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IHO Week 3 (EH) > Anemia > Flashcards

Anemia Flashcards

1
Q

Labs in IDA

A

dec serum iron
inc total iron-binding capacity
dec ferritin

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2
Q

reduction below normal in hgb or RBC

A

anemia

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3
Q

Symptoms of anemia

A 
Pale skin, mucous membranes
Jaundice (if hemolytic)
Tachycardia
Breathlessness
Dizziness
Fatigue
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4
Q

atrophic glossitis

A

red swollen tongue w/ misshapen papillae

megaloblastic anemia

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5
Q

koilonychia

A

spoon shaped nails

IDA

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6
Q

jaundice

A

yellow tinge in sclera/skin d/t excess bile

hemolytic anemia

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7
Q

3 ways to get anemia

A

Lose blood
Destroy too much blood
Make too little blood

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8
Q

Reasons for destroying too much blood (vague)

A

Intracorpuscular vs extracorpuscular

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9
Q

Reasons to make too little blood

A

Too few building blocks
Too few erythroblasts
Not enough room

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10
Q

three morphological groups of anemia

A

weird size
weird shape
normal size and shape

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11
Q

which anemias are “Weird size”

A

IDA
Thalassemia
Megaloblastic

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12
Q

Most important cause IDA

A

GI bleeding

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13
Q

Microcytic, hypochromic anemia

A

IDA

also thalassemia

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14
Q

IDA is a ____cytic, _____chromic anemia

A

microcytic

hypochromic

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15
Q

IDA has increased ____ and _____ (morphology), and _____ (lab)

A

anisocytosis and poikilocytosis

abnormal iron studies

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16
Q

most of our iron is in

A

hgb

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17
Q

Iron absorption

A

duodenum/proximal jejunum

binds to transferrin

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18
Q

Iron circulation

A

transferrin carries iron

iron goes to red cell precursors, organs

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19
Q

Structure of Hemoglobin

A

4 globin chains
4 heme molecules

globin - 2a and 2b chains
heme - iron molecule in protoporphyrin ring

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20
Q

iron only binds O2 in what state

A

ferrous (fe2+)

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21
Q

methemoglobin

A

ferric (fe3+)

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22
Q

Iron metabolism (where does it go)

A

most goes to RBCs

rest goes to macrophages

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23
Q

Iron storage

A

ferritin: quick in, quick out
hemosiderin: more stable

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24
Q

Causes of iron deficiency (Vague)

A

decreased iron intake
increased iron loss
increased iron requirement

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25
Q

reasons for decreased iron intake

A

bad diet

bad absorption

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26
Q

reasons for increased iron loss

A

GI bleed
menses
hemorrhage (slow)

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27
Q

reasons for increased iron requirement

A

pregnancy, fast growth

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28
Q

bottom line in IDA:
premenopausal women think ___
everyone else think ____

A

menorrhagia

GI blood loss

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29
Q

IDA sxs

A

asymptomatic
or fatigue, dizziness
Pica

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30
Q

IDA signs

A

pale
spoon nails
smooth tongue

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31
Q

morphology IDA - blood

A 
hypochromic, microcytic anemia
anisocytosis
poikilocytosis
dec reticulocytes
inc platelets
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32
Q

morphology IDA - bone marrow

A

erythroid hypoplasia
dyserythropoiesis
decreased iron stores

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33
Q

treatment IDA

A

find out why!

oral iron

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34
Q

megaloblastic anemia - underlying cause

A

Defective DNA synthesis
Nuclear/cytoplasmic asynchrony
Dec B12/folate

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35
Q

Macrocytic anemia with oval macrocytes and hypersegmented neutrophils

A

megaloblastic anemia

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36
Q

Megaloblastic: _____cytic anemia with ____ _____cytes and _____ ________

A

Macrocytic anemia with oval macrocytes and hypersegmented neutrophils

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37
Q

What is slow/not slow in megaloblastic anemia that leads to big cells?

A

Slow DNA synthesis (not enough dTMP from dec. B12/folate)

Normal RNA synthesis –> normal cytoplasm w/ immature nucleus

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38
Q

B12 sources

A

meat, dairy, cereal NOT VEGGIES

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39
Q

B12 absorption, transport

A

Binds to IF (from parietal cells)
Absorbed in distal ileum
Carried in blood by transcobalamin II

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40
Q

Causes of B12 deficiency

A 
Diet (rare)
Lack of IF
Pancreatic damage
Ileal damage
Tapeworm
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41
Q

What else is B12 good for?

A

homocysteine –> methionine

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42
Q

homocysteinemia —>

A

atheroscelosis, thrombosis (from dec. B12)

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43
Q

dec methionine –>

A

myelin damage –> subacute combined degeneration

from dec. B12

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44
Q

In a patient w/ macrocytosis, always check for

A

B12 deficiency (even if folate is low)

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45
Q

folate sources

A

lots

green leafy veggies

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46
Q

folate absorption, transport

A

Absorbed in jejunum
Converted to methyl-FH4
Transported freely to liver, red cells

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47
Q

causes of folate deficiency

A

Diet (small reserve)
Alcohol abuse
Jejunal damage
Drugs

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48
Q

morphology of megaloblastic anemia - blood

A

Macrocytic anemia
Oval macrocytes
Hypersegmented neutrophils

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49
Q

morphology of megaloblastic anemia - bone marrow

A

Megaloblastic erythroblasts

Megaloblastic neutrophils

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50
Q

How to test for Pernicious anemia

A

Schilling test

  1. drink radiolabeled B12
  2. Intramuscular injection of B12 (to saturate tissue stores with normal B12, so that if you absorb the radioactive B12, it won’t bind in the tissues, but will be passed into the urine.
  3. Collect urine, see how much radiolabeled B12 there is in it.
  4. If there’s no radioactive B12 in the urine (all passed in feces - not absorbed), try the test again, giving some IF along with the b12….
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51
Q

weird shape anemias are

A 
Hereditary spherocytosis
Autoimmune hemolysing anemia
Sickle cell anemia
G6PD deficiency
MAHA
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52
Q

Types of hemolytic anemia (time)

A

Chronic - usually congenital

Acute - usually acquired

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53
Q

symptoms chronic hemolytic anemia

A

well-compensated, sometimes w/ crises

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54
Q

sxs acute hemolytic anemia

A

Back, abdominal, limb pain
Headache, malaise, fever
Jaundice, pallor, tachycardia

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55
Q

types of hemolytic anemia (how to get them)

A

inherited

Acquired

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56
Q

causes of inherited hemolytic anemia

A

Membrane defects
Enzyme deficiencies
Globin defects

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57
Q

causes of acquired hemolytic anemia

A

Autoimmune hemolytic anemia
Microangiopathic hemolytic anemia
Infection-related
Drug-related

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58
Q

Increased red cell destruction –>

bottom line re: hemolytic anemia

A

increased red cell production

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59
Q

Signs of inc. RBC destruction

A

Inc. serum bilirubin
Inc. LDH
Dec. haptoglobin
Hemoglobinemia/-uria

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60
Q

Signs of inc. RBC production

A

Reticulocytosis

Nucleated red cells in blood

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61
Q

Test to see if Hemolytic anemia is autoimmune

A

Direct antiglobulin test

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62
Q

Direct antiglobulin test

A

Looks for antibody/c’ on RBC surface
Positive result means immune process

take red cells + AHG = agglutination = +
means there are already abs on RBCs

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63
Q

Osmotic fragility test

A

Measures fragility of red cells
Positive result means spherocytes present

Doesn’t give us a lot more information

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64
Q

morphology hemolytic anemia

A 
Normochromic, normocytic anemia
Spherocytes
Other poikilocytes:
targets
sickles
fragmented red cells
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65
Q

How to diagnose hemolytic anemia

A 
Look for signs of hemolysis (destruction, production)
Determine cause (DAT)
66
Q

hereditary spherocytosis has what distinctive cells

A

spherocytes

67
Q

what is the defect in hereditary spherocytosis

A

spectrin

68
Q

what is the cure/tx for hereditary spherocytosis

A

splenectomy

69
Q

triad of HS

A

anemia, jaundice, splenomegaly

70
Q

age of onset, severity HS

A

variable

71
Q

Do HS have crises?

A

Yes

Often with parvovirus

72
Q

pathogenesis HS

A

Abnormal RBC cytoskeleton
Loss of surface area
Spleen removes spheres

73
Q

Morphology of HS

A

Mild normochromic, normocytic anemia

Numerous spherocytes

74
Q

Tx HS

A

splenectomy, or RBC transfusions PRN

75
Q

Warm AIHA

3 main words/hallmarks

A

IgG
Spleen
Spherocytes

76
Q

Warm AIHA - secondary

A 
Leukemia/lymphoma
Other malignancies
Autoimmune disorders
Infections
Drugs
77
Q

pathogenesis WAIHA

A

IgG coats red cells
Macrophages either:
wolf red cells down whole (cells disappear)
nibble at red cells (cells become spherocytes)

78
Q

morphology WAIHA

A

spherocytosis

79
Q

dx WAHA

A

DAT

80
Q

tx WAHA

A

steroids

splenectomy

81
Q

cold AIHA

4 words/hallmarks

A

IgM, complement
Some intravascular hemolysis
Mostly spleen
Agglutination

82
Q

where does hemolysis happen in warm AIHA

A

spleen

83
Q

what kind of Ab for WAHA

A

IgG

84
Q

what kinds of Ab for CAHA

A

IgM, complement

85
Q

Secondary CAHA

A

Infections

Lymphoproliferative diseases

86
Q

Pathogenesis of CAHA

A

IgM, complement coat red cells
IgM falls off in warm body parts
IgM bridges red cells (agglutination)
Complement may lyse red cells (in blood) but usually just opsonizes them (and macrophages in spleen eat them)

87
Q

where does hemolysis happen in CAHA

A

some in intravascular, mostly spleen

88
Q

clinical picture of CAHA

A

Chronic hemolysis aggravated by cold

Pallor, cyanosis in cold body parts

89
Q

morphology CAHA

A

Red cell agglutinates

Rare spherocytes

90
Q

dx CAHA

A

DAT

91
Q

Tx CAHA

A

keep pt warm

treat underlying cause

92
Q

what is wrong in hemoglobinopathies

A

qualitative hemoglobin abnormality

93
Q

what is the most important hemoglobinopathy

A

sickle cell

94
Q

what do sickle cells cost?

A

hemolysis, vaso-occlusion

95
Q

best lab test for hemoglobinopathies

A

hgb electrophoresis

96
Q

which direction does hgb run in electrophoresis

A

towards the anode (+ end)

97
Q

what does sickle cell/sickle trait look like on electrophoresis

A

sickle cell anemia does not run as far

sickle train has one that runs normal, one that runs short

98
Q

underlying cause sickle cell

A

point mutation in b chain genes
substitution of valine for glutamate

aggregates and polymerizes on deoxygenation - red cell becomes sickle shaped - clog up vessels and are fragile

99
Q

clinical findings/sxs in sickle cell anemia

A

chronic hemolysis
vaso-occlusive
increased infections (autosplenectomy)
foot ulcer

100
Q

morphology of sickle cell anemia

A

sickle cells

post-splenectomy blood picture = nucleated RBCs, targets, howell jolly bodies, pappenheimer bodies, incr. platelet count

101
Q

howell jolly bodies

A

basophilic nuclear remnants (clusters of DNA) in circulating erythrocytes. (blue)

102
Q

pappenheimer bodies

A

abnormal granules of iron found inside red blood cells on routine blood stain

103
Q

tx sickle cell

A

prevent triggers
vaccinate against encapsulated bugs (s. pneumo, H. influ)
blood transfusions
bone marrow transplantation

104
Q

triggers sickle cell anemia

A

infection, fever, dehydration, hypoxemia

105
Q

Thalassemia - can’t make enough

A

alpha or beta chains

106
Q

thalassemia disease severity

A

variable

107
Q

Hypochromic, microcytic anemia with increased RBC and target cells

A

thalassemia

108
Q

Thalassemia: _____hromic, _____cytic anemia with increased ____ and ____ cells

A

Hypochromic, microcytic anemia with increased RBC and target cells

109
Q

hemoglobin chain development

A

Hgb F = a2g2
Hgb A2 = a2d2
Hgb A = a2b2

110
Q

normal globin genes

A

4 a-chain genes

2 b-chain genes

111
Q

globin genes in alpha thal

A

deletion of a-chain genes –> decreased amount a-chains

112
Q

globin genes in beta thal

A

defective b-chain genes –> decrease amount b-chains

113
Q

problem with the genes in b-thal

A

defective transcription, translation,

or processing of mRNA of -chain gene

114
Q

severity of defect - b-thal

A

B gene: normal gene
B+ gene: produces some B chains
B0 gene: produces no B chains

115
Q

3 kinds of b-thal

A

b-thal minor (asymptomatic)
b-thal intermedia (less severe)
b-thal major (severe)

116
Q

problem with genes in a-thal

A

a-chain genes are absent

117
Q

4 kinds of a-thal

A

silent
a-thal train
HbH disease (only one a-gene)
Hydrops fetalis

118
Q

what causes the anemia in a-thal

A

not enough a chains

excess unpaired b, g, d chains (newborns make g4 = Hb barts, adults make b4 = HbH)

119
Q

what causes anemia in b-thal

A

not enough b chains

excess unpaired a chains

120
Q

morphology of thalassemia

A

hypochromic, microcytic

minimal to marked anisocytosis and poikilocytosis

target cells, basophilic stippling

121
Q

medullary expansion happens in

A

thalassemia

122
Q

clinical findings a thal population

A

asians, blacks

123
Q

population b-thal

A

mediterraneans, blacks, asians

124
Q

what leads to cell lysis in G6PDD

A

dec G6PD –> inc. perosides –> cell lysis

oxidant exposure

125
Q

what kinds of cells do you see in G6PDD exclusively

A

Bite cells (removal of heinz bodies)

126
Q

inheritance G6PDD

A

x-linked

127
Q

what does G6PD do

A

G6P –> 6PG (PPP) also sending NADP to NADPH, replenishing NADPH for GSSG –> GSH = antioxidant

128
Q

why do G6PDD cells die

A 
They can’t reduce nasties
Nasties attack hemoglobin bonds
Heme breaks away from globin
Globin denatures, sticks to red cell membrane (“Heinz body”)
Spleen bites out Heinz bodies
129
Q

Highest incidence of G6PD is in areas where

A

malaria is epidemic (endemic?)

130
Q

triggers G6PDD

A

broad beans (fava), drugs (antibiotics, aspirin)

131
Q

tx G6PDD

A

spontaneous resolution

132
Q

morphology G6PDD

A

w/o exposure: no anemia
after exposure: acute hemolysis
bite cells, fragments
heinz bodies

133
Q

microangiopathic hemolytic anemia - anemia caused by

A

physical trauma to red cells

134
Q

causes of MAHA

A

artificial heart valve

anything causing DIC, TTP, HUS

135
Q

morphology MAHA

A

schistocytes

triangulocytes

136
Q

anemias of normal size and shape

A

anemia of blood loss
chronic disease
kidney, liver disease
aplastic anemia

137
Q

cause of anemia of blood loss

A

traumatic, acute blood loss

138
Q

morphology in anemia of blood loss

A

at first - normal hgb

after 2-3 days, see reticulocytes

139
Q

chronic vs acute blood loss anemia

A

chronic –> IDA

acute –> A of blood loss

140
Q

what causes AOCD

A

infections, inflammation, malignancy

141
Q

pathogenesis AOCD

A

iron metabolism - absorption is okay, but release is screwed up- cannot get iron into hgb because hepcidin is overproduced

shortened RBC survival, impaired marrow response to anemia

142
Q

AOCD: ___ chromic, _____ cytic

A

normochromic normocytic

143
Q

anemia severity in AOCD

A

usually mild (other CD more a problem)

144
Q

abnormalities in red cell in AOCD

A

none

145
Q

labs in AOCD vs IDA

A 
AOCD:
dec serum iron
dec/normal TIBC
inc ferritin
inc marrow storage iron
IDA:
dec serum iron
inc. TIBC
dec ferritin
dec marrow storage iron
146
Q

what does hepcidin do

A

Hepcidin inhibits iron transport by binding to the iron export channel ferroportin which is located on the basolateral surface of gut enterocytes and the plasma membrane of reticuloendothelial cells (macrophages).
Stuck in cells

147
Q

labs AOCD

A

dec serum iron (stuck in cells)
dec/nl TIBC (can’t transport but want to)
inc. ferritin (have to store it)
inc. marrow storage iron

148
Q

anemia of renal disease: things you must know

A

end-stage renal failure
cause: lack of EPO
may see echinocytes

149
Q

what do you see in anemia of renal disease

A

echinocytes (pointy)

150
Q

cause of anemia of renal disease

A

EPO

151
Q

anemia severity of anemia of renal disease

A

roughly correlates w/ degree of renal failure

152
Q

mgt anemia of renal disease

A

if mild, none

if severe, replace EPO

153
Q

anemia of liver disease: things you must know

A

frequent in liver disease
multiple causes
“uncomplicated” cases are rare
may see acanthocytes (weird little offshoots), targets

154
Q

why is anemia of liver disease rarely uncomplicated

A

get other kinds of anemia - ie inflammation, or slow bleed from esophageal varices, folate deficiency

155
Q

causes of uncomplicated liver disease anemia

A

dec RBC survival and impaired marrow response

156
Q

morphology uncomplicated liver disease anemia

A

mild anemia
usually normocytic - sometimes macrocytic
poikilocytosis (targets, acanthocytes)

157
Q

morphology complicated liver disease anemia

A

megaloblastosis (from folate)

microcytosis (from IDA)

158
Q

aplastic anemia: things you must know

A

pancytopenia
empty marrow
most are idiopathic

159
Q

causes of aplastic anemia

A 
Idiopathic
Drugs
Viruses
Pregnancy
Fanconi anemia
160
Q

clinical findings in aplastic anemia

A

Pallor, dizziness, fatigue (anemia)
Recurrent infection (leukopenia)
Bleeding, bruising (thrombocytopenia)

161
Q

morphology of aplastic anemia

A

blood - empty

bone marrow - empty

162
Q

tx aplastic anemia

A

avoid exposure/trigger
give blood products
drugs: G-CSF, prednisone, ATG
bone marrow transplant as last resort

IHO Week 3 (EH) (5 decks)

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