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pathophys, GI / Heme > Heme > Flashcards

Heme Flashcards

1
Q

A bone marrow stem cell that has the potential to become any blood cell

A

Hematocytoblast ( >myelobast or >lymphoblast)

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2
Q

Monoblast

A

Monocyte/Macrophage

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3
Q

WBC to RBC precursors in bone marrow

A

3:1

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4
Q

Main growth factor for erythrocytes.

Increases 1000 fold in presence of hypoxia

A

Erythropoietin

peptide hormone, produced in kidneys by peritubular capillary cells

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5
Q

Main growth factor for thromboblasts

A

Thrombopoietin

Also GM-CSF and Interleukins

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6
Q

Main growth factors for myeloblasts

A

G-CSF (Granulocytes only!)
GM-CSF (granulo + mono + erythro)
IL-3

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7
Q

7 day process of making an RBC

A 
Hematocytoblast > (EPO) > 
Erythroblast > (EPO, GM-CSF) >
NRBC > (loose nucleus) >
Retic > (enter circulation, lose ribosomes) >
Eryth
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8
Q

Hemoglobin, chains

A

1/3 mass of RBC

2 alpha chains, 2 beta chains

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9
Q

95% of adults hemoglobin

A

A1 (Alpha 2, Beta 2)

α2β2

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10
Q

1.5-3.5% adults hemoglobin

A

A2 (alpha 2, Delta 2)

α2δ2

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11
Q

Fetal Hemoglobin

A

F (α2γ2)

Can be elevated in sickle cell or beta thalassemia

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12
Q

Large chemical group called a PORPHYRIN, made of 4 rings attached to a central iron ion

A

Heme

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13
Q

Other uses for Heme

A

Myoglobin
Nitric Oxide Synthesis
Cytochromes (mitochondria, smooth ER)
Catalase

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14
Q

Heme synthesis

A

LIVER AND BONE MARROW

  1. Glycine + Succ CoA = D-ALA&raquo_space; PORPHOBILINOGEN (PBG)
  2. Four porphobilinogens = PORPHYRIN
  3. Porphyrin + Fe2 = HEME

NEEDS FOLIC ACID AND ZINC

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15
Q

Inherited disorder of heme production

Muscular disorders / pain
Tooth changes
Increased hair growth
Sun intolerance
Personality changes
Neuropathies
A

Porphyria

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16
Q

IRON -
absorbed in___ by___
Stored as ___
travels as ___

A

Duodenum, enterocytes
Ferritin
Transferrin

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17
Q

Reticuloendothelial System

A

Liver
Spleen
Bone Marrow
Lymph Nodes

and their macrophages

RBC BREAKDOWN

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18
Q

HEMOGLOBIN BREAKDOWN in RES

A

Globin&raquo_space; amino acid recycle

Heme > Conjugate, send to liver >
> Biliverdin > Bilirubin > Bile > Urobilinogen > Feces as Stercobilin / reabsorbed recycled

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19
Q

Hemoglobin α2β2, with β abnormal chains (β 6Glu-Val) which tend to change shape at lower pH and/or upon accepting O2

A

HbSS / HbAS

Sickle Cell

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20
Q

Missing one or more of the 4 alpha globin genes

A

Alpha ThaLESSemia (“less” one type of globin chain)

Hemoglobin H (HbH): 
Four β chains joined together (β4)
minor = heterozygous
major = homozygous / missing all normal genes
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21
Q

Missing one or both of 2 beta glob in genes

A

Beta ThaLESSemia

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22
Q 
Hemoglobin H (HbH): 
Four β chains joined together (β4)

or

Hemoglobin Barts (HbBarts):
Four γ chains joined together (Υ4)
A

Alpha ThaLESSemia Major

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23
Q

Genetic Methemoglobinemia

A

Defective Cytochrome B5 Reductase

24
Q

HbM

A

Methemoglobin (normal = 1-2% of heme at a time)

Fe3+ instead of Fe2+

Occurs in presence of oxidative stressors, normally corrected by NADH >(Ctyo B5)> NAD+

Fe3+ does not hold O2, in permanent “deoxy” shape

25
See cyanotic skin discoloration when HbM is
10-20%
26
Oxidizing chemicals that can cause methemoglobinemia
``` Nitrates Benzocaine (local anesthetic) Dapsone (antibiotic) Prilocaine (local anesthetic) Trimethoprim, sulfa drugs ```
27
Glycolysis pathway in RBC
Emden Myerhoff Pathway GLUCOSE ONLY NET: 2 ATP, 2 LACTATE MOLECULES FOR EVERY GLUCOSE MOLECULE 1. Invest 2 ATP 2. G6PD 3. First "payoff" 2 ATP 3. NADH > NAD+ 4. Pyruvate 5. Second "payoff" 2 ATP
28
G6PD detour - follows this pathway instead of glycolysis Generates NADH ** for RBCs (no mitochondria)
Hexose Monophosphate Shunt G6PD makes NADH > NADH refuels Glutathione > DETOX
29
How NADH works to decrease oxidative stress
Refuels GLUTATHIONE (which detoxes oxidized molecule)
30
G6PD Deficiency
**Most common enzyme deficiency in the world** X LINKED Can't produce NADH via HMP shunt (for RBCs) HEMOLYTIC ANEMIA RESULTS
31
G6PD Deficiency Triggers
``` Drugs Infections Fava Beans Diabetic Ketoacidosis Some chemicals (moth balls, methylene blue, HENNA) ``` **MAY PROTECT AGAINST MALARIA**
32
Platelet Lifespan and Growth Factors
10 days GM - CSF Interleukins 3, 6, 11
33
Dysfunctional stem cell lines in bone marrow. Precursor to AML. Requires bone marrow transplant
Myelodysplastic Syndrome
34
Autoimmune destruction of myeloid elements in peripheral blood by out-of-control macrophages. Bone marrow liver and spleen show macrophages that have eaten up all the RBCs. Decrease in all myelocytic lines, hepatosplenomegaly, anemia
Idiopathic Pancytopenia aka Hemophagocytic Syndrome
35
Total dysfunction of bone marrow stem cells. Bone marrow biopsy will show significant decrease ins ten cells, replaced by fat.
Aplastic Anemia (Idiopathic, chemo, drugs, viruses
36
Trifecta of Hemostasis
Vasoconstriction Platelet Aggregation Stasis
37
What causes vasoconstriction in the platelet aggregation pathway?
Thromboxane A2 (TXA2) Exposed collagen of endothelium triggers platelets to aggregate and produce TXA2, which directly causes vasoconstriction LOCALLY at the site of injury
38
How is TXA2 localized?
Endothelial cells around the clot produce PGI2 (also from arachinodic acid) which counteracts TXA2
39
How does aspirin help prevent heart attacks?
Inhibits the COX 1 enzyme in platelets, which decreases TXA2, and thus decreases vasoconstriction and platelet aggregation
40
Extrinsic vs Intrinsic Pathway
Extrinsic is more common, requires damage to endothelium (Tissue Factor) - starts at VII **MEASURED w PT/INR** **Extrinsic requires something Extra (TF)* Intrinsic is "Contact Activation" - starts at XII **MEASURED w PTT**
41
Intrinsic Pathway Heparin - PTT
XII > XI > IX > (VIII) > X > (V) > II > I 12 > 11 > 9 > (8) > 10 > (5) > 2 > 1
42
Extrinsic Pathway Warfarin / Coumadin - PT /INR
VII > IX > (VIII) > X > (V) > II > I 7 > 9 > (8) > 10 > (5) > 2 > 1
43
Genetic disorder characterized by deficiency in clotting factors, usually VIII
Hemophilia
44
PT / INR measures
EXTRINSIC PATHWAY WARFARIN / COUMADIN Vitamin K deficiency *** NOT IX
45
PTT measures
INTRINSIC PATHWAY HEPARIN GOOD FOR CHECKING VIII
46
Vitamin K Dependent Factors
II VII IX X
47
Common genetic factor deficiencies
Hemophilia A (VIII) Von Willebrands (vWF)
48
X-linked trait, usually diagnosed by 3 yrs age Trait: Bleeding into joint spaces after benign injury
Hemophilia A (VIII)
49
Autosomal, most common inherited bleeding disorder Bleeding gums, nosebleeds, menorrhagia
Von Willebrands vWF >> carries VIII
50
Unbound thrombin inactivated by
Antithrombin III | Protein C
51
Natural Heparin
Within granules of mast cells / basophils / surface of endothelial cells Enhances Antihrombin III and inhibits Intrinsic Pathway
52
Turns off amplification activity of V and VIII
Protein C **needs Protein S to function**
53
When Factor V can't be controlled by Protein C
Factor V Leiden Mutation Diagnose w RVV test (Russel Viper Venom)
54
Virchow's Triad
Stasis Endothelial Injury Hypercoagulability
55
Clot Buster
Plasminogen TPA (Tissue Plasminogen Activator)

pathophys, GI / Heme (2 decks)

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