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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
Q

See cyanotic skin discoloration when HbM is

A

10-20%

26
Q

Oxidizing chemicals that can cause methemoglobinemia

A 
Nitrates
Benzocaine (local anesthetic) 
Dapsone (antibiotic)
Prilocaine (local anesthetic) 
Trimethoprim, sulfa drugs
27
Q

Glycolysis pathway in RBC

A

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
  4. NADH > NAD+
  5. Pyruvate
  6. Second “payoff” 2 ATP
28
Q

G6PD detour - follows this pathway instead of glycolysis

Generates NADH ** for RBCs (no mitochondria)

A

Hexose Monophosphate Shunt

G6PD makes NADH > NADH refuels Glutathione > DETOX

29
Q

How NADH works to decrease oxidative stress

A

Refuels GLUTATHIONE (which detoxes oxidized molecule)

30
Q

G6PD Deficiency

A

Most common enzyme deficiency in the world

X LINKED

Can’t produce NADH via HMP shunt (for RBCs)

HEMOLYTIC ANEMIA RESULTS

31
Q

G6PD Deficiency Triggers

A 
Drugs
Infections
Fava Beans
Diabetic Ketoacidosis 
Some chemicals (moth balls, methylene blue, HENNA)

MAY PROTECT AGAINST MALARIA

32
Q

Platelet Lifespan and Growth Factors

A

10 days

GM - CSF
Interleukins 3, 6, 11

33
Q

Dysfunctional stem cell lines in bone marrow. Precursor to AML. Requires bone marrow transplant

A

Myelodysplastic Syndrome

34
Q

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

A

Idiopathic Pancytopenia

aka Hemophagocytic Syndrome

35
Q

Total dysfunction of bone marrow stem cells. Bone marrow biopsy will show significant decrease ins ten cells, replaced by fat.

A

Aplastic Anemia

(Idiopathic, chemo, drugs, viruses

36
Q

Trifecta of Hemostasis

A

Vasoconstriction
Platelet Aggregation
Stasis

37
Q

What causes vasoconstriction in the platelet aggregation pathway?

A

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
Q

How is TXA2 localized?

A

Endothelial cells around the clot produce PGI2 (also from arachinodic acid) which counteracts TXA2

39
Q

How does aspirin help prevent heart attacks?

A

Inhibits the COX 1 enzyme in platelets, which decreases TXA2, and thus decreases vasoconstriction and platelet aggregation

40
Q

Extrinsic vs Intrinsic Pathway

A

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
Q

Intrinsic Pathway

Heparin - PTT

A

XII > XI > IX > (VIII) > X > (V) > II > I

12 > 11 > 9 > (8) > 10 > (5) > 2 > 1

42
Q

Extrinsic Pathway

Warfarin / Coumadin - PT /INR

A

VII > IX > (VIII) > X > (V) > II > I

7 > 9 > (8) > 10 > (5) > 2 > 1

43
Q

Genetic disorder characterized by deficiency in clotting factors, usually VIII

A

Hemophilia

44
Q

PT / INR measures

A

EXTRINSIC PATHWAY

WARFARIN / COUMADIN

Vitamin K deficiency ***

NOT IX

45
Q

PTT measures

A

INTRINSIC PATHWAY

HEPARIN

GOOD FOR CHECKING VIII

46
Q

Vitamin K Dependent Factors

A

II
VII
IX
X

47
Q

Common genetic factor deficiencies

A

Hemophilia A (VIII)

Von Willebrands (vWF)

48
Q

X-linked trait, usually diagnosed by 3 yrs age

Trait: Bleeding into joint spaces after benign injury

A

Hemophilia A (VIII)

49
Q

Autosomal, most common inherited bleeding disorder

Bleeding gums, nosebleeds, menorrhagia

A

Von Willebrands

vWF&raquo_space; carries VIII

50
Q

Unbound thrombin inactivated by

A

Antithrombin III

Protein C

51
Q

Natural Heparin

A

Within granules of mast cells / basophils / surface of endothelial cells

Enhances Antihrombin III and inhibits Intrinsic Pathway

52
Q

Turns off amplification activity of V and VIII

A

Protein C

needs Protein S to function

53
Q

When Factor V can’t be controlled by Protein C

A

Factor V Leiden Mutation

Diagnose w RVV test (Russel Viper Venom)

54
Q

Virchow’s Triad

A

Stasis

Endothelial Injury

Hypercoagulability

55
Q

Clot Buster

A

Plasminogen

TPA (Tissue Plasminogen Activator)

pathophys, GI / Heme (2 decks)

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