Lecture 8 AI generated

Question 1

Describe the different types of muscle cells mentioned in the content.

Answer 1

The different types of muscle cells are skeletal muscle cells, smooth muscle cells, and heart muscle cells.

Question 2

Define myofibrils and sarcomeres.

Answer 2

Myofibrils are composed of proteins like actin, myosin, and titin, organized into thick and thin filaments called myofilaments. Sarcomeres are the basic contractile units of the myocardium.

Question 3

How do muscles contract according to the content?

Answer 3

Muscles contract by sliding the thick (myosin) and thin (actin) filaments along each other.

Question 4

Describe the composition of thin filaments in myofibrils.

Answer 4

Thin filaments consist primarily of the protein actin, coiled with nebulin filaments.

Question 5

Explain the structure of thick filaments in myofibrils.

Answer 5

Thick filaments consist primarily of the protein myosin, held in place by titin filaments.

Question 6

What is the role of myosin in muscle contraction?

Answer 6

Myosin is responsible for force generation in muscle contraction.

Question 7

Describe the role of calcium in muscle contraction.

Answer 7

Calcium ions bind to troponin, exposing binding sites for myosin heads to form cross-bridges with actin filaments, initiating muscle contraction.

Question 8

What is the function of ATP in muscle contraction?

Answer 8

ATP binds to myosin heads, breaking cross-bridges between actin and myosin, causing myosin heads to change position and move towards the next actin binding site.

Question 9

Define atrial fibrillation.

Answer 9

Atrial fibrillation is the most common heart arrhythmia characterized by rapid and irregular activation of the atrium.

Question 10

How does atrial fibrillation differ from a normal ECG?

Answer 10

Atrial fibrillation ECG shows more beats per minute and irregular PQRS compared to a normal ECG.

Question 11

Describe the risk factors associated with atrial fibrillation.

Answer 11

Risk factors for atrial fibrillation include obesity, diabetes, hypertension, valvular heart disease, heart failure, and chronic kidney disease.

Question 12

How should interventions for managing risk factors in atrial fibrillation be approached?

Answer 12

Interventions should be patient-centered, tailored to individual needs, and focus on lifestyle modifications and treatment targeting underlying conditions.

Question 13

Explain the mechanism by which myosin heads move actin filaments during muscle contraction.

Answer 13

Myosin heads bind to new actin sites, swivel, and return to their original conformation, dragging actin along the myosin in a sliding mechanism similar to how an oar propels a rowboat.

Question 14

Describe the different stages of atr fibrillation mentioned in the content.

Answer 14

The stages are normal, paroxysmal, persistent, long-standing persistent, and permanent.

Question 15

What are the current treatments mentioned for atrial remodelling in the content?

Answer 15

Electrical cardioversion or pharmacological cardioversion.

Question 16

Define atrial remodelling as per the content.

Answer 16

Atrial remodelling is defined as pathological changes in the atria (electrical, structural, and metabolic) that lead to the onset and progression of atrial fibrillation.

Question 17

How is structural remodelling described in the content?

Answer 17

Patients with permanent atrial fibrillation show structural changes in the cardiomyocytes, leading to contractile dysfunction and AF progression.

Question 18

Describe tachypacing as mentioned in the content.

Answer 18

Tachypacing is a rapid electrical stimulation used in experimental models for atrial fibrillation.

Question 19

What are the two models of tachypacing mentioned in the content?

Answer 19

Atrial cardiomyocytes and Drosophila prepupae.

Question 20

Describe the Drosoph model for atrial fibrillation (AF).

Answer 20

Drosophila is used as an in vivo model for AF, particularly in the prepupa stage where larvae are immobile and transparent, allowing observation of heart contractions.

Question 21

What is the role of contractile proteins in AF progression?

Answer 21

Reduced number of contractile proteins in patients with AF leads to contractile dysfunction and disease progression.

Question 22

How can the amount of contractile be measured in research studies?

Answer 22

The amount of contractile can be measured using antibodies in a western blot or through immunoflucent coloring.

Question 23

Define Heat Shock Proteins (HSP and their role in AF treatment.

Answer 23

HSP are proteins that to contractile proteins, stabilizing them. Increasing HSP levels can against myolysis in AF.

Question 24

What is the of diet in disease prevention according to the provided content?

Answer 24

The suggests that optimal prevention of diseases involves focusing on nutrition, highlighting the of diet over medication.

Question 25

How does glutamine supplementation benefit athletes to the content?

Answer 25

Glutamine supplements are taken by athletes prevent muscle breakdown and enhance immune system functioning during physical stress.

Question 26

role do Vitamin B3, C, and E play in AF prevention or according to the content?

Answer 26

Vitamins B3, C and E are suggested to potentially help in curing or preventing AF, as mentioned the content.

Question 27

Describe the role of NAD+ in metabolism.

Answer 27

NAD+ is a coenzyme present in all living cells that accepts or donates electrons in redox reactions, crucial for ATP production.

Question 28

What is the function of Poly-ADP-ribose polymerase (PARP) in relation to NAD?

Answer 28

PARP uses NAD as a substrate to produce poly ADP-ribose (PAR), with PARP1 being the primary enzyme consuming NAD.

Question 29

How does PARP activation impact cardiovascular diseases like AF?

Answer 29

PARP activation, triggered by DNA damage, leads to NAD depletion and is implicated in conditions such as Hypertrophy, Heart failure, and Myocardial ischemia/reperfusion.

Question 30

Define the protective role of Nicotinamide (PARP inhibitor) in AF.

Answer 30

Nicotinamide, a PARP inhibitor, safeguards against contractile dysfunction in models of AF by preserving NAD levels.

Question 31

Describe the relationship between AF, DNA damage, and atrial remodelling.

Answer 31

In AF, DNA damage can trigger PARP overactivation, leading to NAD depletion, which is essential for ATP production and ion channel function, ultimately contributing to atrial remodelling.