RAD 204 PATHOLOGY

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RAD 204 PATHOLOGY

• COLLEGE OF MEDICAL SCIENCES/RADIOLOGICAL SCIENCES
  DEPT
• LECTURE 5 CARDIOVASCULAR PATHOLOGY
• WEEK OF OCTOBER 6, 2013
• DR SHAI

part 1 of 2
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STRUCTURE OBJECTIVES

• Companion lecture to this lecture link
  available on http//health141.yolasite.com/
• you are required to have a print or e-version of
  the companion lecture during this lecture
• congenital abnormalities of the heart
• atherosclerosis, ischaemic heart disease,
  hypertension
• valve disorders aneurysms
• diseases of the myocardium, pericardium
• inflammatory and neoplastic disease
• radiological diagnostics in cardiovascular
  pathology FORMAL PROJECT 1 Due November 5,
  2013
• mid term exam 2nd week after Hajj holiday, in
  class, during class time. mcq, short answer

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the project

• http//emedicine.medscape.com/radiology
• gt CARDIAC
• choose from list of cardiac imaging list and use
  (but do not copy/paste) this site, as ONE OF MANY
  credible references gt submit a formal report with
  references on the pathology of the condition and
  a COMPREHENSIVE explanation of
• imaging techniques used in the condition
• radiological diagnostic and therapeutic
  interventions
• OR
• http//my.americanheart.org/professional/Education
  /Professional-Education_UCM_426265_WidgetListPage.
  jsp (MAIN PAGE) CLICK imaging techniques
  application gtgt register and take this course
• http//learn.heart.org/ihtml/application/student/i
  nterface.heart2/index2.html?searchstring5670
• register and complete coursegt take screen shot
  of your progress results gt submit

DUE NOVEMBER 5, 2013
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mid term exam

• WHEN 2nd week after Hajj holiday
• WHERE in class, during class time
• TOPICS terminology, basic pathology, cell
  damage, repair, response to injury,
  inflammation and healing, CVS pathology
• STYLE Multiple Choice Questions, Short Answer
  Questions, Read an Article answer questions on
  the article
• TIPS see the http//health141.yolasite.com/ for
  lectures and articles

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congenital heart abnormalities

• define congenital
• prevalence 8/1000 live births
• aetiology
• idiopathic/sporadic most cases
• maternal rubella, alcohol abuse, intrauterine
  radiation, drugs eg thalidomide
• genetic/ chromosomal eg. Trisomy 21 Downs
  Syndrome
• clinical presentation apparent at or shortly
  after birth heart failure sequelae gt cyanosis,
  dyspnoea, feeding difficulties, failure to thrive

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types of congenital HD

• abnormal shunting of blood b/w LEFT RIGHT sides
  of heart
• left - to - right more common b/c high pressure
  in lt heart
• right - to left shunts from increased resistance
  to blood moving out of rt heart
• obstruction to blood flow

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left - to - right shunts

• malformations gt shunting blood from left to right
  side of heart
• commonest group of congenital heart abnormalities
• from high pressure in lt. side
• blood does NOT bypass lungs so no cyanosis

type of all CHD abnormalities
Ventricular Septal Defect 25-30
Atrial Septal Defect 10-15
Patent Ductus Arteriosus 10-15
AV Septal Defect 5
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ventricular septal defects

• VSD defect of INTERventricular septum
• INTERventricular septum membranous (fibrous)
  portion muscular portion
• size site of defect determines extent of shunt
• presents as cardiac failure in infants or murmur
  in older children/adults
• signs
• pansystolic murmur flow from high pressure left
  ventricle to low pressure right ventricle during
  systole
• tachypnoea (increased respiratory rate)
• indrawing of lower ribs on inspiration
• Management small defect no treatment, close
  spontaneously. large defects surgical repair.

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atrial septal defects

• females more than males 21
• defect of INTERatrial causing shunting to RIGHT
  with enlargement of RT heart pulmonary arteries
• usually at fossa ovalis (incompletely closed
  ostium secundum defect)
• clinical features most children are symptom
  free for years, detected at routine clinical exam
  CXR
• some children dyspnoea, chest infections, cardiac
  failure, arrythmia (eg atrial fibrillation)
• signs from volume overload of rt ventricle
• systolic flow murmur over pulmonary valve
• wide splitting of 2nd Heart Sound (delayed
  closure of pulmonary valve, from increased stroke
  volume and Rt Bundle Branch Block)
• diastolic rumbling murmur (increased flow across
  tricuspid valve)
• Mgmt surgical closure otherwise RV hypertrophy
  pulm. hypertension

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patent ductus arteriosus

• persistence of embryological connection between
  AORTA pulmonary trunk Lt. main pulmonary
  artery
• OPEN ductus arteriosus in 10 CHD, females more
  than males
• associated with maternal Rubella infection
• EMBRYOLOGY intra uterine life
• ductus arteriosus allows Oxygenated Placental
  Blood to flow from Pulm. Artery to Aorta
  (BYPASSING LUNGS)
• _at_ birth pulmonary vasculature resistance
  declines, blood is diverted to lungs for
  oxygenation and ductus arteriosus closes within
  1st few days of life
• BUT if ductus stays patentgt blood continually
  shunted from aorta to pulm artery
• up to 50 LV output may be recirculated through
  lungs, with increase work on heart

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pda

• clinical features depends on size of the left -
  to right shunt
• small shunts asymptomatic , large retarded
  growth development gt cardiac failure
• signs continuous machinery murmur at HS2
• mgmt surgical in childhood

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atrioventricular septal defect

• septal defect with both atrial and ventricular
  component
• from failure of endocardial cushions to fuse
  together
• AV canal persists resulting in a single heart
  chamber, separated by abnormal valve leaflets

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right - to - left shunts

• resultgt blood bypasses lungs to enter systemic
  circulation gt cyanosis

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RT TO LT

• Tetralogy of Fallot
• commonest cause of cyanosis in lt 1 yr olds,
  1/2000 live births
• tetra FOUR
• i) Ventricular Septal Defect
• ii) Over riding aorta (receives blood from rt
  lt ventricles)
• iii) pulmonary stenosis (from thickening of
  subvalvar muscle or stenosis in valve cusps)
• Rt Ventricular Hypertrophy

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tetralogy of fallot

• AETIOPATHOGENESIS defects from embryological
  abnormality in bulbar septum, which normally
  separates ascending aorta from pulm. artery, and
  which fuses with interventricular septum
• pulm stenosisgt inadequate perfusion of lungs
• overriding aortagt receives blood from BOTH
  ventricles
• net result gt systemic circulation w/
  DEOXYGENATED blood gt CYANOSIS
• cyanosis esp. after feeding or crying attack,
  results in growth stunting, digital clubbing,
  polycythaemia
• children feel RELIEF from squatting
• loud ejection systolic murmur from VSD or PS
• MGMT surgical closure of septal defect,
  rechannel blood to aorta from LV
• COMPLICATIONS BACterial endocarditis, cerebral
  infarct/abcess

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transposition of great arteries

• malformation whereby connections between RT LT
  ventricle, aorta, pulm. artery are DISORDERED
• aorta emanates from RV, pulm art from LV
• prognosis possible if there IS ONE OR MORE OF
• ASD
• VSD
• PDA
• mgmt surgical correction

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persistent truncus arteriosus

• EMBRYO aorta pulm art develop from same
  single tube (TRUNCUS ARTERIOSUS)
• persistence by failure of conotruncal RIDGES to
  fuse and descend towards ventricles
• so, pulm. artery arises away from origin of
  undivided truncus
• there is always defective interventricular
  septum
• undivided truncus overrides both ventricles and
  receives blood from both sides.

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tricuspid atresia

• rare, absent tricuspid orifice , always
  associated with
• Patent foramen ovale
• VSD
• Underdeveloped RV
• Hypertrophy of LV
• pathophysio blood shunted from RA to LA, then
  small amount shunted from LV to RV via defect
• some deoxygenated bloodenters systemic
  circulation gt cyanosis
• mgmt surgical correction

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obstructive congenital defects

• COARCTATION OF AORTA
• stenosis of aorta, at or just beyond ductus
  arteriosus
• females 2 males 1, 1/4000 live births
• clinical features form stricture of aorta
• Hypertension (proximal to stenosis) gt headache,
  dizzy
• Hypotension (distal to stenosis) gt weakness, low
  circulation

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coarctation of aorta

• BP raised in upper body, normal or low in legs
• large pulsations in upper body, lower body weak
  pulses
• systolic murmur
• untreated
• LV failure from HTN, cerebral hemorrhage,
  bacterial endocarditis, dissection of aorta

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ATHEROSCLEROSIS

• ARTERIOSCLEROSIS thickening loss of
  elasticity of arteries from ANY condition.
• commonest type is AtheroSclerOsis hardening or
  loss of elasticity due to atheroma formation
• involves intima of large - medium sized arteries
• other type Monckebergs medial calcific
  sclerosis media of medium muscular arteries,
  esp in limbs, lumen size normal
• other type arteriolar sclerosis thickening of
  walls of small arteries and arterioles

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consequences of arteriosclerosis

• vessel thickening narrow lumengt poor tissue
  perfusion
• inelasticity of vessels vessel rupture gt
  haemorrhage
• altered endothelium risk thrombosis define
• arteriosclerosis leads to MI, angina pectoris,
  stroke, TIA, ischaemic colitis, claudication

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atherosclerosis

• degenerative dz. of large med arteries
• accumulation of lipids in intima (tunica intima)
  of arteries gt cell reactions
• commonest aorta (abd. aorta), coronary
  arteries, cerebral arteries, iliac/femoral art
• risk factors
• constitutional genetic traits, race, gender (up
  to 55 males more), age
• hard hypercholesterolaemia (LDL), Hypertension,
  Diabetes mellitus, smoking
• soft lack of exercise, obesity, stress
  personality traits

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pathogenesis

• plaques gt low grade chronic endothelial injury
  from risk factors
• atheroma (atherosclerotic plaques) from
• endothelial injury platelet adhesion to endo.,
  diffusion of plasma proteins including LDL into
  intima of arteries, migration of monocytes into
  intima
• platelets release PDGF gt proliferation of smooth
  muscle cells
• musc cells deposit excess collagen elastin in
  intima
• macrophages phagocytose LDL and release free lipis

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useful links

• http//www.brown.edu/Courses/Digital_Path/systemic
  _path/cardio.html
• https//web.duke.edu/pathology/Week13/Week13.html

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hypertension

• elevated blood pressure important and treatable
  cause of cardiac failure
• also a risk factor for atherosclerosis cerebral
  haemorrhage
• DEFINITION sustained rise of systemic BP gt 160
  mmHg and / or diastolic gt 95 mmHg
• borderline hypertension 140-160 mmHg systolic
  and/or 90-95 mmHg diastolic
• AETIOLOGICAL CLASSIFICATION
• PRIMARY essential / idiopathic raised BP with
  age, 90 cases, raise peripheral vascular
  resistance (genetic, socio-economic, dietary,
  hormonal, neurological sns)
• SECONDARY raised BP NO, renal disease, adrenal
  dz, endocrine dz, shunts, drugs, preeclampsia

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patho classification htn

• BENIGN stable elevation BP/ years
• MALIGNANT dramatic increase BP / short period
  time

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benign

• vessel changes gradually respond to persistent
  stable elevated BP
• histologically
• hypertrophy thickening of muscular media
• thickening of elastic lamina
• fibro elastic thickening of intima
• hyaline deposition in arteriole wall (hyaline
  arteriosclerosis)
• effects
• reduced vessel lumen leads to tissue iscahemia
• rigidity leads to limited expansion
• fragility of vessels leads to haemorrhage

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malignant

• acute destructive changes in walls of small
  arteries when BP SUDDENLY rises
• effects
• necrosis of vessel wall (fibrinoid necrosis)
• infiltration by fibrin in vessels
• leads to lack of blood flow to kidney.

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COMPLICATIONS OF HTN

• VASCULAR
• hyaline deposition in arteries
• fibrinous deposition in arteries
• HEART
• LV Hypertrophy
• BRAIN
• intracerebral haemorrhage small vessel ,
  microinfarct, fluid lacunae
• KIDNEY
• ischaemia of nephrons, chronic renal failure,
  benign hypertensive nephrosclerosis, renal failure

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pulmonary hypertension

• pulmonary arterial pressuRe gt 30 mmHG
• precapillary, capillary, post capillary causes
• effects transudation fluid from pulm
  capillaries INTO alveoli gt dyspnoea,
  expectoration of blood stained watery fluid
• chronic effects hyperplastic arteriosclerosis
  (muscular hypertrophy dilation of pulm
  arteries),
• necrotizing arteriolitis inc pressure in pulm
  arteries haemorrhae in alveolar spaces with
  haemosiderin laden macrophages
• cor pulmonale RT ventriular hypertrophy from inc
  workload

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ischaemic heart disease

• condition caused by a reduction / cessation in
  blood supply to myocardium myocardial ischaemia
• usually from atherosclerosis, sometimes from
  coronary emboli
• leading cause of death in western world
• results in 4 syndromes
• stable angina (chronic)
• unstable angina (Acute)
• myocardial infacrtion (acute)
• sudden cardiac death (acute)

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angina pectoris

• episodic chest pain, from ischaemia to myocardium
  following exercise
• usually from stenosis of 1gt coronary arteries,
  red. blood to myocardium
• stenotic coronary arteries are either
• eccentric fibrolipid plaques affect 1 side of
  wall, vasodilataory drugs may help
• concentric colagenous plaques affect whole art
  wall, circumferential.

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stable angina

• predictable , occurs at fixed level of exercise
  from inc. heart workload
• pain relieved in 2 minutes of rest
• stenosis of at least 75 need to reproduce angina
  on exercise

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unstable angina

• unpredictable, not related to exercise
• reflects reversible ischaemia due to variable
  luminal stenosis
• caused by variations in vasomotor tone by plaques
  or emboli causing occlusion

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prinzimental angina

• vasospastic angina
• at rest
• from increase in coronary vasomotor tone
• unknown mechanism
• common in early morning
• severe but self limiting pain
• rarely lead to MI

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mgmt angina

• avoid risk factors
• drug therapy ( nitrates, b blockers)
• surgery (coronary angioplasty, bypass)

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myocardial infarction

• necrosis of myocardium as a result of severe
  ischaemia
• COMMON, 15 of all deaths worldwide, 60 sudden
  deaths.
• middle age, 50 , but 10 in 35-50 yr olds
• features chest pain, breathlessness, vomitting,
  collapse or syncope
• types
• regional (90) infarct in are supplied by ONE
  major coronary artery
• diffuse (10) cases, relates to overall
  myocardial poor perfusion

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patho features

• macro site of regional infarct shows
  circumferential necrosis from ppor perfusion
• histo NECROSIS Acute Inflammation
• necrotic tissue replaced by collagenous scar
• process takes 7 weeks, necrosis causes enzyme
  release and proteins which are used as markers
  CK-MB, troponin T, lactic dehydrogenase

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outcomes of MI

• IMMEDIATELY sudden cardiac death
• Short Term
• arrythmias (if involves conduction tissue)
• LV Failure necrotic wall softens, cardiac
  dilation
• rupture blood bursts into pericardial cavity
• papillary muscle dysfunction 1 gt valve leaflets
  canot close in systole
• mural thrombus on the inflamed endocardium over
  infarcted area
• acute pericarditis from inflammation over
  infarct surface

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long term

• chronic Left hEART FAILURE inadequate LV
  pumping action
• ventricular aneurysm distension of weakened
  fibrotic part of LV
• recurrent MI SECONDARY MI
• Dresslers Syndrome AutoImmune pericarditis,
  raised ESR

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part 2 will be sent next week

• happy studying!