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RHS > L18- RBC Pathology III > Flashcards

L18- RBC Pathology III Flashcards

1
Q

list the types of Extrinsic causing hemolytic anemias

A

IHA / immunohemolytic anemia: Abs bind RBC Ags

  • Warm Ab IHA
  • Cold Ab IHS: cold agglutinin, cold hemolysin

Non-immune Hemolytic anemia:

  • mechanism trauma
  • infections (mainly malaria)
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2
Q

(1) is the most common IHA, where (2)% are primary causes due to (3) mechanism and (4)% are secondary due to (5) diseases.

A 
1- warm Ab IHA
2- 50% primary
3- idiopathic
4- 50% secondary
5- autoimmune disease (SLE), B-cell neoplasms (CLL, lymphoma), drug rxns (methyldopa, penicillin)
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3
Q

In warm antibody IHA, most Abs are in the (1) form and they will coat, remove, lyse RBCs via (2). (2) can also only partially occur leaving (3).

A

1- IgG
2- Extravascular Hemolysis- erythrophagocytosis in the spleen
3- (following partial membrane removal) spherocyte, destroyed on subsequent cycles

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4
Q

Warm antibody IHA:

  • (1) Sxs / signs
  • (2) Tx
A

1- chronic mild anemia, splenomegaly

2- supportive, removal of offending agent, immuno-suppression

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5
Q

Cold Ab IHA:

  • (1) type uses IgM, (2) type uses IgG
  • (1) type causes (3) effect on RBCs in (4) location
  • (2) type causes (5) effect on RBCs in (6) location
A

1- cold agglutinin
2- cold hemolysin
3- agglutination b/c IgM –> fixes complement
4- peripheral circulation, <30C
5- IgG causes direct RBC lysis via complement
6- peripheral circulation

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6
Q

Cold agglutinin Ab IHA:

  • pathological response to (1) or (2), include e.g.
  • (3) occurs in periphery as a result of agglutination and complement fixation due to IgM
  • (4) occurs as a result of warming / recirculation, although significant deposition of (5) on RBCs is sufficient for (6) to occur
A

1- infections: mycoplasma, EBV, HIV, CMV, influenza
2- meoplastic growths: B-cell lymphomas
3- sludging of blood –> acrocyanosis / Raynaud phenomenon
4- release of IgM from RBC (before complement mediated hemolysis)
5- (transient interaction of IgM-RBC allows…) C3b deposition / opsonization
6- splenic removal / extravascular hemolysis

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7
Q

Cold hemolysin Ab IHA:

  • (1) type autoantibodies cause entity termed (2)
  • (3) occurs in periphery
  • (4) occurs upon rewarming
  • this process is usually preceded by (5)
A

1- IgG
2- paroxysmal cold hemoglobinuria
3- complement fixation
4- intravascular hemolysis and hemoglobinuria
5- viral infections in children, or alone as autoimmune phenomenon

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8
Q

(1) is the main test for diagnosing IHAs. The direct form takes sample RBCs, places them in (2) and (3) indicates a positive result. The indirect form takes sample serum to test for (4). (5) dependence determines the type of IHA.

A

1- coombs test

(detects Abs / complement on RBC surface)
2- RBCs incubated with Abs against human Ig / complement
3- agglutination

(detects Abs in serum)
4- serum causes agglutination of RBCs

5- temperature: warm or cold

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9
Q

list the the types of nonimmune hemolytic anemia

A

Mechanical Damage => hemolysis

i) cardiac valve prostheses: artificial > bioprothetic
ii) microangiopathic hemolytic anemia –> following partial microvascular obstruction like in DIC, malignant HTN, TTP/HUS, SLE

Infections (malaria)
-intracellular RBC parasite => hemolysis of variable severity

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10
Q

______ is evidence of microangiopathic hemolysis on a peripheral blood smear

A

schistocytosis: mechanical fragmentation of RBCs –> varying cell shapes / schistocytes (Burr cells, helmet cells, triangle cells)

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11
Q

list the types of anemias due to impaired RBC production

A

Failure of Proliferation / Maturation of RBC precursors:

  • defect dna synthesis = Megaloblastic
  • defect heme synthesis = Fe deficient
  • defect globin synthesis = thalassemia

Failure of stem cells:
= aplastic anemia

Unknown / multiple mechanisms:
-anemia of chronic disease like cirrhosis, CRF

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12
Q

Megaloblastic anemia:

  • (1) and (2) are the main causes
  • (1)/(2) will both cause (3) progression
A

1- B9/folate deficiency
2- B12/cobalamin deficiency

3- dec thymidine synthesis –> dec DNA synthesis –> defective nuclear maturation (normal RNA, protein synthesis) –> **nuclear-cytoplasmic asynchrony

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13
Q

Megaloblastic anemia:

  • (1) are the three peripheral blood findings
  • (2) are the bone marrow findings
A

1:

i) pancytopenia
ii) macrocytic / MCV >100fL, dec reticulosyte count
iii) hypersegmented neutrophils (>5 lobes)

2:
- hypercellular (although ineffective) hematopoiesis
- Megaloblastic changes: large RBC/WBC precursors, large megakaryocytes defined by large immature nuclei / inc nuclear lobes

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14
Q

B12 absorption:

1) after ingestion, (1) releases B12 from food so (2) salivary protein can bind to it
2) B12-(2) complex is dissociated due to (3, include location)
3) B12 will now bind (4, include site of production)
4) as the B12-(4) complex travels, it will be absorbed in (5) location
5) B12 is transported by (6) to (7) locations

A 
1- gastric pepsin
2- haptocorrin
3- pancreatic proteases, duodenum
4- IF (intrinsic factor), via gastric parietal cells
5- distal illeum
6- transcobalamin
7- liver + other cells
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15
Q

list the causes of B12 deficiency

A

1) dec intake (only strict vegans, abundant in animal products)
2) impaired GI absorption: pernicious anemia (no IF from parietal cells), malabsorption syndrome, GI surgery (gastric or ileal resections), fish tapeworm
3) genetic disorders: very rare, but mutations in a factor related to B12 absorption

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16
Q

(1) is the most common cause of B12 deficient anemia, It is due to (2) process which yields a failure to produce (3) to help absorb B12, to cause (4) type of anemia. It has a (rapid/insidious) onset, therefore patients usually present with (mild/moderate/severe) anemia. (7) is also another key histological finding.

A 
1- pernicious anemia
2- autoimmune destruction of gastric mucosa / parietal cells
3- IF (intrinsic factor)
4- megaloblastic anemia
5- insidious
6- severe
7- chronic atrophic gastritis
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17
Q

B12 deficient anemia, diagnosis and lab findings:

  • clinical history for (1) findings
  • (2) CBC findings
  • (3) peripheral blood and bone marrow findings
A

1- B12 deficiency risk factors
2- low Hb, high MCV, pancytopenia
3- megaloblastic anemia features, low reticulocyte count

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18
Q

list some of the serums tests and results for B12 deficient anemia (hint- 5)

A
  • Serum low B12, normal B9
  • Serum homocyteine, elevated
  • Serum methylmalonic acid, elevated
  • Serum IF Abs / gastric biopsy
  • Schillin Test
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19
Q

never treat B12 deficient anemia with…..

A

B9/folate supplements, as it will worsen the neurological symptoms

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20
Q

describe the role and reason for testing serum Methylmalonic acid levels

A
  • methyl malonyl coenzyme A conversion –> succinyl coA requires B12
  • B12 deficiency => inc plasma and urine methyl malonic acid levels
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21
Q

describe schilling test

A
  • directly tests B12 absorption
  • administer oral dose of B12
  • measure absorption via urinary B12
22
Q

B12 deficienct anemia Tx

A
  • B12 injections, IM (usually, but depends on cause)

- reticulocyte response and improvement seen ~5days after B12 injections

23
Q

Folic Acid, B9:

  • (1) sources
  • (2) daily requirements
  • (3) site of absorption
A

1- green veggies and some fruits (in raw form, 95% destroyed by cooking)
2- 0.4-0.8 mg
3- proximal jejunum

24
Q

B9 stores can last up to (1), takes (1) time for depletion

B12 stores can last up to (2)

A

B9- 6-8 wks

B12- 2 yrs

25
Q

list the causes of B9 deficient anemia

A

1) dec intake- low green veggie intake, often in alcoholics
2) impaired GI absorption
3) inc requirements: pregnancy, infancy, disseminated cancer, drugs (MTX, trimethoprim)

26
Q

B9 deficient anemia Tx

A
  • identify cause, but usually B9 supplementation
  • must exclude B12 deficiency as cause b/c B9 therapy => transient correction of anemia –> depletion of little remaining B12 –> worsening neurological Sxs
27
Q

(1) is the most common nutritional deficiency and the most common anemia in (2) type countries. It is most often seen in (3) people.

  • (4) is usual cause in undeveloped countries
  • (5) is usual cause in developed countries
A

1- Fe deficiency
2- underdeveloped / developing countries
3- children, reproductive females, elderly

4- dietary deficiency
5- chronic blood loss

28
Q

Iron in diet mostly comes from (1) sources. It is mostly absorbed in (2) where it will then follow (3) or (4) pathway. In situations of high Fe levels, (5) released from the liver will inhibit uptake via (2) cells.

A 
1- animals (heme form is 20% absorbable, virtually no absorption from inorganic / vegetable form)
2- duodenum
3- transport to blood
4- storage as mucosal Fe
5- Hepcidin (peptide)
29
Q

describe storage of Fe

A

(free Fe is toxic)
-Fe stored in duodenal mucosa or in liver, spleen, BM, skeletal muscle

Forms:

  • ferritin: Fe-protein complex
  • hemosiderin: partially degraded aggregates of ferritin
30
Q

describe the transport of Fe

A

-plasma, bound to transferrin (inc w/ deficiency)

Note:

  • capacity of transferrin to bind Fe = TIBC (total iron binding capacity)
  • normal is 33% transferrin is saturated with Fe
31
Q
  • (1) normal serum Fe
  • (2) normal TIBC
  • (3) daily requirements of Fe
A

1- 100-120 µg/100ml
2- 300-350 mg/ml
3- 7-10mg men, 7-20mg women

32
Q

describe the distribution of functional Fe

A

80% in Hb

20% in Myoglobin + Fe-containing enzymes (catalase, cytochromes)

33
Q

list the causes of Fe deficiency anemia (IDA)

A

1) dietary deficiency
2) impaired absorption
3) inc requirements: children, premenopausal women, pregnancy
4) chronic blood loss (usually chronic GI blood loss)

34
Q

describe the stages of IDA

A

1- Fe deficiency absent anemia
2- Fe deficiency with mild anemia
3- severe Fe deficiency with severe anemia

-dec serum ferritin, absent bone marrow iron are earliest changes –> followed by dec transferritin saturation

35
Q

IDA clinical features:

  • (1) simple anemia Sxs
  • (2) hallmark Sxs
  • (3) rare associations
A

1- fatigability, dyspnea, palpitations

2- Pica / Ice cravings: inc ice cravings + desire to eat non-food substances (clay, paper, chalk, charcoal)

3- restless leg syndrome, Plummer-Vinson syndrome (i) dysphagia, ii) esophageal web, iii) IDA)

36
Q

list the clinical signs of IDA

A
  • pallor
  • dry / rough skin
  • atrophic glossitis- loss of tongue papillae
  • angular cheilitis
  • Koilonychia (spoon nails)
37
Q

IDA, diagnosis and lab findings:

  • clinical history for (1) findings
  • (2) CBC findings
  • (3) peripheral blood findings
  • (4) bone marrow findings
  • (low/normal/high) reticulocytes
A

1- IDA risk factors
2- low Hb, low MCV, low MCH, high RDW
3- microcytic hypochromic anemia, severe cases –> poikilocytosis / ‘pencil cells’
4- no stainable Fe via Prussian blue ***gold standard, but not routinely done
5- low reticulocyte count

38
Q

describe the Serum Iron studies in IDA

A

Ferritin: low (possible to see false high ferritin, b/c it’s an acute phase protein, so elevated in inflammation)

Iron: low (not diagnostic b/c fluctuates with intake)

TIBC: high (inc transferritin –> inc TIBC also)

Transferritin saturation: low, serum Fe:TIBC ratio is low

39
Q

IDA Tx

A
  • underlying cause, treat if there is or is not anemia
  • Fe replacement therapy: oral v IV; reticulocytes peak in 7-10 days, Hb normalizes by 6-8 wks, Tx for >3 mos after Hb normalization (replenish body stores)
40
Q

ACD = (1):

-list the causes

A

anemia of chronic disease or anemia of chronic inflammation:

  • chronic bacterial infections (lung abscesses, osteomyelitis, endocarditis)
  • chronic immune disorders (RA)
  • malignant tumors (lymphoma, lung/breast CA)
41
Q

ACD pathogenesis:

  • (1) impairment, dec (2) production
  • during inflammation, there is an inc in (3) and a dec in (4) levels
  • (3), (4) leads to dec transfer of iron in (5) process
  • the end result dec (6) in total, accompanied by low (4)
A

(ACD- enough total Fe, just not in the right place)
1- Fe utilization impaired
2- RBC
3- hepcidin
4- EPO
5- dec Fe transfer from BM macrophages in duodenum to RBC precursors
6- dec erythropoiesis

42
Q

ACD, diagnosis and lab findings:

  • (1) in the clinical history
  • (2) CBC results
  • (3) peripheral blood smear results
  • (4) bone marrow results
  • (high/low/normal) EPO levels
A

1- chronic medical condition
2- low Hb, low-normal MCV
3- normocytic normochromic anemia // (sometime hypochromic microcytic)
4- normal or inc levels of stainable Fe (prussian blue, not often done)
5- inappropriately low

43
Q

describe the Serum Iron studies in ACD

A

Ferritin: high, inc Fe stores but in the wrong place = functional IDA

Fe: low, sequestered from circulation

TIBC: low, Fe is fully bound to transferrin

Transferrin saturation: normal, iron:TIBC stays the same as both dec

44
Q

Compare ACD and IDA:

  • (1) serum ferritin
  • (2) serum iron
  • (3) transferrin saturation (Fe:TIBC ratio)
  • (4) TIBC
A 
ACD:
1- normal / high
2- low
3- normal
4- low
IDA:
1- low
2- low
3- low
4- inc
45
Q

Aplastic anemia:

  • caused by defect in (1)
  • evident by (2) in labs
  • affects (M/F) more
  • causes are mostly (hereditary/acquired)
A

1- HSC (hematopoietic stem cells)
2- pancytopenia
3- M = F
4- acquired > hereditary

46
Q

list the causes of aplastic anemia

A
  • idiopathic, 65%
  • Drugs: dose-related and predictable OR idiosyncratic (kills stem cells)
  • Irradiation (kills stem cells)
  • Viral Infections (destroys HSCs)
  • Inherited genetic abnormalities: Fanconi anemia
47
Q

list the clinical features of Aplastic anemia

A
  • anemia Sxs (fatigue, HA, etc)
  • recurrent infections (neutropenia)
  • mucosal hemorrhage, menorrhagia (thrombocytopenia)
  • NO Organomegaly
48
Q

Aplastic anemia, diagnosis and lab findings:

  • (1) in clinical history
  • (2) CBC findings
  • (3) peripheral blood findings
  • (4) bone marrow findings
A

1- cause maybe from clinical history
2- pancytopenia
3- pancytopenia, normochromic normocytic anemia, very low reticulocyte count
4- hypocellular: fat cells, few lymphocytes, plasma cells (must r/o other causes of pancytopenia)

49
Q

Aplastic anemia:

  • (1) outcome
  • (2) Tx
A

1- spontaneous remission is UNcommon in adults (children is mostly viral causation –> full recovery)

2- bone marrow transplant (younger pts), immunosuppression (older adults)

50
Q

Bone Marrow Failure:
-(1) is where bone marrow is replaced by abnormal infiltrates that disturb its architecture, usually via (2)

  • (3) organ disease may cause marrow hypofunction, affecting (4) most
  • (5) organ failure may cause anemia via (6)
A

1- myelophthisic anemia
2- fibrosis
i.e. metastatic cancer, granulomatous inflammation => leucoerythroblastic blood picture

3- diffuse liver disease
4- RBCs (multifactorial etiology)

5- CRF
6- multifactorial anemia including dec EPO

RHS (35 decks)

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