blood part 3 bleeding disorders, blood type Flashcards
Hemostasis
Fast series of reactions for stoppage of bleeding
Hemostasis steps
Vascular spasm
Platelet plug formation
Coagulation (blood clotting)
Vascular Spasm
Vasoconstriction (blood vessel constriction) of damaged blood vessel
triggers for vascular spasm
Direct injury
Chemicals released by endothelial cells and platelets
Pain reflexes
is Platelet Plug Formation positive or negatuve feedback loop
positive feedback cycle
Platelet Plug Formation: At site of blood vessel injury, platelets
Stick to exposed collagen fibers with the help of von Willebrand factor (plasma protein)
Swell, become spiked and sticky, and release chemical messengers
in platelet plug formation ADP
causes more platelets to stick and release their contents
in platelet plug formation Serotonin and thromboxane
enhance vascular spasm and more platelet aggregation
coagulation
A set of reactions in which blood is transformed from a liquid to a gel
Reinforces the platelet plug with fibrin threads
Three phases of coagulation
Prothrombin activator is formed (intrinsic and extrinsic pathways)
Prothrombin is converted into thrombin
Thrombin catalyzes the joining of fibrinogen (soluble form) to form a fibrin mesh (insoluble form)
coagulation intrinsic pathway
Is triggered by negatively charged surfaces (activated platelets, collagen, glass)
Uses factors present within the blood (intrinsic)
coagulation extrinsic pathway
outside blood, Is triggered by exposure to tissue factor (TF)
Bypasses several steps of the intrinsic pathways so Faster
how long does it take clot to form
3-5 minutes
Clot Retraction
Actin and myosin in platelets contract within 30–60minutes
Platelets pull on the fibrin strands, squeezing serum from the clot
Clot Repair PDGF
Platelet-derived growth factor (PDGF) stimulates division of smooth muscle cells and fibroblasts to rebuild blood vessel wall
clot repair VEGF
Vascular endothelial growth factor (VEGF) stimulates endothelial cells to multiply and restore the endothelial lining (inside wall)
Fibrinolysis
break down fibrin
Plasminogen in clot is converted to plasmin
Plasmin is a fibrin-digesting enzyme
hemostasis full steps
vascular spasm (close off side of vessel)
platelet plug (ADP, Thromboxan)
coagulation (extrinsic or intrinsic) forms prothrombin activator
prothrombin to thrombin
firbrogin to fibrin
‘forms cross linked fibrin mesh
clot retraction (squeeze out fluid)
clot repair (endotheial GF replaces inner wall, platelet GF replaces vessel wall)
fibrinolysis
plasminogen turns into plasmin
break down fibrin
Two homeostatic mechanisms prevent clots from becoming large
Swift removal and dilution of clotting factors
Inhibition of activated clotting factors
why can we run out of thrombin
Most thrombin is bound to fibrin threads, and prevented from acting elsewhere
inhibition of clotting factors
thrombin not being able to be reused
heparin (anticoagulant that inhibits thrombin)
Platelet adhesion (preventing undesirable clotting) is prevented by
Smooth endothelial lining of blood vessels
Antithrombic substances nitric oxide and prostacyclin secreted by endothelial cells
Thromboembolytic disorders
undesirable clot formation
Bleeding disorders
abnormalities that prevent normal clot formation
Thrombus
clot that develops and persists in an unbroken blood vessel
May block circulation, leading to tissue death
Embolus
a thrombus freely floating in the blood stream
Pulmonary emboli
impair the ability of the body to obtain oxygen
Cerebral emboli
can cause strokes
Thromboembolytic Conditions are prevented by
blood thinners
asprin, heparin, warfarin
Disseminated Intravascular Coagulation (DIC)
Widespread clotting blocks intact blood vessels
Severe bleeding occurs because residual blood unable to clot
1,001 cuts and dies
Disseminated Intravascular Coagulation (DIC) most common in
pregnancy, septicemia, or incompatible blood transfusions
Thrombocytopenia
deficient number of circulating platelets
Thrombocytopenia due to and treated with
Due to suppression or destruction of bone marrow (e.g., malignancy, radiation)
Treated with transfusion of concentrated platelets
bleeding disorder Impaired liver function
Inability to synthesize procoagulants
Liver disease can also prevent the liver from producing bile, impairing fat and vitamin K absorption
liver impair causes
Causes include vitamin K deficiency, hepatitis, and cirrhosis
Hemophilias
include several similar hereditary bleeding disorders, caused by specific missing clotting factor
hemophilia most common
type A
hemophilia symptoms
prolonged bleeding, especially into joint cavities
hemophilia treatment
Treated with plasma transfusions and injection of missing factors
Whole-blood transfusions are used when
are used when blood loss is substantial
example shark attack, loss of limb
Packed red cells transfusion
(plasma removed) are used to restore oxygen-carrying capacity
what happens with Transfusion of incompatible blood
it can be fatal
spirocytosis use what transfusion
packed red blood cells
sickle cell anemia use what transfusion
packed red blood cells
lack of clotting factors use what transfusion
plasma transfusion
aplastic anemia use what transfusion
packed reed blood cells
what happens with hemorrage and use packed red blood cell transfusion
increase viscosity and can cause shock and stroke
how do you classify blood cells into different groups
Presence or absence of each antigen is used to classify blood cells into different groups
Agglutinogen
antigen
agglutinin
antibody
blood types
Types A, B, AB, and O
Based on the presence or absence of two agglutinogens (A and B) on the surface of the RBCs
blood testing in different antigens
if clump, the opposite of that anitigen is present
ex antigen A clumps, means type A
type A
antigen b, recieve only A,O
type B
antigen A, recieve only B,O
Type AB
no antigens, recieve all
Type O
all antigens, recieve only O
Rh Blood Groups
There are 45 different Rh agglutinogens (Rh factors)
C, D, and E are most common
rH D indicates
positive if clumps
How are anti-Rh bodies formed
When anRh- individual receives Rh+ blood, and a second exposure will cause problems
erythroblastosis fetalis
Rh– mother becomes sensitized when exposure to Rh+ blood causes her body to synthesize anti-Rh antibodies
Anti-Rh antibodies cross the placenta and destroy the RBCs of an Rh+ baby
`erythroblastosis fetalis treatment
The baby can be treated with prebirth transfusions and exchange transfusions after birth
a serum containing anti-Rh can prevent the Rh– mother from becoming sensitized
what happens if mismatched blood is transfused
Donor’s cells
Are attacked by the recipient’s plasma agglutinins
Agglutinate and clog small vessels
Rupture and release free hemoglobin into the bloodstream
what does a mismatch transfusion result in
Diminished oxygen-carrying capacity
Hemoglobin in kidney tubules and kidney failure
difference between wrong small transfusions and wrong large transfusino
small hurt you
large kill you
Death from shock may result from
low blood volume
low blood volume from shock must be replaced
Normal saline or multiple-electrolyte solution that mimics plasma electrolyte composition
Plasma expanders
plasma expanders
Mimic osmotic properties of albumin
More expensive and may cause significant complications
why is adding more RBCs when you have a low blood volume counterproductive
increase blood viscosity
Diagnostic Blood Tests
Hematocrit Blood glucose tests Microscopic examination hemoglobin hbA1c test (blood gluose over past months) CMP, a blood chemistry profile
Complete blood count (CBC)
CBC = RBC + WBC
RBC average count
4.5 million
WBC average count
5-10 million
if bilirubin high means
liver or bile duct problem
high GGT and AP means
bile duct blockage
high BUN means
means something wrong with kidneys
high arcatinine means
something wrong with kidneys
protein in urine means
shot kidneys
