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Yr 2 - IBMS > Blood and Haemostasis > Flashcards

Blood and Haemostasis Flashcards

1
Q

State the Components of Blood

A

55% plasma
45% RBC
less than 1% WBC and platelets

serum = water, salts, glucose
plasma = serum + clotting factors

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2
Q

State the Layers of the Structure of Blood Vessels

A

Tunica Externa - external elastic membrane
Tunia Media - smooth muscle
Tunica Intima - internal elastic membrane and endothelium

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3
Q

In terms of Structure, what do Larger Arteries Lack?

A

smooth muscle

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4
Q

What are the 3 Components of Virchow’s Traid

A

Vessel Wall
Blood Flow
Coagulation Factors

all 3 make clotting more or less likely

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5
Q

Describe what does the Vessel Wall and internal elastic membrane contain, and what do they express

A

collagen and express’ Von Willebran Factor

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6
Q

Describe what Happens when the Endothelium gets Damaged. (4) Describe the end result (2)

A
  • platelets and collagen in the blood are exposed to Von Willebrand Factors in the vessel wall
  • VWF bind to platelets
  • platelets are activated
  • platelet changes shape from circle to star-shaped (increase SA)
  • platelets bind to each other
    = platelet plug

leads to
- platelet aggregation
- trapped fibrinogen

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7
Q

What is Von Willebrand’s Disease

A

a blood disorder in which blood does not clot properly as it lacks VWF

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8
Q

What is a Vascular Spasm?

A

a broken vessel wall
- smooth muscle contracts
- smaller
- less blood flow
- allows clot to form

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9
Q

What are Coagulation Factors?

A

proteins in the blood

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10
Q

Which Coagulation Factors are made in the liver?

A

2
7
9
10

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11
Q

What are the 3 Pathways for Coagulation Factors to Take and Explain.

A

Extrinsic Pathway
- activtated by factors outside the vessel wall
- F3 is expressed outside the vessel wall
- exposure of F3 to blood activates F7
- F7 catalyses the conversion of FX TO FXa
- allows the conversion of prothrombin to thrombin

Instrinic Pathway
- activated by factors inside the vessel wall if there are foreign particles
- F12 gets activated and cascades the activation of F11, F9
- F8 is also part
- allow to the conversion of prothrombin to thrombin

Final Pathway
- thrombin allows the conversion of fibrinogen into fibre
= cross linking fibre network

  • the result of factors:
  • F10 into F10a
  • prothrombin into thrombin
  • fibrinogen into fibrin
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12
Q

What does Irregular or Slow Blood Flow lead to? Which Conditions can it Lead to?

A

coagulation
- atrial fibrillation
- deep vein thrombosis

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13
Q

What is Arterial Fibrillation?

A

a heart condition that causes an irregular and abnormal fast heart rate

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14
Q

Describe Steps of Arterial Fibrillation.

A
  • SAN and conduction of cardiac impulse = abnormal
  • atrial wall doesn’t contract well and at different times
    = turbulent flow
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15
Q

What is the Cause of Pulmonary Embolism?

A

Deep Vein Thrombosis

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16
Q

What does Deep Vein Thrombosis lead to?

A

Pulmonary Embolsim

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17
Q

How does Deep Vein Thrombosis come about?

A

people sat for long time
blood pools beneath lower limbs
clot develop
can end up in pulmonary circuit
= pulmonary embolism

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18
Q

How can you Prevent Blood Clots in the Vessel Wall? (5)

A
  • prevent platelet activation
  • metabolise cyclooxygenase
  • warfarin and heparin = anticoagulants
  • clopirdogel and aspirin = anti-platelet medicine
  • artificial heart valve
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19
Q

What type of Medicine is Clopidrogel?

A

anti-platelet - prevent binding of platelet
similar to aspirin

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20
Q

How long do Warfarin, Aspirin and Clopidrogel last?

A

the lifetime of the platelet - its irreversible

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21
Q

How long do Warfarin, Aspirin and Clopidrogel last?

A

the lifetime of the platelet - its irreversible

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22
Q

Which Medicine is Similar to Heparin

A

Warfarin

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23
Q

How can you Prevent DVT?

A
  • activity
  • compression stockings
  • Heparin and Warfarin (anticoagulants)
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24
Q

How can you Prevent Atrial Fibrillation?

A
  • correct fibrillation
  • heparin and warfarin (anticoagulants)
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25
Q

How does Heparin work? Delivery and Monitoring. How Long Lasting is it and can it be Reversed?

A
  • prevents activation of F10
  • prevents cross linking fibrin network forming
  • delivered via injection
  • monitored via APTT
  • short lasting
  • reversed by protamine sulphate
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26
Q

How does Warfarin Work? (4) Delivery and Monitoring. How Long Lasting is it and can it be Reversed?

A
  • prevents metabolism of Vitamin K in the liver
  • prevents conversion of F9 into F8
  • prevent catalytic conversion of F7
    = prevent prothrombin into thrombin
  • delivered via oral tablet
  • monitored by checking PT or INR
  • long lasting, take a while for effect
  • reversed by Vitamin K
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27
Q

List some other Anti-Coagulant Drugs and 3 Features.

A

apixaban
rivaroxaban
edoxaban
- prevent conversion of F10

dabigratran
- prevent conversion of fibrinogen

  • all taken orally
  • short acting
  • cannot be reversed
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28
Q

What can Blood Clots lead to in the Brain, Lungs, Limbs, Gut, Heart, Veins

A

Brain - stroke
Lungs - pulmonary embolism
Limbs - ischemia
Gut - gut ischemia
Heart - myocardial ischaemia
Veins - DVT

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29
Q

How can Atherosclerosis lead to Clotting?

A
  • plaque formation under the blood vessel endothelium
  • obstructs the vessel
  • if rupture can introduce extrinsic and intrinsic pathway to occur
  • clotting
  • stroke
30
Q

How can Liver Disease lead to Abnormal Bleeding?

A
  • produces a lot of clotting factors and metabolises vitamin K
31
Q

What are Questions to ask a Patient in Relation to Abnormal Bleeding?

A
  • personal and family history
  • medication
  • do they bruise easily, bleed a lot if theres a cut
32
Q

Describe 5 Tests that Measure Abnormal Bleeding.

A

Extrinsic Pathway Test = Prothrombin Time (PT)
- sample of plasma
- add F3
- set timer for fibrin clot to form

INR = same test as external but international normalised ratio

Instrinic Pathway Test = Activated Partial Thromboplastin Time (APTT)
- sample of plasma
- add foreign material
- F12 activated and cascade
- set timer to fibrin clot to form
- the rests are in a ratio
- if less than 1 = little time to clot
- if more than 1 = more time to clot

Platelet Count Test
- 150,000-400,000 is normal
concern if less than 100k
action required if less than 80k

Individual Factor Assays
- done by haemotology

33
Q

How Do You Stop Blood Clotting

A

breakdown fibrin

34
Q

Why is Blood Clotting Relevant to Dentistry? What can be Provided?

A

need to be careful when extracting teeth
- if no healing can given the patient
- tranexamic acid as a mouthwas
- prevents breakdown of fibrin and allows clot

35
Q

Define Haematopoeisis.

A

blood cell production

36
Q

What is the Function of Haemocytoblasts? What are they also known as?

A

give rise to the formed elements in blood

pluripotential haemopoietic stem cells

37
Q

What is the Function of Blood? (4)

A
  • deliver oxygen, remove carbon dioxide
  • maintain temp, pH and fluid volume
  • prevent infection
  • transport hormones and nutrients
38
Q

What are the 3 Types of Haemoglobin?

A

HbA = most common
HbA2 = small amounts
HbF = foetal haemoglobin

39
Q

When does Haemoglobin Appear Red and then Purple/Blue?

A

when its oxygenated then deoxygenated

40
Q

How are Blood Cells Produced?

A

haematopoeisis derived from bone marrow stem cells

41
Q

Which Hormone Enhances Erythopoiesis?

A

Testosterone

42
Q

What is the Name for Erythocyte Cell Death?

A

Eryptosis

43
Q

What can it mean if Urine/Faeces appear Dark?

A

more red blood cell death

44
Q

Provide 5 Types of Red Blood Cell Associated Disease

A
  • Anaemia
  • Pernicious Anaemia
  • Haemoglobinopathis
  • Sickle Cell Anaemia
  • Thalassaemia
45
Q

…. means blood cell production

A

haematopoiesis

46
Q

what cells allow elements to form in the blood?

A

haemocytoblasts AKA pluripotential haemopoietic stem cells

47
Q

What Regulates Plasma Production?

A

Thrombopoeitin

48
Q

Describe the Appearance of Platelets.

A

purple granules
blue-staining outer region

  • bi-concave disc
  • 2/3µm
49
Q

What are the Constituents of Platelets?

A

serotonin
Ca2+ enzymes
ADP
platelet derived growth factor

50
Q

What are the Components of Plasma, Percentages, Solutes (6)

A

water = 90%
solutes = 8%
- proteins
- gas
- electrolytes
- organic nutrients
- hormones
- metabolic waste

51
Q

What are the Blood Types, their Corresponding Antigens and Antibody’s?

A

Type A = A antigen, Anti-B

Type B = B antigen, Anti-A

Type AB = A and B antigens, no antibodies
= CODOMINANT

Type O = Neither A or B antigens, Anti-A and Anti-B
= RECESSIVE

52
Q

What is Rhesus factor?

A

protein that can be found on the surface of the red blood cell
two types:
positive = 85% dominance
negative = 15% recessive

  • the positive or negative sign next to the blood group is the Rhesus factor
53
Q

What is Haemolytic Disease? How can it be Detected?

A

When there is a +Rh foetus and -Rh mother
- lead to anti-rhesus antibodies from mother attacking the foetal blood cells
= haemolytic anaemia

  • take a RhoGAM test at 28 weeks
54
Q

What is the Most Common Rh blood type?

A

+Rh Type O

55
Q

What is the Least Common Rh Blood Type?

A

-Rh Type AB

56
Q

Define Thrombus

A

A structured solid mass or plug of blood constituents formed within the heart of blood vessels

57
Q

Define Thrombosis

A

the process of thrombus formation

58
Q

What are the 3 Types of Thrombus

A
  1. Arterial
    - usually at site of endothelial injury
    - common sites = corony, cerebral, femoral
  2. Cardia aka Mural Thrombi
    - over areas of myocardial injury
    - also with arrhythmias and cardiomyopathy
  3. Venous
    - sites of vascular stasis
    - lower limbs, DVT
59
Q

What are the Outcomes of Thrombus, Considering the Patient had Survived the Immediate Effect of Obstruction

A
  • propagation
  • embolism
  • dissolution
  • and/or organisation/recanalisation
60
Q

What are the Primary and Secondary Predisposing Conditions to Thrombus? SASAPMDOWN

A

Primary - genetic
- protein C or S deficient
- antithrombin deficient
- F5 Mutations
- prothrombin mutations

Secondary - environmental
- Stasis - no movements - coagulation facts are not cleared, platelets clump
- Atherosclerosis - damage to vessel wall and lumen lining
- Smoking - increase prothrombin biomarkers
- Atrial Fibrillation - blood pooling
- Prosthetic Heart Valves - negative change can activate intrinsic pathway
- MI and Vasculitis - damage to vessel wall
- Neoplasia - malignancy induced abnormal coagulation
- Oral Contraceptives - increase in circulating fibrinogen
- Disseminate Intravascular Coagulation
- widespread activation of clotting cascade

61
Q

How do you Prevent Thrombosis?

A

Aspirin - for stroke and MI
Heparin - prevent post-op DVT
Warfarin -
newer therapeutics
- anticoagulants = rivaroxaban, apixaban, betrixaban
- antiplatelt = clopidrogel

62
Q

Describe Thrombolysis

A

thrombolysis
- streptokinase and tissue type plasminogen actiavtor
- activates the body natural fibrinolytic system to break down thrombus

63
Q

What is an Embolus?

A

an abnormal mass of material which is carried in the bloodstream from one part of the circulation to another, impacting in a vessel which calibre is too small to allow it to pass

64
Q

What is an Emboli?

A

plural of embolus

65
Q

Describe the Types of Thromboembolism

A

Pulmonary
- originate from detached piece of thrombus in the deep vein of the leg
- travel via venous system
- to the heart
- out of the pulmonary artery
- GETS STUCK in pulmonary arterial tree

Systemic
- originate from detached piece of mural thrombus
- travels via aorta into systemic arterial circulation
- GETS STUCK in lower limbs, brain, kidney, gut

Cerebral
- originate from detached piece of thrombus in common carotid artery
- travels via arterial system to brain
- GETS STUCK in cerebral vasculature - stroke

Lower Limb/Renal
- originate from detached piece of thrombus in abdominal aorta
- GETS STUCK in arteries - renal or lower lim

66
Q

What is a Paradoxical Embolism?

A

embolism that originates in the systemic veins and enters system arterial circulation

  • travel expected from right heart to pulmonary artery
  • travels from right heart to aorta
67
Q

Define Ischemia

A

an inadequate blood supply to an organ or part of the body

  • heart - coronary artery - get angina
  • legs - intermittent claudication (femoral, iliac and popliteal arteries)
  • gut - mesenteric artery - ischemic bowel
68
Q

Define Infarction

A

death of an area of tissue due to ischemia
- heart - MI
- brain - cerebrovascular accident, stroke
- bowl - bowel infarction

69
Q

What is Shock? Describe the 9 Steps. Shock Hurts Very Lovely and Exciting Peeps And People

A

a life threatening condition of low blood perfusion to tissues resulting in cellular injury and inadequate tissue function

  1. failure of pre-capillary sphincters
  2. cell hypoxia
  3. vasoconstriction
  4. lactic acid and fall in pH
  5. metabolic acidosis
    - cell mem dysfunction
    - influx of sodium and water, efflux of potassium
    - toxic substances enter circulation
    - capillary endothelium damage
    - cell death
  6. energy deficit
  7. inadequate perfusion
  8. anaerobic respiration
  9. peripheral pooling of blood
70
Q

What are the 4 Types of Shock?

A

Cardiogenic Shock
- distended jugular vein due to venous pressure
- weak or absent pulse
- arrhythmia
- reduces blood pressure
- causes: prevention of heart pumping properly

Obstructive Shock
- cardiac tymponade
- pulmonary embolsim
- aortic stenosis
- causes: obstruction of blood flow outside heart

Hypovolaemic Shock
- rapid, weak pulse
- tachycardia
- cool, clammy skin - vasoconstriction
- hypothermia
- thirst and xerostomia
- causes: insufficient fluid circulation
- adults - haemorrhage
- children - vomiting, diarrhoea, burns, excess urine

Distributive Shock
- causes:
- infectious - septic shock - dilation lead to hypotension
- anaphylactic - vasodilation - hypotension and increased capillary permeability
- neurogenic causes
- typically present with systemic inflammatory response syndrome
- high resp rate, high body temp, tachycardia, low or very high WBC count

71
Q

How is Shock Treated

A

ABCDE
- oxygen and bolus of fluid
- meds - vasopressors
- prognosis is poor
- with cariogenic - 70-90% mortality
- with septic shock - 30-50% mortality

72
Q

Define Antiphospholipid Syndrome

A

= connective tissue disease
- body produces antibodies attacking phospholpids
- can generate blood clots
- linked to rheumatoid arthritis

Yr 2 - IBMS (21 decks)

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