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RHS > L14- RBC Pathology I > Flashcards

L14- RBC Pathology I Flashcards

(49 cards)

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1
Q

define the following:

(1) reticulocytosis
(2) erythroid hyperplasia
(3) pancytopenia

A

1- elevated serum reticulocytes
2- excess precursor cells in bone marrow
3- low RBCs, low WBCs, low platelets

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2
Q

Hb makes up __% of the dry weight of RBCs (include why that is important to lab testing)

A

95%- means there cannot be hyperchromatic RBCs since there really can’t be that much more Hb in RBCs

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3
Q

describe the breakdown of Hb

A

HbA, α2β2, 95%
HbA2, α2δ2, ~2%
HbF, α2γ2, ~2 (may slightly inc during pregnancy)

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4
Q

what are the advantages of the RBC shape

A

Biconcave Disc
=> large SA for Hb-O2 interactions –> reach maximal saturation of Hb
-allows for deformability and passage through small capillaries and splenic sinusoids

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5
Q

Define Anemia, then give the practical evaluation of anemia in a clinical setting

A

Defn: reduction (below normal limits) of total circulating RBC mass

  • in practice it is determined throught [Hb] OR packed cell volume / Hematocrit
  • normal [Hb] = 12-15 g/dL
  • normal Hc = ~45%

Note- [Hb]:Hc is about 1:3

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6
Q

define MCV

A

mean cell volume

-average volume of RBC in femtoliters (10^-15L)

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7
Q

define MCH

A

mean cell hemoglobin

-average Hb content per RBC in picograms

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8
Q

define MCHC

A

mean cell hemoglobin concentration

-average [Hb] in given volume of packed RBCs in g/dL

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9
Q

define RDW

A

red cell distribution width
-coefficient of variation of RBC volume (since older RBCs have dec volume)

-normal ~12.5, it will inc with hemolysis

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10
Q

Give the symptoms of Anemia at different severities

A

Mild: asymptomatic

Moderate (poor O2 supply to tissues): easy fatigability, loss of energy, HAs, fainting/dizziness, SOB, palpitations
(more prominent during exercise)

Severe: angina, CHF, confusion

Note- Sxs are more prominent in rapid onsets; in slow onsets, even severe anemia can be asymptomatic

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11
Q

list the clinical signs of anemia

A
  • pallor
  • nail changes
  • hemic murmurs
  • Inc pulse rate and RR –> inc SV –> high output cardiac failure (if severe enough)
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12
Q

how are anemias classified

A
  • morphological changes of RBCs

- pathophysiological mechanisms causing anemia

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13
Q

what are the morphological classifications of anemia

A

1) Normo-, Hypo-chromic: degree of hemoglobinization (or pinkness of) of RBCs
2) Macro-, Normo-, Micro-cytic: based on RBC size

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14
Q

list the 3 morphological classifications of anemia seen in practice (include blood work results)

A

Microcytic Hypochromic anemias: low intracellular [Hb], low MCV

Normochromic Normocytic anemia: normal intracellular [Hb], normal MCV

Normochromic, Macrocytic anemia: normal intracellular [Hb], high MCV

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15
Q

list the microcytic hypochromic anemias

A
  • Fe deficiency
  • anemia of chronic disease (also in normochromic, normocytic)
  • Pb poisoning
  • thalassemia
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16
Q

list the normochromic normocytic anemias

A
  • acute blood loss
  • hemolytic anemia
  • anemia of chronic disease (also in hypochromic, microcytic)
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17
Q

list the normochromic macrocytic anemias

A
  • cobalamin/B12 deficiency

- folate/B9 deficiency

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18
Q

what are the mechanism classifications of anemia

A

1) Accelerated RBC loss/destruction: blood loss, inc destruction / hemolytic anemia
2) Impaired RBC production: defective stem cell, abnormal RBC proliferation / maturation, bone marrow replacement, others

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19
Q

response of body to blood loss depends on….

A
  • rate of blood loss

- internal v external loss

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20
Q

Anemia due to blood loss is divided into….

Study These Flashcards
A
  • acute bleeding (hemorrhage)

- chronic blood loss (in stool, menses, etc)

21
Q

Anemia due to acute hemorrhage:

  • (1) is the immediate concern
  • (2) type of anemia
  • (3) compensation
Study These Flashcards
A

1- hypovolemia
2- normocytic, normochromatic anemia
3- rise in EPO –> reticulocytosis

22
Q

describe the mechanism of anemia in chronic blood loss (include type of anemia)

Study These Flashcards
A

(note- hypovolemia is not a concern)

  • Fe stores are gradually depleted –> underproduction of RBCs
  • microcytic hypochromatic anemia
23
Q

(1) list the common features of hemolytic anemias

(2) how are hemolytic anemias classified

Study These Flashcards
A

1- shortened RBC life span –> inc EPO / erythropoiesis + accumulation of Hb breakdown products

2:
i) by site, intravascular or extravascular
ii) by cause, intrinsic or extrinsic to RBCs

24
Q

list and provide some examples of the 3 causes Intravascular Hemolysis

Study These Flashcards
A
  • Mechanical Injury: defective cardiac valves, microvascular thrombi, heat
  • Complement Fixation: Ab coated RBCs
  • Infections: intracellular parasites (malaria), microbial toxins (clostridia)
25
Extravascular Hemolysis: - caused by defects that will cause (1) by (2) cells in the (3), therefore it is associated with (4) in relation to (3) - (5) and (6) are the common mechanisms by which (1) occurs
1- RBC destruction 2- phagocytes 3- spleen 4- splenomegaly 5- RBCs rendered less deformable (spherocytosis, sickle cell) 6- RBCs rendered foreign (immune mechanism- Ab coating)
26
Peripheral Blood test results that show evidence of hemolytic anemia
normochromic normocytic anemia with polychromasia (bluish tinge) +/- nucleated RBCs
27
Bone Marrow test results that show evidence of hemolytic anemia
(not usually done) | erythroid hyperplasia
28
Plasma/Serum test results that show evidence of hemolytic anemia
- elevated unconjugated bilirubin - elevated LDH - elevated free Hb levels (ntravascular hemolysis -dec or absent Haptoglobin levels
29
Urine test results that show evidence of hemolytic anemia
- hemosiderinuria | - hemoglobinuria (intravascular hemolysis)
30
Intravascular Hemolysis: (1) bilirubin levels (2) haptoglobin levels (3) hemoglobinuria (4) hemosiderinura (5) reticulocyte levels (6) LDH levels (7) free Hb levels (8) splenomegaly (9) Fe recycling
``` 1- inc 2- absent 3- positive 4- positive 5- inc 6- inc 7- large inc 8- absent 9- minimal ```
31
Extravascular Hemolysis: (1) bilirubin levels (2) haptoglobin levels (3) hemoglobinuria (4) hemosiderinura (5) reticulocyte levels (6) LDH levels (7) free Hb levels (8) splenomegaly (9) Fe recycling
``` 1- large inc 2- dec 3- negative 4- negative 5- inc 6- inc 7- inc 8- present 9- maximal ```
32
list the common Intrinsic RBC defects causing hemolytic anemia
(usually hereditary) -Membrane Defect: hereditary spherocytosis - Enzyme Defect: G6PD deficiency - Hb Defect: sickle cell, thalassemia - PNH (paroxysmal nocturnal hemoglobinuria)- ONLY ACQUIRED ONE
33
list the common Extrinsic RBC defects causing hemolytic anemia
(usually acquired) Immune mediated damage: autoimmune, drug-associated, transfusion reaction Non-immune damage: mechanical trauma, infections, chemicals, hypersplenism
34
Hereditary spherocytosis stems from a defect in (1) in the RBC leading them to have (2) shape and a (3) life span. - highest incidences in (4) part of the world - usually inherited in (5) pattern
1- membrane skeleton 2- spheroid shape --> less deformable 3- 10-20 days 4- northern Europe 5- AD (75% of cases)
35
Hereditary spherocytosis: - (1) list affected proteins - (2) pathogenesis (hint- 5 steps)
1- ankyrin, band 3, spectrin, band 4.2 2- reduced membrane stability --> loss of fragments (normal shearing forces in circulation) --> more spherical RBCs --> cannot transverse splenic sinusoids --> phagocytosis / destruction by splenic macrophages (=> splenomegaly)
36
list the clinical features of Hereditary Spherocytosis (Sxs)
Anemia: mild to moderate, 25% asymptomatic, minority are severely anemic from birth Splenomegaly Jaundice: unconjugated hyperbilirubinemia (continous hemolysis)
37
_____ along with hereditary spherocytosis can induce aplastic / hemolytic crises
parvovirus B19 infection
38
hereditary spherocytosis Tx
- supportive | - splenectomy --> corrects anemia, spherocytosis persists
39
Hereditary Spherocytosis diagnosis and lab findings
- FHx - CBC for anemia - evidence of hemolysis - elevated MCHC - positive Osmotic fragility test - negative Coombs test Peripheral blood: normochromic normacytic anemia, spherocytes, polychromatic cells (w/ or w/o nucleated RBCs), Howell-Jolly bodies (post-splenectomy)
40
explain osmotic fragility test
- confirms presence of spherocytes | - spherocytic RBCs lyse prematurely when exposed to inc hypotonic salt solutions
41
explain the coombs test for hereditary spherocytosis
- spherocytes are seen in hereditary spherocytosis and in autoimmune - Neg. coombs test confirms hereditary spherocytosis Test is specifically for autoimmune hemolysis
42
G6PD deficiency is inherited in (1) fashion. List the specific alleles / variants for G6PD, (2).
1- X-linked (affects mainly males) 2: - G6PD A+, high enzyme levels, no hemolysis - G6PD A-, lower enzyme levels, acute intermittent hemolysis - G6PD Mediterranean, more severe than other A- variants - G6PD B, normal variant
43
G6PD A- variant: - normally seen in (1) people - characterized by (2)
1- 10% of american blacks | 2- normal enzyme activity, but dec half-life
44
G6PD Mediterranean variant: - normally seen in (1) people - (2) is the reason why it may have high persistance
1- Middle Eastern populations | 2- protects against malaria
45
describe the parameters that allow for the pathogenesis of G6PD deficiency event to occur
Parameters: - abnormal enzyme are misfolded --> prone to proteolytic degradation - enzyme is not made, no nucleus in RBC - Note: G6PD A- half-life is moderately reduced, Mediterranean is severely reduced
46
describe the pathogenesis of a G6PD deficiency event
1) RBC exposed to oxidants / oxidative stress 2) SH-groups on globin chains of Hb are oxidized 3) precipitation of denatured globins on RBC membrane 4) Heinz body formation 5a) for severe membrane damage --> intravascular hemolysis occurs 5b) less affected RBCs go to spleen --> macrophages 'bite out' inclusions => bite cells ---> extravascular hemolysis
47
describe the clinical presentation of G6PD deficiency
- Acute Hemolysis: intravascular hemolysis 2-3 days after exposure to infection, drugs (antimalarials, Sulfas), foods (fava beans) - Neonatal jaundice, uncommon - Chronic low grade anemia, uncommon: lacks known environmental triggers
48
Triggers for G6PD deficiency: (1) common drugs (2) common foods
1- antimalarials (primaquine), sulfonamides 2- fava beans
49
Diagnosis of lab findings for G6PD deficiency
- clinical Hx - CBC w/ anemia + evidence of hemolysis - Peripheral blood: normochromic, normocytic anemia, heinze bodies, polychromatic cells (+/- nucleated RBCs), bite cells - G6PD enzyme assay (complete during hemolytic episodes, repeat 3 mos. after)

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