Module 2 - Leukocytes Flashcards
Leukocytosis
WBC count is high
*Normal protective response to physiological stress
Leukopenia
WBC count is low
Lack of neutorphils
*this is never normal
Absolute WBC count below 4 x 10^9/L
List causes of LEUKOPENIA
Radiation
Chemotherapy
anaphylaxis
auto-immune disorders
Immune deficiencies
List the causes of LEUKOCYTOSIS
Normal response to infection/inflammation
Malignancies
surgery
pregnancy
injury
exercise
emotional stress
Medicaitons, hormones, toxins
Define Neutrophilia
Early stage of infection or inflammation
Absolute count exceeds 7.5 x 10^9/L
What is “Shift to the left”
Release of immature neutrophils
Occurs when demand > supply (severe infection)
Define Neutropenia
Decrease in circulating neutrophils
Defined a a count less than 2 x 10^9/L
Can result from prolonged infection
Define Eosinophilia
> 4.5 x 10^9/L
Allergic disorders type I (asthma) and dermatological disorders
Define Basophilia
increase in circulating basophils
response to inflammation and hypersensitivity reactions
release histamines
Define Monocytosis
increase in number of circulating monocytes (macrophages)
Usually occurs in later stage of infection, with chronic infection, when phagocytosis is needed and neutropenia
Define Thrombocytopenia
Decrease in number of platelets
< 150 x 10^9/L
What are the CAUSES of thrombocytopenia
Increase consumption of platelets
decrease in production of platelets
What is HIT
Heparin Induced Thrombocytopenia
What is the pathophysiology of HIT
Immune mediated adverse drug reaction
IgG antibodies against heparin-patlet factor 4 complex leading to platelet activation
Results in increased clotting, decreased platelet count
When does HIT occur
5-10 days after starting heparin treatment
What are the SYMPTOMS of HIT
Platelet consumption and clots
decrease in platelet count 5-10 days after initiation of heparin
Bleeding is rare
What does DIC stand for
Disseminated Intravascular Coagulation
What is DIC
Acquired clinical syndrome characterized by wide spread activation of coagulation resulting in fibrin clots to medium and small vessels throughout the body. Can lead to multi-system organ failure and bleeding
Causes of DIC
Retaining pregnancy tissues
Sepsis
Widespread trauma
Cancer
What is the PATHOPHYSIOLOGY of Disseminated Intravascular coagulation
Excessive widespread exposure to TF (tissue factor)
Tissue factor binds and activates VII which activates the extrinsic clotting pathway leading to fibrin and thrombin
Why does haemorrhage occur in DIC
consumption of platelets for clotting exceeds production
What laboratory test can be used to diagnose DIC
Clinical symptoms
D-Dimers
Produced in the degredation of fibrin clots by plasmin
What is the TREATMENT of DIC
(1) end the underlying pathology
(2) Support organ function
(3)control thrombosis
- heparin?
- replace clotting factors?
- fluids (restore BP, UO, CO)
What is a Thrombus
A clot that is attached to the vessel wall
What is the difference between VENOUS thrombi and ARTERIAL thrombi
Venous thrombi - RBC and fibrin, low flow
Arterial thrombi - platelets and firbin, high flow
What is the TREATMENT for Thrombi
(1) Anticoagulant therapy - Venous thrombus only
(2) Remove the clot
What medications activate fibrinolysis
And what is the risk of these medications
Urokinase
streptokinase
alteplase
*risk of hemorrhage
What is the PATHOPHYSIOLOGY of arterial thrombus formation
- atheroscelerosis plaque
- turbulent blood flow
- exposure of basal lamina (collagen)
- slowing of blood flow
- activation of platelets
What is the PATHOPHYSIOLOGY of venous thrombus formation
- stasis of blood flow
- slows down, platelets contact with endothelium for long periods
What are the most common clinical conditions that predispose someone to venous stasis
- surgery
- bed rest > 1 week
- paralysis
- malignancy
- MI, heart surgery
- age
