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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
What does QRS mask
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
26
why is p wave smaller than QRS
atria have a much smaller muscle mass than ventricles
27
where is there no current flow
PR Segment ST Segment TP interval
28
strength of cardiac muscle contraction and accordingly SV
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)
29
Increase EDV increase SV
Intrinsic control of SV depends on the direct correlation between EDV and SV this is length-tension relationship of cardiac muscle
30
The intrinsic relationship matching SV with venousreturn has two major advantages
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
Cellular basis of Frank-Starling mechanism
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
SV is also subject to extrinsic control by i) sympathetic stimulation and ii) adrenaline
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
what is used to estimate contractile state of myocardium
max dP/dT analyse of pressure waveform during isometric contraction phase
34
what do the arteriolar walls
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
Contraction and relaxation
Decrease radius increase resistance decrease local blood flow = vasoconstrcition Relaxation - increase radius , decrease resistance , increase local blood flow = vasodilation
36
what is vascular tone
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
what is tachycardia and bradycardia
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
chronotropic effect
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
cAMP 2nd messenger pathway of neurotransmitter
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
Parasympathetic NS decreases heart rate through 2effects on pacemaker tissue
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
other effects of parasympathetic stimulation on heart activity
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
Sympathetic NS speeds up heart rate through its effect on pacemaker tissue
main effect is to speed up depolarisation so threshold is reaches more rapidly NorAd augments If and T type channel activity
43
other effects of sympathetic stimulation on the heart activity
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
Overall effect of sympathetic stimulation on the heart is to improve its effectiveness as a pump
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
what is anaphylaxis
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
plasma volume alters what
salt excretion by RAAS antidieutric hormone atrial natiruetric peptide
47
RAAS
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
Angiotensin II stimulates
Alodesterone generlasied vasonstriction thirst
49
Angiotensin II and Aldosterone
alodestrone - adrenal cortex stimautles Na+ - NaK pump and Na channel osmosis - plasma volume and blood pressure
50
Angiotensin II binds to AT1 receptors
Angiotensin II binds to AT1 receptor on vascular cells stimulates contraction and therefore, vasoconstriction contributes to changes in total peripheral resistance (TPR)
51
Hypertension Increase renal sympathetic nervous sytem activity A fall in NaCl concentration
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
What does ACEi
prodcues II narrowing vessels circualtory blood volume and chnage in blood pressure
53
what does ventricualr volume chnages at increased heart rate
rapid filling and reduced filling filling caused by atrial contraction
54
Metabolic hyperaemia
increase Metabolic activity increase adenosine vasodilation of coronary vessels increase blood flow oxygen available increases
55
VE and VO2
Note that a higher works loads Ve increases disproportionately to VO2 VO2 exactly matches workload until VO2 is reached
56
Tunica Intima
Inner lining single endothelial layer supported by connective tissue Endothelium subendothelium basement membrane
57
Tunica Media
Middle layer largely smooth muscle helps vessel to contract and expand elastin fibres keep flowing in one direction
58
Tunica Adevntita
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
Embryonic
Primordial lung develop as bud which extend outwards from fetal foregut
60
Pseudoglandular
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
Canalicular
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
Saccular
branching growth / primitve alvoelar ducts thinning stroma brings capillaries type I pneumocytes from type II like blood gas barrier
63
Alveolar
parenchyma Na+ driven fluid absoprotion from the lumen clears the lung of fluid and maintains a thin film of liquid on the surface
64
poor and good ventilation
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
Pulmonary surfactant composed of what and secreted by
Composed of Dipalmitoyl phosphatidyl choline (DPPC)packaged around surfactant proteins (A-D) Secreted by type II alveolar epithelial cells
66
reduces surfce tension in alveoli
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
Effects of surfactant on stability of alveoli
fall r surfacnt molecules croded together surface tension reduced smaller alveolous stabilised alveoli also stabilised by mechanical interactions between neighbouring alveoli
68
Chemoreceptive
inputs monitor plasma and cerebral spinal fluid composition to maintain ventilatory homeostasis
69
Dorsal Respiratory Group
Inspiratory control Nucleus tractus solitarius and is dorsal to the VRG sensory information input chemoreceptors input premotor neurons
70
ventral respiratory group medulla
Rostral - expiration control Intermediate - inspiration control is mediated by pre botzinger complex and has RPG Caudal - expiration control
71
what is cranial motorneurons
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
Model of the RRG in the brian stem
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
increase total ventilation volume
Total ventilation volume = increase Tidal volume + increase frequency
74
spirograph and vitalograph
measures breathing volume at rest measures peak flow on maximal exhaltion

BS22001 Human Physiology and Pharmacology (16 decks)

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