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DEN1DSA > Blood > Flashcards

Blood Flashcards

1
Q

2 main components of blood

A

Plasma (55%)
Formed Elements (45%)

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2
Q

6 components of plasma

A

proteins
amino acids
wastes
nutrients
gases
electrolytes

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3
Q

Formed Elements

A

Includes erythrocytes (red blood cells), leukocytes (white blood cells) and platelets.

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4
Q

Function of Erythrocytes (Red Blood Cells)

A
  • Deliver Oxygen to Cells
  • Remove Carbon Dioxide from Cells
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5
Q

Function of Leukocytes (White Blood Cells)

A
  • Defends the body from diseases (foreign pathogens, toxins, bacteria).
  • Divided into granulocytes and agranulocytes.
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6
Q

Granulocytes

A
  • Cytoplasm CONTAINS very fine granules .
  • Consist of neutrophils, basophils and eosinophils.
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7
Q

Agranulocytes

A
  • Cytoplasm DOES not contain granules .
  • Consist of lymphocytes and monocytes.
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8
Q

Neutrophils

A

Recognise, engulf snd destroy pathogens via phagocytosis
Release preformed granules ( hydrolytic enzymes, antimicrobial
proteins).

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9
Q

Eosinophils

A
  • target extracellular pathogens that are too large to be engulfed by phagocytosis eg. parasites
  • Facilitate allergic Reactions
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10
Q

Basophils

A

Contains granules of histamine which are released to initiate an allergic response

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11
Q

Lymphocytes

A

Specialised WBC that defends against specific pathogens

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12
Q

7 Function of Platelets

A
  • Secrete vasoconstrictors that constrict blood vessels when damaged
  • Form temporary platelet plugs to stop bleeding
  • Includes clotting factors to promote blood clotting
  • Dissolve blood clots when no longer needed
  • Digest and destroy bacteria
  • Secrete chemicals that attract neutrophils and monocytes to sites of inflammation
  • Secrete growth factors to maintain the lining of blood vessels
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13
Q

What happens if there are too few red blood cells

A
  • Reduced oxygen carrying capacity
  • Increased risk of hypoxia (oxygen deprivation)
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14
Q

What happens if there are too many red blood cells

A
  • Increases blood viscosity
  • Increases resistance to flow through blood vessels
  • Increases risk of blood clotting
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15
Q

Steps for Feedback Loop of RBC

A
  1. Stimulus: Decrease O2 carrying ability.. Due to ..
    - Decreased RBC Count
    - Decreased amount of haemoglobin
    - Decreased availability of O2
  2. Receptors: Receptors in the Kidney respond to low oxygen levels.
    - Kidney’s increase EPO secretion into the bloodstream.
    - EPO circles in higher numbers.
  3. Control Center: Stimulates proerythroblasts activating bone marrow to produce reticulocytes (immature RBC).
  4. Effectors: Reticulocytes enter circulating blood resulting in a larger number of red blood cells in circulation.
  5. Response: Increased oxygen delivery to tissues
  6. Return to homeostatic levels.
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16
Q

3 Steps in Haemostasis

A
  1. Vascular Spasm
  2. Platelet Plug Formation
  3. Coagulation
17
Q

Vascular Spasm

A
  • Blood vessels respond to injury by contracting (vasoconstriction)
  • Acts to decrease blood flow to the area of injury (restricts blood loss) enabling for other steps of
    haemostasis to occur
18
Q

Platelet Plug Formation

A
  • Occur via a positive feedback cycle.
  • Platelets come into contact with exposed collagen.
  • Platelets adhere to exposed collagen. Platelets develop
    pseudopods
  • Cytokines are released (Thromboxane, ADP, 5HT)
  • Cytokines activates and attract more platelets to the site
    of injury
  • More platelets aggregate into the region resulting in
    formation of plug
  • Act through positive feedback loop to activate more
    platelets
19
Q

Coagulation

A

Phase 1:
- Both pathways are triggered by tissue damaging events and vitamin K is necessary for normal clotting factor production
- Both pathways lead to production of factor X
- Intrinsic (slower) = activated by injury that occurs within the blood vesse. This begins the activation of factor XII (12)
- Extrinsic (Faster) = Activated by exposed blood to tissue (RELEASES, factor 7). Production of factor X that similarly produces prothrombin activator

Phase 2: Common Pathway to Thrombin
- The production of factor X and Prothrombinactivator cleaves Prothrombin to Thrombin. 3.

Phase 3: Common Pathway to Fibrin Mesh
- Thrombin catalyses the transformation of Fibrinogen to Fibrin.
- Fibrin molecules band together to form long hair-like insoluble strands
- Glue platelets together to form a structural web
- In presence of calcium, factor XIII (crosslinking enzyme), tightly binds fibrin to stabilise the fibrin
mesh.

20
Q

Fibrinolysis

A
  • Process that removes unneeded clots when healing has occurred
  • Crucial process as clots continually form and need to be degraded to prevent clogging of blood vessels
21
Q

Antithrombotic Drugs

A
  • reduce the formation of blood clots
  • For Example: Warfarin, and Aspirin
22
Q

Warfarin Action

A

Warfarin blocks Vitamin K epoxide reductase, and prevents the activation of the vitamin K related factors such as prothrombin which is involved in clotting cascade.

23
Q

Aspirin Action

A
  • Aspirin blocks cyclooxygenase enzymes, preventing the release of thromboxane.
  • Decreases the amount of platelet activation and aggregation.
24
Q

Monocytes

A

Monocytes in blood differentiate into macrophages

25
Q

HAEMOSTASIS

A

A mechanism that leads to the cessation of bleeding from a blood vessel.
Fast, localised and controlled.

26
Q

STEPS OF HAEMOSTASIS:

A

(1) INJURY TO THE BLOOD VESSEL
- causes disruption to the endothelium, exposing the connective tissue under the endothelium.
- Causes collagen fibres to be exposed to blood and platelets.

(2) PLATELET PLUG FORMATION
- Platelets resultantly become activated (because of exposure to collagen fibres).
- Platelets RELEASE ADP, which activates other platelets.
- Causes platelets to swell and stick together to form a plug – positive feedback cycle.
- Reduces the blood loss at the site of injury.

(3) COAGULATION (process of a liquid changing to a solid/semi-solidstate.)
- Fibrin forms a mesh that traps RBC and platelets, allowing the formation of a clot.
- Activation of Fibrogen to fibrin. Fibrin covalently linked mesh that
contracts and retards RBC movement.
- COAGULATION CASCADE – release of clotting factors. Blood goes from liquid to a gel.

DEN1DSA (16 decks)

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