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PY4010 Revision KU

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The Human Body (PY4010)

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Kingston University

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THE SIGNALLING PATHWAY OF BETA-ADRENERGIC RECEPTOR ACTIVATION (NEED TO KNOW THE DETAILS OF THIS SIGNALLING

THE BARORECEPTOR REFLEX
WHAT IS BLOOD PRESSURE? - -
THE MECHANISMS FOR BP HOMEOSTASIS
WHAT ARE BARORECEPTORS? - - -
HOW DO BARORECEPTORS WORK TO RESTORE BLOOD PRESSURE?
THE AUTONOMIC NERVOUS SYSTEM
BRANCHES OF THE NERVOUS SYSTEM
NEUROTRANSMITTER RELEASE BY EFFERENT FIBRES
THE SEVEN PROCESSES IN NEUROTRANSMITTER RELEASE
HOW IS NORADRENALINE SYNTHESISED AND RELEASED FROM THE NERVE TERMINAL?
NORADRENALINE CAUSED BY ADRENALINE TO BE RELEASED BY THE ADRENAL MEDULLA
CATECHOLAMINES
HOW DOES NORADRENALINE AFFECT VARIOUS TISSUES AND ORGANS?
ADRENERGIC PHARMACOLOGY
HOW DOES ACETYLCHOLINE (PARASYMPATHETIC STIMULATION) AFFECT VARIOUS TISSUES AND ORGANS?
TYPES (AND SUBTYPES) OF ADRENERGIC RECEPTORS
PATHWAY E. DISSOCIATION OF G-PROTEIN, ACTIVATION OF ADENYLATE CYCLASE, PRODUCTION OF CAMP AND PKA...)
SIGNALLING PATHWAY E. ACTIVATION OF PHOSPHOLIPASE C, PRODUCTION OF IP3 AND DAG... THE SIGNALLING PATHWAY OF POST-SYNAPTIC ALPHA-ADRENERGIC RECEPTOR ACTIVATION (NEED TO KNOW THE DETAILS OF THIS
ACTIVATION OF ALPHA-ADRENERGIC ON THE PRE-SYNAPTIC MEMBRANE INHIBITS FURTHER NORADRENALINE RELEASE.
THE EFFECT OF ADRENERGIC STIMULATION DEPENDS ON THE SUBTYPE OF ADRENERGIC RECEPTOR ACTIVATED
CHOLINERGIC PHARMACOLOGY
TYPES OF ACETYLCHOLINE RECEPTORS AND WHERE THEY ARE EXPRESSED
THE EFFECTS OF PARASYMPATHETIC STIMULATION ON VARIOUS TISSUE AND ORGANS
EXAMPLES OF MUSCARINIC RECEPTOR AGONSITS/ANTAGONISTS — PHYSIOLOGICAL/THERAPEUTIC EFFECTS
HOW IS ACETYLCHOLINE SYNTHESISED, STORED, RELEASED AND DEGRADED?
NICOTINIC RECEPTORS ARE LIGAND-GATED ION CHANNELS
NEUROMUSCULAR JUNCTION COMPARE AND CONTRAST THE PROPERTIES OF NICOTINIC RECEPTORS EXPRESSED AT THE POSTSYNAPTIC GANGLIA VS
PHYSIOLOGICAL EFFECTS OF NICOTINE
EFFECTS OF CHOLINESTERASE INHIBITORS, AND THEIR ROLE IN THE TREATMENT OF MYASTHENIA GRAVIS
THE SKELETAL MUSCLE
WHAT HAPPENS AT THE NEUROMUSCULAR JUNCTION?
EXCITATION–CONTRACTION COUPLING
STRUCTURE AND TYPES OF SKELETAL MUSCLE
THE STRUCTURE OF THE SARCOMERE
THE INTERACTION BETWEEN THE THIN FILAMENT, TROPOMYOSIN, THE TROPONIN COMPLEX AND THE THICK FILAMENT
WHAT IS THE SARCOLEMMA
WHAT IS THE FUNCTION OF THE T-TUBULES?
WHAT IS THE SARCOPLASMIC RETICULUM?
THE SMOOTH MUSCLE
CHARACTERISTICS OF SMOOTH MUSCLE (VS STRIATED MUSCLE)
TYPES OF SMOOTH MUSCLE
MECHANISMS OF SMOOTH MUSCLE CONTRACTION/RELAXATION
VASCULAR SMOOTH MUSCLE CONTRACTION AND VASOCONSTRICTION SEQUENCE OF EVENTS FOLLOWING THE ACTIVATION OF ANGIOTENSIN II RECEPTORS/ ENDOTHELIN 1 RECEPTORS LEADING TO
THE ROLE OF RHO-KINASE IN MUSCLE CONTRACTION
RESPIRATORY PHYSIOLOGY
WHAT IS BULK FLOW
BOYLES LAW AND HOW IT RELATES TO BREATHING
HOW AIRFLOW RESISTANCE AND LUNG COMPLIANCE CONTRIBUTE TO VENTILATION
WHAT INFLUENCES LUNG COMPLIANCE
ACID–BASE BALANCE
THE BODY NEEDS TO MAINTAIN BLOOD PH WITHIN NORMAL RANGE (PH 7)
WHAT REGULATE BLOOD PH
WHAT BUFFERS HYDROGEN IONS (H+)
THE BICARBONATE BUFFER SYSTEM
THE PHOSPHATE BUFFER SYSTEM
THE PROTEIN BUFFER SYSTEM
CO2 IN THE BLOOD
WHAT IS THE HALDANE EFFECT?
ACIDOSIS VS ALKALOSIS (DEFINITION)
- CAUSES OF METABOLIC/RESPIRATORY ACIDOSIS AND METABOLIC/RESPIRATORY ALKALOSIS, AND COMPENSATORY MECHANISMS
THE RENAL SYSTEM
THE CARDIOVASCULAR SYSTEM
CONTROL OF BLOOD GLUCOSE
HOW IS GLUCOSE TRANSPORTED ACROSS PLASMA MEMBRANES?

THE BARORECEPTOR REFLEX

WHAT IS BLOOD PRESSURE?

Blood pressure is the pressure blood exerts on the arterial walls.

THE MECHANISMS FOR BP HOMEOSTASIS

Diastolic Blood Pressure Minimum pressure in the arteries. Occurs when the heart is not contracting, when the ventricles are filled with blood 60 – 80 mmHg Systolic Blood Pressure Peak pressure in the arteries Occurs during cardiac contraction 90 – 120 mmHg BP – Blood Pressure CO – Cardiac Output TPR – Total Peripheral Resistance SV – Stroke Volume HR – Heart Rate CV – Circulating Volume BP = CO x TPR CO = SV x HR TPR = contractility/radius vessels & CV Pulse Pressure = (SYSTOLIC BP) — (DIASTOLIC BP) Mean Arterial Pressure (MAP), mmHg = (1/3 pulse pressure) + (DIASTOLIC BP) ^ an average blood pressure in an individual during a single cardiac cycle Long–Term Renal/Hormonal Regulation

Determined by Renin-Angiotensin-Aldosterone System
RAAS plays a role in regulating blood volume, systemic vascular resistance which together influence cardiac output and arterial pressure Short–Term Neuronal Control
Achieved through the role of cardiovascular centres and baroreceptor stimulation
Baroreceptors respond to pressure caused by the blood  stimulates impulses to be sent to cardiovascular centre  activates the SNS/PNS

WHAT ARE BARORECEPTORS?

Type of mechanoreceptor located in the blood vessels. Detect the blood pressure, can send messages to the CNS to increase/decrease total peripheral resistance and cardiac output.

THE CARDIOVASCULAR CENTRE o Stimulates cardiac function by regulating heart rate and stroke volume o Via sympathetic stimulation from the cardiac accelerator nerve
THE CARDIO-INHIBITOR CENTRE o Slows cardiac function by decreasing heart rate and stroke volume o Via parasympathetic stimulation from the vagus nerve
THE VASOMOTOR CENTRE o Control’s vessel tone or contraction of the smooth muscle in the tunica media o Changes in vessel diameter affect peripheral resistance, pressure and flow  affect cardiac output

THE AUTONOMIC NERVOUS SYSTEM

BRANCHES OF THE NERVOUS SYSTEM

NEUROTRANSMITTER RELEASE BY EFFERENT FIBRES

Ganglion Collection of nerve endings Sympathetic Nervous System: Preganglionic — SHORT Postganglionic — LONG Parasympathetic Nervous System: Preganglionic — LONG Postganglionic — SHORT Sympathetic and parasympathetic nervous systems, for the majority, work to oppose each other. Nerve ending  release of neurotransmitter EFFERENT — away from CNS PREGANGLIONIC POSTGANGLIONIC parasympathetic some POSTGANGLIONIC sympathetic (acetylcholine) POSTGANGLIONIC sympathetic (noradrenaline/norepinephrine) Targets for Pharmacological Intervention:

Synthesis
Storage
Release
Activation of receptors
Termination of action

NORADRENALINE CAUSED BY ADRENALINE TO BE RELEASED BY THE ADRENAL MEDULLA

Medulla Sympathetic Effects: FIGHT, FRIGHT OR FLIGHT o Noradrenaline (NAdr) — postganglionic fibres o Adrenaline (Adr) — adrenal medulla NAdr from postganglionic fibres moves to adrenal medulla (adrenal gland) which causes adrenaline to be released.

CATECHOLAMINES

Noradrenaline
Adrenaline
Dopamine

HOW DOES NORADRENALINE AFFECT VARIOUS TISSUES AND ORGANS?

Sympathetic Effects:

Mass activation prepares for intense activity o Heart rate increase o Bronchioles dilate o Blood energy sources increase
GI motility decreases
Contraction of sphincters o Muscles surrounding and able to contract/close a bodily passage/opening o BLADDER
Relaxation of: o Detrusor muscle o Ciliary muscle
Mydriasis o Pupil dilation Adrenergic Transmission Metyrosine can inhibit the conversion (tyrosine  dopa) Transport of the transmitter into vesicles inhibited by reserpine NA reuptake blocked by cocaine or tricyclic anti-depressants Termination of transmission:
Diffusion away from receptors
Reuptake into the nerve terminal
Enzymatic breakdown

ADRENERGIC PHARMACOLOGY

HOW DOES ACETYLCHOLINE (PARASYMPATHETIC STIMULATION) AFFECT VARIOUS TISSUES AND ORGANS?

Tissues and Organs?

TYPES (AND SUBTYPES) OF ADRENERGIC RECEPTORS

The signalling pathway of Beta-adrenergic receptor activation (need to know the details of this signalling pathway e. dissociation of G-protein,

PATHWAY E. DISSOCIATION OF G-PROTEIN, ACTIVATION OF ADENYLATE CYCLASE, PRODUCTION OF CAMP AND PKA...)

The signalling pathway of post-synaptic alpha-adrenergic receptor

SIGNALLING PATHWAY E. ACTIVATION OF PHOSPHOLIPASE C, PRODUCTION OF IP3 AND DAG... THE SIGNALLING PATHWAY OF POST-SYNAPTIC ALPHA-ADRENERGIC RECEPTOR ACTIVATION (NEED TO KNOW THE DETAILS OF THIS

activation of phospholipase C, production of IP3 and DAG...

ACTIVATION OF ALPHA-ADRENERGIC ON THE PRE-SYNAPTIC MEMBRANE INHIBITS FURTHER NORADRENALINE RELEASE.

further noradrenaline release.

THE EFFECT OF ADRENERGIC STIMULATION DEPENDS ON THE SUBTYPE OF ADRENERGIC RECEPTOR ACTIVATED

receptor activated (need to know which subtype does what)

THE SKELETAL MUSCLE

WHAT HAPPENS AT THE NEUROMUSCULAR JUNCTION?

(how does the nervous system communicate with the skeletal muscle and brings about muscle contraction)

EXCITATION–CONTRACTION COUPLING

STRUCTURE AND TYPES OF SKELETAL MUSCLE

THE STRUCTURE OF THE SARCOMERE

THE INTERACTION BETWEEN THE THIN FILAMENT, TROPOMYOSIN, THE TROPONIN COMPLEX AND THE THICK FILAMENT

complex and the thick filament (arrangement, the sliding filament theory, cross-bridge cycling, where ATP is needed)

WHAT IS THE SARCOLEMMA

WHAT IS THE FUNCTION OF THE T-TUBULES?

WHAT IS THE SARCOPLASMIC RETICULUM?

THE SMOOTH MUSCLE

CHARACTERISTICS OF SMOOTH MUSCLE (VS STRIATED MUSCLE)

TYPES OF SMOOTH MUSCLE

MECHANISMS OF SMOOTH MUSCLE CONTRACTION/RELAXATION

Sequence of events following the activation of angiotensin II receptors/

VASCULAR SMOOTH MUSCLE CONTRACTION AND VASOCONSTRICTION SEQUENCE OF EVENTS FOLLOWING THE ACTIVATION OF ANGIOTENSIN II RECEPTORS/ ENDOTHELIN 1 RECEPTORS LEADING TO

vasoconstriction

THE ROLE OF RHO-KINASE IN MUSCLE CONTRACTION

o Lungs produce lipid surfactant that (reduces cohesive forces) breaks the surface tension of the water in the alveolus

Laplace’s Law PressureINSIDE = ( 2 * Surface Tension ) / (radius or tension) = PR/
RDS: Respiratory Distress Syndrome of New-Born o Premature babies  no surfactant  poor lung compliance  difficulty breathing  exhaustion  inability to breathe  lung collapse  death
How to calculate total/alveolar ventilation (the relationship between tidal volume, breathing frequency and dead space)
Dead space: residual air lef in airways (so, airways don’t completely collapse/inhalation easier) TOTAL VENTILATION = tidal volume * frequency ALVEOLAR VENTILATION = (tidal volume – dead space) * frequency mL/min, L/min = volume in alveoli * frequency ^ the volume of fresh air entering the alveoli per minute tidal volume — volume we breathe in New air will mix with old air  decrease the [oxygen]
Dynamics of normal breathing cycle (need to know what all the terms mean)
TLC/TLV: total lung volume
RV: the volume remaining in the lungs afer maximum, forceful expiration. It is the volume of air that cannot be expelled, thus causing the alveoli to remain open at all times.
ERV: the amount of extra air exhaled during a forceful exhale
Vital capacity: if you were to breathe out all air in lungs
FRC: the volume remaining in the lungs afer a normal, passive exhalation
VC: the maximum amount of air a person can expel from the lungs afer a maximum inhalation
IRV: the amount of extra air inhaled above the tidal volume, during a forceful inhalation SUMMARY OF MECHANICS
A pressure gradient between the atmosphere and alveoli must be established to move air into or out of the alveoli.
During inspiration, alveoli expand passively in response to an increased transmural pressure gradient; during quiet expiration the elastic recoil of the alveoli returns them to their original volume.
The volume if gas in the lungs at the end of a normal tidal expiration (FRC) is determined by the balance point of the inward recoil of the lungs and the outward recoil of the chest wall.
During forced expiration, when intrapleural pressure becomes positive, small airways are compressed (dynamic compression) and may even collapse.
The two main components of the work of breathing are the elastic recoil of the lungs and
Factors affecting the volume of gas moving across the alveolar capillary barrier
Efficient external respiration requires: o Surface area of structure o Partial pressure gradient between alveoli and capillaries o V / Q match
The volume of gas per unit of time moving across the alveolar capillary barrier is: o Directly proportional to the area of the barrier o Is inversely proportional to barrier thickness o The difference in concentration of the gas between the two sides of the barrier o The diffusivity of the gas in the barrier
Factors affecting alveolar PO 2
PO 2 of atmospheric air
Rate of alveolar O 2 consumption
Alveolar ventilation
Gas tension at equilibrium Inspired air mixes with the dead space which decreases the PO 2 (160  104 mmHg). This further decreases as the air reaches the tissue cells (as low as 20 mmHg). PCO 2 0 mmHg, increases as it mixes with the alveolus. In the blood this decreases but will increase in the tissues. PCO 2 higher levels in pulmonary capillaries creates a gradient for gas exchange.

Once these chemoreceptors start firing  - Reflex via medullary respiratory neurones  - Respiratory muscles increase contractions  - Increase in ventilation  - Return of alveolar and arterial PCO 2 toward normal o Return of brain ECF H+ and PCO 2 toward normal o Return of arterial H+ toward normal - CO2 drives respiration - CO 2 is the most important factor controlling the rate and depth of breathing in the central chemoreceptors o Central chemoreceptors o [H+] in extracellular fluid (detects this ^) o Detected in the medulla – stimulated by increased PCO 2  increase [H+]

ACID–BASE BALANCE

THE BODY NEEDS TO MAINTAIN BLOOD PH WITHIN NORMAL RANGE (PH 7)

WHAT REGULATE BLOOD PH

WHAT BUFFERS HYDROGEN IONS (H+)

The bicarbonate buffer system The phosphate buffer system The protein buffer system

CO2 IN THE BLOOD

WHAT IS THE HALDANE EFFECT?

ACIDOSIS VS ALKALOSIS (DEFINITION)

Causes of metabolic/respiratory acidosis and metabolic/respiratory alkalosis, and compensatory mechanisms

Multiple Choice

Multiple Choice

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