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MCAT PHGY > Circulatory > Flashcards

Circulatory Flashcards

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1
Q

What is perfusion?

A

the transfer / administration of blood flow through a tissue.

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2
Q

what is ischemia?

A

ischemia occurs when an individual has poor blood flow to a tissue. this may cause the accumulation of waste and inadequate supply of nutrients.

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3
Q

what is hypoxia, what is hypoxemia?

A

hypoxia: inadequate oxygen supply at the tissue level
hypoxemia: low levels of oxygen partial pressure in the blood

hypoxemic hypoxia is low tissue O2 due to low blood O2

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4
Q

what is anemia?

A

deficiency in RBC’s or hemoglobin

therefore anemic hypoxia would be low tissue O2 due to low O2 saturation or low blood content.

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5
Q

where does perfusion take place within the vascular system?

A

only within capillaries which are one cell thick called endothelial cells

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6
Q

what is angiogenesis?

A

formation of new blood vessles

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7
Q

What is the pulmonary and systemic circuit? what side of the heart deals with each? where does the blood return?

A

Pulmonary: blood is pumped from the Right ventricle to the lungs and back to the left atrium

Systemic: blood is pumped from the LEFT ventricle to the body and back right atrium

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8
Q

What are the two large veins that dump into the right atrium?

A

superior and inferior vena cava

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9
Q

What is the coronary sinus? what is special about it?

A

the coronary sinus is where all of the coronary veins pool their deoxygenated blood. This is the only deO2 blood that does not enter either vena cavae

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10
Q

what are the 4 valves of the heart? Where are they located?

A

Atrioventricular (AV) valves

  1. tricuspid valve between right atrium and ventricle
  2. Bicuspid / mitral Valve between the left atrium and ventricle

semilunar valves: between arteries and ventricles

  1. pulmonary
  2. aortic
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11
Q

what are varicose veins?

A

a result of valve failure in the venous system

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12
Q

Cardiac cycle: what are diastole and systole

A

they represent the relaxation and contraction of the ventricles

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13
Q

Cardiac cycle: what marks the initiation of systole?

A

at the very end of diastole, the ventricles contract and systole has begun

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14
Q

explain what occurs during systole?

A
  1. the rapid onset of pressure as the ventricles contract causes the AV valves to both slam shut (lub sound)
  2. the pressure continues to rise within the ventricles which eventually opens up the semi-lunar valves
  3. with arterial pressure is high enough the semi-lunar valves slam shut (dub)
  4. the ventricles are relaxing, decreasing pressure which allows blood to flow from the atria to the ventricles again
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15
Q

explain HR, SV, and CO?

A

HR is heart rate measured as beat per minute
SV is stroke volume which is the amount of blood ejected per systole
CO is the amount of blood pumped per minute (cardiac output)

CO = SV x HR

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16
Q

which has a higher cardiac output, Right or left ventricle?

A

neither!! they pump out the same amount of blood but battle against different amounts of pressure. (the higher pressure change for left V makes it larger)

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17
Q

What are some mechanisms that facilitate venous return?

A
  1. venous valves prevent back flow
  2. skeletal muscle pump propels blood upward
  3. respiration uses changing pressures in the chest to draw blood up
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18
Q

what are 3 ways to increase Cardiac output?

A

to increase cardiac output we must either increase HR or SV or both.

Frank-starling mechanism says that if you fill the heart with more blood, it will expand more. Therefore a greater venous return will fill the heart more. Muscle fibres will detect this and contract more forcefully produces a greater stroke volume.

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19
Q

what are two ways to use the frank-starling mechanism?

A

we need to increase venous return to the heart.

  1. we either retain more water so that more blood is in our circulation
  2. contraction of larger veins that pool into our heart
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20
Q

what is a functional syncytium?

A

A functional syncytium is a tissue in which all of the cells can communicate through gap junctions. Cardiac contractile cells are syncytium’s in which they are stimulated by neurons and then all contract at once.

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21
Q

where are the gap junctions of the heart found?

A

between all cardiac muscle cells there are intercalated disks where gap junctions are found

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22
Q

what is the cardiac conduction system

A

the cardiac conduction system is the wave of polarization that goes from the atrial syncytium to the Ventricle syncytium (they are separated neurally and by gap junctions )

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23
Q

Explain the cardiac conduction system of the heart (order and control)

A
  1. Sinoatrial node (SA node) fires through the atria
  2. the signal descends to the atrioventricular node (AV)
  3. This further descends the atrioventricular bundle
  4. spreads through the purkinjie fibres of the ve`ntricles
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24
Q

what are the V-G sodium and calcium ion channels of the heart muscle cell?

A

the V-G sodium channel is the same channel seen in neurons. This is also called the fast sodium channel

the V-G calcium channel is another voltage gated channel which allows for further depolarization of the heart at a certain threshold. Additionally, the calcium that rushes in induces the actin-myosin contraction action to occur

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25
Q

what are fast sodium channels and slow calcium channels?

A

fast sodium channels are the voltage gated channels in neurons and skeletal muscle cells. They cause depolarization

the slow V-G Calcium channels are the channels which open in phase 2 of the caridac myocyte action potential and cause the plateau phase of the action potential

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26
Q

What is a major direct result of the long depolarization of the heart contractile cells?

A

due to the slow calcium channels, the heart stays contracted for a longer amount of time which strengthens the force of contraction

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27
Q

what are t-tubules?

A

these are divot’s within the muscle cell membranes where where more V-G calcium channels exist. The entry of calcium here induces the release of more calcium from the sarcoplasmic reticulum.

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28
Q

how is the absolute refractory period affected by slow calcium channels?

A

the absolute refractory period will be longer since the heart remains fully depolarized for a longer amount of time

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29
Q

how does the amount of calcium in the extracellular environment affect heart contraction?

A

more of it will cause a stronger contraction

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30
Q

is the heart directly stimulated to keep beating by hormonal or neuronal control?

A

no!! it is intrinsic to specialized heart cells!

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31
Q

explain the activity of the SA node

A

certain cells of the heart in localized regions contain sodium leak channels. These channels are always open and allow for gradual depolarization. Eventually the cell will reach the threshold for CALCIUM V-G CHANNELS allowing calcium to rush in an depolarize the cell. This action potential is transmitted to other conductance pathways and through the intercalated discs

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32
Q

What are two major differences between the AP of nodal heart cells and regular muscle cells?

A
  1. nodal heart cells reach depolarization through sodium leak channels. At threshold the main regulator of depolarization is VG calcium channels
  2. skeletal myocytes reach threshold due to a neural synapse which causes VG sodium channels to reach threshold.
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33
Q

how does repolarization work of nodal heart cells?

A

VG calcium channels shut and K+ VG channels open

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34
Q

why doesn’t the AV node or purkinjie fibres depolarize on their own?

A

they do contain leaky sodium channels but they have fewer then the SA node. Resultantly, the SA node fires first and sets the pace for the heart

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35
Q

what is the resting potential for a cardiac muscle cell (contractile cell)

A

-90mv

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36
Q

explain the AP of a heart contractile cell starting from the nodal AP arriving to the contractile cell.

A

nodal AP arrives

phase 0 –> VG sodium channels reach threshold and
depolarize the cell (just like normal neurons but unlike nodal heart cell which use Ca++ only).

Phase 1 –> called the initial repolarization phase, the sodium channels close and the K+ channels open causing the membrane potential to drop slightly.

HOWEVER, calcium channels opened during depolarization which balance the efflux of potassium causing phase 2 aka the plateau phase

phase 3 –> calcium channels close, potassium channels persist

phase 4: RMP dictated by Na+/K+ ATPase and K+ leak channels

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37
Q

what are the internodal tract and bundle of his?

A

internodal tract connects the SA node with the AV node. When this impulse occurs, the signal is slightly delayed in the AV node to permit atrial filling/contraction.

Bundle of his which is just the AV bundle extending down to the purkinjie fibres.

38
Q

Why is the average heart rate 60-80 bbm if the SA node fires at a rate of 120 bbm?????

A

parasympathetic inhibition releases acetylcholine to receptors on nodal cells which constantly inhibits SA node depolarization.

39
Q

what nerve is primarily responsible for parasympathetic inhibition of the heart?

A

the vagus nerve, bitch… which creates the vagal tone of the heart

40
Q

how does the SNS affect the heart? 2 ways, 2 molecules

A
  1. SNS post-ganglionic fibres directly innervate the heart and release norepinephrine
  2. adrenal medulla hormone epinephrine goes through the blood and binds receptors

both increase HR and contractility force

NOTE: sympathetic pre-ganglionic neuron releases ACH and has a short axon. Post-ganglionic neuron releases NE and has a long axon

PARA LONG PRE

41
Q

what are baroreceptors? if blood pressure is too high what occurs via the CNS?

A

baroreceptors detect blood pressure in the aortic arch and the carotid arteries (arteries that supply the head)

if BP is high the CNS will respond by decreasing SNS activity and increasing vagal tone

42
Q

what is ohms law

A

V=IR

v voltage, i current, R resistance (inversely related with radius)

43
Q

explain

deltaP = CO x R

A

the change in pressure from two points equals our caridac output (blood flow) multiplied by resistance

44
Q

how would an increase in stroke volume influence BP?

A

increased SV means increased CO. an increased CO means increased BP

45
Q

how can we change blood flow through our body? there are two fundamental properties that can be altered?

A

resistance and cardiac output

46
Q

what are pre-capillarly sphincters?

A

these control resistance which are essentially just arteriole smooth muscle

47
Q

what is peripheral resistance and how is it calculated?

A

PR is a measure of total resistance in the cardiac system which is found by:

PR = P / Q
Q is blood flow
P is pressure
note: blood flow is just volume / time aka CO

48
Q

explain the CNS activity involved in peripheral resistance!!

A

The SNS is the only division that effects peripheral resistance.
The SNS is constantly innervating pre-capillary sphincters of arterioles by releasing norepinephrine. this produces the ADRENERGIC TONE of the body’s circulation.

The SNS can also directly alter its synapse in certain area’s to promote blood flow. (e.g. it causes vasoconstriction in the gut and vasodilation in skeletal muscle for flight or fight)

49
Q

What is systolic, diastolic, and pulse pressure?

A 
systolic = blood pressure during ventricle contraction 
diastolic = blood pressure during ventricle relaxation

pulse P: difference of the above two

120-80 = pp of 40mmHg

50
Q

explain how a sphygmomanometer works? (4 steps)

A
  1. inflate a cuff around the arm until blood flow is cut off (stethoscope hears nothing)
  2. gradually release pressure
  3. the point when you first hear a noise in the stethoscope is the point when systolic pressure slightly beats cuff pressure (our 120)
  4. when the noise becomes almost inaudible this is our diastolic pressure (80)
51
Q

true or false, 80mmHG is the lowest pressure possible our circulatory system for a normal person?

A

false, 80mmHg is the lowest artery pressure, pressure in the vena cava is almost zero

52
Q

when the ventricles contract, the arteries distend like balloons (they are highly elastic and muscular)

A

true

53
Q

explain auto-regulation of the circulatory system.

A

the SNS does not directly get info from all tissue to see what needs the most blood. Instead, waste products of tissue activate arteriole smooth muscle to relax which causes vasodilation.

therefore, if a tissue is under perfused, waste builds up and vasoD occurs naturally

54
Q

there are 4 blood proteins that are dissolved in the water of plasma, what are they?

A
  • albumin
  • immunoglobulins
  • fibrinogen
  • lipoproteins
55
Q

what is albumin?

A

a plasma protein which is essential for creating oncotic pressure (osmotic pressure due to the presence of proteins alone)

56
Q

what is immunoglobulin?

A

antibodies of immune system

57
Q

what is fibrinogen?

A

essential for blood clotting

58
Q

what are lipoproteins?

A

responsible for transporting other molecules within the blood stream

urea - just a nitrogen waste carrier

59
Q

what is hematocrit?

A

the volume of blood taken up by your erythrocytes (RBC’s)

60
Q

what is erythropoietin

A

this is a hormone produced in the kidney which stimulates RBC production in bone marrow

61
Q

what is unique about RBC’s?

A

They contain no nucleus or mitochondria. However they do require ATP through glycolysis

62
Q

explain blood type groups, they’re inheritance properties, and how they may be combined?

A

There are two blood type groups

1) ABO group which originate from the genes I(A), I(B), and i. Type A and B exhibit co-dominance. If A or B is paired with i, the pair exhibits classical dominance. if ii i is paired you get type O

2) Rh factor which exhibits only classical dominance.
RR and Rh make you Rh+. rr makes you Rh-

groups 1 and 2 are combined to give different forms of blood such as A+ which would arise from I(A)I(A) or I(A)i and from Rr or RR

63
Q

Explain why A and B blood types cause problems in transfusion of blood. Why does Rh not cause immediate problems upon transfusion?

A

Early in infancy, antibodies to A or B develop without being exposed to them. If a type A person is transfused with type B blood they will react negatively right away.
(note: the blood type you are means you do not have those antibodies)

Rh does not cause problems the first time since the antibodies do not arise in infancy. However if an Rh- person is transfused with Rh+ blood, they will develop antibodies to it. This is called sensitization. subsequent exposure to Rh+ will cause the transfusion rxn

64
Q

explain why Rh+ exposure effects mothers who are Rh-. What is the developing disease called ?

A

if an Rh- mom gives birth to an Rh+ kid, blood may mix at birth and the mom will develop Rh+ antibodies. When the mom gives birth to the next child, if it is also Rh+, if blood mixes from mom to child, the Rh+ antibodies will attack the child’s blood cells!

this is called hemolytic disease of the newborn or erythroblastosis fetalis

65
Q

how do you prevent hemolytic disease of a newborn?

A

inject the mom anti-Rh antibodies upon parturition of the first child. This will destroy any Rh+ cells from the child before the mom can mount an antibody build up. Prevents sensitization.

66
Q

what are the universal recipient and donor blood types?

A

donor –> universal D is O-

recipient –> universal R is AB+

67
Q

what is a key difference between erythrocytes and leukocytes?

A

RBC’s have no nucleus or major organelles and carry oxygen

WBC’s are normal eukaryotic cells which are involved in clean up and Immunity

68
Q

what are monocytes, lymphocytes, and granulocytes?

A

different types of white blood cells

69
Q

Explain WBC: monocytes

A

there is only one type of monocyte called

Macrophages –> phagocytosis via amoeboid motility (crawling around)

70
Q

Explain WBC: lymphocytes

A

B cells –> mature into plasma cells and produce antibodies

T-cells –> control immune response

71
Q

Explain WBC: granulocytes

A

neutrophil’s –> phagocytosis which makes pus

eosinophil –> destroy parasites + allergic rxns

basophil –> releases histamine: allergies

72
Q

what is hemostasis, what is responsible for it?

A

hemostasis is the bodies prevention of bleeding which is performed by platelet cells and fibrin protein

73
Q

explain the general process of hemostasis

A
  1. you get cut
  2. platelets begin to aggregate in the area of lesion
  3. protein called thrombin converts fibrinogen to fibrin
  4. fibrin coats the platelets and seals them
74
Q

what is a thrombus?

A

after a scab (platelets +thrombin) has formed it may eventually break off the side of the vessel and become mobile. This is called a thrombus and may cause a blood clot.

75
Q

explain cooperative binding of the heme group in hemoglobin.

A

one hemoglobin has one heme group which has 4 binding sites for oxygen. When NO O2 is bound all 4 sites have a tense position. In area’s of high O2 content such as the lungs, an O2 manages to bind the heme group. When this occurs the other areas adopt a relaxed state which increases their affinity for O2.

this explains why O2 is easily released in the tissues (where O2 content is low)

76
Q

Explain what the Bohr effect is of hemoglobin affinity.

A

Bohr effect explains that certain conditions increase the stability of the tense state of heme binding sites.

  1. increased temperature
  2. increased CO2 partial pressure
  3. decreased pH (therefore increased H+ conc.)

these are the characteristics of working tissue!! (why O2 goes into them from heme)

77
Q

what is percent saturation of hemoglobin?

A

percent saturation is a way to see how much oxygen is bound to the heme groups. 100% indicates every heme group is bound

to find it we use:

%sat = # of O2 molecules bound / # of binding sites

(# binding sites = # of h=Hb x 4)

78
Q

how can we make the oxygen-Hb dissociation curve shift to the right? what is the effect of this shift?

A

this is just the Bohr effect

  1. decreased pH
  2. increased temp
  3. increased PCO2

all of these will decrease the saturation of Hb for every partial pressure of oxygen, therefore more O2 will be released.

79
Q

what enzyme facilitates the conversion of CO2 and H2O into carbonic acid?

A

carbonic anhydase

80
Q

explain how CO2 is transported through the blood.

A

73% is turned to bicarbonate as a buffer
20% is integrated into RBC’s
7% is dissolved

81
Q

what is an intercellular cleft?

A

within capillaries there are gaps between endothelial cells which permit nutrients, waste, and leukocytes to pass thru them

82
Q

explain the absorption of glucose and AA’s and how they are integrated into the blood stream and then the tissue.

A

glucose and AA’s are absorbed by the intestine and enter the HEPATIC PORTAL VEIN which connects two capillary beds (intestine with liver) to allow these molecules to enter the liver.

83
Q

What are chylomicrons?

A

chylomicrons are what original absorbed fats are packaged into.

84
Q

explain the absorption of fats and how they are integrated into the blood stream and then the tissue.

A

unlike AA’s and glucose, fats get to by-pass the hepatic portal vein.

Fats are absorbed by the intestine and packaged into chylomicrons. These are sent into lacteals which connect into lymphatic vessels that drain into a vein by the neck. They complete circultion and end up back at the liver where the chylomicrons are converted into a different lipoprotein.

This new lipoprotein carries fats to adipocyte cells for fat storage.

85
Q

what two types of leukocytes can pass thru intercellular clefts of capillaries? why?

A
  1. neutrophils (granulocyte) which has phagocytic functions
  2. Macrophages ( monocytes) which have “”

due to their amoeboid motility (crawling)

86
Q

what two pressures encourage water to leave capillary intercellular clefts?

A
  1. hydrostatic pressure from the heart beats.

2. tissues high osmolarity (hypertonicity)

87
Q

how does the body try prevent water from leaving capillaries? what special molecule is involved.

A

to prevent h2o leaving, the plasma must have a high osmolarity too.

proteins such as albumin create an oncotic pressure which helps retain water

88
Q

explain what occurs in inflammation.

A

if an area has a pathogen or has been cut, the surrounding capillaries dilate which makes their open clefts circumference increase. This allows leukocytes to fit through. However, this also allows a lot of water through causing an edema.

89
Q

what is an edema?

A

fluid in tissue causing swelling

90
Q

Albumin is produced in the liver, alcoholics may have a decreased albumin production which lowers their oncotic pressure in capillaries. What may the result be?

A

less fluid retention in capillaries which will lead to a body wide edema!!

MCAT PHGY (8 decks)

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