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Microanatomy > Blood 1 > Flashcards

Blood 1 Flashcards

1
Q

Put the following in order from least to most abundant: platelets, erythrocytes, leukocytes

A

leukocytes (least), platelets, erythrocytes (most)

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2
Q

Put the following in order from least to most abundant: monocytes, basophils, neutrophils, lymphocytes, eosinophils

A

basophils (least), eosinophils, monocytes, lymphocytes, neutrophils (most)

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3
Q

What does the suffix, “-penia” indicate?

What about the suffix, “-cytosis/-philia?

A 
Too few (feel free to add your own memory tool about too few penises here . . . hehehe)
Too many
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4
Q

What is hematocrit? What is the normal value?

A

% of blood volume occupied by packed erythrocytes after centrifugation
42-45%

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5
Q

What can cause a deviation of hematocrit? What is the irregular value?

A

Polycythemia vera, 70-80%

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6
Q

What is the “buffy coat” in relation to blood?

A

thin layer (containing leukocytes & platelets) that lies just above the red cells after centrifugation.

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7
Q

What is the difference between plasma and serum?

A

Plasma = Serum + Clotting Factors

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8
Q

Where does the protein component of plasma come from? What does plasma protein do?

A 
Liver (albumin, fibrinogen)
Plasma Cells (antibodies)
Maintains the osmotic pressure of blood and acts as a carrier molecule
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9
Q

What is the clinical correlation between liver disease and edema?

A

Most liver disease = decreased albumin production = decrease in osmotic pressure = movement of too much water into extravascular tissues (edema)

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10
Q
  1. What special dye does a blood smear use?

2. What do they stain?

A
  1. Romanovsky (ex.s: Wrights, Giemsa)
  2. a) Methylene Blue: stains nuclei, ribosomes, specific granules purple
    b) Azure: stains azurophilic granules of leukocytes reddish purple
    c) Eosin: stains RBC pink & specific granules red
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11
Q

How is carbon dioxide carried in plasma?

A

bound to heme as bicarbonate

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12
Q

In what lifecycle stage are RBCs released into the blood? What does an increase of this stage of cell indicate?

A

reticulocytes

Hemolytic anemia

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13
Q

What is the average lifespan of a RBC?

A

120 days

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14
Q

What does the biconcave shape of the RBC provide?

A

large surface area

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15
Q

What does the erythrocyte cytoskeleton consist of?

A

spectrin tetramers, linked by protein complexes containing actin or ankyrin

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16
Q

How do transmembrane proteins function in the erythrocyte cytoskeleton?

A

Glycophorin C & band 3 do 2 things:

  1. anchor the cytoskeleton to the membrane
  2. carry the ABO blood group antigens on their extracellular domains
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17
Q

What is poikilocytosis? What are the specific types?

A

Abnormality in erythrocyte shape; spherocytes, elliptocytes, & drepanocytes (sickle cells)

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18
Q

Name the 2 types of defects that cause poikilocytosis and examples of each

A
  1. Defects in the cytoskeleton (spectrin or the anchoring protein complexes)
    - hereditary spherocytosis
    - hereditary elliptocytosis
  2. Defects in hemoglobin
    - sickle cell anemia (HbS polymerizes into long rods = deforms the RBCs = blockage of larger vessels; = stroke if it occurs in the brain)
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19
Q

What is anisocytosis? What are the 2 types and when do they occur?

A

Abnormalities in erythrocyte size

  1. Macrocytes – abnormally large; due to Vitamin B12 or folate deficiency
  2. Microcytes – abnormally small; due to iron deficiency anemia
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20
Q

What is anisochromasia? What are the 2 types?

A

Abnormalities in erythrocyte staining intensity

  1. Hyperchromic – stain darker than normal, with central pale area smaller than normal or absent
  2. Hypochromic – stain lighter than normal, with central pale area enlarged
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21
Q

What is anemia?

A

decrease in the oxygen carrying capacity of the blood, due to less RBCs or less hemoglobin/cell

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22
Q

What is thrombocytopenia?

What about primary thrombocytopenic purpura?

A 
abnormally low platelet count; characterized by frequent nosebleeds, petechial rash, or larger bruise-like areas (ecchymoses)
One form (primary thrombocytopenic purpura) is an autoimmune disease where anti-platelet antibodies
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23
Q

What is thrombocytosis?

A

excessive #s of platelets

seen in bone marrow disorder or slenectomy

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24
Q

What are the 2 regions of a platelet?

A
  1. hyalomere- clear outer region

2. granulomere- centromere, shows basophilic stippling

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25
Q

What are the 3 types of membrane-bounded “granules” that a granulomere contains:

A
  1. Alpha granules
  2. Delta granules
  3. Lysosomes
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26
Q

What do 4 things do alpha granules contain?

A
  1. Von Willebrand factor (vWF; for platelet adhesion to damaged endothelium)
  2. Platelet-derived growth factor (PDGF; a mitogen for vessel repair)
  3. Fibrinogen (not made by the platelet; cross-links platelets at sites of vessel injury; is converted to fibrin during blood clotting)
  4. P-selectin (a vascular adhesion molecule that stimulates leukocyte adhesion near areas of vascular damage)
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27
Q

What do delta granules contain?

A
  1. Small molecules that promote platelet aggregation (ADP, ATP, & Ca++)
  2. Serotonin (taken up from the plasma) – causes vasoconstriction
28
Q

2 systems of membrane-bounded channels that function in secretion of granule contents

A
  1. Open canalicular system: invaginations of the plasma membrane; granules fuse with the invaginations for rapid secretion
  2. Dense tubular system: stores Ca++ needed for exocytosis of granules; not continuous with plasma membrane
29
Q

What are the 6 platelet-mediated events in damaged vessels?

A
  1. Adhesion
  2. Aggregation
  3. Activation
  4. Clot retraction
  5. Clot resorption
  6. Repair of vessel wall
30
Q

What occurs during platelet adhesion?

A

single layer of platelets forms at sites of endothelial damage, they bind directly to exposed collagen in the basement membrane (BM), vWF links platelets to components of the BM exposed at the site of damage (e.g., laminin)

31
Q

What occurs during platelet aggregation?

A

Fibrinogen from the plasma (made by hepatocytes) links the platelets together in a multilayered primary hemostatic plug that fills the defect in the vessel wall

32
Q

What occurs during platelet activation?

A
  • Secretion of mediators stored in granules
  • Synthesis and release of new mediators (e.g., thromboxane A2)
  • Change of platelet shape
33
Q

What does the release of mediators during platelet activation cause?

A
  • adhesion & aggregation of additional platelets
  • vasoconstriction
  • blood coagulation
  • meshwork of fibrin (stabilizes the platelet plug & forms the secondary hemostatic plug)
34
Q
  1. What occurs during clot retraction?

2. How does it occur?

A
  1. The platelets contract, causing the platelet plug to shrink & flatten against the vascular wall to helps re-establish blood flow
  2. The actin-myosin interaction
35
Q

What mediates clot resorption?

A

enzymes from lambda granules

36
Q

What mediates the repair of the vessel wall?

A

PDGF (strongly mitogenic for the endothelial cells), fibroblasts, and smooth muscle cells

37
Q

What are the 2 ways that platelet activation is prevented in normal tissue?

A
  1. Collagen & laminin in the basement membrane are not exposed (vWF & platelets can’t bind)
  2. Healthy endothelial cells produce factors that inhibit platelet aggregation, e.g., prostacyclin
38
Q

How does Aspirin work?

A

It inhibits . . .

  1. platelet function
  2. Cyclooxygenase activity (prolongs bleeding times)
39
Q

What are the 3 platelet pathologies? What is defective/deficient in them? What process is affected?

A
  1. Von Willebrand’s disease (most common); deficient von Willebrand factor; adhesion
  2. Bernard-Soulier syndrome; defective platelet receptor for von Willebrand factor; adhesion
  3. Glanzmann’s thrombasthenia; defective platelet receptor for fibrinogen; aggregation
40
Q

What are 2 subclasses of White Blood Cells? What are cells are included in these subclasses?

A

Granulocytes: Neutrophils, eosinophils, basophils Agranulocytes: Lymphocytes and monocytes

41
Q

What granules do all leukocytes contain? What granules do agranulocytes lack?

A

azurophilic granules; specific granules

42
Q

What 3 things does leukocyte function involve?

A

diapedesis, chemotaxis, and activation

43
Q

What 2 processes proceed diapedesis?

A
  1. Rolling along the endothelium; mediated by weak interactions (between L-selectins- on leukocytes- and their receptors- on endothelium), which break and form again
  2. Firm adhesion; additional inflammatory stimuli cause the expression of ligands and receptors that form stronger interactions; involves integrins (on leukocytes) & P-selectins & E-selectins (on inflamed endothelial cells)
44
Q
  1. What is diapedesis?
  2. When and where does it occur most frequently?
  3. What does mast cells release? What does it do?
A
  1. Leukocytes pass between endothelial cells to enter the extravascular tissues
  2. During inflammation or infection; postcapillary venules
  3. Histamine; widens the intercellular spaces between endothelial cells
45
Q

What process do Leukocyte Adhesion Deficiencies inhibit?

What is missing in LAD1?

A

Diapedesis

Integrin expression on the leukocytes

46
Q

What is chemotaxis?

A

migration along a concentration gradient of chemotactic factors

47
Q

What is a respiratory burst? What does it produce?

A

A series of enzymatic reactions that uses oxygen; highly reactive forms of oxygen that are microbicidal

48
Q

What cells are usually the first cells to arrive at a site of acute inflammation?

A

neutrophils

49
Q

What is a Barr body?

A

a drumstick appendage visible in some nuclei, which are the inactivated X chromosome (in females)

50
Q

What are hypersegmented neutrophils?

A

neutrophils with > 5 nuclear lobes

51
Q

What are the 2 types of granules in neutrophils?

A
  1. Azurophilic granules (= primary granules): Produced earlier than specific granules, stained histochemically for peroxidase activity (due to their content of myeloperoxidase)
  2. Specific granules (= secondary granules)
52
Q

Where are the most neutrophils . . . bone marrow or blood?

A

Bone marrow - the reserve of mature cells is bigger than neutrophils circulating in the blood

53
Q

What are the neutrophils’ chemotactic factors?

A

-Histamine
-Chemotactic cytokines (e.g. IL-8) produced by
cells such as macrophages
-Bacterial peptides (which begin with N-formyl-methionyl residues)
-Some fragments of activated complement proteins (e.g. C5a)

54
Q

What are the 4 types of neutrophils receptors?

A
  1. Fc receptors
  2. Complement receptors
  3. Scavenger receptors
  4. Toll-like receptors (TLRs), also called pattern recognition receptors or PRRs)
55
Q

What do Fc receptors on neutrophils do?

A

They bind the Fc portion of IgG antibodies that are part of an antigen-antibody complex. This greatly enhances the rate of phagocytosis

56
Q

What are opsonins? Opsonization?

A

Molecules that form the cross-link between bacterial surfaces and phagocyte
The process of binding the opsonins to the target

57
Q

What do complement receptors on neutrophils do?

A

Recognize several fragments of activated complement proteins (act as opsonins)

58
Q

What do scavenger receptors on neutrophils do?

A

Bind to modified forms of low-density lipoproteins (found on bacteria and apoptotic bodies)

59
Q

What do TLRs receptors on neutrophils do?

A
  1. Bind to PAMPs (sequences important for functioning of the bacterium pathogens and endotoxins)
  2. Produce fever: TLR-mediated phagocytosis = IL-1 secretion (by phagocyte) = fever by inducing synthesis of prostaglandins (which act on the hypothalamus to reset the body’s thermostat to a higher temperature)
60
Q

What are the 3 ways neutrophils kill?

A
  1. respiratory burst
  2. antimicrobial mediators in specific granules & azurophilic granules
  3. Neutrophil extracellular traps (NETs)
61
Q

What are the 2 important enzymes involved in the respiratory burst? What steps do they catalyze?

A
  1. NADPH oxidase: in the first step of the respiratory burst

2. Myeloperoxidase: produces hypochlorous acid (HOCl) from H2O2. It dissociates to highly toxic hypochlorite (OCl-)

62
Q

What is Chronic Granulomatous Disease?

What are the consequences?

A

caused by genetic defects; characterized by a decreased/absent respiratory burst = recurrent bacterial/fungal infections & shortened life expectancy

63
Q

Which antimicrobial mediators do specific granules contain?

A
  • lysozyme (attacks cell walls of bacteria, esp. gram + bacteria)
  • lactoferrin (bacteriostatic protein- competes with bacteria for iron and copper . . . required for bacterial replication)
  • collagenase (degrade the ECM, allows access of the neutrophil to the site of inflammation/infection)
64
Q

Which antimicrobial mediators do azurophilic granules contain?

A
  • myeloperoxidase: catalyzes production of hypochlorous acid
  • bactericidal/permeability-increasing protein: damages the membranes of gram - bacteria
  • additional lysozymes
  • defensins: small cationic proteins; form pores
  • neutrophil elastase: helps digest the ECM
65
Q

What is Chediak-Higashi syndrome?

A

A genetic defect interferes with targeting of proteins to azurophilic granules; this leaves neutrophils without the mediators necessary to kill bacteria. Thus, neutrophils contain abnormally large vacuoles (from fusion of azurophilic granules with one another). Often fatal in childhood.

66
Q
  1. What is Neutrophil extracellular traps (NETs)? 2. Where do they form in sepsis? in preclampsia?
A
  1. Extracellular webs composed of strands of neutrophil chromatin with antimicrobial granule proteins adhering to them
  2. In sepsis, NETs form within blood vessels. In preeclampsia, they form in the intervillous spaces of the placenta
67
Q

What factors result in increased hematocrit?

A
  • males higher than females
  • newborns higher than normal
  • exercise
  • higher altitude
  • burns

Microanatomy (6 decks)

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