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Block 7 Week 3 > Usera: Red Blood Cell Disorders > Flashcards

Usera: Red Blood Cell Disorders Flashcards

1
Q

What stimulates the production of red blood cells in the bone marrow?

A

EPO release from interstitial cells in the peritubular capillaries of the renal cortex

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2
Q

What are 3 stimuli for EPO release from the kidney?

A

hypoxemia
anemia
left shift in O2 binding curve

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3
Q

What happens to the O2 binding curve when you:

Increase/decrease pH?
Increase/decrease DPG?
Increase/decrease temp?

A

increase pH, left shift
decrease pH, right shift

decrease DPG, left shift
increase DPG, right shift

decrease temp, left shift
increase temp, right shift

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4
Q

Ectopic production of epo leads to…

A

erythropoiesis

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5
Q

This is a sign of active erythropoiesis…

A

reticulocytes

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6
Q

So, what do reticulocytes in the blood tell you?

A

that your marrow is working fine - erythropoiesis is occuring

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7
Q

What happens to the reticulocyte count in anemia?

A

it is falsely increased - must be corrected for

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8
Q

How do you correct the reticulocyte count?

A

(Actual Hct/45) * retic count

ex: Hct = 20%, retic 15%
True retic = (20/45) * 15% = 6.6%

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9
Q

What is polychromasia? What does it imply? How do you correct for it?

A

difference in palor in RBCs; implies that reticulocytes are present; correct by dividing corrected reticulocyte count by 2

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10
Q

If your reticulocyte is greater than (blank), then your bone marrow is good to go. If your reticulocyte is less than (blank), it is ineffective.

A

3; 3

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11
Q

This is one rather obscure compensatory response to anemia

A

extramedullary hematopoiesis - your body pumps out EPO to compensate for the anemia, which increases hematopoietic stem cell division in the liver, spleen, and bone marrow - can lead to hyperplasia in the bones (ex: in the skull)

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12
Q

Extramedullary hematopoiesis is naturally present in what population?

A

babies and young children

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13
Q

Things included in a CBC?

A 
hemoglobin
Hct (how much of whole blood is RBCs)
RBC count
RBC indices
WBC count w differential
platelet count
morphology
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14
Q

In general, newborns have (blank) normal ranges than children and infants

A

higher

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15
Q

Fetal hemoglobin is HbF. What does it do to the O2 binding curve?

A

shifts it to the left

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16
Q

What happens to HbF over 6-9 months time?

A

the HbF cells are replaced by HbA and HbA2

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17
Q

WHY do children have a lower Hb than adults?

A

higher phosphorus levels in children increase the synthesis of 2,3-BPG and cause a right-shifted O2 binding curve

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18
Q

Why do men have a higher Hb than females?

A

testosterone and lack of cyclic bleeding

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19
Q

What Hb level constitutes anemia for males? Non-pregnant females? Pregnant females?

A

male: Hb < 13.5g/dL
non-preg female: Hb < 12.5g/dL
pregnant female: Hb < 11g/dL

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20
Q

Why do pregnant females have lower normal Hb ranges?

A

increased plasma volume during pregnancy causes a dilutional effect

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21
Q

What is one general difference between sickle cell anemia and thalassemias?

A

sickle cell is a qualitative defect - abnormal structure of RBC

thalassemias are quantitative defects - abnormal synthesis of Hb

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22
Q

List 6 clinical findings in anemia

A 
concentration difficulties
fatigue
dyspnea
dizziness
pallor
pulmonary flow murmur
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23
Q

How do you calculate the mean corpuscular volume and what does this measure?

A

Hct * 1000/RCB

measures the average volume of a red cell

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24
Q

What does the mean corpuscular hemoglobin content measure? What does it mean if it’s low? High?

A

the concentration of Hb within the actual RBCs (Hb/Hct); low MCHC implies that there is a defect in Hb synthesis, like in microcytic anemias; high MCHC implies spherocytosis (too much Hg packed into RBCs)

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25
What does the red cell distribution width measure? When is this value useful?
how much the RBCs vary in size (anisocytosis); only really useful when it's increased *more variation, higher RDW (ex: can be seen in anemic transfusion recipients bc they have two distinct populations of cells)
26
Do mature RBCs have mitochondria? So how do they produce energy? What do they need to prevent damage by free radicals?
no mitochondria, no TCA, beta ox or ketone body synthesis; they use the cori cycle and anaerobic glycolysis; need glutathione synthesis from PPP
27
Soluble iron binding storage protein
ferritin
28
How is ferritin synthesized?
by macrophages in response to IL-1 and TNF-alpha
29
T/F: Serum levels of ferritin can be used to determine ferritin stores in the marrow macrophages
True
30
Decreased ferritin is diagnostic for (blank), while increased ferritin could be (blank)
iron deficiency; anemia of chronic disease or iron overload
31
The serum iron represents iron bound to (blank)
transferrin
32
Where is transferrin synthesized?
in the liver
33
What is normal iron level?
100ug/dL
34
What is the total iron-binding capacity? What does it correlate with? What is a normal TIBC?
total iron-binding capacity is a measure of the max amount of iron the blood can carry; it correlates with the concentration of transferrin; 300ug/dL
35
What is the iron saturation %? What is normal?
percentage of transferrin bound by iron; serum iron/TIBC *100; should be about 33% (means that
36
So what is the difference between ferritin and transferrin?
ferritin is the protein that stores iron in the tissues and bone marrow (can't escape into the serum when bound to ferritin); transferrin is the protein that carries iron in the blood
37
If ferritin is high, what happens to the liver production of transferrin? What about in an iron deficient state?
it decreases - don't need any more iron in the blood; it increases in iron deficiency to pump out more transferrin and get more iron circulating in the bloodstream
38
4 types of microcytic anemias
iron deficiency ACD thalassemia (alpha and beta) sideroblastic anemia
39
10% of dietary iron is resorbed in the (blank); when iron is (blank), it cannot be resorbed
duodenum; oxidized (Fe3+)
40
What two things can free elemental iron from its oxidized (ferric) form?
gastric acid frees it and vit C reduces ferric form of iron
41
Most body iron in incorporated into (blank)
hemoglobin
42
Most common anemia and most common nutritional deficiency worldwide
iron deficiency anemia
43
Which populations get iron deficiency anemia?
toddlers (1-2yo) | females (12-49yo) due to menstruation
44
What are 3 general categories of causes of iron deficiency anemia? What are some examples?
1. blood loss: GI bleed, hookworm infection, NSAIDs/uclers 2. inadequacy: prematurity, restricted diets, malabsorption 3. Other: overutilization, pregnancy/lactation, destroyed in hemolytic anemia
45
4 weird clinical findings in iron deficiency anemia?
esophageal web achlohydria (low or no HCl gastric acid in stomach) glossitis (big tongue) koilonychia (spooned toenails)
46
What happens to the following in iron deficiency anemia? ``` MCV? Serum iron, iron sat? Serum ferritin? TIBC? RDW? Platelets? ```
``` decreased (microcytic) decreased decreased TIBC increased (increased transferrin) RDW increased due to reticulocytes most likely increased platelets ```
47
Most common anemia in a hospital setting
anemia of chronic disease
48
Anemia of chronic disease occurs with chronic (blank) due to arthritis, infection, malignancy, alcoholism, etc
inflammation **production of hepcidin, which is an acute phase reactant
49
What happens to the following in anemia of chronic disease? heme synthesis? renal secretion of EPO? hepcidin secretion by liver?
decreased heme synthesis inadequate renal secretion of EPO hepcidin secreted by liver in response to inflammation, which prevents the release of iron to transferrin
50
What does hepcidin secretion by the liver do?
prevents iron from getting out of marrow macs and into bloodstream to transferrin
51
What happens to the following in anemia of chronic disease? ``` MCV? serum iron? TIBC? iron sat? serum ferritin? ```
``` decreased decreased decreased decreased increased serum ferritin (due to chronic inflammation) ```
52
Thalassemias are a (blank) abnormality of normal globin chains
QUANTITATIVE (not enough produced)
53
In what regions are thalassemias most common?
Mediterranean Africa SE Asia
54
How many copies of the beta globin gene are on each chromosome? Which chromosome? Alpha globin gene? Which chromosome?
one copy of beta gene on each chromosome 11 (two total loci); 2 copies of alpha gene on each chromosome 16 (4 total loci)
55
What is the problem on a genomic level with beta-thalassemia?
defective upstream PROMOTER region of beta-globin gene (gene is OK, but promoter is defective, so no transcription)
56
What happens to the following in B-thalassemia? ``` MCV? Hb? Hct? RBC count? RDW and ferritin? ```
``` MCV: mildly decreased Hb: decreased Hct: decreased RBC count: increased (trying to compensate for nonfunctional hemoglobin) RDW/ferritin are normal ``` **lab values are the same for alpha-thal
57
What hemoglobin types will you see an increase in in B-thalassemia?
HbA2 (2alpha, 2 gamma) | HbF (fetal hemoglobin)
58
Should you treat a patient w beta-thalassemia?
No! You have the risk of iron overload
59
What happens in Beta-thalassemia major on a genetic level?
Defects in BOTH chromosome 11's coding for the Beta-chain, so you get ZERO HbA (2alpha2beta)
60
What does Beta-thalassemia lead to?
severe hemolytic anemia **not making enough of the beta chain, so body compensates by increasing RBCs – pumps out abnormal RBCs which are eaten up and hemolyzed by splenic macrophages
61
What happens to RDW and reticulocytes in beta-thalassemia?
both are increased bc the body is trying to compensate for lack of beta globin
62
What is the problem genetically in alpha thalassemias?
one chromosome deletion - does not cause anemia
63
2 gene deletions in the alpha globin gene results in (blank)
alpha-thalassemia trait
64
How does alpha-thalassemia differ in blacks vs Asians?
Blacks (α/- α/-) – mild anemia | Asians (-/- α/α) – increased risk for more serious forms **one chromosome w both alpha globin segments defective
65
What is hydrops fetalis?
two dysfunctional chromosome 16's; all four alpha loci are messed up - incompatible with life
66
List 4 things that can lead to sideroblastic anemia
chronic alcoholism Vit B6 (pyridoxine) deficiency lead poisoning iron overload
67
What is the problem that is occuring in sideroblastic anemia?
defect in protoporphyrin (ultimately, heme) synthesis within mitochondria = iron cannot be incorporated into heme so iron is trapped in the mito
68
What is the rate limiting step in heme synthesis? What cofactor is required?
Converting succinyl-CoA to aminolevulinic acid via ALAS; Vit B6 required for ALAS
69
How does chronic alcoholism lead to sideroblastic anemia?
ETOH is a mitochonrial toxin **30% of hospitalized alcoholics will have sideroblastic anemia
70
Why does vitamin B6 (pyridoxine) deficiency cause sideroblastic anemia?
Vit B6 is a cofactor for the ALAS enzyme (rate-limiting step in heme synthesis)
71
Vitamin B6 deficiency can be seen in alcoholics and those taking (blank) for TB
isoniazid **it complexes with pyridoxine
72
Most common cause of sideroblastic anemia in kiddos ages 1-5yo
lead poisoning **lead-based paint, batteries, etc
73
3 enzymes that are denatured in lead poisoning? What is the bottom line...like these enzymes are denatured, so what cannot proceed normally?
ferrochelatase: iron can't bind w protoporphyrin ALA dehyrase: increase in alpha-ALA ribonuclease: ribosomes can't break down **you can't incorporate iron into heme
74
Clinical findings of lead poisoning?
Burton's line (blue line on gums) abdominal colic (lead deposited in enterocytes) encephalopathy growth retardation (lead deposits in epiphyses of long bones) peripheral neuropathy nephrotoxicity
75
What happens to the following in lead poisoning? Lead levels in urine? Iron, iron sat? Ferritin? MCV and TIBC?
``` elevated lead in urine **urine test is the best test increased iron, iron sat increased ferritin (stored) decreased MCV decreased TIBC (too much ferritin) ```
76
What will you find in the bone marrow of lead poisoning patients?
ringed-sideroblasts (pink cells with blue dots clustered around the perimeter)

Block 7 Week 3 (5 decks)

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