Review posters 06/05/2016 Flashcards

1
Q

Which nerve has the parasympathetic supply to the heart?

A

Vagus

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2
Q

Which neurotransmitter is released on parasympathetic stimulation and where does it act?

A

Neurotransmitter is acetyl choline. It acts on M2 muscirinic receptors.

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3
Q

What does stimulation of the parasympathetic supply to the heart cause?

A

Decreased heart rate and increased AV nodal delay

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4
Q

Name and describe the constant influence the parasympathetic nerves have on the heart?

A

Vagal tone- constantly over the SA and AV node. Brings intrinsic heart rate down from 100bpm to 70bpm.

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5
Q

Stimulation of the sympathetic supply to the heart.

A

Causes increased HR and decreased AV nodal delay. Also increases the force of contraction

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6
Q

Where do the sympathetic nerves supply?

A

Myocardium, AV node and SA node

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7
Q

Where do the parasympathetic nerves supply?

A

AV and SA node.

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8
Q

Name the neurotransmitter and the receptor to which it binds in the sympathetic supply to the heart

A

Nor-adrenaline

Binds to b1 adrenoceptors.

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9
Q

Name the 5 stages of the cardiac cycle

A
Passive filling
Atrial contraction
Isovolumetric ventricular contraction 
Ventricular ejection
Isovolumetric ventricular relaxation.
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10
Q

Describe passive filling

A

Pressure in atria and ventricles close to 0. Atrioventricular valve (mitral or tricuspid) open. Blood flows from SVC and IVC straight into ventricles. They become 80% filled.

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11
Q

Describe atrial contraction

A

To get the remaining 20% of the blood from the atria to the ventricles, the atria contract. This completes the end diastolic volume.

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12
Q

Describe isovolumetric ventricular contraction.

A

Ventricles begin to contract. When pressure in the ventricles rises above the pressure in the atria- the AV valves close. The aortic/pulmonary valves are also closed so the ventricles are a closed space.

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13
Q

Ventricular ejection

A

When the pressure in the ventricles exceeds the pressure in the aorta- the aortic/pulmonary valve opens and the blood leaves the ventricles.
Stroke volume is ejected by each ventricle.
The blood left behind is the end systolic volume.

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14
Q

Isovolumetric ventricular relaxation

A

The ventricles start to relax so the pressure in the ventricles starts to decrease. The aortic/pulmonary valve shut and the AV valves open when the pressure in the ventricles is less than the pressure in the atria.

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15
Q

JVP

A
a= atrial contraction
c= tricuspid valve bulging into the ventricles when the ventricles contract
v= rise in atrial pressure during atrial filling
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16
Q

Describe the general process of oxidative phosphorylation

A

Electrons are brought to the electron transport chain on NADH and FADH. Here, the electrons are released and travel down a series of complexes via a series of oxidation and reduction reactions. These reactions provide the energy to pump H+ ions against their concentration gradient across the mitochondrial membrane into the intermembranous space. The final electron acceptor in the chain is oxygen which is reduced to form water.
The H+ ions then flow back down the concentration gradient through ATP synthase, phosphorylating ADP to ATP.

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17
Q

How does NADH and FADH get into the mitochondrial matrix from the cytoplasm?

A

Aspartate malate co-transporter.
Oxaloacetate and NADH combine to form Malate. Malate is then transported into the mitochondrial matrix where it breaks back down into oxaloacetate and NADH.

18
Q

Why do we need NADH and FADH in the mitochondrial matrix?

A

NADH cannot cross the lining

Also NAD+ can’t be used in oxidative phosphorylation.

19
Q

How are NADH and FADH linked to ATP?

A

Electron transfer from NADH and FADH ultimately is converted to the phosphoryl transfer of ATP

20
Q

What is a redox potential?

A

Reduced substance (X)- tendency to release electrons in comparison with hydrogen (h2)

21
Q

Describe trends in redox potentials and how they are related to E0

A

As the E0 becomes more negative- it is more likely to be oxidised- therefore acting as a reducing agent.
As the E0 becomes more positive- it is more likely to be reduced- therefore acting as a oxidising agent.

22
Q

What are the two steps to oxidative phosphorylation and what do they consist of?

A

Electron transfer- electrons from NADH and FADH ultimately transferred to O2.
Respiratory chain
Energy used to pump H+

ATP synthesis- electrochemical gradient of H+
Flow through ATP synthase energy used to phosphorylate ADP

23
Q

What are cytochromes?

A

Proteins with haem groups. Haem groups contain iron which can reversibly bind to electrons.

24
Q

Which complex does NADH release its electrons too?

A

1

25
Q

Which complex does FADH release its electrons too?

A

2

26
Q

Which complexes are cytochromes?

A

3 and 4

27
Q

Which complex does not pump H+ across the membrane?

A

2

28
Q

How does ATP synthase convert the flow of H+ to phosphorylating energy?

A

Flow of protons turns the rotor (made up of gamma, e and c subunits). This produces energy

29
Q

Uncoupling protein

A

Allows ‘short circuiting’ of the mitochondrial respiration.

30
Q

Where is uncoupling protein found?

A

Brown adipose tissue. Used in hibernating animals and newborns.

31
Q

Neural control of respiration

A

Pre-botzinger complex (in the medulla) stimulates rhythm. This causes the dorsal respiratory group of neurones to fire action potentials to the muscles of inspiration.

32
Q

What happens if the dorsal respiratory group fire too often (hyperventilation)?

A

This stimulates a second respiratory group of neurones called the ventral respiratory group- they fire action potentials which stimulate accessory muscles and cause a forced expiration.

33
Q

What role does the PONS play in respiration?

A

PONS alters signals. Pneumotaxic centre will be stimulated to stop long periods of inspiration with short expiratory gasps (apneusis). The apneustic centre does the opposite.

34
Q

How are the respiratory sensors influenced?

A

Stretch receptors (Hering Bruer reflex)
Joint receptors (movement of joints increases breathing)
Juxtapulmonary receptors (stimulated by pulmonary cappilary congestion or oedema)
Baroreceptors
Higher brain influence

35
Q

How does exercise influence respiration?

A
Increased joint movement- increases breathing
Adrenaline release
Accumulation of carbon dioxide
Increased body temp
Cerebral cortex
36
Q

Cough reflex

A
Short inhalation
Followed by closure of the trachea
Contraction of abdominal muscles
Opening of the trachea
Sharp expiration
37
Q

What is the hypoxic drive?

A

Driven by peripheral chemoreceptors. When O2 saturations in the blood get below 8kpa. Important in patients with COPD

38
Q

Hypercapnia and ventilation

A

Fast response- as carbon dioxide levels rise, ventilation increases massively

39
Q

Hypoxia and ventilation

A

O2 levels become very low before the peripheral chemoreceptors catch on- not as reactive to oxygen as it is to carbon dioxide.

40
Q

Acute effects of altitude training

A

Decreased partial pressure of oxygen means that hyperventilation and increased cardiac output occur.

41
Q

Chronic effects of altitude training

A

increased RBC
Increased mitochondria
Increased capillaries
Increased 2-3 BPG