Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
128 Cards in this Set
- Front
- Back
|
fas is cd
|
95
|
|
|
cd95 is
|
fas
|
|
|
cd95
|
is fas
|
|
|
superoxide dismutase does what
|
turns superoxide anions to h2o2
|
|
|
what form of iron binds transferrin
|
the oxidized ferric plus 3
|
|
|
what form of iron binds transferrin
|
the oxidized ferric plus three
|
|
|
lymphoidfollicles are where
|
the cortex where isotype switching is performed
|
|
|
the cortex of the lymphnode
|
is where the isotype swithcing is performed
|
|
|
do not require phosporylation by virla kinases
|
Non nucleoside RT inhibitors like nevirapine, efivirenz and delaverdine....severe hepatotoxicity is most likely to occur within the first week
|
|
|
do not require phosporylation by virla kinases
|
Non nucleoside RT inhibitors like nevirapine, efivirenz and delaverdine....severe hepatotoxicity is most likely to occur within the first week
|
|
|
do not require phosporylation by virla kinases
|
Non nucleoside RT inhibitors like nevirapine, efivirenz and delaverdine....severe hepatotoxicity is most likely to occur within the first week
|
|
|
do not require phosporylation by virla kinases
|
Non nucleoside RT inhibitors like nevirapine, efivirenz and delaverdine....severe hepatotoxicity is most likely to occur within the first week
|
|
|
do not require phosporylation by virla kinases
|
Non nucleoside RT inhibitors like nevirapine, efivirenz and delaverdine....severe hepatotoxicity is most likely to occur within the first week
|
|
|
podophyllin
|
is what makes etoposide which is a topoisomerase II inhibitor
|
|
|
podophyllin
|
is what makes etoposide which is a topoisomerase II inhibitor
|
|
|
how does topoisomerase II work
|
induces transient breaks in both DNA strands to relieve both positive and negative supercoiling as well as reseal the breaks---etoposide inhibits the resealing specifically
|
|
|
how does topoisomerase II work
|
induces transient breaks in both DNA strands to relieve both positive and negative supercoiling as well as reseal the breaks---etoposide inhibits the resealing specifically
|
|
|
how does topoisomerase II work
|
induces transient breaks in both DNA strands to relieve both positive and negative supercoiling as well as reseal the breaks---etoposide inhibits the resealing specifically
|
|
|
how does topoisomerase II work
|
induces transient breaks in both DNA strands to relieve both positive and negative supercoiling as well as reseal the breaks---etoposide inhibits the resealing specifically
|
|
|
name the antimetabolites that inhibit thymidilate synthase
|
5-doxyuridine, and 5-fluorouracil
|
|
|
5-deoxyuridine and 5-fluorouracil
|
inhibit thymidylate synthase
|
|
|
inhibit thymidylate synthase
|
5-doxyuracil and 5-fluorouracil
|
|
|
inhibit topo I
|
ironotecan topotecan
|
|
|
inhibit topo I
|
ironotecan topotecan
|
|
|
inhibit topo I
|
rionotecan and topotecan
|
|
|
iron chelating agent that can prevent cardiotoxicity of anthracycline
|
dexrazoxane
|
|
|
iron chelating agent that can prevent cardiotoxicity of anthracycline
|
dexrazoxane
|
|
|
the MDR1 gene of chemoresistant tumor cells is a what
|
an atp-dependent transporter
|
|
|
the MDR1 gene of chemoresistant tumor cells is what
|
an ATP-dependent transporter
|
|
|
the MDR1 gene of chemoresistant tumor cells is what
|
an ATP-dependent transporter
|
|
|
iron chelating agent that can prevent cardiotoxicity of anthracycline
|
dexrazoxane
|
|
|
iron chelating agent that can prevent cardiotoxicity of anthracycline
|
dexrazoxane
|
|
|
the MDR1 gene of chemoresistant tumor cells is a what
|
an atp-dependent transporter and the prototype product of this gene is P-glcoprotein
|
|
|
the MDR1 gene of chemoresistant tumor cells is what
|
an ATP-dependent transporter and the prototype product of this gene is P-glycoprotein
|
|
|
the MDR1 gene of chemoresistant tumor cells is what
|
an ATP-dependent transporter and the prototype product of this gene is P-glycoprotein
|
|
|
example of a gene responsible for cell adhesion
|
APC
|
|
|
example of a gene responsible for cell adhesion
|
APC
|
|
|
example of a gene responsible for cell adhesion
|
APC and its mutation is associated with decreased expression of e-cadherins
|
|
|
example of a gene responsible for cell adhesion
|
APC and its mutation is associated with decreased expression of e-cadherins
|
|
|
deficiencies of what cause PT prolongation
|
2 5 7 10 and fibrinogen
|
|
|
deficiencies of what cause PT prolongation
|
2 5 7 10 and fibrinogen
|
|
|
deficiencies of what cause PT prolongation
|
2 5 7 10 and fibrinogen
|
|
|
deficiencies of what cause PT prolongation
|
2 5 7 10 and fibrinogen
|
|
|
deficiencies of what cause PT prolongation
|
2 5 7 10 and fibrinogen
|
|
|
deficiencies of what cause PT prolongation
|
2 5 7 10 and fibrinogen
|
|
|
deficiencies of what cause PT prolongation
|
2 5 7 10 and fibrinogen
|
|
|
deficiencies of what cause PT prolongation
|
2 5 7 10 and fibrinogen
|
|
|
deficiencies of what cause PT prolongation
|
2 5 7 10 and fibrinogen
|
|
|
deficiencies of what cause PT prolongation
|
2 5 7 10 and fibrinogen
|
|
|
the thrombin time measures the rate of conversion of
|
fibrin to fibrinogen
|
|
|
the thrombin time measure the rate of conversion of
|
fibrin to fibrinogen
|
|
|
the throbin time measures the rate of conversionof
|
fibrin to fibrinoge
|
|
|
Myosis fungoides is when
|
proliferating CD4 lymphocytes infiltrate the dermis and epidermis where they form pautrier microabsesses the condition manifests with plaques that may be confused as psoriasis or eczema
|
|
|
Myosis fungoides is when
|
proliferating CD4 lymphocytes infiltrate the dermis and epidermis where they form pautrier microabsesses the condition manifests with plaques that may be confused as psoriasis or eczema
|
|
|
Myosis fungoides is when
|
proliferating CD4 lymphocytes infiltrate the dermis and epidermis where they form pautrier microabsesses the condition manifests with plaques that may be confused as psoriasis or eczema
|
|
|
Myosis fungoides is when
|
proliferating CD4 lymphocytes infiltrate the dermis and epidermis where they form pautrier microabsesses the condition manifests with plaques that may be confused as psoriasis or eczema
|
|
|
Myosis fungoides is when
|
proliferating CD4 lymphocytes infiltrate the dermis and epidermis where they form pautrier microabsesses the condition manifests with plaques that may be confused as psoriasis or eczema
|
|
|
Myosis fungoides is when
|
proliferating CD4 lymphocytes infiltrate the dermis and epidermis where they form pautrier microabsesses the condition manifests with plaques that may be confused as psoriasis or eczema
|
|
|
cd55 and cd59 deficiency is diagnostic of
|
PNH
|
|
|
cd55 and cd59 def. is diagnostic of
|
PNH
|
|
|
diagnostic of PNH
|
cd55 and cd59
|
|
|
diagnostic of PNH
|
cd55 and cd59
|
|
|
whenever you see what clinically you should thin of PNH
|
hemolytic anemia, hypercoagulable state, and decreased blood count
|
|
|
whenever you see what clinically you should think of PNH
|
hemolytic anemia, hypercoagulable state, adn decreased blood count
|
|
|
whenever you see what clinically you should think of PNH
|
hemolytic anemia, hypercoagulable state and decreased blood count
|
|
|
follicular lymphoma on low power looks like
|
packed follicles that obscure the lymphnode architecture
|
|
|
follicular lymphoma on low power looks like
|
packed follcles that obscure the lymphnode architecture
|
|
|
follicular lymphoma at low power loos like what
|
packed follicles that obscure the lymph node architecture
|
|
|
the C-myc gene is located on wht csome
|
8
|
|
|
the c-myc gene is located on what csom
|
8
|
|
|
the cmyc gene is located on what csom
|
8
|
|
|
when active what does antithrombin do?
|
binds to factor 10a and stops factor 10a from converting prothrombin to thrombin
|
|
|
when active what does antithrombin do?
|
binds to factor 10a and stops factor 10a from converting prothrombin to thrombin
|
|
|
when active what does antithrombin do?
|
binds to factor 10a and stops factor 10a from converting prothrombin to thrombin
|
|
|
when active what does antithrombin do?
|
binds to factor 10a and stops factor 10a from converting prothrombin to thrombin
|
|
|
when active what does antithrombin do?
|
binds to factor 10a and stops factor 10a from converting prothrombin to thrombin
|
|
|
when active what does antithrombin do?
|
binds to factor 10a and stops factor 10a from converting prothrombin to thrombin
|
|
|
when active what does antithrombin do?
|
binds to factor 10a and stops factor 10a from converting prothrombin to thrombin
|
|
|
when active what does antithrombin do?
|
binds to factor 10a and stops factor 10a from converting prothrombin to thrombin
|
|
|
when active what does antithrombin do?
|
binds to factor 10a and stops factor 10a from converting prothrombin to thrombin
|
|
|
when active what does antithrombin do?
|
binds to factor 10a and stops factor 10a from converting prothrombin to thrombin
|
|
|
platelets aggregate normally in response to adp but not with addtion of rstocetin...this is a deficiency of what
|
vWF
|
|
|
platelets aggregate normally in response to adp but not with addtion of rstocetin...this is a deficiency of what
|
vWF
|
|
|
platelets aggregate normally in response to adp but not with addtion of rstocetin...this is a deficiency of what
|
vWF
|
|
|
platelets aggregate normally in response to adp but not with addtion of rstocetin...this is a deficiency of whatplatelets aggregate normally in response to adp but not with addtion of rstocetin...this is a deficiency of what
|
vWF
|
|
|
platelets aggregate normally in response to adp but not with addtion of rstocetin...this is a deficiency of what
|
vWF
|
|
|
vWF binds to what
|
gpIb receptors on the platelet membran
|
|
|
gpIb receptors on the platelet membrane bind to
|
vWF
|
|
|
vWF binds to
|
gpIb receptors on the platelet membran
|
|
|
hereditary def. of GpIIb/IIIa
|
glanzmans - platelet aggregation in response to ristocetin is normal but decreased in response to ADP...this disease manifests with mucocutaneous bleeding and an increased bleeding time
|
|
|
hereditary def. of GpIIb/IIIa
|
glanzmans - platelet aggregation in response to ristocetin is normal but decreased in response to ADP...this disease manifests with mucocutaneous bleeding and an increased bleeding time
|
|
|
hereditary def. of GpIIb/IIIa
|
glanzmans - platelet aggregation in response to ristocetin is normal but decreased in response to ADP...this disease manifests with mucocutaneous bleeding and an increased bleeding time
|
|
|
hereditary def. of GpIIb/IIIa
|
glanzmans - platelet aggregation in response to ristocetin is normal but decreased in response to ADP...this disease manifests with mucocutaneous bleeding and an increased bleeding time
|
|
|
hereditary def. of GpIIb/IIIa
|
glanzmans - platelet aggregation in response to ristocetin is normal but decreased in response to ADP...this disease manifests with mucocutaneous bleeding and an increased bleeding time
|
|
|
glanzmans - platelet aggregation in response to ristocetin is normal but decreased in response to ADP...this disease manifests with mucocutaneous bleeding and an increased bleeding time
|
hereditary def. of GpIIb/IIIa
|
|
|
glanzmans - platelet aggregation in response to ristocetin is normal but decreased in response to ADP...this disease manifests with mucocutaneous bleeding and an increased bleeding time
|
hereditary def. of GpIIb/IIIa
|
|
|
glanzmans - platelet aggregation in response to ristocetin is normal but decreased in response to ADP...this disease manifests with mucocutaneous bleeding and an increased bleeding time
|
hereditary def. of GpIIb/IIIa
|
|
|
ristocetin does what
|
activates gpI -IX receptors on platelets making them available to bind vWf (carries8)
|
|
|
ristocetin does what
|
activates gpIb-IX receptors on platelets making them available to bind vWF (carries 8)
|
|
|
ristocetin does what
|
activates gpIb-IX receptors on platelets making them available to bind vWF (carries8)
|
|
|
ristocetin does what
|
activates gpIb-IX receptors on platelets making them availble to bind vWF (carries 8)
|
|
|
ristocetin does what
|
activates gpIb -IX receptors on platelets making them available to bind vWF (carries 8)
|
|
|
how do you treat vWF disease
|
desompressin which releases vWF
|
|
|
how do you treat vWF disease
|
desmopressin which releases vWF
|
|
|
how do you treat vWF disease
|
desmopressin which releases vWF
|
|
|
how do you treat vWF disease
|
desmopressin which releases vWF
|
|
|
defect in the alpha-5 chain of type IV collagen
|
alports
|
|
|
alports
|
defect in the alpha-5 chain of type IV collagen
|
|
|
alports is a what
|
defect in the alpha-5 chain of type IV collagen
|
|
|
alports is what
|
defect in the alpha-5 chain of typeIV collagen
|
|
|
what is the classic histological picture of poststrep G-nephritis
|
enlarge hypercellular glomeruli with subepithelial electron dense deposits giving rise to a lumpy bump appearace....patents typically present with perorbital edema, red face dark hematuria in a 6-10 year old
|
|
|
what is the classic histological picture of poststrep G-nephritis
|
enlarge hypercellular glomeruli with subepithelial electron dense deposits giving rise to a lumpy bump appearace....patents typically present with perorbital edema, red face dark hematuria in a 6-10 year old
|
|
|
what is the classic histological picture of poststrep G-nephritis
|
enlarge hypercellular glomeruli with subepithelial electron dense deposits giving rise to a lumpy bump appearace....patents typically present with perorbital edema, red face dark hematuria in a 6-10 year old
|
|
|
what is the classic histological picture of poststrep G-nephritis
|
enlarge hypercellular glomeruli with subepithelial electron dense deposits giving rise to a lumpy bump appearace....patents typically present with perorbital edema, red face dark hematuria in a 6-10 year old
|
|
|
what is the classic histological picture of poststrep G-nephritis
|
enlarge hypercellular glomeruli with subepithelial electron dense deposits giving rise to a lumpy bump appearace....patents typically present with perorbital edema, red face dark hematuria in a 6-10 year old
|
|
|
what is the classic histological picture of poststrep G-nephritis
|
enlarge hypercellular glomeruli with subepithelial electron dense deposits giving rise to a lumpy bump appearace....patents typically present with perorbital edema, red face dark hematuria in a 6-10 year old
|
|
|
what is the classic histological picture of poststrep G-nephritis
|
enlarge hypercellular glomeruli with subepithelial electron dense deposits giving rise to a lumpy bump appearace....patents typically present with perorbital edema, red face dark hematuria in a 6-10 year old
|
|
|
are there RBCs or RBC casts in the urine of patients with nephrotic syndrome
|
no but there is over 3.5 grams of protein lost
|
|
|
are there RBCs or RBC casts in the urine of patients with nephrotic syndrome
|
no but there is over 3.5 gm of protein lost
|
|
|
what is the pathogenesis of analgesis nephropathy
|
nsaids concentrate in the renal medulla, allowing higher levels in the papilla than the cortex, decreased prostaglindins also facilitates constriction of the medullry vasa recta promoting ischemia..all this results in patchy interstitial inflammation, with subsequent fibrosis, necrosis and scarring of the ppillae, distortion of the calciceal architecture and tubular atrohpy
|
|
|
what is the pathogenesis of analgesis nephropathy
|
nsaids concentrate in the renal medulla, allowing higher levels in the papilla than the cortex, decreased prostaglindins also facilitates constriction of the medullry vasa recta promoting ischemia..all this results in patchy interstitial inflammation, with subsequent fibrosis, necrosis and scarring of the ppillae, distortion of the calciceal architecture and tubular atrohpy
|
|
|
what is the pathogenesis of analgesis nephropathy
|
nsaids concentrate in the renal medulla, allowing higher levels in the papilla than the cortex, decreased prostaglindins also facilitates constriction of the medullry vasa recta promoting ischemia..all this results in patchy interstitial inflammation, with subsequent fibrosis, necrosis and scarring of the ppillae, distortion of the calciceal architecture and tubular atrohpy
|
|
|
what is the pathogenesis of analgesis nephropathy
|
nsaids concentrate in the renal medulla, allowing higher levels in the papilla than the cortex, decreased prostaglindins also facilitates constriction of the medullry vasa recta promoting ischemia..all this results in patchy interstitial inflammation, with subsequent fibrosis, necrosis and scarring of the ppillae, distortion of the calciceal architecture and tubular atrohpy
|
|
|
what is the pathogenesis of analgesis nephropathy
|
nsaids concentrate in the renal medulla, allowing higher levels in the papilla than the cortex, decreased prostaglindins also facilitates constriction of the medullry vasa recta promoting ischemia..all this results in patchy interstitial inflammation, with subsequent fibrosis, necrosis and scarring of the ppillae, distortion of the calciceal architecture and tubular atrohpy
|
|
|
what is the pathogenesis of analgesis nephropathy
|
nsaids concentrate in the renal medulla, allowing higher levels in the papilla than the cortex, decreased prostaglindins also facilitates constriction of the medullry vasa recta promoting ischemia..all this results in patchy interstitial inflammation, with subsequent fibrosis, necrosis and scarring of the ppillae, distortion of the calciceal architecture and tubular atrohpy
|
|
|
what is the pathogenesis of analgesis nephropathy
|
nsaids concentrate in the renal medulla, allowing higher levels in the papilla than the cortex, decreased prostaglindins also facilitates constriction of the medullry vasa recta promoting ischemia..all this results in patchy interstitial inflammation, with subsequent fibrosis, necrosis and scarring of the ppillae, distortion of the calciceal architecture and tubular atrohpy
|
|
|
what is the pathogenesis of analgesis nephropathy
|
nsaids concentrate in the renal medulla, allowing higher levels in the papilla than the cortex, decreased prostaglindins also facilitates constriction of the medullry vasa recta promoting ischemia..all this results in patchy interstitial inflammation, with subsequent fibrosis, necrosis and scarring of the ppillae, distortion of the calciceal architecture and tubular atrohpy
|
|
|
what is the pathogenesis of analgesis nephropathy
|
nsaids concentrate in the renal medulla, allowing higher levels in the papilla than the cortex, decreased prostaglindins also facilitates constriction of the medullry vasa recta promoting ischemia..all this results in patchy interstitial inflammation, with subsequent fibrosis, necrosis and scarring of the ppillae, distortion of the calciceal architecture and tubular atrohpy
|
