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Heart Failuer

Dua Ga English 150 cards

Cards in this deck (150)

  1. 1What is heart failuer?1-Pump failure
    2-Inability of ventricle to maintain adequate circulation->symptoms on exercise\rest
    3-Forward failure + backward failure
    4-Adaptive mechanisms->maintain arterial blood pressure and perfusion of vital organs
  2. 2How does the heart ADAPT in HF?1-Frank startling mechanism (INC stretch-> INC force of contraction)
    2-Myocardial adaptations (hypertrophy/dilatation)
    3-Neurohumoral systems (noreepinephrine/Renin/ANP)
  3. 3What happens (physiology) which lead to HF?-failing to maintain CO+perfusion-> compensatory mechanisms->INC CO BUT LOAD+DEMAND OF HEART INC-
    -INC stretch? by:
    1-frank starling
    2-Inc myocardium size:
    *concentric Hypertrophy (adaptation- HTN)
    *MI->dead tissue->non dead tissue INC size(remodelling)
    3-Neurohormonal
  4. 4explain the neurohormonal mechanism?hormones->INC contraction+HR -> keep CO up
    Renin->vasoconstrict+retain fluid + ANP-> balance vascular tone
  5. 5Why do we have all these componsatory mechanisms and what happens if they fail?1-to maintain the pump
    2-fails -> decompensated heart failure
  6. 6What are the causes of HF?1)Loss of the continuity of the circulatory system (gunshot through thoracic aorta).
    2) conduction disorders (heart block\arrhythmias )
    3)A valvular lesion (stenosis\aortic coarctation->obstructs forward flow. regurgitation->outflow reflux backward; BOTH->myocardial stress.
    4)Failure of the pump itself:Damaged muscle (MI), inflammation+ toxic degeneration, infiltration(amyloid), cardiomyopathy.
  7. 7How can the pattern of hypertrophy indicate the stimuli?1-Pressure-overloaded ventricles (HTN\aortic stenosis)->CONCENTRIC HYPERTROPHY+INC ratio of wall thickness to cavity radius.
    2-volume-overloaded ventricles (mitral regurgitation) ECCENTRIC HYPERTROPHY(DILATATION) + proportionate INC radius and wall thickness.
  8. 8CHF is classified into?1. Systolic dysfunction: (ischemic injury, pressure\volume overload, DCM)
    2. Diastolic dysfunction:(massive lt. ventricular hypertrophy, myocardial fibrosis, amyloid deposition, constrictive pericarditis)
  9. 9what are the charectaristics of all CHF?1-diminished cardiac output (called forward failure)
    2-damming back of blood in the venous system (called backward failure)
    3-both.
  10. 10LEFT SIDED HF START HERE What are the causes of Lt sided HF?(1) Ischemic heart disease.
    (2) Hypertension.
    (3) Aortic and mitral valvular diseases ( calcific aortic stenosis+rheumatic heart disease)
    (4) Myocardial diseases.
    (5) DCM
    (6) MI
    (7) RCM
  11. 11What is the treatment of Lt sided HF ?- dieuretics
    - ACE inhibitors
    - B-blockers
  12. 12What causes the clinical features of Lt sided HF?(DEC forward perfusion+pulmonary congestion)
    Will be explained for every organ later
  13. 13Explain the gross pic of the HEART?1-Except with obstruction at\mitral valve or other restricters of size of lt ventricle, ->chamber usually hypertrophied+often dilated(massively sometimes)
    2-Secondary enlargement of lt atrium is frequently present.
    3-Atrial fibrillation->stasis+thrombus formation+Inc risk of embolic stroke.
  14. 14explain the gross pic of the LUNGS?1. Pulmonary edema:
    a. Perivascular and interstitial transudate(esp interlobular septa)
    b.Progressive edematous widening of alveolar septa.
    c.Accumulation of edema fluid in alveolar spaces.
    d.HF CELLS in alveoli->indicate previous edema.
    (Transferrin(edema fluid) + erythrocytes Hb(congested capillaries)->macrophages phagocytosis->hemosiderin).
  15. 15What are the clinical features of pulmonary edema and congestion?1.Cardiac Dyspnea(earliest cardinal complaint)
    2.Orthopnea(dyspnea on lying down\ relieved by sitting or standing.)
    needs to sleep sitting upright\raising head and chest with pillows.
    3.Paroxysmal nocturnal dyspnea: extreme dyspnea at night wakes patient from sleep
    4.Cough(chronic venous congestion of lungs->cough blood (Hemoptysis) )
  16. 16explain the gross picture of the KIDNEY?1.DEC CO-> DEC renal perfusion->renin-angiotensin-aldosterone->retention of salt and water->expansion ofinterstitial fluid (Oedema)+blood volumes (hypertension).
    2.DEC CO->ischemic acute tubular necrosis+impaired excretion of nitrogenous products->prerenal azotemia.
  17. 17what are the Clinical features of kidney hypoperfusion?1. Oedema
    2. Hypertension
    3. Acute renal failure ( azotemia).
  18. 18Explain the gross pictur of the BRAIN?far-advanced CHF, cerebral hypoxia-> hypoxic encephalopathy
  19. 19what are the Clinical features of Brain hypoperfusion?1. Irritability,
    2. Lack of concentration,
    3. Restlessness,
    4. Coma.
  20. 20What is the forward effect of lt pump failuer?less perfusion->renal hypoperfusion->pre-renal azotemia (renal failure) + renin->INC constriction+fluid+edema
    syncope\dizziness\loss of consciousness
    angina\ischemia(depend on organ affected)
  21. 21what is the What is the backward effect of lt pump failuer?-INC hydrostatic pressure in pulmonary vessels->edema+congestion(widening of interalveolar spaces+engorgement of vessels in IA septa with blood+fluid leak into alveol->heart failure cells.
    -This->INC workload on rt heart->right heart failure (most common way)cuz right side can not pump against edematous lungs->failuer
    -chronic lung/pulmonary disease?rt side fail =core pulmonale(Left->right shunt +pulmonary HTN) ->peripheral edema +congested nutmeg liver\ hepatosplenomegaly
    -effusion in serous cavities CUZ OF systemic congestion.
  22. 22RIGHT SIDED HF START HERE What are the causes of rt sided HF?1-left sided heart failure
    2-core-pulmonale (left->right shunt+chronic lung disease)
    3-Constrictive pericarditis
    CAUSES OF THIS BITCH MUST INCLUDE ALL THE CAUSES OF LT BETCH
  23. 23Explain lt sided hf as a cause?inc pressure in pulmonary circulation incident to left-sided failure->INC burden on right side of the heart.
  24. 24Explain cor pulmonale as a cause of PURE rt sided HF?intrinsic disease of the lungs or pulmonary vasculature->rt ventricular pressure overload->burdened by inc resistance in pulmonary circulation-> dilatation confined to rt ventricle & atrium.
    -In chronic right-sided overload(COPD) Rt ventricle hypertrophy present.
  25. 25explain constrictive pericarditis as a cause of rt sided HF?restricts filling->dams blood back into the systemic venous system
  26. 26what is the major morphologic and clinical effects of pure right-sided failure differ from those of left-sided failure?1-MINIMUM pulmonary congestion
    2-MAXIMUM engorgement of systemic+ portal venous systems
  27. 271-LIVER as major organ affected?1. chronic passive congestion:
    congested red centers of liver lobules surrounded by paler(maybe fatty) peripheral regions.
    Centrilobular necrosis+sinusoidal congestion seen.
    2.sever+rapid rt sided hf? sinusoids rupture->central hemorrhagic necrosis.
    3.long-standing severeRSHF->central areas+time->fibrotic->cardiac sclerosis.
  28. 28what are the Clinical features of liver congestion?1.Congestive Hepatomegaly: tenderness in the right hypochondrium+abnormal LFT
  29. 292-KIDNEY as major organ affected+Clinical features of kidney congestion?-MORE COMMON IN RT SIDED
    1-Greater fluid retention.
    2-Peripheral edema,
    3-Severe azotemia (accumulation of BUN in blood).
  30. 303-Portal System of Drainage:+Clinical features of impaired Portal System of drainage?-INC pressure in portal vein+tributaries. 1.Congestive splenomegaly: Microscopically->sinusoidal dilatation, +areas of recent hemorrhage.enlarged spleen->500 to 600 gm (normal150 gm), +long-standing edema->fibrous thickening of sinusoidal walls
    2.impaired venous drainage of the gastric mucosa->Acute gastritis
    3.congestion of the viscera+later portal hypertension+liver cell failure+DEC synthesis of proteins-> ASCITIS (abnormal accumulations of transudate in peritoneal cavity)
  31. 314.Subcutaneous TissuesPeripheral pitting edema of dependent portions of the body
    -severe\chronic cases->edema quite massive+generalized(ANASARCA)
  32. 32What is the mechanism of edema in congestive heart failure?a.INC ­central venous pressure->INC pressure at venous end of capillaries-> transudate
    b.DEC BV(cuz of transudate)->stimulate ADH+aldosterone->retention.
    c. sympathetic overactivity->stimulate reabsorption of Na by tubules->point D
    d.->renal vasoconstriction->renin-angiotensin system->aldosterone-> retention.
  33. 335- INC venous pressureDistension of the jugular veins in the semi-sitting position due to elevated pressure.
  34. 34effects of rt sided hf in general?• Systemic and portal congestion… …congestive hepatospleenomegaly(nut meg liver)/pleural, pericardial and peritoneal effusions/dependant pitting EDEMA/congestion of the kidney and brain
  35. 35TAKE A BREAK MFWE GOING PERICARDIYUMMY YUMMY
  36. 36Diseases of The Pericardium are assosiated with?1-disease in other portions of the heart\ surrounding structures
    2-secondary to a systemic disorder.
  37. 371-of Fluid in the Pericardial sac (a-PERICARDIAL EFFUSION)-Normall 30 to 50 ml of thin, clear, straw-colored, translucent fluid in the pericardial space.
    if accumulate it gets more than 500 ml
    1.Serous effusion(most common in HF) fluid clear\straw colored\sterile in serosal surface->smooth & glistening.
    2.Serosanguineous: mixed with blood ( blunt chest trauma)
    3.Chylous effusions(mild lipid droplets) due to lymphatic obstruction due to benign\ malignant mediastinal neoplasms
  38. 381-Accumulations of Fluid in the Pericardial sac (b-HEMOPERICARDIUM)#pure blood in pericardial sac
    #Causes:
    1.MI->Rupture of heart wall
    2. Traumatic perforation\rupture of intrapericardial aorta(blood rapidly fills sac under greatly inc pressure->cardiac tamponade)
    3. Trauma during cardiopulmonary resuscitation(marked hemorrhage is unusual. )
  39. 392-PERICARDITISsecondary to a variety of cardiac diseases\systemic disorders\metastases from neoplasms arising in remote sites.
    Primary pericarditis is unusual and almost always of viral origin.
  40. 402-PERICARDITIS (a-ACUTE) I-SEROUS PREICARDITISSerous inflammatory exudates produced by:
    a)Noninfectious inflammations(RF, SLE, Scleroderma, Tumors, Uremia)
    b)infection in tissues contiguous to pericardium(Bacterial pleuritis), well-defined viral infection elsewhere serves as primary focus of infection (Upper respiratory tract, Pneumonia, Parotitis ( inflammation of the parotid gland ))
  41. 412-PERICARDITIS (a-ACUTE) I-SEROUS PREICARDITIS morphology?-Inflammatory reaction in epicardial+ pericardial surfaces with scant numbers of polymorphs, lymphocytes, and histiocytes.
    -volume of fluid is not large (50 to 200 ml) + accumulates slowly.
  42. 422-PERICARDITIS (a-ACUTE) II-FIBRINOID+SEROFIBRINOUS-most frequent types
    -more\less serous fluid w\ fibrinous exudate.
    Causes:
    1.AMI ; postinfarction (Dressler’s) syndrome (autoimmune-appears several weeks afterMI).
    2.Uremia.
    3.Chest radiation.
    4.RF-SLE-TRUMA
    5.Pneumonia or empyema
    7. fibrinous reaction following routine cardiac surgery.
  43. 432-PERICARDITIS (a-ACUTE) II-FIBRINOID+SEROFIBRINOUS morphology?-Serosal surface: dry granular
    -Exudate: more+thicker, Yellow(cuz of leucocytes, RBCs and fibrin.)
    -Fibrin->EITHER digested with resolution of exudate, OR become organized.
  44. 442-PERICARDITIS (a-ACUTE) II-FIBRINOID+SEROFIBRINOUS clinically?-loud pericardial friction rub isTHE MOST striking characteristic of fibrinous pericarditis.
    if collection of serous fluid separates two PERICARDIUM layers-> NO RUB
    -Pain, fever, and signs of cardiac failure
  45. 452-PERICARDITIS (a-ACUTE) III-PURULENT\SUPPURATIVEinvasion by infective organisms THAT may reach the pericardial cavity by several routes:
    1.Direct extension from neighboring inflammations(Empyema of pleural cavity, Lobar pneumonia, Mediastinal infections)
    2.Extension of a ring abscess through myocardium\aortic root in IE ->Seeding from blood
    3.Lymphatic extension
    4.Direct introduction during cardiotomy.
  46. 462-PERICARDITIS (a-ACUTE) III-PURULENT\SUPPURATIVE morphology?-Exudate - from thin\creamy pus - up to 400 to 500 ml.
    -Serosal surfaces: reddened, granular, coated with exudate.
    -Microscopically: acute inflammation
    which may extends to surrounding structures->mediastinopericarditis.
    -Organization is the usual outcome
    ->CONSTRICTIVE PERICARDITIS
  47. 472-PERICARDITIS (a-ACUTE) IV-HEMORRHAGICexudate(blood+fibrinous\suppurative effusion) CUZ OF:
    1.TB
    2.Direct malignant neoplastic involvement of pericardial space.
    3.Bacterial infections .
    4.Pericarditis in patients with underlying bleeding condition.
    5.Follows cardiac surger+MAYBE responsible for significant blood loss\tamponade->need to do “second-look” operation.
  48. 482-PERICARDITIS (a-ACUTE) V-CASEOUS-Caseation is TB in origin until proved otherwise.
    -caused by direct spread from tracheobronchial nodes.
    - anatomic changes are typical of TB elsewhere
    -most frequent cause of fibrocalcific, chronic constrictive pericarditis.
  49. 492-PERICARDITIS (B-CHRONIC\HEALED)-healed stage of forms of pericarditis
    -Isome cases->organization->plaque-like fibrous thickenings of the serosal membranes (“soldier’s plaque”) OR thin, delicate adhesions.
    -other cases->organization->complete obliteration of pericardial sac->restricts cardiac action.
    -some cases->healed pericarditis can be clinically important(when it takes the form of adhesive mediastinopericarditis OR constrictive pericarditis.)
  50. 502-PERICARDITIS (B-CHRONIC\HEALED) I-ADHESIVE MEDIASTINOPERICARDITISCAUSES:
    -a suppurative or caseous pericarditis,
    -previous cardiac surgery
    -irradiation to the mediastinum.
    -simple fibrinous exudation.
  51. 512-PERICARDITIS (B-CHRONIC\HEALED) I-ADHESIVE MEDIASTINOPERICARDITIS morphology?pericardial sac is obliterated+adherence of external parietal layer to surrounding fixed structures->great strain on cardiac function.
    each systolic contraction->heart is pulling against parietal pericardium +attached surrounding structures->INC workload->hypertrophy and dilatation.
  52. 522-PERICARDITIS (B-CHRONIC\HEALED) II-CONSTRICTIVEHeart encased in dense, fibrous, or fibrocalcific scas-> limits diastolic expansion+restricts CO
    Causes:
    Previous serofibrinous, suppurative, hemorrhagic, or caseous (tuberculous) pericarditis, but more often the cause is uncertain.
  53. 532-PERICARDITIS (B-CHRONIC\HEALED) II-CONSTRICTIVE morphology?- pericardial space is obliterated+heart surrounded by dense, adherent layer of scar or calcification(0.5-1 cm thick), that resemble a plaster mould in extreme cases (concretio cordis).
    -hypertrophy and dilatation cannot occur(why?) dense enclosing scar+heart is consequently quiet with reduced output.
    -major therapy? surgical removal of the shell of constricting fibrous tissue (pericardiectomy).
  54. 54SUMMERY OF PREVIOUS BITCH• SEROUS: Rheum. Fever (RF), SLE, scleroderma, tumors, uremia
    • FIBRINOUS: MI (Dressler), uremia, radiation, RF, SLE, s/p open heart surgery
    • PURULENT: infective, bacterial
    • HEMORRHAGIC: Malignancy, TB
    • CASEOUS: TB
    • CHRONIC: (ADHESIVE, CONSTRICTIVE)
  55. 55TAKE A BREAK HOEWE GOING MYOCARSKRRT SKRRTTT
  56. 56MYOCARDITIScan be one of the cause of dilated CMPathy
    Most imp causative agents are coxackie A and B viruses – drugs – amyloidosis – hypo/hyperthyroidism
  57. 57Myocarditis A) Immune mediated reactions1.Post-streptococcal ( Rheumatic )
    2. Post-viral autoimmune reaction.
    3. SLE
    4. Drug hypersensitivity (Methyl dopa, Sulfonamides).
    5. Transplant rejection
  58. 58Myocarditis B) Infections1.Viruses ( coxackie B virus, HIV, CMV, mumps, influenza, polio, varicella, measles): diffuse infiltration of interstitial tissue by lymphocytes, plasma cells and macrophages.
    2.Chlamydia
    3. Rickettsia: (typhus fever)
    4. Bacterial
  59. 59Myocarditis B) Infections BACTERIALA.TB myocarditis : part of generalized miliary tuberculosis, rare site of TB, multiple small tubercles between myocardial fibers.
    B.Syphilitic myocarditis:
    1.Gumma of the septum->heart block
    2.Diffuse syphilitic
    C. Suppurative myocarditis:
    in course of septicaemia\pyaemia OR as a complication of acute bacterial endocarditis ( ring abscess )
    D. Diphtheria: injury caused by toxins released from the bacteria into the circulation->myocardium DOESN'T contain bacteria. macrophages infiltrate damaged myocardium->remove necrotic tissue.
    5. Protozoa: Trypansoma cruzi (Chagas disease)
    6. Helminthic: Trichinosis.
  60. 60SUMMERY OF PREVIOUS MF IMP STUFF IN {}NFLAMMATION of MYOCARDIUM
    • Chiefly microbial
    – {COXACKIE A & B}, CMV, HIV
    – Trypanosoma cruzi (Chagas dis.), 80%
    – Trichinosis
    – Toxoplasmosis
    – Lyme disease (5%)
    – Diphtheria
    • {IMMUNE}: Post-viral, rheumatic, SLE, drug hypersensitivityalpha-methyl dopa, sulfas
    • Adriamycin
    • Cyclophosphamide
    • Catecholamines (Pheochromocytomas)
    • {Amyloid}, systemic or primary cardiac
    – Congo red stain: green birefringence with polarization
    • Amyloid, aging
    – Congo red stain: green birefringence with polarization
    • Hemochromatosis Prussian Blue
    • {BOTH HYPER-, HYPO- -thyroidism}
  61. 61TAKE A THIRD BREAK MFWE GOING TUUuuUUuUuuUUMOURS
  62. 62TUMOURS OF THE HEART-Primary tumors of heart are rare, metastatic to heart occur in 5% of patients dying of cancer.
    -most common primary tumors, in descending order of frequency, are: myxomas, fibromas, lipomas, papillary fibroelastomas, rhabdomyomas, angiosarcomas, and other sarcomas.
    -The five most common all are benign and account collectively for 80 to 90% of primary tumors of the heart.
  63. 63Primary Cardiac Tumors (1. Myxoma)-most common primary tumor in adults
    -Benign mesenchymal
    -90% are located in the atria, with a left-to-right ratio of approximately 4:1 .
    -major clinical manifestations due to ?valvular “ball-valve” obstruction, embolization,
    -fever and malaise due to? elaboration ofIL-6(major mediator of Acute systemic inflammation by some myxomas)
  64. 64Primary Cardiac Tumors (1. Myxoma) morphology?-almost always single, range from small to large, sessile or pedunculated masses, vary from globular and hard lesions mottled with hemorrhage to soft, translucent, papillary, or villous lesions having a myxoid appearance.
    -pedunculated: mobile->move into\ through AV valves during systole-> intermittent+position-dependent obstruction->damaged leaflets.
  65. 65Primary Cardiac Tumors (1. Myxoma) histology?-stellate or globular myxoma cells(clusters or single) embedded within an abundant acid mucopolysaccharide ground substance and covered by endothelium
    -IT IS ATTACHED BY A PEDICLE
    -gelatinous appearance and abundant ground substance
  66. 66Primary Cardiac Tumors (1. Myxoma) Atrial myxoma?large Single pedunculated lesion arising from the area of the fossa ovalis and extents into the mitral valve orifice
    (usually lt atrium)
  67. 67what happens if myxoma occlude mitral valve?SYNCOPE
  68. 68Primary Cardiac Tumors (2. Lipoma)in the subendocardium\subepicardium\ wihin myocardium
    -localized, poorly encapsulated masses, which may be asymptomatic,
    -can create ball-valve obstructions
    -can lead to arrhythmias.
    -most often located in lt ventricle, rt atrium, or atrial septum
  69. 69Primary Cardiac Tumors (3. Rabdomyoma)-Benign hamartoma of cardiac muscle
    -most frequent primary tumor of the heart in infants and children
    -frequently discovered in the first years of life because of obstruction of a valvular orifice or cardiac chamber.
    -mostly affects ventricles
    -ASSOSIATED WITH TB
  70. 70Primary Cardiac Tumors (3. Rabdomyoma) morphology?small, gray-white myocardial masses up to several centimeters in diameter located on either the left or the right side of the heart, protruding into the ventricular chambers.
  71. 71Primary Cardiac Tumors (3. Rabdomyoma) histology?mixed population of cells, most characteristic(large, rounded, or polygonal w\ numerous glycogen-laden vacuoles) separated by strands of cytoplasm running from the plasma membrane to the more or less centrally located nucleus
    SPIDER CELLS MF
    -shown to have myofibrils., probably hamartomas and associated with tuberous sclerosis.
  72. 72MALIGNANT CARDIAC TUMOR (SARCOMA)Cardiac angiosarcomas and other sarcomas are not distinctive from their counterparts in other locations
  73. 73SUMMERY OF PREVIOUS?Cardiac tumors beside myxoma include:
    Benign
    1. Fibroma
    2. Lipoma
    3. Rabdomyoma
    Malignant
    1. Secondaries (lung, lymphoma, breast, melanoma )-Most commonly involve the pericardium, resulting in a pericardial effusion
    2. Angiosarcoma
  74. 74ANOTHER BREAK MFWOOOOOP WOOOOP
  75. 75TUMORS OF THE BLOOD VESSELS AND LYMPHATICSrange from completely benign tumors (angiomas) to intermediate grade/locally aggressive tumors to highly malignant tumors (angiosarcoma)
  76. 76Vascular TUMORS•BENIGN\NEVER metastasize, in fact some are not even TRUE neoplasms, but hamartomas)
    •INTERMEDIATE (rarely metastasize)
    •MALIGNANT (FREQUENT and EARLY metastases, like any other sarcoma->lung)
  77. 77Vascular TUMORSfollow the same diagnostic patterns of other mesenchymal ( “soft” tissue) tumors.
    -KEY difference: “endothelium” lined blood filled spaces\identification of endothelial cells by antigenic markers(factor VIII)
  78. 78Vascular TUMORS (1-HEAMANGIOMA)•ANY benign blood vessel tumor
    -looks like a wa7ma or birthmark
    -collection of blood vessels by the size of capillaries, surrounded by stroma
    -common in infancy & childhood, commonly present at birth often regresses during childhood
    -Mostly in the head and neck region, may also occur in the liver and affects skin.
  79. 79Vascular TUMORS (1-HEAMANGIOMA) Capillary hemangioma (SMALL vascular spaces)-“juvenile”, often called “birth marks”
    –Usually regress with age
    -Most common vascular tumo(seen in skin,SC tissue, mucus membrane of oral cavity & lips)
    -Morphology: Variable size – few millimeters-several centimeters.
    Bright red-blue in color, elevated sometimes
    Histology – lobulated, unencapsulated, of closely packed, thin walled blood filled capillaries, lined by flat endothelium
  80. 80Vascular TUMORS (1-HEAMANGIOMA) CAVERNOUS hemangioma (LARGE vascular spaces)-adult”
    –Usually do NOT regress
    -large dilated vascular channels
    -Morphology – reddish blue, soft mass. occur:face, extremities\deeper structures (liver, brain and others).
    -Histology – not encapsulated, spaces separated by CT bundles.
    -Complications – vulnerable to trauma – may ulcerate/bleed\rupture
    In the brain->pressure symptoms
  81. 81SOME STUFF BOUT HEME MFPICS HERE IN RAHAF NOTES
    -capillary hemangioma: lobulated neoplasm of thin walled small capillaries+scant stroma in between
    -cavernous hemangioma: large dilated vascular spaces separated by CT stroma
    -small empty spaces IN HISTO are BVs
    -has to be properly identified and diagnosis(DO NOT stick a needle for a biopsy bcz it will bleed profusely-> contrindicated)
  82. 82Vascular TUMORS (2-LYMPHANGIOMA)• Small 1-2 mm
    • 90% Head and neck region in kids <2
    • Generally……RARE
    • When large size and/or spaces present often called “CYSTIC HYGROMA"
    • Surgically treated
  83. 83Vascular TUMORS (2-LYMPHANGIOMA)benign tumors of lymphatic channels.
    1.Simple (capillary) –small lymphatic channels.
    2.Cavernou/ cystic hygroma –IN neck/axilla of children. consists of dilated lymphatic spaces, lined by endothelium, w\ pink coagulated lymph. difficult to remove surgically cuz not encapsulated.
    3. Glomus tumor/Glomangioma – benign painful tumor from thermoregulatory organ,seen at the distal portion of digits(esp under fingernails.)
  84. 84Vascular TUMORS (3-ANGIOSARCOMA)A. Malignant proliferation of endothelial cells; highly aggressive
    B. Common sites include skin, breast, and liver(liver associated with exposure to polyvinyl chloride, arsenic, and Thorotrast)
    C.May not look “vascular” at all
    D.Severe atypia
    E.Frequent and often bizarre mitoses
    F.Behave as any sarcoma, i.e., early pulmonary metastases
  85. 85Vascular TUMORS (4-KAPOSI'S SARCOMA)-low grade malignant/intermediate grade tumor.
    -Classic/ European KS.
    -Lymphadenopathic / African KS.
    -Transplant associated –due to immunosuppression.
    -AIDS associated –most common malignancy in AIDS patients.
    -Vascular ectasia / Telangiectasia: non neoplastic localized dilatation of vessels, which maybe:
    A-Congenital:relation w\ bleeding from nose
    B-Acquired – ‘spider nevi’ –seen in pregnancy and liver cirrhosis, CUZ INC estrogen
  86. 86Vascular TUMORS (4-KAPOSI'S SARCOMA)1) Classic European, described 1872, NON-HIV-> better prognosis
    2) EndemicAfrican, poor prognosis
    3) Transplant associated, HIV-(immunocomprimised)
    4) AIDS KS, caused by HHV-8, aka KSHV
    –PATCH->PLAQUE->NODULE
    -Note LACK of a malignant sounding name.
    -viral-induced BY HHV 8 attack endothelial cells->proliferation->tumor
  87. 87Vascular TUMORS (4-KAPOSI'S SARCOMA)A. Low-grade malignant proliferation of endothelial cells; associated with HHV-8
    B. Presents as purple patches, plaques, and nodules on the skin (Fig. 7.15); may also involve visceral organs
    C. Classically seen in
    1. Older Eastern European males—tumor remains localized to skin; treatment involves surgical removal.
    2. AIDS—tumor spreads early; treatment is antiretroviral agents (to boost immune system).
    3. Transplant recipients—tumor spreads early; treatment involves decreasing
    immunosuppression.
  88. 88TAKE A LONG FKING BREAK BITCHWE GOING GOOGOO GAAGAA
  89. 89Congenital heart diseases-Most common heart diseases in childhood
    -Abnormalities of the heart or great vessels that are present from birth.
    -Incidence is higher among premature infants
    -1% oflive births
    -Most detects are sporadic.
    -Faulty embryogenesis (3rd -8th week)
    -some asymptomatic til adult life-30s (ASD, coarctation of the aorta)
    •INC early detection via non invasive methods(US, MRI, CT)
  90. 90what is the Etiopathogenesis\causesof CHD?-Unknown in> 90%
    1.sporadic genetic abnormalities
    2.environmental factors:(alone\combination with genetic) congenital rubella infection, gestational diabetes, teratogens (including some therapeutic drugs). LOOK SLIDE 5\4\3 RAHAF FOR TABLE
  91. 91Explain the genetic abnormalities in releation ot CHD?(single gene mutations, small chromosomal deletions, trisomies\monosomies).
    affect genes encoding transcription factors for development.
    -Most->NO IDENTIFIABLE GENETIC FACTOR
  92. 92What are the most common genetic cause of congenital heart diseases?· Trisomy 21 (Down syndrome)
    · Deletion of chromosome 22q11.2 - DiGeorge syndrome.
    · Turner syndrome (monosomy X) and trisomies 13, 18, and 21
  93. 93Classify CHD?1-OBSTRUCTION:
    COARCTATION OF AORTA
    Ao\Pulmonay STENOSIS
    2-SHUNTS:
    A)LEFT->RIGHT(late cyanosis)
    -ASD\VSD\PATENT DUCT ART
    B)RIGHT->LEFT(early cyanosis)
    -ToF\Transposition of great vessels\persistant truncus arteriosus
  94. 94Defects with Left->Right shunt?-asymptomatic at birth BUT
    shunt can eventually reverse.
    1. Increased Flow through pulmonary circulation->pulmonary vessels hypertrophy-> pulmonary hypertension.(if significant? IRREVERSIBLE and might develop rt sided HF)
    2,INC pulmonary resistance->reversal of shunt-> late cyanosis (Eisenmenger syndrome) +Rt ventricular hypertrophy+
    polycythemia+clubbing.
  95. 95Defects with Right->Left shunt?cyanosis shortly after birth.
    -VENOUS EMBOLI become SYSTEM
    ALL Ts
    • Tetralogy Of Fallot
    • Transposition of
    the great vessels
    • Truncus arteriosus
    • Total anomalous
    Pulm. venous connections
    • Tricuspid atresia
  96. 96Notice THATLT->RT SHUNT THE PROBLEM IS WITH THE PRESSURE CHANGES DUE TO THE FLOW NOOOOTTT THE OXYGENATED BLOOD MOVING
  97. 97ATRIAL SEPTAL DEFECTS-gross: smooth surface is atria, ventricle rough+large hole in the septum
  98. 98What is ATRIAL SEPTAL DEFECTS?-Fixed opening in atrial septum (ostium secondum90%- ostium primum 5%-sinus venosus 5%) -> free communication of blood between atrias.
    -Ostium primum&Down syndrome.
    -lead to lt->rt shunt+split S, on auscultation (increased blood in right
    heart->delays closure of pulm valve)
    -Paradoxical emboli are important complication.
    - 8% of all CHD
  99. 99What is the morphology of ATRIAL SEPTAL DEFECTS?1.L->R shunt,CUZ pulm BP (24/8 mm Hg) Lt ventricle. Pulmonary flow may 2x-4x normal.
    2.murmur often present cuz of excessive flow through tricuspid valve
    3.INC flow through pulm valve and circulation-> rt atrium and ventricle Volume hypertrophy
    4.Compensatory INC in muscular thickness of the small arteries and arterioles with vasoconstriction-> irreversible pulmonary hypertension develops in <10% of subjects with an isolated unoperated defect..
  100. 100What is the morphology of ATRIAL SEPTAL DEFECTS?5.Eisenminger Syndrome: severe pulmonary hypertension->reversal of the shunt (rt->lt)+late cyanosis, polycythemia and clubbing of fingers due to chronic hypoxia cuz of perfusion of the tissues by deoxygenated blood. Respiratory difficulties, and cardiac failure occur progressively
    6.IE rare cuz low-pressure gradients+ sluggish flow, but paradoxic embolism\ brain abscess occur when flow is reversed.
  101. 101What is the morphology of ATRIAL SEPTAL DEFECTS?1-Clinically:
    – Asymptomatic until adulthood (30y)
    – mild systolic murmur,
    – Splitting of S2
    2-Complications :
    • Pulmonary vascular changes …PHT…ESINMINGER SYNDROME
    • Paradoxical emboli
    • Heart failure
  102. 102What are the hemodynamic changes of ATRIAL SEPTAL DEFECTS?-flow from lt (high P)->Rt->VOLUME overload in this part
    -more blood ->right ventricle+ pulmonary artery+ pulmonary circulation
    -Only detected when complications And can close spontaneously->give it a chance before surgery
    -volume overload->hypertrophy of the media->irreversible pulmonary hypertension->Rt sided HF "ESINMENGER’S SYNDROME"-> secondary volume hypertension cuz VOLUME overload IN PULMONARY CIRCULATION secondary to the ASD
  103. 103why is the murmur systolic in ASD and not diastolic?cuz greater flow of blood In the pulmonary vessels and valves->mild systolic murmur
  104. 104AVSD• Associated with defective, inadequate AV valves
    • partial, or COMPLETE (ALL 4 CHAMBERS FREELY COMMUNICATE)‏
    • very rare In which we have huge opening in AV septum
  105. 105VSD-abnormal opening in the ventricular septum that allows free communication between right and left ventricles. It represents 30 % of all types of congenital heart diseases.
    -Most common congenital heart defect
    -Associated with fetal alcohol syndrome
  106. 106VSD-Results in left-to-right shunt; size of defect determines extent of shunting and age at presentation. Small defects ->Asymptomatic. Large ->Eisenmenger
    -Treatment involves surgical closure; small defects may close spontaneously.
  107. 107VSD classification (accord to size of defect)1.Small defects (less than 0.5 cm in diameter) are known as Roger’s disease, and most are muscular.
    2.Large defects are usually membranous\infundibular+remain patent and permit a significant left-to-right flow->rt ventricular hypertrophy +early pulmonary hypertension. This is followed by:
    Eisenminger syndrome, shunt reversal, late cyanosis, clubbing, polycythemia.
  108. 108VSD classification (accord to location of defect)1.Membranous:90% (membranous VSD) and are therefore close to the AV (His) bundle of conduction system.
    2.Muscular: remainder lie below the pulmonary valve (infundibular, supracristal, or subarterial ) or are located within the muscular septum. Although most often single, VSDs in the muscular septum may be multiple (so-called “Swiss-cheese septum”).
  109. 109VSD-upper part of the ventricular wall closer to the atria = membranous
    -muscular part, it takes the swiss-cheese appearance (multiple holes), but when in membranous parts, it is usually one hole only.
  110. 110VSD clinincally and complication•Clinically
    –30-50% spontaneous closure (delay Rx)
    –Harsh pan systolic murmur
    •Complications
    –PHT…EISINMINGER..cyanosis
    –Increases risk of endocarditis
  111. 111VSD hemodynamic changes?-EARLY STAGE: asymptomatic, with only the systolic murmur cuz INC flow in pulmonary artery\might close on their own after some chance, Otherwise quick correction cuz of consequences
    -LATE STAGES:reversal of the shunt when pulm HTN INC->INC rt ventricular pressure higher than Lt->late cyanosis->Esinmenger’s(less common in ASD bcz less volume (no pressure overload))
  112. 112what is the first stage of pulmonary HTN?HYPERPLASIA OF MEDIA
    (whenever the HTN is established-> irreversible.)
  113. 113PATENT DUCTUS ARTERIOSUS:-Ductus arteriosus remains open after birth.
    -8% of all types of CHD.
    -associated with congenital rubella
    -Results in left-to-right shunt between the aorta and the pulmonary artery
  114. 114Compare normal closure OF THAT MF?1-Normally, after birth, with left-to-right flow->primary stimulus for closure of the ductus is INC NEONATAL BLOOD O2+DEC PROSTAGLANDINS-> ductal muscular contraction
  115. 115INFANTS WITH PDA?-full-term infant->closes functionally within the first day or two of life.
    -full-term infants+PDA=true structural wall defect.
    -premature respiratory distress syndrome at birth (hypoxemia)->MAY remain patent.
  116. 116NOTICE THAT...In some cases->Patency of the ductus arteriosus may be necessary in some patients with complex forms of congenital heart disease ->GIVE PGs ->keep PDA open.
    ((Prostaglandin E1) in case of TGA, TA, TAPVC, PA, AA)
  117. 117WHY CAN PDA be life threatning\Life saving?-Threatning:(hypoxia+ tissue ischemia -> polycythemia)
    -Saving:(no other connection in the heart:Transposition of great vessels = separate systemic and pulmonary circulations = aorta coming from right ventricle and pulmonary trunk coming from left ventricle->no oxygen to limbs And all P2->lungs)
    PDA: connection to keep baby alive otherwise death at birth
  118. 118What is the morphology of PDA?-85 to 90% of PDAsare isolated
    -Rest? w\ VSD, coarctation,pulm\Ao stenosis, hypoplastic Lt heart syndrome [HLHS], pulmonary atresia, transposition of the great vessels
    -No cyanosis at first?cuz Lt->Rt
    -Why do we heat Loud machinery HOLOSYSTOLIC murmur?continuous flow from aorta-> pulmonary artery.
  119. 119What is the morphology of PDA?-Obstructive pulmonary vascular disease (pulm HTN)+ultimate Eisenminger syndrome+flow reversal+late cyanosis(especially lower extremeities), clubbing, polycythemia, and Rt ventricular faliuer
    ->lesion? INOPERABLE
  120. 120explain the diffrence between PDA early and late stage?1-EARLY:No cyanosis and machinery murmur UNTIL->pulm artery gets abnormal pressures->compensatory mechanism (hypertrophy of media
    2-LATE:pulm HTN->reverse shunt->deO2 blood->aorta->lower body differential cyanosis
  121. 121Why is there diffrential cyanosis in PDA?Cuz unoxygenated blOOd enters aorta below suclavian artery DISTAL TO BREANCHING OF MAJOR ARTREIES->ESCAPES UL
  122. 122How do u treat PDA?-rostaglandin inhibitors (NSAIDS)\indomethacin\Surgery>close the ductus.
    (PGs MAINTAIN PATENCY)
  123. 123Take a break mfwe still got a long ass way to go
  124. 124some thigns bout RT->LT shunt before we start1-transposition = aorta& pulm trunk switch places
    2-Truncus arteriosus = ONLY ONE trunk out of ventricles->branches=>all heart branches=>No separation between aorta and pulmonary-> cyanosis
    3-Total A.V.C = pulmonary veins empty to the right atrium->no oxygen to Lt heart + body->atrophy of Lt heart
    4-Tricuspid atresia = very severe stenosis of tricuspid valve may completely closed
  125. 125some things bout RT->LT shunt before we start-Pradoxical emboli = emboli from one side of the circulation to the other ( from venous side then passes through right to left to systemic)
    -Clubbing = manifestation of hypoxia
    -Polycythemia…react to hypoxia
  126. 126TETRALOGY OF FALLOT-10 % of all types of CHD
    -most common form of cyanotic congenital heart disease.
  127. 127What are The four features of Fallot’s tetralogy?(1) VSD
    (2) Obstruction to the right ventricular outflow tract ( subpulmonary stenosis cuz pulmonary valve close to VSD-> stenosis below valve )
    (3) Overriding of the aorta to the VSD (blood from both sides of ventricles-> O2+DeO2)
    (4) Right ventricular hypertrophy(bcz of stenosis of pulm artery->pressure overload)
  128. 128What are The clinical features of Fallot’s tetralogy?– Onset of cyanosis at 3 months
    – SURVIVAL DEPENDS on SEVERITY of SUBPULMONIC STENOSIS
    – PINK tetrology if pulmonic obstruction is small
  129. 129What is The morphology of Fallot’s tetralogy?1-greater resistance to Rt ventricular outflow+pulmonary stenosis.
    2-right-to-left shunting predominates -> cyanosis.
    3-pulmonary arteries->progressively smaller\thinner walled (hypoplastic)+ aorta progressively LARGER in diameter.
    4- child grows->INC heart size-> pulmonic orifice DOESN'T expand proportionally->worst obstruction.
    5-subpulmonary stenosis->protects lungs from pressure overload
  130. 130What is The morphology of Fallot’s tetralogy?6-most cyanotic from birth\soon thereafter.
    7-Hypoxemic spells ( bouts) with deeper cyanosis and dyspnea. Loss of consciousness and fainting attacks may occur
    8-Retardation of growth\clubbing of fingers cuz of systemic chronic hypoxia
    9-Squatting position is done by older children to relieve hypoxemic spell
    10-heart enlarged\may be “boot-shaped” cuz right ventricular hypertrophy(particularly apical region.)
  131. 131Why is Rt ventricular failuer rare in ToF?cuz the right ventricle is decompressed ( pump the blood) into the left ventricle and aorta.
  132. 132What is the use of squatting?increased arterial resistance
    decreases shunting and allows more blood to reach the lungs.
  133. 133what is the most important factor of severity of ToF and WHY?degree of subplumonic stenosis
    -will decide whether blood go to pulm trunk\overriding aorta
    -very minimal?Pink fallot w\ no symp
    -severe (most cases)?->high pressure in Rt ventricle->blood go through VSD to ->left->aorta->Cyanosis!
    -Should be corrected asap bcz of consequences of hypoxia (hypercoagulability, thromboemoboli)
  134. 134TRANSPOSITION OF GREAT VESSELS?We NEEDED a shunt from left to right, else, incompatible with life(need ASD, VSD, PDA)
  135. 135Transposition of great MFs definition and leads to?1-Abnormal development of trunco-conal septum
    2-resulting in:
    -aorta arises from right ventricle
    -pulmonary artery from left ventricle
    -early cyanosis+Rt ventricular hypertrophy+Lt ventricle ATROPHY
    -Poor prognosis without surgery
  136. 136Transposition of great MFs:-Associated with maternal diabetes
    -pulmonary+systemic circuits DON'T mix.
    -Creation oF shunt (allowing blood to mix) aFter birth is REQUIRED for survival.
    -PGE->administered to maintain a PDA until definitive surgical repair is
    performed.
  137. 137TRUNCUS ARTERIOSIS-Failure of development of dividing septum between aorta and pulmonary artery with common trunk->combined in one large Truncus Arteriosus
    -Usually VSD is also present
    -Massive flow of blood to lungs-> pulmonary HTN
    -early cyanosis+CHF
    -Poor prognosis W\O surgery
  138. 138TRICUSPID ATRESIAA-Tricuspid valve orifice fails to develop -> hypoplastic RT ventricle
    B-Needs a shunt, ASD, VSD, or PDA, Often associated with ASD
    -early cyanosis
  139. 139Total Anomalous Pulmonary Venous Connection (TAPVC)-pulmonary veins anomalous\abnormal with respect to how they return to heart.
    -O2ed blood goes to right heart
    • Needs a PFO (patent foramen ovale) or VSD
    • HYPOPLASTIC LA
  140. 140ANOTHER BREAK MFLAST MFING PART
  141. 141OBSTRUCTVE CHD\without shunt• COARCTATION OF THE AORTA
    • PULMONARY STENOSIS/ ATRESIA
    • AORTIC STENOSIS/ATRESIA
  142. 142Coarctation of Aorta•M>F BY 3X-4X
    •INFANTILE FORM (proximal to PDA) (SERIOUS)‏
    •ADULT FORM (CLOSED DUCTUS, i.e., NO PDA)‏
    •Bicuspid aortic valve 50% of the time
  143. 143Coarctation of Aorta-females with Turner’s syndrome frequently have a coarctation.
    -6% of all types of CHD
    -Two classic forms:
    (1)“infantile” form (tubular hypoplasia of the aortic arch proximal to a patent ductus that is often symptomatic in early childhood)
    (2)“adult” postductal(discrete ridge-like infolding of the aorta, just opposite to ligamentum arteriosum)
  144. 144What are the effects of Coarctation of Aorta?1.Preductal coarctation:
    -Early signs and symptoms (immediately after birth).
    -head and upper extremities are hypoxic and lower parts of body are cyanotic.
    -Many infants with this anomaly do not survive the neonatal period without surgical intervention ( Hence; infantile)
  145. 145What are the effects of Coarctation of Aorta?2. postductal coarctation:
    -Most of children are asymptomatic
    -Typically UL HTN, but there are WEAK PULSE+lower BP in lower extremities, associated with manifestations of arterial insufficiency (i.e., claudication and coldness).
  146. 146What are the effects of Coarctation of Aorta IN ADULT?-collateral circulation between pre-coarctation+post-coarctation arteries->intercostal+internal mammary arteries->enlargedat at sites of anastomosis+radiographically visible erosions (“notching”) of the undersurfaces of ribs.(last line imp)
    -NOT associated with a PDA->coactation distal to aortic arch.
    -Associated with bicuspid aortic valve
    -UL HTN, but there are WEAK PULSE
  147. 147What are the effects of Coarctation of Aorta IN INFANTILE?-associated with a PDA; coarctation lies distal to aortic arch, but proximal to PDA.
    -Presents as lower extremity cyanosis in infants, often at birth
    -Associated with Turner syndrome
  148. 148Pulmonary Stenosis or Atresia with Intact Ventricular Septum-If 100% atretic, hypoplastic RV with
    ASD
    -Clinical severity ~ stenosis severity
    -Relatively frequent malformation represents an obstruction at pulmonary valve.
    -may occur as isolated defect\part of a more complex anomaly (ToF\transposition->valve usually bicuspid but occasionally unicommissural\dysplastic tricuspid)
  149. 149Aortic Stenosis and Atresia-little functional significance early in life BUT predisposed to calcification in adult life .
    -Rarely there is a single cusp-> surprisingly compatible with survival.
    -severe congenital aortic stenosis\ atresia
    -obstruction of Lt ventricular outflow tract->underdevelopment (hypoplasia) of Lt ventricle+ascending aorta.
    -ductus must be open to allow blood flow to aorta and coronary arteries.
    -hypoplastic left heart syndrome->nearly always fatal in the first week of life, when the ductus closes.
    -Surgical repair is possible but carries a relatively high mortality rate.
  150. 150AORTIC STENOSIS/ATRESIA•VALVULAR:
    –If severe, hypoplastic LVfatal
    •SUB-valvular (subaortic):‏
    –Aortic wall THICK BELOW cusps
    •SUPRA-valvular:
    –Aortic wall THICK ABOVE cusps in ascending aorta
    - Would you expect LVH in all cases? YES

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Flashcards on Heart Failuer, created by Dua Ga on 10/10/2018.
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