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Med Yr2 > ABC > Flashcards

ABC Flashcards

1
Q

Erythrocytes: basic properties (3)
- Structure
- Lifespan
- Clearance by ….

A
  • Biconcave disc shape, anucleate
  • 90 -120 days
  • Reticuloendothelial system (spleen)
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2
Q

Erythrocytes: function

A
  • Transport of O2 and CO2 around the body
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3
Q

Platelets (thrombocytes): function

A
  • Blood coagulation upon vasculature injury
  • Release granules and activate clotting cascade
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4
Q

Platelet structure:

A
  • Surface coated with glycoproteins for adhesion/aggregation
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5
Q

Platelets: interactions
1. Platelet-platelet
2. Platelet-endothelium

A
  1. bind to fibrinogen for platelet-platelet adhesion
  2. bind to von WIllibrand Factor (vWF) for platelet endothelium adhesion
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6
Q

Myeloid cells:
- definiton
- Types

A
  • Blood cells that originate from progenitor cells born in bone marrow
  • Monocytes, granulocytes, erythrocytes, megakaryocytes
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7
Q

Monocytes: definition

A
  • Undifferentiated leukocytes that differentiate into:
    1. Macrophages
    2. Dendritic cells
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8
Q

Granulocytes:
- Definition
- Types (4)

A
  • Cells characterised by specific granules in their cytoplasm
    1. Neutrophils
    2. Eosinophils
    3. Basophils
    4. Mast cells
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9
Q

Neutrophils: role

A
  • Phagocytose, degranulate and release NETs to kill bacteria and fungi
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10
Q

Neutrophils: development
- Location
- Requires …..

A
  • Mature in bone marrow prior to circulation
  • G-csf for proliferation/differentiation
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11
Q

Neutrophils: basic properties
- Structure
- Lifespan
- Clearance

A
  • Multi-lobed nucleus (1-5), granular cytoplasm
  • 6-10 hours
  • Reticuloendothelial system (spleen)
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12
Q

Types pf phagocytes: (3)

A
  • Monocyte/macrophage
  • Neutrophils
  • Dendritic cells
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13
Q

Monocytes: basic properties
- Size
- Functions
- Lifespan

A
  • Largest leucocyte
  • Diverse subsets and functions
  • 1-2 days
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14
Q

Monocyte development:
- Requires (2)
- Shares common progenitor with ….
- Develops into …..

A
  • GM-CSF, M-CSF
  • granulocytes
  • Macrophages and dendritic cells in tissue
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15
Q

Monocytes: function

A
  • Differentiate into macrophages and dendritic cells
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16
Q

Eosinophils: function

A
  • Target larger parasites and modulate allergic reactions
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17
Q

Basophils: function

A
  • Release histamines for inflammatory responses and ALLERGIC REACTIONS
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18
Q

Mast cell: function

A
  • Release histamines and serotonin to modulate allergic reactions and INFLAMMATORY RESPONSE
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19
Q

Lymphoid cells:

A
  • blood cells that arise from progenitor cells born in the bone marrow but must migrate to the lymphatic organs to differentiate
  • B & T -lymphocytes
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20
Q

B-lymphocyte function: (2)

A
  • function in the humoral immunity component of the adaptive immune system
  • Produce plasma cells that produce antibodies
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21
Q

T-lymphocytes:
- Function
- Subsets (2)

A
  • Function in the adaptive immune response
  • Cytotoxic T cells and Helper T cells
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22
Q

Normal blood cell production: start point

A
  • Multipotent hematopoietic stem cell
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23
Q

Blood cell production: myeloid pathway start

A
  • Multipotent hematopoietic stem cell -> Common myeloid progenitor
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24
Q

Myeloid production: Megakaryocyte
- Route
- Via

A
  • Common myeloid progenitor -> Megakaryocyte
  • Via Thrombopoietin (TPO) prod. by liver
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25
Q

Myeloid production: Erythrocyte
- Via

A
  • Erythropoietin (EPO) prod. by kidneys
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26
Q

Myeloid production: granulocytes

A

Myeloblast -> granulocytes
- Via granulocyte colony stimulating factor (G-CSF)

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27
Q

What does the full blood count (FBC) measure?: (4)

A
  • RBC’s
  • WBC’s
  • WBC differentiation
  • Platelets
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28
Q

Reticulocyte count: definition

A
  • The number of developing RBC’s
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29
Q

Relevancy of reticulocyte count in differential diagnosis of anaemia: (2)

A
  • Increased RC: Reduced RBC survival (haemolysis or bleeding)
  • Reduced RC: problem with production
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30
Q

Blood film definition:

A
  • Snapshot of the cells that are present in the blood at the time that the sample is obtained
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31
Q

Blood film diagnostic uses: (2)

A
  • Assess red cell, platelet and white cell (numbers, size, colour and morphology)
  • View any abnormal cells
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32
Q

Haemostasis: blood vessel wall
- Endothelial cell role

A
  • Contains negative regulators to reduce haemostasis
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33
Q

Negative regulators in endothelial cells:
- Soluble mediator
p

A

Soluble mediators:
- Prostacyclin

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34
Q

Negative regulators in endothelial cells:
- Surface mediators (3)
E
T
H

A

Surface mediators
- Endothelial protein C receptor
- Thrombomodulin
- Heparens

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35
Q

Haemostasis: blood vessel wall
- Sub-endothelial cells

A
  • Have activators that enhance haemostasis
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36
Q

Sub- endothelial cell activators for haemostasis: (3)

A
  • Collagen
  • Tissue factor
  • Von Willebrand Factor (VWF)
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37
Q

Role of platelets in haemostasis:
Adhere …
Activate ….
Support …..

A
  • Adhere to sub-endothelial proteins after vascular damage
  • Activate and aggregate other platelets
  • Support activation of coagulation factors
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38
Q

Role of VWF in haemostasis:

A
  • Binds platelet surface proteins to mediate platelet adhesion
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39
Q

Role of coagulation factors in haemostasis:

A
  • Series of plasma proteins which convert prothrombin to thrombin
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40
Q

Roles of fibrinogen in hameostasis:
- Binds…..
- Polymerised …..

A
  • Binds platelet surface integrins to mediate platelet aggregation
  • Polymerised to thrombin to form fibrin clot
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41
Q

Cell based model of haemostasis:

A
  • all the components of haemostasis interact in a regulated way to generate clot only at the site of vascular injury
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42
Q

Thrombin:
- Definition
- Role

A
  • An activated coagulation factor that is the main effector of haemostasis
  • Thrombin polymerises fibrinogen to FIBRIN and fully activates PLATELETS
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43
Q

Haemostasis - step 1: trigger
(2)

A
  1. Collagen and tissue factor exposed
  2. Von Willebrand Factor (vWF) binds collagen
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44
Q

Hameostasis - step 2: Primary Haemostasis
(2)

A
  1. Platelets adhere to vWF-collagen
  2. Platelets activate and aggregate
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45
Q

Haemostasis - step 3: Thrombin generation

A
  1. Tissue factor initiates rapid thrombin generation on activated platelets
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46
Q

Hameostasis - step 4: consolidation

A
  1. Thrombin converts fibrinogen to fibrin and completes platelet activation
  2. Stable fibrin-platelet clot is formed
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47
Q

Regulation of haemostasis: clot formation
1. vWF adhesivity is regulated by …….

A

ADAMTS 13

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48
Q

Regulation of haemostasis: clot formation
2. Thrombin is regulated by ……. (2)

A
  • Antithrombin
  • Activated protein c system
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49
Q

Regulation of haemostasis: fibrinolysis

A
  • Thrombin converts enzyme plasminogen to plasmin
  • Plasmin cleaves fibrin to degradation products (D-dimer)
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50
Q

Core laboratory tests of haemostasis: (4)

A
  1. Platelet count + blood screen
  2. Coagulation screen (PT + APTT)
  3. Fibrinogen level
  4. D Dimer level
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51
Q

PT + APTT tests principles: (3)

A
  1. Add activator (phospholipid+Ca2+) to anticoagulated blood
  2. Incubate at 37*C
  3. Measure time to fibrin clot formation
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52
Q

Indications of prolonged PT or APTT: (3)

A
  1. Reduced levels of coagulation factors (bleeding disorders)
  2. Reduced function of coagulation factors (anticoagulant drugs)
  3. Laboratory artefact (human error)
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53
Q

Isolate prolonged PT?:

A
  • Factor VII issue (extrinsic pathway)
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54
Q

Isolated prolonged APPT?:

A
  • Issues with factors VIII, IX, XI (intrinsic pathway)
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55
Q

Long PT and APTT?:

A
  • Multiple factor defects; II, V, X, fibrinogen (common pathway)
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56
Q

What does high fibrinogen levels indicate?:

A
  • Acute phase response, pregnancy
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57
Q

What do low fibrinogen levels indicate?:
A
L
M

A
  • Acquired bleeding disorders
  • Liver disease
  • Massive transfusion
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58
Q

What does an elevated D-dimer level indicate?:
D I C
V
Multiple

A
  1. Disseminated intravascular coagulation
  2. Venous thrombosis
  3. Pregnancy, liver/kidney disease, sepsis
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59
Q

Point-of-care tests of haemostasis:
- Example
- Importance

A
  • Thromboelastometry
  • Quick and easy to perform and interpret, useful in urgent clinical settings
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60
Q

Virchow’s triad:

A
  1. Hypercoagulability
  2. Endothelial injury
  3. Venous stasis
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61
Q

Risk factors for VTE: physiological factors (4)

A
  1. Dehydration
  2. Obesity
  3. Pregnancy
  4. Old age
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62
Q

Risk factors for VTE: other factors (3)

A
  • Medical comorbidities
  • Significant reduction in mobility
  • Vascular access and devices
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63
Q

Risk factors for VTE: medications (3)

A
  • Hormone replacement therapy
  • Some cancer treatments
  • Oestrogen-containing contraceptives
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64
Q

Risk factors for VTE: hospital/surgery (3)

A
  • Surgery with general anaesthetic + time > 90mins
  • Critical care admission
  • Hospital admission
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65
Q

DVT signs and symptoms:
L
S
T
D
P O

A
  • Leg pain
  • Swelling
  • Tenderness
  • Discolouration
  • Pitting oedema
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66
Q

VTE ‘atypical’ presentations:
B L S
A
D
P

A
  • Bilateral leg swelling
  • Asymptomatic
  • Death
  • Pyrexia of unknown origin
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67
Q

Diagnosis: DVT^1,2: (2)

A
  • Confirmatory test:
    1. Venous ultrasonography
    2. MRV or CTV for VTE at unusual sites
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68
Q

Diagnosis: PE^2-4:

A
  • Confirmatory tests:
    1. CT pulmonary angiogram
    2. Ventilation-perfusion scan
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69
Q

D-dimer test for VTE:
- Use
- False negatives if. …..

A
  • Increased levels in VTE and other diseases/conditions
  • False negative: patient on anticoagulants, take blood before starting anticoagulants
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70
Q

Screening thrombophilia to see if it is….. (2)

A
  • Inherited thrombophilia
  • Acquired thrombophilia: screening for antiphospholipid syndrome
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71
Q

Antiphospholipid syndrome:
- Description
- Associations

A
  • Autoimmune, acquired prothrombotic condition
  • Associated with systemic lupus erythematosus (SLE)
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72
Q

Antiphospholipid syndrome: clinical features
A T
V T
M T
P L
L R
T

A
  • Arterial thrombosis
  • VTE
  • Microvascular thrombosis
  • Pregnancy loss
  • Livedo reticularis (red-blue rash)
  • Thrombocytopenia
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73
Q

Antithrombotics:
- definition
- potential side effect for all

A
  • Used to treat and prevent thrombotic complications
  • Bleeding
74
Q

Anticoagulant examples: (3)

A
  • Heparin
  • Warfarin
  • DOACs (Direct Oral Anticoagulants)
75
Q

Commonest clinical indications for anticoagulation:
V
V P
S P
M

A
  • VTE (TD)
  • VTE prevention
  • Stroke prevention in AF (TD)
  • Mechanical heart valves - Warfarin (TD)
76
Q

Anticoagulants: Warfarin
- Mechanism
- Half-life
- Renal clearance

A
  • Inhibits vitamin K metabolism, reducing factors II, VII, IX and X
  • 40 Hrs
  • Renal clearance: 8% (low)
77
Q

Anticoagulants: Dabigatran (DOAC)
- Mechanism
- Half-life
- Renal clearance

A
  • Direct thrombin inhibitor
  • 12-18 hrs
  • 85% (high)
78
Q

DOACs: direct fator Xa inhibitors (3)
A
R
E

A
  • Apixaban
  • Rivaroxaban
  • Edoxaban
79
Q

Apixaban:
- Action
- Half-life
- Renal clearance

A
  • Direct factor Xa inhibitor
  • 12 Hrs
  • 27%
80
Q

Rivaroxaban:
- Action
- Half-life
- Renal clearance

A
  • Direct factor Xa inhibitor
  • 5-9hrs young 11-13 hrs old
  • 33%
81
Q

Edoxaban:
- Action
- Half-life
- Renal clearance

A
  • Direct factor Xa inhibitor
  • 10-14hrs
  • 50%
82
Q

Anticoagulants: Heparin
- Action
- Half-life
- Renal clearance

A
  • Direct factor Xa and thrombin inhibitor
  • 4-5 hrs
83
Q

Warfarin:
- Characteristics
- Effect on coagulation time
- Monitored by…….

A
  • Slow onset and long half life
  • Increases PT and APTT
  • Monitoring using INR (patient PT/control PT)
84
Q

Warfarin is used for: (4)
M H V
S R F
A S
A F with

A
  • Mechanical heart valves
  • Severe renal failure
  • Antiphospholipid syndrome
  • AF with rheumatic mitral stenosis
85
Q

Warfarin:
- Interactions
- Reversals

A
  • Many medications and food (Vit K in veg, alcohol)
  • Vitamin K (6h) or po(24h)
86
Q

Heparin: LMWH
- Administration
- Lab measure
- Onset
- t1/2

A
  • Sub cutaneous
  • antiXa
  • Fast onset (3hr peak)
  • 4-5hr
87
Q

Heparin: UFH
- Administration
- Lab measure
- t1/2

A
  • Iv or SC
  • APTT or antiXa
  • t1/2 = 1-2Hr
88
Q

DOACs: PROS
- Convenient
- onset & t1/2
- Risks reduction

A
  • Convenient: fixed dose, no/few food/drug interactions, no need to monitor
  • Quick onset and t1/2
  • Lower risks of intracranial haemorrhage, fatal haemorrhage and major bleeding
89
Q

DOACs: CONS (3)

A
  • Multiple drugs needed at once
  • Need for good compliance
  • Follow up still needed
90
Q

Anticoagulation treatment for VTE:
- Duration
- Decision

A
  • Three months for acute thrombosis
  • Then decision to be made: recurrence vs bleeding
91
Q

Assessing bleeding risk in VTE: Acute VTE (proximal DVT or PE)

A
  • Anticoagulate unless significant obvious contraindication (e.g. active significant
    bleeding)
  • Optimise modifiable bleeding risks (e.g. Hypertension, other medications e.g. aspirin, NSAIDs, alcohol)
92
Q

Who should be considered for long term anticoagulants?:

A
  • Unprovoked cases: medium chance of recurrence
  • Persistent significant risk factor: HIGH RISH
93
Q

Primary haemostasis disorders are caused by defects in: (3)

A
  • Platelets
  • VWF
  • Vessel wall
94
Q

Coagulation disorders are caused by defects in: (2)

A
  • Coagulation factors
  • Fibrinogen
95
Q

Bleeding types more prevalent in Primary haemostasis disorders: (2)

A
  • Abnormal skin bleeding
  • Abnormal nose and mouth
96
Q

Bleeding types more common in Coagulation disorders:

A
  • Joint bleeds (haemarthrosis)
  • Soft tissue bleeds (haematoma)
97
Q

Bleeding types equally common between primary haemostasis & coagulation disorders: (3)

A
  • Heavy menstrual bleeding
  • Obstetric and surgical bleeding
  • CNS and gut bleeds
98
Q

ISHT bleeding assessment tool:

A
  • 9 possible bleeding sites are scored on a severity of 1-4 each
99
Q

Clinical history and examination -> Active bleeding
- Factors to asses (3)

A
  • PTT, APTT and PLT count
  • Fibrinogen
  • Haemoglobin
100
Q

Clinical history and examination -> elective investigation: first line tests

A
  • PT, APTT and PLT count
101
Q

Clinical history and examination -> elective investigation: Second line tests

A
  • Fibrinogen levels
  • VWF levels
  • PLT function
102
Q

Approach to abnormal coagulation test results:

A
  • Common in patients with no bleeding, must be considered in the clinical context
103
Q

Genetic diseases in haemostasis: (4)
V
H
F
HPFD

A
  • VWF disease
  • Haemophilia A & B
  • Factor XI deficiency
  • Heritable platelet function disorder
104
Q

Difference between haemophilia A and B:

A

Haemophilia A = Factor VIII deficiency
Haemophilia B = Factor IX deficiency

105
Q

Haemophilia features:
- Inheritance

A
  • X linked recessive
106
Q

Haemophilia features:
- Coagulation pathway bleeding symptoms

A
  • Soft tissue and joint bleeding
  • Bleeding after surgery/dental extraction
107
Q

Haemophilia features: laboratory

A
  • Increased APTT
  • Decreased factor VIII or factor IX
  • Pathogenic variants in F8 or F9
108
Q

Causes of acquired bleeding diseases: reduced synthesis (3)

A
  • LIVER DISEASE
  • Vit K deficiency
  • Immune thrombocytopenia
109
Q

Causes of acquired bleeding diseases: Impaired function (3)

A

_ CKD
- LIVER DISEASE
- Heparin, DOACs, NSAIDs

110
Q

General affect of liver disease on clotting:

A
  • Liver synthesises most haemostasis proteins and regulates PLT production in the marrow
111
Q

Effect of liver disease due to reduced protein synthesis:

A
  • Decreased clotting factor
  • Decreased fibrinogen
  • Decreased regulator levels
112
Q

Effect of liver disease due to cholestasis:

A
  • Decreased clotting factor function due to vitamin K malabsorption
113
Q

Effect of liver disease on thrombopoietin (TPO):

A
  • Reduced TPO synthesis decreases PLT numbers
114
Q

Effect of liver disease on metabolism:

A
  • Metabolic disturbance causes a decrease in PLT function
115
Q

Extra detrimental effect of liver disease:
- Clue: Increased Fi……..

A
  • Increased fibrinolysis
116
Q

Liver disease symptoms relating to bleeeding: (3)

A
  • Skin and soft tissue bleeds
  • Acute GI tract bleeding due to oesophageal varices
  • Retinal bleeds
117
Q

Laboratory signs of liver disease:
- PT/APTT
- Fibrinogen
- PLT
- D-dimer

A
  • Increased PT and APTT
  • Decreased fibrinogen
  • Decreased PLT count
  • Increased D-dimer
118
Q

Complex multisystem disorder in haemostasis:
- Examples of what may trigger DIC (3)

A
  • Sepsis
  • Cancer
  • Trauma
119
Q

Disseminated Intravascular coagulation (DIC): defintion

A
  • Combination of thrombosis and bleeding disorder
120
Q

Pathogenesis of DIC: (2)

A
  • Increase in prothrombotic protein
  • Loss of negative haemostasis regulators
121
Q

Effects of DIC:
- Leads to ……
- Symptom
- Consumption of …

A
  • Leads to widespread and dysregulated haemostasis activation
  • Fibrin and platelet microvascular thrombi
  • Consumption of PLT, coagulation factors and fibrinogen
122
Q

Pathogenesis of DIC:
- PT/APTT
- PLT count
- D-dimer count
- Extra sign

A
  • Increased PT and APTT
  • Decreased PLT
  • Increased +++ D-dimer
  • Usually anaemia
123
Q

Principles of treatment for abnormal bleeding: (3)

A
  1. Avoid/control causes of bleeding (local measures)
  2. Pro-haemostatic drugs
  3. Replace missing content
124
Q

Replacing missing content in abnormal bleeding:
- Blood products from donor (2)
- Factor concentrates: (2)

A
  • Blood products from donor: fresh frozen plasma, platelet transfusion
  • Factor concentrates: plasma derived, recombinant
125
Q

Pro-haemostatic drugs: tranexamic acid
- Action
- Effective in …..

A
  • Blocks plasmin binding and activation of fibrin, reducing FIBRINOLYSIS
  • Effective in genetic and acquired bleeding disorders and major haemorrhage
126
Q

Pro-haemostatic drugs: Desmopressin (DDAVP)
- Action
- Effective in ….

A
  • Release factors VIII and VWF
  • Mild haemophilia A and VWF deficiency (also in other mild bleeding disorders)
127
Q

Blood products from donor: fresh frozen plasma
- Contains ……
- Indications (3)

A
  • All soluble coagulation factors and proteins
  • Bleeding in severe liver disease
  • Massive transfusion
  • Disseminated intravascular coagulation
128
Q

Blood products from donor: platelet transfusion
- Contains

  • Indications (4)
  • B M F
  • Exposure to …
  • T,D,M T
  • G
A
  • Platelets and small amount of RBC
  • Bone marrow failure
  • Exposure to anti-PLT drugs
  • Trauma, DIC, massive transfusion
  • Genetic PLT disorders
129
Q

Factor concentrates: plasma derived (4)

A
  • VWF
  • Fibrinogen
  • Factor XI
  • Factor XIII
130
Q

Factor concentrates: recombinant (3)

A
  • Factor VIII
  • Factor IX
  • Factor VIIa
131
Q

Brief summary of a blood donation:

A
  • Replacement of substances in the recipient from donated blood (cells, plasma, protein)
132
Q

Separation of blood into components following donation:
- Depletion
- Split

A
  • Leukocyte depletion (to prevent immune response)
  • Split into RBCs/PLTs (for bacteria testing) /plasma
133
Q

What is plasma used for once it is separated from the rest of the blood?: (3)
- F P P
- F F P
-C (F)

A
  • Plasma is used for:
    1. fractionated plasma proteins
    2. fresh frozen plasma (clotting factors)
    3. cryoprecipitate (fibrinogen)
134
Q

Transfusion incompatability: Major

A
  • Recipient has antibodies against transfused blood
135
Q

Transfusion incompatibility: Minor

A
  • Transfused blood has antibodies against recipient
136
Q

Red cell compatibility: recipient blood group O
- Antibodies formed
- Red cells for transfusion

A
  • Anti-A, Anti-B
  • Group O only
137
Q

Red cell compatibility: recipient blood group A
- Antibodies formed
- Red cells for transfusion

A
  • Anti-B
  • Group A or O
138
Q

Red cell compatibility: recipient blood group B
- Antibodies formed
- Red cells for transfusion

A
  • Anti-A
  • Group B or O
139
Q

Red cell compatibility: recipient blood group AB
- Antibodies formed
- Red cells for transfusion

A
  • None
  • Groups AB, A ,B or O
140
Q

Donor plasma compatibility:
- explanation
- universal donor
- universal recipient

A
  • The recipient patient cannot receive plasma containing anti-bodies against there blood type
  • Group AB (no ABO antibodies)
  • Group O (no antigens)
141
Q

Rhesus (Rh) factor rule: Rh+
- Definition
- Receive
- Donate

A
  • you have Rh antigen and will not make antibodies for it
  • can receive Rh- or Rh
  • can only donate to Rh+
142
Q

Rhesus (Rh) factor rule: Rh-
- Definition
- Receive
- Donate

A
  • You do not have Rh antigen and will make antibodies for it
  • Can only receive Rh-
  • Can donate to Rh- and Rh+
143
Q

Acute transfuse reactions: (2)

A
  • Acute haemolysis
  • Bacteria contamination
144
Q

Acute breathlessness due to transfusion: (3)

A
  • Fluid overload
  • Anaphylaxis
  • Transfusion related lung injury
145
Q

Minor reactions to transfusions: (2)

A
  • Rash
  • Febrile reaction
146
Q

Transfusion transmitted diseases: (4)

A
  • Viral
  • Bacterial
  • Protozoa
  • CJD
147
Q

Risk factors for arterial thrombosis:
S
H
H
D
O/S
M/D
A

A
  • Smoking
    o Hypertension
    o Hyperlipidaemia
    o Diabetesmellitus
    o Obesity/sedentarylifestyle
    o Mentalstress/depression
    o Advancing age
148
Q

Novel markers for arterial thrombosis:

A
  • High sensitivity CRP
  • Homocysteine
  • Lipoprotein
149
Q

Presentations of arterial thrombosis: Cerebrovascular event (3)

A
  • Carotid stenosis (blockage)
  • Thromboembolic (clot)
  • Haemorrhagic (rupture)
150
Q

Presentations of arterial thrombosis: Acute coronary syndrome (3)

A

o Plaque rupture
o Plaque erosion
o Calcific nodule

151
Q

Presentations of arterial thrombosis: peripheral artery disease (2)

A
  • Claudication (reduced blood flow to limbs)
  • Acute ischaemia
152
Q

Pathophysiology of arterial thrombosis:
- Existing plaque due to formation of atherosclerosis ……. (5)

A
  1. Plaque disruption
  2. Collagen exposure
  3. Platelet activation
  4. Platelet aggregation
  5. Vessel occlusion
153
Q

Aetiology of atherosclerosis: what initiates the process?
- What does it cause?
- Risk factors for this? (S,H,H,)

A
  • Oxidative stress
  • Endothelial cell dysfunction
  • Smoking, hyperlipidaemia, hypertension, stress
154
Q

Aetiology for atherosclerosis: chain of events due to endothelial cell dysfunction (6)
L A
I of L
P of S ….
V
F C F
A

A

Leucocyte adhesion →
infiltration of LDL →
proliferation of smooth muscle cells →
vasoconstriction→
foam cell formation (oxidised LDL)→apoptosis

155
Q

Consequences of atherosclerosis: heart (3As)

A
  • Angina
  • ACS - plaque rupture/erosion, calcific nodule
  • AF
156
Q

Consequences of atherosclerosis: Brain (2)

A

▪ Cerebrovascular accident – carotid stenosis, thromboembolic, haemorrhagic
▪ Vascular dementia

157
Q

Consequences of atherosclerosis: peripheral (4)
R
A A
P
I

A

▪ Renal artery stenosis
▪ Aortic aneurysm
▪ Peripheral artery disease – claudication, acute ischaemia
▪ Impotence

158
Q

Acute ST-elevation therapy: first line treatment

A
  • Rapid revascularisation + anti-thrombotic therapies
159
Q

Acute ST-elevation therapies: (2)

A
  • Thrombolysis: pre-hospital/during
  • Percutaneous coronary intervention
160
Q

Percutaneous coronary intervention:
- primary

A
  • Emergency procedure to widen narrowed blood vessels
161
Q

Percutaneous coronary intervention:
- Facilitated

A
  • Fibrinolytic therapy to stabilize the patient while transport is being arranged to primary PCI facility
162
Q

Platelet activation/deactivation pathway:
- Initial reaction
- Activation
- Deactivation

A
  • Arachidonic acid (AA) -> PGH2 via COX1/2 enzymes
  • PGH2 acts upon TXA2
  • PGH2 acts upon PGI2
163
Q

Aspirin mechanism of action: (3)
- Action
- Effects (2)

A
  • Inactivates COX1/2
  • Decreases TXA2 levels (an activator)
  • Continued production of PGI2 (inactivator)
164
Q

Aspirin: use

A
  • In acute MI in combo with fibrinolytic drugs
165
Q

P2Y12 receptor:
- Relation to PLTs
- Function

A
  • P2Y12 highly expressed on PLT
  • Binding site of VWF, collagen, TXA2 and thrombin to induce platelet aggregation
166
Q

P2Y12 receptor antagonist:
- Action
- Use

A
  • Blocks the P2Y12 receptor, reducing platelet aggregation
  • Strokes and MI’s
167
Q

Example of Py12 receptor antagonists: Irreversible

A
  • Clopidogrel
168
Q

Examples of Py12 receptor antagonists: Reversible (2)

A
  • Ticagrelor
  • Cangrelor
169
Q

αIIbβ3: mechanism

A
  • Cross linking of platelets via fibrin
170
Q

αIIbβ3 antagonists: mechanism

A
  • prevent fibrin binding to these receptors, stopping platelet aggregation
171
Q

αIIbβ3 antagonist: uses

A
  • Acute MI
  • MI prevention
  • Coronary bypass
172
Q

αIIbβ3 antagonist: examples
- Abc….
- Tiro….
- Eptif…..

A
  • Abciximab
  • Tirofiban
  • Eptifibatide
173
Q

Fibrinolytic therapy: mechanism of action (2)

A
  • Promotes conversion of plasminogem to plasmin
  • Plasmin proteolytic enzyme degrades fibrin to fibrinogen
174
Q

Endogenous plasminogen activators (PA):
S
t
U

A
  • Streptokinase-plasminogen complex
  • tPA
  • Urokinase
175
Q

Fibrinolytic therapy: Uses
A M
A T
A A T

A
  • Acute MI (within 12 hrs onset)
  • Acute thrombotic stroke
  • Acute arterial thromboembolism
176
Q

Fibrinolytic drug examples:
S
R
T

A
  • Streptokinase
  • Reteplase
  • Tenectplase
177
Q

Mechanism of Tranexamic acid:

A
  • Inhibits plasminogen activation
178
Q

Mechanism of Aprotinin:

A
  • Inhibits plasmin
179
Q

Aprotinin use:

A
  • Used in patients with a high risk of blood loss (i.e. after open heart surgery)
180
Q

Tranexamic acid use:

A
  • Increased risk of bleeding (dental extraction / prostatectomy)

Med Yr2 (12 decks)

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