Golj Patho: Cell injury and inflammation Flashcards
Myeloperoxidase deficiency
NBT dye test:
Respiratory burst present:
FA 208
NBT dye test is positive - blue color because Respiratory burst is present.
Lack MPO which: Cl- + peroxide into bleach.
usually asymptomatic but more prone to candida infections.
Chronic granulomatous disease
what enzyme is defective?
this renders child susceptible to what type of bacteria?
fa 215
X-linked R
Lack NADPH oxidase which is responsible for respiratory burst using Oxygen.
Boy is susceptible to catalase + bacteria (staph, aspergillus), but can use the peroxide created in catalase - bacteria (strep) to kill it.
Umbilical cord does not fall off.
defect in what surface protein?
what cell uses this?
FA 227
beta integrin defect / CD18 integrin
Neutrophils use it for tight binding to umbilical cord endothelium
Why is angioedema a complication of ACE inhibitor?
FA 386, 555
ACE normally degrades bradykinin, a kinin that increases vessel permeability and hence swelling of tissues. (also increases pain, vasodilation)
ACE inhibitors also cause cough.
Actinic keratosis
cause
what type of cell change
FA 443
UV-b light damage of skin
causes predisposition of skin cells to squamous cell carcinoma; type of dysplasia
H. Pylori
causes what type of cell change in the stomach?
FA 360
glandular metaplasia, precursor for adenocarcinoma of the stomach
stomach should not have glands
Virchow gland is found (left supraclavicular node)
Mechanism of methotrexate use in psoriasis
FA 63
methotrexate blocks dihydrofolate reductase, prevents dTMP from being created for DNA synthesis
this blocks S phase
Budd-Chiari syndrome
cause and effect?
FA 370
thrombosis or compression of hepatic veins causing necrosis in liver -> congestive liver disease
will see caput medusa (varices), nutmeg liver
nutmeg liver
FA 370
may be seen in congestive liver disease; also seen in right heart failure; caused by thrombosis in hepatic vein, which backs the flow of blood.
will see varices as well
cherry-red appearance of skin, decreased SaO2 (oxygen saturation), and headache
FA 257, 605
classic presentation of CO poisoning
Co binds to hb therefore not all RBC’s bound to O2; decreased SaO2
cherry-red because Hb is tightly bound to something
what do you ask a patient who was in a fire?
do you have headache or confusion?
early signs of CO poisoning, important to ask
membrane blebbing is an example of what cellular damage
it is reversible cellular injury caused by hydropic / cell swelling, which was due to hypoxia which impairs oxidative phosphorylation
cardiac troponin in pt is elevated. what has occurred morphologically to their heart myocytes?
FA 224
lack of ATP results in sodium build up and hydropic damage (swelling)
plasma membrane damage results in leaking of enzymes and additional calcium will enter cell.
myocytes release CK-MB and troponin
FA 224
three phases of cell death of loss of nucleus
nuclear condensation (pyknosis)
fragmentation (karyorrhexis)
dissoluation (karyolysis)
ischemic infarction of brain leads to what necrosis pattern
liquefactive necrosis
microglia contain proteolytic enzymes and due to brain’s increased fat content
granulomatous infection in TB resembles what type of necrosis
FA 223
caseous necrosis
FA 223
female undergoes trauma to breast in car accident
what type of necrosis ensues and what is the mechanism
FA 223
fat necrosis, nonenzymatic in this case.
deposition of calcium allows fatty acid released from trauma to undergo saponification
this would be dystrophic calcification
FA 223
30 y/o pregnant female with preeclampsia
will damage placenta via what necrosis
FA 581 233
fibrinoid necrosis of the umbilical cord vessel wall
caused by high blood pressure in mother (preeclampsia)
FA 581, 223
necrotic damage to blood vessel wall; immune reactions in vessels
immune complexes with fibrin
FA 233
fibrinoid necrosis
examples are palpable purpura, necrotizing vasculitis
FAA 223
endometrial shedding during menstrual cycle is an example of what cellular process
apoptosis
cellular injury, DNA damage, or decreased hormonal stimulation will lead to the inactivation of what factor?
FA path section
Bcl-2, which is anti-apoptotic. removal of it will release cytochrome C from mitochondria
CD14 location and what does it bind to
Macrophage surface receptor that recognizes lipopolysaccharide (LPS) on the surface of gram negative bacteria
effects of LTC4, LTD4, and LTE4
slow reacting substances of anaphylaxis 1 vasoconstriction 2 bronchoconstriction / spasm 3 increased vascular permeability all are smooth muscle contraction
this leukocyte is involved in type I hypersensitivity
releases its granules via IgE crosslinking
can be activated via C3a and C5a
mast cells
poma p11
what is the second phase of the mast cell response?
i.e. how is the acute inflammatory response continued (delayed response)
poma 12
Leukotrienes
maintain the acute inflammatory response
poma p12
role of C3b
opsonization
this inactive proinflammatory protein - once exposed to subendothelial or tissue collage - activates coagulation and kinin system
Hageman factor or F XII
what mediates redness and warmth (rubor and calor)
what three important molecules
Histamine, prostaglandins, and bradykinin mediate vasodilation which increases blood flow
NOT leukotrienes - these mediate vasoconstriction
where does exudate leak from and what mediates its leakage
poma 12
swelling (tumor) is leakage of exudate (protein and liquid) from postcapillary venules
mediated by histamine - which causes endothelial cell contraction - and tissue damage
what mediates pain (dolor) and how
bradykinin and PGE2 mediate pain by sensitizing sensory nerve endings
what mediates fever?
two are things released from a certain leukocyte
poma 13
TNF and IL-1 are released from MQ in contact with pyrogens (for example, LPS from bacteria) and cause the perivascular cells of hypothalamus COX enzymes to increase activity -> this leads to PGE2 production
PGEEEE - FEEEVER
poma 13
How does aspirin lower fever
poma 13
inhibits cyclooxygenase so that PGE2 cannot be formed in the hypothalamus which would otherwise increase the body’s temperature set point
P-selectin is released from what specific intracellular structure upon stimulation by histamine?
Weibel=Palode bodies
what induces E selectin formation on endothelial cells
TNF and IL-1
where is CD11/18 integrin (beta integrin) located and what upregulates its expression
what are the two integrins called
FA 227
located on neutrophils, stimulated by C5a and LTB4 (which also happen to be neutrophil chemotactic factors)
The two integrins are LFA-1 and Mac-1
FA 227
leukocyte adhesion deficiency is due to defect of
FA 215
the CD18 subunit on LFA-1 integrin
FA 215
pt lacks pus formation
FA 215
leukocyte adhesion deficiency
CD18 subunit
FA 215
pt presents with recurrent pyogenic infections, partial albinism.
what is the mechanism of this disease
FA 215
Chédiak-Higashi syndrome is defect in lyososomal trafficking regulator gene (LYST)
can’t fuse phagosome-lyososomes, therefore bacteria that are phagocytosed
pyogenic infections are by staphylococci and streptococci
FA 215
Chediak-Higashi syndrome
FA 215, poma 13
LYST lysosomal trafficking regulator gene is defective
sx include light albinism, pyogenic infections by staphyloocci and streptococci, peripheral neuropathy
giant granules are seen in granulocytes, there is pancytopenia, mild coagulation defects.
fa 215, poma 13
Role of superoxide dismutase
FA 208
convert superoxide O2- to H2O2
FA 208
myeloperoxidase role
FA 208
H2O2 converted into bleach HOCl
FA 208
oxidative / respiratory burst
O2 - > O2- superoxide via NADPH oxidase
Neutrophils and monocytes only
Nitroblue tetrazolium test in:
chronic granulomatous disease
MPO deficiency
negative (in CGD, do not have NADPH oxidase and therefore no respiratory burst)
positive (have NADPH oxidase)
name bacteria that pts with Chronic granulomatous disease are susceptible to
FA 215
susceptible to catalase positive bacteria such as:
staph aureus
Pseudomonas cepacia (very important, because all students already know staph aureus)
Aspergillus
Need PLACESS
FA 215
pt with higher risk of candida infections
what enzyme is lacking
FA 208, poma 14
MPO myeloperoxidase deficiency usually asymptomatic NBT dye test is positive - have resp burst FA 208, poma 14
how do macrophages call in more neutrophils to an inflammatory site
produce IL-8
how is chronic inflammation initiated
what main cell types mediate this type of inflammation
MQ’s ingest the viral microbe, present MHC-II on their surface to activate T helper cells
macrophages and fibroblasts
FA 225, poma 14
chronic inflammation is characterized by what
FA 225, poma 14
persistant destruction and repair via fibroblasts and mq’s;
call in lymphocytes and plasma cells into tissue
associated with blood vessel proliferation, fibrosis.
FA 225, poma 14
describe what signals CD4+ T cell activation
FA 203, poma 15
B7 on DC binds to CD28
TCR along with CD3 binds to antigen presented on MHCII
FA 203, poma 15
describe what signals B cell activation
FA 203
Thelper cell binds to MHCII on B cell
CD40L on Thelper cell binds to CD40 on B cell
Th cell then releases cytokines that determine Ig class switching of that B cell
FA 203
Th1 cell secretion
what stimulates Th1 creation
FA 202
IFN-gamma - which activates MQ’s and CD8+ T cells
activated by IFN-gamma and IL-12
FA 202
Th2 cell secretion
what stimulates Th1 creation
secretes IL-4 (IgE), IL-5 (eosinphilic cell chemotaxis and activation) and IL-10
IL-4 activates Th2 cells
inhibited by IFN- gamma
FA 202
in what ways to CD8+ cells mediate killing?
FA202
perforins and granzyme B
perforins create holes for granzymeB to enter and activate caspases
Expression of FasL, which binds to Fas on target cells activating apoptosis
FA 202, poma 15
what is the key characteristic of a granuloma?
FA 225
epitheloid histiocytes / epitheloid macrophages
(macrophage with abundant pink cytoplasm)
FA 225
what are noncaseating granulomas
poma 15
granulomas that lack central necrosis
remember that caseous necrosis has necrosis in the middle of a granuloma
poma 15
what are caseating granulomas
granulomas with central necrosis
characteristic of TB, fungal infections
histologic hallmark of Crohn’s disease
hallmark of ulcerative colitis
FA 362
noncaseating granulomas is Crohn’s (Th1 mediated)
crypt abscesses with ulcers is ulcerative colitis (neutrophils, remember abscesses are neutrophils)
FA 362
key differentials for caseating granulomas are
FA 223
TB, fungal infections, mycobacterium
FA 223
list steps involved in granuloma formation
FA 230, poma 16
MQ’s process and present antigen via MHC class II to CD4+ T cells
MQs secrete IL-12 which makes Th1 subtype
Th1 cells secrete IFN-gamma which converts MQ’s to epitheloid histiocytes and giant cells
TNF alpha from mq’s induces and maintains granuloma formation
FA 230, poma 16
22q11 microdeletion
third and fourth pharyngeal pouches fail to form
what are symptoms
T cell deficiency due to lack of thymus, hypocalcemia (lack of parathyroids), abnormalities of heart, great vessels, face (velocardial syndrome)
DiGeorge Syndrome
FA 214
MCC of severe combined immunodeficiency
what’s the other cause
defective IL-2R gamma chain (X linked, therefore seen in boys often)
and adenosine daminase deficiency (autosomal recessive)
FA 215, poma 16
what enzyme deaminates adenosine and deoxyadenosine for secretion because they would otherwise be toxic to cell?
FA 215, poma 16
adenosine deaminase deficiency
in ADA deficiency, these two products accumulate and is toxic to lymphocytes which are making DNA and dividing often
FA 215, poma 16
ADA deficiency causes
severe combined immunodeficiency syndrome
(SCIDS)
build up of adenosine and deoxyadenosine
symptoms of SCIDS
failure to thrive, infections by fungal, viral, baceterial, protozoal infections
FA 215, poma 16
lack of B cell maturation and defect of BTK (a tyrosine kinase gene) is characteristic of
X-linked (Bruton’s) agammaglobulinemia
recurrent bacterial and enteroviral / giardial (no IgA in intestinal mucosa) infections after 6 months when mother’s IgG antibodies are gone
poma 16, FA214
findings of Bruton’s agammaglobulinemia
FA 214
- absent B cells in peripheral blood
- decreased Ig of all classes
absent lymph nodes and tonsils
FA 214
pt’s serum ab’s are low in IgA, and NL IgG, IgM levels
pt has anaphylaxis to IgA contain products
what dz
FA 214
selective IgA deficiency
most common immunodeficency, cause is unknown
FA 214
what is the defect in common variable immunodeficiency
defect in B cell differentiation, many causes
decreased plasma cells and immunoglobulins
pt’s with IgA selective deficiency have increased risk of what types of diseases
anaphylaxis to what?
autoimmune; celiac disease; GI infections
anaphylaxis to IgA-containing products
X-linked recessive disease that causes increased IgM in serum. Dz?
what is the genetic defect
FA 215, poma 17
hyper-IgM syndrome
Defective CD40L on Th cells -> therefore, B cells cannot class switch out of IgM.
FA 215, poma 17
serum findings include increased IgM, low IgG, IgA, IgE
how do these patients typically present?
FA 215, poma 17
severe pyogenic infections early in life
opportunistic infection with Pneumocystis, Cryptosporidium, CMV
poor opsonization
FA 215, poma 17
presentation of Wiskott-Aldrich syndrome
FA 215, poma 17
Thrombocytopenic purpura Eczema Recurrent Infections W-A-T-E-R FA 215, poma 17
boy child has mutation in WAS gene, rendering T cells unable to reorganize actin cytoskeleton
dz
FA 215
Wilskott-Aldrich
X-linked recessive
FA215
Neisseria infection susceptibility
C5-C9 deficiency
FA 206
pt presents with angioedema (periorbital), and mucosal surfaces hereditary angioedema what dz what drug is contraindicated FA 206, poma 17
C1 esterase inhibitor deficiency
ACE inhibitors are contraindicated
FA 206, poma 17
AIRE mutation results in
poma 17
autoimmune polyendocrine syndrome
AIRE is part of negative selection of T cells and allows medullary dendritic cell to present self antigen; if it cannot, T cell can get through and cause autoimmune destruction
poma 17
pt presents with triad of
hypoparathyroidism, adrenal insufficiency (addisons), and candida infections due to autoimmunity
what is defective and what is the dz
FA 324, poma 17
defective AIRE protein in medulla of thymus
autoimmune polyendocrine syndrome
FA 324, poma 17
self reactive T cell binds to self cell and there is no costimulation
what occurs
anergy - that T cell is shut off
can also undergo apoptosis by having its FAS (CD95) receptor bound to FasL by the self cell it is trying to bind to
FA 209, poma 17
CD25 polymorphism.
what cell type does it effect?
what is it associated with?
FA 202, poma 17
effects Tregs (CD25 is IL-2R) associated with autoimmune disorders such as MS, Type I DM FA 202, poma 17
Pt presents with an X-linked syndrome that is immune dysregulation.
have diarrhea, damage to thyroid and pancreas
hint.
FA202, poma 17
IPEX
mutation of FOXP3 rendering Tregs defected
polyendocrinopathy (thyroid gland and pancreas damage, could lead to DM), enteropathy (hence the diarrhea)
FA202, poma 17
women are more commonly affected by autoimmune disorders; why?
poma 17
estrogen reduces apoptosis of self-reactive B cells
poma 17
what specific trigger events are required for autoimmunity to actually take place
genetic predisposition so that self reactive lymphocytes are present
then environmental trigger either by bystander activation or molecular mimicry ( that is, an antigen activates the leukocyte)
what ages does bruton’s agammaglobulinemia usually present?
what gene is defective
FA 215
bruton’s tyrosine kinase BTK defective in b cells
presents after 6 months after mother’s antibodies have gone away; pt will get recurrent bacterial and enteroviral infections
histological findings of amyloidosis
FA 231
congo red
apple green birefringence under polarized light
define labile tissue.
FA 72, poma
tissue contain stem cells that constantly reproliferate and grow back. eg. bone, lung, skin
what type of tissue is liver?
Labile, stable, or permanent?
FA 72
Stable; hepatocytes will regenerate if damaged
what are the labile stem cells of small and large bowel located?
FA 72, poma 21
mucosal crypts
where are stem cells of skin located?
FA 72, poma 21
located in the basal layer
The bone marrow stem cells are called …
what is their cell surface marker?
poma 21
hematopoeitic stem cells, surface marker is CD 34
what are the stem cells of the lung?
FA 600, poma 21
Type II pneumocytes
How does permanent tissue repair it is damaged if it can regenerate cells?
poma 21, FA 229
repairs via fibrous scar;
for example, post MI myocardial tissue will form fibrous scar
deep cuts heal with fibrous scar. why?
poma 21
because a deep cut through the dermal layer will cut through the basal cells
what three main things consist granulation tissue? what is each one’s role?
poma 21, FA 229
fibroblasts (deposit type III collagen)
Capillaries (nutrient flow)
myofibroblasts (contract the wound)
a scar is what type of collagen? what was replaced and how was it replaced?
poma 21
Type I collagen which has higher strength.
Type III collage was initially part of the granulation tissue and is removed via collagenase, which requires Zn as cofactor
cofactor required for collagenase?
poma 21, FA 229
Zinc
role of TGF-beta in wound healing?
poma 21, FA 229
decrease inflammation, and it is a fibroblast growth factor
Role of PDGF in wound healing? secreted by?
poma 21, FA 229
secreted by platelets and macrophages.
helps in vascular remodeling and stimulates endothelium, smooth muscle, and fibroblasts for collagen formation
Role of FGF
poma 21, FA 229
Angiogenesis
role of VEGF?
poma 21, FA 229
Angiogenesis
Pt has scar that is healed by secondary intention. 6 months later, the wound has gotten a lot smaller. what is the mechanism?
FA 229, poma 21
myofibroblasts contraction of wound
what can cause delayed wound healing?
vitamin C deficiency, infection, diabetes, foreign body
what specific step in wound healing / collagen synthesis is delayed by a deficiency of vitamin C?
FA 76, poma 22
hydroxylation of pro/lys residues on collagen alpha helix
what step does copper deficiency delay wound healing ?
poma 22, FA 76
lysyl oxidase which covalently crosslinks lysein-hydroxylysine on collagen fibers
pt presents with delayed healing of wound.
they are deficient in Zn. what is the mechanism by which wound healing is delayed
poma 21
Type III collagen is not being replaced by type I collagen due to inactivity of collagenase which requires zn as cofactor
The rupture of a wound - that is commonly seen post abdominal surgery - is called
dehiscence
Pt has scar that appears raised but is confined in boundaries. what type of collagen and what is it called?
FA 229, poma 21
Hypertrophic scar; too much type I collagen
following resection on the face of an african american patient, the wound becomes out of proportion of scar’s boundaries.
what type of collagen?
FA 229, poma 21
Keloid scar - Type III collagen is deposited too much by fibroblasts
Defect in platelet plug formation due to decreased GpIIb/IIIa?
FA 397
Glanzmann thrombasthenia
lack of platelet to platelet plugging
anemia of chronic disease is due to release of what from the liver?
what is the mechanism of this anemia?
FA 393
chronic inflammation increases hepcidin release from liver.
hepcidin binds ferroportin in macrophages and intestinal mucosal cells.
RBC’s now lack iron.
Erythrocyte sedimentation rate of patient with chronic inflammation is elevated.
What is the mechanism?
FA 230
products of inflammation (e.g. fibrinogen) coat RBCs and cause aggregation.
Denser RBC’s therefore fall at faster rate in pipette.
what enzymes are contained with azurophilic granules of neutrophil? (also called lysosomes)
FA 382
proteinases, acid phosphatase, myeloperoxidase (gives blue-green color), beta glucuronidase
what enzymes are contained within specific granules of neutrophils?
FA 382
ALP (alkaline phosphatase), collagenase, lysozyme, and lactoferrin.
role of IL-10; what cells does it inhibit?
what is the mechanism?
FA 207
inhibits activated macrophages and dendritic cells. decreases expression of MHC class II and Th1 cytokines
what HLA subtype predisposes a patient to ankylosing spondylitis ?
FA 201, 637
HLA-B27
why does a deficiency of early complement proteins increase the risk of systemic lupus erythematous?
FA 433, poma 18
because they help in the removal / opsonization of apoptotic bodies.
if they are not present, the antibody-antigen complexes will not be removed from blood and deposit into tissue causing damage.
Malar “bufferfly” rash is seen over pt’s cheek bones after sunlight exposure.
dz?
FA 433, poma 18
SLE
pt presents with orthopnea, and heart failure cells are seen in lungs.
what cells were these originally and what is the mechanism?
FA 297
dust cells (MQ’s of the lungs) engulfed RBC’s during pulmonary edema, and they are now hemosiderin-laden macrophages, which gives them an organ-brown appearance.
pt findings include hypercoagulability, endothelial damage, and blood stasis.
what is the association?
FA 637, 608
Virchow triad, increased risk of thrombosis.
will commonly present with DVT
what is the main mechanism of damage in systemic lupus erthematous?
what type of hypersensitivity reaction is this?
fa 433, poma 18
antigen-antibody complexes deposit and damage multiple tissues.
this is Type III HSY.
what is the cardiac manifestation of lupus?
FA 636, FA 433, poma 18
nonbacterial thrombotic endocarditis.
this is when there are nonbacterial, wart-like vegetations on both sides of valve.
pt presents with raynaud phenomenon, malar bufferfly rash, and is developing diffuse proliferative glomerulonephritis.
what lab test would confirm the diagnosis?
FA 433, poma 18
anti-dsDNA antibodies and anti-smith antibodies.
antinuclear antibodies are sensitive but not specific to SLE; they can be found in other autoimmune diseases.
what is the most common cause of death in patients with SLE?
is this true for drug induced SLE?
FA 433, FA 636,
lupus nephropathy. nephritic and nephrotic syndromes.
drug induce SLE typically does not result in renal or CNS involvement. poma 19
mother is found to have anti-SSA antibodies.
what is the hypersensitivity type of her disease?
what will her child have increased risk of developing?
poma 19, FA 430
Sjogren syndrome
Type IV hypersensitivity because antibodies are against own tissues.
child will have increased risk of developing neonatal lupus which includes congenital heart block.
pt develops enlarged parotid gland and dry eyes.
what other autoimmune disorder can be expected in this patient?
what type of antibodies will be found?
Sjogren syndrome: pt may also have rheumatoid arthritis or SLE.
anti-SSA / anti-SSB (it spells out sjogren syndrome)
FA 430, poma 19
pt presents with dry eyes and dry mouth.
what would you see on biopsy and what would you see that would be diagnostic for sjrogen syndrome?
lymphocytic sialadenitis on lip biopsy would be diagnostic for sjrogen syndrome.
would see lymphocytic infiltrations in the histo section.
poma 19, poma 20, FA 430
what autoantibody is seen in mixed connective tissue disease?
anti-U1 RNP (ribonucleoprotein)
poma 20, FA 213
anti-U1 RNP is specific for what disease?
mixed connective tissue disease
poma 20, FA 213
What type of HSR is the Arthus reaction?
What are its characteristics?
Give an example.
local, subacute antibody mediated hypersensitivity reaction.
Type III.
Characterized by edema, necrosis, and activation of complement.
Antigen-antibody complexes in the skin.
(FA 211)
Arthus reaction (e.g. swelling and inflammation following tetanus vaccine) (FA 212)
What is the mechanism of serum sickness?
what type of HSR?
immune complex disease in which antibodies to foreign proteins are produced (5 days)
Complexes deposited in membranes, where they fix complement (leads to tissue damage)
FA 211
Type III
48 hours after PPD test, pt notices indurated, raised, erythematous area.
What lymphocyte is responsible?
What type of HSR?
Type IV
Delayed T-cell-mediated type - sensitized T cells encounter antigen and then release cytokines (leads to MQ activation; no antibody involved)
FA 211
How long does acute transplant rejection take to occur?
What is the pathogenesis (what type of cells)
FA 217
weeks to months, CD8+
Pt receives second blood transfusion and undergoes anaphylactic shock.
Disease?
What other problems would these patients present with?
IgA deficiency, Selective IgA deficiency
GI infections, autoimmune diseases, anaphylaxis to IgA containing products (Blood transfusion)
FA 624, 214
24 y/o with increasing malaise; skin facial lesion over cheeks. PE shows mild pitting edema. On auscultation, friction rub is audible over chest.
Lab findings show pancytopenia and serum creatinine of 3 mg/dL.
Urinalysis shows hematuria and proteinuria.
Serologic test for syphilis yields false-positive result.
Renal biopsy shows granular deposits of IgG and complement in the mesangium and along basement membrane.
Mechansim of disease?
will likely develop what life-threatening disease?
Defective clearance of apoptotic nuclei (UV light damage)
renal failure / lupus nephropathy
FA 433, SLE
24 y/o with increasing malaise; skin facial lesion over cheeks. PE shows mild pitting edema. On auscultation, friction rub is audible over chest.
Lab findings show pancytopenia and serum creatinine of 3 mg/dL.
Urinalysis shows hematuria and proteinuria.
Serologic test for syphilis yields false-positive result.
PT and PTT are elevated.
What is this patient at risk for?
What autiantibodies are likely to be found in serum?
Antiphospholipid syndrome
Anticardiolipin antibodies and lupus anticoagulant
risk of thrombosis
FA 433
