1b. BLOOD VESSELS AND HEART LECTURE.pptx 2.pdf

Anapath

1. Heart and Blood vessels- Lecture,
MBChB III
23/03/25
Dr Nthabiseng E Mothata
Registrar
Anatomical pathology department

2. BLOOD VESSELS
Vascular diseases are responsible for some of the most
common and lethal conditons afictnt mankind.
Althouth most clinically sitnifcant disorders involve arterial
lesions, venous patholoties also can wreak havoc.
Vascular disease develops throuth two principal mechanisms:
• Narrowint or complete obstructon of vessel lumina, occurrint
either protressively (e.t., by atherosclerosis) or
acutely (e.t., by thrombosis or embolism)
• Weakenint of vessel walls, causint dilaton and/or
rupture

3. STRUCTURE AND
FUNCTION OF
BLOOD VESSELS

4. Endothelial cells
•Endothelium is a contnuous
sheet of cells linint the entre
vascular tree that retulates
many aspects of blood and
blood vessel functon.
•Restnt ECs maintain a non-
thrombotenic blood-tssue
interface, modulate
infammaton, and infuence
the trowth and behavior of
other cell types, partcularly
SMCs.

5. Blood pressure regulation

6. Hypertensive vascular
disease
•Hypertension is a common disorder afectnt 25% of the populaton
•it is a major risk factor for atherosclerosis, contestve heart failure, and renal
failure.
•Hypertension may be primary (idiopathic) or less commonly secondary to an
identfable underlyint conditon.
•In close to 95% of cases hypertension is idiopathic or “essental.” The remainint
cases (secondary hypertension) are due to primary renal disease, renal artery
narrowint (renovascular hypertension), or adrenal disorders.
•Essental hypertension represents 95% of cases and is a complex, multfactorial
disorder, involvint both environmental infuences and tenetc polymorphisms
that may infuence sodium resorpton, aldosterone pathways, the adrenertic
nervous system, and the renin-antiotensin system.
•Hypertension occasionally is caused by sintle-tene disorders or is secondary to
diseases of the renal arteries, kidneys, adrenal tlands, or other endocrine ortans.

7. Histology
Hyaline arteriolosclerosis.
Hyperplastc arteriolosclerosis
(“onion-skinning”) (arrow)

8. Vascular wall response to
injury

9. Arteriosclerosis
•Arteriosclerosis literally means “hardenint of the arteries”;
•it is a teneric term refectnt arterial wall thickenint and loss of elastcity.
•Four distnct types are recotnized, each with diferent clinical and patholotic causes and
consequences:
• Arteriolosclerosis afects small arteries and arterioles and may cause downstream
ischemic injury.
•Mönckeberg medial sclerosis is characterized by the presence of calcifc deposits in
muscular arteries, usually centered on the internal elastc lamina, and typically in
individuals older than 50 years of ate. The lesions do not encroach on the vessel lumen
and usually are not clinically sitnifcant.
•Fibromuscular intmal yperplasia is a non-atherosclerotc process that occurs in
muscular arteries larter than lesion driven by infammaton (as in a healed arterits or
transplant-associated arteriopathy, or by mechanical injury (e.t., associated with stents or
balloon antioplasty, see later).
•Such a healint response can cause substantal stenosis of the vessel; indeed, such intmal
hyperplasia underlies in-stent restenosis and is the major lont-term limitaton of solid
ortan transplants.

10. Atherosclerosis
•Atherosclerosis is characterized by intmal lesions
called atheromas (or atheromatous or
atherosclerotc plaques) that impinte on the
vascular lumen and can rupture to cause sudden
occlusion.
•It underlies the pathotenesis of coronary, cerebral,
and peripheral vascular disease, and causes more
morbidity and mortality (routhly half of all deaths)
in the Western world than any other disorder.

12. Morphology

13. Microscopy

14. Atherosclerotic plaques are susceptible to several
clinically
important changes:
•Rupture, ulceraton, or erosion
•Hemorrhate into a plaque.
• Atheroembolism
•Aneurysm formaton.

16. Aneurysms and dissections
•Aneurysms are contenital or acquired dilatons of blood vessels or the heart
• “True” aneurysms involve all three layers of the artery (intma, media, and adventta) or the
attenuated wall of the heart; these include atherosclerotc and contenital vascular aneurysms,
as well as ventricular aneurysms resultnt from transmural myocardial infarctons.
•By comparison, a false aneurysm (pseudoaneurysm) results when a wall defect leads to the
formaton of an extravascular hematoma that communicates with the intravascular space
(“pulsatnt hematoma”).
• Examples are ventricular ruptures contained by pericardial adhesions and leaks at the juncton
of a vascular traf with a natural artery.
• In arterial dissectons, pressurized blood tains entry to the arterial wall throuth a surface
defect and then pushes apart the underlyint layers. Aneurysms and dissectons are important
causes of stasis and subsequent thrombosis; they also have a propensity to rupture—ofen with
catastrophic results.
•Aneurysms can be classifed by shape
•Saccular aneurysms are discrete outpouchints rantint from 5 to 20 cm in diameter, ofen with a contained
thrombus.
•Fusiform aneurysms are circumferental dilatons up to 20 cm in diameter; these most commonly involve
the aortc arch, the abdominal aorta, or the iliac arteries.

18. Thoracic and abdominal
aneurysms
•Aneurysms occurrint because of atherosclerosis form most
commonly in the abdominal aorta and common iliac
arteries, and may also involve the aortc arch and
descendint thoracic aorta.
•Abdominal aortc aneurysms (AAAs) occur more frequently
in men and in smokers and rarely develop before 50 years
of ate.
•Atherosclerosis is a major cause of AAA, but other factors
clearly contribute, since the incidence is less than 5% in
men older than 60 years of ate despite the almost universal
presence of abdominal aortc atherosclerosis in this
populaton.

19. •The clinical consequences of AAA include the followint:
• Obstructon of a vessel branc ing of t e aorta (e.t., the renal,
iliac, vertebral, or mesenteric arteries), resultnt in ischemia of the
kidneys, lets, spinal cord, or tastrointestnal tract, respectvely
•Embolism of at eromatous material (e.t., cholesterol crystals) or
mural thrombus
•Impingement on adjacent structures (e.t., compression of a
ureter or erosion of vertebrae by the expandint aneurysm)
•An abdominal mass (ofen palpably pulsatnt) that simulates a
tumor
•Rupture into the peritoneal cavity or retroperitoneal tssues,
leadint to massive, ofen fatal emorr age

20. AAA

21. Thoracic aorta aneurysm
•Thoracic aortc aneurysms most commonly are associated with
hypertension, bicuspid aortc valves, and Marfan syndrome.
•Less commonly, disorders caused by mutatons in the TGF-β sitnalint
pathway are causatve.
•These aneurysms manifest with the followint sitns and symptoms:
•Respiratory or feedint difcultes due to airway or esophateal
compression, respectvely, because of encroachment on mediastnal
structures
•Persistent couth from irritaton of the recurrent larynteal nerves
•Pain caused by erosion of bone (i.e., ribs and vertebral bodies)
•Cardiac disease due to valvular insufciency or narrowint of the
coronary osta; heart failure induced by aortc valvular incompetence
•Aortc dissecton or rupture

22. Aortic dissection
•Aortc dissecton occurs when blood splays apart the laminar planes of the media
to form a blood-flled channel within the aortc wall.

23. Vasculitis
•Vasculits is a teneral term for vessel wall infammaton.
•The two most common pathotenic mechanisms of vasculits are
immune-mediated infammaton and direct vascular invasion by
infectous pathotens.
• Infectons also can indirectly precipitate immune-mediated
vasculits (e.t., by teneratnt immune complexes or tritterint
crossreactvity).
•In any tiven patent, it is critcal to distntuish between infectous
and immunolotic mechanisms because immunosuppressive
therapy is appropriate for immunemediated vasculits but could
exacerbate infectous vasculits.
•Physical and chemical injury, includint that due to radiaton,
mechanical trauma, and toxins, also can cause vasculits.

24. Classifcation of vasculitis

25. Giant cell artetitis

26. Tumours

27. Hemangiomas
•Hemantiomas are very common tumors composed of blood-flled
vessels These lesions consttute 7% of all benitn tumors of infancy and
childhood; most are present from birth and initally increase in size, but
many eventually retress spontaneously .
•While hemantiomas typically, are localized lesions confned to the head
and neck, they occasionally may be more extensive (antiomatosis) and
can arise internally.
•Nearly one third of these internal lesions are found in the liver.
•Malitnant transformaton is rare. Several histolotic and clinical variants
have been described:
•Capillary hemantioma
•Juvenile hemantiomas (so-called “strawberry hemantiomas”)
•Pyotenic tranulomas

29. Kaposi sarcoma
•Kaposi sarcoma (KS) is a vascular neoplasm caused
by Kaposi sarcoma herpesvirus (KSHV, also known
as human herpesvirus-8, or HHV-8).
•Althouth it occurs in a number of contexts, it is
most common in patents with AIDS; indeed, its
presence is used as a criterion for the diatnosis.

31. Heart
overview of heart diseases
•Failure of t e pump.
•In the most common situaton, the cardiac muscle contracts weakly and the chambers cannot empty properly—so-
called “systolic dysfuncton.” In some cases, the muscle cannot relax sufciently to permit ventricular fllint,
resultnt in diastolic dysfuncton.
•Obstructon to fow.
•Lesions that prevent valve openint (e.t., calcifc aortc valve stenosis) or cause increased ventricular chamber
pressures (e.t., systemic hypertension or aortc coarctaton) can overwork the myocardium, which has to pump
atainst the obstructon.
• Regurgitant fow.
•Valve patholoty that allows backward fow of blood results in increased volume workload and may overwhelm the
pumpint capacity of the afected chambers.
•S unted fow.
•Defects (contenital or acquired) that divert blood inappropriately from one chamber to another, or from one vessel
to another, lead to pressure and volume overloads.
•Disorders of cardiac conducton.
•Uncoordinated cardiac impulses or blocked conducton pathways can cause arrhythmias that slow contractons or
prevent efectve pumpint altotether.
•Rupture of t e eart or major vessel.
•Loss of circulatory contnuity (e.t., a tunshot wound throuth the thoracic aorta) may lead to massive blood loss,
hypotensive shock, and death.

32. Heart failure
•Heart failure, ofen referred to as contestve heart failure
(CHF),
•is the common end point for many forms of cardiac
disease and typically is a protressive conditon with a
poor protnosis.
•Routhly one half of patents die within 5 years of
receivint a diatnosis of CHF, and 1 in 9 deaths in the
United States include heart failure as a contributory
cause.
•Heart failure may result from systolic or diastolic
dysfuncton.

34. •Lef-sided heart failure is most commonly secondary to
ischemic heart disease, systemic hypertension, mitral or
aortc valve disease, or primary diseases of the
myocardium;
•Symptoms are mainly a consequence of pulmonary conteston
and edema, althouth systemic hypoperfusion can cause renal
and cerebral dysfuncton.
•Ritht-sided heart failure is due most ofen to lef-sided
heart failure and, less commonly, to primary pulmonary
disorders;
•sitns and symptoms are related chiefy to peripheral edema and
visceral conteston.

35. Congenital heart diseases
•Contenital heart diseases are abnormalites of the heart or treat vessels
that are present at birth.
•They account for 20% to 30% of all birth defects and include a broad
spectrum of malformatons, rantint from severe anomalies incompatble
with intrauterine or perinatal survival, to lesions that produce few or no
symptoms, some of which to completely unrecotnized durint life.
•Contenital heart disease afects nearly 1% of newborns (or routhly 40,000
infants per year in the United States).
•The incidence is hither in premature infants and in stllborns,
approximately one fourth of which have sitnifcant cardiac malformatons.
•Defects that permit live birth usually involve only sintle chambers or
retions of the heart.
•Twelve enttes account for 85% of contenital heart disease

36. Clinical features
•The various structural anomalies in contenital heart
disease can be assitned to three major troups
based on their hemodynamic and clinical
consequences:
•(1) malformatons causint a lef-to-ritht shunt;
•(2) malformatons causint a ritht-to-lef shunt
(cyanotc contenital heart diseases); and
•(3) malformatons causint obstructon.

37. Left to right shunt
malformation
•Disorders associated with Lef-to-ritht shunts are the most
•common types of contenital cardiac malformatons.
•They include atrial septal defects (ASDs), ventricular septal
defects (VSDs), and patent ductus arteriosus (PDA).
•ASDs typically increase only ritht ventricular and pulmonary
outlow volumes, while VSDs and PDAs cause both increased
pulmonary blood fow and pressure.
•Manifestatons of these shunts rante from completely
asymptomatc to fulminant heart failure.
•Cyanosis is not an early feature of these defects.
•However, as discussed earlier, prolonted lef-to-ritht

38. Complicatio
ns
•pulmonary hypertension
•the systemic circulaton, a
chante marked by the
appearance of cyanosis
(Eisenmenter syndrome).

39. Right to left shunt
malformation
•Cardiac malformatons associated with ritht-to-lef shunts
are distntuished by early cyanosis.
•This occurs because poorly oxytenated blood from the ritht
side of the heart fows directly into the arterial circulaton.
•Two of the most important conditons associated with
cyanotc contenital heart disease are tetraloty of Fallot and
transpositon of the treat vessels.
•Clinical consequences
•of severe, systemic cyanosis include clubbint of the tps of the
fnters and toes (hypertrophic osteoarthropathy), polycythemia,
•and paradoxical embolizaton.

40. •TOF
•Transpositon of treat
arteries

41. Tetralogy of fallot
•Tetraloty of Fallot is the most common cause of cyanotc
contenital heart disease.
•It accounts for about 5% of all contenital cardiac
•The four cardinal features are;
• VSD
•Ritht ventricular outlow tract obstructon (subpulmonic stenosis)
•Overridint of the VSD by the aorta
•Ritht ventricular hypertrophy
•All the features result from anterosuperior displacement of
the infundibular septum leadint to abnormal septaton
between the pulmonary trunk and the aortc root.

42. Obstructive lesions
•Contenital obstructon of blood fow can occur at
the level of the heart valves or more distally within
a treat vessel.
•Obstructon can also occur proximal to the valve, as
with subpulmonic stenosis in tetraloty of Fallot.
•Relatvely common examples of contenital
obstructons are pulmonic valve stenosis, aortc
valve stenosis or atresia, and coarctaton of the
aorta.

43. CoA
•Coarctaton (narrowint, or constricton) of the aorta is a common
form of obstructve contenital heart disease.
•Males are afected twice as ofen as females, althouth females with
Turner syndrome frequently have coarctaton.
•There are two classic forms (Fit. 11.5):
• An “infantle” preductal form featurint hypoplasia of the aortc arch
proximal to a PDA
•An “adult” postductal form consistnt of a discrete ridtelike infoldint of the
aorta, adjacent to the litamentum arteriosum
•Coarctaton can occur as a solitary defect, but in more than half of
the cases is accompanied by a bicuspid aortc valve.
•Aortc valve stenosis, ASD, VSD, or mitral returtitaton also, can be
present.

44. CoA

45. MI
•Myocardial infarcton (MI), also commonly referred to as “heart attack,”
is necrosis of the heart muscle resultnt from ischemia.
•The major underlyint cause of IHD is atherosclerosis; while MIs can
occur at virtually any ate, the frequency rises protressively with atint
and with increasint risk factors for atherosclerosis.
•Nevertheless, approximately 10% of MIs occur before 40 years of ate,
and 45% occur before 65 years of ate.
•Blacks and whites are equally afected. Men are at treater risk than
women, althouth the tap protressively narrows with ate.
•In teneral, women tend to be protected atainst MI durint their
reproductve years. However, menopause—with declinint estroten
producton—is associated with exacerbaton of coronary artery disease,
and IHD is the most common cause of death in older adult women.

46. •Coronary Artery Occlusion
•In a typical MI, the followint sequence of events takes
•place:
• An atheromatous plaque is eroded or suddenly disrupted by endothelial
injury, intraplaque hemorrhate, or mechanical forces, exposint
subendothelial collaten and necrotc plaque contents to the blood.
•Platelets adhere, attretate, and are actvated, releasint thromboxane
A2, adenosine diphosphate (ADP), and serotonin—causint further
platelet attretaton and vasospasm.
•Actvaton of coatulaton by exposure of tssue factor and other
mechanisms adds to the trowint thrombus.
•Within minutes, the thrombus can evolve to completely occlude the
coronary artery lumen.

47. •Clinical Features
•The classic MI is heralded by severe, crushint
substernal chest pain (or pressure) that can radiate
to the neck, jaw, epitastrium, or lef arm.

49. •Patterns of Infarcton
•The locaton, size, and morpholotic features of an
acute myocardial infarct depend on multple factors:
•Size and distributon of the involved vessel (Fit. 11.9)
•Rate of development and duraton of the occlusion
•Metabolic demands of the myocardium (afected, for
example, by blood pressure and heart rate)
•Extent of collateral supply

50. Acute
MI

51. Microscopic features

53. Complications

54. Vulvular heart
disease
•Valvular disease may result in stenosis,
insufciency (returtitaton or
incompetence), or both.

55. Rheumatic heart disease
•Rheumatc heart disease results from ant-
streptococcal antbodies that cross-react with
cardiac tssues; it most commonly afects the mitral
valve and is responsible for almost all cases of
acquired mitral stenosis.
•The most important functonal consequence of
rheumatc heart disease is valvular stenosis and
returtitaton; stenosis tends to predominate.

57. Infective endocarditis
•Infectve endocardits (IE) is a microbial infecton of the heart valves
or the mural endocardium that leads to the formaton of vetetatons
composed of thrombotc debris and ortanisms, ofen associated
with destructon of the underlyint cardiac tssues
•Acute endocardits refers to tumultuous, destructve infectons,
frequently involvint a hithly virulent ortanism attackint a previously
normal valve. It is associated with of substantal morbidity and
mortality, even with appropriate antbiotc therapy and/or surtery.
•Subacute endocardits refers to infectons by ortanisms of low
virulence afectnt a previously abnormal heart, especially scarred or
deformed valves. The disease typically appears insidiously and—
even if untreated— follows a protracted course of weeks to months;
most patents recover afer appropriate antbiotc therapy.

60. Noninfectious IE

61. Cardiomyopathy
•Cardiac disease due to intrinsic myocardial dysfuncton are termed
cardiomyopathies (literally, “heart muscle diseases”); these can be primary—
that is, principally confned to the myocardium—or secondary presentnt as the
cardiac manifestaton of a systemic disorder.
•Cardiomyopathies can be classifed accordint to a variety of criteria, includint
the underlyint tenetc basis of dysfuncton; indeed, some of the arrhythmia-
inducint channelopathies that are included in some classifcatons of
cardiomyopathy were alluded to earlier. For purposes of teneral diatnosis and
therapy, however, three tme honored clinical, functonal, and patholotic
patterns are recotnize):
•Dilated cardiomyopathy (DCM) (includint arrhythmotenic ritht ventricular
cardiomyopathy)
•Hypertrophic cardiomyopathy (HCM)
•Restrictve cardiomyopathy
•Of the three major patterns, DCM is most common (90% of cases), and
restrictve cardiomyopathy is the least frequent.

65. Pericardial diseases
•Pericardial lesions typically are associated with a
patholotic process elsewhere in the heart or surroundint
structures, or are secondary to a systemic disorder.
•Pericardial disorders include efusions and infammatory
conditons, sometmes resultnt in fbrous constricton.
•Normally, the pericardial sac contains less than 50 cc of
thin, clear, straw-colored fuid.
•Under various circumstances, the pericardial sac may be
distended by accumulatons of serous fuid (pericardial
efusion), blood (hemopericardium), or pus (purulent
pericardits).

66. •Pericardial efusions and their
causes include the followint:
•Serous: Contestve heart
failure, hypoalbuminemia
of any cause
•Serosantuineous: Blunt
chest trauma, malitnancy,
ruptured MI, or aortc
dissecton
•Chylous: Mediastnal
lymphatc obstructon

67. Tumours
•Primary cardiac tumors are uncommon; moreover,
most also are (fortunately) benitn.
•The fve most common have no malitnant potental
and account for 80% to 90% of all primary heart
tumors.
•In descendint order of frequency, these are
myxomas, fbromas, lipomas, papillary
fbroelastomas, and rhabdomyomas.
•Antiosarcomas consttute the most common
primary malitnant tumor of the heart.

68. •Myxomas are the most common primary tumors of the adult
heart (Fit. 11.30).
•Routhly 90% are atrial, with the lef atrium accountnt for 80% of those.
•Rhabdomyomas are the most frequent primary tumors of the
heart in infants and children; they frequently are discovered
owint to valvular or outlow obstructon.
•Cardiac rhabdomyomas occur with hith frequency in patents with
tuberous sclerosis caused by mutatons in the TSC1 or TSC2 tumor
suppressor tenes; loss of TSC-1 and TSC-2 actvity leads to myocyte
overtrowth.
•Because they ofen retress spontaneously (for unknown reasons),
rhabdomyomas are sometmes considered to be hamartomas rather
than true neoplasms.