Sean power Flashcards
Describe cardiac muscle
*An involuntary muscle
* Muscle fibres are branched and surrounded by endomysium.
*Presence of sarcomeres gives striated appearance.
*Centrally located nuclei - mononucleated or binucleated
*T-tubules run along the sarcolemma to make contact with the sarcoplasmic reticulum
*Intercalated disks between the myocytes composed of 3 main parts:
–>Desmosomes
–>Adherens junctions
–>Gap junction.
Describe the intercalated disk
- Adherens Junctions:
-Forms a “belt around cells” holding them
together.
-Cadherin attached to actin filaments
-Anchorage site for actin - Gap Junctions:
-Formed by connexons made of connexin proteins.
-Allows passage of small molecules only
-Allows for rapid propogation of action potentials - Desmosomes:
-Cadherin linker proteins between adjacent plasma membranes.
-Attached to intercellular keratin intermediate filaments.
-Prevents separation of myocytes during contraction
Describe the pathway relaying cardiac ischemia pain
*Afferents from activated nociceptors in heart travel back to sympathetic trunk via C-fibres.
*They enter the cervical regions of the sympathetic trunk.
*They descend within the trunk to levels T1-T4 (sometimes T5)
*They then exit the trunk via the ramus communicans and enter the proximal portion of the spinal nerve at the level.
*They synapse on 2nd order neurons of the spino-thalamic tract within the dorsal horn of SC which then relay the information to the somatosensory cortex
*Because these synapse on the same 2nd order neurons as those relaying somatic pain, the brain cannot localise the location of initial visceral nociception activation.
*The pain is therefore perceived in the T1-T4(5) dermatomes.
What is the most sensitive protein measured to detect MI?
Cardiac troponins T + I
Most sensitive as it is specific to cardiac muscle and not found elsewhere.
Both Troponin T and I are involved in the contraction process of myocardium
Troponin levels begin to rise 2-4 hours from symptom onset, peak around 24 hours and remain elevated for 7-10 days.
Give 2 options for reperfusion of coronary artery during STEMI
Pharmacological: Thrombolytics
Surgical: Percutaneous Coronary Intervention
Thrombolytics (fibrinolytic) should be used if time to PCI is > 90 mins.
MOA of thrombolytics
Alteplase, Reteplase, Streptokinase
-Binds to fibrin component of clot
-Activates plasminogen which is then converted to plasmin
-Plasmin dissolves clot by degrading fibrin
- inactivates fibrinogen, prothrombin and factors V + XII
-Therefore increases PT (Prothrombin time) and PTT (Partial thromboplastin time)
What is meant by Prothrombin Time, how is it measured and what is the normal PT?
List 3 things that can affect PT
-Prothrombin time refers to how quickly a blood clot can form following initiation of coagulation with thromboplastin.
-Assesses function of Extrinsic + Common pathway
-Can detect abnormalities in Factors II, V, VII, X
-Normal PT is between 10-13s (INR 0.8-1.1) if not on anti-coagulant medication
(1) Liver disease
(2) Vitamin K deficiency
(3) Genetic abnormalities resulting in Factor deficiency.
What is meant by partial thromboplastin time, how is it measured and what is the normal PTT?
Partial thromboplastin time (PTT) refers to how quickly blood can form a clot following initiation of the intrinsic pathway of clotting cascade.
Assesses for function of all factors except VII and XIII
Calcium and activating substances (Kaolin and Cephalin) are added to sample to initiate the intrinsic pathway.
Normal time is around 25-35 s
4 contraindications to Thrombolysis
- Active bleeding
- Recent sx
- Recent hx of intracranial haemorrhage
- Severe uncontrolled HTN
List 3 Nitrovasodilators and outline MOA
Nitro-glycerine
Isosorbide Dinitrate
Isosorbide mononitrate
-Usually given sublingually
-Converted to Nitric oxide in the body
-Increases cGMP
-Inhibits inositol phosphate pathway
-inhibits calcium influx in SMC
-Inhibits myosin light chain kinase
-inhibts cross-bridge cycling and promotes vasodilaton.
List 4 anti-platelet drugs
Aspirin
Clopidogrel / Prasugrel
Abciximab
Used in conditions involving endothelial damage to prevent platelets from sticking to area of damage i.e. Ischemic heart disease
MOA of Aspirin (Anti-platelet)
-Irreversibly inhibits COX 1 + 2
-Inhibits prostaglandin, prostacyclin + TXA2 production
-Decreases platelet activation + inflammation.
MOA of Clopidogrel / Prasugrel (Antiplatelet)
-Irreversibly binds to receptor sites for ADP on P2Y12 (P2Y12 antagonist)
-This prevents ADP from binding thereby preventing GIIb/IIIa expression.
-Inhibits platelet activation +aggregation
MOA abciximab (Antiplatelet)
G-IIb/IIIa receptor antagonist
-Prevents binding of fibrinogen
-prevents platelet aggregation + fibrinogen cross-linking
4 contraindications to anti-platelet drugs
- Acute bleeding
- Recent Sx
- Significant thrombocytopenia
- Hx of intracranial hemorrhage
