Pathophysiology-Blood/hematology

Front 1

Blood is made up of a liquid component and a cellular component. The liquid component is called _____.

Back 1

Plasma

Front 2

The cellular component of blood is made up of erythrocytes, ________, and thrombocytes all suspended in plasma.

Back 2

leukocytes

Front 3

Thrombocytes are also called ....?

Back 3

platelets

Front 4

what is the role of plasma?

Back 4

carries antibodies and nutrients to tissues and carries waste away

Front 5

Polycythemia is ....?

Back 5

an increase in RBC's

Front 6

A decrease in RBC's is called ______?

Back 6

Anemia

Front 7

The percentage of blood that is actually cells is called ...? What are the percentages for males/females?

Back 7

Hematocrit.
42-52% for males
37-47% for females

Front 8

Causes of elevated hematocrit....?

Low hematocrit?

Back 8

Dehydration, excess red blood cells

Blood loss, anemia

Front 9

Plasma consists of mainly _____, globulin, and _____ held in aqeous suspension.

Back 9

proteins, globulin, and fibrinogen

Front 10

Albumin is produced where and regulates what?

Back 10

Albumin is produced in the Liver and regulates colloidal osmotic pressure of blood.

Front 11

Thrombin converts Fibrinogen into Fibrin during coagulation. Where is Fibrinogen produced?

Back 11

The liver

Front 12

_________ secretion from the kidneys increases RBC production.

Back 12

erythropoieitin-EPO

Front 13

Red blood cells are produced in the ______ in adults.

Back 13

bone marrow

Front 14

the normal lifespan of a RBC is?

Back 14

120 days

Front 15

the requirements to produce a healthy red blood cell include; vitamin B12, ______, and minerals such as copper, cobalt, and especially ______.

Back 15

vitamin B12, folic acid, and minerals such as copper, cobalt, and especially iron.

Front 16

Iron is absorbed where in the digestive system?

Back 16

the duodenum and the upper jejunum

Front 17

After absorption Iron is transported to the bone marrow (Hemoglobin synthesis) and muscle (myoglobin synthesis). Unused Iron is temporarily stored as ______ and _______ in specialized cells called reticuloendothelial cells until released for use in bone marrow for new RBC's.

Back 17

ferritin and hemosiderin

Front 18

Hemoglobin consists of ____ heme groups.

Back 18

4 heme groups each containing a ferrous atom to which the oxygen molecule can attach.

Front 19

The two classifications of WBC's are called?

Back 19

Granular leukocytes and Nongranular leukocytes.

Front 20

Granular leukocytes are also called?

Back 20

Granulocytes

Front 21

the granular leukocytes (granulocytes) are ...?

Back 21

neutrophils, eosinophils & basophils
"NEB"

Front 22

the nongranular leukocytes are the ...?

Back 22

monocytes and lymphocytes

Front 23

t-lymphocytes complete their maturation in the ________. b-lymphocytes in the ________.

Back 23

thymus, lymph nodes

Front 24

60-30-8-3-0
"Never-Let-My-Engine-Blow"

Back 24

neutrophils 60%, lymphocytes 30%, monocytes 8%, eosinophils 3%, basophils 0%

Front 25

the lifespan of platelets is ____?

Back 25

7-10 days

Front 26

which granulocyte phagocytize bacteria?

Back 26

neutrophils

Front 27

lymphocytes are nongranular leukocytes responsible for eliminating ______?

Back 27

viruses.

via t lymphocytes (regulate cell-mediated immunity) and b lymphocytes (antibodies).

Front 28

An abnormal or pathologic condition of the blood is called _______?

Back 28

dyscrasia

Front 29

Blood disorders may be primary or secondary and quantitative or _______?

Back 29

qualitative.

Front 30

what is pancytopenia?

Back 30

decreased levels in all blood cells. (RBC, WBC, and platelets)

Front 31

a low platelet count is also called?

Back 31

thrombocytopenia (thrombocytes is another name for platelets)

Front 32

what are the most common WBC deficiencies?

Back 32

neutropenia (low neutrophils) and lymphocytopenia (low lymphocytes)

Front 33

The platelet disorder Thrombocytopenia is what?

Back 33

too few platelets

Front 34

The platelet disorder Thrombocytosis is what?

Back 34

too many platelets

Front 35

Dysfunctional platelets is a disorder called ...?

Back 35

Thrombocytopathy

Front 36

A decrease in red blood cell number or function causes what?

Back 36

Anemia

Front 37

___________ out-competes oxygen (200x). It binds tightly to the Iron causing fatal hypoxia.

Back 37

Carbon Monoxide

Front 38

Irritability=typically oxygen deprivation of the brain. True or False?

Back 38

True

Front 39

What could affect bone marrow production of RBC's?

Back 39

A problem with the kidneys as this is where Erythropoietin is made (a small percentage is made in the liver as well)

Front 40

hematopoietic cells are also called?

Back 40

stem cells

Front 41

Aplastic Anemia is a loss of _____ cells. Leading to ______.

Back 41

stem cells (hematopoietic cells)

a loss in all blood cell types (pancytopenia)

Front 42

Iron Deficient Anemia results in a reduction of _______ transported in the blood.

Back 42

oxygen

Front 43

hypochromic red blood cells are ____.

Back 43

pale

Front 44

small red blood cells can result from Iron deficiency. These are called _____ RBC's.

Back 44

mycrocytic red blood cells

Front 45

Hemoglobin gives RBC's their _____ and _______.

Back 45

red colour and full shape.

Front 46

What is Hypochromic Microcytic Anemia?

Back 46

pale, small red blood cells.

Front 47

Hypochromic Microcytic Anemia is most common in males or females?

Back 47

females (1 in 5 women)

Front 48

In a healthy individual how much dietary Iron is absorbed? In someone with Iron Deficient Anemia this rise to ____.

Back 48

5-10%

Rises to 20% in those w/ Iron Deficient Anemia

Front 49

Name 2 signs/symptoms of Iron Deficient Anemia.

Back 49

1.Pallor of skin and mucous membranes
2.fatigue, lethargy, cold intolerance
3.irritability (low oxygen to brain)
4.degenerative changes-brittle hair, concave and rigid nails
5.menstrual irregularities
6.delayed healing
7.tachycardia, heart palpitations, dyspnea, syncope (loss of consciousness)

Front 50

Pernicous Anemia is caused by a deficiency in which vitamin?

Back 50

B12

Front 51

This class of hematologic disorders is characterized by very large, immature, nucleated erythrocytes.

Back 51

Megaloblastic Anemia

Front 52

The most common form of Megaloblastic Anemia is _______.

Back 52

Pernicious Anemia

Front 53

Malabsorption of B12 owing to lack of ________ produced in the glands (parietal cells) of the gastric mucosa.

Back 53

Intrinsic Factor

Front 54

Vitamin B12 must bind w/ _______ for absorption to take place in the terminal ileum. The terminal Ileum happens to be the most common place for _____ disease. This could be affecting absorption.

Back 54

Intrinsic Factor

Crohn's

Front 55

B12 deficit leads to impaired maturation of __________.

Back 55

erythrocytes (RBC's)

Front 56

the large erythrocytes encountered in Pernicious Anemia are destroyed prematurely (before 120 days)? True or False?

Back 56

True

Front 57

B12 deficit is not a cause of demyelination? True or False

Back 57

False. B12 deficiency causes demyelination.

Front 58

Signs and Symptoms of Pernicious Anemia include;

Back 58

1. enlarged, red, sore, and shiny tongue due to papillae atrophy.
2. A decrease in gastric acid-leads to digestive discomfort
3. neurological effects-tingling and burning sensations in extremities, loss of coordination, and position sense (proprioception).
4. Mucous membranes of stomach shrink, decreased HCL production (no release of IF w/o HCL)
5. diplopia (double vision)-optic nerve shrinks
6. hearing problems-otic nerve shrinks
7. decreased taste
8. poor memory, mood changes, dementia
9. irritability-hypoxia of CNS
10. headache-hypoxia of brain+C02 building up

Front 59

Pernicious Anemia complications include; possible permanent CNS problems, heart failure, and _____ cancer (due to inadequate ____).

Back 59

stomach cancer-due to inadequate HCL, allowing bacteria to grow and affecting normal cell division

Front 60

Are B vitamins water soluble?

Back 60

Yes they are water soluble and not stored.

Front 61

Folic Acid Deficiency Anemia is a deficiency in Folic Acid, also referred to as vitamin ____.

Back 61

Folic Acid=Vitamin B9 (Folate)

Front 62

Folic Acid: B9 (Folate) is needed to make _____ and ____, the building blocks of cells.

Back 62

DNA and RNA

Front 63

Since Folic Acid (B9) is water soluble it comes from the diet. Sources of it include; ____________?

Back 63

leafy green vegetables, citrus fruits, and dried peas and beans.

Front 64

The most common cause of Folic Acid Deficiency Anemia is _______.

Back 64

Alcohol abuse that suppresses the metabolic effects of folate.

Front 65

Must have folic acid to produce good RBC's. Otherwise there is inadequate ________ synthesis.

Back 65

hemoglobin

Front 66

Folic acid deficiency during the first two months of pregnancy increase the risk of _________.

Back 66

spina bifida

Front 67

What are the two megaloblastic anemias?

Back 67

Pernicous Anemia and Folic Acid Deficiency Anemia

Front 68

Hemolytic Anemias result from excessive destruction of _____.

Back 68

RBC's. Destruction of red blood cells (hemolysis)

Front 69

Sickle Cell Anemia is a genetically inherited characteristic in which there is abnormal hemoglobin. True or False?

Back 69

True

Front 70

the lifespan of a sickled RBC is approx. _____.

Back 70

20 days

Front 71

Sickle Cell Anemia: "when this altered hemoglobin is deoxygenated it crystallizes and changes the shape of RBC from disc to _______ shape.

Back 71

crescent "sickle" shape

Front 72

HbS (sickle RBC) can't transport oxygen in a normal fashion. True or False?

Back 72

False. Sickled RBC's can transport oxygen in the same way that disc shaped RBC's can.

Front 73

Sickle Cell Anemia: _________ count is very low resulting in low hemoglobin levels.

Back 73

Red Blood Cell (erythrocyte)

Front 74

Fetal hemoglobin is replaced by regular hemoglobin (or sickle cell hemoglobin) at ____ old.

Back 74

at 12 months old; fetal hemoglobin is replaced by Hb or HbS

Front 75

Signs and Symptoms of Sickle Cell Anemia:

Back 75

1. pallor, weakness, tachycardia, dyspnea,
2. cardiomegaly, hepatomegaly, jaundice, splenomegaly,
3. delayed growth and development (late puberty is common, late tooth eruption, intellectual development is usually impaired)
4. vascular occlusions and infarctions
5. gallstones from elevated levels of bilirubin caused by hemolysis
6. asplenia, renal failure

Front 76

Is there an advantage to sickle cell anemia? Explain.

Back 76

Yes. Those w/ sickle cell anemia are much more resistant to malaria (plasmodium flaciparum). The HbS in RBC's interferes with the ability of the parasite to reproduce.

Front 77

Treatment of Anemia will depend on underlying etiology and severity. If anemia is the result of an underlying disease-the primary disease must be treated first.

Back 77

Iron, folate, and b12 anemia may use supplementation to treat deficiency. In severe cases-transfusion.

Front 78

The coagulation system has 2 main components. These are _____ and _____.

Back 78

platelets and coagulation factors.

Front 79

Clotting factors are ______, many of which are synthesized in the _____ and circulate in the plasma in inactive form.

Back 79

proteins

Liver

Front 80

Which clotting factors need vitamin K for their synthesis?

Back 80

Clotting factors 2,7,9,10 need vitamin K for their synthesis.

Front 81

deficiencies in clotting factors can occur from liver failure, ______ deficiency or as with any protein a genetic mutation leading to dysfunctional protein or inadequate amounts of it.

Back 81

vitamin K

Front 82

vitamin K is fat soluble. True or False?

Back 82

True. Vitamin K is fat soluble

Front 83

there are two clotting pathways, Extrinsic and ______.

Back 83

Intrinsic

Front 84

The Intrinsic clotting factor is initiated when there is damage on the inside of a blood vessel. When is the Extrinsic factor initiated?

Back 84

When there is tissue injury which exposes clotting factor to the circulation.

Front 85

Both clotting pathways feed into a common pathway. True or False?

Back 85

True! Both the Extrinsic and Intrinsic clotting pathways feed into the common pathway.

Front 86

Factors involved in the Extrinsic Clotting Pathway:

Back 86

Tissue Factor
Fator VII
Factor X

Front 87

Factors involved in the Intrinsic Clotting Pathway:

Back 87

Tissue Factor
Factor XI
Factor IX
Factor VIII
Factor X

Front 88

Classic Hemophilia is also called ________.

Back 88

Hemophilia A

Front 89

Hemophilia A (classic hemophilia) is caused by a decrease in amount or functional ability of factor ___.

Back 89

Hemophilia A: decrease in amount or functional ability of Factor VIII. Factor X is not triggered in the clotting cascade due to decreased or less functional Factor VIII.

Front 90

Hemophilia A makes up __% of people who have hemophilia.

Back 90

80%

Front 91

Hemophilia B is also called ________.

Back 91

Christmas Disease

Front 92

Hemophilia B (Christmas Disease) is caused by a decrease in amount or functional ability of factor ___.

Back 92

Factor IX. Factor X is not triggered in the clotting cascade preventing fibrinogen from converting to fibrin (which produces a clot at the site of bleeding)

Front 93

Which type of Hemophilia is an inherited autosomal dominant trait?

Back 93

Von Willebrand's Disease

Front 94

What is "Von Willebrand's Disease"?

Back 94

defect in the platelet function due to lack of Von Willebrand's factor AND decreased amount of Factor VIII.

Front 95

Decreased Von Willebrands factor causes decreased adherence of platelets to vessel wall. Is this true?

Back 95

Yes.

Front 96

When damage to small blood vessels and capillaries occurs there are three main mechanisms that promote hemostasis (or stoppage of bleeding). These are

1. vasoconstriction
2. ___________
3.attraction of more Platelets

Back 96

Platelet adherance

Front 97

Clotting Process: When platelets adhere to a damaged vessel, they undergo degranulation and release cytoplasmic granules, which contain _______, a vasoconstrictor, and ADP and _________.

Back 97

Serotonin-a vasoconstrictor

Thromboxane A2

Front 98

During clotting ADP (Adenosine diphosphate) attracts more _______ to the area.

Back 98

platelets

Front 99

During clotting, Thromboxane A2 promotes platelet aggregation, _______, and vasoconstriction.

Back 99

degranulation

Front 100

Points to remember:

To make a clot:
1.Platelets need to adhere to the vessel wall
2.Secrete substances to call more platelets to the site
3.Then stick to each other to form an aggregate clot

Back 100

Adhesion to the vessel wall requires von Willebrand's factor, which serves as a bridge from the vessel wall to the platelet.

Front 101

Clotting and Hemorrhage occurring at the same time in the vascular system is a condition called ______ ______ Coagulation.

Back 101

Disseminated Intravascular Coagulation

Front 102

DIC (Disseminated Intravascular Coagulation) causes small blood vessel blockage, organ tissue damage (necrosis), depletion of circulating clotting factors and platelets, and activation of a clot-dissolving process called ______. This in turn can lead to severe hemorrhage.

Back 102

fibrinolysis

Front 103

What is fibrinolysis?

Back 103

A clot-dissolving process. "lysis of fibrin"

Front 104

There are 5 major causes of DIC. These are: Infection, Obstetric complications, Neoplastic disease (acute leukemia, metastatic carcinoma, lymphomas), disorders that produce necrosis, other conditions associated w/ massive insult to the body. Is it understood as to why these conditions and disorders lead to DIC?

Back 104

No. This is not clearly understood.

Front 105

DIC usually develops in association w/ 3 pathologic processes.

1. Damage to the endothelium
2. Release of tissue thromboplastin
3. ____________

Back 105

Activation of factor X

Front 106

The most significant clinical feature of DIC: ________

Other signs: cutaneous oozing, petechiae (microhemorrhages on the skin), bleeding from surgical or IV sites, bleeding from GI tract, cyanosis of extremities (not enough oxygen to the tissues=pale skin colour)

Back 106

abnormal bleeding w/o a history of serious hemorrhage disorder.

Front 107

DIC prognosis: __-__ will die. DIC w/ sepsis has a significantly higher rate of death than DIC associated w/ trauma.

Back 107

10-50% will die