Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
296 Cards in this Set
- Front
- Back
THE AVERAGE YOUNG ADULT HAS HOW MUCH 'BLOOD'? (*VOLUME)
|
6 LITERS
|
|
'BLOOD' is separated into 2 different components. What are the 2 components?
|
1. CELLS
2. PLASMA |
|
What 3 types of 'CELLS' are found in 'BLOOD' composition?
|
1. ERYTHROCYTES
2. LEUKOCYTES 3. THROMBOCYTES |
|
WHAT IS ANOTHER NAME FOR 'ERYTHROCYTES'?
|
RED BLOOD CELLS (RBCs)
|
|
WHAT IS ANOTHER NAME FOR 'LEUKOCYTES'?
|
WHITE BLOOD CELLS (WBCs)
|
|
WHAT IS ANOTHER NAME FOR 'THROMBOCYTES'?
|
PLATELETS
|
|
In 'BLOOD', 'PLASMA' can be separated into 2 main sub-groups. What are the 2 main sub-groups?
What percentages does each make up of the 'PLASMA'? |
1. WATER (90-92%)
2. SOLIDS (7-9%) |
|
What are the 5 functions of 'BLOOD'?
|
1. CARRIAGE OF O2 TO CELLS
2. TRANSPORT OF HORMONES IN BODY 3. REMOVAL OF CO2 FROM CELLS 4. DEFENSE AGAINST DISEASE 5. REGULATE ACID/BASE BALANCE |
|
What 'PROTEIN' is found in the most abundance in blood plasma?
|
ALBUMIN
|
|
'ALBUMIN' accounts for what percentage of the total amount of 'protein' found in blood plasma?
|
ALBUMIN = 55% OF 'BLOOD PLASMA PROTEIN' CONCENTATION
|
|
What is considered to be the 'NORMAL' hematocrit?
|
45% = NORMAL
|
|
What is the normal 'HEMATOCRIT' range for males?
|
42-48% = MALES
|
|
What is the normal 'HEMATOCRIT' range for females?
|
38-44% = FEMALES
|
|
When blood is placed in centrifuge and spun down, there are 2 different sections. What is the 'BOTTOM' portion referred to as and what is the 'TOP' portion referred to as?
|
FORMED ELEMENTS = 'BOTTOM'
PLASMA = 'TOP' |
|
'PLASMA' minus the 'coagulation factors' is referred to as what?
|
SERUM
|
|
What causes a sample of blood to clot?
|
COAGULATION FACTORS / CLOTTING FACTORS
|
|
What is the ratio of 'RED BLOOD CELLS' to other 'BLOOD CELLS'?
|
500:1
|
|
There are many organic/inorganic substances that are dissolved in blood. What are 9 examples of these?
|
1. PROTEINS
2. ELECTROLYTES 3. GLUCOSE 4. AMINO ACIDS 5. LIPIDS 6. VITAMINS 7. HORMONES 8. GASES 9. WASTE PRODUCTS |
|
'PLASMA PROTEINS' can be separated into 4 basic groups. What are the 4 basic groups?
|
1. ALBUMIN
2. GLOBULINS (ALPHA/BETA/GAMMA) 3. CLOTTING FACTORS 4. OTHERS (ENZYMES/HORMONES) |
|
WHERE ARE THE 'ALPHA/BETA' GLOBULINS FORMED?
|
IN THE LIVER
|
|
What is the main function of 'ALBUMIN' proteins found in the blood?
What is a important characteristic of this protein? |
OSMOTIC PRESSURE REGULATION
IS THE 'SMALLEST' MOST 'ABUNDANT' PLASMA PROTEIN |
|
What are the functions of the 'ALPHA/BETA' globulins?
How do they work? |
CARRIER VEHICLES
PREVENT SUBSTANCES IN BLOOD FROM LEAVING THE CAPILLARY TOO QUICKLY. |
|
What is the function of 'GAMMA' globulins as a blood plasma protein?
What 2 types of this are possible? |
ANTIBODY PRODUCTION
1. NATURAL IMMUNITY 2. ACQUIRED IMMUNITY |
|
Where are 'GAMMA GLOBULINS' formed?
|
IN LYMPHOID TISSUES
|
|
What is the function of the 'RETICULO-ENDOTHEILIAL' system?
What does it produce? |
1. TISSUES/CELLS CAPABLE OF 'PHAGOCYTOSIS'
2. FORMS ANTIBODIES (IMMUNE RESPONSE) TO BACTERIA |
|
'CELLS' connected to the 'RETICULO-ENDOTHELIAL' system can be found in 4 different places in the human body. What are the 4 places?
|
1. BONE MARROW
2. SPLEEN 3. LIVER 4. LYMPH NODES |
|
What are the 4 characteristics of 'ERYTHROCYTES'?
|
1. NO NUCLEUS
2. CANNOT MULTIPLY 3. BICONCAVE DISCS 4. NO ENDOPLASMIC RETICULUM 5. DO NOT SYNTHESIZE PROTEINS |
|
What are the 2 functions of 'ERYTHROCYTES'?
|
1. TRANSPORT HEMOGLOBIN
2. PARTICIPATE IN CO2 TRANSPORT |
|
'MALES' have an average of approximately how many 'ERYTHROCYTES' (RBCs)?
|
5.5 million/mm^3
|
|
'FEMALES' have an average of approximately how many 'ERYTHROCYTES' (RBCs)?
|
4.5 million/mm^3 = FEMALES
|
|
Under what conditions will there be an 'INCREASE' of 'ERYTHROCYTES' (RBCs)?
|
1. ALTITUDE
2. MUSCULAR EXERCISE 3. TEMPERATURE 4. AGE - HIGHER IN INFANTS |
|
The synthesis of 'RED BLOOD CELLS' is known as what?
|
ERYTHROPOIESIS
|
|
The synthesis of 'ALL BLOOD CELLS' is known as what?
|
HEMATOPOIESIS
|
|
During life, the synthesis of 'BLOOD CELLS' is split into different parts of the body.
Where does synthesis take place during the following times of life: - EARLY EMBRYO - MIDDLE PREGNANCY - ADULT |
1. EARLY EMBRYO = YOLK SAC
2. MIDDLE PREGNANCY = LIVER, SPLEEN AND BONE MARROW 3. ADULT = BONE MARROW, VERTEBRAE, RIBS, STERNUM |
|
What is the process of forming a 'RED BLOOD CELL'?
(*There are 5 steps) |
1. STEM CELL
2. PROERYTHROBLAST 3. NORMOBLAST 4. RETICULOCYTE 5. ERYTHROCYTE (MATURE RBC) |
|
What is considered to be the most important step in the process of 'RED BLOOD CELL' synthesis?
Why? |
RETICULOCYTE
Cell leaves marrow and enters blood-stream 'W/OUT' a 'NUCLEUS' |
|
Between what 2 processes does the 'RED BLOOD CELL' lose its nucleus?
|
NORMOBLAST -> RETICULOCYTE
|
|
Without this 'hormone' red blood will not forms and 'stem cells' will NOT be stimulated.
|
ERYTHROPOIETIN
|
|
How is the 'synthesis' of RED BLOOD CELLS regulated?
(*THERE ARE 4 EXAMPLES) |
1. HEMORRHAGE
2. RESPIRATORY/CIRCULATORY DISEASE 3. PARTIAL MARROW DESTRUCTION 4. PHYSICAL ACTIVITY |
|
If the 'OXYGEN' delivery to certain cells of the kidney decreases, what is secreted and from what organ?
|
ERYTHROPOIETIN = SECRETED
SECRETED FROM 'KIDNEYS' (*STARTS 'ERYTHROPOIESIS') |
|
'ERYTHROPOIETIN' (EPO) goes into the blood and stimulates what to become what. Where does this 'generally' occur?
|
STIMULATES 'STEM CELLS' to become 'PROERYTHROBLASTS'
GENERALLY OCCURS IN 'BONE MARROW' |
|
There are 3 other uncommon factors that help regulate 'RED BLOOD CELL' production. What are they?
|
1. COLONY-STIMULATING FACTORS
2. INTERLEUKINS 3. STEM CELL FACTORS |
|
It takes approximately how many days for (RBCs) to increase after 'ERYTHROPOIETIN' is stimulated?
|
5 DAYS
|
|
'ERYTHROPOIETIN' is part of the group of 'CYTOKINES' called what?
|
HEMATOPOEITIC GROWTH FACTORS (HGFs)
|
|
What is 'BLOOD DOPING'?
|
SEPARATING 'RED BLOOD CELLS' AND STORING THEM FOR A CERTAIN AMOUNT OF TIME.
RE-INJECTING THE 'RED BLOOD CELLS' TO CAUSE A HIGHER HEMATOCRIT. THIS CAUSES INCREASED 'ENDURANCE' / 'OXYGEN' CARRYING CAPACITY. |
|
What might happen with an abnormally 'HIGH' hematocrit due to 'BLOOD DOPING'?
|
BLOOD BECOMES 'SLUGGISH' AND 'THICK'.
HEART HAS TO WORK HARDER FOR IT TO MOVE THROUGH BODY. INCREASED CHANGE OF HEART ATTACK. |
|
How do (RBCs) become 'worn out'?
|
THROUGH WEAR/TEAR OF PASSING THROUGH BLOOD VESSELS.
|
|
Approximately how many 'RED BLOOD CELLS' (RBCs) are 'destroyed' each second?
|
~2,500,000 RED BLOOD CELLS / SECOND
|
|
What is 'HEMOGLOBIN'?
|
Substance the can 'reversibly' bind to 'OXYGEN'
|
|
Approximately how many molecules of 'HEMOGLOBIN' are there per 'RED BLOOD CELL'?
|
200 MILLION HEMOGLOBIN MOLECULES / RED BLOOD CELL
|
|
'HEMOGLOBIN' consists of 2 parts. What are the 2 parts?
|
1. GLOBIN (4 POLYPEPTIDE CHAINS)
2. HEME (Fe++ w/ PORPHYRIN) |
|
The 'GLOBIN' portion of 'HEMEGLOBIN' is considered to be a what?
What is it made of? |
PROTEIN
MADE OF 4 POLYPEPTIDE CHAINS. (2 ALPHA CHAINS AND 2 BETA CHAINS) |
|
4 DISK-SHAPED MOLECULES ARE WHAT MAKE UP THIS COMPOUND.
|
'HEME' IN HEMO-GLOBIN
|
|
Each 'HEME' has what molecule in the center?
|
IRON
|
|
When 'IRON' (Fe++) is combined with 'PORPHYRIN', what is the result?
|
A 'HEME' GROUP
|
|
How many 'PEPTIDE' bonds does a 'HEME' molecule have?
|
4 PEPTIDE BONDS
|
|
By 'WEIGHT', what percentage of a RBC is ade of Hb (HEMOGLOBIN)?
|
34% of RBC = HEMOGLOBIN
|
|
In 100 ml of 'BLOOD' there are approximately how many 'GRAMS' of 'HEMOGLOBIN'?
|
15 GRAMS
|
|
What amount of 'OXYGEN' in 'ml' will combine on a 'per gram' basis with 'HEMOGLOBIN'?
|
1.34 ml OXYGEN / 1g Hb
|
|
What is 'OXYHEMOGLOBIN' defined as?
What color(s) does it have? Does it change? If so, when? |
HEMOGLOBIN that is 'SATURATED' with O2 (OXYGEN)
COLOR = CHERRY (W/ OXYGEN) COLOR = PURPLE-BLUE (W/OUT OXYGEN) |
|
Hb (HEMOGLOBIN) can combine with 2 other molecules. What are the 2 moelcules?
Which one does 'COMPETE' for the OXYGEN binding Hb spot? |
1. CARBON DIOXIDE (CO2)
2. CARBON MONOXIDE (CO) CARBON MONOXIDE (CO) 'DOES' COMPETE FOR THE SAME 'OXYGEN' (O2) BINDING SPOT. |
|
Why is 'CARBON MONOXIDE' such a dangerous gas?
|
BECAUSE IT 'COMPETES' FOR THE SAME LOCATION 'OXYGEN' BINDS TO ON 'HEMOGLOBIN'
HAS 200X AFFINITY FOR Hb THAN OXYGEN |
|
When 'HEMOGLOBIN' combines with CO2 (CARBON DIOXIDE), what is the molecule called?
|
CARBAMINO HEMOGLOBIN
|
|
When 'HEMOGLOBIN' combines with CO (CARBON MONOXIDE), what is the molecule called?
|
CARBOXY HEMOGLOBIN
|
|
This molecule has '200x' the affinity for 'HEMOGLOBIN' (Hb) than 'OXYGEN' does.
|
CARBON MONOXIDE
|
|
TRUE OR FALSE
The 4 'POLYPEPTIDE' chains formed on the globin protein in a 'HEMOGLOBIN' molecule can NOT be re-used again. |
FALSE
POLYPEPTIDE BONDS CAN BE USED 'AGAIN' OR FOR 'AMINO ACIDS' (*HUMAN BODY IS EFFICIENT) |
|
What happens to 'HEMOGLOBIN' when RBCs are worn out and destroyed? What is this referred to as?
|
CATABOLISM (BREAKDOWN) OF HEMOGLOBIN
|
|
When 'HEMOGLOBIN' (Hb) is 'catabolized' or broken down. There are 4 steps that occur for a complete breakdown. What are they?
|
1. Hb goes to (HEME + GLOBIN)
2. GLOBIN is 'reused' in AMINO ACIDS or in another HEMEGLOBIN 3. HEME goes to (Fe++ and PORPHYRIN) 4. IRON in the PORPHYRIN is 'REDUCED' |
|
After 'catabolism' of a 'HEMOGLOBIN' molecule, what happens to the 'PORPHYRIN' portion?
(*THERE ARE 2 STEPS) |
1. IRON IS REMOVED FROM CENTER
2. RING STRUCTURE CHANGES TO CHAIN STRUCTURE CALLED 'BILIVERDIN' |
|
What is 'BILIVERDIN' a result of?
|
RESULT FROM THE BREAKDOWN (CATABOLISM) OF A 'HEME' GROUP DUE TO 'HEMOGLOBIN'/'RBC' DESTRUCTION.
|
|
'BILIVERDIN' is converted to what molecule when it is being broken down by the body?
|
BILIRUBIN (YELLOW COLOR)
|
|
What is 'BILIVERDIN'?
|
THE BY-PRODUCT OF THE 'CATABOLISM' OF THE 'HEME' GROUP FROM A 'HEMOGLOBIN' MOLECULE THAT HAS BEEN DESTROYED.
|
|
What is the process for 'HEMOGLOBIN' destruction?
(*3 STEPS) |
1. HEMOGLOBIN -> HEME + GLOBIN
GLOBIN = REABSORBED/REUSED 2. HEME -> IRON + PORPHRYIN IRON = REABSORBED 3. PORPHYRIN -> BILIVERDIN -> BILIRUBIN -> SECRETED FROM BODY |
|
Where is 'BILIRUBIN' delivered to?
|
LIVER
|
|
After 'BILIRUBIN' has been delivered to the 'LIVER', what is its function?
|
EXCRETED FROM LIVER WITH 'BILE'
|
|
'BILIRUBIN', once in the 'LIVER' and secreted with 'BILE' has 2 options/pathways. What are they?
|
1. EXCRETION VIA 'FECES'
2. EXCRETION VIA 'URINE' |
|
What do 'FECES' and 'URINE' owe their normal 'brown/yellowish' color to?
|
BILIRUBIN PRODUCTS
|
|
When 'BILIRUBIN' is excreted in the form of 'FECES' what is it called?
|
STERCOBILIN
|
|
When 'BILIRUBIN' is reabsorbed back into the blood, delivered to 'KIDNEYS' and excreted in the form of 'URINE' what is it called?
|
UROBILIN
|
|
What is it called when the 'YELLOWISH' colored 'BILIRUBIN' accumlates in the blood to an abnormally 'HIGH' degree?
|
JAUNDICE (HYPERBILIRUBINEMIA)
HIGH BLOOD BILIRUBIN LEVELS |
|
There are 3 causes of 'JAUNDICE', what are they?
|
1. LIVER DISEASE
2. EXCESS RED CELL DESTRUCTION 3. BILE DUCT OBSTRUCTION |
|
What is 'ANEMIA' defined as?
|
ANY CONDITION THAT RESULTS IN A 'DECREASED' OXYGEN-CARRYING CAPACITY OF THE BLOOD.
|
|
There are 2 main 'CAUSES' of 'ANEMIA', what are they?
|
1. DECREASED NUMBER OF RBCs
2. DECREASED HEMOGLOBIN/CELL |
|
What are the 3 'SYMPTOMS' of 'ANEMIA'?
|
1. PALE SKIN COLOR
2. FATIGUE 3. RAPID HEART RATE |
|
Why do 'NEWBORN BABIES' develop 'JAUNDICE' more commonly than adults?
|
BABIES HAVE A HIGHER HEMATOCRIT WHEN BORN.
RBCs ARE DESTROYED AT HIGH RATE AFTER BIRTH TO REACH A BALANCED LEVEL. INCREASED RBC DESTRUCTION CAUSES 'HIGH' BILIRUBIN LEVELS |
|
TRUE OR FALSE
'BABIES' develop a 'BLOOD BRAIN BARRIER' at a very young age. |
FALSE
'BABIES' do 'NOT' have a well developed 'BLOOD BRAIN BARRIER' until they are much older. |
|
What are the 4 basic 'TYPES' of 'ANEMIA'?
|
1. HEMORRHAGIC
2. APLASTIC 3. NUTRITIONAL 4. HEMOLYTIC |
|
What is 'HEMORRHAGIC ANEMIA' defined as?
|
'ANEMIA' DUE TO BLOOD LOSS
|
|
What is 'APLASTIC ANEMIA' defined as?
|
'ANEMIA' DUE TO BONE MARROW DESTRUCTION
(*LEAST COMMON) |
|
What are some of the 'CAUSES' for 'APLASTIC ANEMIA'?
(*THERE ARE 4) |
1. CANCER
2. EXCESSIVE X-RAY EXPOSURE 3. CERTAIN CHEMICALS 4. SOME DRUGS |
|
What is 'NUTRITIONAL ANEMIA' defined as?
What 2 'SUB-GROUPS' are included in this type of 'ANEMIA'? |
ANEMIA DUE TO A 'LACK' OF VITAMINS/PROTEINS IN THE BODY.
(IRON DEFICIENCY ANEMIA) |
|
What 'PROTEIN' is 'IRON' bound to in the body? What does it serve as?
|
IRON IS BOUND TO 'FERRITIN' PROTEIN
SERVES AS BUFFER TO FIGHT AGAINST 'IRON DEFICIENCY' |
|
What is considered to be the 'MOST COMMON' type of 'ANEMIA'?
|
NUTRITIONAL ANEMIA
|
|
What is the definition of 'FOLIC ACID DEFICIENCY ANEMIA'? What specific type of 'ANEMIA' does this fall under?
|
NUTRITIONAL ANEMIA
Folic Acid = REQUIRED FOR 'MITOSIS'. WITHOUT 'FOLIC ACID', CELL DIVISION IMPAIRMENT OCCURS. IMPACTS GREATER ON 'RBC' PRODUCTION |
|
What is 'PERNICIOUS ANEMIA'? What type of 'ANEMIA' is this considered to be?
|
NUTRITIONAL ANEMIA
VITAMIN B12 DEFICIENCY FAILURE OF VITAMIN B12 TO BE 'ABSORBED' FROM THE G-I TRACT. |
|
What is the process in which 'PERNICIOUS ANEMIA' occurs?
|
PARIETAL CELLS -> INTRINSIC FACTOR -> VITAMIN B12 ABSORPTION -> MITOSIS (RBC) PRODUCTION
|
|
What is 'HEMOLYTIC ANEMIA' defined as?
|
RBC DESTRUCTION
|
|
What are 3 causes of 'HEMOLYTIC ANEMIA'?
|
1. SICKLE CELL ANEMIA
2. ERYTHROBLASTOSIS FETALIS 3. LEAD/ARSENIC POISONING 4. SICKEL CELL ANEMIA |
|
What happens in 'SICKEL CELL ANEMIA'?
|
THE #6 'AMINO ACID' IS SUBSTITUTED.
(GLUTAMIC ACID CHANGED TO VALINE) |
|
What is the definition of 'POLYCYTHEMIA'?
|
'INCREASED' RBC NUMBERS 'ABOVE' NORMAL LEVELS
(*HINT - BLOOD DOPERS. HIGH HEMATOCRIT) |
|
What are the 2 different types of 'POLYCYTHEMIA'?
|
1. PHYSIOLOGIC/SECONDARY
2. POLYCYTHEMIA VERA |
|
What are the 'CHARACTERISTICS' of 'PHYSIOLOGIC/SECONDARY' 'POLYCYTHEMIA'?
(*THERE IS ONLY 1) |
NO ACTUAL RBC PATHOLOGY
RESIDING AT HIGH ALTITUDES NORMAL RESPONSE TO LOW OXYGEN PRESSURE. COUNTS OF 6-8 MILLION CELLS ARE COMMON. THERE ARE 'NO' SIGNIFICANT ADVERSE REACTIONS. |
|
What is 'POLYCYTHEMIA VERA' also known as? What is it caused by?
|
KNOWN AS 'ERYTHREMIA'
CAUSED BY 'TUMOR OF THE BONE MARROW' |
|
What are some of the 'CHARACTERISTICS' of 'POLYCYTHEMIA VERA' (ERYTHREMIA)?
(*THERE ARE 5 OF THEM) |
1. 11 MILLION CELLS/MM^3 (RBCs)
2. HEMATOCRIT = 80% 3. BLOOD IS VERY VISCOUS/SLUGGISH 4. HIGH BLOOD PRESSURE 5. HIGH RISK OF STROKE/HEART ATTACK |
|
What is the 'average' number of 'LEUKOCYTES' in a person?
|
6,000 - 12,000 /mm^3 (1/500 of RBC count)
|
|
TRUE OR FALSE
Though 'LEUKOCYTE' numbers are low, 'PRODUCTION RATE' is equal to or great than that of RBC's. |
TRUE
'PRODUCTION RATE' IS EQUAL TO OR GREATER THAN 'RBC' PRODUCTION. |
|
What is the range of 'LIFE SPAN' of a 'LEUKOCYTE'?
|
4 DAYS to MONTHS (DEPENDS ON TYPE)
|
|
Where are the 'MAJORITY' of 'LEUKOCYTES' found?
|
OUTSIDE CIRCULATION
|
|
What 3 types of 'LEUKOCYTES' are considered to be 'GRANULOCYTES' and what are their percentages?
|
1. NEUTROPHILS (65-70%)
2. ESOINOPHILS (1-2%) 3. BASOPHILS (0-.5%) (*HINT - 'Granny N.E.B'. All the '-phil' cells are part of the same family) |
|
What 2 types of 'LEUKOCYTES' are considered to be 'AGRANULOCYTES' and what are their percentages?
|
1. LYMPHOCYTES (20-24%)
2. MONOCYTES (5%) (*HINT - [ALMs]) |
|
Where are 'AGRANULOCYTES' formed?
|
IN THE 'LYMPH NODES'
|
|
Where are 'GRANULOCYTES' formed?
|
BONE MARROW
|
|
Which 'LEUKOCYTE' is 'MOST' common in fighting 'INFECTION'?
What group does it belong to? |
NEUTROPHILS
GRANULOCYTE FAMILY |
|
What is the definition of 'DIFFERENTIAL WHITE BLOOD CELL COUNT'?
|
PERCENTAGE DISTRIBUTION OF TYPES OF 'WBCs'
(*OUT OF 100 WBCs RATIO IS DETERMINED) |
|
Where are the 'LEUKOCYTE' production sites for an 'EMBRYO'?
(*THERE ARE 3 SITES) |
1. BONE MARROW
2. LIVER 3. SPLEEN |
|
Where are the 'LEUKOCYTE' production sites for an 'ADULT'?
(*THERE ARE 2 DIFFERENT SITES) (*HINT - EACH FAMILY HAS A DIFFERENT PRODUCTION SITE) |
1. GRANULOCYTES = BONE MARROW
2. AGRANULOCYTES = LYMPHOID TISSUES |
|
What is the definition of 'PHAGOCYTOSIS'? What cells 'commonly' participate in this?
|
ABILITY TO 'ENGULF' FOREIGN BODIES
'WHITE BLOOD CELLS' (LEUKOCYTES) |
|
What is 'DIAPEDESIS'?
What cells 'commonly' participate in this? |
ABILITY TO 'SQUEEZE' THROUGH CAPILLARY WALLS
'WHITE BLOOD CELLS' (LEUKOCYTES) |
|
What is 'AMEBOID MOTION' described as?
What cells 'commonly' participate in this? |
ABILITY TO MOVE ONCE CIRCULATION HAS BEEN LEFT.
CYTOPLASM STREAMS SIMILAR TO AN 'AMOEBA' 'WHITE BLOOD CELLS' (LEUKOCYTES) |
|
What is 'CHEMOTAXIS' defined as?
|
LEUKOCYTES ARE 'DRAWN' TOWARD AN AREA OF 'INFECTION'.
|
|
What is the 'PROCESS' for 'CHEMOTAXIS'?
|
1. INJURED CELL RELEASES 'LEUCOTAXINE'
2. INCREASED CAPILLARY PERMEABILITY 3. LEUCOTAXIN ATTRACTS 'NEUTROPHILS' 4. 'NEUTROPHILS' INITIATE PHAGOCYTIC PROPERTIES |
|
What is 'LEUCOTAXINE'?
|
A 'CHEMOTAXIC' SUBSTANCE RELEASED BY AN 'INJURED CELL'
ATTRACTS 'NEUTROPHILS' |
|
What are the characteristics of 'NEUTROPHILS'?
(*THERE ARE 3 OF THEM) |
GRANULOCYTE
1. ACUTE CONDITION DEFENSE 2. PHAGOCYTIC SPECIALISTS 3. RELEASE 'NETs' (NEUTRPHIL EXTRACELLULAR TRAPS) TO CONTAIN BACTERIA-KILLING CHEMICALS |
|
What are the characteristics of 'EOSINOPHILS'?
(*THERE ARE 3 OF THEM) |
GRANULOCYTE
1. INCREASE DURING 'ALLERGIC' CONDITIONS (HAYFEVER and ASTHMA) 2. ATTRACTED TO SITES WHERE ALLERGIC REACTIONS HAVE OCCURRED. 3. MAST CELLS / BASOPHILS RELEASE 'EOSINOPHIL CHEMOTACTIC FACTOR) DURING ALLERGIC REACTION |
|
This 'LEUKOCYTE' is involved during 'ACUTE CONDITIONS' to fight off 'INFECTION'.
Examples are, appendicitis, sore throat, and pneumonia. |
NEUTROPHILS
|
|
These 'LEUKOCYTES' 'INCREASE' in number during an 'ALLERGIC' reaction.
|
EOSINOPHILS
|
|
What are the characteristics of 'BASOPHILS'?
(*THERE IS ONLY 1) |
1. SECRETE 'ANTICOAGULANT'
(HEPARIN and HISTAMINE) DURING ALLERGIC REACTION |
|
These 'LEUKOCYTES' release 'HISTAMINE' and 'HEPARIN'.
|
BASOPHILS
|
|
These 'LEUKOCYTES' are 'very active' in an 'IMMUNE RESPONSE'.
|
AGRANULOCYTES
LYMPHOCYTES |
|
What are the 2 types of 'LYMPHOCYTES'?
|
1. B-LYMPHOCYTES
2. T-LYMPHOCYTES |
|
What are the functions of 'B-LYMPHOCYTES'?
|
1. PRODUCE ANTIBODIES (ANTIBODIES ALSO PRODUCED BY PLASMA CELLS)
(*HINT - 'B' STANDS FOR 'BODIES-BUILDER') |
|
What are the functions of 'T-LYMPHOCYTES'?
|
DIRECTLY 'DESTROY' SPECIFIC TARGET CELLS
CELLS DESTROYED THAT HAVE BEEN INVADED BY VIRUS/CANCER. PROCESS IS CALLED 'CELL-MEDIATED IMMUNITY' (*HINT - 'T' STANDS FOR 'TERMINATOR') |
|
What are the 'CHARACTERISTICS' of 'MONOCYTES'?
(*THERE ARE 4 OF THEM) |
1. 'CHRONIC CONDITION' DEFENSE
2. ACTIVE IN PHAGOCYTOSIS 3. BECOME 'MACROPHAGES' 4. LIVE FOR 'MONTHS' EVEN 'YEARS' |
|
These type of 'LEUKOCYTES' 'INCREASE' during 'CHRONIC' conditions (e.g., tuberculosis/venereal disease).
|
MONOCYTES
|
|
These type of 'LEUKOCYTE' become 'MACROPHAGES' and are 'very active' in 'PHAGOCYTOSIS'. They can live for months and even years.
|
MONOCYTES
|
|
What is 'LEUKEMIA' defined as?
|
MALIGNANT 'BLOOD DISEASE'
'INCREASED' NUMBER OF 'LEUKOCYTES' *IMMATURE TO FIGHT OFF INFECTION |
|
With 'LEUKEMIA', what could be considered to be 'FATAL'?
Why? |
A SMALL 'INFECTION'
INCREASED NUMBER OF 'LEUKOCYTES' ARE VERY 'IMMATURE' AND ARE UNABLE TO FIGHT OFF INFECTION. |
|
During 'LEUKEMIA', the 'WBC' count may reach what number?
|
500,000/mm^3 'WBCs'
|
|
What are considered to be the 'most common' reasons for death among 'LEUKEMIA' patients?
*There are 2 of them |
1. INFECTIONS
2. HEMORRHAGE |
|
What is 'LEUKOPENIA' defined as?
|
DECREASED PRODUCTION OF 'WHITE BLOOD CELLS' (LEUKOCYTES).
|
|
What are the 3 possible causes for 'LEUKOPENIA'?
|
1. RADIATION
2. DRUGS 3. CHEMICALS |
|
What is the 'AVERAGE' number of 'THROMBOCYTES' (PLATELETS) in the body?
|
150,000-350,000/mm^3 PLATELETS (THROMBOCYTES)
|
|
What are 'THROMBOCYTES' also referred to as?
|
PLATELETS
|
|
What is a 'MEGAKARYOCYTE'?
|
VERY LARGE 'BONE MARROW CELL'
|
|
How are 'THROMBOCYTES' (PLATELETS) formed?
|
PIECES OF 'CYTOPLASM' THAT ARE SAID TO 'CHIP' OFF.
|
|
What is the name of the 'recently' identified 'HORMONE' that is said to 'INCREASE' the number of 'MEGAKARYOCYTES'?
|
THROMBOPOIETIN
|
|
What produces 'PLATELETS'?
|
MEGAKARYOCYTES
|
|
Where does the 'DESTRUCTION' of 'PLATELETS' occur?
|
IN THE 'SPLEEN'
|
|
What is the 'LIFE SPAN' range of 'PLATELETS' (THROMBOCYTES)?
|
8 DAYS TO MANY MONTHS
|
|
What do 'PLATELETS' play an important role in?
|
BLOOD CLOTTING
|
|
How do 'PLATELETS' perform 'BLOOD CLOTTING'?
|
'PLATELET PLUG' IS FORMED
'PLATELET PLUG' STOPS BLEEDING BEFORE ACTUAL CLOT IS FORMED |
|
TRUE OR FALSE
'PLATELET PLUGS' are formed 'many' times during the day. |
TRUE
'PLATELET PLUGS' are formed 'many' times during the day. THIS IS DUE TO SMALL SITES OF INJURY IN VESSELS IN THE BODY. |
|
Why do 'PLATELETS' not form in the 'BLOOD VESSELS'?
|
BLOOD VESSELS ARE EXTREMELY SMOOTH WHICH DO 'NOT' ALLOW PLATELETS TO STICK TOGETHER.
|
|
When do 'PLATELETS' begin to stick together?
|
WHEN EXPOSED TO 'COLLAGEN' (A PROTEIN)
|
|
As 'PLATELETS' begin to stick together, 3 things are released. What are the 3 substances?
|
1. ADP
2. SEROTONIN 3. PROSTAGLANDIN (THROMBOXANE A2) |
|
The 'chemicals' that are released upon the formation of a 'PLATELET PLUG' stimulate what process to occur?
|
STIMULATE 'VASOCONSTRICTION'
OTHER 'PLATELETS' BECOME STICKY |
|
'PLATELETS' also contain a very high concentration of what 2 molecules that are also found in muscle tissue?
|
1. ACTIN
2. MYOSIN |
|
Because of the 'ACTIN' and 'MYOSIN', 'PLATELETS' have the ability to do what in 'aggregated platelets'?
|
CONTRACT
|
|
The 'PLATELET PLUG' does 'NOT' expand and spread from damaged endothelium. Why does this happen?
|
UNDAMAGED 'ENDOTHELIAL CELLS' secrete 'PROSTAGLANDIN I2' (PGI2).
THIS INHIBITS 'PLATELET AGGREGATION' |
|
'PROSTAGLANDIN I2' (PGI2) is also known as what?
|
PROSTACYCLIN
|
|
There are 2 chemicals that the body secretes in order to 'INHIBIT' 'PLATELET AGGREGATION' on 'undamaged endothelial cells'. What are the 2 chemicals?
|
1. PROSTACYCLIN (PGI2)
2. NITRIC OXIDE (NO) |
|
'NITRIC OXIDE' has the ability to do 4 things with regards to 'PLATELET AGGREGATION'. What are they?
|
1. CAUSES VASODILATION
2. INHIBITS PLATELET ADHESION 3. ACTIVATION 4. AGGREGATION |
|
What is the definition of 'THROMBOCYTOPENIA'?
|
ABNORMALLY 'LOW' NUMBER OF PLATELETS
(50,000 AND BELOW) |
|
What is one of the 'SYMPTOMS' of 'THROMBOCYTOPENIA'?
|
EXCESS BLEEDING
|
|
'THROMBOCYTOPENIA' may result from 2 causes. What are the 2 causes?
|
1. IDIOPATHIC THROMBOCYTOPENIA (UNKNOWN CAUSES)
2. AUTOIMMUNITY ATTACK ON PLATELETS |
|
What numbers of 'PLATELETS' (THROMBOCYTES) is considered to be 'LETHAL'?
|
~10,000/mm^3 PLATELETS
|
|
The 'BLEEDING' from many small vessels is known as what?
|
THROMBOCYTOPENIA PURPURA
(*HINT - 'PURPURA' = PURPLE) |
|
How can 'THROMBOCYTOPENIA' be treated?
|
TRANSFUSIONS OF PACKETED PLATELETS
|
|
When the 'ENDOTHELIAL LINING' of a vessel is exposed to 'COLLAGEN PROTEINS', a process of 3 separate but overlapping mechanisms occurs. What are they?
|
1. VASOCONSTRICTION
2. PLATELET PLUG FORMATION 3. FORMATION OF BLOOD CLOT |
|
'VASOCONSTRICTION' is 'STIMULATED' by what during the 'BLOOD CLOTTING' process?
|
SEROTONIN
|
|
What causes 'VASOCONSTRICTION' during 'BLOOD CLOTTING'? What are some of the characteristics?
(*There are 3 things) |
1. VESSEL WALL IS CUT OR BROKEN
2. MUSCLES STIMULATED TO CONTRACT 3. BLOOD LOSS IS 'DECREASED' |
|
TRUE OR FALSE
In the absence of 'VESSEL DAMAGE', platelets are attracted to each other. |
FALSE
'PLATELETS' are 'repelled' from each other during 'VESSEL DAMAGE' |
|
What does the 'PLATELET PLUG' temporarily do?
|
TEMPORARILY 'CLOSES' THE VESSEL UNTIL CLOTTING MECHANISMS CAN FORM A CLOT.
|
|
What is the 'PLATELET PLUG' strengthened by?
|
PROTEIN FIBERS CALLED 'FIBRIN'
|
|
What are the two 'pathways' that result in the formation of 'FIBRIN'?
|
1. INTRINSIC PATHWAY (Inside)
2. EXTRINSIC PATHWAY (Outside) |
|
What is the main difference between 'EXTRINSIC' and 'INTRINSIC' pathways?
|
1. EXTRINSIC = TISSUE DAMAGE
2. INTRINSIC = VASCULAR DAMAGE |
|
What 'CLOTTING FACTORS' does the 'INTRINSIC PATHWAY' have that the 'EXTRINSIC PATHWAY' does not?
|
FACTOR 9, 11 AND 12
|
|
Where are 'PROTHROMBIN' and 'FIBRINOGEN' made?
(*Hint - They are 'PLASMA PROTEINS') |
MADE IN THE LIVER
|
|
What 'CONVERTS' 'PROTHROMBIN' to 'THROMBIN'?
|
CALCIUM
|
|
When 'THROMBIN' reacts with 'FIBRINOGEN' what is the result?
|
FIBRIN CLOT
|
|
What is the 'COLOR' of a 'CLOT'?
|
NO COLOR
CLOT IS DERIVED FROM 'PLASMA' CONSTITUENTS *THE RED COLOR COMES FROM 'RBCs' THAT BECOME TRAPPED. |
|
'PLATELETS' play a role in bringing what closer together?
|
FIBRIN THREADS CLOSER TOGETHER
|
|
TRUE OR FALSE
CLOTS DO NOT SHRINK IN SIZE |
FALSE
'CLOT RETRACTION' OR 'SYNERESIS' OCCURS BY BRINGING 'FIBRIN' THREADS CLOSER TOGETHER. |
|
What is the clotting factor 'NUMBER' for 'FIBRINOGEN'?
|
I
|
|
What is the clotting factor 'NUMBER' for 'PROTHROMBIN'?
|
II (2)
|
|
What is the clotting factor 'NUMBER' for 'TISSUE THROMBOPLASTIN'?
|
III (3)
|
|
What is the clotting factor 'NUMBER' for 'CALCIUM'?
|
IV (4)
|
|
What is the clotting factor 'NUMBER' for 'ANTIHEMOPHILIC GLOBULIN'?
|
VIII (8)
|
|
What is the clotting factor 'NUMBER' for 'CHRISTMAS FACTOR'?
|
IX (9)
|
|
What is the clotting factor 'NUMBER' for 'FIBRIN STABILIZING FACTOR'?
|
XIII (13)
|
|
What is the 'NAME' for clotting factor 'I'?
|
FIBRINOGEN
|
|
What is the 'NAME' for clotting factor 'II'?
|
PROTHROMBIN
|
|
What is the 'NAME' for clotting factor 'III'?
|
TISSUE THROMBOPLASTIN
|
|
What is the 'NAME' for clotting factor 'IV'?
|
CALCIUM
|
|
What is the 'NAME' for clotting factor 'VIII'?
|
ANTIHEMOPHILIC GLOBULIN
|
|
What is the 'NAME' for clotting factor 'IX'?
|
CHRISTMAS FACTOR
|
|
What is the 'NAME' for clotting factor 'XIII'?
|
FIBRIN STABILIZING FACTOR
|
|
What 'CLOTTING FACTOR' is the cause of 'HEMOPHILIA'?
|
FACTOR VIII (8)
ANTIHEMOPHILIC GLOBULIN |
|
What do 'ANTICOAGULANTS' do?
|
PREVENT 'BLOOD CLOTTING'
|
|
'ANTICOAGULANTS' are also referred to as what?
|
'BLOOD THINNERS'
|
|
What is 'DICOUMARAL' (COUMADIN)?
How does it function? |
ANTICOAGULANT (BLOOD THINNER)
INTERFERES WITH 'VITAMIN K' WHICH ALSO AFFECTS FACTORS VII, IX, AND X. *LIVER 'MUST' HAVE VITAMIN K TO PRODUCE CLOTTING FACTORS |
|
What is 'HEPARIN'?
How does it function? |
INTERFERES WITH THE FORMATION OF 'THROMBIN' FROM 'PROTHROMBIN'
*HEPARIN SHOTS GIVEN TO PATIENTS BEFORE SURGERY TO 'PREVENT' CLOTTING DURING/AFTER SURGERY. |
|
How do 'CITRATES', 'OXALATES' and 'EDTA' work as 'ANTICOAGULANTS?
|
TIE UP CALCIUM
|
|
Where is 'VITAMIN K' produced (greatest source)?
Where is it 'STORED'? |
PRODUCED = 'G.I. TRACT VIA BACTERIA'
STORED = 'LIVER' |
|
'NEWBORN BABIES' do 'NOT' have 'BACTERIA' in their G.I. tract. Because of this, what usually happens after a baby is delivered?
|
INJECTED WITH A 'VITAMIN K' SHOT
|
|
What is the definition of 'FRIBRINOLYSIS'?
|
LYSIS OF CLOTS
|
|
How does the 'FIBRINOLYSIS' begin?
|
CLOT STIMULATES RELEASE OF A SUBSTANCE FROM THE 'WALL' OF A BLOOD VESSEL
|
|
There is an 'ACTIVATOR' located in the 'PLASMA' which stimulates what to occur? With what protein does this start with?
|
LYSIS OF CLOTS
STARTS WITH 'PLASMINOGEN' PROTEIN |
|
When an 'ACTIVATOR' is stimulated after a clot is formed, what is the 'PATHWAY' for the clot to decompose?
(*There are 4 steps) |
'PLASMINOGEN' -> 'PLASMIN' -> 'FIBRIN' -> DEGRADED FIBRIN PRODUCTS
|
|
What is the 'NATURALLY' ocurring agent in the body that breaks up clots?
|
'PLASMIN'
|
|
TRUE OR FALSE
'PLASMIN' is very 'QUICK' at removing clots in the body. |
FALSE
'PLASMIN' is natural but 'NOT' quick. |
|
What are the 4 conditions that can cause 'EXCESSIVE' bleeding in humans?
|
1. LIVER DISEASE
2. VITAMIN K DEFICIENCY 3. HEMOPHILIA 4. THROMBOCYTOPENIA |
|
When 'LIVER DISEASE' is a factor in excessive bleeding, what is happning?
|
LIVER IS 'DECREASING' PRODUCTION OF 'CLOTTING FACTORS'
|
|
Where are the 'MAJORITY' of clotting factors produced?
|
LIVER
|
|
Someone diagnosed with a 'VITAMIN K' deficiency may have what symptoms?
Why? |
EXCESSIVE BLEEDING
LACK OF 'VITAMIN K' DECREASES FORMATION OF: 1. PROTHROMBIN 2. OTHER FACTORS |
|
What is 'HEMOPHILIA' defined as?
What 2 types are there? |
LACK OF FACTOR VIII (8)
(ANTIHEMOPHILIC GLOBULIN) |
|
When 'HEMOPHILIA' is diagnosed, what is its most 'COMMON' form?
|
HEMOPHILIA A
(LACK OF FACTOR VIII (8)) |
|
Someone who is lacking 'FACTOR IX (9)' would be diagnosed with what?
(*FACTOR 9 = CHRISTMAS FACTOR) |
HEMOPHILIA B
|
|
What is a 'THROMBUS' defined as?
|
CLOT THAT IS 'ATTACHED' TO A BLOOD VESSEL WALL
|
|
What is an 'EMBOLUS' defined as?
|
CLOT THAT 'DETACHES' from the wall and floats freely in the circulation.
|
|
'THROMBUS' formation is usually due to what 3 causes?
|
1. TRAUMA (INJURY) TO BLOOD VESSEL
2. SLOW BLOOD FLOW (USUALLY IN VEINS) 3. ROUGH SURFACE ON INSIDE OF BLOOD VESSELS (ARTERIOSCLEROTIC PLAQUES) |
|
What is 'THROMBOCYHTEMIA' defined as?
|
EXCESS PLATELETS
50,000 mm^3 OR LESS |
|
How does 'ASPIRIN' help fight against 'HEART ATTACKS'?
|
INHIBITS PLATELET AGGREGATION AND THE RELEASE OF PLATELET CLOTTING FACTORS
THEREBY 'DECREASES CLOT FORMATION' |
|
There are 3 general 'LINES OF DEFENSE' in the body. What are they?
|
1. EXTERNAL DEFENSE
2. PHAGOCYTIC CELLS 3. IMMUNITY |
|
What is the 'MAIN' source of 'EXTERNAL DEFENSE' in the body?
|
SKIN
|
|
What is 'LYSOZYME'?
|
'ENZYME' secreted from the skin that 'DESTROYS' bacteria.
|
|
There are 4 'MECHANISMS' in the body for modes of 'EXTERNAL DEFENSE'. What are they?
|
1. SKIN
2. DIGESTIVE TRACT 3. RESPIRATORY TRACT 4. GENITOURINARY TRACT |
|
What are the 2 types of 'IMMUNITY'?
|
1. NON-SPECIFIC
2. SPECIFIC |
|
What is 'NON-SPECIFIC IMMUNITY' defined as?
|
IMMUNITY THAT NON-SELECTIVELY DEFEND AGAINST DIESEASE.
|
|
What are the 5 different types of 'NON-SPECIFIC IMMUNITY'?
|
1. INFLAMMATION
2. INTERFERON 3. FEVER 4. NATURAL KILLER CELLS 5. COMPLEMENT SYSTEM |
|
How is 'INFLAMMATION' help as defense against disease in 'NON-SPECIFIC IMMUNITY'?
(*THERE ARE 3 REASONS) |
1. HELPS ISOLATE, DESTROY, INACTIVATE INVADING AGENTS.
2. REMOVE DEBRIS 3. PREPARE FOR HEALING AND REPAIR |
|
What are 'INTERFERONS' and how do they help as defense against disease in 'NON-SPECIFIC IMMUNITY'?
(*THERE ARE 3) |
PROTEINS THAT ARE RELEASE FROM VIRUS-INFECTED CELLS.
PROVIDES PROTECTION TO OTHER CELLS THAT MAY BE INFECTED BY THE 'VIRUS' |
|
How does 'FEVER' help as defense against disease in 'NON-SPECIFIC IMMUNITY'?
(*THERE ARE 2 REASONS) |
INHIBITS 'BACTERIA GROWTH'
MAY AID IN RECOVERY FROM INFECTION |
|
What are 'NATURAL KILLER CELLS' and how do they help as defense against disease in 'NON-SPECIFIC IMMUNITY'?
|
LYMPHOCYTE-LIKE CELLS THAT DESTROY VIRUS-INFECTED CELLS/CANCER CELLS
|
|
What is the 'COMPLEMENT SYSTEM' and how is it a help as defense against disease in 'NON-SPECIFIC IMMUNITY'?
|
PLASMA 'PROTEINS' THAT DESTROY FOREIGN CELLS BY ATTACKING THEIR PLASMA MEMBRANES
|
|
What is 'SPECIFIC IMMUNITY' defined as?
How does it work? |
SYSTEM THAT RESPONDS 'SELECTIVELY' TO INVADING AGENTS
'ANTIBODIES' ARE FORMED FROM PREVIOUSLY EXPOSED DISEASE. 'ANTIBODIES' SELECTIVE TARGET INVADERS AND DESTROY THEM. |
|
Why in 'SPECIFIC IMMUNITY' does the first exposure cause harm to the individual whereas the second exposure does not?
|
TAKES BODY SEVERAL DAYS TO MOUNT AN 'IMMUNE RESPONSE'
'ANTIBODIES' (SPECIFIC PROTEINS) ARE FORMED TO COMBINE WITH 'ANTIGEN' AFTER 1st EXPOSURE |
|
What is an 'ANTIGEN'
|
AN 'INVANDING AGENT' THAT INITATES A 'SPECIFIC IMMUNITY' RESPONSE
|
|
What is the 2nd exposure of the reaction between an 'ANTIGEN' and an 'ANTIBODY' called?
|
IMMUNE REACTION
|
|
There are 2 'BROAD TYPES' of 'SPECIFIC IMMUNE RESPONSES'. What are they?
|
1. HUMORAL IMMUNITY
2. CELL-MEDIATED IMMUNITY |
|
What is 'HUMORAL IMMUNITY' defined as?
|
HUMORAL = FLUID = BONE MARROW = (B-LYMPHOCYTES)
B-LYMPHOCYTES COMBAT INFECTION / BACTERIA |
|
What is 'CELL-MEDIATED IMMUNITY' defined as?
|
DESTRUCTION BY THE 'T-LYMPHOCYTES'
CELLS THAT ARE IN 'CLOSE PROXIMITY' OR HAVE 'PHYSICAL CONTACT' WITH THE VICTIM CELL TO DESTROY IT. |
|
TRUE OR FALSE
T-CELLS DO 'NOT' SECRETE ANTIBODIES |
TRUE
THEY DO 'NOT' SECRETE ANTIBODIES |
|
What is 'SELF-RECOGNITION' or 'TOLERANCE' defined as?
What is an example where this is important? |
ABILITY TO 'DISTINGUISH' MATERIAL THAT IS 'SELF' FROM MATERIAL THAT IS 'NON-SELF'
EXAMPLE = ORGAN TRANSPLANTS |
|
What is 'AUTOIMMUNITY' defined as?
|
FORMATION OF 'ANTIBODIES' AGAINST A PERSON'S OWN TISSUES
|
|
What are some examples of 'AUTOIMMUNE' diseases?
(*THERE ARE 2 OF THEM) |
1. RHEUMATIC FEVER
2. GRAVE'S DISEASE |
|
What is 'RHEUMATIC FEVER' defined as?
|
ANTIBODIES THAT ARE PRODUCED AGAINST 'STREPTOCOCCUS BACTERIA' CROSS REACT WITH THE HEART AND KIDNEY TISSUES.
'AUTOIMMUNE DISEASE' |
|
What is 'GRAVE'S DISEASE'?
|
ANTIBODIES STIMULATE THYROID GLAND WHICH MIMIC 'THYROID STIMULATING HORMONE (TSH)'.
|
|
What is 'ACTIVE IMMUNITY'?
|
THE BODY 'ACTIVELY' FORMS ANTIBODIES AGAINST ANTIGENS THAT IT HAS BEEN PREVIOUSLY EXPOSED TO.
(SELF PRODUCING) |
|
What are some examples of 'ACTIVE IMMUNITY'?
(*THERE ARE 4 OF THEM) |
1. MEASELS
2. CHICKEN POX 3. MUMPS 4. VACCINE |
|
What is a 'VACCINE'?
|
DEAD PIECES OF THE INVADER
ANTIBODIES CREATED FROM DEAD 'ANTIGENS' |
|
What is 'PASSIVE IMMUNITY'?
|
TRANSFUSING A PERSON WITH 'ANTIBODIES' IN PLASMA FROM SOMEONE ELSE THAT HAS BEEN ACTIVELY IMMUNIZED AGAINST A 'SPECIFIC ANTIGEN'.
|
|
What is the problem with 'PASSIVE IMMUNITY'?
|
'ANTIBODIES' DO NOT LAST LONG AND START TO DEGRADE SO IMMUNITY IS 'NOT' PERMANENT.
|
|
What are some examples of 'PASSIVE IMMUNITY'?
|
1. RHOGAM SHOT
2. MOTHER'S MILK |
|
TRUE OR FALSE
Passive Immunization with antibodies can 'ONLY' be accomplished with human immunoglobulins. |
FALSE
HUMAN IMMUNOGLOBULINS (ANTIBODIES) 'AND' ALSO ANIMAL IMMUNOGLOBULINS |
|
When is 'PASSIVE IMMUNITY' beneficial?
|
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) |
|
A person with type 'A' blood has what type of 'ANTIGENS' on the surface of each red blood cell?
|
TYPE A ANTIGENS
|
|
A person with type 'B' blood has what type of 'ANTIGENS' on the surface of each red blood cell?
|
TYPE B ANTIGENS
|
|
A person with type 'AB' blood has what type of 'ANTIGENS' on the surface of each red blood cell?
|
TYPE AB ANTIGENS
|
|
A person with type 'O' blood has what type of 'ANTIGENS' on the surface of each red blood cell?
|
'NO' ANTIGENS
|
|
Approximately how long after 'BIRTH' does the body begin to produce 'ANTIBODIES' in their 'blood'?
|
2-8 MONTHS AFTER BIRTH
|
|
'ANTIBODIES' in the 'BLOOD' are also called what?
|
AGGLUTININS
|
|
Where are 'ANTIGENS' located with regards to 'BLOOD'?
|
'ON' THE RED BLOOD CELL
|
|
What do 'ANTIBODIES/AGGLUTININS' do?
|
REACT W/ ANTIGENS OF OTHER BLOOD
|
|
What is considered to be the 'UNIVERSAL RECIPIENT'?
|
AB BLOOD TYPE
|
|
What is considered to be the 'UNIVERSAL DONOR'?
|
O
|
|
What happens if 'BLOOD TYPES' do not match during a 'TRANSFUSION'?
|
RECIPIENT'S ANTIBODIES 'ATTACH' TO THE DONOR'S RED BLOOD CELL 'ANTIGENS'
CELLS BEGIN TO 'AGGLUTINATE' |
|
What is 'HEMOLYSIS'?
|
RED BLOOD CELLS RUPTURE (LYSE)
CAUSED BY 'AGGLUTINATION' IN THE BLOOD FROM TRANSFUSION ERRORS |
|
How many types of 'Rh' antigens are there? Which is the most common?
|
6 COMMON TYPES OF 'Rh' ANTIGENS. ALSO CALLED 'Rh FACTOR'
TYPE 'D' IS MOST PREVALENT |
|
Are more people 'Rh-' or 'Rh+'?
|
MORE ARE 'Rh+'
|
|
Which factor in the 'BLOOD' next to the (ABO) group system has the greated 'clinical' importance?
Why? |
'Rh GROUP'
THIS GROUP HAS THE ABILITY TO CAUSE: HEMOLYSIS (HEMO=BLOOD, LYSIS=BREAK OPEN) OTHER 'HEMOLYTIC' DISEASES TO 'NEWBORNS' (e.g., ERYTHROBLASTOSIS FATALIS) |
|
When the 'Rh GROUP' is 'NOT' compatible during pregnancy and the 'MOTHER'S' antibodies attack the 'ANTIGENS' of the baby, what is this called?
|
'ERYTHROBLASTOSIS FETALIS'
|
|
Which form of the 'Rh GROUP' is the only one to 'PRODUCE ANTIBODIES'?
|
ONLY 'Rh -' CREATES ANTIBODIES
|
|
What is 'ERYTHROBLASTOSIS FETALIS' defined as?
|
'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' |
|
What would be the result of the following situation during a pregnancy:
MOTHER = 'Rh +' BABY = 'Rh -' FATHER = 'Rh -' |
NO 'ANTIBODIES' CREATED
(*ONLY 'Rh -' BLOOD TYPE CREATES ANTIBODIES) |
|
What would be the result of the following situation during a pregnancy:
MOTHER = 'Rh +' FATHER = 'Rh -' BABY = 'Rh +' |
NO 'ANTIBODIES' CREATED
|
|
What would be the result of the following situation during a pregnancy:
MOTHER = 'Rh +' FATHER = 'Rh +' BABY = 'Rh +' |
NO 'ANTIBODIES' CREATED
|
|
What would be the result of the following situation during a pregnancy:
MOTHER = 'Rh -' FATHER = 'Rh -' BABY = 'Rh -' BABY = 'Rh +' |
NO 'ANTIBODIES' CREATED
|
|
What would be the result of the following situation during a pregnancy:
MOTHER = 'Rh -' FATHER = 'Rh +' BABY = 'Rh +' |
'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'. |
|
What would be the result of the following situation during a pregnancy:
MOTHER = 'Rh -' FATHER = 'Rh +' BABY = 'Rh -' |
NO 'ANTIBODIES' CREATED
|
|
What does a woman who is 'Rh -' need to be injected with after giving birth to a 'Rh +' baby?
Why? |
'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' |
|
'A BLOOD' type has what kind of 'ANTIGENS' and what type of 'ANTIBODIES'?
|
'A BLOOD TYPE'
'A ANTIGENS' 'ANTI-B ANTIBODIES' |
|
'B BLOOD' type has what kind of 'ANTIGENS' and what type of 'ANTIBODIES'?
|
'B BLOOD TYPE'
'B ANTIGENS' 'ANTI-A ANTIBODIES' |
|
'AB BLOOD' type has what kind of 'ANTIGENS' and what type of 'ANTIBODIES'?
|
'AB BLOOD TYPE'
'A & B ANTIGENS' 'NO ANTIBODIES' (*UNIVERSAL RECIPIENT) |
|
'O BLOOD' type has what kind of 'ANTIGENS' and what type of 'ANTIBODIES'?
|
'NO ANTIGENS'
'ANTI-A & ANTI-B ANTIBODIES' (*UNIVERSAL DONOR) |
|
Where are the 'ANTIBODIES' for a specific blood type located?
|
ANTIBODIES = 'PLASMA'
|
|
Where are the 'ANTIGENS' for a specific blood type located?
|
ANTIGENS = 'ATTACHED TO BLOOD CELL'
|
|
A 'NORMAL' HEMATOCRIT IS:
1. 45% 2. 35% 3. 55% 4. 60% |
1. 45%
|
|
HOW MANY 'RED BLOOD CELLS' ARE PRODUCED EVERY SECOND?
1. 250,000 2. 1 MILLION 3. 2.5 MILLION 4. 500,000 |
3. 2.5 MILLION
|
|
WHICH HORMONE STIMULATES 'RED BLOOD CELL' PRODUCTION?
1. OXYTOCIN 2. ESTROGEN 3. ERYTHROPOIETIN 4. ADH |
3. ERYTHROPOIETIN
|
|
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 |
1. PERNICIOUS ANEMIA
|
|
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 |
3. LYMPHOCYTES ANO MONOCYTES
|
|
WHICH OF THE FOLLOWING DOES 'NOT' STIMULATE 'VASOCONSTRICTION'?
1. ADP 2. PLASMIN 3. SEROTONIN 4. THROMBOXANE A2 |
2. PLASMIN
|
|
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 |
3. A BLOOD CLOT THAT DETACHES FROM A BLOD VESSEL WALL AND FLAOTS FREELY
|
|
FORMATION OF 'ANTIBODIES' AGAINST A PERSON'S OWN TISSUE IS:
1. NON-SPECIFIC IMMUNITY 2. CELL-MEDIATED IMMUNITY 3. PASSIVE IMMUNITY 4. AUTO IMMUNITY |
4. AUTO IMMUNITY
|
|
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 |
2. TYPE AB
(*UNIVERSAL RECIPIENT) |