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Cardiac Flashcards

(53 cards)

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1
Q

Which pathway is linked to heart development

A

Wnt/B catenin pathway

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2
Q

What happens when Wnt pathway is activated

A

Heart cells formation is blocked

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3
Q

How is Wnt pathway blocked?

A

Node releases proteins which blocks this pathway, so heart cells can now form proprely

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4
Q

What are the stages of heart formation

A

1- Starts as a long tube
PHF- makes the first part of cell
SHF- adds more parts later
2- Tube grows and bends
3- Helper cells (neural crest cells) move into the heart and separate tubes into 2 parts: 1 into lungs, 1 into heart
4- Heart splits into 4 chambers
5- Vessels form

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5
Q

Which gene is associated with heart development

A

NKX2-5
When this is mutated, it can’t bind to the dna
As a result important genes cant be turned on
This leads to congenital heart defect

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6
Q

NKX2-5 is involved in?

A

Atrial septation, ventricle septation and great blood vesells formation

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7
Q

Risk factors of Congenital HD?

A

1- Family history and genetics
2- Turner, Down’s Syndrome, Phenulketonuria
3- Alcohol intake during preg or exposure to smoke
4- Medicines like ACE inhibitors for high blood pressure, retinoic acids, anti-seizure medicines and ibuprofen
5- Diabetes
6- Cousin marriages

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8
Q

Treatments for CHD?

A
  • If CHD is not severe, the patient may have regular check-ups
    -If it is severe, surgery or a catheter (small thin tube into a blood vessel)
    -Medications like duireetics help remove extra water from the body, making it easier to breathe and Dixogin slows down the heart and makes the heart beat stronger
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9
Q

What is tetralogy of fallot?

A

Means there are 4 things wrong with the heart:
1) Ventricular Septal defect
There’s a hole between the two bottom chambers (ventricles).
➔ Blood mixes between right and left sides
2- Pulmonary stenosis- path to the lungs is narrowed
3- Overrding aorta- Aorta is sitting in the wrong place, taking blood from both sides of the heart
4- Right ventricular hypertrophy- right ventricle gets thick as its working hard to pump blood to the narrow lung valve

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10
Q

Does heart generates its own electrical stimulation

A

yes

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11
Q

What is the SA node?

A

Primary pacemaker of the heart
Initiates all heartbeats and controls heart rate

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12
Q

Where are pacemaker cells found

A

SA node
AV node
Bundle of his
These do not require external stimulus to trigger an action potential, they are capable of triggering their own

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13
Q

What are 3 phases of pacemaker action potentials

A

Phase 4- pacemaker potential
Phase 0- depolarisation
Phase 3- Repolarisation

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14
Q

Define pacemaker potential (-60)

A

The inside of the membrane is more negative, compared to outside.
Na+ ions leak into the cell through funny channels, making inside more positive.
The membrane potential steadily becomes more positive, until it reaches a certain threshold (-40) that triggers the next phase.

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15
Q

Define depolarisation
(+10)

A

Membrane potential increases sharply.
Rapid influx of Ca2+ ions through Ca+ channels, which causes rapid depolarisation

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16
Q

Repolarisation

A

Membrane potential returns to a negative resting state.
K+ channels open to flow K+ ions out of the cell, which causes the cell to become more negative, resulting in repolarisation

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17
Q

How many stages do cardiac myocytes have?

A

5 phases:
Resting potential
Depolarisation
Initial repolarisation
Plateu
Final depolarisation

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18
Q

Define resting membrane potential?

A

Cell is at rest and not actively firing an action potential
Resting potential is at -90mV.
The inside is more negative due to K+ ions, while the outside is more positive due to Na+ and Ca2+

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19
Q

Define depolarisation

A

Na+ channels open, allowing Na+ ions in, making the inside of the cell more positive.
From -90 to +40

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20
Q

Define initial repolarisation

A

Na+ chanels close.
K+ ions channels open, allowing K+ to flow out of the cell.
Membrane potential returns to more - value, but doesn’t yet reach resting potential

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21
Q

Define plateu

A

Cell remains depolarised for a longer time, important for sustaining contraction.

Ca2+ is open allowing Ca2+ to enter inside.
The influx of Ca2+ ions inside is maintained by outflow of K+ ions out
remains stable at 0 mV

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22
Q

Define repolarisation

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A

Ca2+ channels close while K+ remain open
Membrane potential becomes negative again (-90)

23
Q

Diff between absolute and relative refractory period

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A

Absolute- the time in which no new action potential can be initiated as Na+ channels are inactive
Relative- another action potential can be activated but requires stronger than normal stimulus as Na+ are already open

24
Q

What does ECG measure?

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A

electrical impulses which trigger the heart to contract

25
What does P wave suggest
Atrial depolarisation (atrial contraction)
26
What does QRS wave suggest?
Ventricular depolarisation (ventricles contracting)
27
What does T wave represent
Ventricular repolarisation
28
Define atrial fibrillation
Atrial fibrillation is when the heart beats irregularly and too fast
29
What happens in atrial fibrillation
Normally the SA node sends organised, regular electrical impulses to make atria contract properly. In Afib, atria have random electrical signals coming through, causing irregular contractions.
30
Which wave is not seen in afib?
P wave
31
Risk factors for AFib?
Old age Family history and genetics Lifestyle factors i.e. alcohol intake, smoking, stress Medical conditions like CKD, diabetes, obesity Over the counter med Surgery
32
Treatments for Afib?
Treating the underlying cause i.e. if due to overactive hyperthyroidism- curing it may also cure Afib Medicines to reduce the risk of stroke as blood clots can form Restoring normal heart rate through beta-blockers (heart rate should be 90 min when resting) Restoring rhythm through anti-arrynthymic drugs like flecainidine Procedures: Electrical Cardioversion - shock the heart to resit it back to normal rhythm Catheter ablation- insert into heart and burn small areas causing abnormal signals Pacemaker
33
Define ventricular fibrillation
Abnormal heart rhythm that makes ventricles contract in a rapid and uncoordinated manner, resulting in no blood being pumped at all to the body
34
Which waves are absent in ventricular fibrillation
All waves are disorganised
35
Risk factors for ventricular fibrillation
Heart diseases like heart attack or angina- diseases which change the structure of heart by making it walls thicker or weaker Other arrhythmias Heart surgery Medications Electrolyte imbalance- too low or too high K in the blood Electrical shock Being hit in a chest with small-fast moving objects
36
Treatments for VFib
Automated External Defibrillator- delivers a shock to stop inorganised electrical activity and resarts the normal rhythm (Without the shock, VFib is fatal) if given within 3 minutes it can increase survival rates upto 95%. Antiarrhythmic medications Implanted devices- Most people who suffer from Vfib, have ICD placed which can detect arryhtmias and deliver electral shock to resort the heart to normal rhythm
37
Clinical consequences of AFib
Blood clots in heart rate Increased risk of stroke, heart failure Fast, pouding hearbeat Shortness of breath
38
Clinical consequences of VFib?
Ventricles not pumping blood at all Sudden cardiac arrest, causing death in a few mins without proper care
39
Features of skeletal muscle
Striated Multi-nucleated Attached to skeleton Voluntary
40
Features of cardiac msucle
Striated Multi-nucleated Branched Involunatry In the walls of heart
41
Define cardiomyopathy
Diseases of the heart muscles, where the walls of the hearts become thickened, weake or stiffer
42
Dilated cardiomyopathy (most common)
When the heart chambers especially, LV becomes enlarged and weaker
43
Hyperthrophic cardiomyopathy
LV becomes thickened, walls become thickened
44
Restrictive cardiomyopathy
Heart walls are stiffened
45
Arrhythmogenic right ventricular cardiomyopathy
Irregular rythms and fibrous scarring especially in RV
46
Takotsubo
Temporary heart dysnfunction after emotional or physical stress
47
Define cardiac remodelling
structural and functional changes in hearts size, shape and function after injury or stress
48
What happens in remodelling
After injury, heart cells die Compensation through: Surviving muscle cells become bigger (hypertrophy) Heart walls stretch to maintain stroke volume Over time ➔ fibrosis builds up ➔ heart becomes stiff, inefficient ➔ heart failure
49
Eccentric vs concentric hypertrophy
E- heart muscle fibres stretch and the heart chamber increases in size C- heart muscles become thicker without change in size of heart chamber
50
Risk factors for heart failure
CHD Heart valve disease HBP Arrhythmias CHD- congenital diabetes and obesity Viral infections Old age Alcohol use Smoking Some medications used to treat diabetes increase the risk of HF. Nonsteroidal anti-inflammatory drugs can also increase HF
51
Treatments for HF
lifestyle changes Medicines- diuretics, beta-blockers, vasodilators Devices implanted into heart to control rhythm Surgery
52
Symptoms of HF
Heart does not supply enough blood to meet your body's needs. - Shortness of breath with activity or when lying down. - Fatigue and weakness. - Swelling in the legs, ankles, feet and belly area. - Rapid or irregular heartbeat. - Reduced ability to exercise. - Very rapid weight gain from fluid buildup. - Nausea, fainting and lack of appetite. - Difficulty concentrating or decreased alertness. - Chest pain if heart failure is caused by a heart attack.
53
What organs can HF affect
Kidney damage or failure. Heart failure can reduce the blood flow to the kidneys. Untreated, this can cause kidney failure. Kidney damage from heart failure can require dialysis for treatment. Other heart problems. Heart failure can cause changes in the heart's size and function. These changes may damage heart valves and cause irregular heartbeats. Liver damage. Heart failure can cause fluid buildup that puts too much pressure on the liver. This fluid backup can lead to scarring, which makes it more difficult for the liver to work properly. Sudden cardiac death. If the heart is weak, there is a risk of dying suddenly due to a dangerous irregular heart rhythm.

Cellular Science (11 decks)

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