Final Exam Review Flashcards
(425 cards)
1
Q
3 primary regions of the brain
A
forebrain, brainstem, cerebellum
2
Q
right side of brain controls
A
left side movement of body, left side sensory perception, spatial orientation, creativity, face recognition, music, dreams, philosophy, intuition
3
Q
left side of brain controls
A
right side movement, sensory perception. Logic, analytical processing, language and math skills
4
Q
functions of the thalamus
A
relay station for all sensory information except smell. Relay for all motor pathways. Interpretation center for sensory information (the modality (pain, heat, cold, touch pressure), but not the location or intensity)
5
Q
functions of basal nuclei
A
inhibition of muscle tone, coordination of slow, sustained movements, selecting purposeful patterns of movement and supressing useless patterns
6
Q
Reflex
A
response to a stimulus that occurs without conscious effort
7
Q
four basic reflex categories
A
level of neural processing (spinal or cranial)
efferent division controlling (somatic or autonomic)
developmental pattern (innate or conditioned)
Number of synapses (monosynaptic, postsynaptic)
8
Q
5 components of reflex arc
A
sensory receptor
affarent pathway
integrating center
efferent pathway
effector
9
Q
knee jerk reflex
A
affarent neuron to efferent neuron, isn’t processed by the brain first
10
Q
functions of hypothalamus
A
regulates: body temp, osmolarity of fluids, food intake, rage, agression, Anterior pituitary function, uterine contractility and milk ejection, sleep/wake cycles
11
Q
cardiac center (medulla
A
controls heart rate and strength of contraction
12
Q
vasomotor center (medulla)
A
controls blood pressure
13
Q
respiratory centers (medulla and pons)
A
controls rate and depth of respiration
14
Q
digestive center (medulla)
A
controls vomiting, swallowing, coughing, sneezing
15
Q
infant sleep
A
17 hrs
16
Q
teen sleep
A
9 hrs
17
Q
adult sleep
A
6-8 hrs
18
Q
reticular activating system
A
regulation of sleep and awakefulness
makes cortex more receptive to signals, inhibited by cocaine and amphetamines.
19
Q
afferent division of PNS
A
sensory and visceral stimuli
20
Q
efferent division of pns
A
somatic and autonomic nervous systems
21
Q
affarent fibers enter spinal cord via
A
dorsal root
22
Q
efferent fibers leave spinal cord via
A
ventral root
23
Q
Functions of the hypothalamus
A
TO FAR PUMAS
Temperature Osmolarity Food intake Agression Rage Pituitary Uterine Contractions Milk ejection Sleep/Wake
24
Q
Medulla oblongata
A
cardiac center (controls heart rate, strength of contraction), vasomotor center (controls blood pressure), respiratory centers (controls rate and depth of respiration, Digestive center (vomiting, swallowing, caughing, sneezing)
25
define sleep (clinical)
a state of decreased (not complete loss) of motor activity and perception
26
Sleep requirements for infants, teens, and adults
Infants- 17 hr/day
Teens- 9 hr/day
Adults 6/8 hr/day
27
Reticular formation
a nerve network in the brainstem that plays an important role in controlling sleep/wake
Makes the cortex more receptive to incoming signals
Uses acetylcholine, norepinephrine, dopamine, histamine
Cocaine and amphetamines target this region of the brain
Antihistamines block signaling in hypothalamus through competitive binding to histamine receptors
connects the spinal cord, cerebrum, and cerebellum and controls overall state of consciousness
28
How do afferent fibers enter the spinal cord?
via the dorsal root
29
How do efferent fibers leave the spinal cord?
ventral root
30
What is the ganglion?
collection of cell bodies outside of CNS
31
Do sensory receptors use neurotransmitter?
no
32
What do photoreceptors sense?
light
33
what do chemoreceptors sense?
chemicals dissolved in saliva (taste)
Chemicals in mucus (smell)
Chemicals in extracellular fluid (pain)
34
What do thermoreceptors do?
detect changes in temperature
35
What do mechanoreceptors do?
respond to pressure (vibration), sound waves (noise), and acceleration (balance and equilibrium)
36
define synesthesia
Refers to cross-sensory experience (i.e., a color has a taste)
Stimulus of one pathway leads to automatic involuntary stimulus of a second pathway
37
What is the purpose of sensory pathways?
primarily a protective mechanism meant to bring a conscious awareness that tissue damage is occuring or is about to occur
storage of experiences in our memory helps us avoid potentially harmful events in future
38
How does the brain sense the intensity of a stimulus?
frequency of action potentials. More frequent the AP's, the more intense the stimulus. Rapid firing of AP's add up to reach threshold easily and fire, presenting a strong stimulus
39
population coding
representation of a particular object by the pattern of firing of a large number of neurons. The stronger the stimulus will fire more neurons. Each overlapping neuron is connected by inhibitory neurons, the area where the stimulus is greatest will fire the most AP's and activate the inhibitory neurons on the other neurons, so the sensation is perceived in the correct spot. PRE-SYNAPTIC INHIBITION
40
define two point discrimination
the ability to discern that two nearby objects touching the skin are truly two distinct points, not one. Different in different areas of the body. Lips/Fingers best at it, upper arm and calf worst
41
lateral inhibition
The pattern of interaction among neurons in the visual system in which activity in one neuron inhibits adjacent neurons' responses.
42
fear of pain
algophobia
43
why is pain a good thing?
protective mechanism meant to bring a conscious awareness that tissue damage is occurring or is about to occur
Storage of painful experiences in memory help us avoid potentially harmful events in future
44
receptor for pain
nociceptor
45
pain neurotransmitters
Substance P (activates ascending pathways that transmit nocioceptor signals) and glutamate (excitatory neurotransmitte
46
Fast pain
sharp, acute pain. Transmitted on fast (A-Delta) fibers which are mylenated (12-30 mps)
47
Slow pain
dull, achey. Persists chronically. Transmitted on slow (C-fibers) fibers which are unmylenated (.2-1.3 mps)
48
gate-control theory
the theory that the spinal cord contains a neurological "gate" that blocks pain signals or allows them to pass on to the brain. The "gate" is opened by the activity of pain signals traveling up small nerve fibers and is closed by activity in larger fibers or by information coming from the brain.
SLow pain inhibits inhibitory neurons, so the pain is perceived in the brain.
When another stimulus comes along, it activates the inhibitory interneuron on the nocioceptor so pain conduction is stopped
49
Endogenous Opiates
natural morphine-like substances in the body that modulate pain transmission by blocking receptors for substance P.
Bind opioid receptors on postsynaptic neuron and induce an inhibitory membrane potential shift
Bind to opioid receptors on the afferent nocireceptor neuron and inhibits the release of substance P
Depends on presence of opiate receptors. Endorphins, enkephalins, dynorphin
50
Endogenous opiates depend on
presence of opiate receptors
51
prostaglandins
released from damaged tissue that sensitizes nocireceptors and cause pain.
Lower the threshold for AP in nocioceptor so moe are fired. Can use NSAIDS to inhibit them (including celebrex!)
52
How do sensory receptors work?
detect energy in "modalities", function w/o neurotransmitter!
53
Sensory receptor pathway (1,2,3 order neurons)
1st order neuron to CNS to 2nd order neuron to Thalamus to 3rd order neuron to cortex. Information sensed and stored for future use
54
Pain gene
SCN9-A
55
Draw out the pain pathway
draw
56
What are catecholamines?
epinephrine and norepinephrine
57
Sympathetic nervous system characteristics
increases during active states, fight or flight, increases heart rate, increases metabolism for energy, takes blood to the muscles and away from digestive system to fuel movement
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parasympathetic nervous system characteristics
rest and digest, lowers heart rate, lowers blood flow to muscles and increases it to GI tract, lowers rate of metabolism to store it for when its needed
59
Where is the sympathetic nervous system located?
T1-L2
60
Where is the parasympathetic nervous system located?
Cranial nerves 7,9,10, s2-s4
61
How many neurons are involved in autonomic processes?
2, one preganglionic in the spinal cord, one postganglionic that goes to the effector organ
62
Preganglionic neurons in sympathetic neurons
cholinergenic, post ganglionic has a nicotinic receptor
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Postganglionic neurons in sympathetic nervous system
adrenergenic neuron, releases nor/epinephrine to target organs that have adrenergenic receptors
64
Preganglionic neurons in parasympathetic
cholinergenic, release ACh to nicotinic receptor
65
Post Ganglionic in parasympathetic
cholinergenic, release ACh to Muscarinic receptor on target organ
66
Nicotinic receptors
respond to acetylcholine, 4 types, goes to adrenal medulla, skeletal muscle, ion channel opening, generally excitatory
67
muscarinic receptors
respond to ACh, 5 types, effector organs in PSNS, G-linked receptors, excitatory or inhibitory
68
Nicotinic receptor at the synapse sequence of events
ACh binds receptor, NaK channel opens, Na diffuses into cell
69
Muscarinic receptor in heart
ACh binds receptor
Gprotein subunits dissociate
G protein binds to K+ channel, opens it
K+ diffuses out of cell
70
Adrenergenic receptor
alpha and beta types, inhibitory or excitatory. G protein linked
71
Nicotinic and muscarinic- which is fast, slow?
Nic is fast, musc is slow
72
Secondary messenger system of muscarinic receptors
Neurotransmitter binds receptor
Activates G protein
Activates or inhibits enzyme
enzyme makes secondary messenger if stimulated
messenger opens/ closes ion channels or initiates other responses
73
alpha one andrenergic receptor pathway
responds to norepinephrine/epinephrine, alpha subunit binds to phospholipase C. PhC turns PIP2 into IP3 and DAG. IP3 goes to the ER and causes calcium release. DAG activates PKC which phosphorylates proteins and causes a response.
74
Neuron that acts on adrenal medula
cholinergenic, releases ACh at medulla which acts on endocrine cells to release epinephrine
75
alpha 2/Beta balance
alpha 2 is inhibitory, B1 is activator. if alpha is activated, the alpha protein binds to enzyme and inhibits it. If beta is activated, its alpha portion binds to enzyme, turns ATP to cAMP, activates PKA.
76
Varicosities
swellings on axons in neuroeffector junctions, contain vessicles. Varicosities are far away, their NT spreads out and binds to receptors all over the target organ. NT is either diffused away, degraded, or taken back up into presynaptic neuron
77
Somatic nervous system
innervates skeletal muscle, mostly voluntary, contains a single motor neuron
78
muscle makeup levels
fascicles, musclue fibers, sarcolemma, myofibrils, sarcomeres
79
Each myofiber is connected to
one motor neuron
80
motor end plate
invaginations containing large numers of nicotinic receptors
81
primary neurotransmitter of somatic NS
ACh
82
what does acetylcholinesterase do?
found between the invaginations of the motor end plate, terminates the signal allowing the muscle to relax
83
firing of a motor neuron process
AP opens calcium channels which triggers release of acetylcholine, ACH binds to nicotinic receptors, causing cation channels to open. Sodium flows into muscle and causes depolarization
84
Myasthenia gravis
inability to properly signal at NMJ. Leads to general muscle weakness
85
Where is myosin anchored?
m
86
Where is actin anchored?
z line
87
crossbridges
myosin heads
88
What happens to the IHZA lines/bands during contraction?
IHZ shorten, A stays the same
89
How does contraction happen?
AP runs down T tubules causing depolarization, DHP receptors change with depolarization and open ryanodine receptors. Calcium flows from SR through ryanodine receptors to sarcomeres
90
Cross bridge cycle
Calcium binds to troponin which binds to and releases tropomyesin
energized myosin (ADP + Pi) binds to actin
Pi is released, myosin binds and pulls actin
ADP is released, MA still bound together
New ATP binds, MA dissociate
ATP hydolyzed, myosin head is "cocked"
91
How does relaxation occur?
DHP receptor plugs ryanodine receptor
SERCA pumps take calcium back into SR (primary active transport)
Calsequestrin binds free calcium in SR
NaK pump moves Calcium into SR (secondary active transport)
92
Why is ATP needed during relaxation?
Provides energy for SERCA pumps
Binds to Myosin heads (to release from actin)
Indirect use through NaK pumps to antiport calcium
93
What is a twitch?
fast weak contraction
94
what is the latent period?
delay between AP and start of twitch. Happens becaue excitation events must occur before twitch happens
95
How is the amount of force generated by a muscle determined?
of cross bridges
96
twitch summation
multiple twitches occur, add up, lead to a lot of calcium release and caue a contraction
97
force produced by individual fibers caused b
frequency of stimulation
fiber length
fiber diameter
98
What causes muscle fatigue?
Loss of ATP, accumulation of metabolites, loss of nerve signaling, low oxygen, stress
99
what are satalite cells?
repair damaged muscle. located between sarcolamma and basolateral membrane. This is why muscle cells are multi nucleated. Satellite cells fuse to myofibers to regenerate them.
100
Hypertrophy (satellite cells)
increase in cell size. Satellite cells are responsible for muscle growth!
101
Free radical theory of aging
as we age, free radical generation goes up, muscle mass can be lost. Physical activity prevents loss of muscle mass.
102
Motor unit
one motor neuron plus all the muscle fibers it innervates (spread out throughout the muscle, not right next to each other)
As increased force is required, more motor units are recruited
103
Easiest to generate an action potential in a neuron with a _____ cell body
small
104
motor unit summation
Recruitment of more motor units with stronger stimuli. Will continue until a muscle generates enough force to move a load or it generates a maximum contraction
105
Orderly recruitment of motor neurons
Motor neurons that innervate many muscle fibers are bigger than those that innervate only a few fibers.
Small neurons are easier to depolarize than big ones
Recruitment of motor units occurs on a small/medium/large basis, depending on the magnitude of the stimuli.
This is how you're able to pick up a pencil and control it- only small motor units are being activated
106
isotonic contraction
muscle is allowed to shorten as it contracts
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isometric contraction
muscle not allowed to shorten, but there is tension
108
What effects the speed of a contraction?
Is the muscle slow or fast twitch?
How does it get its ATP?
109
eccentric contraction
muscle lengthens
110
concentric contraction
muscle shortens
111
How do fast twitch muscles get ATP?
glycolytic pathway (don't need oxygen!)
112
How do slow twitch muscles get ATP?
oxidative phosphorylation- require oxygen
113
Type I (slow oxidative) muscle fibers characteristics
```
High oxidative capacity
low glycolytic capacity
slow speed of contraction
low myosin ATPase
High mitochondrial count
High capillary density
High myoglobin content
High resistance to fatigue
Thin fiber diameter
Small motor unit size
Low force generating
```
114
Type IIA (fast oxidative) muscle fiber characteristics
```
High oxidative capacity
Intermediate glycolytic capacity
Intermediate speed of contraction
Intermediate myosin ATPase
High mitochondrial density
High capillary density
high myoglobin content
intermediate resistance to fatigue
intermediate fiber diameter
intermediate motor unit size
intermediate force generating capability
```
115
Type IIX (fast glycolytic) muscle fibers
```
Low oxidative capacity
High glycolytic capacity
Fast speed of contraction
High myosin ATPase activity
Low mitochondrial density
Low capillary density
Low myoglobin content
low resistance to fatigue
Large fiber diameter
Large motor units
High force generating capacit
```
116
What does training do for your muscle fiber types?
Can help you use each one better. Can increase mitochondria count, decrease lactate production, and improve motor skills. Probs won't change your natural count of slow/fast fibers though
117
Do mitochondria themselves change during training?
Yes, it looks like they become more efficient and the enzymes within them do as well
118
differences between fetal and newborn circulation
fetus doesn't need to pump blood to the lungs to be oxygenated.
Foramen ovale (connects right and left atria)
Ductus arteriosis (connects aorta and pulmonary artery)
Ductus venosus (connects umbilical blood and vena cava, bypassing the liver)
All close within 30 minutes of birth due to an increase in pressure on the left side of the heart
119
Heart disease
blood supply to the heart is blocked
120
how do they measure if you're having a heart attack
measure cardiac enzymes in blood, high levels are bad
121
how does high blood pressure cause heart attacks
stretches blood vessels, cholesterol comes to try and fix micro tears in the stretched vessels and that causes plaque buildup
122
Myogenic contraction
cardiac muscle automatically contracting without innervation from any neurons
123
purpose of autonomic innervation
increase rate and strength of contraction (sympathetic)
Decrease rate of contraction (parasympathetic)
124
Pacemaker cells
initiate action potentials
125
conduction fibers
transmit action potentials throughout the heart for coordination
126
Where are pacemaker cells concentrated?
In the SA/AV nodes
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Gap junctions
Permit rapid conduction of AP's from pacemaker cells to conduction fibers by permitting current to pass in the form of ions from one cell to another. Keep the myocardium from stretching when filled with blood
128
AV nodal delay
refractory period that hits AV node when action potentials from SA node get there. Makes sure the atria and ventricles don't contract at the same time, coordinated heartbeat
129
Gap junctions
Permit rapid conduction of AP's from pacemaker cells to conduction fibers by permitting current to pass in the form of ions from one cell to another. Keep the myocardium from stretching when filled with blood
130
Steps of a heartbeat (action potentials)
```
AP generated in SA node
AP's travel from SA to atria
AP's spread throughout atria to AV node
AP's travel to apex of the heart
Ap's spread upward through ventricles
Resting state
```
131
why can pacemaker cells generate their own action potentials?
they don't have steady resting potentials, they depolarize very slowly.
132
Steps of a generation of an action potential in the heart
+1. K+ channels close and "funny" channels open (NaK channel) until membrane potential hits -55 (short of AP threshold)
2. Influx of Na triggers opening of voltage gated Ca++ channels (t-type) that depolarize to -50 (threshold) then close
3. Threshold causes opening of L-type Ca++ channels that cause rapid depolarization
4. K+ channels open repolarizing the cell, Ca++ channels close
133
Why do the SA node, AV node, and Purkinje Fibers all have different rates?
So there is no competition between them, a good backup system
134
Differences between the generation of contractile AP's in cardiac tissue and skeletal tissue
AP of cardiac muscle causes DECREASE in pk
Depolarization causes opening of Ca++ voltage gated channels
Cardiac AP just as long as twitch so its impossible to tetanize heart. CANT be summated
135
Phases of the generation of contractile action potentials in cardiac muscle
Phase 0- depolarization causes opening of Na+ channels. MP peaks at +30-40
Phase 1- Opened Na+ channels close, deoplarization also caused closure of K+ channels, opening of L-type Ca++ channels
Phase 2- K+ channels stay closed, Ca++ channels open, stays depolarized.
Phase 3- K+ channels open. Begin to repolarize slowly. Ca++ channels close, AP terminated
Phase 4- Pk, Pna, Pca resting MP at -90 mv
136
Contraction of cardiac muscle steps
current spreads across gap junction
AP opens L-type calcium channel, calcium flows into cell
calcium binds to ryanodine channel, releasing more calcium (calcium induced calcium release)
Ca binds to troponin, etc
137
How is Ca++ removed from cardiac muscle?
SERCA pumps
Plasma membrane calcium ATPase
NaCa membrane exchanger (countertransport)
138
Phases of the cardiac cycle
1- blood returns to heart, passes through atria and into ventricles. Atria contract, driving more blood into the ventricles
2- ventricles begin to contract, when ventrical pressure is greater than atrial, AV valves close. Semilunar valves remain closed.
3- When ventrical pressure is high enough, semilunar valves open, blood flows out. When ventricle pressure falls below aortic pressure, the semilunar valves close again
4- All valves are closed, blood volume is constant, ventricles still relaxing. When ventricle pressure falls below atrial pressure, AV valves open again
139
Dicrotic notch
brief rise in aortic pressure caused by backflow of blood rebounding off semilunar valves. Ensures they stay closed
140
Which is longer, systole or diastole?
Diastole, lets the heart rest longer
141
Atrial fibrilation
action potentials generated from places other than SA node around the atria causing a quivering, not contraction, of the atria. Some of these action potentials cause depolarization and contraction of the ventricles, but it is very irregular. Forms clots in the atria from incomplete pumping that can travel in bloodstream
142
p wave
atrial depolarization
143
QRS complex
ventricular depolarization
144
T wave
ventricular repolarization
145
what's missing from ekg?
atrial repolarization
146
stroke volume
The amount of blood ejected from the heart in one contraction.
SV= end diastolic volume- end systolic volume
147
cardiac output
heart rate x stroke volume
148
What are the two ways in which cardiac output is regulated?
Regulating heart rate
Regulating stroke volume
149
Where does the parasympathetic nervous system innervate the heart?
At the SA and AV nodes
150
Where does the sympathetic nervous system innervate the heart?
At the SA and AV nodes, and at the ventricular myocardium
151
What neurotransmitter does the sympathetic NS release on the heart? What is it's affect?
Releases Norepinephrine, which modifies the initial depolarization under threshold. It causes Funny channels and T-type channels to be more open, causing an increased heart rate
152
How does norepinephrine open Funny and T-type channels?
Binds to a g-protein linked receptor, who's G subunit binds to Adenylate Cyclase (turning ATP to cAMP), which activates Protein Kinase, which phosphorylates the channels causing them to be more open and leading to more depolarization of the heart.
153
What nerve from the Parasympathetic NS innervates the heart?
Vagus Nerve
154
What does the parasymp release on the heart and what is it's effect?
Releases ACh at the SA and AV nodes. Decreases heart rate by making it take longer to reach threshold
155
How does acetylcholine slow the heart rate?
Binds to a muscarinic cholinergic receptor with two g linked proteins. One protein closes T-type channels while the other opens K+ channels, allowing it to leave the cell and hyperpolarize.
156
Which branch of the NS controls stroke volume?
Sympathetic
157
What are the factors that regulate stroke volume?
Venous return (raising the end-diastolic volume), and Sympathetic activity (epinephrine), causing harder contractions of the heart
158
How does the sympathetic nervous system cause a higher stroke volume?
Norepinehprine binds to g protein linked receptor, binds to adenylate cyclase (ATP to cAMP), Protein Kinase opens up L type calcium channels, opens Ca++ channels in Sarcoplasmic retticulum, increases activity of Ca++ ATPase bringing calcium back into Sarcoplasmic Retticulum, and causes more of an optimal overlap between actin and myosin. Overall, creates more cross bridges!
159
Frank-Starling Law of the Heart
When the rate at which the blood flows into the heart from the veins changes, the stretch on the ventricular myocardium changes, causing the ventricle to contract with greater or lesser force so that stroke volume matches venous return
More venous return, harder contraction
This is due to more optimum overlap of actin and myosin filaments when the heart is stretched
160
Resting cardiac output
5 L/min
161
Exercise cardiac output
25 L/min
162
Arteries
carry blood away from the heart. Low resistance, large diameter, elastin and collagen
163
Veins
Blood vessels that carry blood back to the heart
164
Arterioles
small vessels that receive blood from the arteries. Resistance vessels. Smooth muscle rings regulate radius and resistance.
165
Capilaries
microscopic blood vessels that connect arteries and veins. Site of nutrient exchange
166
Venules
small vessels that gather blood from the capillaries into the veins
167
blood pressure
the force exerted by blood on the walls of blood vessels
168
Formula for flow
Flow = change in pressure/resistance
169
What is the change in pressure in the systemic circuit?
85 mmHg
| pressure in aorta-pressure in vena cava
170
Pressure gradient in pulmonary circuit
| pulmonary artery-pulmonary vein
15 mm Hg
171
If pressure is so much lower in the pulmonary circuit, how can flow be equal?
Resistance must be much higher in systemic circuit and much lower in pulmonary circuit
172
Factors affecting resistance to flow. Which one can we control?
Viscosity of fluid
Length of the vessel
Radius of the vessel (MOST IMPORTANT)
173
Characteristics (muscle layers) in arteries and veins
arteries have smaller lumens but a large muscle layer, veins have large lumens and a small muscle layer
174
Does making the lumen smaller = lower or higher resistance?
higher. The blood must contact more of the surface of the vessel wall.
175
How much does vessel diameter affect resistance? (Formula)
R/r^4, if you double the size of the vessel, the resistance reduces by a factor of 16
176
Ischemia
restriction of blood flow to tissues resulting in a shortage of oxygen and glucose to keep cells alive (buildup of plaques)
177
Symptoms of Ischemic heart disease
angina, acute myocardial infarction, sudden death
178
Treatments for Ischemic heart disease
Blood thinners. Nitroglycerine as a vasodilator at the hospital, but prolonged exposure whould mean you would lose the ability to constrict all blood vessels
179
Normal blood pressure
120/80
180
Pulse pressure. Problems with it?
Systolic-diastolic. Doesn't take into account the starting pressures. Someone with very high BP could have the same pulse pressure as someone with very low BP
181
Calculating Mean Arterial Pressure (MAP)
Systolic + (2xDiastolic) all over 3
182
Why does blood flow slow in the capilaries?
pressure decreases over the vessel but resistance increases. They also have the greatest combined cross-sectional area, meaning the flow must slow to maintain an equal amount of fluid passing a point per unit time
183
Purpose of elastin and collagen in arteries
elastin allows arteries to stretch, collagen holds them firm at a certain stretching point. When blood contacts collagen, that is the start of heart disease
184
How do arteries act as a pressure reservoir?
They stretch when the heart pumps blood and then snap back, holding the pressure in their walls
185
Why do we get arteries and not vein disease?
arteries stretch and micro-tear. Veins have super low pressure so they don't stretch
186
What happens if you lose elastin?
hardened arteries, increase in BP
187
Tthis?otal peripheral resistance. How does constriction/dilation affect
Combined resistance of all blood vessels within the systemic circuit. Vasoconstriction causes increased resistance, dilation causes decreased resistance
188
What can and cannot cross through a capillary wall?
lipid soluble substances pass through wall
water soluble substances pass through pores
Exchangable proteins are moved by vesicular transport
Plasma proteins are stuck
189
Where does most absorption and filtration occur in the capilary?
Filtration occurs at the arteriole end, absorption at the venule end
190
Values for pcap, piif, picap, and piif at arteriole end
pcap=38
piif=0
picap=25
Pif=1
Net= +12 (more filtration)
191
Values at venule end
pcap= 16
piif=0
picap=15
pif=1
Net 16-26= -10 (more absorption). Overall, we filter more than we absorb
192
How to measure blood pressure
inflate BP cuff until flow of blood stopped, put stethoscope below cuff on artery, cuff deflated until blood can pass through (first sound is systolic BP), as the cuff deflates the sound becomes less audible until it disappears (diastolic BP)
193
Describe how standing up causes a lower arterial pressure
standing leads to pooling of the blood in the veins of the legs. This lessens venous return, which, via the frank starling law, says the heart will beat softer because not as much blood is reaching it. Decreased stroke volume means decreased cardiac output means decreased arterial pressure= light headedness.
194
Formula for mean arterial pressure
MAP= Cardiac Output x TPR
CO= heart rate x stroke volume
TPR= sum of all resistance in all vessels of the systemic circulation
195
How can you change cardiac output?
change rate or strength of contractions
196
How do you change TPR?
constrict or dilate vessels
197
Normal cerebral blood pressure
between 60-140 mmHg. Under 60, body can't adjust so you feel light headed.
198
Vasomotor center in medulla
controls sympathetic vasoconstrictor neurons. Its active, sending action potentials to sympathetic neurons innervating arteriols
199
Baroreceptors
Monitor blood pressure. ONe located in aortic arch and one in the carotid sinus
If pressure is too high, they fire many AP's to make it lower
If pressure is too low, they fire few AP's to make it higher
200
How does the baroreceptor work?
Its neuron is connected to three other ones. It is continually firing. If its firing quickly, its blocking AP's from the sympathetic nervous system wanting to put norepinephrine on the heart. If its firing slowly, those AP's get through. If it fires fast, it activates an acetylcholine neuron. SEE PICTURE ON SLIDE 13
201
Via the baroreceptor, the parasympathetic nervous system can control
action potential frequency. Heart rate.
202
Via the baroreceptor, the sympathetic nervous system can control
Action potential frequency, contractility, venomotor tone, and vasoconstriction
203
Factors affecting venous return
low pressure gradient
veins have low flow resistance
one way valves in veins protect backflow
muscle pump= contraction of muscle pushes blood toward heart through veins
204
varicose veins
abnormally swollen, twisted veins with defective valves; most often seen in the legs
205
the muscle pump
The rhythmic mechanical compression of the veins that occurs during skeletal muscle contraction in many types of movement and exercise, for example during walking and running, and assists the return of blood to the heart.
206
Respiratory movements and blood flow
pressure in the thorax decreases when you breathe in- this causes blood to rush into the chest. One way valves prevent backflow.
207
Sympathetic vasoconstriction
vasoconstriction pushes blood back toward the heart
208
venomotor tone
smooth muscle tension in the veins
209
What are the three layers of blood after centrifuging?
Erythrocytes, Buffy coat, plasma
210
What does the buffy coat have in it?
White blood cells and platelets
211
What is plasma made of?
Primarily water (91%), but 7-9% plasma proteins. Albumin is the most abundant
212
function of albumin in plasma
maintains osmotic pressure in blood (prevents edema), serves as a carrier for fatty acids and other hydrophobic substances
213
What do globulins do? (plasma protein)
blood clotting, immunodefense
214
What does fibrinogen do? (plasma protein)
Blood clotting
215
What pressure is due to albumin concentration in the plasma?
Picap and Piif, the flow of solutes in and out of the capillary
216
Characteristics of erythrocytes
No nucleus or organelles, but do have glycolytic enzymes. Hemoglobin to transport oxygen and CO2.
217
How long do erythrocytes live?
about 120 days
218
Where are erythrocytes produced?
bone marrow (cranial, costal, and sternal in adults)
219
Sickle cell anemia- causes, symptoms, evolutionary reason
Recessive mutation in hemoglobin gene causes oddly shaped and sharp erythrocytes
mostly found in persons of African descent
Cells don't carry oxygen well and are "sticky", they cannot travel well through blood vessels and often clot.
Patients experience painful crises that can last days
Developed as an evolutionary advantage against malaria
220
hematocrit
percentage of blood volume occupied by red blood cells
42-52 normal for men 37-47 normal for women.
calculated by height of erythrocytes/height of whole column
221
anemia
low RBC count leads to decreased oxygen carrying capacity. (<40 in men, <37 in women)
Symptoms: Dyspnea (difficulty breathing), Tachycardia (super fast heart rate), fatigue
222
Hemorrhagic anemia
loss of blood
223
pernicious anemia
nutritional deficiency- not enough vit B12
224
Renal anemia
kidney disease leads to decreased erythropoietin production
225
Aplastic anemia
bone marrow cells destroyed by radiation/ drugs
226
How are erythrocytes produced?
1. Kidneys detect reduced O2 (due to lower O2- carrying capacity of blood) and release erythropoietin (EPO).
2. EPO stimulates erythropoiesis by bone marrow.
3. Additional erythrocytes increase oxygen carrying capacity decreased EPO release by kidneys
227
What happens when an RBC is broken down?
biliruben goes to the liver, joins with bile and stool (what makes it brown)
228
Polycythemia
too many RBC's
229
primary polycythemia
bone marrow tumor
230
secondary polycythemia
chronic hypoxia (high altitude)
231
Blood doping
inject RBC's or erythropoietin, increases oxygen carrying capacity of blood. Also makes it more viscous and decreases flow, so the heart must work harder to pump it. Could cause stroke or heart attack
232
How does the hematocrit change is anemic? Polycythemic? Dehydrated?
Amemic- much lower than normal
Polycythemia- much higher than normal
Dehydration- much higher than normal
233
Hemostasis (and steps)
cessation of bleeding
Vasoconstriction
Formation of platelet plug
formation of fibrin mesh
234
what are platelets?
Small fragments of cells made from stem cells
235
1st step of hemostasis
vascular spasm- damage activates sympathetic nervous system which causes constriction. Less blood flow to area means less blood loss
236
Platelet plug formation
Healthy cells secrete nitric oxide and prostacyclin, but a damaged vessel doesn't. When floating platelets come in contact with collagen, they area activated and become "sticky". They release ADP to stimulate agregation and then thromboxane A, inducing more cells to release ADP and thromboxane A. Positive feedback!
Platelet plug releases seratonin and epinephrine ( constriction, smaller hole in vessel, less bleeding)
Thromboxane A and prostacyclin are both derrivatives of arachadonic acid
237
Blood clot formation
Exposure of plasma to collagen initiates reactions that convert fibrinogen to its active form of fibrin. Fibrin forms a meshwork with bloodcells trapped between fibers that reinforces the platelet plug
238
What does thrombin do?
converts fibrinogen to fibrin.
A phospholipid on the surface of activated platelets activates thrombin
239
Intrinsic fibrin formation
7 steps, all chemicals necessary for this pathway are found in the blood
240
Extrinsic fibrin pathway
4 steps, chemicals released by damaged tissue initiates shortcut
both pathways work together, intrinsic in the vessel, extrinsic in surrounding tissues
241
Blood clotting feedback
Thrombin is activated and activates fibrinogen which activates more proteins that activate thrombin. Positive feedback.
242
What surrounds the alveoli?
capillaries
243
flow rate through airways
change in pressure/resistance
244
COPD (chronic obstructive pulmonary disease)
A group of lung diseases that block airflow and make it difficult to breathe.
Bronchioles lose their shape and become clogged with mucus, walls of alveoli are destroyed, forming fewer, larger alveoli.
245
muscles involved in breathing
diafragm, intercostal muscles, abdominal wall.
246
How is air moved in and out of the lungs?
When the diafragm and other muscles contract it creates a pressure difference with the air outside the body. In order to equilibrate, air rushes into the lungs. Reverse is true for exhaling
247
transmural pressure
alveolar pressure - intrapleural pressure.
If not maintained breathing can't occur. Intrapleural pressure is always -, and intraalveolar pressure isn't
248
How does Boyle's law explain breathing
When you inhale volume increases so pressure must decrease, air flows in.
When you exhale volume decreases so pressure increases and air flows out
249
Pressures during inspiration and expiration
at rest, lungs at 760 mmHg
after diaphragm contracts, 759 mmHg
during expiration, 761 mmHg
250
vital capacity
The total volume of air that can be exhaled after maximal inhalation.
251
closed pneumothorax
no associated external wound. Spontaneous pneumothorax. Can be caused by rupture of blebs on the visceral pleura.
252
open pneumothorax
An open or penetrating chest wall wound through which air passes during inspiration and expiration, creating a sucking sound; also referred to as a sucking chest wound.
253
tension pneumothorax
a type of pneumothorax in which air that enters the chest cavity is prevented from escaping
254
How is the rate of airflow through the lungs regulated?
Changing the resistance!
Sympathetic: relaxation of smooth muscle leads to bronchodilation
Parasympathetic: contraction of smooth muscle leads to bronchoconstriction
255
compliance
ease with which the lungs expand under pressure
How much effort is required to move the lungs? The less compliant, the more work required to produce a breath
256
elasticity
tendency to return to initial size after being stretched
due to high elastin content. Elastic tension increases during inspiration
257
Pulmonary fibrosis
formation of scar tissue in the connective tissue of the lungs. Compliance is lost. Leads to death.
258
surfactant
produced by type II alveolar cells, decreases surface tension within the alveoli. Leads to increased compliance and decreased tendency to recoil.
259
Respiratory distress syndrome
Premature infant not born with enough surfactant, cannot inflate lungs. Tend to collapse. Treatment includes an oxygen tube delivering 95% oxygen to the lungs
260
tidal volume
Amount of air that moves in and out of the lungs during a normal breath
Vt
261
Inspiratory reserve volume
Amount of air that can be forcefully inhaled after a normal tidal volume inhalation
IRV
262
Expiratory reserve volume
Amount of air that can be forcefully exhaled after a normal tidal volume exhalation
263
Residual volume
Amount of air remaining in the lungs after a forced exhalation
RV
264
inspiratory capacity
tidal volume + inspiratory reserve volume
IC
265
Vital capacity
The total volume of air that can be exhaled after maximal inhalation.
Tidal volume + IRV + ERV
266
Functional residual capacity
expiratory reserve volume + residual volume
FRC
267
Total lung capacity
Vt + ERV + IRV + RV
268
How do these measurements help in determining respiratory diseases?
Can compare graphs to normal values. Obstructive diseases reach max volume expired but in much more time. Restrictive reaches about half the normal.
269
Breathing requires __ of all energy during a day
3%.
270
Work of breathing is increased when _____
pulmonary compliance is decreased (respiratory distress syndrome), airway is restricted (COPD), elasticity is lost (fibrosis), and exercise
271
dead space
The portion of the tidal volume that does not reach the alveoli and thus does not participate in gas exchange.
150 ml
272
Minute Alveolar Ventilation MAV formula
Rate x (Tidal Volume - Dead Space)
Amount of new air entering alveoli each minute
273
Which is better to increase MAV- respiratory rate or tidal volume?
Tidal volume, because the dead space never changes
274
minute respiratory volume
the total amount of gas that flows in and out of the lungs in one minute
275
Obstructive lung disease
Narrowed airways result in resistance to airflow during breathing. Examples are asthma, bronchiectasis, COPD, and cystic fibrosis.
276
restrictive lung disease
disease of the lung that causes a decrease in lung volumes
277
Alveolar ventilation
movement of air into and out of the alveoli. CO2 coming from tissues and O2 going to tissues
278
Major constituents of dry ai
Nitrogen (78%) and Oxygen (21%)
279
partial pressure of oxygen in normal air
160 mmHg
280
Why is the partial pressure O2 only 100 mmHg in the alveolus?
The difference in partial pressures moves the gas. PCO2 is greater so it drives O2 through the circuit and CO2 out of it
281
Two ways to transport oxygen in blood
Physical: .3 ml O2/100ml blood
Hemoglobin: 1 g Hb = 1.34 ml O2
282
How much hemoglobin do we have?
men: 13.8 to 18.0 g/dl
Women: 12.1 to 15.1 g/dl
Pregnant: 11 to 14 g/dl
283
How does Heme bind O2?
The iron center
284
Max oxygen carrying capacity of blood
15 g hemoglobin/ 100 ml blood and 1 g Hb/ 1.24 ml blood, so max capacity is
20 ml O2/100 ml blood
285
What determines how much oxygen is bound to hemoglobin?
Partial pressure of O2. The higher the pressure the more saturated it is
286
How to calculate oxygen content of blood
calculate oxygen carrying capacity (HB x 1.34 ml oxygen/g Hb)
Obtain % saturation of Hb from curve
Multiply capacity % by saturation
287
What is the PO2 in a tissue that needs oxygen? Why?
40 mmHg. The lower pressure means oxygen will dissociate into the tissue, but it will not all be used. Theres still a lot leftover in the blood after all the tissues get oxygen. This way if they need more, the body can compensate
288
Four things that influence HB's affinity for O2
Temperature
pH (bohr effect)
Pco2
2,3 bpg
289
How does temperature change O2 affinity for hemoglobin?
Increasing T decreases HB's affinity for oxygen but reducing temperature increases it.
HB tertiary structure is temperature sensitive and can be altered to increase or decrease O2 affinity
When you exercise your muscles heat up so HB delivers more oxygen to them
290
How does pH change O2 affinity for HB?
When O2 binds to Hb there is a proton release. So at lower pH's it has decreased affinity, at higher pH it has an increased affinity
291
What percentage of O2 is unloaded to tissue?
25%, Hemoglobin retains 75% of bound oxygen
292
What to right and left shifts mean in the O2 HB curve?
shift rightward is decreasing affinity
leftward is increasing affinity
293
How does pCO2 effect how O2 binds to HB?
AN increase in pCO2 occurs when metabolic activity is increased. CO2 can bind to hemoglobin and when it does it decreases its affinity for oxygen via a conformational change.
294
How does 2,3 BPG affect O2 and HB?
When oxygen levels are low, 2,3 BPG synthesis occurs and it decreases O2/HB affinity (increasing the amount of O2 released to tissue)
High oxyhemoglobin inhibits 2,3 BPG production
295
3 forms of CO2 in blood
directly dissolved
bound to hemogloboin
disguised as bicarbonate (predominant form)
296
How is CO2 converted to bicarbonate?
when CO2 enters the blood stream, it is picked up by carbonic anhydrase; this enzyme converts the CO2 and water into carbonic acid; carbonic acid is a weak acid... it will dissociate into a proton and a bicarbonate ion.
Erythrocytes contain carbonic anhydrase
297
How is CO2 (bicarbonate) transferred in the blood?
Partial pressure pushes it from tissues into interstitial fluid into plasma into erythrocytes where it is converted to bicarbonate. Once converted, it is exchanged with a chloride ion (chloride shift) from the plasma so the bicarbonate is carried in the plasma.
298
How is CO2 breathed out?
When blood reaches the capilaries next to the alveoli, the CO2 dissolved in the bloodstream moves down its pressure gradient into the alveoli. This causes the bicarbonate and dissolved hydrogens to combine forming carbonic acid, which is converted to CO2 by carbonic anhydrase. It then moves down the pressure gradient to the alveoli and is breathed out
299
Important CNS structures in control of breathing
Medulla oblongata and pons
chemoreceptors
Pulmonary receptors
300
Where are the respiratory centers located?
medulla and pons
301
Dorsal respiratory group
medulla, inspiratory neurons stimulate phrenic nerve, causing inspiration
302
Ventral respiratory group
has inspiratory and expiratory neurons, quiet during normal breathing, activating during heavy breathing
303
Peripheral/ central (in the brain) Chemoreceptors and control of breathing
H+, Co2, low O2 stimulate receptors located in the aorta and carotid artery. (H+ is the most important in regulation of respiration, much of it comes from CO2)
They fire impulses on the dorsal respiratory group to contract the diaphragm
304
Difference between peripheral and central chemoreceptors
peripheral are rapid acting
central are activated slowly but have a more prolonged effect, the most important in regulating long-term breathing rate
305
Pulmonary receptors
receptors that detect irritants and stimulate coughing. Stimulate Hering Breuer reflex.
306
Hering Breuer reflex
A protective mechanism that terminates inhalation, thus preventing overexpansion of the lungs.. Activated by stretching of the lungs, inhibits respiratory control centers making further respiration difficult
307
Central pattern generator
Pacemaker cells generate breathing rhythm
308
Pontine respiratory group
Helps with transition between expiration and inspiration
309
DRG neurons innervate the _____ via the ______
diaphragm, phrenic nerve.
310
contraction of the _____ causes inspiration
diaphragm
311
central chemoreceptors are located in the
medulla
312
central chemoreceptors sense
increase in H+ in CSF. Blood brain barrier doesn't let hydrogens in, so it measures the amount of CO2 in the blood to sense the H+ concentration. High CO2 signals a low pH and it sends signals to start breathing faster
313
peripheral chemoreceptors sense
low pO2 and high pCO2
314
Components of the nephron
Vascular and tubular components
```
Tubular components:
Bowmans capsule
Proximal tubule
Loop of Henle
Distal Tubule
Collecting Duct
```
Vascular component:
Afferentarteriole, glomerulus, efferent arteriole, peritubular capilaries
315
What do your kidneys do?
regulate plasma: ionic composition, volume and blood pressure, osmolarity, pH, and removal of waste
316
4 basic renal processes
glomerular filtration
tubular reabsorption
tubular secretion
excretion
317
Glomerular filtration
Fluid filtered from glomerulus into bowmans capsule passes through 3 layers of glomerular membrane
Glomerular capillary wall (permeable to water and solutes)
Basement membrane (collagen)
Inner layer- podocytes (form slit pores)
318
4 forces that determine glomerular filtration pressure (GFP)
Bowmans capsule hydrostatic and osmotic pressure
Glomerular hydrostatic and capillary osmotic pressure
319
Which forces favor filtration?
Glomerular capillary hydrostatic (Pgc)
Bowmans capsule osmotic (Pibc)
320
Which forces oppose filtration?
Bowmans capsule hydrostatic (Pbc)
Glomerular capillary osmotic pressure (Pigc)
321
Total glomerular filtration pressure
16 mmhg favoring filtration
322
Total renal plasma flow
625 ml/min
323
Glomerular filtration rate
volume of plasma filtered per unit time. Typically 125 ml/min. Depends on filtration pressure
324
Filtration fraction
Glomerular filtration rate/ plasma flow rate
325
under normal conditions, how long does it take the body to filter all of your plasma?
22 minutes!
326
How is glomerular filtration rate regulated?
by regulating the pressure. Mostly by glomerular capillary hydrostatic pressure
327
What is the kidney's "sweet spot" for GFR?
between 80-180 mmHg. Graph has a flat section so your normal body functions can fluctuate without effecting the filtration rate
328
two types of intrinsic control of GFR
Myogenic regulation and tubuloglomerular feedback
329
Myogenic regulation
Can increase map, which stretches the afferent arteriole causing a contraction. Contraction means lower pressure and flow past the arteriole, lower filtration rate.
330
Tubuloglomerular feedback
macula densa cells detect change in GFR. When GFR increases macula densa cells release adenosine which constricts the arterioles, decreasing GFR
331
Extrinsic control of GFR
Regulation of fluid output by sympathetic nervous system. More important if MAP is way out of the normal. Increases Map, decreases urine flow and fluid loss
332
Filtered load
quantity of a given solute that is filtered per unit time
333
Tubular reabsorption
movement of solutes and water from the kidney tubules back into the blood of the peritubular capillaries
334
Active reabsorption
movement from tubular lumen across epithelial cells against concentration gradient (requires energy)
335
Passive reabsorption
no energy is required for the substances net movement, occurs down electrochemical or osmotic gradients
336
What is reabsorbed in the proximal tubules?
glucose, amino acids, sodium. (water follows)
337
What is actively transported from the distal tubule?
sodium (water follows it)
338
Reabsorption rates
Kidneys only have a certain number of transporters available to put things back into the blood, so once they're all operating at their max rate, you don't get any more reabsorption. It stays in the blood and water stays there too. (excess sugar or salt means you'll have to pee more)
339
tubular secretion
active transport of substances into the lumen of the kidney tubules from the blood. H+, K+, and drugs can be removed by this mechanism.
340
What is plasma clearance?
measure of the rate at which substances are cleared from the plasma (ml/min)
341
Why is plasma clearance clinically important?
Medications. Ones that last too long or too short in the bloodstream won't be effective.
342
first step to calculating plasma clearance
How much of the substance enters the urine each minute?
Rate of urine formation (ml/min) x concentration of substance in urine (mg/ml)= mg/minute
343
Second step in calculating plasma clearance
What is the substance concentration in the plasma?
Calculation from step one/ plasma concentration of substance= ml/minute cleared
344
Application of inulin clearance
Body doesn't produce inullin so if injected it will all enter the urine. The clearance of any substance neither reabsorbed or secreted is equal to the glomerular filtration rate.
345
Clinical application of PAH clearance
Pah is filtered at glomerulus and not reabsorbed, but any remaining is secreted. Clearance of PAH is equal to the plasma flow in the kidneys (renal plasma flow). Can easily be converted into renal blood flow.
346
Creatinine clearance function
estimate GFR
347
How much of a normal water output is due to urine excretion?
60%
348
What are the clinical consequences of dehydration?
Decreased MAP
Increased plasma osmolarity
349
How is renin released?
Drop in blood pressure activates juxtaglomerular (JG) cells and renin is released from them
350
Where are juxtaglomerular cells located?
in the walls of the afferent arterioles
351
Describe the renin-angiotensin-aldosterone system
decreased blood pressure causes release of renin which converts angiotensin into angiotensin I. ACE converts angiotensin I to angiotensin II. Angiotensin 2 acts on adrenal gland to secrete aldosterone, which causes salt and water retention, raising blood pressure.
352
4 mechanisms by which angiotensin II affects blood pressure
1. causes vasoconstriction
2. release of aldosterone which causes sodium reabsorption
3. Acts on posterior pituitary to release ADH, increasing water re absorption in distal tubules and collecting ducts
4. stimulates thirst
353
How does aldosterone increase Na+ reabsorption?
increased opening of NaK channels on luminal membrane (mostly at collecting duct)
Synthesis of NaK channels on luminal membrane
Synthesis of NaK pumps
354
Effects of high aldosterone
high plasma volume, blood pressure, and sodium levels. Low plasma potassium levels.
355
Where is ACE found?
bound to the inner surfaces of capillaries throughout the body but particularly abundant in the lungs
356
combine inulin and PAH into something significant
inulin plasma clearance/PAH plasma clearance=
GFR/Renal Plasma Flow= Filtration Fraction
357
Why does the body need to be able to modify the concentration of urine?
Extracellular fluid osmolarity normally 300 mOsm- must keep that in homeostasis by regulating fluid volume in plasma and amount that leaves in urine
358
If interstitial fluid concentration is normally 300 miliosmolar, what concentration would urine be?
300 miliosmolar
359
Osmotic gradient
osmolarity of interstitial fluid gets progressively greater from cortex to medulla
360
what preserves the osmotic gradient?
vasa recta
361
Countercurrent multiplication
mechanism by which the solute concentration of interstitial fluid of the kidney becomes progressively greater from cortex to medulla
362
Which kind of nephron is most important in concentrating urine?
juxtamedullary nephron
363
Descending limb is premeable to _____ and does not reabsorb _____
water, NaCl
364
Ascending limb is impermeable to _______ activley transports _______
water, NaCl
365
How does the vasa recta maintain the medullary osmotic gradient?
Bloodflow runs in the opposite direction as the nephron, so at a region where water is leaving the interstitial fluid, the vasa recta is pumping it back in. Keeps the concentration relatively constant.
366
ADH where made and secreted
hypothalamus, posterior pituitary
367
What does ADH do?
increases water permeability of the collecting duct (reabsorbtion)
368
Dehydration and ADH
Low water content activates ADH, urine volume will be small and concentrated
369
How does ADH increase water reabsorption?
ADH binds receptors on renal tubule cells. Receptors are G protein coupled, activates adenylate cyclase, turns ATP to cAMP, activates PKA, inserts aquaporin 2's into the membrane. Also synthesizes new aquaporins. Water flows out.
370
Regulation of ADH
baroreceptors and osmoreceptors send feedback about blood pressure, volume, and osmolarity. High osmolarity increases secretion of ADH
371
Diabetes insipidus cause
kidneys either don't respond to ADH or not enough adh is made
372
Types of diabetes insipidus
Nephrogenic- kidneys don't respond to ADH
Neurogenic- Hypothalamus doesn't make enough ADH
373
without adh, collecting ducts are normally
impermeable to water
374
how is micturition regulated?
bladder fills, wall expands and activates stretch receptors
sympathetic- relaxes internal sphincter
parasympathetic- contracts detrusor muscle
somatic- relaxation of external sphincter
375
functions of saliva
moistens and lubricates food
salivary amylase begins digestion of carbohydrates
antibacterial action
solvent for taste
buffers acids
376
controls for saliva production
chemoreceptors in mouth, salivary glands send feedback to cortex
377
Basic functions of the stomach
stores food, contracts muscle and grinds food into chyme
378
secretions of the stomach
mucus, pepsinogen, HCl, intrinsic factor, gastrin, somatostatin, histamine
379
Digestion in the stomach
pepsinogen breaks down proteins
380
absorption in the stomach
no food, some drugs
381
Gastric pits contain
gastric glands, chief cells, parietal cells
382
chief cells
secrete pepsinogen
383
parietal cells
secrete HCl and intrinsic factor
384
goblet cells
secrete mucus
385
d cells
secrete somatostatin (inhibits acid secretion)
386
G cells
secrete gastrin (stimulates acid secretion)
387
Pepsinogen
reacts with HCl to become pepsin, then cleaves pepsinogen into pepsin. Breaks proteins into fragments (at large aromatic side chains or hydrophobic groups
most active at pH 2 but inactive at pH 6.5, permanent deactivation at pH 8
388
Why and how do we vomit?
vomition center in the medulla is innervated by nerves on the GI tract. Overstretching, fear and anxiety, etc can stimulate the nerves and cause us to vomit
389
Drugs that inhibit vomiting
Chemoreceptors that regulate vomition center
390
functions of HCl in stomach
activates pepsinogen
breaks down connective tissue and food particles
denatures proteins
kills microorganisms
391
intrinsic factor
important in vitamin b12 absorption
392
GERD
esophageal sphincter doesn't close all the way, allows stomach acid up the esophagus causing discomfort and ulcers. Leaads to increased proliferation of esophageal cells which can become cancerous
393
Describe how parietal cells secrete HCl
CO2 and water in the cell react via carbonic anyhydrase, forming bicarbonate and H+. Bicarbonate leaves into the bloodstream in exchange for a - chloride ion which passes through a channel. An active pump using ATP switches H+ for K+ and Cl- uses the transporter to get into the lumen.
394
How does prilosec work?
blocks proton pump that sends H+ into lumen of stomach
395
how does zantac work?
antihistamine, blocks H2 receptors so bicarbonate cant leave and cl- cant come in
396
migrating motility complex
cleans out small intestine between meals when absorption isn't happening
397
secretions of the small intestine
juice of the intestine (protects and lubricates, has water for hydrolysis), but no digestive enzymes
398
How is digestion accomplished in small intestine?
pancreatic enzymes, bile, and brush border enzymes
399
Pancreatic secretions
bicarbonate (neutralizes chyme from stomach)
trypsinogen
chymotrypsinogen
procarboxypeptidase
pancreatic amylase (breaks down polysaccharides to maltose)
Pancratic lipase (triglycerides to monoglycerides, FA's)
400
How are Trypsinogen, chymotrypsinogen, and procarboxypeptidase activated in the pancreas?
enterokinase converts trypsinogen to trypsin then trypsin converts the rest to active form
401
Gastrin
secreted by G cells
stimulates parietal cells to make more HCl
stimulates chief cells to make pepsinogen
stimulates stomach walls to contract
increases bloodflow to stomach and maintains mucous lining
stimulates closing of esophageal sphincter
release is inhibited by low pH
402
Cholecystokinin
produced by the small intestine from I-cells
Promotes release of digestive enzymes from pancreas and bile from gallbladder
403
Secretin
Produced by duodenum in S cells
Increased when small intestine pH is low
Inhibits gastrin release
regulates pH in small intestine by inhibiting parietal cells withing the stomach and stimulating production of bicarbonate
see table on slide 22
404
hormonal control of bile release
CCK increases bile secretion
Secretion decreases it
405
Functions of bile
excretion of biliruben, emulsification of fat
406
what acts on the surface of fat droplets?
pancreatic lipase
407
Brush border
folds and villi increase surface area for absorption
contains enterokinase, maltase, sucrase, lactase, aminopeptidase
408
celiac disease
destruction of the vili due to inflammatory reactions. Results in diarrhea, weight loss, anemia, calcium and vit D deficiency, blahblahblah
409
Draw out carbohydrate digestion pathway
Polysaccharides to disaccharides (amylase)
| Dissacharides to monosacharides (lactase, maltase, sucrase)
410
absorbtion of carbohydrates
facilitated diffusion of secondary active transport with Na
411
trypsin
cleaves @ carboxyl sides of lysine/arginine except when followed by proline
412
chymptrypsin
carboxyl end of aromatics
413
carboxypeptidase
branched chain AA's
414
exogenous protein digestion (dietary proteins)
polypeptides to small peptides (pepsin and pancreatic enzymes)
small peptides to amino acids (amino peptidases and intracellular peptidases)
415
absorption of proteins
coupled to Na/H exchanger
416
fat absorption
Absorption of fat and other substances from digestive tract via lacteals. Broken down into micelles, taken up by lacteals, reform TAG's, form chilomicrons, enter lymph
417
HDL cholesterol
```
builds membranes
manufactures bile
absorbs ADEK
insulates neurons
production of adrenal/sex hormones
```
418
LDL cholesterol
clogs arteries, heart attacks, strokes, death
419
Gastrocolic reflex
increased peristalsis of the colon after food has entered the stomach
420
secretions of large intestine
mucus and bicarbonate to lubricate lumen and neutralize acid.
421
Absorptions of large intestine
salt and water
422
fecal composition
dead bacteria, fat, organic/inorganic waste, protein, roughage. Mostly bacteria and roughage.
423
borborgymi
hyperactive bowel sounds
424
composition of flatus
stomach- NO from air
SI- CO2 and NaCO3 from HCl and HCO3-
LI- CO2, methane, NO
425
fat digestion performed by
pancreatic lipase
