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Hemostasis Flashcards

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1
Q

What is the first step of hemostasis? What are the two mediators of this?

A

Transient vasoconstriction mediated by a neural reflex arc and endothelin release

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2
Q

What is the molecule that is on endothelium and causes vasoconstriction?

A

Endothelin

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3
Q

What is the molecule on platelets that binds vWF?

A

GPIb

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4
Q

Where does vWF come from (which cells)? (2)

A
  • Weibel-Palade bodies within Endothelium

- Platelets

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5
Q

What is step II of hemostasis?

A

vWF binding to GPIb

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6
Q

What is in Weibel-Palade bodies?

A

vWF

P-selectin

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7
Q

What is released from platelets when the bind vWF?

A

ADP

TXA2

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8
Q

What is the enzyme that makes TXA2?

A

COX

platelet cyclooxygenase

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9
Q

What is the receptor on platelets that ADP induces? What does this do?

A

GpIIb/IIIa

Causes platelet-platelet binding

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10
Q

What does TXA2 do in platelets?

A

Causes platelet linking

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11
Q

What is the linker molecule between platelets that is used in aggregation?

A

fibrinogen + GPIIb/IIIa

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12
Q

What are the two, broad types of disorders of primary hemostasis?

A

Qualitative

Quantitative

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13
Q

What is the most common symptom of hemostasis disorders?

A

Mucosal and skin bleeding (epistaxis, hemoptysis etc)

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14
Q

What is the most feared complication of platelet defects?

A

Intracranial bleeding

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15
Q

Are petechia usually seen in qualitative or quantitative disorders?

A

Quantitative (thrombocytopenia)

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16
Q

Petechiae are characteristic of what hematological defect?

A

Quantitative Platelet issues

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17
Q

What is the drug that binds to and inhibits GpIIa/IIIb?

A

Abciximab

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18
Q

Define primary and secondary hemostasis

A 
Primary = platelet plug
Secondary = Fibrinogen cross linking
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19
Q

What are the four useful lab studies for hemostasis disorders?

A
  • Platelet count
  • Bleeding time
  • Blood smear
  • Bone marrow biopsy
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20
Q

What are the cells that produce platelets?

A

Megakaryocytes

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21
Q

What is immune thrombocytopenic purpura (ITP)?

A

Autoimmune production of IgG against platelet antigens (e.g. GPIIb/IIIa)

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22
Q

What is the most common cause of thrombocytopenia in adults?

A

ITP

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23
Q

What organ makes the IgG in ITP?

A

Spleen

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24
Q

What is the acute form of ITP? What is the treatment?

A

Develops weeks after viral infection/immunization

Usually self-limited, thus supportive treatment

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25
What is the chronic form of ITP? Who is this usually seen in (disease/age group)?
Usually women of childbearing age, associated with SLE.
26
What is the problem with ITP in pregnant women?
IgG that is produced can cross the placenta, and resulting in thrombocytopenia in fetus
27
What is the platelet count in ITP (up, down, or normal)?
Down
28
What is the PT/PTT in ITP (up, down, or normal)?
Normal
29
What is the megakaryocyte count in ITP (up, down, or normal)?
Up
30
What is the treatment for the fetus in ITP?
Corticosteroids
31
What is the treatment for symptomatic ITP? Why does this work?
IVIG--causes macrophages to eat IG, not bound to platelets (effect is short lived)
32
What is the treatment of refractory ITP? Why?
Splenectomy--eliminates the site of antibody production, and the site of destruction
33
What is microangiopathic hemolytic anemia?
Pathologic formation of platelet microthrombi in small vessels, causing RBCs to rupture d/t platelet microthrombi
34
What is the characteristic finding of a blood smear in microangiopathic hemolytic anemia?
Sheared RBCs (schistocytes)
35
Helmet cell = ?
Schistocyte (seen in microangiopathic anemia)
36
What are the two diseases that cause microangiopathic anemia?
Thrombocytopenic purpura (TTP) Hemolytic uremic syndrome (HUS)
37
What is the deficient enzyme in TTP? What does this do?
Decrease in ADAMTS13 enzyme, which normally cleaves vWF for degradation, causing abnormal platelet adhesion on uncleaved monomers
38
What causes the decrease in ADAMS-13 in TTP?
Acquired antibody; most commonly seen in females
39
What causes HUS?
E.coli OH157:H7 verotoxin damages endothelial cells, resulting in platelet microthrombi
40
What is the bacteria that causes HUS? Who is affected, and where does this bacteria come from?
E.coli OH157:H7 Children affected when eating undercooked beef
41
What are the clinical findings of HUS? (4)
- Dysentery - Skin and mucosal bleeding - Renal damage - CNS dysfunction
42
What is the predominant problem in TTP and HUS respectively?
``` TTP = CNS dysfunction HUS = Renal insufficiency ```
43
Why is the PT/PTT normal in HUS/TTP?
No activation of the coagulation cascade
44
What are the findings of a blood smear with TTP/HUS?
Schistocytes
45
What are the findings of a bone biopsy with TTP/HUS?
Increased megakaryocytes
46
What happens to bleeding time with TTP/HUS?
Increased
47
What is the treatment for TTP?
Plasmapheresis and corticosteroids
48
What is the cause of Bernard-Soulier syndrome?
Genetic GP1b deficiency; platelet adhesion is impaired
49
What are the findings of a blood smear with Bernard-Soulier syndrome?
Mild thrombocytopenia with enlarged platelets | **(Big Suckers with Bernard-Soulier)**
50
What is the cause of Glanzmann thrombasthenia?
Genetic GIIb/IIIa causing platelet aggregation impairment
51
What is the MOA of ASA in preventing platelet aggregation?
Lack of TXA2 d/t irreversible inhibition of COX
52
***What is the coagulation problem with uremia?***
***Uremia disrupts platelet function; both adhesion and aggregation is impaired***
53
What is the goal of secondary hemostasis?
Stabilize the platelet plug
54
What is the end product of coagulation?
Thrombin/fibrin
55
What protein connects the GPIIb/IIIa proteins on platelets together? What forms this, and what enzyme activates it?
Fibrin, which is formed from fibrinogen by thrombin
56
What produces fibrinogen, and where does it go (before activation?
Liver, floats around in the blood stream until activated
57
What are the three things that are needed to activate the coagulation cascade?
1. Activating substance 2. Ca 3. Phospholipid surface of platelets
58
What are the two activating substances of the coagulation cascade?
1. Tissue thrombin activator (VII) | 2. Subendothelial collagen activates factor XII
59
What causes disorders of secondary hemostasis?
Usually d/t factor abnormalities
60
What are the clinical features of secondary hemostasis disorders?
- Deep tissue bleeding into muscles/joints | - Rebleeding after procedures
61
What does PT measure (intrinsic or extrinsic pathway)?
The extrinsic pathway
62
What does PTT measure (intrinsic or extrinsic pathway)?
The intrinsic pathway ("has more factors, so has an extra T")
63
What are the factor steps of the intrinsic pathway?
12, 11, 9, 8, 10
64
What are the factor steps of the extrinsic pathway? Common pathway?
3, 7, 10 Common = 5, 2, 1
65
What activates factor 12?
Subendothelial collagen
66
What activates the extrinsic pathway?
Tissue thromboplastin (factor 3)
67
Which lab value measures the effect of heparin (PT or PTT)?
PTT (HEP and PTT both have three letters)
68
Which lab value measures the effect of warfarin (PT or PTT)?
PT
69
What is the factor that has a genetic defect in hemophilia A?
Factor VIII ("Hemophilia aaa--eeeight")
70
What is the inheritance pattern of hemophilia A?
X-linked recessive or new mutation
71
What are the PT and PTT findings of hemophilia A?
Increased PTT | Normal PT
72
What is the platelet count and bleeding time in hemophilia A? (up, down, normal)
Normal
73
What is the treatment for hemophilia A?
Recombinant factor 8
74
What is the factor deficiency for hemophilia B ("Christmas disease")?
Factor IX
75
What is the cause of coagulation factor inhibitor? Which factor is affected most commonly?
Acquired antibody against coagulation factor, resulting in impaired factor function Factor VIII most commonly affected
76
How do you distinguish between hemophilia A caused by a coagulation factor inhibitor vs a factor deficiency (since both have increased PTT)?
PTT does not correct upon mixing normal plasma with pts plasma (mixing study) if caused by a coagulation factor inhibitor (since antibodies are in serum)
77
What is von Willebrand disease? Symptoms?
Deficiency of vWF Mucosal and skin bleeding
78
What is the most common inherited coagulation factor disorder?
Genetic vWF deficiency
79
What is the most common type of vWF disease? Inheritance pattern?
AD decrease in vWF levels (quantitative, not qualitative defect)
80
What happens to bleeding time, PTT, and PT in vWF disease?
- Increased bleeding time - Increased PTT - Normal PT
81
Why does the PTT increase in vWF disease?
vWF is needed to stabilize factor 8
82
What is the ristocetin test, and what is the result in vWF disease?
Ristocetin induces platelet agglutination by causing vWF to bind to platelet GPIb; thus abnormal test
83
What is the treatment for vWF disease? MOA?
desmopressin | Increases the release of vWF from WP bodies
84
What are the factors that need vitamin K for gamma carboxylation?
10, 9, 7, 2 (vitamin K was born in 1972) | protein C and S
85
Why are newborns susceptible to vitamin K deficiency, as well as pts on long term abx?
Lack of bacterial colonization in the gut that make vit K
86
How does liver failure lead to coagulation disorders? How about abx therapy? Malabsorption?
- Decreased production of coagulation factors - Decreased vit K from bacteria - Decrease in fat soluble vitamin (K) absorption
87
What is the enzyme the liver produces that activates vitamin K?
Epoxide reductase
88
What lab value is followed in liver damage-caused coagulation disorders?
PT (same as warfarin)
89
***Why does large volume transfusion cause secondary coagulation defects?***
***Dilution of coag factors***
90
What is the cause of heparin induced thrombocytopenia (HIT)?
Antibodies to Hep-PF4 complex Fragments of destroyed platelets may activated remaining platelets, leading to thrombosis
91
What, generally, is DIC caused by?
Pathologic activation of the coagulation cascade, leading to the consumption of factors and platelets
92
What are the two major problems with DIC?
1. Widespread microthrombi | 2. Thrombocytopenia
93
What causes DIC in sepsis?
Cytokines and induction of coag by bacteria
94
What happens to platelet count in DIC (up, down, nl)?
Goes down
95
What happens to PT/PTT in DIC (up, down, nl)?
Up
96
What happens to fibrinogen in DIC (up, down, nl)?
Goes down
97
What is the screening lab test for DIC?
D-Dimer (elevated fibrin split products)
98
Microangiopathic hemolytic anemia is found in DIC. What is the blood smear finding to confirm this?
Schistocytes
99
What is the treatment for DIC?
Transfuse blood products or cryoprecipitate
100
What is the function of fibrinolysis normally?
Remove thrombus after damaged vessel heals
101
What is the function of plasmin? (3)
- Degrades fibrin/fibrinogen - Shuts down clotting factors - Blocks platelet aggregation
102
What do endothelial cells release to activate plasmin from plasminogen?
tPA
103
What is the endogenous molecule that inactivates plasmin?
alpha-2-antiplasmin
104
What are disorders of fibrinolysis caused by, generally?
Plasmin overactivity, resulting in excessive cleavage of fibrinogen
105
What is the chemical released during a radical prostatectomy that activates plasmin?
Urokinase
106
Why does liver cirrhosis lead to fibrinolysis disorder?
Loss of alpha-2 antiplasmin
107
Disorders of fibrinolysis present similar to what other process?
DIC
108
What are happens to PT/PTT with disorders of fibrinolysis? Why?
increase--cleavage of coaulation factors
109
What happens to bleeding time and platelet count with disorders of fibrinolysis? Why?
Increased bleeding time | Normal platelet count--inhibition of platelet aggregation
110
What is the difference between DIC and fibrinolysis disorders in terms of platelet count? D-dimer?
DIC has reduced platelets with increased d-dimer Both normal with fibrinolysis
111
Why is the d-dimer not elevated with disorders of fibrinolysis?
No clot formed, just overactivation of plasmin
112
***What is the treatment for disorders of fibrinolysis? MOA?***
***Aminocaproic acid--blocks activation of plasminogen***
113
What are the two characteristics that distinguish a thrombus from a post mortem clot?
- Lines of Zahn | - Attachment to the blood vessel walls
114
What are the three major risk factors for thrombosis?
1. Disruption of blood flow 2. Endothelial cell damage 3. Hypercoagulable state
115
What protects blood vessels from thrombosis? (4)
1. Barrier via endothelial cells does not allow attachment 2. PGI2 3. NO 4. Heparin-like molecules
116
What is the function of PGI2 that endothelial cells release?
Prevents coagulation and dilates vessels
117
What is the function of antithrombin III?
Inactivates thrombin and coagulation factors
118
What are lines of Zahn?
Alternating layers of RBCs, platelets, and fibrin in a thrombus
119
What is the function of tPA that endothelial cells secrete?
Activates plasminogen to plasmin, which will cleaves fibrin and fibrinogen to prevent clot formation
120
What is the function of plasmin? (3)
1. Cleaves fibrin & fibrinogen 2. Destroys coag factors 3. Blocks platelet aggregation
121
What is the function of thrombomodulin?
Redirect thrombin to activate protein C
122
What is the action of protein C once activated by thrombomodulin/thrombin?
Inactivates factors V and VIII
123
What are the ways that we can develop elevated levels of homocysteine? (recall that this damages endothelial cells)
1. Vitamin B12/folate deficiency | 2. Cystathionine beta synthase (CBS) deficiency (homocysteine)
124
Why does a Vit B12/folate deficiency lead to increased levels of homocysteine?
THF needs to hand off a methyl group to vit B12, which hands off to homocysteine, which produces methionine
125
What is the enzymatic deficiency that leads to high levels of homocysteine, and is the cause of homocystinuria?
Cystathionine beta synthase (CBS)
126
What are the symptoms of homocystinuria?
- Vessel thrombosis - MR - Long, slender fingers - Lens dislocation
127
What are the two ways that can result in a hypercoagulable state?
1. Excessive procoagulant factors | 2. Lack of anticoagulant factors
128
What is the classic presentation for patients with a hypercoagulable state?
Recurrent DVTs, or DVTs at a young age
129
Deficiencies in protein C or S leads to what? Why? How is this inherited?
Hypercoagulable state, since protein C will not block factors 5 and 8. AD
130
Patients with deficiencies in protein C or S are more likely to have a complication with what drug? Why?
Warfarin (coumadin) since protein C and S are lost first, and these are already defective or deficient
131
What is the treatment that we start patients with when starting coumadin?
Heparin first
132
What is factor V leiden? Does this lead to a hypercoagulable state or a bleeding disorder?
Mutated form of factor V that prevents deactivation by protein C Leads to a hypercoagulable state
133
What is the most common cause of a hypercoagulable state?
Factor V leiden
134
What is the prothrombin 20210A defect?
Inherited point mutation in prothrombin, leading to increased gene expression, and thus a hypercoagulable state
135
What does an antithrombin III deficiency lead to?
Decreases the protective effect of heparin-like molecules produced by the endothelium, increasing the risk for thrombus
136
What normally activates antithrombin III? What does activation of antithrombin III lead to?
Heparin like molecules activates it inactivates thrombin and coagulation factors
137
Why doesn't the PTT rise when patients with antithrombin III deficiency are given heparin? What is given to these patients instead?
Limited number of ATIII Warfarin
138
***Why are oral contraceptives associated with a hypercoagulable state?***
***Estrogen induces an increased production of coagulation factors***
139
What is an atheroscleotic embolus? How can you differentiate this from a normal embolus?
One that results from an arthresclerotic plaque Will see cholesterol crystals in the embolus
140
Fat emboli are associated with what?
Bone fractures
141
What are the signs/symptoms of a fat embolus?
-Dyspnea and petechiae on the skin overlying the chest
142
Gas emboli are classically seen in what condition?
Decompression sickness
143
What causes decompression sickness?
N gas precipitates out of the blood due to rapid ascent by a diver
144
What are the two symptoms that decompression sickness can present with?
Bends or the chokes
145
What is Caisson's disease?
Chronic form of gas emboli that is characterized by multifocal ischemic necrosis of bone
146
Why can gas emboli result from laparoscopic surgery?
Air is pumped into the abdomen
147
What are the symptoms that occur when amniotic fluid enters maternal circulation?
- Dyspnea - DIC - Neuro symptoms
148
What is found within amniotic fluid that causes an embolism?
-**Tissue thromboplastin** -Squamous cells Keratin debris
149
What are the three veins usually associated with DVTs?
Iliac Popliteal Femoral
150
Why are PEs usually silent? (2)
1. Dual blood supply to the lung | 2. Usually small embolus
151
When do pulmonary infarction usually occur with PEs?
Obstruction of medium to large vein Pre-existing cardiopulmonary compromise
152
Why is the D-dimer elevated with DVTs or a PE?
Clot is actively being lysed, resulting in fibrin breakdown products
153
Why is the characteristic shape of infarcts caused by PEs? Why is it hemorrhagic?
Wedge Hemorrhagic d/t other blood supply and loose CT d/t infarct
154
What is a saddle embolus?
Blockage of both pulmonary arteries by a clot
155
What is the major complication of chronic pulmonary emboli?
Pulmonary HTN (type IV)
156
What is the most common cause of a systemic thromboembolism?
Thrombus that arose from the left heart
157
What drug should never be given to patients with HIT?
Coumadin
158
What causes DIC in the obstetric setting?
Amniotic fluid contains tissue thromboplastin, which can activate the coag cascade if exposed in maternal blood
159
How can adenocarcinoma cause DIC?
Mucin production causes activation of coagulation cascade
160
How can acute promyelocytic leukemia cause DIC?
Auer rods in cells leak out of cells and activate the coagulation cascade
161
How can rattle snake bite cause DIC?
Toxin causes activation of coag
162
What is the MOA of heparin?
Binds to and activates ATIII
163
What is the MOA of vincristine and vinblastine? Use? Side effects?
bind to beta-tubulin, and inhibit polymerization into microtubules Solid tumors, leukemias/lymphomas Neurotoxic and myelosuppression
164
What is the MOA, use, and side effects of: paclitaxel and other taxols?
- Hyper Stabilize polymerized tubules - Ovarian and breast cancer - Myelosuppression and alopecia
165
What is the MOA, use, and side effects of: cisplatin and carboplatin?
- Cross link DNA - Testicular, bladder, and ovarian cancer - Nephrotoxic and acoustic nerve damage
166
What is the MOA, use, and side effects of: Irinotecan and topotecan?
- Topoisomerase II inhibitors - Solid tumors - Myelosuppression, alopecia
167
What is the MOA, use, and side effects of: hydroxyurea
Inhibits ribonucleotide reductase (S phase specific) - Melanoma, CML - Myelosuppression
168
What is the MOA, use, and side effects of: cyclophosphamide
- Covalently linking DNA - Solid tumors - Myelosuppression, hemorrhagic cystitis
169
What is the MOA, use, and side effects of: Nitrosoureas (carmustine, lomustine)
- Cross BBB and covalently links DNA - Brain tumors - CNS toxicity
170
What is the MOA, use, and side effects of: busulfan
- Cross links DNA - CML, and bone marrow ablation - Pulmonary fibrosis
171
What is the MOA, use, and side effects of: bleomycin
- Induces free radical damage to cause breaks in DNA - Testicular cancer - Pulmonary fibrosis
172
What is the MOA, use, and side effects of: doxorubicin
- Generates free radicals and intercalates DNA - Solid tumors, leukemia - Cardiotoxic
173
What is dexrazoxane used for?
Prevent cardiotoxicity from doxorubicin
174
What is the MOA, use, and side effects of: 5-FU
- Pyrimidine analog, inhibits thymidylate synthase - Colon cancer - Photosensitivity and myelosuppression
175
What is the MOA, use, and side effects of: ritixumab
- Anti CD20 - RA, non-hodgkin's lymphoma - PML
176
What is the MOA, use, and side effects of: Vemurafeib
- BRAF kinase inhibitor | - Metastatic melanoma
177
What is the MOA, use, and side effects of: bevacizumab
- Monoclonal ab against VEGF - Solid tumors - Hemorrhage
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