Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

SBL Block 1 > Red Blood Cells > Flashcards

Red Blood Cells Flashcards

1
Q

Anemia Classifications
Size (3) Hemoglobin (2) Shape (2)
Measurements (4)

A

Normocytic, Microcytic, Macrocytic

Normochromic, Hypochromic

Poikilocytic, Non-Poikilocytic

Mean Cell Volume
Mean Cell Hemoglobin
Mean Cell Hemoglobin Concentration
Red Cell Distribution Width

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q 
Acute Blood Loss
Compensatory Changes (4)
A 
Increased CFU-E cells (RBC progenitors)
Become Reticulocytes (5 days)

Leukocytosis and Thrombocytosis also occur

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

Hemolytic Anemias

Extravascular (2) Intravascular (6) Unique Characteristics

A

Extravascular:
Splenomegaly
Caused by decreased RBC deformability

Intravascular:
Hemoglobinemia, Hemoglobinuria
Caused by mechanical injury to normal cells
Also caused by toxins, parasites and complement

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

Hemolytic Anemias

Common Clinical Features (3) Lab Features (3) Blood Smear (2)

A

Anemia
Jaundice
Cholelithiasis

Decreased Haptoglobin
Unconjugated bilirubinemia
Hemosiderinuria

Increased normoblasts
Reticulocytosis

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

Hereditary Spherocytosis

Pathogenesis (3) Diagnosis (2) Presentation (3) Crisis Syndromes (2)

A

Mutated cell membrane proteins ankyrin and spectrin
Cells become spheroid and less deformable
Spleen traps and destroys RBCs

Increased sensitivity of RBCs to osmotic lysis (osmotic fragility test)
Increased mean cell hemoglobin concentration

Anemia, Splenomegaly, Jaundice

Aplastic Crisis: caused by Parvovirus destruction of RBC progenitors

Hemolytic Crisis: caused by increased splenic RBC destruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

G6PD Deficiency

Pathogenesis (2) Morphology, Presentation (4) Worse Variant

A

Decreased NADPH causes decreased protection against oxidative stress
ROS cause intra/extravascular hemolysis

Heinz Bodies

Episodic Hemolysis:
Following Infection, Drugs, Fava beans

Mediterranean variant shows worse hemolysis

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

Sickle Cell Disease

Pathogenesis (4) Blood Smear (3) Complications (4)

A

Point mutation of beta-globin
Glutamate to Valine substitution creates HbS
Increased MCHC, decreasaed pH and slow blood flow increase sickling
Mononuclear cells phagocytose sickled cells causing extravascular hemolysis

Irreversibly sickled cells
Target cells
Howell-Jolly bodies in RBCs

Autosplenectomy
Priapism
Stroke
Retinopathy

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

Vaso-Occlusive Sickle Cell Crises
Pathogenesis, Examples with Descriptions
Hand-Foot, Acute Chest (2)

A

Hypoxic injury and infarction

Hand-Foot Syndrome: bone pain in kids
Acute Chest Pain: caused by lung infection, life threatening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Non-Occlusive Sickle Cell Crisis Descriptions

Sequestration (3) Aplastic

A

Sequestration Crisis: in kids, entrapment of RBCs in spleen, can cause life threatening shock

Aplastic: Parvovirus B19 RBC progenitor infection

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

Thalassemia Syndromes

Genetics (4) General Pathogenesis and Presentation

A

Genetics:
Beta - Point mutations of single Beta-globin gene on Chromosome 11
Alpha - Deletions of a pair of Alpha-globin genes on Chromosome 16

Anemia caused by decreased RBC production and lifespan

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

Beta-Thalassemia

Pathogenesis (2) Secondary Complication, Blood Smear (4)

A

Anemia caused by two mechanisms:
Decreased HbA synthesis
Imbalanced alpha-beta synthesis causes membrane damage that decreases RBC survival (EV hemolysis)

Secondary Hemochromatosis from ineffective erythropoiesis

Anisocytosis (varying size)
Poikilocytosis
Hypochromia
Microcytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q 
Beta-Thalassemia Major vs Minor
Clinical Features (5/2) Lab Values (1/1) Major Treatment (3)
A

Major Clinical:
Anemia starting 6-9 months after birth (HbA needed)
Growth retardation and death at early age
Enlarged bones
Hepatosplenomegaly
Cardiac failure from hemochromatosis

Minor Clinical:
Usually asymptomatic
Mild anemia

Lab values
Major: Elevated HbF
Minor: Elevated HbA2

Treat Major with Iron chelation and blood transfusions
May cure with hematopoietic stem cell transplant

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

alpha-Thalassemia
Types with Descriptions
Silent Carrier (2) a-Thalassemia Trait (3) HbH Disease (4) Hydrops Fetalis (4)

A

Silent Carrier:
Missing one alpha-globin gene
Asymptomatic

Trait:
Missing two alpha-globin genes
Minimal microcytic anemia
If both deleted from one chromosome, can cause symptomatic a-Thalassemia in offspring

HbH Disease:
Missing three alpha-globin genes
Forms Beta tetramers
Tissue hypoxia disproportionate to level of HgB
Can cause Sequestration Crisis

Hydrops Fetalis:
Caused by four missing alpha-globin genes
Formation of Hemoglobin Barts (gamma tetramers)
Fetus shows edema, hepatosplenomegaly, pallor
Lifelong chelation and transfusion dependence

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

Paroxysmal Nocturnal Hemoglobinuria

Genetics (2) Pathogenesis (3) Complications (3) Diagnosis, Treatment

A

Phosphatidylinositol glycan complementation group A (PIGA) gene mutation
Only hemolytic anemia caused by acquired defect

Mutation causes GPI-linked protein deficiency
RBCs susceptible to lysis via C5b-C9 MAC
Causes intravascular hemolysis

Hemosiderinuria causing iron deficiency
Venous thrombosis (leading cause of death)
Acute myeloid leukemia or myelodysplastic syndrome

Diagnose with flow cytometry

Treat with Eculizumab

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

Warm Antibody Immunohemolytic Anemia
Etiologies: Primary/Secondary (3) Pathogenesis (3)
Drug-Induced Mechanisms (2)

A

Primary idiopathic
Secondary - Lupus, Drugs, Lymphoid neoplasms

IgG coats RBCs
Phagocytes remove membrane, forming spherocytes
Spleen destroys spherocytes

Drug Antigens bind RBCs and are attacked
Drugs induce the production of auto-Abs against RBCs

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

Cold Agglutinin Immunohemolytic Anemia

Etiologies: Acute (2) Chronic (2) Pathogenesis (3) Presentation (2)

A

Acute: mycoplasma pneumoniae, mononucleosis
Chronic: idiopathic, lymphoid neoplasms

IgM binds RBCs in cold periphery
C3b deposited on RBCs
Phagocytes destroy RBCs in liver/spleen/BM

Raynaud phenomenon
Cyanosis in extremities

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

Cold Hemolysin Immunohemolytic Anemia

Etiology, Pathogenesis (2)

A

Post-Viral infection (in kids)

IgG binds P antigen on RBCs in cold periphery
Once in warm areas, complemented-mediated hemolysis

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

RBC Trauma Hemolytic Anemia

Etiologies (2) Pathogenesis (2) Blood Smear (4)

A

Cardiac Valve Prosthetics (artificial mechanical)
Microangiopathic disorders: DIC

Microvascular lesion causing fibrin/platelet deposition
Luminal narrowing increases shear forces on RBCs

Shistocytes (RBC fragments)
Burr cells
Helmet cells
Triangle cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Megaloblastic Anemias

Etiologies (2) Blood Smear (5)

A

Vit B12 deficiency
Folate Deficiency

Macro-Ovalocytes
Nuclear Hypersegmentation of Neutrophils
Hypercellular bone marrow
Giant Metamyelocytes
Band cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Normal B12

Metabolism (4) and Functions (4)

A

Pepsin breaks B12 from natural binding protein
Haptocorrin picks B12 up and carries to SI
Proteases break B12 from Haptocorrin
Intrinsic Factor picks B12 up and sends it to blood in Ileum

Helps synthesize methionine
Important for Folate synthesis and then Thymidine

Helps synthesize Succinyl CoA
Important for proper synthesis of neuronal lipids

21
Q

Pernicious Anemia

Pathogenesis (3) Morphology (2) Complications (2) Clinical Diagnostic Features (4) Treatment

A

T cell mediated AI damage of gastric epithelium
Triggers formation of auto-Abs
Abs destroy intrinsic factor secreting cells, blocking B12 absorption

Fundic gland atrophy
Stomach metaplasia (intestinalization)
Atrophic glossitis (beefy, shiny tongue)
Demyelination of dorsal and lateral spinal tracts

Megaloblastic anemia
Leukopenia with hypersegnmentation
Low serum B12
Elevated homocysteine and methymalonic acid

Can treat megaloblastic anemia with Folate supplementation (does not treat demyelination)

22
Q

Non-Pernicious Anemia Causes of B12 Deficiency (4)

A

Decreased Pepsin
Ileal resection
Gastrectomy (decreased IF)
Tapeworms

23
Q 
Folate
Normal Functions (3) Causes of Deficiency (3) Presentation
A

Purine synthesis
Converts homocysteine to methionine
dTMP synthesis (Thymidine)

Decreased intake (alcoholics)
Increased requirements (pregnancy, cancer, anemias)
Impaired utilization (Methotrexate)

Megaloblastic anemia identical to B12 deficiency

24
Q

Iron Physiology

Distribution (2) Transport, Absorption Regulation (2)

A

Most iron is in heme and enzymes
About 20% is stored as ferritin

Free iron is toxic, Transferrin used to transport instead

Absorption decreased by hepcidin
In response to elevated intrahepatic iron

25
Q

Iron Deficiency Anemia

Etiologies (4) Morphology, Clinical Features (4) Labs (4) Associated Syndrome with Presentation (3)

A 
Dietary lack (infants, elderly, impoverished)
Impaired absorption (sprue, chronic diarrhea)
Increased demand (children, pregnancy)
Chronic blood loss (most common)

Hypochromic Microcytic anemia

Koilonychia (spoon nails)
Fatigue
Alopecia
Glossitis

Elevated Total Iron Binding Capacity (TIBC)
Decreased HCT, Ferritin, Hepcidin

Plummer Vinson Syndrome: Esophageal webs, anemia, glossitis

26
Q

Anemia of Chronic Disease

Etiologies (3) Pathogenesis (3) Labs (6)

A

Chronic Microbial Infections: osteomyelitis, endocarditis
Chronic Immune Disorders: Rheumatoid Arthritis
Neoplasms

Chronic inflammation causes increased IL-6
IL-6 causes increased hepcidin
Increased hepcidin decreases iron absorption and decreases ferroportin function

Decreased TIBC, serum iron, EPO
Elevated Ferritin, Hepcidin, Macrophage Iron

27
Q

Aplastic Anemia

Etiologies (5) Pathogenesis (2) Diagnosis, Clinical Features (5) Prognosis

A 
Acquired - Idiopathic
Chemicals - Chemo drugs
Physical Agents - Viral infections
Whole body Irradiation
Inherited: Telomerase Defects, Fanconi anemia

Extrinsic immune mediated suppression of marrow progenitors
Intrinsic abnormalities of hematopoietic stem cells

“Dry” bone marrow tap devoid of hematopoietic stem cells (hypocellular)

Pancytopenia:
Reticulocytopenia**
Macrocytic Normochromic Anemia
Petechiae and Ecchymoses (thrombocytopenia)
Frequent Infections (neutropenia)

Good prognosis with bone marrow transplant

28
Q

Pure Red Cell Aplasia

Etiologies (3) Clinical Feature

A

Thymoma
Large Granular Lymphocytic Leukemia
Parvovirus Infection (can persist if immunocompromised)

Primary bone marrow disorder causing only loss of RBCs

29
Q

Myelophthisic Anemia

Etiologies (2) Pathogenesis, Blood Smear (2)

A

Most often from Metastasis
Myeloproliferative disorders

Space occupying lesions replace normal bone marrow elements

Leukoerythroblastosis
Teardrop shaped RBCs

30
Q

Chronic Diseases Associated with Anemia (3)

A

Chronic Renal Failure
Hepatocellular disease
Hypothyroidism

31
Q

Polycythemia
Clinical Description (2) Relative vs Absolute
Primary vs Secondary

A

Abnormally high red blood cell count
Increased Hgb level

Relative: caused by dehydration that decreases plasma volume
Absolute: caused by increased hematopoietic progenitor cells

Primary: Polycythemia vera
EPO-independent growth of RBC progenitors

Secondary: compensatory of pathologic increase in EPO

32
Q

Excessive Bleeding

Causes (3) and Tests with Descriptions (4)

A

Increased vessel fragility
Platelet deficiency or dysfunction
Coagulation issues

Prothrombin Time: Extrinsic, Common coagulation paths
Partial Thromboplastin Time: Intrinsic and Common
Platelet counts
Platelet Function Tests: thrombin, vWf tests

33
Q

Vessel Wall Defects Causing Bleeding

Examples (6)

A

Infections: meningococcemia

Drug Reactions: hypersensitivity reactions

Collagen Defects: Scurvy, Ehlers Danlos

Immune Complex Deposition: Henoch Schonlein

Hereditary Hemorrhagic Telangiectasia

Perivascular Amyloidosis

34
Q 
Thrombocytopenia
Lab Values (3) Causes (4)
A

<100,000 is thrombocytopenia
<20,000 can cause spontaneous bleeding
Normal PT/PTT

Decreased Production: Bone Marrow defects, HIV

Decreased Platelet Survival: Immune-Mediated, DIC, Thrombotic Microangiopathies

Sequestration: Splenomegaly

Dilution: Blood transfusions

35
Q

Chronic Immune Thrombocytopenic Purpura

Pathogenesis, BM/Blood Findings (2) Clinical Features (4) Treatment

A

IgG autoantibodies opsonize membrane glycoproteins IIb/IIa or Ib/IX
Spleen removes opsonized platelets

Increased megakaryocytes
Megathrombocytes in peripheral blood

Petechiae
Ecchymoses
Melena
Hematuria

Glucocorticoids

36
Q

Acute Immune Thrombocytopenic Purpura

Pathogenesis (2) Clinical Features (2)

A

IgG autoantibodies opsonize membrane glycoproteins IIb/IIa or Ib/IX
Spleen removes opsonized platelets

Occurs in Kids after viral illness
Spontaneously regresses

37
Q 
Heparin Induced Thrombocytopenia
Type I (2) and Type II (4)
A

Type I
Occurs right after initiation of therapy
Spontaneously resolves

Type II
Occurs 5-14 days after heparin started
Causes arterial/venous thromboses
Caused by auto-Abs to Heparin-PF4 complexes 
Complexes activate platelets
38
Q

Thrombotic Thrombocytopenic Purpura

Pathogenesis (2) Clinical Pentad

A

ADAMTS13 deficiency
vWF multimers accumulate and activate platelets

Fever
Thrombocytopenia
Microangiopathic Hemolytic Anemia
Transient Neurological Defects
Renal Failure
39
Q 
Hemolytic Uremic Syndrome 
Typical Pathogenesis (2) Atypical Pathogenesis (3) Common Pathologic Feature, Presentation (5)
A

Shiga-like toxin absorbed into circulation
Toxin alters endothelial cells which activates platelets

Atypical HUS
Defects in Complement Factor H, CD46 or Factor I

Both types characterized by excessive activation of complement

Bloody diarrhea followed by:
Fever
Thrombocytopenia
Renal Failure
Microangiopathic Hemolytic Anemia
40
Q

Defective Platelet Function Bleeding
Inherited Etiologies with Examples (3)
Acquired Etiologies (2)

A

Defective Platelet Adhesion:
Bernard Soulier - glycoprotein Ib-IX defect

Defective Platelet Aggregation:
Glanzmann Thrombasthenia - glycoprotein IIb-IIIa defect

Defective Platelet Secretion (storage pool disorders):
Defective TxA2 and ADP release

Aspirin/MSAID induced
Uremia

41
Q

Clotting Factor Deficiencies
Clinical Features (2)
Most Common Inherited Deficiencies (3)
Acquired Deficiencies (2)

A

Large Post-traumatic ecchymoses or hematomas
Prolonged bleeding after any laceration

Factor VIII (hemophilia A)
Factor IX (hemophilia B)
von Willebrand Factor

Vitamin K Deficiency (impaired II, VII, IX, X and Protein C)
Disseminated Intravascular Coagulation

42
Q

von Willebrand Disease
Presentation (3) Lab Values (2)
Type 1 (2) Type 2 (2) Type 3 (3)

A

Mucosal bleeding
Excessive wound bleeding
Menorrhagia

Prolonged PTT and Bleed Time
Reduced ristocetin cofactor activity

Type 1: Autosomal dominant point mutations
Mild deficiency in vWF

Type 2: Missense mutations cause defective multimer formation

Type 3: Autosomal recessive deletions/frameshift
Very low vWF and severe bleeding

43
Q

Hemophilia A

Pathogenesis (3) Lab Value, Diagnosis, Clinical Features (3)

A

X linked recessive Factor VIII mutations
X inversion causes most severe deficiency
May develop antibodies to Factor VIII

Prolonged PTT

Factor VIII assays

Most common cause of life threatening bleeding
Spontaneous hemorrhage
Hemarthroses

44
Q 
Hemophilia B (Christmas Disease)
Pathogenesis, Lab Value, Diagnosis, Clinical Features (2)
A

X linked recessive Factor IX mutations

Prolonged PTT

Factor IX assays

Spontaneous hemorrhage
Hemarthroses

45
Q

Disseminated Intravascular Coagulation

Etiologies (4) Pathogenesis (2) Complications (5) Lab Values (4) Associated Syndromes (2)

A

Obstetric complications
Sepsis (endotoxins)
Malignancies
Major trauma

Release of tissue factor that combines with Factor VII
Endothelial cell injury which increases tissue factor and decreases anticoagulant thrombomodulin

Hypoxia (fibrin deposition)
Microangiopathic hemolytic anemia (fibrin deposition)
Hemorrhage (platelets consumed)
Widespread thrombi in organs
Bilateral renal cortical necrosis

Prolonged PT and PTT
Low fibrinogen
Elevated D Dimer

Waterhouse Friderichsen Syndrome (N meningitidis)
Kasabach-Merritt Syndrome (giant hemangiomas)

46
Q

Febrile Non-hemolytic Reaction

Etiology, Clinical Features (3) Pathogenesis

A

Most common adverse reaction to blood transfusion

Fever
Chills
Dyspnea

Caused by inflammation from donor leukocytes

47
Q 
Blood Transfusion Allergic Reactions
Associated Deficiency (2) Urticaria (2)
A

IgA deficiency predisposes reaction
Caused by IgG-mediated reaction to donor IgA

Urticarial reaction seen if IgE recognizes allergens in donor blood
Responds to antihistamines

48
Q

Hemolytic Transfusion Reactions
Acute: Pathogenesis (2) and Presentation (5) Test
Delayed: Pathogenesis (2) Prognosis

A

Acute
IgM mediated complement attack on donor RBCs
Caused by ABO incompatibility
Fever, shaking, chills, flank pain (severe causes DIC)
(+) Coombs test

Delayed
IgG mediated attack on previously sensitized Ags
Sensitized from prior blood transfusions
Complement activation can be fatal

49
Q

Transfusion Related Acute Lung Injury

Pathogenesis (3) Clinical Features (4)

A

Two Hit Hypothesis:
Primer causes sequestered, sensitized neutrophils in lung microvasculature
Neutrophils activated by MHC I Abs in donor blood
More likely with donations containing high levels of Abs such as fresh frozen plasma and platelets

Sudden onset respiratory failure
Diffuse bilateral lung infiltrates
Hypoxemia
Hypotension

SBL Block 1 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions