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STEP 1 Pathoma > Chapter 5 > Flashcards

Chapter 5 Flashcards

1
Q

How does anemia present (decreased circulating RBC mass)?

A

-weakness, fatigue, and dyspnea

pale conjunctiva

HA

Angina

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2
Q

How is anemia defined?

A

Hb less than 13.5 g/dL in males and 12.5 g/dL in females (normal Hb is 13.5-17.5 in males and 12.5-16 in females)

Based on MCV, anemia can be classified as microcytic (MCV less than 80), normocytic (80-100), or macrocytic (MCV= 100+)

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3
Q

Principles of microcytic anemias

A

Anemia with MCV less tahn 80

Due to decreased production of hemoglobin (RBC progenitor cells in the bone marrow are large and normally divide multiple times to produce smaller mature cells, and microcytosis represents an extra division to maintain hemoglobin concentration

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4
Q

What is hemoglobin made of?

A

heme and globin; heme is made or iron and protoporphyrin- a decrease in any of these leads to a microcytic anemia

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5
Q

What are the microcytic anemias?

A

1) iron deficiency anemia
2) Anemia of chronic disease
3) Sideroblastic anemia
4) thalassemia

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6
Q

Describe iron deficiency anemia

A

Due to decreased levels of iron (most common form of anemia)

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7
Q

How is iron absorbed?

A

Absorption occurs in the duodenum. Enterocytes have heme and non-heme (DMT1) transporters; the heme form is more readily absorbed

Enterocytes transport iron across the cell membrane into blood via ferroportin. Transferrin trasports iron in the blood and delivers it to liver and bone marrow amcrophages for storage. Stored intracellular iron is bound to ferritin, which prevents irons from forming free radicals via the Fenton rxn

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8
Q

What are some lab measures of iron status?

A

1) Serum iron
2) Total iron-binding capacity- measure of transferrin molecules in the blood
3) % saturation- percentage of transferrin molecules that are bound by iron (normal is 33%)
4) Serum ferritin-reflects iron stores in macrophages and liver

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9
Q

What are some common causes of iron deficiency?

A

Infants breat feeding- human milk is low in iron

poor diet

Adults (20-50)- peptic ulcer disease in males and menorrhagia or pregnancy in females

Elderly- colon polyps/carcinoma or hookworm (Ancylostoma duodenale or Necator americanus) in the developing world

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10
Q

What is the progression of iron loss?

A
  1. Storage iron is depleted leading to decreased ferritin and increased TIBC
  2. Serum iron is depleted leading to decreased serum iron and decreased % saturation
  3. Normocytic anemia- bone marrow makes fever, but normal sized RBCs
  4. Microcytic, hypochromic anemia
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11
Q

Signs of iron deficiency anemia?

A

pica, koilonychia (below)

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12
Q

Lab findings of iron deficient anemia

A

Microcytic, hypochromic RBCs with increased red cell distribution width

decreased ferritin , % saturation, and serum iron

increased TIBC and free protoporphyrin (FEP)

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13
Q

How is iron deficient anemia tx?

A

ferrous sulfate

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14
Q

What is Plummer-Vinson Syndrome?

A

Triad of anemia, dysphagia, and beefy-red tongue

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15
Q

What is anemia of chronic disease?

A

Anemia associated with chronic inflammation (eg endocarditis or autoimmune conditions) or cancer.

Occurs because chronic disease results in production of acute phase reactants fromthe liver, including hepcidin and hepcidin sequesters iron in storage sites by limiting iron transfer, and suppressing EPO in order to prevent bacteria form accessing iron

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16
Q

What are the lab findings of anemia of chronic disease?

A

elevated ferrtitin

decreased TIBC, serum iron, and % saturation

elevated free protoporphyrin (FEP)

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17
Q

What causes sideoblastic anemia?

A

Anemia due to defective protoporphyin synthesis leading to less heme and a microcytic anemia

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18
Q

How is protoporphyrin made?

A

Aminolevulinic acid synthase (ALAS) converts succinyl CoA to aminolevulinic acid (ALA) using vitB6 as a cofactor

Aminolevulinic acid dehydratase converts ALA to porphobilinogen, and then porphobilinogen is converted to protoporphyrin

Ferrochelatase attached protoporphyrin to iron to make heme (occurs in the mitochondria)

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19
Q

Note that iron is transferred to erythroid precursors and enter the mitochondria to from heme. If protoporphyrin is deficienct, iron remains trapped in mitochondria and these iron-laden mitochondria form a ring around the nucleus of erythroid precursors (aka sideroblasts)

How can sideoblastic anemia occur?

A

can be congenital or acquired:

Congenitally mostly via ALAS defect

Acquired via alcoholism (mitochondrial poison), Lead poisoning (inhibits ALAD and ferrochelatase), vitB6 deficiency (seen with isoniazid therapy)

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20
Q

What are the lab findings of sideoblastic anemia?

A

elevated ferritin, serum iron, and % saturation

decreased TIBC

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21
Q

What is a normal TIBC?

A

300 ug/dL

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22
Q

What is a normal serum iron?

A

100 ug/dL

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23
Q

What is a normal % saturation?

A

33%

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24
Q

What are thalassemias?

A

Anemia due to decreased synthesis of the globin chanins of hemoglobin leading to microcytic anemia

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25
Q

What are the normal types of hemoglobin?

A

HbF (a2Y2), HbA (a2b2), and HBA2 (a2delta2)

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26
Q

What causes a-thalassemia?

A

usually due to gene deletion; normally, 4 alpha genes are present on chromosome 16

One gene deleted= asymptomatic

Two genes deleted= mild anemia with elevaed RBC count; cis deletion is associated with an icnreased risk of severe thalassemia in offspring (seen in Asians); trans deletions seen in Africans

Three genes deleted= severe anemia; B chains form tetramers (HbH) that damage RBCs; HbH seen on electrophoresis

  1. Four genes deleted= lethal in utero due to hydrops fetalis; y chains form tetramers (Hb barts)
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27
Q

What causes B-thalassemia?

A

usually due to gene mutations (point mutations in promoter or splicing sites); seen in African and Mediterranean deescent pts.

There are two B genes present on chromosome 11 and mutations result in absent (Bo) or diminished (B+) production of the B-globin chain

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28
Q

How does B-thalassemia minor (B/B+) present?

A

Mildest form of disease and is usually asymptomatic with an increased RBC count

will see microcytic, hypochromic RBCs and target cells on blood smear

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29
Q

How does B-thalassemia minor (B/B+) present on electrophoresis?

A

slightly decreased HbA with increased HBA2 (5%, normal 2.5%) and HbF (2%, normal 1%)

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30
Q

How does B-thalassemia major (Bo/Bo) present?

A

most severe forms of disease and present with severe anemia a few months after birth

there is high HbF (a2y2) at birth and is temporarily protective

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31
Q

More on B-thalassemia major (Bo/Bo)

A

Unpaired a chains precipitate and damage RBC membranes, resulting in ineffective eryhtrooiesis and extravascular hemolysis (removal or circulating RBCs by the spleen)

Massive erythroid hyperplasia ensues resulting in expansion of hematopoiesis into the skill (resulting in crewcut appearance- below) and facial bones (leading to chipmunk facies), as well as extramedullary hematopoiesis wth HSM, and risk of aplastic crisis with parvovirus B19 infection

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32
Q

B thalassemia major chipmunk facies

A
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33
Q

How is B thalassemia major tx?

A

major tranfusions often needed leading to a risk of secondary hemochromatosis

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34
Q

What does electrophoresis show with B thalassemia major?

A

HBA2 and HbF with little to no HbA

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35
Q

What most commonly causes macrocytic anemia (MCV 100+)?

A

vitB12 or folate deficiency (megaloblastic anemia)

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36
Q

What are folate and B12 needed for?

A

synthesis of DNA precursors- folate circulates as methyl THF and removal of the methyl roup and tranfer to vitB12 allows for participation in synthesis of DNA precursors

vitB12 then transfers the methyl group to homocysteine, producing methionine

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37
Q

What does lack of folate or B12 cause?

A

Impaired division and enlargemnt of RBC precursors leads to megaloblastic anemia and impaired division of grnaulocytes leads to hypersegmented neutrophils

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38
Q

Folate

A

Gained in diet from green veggies and fruits and absorbed in the jejunum. Folate deficiencies only take months to develop as body stores are minimal

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39
Q

Main causes of Folate deficiency?

A

poor diet (e.g. alcoholics and elderly),

increased demand (e.g. pregnancy, cancer, and hemolytic anemias)

and folate antagonist use (methotrextate, etc.)

40
Q

How does folate deficiency present?

A

macrocytic RBCs and hypersgemented neutrophis (5+ lobes)

Glossitis

decreased serum folate and increased serum homocysteiene (risk of thrombosis)

normal methylmalonic acid

41
Q

How is VitB12 processed and absorbed?

A

Gained in diet in animal proteins.

Salivary gland enzymes such as amylase liberate vitB12 which is then bound by R-binder (also from the salivary gland) and carried through the stomach

Pancreatic proteases in the duodenum detach vitB12 from R-binder and vitB12 binds to intrinsic factor from gastric parietal cells in the small bowel.

The B12-IF complex is absorbed in the ileum

42
Q

Note that VitB12 deficiencies are less common than folate deficiency and takes years to devleop due to large hepatic stores of B12

A
43
Q

Causes of VitB12 deficiency?

A

Pernicious anemia (autoimmune destruction of parietal cells)

Pancreatic insufficiency and damage to the terminal ileum (Crohn disease and Diphyllobothrium latum)

44
Q

What are the findings of VitB12 deficiency?

A

Macrocytic RBCs with hypersgemented neutrophils

Glossitis

Subacute combined degeneration of the spinal cord (dorsal columns and coritcopsinal tracts)

decreased serum B12

elevated homocysteine and methylmalonic acid

45
Q

What causes Subacute combined degeneration of the spinal cord?

A

vitB12 is a cofactor for the conversion of methylmalonic acid to succinyl CoA and its deficiency results in increased levels of methelmalonic acid, which impairs spinal cord myelinization resultin in poor proprioception and vibratory sensation and spastic paresis

46
Q

Normocytic anemias are mostly due to ______

A

increased peripheral destruction or underproduction (reitculocyte count helps to distinguish these)

47
Q

Reticulocytes

A

Young RBCs are released from the bone marrow and ID’d on a blood smear as larger cells with a bluish cytoplasm due to residual RNA

NOTE: The normal reticulocyte count is 1-2% and the normal RBC life-span is 120 days and each day roughyl 1-25 are removed from circulatio and replaced by reitculocytes

48
Q

A properly functioning marrow responds to anemia by increasing the RC to 3+%, but this number is falsely elevated in anemia due to the decrease in no. of RBCs. Thus, RC must be corrected, how?

A

by multiplying RC * HCt/45

Corrected count 3+% indicated good marrow response and sugegst peripheral destruction while corrected RC of less than 3% indicates underproduction due to marrow issues

49
Q

What are the peripheral destruction causes of normocytic anemia?

A

divided into extravascular and intravascular hemolysis- both result in anemia with an appropriate marrow response

50
Q

Describe extravascular hemolysis

A

This involves RBC destruction by the RES (macrophages of the spleen, liver, and lymph nodes).

In this system, macrophages consume RBCs and break down hemoglobin (globin to AAs, heme to iron and protoporphyrin (iron is recycled and protoporphryin is bronw down into unconjugated bilirubin, which is bound to serum albumin and delivered to the liver for conjugation andexcretion into bile)

51
Q

What are the findings of extravascular hemolysis?

A

Anemia with splenomgealy, jaundice due to unconjugated bilrubin, and increased risk for bilirubin gallstones

marrow hyperplasia with corrected reticulocyte count of 3+%

52
Q

Describe intravascular hemolysis

A

Involves destruction of RBCs within vessels with findings of hemoglobinemia, hemoglinuri, hemosiderinuria, and decreased serum haptoglobin

53
Q

Why does intravascular hemolysis cause hemosiderinuria?

A

Renal tubular cells pick up some of the hemoglobin that is filtered into the urine and break it down into iron, which accumulates as hemosiderin; tubular cells are eventually shed resulting in hemosideruria

54
Q

What are some normocytic anemias with predominantly extravascular hemolysis?

A

1) Hereditary spherocytosis
2) Sickle cell anemia
3) hemoglobin C

55
Q

What causes Hereditary spherocytosis?

A

inherited defect in RBC cytoskeleton-membrane tethering proteins such as ankyrin, spectrin, or band 3. This causes membrane blebs to form and bleb over time, resulting in a round instead of disc shaped RBC and these spherocytes are les able to maneuver through splenic sinusoids and are consumed by splenic macrophages, resulting in anemia

56
Q

What are the lab findings of Hereditary spherocytosis?

A

Spherocytes with loss of central pallor

Elevated RDW and MCHC

Splenomegaly, jaundice with uncnjugated bilirubin, and risk for bilirubin gallstones

Risk of aplastic crisis with parvovirus B19

57
Q

How is Hereditary spherocytosis diagnosed?

A

osmotic fragility test, which reveals increased spherocyte fragility in hypotonic solution

58
Q

How is Hereditary spherocytosis tx?

A

splenectomy- anemia resolves by spheroytes persist and Howell-Jolly bodies (fragments of nuclear materal) emerge on blood smear

59
Q

What causes Sickle cell anemia?

A

AR mutation in B chain of hemoglobin due to a single AA change from glutamic acid (hydrophilic) to valine (hydrophobic)- gene carried by 10% of AA due to malaria protection

Sickle cell disease arises when two abnormal B genes are present; resulting in 90% of HbS in RBCs

60
Q

What happens to HbS in sickle cell?

A

It polymerizes when deoxygenated and the polymers aggregate into needle-like structures, resulting in sickle cells (increased sickling with hypoxemia, dehydration, and acidosis)

61
Q

What is one tx for sickle cell?

A

Hydroxyurea, which increases protective HbF (which is fetal and protective for the first few months of life)

62
Q

More on the pathogenesis of SCD

A

cells continuously sickle and de-sckle passing through microciruclation reustin in complications related to RBC membrane damage including:

  1. Extravascular hemolysis-RES removes RBCs with damaged mebranes, leading to anemia, jaundice with unconjugated hyperbilirubinemia, and increased risk for bilirubin gallstones
  2. Intravascular hemolysis
  3. Masive erythroif hyperplasia resultin expansion of hematopoiesis into the skull (crewcut) and chipmunk facies, extramedullary hematopoiesis with HSM, and risk of aplastic crisis with B19
63
Q

Extensive sickling in SCD leads to complication of vaso-occlusion, including:

A
  1. Dactylitis- swollen hands and feet due to vaso-occlusive infarcts in bones (common presenting sign in infants)
  2. Autosplenectomy- fibrotic spleen
  3. Acute chest syndrome- vaso-occlusion in pulmonary microcirculation presenting with chest pain, SOB, and lung infiltrates (common cause of death in adult pts.)
  4. Pain crises
  5. Renal paillary necrosis-resulting in gross heamturia and proteinuria
64
Q

What risks come with the Autosplenectomy seen in SCD?

A

Risk of infection with encapsulated organisms such as N. meningitidis, S. pneumo, and H. influenzae (most common cause of death in children)

Risk of Salmonella paratyphi osteomyelitis

Howell-Jolly bodies on blood smear

65
Q

What is sickle cell trait?

A

The presence of one mutated and one normal B chain resulting in less than 50% HbS in RBCs (HbA is slightly more efficiently produced than HbS)

These pts are generally asymptomatic with no anemia; RBCs with less than 50% HbS do not sickle in viva except in the renal medulla due to extreme hypoxia and hypertonicity, which results in microinfarction leading to microscopic hematura and eventually decreased ability to concentrate urine

66
Q

Lab findings of SCD?

A

Sickle cells and target cells on blood smear in SCD but not in sickle cell trait

Metabilsufite screen causes cells with any amount of HbS to sickle; positive in both disease and trait

Hb electrophoresis confirms the presence and amount of HbS (Disease = 90% HbS, 8% HbF, 2% HbA2 (no HbA); Trait= 55% HbA, 42% HbS, 2% HbA2)

67
Q

What is Hemoglobin C?

A

AR mutation in the B chain of hemoglobin where the normal glutamic acid is replaced by lysine (less common than SCD)

Present with mild anemia due to extravascular hemolysis

Characteristic HbC crystials in RBCs in blood smear

68
Q

What are the normocytic anemias with predominantly intravascular hemolysis?

A

1) Paroxysmal nocturnal hemoglobinuria (PNH)
2) G6PD deficiency
3) Immune hemolytic anemia
4) Microangiopathic hemolytic anemia
5) Malaria

69
Q

What causes Paroxysmal nocturnal hemoglobinuria (PNH)?

A

acquired defect in myeloid stem cells resulting in absent glycosylphosphatidylionsoital (GPI) which renders cells suceptible to destruction by complement- note that red cells coexist with complement, and decay accelerating factor (DAF) on the surface of blood cells protects against complement-mediated damage by inhibiting C3 convertase. DAF is secured by GPI, an anchoring glycolipid, and the absence of GPI= absence of DAF

70
Q

How does PNH present?

A

Intravascular hemolysis occurs episodically, often at night during sleep because at night mild respiratory acidosis develops with shallow breathing and activates complement, causing RBCs, WBCs, and platelets to be lysed.

This intravascular hemolysis leads to hemoglobinemia and hemoglobinuria (especailly in the morning) and hemosiderinuria seen days after hemolysis.

71
Q

How is PNH screened for?

A

Sucrose test (confirmed via the acidified serum test or flow cytometry to detect lack of CD55 (DAF) on blood cells

72
Q

What is the main cause of death in PNH?

A

thrombosis of the hepatic, portal, or cerebral veins (destroyed platelets release cytoplasmic contents into circulation, inducing thrombosis)

complications include iron defic. anemia (due to chronic loss of hemoglobin in the urine) and acute myeloid leukemia (AML) in 10% of pts.

73
Q

What causes G6PD deficiency?

A

X-linked recessive disorder resulting in reduced half-life of G6PD, rendering cells suceptible to oxidative stresses because glutathionine normally neutralizes hydrogen peroxide, but becomes oxidized in the process, and NAPDH, a byproduct of G6PD, is needed to regenerate reduced glutathionine (this leads to intravascular hemolysis)

74
Q

What are the major variants of G6PD deficiency?

A
  1. African variant- mildly reduced half life of g6PD leading to mild intravascular hemolysis with oxidative stress
  2. Mediterranean variant marked by markedly reduced half-life of G6PD leading to severe hemolysis
75
Q

What does G6PD deficiency result in?

A

Oxidative stress precipitates Hb as Heinz bodies (below) (especially in the setting of infections, drugs including primaquine, sulfa drugs, and dapsone, and fava beans)

76
Q

What happens to the Heinz bodies seen in G6PD deficiency?

A

the spleen removes them resulting in bite cells

77
Q

How does G6PD deficiency present?

A

IV hemolysis

hemoglobinuria and back pain hours after exposure to oxidative stress

78
Q

How is G6PD deficiency daignosed?

A

Heinz prep used to screen and enzyme studies to confirm

79
Q

What causes immune hemolytic anemia (IHA)?

A

Antibody mediated (IgG or IgM) destruction of RBCs

80
Q

Describe IgG mediated IHA

A

-mainly involves extravascular hemolysis in which IgG binds RBCs in the relatively warm temps of the central body (warm agglutinin) and the membrane of these AB-bound RBCs are consumed by splenic macrophages resulting in spherocytes

81
Q

IgG mediated IHA is associated with what?

A

SLE (most common cause), CLL, and drugs like penicillin and cephalosporins

Drugs may attach to the RBC membrane with sequent binding of Ab to the complex

82
Q

Describe IgM mediated IHA

A

Mainly involves intravascular hemolysis in which IgM binds to RBCs and fixes complement in the relatively cold temps of the extremities

RBCs inactivate complement, but the residual C3b serves as an opsonin for splenic macrophages resulting in spherocytes

83
Q

IgM mediated IHA is associated with _________

A

M. pneumoniae and infectius mono

84
Q

How can IHA be diagnosed?

A

Coombs test (direct or indirect)

85
Q

Describe a Direct Coombs test

A

Confirms the presence of Ab or complement coated RBCs. When anti-IgG/complement is added to the pts. RBCs, agglutination occurs if RBCs are already coated with IgG or complement.

86
Q

Describe an Indirect Coombs test

A

Anti-IgG and test RBCs are mixed with the pt. serum and agglutination occurs if serum Abs are present

87
Q

What is microangipathic hemolytic anemia?

A

Intravascular hemolysis that results from vascular pathology; RBCs are destroyed as they pass through the circulation

Occurs with microthombi (TTP-HUS, DIC, HELLP), prosthetic heart valves, and aortic stenosis; when presnet, microthrombi produce schistocytes on blood smear

88
Q

How does malaria cause disease?

A

Infection of RBCs and liver with Plasmodium; transmitted by the female Anopheles mosquit

RBCs rupture as part of the Plasmodium life-cycle, resultin intravascular hemolysis and cyclical fever

89
Q

Describe the fever of different types of malaria?

A

P. falciparum- daily fever

P. vivax and ovale- Fever every other day

90
Q

Describe anemia due to underproduction

A

Decreased production of RBCs by the bone marrow characterized by low corrected RC

91
Q

What are the causes of anemia due to underproduction?

A
  1. Parvovirus B19
  2. Aplastic anemia
  3. Myelophthisic processes
92
Q

How does Parvovirus B19 cause underproduction anemia?

A

It infects progenitor red cells and temporarily halts erythropoiesis leading to significant anemia

tx is supportive

93
Q

What is aplastic anemia?

A

Damage to hematopoietic stem cells resulting in pancytopenia with low RC

Biopsy reveals an empty, fatty marrow (below)

94
Q

What is this?

A

Malaria

95
Q

How is aplastic anemia tx?

A

Cessation of caustive drugs and supportive care with transfusions and marro-stimulatin factors such as EPO, GM-CSF, and G-CSF

Immunosuppression may be helpful as some idiopathic cases are due to abnormal T-cell activation with release of cytokines

96
Q

What is a Myelophthisic process?

A

Pathologic process (e.g. cancer) that replaces bone marrow resulting in pancytopenia

STEP 1 Pathoma (18 decks)

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