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PD BIO 305 > Blood 2 > Flashcards

Blood 2 Flashcards

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2
Q

The ‘BLEEDING’ from many small vessels is known as what?

A

THROMBOCYTOPENIA PURPURA

*HINT - ‘PURPURA’ = PURPLE

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3
Q

How can ‘THROMBOCYTOPENIA’ be treated?

A

TRANSFUSIONS OF PACKETED PLATELETS

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4
Q

When the ‘ENDOTHELIAL LINING’ of a vessel is exposed to ‘COLLAGEN PROTEINS’, a process of 3 separate but overlapping mechanisms occurs. What are they?

A
  1. VASOCONSTRICTION
  2. PLATELET PLUG FORMATION
  3. FORMATION OF BLOOD CLOT
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5
Q

‘VASOCONSTRICTION’ is ‘STIMULATED’ by what during the ‘BLOOD CLOTTING’ process?

A

SEROTONIN

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6
Q

What causes ‘VASOCONSTRICTION’ during ‘BLOOD CLOTTING’? What are some of the characteristics?

(*There are 3 things)

A
  1. VESSEL WALL IS CUT OR BROKEN
  2. MUSCLES STIMULATED TO CONTRACT
  3. BLOOD LOSS IS ‘DECREASED’
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7
Q

TRUE OR FALSE

In the absence of ‘VESSEL DAMAGE’, platelets are attracted to each other.

A

FALSE

‘PLATELETS’ are ‘repelled’ from each other during ‘VESSEL DAMAGE’

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8
Q

What does the ‘PLATELET PLUG’ temporarily do?

A

TEMPORARILY ‘CLOSES’ THE VESSEL UNTIL CLOTTING MECHANISMS CAN FORM A CLOT.

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9
Q

What is the ‘PLATELET PLUG’ strengthened by?

A

PROTEIN FIBERS CALLED ‘FIBRIN’

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10
Q

What are the two ‘pathways’ that result in the formation of ‘FIBRIN’?

A
  1. INTRINSIC PATHWAY (Inside)

2. EXTRINSIC PATHWAY (Outside)

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11
Q

What is the main difference between ‘EXTRINSIC’ and ‘INTRINSIC’ pathways?

A
  1. EXTRINSIC = TISSUE DAMAGE

2. INTRINSIC = VASCULAR DAMAGE

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12
Q

What ‘CLOTTING FACTORS’ does the ‘INTRINSIC PATHWAY’ have that the ‘EXTRINSIC PATHWAY’ does not?

A

FACTOR 9, 11 AND 12

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13
Q

Where are ‘PROTHROMBIN’ and ‘FIBRINOGEN’ made?

*Hint - They are ‘PLASMA PROTEINS’

A

MADE IN THE LIVER

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14
Q

What ‘CONVERTS’ ‘PROTHROMBIN’ to ‘THROMBIN’?

A

CALCIUM

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15
Q

When ‘THROMBIN’ reacts with ‘FIBRINOGEN’ what is the result?

A

FIBRIN CLOT

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16
Q

What is the ‘COLOR’ of a ‘CLOT’?

A

NO COLOR

CLOT IS DERIVED FROM ‘PLASMA’ CONSTITUENTS

*THE RED COLOR COMES FROM ‘RBCs’ THAT BECOME TRAPPED.

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17
Q

‘CLOT RETRACTION’ is also referred to as what?

A

SYNERESIS

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18
Q

‘PLATELETS’ play a role in bringing what closer together?

A

FIBRIN THREADS CLOSER TOGETHER

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19
Q

Why is ‘CLOT RETRACTION’ important?

A

DURING ‘INTRAVASCULAR CLOTS’ THE CLOT IS ABLE TO PULL AWAY FROM THE WALL AND ‘RESTORE BLOOD FLOW’

ALLOWS CLOT TO ‘SHRINK IN SIZE’ AFTER TIME

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20
Q

TRUE OR FALSE

CLOTS DO NOT SHRINK IN SIZE

A

FALSE

‘CLOT RETRACTION’ OR ‘SYNERESIS’ OCCURS BY BRINGING ‘FIBRIN’ THREADS CLOSER TOGETHER.

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21
Q

What is the clotting factor ‘NUMBER’ for ‘FIBRINOGEN’?

A

I

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22
Q

What is the clotting factor ‘NUMBER’ for ‘PROTHROMBIN’?

A

II (2)

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23
Q

What is the clotting factor ‘NUMBER’ for ‘TISSUE THROMBOPLASTIN’?

A

III (3)

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24
Q

What is the clotting factor ‘NUMBER’ for ‘CALCIUM’?

A

IV (4)

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25
Q

What is the clotting factor ‘NUMBER’ for ‘ANTIHEMOPHILIC GLOBULIN’?

A

VIII (8)

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26
Q

What is the clotting factor ‘NUMBER’ for ‘CHRISTMAS FACTOR’?

A

IX (9)

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27
Q

What is the clotting factor ‘NUMBER’ for ‘FIBRIN STABILIZING FACTOR’?

A

XIII (13)

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28
Q

What is the ‘NAME’ for clotting factor ‘I’?

A

FIBRINOGEN

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29
Q

What is the ‘NAME’ for clotting factor ‘II’?

A

PROTHROMBIN

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30
Q

What is the ‘NAME’ for clotting factor ‘III’?

A

TISSUE THROMBOPLASTIN

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31
Q

What is the ‘NAME’ for clotting factor ‘IV’?

A

CALCIUM

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32
Q

What is the ‘NAME’ for clotting factor ‘VIII’?

A

ANTIHEMOPHILIC GLOBULIN

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33
Q

What is the ‘NAME’ for clotting factor ‘IX’?

A

CHRISTMAS FACTOR

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34
Q

What is the ‘NAME’ for clotting factor ‘XIII’?

A

FIBRIN STABILIZING FACTOR

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35
Q

What ‘CLOTTING FACTOR’ is the cause of ‘HEMOPHILIA’?

A

FACTOR VIII (8)

ANTIHEMOPHILIC GLOBULIN

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36
Q

What do ‘ANTICOAGULANTS’ do?

A

PREVENT ‘BLOOD CLOTTING’

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37
Q

‘ANTICOAGULANTS’ are also referred to as what?

A

‘BLOOD THINNERS’

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38
Q

What is ‘DICOUMARAL’ (COUMADIN)?

How does it function?

A

ANTICOAGULANT (BLOOD THINNER)

INTERFERES WITH ‘VITAMIN K’ WHICH ALSO AFFECTS FACTORS VII, IX, AND X.

*LIVER ‘MUST’ HAVE VITAMIN K TO PRODUCE CLOTTING FACTORS

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39
Q

What is ‘HEPARIN’?

How does it function?

A

INTERFERES WITH THE FORMATION OF ‘THROMBIN’ FROM ‘PROTHROMBIN’

*HEPARIN SHOTS GIVEN TO PATIENTS BEFORE SURGERY TO ‘PREVENT’ CLOTTING DURING/AFTER SURGERY.

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40
Q

How do ‘CITRATES’, ‘OXALATES’ and ‘EDTA’ work as ‘ANTICOAGULANTS?

A

TIE UP CALCIUM

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41
Q

Where is ‘VITAMIN K’ produced (greatest source)?

Where is it ‘STORED’?

A

PRODUCED = ‘G.I. TRACT VIA BACTERIA’

STORED = ‘LIVER’

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42
Q

‘NEWBORN BABIES’ do ‘NOT’ have ‘BACTERIA’ in their G.I. tract. Because of this, what usually happens after a baby is delivered?

A

INJECTED WITH A ‘VITAMIN K’ SHOT

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43
Q

What is the definition of ‘FRIBRINOLYSIS’?

A

LYSIS OF CLOTS

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44
Q

How does the ‘FIBRINOLYSIS’ begin?

A

CLOT STIMULATES RELEASE OF A SUBSTANCE FROM THE ‘WALL’ OF A BLOOD VESSEL

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45
Q

There is an ‘ACTIVATOR’ located in the ‘PLASMA’ which stimulates what to occur? With what protein does this start with?

A

LYSIS OF CLOTS

STARTS WITH ‘PLASMINOGEN’ PROTEIN

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46
Q

When an ‘ACTIVATOR’ is stimulated after a clot is formed, what is the ‘PATHWAY’ for the clot to decompose?

(*There are 4 steps)

A

‘PLASMINOGEN’ -> ‘PLASMIN’ -> ‘FIBRIN’ -> DEGRADED FIBRIN PRODUCTS

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47
Q

What is the ‘NATURALLY’ ocurrig agent in the body that breaks up clots?

A

‘PLASMIN’

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48
Q

TRUE OR FALSE

‘PLASMIN’ is very ‘QUICK’ at removing clots in the body.

A

FALSE

‘PLASMIN’ is natural but ‘NOT’ quick.

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49
Q

What are the 4 conditions that can cause ‘EXCESSIVE’ bleeding in humans?

A
  1. LIVER DISEASE
  2. VITAMIN K DEFICIENCY
  3. HEMOPHILIA
  4. THROMBOCYTOPENIA
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50
Q

When ‘LIVER DISEASE’ is a factor in excessive bleeding, what is happning?

A

LIVER IS ‘DECREASING’ PRODUCTION OF ‘CLOTTING FACTORS’

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51
Q

Where are the ‘MAJORITY’ of clotting factors produced?

A

LIVER

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52
Q

Someone diagnosed with a ‘VITAMIN K’ deficiency may have what symptoms?

Why?

A

EXCESSIVE BLEEDING

LACK OF ‘VITAMIN K’ DECREASES FORMATION OF:

  1. PROTHROMBIN
  2. OTHER FACTORS
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53
Q

What is ‘HEMOPHILIA’ defined as?

What 2 types are there?

A

LACK OF FACTOR VIII (8)

ANTIHEMOPHILIC GLOBULIN

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54
Q

When ‘HEMOPHILIA’ is diagnosed, what is its most ‘COMMON’ form?

A

HEMOPHILIA A

LACK OF FACTOR VIII (8)

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55
Q

Someone who is lacking ‘FACTOR IX (9)’ would be diagnosed with what?

(*FACTOR 9 = CHRISTMAS FACTOR)

A

HEMOPHILIA B

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56
Q

What is a ‘THROMBUS’ defined as?

A

CLOT THAT IS ‘ATTACHED’ TO A BLOOD VESSEL WALL

57
Q

What is an ‘EMBOLUS’ defined as?

A

CLOT THAT ‘DETACHES’ from the wall and floats freely in the circulation.

58
Q

‘THROMBUS’ formation is usually due to what 3 causes?

A
  1. TRAUMA (INJURY) TO BLOOD VESSEL
  2. SLOW BLOOD FLOW (USUALLY IN VEINS)
  3. ROUGH SURFACE ON INSIDE OF BLOOD VESSELS (ARTERIOSCLEROTIC PLAQUES)
59
Q

What is ‘THROMBOCYHTEMIA’ defined as?

A

EXCESS PLATELETS

50,000 mm^3 OR LESS

60
Q

How does ‘ASPIRIN’ help fight against ‘HEART ATTACKS’?

A

INHIBITS PLATELET AGGREGATION AND THE RELEASE OF PLATELET CLOTTING FACTORS

THEREBY ‘DECREASES CLOT FORMATION’

61
Q

There are 3 general ‘LINES OF DEFENSE’ in the body. What are they?

A
  1. EXTERNAL DEFENSE
  2. PHAGOCYTIC CELLS
  3. IMMUNITY
62
Q

What is the ‘MAIN’ source of ‘EXTERNAL DEFENSE’ in the body?

A

SKIN

63
Q

How does ‘SKIN’ work as an ‘EXTERNAL DEFENSE’ mechanism?

A

ANATOMICAL BARRIER TO PENETRATION BY ‘PATHOGENS’

THERE ARE SECRETIONS WITH ‘LYSOZYME’ WHICH DESTROY BACTERIA

64
Q

What is ‘LYSOZYME’?

A

‘ENZYME’ secreted from the skin that ‘DESTROYS’ bacteria.

65
Q

There are 4 ‘MECHANISMS’ in the body for modes of ‘EXTERNAL DEFENSE’. What are they?

A
  1. SKIN
  2. DIGESTIVE TRACT
  3. RESPIRATORY TRACT
  4. GENITOURINARY TRACT
66
Q

Why is the ‘DIGESTIVE TRACT’ considered to be an ‘EXTERNAL DEFENSE’?

A

THERE IS A ‘HIGH ACIDITY’ IN STOMACH ACID (pH=1 or 2)

67
Q

Why is the ‘RESPIRATORY TRACT’ considered to be an ‘EXTERNAL DEFENSE’?

A

MOVEMENT OF MUCUS BY CILIA

ALVEOLAR ‘MACROPHAGES’

68
Q

What is the ‘GENITOURINARY TRACT’ and how is it an ‘EXTERNAL DEFENSE’ mechanism?

A

ACIDITY OF ‘URINE’

ACIDITY OF ‘VAGINAL LACTIC ACID

69
Q

There are 5 types of ‘PHAGOCYTIC CELLS’ involved in defense against disease. What are they and where are they?

A
  1. NEUTROPHILS (WBCs - BLOOD)
  2. MONOCYTES (WBCs - BLOOD)
  3. KUPFFER CELLS (LIVER)
  4. ALVEOLAR MACROPHAGES (LUNGS)
  5. MICROGLIA (CNS - CENTRAL NERVOUS SYSTEM)
70
Q

What are the 2 types of ‘IMMUNITY’?

A
  1. NON-SPECIFIC

2. SPECIFIC

71
Q

What is ‘NON-SPECIFIC IMMUNITY’ defined as?

A

IMMUNITY THAT IS ‘INHERIT AGAINST DISEASE’

72
Q

What are the 5 different types of ‘NON-SPECIFIC IMMUNITY’?

A
  1. INFLAMMATION
  2. INTERFERON
  3. FEVER
  4. NATURAL KILLER CELLS
  5. COMPLEMENT SYSTEM
73
Q

How is ‘INFLAMMATION’ help as defense against disease in ‘NON-SPECIFIC IMMUNITY’?

(*THERE ARE 3 REASONS)

A
  1. HELPS ISOLATE, DESTROY, INACTIVATE INVADING AGENTS.
  2. REMOVE DEBRIS
  3. PREPARE FOR HEALING AND REPAIR
74
Q

What are ‘INTERFERONS’ and how do they help as defense against disease in ‘NON-SPECIFIC IMMUNITY’?

(*THERE ARE 3)

A

PROTEINS THAT ARE RELEASE FROM VIRUS-INFECTED

PROVIDES PROTECTION TO OTHER CELLS THAT MAY BE INFECTED BY THE ‘VIRUS’

75
Q

How does ‘FEVER’ help as defense against disease in ‘NON-SPECIFIC IMMUNITY’?

(*THERE ARE 2 REASONS)

A

INHIBITS ‘BACTERIA GROWTH’

MAY AID IN RECOVERY FROM INFECTION

76
Q

What are ‘NATURAL KILLER CELLS’ and how do they help as defense against disease in ‘NON-SPECIFIC IMMUNITY’?

A

LYMPHOCYTE-LIKE CELLS THAT DESTROY VIRUS-INFECTED CELLS/CANCER CELLS

77
Q

What is the ‘COMPLEMENT SYSTEM’ and how is it a help as defense against disease in ‘NON-SPECIFIC IMMUNITY’?

A

PLASMA ‘PROTEINS’ THAT DESTROY FOREIGN CELLS BY ATTACKING THEIR PLASMA MEMBRANES

78
Q

What is ‘SPECIFIC IMMUNITY’ defined as?

How does it work?

A

SYSTEM THAT RESPONDS ‘SELECTIVELY’ TO INVADING AGENTS

‘ANTIBODIES’ ARE FORMED FROM PREVIOUSLY EXPOSED DISEASE.

‘ANTIBODIES’ SELECTIVE TARGET INVADERS AND DESTROY THEM.

79
Q

Why in ‘SPECIFIC IMMUNITY’ does the first exposure cause harm to the individual whereas the second exposure does not?

A

TAKES BODY SEVERAL DAYS TO MOUNT AN ‘IMMUNE RESPONSE’

‘ANTIBODIES’ (SPECIFIC PROTEINS) ARE FORMED TO COMBINE WITH ‘ANTIGEN’ AFTER 1st EXPOSURE

80
Q

What is an ‘ANTIGEN’

A

AN ‘INVANDING AGENT’ THAT INITATES A ‘SPECIFIC IMMUNITY’ RESPONSE

81
Q

What is the 2nd exposure of the reaction between an ‘ANTIGEN’ and an ‘ANTIBODY’ called?

A

IMMUNE REACTION

82
Q

There are 2 ‘BROAD TYPES’ of ‘SPECIFIC IMMUNE RESPONSES’. What are they?

A
  1. HUMORAL IMMUNITY

2. CELL-MEDIATED IMMUNITY

83
Q

What is ‘HUMORAL IMMUNITY’ defined as?

A

HUMORAL = FLUID = BONE MARROW = (B-LYMPHOCYTES)

B-LYMPHOCYTES COMBAT INFECTION / BACTERIA

84
Q

What is ‘CELL-MEDIATED IMMUNITY’ defined as?

A

DESTRUCTION BY THE ‘T-LYMPHOCYTES’

CELLS THAT ARE IN ‘CLOSE PROXIMITY’ OR HAVE ‘PHYSICAL CONTACT’ WITH THE VICTIM CELL TO DESTROY IT.

85
Q

TRUE OR FALSE

T-CELLS DO ‘NOT’ SECRETE ANTIBODIES

A

TRUE

THEY DO ‘NOT’ SECRETE ANTIBODIES

86
Q

What is ‘SELF-RECOGNITION’ or ‘TOLERANCE’ defined as?

What is an example where this is important?

A

ABILITY TO ‘DISTINGUISH’ MATERIAL THAT IS ‘SELF’ FROM MATERIAL THAT IS ‘NON-SELF’

EXAMPLE = ORGAN TRANSPLANTS

87
Q

What is ‘AUTOIMMUNITY’ defined as?

A

FORMATION OF ‘ANTIBODIES’ AGAINST A PERSON’S OWN TISSUES

88
Q

What are some examples of ‘AUTOIMMUNE’ diseases?

*THERE ARE 2 OF THEM

A
  1. RHEUMATIC FEVER

2. GRAVE’S DISEASE

89
Q

What is ‘RHEUMATIC FEVER’ defined as?

A

ANTIBODIES THAT ARE PRODUCED AGAINST ‘STREPTOCOCCUS BACTERIA’ CROSS REACT WITH THE HEART AND KIDNEY TISSUES.

‘AUTOIMMUNE DISEASE’

90
Q

What is ‘GRAVE’S DISEASE’?

A

ANTIBODIES STIMULATE THYROID GLAND WHICH MIMIC ‘THYROID STIMULATING HORMONE (TSH)’.

91
Q

What is ‘ACTIVE IMMUNITY’?

A

THE BODY ‘ACTIVELY’ FORMS ANTIBODIES AGAINST ANTIGENS THAT IT HAS BEEN PREVIOUSLY EXPOSED TO.

(SELF PRODUCING)

92
Q

What are some examples of ‘ACTIVE IMMUNITY’?

*THERE ARE 4 OF THEM

A
  1. MEASELS
  2. CHICKEN POX
  3. MUMPS
  4. VACCINE
93
Q

What is a ‘VACCINE’?

A

DEAD PIECES OF THE INVADER

ANTIBODIES CREATED FROM DEAD ‘ANTIGENS’

94
Q

What is ‘PASSIVE IMMUNITY’?

A

TRANSFUSING A PERSON WITH ‘ANTIBODIES’ IN PLASMA FROM SOMEONE ELSE THAT HAS BEEN ACTIVELY IMMUNIZED AGAINST A ‘SPECIFIC ANTIGEN’.

95
Q

What is the problem with ‘PASSIVE IMMUNITY’?

A

‘ANTIBODIES’ DO NOT LAST LONG AND START TO DEGRADE SO IMMUNITY IS ‘NOT’ PERMANENT.

96
Q

What are some examples of ‘PASSIVE IMMUNITY’?

A
  1. RHOGAM SHOT

2. MOTHER’S MILK

97
Q

TRUE OR FALSE

Passive Immunization with antibodies can ‘ONLY’ be accomplished with human immunoglobulins.

A

FALSE

HUMAN IMMUNOGLOBULINS (ANTIBODIES) ‘AND’ ALSO ANIMAL IMMUNOGLOBULINS

98
Q

When is ‘PASSIVE IMMUNITY’ beneficial?

A
  1. INDIVIDUALS UNABLE TO FORM ANTIBODIES
  2. PREVENTION OF DISEASE WHEN TIME DOES NOT PERMIT ACTIVE IMMUNIZATION (AFTER EXPOSURE)
  3. TREATMENT OF CERTAIN DISEASES (e.g., TETANUS)
  4. TREATMENT OF CONDITIONS WHERE ACTIVE IMMUNIZATION IS ‘UNAVAILABLE’ OR ‘IMPRACTICAL’ (e.g., SNAKE BITE)
99
Q

A person with type ‘A’ blood has what type of ‘ANTIGENS’ on the surface of each red blood cell?

A

TYPE A ANTIGENS

100
Q

A person with type ‘B’ blood has what type of ‘ANTIGENS’ on the surface of each red blood cell?

A

TYPE B ANTIGENS

101
Q

A person with type ‘AB’ blood has what type of ‘ANTIGENS’ on the surface of each red blood cell?

A

TYPE AB ANTIGENS

102
Q

A person with type ‘O’ blood has what type of ‘ANTIGENS’ on the surface of each red blood cell?

A

‘NO’ ANTIGENS

103
Q

Approximately how long after ‘BIRTH’ does the body begin to produce ‘ANTIBODIES’ in their ‘blood’?

A

2-8 MONTHS AFTER BIRTH

104
Q

‘ANTIBODIES’ in the ‘BLOOD’ are also called what?

A

AGGLUTININS

105
Q

Where are ‘ANTIGENS’ located with regards to ‘BLOOD’?

A

‘ON’ THE RED BLOOD CELL

106
Q

What do ‘ANTIBODIES/AGGLUTININS’ do?

A

REACT W/ ANTIGENS OF OTHER BLOOD

107
Q

What is considered to be the ‘UNIVERSAL RECIPIENT’?

A

AB BLOOD TYPE

108
Q

What is considered to be the ‘UNIVERSAL DONOR’?

A

O

109
Q

What happens if ‘BLOOD TYPES’ do not match during a ‘TRANSFUSION’?

A

RECIPIENT’S ANTIBODIES ‘ATTACH’ TO THE DONOR’S RED BLOOD CELL ‘ANTIGENS’

CELLS BEGIN TO ‘AGGLUTINATE’

110
Q

What is ‘HEMOLYSIS’?

A

RED BLOOD CELLS RUPTURE (LYSE)

CAUSED BY ‘AGGLUTINATION’ IN THE BLOOD FROM TRANSFUSION ERRORS

111
Q

How many types of ‘Rh’ antigens are there? Which is the most common?

A

6 COMMON TYPES OF ‘Rh’ ANTIGENS. ALSO CALLED ‘Rh FACTOR’

TYPE ‘D’ IS MOST PREVALENT

112
Q

Are more people ‘Rh-‘ or ‘Rh+’?

A

MORE ARE ‘Rh+’

113
Q

Which factor in the ‘BLOOD’ next to the (ABO) group system has the greated ‘clinical’ importance?

Why?

A

‘Rh GROUP’

THIS GROUP HAS THE ABILITY TO CAUSE:

HEMOLYSIS (HEMO=BLOOD, LYSIS=BREAK OPEN)

OTHER ‘HEMOLYTIC’ DISEASES TO ‘NEWBORNS’ (e.g., ERYTHROBLASTOSIS FATALIS)

114
Q

When the ‘Rh GROUP’ is ‘NOT’ compatible during pregnancy and the ‘MOTHER’S’ antibodies attack the ‘ANTIGENS’ of the baby, what is this called?

A

‘ERYTHROBLASTOSIS FETALIS’

115
Q

Which form of the ‘Rh GROUP’ is the only one to ‘PRODUCE ANTIBODIES’?

A

ONLY ‘Rh -‘ CREATES ANTIBODIES

116
Q

What is ‘ERYTHROBLASTOSIS FETALIS’ defined as?

A

‘HEMOLYTIC ANEMIA’ IN NEWBORN ‘Rh +’ BABY.

CAUSE IS FROM ‘MATERNAL ANTIBODIES’ THAT ARE AGAINST THE ‘Rh FACTOR’ OF THE NEWBORN.

‘MOTHER’S ANTIBODIES’ CROSS THE PLACENTA AND INTERACT WITH BABY ‘Rh FACTOR’

117
Q

What would be the result of the following situation during a pregnancy:

MOTHER = 'Rh +'
BABY = 'Rh -'
FATHER = 'Rh -'
A

NO ‘ANTIBODIES’ CREATED

*ONLY ‘Rh -‘ BLOOD TYPE CREATES ANTIBODIES

118
Q

What would be the result of the following situation during a pregnancy:

MOTHER = 'Rh +'
FATHER = 'Rh -'
BABY = 'Rh +'
A

NO ‘ANTIBODIES’ CREATED

119
Q

What would be the result of the following situation during a pregnancy:

MOTHER = 'Rh +'
FATHER = 'Rh +'
BABY = 'Rh +'
A

NO ‘ANTIBODIES’ CREATED

120
Q

What would be the result of the following situation during a pregnancy:

MOTHER = 'Rh -'
FATHER = 'Rh -'
BABY = 'Rh -'
BABY = 'Rh +'
A

NO ‘ANTIBODIES’ CREATED

121
Q

What would be the result of the following situation during a pregnancy:

MOTHER = 'Rh -'
FATHER = 'Rh +'
BABY = 'Rh +'
A

‘ANTIBODIES’ ARE CREATED

‘ERYTHROBLASTOSIS FETALIS’ WILL OCCUR ON NEXT (Rh +) PREGNANCY UNLESS MOTHER IS GIVEN A ‘RHOGAM SHOT’ WHICH WILL INDUCE ‘PASSIVE (SHORT TERM) IMMUNITY’ TO ‘Rh + ANTIGENS’.

122
Q

What would be the result of the following situation during a pregnancy:

MOTHER = 'Rh -'
FATHER = 'Rh +'
BABY = 'Rh -'
A

NO ‘ANTIBODIES’ CREATED

123
Q

What does a woman who is ‘Rh -‘ need to be injected with after giving birth to a ‘Rh +’ baby?

Why?

A

‘RHOGAM SHOT’

THIS CREATES ‘PASSIVE IMMUNITY’ WHICH IS SHORT TERM. IF NOT, MOTHER WILL CREATE ‘ANTIBODIES’ AGAINST ‘Rh + FACTOR’ CAUSING ALL FUTURE PREGNANCIES WITH ‘Rh + TYPE BLOOD’ TO GO THROUGH ‘ERYTHROBLASTOSIS FETALIS’

124
Q

‘A BLOOD’ type has what kind of ‘ANTIGENS’ and what type of ‘ANTIBODIES’?

A

‘A BLOOD TYPE’

‘A ANTIGENS’

‘ANTI-B ANTIBODIES’

125
Q

‘B BLOOD’ type has what kind of ‘ANTIGENS’ and what type of ‘ANTIBODIES’?

A

‘B BLOOD TYPE’

‘B ANTIGENS’

‘ANTI-A ANTIBODIES’

126
Q

‘AB BLOOD’ type has what kind of ‘ANTIGENS’ and what type of ‘ANTIBODIES’?

A

‘AB BLOOD TYPE’

‘A & B ANTIGENS’

‘NO ANTIBODIES’

(*UNIVERSAL RECIPIENT)

127
Q

‘O BLOOD’ type has what kind of ‘ANTIGENS’ and what type of ‘ANTIBODIES’?

A

‘NO ANTIGENS’

‘ANTI-A & ANTI-B ANTIBODIES’

(*UNIVERSAL DONOR)

128
Q

Where are the ‘ANTIBODIES’ for a specific blood type located?

A

ANTIBODIES = ‘PLASMA’

129
Q

Where are the ‘ANTIGENS’ for a specific blood type located?

A

ANTIGENS = ‘ATTACHED TO BLOOD CELL’

130
Q

A ‘NORMAL’ HEMATOCRIT IS:

  1. 45%
  2. 35%
  3. 55%
  4. 60%
A
  1. 45%
131
Q

HOW MANY ‘RED BLOOD CELLS’ ARE PRODUCED EVERY SECOND?

  1. 250,000
  2. 1 MILLION
  3. 2.5 MILLION
  4. 500,000
A
  1. 2.5 MILLION
132
Q

WHICH HORMONE STIMULATES ‘RED BLOOD CELL’ PRODUCTION?

  1. OXYTOCIN
  2. ESTROGEN
  3. ERYTHROPOIETIN
  4. ADH
A
  1. ERYTHROPOIETIN
133
Q

THE TYPE OF ‘ANEMIA’ CAUSED BY DEREASED SECRETION OF THE ‘INTRINSIC FACTOR’ IS:

  1. PERNICIOUS ANEMIA
  2. HEMORRHAGIC ANEMIA
  3. APLASTIC ANEMIA
  4. SICKLE CELL ANEMIA
A
  1. PERNICIOUS ANEMIA
134
Q

WHICH TWO TYPES OF ‘WHITE BLOOD CELLS’ ARE PRODUCED IN ‘LYMPH NODE TISSUES’?

  1. LYMPHOCYTES AND BASOPHILS
  2. NEUTROPHILS AND MONOCYTES
  3. LYMPHOCYTES AND MONOCYTES
  4. LYMPHOCYTES AND NEUTROPHILS
A
  1. LYMPHOCYTES ANO MONOCYTES
135
Q

WHICH OF THE FOLLOWING DOES ‘NOT’ STIMULATE ‘VASOCONSTRICTION’?

  1. ADP
  2. PLASMIN
  3. SEROTONIN
  4. THROMBOXANE A2
A
  1. PLASMIN
136
Q

AN ‘EMBOLISM’ IS:

  1. A BLOOD CLOT ATTACHED TO A BLOOD VESSEL WALL
  2. A BLOOD CLOT FORMED IN PULMONARY ARTERIES ONLY
  3. A BLOOD CLOT THAT DETACHES FROM A BLOOD VESSEL WALL AND FLOATS FREELY
  4. A BLOOD CLOT FORMED IN THE HEART
A
  1. A BLOOD CLOT THAT DETACHES FROM A BLOD VESSEL WALL AND FLAOTS FREELY
137
Q

FORMATION OF ‘ANTIBODIES’ AGAINST A PERSON’S OWN TISSUE IS:

  1. NON-SPECIFIC IMMUNITY
  2. CELL-MEDIATED IMMUNITY
  3. PASSIVE IMMUNITY
  4. AUTO IMMUNITY
A
  1. AUTO IMMUNITY
138
Q

A PERSON WHO HAS ‘NEITHER’ A NOR B ALLGUTININS IN HIS OR HER BLOOD IS WHICH BLOOD TYPE?

  1. TYPE O
  2. TYPE AB
  3. TYPE A
  4. TYPE B
A
  1. TYPE AB

*UNIVERSAL RECIPIENT

PD BIO 305 (19 decks)

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