Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

SBL 1 > Pathology of RBC and Bleeding Disorders > Flashcards

Pathology of RBC and Bleeding Disorders Flashcards

(53 cards)

Start Studying
1
Q

Hematocrit?

A

Percentage of whole blood voume occupied by RBC’s

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

MCV equation?

A

MCV= HCT/RBC

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

MCH?

A

MCH=Hgb/RBC

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

MCHC?

A

MCHC=Hgb/Hct

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

Describe the values for acute blood loss.

A
  • Normal MCV and MCH
  • Retic count will be low initially and will slowly rise to compensate for anemia in 6-7 days
  • Annemia will show through low Hgb and Hct after 6 to 12 hrs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What anemias are in the catergory of Hemolytic?

A
  • HS
  • G6PD def
  • SC
  • Thalassemia
  • PNH
  • Immunohemolytic anemia
  • Hemolytic anemia due to trauma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is HS? How to treat? How does it present?

A
  • unstable membrane skeletal proteins on RBC’s
  • travel through the spleen where they are destroyed due to their lack of flexibility
    • Hypersplenism
  • Remove the spleen to increase the lifespan of the RBC’s
    • Howell Jolly bodies present with spleen removed
  • Anemia, Jaundice, Splenomegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where is G6PD deficiency common?

A
  • Sub sarahan africa
  • Middle east
  • Mediterranean
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What happens in G6PD deficiency?

A
  • Episodic hemolysis due to oxidative stress caused by:
    • drugs
    • stress
    • infection
    • fava beans
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are heinz bodies?

A
  • precipitation of denatured Hbg and other stromal proteins due to oxidative damage
  • Cells with heinz bodies can’t go through spleen and either get destroyed or heinz bodies removed leading to Bite Cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What mutation causes Sickle cell?

A
  • Mutation in B chain of Hbg
    • GAG to GTG (Glu to Val)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What makes polymerization of Sickle Cell more likely?

A
  • Hypoxia
  • Intracell dehydradation
  • Low pH
  • Sluggish blood flow
  • Sickled cells undergo vascular hemolysis
  • Vaso occlusion leads to under perfusion looping back around to hypoxia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

In what disease will you see target cells?

A
  • SC disease, a milder disease than Sickle Cell
  • The Hbg C can crystalize but it doesn’t polymerize
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What drug is used to treat sickle cell?

A

Hyrdoxyurea, it increases HgbF

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

B Thal Major?

A
  • Severe anemia
  • Preferential switch to Hgb F
  • Dramatic medullary and extramedullary hematopoiesis
  • See “crew cut” from bonw marrow expansion on x ray
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What disease is indicated

A

B Thal Major

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

B Thal Minor?

A
  • Microcytic anemia
  • Mild and asymptomatic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

a-Thalassemia 3 genes?

A
  • HbH disease
  • High oxygen affinity
  • Hemolytic and Microcytic anemia and splenomegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

a-Thalassemia 4 genes?

A

Hb Barts (Hydrops Fetalis)

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

Parozysmal Nocturnal Hemoglobinuria?

A
  • PIGA mutations affecting HSC so all derived cells are affected
  • Cells lack CD55 and CD59 to protect them from lysis by complement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is PNH a risk factor for?

A

MDS/AML

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

How do you treat PNH?

Study These Flashcards
A
  • Eculizamab, a targeted therapy that blocks C5 and C5a
23
Q

What is a “Warm Ab”?

Study These Flashcards
A
  • IgG
  • Idiopathic: autoimmune hemolytic anemia
  • Secondary:
    • CLL
    • Lymphoma
    • SLE
    • Drug related
24
Q

Cold Ab?

Study These Flashcards
A
  • Idiopathic: Chronic hemagglutinin disease
  • Secondary:
    • Mono
    • Mycoplasma pneumonia
    • Lymphoma
25
What is a direct Coombs test?
* Detects presence of Ab bound to red cell surface
26
What is the indirect Coombs test?
Detects Ab in the plasma
27
Warm Hemolytic anemia?
* IgG * Opsonized cells are phagocytosed in the spleen or they gradually lose their membranes * Autoimmune or drugs
28
Cold hemolytic anemia?
* IgM * Strong affinity at lower temp * More likely to manifest in the nose and fingertips (raynaud) * IgM leads to C3b deposition and the liver spleen and bone marrow remove the cells
29
what is indicated if you have a high retic count? (general)
* Bleeding or destruction of RBC's
30
What is indicatetd if you have a low retic count?
* RBC production problem
31
What causes megaloblastic anemia?
* Impaired DNA synthesis * Anemia occurs as a result of not being able to produce RBC's and growth factor production increases * Marrow hyperplasia occurs but hematopoiesis is ineffective
32
With megaloblastic anemia what is seen in the peripheral blood?
* Hypoproliferative (low retic) * Macrocytic (high MCV) * Ovalocytes * Neutrophil hypersegmentation
33
What is pernicious anemia?
* Megaloblastic anemia caused by autoimmunity typically seen in older adults * Abs directed against parietal cells which secrete Intrinsic Factor * IF needed for B12 absorption * B12 needed for DNA synthesis * Chronic atrophic gastritis can lead to megaloblastic anemia * which can lead to spinal (and brain/peripiheral nerves) demyelination
34
What byproduct of DNA synthesis is high in Pernicious anemia?
* High levels of homocysteine/ MM Co-A
35
Iron Deficiency Anemia * hypoproliferative * Microcytic * Hypochromic * Anisocytosis
36
Physical manifestations of Iron deficiency anemia?
* Koilonychia * Alopecia * Atrophic glossitis * [Angular chelitis
37
With IDA what will iron studies show?
* Low serum iron * Low serum ferritin * Low Hepcidein * Increased TIBC
38
What is Anemia of chronic disease?
* Impaired RBC production/iron utilization in chronic illnesses * Chronic illness makes the body horde iron instead of utilizing it * Looks similar to IDA
39
What will an Iron study show with Anemia of chronic disease?
* Low serum iron * Reduced TIBC * Increased ferritin * Abundant iron in the tissues
40
A: normal bone marrow B: Aplastic Anemia
41
How do you diagnose Aplastic anemia?
* Anemia * Thrombocytopenia * Leukopenia * Bone marrow full of adipose
42
when do you see pure red cell aplasia?
* Very rare, seen with thymomas * Parvovirus B19 when there is hemolytic anemia * The BM shows decreased erythroid precursors
43
What is Myelophthisic anemia?
* Space occupation in the bone marrow seen in metastatic cancer, fibrosis,inflammation, and necrosis replacing the normal hematopoietic cells * Abnormal release of erythroid and granulocyte precursors results in leukoerythroblastosis (pic)
44
Periorbital bruising can be a sign of what cancer?
Myeloma with perivasscular amyloid deposition
45
What will a patient with Immune thrombocytopenic purpura present with? How do you treat?
* Petechiae and purpura * CBC shows thrombocytopenia, and potentially Ab's to platelets * BM shows increased megakaryocytes due to the lack of platelets * Tx by reducing the immune response with corticosteroids, IVIg, and Rituximab (anti-CD20)
46
What is the pentad of Thrombotic thrombocytopenic purpura?
* Fever * Thrombocytopenia * Microangiopathic hemolytic anemia * Neuro defects * Renal failure
47
What causes TTP? How to treat?
* ADAMTS13 is defective, this is the metalloproteinase that breaks down the multimers of vWF and without this we get massive sized platelet aggregations * Plasma exchange therapy
48
What is the typical presesntation of Hemolytic Uremic Syndrome? and atypical?
* Shiga like toxin elaborated by E. coli O157:H7 (bloody diarrhea) * atypical is variable linked to complement dysfunction * Tx is supportive
49
What is Bernard Soulier and Glanzmann thrombasthenia?
* BS: no adhesion occurs * GT: no aggregation occurs
50
vWF disease type 2 and 2A?
* 2: qualitative defects defined by lack of appropriate interaction with ligands * 2A is most common and defined by a lack of multimer assembly
51
Who is the universal red cell donor and recipient?
* Donor is O * Recipient is AB
52
Who is the universal Plasma donor and recipient?
* Donor: AB * Recipient: O
53
What is a TRALI?
* Acute respiratory failure during or after a transfusion with diffuse bilateral pulmonary infiltrates * May have fever or hypotension and can be fatal

SBL 1 (8 decks)

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