GenPath Manual Revised Again

[G E N E R A L P A T H O L O G Y | L A B O R A T O R Y M A N U A L] AY: 2022-2023
MINDANAO STATE UNIVERSITY - GENERAL SANTOS

CITY COLLEGE OF MEDICINE
ESTABLISHED 2021
VISION
MSU General Santos City College of Medicine will become a globally competitive
medical institution promoting peace and development in Southern Mindanao by
improving the health condition of the community.
MISSION
MSU General Santos City College of Medicine will provide competent, excellent,
compassionate, humane physicians engaged in clinical, academic, research, and
primary care dedicated to improve the health status and promote peace in
SOCCSKSARGEN area regardless of religion, social status, and ethnicity.
MOTTO
“COMCECH: Competence, Excellence, Compassion, and Humanity ”
CORE VALUES
Competence, Compliance, Compassion,
Cooperation, and Collaboration
M I N D A N A O S T A T E U N I V E R S I T Y – G E N E R A L S A N T O S CITY | 2
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TABLE OF CONTENTS
Activity 1: General Aspects Of Diseases................................................2
Activity 2: Cell Injury And Necrosis..........................................................2
Activity 3: Genetic Disorders.....................................................................2
Activity 4: Neoplasia – Gross And Microscopy......................................2
Activity 5: Environmental And Nutritional Disorders.............................2
Activity 6: Diseases Of Infancy And Childhood.....................................2
Activity 7: Cardiovascular System Pathology.........................................2
Activity 8: Hematopathology.....................................................................2
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ACTIVITY 1: GENERAL ASPECTS OF DISEASES
Name: _________________________________ Date: ________________ Score: _________
Course & Year Level: ____________________________ Group: _______________________
1. Define, illustrate, make a diagram, draw or attach pictures, and use in proper context.
a. Brain death
b. Diagnosis
c. Differential Diagnosis
d. Disease
e. Etiology
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f. Exacerbation
g. Factitious
h. Functional
i. Abnormality
j. Iatrogenic
k. Idiopathic
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l. Lesion
m. Morphology
n. Mortality rate
o. Natural history
p. Nosocomial
q. Pathogenesis
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r. Pathognomonic
s. Prognosis
t. Psychosomatic
u. Remission
v. Sign
w. Somatic death
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x. Structural abnormality
y. Symptom
z. Syndrome
2.Distinguish between disease and non-disease.
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3. Outline a classification of causes of disease, basic responses of the body to injury, and
manifestations of disease; and classify common examples in each category.
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References:
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ACTIVITY 2: CELL INJURY AND NECROSIS
Name: _________________________________ Date: ________________ Score: _________
1. Define, illustrate, make a diagram, draw, or attach an image or picture and use in proper
context:
1) Agenesis
2) Anthracosis
3) Aplasia
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4) Apoptosis
5) Atrophy
6) Autolysis
7) Autophagy
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8) Bilirubin
9) Cellular swelling (hydropic change)
10) Dysplasia
11) Gangrene
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12) Heat-shock proteins
13) Hemosiderin
14) Hemosiderosis
15) Heterophagy
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16) Homeostasis
17) Hyaline
18) Hyperplasia
19) Hypertrophy
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20) Hypoplasia
21) Hypoxia
22) Infarct
23) Ischemia
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24) Karyolysis
25) Karyorrhexis
26) Lipofuscin
27) Melanin
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28) Metaplasia
29) Necrosis
 Coagulative Necrosis
 Liquefactive Necrosis
 Fat Necrosis
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 Caseous Necrosis
 Fibrinoid Necrosis
 Gangrenous Necrosis
30) Neoplasia
31) Pyknosis
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32) Steatosis
2. Compare cell and tissue adaptation, reversible cell injury, and irreversible cell injury (cell death)
on the basis of:
a) Etiology
b) Pathogenesis
c) Morphologic Appearance (ultrastructural and histologic)
Feature Cell and Tissue Reversible Cell Injury Irreversible Cell Injury
Adaptation
Etiology
Pathogenesis
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Ultrastructura
l Appearance
Histologic
Appearance
3. Compare and contrast cell death and somatic death in terms of:
a) Causes
b) Pathogenesis
c) Histologic Appearance
Feature Cell Death Somatic Death

Causes
Pathogenesis
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Histologic
Appearance
4. Outline the relationship between:

a) Biochemical
b) Light Microscopic
c) Ultrastructural changes in the process of cell injury and cell death
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5. Compare coagulative necrosis, liquefactive necrosis, gangrenous necrosis, caseous

necrosis, fat necrosis, fibrinoid necrosis, and apoptosis .
A. Coagulative Necrosis
Common sites or tissues involved Common causes or causative mechanisms
Gross Appearance Microscopic Appearance
Types Extent of Healing
B. Liquefactive Necrosis
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C. Gangrenous Necrosis
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D. Caseous Necrosis
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E. Fat Necrosis
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F. Fibrinoid necrosis
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G. Apoptosis
6. Compare and contrast the following types of cell injury:
Feature Reperfusion Injury Free-Radical Induced Injury Chemical Injury

Biochemica
l
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Mechanism
Molecular
mechanism
7.List the types of subcellular alterations that can occur in cell injury, with respect to the
following organelles:
a) Lysosomes
b) Endoplasmic reticulum
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8.Discuss the significance of intracellular accumulation of:

a) Lipids
b) Proteins
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c) Glycogen
d) Pigments
9.Compare fatty change (steatosis) and fatty infiltration.
Feature Fatty change Fatty infiltration

Causes
Pathogenesis
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Organs involved
Histologic
appearance
10.Compare dystrophic and metastatic calcification
Feature Dystrophic Calcification Metastatic Calcification

Etiology
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Pathogenesis
Morphologic
Appearance
Sites
Associated
Diseases
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Clinical
Significance
References:
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ACTIVITY 3: GENETIC DISORDERS
Name: _________________________________ Date: ________________ Score: _________
Complete the table of the following genetic disorders:
Disease Gene/Defect Inheritance Clinical Features

1.Congenital Adrenal
Hyperplasia
2 Congenital
Hyperinsulinism
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3. Central Diabetes
insipidus
4. Prader-Willi
Syndrome
5. Neonatal Diabetes
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6. Rett Syndrome
7. Smith-Magenis
Syndrome
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8. Acute
Lymphobastic
Leukemia
9. Retinoblastoma
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10. Glioma
11. Wilms Tumor
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12. Hodgkin’s
Lymphoma
13. Juvenile
Idiopathic Arthritis
14. Takayasu
Arteritis
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15. Systemic Lupus

Erythematosus
16. Juvenile
Systemic Sclerosis
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17. Polyarteritis
Nodosa
18. Melioidosis
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19. Lyme Disease
20. Cat-Scratch
Disease
21. Inflammatory
Bowel Disease
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22. Idiopathic
Neonatal Hepatitis
23. Biliary Atresia
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24. Choledochal Cyst
25. Eosinophilic
Colitis
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26. Mucopoly-
saccharisodes
27. Gaucher Disease
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28. Pompe Disease
29. Osteogenesis
imperfect
30. Maple Syrup

Urine Disease
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31. Conjoined twins
32. Gonadal
Dysgenesis
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33. Herlyn-Werner-
Wunderlich
Syndrome (OHVIRA)
Obstructed
Hemivagina and
Ipsilateral Renal
agenesis
34. Primary Fallopian

tube cancer
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35. Sertoli-Leydig
Cell Tumor
36. Uterine Sarcoma
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37. Unicornuate
Uterus
38. Distal Vaginal

Agenesis
39. Galactosemia
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40. Mucormycosis in
Pregnancy
41. HIV in pregnancy
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42. Fowler’s
syndrome
43. Sesame
syndrome
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44. Ochoa syndrome
45. Cloacal
Malformation
(Persistent Cloaca)
46. Exstrophy of the

Bladder
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47. Aneurysms in
Children
48. Syndromic
Craniosynostosis
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49. DAVF in children
50. X-linked Dystonia

(Lubag)
51. Erdheim Chester
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Disease
52. Basal Cell Nevus

Syndrome (Gorlin
Goltz Syndrome)
53. Epidermolysis
Bullosa
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54. Generalized
Pustular Psoriasis
55. Icthytotic Skin

Disorders
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56.
Neurofibromatosis
type 2
57. Primary Systemic

Vasculitis
58. IgG4 Related

Disease
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59. Achalasia
60. Gastrointestinal
Stromal Tumor
(GIST)
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61. Yaws (Endemic

Treponematoses)
62. Mycetoma
63. X-linked
Agammaglobulinemia
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64. Chronic
Granulomatous
Disease
65. Wiskott-Aldrich
Syndrome
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66. Severe
Combined
Immunodeficiency
67. Hyper IgE

Syndrome/Job’s
Syndrome
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68. Gastric Cancer
69. Pancreatic
Cancer
70. Bladder Cancer
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71. Primary CNC

Cancer
72. Laryngeal Cancer
73. Scleroderma
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74. Immune
Mediated
Inflammatory
Myopathies
75. Diamond
Blackfan Anemia
76. Aplastic Anemia
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77. Polycythemia
vera
78. Langerhans Cell

Histiocytosis
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79. Behcet Disease
80. Primary
Congenital Glaucoma
81. Spinal Muscular

Atrophy
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82. Congenital
Central
Hypoventilation
Syndrome
83. Interstitial Lung

Disease
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84. Hemophilia B
85. Evans Syndrome
86. Hutchinson-
Gilford Progeria
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87. Serous Ovarian

Cancer
88. Juvenile Breast

Atrophy
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89. Achard-Thiers
Syndrome (Diabetic
Bearded Woman
Syndrome)
90. Neuroendrocrine
Tumor, Cervix
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91. Uterine
Leiomyosarcoma
92. Malignant
Melanoma
93. Vulvar Adenoid
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Cystic Carcinoma
94. Rectal
Gastrointestinal
Stromal Tumor
95. Pseudomyxoma
Peritonei
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96. Idiopathic
Pulmonary Arterial
Hypertension
97. Achondroplasia
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98. Cystic Fibrosis
99. Duchenne
Muscular Dystrophy
100. Hypercholes-
terolemia
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101. Glucose-6-
Phosphate
Dehydrogenase
Deficiency
102. Hemochroma-
tosis
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103. Holoprosen-
cephaly
104. Huntington
Disease (and
Huntington Chorea)
105. Klinefelter
Syndrome
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106. Marfan
Syndrome
107. Myoclonic
Epilepsy with Ragged
Red Fibers (MERRF)
108. Myotonic
Dystrophy
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109. Neurofibro-
matosis
110. Phenylketonuria
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111. Polycystic
Kidney Disease
112. Sex Reversal
113. Tay-Sachs
Disease
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114. Thalassemia
115. Turner
Syndrome
116. Xeroderma
Pigmentosum
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References:
ACTIVITY 4: NEOPLASIA – GROSS AND MICROSCOPY
Name: _________________________________ Date: ________________ Score: _________
Gross Dissection:
Dissected Organ Description
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Microscopic Slides:
Slide # and Specimen Scanner view (40x) Low-power view (100x) High-power view (s)
15 -
Description
16 -
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ACTIVITY 5: ENVIRONMENTAL AND NUTRITIONAL DISORDERS
Name: _________________________________ Date: ________________ Score: _________
1. Define the following and give illustration/s or examples.

DEFINITION ILLUSTRATION
1. Adverse Drug Reactions
2. Alcoholism
3. Analgesic Nephropathy
4. Anthracosis
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5. Asbestos
6. Asbestosis
7. Bagassosis
8. Berylliosis
9. Biologic Effective Dose
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2. Based on your reference/s, list the top 10 most common environmental and nutritional
disorders including their etiology, epidemiology, pathogenesis and pathophysiology, and clinical
manifestations.
TOP 1 DISEASE:
Etiology Epidemiology
Pathogenesis and Pathophysiology:
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Clinical Manifestations
TOP 2 DISEASE:
Pathogenesis and Pathophysiology
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TOP 3 DISEASE:
TOP 4 DISEASE:
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TOP 5 DISEASE:
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TOP 5 DISEASE:
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TOP 6 DISEASE:
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TOP 7 DISEASE:
TOP 8 DISEASE:
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TOP 9 DISEASE:
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TOP 10 DISEASE:
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References:
REFLECTION & REACTION

Your insights and reflection for this chapter:
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ACTIVITY 6: DISEASES OF INFANCY AND CHILDHOOD
Name: _________________________________ Date: ________________ Score: _________
Complete the tables by focusing on each condition’s definition, etiology, pathogenesis and
pathophysiology, and clinical manifestations.
A. Malformations
POLYDACTYLY AND SYNDACTYLY

Definition: Etiology:
Clinical Manifestations:
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CLEFT LIP
SEVERE LETHAL MANIFESTATIONS

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B. Disruptions
DISRUPTION BY AN AMNIOTIC BAND


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C. Sequence
OLIGOHYDRAMNIOS
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D. Prematurity
RESPIRATORY DISTRESS SYNDROME

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NECROTIZING ENTEROCOLITIS
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E. Fetal Hydrops
KERNICTERUS
HYDROPS FETALIS
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F. Inborn Errors of Metabolism and Other Genetic Disorders
CYSTIC FIBROSIS
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G. Tumors and Tumor-like Lesions
CONGENITAL CAPILLARY HEMANGIOMA

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NEUROBLASTOMA
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SACROCOCCYGEAL TERATOMA
WILMS TUMOR
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ACTIVITY 7: CARDIOVASCULAR SYSTEM PATHOLOGY
Name: _________________________________ Date: ________________ Score: _________
1. Cardiovascular Pathology Slides

Complete the tables by focusing on each condition’s definition, etiology, pathogenesis
and pathophysiology, and clinical manifestations.
Case 1 Normal aorta - intima
The aortic intima shows a “tree-bark” appearance with focal

areas of intimal thickening which appears as white and shiny.
Etiology Normally the aortic intima is smooth and thin, and there is no evidence
of irregularity, protrusion, calcification, or ulceration.
Numerous factors promote the formation of intimal hyperplasia such as
vascular wall injury, aging and inflammation, non-laminar shear stress,
particularly at branch points in the vasculature, results in a mild form of
intimal hyperplasia often referred to as intimal thickening
Pathogenesis +
pathophysiology A normal aorta has three
distinct layers: the tunica
intima, media, and
adventitia. A healthy
intima contains a single
layer of endothelial cells
and a small amount of
extracellular matrix with
rare mesenchymal cells.
It is bordered by the
internal elastic lamina.
Clinical Absence of chest pain, no headaches, and normal blood pressure

Manifestation level.
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References Kronzon, I. &Tunick, P.A. Chapter 39 - Aortic Atherosclerosis

and Embolic Events, Editor(s): Lang, R.M., Goldstein, S.A.,
Kronzon, I. & Khandheria, B.K. Dynamic Echocardiography,
W.B. Saunders, 2011, Pages 180-182, ISBN 9781437722628,
Retrieved on December 27, 2022 from
https://doi.org/10.1016/B978-1-4377-2262-8.00039-6.
(https://www.sciencedirect.com/science/article/pii/B97814377226
28000396)
Case 2 Minimal amount of fatty streaks and dots
The faint reddish staining is from hemoglobin that leaked from

RBC's following death. The surface is quite smooth, with only
occasional faint small yellow lipid streaks visible.
The white arrow denotes the most prominent fatty streak in the
photo, but there are other fatty streaks scattered over the aortic
surface.
Grossly, fatty streaks are flat or minimally elevated, 3- to 5-mm,

yellow foci along the intimal aortic surface. Microscopically,
islands of intracellular and extracellular lipid accumulation are
seen in the intima. The cells within the intima, derived from
smooth muscle cells and macrophages, are filled with lipid
droplets, creating "foam cells." These foci stain strongly with Oil
Red O (a lipophilic stain). There is no collagen deposition in
these lesions.
Etiology Fatty streaks is the earliest visible lesion of atherosclerosis,

which is due to an accumulation of lipid-laden foam cells in the
intimal layer of the artery. With time, the fatty streak evolves into
a fibrous plaque, the hallmark of established atherosclerosis.
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Pathogenesis +
pathophysiology
1. The monocytes that moved to the artery turn into cells

called macrophages. Macrophages surround and
consume invaders to get rid of them. In this case, the
macrophages consume the cholesterol.
2. As the macrophages fill up with cholesterol, it takes on a
foamy appearance. So, it is then called “foam cells.”
3. After the foam cells consume cholesterol, it dies.
4. As the foam cells die, the body sends more and more
white blood cells to the area. Those cells continue
consuming cholesterol, get foamy and die. As this
process continues, it damages the endothelium more.
All the dead foam cells form a bulge underneath the

endothelium. This “fatty streak” is the beginning of plaque
formation.
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Clinical Manifestation  Chest pain (angina) while exercising, and the pain stops after
rest.
 Leg cramps when walking (intermittent claudication).
 Transient ischemic attack (TIA).
References Klatt, E. C., MD. (n.d.-a). Cardiovascular Pathology. Edward C.

Klatt MD. https://webpath.med.utah.edu/CVHTML/CV114.html
Crowther, M. A. (2005, January 1). Pathogenesis of
Atherosclerosis. American Society of Hematology.
https://ashpublications.org/hematology/article/2005/1/436/19259/
Pathogenesis-of-Atherosclerosis
Atherosclerosis: Causes, Symptoms, Risks & Tests. (n.d.).
Cleveland Clinic.
https://my.clevelandclinic.org/health/diseases/16753-
atherosclerosis-arterial-disease
Case 3 Fatty dots that have become confluent in some areas in the
ascending aorta.
Etiology Atherosclerosis begins in the intima with deposition of thrombus

and its subsequent organization by the infiltration of fibroblasts and
secondary lipid deposition.
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Pathogenesis +
pathophysiology
Clinical Manifestation  Chest pain (angina)

 Cold sweats
 Dizziness
 Extreme fatigue
 Heart palpitations
 Shortness of breath
 Nausea
 Weakness
References Kelly K.L. (2015). The vascular system. Reisner H.M.(Ed.),

Pathology: A Modern Case Study. McGraw Hill.
https://accessmedicine.mhmedical.com/Content.aspx?
bookid=1569&sectionid=95968984
Shah, N. D. S. O. (2022, July 1). Coronary Artery Atherosclerosis:
Practice Essentials, Background, Anatomy.
https://emedicine.medscape.com/article/153647-overview
Stary, H. C., Chandler, A. B., Glagov, S., Guyton, J. R., Insull, W.,
Rosenfeld, M. E., Schaffer, S. A., Schwartz, C. J., Wagner, W. D., &
Wissler, R. W. (1994). A definition of initial, fatty streak, and
intermediate lesions of atherosclerosis. A report from the
Committee on Vascular Lesions of the Council on Arteriosclerosis,
American Heart Association. Circulation, 89(5), 2462–2478.
https://doi.org/10.1161/01.cir.89.5.2462
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Case 4 Atheromatous plaque of aorta showing confluent elevated yellow

granular surface in intima. Uncomplicated plaque
Etiology Etiology of atherosclerosis is unknown, but there are multiple factors that
contribute to atherosclerotic plaque progression like genetic,acquired
and environmental factors.
Pathogenesis + Hypercholesterolemia results to endothelial permeability of lipids into the

pathophysiology arterial wall.
Clinical chest pain, weakness, fatigue, sweating

Manifestation jaw, abdominal, and/or arm pain.
References
Ladich, E. R. (2022, June 15). Atherosclerosis pathology. Definition,
Etiology, Epidemiology. Retrieved December 26, 2022, from
https://reference.medscape.com/article/1612610-overview#a1
Bergheanu, S. C., Bodde, M. C., & Jukema, J. W. (2017).

Pathophysiology and treatment of atherosclerosis : Current view and
future n perspective on lipoprotein modification treatment. Netherlands
heart journal : monthly journal of the Netherlands Society of Cardiology
and the Netherlands Heart Foundation, 25(4), 231–242.
https://doi.org/10.1007/s12471-017-0959-2
Case 5
Cross section shows that the atheromatous lesion is
related to fatty and atheromatous deposits with fibrous
cap of the intima. The buffy brown elastic muscular media
becomes attenuated under the atheromatous plaque.
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Etiology Etiology of atherosclerosis is unknown, but there are

multiple factors that contribute to atherosclerotic plaque
progression like genetic,acquired and environmental
factors.
Pathogenesis + Hypercholesterolemia results to endothelial permeability

pathophysiology of lipids into the arterial wall and focal macrophage
infiltration into areas of lipid pools with an overlying fibrous
cap.
Clinical Manifestation chest pain, weakness, fatigue, sweating

jaw, abdominal, and/or arm pain.
References
Ladich, E. R. (2022, June 15). Atherosclerosis
pathology. Definition, Etiology, Epidemiology.
Retrieved December 26, 2022, from
https://reference.medscape.com/article/1612610-
overview#a1
Bergheanu, S. C., Bodde, M. C., & Jukema, J. W.

(2017). Pathophysiology and treatment of
atherosclerosis : Current view and future
perspective on lipoprotein modification treatment.
Netherlands heart journal : monthly journal of the
Netherlands Society of Cardiology and the
Netherlands Heart Foundation, 25(4), 231–242.
https://doi.org/10.1007/s12471-017-0959-2
Case 6
An oil red 0 stain staining fat. The red areas are fatty
being atheromatous deposits and the white areas around
the intercostal arterial ostea are fibrous plaques.
Etiology Etiology of atherosclerosis is unknown, but there are multiple
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factors that contribute to atherosclerotic plaque progression like

genetic,acquired and environmental factors.
Pathogenesis + Hypercholesterolemia results to endothelial permeability of

pathophysiology lipids into the arterial wall and collagen-rich plaque formation
with significant luminal stenosis; lesions may contain large
areas of calcification with few inflammatory cells and minimal or
absence of necrosis
Clinical manifestation Chest pain, weakness, fatigue, sweating

jaw, abdominal, and/or arm pain.
References:
Ladich, E. R. (2022, June 15). Atherosclerosis pathology.
Definition, Etiology, Epidemiology. Retrieved December 26,
2022, from https://reference.medscape.com/article/1612610-
overview#a1
CASES 7-9
Atherosclerosis (Plaques)
SLIDE 7
Complicated atherosclerosis showing ulceration of the
plaques superimposed with thrombotic deposition. Note the
whitish fibrous plaques and wrinkling of the intimal surface.
SLIDE 8
Transverse sections of normal coronary artery embedded in
the epicardial fat, which obscures the vascular wall in the
illustration.
SLIDE 9
Multiple cross sections of coronary artery showing extensive
atherosclerosis, and recent thrombotic occlusion in some
segments. There is variation between different sections in
morphologic appearance and severity (degree of lumen
narrowing).
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Etiology Gradual plaque buildup due to risk factors including high

cholesterol and triglyceride levels, high blood pressure,
smoking, diabetes, obesity, lack of exercise and a diet high in
saturated fats
Pathogenesis +
pathophysiology
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Clinical Manifestation Claudication (sudden numbness or weakness in arms or legs)

and angina
References LaMorte, W. (2016). Pathogenesis of Atherosclerosis. Boston

University School of Public Health.
https://sphweb.bumc.bu.edu/otlt/mph-modules/ph/ph709_hea
rt/ph709_heart3.html
Pahwa R, Jialal I. (2022). Atherosclerosis. In: StatPearls

[Internet]. Treasure Island (FL): StatPearls Publishing.
Available from:
https://www.ncbi.nlm.nih.gov/books/NBK507799/
Yelle, D. (2018). Atherosclerosis. McMaster Pathophysiology

Review. Retrieved from:
http://www.pathophys.org/atherosclerosis/
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Case 10
Severe coronary atherosclerosis with old thrombotic occlusion
which has undergone organisation and been replaced by semi-
translucent fibrous tissue. Many segments have pinpoint
lumens (recanalization)
Etiology Etiologic factors can be broadly categorized into non-modifiable

and modifiable factors.
 Non-modifiable factors include gender, age, family
history, and genetics.
 Modifiable risk factors include smoking, obesity, lipid
levels, and psychosocial variables.
Pathogenesis +
Pathophysiology
subendothelial deposition of lipid-laden macrophages—

>formation of a "fatty streak." —>vascular insult occurs, the
intima layer breaks —>monocytes migrate becoming
macrophage →macrophages take up oxidized low-density
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lipoprotein (LDL) particle →T cells get activated, which releases

cytokines →Growth factors released→increase the population
of foam cells→formation of subendothelial plaque→ plaque
grow in size → fibrous cap will form, and the lesion will become
calcified →not enough blood would reach the myocardial tissue
Clinical Manifestation
References
Dalen JE, Alpert JS, Goldberg RJ, Weinstein RS. The epidemic
of the 20(th) century: coronary heart disease. Am J Med. 2014
Sep;127(9):807-12
Brown JC, Gerhardt TE, Kwon E. StatPearls [Internet].

StatPearls Publishing; Treasure Island (FL): Jun 5, 2022. Risk
Factors For Coronary Artery Disease.
Case 11
Abdominal aneurysm with rupture
Etiology  Atherosclerosis (most common), smoking, advanced
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age, male gender, White race, family history

 hypertension, hypercholesterolemia, and prior history
of aortic dissection
Pathogenesis +
Pathophysiology
Clinical Manifestation  Pain in the chest, belly (abdomen), lower back, or

flank (over the kidneys)
 A pulsating feeling in the belly
 A "cold foot" or a black or blue painful toe
 Fever or weight loss, if the aneurysm was caused by
infection or inflammation (inflammatory aortic
aneurysm)
References
Abdominal aortic aneurysms (AAA). Merck Manual
Professional
Version.https://www.merckmanuals.com/professional/cardiova
scular-disorders/diseases-of-the-aorta-and-its-branches/
abdominal-aortic-aneurysms-aaa
Powell JT, Sweeting MJ, Brown LC, Gotensparre SM, Fowkes
FG, Thompson SG. Systematic review and meta-analysis of
growth rates of small abdominal aortic aneurysms. Br J Surg.
2011 May;98(5):609-18
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Kent KC, Zwolak RM, Egorova NN, Riles TS, Manganaro A,

Moskowitz AJ, Gelijns AC, Greco G. Analysis of risk factors for
abdominal aortic aneurysm in a cohort of more than 3 million
individuals. J Vasc Surg. 2010 Sep;52(3):539-48.
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Case 12
In situ view showing retroperitoneal hemorrhage involving
the left paracolic region
Etiology  penetrating and blunt trauma, typically of the

abdomen and pelvis
 patients undergoing anticoagulation or those on
fibrinolytic therapy
 hemorrhagic pancreatitis, renal or adrenal
malignancies, gynecological complications, and
aneurysmal dilations of the aortic and renal arteries
Pathogenesis +
Pathophysiology
Clinical Manifestation Sudden onset of flank or abdominal pain with fullness,

guarding, and hypotension
Infection/sepsis
Symptomatic anemia
Exsanguination
Abdominal compartment syndrome
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References
Kasotakis G. Retroperitoneal and rectus sheath hematomas.
Surg Clin North Am. 2014 Feb;94(1):71-6.
Feliciano DV. Management of traumatic retroperitoneal

hematoma. Ann Surg. 1990 Feb;211(2):109-23.
AAA-clinical-findings-and-complications: Calgary guide. The

Calgary Guide to Understanding Disease. (2021, February
28). Retrieved December 27, 2022, from
https://calgaryguide.ucalgary.ca/aaa-clinical-findings-and-
complications/aaa-clinical-findings-and-complications/
Case 13 Atherosclerotic aortic aneurysm

Atherosclerotic aortic aneurysm which has been opened and has
exposed the lumen, which is filled with a massive amount of
thrombus. Notice the severe degree of complicated atherosclerotic
change in the segment above the aneurysm.
Etiology
A multifactorial disease, with both genetic and environmental risk
factors contributing to the underlying pathobiology. Aortic
aneurysms are atherosclerotic in origin, in older patients.
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Pathogenesis &
Pathophysiology
Reference
Golledge, J. & Norman, P.E. (2010) Atherosclerosis and Abdominal
Aortic Aneurysm; Retrieved from:
https://www.ahajournals.org/doi/10.1161/ATVBAHA.110.206573
Jones, G. (2011). The Pathohistology of Abdominal Aortic

Aneurysm. In (Ed.), Diagnosis, Screening and Treatment of
Abdominal, Thoracoabdominal and Thoracic Aortic Aneurysms.
IntechOpen. https://doi.org/10.5772/intechopen.84036
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Case 14 Abdominal aortic aneurysm
Cross section of lower abdominal aorta and common iliac artery

showing aortic aneurysm (fusiform in shape) with mural thrombosis
resulting in marked lumen stenosis. The old thrombus tends to
become yellow-brown and semi translucent due to disintegration of
blood elements.
Etiology
May be caused by multiple factors that result in the breaking down
of the well-organized proteins of the aortic wall that provide support
and stabilize the wall. The exact cause is not fully known.
Pathogenesis &
Pathophysiology
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Reference
Silverstein, M.D., Pitts, S., Chaikof, E.l., & Ballard, D.J. (2005)
Abdominal Aortic Aneurysm(AAA): Cost-Effectiveness of
Screening, Surveillance of Intermediate-Sized AAA, and
Management of Symptomatic AAA; Retrieved from:
https://www.researchgate.net/publication/7514800_Abdominal_Aort
ic_Aneurysm_Aaa_Cost-
Effectiveness_of_Screening_Surveillance_of_Intermediate-
Sized_Aaa_and_Management_of_Symptomatic_Aaa
Kuivaniemi H., Ryer, E.J., Elmore J.R., & Tromp, G. (2015)

Understanding the Pathogenesis of abdominal aortic aneurysms;
Retrieved from: http://europepmc.org/article/MED/26308600
Shimizu, K., Mitchell, R.N., & Libby, P. (2006) Inflammation and

cellular immne response in Abdominal aortic Aneurysms; retrieved
from:
https://www.ahajournals.org/doi/10.1161/01.atv.0000214999.12921
.4f#d1e533
Case 15 Thoracic aortic aneurysm

Massive extrapleural hematoma of left chest due to rupture
of thoracic aortic aneurysm.
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Etiology
Causes of Thoracic Aortic Aneurysms may include:
 Hardening of the arteries (atherosclerosis)

 Genetic conditions
 Blood vessel inflammation
 Irregular aortic valve
 Untreated infection
 Traumatic injury
Pathogenesis &
Pathophysiology
Clinical Manifestation  Back pain

 Cough
 Weak, scratchy voice (hoarseness)
 Tenderness or pain in the chest
 Sharp, sudden pain in the upper back that spreads
downward
 Pain in the chest, jaw, neck or arms
 Difficulty breathing
 Low blood pressure
 Loss of consciousness
 Trouble swallowing
Reference
Mayo clinic (2022) Thoracic Aortic Aneurysm; Retrieved
from:
https://www.mayoclinic.org/diseases-conditions/thoracic-
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aortic-aneurysm/symptoms-causes/syc-20350188
CASE 16 - 17
Thoracic Aortic Aneurysm
There are two thoracic aneurysms with the proximal one

ruptured. Extensive atherosclerotic changes in mural
thrombi are present. The underlying process may be
syphilitic in nature
A dissecting aneurysm shown in the thoracic aorta.
Etiology
Male gender, increased age, history of hypertension,
chronic obstructive pulmonary disease (COPD), coronary
artery disease, smoking, and previous aortic dissection are
risk factors of thoracic aortic aneurysm.
Faiza Z, Sharman T. Thoracic Aorta Aneurysm. [Updated

2022 May 8]. In: StatPearls [Internet]. Treasure Island (FL):
StatPearls Publishing; 2022 Jan-. Available from:
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Case 21-22 Daig Syphilitic aortitis
 Severe degree of atherosclerosis with dilation and

aneurysm formation of ascending aorta and
thoracic aorta, typical for syphilitic aortitis.
 The so-called "tree-bark" appearance of intima of

syphilitic aortitis.
Etiology  Associated with the tertiary stage of syphilis caused

by Treponema pallidum
 Aortitis is a representative of a cluster of large-
vessel diseases that have various or unknown
etiologies.
Pathogenesis and  Unknown factors T. Pallidum can produce an

Pathophysiology inflammatory process in the vasa vasorum, the
inner layer of the aorta, which can result in
strictures after infecting the body and spreading
through vascular dissemination. Additionally, there
is blockage as a result of granuloma formation,
focal necrosis of the elastic and muscular layers,
and the replacement of fibrotic tissue with calcified
tissue (syphilitic aorta). Continuation of this process
may result in severe strictures with saccular or
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fusiform aneurysms. Dissection-related rupture is

extremely rare to happen because of the severe
media layer scarring, in contrast to non-syphilitic
aortic aneurysms where the rupture is the primary
cause of death.
Clinical manifestation  When the coronary ostia are blocked, the clinical
manifestations may be:
o angina, dyspnea, or aortic failure.
o However, due to the luetic aneurysm's
rapid enlargement, chest discomfort is the
most prevalent clinical complaint.
References
de Araujo DB, Oliveira DS, Rovere RK, de Oliveira Filho
UL. Aortic aneurysm in a patient with syphilis-related spinal
pain and paraplegia. Reumatologia. 2017;55(3):151-153.
doi: 10.5114/reum.2017.68916. Epub 2017 Jul 18. PMID:
28769140; PMCID: PMC5534511
Braz J Cardiovasc Surg - Syphilitic aortitis: diagnosis and

treatment. Case report. (n.d.). Www.bjcvs.org. Retrieved
January 1, 2023, from https://www.bjcvs.org/article/524/en-
US/syphilitic-aortitis--diagnosis-and-treatment--case-
report#:~:text=The%20clinical%20presentation%20may
%20be
Case 23 Atheroembolic Kidney Disease
An interlobar renal artery is occluded by an atheromatous

emboli that contains cholesterol (clefts left in tissue
following lipid extraction during processing), foreign body
reaction and some fibrosis.
Etiology  Occurs in patients with atherosclerotic vascular

disease with atherosclerotic plaques in the aorta
and large to medium-sized vessels that have
ulcerated
 Kidneys are in proximity to the abdominal aorta,
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high renal blood flow makes them the most

frequent target organ
 Most often an iatrogenic disease, following surgical
and vascular procedures (coronary artery bypass
grafting, abdominal aortic aneurysm repair,
angiography, angioplasty, endovascular grafting)
Pathogenesis &
Pathophysiology
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Clinical Manifestations  Livedo reticularis

 Blue toe/purple toe syndrome
 Abdominal pain
 Neurological deficits
References: Vaidya,P.N.,& Finnigan,N.A.(2022). Atheroembolic kidney

disease. Retrieved on December 28, 2022,from
Case 24 Occlusive Peripheral Arterial Disease
Gangrene of the third and fifth toes with atrophic skin

change in peripheral circulatory insufficiency due to
occlusive atherosclerosis.
Etiology  Usually caused by Atherosclerosis

 Other causes:
o Inflammation of the blood vessels
o Injury
o Radiation exposure
 Risk factors:
o Diabetes
o Smoking
o Obesity
o High blood pressure
o High cholesterol
o Increasing age (50 and above)
o Family history of peripheral artery disease,
heart disease, stroke
o High levels of homocysteine
Pathogenesis &
Pathophysiology
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Clinical Manifestations  Claudication

 Ischemic rest pain
 Erectile dysfunction
 Loss of pulses
 Pain on palpation
 Pallor
 Muscle atrophy and loss of hair
 Cool and cyanotic skin
 Presence of bruit
References: Zemaitis,M.R., Boll,J.M., & Dreyer, M.A.(2022). Peripheral

arterial disease. Retrieved on December 28, 2022, from
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Case 32
A roughened brown patch with a linear tear on the epicardial
surface is the site of rupture due to transmural infarction.
A transmural myocardial infarction refers to a myocardial

infarction that involves the full thickness of the myocardium. It was
one believed that the development of Q waves indicated the
infarction was “transmural;” however, autopsy studies failed to
confirm this.
Etiology
Cardiovascular disease is considered the major cause of morbidity
and mortality throughout the world. Also myocardial infarction is
the main health problem. In 2015, about 15.9 million myocardial
infarctions occurred throughout the world. In the United States
about one million people have an MI each year. Modifiable risk
factors include high blood pressure, smoking, diabetes, lack of
exercise, obesity, depression, high blood cholesterol, poor diet,
lifestyle and excessive alcohol intake. Family history is also
responsible for cardiovascular disease.
Pathogenesis and
Pathophysiology
The major cause of acute myocardial infarction (MI) is coronary

atherosclerosis with superimposed luminal thrombus, which
accounts for more than 80% of all infarcts. MIs resulting from
nonatherosclerotic diseases of the coronary arteries are rare.
Clinical manifestations
Patients can present with chest discomfort or pressure that can
radiate to the neck, jaw, shoulder, or arm. In addition to the history
and physical exam, myocardial ischemia may be associated with
ECG changes and elevated biochemical markers such as cardiac
troponins. Transmural infarcts involve the whole thickness of
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myocardium from epicardium to endocardium and are usually

characterized by abnormal Q waves on ECG.
References
Ojha N, Dhamoon AS, Chapagain R. Myocardial Infarction
(Nursing). 2022 Aug 8. In: StatPearls [Internet]. Treasure Island
(FL): StatPearls Publishing; 2022 Jan–. PMID: 33760446.
Saleh M, Ambrose JA. Understanding myocardial infarction.

F1000Res. 2018 Sep 3;7:F1000 Faculty Rev-1378. doi:
10.12688/f1000research.15096.1. PMID: 30228871; PMCID:
PMC6124376.
Romero M.E., & Fernandez-Jimenez R, & Ladich E, & Fuster V, &

Ibanez B, & Virmani R (2017). Pathology of myocardial infarction
and sudden death. Fuster V, & Harrington R.A., & Narula J, &
Eapen Z.J.(Eds.), Hurst's The Heart, 14e. McGraw Hill.
https://accessmedicine.mhmedical.com/content.aspx?
bookid=2046&sectionid=176555698
Case 33
Hemopericardium as seen in-situ. The pericardium is
opened to reveal blood in the cavity, surrounding the
heart.
Hemopericardium refers to the presence of blood within

the pericardial cavity, i.e. a sanguineous pericardial
effusion.
Etiology
Hemopericardium and resulting tamponade can result
from any form of chest trauma, free wall rupture following
myocardial infarction, retrograde bleeding into the
pericardial sac following a type A aortic dissection, and as
a complication of any invasive cardiac procedure.
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Pathogenesis and
Pathophysiology
Cardiac tamponade results from an accumulation of
pericardial fluid under pressure, leading to impaired
cardiac filling and hemodynamic compromise. Findings
during physical examination are included in Beck´s triad
(sinus tachycardia, elevated jugular venous pressure, low
blood pressure) and pulsus paradoxus.
References
Jensen, J.K. & et.al (2017). Cardiac Tamponade: A
Cardiac Challenge. The European Society of Cardiology:
Vol. 15, N° 17
Case 34
Infarct, two weeks prior to death, showing resorption of
necrotic fibers, replacement by fibroblasts. There is
mixed neutrophil and monocyte infiltration. Residual
necrotic muscle fibers are still identifiable.
Myocardial infarction (MI), colloquially known as "heart

attack," is caused by decreased or complete cessation of
blood flow to a portion of the myocardium.
Etiology
Myocardial infarction may be"silent," and go undetected,
or it could be a catastrophic event leading to
hemodynamic deterioration and sudden death. Closely
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associated with coronary artery disease. The most

common cause of death and disability in the western
world and worldwide is coronary artery disease
Pathogenesis and
Pathophysiology
The acute occlusion of one or multiple large epicardial

coronary arteries for more than 20 to 40 minutes can lead
to acute myocardial infarction. The occlusion is usually
thrombotic and due to the rupture of a plaque formed in
the coronary arteries. The occlusion leads to a lack of
oxygen in the myocardium, which results in sarcolemmal
disruption and myofibril relaxation. These changes are
one of the first ultrastructural changes in the process of
MI, which are followed by mitochondrial alterations. The
prolonged ischemia ultimately results in liquefactive
necrosis of myocardial tissue.
Clinical manifestation
The symptoms of MI include chest pain, which travels
from left arm to neck, shortness of breath, sweating,
nausea, vomiting, abnormal heart beating, anxiety,
fatigue, weakness, stress, depression, and other factors.
References
Lu L, Liu M, Sun R, Zheng Y, Zhang P. Myocardial
Infarction: Symptoms and Treatments. Cell Biochem
Biophys. 2015 Jul;72(3):865-7. doi: 10.1007/s12013-015-
0553-4. PMID: 25638347.
Ojha N, Dhamoon AS. Myocardial Infarction. [Updated

2022 Aug 8]. In: StatPearls [Internet]. Treasure Island
(FL): StatPearls Publishing; 2022 Jan-. Available from:
Case 35
Close-up view of rupture of a left ventricular infarct. Note
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the sinuous tract that opens at the epicardial surface. The

infarcted myocardium exhibits yellow color.
Etiology
Risk factors
 Tobacco smoking
 Hypertension
 Drug abuse
 Obesity
 Stress
 Alcohol
 Diabetes
 Hyperlipoproteinemia
 Chronic kidney disease
Pathogenesis &
Pathophysiology
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Clinical Manifestations  Chest pain/ chest discomfort

 Dyspnea
 Fatigue
 Increased sweating
 Weakness
 Nausea
 Vomiting
 Lightheadedness
 Palpitation
 Anxiety
 Arrhythmia
References:
Botleroo, R. A., Bhandari, R., Ahmed, R., Kareem, R.,
Gyawali, M., Venkatesan, N., Ogeyingbo, O. D., &
Elshaikh, A. O. (2021, August 9). Stem cell therapy for the
treatment of myocardial infarction.
Case 37
Recent myocardial infarct involving the left myocardial
apical region, showing thinning of the wall, and presence of
an overlying mural thrombus. The ventricle is dilated.
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Etiology
Myocardial infarct
 Lifestyle
 Age
 Diabetes
 hyperlipoproteinemia
Mural thrombus
 Abnormal myocardial contractions

 Arrhythmias
 Dilated cardiomyopathy
 Endomyocardial injury (myocarditis)
Pathogenesis &
Pathophysiology
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Clinical Manifestations  Weakness

 Arrhythmia
 Fatigue
 Chest pain
 weakness
References:
Albakri, A. (2018). Ischemic cardiomyopathy: A review of
literature on clinical status and meta-analysis of Diagnostic
and Clinical Management. Biology, Engineering and
Medicine, 3(5). https://doi.org/10.15761/bem.1000151
Case 39
Mural thrombus in the posterior wall, where dilatation has
developed consequent to an infarct.
Etiology  Age
 Lifestyle
 Platelet roles
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 Acute plaque rupture

 Hyperlipoproteinemia
 Family history
Pathogenesis +
Pathophysiology
Abnormal myocardial contractions such as arrhythmias, dilated
cardiomyopathy, endomyocardial injury, and myocardial
infarction.
References  Md, E. K. C., & FRCPath, K. V. M. M. (2021c).

Robbins and Cotran Review of Pathology (Robbins
Pathology) (5th ed.). Elsevier.
 Sudden cardiac death. (n.d.).
https://www.pathologyoutlines.com/topic/heartsuddend
eath.html
Case 40
Marked left ventricle dilatation and endocardial
fibroelastosis. Notice the diffuse thinning of the ventricular
wall.
Etiology
Familial, primary without family history, or secondary
(associated with or caused by other conditions). This could
also be due to bacterial or viral infections such as
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coxsackievirus, adenovirus, parvovirus, and human

immunodeficiency virus (HIV). lifestyle is also a big factor
in the development of the condition. Arrhythmias,
hemochromatosis and excess iron in the heart also
contribute to the problem.
Pathogenesis +
Pathophysiology
Clinical manifestations  Congestive heart failure

 Valvular heart disease
 Abnormal cardiac rhythms
 Sudden cardiac death
 Thromboembolism
References Mahmaljy H, Yelamanchili VS, Singhal M. Dilated

Cardiomyopathy. [Updated 2022 Aug 8].
Cases 41 - 42 41. Marked endocardial fibrosis and thin myocardial wall.
42 Focal endocardial and myocardial fibrosis in an area of old

infarct, which has resulted in a ventricular aneurysm.
41.
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42.
Etiology The exact cause of the fibrotic process of endomyocardial

fibrosis remains currently unknown. Nonetheless, multiple
factors have been proposed. These factors include
eosinophilia, Infections, exposure to environmental factors,
immunologic factors and genetics.
Pathogenesis +
Pathophysiology
Clinical Manifestation  Cardiogenic shock

 Heart failure
 Arrhythmias
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 Thromboembolic disease.
 Ascites
 Hepatomegaly
 Lower extremities edema
 High jugular venous pressure
 Tricuspid regurgitation
 Dyspnea
 Cachexia
 Fatigue
 pulmonary hypertension
 S3, S4 gallop
References Sovari, A. A., MD. (2020, December 29). Endomyocardial

Fibrosis: Background, Pathophysiology, Etiology.
https://emedicine.medscape.com/article/154931-overview
Case 43 Ventricular aneurysm on external view
Etiology Heart attacks are the top cause of ventricular aneurysms.
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Pathogenesis and
Pathophysiology
A cardiac attack causes heart muscle to die. Scar tissue

forms on the damaged area. Over time, this scar tissue
can stretch and become thinner, causing a weakened
section of heart muscle.
Rarely, a ventricular aneurysm is present at birth. This is a
congenital heart condition or birth defect. The aneurysm
may go undetected until it causes problems during
adulthood. Aneurysms form when the intraventricular
tension stretches the non-contracting, infarcted heart
muscle, resulting in an expansion of the thin layer of
necrotic muscle and fibrous tissue, which bulges with each
cardiac contraction. The wall of a mature aneurysm is a
white fibrous scar. It becomes more densely fibrotic as the
time passes, and bulges outward with each cardiac
contraction, resulting in a reduction of the left ventricular
stroke volume. On microscopy, hyalinized fibrous tissue is
the predominant finding. It usually takes 1 month for
fibrous tissue to form.
Clinical Manifestation Left ventricular aneurysms may not cause symptoms,

especially if the weakened area is small. Some people
experience symptoms like:
 Angina (chest pain or pressure).
 Edema (fluid retention).
 Fatigue.
 Heart palpitations.
 Shortness of breath.
 Stroke (due to a blood clot which may form in the
aneurysm).
References Ventricular Aneurysm: Causes, Symptoms and Treatment.

(n.d.). Cleveland Clinic.
https://my.clevelandclinic.org/health/diseases/23286-
ventricular-aneurysm
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Case 44 An infarct, ventricular aneurysm, and rupture of the posterior

papillary muscle consequent to the recent infarct
Etiology The most common cause of papillary muscle rupture is secondary

to myocardial infarction. This usually occurs 2 to 7 days post-
ischemic event. Rupture occurs more commonly with ST-segment
elevation myocardial infarctions but also occurs less frequently
with non-ST segment elevation infarctions. Other possible
documented etiologies of rupture include trauma, syphilis,
periarteritis nodosa, vegetating valvulitis, myocardial abscess,
iatrogenic, and cocaine use.
Pathogenesis and Rupture of the papillary muscle can be both partial and complete.
Pathophysiology Partial rupture (occurring at one of the muscle heads) causes
fewer leaflets to flail and has less valvular regurgitation. These are
hemodynamically better tolerated than a complete rupture. Partial
rupture has been documented to occur up to 3 months after
infarction. Complete rupture of the papillary trunk, which usually
occurs within 1-week post-infarction, leads to rapid clinical
deterioration.
Clinical Manifestation Sudden acute heart failure symptoms. Rapid, severe regurgitation
from papillary muscle failure causes atrial dilatation secondary to
an abrupt increase in atrial pressure. This coupled with a
hyperactive precordium, and insufficient turbulence of blood
through the regurgitant valve makes diagnosis clinically difficult at
times because, often, there is not a stethoscopically audible
regurgitant murmur. Patients who do have murmurs can have
mid, late, or holosystolic murmurs. Symptoms and physical
findings are determined by the valve affected. The most papillary
muscle chordae tendineae complex affected is the posterior-
medial papillary muscle of the mitral valve involved, and thus
acute left-sided heart failure symptoms are found which include
rapidly progressive pulmonary edema and hypoxia. Cardiogenic
shock with hypotension is also commonly observed. Chest pain
has also been cited as a symptom in some patients.
References Papillary Muscle Rupture. (22 C.E., July 7). National Center for
Biotechnology Information.
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Case 45 Old septal infarct exhibiting white fibrous scar
Etiology Septal infarct is usually caused by an inadequate blood

supply during a heart attack (myocardial infarction). In
the majority of cases, this damage is permanent.
Pathogenesis and Septal infarct is a patch of dead, dying, or decaying

Pathophysiology tissue on the septum. The septum is the wall of tissue
that separates the right ventricle of your heart from the
left ventricle. Septal infarct is also called septal
infarction.
Heart attacks often produce sudden symptoms like
dizziness and chest pain. However, sometimes a heart
attack causing septal infarct produces no symptoms and
goes undetected. The only way it may be detected is
during heart surgery or an electrocardiogram (ECG)
exam.
If the finding on an ECG is “septal infarct, age
undetermined,” it means that the patient possibly had a
heart attack at an undetermined time in the past. A
second test is typically taken to confirm the finding,
because the results may instead be due to incorrect
placement of electrodes on the chest during the exam.
Clinical Manifestation For many people, a septal infarct goes unnoticed until
discovered during surgery or an ECG.
The symptoms of a heart attack that results in a septal
infarct can be either minimal enough to go unperceived
or the same as in any other heart attack:
 pressure, pain, or aching in the chest or arms
 pressure, pain, or aching in the neck, jaw, or
back
 nausea
 indigestion or heartburn
 abdominal pain
 lightheadedness
 dizziness
 shortness of breath
 cold sweat
 fatigue
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References Frothingham, S. (2020, May 30). Septal Infarct.

Healthline. https://www.healthline.com/health/septal-
infarct
Case 46 Rupture of papillary muscle consequent to infarction
Etiology Secondary to myocardial infarction (most common cause),

trauma, syphilis, periarteritis nodosa, vegetating valvulitis,
myocardial abscess, iatrogenic, and cocaine use.
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Pathogenesis +
pathophysiology
Clinical manifestations Abrupt onset of shortness of breath and pulmonary edema;

hypotension
Reference Papillary muscle rupture - StatPearls - NCBI bookshelf. (2022,

July 7). National Center for Biotechnology Information.
Case 47 Concentric hemorrhagic necrosis of left ventricle that

developed during extracorporeal circulation for
valvular repair. The coronary angiogram
demonstrates paucity of intramyocardial vessels.
Such a lesion develops as a result of inadequate
perfusion. Following infarction, reperfusion results in
hemorrhagic appearance.
Etiology Aortic stenosis (AS), organic and ischemic

(functional) mitral regurgitation, and tricuspid
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regurgitation
Pathogenesis + pathophysiology
Clinical manifestation • Dyspnea on extortion, orthopnea and PND.

• Acute pulmonary edema may be precipitate
by uncontrolled AF, exercise, chest infection,
anesthesia and pregnancy.
• fatigue is due to reduce cardiac out put
reserve and is common in mild or moderate
stenosis.
• Hemoptysis can occur for a Varity of reasons.
• Alveolar capillary rupture (pink frontally
pulmonary oedema)
• Bronchial vein rupture (large hemorrhage)
• Blood stained sputum of chronic bronchitis
• Horse voice (left recurrent laryngeal nerve
Compression - Ortner's sign )
• Dysphagia (esophageal compression)
• Left lung collapse (left main bronchus
compression)
Reference Teaching and Training. (n.d.). Valvular heart disease.

Share and Discover Knowledge on SlideShare.
Case 48 Interstitial myocardial fibrosis. May be seen in chronic

ischemic heart disease or hypertension.
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Etiology Coronary heart disease, aortic stenosis and hypertension
Pathogenesis +
pathophysiology
Clinical manifestations Diffuse interstitial fibrosis, left ventricular hypertrophy,

cardiac failure, sudden death,cardigan arrhythmia
References Espeland, T., Lunde, I. G., Amundsen, B. H., Gullestad,

L., & Aakhus, S. (2018, October 12). Myocardial fibrosis.
Tidsskrift for Den Norske Legeforening.
https://tidsskriftet.no/en/2018/10/oversiktsartikkel/myocar
dial-fibrosis
Case 50 Cross section demonstrates marked left ventricular

thickening and obliteration of the ventricular lumen, thus, a
concentric hypertrophy, typical longstanding hypertension.
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Etiology  Chronic high blood pressure

 Aging, complex interplay between genetic and
environmental factors.
 Risk factors:obesity, high sodium diets (greater than
3g/day), physical inactivity, excessive alcohol
consumption
Pathogenesis + Pathophysiology
Clinical Manifestation  Arrhythmia

 Chest Pain
 Fatigue
 Fluttering or pounding in the chest
 Heart Murmur
 Dizziness
 Fainting
 Shortness of Breathe
 Swelling in the feet, ankle, legs, belly, or neck
References Tackling G, Borhade MB. Hypertensive Heart Disease.

[Updated 2022 Jun 27]. In: StatPearls [Internet]. Treasure
Island (FL): StatPearls Publishing; 2022 Jan-. Available
from: https://www.ncbi.nlm.nih.gov/books/NBK539800/
Case 51 Fine granularity of renal cortex due to underlying

arteriolo-nephrosclerosis, which is the result of
longstanding hypertension.
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Etiology Chronic, poorly controlled hypertension
Pathogenesis+ Pathophysiology
Clinical Manifestation impaired vision, blood in the urine, loss of weight,

and the accumulation of urea and other
nitrogenous waste products in the blood, a
condition known as uremia.
References Hill G. S. (2008). Hypertensive nephrosclerosis.

Current opinion in nephrology and hypertension,
17(3), 266–270.
https://doi.org/10.1097/MNH.0b013e3282f88a1f
Case 52 Arteriolosclerosis of renal arterioles showing

eosinophilic hyaline deposits subendothelially. Notice
renal tubular atrophy and interstitial fibrosis.
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Etiology It is mainly caused by malignant hypertension

exacerbated by a number of factors including:
 High cholesterol
 High triglycerides
 Insulin resistance or diabetes
 Obesity
 Smoking or use of other tobacco products
 Inflammation from other diseases
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Clinical Manifestations  Chest pain or pressure (angina)

 Sudden arm or leg weakness or numbness.
 Slurred speech or difficulty speaking.
 Brief loss of vision in one eye.
 Drooping facial muscles.
 Pain when walking.
 High blood pressure.
 Kidney failure
References Burchell HB, Allen EV, Moersch FP. Clinical

Manifestations Of Arteriosclerosis. Jama.
1951;147(16):1511–1514.
doi:10.1001/jama.1951.03670330003002
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Case 53 An onion-skin like intimal thickening of a small

muscular artery, seen in accelerated or
malignant hypertension typical of hyperplastic
arteriolosclerosis.
Etiology Malignant hypertension, aging, diabetes mellitus
Pathogenesis + Pathophysiology Malignant hypertension -> endothelial injury ->

concentric proliferation of smooth muscle cells
with thickened, reduplicated basement
membrane
Clinical manifestations  Chest pain (angina) while exercising

 Leg cramps when walking (intermittent
claudication).
 Transient ischemic attack (TIA)
 Heart attack or stroke (sudden
blockage)
References Kumar, V., Abbas, A., Aster, J., & Turner, J.

(2021). Robbins & Cotran Pathologic Basis of
Disease (10th ed.). Elsevier.
Case 54 The "flea-bitten" kidney exhibiting punctate hemorrhages

seen in malignant hypertension.
Etiology  Malignant nephrosclerosis

 Acute post-streptococcal GN
 Rapidly progressive GN
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 Haemolytic-Uraemic Syndrome
 Thrombotic thrombocytopenic purpura
 Henoch-Schonlein purpura
Pathogenesis +
Pathophysiology
Clinical manifestations  Usually associated with pre-existing hypertension,

glomerulonephritis or reflux nephropathy
 Rarely caused by juxtaglomerular cell tumor
 1 - 5% of patients with hypertension; higher frequency in
young men, African-Americans
 Symptoms: diastolic blood pressure 130 mm or more,
cardiac symptoms, encephalopathy, headache, nausea,
vomiting, loss of consciousness, proteinuria and renal
failure
 Treatment: antihypertensive therapy before irreversible
renal lesions develop
 Renal survival has improved; mean proteinuria is
important prognostic factor
References Malignant hypertension and accelerated nephrosclerosis.

(n.d.). https://www.pathologyoutlines.com/topic/kidneymalig
nanthyper.html
Case 55 Necrotizing arteritis (fibrinoid necrosis) of glomerular

afferent arteriole and ischemic glomerulus in malignant
hypertension.
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Etiology Any condition that damages blood vessels can cause it.
For example, extremely high blood pressure, such as
malignant hypertension (or hypertensive crisis), can lead
to fibrinoid necrosis.
Pathogenesis +
Pathophysiology
Clinical manifestations Cutaneous small vessel vasculitis limited to the skin:

(a) palpable purpura and necrotic ulcers in the
lower limbs;
(b) necrosis of endothelial cells from superficial
papillary dermis with fibrin deposition, neutrophil
infiltration, and leukocytoclasia.
Reference Fibrinoid Necrosis: Causes, Symptoms & Treatment.

(n.d.). Cleveland Clinic. https://my.clevelandclinic.org
/health/diseases/24455-fibrinoid-necrosis
Case 56 Apoplexy - hypertensive hemorrhage in the internal

capsule with rupture into the ventricle
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Etiology
Pathogenesis +
Pathophysiology
The main symptoms and consequences of apoplexy

are due to the increased pressure present within the
bony walls of the sella turcica in which the pituitary
resides. A sudden increase in the sella contents due
to blood and edema results in increased pressure.
This increased pressure and meningeal irritation are
responsible for the neurologic symptoms including
the increased pressure in the cavernous sinus and
the cranial nerve palsies as well as bitemporal-
hemianopsia. Extravasation of blood into the
subarachnoid space causes meningeal irritation.
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Clinical manifestations
References Hannoush ZC, Weiss RE. Pituitary Apoplexy. [Updated

2018 Apr 22]. In: Feingold KR, Anawalt B, Blackman MR,
et al., editors. Endotext [Internet]. South Dartmouth (MA):
MDText.com, Inc.; 2000-. Available from:
Case 57 Adrenal cortical adenoma (functional) - there is atrophy of

adjacent adrenal cortex. A cause of "secondary"
hypertension, potentially curable by surgery.
Etiology There are specific genetic mutations associated with

hormonally active and inactive adrenal adenomas.
However, the exact pathogenesis is not entirely clear.
Mutations of CTNNB1 genes which provide instructions for

making beta-catenin (Wnt/beta-catenin pathway) are
associated with the larger and non-secreting adrenocortical
adenomas.
The mutations associated with cortisol-producing adrenal

nodules include PRKACA (cortisol producing adenoma)
GNAS1 (McCune Albright syndrome), MENIN (multiple
endocrine neoplasm type 1 ) and ARMC5 (hereditary
bilateral adrenal adenoma).
The mutations associated with aldosterone-producing
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adrenal adenomas include KCNJ5, ATP1A1, ATP2B3,

CACNA1D and CTNNB1.
Pathogenesis +
Pathophysiology
It can occur due to neoplastic proliferation of adrenal

cortical cells. May arise from any of the three layers, but
zona fasciculata is the most common.
Approximately 90% of ACAs are nonfunctional When
functional, may secrete one or more of the 3 major classes
of adrenal steroids (from external to internal layers):
 Zona glomerulosa: mineralocorticoids (aldosterone)

 Zona fasciculata: glucocorticoids (cortisol)
 Zona reticularis: androgens (testosterone,
dihydrotestosterone [DHT], androstenedione,
dihydroepiandosterone [DHEA])
Hyperaldosteronism/Conn's syndrome: ↑aldosterone →

impacts distal tubules & collecting ducts of nephron → ↑
sodium and water retention, ↓ potassium retention → ↑
blood pressure
Hypercortisolism/Cushing's syndrome: ↑cortisol → ↓

corticotropin releasing hormone (CRH), ↓
adrenocorticotropic hormone (ACTH), ↑ blood glucose
Virilization: ↑ DHEA, ↑ DHEA-sulfate (DHEA-S), ↑

androstenedione, ↑ testosterone, ↑ DHT → ↑ urinary 17-
ketosteroids (metabolic product)
Feminization: ↑ androgens → aromatization → ↑

estrogen, ↑ estradiol → ↑ urinary 17-ketosteroids
(metabolic product)
Children: predisposing genetic factors are present in ~50%
of children with adrenal cortical tumors, most commonly Li-
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Fraumeni syndrome and Beckwith-Wiedemann syndrome;

may arise due to defective apoptosis
Clinical manifestations Minority are functional, may produce a pure or mixed

endocrine syndrome (from most to least common):
 Hyperaldosteronism/Conn's syndrome:
hypertension, proximal muscle weakness, headache,
polyuria, tachycardia with/without palpitation,
hypokalemia, hypocalcemia
 Hypercortisolism/Cushing's syndrome: central
obesity, moon facies, plethora, striae, thin skin, easy
bruising, hirsutism, telangiectasias, hyperhidrosis
 Virilization:
o Females: increased muscle mass (Herculean
habitus), clitoromegaly, facial hair, deep voice,
pubic hair
o Males: penile enlargement, pubic hair
 Feminization: gynecomastia, impotence
References Begum, MD, J. (2021, November 30). Cancer. WebMD.

https://www.webmd.com/cancer/adrenal-gland-adenoma
Mahmood E, Anastasopoulou C. Adrenal Adenoma.

[Updated 2022 Jul 24]. In: StatPearls [Internet]. Treasure
Case 58 Coarctation of aorta
“Narrowing of descending aorta”
Etiology The exact cause of coarctation of the aorta is unknown. It

is thought to be caused by heart defects at birth, either
occurring due to gene defect, a chromosome abnormality,
environmental exposure, traumatic injury or combination
of genes and other risk factors.
Pathogenesis + Pathogenesis
Pathophysiology
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The exact mechanism by which aortic coarctation is

produced is not clearly understood. The most commonly
invoked hypotheses include hemodynamic and ectopic
ductal tissue theories. In the hemodynamic theory, an
abnormal preductal flow or abnormal angle between the
ductus and aorta that increases right-to-left ductal flow
and decreases isthmic flow potentiates development of
coarctation. Postnatal spontaneous closure of the ductus
arteriosus completes the development of aortic
obstruction.
Abnormal extension of ductal tissue into the aorta
(ectopic ductal tissue) has been postulated to create the
coarctation shelf and, with ductal closure, development of
aortic obstruction. This theory, however, does not explain
the variable degrees of isthmus and aortic arch
hypoplasia associated with coarctation of the aorta.
Pathophysiology
Coarctation of the aorta causes an increase in the upper

extremity blood pressure, resulting in two common
presentations. The first is the neonatal presentation that
is associated with left ventricular dysfunction and shock
from the neonatal myocardium's intolerance of the sudden
increase in afterload that occurs with closure of the
ductus arteriosus. This presentation often occurs within
the first one to two weeks after birth. In patients with
neonatal coarctation evolving while the patent ductus
arteriosus is closing, the lower extremity saturation can be
low as perfusion to the lower body can be maintained by
ductal patency. In the era of lower extremity pulse
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oximetry screening in newborns, a neonate could often

pass with an acceptable saturation as it is less common
for the ductus to contribute significantly unless other left
heart structures are hypoplastic. The second
presentation occurs in older children and adults.
Coarctation of the aorta in this scenario results in upper
extremity hypertension, leading to early coronary artery
disease, aortic aneurysm, and cerebrovascular disease.
Hemodynamics of simple coarctation of the aorta (CoA)

and complex CoA. a Hemodynamics of simple CoA.
Closure of the ductus arteriosus leads to left ventricular
pressure overload, resulting in left ventricular dysfunction.
b In complex CoA, blood flow from the left ventricle to the
right ventricle through the ventricular septal defect causes
left ventricular volume overload. Subsequent increase in
left ventricular endo-diastolic pressure leads to pulmonary
venous and arterial hypertension
Clinical manifestations Coarctation of the aorta is usually diagnosed after the

baby is born. Newborn screening using pulse oximetry
during the first few days of life may or may not detect
coarctation of the aorta.
In infants where the coarctation of the aorta is severe or

moderate, symptoms can include:
 labored or rapid breathing

 weak femoral artery pulse (taken in the groin
area)
 heavy sweating
 poor growth
 pale or gray appearance
 heart murmur
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If the narrowing is mild, coarctation of the aorta symptoms

may go unnoticed until the child is older or even an adult.
In those cases, symptoms can include:
 high blood pressure

 cold feet or legs
 difficulty exercising (gets out of breath quickly)
 dizziness
 fainting
 nosebleeds
 headaches
 leg cramps
 heart murmur
References Coarctation of the Aorta. (n.d.). Children’s Hospital of

Philadelphia. Retrieved January 3, 2023, from
https://www.chop.edu/conditions-diseases/coarctation-
aorta
Law MA, Tivakaran VS. Coarctation of the Aorta.

[Updated 2022 Aug 8]. In: StatPearls [Internet]. Treasure
Patnana, S. R. (2018, November 20). Coarctation of the

Aorta: Background, Pathophysiology, Prognosis.
Medscape.
https://emedicine.medscape.com/article/895502-
overview#a4
Standford Medicine, Health Care. (n.d.). Coarctation of

the Aorta Causes. Stanford Health Care. Retrieved
January 3, 2023, from
https://stanfordhealthcare.org/medical-conditions/blood-
heart-circulation/coarctation-aorta/causes.htm
Case 59 Pheochromocytoma of adrenal medulla showing hemorrhagic

features in the tumor tissue.
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Etiology Sporadic (90%) and familial (10%).

The tumor develops in specialized cells, called chromaffin
cells, located in the center of an adrenal gland. These
cells release certain hormones, primarily adrenaline
(epinephrine) and noradrenaline (norepinephrine).
Pathogenesis +
Pathophysiology
Clinical Manifestation  Classical pentad symptoms (headache, palpitation,

perspiration, pallor, and orthostasis)
 Hypertension – the most common presenting feature
Hammer, G.D. & McPhee, S.J. (2019).

Pathophysiology of Disease: An Introduction to
References Clinical Medicine (8th ed.). McGraw-Hill Education.
Case 61 Rheumatic mitral stenosis with marked left atrial dilatation

and endocardial fibrosis. Valve viewed from atrial aspect.
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Etiology Results as a sequela of rheumatic heart disease
Clinical Manifestation  Shortness of breath

 Hemoptysis
 Orthopnea
 Palpitations
 Neurologic symptoms
Reference Hammer, G.D. & McPhee, S.J. (2019). Pathophysiology of

Disease: An Introduction to Clinical Medicine (8th ed.).
McGraw-Hill Education.
Case 62
Chronic rheumatic mitral valvulitis with stenosis, which can

pass a probe of 3.5 cm circumference. Notice the fibrous
thickening and fusion of chordae tendineae.
Etiology Functional abnormalities due to

 alteration in matrix architecture
 cellular components impair the proper directionality
of blood flow through the heart chambers resulting
in heart failure
 Overall, HVD are slowly progressive disorders that
affect mainly the aging population (>65 years),
reaching epidemic proportions worldwide
 Despite increased life expectancy over the last
several decades, calcific aortic valve disease
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(CAVD), and degenerative mitral valve disease are

the two most common types of non-rheumatic valve
disease
 Due to vast health impact in developed world,
CAVD has sustained significant research interest
and a greater number of studies as compared to the
other valvular disorders.
Pathogenesis and
Pathophysiology
Case 63
Chronic rheumatic mitral valvulitis showing fibrous

shortening of the leaflets, and retraction of chordae;
consequently, insufficiency of the valve.
Etiology  Rheumatic heart disease results from either a

single or repeated attacks of rheumatic fever that
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results in rigidity and deformity of valve cusps,

the fusion of the commissures, or shortening
and fusion of the chordae tendineae.
 Over 2 to 3 decades, valvular stenosis and/or
regurgitation results. In chronic rheumatic heart
disease, the mitral valve alone is the most
commonly affected valve in an estimated 50% to
60% of cases. Combined lesions of both the aortic
and mitral valves occur in 20% of cases.
Involvement of the tricuspid valve occurs in about
10% of cases but only in association with mitral or
aortic disease. Tricuspid valve cases are thought
to be more common when recurrent infections
have occurred. The pulmonary valve is rarely
affected.
Case 64
Rheumatic mitral stenosis leading to marked left atrial

dilatation. A huge (about 5 cm diameter) ball thrombus is
attached to the atrial wall. Dislodgement of such mural
thrombus will completely and fatally obstruct the mitral
orifice.
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Etiology The most common cause of mitral stenosis is rheumatic

fever. Uncommon causes of mitral stenosis are calcification
of the mitral valve leaflets and congenital heart disease.
Other causes of mitral stenosis include infective
endocarditis, mitral annular calcification, endomyocardial
fibroelastosis, malignant carcinoid syndrome, systemic
lupus erythematosus, Whipple disease, Fabry disease, and
rheumatoid arthritis.
Pathogenesis and
Pathophysiology
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Case 65 Acute rheumatic valvulitis, with dew-drop like

verrucae along the valvular Margin.
Etiology Valvulitis is the inflammation of the heart

valves which is a common complication of
Acute Rheumatic Fever that stems from an
infection with Group A Streptococcus bacteria
Pathogenesis + Pathophysiology Untreated Group A Streptococci Infection

(Acute tonsillitis/pharyngitis) —> Development
of Antibodies —> Molecular Mimicry —> Type
II Hypersensitivity reaction —-> Inflammation
and cell damage (including valvulitis)
Clinical manifestations Most common in children between the ages of

5 to 15, the symptoms of Acute Rheumatic
Fever with Valvulitis include chest pain and
heart inflammation
Reference Acute Rheumatic Fever With Valvulitis:

Disease Bioinformatics. Novus Biologicals,
LLC. Retrieved from
https://www.novusbio.com/diseases/acute-
rheumatic-fever-with-
valvulitis#:~:text=Valvulitis%20is%20the
%20inflammation%20of,repair%20or
%20replace%20heart%20valves.
Case 66 Acute superimposed upon chronic mitral

rheumatic valvulitis. Notice the vegetations on
the valve and some fibrous thickening of the
valve leaflets, as well as the chordae.
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Etiology Valvulitis is the inflammation of the heart

valves which is a common complication of
Acute Rheumatic Fever that stems from an
infection with Group A Streptococcus
Pathogenesis + Pathophysiology Pharyngeal infection with Streptococcus

pyogenes → presentation of antigens to the
immune T and B cells → Activation of CD4+
cells leads to the production of specific acute
and chronic phase antibodies (IgM and IgG,
respectively) by B lymphocytes → antibodies
and activated T cells react with structurally
similar proteins or peptides in heart tissue,
resulting to heart inflammation → inflammation
of the valve tissue with the growth of new blood
vessels
Clinical manifestations Heart murmur due to narrowed mitral valve;

Fatigue
Reference Mutithu, D. W., Roberts, R., Manganyi, R., &

Ntusi, N. A. B. (2022). Chronic rheumatic heart
disease with recrudescence of acute rheumatic
fever on histology: a case report. European
Heart Journal - Case
Reports, 6(7). https://doi.org/10.1093/ehjcr/yta
c278
Case 67 Aortic rheumatic valvulitis - thickening and
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fusion of the leaflets
Etiology Rheumatic heart disease is caused by

rheumatic fever, an inflammatory disease that
can affect many connective tissues, especially
in the heart, joints, skin, or brain.The heart
valves can be inflamed and become scarred
over time.
Pathogenesis + Pathophysiology Rheumatic heart disease results from either a

single or repeated attacks of rheumatic fever
that results in rigidity and deformity of valve
cusps, the fusion of the commissures, or
shortening and fusion of the chordae
tendineae. Over 2 to 3 decades, valvular
stenosis and/or regurgitation results. In chronic
rheumatic heart disease, the mitral valve alone
is the most commonly affected valve in an
estimated 50% to 60% of cases. Combined
lesions of both the aortic and mitral valves
occur in 20% of cases. Involvement of the
tricuspid valve occurs in about 10% of cases
but only in association with mitral or aortic
disease. Tricuspid valve cases are thought to
be more common when recurrent infections
have occurred. The pulmonary valve is rarely
affected.
Rheumatic heart disease is the result of

valvular damage caused by an abnormal
immune response to Streptococcus pyogenes
infection, which is classified as a group A
streptococcus that causes acute rheumatic
fever.After multiple episodes of rheumatic
fever, progressive fibrosis of heart valves can
occur, which can lead to rheumatic valvular
heart disease. If valvular heart disease remains
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untreated, then heart failure or death may

occur.
Clinical manifestations Carditis is the most serious presentation of

rheumatic fever. The symptoms and signs of
carditis are dependent on the areas of the
heart involved, which include the pericardium,
myocardium, or heart valves. The presentation
of a pericardial friction rub on auscultation
leans toward the diagnosis of pericarditis. The
presence of signs of congestive heart failure
points toward a diagnosis of myocarditis, which
includes but is not limited to lower extremity
edema, shortness of breath with exertion or
rest, abdominal distension, or inability to lay flat
due to shortness of breath (orthopnea).
Myocarditis in the absence of valvular disease
is unlikely to be rheumatic in origin. Therefore,
an apical systolic or basal diastolic murmur
should be auscultated on physical exam. Mitral
regurgitation is the most common valvular
lesion, which is an apical pan-systolic murmur
on auscultation. Aortic regurgitation is less
common. If patients have a known history of
rheumatic heart disease, a change in the
character of the murmur or the presence of a
new murmur on auscultation leads to the
diagnosis of acute rheumatic heart fever.
Rheumatic heart disease predominantly affects
the left-sided cardiac valves. The tricuspid
valve and rarely pulmonary valve can be
affected, but very unlikely without mitral valve
involvement.
References “Rheumatic Heart Disease.” Rheumatic Heart

Disease | Johns Hopkins Medicine, 8 Aug.
2021,
www.hopkinsmedicine.org/health/conditions-
and-diseases/rheumatic-heart-disease.
Case 68 Fibrinous pericarditis of rheumatic pancarditis.
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Etiology
Injury to the pericardium leads to the release of
inflammatory cells, fibrin, and fluid. Most
commonly, acute pericarditis is idiopathic, and
in 90% of the cases, an etiology remains
undetermined. The remaining 10% are
secondary to bacterial and viral infections,
autoimmune disease, uremia, myocardial
infarction, cardiac surgery, malignancy,
trauma, and radiation.
Malignancies associated with fibrinous
pericarditis include lung and breast cancer,
lymphomas, leukemia, and metastatic disease.
Tuberculosis is one of the common causes of
pericarditis in countries where tuberculosis is
endemic. Several autoimmune and
inflammatory conditions like lupus,
scleroderma, rheumatoid arthritis, and mixed
connective tissue disorder are known to cause
pericarditis.
The normal pericardium sac contains
anywhere from 20-50 ml of plasma. A sudden
increase in the pericardial fluid can increase
pressure on the right atria and right ventricles,
which can compromise right atrial filling,
reduce stroke volume, and diminish cardiac
output. It is not the volume of pericardial fluid
that is important but the speed of
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accumulation. With gradual accumulation of

fluid, the pericardium has time to stretch and
accommodate the increase in fluid.
Pericardial effusion may impede diastolic filling
of the right heart if it accumulates too quickly,
and it may also result in constriction of the
heart if the accumulation is persistent. This
fluid accumulation may result in pericardial
tamponade.
Inflammation of the pericardium produces a
serous or purulent discharge. For example, in
viral pericarditis, the fluid is serous. Purulent
discharge can present in neoplastic or
tuberculous associated episodes of pericarditis
In most cases of acute pericarditis, the
inflammatory exudate and influx of neutrophils
result in a fibrinous reaction with adhesions
and fluid accumulation.
Clinical manifestation
Acute retrosternal chest pain that is sharp and
pleuritic presents in over 95% of cases of acute
pericarditis. The chest pain is classically
pleuritic and worsened by coughing, breathing,
and sitting up-right.Chest pain is often relieved
by leaning forward.
The most important physical sign in pericarditis
is the pericardial friction rub.The friction rub is
best heard while the patient is upright and
leaning forward. It is a high pitched, scratching
sound best heard at the left lower sternal
border during expiration. The pericardial friction
rub has three distinct components that
correspond to the cardiac cycle. These
components are heard during atrial systole,
ventricular systole, and rapid ventricular filling
during early diastole. It can be best heard with
the patient sitting or leaning forward. Other
critical clinical signs to be aware of are signs of
tamponade such as raised jugular venous
pressure (JVP), muffled heart sounds, and
decreased blood pressure. If pericardial
tamponade is concerned, checking for a pulsus
paradoxus is recommended. It is defined as a
drop of systolic blood pressure by more than
10 mm hg during inspiration.
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Reference Snyder MJ, Bepko J, White M. Acute

pericarditis: diagnosis and management. Am
Fam Physician. 2014 Apr 01;89(7):553-60.
Case 69 Acute rheumatic valvulitis showing fibrin

(acellular, eosinophilic) deposition on the
denuded endocardial surface. Underneath are
proliferative lesions of Aschoff bodies with
moderate edema of the tissue of the valve.
Etiology Acute rheumatic fever (ARF) results from the

body’s autoimmune response to a throat
infection caused by Streptococcus pyogenes,
also known as the group A Streptococcus
bacteria.
Overview of the pathogenesis of acute

rheumatic fever (GAS: group A Streptococcus;
BCR: B cell receptor; TCR: T cell receptor)
Figure reproduced with permission from
(Carapetis, et al., 2016).
Clinical manifestation ARF can present with several different clinical

manifestations in the weeks following an
episode of S. pyogenes pharyngitis (Special
Writing Group of the Committee on Rheumatic
Fever, Endocarditis, and Kawasaki Disease of
the Council on Cardiovascular Disease in the
Young of the American Heart Association,
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1992; Gewitz, et al., 2015). The most common

presenting features of ARF are fever (>90% of
patients) and arthritis (75% of patients). The
most serious manifestation is carditis (>50% of
patients) because it can lead to chronic
rheumatic heart disease—while all other
clinical features fully resolve, often within
weeks.
There are four other clinical features that are

considered minor manifestations of ARF: fever,
arthralgia, elevated acute phase reactants, and
prolonged PR interval on electrocardiogram
(Gewitz, et al., 2015).
References Sika-Paotonu D, Beaton A, Raghu A, et al.

Acute Rheumatic Fever and Rheumatic Heart
Disease. 2017 Mar 10 [Updated 2017 Apr 3].
In: Ferretti JJ, Stevens DL, Fischetti VA,
editors. Streptococcus pyogenes : Basic
Biology to Clinical Manifestations [Internet].
Oklahoma City (OK): University of Oklahoma
Health Sciences Center; 2016
Case 70 Rheumatic carditis

High magnification of Aschoff body showing the
nuclear peculiar features of Anitschow myocytes
Etiology Rheumatic heart disease results from either a

single or repeated attacks of rheumatic fever
that results in rigidity and deformity of valve
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cusps, the fusion of the commissures, or

shortening and fusion of the chordae tendineae.
Over 2 to 3 decades, valvular stenosis and/or
regurgitation results. In chronic rheumatic heart
disease, the mitral valve alone is the most
commonly affected valve in an estimated 50% to
60% of cases. Combined lesions of both the
aortic and mitral valves occur in 20% of cases.
Involvement of the tricuspid valve occurs in
about 10% of cases but only in association with
mitral or aortic disease. Tricuspid valve cases
are thought to be more common when recurrent
infections have occurred. The pulmonary valve
is rarely affected.
Clinical manifestation Rheumatic heart disease has a variety of clinical

manifestations including myocarditis,
decompensated congestive heart failure,
arrhythmias (i.e., atrial fibrillation), and valvular
heart disease.
Swollen, tender, red and extremely painful joints

— particularly the knees and ankles. Nodules
(lumps under the skin) Red, raised, lattice-like
rash, usually on the chest, back, and abdomen.
Shortness of breath and chest discomfort.
References Dass C, Kanmanthareddy A. Rheumatic Heart

Disease. [Updated 2022 Jul 25]. In: StatPearls
[Internet]. Treasure Island (FL): StatPearls
Publishing; 2022 Jan-. Available from:
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Case 71 An exudative and proliferative Aschoff body.

Notice the eosinophilic fibrinoid necrosis of
collagen (or exudate), edema of the tissue (wide
spaces between the cells) and the so-called
Anitschow myocytes showing typical caterpillar-
like nuclear chromatin pattern or "owl-eye"
appearance when seen on cross sections.
Multinucleation of these cells may occur.
Etiology Valvular damage caused by an abnormal

immune response to Streptococcus pyogenes
infection, which is classified as a group A
streptococcus that causes acute rheumatic
fever.
Clinical Manifestations Echocardiography is the primary evaluation tool

for patients with suspected and confirmed RHD,
as it delineates the distribution and severity of
valvular involvement and excludes alternate
pathology (Saxena, 2013). While the carditis
associated with ARF is a pancarditis, valvular
pathology almost exclusively dominates chronic
RHD. Left-sided cardiac involvement is most
commonly seen; it involves the mitral valve
almost 100% of the time and involves the aortic
valve in 20–30% of cases. The tricuspid valve is
affected histologically in 15–40% of patients with
RHD (Kitchin & Turner, 1964; Roguin,
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Rinkevich, Milo, Markiewicz, & Reisner, 1998;

Chopra & Bhatia, 1992), but this finding is rarely
of clinical importance except in the most severe
cases (Kitchin & Turner, 1964; Carpentier, et al.,
1974). The pulmonary valve is almost never
affected, though there are reports of pulmonary
autografts, which have been used in the aortic
position during a Ross procedure, subsequently
developing graft failure and showing signs of
rheumatic carditis (Choudhary, et al., 1999).
Reference Sika-Paotonu D, Beaton A, Raghu A, et al.

Acute Rheumatic Fever and Rheumatic Heart
Disease. 2017 Mar 10 [Updated 2017 Apr 3]. In:
Ferretti JJ, Stevens DL, Fischetti VA, editors.
Streptococcus pyogenes : Basic Biology to
Clinical Manifestations [Internet]. Oklahoma City
(OK): University of Oklahoma Health Sciences
Center; 2016-. Available from:
Case 73 A marantic thrombus on a normal mitral valve leaflet
Etiology Most commonly associated with pancreatic cancer

to adenocarcinoma of the lungs, SLE systemic
lupus erythematosus. Other associations include
autoimmune disorders, hyper coagulate states,
septicemia, severe burns or chronic disease such
as tuberculosis, uremia or AIDS.
Pathogenesis + Pathophysiology Endothelial injury in the setting of hypercoagulability

leading to primary and secondary clotting cascade
activation involving platelets, clotting factors and
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inflammatory mediators leading to the formation of

thrombi and vegetation on the affected valves. It
has greater propensity to affect left sided valves.
Clinical manifestations Cerebrovascular events:

 Strokes
 Transient ischemic attacks
Emboli affecting any arterial system:
 Critical limb ischaemia
 Splenic and renal infarcts
 Acute mesenteric ischaemia
Weight loss
Night sweats
Anorexia
Patients with SLE:
 Rashes
 Arthralgia
 Renal impairment
Patients with antiphospholipid syndrome:
 Recurrent deep vein thrombosis
 miscarriage
Reference Iris publishers. (2019). Marantic or Non-Bacterial

Thrombotic Endocarditis. Iris Publishers LLC.
https://doi.org/10.33552/OJCR.2019.01.000519
Case 74 Subacute bacterial endocarditis showing

thrombotic deposition on deformed valve
Etiology Subacute bacterial endocarditis is a type of

infective endocarditis. It is an infection that
occurs when bacteria (usually streptococci that
thrive in the mouth and throat) enter the
bloodstream and attack the lining of the heart
valves. Bacteria colonize the heart valves forming
vegetations.
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Clinical manifestations Signs & Symptoms

 Fever
 Heart murmur
 Worsening of old murmur
 Hematuria
 Vascular embolic event
 Splenomegaly
 Splinter hemorrhages
 Osler nodes
 Janeway lesions
 Roth spots
Complication:
 Stroke
 Non-stroke embolization
 Heart failure
References Brennan. (2021, April 13). What Is Subacute

Bacterial Endocarditis? WebMD. Retrieved
December 29, 2022, from
https://www.webmd.com/heart-disease/what-is-
subacute-bacterial-endocarditis
Case 75 Thickened aortic valves of rheumatic origin,

superimposed with subacute bacterial
endocarditis that presents a large amount of
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thrombotic vegetation
Etiology  A congenitally abnormal valve with

superimposed calcification
 Rheumatic valve disease is the most
common cause
 causes include calcification of the tri-leaflet
valve, alkaptonuria, systemic lupus
erythematosus, ochronosis, irradiation,
homozygous type II lipoproteinemia, and
metabolic diseases such as Fabry disease
With time, the ventricle can no longer

compensate, causing secondary LV cavity
enlargement, reduced ejection fraction (EF),
decreased cardiac output, and a misleadingly
low gradient across the aortic valve (low-
gradient severe AS).
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Reference Nkomo VT, Gardin JM, Skelton TN, Gottdiener

JS, Scott CG, Enriquez-Sarano M. Burden of
valvular heart diseases: a population-based
study. Lancet. 2006 Sep 16;368(9540):1005-11
Case 76 Close-up view of thrombotic vegetation gingerly

attached to the closure margin of aortic valves.
Etiology  Clinically undetectable or become a nidus for

infection
 Caused by Catheters passed through the right
side of the heart may injure the tricuspid and
pulmonic valves, resulting in platelet and fibrin
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attachment at the site of injury

 Disorders such as systemic lupus
erythematosus (SLE)
Pathogenesis and pathophysio
Clinical Manifestations Vegetations themselves rarely cause symptoms

unless their size and location cause valvular
dysfunction, sometimes causing dyspnea and/or
palpitations. Symptoms result from embolization
and depend on the organ affected (eg, brain,
kidneys, spleen, digits). Fever and a heart
murmur are sometimes present
Reference
Hurrell H, Roberts-Thomson R, Prendergast BD:
Non-infective endocarditis. Heart 106(13):1023–
1029, 2020. doi: 10.1136/heartjnl-2019-315204
Case 79 Colonies of bacteria embedded in fibrin

meshwork, and acute inflammatory exudates in
subacute bacterial endocarditis.
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Etiology Subacute bacterial endocarditis is usually

caused by streptococcal bacteria. This form of
the disease usually develops on damaged
valves after dental surgery involving infected
gums, reproductive or urinary (genitourinary
tract) surgery or operations on the
gastrointestinal tract. A history of a preceding
dental, genital or urologic procedure is common.
Pathogenesis + Pathophysiology Subacute bacterial endocarditis occurs typically

in patients who have valvular disease, usually
rheumatic, but who have acquired a high degree
of immunity, so that reinfection, recurrent
endocarditis or pancarditis, and congestive heart
failure do not occur. This increased immunity is
responsible for the fact that the patient is not
heart-conscious even during the attack of acute
valvular infection. Then a transient bacteremia,
caused by an upper respiratory infection,
tonsillectomy, the extraction of an infected tooth,
or pyelitis, permits secondary invasion and
implantation of bacteria (usually the
ubiquitousStreptococcus viridans) on the
damaged valve. A careful history will reveal that
some infection which lowered the general body
resistance is usually the beginning of an illness
that later develops into subacute bacterial
endocarditis. Although the bacteria are able to
implant themselves on the damaged valves,
they find in the valve an altered tissue reactivity
which does not permit much local damage, such
as ulceration or extension into the myocardium
or pericardium.
Clinical Manifestations  Heart murmur not previously present or a

changed heart murmur
o Presents in 80% of endocarditis
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patients
 A higher fever of 100 – 103 degrees F
 Flu-like symptoms including chills
 Shortness of breath at rest
 Night sweats
 Chest pain while breathing
 Swelling in the feet, legs or abdomen
 Rapid heartbeat (tachycardia)
 Loss of appetite leading to weight loss
 Blood or blood cells in the urine
(hematuria)
 Small red spots in the conjunctiva of the
eyes and fingernails (splinter
hemorrhages)
 Small painless spots on the palms of the
hands or soles of the feet (Janeway
lesions)
 Pain nodules in the fingertips (Osler
nodes)
References Held, I. W., & Lieberson, A. (1943).

Pathogenesis of subacute bacterial endocarditis.
American Heart Journal, 25(4), 478–485.
https://doi.org/10.1016/s0002-8703(43)90487-9
Case 81 A metastatic pyemic abscess in myocardium
Etiology Commonly thought to occur primarily by the extent

of a pre-existing cardiac infection, such as
infective endocarditis (IE).
Secondary causes of cardiac abscess are
believed to be due to bacteremia (persistent or
transient) without a known cardiac source, as well
as susceptible heart tissue soon after myocardial
infarction (MI), or prosthetic valve disease,
usually in the setting of bacteremia.
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Pathogenesis + Pathophysiology The number one predisposing factor for a cardiac

abscess is current or prior infective
endocarditis. S. aureus, the most commonly
involved causative agent, is present in up to one-
third of all cases and has an even higher
incidence in patients with prosthetic valves.
Clinical manifestations  Fever

 Anorexia
 Myalgias
 Headache
 Dyspnea
 Joint pain
 Rashes
 Cough
 Chest pain
 Heart attack or stroke (sudden blockage)
References Ramos Tuarez FJ, Yelamanchili VS, Law MA.

Cardiac Abscess. [Updated 2022 Jul 18]. In:
StatPearls [Internet]. Treasure Island (FL):
StatPearls Publishing; 2022 Jan-. Available from:
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Case 82 Calcific aortic stenosis showing rigidity and

thickening of the aortic valve.
Etiology CONGENITAL
Aortic valve stenosis that's related to increasing
age and calcium deposit buildup usually doesn't
cause symptoms until age 70 or 80. However, in
some people — particularly those with congenital
aortic valve defects — calcium deposits result in
stiffening of the valve cusps at a younger age.
ACQUIRED
Rheumatic valve disease is the most common
cause in developing countries.
the commissures of the leaflets fuse to leave a
small central orifice.
Clinical manifestations  Fatigue

 Heart palpitations
 Swelling in your feet
 ankles or lower legs
 Chest pain (angina)
 Dizziness, lightheadedness or fainting
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References Pujari SH, Agasthi P. Aortic Stenosis. [Updated

2022 Oct 1]. In: StatPearls [Internet]. Treasure
Island (FL): StatPearls Publishing; 2022 Jan-.
Available from:
2. Case Problems
Answer the following cases using the format below:
Case A.
A 9-year-old female had two previous attacks of rheumatic fever. She entered the
hospital for the third time with painful swollen joints, fever, and pulmonary edema.
She died with signs of progressive heart failure.
Diagnosis:
Etiology:
Pathogenesis:
Gross Findings:
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Histologic Morphology
Pathophysiology of Clinical Manifestations:
Case B.
A 67 year old male had rheumatic heart disease for thirty years. Three months
prior to death he began to have episodes of fever and chills accompanied by
signs of worsening congestive heart failure. Splinter hemorrhages and purpuric
skin rashes were noted three weeks before death.
Diagnosis:
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Etiology:
Pathogenesis:
Gross Findings:
Pathophysiology of Clinical Manifestations:
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Case C.
This 45 year old man had been well until he was awakened by chest pain that
radiated to both arms and neck and was associated with diaphoresis. His blood
pressure was 160/110. He was treated with diuretics (Lasix), but he continued to
gain weight. He developed a friction rub. Two days after the onset of the chest
pain he had a cardiac arrest and died.
Diagnosis:
Etiology:
Pathogenesis:
Gross Findings:
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Pathophysiology of Clinical
Manifestations:
Case D.
This 64 year old male had two episodes of myocardial infarction followed by
congestive heart failure during the eight months prior to death. Death was
preceded by arrhythmia.
Diagnosis:
Etiology:
Pathogenesis:
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Gross Findings:
Pathophysiology of Clinical
Manifestations:
3. Multiple Choice
Choose the letter of the correct answer and explain its etiology, pathogenesis and
pathophysiology, and its gross and histologic findings.
A.Causes of Syncope
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Choices:
a. Hypoglycaemia.
b. Grand mal seizure.
c. Sinus arrest.
d. Complete heart block.
e. Ventricular tachycardia.
f. Vasovagal (neurocardiogenic) syncope.
g. AS.
h. Atrial myxoma.
i. Transient ischaemic attack.
j. MS.
k. Aortic dissection.
1) An 80 - year - old male with breathlessness, fatigue and exertional syncope.

A quiet systolic murmur is heard on examination.
Answer:
Etiology:
Gross Findings:
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Histologic Findings:
2) A 25 - year - old woman witnesses a car accident. There is a 2 - minute

prodrome of feeling nauseated, pale and clammy before collapsing.
Answer:
Etiology:
Gross Findings:
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3) A 74 - year - old type 2 diabetic on metformin with a past history of

myocardial infarctions, coronary artery bypass surgery and left ventricular
ejection fraction of 25%. Syncope occurs while sitting with no warning and
with a quick recovery after 20 seconds.
Answer:
Etiology:
Gross Findings:
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4) A 65 - year - old woman with previous aortic valve replacement surgery, a

blood pressure of 200/100 mmHg, sinus rhythm, PR interval 0.25 seconds,
RBBB and left - axis deviation, has syncope without warning.
Answer:
Etiology:
Gross Findings:
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5) A 78 - year - old woman with paroxysmal atrial fibrillation, recently started

on sotalol, has a 20 - minute episode of irregular palpitations which ends
with a sudden 5 - second loss of consciousness resulting in a collapse.
Answer:
Etiology:
Gross Findings:
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B. Palpitations
Choices:
A. Ectopic beats
B. Sinus rhythm
C. Sinus tachycardia
D. Atrial fifibrillation
E. Atrial flflutter
F. Automatic atrial tachycardia
G. Wolff - Parkinson - White syndrome
H. Mobitz 1 (Wenckebach) second - degree heart block
I. AV - nodal reciprocating tachycardia
J. Ventricular tachycardia
K. Torsades de pointes
1) A cause of syncope or sudden cardiac death in patients with

congenital or acquired LQTS.
Answer:
Etiology:
Gross Findings:
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2) A regular rhythm at 150 bpm, associated with hypertension and

increasing age and a risk factor for thromboembolic stroke.
Answer:
Etiology:
Gross Findings:
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3) Found in 1 in 1000 people, usually causing a sudden - onset regular

tachycardia but may also rarely result in ventricular fibrillation.
Answer:
Etiology:
Gross Findings:
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4) A common form of palpitation, usually worse at times of rest,

causing a heavy thumping or sensation of “missed beats” .
Answer:
Etiology:
Gross Findings:
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5) A sudden - onset, rapid, regular rhythm at 170 bpm, presenting for

the fifirst time in a 25 - year - old woman, terminated with carotid
sinus massage, with a normal 12 - lead ECG appearance during
sinus rhythm.
Answer:
Etiology:
Gross Findings:
C. Physical Signs
Choices:
a. A collapsing ‘ waterhammer ’ pulse.
b. An irregularly irregular pulse.
c. An ejection systolic murmur radiating to the carotid arteries.
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d. A mid - systolic click and late - systolic murmur loudest at the apex.
e. Fixed splitting of the second heart sound.
f. A fall in blood pressure of >10 mmHg during inspiration.
g. A pericardial rub.
h. Fine inspiratory crackles at both lung bases.
i. Radial – femoral delay.
j. A low, rumbling mid - diastolic murmur, loudest when lying on the left side.
k. A palpable thrill over the left sternal edge.
l. Central cyanosis.
m. A pulsatile liver.
n. Pitting oedema in the lower limbs.
1) Viral pericarditis
Answer:
Etiology:
Gross Findings:
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2) A small VSD.
Answer:
Etiology:
Gross Findings:
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3) Mitral valve prolapse with moderate MR.
Answer:
Etiology:
Gross Findings:
4) Atrial fibrillation
Answer:
Etiology:
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Gross Findings:
5) Severe TR
Answer:
Etiology:
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Gross Findings:
D. Causes of Systolic Murmur
Choices:
a. Severe AS.
b. MR.
c. VSD.
d. Innocent murmur.
e. Aortic coarctation.
f. Mitral valve prolapse.
g. HOCM.
h. Bicuspid aortic valve (mildly stenosed).
i. TR.
j. Functional MR due to a dilated cardiomyopathy.
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1) A 32 - year - old woman presents with palpitations,which she describes as

having a pause and thump pattern. She is otherwise well and plays squash on a
regular basis without limitation. On examination,she looks well. Her pulse is
normal in character and volume. Blood pressure is 110/70 mmHg. JVP is not
elevated. Apex beat is normal. There is a mid – to late - systolic murmur, heard
best at the apex.
Answer:
Etiology:
Gross Findings:
2) A 72 - year - old man presents with breathlessness on exertion after 100 m. He

has a history of hypertension treated with enalapril 20 mg po bd. On examination,
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he has a small volume pulse, blood pressure is 100/80 mmHg, his JVP is visible
mid - neck. The apex beat is easily palpable but not displaced. Auscultation
reveals a systolic murmur heard throughout the precordium and which radiates to
the neck. The second sound is inaudible.
Answer:
Etiology:
Gross Findings:
3) A 50 - year - old woman presents with breathlessness and leg oedema. Her
sister and father also have breathing problems ’ felt to be heart related. On
examination, she is overweight; she has a tachycardia of 100 bpm in atrial
fibrillation with a small volume pulse. Blood pressure is 90/70 mmHg.The JVP is
elevated to the angle of the jaw. The apex beat is displaced to the anterior axillary
line. On auscultation, the heart sounds are soft, there is a soft apical pansystolic
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murmur and an added third heart sound. The liver is palpable but not pulsatile.
She has oedema to the knees.
Answer:
Etiology:
Gross Findings:
4) A 20 - year - old woman is referred by her GP having been found to have a

murmur when being examined for an exacerbation of her asthma. She is well.
Pulse is normal; blood pressure is 110/70 mmHg; JVP is not elevated. The apex
beat is not displaced. There is a mid - systolic murmur, heard best at the left
sternal edge with the patient lying flat; the murmur does not radiate. The rest of
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the clinical examination is normal. Her ECG shows a sinus bradycardia of 55 bpm
but is otherwise normal.
Answer:
Etiology:
Gross Findings:
5) A 5 - year - old boy is seen in A & E with a fractured humerus. On auscultation,

he has a loud pansystolic murmur, heard best at the left sternal edge. There are
no other abnormal physical signs. His parents report that he was noted to have a
murmur at birth and they were told it would probably go when he got older.
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Answer:
Etiology:
Gross Findings:
E. Causes of Left Hemiparesis
Choices:
a. Infective endocarditis.
b. Left ventricular mural thrombus.
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c. Carotid artery stenosis.

d. Paroxysmal atrial fi brillation.
e. Left atrial myxoma.
f. Paradoxical embolism.
g. Decompression sickness.
h. Haemorrhagic stroke.
i. Cerebral secondaries.
j. Subdural haematoma.
1) A 60 - year - old diabetic man with a 30 - pack year history of smoking who
describes waking up at night very short of breath and ‘ tight chested ’ a week
before. He presents with a sudden onset of a left hemiparesis and the ECG shows
Q waves in the anteroseptal leads.
Answer:
Etiology:
Gross Findings:
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2) A 45 - year - old man gives a history of being generally unwell over the past 3
weeks. He has lost 1 kg in weight. On examination, there are no peripheral
stigmata of endocarditis. He looks anaemic and is pyrexial at 38° C. Pulse is 100
bpm in sinus rhythm and collapsing in nature; blood pressure is 180/40 mmHg.
Auscultation reveals an early diastolic murmur, heard best in inspiration at the left
sternal edge.
Answer:
Etiology:
Gross Findings:
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3) A 78 - year - old man with a 30 - pack year history of smoking and a past history
of a left femoropopliteal bypass operation presents with a week ’ s history of
intermittent weakness affecting the left arm. His wife notices that the left side of
his face droops with each episode and lasts approximately 30 minutes. On
examination, his pulse is 70 bpm and regular; blood pressure is 130/70 mmHg;
heart sounds are normal. Both carotids are palpable and there are no carotid
bruits. He has bilateral femoral artery bruits and his pulses are absent below the
femoral arteries.
Answer:
Etiology:
Gross Findings:
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4) A 69 - year - old woman gives a long - standing history of poorly controlled

hypertension. She presents with a sudden onset of left - sided weakness. On
examination, pulse is 120 bpm in atrial fibrillation; blood pressure is 200/120
mmHg; heart sounds are normal. A CT scan performed within 2 hours of the onset
of symptoms is reported as normal.
Answer:
Etiology:
Gross Findings:
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5) A 50 - year - old man presents to the vascular surgeons with a painful cold right
foot. He has been previously quite fi t but on questioning gives a history of two
episodes of syncope over the past 2 weeks. He has no cardiovascular risk factors
and is very fit and well. He undergoes a successful removal of a large left femoral
embolus; however, 3 days later he develops a sudden onset of a left hemiparesis.
On examination, he is apyrexial; pulse 70 bpm with normal character; blood
pressure 130/90 mmHg. The apex is not displaced. Heart sounds reveal an apical
diastolic ‘ plop. Blood tests have revealed a normochromic normocytic anaemia
and an ESR of 100 mm/h
Answer:
Etiology:
Gross Findings:
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F. Causes of an elevated troponin
Choices:
a. Pericarditis.
b. Non- STEMI.
c. Pulmonary embolism.
d. Hypertensive crisis.
e. Myocarditis.
f. Ischaemic cardiomyopathy with acute left ventricular failure.
g. Septic shock.
h. Amyloid heart disease.
i. Cardiac arrest.
j. Tachyarrhythmia.
k. Cardiac contusion.
1) A 40 - year - old woman presenting with central chest pain. Clinical examination
is normal. ECG on presentation is shown in Figure EMQ 8.1 .
Answer:
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Etiology:
Gross Findings:
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2) A 50 - year - old man with a history of alcohol abuse presents having collapsed
at home. He lives alone. On arrival he is delirious. He is warm peripherally. O2
saturations on air are 86%. Pulse 120 bpm; blood pressure 80/30 mmHg; JVP is
just visible lying flat. Heart sounds cannot be heard as a result of coarse breath
sounds. His ECG shows a sinus tachycardia and a CXR shows bilateral airspace
shadowing with air bronchograms.
Answer:
Etiology:
Gross Findings:
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3) An 18 - year - old man presents with a history of breathlessness chest pain and
fatigue over the past 3 days. On examination, he is apyrexial. He looks unwell
slightly jaundiced and is cool peripherally. Pulse is 120 bpm in sinus rhythm;
blood pressure 90/70 mmHg with no paradox; JVP elevated to the angle of the jaw
with a normal wave form. The apex beat is displaced to the anterior axillary line.
Auscultation reveals third and fourth heart sounds and a soft apical systolic
murmur. Auscultation of the chest reveals crepitations to the mid -zones and he
has bilateral pitting oedema. His ECG demonstrates non - specific ST
abnormalities in the lateral chest leads.
Answer:
Etiology:
Gross Findings:
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4) A 60 - year - old woman presents 5 days following a total knee replacement with
breathlessness. She arrests in the ambulance and is resuscitated. On
examination, her pulse is 120 bpm in sinus rhythm; blood pressure 60/40 mmHg,
O2 saturations on air 90%. Heart sounds are normal and chest is clear. The ECG is
shown in Figure EMQ 8.2 .
Answer:
Etiology:
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Gross Findings:
5) A 40 - year - old man with an ECG shown in Figure EMQ 8.3 after an aortic
aneurysm repair.
Answer:
Etiology:

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Gross Findings:
G. Causes of Chest Pain
Choices:
a. Aortic dissection.
b. Pericarditis.
c. Pulmonary embolism.
d. Oesophageal refl ux.
e. ACS – unstable angina.
f. Paroxysmal SVT.
g. Pleurisy.
h. Musculoskeletal.
i. Gall stones.
j. Stable angina.
k. ACS – myocardial infarction.
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1) A 70 - year - old man presenting with severe central chest pain of sudden onset.
On examination he has a right hemiparesis. Blood pressure is 180/80 mmHg. On
auscultation he has an early diastolic murmur.
Answer:
Etiology:
Gross Findings:
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2) A 40 - year - old woman with a history of chest pain on exertion over the past 3
months presenting with a sudden deterioration and chest pain after walking 10 m.
Answer:
Etiology:
Gross Findings:
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3) A 60 - year - old diabetic presents with syncope followed by breathlessness

with vomiting and sweating on the background of a 6 - month history of declining
exercise tolerance with associated chest tightness. A CXR demonstrates features
of pulmonary oedema.
Answer:
Etiology:
Gross Findings:
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4) A 20 - year - old man with a history of cough productive of green sputum and a
3 - day history of central chest pain, which is relieved on sitting forwards.
Answer:
Etiology:
Gross Findings:
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5) A 40 - year - old woman with a history of severe central chest pain presenting at
rest. There is a 10 - year history of nocturnal chest pain last up to 1 hour. An ECG
performed during pain is normal.
Answer:
Etiology:
Gross Findings:
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H. Cardiac Causes of Dyspnea
Choices:
a. Diastolic heart failure.

b. Ischaemic heart disease.
c. Acute myocardial infarction.
d. Paroxysmal atrial fibrillation or flutter.
e. Valvular heart disease.
f. Dilated cardiomyopathy.
g. Mobitz type 2 second - degree or third - degree heart block.
h. Sustained atrial fibrillation or flutter.
i. Pericardial tamponade.
j. Constrictive pericarditis.
k. Restrictive cardiomyopathy.
l. Pulmonary embolism.
m. Pulmonary hypertension.
n. Congenital heart disease.
o. Uncontrolled hypertension.
p. Sinus node disease with bradycardia.
q. HOCM.
1) A 50 - year - old woman with a history of breathlessness on exertion over the

past 12 months. Upon examination, she is mildly centrally cyanosed. Pulse is 80
bpm, normal volume and character. JVP is elevated to the angle of the jaw. There
is a right ventricular heave and a loud pulmonary second sound but auscultation
is otherwise normal. Her chest is clear and she has mild peripheral oedema. An
ECG demonstrates tall R waves in the anteroseptal leads.
Answer:
Etiology:
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Gross Findings:
2) A 40 - year - old woman with a history of breast cancer, treated with

radiotherapy and chemotherapy 6 months previously, presents with fatigue and
breathlessness over the past 3 weeks. There is no cardiac history and she has no
risk factors for cardiac disease. On examination, she is cool peripherally. Pulse is
100 bpm in atrial fibrillation; blood pressure 100/80 mmHg; JVP is elevated to the
angle of the jaw. Heart sounds are quiet and the apex beat is impalpable. An ECG
demonstrates small complexes. CXR shows a globular cardiac outline.
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Answer:
Etiology:
Gross Findings:
3) A 60 - year - old diabetic woman with a long –standing history of hypertension

presents with increasing breathlessness on exertion over the past 2 years. Her
exercise tolerance is now 20 m but she is not breathless at rest. Her cardiac
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examination is normal with the exception of a soft fourth heart sound. Blood
pressure is 140/80 mmHg on medication. Her chest is clear. An ECG demonstrates
left ventricular hypertrophy and strain and a stress echocardiogram reveals
normal wall motion at rest and stress. BNP is elevated.
Answer:
Etiology:
Gross Findings:
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4) A 45 - year - old man with a history of hypertension presents with a history of

four episodes of acute breathlessness over the past 6 months. The episodes
occur predominantly at rest and last between 15 and 20 minutes. Between these
episodes he has a normal exercise tolerance and he plays tennis on a regular
basis to a high standard. Cardiac examination is normal. An echocardiogram
demonstrates normal left ventricular function; the left atrium is reported as
dilated.
Answer:
Etiology:
Gross Findings:
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5) A 48 - year - old woman presents with fatigue and breathlessness, which has
progressed over the past 6 months. She is usually quite sedentary but now has an
exercise tolerance of less than 50 m. She has had three episodes of acute
dyspnoea at night. There are no risk factors for cardiac disease other than a
family history of early cardiac death on her father’s side. On examination, she has
a pulse of 80 bpm in sinus rhythm with a small volume; blood pressure is 110/70
mmHg; JVP is elevated to the middle of the neck. The apex beat is displaced to
the anterior axillary line. Auscultation is normal. She has pitting oedema to the
mid - calf. Her ECG demonstrates non - specific ST changes in the lateral chest
leads.
Answer:
Etiology:
Gross Findings:
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References:

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ACTIVITY 8: HEMATOPATHOLOGY
Name: _________________________________ Date: ________________ Score: _________
Solve the following cases presented and come up with the appropriate diagnosis, a
etiology, pathogenesis, pathophysiology, and gross and histologic findings.
Case 1:
Diagnosis:
Etiology:
Gross Findings:
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Case 2:
Diagnosis:
Etiology:
Gross Findings:
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Case 3:
Diagnosis:
Etiology:
Gross Findings:
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Case 4:
Diagnosis:
Etiology:
Gross Findings:
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Case 5:
Diagnosis:
Etiology:
Gross Findings:
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Case 6:
Diagnosis:
Etiology:
Gross Findings:
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Case 7:
Diagnosis:
Etiology:
Gross Findings:
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Case 8:
Diagnosis:
Etiology:
Gross Findings:
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Case 9:
Diagnosis:
Etiology:
Gross Findings:
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Case 10:
Diagnosis:
Etiology:
Gross Findings:
Case 11:
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Diagnosis:
Etiology:
Gross Findings:
References:
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[G E N E R A L P A T H O L O G Y | L A B O R A T O R Y M A N U A L] AY: 2022-2023

MINDANAO STATE UNIVERSITY - GENERAL SANTOS

Activity 1: General Aspects Of Diseases................................................2

Activity 2: Cell Injury And Necrosis..........................................................2

Activity 3: Genetic Disorders.....................................................................2

Activity 4: Neoplasia – Gross And Microscopy......................................2

Activity 5: Environmental And Nutritional Disorders.............................2

Activity 6: Diseases Of Infancy And Childhood.....................................2

Activity 7: Cardiovascular System Pathology.........................................2

ACTIVITY 1: GENERAL ASPECTS OF DISEASES

Name: _________________________________ Date: ________________ Score: _________

Course & Year Level: ____________________________ Group: _______________________

2.Distinguish between disease and non-disease.

ACTIVITY 2: CELL INJURY AND NECROSIS

Name: _________________________________ Date: ________________ Score: _________

Course & Year Level: ____________________________ Group: _______________________

9) Cellular swelling (hydropic change)

12) Heat-shock proteins

Feature Cell Death Somatic Death

4. Outline the relationship between:

5. Compare coagulative necrosis, liquefactive necrosis, gangrenous necrosis, caseous

Gross Appearance Microscopic Appearance

Types Extent of Healing

Gross Appearance Microscopic Appearance

Types Extent of Healing

Gross Appearance Microscopic Appearance

Types Extent of Healing

Gross Appearance Microscopic Appearance

Types Extent of Healing

Gross Appearance Microscopic Appearance

Types Extent of Healing

Gross Appearance Microscopic Appearance

Types Extent of Healing

Gross Appearance Microscopic Appearance

Types Extent of Healing

6. Compare and contrast the following types of cell injury:

Feature Reperfusion Injury Free-Radical Induced Injury Chemical Injury

8.Discuss the significance of intracellular accumulation of:

9.Compare fatty change (steatosis) and fatty infiltration.

Feature Fatty change Fatty infiltration

10.Compare dystrophic and metastatic calcification

Feature Dystrophic Calcification Metastatic Calcification

ACTIVITY 3: GENETIC DISORDERS

Name: _________________________________ Date: ________________ Score: _________

Course & Year Level: ____________________________ Group: _______________________

Complete the table of the following genetic disorders:

Disease Gene/Defect Inheritance Clinical Features

11. Wilms Tumor

15. Systemic Lupus

19. Lyme Disease

23. Biliary Atresia

24. Choledochal Cyst

27. Gaucher Disease

28. Pompe Disease

30. Maple Syrup

31. Conjoined twins

34. Primary Fallopian

36. Uterine Sarcoma

38. Distal Vaginal

41. HIV in pregnancy

44. Ochoa syndrome

46. Exstrophy of the

49. DAVF in children

Name: _________________________ Date: Score: _

Course & Year Level: ______ Group: _

Name: _________________________ Date: Score: _

Course & Year Level: ______ Group: _

Name: _________________________ Date: Score: _

Course & Year Level: ______ Group: _

Name: _________________________ Date: Score: _

Course & Year Level: ______ Group: _

Name: _________________________ Date: Score: _

Course & Year Level: ______ Group: _

Name: _________________________ Date: Score: _

Course & Year Level: ______ Group: _