UA WI18-Chapter 10 Blood Disorders Part 1 Flashcards Preview

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Flashcards in UA WI18-Chapter 10 Blood Disorders Part 1 Deck (131):
1

A decrease in the number of RBC or less than normal quantity of Hb in blood.

Anemia

2

Increased amount of RBC in blood.

Polycythemia

3

What are the three main classes of anemia?

Excessive blood loss

Deficient RBC production

Excessive blood cell destruction

4

Sx. Common to all anemia.

Weakness, fatigue, pallor, malaise, dyspnea, tachycardia, murmur(systolic), low blood pressure, dizziness, headaches coldness, weak pulse etc.

5

Acute blood loss is caused _______ and results in _______.

Trauma, surgery, GI tract lesions, Gynecolgic disturbance


Results in hypovolemia

6

Term for decreased blood volume

Hypovolemia

7

In an acute blood loss case report, what would be found?

Decreased platelet

Increased neutrophils (shift left)

Changes in RBC morphology: normal initially—> hypochromic once volume restored

8

Chronic blood loss is caused by______.

When do symptoms appears?

Cancer, menstruation, fibroids in older women and angiodysplasia.

When iron store is depleted

9

In a chronic bleeding case report, what is reported?

Elevated platelets

Leukopenia

RBC morphology: Normocytic or microcytic/ hypochromic

10

What are the causes of deficient RBC production?

Iron-deficiency anemia

Vit. Deficiency anemia

Bone marrow or stem cell problem

Health disorders: i.e renal insufficiency

11

Iron deficient anemia is described as?

Low RBC amount or low Hb

12

Iron deficiency anemia causes?

Insufficient intake

Duodenal malabsorption

Iron loss from bleeding

Increased need- e.g growth spurt

13

Iron deficiency clinical presentation?

PICA
Koilonychia-spoon shaped brittle nails
Sleepiness
Angular cheilitis
Mouth ulcers
Hair loss
Missed menstrutation
Depression

14

Iron deficiency hematology report?

HYPOCHOMIC/MICROCYTIC

Anisocytosis/poikilocytosis

Leukocytes unaffected

15

Megaloblastic anemia is described as?

A condition is which the bone marrow produces unusually large, structurally abnormal immature RBC

16

Causes of megaloblastic anemia

Vit. B12 , Vit. B9 or both

(Both needed for maturation of blood cell and normal nerve cell function)

17

Abnormal DNA synthesis and Delayed cell division, with normal Hb & RNA synthesis in megaloblastic anemia is a result of ?

B9 and B12 deficiency

18

Etiological factors of B12 deficiency

Deficient intake

Lack of IF

Malabsorption syndrome-ileum

Worm infection

Increased used (pregnancy)

19

Etiological factors of B9 deficiency

Deficient intake

Alcoholism

Malabsorption- duodenum, jejunum

Increased use (pregnancy)

20

Clinical manifestation of megaloblastic anemia a/w B12 deficiency?

Fatigue, dyspnea, muscle weakness, glossitis, GI problems

21

Megaloblastic anemia a/w with B12 deficiency will result in _______ which is characterized by_______.

Result in: irreversible nervous system pathology collectively know as Subacute combined degeneration of spinal.

Characterized by: Demyelination of posterior and lateral columns and psychological problems.

22

What is the AKA term for subacute combined degeneration of spinal cord?

Lichtheim disease

23

Lichtheim disease is clinically manifested by:

Numbness/tingling in fingers extremities

Loss of balance, vibration and ataxia

Paraplegia

Depression, dementia

24

Tx for megaloblastic anemia a/w B12 deficiency

B12 by supplement

Injection of b12

25

Autoimmune disorder in which the body can’t make enough healthy RBC because it can’t absorb sufficient amounts og B12.

Pernicious anemia

26

Pernicious anemia produces Ab against_____?

Parietal cells

Intrinsic factor

Intrinsic factor receptors in ileum

27

Congenital pernicious is described as

Pernicious anemia passed down.

-Babies w/ this can’t make enough IF or absorb B12 in small intestines so tx requires intramuscular B12 shots-

28

Megaloblastic anemia a/w B9 clinical manifestation

Angular cheilitis/glossitis, fatigue, dyspnea, muscle weakness, GI problems and Depression.

No Neurological symptoms

29

Megaloblastic anemia a/w B9 affects pregnancy in what way?

Neural tube defects

Low birth rates

30

Megaloblastic anemia hematology

Pancytopenia

Hypersegmented neutrophils (senile)

Morphology: Macrocytic, anisocytosis/poikilocytosis- Howell-jolly bodies

MCV/ MCH increase or normal

LDH increased

31

Disease in which the bone marrow and the blood stem cells are damaged.

Aplastic anemia

32

Causes of aplastic anemia

50% idiopathic

Infection: Ds- hepatitis B/C, Epstein-Barr, Ss-parvovirus

Ionizing radiation

AI (e.g SLE)

Drugs

33

Aplastic anemia clinical manifestations

Fatigue, pallor, tachycardia/palpitations/dyspnea, weakness

34

Thrombocytopenia results from aplastic anemia, what are associated risk?

Hemorrhage

Bruising

Petechiae

35

Leukopenia in aplastic anemia is associated with what risk?

Risk of Infection

36

Definition: low counts of immature RBC/reticulocytes

Reticulocytopenia

(Result of Aplastic anemia)

37

Aplastic anemia laboratory findings

Pancytopenia

Normochromic/normocytic

Decreased granulocytes (WBC)

Increased serum ion (no RBC to take them)

38

Anemia in which the bone marrow and liver produce ringed sideroblast rather than healthy red blood cells.

Sideroblastic anemia

39

Define a sideroblast

Atypical abnormal uncleared erythoblast w/ iron granules

40

Why do sideroblast form ?

Due to reduce porphyria synthesis which helps incorporate iron into heme

41

Sideroblastic anemia etiology

50% idiopathic

30% acquired (MM, SLE, Liver cirrhosis etc)

20% hereditary (X-linked)

42

Sideroblastic anemia Sx/signs

Enlarged liver and spleen (MC)

Skin paleness

Fatigue

Dizziness

43

Sideroblastic anemia lab finding

Ring sideroblast in bone marrow

Anisocytosis/poikilocytosis/ basophillic stippling, target cells

Increased serum iron & transferrin saturation

44

Anemia due to hemolysis, the abnormal breakdown of RBC

Hemolytic anemia

(Intravascular or extravascular)

45

Intrinsic etiology of hemolytic anemia include

Defect of RBC membrane production

Defect in hemoglobin production

Defective RBC metabolism

46

Extrinsic etiology of hemolytic anemia include

Immune-mediated disorders

Drug side effects

Trauma

47

Sx of hemolytic anemia

Fatigue

Shortness of breath

Jaundice

Gallstone (due to increased bilirubin)

Pulmonary hypertension (due to abnormal bilirubin)

48

Hemolytic anemia lab findings

Increased serum bilirubin (feces and urinary as well)

Anisocytosis/poikilocytosis/ reticulocytosis

Elevated LDH

49

Intrinsic hemolytic anemia characterized by the production of RBCs that are sphere-shaped and prematurely breakdown.

Hereditary spherocytic anemia

50

The sphere shaped RBC a/w hereditary spherocytic anemia is a result of ?

Membrane lipoprotein defects

51

Sx of hereditary spherocytosis

Fatigue, dyspnea

Jaundice

Gallstones

Pulmonary hypertension

Splenomegaly

Aplastic crisis (temporary)

52

Hereditary spherocytosis lab

RBC- microcytic, hyperchromic

MCV low/ MCH normal

Increased unconjugated bilirubin in blood

Increased urobilinogen in ruins and stool

53

Intrinsic anemia disorder a/w an inherited autosomal recessive hemoglobinopathy, characterized by structurally abnormal Hb.

Qualitative defects

Sickle cell (group of disorders)

54

Sickle cell occurs when the _____, ______ on the ______ in the Hb molecule is replaced by other amino acids

Sixth amino acid

Glutamic acid

Beta-globin chain

55

The three detected mutation of sickle cells are

HbS- glutamic replaced with valine (E6V)

HbC- glutamic replaced with lysine (E6K)

HbE- Glutamic replaced with lysine on the 26 position on beta globin (E26K)

56

Sickle cell disease found in which geographic locations?

African, Caribbean, Mediterranean, middle eastern, East Indian ancestries

57

Sickle cell type that is the most common and occurs when copies of Hb S gene are inherited from both parents.

Hb SS sickle cell anemia AKA E6V

58

Sickle cell type that is the second most common and occurs when the Hb C gene is inherited from one parent and the Hb S from another

E6K AKA Hb SC sickle cell

(Less severe)

59

Sickle cell type that occurs when the Hb S gene is inherited from one parent and the Hb E from another.

Hb SE AKA E26K

(Very severe)

60

Sickle cell type that occurs when hemoglobin C is inherited from both parents.

Hb CC sickle cell AKA E6K

61

Sickle cell trait (SCT) is characterized by

Inheritance of Hb S and a normal gene Hb A- don’t have symptoms but can pass it on

62

Clinical manifestation of Sickle cell characterized by severe anemia.

(Not present younger than 4-6months)

Due to hemolysis-Fatigue, tachycardia, jaundice, dyspnea, paleness

63

Clinical manifestation of sickle cell characterized by vasooclusion:

(Not present younger than 4-6months)

Painful crisis & Tissue ischemia

low back pain, joint pain

Hand-foot syndrome/ SC dactylitis

Chest/abdominal pain

Bone infarcts

64

Sickle Lab findings

Sickle cell

Target cell

Increased sickle cell Hb, decreased normal

Howell jolly bodies

High reticulocyte count

65

Blood disorder that is autosomal recessive characterized by abnormal forms of hemoglobin resulting in weakening and destruction of RBC.

Quantitative defect

Thalassemia

66

Two types of thalassemia based on part of O2 carrying protein RBC is lacking

Alpha- severe

Beta- less severe

67

Both alpha and beta forms of thalassemia include the following form.

Major (from both parents)

Minor ( one parent)

68

In which form of thalassemia are children normal at birth, then exhibit severe anemia.

Also it is more prevalent in Mediterranean people known as Cooley’s anemia

Beta-thalassemia major

69

In which form of thalassemia can unborn babies die

Alpha-thalassemia major

70

The alpha and beta thalassemia minor are characterized by:

No Sx

Microcytic RBC

71

Beta-thalassemia major is manifested by:

Anemia

Iron overload

Bone deformities

Jaundice

Splenomegaly

Increased risk of infection

72

Bone deformities a/w thalassemia

Hair on end skull- accentuated trabeculae

Honeycomb pattern- destruction due to multiple bone infarcts

73

Thalassemia lab findings:

Decreased Hb, RBC, MCV, MCH, MCHC

Hypochromic microcytic, poikilocytosis, target cells, Cabot rings, ovalocytosis, Howell jolly bodies

Increased bilirubin, iron, ferritin

74

Tx of thalassemia

Major forms-regular blood transfusion, folate supplements, bone marrow transplant, chelation therapy (reduce iron)

75

X-linked recessive genetic disorder that predisposes to spontaneous destruction of RBC and resultant jaundice in response to triggers like:

Illness, food, medication

G6PDH deficiency AKA Favism

76

G6PDH function

Maintains pathway that produces gluthione, an antioxidant

77

G6PDH deficiency clinical manifestion

Paleness

Jaundice

Dark urine

Fatigue

Shortness of breath

Tachycardia

78

G6PDH deficiency lab

Normocytic, normochromic

Bite RBC (Degmacytes)

Heinz bodies w/ inclusions

WBC increase/platelet unaffected

Increased indirect bilirubin, LDH

Hematuria

79

Extrinsic hemolytic anemias etiological factors

Chemical poisoning
Physical
AI
Paroxysmal nocturnal hemoglobinuria
Infection
Erythroblastosis fetalis

80

Erythroblastosis fetalis is described as

An occurrence when an Rh(-) mother gives birth to Rh(+) .

Her body synthesis Ab against Rh(+), next Rh(+) is not conceived

81

State in which the proportion of blood volume that is occupied by red blood cells increases

Polycythemia

82

Two forms of polycythemia

Absolute- absolute #RBC increased

Relative- decrease in volume of plasma w/ normal absolute RBC

83

What is the hallmark of polycythemia?

Elevated hematocrit w/ normal MCV

84

Polycythemia present when excessive amount of red blood cells is produced as a
result of an abnormality of the bone marrow.

Absolute primary polycythemia AKA polycythemia Vera

85

Sx of polycythemia Vera

Itching/redness of skin

Sudden severe burning pain in hands and feet

Headache and vertigo

Hepatoslpenomegaly

ESR decreased

86

Polycythemia caused by either natural or artificial increases in the production of erythropoietin.

Characterized only by increased production of RBC

Absolute secondary polycythemia/ Physiological polycythemia

87

Two conditions associated with absolute secondary polycythemia

1. Conditions that result in physiological appropriate polycythemia (adaptation)

2. Conditions that don’t result as a manifestation of physiological adaptation

88

Relative polycythemia results from

Loss of body fluid - burns, dehydration, stress.

89

Type of cancer of blood, bone marrow and lymphoid system characterized by an abnormal increase in immature or mature abnormal white blood cells

Leukemia

90

Leukemia is a broad base of diseases also know as?

Hematological neoplasms

91

Classification of leukemia characterized by a rapid increase in the number of immature blood cells due to bone marrow disorder

Acute (MC in young/middle aged people)

92

Classification of leukemia characterized by the excessive building up of RELATIVELY mature and still abnormal WBC

Chronic leukemia (MC in older people)

93

Leukemia classified based on Lymphocytes being affected

Lymphocytic / lymphoblastic leukemia’s

94

Leukemia classified based on RBC, some WBC and platelets being affected.

Myeloid/myelogenous leukemia

95

What are the general clinical manifestations of acute forms of leukemia

Generally non-specific
Flu-like symptoms:fatigue, fever, malaise
Anorexia
Secondary infection
Anemia/excessive bleeding
Hepatosplenomegaly
Lymphadenopathy

96

Acute lymphocytic leukemia described as?

Malignant immature lymphocytes growing w/in bone marrow.

Affects young children

Blood shows undifferential immature lymphocytes- (blueberries)

97

Acute myeloid leukemia is described as ?

Rapid growth of abnormal non-differentiated granulocytes, abnormal myeloblasts (WBC) accumulating in bone marrow causing a drop in RBC, Platelets and normal WBC amount.

More often adults, avg age 67 year/ MC in males

98

Clinical manifestation of chronic leukemia’s

Insidious onset
Non specific Sx
Anemia
Anorexia
Bacterial, viral, fungal infection due to immunosuppression

99

Chronic lymphocytic leukemia is described as?

Abnormal growth of B cells in the bone marrow that most often affects middle-age adults or elder over the age of 55 and never children

100

Most people Dx with Chronic lymphocytic leukemia are diagnosed without sx as a result of what

As a result of routine blood test that returns high in WBC count

101

Form of leukemia classified by the increased and unregulated growth of predominantly myeloid cells (granulocytes) in bone marrow and the accumulation of these cells in the blood, lymphnodes and spleen

Chronic myeloid leukemia

102

Most people dx with CML have a genetic abnormality in their blood cells called Philadelphia (Ph) chromosome.

Describe the Ph chromosome

The Ph chromosome cause the production of the enzyme tyrosine kinase protein that is always on causing the cell to divide uncontrollably

103

What is the affect of CML on cells?

Increased granulocytes of all types including mature myeloid cells.

Basophils and eosinophils increased

104

Cancer of the lymph tissue that happens when B or T cells divide faster than normal and live longer than normal

Lymphoma

105

Two main types of lymphoma

Hodgkin lymphoma

Non-Hodgkin lymphoma (MC)

106

Risk factors for lymphoma

- exposure to virus (e.g. hepatitis B, C, Epstein-Barr)
- exposure to Helicobacter pylori
- exposure to chemical (e.g. herbicides) and radiation
- autoimmune diseases (e.g. Sjögren syndrome, SLE)

107

Clinical manifestation of lymphoma that is characterized by
-painless enlargement of nodes
-rubbery and swollen when examined
-nodes of the cervical, supraclavicular, chest, groin, and across whole body

Lymphadenopathy

108

DDx between lymphomas:
1. One type
2. Begins w/ B cells
3. Age 15-35 &over 50
4. MC in Females
5. Lymphadenopathy begins in upper body and spreads to lower
6. Lymphnodes painful after alcohol consumption
7. In biopsy of lymphnodes: Reed-Steinberg cells found

Hodgkin lymphoma

109

Reed Sternberg cells are described as ?

Found in hodgkins lymphoma

LArge often bi-uncleared cells with prominent nucleoli, originating from B-lymphocytes

110

Hereditary clotting factor disorders

Von willebrand disease

Hemophilia

111

Acquired clotting factor disorders

Disseminated intravascular coagulation

Circulating anticoagulants

112

Von Willebrand disease is described as?

The most common hereditary coagulation abnormality described in humans, developed through von willebrand factor deficiency

113

Von willebrand disease results in

Non formation of platelet plus and excessive bleeding

114

Von willebrand disease is a/w an autosomal dominant inheritance of which chromosome

12- always one parent with disease

115

Clinical manifestation of vWD

Bruising-nosebleed-gumbleeds

Recurring GI bleeding

Intensive menstruation hemorrhage (menorrhagia)

Prolonged bleeding and unaffected platelet count

116

Hemophilia is described as?

Rare genetic disorder that prevents the blood from clotting properly due to lack of clotting factors 8, 9, & 11

117

Types of hemophilia and their associated factor

Hemophilia A- VIII (80% of cases)

Hemophilia B/Christmas dz-lack of CF 9

Hemophilia C- deficiency of factor 11

118

T/F: Hemophila affects both genders equally

True

119

Hemophilia patients have parents that are affected/unaffected by bleeding disorder

Unaffected

120

Clinical manifestation of hemophilia

Usually discovered before 18 months old

Bleeding larger in weight bearing joints—>hemarthrosis

Bleeding tongue may close airway

121

Disseminated intravsacular coagulation is described as

Disorder in which CF become overreactive resulting is small clots in small vessels in the entire body

122

Explain whether or not DIC is a primary or secondary disorder.

DIC is a secondary disorder due to the fact it accompanies an underlying condition usually with critical illness

123

Clinical manifestation of DIC

Bleeding
Drop in BP
Dysfunction of all organs

124

Disorder where there is abnormally low platelets

Thrombocytopenia- regular platelet count should be between 150,000-450,000

125

Causes of thrombocytopenia

Nutrient deficiencies
Hereditary syndromes
Increased platelet destruction
Drugs
Various blood disorders

126

Clinical manifestations of thrombocytopenia

Low platelets
Petechiae
Purport
Nosebleeds
Bleeding gums

127

Rare disorder, causing extensive microscopic clots to form in the small blood vessels throughout the body

Thrombotic thrombocytopenic purpura

128

Five features of Thrombotic thrombocytopenic purpura

Thrombocytopenia

Microangiopathic hemolytic anemia

Neurologica Sx

Kidney failure

Fever

129

A disorder that usually occurs when an infection in the digestive system produces toxic substances that:

destroy RBCs
cause kidney injury
form blood clots in small blood vessels

Hemolytic-uremic syndrome (one of the TTP)

130

What is the common causative factor of hemolytic uremic syndrome

Post GI infection with E.coli

131

Clinical manifestation of Hemolytic syndrome

MC cause of acquired acute renal failure in childhood

GI problems

Kidney failure

Systemic problems