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Physio II > anemia > Flashcards

anemia Flashcards

1
Q

Pyrroles is synthesized from

A

succinyl coA and glycine

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2
Q

Synthesis of hemoglobin begins with and ends with

A

Synthesis of hemoglobin begins in the proerythroblasts and continues even into the reticulocyte stage of the RBCs.

when reticulocytes leave the bone marrow and pass into the blood stream they continue to form hemoglobin for another day or to until they become mature erythrocytes

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3
Q

protoporphyrin IX is synthesized from

A

b. 4 pyrroles

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4
Q

of iron forms from

A

Heme and protoporphyrin IX

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5
Q

hemoglobin chain (alpha or beta)

A

formed from polypeptide and heme

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6
Q

what is hemoglobin A synthesized form

A

2 alpha chains 2 beta chains

4 subunits

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7
Q

anemia define

A

Abnormally low number of circulating red blood cells or level of hemoglobin, or both, resulting in diminished oxygen-carrying capacity.”

sign nOT dz

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8
Q

major function of RBC

A

also known as erythtrocytes is to transport hemoglobin which carries oxygen form the lungs to the tissues

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9
Q

functions of the RBC

A

transport hemoglobin so it doesn’t leak through capillary membranes

contain carbonic anhydrase whihc catalyzes the reaction betwen CO2 and water –>carbonic acid

H2CO3

hemoglobin also serves as a acid base buffer and therefore RBC at large are great for acid base buffering

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10
Q

role of carbonic anhydrase

A

makes it possible for the water of the blood to transport enormous quantities of CO2 in the form of bicarbonate ion (HCO3−)

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11
Q

three “dz” that are very similar

A

Thyroid, Depression, Anemia present VERY similarly

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12
Q

reduced oxygen capacity could be caused by

A

imparied oxygen transport (i.e. hemoglobin)
or reduced red cells

Condition typically results from red cell loss (hemolysis/hemorrhage), deficient erythropoiesis, or deficient hemoglobin production

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13
Q

physical effects of hypoxia and sxs assoicated with anemia

A

i. Fatigue
ii. Weakness
iii. Dyspnea
iv. Angina
v. HA, faintness, dim vision

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14
Q

skin effects of hypoxia

A

Pallor of skin, mucus membranes, conjunctiva, nails

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15
Q

what could blue mucus membranes in the nose indicate

A

allergies or anemia

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16
Q

Normocytic

A

normal-sized rbc but ↓ amount í MCV 80-100 fl

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17
Q

Macrocytic

A

presence of large rbc in peripheral smear í MCV>100 fl

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18
Q

Microcytic

A

presence of small, often hypochromic, rbc in peripheral blood smear í MCV<80 fl

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19
Q

anemia usually characterized by a low MCV

A

Microcytic

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20
Q

etiologies of microcytic anemia

A

” IDA: Iron Deficiency Anemia

“ Thalassemia

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21
Q

etiologies of normocytic anemia

A

” ACD: anemia of chronic disease (or anemia of inflammation)

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22
Q

etiologies of Macrocytic anemia

A

” B12/Folate deficiency

“ w/ ↑ reticulocyte: hemolysis

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23
Q

diagnostic that tells you O2 carrying capactiy

A

Hgb

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24
Q

Hct tells you

A

% of intact RBCs and RBC count

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25
Q

Any time you have an increased reticulocyte count, you need to think

A

why is the person working so hard to push RBCs into the blood before they are ready?

What are they replacing? What are they trying to adapt to?

this is seen with hemolytic anemia

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26
Q

Possible jaundice think

A

might be producing more bilirubin than they can handle

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27
Q

Hgb content can refer to

A

normochromic-normal hemoglobin

hypochromic- less hemoglobin

Typically don’t see hyperchromic anemias

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28
Q

Iron deficiency

A

can’t make heme and so red cells are smaller (microcytic)

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29
Q

If acute blood loss, and anemic tend to see what in terms of cell morphology

A
  • tend to have normal cell morphology (normal cell size and normal Hgb content)
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30
Q

If you lose blood over long period of time - you become

A

iron deficient and get small cells

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31
Q

acute blood loss think

A

think hypovolemia/shock

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32
Q

sxs associated with acute blood loss

A

Will feel symptoms consistent w/ anemia at relatively high hemoglobin levels - don’t usually get as low as you will with chronic loss

could feel this at 9 or 10

Fluid enter compartment, dilutes blood, Hgb/Hct fall with normal cell morphology
iv. Chronic loss leads to iron

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33
Q

chronic blood loss leads to

A

Chronic loss leads to iron deficiency anemia over time, NO volume depletion (microcytic anemia)

Your body adapts to that blood loss so your hemoglobin can be down to 6

usually
13.5 to 17.5 grams men
For women, 12.0 to 15.5

34
Q

what labs are important when assessing anemia

A

red cell indicies/Hgb is usually ordered as part of a cbc

used to diagnose the cause

Average red blood cell size (MCV)
Hemoglobin amount per red blood cell (MCH)
The amount of hemoglobin relative to the size of the cell (hemoglobin concentration) per red blood cell (MCHC

35
Q

chronic kidney disease anemia

A

secondary to loss of erythropoietin

36
Q

why is tachycardia seen as a sx of anemia

A

cycling the RBC you have faster for quicker oxygenation

might also increase your ventilation rate

37
Q

in the developed world iron deficiency anemia is related to

A

diet

38
Q

in the developed world iron deficiency anemia is related to

A

bleeding

39
Q

pathophys of hereditary spherocytosis

A

Deficiency of red cell membrane proteins (spectrin, ankyrin) that helps maintain the disc shape

get a little beach ball

loss of surface area
loss of disc results in the impeded ability to travel through small spaces and the result is damage

40
Q

what happens to the body in hereditary spherocytosis

A

Signs include jaundice- bilirubin accumulation from distruction
splenomegaly- destruction occurs in the spleen
bilirubin stones

41
Q

tx for hereditary spherocytosis

A

take out the spleen where most of the hemolysis is happening

keep red cells a little bit longer and stave off destruction to the bone marrow

42
Q

why would we see a aplastic crisis with hereditary spherocytosis

A

g. Aplastic crisis when red cell production disrupted as by virus

43
Q

what can put a sickle cell pt into crisis

A 
exertion
cold stress
altitude 
stress
dehydration
acidosis

Low oxygen tension leads to sickling

can all result in a lot of occlusive damage to the vasculature with the cells get caught

44
Q

Sickle Cell Anemia

A

Point mutation in beta chain of hemoglobin, abnormal substitution

transmitted in by recessive pattern

45
Q

what % of pts present with heterozygotic sickling

A

40% sickling with heterozygotic trait

46
Q

Thalassemias

A

seen in (MEDITERRANEAN population

47
Q

Thalassemias

A

Alpha: result of deletion of alpha subunit on Chromosome 16

severe disease Hgb H formed

Beta: usually caused by point mutations in b subunit. Relative increases in Hgb A2 and F.

48
Q

Thalassemias tests

A

Diagnosis – Electrophoresis í get a hemoglobin electrophoresis and it tells you different proportions of different hemoglobin
i. Normal pt’s don’t Hgb H

49
Q

Microcytosis out of proportion to the degree of anemia

A

Thalassemias

50
Q

MCC worldwide

A

(dietary deficiency or bleeding)

IDA

microcytic hypochromic anemia

51
Q

Anisocytosis

A

red cells are all different sizes, they are not similar to each other

seen in IDA because of increased production to make up for low hemoglobin

52
Q

Poikilocytosis

A

abnormally shaped red blood cells

seen in IDA because of increased production to make up for low hemoglobin

53
Q

this type of anemia results from impaired nucleic acid synthesis when the cells are turning over

A

Megaloblastic Anemias

not till the very end that the precursor cell losses the nucleus

54
Q

MCC of megaloblastic Anemias

A

MCC: B12 or folate deficiency

can’t turnover the DNA as fast as you normally would

cell is getting bigger and bigger as it’s waiting for nucleus to turn over DNA

generating more and more cytoplasm but doesn’t’ have the cofactors it needs to turnover the DNA

offspring are bigger

55
Q

B12 is absorbed and stored where

A

a. Bound to intrinsic factor in stomach
b. Absorbed at terminal ileum
c. Stored in liver (sufficient for 3 years without intake)

56
Q

Microcytic Anemia (MCV <80fL)

MC and 2nd MC

A

IDA MC

2nd: thalassemia

57
Q

AKA bone marrow depression

A

Aplastic Anemia

Fatty replacement of bone marrow - loss of all 3 stem cell lines

results in loss of all products
pancytopenia

58
Q

pancytopenia

A

reduction in all blood cell numbers seen with bone marrow depression (aplastic anemia)

59
Q

sxs with aplastic anemia

A

e. Petechiae and bruising from loss of platelets, and infections from WBC loss

60
Q

causes of aplastic anemia

A

Often caused by exposures (radiation, chemicals, Felbamate & tegretol [AED])

and chronic liver disease (where clottng factors are made)

61
Q

tx of aplastic anemia

A

May require BMT (bone marrow transplant)

62
Q

ACD: Chronic Disease theory

A

a. Common result of chronic infections (eg AIDS, RA, SLE, Hodgkin’s)

Theory focuses on macrophage and lymphocyte role in sequestering iron, destroying red cells, chemical suppression of EPO response, inhibited precursor cells, reduced Fe transport
Similar to IDA (microcytic/hypochromic) - separate from CRF (normocytic/normochromic)

63
Q

the capacity of a red cell is about ____ hbg

A

1/3

MCHC (mean corpuscular hmg content) should always be around 33%)

64
Q

RDW

A

reticulocyte distribution width aka variability in size

standard deviation of red cell size
when this is high it means that you have a lot of different size red cells

(Reticulocytes and epo are high trying to repair)
1. Reference range = 11-14.5

65
Q

measure aka variability in size

A

reticulocyte distribution width (RDW)

66
Q

average volume of RBC

A

v. MCV

67
Q

if I say MCV you say

A

cell size

68
Q

MCV If low = then microcytic

A
  1. If low = then microcytic
69
Q

mcv If high

A

= then macrocytic

70
Q

MCV if normal

A

If normal = normocytic

71
Q

vi. MCH

A

= Mean corpuscular hemoglobin

72
Q

how to tell if you have a good sample of blood

A

with rule of 3’r

(red count, Hgb content and Hematocrit should be roughly mupltiples of 3)

if it fits= good specimen

73
Q

Evaluate anemia

A

good specimen= rule of 3’s

i. Hgb/Hct
1. 14-18 men
2. 12-16 women
ii. Check MCV and classify
iii. Check RBC count

74
Q

if you see microcytic hpochromic anemia

what should you suspect and hwta labs would you get

A

IDA
iron studies
Total iron binding capacity (TIBC)
Ferritin

75
Q

Ferritin

A

how we store iron (MOST important one)

  1. Below 15 is diagnostic of iron deficiency anemia even if we don’t see anything else
  2. Last thing she restores is the
76
Q

if iron level is low

A

if iron level is low, binding capacity is high

77
Q

with macrocytic anemia order

A

i. Get a B12 level
ii. Get a folate level

iii. Iron studies are NOT indicated but do it anyway to r/o
1. Since it is macrocytic there is not reason for them to Iron deficient

78
Q

hallmark of Thalassemia

A

hallmark if microcystosis out of proportion to the presentation

MCV will be super low without fatigue

79
Q

Thalassemia dx test

A

Hemoglobin Electrophoresis

80
Q

the goal with IDA

A

to repair ferritin level

81
Q

who gets macrocytic anemia due to B12 deficiency

A

” Pernicious anemia (MC); gastrectomy = ↓production of intrinsic factor (can’t absorb B12)
“ H. Pylori infxn
“ Competition for Vit B12 in gut
“ Pancreatic insufficiency
“ Decr ileal absorption of B12 = surgical resection, Crohn’s MC
“ Dietary & transcobalamin II deficiencies = RARE cause

Physio II (18 decks)

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