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Test your basic knowledge |
MCAT Biology Circulatory System
Start Test
Study First
Subjects
:
mcat
,
health-sciences
Instructions:
Answer 50 questions in 15 minutes.
If you are not ready to take this test, you can
study here
.
Match each statement with the correct term.
Don't refresh. All questions and answers are randomly picked and ordered every time you load a test.
This is a study tool. The 3 wrong answers for each question are randomly chosen from answers to other questions. So, you might find at times the answers obvious, but you will see it re-enforces your understanding as you take the test each time.
1. Purpose of erythrocytes?
to transport O2 to tissues and CO2 to the lungs
varicose veins
atria and ventricles
WBC
2. Pump blood out of the heart at high pressures into arteries
oncotic pressure
ventricles
increased hydrostatic pressure in the capillaries - which increases the fluid that leaks out of the capillaries into the interstitum
pulse pressure
3. Tissue which the cytoplasm of different cells communicate via gap junctions
Functional syncytium
heart rate
neutrophil
Diastole
4. When do semilunar valves close?
Arterial pressure=ventricular pressure
Rh blood group
Glucose
CNS decreases vagal signal and sympathetic input increases
5. Muscular pump that forces blood through series of branching vessels
Hepatic portal vein
serum
Intercalated discs
heart
6. Why is the SA node the primary pacemaker?
It has the most Na leak channels - allowing to reach threshold potential first; all other nodes leak - but rate at as quick of a rate
Na leak channels
systemic arterial blood pressure
coronary sinus
7. Universal donor
amino acids and glucose
SA node
Waste
O- since there are no surface antigens for antibodies to bind to...
8. Difference in pressure=blood flow (L/min)*resitance ^P=Q*R
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9. Response by CNS when blood pressure is too high
heart
AV node
increase vagal signal and inhibits sympathetic input
systemic arterial blood pressure
10. Breakdown product of the hemogloblin heme group
bilirubin
systolic blood pressure
5 phases of cardiac muscle cell contraction
hypoxia
11. Allow Na to leak across membrane - causing cell potential to get closer to threshold potential; allow threshold to be reached for Ca channels to open let Ca into the cell
Na leak channels
Capillaries
Vagal Signal
macrophage
12. Inadequate blood flow - resulting in tissue damage due to shortage of O2 and nutrients - and increase of metabolic waste
venous blood pressure
AV node
Ischemia
Inflammation
13. 3 factors that dictate the affinity of hemoglobin for O2
heart
Temperature or metabolic rate
Granulocytes
varicose veins
14. What is the direct cause of edema?
Slow Ca channels
venous blood pressure
It is the same - otherwise it would lead to fluid backup
increased hydrostatic pressure in the capillaries - which increases the fluid that leaks out of the capillaries into the interstitum
15. Voltage - gated channels that stay open longer than Na channels and open later responsible for the plateau phase of cardiac muscle contraction
Slow Ca channels
nutrients - wastes - and WBC
CNS decreases vagal signal and sympathetic input increases
to transport O2 to tissues and CO2 to the lungs
16. Protein in RBC that transport O2 though the blood since O2 is too hydrophobic in plasma; protein has 4 subunits that change confirmation cooperatively depending on the concentration of O2
Hemoglobin
Coronary veins
cardiac output (L/min)
atria
17. Which is longer - diastole or systole?
Coronary arteries
Diastole is longer
5 phases of cardiac muscle cell contraction
hepatic portal system and hypothalamic - hypophosial portal system
18. AV valve between left atrium and left ventricle
fats
bicuspid (mitral) valve
coronary sinus
Repolarization of nodes
19. Blood clot or scab circulating in bloodstream
basophil
bilirubin
Thrombus
Sympathetic regulation of heart
20. Reservoirs where blood collects from veins
Erythrocytes
atria
Diastole is longer
Temperature or metabolic rate
21. Valves between the ventricle and the atria to prevent back flow
Frank - Starling Effect
Ohm's law
Hemoglobin
atrioventricular valves
22. Body's mechanism of preventing bleeding
Frank - Starling Effect
eosinophil
hemostasis
arteries
23. At the end of the capillary - is the osmotic pressure high or low?
High since the concentration of plasma proteins has increased due to movement of water
nutrients - wastes - and WBC
heart
fats
24. Adequate circulation - but O2 supply is reduced (no build up waste products or loss of nutrients)
hypoxia
nutrients - wastes - and WBC
Coronary arteries
basophil
25. Receptors in the carotid arteries and aortic arch that notify CNS if blood pressure is high or low
Baroreceptors
primary bicarbonate generated from CO2.
veins
Hemoglobin
26. Store and release histamine and are involved in allergic rxns
nutrients
Immunoglobulins (antibodies)
basophil
increased hydrostatic pressure in the capillaries - which increases the fluid that leaks out of the capillaries into the interstitum
27. 2 ways to increase venous return
1. increase total blood volume by retaining more H2O 2. Contraction of large veins - propelling blood toward the heart
urea
atrioventricular valves
ABO blood group
28. AV valve between right atrium and right ventricle
Baroreceptors
Valves of the venous system
tricuspid valve
It is the same - otherwise it would lead to fluid backup
29. Ensure the one - way flow through the circulatory system
valves
Third transportation of CO2 in the blood
Slow Ca channels
hypoxia
30. Where do all components of the blood develop from?
urea
bone marrow
nutrients - wastes - and WBC
adipocytes
31. 2 chambers of the heart
Slow Ca channels
atria and ventricles
Hemolytic disease of a newborn
Ischemia
32. 1. depolarization caused by fast Na channels - where action potential through intercalated discs reaches threshold potential - opening Na channels 2. initial depolarization with Na channels closing and k channels opening - but Ca channels also open 3
Inflammation
5 phases of cardiac muscle cell contraction
high osmolarity of tissues
venous return
33. Because the veins have essentially 0 pressure - these valves ensure one - way flow - skeletal muscle contraction encourages flow through veins
Hemoglobin
Valves of the venous system
AV node
Frank - Starling Effect
34. Where blood passes through 2 sets of capillaries before returning to the heart; Evolved as direct transport routes
1. increase total blood volume by retaining more H2O 2. Contraction of large veins - propelling blood toward the heart
Hemolytic disease of a newborn
atria
Portal systems
35. Open when threshold is reached causing membrane potential to increase/depolarize; operate slower than Na channels
bone marrow
venous return
Ca channels
Lipoproteins
36. Mother has Rh - blood with Rh+ antibodies that attack the babies Rh+ blood
Hepatic portal vein
Hemolytic disease of a newborn
Pulmonary and aortic semilunar valves
Baroreceptors
37. First branches from the aorta that provide the heart's blood supply
Na leak channels
T- tubules
Coronary arteries
Inflammation
38. Resting membrane potential of -90mV and have long duration action potentials
glycolysis. RBC have no ETC - FA oxidation - or TCA cycle
hemostasis
Inflammation
Cardiac muscle cells
39. Amount of blood pumped w/ each systolic contraction
stroke volume
Capillaries
to transport O2 to tissues and CO2 to the lungs
Portal systems
40. Essentially 0 mmHg - which results b/c of branching of vessels dissipating pressure to overcome resistance
Na leak channels
Tense
venous blood pressure
Rh blood group
41. Vessels where deoxygenated blood from coronary sinus continue to flow into heart
Ca channels
when person that is Rh - is exposed to blood that is Rh+
Coronary veins
fats
42. Neural sympathetic input by postganglionic neuron of norepinephrine innervating arterial smooth muscle
chylomicrons
adrenergic tone
fibrinogen
to transport O2 to tissues and CO2 to the lungs
43. Capillaries dilate - increasing the cleft size - which allows more H2O to move through to tissues
Inflammation
varicose veins
tricuspid valve
glycolysis. RBC have no ETC - FA oxidation - or TCA cycle
44. Where are RBCs broken down?
Spleen and liver
cardiac output (L/min)
tricuspid valve
Vagal Signal
45. Active form of fibrinogen - protein forms a mesh that holds platelet plug together to protect wound - ibrinogen is converted to (blank) by thrombin
AB+ since no antibodies are made to any blood type
fibrin
Coronary arteries
valves
46. Connected to SA node via internodal tract - and passes signal to Common bundle of His to contract ventricles
tricuspid valve
AV node
urea
heart rate
47. Contraction of the ventricles - where pressure increases rapidly - causing AV valves to close - Marks the beginning of the 'lub' sound
nutrients - wastes - and WBC
valves
Systole
AV node
48. What is the only process RBC use to generate ATP?
adipocytes
arteries
Thrombus
glycolysis. RBC have no ETC - FA oxidation - or TCA cycle
49. Request by tissues to increase blood flow - where build up of metabolic waste causes arterioles to dialate
bicuspid (mitral) valve
Internodal tract
Pulmonary and aortic semilunar valves
local autoregulation
50. Glycoproteins that are coded for by 3 alleles (A - B - i)
Hemoglobin
WBC
ABO blood group
increase vagal signal and inhibits sympathetic input