Heme/Onc basics Flashcards
RBCs
- nuclei +/-
- shape
- filled with what
- life span
no nuclei
biconcave– filled with hemoglobin
life span=120 days
Neutrophils
- Nucleus +/-
- contain?
- function
- life span
- 3-5 nuclear lobes
- cytoplasm with pale, lilac colored granules
- phagocytes
- provide protection from acute infections
- life span 5 hours-few days
Basophils
- nucleus +/-
- role
lack nuclear segmentation–dots everywhere
role=similar to eosinophils
- phagocytic
- help fight acute infections
eosinophils
- nucleus +/-
- role?
two nuclear lobes
roles
-chronic immune responses–>helminth worm infections, asthma and allergies
Monocytes
- nucleus +/-
- roles
- life span
kidney shaped nucleus in light blue cytoplasm
- highly phagocytic
- life span is long
- keep “watch” detecting danger signals produced by infection or tissue injury
Lymphocytes
- key role in?
- structure
- types
key role in adaptive immunity
- condensed nuclei and scant cytoplasm
- B cells
- t cells
- NK cells
where are B cells made
where are T cells made
B cells–>bone marrow
T cells–>thymus (transformed in thymus)
eosinophil
monocyte
lymphocyte
neutrophil
basophil
bone marrow produces how much:
- rbc
- platlets
- neutrophils
RBC= 200 billion
platelets=100 billion
neutrophils=60 billion
define hematopoiesis
production of RBCs and platelets in the bone marrow
cytopenia
too few blood cells
cytoses
too many blood cells
what maintains hematopoeisis
hematopoietic stem cells (HSCs)
what is technically transplanted
hematopoietic stem cells
define hemostasis
stopping of blood flow
clot formation starts with
platelet plug at the site of vessel injury–> PRIMARY PLAT PLUG
steps in hemostasis
- primary platelet plug
- once platelets adhere to vessel wall—triggers platelet activation–>changes plat shape from circle to a spiky sea urching shape–>incrs surface area of platelet + changes platelet membrane glycoproteins—->allows it to bind to fibrinogne
- plat activation results in release of arachidonic acid–>converted to thromboxane A2 (protent inducer of platelets via series of enzymes Cyclooxygenase)
what happens after platelets are activated during hemostasis
- shape changes from circle–>spiky sea urchin
- surface area incrs with shape change
- shape change also changes plats membrane glycoproteins–lets them bind to fibrinogen
- arachidonic acid released–>converted to Thromboxane A2–>inducer of platelets via series of enzymes including Cyclooxygenase
cyclooxygenase
- what is it
- what activates it
enzyme that activates platelets
**thromboxane A2 activates platelets thru this enzyme
ASA contains what
cyclooxygenase inhibitors
-why ASA is used to suppress platelet activation
coagulation cascade
-three pathways and their factors invovled + lab work to test for the pathway
- INTRINSIC PATHWAY
TEST=aPartial Thromboplastin Time (aPTT)
*FACTORS: XII, XI, IX, VIII, X
12, 11, 9, 8, 10 - EXTRINSIC
TEST= prothrombin time (PT)
FACTORS: VII, X
7 and 10 - COMMON PATHWAY
X from extrinsic and intrinsic
X–> Xa–>prothrombin (II) + thrombin–>Fibrinogen (I)–> FIBRIN CLOT
Lab assessments of the coagulation cascade
-what are the initial tests of blood coagulation cascade
INITIAL TESTS
- Plat count
- prothrombin time (PT)
- partial thromboplastin Time (PTT) aka aPTT
Platelet Count
- normal?
- below normal means? s/s?
> 100,000 per microliter
BELOW= takes LONGER time to clot
s/s: purpura + mucosal bleeding
Prothrombin Time (PT)
- normal?
- this is testing what?
- abnormal time?
- testing of the extrinsic pathway
- Normal 10-13 seconds— time it takes for blood to clot
- LONGER=deficiency in one or more of the clotting factors in extrinsic pathway–>aka FACTORS VII****, X,
INR
- stands for
- dervied from?
international normalized ratio
- derived from PT
- same as PT— but it is “standardized” by taking into account the potency of the tissue factor—–whifh is what is added to the plasma to perform the PT used
aPTT
- stands for
- normal?
- what is added
- which pathway
Activated PARTIAL thromboplastin TIME
- normal (time takes for blood to clot) is 25-35 secs
- Kaolin is added to plasma–>activates factor XII–>starts INTRINSIC cascade (factors XII, XI, IX, VIII, X, prothrombin and fibrinogen)
Thrombin TIme
- when is this done
- tests?
- extra test— only done if there is a coagulation problem
* THROMBIN TIME (TT)–>tests functionality of fibrinogen and presence of thrombin inhibitors (heparin, etc)
patients with inherited bleeding disorders usually have ____ deficiencies present
only a single
patients with an acquired bleeding problem, they will have _____ deficiencies
multiple
***acquired problems like vit K deficiency or liver dz
list the common anticoag drugs
- VIT K ANTAGONISTS–warfarin
- HEPARIN
- LOW MOLECULAR WEIGHT HEPARIN
vitamin K anatagonist
- what do they do
- MC ? route?
- what is monitored when pt on this
**block or slow down clotting by affecting VII, IX and X and prothrombin–>bc they all need vit K for carboxylation
MC=warfarin–PO
-pt must be monitored closely–PT/INR testing–>make sure anti-coagulation is within therapeutic range
Heparin
- moa
- route
activates anithrombin
- inhibits several steps in cascade
- IV***
low molecular weight heparin
- route
- moa
sc
*doesnt require intensive monitoring—but also doesnt work as fast
direct inhibitor drugs
- what are they
- general moa
new oral anticoags that directly inhibit activated coagulation factors—— INDIRECTLY affects many parts of the coag cascade
define sequestration
- where is it done
- can cause?
- spleen
- spleen takes 1/3 of body’s platelets to store them
- pt with splenomegaly have higher proportion of their platelets entrapped along with RBCs and WBCs
- significant reduction in one or more of peripheral blood counts due to sequsetration is called–>HYPERSPLENISMh
hypersplenism
- what is it
- what happens to plat count
sig reduction in one or more of the peripheral blood counts by splenic sequestration
**PTs with it generally have plat counts of 50,000-120,000 per microliter—- not really low enough to pose a serious risk of hemorrhage
