CVS Theme 4

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  • Created by: Splodge97
  • Created on: 21-05-17 09:48
What does the peripheral circulation serve?
Projects to the walls and contact surfaces of the body - serves the upper and lower regions, skin, alveolar membranes and intestinal epithelium
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Why does hypoxia lead to hypercapnia?
Hypoxia (low O2 supply) leads to hypoxaemia (low plasma O2) and then hypercapnia when less CO2 is removed by Hb due to reduced blood flow
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What occurs in hypoxic pulmonary vasoconstriction?
Hypoxia reduces flow in pulmonary circulation (slowing for better diffusion). Only in pulmonary (not systemic) as expresses more K+ channels with O2 receptors (more in better ventilated areas); in O2 deficit less hyperpolarisation allows contraction.
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What is hypoxic systemic vasoconstriction?
Hypoxia increases flow in the systemic circulation by causing vasodilation (having large effect as r major influence of F); allows faster perfusion to tissues
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What is the tunica intima?
Internal layer of arteries and veins, comprised of an endothelium (controlling transport) and a sub-endothelial layer (containing collagen and elastin)
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What is the tunica media?
Middle layer of arteries and veins, contains smooth muscle (one cell wrapped around arterioles, many cell layers in arteries)
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What is the tunica externa?
External layer of both arteries and veins, permeated by small vessels called vasa vascrum which supply blood to the outer layers of the vessel walls. Capillaries also emerge from this layer.
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What extra layers are present in arteries?
Internal elastic lamina (between intima and media), a dense film of collagen fibres; has perforations allowing transport from endothelium to smooth muscle. External elastic lamina (between media and externa), same but no perforations.
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What is the triple response of Lewis?
Red reaction (line through local vasocaonstriction via histamine/cytokines) --> Flare (redness spreads through PNS action) --> Wheal (localised oedema through increased capillary permeability via histamine)
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How is histamine produced?
In decarboxylation reaction from histidine catalysed by histidine decarboxylase, where carboxyl group lost and CO2 released
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How does vascular smooth muscle contract?
Threshold met by Na+ influx --> Na+VGC's cause depolarisation (slower than in cardiomyocytes as fewer) --> L-type Ca2+VGC's open --> Ca2+ binds to ryanodine receptors on SR --> Ca2+ binds to CaM --> MLCK activated (phosphorylates myosin heads)
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Give examples of vasoconstrictors released from the vascular endothelium
Endothelin-1, prostaglandins, angiotensin II and reactive O2 species - all increase Ca2+
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Give examples of vasodialtors released from the vascular endothelium
NO (acts via cGMP), prostaglandins (acts via cAMP) and EDHF (endothelium derived hyperpolarisation factor, opens K+ channels)
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Why does vascular smooth muscle naturally constrict (if the endothelium was removed)?
Ach would bind directly to cholinergic Ca2+ receptors on smooth muscle to cause calcium influx, initiating contraction - NO is constantly released from the endothelium to prevent this
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What are the functions of nitric oxide (NO)?
Vasodilation, reducing blood cell agglutination (so platlets don't block vessels), inhibiting proliferation/migration/differentiation of endothelium and smooth muscle, interacting with DNA and reducing harmful superoxide radicals
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What nitric oxide synthases are used in endogenous NO synthesis?
n(neuronal)NOS which acts as a neurotransmitter, i(inducible)NOS which increases smooth muscle Ca2+ in inflammation and e/c(endothelial/constitutive)NOS which increases endothelial Ca2+
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How is NO released from the vascular endothelium via the receptor stimulated pathway?
Ach binds to cholinergic receptors on G-protein linked channels --> channels phosphorylate IP3 --> IP3 binds to complementary Ca2+ receptors on SR --> Ca2+ combines with CaM --> activates eNOS, catalyses L-arginine+O2+NADPH to citruilline+NO+NADP+
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How is NO released from the vascular endothelium via the shear stress (flow dependant) pathway?
Increase in blood flow through hypertension/hypervolaemia/vasoconstriction --> stimulates mechanoreceptors to activate nNOS --> causes production and release of NO from endothelium
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How does NO act on vascular smooth muscle?
NO enters --> binds to guanylate cyclase, catalyses GTP to cGMP --> activates PKG --> stimulates BK proteins (remove K+), stimulates Ca2+ removal by SERCA/Ca2+ATPase, inhibits Ca2+ influx via IP3 Ca2+ channels/L-Ca2+VGC's and (with PKA) inhibits MCLK
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Give an example of an artificial nitrovasodilator. What can it be used for?
Glycerol trinitrate (GTN), separates to glycerine (stored in blood) and 3NO. Produces same vasodilation to treat pulmonary hypertension, heart failure, asthma, bronschospastic disease and sickle cell anaemia.
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How is vascular smooth muscle contraction initiated via the cAMP pathway (less typical)?
Ach binds to endothelium, activating IP3 --> binds to Ca2+ channels on SR --> activates anachidronic acid --> stimulates COX to produce prostaglandins I+E --> activate adenylate cyclase in smooth muscle --> PKA (via cAMP) reduces Ca2+/inhibits MLCK
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How is blood pressure normally expressed?
As systolic pressure/diastolic pressure (e.g. 120/80mmHg)
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How acn blood pressure be calculated?
Via a rearrangement of Ohms law (Diff P = F x R)
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What factors cause blood pressure to vary?
Emotional state, activity and level of health
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How is blood pressure measured using a Korotkov sphygomamometer?
Cuff at top of arm inflated to stop blood flow (so no sound when stethoscope over brachial artery) --> pressure drops below 120mmHg so flow obstructed, creating Korotkov sounds when artery oscillates --> pressure reduces and flow free so sounds stop
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How is blood pressure controlled in the short term?
This is achieved by a reflex response, where receptors (baroreceptors/chemoreceptors) in arterial walls synapse in ventral horn of spinal cord, signalling efferents to send impulses to the smooth muscle of the tunica media. It is active in secs/mins.
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What are the features of baroreceptors?
Stretch receptors, detect between 60-100mmHg, in carotid sinus (of internal carotid), arch of the aorta and bifurcation of common carotid. Send impulses to medulla, in turn sends to SAN (para and sympa) and ventricles/tunica media (symp).
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What are the features of chemoreceptors?
Less impact on short term BP control than baroreceptors - present in coronary sinus and arch of aorta, sensitive to pH, maintain BP between 40-60mmHg
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What is the ischemic nervous response to maintain blood pressure?
Acts in severe wounds/disease when blood pressure drops below 40mmHg (so not sensed by baro/chemoreceptors) and causes extremely low BF to the brain
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How is blood pressure controlled in the long term?
Via the renin-angiotensin pathway generating angiotensin II when low tubular pressure is detected by macula densa cells. However, requires long time to create an effect.
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How does angiotensin II increase blood pressure?
Increases sympathetic innervation to the heart so bpm increases. In smooth muscle binds to receptor on Gg-linked channels, stimulating phospholipase C; activates PIP2 to form DAG (stays at membrane as hydrophobic) and IP3 (goes to SR to release Ca2+)
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Why is blood pressure lower in the capillaries?
To increase time for transport and prevent rupture
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Where doess the cardiovascular centre (CVC) of the medulla recieve signals from?
Cerebral cortex, limbic system, hypothalamus, proprioceptors, chemoreceptors and baroreceptors
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How does the cardiovascular centre initiate sympathetic and parasympathetic responses?
Sympathetic via release of catecholamines (dopamine in the CNS, nor-adrenaline in the CNS and PNS - bind to adrenergic receptors) and parasymapthetic via release of acetylcholine (binds to muscarininc receptors)
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What sympathetic response does the CVC cause in vascular smooth muscle?
Catecholamines bind to either 1) Gg alpha-1 to activate phospholipase C (activates IP3 so constriction) 2) Gi alpha-2 to inhibit adenylate cyclase (constriction as no PKA) or 3) Gs beta receptors to activate adenylate cyclase (PKA so dilation)
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What sympathetic response does the CVC cause in cardiomyocytes?
Catecholamines bind to Gs coupled beta receptors to activate adenylate cyclase; PKA produced phosphorylates PLB so SERCA can operate to more rapidly remove Ca2+ (increasing HR and contractile force)
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What parasympathetic response does the CVC cause in vascular smooth muscle?
Ach binds to muscarinic Gq coupled M3 receptors to activate phospholipase C (generating IP3 so contraction)
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What parasympathetic response does the CVC cause in cardiomyocytes?
Ach binds to muscarinic Gi coupled M2 receptors to inhibit adenylate cyclase; this reduces PKA so PLB not posphorylated, meaning SERCA inactive (so slower removal of Ca2+ reduces HR and contractile force)
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How is venous return maintained?
Mainly by the skeletal muscle pump (muscle contraction in exercise) and respiratory pump. Also maintained by gravity (in upper extremities passing blood to superior vena cava), valves and venous smooth muscle contractions (mainly in abdomen).
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How does the respiratory pump operate to maintain venous return?
In inspiration pressure in abdomen increased so veins compressed and pressure drop in pleural cavities pulls blood into inf vena cava. In expiration raised pressure/shrinkage of thorax pushes blood into RA from sup vena cava.
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Other cards in this set

Card 2

Front

Why does hypoxia lead to hypercapnia?

Back

Hypoxia (low O2 supply) leads to hypoxaemia (low plasma O2) and then hypercapnia when less CO2 is removed by Hb due to reduced blood flow

Card 3

Front

What occurs in hypoxic pulmonary vasoconstriction?

Back

Preview of the front of card 3

Card 4

Front

What is hypoxic systemic vasoconstriction?

Back

Preview of the front of card 4

Card 5

Front

What is the tunica intima?

Back

Preview of the front of card 5
View more cards

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