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D&T:1 > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

Symptoms of Pulmonary Edema

A

Dyspnea

Orthopnea

Paroxysmal nocturnal dyspnea

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2
Q

Heart Failure Cells

A

Hemosiderin-laden macrophages in the alveolar spaces that can be seen w/ chronic pulmonary congestion

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3
Q

Process of ecchymosis healing

A

Hemoglobin (red-blue) =» Bilirubin (blue-green) =» Hemosiderin (gold-brown)

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4
Q

Hemorrage

A

Can manage up to 20% loss before shock occurs

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5
Q

Sentinal Node Biopsy

A

Reduces the number of axillary dissections needed for breast-cancer staging =» reduced comorbidity of breast cancer

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6
Q

PFA

A

Prolonged collagen/EDI; normal collagen/ADP =» Drug induced issue

Prolonged both =» platelet abnormality (possible vWF)

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7
Q

Leukocytoclastic vasculitis

A

Destruction of the vascular wall due to the deposition of drug-induced immune complexes

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8
Q

Henoch-Schonlein Purpura

A

Systemic hypersensitivity disease in which immune complexes deposit in the vascular wall

*Colicky abdominal pain, AGN, polyarthralgia

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9
Q

Immune Thrombocytopenic Purpura

A

Chronic: IgG autoab against platelet that are prominently removed by the spleen (will be congested and have fulminant macros)
*BM will have increased megakaryocytes w/ left-shifted maturation

Treatment: Immunosuppression, rituximab

Acute: Abrupt, normally self-limiting but can progress to acute

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10
Q

Heparin Induced Thrombocytopenia

A

Type I: Direct platelet aggregation caused by heparin a couple days after administration; common and clinically insignificant

Type II: Abs directed against Platelet Factor 4 complex result in agglutination and thrombosis; **can be life-threatening
-LMW heparin is LESS LIKELY to cause but cannot cure it

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11
Q

TTP

A

Caused by an ADAMTS deficiency =» accumulation of HMW multimers of vWF and aggregation

Classic pentad: 1. Fever

                       2. Thrombocytopenia 
                       3. Microangiopathic hemolytic anemia 
                       4. Renal failure 
                       * 5. Neurologic symptoms

Treatment: Plasma exchange to remove antibody
*DO NOT GIVE PLATELETS; MAKES IT WORSE

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12
Q

Hemolytic Uremic Syndrome

A

Presents as bloody diarrhea and subsequent renal failure following an infection by E.coli 0157:H7

Treatment: Supportive care; plasma exchange

Can suffer irreparable renal damage

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13
Q

Bernard-Soulier Syndrome

A

Deficiency of platelet Gp-Ib complex where platelets bind to vWF; AR inheritance

*Giant platelets

Labs: Everything can cause aggregation except ristocetin

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14
Q

Glanzmann’s Thrombasthenia

A

Deficiency of Gp-IIIb-IIa where fibrinogen crosslinks platelets

Labs: Only ristocetin can cause aggregation

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15
Q

vonWillebrand Disease

A

Most common bleeding disorder that presents as prolonged bleeding from cuts, menorrhagia, and GI bleeding

-Abnormal PFA and PTT

Type I and III =» quantitative (III more severe)

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16
Q

Hemophilia A

A

Factor VIII deficiency that presents w/ easy bruising, menorrhagia, and *hemarthrosis

Labs: Prolonged PTT

-Will not see mucous membrane bleeding or petechiae

Treatment: Humate P/ recombinant Factor VIII

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17
Q

Christmas Disease

A

Clinically identical to Hemophilia A but is due to altered/deficient Factor IX

-Prolonged PTT

Treatment: recombinant Factor IX

18
Q

DIC

A

Presents as a microangiopathic hemolytic anemia that progresses to SOB, respiratory failure, **RENAL FAILURE, circulatory shock (all related to hypoxia of areas affected)

-Can originate from meningococcemia, APML, Adenocarcinoma, placenta abruption, massive tissue injury
=»Tissue injury and massive Thrombin release cause excessive activation of coag cascade and fibrin deposits in vasculature

Labs: Decreased platelets, fibrinogen
Prolonged PTT and PT
Increased D-dimer
PB: Schistocytes, reticulocytosis, leukocytosis, left shift, thrombocytopenia

*Can cause Waterhouse-Friedrichson Syndrome (meningococcemia) and Sheehan Syndrome along w/ thrombi affecting other areas

19
Q

Sheehan Sydrome

A

Postpartum pituitary necrosis; can be caused by DIC

20
Q

SIRS

A

“Systemic Inflammatory Response Syndrome”

Exaggerated response of a local inflammatory reaction mediated by TNF-a, IL-1, IL-6 and excessive endothelial cell activation

-Diagnosed by two or more signs of the following: fever, tachcardia, tacypnea, leukocytosis, leukopenia

21
Q

Trigger for septic shock

A

Bacterial products that activate TLRs on PMNs

22
Q

Endothelial Cell Activation during Septic Shock

A

3 major effects

  1. Thrombosis (DIC)- Inflammatory mediators stimulate PAI-1 and TF prod.; also decrease TFPI, Protein C, thrombomodulin
  2. Increased Vascular Permeability- Increases interstitial fluid decreasing the amount of fluid available to the tissues =» hypoxia
  3. Vasodilation- Increased NA and TXA2
23
Q

Adult Respiratory Distress Syndrome (Shock)

A

Can be induced by septic shock when decreased perfusion of the heart =» decreased contractility =» increased pulmonary edema =» lung damage

*Septic shock also damages the kidneys, liver, lungs

24
Q

Stages of Shock

A

Nonprogressive- Tissue perfusion is maintained after reflex mechanisms compensate (SIRS)

Progressive- Worsening circulator and metabolic imbalances cause acidosis and organ/tissue damage

Irreversible- Extent of tissue damage is too bad and pt. is done for

25
Q

Treatment of Septic Shock

A

Control fluid infection

Vasopressors

Insulin therapy (for induced hyperglycemia and insulin resistance)

Protein C (decrease thrombosis)

Anti-inflammatories

Corticosteroids

26
Q

Heparin

A

Reversibly binds to ATIII at an Arg-Ser residue (Coag factors irreversibly bind); must be given IV or subcutaneous injection (IM causes hematoma)

-Also increases LPL activity =» lipid clearance

Indications: Venous thrombosis, pulmonary thromboembolism; **can be given in pregnancy

-Can cause Heparin-Induced Thrombocytopenia

27
Q

Protamine

A

Heparin antidote that binds and disables activity

-May be cross-allergic w/ NPH insulin and fish allergies

28
Q

Enoxaparin (Daltaparin, Tinzaparin)

A

LMW heparin that is too small to simultaneously bind ATIII and thrombin; is as safe and effective as unfractionated heparin

*Used in pregnant women AND with outpatients

Indications: Prophylaxis and acute thromboembolism

29
Q

Fondaparinaux

A

Works the same as enoxaparin (specific inactivation of Factor Xa after binding ATIII; is a pentasaccharide synthetic

Indications: Prophylaxis and acute DVT

*Used in pregnant women

30
Q

Warfarin

A

Inhibits the synthesis of BIOLOGICALLY ACTIVE Vitamin-K dependent factors (they are still present tho); does not inhibit clotting in vitro

Indication: Arterial thromboembolism from A-fib prophylactic; post-op on prosthetic heart valves; venous thromboembolism; pulmonary embolism

⭐️DOC ORAL ANTICOAGULANT
Therapeutic INR goal= 2.0-3.0 (+.5 for heart valve replacement)

Drugs that increase effect: Ketoconazole, cephalosporin, Bactrim, cimetidine

…decrease effect: **Rifampin, cholestyramine, penobarbitol, cigarettes
*CYP2C9 mutations, VKORC

31
Q

Warfarin during pregnancy

A

1st trimester =» nasal hypoplasia

Later=» CNS issues/death

32
Q

Argatroban

A

Directly inhibits the active site of ATIII;

⭐️used in pts. w/ possible HIT

33
Q

Dagibatran

A

Pro-form of argibatran (directly inhibits ATIII); pro-drug converted to active form by plasma esterases

-Has less drug interactions as it does not react w/ CYP2C9 but it is a substrate for p-glycoprotein

Indications: Prevention of thrombotic stroke; prevention of stroke due to A-fib

***NO ANTIDOTE =» CAUTION W/ DECREASED RENAL FNXN

34
Q

Dipyridamole

A

Inhibits platelet PDE =» Increased cAMP levels
=»inhibition of platelet aggregation

-Commonly used alongside Warfarin

35
Q

Ticlopidine/Clopidogrel

CLOPY

A

Binds irreversibly to the ADP P2Y12 receptor (platelets need this and another ADP receptor to activate the GpIIIb-IIa complex)
-form disulfide links on a CYS residue

Indications: Reduced risk of stroke; (clopidogrel) acute coronary syndrome

*Ticoplidine ARs include: agranulocytosis, life-threatening thrombocytopenia

=»Clopidogrel PREFERRED

36
Q

Cangrelor

A

Reversibly binds to ADP P2Y12 receptor on platelets; very brief half-life

37
Q

Abciximab/Eftifibatide

A

Ab that binds the IIb/IIIa receptor; competitive reversible inhibition used w/ unstable angina or angioplasty procedures

  • Abciximab has 24hr half life and much stronger anticoagulant
  • Do not use w/ bleeding, Warfarin, thrombocytopenia, surgery
38
Q

Streptokinase

A

Forms a complex w/ plasminogen to activate other plasminogen molecules

Indications: Reperfusion of coronary arteries following an MI (use in 4-6hrs)

ARs: Tombolytic state (a2-antiplasmin is overwhelmed), FEVER, bleeding

-Do not use w/ intracranial trauma or diastolic pressure of >110mmHg

39
Q

Antistreplase

A

Combination of streptokinase-plasminogen and acylated active site

-Acyl group removed by plasma esterases; induces a less lytic state than streptokinase

40
Q

Alteplase

A

rt-PA that activates platelet-bound plasminogen and induces less of a lytic state due to its high specificity

Indications: Reperfusion of coronary arteries following MI, pulmonary thromboembolism

*Tenecteplase= geneticall engineered recombinant w/ even more specificity; more resistant to PAI-1

41
Q

Aminocaproic acid

A

Inhibitor of fibrinolysis; competes for lysine binding sites on plasminogen and plasmin =» deactivation

D&T:1 (6 decks)

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