Path Flashcards
0
Q
Infections that cause pseudo membranous inflammation
A
Diphtheria, clostridium difficile
1
Q
Most common cause if a skin abscess
A
s aureus
2
Q
What causes serous inflammation
A
Blister in second degree burns, viral pleuritis
3
Q
What do lipoxins do
A
Inhibit transmigration/chemotaxis, enhance apoptosis, anti inflammatory mediators
4
Q
What do resolvins do
A
Inhibit recruitment of inflammatory cells
5
Q
Most common cause of chronic inflammation
A
Infection (tb, leprosy, hep c)
7
Q
Most common cause of impaired wound healing
A
Infection
8
Q
ST segment depression on ECG indicates:
A
subendocardial ischemia
9
Q
(reversible/irreversible) change to cell: Na/K ATPase pump impaired
A
reversible
10
Q
(reversible/irreversible) change to cell: CaATPase pump impaired
A
irreversible–cannot pump Ca2+ out of cytosol
11
Q
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.
A
Ca2+
12
Q
NADPH oxidase is found in ____ cell membranes (type of cell)
A
phagocyte–neutrophils and monocytes
13
Q
Consequences of free radical injury include cirrhosis and exocrine/endocrine dysfunction of the
_____ (organ).
A
pancreas
14
Q
Salicylates, alcohol damage mitochondria; produce megamitochondria in ______ (cell type)
A
hepatocytes
15
Q
(decreased/increased) drug detoxification causes lower than expected therapeutic drug levels.
A
increased detox > lower therapy
16
Q
Induction of enzyme synthesis in the cytochrome P450 system produces _______ (organelle) hyperplasia
A
SER
17
Q
name disease: defect in posttranslational modification lysosomal enzymes; deficient phosphotransferase
A
Inclusion (I)-cell disease
18
Q
name disease: giant lysosomal granules (fusion defect); defect in formation of phagolysosomes
A
Chediak-Higashi
19
Q
(dystrophic/metastatic) calcification: serum calcium and serum phosphate are normal
A
dystrophic
20
Q
(dystrophic/metastatic) calcification: serum calcium is increased and/or phosphate
A
metastatic
21
Q
(hypertrophy/hyperplasia) depends on the regenerative capacity of different cell types
A
hyperplasia
22
Q
Barrett esophagus: ____ to ____ epithelium due to acid reflux in distal esophagus
A
squamous > glandular
23
Q
bronchus in smoker, endocervix: _____ to _____ epithelium
A
glandular > squamous
24
Q
(pale/hemorrhagic) infarctions: loose tissue, lung, bowel, testicle
A
hemorrhagic
25
(pale/hemorrhagic) infarctions: dense tissue, heart, kidney, spleen
pale
26
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
27
______necrosis: lysosomal enzyme destruction tissue by neutrophils
Liquefactive
28
cerebral infarction: (liquefactive/coagulative) necrosis
liquefactive
29
wet gangrene: (liquefactive/coagulative) necrosis
liquefactive
30
enzymatic fat necrosis leads to:
acute pancreatitis
31
______: calcium combined with fatty acids; dystrophic calcification
Saponification
32
(intrinsic/extrinsic) pathway of apoptosis requires TNF-a
extrinsic
33
main source of TNF-a
macrophages
34
_____: proinflammatory cell death using caspase-1
Pyroptosis
35
Microbial pathogens that may be killed by ______ include Salmonella typhimurium, Shigella flexneri, Legionella pneumophila
pyroptosis
36
(histamine/PGE2 and bradykinin) mediated: rubor, calor, tumor
histamine
37
(histamine/PGE2 and bradykinin) mediated: dolor
bradykinin and PGE2
38
the primary leukocytes in acute inflammation
neutrophils
39
(selectins/B-integrins): activated by IL-1 and TNF
selectins
40
(selectins/B-integrins): firm adhesion of neutrophils, activated by C5a and LTB4
B-integrins
41
Catecholamines and corticosteroids (stimulate/inhibit) activation of these neutrophil adhesion
molecules.
inhibit
42
```
Inhibition of neutrophil β2-integrins, leads to an increase in the peripheral blood
neutrophil count (called ______)
```
neutrophilic leukocytosis
43
(neutrophilic leukocytosis/neutropenia): enhanced activation of neutrophil β2-integrins causes the total circulating neutrophil count to decrease
neutropenia
44
_____ (process) mediators: C5a, LTB4, bacterial products, IL-8
chemotaxis
45
opsonins __ and __: enhance neutrophil ability to ingest bacteria and recognize/attach
IgG and C3b
46
MPO=
myeloperoxidase system--oxygen dependent neutrophil killing of bacteria/fungi
47
(SOD/Fenton rxn) converts superoxide free radicals to H2O2
SOD
48
(SOD/Fenton rxn) converts peroxide to hydroxyl free radicals by iron
Fenton
49
end product of oxygen dependent MPO system:
bleach
50
____ (enzyme) deficiency: lack of NADPH interferes with normal function of the O2-dependent MPO system
G6PD--glucose 6 phosphate DHase
51
(chronic granulomatous dz/myeloperoxidase def): XLR
CGD
52
(chronic granulomatous dz/myeloperoxidase def): AR
MD
53
(chronic granulomatous dz/myeloperoxidase def): NADPH oxidase is absent
CGD
54
(chronic granulomatous dz/myeloperoxidase def): myeloperoxidase is absent
MD
55
(chronic granulomatous dz/myeloperoxidase def): respiratory burst is absent
CGD
56
(chronic granulomatous dz/myeloperoxidase def): peroxide is absent
CGD
57
(chronic granulomatous dz/myeloperoxidase def): bleach is absent
both
58
(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
59
(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
60
(IL-8/IL-6): chemotaxis
IL-8
61
(histamine/NO): vasodilation, bactericidal
NO
62
(histamine/NO): vasodilation, increased vascular permeability
histamine
63
(complement/chemokines): synthesized in liver
complement
64
(complement/chemokines): produced by leukocytes, endothelial cells
chemokines
65
(chemokines/bradykinin): product of kinin system activation by activated factor XII
bradykinin
66
source of leukotrines (cell type)
leukocytes--converted from arachidonic acid by lipoxygenase-mediated hydroxylation
67
(prostaglandin/thromboxane A2): platelet aggregation
thromboxane A2
68
(prostaglandin/thromboxane A2): inhibits platelet aggregation
prostaglandin I2
69
histamine, NO, PGI2 participate in vaso (dilation/constriction)
vasodilation
70
thromboxane A2 participates in vaso (dilation/constriction)
constriction
71
histamine, bradykinin, LTC4, LTD4, LTE4, C3a, C5a participate in (producing pain/increasing venular permeability)
increasing venular permeability
72
PGE2, bradykinin participate in (producing pain/increasing venular permeability)
producing pain
73
PGE2, IL-1, TNF participate in (chemotaxis/producing fever)
producing fever
74
C5a, LTB4, IL-8 participate in (chemotaxis/producing fever)
chemotaxis
75
IL-_ stimulates acute phase reactant synthesis by liver
IL-6
76
two examples of noninfectious granulomatous inflammation
sarcoidosis, Crohn dz
77
two examples of granulomatous infections
TB, systemic fungi (histoplasmosis)
78
serum protein electrophoresis in acute inflammation: albumin (increases/decreases), no alteration in gamma-globulin peak
decreases
79
(increase/decrease) in gamma-globulin in chronic inflammation is due to the marked (increase/decrease) of synthesis of IgG in chronic inflam
increase, increase
80
stack of coins appearance
Rouleau RBCs stack
81
RBC rouleau: (increase/decrease) of fibrinogen/immunoglobulins, erythrocyte sed rate
increase all
82
C reactive protein is a marker of:
necrosis and disease activity
83
(IgM/IgG) predominant immunoglobulin in acute inflam
IgM
84
(IgM/IgG) predominant immunoglobulin in chronic inflam
IgG--increased serum IgG is key finding in chronic inflam
85
lung injury primary repair cell
type II pneumocyte
86
brain injury repair cells
astrocytes and microglial cells
87
primary cell in peripheral nerve transsection repair
Schwann
88
repair process in cardiac muscle damage
fibrosis (permanent tissue)
89
repair cell in muscle post exercise
satellite
90
glucocorticoids (simulate/inhibit) scar formation
inhibit
91
p53 protein product: inhibits Cdk4 (cell arrested in __ phase)
G1
92
most critical phase in cell cycle
G1 to S phase
93
proteins that control G1 to S phase in cell cycle (two)
cyclin D, Cdk4
94
(IL-1/TNF): Activates macrophages; stimulates release of acute phase reactants
TNF
95
(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
96
(IL-1/TNF-a) is important in the formation and maintenance of TB and systemic fungal granulomas.
TNF-a. recruits cells for granuloma formation
97
Multinucleated giant cell nuclei are usually located at the (center/periphery) of the granuloma.
periphery
98
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
99
(acute/chronic) inflam: serum protein electrophoresis=mild hypoalbuminemia
acute
100
(acute/chronic) inflam: serum protein electrophoresis=polyclonal gammopathy, greater degree of hypoalbuminemia
chronic
101
(acute/chronic) inflam: neutrophilic leukocytosis
acute
102
(acute/chronic) inflam: monocytosis
chronic
103
(acute/chronic) inflam: scar tissue formation, amyloidosis
chronic
104
(acute/chronic) inflam: complete resolution or abscess formation
acute (or progresses to chronic inflam)
105
(acute/chronic) inflam: scar tissue present
chronic
106
(acute/chronic) inflam: necrosis is prominent
acute
107
(acute/chronic) inflam: histamine is key mediator, along with prostaglandins and leukotriene
acute
108
(acute/chronic) inflam: monocytes/macrophages are key mediators, also B and T lymphocytes, plasma cells, fibroblasts
chronic
109
(mast cells/eosinophils): receptors for IgE
eosinophils
110
(TLR/NK cells/NFκβ/PAMPs): “master switch” to nucleus for induction of inflammation
NFkB
111
(TLR/NK cells/NFκβ/DAMPs/PAMPs): heat shock protein, chromatin-associated HMGB1, purine metabolites (ATP, adenosine, uric acid)
DAMPs
112
Inflammosomes activate caspase-1 → (increase/decreases) secretion IL-1β and IL-18 → attract immune cells to sites of infection
increases
113
(hemosiderin/ferritin/transferrin/hepcidin) keeps iron away from bacteria
hepcidin
114
IFN-(α and β/γ): activation of macrophages
gamma
115
IFN-(α and β/γ): inhibition of viral growth
alpha and beta
116
CD40 ligands, cytokines, and (CD4/CD8) T cells are involved in isotype switching
CD4 helper T cells
117
on which chromosome is the HLA system
(Major Histocompatiblity Complex=HLA): chromosome 6
118
Type (I/II/III/IV) hypersensitivity: IgE antibody mediated activation of mast cells or basophils followed by acute inflammatory rxn
I
119
IL-(4/5) causes plasma cells to switch from IgM to IgE synthesis.
4
120
IL-(4/5) stimulates the production and activation of eosinophils.
5
121
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
122
Type (I/II/III/IV) hypersensitivity: rhinitis and conjunctivitis, asthma, dermatitis, vomiting, diarrhea, anaphylaxis, edema, hives
I
123
Type (I/II/III/IV) hypersensitivity: atopic (allergens), drug hypersensitivity (penicillin), transfusion rxn in IgA immunodef
I
124
Type (I/II/III/IV) hypersensitivity: complement dependent antibody reactions
II
125
Type (I/II/III/IV) hypersensitivity: cell lysis mediated by IgM or IgG, phagocytosis, IgE dependent cell-mediated cytotoxicity, Graves, myasthenia Gravis
II
126
Type (I/II/III/IV) hypersensitivity: Goodpasture, pernicious anemia, ABO hemolytic dz of the newborn
II
127
Type (I/II/III/IV) hypersensitivity: SLE, Arthus rxn (farmer's lung), serum sickness
III
128
Type (I/II/III/IV) hypersensitivity: Poststreptococcal glomerulonephritis,
III
129
Type (I/II/III/IV) hypersensitivity: CD4 Helper T cell mediate granuloma formation
IV
130
Type (I/II/III/IV) hypersensitivity: CD8 cytotoxic destruction of virus infected, neoplastic, or donor graft cells
IV
131
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
132
Type (I/II/III/IV) hypersensitivity: late phase mediators= prostaglandins, leukotrienes, platelet activating factor
I
133
Type (I/II/III/IV) hypersensitivity: antibody directed against antigens on cell membrane or in ECM
II
134
Type II hypersensitivity: (IgM/IgG) cell lysis--cold IHA, ABO mismatch
IgM
135
Type II hypersensitivity: (IgM/IgG) cell lysis--Goodpasture, acute rheumatic fever
IgG
136
Type (I/II/III/IV) hypersensitivity: circulating antigen-antibody complexes that damage tissue
III
137
____ rxn in Type III hypersensitivity: formation of immunocomplexes at a localized site. Ex: farmer's lung
Arthus rxn
138
Type (I/II/III/IV) hypersensitivity: T cell-mediated immunity, often delayed
IV (DTH-delayed type hypersensitivity)
139
Type (I/II/III/IV) hypersensitivity: controls TB infection, graft rejection, tumor surveillance
IV
140
Type (I/II/III/IV) hypersensitivity: allergic contact dermatitis--poison ivy, topical drugs, rubber, chemicals
IV
141
(cornea/kidney/bone marrow) transplant: best allograft survival rate
cornea
142
(cornea/kidney/bone marrow) transplant: danger of transmitting Creutzfeldt-J-Dz
cornea
143
(cornea/kidney/bone marrow) transplant: better survival if donor is living than cadaver
kidney
144
(cornea/kidney/bone marrow) transplant: danger of graft-vs-host rxn and CMV infection
bone marrow
145
most important requirement for successful transplantation
ABO blood grp compatibility
146
hyperacute transplant rejection: Type II hypersensitivity, (reversible/irreversible)
irreversible
147
acute transplant rejection: type II/IV, (reversible/irreversible)
reversible
148
key cell in donor graft: (CD4/CD8/dendritic)
dendritic
149
most common infection in transplant recipients
CMV
150
solid organ transplantation: (Candida/Aspergillus) most common infection
candida
151
bone marrow transplantation: (Candida/Aspergillus) most common infection
aspergillus
152
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
153
approx 90% of all autoimmune dz occurs in (men/women)
women (hormones thought to play a role)
154
rheumatic fever: produced by (S pyogenes/Chlamydia trachomatis)
S pyogenes
155
Reiter syndrome: produced by (S pyogenes/Chlamydia trachomatis)
chlamydia t
156
Bacterial triggers of _______: S. pyogenes,
| C. trachomatis, M. pneumoniae, C. jejuni
autoimmune dz
157
Viruses as triggers of _______: coxsackievirus, measles virus, CMV, EBV, HHV-6, influenza virus
autoimmune dz
158
SLE affects (older women/women of childbearing age/children)
mostly women of childbearing age
159
most common visceral organ involved in SLE
kidney
160
how do you differentiate between drug induced lupus and SLE
antihistone antibodies, ↓incidence renal/CNS disease, symptoms disappear when drug removed
161
best screen for SLE
ANA (high sensitivity, not great specificity)
162
(screen/confirm) for SLE: anti- dsDNA/anti-Sm antibodies; high specificity
confirm
163
(SLE/Systemic sclerosis): ↑CD4 TH2 cells; ↑DNA-topoisomerase, centromere antibodies
systemic sclerosis
164
most common initial sign of systemic sclerosis
raynaud
165
what does CREST stand for
calcinosis, Raynaud, esophageal dysmotility, sclerodactyly, telangiectasia
166
(infectious/noninfectious) inflammatory myopathies: polymyositis, dermatomyositis
noninfectious
167
(polymyositis/ dermatomyositis): muscle atrophy is a prominent feature
dermatomyositis
168
use corticosteroids to treat (polymyositis/ dermatomyositis)
both
169
renal dz is (common/uncommon) in mixed connective tissue disease)
uncommon
170
HIV is cytotoxic to CD (4/8) cells
4
171
where is complement synthesized
in liver
172
Complement: (C3a and C5a/C3b/C5b-C9): stimulate mast cell release of histamine
C3a and C5a
173
Complement: (C3a and C5a/C3b/C5b-C9): opsonization
C3b
174
Complement: (C3a and C5a/C3b/C5b-C9): cell lysis
C5b-C9
175
Complement: (C3a/C5a): activation of neutrophil adhesion molecules, neutrophil chemotaxis
C5a
176
(classical/alternative) complement pathway: C1, C4, C2; activated by ICs; requires antibody for activation
classical
177
(classical/alternative) complement pathway: factor B, properdin, factor D; activated by endotoxins
alternative
178
____ (complement) pathway: important in destruction of bacteria, fungi, viruses, does not require antibodies for activation
Lectin
179
most common complement def (C2/C6-C9)
C2
180
(C2/C6-C9) complement def: Increased susceptibility to disseminated Neisseria gonorrhoeae or Neisseria meningitidis infections
C6-C9 def
181
most common overall organ involved in amyloidosis
kidney
182
most common cause of death in shock
multiple organ dysfunction syndrome
183
_____ produces fibrin thrombi in the microvasculature of most organs, leading to
tissue damage.
DIC
184
(transudate/exudate): protein poor and cell poor fluid
transudate
185
(transudate/exudate): protein rich, cell rich fluid
exudate
186
(transudate/exudate): pitting edema, body cavity effusions, alteration in Starling Forces (HP, OP)
transudate
187
(transudate/exudate): no pitting edema
exudate
188
(oncotic/hydrostatic) pressure: favors movement of fluid (transudate) out of capillaries/venules.
hydrostatic
189
(oncotic/hydrostatic) pressure: equates with the serum albumin level and opposes filtration of fluid out of
capillaries/venules.
oncotic
190
in normal circumstances, (oncotic/hydrostatic) pressure is higher
OP is greater than HP
191
(increased hydrostatic/decreased oncotic): pulmonary edema in LHF, peripheral pitting edema in RHF, portal HTN
increased hydrostatic
192
(increased hydrostatic/decreased oncotic) pressure: nephrotic syndrome, malnutrition, cirrhosis, malabsorption
decreased oncotic pressure
193
ascites in cirrhosis: increase in (hydrostatic/oncotic) pressure, decrease in (hydrostatic/oncotic) pressure
increase HP, decrease OP (hypoalbuminemia)
194
in lymphatic obstruction, T cell cytokines stimulate _____ (cell type) to synthesize hyaluronic acid
fibroblasts
195
example of activated coagulation system in thrombosis
DIC: disseminated intravascular coagulation
196
(heparin and warfarin/plasmin) breaking down the thrombus to restore blood flow
plasmin (fibrinolytic system)
197
(heparin and warfarin/plasmin) preventing formation of venous thrombi, not dissolving thrombi but preventing further formation
heparin and warfarin
198
most common (venous/arterial) thrombus: coronary artery thrombus overlying an atherosclerotic plaque
arterial
199
(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
200
(gas/fat/paradoxical/systemic) embolism: majority originate in left side of heart
systemic
201
(gas/fat/paradoxical/systemic) embolism: most often due to traumatic fracture of long bones (femur) or pelvis
fat
202
fat embolism patients are symptomatic in (most/few) cases
few (10%)
203
(gas/fat/paradoxical/systemic) embolism: hypoxemia, increased A-a gradient, thrombocytopenia
fat
204
____ embolism: occurs during labor or immediately postpartum
amniotic fluid--maternal mortality is 80%
205
in amniotic fluid embolism: (dyspnea/bleeding) is due to DIC
bleeding
206
in amniotic fluid embolism: (dyspnea/bleeding) is due to ARDS
dyspnea. also due to ARDS
207
decompression sickness is a form of (fat/gas/paradoxical/systemic) embolism
gas--scuba and deep sea diving
208
____ embolism: ↑pressure on lower extremity veins → stasis → thrombosis → embolism; dyspnea, pleuritic chest pain
pulmonary
209
caisson disease caused by persistence of gas emboli in bone: (acute/chronic)
chronic
210
loss of more than __% of blood produces shock
20%
211
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
212
best indicator of tissue hypoxia: mixed (arterial/venous) oxygen content
decreased mixed venous oxygen content
213
_____ shock: increased anion gap type of metabolic acidosis due to lactic acidosis
hypovolemic
214
(septic/hypovolemic) shock: warm skin, strong peripheral pulses, hypotension, DIC
septic
215
(septic/hypovolemic) shock: cold/clammy skin, hypotension, tachycardia, ↓urine output
hypovolemic
216
most common cause of cardiogenic shock
acute MI
217
(cardiogenic/septic) shock: ↑CO, ↓LVEDP, ↓PVR, ↑MVO2
septic (initial phase)
218
(cardiogenic/septic) shock: ↓CO, ↑LVEDP, ↑PVR, ↓MVO2
cardiogenic
219
most common site for infection leading to sepsis
lungs
220
endotoxins (LPS) are released by gram (+/-) bacteria
negative
221
endotoxins (LPS) activate macrophages, releasing IL-1 and TNF. (IL-1/TNF) produces fever
IL-1
222
endotoxins (LPS) activate macrophages, releasing IL-1 and TNF. (IL-1/TNF) damages endothelial cells, causing them to release vasodilators
TNF
223
endotoxins activate the (classical/alternative) complement pathway. Anaphylatoxins C3a and C5a are produced which stimulate mast cells to release histamine
alternative
224
MCC sepsis due to gram- (+/-) organisms (coagulase-negative Staphylococci)
positive
225
E coli: most common cause of gram-(+/-) septic shock
negative
226
Endotoxins damage tissue, causing the release of tissue thromboplastin, which activates the extrinsic coagulation system producing _____
DIC
227
most common fungal cause of septic shock
Candida
