Path Flashcards
Infections that cause pseudo membranous inflammation
Diphtheria, clostridium difficile
Most common cause if a skin abscess
s aureus
What causes serous inflammation
Blister in second degree burns, viral pleuritis
What do lipoxins do
Inhibit transmigration/chemotaxis, enhance apoptosis, anti inflammatory mediators
What do resolvins do
Inhibit recruitment of inflammatory cells
Most common cause of chronic inflammation
Infection (tb, leprosy, hep c)
Most common cause of impaired wound healing
Infection
ST segment depression on ECG indicates:
subendocardial ischemia
(reversible/irreversible) change to cell: Na/K ATPase pump impaired
reversible
(reversible/irreversible) change to cell: CaATPase pump impaired
irreversible–cannot pump Ca2+ out of cytosol
increased cytosolic __ (ion): (a) Activation of phospholipase increases cell and organelle membrane permeability. (b) Activation of proteases damages the cytoskeleton.
(c) Activation of endonucleases causes fading of nuclear chromatin (karyolysis).
(d) Activation of ATPase leads to ↓ATP.
(e) activates caspases causing apoptosis of the cell.
Ca2+
NADPH oxidase is found in ____ cell membranes (type of cell)
phagocyte–neutrophils and monocytes
Consequences of free radical injury include cirrhosis and exocrine/endocrine dysfunction of the
_____ (organ).
pancreas
Salicylates, alcohol damage mitochondria; produce megamitochondria in ______ (cell type)
hepatocytes
(decreased/increased) drug detoxification causes lower than expected therapeutic drug levels.
increased detox > lower therapy
Induction of enzyme synthesis in the cytochrome P450 system produces _______ (organelle) hyperplasia
SER
name disease: defect in posttranslational modification lysosomal enzymes; deficient phosphotransferase
Inclusion (I)-cell disease
name disease: giant lysosomal granules (fusion defect); defect in formation of phagolysosomes
Chediak-Higashi
(dystrophic/metastatic) calcification: serum calcium and serum phosphate are normal
dystrophic
(dystrophic/metastatic) calcification: serum calcium is increased and/or phosphate
metastatic
(hypertrophy/hyperplasia) depends on the regenerative capacity of different cell types
hyperplasia
Barrett esophagus: ____ to ____ epithelium due to acid reflux in distal esophagus
squamous > glandular
bronchus in smoker, endocervix: _____ to _____ epithelium
glandular > squamous
(pale/hemorrhagic) infarctions: loose tissue, lung, bowel, testicle
hemorrhagic
(pale/hemorrhagic) infarctions: dense tissue, heart, kidney, spleen
pale
name disease: _______ of the toes in individuals with diabetes mellitus is a form of infarction that results from ischemia. Coagulation necrosis is the primary type of necrosis that is present in the dead tissue
dry gangrene
______necrosis: lysosomal enzyme destruction tissue by neutrophils
Liquefactive
cerebral infarction: (liquefactive/coagulative) necrosis
liquefactive
wet gangrene: (liquefactive/coagulative) necrosis
liquefactive
enzymatic fat necrosis leads to:
acute pancreatitis
______: calcium combined with fatty acids; dystrophic calcification
Saponification
(intrinsic/extrinsic) pathway of apoptosis requires TNF-a
extrinsic
main source of TNF-a
macrophages
_____: proinflammatory cell death using caspase-1
Pyroptosis
Microbial pathogens that may be killed by ______ include Salmonella typhimurium, Shigella flexneri, Legionella pneumophila
pyroptosis
(histamine/PGE2 and bradykinin) mediated: rubor, calor, tumor
histamine
(histamine/PGE2 and bradykinin) mediated: dolor
bradykinin and PGE2
the primary leukocytes in acute inflammation
neutrophils
(selectins/B-integrins): activated by IL-1 and TNF
selectins
(selectins/B-integrins): firm adhesion of neutrophils, activated by C5a and LTB4
B-integrins
Catecholamines and corticosteroids (stimulate/inhibit) activation of these neutrophil adhesion
molecules.
inhibit
Inhibition of neutrophil β2-integrins, leads to an increase in the peripheral blood neutrophil count (called \_\_\_\_\_\_)
neutrophilic leukocytosis
(neutrophilic leukocytosis/neutropenia): enhanced activation of neutrophil β2-integrins causes the total circulating neutrophil count to decrease
neutropenia
_____ (process) mediators: C5a, LTB4, bacterial products, IL-8
chemotaxis
opsonins __ and __: enhance neutrophil ability to ingest bacteria and recognize/attach
IgG and C3b
MPO=
myeloperoxidase system–oxygen dependent neutrophil killing of bacteria/fungi
(SOD/Fenton rxn) converts superoxide free radicals to H2O2
SOD
(SOD/Fenton rxn) converts peroxide to hydroxyl free radicals by iron
Fenton
end product of oxygen dependent MPO system:
bleach
____ (enzyme) deficiency: lack of NADPH interferes with normal function of the O2-dependent MPO system
G6PD–glucose 6 phosphate DHase
(chronic granulomatous dz/myeloperoxidase def): XLR
CGD
(chronic granulomatous dz/myeloperoxidase def): AR
MD
(chronic granulomatous dz/myeloperoxidase def): NADPH oxidase is absent
CGD
(chronic granulomatous dz/myeloperoxidase def): myeloperoxidase is absent
MD
(chronic granulomatous dz/myeloperoxidase def): respiratory burst is absent
CGD
(chronic granulomatous dz/myeloperoxidase def): peroxide is absent
CGD
(chronic granulomatous dz/myeloperoxidase def): bleach is absent
both
(IL-1 and TNF/IL-6): Initiate PGE2 synthesis in the anterior hypothalamus, leading to production of fever
Activate endothelial cell adhesion molecules
IL-1 and TNF
(IL-1 and TNF/IL-6): Primary cytokines responsible for increased liver synthesis of acute phase reactants (APRs), such as ferritin, coagulation factors (e.g., fibrinogen), and C-reactive protein
IL-6
(IL-8/IL-6): chemotaxis
IL-8
(histamine/NO): vasodilation, bactericidal
NO
(histamine/NO): vasodilation, increased vascular permeability
histamine
(complement/chemokines): synthesized in liver
complement
(complement/chemokines): produced by leukocytes, endothelial cells
chemokines
(chemokines/bradykinin): product of kinin system activation by activated factor XII
bradykinin
source of leukotrines (cell type)
leukocytes–converted from arachidonic acid by lipoxygenase-mediated hydroxylation
(prostaglandin/thromboxane A2): platelet aggregation
thromboxane A2
(prostaglandin/thromboxane A2): inhibits platelet aggregation
prostaglandin I2
histamine, NO, PGI2 participate in vaso (dilation/constriction)
vasodilation
thromboxane A2 participates in vaso (dilation/constriction)
constriction
histamine, bradykinin, LTC4, LTD4, LTE4, C3a, C5a participate in (producing pain/increasing venular permeability)
increasing venular permeability
PGE2, bradykinin participate in (producing pain/increasing venular permeability)
producing pain
PGE2, IL-1, TNF participate in (chemotaxis/producing fever)
producing fever
C5a, LTB4, IL-8 participate in (chemotaxis/producing fever)
chemotaxis
IL-_ stimulates acute phase reactant synthesis by liver
IL-6
two examples of noninfectious granulomatous inflammation
sarcoidosis, Crohn dz
two examples of granulomatous infections
TB, systemic fungi (histoplasmosis)
serum protein electrophoresis in acute inflammation: albumin (increases/decreases), no alteration in gamma-globulin peak
decreases
(increase/decrease) in gamma-globulin in chronic inflammation is due to the marked (increase/decrease) of synthesis of IgG in chronic inflam
increase, increase
stack of coins appearance
Rouleau RBCs stack
RBC rouleau: (increase/decrease) of fibrinogen/immunoglobulins, erythrocyte sed rate
increase all
C reactive protein is a marker of:
necrosis and disease activity
(IgM/IgG) predominant immunoglobulin in acute inflam
IgM
(IgM/IgG) predominant immunoglobulin in chronic inflam
IgG–increased serum IgG is key finding in chronic inflam
lung injury primary repair cell
type II pneumocyte
brain injury repair cells
astrocytes and microglial cells
primary cell in peripheral nerve transsection repair
Schwann
repair process in cardiac muscle damage
fibrosis (permanent tissue)
repair cell in muscle post exercise
satellite
glucocorticoids (simulate/inhibit) scar formation
inhibit
p53 protein product: inhibits Cdk4 (cell arrested in __ phase)
G1
most critical phase in cell cycle
G1 to S phase
proteins that control G1 to S phase in cell cycle (two)
cyclin D, Cdk4
(IL-1/TNF): Activates macrophages; stimulates release of acute phase reactants
TNF
(IL-1/TNF): Stimulates synthesis of metalloproteinases (i.e., enzymes containing trace metals)
Stimulates synthesis and release of acute phase reactants from the liver
IL-1
(IL-1/TNF-a) is important in the formation and maintenance of TB and systemic fungal granulomas.
TNF-a. recruits cells for granuloma formation
Multinucleated giant cell nuclei are usually located at the (center/periphery) of the granuloma.
periphery
Cell types in TB granuloma: Epithelioid cells (activated macrophages) and mononuclear cells consisting of
CD(4/8) T cells, specifically, TH cells of the TH(1/2) type (memory T cells)
CD4 helper T cells
TH1
(acute/chronic) inflam: serum protein electrophoresis=mild hypoalbuminemia
acute
(acute/chronic) inflam: serum protein electrophoresis=polyclonal gammopathy, greater degree of hypoalbuminemia
chronic
(acute/chronic) inflam: neutrophilic leukocytosis
acute
(acute/chronic) inflam: monocytosis
chronic
(acute/chronic) inflam: scar tissue formation, amyloidosis
chronic
(acute/chronic) inflam: complete resolution or abscess formation
acute (or progresses to chronic inflam)
(acute/chronic) inflam: scar tissue present
chronic
(acute/chronic) inflam: necrosis is prominent
acute
(acute/chronic) inflam: histamine is key mediator, along with prostaglandins and leukotriene
acute
(acute/chronic) inflam: monocytes/macrophages are key mediators, also B and T lymphocytes, plasma cells, fibroblasts
chronic
(mast cells/eosinophils): receptors for IgE
eosinophils
(TLR/NK cells/NFκβ/PAMPs): “master switch” to nucleus for induction of inflammation
NFkB
(TLR/NK cells/NFκβ/DAMPs/PAMPs): heat shock protein, chromatin-associated HMGB1, purine metabolites (ATP, adenosine, uric acid)
DAMPs
Inflammosomes activate caspase-1 → (increase/decreases) secretion IL-1β and IL-18 → attract immune cells to sites of infection
increases
(hemosiderin/ferritin/transferrin/hepcidin) keeps iron away from bacteria
hepcidin
IFN-(α and β/γ): activation of macrophages
gamma
IFN-(α and β/γ): inhibition of viral growth
alpha and beta
CD40 ligands, cytokines, and (CD4/CD8) T cells are involved in isotype switching
CD4 helper T cells
on which chromosome is the HLA system
(Major Histocompatiblity Complex=HLA): chromosome 6
Type (I/II/III/IV) hypersensitivity: IgE antibody mediated activation of mast cells or basophils followed by acute inflammatory rxn
I
IL-(4/5) causes plasma cells to switch from IgM to IgE synthesis.
4
IL-(4/5) stimulates the production and activation of eosinophils.
5
Type I hypersensitivity: APCs release IL-4 which induces CD4 T cells to become CD4 TH(1/2) cells that produce IL-4 and IL-5
TH2
Type (I/II/III/IV) hypersensitivity: rhinitis and conjunctivitis, asthma, dermatitis, vomiting, diarrhea, anaphylaxis, edema, hives
I
Type (I/II/III/IV) hypersensitivity: atopic (allergens), drug hypersensitivity (penicillin), transfusion rxn in IgA immunodef
I
Type (I/II/III/IV) hypersensitivity: complement dependent antibody reactions
II
Type (I/II/III/IV) hypersensitivity: cell lysis mediated by IgM or IgG, phagocytosis, IgE dependent cell-mediated cytotoxicity, Graves, myasthenia Gravis
II
Type (I/II/III/IV) hypersensitivity: Goodpasture, pernicious anemia, ABO hemolytic dz of the newborn
II
Type (I/II/III/IV) hypersensitivity: SLE, Arthus rxn (farmer’s lung), serum sickness
III
Type (I/II/III/IV) hypersensitivity: Poststreptococcal glomerulonephritis,
III
Type (I/II/III/IV) hypersensitivity: CD4 Helper T cell mediate granuloma formation
IV
Type (I/II/III/IV) hypersensitivity: CD8 cytotoxic destruction of virus infected, neoplastic, or donor graft cells
IV
Type (I/II/III/IV) hypersensitivity: initiated by the introduction of an allergen, which stimulates CD4 TH2 reactions and immunoglobulin E (IgE) production. IgE binds to Fc receptors on mast cells
I
Type (I/II/III/IV) hypersensitivity: late phase mediators= prostaglandins, leukotrienes, platelet activating factor
I
Type (I/II/III/IV) hypersensitivity: antibody directed against antigens on cell membrane or in ECM
II
Type II hypersensitivity: (IgM/IgG) cell lysis–cold IHA, ABO mismatch
IgM
Type II hypersensitivity: (IgM/IgG) cell lysis–Goodpasture, acute rheumatic fever
IgG
Type (I/II/III/IV) hypersensitivity: circulating antigen-antibody complexes that damage tissue
III
____ rxn in Type III hypersensitivity: formation of immunocomplexes at a localized site. Ex: farmer’s lung
Arthus rxn
Type (I/II/III/IV) hypersensitivity: T cell-mediated immunity, often delayed
IV (DTH-delayed type hypersensitivity)
Type (I/II/III/IV) hypersensitivity: controls TB infection, graft rejection, tumor surveillance
IV
Type (I/II/III/IV) hypersensitivity: allergic contact dermatitis–poison ivy, topical drugs, rubber, chemicals
IV
(cornea/kidney/bone marrow) transplant: best allograft survival rate
cornea
(cornea/kidney/bone marrow) transplant: danger of transmitting Creutzfeldt-J-Dz
cornea
(cornea/kidney/bone marrow) transplant: better survival if donor is living than cadaver
kidney
(cornea/kidney/bone marrow) transplant: danger of graft-vs-host rxn and CMV infection
bone marrow
most important requirement for successful transplantation
ABO blood grp compatibility
hyperacute transplant rejection: Type II hypersensitivity, (reversible/irreversible)
irreversible
acute transplant rejection: type II/IV, (reversible/irreversible)
reversible
key cell in donor graft: (CD4/CD8/dendritic)
dendritic
most common infection in transplant recipients
CMV
solid organ transplantation: (Candida/Aspergillus) most common infection
candida
bone marrow transplantation: (Candida/Aspergillus) most common infection
aspergillus
in ____ rxn, donor T cells attack host MHC antigens located in the skin, bile duct epithelium, and mucosa of the GI tract.
Graft-vs-Host
approx 90% of all autoimmune dz occurs in (men/women)
women (hormones thought to play a role)
rheumatic fever: produced by (S pyogenes/Chlamydia trachomatis)
S pyogenes
Reiter syndrome: produced by (S pyogenes/Chlamydia trachomatis)
chlamydia t
Bacterial triggers of _______: S. pyogenes,
C. trachomatis, M. pneumoniae, C. jejuni
autoimmune dz
Viruses as triggers of _______: coxsackievirus, measles virus, CMV, EBV, HHV-6, influenza virus
autoimmune dz
SLE affects (older women/women of childbearing age/children)
mostly women of childbearing age
most common visceral organ involved in SLE
kidney
how do you differentiate between drug induced lupus and SLE
antihistone antibodies, ↓incidence renal/CNS disease, symptoms disappear when drug removed
best screen for SLE
ANA (high sensitivity, not great specificity)
(screen/confirm) for SLE: anti- dsDNA/anti-Sm antibodies; high specificity
confirm
(SLE/Systemic sclerosis): ↑CD4 TH2 cells; ↑DNA-topoisomerase, centromere antibodies
systemic sclerosis
most common initial sign of systemic sclerosis
raynaud
what does CREST stand for
calcinosis, Raynaud, esophageal dysmotility, sclerodactyly, telangiectasia
(infectious/noninfectious) inflammatory myopathies: polymyositis, dermatomyositis
noninfectious
(polymyositis/ dermatomyositis): muscle atrophy is a prominent feature
dermatomyositis
use corticosteroids to treat (polymyositis/ dermatomyositis)
both
renal dz is (common/uncommon) in mixed connective tissue disease)
uncommon
HIV is cytotoxic to CD (4/8) cells
4
where is complement synthesized
in liver
Complement: (C3a and C5a/C3b/C5b-C9): stimulate mast cell release of histamine
C3a and C5a
Complement: (C3a and C5a/C3b/C5b-C9): opsonization
C3b
Complement: (C3a and C5a/C3b/C5b-C9): cell lysis
C5b-C9
Complement: (C3a/C5a): activation of neutrophil adhesion molecules, neutrophil chemotaxis
C5a
(classical/alternative) complement pathway: C1, C4, C2; activated by ICs; requires antibody for activation
classical
(classical/alternative) complement pathway: factor B, properdin, factor D; activated by endotoxins
alternative
____ (complement) pathway: important in destruction of bacteria, fungi, viruses, does not require antibodies for activation
Lectin
most common complement def (C2/C6-C9)
C2
(C2/C6-C9) complement def: Increased susceptibility to disseminated Neisseria gonorrhoeae or Neisseria meningitidis infections
C6-C9 def
most common overall organ involved in amyloidosis
kidney
most common cause of death in shock
multiple organ dysfunction syndrome
_____ produces fibrin thrombi in the microvasculature of most organs, leading to
tissue damage.
DIC
(transudate/exudate): protein poor and cell poor fluid
transudate
(transudate/exudate): protein rich, cell rich fluid
exudate
(transudate/exudate): pitting edema, body cavity effusions, alteration in Starling Forces (HP, OP)
transudate
(transudate/exudate): no pitting edema
exudate
(oncotic/hydrostatic) pressure: favors movement of fluid (transudate) out of capillaries/venules.
hydrostatic
(oncotic/hydrostatic) pressure: equates with the serum albumin level and opposes filtration of fluid out of
capillaries/venules.
oncotic
in normal circumstances, (oncotic/hydrostatic) pressure is higher
OP is greater than HP
(increased hydrostatic/decreased oncotic): pulmonary edema in LHF, peripheral pitting edema in RHF, portal HTN
increased hydrostatic
(increased hydrostatic/decreased oncotic) pressure: nephrotic syndrome, malnutrition, cirrhosis, malabsorption
decreased oncotic pressure
ascites in cirrhosis: increase in (hydrostatic/oncotic) pressure, decrease in (hydrostatic/oncotic) pressure
increase HP, decrease OP (hypoalbuminemia)
in lymphatic obstruction, T cell cytokines stimulate _____ (cell type) to synthesize hyaluronic acid
fibroblasts
example of activated coagulation system in thrombosis
DIC: disseminated intravascular coagulation
(heparin and warfarin/plasmin) breaking down the thrombus to restore blood flow
plasmin (fibrinolytic system)
(heparin and warfarin/plasmin) preventing formation of venous thrombi, not dissolving thrombi but preventing further formation
heparin and warfarin
most common (venous/arterial) thrombus: coronary artery thrombus overlying an atherosclerotic plaque
arterial
(gas/fat/paradoxical/systemic) embolism: Most frequently due to venous emboli passing through an atrial septal defect (ASD) or a ventricular septal defect (VSD) into the systemic circulation.
paradoxical
(gas/fat/paradoxical/systemic) embolism: majority originate in left side of heart
systemic
(gas/fat/paradoxical/systemic) embolism: most often due to traumatic fracture of long bones (femur) or pelvis
fat
fat embolism patients are symptomatic in (most/few) cases
few (10%)
(gas/fat/paradoxical/systemic) embolism: hypoxemia, increased A-a gradient, thrombocytopenia
fat
____ embolism: occurs during labor or immediately postpartum
amniotic fluid–maternal mortality is 80%
in amniotic fluid embolism: (dyspnea/bleeding) is due to DIC
bleeding
in amniotic fluid embolism: (dyspnea/bleeding) is due to ARDS
dyspnea. also due to ARDS
decompression sickness is a form of (fat/gas/paradoxical/systemic) embolism
gas–scuba and deep sea diving
____ embolism: ↑pressure on lower extremity veins → stasis → thrombosis → embolism; dyspnea, pleuritic chest pain
pulmonary
caisson disease caused by persistence of gas emboli in bone: (acute/chronic)
chronic
loss of more than __% of blood produces shock
20%
in hypovolemic shock, there (is/is not) an initial drop in Hb and Hct concentration
is not because there is an equal loss of RBCs and plasma
best indicator of tissue hypoxia: mixed (arterial/venous) oxygen content
decreased mixed venous oxygen content
_____ shock: increased anion gap type of metabolic acidosis due to lactic acidosis
hypovolemic
(septic/hypovolemic) shock: warm skin, strong peripheral pulses, hypotension, DIC
septic
(septic/hypovolemic) shock: cold/clammy skin, hypotension, tachycardia, ↓urine output
hypovolemic
most common cause of cardiogenic shock
acute MI
(cardiogenic/septic) shock: ↑CO, ↓LVEDP, ↓PVR, ↑MVO2
septic (initial phase)
(cardiogenic/septic) shock: ↓CO, ↑LVEDP, ↑PVR, ↓MVO2
cardiogenic
most common site for infection leading to sepsis
lungs
endotoxins (LPS) are released by gram (+/-) bacteria
negative
endotoxins (LPS) activate macrophages, releasing IL-1 and TNF. (IL-1/TNF) produces fever
IL-1
endotoxins (LPS) activate macrophages, releasing IL-1 and TNF. (IL-1/TNF) damages endothelial cells, causing them to release vasodilators
TNF
endotoxins activate the (classical/alternative) complement pathway. Anaphylatoxins C3a and C5a are produced which stimulate mast cells to release histamine
alternative
MCC sepsis due to gram- (+/-) organisms (coagulase-negative Staphylococci)
positive
E coli: most common cause of gram-(+/-) septic shock
negative
Endotoxins damage tissue, causing the release of tissue thromboplastin, which activates the extrinsic coagulation system producing _____
DIC
most common fungal cause of septic shock
Candida
