Medical Physiology Exam 1

Front 1

What is the main goal of a Negative Feedback System?

Back 1

Diminish the Difference

(thermostat: match the set and actual temperature)

Front 2

When does baroreceptor firing increase, when BP is low or high?

Back 2

BP high

(more firing with higher BP)

Front 3

What is the main goal with positive feedback system?

Back 3

Excentuate the change

Front 4

What are the effectors of maintenance of blood glucose levels?

Back 4

insulin/ glucagon

negative feedback system

Front 5

What is the purpose of an effector?

Back 5

to bring about a change

Front 6

What unit is missing from positive feedback compared to negative feedback?

Back 6

a controller

sensor directly affects the effector

Front 7

What is an example of a positive feedback system?

Back 7

LH surge during a menstrual cycle

estrogen is the effector and ovaries are the sensors

Front 8

What is the downfall of a feedforward system?

Back 8

no back pathway

Front 9

What is the purpose of feedforward system?

Back 9

respond in anticipation of a disturbance

Front 10

What are two methods for movement of molecules?

Back 10

diffusion
bulk flow

Front 11

What is needed for bulk flow?

List 2 examples

Back 11

Driving Force

Lungs - air movement
Heart - blood movement

Front 12

Factors that determine membrane permeability

Back 12

-size
-charge
-lipid solubility

Front 13

Factors of Rate of diffusion

Back 13

Area available
Concentration Difference
Lipid solubility (size and charge)

Front 14

Hydrophobic

Back 14

permeable

Front 15

Frick's Law

Back 15

rate of diffusion is proportional to concentration difference

J = P.A. (C1-C2)
net rate of membrane transport = permeability coefficient* concentration difference

Front 16

Secondary active transport

Back 16

co-transport with Na+ ions

(symport or antiport)

Front 17

How does a parietal cell utilize channels, transporters and pumps?

Back 17

transports Cl from the blood to the stomach lumen and H+ with utilization of the bicarbonate ion

Front 18

What does the drug omeprazole inhibit?

Back 18

H+/K+ ATPase in the parietal cell
(inhibiting H+ secretion into the stomach lumen)

Front 19

3 diseases from disordered cell membrane transport

Back 19

1. hexo-malabsorption
2. cystic Fibrosis (lung consolidation)
3. diabetes insipidus (unable to reabsorbe H2O)

Front 20

Amount and % of total body water

Back 20

42 L
60%

Front 21

Amount and % of Intracellular water

Back 21

28L
40%

Front 22

Amount and % of interstital/ lymph water

Back 22

10.5L
15%

Front 23

Amount and % of plasma water

Back 23

3.5L
5%

Front 24

Amount and % of extracellular water

Back 24

14L
20%

Front 25

What is unique about transcellular water

Back 25

contained within an epithelial layer

(ex. cerebrospinal fluid, ocular fluid, joint fluid)

Front 26

Equation for Volume distribution

Back 26

V distribution = (m. of indicator injected - m. of indicator lost)/ concentration in plasma

Front 27

Equation for mass of indicator excreted (lost)

Back 27

mass of indicator excreted = urine volume*indicator concentration in urine

Front 28

Indicator for total body water

Back 28

antipyrine, D2O, HTO

Front 29

Indicator for plasma H2O

Back 29

Evans blue, I-Albumin

Front 30

Indicator for extracellular H2O (PW & ISW)

Back 30

Impermeate ions (overestimate H2O)

Inert sugars (underestimate H2O)

Front 31

Determine intracellular Fluid Volume

Back 31

total body water - extracellular body water

Front 32

Determine interstitial fluid volume

Back 32

extracellular body water - plasma water

Front 33

tonicity

Back 33

effective osmolality with regard to a reference solution

Front 34

Adrenal Insufficiency

Back 34

decrease in aldosterone -> decrease in Na reabsorption

Hyposmotic volume contration

(loss of Na and water, but kidneys excrete more Na than water)

Front 35

SIADH

Back 35

Syndrome of Inappropriate Antidiuretic Hormone

Hyposmotic Volume Expansion

too much ADH secreted -> not much urine, instead reabsorbing lots of H2O

Front 36

Sweating, fever, diabetes insipidus

Back 36

Hyperosmotic volume contraction

Front 37

High NaCl intake

Back 37

Hyperosmotic volume expansion

Front 38

Diarrhea

Back 38

Isomotic volume contraction

Front 39

Isotonic NaCl infusion

Back 39

Isosmotic volume expansion

Front 40

4 responses to decrease in blood volume

Back 40

1. inc. RAAS
2. inc. sympathetic outflow (SNS)
3. inc. Arginine vasopressin AVP... ADH
4. dec. atria natriutetic peptide (ANP)

->all reabsorb sodium

Front 41

Ways to regulate ECF osmolality

Back 41

1. release of AVP or ADH
2. trigger thirst

Front 42

Ion movement depends on ______ ______ and ______ _____

Back 42

electrical gradient and concentration gradient

Front 43

What 2 factors constitute the net 'driving force'?

Back 43

Concentration gradient and electrical gradient

Front 44

How does the Nernst Potential relate to the driving force

Back 44

Nernst Potential is where there is ZERO driving force

Front 45

Nernst Equation

Back 45

Eion = 61/z * log[ion]o/[ion]i

Front 46

[K+] inside and outside of cell

Back 46

[K+]inside = 140mM
[K+]outside = 5mM

Front 47

[Na+] inside and outside of cell

Back 47

[Na+]inside = 10mM
[Na+]outside = 140mM

Front 48

[Ca2+] inside and outside of cell

Back 48

[Ca2+]inside = 0.0001mM
[Ca2+]outside = 1mM

Front 49

[Cl-] inside and outside of cell

Back 49

[Cl-]inside = 20mM
[Cl-]outside = 116mM

Front 50

Equilibrium potential (Ek)

Back 50

-88mV

Front 51

Equilibrium potential for sodium (Ena)

Back 51

+70 mV

Front 52

Equilibrium potential for calcium (Eca)

Back 52

+122 mV

Front 53

Equilibrium potential for chloride (Ecl)

Back 53

-47 mV

Front 54

What causes a membrane to be selectively permeable to a specific ion

Back 54

an open channel

Front 55

A membrane at rest is most permeable to _____ ions

Back 55

K+ (potassium)

Front 56

2 factors that determine membrane potential

Back 56

1. Nernst Potential
2. Permeabilities

Front 57

What does the Goldman- Hodgkin-Katz equation determine

Back 57

membrane potential (Em)

Front 58

How permeable is Cl- in neurons and skeletal muscle cell

Back 58

neurons -> negligible permeability
skeletal m. cell -> significant

Front 59

What structure maintains the membrane potential?

Back 59

Na+/K+ ATPase

Front 60

Hyperkalemia

Back 60

depolarize membrane potential

increase sodium channel inactiviation -> inexcitability

Front 61

Hypokalemia

Back 61

hyperpolarization

increase concentration gradient

Front 62

Excitable cells

Back 62

nerves and all three muscle types

Front 63

Start and stop of action potential duration

Back 63

start: threshold
stop:upon return to resting potential (before hyperpolarize phase)

Front 64

What produces an electrical current

Back 64

flow of ions across a membrane

Front 65

g(Na) > g(K)

Back 65

ion conductance for upstroke of AP

Front 66

g(Na) = g(K)

Back 66

conductance at the peak of an AP

Front 67

g(Na) < g(K)

Back 67

conductance for the downstroke of an AP

Front 68

What causes the threshold?

Back 68

voltage-gated Na+ channels

Front 69

Na+ channels open in a fast, _______ feedback process

Back 69

positive

Front 70

To initiate an AP, the resting ____ efflux must be overcome

Back 70

K+

potassium moving out tries to keep the cell negative

Front 71

Hyperparathyroidism

Back 71

Hypercalcemia

reduced excitability -> muscle weakness

Front 72

Hypoparathyroidism/ Chronic Renal Failure

Back 72

Hypocalcemia

increased excitability -> spontanous m. twitching

Front 73

What happens to the sodium driving force at the peak of an AP?

Back 73

decreases

Front 74

Where in the AP is the inactivation gate closed?

Back 74

peak and downstroke of an AP

Front 75

Where in an AP is the activation gate open?

Back 75

upstroke and peak of an AP

Front 76

What explains the refractory period?

Back 76

recovery from inactivation

Front 77

___________ can increase Na+ channel inactivation and cause inexcitability

Back 77

Hyperkalemia

Front 78

What 2 channels contribute to the cell K+ efflux

Back 78

inward rectifier - open at negative potentials (resting)

Voltage gated - open at depolarized potentials (causes repolarization)

Front 79

What does a smaller K+ current do to the AP duration

Back 79

makes it longer

Front 80

What happens to a passive current as it passes down an excitable cell?

Back 80

magnitude of current decreases due to leakiness

Front 81

Passive current spreak triggers ____ ____ _______

Back 81

action potential regeneration

Front 82

What affects how far a current spreads passively?

Back 82

the extent of leakiness

Front 83

length or space constant

Back 83

measure of the leakiness of a cell

(37% of initial voltage)

Front 84

What does increasing the radius do to the internal resistance?

Back 84

decreases the internal resistance

Front 85

large space constant = _____ ______ velocity

Back 85

faster conduction

Front 86

What does myelination do?

Back 86

increases membrane resistance -> reducing leakiness

Front 87

2 types of synapses

Back 87

electrical and chemical

Front 88

What is needed at an electrical synapse?

Back 88

direct connection - connexon make a gap junction

Front 89

What 3 things possess gap junctions

Back 89

neurons, cardiac myocytes, and smooth muscle

Front 90

What does ischemia do to gap junctions?

Back 90

gap junction become uncoupled/ closed

Front 91

What would decreasing the pH and increasing the intracellular [Ca2+] do to a gap junction?

Back 91

cause it to close

Front 92

What causes an increase in [Ca2+] within the terminal of an axon?

Back 92

opening of voltage gated calcium channels due to depolarization caused by open sodium channels

Front 93

What does the drug SSRI affect?

Back 93

neurotransmitter reuptake channel on the pre-synaptic axon

Front 94

Difference between ionotropic and metabotropic receptors?

Back 94

ionotropic receptor is permeable to ions upon ligand binding

metabotropic receptor is a G coupled receptor, slower response

Front 95

Which neurotransmitter produces effect through both ionotropic and metabotropic receptors?

Back 95

Acetylcholine

Front 96

Nicotinic receptor

Back 96

ionotropic receptor

Front 97

Muscarinic receptor

Back 97

metabotropic receptor

Front 98

What movement of ions cause an inhibitory postsynaptic respose?

Back 98

Cl- ions in
K+ ions out

Front 99

Acetylcholine

Back 99

parasympathetic Neurotransmitter

Front 100

Nitric oxide

Back 100

parasympathetic Neurotransmitter

Front 101

Norepinephrine

Back 101

sympathetic neurotransmitter

Front 102

Epinephrine

Back 102

sympathetic neurotransmitter

Front 103

3 Neurotransmitters found in the brain

Back 103

Dopamine
Histamine
Serotonin

Front 104

2 excitatory amino acid neurotransmitters

Back 104

Glutamate
Aspartate

Front 105

2 inhibitory amino acid neurotransmitters

Back 105

Glycine
GABA

Front 106

Where does neuromuscular transmission occur?

Back 106

motor end plate

Front 107

motor neuron

Back 107

1 motor axon with corresponding muscle fibers it innervates

Front 108

What is the neurotransmitter and receptor at the neuromuscular junction

Back 108

receptor: nicotinic ACh receptor

neurotransmitter: acetylcholine

Front 109

End plate potential (EPP)

Back 109

results in muscle fiber upon motor nerve stimulation and can possibly lead to an AP

Front 110

What determine the magnitude of an EPP

Back 110

dependent upon the extent of ACh release

Front 111

What make up the end plate current?

Back 111

mixture of Na+(in) and K+(out) => net flow of ions

Front 112

What terminates an EPP

Back 112

degradation of ACh by acetylcholinesterase

Front 113

How is ACh resynthesized?

Back 113

choline is transported back into the nerve terminal via Na+/choline symport -> then choline is connected to acetyl group via choline-acetyl transferase

Front 114

Myasthenia Gravis

Back 114

autoimmune disease affecting ACh receptors

(antibodies that block ACh receptors)
treatment: Neostigmine - block AChesterase

Front 115

Lambert-Eaton syndrome

Back 115

autoimmune disease that attacks presynaptic Ca2+ channels

-> decreasing ACh release

Front 116

Cobra Venom

Back 116

paralysis via blocking nicotinic ACh receptors

Front 117

2 v-SNARES

Back 117

synaptotagmin - calcium sensor
synaptobrevin - intertwine

Front 118

2 t-SNARES

Back 118

SNAP-25
Syntaxin

Front 119

How does Botulinum toxin reduce vesicle release

Back 119

cleave SNARE proteins

unable to dock vesicles

Front 120

How does Tetanus toxin reduce vesicle release

Back 120

cleaving synaptobrevin

unable to dock vesicle

Front 121

How does tetanus toxin reduce vesicle release?

Back 121

cleaves synaptobrevin -> vesicle unable to dock

Front 122

How does tetanus toxin cause 'lock jaw'?

Back 122

inhibits vesicle release in the inhibitory internueron -> motor axon active all of the time

Front 123

Spatial Summation

Back 123

postsynaptic potentials sum when they collide within the soma

different inputs that fire at the same time

Front 124

Temporal Summation

Back 124

rapid EPSPs from a single input that sum if close enough in time

Front 125

Synaptic Facilitation

Back 125

increase in EPSP magnitude caused by repetitive synaptic transmission

Front 126

Skeletal m.: velocity, duration, fatigability

Back 126

rapid velocity
relatively long duration
variable fatigability

Front 127

Cardiac m.: velocity, duration, fatigability

Back 127

rapid velocity
short duration
no fatigue

Front 128

Smooth m.: velocity, duration, fatigability

Back 128

slow velocity
long duration
no fatigue

Front 129

myogenic

Back 129

no axon is needed for initiation

Front 130

A Band

Back 130

entire myosin molecule

Front 131

I Band

Back 131

only actin, including Z line

Front 132

H Band

Back 132

only myosin, including M line

Front 133

What does Myosin Light chain kinase do?

Back 133

phosphorylates myosin -> allowing myosin to bind to actin

Front 134

Where does the triad fall in skeletal m.?

Back 134

along A-I junction

Front 135

Where does the Dyad fall in cardiac m.?

Back 135

along the Z line

Front 136

What do Ryanodine receptors (RyR) span?

Back 136

t-tubule and SR

Front 137

Dihydropyridine receptors (DHPR)

Back 137

Ca2+ voltage gated channels within the t-tubule

Front 138

__ DHPR : ___ RyR in skeletal and cardiac m.

Back 138

2:1 in skeletal m.
1:~4 in cardiac m.

Front 139

How does Ca2+ cause contraction

Back 139

by binding to Troponin C

Front 140

3 ways of removing Ca2+ from the cell

Back 140

1. SERCA pump
2. Na-Ca exchanger
3. Ca-ATPase

Front 141

Malignant Hyperthermia

Back 141

mutation that prevents termination of Calcium release by high [Ca]

Front 142

How is contractile force increased in a single skeletal muscle fiber?

Back 142

increase twich frequency

Front 143

How is contractile force increased in whole skeletal muscle?

Back 143

increase number of motor units

Front 144

How is contractile force increased in cardiac muscle?

Back 144

increase [Ca] in cytosol from SR

Front 145

What do Golgi Tendon Organs sense?

Back 145

Tension

Front 146

What do muscle spindles sense?

Back 146

length

Front 147

Afferent neuron of GTOs

Back 147

Ib

Front 148

Afferent neurons of Muscle Spindles

Back 148

II and Ia

Front 149

Myotatic (Stretch) Reflex

Back 149

muscle stretch triggers contraction of the stretched muscle

Front 150

Major players in control of posture

Back 150

muscle spindles and stretch reflex

Front 151

Inverse Myotatic Reflex

Back 151

muscle tension triggers muscle relaxation

Front 152

Flexor Reflex

Back 152

produces coordinated responses in ipsilateral and contralateral limbs

Front 153

Importance of Muscle Spindles

Back 153

sense muscle length
-stretch reflex
-posture
-position sense

Front 154

2 Main types of Smooth Muscle

Back 154

1. Single Unit (phasic)
2. Multi-unit (tonic and fine control)

Front 155

Smooth m. in the bladder

Back 155

well coupled, 1 functional unit

Front 156

smooth m. in blood vessels

Back 156

less coupling, lots of small units

Front 157

Difference in cross-bridges in smooth m. compared to skeletal m.

Back 157

smooth m. cross bridges have a longer attachment time due to lower contration velocity and more force/ cross-bridge

Front 158

2 examples of tonic smooth muscle

Back 158

spincter and blood vessels

Front 159

2 examples of phasic smooth m.

Back 159

intestines and bladder

Front 160

What is the electrical activity of phasic smooth m.?

Back 160

action potentials

Front 161

electrical activity of tonic smooth m.?

Back 161

graded changes in Em or Independent of Em

Front 162

Myosin Light Chain Phosphatase

Back 162

dephosphorylates myosin causing relaxation