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PHYSIOLOGY II > BLOOD (WEEK II) > Flashcards

BLOOD (WEEK II) Flashcards

1
Q

Describe the Erythrocyte structure

A
  • BICONCAVE SHAPE provides a LARGE SURFACE AREA for diffusion of O2
  • THINNESS enables O2 to diffuse rapidly between the exterior and innermost regions of the cell
  • FLEXIBLE MEMBRANE allows to squeeze through narrow capillaries
  • HAEMOGLOBIN allows transport of O2
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2
Q

Describe the structure of Haemoglobin

A
  • Haemoglobin has two parts: GLOBIN PORTION (four highly folded polypeptide chains) & FOUR HEME GROUPS (non-protein that bind to each polypeptide)
  • Each of the four iron atoms combine reversibly with one molecule of O2
  • Haemoglobin can also combine with CO2, H+ portion of Carbonic Acid, CO, & NO
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3
Q

Why is 98.5% of O2 carried in the blood bound to haemoglobin?

A

Since O2 is poorly soluble in plasma

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4
Q

Why do Red blood cells not contain a nucleus or organelles?

A

To make room for more haemoglobin to carry more O2

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5
Q

Which enzymes remain within a mature erythrocyte?

A

Glycolytic enzymes & Carbonic anhydrase

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6
Q

Why are Glycolytic enzymes necessary in Erythrocytes?

A
  • To generate the energy needed to fuel active transport mechanism involved in maintaining proper ionic concentrations within a cell
  • Erythrocytes cannot use O2 since have no mitochondria so rely entirely on GLYCOLYSIS for ATP formation
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7
Q

What are the two ways that Carbonic anhydrase contribute to CO2 transport?

A
  • Carriage on haemoglobin
  • Metabolically producing CO2 into bicarbonate ion (HCO3-)
    [the primary form in which CO2 is transported in the blood]
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8
Q

Why do red blood cells have a small life span?

A

Red blood cells don’t contain a nucleus or organelles therefore the lack of DNA, RNA and Ribosomes means that they cannot synthesise proteins for cell repair, growth and division

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9
Q

Where does the cell cycle of an erythrocyte end?

A

In the Spleen

As a red blood cell ages, its plasma membrane which cannot be repaired becomes fragile and prone to rupture as the cell squeezes through tight spots in the vascular system. The spleen has narrow, winding capillaries which is a tight fit for the fragile cells.

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10
Q

What are special functions of the spleen?

A
  • Remove old erythrocytes from circulation
  • Limited ability to store healthy erythrocytes
  • Reservoir for platelets
  • Contains lots of lymphocytes
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11
Q

Describe what happens when there is reduced O2 delivery to the kidneys

A

1) Reduced O2 delivery to the kidneys stimulates them to secrete ERYTHROPOIETIN into the blood which stimulates ERYTHROPOIESIS by the red marrow
2) Erythropoietin act on undifferentiated stem cells stimulating their maturation into mature erythrocytes
3) Increased erythropoietic activity elevates the number of circulating RBCs increasing O2 carrying capacity of blood and restoring O2 delivery to tissues to normal
4) Once O2 to tissues is normal, EPO secretion is turned down

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12
Q

Why do red blood cells require Erythropoiesis?

A

RBCs cannot divide to replenish their own numbers so the old ruptured cells must be replaced by new cells produced in the bone marrow (ERYTHROPOIESIS)

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13
Q

Where were red blood cells formed during development before the bone marrow?

A

In the yolk sac then in developing liver and spleen

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14
Q

Where does erythropoiesis occur in adults?

A
  • Sternum
  • Ribs
  • Pelvis
  • Upper ends of limb bones
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15
Q

What are Reticulocytes?

A

Reticulocytes are immature erythrocytes that are released in large numbers by the bone marrow when demands for RBC production are high (e.g hemorrhage)

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16
Q

How are Lab-produced erythropoietin used clinically?

A

Used to boost RBC production in patients with suppressed erythropoietic activity (e.g kidney failure, chemotherapy)

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17
Q

What is Anemia and how is it caused?

A

Anemia is a below normal O2-carrying capacity of the blood which is characterised by a low hematocrit.

CAUSES:
- decreased rate of erythropoiesis
- excessive losses of erythrocytes
- deficiency in hemoglobin content of erythrocytes

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18
Q

What are the six types of Anemia?

A
  • NUTRITIONAL ANEMIA (dietary deficiency for a factor needed for erythropoiesis)
  • PERNICIOUS ANEMIA (inability to absorb enough ingested vitamin B12 from the digestive tract due to deficient intrinsic factor)
  • APLASTIC ANEMIA (bone marrow not producing enough RBCs despite all ingredients being available)
  • RENAL ANEMIA (kidney disease -> inadequate kidney function, inadequate erythropoietin secretion)
  • HEMORRHAGIC ANEMIA (losing lots of blood)
  • HEMOLYTIC ANEMIA (rupture of too many circulating erythrocytes)
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19
Q

What is Polycythemia?

A

Too many circulating RBCs and an elevated hematocrit

20
Q

What is the difference between Primary Polycythemia and Secondary Polycythemia?

A

PRIMARY POLYCYTHEMIA = tumorlike condition of the bone marrow in which erythropoiesis proceeds at an excessive, uncontrolled rate.
[excessive RBCs increases blood’s viscosity causing sluggish blood flow which reduces O2 delivery to tissues. Increased viscosity increases total peripheral resistance which may elevate blood pressure]

SECONDARY POLYCYTHEMIA = an appropriate erythropoietin-induced adaptive mechanism to improve blood’s O2 carrying capacity in response to a prolonged reduction in O2 delivery to the tissues
[slightly different since number of circulating RBCs is not increased, simply concentrated in a smaller plasma volume]

21
Q

Who discovered human blood groups?

A

Karl Landsteiner

22
Q

What are the differences in human blood due to?

A

The presence or absence of certain protein molecules called ANTIGENS and ANTIBODIES.
Antigens are located on the surface of RBCs and antibodies are in the blood plasma.

23
Q

What are the different combinations or Agglutinins?

A
  • TYPE O = no agglutinogens, contain both anti-A and anti-B agglutinins
  • TYPE A = type A agglutinogens & anti-B agglutinins
  • TYPE B = type B agglutinogens & anti-A agglutinins
  • TYPE AB = A & B agglutinogens but no agglutinins
24
Q

Describe blood group A

A

If you belong to blood group A, you have A antigens on the surface of your RBCs and B antibodies in your blood plasma

25
Q

Describe blood group B

A

If you belong to blood group B, you have B antigens on the surface of your RBCs and A antibodies in your blood plasma

26
Q

Describe blood group AB

A

If you belong to blood group AB, you have both A and B antigens on the surface of your RBCs and no A or B antibodies in your blood plasma

27
Q

Describe blood group O

A

If you belong to blood group O, you have neither A or B antigens on the surface of your RBCs and both A and B antibodies in your blood plasma

28
Q

What are the properties of the ABO gene?

A
  • ABO gene is autosomal
  • ABO gene is located on chromosome 9
  • A and B blood groups are dominant over the O blood group
  • A and B group genes are CO-DOMINANT
  • Each person has two copies of genes coding for their ABO blood group
29
Q

What are Rhesus (Rh) antigens?

A

Transmembrane proteins with loops exposed at the surface of red blood cells. They are used for the transport of CO2 and/or ammonia across the plasma membrane.

30
Q

Why is an Rh incompatibility so dangerous when ABO incompatibility is not during pregnancy?

A
  • Most anti-A or anti-B antibodies are of the IgM class (large molecules) which DO NOT cross the placenta
  • anti-A and anti-B antibodies destroy any foetal cells that enter mother’s blood
  • Shortly after each birth of an Rh+ baby, the mother is given an injection of anti-Rh antibodies. These destroy any foetal cells that got into her circulation before an active immune response is activated.
31
Q

What is Serology?

A

A direct detection of the ABO antigens
[main method used in blood transfusion centres and hospital blood banks]

32
Q

What does Serology involve?

A
  • Antibodies specific at detecting particular ABO antigens on RBCs
  • Cells that are of a known ABO group that are agglutinated by naturally occurring antibodies in the person’s serum
33
Q

What is Erythroblastosis Fetalis?

A

A hemolytic anemia in the foetus or neonate caused by trans-placental transmission of maternal antibodies to foetal RBCs. The disorder usually results from incompatibility between maternal and foetal blood groups, often Rh antigens.

34
Q

Describe how an Rh-Negative mother and an Rh-Positive foetus can be fatal

A

1) RBCs from the foetus can go into the mother’s bloodstream through the PLACENTA.
2) The Rh-Negative mother’s immune system treats the Rh-Positive fatal cells as a foreign substance and makes antibodies against them.
3) Anti-Rh antibodies may cross the placenta into the foetus where they destroy the foetus’ circulation red blood cells

35
Q

What are the signs of Rh incompatibility?

A

MOTHER:
- POLYHYDRAMNIOS (presence of excessive amniotic fluid surrounding the foetus)

BABY:
- PALLOR (unhealthy pale appearance)
- HEPATOSPLENOMEGALY
- Jaundice NOT at birth
- HYPOTONIA (decreased muscle tone)
- Mental retardation and hearing problems

36
Q

What are Exam/test indications for Rh incompatibility in foetus’?

A
  • A positive Coombs’ test result (Direct and Indirect Coomb’s test)
  • Fetal Blood Sampling for Rh sensitisation during pregnancy
  • A high level of bilirubin in the baby’s cord blood
37
Q

What is the Coombs’ Test?

A

A test that looks for antibodies that may bind to fetal blood cells and cause premature RBC destruction

38
Q

What is the difference between Indirect and Direct Coomb’s test?

A

INDIRECT COOMB’S TEST (mother) = for unbound circulating antibodies against red blood cells and is used to determine if the person has a reaction to blood transfusion

DIRECT COOMB’S TEST (baby) = to detect antibodies that are already bound to the surface of red blood cells in the baby

39
Q

What is Fetal Blood Sampling for Rh sensitisation?

A

Used to look at a foetus’ red blood cell count and oxygen level & looks for signs that your immune system is destroying fetal red blood cells

40
Q

What are the properties of Fetal blood sampling?

A
  • Directly from the umbilical cord or fetus
  • Tested for signs of anemia
  • Also known as CORDOCENTESIS or PERCUTANEOUS UMBILICAL CORD BLOOD SAMPLING
41
Q

Describe the prevention method for Rh incompatibility

A

Rh immune globulin

Rh immune globulin contains antibodies to the Rh factor in blood. Giving these Rh antibodies to an Rh-Negative pregnant woman will prevent her immune system from producing its own anti-Rh antibodies which would attack the Rh-Positive red blood cells of the foetus

42
Q

When should Rh immune globulin be given to an Rh-negative woman to prevent sensitisation?

A
  • After amniocentesis, fatal blood sampling or CVS
  • When bleeding occurs in the second or third trimester of pregnancy
  • At 28 weeks of pregnancy
  • After an external cephalic version of a breech foetus
  • After abdominal trauma during pregnancy
  • Within 72 hours after delivery of an Rh-positive infant
  • After a threatened or complete miscarriage or an induced abortion
  • Before or immediately after treatment for ectopic pregnancy or a partial molar pregnancy
43
Q

What is the treatment for Rh incompatibility (foetus)?

A
  • Aggressive hydration
  • Early phototherapy
  • Early exchange transfusion if required
44
Q

What is the treatment for Rh incompatibility (foetus)?

A
  • Aggressive hydration
  • Early phototherapy
  • Early exchange transfusion if required
45
Q

What does Early exchange transfusion do?

A
  • Removes Biliburin
  • Removes antibodies
  • Removes sensitised cells which are liable to be haemolysed
  • Replaces RBC numbers
46
Q

What is the antenatal management for Rh incompatibility?

A
  • Mother’s rise in titres
  • Giving anti D to the mother
  • Amniotic fluid bilirubin levels to looks at early delivery
  • Foetal transfusion to prevent onset of severe anemia and cardiac failure
47
Q

What are the properties of Fetal blood transfusions?

A
  • Can be given through the fatal umbilical vein
  • Intrauterine transfusion provides blood to Rh-positive foetus when fatal red blood cells are being destroyed by Rh antibodies
  • Keeps foetus healthy until it is mature enough to be delivered

PHYSIOLOGY II (15 decks)

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