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402-Exam 1 > RBCs, WBCs, platelets > Flashcards

RBCs, WBCs, platelets Flashcards

1
Q

What needs to be protected for Hgb function?

A

Hgb oxidizes, degrades in solution, and is damaging to tissues if they are free (not bound to O2). Unbound O2 is free oxygen radical.

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1
Q

What is primary purpose of blood?

A

Primary function of erythrocyte is to transport hemoglobin, which carries oxygen to the tissues.

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2
Q

What are the components for a proper hemoglobin/O2 transport?

A
  • Normal red cell amounts
  • Normal Hgb structure and function
  • Normal red cell mass

Any of them are diseased, it can result in anemia and hypoxmia.

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3
Q

What makes the blood red?

A

Iron complexed with O2 reflects light in the red spectrum.

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4
Q

How many oxygen molecule can a hemoglobin carry?

A

4

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5
Q

What kind of iron that can bind O2?

A

Ferrous (2+) iron binds O2, then releases to the tissues. Ferric (3+) cannot bind O2. Think icky!

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6
Q

Explain Hgb-O2 binding affinity and the difference in different tissues/organs.

A
  • Lower pH and lower O2 content facilitates unloading of O2 (low affinity). = in metabolizing tissues.
  • Higher pH and high O2 content facilitates loading of O2 (higher facility). = in lungs.
  • 2,3-DPG takes part in releasing or not releasing O2.
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7
Q

What happened when O2-HgB dissociation curve when shift to the RIGHT?

A

Optimize O2 unloading by decreased affinity
- decrease pH
- Increase 2-3 DPG
- Increase CO2
- Increase temperature

Think of any that requires physical activity. Think exercise always RIGHT.

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8
Q

What happened when O2-HgB dissociation curve when shift to the LEFT?

A

Optimize O2 loading by decreased affinity
- increase pH [alkaline]
- decrease 2-3 DPG
- decrease CO2
- decrease temperature [hypothermic]

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9
Q

What is the adaptation of animals to high altitudes. Compare min-hrs to days-weeks.

A
  • Immediate (min-hrs): hyperventilation (left shift), splenic contraction.
  • Acclimation (days-weeks): increased 2,3 DPG (right shift), increase red cell mass due to EPO stimulation.
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10
Q

LEFT or RIGHT shift:
1- Horse finishing a 24-hr endurance ride.
2- Stored RBCs in the blood bank, with depletion of 2,3-DPG.
3- A cow with metabolic alkalosis due to abomasal displacement.
4- A intrepid Poodle, climbing Mt. Everest.

A

1- R
2- L
3- high pH = L
4- R

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11
Q

List the 3 important pathway red cell metabolic pathways, and say why each is important.

A
  • Methemoglobin reductase pathway = red cell function.
  • Rapaport-lubering pathway = important in 2,3 DPG synthesis.
  • Pentose phosphate shunt = antioxidant systems in regards to Glutathione.
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12
Q

What does methemoglobin reductase pathway do?

A

Using NADH to convert Fe3+ back to Fe2+, aka antioxidant to keep heme iron in ferrous Fe2+ state.

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13
Q

What does Rapaport-lubering pathway do?

A

Ramp up or ramp down 2,3-DPG which is important in regulating hemoglobin oxygen affinity.

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14
Q

Why are cats sensitive to oxygenation?

A

Because cats Hgb contains 8 sulfhydryl (SH) groups.

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15
Q

What are the abnormalities in heme synthesis?

A
  • Porphyrias: inherited enzyme defects in porphyrin synthesis (i.e.: abnormal porphyrins in teeth, photosensitization, red pigment in urine).
  • Dyserythropoiesis: acquired defects (lead toxicity)
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16
Q

What are the consequences of lead toxicity?

A
  • Nucleated RBCs
  • Basophilic stippling: interfere ability to synthesize globin and break down RNA.
  • DYSerythropoiesis (process formation of RBCs).
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17
Q

How is iron transported? Where is iron stored? And in what form is iron stored as?

A
  • Iron is transported on the serum protein called TRANSFERRIN.
  • Iron is stored in BONE MARROW MACROPHAGE as FERRITIN (more readily available) and HEMOSIDERIN.
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18
Q

Walk me through iron absorption in the gut and how iron is utilized in erythropoiesis.

A
  • Absorption: Fe2+ are brought into enterocyte in duodenum, packaged, and stored as ferritin. Some goes to transporter Ferroportin (regulated by Hepcidin). Ferroportin passes iron to blood (binds to Transferrin) to deliver to body.
  • Erythropoiesis: Transferrin receptor receive Fe2+, internalized them, push it through Ferroportin which push it to erythroid precursor cells for development. Some Fe2+ is stored internally as ferritin or hemosiderin (either internal or external of macrophage).
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19
Q

What regulates Ferroportin? What is the function?

A

Hepcidin - a key regulator of iron homeostasis.
- Synthesized in liver, regulate the iron coming in and out of GI tract and storage.
- Inflammation leads to high hepcidin => iron got locked up in macrophages => anemia of inflammation.
- High hepcidin (in a well oxygenated state), ability to move iron decreases because ferroportin is internalized and degraded: decrease absorption in the intestine; block release of iron from macrophages to developing erythroid cells.

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20
Q

How can iron being recycled?

A

Old red cells got pulled out of circulation for macrophage to phagocytose, then recycle the Fe2+. Fe2+ is transferred to ferroportin and the cycle repeats.

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21
Q

Effects on Hepcidine (a), effect on iron avail (b), effect on erythropoiesis (c) in the following:
1- Hemorrhage
2- Large iron stores
3- Iron deficiency
4- inflammation

A

1- a/d; b/i; c/i
2- a/i; b/d; c/d
3- a/d; b/i; c/i
4- a/i; b/d; c/d

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22
Q

What is HCT? How is it different from PCV?

A

Hematocrit (%) - percent of blood that is occupied by RBCs. PCV is the microhematocrit which is essentially the same thing with the number fluctuate ~2 units. If HCT = 40%, then PCV should be around 38-42.

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23
Q

What is HGB?

A

Hemoglobin concentration measure the amount of HgB.

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24
Q

Who got high RBC mass? Who got low RBC mass?

A

Slighthounds, horses, beef cattle OR male have high RBC mass
Young animals OR pregnant have low RBC mass

25
Q

MCV means? Types?

A

Mean cell volume
normocytic, microcytic, macrocytic

26
Q

MCH means? What’s one special thing about MCH?

A

Mean cell hemoglobin = average amount of Hgb within EACH red cell (= HgB/RBC count)
Normochromic, hypochromic, NEVER hyperchromic

27
Q

MCHC means? Categories?

A

Mean cell hemoglobin concentration = average amount of hemoglobin in proportion to the red cell mass (= HgB/Hct)
Normochromic, hypochromic

28
Q

What kind of dog breed have microcytic RBCs? What kind have macrocytic RBCs? How about age?

A
  • Akita, Husky, Shiba, Sharpei = microcytic RBCs.
  • Slighthounds = macrocytic RBCs.
  • Young = microcytic RBCs (in foals and calves, microcytosis until 1 yoa)
29
Q

Describe red cell membrane

A
  1. Cytoskeleton: determine and maintain RBC shape, viscoelastic properties, delimit deformability.
  2. Lipid bilayer: permeability barrier, in equilibrium with plasma lipids, noncompressible.
30
Q

What kind of cell present often in the outer leaflet of lipid bilayer? And what is the function of it?

A

Cholesterol.
Increased rigidity of the RBCs to protect the structure of red cell. Less = red cell more fragile. More = red cell cannot bend properly because too rigid.

Also electrolyte transporters also nest on the inner leaflet form.

31
Q

What does ATP function for RBC?

A

ATP production maintain membrane shape, cation pump (Ca2+ and Na/K), and ionic gradient. Any changes will reflect on shape changes to RBCs.

32
Q

What are the 2 categories of RBC membrane abnormalities? What are the consequences?

A
  • Structural abnormality (lipids or proteins)
  • Metabolic abnormality (ATP, Ca2+)

Consequences:
- Decreased deformability
- Poikilocytosis (shape change)
- Hemolysis

33
Q

What are the spleen roles?

A
  • Narrow sinusoidal passages to inhibit deformed red cell to pass through
  • Remove inclusions
  • Splenic macrophages phagocytose damaged RBCs.
34
Q

Define echinocytes. Normal vs. pathologic.

A
  • Pointy ends, small spikes across red cells. Looking like an HIV virus.
  • Norm/artifact: drying artifact in smear prep (water evap), prolonged storage in EDTA or too little blood in EDTA tube.
  • Path: electrolyte abnorm, uremia, rattlesnake envenomation.
35
Q

Define acanthocytes. Normal vs. Path.

A
  • Irregular projectiles, cell doesn’t have the round shape. Looking like a blob.
  • Normal: in pigs, calves, rabbits.
  • Path: hepatic dz (change in cholesterol in leaflet), lipid abnormalities, red cell fragmentation (from fibrin clot shatter), neoplasia (hemangiosarcoma, osteosarcoma, lymphoma).
36
Q

Define codocytes or leptocytes. Normal vs. path.

A
  • AKA target cells. Appear like Target logo.
  • Normal: drying artifact in smear preparation.
  • Pathologic: anemia (nonspecific), iron deficiency anemia (COMMON!), hepatobiliary dz.
37
Q

Define schistocytes. Normal vs. Path?

A
  • Red cell that has been fragmented.
  • Normal: none.
  • Path: red cell fragmentation. Physical vs. mechanical anemia. Fibrin strands tear and fragment erythrocytes.
38
Q

Define keratocytes. Normal vs. Path?

A
  • Cell with a blister that pops leaving two projectile looking like devil cells.
  • Normal: none.
  • Path: red cell fragmentation (mechanical trauma).
39
Q

Define spherocyte. Normal vs. Path? How does it relate to agglutination.

A
  • No central palor, dense.
  • Normal: none.
  • Path: IMHA (when spherocyte is abundant);

Mechanism: phagocytosis remove RBC membrane leading to remaining membrane reseals around the cytosol, forming spherocyte.

Go hand in hand with agglutination. Hallmark of IMHA.

40
Q

Define Heinz bodies. Normal vs. Path?

A
  • Result of oxidation (@ early stage) of globin chains, clump and bind to the inner red cell membrane, protruding from the surface.
  • Path: feline Hgb is oxidant-sensitive because they have double as much SH (sulfur) group as any other species.
41
Q

Define eccentrocytes. Normal vs. Path?

A
  • Hgb shifted to one side. Like a half moon.
  • Normal: none.
  • Path: oxidative damage (ie: onion-induced hemolysis) @ late stage.
42
Q

RBC pathway: pentose phosphate shunt. Function?

A
  • Antioxidant, reduces SH groups on globin. Heal and repair heinz body and eccentrocytes.
43
Q

Lifespan of RBCs?

A
  • Most mammals, RBC lasts 100-150 days (except cats and rabbits with shorter).
44
Q

Red cell and Hgb degradation pathway?

A

1a) Globin turns into amino acids (push out into blood and use for new cells).
1b) Fe: iron popped off and recycle.
1c) Heme: breakdown process by heme oxygenase to turn into BILIVERDIN. In birds and reptiles, this is an endpoint.

4) Biliverdin is turned into BILIRUBIN by biliverdin reductase (in mammals). End break down products of heme in mammals.
5) BIL is pushed to blood, carried by ALB through blood to get to liver.
6) BIL was taken internally in liver to conjugate to glucuronide (water soluble) to be able to dissolved.
6) BIL is pushed down in bile secreted by intestine, excreted in feces.

45
Q

How to get rid of RBCs in disease state?

A

Same as healthy state, but go to kidney for filter/secretion.
- Kidney = pop-up vale.
- When see bilirubinuria (not usually seen), use as evidence of hemolysis. `
- Can by pass GI tract.

46
Q

What is ALB?

A
  • Highest concentration of protein in plasma.
  • Maintain oncotic pressure
  • Carrier protein
  • Synthesized by HEPATOCYTES
47
Q

What is GLOB?

A
  • Is the other plasma proteins.
    1) Immunoglobulins (gamma) synthesized by plasma cells, account most GLOB in plasma. (i.e.: infectious species tend to have allergic immunoglobulins react).

2) Other alpha, beta globulins synthesize by hepatocytes (i.e.: animals with liver dz has low ALB)

48
Q

Why does plasma yields higher number than serum?

A

Because plasma include all proteins including fibrinogen and clotting factors. Therefore, trend the same value.

49
Q

How does plasma measure?

A
  • By refractometry
  • Measure total plasma protein (TPP), fibrinogen, Prot:Fib ratio.
50
Q

What can cause false reading of TPP?

A
  • High concentrations of glucose, sodium or urea can increase TPP.
  • Hemolysis and lipemia can interfere with reading.
51
Q

How globulins are calculated?

A

GLOB = TP - ALB
*Species specific

52
Q

What terms refer to high of both ALB and GLOB?

A

Panhyperproteinemia

53
Q

Compare relative vs. true changes in protein concentration.

A

Relative change is change in plasma water volume (see in dehydration and overhydration) vs. true change is change in actual protein concentration (as in protein synthesis, protein loss or change in protein intake/utilization).

54
Q

Mech of HYPERalbuminemia

A

ONLY dehydration
(liver never synthesizes too much ALB)

55
Q

Mech of HYPERglobulinemia

A
  • Dehydrtion
  • Increased production of immunoglobulins (HYPERgammaglobulinemia) in chronic inflammation (polyclonal gammopathy) and lymphoid neoplasia (monoclonal gammopathy).
56
Q
A
57
Q

Define leukocyte

A

Nucleated cell that travels through the blood to get to the tissues, where it functions

58
Q

What’s “leukon”?

A

ALL leukocytes in body including marrow precursors, leukocytes in blood, leukocytes and leukocyte derived cells in tissues

59
Q

Define leukogram

A

Blood test evaluating leukocytes, usually part of the complete blood count (CBC).

60
Q

Define leukocytosis

A

Increase in leukocyte numbers above the reference limit (neutrophilia or heterophilia is the usual cause)

61
Q
A

402-Exam 1 (3 decks)

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