Review set 6 Flashcards

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1
Q

Atria

A

receiving chambers (pump blood into ventricles at the SAME time)

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2
Q

Ventricles

A

pumping chambers (highly muscular, left ventricle = thickest walls) - pump blood OUT of heart into arteries at the SAME time

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3
Q

Coronary arteries

A

supply oxygen and glucose to heart muscle (aerobic respiration) for pumping action – if a coronary artery is blocked, a heart attack may occur

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4
Q

Flow of blood into, through, and out of the heart

A
  1. Vena cava delivers deoxygenated from body to right atrium
  2. Blood passes through right atrioventricular (AV) valve into right ventricle, which pumps it through the right semilunar valve into the pulmonary arteries which take it to the lungs to be oxygenated (pulmonary circulation)
  3. Oxygenated blood returns to the left atrium of the heart through the pulmonary veins
  4. Blood passes through left AV valve into left ventricle, which pumps it through left semilunar valve into the aorta which takes it to the body (systemic circulation)
    Note: Heart valves (and valves in veins) maintain one-way blood flow!
    a. Atrial contraction builds atrial pressure and opens AV valves (blood flows into ventricles)
    b. Ventricle contraction closes AV valves and opens semilunar valves (blood flows into arteries – as
    arterial pressure increases, semilunar valves close)
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5
Q

Diagram the heart and check it from ms. manns slides

A

how do you feel?

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6
Q

Myogenic

A

signal for cardiac contraction arises in heart muscle itself

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7
Q

SA (sinoatrial) node works/process/ PACE MAKING

A
  1. SA (sinoatrial) node (pacemaker – specialized collection of nerves) in right atrium generates impulse, stimulating atria to contract (top to bottom)
  2. Impulse reaches junction between atria and ventricles and activates AV (atrioventricular) node
  3. AV node waits ~0.1 sec then sends signals causing ventricles to contract (from the bottom – apex of heart – up, so that blood is pushed up and out of ventricles to arteries)
    *This sequence of events ensures delay
    between atrial and ventricular contraction
    (maximizing blood flow
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8
Q

The RATE at which this sequence of events happens is your

A

RESTING( myogenic) heart rate

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9
Q

SA node is controlled by the

A

Medulla, Adrenal gland (on top of kidney) can also speed up heart rate by releasing adrenaline into bloodstream

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10
Q

IF CO2 levels rise what does the medulla do?

A

medulla sends signal to SA node through cardiac nerve to cause SA node to fire more frequently (increase heart rate)

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11
Q

As CO2 levels decrease what does the medulla do

A

medulla sends signal to SA node through vagus nerve to cause SA node to fire less frequently (decreasing heart rate/ returning to normal/ resting)

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12
Q

The Cardiac Cycle is

A

the series of events that take place in the heart over the course of ONE HEARTBEAT

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13
Q

Cardiac Cycle

A

Involves Systole (contraction – higher blood pressure reading) and Diastole (relaxation - lower blood pressure reading)
a. Blood flows freely from atria to ventricles (diastole) until ventricles almost full (~70%). This occurs due to slightly higher pressure in the atria than in ventricles
b. SA node fires, causing atria to contract (atrial systole), which causes higher pressure in atria in order to fill ventricles to maximum capacity (both atria contract at same time)
Note: atria have relatively thin walls, so the pressure produced by atrial systole is not very high, but because most of the volume of blood has already passively moved into each ventricle, atrial systole does not need to generate much pressure.
c. AV node is activated, “waits” for 0.1 sec, then sends signals to cause ventricles to contract (ventricular systole) - from bottom to top
d. Increased ventricular pressure causes AV valves to close (between atria and ventricles) causing first heart sound (“lub”) - the closing of these valves prevents backflow of any blood to the atrium.
e. High ventricular pressure overcomes the high pressures in arteries, causing semilunar valves to open and blood flows away from heart.
f. Pressure increases in the pulmonary arteries and aorta and decreases in the ventricles, which causes the semilunar valves to close, causing the second heart sound = “dub”)
g. Blood flows freely into the atria (atrial diastole)
h. Pressure in ventricles drops below pressure in atria (ventricular diastole), allowing AV valves to reopen and cardiac cycle starts again

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14
Q

Arteries, Pressure, Diameter and Vessel Wall thickness, Vessel Wall Features, Additional features

A

Pressure: High
Diameter and vessel wall thickness: Narrow Lumen surrounded by a thick wall (3 layers)
Vessel wall features: 3 layers; middle layer of wall is thick layer of smooth muscle/elastic fibers to maintain pressure between heart beats- high elasticity allows for elastic recoil to help push blood.
Additional features: Outer layer of wall contains collagen to prevent artery from rupturing under high pressure (no valves)

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15
Q

Capillaries, Pressure, Diameter and Vessel Wall thickness, Vessel Wall Features, Additional features

A

Pressure: Low
Diameter and Vessel Wall thickness: Narrow diameter with walls only one cell thick (decrease diffusion distance/ increase rate)
Vessel Wall Features: Some Contain pores/ fenestrations
Additional features: Involved in material and gas exchange between blood and tissues, so narrow to increase SA/V ratio for diffusion

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16
Q

Veins, Pressure, Diameter and Vessel Wall thickness, Vessel Wall Features, Additional features

A

Pressure: Low
Diameter and Vessel Wall thickness: Wide lumen (low pressure decrease resistance and increase blood flow) surrounded by a thin wall
Vessel Wall Features: 3 layers; thin walls because blood not traveling in pulses less muscle than arteries easier to compress and misshape
Additional features: Contain valves to prevent pooling of blood and maintain one way blood flow

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17
Q

What is blood composed of?

A

is a TISSUE, composed of plasma (fluid ~55%), erythrocytes (RBC’s ~45%), leucocytes (WBC’s = phagocytes – nonspecific immunity, and lymphocytes – specific immunity) and platelets (less than 1% for WBC’s + platelets)

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18
Q

What does blood transport?

A

nutrients (glucose, lipoproteins), oxygen, carbon dioxide, hormones, antibodies, urea and heat.

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19
Q

Atherosclerosis

A

build-up of plaque deposits (fats, cholesterol, cell debris etc.) in arteries
Atherosclerosis can cause partial or complete occlusions; plaque deposits are so substantial that vessel can no longer
supply even a minimally healthy amount of blood to the tissue.
Plaque deposits cause increased blood pressure (narrower lumen) in arteries, which causes chronic inflammation (swelling) and damages endothelial wall
Chronic inflammation leads to lipid, cell debris, calcium and cholesterol accumulation (rough/ hardened walls)
Fatty deposits (atheromas) develop in the arteries, narrowing the lumen (stenosis) and reducing elasticity of the arterial wall (more prone to rupture b/c cannot stretch as well under pressure)
If plaques break off of original deposits, they damage artery walls and cause clots to form (called a thrombosis)

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20
Q

If a thrombosis develops in a coronary artery what occurs?

A

coronary thrombosis) it can reduce blood flow/ oxygen and lead to a heart attack (an acute myocardial infarction)

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21
Q

risk factors for coronary heart disease

eggsoda

A
Exercise(lack of)
Genetics
Gender (male lower estrogen)
Smoking
Obesity 
Diet 
Age
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22
Q

Respiration

A

transport of oxygen to cells producing energy;

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23
Q

Respirations 3 processes

A
  1. Ventilation: Exchange of air between lungs and atmosphere (through breathing)
  2. Gas exchange: Exchange of oxygen and carbon dioxide in alveoli (lungs) and in bloodstream (by diffusion)
  3. Cell Respiration: Release of ATP from organic molecules (enhanced by oxygen – aerobic respiration)
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24
Q

Ventilation

A

Exchange of air between lungs and atmosphere (through breathing)

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25
Q

Gas exchange

A

Exchange of oxygen and carbon dioxide in alveoli (lungs) and in bloodstream (by diffusion)

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26
Q

Cell respiration

A

Release of ATP from organic molecules (enhanced by oxygen – aerobic respiration)

27
Q

Why is ventilation system needed

A

Maintains concentration gradient of oxygen (high) and carbon dioxide (low) in the alveoli of the lungs, so that oxygen diffuses from lungs into blood and CO2 diffuses from blood into lungs. Ventilation system allows continual cycling of air in lungs with atmosphere to maintain concentration gradients

28
Q

Alveoli structure and adapted to function

A

*Thin wall – Single layer of cells (small diffusion distance)
*Rich capillary network – maintain concentration gradients, and only one cell thick too
*Increased SA:V ratio – small, spherically shaped to increase surface area and decrease volume
*Moist – cells in lining secrete fluids to allow gases to dissolve so it
diffuses easier into blood (and to prevent alveoli from collapsing
on selves!

29
Q

Alveoli cells are

A

pneumocytes

30
Q

The 2 types of Alveoli cells or pneumocytes:

A

Type I: Gas Exchange (flattened/ thin to increase SA)
Type II: Secrete pulmonary surfactant - decreases surface tension so all alveoli expand at same rate under unequal pressure (prevent cells from collapsing in on/ sticking to themselves) - cube shaped

31
Q

The human ventilation system includes

A

the trachea, lungs, bronchi (singular = bronchus), bronchioles, and alveoli

32
Q

Ventilation what it uses

A

(exchange of air between lungs and atmosphere through breathing) involves the internal and external intercostal muscles (between ribs), the diaphragm (below lungs) and abdominal wall muscles, and it is driven by a negative pressure mechanism

33
Q

Inspiration

A

Diaphragm muscles contract (flatten downwards) and external (on outside) intercostal muscles contract (pull ribs up and out)
Thoracic cavity volume and lung volume increase (pressure of air in lungs drops below atmospheric pressure – air rushes in to equalize)

34
Q

Expiration

A

Diaphragm muscles relax (curve upward), abdominal wall muscles contract (pushing diaphragm up), external intercostal muscles relax (ribs fall), and internal (on inside) intercostal muscles contract (pulling ribs down)
Thoracic cavity volume and lung volume decrease (pressure of air in lungs rises above atmospheric pressure – air rushes out to equalize)

35
Q

How to measure ventilation/ ventilation rate?

A
  1. Count number of breaths (per minute)
  2. Chest belt and pressure meter (records ventilation rate by recording
    number of times chest rises and falls)
  3. Spirometer (measures volume of gas inhaled/ expelled per breath) -
    Note: changes in volume are shown as increasing (breathing in) or
    decreasing (breathing out) over time on a graph and each breath is one
    “wave” (shows tidal volume = amount of oxygen taken in in one
    breath = highest value (top of wave) - lowest value (bottom of wave))
36
Q

whats the science behind Ventilation rate changes with exercise

A

Exercise increases aerobic respiration and decreases blood pH (more CO2 in the blood), which ↑demand for oxygen; this causes breathing center in brain (medulla) to send signals to diaphragm and intercostal muscles to increase contractions to ↑ventilation rate (more breaths per minute), and/ or ↑ tidal volume (volume of air exchanged - taken in or out - with each breath)

37
Q

Emphysema

A

is a chronic/progressive disease where the walls of the alveoli are damaged (feeling of shortness of breath) - a form of COPD (chronic obstructive pulmonary disease)
Healthy alveoli turn into large, irregularly shaped structures with gaping holes, ↓ elasticity (so ↑ total lung volume at rest)
↓ SA, ↓O2 can reach the bloodstream
Causes: tobacco/marijuana/fumes/coal dust/air pollution

38
Q

Lung Cancer

A

is a cancerous growth (uncontrolled cell division) within the lungs.
Malignant cancer cells can take over healthy tissues of the bronchioles and alveoli – then eventually spread (metastasize) to the brain/bones/liver/adrenal gland
Lung tissues become dysfunctional can lead to internal bleeding, coughing up blood, wheezing, respiratory distress and weight loss
Causes: carcinogens (smoking, asbestos)/air pollution/ certain infections/genetic predispositions

39
Q

A pathogen

A

is a disease-causing (disrupts normal physiology) agent (bacteria, virus, fungus, prion etc.) - most are species-specific, but some can cross species barriers

40
Q

1st line of defense (non-specific = block all pathogens):

A

kin and Mucous Membranes
Skin and mucous membranes = surface barriers (1st line of defense – NONSPECIFIC) = prevent entry of pathogens into the body
Skin: Dry/ thick (15-20 layers of mostly dead cells), lower pH (slightly acidic due to sweat to prevent bacterial growth), biochemical secretions from glands (ex: sebaceous glands – secrete chemicals/ oils that inhibit bacterial growth), natural microflora to protect
Mucous membranes: Thin layer of living cells lining bodily tracts and eyes; secrete mucous to trap/ wash away pathogens to protect internal structures, mucous contains enzyme lysozyme (lysis of pathogens), may also contain ciliated structures to aid in movement of pathogens out of bodily tracts (respiratory system)

41
Q

2nd line of defense against pathogens

A

Phagocytic Leucocytes: WBC’s that ingest pathogens in the blood and in body tissues (non-specific = ingest ALL pathogens).

  • Phagocytic leucocytes (“wandering macrophages”) are NONSPECIFIC (2nd line of defence in addition to fever/ inflammation)
  • Phagocytic leucocytes move throughout blood vessels and tissues
  • Identify cells as “self” (MHC’s) or “nonself” by membrane proteins in cell surface (foreign surface proteins = antigens)
  • If antigens identified, leucocytes change shape (amoeboid movement) to engulf foreign substance/ cell (endocytosis)
  • Phagocytosed substances contained in vesicles that fuse with lysosomes for lysis/ breakdown (inside leucocyte)
42
Q

3rd line of defense against pathogens

A

SPECIFIC = production of ANTIBODIES by plasma cells - to target specific pathogens)
In a PRIMARY INFECTION (first exposure to a pathogen): Macrophages identify “non-self” antigens and engulf/ ingest pathogens
Antigens (or pieces of them) from the pathogen remain in the macrophage and are “displayed” or “presented” on the macrophage cell membrane to WBC’s called helper-T cells (TH cells) - this “activates” the TH cells
Helper-T cells release cytokines to activate specific B cells (B lymphocytes – produced in bone marrow – millions of different types) in the body that are able to produce the specific antibody that is needed for that specific pathogen
Because B cells exist in VERY small numbers in the bloodstream, once they are activated, they begin to divide rapidly (mitosis – exact copies) so that there are enough of them to produce the proper antibody in large enough amounts to be effective – this is called B cell cloning (aka clonal selection)

43
Q

What are the two types of cells that b cell cloneing produce?

A

Antibody-secreting plasma cells

Memory cells

44
Q

Antibody-secreting plasma cells:

A

make and secrete antibodies (~2000
secreted into the bloodstream every second) immediately to “target” the
(primary) infection for destruction

45
Q

Memory cells

A

long-lived cells which do not secrete antibodies initially. Instead, they
remain in the bloodstream to provide LONG-TERM IMMUNITY - will secrete antibodies if a subsequent (secondary) infection occurs (providing your body with immunity from the same pathogen should it invade again)

46
Q

Shape of Antibodies

A

Antibodies are Y-shaped proteins (also called IMMUNOGLOBULINS) that
are SPECIFIC to one type of antigen (like a lock and key) - constant region branches into two forks and these ends (of each “Y”) contain SPECIFIC antigen-binding sites (both ends bind to the same antigen). When antibodies bind to an antigen they “tag” it for phagocytosis and lysis (opsonization) or cause pathogen to agglutinate (stick together)

47
Q

Acquired immunity

A

is either active or passive and can be acquired through natural or artificial means:

48
Q

Active immunity

A

immunity due to the production of antibodies by the organism itself due to exposure to pathogen/ antigen

49
Q

Passive immunity:

A

immunity due to acquisition of antibodies from another organism/ source (placenta, colostrum, injection) - short -term immunity (as NO MEMORY CELLS/ OWN ANTIBODIES PRODUCED by this process)

50
Q

Vaccines explain

A

(containing weakened forms of pathogens or their antigens) confer active, long-term immunity.

  • Injected into body to trigger production of antibodies and memory cells in person’s body (triggers a primary response)
  • Vaccine contains weakened form of pathogen, injected into bloodstream of individual triggering primary immune response – B cell activation (antibodies) and memory cell formation (for long-term immunity if exposed to real/ live pathogen in future) - cause a FASTER, more INTENSE response if pathogen is encountered by body again.
51
Q

Passive immunity

A

Producing antibodies for commercial use

-Monoclonal antibodies (pregnancy tests, detection/diagnosis of disease, create injections for rabies/venoms etc.)

52
Q

How to produce monoclonal antibodies

A
  1. Inject lab animal with specific antigen and allow immune response to occur
  2. Harvest spleen (blood cells) and identify/ isolate specific B lymphocytes (plasma cells)
  3. Grow B lymphocytes (plasma cells) with myelomas (cancerous/ divide forever) and will fuse to create hybridomas
  4. ELISA test (antigen bound to enzyme that will change color if antibody binds) identifies hybridomas making specific antibodies and those continue to divide forever, producing desired antibodies indefinitely
53
Q

What are Antigens and what do they do?

A

Antigens can cause specific plasma cells to produce an antibody called IgE (primary exposure)
-If antigen is encountered again, IgE binds to mast cells (WBC’s) and they release histamines

54
Q

What does a histamine do?

A

-Histamines cause an inflammatory response (blood vessels dilate and become more permeable to leukocytes - so they can “get in there” and “fight” the foreign invaders better/ faster, which then causes swelling, pain, redness, and possibly a drop in blood pressure); histamine also causes congestion/ extra mucus production, sneezing, excess tear production, fever, and itching

55
Q

RBC’s

A

do NOT have nucleii, so they have BASIC surface proteins (antigens) - no MHC’s, just IA, IB, and/ or Rh
-RBC antigens can cause antibody production/ agglutination of cells/ clumping if transferred between incompatible individuals

56
Q

What do antibodies help determine

A

Antibodies used to determine blood type too (“clumping in a blood sample is a POSITIVE result for presence of that antigen - Ex: Anti-A Sera contains “A” antibodies that BIND to A proteins on the surface of RBC’s and cause clumping in the blood sample. IF clumping occurs, that protein IS present. NO clumping = that protein is NOT present)
-Note that “Anti-D” tests for the Rh factor (it is
either present + or absent -)

57
Q

Blood clotting

A

Blood clotting seals damaged blood vessels to prevent blood loss and prevent pathogen entry into body

58
Q

What occurs during blood clotting

A

Damaged cells release chemicals causing platelets to “stick” to it (primary plug) and platelets/ damaged tissue release “clotting factors”

  • Clotting factors convert prothrombin into thrombin
  • Thrombin catalyzes conversion of fibrinogen (soluble) into fibrin (insoluble)
  • Fibrin forms an insoluble “mesh” of fibers around damaged area to stabilize/ catch more “debris” to solidify
59
Q

Antibiotics are effective against what but not what? WHY?

A

Antibiotics are effective against bacteria but not against viruses.

  • Antibiotics are substances that kill/ inhibit bacteria by targeting/ blocking prokaryotic metabolic pathways (target key enzymes/ 70S ribosomes/ DNA replication/ RNA polymerase/ cell wall production etc.)
  • Human cells are EUKARYOTIC and do not have these features, so bacteria (prokaryotes) easy to target
  • Some bacteria have antibiotic resistance gene(s) - antibiotics ineffective on them, so they survive, reproduce, and pass on antibiotic resistance genes and more and more of population has resistance over time (can be conferred through transfer of plasmids between bacteria too)
  • Viruses takeover host cells and use host cell metabolic pathways – they do NOT have their own metabolic pathways -therefore, antibiotics are ineffective against them (instead – antivirals used to target viruses – ex: target reverse transcriptase in retroviruses)
60
Q

What does HIV do to the immune system?

A

HIV is a retrovirus (RNA), transmitted through exchange of bodily fluids, infecting helper-T cells; uses reverse transcriptase to convert RNA into DNA to infect host-cell genome; becomes dormant for many years then activates, destroying helper T cells (helper-T cells begin to die off, causing B cells to remain inactivated during infection = no antibodies and no memory cells) - this causes symptoms of AIDS(final stages of the infection), as person is no longer able to fight off pathogens the same way they did before. Because of this, secondary infections usually kill individuals with AIDS, as they have no long-term immunity anymore.

61
Q

William Harvey

A

Valves (in veins) ensure unidirectional blood flow; Heart pumps blood to body through arteries; Blood returned to heart through veins; Heart is a pump for blood; Blood flows in a single, connected blood network.

62
Q

Alexander Fleming

A

Penicillin: Discovery was serendipitous (happy accident) - mold began to grow on bacterial plate and secreted a “substance” (penicillin) that inhibited bacterial growth (antibiotic).

63
Q

Florey and Chain

A

Penicillin: Tested as antibiotic for medical use - used 8 mice; all injected with pathogenic streptococcus then 4 also injected with penicillin. Mice with penicillin lived, showing medical antibiotic applications of penicillin (mice without penicillin died). Then, started giving to sick humans! Now, it’s test on animals, test on healthy patients, test on sick patients.

64
Q

Jenner

A

Smallpox Vaccine: Jenner developed vaccine by testing on the 8-year old son of one of his servants. He purposefully infected the boy with cowpox (related to smallpox), let him react/ get sick and get better, and then purposefully infected him with smallpox (which killed about 30% of people at the time) - boy never became infected, so tested on a few more people, then smallpox vaccine accepted/ developed and given throughout 19th and 20th centuries until smallpox eradicated (first disease to be eradicated by a vaccine)!