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BIO 313 > Exam 2: Blood, Immune System, and Respiratory System > Flashcards

Exam 2: Blood, Immune System, and Respiratory System Flashcards

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1
Q

What is the average total blood volume & the relative volumes of erythrocytes & plasma (hematocrit)?

A

5 liters, 50-60% plasma, 40-50% formed elements (99% erythrocytes, <1% buffy coat (white blood cells, platelets))

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2
Q

How do we use hematocrit to measure health?

A

?

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3
Q

Major constituents of Plasma

A

Plasma proteins (7%) [Albumins (60%), Globulins (35%), Fibrinogen (4%), Regulatory Proteins (<1%)] water (92%), and other solutes (1%) (electrolytes, organic nutrients and wastes)

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4
Q

Function of erythrocytes and hemoglobin

A
  • Transport of O2 and CO2

- specialized protein with high affinity for binding to O2 and CO2

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5
Q

Where are erythrocytes produced (hematopoeisis)?

A

In red bone marrow

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6
Q

What are the dietary requirements for erythropoeisis?

A

Amino acids, Iron, Vitamin B12, folic acid, and many other nutrients

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7
Q

Why is iron balance important?

A

To make sure O2 levels remain high enough for respiration

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8
Q

Life Span of Erythrocytes

A

Formed in the bone marrow, then circulate in the blood for ~120 days, then erythropoeitin is stimulated to break down RBCs which swallowed up my macrophages in spleen, liver and bone marrow (AA’s and Fe go back to bones via transferrin) heme gets converted to bilirubin (very toxic to cells; cause of jaundice) which is sent to the liver and kidneys and eliminated in urine and feces

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9
Q

How is erythropoeisis regulated and stimulates erythropoeitin?

A

When O2 levels are low, the kidneys signal to make erythropoeitin, which triggers erythropoeisis in the bone marrow, which releases more RBCs, which raises O2 levels and shuts of the kidney’s synthesis of erythropoeitin

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10
Q

Polycythemia

A

higher than normal hematocrit (increase in RBCs), could be the result of EPO doping

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11
Q

Nutritional Anemia

A
  • low hemoglobin

- dietary deficiency in iron, B vitamins, or folic acid

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12
Q

Pernicious Anemia

A
  • low hemoglobin

- “intrinsic factor” not produced by stomach, thus Vitamin B12 not absorbed

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13
Q

Renal Anemia

A
  • reduced number of RBCs

- insufficient amount of EPO from the kidneys

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14
Q

Aplastic Anemia

A
  • reduced number of RBCs
  • hematopoietic stem cell failure; often due to destruction by toxic chemicals, radiation, cancer
  • could need bone marrow transplant
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15
Q

Hemorrhagic Anemia

A
  • reduced number of RBCs
  • caused by excessive bleeding
  • generally very short time
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16
Q

Hemolytic Anemia

A
  • reduced number of RBCs
  • rupture of excessive number of RBCs
  • could be caused by transfusion of wrong blood type
  • can cause death quickly, sometimes no treatment
  • 2nd transfusion ASAP, massive blood clots
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17
Q

Sickle Cell Anemia

A
  • abnormal hemoglobin caused by recessive alleles
  • lethal eventually (slow and painful)
  • rare in many populations except Africa and tropical areas
  • coexists with malaria
  • incomplete dominance = weird shapped cells, but immunity to malaria, high fitness
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18
Q

leukocytes

A

?

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19
Q

How are platelets formed?

A

cell fragments of megakaryote

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20
Q

Events of platelet plug formation

A

?

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21
Q

How is the platelet plug formation kept localized?

A

Prostacyclin keeps platelets from aggregating

  • present until injury
  • made by normal epithelium
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22
Q

What is the importance of the platelet plug in clot formation

A

temporary seal that promotes formation of blood clot

23
Q

Steps of the clotting cascade

A

Tissue factor 3 or platelet factor 3 trigger factor 10, and activates prothrombin activator which converts prothrombin to thrombin, thrombin then converts fibrinogen to fibrin that covers the platelet plug

24
Q

what is the function of thrombin

A

converting fibrinogen to fibrin

25
Q

Intrinsic vs extrinsic pathways

A

Intrinsic-platelet triggered

Extrinsic-tissue trauma releases Tissue Factor 3, can recruit intrinsic pathway

26
Q

how is the liver important in homeostaisis

A

it produces many of the clotting factors

27
Q

Mechanisms for clot formation limitation and clot removal

A

Fibrinolysis-removal of clot
-tissue plasminogen activator (t-PA) released from endothelial cells near clot activates Plasminogen (plasma protein trapped in clot) to convert to plasmin, which is an active enzyme that dissolves fibrin meshwork

28
Q

How are drugs that prevent clotting clinically useful?

A

after surgery to prevent blood clots - thrombolytic drugs

29
Q

Aspirin

A

prevents platelets from sticking by inhibiting synthesis of thromboxain, which tells the platelets to plug
-good blood thinner

30
Q

Antigen

A

molecule that stimulates immune response

31
Q

Antibody

A
  • protein produced by defense cells

- binds to antigen and promotes it destruction

32
Q

Antigenic determinant

A

the recognized part of the antigen

33
Q

What is immunogenicity and reactivity?

A
  • ability to stimulate proliferation of specific lymphocytes and antibody production
  • ability to react with products of activated lymphocytes and the antibodies released in response to them
34
Q

What is immunocompetence? Self-tolerant?

A

?

35
Q

How do cell surface antigens determine common human blood types?

A

The type of antigens located on the RBCs determines what type of blood you have
ex: antigen A = Type A

36
Q

Why do we make anti-A and anti-B antibodies beginning in infancy when normally we have to be exposed to an antigen before large scale production of antibodies?

A

?

37
Q

RhoGAM

A
  • kills fetal RBCs to prevent exposure for mother to Rh positive
  • prevents mother’s antibodies from attacking fetus
  • given right before and after birth
38
Q

Innate immunity

A

non-specific, no memory

-surface barriers & internal defenses

39
Q

Mechanisms for protection

A
  1. barriers at body surface
  2. Innate immune responses
  3. Specific immune responses (adaptive)
40
Q

Adaptive immunity

A

very specific, long-term protection, fast response

-immunizations

41
Q

Humeral Immunity

A

?

42
Q

Naive B Lymphocytes

A

primary response to antigen

  • genetically predisposed 1 per antigen
  • once exposed, memory B cells will come
43
Q

Memory B Lymphocytes

A
  • produced after first exposure to antigen

- produces strong immune response from 2nd exposure on, shorter effect of illness

44
Q

Natural Active Immunity

A

Naturally contracted, immunity coming from inside the body

Infection; contact with pathogen

45
Q

Natural Passive Immunity

A

Naturally contracted, immunity coming from outside of the body
antibodies pass from mother to fetus via placenta; or to infant via breast milk

46
Q

Artificial Active Immunity

A

Artificially acquired, immunity made inside the body

vaccine; dead or attenuated pathogens

47
Q

Artificial Passive Immunity

A

Artificially contracted, immunity made outside the body

injection of immune serum (gamma globulin)

48
Q

Functions of the respiratory system

A
  1. Provides O2
  2. Eliminates CO2
  3. Regulates blood pH along with kidneys
  4. forms speech sounds
  5. defends against microbes
  6. Influences atrial contractions
  7. Traps and dissolves blood clots from systemic circuit
49
Q

Conduction zone

A

Trachea thru terminal bronchioles

50
Q

Respiratory zone

A

respiratory bronchioles thru alveolar sacs

51
Q

Alveoli

A
  • most found in alveolar sacs
  • large surface area to volume ratio
  • surrounded by pulmonary capillaries
  • maximum gas exchange
52
Q

type I vs type II alveoli

A

?

53
Q

Boyle’s Law

A

gas will always conform to and fill its container

  • ideal gas law
  • V1P1=V2P2
  • when volume changes, pressure will change and vice versa
    ventilation: diaphragm contracts to increase volume, pressure drops, which brings air in and just the opposite for expiration

BIO 313 (1 decks)

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