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PNB 2265 > Unit 1: Blood > Flashcards

Unit 1: Blood Flashcards

Understand function and makeup of blood

1
Q

What is the Plasma Made of?

A

Water (92%)

Plasma Protein (7%)
1. Albumin: Transport Isotonic Environment (60%)
2. Globulins: Immune, Makes Antibodies (35%)
3. Fibrinogens: Blood Clotting (4%)
4. Regulatory Proteins (1%)

Other Solutes (1%) → electrolytes/ ions, hormones

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2
Q

What are the formed Elements of Blood?

A

Erythrocytes: RBC –> O2 transport
Leukocytes: Immune function

Thrombocytes: Clotting

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3
Q

Properties of Erythrocytes

A

Transport O2 → Biconcave Shape:
Flexible, ↑ SA, can stack & move through the capillaries
↓ SA = bad O2 transport
Loose shape = sticky → blockages
Hb = ⅓ mass of cell (LOTS)

  • Created by EPO (connection to Testosterone)
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4
Q

Describe the Hematocrit Test

A

Can see big dif. In Plasma vs formed elements: About 50/50 but more Plasma

Formed Elements (pellet), buffy coat, plasma (supernatant)

Hemat. Looking at ratios
* Polycythemia
* Anemias
*Dehydration

Limitation: Can’t see individual cells (morphology, or exact type)

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5
Q

Describe Complete Blood Count

A

Splits into individual cell types
Looks at #, size, morphology
Mean Corpuscular Volume (MCV) Avg. vol. RBC in a sample (size)

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6
Q

Describe Compete Blood Count Differential

A

Repeat CBC over and over until all WBC types accounted for

Lymphocytes → HIV (effect Helper-T) this is not a very effective test, want to do genetic testing to see if the virus is there

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7
Q

Define Antigen

A

A protein on cells, help tag them as self, or non-self
* connection to blood typing/ immunity

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8
Q

Define Antibody

A

An immune system cell that attacks non-self proteins

leads to Agglutination in non-compatible blood transfusions

Anti-RH (D-antibody) = can Cross the membrane (Placental) → IgG-monomer (small) → Hemolytic Disease of the new born

Anti A/B = to big, can’t cross membrane → IgM-Pentamer (exposed from food)

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9
Q

Explain Bombay Blood

A

Bombay Blood = H-Antigen (immune response to H antigen → has H-antibodies)

(H antigen =precursor for A&B)
- So in ABO tests can appear at O -

Ways to test for Bombay Blood =????

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10
Q

Explain the Common Clotting Pathway

A

Thrombin → fibrinogen → fibrin

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11
Q

Explain the Extrinsic Clotting Pathway

A

Tissue factors from damage to vessel → activates common:
Thrombin → fibrinogen → fibrin

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12
Q

Explain the Intrinsic Clotting Pathway

A

Collagen → Common Pathway

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13
Q

What are the 3 phases of the Injury Clotting Pathway

A
  1. Vascular Spasm (Damage blood vessel, contracts)
  2. Platelet Phase (Platelets activated at injury) → pos. feedback

3.Coagulation phase: convert fibrinogen (soluble) to fibrin (insol.) = clot

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14
Q

Explain Vascular Spasm

A

Phase 1 in the Injury Clotting Process
Vascular Spasm (Damage blood vessel, contracts)

Signaling factors released from endothelial cells → attract/ activate platelets

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15
Q

Explain the Platelet Phase

A

Phase 2 in the Injury Clotting Process
Platelet Phase (Platelets activated at injury) → pos. feedback
Aggregation, Adhesion, Plug formation, Assist clot formation; also signal more platelets

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16
Q

Explain the Coagulation Phase

A

Phase 3 in the Injury Clotting Process

Coagulation phase: convert fibrinogen (soluble) to fibrin (insol.) = clot
Now w/ Fibrin mesh to hold cells together = clot

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17
Q

Define Thrombocytopenia

A

Low Platelet count → problems clotting

18
Q

Define Thrombocytosis

A

High Platelet count → Clots

19
Q

What are Platelets and what are their properties

A

cell fragments
- sticky
- contractile properties (can change size safely)

Important for clotting

20
Q

What are the ways we Regulate clotting

A
  1. Fibrinolysis = Dissolve thrombus (clot), need plasmin that dissolves insoluble = clot-busting drug
  2. Anticoagulant = inhibits Thrombin ( no clot formed); Heparin to thin blood
21
Q

Define Anemia

A

When you are not able to transport O2 nicely

22
Q

What is Macrocytic Anemia and it’s causes

A

Large RBC’s

Large MCV
Cause: Vit. B12 deficiency
Pernicious Anemia → can be caused by gastric bypass
(no intrinsic factor for B12 absorption)

23
Q

What is Microcytic Anemia and it’s causes

A

Microcytic Anemia: small cell size
Smaller MCV
Cause: Hb mutation, Fe deficiency

24
Q

What is Polycythemia and its causes

A

Elevated RBC levels (↑ Hematocrit) = Increased O2 capacity + transport

Areas of High altitude
Blood Doping (artificial)

25
What is Normocitic Anemia and its causes
Normocitic anemia (normal size RBC; not enough of them) When Erythropoiesis not regulated enough | Regulated by:
26
Name and define all acronyms of CBC / CBD Diff.
27
Describe Erythropoiesis
The process of creating RBC→ need components of RBC ( B12, and Fe) also need Hormone (EPO) EPO: Made from Kidneys; HIIF (low oxygen factors) cause EPO release→ signals more RBC production * Testosterone also stimulates EPO * So men have more RBC's = a higher hematocrit EPO Binds to hematopoietic cells → precursor (Proerythroblast) → more binding on pro. → RBC * Color change → gene expression; Hb Organelles/ nucleus ejected for Biconcave shape * Can now migrate out of bone marrow ## Footnote RBC Life span (2-3 months)
28
# Thinking abt. Erythopoiesis How can we treat blood related dieases
CRISPR cas 9 → edit genes, to address progenitor RBC cells | RBC don't have nucleus, have to go further back in development to adress
29
Describe Sickle Cell Anemia
Anemia from a single point mutation in beta chain (Causes miss folding now sticking to other Hb like rods) ↓ O2 capacity of Hb + Life expectanty *Cells Stick to cell wall = blockages (AKA Vaso-Occlusive Crisis) Stroke, pain ## Footnote Protection from Malaria; changes to actin cytoskeleton + molecular compounds
30
Describe Carbonmonoxide and Cyanide Poisoning ## Footnote CO and CN-
CO = binds better at O2 spot on Hb Prevents O2 transport Can’t detect Hyperbaric chamber: changes partial pressure of O2 to outcompete CO CN- = binds non-competitively Brought to tissues & stops ATP cycle
31
Describe Hemolytic Disease of the new born
Mom (-), Baby (+) for Rh (D-ant.) 1st preg. Mom = not exposed to D yet Placental Membrane; circulations separate During birth mom exposed to D → sensitized now has D-antibodies 2nd preg = potential Miscarriage if baby is (+) ## Footnote becasue the now present Anti-D antibodies are small and can cross the pacental membrane, and attack fetus
32
Define Catabolism
Breakdown of cells
33
Describe normal catabolism of Erythrocytes
Normal Catabolism Separates Hb (protein component) & Fe WBC phagocytosis RBC, it get's engulfed 1. Heme > Biliverdin > Bilirubin > liver as bile > excreeted 2. Fe recycling; Transferrin (a trasnport protein) brings to bone marrow, Ferritin & Hemosiderin in cell ## Footnote Ferritin and Hemssiderin = How reactive Fe is stored in cells before its bound again to Heme group; cause Fe is so reactive w/o always being bound will damage cell
34
What is Hemolysis | Think about Catabolism of RBC
The uncontrolled lysis (bursting) of RBC Problem: There are not enough WBC to engulf the bursing cells Hb released = Fe released; reactive → cell damage Try to excrete w/ Kidneys *can result in kidney failure/ damage
35
Define Hemogobinuria and Hematuria, what happens as a reault of these conditions?
Hemoglobinuria: Hb in urine Hematuria: Blood in Urine Kidney Damage/Failure
36
Define Jaundice its characteristics and causes
Jaundice: Yellow skin → Bilirubin in tissues Cause: Liver Failure → can’t excrete enough bilirubin Bilirubin = usually in Bile liver not working → instead builds up in tissues ## Footnote Bilirubin = Yellow protein ( was heme, converted to biliverdin (green) then into Bilirubin (yellow), It gets excreted by the liver as bile → helps with fat digestion
37
What are the types of synthetic blood, and the problems associated with each
Synthetic Blood: (no good, blood transfusion/banking = best) 1. Hb directly to body → Problem: Recreate effects of uncontrolled catabolism (free Hb + Fe floating around) 2. Molecules not based on Fe → Tried fluorine, good at binding/ transport. O2 but don’t let O2 go ## Footnote Uncontroled catabolism = Hemolysis
38
Describe the different types of Hemoglobin | Its make up, Fetal Hb, Conformation Changes
Hemoglobin = 2 alpha, 2 beta chains → IRON (4) * the globin groups * The Heme (Fe) Fetal = Alpha and Gamma Bind to Hb; conformation changes = diff. Affinities → Cooperative Binding: * Nothing bound = DeoxyHb * Oxygen Bound = OxyHb * CO2 Bound= Carbamino ## Footnote Fetal Hb: Has a higher binding afinity, to pull O2 through placenta/ hold on to it better
39
Compare and Contrast the Bohr Effect and the Haladane Effect ## Footnote Both are kinda saying the same thing
Bohr Effect: Co2 binds = releasing O2 (offloading O2 Haldane Effect: Easier for CO2 to bind if no O2
40
Explain the Hemoglobin-Dissociation Curve ## Footnote AKA Hb-Saturation Curve
CADET face right (increase p50: release O2) FIBB (decrease p50: Load O2)
41
Define P50
42
Testing for HIV | Human Immunodeficiency Virus
Want to do a genetic test, to see if the virus is present. or CBD DIff. would be better --> can see the whole WBC Profile ## Footnote HIV destroys white blood cells; by attacking Helper T-Lymphocytes; Disease that causes AIDS. There is now good pharmocuticals for this.

PNB 2265 (3 decks)

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