CR2

118 flashcards · Other · by Harry Temple

1. Where are the sites of RBC production in children and adults?

   <5yo - bone marrow of all bones 5-25yo - marrow of long bones >25yo - marrow of membranous bones (ribs, sternum, vertebrae)

2. What makes up the cardiac plexus and what is the function of each?

   Vagus, sympathetics and GVAs Vagus - decrease rate of firing Sympathetics (T1-5) - increase rate of firing GVAs - run with sympathetics to synapse in spinal cord at T1-5

3. What are the branches of RCA and LCA?

   RCA - marginal and PDA LCA - LAD and circumflex (gives off left marginal)

4. How do the RCA and LCA appear on angiogram?

   RCA - C shaped LCA - M shaped

5. What is the MOA of heparin and how is it administered?

   Binds to and activates antithrombin Inhibits thrombin and Xa Given parenterally as not absorbed in gut Short half life so given regularly/continuously

6. What is the MOA of warfarin and what is it's effect on clotting tests?

   Vit K antagonist Increases PT and INR

7. What is the MOA of DOACs, when should you be careful and how are they reversed?

   Direct thrombin inhibitors (dabigatran) or Xa inhibitors (apixaban, rivaroxaban) Careful in pts with kidney problems Idarucizumab reverses dabigatran

8. What is D-dimer?

   Protein fragment of fibrin breakdown Tested in patients with ?thrombotic disorders

9. What is the function of plasmin and how does it work?

   Breaks down clots From inactive plasminogen which then binds to platelet plugs a2-antiplasmin from damaged endothelium prevents conversion before full wound healing When healing complete, a2-antiplasmin release ceases and tPA released

10. What is haemophilia B?

    Deficient factor IX Less common Reduces +ve feedback loop producing thrombin

11. What is haemophilia A?

    Deficient factor VIII More common Reduces +ve feedback loop producing thrombin

12. What do PT, activated partial thromboplastin time, bleeding time and INR assess?

    PT - extrinsic and common pathways APTT - intrinsic and common pathways Bleeding time - platelet function INR - derived from PT

13. What is the function of XIIIa?

    Increases fibrin cross-linking to form a mechanically stable clot

14. What is the function of kallikreins and one of the products and how does a clotting factor affect this?

    Cleave kinins from inactive kininogen precursors XIIa increases kallikrein levels Bradykinin dilates arterioles and constricts veins so causes local oedema and swelling

15. What artery supplies SAN and AVN and bundle branches and what are right/left dominant hearts?

    SAN/AVN - RCA Bundle branches - descending arteries Right dominant (most common) where PDA comes from RCA

16. What is the effect of an ischaemic bundle branch?

    Ischaemic bundle branch doesn't properly conduct --> uses different pathway through myocytes --> slower conduction speed --> prolongs QRS --> loss of ventricular synchrony

17. Where do MIs most commonly occur and what vessels does a CABG use?

    LAD > RCA > circumflex Portion of great saphenous vein or redirects mammary artery

18. What ECG leads give left, anterior and inferior views and what CA supplies each region?

    Left (circumflex) - aVL, I, V5-6 Anterior (LAD) - V1-4 Inferior (RCA) - aVF, II, III

19. What is mitral regurgitation?

    Most common valvular heart disease Systolic murmur as blood flows back into atria

20. What is aortic stenosis?

    Systolic murmur as turbulence when blood pushed through valve More severe in late systole as more time taken to generate pressure to pass through valve

21. What is mitral stenosis?

    Soft, rumbling diastolic murmur Not very loud as ventricular filling usually passive

22. What is aortic regurgitation?

    Diastolic murmur Decreases CO and elevates preload and afterload

23. What is preload and when does it increase?

    Volume of blood in ventricles at end of diastole Hypervolaemia, regurgitation or HF

24. What is afterload and when does it increase?

    Resistance to outflow HTN, valve or outflow stenosis, vasoconstriction

25. What causes concentric hypertrophy and what does this cause?

    Increased afterload (chronic HTN or stenosis) Wall thickness increases and filling reduces so volume overload and eccentric hypertrophy as a result

26. What causes eccentric hypertrophy and what is the effect of this?

    Increased preload (regurgitation, systolic dysfunction or hypervolaemia) Increases O2 demand as less mechanical efficacy

27. What is the effect of atrial remodelling and how is LA enlargement seen on CXR?

    Increases AF risk Double density as it pushes behind right cardiac shadow

28. How is the primitive heart tube formed and where does the blood enter/exit?

    Blood islands aggregate to form R/L endocardial tubes which then fuse into primitive heart tube Enters inferiorly and exits superiorly

29. What do the parts of the primitive heart tube go on to form?

    Truncus arteriosus - proximal aorta and pulmonary artery Bulbus cordis - RV and ventricular outflow Primitive ventricle - LV Primitive atria - RA and LA Sinus venosus - coronary sinus and smooth wall of atria

30. What limits primitive heart growth and what happens if heart looping occurs incorrectly?

    Pericardium Heart has to fold to align structures properly Dextrocardia

31. What is the intrinsic pathway in clotting and how is XII activated?

    Factor sequence - 12 - 11 - 9 - 10 Polyphosphate anions released from activated platelets

32. How are separate AV canals formed from primitive heart?

    Endocardial cushions grow to separate atrioventricular canal

33. How does the atrial septum form?

    Septum primum grows and forms ostium primum --> ostium secundum forms before ostium primum fully closes --> septum secundum develops superior to inferior but leaves foramen ovale

34. What is the function of the foramen ovale and what happens at birth?

    Shunts blood from RA to LA Closes as RA pressure decreases

35. What causes ASD?

    Failure of septum primum/secundum to form properly

36. How does the ventricular septum form and what causes most VSDs?

    Muscular IVS grows from floor and membranous IVS grows from endocardial cushion Failure of membranous portion to grow

37. How do the heart outflow tracts separate?

    Truncoconal swellings in truncus arteriosus grow towards each other in spiral structure

38. Outline the foetal circulation

    Blood enters through umbilical vein and shunts into IVC by ductus venosus (bypasses liver) Most shunted by foramen ovale but some shunted by ductus arteriosus

39. What do the ductus venosus, foramen ovale, ductus arteriosus and umbilical arteries become?

    Ductus venosus - ligamentum teres Foramen ovale - fossa ovale Ductus arteriosus - ligamentum arteriosum Umbilical arteries - medial umbilical ligaments

40. What causes cyanotic and acyanotic lesions?

    Cyanotic - R --> L shunting Acyanotic - L --> R shunting

41. What are examples of acyanotic lesions?

    ASD, VSD, patent ductus arteriosus and coarctation of the aorta

42. What are examples of cyanotic lesions?

    Tetralogy of Fallot, transposition of the great vessels and persistent truncus arteriosus

43. What is patent ductus arteriosus and how is it treated?

    Blood shunted from aorta to PA Prostaglandin inhibitor (eg. ibuprofen) or surgery if fails to close

44. What is the common pathway in clotting and what is DIC?

    Prothrombin --> thrombin which catalyses fibrinogen --> fibrin to form strong, stable clot DIC - clots form in intact blood vessels

45. What is coarctation of the aorta?

    Narrowing of aorta above or below ductus arteriosus Pre-ductal - ductus persists to retain blood flow Post-ductal - collateral circulation must develop Causes high pressure in upper limb and low pressure in lower limb

46. What are the features of tetralogy of Fallot?

    VSD, overriding aorta, pulmonary stenosis and RV hypertrophy

47. What is persistent truncus arteriosus?

    One outflow supplies aorta and PA Has a large VSD below truncal valve to allow mixing of blood

48. What causes transposition of the great vessels?

    Conotruncal septum runs straight down rather than in spiral

49. How does a +ve feedback loop of thrombin formation occur?

    Small amount of thrombin activates V, VIII and IX Va stimulates thrombin formation from prothrombin VIIIa and IXa increase X --> Xa

50. What is the extrinsic pathway in clotting?

    Thrombin formation triggered by vessel injury Factor sequence - 3 (tissue factor) - 7 - 10 Factor Xa converts small amount of prothrombin --> thrombin

51. How is aspirin an anticoagulant?

    Inhibits COX --> reduces TXA2 formation --> fewer platelets stick together

52. What is the function of TXA2 and what is bleeding time?

    Activates +ve feedback loop until platelet plug is formed Time to form effective platelet plug and stop initial haemorrhage (normal <10mins)

53. What happens once platelets become activated?

    Change shape and become spiky and entangled Release ADP, TXA2 and 5-HT ADP and TXA2 induces platelet GP2b/3a expression so more platelets bind

54. How does a platelet cluster form in a blood vessel?

    Platelets bound to VWF express GP2b/3a --> receptors bind to fibrinogen --> binds more platelets Fibrinogen binding activates platelets

55. How does endothelial damage start platelet binding?

    VWF binds to exposed collagen --> platelets bind to VWF by GP1b

56. How does blood flow reduce to a damaged vessel?

    Blood vessel stops normal secretion of NO and PGI2 (usually relax smooth muscle) Endothelin release causes vasoconstriction Damage to sympathetic nerve endings releases norad

57. How is platelet production regulated and what is the name of low and high platelet counts?

    Thrombopoietin Low - thrombocytopenia High - thrombocytosis

58. What cells do megakaryocytes come from, what are platelets and what is their lifespan?

    Common myeloid progenitors Sheds of cytoplasm from megakaryocytes 10 days

59. What are the definitions of haemostasis, 1y and 2y haemostasis?

    Haemostasis - cessation of bleeding at vascular injury site by thrombus formation 1y - formation of platelet plug 2y - formation of fibrin clot

60. What causes ST depression?

    Reciprocal response to ST elevation in other leads Also coronary ischaemia or hypokalaemia

61. What causes ST elevation in STEMIs?

    Failure of ventricular AP to propagate into some parts of ventricular muscle ST elevated above normal in 2 or more adjacent leads

62. What is bundle branch block and ECG features?

    Abnormal conduction through bundle branches Prolonged QRS and notch in R wave

63. What is junctional rhythm and ECG features?

    Damage to SAN or block in atrial conduction so AVN takes over Bradycardia and absent/inverted P wave

64. What is atrial flutter?

    Re-excitation of impulses in atria from one excitatory focus (usually not SAN) High rate, regular, P wave replaced with F (flutter waves)

65. What is AF, ECG features and symptoms?

    Sites other than SAN create pacemaker impulses Features - high rate, irregularly irregular and no distinguishable P waves Sx - palpitations, fainting, chest pain, CHF

66. What is 3rd degree heart block and ECG features?

    P waves present but unsynchronised with QRS complex Ventricles create own slow escape beats so bradycardia present and exercise intolerant Adrenaline increases inotropy but not HR

67. What are ECG features of 2nd degree heart block type II and how is it treated?

    Mobitz type II P waves regular but AVN randomly fails to respond Ventricular rate irregularly irregular and may progress to complete heart block Implanted pacemaker

68. What are ECG features of 2nd degree heart block type I?

    Wenkenbach PR interval gradually increases until P wave not followed by QRS System then resets and repeats

69. What are ECG features of 1st degree heart block?

    PR interval fixed constant duration >200ms with regular rate

70. What is ventricular fibrillation, ECG features and how is it treated?

    Irregular, high rate, unrecognisable QRS and no P wave Irregular rhythm and amplitude with little/no CO Immediate defibrillation

71. What is ventricular tachycardia, ECG features and causes?

    180-190bpm with prolonged QRS but regular rhythm and amplitude Poor CO and risk of arrest Causes - coronary artery disease, cardiomyopathy, heavy caffeine/drug/alcohol

72. What is sinus tachycardia?

    >100bpm with normal PR interval

73. What is sinus bradycardia and when is it seen?

    <60bpm Usually benign but found in athletes, patients on beta blockers or increased vagal tone

74. What causes abnormally large T waves?

    Hyperkalaemia

75. How does ischaemia cause T wave inversion?

    Inner muscle more susceptible to ischaemia (reduces endocardial AP duration) If outer muscle has normal AP duration then inverted T wave as endocardial AP now shorter

76. How do differences in heart muscle depolarisation create the T wave?

    Endocardial muscle depolarises before and for longer than epicardial muscle T wave due to epicardial muscle repolarising while endocardial muscle still contracting

77. What is the QRS duration, normal duration and what does prolonged QRS show?

    Start to end of QRS complex <120ms Slow/desynchronised ventricular depolarisation

78. What is the PR interval, normal duration and when is it prolonged?

    Start of P wave to start of QRS 120-200ms Heart block, hypokalaemia, acute rheumatic fever, carditis

79. What is sinus rhythm and the characteristics of the P wave?

    P wave before every QRS complex with a normal shape Upright in II and biphasic in V1 and normally 80ms

80. What should you look at when interpreting an ECG?

    1. Rate 2. Rhythm 3. P waves present? One before each QRS? Normal duration? 4. PR interval normal duration? 5. QRS complex normal duration? 6. ST interval elevated/depressed? QT interval normal? T wave inverted?

81. How can autoantibodies cause haemolytic anaemia and how can this be tested?

    IgG binds to RBC and labels for destruction by spleen Coombs test - add antihuman Ab to blood sample to test for presence of IgG, RBCs agglutinate if +ve Causes - idiopathic, drugs (penicillin), SLE or transfusion

82. What is G6PD deficiency?

    Reverses oxidation of Hb and prolongs RBC lifespan X-linked Carriers don't show symptoms unless exposed to trigger (food, infection or drugs (dapsone or cotrimoxazole)

83. What is hereditary spherocytosis and the clinical features?

    Defect in proteins of cytoskeleton so cell contracts to sphere High fragility so more prone to degradation when passing through capillaries Features - autosomal dominant, spherocytes in blood film, ↑LDH, ↑bilirubin, ↓Hb

84. What are the different causes of haemolytic anaemias?

    Membrane - autoantibody, spherocytosis, oxidising agents Hb - abnormal structure (eg. sickle cell) or imbalance in a:b synthesis (thalassaemia) Enzyme - G6PD deficiency

85. What are haemolytic anaemias, how does this cause jaundice, what is the presentation and labs?

    Shortened RBC survival (present if lifespan < 120 days) Increased bilirubin causes jaundice or gall-stones if long-standing Presentation - pallor, signs/symptoms of anaemia, jaundice, gallstones, splenomegaly Labs - ↑LDH, ↑bilirubin, ↑reticulocytes, ↑RBCs in marrow

86. What are the causes of folate deficiency and how is it treated?

    Nutritional - old age, poverty, alcoholism Malabsorption - coeliac, Crohn's Excess utilisation - pregnancy, lactation Other - anticonvulsants Treatment - oral folic acid

87. What are the causes of B12 deficiency?

    Nutritional (eg. vegan) Malabsorption - gastric (pernicious anaemia, surgical gastrectomy) or intestinal (Crohn's)

88. What are the clinical features, treatment and results of investigations for pernicious anaemia?

    Features - insidious, anaemia, glossitis, mild jaundice, neurological symptoms Treatment - IM B12 every 3 months for life Investigations - macrocytic anaemia, hypersegmented neutrophils and reduced serum B12

89. What is pernicious anaemia and what does it cause?

    Autoantibody against parietal cells so reduced IF and B12 absorption Gastric atrophy, ↓ acid and IF production

90. What are the findings of B12 deficiency anaemia on blood count, biochemistry and blood film?

    Blood count - ↓Hb, ↑MCV, ↓ WBCs Biochemistry - ↑LDH, ↑ bilirubin Blood film - hypersegmented neutrophils

91. Why does B12 deficiency cause macrocytic RBCs?

    Impaired DNA synthesis --> cells fail to divide --> overlarge RBCs

92. How long can B12 be stored and how do we get folate in diet?

    Long time (3 years) Greens but destroyed by cooking

93. Why is B12 important and how can folate be used for this?

    Cofactor for tetrahydrofolate (THF - cofactor for nucleic acid formation) synthesis THF may be obtained from dietary folate without need for B12

94. How can you assess B12 levels?

    Indirectly by serum methylmalonic acid (MMA)

95. How is B12 absorbed and what often causes B12 deficiency anaemia?

    Binds to haptocorrin in stomach (protects from acid) --> binds to IF in duodenum --> absorbed in terminal ileum --> transported by transcobalamin II Deficient/absent IF

96. What is B12 needed for, what is the effect of low B12 and how do we get B12 in diet?

    DNA and myelin synthesis Affects cells with high turnover (eg. RBCs) and prolonged deficiency can cause irreversible nervous system damage Meat proteins (not destroyed by cooking)

97. What is the role of the stomach in Fe absorption and how can drugs affect this?

    Stomach acid aids absorption PPIs decrease acids so decrease Fe absorption

98. What regulates Fe entry into blood and how and how can this cause anaemia?

    Hepcidin breaks down ferroportin to inhibit Fe release into blood Hepcidin increased in chronic disease (eg. cancer) to cause anaemia of chronic disease

99. How is Fe transported basolaterally and transported in plasma?

    Ferroportin Bound to transferrin

100. How is iron stored in enterocytes and what is the function of this?

     Stored in ferritin as inactive Fe3+ Acts as a buffer to release Fe when needed Serum ferritin is a diagnostic test for iron deficiency anaemia