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Anatomy > blood part 3 bleeding disorders, blood type > Flashcards

blood part 3 bleeding disorders, blood type Flashcards

1
Q

Hemostasis

A

Fast series of reactions for stoppage of bleeding

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2
Q

Hemostasis steps

A

Vascular spasm
Platelet plug formation
Coagulation (blood clotting)

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3
Q

Vascular Spasm

A

Vasoconstriction (blood vessel constriction) of damaged blood vessel

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4
Q

triggers for vascular spasm

A

Direct injury
Chemicals released by endothelial cells and platelets
Pain reflexes

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5
Q

is Platelet Plug Formation positive or negatuve feedback loop

A

positive feedback cycle

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6
Q

Platelet Plug Formation: At site of blood vessel injury, platelets

A

Stick to exposed collagen fibers with the help of von Willebrand factor (plasma protein)
Swell, become spiked and sticky, and release chemical messengers

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7
Q

in platelet plug formation ADP

A

causes more platelets to stick and release their contents

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8
Q

in platelet plug formation Serotonin and thromboxane

A

enhance vascular spasm and more platelet aggregation

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9
Q

coagulation

A

A set of reactions in which blood is transformed from a liquid to a gel
Reinforces the platelet plug with fibrin threads

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10
Q

Three phases of coagulation

A

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)

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11
Q

coagulation intrinsic pathway

A

Is triggered by negatively charged surfaces (activated platelets, collagen, glass)
Uses factors present within the blood (intrinsic)

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12
Q

coagulation extrinsic pathway

A

outside blood, Is triggered by exposure to tissue factor (TF)
Bypasses several steps of the intrinsic pathways so Faster

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13
Q

how long does it take clot to form

A

3-5 minutes

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14
Q

Clot Retraction

A

Actin and myosin in platelets contract within 30–60minutes

Platelets pull on the fibrin strands, squeezing serum from the clot

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15
Q

Clot Repair PDGF

A

Platelet-derived growth factor (PDGF) stimulates division of smooth muscle cells and fibroblasts to rebuild blood vessel wall

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16
Q

clot repair VEGF

A

Vascular endothelial growth factor (VEGF) stimulates endothelial cells to multiply and restore the endothelial lining (inside wall)

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17
Q

Fibrinolysis

A

break down fibrin
Plasminogen in clot is converted to plasmin
Plasmin is a fibrin-digesting enzyme

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18
Q

hemostasis full steps

A

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

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19
Q

Two homeostatic mechanisms prevent clots from becoming large

A

Swift removal and dilution of clotting factors

Inhibition of activated clotting factors

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20
Q

why can we run out of thrombin

A

Most thrombin is bound to fibrin threads, and prevented from acting elsewhere

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21
Q

inhibition of clotting factors

A

thrombin not being able to be reused

heparin (anticoagulant that inhibits thrombin)

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22
Q

Platelet adhesion (preventing undesirable clotting) is prevented by

A

Smooth endothelial lining of blood vessels

Antithrombic substances nitric oxide and prostacyclin secreted by endothelial cells

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23
Q

Thromboembolytic disorders

A

undesirable clot formation

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24
Q

Bleeding disorders

A

abnormalities that prevent normal clot formation

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25
Q

Thrombus

A

clot that develops and persists in an unbroken blood vessel

May block circulation, leading to tissue death

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26
Q

Embolus

A

a thrombus freely floating in the blood stream

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27
Q

Pulmonary emboli

A

impair the ability of the body to obtain oxygen

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28
Q

Cerebral emboli

A

can cause strokes

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29
Q

Thromboembolytic Conditions are prevented by

A

blood thinners

asprin, heparin, warfarin

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30
Q

Disseminated Intravascular Coagulation (DIC)

A

Widespread clotting blocks intact blood vessels
Severe bleeding occurs because residual blood unable to clot
1,001 cuts and dies

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31
Q

Disseminated Intravascular Coagulation (DIC) most common in

A

pregnancy, septicemia, or incompatible blood transfusions

32
Q

Thrombocytopenia

A

deficient number of circulating platelets

33
Q

Thrombocytopenia due to and treated with

A

Due to suppression or destruction of bone marrow (e.g., malignancy, radiation)
Treated with transfusion of concentrated platelets

34
Q

bleeding disorder Impaired liver function

A

Inability to synthesize procoagulants

Liver disease can also prevent the liver from producing bile, impairing fat and vitamin K absorption

35
Q

liver impair causes

A

Causes include vitamin K deficiency, hepatitis, and cirrhosis

36
Q

Hemophilias

A

include several similar hereditary bleeding disorders, caused by specific missing clotting factor

37
Q

hemophilia most common

A

type A

38
Q

hemophilia symptoms

A

prolonged bleeding, especially into joint cavities

39
Q

hemophilia treatment

A

Treated with plasma transfusions and injection of missing factors

40
Q

Whole-blood transfusions are used when

A

are used when blood loss is substantial

example shark attack, loss of limb

41
Q

Packed red cells transfusion

A

(plasma removed) are used to restore oxygen-carrying capacity

42
Q

what happens with Transfusion of incompatible blood

A

it can be fatal

43
Q

spirocytosis use what transfusion

A

packed red blood cells

44
Q

sickle cell anemia use what transfusion

A

packed red blood cells

45
Q

lack of clotting factors use what transfusion

A

plasma transfusion

46
Q

aplastic anemia use what transfusion

A

packed reed blood cells

47
Q

what happens with hemorrage and use packed red blood cell transfusion

A

increase viscosity and can cause shock and stroke

48
Q

how do you classify blood cells into different groups

A

Presence or absence of each antigen is used to classify blood cells into different groups

49
Q

Agglutinogen

A

antigen

50
Q

agglutinin

A

antibody

51
Q

blood types

A

Types A, B, AB, and O

Based on the presence or absence of two agglutinogens (A and B) on the surface of the RBCs

52
Q

blood testing in different antigens

A

if clump, the opposite of that anitigen is present

ex antigen A clumps, means type A

53
Q

type A

A

antigen b, recieve only A,O

54
Q

type B

A

antigen A, recieve only B,O

55
Q

Type AB

A

no antigens, recieve all

56
Q

Type O

A

all antigens, recieve only O

57
Q

Rh Blood Groups

A

There are 45 different Rh agglutinogens (Rh factors)

C, D, and E are most common

58
Q

rH D indicates

A

positive if clumps

59
Q

How are anti-Rh bodies formed

A

When anRh- individual receives Rh+ blood, and a second exposure will cause problems

60
Q

erythroblastosis fetalis

A

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

61
Q

`erythroblastosis fetalis treatment

A

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

62
Q

what happens if mismatched blood is transfused

A

Donor’s cells
Are attacked by the recipient’s plasma agglutinins
Agglutinate and clog small vessels
Rupture and release free hemoglobin into the bloodstream

63
Q

what does a mismatch transfusion result in

A

Diminished oxygen-carrying capacity

Hemoglobin in kidney tubules and kidney failure

64
Q

difference between wrong small transfusions and wrong large transfusino

A

small hurt you

large kill you

65
Q

Death from shock may result from

A

low blood volume

66
Q

low blood volume from shock must be replaced

A

Normal saline or multiple-electrolyte solution that mimics plasma electrolyte composition
Plasma expanders

67
Q

plasma expanders

A

Mimic osmotic properties of albumin

More expensive and may cause significant complications

68
Q

why is adding more RBCs when you have a low blood volume counterproductive

A

increase blood viscosity

69
Q

Diagnostic Blood Tests

A 
Hematocrit
Blood glucose tests
Microscopic examination
hemoglobin hbA1c test (blood gluose over past months)
CMP, a blood chemistry profile
70
Q

Complete blood count (CBC)

A

CBC = RBC + WBC

71
Q

RBC average count

A

4.5 million

72
Q

WBC average count

A

5-10 million

73
Q

if bilirubin high means

A

liver or bile duct problem

74
Q

high GGT and AP means

A

bile duct blockage

75
Q

high BUN means

A

means something wrong with kidneys

76
Q

high arcatinine means

A

something wrong with kidneys

77
Q

protein in urine means

A

shot kidneys

Anatomy (29 decks)

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