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Clin Med II > Hematology- Jaynstein > Flashcards

Hematology- Jaynstein Flashcards

1
Q

What is the cut off for macrocytic anemia

A

>100fl

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2
Q

What is the cut off for microcytic anemia

A

<80fl

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3
Q

What does a high retic indicate

A

Hemolysis
Acute blood loss

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4
Q

What is the NR for Plt count

A

150,000-450,000/mcL

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5
Q

What is the Hgb of a mild anemia

A

8-10

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6
Q

What is the Hgb level in a moderate anemia

A

6-8

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7
Q

What is the Hgb in a severe anemia

A

<6

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8
Q

What is the severity of an anemia largely dependent on

A

symptoms

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9
Q

What are the s/s of anemia

A

Fatigue
Tachycardia (due to compensation)
HSM
DOE
Pallor
Bone Tenderness (if applicable to underlying cause)

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10
Q

What do the MCH and MCHC determine

A

They describe the Hgb concentration- varying levels will tell you if an RBC is normochromic, hypochromic, or hyperchromic

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11
Q

What are the microcytic anemias

A

IDA
Thalassemia
Anemia of chronic disease (if they have had it long enough)
Sideroblastic anemia

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12
Q

What are the normocytic anemias

A

anemia of chronic disease (early on)
aplastic anemia
hemolytic anemia

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13
Q

What are the macrocytic anemias (megaloblastic)

A

B12 deficiency
Folate deficiency

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14
Q

Where is the majority of iron absorbed

A

duodenum

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15
Q

How is iron transported in the body

A

Transferrin

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16
Q

What is the storage form of iron

A

ferritin

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17
Q

Where is iron stored

A

Liver
Spleen
Bone marrow
Muscle

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18
Q

What is the leading cause of anemia world wide

A

IDA

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19
Q

What causes IDA

A

Insufficient dietary intake
Poor absorption of iron
Chronic blood loss

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20
Q

What pts are more prone to IDA

A

women

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21
Q

What should you always do if a pt presents with IDA

A

search for evidence of blood loss (don’t forget DRE)

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22
Q

What are the sx of IDA

A
  • Tachycardia
  • DOE
  • Fatigue
  • Pale skin and mucosa
  • Brittle nails
  • Angular cheilitis
  • Pruritis
  • Pica
  • Anxiety/tingling/numbness
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23
Q

What are the iron studies in order of most to least sensitive for detecting IDA

A

Ferritin

TIBC

Transferrin Sat

Serum Iron

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24
Q

What does the Ferritin test look for

A

stored iron

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25
Q

What is the first lab to decrease in IDA

A

Ferritin

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26
Q

If a pt has a Ferritin of <30mcg/dL with a decrease H/H, what is the diagnosis

A

IDA

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27
Q

What does the TIBC measure

A

capacity to bind iron

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28
Q

What are the NR for TIBC

A

240-450 mcg/dL

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29
Q

Is TIBC increased, decreased, or normal in IDA

A

increased (less free floating Iron to bind)

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30
Q

Will Transferrin Sat % be high, low, or normal in IDA

A

Low

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31
Q

What will serum iron levels be in IDA

A

normal to possibly slightly decreased

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32
Q

Why is serum iron not an ideal test for dx IDA

A

It can have considerable daily variation so it isn’t that useful

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33
Q

What are the treatments for IDA

A

PO→Diet or ferrous sulfate tablets

Parental→IV

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34
Q

Why do you want to start a pt on low dose of ferrous sulfate

A

It is poorly tolerated and upsets GI tract

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35
Q

How long does it take for Hct to get halfway to normal when tx IDA with ferrous sulfate

A

about 3 weeks

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36
Q

When will tx of IDA with ferrous sulfate return a pt to normal HCT levels

A

2 months

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37
Q

When would you admin ferrous sulfate IV

A

If pt is super intolerant PO or has a GI disease inhibiting absorption

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38
Q

Why is it important to ask fhx in a pt with new dx of anemia

A

To r/o thalassemias

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39
Q

What kind of anemia is a ild to moderate thalassemia

A

microcytic/hypochromic

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40
Q

What is the retic of a pt with a thalassemia

A

elevated- bone marrow is attempting to compensate

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41
Q

What are the iron studies for a pt with thalassemia

A

normal

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42
Q

What disorder is known to show target cells on a smear

A

Thalassemia

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43
Q

What is the definitive lab to dx thalassemia

A

Electrophoresis

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44
Q

What are the s/s of a severe thalassemia

A

Pallor

HSM

Growth failure

Bone deformities

Jaundice

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45
Q

What is the tx for mild thalassemia

A

No specific tx just monitoring

Folate supplements (to try and aid in synthesis)

Avoid iron supplements and sulfonamides

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46
Q

What is the tx for major thalassemias

A

May require transfusion

splenectomy

bone marrow transplants

avoid iron/sulfonamides

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47
Q

What is the cure for thalassemia major

A

allogenic stem cell transplant

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48
Q

What are the complications associated with thalassemias

A

iron overload

increased risk of infection (especially if tx with splenectomy)

Bone deformities

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49
Q

How do you tx iron overload

A

chelating agents

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50
Q

What is sideroblastic anemia

A

Anemia cuased by reduced Hgb synthesis because of failure to incorporate iron

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51
Q

What causes sideroblastic anemia

A

Alcoholism

lead

copper

zinc

dietary B6 or Cu deficiency

OCP

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52
Q

What is a characteristic sign of lead poisoning associated with sideroblastic anemia

A

basophilic stippling

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53
Q

What is characteristic on a periph smear for sideroblastic anemia

A

ringed sideroblasts

and if caused by lead poisoning, basophilic stippling

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54
Q

What is the tx for sideroblastic anemia

A

rarely requires tx, just tx underlying cause

on rare occasion can transfuse if necessary

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55
Q

What are the causes of megaloblastic anemias

A

B12 or folate deficiency

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56
Q

What is the most common cause of B12 deficiency

A

Pernicious anemia

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57
Q

What leads to pernicious anemia

A

Hereditary loss of gastric cells that help absorb B12

or

GI surgery that leads to loss of gastric cells (bariatric)

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58
Q

What pt population is prone to B12 deficiency and why

A

Vegans, it is found in foods of animal origin

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59
Q

What are the s/s of vit B12 deficiency

A

Fatigue

Pallor

CNS complaints- loss of vibratory sense, parasthesias, loss of balance

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60
Q

What labs will be out of range for vit b12 deficiency

A

elevated MCV

Low B12

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61
Q

What is the tx for B12 deficiency anemia

A

B12 IM injections

or

cobalamin PO

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62
Q

What does the body use folic acid for

A

DNA synthesis and repair

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63
Q

What foods contain folate

A

fruits and veggies

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64
Q

Why is folic acid so important to supplement

A

you can’t synthesize it and must come from your diet

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65
Q

What drugs can decrease folate absorption

A

phenytoin

sulfonamides

methotrexate

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66
Q

What are the s/s of folic acid deficiency

A

regular anemia sx

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67
Q

What labs will be out of NR for folic acid deficiency

A

Elevated MCV

Low folate

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68
Q

What is the tx for folic acid deficiency

A

Folic acid supplementation- 1mg PO daily

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69
Q

What is B9

A

folic acid

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70
Q

What normocytic anemias have low retic counts

A

anemia of chronic disease

anaplastic anemia

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71
Q

What normocytic anemia(s) have high retics

A

hemolytic anemia (there is attempted compensation by the marrow)

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72
Q

What are the most common causes of anemia of chronic disease

A

Chronic infxn/inflammation/cancer/liver disease

or

Renal failure leading to decreased epo production/reduced RBC production

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73
Q

What age group is more prone to anemia of chronic disease

A

>85 years old

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74
Q

How do you tx anemia of chronic disease

A

Tx the comorbidity

ir bad enough can tx with transfusion or EPO

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75
Q

What causes aplastic anemia

A

Bone marrow failure due to injury or abnormal expression of stem cells

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76
Q

What are the autoimmune cause(s) of aplastic anemia

A

SLE

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77
Q

What kind of trauma leads to aplastic anemia

A

radiation

chemo

toxins

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78
Q

What kinds of drugs lead to aplastic anemia

A

sulfonamides

phenytoin

carbamazepine

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79
Q

What are the s/s of aplastic anemia

A

fatigue

pallor

freq infxn

bleeding

purpura

petechiae

HSM

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80
Q

What are the lab changes associated with aplastic anemia

A

Pancytopenia

normocytic early on

decreased retic (no compensation)

normal smear just decreased numbers

bone marrow is hypocellular

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81
Q

What is the tx of mild aplastic anemia

A

blood and plt transfusions

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82
Q

What is the tx of severe aplastic anemia

A

bone marrow transplant

immunosuppression

83
Q

What is the prognosis of severe aplastic anemia

A

typically live about 6 months if not aggresively tx

84
Q

What do pts with aplastic anemia usually die from

A

infxn

85
Q

What are the most common hemolytic anemias

A

G6PD deficiency

Sickle Cell

86
Q

Why are sx of hemolytic anemias commonly delayed

A

Bone marrow production of erythrocytes will increase initially to compensate

87
Q

What are the sx specific to hemolytic anemia

A

jaundice

splenomegaly

88
Q

What will labs show for hemolytic anemias

A

elevated retic

elevated bilirubin

elevated LDH

urobilinogen

89
Q

What is the tx for hemolytic anemias

A

transfusions

90
Q

What is G6PD deficiency anemia

A

hereditary enzyme defect leading to episodic hemolytic anemia because RBCs cannot cope with oxidative stress

91
Q

What is a characteristic of RBCs that is specific to G6PD deficiency

A

Heinz bodies

92
Q

What are heinz bodies

A

markers for RBC destruction as a result of the body’s inability to handle oxidation

93
Q

What pt population does G6PD def. commonly affect

A

african american men

94
Q

What meds/foods can put a pt with G6PD def. into anemia

A

dapsone

quinine

primaquine

quinidine

sulfonamide

nitrofurantoin

fava beans

95
Q

What are the s/s of G6PD def

A

fatigue

splenomegaly

96
Q

What lab changes will be seen with G6PD Def

A

elevated bilirubin

elevated retic

heinz bodies

97
Q

How do you tx G6PD def

A

avoid known oxidative drugs

98
Q

How common is sickle cell and who does it affect

A

1:400 american blacks

99
Q

What provokes sickle cell crisis

A

infxn

dehydration

hypoxia

can be spontaneous

100
Q

What is the typical cause of pain for a pt in sickle cell crisis

A

ischemia to organs

101
Q

What are the s/s specifically for sickle cell anemia

A

chronically ill appearing

jaundice

splenomegaly

systolic murmur

non-healing ulcers

102
Q

When do s/s of sickle cell usually manifest in a pt

A

within 6 months of life

103
Q

What lab changes can be seen in pts with sickle cell

A

anemia

elevated retic

sickled cells on smear

howell-jolly bodies

target cells

104
Q

How do you confirm dx of sickle cell

A

Hgb S on electrophoresis

105
Q

What is the tx for sickle cell

A

prophylaxsis with hydroxyurea (stimulates epo)

UTD on vaccines

folic acid supplements

blood transfusions when necessary

106
Q

Is there a cure for sickle cell

A

no

107
Q

How do you tx sickle cell in acute crisis

A

tx pain

identify and remove ppt

tx infxn and ischemia

admin exchange transfusions

108
Q

What are the complications associated with sickle cell disease

A

strokes, PE, DVTs

increased infxn

leg ulcers

osteo-necrosis

gallstones

kidney damage

priapism

splenic squestration/rupture

eye damage

delayed growth

acute chest syndrome

109
Q

What occurs in primary hemostasis

A

plt adhesion

activation

aggregation into hemostatic plug

110
Q

What occurs in secondary hemostasis

A

clotting factors are activated to form a fibrin complex that then stabilizes the plt plug

111
Q

What is the only test that evaluates plts

A

bleeding time

112
Q

What does the aPTT test

A

Evaluates the intrinsic pathway

113
Q

What can prolong the aPTT

A

heparin

hemophilia

DIC

APS

114
Q

What does the PT evaluate

A

The extrinsic pathway

115
Q

What can prolong the PT

A

warfarin

liver dysfunction

vit k def

DIC

116
Q

What does fibrinogen test measure

A

protein precursor to fibrin

117
Q

What does a decrease in fibrinogen indicate

A

greater bleeding risk

118
Q

What does the d-dimer measure

A

measures a product of clot breakdown

119
Q

When would you start to be concerned about a pts plt level

A

when it gets below 50,000/mL

120
Q

At what plt level does spontaneously bleeding start to be a concern

A

about 20,000/mL

121
Q

What are the ss of thrombocytopenia

A

vary based on cause but commonly there is:

petechia (<3mm)

purpura (3-10mm)

Ecchymosis (>10m)

Long bleeding time or easy bruising

mild gingival and nasal bleeds

122
Q

What are the most common causes of thrombocytopenia

A

decreased plt production

increased plt destruction

sepsis/blood loss

123
Q

What labs will be abnormal if there is thrombocytopenia due to decreased plt production

A

bleeding time will be increased

124
Q

How do you tx thrombocytopenia due to decreased plt production

A

address underlying cause (remove offending med etc)

bone marrow stimulation

125
Q

How do you dx thrombocytopenia of decreasd plt production if there is no obvious cause

A

CA eval

bone marrow asp.

126
Q

What is idiopathic thrombocytopenic purpura

A

Autoimmune disease characterized by an abnormal decrease in the number of plts→IgG tagged plts

127
Q

What pt population is it common and unconcerning to see idiopathic thrombocytopenic purpura in?

A

children post-viral infxn

it is usually self limited

128
Q

When is Idiopathic Thrombocytopenic purpura (ITP) concerning

A

When acquired as an adult- this is less likely to resolve

129
Q

What is the pt presentation for ITP

A

rash

mucosal bleeding

easy bruising

130
Q

How do you dx ITP

A

Made by an isolated low plt count of less than 10k- dx of exclusion and you have ruled out all other causes

131
Q

What labs will be altered with ITP

A

thrmobocytopenia

prolonged bleed time

132
Q

What is the tx for ITP

A

in kids- only monitor

BUT

in adults-

if plt is >20k and there is no bleed, dont treat

If plt is <20k or there is a bleed admin prednisone, IVIG and splenectomy if persistent

133
Q

When would a pt with ITP get a plt transfusion

A

If they are at severe bleed risk, otherwise it is a pointless tx

134
Q

What is TTP (thrombotic thrombocytopenic purpura)

A

Autoimmune process characterized by extensive microscopic intravascular clotting, leading to plt clumping, thrombocytopenia, and easy bleeding

135
Q

Why does TTP lead to RBC lysis

A

The thrmobosis leads to shearing of RBCs

136
Q

What disease can be caused by an ADAMTS13 enzyme defect

A

TTP

137
Q

What can trigger TTP

A

meds

bacterial infxn

pregnancy

SLE

bone marrow transplants

138
Q

What is the pt demo that commonly gets TTP

A

90% occur in adulthood

women

139
Q

What labs will be altered with TTP

A

Plt count <50,000

Anemia

unconjugated bili

LDH elevation

evidence of renal failure

urine with hematuria and proteinuria

smear with frag RBCs

140
Q

What is the tx for TTP

A

EMERGENT-

admit

corticosteroids

pRBCs

plasmapharesis (to get rid of vWF)

ASA

Splenectomy

141
Q

What usually causes HUS

A

GI infections of E. coli, shigella, or salmonella

142
Q

What is the disease process of HUS

A

bacterial toxins damage vascular endothelium leading to thrombus formation and eventually thrombocytopenia

143
Q

What organ does HUS usually attack

A

kidney

144
Q

What pt population is commonly affect by HUS

A

kids

145
Q

What disease should you suspect if a child has renal failure associated with diarrhea

A

HUS

146
Q

What is the sx triad of HUS

A

thrombocytopenia

renal failure

hemolytic anemia

147
Q

What are the lab changes in HUS

A

plt count <50k

anemia

uncon. bili

LDH elevated

renal failure signs

blood and protein in urine

frag RBCs

148
Q

How do you tx HUS

A

Kids: Admit for observation and give IVF

Adults: tx like TTP

149
Q

What meds do you want to avoid when tx HUS

A

Abx- they increase bacterial lysis leading to increase release of toxin and increase clotting

150
Q

What does HELLP stand for

A

Hemolysis

Elevated Liver enzymes

Low PLT count

151
Q

What causes HELLP

A

complication of pregnancy that usually accompanies preeclampsia or eclampsia

152
Q

What are the s/s of HELLP

A

nonspecific:

fatigue

n/v

HA

RUQ abd pain

blurry vision

epistaxis

153
Q

What are the lab changes associated with HELLP

A

thrmobocytopenia

low h/h

elevated bili

elevated LDH

elevated LFTs

154
Q

What complications are associated with HELLP for the mother

A

1% mortality risk

DIC

renal failure

liver damage

155
Q

What complications are associated with pregnancy with HELLP

A

placental abruption

iatrogenic prematurity

156
Q

How do you tx HELLP

A

delivery (if 34 weeks or more)

157
Q

What is DIC

A

An “acquired bleeding disorder” caused by abnormal acceleration of the coag cascade leading to thrombosis and depletion of clotting factors leading to simulatenous bleeding

bleed and clot happening at once

158
Q

What are the s/s of DIC

A

Bleeding from multiple sites

ecchymossis/petechiae/purpura

cool and/or mottled extremities

dyspnea

hematuria

159
Q

What lab changes are present in DIC

A

All the bleeding and clotting tests will be abnormal, if you see everything is abnormal think DIC

160
Q

What is the tx for DIC

A

supportive care (ABC mgmt, cardiopulm support)

tx underlying d/o

transfuse only if absolutely necessary for bleed

heparin may or may not be helpful (case by case)

161
Q

What is HIT

A

The development of thrombocytopenia after the admin of heparin

162
Q

When does HIT usually form

A

after about 5 days of admin of heparin

163
Q

How do you dx HIT

A

Decrease of plt count by 50% or more with admin of heparin

164
Q

What are the sx of HIT

A

Pt are rarely symptomatic but if they display symptoms it is more likely to be clotting symptoms than bleeding

165
Q

What is the tx for HIT

A

Stop heparin and initiate another anticoag NOT WARFARIN

Avoid heparin indefinitely

plt tranfusion is not usually necessary

166
Q

Why do only males get hemophilia

A

It is a sex linked trait so women are only carriers

167
Q

What factor deficiency leads to hemophilia A

A

Factor 8

168
Q

What factor deficiency leads to hemophilia B

A

Factor 9

169
Q

What does the severity of hemophilia depend on

A

The amount of active protein produced

170
Q

How does a pt with mild hemophilia usually discover the disease

A

after a trauma or surgery (no spontaneous bleeds)

171
Q

What are common sites of random bleeds in pts with hemophilia

A

joints

soft tissue

urine/stool

brain

172
Q

What lab values will be abnormal in pts with hemophilia

A

aPTT- usually prolonged

Factor assay is low (8 or 9 depending on type of hemophilia)

173
Q

How do you tx hemophilia

A

avoid drugs that can interfere with clotting- ASA and NSAIDS

prophylaxis with factor replacement before surgery

lifestyle mods

174
Q

What is the most common congenital coagulopathy

A

Von Willebrand’s Disease

175
Q

What are the s/s of Von Willebrand’s Disease

A

epistaxis

gingival bleeding

menorrhagia

Gi bleed

or incidentally noticed after dental procedure

176
Q

Is Von Willebrand’s Disease a d/o with a high bleed risk/concern

A

no

177
Q

What labs values will be out of range in Von Willebrand’s Disease

A

prolonged bleeding time (spontaneously or after ASA challenge)

Low plasma vWF

Factor VIII might also be low

178
Q

What role does vWF play with Factor VIII

A

It prevents degradation of Factor VIII

179
Q

What is the tx for Von Willebrand’s Disease

A

Majority of cases are mild and require little to no tx

avoid ASA

supplement with desmopressin prior to surgery to release any stored vWF

180
Q

What clotting factor is not produced in the liver

A

Factor VIII (8)

181
Q

When trying to diagnose liver dysfunction, what is an effective test

A

PT/INR- pts with liver issues will have increased levels

182
Q

If a pt has a coagulopathy of the liver, how can you prophylax them for procedures

A

tx with FFP transfusion so they can supplement missing factors

183
Q

What factors require Vit K

A

Factor 2,7,9, and 10

184
Q

Why does Vit K deficiency prolong the PT and aPTT

A

It is involved in both the intrinsic and extrinsic pathway

185
Q

When should you check for clotting disorders

A

When a pt has an unprovoked PE or DVT

186
Q

What are the 4 clotting disorders you can screen for

A

antiphosphlipid antibody syndrome

Factor V Leiden

Protein C and S deficiency

Polycythemia Vera

187
Q

What do all clotting disorders put a pt at risk of

A

DVT

PE

CVA

MI

Miscarriage

188
Q

What is the acute tx of any and all hypercoagulable states

A

heparin/lmwh

thrombectomy or thrombolysis if indicated

189
Q

What is the preventative tx for any and all clotting disorders

A

anticoagulants or aspirin

Avoiding OCP

Minimizing risk like cigarettes, and mgmt of comorbities

190
Q

What is antiphospholipid antibody syndrome (APS)

A

An autoimmune disease in which people produce abnormal proteins called APA that create turbulent and stagnate blood flow leading to thrombi

191
Q

What disease is antiphospholipid antibody syndrome commonly associated with

A

SLE

192
Q

What other diseases are commonly associated with antiphospholipid antibody syndrome

A

miscarriage

DVT/PE

193
Q

How do you tx antiphospholipid antibody syndrome

A

same as tx of all hypercoagulability states (in another notecard)

194
Q

What is the most common inherited form of coagulopathy

A

Factor V Leiden

195
Q

How do you dx factor V leiden

A

Activated Protein C resistance test

PCR

196
Q

What is Protein C deficiency

A

A genetic coagulopathy disease

197
Q

What lab is used to dx Protein C Deficiency

A

Protein C Assay

198
Q

What is Protein S deficiency

A

A genetic coagulopathy disease

199
Q

How do you dx Protein S deficiency

A

Protein S assay

200
Q

What are the s/s of polycythemia vera

A

Pruritis (unexplained and provoked by things like showering)

HA

Fatigue

Splenomegaly

201
Q

What labs can diagnose polycythemia vera

A

Crit >60%

202
Q

What is Polycythemia vera

A

An acquired myeloproliferative d/o causing increased RBC and PLTs leading to hypercoagulability

203
Q

What is the tx for PV

A

one unit of blood weekly until crit <45% then PRN

Clin Med II (8 decks)

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