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Unit 3: LGS > Week 3 > Flashcards

Week 3 Flashcards

1
Q

Limitations of RBC

A
  • Do not have any organelles: cannot replicate or make ATP aerobically
  • Do not have ribsomes; cannot make proteins; the proteins originate in the cell; the RBC is packed with what they need to survive for 120 days
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2
Q

What is the role of glycolysis in RBC’s?

A

To produce ATP (4 in total, 2 to use)

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3
Q

End product of glycolysis?

A

Lactate; reduction reaction because NADH gives hydrogen to pyruvate to create lactate; enzyme is lactate - dehydrogenase

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4
Q

What is fate of NADH produced by glycolysis in RBC?

A

○ Reduces methemoglobin to ferrous iron;

○ used to convert pyruvate to lactate

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5
Q

What occurs with high NADH level produced by RBC?

A

the NADH/NAD ratio will go up stopping ETC, TCA, and pushing cells to anaerobic respiration

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6
Q

Different fates of G6P in RBC

A
  • glycolysis

- pentose phosphate pathway

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7
Q

Pentose Phosphate Pathway

A
  • will make ribose-5-phosphate (make 5 carbon sugar) and NADPH; rate limiting enzyme to shunt G6P to PPP is G-6-P dehydrogenase
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8
Q

What happens to the 5 carbon sugars?

A

used to make nucleic acid in other cells but in RBC they will be shunted back into glycolysis as Fructose-6-P or Glyceraldehyde-3-P (Hexose monophosphate shunt); enzymes are transketolase (co-enzyme: thiamine–Vit B1) and transaldelase

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9
Q

What is the role of NADPH in RBC’s

A

Maintains glutathione in reduced state so glutathione can protect RBC from reactive oxygen

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10
Q

Glutathione

A

: principle anti-oxidant enzyme at cellular levels; neutralizes free radicals (hydrogen peroxide to water and oxygen AND hydroxyl radical); reduced form is GSH will be oxidized to GSSG

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11
Q

What occurs with high free radical production?

A
  • cell lysis due to lipids and proteins being attacked in cell membrane
  • Will create permanent damage due to RBC not being able to make and replace damaged proteins
  • Will oxidize Fe+2 to Fe+3
  • Modifies hemoglobin to make heinz bodies
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12
Q

What is the role of 2,3 BPG shunt in RBC?

A

○ Only some glucose will shunt
○ Will produce 2,3 BPG which will help hemoglobin release oxygen by stabilizing deoxygenated form of hemoglobin
○ Lower the pH in the tissue, the higher the binding of BPG to hemoglobin

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13
Q

How does oxygen bind to hemogblobin?

A

Oxygen forces out hydrogen ion bound to hemoglobin therefore there is less hydrogen ion allowing for oxygen to bind to hemoglobin

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14
Q

Fetal vs Adult hemoglobin

A
  • HbF less able to bind to 2,3 BPG
  • Gamma chain has less binding spots for 2,3 BPG to bind as tightly as beta chain does in adult
  • Fetal cells are less metabolically active than normal cells, which means it is less acidic (so less Hydrogen), will cause less tight binding of hemoglobin to 2,3 BPG
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15
Q

G6PD deficiency

A
  • Low G6PD so glucose is not going to PPP so it is not creating NADPH which will prevent cell from being able to reduce glutathione and protect cell from oxidative insult
  • High levels of bili-rubin is causing jaundice symptoms and is due to cell lysing because of oxidative insult
  • Elevated lactate dehydrogenase is causing increased lactate which is causing decreased blood pH
  • Anemia is caused by cells lysing due to oxidative insult because of low G6PD
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16
Q

A quantitative deficiency of the enzyme tansketolase will affect RBC metabolism by which of following mechanisms?

A

the oxidative part would work fine it would only affect the 5 carbon sugar going back into glucose so ATP production would decrease

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17
Q

What happens when GSSG increases?

A
  • caused because of G6PD deficiency
  • will decrease hydrogen peroxide from being broken down into water and Oxygen, which will increase oxidative stress in cell. The radicals will attack the proteins and lipids in cell membrane, causing it to rupture and causing the cell to lyse.
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18
Q

Heme

  • function
  • made from
  • made
  • rate limiting enzyme
A
  • houses ferrous enzyme
  • made from glycine (hydrophobic, allyphatic) and succinyl CoA ( in TCA)
  • Made in bone marrow and liver
  • Delta alla synthase is rate limiting enzyme; controlled by amount of heme
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19
Q

Hemoglobin degradation in normal state

A
  • RBC lives for 120

- Macrophages will eat RBC and take to spleen

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20
Q

Steps of Hemoglobin degradation in normal state

A
  • heme and globin separated
  • heme will be oxidized (heme oxygenase) into billiverdin and then reduced (biliverdin reductase) into unconjugated bilirubin; globin will be changed into AA
  • bilirubin will combine with albumin to be taken from spleen through the blood into the liver
  • in the liver the bilirubin will loose albumin and gain UDP-glucouronate which will convert it to bilirubin diglucuronide
  • bilirubin diglucuronide will be excreted into digestive system and bacteria will ferment into urobilinogen
  • urobilinogen will then be excreted in feces and urine
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21
Q

Hemoglobin degradation in diseased state

A
  • There will be a lot of hemoglobin in blood, and kidney will try to eliminate a lot of it stressing it out
  • Body gets rid of Hgb in blood by having proteases chop it up into dimers, then haptoglobin will bind to hemoglobin dimers and takes them to macrophages and liver to be broken down as normal
  • Free haptoglobin would be low in blood because they would be bound to the hemoglobin that spilled into the blood
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22
Q

Iron Hemostasis

  • comes from
  • converted to
  • stored in
A
  • Iron comes in through diet (meat) in ferric form
  • Fe3+ (ferric) cannot get into cell and is converted into Fe2+ (ferrous) and is brought into enterocytes of the intestine through DMT1
  • stored in cells through ferritin
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23
Q

Hepsidin

A

causes iron to be trapped in cells (enterocytes and macrophages in particular)

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24
Q

How is iron transported in blood?

A

When iron is transported in blood it is converted back to ferric form and combines with apotransferrin, which makes transferrin (free iron is toxic in blood and must be bound)

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25
Q

Hemosyderine

A

seen in iron overload

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26
Q

How is iron lost from body?

A

Iron builds up in cells and when those cells are sloughed off, iron is lost with cell

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27
Q

Anemia

A

low hemoglobin or hematocrit

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28
Q

Iron deficiency anemia

  • Serum iron:
  • Ferritin:
  • TIBC:
  • % Iron Saturation:
  • Hepcidin:
A
  • Serum iron: low
  • Ferritin: low
  • TIBC: high
  • % Iron Saturation: low
  • Hepcidin: low
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29
Q 
- Anemia of chronic disease
○ Serum iron: 
○ Ferritin 
○ TIBC
○ % Iron Saturation: 
-Hepcidin
A 
○ Serum iron: low
○ Ferritin: high
○ TIBC: low or normal
○ % Iron Saturation: low
-Hepcidin: high; iron trapped in cells
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30
Q

hematocrit

A

the ratio of the volume of red blood cells to the total volume of blood.

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31
Q

Total iron binding capacity

A

blood test to see if you have too much or too little iron in your blood. Iron moves through the blood attached to a protein called transferrin. This test helps your health care provider know how well that protein can carry iron in your blood.

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32
Q

Why is hepcidin increased with anemia of chronic disease

A
  • With inflammation there is increased IL-6 which increases hepcidin, which keeps iron in cells
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33
Q

Antigen

A

something that elicits an immune response, something that the antibody binds too (most common definition); can be inside the cell, outside the cell

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34
Q

Antibody

A

something produced to counter act foreign substances

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35
Q

Difference b/w A and B

A

If you have a galnac then youre A; galactose then youre B

36
Q

Agglutination

A

Clumping of cells together; typically occurs in lab

37
Q

Which antibody isotype causes RBC agglutination?

A
  • IgM; one antibody is binding more than one RBC because it contains more binding sites which results in clumping of cells;
  • other isotypes can bind to RBCs but they won’t clump together
  • agglutination is only in lab, it is called transfusion reaction
38
Q

Blood Types

A

A: has anti-B antibodies
B: has anti-A antibodies
AB: has no antibodies
O: has anti-A and anti-B antibodies

39
Q

Prediction of childs blood type

  • M:A, F:O
  • M:B, F:A
  • M:AB; F:A
  • M:O, F:AB
A
  • AO or OO
  • AB, A, B, O
  • AB, A, B
  • A, B
40
Q

Forward blood typing

A
  • blood is added to serum with known antibodies, if antigen is present on RBC then you will get agglutination
  • always using IgM
  • Antibodies come from stock or commercially developed antibodies
  • patients blood type will show positive agglutination
41
Q

Back blood typing

A
  • patients serum is mixed with RBC’s of known ABO type
  • You don’t make antigens against your own antibodies so patients blood type will be positive for whatever type does NOT agglutinate
42
Q

How do you form antibodies to antigens that aren’t in your body?

A
  • naturally occuring antibodies
  • Theory: over time exposed to diff. animal antigens in food particles that help dev. These other antibodies
  • Carbohydrates tend to form IgM; Protein forms more IgE
43
Q

What is universal donor? Why?

A
  • Type O neg: there is no surface antigens on RBCs; mainly giving RBCs w/o the plasma so don’t really get antibodies
  • transfusion of RBCs - want to protect RBCs that you’re transfusing; don’t want to lyse RBCs
44
Q

What is universal acceptor?

A

ABO; do not contain any antibodies in plasma

45
Q

Rh antigen

A
  • is IgG so it can cross placental barrier and this is b/c it’s a protein antibody
  • Require prior exposure to be expressed
  • prior exposures usually occur from prior pregnancies through fetus blood
46
Q

rhogam

A

Rh antibodies that bind all of babies RBCs before mom has a chance to make antibodies

47
Q

What is typically seen when baby is Rh positive and mom is Rh negative?

A
  • If mom has had previous exposure to Rh antigen from previous pregnancies then she has probably made an Rh anti-body
  • The baby will usually be anemic
  • Can cause fetal hydrops: fluid build up in babies
  • Will treat mom with rhogam which will produce fake RH negative antibodies that will bind to any of the RH antigen from babies blood that was mixed labor so that mom will not produce own antibodies
48
Q

What can occur with moms that have O blood and baby has A, B, or AB?

A

-O mothers can also express A and B antigens that are IgG and can cross the border and attack a baby if there are A or B; this is a lot milder than O neg and O pos

49
Q

How to treat fetal anemia?

A
  • intravascular intrauterine fetal transfusion of O negative blood
  • O negative will help baby and not hurt mother
50
Q

spherocytes

A

erythrocytes (red blood cells) that are sphere-shaped rather than bi-concave disk shaped as normal
- abnormal shape gets them stuck in the fenestrated capillaries of the spleen which causes them to lyse; unable to deform and squeeze thru tiny cords

51
Q

Direct antibody

A

when you make an antibody for the auto-immune antibody; testing for auto-antibodie

52
Q

allo-antibodies

A

antibodies directed against non-self antigens

53
Q

Steps of direct antibody testing (DAT/ coombs test)

A
  • Start off w/ patients RBCs w/ antibodies attached
  • Wash the serum to wash off any other things on it
  • Add in a special antibody to the Fc portion and if there’s agglutination then we know they have antibodies bound to the RBC’s (auto-antibodies b/c no previous transfusion or anything)
  • Therefore probably autoimmune hemolytic anemia
54
Q

Extravascular hemolysis

A
  • Lysing of RBC in spleen/liver
  • Macrophages phagocytose Heinz bodies (RBC that look like they have a bite taken out of them)
  • If the cell w/ the bite survives and gets back into circulation then the membrane fuses and forms a spherocyte
  • Macrophages have Fc receptors that recognize antibodies and will opsonize them or tag them
  • elevated unconjugated bilirubin
55
Q

Intravascular hemolysis

A

Lysing of RBC in vessels

  • decreased haptoglobin (binds to free Hgb dimers and takes them back to liver)
  • increased lactate dehydrogenase (not using in glycolysis bc lysing)
  • more acute problems because dimers can cause hemoglobinuria and lactate can damage kidneys
56
Q

Mechanisms of hemolysis

A
  • Hereditary spherocytosis: extravascular hemolysis
  • Auto-immune hemolytic anemia: predominantly extravascular, severe cases can cause intravascular
  • G6PD thalassemia: both
  • Hemolytic transfusion reaction: intravascular
  • Mechanical: intravascular
57
Q

How is anemia defined

A

Reference range is used to identify if patient has low values or high values and these ref. ranges can vary from site to site, sex, age, certain stages like pregnancy

58
Q

Hgb reference range in males vs females

A

-reference range in males tend to be higher due to higher mass because they need more oxygen to supply their higher mass, so they will have increased amount of RBC’s

59
Q

Ways body compensates for anemia

A
  • Inc. cardiac output which will inc. o2 and blood flow,
  • inc. 2,3 BPG to make O2 more available to the tissues so there is a higher percentage of oxygen that presents to the tissue
  • altered blood flow: vasoconstriction which allows blood to be shunted to vital organs like the heart and brain
60
Q

Fick equation

A

O2 delivery=blood flow*Hgb concentration * (asat-vsat)

61
Q

Ways to categorize anemia

A
  • Morphologic: MCV( will tell you about size and morphology); RBC shape on peripheral smear
  • Pathophysiologic: decreased production or increased destruction; reticulocyte count
62
Q

Causes of microsidic anemia

A

-iron deficiency and thalacemia

63
Q

Normologic approach to categorize anemia

A

-based on size

64
Q

Causes of macrosidic anemia

A

-B12 and folate deficiency (really large RBC), spherocytosis with increased reticulocytes

65
Q

Normosidic anemia

A
  • anemia of chronic disease

- nutritional deficiency (will have really large and small sized cells so will have normal mean size)

66
Q

Orthostatic hypotension

A

-hypovolemic, can occur when patient has bleed

67
Q

How to treat upper GI bleed

A
  • normal saline to help with volume

- upper endoscope to pin-point bleeding and stop

68
Q

Drop in H&H after treatment of GI bleed

A
  • hemodilution due to fluids being pumped to help with hypovolemia, the hgb concentration is diluted
  • blood was continually lost during procedure
69
Q

Why do you have increased TIBC in iron deficiency anemia?

A
  • correlates what is occurring with transferrin

- will have low transferrin because have low iron

70
Q

Colorecto carcinoma

A

weakness, dizziness, light headedness with iron deficiency anemia

71
Q

Iron supplementation

A
  • oral: can cause GI issues; if patient is on medication that inhibits acid production, the iron needs to be given before for better absorption
  • IV: better for older patients that cannot tolerate iron PO
  • IM: better because GI has poor absorption
72
Q

Flow murmur

A

-can be caused by anemia that has been present for a while

73
Q

Rheumatoid Arthritis and anemia

A

-chronic inflammation leads to hepsidin which leads to increased storage of iron which causes an anemia, due to impeding iron from leaving macrophage and enterocyte

74
Q

Treatment for anemia of chronic inflammation

A

-treat underlying disease and decrease inflammation so hepsidin can be lowered

75
Q

Lupus

A
  • autoimmune disease where immune system attacks own tissues

- will present with butterfly rash on face

76
Q

Pans-cytopenia

A

-leukopenia, thrombocytopenia, anemic

77
Q

Peripheral blood smear with lupus

A
  • looking for reticulocytes to indicate hemolysis which causes immature RBC’s to be released to try and help keep up
  • looking for spherocytes due to autoimmune
78
Q

elevated LDH and auto-immune disease

A

-check haptoglobin, low=hemolysis

79
Q

auto-immune hemolytic anemia in setting of anemia due to chronic inflammation

A
  • caused by lupus

- increased haptoglobin and hepsidin

80
Q

Valvular etiology of anemia

A
  • will need to look at echo to evaluate valve for retrograde flow
  • valve has metallic components and RBC are being lysed on foreign material
  • at higher risk for having hemolysis, baseline will have elevated hemolysis
81
Q

Rapport luebering shunt

A

will tun 2,3-BPG to 3 phosphoglycerate through phosphatase

82
Q

How to change ferric to ferrous iron

A

-NADH produced from G3p being changed to 1-3 BPG is used to reduce oxidized cytorchrome b5 to reduced cytochrome b5 with the help of cytochroms b5 reductase. Reduced cytochrome b5 will give its hydrogen to Fe3 to turn it into Fe2, making oxidized cytochrome b5

83
Q

Microcytic anemia (decreased MCV)

A
  • Iron deficiency
  • Thalessemia: inherited blood disorder characterized by less hemoglobin and fewer red blood cells in your body than normal.
84
Q

Normocytic anemia (normal MCV)

A

-anemia of chronic disease

85
Q

Macrocytic anemia (elevated MCV)

A
  • megaloblastic anemia (caused by B12-folate deficiency)

- hemolytic anemia (with reticulocytes)

Unit 3: LGS (7 decks)

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