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Medicine Foundation + Case 1 > Case 1 - The heart > Flashcards

Case 1 - The heart Flashcards

1
Q

What is the smooth area of the atria called?

A

Sinus venarum

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2
Q

What do the primary and secondary heart field and the cardiac neural crescent cells do?

A

PHF- forms the heart tube
SHF- adds to the heart
CNCC- migratory and form the septa and vessels

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3
Q

What are the fetal cardiac shunts?

A

Foramen ovale- between 2 atria

Ductus arteriosus- between pulmonary artery and aorta

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4
Q

What is tetralogy of fallot?

A

VSD, over-riding aorta, hypertrophy of RV and pulmonary stenosis.

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5
Q

What is the oblique sinus?

A

The reflection surrounding the veins.

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6
Q

What is the transverse sinus?

A

The hole between the 2 sites of reflection.

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7
Q

What does the right coronary artery supply?

A

RV, RA, AVN, SAN, interatrial septum and part of LA, LV and interventricular septum.

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8
Q

What does the left coronary artery supply?

A

Most of the LA, LV, interventrivular septum and AV bundle.

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9
Q

Describe the action potential of a SAN cell.

A

The funny sodium channels open at -60, so sodium moves into the cell and you get slow depolarisation. When it reaches the threshold the L type VG calcium channels open and calcium moves in and you get an action potential. When it reaches 0 the calcium channels close and potassium channels open and the cell is repolarised.

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10
Q

How does the parasympathetic NS slow the heart rate?

A

It activates special potassium channels which increase the movement of potassium so it takes longer to reach the threshold.

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11
Q

Describe the action potential of a ventricular muscle cell.

A

Sodium channels open and the cell is depolarised then starts to repolarise. Then the calcium channels open and calcium moves in so the graph plateus as you get contraction. The calcium channels then close and potassium ones open and the cell is repolarised.

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12
Q

What are the 5 types of cardiomyopathy?

A

Dilated, restrictive, hypertrophic, arrhythmogenic and takotsubo.

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13
Q

What is the intrinsic mechanism for regulating contraction and why does it occur?

A

This suggests that the force of contraction is proportional to the initial fibre length in diastole. The more blood is in the heart, the more the fibres stretch so the bigger the next contraction. This occurs because increasing fibre length means there is more overlap of actin and myosin and also increased fibre length increases sensitivity of the contractile proteins to calcium.

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14
Q

What is the extrinsic mechanism for regulating contraction?

A

The sympathetic nervous system releases noradrenaline onto the cells which activates the cAMP second messenger system. Protein kinase A is activated which phosphorylates the L type calcium channels so they stay open longer, increase the amount of calcium coming out of the SR and increase actin myosin interactions.

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15
Q

What is hyperplasia?

A

An increase in the number of cells.

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16
Q

What is hypertrophy and atrophy?

A

Hypertrophy is an increase in the size of cells, atrophy is a decrease in the size of cells.

17
Q

What is metaplasia?

A

An abnormal change in the nature of cells.

18
Q

What are the causes of cell injury?

A

Hypoxia, infection, autoimmune, free radicals, irradiation and chemicals.

19
Q

How do free radicals cause damage?

A

They oxidise DNA, cell membranes and proteins meaning they don’t function properly.

20
Q

What is the response to sublethal injury?

A

It is reversible and includes cellular swelling and fatty change.

21
Q

What is necrosis?

A

Cell death, the cell swells and lysosomes burst open so the lysozymes start destroying the cell. The cell membrane bursts open and everything spills out.

22
Q

What is pyknosis?

A

When the nucleus thickens into a dense mass.

23
Q

What is apoptosis?

A

Active and controlled cell death, enzymes hydrolyse the cell and you get the formation of apoptotic bodies which are phagocytosed by neighbouring cells. There is no swelling and the cell membrane remains in tact.

24
Q

Where are the 6 chest electrodes placed in an ECG?

A 
V1- right 4th ICS
V2- left 4th ICS
V3- between V2 and V4
V4- 5th ICS, mid-clavicular line
V5- left anterior axillary line
V6- left mid-axillary line
25
Q

What view do you get from lead V1 and V2?

A

Septal view.

26
Q

What view do you get from lead V3 and V4?

A

Anterior view.

27
Q

What view do you get from lead V5 and V6?

A

Lateral view.

28
Q

What are the limb leads?

A 
Lead 1: LA-RA lateral view
Lead 2: RA-LL inferior view
Lead 3: LA-LL inferior view
avR: LA+LL-RA lateral view
avL: RA+LL-LA lateral view
avF: RA+LA-LL inferior view
29
Q

How do you know if the electrical activity is traveling towards the lead?

A

There will be a positive deflection or the R wave will be bigger than the S wave.

30
Q

How do you know if electrical activity is traveling away from the lead?

A

There will be a negative deflection or the S wave will be bigger than the R wave.

31
Q

How do atheroma’s develop?

A

First is endothelium dysfunction, the artery wall endothelium become damaged. Then oxidised lipoproteins enter the wall and this causes an inflammatory response. Monocytes arrive and become macrophages and try to digest the lipoproteins. The macrophages become foam cells. The foam cells degenerate and release their products which form the fatty streak which is a slightly elevated zone. The smooth muscle cells then migrate to the area and form a layer over the top containing lots of collagen, this is the advanced fibrinoid plaque. The plaque might then grow slowly or rupture and result in thrombosis.

32
Q

What are the main clinical effects of atheroma formation?

A

Heart disease (angina, MI), cerebrovascular disease (stroke, TIA), vascular dementia and peripheral arterial disease.

Medicine Foundation + Case 1 (4 decks)

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