ABC Flashcards
1
Q
Erythrocytes: basic properties (3)
- Structure
- Lifespan
- Clearance by ….
A
- Biconcave disc shape, anucleate
- 90 -120 days
- Reticuloendothelial system (spleen)
2
Q
Erythrocytes: function
A
- Transport of O2 and CO2 around the body
3
Q
Platelets (thrombocytes): function
A
- Blood coagulation upon vasculature injury
- Release granules and activate clotting cascade
4
Q
Platelet structure:
A
- Surface coated with glycoproteins for adhesion/aggregation
5
Q
Platelets: interactions
1. Platelet-platelet
2. Platelet-endothelium
A
- bind to fibrinogen for platelet-platelet adhesion
- bind to von WIllibrand Factor (vWF) for platelet endothelium adhesion
6
Q
Myeloid cells:
- definiton
- Types
A
- Blood cells that originate from progenitor cells born in bone marrow
- Monocytes, granulocytes, erythrocytes, megakaryocytes
7
Q
Monocytes: definition
A
- Undifferentiated leukocytes that differentiate into:
1. Macrophages
2. Dendritic cells
8
Q
Granulocytes:
- Definition
- Types (4)
A
- Cells characterised by specific granules in their cytoplasm
1. Neutrophils
2. Eosinophils
3. Basophils
4. Mast cells
9
Q
Neutrophils: role
A
- Phagocytose, degranulate and release NETs to kill bacteria and fungi
10
Q
Neutrophils: development
- Location
- Requires …..
A
- Mature in bone marrow prior to circulation
- G-csf for proliferation/differentiation
11
Q
Neutrophils: basic properties
- Structure
- Lifespan
- Clearance
A
- Multi-lobed nucleus (1-5), granular cytoplasm
- 6-10 hours
- Reticuloendothelial system (spleen)
12
Q
Types pf phagocytes: (3)
A
- Monocyte/macrophage
- Neutrophils
- Dendritic cells
13
Q
Monocytes: basic properties
- Size
- Functions
- Lifespan
A
- Largest leucocyte
- Diverse subsets and functions
- 1-2 days
14
Q
Monocyte development:
- Requires (2)
- Shares common progenitor with ….
- Develops into …..
A
- GM-CSF, M-CSF
- granulocytes
- Macrophages and dendritic cells in tissue
15
Q
Monocytes: function
A
- Differentiate into macrophages and dendritic cells
16
Q
Eosinophils: function
A
- Target larger parasites and modulate allergic reactions
17
Q
Basophils: function
A
- Release histamines for inflammatory responses and ALLERGIC REACTIONS
18
Q
Mast cell: function
A
- Release histamines and serotonin to modulate allergic reactions and INFLAMMATORY RESPONSE
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
20
Q
B-lymphocyte function: (2)
A
- function in the humoral immunity component of the adaptive immune system
- Produce plasma cells that produce antibodies
21
Q
T-lymphocytes:
- Function
- Subsets (2)
A
- Function in the adaptive immune response
- Cytotoxic T cells and Helper T cells
22
Q
Normal blood cell production: start point
A
- Multipotent hematopoietic stem cell
23
Q
Blood cell production: myeloid pathway start
A
- Multipotent hematopoietic stem cell -> Common myeloid progenitor
24
Q
Myeloid production: Megakaryocyte
- Route
- Via
A
- Common myeloid progenitor -> Megakaryocyte
- Via Thrombopoietin (TPO) prod. by liver
25
Myeloid production: Erythrocyte
- Via
- Erythropoietin (EPO) prod. by kidneys
26
Myeloid production: granulocytes
Myeloblast -> granulocytes
- Via granulocyte colony stimulating factor (G-CSF)
27
What does the full blood count (FBC) measure?: (4)
- RBC's
- WBC's
- WBC differentiation
- Platelets
28
Reticulocyte count: definition
- The number of developing RBC's
29
Relevancy of reticulocyte count in differential diagnosis of anaemia: (2)
- Increased RC: Reduced RBC survival (haemolysis or bleeding)
- Reduced RC: problem with production
30
Blood film definition:
- Snapshot of the cells that are present in the blood at the time that the sample is obtained
31
Blood film diagnostic uses: (2)
- Assess red cell, platelet and white cell (numbers, size, colour and morphology)
- View any abnormal cells
32
Haemostasis: blood vessel wall
- Endothelial cell role
- Contains negative regulators to reduce haemostasis
33
Negative regulators in endothelial cells:
- Soluble mediator
p
Soluble mediators:
- Prostacyclin
34
Negative regulators in endothelial cells:
- Surface mediators (3)
E
T
H
Surface mediators
- Endothelial protein C receptor
- Thrombomodulin
- Heparens
35
Haemostasis: blood vessel wall
- Sub-endothelial cells
- Have activators that enhance haemostasis
36
Sub- endothelial cell activators for haemostasis: (3)
- Collagen
- Tissue factor
- Von Willebrand Factor (VWF)
37
Role of platelets in haemostasis:
Adhere ...
Activate ....
Support .....
- Adhere to sub-endothelial proteins after vascular damage
- Activate and aggregate other platelets
- Support activation of coagulation factors
38
Role of VWF in haemostasis:
- Binds platelet surface proteins to mediate platelet adhesion
39
Role of coagulation factors in haemostasis:
- Series of plasma proteins which convert prothrombin to thrombin
40
Roles of fibrinogen in hameostasis:
- Binds.....
- Polymerised .....
- Binds platelet surface integrins to mediate platelet aggregation
- Polymerised to thrombin to form fibrin clot
41
Cell based model of haemostasis:
- all the components of haemostasis interact in a regulated way to generate clot only at the site of vascular injury
42
Thrombin:
- Definition
- Role
- An activated coagulation factor that is the main effector of haemostasis
- Thrombin polymerises fibrinogen to FIBRIN and fully activates PLATELETS
43
Haemostasis - step 1: trigger
(2)
1. Collagen and tissue factor exposed
2. Von Willebrand Factor (vWF) binds collagen
44
Hameostasis - step 2: Primary Haemostasis
(2)
3. Platelets adhere to vWF-collagen
4. Platelets activate and aggregate
45
Haemostasis - step 3: Thrombin generation
5. Tissue factor initiates rapid thrombin generation on activated platelets
46
Hameostasis - step 4: consolidation
6. Thrombin converts fibrinogen to fibrin and completes platelet activation
7. Stable fibrin-platelet clot is formed
47
Regulation of haemostasis: clot formation
1. vWF adhesivity is regulated by .......
ADAMTS 13
48
Regulation of haemostasis: clot formation
2. Thrombin is regulated by ....... (2)
- Antithrombin
- Activated protein c system
49
Regulation of haemostasis: fibrinolysis
- Thrombin converts enzyme plasminogen to plasmin
- Plasmin cleaves fibrin to degradation products (D-dimer)
50
Core laboratory tests of haemostasis: (4)
1. Platelet count + blood screen
2. Coagulation screen (PT + APTT)
3. Fibrinogen level
4. D Dimer level
51
PT + APTT tests principles: (3)
1. Add activator (phospholipid+Ca2+) to anticoagulated blood
2. Incubate at 37*C
3. Measure time to fibrin clot formation
52
Indications of prolonged PT or APTT: (3)
1. Reduced levels of coagulation factors (bleeding disorders)
2. Reduced function of coagulation factors (anticoagulant drugs)
3. Laboratory artefact (human error)
53
Isolate prolonged PT?:
- Factor VII issue (extrinsic pathway)
54
Isolated prolonged APPT?:
- Issues with factors VIII, IX, XI (intrinsic pathway)
55
Long PT and APTT?:
- Multiple factor defects; II, V, X, fibrinogen (common pathway)
56
What does high fibrinogen levels indicate?:
- Acute phase response, pregnancy
57
What do low fibrinogen levels indicate?:
A
L
M
- Acquired bleeding disorders
- Liver disease
- Massive transfusion
58
What does an elevated D-dimer level indicate?:
D I C
V
Multiple
1. Disseminated intravascular coagulation
2. Venous thrombosis
3. Pregnancy, liver/kidney disease, sepsis
59
Point-of-care tests of haemostasis:
- Example
- Importance
- Thromboelastometry
- Quick and easy to perform and interpret, useful in urgent clinical settings
60
Virchow's triad:
1. Hypercoagulability
2. Endothelial injury
3. Venous stasis
61
Risk factors for VTE: physiological factors (4)
1. Dehydration
2. Obesity
3. Pregnancy
4. Old age
62
Risk factors for VTE: other factors (3)
- Medical comorbidities
- Significant reduction in mobility
- Vascular access and devices
63
Risk factors for VTE: medications (3)
- Hormone replacement therapy
- Some cancer treatments
- Oestrogen-containing contraceptives
64
Risk factors for VTE: hospital/surgery (3)
- Surgery with general anaesthetic + time > 90mins
- Critical care admission
- Hospital admission
65
DVT signs and symptoms:
L
S
T
D
P O
- Leg pain
- Swelling
- Tenderness
- Discolouration
- Pitting oedema
66
VTE 'atypical' presentations:
B L S
A
D
P
- Bilateral leg swelling
- Asymptomatic
- Death
- Pyrexia of unknown origin
67
Diagnosis: DVT^1,2: (2)
- Confirmatory test:
1. Venous ultrasonography
2. MRV or CTV for VTE at unusual sites
68
Diagnosis: PE^2-4:
- Confirmatory tests:
1. CT pulmonary angiogram
2. Ventilation-perfusion scan
69
D-dimer test for VTE:
- Use
- False negatives if. .....
- Increased levels in VTE and other diseases/conditions
- False negative: patient on anticoagulants, take blood before starting anticoagulants
70
Screening thrombophilia to see if it is..... (2)
- Inherited thrombophilia
- Acquired thrombophilia: screening for antiphospholipid syndrome
71
Antiphospholipid syndrome:
- Description
- Associations
- Autoimmune, acquired prothrombotic condition
- Associated with systemic lupus erythematosus (SLE)
72
Antiphospholipid syndrome: clinical features
A T
V T
M T
P L
L R
T
- Arterial thrombosis
- VTE
- Microvascular thrombosis
- Pregnancy loss
- Livedo reticularis (red-blue rash)
- Thrombocytopenia
73
Antithrombotics:
- definition
- potential side effect for all
- Used to treat and prevent thrombotic complications
- Bleeding
74
Anticoagulant examples: (3)
- Heparin
- Warfarin
- DOACs (Direct Oral Anticoagulants)
75
Commonest clinical indications for anticoagulation:
V
V P
S P
M
- VTE (TD)
- VTE prevention
- Stroke prevention in AF (TD)
- Mechanical heart valves - Warfarin (TD)
76
Anticoagulants: Warfarin
- Mechanism
- Half-life
- Renal clearance
- Inhibits vitamin K metabolism, reducing factors II, VII, IX and X
- 40 Hrs
- Renal clearance: 8% (low)
77
Anticoagulants: Dabigatran (DOAC)
- Mechanism
- Half-life
- Renal clearance
- Direct thrombin inhibitor
- 12-18 hrs
- 85% (high)
78
DOACs: direct fator Xa inhibitors (3)
A
R
E
- Apixaban
- Rivaroxaban
- Edoxaban
79
Apixaban:
- Action
- Half-life
- Renal clearance
- Direct factor Xa inhibitor
- 12 Hrs
- 27%
80
Rivaroxaban:
- Action
- Half-life
- Renal clearance
- Direct factor Xa inhibitor
- 5-9hrs young 11-13 hrs old
- 33%
81
Edoxaban:
- Action
- Half-life
- Renal clearance
- Direct factor Xa inhibitor
- 10-14hrs
- 50%
82
Anticoagulants: Heparin
- Action
- Half-life
- Renal clearance
- Direct factor Xa and thrombin inhibitor
- 4-5 hrs
83
Warfarin:
- Characteristics
- Effect on coagulation time
- Monitored by.......
- Slow onset and long half life
- Increases PT and APTT
- Monitoring using INR (patient PT/control PT)
84
Warfarin is used for: (4)
M H V
S R F
A S
A F with
- Mechanical heart valves
- Severe renal failure
- Antiphospholipid syndrome
- AF with rheumatic mitral stenosis
85
Warfarin:
- Interactions
- Reversals
- Many medications and food (Vit K in veg, alcohol)
- Vitamin K (6h) or po(24h)
86
Heparin: LMWH
- Administration
- Lab measure
- Onset
- t1/2
- Sub cutaneous
- antiXa
- Fast onset (3hr peak)
- 4-5hr
87
Heparin: UFH
- Administration
- Lab measure
- t1/2
- Iv or SC
- APTT or antiXa
- t1/2 = 1-2Hr
88
DOACs: PROS
- Convenient
- onset & t1/2
- Risks reduction
- 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
DOACs: CONS (3)
- Multiple drugs needed at once
- Need for good compliance
- Follow up still needed
90
Anticoagulation treatment for VTE:
- Duration
- Decision
- Three months for acute thrombosis
- Then decision to be made: recurrence vs bleeding
91
Assessing bleeding risk in VTE: Acute VTE (proximal DVT or PE)
- 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
Who should be considered for long term anticoagulants?:
- Unprovoked cases: medium chance of recurrence
- Persistent significant risk factor: HIGH RISH
93
Primary haemostasis disorders are caused by defects in: (3)
- Platelets
- VWF
- Vessel wall
94
Coagulation disorders are caused by defects in: (2)
- Coagulation factors
- Fibrinogen
95
Bleeding types more prevalent in Primary haemostasis disorders: (2)
- Abnormal skin bleeding
- Abnormal nose and mouth
96
Bleeding types more common in Coagulation disorders:
- Joint bleeds (haemarthrosis)
- Soft tissue bleeds (haematoma)
97
Bleeding types equally common between primary haemostasis & coagulation disorders: (3)
- Heavy menstrual bleeding
- Obstetric and surgical bleeding
- CNS and gut bleeds
98
ISHT bleeding assessment tool:
- 9 possible bleeding sites are scored on a severity of 1-4 each
99
Clinical history and examination -> Active bleeding
- Factors to asses (3)
- PTT, APTT and PLT count
- Fibrinogen
- Haemoglobin
100
Clinical history and examination -> elective investigation: first line tests
- PT, APTT and PLT count
101
Clinical history and examination -> elective investigation: Second line tests
- Fibrinogen levels
- VWF levels
- PLT function
102
Approach to abnormal coagulation test results:
- Common in patients with no bleeding, must be considered in the clinical context
103
Genetic diseases in haemostasis: (4)
V
H
F
HPFD
- VWF disease
- Haemophilia A & B
- Factor XI deficiency
- Heritable platelet function disorder
104
Difference between haemophilia A and B:
Haemophilia A = Factor VIII deficiency
Haemophilia B = Factor IX deficiency
105
Haemophilia features:
- Inheritance
- X linked recessive
106
Haemophilia features:
- Coagulation pathway bleeding symptoms
- Soft tissue and joint bleeding
- Bleeding after surgery/dental extraction
107
Haemophilia features: laboratory
- Increased APTT
- Decreased factor VIII or factor IX
- Pathogenic variants in F8 or F9
108
Causes of acquired bleeding diseases: reduced synthesis (3)
- LIVER DISEASE
- Vit K deficiency
- Immune thrombocytopenia
109
Causes of acquired bleeding diseases: Impaired function (3)
_ CKD
- LIVER DISEASE
- Heparin, DOACs, NSAIDs
110
General affect of liver disease on clotting:
- Liver synthesises most haemostasis proteins and regulates PLT production in the marrow
111
Effect of liver disease due to reduced protein synthesis:
- Decreased clotting factor
- Decreased fibrinogen
- Decreased regulator levels
112
Effect of liver disease due to cholestasis:
- Decreased clotting factor function due to vitamin K malabsorption
113
Effect of liver disease on thrombopoietin (TPO):
- Reduced TPO synthesis decreases PLT numbers
114
Effect of liver disease on metabolism:
- Metabolic disturbance causes a decrease in PLT function
115
Extra detrimental effect of liver disease:
- Clue: Increased Fi........
- Increased fibrinolysis
116
Liver disease symptoms relating to bleeeding: (3)
- Skin and soft tissue bleeds
- Acute GI tract bleeding due to oesophageal varices
- Retinal bleeds
117
Laboratory signs of liver disease:
- PT/APTT
- Fibrinogen
- PLT
- D-dimer
- Increased PT and APTT
- Decreased fibrinogen
- Decreased PLT count
- Increased D-dimer
118
Complex multisystem disorder in haemostasis:
- Examples of what may trigger DIC (3)
- Sepsis
- Cancer
- Trauma
119
Disseminated Intravascular coagulation (DIC): defintion
- Combination of thrombosis and bleeding disorder
120
Pathogenesis of DIC: (2)
- Increase in prothrombotic protein
- Loss of negative haemostasis regulators
121
Effects of DIC:
- Leads to ......
- Symptom
- Consumption of ...
- Leads to widespread and dysregulated haemostasis activation
- Fibrin and platelet microvascular thrombi
- Consumption of PLT, coagulation factors and fibrinogen
122
Pathogenesis of DIC:
- PT/APTT
- PLT count
- D-dimer count
- Extra sign
- Increased PT and APTT
- Decreased PLT
- Increased +++ D-dimer
- Usually anaemia
123
Principles of treatment for abnormal bleeding: (3)
1. Avoid/control causes of bleeding (local measures)
2. Pro-haemostatic drugs
3. Replace missing content
124
Replacing missing content in abnormal bleeding:
- Blood products from donor (2)
- Factor concentrates: (2)
- Blood products from donor: fresh frozen plasma, platelet transfusion
- Factor concentrates: plasma derived, recombinant
125
Pro-haemostatic drugs: tranexamic acid
- Action
- Effective in .....
- Blocks plasmin binding and activation of fibrin, reducing FIBRINOLYSIS
- Effective in genetic and acquired bleeding disorders and major haemorrhage
126
Pro-haemostatic drugs: Desmopressin (DDAVP)
- Action
- Effective in ....
- Release factors VIII and VWF
- Mild haemophilia A and VWF deficiency (also in other mild bleeding disorders)
127
Blood products from donor: fresh frozen plasma
- Contains ......
- Indications (3)
- All soluble coagulation factors and proteins
- Bleeding in severe liver disease
- Massive transfusion
- Disseminated intravascular coagulation
128
Blood products from donor: platelet transfusion
- Contains
- Indications (4)
- B M F
- Exposure to ...
- T,D,M T
- G
- Platelets and small amount of RBC
- Bone marrow failure
- Exposure to anti-PLT drugs
- Trauma, DIC, massive transfusion
- Genetic PLT disorders
129
Factor concentrates: plasma derived (4)
- VWF
- Fibrinogen
- Factor XI
- Factor XIII
130
Factor concentrates: recombinant (3)
- Factor VIII
- Factor IX
- Factor VIIa
131
Brief summary of a blood donation:
- Replacement of substances in the recipient from donated blood (cells, plasma, protein)
132
Separation of blood into components following donation:
- Depletion
- Split
- Leukocyte depletion (to prevent immune response)
- Split into RBCs/PLTs (for bacteria testing) /plasma
133
What is plasma used for once it is separated from the rest of the blood?: (3)
- F P P
- F F P
-C (F)
- Plasma is used for:
1. fractionated plasma proteins
2. fresh frozen plasma (clotting factors)
3. cryoprecipitate (fibrinogen)
134
Transfusion incompatability: Major
- Recipient has antibodies against transfused blood
135
Transfusion incompatibility: Minor
- Transfused blood has antibodies against recipient
136
Red cell compatibility: recipient blood group O
- Antibodies formed
- Red cells for transfusion
- Anti-A, Anti-B
- Group O only
137
Red cell compatibility: recipient blood group A
- Antibodies formed
- Red cells for transfusion
- Anti-B
- Group A or O
138
Red cell compatibility: recipient blood group B
- Antibodies formed
- Red cells for transfusion
- Anti-A
- Group B or O
139
Red cell compatibility: recipient blood group AB
- Antibodies formed
- Red cells for transfusion
- None
- Groups AB, A ,B or O
140
Donor plasma compatibility:
- explanation
- universal donor
- universal recipient
- The recipient patient cannot receive plasma containing anti-bodies against there blood type
- Group AB (no ABO antibodies)
- Group O (no antigens)
141
Rhesus (Rh) factor rule: Rh+
- Definition
- Receive
- Donate
- you have Rh antigen and will not make antibodies for it
- can receive Rh- or Rh
- can only donate to Rh+
142
Rhesus (Rh) factor rule: Rh-
- Definition
- Receive
- Donate
- You do not have Rh antigen and will make antibodies for it
- Can only receive Rh-
- Can donate to Rh- and Rh+
143
Acute transfuse reactions: (2)
- Acute haemolysis
- Bacteria contamination
144
Acute breathlessness due to transfusion: (3)
- Fluid overload
- Anaphylaxis
- Transfusion related lung injury
145
Minor reactions to transfusions: (2)
- Rash
- Febrile reaction
146
Transfusion transmitted diseases: (4)
- Viral
- Bacterial
- Protozoa
- CJD
147
Risk factors for arterial thrombosis:
S
H
H
D
O/S
M/D
A
- Smoking
o Hypertension
o Hyperlipidaemia
o Diabetesmellitus
o Obesity/sedentarylifestyle
o Mentalstress/depression
o Advancing age
148
Novel markers for arterial thrombosis:
- High sensitivity CRP
- Homocysteine
- Lipoprotein
149
Presentations of arterial thrombosis: Cerebrovascular event (3)
- Carotid stenosis (blockage)
- Thromboembolic (clot)
- Haemorrhagic (rupture)
150
Presentations of arterial thrombosis: Acute coronary syndrome (3)
o Plaque rupture
o Plaque erosion
o Calcific nodule
151
Presentations of arterial thrombosis: peripheral artery disease (2)
- Claudication (reduced blood flow to limbs)
- Acute ischaemia
152
Pathophysiology of arterial thrombosis:
- Existing plaque due to formation of atherosclerosis ....... (5)
1. Plaque disruption
2. Collagen exposure
3. Platelet activation
4. Platelet aggregation
5. Vessel occlusion
153
Aetiology of atherosclerosis: what initiates the process?
- What does it cause?
- Risk factors for this? (S,H,H,)
- Oxidative stress
- Endothelial cell dysfunction
- Smoking, hyperlipidaemia, hypertension, stress
154
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
Leucocyte adhesion →
infiltration of LDL →
proliferation of smooth muscle cells →
vasoconstriction→
foam cell formation (oxidised LDL)→apoptosis
155
Consequences of atherosclerosis: heart (3As)
- Angina
- ACS - plaque rupture/erosion, calcific nodule
- AF
156
Consequences of atherosclerosis: Brain (2)
▪ Cerebrovascular accident – carotid stenosis, thromboembolic, haemorrhagic
▪ Vascular dementia
157
Consequences of atherosclerosis: peripheral (4)
R
A A
P
I
▪ Renal artery stenosis
▪ Aortic aneurysm
▪ Peripheral artery disease – claudication, acute ischaemia
▪ Impotence
158
Acute ST-elevation therapy: first line treatment
- Rapid revascularisation + anti-thrombotic therapies
159
Acute ST-elevation therapies: (2)
- Thrombolysis: pre-hospital/during
- Percutaneous coronary intervention
160
Percutaneous coronary intervention:
- primary
- Emergency procedure to widen narrowed blood vessels
161
Percutaneous coronary intervention:
- Facilitated
- Fibrinolytic therapy to stabilize the patient while transport is being arranged to primary PCI facility
162
Platelet activation/deactivation pathway:
- Initial reaction
- Activation
- Deactivation
- Arachidonic acid (AA) -> PGH2 via COX1/2 enzymes
- PGH2 acts upon TXA2
- PGH2 acts upon PGI2
163
Aspirin mechanism of action: (3)
- Action
- Effects (2)
- Inactivates COX1/2
- Decreases TXA2 levels (an activator)
- Continued production of PGI2 (inactivator)
164
Aspirin: use
- In acute MI in combo with fibrinolytic drugs
165
P2Y12 receptor:
- Relation to PLTs
- Function
- P2Y12 highly expressed on PLT
- Binding site of VWF, collagen, TXA2 and thrombin to induce platelet aggregation
166
P2Y12 receptor antagonist:
- Action
- Use
- Blocks the P2Y12 receptor, reducing platelet aggregation
- Strokes and MI's
167
Example of Py12 receptor antagonists: Irreversible
- Clopidogrel
168
Examples of Py12 receptor antagonists: Reversible (2)
- Ticagrelor
- Cangrelor
169
αIIbβ3: mechanism
- Cross linking of platelets via fibrin
170
αIIbβ3 antagonists: mechanism
- prevent fibrin binding to these receptors, stopping platelet aggregation
171
αIIbβ3 antagonist: uses
- Acute MI
- MI prevention
- Coronary bypass
172
αIIbβ3 antagonist: examples
- Abc....
- Tiro....
- Eptif.....
- Abciximab
- Tirofiban
- Eptifibatide
173
Fibrinolytic therapy: mechanism of action (2)
- Promotes conversion of plasminogem to plasmin
- Plasmin proteolytic enzyme degrades fibrin to fibrinogen
174
Endogenous plasminogen activators (PA):
S
t
U
- Streptokinase-plasminogen complex
- tPA
- Urokinase
175
Fibrinolytic therapy: Uses
A M
A T
A A T
- Acute MI (within 12 hrs onset)
- Acute thrombotic stroke
- Acute arterial thromboembolism
176
Fibrinolytic drug examples:
S
R
T
- Streptokinase
- Reteplase
- Tenectplase
177
Mechanism of Tranexamic acid:
- Inhibits plasminogen activation
178
Mechanism of Aprotinin:
- Inhibits plasmin
179
Aprotinin use:
- Used in patients with a high risk of blood loss (i.e. after open heart surgery)
180
Tranexamic acid use:
- Increased risk of bleeding (dental extraction / prostatectomy)
