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First Aid Yellow > Heme > Flashcards

Heme Flashcards

1
Q

No color in the iris, bircornuate uterus, mental disability

A 
Wilm's Tumor
WAGR
Wilms
Aniridia
Genitourinary malformation
Retardation
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2
Q

What is responsible for RBC concavity and flexibility

A

Spectrin

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3
Q

Varying sizes of RBCs

A

Anisocytosis

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4
Q

Vary shapes of RBC

A

Poikilocytosis

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5
Q

Immature RBCs

A

Reticulocytes

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6
Q

Deficiency of Factor VIII

A

Hemophilia A

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7
Q

Deficiency of Factor IX

A

Hemophilia B

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8
Q

Rate Limiting Step in Coag Cascade

A

X to Xa

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9
Q

PT measures which path

A

Extrinsic Path

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10
Q

PTT measures which path

A

Intrinsic Path

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11
Q

Other paths XIIa works on

A

Converts Prekallikrein to Kallikren (converts plasmingogen to plasmin) (converts HMWK to bradykinin)

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12
Q

Women with history of recurrent pregnancy loss and history of DVTs

A

Factor V Leiden

-mutant factor V resistant to degradation by protein C

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13
Q

THrombotic skin necrosis with hemorrhage after adminstration of warfarn

A

Protein C or S deficiency

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14
Q

G20290A mutation

A

Prothrombin gene mutation

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15
Q

Anticoag you follow using PTT

A

Heparin

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16
Q

cofactor for activation of antithrombin

A

Heparin

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17
Q

Antidote for Heparin OD

A

Protamine Sulfate

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18
Q

LMWH work more on facotr

A

Xa

  • longer halflife
  • can be adminitored subcutaneously
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19
Q

Why no monitoring of LMWH

A

Dosage is based on body weight

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20
Q

What cuases Heparin-induced Thrombocytopenia

A

Development of IgG antibodies against heparin-bound platelet factor 4 (PF4) –> Ab-hepatrin PF4 complex activates plateles –> thrombosis and thrombocytopenia

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21
Q

Treatment for HIT?

A

Direct thrombin inhibitors

-Bivalirudin (you were so RUDe to cause a HIT)

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22
Q

inhibits epoxide reductase

A

Warfarin

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23
Q

Monitored using PT

A

Warfarin

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24
Q

MOA of Warfarin

A

Intererferes with gamma-carboxylation of vit K-dept clotting factors (10,9,7,2) and proteins C & S
-blocks C and S first why you need to start with heparin as well

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25
Q

Anticoag you can give during pregnancy

A

Heparin

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26
Q

Teratogenic affects of Warfarin

A

Bone and cartilate problems, nasal hypoplasia

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27
Q

OD of Warfarin

A

Vit K, fresh frozen plasma

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28
Q

Apixaban, Rivaroxaban

A

Xa inhibitors direct

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29
Q

Aids in the coversion of plasminogen to plasmin (medication)

A

Thrombolytics (tPA, rPA, streptokinase, tenecteplase)

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30
Q

Nephritis, deafness, cataracts

A

Alport Syndrome

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31
Q

IF: granular pattern of immune complex deposition, LM: hypercellular glomeruli

A

PSGN

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32
Q

Deficiency of Aldolase B

A

Fructose Intolerance

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33
Q

Deficiency of Cystathionine Synthase

A

Homocystinuria

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34
Q

Galactose-1-phosphate uridyltransferase def

A

Intellectual disability, HSM, cataracts

Classic Galactosemia

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35
Q

Deficiency of Tyrosinase

A

Albinism

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36
Q

What do you administer Anti-D IgG (RhoGAM) for?

A

Rh negative women during the third trimester to prevent maternal anti-D IgG production to avoid erthyroblastosis fetalis

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37
Q

Anti-Rh-D

A

Erythroblastosis Fetalis

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38
Q

RBC form in lead poisoning

A

microcytic anemia with basophilic stippling

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39
Q

RBC form in bone marrow infiltration (myelofibrosis)

A

Teadrop cell

Dacrocyte

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40
Q

RBC form G6PD def

A

Heinz bodies bite cells (Degamyte)

-because of that oxidized Hg, someone dug in that RBC with all their might (and by someone I mean MP)

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41
Q

Burr cell

A

Echinocyte (more evenly spaced and even length spurs compared to acanthocytes)

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42
Q

RBC form End-stage renal disease

A

Burr cell (Echinocyte)

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43
Q

RBC form Pyruvate Kinase deficiency

A

Burr cell (echinocyte)

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44
Q

Pencil shaped RBCs

A

Elliptocyte

  • Hereditary elliptocytosis
  • mutation in RBC membrane protein (spectrin)
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45
Q

RBC form in Disorders of heme synthesis

A

Ringed sideroblasts

-Sideroblastic anemia

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46
Q

RBC form in DIC

A

Schistocytes

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47
Q

RBC form in TTP/HUS

A

Schistocytes

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48
Q

Target cells are seen in which path?

A 
HALT said the hunter to the target
H: HbC disease
A: Asplenia
L: Liver disease
T: Thalassemia
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49
Q

RBC form seen in patients with functional hypospelnia or asplenia

A

Howell-Jolly bodies

-basophilic nuclear remnants found in RBCs (normally removed by splenic MP)

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50
Q

Causes of Heinz bodies in G6PD

A 
Spleen Purges Nasty Inclusions From Damaged Cells
Sulfonamids
Primaquine
Nitrofurantoin
Isoniazid
Fava beans
Dapsone
Chloroquine
TB & malaria drugs, fava beans and sulfonamides
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51
Q

Fetal erythropoiesis

A

York sac
Liver
Spleen
Bone marrow

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52
Q

Lead poisoning inhibits which enzymes

A

Ferrochelatase and ALA dehydratase

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53
Q

Treatment for Lead poisoning

A

Succimer and EDTA

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54
Q

Symptoms of LEAD poisoning

A 
LEAD
Lead Lines on gums and on long bones
Encephalopathy and Erythrocyte Basophilic stippling
Abdominal colic and sideroblastic Anemia
Drops: write and foot drops
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55
Q

What inhibits gamma-aminolevuliinic acid synthase?

A

Glucose and heme

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56
Q

What cofactor is required for gamma-aminolevulinic acid synthase?

A

B6

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57
Q

Defective Prophobilinogen deaminase

A

Acute intermittent prophyria

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58
Q

dark reddish urine, colicky abdominal pain, psychological disturbances, polyneuropathy

A

Acute intermittent porphyria

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59
Q

Treatment of Acute intermittent porphyria

A

Glucose and heme (blocks ALA anythase)

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60
Q

Symptoms of acute intermittent porphyria

A 
5 P's
Painful abdomen
Port wine-colored urine
Polyneuropathy
Psychological disturbances
Precipitated by drugs, alcohol, starvation
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61
Q

Build up of porphobilinogen, gama-ALA, coprophiobilinogen

A

Acute intermittent porphyria

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62
Q

Blistering cutaneous photosensitivity, excessive hair growth, facial hyperpigmentation, increased LFTs, tea-colored urine

A

Porphyria Cutanea Tarda

“werewolves”

63
Q

Defective Uropophyrinogen Decarboxylase

A

Porphyria Cutanea Tarda

64
Q

Tumors that release EPO

A 
Potentially Really High Hematocrit
P: Pheochromocytoma
R: Renal Cell Carcinoma
H: Hepatocellular Carcinoma
H: Hemangioma
65
Q

Relative erythrocytosis

A

Normal number of RBCs and decreased plasma volume

66
Q

Mutation in Sickle Cell Hemoglobin

A

Glutamate to Valine in Beta Chain

67
Q

Mutation in Hemoglobin C disease

A

Glutamate to Lysine in Beta Chain

68
Q

Medication inhibiting alcohol dehydrogenase

A

Fomepizole

69
Q

Uses for Fomepizole

A

Methylene and ethylene glycol poisoining

70
Q

50 year old patient with iron deficiency anemia check for what

A

Colon cancer

71
Q

microcytosis and hypochromasia with GI bleeding

A

Iron deficiency

72
Q

Iron deficiency anemia, esophageal webs, dysphagia

A

Plummer Vinson Syndrome

-Glossitis

73
Q

Fatigue, light conjunctiva, pica, spoon nails

A

Iron deficiency anemia

74
Q

HbH

A

four beta-globin forms

-In 3 allele deletion alpha-thalassem;ia

75
Q

Causes hydropsfetalis

A

4 allele deletion in alpha thalassemia

76
Q

Hb Barts

A

4 gamma globin forms

  • incompatible with life
  • due to 4 allele deletion in alpha thalassemia
77
Q

Alpha thalassemia more common in what population

A

Asians and Africans

78
Q

Beta thalassemia more common in what population

A

Mediterranean

79
Q

Increases HbA2

A

Beta-thalassemia minor

-beta chain underproducted

80
Q

microcytic, hypochromic anemia withtarget cells and increased anisopoikilocytosis

A

Beta-thalassemia major

81
Q

“crew cut” on skull x ray and “chip munk” facies

A

Beta-thalassemia major

82
Q

What is important to monitor with beta-thalassemia

A

Iron levels b/c contast blood transfusions

83
Q

Defect in delta-ALA synthase gene

A

Sideroblastic anemia

84
Q

Treatment for sideroblastic anemia

A

B6 (pyridoxine)

85
Q

Test to diagnose Beta-thalassemia minor

A

Hg electrophoresis (look for increased A2)

86
Q

Blood iron tests in anemia of chronic disease

A

Decreased iron, decreased TIBC (not main concern of body to increase iron), increased ferittin, normal % trasnferrin saturation

87
Q

Iron studies in sideroblastic anemia

A

increasaed iron, decreased TIBC, increased ferritin, normal or increased % transferrin saturation
-impaired heme synthesis so extra iron is lying around

88
Q

RBC macrocytosis with hypersegmented NP and glossitis

A

Megaloblastic anemia

  • Folate def
  • B12 def
  • Orotic aciduria
  • Diamond-Blackfan anemia
89
Q

Cause of megaloblastic anemia (general)

A

Impaired DNA synthesis –> maturation of nucleus is delayed to rest of RBC maturation, causing RBCs to expand

90
Q

Increased homocystiene, normal methylmalonic acid, no neurological symptoms, macrocytic anemia

A

Folate deficiency

91
Q

Methotrexate and Trimethoprim cause what type of anemia

A

Folate deficiency Macrocytic megaloblastic anemia

92
Q

Anemia in vegans

A

B12 deficiency macrocytic megaloblastic anemia

93
Q

Increased homocystiene, increased methylmalonic acid, neurological symptoms, macrocytic anemia

A

B12 deficiency megaloblastic macrocytic anemia

-Methylmalonic acid: impairs myelin synthesis

94
Q

Macrocytic anemia, failure to thrive, developmental delay, no response to folate and B12

A

Orotic aciduria megaloblastic macrocytic anemia

-Defect in UMP synthase

95
Q

Treatment for Orotic aciduria

A

Uridine monophosphate

96
Q

Macrocytic anemia rapid-onset within 1st year of life

A

Diamond-Blackfan anemia

-intrinsic defect in erythroid progenitor cells

97
Q

RBC macrocytosis without hypersegmented neutrophils

A

Nonmegaloblastic anemia

-causes: alcholism, and liver disease

98
Q

MOA of anemia of chronic disease

A

Inflammation –> increase in hepcidin (binds ferroportin on MP and intestinal mucosal cels inhibiting iron transport) –> decreased release of iron from MP and decreased iron absorption from gut

99
Q

Treatment of anemia of chronic disease

A

EPO

100
Q

normocytic anemia, increased EPO, panyctopenia

A

Aplastic anemia (nonhemolytic, normocytic anemia)

101
Q

Causes of aplastic anemia

A
  • radiation
  • benzene and cancer drugs
  • Parovirus B19, EBV, HIV, hepatitis
  • Fanoconi anemia
  • idiopathic
102
Q

DNA repair defect causing bone marrow failure

A

Fanconi anemia

103
Q

normocytic anemia, increased indidence of tumors, cafe au lait spots, thumb and arm defects

A

Fanconi anemia

104
Q

Treatment of aplastic anemia

A

GM-CSF bone marrow stimulation

105
Q

Rate limiting enzyme of beta-oxidation of FA

A

Carnitine acyltransferase I

106
Q

Result of glycolytic enzyme deficiency

A

Hemolytic anemia

107
Q

Def in pyruvate dehydrogenase

A

Neurological defects

108
Q

Defect in akyrin and specrin

A

Hereditary Spherocytosis

109
Q

Causes an aplastic crisis with Parvovirus B10

A
  • Hereditary Spherocytosis

- Sickle cell anemia

110
Q

Positive osmotic fragility test

A

Hereditary spherocytosis (normocytic hemolytic anemia)

111
Q

Anemiawith increased MCHC and increased RWD

A

Hereditary spherocytosis (normocytic hemolytic anemia)

112
Q

G6PD causes what kind of hemolysis

A

Extravascular and Intravascular

113
Q

MOA of Pyruvate Kinase deficiency

A
  • Auto rec

- Defect in pyrovute kinase (RBCs cannot complete glycolysis) -> decreased ATP -> rigid RBCs -> extravascular hemolysis

114
Q

Hemolytic anemia in a newborn

A

Pyruvate Kinase def (normocytic hemolytic anemia)

115
Q

Blood smear shows hemoglobin crystals inside RBCs and target cells

A

HbC disease (normocytic hemolytic anemia)

116
Q

MOA of Paroxysmal Nocturnal Hemoglobinuria

A

Increased completement mediated RBC lysis (impaired synthesis of GPI anchor for decay-accelerating factor that protects RBC membrane from complement) CD55/59 negative

117
Q

CD55/CD59 negative

A

Paroxysmal noctural Hemoglobinuria (normocytic hemolytic anemia)

118
Q

Eculizumab treats what

A

Paroxysmal nocturnal hemoglobinuria (normocytic hemolytic anemia)

119
Q

Positive Ham’s test

A

Paroxysmal nocturnal hemoglobinuria (normocytic hemolytic anemia)

120
Q

Precipitates sickling of cells in SCD

A

low oxygen, high altitude, acidosis

121
Q

Painful crises that occur inSCD and why

A
  • Vaso-occlusive
  • dactylitis
  • priapism
  • acute chest syndrome
  • avascular necrosis
  • stroke
122
Q

Treatment for SCD

A

Hydroxyurea (increases HgF)

123
Q

RBCs are damaged when passing through obstructed or narrowed vessel lumina

A

Microangiopathic anemia (normocytic hemolytic anemia)

124
Q

RBCs damaged from prosthetic heart valves and aortic stenosis

A

Macroangiopathic anemia (normocytic hemolytic anemia)

125
Q

Coombs +, anemia with SLE, increased IgG

A

Autoimmune hemolytic anemia

-Warm

126
Q

Coombs +,anemia triggered by cold, and Myoplasma pneumonia, blue fingers and toes from cold

A

Autoimmune hemolytic anemia

-Cold

127
Q

Anti=Ig antibody added to patients blood, RBCs agglutinate if RBCs are covered with Ig

A

Direct Coombs test

128
Q

normal RBCs added to patient’s serum, if serum has anti-RBC surface Ig, they agglutinate

A

Indirect Coombs

129
Q

Uses for indirect Coombs

A

Blood typing, screen for maternal Ab in fetal blood

130
Q

interacts with vWF on platelet

A

GP1b

131
Q

After ADP binds ADP receptor whatmoves to surface

A

GPIIb/IIIa

132
Q

What binds to GPIIb/IIIa

A

Fibrinogen

133
Q

after endothelial damage how to blood vessels respond

A

vasoconstriction (neural stimulation)

-platelets to move slower and stay in area

134
Q

After platelets adhere and bind vWF what do they release

A

Ca (necessary for coag cascade) and ADP

TXA2 (vasoconstriction and promotes platelet aggregation

135
Q

MOA of aspirin and coag cascade

A

Apsirin irreverisbily inhibits cyclooxegenase preventing TXA2 production –> no vasoconstriction and harder for platelets to aggregate

136
Q

Clopidogrel, Pasgugrel, Ticagrelor, Ticlopidine

A

ADP receptor inhibitors

  • preent expression of glycoproteins IIb/IIIa on sufrace
  • no release of glycoproteins, staying grey (GRE)
137
Q

Abciximab, Eptifibatide, Tirofiban

A

Glycoprotein IIb/IIIa inhibitors

  • bind to the glycoprotein receptor IIa/IIIb on activated platelets, preventing aggregation
  • FIB (prevent FIBrinogen frombinding)
138
Q

Lifespan of platelet

A

8-10 days

139
Q

Hemosidinuria and thrombosis

A

Paroxysmal nocturnal hemoglobinuria

140
Q

Thyroid cells with optically clear nuclei

A

Papillary thyroid carcinoma

141
Q

Signs of platelet abnormalities

A

microhemorrhages: mucous membrane bleeding, epistaxis, petechiae, purpura, increased bleeding time, decresed platelet count

142
Q

Defect in GpIb, so platelet can’t adhere to vWF

A

Bernard-Soulier Syndrome

143
Q

Defect in GpIIb/IIIa, defect in platelet to platelet aggreation

A

Glanzmann Thrombasthenia

144
Q

Thrombocytopenia,Microangiopathic Hemolytic anemia, acute renal failure

A

Hemolytic-Uremic Syndrome

-Treat with plasmapheresis

145
Q

Anti-GpIIb/IIIa antibodies

A

Immune thrombocytopenia

146
Q

Incrased megakaryoctytes with microhemorrages

A

Immune Thrombocytopenia

-Trying to increase platelets because platelet-Ab complex begin consumed by splenic MP

147
Q

Deficiency of ADAMTS13

A

vWFmetalloprotease –> decreased degradation of vMF multilers –> increased platelet aggregation and thrombosis
Thrombotic Thrombocytopenic purpura

148
Q

Fever, anemia, neurological symptoms, thrombocytopenia, renal failure

A 
TPP
HUNT For The Toilet Paper
H: hemolysis
U: uremia
N: neurological symptoms
T: thrombocytopenia
TTP
149
Q

No platelet aggregationwith ristocetin cofactor assay

A

von Willebrand Disease

  • decreased vWF causes increased PTT
  • defect in platelet plug formation
150
Q

Treatment for von Willebrand disease

A

Desmopressin

151
Q

Schistocytes, increased d-dimers, decreased fibrinogen, decreaesd factor V and VIII

A

DIC

152
Q

Causes of DIC

A 
STOP Making New Thrombi
S: sepsis (G-)
T; trauma
O: Ob complications
P: pancreatitis
M: malignancy
N: nephrotic syndrome
T: transfusion
153
Q

Antiplatelet antibodies

A

Immune thrombocytopenia

154
Q

Most common inherited bleeding disorder

A

von Willebrand disease

First Aid Yellow (4 decks)

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