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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
Q

Hemophilia

A 
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
Q

Hemophilia A vs B

A

A: Factor 8 deficiency
B: Factor 9 deficiency

27
Q

Hemophilia factor level and clinical manifestation:
<1
1-5
5-10

A

< 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
Q

3 granulocytes

A

Neutrophils
Eosinophils
Basophils

29
Q

Neutrophils

A

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
Q

Neutrophils primary versus secondary granule contents

A

Primary: lysozyme, hydrolytic enzymes, myeloperoxidase
Secondary: defensins, lysozyme

31
Q 
What does
1. Phagocyte NADPH oxidase
2. Myeloperoxidase
3. NO synthase
make?
A
  1. O2- (superoxide anion)
  2. CLO- (hyperchlorite anion)
  3. NO (nitric oxide)
32
Q

Chronic granulomatous disease

A

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
Q

Basic steps of neutrophil migration

A
  1. Rolling (mucin CAM and E-selectin)
  2. Activation (IL-8)
  3. Arrest/adhesion (LFA-1)
  4. Transendothelial migration
34
Q

Leukocyte adhesion deficiency

A

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
Q

Eosinophils

A

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
Q

Basophils

A

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
Q

Monocytes

A 
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
Q

Monocyte/macrophage function

A

Phagocytosis of microorganism

Killing of ingested microorganisms

39
Q

2 functions of macrophages that monocytes do not do

A

Recruitment of immune cells into inflammatory site (secrete cytokines and chemokines)
Present antigen to T cells

40
Q

Changes involved in differentiation from monocytes to macrophages

A

Increase in size
Increased numbers and complexity of organelles
Increased phagocytic activity
Increased levels of hydrolytic enzymes

41
Q

2 ways complement can be activated

A
  1. Antibody antigen complexes (classical)

2. Microbial cell wall components (alternative and lectin pathways)

42
Q

3 things generated from complement activation

A
  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
Q

3 ways host cells are spared from complement

A
  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
Q

Paroxysmal Noctural Hemoglobinuria (PNH)

A 
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
Q

Amounts of lymphocytes

A 
T cells (70-80%, CD4:CD8 in 2 to 1 ratio)
B cells (10-20%)
NK cells (5-10%)
46
Q

T cell function

A

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
Q

B cells

A

Acquired immunity
Formed and matured in bone marrow
Produce and secrete antibody

48
Q

NK cells

A

Innate immunity
Formed and matured in the bone marrow
Kill virally infected cells and cancer cells

49
Q

Severe combined immunodeficiency

A

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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