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POS 1: HEMATO > 8. Alteraciones Y Farma Hemostasia Primaria > Flashcards

8. Alteraciones Y Farma Hemostasia Primaria Flashcards

1
Q

¿Qué observamos?

A

En esta imagen de un brazo, se observa el “signo de Rumpel Leede” → formación de petequias. Al tomar la tensión y aumentar la presión sanguínea en el antebrazo, si tenemos una alteración de la hemostasia primaria (por trombocitopenia sobre todo), se forman petequias.

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2
Q

¿Qué observamos?

A

SÍNDROME DE MARFAN= alteración hemostasia (tejido conectivo) por mutación fibrilina 1.

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3
Q

¿Qué observamos?

A

Síndrome de Ehler-Danlos: alteraciones tejido conectivo por mutaciones del gen colágeno tipo V o colágeno tipo III

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4
Q

¿Qué observamos?

A

Malformación vascular hereditaria:
Síndrome de Rendu-Osler-Weber: también llamado “telangiectasia hemorrágica hereditaria’’.

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5
Q

¿Qué observamos?

A

Hemangioma cavernoso hepatico (raramente sangra)
Pertenece al grupo de alteraciones de la hemostasia primaria de causa vascular hereditaria

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6
Q

¿Qué observamos?

A

ESCORBUTO: síndrome hemorragico vascular adquirido.
Déficit de vitamina C que altera la síntesis de colágeno. Observamos pequeñas hemorragias puntiformes.

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7
Q

¿Qué observamos?

A

PÚRPURA SENIL: disminución de colágeno en ancianos. Manchas en manos

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8
Q

¿Qué observamos?

A

VASCULITIS: síndrome hemorragico vascular adquirido.
Púrpura palpable (vaso inflamado) por hipersensibilidad.

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9
Q

PTI

A
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10
Q

Trombocitopenias farmacológicas

A

ACTIVACIÓN DEL COMPLEMENTO

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11
Q

Trombocitopenia inducida por heparina

A

FACTOR PLAQUETAR 4 SE UNE A HEPARINA, SE GENERA TROMBOSIS

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12
Q

Púrpura trombotica trombocitopénica

A

Deficiencia de ADAMS-13, no se corta VWfactor, formación de trombos.
RETICULOCITOS Y ESQUISTOCITOS

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13
Q

Fármacos análogos de la trombopoyetina, agonistas a su R en megacariocitos que promueven la síntesis de plaquetas
TRATAMIENTO TROMBOCITOPENIAS AUTOINMUNES

A

AVATROMBOPAG, ELTROMBOPAG, LUSUTROMBOPAG

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14
Q

Fármacos análogos de la trombopoyetina, agonistas a su R en megacariocitos que promueven la síntesis de plaquetas, en concreto en pacientes con anemia aplásica grave
TRATAMIENTO TROMBOCITOPENIAS AUTOINMUNES

A

ELTROMBOPAG

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15
Q

Fármacos análogos de la trombopoyetina, agonistas a su R en megacariocitos que promueven la síntesis de plaquetas. En concreto, en pacientes adultos con enfermedad hepática crónica que tengan programada una intervención masiva.
TRATAMIENTO TROMBOCITOPENIAS AUTOINMUNES

A

AVATROMBOPAG Y LUSUTROMBOPAG

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16
Q

RAM de AVATROMBOPAG, ELTROMBOPAG Y LUSUTROMBOPAG

A

TROMBOSIS Y HEPATOTOXICIDAD

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17
Q

Fármaco inhibidor de la tirosina-cinasa esplénica (SYK) que ejerce su actividad a través de su metabolito principal R406.
REDUCE LA DESTRUCCIÓN DE LAS PLAQUETAS MEDIADA POR ANTICUERPOS.

A

FOSFATINIB

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18
Q

RAM FOSFATINIB

A

HTA, diarrea, náuseas, deposiciones frecuentes, dolor abdominal…

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19
Q

Molécula de fusión con capacidad de unirse al R de la trombopoyetina y aumentar producción de las plaquetas.
TRATAMIENTO DE ELECCIÓN PARA LA PTI.

A

ROMIPLOSTIM

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20
Q

RAM ROMIPLOSTIM

A

TROMBOSIS VENOSA Y ARTERIAL

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21
Q

Formación trombo plaquetario

A
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22
Q

Formación trombo plaquetario

A
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23
Q

Fármacos antiagregantes

A
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24
Q

INHIBIDORES DE LA COX

A

ÁCIDO ACETILSALICÍLICO Y TRIFLUSAL

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25
Q

Fármacos antiagregantes que interfieren en el complejo GPIIB/IIIA, por inhibición de mecanismos dependientes de ADP

A

TICLOPIDINA, CLOPIDOGREL, PRASUGREL

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26
Q

Fármacos antiagregantes que interfieren en el complejo GPIIB/IIIA, siendo antagonista del complejo

A

ABCIXIMAB, TIROFIBÁN, EPTIFIBATIDA

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27
Q

Fármacos antiagregantes que modulan mecanismos relacionados con el AMPc y el GMPc

A

EPOPROSTENOL, ILOPROST, DIPIRIDAMOL Y CILOSTAZOL

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28
Q

Fármaco antiagregante inhibidor irreversible de COX (disminuye niveles tromboxano)
Efecto potente y dosis bajas (única dosis diaria, 75-100 mg)

A

ÁCIDO ACETILSALICÍLICO

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29
Q

RAM ÁCIDO ACETILSALICÍLICO

A

HEMORRAGIA GI

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30
Q

DERIVADO DE AAS

A

TRIFLUSAL

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31
Q

TICLOPIDINA, clopidogrel y prasugrel son…

A

PROFÁRMACOS (tardan en activarse y en desactivarse)

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32
Q

Segundo fármaco antiagregante más usado después de AAS

A

CLOPIDOGREL

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33
Q

Fármacos antiagregantes antagonistas receptores GPIIb/IIIa, administración por vía endovenosa (uso intrahospitalario), complemento de heparina

A

ABCIXIMAB, TIROFIBÁN, EPTIFIBATIDA

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34
Q

Prostacyclins sintética que inhibe la expresión del receptor GPIIb/IIIa. Tiene administración parenteral (diálisis renal) asociado a heparina.

A

EPOPROSTENOL

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35
Q

Fármaco antiagregante análogo de la prostaciclina que se administra por vía inhalatoria

A

ILOPROST Y TEPROSTINILO

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36
Q

Fármacos antiagregantes que aumentan AMPc y GMPc. Se recomienda su asociación a dosis bajas de AAS.

A

DIPIRIDAMOL Y CILOSTAZOL

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37
Q

Enfermedad vW

A
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38
Q

ESTIMACIÓN F VW

A
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39
Q

¿Qué son las alteraciones de la hemostasia primaria?

A

Hemorragias cutáneas y mucosas como petequias y epistaxis.

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40
Q

¿Qué son las alteraciones de la hemostasia secundaria?

A

Hemorragias profundas como hematomas y hemartrosis.

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41
Q

¿En qué consiste el tiempo de hemorragia (Ivy)?

A

Hacer una pequeña incisión y medir el tiempo que tarda en cesar la hemorragia.

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42
Q

¿Por qué es importante el recuento plaquetar en la hemostasia primaria?

A

Es fundamental para la formación del trombo plaquetario.

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43
Q

¿Qué se estudia en el estudio de factor Von-Willebrand (VWf)?

A

La alteración más frecuente de la hemostasia primaria.

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44
Q

¿Qué indica el ‘signo de Rumpel Leede’?

A

Formación de petequias al aumentar la presión sanguínea en el antebrazo.

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45
Q

¿Qué se necesita para realizar estudios de agregación plaquetar?

A

Plasma rico en plaquetas y un quelante del calcio como EDTA.

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46
Q

¿Cómo se obtiene el plasma rico en plaquetas?

A

Centrifugando una muestra de sangre en un tubo EDTA a baja velocidad.

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47
Q

¿Qué ocurre al añadir estímulos como epinefrina y ADP al plasma rico en plaquetas?

A

Las plaquetas se agregan y el plasma deja de estar turbio.

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48
Q

¿Cuál es el propósito de medir la transmisión de luz durante el estudio de agregación plaquetaria?

A

Analizar la agregación plaquetaria a medida que coagula la sangre.

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49
Q

Fill in the blank: La hemostasia primaria se caracteriza principalmente por la formación de _______.

A

trombo plaquetario.

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50
Q

True or False: Las alteraciones de la hemostasia primaria incluyen hemorragias profundas.

A

False.

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51
Q

¿Qué indican los cambios de luminiscencia o turbidez en la agregación plaquetaria?

A

La formación de agregados plaquetarios relativamente grandes

Esto refleja la actividad en la agregación de plaquetas.

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52
Q

¿Cuántas fases distintas tiene la curva típica de la agregación plaquetaria?

A

Cinco fases distintas

La curva presenta dos curvas a lo largo de estas fases.

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53
Q

¿Qué ocurre al añadir sustancias como Epinefrina y ADP en la agregación plaquetaria?

A

Se produce una parte inicial curva que es reversible

Esto indica que se necesita la liberación de ADP para la activación.

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54
Q

¿Cuál es el primer incremento en la curva de agregación plaquetaria?

A

Incremento inicial de la transmisión de la luz

Atribuible a la dilución del plasma rico en plaquetas.

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55
Q

¿Qué ocurre durante la segunda fase de la curva de agregación plaquetaria?

A

Leve disminución de la transmisión a medida que las plaquetas cambian de forma

Esto refleja la morfología de las plaquetas durante la activación.

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56
Q

¿Qué representa el tercer incremento en la curva de agregación plaquetaria?

A

Incremento agudo inicial de la transmisión a medida que las plaquetas se agregan

Este es un indicador de la agregación plaquetaria efectiva.

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57
Q

¿Qué caracteriza la meseta breve o disminución de la agregación en la curva?

A

Una breve estabilización antes de continuar con la agregación secundaria

Esto ocurre antes de la segunda curva de agregación.

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58
Q

¿Qué causa la segunda curva de agregación plaquetaria?

A

Agregación secundaria estimulada por la secreción de gránulos plaquetarios

Esto es resultado de la activación plaquetaria y liberación de ADP.

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59
Q

¿Qué papel juega el ADP en la activación plaquetaria?

A

Recluta y activa más plaquetas

Es esencial para la agregación plaquetaria posterior.

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60
Q

¿Cuáles son algunos de los múltiples estímulos que dependen de la activación plaquetaria?

A

Trombina, tripsina, colágeno, ADP, epinefrina, metabolitos del ácido araquidónico, factor activador de plaquetas

Estos factores pueden activar las plaquetas y desencadenar su función.

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61
Q

¿Qué ocurre si las plaquetas no liberan suficiente ADP?

A

No observaremos la segunda curva, indicando que algo falla

Esto sugiere un problema en la activación o reclutamiento plaquetario.

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62
Q

¿Cómo son las curvas generadas por otros agonistas como Colágeno y Ristocetina?

A

Típicamente unimodales, con una sola curva

Esto difiere de las curvas observadas con ADP.

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63
Q

¿Cuáles son los dos tipos de alteraciones de la hemostasia primaria?

A

Causa vascular y alteraciones de las plaquetas

Estas alteraciones pueden afectar la función hemostática.

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64
Q

¿Qué tipo de origen puede tener la afectación vascular?

A

Hereditario o adquirido

Esto incluye síndromes hemorrágicos y alteraciones del tejido conectivo.

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65
Q

¿Qué es el síndrome de Marfan?

A

Mutación de la fibrilina 1

Se relaciona con alteraciones del tejido conectivo y riesgo de aneurisma de aorta.

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66
Q

¿Cuáles son algunos fenotipos asociados al síndrome de Marfan?

A

Aracnodactilia, luxación del cristalino

Estos signos son consecuencia de la alteración del tejido conectivo.

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67
Q

What is the Ehler-Danlos syndrome associated with?

A

Alteraciones del gen colágeno tipo V o colágeno tipo III

This alteration confers hyperlaxity, with the risk of rupturing large vessels and causing hemorrhages.

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68
Q

What are the main characteristics of Ehler-Danlos syndrome?

A

Hiperlaxitud articular e hiperelasticidad cutánea

This syndrome includes joint hyperlaxity and skin hyperelasticity.

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69
Q

What is the Rendu-Osler-Weber syndrome also known as?

A

Telangiectasia hemorrágica hereditaria

This syndrome is characterized by the presence of multiple telangiectasias.

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70
Q

Where do telangiectasias typically occur in Rendu-Osler-Weber syndrome?

A

Fosas nasales, labios, boca

These are common sites where spontaneous bleeding may occur due to thin vessel walls.

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71
Q

What is a hemangioma?

A

Un tumor vascular benigno

Hemangiomas can appear in any location and are generally benign.

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72
Q

What type of hemangioma can be very large and occasionally bleed?

A

Hemangiomas cavernosos

These cavernous hemangiomas can be quite large and may bleed, although it is rare.

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73
Q

What is purpura simple?

A

Fragilidad capilar de causa desconocida

This condition leads to spontaneous bruising.

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74
Q

What is purpura senil commonly associated with?

A

Ancianos y alteración del colágeno

This condition is frequent in the elderly due to changes in collagen.

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75
Q

What vitamin deficiency causes scurvy?

A

Déficit de Vitamina C

This deficiency affects collagen synthesis, leading to specific hemorrhagic manifestations.

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76
Q

What are small punctate hemorrhages in scurvy called?

A

Púrpuras centradas en un folículo piloso

These appear as small, pinpoint-like hemorrhages.

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77
Q

What does the suffix ‘-itis’ indicate in vasculitis?

A

Lesiones inflamatorias de los vasos sanguíneos

Vasculitis refers to the inflammation of blood vessels.

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78
Q

What are the symptoms of small vessel vasculitis?

A

Púrpura palpable

This condition manifests with palpable purpura due to inflamed vessels.

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79
Q

What is thrombocytopenia?

A

Disminución en el n° de plaquetas

It refers to a reduction in platelet count.

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80
Q

What are the two situations related to thrombocytopenia?

A
  • Disminución en el n° de plaquetas
  • Alteración de la función plaquetaria

These represent the quantitative and qualitative aspects of platelet issues.

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81
Q

What is the normal range (VN) for platelet count?

A

150.000 - 400.000 / uL

Counts below this range may indicate bleeding disorders.

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82
Q

What is the clinical significance of a platelet count between 100.000-150.000 / uL?

A

No detectamos clínica ni test de la cuchilla alterado

This range typically does not show clinical manifestations or altered bleeding time.

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83
Q

What is the platelet count range for no clinical symptoms but a prolonged bleeding time?

A

Between 100,000 and 50,000 / uL

A test may detect a slightly abnormal bleeding time in this range.

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84
Q

At what platelet count does the risk of more profuse bleeding after injury increase?

A

Between 20,000 and 50,000 / uL

This range indicates a significant risk for bleeding.

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85
Q

What is the platelet count threshold for spontaneous bleeding?

A

Less than 20,000 / mL

This level is critical for monitoring patient safety.

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86
Q

Name two types of bleeding associated with low platelet counts.

A
  • Petechiae
  • Ecchymosis

These are common manifestations of thrombocytopenia.

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87
Q

What is the risk of bleeding in the central nervous system (CNS) when platelet counts drop below 5,000 / uL?

A

Significant risk

Very low platelet counts pose serious risks to CNS health.

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88
Q

Define thrombocytopenia.

A

A condition characterized by low platelet count

It can be caused by various factors including production failure and increased destruction.

89
Q

What are the potential causes of thrombocytopenia?

A
  • Production failure
  • Combined factors
  • Isolated factors
  • Viral infections
  • Alcohol
  • Dilutional causes
  • Distributive causes (hypersplenism)

Each cause can lead to different clinical scenarios.

90
Q

What is dilutional thrombocytopenia?

A

Thrombocytopenia due to massive hemorrhage without platelet replacement

This occurs when blood and plasma are replaced but not platelets.

91
Q

What describes distributive thrombocytopenia?

A

Thrombocytopenia caused by hypersplenism

This condition involves the retention of platelets in the spleen.

92
Q

What conditions can lead to isolated low platelet production?

A
  • Alcohol toxicity
  • Certain viral infections

These factors affect platelet production without impacting other blood components.

93
Q

What does combined low platelet production indicate?

A
  • Infiltration (e.g., myeloproliferative syndromes)
  • Primary bone marrow failure (e.g., aplastic anemia)

This suggests a more complex underlying condition affecting multiple blood cell lines.

94
Q

What is pseudothrombocytopenia?

A

A false low platelet count due to platelet aggregation in blood samples

This can be resolved by measuring platelets in citrate instead of EDTA.

95
Q

What is the significance of splenic pooling in thrombocytopenia?

A

It can lead to a lower percentage of circulating platelets due to retention in the spleen

For example, patients with splenomegaly may have significant retention of platelets.

96
Q

What is the range of circulating platelets in patients?

A

10-40%

This percentage reflects the variability in platelet counts among individuals.

97
Q

What are the two diagnostic situations found in low platelet counts?

A
  • Low production of platelets
  • Increased destruction or sequestration of platelets

Identifying the cause is essential for appropriate management.

98
Q

What are myeloproliferative syndromes?

A

Disorders characterized by excessive production of blood cells from the bone marrow

They can lead to complications including thrombocytopenia.

99
Q

What is the relationship between megaloblastic anemia and thrombocytopenia?

A

Megaloblastic anemia can lead to bone marrow failure, affecting platelet production

This condition is often linked with vitamin deficiencies.

100
Q

¿Qué es el aumento del consumo de plaquetas?

A

Es la disminución de plaquetas debido a causas inmunes o infecciosas.

Incluye condiciones donde el sistema inmune ataca a las plaquetas o infecciones como la sepsis que puede causar trombopenia.

101
Q

¿Cuáles son las causas inmunes del aumento del consumo de plaquetas?

A

Las causas inmunes incluyen:
* Fármacos
* Púrpura trombocitopénica idiopática (PTI)

PTI es una condición en la que el sistema inmune ataca las plaquetas.

102
Q

¿Qué infecciones pueden causar trombopenia?

A

La sepsis es un ejemplo frecuente de infección que puede causar trombopenia.

La trombopenia es la disminución del número de plaquetas en la sangre.

103
Q

¿Qué son las microangiopatías trombóticas?

A

Son condiciones que incluyen:
* Coagulación intravascular diseminada (CID)
* Púrpura trombótica trombocitopénica (PTT)
* Síndrome hemolítico urémico (SHU)

Estas condiciones se caracterizan por la activación anormal de la coagulación en pequeños vasos sanguíneos.

104
Q

¿Qué son las trombocitopenias por fallo medular?

A

Son trombocitopenias causadas por problemas en la producción de plaquetas en la médula ósea.

Incluyen dos categorías: amegacariocíticas y megacariocíticas.

105
Q

¿Cuáles son las causas de las trombocitopenias amegacariocíticas?

A

Las causas incluyen:
* Depresión medular (infecciones, tóxicos, radiaciones)
* Invasión/infiltración (leucemia, tumores)
* Insuficiencia medular (aplasias)

La depresión medular puede resultar de múltiples factores que afectan la producción celular en la médula ósea.

106
Q

¿Qué caracteriza a las trombocitopenias megacariocíticas?

A

El número de megacariocitos es correcto, pero hay fallo en la maduración de las plaquetas.

Esto puede ser causado por consumo de alcohol, anemias megaloblásticas y síndromes mielodisplásicos.

107
Q

¿Qué es la púrpura trombocitopénica idiopática (PTI)?

A

Es una enfermedad donde el sistema inmune ataca las plaquetas mediante un mecanismo de hipersensibilidad tipo II.

Esto implica la formación de anticuerpos IgG contra glicoproteínas en las plaquetas.

108
Q

¿Qué enfermedades pueden estar asociadas con anticuerpos antiplaquetarios?

A

Incluyen:
* Lupus eritematoso sistémico (LES)
* Infecciones como VIH
* Vacunas
* Fármacos como quinina, heparina, y sales de oro

Estas condiciones pueden resultar en la destrucción de plaquetas.

109
Q

¿Cómo actúan los fármacos en la trombocitopenia farmacológica?

A

Los fármacos pueden unirse a proteínas plasmáticas, haptenizarse y provocar la producción de anticuerpos.

Esto puede llevar a la activación del complemento, dañando las plaquetas.

110
Q

¿Verdadero o falso? La insuficiencia medular puede causar trombocitopenia.

A

Verdadero.

La insuficiencia medular se refiere a la incapacidad de la médula ósea para producir suficientes células sanguíneas.

111
Q

What is the main cause of thrombocytopenia induced by heparin?

A

Thrombocytopenia secondary to heparin

This condition can paradoxically lead to thrombosis despite causing low platelet counts.

112
Q

Is thrombocytopenia induced by heparin common or rare?

A

Infrequent

This is especially the case with low molecular weight heparins used today.

113
Q

What mechanism causes heparin-induced thrombocytopenia?

A

Same mechanism that causes thrombosis after COVID vaccination

Involves immune response and platelet activation.

114
Q

What does a normally activated platelet secrete?

A

Contents of its granules, including platelet factor IV (PF4)

PF4 plays a key role in the immune response to heparin.

115
Q

What happens to platelet factor IV when it binds to circulating heparin?

A

It undergoes a conformational change and becomes haptenized

This alteration triggers an immune response.

116
Q

What do antibodies against PF4 bind to?

A

Platelets

They bind via Fc receptors, leading to platelet aggregation and thrombus formation.

117
Q

What is the consequence of activated platelets binding to heparin and PF4?

A

Formation of a thrombus

This process is facilitated by the binding of antibodies.

118
Q

What are the types of antibodies associated with post-transfusion reactions?

A

Antiplatelet antibodies

These can lead to complications in transfusion scenarios.

119
Q

What condition is characterized by a deficiency of ADAMTS13?

A

Thrombotic thrombocytopenic purpura (TTP)

This deficiency can be congenital or acquired.

120
Q

What is the role of ADAMTS13?

A

To lyse von Willebrand factor (VWf)

It prevents the formation of excessively large VWf complexes.

121
Q

What happens when there is a lack of ADAMTS13?

A

Formation of excessively large VWf multimer complexes

This leads to excessive platelet aggregation and microangiopathy.

122
Q

What are the consequences of excessive platelet aggregation due to large VWf complexes?

A

Thrombi formation and vascular damage

This results in consumption of platelets and subsequent thrombocytopenia.

123
Q

What is TTP?

A

Thrombotic Thrombocytopenic Purpura

A condition characterized by microangiopathic hemolytic anemia, thrombocytopenia, and organ injury, often due to ADAMTS13 deficiency.

124
Q

What does ADAMTS13 do?

A

It is a von Willebrand factor-cleaving protease

Its deficiency leads to the accumulation of large von Willebrand factor multimers, causing excessive platelet aggregation.

125
Q

What are the two main types of TTP?

A
  • Acquired TTP
  • Familial TTP

Acquired TTP is often associated with autoantibodies against ADAMTS13, while familial TTP is due to genetic mutations.

126
Q

What is Disseminated Intravascular Coagulation (DIC)?

A

A complex disorder characterized by systemic activation of coagulation

It leads to the formation of blood clots throughout the small blood vessels, resulting in organ damage and bleeding.

127
Q

What is the main cause of acute renal failure in children related to TTP?

A

Hemolytic Uremic Syndrome (HUS)

HUS often presents with thrombocytopenia, renal impairment, and is frequently associated with E. coli O157:H7 infection.

128
Q

What are the consequences of endothelial damage in TTP?

A
  • Formation of microthrombi
  • Consumption of platelets

Microthrombi formation leads to platelet consumption and mechanical damage to red blood cells.

129
Q

What is the treatment approach for TTP?

A
  • Supportive care
  • Plasmapheresis/IVIG
  • Management of DIC
  • Control of bleeding

Plasmapheresis helps remove the inhibitory antibodies against ADAMTS13 and replenish the enzyme.

130
Q

What is Kasabach-Merritt syndrome?

A

A condition associated with vascular tumors causing thrombocytopenia

It involves activation of coagulation mechanisms leading to consumption of platelets.

131
Q

What are thrombocytopathies?

A

Disorders affecting platelet function

They can be congenital or acquired and affect mechanisms such as adhesion, secretion, and aggregation.

132
Q

Fill in the blank: The main factor involved in platelet adhesion is _______.

A

Factor von Willebrand

It is crucial for the initial attachment of platelets to the damaged endothelium.

133
Q

What role does fibrinogen play in platelet function?

A

It acts as a bridge between platelets

Fibrinogen binds to glycoprotein IIb/IIIa on platelets, facilitating aggregation.

134
Q

What happens during the activation of platelets?

A

They secrete granule contents, including thromboxane

This secretion promotes further platelet activation and aggregation.

135
Q

True or False: Thrombocytopenia can result from excessive platelet consumption.

A

True

Increased consumption occurs in conditions like TTP and DIC.

136
Q

What are schistocytes?

A

Fragmented red blood cells

They are often seen in microangiopathic hemolytic anemias, indicating mechanical destruction.

137
Q

Fill in the blank: The process of platelet recruitment and activation is crucial for _______.

A

Thrombus formation

Activation leads to a cascade of events necessary for forming a stable blood clot.

138
Q

¿Qué alteraciones en la adhesión se observan en las trombocitopatías hereditarias?

A

El Test de agregación plaquetaria de ristocetina tendrá tiempo aumentado. La agregación con ADP y colágeno se mantiene normal.

Esto indica un fenómeno VW dependiente.

139
Q

¿Cuál es la trombocitopatía más frecuente?

A

La enfermedad de Von Willebrand (VWf)

Existen tres tipos de enfermedad de VW: tipo 1, tipo 2 y tipo 3.

140
Q

¿Cómo se clasifica la enfermedad de Von Willebrand?

A
  1. VW tipo 1: hay menos VW de lo normal
  2. VW tipo 2: hay cantidades normales de VW
  3. VW tipo 3: no hay apenas o nada de VW

Cada tipo se caracteriza por diferentes niveles de factor von Willebrand.

141
Q

¿Qué receptor se ve afectado en la enfermedad de Bernard-Soulier?

A

La glicoproteína 1b (GP 1b)

Este receptor es el que permite la adhesión de las plaquetas al endotelio.

142
Q

¿Cuál es el diagnóstico diferencial cuando se observa un patrón de curva de ristocetina alterada?

A

Enfermedad de Von Willebrand y Bernard-Soulier

La diferencia se evidencia al estudiar la actividad del factor VIII.

143
Q

¿Qué efecto tienen las alteraciones de la secreción plaquetar en el tiempo de hemorragia?

A

Presentan un leve aumento del tiempo de hemorragia.

Esto se debe a la ausencia de agregación inducida con colágeno, epinefrina o ADP a bajas dosis.

144
Q

En las alteraciones de la secreción plaquetar, ¿cómo se comporta la agregación inducida por ristocetina?

A

Será normal, ya que mide unión GP1b-VWf.

Sin embargo, la agregación con colágeno, epinefrina o ADP será reversible.

145
Q

¿Qué ocurre con la agregación inducida por otros estímulos en el caso de alteraciones de la secreción plaquetar?

A

Se observará una agregación inicial pero reversible.

Solo veremos la primera onda, ya que no se produce la liberación del contenido de los gránulos.

146
Q

¿Qué se necesita para que la agregación sea irreversible en las alteraciones de la secreción plaquetar?

A

Administrar dosis altas de estímulos de ADP.

Esto permite no solo la unión inicial, sino también más reclutamiento de plaquetas.

147
Q

¿Qué se relaciona con las alteraciones de los gránulos y almacenamiento de ADP?

A

La reducción de síntesis de TXA2 por deficiencia de COX y falta de respuesta ante TXA2 por defecto en el receptor de membrana plaquetar.

Esto afecta la función plaquetaria y la formación de trombos.

148
Q

¿Qué se observa en la agregometría plaquetaria en un paciente con afectación de los gránulos?

A

Se verá solo una onda de agregación inicial pero reversible.

Esto se debe a la falta de liberación de contenido de los gránulos.

149
Q

What is Afibrinogenemia?

A

No se produce fibrinógeno

Afibrinogenemia es una condición que resulta en la ausencia de fibrinógeno, lo que afecta la coagulación sanguínea.

150
Q

What characterizes Trombastenia o Enfermedad de Glanzmann?

A

Falta de glicoproteína 2b3a en plaquetas

Esta condición impide la agregación plaquetaria y es grave, presentando crisis hemorrágicas severas.

151
Q

What is the result of a prolonged bleeding time?

A

Gran prolongación del tiempo de hemorragia

Esto indica problemas en la función plaquetaria, como en la Trombastenia.

152
Q

Which test does not show aggregation in Trombastenia except with ristocetina?

A

Test de agregación

Este test no muestra agregación con colágeno, epinefrina, o ADP, salvo con ristocetina.

153
Q

What is the most common acquired thrombocytopathy?

A

ENFERMEDAD DE VON WILLEBRAND

Es importante clasificarla en tres tipos: tipo I, II y III.

154
Q

What defines ENFERMEDAD DE VON WILLEBRAND tipo I?

A

Deficiencia cuantitativa parcial de vWF

Representa el 70% de los casos y generalmente causa diatesis hemorrágicas leves.

155
Q

What characterizes ENFERMEDAD DE VON WILLEBRAND tipo II?

A

Deficiencia cualitativa de vWF

Este tipo se divide en subtipos (IIA, IIB, IIM, IIN) y representa el 25% de los casos.

156
Q

What is the distinction of ENFERMEDAD DE VON WILLEBRAND tipo III?

A

Deficiencia cuantitativa total de vWF

Es muy grave y representa el 5% de los casos.

157
Q

What is the clinical presentation of VW tipo I and II?

A

Diatesis hemorrágicas leves

Incluyen epistaxis, metrorragias y episodios hemorrágicos más frecuentes.

158
Q

What occurs in VW tipo 2a?

A

Multímeros de VWf más pequeños

Esto resulta en una menor capacidad de agregación plaquetaria.

159
Q

What is the effect of VW tipo 2b?

A

Mayor reactividad y afinidad por la GPIb

Esto puede traducirse en depleción plaquetar y aumento de agregación por ristocetina.

160
Q

Fill in the blank: VW tipo 1 es una enfermedad _______.

A

cuantitativa parcial de vWF

Esto implica que hay una cantidad reducida de vWF en el organismo.

161
Q

True or False: ENFERMEDAD DE VON WILLEBRAND tipo III has a total or near total quantitative deficiency of vWF.

A

True

Esta condición es la más grave de las tres tipos de enfermedad de von Willebrand.

162
Q

What is the clinical implication of ENFERMEDAD DE VON WILLEBRAND tipo II?

A

Presenta cantidades normales de vWF

Sin embargo, la funcionalidad de vWF está alterada, afectando la agregación plaquetaria.

163
Q

What does the screening test for platelet aggregation with ristocetin measure?

A

It measures aggregation by inducing interaction between GPIb and VWf

164
Q

What is the result for Type 1 in the ristocetin aggregation test?

A

Prolonged ristocetin time

165
Q

What is the result for Type 2a in the ristocetin aggregation test?

A

Prolonged ristocetin time

166
Q

What is the result for Type 2b in the ristocetin aggregation test?

A

Increased interaction by ristocetin (unclear mechanism)

167
Q

What does low levels of VWf indicate about factor VIII levels?

A

Low levels of factor VIII

168
Q

What are the factor VIII levels in VW type 1?

A

Low factor VIII levels

169
Q

What are the factor VIII levels in VW type 2a and 2b?

A

Normal or low factor VIII levels

170
Q

What test measures the intrinsic pathway of coagulation related to factor VIII?

A

Cefalina-Caolín time (TCK)

171
Q

What is the TCK result for VW type 1?

A

Prolonged TCK

172
Q

What is the TCK result for VW type 2a and 2b?

A

Normal TCK

173
Q

What is the first step to study VW disease types I and II?

A

Study aggregation with ristocetin (deficit VW = prolonged time)

174
Q

What can be used to quantify VW protein levels?

A

Antigen testing

175
Q

What does SDS agarose electrophoresis analyze in VW disease?

A

Different multimers of VW

176
Q

What is the electrophoresis result for VW type 1?

A

Small band (low quantity, but normal structure)

177
Q

What is the electrophoresis result for VW type 2a?

A

Band comparable to normal, but small multimers

178
Q

What is the electrophoresis result for VW type 2b?

A

Normal/abnormal size multimers with normal quantities

179
Q

What is a characteristic of Type 2b VW disease?

A

Increased reactivity and consequent platelet depletion

180
Q

What is the platelet count in types 1 and 2b of VW disease?

A

Normal or low platelet count in type 2b

181
Q

What is the characteristic of VW disease type III?

A

Rare, recessive, severe with almost total absence of VW factor

182
Q

How does VW disease type III behave in relation to hemostasis?

A

Behaves as a secondary hemostasis disorder

183
Q

What are the VWf and factor VIII levels in VW type III?

A

Very low VWf and very low factor VIII levels

184
Q

What is the ristocetin aggregation test result for VW type III?

A

Prolonged time

185
Q

What is the TCK result for VW type III?

A

Prolonged TCK

186
Q

What is the initial assessment for a patient presenting with cutaneous and mucosal hemorrhages?

A

Recuento plaquetario y pruebas de tiempo de hemorragia

This assessment helps identify potential causes of bleeding.

187
Q

What does a normal platelet count and normal bleeding time indicate?

A

Otra causa (diátesis hemorrágica angiopática)

Indicates that the bleeding may not be due to platelet issues.

188
Q

What does a decreased platelet count and abnormal bleeding time suggest?

A

Diátesis hemorrágica trombopénica

This condition indicates a problem with platelet production or survival.

189
Q

What additional tests should be conducted if the platelet count is decreased?

A

Volumen plaquetario medio, presencia de esplenomegalia, estudios de la médula ósea

These tests help further evaluate the cause of thrombocytopenia.

190
Q

What does a normal platelet count and abnormal bleeding time indicate?

A

Diátesis hemorrágica trombocitopática y Enfermedad de von Willebrand

Indicates issues with platelet function rather than quantity.

191
Q

What is the most common thrombocytopathy?

A

Enfermedad de von Willebrand

This condition affects platelet function and is often tested for in cases of abnormal bleeding.

192
Q

What are the two main tests for evaluating primary hemostasis?

A

Recuento plaquetario y tiempo de hemorragia

These tests are crucial for diagnosing bleeding disorders.

193
Q

Fill in the blank: A normal platelet count with an abnormal bleeding time suggests _______.

A

Diátesis hemorrágica trombocitopática

This indicates a problem with platelet function.

194
Q

True or False: Splenomegaly can indicate distributive thrombocytopenia.

A

True

Splenomegaly can lead to increased sequestration of platelets.

195
Q

What is the initial assessment for a patient presenting with cutaneous and mucosal hemorrhages?

A

Recuento plaquetario y pruebas de tiempo de hemorragia

This assessment helps identify potential causes of bleeding.

196
Q

What does a normal platelet count and normal bleeding time indicate?

A

Otra causa (diátesis hemorrágica angiopática)

Indicates that the bleeding may not be due to platelet issues.

197
Q

What does a decreased platelet count and abnormal bleeding time suggest?

A

Diátesis hemorrágica trombopénica

This condition indicates a problem with platelet production or survival.

198
Q

What additional tests should be conducted if the platelet count is decreased?

A

Volumen plaquetario medio, presencia de esplenomegalia, estudios de la médula ósea

These tests help further evaluate the cause of thrombocytopenia.

199
Q

What does a normal platelet count and abnormal bleeding time indicate?

A

Diátesis hemorrágica trombocitopática y Enfermedad de von Willebrand

Indicates issues with platelet function rather than quantity.

200
Q

What is the most common thrombocytopathy?

A

Enfermedad de von Willebrand

This condition affects platelet function and is often tested for in cases of abnormal bleeding.

201
Q

What are the two main tests for evaluating primary hemostasis?

A

Recuento plaquetario y tiempo de hemorragia

These tests are crucial for diagnosing bleeding disorders.

202
Q

Fill in the blank: A normal platelet count with an abnormal bleeding time suggests _______.

A

Diátesis hemorrágica trombocitopática

This indicates a problem with platelet function.

203
Q

True or False: Splenomegaly can indicate distributive thrombocytopenia.

A

True

Splenomegaly can lead to increased sequestration of platelets.

204
Q

What are the clinical manifestations associated with primary hemostasis?

A

Diátesis hemorrágicas en piel y mucosas

These manifestations indicate issues with primary hemostasis.

205
Q

What are the clinical manifestations associated with secondary hemostasis?

A

Hematomas profundos, diátesis en masas musculares y hemartros

These manifestations are similar to those seen in hemophilia.

206
Q

What is the role of Weibel-Palade bodies?

A

Storage and release of von Willebrand factor (VWF)

Weibel-Palade bodies are specialized organelles found in endothelial cells.

207
Q

What does VWFpp stand for?

A

Von Willebrand factor propeptide

VWFpp is a precursor to the active von Willebrand factor.

208
Q

What is Type 3 VWD characterized by?

A

Undetectable vWF levels

This type represents the most severe form of von Willebrand disease.

209
Q

What are the characteristics of VWD Type 1?

A

Low VWF levels and normal VWF multimers

This is the mildest form of von Willebrand disease.

210
Q

What is a key feature of VWD Type 2A?

A

Low VWF-collagen binding and abnormal vWF multimers

This type involves qualitative defects in vWF.

211
Q

What distinguishes VWD Type 2B?

A

Enhanced VWF-platelet binding and abnormal vWF multimers

This type is characterized by increased affinity of vWF for platelets.

212
Q

What are acquired thrombocytopathies?

A

Alteraciones enzimáticas, daño plaquetar por anticuerpos, recubrimiento de plaquetas, déficit de COX, unión de PDFs, toxinas, enfermedad de VW adquirida

These conditions can lead to impaired platelet function.

213
Q

What causes the platelet damage in lupus?

A

Antibodies against platelets

This immune response can lead to thrombocytopenia.

214
Q

What is the effect of aspirin on platelet function?

A

Déficit de COX

Aspirin inhibits cyclooxygenase, affecting platelet aggregation.

215
Q

What is the mechanism of action in the context of disseminated intravascular coagulation (DIC)?

A

Unión de productos de degradación del fibrinógeno (PDFs) al receptor GPIIb/IIIa

This inhibits platelet aggregation, contributing to bleeding.

216
Q

What is the Heyde syndrome associated with?

A

Estenosis aórtica

This syndrome affects von Willebrand factor and can lead to bleeding complications.

217
Q

How does estenosis aórtica affect von Willebrand factor?

A

Produce turbulencias que desenrollan los factores VW, haciéndolos más sensibles a ADAMTS13

This leads to the breakdown of vWF into smaller multimers.

218
Q

True or False: VWD Type 2B is characterized by low VWF-platelet binding.

A

False

VWD Type 2B is characterized by enhanced VWF-platelet binding.

POS 1: HEMATO (18 decks)

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