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Derm, infectious disease, topical drugs, RBC disorders > Red Blood Cell Disorders > Flashcards

Red Blood Cell Disorders Flashcards

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1
Q

What is the stimulation for EPO release

A

Hypoxemia
Anemia
Left shift of oxygen binding curve

it is released from Interstitial cells in peritubular capillaries of renal cortex

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2
Q

What 3 things cause left shift in oxygen binding curve

A

increased pH
decreased DPG
decreased temp

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3
Q

what 3 things cause a right shift in the oxygen binding curve

A

decreased pH
increased DPG
increased temperature

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4
Q

reticulocyte count

A

Recorded as a % of normal (normal 3> ineffective

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5
Q

extramedullary hematopoeisis

A

Naturally present in babies and young children - Liver and spleen
Compensatory response to anemia
-Hepatosplenomegaly
-Bone marrow expansion in active marrow

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6
Q

hemoglobin in newborns

A

Higher normal ranges than children and infants
Fetal hemoglobin – HbF (2α2γ) – shifts OBC to the left
Over 6-9 months, HbF cells are replaced by HbA (97%), HbA2 (2.5%), and HbF (<1%)

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7
Q

hemoglobin in children

A

lower than adults. Higher phosphorus levels increase synthesis of 2,3 DPG – leading to right shifted OBC

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8
Q

hemoglobin in adults

A

Men have higher Hb due to testosterone, and lack of cyclic bleeding
Anemia in adult male = Hb < 12.5 g/dL
PREGNANCY: lower normal ranges due to increased plasma volume (dilutional effect)
Anemia in pregnancy = Hb < 11g/dL

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9
Q

hemoglobin electrophoresis is used to…

A 
detect hemaglobinopathies:
Abnormal structure (sickle cell anemia)
Abnormal synthesis (Thalassemias)
HbA 2α2ß  (97% in adults)
HbA2 2α2δ (2.5% in adults)
HbF 2α2γ (1% in adults)
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10
Q

clinical findings in anemia

A 
Fatigue
Dyspnea
Concentration difficulties
Dizziness
Pallor
Pulmonary flow murmur
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11
Q

what are the calculated RBC indices

A

MCV – mean corpuscular volume (Hct x 1000/RBC)
Useful for classifying anemias (see next slide)
-Microcytic = 100 um3
MCHC – Mean corpuscular Hemoglobin content
RDW – Red cell distribution width

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12
Q

MCV

A

MCV – mean corpuscular volume (Hct x 1000/RBC)
Useful for classifying anemias (see next slide)
Microcytic = 100 um3

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13
Q

MCHC – Mean corpuscular Hemoglobin content

A

average Hb concentration (Hb/Hct)
Low – implies defect in Hb synthesis: microcytic anemias
High - spherocytosis

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14
Q

RDW – Red cell distribution width

A

Reflects variation in size (anisocytosis)
Not very useful unless its increased
E.g. iron deficiency

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15
Q

mature RBC characteristics

A

Lack mitochondria
No TCA
No beta-ox
No ketone body synthesis
Rely on anaerobic glycolysis – cori cycle
Pentose phosphate pathway – synthesizes glutathione

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16
Q

Ferritin

A

Soluble iron binding storage protein
Serum levels correlate with ferritin stores in marrow macs
Synthesized by macs, driven by Il-1 and tnf-α
Decreased ferritin diagnostic of iron deficiency
Increased ferritin:
-Anemia of chronic disease
-Iron overload

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17
Q

Serum Iron

A 
Serum iron represents iron bound to transferrin
Synthesized in liver
Normal iron ~100 ug/dL
Decreased iron
-Iron def
-ACD
Increased iron
Iron over load (transfusions, sideroblastic, hemochromatosis)
18
Q

Total Iron Binding Capacity

A

Correlates with [transferrin]

Normal ~300 ug/dL

19
Q

iron saturation percentage

A

Percentage of iron binding sites on transferrin
=serum iron/TIBC x 100
Normal is ~33%

20
Q

Ferritin storage and transferrin synthesis relationship

A

Decreased ferritin stores cause increased transferrin synthesis in the liver. Increased ferritin leads to decreased transferrin synthesis.

21
Q

Microcytic Anemias

A

MCV<80

Iron deficiency
ACD
Thalassemia (α and ß)
Sideroblastic Anemia

22
Q

Iron Deficiency Anemia

A 
10% dietary iron resorbed in duodenum
Oxidized form (ferric Fe+3) cannot be resorbed in the duodenum

Gastric acid frees elemental iron

Vitamin C reduces ferric iron

Most body iron is incorporated into hemoglobin

  • Remainder is stored in marrow macs (~1,000 mg in men, ~400 mg in women)
  • Myoglobin
  • Enzyme cofactors
23
Q

How common is iron deficiency anemia and who is at highest risk?

A

Most common anemia, and most common nutritional deficiency worldwide
Toddlers 1-2 years of age
Females 12-49 due to menstrual loss

24
Q

Three groups of causes for iron deficiency anemia

A 
BLOOD LOSS
GI bleed
PUD
Hookworm infection
NSAIDS/Ulcers
Meckels
Menorrhagia
INADEQUACY
Prematurity
Restricted diets
Malabsorption
 (e.g. celiac)

OTHER
Overutilization: Pregnancy/lactation

Destruction:

  • Hemolytic anemias
  • PNH
25
Q

Iron deficiency anemia clinical findings

A 
Plummer-Vinson syndrome:  
esophageal web
Achlohydria (decreased or absent stomach acid production)
Glossitis
koilonychia (spoon nails)
26
Q

lab findings with iron deficiency anemia

A 
Decreased MCV
Decreased serum iron, iron sat
Decreased serum ferritin
Increased TIBC, RDW
Thrombocytosis – reactive
27
Q

Anemia of chronic disease

A

Most common anemia in hospital setting
–Chronic inflammation (e.g. arthritis, infections, malignancy, alcoholism)
Decreased synthesis of heme
Inadequate renal secretion of EPO
Hepcidin secretion by liver – response to inflammation
–Prevents the release of iron to transferrin (iron is in Macs, just can’t get out)

28
Q

What is Hepcidin

A

secreted by liver in response to inflammation. it presents the release of iron to transferrin, keeping iron in macrophages

29
Q

Lab findings with ACD

A

Decreased MCV
Decreased serum iron, TIBC, and iron sat
Increased serum ferritin

30
Q

thalassemias

A

Autosomal recessive traits
Quantitative abnormality of normal globin chains
Most common in Mediterranean, Africa and southeast Asia . . .
One copy of ß gene on each chromosome 11 (2 total loci)
2 copies of α gene on each chromosome 16 (4 total loci)

31
Q

Beta thalassemia

A 
DEFECTIVE UPSTREAM PROMOTER REGION OF ß GLOBIN GENE
Mild microcytic anemia
Decreased MCV, Hemoglobin and hct
Increased RBC count
Normal RDW and ferritin
--Decreased HbA 2α2ß  
--Increased HbA2 2α2δ and HbF 2α2γ

DO NOT TREAT

32
Q

beta thalassemia major

A

Aka cooley’s anemia ß0ß0

Severe hemolytic anemia
Rbc’s accumulate α chain inclusion, and are removed by splenic macrophages
Increased RDW and reticulocytes
ZERO HbA 2α2ß  
Increased HbA2 2α2δ and HbF 2α2γ

REQUIRES LONG TERM TRANSFUSION

33
Q

alpha thalassemias

A 
GENE DELETION
ONE DELETION DOES NOT CAUSE ANEMIA
2 GENE DELETION IS α–THAL TRAIT
Blacks (α/- α/-) – mild anemia
Asians (-/- α/α) – increased risk for more serious forms

Decreased MCV, Hb, Hct
Increased RBC count
Normal RDW, ferritin

34
Q

causes of sideroblastic anemia

A 
Chronic alcoholism
Pyridoxine deficiency (vit b6)
Lead poisoning
Iron overload
Hereditary – x-linked recessive (rare)
35
Q

sideroblastic anemia in chronic alcoholics

A

Etoh is a mitochondrial toxin

30% of hospitalized alcoholics will have sideroblastic anemia

36
Q

sideroblastic anemia in pyridoxine deficiency (vitamin B6)

A

Co-factor for δ–aminolevulinic acid synthase (δ–ALA)
Rate-limiting step in heme synthesis
Deficiency see in alcoholics and Isoniazid (INH) therapy
INH used to treat Tuberculosis, complexes with pyridoxine

37
Q

lead poisoning and sideroblastic anemia

A

Most common cause in little dudes 1-5 years of age
Eating lead-based paint
Battery and ammunition factories

Lead denatures critical enzymes:
Ferrochelatase: therefore iron cannot bind with protoporphyrin
ALA Dehydrase: causes increase in δ–ALA
Ribonuclease: prevents the breakdown of ribosomes, causing basophilic stippling

38
Q

what critical enzymes does lead denature?

A

Ferrochelatase: therefore iron cannot bind with protoporphyrin

ALA Dehydrase: causes increase in δ–ALA

Ribonuclease: prevents the breakdown of ribosomes, causing basophilic stippling

39
Q

clinical finding with sideroblastic anemia

A

Abdominal colic
Encephalopathy (due to increased δ–ALA)
growth retardation (maybe not in Tommy boy’s case though)
Peripheral neuropathy
Nephrotoxicity
Burton’s line (blue lining of gums at base of teeth)

40
Q

lab findings with sideroblastic anemia

A

Elevated lead levels (urine is the best test)
Increased iron, iron sat, and ferritin
Decreased MCV and TIBC
Ringed-sideroblasts in marrow

Derm, infectious disease, topical drugs, RBC disorders (8 decks)

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