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1. symptoms > bleeding > Flashcards

bleeding Flashcards

1
Q

Normal Hemostasis (clotting)

A

Primary- Vasculature, blood flow, platelet count and function, extracellular matrix proteins–> Platelet plug

Secondary- coagulation factors–> fibrin clot

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2
Q

intinal steps vascular injury

A

vasoconstriction (Reduces blood flow, mediated by endothelin)

Exposure of subendothelium collagen and von willebrand factor (vWF)

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3
Q

Primary hemostasis

A

platelet adhesion
Platelet activation (shape change, granule release) (vW binds platelet glycoprotein 1 b) platelets binding together (binding– platelet glycoprotein 1b (Gp 1b) to vWf and exposed collagen
bind

Recruitment
Aggregation

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4
Q

primary hemostasis: platelet adhesion

A

platelet adhesion- binding of platelet glycoprotein 1 b (Gp1b) to vWF and exposed collagen

Platetls sticking to fibrinogen to stick to each other

Deficiency of Gp2b3a: glanzmann thrombasthenia

Deficiency of Gp1b: bernard- soulier syndrome

vWF deficiency- von Willebrand disease

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5
Q

Primary hemostasis (shape change)

A

Shape change

Increasing their surface area, move negatively charged phospholipids to the surface (for binding Ca++)

Conformational change in platelet glycoprotein 2b/3a

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6
Q

Primary hemostasis (granule release)

A

a- granules (fibrinogen, clotting factors, vWF, platelet factor 4, platelet-derived growth factor, fibronectin)

Dense granules- ADP, ATP, Calcium, serotonin, epinephrine

Stimulate platelet activation

Recruitment

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7
Q

Primary hemostasis (aggregation)

A

Gp2b/3a binds fibrinogen, forming bridges between platelets

initial wave is reversible

Thrombin stimulates: irreversible platelet contraction

Conversion of fibrinogen to insoluble fibrin

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8
Q

Bleeding disorders defects in primary hemostasis and secondary hemostasis

A

Defects in primary hemostasis- SKin and mucosal membrane hemorrhages (petechiae, epistaxis, menorrhagia) are common), vascular abnormalities (ehlers-danlos), thrombocytopenia, platelet function disorders, von Willebrand disease

Defects in secondary hemostasis- bleeds into soft tissues or joints Clotting factor deficiencies (hemophilia, liver disease)

Exogenous- anticoagulants

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9
Q

thrombocytopenia

A

Usually defined as <100,000/ul

Differential diagnosis: decreased bone marrow production, Increased destruction (immune mediated, non immune mediated)

Dilutional, sequestration

Mostly small vessel bleeds butrisk for intracranial hemorrhage when PLTs <10,000ul

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10
Q

defects of platelet adhesion

A

Co factor abnormal- Von Willebrands disease

Platelet abnormal- Bernard Soulier Syndrome

Substrate Abnormal- Ehlers Danlos Syndrome, Scurvy, Pseudoxanthoma Elasticum

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11
Q

Defects of platelet secretion

A

Prostaglandin defects- phospholipase defect, cyclooxygenase defect, thromboxane synthase defect

Storage pool defect- Alpha SPD, Delta SPD, Alpha Delta SPD

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12
Q

causes of thrombocytopenia

A

increased destruction- Immune mediated: Immune thrombocytopenia purpura (ITP), heparin-induced thrombocytopenia (HIT), Transfusion/pregnancy associated allo immune thrombocytopenia. Drug (linezolid, vancomyvin)

Non-immune mediate- Disseminated intravascualr coagulation (DIC) thrombotic thrombocytopenic purpura (TTP), hemolytic uremic syndrome (HUS), Drug

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13
Q

Immune thrombocytopenia purpura ITP

A

caused by autoantibodies made against PLT antigens (Gp2b/3a, Gp1b)

Destruction of PLTs occurs by phagocytosis- FcR mediated, site is the spleen

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14
Q

Primary vs Secondayr ITP

A

Categorization: Primary (unknown etiology), Secondary (Associated with- lupus, leukemia/lymphoma CLLSLL, drugs, viruses HIV, hepatitis)

Clinical features- skin, mucosal bleeds, normal spleen size, Variants (Acute self limited, <6 months, post viral, children), chronic (adult, usually females, persistent, >6 months

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15
Q

ITP pathophys and diagnosis

A

Pathologic findings- Thrombocytopenia (often quite low), large platelets, Normal to increased megakaryocytes in marrow, White pulp expansion

Diagnosis- presumptive, diagnosis of exclusion, no diagnostic test, normal clotting tests, bone marrow not required

Treatment0 may not be needed in kids with self limited disease
Immunosuppressant therapy (steroids, Intravenous Immunoglobulin (IVIG), anti CD20 antibody (rituximab)
Thrombopoietin agonist, Splenectomy

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16
Q

Aspirin effects

A

Aspirin decreases platelet aggregationby inhibition in COX1

Results in decreased thromboxane formation

Thromboxane regulates patelet aggregation through mediating glycoprotein 2b3a

17
Q

Secondary hemostasis

A

Goal is to generate thrombin (F2A)

Enzymatic reaction requiring: Phospholipid membranes of platelets (negative surface), inactivate substrate (factors), Calcium, Activate enzyme (activate factor), positive feedback (F2a)

End result: fibrin clot

18
Q

secondary hemostasis clotting factors

A

Produced in the liver hepatocytes (Exception F8- made in epithelial cells of liver sinusoids

Circulating in inactive, functional Form

Active forms produced during cascade

Some are vitamin K dependent (2 7 9 10) Protein C and S

19
Q

Extrinsic or Pt pathway

A

7 (Tissue factor)–> 7a
7a–> 10a
10a (5)–> 2a

2a–> Fibrinogen to fibrin

20
Q

Intrinsic pathway

A

12–> 12a
11–> 11a
9–> 9a
10–> 2–> fibrin

21
Q

Prothrombin time

A

Combine tissue factor, lots of phospholipid, and calcium

test the extrinsic and common pathway (7, 10, 2 5 fibrinogen)

Uses- screening for factor deficiencies, Warfarin monitoring

Reported in secs and INR (normalizes for variability across labs)

Not prolonged with heparin

22
Q

APTT

A

COmbines activator, low phospholipid, calcium

Tests the intrinsic and common pathway (12 11 10 9 8 2 5 and fibrinogen

Uses- Screen for factor deficiency, lupus anticoagulant, heparin monitoring

Variably sensitive to warfarin

23
Q

Mixing studies (the anser on the exam)

A

Can be done with PT or aPTT

Mix 1 part of patient sample with 1 part normal plasma

Corrects with factor deficiencies

Fails to correct with inhibitors (drugs, lupus anticoagulantS)

24
Q

Isolated prolonged apTT but a normal Pt

A

12, 11, 9, 8 deficiencies

Lupus anticoagulant

heparin

25
Q

Isolated Prolonged PT with a normal aPTt

A

factor 7 deficiency

Aka Warfarin deficiency

26
Q

Isolated prolonged thrombin Time

A 
A fibrinogenemia
Hypofibrinogenemia
Dysfibrinogenemia
Inhibitors against F2
(rare)
27
Q

Bleeding with normal PT, aPTT, Vw testing

A 
Mild factor deficiency
Thrombocytopenia
Platelet dysfunction
Vascular abnormality (survy, collagen defects)
Factor 8 deficiency
Antiplasmin deficiency
28
Q

hemophilia

A

Hemophilia is an inherited bleeding disorder in which there is a deficiency or lack of factor 8 (hemophilia A) A8

or factor 9 (B-9)

29
Q

inheritance of hemophilia

A

Hemophilia A and B are X linked recessive disorders

Hemophilia is typically expressed in males and carried by females

Severity level is consisten between family members

30% of cases of hemophilia are new mutations

1. symptoms (11 decks)

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