Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MOHDIII - Unit 2 > Bleeding Disorders > Flashcards

Bleeding Disorders Flashcards

1
Q

Assessment of intrinsic pathway

A
  • partial thromboplastin time (PTT or APTT)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Assessment of extrinsic pathway

A
  • prothrombin time (PT)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How to do prothrombin time

A
  • add thromboplastin and calcium to plasma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Prothrombin time uses

A
  • monitor warfarin (coumadin) therapy
  • evaluate liver disease
  • evaluate vitamin K deficiency
  • evaluate disseminated intravascular coagulation (DIC)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

International normalized ratio (INR)

A
  • uses international sensitivity index (ISI) to normalize PT time
  • ISI=measure of the sensitivity of the thromboplastin the lab is using
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How to do PTT

A
  • add activator, calcium, & phospholipid to plasma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Reasons for prolonged PTT

A
  • heparin
  • factor deficiency that may cause bleeding
  • factor deficiency w/ no clinical significance (factor XII)
  • specific factor inhibitor - most commonly to factor VIII
  • antiphospholipid antibody
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Mixing study

A
  • used in evaluation of a prolonged PTT or PT
  • patients sample mixed w/ equal volume of normal plasma
  • correction to normal = FACTOR deficiency
  • continued prolongation = INHIBITOR (aka antibody)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Fibrinogen

A
  • measured by addition of thrombin to plasma
  • may have either quantitative or qualitative abnormalities of fibrinogen
  • DECREASED in DIC, liver disease, congenital absence of fibrinogen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

D-dimer

A
  • D-dimer assay detects excess generation of cross linked fibrin by plasmin
  • useful in evaluation of DIC
  • used in evaluation of venous thrombosis & pulmonary embolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

PFA-100 closure times

A
  • evaluates platelets
    1. col/epi & col/ADP - normal = no platelet abnormality
    2. col/epi long & col/ADP normal = aspirin effect
    3. col/epi & col/ADP abnormal = platelet defect or von willebrand disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Causes of hemorrhage

A
  • trauma, tumor, ulcer, necrosis, depletion of hemostatic factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Petechia

A
  • pinpoint hemorrhages in skin

- sign of platelet disorder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Purpura

A
  • slightly larger hemorrhages than petechia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Ecchymoses

A
  • large areas of hemorrhage into skin

- aka large bruises

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Hematoma

A
  • localized collection of clotted blood into a space or potential space
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Platelet

A
  • produced in marrow from megakaryocytes
  • normal number 150,000-450,000/uL
  • remain in circulation 7-10 days
  • QUANTITATIVE problems more common than qualitative
  • typically causes mucocutaneous bleeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Platelet counts & bleeding risk

A
  • minimal bleeding: >50,000
  • minor bleeding: 20-50,000
  • spontaneous:
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Thrombocytopenia causes

A
  • decreased platelet production
  • ineffective platelet production
  • splenic sequestration of platelets
  • increased peripheral destruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Bone marrow appearance in aplastic anemia

A
  • all FAT no cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Increased platelet destruction causes

A
  • non immune destruction: DIC, other microangiopathic hemolytic anemias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Immune mediated thrombocytopenia

A
  • alloimmune destruction: maternal fetal incompatability, blood transfusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Drug induced thrombocytopenia

A
  • drug or metabolite attached to platelet surface
  • development of antibodies to platelet-drug complex
  • platelets removed by macrophages in liver/spleen
  • QUININE is prototypic drug
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Heparin induced thrombocytopeina

A
  • caused by antibody directed against heparin & platelet factor 4
  • causes platelet AGGREGATION & thrombocytopenia
  • may cause life threatening THROMBOSIS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Acute immune thrombocytopenia purpura

A
  • CHILDREN: 2-6 yrs old
  • antecedent viral illness
  • increased incidence in fall/winter
  • ABRUPT onset
  • self limited course, most completely recover
  • Rx: steroids, IV IgG, Rh immune globulin
26
Q

Chronic immune thrombocytopenia purpura

A
  • ADULTS: 20-40 yrs old
  • FEMALES greater than males, 3:1
  • GRADUAL onset
  • remission and RELAPSES over years
27
Q

Thrombotic thrombocytopenia purpura

A
  • PENTAD of features: microangiopathic hemolytic anemia, thrombocytopenia, neurologic abnormalities, fever, renal dysfunction
28
Q

TTP histologic findings

A
  • thrombi w/in glomerular capillaries

- schistocytes in peripheral blood

29
Q

TTP etiology & treatment

A
  • deficiency of a protease (ADAMTS13): cleaves large von willebrand multimers
  • multimers aggregate platelets leading to thrombi
  • treatment: plasmapheresis & infusion of fresh frozen plasma
  • *FATAL unless they undergo treatment**
30
Q

Drug induced platelet dysfuntion

A
  • aspirin: IRREVERSIBLY acetylates COX
  • NSAIDs: REVERSIBLY inhibit COX
  • clopidogrel: blocks ADP receptor (P2Y12)
31
Q

Disease-related platelet dysfunction

A
  • uremia: global platelet dysfunction
  • paraproteins (plasma cell myeloma)
  • myeloproliferative disorders
  • after extracorporeal platelet circulation (cardiac bypass pump)
32
Q

Hemophilia A (classic hemophilia)

A
  • factor VIII deficiency
  • sex linked: men effected, women carriers
  • incidence: 1/10,000 males
  • MOST common hereditary disease
  • most severe hemophiliacs have inversion mutation in X chromosome
33
Q

Type of bleeding with hemophilia

A
  • bleeding into JOINTS, hematomas
34
Q

Signs & symptoms of severe hemophilia

A
  • delayed bleeding from small wounds b/c platelets are normal
  • hematomas, hemarthrosis, hematuria
  • joint destruction & muscle atrophy
  • death from bleeding into vital areas, complications of therapy
  • lab abnormalities: prolonged PTT, normal PT, normal PFA-100
35
Q

Treatment of hemophilia

A
  • treatment of hemophilia A is factor VIII replacement

- 5-15% of patients will develop factor VIII inhibitor (antibody)

36
Q

Hemophilia B

A
  • factor IX deficiency
  • sex linked, incidence: 1/50,000 males
  • cause: failure of synthesis or synthesis of defective factor IX
  • treatment: factor IX
  • lab abnormalities: prolonged PTT, normal PT
37
Q

Other coagulation factor deficiencies

A
  • most are rare

- deficiency in factor XII: benign disorder, NO increased risk of bleeding, prolonged PTT

38
Q

Von willebrand disease

A
  • autosomal dominant
  • deficiency of von willebrand factor
  • relatively common (1% population): bleeding occurs in less than 10% of these patients
  • signs/symptoms: mucocutaneous bleeding, epistaxis, menorrhagia
39
Q

Diagnosis of von willebrand disease

A
  • prolonged PFA-100 closure time
  • decreased factor VIII level
  • decreased von willebrand factor antigen activity
40
Q

Subtypes of von willebrand disease

A

Type I: 70% moderate reduction in vWF levels in plasma
Type II: qualitative defects in vWF
Type III: autosomal recessive-vWF absent, present like hemophiliacs

41
Q

Treatment of von Willebrand disease

A
  • avoid aspirin
  • DDAVP (desmopressin), synthetic analog of vasopressin
  • humate P: contains factor VII and vWF
42
Q

Changes in hemostasis in liver disease (vWF & factor VIII)

A
  • increased levels of vWF & factor VIII due to endothelial cell activation
43
Q

Lab abnormalities in liver disease

A
  • increased PT, PTT
  • increased D-dimers/FDPs (don’t clear them)
  • decreased fibrinogen level
  • increased factor VIII level
  • decreased platelet count
44
Q

Treatment for liver disease

A
  • fresh frozen plasma but don’t just treat numbers
45
Q

Disseminated Intravascular Coagulation (DIC)

A
  • intravascular thrombin formation
  • deposition of fibrin in microvasculature
  • inhibitors consumed (AT, protein C/S) but fail to control process
  • fibrinolysis initiated, fails to remove all the fibrin
  • platelet consumption
46
Q

Signs of DIC

A
  • schistocytes due to thrombosis and vascular occlusion

- increased bleeding due to platelet consumption

47
Q

Causes of DIC

A
  • sepsis, trauma, cancer (AML)
  • obstetrical complications
  • vascular disorders
  • toxins: SNAKE VENOM, drugs
48
Q

Lab abnormalities in DIC

A
  • increased PT, PTT
  • decreased fibrinogen
  • increased D-dimer/FDPs
  • decreased platelet count
  • fragmented RBCs in blood smear
49
Q

Treatment of DIC

A
  • treat UNDERLYING disorder

- blood product replacement in patients who are bleeding

50
Q

Factors requiring vitamin K

A
  • II, VII, IX, X

- protein C & S

51
Q

Vitamin K deficiency

A
  • hemorrhagic disease of newborn (HDN): prevented by giving vitamin K at birth
  • warfarin (coumadin)
  • oral antibiotic therapy: decreased gut flora
  • poor absorption of vitamin K: biliary tract obstruction, bowel disease
52
Q

Acquired coagulation abnormalities

A
  • post Op state, bed rest, pregnancy, oral contraceptives, myeloproliferative disorders, cancer, antiphospholipid antibody syndrome (lupus anticoagulant)
53
Q

Antiphospholipid antibody syndrome

A
  • most common cause of acquired thrombophilia
  • development of antibodies against plasma proteins w/ affinity for anionic phospholipids: most commonly Beta2-glycoprotein 1
54
Q

Antiphospholipid antibody syndrome: clinical findings

A
  • venous/arterial thrombosis
  • recurrent fetal loss
  • thrombocytopenia
55
Q

Lupus anticoagulant

A
  • antibody that prolongs phospholipid dependent coagulation tests (PTT)
  • may occur in presence OR absence of SLE
  • INCREASED risk of clotting even with increased PTT
56
Q

Factor V Leiden

A
  • mutation in factor V: unable to be cleaved by activated protein C
  • prevalence: 3-7% in caucasians
  • heterozygous state: only a mild risk factor
57
Q

Inherited thrombophilias

A
  • prothrombin gene mutation: increased prothrombin
  • protein C or S deficiency
  • anithrombin deficiency
  • hyperhomocyteinemia
  • dysfibrinogenemia
58
Q

Clinical features of thrombophilic patient

A
  • FAMILY HISTORY of thrombosis
  • thrombosis at young age
  • idiopathic thrombosis
  • thrombosis in an unusual site
59
Q

Morphology of thrombi

A
  • arterial thrombi: platelets & fibrin (WHITE thrombus)
  • venous thrombi: cellular elements & thrombin (RED thrombus)
  • mural thrombus: attached to wall (LINES OF ZAHN imply thrombus at site of blood flow)
60
Q

Fates of thrombus

A
  • propagation: extension leading to vessel obstruction
  • embolization: travel to other sites
  • dissolution: removed by fibrinolysis
  • organization: ingrowth of endothelial cells, smooth muscle fibroblasts, vascular flow may be re-established
61
Q

Clotting cascade pathways

A
  • intrinsic: factors VIII, IX, XI, XII
  • extrinsic: factor VII
  • common: factor X & II (thrombin)

MOHDIII - Unit 2 (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions