb)
nfkb
responsible for cytokine production, connected to microbial recognition
renal plasma flow
decreased by angiotensin 2, epinephrine, norepinephrine
myxoma
constitutional symptoms (myxoma produces IL-6 –> fever, weight loss), mid-diastolic rumble over apex, positional CV sx (syncope, dyspnea)(valvular obstruction depends on position), embolic sx, large pedunculated mass on LA; histology = scattered cells within mucopolysaccharide stroma, abnormal blood vessels (myxoma produces a lot of vascular endothelial growth factor), hemorrhaging
endocarditis
risk factors: prosthetic valves, valvular disease, IVDU, immunosuppression, vegetations seen on echo, typically a regurgitant murmur
AML
pancytopenia (anemia, neutropenia, thrombocytopenia)
light from optic tract –>
mainly lateral geniculate nucleus, also suprachiasmatic nucleus (circadian rhythms), pretectal areas (light reflex), superior colliculus (reflex gaze); from lateral geniculate nucleus –> optic radiations (meyer’s loop + baum’s loop) –> primary visual cortex
damage to meyer’s loop
contralateral superior quadrantanopia
temporal lobe lesions
aphasia (dominant hemisphere lesions), memory deficits, hallucinations (visual, sensory, auditory), seizures (complex partial and tonic-clonic)
heart failure cells
pulmonary HTN –> RBCs extravasate into alveoli –> digested by macrophages, iron-containing macromolecules converted to hemosiderin –> hemosiderin-containing alveolar macrophages = heart failure cells = indicate pulmonary congestion/edema associated with heart failure
golden or brown cytoplasmic granules
hemosiderin or lipofuscin, use Prussian blue stain to differentiate
Prussian blue stain
detects intracellular iron (turns blue)
pulmonary htn associated with congestion of pulmonary capillaries
only when HTN is distal to capillaries (LH failure); if proximal to capillaries, then capillary pressures are okay (ex: COPD, interstitial lung disease, pulmonary embolism, autoimmune vasculitis; airway obstruction –> pulmonary arterial hypertension)
granulomas in lung tissue
TB, fungal infections, inhalation of foreign particles, beryllium, wegener’s, sarcoidosis, histiocytosis
non-caseating granulomas in lung tissue - appearance
tightly clustered macrophages surrounded by rim of mononuclear cells, multinucleated giant cells
barrett’s esophagus
intestinal columnar epithelium with goblet cells = should not be there (esophagus normally has stratified squamous epithelium), metaplasia adaptive at first but increases risk of adenocarcinoma; acid –> inflammation and necrosis of normal esophageal epithelium
risks for squamous carcinoma of esophagus
alcohol, smoking, achalasia, nitrosamine-containing foods, plummer-vinson syndrome
neurofibromas
short, sessile, or pedunculated cutaneous lesions, associated with NF-1 mutation (autosomal dominant), tumors of schwann cells (derived from neural crest), cutaneous and subcutaneous, rubbery texture
Neurofibromatosis 1
cafe-au-lait spots (smooth or irregular borders), lisch nodules (pigmented hamartomas of iris = asx), optic gliomas (can cause blindness), other brain tumors (weakness, headaches, different sx)
conus medullaris syndrome (damage to L2)
flaccid paralysis of bladder and rectum, impotence, and saddle anesthesia (S3-S5)
cauda equina syndrome
cauda equina has 18 spinal/peripheral nerves: low back pain radiating to one or both legs, saddle anesthesia and loss of anocutaneous reflex (S2-S4, pudendal nerve), bowel and bladder dysfunction (S3-S5)
T12
where lumbar spinal nerves originate
achilles reflex
S1 and S2, tests integrity of sciatic nerve (S1 and S2 also do sensation of posterior leg and thigh)
knee jerk reflex
L3 and L4 (part of femoral nerve)
Wernicke korsakoff syndrome
if give dextrose infusion without thiamine to alcoholic/malnourished patient –> drop in thiamine concentration –> pyruvate DH needs thiamine –> brain can’t metabolize glucose –> necrosis of mammillary body
thalamus
responsible for relaying information between spinal cord and cortex
chronic thiamine deficiency
korsakoff psychosis
Mammillary body
part of Papez circuit (part of limbic system, does emotion and memory)
c-ANCA
antibodies against lysosomal enzymes in neutrophils and monocytes, found in Wegener’s = necrotizing granulomatous vasculitis
Wegener’s
triad: pulmonary sx (necrotizing granulomas in the lung), upper respiratory tract (mucosal granulomas that ulcerate, sinusitis), renal dz (RPGN)
RPGN associated with wegener’s
type 3 = pauci-immune, high c-ANCA in blood, no antibodies/complement/immune complexes found in the kidney (unlike goodpasture’s)
IgA nephropathy
2-3 days after respiratory infection (much sooner than PSGN), also kids and young aduls (like PSGN)
myxomatous degeneration/mitral valve prolapse
MC abnormality predisposing to native valve bacterial endocarditis in the US (not rheumatic fever anymore due to antibiotics); MVP predisposes to infected vegetations (fibrin collects on MVP, bugs collect on fibrin during periods of bacteremia) –> vegetations can throw thrombi
native valve bacterial endocarditis
most commonly involves mitral valve (most common abnormality = MVP), predisposing factors: mitral regurgitation (in the US, MR used to be most frequently caused by rheumatic fever, now it’s most frequently caused by myxomatous degeneration)
nonbacterial endocardial thrombus formation
high pressure against endocardial endothelium (mitral regurg: from high pressure to low pressure compartment)
calcification of mitral annulus
most common in older people, hx of myxomatous degeneration or high ventricular pressures
hemangioma
well-circumcised masses of spongy tissue; cavernous, blood filled vascular spaces of various sizes, lined by epithelial layer, mostly benign
idiopathic membranous nephropathy
associated with IgG4 antibodies against phospholipase A2 receptor (only applies to idiopathic, not SLE membranous nephropathy)
amyloidosis of kidney related to multiple myeloma
related to deposition of light chains
systemic/multi organ amyloidosis in primary systemic amyloidosis
deposition of immune globulin light chains; primary systemic amyloidosis associated with monoclonal B cell proliferation (multiple myeloma)
respiratory drive
respiratory rate set by medullary respiratory center, input from central and peripheral chemoreceptors; CO2 readily diffuses across blood-brain barrier, creates H+, activates medullary respiratory center
respiratory drive in pt with COPD
chronic hypercapnea –> medullary respiratory center no longer responds to high levels of CO2, only drive to breathe is low O2 –> giving O2 is dangerous because it can eliminate their drive to breathe
carotid sinus
internal carotid artery
central chemoreceptors
indirectly sense arterial CO2, directly sense H+ (created by CO2 that has crossed the blood brain barrier)
minimal change disease
immune mediated: responds to steroids, associated with infection; increase in anionically charged proteins (albumin)
disruption of glomerular basement membrane
alport
diabetic glomerulonephropathy
hyaline masses in mesangium, eosinophilic
focal tubular necrosis and epithelial shedding
acute tubular necrosis, often accompanied with rupture of basement membranes
heteroplasmy
mitochondria are distributed unevenly to daughter cells –> some cells have mostly NL or abNL mitochondria –> creates variety in disease expression
mitochondrial encephalopathy
with lactic acidosis and stroke-like episodes
variable expressivity
differences in phenotype of an autosomal dominant disorder
complement-mediated cytotoxicity
IgG, IgM; IgM can effectively activate C1 because C1 needs to bind 2 or more antibodies (IgM = pentamer)
anaphylaxis
systemic version of allergic reaction
type 1 hypersensitivity MOA
first contact –> B cells undergo class switching to IgE –> IgE bind to IgE Fc receptors on basophils and mast cells –> second exposure –> cross-linking, degranulation, release of histamine, heparin, leukotrienes, others –> systemic vasodilation, increase in vascular permeability, bronchoconstriction –> hemodynamic and respiratory instability
type 1 hypersensitivity clinical situations
asthma, anaphylaxis
superior mesenteric artery
leaves aorta at L1; SMA syndrome: SMA and aorta trap/obstruct the transverse duodenum because of decreased angle between SMA and aorta (aortomesenteric angle decreases secondary to diminished mesenteric fat, pronounced lordosis, or surgical correction of scoliosis)
transverse duodenum
courses horizontally at L3, between aorta (posterior) and SMA (anterior)
renal arteries
originate from aorta at L1, IVC (formed by right and left common iliac veins at L4-L5) is anterior to right renal artery
thoracic duct
empties into left subclavian
anal fissure
fear in mucosa, majority occur at posterior midline of anal verge (distal to pectinate line, line between anal skin and perianal skin), posterior anal canal relatively poorly perfused (more sensitive); anal fissures associated with constipation; severe tearing pain; may have a skin tag
obstructive PFT profile
decreased FEV1/FVC, increase in TLC and RV
restrictive PFT profile
decreased TLC and FVC due to decreased lung expansion
COPD clinical
progressive exertional dyspnea (emphysema), frequent respiratory infections (chronic bronchitis)
heart failure
heart cannot pump enough blood, or it can only do so with elevated ventricular filling pressure
diastolic heart failure pathophysiology
decreased ventricular relaxation/compliance, increased ventricular stiffness, caused by HTN/LVH and MI
diastolic heart failure, pressure/volume curve
bottom curve moves up and to the left; EF remains the same, LVEDP increases to abnormally high in order to achieve near-normal LVEDV/stroke volume (always trying to normalize CO/BP)
systolic dysfunction
decreased EF, reduced CO at normal LVEDV, increases to abnormally high LVEDV/LVEDP in order to increase CO (always try to normalize CO and BP during compensation)
diastolic vs. systolic
diastolic only increases LVEDP (normal LVEDV, normal contractility), systolic failure increases LVEDP and LVEDV (abnormal contractility)
enlargement of LA can compress
left recurrent laryngeal nerve (loops behind ligamentum arteriosum, underneath and around aortic arch, back up alonside trachea to the larynx = Ortner syndrome: neurapraxia –> left vocal cord paresis and hoarseness
hoarseness
vocal cord disease or malfunction
x-linked agammaglobulinemia
increased risk for streptococci and staphylococci; normal responses to listeria and viruses (intracellular), and fungi
neonates up to 3 months
not yet fully developed cell-mediated immunity, at risk for listeria (rarely causes disease in normal healthy adult)
candida
normal skin and mucous membrane flora; causes systemic illness in immunecompromised (opportunistic); skin and mucous infections if pt doesn’t have local pre-formed T cells (cutaneous candidiasis, oral thrush, esophageal candidiasis, vulvovaginitis); systemic infections if pt doesn’t have neutrophils (right-sided endocarditis, kidney and liver abscesses, candidemia); polymorphic (seen as budding yeast or pseudohyphae)
deficiency in complement
SLE-like disease, neisseria gonorrhea, neisseria meningitis
blastomyces dermatitidis
ohio and mississippi river valleys, great lakes region, pulmonary: PNA; disseminated: common and severe; bx: large round yeast and single broad based bud
dimorphic fungi (molds with hyphae in RT/25-30, yeast in body temp 35-37)
blastomyces, coccidioides (paracoccidioides), spirothrix, histoplasma
sporothrix schenkii
gardening/thorn prick, pustules, ulcers, subcutaneous nodules along lymphatics, culture: branching hyphae, bx: round or cigar-shaped budding yeast
coccidioides immitis
southwestern states, mold form in soil, pulmonary form: flu-like illness, cough, erythema nodosum, disseminated form: affects skin, bones, lungs; bx: doubly refractile thick-walled spherules filled with endospores
histoplasma capsulatum
ohio and mississippi river valleys, soil, bird, bat droppings; pulmonary: similar to tb (lung granulomas); disseminated: lungs, spleen, liver; bx: oval yeast cells within macrophages
paracoccidiodes
central and south america, mucocutaneous or cutaneous ulcers, can progress to LNs/lungs, bx: cells covered in budding blastoconidia
aspergillus
mold form only, septate hyphae with acute angles, mainly immunocompromised pts
malassezia furfur
cutaneous mycosis (hypopigmented patches), KOH preparations of skin scrapings = short hyphae and spores = spaghetti and meatballs
rhizopus, mucor, absidia
saprophytic fungi, causes mucormycosis in immunocompromised; mold form of rhizopus and mucor = nonseptate hyphae and wide angles, paranasal infxn in diabetic pts
fungal sinus infections
aspergillus, mucor (mucor in diabetics and immunocompromised)
hemochromatosis genetic mechanism
HFE mutation, abnormally high iron intestinal absorption, HFE expressed on basolateral side - binds transferrin and takes in iron –> amount of iron taken into the cell regulates cell’s uptake of iron from the gut
hemochromatosis clinical presentation
affects heart, pancreas, liver - cirrhosis, HCC
iron deficiency anemia
celiacs
basal ganglia atrophy
wilson’s disease
mycobacterial infections
require IFN-g; infected macrophages –> secrete IL-12 –> Th1 cells secrete IFN-g –> helps with phagocytosis; defects in this pathway –> disseminated mycobacterial infections, require lifelong antimycobacterial agents
x-linked agammaglobulinemia
predisposed to lower respiratory infections and giardia
s epidermidis
ubiquitous on skin, attaches to foreign objects in the body, synthesis biofilm (extracellular polysaccharide matrix) that protects bugs from antibiotics, opsonization, neutrophil migration, t-cell activation –> can then release bugs into the bloodstream –> must remove foreign object infected with biofilm; MCC of endocarditis with prosthetic valves and septic arthritis for joint replacement
tx s epidermidis
should treat aggressively pending organism identification and antimicrobial susceptibility; initial empiric treatment with vancomycin +/- rifampin or gentamicin due to widespread antibiotic resistance of s. epidermidis (especially in nosocomial infxns)
staphylococcal tx
ciprofloxacin resistance seems to accompany methicillin resistance; methicillin resistance likely means cephalosporin resistance bc methicillin resistance = alteration of penicillin binding protein (same protein bound by cephalosporin)
obligate intracellular organisms
chlamydia, rickettsia
facultative intracellular organisms
legionella, listeria, mycobacteria, salmonella, neisseria
Staph aureus
most pathogenic staph (coagulase positive = able to clot blood); produces yellow pigment; endocarditis in IVDU; MCC osteomyelitis
staph aureus protein A
cell wall component, binds Fc portion of IgG, prevents complement fixation and phagocytosis
food poisoning by staph
staphylococcal enterotoxin
enveloped viruses
susceptible to ethers and other organic solvents which dissolve the envelope –> lose infectivity
viral heat stability
destroyed by heating 50-60degrees for 30 minutes
death by diarrhea
MCC in 3rd world = viruses;
staph vs. strep
staph = clusters; strep = chains
catalase test
differentiates staph (positive) vs. strep (negative)
neisseria meningitidis
GN kidney-bean shaped cocci; lipooligosaccharid (LOS) correlates with morbidity and mortality, outer membrane LOS acts like LPS of enteric GNRs, sepsis by inducing systemic inflammatory response, cutaneous petechiae/hemorrhagic bullae, lacks O-antigen of LPS, capsule helps resist phagocytosis but is not associated with morbidity/mortality, protective antibodies are directed against capsular polysaccharide (vaccine = capsule polysaccharides); URI, meningitis, meningococcemia
lancet shaped
strep pneumo
