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Pathology Post Midterm > Module 1: Anemia of Chronic Disease, Aplastic, Megaloblatic > Flashcards

Module 1: Anemia of Chronic Disease, Aplastic, Megaloblatic Flashcards

1
Q

Anemia of chronic disease is usually normocytic, non hemolytic anemia, what can it also be?

A

Hypochromatic and microcytic

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2
Q

Anemia of chronic disease is the most common anemia in what population?

A

Hospitalized patients

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3
Q

What is the etiology of anemia of chronic disease?

A
  1. Chronic bacterial infection (lung abscess, TB, endocarditis)
  2. Chronic Immune Disorders (RA)
  3. Malignant Tumors
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4
Q

What is the pathogenesis for anemia of chronic disease?

A

Production of acute phase reactants (Hepcidin) from the liver
—inflammation – increased hepcidin sequesters iron in storage sites by: limiting iron transfer from macrophages to erythroid precursors and suppressing EPO production

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5
Q

What are the lab values for anemia of chronic diseases?

A

Increased ferritin
Decreased TIBC
Decreased MCV (microcytic)
Normal reticulocytes

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6
Q

Aplastic Anemia is a normochromic, normocytic anemia, what is the problem in this anemia?

A

Decreased number due to destruction

–defect in multipotent hematopoeitic stem cell

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7
Q

Aplastic Anemia affects all myeloid cells, what does this mean?

A

Pancytopenia (WBC,RBC, and platelets)

–destroys myeloblast, monocytes and megakaryocytes

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8
Q

What is the etiology for aplastic anemia?

A

Primary: idiopathic
Secondary: PMH (intravascular), Viruses (EBV,CMV,HIV,Hep E/TT/G), Drugs (chloramphenicol- abx, anti-thyroid -PTU) and Myelotoxic chemical (benzene, toluene and insecticides- DDT) and whole body radiation

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9
Q

What is the pathogenesis for aplastic anemia?

A

Autoreactive T cell destroying pluripotent myeloid stem cells in the bone marrow and in the extramedullary sites
–patients are not able to compensate via extramedullary hematopoiesis, so they get splenomegaly and hepatomegaly

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10
Q

What is the presentation for a patient with aplastic anemia?

A 
Fatigue (normochromic normocytic anemia)
Infections (granulocytopenia) 
Monocytopenia 
Bleeding - thrombocytopenia 
Petechiae, purpura, and ecchymosis 
Reticulocytopenia
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11
Q

What investigations are done for aplastic anemia?

A
  1. Bone marrow aspirate –Dry tap (due to more fat cells then actual hematopoietic cells
  2. Bone Marrow biopsy (Best investigation): hypocellular and more fat than hematopoietic cells and lymphocytes and reticulocytopenia
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12
Q

What is the most common cause of death for patients with aplastic anemia?

A

Recurrent infections because again pancytopenia

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13
Q

What are the other complications for aplastic anemia?

A
  1. CHF (due to chronic anemia)
  2. Bleeding due to thrombocytopenia
  3. Gingival bleeding
  4. Vaginal bleeding
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14
Q

What is the treatment for aplastic anemia?

A

Bone marrow transplant is definitive

  • -also give immunosuppression drugs that target T cells
  • -treat underlying cause
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15
Q

The next type of anemia that is to be discussed is megaloblastic anemia. What are the two types?

A
  1. Folate deficiency – presents earlier, because we dont have a large store
  2. B12 deficiency
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16
Q

First lets discuss the etiologies for Folate Deficiencies.

A
  1. Nutritional (if a patient lacking raw greens in the diet, aka an older person living off toast)
  2. Malabsorption Diseases (absorption occurs in the jejunum): Celiac, Crohn’s, Tropical Sprue, and Whipple’s
  3. Folate Holding Drugs: Phenytoin (anti-epileptic) and Methotrexate (immunosuppressant for RA)
  4. Increased demand: in pregnant women and chronic hemolytic anemias
17
Q

Now what are the etiologies for B12 anemia?

A
  1. Pernicious Anemia (type 2 HSR) –most common cause of B12 deficiency
  2. Resection of Terminal Ileum
  3. Partial Gastrectomy
  4. Whipple’s
  5. Crohn’s
  6. Celiac
  7. Tropical Sprue
  8. Chronic Pancreatitis
  9. Nutritional (vegans and veggies will get B12 deficiency but this takes years due to stores)
18
Q

What is pernicious anemia?

A

Antibodies are destroying intrinsic factor (type 2 HSR – autoimmune disorder)

19
Q

What other autoimmune disorders can pernicious anemia co-exist with?

A 
RA
Lupus
Type I DM
Sjogrens Syndrome 
Graves
20
Q

Pernicious Anemia targets parietal cells and destroys them, what effect does this have on the stomach?

A

Parietal cells make HCl therefore makes the stomach an acidic environment
-therefore patients go into a state of hypochlorhydria (decreased acid in the stomach)

21
Q

What are the complications of pernicious anemia?

A
  1. Chronic atrophic gastritis –leads to intestinal metaplasia — intestinal dysplasia —intestinal gastric adenocarcinoma (in the body and fundus)
  2. Type I gastric carcinoid tumor: no acid therefore no G cells to make gastrin which stimulates neuroendocrine cells to make histamine this goes to partial cells to send a signal to make acid, however, there is a lack of parietal cells so you body is in a chronic state of G cell hyperplasia leading to the tumor
22
Q

A mentioned earlier chronic pancreatitis was an etiology for B12 deficiency. Explain the pathogenesis behind this

A

Pancreatic enzymes free up R binders from vitamin B12 otherwise intrinsic factor can not bind and free B12 can not be released

  • –pancreatic enzymes are also needed for the fat soluble vitamins so ADEK malabsorption
  • -pancreatic enzymes are not needed for iron or folate
23
Q

Now on to presentation, how does Folate deficiency present?

A

Folate:

  • -fatigue
  • -there are no neurological symptoms!
24
Q

How does Vitamin B12 deficiency present?

A

B12:

  • -Fatigue
  • Neurological symptoms: accumulation of methylmalonic acid in the blood causing peripheral neuropathy followed by proprioception and vibration (due to degeneration of dorsal or posterior columns)
  • -also get weakness due to the damaged peripheral nerves
25
Q

What are the investigations for Folate deficiency ?

A

Folate:
RBC folate is most accurate investigation
–elevated homocysteine in the serum
—no methylmalonic acid seen

26
Q

What are the investigations for B12 deficiency?

A

B12:
Serum B12 is most accurate investigation
—antibodies to parietal cells/intrinsic factor
–elevated homocysteine levels
–elevated methylmalonic acid

27
Q

What is seen on peripheral blood smear for megaloblastic anemia?

A

Hypersegmented neutrophils (more than 5 lobes) (slide 8a)
Macro-ovalocytes (macrocytes)
–bigger than normal
–high MCV

28
Q

What is seen in bone marrow for megaloblastic anemia?

A

Megaloblasts
–erythroid precursors with immature nucleus but mature cytoplasm (need B12 and folate for DNA maturation) called nuclear cytoplasmic asynchrony
seen on slide 8b

29
Q

What is the schilling’s test and how does it work?

A

Test for malabsorption of B12

  • -testing pernicious anemia vs. terminal ileal disease
    1. Give patient radiolabeled B12 to drink
    2. Give patient oral intrinsic factor
    3. Give patient IM B12 (buffers stores of B12 in the body)
  • -if you see B12 in the urine —absorbed successfully (and therefore dx is pernicious anemia because after given intrinsic factor b12 was absorbed)
  • -if you see no B12 in the urine —- terminal ileal disease or chronic pancreatitis (Ends up in poop)
30
Q

What are complications of both B12 and folate deficiency?

A
  1. CHF
  2. Chronic: neutropenia and thrombocytopenia (WBCs and platelets need DNA maturation but cant do it without B12 and folate)
31
Q

What are additional complications for B12 deficiency?

A
  1. Adenocarcinoma in the body and fundus of the stomach from chronic gastritis
  2. Gastric Carcinoid tumor
  3. Degeneration of dorsal columns (vibration and proprioception lost)
32
Q

What are the treatments for megaloblastic anemia?

A

Folate: give folate (orally)
B12: give B12 (IM)
–do not ever give folate to a patient with B12 deficiency it will worsen the symptoms due to trapping of the methylmalonic acid

33
Q

Now the next anemias that will be discussed are the immune hemolytic anemias which involves Ab mediated destruction of RBCs. The first is IgG mediated, which is the most common. Explain what this involves?

A

IgG mediated: extravascular hemolysis

  • -binds RBCs in warm temperature of central body
  • -associated with SLE, CLL and drugs (penicillin and cephalosporin) (Secondary causes)
  • -primary cause is idiopathic
34
Q

The next autoimmune hemolytic anemias is IgM mediated, explain what this involves.

A

IgM mediated: Intravascular hemolysis

  • -Binds RBCs and fixed complement in cold temperature extremities
  • -Associated with mycoplasma pneumoniae, infectious Mono, CMV, influenza, and HIV (again these are secondary causes)
35
Q

The last immune hemolytic anemia is Paroxysmal cold hemoglobinuria, what does this involve?

A

Least frequent

  • -secondary causes syphilis and virus
  • -more severe in children 1/3rd of cases
36
Q

A good way to test these immune hemolytic anemias is via a Coomb’s test. Explain how the direct coombs test works

A

Direct Coombs Test (direct antiglobulin test)

  • –detection of Abs +/- complement on patients RBC
  • -patients RBCs are incubated with Abs against the Anti-RBC Abs —- RBC agglutination
37
Q

Explain how the indirect coombs test works?

A

Indirect Coombs Test (Indirect Antiglobulin Test)

  • -patients serum is tested for its ability to agglutinate test RBCs that have known Abs bound to them.
  • -temperature dependence defines warm and cold

Pathology Post Midterm (50 decks)

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