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YEAR 2 TOPICS TO STUDY > Life Science - For exam! > Flashcards

Life Science - For exam! Flashcards

0
Q

Glial Cells (Neuroglia)

A

Support communication work carried out by neurons.

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1
Q

Function of the Nervous System

A

Rapid communication system which coordinates and regulates body functions.

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2
Q

Anatomical Divisions of the Nervous System

A
  1. Central Nervous System (Brain and Spinal Cord)

2. Peripheral Nervous System (Cranial and Spinal Nerves)

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3
Q

Two Functional Divisions of the PNS

A
  1. Afferent (sensory)

2. Efferent (motor)

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4
Q

2 Divisions of the Efferent Division of the PNS

A
  1. Somatic (Voluntary)

2. Autonomic (Involuntary)

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5
Q

Functions of the Somatic Division of the PNS

A

Controls skeletal muscle contractions. Making a conscious choice to move your body.

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6
Q

Function of the Autonomic Division of the PNS

A

Subconscious control of motor functions. This includes reflexes, organs and body tissues not under conscious control (heart, etc.)

Controls the activity of smooth muscle such as the walls of airways or blood vessels, cardiac muscles and glands.

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7
Q

Functions of the Efferent Division of the PNS

A

Passes motor commands from the CNS to effector organs.

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8
Q

Functions of the Afferent Division of the PNS

A

Sends sensory data from sense organs to CNS.

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9
Q

Divisions of the Autonomic Nervous System

A
  1. Sympathetic (fight or flight)

2. Parasympatheic (resource storage and acquisition)

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10
Q

Function of Sympathetic Division of PNS

A

Responsible for mobilizing the body to deal with stressful situations. Fight or flight response. Predominates during stressful situations.

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11
Q

Function of Parasympathetic Division of PNS

A

Responsible for acquisition and storage of resources. Predominates when the body is at rest.

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12
Q

Four Anatomical Brain Parts

A
  1. Cerebrum
  2. Diencephalon
  3. Brain stem
  4. Cerebellum
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13
Q

INSERT DIAGRAM of 4 BRAIN PARTS HERE

A

here

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14
Q

The Cerebrum

A

Largest structure of the human brain.

Divided into two cerebral hemispheres which control colateral sides of the body.

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15
Q

Structure of the Cerebrum

A

Contains folds (gyri), gaps (sulci) and larger gaps (fissures).

Contains two type of brain tissue: white matter and gray matter.

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16
Q

Gyri

A

Folds found in the cerebrum.

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17
Q

Sulci

A

Large gaps of space found in the cerebrum.

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18
Q

Fissures

A

Large gaps of space between gyri in the cerebrum.

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19
Q

Composition of Gray Matter

A

Composed mainly of neuron cell bodies.

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20
Q

Composition of White Matter

A

Composed mainly of neuron axons.

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21
Q

Cerebral Cortex Anatomy

A

Layer of gray matter on the surface of the cerebral hemispheres.

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22
Q

Function of the Cerebral Cortex

A

Receives sensory information, initiates and controls voluntary movement, site of higher functions including information processing, understanding, thinking, memory and personality.

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23
Q

Basal Ganglia

A

Small areas of gray matter located deep within the cerebral hemispheres.

Involved in fine control and regulation of voluntary movement.

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24
Q

Lobes of the Cerebral Hemisphere

A
  1. Frontal
  2. Parietal
  3. Occipital
  4. Temporal
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25
Q

Functions of the Frontal Lobe of the Cerebral Hemisphere

A
  1. Motor cortex and motor planning area
  2. Associated with higher functions including integrated thought, personality, motivation and regulation of emotional behavior and mood.
  3. Functional center for aggression.
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26
Q

LOCATIoN oF LOBES OF THE cEREBRAL HEMISPHERES

A

INSERT PH(OTO HERE

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27
Q

Function of the Parietal Lobe

A

Receives sensory information from the body. Responsible for understanding speech and perception.

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28
Q

Function of the Occipital Lobe

A

Receives visual information from sensory organs.

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29
Q

Function of the Temporal Lobe

A

Receives auditory information from sensory organs.

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30
Q

Composition of the Diencephalon

A

Composed of the Thalamus and Hypothalamus.

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31
Q

Function and Anatomy of the Thalamus

A
  1. Comprises clusters of neurons.
  2. Acts as the main relay center for sensory information arriving in the brain.
  3. Begins the processing of sensory information and filters out unimportant information before routing significant signals to the cerebral cortex.
  4. Plays and important role in voluntary movement.
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32
Q

Function and Anatomy of the Hypothalamus

A
  1. Lies beneath the thalamus.
  2. Physically connected to the pituitary gland.
  3. Made up of a large number of clusters of which carry out the functions of the hypothalamus.
  4. Responsible for regulation of sleep and wake cycles, appetite, thirst, water balance, sexual behavior, body temperature.
  5. Controls the Autonomic Nervous System.
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33
Q

Structures of the Brain Stem

A
  1. Medulla Oblongata
  2. Pons
  3. Midbrain
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34
Q

Medulla Oblongata

A

An enlarged upright extension of the spinal cord.

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35
Q

Pons

A

Connects the cerebral cortex with the medulla oblongata.

It also serves as a communications and coordination center between the two hemispheres of the brain. As a part of the brainstem, the pons helps in the transferring of messages between various parts of the brain and the spinal cord.

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36
Q

Midbrain

A

Acts as a relay information system for the auditory, visual, and motor systems of the body.

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37
Q

INSERT IMAGE OF BRAIN STEM AND CEREBELLUM

A

PG 9

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39
Q

Reticular Formation

A

Small clusters (nuclei) of gray matter scattered throughout the brain stem.

The neurons of the reticular formation receive sensory input from a wide range of sources and the cerebral cortex and cardiovascular and respiratory systems.

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40
Q

Function of the Brain Stem

A

Functions as a two way conduction system. Sensory pathways conduct signals up from the spinal cord to the rest of the brain. Motor pathways conduct signals down from the brain to the spinal cord. Some nerve fibres pass through, most actually synapse in the brain stem.

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41
Q

Tissue of the Brain Stem

A

Consists mainly of white matter with small clusters of grey matter (nuclei) scattered throughout.

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42
Q

Where do most nerve signals synapse?

A

In the brain stem

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43
Q

Reticular Activating System (RAS)

A

Arouses and maintains consciousness.

Stimulation of RAS nerves maintains alertness and attention (ie. bright lights, loud noise or noxious smells arouse consciousness)

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44
Q

How do general anesthetics function?

A

By suppressing the reticular activating system (RAS).

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45
Q

How is clinical brain death established?

A

Through a lack of electrical activity in the brain stem.

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46
Q

Vital centers in the brain stem

A
  1. Cardiovascular center
  2. Respiratory Center
  3. Reflex centers
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47
Q

Cardiovascular Center of the Brain Stem

A

Controls the rate and force of contraction of the heart.

Also contained the vasomotor center which controls diameter of blood vessels.

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48
Q

Respiratory Center of the Brain Stem

A

Controls the rate and depth of breathing. Functions in association with similar nuclei in the pons.

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49
Q

Reflex Center of the Brain Stem

A

Activated by irritants to the airways or stomach which activate reflex centers in the medulla to induce coughing, vomiting, or sneezing to remove the irritant.

Swallowing and blinking reflexes are also associated with the medulla.

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50
Q

Decussation of the Pyramids

A

Motor nerve axons descending from the cortex to the spinal cord which cross over in the medulla.

This accounts for the contralateral effect of the cerebrum controlling the opposite side of the body.

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51
Q

Function of the Cerebellum

A

To coordinate voluntary movement, posture, balance and motor learning. Ensures smooth fluid body movement. It receives sensory information from voluntary muscles, eyes and ears.

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52
Q

Proprioception

A

Information received from the body enables the cerebellum to determine where the limbs are in relation to the rest of the body; the eyes and ears provide information on where the head is in space.

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53
Q

How does the cerebellum maintain posture and balance?

A

Through sensory information received through proprioception.

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54
Q

Damage to the cerebellum

A

Causes uncoordinated, clumsy movement and staggering. May also cause inability to learn new complex movement.

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55
Q

Spinal Cord

A

A column of nerve tissue carrying sensory information to the brain and motor information from the brain.

Also responsible for certain reflexes.

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56
Q

How many spinal nerves are there?

A

31 pairs of spinal nerves

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57
Q

What types of spinal nerves are there?

A 
8 pairs - cervical
12 pairs - thoracic
5 pairs - lumbar 
5 pairs - sacral
1 pair - coccygeal
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58
Q

Nerves in the spinal cord

A

Nerves enter and leave the spinal cord through spinal nerves.

Sensory nerves enter by the dorsal root.
Motor nerves leave by the ventral root.

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59
Q

Dorsal Root

A

Sensory nerves enter the spinal cord through this root.

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60
Q

Ventral root

A

Motor nerves leave the spinal cord through this root.

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61
Q

Sensory Nerve Pathway

A

Sensory information travels to the cerebral cortex by a three neuron pathway crossing over to the contralateral side of the brain.

  1. Posterior column
  2. Anterior and lateral spinothalmic tracts
  3. Spinocerebellar tract.
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62
Q

First, second, and third order neurons

A

First order - carry signal from the sense organ to the spinal cord.

Second order - relays information from the spinal cord to the thalamus.

Third order - Transmit information from the thalamus to the primary sensory cortex where the information is processed.

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63
Q

Motor Nerve Pathways

A

Motor commands travel from the cerebral cortex by direct or pyramidal pathway which involves two neurons (upper and lower motor neurons).

Decussation passes the signal to the opposite side of the body.

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64
Q

Major Motor Nerve Tracts

A

Anterior and Lateral corticospinal and corticobulbar tracts.

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65
Q

Spinal Reflexes

A

A movement which involves no command from the brain.

Function is mainly protective.

Sensory receptors send an action potential to an association or interneuron in the spinal cord which stimulates a motor neuron signaling a reflex muscle contraction.

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66
Q

Examples of spinal reflexes

A
  1. Patellar reflex
  2. Plantar flexion reflex
  3. Withdrawal reflex
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67
Q

Protection for the Central Nervous System

A

Provided by bone, meninges (protective, three layer membrane), and cerebrospinal fluid (CSF).

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68
Q

Meninges

A

A protective membrane for the central nervous system. Made up of three layers:

  1. Dura Mater (top)
  2. Arachnoid (middle)
  3. Pia Mater (bottom)
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69
Q

Cerebrospinal Fluid (CSF)

A

Found within the subarachnoid space and in the four ventricles of the brain and the central canal of the spinal cord.

Acts as a mechanical buffer (shock absorber) and controls the chemical environment of the brain; exchanging nutrients and waste products.

It is reabsorbed into the venous blood through the arachnoid villi.

70
Q

How is Cerebrospinal Fluid (CSF) produced?

A

It is filtered from the blood by a network of capillaries which project from the pia matter into the cerebral ventricles.

71
Q

What is CSF composed of?

A 
Water
Salts
Glucose
Plasma proteins
Creatinine
Urea
White blood cells
72
Q

Arachnoid villi

A

Reabsorb CSF into the venous blood.

73
Q

Identify the different parts of the neuron structure

A

INSERT PAGE 14 IMAGE HERE

74
Q

Dendrites

A

Part of the nerve cell which receives incoming signals and passes it on to the cell body.

75
Q

Cell Body

A

Contains nucleus and other organelles.

76
Q

Axon

A

Single large projection running between the cell body and to the axon terminal.

Conducts the electrical signal along it.

77
Q

Unidirectional signaling

A

Signaling by the nervous system only takes place in one direction.

78
Q

Action potential

A

Electrical impulse passed through a nerve cell.

79
Q

Resting Potential

A

Electrical imbalance of -70mV between the plasma membrane of a nerve cell. The neuron is not transmitting a signal at this point.

At resting potential the inside of the membrane is - while the outside is more +.

80
Q

Action Potential

A

A change in the potential difference across the neuronal membrane from -70mV (resting potential) to approximately 30-50mV.

This change occurs due to the movement of NA+ and K+ ions through ion channels.

81
Q

Depolarization

A

Sodium channels open and + charged sodium ions flood into the membrane making it more + charged than outside the membrane.

82
Q

Threshold potential

A

As the inside of the membrane becomes more + this is reached and the action potential will proceed at this point.

83
Q

Repolarization

A

When 30mV is reached the sodium channels close and the potassium channels open allowing + charge potassium to leave the neuron making the inside more - than the outside.

84
Q

Refractory period

A

When the neuron is resistant to further stimulation during the process of depolarization and repolarization to ensure the action potential travels in only one direction.

85
Q

Myelinated Axon

A

A protective coating on the axon (by the Schwann cell) that prevents it from touching the extracellular fluid and prevents ions from passing across it.

This results in the action potential jumping between the Nodes of Ranvier.

86
Q

Node of Ranvier

A

Axon cell membrane that is bare and exposed to extracellular fluid.

87
Q

Saltatory Conduction

A

When the action potential jumps from one Node of Ranvier to the next along the axon greatly increasing the speed of nervous transmission.

88
Q

Synapse

A

The meeting point between the end of one neuron and the beginning of another neuron, muscle or gland.

89
Q

Neurotransmitters

A

Chemicals which carry the signal from the giving to the receiving cell.

90
Q

Presynaptic Neuron

A

Neuron passing the action potential to the next cell.

91
Q

Post synaptic receptors

A

Receptors on the receiving cells that allow the neurotransmitters to bind to the postsynaptic cell and release

92
Q

Effect of a neurotransmitter binding to the receptor

A

Can have either an excitatory or inhibitory affect on the postsynaptic cell.

93
Q

What happens to neurotransmitters once they have acted?

A

They are removed from the synaptic cleft or they will continue to signal indefinitely.

The neurotransmitter is either broken down by an enzyme or transported back to the presynaptic neuron which released it.

94
Q

What does Alzheimer’s Disease physically do to the brain?

A

There is a development of plaques and tangles and significant cell death.

95
Q

Nerve death in Alzheimer’s Disease

A

Cell death is widespread throughout the brain. It mainly affects cholinergic neurons (those which release the neurotransmitter acetylcholine) of the cerebral cortex.

96
Q

Which neurotransmitter is affected in Alzheimer’s disease?

A

Acetylcholine.

97
Q

Symptoms of Alzheimer’s disease

A

STAGE 1

  1. Impaired short term memory.
  2. Disorientation
  3. Impaired cognition.
  4. Impaired concentration
  5. Fatigue
  6. Decline in spatial perception

STAGE 2

  1. Memory failure
  2. Emotional blunting
  3. Personality changes
  4. Decline in intellectual functions

STAGE 3

  1. Gross disturbance of all intellectual functions
  2. Vegetative State
  3. Death within a few years
98
Q

Therapies for Alzheimer’s Disease

A

Includes the following inhibitors of acetylcholine esterase (the enzyme that breaks down the neurotransmitter acetylcholine).

- Donepezil
- Galantamine
- Rivastigmine

As well as an agonist of glutamate receptors:
- Mematine

99
Q

What enzyme is responsible for the breakdown of acetylcholine?

A

Acetylcholine esterase.

100
Q

Acetylcholine Esterase Inhibitors for the treatment of Alzheimers

A

Used to treat mild to moderate dementia.

Prevent the breakdown of acetylcholine.

Slow the development of symptoms by slowing the decline of acetylcholine in the cerebral cortex.

Eventually symptoms will worsen as there will be very little acetylcholine produced.

101
Q

Use of Antagonist Glutamate Receptors to treat Alzheimer’s disease

A

Used for moderate to severe dementia.

Blocks the damaging effects of excess glutamate on neurons.

102
Q

Parkinson’s Disease

A

Occurs due to death of doperminergic neurons in the substantia nigra of the mid-brain.

Cause by a lack of the nuerotransmitter dopamine.

103
Q

What condition is caused by a lack of dopamine in the brain?

A

Parkinson’s Disease

104
Q

What condition is caused by a lack of acetylcholine in the brain?

A

Alzheimer’s Disease

105
Q

Treatment for Parkinson’s Disease

A

Normally treated with levodopa, a replacement for the dopamine lost in the brain.

106
Q

Generalized Anxiety Disorder (GAD)

A

Includes a number of conditions including:

  • panic disorder
  • obsessive-compulsive disorder
  • phobias

Generally affects the forebrain and the limbic system.

107
Q

Causes of Anxiety

A

Is not well understood but a chemical imbalance in the brain and genetic predisposition is possible.

108
Q

Treatment of Anxiety Disorders

A
  1. Barbiturates - can cause dependence and suicide, not used since 1960s
  2. Benzodiazepines (diazepam, lorazepam,etc) - Activate GABA receptor proteins by the neurotransmitter GABA which inhibits neurons from firing (much less likely to fire an action potential). These drugs bind to GABA receptors, inhibiting nervous transmission thus reducing anxiety and aggression. Can induce sleep, amnesia, and sedate.

Only to be used for short-term “severe” anxiety due to possible dependence and withdrawal symptoms.

  1. Buspirone - A 5-HT1a receptor agonist. Activating theses receptors on nerve terminals which inhibits the release of serotonin from the affected neurons decreasing the concentration of serotonin in the synapse.
  2. Beta-blockers - are agonists of beta-adrenoreceptors; they prevent the activation of receptors by noradrenaline and adrenaline. Not effective on psychological symptoms of anxiety but are used to treat some physical symptoms.
109
Q

Why should benzodiazepines be used only for short-term treatment of anxiety?

A

Because there is a possibility of dependence as well as withdrawal symptoms when the drug is stopped.

110
Q

Barbiturates

A

Used to treat anxiety disorders prior to 1960s

111
Q

Buspirone

A

A 5-HT1a receptor agonist used to treat anxiety.

Activating theses receptors on nerve terminals which inhibits the release of serotonin from the affected neurons decreasing the concentration of serotonin in the synapse.

112
Q

Beta-blockers

A

Used to treat anxiety, beta-blockers are agonists of beta-adrenoreceptors; they prevent the activation of receptors by noradrenaline and adrenaline. Not effective on psychological symptoms of anxiety but are used to treat some physical symptoms.

113
Q

Depression

A

May be caused by reduced levels of the neurotransmitter amine.

Severe depression is thought to be genetically linked.

114
Q

Treatment of Depression

A

Anti-depressants increase the levels of noradrenaline or serotonin or both within the brain. Treatment inhibits the re-uptake of the neurotransmitter from the synapse or by preventing the breakdown of the transmitter within the neurons.

115
Q

What condition is caused by a lack of amine in the brain?

A

Depression

116
Q

What condition is treated with noradrenaline or serotonin?

A

Depression

117
Q

What condition uses beta blockers for treatment?

A

Anxiety

118
Q

What condition uses benzodiazepines for treatment?

A

Anxiety

119
Q

What condition was treated with barbiturates in the past?

A

Anxiety

120
Q

What condition is treated with dopamine agonists?

A

Parkinson’s Disease

121
Q

What condition is treated with acetylcholine esterase inhibitors?

A

Alzheimers

122
Q

Tri-cyclic anti-depressants (TCAs)

A

Used to treat depression.

Examples:
Amitriptyline, Dosulepin, Imipramine

Block the transport proteins which remove noradrenaline and serotonin from the synapses therefore increasing the concentration of noradrenaline and serotonin at the synapse.

123
Q

SSRIs

Selective Serotonin Re-uptake Inhibitors

A

Used to treat depression.

Examples:
Fluoxetine (prozac), paroxetine, sertraline.

Block the transport proteins responsible for removing serotonin from the synapse, thereby increasing the concentration of serotonin at the synapse.

124
Q

Serotonin and Noradrenaline Re-uptake Inhibitors

A

Used to treat depression.

Examples:
Venlafaxine and Duloxetine

Block the transport proteins which remove noradrenaline and serotonin from the synapses therefore increasing the concentration of noradrenaline and serotonin at the synapse.

Fewer side effects than TCAs.

125
Q

Monoamine Oxidase Inhibitors (MAOIs)

A

Used to treat depression.

Examples:
Phenelezine, isocarboxazid, tranylcypromine, moclobemide.

Monoamine oxidase breaks down unused or recycled neurotransmitter molecules, therefore inhibiting this enzyme increases the number of neurotransmitters found at the axon terminal.

126
Q

Symptoms of Schizophrenia

A

Positive symptoms:

  • hallucinations
  • delusions
  • disorganized speech
  • bizzare behavior

Negative symptoms:

  • poverty of speech
  • blunting of emotions
  • lack of drive
  • inability to enjoy things
127
Q

Cause of Schizophrenia

A

The cause is unknown but may be caused by excessive amounts of dopamine in the brain.

128
Q

Treatment for Schizophrenia

A

Anti-psychotic drugs are dopamine receptor agonists which block the activation of dopamine receptors in the brain.

Typical (older drugs with higher side effects):

  • chlorpromazine
  • haloperidol

Atypical (new drugs with lower risk of serious side-effects)

  • clozapine
  • risperidone

These drugs generally induce apathy, reduce initiative, slow responses, inhibit aggression and make the individual drowsy.

129
Q

Side effects of Schizophrenic drugs

A
  • Involuntary movement (muscle spasm)
  • face and tongue movement
  • breast swelling, pain & lactation (both sexes)
130
Q

Multiple Sclerosis

A

An inflammatory condition in which the myelin sheaths of the axon is progressively damaged resulting in loss of sensation and motor control due to ineffective conduction of action potentials.

131
Q

Three main characteristics of MS

A
  1. Destruction of myelin
  2. Formation of lesions/plaques in the central nervous system
  3. Inflammation
132
Q

Cause of MS

A

No definitive cause has been identified but is thought to be a mix of genetic and environmental factors.

133
Q

Name the types of MS

A
  1. Relapsing MS
  2. Secondary Progressive
  3. Primary Progressive
134
Q

Relapsing MS

A

Symptoms appear and then partially or completely fade.

135
Q

Secondary Progressive MS

A

Comes after relapsing MS.

Characterized by a build up of disability.

136
Q

Primary Progressive MS

A

Symptoms continue to get worse over time rather than phases ore relapse and remittance.

137
Q

Symptoms of Multiple Sclerosis

A
  1. Muscle weakness and tightness
  2. Numbness and tingling
  3. Blurry vision
  4. Poor mobility and balance
138
Q

Treatments for MS

A
  1. Beta interferons
  2. Glatiramer acetate
  3. Tysabri
  4. Gilenya
139
Q

Beta Interferons

A

Used for the treatment of MS.

Acts to reduce inflammation causing damage to nerve fibers.

Used for relapsing-remitting and secondary progressive.

140
Q

Glatiramer acetate

A

Used for the treatment of MS.

Thought to act as a decoy to prevent immune cells from attaching.

Used for relapsing-remitting MS.

141
Q

Tysabri

A

Used for treatment of MS.

Antibody which binds immune cells and prevents them leaving the blood stream and crossing the blood-brain barrier.

Used for treating aggressive MS.

142
Q

Gilenya

A

Used for treatment of MS.

Prevents T cells (immune cells) leaving the lymph node.

Used for treating relapsing-remitting MS.

143
Q

Ischemic stroke

A

Caused by an artery occlusion.

  • atheroscleorotic build up of plaque
  • embolism arising from a thrombus elsewhere
144
Q

Transient Ischemic Attack (TIA)

A

When and ischemic blockage resolves spontaneously within a few minutes.

Neurological symptoms are present for less than 24 horus.

145
Q

Hemorrhagic Stroke

A

Caused by a rupture of a small aneurism within the brain tissue or subarachnoid space.

146
Q

Risk factors for stroke

A
  1. Hypertension
  2. Atrial fibrillation
  3. Myocardial infarction
  4. Diabetes
  5. Smoking
  6. Previous ischemic attack
147
Q

Symptoms of Stroke

A
  1. Facial weakness
  2. Arm weakness
  3. Speech problems
148
Q

Long term problems associated with stroke

A
  1. Cognitive problems
  2. Depression/emotional problems
  3. Fatigue
  4. Weakness and paralysis
  5. Visual problems
149
Q

Preventative Treatment for stroke

A
  1. Treatment of hypertension, diabetes
  2. Stop smoking (counselling)
  3. Surgery to remove arterial obstruction.
150
Q

Treatment for stroke

A

Reducing the risk of embolism through the use of anticoagulants, anti-platelet drugs, and thrombolytic drugs.

151
Q

Vasospasm

A

Complication of hemorrhagic stroke where a nearby blood vessel constricts closing the vessel completely leading to brain damage.

Nimodipine can be used to prevent this working as a vasodilator.

152
Q

Diabetes

A

Caused by insufficient or absent production of the hormone insulin by the pancreas or because the tissues are resistant to the effects.

153
Q

Insulin Function and Production

A

Insulin in produced and stored by Beta Cells within the Islets of Langerhan in the Pancreas in response to rising glucose levels in the blood.

Insulin promotes glucose absorption into the liver and muscle cells where it is converted into energy.

154
Q

Symptoms of Diabetes

A

Caused by high blood sugar.

  1. Thirst
  2. Frequent urination
  3. Increased hunger

Can also affect eyesight.

155
Q

Type 1 Diabetes

A

Caused by an autoimmune response by the body’s immune system against Beta Cells.

Beta cells are destroyed and cannot produce insulin.

Insulin must be supplied through regular injections or an insulin pump.

(Previously called insulin dependent)

156
Q

Type 2 Diabetes

A

The receptors and the liver and muscle cells for insulin no longer recognize and respond to binding insulin. The body does produce insulin, but it is not recognized.

Caused by genetic and lifestyle factors.

Managed with diet and exercise.

157
Q

Anatomy of the liver

A

Made up of 2 main lobes.

The right lobe is larger and made up of 3 smaller lobes.

Functional unit is a lobule.

Instead of capillaries the liver has sinusoids which are lined with phagocytic Kupffer cells.

158
Q

Functions of the Liver

A

Processing food.
Detoxification of waste products
Drug metabolism

159
Q

Metabolism of Alcohol by the Liver

A
  1. Alcohol is absorbed by the stomach and intestines into the blood.
  2. In the liver, the enzyme alcohol dehydrogenase (ADH) converts alcohol to acetylaldehyde.
  3. The acetylaldehyde is then broken down into acetate, then to CO2 and water.

A small portion of alcohol remains unmetabolized and remains on the breath and in the blood.

160
Q

Stages of Alcoholic Liver Disease

A
  1. Alcoholic Fatty Liver Disease
  2. Alcoholic Hepatitis
  3. Cirrhosis
161
Q

Acute Liver Damage

A

Caused by excessive drinking over a few months

162
Q

Chronic Liver Damage

A

Caused over a period of years.

163
Q

Why alcohol damages the liver?

A

It is thought that alcohol causes oxidative stress leading to cell damage, inflammation and scarring.

164
Q

Alcoholic Fatty Liver Disease

A

Excessive alcohol consumption leads to a build-up of fatty acids in the liver.

There are usually no symptoms and can be reversed within 2 weeks of sobriety.

165
Q

Alcoholic Hepatitis

A

Continual consumption leads to inflammation of the liver. This can also occur through binge drinking.

Can be reversed by ceasing alcohol consumption.

166
Q

Cirrhosis

A

Sustained inflammation leads to scarring of the liver and loss of function. This damage is non-reversible.

167
Q

Complications of Alcoholic Liver Disease

A

Portal hypertension - scarring causes blood vessels to narrow causing an increase in blood pressure in the liver. This can lead to varicose veins to bypass blocked vessels which can rupture (variceal bleeding)

Jaundice - the liver is unable to remove pigments such as billirubin.

168
Q

In what part of the brain is the reflex center found?

A

In the medulla oblongata.

169
Q

What type of neurotransmitter do benzodiapines affect?

A

GABA neurotransmitters

170
Q

Benzodiazepines

A

Used to treat anxiety disorders.

Binds to GABA receptor proteins making the receptor more sensitive to the effects of the GABA neurotransmitter and inhibiting nervous transmission (making it less likely that an action potential will fire).

171
Q

Name 2 neurotransmitters released by the autonomic nervous system.

A

Noradrenaline and acetylcholine.

172
Q

What is an aneurism?

A

A bulge in a blood vessel caused by a weakness in the vessel wall. As blood passes through the vessel it causes it to bulge like a balloon.

YEAR 2 TOPICS TO STUDY (10 decks)

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