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CMOD Week 1 > Structure and Function of Blood Cells > Flashcards

Structure and Function of Blood Cells Flashcards

1
Q

How can you prevent blood from clotting?

A

by removing free calcium ions with a chelating agent such as EDTA (lavender top tube) or citrate (blue top tube)

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2
Q

What is eosin used for?

A

Can be used for staining red blood cells in order to identify any abnormal shapes and is effective because the iron at the center of heme is positively charged and eosin sticks to it (negatively charged with a COO- group)

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3
Q

What are some of the key morphologic features of normal red cells?

A

They are bi-concave disks, fairly uniform in size, and the area of central pallor occupies about a third of the diameter of the disk

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4
Q

How does the morphology for red cells change in iron deficiency anemia?

A

the area of central pallor is enlarged

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5
Q

What are the first two elements of differential diagnosis of eosinophilia?

A

allergies and infections with parasites

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6
Q

What are roles of eosinophils?

A
  1. protect against parasites (helminths, mostly)-(this is why eosinophilia is a result of infections with parasites). Does this using major basic protein (MBP) found in its granules

NOTE: eosinophils are rare in blood (less than 5% of leukocytes)

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7
Q

What does methylene blue stain?

A

hydrophobic acidic macromolecules (nucleic acids and some proteins). It’s positively charged

Soluble in water and methanol

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8
Q

What is the role of histamine in inflammation?

A

increases permeability of small blood vessels

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9
Q

What is/are the roles of basophils?

A
  1. protect against parasites (helminths, mostly). Does this by secreting histamine in response to IgE-bound antigens
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10
Q

Basophil density increases under what circumstances?

A

allergies reactions

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11
Q

What is/are the roles of monocytes?

A

Initiate the immune response to foreign antigens. Does this by phagocytosing invading organisms and presenting their antigens to helper T cells (CD4+) via MHC-II

Most macrophages (not all) are derived from monocytes

represent 3-8% of blood leukocytes

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12
Q

What is the best way to tell a lymphocyte from a monocyte?

A

the shape of the nucleus. Lymphocyte nuclei are usually round or oval, while monocyte nuclei are usually irregular, S-shaped, or amoeboid.

lymphocytes represent 20-30% of blood leukocytes

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13
Q

What are pseudonyms for neutrophils?

A

segs, polymorphonuclear cells, or ‘PMNs’

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14
Q

What is/are the roles of neutrophils?

A

ingest and kill invading organisms, secrete mediators (via degranulation) which can lyse bacteria (such as lysozyme)

They commit suicide within a day, but even dead neutrophils can help to kill bacteria

represent 40-70% of blood leukocytes

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15
Q

How can neutrophils help kill bacteria even after death?

A

their chromatin contributes to the formation of ‘neutrophil extracellular traps (NETs)’ which can assist in controlling sepsis.

NOTE: this process can also result in sepsis-associated conditions like pre-eclampsia (a term for a syndrome of severe hypertension that can occur during pregnancy)

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16
Q

What clinical situation would cause neutrophil density to fall rapidly if left unchecked?

A

chemotherapy. Numbers drop due to the fast turnover of neutrophils

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17
Q

How are neutrophils recruited to the site of an infection?

A

Ex. tissue macrophages encounter pathogen (innate immunity) and secretes IL-8. Neutrophils respond by migrating toward the macrophage.

Ex. Endothelial cells transmit danger signals in the forms of ICAM-1 expression. Neutrophils adhere to the ICAM-1 ligands via LFA-1, then migrate between the cells to the combat

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18
Q

What is leukocyte adhesion defect?

A

a congenital disease caused by a defect in a component of lymphocyte function associated antigen 1, “LFA-1” (CD-18) resulting in immunodeficiency and characterized by children with severe recurrent infections

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19
Q

What are the ways in which neutrophils can recognize foreign invaders?

A

via toll-like receptors as part of the innate immune system, via complement fixation (operates in the context of either innate or acquired immunity), or via the adaptive immune system (Fc receptors that recognize antibodies bound to targets)

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20
Q

What are the key granular contents of neutrophils?

A

myeloperoxidase (MPO)
defensins
lysozyme

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21
Q

What does myeloperoxidase (MPO) do?

A

enzyme involved in making hypochlorite (bleach) to kill micro-organisms. Intracellular mechanism

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22
Q

What does lysozyme do?

A

breaks down the cell walls of bacteria

23
Q

What is chronic granulomatous disease?

A

defect in the hypochlorite generating system of neutrophils resulting in immunodeficiency in which neutrophils migrate toward infectious agents but cannot kill them. Characterized by children with severe recurrent infections

24
Q

How can pathologists tell if a neoplastic cell is a neutrophil?

A

using immunostain with an antibody to MPO

25
Q

What are the roles of platelets?

A
  1. primary hemostatic plug
  2. stimulate coagulation cascade (fibrin formation, etc.)
  3. stimulate would healing (fibroblast growth/migration)
  4. Immune function (including pathogen inactivation)

platelets are found in very high concentration in the body (100 times that of white cells). 9-10 day lifespan

26
Q

How does platelet adherence work?

A

Damage to a blood vessel causes exposure to sub endothelial collagen. Platelets adhere either directly or via a circulating adaptor protein called von Willebrand factor (vWF). Adherence induces ‘platelet activation’

27
Q

Can platelets function without vWF?

A

Yes, however it is a critical component of adherence

28
Q

How does vMF work?

A

vMF is a coiled cable floating in plasma. it’s a multiuser put together from several identical subunits assembled in sequence. When it encounters exposed sub endothelial collagen, it uncoils to expose a number of platelet binding sites (one on each monomer). Platelets then bind to the vMF via a surface receptor.

29
Q

What is the name of the surface receptor needed for platelets to bind to vMF during adherence?

A

GP1b

30
Q

What is Bernard-Soulier syndrome?

A

defect in GP1b causing mild bleeding in mucocutaneous locations (skin, oral mucosa) in kids

31
Q

What is von Willebrand’s syndrome?

A

defect in vMF causing mild bleeding in mucocutaneous locations (skin, oral mucosa) in kids

32
Q

How are platelets activated?

A

binding of platelets to vMF increases binding affinity for collagen, vMF, and fibrinogen. This increased affinity is caused primarily due to a conformational change in a platelet surface protein complex called GPIIb/IIIa

33
Q

The products of platelets are categorized based on the two types of intraplatelet granules from which they originate. What are the names of these granules?

A

dense granules and alpha granules

34
Q

How does autocatalytic activation of platelets occur?

A

ADP is stored in platelet dense granules, and when secreted can bind to ADP adaptors on the platelet surface and augment still more release of itself and other mediators

35
Q

What type of drug can be used to block the binding of ADP to its receptor on the platelet surface during autocatalytic activation?

A

clopidogrel

36
Q

What role does thromboxane A2 play in platelet activation?

A

it is lipid. Platelet adherence ramps up its production from a precursor in the platelet membrane. It can then bind to its platelet surface receptors and augment both granule secretion and its own production

37
Q

What type of drug can be used to block the binding of thromboxane A2 to its receptor on the platelet surface during autocatalytic activation?

A

Aspirin

38
Q

How do activated platelets augment the coagulation cascade?

A
  1. secretion of proenzymes (specifically factor V), as well as vMF and fibrinogen
39
Q

Where are factor V, vMF, and fibrinogen stored in platelets until they are activated?

A

in alpha granules

40
Q

How does cross linking of platelets occur?

A

it is mediated by bound fibrinogen, each molecules of which has multiple platelet binding sites. The cross linked platelets then get cemented into place as a mature clot when the coagulation cascade generates fibrin from fibrinogen

41
Q

What factors affect the saturation ability of hemoglobin near its target organs?

A

Lactate and diphosphoglycerol (2,3-DPG), an intermediate of glycolysis (aka bisphosphogylcerate (2,3-BPG)), help to lower the pH, thus lowering the affinity of hemoglobin for oxygen

42
Q

What are some of the design requirements for red cell survival?

A

flexible shape, durable membrane, maximum Hgb/o2 carrying capacity, must offset osmotic pressure and the tendency for water to want to enter the cell (needs energy), needs an anti-oxidant system

43
Q

What gives RBCs their flexible shape?

A

their biconcave disc shape can and does fold along any axis. Impaired if hemoglobin precipitates

44
Q

What gives RBCs their durable membrane?

A

cables like spectrin anchor at transmembrane proteins distributed in the membrane

45
Q

What causes chronic hemolytic anemia?

A

individuals who carry two mutated alleles in spectrum or ankyrin have RBCs with shortened survival times (cells lose their concave shape and end up spherical)

46
Q

Why is maintaining the correct structural composition of hemoglobin so vital?

A

RBCs are packed with hemoglobin so any change will cause it to precipitate and rupture the RBC.

47
Q

What micro-organisms thrive on hemoglobin?

A

primarily those in the Plasmodium family of protozoa. This family is responsible for malaria

48
Q

How do RBCs counter the natural want of water to influx into the cell?

A

they actively pump sodium ions out of the cells, requiring ATP. If it fails, the RBC will swell and burst

49
Q

Why is an anti-oxidant system needed by RBCs?

A
  1. oxidized SH groups on hemoglobin can become cross linked causing Hgb denaturation and/or precipitation
  2. Oxidized iron (Fe3+) cannot carry O2
50
Q

Hemoglobin with oxidized iron (Fe3+) is called what?

A

methemoglobin. the disease state caused by the presence of this is called methemoglobinemia and results in hypoxia

51
Q

How does an effective anti-oxidant system work on RBCs?

A
  1. Glutathione (GSH) eliminates peroxide before it can damage the RBC (it becomes oxidized as hydrogen peroxide becomes reduced and then is reduced using NADPH)
  2. Cytochrome b5 reductase reduces Methemoglobin back to normal hemoglobin

Failure of these systems to work result in increased oxidative stress that cause clumping of RBCs

52
Q

What is another mechanism employed by the body in the event of a defective anti-oxidant system for RBCs?

A

tissue-based macrophages called bite cells can remove large clumps from the membrane and, somehow, the cell can reform its disc shape

53
Q

Why would defects in glycolytic enzymes result in hemolytic anemia in children?

A

RBCs depend on ATP to power their sodium/K+ pump to combat osmotic influx. A deficiency in a glycolytic enzyme would decrease the amount of available ATP, resulting in swelling and lysing of RBCs

CMOD Week 1 (18 decks)

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