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phase 1 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Platelet biochemistry

What is the action of prostacyclin on platelet activation/ adhesion/ aggregation in undamaged areas?

A

Inhibition

Prostacyclin inhibits platelet activation/ adhesion/ aggregation in undamaged areas

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2
Q

Platelet biochemistry

Damage to the endothelium of blood vessels causes what to be exposed?

A

Collagen

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3
Q

Platelet biochemistry

What is adhesion?

A

Platelets binding to exposed collagen

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4
Q

Platelet biochemistry

Which receptors/ intermediate molecules help during initial adhesion?

A

During intial adhesion GP1B receptors on platelets bind to the intermediary Von Willebrand factor (VWF) on the exposed collagen

Platelet - GP1B - VWF - Collagen

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5
Q

Platelet biochemistry

Which receptors/ intermediate molecules help during stable adhesion?

A

GPVI receptors on activated platelets help them bind to collagen directly

Platelet - GPVI - Collagen

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6
Q

Platelet biochemistry

How do platelets adhere to each other? (Mention receptors/ intermediate molecules)

A

Platelets adhere to eachother using GP2b/3a receptors and fibrinogen as an intermediate

Platelet - GP2b/3a - Fibrinogen - GP2b/3a - Platelet

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7
Q

Platelet biochemistry

The binding of platelets to collagen releases the contents of their secretory vesicles via exocytosis.

Which molecules are released?

A
  • Thromboxane A2
  • Thrombin
  • ADP
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8
Q

Platelet biochemistry

Where is thromboxane A2 derived from?

A

Arachidonic acid is converted into Prostaglandin H2 by the COX 1 enzyme.

Prostaglandin H2 is converted into Thromboxane A2.

This is done in platelets.

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9
Q

Platelet biochemistry

What is the action of Thromboxane A2?

A

It causes vasoconstriction and further platelet acitvation and aggregation.

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10
Q

Platelet biochemistry

Where is thrombin derived from?

A

Thrombin (a.k.a factor 2a) is the activated version of Prothrombin (factor 2).

Prothrombin is a protein that comes from the liver.

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11
Q

Platelet biochemistry

What is the action of thrombin?

A

Thrombin binds to PAR1 and PAR4 (both are receptors on platelets).

This activates platelets and induces further thrombin release (positive feedback).

It also leads to the release of ADP from electron dense granules.

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12
Q

Platelet biochemistry

What happens specifically when thrombin binds to PAR1?

A

Intracellular stores release Ca2+ which results in the inhibition of translocase and activation of the scramblase protein.

This causes the aminophospholipids present on the inner membrane of the platelets to be expressed on the outer membrane.

This leads to the assembly of prothrombinase and allows for prothrombin to be converted into thrombin.

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13
Q

Platelet biochemistry

What is the function of ADP (released from electron dense granules)?

A

Binds to P2Y1 and P2Y12

P2Y1- leads to further activation of platelets
P2Y12- leads to further aggregation of platelets

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14
Q

Platelet biochemistry

What are the effects of platelet activation?

A

Platelets change shape from smooth discoid to spiculated with psuedopodia

The number of GP2b/3a receptors increase (leading to more platelet aggregation) and their affinity to fibrinogen also increases.

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15
Q

Platelet biochemistry

What are the different types of granules in platelets?

A

Electron dense granules
Alpha granules

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16
Q

Platelet biochemistry

What molecules do electron dense granules release?

A

Ca2+
ADP/ATP
Serotonin

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17
Q

Platelet biochemistry

What molecules do alpha granules release?

A

Fibrinogen
VWF
Platelet derived growth factor

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18
Q

Platelet biochemistry

What does serotonin do?

A

Stimulates vasoconstriction

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19
Q

Platelet biochemistry

Which two molecules stimulate vasoconstriction?

A

Thromboxane A2
Serotonin

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20
Q

Platelet biochemistry

What is the primary haemostatic plug?

A

The primary hemostatic plug is the initial platelet-rich clot that forms at the site of a vascular injury, temporarily stopping blood flow.

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21
Q

Platelet biochemistry

Put these in order and summarise them:
Aggregation, Injury, Activation, Adhesion

A
  1. Injury- Vasoconstriction via endothelin release
  2. Adhesion- Platelets binding to exposed collagen
  3. Activation- Pseudopodia and granule release
  4. Aggregation- Platelets binding to platelets using GP2b/3a receptors and fibrinogen
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22
Q

Platelet biochemistry

Where is prostaglandin H2 derived from?

A

Arachidonic acid is converted into prostaglandin H2 via COX1 and COX2 enzymes

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23
Q

Platelet biochemistry

What can prostaglandin H2 be converted into?

A

Thromboxane A2 or Prostacyclin

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24
Q

Platelet biochemistry

How do Thromboxane A2 and Prostacyclin differ?

A

Thromboxane A2 is a vasoconstrictor and promotes platelet activation

Prostacyclin is a vasodilator and inhibits platelet activation/ adhesion/ aggregation

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25
Q

Clotting cascade

What is the clotting cascade?

A

A series of events that results in a stable blood clot that stops bleeding

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26
Q

Clotting cascade

What is the difference between the intrinsic and extrinsic pathways?

A

The intrinsic pathway responds to spontaneous, internal damage of the vascular endothelium, whereas the extrinsic pathway becomes activated secondary to external trauma.

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26
Q

Clotting cascade

Explain the extrinsic pathway

A

When the endothelium is damaged the endothelial cells release tissue factor.

Tissue factor along with factor 7a activates factor 10 into 10a.

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27
Q

Clotting cascade

Explain the intrinsic pathway.

A

Exposed collagen activates factor 12 into 12a.

Factor 12a activates factor 11 into 11a.

Factor 11a activates factor 9 into 9a.

Factor 9a activates factor 8 into 8a.

Factor 8a, along with factor 5a, converts factor 10 into 10a.

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28
Q

Clotting cascade

Explain the common pathway

A

Factor 10a converts prothrombin (factor 2) into thrombin (factor 2a).

Thrombin converts fibrinogen (factor 1) into fibrin (factor 1a).

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29
Q

Clotting cascade

What coagulation factors does the liver produce?

A

Every factor except 3, 4 and 8.

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30
Q

Clotting cascade

Where is VWF produced?

A

Liver

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31
Q

Clotting cascade

What is blood serum?

A

Blood plasma without clotting factors

32
Q

Clotting cascade

What are the vitamin K dependant coagulation factors?

A

10, 9, 7 and 2

Remember as 1972

33
Q

Clotting cascade

Describe the fibrinolytic system

A

Tissue plasminogen converts plasminogen into plasmin.

Plasmin degrades the fibrin mesh in the clot into fibrin degradation products, dissolving the clot.

34
Q

Structures and functions of RBCs, WBCs and platelets

Describe the structure of haemoglobin

A

4 globin chains in total
Each chain has a haem group
Each haem group has an iron ion in the centre that oxygen binds to.

35
Q

Structures and functions of RBCs, WBCs and platelets

Give 4 examples of haemoglobin types

A

HbA- Alpha haemoglobin
HbB- Beta haemoglobin
HbF- Foetal haemoglobin
HbS- Sickle haemoglobin

36
Q

Structures and functions of RBCs, WBCs and platelets

What chains make up adult haemoglobin?

A

2 HbA, 2 HbB

37
Q

Structures and functions of RBCs, WBCs and platelets

What chains make up foetal haemoglobin?

A

2 HbA, 2 HbF

38
Q

Structures and functions of RBCs, WBCs and platelets

What chains make up the haemoglobin sickle cell anaemia patients?

A

2 HbA, 2 HbS

39
Q

Structures and functions of RBCs, WBCs and platelets

Leukocytes are split into which groups?

A

Granulocytes
Agranulocytes

40
Q

Structures and functions of RBCs, WBCs and platelets

What are granulocytes?
Give examples

A

Cells that can release content of their granules via degranulation.
- Neutrophils
- Basophils
- Eosinophils
- Mast cells

41
Q

Structures and functions of RBCs, WBCs and platelets

What are agranulocytes?

A

A type of Leukocytes that don’t have any granules in their cytoplasm.

  • Lymphocytes (B & T cells)
  • Monocytes (Antigen presenting macrophages)
42
Q

Structures and functions of RBCs, WBCs and platelets

What type of cells can monocytes differentiate into?

A
  • Kuppfer cells
  • Dendritic cells
  • Alveolar macrophages
  • Microglia
43
Q

Structures and functions of RBCs, WBCs and platelets

Where do T-lymphocytes originate?

A

Bone marrow

44
Q

Structures and functions of RBCs, WBCs and platelets

Where do B-lymphocytes originate?

A

Bone marrow

45
Q

Structures and functions of RBCs, WBCs and platelets

Where do T- lymphocytes mature?

A

Thymus gland

46
Q

Structures and functions of RBCs, WBCs and platelets

Where do B-lymphocytes mature?

A

Bone marrow

47
Q

Structures and functions of RBCs, WBCs and platelets

After maturation where do T-lymphocytes circulate?

A

Mucosal and cutaneous lymphoid tissues

48
Q

Structures and functions of RBCs, WBCs and platelets

After maturation where do B-lymphocytes circulate?

A

Lymph nodes and the spleen

49
Q

Constituents of plasma protein

What is plasma?

A

A transport medium that contains salt, water, glucose and proteins

50
Q

Constituents of plasma protein

What is the main function of albumin?

A

Keeps intravascular fluid within the blood vessels

51
Q

Constituents of plasma protein

What proteins exist in plasma?

A
  • Albumin
  • Carrier proteins
  • Coagulation factors
  • Immunoglobulins
52
Q

Constituents of plasma protein

What are the different immunoglobulin types and their functions?

A
  • IgM- Produced in primary immune response
  • IgG- Produced in secondary immune response
  • IgA- Present in mucosal secretions (e.g. tears, saliva, etc.) to prevent pathogen entry
  • IgE- Allergic reactions
  • IgD- Unknown function

Remember as MAGE/GAME (since IgD’s function is unknown)

53
Q

Constituents of plasma protein

What is serum?

A

Blood plasma without any clotting factors

54
Q

Blood groups and the rhesus system

What determines the difference between blood types?

A

The sugar on the antigen

55
Q

Blood groups and the rhesus system

Describe the production of antibodies in infants

A

Infants below 3 months produce few antibodies and use maternal antibodies
After 3 months they produce their first true antibodies.

56
Q

Blood groups and the rhesus system

out of IgM and IgG, which can cross the placenta?

A

IgG can cross the placenta

57
Q

Blood groups and the rhesus system

What antibodies do people with type A blood produce?

A

Anti-B antibodies

58
Q

Blood groups and the rhesus system

What antibodies do people with type B blood produce?

A

Anti-A antibodies

59
Q

Blood groups and the rhesus system

What antibodies do people with type AB blood produce?

A

None

60
Q

Blood groups and the rhesus system

What antibodies do people with type O blood produce?

A

Both anti-A and anti-B antibodies

61
Q

Blood groups and the rhesus system

What antigens do people with type O blood have?

A

No antigens

62
Q

Blood groups and the rhesus system

Which blood group is the universal acceptor and why?

A

AB because they have no antibodies

63
Q

Blood groups and the rhesus system

Which blood group is the universal donor and why?

A

O because they have no antigens

64
Q

Blood groups and the rhesus system

Who produces anti-D immunoglobulin?

A

People who are RhD+

65
Q

Blood groups and the rhesus system

When is the anti-d immunoglobulin produced?

A

When RhD- people are exposed to RhD+ blood

66
Q

Blood groups and the rhesus system

What is HDFN?

A

Haemolytic disease of the foetus and new-born

67
Q

Blood groups and the rhesus system

How does rhesus disease occur?

A
  1. A baby with a RhD negative mother and RhD positive father might be RhD positive.
  2. The mother makes RhD antibodies for the first pregnancy, but these antibodies are IgM and cannot cross the placenta.
  3. If the second pregnancy is also one with a RhD positive baby, the mother will make IgG RhD antibodies (secondary immune response).
  4. The IgG antibodies can cross the placenta and cause haemolysis in the baby so it may become anaemic.
68
Q

Blood groups and the rhesus system

What is the prevention for rhesus disease and how does it work?

A

Anti-D immunoglobulin injections, this prevents the mother from making her own anti-D immunoglobulins and prevents sensitisation.

69
Q

Blood groups and the rhesus system

When does the prevention for rhesus disease not work and why?

A

If the mother has already developed anti-D antibodies in previous pregnancies it is harder to use the injection and the baby will have to be monitored.

70
Q

Cardiac cycle

What does the P wave on an ECG represent?

A

Atrial depolarisation

71
Q

What stimulates atrial depolarisation?

A

Firing of the SAN

72
Q

Why does atrial contraction only account for a fraction of ventricular filling?

A

Because the ventricles are already almost full due to passive blood flow through the AV valves.

73
Q

What causes the AV valves to close?

A

Atrial contraction completes so atrial pressure begins to fall, reversing the pressure gradient across the AV valves.

74
Q

What is the first heart sound (S1)?
What does it mark?

A

The closing of the AV valves

It marks the beginning of systole

75
Q

What does the QRS complex represent?

A

Ventricular depolarisation

76
Q

What is isovolumetric contraction?
When does it happen?

A

It is a phase in early systole when the ventricles begin to contract but both the AV valves and the semi-lunar valves remain shut.

It is called isovolumetric because no blood is ejected and ventricular volume remains unchanged.

77
Q

When does ventricular ejection begin?

A

When ventricular pressures exceed the pressures within the aorta and pulmonary artery.

78
Q
A

phase 1 (8 decks)

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