Neuro Final

Front 1

In plasma protein disorders, dx is difficult due to:

Back 1

variable bleeding times,
wide range of PLT abnormalities
wide range of PTT

Front 2

In plasma protein disorders like vWD, PT is:

Back 2

normal

Front 3

In plasma protein disorders like vWD, PTT is:

Back 3

prolonged in severe

Front 4

Type III plasma protein disorder is the _____ of vWF and is most ______.

Back 4

absence, severe

Front 5

vWD affects what factor?

Back 5

8

Front 6

How do you define disease level in VWD?

Back 6

Factor 8 Level & vWF antigen determination

Front 7

In VWD, CBC is:

Back 7

normal

Front 8

If you have type 1 vWD, tx =

Back 8

DdAVP - stimulate release of endothelial stores of vWF

Front 9

If you have type 2 & 3 vWD, tx =

Back 9

Cryoprecipitate

Front 10

if acquired vWD, tx with:

Back 10

Cryoprecipitate (severe) or DdAVP (mild)

Front 11

PT checks

Back 11

factor VII dependent pathways

Front 12

abnormalities of PT are due to

Back 12

- Vit K deficiency & warfarin
- liver disease
- DIC
- factor deficiency (7, 5, 10, 2 [1572])
- factor inhibitor

Front 13

PTT measures:

Back 13

Factor 10, 9, & 8 dependent pathways

Front 14

PTT can be abnormal due to:

Back 14

- heparin
- DIC
- lupus anticoagulant
- factor deficiency ( 11, 9, 8, 5, 10, 2)
- factor inhibitor

Front 15

THrombin time measures

Back 15

fibrinogen

Front 16

Thrombin time is abnormal due to:

Back 16

- heparin
- DIC
- hypofibinogenemia
- dysfibrinogenemia

Front 17

Platelet function analysis is tested:

Back 17

- platelet
- vWF

Front 18

A mixing study is tested by:

Back 18

presence of an inhibitor

Front 19

Platelet function analysis is abnormal due to:

Back 19

aspirin
vWD
storage pool disease

Front 20

An abnormal mixing study may be due to:

Back 20

abnormal clotting time corrects with deficiency; does not correct with an inhibitor

Front 21

1 unit of platelets transfused raises platelets:

Back 21

10K

Front 22

platelets form hemostatic plug; platelets form from:

Back 22

megakaryocytes

Front 23

megakaryocytes matures in bone marrow in response to lineage specific cytokine,

Back 23

thrombopoietin

Front 24

Extrinisic Pathway =

Back 24

initial pathway:
7a to 7
7 to 9 to 9a
7 to 10 to 10a in presence of Ca++

Front 25

the extrinisic pathway is downregulated by:

Back 25

tissue pathway factor inhibitor (TPFI)

Front 26

TPFI bins to:

Back 26

7a & 10

Front 27

what is needed to stimulate intrinsic factors?

Back 27

extrinisic factors

Front 28

Secondary hemostasis is

Back 28

the development of a fibrin clot

Front 29

extrinisic hemostasis is:

Back 29

tissue thromboplastin

Front 30

intrinsic hemostatis is:

Back 30

platelet thromboplastin

Front 31

primary coagulation is

Back 31

the formation of a platelet plug

Front 32

Secondary hemostasis

Back 32

is extrinisic, intrinsic & common pathways - fibrin plug

Front 33

Sustained procoagulant response requires incorporation of components of:

Back 33

intrinsic pathway

Front 34

Intrinsic pathway:

Back 34

thrombin activates 11, 5, 8
11a activates 9 which activates 9a
9a + 8a & Ca++ and phospholipid to form IF 10a-ase complex
Xa interacts with 5a (+Ca) to form prothrombinase
Prothrombinase turns prothrombin into thrombin

Front 35

Prothrombinase complex turns what into what

Back 35

prothrombin into thrombin

Front 36

Thrombin cleaves

Back 36

fibrinogen to form fibrin

Front 37

Fibrin is cross linked by ____ to result in a clot that is:

Back 37

8a
resistant to lysis

Front 38

Thrombin functions

Back 38

activates: 5, 8, 9
activates platelet exposing procoag phospholipid
involves release of PLT activating substance - thromboxane, Ca, ADP, vWF
activates 13
activates protein C

Front 39

Drugs that strongly inhibit/affect platelet fxn

Back 39

strong inhibitors:
Clopidigrel
Abciximab
ASA
NSAIDS

"Strong inhibitions are lost in CanAAN"

Front 40

Drugs that moderately inhibit platelet fxn

Back 40

Moderate

Heparin
Abx (PCN, cephalosporin, nitrofurantoin)
Dextran
Fibrinolytics
Hetastarch

"I was moderately inhibited when I HAD to give my FH"

Front 41

Drugs that are weak platelet inhibitors

Back 41

Weak

- alcohol
- nitroglycerin
- nitroprusside

ANN is weakly inhibited when she drinks

Front 42

Liver is the site of what coag proteins

Back 42

many - esp. 5 & 7

Front 43

T/F
Liver is not responsible for coag factor 8 production

Back 43

True

Front 44

What factors require Vit K for activity?

Back 44

1972
(2, 10, 9, 7)
and protein c & S

Front 45

What factors do not require vitamin K for activity?

Back 45

5, 11, 12, fibrinogen, antithrombin 3

Front 46

In liver disease, what increase?

Back 46

Factor 8, vWF

Front 47

Liver disease has a ___ PT and a ___ PTT

Back 47

Increased PT
Normal PTT unless severe

Front 48

If problems with secondary hemostatis, bleeding problems much more severe and result in:

Back 48

joint/muscle hemorrhage - hemarthrosis
easy bruising
bleeding after trauma/surgery

Front 49

TCT

Back 49

thrombin clot time

Front 50

Bleeding time is used to assess what coag system

Back 50

primary

Front 51

bleeding time looks at what fxn?

Back 51

platelet

Front 52

INR is a measurement of:

Back 52

PT/Vitamin K activity that has been corrected for lab variation

Front 53

INR WNL =

Back 53

1

Front 54

INR 2 -3 =

Back 54

therapeutic in CVT (cerebral venous thrombosus?)

Front 55

INR 2.5 - 3.5

Back 55

therapeutic for valvular

Front 56

TCT or thrombin clot time is a measure of

Back 56

acitivity of fibrinogen

Front 57

T/F
Factor 7 is in the intrinsic pathway

Back 57

false!
in extrinsic

Front 58

Antiplatelet therapies include:

Back 58

ASA
NSAIDS
Clopidigrel
Dypyridamole
Prostacyclin
Abciximab
Integrillin
Lamifiban
Tirofiban
Xemilofiban

Front 59

In Hemophilia A(8), what is the PT, PTT, TT

Back 59

PT = normal
PTT= prolonged
TT = normal

Front 60

In Hemophilia B (9), what is the PT, PTT, TT

Back 60

PT =normal
PTT= prolonged
TT = normal

Front 61

Hemophilia 8 is x-linked recessive yet its manifestations depend on the amount of:

Back 61

Factor 8 deficiency

Front 62

What characteristics are found in both hemophilia 8 & 9:

Back 62

x-linked recessive
increased PTT
WNL - PT, BT, fibrinogen
No NSAIDS or ASA
Avoid IM injections
Hemarthrosis

Front 63

What is the hallmark of hemophilia A?

Back 63

prolonged PTT

Front 64

What is the management of Hemophilia A?

Back 64

DdAVP - increases factor 8 activity

Front 65

patients with severe Hemophilia 8 get what tx

Back 65

cryoprecipitate

Front 66

What should pt with hemophilia A avoid

Back 66

ASA
antiplatelets
IM injections

Front 67

What is leading COD with hemophilia?

Back 67

AIDS
HEP B
HEP C

Front 68

T/F
Hemophilia B is clinically identical to Hemophilia A

Back 68

True

Front 69

Deficiency of Factor V leads to ___ PT, ___ PTT

Back 69

Increased PT
Increased PTT

Front 70

What is etiology of Factor V deficiency?

Back 70

liver disease in some cases

Front 71

Tx of Factor V deficiency =

Back 71

FFP or platelets

Front 72

Deficiency of Factor VII is ____ and has a ___ PT, ____ PTT, ____TCT

Back 72

rare
Increased PT
normal PTT
normal TCT

Front 73

Defciency of factor X is ____ and has a ___ PT, ____ PTT.

Back 73

rare
Increased PT
Increased PTT

Front 74

Tx of factor X =

Back 74

plasma

Front 75

patients with severe Hemophilia 8 get what tx

Back 75

cryoprecipitate

Front 76

What should pt with hemophilia A avoid

Back 76

ASA
antiplatelets
IM injections

Front 77

What is leading COD with hemophilia?

Back 77

AIDS
HEP B
HEP C

Front 78

T/F
Hemophilia B is clinically identical to Hemophilia A

Back 78

True

Front 79

Deficiency of Factor V leads to ___ PT, ___ PTT

Back 79

Increased PT
Increased PTT

Front 80

What is etiology of Factor V deficiency?

Back 80

liver disease

Front 81

Tx of Factor V deficiency =

Back 81

FFP or platelets

Front 82

Deficiency of Factor VII is ____ and has a ___ PT, ____ PTT, ____TCT

Back 82

rare
Increased PT
normal PTT
normal TCT

Front 83

Defciency of factor X is ____ and has a ___ PT, ____ PTT.

Back 83

rare
Increased PT
Increased PTT

Front 84

Tx of factor X =

Back 84

plasma

Front 85

T/F
newborns are often deficient in Vit K

Back 85

Ture

Front 86

Halmark of Vit K deficiency =

Back 86

increased PT due to short 1/2 life of VII - thus cannot activate extrinisic pathway & increased PT

Front 87

Vitamin K is responsible for the activation of:

Back 87

7, 9, 10, 2

Front 88

If Vit K deficiency is due to liver disease, waht will labs look like?

Back 88

Increased AST/ALT
Increased bili
Increased PT
Normal PTT

Front 89

In prolonged Vit K deficiency, what gets messed up in intrinsic pathway

Back 89

2, 3, 9, 10

also has prolonged PTT

Front 90

Manifestations of Vit K deficiency =

Back 90

bleeding

Front 91

Tx of VIt K deficiency

Back 91

replace Vit K - AquaMEPHYTON

Front 92

What is the best way to deliver K in Coumadin excess?

Back 92

oral

Front 93

In emergency vit K deficiency/coumadin OD, what can you use

Back 93

FFP

Front 94

Propagation of DIC due to failure to:

Back 94

clear activated factors and due to reduced regulatory proteins (ATIII, protein C)

Front 95

In liver disease, platelet dysfunction due to:

Back 95

abnormal proteins, enzymes

Front 96

Liver disease has increased fibrinolysis due to:

Back 96

increased tPA

Front 97

What is the best indicator of acute liver function?

Back 97

Increased PT - b/c factor 7 short half life

Front 98

In liver disease, what do labs look like?

Back 98

Increased PTT (severe)
Increased fibrin split
Decreased platelets
All coag factors down but 8

Front 99

If factor 8 is decreased in liver disease, what should you do?

Back 99

think of another dx

Front 100

what are other good measure of liver fxn?

Back 100

Prealbumin & albumin

Front 101

Causes of DIC

Back 101

gram - bacteremia
trauma
closed head injury
burns
hypotension/hypoperfusion
adenocarcinoma
acute promyelocytic leukemia
vasculitis
giant hemangioma
aortic aneurysm
cardiac mural thrombus
snake venom
activated factor infusions

Front 102

What gets activated in DIC

Back 102

intrinsic in coag
extrinsic in CA and tumor mass

Front 103

In DIC, the procoagulant response is activated intravascularly which leads to:

Back 103

diffuse thrombin production

Front 104

In DIC you see multiple_____, _____ and ______.

Back 104

multiple fibrin thrombi, tissue ischemia, end organ damage

Front 105

DIC also activates what:

Back 105

fibrinolytic pathway - leads to fibrin degradation

Front 106

Labs in DIC

Back 106

Increased PT
Increased PTT
Decreased PLT
Increased fibrin split products - d dimers +
Schistocytes on peripheral smear

Front 107

How do you tx DIC

Back 107

tx underlying disease
replace clotting factor
Heparin contraversial but often used (destabilize clots before ischemia)

Front 108

Trousseau's -

Back 108

malignancy associated with DIC; proteins w/both primary & secondary

Front 109

What is the counter to coagulation?

Back 109

natural anitcoagulants & fibrinolytic pathway

Front 110

natural anitcoagulants & fibrinolytic pathway exist to

Back 110

downregulate each step of procoag response

Front 111

TFPI down regulates:

Back 111

initial step - via antithrombin 3 & protein C

Front 112

Antithrombin 3 neutralizes:

Back 112

2a
10a
11a
12a

Front 113

Protein C inactivates

Back 113

5a
8a

Front 114

Mechanism for clot removal during course of vascular repair =

Back 114

plasminogen - plasmin via tPA
Plasmin degrades fibrin clot

Front 115

Inherited causes of thrombophilia

Back 115

Activated protein C resistance/factor 5
Homocystelinemia
Prothrombin 20210A
Antithrombin 3 deficiency
Protein C
Protein S
TPA deficiency
Plasminogen activator inhibitor excess
Dysfibrinogenemia
Decreased plasminogen

Front 116

Meds that are acquired causes of thrombosis

Back 116

HIT
OCPs
HRT
Prothrombin complexes

Front 117

Lab evaluatio of venous thrombosis will point to:

Back 117

Factor V (biggest)
Lupus anticoag
anticardiolipin
homocysteine level
prothrombin 20210A
Antithrombin 3 activity
Protein C activity
Protein S activity

Front 118

T/F hemolytic anemia causes increased thrombosis

Back 118

true

Front 119

T/F nephrotic syndrome causes increased thrombosis

Back 119

true

Front 120

T/F artificial heart valves cause increased thrombosis

Back 120

true

Front 121

Risk of getting cancer

Back 121

1:2 men
1:3 women

Front 122

#1 death rate in women & men

Back 122

lung CA

Front 123

what are the good things that protect us from cancer and the bad things that allow cancer to get turned on?

Back 123

good = tumor suppressor genes

bad = oncogenes

Front 124

Tobacco CA effects

Back 124

lung
bronchus
esophagus
head & neck
stomach
pancreas
kidney
bladder
cervical
prostate

Front 125

Inherited causes of thrombophilia

Back 125

Activated protein C resistance/factor 5
Homocystelinemia
Prothrombin 20210A
Antithrombin 3 deficiency
Protein C
Protein S
TPA deficiency
Plasminogen activator inhibitor excess
Dysfibrinogenemia
Decreased plasminogen

Front 126

Meds that are acquired causes of thrombosis

Back 126

HIT
OCPs
HRT
Prothrombin complexes

Front 127

Lab evaluatio of venous thrombosis will point to:

Back 127

Factor V (biggest)
Lupus anticoag
anticardiolipin
homocysteine level
prothrombin 20210A
Antithrombin 3 activity
Protein C activity
Protein S activity

Front 128

T/F hemolytic anemia causes increased thrombosis

Back 128

true

Front 129

T/F nephrotic syndrome causes increased thrombosis

Back 129

true

Front 130

T/F artificial heart valves cause increased thrombosis

Back 130

true

Front 131

Risk of getting cancer

Back 131

1:2 men
1:3 women

Front 132

#1 death rate in women & men

Back 132

lung CA

Front 133

what are the good things that protect us from cancer and the bad things that allow cancer to get turned on?

Back 133

good = tumor suppressor genes

bad = oncogenes

Front 134

Tobacco CA effects

Back 134

lung
bronchus
esophagus
head & neck
stomach
pancreas
kidney
bladder
cervical
prostate

Front 135

high etoh causes what kinds of Ca

Back 135

liver
rectum
breast
oralcavity
pharynx
larynx
esophagus

Front 136

being obese or having a high fat diet increases your risk of CA where?

Back 136

colon
breast
endometrium
kidney
pancreas
esophagus

Front 137

#1 environmental carcinogen

Back 137

tobacco

Front 138

alkylating agents for chemo can induce

Back 138

AML

Front 139

What induces lymphoma

Back 139

immunosuppressants, radiation

Front 140

what CAs do statins protect agains

Back 140

breast
colon
prostate

Front 141

OCPs protect against what CA

Back 141

ovarian

Front 142

what is protective in colon CA

Back 142

folic acid
NSAIDS
Statins

Front 143

good cost benefit in cancer screening

Back 143

mammo & pap

Front 144

bad cost benefit

Back 144

CEA
BRCA 1 & 2

Front 145

loss or suppression of TP53 can lead to what CA

Back 145

sarcoma, breast, brain, adrenal

Front 146

c-myc mutation can lead to

Back 146

Burkitt's lymphoma, neuroblastoma

Front 147

CLL has a mutation of

Back 147

bcl2

Front 148

If pt has increased ACTH, what CA might he have?

Back 148

oat cell

Cushing:oat

Front 149

If pt has increased ADH, what CA might he have?

Back 149

Small cell lung

SIADH: lung

Front 150

If pt has increased HcG, what CA might he have?

Back 150

germ cell tumors, lung CA

hCG: germ-lung

Front 151

What can happen in CA that effects the kidneys that is a medical emergency?

Back 151

hypercalcemia

Front 152

In radiation how is the following affected in early and late complications?

Bone marrow

Back 152

early - aplasia

late - leukemia, myelodysplasia

Front 153

In radiation how is the following affected in early and late complications?

Heart

Back 153

Early - none

Late - pericarditis, cardiomyopathy, coronary disease

Front 154

In radiation how is the following affected in early and late complications?

Rectum

Back 154

early - diarrhea, tesemsus

late - stricture, obstruction

Front 155

chemo sis the major tx inL

Back 155

60% of Ca

Front 156

doxorubicin side effects =

Back 156

alopecia
cardiomyopathy

Front 157

MXT side effects =

Back 157

stomatitis - give folic acid

Front 158

Cisplatin side effects =

Back 158

renal failure

Front 159

what cancers are more likely to get hypercalcemia

Back 159

breast, MM (#1), osteolytic CA

Front 160

chemo sis the major tx inL

Back 160

60% of Ca

Front 161

doxorubicin side effects =

Back 161

alopecia
cardiomyopathy

Front 162

MXT side effects =

Back 162

stomatitis - give folic acid

Front 163

chemo sis the major tx inL

Back 163

60% of Ca

Front 164

chemo sis the major tx inL

Back 164

60% of Ca

Front 165

Cisplatin side effects =

Back 165

renal failure

Front 166

doxorubicin side effects =

Back 166

alopecia
cardiomyopathy

Front 167

doxorubicin side effects =

Back 167

alopecia
cardiomyopathy

Front 168

what cancers are more likely to get hypercalcemia

Back 168

breast, MM (#1), osteolytic CA

Front 169

MXT side effects =

Back 169

stomatitis - give folic acid

Front 170

MXT side effects =

Back 170

stomatitis - give folic acid

Front 171

Cisplatin side effects =

Back 171

renal failure

Front 172

Cisplatin side effects =

Back 172

renal failure

Front 173

what cancers are more likely to get hypercalcemia

Back 173

breast, MM (#1), osteolytic CA

Front 174

what cancers are more likely to get hypercalcemia

Back 174

breast, MM (#1), osteolytic CA

Front 175

Use hormone therapy when:

Back 175

estrogen receptor + disease
lymph node, skin, bone, mets
>2 y from completion of adjuvant therapy

Front 176

use chemi when:

Back 176

receptor - disease
lung/liver involvement
< 2 y from completion of adjuvant therapy
progression after use of 1st & 2nd line chemo

Front 177

EBV increases risk of

Back 177

Burkitts

Front 178

Conjugate estrogens taken ____ y = increased risk of what?

Back 178

< 5-10
breast and endometrial cancer
5x if no progesterone taken

Front 179

Management of hypercalcemia =

Back 179

IV fluids
good urine output
pamidronate