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KHI > Sean power > Flashcards

Sean power Flashcards

1
Q

Describe cardiac muscle

A

*An involuntary muscle
* Muscle fibres are branched and surrounded by endomysium.
* numerous nuclei - dependance on aerobic metabolism
*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.

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2
Q

Describe the intercalated disk

A
  1. Adherens Junctions:
    -Forms a “belt around cells” holding them
    together.
    -Cadherin attached to actin filaments
    -Anchorage site for actin
  2. Gap Junctions:
    -Formed by connexons made of connexin proteins.
    -Allows passage of small molecules only
    -Allows for rapid propogation of action potentials
  3. Desmosomes:
    -Cadherin linker proteins between adjacent plasma membranes.
    -Attached to intercellular keratin intermediate filaments.
    -Prevents separation of myocytes during contraction
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3
Q

Describe the pathway relaying cardiac ischemia pain

A

*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.

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4
Q

What is the most sensitive protein measured to detect MI?

A

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 24-48 hours and remain elevated for 7-10 days.

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5
Q

Creatinine kinase and MI

A

Creatinine kinase also found in skeletal muscle/brain

More specific is the creatinine kinase-myocardial isoform

Rise 2-4 hours
Peak - 24
normal: 48-72hr

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6
Q

Give 2 options for reperfusion of coronary artery during STEMI

A

Pharmacological: Thrombolytics
Surgical: Percutaneous Coronary Intervention

Thrombolytics (fibrinolytic) should be used if time to PCI is > 90 mins.

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7
Q

MOA of thrombolytics

A

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)

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8
Q

What is meant by Prothrombin Time, how is it measured and what is the normal PT?

List 3 things that can affect PT

A

-Prothrombin time refers to how quickly a blood clot can form following initiation of coagulation with thromboplastin/tissue factor.

-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.
(4) Warfarin

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9
Q

What is meant by partial thromboplastin time, how is it measured and what is the normal PTT?

A

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

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10
Q

4 absolute contraindications to Thrombolysis

A
  1. Active bleeding
  2. Recent sx/trauma/head injury in last 3 weeks
  3. hx of intracranial haemorrhage
  4. Ischemic stroke in last 6 months
  5. GI bleed in last month
  6. CNS neoplasm
  7. Severe uncontrolled HTN
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11
Q

List 3 Nitrovasodilators and outline MOA

A

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.

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12
Q

List 4 anti-platelet drugs

A

Aspirin

Clopidogrel / Prasugrel

Abciximab

Used in conditions involving endothelial damage to prevent platelets from sticking to area of damage i.e. Ischemic heart disease

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13
Q

MOA of Aspirin (Anti-platelet)

A

-Irreversibly inhibits COX 1 through acetylation of serine residues.
-Inhibits prostaglandin, prostacyclin + TXA2 production
-Decreases platelet activation + inflammation.

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14
Q

MOA of Clopidogrel / Prasugrel (Antiplatelet)

A

-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

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15
Q

MOA abciximab (Antiplatelet)

A

G-IIb/IIIa receptor antagonist

-Prevents binding of fibrinogen
-prevents platelet aggregation + fibrinogen cross-linking

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16
Q

4 contraindications to anti-platelet drugs

A
  1. Acute bleeding
  2. Recent Sx
  3. Significant thrombocytopenia
  4. Hx of intracranial hemorrhage
17
Q

Name 2 groups of DOACS and drug examples for each

A
  1. Direct Xa inhibitors
    -Apixiban
    -Rivaroxaban
  2. Direct thrombin inhibitors
    -Dabigatron
18
Q

MOA of direct Xa inhibitors

A

Apixaban/ Rivaroxaban

-Binds to active site of Factor Xa
-stops the formation of pro-thrombinase complex.
-there prevents activation of prothrombin to thrombin.

19
Q

MOA of direct thrombin inhibitors

A

Dabigatron

-Directly inhibits activity of free and clot associated thrombin.
-Prevents activation fibrinogen -> fibrin as well as further activation of platelets, factors V, VIII, IX

20
Q

Morphological changes following MI

A

(1) 30mins - 4hours
–> Wavy muscle fibres
–> Sarcolemma disruption
–> Dense mitochondria

(2) 12-24 hours
–> Dark mottling
–> Coagulative necrosis
–> Eosinophils at infarct site

(3) 1-3 days
–> Mottling with yellow-tan appearance at centre of infarct
–> PMN infiltrate
–> Loss of nuclei + striations

(4) 3-7days
–> Hyperemic border
–> Dying neutrophils
–> Phagocytosis by macrophages

(5) 3 weeks
–> Granulation tissue in periphery of infarct
–> Necrotic debris removed
–> collagen deposition

(6) After 3 months
–> Scar tissue

21
Q

After how many minutes of onset of ischemia is there irreversible damage?

A

after 40mins

22
Q

After how many hours is there loss of tissue viability?

A

6-12hrs

23
Q

4 things affected stroke vol

A

(1) Cardiac size
(2) contractility
(3) Afterload
(4) Preload

24
Q

4 Signs of hyperkalemia on ECG

A

(1) Tall T waves
(2) Loss of P waves
(3) Broad QRS complex
(4) Ventricular fibrillation

25
Q

4 signs of hypokalemia on ECG

A

(1) U waves
(2) Small T waves
(3) Prolonged PR interval
(4) ST Depression

26
Q

Inferior wall/base of heart infarction - usually involves occlusion of what artery?

A

Rt coronary artery

27
Q

What does the ST region of an ECG represent?

A

The ST segment encompasses the region between the end of ventricular depolarization and beginning of ventricular repolarization on the ECG. In other words, it corresponds to the area from the end of the QRS complex to the beginning of the T wave.

28
Q

Explain the underlying physiology on an ST elevation

A
  • ST elevation on an ECG is indicative of a transmural infarction, meaning an infarct that affects the entire thickness of the heart wall.
  • This type of infarction disrupts the normal process of repolarization in the affected myocardial cells.
  • Normally, the ST segment represents the period when the ventricles are depolarized and beginning to repolarize. In the case of a transmural infarction, the injured myocardium remains depolarized even after the rest of the ventricles have started to repolarize. This discrepancy causes the ST segment to appear elevated on the ECG. Therefore, an elevated ST segment is a sign of incomplete and abnormal repolarization of the ventricular myocardium, typically indicating a significant myocardial injury such as a transmural infarction.
29
Q

list 4 complications of MI

A
  1. Arrythmias (especially ventricular)
  2. Rupture -> tamponade (usually 3-5 days)
  3. Embolism due to stasis in flow
  4. Heart failure due to “stunned myocardium” - impaired contractility
  5. Valve dysfunction
30
Q

outline the sequence of events leading to an MI

A
  1. Intraplaque hemorrhage or mechanical force results in atheromatous plaque disruption -> subendothelial collagen and necrotic plaque exposed to blood.
  2. Platelets adhere, activate and aggregate releasing ADP, TXA2 and serotonin -> occlusion and vasospasm
  3. Tissue factor exposure causes activation of coagulation -> growing thrombus
  4. Occlusion of blood flow causes switch from aerobic -> anaerobic respiration leading to depletion of ATP and build of lactic acid -> myocyte dysfunction and loss of contractility (within seconds)
  5. After 40 mins, irreversible injury occurs and the process of coagulative necrosis begins.

KHI (20 decks)

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