Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

PathoPharm 2 > Hematology > Flashcards

Hematology Flashcards

(122 cards)

Start Studying
1
Q

megaloblastic anemias

A

Macrocytic-Normochromic Anemias
Pernicious anemia
folate deficiency anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Methylmalonic acid and homocysteine levels are elevated early in the disease

A

pernicious anemia evaluation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Folate (folic acid) deficiency anemia s/s

A

Severe cheilosis: Scales and fissures of the lips and corners of the mouth
Stomatitis: Mouth inflammation
Painful ulcerations of the buccal mucosa and tongue: Characteristic of burning mouth syndrome
Dysphagia (difficulty swallowing), flatulence, and watery diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Folate (folic acid) deficiency anemia and CNS s/s

A

usually not seen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pernicious anemia s/s

A

Weakness, fatigue
Paresthesias of the feet and fingers, difficulty walking
Loss of appetite, abdominal pains, weight loss
Sore tongue that is smooth and beefy red, secondary to atrophic glossitis
“Lemon yellow” (sallow) skin as a result of a combination of pallor and icterus
Neurologic symptoms from nerve demyelination - Not reversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  • Most common type of anemia worldwide
A

Iron-deficiency anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Sideroblastic anemia cause

A

defect in mitochondrial heme synthesis. Altered mitochondrial metabolism causes ineffective iron uptake and results in dysfunctional hemoglobin synthesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

o Sideroblasts

A

Erythroblasts contain iron granules that have not been synthesized into hemoglobin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
  • Reversible sideroblastic anemia a/w
A

Associated with alcoholism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Sideroblastic anemia s/s

A

o Iron overload (hemochromatosis)
o Enlarged spleen (splenomegaly) and liver (hepatomegaly)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Sideroblastic anemia diagnostic

A

o Dimorphism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

o Dimorphism

A

Normocytic and normochromic cells concomitantly observed with microcytic-hypochromic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Sideroblastic anemia tx (hereditary)

A

Pyridoxine (B6) therapy; life-long maintenance therapy at a lowered dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Sideroblastic anemia tx (congenital)

A

Stem cell transplantation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Sideroblastic anemia tx (myelodysplastic synd (decreased RBC production))

A

Recombinant human erythropoietin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q
  • Pancytopenia
A

Reduction or absence of all three types of blood cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q
  • Most aplastic anemias are
A

autoimmune disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Aplastic anemia patho

A

Hypocellular bone marrow that has been replaced with fat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q
  • Paroxysmal nocturnal hemoglobinuria: deficiency in
A

CD55 and CD59: Cause complement-mediated intravascular lysis and release of hemoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

hapten model

A

Drug-induced hemolytic anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Drug-induced hemolytic anemia most common cause

A

cephalosporins. others also PCN and hydrocortisone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

hemolytic anemia s/s

A

o May be asymptomatic
o Jaundice (icterus)
o Splenomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

hemolytic anemia tx first line

A

Corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

hemolytic anemia tx 2nd line

A

Splenectomy and Rituximab (Rituxan) (monoclonal antibody)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
o Paroxysmal nocturnal hemoglobinuria tx
Eculizumab (Solaris)
26
* Polycythemia vera: acquired mutation in
Janus kinase 2 (JAK2) - * Negates the self-regulatory activity of JAK2 that allows the erythropoietin receptor to be constitutively active, regardless of the level of erythropoietin.
27
Polycythemia vera can convert to
acute myeloid leukemia (AML)
28
Polycythemia vera s/s
splenomegaly. painful itching by heat or water
29
Polycythemia vera tx
phlebotomy )300-500cc). spirin, interferon-a, hydroxyurea, radioactive phosphorus
30
* Hereditary hemochromatosis: autosomal...
recessive
31
Hereditary hemochromatosis
increased gastrointestinal iron absorption with subsequent tissue iron deposition
32
Hereditary hemochromatosis s/s
 Hepatomegaly, abnormal liver enzymes, bronzed skin, diabetes, and cardiomegaly
33
Hereditary hemochromatosis tx
Phlebotomy; refrain from taking iron and vitamin C supplements and consuming raw shellfish; alcohol use in moderation
34
AML mutation
tyrosine kinase FLT3
35
ALL genetic anomoly
Philadelphia chromosome on chromosome 9and 22
36
CML genetics
Philly chromosome present and BCR-ABL1 causes intiaiton
37
CLL most common s/s
lymphadenopathy
38
CML cure
no cure
39
non hodgkins lymphoma cells
B cells, T cells, and NK cells
40
more localized: hodgkins or non?
hodgkins
41
Burkitt lymphoma
highly aggressive B-cell non-hodgkin lymphoma of jaw. EBV 90%. abd swelling. Rituximab tx
42
lymphoblastic lymphoma
rare non-hodgkin type.
43
lymphoblastic lymphoma population
1/3 in male children and adolescents
44
lymphoblastic lymphoma origin
T-cell in thymus 85%
45
lymphoblastic lymphoma first s/s
painless lymphadenopathy in neck
46
multiple myeloma translocation
imglobulin heavy chain on chromo 14
47
multiple myeloma patho
production of too much M protein (abnorm antibody). Light chains (Bence Jones proteins) pass through glomerulus and cause kidney damage
48
multiple myeloma s/s
hypercalc, renal failure, anemia, lytic lesions, infections
49
Occurs before multiple myeloma
Monoclonal Gammopathy of Undetermined Significance
50
Monoclonal Gammopathy of Undetermined Significance diagnosis
presence of an M protein in the blood or urine without additional evidence of multiple myeloma
51
Waldenström Macroglobulinemia
lymphoplasmacytic lymphoma. rare type of slow-growing plasma cell tumor that secretes a monoclonal immunoglobulin M (IgM) molecule. Arises from plasma cells that have genetic rearrangement of region genes (V, D, J)
52
Thrombocytosis
Plt >400k
53
Immune thrombocytopenic purpura: Ig_ antibody targets platelet _.
IgG, glycoprotein
54
procoagulant factors
7,9,10
55
vitamin K makes
prothrombin, procoag factors 79,10), and protein c and s (anticoags)
56
DIC patho
release of tissue factor leading to increased fibrin and thrombin activity. and increased fibrinolysis. overconsumption of platelets and clotting factors
57
primary thrombophilia
hereditary. defect in proteins for hemostasis
58
secondary thrombophilia
acquired. decreased anticoag proteins
59
hereditary thrombophilia (primary) are mostly autosomal...
dominant
60
antiphospholipid syndrome
autoimmune antibodies against plasma membrane phospholipids. tx: heparin with aspirin
61
normal rbc lifespan for full term infants
60-80 days
62
rbc lifespan for preemies
20-30 days
63
when are normal adult hgb % established
6-12 M
64
when do erythrocyte production begin in bone marrow
5 M gestation
65
hemolytic disease of newborn
erythroblastosis fetalis. alloimmune disease. Maternal blood and fetal blood incompatibility.
66
hemolytic disease of newborn test and prevention
Coombs test. Rhogam
67
glucose 6 phosphate dehydrogenase deficiency: genetics
x-linked, recessive
68
glucose 6 phosphate dehydrogenase deficiency
G6PD maintains RBC metabolic processes. Deficiency shortens lifespan. Only happens when stressors are present
69
Heinz bodies
denatures hgb in RBCs. seen in glucose 6 phosphate dehydrogenase deficiency.
70
Hereditary spherocytosis
congenital hemolytic anemia causing abn proteins and increased intracellular Na+. no hemoglobin abnormality exists
71
Hereditary spherocytosis is autosomal...
dominant
72
Hereditary spherocytosis s/s and tx
anemia, jaundice, splenomegaly. Folic acid and partial splenectomy.
73
Sickle cell genetics
valine is replaced with glutamic acid. Autosomal recessive
74
aplastic crisis
occurs d/t a viral infxn in sickle cell disease
75
Thalassemias are autosomal...
recessive
76
beta-thalassemia minor
mild-mod microcytic-hypochromic anemia.
77
alpha-thalassemia minor
2 genes
78
alpha-thalassemia major
4 genes, fatal
79
hgb H disease
3 genes
80
Hemophilia A
Factor 8 deficiency. X-linked
81
Hemophilia B
Xmas disease. Factor 9 deficiency
82
Hemophilia C
Factor 11 deficiency
83
von wilibrand disease
autosomal dominant. factor 8 defiency
84
Primary use for cryo
Hemophilia A. Blood factor 8
85
What increases factor 8 activity
Desmopressin (ADH)
86
Heparin requires what for action
antithrombin 3
87
Heparin inhibits what factors
9a, 10a, 11a, 12a, and thrombin (2)
88
t1/2 of heparin increases with
liver or renal disease
89
heparin is found in
mast cell and nerve terminal vesicles
90
heparin structure
glycosaminoglycan
91
dextran -_ is fromed from dextran -_
40,70
92
dextran-40 is removed in
the glomerulus
93
dextran-70 is converted to
glucose
94
which blood sub is actual O2 carrying
perfluorocarbons. not in market d/t surfactant destruction
95
the platelet plug is strengthened by the addition of
fibrin via coag cascade
96
PG-I2 produced by and action
COX-2. inhibits plt aggreg and vasodilates
97
TX-A2 produced by and action
COX1. plt aggreg and vasoconstricts
98
apsirin is covalently bonded to
COX-1> COX-2
99
high CAMP levels _ aggregation
inhibits
100
CAMP is controlled by
TX-A2 and others
101
Diprydamole
PDE-5 inhibitor. weaky anitplt. given with warfarin. can induce angina
102
ADP inhibitor MOA and examples
blocks decrease in CAMP by P2Y12 proteins - clopidogrel: prodrug - ticlopidine: prodrug -Cangrelor -Ticagrelor -Prasugrel
103
ADP inhibitor who cant tolerate aspirin
ticlopidine
104
irreversible oral ADP Inhibitor
prasugrel
105
reversible oral ADP Inhibitor
ticagrelor
106
glycoprotein 2b/3a receptors. Inhibitors ex:
where fibrinogen binds on plts -abciximab -eptifibatide: peptide -tirofiban: non peptide tyrosine
107
Hirudin
thrombin inhibitor. peptide. doesnt need AT3 like heparin and can replace heparin
108
bivalirudin
similar to hirudin
109
Argotraban. What does it trigger?
thrombin inhibitor. arginine derivative. Triggers nitric oxide release
110
does heparin cross placenta?
no
111
LMWH
Lovenox. requires PENTAsacchiride like heparin
112
fondaparinux inhibits?
LMWH. acts with AT3 to inhibit 10a, not thrombin
113
warfarin reversal
vit K or FFP to provide prothrombin
114
warfarin clearance rated decreased by
amio, cimetadine, omeprazole
115
does warfarin cross the placenta?
yes
116
Dabigatran
esterase prodrug activated by by plasma and liver esterases
117
-XABANs MOA
inhibitors of factor 10a
118
apixaban also inhibits
prothrombinase which converts prothrombin (factor 2) to thrombin (2a)
119
Adexanet alfa
reverses factor 10a inhibitors
120
Thrombolytic agents
streptokinase, alteplase
121
streptokinase isoalted from
beta-hemolytic streptococci. possible allergic reaction
122
alteplase
Tissue plasminogen activator (TPA)

PathoPharm 2 (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions