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Human Biology ATAR > Unit 3 Human Biology > Flashcards

Unit 3 Human Biology Flashcards

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1
Q

Meninges

A

Layer of tissue between skull & brain for protection & cushioning.

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2
Q

Meningitis

A

Inflammation of meninges. Meningococcol vaccine used to prevent it.

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3
Q

Dura Mater

A

Outer layer.
Dense, irregular, fibrous tissue.
Attached to outside of cranium.
Dura extends between lobes of the brain & forms a supportive, protective partition.
Extends to base of spinal column.

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4
Q

Arachnoid Mater

A

Middle meninges.
Spider-web like collagen & elastic fibre found there.
Thin membrane that lacks blood vessels.
Thin strands extend from underside & attach to pia mater.

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5
Q

Pia Mater

A

“Gentle/little mother”
Innermost layer.
Thin, almost transparent layer.
Many nerves & blood vessels.
Closely follows the contours of the brain & spinal cord.

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6
Q

Cerebrospinal Fluid (CSF)

A

Brain & spinal cord are protected & nourished by CSF.
Mechanical protection (shock absorber).
Chemical protection (optimum chemical environment for impulse transmission & pH controls breathing).
Circulation (brings brain nutrients from blood).
Formed in ventricles of brain.

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7
Q

Ventricles

A

Where CSF is produced in brain.
Four ventricles:
Two lateral in centres of cerebral hemispheres.
One above hypothalamus & between halves of thalamus.
One located between brain stem & cerebellum.

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8
Q

Hydrocephalus

A

Too much CSF produced than what is being absorbed by the body.
Large head, headache & increased pressure.
Treatment is draining CSF - no cure.

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9
Q

Limbic System

A

Located in cerebral hemispheres & diencephalon.
Governs emotional aspects of behaviour & aids in memory - events which produce a strong emotional response are remembered better.
Damage can result in short term memory loss.
Known as the ‘emotional brain’.

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10
Q

Stroke

A

Reduced or blocked blood flow.
Haemorrhages & blood clots increase intracranial pressure.
Brain tissue dies.
Risk: high blood pressure, cholesterol, heart disease, diabetes, smoking, high alcohol intake, obesity.

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11
Q

Transient Ischemic Attack (TIA/Ministroke)

A

May last minutes.
Flow reduced & brain tissue suffers temporarily.
Blood flow reestablished after a while.

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12
Q

Alzheimers (degenerative)

A

Widespread cognitive deficits (disorientation, short attention span, short term memory loss).
Death from secondary causes (bedridden, etc).
Difficult diagnosis (loss of neurons in specific regions; abnormal proteins deposited in brain tissue; tangled nerve masses)
Damage generally limited to cerebral cortex affecting memory, sensory perception & motor movement.
Cortex decreases in size, ventricles increase.

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13
Q

Parkinson’s (Degenerative)

A

Progressive disorder of CNS.
Tremor & rigidity (continuous contraction)
Motor performance impaired by bradykinesia (slow motion) & hypokinesia (reduced range of motion).
Treatments aim to increase dopamine & decrease acetylcholine (ACh) with therapeutic drugs or experimental implantation of foetal brain cells (stem cells).

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14
Q

Cerebral Palsy (Traumatic)

A

Damage to motor areas of brain during foetal life, after birth or during infancy.
Generally due to oxygen deprivation.
Poor control & coordination of voluntary muscle movement, little/no intellectual impact.
Irreversible but not progressive.

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15
Q

Spinal Cord

A

Extension of medulla oblongata in brain.
Thin cord that passes through vertebral foremen to level of second lumbar vertebra.

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16
Q

Dorsal & Ventral Branch

A

Close to spinal cord, the mixed spinal nerve splits into a dorsal branch (root) & ventral branch.
Dorsal branch carries afferent (sensory) neurons.
Swelling of dorsal branch known as dorsal root ganglion, which contains the cell bodies of the sensory neurons.
Ventral branch carries efferent (motor) neurons.

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17
Q

Neuron Structure

A

Consists of cell body, dendrites and axon.
Neurons have several dendrites but only one axon.
One way flow of information.

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18
Q

Efferent (Motor) Neurons

A

Take impulse from CNS to effectors.
Mostly multipolar with single long axon.
Cell body in grey matter of SC.
Pass through ventral root of spinal nerves.
Dendrites synapse with connector neurons in spinal cord.
Can be somatic (voluntary) or autonomic (involuntary).

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19
Q

Afferent (Sensory) Neurons

A

Take nerve impulses from receptor to CNS.
Mostly unipolar with cell body lying to once side of axon.
Cell body in dorsal root ganglion.
Passes through dorsal root of spinal nerves.
Sensory receptors occur at end of dendrites.
Axons synapse with connector neurons in spinal cord.

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20
Q

Myelination

A

Most axons surrounded by myelin sheath.
Made of lipid & protein & acts as an insulator during conduction of electrical impulses through nerves & increases the speed at which the impulse is sent.
Made of Schwann cells in the peripheral NS which is flattened and wrapped around the axon.
Outermost layer contains cytoplasm & nucleus. Layer is called the neurolemma & aids in regrowth of damaged axons.
Gaps between Schwann cells are called nodes of ranvier/neurofibril nodes. Occur 1mm apart.
Unmyelinated axons have a thin covering of neurological plasma membrane.

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21
Q

Multiple Sclerosis

A

Disease that affects myelin sheaths of neurons in CNS.
Sheaths deteriorate & form plaques/scleroses.
Loss of sheath causes nerves to ‘short circuit,’ causing muscle weakness, loss of coordination, visual impairment & speech disturbances.
Most common in women between 20-40.
Attacks alternatively with periods of remission with improvement in symptoms.
Progressive loss of function.
May be in autoimmune response following viral infection.

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22
Q

Grey & White Matter

A

White: consists of myelinated processes of axons.
Grey: contains cell bodies, dendrite, unmyelinated axons & neuroglia.
In spinal cord, grey matter forms a central H in the cord.
In the brain, thin outer shell of grey matter forms over cerebral hemispheres.
Deep in cerebrum are areas of grey matter called nuclei.
Most nerves in the PNS & all tracts in CNS are white matter.

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23
Q

Multipolar

A

Several dendrites & one axon - neurons of CNS are mostly multipolar.

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24
Q

Unipolar

A

One process & are always sensory neurons.
Axon terminals are in CNS & cell bodies in ganglia outside CNS.
Cell body attached to side of axon.

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25
Q

Bipolar

A

One main dendrite & one axon. Usually found in special sense organs.

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26
Q

Functional Classification of Neurons

A

Sensory/afferent neurons: transmit sensory impulses, have specialised receptor ends at tips of dendrites or the dendrites are in contact with specialised receptor cells in the skin/sense organs. (Most unipolar, some bipolar)
Motor/efferent neurons: transmit motor nerve impulses from CNS to effectors. (Accelerator neurons - increase activity; inhibitory neurons - slows rate of activity).

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27
Q

Interneurons / Association Neurons

A

Multipolar neurons in CNS that form links between other neurons.

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28
Q

Regeneration of Nerve Fibres

A

At 6 months, neurons lose their ability to divide.
If cell body is injured, the cell dies.
If peripheral axon is cut, it may regenerate.
Distal portion (axon terminals) of axon & myelin sheath die, but neurolemma remains.
Proximal axon (axon hillock) develops sprouts, one of which forms into tube.
Remaining Schwann cells divide & form a regeneration tube.

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29
Q

Reflex Arc

A

Rapid, predictable, automatic response to a stimulus.
Unlearned, unpremeditated & involuntary.
One is conscious of somatic reflexes only after they occur.
Two types:
Somatic: involves contraction of skeletal muscle.
Autonomic: involves responses of smooth muscle, cardiac muscle & glands.

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30
Q

5 Components of Reflex Arc (RSIME)

A
  1. Receptor: sensory structures respond to changes in the environment.
  2. Sensory neuron: conducts an impulse from a receptor to its axon terminals.
  3. Integrating centre: some region within the CNS.
  4. Motor neuron: impulses from integrating centre to an effector.
  5. Effector: body part which responds to the motor nerve impulse (muscle or gland).
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31
Q

Neurophysiology

A

Plasma membrane has a resting membrane potential, an electric voltage difference across the membrane.
The membrane is polarised because of the separation of charges.
Ions moved in & out of the cell by active transport - Na/K pumps.

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32
Q

Passive Ion Channels (Location)

A

Found on dendrite, cell body & axon.
Passive channels are responsible for the resting membrane potential.

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33
Q

Chemically Gated Ion Channels

A

Found on dendrites & cell body.
Responsible for the synaptic potentials, the incoming signals to the neuron.

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34
Q

Voltage Gated Ion Channels (Location)

A

Found on axon hillock unmyelinated axons & nodes of Ranvier on myelinated axons.

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35
Q

Potential Difference

A

Difference in electrical charge between two points.
Represents stored energy & is measured in volts.

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36
Q

Ion Channels

A

Purpose is to send nerve impulse or action potential down cell membrane.
Flow of charged particles known as current.
Current is caused by the movement of positively charged ions rather than flow of electrons.
If membrane is polarised, it is in its resting state.

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37
Q

Nerve Transmission/Impulse

A
  • Due to different permeability to Na & K, there is a weak electrical charge across the membrane of the neuron (resting potential). Membrane is said to be polarised.
  • When the neuron is stimulated, the action of the Na & K membrane pumps are briefly interrupted. Changes to the permeability of the membrane allows Na to diffuse into the cell & K to diffuse out.
  • This reverses the electrical charge across the membrane (action potential). The cell membrane is said to be depolarised.
  • Depolarisation sweeps down the nerve fibre in a sequence of small steps - nerve impulse.
  • As soon as the nerve impulse passes, the membrane pumps are reactivated & the resting potential restored.
  • In myelinated fibres, the impulse leap-frogs from node to node, known as saltatory conduction.
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38
Q

Speed of Transmission in Neuron Cell (Factors Affecting)

A

Affected by diameter of nerve fibre (thicker = faster) & myelination (saltatory conduction in myelinated fibres = faster than continuous conduction).

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39
Q

Action Potential (Impulse)

A

A series of rapidly occurring events that decrease & reverts the polarity of the membrane.
These impulses can travel long distances without dying out.
Action potentials rely on two types of gated ion channels - Na to enter & K to leave.
When a depolarisation equals or exceeds the threshold amount, many voltage gated Na channels open & Na diffuses into the cell.
As Na rushes into the cell, the membrane potential reaches 0 & momentarily becomes positive.
These gates remain open for only a few 1/10 000 of a second, & are closed by an inactivation gate.
The same depolarisation that opened the Na channels also causes K channels to open, but they open more slowly so that they open about the same time that the Na channels are closing.
K diffuses out of the cell due to a high concentration out of the cell & high concentration inside the cell. The resting membrane potential is reestablished.
Na/K pumps pump K into the axon & Na back out to maintain the concentration gradient.

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40
Q

Na Channels

A

Have two gates - at rest, one is closed (activation gate) & the other is open (inactivation gate).
Depolarisation affects both gates.
FINISH

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41
Q

Action Potential

A
  1. Resting potential: Cell is polarised (-70mv).
  2. Threshold: Stimulus reaches the threshold potential. Stimulus strength reaches threshold limit (-55mv).
  3. Depolarisation: Na+ channels open; K+ channels close. Voltage gated Na+ channels open. Na+ flows into the cytoplasm. More voltage gated Na+ channels open (positive feedback).
  4. Repolarisation: Na+ channels close; K+ channels open. Membrane remains hyperpolarised until K+ channels close, causing the relative refractory period.
  5. Hyperpolarisation: K+ channels close slowly. Causes the mv value to exceed below -70mv, & adjusts to return to 70mv.
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42
Q

Absolute Refractory Period

A

During time between opening of Na channel activation gate & opening of the inactivation gate, a Na channel cannot be stimulated.
This is known as absolute refractory period.
A Na channel cannot be involved in another action potential until the inactivation gate has been reset.
Another action potential cannot be stimulated.

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43
Q

Relative Refractory Period

A

An action potential can be generated during hyperpolaristion which requires the second stimulus to be much stronger.
Because of the refractory period, a nerve fibre cannot be continually stimulated.
Nerve impulse conduction is an all-or-nothing response.
CNS perceives a stimulus as weak or strong based on the frequency of the action potentials in the axon.

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44
Q

Synapse

A

The junction between two neurons, or between a neuron & a muscle gland.
Nerve impulse transmission occurs because special neurotransmitter chemicals are released into the tiny gap (synaptic cleft) which separates the two nerve cells.
Acetylcholine & noradrenaline are the neurotransmitters of the PNS.

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45
Q

Synapse Process

A

Action potential occurs.
An impulse travels down an axon of a presynaptic neuron and reaches the synaptic end bulb. This opens Ca VGICs located at the end of the neuron.
Ca diffuses into the cell & through a series of reactions, causes synaptic vesicles of neurotransmitters to fuse with the cell membrane.
The neurotransmitters are released from the presynaptic neuron into the synapse via exocytosis.
Neurotransmitters diffuse across synapse & bind to receptors on the postsynaptic neuron. This causes Na CGICs to open and Na to travel into the postsynaptic neuron.

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46
Q

Neurotransmitters

A

Acetylcholine (transmits signal to skeletal muscle).
Epinephrine/adrenaline & norepinephrine (fight or flight response).
Serotonin (widespread in brain, affects mood, sleep, attention & learning).
Dopamine (widespread in brain, affects mood, sleep, attention & learning. Lack associated with Parkinson’s. Excessive amounts linked to schizophrenia).
Gasses (carbon monoxide), mood altering drugs (amphetamines, caffeine, nicotine, alcohol), hallucinogenic drugs and poisons/venoms can affect neurotransmitters and their function.

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47
Q

Homeostasis

A

The process whereby the body’s internal environment in maintained in a steady state (ie. within normal tolerance limits).
Is regulated by the nervous & endocrine systems.
Autonomic NS has control over digestion, respiration, circulation, hormone secretion, maintaining body temperature & water balance.

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48
Q

Negative Feedback Loop

A

Homeostasis is regulated & maintained by negative feedback loops (the response neutralises/reverses the original stimulus).

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49
Q

Control Mechanisms of Homeostasis

A
  1. Control centre:
    Mainly brain & other parts of the CNS.
    Sets values at which the controlled system should be maintained.
  2. Receptor:
    Monitors changes in the controlled condition & sends information to control centre.
  3. Effectors:
    Receives information from controlled centre & produces response to correct stimuli.

Stimuli → Receptor → Modulator → Transmission → Effector → Response → Feedback

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50
Q

Why is homeostasis important?

A

Maintains conditions under which cells perform most efficiently.

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51
Q

Tolerance Limits

A

The range of conditions in which the body can function.
If the condition changes beyond the tolerance limits, the body systems cannot function properly, resulting in sickness/death.
ICU provides equipment that can carry out homeostatic balance.

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52
Q

Tissue Fluid Properties/Functions

A

Regulates body temperature, blood pressure, fluid concentrations, acidity, concentration of nutrients/wastes/gasses.

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53
Q

Physical Heat Exchange Processes

A

Radiation: no direct contact, can result in heat gain or loss. Eg: sun, fire.
Convection: hot or cold air passes over a body, can result in heat gain or loss. Eg: fan.
Conduction: direct contact with heat source, can result in heat gain or loss. Eg: standing on hot sand.
Evaporation: transformation of water from its liquid state to gaseous state, results in only heat loss. Eg: steam or water vapour.

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54
Q

Feedback Loop: Temperature >37ºC

A

Stimulus: Core body temperature >37ºC.
Receptor: Thermoreceptors on skin & hypothalamus.
Modulator: Thermoregulatory centre in hypothalamus.
Transmission: ANS
Effector: Sweat glands & cutaneous arterioles.
Response: Sweating & vasodilation.
Feedback: Increased heat loss & decreased heat loss results in decreased core body temperature to set point.

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55
Q

Feedback Loop: Temperature <37ºC

A

Stimulus: Core body temperature <37ºC.
Receptor: Thermoreceptors on skin & hypothalamus.
Modulator: Thermoregulatory centre in hypothalamus.
Transmission: ANS
Effector: Cutaneous arterioles & skeletal muscles.
Response: Shivering & vasoconstriction.
Feedback: Decreased heat loss & increased heat production results in increased core body temperature to set point.

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56
Q

Thermoneutral Zone

A

The temperature range bounded by the lower critical temperature (point where shivering starts) and upper critical temperature (point where sweating starts).

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57
Q

Increasing Heat Production

A

Increased metabolic activity (more muscular work) increases heat production.
Shivering reflex involves groups of antagonistic muscles surrounding vital organs being stimulated simultaneously which results in shaking (shivering), increasing heat production.
The hormones adrenaline & thyroxine increase the metabolic rate & thus heat production.

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58
Q

Reducing Heat Loss

A

Loss of heat can be reduced by vasoconstriction of the cutaneous arterioles (blood vessels) & piloereaction (arrector pili muscles contract, increasing thickness of ‘dead air’ around the body).

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59
Q

Increasing Heat Loss

A

Above TNZ, the body produces more heat into the environment through sweating, vasodilation.
Thyroxine used to increase or decrease heat loss.
Sweat glands secrete sweat which is carried out by sweat ducts onto the skin surface, and evaporated.

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60
Q

Voluntary Responses (Heat Change)

A

Response to heat change - clothes on/off, hot/cold food consumption, exercise, etc.

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61
Q

Kidney Function

A

Fluid/salt balance, removal of wastes (urea), pH balance.

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62
Q

Fluid Circulation

A

Substances enter & leave the blood stream via the permeability capillaries.
At the arterial end of a capillary there is a mass flow of plasma & nutrients from the bloodstream into the tissue fluid.
This occurs because the blood pressure is greater than the osmotic pressure (working in the opposite direction).
As the blood is forced through the capillary the blood pressure drops.
At the venous end of a capillary there is a mass flow of tissue fluid & wastes from the tissues into the bloodstream.
This occurs because the blood pressure is now less than the osmotic pressure.
Around 55% of body fluids is water, 45% organic & inorganic components.
Of bodily fluids, 55% is intracellular fluid, 8% is plasma, 36% is tissue fluid & 1% is extracellular fluids.

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63
Q

Urine Formation

A

Filtration (renal corpuscle), selective reabsorption (PCT, Loop of Henle, DCT & collecting duct), tubular secretion (PCT & DCT).

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64
Q

Filtration

A

Structure: renal corpuscle.
Substance: water, urea, glucose, amino acids, vitamins, salts (Na, Cl).
Transport: passive.

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65
Q

Selective Reabsorption

A

Structure: PCT/LoH/DCT/CD.
Substance: water, salts, glucose, w amino acids, vitamins/water, Na, Cl/water, Na, Cl/water
Transport: osmosis & active/osmosis & active/osmosis & active/passive.

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66
Q

Tubular Secretion

A

Structure: PCT & DCT.
Substance: H+, NH4+, creatinine, toxins, drugs, neurotransmitters.
Transport: active.

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67
Q

Selective Water Reabsorption

A

Can be divided into two phases:
1. Reabsorption of salt under influence of aldosterone.
2. Reabsorption of water under influence of ADH, targeting ascending limb & DCT.

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68
Q

Feedback Loop: Reabsorption of Salt / Decreased Blood Pressure

A

Stimulus: decreased blood volume (decreased blood pressure).
Receptor: baroreceptors in renal artery.
Modulator: hypothalamus.
Transmission: stimulates AP to secrete ACTH to stimulate adrenal cortex to secrete aldosterone.
Effector: Na pumps in LH to the DCT of the nephron.
Response: Na reabsorbed.
Feedback: Creating osmotic gradient & water diffuses back into the blood.

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69
Q

Feedback Loop: Influence of ADH

A

Stimulus: decreased blood volume, reduced blood pressure, increased osmotic pressure.
Receptor: osmoreceptors in hypothalamus.
Modulator: hypothalamus/trigger thirst reflex (→ feedback).
Transmission: nerve signals to posterior pituitary gland, ADH secreted into bloodstream.
Effector: DCT & collecting duct of nephron.
Response: increases permeability of DCT & collecting duct.
Feedback: water reabsorbed, osmotic pressure maintained or reduced, decrease in urine production.

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70
Q

Glucose Concentration

A

Normal: 80-120 mg/100cm^-3.
Below 60 = coma.
Above 180 = exceeds renal threshold & glucose appears in urine.

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71
Q

Carbohydrate Metabolism

A

Glycogenesis
- Glucose absorbed across membrane by facilitated diffusion.
- Glucose stored as glycogen.
Glycogenolysis
- Glycogen broken down to glucose.
- Glucose diffuses out of cell through protein carriers.

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72
Q

Glucose Storage (Decreasing Blood Glucose)

A

Glucose concentration in blood increases.
Beta cells in pancreas release insulin.
Insulin stimulates liver cells to store glucose as glycogen.
Insulin stimulates lipid synthesis.
Insulin helps to conserve resources.

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73
Q

Energy/Glycogen Storage

A

Glycogen storage: glucose polymer in liver & muscle cells.
If glycogen stores are full & caloric intake still exceeds caloric expenditure, excess stored as fat - synthesis pathway.

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74
Q

Insulin

A

Decreases blood glucose level.
If glucose rises above set point, pancreas secretes insulin.
Promotes transport of glucose into cells & storage of glucose as glycogen in liver & muscle cells.

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75
Q

Glucagon

A

Increases blood glucose levels.
When glucose levels drop below set point, pancreas secretes glucagon.
Promotes breakdown of glycogen & releases glucose into the blood.

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76
Q

Adrenaline

A

Increases blood glucose levels.
Promotes breakdown of glycogen in the liver (glycogenolysis) & release of glucose into blood.
Promotes production of glucose in the liver (gluconeogenesis) & release of glucose into the blood.
Raises blood glucose levels.

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77
Q

Cortisol

A

Increases blood glucose level.
Increases resistance of fat & muscle cells to insulin.
Promotes breakdown of glycogen in the liver (glycogenolysis) & release of glucose into the blood.
Promotes production of glucose in the liver (gluconeogenesis) & release of glucose into the blood.
Raises the blood glucose levels.

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78
Q

Feedback Loop: Rising Blood Glucose

A

Stimulus: rising blood glucose level.
Receptor: chemoreceptors in pancreas, islets of langerhans, beta cells.
Modulator: islets of langerhans, beta cells, production of insulin.
Transmission: insulin secreted into the blood.
Effector: somatic cells & liver.
Response: somatic cells take up more glucose/more permeable, liver takes up more glucose & stores it as glycogen (glycogenesis).
Feedback: blood glucose levels decrease to set point, insulin release diminishes.

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79
Q

Feedback Loop: Decreased Blood Glucose

A

Stimulus: decreased blood glucose levels.
Receptor: chemoreceptors in pancreas, islets of langerhans, alpha cells.
Modulator: islets of langerhans, alpha cells producing glucagon.
Transmission: glucagon secreted into blood.
Effector: liver.
Response: liver breaks down glycogen & releases glucose into the blood (glycogenolysis).
- adrenal medulla releases adrenaline/noradrenaline for glycogenolysis/breakdown of glycogen into glucose.
- adrenal cortex releases cortisol for glycogenolysis.
- cortisol also triggers removal of amino acids from muscle cells, sending them to liver to be converted to glucose (gluconeogenesis).
- lipolysis also helps aid with gluconeogenesis.
Feedback: blood glucose level rises to set point, glucagon release diminishes.

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80
Q

Blood Pressure

A

Pressure of the circulating blood against walls of blood vessel.
Pressure is highest when the ventricles in heart contract (systole) and lowest when they relax (diastole).
Adult BP is normal at around 120/80.

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81
Q

Sinoatrial Node

A

Heart contains conductive tissue which regulates heart beat.
SA node/pacemaker is a cluster of specialised cardiac cells in the wall of the right atrium which initiates the heart beat.
The atrioventricular node (AV node) is the secondary pacemaker which regulates the beating of the ventricles.

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82
Q

Cardiac Output

A

Total volume of blood being pumped out of the heart over a particular period of time.
Affected by stroke volume & heart rate.
CA = stroke volume x heart rate

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83
Q

Factors affecting Stroke Volume

A

Venous return (F-S Law)
Autonomic NS (sympathetic stimulation increases stroke volume)
Hormones (thyroxine, adrenaline/noradrenaline, glucagon)
Ca & K levels

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84
Q

Frank-Sterling Law of the Heart

A

Greater volume of blood entering the heart during diastole, the greater volume of blood ejected during systolic contraction (stroke volume).

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85
Q

Feedback Loop: Increased Heart Rate/Blood Pressure

A

Stimulus: blood pressure/heart rate increases.
Receptor: baroreceptors in right atrium, aorta & carotid artery.
Modulator: cardiac centre in medulla oblongata.
Transmission: vagus nerve.
Effector: heart (SA node).
Response: parasympathetic stimulation slows down heart rate.
Feedback: decreased blood pressure to set point

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86
Q

Feedback Loop: Decreased Heart Rate/Blood Pressure

A

Stimulus: blood pressure/heart rate decreases.
Receptor: baroreceptors in right atrium, aorta & carotid artery.
Modulator: cardiac centre in medulla oblongata.
Transmission: cardiac nerve.
Effector: heart (SA node).
Response: sympathetic stimulation speeds up heart rate.
Feedback: blood pressure/heart rate increases.

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87
Q

Control of Breathing

A

Can be voluntary or involuntary.
Control centres occur in brain stem:
- Medullary rhythmicity centre (normal breathing).
- Apneustic centre (rate of breathing).
- Pneumotaxic centre (depth of breathing).
Nerve impulses activate respiratory muscles:
- Diphragm
- Intercostal muscles (internal & external).

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88
Q

Respiratory Cycle

A

Quiet breathing:
- Inhalation (active)
- Exhalation (passive)
→ Diaphragmatic (deep breathing)
→ Costal (shallow breathing)
Forced breathing:
- Inhalation & exhalation (active)

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89
Q

Regulation of Normal Breathing Cycle

A

Quiet Breathing:
- Inspiration (2 sec)
- Inspiratory nucleus activated.
- Nerve impulses sent to respiratory muscles.
- Respiratory muscles contract.
- Exhalation (3 sec)
- Inspiration nucleus suppressed.
- Respiratory muscles relax.

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90
Q

Regulation of Forced Breathing

A
  • Inspiration
    • Inspiratory nucleus activated/expiration nucleus suppressed.
    • Nerve impulses sent to respiratory muscles.
    • Inspiratory muscles contract/expiration muscles relax.
  • Expiration
    • Expiratory nucleus activated/Inspiratory nucleus suppressed.
    • Nerve impulses sent to respiratory muscles.
    • Expiratory muscles contract/inspiratory muscles relax.
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91
Q

Respiratory Reflexes

A

Normal breathing modified by:
- Changes in levels of oxygen & carbon dioxide.
- Changes in blood pressure.
- Stretch receptors in lungs.
- Irritants (sneezing, coughing, etc).
- Sensations (such as cold, pain, etc).
Basic rhythm of ventilation controlled by medullary rhythmicity area (medulla oblongata).
Inspiratory area (dorsal resp. group).
- Determines basic rhythm of breathing.
- Causes contraction of diaphragm & external intercostals.
Expiratory area (ventral resp. group)
- Inactive during normal quiet breathing.
- Activates the inspiratory area during forceful breathing.
- Causes contraction of internal intercostals & abdominal muscles.

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92
Q

Feedback Loop: Breathing/Low & High CO2

A

Stimulus: high CO2 (low pH or high H+) or Low O2
Receptor: chemoreceptors in the aorta (high CO2 or low O2), carotid artery (high CO2 or low O2) and medulla oblongata (high CO2 only).
Modulator: respiratory centers in brain stem (medulla oblongata and pons).
Transmission: reflexes involving somatic nerves.
Effector: respiratory muscles (diaphragm and intercostal muscles).
Response: increase rate and depth of breathing.
Feedback: levels of CO2 decrease and O2 increase return to normal.

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93
Q

Steady State Control Mechanisms

A

Sweating, shivering, vasoconstriction, vasodilation: body temperature.
Breathing rate: oxygen & carbon dioxide levels, pH.
Cardiac output: most homeostatic functions.
Kidney function: fluid balance, pH, getting rid of wastes.

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94
Q

Diabetes

A

A disease characterised by abnormally high levels of blood glucose.
Results in the body’s inability to produce sufficient insulin to maintain blood sugar level in homeostatic balance.

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95
Q

Insulin

A

Hormone that lowers blood glucose.

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96
Q

Glucagon

A

Hormone that raises blood glucose level.

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97
Q

Glucose

A

Simple carbohydrate (basic carbohydrate building block).

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98
Q

Glycogen

A

Complex carbohydrate (stored in liver & muscles).

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99
Q

Glycogenesis

A

Formation of glycogen from glucose, or from breaking down lipids/proteins.

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100
Q

Glycogenolysis

A

Breakdown of glycogen to glucose.

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101
Q

Lipogenesis

A

Formation of fats from carbohydrates.

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102
Q

Glycaemia

A

Blood glucose level.

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103
Q

Feedback Loop: Low Blood Sugar

A

Stimulus: blood glucose below threshold (<90mg/dl).
Receptor: α-cells of Islets of Langerhans (pancreas)
Modulator: α-cells secrete glucagon.
Transmission: glucagon secreted into bloodstream.
Effector: skeletal muscles, liver & fat.
Response: liver & skeletal muscles - glycogen converted to glucose. Fat - increases fat mobility.

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104
Q

Feedback Loop: High Blood Glucose

A

Stimulus: blood glucose above threshold (>90mg/dl)
Receptor: β-cells in Islets of Langerhans (pancreas).
Modulator: insulin secreted from β-cells.
Transmission: insulin secreted into bloodstream.
Effectors: somatic cells & liver.
Response: somatic cells become more permeable to glucose; liver - converts glucose to glycogen.

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105
Q

Type 1 Diabetes

A

Body produces no/too little insulin.
Treated with regular insulin injections.
Early onset.

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106
Q

Type 2 Diabetes

A

Late onset - generally occurs after 30.
Body’s cells become resistant to insulin and/or too little insulin produced.
Treated by dietary control, regular exercise, medication such as insulin injection can be used.
Life threatening if left untreated.

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107
Q

Diabetes Symptoms

A

Excessively thirsty.
Passing more urine.
Feeling tired & lethargic.
Always feeling hungry.
Having cuts that heal slowly.
Itching, skin infections.
Blurred vision.
Weight change (T1 - loss, T2 - gain).

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108
Q

Diabetes - If Homeostasis is not Restored

A

Blindness
Kidney failure
Cardiovascular disease
Loss of sensation
Ulcers & gangrene sometimes requiring amputation of toes or foot.

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109
Q

Ketoacidosis

A

People with T1 diabetes cannot use glucose as an energy source so their body burns fat & proteins instead.
Toxic compounds called ketones are a byproduct.
If ketones accumulate in the body a life threatening condition known as ketoacidosis can occur.
If it remains untreated, it results in total homeostatic disruption, followed by coma or death.

110
Q

Hyperthermia

A

Failure of the body’s homeostatic mechanisms to control body temperature within the TNZ.
Failure to lower the temperature results in heat stroke & ultimately death.

111
Q

Heat Exhaustion

A

At temperatures between 38-40ºC people sweat, become flushed & feel increasingly uncomfortable. Their heart rate increases & they may experience nausea, headache & may feel dizzy, become confused or faint.
Heat exhaustion is treated by resting in a cool area & drinking water.

112
Q

Heat Stroke

A

At temperatures above 41ºC people experience heat stroke.
The heart rate becomes very fast, sweating stops & the skin becomes dry & hot.
Beyond this point, it is difficult for the body to maintain homeostatic balance & the temperature rises rapidly.
Above 42ºC people are likely to lapse into a coma & will die if their temperature rises above 43-44ºC.

113
Q

Renal Failure

A

When kidneys stop working, homeostatic disruption is so widespread that the person may die unless they receive urgent medical treatment.

114
Q

Causes of Renal Failure

A

Acute (sudden): resulting from causes such as toxic drugs, blockage or injury.
Chronic (gradual): resulting from problems such as diabetes, cancer, high blood pressure or polycystic kidney disease.

115
Q

Consequences of Renal Failure

A

In both acute & chronic renal failure, urine production is disrupted. Water, salts & metabolic wastes are retained in the body.
This causes widespread homeostatic problems which affect almost every system of the body.
The most common cause of death is cardiovascular disease.

116
Q

Treatment for Renal Failure

A

In many instances, there is no cure for renal failure.
Many people with renal failure have to undergo regular haemodialysis treatment to purify their blood (conventionally three times a week).
Sometimes a kidney transplant is an option.

117
Q

Haemodialysis

A

Blood is removed from an artery, toxic substances, metabolic wastes & excess fluid are removed & then the blood is returned to the body.

118
Q

Kidney Transplant

A

People with renal failure can receive a kidney transplant if a matching donor kidney is available.
The transplanted kidney is lower in the pelvis & attached to the common iliac artery & vein.

119
Q

Menopause

A

When the ovaries stop working, oestrogen is no longer produced.
Menopause is the permanent cessation of menstruation generally occurring between the ages of 40-60. Average age is 51 years old.
Results from declining oestrogen levels & can cause vaginal dryness, hot flashes, headaches & joint pain.
Menopausal women may see an increase in risk of heart disease & osteoporosis.
Hormone replacement therapy (HRT) has long been prescribed to reduce menopausal symptoms & risk of heart disease & osteoporosis.
Recent findings suggest the HRT may increase risk of breast cancer, stroke, heart attack & blood clots.
Body becomes more sensitive to changes in core body temperature.

120
Q

Consequences of Oestrogen Loss

A

→ Early symptoms:
Hot flashes
Insomnia
Irritability
Mood disturbances
→ Physical changes (intermediate):
Vaginal atrophy
Stress (urinary) incontinence
Skin atrophy
→ Disease (late):
Osteoporosis
Cardiovascular disease
Dementia (alzheimer’s disease)
Cancers

121
Q

Osteoporosis

A

Oestrogen deficiency
Peak bone mass at 30-35 years old.
Bone loss at a rate of 0.5-1% per year afterwards.
Bone loss at a rate of 2-3% per year for 10 years after menopause.
Osteoporosis is associated with fracture (femoral neck, vertebral body & distal radius).

122
Q

Preventing Osteoporosis

A

Change lifestyle risk factors
Exercise
Adequate calcium/ Vitamin D intake
Hormone replacement therapy (HRT)
Alendronate
Raloxifene

123
Q

Cardiovascular Disease

A

Rapid increase in mortality & morbidity from cardiovascular disease after menopause.
Epidemiological evidence suggests that HRT is associated with 50% reduction in cardiovascular risk in menopausal women.
There is no prospective randomised data to show that HRT is effective in the primary prevention of cardiovascular disease.

124
Q

Preventing Cardiovascular Disease

A

Healthy lifestyle
Diet
Avoid smoking
Control of hypertension, diabetic & hyperlipidanaemia
HRT (not effective for secondary prevention)

125
Q

Lymphatic System

A

Comprised of lymph, lymph nodes, lymph vessels, the spleen, tonsils & thymus.
Plays a vital role in protecting the body from pathogens & cancer cells, & removing debris (eg. old blood cells) from the circulation.

126
Q

Elephantiasis

A

A disease found often in tropical countries in which a small roundworm blocks lymphatic vessels, usually in the legs or scrotum.

127
Q

Three Lines of Defence

A

First (external)
Second (internal)
Third (specific, slower response to specific microbes)

128
Q

First Line of Defence

A

Skin, mucous membranes, secretions of skin.
Eg. HCl in stomach, vomiting.

129
Q

Second Line of Defence

A

Phagocytic WBCs, antimicrobial proteins, inflammatory response, natural killer cells.

130
Q

Third Line of Defence

A

Specific/acquired defence mechanisms.
Slower response to specific microbes.
Cytotoxic lymphocytes (cell-mediated response), antibodies (humoral response).

131
Q

Innate Immunity

A

Present before any exposure to pathogens & is effective from the time of birth.
Involves non specific responses to pathogens.

132
Q

External Defences

A

Intact skin & mucous membranes form physical barriers that bar the entry of microorganisms & viruses.
Certain cells of the mucous membranes produce a mucus - a viscous fluid that traps microbes & other particles.

133
Q

Phagocytosis

A

If cells are under attack, they release histamine.
Histamine plus chemicals from pathogens mean neutrophils are attracted to the site of attack.
Pathogens are attached to antibodies & neutrophils have antibody receptors.
Endocytosis of neutrophil membrane → phagocytic vacuole.
Lysosomes attach to phagocytic vacuole → pathogen digested by proteases.

134
Q

Phagocytic Cells

A

Phagocytes attach to their pray via surface receptors & engulfs them, forming a vacuole that fuses with a lysosome.

135
Q

Neutrophils

A

60% of WBCs.
Patrol tissues as they squeeze out of the capillaries.
Large numbers are released during infections.
Travel through capillaries & consume any pathogen.
Short lived - die after digesting bacteria.
Dead neutrophils make up a large proportion of pus.

136
Q

Macrophages

A

Are a specific type of phagocyte - can be found migrating through the body or in various organs of the lymphatic system, not the blood.
Larger than neutrophils.
Made in bone marrow as monocytes, called macrophages once they reach organs.
Long lived - can consume many more pathogens before dying.
Initiate immune responses as they display antigens from the pathogens to the lymphocytes.

137
Q

Natural Killer Cells

A

Patrol the body & attack virus-infected body cells & cancer cells.
Trigger apoptosis in the cells they attack.

138
Q

Effects of Inflammation

A

Increased blood flow results in increased local temperature & local cellular metabolism.
Increased capillary permeability & phagocytic migration to the injured tissue.

139
Q

Inflammatory Response

A

Mast cells release histamine & heparin.
Histamine increases blood flow to area/walls of capillaries, making them become more permeable.
Heparin prevents clotting in immediate area/clot forms around damaged area to prevent spread.
Chemicals released by mast cells attract phagocytes, consume debris.
Abnormal conditions stimulate pain receptors.
Phagocytes filled with bacteria die to form pus.
New cells produced by mitosis repair damaged tissue.

140
Q

Fever

A

Upon infection, the inflammatory response brings white blood cells to the area.
White blood cells release pyrogens which stimulate the hypothalamus to raise the body’s core temperature.
It sets the thermoregulatory centre higher which causes muscles to shiver to produce more heat & vessels to vasoconstrict to reduce heat loss.
A high body temperature can inhibit the growth of (some) bacteria (& viruses).
Some prefer warmer temperatures.

141
Q

Swollen Lymph Nodes

A

Lymph fluid containing the bacteria enter the lymph nodes & pass through a mesh work of fibres/lymphoid tissue which traps/captures the bacteria.
Then the macrophages in the lymph nodes ingest the bacteria by phagocytosis.
Once the pathogen is gone, the thermoregulatory centre is reset to 37ºC & body temperature is lowered by vasodilation & sweating.

142
Q

Acquired Immunity

A

Develops only after exposure to inducing agents such as microbes, toxins or other foreign substances.
Involves a very specific response to pathogens.
Is the body’s second major kind of defence involving the activity of lymphocytes.

143
Q

Specific Immunity

A

Protects the body against specific substances (antigens).
There are two types of SI: cellular immunity & antibody mediated (humoral) immunity.
Specific immunity is acquired through natural infection or immunisation.

144
Q

Antigen

A

Any foreign molecule that is specifically recognised by lymphocytes & elicits a response from them.

145
Q

Antibody

A

A globular protein that is produced by B lymphocytes (plasma cells) & interact with specific antigens.

146
Q

Lymphocytes

A

Recognises & binds to just a small, accessible portion of the antigen.

147
Q

Epitopes

A

Antigenic determinants where antibodies bind to the antigen.

148
Q

B & T Cells

A

Both types are produced in bone marrow from stem cells.
Newly formed lymphocytes are all alike, but they later develop into B or T cells, depending on where they continue their maturation.
B lymphocytes are ‘educated’ (acquire immunological competence) in bone marrow.
Umbrella term - can differentiate into different types (such as plasma).
T lymphocytes are ‘educated’ in the thymus.

149
Q

Thymus

A

A mass of glandular tissue located in the upper chest, under the breastbone.
The thymus is most active during puberty, but atrophies (decreases in size) in adults.

150
Q

Branches of Acquired Immunity

A

Humoral immune response involves the activation & clonal selection of B cells, resulting in the production of secreted antibodies.
The cell-mediated immune response involves the activation & clonal selection of killer T cells.
Both happen at the same time.

151
Q

Major Histocompatibility Complex (MHC)

A

A group of genes that are unique to each individual.
Code for small protein molecules that act as ‘self’ markers on all body cells.
MHC molecules initiate the immune response by presenting antigen fragments to T cells.

152
Q

Antigen Presenting Cells

A

A cell that presents antigens.
Two types of MHC classes:
- Class I MHC - self & non-self antigen found on all cells.
- Class II MHC - antigen presenting cells (APCs).
APCs engulf pathogens & display the antigen on their cell membranes (on their class II MHC)
From there it will initiate acquired immunity.

153
Q

APC Exposure (4-Step Process)

A
  1. Pathogen ingested by APC.
  2. Pathogen digested by APC.
  3. Antigen presented on MHC complex.
  4. T cell with complimentary antigen receptor site attaches.
154
Q

T Cell Receptors for Antigens & Role of MHCs

A

A fragment of foreign protein (antigen) inside the cell associates with an MHC molecule & is transported to the cell surface.
The combination of MHC molecule & antigen is recognised by a T cell, altering it to the infection.

155
Q

Humoral Immunity

A

Antigens on foreign cells, such as bacteria, are recognised by receptors on specific B cells.
The antigen is digested by an APC. Antigen fragments are displayed on the cell surface (on the class II MHC).
Helper T cells with matching receptors become activated when they lock onto the antigen fragment.
The activated helper T cell secretes cytokines - messenger proteins that regulate the immune system.
Cytokines stimulate the B cell to divide, producing number of plasma cells & memory B cells.
The plasma cells secrete antibodies into circulation.
Memory B cells help undergo clonal selection faster when there is a second exposure to the pathogen.

156
Q

Clonal Selection of Lymphocytes

A

In a primary immune response, binding of antigens to a mature lymphocyte induces the lymphocytes division & differentiation, a process called clonal selection.
1. After a macrophage engulfs & degrades a bacterium, it displays an antigen complex with a class II MHC module. A helper T cell that recognises the displayed complex is activated with the aid of cytokines secreted from the macrophage, forming a clone of the activated helper T cells.
2. A B cell that has taken up & degraded the same bacterium displays class II MHC-antigen complexes. An activated helper T cell bearing receptors specific for the displayed antigen binds to the B cell. This interaction, with the aid of cytokines from the T cell, activates the B cell.
3. The activated B cell proliferates & differentiates into memory B cells & antibody-secreting plasma cells. The secreted antibodies are specific for the same bacterial antigen that initiated the response.

157
Q

Antibody Mediated Immunity

A
  1. Pathogen displaying antigens.
  2. Antigen recognised by compatible antibody.
  3. B cell digests antigen & displays antigen fragments.
  4. T helper cell recognises antigen.
  5. Activated T helper cell releases cytokines.
  6. Cytokines cause B cell to mature into plasma cell.
  7. Plasma cell secretes antibody.
158
Q

B Cells: Response to Extracellular Pathogens

A

Activation of B cells is aided by cytokines & antigen binding helper T cells.
The clonal selection of B cells generates antibody-secreting plasma cells.

159
Q

Antibody-Mediated Disposal of Antigens

A

The binding of antigens is also the basis of several antigen disposal mechanisms.
Leads to elimination of microbes by phagocytosis & complement-mediated lysis.

160
Q

Agglutination

A

When antibodies come into contact with target antigens they lock onto them.
This causes the antigen-bearing cells (often pathogens) to bind together (agglutinate), thus rendering them harmless.

161
Q

PLAN BCDE

A

Precipitate - make soluble substances insoluble.
Lysis - make pathogen membranes more permeable.
Agglutination - antigen-bearing cells bind together.
Neutralisation - combines with foreign bacterial toxins.
Binding - to surface of viruses & prevent them from entering cells.
Coating bacteria
Dissolve organisms
Enhance phagocytosis

162
Q

Primary & Secondary Response

A

Primary response takes about two weeks to peak & antibody levels do not remain high.
During the secondary response, antibody levels rise faster, reach higher concentrations & remain elevated for an extended period.

163
Q

Cell Mediated Immunity

A

A ‘sick’ cell is ingested by an antigen presenting cell (macrophage or dendritic cell).
Antigen fragments bound to MHC molecules are displayed on the surface of APCs.
Compatible helper T cells lock onto antigen MHC complex & secrete cytokines.
The activated helper T cells secrete cytokines (messenger proteins that regulate the immune system).
Cytokines stimulate the T cell to divide, producing numerous killer T cells, more helper T cells, suppressor T cells & memory cells.
The killer T cells kill any infected cells via apoptosis.
Memory T cells help undergo clonal selection faster when there is a second exposure to the pathogen.

164
Q

Cytokines

A

Stimulate T cells to divide & differentiate into killer cells, helper & memory cells.

165
Q

Killer Cells (Cytotoxic T Cells):

A

Destroy body cells infected by viruses or transformed by cancer.

166
Q

Suppressor T cells

A

Slows down the immune response.

167
Q

Helper T Cells

A

Perform many immune functions. They are essential in activating cytotoxic T & B cells.

168
Q

Memory Cells

A

Remain in the body & enable the immune system to react rapidly should it encounter those same antigens again.

169
Q

Cellular Immunity

A
  1. Pathogen ingested by macrophage or dendritic cell.
  2. Pathogen digested & fragments presented to T cells.
  3. Helper T cells secrete cytokines.
  4. Cytokines activate B pathway
  5. Cytokines stimulate killer T cells to divide.
  6. Killer T cells hunt & destroy infected cells.
170
Q

Helper T Cells: Response to Most Antigens

A

Helper T cells produce CD4, a surface protein that enhances their binding to class II MHC molecule-antigen complexes on antigen-presenting cells.
Activation of the helper T cell then occurs.
Activated helper T cells secrete several different cytokines that stimulate other lymphocytes.

171
Q

Role of Helper T Cells

A
  1. After a dendritic cell engulfs & degrades a bacterium, it displays bacterial antigen fragment (peptides) complexes with a class II MHC molecule on the cell surface. A specific helper T cell binds to the displayed complex via its TCR with the aid of CD4. This interaction promotes secretion of cytokines by the dendritic cell.
  2. Proliferation of the T cell, stimulated by cytokines from both the dendritic cell & the T cell itself, gives rise to a clone of activated helper T cells (not shown), all with receptors for the same MHC-antigen complex.
  3. The cells in this clone secrete other cytokines that help activate B cells & cytotoxic T cells.
172
Q

Killer/Cytotoxic T Cells

A

Make a surface protein that enhances the interaction between a target cell & a cytotoxic T cell.
Bind to infected cells, cancer cells & transplanted tissues.
Activates a cytotoxic T cell & differentiates it into an active cell.
The activated cytotoxic T cells secretes proteins that destroy the infected target cells:
1. A cytotoxic T cell binds to a class I MHC antigen complex on a target cell. This interaction, along with cytokines from helper T cells, leads to the activation of the cytotoxic cell.
2. The activated T cell releases performing molecules, which form pores in the target cell membrane, & proteolytic enzymes, which enter the target cell by endocytosis.
3. The enzymes initiate apoptosis within the target cells, leading to fragmentation of the nucleus, release of small apoptosis bodies, & eventual cell death. The released cytotoxic T cell can attack other target cells.

173
Q

Active Immunity

A

Develops naturally in response to an infection.
Can also develop following immunisation, also called vaccination.
In immunisation, a non pathogenic form of a microbe or part of a microbe elicits an immune response to an immunological memory for that microbe.

174
Q

Passive Immunity

A

Provides immediate, short term protection.
Is conferred naturally when IgG crosses the placenta from mother to foetus or when IgA passes from mother to infant through breast milk.
Can be conferred artificially by injecting antibodies into a non-immune person.

175
Q

Vaccine (Artificial Immunity)

A

A preparation made of weakened or dead pathogenic cells injected into the body in order to stimulate the production of antibodies.

176
Q

Dead Vaccines

A

Contains killed microorganisms (using chemicals or heat).
Eg: vaccines against flu, cholera & hepatitis A.

177
Q

Attenuated Vaccines

A

Use live microorganisms that have been disabled or closely related organisms that are less dangerous.
Attenuated vaccines generally produce a more durable immunological response but are less stable than dead vaccines.
Eg: vaccines against measles, rubella & mumps.

178
Q

Tissue & Organ Transplants

A

MHC molecules are responsible for stimulating the rejection of tissue grafts & organ transplants.
The changes of successful transplantation are increased:
If the donor & recipient MHC tissue types are well matched.
If the recipient is given immunosuppressive drugs.
Lymphocytes in bone marrow transplants may cause a graft versus host reaction in recipients.
The immune system can wage war against cells from other individuals.
Transplanted tissues are usually destroyed by the recipient’s immune system.
Drugs are given that suppress the immune response to reduce the risk of graft versus host reaction.

179
Q

Immune Dysfunction

A

Exaggerated, self-directed or diminished immune responses can cause disease.
If the delicate balance of the immune system is disrupted, the effects on the individual can range from minor to often fatal consequences.

180
Q

Allergies

A

Exaggerated (hypersensitive) responses to certain antigens called allergens.
These include pollen, skin cells (dander), dust mites, peanuts, eggs.
In localised allergies such as hay fever, IgE antibodies produced after first exposure to an allergen attach to receptors on mast cells.
The next time the allergen enters the body it binds to the mast cell - associated IgE molecules.
The mast cells then release histamine & other chemicals that cause vascular changes & typical symptoms.

181
Q

The Allergic Response

A
  1. IgE antibodies produced in response to initial exposure to an allergic bond to receptors or mast cells.
  2. On subsequent exposure to the same allergen, IgE molecules attached to a mast cell recognise & bind to the allergen.
  3. Degranulation of the cell, triggered by cross-linking of adjacent IgE molecules, releases histamine & other chemicals, leading to allergy symptoms.
    - An acute allergic response sometimes leads to anaphylactic shock.
    - A whole-body, life-threatening reaction can occur within seconds of exposure to an allergen.
182
Q

Autoimmune Diseases

A

The immune system loses tolerance for self & turns against certain molecules of the body.
Eg. rheumatoid arthritis, systemic lupus, erythematosus, multiple sclerosis, insulin-dependent diabetes.

183
Q

Rheumatoid Arthritis

A

Autoimmune disease that leads to damage & painful inflammation off the cartilage & bone joints.

184
Q

Immunodeficiency Diseases

A

An inborn primary immunodeficiency results from hereditary or congenital defects that prevent proper functioning of innate, humoral &/ cell-mediated defences.
An acquired or secondary immunodeficiency results from exposure to various chemical & biological agents.

185
Q

Inborn (Primary) Immunodeficiencies

A

In severe combined immunodeficiency (SCID), both the humoral & cell-mediated ranges of acquired immunity fail to function.

186
Q

Acquired (Secondary) Immunodeficiency

A

In severe combined immunodeficiency (SCID), both the humoral & cell-mediated ranges of acquired immunity fail to function.

187
Q

Acquired Immunodeficiency Syndrome

A

People with AIDS are highly susceptible to opportunistic infections & cancers that take advantage of an immune system in collapse.
Because AIDS arises from the loss of helper T cells, both the humoral & cell-mediated immune responses are impaired.

188
Q

Pathogens

A

Infectious diseases are caused by pathogens.
Is a disease causing organism, usually a microorganism.
Includes bacteria, viruses, Protozoa, fungi.
Not all microorganisms are pathogens.

189
Q

Bacteria

A

Single celled organisms that are prokaryotic (no nuclear membrane).
<1% cause diseases.
Infections make a person noticeably sick.
Reproduce rapidly & many give off toxins which damage body tissue.
Symptoms of infections depend on the type of bacteria, but range from fever, pain, swelling, vomiting, diarrhoea, formation of pus to abortion.
Body fluids can be sampled & cultured to grow & identify the bacterial pathogen.
Antibiotics are the usual treatment for bacterial infections, but treatment can vary.
Bacteria adapt quickly & may become resistant to antibiotics.
Produce disease in one of two ways:
- Using cells for food: break down healthy cells for food, destroying tissues.
- Releasing toxins: produce a toxin (poisonous protein) that is released into the bloodstream where it can travel throughout the body, disrupting normal activity & damaging tissues.

190
Q

Antibiotics

A

Two types: bactericidal & bacteriostatic.

191
Q

Antibiotics: Bactericidal

A

Kills bacteria by changing the structure of the cell membrane.
Disrupts the action of essential enzymes.

192
Q

Antibiotics: Bacteriostatic

A

Prevents further replication by disrupting protein synthesis.
Stops bacteria from reproducing.

193
Q

Viruses

A

A virus is an infectious agent found in virtually all life forms.
Consist of a piece of genetic material (RNA/DNA) housed with a protective coat. Viruses are not cells.
Reproduce by hijacking the cell of another organism (host) & getting the host cell to reproduce more viruses.
Most viruses cause disease & are specific as to which type of cell they will attack.
Consist of genetic material & have a central core either of DNA or RNA.
Although they are infectious agents, they differ from bacteria in that they contain no nucleus or cytoplasm.
They do not feed, excrete or grow.
They cannot reproduce outside of a living cell.
Structure consists of nucleic acids, capsid & envelope.
In order to replicate, they need a host cell. Any living cell can be used.
Without a host cell, they cannot functions (ie. are harmless).
although any cell can theoretically become a host cell, specific viruses will only infect specific cells (eg. HIV will only infect human T cells).

194
Q

Viruses: Process of Infection

A

Attach: the capsid of the virus binds to receptor proteins on the surface of a host cell, tricking the host cell into thinking its not a foreign invader.
Inject: the virus injects its genetic material (DNA or RNA) into the host cell.
Assemble: the viral genes are expressed, turning the host cell into a virus-making factory.
Repeat: the host cell eventually bursts, releasing hundreds of newly formed viruses to infect.

195
Q

Viruses: Treatment

A

Antivirals can only be used to treat certain viral infections.
Does not kill or disarm the virus permanently, only shortens the symptoms by 1-2 days.
Just like antibiotics, there is evidence of antiviral resistance as well.

196
Q

Antiviral Drugs

A

Only a few effective antiviral drugs have been developed.
Work by:
- Altering cell’s genetic material so that the virus cannot multiply.
- Prevents new virus formed from leaving the cell.
Viruses mutate frequently, leaving the antiviral drug ineffective.

197
Q

Reservoirs: Where Pathogens Persist

A

Reservoir: the primary habitat in the natural world from which a pathogen originates.
Source: the individual or object from which an infection is actually acquired.
Living reservoirs
- Carrier: an individual who inconspicuously shelters a pathogen & spreads it to others.

198
Q

Animals as Reservoirs

A

Vector: a live animal that transmits an infectious agent from one host to another.
Majority are arthropods.
Biological vector: actively participates in a pathogens life cycle.
Mechanical vectors: transport the infectious agent without being infected.

199
Q

Zoonosis

A

An infection indigenous to animals but naturally transmissible to humans.
Human does not contribute to the persistence of the microbe.
Can have multi-host involvement.
At least 150 worldwide.

200
Q

Endocrine vs. Exocrine

A

Endocrine: transports their hormones to target tissues via the blood. (Secretes hormones into the blood).
Exocrine: transports their hormones to the target tissues via ducts. (Secretes hormones into ducts).

201
Q

Hypothalamus & Anterior Pituitary

A

The hormones are produced in specialised cells located within the anterior lobe & stored there.
A system of blood vessels connects capillaries in the hypothalamus with capillaries in the anterior lobe.
The hormones are stimulated for release by specialised chemicals known as releasing & inhibiting factors which are produced in the hypothalamus & released into the anterior pituitary.

202
Q

Hypothalamus & Posterior Pituitary

A

The hormones are produced in specialised cell bodies located in the hypothalamus above the the pituitary. The hormones are not produced in the posterior pituitary.
The hormones are transported down the axons of these cells & terminate in the posterior lobe.
The hormones are then stored in the posterior lobe.
When the posterior lobe receives a nerve impulse from the hypothalamus, the hormones are released into the bloodstream.

203
Q

Nervous / Endocrine Systems

A

Communication: electrical / chemical
Speed of Response: quickly (1-10 msec) / slowly (sec - days)
Persistence of Response: stops quickly / may continue for weeks
Area of Effect: targeted & specific / general & widespread
Long Term Stimuli: response declines quickly / responses persists

204
Q

Hormones: Properties

A

One molecule activates thousands of enzyme molecules through a process called enzyme amplification.

205
Q

Hormones: Clearing Response

A

Different hormones vary in their rates of clearance.
Length of time required to clear 50% of the hormone from the blood is the half-life.
Each hormone has a specific half-life, due to:
- Different molecular structure
- Weight
- Bound or unbound to a transport protein.

206
Q

Mechanism of Hormone Action

A

Hormones influence target cells.
They bind to receptors on cell membranes.
Once bound, hormones alter cell activity by:
- Altering plasma membrane potential (opening ion channels).
- Stimulates synthesis of proteins (usually regulatory such as enzymes).
- Activates or deactivates enzymes.
- Stimulates mitosis.

207
Q

Steroid Hormones

A

Lipid soluble
Transported by carriers
Hydrophobic - hormone diffuses through plasma membrane & makes its way to nucleus
Bind to chromatin (DNA)
Initiate transcription

208
Q

Protein/Peptide Hormones

A

Water soluble
Cannot penetrate cell membrane
Binds to plasma membrane receptor
Use 2nd messenger systems
Usually activate/deactivate enzyme systems that are there rather than create more.
Eg: FSH, TSH, LH, ACTH, PTH, Glucagon.

209
Q

Steroid / Peptide Hormones

A

Circulating Form: bound to carrier proteins / not bound to carrier proteins
Membrane Permeable: yes / no
Speed of Response: slow (requires DNA binding & changes in gene transcription) / fast (rapid signal transduction via protein conformational change)
Breakdown: slow (large reserve of hormones since they are mostly hormone bound) / fast (due to enzymatic breakdown)

210
Q

Acromegaly

A

Overproduction (hypersecretion) of growth hormone after the epiphyseal plates have fused.
Bone shapes change & cartilaginous areas of the skeleton enlarge.
Results in broad facial features & an enlarged lower jaw.

211
Q

Cretinism

A

Hyposecretion of thyroid hormone in infancy.
Results in severely stunted mental & physical growth.

212
Q

Goiter

A

Thyroid hyposecretion due to nutritional iodine insufficiency.
Results in the growth of a goiter, or the enlargement of the thyroid gland.
Decreased metabolism results in the increase of TSHrf being released from the hypothalamus, resulting in an increased production of TSH from the AP reaching the thyroid gland, the amount of thyroxine produced is low due to iodine deficiency, resulting in a lower metabolism.

213
Q

Addison’s Disease

A

Caused by hyposecretion of corticosteroids, especially gluconeocorticoids.
Pigment change results from stimulation of melanocytes by ACTH, which is structurally similar to MSH.

214
Q

Cushing’s Disease

A

Caused by hypersecretion of glucocorticoids.
Lipid reserves are mobilised & adipose tissue accumulates in the cheeks & base of neck.

215
Q

Grave’s Disease/Betty Davis Eyes

A

Overactive thyroid gland (hypersecretion).
Person has an elevated metabolic rate, can be nervous, sweaty & lose weight despite great appetite.
Often protrusion of eyes. More common in women.
Treatment: surgery or radioactive I which destroys some thyroid cells (radioactive I is a medication the same shape as iodine. Thyroid gland absorbs it & it then destroys some thyroid cells).

216
Q

Triplet

A

Three bases in a DNA strand.

217
Q

Codon

A

The bases in the mRNA that match the triplet.

218
Q

Anticodon

A

Three bases in tRNA that match the codon. They match specific amino acids.

219
Q

Operon

A

Genes grouped together with related functions. Consists of structural genes, regulatory genes & regulatory sites.

220
Q

Structural Genes

A

Code for polypeptides.

221
Q

Regualtory Genes

A

Code for depressors or activators.

222
Q

Regulatory Sites

A

Promoter: RNA polymerase binding site. A single promoter controls transcription of all genes in an operon. They are transcribed as one unit & a single mRNA is made.
Operator: DNA binding site of a repressor protein.

223
Q

Repressor Protein

A

Used to turn genes off. Binds to DNA at operator site, blocking RNA polymerase, therefore blocking transcription.

224
Q

RNA

A

A nucleic acid that uses a slightly different sugar (ribose sugar) than DNA & the base uracil in place of thymine.
It is single stranded & there are many types - mRNA, tRNA, rRNA, etc.

225
Q

mRNA

A

Functions in the nucleus, migrates to ribosomes in the cytoplasm.
Carries DNA sequence information to ribosomes.

226
Q

tRNA

A

Functions in the cytoplasm.
Provides linkage between mRNA & amino acids; transfers amino acids to ribosomes.
Has an amino acid attachment site where each amino acid binds prior to being added to the amino acid chain, & an mRNA attachment site where the anticodon matches to the codon.

227
Q

rRNA

A

Functions in the cytoplasm.
Structural component of ribosomes.

228
Q

Transcription

A

Occurs in the nucleus.
Makes an mRNA copy of the DNA.
Introns are edited out.
mRNA leaves the nucleus.
The enzyme RNA polymerase opens the DNA strands & synthesises a new strand of mRNA complementary to only one of the DNA strands.
Transcription starts & stops at distinct sites at the ends of a gene.

229
Q

Post-Transcriptional Processing

A

Primary transcript (mRNA) needs work after transcription - the introns are edited out & the exons are connected in one long sequence.
This forms the mature mRNA.

230
Q

Translation

A

Process produces a polypeptide from the mRNA.
A complicated process that occurs in the cytoplasm.
Involves mRNA, tRNA, rRNA, ribosomes & amino acids.
Many antibiotics block steps in translation within bacterial cells.

231
Q

Ribosomes

A

Made of two large subunits - one large & the other small.
Has three sites that assist in protein synthesis.
P (peptides-tRNA binding) site: holds tRNA carrying growing polypeptide chain.
A (aminoacyl-tRNA binding) site: holds tRNA carrying next amino acid to be added to chain.
E (exit) site: empty tRNA leaves ribosome from exit site.

232
Q

Building a Polypeptide (Steps)

A

Three stages:
- Initiation
- Elongation
- Termination

233
Q

Building a Polypeptide: Initiation

A

Brings together mRNA, ribosome subunits, proteins & initiator tRNA.

234
Q

Building a Polypeptide: Elongation

A

tRNA complexes bind to mRNA codon by forming complementary base pairs with the tRNA anticodon.
The ribosome moves from codon to codon along the mRNA.
Amino acids are added one by one.

235
Q

Building a Polypeptide: Termination

A

Release factor binds to the stop codon.

236
Q

Termination: Release Polypeptide

A

Release factor: release protein binds to the A site & bonds a water molecule to the polypeptide.

237
Q

Restriction Enzymes

A

DNA molecules are very long, often consisting of millions of base pairs.
in order to study DNA structure, molecules are broken into smaller fragments by enzymes known as restriction enzymes.
Restriction enzymes do not bread up the DNA molecule randomly, but cut it at particular intervals.
The fragments cut by the restriction enzymes are called restriction fragments.
The fragments can be separated using gel electrophoresis & recombinant DNA.
Repeated sequences can also be cut out by restriction enzymes.

238
Q

Polymerase Chain Reaction (PCR)

A

Can produce many copies of a specific target segment of DNA.
A three-step cycle - heating, cooling & replication - brings about a chain reaction that produces an exponentially growing population of identical DNA molecules.
Can copy different lengths of DNA, it does not have to copy the whole length of a DNA molecule.
- One gene
- Several genes
- Many genes
Artificial process which imitates natural DNA replication.

239
Q

PCR Process

A

Reagents needed:
- DNA sample which is wanted to be amplified.
- Taq DNA polymerase
- Nucleotides (called dNNTPs)
- Pair of primers
- One primer binds to the 5’ end of one of the DNA strands, the other binds to the 3’ end of the anti-parallel DNA strand.
- Delineate the region of DNA that is wanted to be amplified.
Denaturation: heated briefly to separate DNA strands.
Annealing: cooled to allow primers to form H+ bonds with ends of target sequence.
Extension: DNA polymerase adds nucleotides to the 3’ end of each primer.

240
Q

Recombinant DNA

A

DNA produced by combining DNA from different sources.

241
Q

Vectors

A

In DNA cloning, the plasmid/chromosome used to carry the cloned DNA segment to a desired location.
This is frequently a virus or liposome that is used.

242
Q

Plasmids

A

Circular DNA molecule that is found in bacteria.

243
Q

Recombinant DNA

A

A section of DNA, often in the form of a plasmid, that is formed by joining two DNA sections from two different sources.
For genetic engineering, the gene must be obtained, copied and pasted into a vector, and cell must express gene in protein synthesis.

244
Q

Genetic Engineering Recombinant DNA: Process

A
  1. Plasmid isolated & restriction enzyme cuts once.
  2. DNA isolated & same restriction enzyme cuts DNA twice.
  3. Gene inserted into plasmid. Ligase seals the nick.
  4. Plasmid put into bacterial cell.
  5. Cell multiples with gene of interest.
  6. Cells then placed into agar plate & exposed to bacteria. Only the cells that took up the DNA will be immune to the bacteria - the others will die.
  7. The remaining cells that took up the gene/DNA are cloned.
245
Q

Cutting & Sticking

A

Recombinant DNA made by cutting DNA & sticking it together.
Restriction enzymes from bacteria cut DNA at specific points.
Restriction enzymes cut DNA at the restriction site on the DNA.
Where the restriction enzymes cuts leaves some exposed single strand bases known as a ‘sticky’ end.
Recombinant DNA is made by cutting DNA & sticking it together.
Separate fragments of DNA are joined into plasmid by enzyme DNA ligase.
Both pieces of DNA cut must have been cut by the same restriction enzyme so that the sticky ends are complementary.
The DNA is now called recombinant DNA.

246
Q

Bacterial Cells & Plasmids

A

Plasmids cut with restriction enzyme used to isolate the chosen gene.
Complementary sticky ends are formed.
Plasmid & gene mixed & they combine.
Plasmid then seals & forms recombinant plasmid with help of ligase enzyme.
Plasmids mixed with bacterial cells which take up plasmid.
Less than 1/4 of 1% of bacteria take up the plasmid & are now known as transformed bacteria or transgenic bacteria (changed genes).

247
Q

Resulting Colonies: Examining

A

Three types of colonies will form:
- Bacteria that did not take up the plasmid.
- Bacteria containing a plasmid that did not seal in a copy of the DNA.
- Bacteria containing the new recombinant plasmid, known as transformed bacteria.

248
Q

Identifying Transformed Bacteria

A

Original plasmids have antibiotic resistance gene (used as a genetic marker) for the antibiotics ampicillin & tetracycline.
Plasmids cut in the middle of the tetracycline gene & insulin gene inserted meaning no more resistance to tetracycline.
Bacteria then grown on agar plates.
Then transferred onto plates treated with ampicillin to see if they have the plasmid & will grow.
Then some transferred onto plates treated with tertracycline to see if they still grow or not. If they do not, they contain the insulin gene.
This is called replica plating.

249
Q

Recombinant DNA: Medical Application

A

Production of pharmaceuticals for treatment of diseases (eg. human insulin, interferons).
Production of pharmaceuticals for disease prevention (eg. vaccine such as hepatitis B).

250
Q

Examples of Genetic Engineering

A

If a person is type 1 diabetic & cannot produce insulin, it is possible through genetic engineering to add the insulin gene to the body, so the person can produce insulin.
The first human protein made commercially using engineered bacteria was human insulin, but many other hormones & human proteins are now being produced. In addition, many recombinant vaccines have been produced.
Many human proteins that were formerly extremely expensive to produce because they were found in human tissues only in small amounts can now be made in large amounts from the cloned gene.
Many recombinant vaccines have been produced. These include live recombinant, vector, subunit & DNA vaccines.

251
Q

Functions of the Nervous System (NS)

A

Sensory functions: sense changes (stimuli) within the body & outside the body.
Integrative function: analyses the sensory information, stores some aspects & makes decisions regarding appropriate behaviours.
Motor functions: respond to stimuli by initiating muscular contractions or glandular secretions. These muscles are called effectors.

252
Q

NS: Three Functions

A

Sensory input
- From millions of specialised receptors.
- Receive stimuli.
Integration
- Process stimuli.
- Interpret stimuli.
Motor output
- Cause response.
- At many effector organs.

253
Q

Two Divisions of NS

A

Central NS
Peripheral NS
These two work together as a single coordinated whole.

254
Q

Central NS

A

→ Consists of the brain & spinal cord.
Integrates incoming information.
Generates thoughts & emotions.
Forms & stores thoughts, ideas & actions (muscle memory).
Connected to sensory receptors, muscles & glands in the various parts of the body by the PNS.
Consists of cranial & spinal nerves.

255
Q

The Brain

A

One of the largest organs in the body.
Male brain is approx. 1600gm.
Female brain is approx. 1450gm.
Equivalent in terms of size/body weight.
Average measurement is 1350cc (cm2).
Generally has around 100 bn neurons.
Divided into hemispheres & lobes.
It’s size is not representative of intelligence.
The brain is the anterior expansion of the spinal cord.

256
Q

The Cerebrum

A

Contains:

Sensory areas (perception of sight, hearing, taste, smell, touch, etc).
Motor areas (movement & speech).
Association areas (awareness, memory, etc).

257
Q

Gyri & Sulci

A

The corrugated surface of the cerebrum greatly increases the surface area of the cerebral cortex.
The corrugations consist of gyri (ridges) & sulci (groves).

258
Q

Cerebral Cortex

A

Grey matter consists of synapsing cell bodies.
White matter contains tracts of myelinated nerve fibres.

259
Q

Frontal Lobe (Cerebrum)

A

Contains the motor cortex responsible for voluntary control of muscles.
Responsible for judgement, emotions, motivation & memory.

260
Q

Temporal Lobe (Cerebrum)

A

The temporal lobe contains the olfactory (smell) & auditory (hearing) areas.

261
Q

Occipital Lobe (Cerebrum)

A

The occipital lobe contains the visual areas.
Damage to this area may result in cortical blindness.

262
Q

Parietal Lobe (Cerebrum)

A

Contains the primary sensory strip & sensory association areas.
Damage to this region makes it difficult to understand sensory inputs from the skin.

263
Q

Thalamus

A

Makes up about 80% of diencephalon.
Dumbbell shaped; lobes connected by the isthmus.
Principal relay station for sensory impulses to the cerebral cortex.
Also plays a role in emotions, memory, awareness & cognition.

264
Q

Hypothalamus

A

One of the major regulators of homeostasis.
Control of the autonomic nervous system.
Controls the pituitary gland (“the master gland”).
Regulates eating & drinking.
Controls body temperature (“thermostat”)
Regulation of diurnal rhythms & states of consciousness.
Regulation of emotional & behavioural patterns.

265
Q

Cerebellum

A

Also known as secretary of the brain.
Coordinates fine, controlled motor movement, muscle tone & storing memory for habitual actions (muscle memory).
Receives information from proprioceptors in muscles.
Compares this to other sensory information from the inner ears, eyes, head position.
Sends impulses to the motor area of the brain to contract specific muscles to maintain balance.

266
Q

Brain Stem

A

Connects the spinal cord to the diencephalon.
Made up of medulla oblongata, pons & midbrain.
Midbrain or mesencephalon contains the cerebral aqueduct, & is an area for passage of fibres between areas of the brain & for coordination of muscle activity.

267
Q

Pons

A

Means ‘bridge’.
Connects the spinal cord with the brain & links parts of the brain with one another by way of tracts.
Contains several nuclei that are the origins for cranial nerves.
Works with the medulla to control breathing.
Regulates involuntary actions such as depth of breath, heart rate, etc.

268
Q

Medulla Oblongata

A

Continuous with upper part of the spinal cord.
Most sensory & motor tracts cross over to the other side of the body as they pass through the medulla.
Forms the lower region of the brain stem.
Respiratory, cardiac & vasomotor centres located here.
Contains reflex centres for swallowing, choking, etc.
Controls involuntary actions such as breathing, heart beat.

269
Q

Neurons

A

Highly specialised cells of the nervous system (nerve cells).
Generate electrochemical nerve impulses & carry information from one part of the body to another.
Structure fits function:
Many entry points for signal.
One path out.
Transmits signal through ‘body’.

270
Q

Glial Tissue

A

Around 40% of the brain & spinal cord consists of glial cells.
Support, protect & provide neurones with nutrition & insulate them from each other.

271
Q

Subdural Space

A

Between dura mater & arachnoid mater, filled with interstitial fluid.

272
Q

Subarachnoid Space

A

Between arachnoid mater from pia mater. Filled with CSF.

Human Biology ATAR (2 decks)

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