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Heme/Lymph 1 > Anemia > Flashcards

Anemia Flashcards

1
Q

Healthy Erythron

A

12-15 g/dL
Normal structure
Circulate for 120 days
Kidneys respond to RBC need with erythropoeitin
RBC precursors normal with enough iron and vitamin cofactors
Senescent RBCs cleared by spleen

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2
Q

Normal RBCs

A

Pliable, elastic, anucleate
Membrane is selectively permeable
Large SA to V ration permites RBC to squeeze through capillaries and resume shape

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3
Q

Normal RBC cytoplasm content

A

Hemoglobin A for transport of oxygen to tissues

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4
Q

RBC membrane structure

A 
Phospholipid bilayer and cholesterol 
Internal spectrin cytoskeleton
Transmembrane proteins
Glycopeptides and glycolipids (outer)
GPI-linked proteins (outer)
Absorbed plasma substances (outer)
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5
Q

Interactions of RBC membrane determine

A

Shape, metabolism, trasnport, and survival

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6
Q

Definition of anemia

A

Reduction in RBC mass, numbers, or hemoglobin concentration with corresponding decrease in oxygen carrying capacity of the blood

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7
Q

Compensatory mechs to anemia

A

Circulatory - increase HR, dilation of arterioles to increase tissue perfusion
Biochem - increase 2,3-DPG in RBCs…decreases hemoglobin affinity to increase delivery to tissues
Bone marrow - hyperplasia due to increase in erythropoetin…increase in reticulocytes

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8
Q

When compensation fails (clinical features of anemia)

A 
Pallor
Weakness
Malaise
Headaches
Dyspnea (on exertion at firt)
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9
Q

Later consequences of anemia with resulting hypoxia

A

Angina pectoris and heart failure
Fatty change in liver
Compensatory bone marrow hyperplasia

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10
Q

How do we classify anemia?

A

By RBC morphology

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11
Q

RBC morphology (size, color, appearance)

A

Size - normocytic, microcytic, macrocytic
Color - normochromic, hypochromic
Appearance - spherocytes, target cells, schistocytes, cytoplasmic inclusions

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12
Q

Color reflects

A

Degree of hemoglobinization

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13
Q

Hypochromic microcytic anemia

A

Could be due to iron deficiency

Small red cells contain narrow rim of peripheral hemoglobin

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14
Q

Megaloblastic anemia

A

Enlarged oval RBCs

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15
Q

Spherocyte

A

Membrane loss…loss of SA relative to volume
Loss of central pallor
Typical of extravascular hemolysis
Not all affected

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16
Q

Target cell

A

Membrane excess…def of cytoplasm

Cause might be thalassemias (reduces Intracell Hb but not membrane surface area)

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17
Q

Schistocytes

A

RBCs mechanically fractured in circulation

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18
Q

Cytoplasmic inclusions

A

Could see precipitate of denatured globin in supravital staining
Think G6PD deficiency
Bite cells will be produced as macrophages pluck out

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19
Q

Reticulocytes

A

Larger size with blue tint
Percentage reflects both demand and effective of erythropoiesis
If large, increases MCV

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20
Q

Polychromasia

A

Many reticulocytes

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21
Q

Mechs of anemias

A

Blood loss
Impaired RBC production (nutrient def or marrow disorder)
Increased RBC destruction (hemolytic anemias)

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22
Q

Acute blood loss symptoms depend on

A

Rate of hemorrhage and site of bleeding (int vs ext)

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23
Q

Severe blood loss can

A

Lead to cardiovascular collapse, shock, and death

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24
Q

Acute blood loss compensatory

A

Shift of fluid from extraascular space ot cirulcation—–leads to hemodilution and decreased hematocrit…**hemocrit and hemoglobin values may not reflect magnitude of blood loss because this takes some time

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25
Q

Acute blood loss and renal

A

Renal hypoxia increases production of EPO…leads to increased reticulocytes in peripheral blood

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26
Q

As blood loss increase (urine, mental status, other vitals)

A 
Pulse increases
BP decreases
RR increases
Urine output decrease
CNS goes first to anxious and confused, then lethargic
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27
Q

Chronic blood loss and examples

A

Rate of loss exceeds regen capacity
Iron reserves depleted so iron deficiency anemia
(colon cancer, hookworm, chronic menorrhagia)

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28
Q

Disorders of stem cell proliferation or differentiation

A

Aplastic anemia
Pure red cell aplasia
Anemia due to renal failure
Anemia due to liver dz and endocrine disorders (mild)

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29
Q

Aplastic anemia with mechs

A

Bone marrow aplasia and pancytopenia
Suppression of stem cell activity by activated T cells or intrinsic clonal stem cell abnormalities
Few reticulocytes and no splenomegaly…hyocellular marrow with mostly fat cells (dry tap)

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30
Q

Pathophys of aplastic anemia and tx

A

Damaged stem cells produce
1) profeny expressing neo-antigens that avoke AI response
2) Cloncal pop with reduced prolif capacity
BOTH lead to marrow aplasia

immune suppression and BM trasnplant

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31
Q

PRCA

A

Aplasia of marrow RBC precursors
Reduced reticulocytes and marrow BC precursors
Other marrow lineages normal and present
Associated with thymomas, AI dz and parvovirus B-19

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32
Q

Anemia due to renal failure

A

EPO def
Normocytic and normochromic
Due to reduced production of EPO by kidney likely iwht decrease in renal mass
RBC survivial may be shortened

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33
Q

Myelophthisic anemias

A

Space occupying lesions reducing hematopoetic capcity may include metastases, fibrosis and granulomas
Infiltrating nonhematopoeitic cells can cause varying degrees of anemia
Could be due to toxins or infection

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34
Q

Defects in hemoglobin synthesis

A

Iron def

Sideroblastic anemias

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35
Q

Key steps in synthesis of heme take place in

A

Mitochondria of RBC precursors

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36
Q

Sideroblastic anemias

A

Ringed sideroblasts…formed by abnormal deposition of iron in mitochondria of RBC precurosrs
Common pathological process is through to be disordered heme synthesis

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37
Q

Globin synthesis disorders

A

Hemoglobinopathies (qualitative)

Thalassemias (quantitative)

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38
Q

Iron def casues

A

Dietary lack
Increased requirements
Chronic blood loss
Impaired absorption

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39
Q

Total iron stores normally…trasnport, functional, storage

A

4 grams…intake 10-20 mg
Trnasport - transferrin (33% bound to iron)
Functional - hemoglobin, myoglobin, enzymes
Storage - ferritin (not in circulation), hemoseridin

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40
Q

Iron regulating organ, metabolism

A

Duodenum (absorbed in both heme and non-heme forms)

Controlled by rate of absorption (once absorbed, very little iron excreted)

41
Q

In iron deficiency

A

Serum iron decreases and iron binding capcity increases….ferritin SHOULD be low in iron def and high in excess but could be misleadingly increased if inflammation

42
Q

Iron regulation

A

On luminal side, heme iron is absorbed by heme transporter…non-heme iron is reduced to ferrous form by stomach acid or cytochrome B before absorption…once entering cytoplasm, stored in ferritin…iron that is not absorbed into plasma is lost into fecal stream when enterocyte shed….fraction enters plasma via ferroportin-hephaestin complex which oxidizes back to ferric form for attachment o transferrin in portal blood…when iron nromal and erythropoeisis at steady state, absorption into plasma is minimal

43
Q

When body iron needs to increase,

A

More iron reaches plasma…HFE protein in gut cells plays role

44
Q

Iron cycle

A

Plasma iron bound to transferrin is transported to marrow and transferred to RBC which incorporate it into hemoglobin…RBCs circulate for 120 ays befroe ingested my macros of RES…macros extract iron from hemoglobin and return it to plasma

45
Q

Iron def anemia

A

Microcytic, hypochromic anemia
Low serum iron and ferritin
High total iron binding capcity…surplus transferrin carrying capacity relative ot iron concentratyion

Visible marrow ion stores absent

46
Q

Signs and symptoms of iron-def anemia

A 
Pallor
Irritable 
Fatigue
Tachycard
Sore or swollen tongue 
Koilonychia
Alopecia
Craving for clay or ice 
Plummer-Vision syndrome - hypochromic microcytic anemia, esophageal web, glossitis
47
Q

Anemia of chronic dz

A 
Can be normochromic, normocytic or hypochromic, microcytic 
Low serum iron AND low iron binding capcity  because transferrin concentration decreases in inflammation (distinguishes from iron-def)
Low erythropoeitin (due to IL-1 and TNF)
48
Q

Why is serum iron low in anemia of chronic dz

A

Increased activity of hepcidin in inflam sites…this degrades ferroportin activity and decreases iron absorption

49
Q

Types of megaloblastic anemias

A

B12 def or malabsorption

Folate def

50
Q

Pernicious anemia

A

Folate def anemia

51
Q

B-12 and folate needed for

A

Thymidine synthesis for DNA synthesis

52
Q

Cobalamin def

A

Inhibits metab of folate into form needed to serve as cofactor for thymidine stnehsis

53
Q

Def of B-12 or folate patho

A

Inhibits conversion of homocysteine into methionine, allowing homocysteine to accumulate in serum

54
Q

B-12 other cofactor

A

MMA to succinate…B-12 def allows MMA to accumulate

55
Q

How can you tell difference between folate and B-12 def

A

FOlate - only homocysteine elevate
B-12 - both MMA and homocysteine

Neurologic consequences of B-12 def

56
Q

Most B-12 def due to

A

Impaired absorption

57
Q

Folate vs. B-12 def prevalence

A

Folate more common

58
Q

Megaloblastic anemias morphology, peripheral blood, and bone marrow

A

Morphology- due tp DNA derangement, erythroid precursors are large
Per blood - pancytopenia, anisocytosis, macrocytosis, ovalocytosis, low reticulocyte count, large hypersegmeneted neutrophils
Bone marrow - hypercellularity, megaloblastic cells and ineffevtive erythropoeisis

59
Q

Megaloblastic marrow shows

A

Delayed nuclear maturation due to impaired DNA synthesis

60
Q

B-12 absorption depends on

A

Adeuqate diet
Acid-pepsin in stomach - releases B-12 from protein
Gastric secretion of IF
Pancreatic proteases - liberate from R factor
Ileum with functioning B12-IF receptors

61
Q

Once absorbed in the ileum B-12

A

Bound to transcobalamin 2 and released to plasma

62
Q

B12 population

A

Dietary lack from vegetarians
Increased requirements in pregnancy
Impaired absorption in white people over 50

63
Q

B-12 malabsorption causes

A

Gastric - achlorhydria (gastric juices release B-12 from food)…gastrectomy, parasites, atrophic gastritis/AI pernicious anemia (IF absent)
Ileal - Ileal resection, diffuse intestinal dz, bacterial overgrowth, fish tapeworm

64
Q

Pathogen of pernicious anemia

A

AI destruction of gastric mucosa…loss of parietal cells and chronic inflammatory infiltrate
3 types of ABs - Block binding of B12 to IF
Block binding of B12/IF complex to ileal
AB against gastric proton pump
Associated with other AI disorders (thyroiditis)

65
Q

Morphology of pernicious anemia

A

Bone marrow and peripheral blood changes…GI tract - atrophic glossitsm chronic gastritis with intestinal metaplasia (increased cancer risk)

66
Q

Pernicous anemia due to B12 symtpoms and tx

A

Spinal cord myelin degeneration producing spastic paraparesis, sensory ataxia and parethesias (subacute combined degneeration)
Folate tx can reverse megaloblastic changes but NOT tx neurological symptoms

Must use IV B-12 to tx nervous system

67
Q

Schilling test for B-12

A

Give B-12 orally and easure in 24 hour urine…If over 7% is excreted, then normal

If part 1 low, give B-12 with IF…if increases (greater than 9%, then demonstrates IF missing and diagnoses PA)

68
Q

Folate def anemia

A

Similar to B12 without neurological alterations

Tx with folate

69
Q

Clinical features of hemolytic anemias

A

Abnormal RBC destruction inside or outside spleen
Shortened RBC lifespan
Increased EPO levels and increased compensatory EPO
Accumulation of hemoglobin catabolism products (bilirubin)

70
Q

Classification of hemolytic anemias

A

Intrinsic RBC abnormalities (hereditary or acqwuired)
Extrinsic causes of RBC destruction
Hemolysis may take place inside the circulation (intravascular) or outside (spleen, extravascular)

71
Q

intrinsic RBC abnormalities

A

Cytoskeleton disorders (spherocytosis, elliptocytosis)
Disorders of lipid synthesis (increased membrane lectin)
Glycolytic enzyme disorders (pk def, hexokinase def.)
Hexose monophosphate shunt enzyme disorders (G6PD or glutathione synthetase def)
Thalassemias and hemoglobinopathies

72
Q

Only acquired intrinsic RBC idsorder

A

PNH

73
Q

Extrinsic RBC abnormalities

A

Auto/alloantibodies

Allo - transfusion rxns or hemolytic dz of fetus and newborn

74
Q

Immune mediated hemolysis may or may not

A

Involve complement and MAC…dictates whetehr intravascular, extravascular or both

75
Q

Mechanical trauma to RBCs

A

Microangiopathic hemolytic anemias - produce schistocytes…could also be from IV fluids, chem injry and infections like malaria

76
Q

Intravascaulr hemolysis manifestation

A

Hemoglobinemia
Hemoglobinuria
Jaundice
Decrease serum haptoglobin…haptoglobin binds free hemoglobin and felps prevent urinary excretion

77
Q

Extravascaulr hemolysis

A

Mostly in spleen
Jaundice
RBCs phagocytosed by splenic macrophages
Increased normoblasts, reticulocytes, and spehrocytes

78
Q

Hereditary spehrocytosis

A

Intrinsic cytoskeleton defect - spheroid RBCs, fragile, porrly deformable, vulnerable to splenic sequestration
Mutations to ankyrin, band 3, band 4.2, spectrin
Auto dominant

79
Q

Hereditary spherocytosis morphological

A 
Spherocytes increase
Reticulocytosis
Marrow hyperplasia 
Splenomegaly
Cholelithiasis
80
Q

HS clinical

A

20-30% asymptomatic
Others have aplastic crisis or hemolytic crisis
Splenectomy resolves symptoms but RBC abnormality remains

81
Q

Osmotic fragilty test

A

Suspend Pt RBCs for 24 hours…spherocytes will tolerate saline less well and burst sooner

82
Q

G6PD def general

A

Enzyme dysfunction in hexose monphosphate shunt of glutathione metab…decreases RBC ability to withstand injury
Oxidizes G6P and reduces NADP

83
Q

G6PD def

A

Intra and extra hemoylsis associated with certain drugs
Sensitive to fava beans
X-linked rec
2 variatns

84
Q

G6PD lab

A

Normochromic normocytic anemia with reticulocytosis
Elevated bilirubin
Hemoglobinuria

85
Q

Peripheral blood of G6Pd shows

A

Heinz bodies (denatured precipitated globin chains)…form on oxidant exposure and can cause intravascular hemolysis…can be plucked out by splenic macrophages and produce bite cells

86
Q

PNH

A

Rare intrinsic defect
Mutation in PIGA which is needed for synthesis of GPI
Stem cell clone are prone to lysis because without GPI linakge, important GPI proteins which regulate complement on RBC membranes are missing (DAF, MIRL, C8 binding protein)

87
Q

PNH clinical

A

Usually intravascular hemolysis leading to iron def via urinary hemoglobin loss
Tendency to thrombosis and AML

88
Q

AIHAs

A

Caused by autoantibodies with specificities for RBC antigens which promote intra and extra vascular hemolysis
Can be IgG or IgM

89
Q

DAT

A

Can test for AIHAs

Try to detect IgG on RBCs using AHG

90
Q

AIHA classification

A

Temperature at which AB reacts most strongly…IgG reacts best at higher temps

91
Q

Warm AI HA

A 
37 C 
Most comon 
Can be pirmary or secondary 
IgG causing mostly extravascular hemolysis with partial RBC phagocystis producing spherocytes in peripheral blood 
Splenectomy and immunosuppressants
92
Q

CAS

A

IgM
Can be extra ro intra
Clinically cyanosis of areas exposed to cold and Raynaud phenomenon

93
Q

PCH

A

Intermittent massive intravascular hemolysis with hemoglobinuria following cold expossure
May accompany infections
IgG binds to RBCs at cold temps and fixes complement which lyses them at warming temp

94
Q

Drug induced immune hemolysis mechs

A 
Cross reacting autoABs
Haptens (antigenic)
Immune complexes (bind to RBCs)
Membrane modification 
T cell acitivty suppresssion
95
Q

Microangiopathic hemolytic anemias

A

Due to mechanical trauma

Hallamrk is schistocyte in peripheral blood

96
Q

Common cause of splenomegaly

A

Portal hypertension

97
Q

Splenic pathology in sickle cells dz

A

Spleen sequesters large portion of RBCs…can lead to vascular occlusion…most function asplenically

98
Q

Splenic enlargement infections

A

Mono, malaria, hepatic schistosomiasis

99
Q

Splenic infarction

A

Thromboembolism of splenic artery or branches
Sickle cell, atheromatous, infective endocarditis
Rapid splenic enlargment
LUQ pain, fever, N/V

Heme/Lymph 1 (14 decks)

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