Hematology in special populations (3) Flashcards
(31 cards)
What is the purpose of platelets?
When there is damage to a blood vessels platelets create a plug which forms into a clot to stop the bleeding
What is thrombocytopenia defined as?
Platelet count < 100,000 cells/mm^3
or >50% reduction in platelets from baseline
What does thrombocytopenia present with clinically? (2)
Bruising
Bleeding
(due to the inability to form a clot and stop the leaking of the damaged vessel)
In general, we treat thrombocytopenia based on what?
The underlying condition that is causing the thrombocytopenia (which is why the mechanism behind the thrombocytopenia is important to identify)
What are the 2 broad reasons why platelets may be low?
- Increased platelet destruction (platelets are being made but are being destroyed)
- Decreased platelet production (not enough platelets are being made)
What can cause increased platelet destruction? (3)
- Infection
- Drug induced (DITP) - usually within 5-10 of starting new medication
- Immune mediated (ITP) - immune reaction which causes platelet destruction
What can cause decreased platelet production?
- Usually due to bone marrow failure
- Chronic alcohol use
- Infection
Thrombocytopenia treatment approaches/options (4)
(treatment is based on underlying mechanism/cause)
- Corticosteroids (if there is an immune component)
- Intravenous immunoglobulin (IVIG) (if immune component)
- Stop offending medication (if drug induced)
- Plasma exchange (if needed to clean out antibodies or drug, but then is also treated with additional drug)
Heparin induced thrombocytopenia (HIT) presentation
This is a life threatening condition after heparin exposure
Presents with thrombocytopenia (reduction in platelets) AND new thrombosis (usually DVT or PE)
How does HIT occur?
occurs 5-10 days after heparin exposure
(due IgG antibodies forming immune complexes)
Less likely to happen with LMWH than unfractionated heparin infusion
Dose and duration dependent (DDD)
How is HIT classified? (4 factors)
4Ts classification:
1. Thrombocytopenia level
2. Timing of onset
3. Thrombosis (new vs progression of previous)
4. Other causes
HIT treatment (3 options)
First line: direct thrombin inhibitors
-argatroban, bivalirudin, dabigatran
Warfarin
-not used much, only if platelets are high (>150,000) or if patients have renal impairment (can’t use direct thrombin inhibitors with renal impairment)
Xa inhibitors
-Fondaparinux, edoxaban, rivaroxaban and apixaban
What is pancytopenia? How does it present?
Pancytopenia is when everything is low - RBCs, WBCs, and platelets
So, presents with BIA…
B = bruising and bleeding (due to low platelets)
I = infection (due to low WBCs)
A = anemia (due to low RBCs)
What are causes of pancytopenia (3) Why is this important to know?
Usually bone marrow dysfunction related…
Bone marrow underproduction
-aplastic anemia, toxins, drugs, SLE, radiation
Bone marrow infiltration
-malignancy, nutritional deficiencies (vitamin b12, folate, copper)
Peripheral destruction of blood cells
-immunologically mediated - autoimmune (SLE)
Splenic Sequestration
-occurs in cirrhosis
It is important to know what the cause is because that determines how we treat it
Why is anemia common in cancer patients?
Chemotherapy
-destroys stem cells
-decreases erythrocyte production
-decreases life span of RBCs
Radiation
-decreases RBC production
Tumors
-cause hemorrhage
-can replace bone marrow with malignant cells
-can release cytokines that decrease erythrocyte production
EPO for cancer associated anemia considerations
exogenous erythropoietin (EPO) is an option to increase RBC production in cancer associated anemia
However, it should only be used if cancer is not curative and hemoglobin is < 10 and the patient is suffering
With cancer, bone marrow is suppressed, giving EPO keeps pushing bone marrow to produce RBCs, but it is already week - will not lead to positive outcomes = puts patients at risk of side effects of EPO without the benefit
So can be used as a palliative approach maintain a goal hemoglobin at the lowest concentration needed to avoid transfusions
What is normocytic anemia usually caused by?
Cancer (disease or chemo induced)
or CKD
How can we improve hemoglobin response in patients with normocytic anemia associated with cancer or CKD?
By providing iron
-we want to improve the hgb response and avoid transfusions
What is aplastic anemia?
Occurs when there is direct damage to pluripotent hematopoietic stem cells before they can differentiate into committed stem cells
-results in decreased production of all blood cells (erythrocytes, neutrophils, and platelets)
Can happen at any age, can be mild or severe, gradual or rapid, is difficult to treat
Can be drug induced but this is very rare (The highest incidence occurs in ages 10-25 years old and >60 years old)
Aplastic anemia diagnosis criteria
Diagnosed if at least TWO of the following are present
-Neutropenia - WBC ≤ 3500 cells/mm3
-Platelet count ≤ 55,000 cells/mm3
-Hgb ≤ 10 g/dL
-Reticulocyte count ≤ 30,000 cells/mm3
(everything is low, even reticulocytes, because the stem cells cannot even differentiate into those)
How is aplastic anemia classified?
►Moderate: at least 2 of the following: neutrophils < 1500 cells/mm3, platelets < 50,000 cells/mm3, Hgb < 10 g/dL
►Severe: at least 2 of the following: neutrophils < 500 cells/mm3, platelets < 20,000 cells/mm3, reticulocyte < 1%
►Very severe: severe aplastic anemia with neutrophil count < 200 cells/mm3
How is aplastic anemia treated?
Polyclonal IgG (ATG)
or calcineurin inhibitor (cyclosporine)
Many patients require combination therapy:
ATG + cyclosporine + prednisone + eltrombopag
What are the 2 types of ATG and which one is preferred for aplastic anemia?
(polyclonal IgG antibody)
There are 2 types:
Atgam (horse derived) and Thymoglobulin (rabbit derived)
Atgam (horse derived) is preferred because it has a higher response rate and higher 3 year survival rate
Atgam administration consideration
(this is the horse derived ATG)
A test dose is recommended because patients can experience serum sickness
And patients should be premedicated with acetaminophen, diphenhydramine, and glucocorticoids (to prevent serum sickness)
