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Human Organs and Tissues > Peripheral blood > Flashcards

Peripheral blood Flashcards

1
Q

9 Functions of blood

A

Oxygen delivery via RBCs (hemoglobin)
Carbon dioxide removal via RBCs and HCO3-
Distribute nutrients to cells of the body
Removal of metabolic wastes from cell metabolism
Distribution of hormones, signalling molecules, etc
Regulation of body temperature
Buffer body fluids and osmotic balance
Hemostasis (clotting)
Immune cell circulation, diapedesis, inflammation and protection

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2
Q

Plasma composition

A 
Albumin
alpha, beta and gamma globulin
Clotting factors
Complement factors
Chylomicrons
VLDL
LDL
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3
Q

Albumin

A

From the liver

Functions: Colloid osmotic pressure (allows fluid to stay in the blood), and transport of metabolites and medicine

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4
Q

Alpha and beta globulin

A

From liver

Functions: transport of metal ions and vitamins

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5
Q

Gamma globulin

A

From plasma cells

Antibodies

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6
Q

Complement factors

A

From liver

Functions: destruction of microorganisms and initiation of inflammation

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7
Q

Chylomicrons

A

From intestinal epithelium
Function:
Transport of TAGs from intestine to liver

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8
Q

VLDL and LDL

A

Both from liver
VLDL transports TAGs from liver to body
LDL transports cholesterol from liver to body

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9
Q

2 types of Romanovsky Staining

A

May-Grunwald-Giemsa

Wright-Giemsa

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10
Q

2 components of Romanovsky Staining

A 
Azure B (blue, binds anionic molecules like DNA and histamine)
Eosin Y (pink, binds cationic sites of proteins like hemoglobin and cationic eosinophil protein)
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11
Q

3 zones in peripheral blood smear prep

A 
Thick area (cells are too close together)
Morphology zone (cells are good distance apart, no drying artifact)
Brush border (cells are really far apart and too many artifacts)
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12
Q

Red blood cells

A

Anucleate
Normally have biconcave shape
Approx 7.5 um in diameter
Number in health 3.9-6.0x10^12/L
Wider the depression, the less hemoglobin you have
Functions: oxygen delivery and CO2 removal from tissues, mediated by hemoglobin

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13
Q

Hemoglobin

A

Free hemoglobin is toxic to tissues and is quickly degraded, so RBCs are bags of it
Cannot be made without iron!!
4 subunits
Sigmoidal oxygen delivery

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14
Q

Iron deficiency anemia

A

Hemoglobin cannot be made without iron

Red cells with very little hemoglobin appear pale and small

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15
Q

Hereditary spherocytosis

A

RBCs look like perfect spheres
Genetic mutation
Either cytoskeleton structure defect or defective attachment of cytoskeleton to cell membrane
Can get stuck in the spleen and macrophages can eat them or take part of their membranes

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16
Q

Ankyrin

A

Links cytoskeleton to membrane proteins

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17
Q

Sickle cell anemia

A

Sickle cell crisis is when red cells can’t squeeze through capillaries and instead start sticking to the vessel walls and to each other and clogging up blood vessels
Hemoglobin S is a single substitution in the beta chain
When deoxygenated they bind together
If red cell goes to lung its reversible, but if they stay there too long they can get stuck and form polymers

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18
Q

Platelets

A 
Cytoplasmic fragments of megakaryocytes
Number in health 150-44x10^9/L
Size 2-4um
ADP and Ca lead to platelet activation
Functions: clot formation
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19
Q

2 main platelet receptors

A
  1. GPIbIX receptors: attachment to vWF and activation

2. GPIIbIIIa receptors: attachement to fibrin and activation

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20
Q

2 types of platelet granules and what is found in them

A
  1. Electron dense granule: nucleotides (ADP) and Ca2+

2. Specific alpha granule: fibrinogen, factor V, VWF

21
Q

Steps in platelet clot formation

A
  1. Adhere to site of vessel injury by binding to von Willebrand Factor (GPIbIX) and sub-endothelial collagen
  2. Platelets become activated and aggregate to seal the site of vessel injury
  3. Platelets provide phospholipid surface for activation of clotting factors and formation of fibrin clot
  4. Platelets bind fibrin (GPIIbIIIa) to form stable clot
22
Q

What do PGI2 and NO do?

A

They increase cyclic AMP or GMP during steady state which increases the threshold for platelet activation
So you don’t get clots with no injury

23
Q

What do
1. Aspirin
2. Plavix
block?

A
  1. TxA2 production

2. P2Y12 receptor activation by ADP

24
Q

What is the coagulation cascade? What does in result in the generation of?

A

Series of enzymatic reactions where inactive precursor (proenzyme) is converted to an active enzyme, which then activates next proenzyme in the cascade
Results in generation of fibrin clot

25
Hemophilia
``` X-linked recessive disorder A and B type Clinically identical Incidence (1:5000 males) approx 85% A Strong association between factor level and severity of the disorder ```
26
Hemophilia A vs B
A: Factor 8 deficiency B: Factor 9 deficiency
27
Hemophilia factor level and clinical manifestation: <1 1-5 5-10
< 1: Severe disease, frequent spontaneous bleeding episodes, joint deformity and crippling if not treated adequately 1-5: Moderate disease, post-traumatic bleeding, occasional spontaneous bleeding 5-20: mild disease, post-traumatic bleeding
28
3 granulocytes
Neutrophils Eosinophils Basophils
29
Neutrophils
Most abundant PMN with segmented nucleus (3-4 segments) Produced in bone marrow Released into blood Circulate for 7-10 hours Migrate into tissues and die within 48 hours Generally first cells to arrive at sites of infection May see Barr body in females Primary (large, purple) and secondary (small, orange/pink) granules Function: Phagocytosis of bacteria, fungi, and debris, killing of ingested bacteria
30
Neutrophils primary versus secondary granule contents
Primary: lysozyme, hydrolytic enzymes, myeloperoxidase Secondary: defensins, lysozyme
31
``` What does 1. Phagocyte NADPH oxidase 2. Myeloperoxidase 3. NO synthase make? ```
1. O2- (superoxide anion) 2. CLO- (hyperchlorite anion) 3. NO (nitric oxide)
32
Chronic granulomatous disease
Results from deficiency of phagocyte NADPH oxidase Leads to dysfunctional killing of bacterial and fungal organisms by neutrophils Patients suffer from recurrent bacterial and fungal infections Treat with bone marrow transplant
33
Basic steps of neutrophil migration
1. Rolling (mucin CAM and E-selectin) 2. Activation (IL-8) 3. Arrest/adhesion (LFA-1) 4. Transendothelial migration
34
Leukocyte adhesion deficiency
Results from deficiency of LFA-1 integrin Leads to inability of neutrophils to transmigrate from blood to tissues Most patients with severe LAD die when younger than 1 year. Bacterial infections are responsible for most deaths
35
Eosinophils
Produced in bone marrow and released to blood Segmented nucleus (2 lobes) Spherical pink/orange granules Approx 12-17um in diameter Number in health 0.1-1.0x10^9/L (<1% of WBCs) Increase in parasitic infection or allergy Contain lysosomal and oxygen radical generation enzymes similar to neutrophils and monocytes Contain anti-parasite protein called eosinophil cationic protein
36
Basophils
Produced in bone marrow and released to blood Segmented nucleus (2 lobes) Spherical purple granules Approx 12-17um in diameter Number in health 0.1-0.2x10^9/L (<1% of WBCs) Back up mast cell responses during inflammation Also involved in allergic reactions (contain histamines, make leukotrienes and prostaglandins)
37
Monocytes
``` Horse shoe nucleus Bluish gray cytoplasm often vacuolated Variable number of fine reddish granules Approx 15-18um in diameter Number in health 0.2-1.0x10^9/L (5-10%) Produced in bone marrow and released to blood Circulate for approx 8 hours Migrate into tissues and differentiate into macrophages ```
38
Monocyte/macrophage function
Phagocytosis of microorganism | Killing of ingested microorganisms
39
2 functions of macrophages that monocytes do not do
Recruitment of immune cells into inflammatory site (secrete cytokines and chemokines) Present antigen to T cells
40
Changes involved in differentiation from monocytes to macrophages
Increase in size Increased numbers and complexity of organelles Increased phagocytic activity Increased levels of hydrolytic enzymes
41
2 ways complement can be activated
1. Antibody antigen complexes (classical) | 2. Microbial cell wall components (alternative and lectin pathways)
42
3 things generated from complement activation
1. Anaphylatoxins (C3a and C5a - facilitate activation and recruitment of immune cells) 2. Opsonin (C3b - facilitates phagocytosis of microbes) 3. MAC (C5-9 - forms pores in bacterial cell membranes)
43
3 ways host cells are spared from complement
1. Complement activation and effector function is inactivated by host cell receptors 2. Decay accelerating factor (DAF; CD55 - inhibits formation of C3 convertase) 3. Membrane inhibitor of reactive lysis (MIRL;CD59 - inhibits MAC assembly)
44
Paroxysmal Noctural Hemoglobinuria (PNH)
``` No DAF or MIRL Starts as an autoimmune disease Intravascular hemolysis Free hemoglobin release Blood in urine Renal failure (too many clots from activated platelets) Decrease NO endothelium, thrombosis, and pulmonary hypertension (lung pressure is high = heart failure) Treatment: Anti-C5 mAB, Eculizumab ```
45
Amounts of lymphocytes
``` T cells (70-80%, CD4:CD8 in 2 to 1 ratio) B cells (10-20%) NK cells (5-10%) ```
46
T cell function
Acquired immunity Formed in bone marrow, mature in thymus CD4+: helper cells, generals of the immune response, help to activate or silence CD8+ T cells, B cells, macrophages, and other immune system cells CD8+: cytotoxic T cells, kill virally infected cells
47
B cells
Acquired immunity Formed and matured in bone marrow Produce and secrete antibody
48
NK cells
Innate immunity Formed and matured in the bone marrow Kill virally infected cells and cancer cells
49
Severe combined immunodeficiency
Bubble boy disease Genetic disease Both B and T cells are absent or dysfunctional Due to a defect in one or several genes needed for their development such as IL-2y receptor subunit, RAG 1 or 2 Patients usually die within one year due to severe, recurrent infections Treatment: bone marrow transplant

Human Organs and Tissues (11 decks)

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