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year 1 flash cards > TOPIC 8 - blood bois > Flashcards

TOPIC 8 - blood bois Flashcards

1
Q

what is blood?

A
  • viscous fluid pumped by heart and vascular system
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2
Q

what does blood contain?

A

RBC
WBC (immunoglogy)
platelets (clotting)
contains plasma

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3
Q

volume of blood?

A

5 liters

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4
Q

function of blood

A
  • hydration of tissues
  • delivery of oxygen and nutrients
  • delivery of endocrine hormones
  • regulate body temp+pH
  • fight infection -immune response initiation
  • prevent own blood loss through blood clotting
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5
Q

erythrocytes background check

A
  • most abundant blood cell
  • for oxygen transport mainly - Fe v important in this
  • no nucleas/anucleate
  • no mitochondria= all energy from glucose in glycolytic pathway
  • contain haemoglobin = regulates O2 transport
  • also delivery= glucose, AA, fatty acids, vitamins, minerals
  • collect waste products from tissues to drop off at organs: kidneys and liver
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6
Q

examples of endocrine hormones

A
  • insulin - B cells in pancreas
  • Oestrogen, progesterone, testosterone- overs/testies
  • vasopressin - prosternar pituatary lobe
  • Adrenalin - adrenal medulla
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7
Q

regulating body temp

A
  • absorb heat via vasodilation and constriction
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8
Q

regulating body pH

A
  • maintenance of fluid volume ions and proteins to prevent fluid loss of our blood into inerstitial spaces
  • maintenance pH proteins act as buffers to prevent changes in pH
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9
Q

how do we Prevent blood loss- Haemostasis

A
  • platelets: small and anucleate = clump together

- Blood coagulation;ation pathway: through formation of thrombin clot

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10
Q

common progenitor cell of all blood cells?

A

multi potential haematopoietic stem cell

made in bone marrow

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11
Q

2 major lineages from the multi potential haematopoeitic stem cell?

A

myeloid
lymphoid
both in bone marrow

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12
Q

lineage of myeloid (4 cells) and where formed

A

megakaryocyte (bone marrow)
erythrocyte (blood/lymph)
mast cell (tissue)
myeloblast (bone marrow)

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13
Q

lineage of myeloblast?

A 
basophil
neutrophil
eosinophil
monocyte 
all in blood/lymph
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14
Q

lineage of monocyte?

A

macrophage - in tissue

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15
Q

lineage of lymphoid

A

natural killer cell- eg. large granular lymphocyte
small lymphocyte
all in blood and lymph

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16
Q

lineage of small lymphocyte

A

T cells
B cells – turn to plasma cells
in blood/plasma

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17
Q

how does blood coagulation work?

A 
platelets = activated on exposure of injury
blood coagulation fibrin forms mesh work
traps other cells 
forms haemopoatic plug 
blood cant escape
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18
Q

what test is used for diagnosis of haemotogical diseases ?

A

peripheral blood smears

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19
Q

using blood plasma as diagnostic

A
  • put in tube with anticoagulant = prevent clotting

blood plasma contains blood coagulation and immune system factors

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20
Q

most abundant blood plasma proteins?

A
  • albumin
  • immunoglobulins (for infection)
  • fibrinogen (for clotting)
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21
Q

what is the significance of hematocrit?

A

important component made by RBCs
marker of blood tea;th
changes in this = indicator of disease

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22
Q

using blood serum as diagnostic

A

allowed to clot before centrifuged

has no clotting factors

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23
Q

how are blood groups classified?

A

based on antigens of RBC membrane

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24
Q

what does mixing of incompatible blood groups lead to?

A

endogenous antibodies (self antibodies) react with antigens on RBC membrane
get cross reaction in RBC
RBC carrying a foreign antigen = immune response
= aggregation
=blood vessles blocked
= eventually RBC lysis

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25
Q

what are agglutinogens?

A

antigens

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26
Q

what are agglutinins

A

antibodies in plasma

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27
Q

blood group A features?

A

A antigens on RBC

anti B antibodies in plasma

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28
Q

blood group B features?

A

B antigens on RBC

anti A antibodies in plasma

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29
Q

blood group O?

A

no antigens
anti A and anti B antibodies in plsma
universal donor

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30
Q

blood group AB

A

both A and B antigens
no antibodies
universal receptor

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31
Q

agglutinins function

A

bind to agglutinogens
not carried by RBC
cause agglutination

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32
Q

what is acute haemolytic reaction

A

happens when RBC lysis

due to incompatable blood groups mixing

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33
Q

symptoms of acute hemolytic reaction

A

systemic: chills, fever
vascualr: hypotension, uncontrolable breating
heart: increased heart rate
chest: contracting pain
lumbar region: pain
kidney fialure
bleeding

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34
Q

what are rhesus (Rh) blood groups?

A

based on ion channel antigen on RBC memrbane
Rh+ = common = A+ (has Rh antigen on surface)
Rh- = rare = A- (No Rh antigen on surface)
mixing of two= just don’t do it

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35
Q

Rh- mixing with Rh+

A

RBCs contain no Rh agglutinogens

agglutinins against Rh+ RBCsb produced

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36
Q

how does haemolytic syndrome in the foetus occur?

A

in 1st pregnancy:

  • mother protected by the placenta-blood barrier = not exposed to Rh agglutinogens until time childbirth due to placental tearing
  • anti-Rh agglutinins generate and antibodies circulate
  • in 2nd preganacy: antibodies cross placental barrier- born with severe anemia
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37
Q

what are the three phases to the circulatory haemostatic process?

A

hemorrhage - bleeding
thrombosis - clotting
fibrinolysis - clot dissolution

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38
Q

what systems interact for haemostasis?

A
  • blood vessels
  • platlets
  • coagulation system
  • fibrinolytic system
  • inhibitors of the above
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39
Q

what is a vascular spasm?

A

at the site of injury the blood vessel constricts to reduce blood flow and therefore blood loss

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40
Q

what is the primary response?

A

platelet, endothelial and fibrinogen mediated

- temporary platelet plug forms to prevent blood loss

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41
Q

outline the key steps of the primary response

A

A primary plug forms to stop blood loss

  1. adhesion - platelets stick to exposed collagen at injury site and change shape
  2. secretion - granules containing proteins and factors released, attracting more platelets to the site
  3. aggregation - platelets stick together with fibrinogen
  4. activation of coagulation cascade to consolidate the plug
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42
Q

what is the lifespan of a platelet?

A

7-10 days

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43
Q

how are platelets kept in the unactivated state?

A

endothelial cells release chemicals which keeps them in their resting disc shape

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44
Q

outline the 4 phases of platelet shape change

A
  1. flowing disc shape
    - when collagen exposed, it touches the surface and slows down, begins rolling
  2. rolling ball shaped
    - arms begin to stick out, this allows it to grab onto other platelets and slow down (allows them to aggregate)
  3. hemisphere shaped
    - firm but reversible adhesion - first stage of platelet plug
  4. spreading platelet
    - irreversible adhesion
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45
Q

what are the two types of granules in platelets, and what are their roles?

A

dense granules

  • ATP, ADP, serotonin, Ca2+
  • help platelet activation through positive feedback (attracts more platelets to the area)

alpha granules
- factor IV/4, plasminogen activator inhibitor/PAI-1, growth factor, chemokines, platelet derived growth factor
- help coagulation and aid wound healing
overall both amplify haemostaic response

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46
Q

what is the fibrinogen receptor on an activated platelet?

A

⍺IIbß3 - allows activated platelets to aggregate, using fibrinogen as a ‘glue’
when platelet unactivated A11bB3 unable to bind to fibrinigin

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47
Q

what is the collagen receptor on platelets?

A

⍺2ß1

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48
Q

how is potential infection at a injury site prevented?

A

platelets also release chemicals that attract leucocytes, the platelets then grab onto the leucocytes and hold them in place

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49
Q

what triggers the coagulation cascade?

A

tissue factor is released into the blood stream from damaged cells
noramally TF on inside of cell but when cell damaged TF on outside

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50
Q

what does tissue factor activate?

A

factor VII → factor VIIa

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51
Q

what does factor VIIa activate?

A

factor X → factor Xa

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52
Q

what does factor Xa activate?

A

prothrombin → thrombin

NB- all of this activation on activated platelet surface

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53
Q

what does thrombin activate?

A

fibrinogen → fibrin

thrombin produced close proximity to fibrinogen = produces fibrin rapidly

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54
Q

what role does thrombin have in activation?

A

it feeds back and keeps promoting activation of factors and therefore its own production - massive amplification

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55
Q

why is vitamin K necessary for clotting?

A

needed so that clotting factors can bind to platelet surface via Ca2+

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56
Q

BLOOD DISEASES

A

WELCOME XOXO

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57
Q

what are the 4 main disorders of blood?

A

bleeding
thrombosis
hereditary angioedema
complement deficiency

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58
Q

what are 7 the main diseases of blood cells?

A 
haematological malignancies 
sickle cell anaemia 
thalassaemia 
leukopenia 
thrombocytopenia 
infectious mononucleosis 
haemoglobinopathies
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59
Q

definition of blood diseases?

A

affect the quantity and/or function of cells in the blood or proteins in the blood clotting or immune systems

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60
Q

anaemia?

A

decreased no. RBC

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61
Q

leukopenia?

A

decreased no. WBC

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62
Q

thrombocytopenia?

A

decreased no. platlets

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63
Q

erythrocytosis?

A

increased no. RBC

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64
Q

leukocytosis?

A

increased no WBC

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65
Q

thrombocythemia/thrombocytosis?

A

increased no. platletes

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66
Q

what certain factors will cause severe blood loss?

A 
injury (acute)
disease (chronic)
thrombocytopenia 
coagulation deficiencies ( haemophilia)
vitamin K deficiency 
drugs
liver disease 
infection/sepsis
aneurysm rupture
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67
Q

major causes of thrombosis?

A 
atheroscelosis 
cancer
immobilisation
surgery
hypercoagulability 
thrombosythaemia
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68
Q

can retroviruses cause cancer of blood cells?

A

yes - eg. T-lymphotropic virus (HTLV-1)

associated with leukaemiia

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69
Q

whats Burkitt’s lymphoma

A

diseases caused by translocation between c-MYC gene on chromosome 8 with IgH loci on chromosome 4

70
Q

polycythaemia?

A

increased no of RBC

71
Q

thrombocythaemia?

A

increased no. platletes

72
Q

myelofibrosis?

A

increased no. megakaryocyte

73
Q

what are myeloid malignancies?

A

heterozygous disorders
uncontrolled proliferation
and/or blockage of differentiation abnormal myeloid progenitor cells

74
Q

what is chronic myeloid leukaemia?

A

’ the philadelphia chromosome’
translocation between 22 and 9
= leads consecutively active tyrosine kinase
= uncontrolled cell proliferation

75
Q

what is leukaemia?

A

accumulation WBC in bone marrow

76
Q

what does leukaemia do?

A

lead bone marrow failure

  • decreased RBC
  • decreased platelets
  • increased WBC in blood
  • but soon after decreased WBC due to bone a=marrow failure
77
Q

symptoms of leukaemia

A
  • blood hyper-viscosity due increased WBC = causes respiratory / neurological disorders
  • tiredness
  • anemia
  • bleeding
78
Q

what is lymphoma

A

affects lymph nodes
T/B lymphocyte neoplasia
eg. non-hodgkin or hodgkin
characterised: Reed Sternberg cells

79
Q

what are Reed-Sternberg cells

A

originate from B lymphocytes
become enlarged are multinucleate
or bilobed nucleus

80
Q

what are the symptoms of anaemia?

A 
tiredness 
pallor 
fainting 
tachycardia 
shortness of breath
81
Q

what is anaemia caused by?

A

abnormal RBC production/destruction

82
Q

what does anaemia do?

A 
leads to tissue anoxia 
reduction in O2 delivery to tissues 
sends message to kidney (major source of erthoportin)
kidney stimulates RBC production 
negative feedback loop

NB-often ppl w/ kidney disease have anaemia

83
Q

forms of anemia

A 
mild= thallassemia and sickle cell anaemia 
severe= lethal
84
Q

what is erythropoietin

A

drives RBC production

85
Q

role of erythropoietin: steps in process of rbc production

A
  1. anaemia hypoxia
  2. leads to tissue hypoxia
  3. sends message to kidney
  4. kidney releases erythropoietin
  5. erythropoietin sent bone marrow
  6. leads to erythropoiesis
  7. leads to increased RBC mass
86
Q

what is acute anaemia?

A

loss of large amount of blood

87
Q

what is chronic anaemia?

A

blood loss when volume of blood lost exceeds the capability for haematopoiesis of bone marrow

88
Q

example of chronic anaemia

A

bleeding peptide ulcer

89
Q

what is haemolytic anaemia?

A

increased RBC destruction

  • lifespan from 120 to 20 days
  • bone marrow unable replace sufficient RBC
90
Q

what are the two ways we can get haemolytic anaemia?

A

1) acquired - malaria/sepsis/drug induced

2) inherited - G6P dehydrogenase, Autoimmune Hemolytic Anemia

91
Q

different ways we get acquired anaemia

A
  • drug induced
  • snake venom
  • mechanical (heart valves)
  • infections (malaria)
92
Q

different inherited haemolytic anaemias

A

1) RBC cytoskeletal defects: mutation in a or b spectrin

2) RBC enzyme defects - G6PD deficiency

93
Q

why is iron essential in blood?

A

essential element of haem group in Hb

iron deficiency = most common cause anaemia

94
Q

causes of anaemia - iron deffiency

A
  • diet induced
  • blood loss
  • infection
  • growth spurts
  • pregnancy
95
Q

how does low iron lead to anaemia?

A

leads to microcytic anaemia= pale and small RBCs due to reduced Hb production = hypochromic

96
Q

what is hypochromic?

A

less Hb in each RBC

97
Q

what is megaloblastic anaemia?

A

Vitamin B12 or folate deficiency

98
Q

pathophysiology of megaloblastic anaemia

A
  • vit B12 and folate involved in DNA replication
  • deficiency causes problems w/ mitosis or proerythroblast
  • causes megaloblastic or macrocytic anaemia (large RBCs)
99
Q

what is B12 deficiency caused by?

A

reduced absorption

100
Q

what is folate deficiency caused by?

A

poor nutrition
alcoholism
malabsorption
certain drugs

101
Q

cause of sickle cell anaemia

A
  • mutation in HbB globin gene
  • changes AA glu 6 to Val
  • polymerisation of Hb - distorting RBC
102
Q

effect of sickle cell anaemia

A
  • “sickling of RBC”
  • sickle cell crisis due to blockage of microvasculature
  • heterozygosity confers protection against malaria
103
Q

what is Thalassemia

A
  • microcytic anemia
  • defects in alpha or beta chains of Hb
  • leads to ineffective erthropoiesis or hemolysis
104
Q

factors that decrease effectiveness of erythropoietin

A
  • iron deficiency
  • vit B12 deficiency
  • folate deficiency
  • anaemia or chronic disease
105
Q

do we have other reactions which generate thrombin ?

A

Factor 7a also activates factor 9 which generates factor 10a

106
Q

what is the 3 parts to the haemostatic reponse?

A

1- plug hole where damage is (platelets interacting w/ vessel wall) - not v stable
2- consolidate plug: coagulation cascade
3- dissolve plug after healing

107
Q

why must haemostatic response be localised?

A

so we get physiological and not pathological response

108
Q

which haemostatic response results in immediate bleeding?

A 
1' response 
 as it is:
- platelet mediated 
- endothelial mediated
- fibrinogen mediated
109
Q

which haemostaic response results in delayed bleeding?

A

2’ response - as plug not coagulated

  • circulating enzymes
  • platelet mediated
  • fibrin- mediated
110
Q

what does fibrin ensure?

A

forms meshwork that hold platelets together so makes sure plug is stable and not washed away

NB- if plug washed away/ not stable = embolisms

111
Q

what is a quiescent state of a platelet

A

the resting state
before encounter injury
endothelial release chemical in blood to keep them in this phase

112
Q

how to platelets respond to injury so rapidly?

A

undergo ‘explosive’ activation

  • large no. receptors: interact w/ other cells and each other
  • high no platelets: mass action effect
  • rich signalling proteins
  • positive feedback
113
Q

what is the role of stimulatory agonist

A

activation of platelets - at site of injury to outweigh inhibitory agonists

114
Q

what is the role of inhibitory agonists

A
  • away from site of injury
  • ensure we don’t get activation of platelets where we don’t need it
  • helps it stay localised
115
Q

BLEEDING

A

WELCOMIN

116
Q

What are the 2 types of bleeding?

A

1- induced/acquired: trauma, surgery, infection

2- inherited- linked to coagulopathy disorder

117
Q

what can be the causes of an external bleed?

A

trauma

surgery

118
Q

what can be the causes of an internal bleed?

A

haemophillia
aneurysm rupture
drug induced
gastro intestinal

119
Q

what are some bleeding triggers

A 
trauma
surgery
sepsis 
aneurysm rupture
drugs (anticoagulants, aspirin)
vit K deficiency
120
Q

what happens in DIC- disseminated intravascular coagulation

A

step 1- infection
step 2- sepsis- systemic infection
3- intravascular TF exposure (TF usually inside cells)
4a- systemic coagulation activation leads to microvascular clots - using up clotting factors faster than making them
4b- consumption of clotting factors and platelets in excess leads to bleeding -as liver can’t produce clotting factors fast enough and bone marrow megakaryocytes can’t release platelets fast enough
(4a and 4b happen simultaneously both lead to):
multiple organ failure

121
Q

what is bleeding a consequence of in DIC

A

a systemic infection

122
Q

what happens in AAA- abdominal aortic aneurysm

A
  • progressive dilation of abdominal aorta
  • high risk of rupture if aneurysm too large
  • rupture- major bleeding - 50% deaths
123
Q

why is vit K importnant?

A

-required for processing of factors 2,7,9,10
and proteins C and S
-vit K = cofactor for enzyme in this reaction

124
Q

how does vit K work processing these factors?

A

1-precursor forms of factors 2,7,9,10 and proteins C and S undergo reaction with carboxyglutamic acid
2-enzyme catalyses reaction
3-result in completed forms of above factors and proteins

125
Q

what happens in vit K deficiency?

A
  • ineffective coagualtion factors produced
  • will effect bleeding consequences
  • major impact on coagulation cascade
126
Q

what is warfin and why is it used?

A
  • anticoagulant
  • used when overactive haemostaic response
  • inhibits epoxide reductase = so coagulation cascade
127
Q

consequences of vit K deficiency

A
  • malnutrition
  • fat malabsorption
  • liver disease
  • due to vit K antagonists- eg.warfarin
  • can be reversed by administration of vit K = rapid production coagulation protein by liver
128
Q

what is haemostasis thromcoytopenia/ thrombastenia?

A

loss / dysfunction of platlets

129
Q

through what is thromcoytopenia/ thrombastenia acquired ?

A 
Leukaemia
Blood loss
Disseminated intravascular coagulation (DIC)
Drug-induced
Immune thrombocytopenic purpura (ITP)

All lead to reduced platelet coats = high risk of bleeding

130
Q

what are the 3 primary causes of inherited bleeding?

A
  • Platelet dysfunction
  • Coagulation factor deficiency or haemophilia (severe)
  • Thrombocytopenia (mild)
131
Q

what are the symptoms of a coagulation factor defect?

A
  • large bruising
  • slight bleeding from cuts
  • bleeding day after surgery
132
Q

what are the symptoms of platlets disorders?

A
  • small bruising
  • profuse bleeding from cuts
  • common nosebleeds
  • immediate bleeding after surgery
133
Q

what happens in diseases Von Willebrand syndrome and Bernard-Soulier syndrome?

A

Defects in platelet-platelet interaction.

platelets bind to site of injury but platelets don’t stick together= no aggregation

134
Q

what happens in diseases Glanzmann thrombasthenia.

and Congenital afibrinogenemia.

A

Defects in platelet granules, secretion and signal transduction.
so when platelets aggregate can’t consolidate themselves = no positive feedback

135
Q

is haemophilia A or B an X-linked disorder?

A

both

NB- severity level is consistent between family members as same mutation is carried

136
Q

what happens in haemophilia?

A

insufficient thrombin generation

=major effect on coagulation cascade

137
Q

what are the sevrity levels in haemophillia?

A

-Normal (factor VIII or IX level = 50-150%)
-Mild hemophilia
(factor VIII or IX level = 6-50% )
-Moderate hemophilia
(factor VIII or IX level = 1-5%)
Severe hemophilia
(factor VIII or IX level = <1%)

138
Q

what are the consequences of uncontrolled bleeds in haemophilia?

A
  • bruising
  • joint bleeding and destruction

after repeated joint bleeds= inflammation= stiff joint = lock joint syndrome

139
Q

how can we find out if someone is missing a clotting factor in their blood?

A
  • mix plasma of healthy person and diseased patient
  • clotting time should be restored
  • now we do genetic test
140
Q

which pathway does the APTT- activated partial thromboplastin time test?

A

looks at factors in the intrinsic pathway

141
Q

which pathway does PT - prothrombin time test?

A

factor 7

142
Q

if clotting time is not corrected after mixing with normal plasma- what does this imply?

A

due to inhibitors- has induced autoimmune response

143
Q

THROMBOTIC DISEASE

A

WELCOME X

144
Q

what is thrombosis?

A

formation of a blood clot inside the vessel, blocking blood circulation

145
Q

what are the consequences of thrombosis?

A

ischaemia (tissue death), malfunction, pain or swelling in the organ or tissue affected

146
Q

what are the main thrombotic disorders of arterial thrombosis?

A
  • Myocardial infarction (MI; heart)
  • Atrial fibrillation (AF; heart)
  • Peripheral vascular disease (PVD; leg)
  • Stroke (brain)
147
Q

what are the main thrombotic disorders of Venous thrombosis?

A
  • Deep vein thrombosis (DVT; arm/leg)

- Pulmonary embolism (PE; lungs)

148
Q

what 3 things were included in virchow’s triad?

A
  • stasis
  • vessel wall injury
  • hypercoagulability
149
Q

what happens in the arterial thrombosis disorders?

A

-rupture of the atherosclerotic plaque= uncontrolled platelet activation

150
Q

what is an atherosclerotic plaque?

A

deposition of lipids in from LDL in blood vessel wall: inflammation of the vessel wall with infiltration of macrophages (> foam cells) and fat deposits >

151
Q

is the thrombus of the venous or arterial thrombosis platelet rich?

A
  • thrombus of the arterial thrombosis is platelet rich

- that of the venous is RBC and fibrin rich

152
Q

risk factors of arterial thrombosis?

A
  • Advanced age
  • Smoking
  • Diabetes
  • Hypertension
  • Cholesterol
  • Poor diet
  • Lack of exercise
  • Ethnicity
153
Q

what are the 3 main phases of arterial thrombosis thrombotic response?

A
  • Plaque fissure or rupture
  • Adhesion and activation of platelets
  • Activation of coagulation cascade
154
Q

how does the plaque rupture in arterial thrombosis?

A
  • lipids accumulate + become cytotoxic and oxidised
  • change function of cells on top plaque
  • plaque= unstable = cracks open= thrombus
155
Q

which blood vessels are affected in arterial thrombosis?

A

those supplying heart tissue

Myocardial tissues= starved of oxygen = physical damage = cardiac arrest

156
Q

what are the 2 types of arterial thrombi?

A
  • mural thrombi
  • occlusive thrombi

NB both due to controlled platelet division

157
Q

what are the main features of mural thrombi?

A
  • not occlude vessel
  • unstable angina
  • transient ischaemic attack
158
Q

what are the main features of occlusive thrombi?

A
  • occludes vessel
  • myocardial infarction
  • cerebral infarction
159
Q

arterial thrombosis thrombotic response?

A
  • platelets bind collagen and exposed to oxidised lipids from plaques
  • activation platelets
  • release of ADP and TxA2
  • expansion thrombus
  • reduced availability of endothelial NO and PGI2
  • occlusive thrombi
160
Q

name the 3 factors that drive expansion of thrombus in arterial thrombosis

A
  • ADP (released on dense granuals)
  • TxA2 (from arachidonic acid)
  • thrombin ( coagualtion cascade)
    NB- there action promoted by oxidised lipids
  • they reduce actions of inhibitors- NO and PGI2
161
Q

how do we treat atherothrombosis?

A

Antiplatelets:
–Aspirin - inhibits what drives platelet activation
–Anti aIIbb3 -receptor for fibrinogen and vWF
- Abciximab, Tirofiban
–Anti P2Y
-Clopidogrel, Ticagrelor, Prasugrel
–Fibrinolytics = v.potent = high risk bleeding associated

162
Q

what is DVT and its features?

A 
deep vien thrombosis 
- in area of low blood flow= accumulation of cells- RBC = inflammation 
-platelet activation 
-fibrin generation 
clot = fibrin and RBC
-less damage to blood vessel
- blood clot can break = embolism
163
Q

DVT symptoms

A

calf swelling
pain
associated odema

164
Q

what is odema

A

leaky endothelial cells allows fluid accumulate in vasculature
press test to check for odema

165
Q

RF of DVT

A
  • immobilisation
  • surgery
  • cancer
  • pregnancy
  • contraceptives
  • genetics
166
Q

what is the most common embolism DVT causes

A

pulmonary embolism

  • chest pain
  • lungs stop functioning
  • can be in both lungs
167
Q

treatment for DVT

A

mmediate onset of anticoagulant effect:
–Unfractionated Heparin (intravenous – helps antithrombin to inhibit thrombin and Xa)
–Low Molecular Weight Heparin (LMWH; subcutaneous)
Slow onset:
–VKA, monitored by INR

168
Q

what does the presence of D dimer in blood show?

A

ongoing thrombotic events

produced by breakdown of fibirin

169
Q

what is circulatory stasis?

A

loss laminar flow and pooling around valves gaps between endo cells

170
Q

what happens in endothelial dysfunction?

A

activation and exposure of TF after inflammation

171
Q

what happens in hypercoaguable state?

A

localised inflammation
loss inhibitor function
too much activity of TM and protein C and S = thrombin accumulation

year 1 flash cards (23 decks)

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