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PD Bio 305 > Final Exam Review > Flashcards

Final Exam Review Flashcards

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Biology 101 flashcards
1
Q

3 primary regions of the brain

A

forebrain, brainstem, cerebellum

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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

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3
Q

left side of brain controls

A

right side movement, sensory perception. Logic, analytical processing, language and math skills

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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)

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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

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6
Q

Reflex

A

response to a stimulus that occurs without conscious effort

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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)

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8
Q

5 components of reflex arc

A

sensory receptor

affarent pathway

integrating center

efferent pathway

effector

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9
Q

knee jerk reflex

A

affarent neuron to efferent neuron, isn’t processed by the brain first

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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

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11
Q

cardiac center (medulla

A

controls heart rate and strength of contraction

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12
Q

vasomotor center (medulla)

A

controls blood pressure

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13
Q

respiratory centers (medulla and pons)

A

controls rate and depth of respiration

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14
Q

digestive center (medulla)

A

controls vomiting, swallowing, coughing, sneezing

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15
Q

infant sleep

A

17 hrs

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16
Q

teen sleep

A

9 hrs

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17
Q

adult sleep

A

6-8 hrs

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18
Q

reticular activating system

A

regulation of sleep and awakefulness

makes cortex more receptive to signals, inhibited by cocaine and amphetamines.

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19
Q

afferent division of PNS

A

sensory and visceral stimuli

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20
Q

efferent division of pns

A

somatic and autonomic nervous systems

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21
Q

affarent fibers enter spinal cord via

A

dorsal root

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22
Q

efferent fibers leave spinal cord via

A

ventral root

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23
Q

Functions of the hypothalamus

A

TO FAR PUMAS

Temperature
Osmolarity
Food intake
Agression
Rage
Pituitary
Uterine Contractions
Milk ejection
Sleep/Wake
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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)

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25
Q

define sleep (clinical)

A

a state of decreased (not complete loss) of motor activity and perception

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26
Q

Sleep requirements for infants, teens, and adults

A

Infants- 17 hr/day
Teens- 9 hr/day
Adults 6/8 hr/day

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27
Q

Reticular formation

A

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

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28
Q

How do afferent fibers enter the spinal cord?

A

via the dorsal root

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29
Q

How do efferent fibers leave the spinal cord?

A

ventral root

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30
Q

What is the ganglion?

A

collection of cell bodies outside of CNS

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31
Q

Do sensory receptors use neurotransmitter?

A

no

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32
Q

What do photoreceptors sense?

A

light

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33
Q

what do chemoreceptors sense?

A

chemicals dissolved in saliva (taste)

Chemicals in mucus (smell)

Chemicals in extracellular fluid (pain)

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34
Q

What do thermoreceptors do?

A

detect changes in temperature

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35
Q

What do mechanoreceptors do?

A

respond to pressure (vibration), sound waves (noise), and acceleration (balance and equilibrium)

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36
Q

define synesthesia

A

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

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37
Q

What is the purpose of sensory pathways?

A

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

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38
Q

How does the brain sense the intensity of a stimulus?

A

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

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39
Q

population coding

A

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

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40
Q

define two point discrimination

A

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

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41
Q

lateral inhibition

A

The pattern of interaction among neurons in the visual system in which activity in one neuron inhibits adjacent neurons’ responses.

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42
Q

fear of pain

A

algophobia

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43
Q

why is pain a good thing?

A

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

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44
Q

receptor for pain

A

nociceptor

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45
Q

pain neurotransmitters

A

Substance P (activates ascending pathways that transmit nocioceptor signals) and glutamate (excitatory neurotransmitte

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46
Q

Fast pain

A

sharp, acute pain. Transmitted on fast (A-Delta) fibers which are mylenated (12-30 mps)

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47
Q

Slow pain

A

dull, achey. Persists chronically. Transmitted on slow (C-fibers) fibers which are unmylenated (.2-1.3 mps)

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48
Q

gate-control theory

A

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

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49
Q

Endogenous Opiates

A

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

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50
Q

Endogenous opiates depend on

A

presence of opiate receptors

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51
Q

prostaglandins

A

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!)

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52
Q

How do sensory receptors work?

A

detect energy in “modalities”, function w/o neurotransmitter!

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53
Q

Sensory receptor pathway (1,2,3 order neurons)

A

1st order neuron to CNS to 2nd order neuron to Thalamus to 3rd order neuron to cortex. Information sensed and stored for future use

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54
Q

Pain gene

A

SCN9-A

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55
Q

Draw out the pain pathway

A

draw

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56
Q

What are catecholamines?

A

epinephrine and norepinephrine

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57
Q

Sympathetic nervous system characteristics

A

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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58
Q

parasympathetic nervous system characteristics

A

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

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59
Q

Where is the sympathetic nervous system located?

A

T1-L2

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60
Q

Where is the parasympathetic nervous system located?

A

Cranial nerves 7,9,10, s2-s4

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61
Q

How many neurons are involved in autonomic processes?

A

2, one preganglionic in the spinal cord, one postganglionic that goes to the effector organ

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62
Q

Preganglionic neurons in sympathetic neurons

A

cholinergenic, post ganglionic has a nicotinic receptor

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63
Q

Postganglionic neurons in sympathetic nervous system

A

adrenergenic neuron, releases nor/epinephrine to target organs that have adrenergenic receptors

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64
Q

Preganglionic neurons in parasympathetic

A

cholinergenic, release ACh to nicotinic receptor

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65
Q

Post Ganglionic in parasympathetic

A

cholinergenic, release ACh to Muscarinic receptor on target organ

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66
Q

Nicotinic receptors

A

respond to acetylcholine, 4 types, goes to adrenal medulla, skeletal muscle, ion channel opening, generally excitatory

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67
Q

muscarinic receptors

A

respond to ACh, 5 types, effector organs in PSNS, G-linked receptors, excitatory or inhibitory

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68
Q

Nicotinic receptor at the synapse sequence of events

A

ACh binds receptor, NaK channel opens, Na diffuses into cell

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69
Q

Muscarinic receptor in heart

A

ACh binds receptor
Gprotein subunits dissociate
G protein binds to K+ channel, opens it
K+ diffuses out of cell

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70
Q

Adrenergenic receptor

A

alpha and beta types, inhibitory or excitatory. G protein linked

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71
Q

Nicotinic and muscarinic- which is fast, slow?

A

Nic is fast, musc is slow

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72
Q

Secondary messenger system of muscarinic receptors

A

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

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73
Q

alpha one andrenergic receptor pathway

A

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.

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74
Q

Neuron that acts on adrenal medula

A

cholinergenic, releases ACh at medulla which acts on endocrine cells to release epinephrine

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75
Q

alpha 2/Beta balance

A

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.

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76
Q

Varicosities

A

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

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77
Q

Somatic nervous system

A

innervates skeletal muscle, mostly voluntary, contains a single motor neuron

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78
Q

muscle makeup levels

A

fascicles, musclue fibers, sarcolemma, myofibrils, sarcomeres

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79
Q

Each myofiber is connected to

A

one motor neuron

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80
Q

motor end plate

A

invaginations containing large numers of nicotinic receptors

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81
Q

primary neurotransmitter of somatic NS

A

ACh

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82
Q

what does acetylcholinesterase do?

A

found between the invaginations of the motor end plate, terminates the signal allowing the muscle to relax

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83
Q

firing of a motor neuron process

A

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

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84
Q

Myasthenia gravis

A

inability to properly signal at NMJ. Leads to general muscle weakness

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85
Q

Where is myosin anchored?

A

m

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86
Q

Where is actin anchored?

A

z line

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87
Q

crossbridges

A

myosin heads

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88
Q

What happens to the IHZA lines/bands during contraction?

A

IHZ shorten, A stays the same

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89
Q

How does contraction happen?

A

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

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90
Q

Cross bridge cycle

A

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”

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91
Q

How does relaxation occur?

A

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)

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92
Q

Why is ATP needed during relaxation?

A

Provides energy for SERCA pumps
Binds to Myosin heads (to release from actin)
Indirect use through NaK pumps to antiport calcium

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93
Q

What is a twitch?

A

fast weak contraction

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94
Q

what is the latent period?

A

delay between AP and start of twitch. Happens becaue excitation events must occur before twitch happens

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95
Q

How is the amount of force generated by a muscle determined?

A

of cross bridges

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96
Q

twitch summation

A

multiple twitches occur, add up, lead to a lot of calcium release and caue a contraction

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97
Q

force produced by individual fibers caused b

A

frequency of stimulation
fiber length
fiber diameter

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98
Q

What causes muscle fatigue?

A

Loss of ATP, accumulation of metabolites, loss of nerve signaling, low oxygen, stress

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99
Q

what are satalite cells?

A

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.

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100
Q

Hypertrophy (satellite cells)

A

increase in cell size. Satellite cells are responsible for muscle growth!

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101
Q

Free radical theory of aging

A

as we age, free radical generation goes up, muscle mass can be lost. Physical activity prevents loss of muscle mass.

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102
Q

Motor unit

A

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

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103
Q

Easiest to generate an action potential in a neuron with a _____ cell body

A

small

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104
Q

motor unit summation

A

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

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105
Q

Orderly recruitment of motor neurons

A

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

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106
Q

isotonic contraction

A

muscle is allowed to shorten as it contracts

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107
Q

isometric contraction

A

muscle not allowed to shorten, but there is tension

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108
Q

What effects the speed of a contraction?

A

Is the muscle slow or fast twitch?

How does it get its ATP?

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109
Q

eccentric contraction

A

muscle lengthens

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110
Q

concentric contraction

A

muscle shortens

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111
Q

How do fast twitch muscles get ATP?

A

glycolytic pathway (don’t need oxygen!)

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112
Q

How do slow twitch muscles get ATP?

A

oxidative phosphorylation- require oxygen

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113
Q

Type I (slow oxidative) muscle fibers characteristics

A 
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
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114
Q

Type IIA (fast oxidative) muscle fiber characteristics

A 
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
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115
Q

Type IIX (fast glycolytic) muscle fibers

A 
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
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116
Q

What does training do for your muscle fiber types?

A

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

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117
Q

Do mitochondria themselves change during training?

A

Yes, it looks like they become more efficient and the enzymes within them do as well

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118
Q

differences between fetal and newborn circulation

A

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

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119
Q

Heart disease

A

blood supply to the heart is blocked

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120
Q

how do they measure if you’re having a heart attack

A

measure cardiac enzymes in blood, high levels are bad

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121
Q

how does high blood pressure cause heart attacks

A

stretches blood vessels, cholesterol comes to try and fix micro tears in the stretched vessels and that causes plaque buildup

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122
Q

Myogenic contraction

A

cardiac muscle automatically contracting without innervation from any neurons

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123
Q

purpose of autonomic innervation

A

increase rate and strength of contraction (sympathetic)

Decrease rate of contraction (parasympathetic)

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124
Q

Pacemaker cells

A

initiate action potentials

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125
Q

conduction fibers

A

transmit action potentials throughout the heart for coordination

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126
Q

Where are pacemaker cells concentrated?

A

In the SA/AV nodes

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127
Q

Gap junctions

A

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

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128
Q

AV nodal delay

A

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

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129
Q

Gap junctions

A

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

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130
Q

Steps of a heartbeat (action potentials)

A 
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
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131
Q

why can pacemaker cells generate their own action potentials?

A

they don’t have steady resting potentials, they depolarize very slowly.

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132
Q

Steps of a generation of an action potential in the heart

A

+1. K+ channels close and “funny” channels open (NaK channel) until membrane potential hits -55 (short of AP threshold)

  1. Influx of Na triggers opening of voltage gated Ca++ channels (t-type) that depolarize to -50 (threshold) then close
  2. Threshold causes opening of L-type Ca++ channels that cause rapid depolarization
  3. K+ channels open repolarizing the cell, Ca++ channels close
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133
Q

Why do the SA node, AV node, and Purkinje Fibers all have different rates?

A

So there is no competition between them, a good backup system

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134
Q

Differences between the generation of contractile AP’s in cardiac tissue and skeletal tissue

A

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

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135
Q

Phases of the generation of contractile action potentials in cardiac muscle

A

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

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136
Q

Contraction of cardiac muscle steps

A

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

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137
Q

How is Ca++ removed from cardiac muscle?

A

SERCA pumps
Plasma membrane calcium ATPase
NaCa membrane exchanger (countertransport)

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138
Q

Phases of the cardiac cycle

A

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

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139
Q

Dicrotic notch

A

brief rise in aortic pressure caused by backflow of blood rebounding off semilunar valves. Ensures they stay closed

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140
Q

Which is longer, systole or diastole?

A

Diastole, lets the heart rest longer

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141
Q

Atrial fibrilation

A

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

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142
Q

p wave

A

atrial depolarization

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143
Q

QRS complex

A

ventricular depolarization

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144
Q

T wave

A

ventricular repolarization

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145
Q

what’s missing from ekg?

A

atrial repolarization

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146
Q

stroke volume

A

The amount of blood ejected from the heart in one contraction.

SV= end diastolic volume- end systolic volume

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147
Q

cardiac output

A

heart rate x stroke volume

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148
Q

What are the two ways in which cardiac output is regulated?

A

Regulating heart rate

Regulating stroke volume

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149
Q

Where does the parasympathetic nervous system innervate the heart?

A

At the SA and AV nodes

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150
Q

Where does the sympathetic nervous system innervate the heart?

A

At the SA and AV nodes, and at the ventricular myocardium

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151
Q

What neurotransmitter does the sympathetic NS release on the heart? What is it’s affect?

A

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

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152
Q

How does norepinephrine open Funny and T-type channels?

A

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.

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153
Q

What nerve from the Parasympathetic NS innervates the heart?

A

Vagus Nerve

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154
Q

What does the parasymp release on the heart and what is it’s effect?

A

Releases ACh at the SA and AV nodes. Decreases heart rate by making it take longer to reach threshold

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155
Q

How does acetylcholine slow the heart rate?

A

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.

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156
Q

Which branch of the NS controls stroke volume?

A

Sympathetic

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157
Q

What are the factors that regulate stroke volume?

A

Venous return (raising the end-diastolic volume), and Sympathetic activity (epinephrine), causing harder contractions of the heart

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158
Q

How does the sympathetic nervous system cause a higher stroke volume?

A

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!

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159
Q

Frank-Starling Law of the Heart

A

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

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160
Q

Resting cardiac output

A

5 L/min

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161
Q

Exercise cardiac output

A

25 L/min

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162
Q

Arteries

A

carry blood away from the heart. Low resistance, large diameter, elastin and collagen

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163
Q

Veins

A

Blood vessels that carry blood back to the heart

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164
Q

Arterioles

A

small vessels that receive blood from the arteries. Resistance vessels. Smooth muscle rings regulate radius and resistance.

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165
Q

Capilaries

A

microscopic blood vessels that connect arteries and veins. Site of nutrient exchange

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166
Q

Venules

A

small vessels that gather blood from the capillaries into the veins

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167
Q

blood pressure

A

the force exerted by blood on the walls of blood vessels

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168
Q

Formula for flow

A

Flow = change in pressure/resistance

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169
Q

What is the change in pressure in the systemic circuit?

A

85 mmHg

pressure in aorta-pressure in vena cava

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170
Q

Pressure gradient in pulmonary circuit

pulmonary artery-pulmonary vein

A

15 mm Hg

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171
Q

If pressure is so much lower in the pulmonary circuit, how can flow be equal?

A

Resistance must be much higher in systemic circuit and much lower in pulmonary circuit

172
Q

Factors affecting resistance to flow. Which one can we control?

A

Viscosity of fluid
Length of the vessel
Radius of the vessel (MOST IMPORTANT)

173
Q

Characteristics (muscle layers) in arteries and veins

A

arteries have smaller lumens but a large muscle layer, veins have large lumens and a small muscle layer

174
Q

Does making the lumen smaller = lower or higher resistance?

A

higher. The blood must contact more of the surface of the vessel wall.

175
Q

How much does vessel diameter affect resistance? (Formula)

A

R/r^4, if you double the size of the vessel, the resistance reduces by a factor of 16

176
Q

Ischemia

A

restriction of blood flow to tissues resulting in a shortage of oxygen and glucose to keep cells alive (buildup of plaques)

177
Q

Symptoms of Ischemic heart disease

A

angina, acute myocardial infarction, sudden death

178
Q

Treatments for Ischemic heart disease

A

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
Q

Normal blood pressure

A

120/80

180
Q

Pulse pressure. Problems with it?

A

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
Q

Calculating Mean Arterial Pressure (MAP)

A

Systolic + (2xDiastolic) all over 3

182
Q

Why does blood flow slow in the capilaries?

A

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
Q

Purpose of elastin and collagen in arteries

A

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
Q

How do arteries act as a pressure reservoir?

A

They stretch when the heart pumps blood and then snap back, holding the pressure in their walls

185
Q

Why do we get arteries and not vein disease?

A

arteries stretch and micro-tear. Veins have super low pressure so they don’t stretch

186
Q

What happens if you lose elastin?

A

hardened arteries, increase in BP

187
Q

Tthis?otal peripheral resistance. How does constriction/dilation affect

A

Combined resistance of all blood vessels within the systemic circuit. Vasoconstriction causes increased resistance, dilation causes decreased resistance

188
Q

What can and cannot cross through a capillary wall?

A

lipid soluble substances pass through wall

water soluble substances pass through pores

Exchangable proteins are moved by vesicular transport

Plasma proteins are stuck

189
Q

Where does most absorption and filtration occur in the capilary?

A

Filtration occurs at the arteriole end, absorption at the venule end

190
Q

Values for pcap, piif, picap, and piif at arteriole end

A

pcap=38
piif=0
picap=25
Pif=1

Net= +12 (more filtration)

191
Q

Values at venule end

A

pcap= 16
piif=0
picap=15
pif=1

Net 16-26= -10 (more absorption). Overall, we filter more than we absorb

192
Q

How to measure blood pressure

A

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
Q

Describe how standing up causes a lower arterial pressure

A

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
Q

Formula for mean arterial pressure

A

MAP= Cardiac Output x TPR

CO= heart rate x stroke volume

TPR= sum of all resistance in all vessels of the systemic circulation

195
Q

How can you change cardiac output?

A

change rate or strength of contractions

196
Q

How do you change TPR?

A

constrict or dilate vessels

197
Q

Normal cerebral blood pressure

A

between 60-140 mmHg. Under 60, body can’t adjust so you feel light headed.

198
Q

Vasomotor center in medulla

A

controls sympathetic vasoconstrictor neurons. Its active, sending action potentials to sympathetic neurons innervating arteriols

199
Q

Baroreceptors

A

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
Q

How does the baroreceptor work?

A

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
Q

Via the baroreceptor, the parasympathetic nervous system can control

A

action potential frequency. Heart rate.

202
Q

Via the baroreceptor, the sympathetic nervous system can control

A

Action potential frequency, contractility, venomotor tone, and vasoconstriction

203
Q

Factors affecting venous return

A

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
Q

varicose veins

A

abnormally swollen, twisted veins with defective valves; most often seen in the legs

205
Q

the muscle pump

A

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
Q

Respiratory movements and blood flow

A

pressure in the thorax decreases when you breathe in- this causes blood to rush into the chest. One way valves prevent backflow.

207
Q

Sympathetic vasoconstriction

A

vasoconstriction pushes blood back toward the heart

208
Q

venomotor tone

A

smooth muscle tension in the veins

209
Q

What are the three layers of blood after centrifuging?

A

Erythrocytes, Buffy coat, plasma

210
Q

What does the buffy coat have in it?

A

White blood cells and platelets

211
Q

What is plasma made of?

A

Primarily water (91%), but 7-9% plasma proteins. Albumin is the most abundant

212
Q

function of albumin in plasma

A

maintains osmotic pressure in blood (prevents edema), serves as a carrier for fatty acids and other hydrophobic substances

213
Q

What do globulins do? (plasma protein)

A

blood clotting, immunodefense

214
Q

What does fibrinogen do? (plasma protein)

A

Blood clotting

215
Q

What pressure is due to albumin concentration in the plasma?

A

Picap and Piif, the flow of solutes in and out of the capillary

216
Q

Characteristics of erythrocytes

A

No nucleus or organelles, but do have glycolytic enzymes. Hemoglobin to transport oxygen and CO2.

217
Q

How long do erythrocytes live?

A

about 120 days

218
Q

Where are erythrocytes produced?

A

bone marrow (cranial, costal, and sternal in adults)

219
Q

Sickle cell anemia- causes, symptoms, evolutionary reason

A

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
Q

hematocrit

A

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
Q

anemia

A

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
Q

Hemorrhagic anemia

A

loss of blood

223
Q

pernicious anemia

A

nutritional deficiency- not enough vit B12

224
Q

Renal anemia

A

kidney disease leads to decreased erythropoietin production

225
Q

Aplastic anemia

A

bone marrow cells destroyed by radiation/ drugs

226
Q

How are erythrocytes produced?

A
  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
Q

What happens when an RBC is broken down?

A

biliruben goes to the liver, joins with bile and stool (what makes it brown)

228
Q

Polycythemia

A

too many RBC’s

229
Q

primary polycythemia

A

bone marrow tumor

230
Q

secondary polycythemia

A

chronic hypoxia (high altitude)

231
Q

Blood doping

A

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
Q

How does the hematocrit change is anemic? Polycythemic? Dehydrated?

A

Amemic- much lower than normal

Polycythemia- much higher than normal

Dehydration- much higher than normal

233
Q

Hemostasis (and steps)

A

cessation of bleeding

Vasoconstriction
Formation of platelet plug
formation of fibrin mesh

234
Q

what are platelets?

A

Small fragments of cells made from stem cells

235
Q

1st step of hemostasis

A

vascular spasm- damage activates sympathetic nervous system which causes constriction. Less blood flow to area means less blood loss

236
Q

Platelet plug formation

A

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
Q

Blood clot formation

A

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
Q

What does thrombin do?

A

converts fibrinogen to fibrin.

A phospholipid on the surface of activated platelets activates thrombin

239
Q

Intrinsic fibrin formation

A

7 steps, all chemicals necessary for this pathway are found in the blood

240
Q

Extrinsic fibrin pathway

A

4 steps, chemicals released by damaged tissue initiates shortcut

both pathways work together, intrinsic in the vessel, extrinsic in surrounding tissues

241
Q

Blood clotting feedback

A

Thrombin is activated and activates fibrinogen which activates more proteins that activate thrombin. Positive feedback.

242
Q

What surrounds the alveoli?

A

capillaries

243
Q

flow rate through airways

A

change in pressure/resistance

244
Q

COPD (chronic obstructive pulmonary disease)

A

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
Q

muscles involved in breathing

A

diafragm, intercostal muscles, abdominal wall.

246
Q

How is air moved in and out of the lungs?

A

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
Q

transmural pressure

A

alveolar pressure - intrapleural pressure.

If not maintained breathing can’t occur. Intrapleural pressure is always -, and intraalveolar pressure isn’t

248
Q

How does Boyle’s law explain breathing

A

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
Q

Pressures during inspiration and expiration

A

at rest, lungs at 760 mmHg

after diaphragm contracts, 759 mmHg

during expiration, 761 mmHg

250
Q

vital capacity

A

The total volume of air that can be exhaled after maximal inhalation.

251
Q

closed pneumothorax

A

no associated external wound. Spontaneous pneumothorax. Can be caused by rupture of blebs on the visceral pleura.

252
Q

open pneumothorax

A

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
Q

tension pneumothorax

A

a type of pneumothorax in which air that enters the chest cavity is prevented from escaping

254
Q

How is the rate of airflow through the lungs regulated?

A

Changing the resistance!

Sympathetic: relaxation of smooth muscle leads to bronchodilation

Parasympathetic: contraction of smooth muscle leads to bronchoconstriction

255
Q

compliance

A

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
Q

elasticity

A

tendency to return to initial size after being stretched

due to high elastin content. Elastic tension increases during inspiration

257
Q

Pulmonary fibrosis

A

formation of scar tissue in the connective tissue of the lungs. Compliance is lost. Leads to death.

258
Q

surfactant

A

produced by type II alveolar cells, decreases surface tension within the alveoli. Leads to increased compliance and decreased tendency to recoil.

259
Q

Respiratory distress syndrome

A

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
Q

tidal volume

A

Amount of air that moves in and out of the lungs during a normal breath

Vt

261
Q

Inspiratory reserve volume

A

Amount of air that can be forcefully inhaled after a normal tidal volume inhalation

IRV

262
Q

Expiratory reserve volume

A

Amount of air that can be forcefully exhaled after a normal tidal volume exhalation

263
Q

Residual volume

A

Amount of air remaining in the lungs after a forced exhalation

RV

264
Q

inspiratory capacity

A

tidal volume + inspiratory reserve volume

IC

265
Q

Vital capacity

A

The total volume of air that can be exhaled after maximal inhalation.

Tidal volume + IRV + ERV

266
Q

Functional residual capacity

A

expiratory reserve volume + residual volume

FRC

267
Q

Total lung capacity

A

Vt + ERV + IRV + RV

268
Q

How do these measurements help in determining respiratory diseases?

A

Can compare graphs to normal values. Obstructive diseases reach max volume expired but in much more time. Restrictive reaches about half the normal.

269
Q

Breathing requires __ of all energy during a day

A

3%.

270
Q

Work of breathing is increased when _____

A

pulmonary compliance is decreased (respiratory distress syndrome), airway is restricted (COPD), elasticity is lost (fibrosis), and exercise

271
Q

dead space

A

The portion of the tidal volume that does not reach the alveoli and thus does not participate in gas exchange.

150 ml

272
Q

Minute Alveolar Ventilation MAV formula

A

Rate x (Tidal Volume - Dead Space)

Amount of new air entering alveoli each minute

273
Q

Which is better to increase MAV- respiratory rate or tidal volume?

A

Tidal volume, because the dead space never changes

274
Q

minute respiratory volume

A

the total amount of gas that flows in and out of the lungs in one minute

275
Q

Obstructive lung disease

A

Narrowed airways result in resistance to airflow during breathing. Examples are asthma, bronchiectasis, COPD, and cystic fibrosis.

276
Q

restrictive lung disease

A

disease of the lung that causes a decrease in lung volumes

277
Q

Alveolar ventilation

A

movement of air into and out of the alveoli. CO2 coming from tissues and O2 going to tissues

278
Q

Major constituents of dry ai

A

Nitrogen (78%) and Oxygen (21%)

279
Q

partial pressure of oxygen in normal air

A

160 mmHg

280
Q

Why is the partial pressure O2 only 100 mmHg in the alveolus?

A

The difference in partial pressures moves the gas. PCO2 is greater so it drives O2 through the circuit and CO2 out of it

281
Q

Two ways to transport oxygen in blood

A

Physical: .3 ml O2/100ml blood

Hemoglobin: 1 g Hb = 1.34 ml O2

282
Q

How much hemoglobin do we have?

A

men: 13.8 to 18.0 g/dl

Women: 12.1 to 15.1 g/dl

Pregnant: 11 to 14 g/dl

283
Q

How does Heme bind O2?

A

The iron center

284
Q

Max oxygen carrying capacity of blood

A

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
Q

What determines how much oxygen is bound to hemoglobin?

A

Partial pressure of O2. The higher the pressure the more saturated it is

286
Q

How to calculate oxygen content of blood

A

calculate oxygen carrying capacity (HB x 1.34 ml oxygen/g Hb)

Obtain % saturation of Hb from curve

Multiply capacity % by saturation

287
Q

What is the PO2 in a tissue that needs oxygen? Why?

A

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
Q

Four things that influence HB’s affinity for O2

A

Temperature
pH (bohr effect)
Pco2
2,3 bpg

289
Q

How does temperature change O2 affinity for hemoglobin?

A

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
Q

How does pH change O2 affinity for HB?

A

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
Q

What percentage of O2 is unloaded to tissue?

A

25%, Hemoglobin retains 75% of bound oxygen

292
Q

What to right and left shifts mean in the O2 HB curve?

A

shift rightward is decreasing affinity

leftward is increasing affinity

293
Q

How does pCO2 effect how O2 binds to HB?

A

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
Q

How does 2,3 BPG affect O2 and HB?

A

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
Q

3 forms of CO2 in blood

A

directly dissolved

bound to hemogloboin

disguised as bicarbonate (predominant form)

296
Q

How is CO2 converted to bicarbonate?

A

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
Q

How is CO2 (bicarbonate) transferred in the blood?

A

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
Q

How is CO2 breathed out?

A

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
Q

Important CNS structures in control of breathing

A

Medulla oblongata and pons

chemoreceptors

Pulmonary receptors

300
Q

Where are the respiratory centers located?

A

medulla and pons

301
Q

Dorsal respiratory group

A

medulla, inspiratory neurons stimulate phrenic nerve, causing inspiration

302
Q

Ventral respiratory group

A

has inspiratory and expiratory neurons, quiet during normal breathing, activating during heavy breathing

303
Q

Peripheral/ central (in the brain) Chemoreceptors and control of breathing

A

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
Q

Difference between peripheral and central chemoreceptors

A

peripheral are rapid acting

central are activated slowly but have a more prolonged effect, the most important in regulating long-term breathing rate

305
Q

Pulmonary receptors

A

receptors that detect irritants and stimulate coughing. Stimulate Hering Breuer reflex.

306
Q

Hering Breuer reflex

A

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
Q

Central pattern generator

A

Pacemaker cells generate breathing rhythm

308
Q

Pontine respiratory group

A

Helps with transition between expiration and inspiration

309
Q

DRG neurons innervate the _____ via the ______

A

diaphragm, phrenic nerve.

310
Q

contraction of the _____ causes inspiration

A

diaphragm

311
Q

central chemoreceptors are located in the

A

medulla

312
Q

central chemoreceptors sense

A

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
Q

peripheral chemoreceptors sense

A

low pO2 and high pCO2

314
Q

Components of the nephron

A

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
Q

What do your kidneys do?

A

regulate plasma: ionic composition, volume and blood pressure, osmolarity, pH, and removal of waste

316
Q

4 basic renal processes

A

glomerular filtration
tubular reabsorption
tubular secretion
excretion

317
Q

Glomerular filtration

A

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
Q

4 forces that determine glomerular filtration pressure (GFP)

A

Bowmans capsule hydrostatic and osmotic pressure

Glomerular hydrostatic and capillary osmotic pressure

319
Q

Which forces favor filtration?

A

Glomerular capillary hydrostatic (Pgc)

Bowmans capsule osmotic (Pibc)

320
Q

Which forces oppose filtration?

A

Bowmans capsule hydrostatic (Pbc)

Glomerular capillary osmotic pressure (Pigc)

321
Q

Total glomerular filtration pressure

A

16 mmhg favoring filtration

322
Q

Total renal plasma flow

A

625 ml/min

323
Q

Glomerular filtration rate

A

volume of plasma filtered per unit time. Typically 125 ml/min. Depends on filtration pressure

324
Q

Filtration fraction

A

Glomerular filtration rate/ plasma flow rate

325
Q

under normal conditions, how long does it take the body to filter all of your plasma?

A

22 minutes!

326
Q

How is glomerular filtration rate regulated?

A

by regulating the pressure. Mostly by glomerular capillary hydrostatic pressure

327
Q

What is the kidney’s “sweet spot” for GFR?

A

between 80-180 mmHg. Graph has a flat section so your normal body functions can fluctuate without effecting the filtration rate

328
Q

two types of intrinsic control of GFR

A

Myogenic regulation and tubuloglomerular feedback

329
Q

Myogenic regulation

A

Can increase map, which stretches the afferent arteriole causing a contraction. Contraction means lower pressure and flow past the arteriole, lower filtration rate.

330
Q

Tubuloglomerular feedback

A

macula densa cells detect change in GFR. When GFR increases macula densa cells release adenosine which constricts the arterioles, decreasing GFR

331
Q

Extrinsic control of GFR

A

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
Q

Filtered load

A

quantity of a given solute that is filtered per unit time

333
Q

Tubular reabsorption

A

movement of solutes and water from the kidney tubules back into the blood of the peritubular capillaries

334
Q

Active reabsorption

A

movement from tubular lumen across epithelial cells against concentration gradient (requires energy)

335
Q

Passive reabsorption

A

no energy is required for the substances net movement, occurs down electrochemical or osmotic gradients

336
Q

What is reabsorbed in the proximal tubules?

A

glucose, amino acids, sodium. (water follows)

337
Q

What is actively transported from the distal tubule?

A

sodium (water follows it)

338
Q

Reabsorption rates

A

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
Q

tubular secretion

A

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
Q

What is plasma clearance?

A

measure of the rate at which substances are cleared from the plasma (ml/min)

341
Q

Why is plasma clearance clinically important?

A

Medications. Ones that last too long or too short in the bloodstream won’t be effective.

342
Q

first step to calculating plasma clearance

A

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
Q

Second step in calculating plasma clearance

A

What is the substance concentration in the plasma?

Calculation from step one/ plasma concentration of substance= ml/minute cleared

344
Q

Application of inulin clearance

A

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
Q

Clinical application of PAH clearance

A

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
Q

Creatinine clearance function

A

estimate GFR

347
Q

How much of a normal water output is due to urine excretion?

A

60%

348
Q

What are the clinical consequences of dehydration?

A

Decreased MAP

Increased plasma osmolarity

349
Q

How is renin released?

A

Drop in blood pressure activates juxtaglomerular (JG) cells and renin is released from them

350
Q

Where are juxtaglomerular cells located?

A

in the walls of the afferent arterioles

351
Q

Describe the renin-angiotensin-aldosterone system

A

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
Q

4 mechanisms by which angiotensin II affects blood pressure

A
  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
Q

How does aldosterone increase Na+ reabsorption?

A

increased opening of NaK channels on luminal membrane (mostly at collecting duct)

Synthesis of NaK channels on luminal membrane

Synthesis of NaK pumps

354
Q

Effects of high aldosterone

A

high plasma volume, blood pressure, and sodium levels. Low plasma potassium levels.

355
Q

Where is ACE found?

A

bound to the inner surfaces of capillaries throughout the body but particularly abundant in the lungs

356
Q

combine inulin and PAH into something significant

A

inulin plasma clearance/PAH plasma clearance=

GFR/Renal Plasma Flow= Filtration Fraction

357
Q

Why does the body need to be able to modify the concentration of urine?

A

Extracellular fluid osmolarity normally 300 mOsm- must keep that in homeostasis by regulating fluid volume in plasma and amount that leaves in urine

358
Q

If interstitial fluid concentration is normally 300 miliosmolar, what concentration would urine be?

A

300 miliosmolar

359
Q

Osmotic gradient

A

osmolarity of interstitial fluid gets progressively greater from cortex to medulla

360
Q

what preserves the osmotic gradient?

A

vasa recta

361
Q

Countercurrent multiplication

A

mechanism by which the solute concentration of interstitial fluid of the kidney becomes progressively greater from cortex to medulla

362
Q

Which kind of nephron is most important in concentrating urine?

A

juxtamedullary nephron

363
Q

Descending limb is premeable to _____ and does not reabsorb _____

A

water, NaCl

364
Q

Ascending limb is impermeable to _______ activley transports _______

A

water, NaCl

365
Q

How does the vasa recta maintain the medullary osmotic gradient?

A

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
Q

ADH where made and secreted

A

hypothalamus, posterior pituitary

367
Q

What does ADH do?

A

increases water permeability of the collecting duct (reabsorbtion)

368
Q

Dehydration and ADH

A

Low water content activates ADH, urine volume will be small and concentrated

369
Q

How does ADH increase water reabsorption?

A

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
Q

Regulation of ADH

A

baroreceptors and osmoreceptors send feedback about blood pressure, volume, and osmolarity. High osmolarity increases secretion of ADH

371
Q

Diabetes insipidus cause

A

kidneys either don’t respond to ADH or not enough adh is made

372
Q

Types of diabetes insipidus

A

Nephrogenic- kidneys don’t respond to ADH

Neurogenic- Hypothalamus doesn’t make enough ADH

373
Q

without adh, collecting ducts are normally

A

impermeable to water

374
Q

how is micturition regulated?

A

bladder fills, wall expands and activates stretch receptors

sympathetic- relaxes internal sphincter

parasympathetic- contracts detrusor muscle

somatic- relaxation of external sphincter

375
Q

functions of saliva

A

moistens and lubricates food

salivary amylase begins digestion of carbohydrates

antibacterial action

solvent for taste

buffers acids

376
Q

controls for saliva production

A

chemoreceptors in mouth, salivary glands send feedback to cortex

377
Q

Basic functions of the stomach

A

stores food, contracts muscle and grinds food into chyme

378
Q

secretions of the stomach

A

mucus, pepsinogen, HCl, intrinsic factor, gastrin, somatostatin, histamine

379
Q

Digestion in the stomach

A

pepsinogen breaks down proteins

380
Q

absorption in the stomach

A

no food, some drugs

381
Q

Gastric pits contain

A

gastric glands, chief cells, parietal cells

382
Q

chief cells

A

secrete pepsinogen

383
Q

parietal cells

A

secrete HCl and intrinsic factor

384
Q

goblet cells

A

secrete mucus

385
Q

d cells

A

secrete somatostatin (inhibits acid secretion)

386
Q

G cells

A

secrete gastrin (stimulates acid secretion)

387
Q

Pepsinogen

A

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
Q

Why and how do we vomit?

A

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
Q

Drugs that inhibit vomiting

A

Chemoreceptors that regulate vomition center

390
Q

functions of HCl in stomach

A

activates pepsinogen

breaks down connective tissue and food particles

denatures proteins

kills microorganisms

391
Q

intrinsic factor

A

important in vitamin b12 absorption

392
Q

GERD

A

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
Q

Describe how parietal cells secrete HCl

A

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
Q

How does prilosec work?

A

blocks proton pump that sends H+ into lumen of stomach

395
Q

how does zantac work?

A

antihistamine, blocks H2 receptors so bicarbonate cant leave and cl- cant come in

396
Q

migrating motility complex

A

cleans out small intestine between meals when absorption isn’t happening

397
Q

secretions of the small intestine

A

juice of the intestine (protects and lubricates, has water for hydrolysis), but no digestive enzymes

398
Q

How is digestion accomplished in small intestine?

A

pancreatic enzymes, bile, and brush border enzymes

399
Q

Pancreatic secretions

A

bicarbonate (neutralizes chyme from stomach)

trypsinogen

chymotrypsinogen

procarboxypeptidase

pancreatic amylase (breaks down polysaccharides to maltose)

Pancratic lipase (triglycerides to monoglycerides, FA’s)

400
Q

How are Trypsinogen, chymotrypsinogen, and procarboxypeptidase activated in the pancreas?

A

enterokinase converts trypsinogen to trypsin then trypsin converts the rest to active form

401
Q

Gastrin

A

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
Q

Cholecystokinin

A

produced by the small intestine from I-cells

Promotes release of digestive enzymes from pancreas and bile from gallbladder

403
Q

Secretin

A

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
Q

hormonal control of bile release

A

CCK increases bile secretion

Secretion decreases it

405
Q

Functions of bile

A

excretion of biliruben, emulsification of fat

406
Q

what acts on the surface of fat droplets?

A

pancreatic lipase

407
Q

Brush border

A

folds and villi increase surface area for absorption

contains enterokinase, maltase, sucrase, lactase, aminopeptidase

408
Q

celiac disease

A

destruction of the vili due to inflammatory reactions. Results in diarrhea, weight loss, anemia, calcium and vit D deficiency, blahblahblah

409
Q

Draw out carbohydrate digestion pathway

A

Polysaccharides to disaccharides (amylase)

Dissacharides to monosacharides (lactase, maltase, sucrase)

410
Q

absorbtion of carbohydrates

A

facilitated diffusion of secondary active transport with Na

411
Q

trypsin

A

cleaves @ carboxyl sides of lysine/arginine except when followed by proline

412
Q

chymptrypsin

A

carboxyl end of aromatics

413
Q

carboxypeptidase

A

branched chain AA’s

414
Q

exogenous protein digestion (dietary proteins)

A

polypeptides to small peptides (pepsin and pancreatic enzymes)
small peptides to amino acids (amino peptidases and intracellular peptidases)

415
Q

absorption of proteins

A

coupled to Na/H exchanger

416
Q

fat absorption

A

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
Q

HDL cholesterol

A 
builds membranes
manufactures bile
absorbs ADEK
insulates neurons
production of adrenal/sex hormones
418
Q

LDL cholesterol

A

clogs arteries, heart attacks, strokes, death

419
Q

Gastrocolic reflex

A

increased peristalsis of the colon after food has entered the stomach

420
Q

secretions of large intestine

A

mucus and bicarbonate to lubricate lumen and neutralize acid.

421
Q

Absorptions of large intestine

A

salt and water

422
Q

fecal composition

A

dead bacteria, fat, organic/inorganic waste, protein, roughage. Mostly bacteria and roughage.

423
Q

borborgymi

A

hyperactive bowel sounds

424
Q

composition of flatus

A

stomach- NO from air
SI- CO2 and NaCO3 from HCl and HCO3-
LI- CO2, methane, NO

425
Q

fat digestion performed by

A

pancreatic lipase

PD Bio 305 (10 decks)

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