Bleeding Disorders Flashcards
(255 cards)
1
Q
When should a patient be evaluated for bleeding disorders?
A
Spontaneous bleeding, excessive hemorrhage after surgery or trauma, menorrhagia, bleeding after venipuncture, excessive bleeding after labor/delivery.
2
Q
What co-existing diseases can impair platelet or vessel wall interactions?
A
Renal failure and liver disease.
3
Q
How can malignancy affect coagulation?
A
Recent chemotherapy can cause thrombocytopenia.
4
Q
Which drugs can cause thrombocytopenia?
A
Aspirin, NSAIDs, and certain antibiotics.
5
Q
What are the bleeding patterns associated with thrombocytopenia or platelet disorders?
A
Bleeding from skin and mucosa, GI bleeding, epistaxis, hemoptysis, spontaneous or immediate after trauma.
6
Q
What are the bleeding patterns associated with factor deficiencies?
A
Bleeding from deeper tissue sites, such as hematomas, retroperitoneal hemorrhage, and hemarthroses, with more delayed onset.
7
Q
What are petechiae?
A
Pinpoint skin hemorrhages less than 3mm in size.
8
Q
What initiates the extrinsic pathway in the coagulation cascade?
A
External Vessel damage and tissue factor (TF), trauma/injury to vessel wall, tissue damage, hypoxia, sepsis, inflammation.
9
Q
What is purpura?
A
Skin hemorrhages between 3-10mm, sometimes palpable.
10
Q
What is another name for the extrinsic pathway?
A
Tissue Factor Pathway
11
Q
Which factor is activated in the extrinsic pathway?
A
Tissue Factor III
12
Q
What is the common pathway in the coagulation cascade?
A
The pathway where both intrinsic and extrinsic pathways converge, leading to fibrin formation.
13
Q
What is ecchymosis?
A
A bruise larger than 1cm.
14
Q
What initiates the intrinsic pathway in the coagulation cascade?
A
Contact with subendothelial surface damage
15
Q
What is another name for the intrinsic pathway?
A
Contact Activation Pathway
16
Q
What basic laboratory evaluations are used for bleeding disorders?
A
CBC (Hgb, Platelets), coagulation profile (PT/INR, aPTT), fibrinogen, D-Dimer.
17
Q
What does PT/INR measure?
A
Clotting factors from the extrinsic pathway.
18
Q
Which factors are involved in the intrinsic pathway?
A
HMWK, PK, XII, XI, IX, X,VIII
19
Q
What does ‘a’ signify in the context of coagulation factors?
A
Activated
20
Q
What does aPTT measure?
A
Clotting factors from the intrinsic pathway.
21
Q
What is the role of Factor XIIIa in the common pathway?
A
Cross-links fibrin
22
Q
What is the role of thrombin in the coagulation cascade?
A
Converts fibrinogen to fibrin
23
Q
What are the normal ranges for PT, INR, and aPTT?
A
PT: 11-13.5 sec, INR: ≤ 1.1, aPTT: 21-35 sec.
24
Q
What is the role of antithrombin in physiologic anticoagulation?
A
Inactivates thrombin and other factors
25
What is fibrinogen and where is it synthesized?
A protein synthesized by the liver.
26
What are the major causes of DIC?
Infections, sepsis, immunologic reactions, transfusion reactions, obstetric complications, malignancies, liver failure, acute pancreatitis, envenomation, ARDS, trauma, shock, vascular disorders.
27
What are some examples of immunologic reactions that can cause DIC?
Transfusion reactions and ABO incompatibility.
28
What obstetric complications can lead to DIC?
Septic abortion, retained contents, placental abruption.
29
What is the most common complication of severe hemophilia?
Acute Hemarthrosis
30
What accelerates the action of antithrombin?
Heparin
31
Which malignancies are associated with DIC?
Acute leukemia and adenocarcinoma.
32
What sensation precedes intense pain and swelling in acute hemarthrosis?
Tingling or burning sensation
33
What is the role of proteins C and S in anticoagulation?
Destroy factors V and VIII
34
What are the physical exam findings in acute hemarthrosis?
Hot, swollen, and tender joint with erythema
35
What are the key features of acute DIC?
Introduction of tissue factor into the bloodstream, initiation of the extrinsic pathway, thrombin formation, platelet activation, excess consumption of clotting factors, elevated PT/INR, aPTT, thrombocytopenia, mucosal bleeding.
36
What happens to Vitamin K after it activates clotting factors?
It becomes de-activated.
37
What happens to clotting factors in acute DIC?
Excess consumption of clotting factors, leading to elevated PT/INR and aPTT.
38
What are the symptoms of acute hemarthrosis?
Pain, stiffness, limited mobility, maintained in flexed position
39
How are proteins C and S activated?
By thrombin
40
What does a low fibrinogen level indicate?
Decreased production or excessive clot formation.
41
Why does thrombocytopenia occur in acute DIC?
Bone marrow can't keep up with platelet consumption.
42
Which enzyme re-activates Vitamin K?
Vitamin K reductase.
43
What is the immediate treatment for acute hemarthrosis?
Immediate factor replacement
44
What can deficiencies in anticoagulation mechanisms lead to?
Hypercoagulable state
45
What is D-Dimer?
A fibrin degradation product released when clots dissolve.
46
What does RICE stand for in the context of acute hemarthrosis treatment?
Rest, Ice, Compression, Elevation
47
What are the bleeding manifestations of acute DIC?
Petechiae, purpura, bleeding from mucosal sites, venipuncture sites, wounds.
48
How does Warfarin affect Vitamin K?
It inhibits Vitamin K reductase.
49
What is the mechanism of action of Coumadin (Warfarin)?
Vitamin K antagonist
50
Why is joint aspiration not recommended in acute hemarthrosis?
Risk of infection and worsening bleeding
51
What are the thrombotic manifestations of acute DIC?
Digital ischemia and gangrene, especially in patients on vasopressors.
52
What conditions can elevate D-Dimer levels?
Clot (DVT, PE) or DIC.
53
Why should NSAIDs be avoided in acute hemarthrosis?
They may exacerbate bleeding due to platelet inhibition
54
Which factors require vitamin K for activation?
Factors II, VII, IX, and X
55
What laboratory findings are indicative of DIC?
Prolonged PT/INR, aPTT, thrombocytopenia, increased FDP levels, elevated D-Dimer, decreased fibrinogen.
56
What can result from recurrent or untreated bleeds in hemophilia?
Chronic joint damage
57
What occurs during thrombosis?
Simultaneous activation of platelets and formation of fibrin in response to vessel injury.
58
What does exogenous Vitamin K do in the presence of Warfarin?
It provides the necessary active form of Vitamin K.
59
Which pathway does Warfarin mainly inhibit?
Extrinsic pathway and factor VII
60
What are the features of chronic joint damage in hemophilia?
Cartilage damage with cyst formation, bony erosion, flexion contractures
61
What is primary hemostasis?
Platelet activation.
62
How does chronic DIC differ from acute DIC?
Chronic DIC involves continuous or intermittent exposure to small amounts of tissue factor, is usually associated with malignancies, and is primarily a thrombotic disorder with recurrent superficial and deep venous thromboses.
63
What are the three sources of Vitamin K?
Dietary intake, synthetic drugs, and synthesis by intestinal flora.
64
How is the effect of Warfarin monitored?
By PT/INR
65
What is the primary characteristic of ITP diagnosis?
Isolated thrombocytopenia with normal WBC and RBC and no other cause identified.
66
What is secondary hemostasis?
Clotting factor activation leading to fibrin formation.
67
What is the prophylaxis strategy in severe hemophilia?
Scheduled administration of factors 2-3 times a week
68
What is the primary treatment approach for DIC?
Reverse the underlying cause if possible; all other measures are supportive and temporizing.
69
What percentage of intramuscular hematomas occur in hemophilia patients?
30%
70
What distinguishes primary ITP from secondary ITP?
Primary ITP has no identified trigger, while secondary ITP is preceded by infection or immunologic condition.
71
What role does von Willebrand Factor (vWF) play in hemostasis?
Mediates platelet adhesion to the site of vessel injury.
72
What supportive treatments are used in DIC?
Fresh frozen plasma, platelet transfusion, cryoprecipitate if fibrinogen is low.
73
What are common causes of intramuscular hematomas in hemophilia?
Physical trauma, IM injections
74
When is treatment necessary for ITP in children?
If there is bleeding, platelet counts are below 20,000/μl, or it is a chronic form.
75
What does a prolonged PT/INR indicate?
Vitamin K deficiency
76
What substances do adhered platelets release?
ADP and Thromboxane A2.
77
What is the first-line treatment for ITP?
Corticosteroids/Prednisone.
78
What is the role of heparin in anticoagulation?
Activates antithrombin
79
What conditions can lead to Vitamin K deficiency?
Malabsorption, eradication of gut flora, prolonged antibiotic use, critical care, prolonged NPO, broad-spectrum antibiotics, acute gastroenteritis, and diarrhea.
80
What is the coagulation cascade?
A series of reactions leading to the formation of cross-linked fibrin.
81
What is the fatality rate of intracerebral hemorrhage (ICH) in hemophilia?
30%
82
How long should corticosteroids be used for ITP treatment?
Not more than 3-4 weeks.
83
Why is heparin used cautiously in DIC?
Heparin could exacerbate bleeding and is reserved for DIC associated with malignancy and forms mainly manifested by thrombosis.
84
What activates the intrinsic pathway of the coagulation cascade?
Internal damage to the vessel wall.
85
What is the function of Intravenous Immune Globin (IVIG) in ITP treatment?
It blocks the Fc receptor on macrophages.
86
What activates the extrinsic pathway of the coagulation cascade?
External trauma or injury to the vessel wall, tissue damage, hypoxia, sepsis, inflammation.
87
What is a significant cause of death in liver failure related to coagulopathy?
Bleeding, particularly GI bleeding due to portal hypertension and esophageal varices.
88
Why should non-emergent platelet transfusions be avoided in ITP treatment?
They are not effective and can cause complications.
89
What is the end result of both the intrinsic and extrinsic pathways?
Activation of Factor X, leading to the common pathway.
90
What usually induces intracerebral hemorrhage in hemophilia patients?
Head trauma
91
Which factors does heparin inactivate?
Factors XII, XI, IX, X, and thrombin
92
What laboratory finding is associated with Vitamin K deficiency?
Prolonged PT/INR.
93
What is Rituximab used for in ITP treatment?
It targets B-cells which produce antibodies against platelets.
94
What type of bleeding should be avoided with NSAID use in hemophilia?
GI bleeding
95
Which pathways does heparin mainly inhibit?
Intrinsic and common pathways
96
What type of bleeding is seen with Vitamin K deficiency?
Bleeding with minor trauma, spontaneous bruising, petechiae, and spontaneous internal bleeding.
97
What is the basis for suspecting hemophilia in a patient?
Family and personal bleeding history
98
What coagulation profile tests are used in diagnosing hemophilia?
aPTT, PT/INR
99
How is the effect of heparin monitored?
By aPTT
100
What are the mechanisms of coagulopathy in liver failure?
Impaired clotting factor synthesis, impaired activation of vitamin K-dependent factors, ineffective y-carboxylation, platelet dysfunction, splenomegaly, suppression of thrombopoiesis by alcohol or folate deficiency.
101
What is the final product of the common pathway in the coagulation cascade?
Cross-linked fibrin mesh forming a stable clot.
102
What are the symptoms of HITT?
Hemorrhage or thrombosis, thrombocytopenia without evidence of thrombosis, skin necrosis due to focal thrombosis.
103
What does Thrombopoietin (TPO) Receptor Agonist do in ITP treatment?
Promotes growth and differentiation of platelets and increases production.
104
At what platelet count might bleeding occur with minor trauma?
Less than 50,000.
105
What is another name for the extrinsic pathway?
Tissue Factor Pathway.
106
How is hemophilia confirmed?
Factor VIII and IX assay
107
What is the role of Factor X in the coagulation cascade?
Activation leads to the common pathway and clot formation.
108
When is a high-dose TPO Receptor Agonist given in ITP treatment?
In case of severe bleeding or in chronic form.
109
Why is vitamin K ineffective in treating coagulopathy of liver failure?
The coagulopathy is due to a deficiency in the process of clotting factor synthesis, not a vitamin K deficiency.
110
What are NOACs also known as?
Direct oral anticoagulants (DOACs)
111
At what platelet count does spontaneous bruising and petechiae occur?
Less than 30,000.
112
What are some examples of TPO Receptor Agonists?
Romiplostim (N-Plate), Eltrombopag (Promacta), Avatrombopag (Doptelet).
113
What additional testing is available for hemophilia diagnosis?
Genetic testing
114
What is the typical platelet count in liver failure coagulopathy?
Approximately 50,000.
115
What are the common sites of thrombosis in HITT?
Venous thrombosis, pulmonary embolism, lower limb arterial thrombosis, cerebrovascular incidents, myocardial infarction.
116
What is the goal of clotting factor replacement in hemophilia treatment?
25-30% normal factor activity level
117
When is splenectomy indicated in ITP treatment?
If there is no response to medical management, requires repeated pharmacologic treatment, or severe recurrent hemorrhagic symptoms.
118
Which factor does Dabigatran target?
Factor IIa (Thrombin)
119
What is the patient outcome associated with HITT?
Mortality and morbidity, prolonged hospital stay.
120
What immunizations are required before a splenectomy for ITP?
Meningococcus, pneumococcus, and H. influenza.
121
What factor activity level is targeted before surgery in hemophilia patients?
50%
122
What treatments are used for coagulopathy in liver failure?
Supportive treatments such as FFP and platelet transfusion for active bleeding or prior to procedures.
123
At what platelet count does spontaneous internal bleeding occur?
Less than 10,000.
124
Which factors do Rivaroxaban, Epixaban, and Edoxaban target?
Factor Xa
125
What factors require vitamin K for activation?
Pro-coagulant factors II, VII, IX, X and anticoagulant factors Protein C and S.
126
What factor activity level is required for limb- or life-threatening events in hemophilia?
80-100%
127
What is another name for Factor XI deficiency?
Hemophilia C
128
What are the hallmark features of Thrombotic Microangiopathies (TMAs)?
Microangiopathic Hemolytic Anemia (MAHA), thrombocytopenia, and ischemic tissue damage.
129
What action should be taken when HITT is diagnosed?
Discontinuation of heparin therapy and replacing it with other anticoagulants like rHirudin or danaproid.
130
What are the two main types of TMAs?
Thrombotic Thrombocytopenic Purpura (TTP) and Hemolytic Uremic Syndrome (HUS).
131
In which populations is Factor XI deficiency more prevalent?
Ashkenazi and Iraqi Jewish populations
132
What is the most common acquired thrombophilia?
Autoantibodies against phospholipids in endothelial cell membranes
133
What is the inheritance pattern of Factor XI deficiency?
Autosomal recessive
134
What are the advantages of NOACs over vitamin K antagonists?
Fewer significant bleeding events, no monitoring or dietary restrictions, antidotes available
135
What triggers Thrombotic Thrombocytopenic Purpura (TTP)?
Endothelial injury from an inciting event releases vWF and increases platelet consumption.
136
What are the causes of thrombocytopenia?
Decreased production, increased destruction, immune-mediated, non-immune mediated, platelet consumption, infection/sepsis, and drugs.
137
How does warfarin affect vitamin K?
Warfarin inhibits vitamin K reductase, keeping vitamin K inactive.
138
What are primary hypercoagulable states?
Decreased anticoagulant factors (Protein C, S, Antithrombin) and increased pro-coagulant factors (Factor 5).
139
What type of bleeding is not common in Factor XI deficiency?
Spontaneous hemarthroses
140
What enzyme moderates vWF in TTP?
ADAMTS13.
141
Which antibody is often associated with Lupus?
Lupus Anticoagulant
142
How can the effects of warfarin be reversed?
By administering exogenous vitamin K, which bypasses the action of warfarin.
143
What are some clotting factor disorders?
Hemophilias A, B, C, Von Willebrand Disease, DIC, Liver Failure, Vitamin K deficiency
144
What are examples of immune-mediated platelet disorders?
Immune Thrombocytopenic Purpura (ITP) and Thrombotic Microangiopathies (TMAs).
145
What enzyme reactivates vitamin K?
Vitamin K reductase.
146
What is the most common hereditary bleeding disorder worldwide?
Von Willebrand Disease (vWD)
147
What is Hemophilia A?
Deficiency of clotting factor VIII
148
What can induce auto-antibodies against ADAMTS13 in TTP?
Pregnancy, vasculitis, chemo, bone marrow transplant, drugs, infections (HIV).
149
What are the three main autoantibodies involved in acquired thrombophilia?
Lupus Anticoagulant, Anticardiolipin Ab, Anti B-2 Glycoprotein I
150
What are the presentation signs of acquired TTP?
Marked thrombocytopenia with neurologic abnormalities, fever, and renal failure.
151
What is the inheritance pattern of Von Willebrand Disease?
Autosomal dominant
152
What is Hemophilia B also known as?
Christmas Disease
153
What are secondary hypercoagulable states?
Pregnancy, immobilization, malignancy, post-operative state, OCPs, antiphospholipid syndrome, hyper-homocysteinemia, myeloproliferative disorder.
154
What are the lab findings in TTP?
Normal coags, hemolytic anemia with schistocytes, decreased ADAMTS13 level.
155
With which conditions is acquired thrombophilia commonly associated?
Other autoimmune or rheumatologic conditions, such as Lupus
156
What does Von Willebrand Factor (vWF) mediate?
Platelet adhesion and aggregation, stabilizes Factor VIII
157
What is the treatment for TTP?
Plasma exchange to remove antibodies and replace the enzyme.
158
What percentage of hypercoagulable states are venous?
90%.
159
What does endothelial cell damage lead to in acquired thrombophilia?
Thrombosis (arterial and venous)
160
What are examples of Thrombotic Microangiopathies (TMAs)?
Thrombotic Thrombocytopenic Purpura (TTP) and Hemolytic Uremic Syndrome (HUS).
161
What are the key features of Hemolytic-Uremic Syndrome (HUS)?
Acute renal failure, MAHA, thrombocytopenia.
162
What are the types of Von Willebrand Disease based on?
Different mutations
163
What are the pregnancy-related complications of acquired thrombophilia?
Recurrent pregnancy loss/stillbirth
164
What are the most common sites for venous thromboembolism (VTE)?
Extremity DVT and pulmonary embolism.
165
What is the rarest type of Von Willebrand Disease?
Type 3
166
What is the most frequent cause of HUS?
Shiga-toxin producing E. coli O157:H7 diarrhea.
167
What are the common arterial complications of acquired thrombophilia?
Cerebrovascular events (stroke, TIA)
168
What symptoms did the 30-year-old female present with?
Non-painful rash on lower extremities and mild gingival bleeding.
169
What are some rare sites for VTE?
Mesenteric, cerebral, portal.
170
What is the inheritance pattern of Hemophilias A and B?
X-linked recessive
171
What are the physical exam findings in Von Willebrand Disease?
Petechiae, ecchymoses, hematoma
172
What is the treatment for Shiga-toxin associated HUS (ST-HUS)?
Transfusion support and possibly dialysis.
173
What are the common venous complications of acquired thrombophilia?
DVT, PE
174
When should hypercoagulable states be suspected?
History of recurrent VTE, first VTE under 50 years old, first-degree relative with VTE under 50 years old, unexplained VTE.
175
What percentage of Hemophilia cases arise as spontaneous mutations?
30%
176
What is the treatment for complement-associated HUS (C-HUS)?
Eculizumab (Solaris).
177
What laboratory findings are typical in Von Willebrand Disease?
Normal platelet levels, prolonged aPTT, normal PT/INR
178
What is not usually associated with arterial thrombosis?
Hypercoagulable states.
179
What is the clinical presentation of severe Hemophilia?
<1% of normal factor activity, spontaneous hemarthroses, hematomas, profuse hemorrhage with trauma or surgery
180
What should be checked to distinguish between TTP and HUS?
ADAMTS13 level.
181
What are the three plasma measurements used in diagnosing Von Willebrand Disease?
VWF Antigen, VWF Activity, Ristocetin Cofactor Activity
182
What were the patient's vital signs?
BP 110/70, P 80, R 16, T 97.8, SpO2 100%.
183
What is the misnomer associated with Lupus Anticoagulant?
It is an antibody that prolongs aPTT by binding to phospholipid in the lab assay
184
What is the treatment approach for Von Willebrand Disease?
Correction and prevention of bleeding during trauma, surgery
185
What did the physical exam reveal about the patient's skin?
Multiple small red punctate lesions that do not blanch on bilateral lower extremities.
186
How does Lupus Anticoagulant act in the lab assay?
As an inhibitor, interfering with the test, falsely elevating the result
187
What pharmacologic treatment is used in Type 1 Von Willebrand Disease?
DDAVP – Desmopressin
188
What are the primary hypercoagulable states?
Protein C activity, Protein S activity, Antithrombin III activity, Factor V Leiden, Prothrombin gene mutation, Anticardiolipin antibody, Lupus anticoagulant, B-2 glycoprotein I.
189
What determines the duration of anticoagulation in hypercoagulable states?
Diagnosis.
190
What was the patient's platelet count?
25,000.
191
Is Lupus Anticoagulant clinically a bleeding disorder?
No
192
What is Disseminated Intravascular Coagulation (DIC) also known as?
Consumptive Coagulopathy
193
When should you suspect Lupus Anticoagulant?
With prolonged aPTT (and often INR) with no clinical bleeding, especially with history of thrombosis, miscarriage, or Lupus
194
What characterizes Disseminated Intravascular Coagulation (DIC)?
Both clotting and bleeding
195
When should labs ideally be ordered for hypercoagulable states?
Before initiating anticoagulation or 2 weeks after completing therapy.
196
What is the leading cause of morbidity and mortality in severe Hemophilia?
Intracranial hemorrhage (ICH)
197
What is the most likely diagnosis for the patient?
Immune Thrombocytopenic Purpura (ITP).
198
What causes clotting in Disseminated Intravascular Coagulation (DIC)?
Circulating thrombin
199
What effect does warfarin have on Protein C and S?
Decreases their levels.
200
What are the clinical criteria for diagnosing Antiphospholipid Syndrome?
History of arterial or venous thrombus or pregnancy loss
201
At what age do spontaneous hemarthroses typically occur in severe Hemophilia?
Between 9-18 months
202
What is the typical platelet count in acute ITP?
Less than 20,000/μl.
203
What lab test is used to diagnose Lupus Anticoagulant?
Specific LA assay with elevated titers
204
What effect does heparin have on antithrombin activity?
Decreases measurable activity.
205
What is the clinical presentation of moderate Hemophilia?
1-5% of normal factor activity, hemarthroses develop at 2-5 years of age
206
What causes bleeding in Disseminated Intravascular Coagulation (DIC)?
Depletion of clotting factors and excessive fibrinolysis
207
What is the typical platelet count in chronic ITP?
30,000 - 80,000/μl.
208
What percentage of children with ITP experience spontaneous remission?
83%.
209
Is there any data suggesting different treatment for APLS compared to other VTE?
No
210
What is the clinical presentation of mild Hemophilia?
>5% of normal factor activity, spontaneous bleeding uncommon, severe bleeding after trauma/surgery
211
What are the major causes of Disseminated Intravascular Coagulation (DIC)?
Infections, immunologic reactions, obstetric complications, malignancies, liver failure, acute pancreatitis, envenomation, ARDS, trauma, shock, vascular disorders
212
What is the antepartum prophylaxis for pregnancy in APLS?
ASA, heparin
213
What is the most common complication of severe Hemophilia?
Acute hemarthrosis
214
What percentage of adults with ITP experience spontaneous remission?
2%.
215
What is homocysteine?
An amino acid derivative that interacts with endothelium, predisposing to atherosclerosis, arterial and venous thrombosis
216
What are the types of antithrombin deficiency?
Type I (quantitative deficiency) and Type II (qualitative deficiency).
217
What is the response rate to splenectomy in acute ITP?
71%.
218
What is the prevalence of antithrombin deficiency in VTE cases?
1-2% of all VTE, 2.5% recurrent or age under 45.
219
What gene defect is associated with hereditary hyperhomocysteinemia?
MTHFR gene
220
What are the symptoms of acute hemarthrosis?
Tingling or burning sensation in joint, intense pain, swelling, hot, swollen and tender joint with erythema, pain, stiffness, limited mobility, maintained in flexed position
221
What is the response rate to splenectomy in chronic ITP?
66%.
222
What is the diagnosis method for antithrombin deficiency?
Functional assays and quantitative assays.
223
What is the most common primary thrombophilia?
Factor V Leiden mutation.
224
What are the clinical signs of ITP?
Petechiae on skin, mucous membranes, and GU system.
225
What is the bleeding severity in ITP correlated with?
Platelet counts.
226
What nutritional deficiencies can lead to acquired hyperhomocysteinemia?
B12, folate, pyridoxine
227
What are some drugs associated with thrombocytopenia?
Acetaminophen, acetazolamide, allopurinol, alprenolol, amiodarone, ampicillin, amrinone, antazoline, aspirin, carbamazepine, cephalexin, cephalothin, chlorothiazide, chlorpheniramine, chlorthalidone, cimetidine, diazepam, desipramine, digitoxin, digoxin, diltiazem, diphenylhydantoin, furosemide, gentamicin, gold salts, heparin, heroin, imipramine, iopanoic acid, lidocaine, meprobamate, methicillin, methyldopa, minoxidil, morphine, novobiocin, para-aminosalicylic acid, penicillin, phenylbutazone, procainamide, quinidine, quinine, rifampin, spironolactone, sulfisoxazole, trimethoprim-sulfamethoxazole, valproic acid, vancomycin.
228
What is the second most common primary thrombophilia?
Prothrombin G20210 A.
229
What is the risk of spontaneous intracranial bleeding in ITP with platelet counts less than 5,000/μl?
High risk.
230
What is the incidence of Heparin-induced Thrombocytopenia and Thrombosis (HITT)?
Approximately 6%.
231
What are the treatment options for hypercoagulable states?
Heparin, argatroban, warfarin, direct oral anticoagulants (DOACs) like dabigatran, rivaroxaban, apixaban.
232
How is ITP diagnosed?
By exclusion.
233
Is there evidence that vitamin supplementation reduces thrombosis in hyperhomocysteinemia?
No
234
Is hyperhomocysteinemia routinely checked as part of VTE work-up?
No
235
What factors influence the choice of anticoagulant regimen?
Comorbidities, compliance, side effects, and safety.
236
What lab findings are typical in ITP?
Isolated thrombocytopenia with normal WBC and RBC.
237
What causes HITT?
Antibody reacts with heparin/platelet factor 4 complex.
238
What is primary ITP?
ITP with no identified trigger.
239
What is the duration of treatment for the first VTE episode in primary hypercoagulable states?
6-12 months, then weigh benefit vs. risk of bleeding complications.
240
What are some factors predisposing to thrombosis?
Chronic DIC, immobility, indwelling lines, tumors compressing vessels
241
What is secondary ITP?
ITP preceded by infection or immunologic condition.
242
When does HITT typically onset?
More than 6 days of heparin exposure; amnestic response sooner.
243
What are the most common complications of malignancy related to thrombosis?
DVT and PE
244
When is lifelong therapy recommended in primary hypercoagulable states?
Life-threatening events, unusual sites, more than one inherited deficiency, homozygous Factor V Leiden, recurrent VTE.
245
What are some secondary hypercoagulable states?
Obesity, trauma, OCPs, nephrotic syndrome, diabetes, paroxysmal nocturnal hemoglobinuria
246
What is the prophylactic anticoagulation recommendation for patients with known deficiency but no history of VTE?
During high-risk states like surgery or pregnancy.
247
What happens to the platelet count in HITT?
It drops to half of the baseline, may still be within the normal range.
248
What is the most common acquired thrombophilia?
Antiphospholipid syndrome.
249
Which type of heparin is more likely to cause HITT?
Bovine unfractionated heparin.
250
What are the autoantibodies involved in antiphospholipid syndrome?
Lupus anticoagulant, anticardiolipin antibody, anti B-2 glycoprotein I.
251
What are the symptoms of HITT?
Hemorrhage or thrombosis, skin necrosis, venous thrombosis, pulmonary embolism, lower limb arterial thrombosis, cerebrovascular incidents, myocardial infarction.
252
What conditions are commonly associated with antiphospholipid syndrome?
Other autoimmune or rheumatologic conditions like lupus.
253
What complications are associated with antiphospholipid syndrome?
Recurrent pregnancy loss, stillbirth, cerebrovascular incidents, DVT, PE.
254
What is the outcome for patients with HITT?
Associated with mortality and morbidity; prolonged hospital stay.
255
What is the action to take when HITT is diagnosed?
Discontinuation of heparin therapy and replacing it with other anticoagulants (rHirudin, danaproid).
