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Cardiology

   1. Regarding the electrical activity of the heart
      A. Under normal conditions, the SA node is the dominant pacemaker
      B. Vagal stimulation is negatively chronotropic
      C. Na+ is not required for cardiac action potential generation
      D. The AV node lies in the junction of the right atrium and the SVC
      E. The absolute refractory period follows the relative refractory period

   2. SA node
      A. The intrinsic discharge rate of the SA node is lower than the AV node
      B. Senile amyloidosis may cause sinus node dysfunction
      C. May be supplied by the right coronary artery
      D. SA node dysfunction causes sick sinus syndrome
      E. Sinus tachycardia is when the HR is >100

   3. Heart sounds
      A. S2 refers to the closure of the aortic and the tricuspid valves
      B. Splitting of the second heart sound may be physiological
      C. Splitting of the first heart sound may be physiological
      D. S3 is usually due to rapid ventricular filling in patients under 40
      E. S4 is associated with effective ventricular contraction

   4. Heart murmurs
      A. Can be graded from 0 to 5
      B. A grade 4 murmur can be felt as a thrill
      C. Vasalva murmur decreases the intensity of all murmurs
      D. Pansystolic murmurs are seen in VSD
      E. Middiastolic murmurs are typical of mitral stenosis

   5. The following are causes of atrial fibrillation
      A. Community acquired Pneumonia
      B. Hospital acquired pneumonia
      C. Hyperthyroidism
      D. Atrial myxoma
      E. Smoking

   6. Arrythmias
      A. Atrial flutter is seen as ‘regular sawtooth like’ activity on ECG
      B. Atrial fibrillation are uncommon following open heart surgery
      C. Wollf – Parkinson – White syndrome rarely causes arrhythmias
      D. Mobitz type I is associated with progressive prolongation of the PR interval
      E. First degree heart block may be 2:1 or 3:1

   7. Causes of displaced apex beat are
      A. Dextrocardia
      B. Splenomegaly
      C. Right ventricular hypertrophy
D. Left ventricular hypertrophy
    E. Fibrosis of left upper lung lobe

8. Kussmaul sign is seen in
   A. Cardiac tamponade
   B. Diabetic ketoacidosis
   C. Constrictive pericarditis
   D. Right ventricular myocardial infarction
   E. Restrictive cardiomyopathy

9. Atherosclerosis
   A. Usually develops over a period of months
   B. Homocysteine is protective against plaque formation
   C. Diabetes mellitus promotes plaque formation
   D. May present as intermittent claudication
   E. Statins do not help in increasing the HDL level

10. Ischemic Heart Disease
    A. Atherosclerotic plaques in the heart are commonly seen in the ant. descending coronary art.
    B. Percutaneous coronary intervention (PCI) is indicated in 3 vessel disease
    C. ST elevation is indicative of myocardial infarction
    D. All patients with IHD have stenotic lesions in their coronary arteries
    E. CABG has a higher risk of recurrence as compared to PCI

11. The following are true regarding cardiac tamponade
    A. Caused by neoplastic disease
    B. Presence of pulsus paradoxus
    C. ECG shows large QRS complexes
    D. There will be a drop in JVP
    E. A positive Kussmaul’s sign is sometimes present

12. Cardiomyopathies
    A. May be caused by systemic hypertension
    B. Refers to primary disease of the myocardium
    C. Clinically classified as dilated, obstructive and constrictive
    D. Duchenne progressive muscular dystrophy (DMD) may cause dilated cardiomyopathy
    E. A systolic murmur may be heard in hypertrophic cardiomyopathy

13. The following are risk factors for acute MI
    A. Ethnic origin
    B. BMI >30
    C. Active lifestyle
    D. Family history of premature CHD
    E. Low serum HDL

14. Cardiac markers
    A. Troponin C is used as a cardiac marker for AMI
    B. Myoglobin may be used as a cardiac marker of AMI
C. LDH is highly specific for myocardial infarction
    D. CKMB levels persist in blood longer than the cardiac troponin
    E. A single measurement of raised troponin is insufficient to diagnose AMI

15. The following are complications of thrombolytic therapy
    A. Allergic reactions
    B. Hypotension
    C. Deep Vein Thrombosis
    D. Bone fractures
    E. Bleeding

16. The following are clinical manifestations of heart failure
    A. Hepatomegaly
    B. Cachexia
    C. Cheyne – Stokes respiration
    D. Hepatojugular reflux
    E. Tachycardia
ANSWERS

1. Regarding the electrical activity of the heart
   A) T – In normal heart only one region demonstrates spontaneous electrical electrical activity (as
   pacemaker) (Human physiology Fox ,page 400)
   B) T – vagal activation  release Ach on SA node  decrease pacemaker rate. ( Essential human
   physiology, Amar Chartterjee.page 102)
   C) F – Entry of Na+ predominates and produces a depolarization of pacemaker. ( Human physiology
   Fox, page 400)
   D)F – AV node located at inferior portion of the interatrial septum. SA node is the one located in the
   right atrium, near the opening of SVC. ( Human physiology Fox, page 402)
   E) F – First is absolute refractory period, then relative refractory period. ( Human physiology Fox,
   page 402)

2. SA node
    A. false: The SA node, AV node and the remaining specialized conduction tissue of the heart but
        the SA node is the normal cardiac pacemaker as it is intrinsically faster       discharged rate
        PS: Clinical Anesthesia By Paul G. Barash, Bruce F. Cullen, Robert K. Stoelting, Michael Cahalan,
        P218
            http://books.google.com.my/books
    B. True: senile amyloidosis is an infiltrative disorder usually around 9th decade of life where the
        deposition of amyloid protein in atrial myocardium can result in SA node        dysfunction
        p/s: Harrison's Cardiovascular Medicine By Eugene Braunwald, Joseph Loscalzo, p134-135
        http://books.google.com.my/books
    C. True: SA nodes receive blood supply from sa nodal artery (branch of right coronary artery) in
        59% of patient, 38% patient received blood supply from left circumflex artery,          and 3%
        patient from both artery
        p/s :Hurst's the heart, Book 1 P894
        http://books.google.com.my/books?id
    D. True: sick sinus syndrome is result from fibrous tissue displacement in the SA node p/s:
        Harrison's Cardiovascular Medicine By Eugene Braunwald, Joseph Loscalzo, p134-135
        http://books.google.com.my/books?
    E. True: sinus rate acccelaration >100 is known as sinus tachycardia
        Kumar and clark, p716

3. Heart sounds
    A.      False: S2 is closing of aortic and pulmonary valve, or semilunar valve.
    B.       True: S2 splitting associated with inspiration is physiological. (in inspiration, the blood is
    more in
        R atrium but less in L atrium, t/fore, closer of P2 is delayed)
    C.      False: S1 is usually indicates abnormalities-RBBB, ebstein’s anomaly
    D.      True: S3 may normal in youngsters due to ventricular filling
    E.      False: S4 may heard in elderly due to rigid ventricle(hypertrophy).

4. Heart murmurs
    A. F – Grade 1 to 6 (Talley & Connor, 2nd Edition, pg.55)
    B. T – Grading of Murmur: (Talley & Connor, 2nd Edition, pg.55, Medical Secrets by Zollo, pg 64)
              1: very soft and barely audible intensity (only cardiologist can hear it)
2: soft and low intensity murmur (heard by experienced one)
                3: moderate murmur but no thrill (everyone can hear it)
                4: loud murmur with palpable thrill
                5: loud murmur (still require stethoscope to hear it)
                6: loudest murmur (heard without even placing the stethoscope)
    C. F – Valsalva maneuvers mean forceful expiration against closed glottis. Ask the patient to hold
       his nose, close the mouth and breath out hard and hold as long as possible. It will decrease
       preload thus reducing the intensity of murmur in case of aortic stenosis, mitral regurgitation and
       systolic murmur of hypertrophic cardiomyopathy (Talley & Connor, 2nd Edition, pg.55-56)
    D.      T – Other causes of pansystolic murmur: mitral regurgitation, tricuspid regurgitation, VSD,
            aortopulmonary shunt. (Talley & Connor, 2nd Edition, pg.53)
    E.      T – Mid-diastolic murmur: low pitch, due to impaired ventricular filling mitral stenosis,
       tricuspid stenosis, atrial myxoma (rare)


5. The following are causes of atrial fibrillation
   A. T – dalam infection, selalunye akan ade increase in catecholamine. Catecholamine ni terdiri
   daripada adrenaline and noradrenaline. 2 ekor makhluk ni akan exert sympathetic effect so dekat
   heart, mereka ni akan menyebabkan increase in the force of contraction
   of the heart increasing heart rate, blood pressure, and blood sugar. Tapi bile dah byk sgt 2 ekor ni,
   they can cause overcharging of the cardiovascular system, which can precipitate arrthymia. Sumber:
   http://www.zimbio.com/Catecholamine/articles/2/Beta+Blockers
   B. T – sama seperti di atas.
   C. T - Thyroid hormones upregulate sarcoplasmic Calcium ATPase, myosin heavy chain alfa, voltage
       gated K+ channels, Na+ channels and beta1 adrenergic receptors. These effects result in
       increased heart rate, systolic hypertension, increased ventricular contractility and cardiac
       hypertrophy. Changes in electrophysiological characteristics of atria result in dysrhythmias,
       especially atrial fibrillation, in patients with hyperthyroidism. Sumber:
       http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1431605/
   D. F – atrial myxoma is the commonest heart tumor walaupun heart tumor ni secara umumnya
       sangatlah rare. The most common heart tumor yg boleh present with AF is rhabdomyoma and
       fibroma. Ini kerana mereka ini akan men’damage’kan myocardium or conduction system.
       Sumber: http://resources.metapress.com/pdf-preview.axd?
       code=ekxjgn975qpmexrd&size=largest
   E. T – merokok boleh meningkatkan kandungan catecholamine di dalam darah. Maka, ape yg akan
       berlaku sama seperti di jawapan A tadi.
       http://www.nejm.org/doi/full/10.1056/NEJM197609092951101


6. Arrythmias
   A. True - ECG shows regular sawtooth-like atrial flutter waves
   (F waves) between QRS complexes <--K&C pg. 725
   B. False - Atrial fibrillation occurs in one-third of patients
       after coronary bypass surgery and in more than half of those
   undergoing valvular surgery <---K&C pg 724
   C. T – http://emedicine.medscape.com/article/159222-overview
   D. True -Mobitz I block (Wenckebach block phenomenon) is
       progressive PR interval prolongation until a P wave fails
to conduct. The PR interval before the blocked P wave
            is much longer than the PR interval after the blocked P wave <-- K&C pg 721

       E. False - 2nd degree <--K&C 721

   7. Causes of displaced apex beat are
      A. T : dextrocardia is congenital defect in which position of heart adalah mirror image of its normal
         position. Oleh it, secara automatic apex beat dia adalah displaced
      B. F: spenomegaly menghala kepada inferiomedially ke arah right iliac fossa. Oleh itu, apex beat
         xkan displaced.
      C. T: hypertrophy boleh menyebabkan displaced mengikut buku oxford text book of medicine 4th
         edition page 852 ataupun 2852. Xsure page yg exact coz ade copy online. Kat online die tulis
         P.2.852. Another source http://www.mediscuss.org/examination-cardiac-apex-beat-44.html
      D. T : sama seperti alasan di atas http://www.mediscuss.org/examination-cardiac-apex-
         beat-44.html
      E. T: fibrosis of left upper lung lobe akan menyebabkan mediastinal shift. Kalau ikut muka surat yg
         sama., maka jawapannya adalah true.

   8. Kussmaul sign is seen in
          a. T
          b. F
          c. T
          d. T
          e. T

   Kussmaul's sign is the observation of a rise in JVP on inspiration. Do not confuse with Kussmaul
   breathing, ie a deep and labored breathing pattern often associated with severe metabolic acidosis,
   particularly DKA but also renal failure.

   The classical differential diagnosis are constrictive pericarditis, restrictive cardiomyopathy, cardiac
   tamponade.
   (Ref: http://www.gpnotebook.co.uk/simplepage.cfm?ID=1369047062 )
   Cardiac conditions that may be associated with a positive Kussmaul's sign include right atrial myxoma,
   tricuspid stenosis, constrictive pericarditis, pericardial effusion, restrictive myocardopathy, and severe
   pulmonary hypertension. Overall, the commonest cause is severe right-sided congestive heart failure.
   (Ref: http://www.etsu.edu/com/medicalmystery/KussmaulsSign.aspx)

9. Atherosclerosis
   A. Usually develops over a period of months
      Ans = False
      Reference = Harrison vol II page 1501
      ATH occurs over a period of many years.

   B. Homocysteine is protective against plaque formation
      Ans = False
      Reference = Harrisons vol II page 1508 & http://www.medicinenet.com/homocysteine/article.htm
      Homocysteine is a naturally occurring amino acid found in blood plasma produced by the body, usu
      as a byproduct of consuming meat.
Increased homocysteine – lead to increased risk of ATH cause narrowing & hardening of the arteries.
   So, homocysteine is actually hazardous than protective
C. Diabetes mellitus promotes plaque formation
   Ans = True
   Reference = mama robin page 345 & John’s book of DM (http://books.google.com.my/books?
   id=ohgjG0qAvfgC&pg=PA870&lpg=PA870&dq=How+diabetes+mellitus+promote+plaque+formation
   &source=bl&ots=yIzn5AJ9Is&sig=VCD9rrPVL_ATe8GyZ5y5Zr0WVJ8&hl=en&ei=RUO-
   TaC6M8virAfNm-
   DtBQ&sa=X&oi=book_result&ct=result&resnum=6&ved=0CDMQ6AEwBQ#v=onepage&q&f=false)
   IN DM – thereis hyperglycemia & insulin resistance – lead to increased expression of (E-selectin,
   vascular-cell adhesion molecule-1 VCAM-1, intracellular adhesion molecule-1 ICAM-1) by
   endothelial cells….--- so, promote leucocyte infiltration into arterial wall (endothelial)…----then,
   leucocyte infiltrate into subendothelial by stimulation of monocyte chemoattractant protein-1
   (MCP-1)-----infiltrated monocyte differentiate into macrophages----!!!these are the proatherogenic
   effect by accumulating lipids & releasing proinflammatory cytokines and matrix metalloproteinase
   which likely promotes plaque formation & expansion.

D. May present as intermittent claudication
   Ans = True
   Reference= Harrison vol II page1501
   ATH occur in peripheral circulation can cause intermittent caludication

E. Statins do not help in increasing the HDL level
   Ans = False
   Reference = Harrisons vol II page 2427
   Statin= HMG-CoA reductase inhibitors
   Statin inhibit the HMG-CoA reductase – then inhibit the synthesis of cholesterol. At the same time,
   d/t decrease synthesis of cholesterol in the cell, in menyebabkan hepatic LDL receptor activity on
   the cell increasing & there is accelerated clearance of circulating LDL in the blood so that,
   cholesterol will be transferred in the cell.
   Meaning – main role of statin is LDL lowering agent, but can also reduce TG & have modest HDL
   raising effect.

    10. Ischemic Heart Disease
    A. Atherosclerotic plaques in the heart are commonly seen in the ant. descending coronary art.
        Ans = True
        Reference = Harrisons vol II page 1515
        Common seen in the ant descending artery (L)

    B. Percutaneous coronary intervention (PCI) is indicated in 3 vessel disease
       Ans = False
       Reference = harrisons vol II (page 1525 & 1526 –choice b/w PCI & CABG)
       PCI –ptnts w single @ 2 vessel dis w normal LV fx & anatomically suitable lesions
       CABG – 3 vessel dis @ 2-vessel dis that includes proximal L descending coronary a.

    C. ST elevation is indicative of myocardial infarction
       Ans = False
       Reference = harrisons vol II fig 239-1page 1532 & page 1534
MI can be STEMI @ NSTEMI. So, MI x semestinya ad ST elevation
          Cardiac trop-T(cTnT) & trop-I(cTnI) is indicative and can distinguish from UA & NSTEMI. Levels of
          cTnT and cTnI may remain elevated for 7-10 days after STEMI

    D. All patients with IHD have stenotic lesions in their coronary arteries
       Ans = False
       Reference = harrisons vol II page 1514
       Not all have stenotic lesion because some ptient w IHD can also be due to coronary spasm
       (prinzmetal’s variant angina)

    E. CABG has a higher risk of recurrence as compared to PCI
       Ans = false
       Reference = harrisons vol II page 1526
       PCI is higher compared to CABG

    11.   The following are true regarding cardiac tamponade
    A.    T. Caused by neoplastic disease
    B.    T. Presence of pulsus paradoxus
    C.    F. ECG shows large QRS complexes
    D.    F. There will be a drop in JVP
    E.    F. A positive Kussmaul’s sign is sometimes present

A. 1. “Malignant disease is the most common cause of pericardial effusion with tamponade.”
      http://emedicine.medscape.com/article/759642-overview
   2. “Neoplastic disease, particularly advanced, is the most frequent cause of tamponade in the
      hospitals.”       http://www.heartalex.com/alexheartfiles/undergraduate/lectures
%20notes/Pericardial%20          disease%20r.pdf
B. 1. “Blood pressure may fall (pulsus paradoxical) when the person inhales deeply.”
      http://www.nlm.nih.gov/medlineplus/ency/article/000194.htm
C. 1.  “Electrical alternans is pathognomonic of cardiac tamponade and is characterized by
      alternating levels of ECG voltage of the P wave, QRS complex, and T waves. This is a result of
      the heart swinging in a large effusion.” http://emedicine.medscape.com/article/759642-
      diagnosis
D. 1. “Elevation of jugular venous pressure with a prominent x descent and a diminutive or absent
      y descent”                 http://www.harrisonspractice.com/practice/ub/view/Harrisons
%20Practice/141253/1/cardi ac_tamponade
E. 1. “Kussmaul’s sign is not seen in patients with cardiac tamponade because even though the
      increase in pericardial pressure exerts an inward force compressing the entire heart during
      inspiration, the increase in negative intrathoracic pressure is still able to be transmitted to
      the right side of the heart and subsequent increase in blood flow to the right atrium
      ensues.” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757428/
12. Cardiomyopathies

A) T – http://www.mayoclinic.com/health/cardiomyopathy/DS00519/DSECTION=causesB) T – When
abnormality is primary in and localized to myocardium, the condition is called cardiomyopathy. ( Baby
Robbins Patho, page 307). Tapi, base on definition by AHA, it divides into primary and secondary..so
susah nak cakap, but ikut je definition Dorland, it is a primary disease
http://www.emedicinehealth.com/cardiomyopathy/page2_em.htm#causes
C) F – divided into dilated, hypertrophic and restrictive. ( Baby Robbins Patho, page 307)
D) T – The cause is frequently unknown (idiopathic dilated cardiomyopathy), but some pathology may
contribute, such as genetic defect for example X-linked cardiomyopathy (Duchenne and Becker muscular
dystrophies). ( Baby Robbins Patho, page 307)
E) T – Some of the classic physical findings are ejection systolic murmur (due to left ventricular outflow
obstruction) and pansystolic murmur (due to mitral regurgitation). ( Kumar&Clark Medicine, page 851)


13. The following are risk factors for acute MI
    a. False: no evidence regarding ethnic predisposition
            Ps: kumar and clark, p745
    b. TRUE : 5% male and 6% female death of CAD is due to obesity(bmi>30)
            Ps: kumar and clark, p746
    c. False: sedentary life style
            Ps: kumar and clark, p747
    d. True: first degree relative has developed ishaemic heart disease before age of 50
            Ps: kumar and clark, p745
    e. True: high serum cholesterol with low serum HDL associated strongly with coronary artheroma
            Ps: kumar and clark, p746

14. Cardiac markers
A.False: troponin C is associated with cardiac and skeletal muscle.so, its not used for myocardiac
damage
B.True: myoglobin can be used in it
C:False :LDH is not highly specific cardiac marker as troponin, they are also high in tissue breakdown and
hemolysis
D.False:CKMB persist for about 72 hrs. but troponin can last 7-10 days
E.False: regarding http://emedicine.medscape.com/article/811905-overview, some authorities have
called for a troponin standard alone and recommend eliminating CK-MB..(haa korang bace la sket)

15. The following are complications of thrombolytic therapy
    Thrombolytic therapy: a.k.a fibrinolytic  f(x): dissolve (lyse) blood clots eg: tissue plasminogen
        activator (tPA), streptokinase, urokinase. Complications include bleeding, allergic reactions
        (mostly streptokinase), emboli (http://med-lib.ru/english/oxford/thromb_ther.php: emboli,
        http://ezinearticles.com/?Complications-With-Thrombolytics&id=5367300 : allergic,
        https://www.vascularweb.org/vascularhealth/Pages/thrombolytic-therapy.aspx : hypotension)
A. T mostly streptokinase
B. T complication due to bleeding
C. F salah satu kegunaan thrombolytic utk treat DVT bukan nye thrombolytic menyebabkan DVT
D. F thrombolytic tk menyebabkan fracture!!!
E. T can occur at the site of drug administration, from other puncture sites, or from areas of recent
       surgery

16. The following are clinical manifestations of heart failure
A. T – selalunye berlaku dlm right sided heart failure. Akan ade engorgement of systemic and portal
    venous system. Sumber: papa robin page 563. Severe heart failure causes blood to back up from the
    heart into the inferior vena cava (the large vein that carries blood from the lower parts of the body
    to the heart). Such congestion increases pressure in this vein and other veins that carry blood to it,
    including the hepatic veins (which drain blood from the liver). If this pressure is high enough, the
    liver becomes engorged (congested) with blood and malfunctions. Sumber:
    http://www.merckmanuals.com/home/sec10/ch138/ch138g.html
B. T – wujud satu keadaan yg di panggil cardiac cachexia. Menurutnya, CHF akan menghasilkan TNF yg
    byk. Maka, TNF ini akan impair the synthesis or accelerate the catabolism of proteins in the skeletal
    muscle. Sumber: http://eurheartj.oxfordjournals.org/content/18/2/187.full.pdf
C. T – yes,boleh jd dlm severe heart failure. Sumber: kumar and clark page 688. Instability of
    respiratory control underpins the development of Cheyne-Stokes respiration and results from
    hyperventilation, prolonged circulation time, and reduced blood gas buffering capacity. Sumber:
    http://thorax.bmj.com/content/53/6/514.full
D. T –it is a reflection of a right ventricle that cannot accommodate augmented venous return. Sumber:
    http://www.amjmed.com/article/S0002-9343(00)00443-5/abstract
E. T – in order utk maintain CO, heart akan try utk beat faster.manifest as tachy. Sumber:
    http://www.aafp.org/afp/20000301/1319.html

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Ganyang MCQ Cardiology

  • 1. Cardiology 1. Regarding the electrical activity of the heart A. Under normal conditions, the SA node is the dominant pacemaker B. Vagal stimulation is negatively chronotropic C. Na+ is not required for cardiac action potential generation D. The AV node lies in the junction of the right atrium and the SVC E. The absolute refractory period follows the relative refractory period 2. SA node A. The intrinsic discharge rate of the SA node is lower than the AV node B. Senile amyloidosis may cause sinus node dysfunction C. May be supplied by the right coronary artery D. SA node dysfunction causes sick sinus syndrome E. Sinus tachycardia is when the HR is >100 3. Heart sounds A. S2 refers to the closure of the aortic and the tricuspid valves B. Splitting of the second heart sound may be physiological C. Splitting of the first heart sound may be physiological D. S3 is usually due to rapid ventricular filling in patients under 40 E. S4 is associated with effective ventricular contraction 4. Heart murmurs A. Can be graded from 0 to 5 B. A grade 4 murmur can be felt as a thrill C. Vasalva murmur decreases the intensity of all murmurs D. Pansystolic murmurs are seen in VSD E. Middiastolic murmurs are typical of mitral stenosis 5. The following are causes of atrial fibrillation A. Community acquired Pneumonia B. Hospital acquired pneumonia C. Hyperthyroidism D. Atrial myxoma E. Smoking 6. Arrythmias A. Atrial flutter is seen as ‘regular sawtooth like’ activity on ECG B. Atrial fibrillation are uncommon following open heart surgery C. Wollf – Parkinson – White syndrome rarely causes arrhythmias D. Mobitz type I is associated with progressive prolongation of the PR interval E. First degree heart block may be 2:1 or 3:1 7. Causes of displaced apex beat are A. Dextrocardia B. Splenomegaly C. Right ventricular hypertrophy
  • 2. D. Left ventricular hypertrophy E. Fibrosis of left upper lung lobe 8. Kussmaul sign is seen in A. Cardiac tamponade B. Diabetic ketoacidosis C. Constrictive pericarditis D. Right ventricular myocardial infarction E. Restrictive cardiomyopathy 9. Atherosclerosis A. Usually develops over a period of months B. Homocysteine is protective against plaque formation C. Diabetes mellitus promotes plaque formation D. May present as intermittent claudication E. Statins do not help in increasing the HDL level 10. Ischemic Heart Disease A. Atherosclerotic plaques in the heart are commonly seen in the ant. descending coronary art. B. Percutaneous coronary intervention (PCI) is indicated in 3 vessel disease C. ST elevation is indicative of myocardial infarction D. All patients with IHD have stenotic lesions in their coronary arteries E. CABG has a higher risk of recurrence as compared to PCI 11. The following are true regarding cardiac tamponade A. Caused by neoplastic disease B. Presence of pulsus paradoxus C. ECG shows large QRS complexes D. There will be a drop in JVP E. A positive Kussmaul’s sign is sometimes present 12. Cardiomyopathies A. May be caused by systemic hypertension B. Refers to primary disease of the myocardium C. Clinically classified as dilated, obstructive and constrictive D. Duchenne progressive muscular dystrophy (DMD) may cause dilated cardiomyopathy E. A systolic murmur may be heard in hypertrophic cardiomyopathy 13. The following are risk factors for acute MI A. Ethnic origin B. BMI >30 C. Active lifestyle D. Family history of premature CHD E. Low serum HDL 14. Cardiac markers A. Troponin C is used as a cardiac marker for AMI B. Myoglobin may be used as a cardiac marker of AMI
  • 3. C. LDH is highly specific for myocardial infarction D. CKMB levels persist in blood longer than the cardiac troponin E. A single measurement of raised troponin is insufficient to diagnose AMI 15. The following are complications of thrombolytic therapy A. Allergic reactions B. Hypotension C. Deep Vein Thrombosis D. Bone fractures E. Bleeding 16. The following are clinical manifestations of heart failure A. Hepatomegaly B. Cachexia C. Cheyne – Stokes respiration D. Hepatojugular reflux E. Tachycardia
  • 4. ANSWERS 1. Regarding the electrical activity of the heart A) T – In normal heart only one region demonstrates spontaneous electrical electrical activity (as pacemaker) (Human physiology Fox ,page 400) B) T – vagal activation  release Ach on SA node  decrease pacemaker rate. ( Essential human physiology, Amar Chartterjee.page 102) C) F – Entry of Na+ predominates and produces a depolarization of pacemaker. ( Human physiology Fox, page 400) D)F – AV node located at inferior portion of the interatrial septum. SA node is the one located in the right atrium, near the opening of SVC. ( Human physiology Fox, page 402) E) F – First is absolute refractory period, then relative refractory period. ( Human physiology Fox, page 402) 2. SA node A. false: The SA node, AV node and the remaining specialized conduction tissue of the heart but the SA node is the normal cardiac pacemaker as it is intrinsically faster discharged rate PS: Clinical Anesthesia By Paul G. Barash, Bruce F. Cullen, Robert K. Stoelting, Michael Cahalan, P218 http://books.google.com.my/books B. True: senile amyloidosis is an infiltrative disorder usually around 9th decade of life where the deposition of amyloid protein in atrial myocardium can result in SA node dysfunction p/s: Harrison's Cardiovascular Medicine By Eugene Braunwald, Joseph Loscalzo, p134-135 http://books.google.com.my/books C. True: SA nodes receive blood supply from sa nodal artery (branch of right coronary artery) in 59% of patient, 38% patient received blood supply from left circumflex artery, and 3% patient from both artery p/s :Hurst's the heart, Book 1 P894 http://books.google.com.my/books?id D. True: sick sinus syndrome is result from fibrous tissue displacement in the SA node p/s: Harrison's Cardiovascular Medicine By Eugene Braunwald, Joseph Loscalzo, p134-135 http://books.google.com.my/books? E. True: sinus rate acccelaration >100 is known as sinus tachycardia Kumar and clark, p716 3. Heart sounds A. False: S2 is closing of aortic and pulmonary valve, or semilunar valve. B. True: S2 splitting associated with inspiration is physiological. (in inspiration, the blood is more in R atrium but less in L atrium, t/fore, closer of P2 is delayed) C. False: S1 is usually indicates abnormalities-RBBB, ebstein’s anomaly D. True: S3 may normal in youngsters due to ventricular filling E. False: S4 may heard in elderly due to rigid ventricle(hypertrophy). 4. Heart murmurs A. F – Grade 1 to 6 (Talley & Connor, 2nd Edition, pg.55) B. T – Grading of Murmur: (Talley & Connor, 2nd Edition, pg.55, Medical Secrets by Zollo, pg 64) 1: very soft and barely audible intensity (only cardiologist can hear it)
  • 5. 2: soft and low intensity murmur (heard by experienced one) 3: moderate murmur but no thrill (everyone can hear it) 4: loud murmur with palpable thrill 5: loud murmur (still require stethoscope to hear it) 6: loudest murmur (heard without even placing the stethoscope) C. F – Valsalva maneuvers mean forceful expiration against closed glottis. Ask the patient to hold his nose, close the mouth and breath out hard and hold as long as possible. It will decrease preload thus reducing the intensity of murmur in case of aortic stenosis, mitral regurgitation and systolic murmur of hypertrophic cardiomyopathy (Talley & Connor, 2nd Edition, pg.55-56) D. T – Other causes of pansystolic murmur: mitral regurgitation, tricuspid regurgitation, VSD, aortopulmonary shunt. (Talley & Connor, 2nd Edition, pg.53) E. T – Mid-diastolic murmur: low pitch, due to impaired ventricular filling mitral stenosis, tricuspid stenosis, atrial myxoma (rare) 5. The following are causes of atrial fibrillation A. T – dalam infection, selalunye akan ade increase in catecholamine. Catecholamine ni terdiri daripada adrenaline and noradrenaline. 2 ekor makhluk ni akan exert sympathetic effect so dekat heart, mereka ni akan menyebabkan increase in the force of contraction of the heart increasing heart rate, blood pressure, and blood sugar. Tapi bile dah byk sgt 2 ekor ni, they can cause overcharging of the cardiovascular system, which can precipitate arrthymia. Sumber: http://www.zimbio.com/Catecholamine/articles/2/Beta+Blockers B. T – sama seperti di atas. C. T - Thyroid hormones upregulate sarcoplasmic Calcium ATPase, myosin heavy chain alfa, voltage gated K+ channels, Na+ channels and beta1 adrenergic receptors. These effects result in increased heart rate, systolic hypertension, increased ventricular contractility and cardiac hypertrophy. Changes in electrophysiological characteristics of atria result in dysrhythmias, especially atrial fibrillation, in patients with hyperthyroidism. Sumber: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1431605/ D. F – atrial myxoma is the commonest heart tumor walaupun heart tumor ni secara umumnya sangatlah rare. The most common heart tumor yg boleh present with AF is rhabdomyoma and fibroma. Ini kerana mereka ini akan men’damage’kan myocardium or conduction system. Sumber: http://resources.metapress.com/pdf-preview.axd? code=ekxjgn975qpmexrd&size=largest E. T – merokok boleh meningkatkan kandungan catecholamine di dalam darah. Maka, ape yg akan berlaku sama seperti di jawapan A tadi. http://www.nejm.org/doi/full/10.1056/NEJM197609092951101 6. Arrythmias A. True - ECG shows regular sawtooth-like atrial flutter waves (F waves) between QRS complexes <--K&C pg. 725 B. False - Atrial fibrillation occurs in one-third of patients after coronary bypass surgery and in more than half of those undergoing valvular surgery <---K&C pg 724 C. T – http://emedicine.medscape.com/article/159222-overview D. True -Mobitz I block (Wenckebach block phenomenon) is progressive PR interval prolongation until a P wave fails
  • 6. to conduct. The PR interval before the blocked P wave is much longer than the PR interval after the blocked P wave <-- K&C pg 721 E. False - 2nd degree <--K&C 721 7. Causes of displaced apex beat are A. T : dextrocardia is congenital defect in which position of heart adalah mirror image of its normal position. Oleh it, secara automatic apex beat dia adalah displaced B. F: spenomegaly menghala kepada inferiomedially ke arah right iliac fossa. Oleh itu, apex beat xkan displaced. C. T: hypertrophy boleh menyebabkan displaced mengikut buku oxford text book of medicine 4th edition page 852 ataupun 2852. Xsure page yg exact coz ade copy online. Kat online die tulis P.2.852. Another source http://www.mediscuss.org/examination-cardiac-apex-beat-44.html D. T : sama seperti alasan di atas http://www.mediscuss.org/examination-cardiac-apex- beat-44.html E. T: fibrosis of left upper lung lobe akan menyebabkan mediastinal shift. Kalau ikut muka surat yg sama., maka jawapannya adalah true. 8. Kussmaul sign is seen in a. T b. F c. T d. T e. T Kussmaul's sign is the observation of a rise in JVP on inspiration. Do not confuse with Kussmaul breathing, ie a deep and labored breathing pattern often associated with severe metabolic acidosis, particularly DKA but also renal failure. The classical differential diagnosis are constrictive pericarditis, restrictive cardiomyopathy, cardiac tamponade. (Ref: http://www.gpnotebook.co.uk/simplepage.cfm?ID=1369047062 ) Cardiac conditions that may be associated with a positive Kussmaul's sign include right atrial myxoma, tricuspid stenosis, constrictive pericarditis, pericardial effusion, restrictive myocardopathy, and severe pulmonary hypertension. Overall, the commonest cause is severe right-sided congestive heart failure. (Ref: http://www.etsu.edu/com/medicalmystery/KussmaulsSign.aspx) 9. Atherosclerosis A. Usually develops over a period of months Ans = False Reference = Harrison vol II page 1501 ATH occurs over a period of many years. B. Homocysteine is protective against plaque formation Ans = False Reference = Harrisons vol II page 1508 & http://www.medicinenet.com/homocysteine/article.htm Homocysteine is a naturally occurring amino acid found in blood plasma produced by the body, usu as a byproduct of consuming meat.
  • 7. Increased homocysteine – lead to increased risk of ATH cause narrowing & hardening of the arteries. So, homocysteine is actually hazardous than protective C. Diabetes mellitus promotes plaque formation Ans = True Reference = mama robin page 345 & John’s book of DM (http://books.google.com.my/books? id=ohgjG0qAvfgC&pg=PA870&lpg=PA870&dq=How+diabetes+mellitus+promote+plaque+formation &source=bl&ots=yIzn5AJ9Is&sig=VCD9rrPVL_ATe8GyZ5y5Zr0WVJ8&hl=en&ei=RUO- TaC6M8virAfNm- DtBQ&sa=X&oi=book_result&ct=result&resnum=6&ved=0CDMQ6AEwBQ#v=onepage&q&f=false) IN DM – thereis hyperglycemia & insulin resistance – lead to increased expression of (E-selectin, vascular-cell adhesion molecule-1 VCAM-1, intracellular adhesion molecule-1 ICAM-1) by endothelial cells….--- so, promote leucocyte infiltration into arterial wall (endothelial)…----then, leucocyte infiltrate into subendothelial by stimulation of monocyte chemoattractant protein-1 (MCP-1)-----infiltrated monocyte differentiate into macrophages----!!!these are the proatherogenic effect by accumulating lipids & releasing proinflammatory cytokines and matrix metalloproteinase which likely promotes plaque formation & expansion. D. May present as intermittent claudication Ans = True Reference= Harrison vol II page1501 ATH occur in peripheral circulation can cause intermittent caludication E. Statins do not help in increasing the HDL level Ans = False Reference = Harrisons vol II page 2427 Statin= HMG-CoA reductase inhibitors Statin inhibit the HMG-CoA reductase – then inhibit the synthesis of cholesterol. At the same time, d/t decrease synthesis of cholesterol in the cell, in menyebabkan hepatic LDL receptor activity on the cell increasing & there is accelerated clearance of circulating LDL in the blood so that, cholesterol will be transferred in the cell. Meaning – main role of statin is LDL lowering agent, but can also reduce TG & have modest HDL raising effect. 10. Ischemic Heart Disease A. Atherosclerotic plaques in the heart are commonly seen in the ant. descending coronary art. Ans = True Reference = Harrisons vol II page 1515 Common seen in the ant descending artery (L) B. Percutaneous coronary intervention (PCI) is indicated in 3 vessel disease Ans = False Reference = harrisons vol II (page 1525 & 1526 –choice b/w PCI & CABG) PCI –ptnts w single @ 2 vessel dis w normal LV fx & anatomically suitable lesions CABG – 3 vessel dis @ 2-vessel dis that includes proximal L descending coronary a. C. ST elevation is indicative of myocardial infarction Ans = False Reference = harrisons vol II fig 239-1page 1532 & page 1534
  • 8. MI can be STEMI @ NSTEMI. So, MI x semestinya ad ST elevation Cardiac trop-T(cTnT) & trop-I(cTnI) is indicative and can distinguish from UA & NSTEMI. Levels of cTnT and cTnI may remain elevated for 7-10 days after STEMI D. All patients with IHD have stenotic lesions in their coronary arteries Ans = False Reference = harrisons vol II page 1514 Not all have stenotic lesion because some ptient w IHD can also be due to coronary spasm (prinzmetal’s variant angina) E. CABG has a higher risk of recurrence as compared to PCI Ans = false Reference = harrisons vol II page 1526 PCI is higher compared to CABG 11. The following are true regarding cardiac tamponade A. T. Caused by neoplastic disease B. T. Presence of pulsus paradoxus C. F. ECG shows large QRS complexes D. F. There will be a drop in JVP E. F. A positive Kussmaul’s sign is sometimes present A. 1. “Malignant disease is the most common cause of pericardial effusion with tamponade.” http://emedicine.medscape.com/article/759642-overview 2. “Neoplastic disease, particularly advanced, is the most frequent cause of tamponade in the hospitals.” http://www.heartalex.com/alexheartfiles/undergraduate/lectures %20notes/Pericardial%20 disease%20r.pdf B. 1. “Blood pressure may fall (pulsus paradoxical) when the person inhales deeply.” http://www.nlm.nih.gov/medlineplus/ency/article/000194.htm C. 1. “Electrical alternans is pathognomonic of cardiac tamponade and is characterized by alternating levels of ECG voltage of the P wave, QRS complex, and T waves. This is a result of the heart swinging in a large effusion.” http://emedicine.medscape.com/article/759642- diagnosis D. 1. “Elevation of jugular venous pressure with a prominent x descent and a diminutive or absent y descent” http://www.harrisonspractice.com/practice/ub/view/Harrisons %20Practice/141253/1/cardi ac_tamponade E. 1. “Kussmaul’s sign is not seen in patients with cardiac tamponade because even though the increase in pericardial pressure exerts an inward force compressing the entire heart during inspiration, the increase in negative intrathoracic pressure is still able to be transmitted to the right side of the heart and subsequent increase in blood flow to the right atrium ensues.” http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757428/
  • 9. 12. Cardiomyopathies A) T – http://www.mayoclinic.com/health/cardiomyopathy/DS00519/DSECTION=causesB) T – When abnormality is primary in and localized to myocardium, the condition is called cardiomyopathy. ( Baby Robbins Patho, page 307). Tapi, base on definition by AHA, it divides into primary and secondary..so susah nak cakap, but ikut je definition Dorland, it is a primary disease http://www.emedicinehealth.com/cardiomyopathy/page2_em.htm#causes C) F – divided into dilated, hypertrophic and restrictive. ( Baby Robbins Patho, page 307) D) T – The cause is frequently unknown (idiopathic dilated cardiomyopathy), but some pathology may contribute, such as genetic defect for example X-linked cardiomyopathy (Duchenne and Becker muscular dystrophies). ( Baby Robbins Patho, page 307) E) T – Some of the classic physical findings are ejection systolic murmur (due to left ventricular outflow obstruction) and pansystolic murmur (due to mitral regurgitation). ( Kumar&Clark Medicine, page 851) 13. The following are risk factors for acute MI a. False: no evidence regarding ethnic predisposition Ps: kumar and clark, p745 b. TRUE : 5% male and 6% female death of CAD is due to obesity(bmi>30) Ps: kumar and clark, p746 c. False: sedentary life style Ps: kumar and clark, p747 d. True: first degree relative has developed ishaemic heart disease before age of 50 Ps: kumar and clark, p745 e. True: high serum cholesterol with low serum HDL associated strongly with coronary artheroma Ps: kumar and clark, p746 14. Cardiac markers A.False: troponin C is associated with cardiac and skeletal muscle.so, its not used for myocardiac damage B.True: myoglobin can be used in it C:False :LDH is not highly specific cardiac marker as troponin, they are also high in tissue breakdown and hemolysis D.False:CKMB persist for about 72 hrs. but troponin can last 7-10 days E.False: regarding http://emedicine.medscape.com/article/811905-overview, some authorities have called for a troponin standard alone and recommend eliminating CK-MB..(haa korang bace la sket) 15. The following are complications of thrombolytic therapy Thrombolytic therapy: a.k.a fibrinolytic  f(x): dissolve (lyse) blood clots eg: tissue plasminogen activator (tPA), streptokinase, urokinase. Complications include bleeding, allergic reactions (mostly streptokinase), emboli (http://med-lib.ru/english/oxford/thromb_ther.php: emboli, http://ezinearticles.com/?Complications-With-Thrombolytics&id=5367300 : allergic, https://www.vascularweb.org/vascularhealth/Pages/thrombolytic-therapy.aspx : hypotension) A. T mostly streptokinase B. T complication due to bleeding C. F salah satu kegunaan thrombolytic utk treat DVT bukan nye thrombolytic menyebabkan DVT D. F thrombolytic tk menyebabkan fracture!!!
  • 10. E. T can occur at the site of drug administration, from other puncture sites, or from areas of recent surgery 16. The following are clinical manifestations of heart failure A. T – selalunye berlaku dlm right sided heart failure. Akan ade engorgement of systemic and portal venous system. Sumber: papa robin page 563. Severe heart failure causes blood to back up from the heart into the inferior vena cava (the large vein that carries blood from the lower parts of the body to the heart). Such congestion increases pressure in this vein and other veins that carry blood to it, including the hepatic veins (which drain blood from the liver). If this pressure is high enough, the liver becomes engorged (congested) with blood and malfunctions. Sumber: http://www.merckmanuals.com/home/sec10/ch138/ch138g.html B. T – wujud satu keadaan yg di panggil cardiac cachexia. Menurutnya, CHF akan menghasilkan TNF yg byk. Maka, TNF ini akan impair the synthesis or accelerate the catabolism of proteins in the skeletal muscle. Sumber: http://eurheartj.oxfordjournals.org/content/18/2/187.full.pdf C. T – yes,boleh jd dlm severe heart failure. Sumber: kumar and clark page 688. Instability of respiratory control underpins the development of Cheyne-Stokes respiration and results from hyperventilation, prolonged circulation time, and reduced blood gas buffering capacity. Sumber: http://thorax.bmj.com/content/53/6/514.full D. T –it is a reflection of a right ventricle that cannot accommodate augmented venous return. Sumber: http://www.amjmed.com/article/S0002-9343(00)00443-5/abstract E. T – in order utk maintain CO, heart akan try utk beat faster.manifest as tachy. Sumber: http://www.aafp.org/afp/20000301/1319.html