Brainscape's Knowledge GenomeTM

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


See full index

FU17 Hematology > Anemia > Flashcards

Anemia Flashcards

1
Q

Oxygen carrying unit

A

Heme

Contains iron

Also assists in CO2 transport (can pick up CO, NO)

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

Laboratory definition of anemia

A

Hg < 12 g/dL (women), <13 (men)

Hct < 36%, <40%

Can be asymptomatic or symptomatic

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

General s/s of anemia

A

Pallor (conjunctiva, skin, membranes)
Tachycardia
Orthrostasis
Weakness, fatigue

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

How is anemia diagnosed? (Test and associated)

A

CBC

Using parameters

RBC, MCV, RDW, MCHC

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

MCV

A

Tells us the AVERAGE size of the cells

Microcytic (<85)
Normocytic (85-100)
Macrocytic (100+)

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

What indicies must we use in addition to the MCV to diagnose anima ?

A

RDW

Tells us the distribution of the cells (11-16% is good)

Narrow RDW = less size difference between the cells

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

Retic count

A

Dependent upon degree of anemia

Used in anemia to see if the bone marrow is working

Would expect low if bone marrow not working effectively

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

Corrected retic count

A

Bc anemia will give us a typically higher retic count than average we must correct it

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

Corrected retic > 2%

A

Normal proliferation

Could be hemolytic or due to acute blood loss

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

Corrected retic < 2%

A

Hypoproliferation in bone marrow

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

Tests comprising iron studies (5)

A
  1. Iron (iron levels in serum)
  2. Transferrin (amount of transferrin in blood)
  3. TIBC (available transferrin in blood)
  4. % sat (amount of transferrin with iron)
  5. Ferritin – impacted by inflammation or infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Additional tests to evaluate anemia (after iron studies)

A

B -12 and folate levels

LFTs (specifically LDH)

Haptaglobin

TSH

SPEP/UPEP

DAT

BM bx

Hg.Genetic testing

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

Mild anemia workup

A
  1. Evaluate for heavy blood loss
  2. Order initial work up (iron studies, b-12 and folate)
  3. Treat or move towards urgent eval
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Severe anemia evaluation

A
  1. Evaluate for blood loss (GI bleed – not menstrual at this point)
  2. Order initial work up + LDH, haptaglobin, retic, DAT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Target cells

Peripheral blood smear

A

Caused by membrane defect

Thalassemia or liver dz

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

Peripheral blood smear

Schistocytes

A

Helmet fragments

Seen in INTRAVASCULAR hemolytic processes (DIC)

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

Peripheral blood smear

Basophilic stippling

A

Blue stipples appearance

Seen in lead toxicity (microcytic anemia)

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

Peripheral blood smear

Rouleaux formation

A

RBC staked like coins

Due to high paraprotein in blood

Indicates multiple myeloma

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

Types of microcytic anemias (5)

A
  1. Iron deficiency anemia
  2. Lead poisoning
  3. Anemia of chronic disease
  4. Sideroblastic anemia
  5. Thalassemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Where is iron absorbed from

A

Proximal duodenum and moved thru blood by transferrin to marrow

When RBCs are broken down in liver, iron is recycled and carried to marrow

Small amount of iron is lost daily but most of it is retained

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

MC cause of microcytic anemia

A

Iron deficiency

Typically hypochromia and can cause thrombocytosis

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

Epidemiology of IDA

A

Women of childbearing age (heavy menses)

Vegetarians, infants, pregnancy women, celiac or IBDs

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

Conditions/symptoms associated with IDA

A

PICA

RLS/leg cramps

Cold intolerance

Esophageal webs

Chelitits

Koilonychia

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

Etiology of IDA

A

Iron loss (menstruation, GI bleed, chronic low grade hemolysis)

Insufficient absorption (poor intake, malabsorption by gut)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

IDA

CBC results

A

Hypochromia

microcytic anemia

+/- thrombocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Peripheral smear

IDA

A

No structural abnormalities

Uniform size – just small

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Iron studies

IDA

A

Iron: LOW

** Transferrin: HIGH

TIBC: high

% saturation: LOW

Ferritin: LOW

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

IDA workup (4 steps)

A
  1. Women with heavy periods – begin Fe replacement, check
  2. M/f w/o menses - suspect GI bleed so endoscopy, colonoscopy
  3. No finding of blood loss yet, will do capsule scope to look at SI
  4. Nothing yet, workup for malabsorption (celiac)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

IDA treatment

A

Oral Ferrous sulfate (325 mg) given up to 3x/day

Should be taken with vitamin C on empty stomach (to maximize absorption)

Other formulations are available but not great (parentarel venofer if nec. - low anaphylaxis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How long on IDA treatment before results are seen?

A

Retic count should increase in 5-10 days, HgB should increase 1-2 gm/2 weeks

Typ. Takes 3-4 months to get to normal

Prevention is done by taking supplemental iron (infants, vegetarians, pregnant)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Caution in treating IDA + remedy

A

Iron overload

Can happen in transfusion (200mg/unit PRBC)

Can’t get rid of excess iron so will store in improper organs

TReAMENT: chelation or phlebotomy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Disorder caused by genetic defect causing decrease in alpha or beta chain production

A

Thalassemia

African, Asian, Mediterranean

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Alpha thalassemia

A

Impaired alpha chain production – too many beta chains

May allow malaria prevention

Four subtypes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What does the HgB look like in alpha thalassemia

A

The Beta chains can form stable tetramers so they will get out into the serum (little effect on erythropoiesis)

BUT beta chains have a high O2 affinity so it can hold, but not release oxygen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Types of alpha thalassemia

A
  1. Alpha thalassemia minima
  2. Alpha thalassemia minor/trait
  3. Alpha thalassemia/HgH
  4. Fetal Hydrops
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Alpha thalassemia minima

A

Deletion of 1 alpha gene

Silent carrier

No abnormalities in smear or CBC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Alpha thalassemia Minor

A

2 genes deleted

Minimal anemia with reduced MCV (minor microcytic anemia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Alpha thalassemia/ HgH

A

Significant production of beta tetramers

Microcytic anemia and intravascular hemolysis

Target cells and Heinz bodies on smear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Fetal Hydrops

A

4 alpha genes are missing

Incompatible with life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

HgH disease tetramers (+ symptoms)

A

B chain tetramers

Soluble but not stable when under stress

They precipitate out but are hemolyized in the vessels

Significant anemia, jaundice with papal leaders splenomegdaly

Significant reticulocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Beta thalassemia

A

Suppression of beta chain production resulting in over production of alpha chains

Alpha chains are not able to form tetramers so they are destroyed in the marrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Types of beta thalassemia

A
  1. Beta thalassemia minor

2. Beta thalassemia major

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Beta thalassemia minor

CBC

A

Asymptomatic but significant microcytosis

Normalish Hct, Narrow RDW

High RBC counts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Beta thalassemia
Minor

Peripheral smear

A

Hypochromia

Microcytosis

Target cells and dacrocytes

45
Q

Beta thalassemia major

A

Infants fall ill after 6 months of life (due to production of gamma globulin)

Chronic anemia and hemolysis (moderate to severe)

Pts develop failure to thrive, abdominal swelling and jaundice

Extramedullary RBC production –> craniofacial probelms and hepatosplenomegaly

Iron overload, high output heart failure

46
Q

Thalassemia workup

A

Genetic testing to determine the gene profile and specific mutation

47
Q

Treament of Beta thalassemia major

A

Hypertransfuison therapy (2-4 weeks to suppress extramedullary hematopoiesis)

Iron chelation

Maybe a hematopoietic stem cell transplant

Alphas are monitored and supported

48
Q

Lead poisoning

A

Becoming more rare

Can be found in lead paint (old homes), moonshine consumption, lead fume, contamination

49
Q

Lead poisoning anemia

A

Interference with HgB synthesis and other effects

Cognitive damage, decreased growth, deposition of lead in other dry symptoms

50
Q

Lead poisoning anemia results

A

Microcytic or normocytic anemia with basophilic stippling on smear

Diagnosed by getting lead levels

EDTA chelation treament

51
Q

What must we rule out with lead poisoning

A

Iron deficiency anemia as well bc lead will interfere with iron absorption in the gut

52
Q

Sideroblastic anemia

A

Nucleated red blood cell precursors with iron rods are released into the blood

Diagnosed with BMbx

Caused by aberrations in processing of iron iron by eruthroblast

53
Q

Normocytic anemia causes

A
  1. Anemia of chronic disease
  2. Acute blood loss anemia
  3. Multiple myeloma
  4. Anemia of CKD
  5. Myelofibrosis/myelophthsic anemia
  6. Aplastic anemia
  7. Pure red cell aplasia
  8. Thyroid dz
54
Q

Anemia of chronic disease

A

Occurs secondary to any inflammatory, infectious, or malignant disease of a long standing nature (HIV, hepatitis, RA, CAD, DM)

Normocytic or microcytic

55
Q

ACD pathophysiology

A

Decreased iron + decreased erythropoietin + early RBC death

Inflammation causes increased hepcidin which therefore causes decreased absorption

56
Q

ACD iron studies

A
  1. Serum iron: low
  2. Transferrin: low/normal
  3. TIBC: low/normal
  4. Ferritin : elevated (inflammation)
57
Q

ACD treatment

A

Treatment of underlying condition

Can use ESA but not recommended.

58
Q

Acute blood loss anemia

A

Symptoms of volume depletion ass. With significant blood loss

Falsely elevated H & H until equiliberation

59
Q

What kind of things cause acute blood loss anemia?

A

Surgery
Childbirth
Trauma
GI bleed

60
Q

Anemia due to multiple myeloma

A

Plasma cell overproduction suppresses the other cell lines

Causing normocytic anemia, neutropenia, thrombocytopenia

Bone pain (lytic lesions, renal failure, hypercalcemia)

61
Q

Anemia due to multiple myeloma

Peripheral smear and diagnosis

A

Smear: Rouleaux formation

Diagnosis w/ SPEP/UPEP

Treatment: treat MM + transfusion support

62
Q

Anemia of CKD

A

Normocytic anemia due to decreased erythropoietin
Production in kidney

Only seen once patient is at stage 3 CKD ( GFR < 45%)

63
Q

Anemia of CKD MC in which patients

A

Black, male, older

Bc high rates of CKD

64
Q

Anemia of CKD with multifactorial…

A

Cocontaminant with folate and IDA due to nutrient deficiency

Also due to decreased RBC survive and blood loss on hemodialysis

65
Q

Treatment of anemia due to CKD

A

Titrated erythropoietin stimulation agent (ESA) – keep HgB levels b/t 10-12

Too much ESA can cause cardiac events, raise BP, and cause seizures

66
Q

Myelophthisic Anemia

A

Collection of disorders that infiltrate the bone marrow and crowd out normal cellular precursors of RBCs, WBCs, and platelets therefore causing normocytic anemia

Associated with extramedullary hematopoietisis resulting in splenomegdaly

67
Q

Infiltration processes in myelophthisic anemia

A
  1. Metastatic cancers to bone
  2. Tuberculosis
  3. Lymphoma/myeloma
  4. Lipid storage disorders
68
Q

Symptoms of myelophthisic anemia

A

Suspected in patients with moderately severe normocytic normochromic anemia

Reticulocytosis occurs (not indicated by increased blood regeneration)

69
Q

Myelophthisic anemia

Peripheral smear

A

Immature myeloid cells and nucleated RBCs

Extreme variation in size and shape

70
Q

Myelophthisic anemia diagnosis and treatment

A

BM bx

Treat underlying dz

71
Q

Myeloidfibrosis

A

Normocytic anemia caused by the deposition of scar tissue in the bone marrow

Replaces the cellular line precursor (low RBCs and all other cell lines)

72
Q

Myelofibrosis peripheral smear + BMbx

A

RBC fragments and dacrocytes on smear

Fibrosis in BM - “dry tap_ due to lack of cells

73
Q

Aplastic anemia

A

Normocytic anemia with concomitant pancytopenia

Congenital and acquired forms

Diagnosed with BMbx (hypocellular) and treated by removing offending agent

74
Q

Congenital aplastic anemia

A

Rare

Fanconi

Cafe-at-lait spots, short stature, aplastic anemia, skeletal abnormalities

75
Q

Acquired aplastic anemia

A

Via medications (chemo, sulfa drugs), toxins, infections, radiation, autoimmune

76
Q

Pure red cell aplasia

A

Aplastic anemia w/o pancytopenia

Acquired and congenital (Diamond black)

diagnosed with BMbx - low erythroid precursors w/plenty WBC and megakaryocytes

Treat underlying disorder, test for thymoma

77
Q

Etiologies of acquired pure red cell aplasia

A 
Thymoma 
Neoplasm 
Collagen dz 
Drug (e-mycin, isoniazid) 
Autoimmune 
Infection (parvo, EBV, hepatitis)
78
Q

Normocytic anemia workup

A
  1. Chemistry panel and TSH
  2. SPEP/UPEP
  3. Peripheral smear

If diagnosis still unknown do BMbx (aspiration and trephine)

79
Q

Macrocytic anemia

A

MCV > 100 and corrected retic of <2%

Two categories : megoblastic and non megoblastic

80
Q

Non megoblastic macrocytic anemia (list)

A

Anemia with normal WBC nuclei

  1. Liver dz
  2. Chronic alcohol use
  3. Hypothyroidism
81
Q

Megaloblastic macrocytic anemias

A

Abnormally slow nuclear maturation of RBC precursors and hypersegmented neutrophils

  1. Vitamin B12 def.
  2. Folate def.
  3. Drugs
  4. Myelodysplastic syndrome
82
Q

Medications that cause macrocytosis

A

Chemotheraputic agents

Metformin

Anticonvulsants

83
Q

B-12 absorption

A

Completely thru diet

In terminal ileum

Req. intrinsic factor (secreted by parietal cells in stomach)

Body has many stores of B12 and takes a long time to develop

84
Q

Etiologies of B12 def.

A

Due to malabsorption or dietary deficient

  1. Bacterial overgrowth
  2. Inflammatory disease in terminal ileum (esp. chron’s)
  3. Poor dietary intake (vegans)
85
Q

Pernicious anemia

A

Caused by strophic gastritis and lack of parietal cell production

While the person is consuming enough B12, lack of intrinsic factor means it is not picked up - so it is a lack of b12

86
Q

Atrophic gastritis

A

Typically the cause of pernicious anemia

Body produces auto-antibodies to parietal cells therefore they are tagged by Abs and removed before they can preform their action in the intestine

Can also be seen in patients with partial gastretomy

87
Q

S/s of b12 anemia (CNS)

A

Degeneration of spinal cord before macrocytosis

Symmetrical lower extremity parenthesis, loss of vibratory and proprioception, weakness

Spasticity and Babinski signs (ataxia - esp in dark)

Dementia, irritability, memory loss

88
Q

Other B12 anemia s/s

A

Atrophic glossitits

Flattening fo intestinal villi

Skin change

89
Q

How is b12 def. diagnosed? Treated?

A

Low vitamin b12 levels

Also methylmalonic acid level (if elevated = B12 problems)

Treatment: vitamin b12 intramuscular injection

90
Q

Folate deficiency anemia

A

Rapid macrocytic anemia +/- leukopenia and thrombocytopenia

Cofactors in DNA replication and division

91
Q

Causes of folate def. anemia

A
  1. Nutritional def./malabsorption
  2. Alcoholism/Cirrhosis
  3. Pregnancy
  4. Medications
92
Q

Folate anemia diagnosis and treatment

A

D: RBC folate levels and homocysteine levels (elevated in def.)

T: supplemental folate

93
Q

Myelodysplastic anemia

A

Group of clonal disorders that affect prescursors of RBC, WBC, and platelets

Marrow is hypercellular or hypocellular and maturation is impaired

Causes anemia, +/- pancytopenia

May not be known or secondary to chemotherapty and radiation

94
Q

Diagnosis of myelodysplastic syndrome

A

Typically premalignant, +70

Found incidentally, cytopenia on CBC

Made via BMbx and treated with medications depending on subtype

95
Q

Peripheral smear of Myelodysplastic syndrome

A

Bi-lobed hyposegmented neutrophils –> Pseudo-Pleger Huet Cells

96
Q

Why does liver disease cause macrocytic anemia?

A

Increased cholesterol and phospholipid deposition in the cell wall

97
Q

Alcohol macrocytic anemia

A

Alcohol is toxic to bone marrow – delays maturation

Additionally often have b12 or folate deficiency and liver disease

Symptoms will persist months after cessation

98
Q

Hemolytic anemias

A

Anemia caused by lysis of EBCs

Always associated with elevated corrected retic count if only disease present

Divided by cause of hemolysis: intracorpuscular and extracorpuscular

Or by site of hemolysis: extravascular, intravascular, intramedullary

99
Q

Intracorpuscular hemolytic anemia

A

Hemolysis caused by RBC problem

  1. membrane defects
  2. enzyme defects
  3. hemoglobinopathies
100
Q

Extracorpuscular hemolytic anemia

A

Hemolysis due to extrinsic issue

  1. Autoimmune
  2. Microangiopathic
  3. Mechanical valve
101
Q

Extravascular hemolytic anemia

A

RBCs are removed by liver and spleen prematurely

Seen in autoimmune anemia

102
Q

INTRAVASCULAR hemolytic anemia

A

RBC lysis within the vascular system

Seen in microangiopathic

103
Q

Intramedullary hemolytic anemia

A

Destruction of RBCs within the marrow

Seen in thalassemia major

104
Q

Hemolysis workup (results) 4

A
  1. LDH (elevated)
  2. Indirect Bilirubin (elevated)
  3. Haptaglobin (low/absent)
  4. Retic count (elevated)
105
Q

Following blood workup, next step in hemolytic workup

A

Peripheral smear

106
Q

Spherocytes in peripheral smear of hemolytic anemia suggest which type?

A

extravascular

107
Q

Schistocytes in peripheral smear of hemolytic anemia suggest which type?

A

INTRAVASCULAR

108
Q

ABCs of hemolytic anemia

A

A - Air (low oxygen)

B- shape

C- synthesis

D- defective enzymes

E - hostile environment

FU17 Hematology (10 decks)

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