Cardiology 2

Question 1

What triggers intracellular Ca release to induce contraction of cardiac muscle?

Answer 1

Ca entry through L-type channels binds A-site on Ryr

Question 2

Describe the two binding sites on the Ryr that allow Ca release to be stopped

Answer 2

I1=low affinity inhibition therefore prolonged block

I2= high affinity inhibition therefore transient block

Question 3

What trigger malignant hyperthermia?

Answer 3

volatile anestic binding to unstable Ryr

Question 4

The hypercatabolic state seen in Ryr leak is caused by a mutation in?

Answer 4

Ryr itself and NOT in the L-type sodium channel or Na channel (these more rare)

Question 5

The hyperthermia seen in malignant hyperthermia is caused by

Answer 5

excessive muscle contraction (body temp goes up) in an uncontrolled fashion

Question 6

Signs of malignant hyperthermia include?

Answer 6

tachycardia/arrythmias
skeletal muscle spasm
rapid breathing
metabolic/respiratory acidosis
hypertension followed by hypotension

Question 7

What is dantrolene used to treat

Answer 7

Malignant hyperthermia caused by a mutation in the Ryr

Question 8

How does dantrolene work to treat malignant hyperthermia?

Answer 8

binds to and stabilizes Ryr (therefore if issues is with L-type Ca channels then the dantrolene won’t be effective)

Question 9

Does the Na/Ca exchanger increase or decrease in heart failure?

Answer 9

Increase because Na/Ca exchangers are expressed more during heart failure

Question 10

Explain Ca activation

Answer 10

Ca comes from SR and binds troponin C which releases troponin I block so myosin is able to weakly bind

Question 11

Cross bridges

Answer 11

1. blocked- no Ca actin and myosin separate
2. Ca binds TnC, myosin bindin site exposed
3. Myosin binds actin (initially weak)
4. Myosin adjusts link with actin- strong
5. myosin consumes ATP and energy drives head forward
6. either Ca falls off and myosin binding site blocked again OR if still on will restart actin/myosin binding

Question 12

DCM can be treated with?

Answer 12

Ca sensitizers (pimobendan)- it rescues force impairment of myofilaments

Question 13

What is impaired in DCM?

Answer 13

myofilament force

Question 14

How did the get dATP into the heart

Answer 14

took virus carrying R1R2 and insert it into cells and produce more R1R2 enzyme - get more dATP and when get more dATP get an increase in contractibility

Question 15

An increased in dATP from __% to __% can rescue function of myofilaments in canine DCM

Answer 15

1% —> 2%

Question 16

Mitral valve regurgitation disease

Answer 16

• excess CT stiffens valve
• stiff valves that do NOT seal
• strain on chordae tendonae may rupture

Question 17

Describe all 4 stages of MVR disease

Answer 17

Stage A- at high risk for developing disease but have no identifiable disorder
Stage B- structural heart disease but no clinical signs
Stage C- clinical signs of heart failure
Stage D- clinical signs of heart failure and refractory to standard treatments

Question 18

Stage C heart failure treatment? Stage D

Answer 18

Stage C- ACE inhibitors, pimobendan, furosemide

Stage D- no consensus, increased furosemide and pimobendan

Question 19

How are distended chordae repaired in Japan?

Answer 19

replaced with expanded polytetrafluorethylene (ePTFE)