Hertz CIS Flashcards

(34 cards)

1
Q

koilonychia

A

spoon shaped nails seen in iron deficiency

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2
Q

RDW measures?

A

red cell distribution width– the differences in the red cell sizes

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3
Q

red cell normal, HG low, what do we think?

A

a thalassemia

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4
Q

how to look at the hemogram

A
  1. RBC/ Hgb to look at an anemia
  2. MCV– are we normo, micro, or macrocytic?
  3. RDW- variation in size.
  4. Retic count
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5
Q

Why are MCH and MCHC kind of worthless?

A

they are calculated values, don’t add a whole lot.

When they’re low, the color is low.

THe MCHC is only good in hereditary spherocytosis, when it is elevated. Dead giveaway.

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6
Q

skier hits tree, bleeding into abdomen

A

hemoglobin normal to start, begins to drop

retic stays normal until about 8 days later, rises as hemoblogen gets under 10 g

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7
Q

colon cancer

A

chronic blood loss. retic would be up, hypochromic microcytic anemia. MCV would be like 70. Lower MCV more likeiron deficiency.

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8
Q

Female with post-menopausal bleeding

A

anemia of chronic blood loss

endometrial cancer

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9
Q

extravascular hemolysis triad

A

jaundice, splenomegaly, reticulocytosis

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10
Q

Haptoglobin

A

when red cells get popped or hemolyzed (intravascular), haptoglobin picks up the hemoglobin. (alpha 2).

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11
Q

normal MCHC values

A

33-34

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12
Q

Holly Jowell bodies happen when?

A
splenectomy
nonfunctional spleen when small, stiff RBCs (old)
Sickle cell (due to autosplenectomy)
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13
Q

G6PD

A

HEinz bodies, bite cells

mediterranean is the worst, don’t make any

negative is ok, just diminished.

BOTH intravascular and extravascular hemolysis

wait 2 weeks to test because the G6PD problem cells will be gone for a while (the old ones)

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14
Q

Sickle Cell. What does the C type do?

A

inhibits polymerization, sort of stabilizes the sickle cell and ends up being a milder version than sickle trait

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15
Q

the balance of thalassemia genes

A

4 alphas

2 betas

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16
Q

In beta thalassemia we are making

A

more alpha than beta

aaaa BB (normal)
aaaa  Bb  (minor)
aaaa bb (major)
17
Q

alpha thalassemias

A

missing 1- silent carrier
missing 2- trait
missing 3- H
missing 4- Hydrrops

18
Q

target cells mean

A

hemonglobinopathies like- thalassemia

19
Q

soccer ball cells

A

hemoglobin H- high affinity (hangs on to oxygen)

20
Q

hemosiderin around the kidney tubules

chronic anemia, normochromic, normocytic

A

PNH

test to make sure? flow cytometry
deficiency of CD59

21
Q

downey cells

A

active T cells (seen in mono)

causes agglutination

22
Q

autoimmune diseases DATs?

A

warm agglutination
Ig G

(no blood transfusions are compatible)

23
Q

acute disease DAT?

A

cold agglutination

Ig M

24
Q

zero retics, what would we need to think?

A

folate or B12 deficiency

think even more if you see hypersegmented neutrophils

25
asynchrony in folate/ B12 deficiency
nucleus doesn't develop well but the cytoplasm does
26
4 things that can cause B12 deficiency
Sjogrens atrophic gastritis lack of pancreatic amylase Crohn's disease fish tapeworm loves B12
27
pencil cells mean
iron deficiency anemia
28
3 chronic diseases
infections autoimmune neoplasms
29
primary hemochromatosis
the ferroportin is always open, too much iron always comes in.
30
secondary hemochromatosis
particularly happens in thalassemia | can't make good marrow, --> gut tries to absorb as much iron as possible
31
WBC and platelets low. What do we ask?
what do you do for a living or what drugs? e.g. bone marrow suppression from lead
32
dacryocytes come from
myelophthystic process (space occupying lesion)
33
stuff that leads to myellophthystic stuff
granulomas cancer renal disease (?)
34
renal cell carcinoma makes
EPO! --> erythrocytosis hepatocellular and cerebellar hemangioblastomas can also do this