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organisms respond to changes in their internal and external environments Flashcards

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AP® Biology flashcards Biology 101 flashcards
1
Q

what is a stimulus?

A

detectable change in the environment

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2
Q

what is a stimulus detected by?

A

receptor

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3
Q

what is a tropism?

A

when plants respond via growth to stimuli, they can be positive or negative

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4
Q

what are tropisms controlled by?

A

indoleacetic acid (IAA), a type of auxin that controls cell elongation

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5
Q

IAA causes cell elongation in…

A

shoots

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6
Q

IAA inhibits cell elongation in…

A

roots

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7
Q

positive phototropism in shoots

A
  • shoot tip cells produce IAA
  • this causes cell elongation
  • IAA diffuses to cells on shaded sides
  • resulting in a high conc. in shaded side
  • causing shaded to elongate and bend towards light
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8
Q

negative phototropism in roots

A
  • high conc. of IAA inhibits cell elongation
  • causes root cells to elongate more on lighter side
  • root bends away from the light
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9
Q

negative gravitropism in shoots

A
  • IAA will diffuse from upper side to lower side of shoot
  • causes cell elongate and plant grows upwards
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10
Q

positive gravitropism in roots

A
  • IAA moves to lower side of roots
  • upper side elongates
  • root bends down so anchor plant in
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11
Q

taxis

A

movement of an organisms body towards favourable stimuli or away from unfavourable stimuli (directional response to external stimuli)

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12
Q

kinesis

A

organism changes the speed of movement and the rate it changes the direction (non-directional response)

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13
Q

why do many organisms respond to temperature and humidity via kinesis rather than taxis?

A

often no clear gradient from one extreme to another

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14
Q

simple reflex arc

A
  • receptor detects stimulus
  • sensory neuron
  • relay neuron in CNS
  • motor neuron
  • response by effect
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15
Q

advantages of simple reflex arc

A
  • rapid response to potentially dangerous stimuli
  • instinctive
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16
Q

what are pacinian corpuscles?

A

pressure receptors located deep in skin, mainly in fingers and feet

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17
Q

structure of pacinian corpuscle

A
  • single nerve fibre surrounded by layers of connective tissue which are separated by a viscous gel contained by a capsule
  • stretch-mediated Na+ channels on plasma membrane
  • capillary runs along base layer of tissue
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18
Q

what stimulus does a pacinian corpuscle respond to and how?

A
  • pressure deforms membrane, causing stretch-mediated Na+ ion channels to open due to widening of sodium channels
  • if influx of Na+ ions raises membrane to threshold potential, a generator potential is produced
  • action potential moves along sensory neuron
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19
Q

two types of photoreceptor in retina

A

rods and cones

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20
Q

where are rods located?

A

evenly distrubted around periphery of retina and not in the fovea

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21
Q

where are cones located?

A

central fovea

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22
Q

rod cells

A
  • cannot distinguish different wavelengths of light so process images in black and white
  • can detect light of very low intensities
  • linked by spatial summation
  • low visual acuity
  • conatin only one pigment, rhodopsin
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23
Q

how is a generator potential created in a rod cell?

A
  • rhodopsin is broken down by light energy
  • there is enough low-intensity light to cause this
  • enough pigment has to be broken down for the threshold to be met in the bipolar cell
  • this threshold can be reached because so many rod cells are connected to a single bipolar cell
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24
Q

how does retinal convergence impact rod cells?

A

retinal convergence means that the brain cannot distinguish between separate sources of light (low visual acuity)

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25
Q

cone cells

A
  • three types of cone cell that contain different iodopsin pigment which all absorb different wavelengths of light
  • can only detect high intensity light
  • no spatial summation
  • high visual acuity
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26
Q

why can we not see colour in the dark?

A

only one cone cells connects to a bipolar cell so cones so there is no spatial summation and cones can only respond to high light intensity

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27
Q

why are cones located in the fovea?

A

the fovea receives the highest intensity of light

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28
Q

myogenic definition

A

cardiac muscle is myogenic beacause it contracts within the muscle itself rather than by nervous stimulation

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29
Q

what are the two nodes involved in heart contraction?

A

SAN (sinoatrial node) and AVN (atrioventricular node)

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30
Q

where is the SAN located?

A

wall of the right atrium (also known as the pacemaker)

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31
Q

where is the AVN located?

A

between the border of the right and left ventricle within the two atria

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32
Q

where is the bundle of His located?

A

the septum

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33
Q

where are the Purkyne fibres loacted?

A

walls of the ventricles

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34
Q

how are heartbeats coordinated and initiated?

A
  • SAN releases a wave of depolarisation across the atria, causing it to contract
  • AVN releases wave of depolarisation
  • non-conductive layer between the atria and ventricle prevent the wave travellings to ventricles
  • the budle of His conduct and pass the wave of depolarisation down the septum and the Purkyne fibres in the walls of the ventricles
  • apex and then walls of ventricles contract
  • delay of AVN WOD means atria can pump all blood into ventricles
  • cells repolarise and the cardiac muscles relax
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35
Q

what area of the brain controls heart rate?

A

medulla oblongata, via the ANS

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36
Q

what does the heart rate change in response to?

A

blood pressure and pH

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37
Q

what receptors decect pH change?

A

chemoreceptors

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38
Q

where are the chemoreceptors located?

A

carotid artery and aorta

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39
Q

what receptors detect blood pressure change?

A

baroreceptors

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40
Q

where are the baroreceptors located?

A

carotid artery

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41
Q

how does the body produce an increase in HR?

A

stimulus: low pH/low pressure
receptor: chemo/baroreceptor
coordinator: more action potentials to medulla oblongata
effector: SAN via sympathetic nervous system increases frequency of AP

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42
Q

how does the body produce a decrease in HR?

A

stimulus: high pH/high pressure
receptor: chemo/baroreceptor
coordinator: more action potentials to medulla oblongata
effector: SAN via parasympathetic nervous system increases frequency of AP

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43
Q

describe the general structure of a motor neuron

A
  • cell body that contains organelles and RER
  • dendrons that branch into dendrites which carry AP to cell body
  • axon that is a long unbranched fibre that carries AP down neuron
  • nodes of ranvier that are gaps in myelin which allow for saltatory conduction
  • myelin sheath is a lipid which does not allow charged ions to pass through
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44
Q

what is resting potential?

A

the difference between electrical charge inside and outside of the neuron when there is no AP

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45
Q

what is the value for resting potential?

A

-70mV

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46
Q

how is resting potential established?

A
  • higher concentration of potassium ions inside
    and higher concentration of sodium ions outside
  • membrane contains many Na-K pumps
  • actively transports 3Na+ out and 2K+ in
  • membrane is more permeable to K+
  • creates electrochemical gradient
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47
Q

what is an action potential?

A

when the neurone’s voltage increases beyond a set point beyond the resting potential, creating an electrical impulse

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48
Q

what is the value for an action potential?

A

+40mV

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49
Q

what is the threshold value?

A

-55mV

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50
Q

how is an action potential generated?

A
  • stimulus provides energy to cause voltage-gated sodium channels to open
  • causes Na+ to diffuse into axon whilst K+ diffuses out
  • this increases voltage
  • voltage above -55mV exceeds threshold, providing more energy, so more channels open
  • this is depolarisation
  • peaks at 40mV
  • sodium channels close and voltage-gated potassium channels open
  • decreases voltage as K+ diffuses out (repolarisation)
  • hyperpolarisation occurs when voltage is less than resting
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51
Q

all or nothing principle

A

if depolarisation does not exceed threshold, then an action potential is not produced (nothing). all stimuli that does trigger depolarisation will peak at 40mV (all).

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52
Q

why is the all or nothing principle important?

A

makes sure than animals only respond to large enough stimuli to prevent sensory overload

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53
Q

refractory period

A

no action potential can be generated because sodium channels are recovering and cannot be opened (hyperpolarisation)

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54
Q

why is the refractory period important?

A
  • ensures discrete impulses are produced
  • ensures action potentials travel in one direction
  • limits frequency of action potentials
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55
Q

what factors affect the speed of an action potential?

A
  • myelination and saltatory conduction
  • axon diameter
  • temperature
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56
Q

why does myelination and saltatory conduction affect the speed of an action potential?

A
  • gaps between myelin called NOR
  • action potential jumps from node to node (saltatory conduction)
  • myelin provides electrical insulation
  • in non-myelinated axons, AP occurs along whole length
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57
Q

why does axon diameter affect the speed of an action potential?

A

the wider the diameter, the faster the speed of conduction because there is less leakage of ions and less resistance to the flow of ions

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58
Q

why does temperature affect the speed of an action potential?

A

the higher the temperature, the faster the speed of conduction because the ions diffuse faster and the enzymes involved in respiration work faster (ATP)

59
Q

what is a synapse and what is its function?

A

synapses are gaps between the end of the axon and the dendrite of another neuron. this is where the AP is transmiited as a neurotransmitter.

60
Q

outline the process of synaptic transmission

A
  • depolarisation of synaptic knob membrane
  • voltage gated calcium ion channels open and calcium ions diffuse into synaptic knob
  • synaptic vesicles fuse with with presynaptic membrane and release a neurotransmitter
  • neurotransmitter diffuses down neuron across synaptic cleft
  • binds to complementary receptors on postsynaptic membrane
  • sodium ions diffuse in by sodium ion channels leading to depolarisation
  • neurotransmitter is degraded and released from receptor and resting potential is established
61
Q

why is synaptic transmission unidirectional?

A

vesicles are only found in presynaptic membrane and receptors are only on postsynaptic membrane

62
Q

what is the neurotransmitter in a cholinergic synapse?

A

acetylcholine

63
Q

what enzyme breaks down acetylcholine?

A

acetylcholinesterase

64
Q

what does acetylcholinesterase break acetylcholine into?

A

acetate and choline

65
Q

what is summation?

A

the rapid build up of neurotransmitters in the synapse to help generate an action potential

66
Q

what are the two types of summation?

A

spatial and temporal

67
Q

spatial summation

A

many different presynaptic neurones collectively trigger a new action potential by combining the neurotransmitter they release to exceed threshold

68
Q

temporal summation

A

one neurone releases neurotransmitter repeatedly over a short period of time to add up enough to exceed threshold

69
Q

inhibitory synapses

A

cause chloride ions to move into postsynaptic neurone and potassium ions to move out, hyperpolarising the membrane to make an AP unlikely

70
Q

what is a neuromuscular junction?

A

synapse between a motor neurone and a muscle

71
Q

similarities between neuromuscular junction and cholinergic synapse

A
  • both unidirectional
  • acetylcholine is the neurotransmitter
72
Q

differences between neuromuscular junction and cholinergic synapse

A
  • NJ is only excitatory, CS is excitatory or inhibitory
  • NJ connects a motor neurone to a muscle, CS connects two neurones
  • NJ is the end point of an action potential, CS is where a new action potential is generated in the next neurone
  • NJ acetylcholine binds to receptors on muscle fibre membranes, CS acetylcholine binds to receptors in postsynaptic membrane
73
Q

how might drugs increase synaptic transmission?

A
  • inhibit acetylcholinesterase
  • mimic shape of neurotransmitter
74
Q

how might drugs decrease synaptic transmission?

A
  • inhibit release of neurotransmitter
  • decrease permeability of ions in postsynaptic membrane
  • hyperpolarise postsynaptic membrane
75
Q

what are the three types of muscle in the body and where are they located?

A

cardiac: heart
smooth: walls of blood vessels and intenstines
skeletal: attached to incompressible by tendons

76
Q

what does antagonistic muscle pair mean?

A

as one muscle contracts, the other relaxes

77
Q

what is a myofibril?

A

fused cells that share nuclei and sarcoplasm that have a high number of mitochondria, they are the site of contraction

78
Q

what is the sarcomere?

A

small units of a myofibril

79
Q

what proteins make up myofibril?

A

actin and myosin

80
Q

what is the thick protein in the sarcomere?

A

myosin

81
Q

what is the thin protein in the sarcomere?

A

actin

82
Q

process of sliding filament theory

A
  • depolarisation of muscle causes calcium ions from sarcoplasmic reticulum to diffuse into myofibrils
  • calcium ions causes the protein tropomyosin to move and uncover the binding sites on actin
  • myosin heads attach to binding site on actin to form a cross bridge (creating tension)
  • hydrolysis of ATP (ADP) causes actin to bend
  • attachment of new ATP to myosin head causes it change shape slightly and detaches from actin
  • ATPase from sarcoplasm hydrolyses ATP on myosin head to return to ADP and myosin can return to its orginial position
83
Q

evidence for sliding filament theory

A

H-zone narrows
I-band narrows
Z-line gets closer
A-band remains same

84
Q

what is the role of phosophocreatine in muscle relaxation?

A

phosphorylates ADP into ATP when oxygen for aerobic respiration is limited (anaerobic)

85
Q

what are the 5 sarcomere bands?

A

A-band
H-zone
I-band
M-line
Z-line

86
Q

A-band

A

overlap of actin and myosin (total width of the myosin)

87
Q

H-zone

A

myosin only (no overlap with actin)

88
Q

I-band

A

actin only (no overlap with myosin)

89
Q

M-line

A

middle point of myosin

90
Q

Z-line

A

boundary between sarcomeres (end points)

91
Q

where are slow-twitch muscle fibres found?

A

sites of sustained contraction (e.g calf muscle)

92
Q

where are fast-twitch muscle fibres found?

A

sites of rapid contraction (e.g biceps)

93
Q

structure of STF

A
  • large store of myoglobin (stores lots of oxygen)
  • rich blood supply
  • many mitochondria
94
Q

structure of FTF

A
  • thicker and more myosin filamements
  • large store of glycogen
  • phosphocreatine and enzymes for anaerobic respiration
95
Q

properties of STF

A
  • contract slower
  • can respire aerobically for longer periods of time due to rich blood supply and myoglobin
  • adapted for endurance
96
Q

properties of FTF

A
  • contract faster
  • short bursts of powerful contraction
  • adapted for intense exercise
97
Q

what is homeostasis?

A

when the internal bodily environment is maintained set limits around an optimum by physiological control systems

98
Q

why is it important core temperature remains stable?

A

stable- maintain rate of enzyme controlled reactions and prevent membrane damage
low- insufficient kinetic energy
high- denaturing

99
Q

dangers of too acidic pH

A

H+ ions interact with hydrogen and ionic bonds in tertiary structure of enzymes= no E-S complexes formed

100
Q

why is it important blood glucose concentration remains stable?

A
  • maintains constant water potential
  • constant concentration of respiratory substrate
101
Q

what is negative feedback?

A

self-regulatory mechanisms return internal environment to optimum when there is deviation

102
Q

what is positive feedback?

A

a fluctuation triggers changes that result in an even greater deviation from the normal level

103
Q

factors that affect blood glucose concentration

A
  • carbohydrate digestion
  • glycogenolysis
  • gluconeogenesis
104
Q

what is glycogenesis?

A

process of excess glucose being converted to glycogen when blood glucose levels are higher than normal

105
Q

what is glycogenolysis?

A

hydrolysis of glycogen back into glucose when blood glucose levels are too low

106
Q

what is gluconeogenesis?

A

process of creating glucose from non-carbohydrate stores (amino acids and glycerol)

107
Q

what happens when blood glucose concentration increases?

A
  • blood glucose increases
  • detected by beta cells in islets of Langerhans in pancreas
  • beta cells release insulin
  • liver becomes more permeable to glucose and enzymes are activated to convert glucose to glycogen
  • glucose is removed from the blood and stored as glycogen
108
Q

what happens when blood glucose concentration decreases?

A
  • blood glucose decreases
  • detected by alpha cells in the islets of Langerhans
  • alpha cells release glucagon and adrenal glands release adrenaline
  • second messenger model occurs to activate enzymes to hydrolyse glycogen
  • glycogen is hydrolysed bacl to glucose and more glucose is released back into blood
109
Q

how does insulin decrease blood glucose?

A
  • beta cells
  • attaches to receptors on the surface of liver cells, changing the tertiary structure of channel proteins so more glucose is absorbed
  • more protein carriers are incorporated into cell membranes so more glucose is abosrbed from the blood into cells
  • actiavtes enzymes involved in glycogenesis
110
Q

how does glucagon increase blood glucose?

A
  • alpha cells
  • attaches to receptors in the surface of target cells
  • when glucagon binds adenlylate cyclase is activated and this converts ATP into cyclic AMP which activates protein kinase why hydrolyses glycocen into glucose
  • actiavtes enzymes involved in gluconeogenesis
111
Q

role of adrenaline when blood glucose concentration decreases

A
  • adrenal glands produce adrenaline which binds to receptors on liver cells and activates enzymes for glycogenolysis
  • glucose diffuses into blood stream
112
Q

glucagon second messenger model

A
  • glucagon binds to glucagon receptors
  • this causes a change in the tertiary structure of adenylate cyclase, activating it
  • this converts ATP into cyclic AMP (cAMP)
  • cAMP activates protein kinase
  • protein kinase catalyses the hydrolysis of glycogen to glucose (glycogenolysis)
113
Q

secondary messenger model (with adrenaline)

A
  • adrenaline binds to receptor on target cell
  • protein G is actiavte
  • adenylate cyclase converts ATP into cAMP
  • cAMP actiavtes protein kinase
  • glycogenolysis
114
Q

insulin in type I diabetes

A

body is unable to produce insulin

115
Q

insulin in type II diabetes

A

body stops responding to insulin

116
Q

causes of type I diabetes

A

autoimmune disease where beta cells are attacked

117
Q

causes of type II diabetes

A

obesity and poor diet

118
Q

treatment of type I diabetes

A

insulin injections

119
Q

treatment of type II diabetes

A

regulating carb intake, increase exercise and injections (extreme cases)

120
Q

what is osmoregulation?

A

control of blood water potential via homeostatic mechanisms

121
Q

structure of the nephron

A

-renal capsule which surrounds glomerulus
- proximal convoluted tubule (series of loops surrounded by capillaries, walls made of epithelial cells with microvilli)
- loop of Henle which extends from cortex into medulla
- distal convoluted tubule (similar to PCT but has fewer capillaries)
- collecting duct (DCT from several nephrons empty into collecting duct which leads to renal pelvis)

122
Q

function of a nephron

A

filter blood to remove waste and selectively reabsorb useful substances back into the blood

123
Q

blood vessels associated with a nephron

A
  • wide afferent arteriole from renal artery which forms glomerulus
  • narrow efferent arteriole which forms capllary network
124
Q

process of filtering and reabsorptionin nephron

A
  1. ultrafiltration
  2. selective reabsorption
    3 + 4. maintence of sodium ion gradient
  3. water moving out of DCT
125
Q

ultrafiltration in renal capsule

A
  • blood enters through afferent arteriole which splits into capillaries making glomerulus
  • this causes high hydrostatic pressure of blood
  • this forces water and small molecules (glucose and mineral ions) out of gaps in capillary endothelium and basement membrane to form glomerulus filtrate
  • large proteins and blood cells are too big to leave so remain in blood
  • blood leaves via efferent arteriole
126
Q

selective reabsorption in PCT

A
  • concentration of Na+ ions in the PCT is decreased as they are actively transported out of the PCT cells into the blood in the capillaries
  • Na+ diffuse down concentration gradient from the PCT lumen to the cells lining the PCT
  • cotransport with glucose
  • glucose can now diffuse from PCT epithelial cell into blood
  • glucose has been reabsorbed
127
Q

maintenence of sodium ion conecntration in LOH

A
  • mitochondria in walls of cells provide energy to actively transport Na+ and Cl- ions out of the ascending limb
  • accumluation of Na+ and Cl- ions outside of the nephron lowers the water potential
  • water in the descending limb moves out by osmosis into the interstitial space and then the blood capillaries
  • water is reabsorbed into the blood
  • at the base of the ascending limb some Na+ ions are transported out by diffusion as the solution is very dilute
128
Q

walls of the ascending limb

A

thick walls impermeable to water, where Na+ ions are actively transported out

129
Q

walls of the descending limb

A

thin walls permeable to water so it can be moved out by osmosis

130
Q

why is the loop of Henle longer in desert animals?

A

more sodium ions can be actively transported, making water potential very negative, so more water can move out by osmosis and be reabsorbed in blood

131
Q

reabsorption of water in collecting duct

A
  • filtrate reaches top of the PCT which is very dilute
  • filtrate moves to DCT and collecting duct
  • section of medulla surrounding these two parts are very concentrated
  • so more water moves out of the DCT
  • what remains is transported out and forms urine
132
Q

how is the PCT adapted for selective reabsorption?

A
  • microvilli for a larger SA for cotransporter proteins
  • mitochondria for AT
133
Q

what might cause blood water potential to change?

A
  • sweating
  • water intake
  • ions in diet
134
Q

what does hypotonic blood mean?

A

water potential is too high

135
Q

what does hypertonic blood mean?

A

water potential is too low

136
Q

what are changes in blood water potential detected by?

A

osmoreceptors

137
Q

where are osmoreceptors located?

A

hypothalamus

138
Q

what do osmoreceptors do when blood water potential is too low?

A

water leaves osmoreceptors by osmosis and they shrivel, which stimulates the hypothalamus to produce more ADH

139
Q

what do osmoreceptors do when blood water potential is too high?

A

water enters osmoreceptors by osmosis which stimulates the hypothalamus to produce less ADH

140
Q

role of posterior pituitary gland in osmoregulation

A

stores and secretes ADH into the capillaries and blood

141
Q

role of ADH in osmoregulation

A
  • increases permeability of the walls of the collecting duct and DCT to water
  • means more water leaves the nephron
  • more water is reabsorbed into the blood
  • urine is more concentrated
142
Q

what are aquaporins?

A

protein channels for water to pass through, with more aquaporins, more water leaves the nephron and is reabsorbed in the blood

143
Q

fusing of aquaporins

A

when ADH binds to receptors on cell membrane of DCT and CD, it activates a phosphorylase enzyme in cells. phosphorylase causes vesicles containing aquaporins to fuse with the cell membrane and the aquaporins embed.

biology (21 decks)

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