Download Exam 3 Review KEY

BIOL 256 SI, Molly
Exam 3 Review
3/27/16
1.) Sketch a sarcomere below (this will be useful for later questions). Label each filament, zone,
disc, and line.
2.) Sketch the relationship between calcium, troponin, and tropomyosin below.
3.) A motor neuron and all the myofibers it innervates is called a:
a. Neuromuscular junction
b. Motor end plate
c. Motor unit
d. Sarcomere
4.) As a review from last unit, what was the role of calcium in a neuron? Is it the same function in
muscle contractions? If not, explain.
In a neuron, calcium triggered the release of vesicles filled with neurotransmitters.
In muscle contractions, calcium binds troponin and pulls tropomyosin off the myosin binding
sites on the actin filament.
5.) In 4 steps, describe the role of ATP in a cross-bridge cycle.
a. ATP is bound to myosin, releasing the myosin head from the actin filament
b.
Hydrolysis of ATP causes myosin head to cock back and bind actin
c.
Release of Pi causes a power stroke
d.
Release of ADP from the myosin head leaves myosin bound to actin
6.) Discuss with those around you if a muscle would contract in each of the following scenarios. If
not, explain.
a. ATP and calcium were available - Yes
b. No ATP or calcium were available – No, myosin couldn’t bind to actin
c. ATP was available but calcium wasn’t – No, myosin couldn’t bind to actin
d. Calcium was available but ATP wasn’t – No, myosin head wouldn’t release from actin
7.) Describe the difference between isometric and isotonic contractions. Give an example of each.
Isometric contractions – load doesn’t move/ muscle stays the same length
Isotonic contractions – load moves/ muscle shortens
8.) Place the following ques in the correct boxes. They may be used more than once.
red, white, fast, slow, oxidative, glycolytic, many mitochondria, few mitochondria, lots of
myoglobin, little myoglobin, many blood vessels, few blood vessels, fatigue resistant, fatigue
quickly
Type I
Red
Slow
Oxidative
Lots of myoglobin
Many mitochondria
Many blood vessels
Fatigue resistant
Type IIa
Red
Fast
Oxidative
Lots of myoglobin
Lots of mitochondria
Many blood vessels
Fatigue resistant/quickly
Type IIb
White
Fast
Glycolytic
Few mitochondria
Little myoglobin
Few blood vessels
Fatigue quickly
9.) Muscle fatigue occurs when the strength of a muscle contraction becomes weaker and weaker
until it no longer responds to the stimulus. What factors contribute to muscle weakness?
Decrease in oxygen, ATP, creatine phosphate, glycogen, and release of Ach by motor neuron
Increase in lactic acid
10.) In smooth muscles, how is muscle contraction similar and different than in skeletal muscles?
Smooth muscles don’t have sarcomeres, but they still have actin and myosin that slide over each
other. Also in smooth muscles, calcium ions bind calmodulin, not troponin like in skeletal
muscles.
11.) Blood is:
__55_ % plasma
__45_ % formed elements
__8_ % of body weight
12.) Fill in the missing terms or definitions.
e. __Oxyhemoglobin__ - hemoglobin bound to oxygen
f. Carboxyhemoglobin – carbon monoxide competes with oxygen at the heme, turning it
cherry red, blocking ability of oxygen to bind_____
g. __Carbaminohemoglobin___ - CO2 bound to AA of the hemoglobin
h. __Cyanohemoglobin_ - cyanide binds hemoglobin, turning heme blue
i. Deoxyhemoglobin - ____hemoglobin after losing oxygen______
13.) What happens when there’s too few/too many red blood cells?
Too few = tissue hypoxia
Too many = blood viscosity
14.) Anemia is blood with _abnormally low oxygen-carrying capacity____.
Describe the differences among:
a. Polycythemia – increase in RBC – viscous blood and increased blood pressure
b. Hemorrhagic anemia – result of acute or chronic loss of blood
c. Hemolytic anemia – premature rupture of RBC – increases the rate of RBC destruction,
inherited or acquired, due to fragile RBC or problems with Hb
d. Aplastic anemia – destruction or inhibition of red bone marrow – rare, cause unknown,
deficiency of RBC, WBC, and platelets
15.) Myelolasts develop into: eosinophils, neutrophils, and basophils
16.) Monoblasts develop into: monocytes
17.) Lymphoblasts develop into: lymphocytes
18.) Hemostasis is the process your body goes through to stop bleeding. There are three phases
involved. Name and describe them below:
e. (Phase 1) Vascular spasms – immediate vasoconstriction in response to injury
f.
(Phase 2) Platelet plug formation – Damaged blood vessels secrete the Von Willebrand
factor that allows platelets to adhere to the collagen and form a plug
g. (Phase 3) Coagulation (blood clotting) – blood changes from liquid to gel which blocks
the release of blood from the blood stream
19.) What’s the difference between a thrombus and an embolus?
Thrombus is a clot that is stationary. Embolus is a thrombus or other objects that have broken
away and entered the blood stream.
20.) Describe the path of electrical impulses through the heart. Drawing a diagram may be helpful!
SA node  (atria contract via atria contracting fibers)  atria conducting fibers  AV node 
bundle of His  bundle splits into 2 pathways (right and left) and carry impulse to apex 
Purkinje fibers carry impulse from apex to ventricular walls and up  (ventricles contract via
ventricular contracting fibers)
21.) How does the “all-or-none” law apply to myocardial cells?
In the case of myocardial cells, the “all-or-none” response applies to all the atria or ventricles
contract at the same time, or none of them contract.
22.) Heart block is due to damage of the ___atrioventricular __ node.
23.) Normal heart sounds resemble a “lub-dub” noise. What are the sounds that are abnormal “lubdub” noises?
Heart murmur
24.) Draw out an electrocardiogram output. Label each wave, complex, and interval. Below the
output, describe what is happening at each position listed above.
P wave = depolarization of SA node and atrial contraction
QRS complex = ventricles depolarize and contract/ atria repolarize and relax, but this part on the
graph is masked by the larger ventricles peak
T wave = ventricles repolarize and relax/ chambers are filling
P-Q interval = time impulse from SA node to atria to AV node
S-T segment = ventricles depolarize to the beginning of repolarization
25.) T or F: The heart’s biggest danger is running out of fuel for energy to its cells.
26.) Fill in the blank:
Reduced blood flow to cardiomyocytes usually occurs due to ___atherosclerosis___. This results
in ______decrease of oxygen to the cells____, which in turn increases ____lactic acid___. The
intracellular H+ and Ca2+ increase, which causes the __gap__ junctions to close, isolating the
injured cardiomyocytes. As a result, the individual feels ___angina pectoris___. Eventually, those
isolated cells __die_, causing ____fibrosis___, or weakening of the heart. If the weakening of the
heart persists, the end result is ____myocardial infarction___.
27.) Distinguish among arrhythmias, fibrillation, and ectopic focus.
Arrhythmias are uncoordinated atrial and ventricular contractions.
Fibrillations are rapid, irregular contractions due to the SA node not regulating the heartbeat.
Ectopic focus occurs when the SA node loses the control as pacemaker. Typically the AV node
takes over and sets the rhythm.
28.) Average stroke volume is ____70___ mL/beat. Average cardiac output is ____5.2___ L/min.
29.) Do preload, contractility, and afterload increase or decrease stroke volume as each of them
INCREASES?
As preload increases, SV increases.
As contractility increases, SV increases.
As afterload increases, SV decreases.
30.) Positive chronotropic factors _______increase____ heart rate, while negative chronotropic
factors ______decrease___ heart rate.
31.) Normal heart rate changes with age and with the type of exercise. How does endurance exercise
effect resting heart rate?
Endurance exercise lowers the resting heart rate through hypertrophy of the heart muscle.
32.) Describe angiogenesis.
Angiogenesis is the creation of new blood vessels by either increasing the number of blood
vessels or by enlarging the existing blood vessels.
33.) When body temperature increases, blood vessels near the skin will (vasodilate/vasoconstrict).
34.) An increase in peripheral resistance causes an increase in blood pressure. Place “increase” or
“decrease” beside each of the factors that affect peripheral resistance when each of them
INCREASES.
a. Blood viscosity - increase
b. Total blood vessel length - increase
c. Blood vessel diameter – decrease
35.) List the chemicals that increase blood pressure.
Norepinephrine, epinephrine, antidiuretic hormone (ADH), angiotensin II, endothelin,
prostaglandin-derived growth factor
36.) List the chemicals that decrease blood pressure.
Atrial natriuretic peptide (ANP), nitric oxide (NO), histamine, prostacyclin, kinins, alcohol