• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/33

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

33 Cards in this Set

  • Front
  • Back
3 roles in platelet plug formation
adhesion (vWF on collagen, then GPIb-IX on platelet)
aggregation (via fibrinogen bridges)
secretion
Fibrinogen bridges form between what?
GP IIb-IIIa
Collection of mucocutaneous bleeding locations?
epistaxis, gum, heavy menses, bruising, GI/GU bleeding
Where do petechiae tend to occur? What is going on with platelets?
legs, LE; low platelets
too few platelets
thrombocytopenia
too many platelets
thrombocytosis
Describe pseudothrombocytopenia (platelet clumping)
EDTA-anticoagulation, certain pts have a change that causes platelets to clump together (otherwise no bleeding consequence)

check peripheral blood smear
levels of platelets that need tx or risk for hemorrhage
<20,000
three broad causes of thrombocytopenia
underproduction (don't make them)
peripheral destruction (make before destroyed)
splenic sequestration (hiding out)
Causes of underproduction of thrombocytopenia
marrow failure (myelodysplasia, aplastic anemia, vitamin def.)
marrow infiltration (tumors)
marrow toxins (chemo, radiation, infections, alcohol)
Non-immune mechanisms of peripheral destruction
DIC, TTP
process of abnormal generation of thrombin, consumption of clotting factors, destruction of platelets, and activate fibrinolysis
DIC
Components of DIC diagnosis
elevated PT (using up FVII)
low platelets
low/falling fibrinogen
Inc fibrin degradation (D-Dimer)
maybe schistocytes
Etiologies of DIC
gram- sepsis, severe burns, obstetrical disasters, certain leukemias, shock, insect/snake venoms

regardless, treat underlying cause
-can support with platelets, clotting factors, or fibrinogen
Process with abnormal activation of platelets with vWF and fibrin deposition in microvasculature & peripheral destruction of platelets and RBCs
thrombotic thrombocytopenic purpura
Pentad of Thrombotic thrombocytopenic purpura
MAHA(microangiopathic hemolytic anemia)(MUST HAVE)
-inc LDH, inc bilirubin, schistocytes present
low platelets (MUST HAVE)
fever
neurologic manifestations
renal manifestations
Underlying Cause of TTP
antibody against protease (ADAMTS-13)
-can measure activity levels of ADAMTS-13 or presence of inhibitor to ADAMTS-13
When can TTP occur?
Drugs (ticlopidine, quinine, cyclosporine, tacrolimus, gemcitabine)
inc incidence with pregnancy or AIDS
Tx of TTP
plasma exchange (avoid platelet transfusions, fuels the fire)
Common HUS manifestations
fewer neuro than TTP, more renal manifestations

post diarrheal illness (shiga toxin)

Tx with plasma exchange or supportive care
Drugs that can cause thrombocytopenia immune mechanism
B-lactam antibiotics
Trimeth-sulfa drugs
quinine/quinidine
heparin
What occurs with heparin-induced thrombocytopenia?
about 7-10d after heparin starts, platelets drop by 30-50%.

STOP heparin immediately (can lead to thrombosis)
Diagnosis of immune/idiopathic thrombocytopenic purpura
dx of exclusion (unlike Coombs test in hemolytic a)
-megakaryocytes should be present in marrow
When is ITP treated?
Not in children, usually resolves

In adults, treat below 30,000 w/ corticosteroids
Tx protocol for ITP
2/3 resolve on steroids
1/3 have splenectomy

2/3 respond to splenectomy
1/3 have immunosuppression
Differences between ITP and TTP
TTP has schistocytes; ITP had normal RBCs
How many platelets are normally in spleen?
1/3; if spleen enlarges, platelet count drops
When are platelet transfusions used?
when bleeding or prevent bleeding

NOT TTP
Describe secondary thrombocytosis
working at appropriate reactive responses

inflammation, infection, bleeding, iron deficiency
Describe diseases causing primary thrombocytosis
essential thrombocythemia, polycythemia vera, CML, and myelofibrosis
Qualitative bleeding disorders marked by...
prolonged bleeding time
2 congenital qualitative platelet disorders
Glanzmann's thrombaesthenia (defect in IIb/IIIa)
Bernard-Soulier (defect in Ib/IX)
4 main sources of acquired qualitative platelet disorders
uremia
drugs (ASA, NSAIDs)
Herbs
Myeloproliferative diseases