Blood & Immune Flashcards

1
Q

What are the components of blood?

A

Cells, proteins, lipids, electrolytes, vitamins/hormones, glucose

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2
Q

What cells are present in blood?

A

Erythrocytes, myeloid, lymphoid

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3
Q

What proteins does blood contain?

A

Albumin, haemoglobin, fibrinogen, immunoglobulins

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4
Q

Which lipids are found in blood?

A

HDL, LDL, VLDL

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5
Q

Which electrolytes are found in blood?

A

Salts & minerals - HCO3, Na, Cl, Ca, Mg, K, creatinine, creatine

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6
Q

What are the functions of erythrocytes?

A

O2 transport from lungs to tissue

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7
Q

What are leukocytes?

A

WBCs, multiple forms, immune defence

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8
Q

What is the function of platelets?

A

Coagulation & tissue repair

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9
Q

What is plasma?

A

Viscous liquid - fraction of blood without cells, contains fibrinogen that is removed with coagulation

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10
Q

What is serum?

A

Yellow liquid, less viscous, remains after removal of clot

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11
Q

What is the function of albumin?

A

50% of blood proteins, maintains colloidal osmotic pressure, binds & transports many small molecules, hormones, drugs

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12
Q

What is the function of fibrinogen?

A

7% of blood protein, activated through coagulation cascade to form cross linked fibrin

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13
Q

What are immunoglobulins?

A

Antibodies, antigen binding proteins produced by B lymphocytes

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14
Q

What is the function of complement?

A

9 proteins that coat bacteria targeting them for phagocytosis, covalent bonds

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15
Q

What is coagulation?

A

13 proteins cleaved in an ordered cascade resulting in fibrinogen turning into fibrin, calcium is essential

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16
Q

What are the functions of electrolytes?

A

Isotinicity & buffering, maintain blood ph at 7.4, maintain Ca & K

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17
Q

What is haematopoeisis?

A

Formation of blood cells, haematopoetic stem cells kept in bone marrow

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18
Q

What is the marker on haematopoetic stem cells?

A

CD34+ (cluster differentiation)

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19
Q

What are the 2 lineages that haematopoetic stem cells divide into?

A
  1. Lymphoid cells - produces adaptive response

2. Myeloid cells - produces myeloid, erythroid, thromboid cells, innate immunity

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20
Q

Which cells are in innate immunity?

A

Basophils, neutrophils, easinophils, monocytes

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21
Q

Which cells are in the adaptive immunity?

A

Small lymphocyte forming - T lymphocytes, B lymphocytes, plasma cells derived from B lymphocytes

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22
Q

Haematopoeisis: What is GM-CSF (Granulocyte macrophage colony-stimulating factor)?

A

Produced by macrophages, T cells, endothelial cells & fibroblasts.
Stimulates production of neutrophils, basophils & monocytes.

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23
Q

Haematopoeisis: What is erythropoietin’s (EPO) function?

A

Drives production of erythrocytes, produced mainly by kidney during adulthood & liver in perinatal.

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24
Q

Haematopoeisis: What is G-CSF (Granulocyte colony-stimulating factor)?

A

Produced by many different cells, stimulates production of granulocytes & acts to mature neutrophils

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25
Q

How does oxygen bind to haemaglobin?

A

Heme protein using Fe+, allowing oxygen to bind & unbind depending on the partial pressure of oxygen

26
Q

How many oxygen atoms can 1 Hb molecule carry?

A

4

27
Q

What immunity is the complement cascade from?

A

Innate

28
Q

What does complement do?

A

Forms stable complement convertases on the bacterial surface, myeloid cells recognise the convertases to engulf & phagocytose the bacteria, end product is membrane attack complex which has ability on some bacteria to put holes in the surface of the bacteria to kill them directly

29
Q

What is complement?

A

Proteoloytic activation cascade, essential for innate immunity. C3 is most abdunant. Can be activated by 3 different pathways.

30
Q

What is the classical pathway of complement?

A

Mediated by antibodies IgM or IgG binding to a microbe surface which is then bound by complement C1.

31
Q

What is opsonisation?

A

Chemoattractants such as C5a are released that radiate away from bacteria & sensed by the leading edge of the neutrophil.
Neutrophils migrate up the chemoattractant gradient - polymerising actin filaments at their leading edge & de-polymerising at their trailing edge.
Neutrophils have receptors that bind deposited complement proteins (mainly C3b) on the surface. Deposition of complement on microbes which is essential for phagocytosis, deposited complexes are called convertases which activates more complement that then deposits to coat the surface

32
Q

How are convertases bound?

A

Irreversably bound through covalent bonds

33
Q

What are chemoattractants?

A

Cleavage of C3, C4 & C5 produce small fragments (C3a, C4a & C5a) that are powerful anaphylotoxins that attract & activate neutrophils

34
Q

What happens in the end stage of complement?

A

From C5 onwards, a lytic pore is formed that cause some bacteria to lyse - this is the membrane attack complex (MAC).

35
Q

What are virulence factors?

A

Proteins produced by microbes that inhibit complement cascade

36
Q

What is the enzyme that all anticoagulants work on to prevent thrombin from cleaving fibrinogen to fibrin to form the clot?

A

Thrombin

37
Q

What are the 2 pathways in the coagulation cascade?

A
  1. Intrinsic - caused by contact with surfaces

2. Extrinsic - caused by tissue damage

38
Q

What is the key enzyme that is common to both the coagulation pathways?

A

Factor X (10)

39
Q

What electrolyte is essential to blood clotting?

A

Calcium

40
Q

What is thrombin in the coagulation cascade?

A

The enzyme that cleaves fibrinogen to fibrin which cross-links

41
Q

How is plasminogen used?

A

Converted to active plasmin & dissolves the clot (thrombolysis)

42
Q

What is innate immunity?

A

First line/immediate response to pathogen invasion, more primordial than adaptive immunity. Provided by:

  • Complement
  • Myeloid cells & phagocytosis
  • pattern recognition receptors (PRR)
43
Q

What are viruses?

A

Intracellular pathogens, defence relies on antibodies & cellular immunity, can’t survive on own - has to infect cell to replicate & produce progeny

44
Q

What is bacteria?

A

Mostly extracellular pathogens, defence is primarily mediated by innate mechanisms & phagocytosis, can survive on own & in many different conditions

45
Q

What is protozoa/parasites?

A

Complex multicellular organisms require direct killing by chemical mediators released by specialist myeloid cells, granules filled with cytotoxic chemicals, degranulation releases toxic inflammatory chemicals such as histamine

46
Q

What is gram positive bacteria?

A

Thick peptidoglycan cell wall as defence, requires phagocytosis - not directly killed by complement, stains with gram stain e.g. staph aureas

47
Q

What is gram negative bacteria?

A

Thin peptidoglycan layer surrounded by outer membrane, can be lysed directly by complement membrane attack complex, does not stain with gram stain e.g. E. coli

48
Q

What are the steps in neutrophil extravasation?

A
  1. Activation
  2. Tethering
  3. Adhesion
  4. Diapedesis
  5. Chemotaxis
49
Q

What happens during activation of neutrophil extravasation?

A

Chemokines from tissue injury or inflammation activate the local endothelial cells lining an adjacent capillary wall

50
Q

What happens during tethering of neutrophil extravasation?

A

Neutrophil tethers to inside of capillary wall. Mediated by selections upregulated on endothelial cells & sialyl Lewis X (CHO antigen on neutrophils)

51
Q

What happens during adhesion of neutrophil extravasation?

A

Strong binding between neutrophil integrins & ICAM-1 on the endothelium. Neutrophil immobilises & flattens

52
Q

What happens during diapedesis of neutrophil extravasation?

A

Neutrophil squeezes between endothelial cells into interstitial space

53
Q

What happens during chemotaxis of neutrophil extravasation?

A

Neutrophil migrates along a chemical gradient to the site of infection

54
Q

What are complement receptors?

A

Myeloid cell receptors that bind activated complement components deposited on bacteria.
CR1 (main neutrophil receptor that binds to C3b), CR2, CR3 & CR4. Cross-linking on surface CRs initiates phagocytosis

55
Q

FcR (antibody) mediated phagocytosis

A
  1. Antibody (IgM & IgG) bind to bacterial antigens
  2. Exposes the antibody Fc region
  3. Neutrophil FcR binds multivalent Fc
  4. Activates phagocytosis
  5. Membrane invaginates forming a phagosome
  6. Fuses with lysosome to form phagolysosome
  7. Phagolysosome acidifies & superoxides kill bacteria
56
Q

What is molecular pattern recognition?

A

Innate mechanism in which pattern recognition receptors (PRR) bind complex molecules that are unique to microbes. Best known are TLR

57
Q

What are Toll-Like Receptors (TLR)?

A

Leucine Rich Repeat (LRR) receptors that look like a slinky, activation through TLR stimulates a strong innate response through an important inflammation pathway

58
Q

What are pathogen associated molecular patterns (PAMPs)?

A

Molecules unique to microbes recognised by PRRs, structurally very complex, evolutionary stable, stimulate the power switch for the adaptive immune response

59
Q

What is TLR4?

A

Receptor for lipopolysaccharides (LPS) which is a membrane component of all gram-negative bacteria, tiny amounts induce powerful innate response, LPS is a pyrogen

60
Q

What is adaptive immunity?

A

Has memory, secondary response is stronger & more rapid than the primary response, affinity of B cells towards antigen increases with time & persistence of antigen