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From Flashcardlet > Pathology - Exam 3 - anemia > Flashcards

Pathology - Exam 3 - anemia Flashcards

1
Q

what are the mature cell types that emerge from a myeloid stem cell?

A 
basophil
eosinophil
neutrophil
monocyte
platelets
erythrocyte
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2
Q

which are granulocytes?

A

basophil
eosinophil
neutrophil

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3
Q

what blood test do you use for testing for anemia?

A

CBC

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4
Q

“counts” of WHAT are measured in a CBC?

A

RBC
Hemoglobin (how much in the blood?)
hematocrit (measured as a %) - derived value that isn’t used much anymore bc its really only a rough equivalent to the hemoglobin

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5
Q

what relates to RBC size and HEMO content

A

MCV (size)

MCHC (hemo)

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6
Q

for RBC “size”

A

Mean Corpuscular Value

overall how big are your red cells

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7
Q

to determine amount of hemoglobin

A

mean corpuscular hemoglobin content

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8
Q

what are the 3 different MCVs

A

microcytic
normocytic
macrocytic

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9
Q

what are the 2 MCHC’s

A

hypochromic

normochromic

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10
Q

what is the term for variation in shape

A

poikilocytosis

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11
Q

term for size variation

A

anisocytosis

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12
Q

Anemia definition

A

a reduction below normal in:
hemoglobin or
red blood cell number

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13
Q

Symptoms of Anemia

A 
things that you would expect with low oxygen delivery to tissues:
Pale skin, 
mucous membranes
Jaundice (if hemolytic bc bilirubin will go up)
Tachycardia
Breathlessness
Dizziness
Fatigue
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14
Q

Three Ways to Get Anemic

A

Lose blood
Destroy too much blood
Make too little blood

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15
Q

what are the reasons (ways) to destroy blood?

A

Extracorpuscular reasons

Intracorpuscular reasons

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16
Q

what are the reasons (ways) to make too little blood?

A

Too few building blocks
Too few erythroblasts
Not enough room

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17
Q

Anemia of Blood Loss: cause?

A

Cause: traumatic, acute blood loss

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18
Q

Anemia of Blood Loss: can you test a trauma pt’s hemoglobin right away?

A

NO

have to wait a little bit to test trauma pt hemoglobin bc at first Hemoglobin is normal

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19
Q

Anemia of Blood Loss: what do you see in the blood after 2-3 days

A

After 2-3 days, see reticulocytes

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20
Q

acute blood loss vs chronic blood loss

A 
acute = Hg issue
chronic = causes IRON DEFICIENCY ANEMIA
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21
Q

Hemolytic Anemias: 2 types

A

Intracorpuscular vs. extracorpuscular

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22
Q

Hemolytic Anemias:chronic vs acute

A 
acute = feel crappy / see clinically
chronic = bone marrow ramps up its RBC production so pts' seem normal bc Hg not low and then pt gets infection and see "crisis"
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23
Q

Hemolytic Anemias:Signs of destruction:

A

↑ INC bilirubin (unconjugated),
↑ INC LDH (lactate dehydrogenase),
↓ DEC haptoglobin (carrier molecule for free floating Hg)

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24
Q

Hemolytic Anemias:Signs of production:

A

↑ INC reticulocytes,
nucleated red cells in blood
**(Nucleated RBC’s are only suppose to be in marrow but bc marrow is rushing fast to repair, they get pushed out prematurely)

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25
Q

what type of histological “stain” is used to study Reticulocytes

A

(supravital stain) (slide 20)

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26
Q

Microangiopathic Hemolytic Anemia: how does it happen?

A

physical trauma to RBC’s via fibrin starnds

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27
Q

what fancy named “cell” is formed from the traumatized RBC’s that are ripped?
hint: is unique to Microangiopathic Hemolytic Anemia

A

Schistocytes (slide 24)
these are unique to Microangiopathic Hemolytic Anemia

sometimes “triangulocytes” are formed/seen too (slide 25)

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28
Q

Causes of MAHA

A
  • Artificial heart valve
  • Malignancy
  • Obstetric complications (back flow of amniotic fluid)
  • Sepsis
  • Trauma

“A MOST” - memory trick

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29
Q

why is it called warm vs. cold in Autoimmune hemolytic anemia

A

the temperature at which the antibodies react/bind

30
Q

Autoimmune Hemolytic Anemia: 2 types

A

warm and cold

31
Q

Autoimmune Hemolytic Anemia: WARM
what happens to the RBC”s
where does this occur
what cell shape/type remains

A

IgG (make IgG Ab’s to RBC’s)
spleen
spherocytes (smaller and darker)

32
Q

Autoimmune Hemolytic Anemia: COLD
what happens to the RBC”s
where does this occur
what cell shape/type remains

A

IgM, complement
Intravascular hemolysis
Agglutination (clumps that can plug up little capillaries)

33
Q

Autoimmune Hemolytic Anemia: how do you Dx a COLD AIHA?

A

Direct antiglobulin test (DAT)

34
Q

diseases with Intracorpuscular reasons of destroying too much blood

A

sickle cell anemia
Thalassemia
Hereditary Spherocytosis
Glucose-6-Phosphate Dehydrogenase Deficiency

35
Q

Sickle Cell Anemia: this is part of a larger type (group) of anemia - what is it?

A

Hemoglobinopathy

36
Q

Sickle Cell Anemia: what kind of specific defect in Hg?

A
  • qualitative defect in hemoglobin

* Single amino acid (point mutation) substitution in beta chain of hemoglobin

37
Q

Sickle Cell Anemia: mode of inheritance?

A

Can be:
heterozygous (just have SC trait) or
homozygous (full blown SCA)

38
Q

Sickle Cell Anemia: why are sickle cells nasty

A

Fragile (burst easily)

Get stuck in vessels

39
Q

Sickle Cell Anemia: HgS does what inside the RBC

A

Aggregates and polymerizes on deoxygenation
Red cell becomes sickle shaped
Sickles clog up vessels…
…plus, they are fragile

40
Q

what happens to the spleen from SCA

A

spleen gets fibrotic and non-functional after multiple infarcts caused by the sharp sickled RBC’s that clogged/damaged the spleen

41
Q

if you don’t have a spleen what types of infections are you susceptible to?

A

“capsular bugs”?????? confirm this from stephs notes

42
Q

Clinical Findings in Sickle Cell Anemia: typical pt type??

A

Blacks (8% are heterozygous)

Severity of disease is variable

43
Q

Clinical Findings in Sickle Cell Anemia: what disease/infections are seen?

A

Chronic hemolysis
vaso-occlusive disease
Increase in infections (autosplenectomy)

44
Q

what is a major effect of sickle cell anemia?

A

decreased solubility of the deoxy form of hemoglobin (boards question)

45
Q

Thalassemia: what type of defect in Hgb

A

Quantitative defect in hemoglobin

Variable disease severity

46
Q

Thalassemia: can’t make enough what???

A

Can’t make enough α or β chains

47
Q

Thalassemia: histological findings?

A

Hypochromic,
microcytic anemia
Inc. RBC and
target cells

48
Q

Thalassemia: why is it bad to not have enough alpha chains?

A

if you don’t have enough alpha chains, you don’t have anything to pair with (all types have alpha chain) (slide 44)

49
Q

what unique clinical finding can be seen in Thalassemia (predominantly in children)
hint: if you took a head X-ray

A

Thalassemia: Medullary expansion
“hair on end” - thickened something????
hemopoetic precursors get so desperate to be manufactured that the bones in the face and skull try to pick up the slack.

50
Q

Hereditary Spherocytosis: what type/shape of RBC’s are seen

A

Tons of spherocytes (also in another anemia??)

51
Q

Hereditary Spherocytosis: cytoskeleton is messed up due to what??

A

Spectrin defect ???????? ask steph

52
Q

Hereditary Spherocytosis: what happens to the spleen?

A

gigantic spleen but if take it out….

Splenectomy is curative

53
Q

Glucose-6-Phosphate Dehydrogenase Deficiency: what happens biochemically

A

DEC. G6PD → INC. peroxides → cell lysis

G6PD has a role in glutathione action/production
AND –>
glutathione required for reducing peroxides

54
Q

Glucose-6-Phosphate Dehydrogenase Deficiency: most patients are asymtomatic until what…..

A

Oxidant exposure

55
Q

Glucose-6-Phosphate Dehydrogenase Deficiency: what is seen histologically?

A

Spleen Bites out Heinz bodies

what remains is a “BITE CELL”

56
Q

Glucose-6-Phosphate Dehydrogenase Deficiency: how does it “go away”

A

Self-limiting

57
Q

Clinical Findings in G6PD Deficiency

A

Some patients asymptomatic
Others have episodic hemolysis
Spontaneous resolution
Jaundiced sclera

58
Q

what are the triggers of G6PD deficiency

A

Triggers:
broad beans (favism),
drugs (antibiotics, aspirin)

59
Q

Why Do G6PD-Deficient Red Cells Die? slide 55

A

??

60
Q

if see iron deficiency anemia not in a female menstrating or reproducing… what could it be?

A

Gastrointestinal bleeding

61
Q

Iron-Deficiency Anemia: most dangerous/important cause

A

Most important cause: GI bleeding

62
Q

Iron-Deficiency Anemia: what “type” (cell size/Hgb)

A

Microcytic, hypochromic anemia

63
Q

Iron-Deficiency Anemia: clinical findings

A

Atrophic glossitis
pica (eating weird things)
Koilonychia (tiny curled up nails)

64
Q

Iron-Deficiency Anemia: causes of?

A
  • Decreased iron intake
    - bad diet
    - bad absorption
  • Increased iron loss
    - GI bleed (order a poop smear for Dx)
    - menses
    - hemorrhage
  • Increased iron requirement
    - pregnancy
65
Q

Anemia of Chronic Disease: fall into 3 categories - what are they

A

Infections,
inflammation,
malignancy

66
Q

Anemia of Chronic Disease: what is “wrong”

A

Iron metabolism disturbed

67
Q

Anemia of Chronic Disease: what type of anemia (size/Hgb amount)

A

, normocytic
Normochromic
anemia

68
Q

what is the ONLY macrocytic anemia?

A

Megaloblastic anemia

69
Q

Megaloblastic anemia: what is the root of the problem?

A

Defective DNA synthesis
DEC B12/folate
Macrocytic anemia with oval macrocytes and hypersegmented neutrophils

70
Q

Megaloblastic anemia: what is seen histologically?

A 
"megaloblasts"
= immature nucleus and mature cytoplasm 
(Nuclear/cytoplasmic asynchrony)
=  in any blood cell type
oval macrocytes and 
hypersegmented neutrophils
71
Q

Megaloblastic anemia: why do you need B12?

A
  • to make DNA

* to convert homocysteine –> methionnine which is required to make myelin (see slide 72!!!!!)

72
Q

Megaloblastic anemia: what oral manifestation can be seen?

A

Atrophic glossitis (smooth tongue)

From Flashcardlet (51 decks)

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