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BS22001 Human Physiology and Pharmacology > Unknown For Now > Flashcards

Unknown For Now Flashcards

1
Q

what is angina

A

fixed vessel narrowing and endothelial dysfunction
stable - episodic brought on by excersie
unstable - any time

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2
Q

Channels where is teh relaxation and restoring Ca2+

A

Utilises the Na2+ electrochemical gradient to pump Ca2+ out of the cell
Utilises ATP hydrolysis to actively pump Ca2+ out of the cell
Utilises ATP hydrolysis to actively pump Ca2+ into the SR

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3
Q

what is electromechical coupling

A

opening of plasma membrane voltage actiavtes L type ca cahnnels in response to depolarisation with or without potential generation

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4
Q

what is pharmacomechial coupling

A

agent that causes chnage in smooth muscle tone without a change in membrane potential (production of intracellular second messengers contract or relx) IP3 , cGMP

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5
Q

Flexion withdrawl reflex

A

Pain - flexors contracted extensors relax
Opposite - flexors relax extesnors contracted

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6
Q

golgi tendon reflex

A

muscle contracts
extrafusal shortens
stimualte golgi tendon organ
Ib firing frequey send information to inhibitory interneuons
synpase in a motorneurons
muscle relax firing frequency of group lb deccreasess
syngergists relax and antagonist contract

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7
Q

Stretch myotatic reflex

A

Muscle stretch
1a afferent fibres muscle firing
synapse on the a motorneuron
sensory information relay
cause contraction
decrease firing frequency

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8
Q

What does the tail region do

A

tail portions are a helices that intertwine
hinge region the molecule open to form 2 globular heads
the head region are the cross bridges between thick and thin filament

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9
Q

Elbow Joint

A

Synovial hinge joint only flex extent
lateral / medial collateral ligament

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10
Q

Knee Joint

A

Cruciate ligament collateral ligament do not fit properly and stabilise the joint

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11
Q

Intervertable joints

A

Longitnidal ligaments and ligamentum flvaum
largely stiff inelastic strictures

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12
Q

how do calcium channel blockers

A

Calcium channels blockers act as a l type calcium channel on vascular smooth muscle but also at l type calcium channels in cardiac myocytes

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13
Q

what are the main classes of calcium channel blockers

A

Dihydrropridines - nifedipine and amlodipine
Benzothiasepines - diltiazem
Phenyalkylamines - verapamil

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14
Q

KATP channels openers

A

Hypertension be used with beta blocker and dieutrics
Open channels in smooth muscle cell membrane hyperolarise smooth cells
~ minoxidil and nicorandil

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15
Q

a blockers

A

a 1 adrenoreceptors singalling cascade leads to smooth muscle contraction following activation of sympathetic
prevent signalling cascade therefore leads to vasodilation
~ prazonin

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16
Q

Pacemaker activity of cardiac autorhythmic cells

A

Pakcemaker potential - Na in through funny channels
Trasient type Ca open goes to threshold
Long lasting Ca open very fast depoalrisation
K+ out goes repolarises

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17
Q

Action potential in a cardiac contractile cell

A

Na+ in fast
K+ out fast
Ca2+ in slow
K+ out fast

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18
Q

what is the refractory peroid

A

action potential with then contractile response where no action potential

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19
Q

what is an ECG not

A

not direct recording of electrical acitvity
it is not recording of single action potential in a single cell at a single point in time
comparison in voltage detected but not actual potential

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20
Q

how does the pattern chnage

A

whether upward and downward deflection is recorded is determined electrodes with respect to current flow in heart
different waveforms same electrical activity activity recorded electrodes different body parts

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21
Q

ECG leads

A

6 from limbs
6 chest around the heart

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22
Q

Six limb leads

A

Leads I II III
difference in potentials between the two electrodes
one on left leg acts as a ground
are bipolar

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23
Q

Six Chest Leads

A

are also unipoalr
exploring electrode
electrical potential cardiac muscaulture immediately beneath the electrode in six different locations surrounding the heart

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24
Q

Einthoven’s triangle

A

voltage recording are made between points that form an equilateral tringable over the thorax and any single trace is a recording o the voltage difference measured between any two ventricles

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25
Q

What does QRS mask

A

No separate wave for atrial repoalrisation is visible the electrical activity associated with atrial repoalrisation occurs simultaneously with ventricular depoalrsation and is maksed by QRS

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26
Q

why is p wave smaller than QRS

A

atria have a much smaller muscle mass than ventricles

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27
Q

where is there no current flow

A

PR Segment
ST Segment
TP interval

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28
Q

strength of cardiac muscle contraction and accordingly SV

A

Varying the initial length of the cardiac muscle fibres, which in turn depends upon EDV (intrinsic control)
Varying the extent of sympathetic stimulation (extrinsic control)

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29
Q

Increase EDV increase SV

A

Intrinsic control of SV depends on the direct correlation between EDV and SV
this is length-tension relationship of cardiac muscle

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30
Q

The intrinsic relationship matching SV with venousreturn has two major advantages

A
  1. equalising otput between left and right sides of the heart
  2. increase CO ~ venous return through action of sympathetic NS (increase EDV automatically increases SV)
31
Q

Cellular basis of Frank-Starling mechanism

A
  1. Greater initial length increases the sensitivity of contractile proteins in the myofibrils to Ca2+
  2. Increased initial fibre length may also increase Ca2+ release from the sarcoplasmic reticulum
32
Q

SV is also subject to extrinsic control by i) sympathetic stimulation and ii) adrenaline

A

This increased contractility is due to increased Ca2+ entry triggered by NorAd/Ad.
An increase in inward Ca2+ flux during the plateau phase of the action potential enhances the intracellular calcium store.
Ca2+ is required for excitation-contraction coupling in cardiac muscle cells.
Increase the rate of relaxation of cardiac muscle cells by stimulating Ca2+ pumps – take up Ca2+ from cytoplasm more rapidly – shortening systole

33
Q

what is used to estimate contractile state of myocardium

A

max dP/dT
analyse of pressure waveform during isometric contraction phase

34
Q

what do the arteriolar walls

A

arteriolar walls include a thick layer of smooth muscle that is richly innverated by nerves of the sympathetic nervous system
- also sensitive to local chemical changes in hormones

35
Q

Contraction and relaxation

A

Decrease radius increase resistance decrease local blood flow = vasoconstrcition
Relaxation - increase radius , decrease resistance , increase local blood flow = vasodilation

36
Q

what is vascular tone

A

arteriolar smooth muscle displays a state of partial known as vascular tone
- myogenic activity
- sympathetic activity
tonic activity makes it possible to either increase or decrease contractile activity

37
Q

what is tachycardia and bradycardia

A

Increased activity in the sympathetic nerves to the heart increases HR (Tachycardia)
Increased activity in the parasympathetic nerves to the heart decreases HR (Bradycardia)

38
Q

chronotropic effect

A

These two divisions of the autonomic nervous system affect heart rate by changing the slope of the pacemaker potential. Changes in rate are the chronotropic effect

39
Q

cAMP 2nd messenger pathway of neurotransmitter

A

PNS ACh is coupled to an inhibitory G-protein that reduces activity of the cAMP pathway
SNS NorAd is coupled to a stimulatory G-protein that accelerates the cAMP pathway

40
Q

Parasympathetic NS decreases heart rate through 2effects on pacemaker tissue

A

1) Hyperpolarization of SA node membrane takes longer to reach the threshold
2) Decreases the rate of spontaneous depolarisation
ACh increases K+ permeability by G protein-coupled inwardly rectifying potassium channels

41
Q

other effects of parasympathetic stimulation on heart activity

A

Parasympathetic stimulation decreases the AV node’s excitability which prolongs the transmission of impulses to the ventricle
Shortens the plateau phase of the AP in atrial contractile cells, weakening atrial contraction
Parasympathetic stimulation has little effect on ventricularcontraction

42
Q

Sympathetic NS speeds up heart rate through its effect on pacemaker tissue

A

main effect is to speed up depolarisation so threshold is reaches more rapidly
NorAd augments If and T type channel activity

43
Q

other effects of sympathetic stimulation on the heart activity

A

Sympathetic stimulation of the AV node reduces AVnodal delay by increasing conduction velocity.
Speeds up spread of the AP throughout the specialised conduction pathway.
Increased contractile strength of the atrial and ventricular contractile cells (heart beats more forcefully and squeezes out more blood)
Increased Ca2+ permeability through prolonged opening of L-type Ca2+ channels.
Speeds up relaxation

44
Q

Overall effect of sympathetic stimulation on the heart is to improve its effectiveness as a pump

A

Increasing heart rate,
Decreasing the delay between atrial and ventricular contraction
Decreasing conduction time through the heart,
Increasing the force of contraction, and
Speeding up the relaxation process so that more time is available for filling

45
Q

what is anaphylaxis

A

blood pressure control is exploited
Anaphylaxis is hypersensitivity reaction involving mast cell degranulation which then causes release of vasoactive compounds which amongst other things cause circulatory collapse due to serve hypotension

46
Q

plasma volume alters what

A

salt excretion by RAAS
antidieutric hormone
atrial natiruetric peptide

47
Q

RAAS

A

Decreased renal perfusion pressure aka a decrease in effective circulating volume→ Rise in sympathetic nervous system activity to kidneys→ Decreased NaCl concentration in the macula densa

48
Q

Angiotensin II stimulates

A

Alodesterone
generlasied vasonstriction
thirst

49
Q

Angiotensin II and Aldosterone

A

alodestrone - adrenal cortex
stimautles Na+ - NaK pump and Na channel
osmosis - plasma volume and blood pressure

50
Q

Angiotensin II binds to AT1 receptors

A

Angiotensin II binds to AT1 receptor on vascular cells stimulates contraction and therefore, vasoconstriction contributes to changes in total peripheral resistance (TPR)

51
Q

Hypertension

Increase renal sympathetic nervous sytem activity

A fall in NaCl concentration

A

Juxtaglomerular cells in arterioles inhibited by stretch
Fall in blood pressure causes release

Stimulates renin secretion by activation of adrenergic receptors

Activates cascade starting from macula densa

52
Q

What does ACEi

A

prodcues II narrowing vessels
circualtory blood volume and chnage in blood pressure

53
Q

what does ventricualr volume chnages at increased heart rate

A

rapid filling and reduced filling
filling caused by atrial contraction

54
Q

Metabolic hyperaemia

A

increase Metabolic activity
increase adenosine
vasodilation of coronary vessels
increase blood flow
oxygen available increases

55
Q

VE and VO2

A

Note that a higher works loads Ve increases disproportionately to VO2
VO2 exactly matches workload until VO2 is reached

56
Q

Tunica Intima

A

Inner lining
single endothelial layer supported by connective tissue
Endothelium
subendothelium
basement membrane

57
Q

Tunica Media

A

Middle layer
largely smooth muscle
helps vessel to contract and expand
elastin fibres keep flowing in one direction

58
Q

Tunica Adevntita

A

connective tissue
delivers oxygen and nutrient to the cells helps remove waste
gives structure and support to blood vessels
larger arteries have their own blood vessels

59
Q

Embryonic

A

Primordial lung develop as bud which extend outwards from fetal foregut

60
Q

Pseudoglandular

A

Fluid secretion created pressure which gives 3D mechanical support
airways and vasculture have developed to compelelty fill space
form conducting airways know as respiratory tree

61
Q

Canalicular

A

extensive angiogenesis within mesenchyme surronds distal reach
form a dense capillary network
decrease epithelial thickness more cubodial structure
epithelial cell differentiation
form respiratory acini
differentiation mesenchyme rise to chondrocytes, fibroblasts and myoblasts

62
Q

Saccular

A

branching growth / primitve alvoelar ducts
thinning stroma brings capillaries
type I pneumocytes from type II like
blood gas barrier

63
Q

Alveolar

A

parenchyma
Na+ driven fluid absoprotion from the lumen clears the lung of fluid and maintains a thin film of liquid on the surface

64
Q

poor and good ventilation

A

poor ventilation and large blood flow– need to reduce perfusion - hypoxia constricts pulmonary arterioles
good ventilation and poor blood flow– need to reduce ventilation - low CO2 constricts bronchioles

65
Q

Pulmonary surfactant
composed of what
and secreted by

A

Composed of Dipalmitoyl phosphatidyl choline (DPPC)packaged around surfactant proteins (A-D)
Secreted by type II alveolar epithelial cells

66
Q

reduces surfce tension in alveoli

A

Prevents collapse of alveoli during lung expansion and contraction
effects on surface tension varies with alveolar surface area
reduces pressure requires to inflate lungs

67
Q

Effects of surfactant on stability of alveoli

A

fall r surfacnt molecules croded together surface tension reduced
smaller alveolous stabilised
alveoli also stabilised by mechanical interactions between neighbouring alveoli

68
Q

Chemoreceptive

A

inputs monitor plasma and cerebral spinal fluid composition to maintain ventilatory homeostasis

69
Q

Dorsal Respiratory Group

A

Inspiratory control
Nucleus tractus solitarius and is dorsal to the VRG
sensory information input
chemoreceptors input
premotor neurons

70
Q

ventral respiratory group
medulla

A

Rostral - expiration control
Intermediate - inspiration control is mediated by pre botzinger complex and has RPG
Caudal - expiration control

71
Q

what is cranial motorneurons

A

cranial motorneurones are important for opening/closing glottis, affecting upper airway diameter, flaring nostrils
motorneurones controlling direct muscles of inspiration & expiration are therefore not the only ones active during breathing

72
Q

Model of the RRG in the brian stem

A

Pre I neurons inhibit
Early I neurons inhibit
I neuron ramp fire
Late I neurons feed back to suppress I
Early E - neurons repress I + E
E neurons ramp fire

73
Q

increase total ventilation volume

A

Total ventilation volume = increase Tidal volume + increase frequency

74
Q

spirograph and vitalograph

A

measures breathing volume at rest
measures peak flow on maximal exhaltion

BS22001 Human Physiology and Pharmacology (16 decks)

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