FEU-Dr. Nicanor Reyes Medical Foundation
School of Medicine
Department of Pathology
WORKBOOK FOR LABORATORY EXERCISES
IN SYSTEMIC PATHOLOGY
2019 EDITION
SY 2019-2020
MARI KARR A. ESGUERRA, M.D., MSPH, FPSP
ROGELDA R. GONZALES-BONGAT, M.D., MHPEd, FPSP
RONALD C. DY QUIANGCO, M.D.
FEU-NRMF PRAYER
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i
RESULTS OF EXAMINATIONS
First Preliminary Examinations (20%):
__________
Second Preliminary Examinations (20%):
__________
Final Examinations (24%):
__________
Platings (20%):
1.__________
2.__________
3.__________
4.__________
5.__________
6.__________
7.__________
8.__________
9.__________
10.__________
11.__________
12.__________
13.__________
14.__________
15.__________
Plating Lab Quizzes (5%):
1.__________
2.__________
3.__________
4.__________
5.__________
6.__________
7.__________
8.__________
9.__________
10.__________
11.__________
12.__________
13.__________
14.__________
15.__________
6.__________
7.__________
8.__________
9.__________
10.__________
11.__________
12.__________
13.__________
14.__________
15.__________
CPC Quizzes (9%):
1.__________
2.__________
3.__________
4.__________
5.__________
Manual Grade (2%):
1st Prelim: __________
Midterm: __________
Finals: __________
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ii
SYSTEMIC PATHOLOGY
PREFACE
Systemic Pathology deals with specific responses of specialized organs
and tissues to more or less well-defined stimuli. It consists of a study of specific
disease processes as they affect particular organs and systems.
This manual therefore aims to:
1. reinforce the concepts and facts about gross and microscopic
changes in various diseases;
2. facilitate the understanding and retention of information
regarding major features of important pathologic condition by
means of drawings;
3. encourage understanding of diseases through ClinicoPathologic Correlation;
4. encourage supplementary reading through answers to
questions at the end of each exercises.
Each exercise starts with a general discussion of the diseases of the
particular organ-system in consideration. This is followed by a short description
of the specific disease for study and a short clinical protocol, where warranted.
Spaces are provided for drawings of gross and/or microscopic features of the
diseases included in the manual. Efforts have been exerted to include only
diseases which are commonly encountered by a primary health care physician
and those not so common but interesting conditions. Students are encouraged to
think of the clinical manifestations which may arise from the morphologic findings
found in the diseases and vice versa, that is, think of the possible pathologic
findings giving rise to a patient’s clinical manifestations. Pages of the textbook
where the diseases are discussed were likewise included to facilitate reading on
the topic. The questions at the end of each disease serve to further increase
knowledge and stress certain important points on the topic. Always include a
landmark in your drawing to help you identify the organ of involvement.
This manual serves as a guide in the laboratory and does not replace the
textbook in any way.
Requirements:
Colored pencils - individual
Robbins and Cotran Pathologic Basis of Disease by Kumar, Abbas,
and Aster; 9th Edition – one per group
Textbook of Histology by de Fiore – one per group
M.A.E.
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R.D.Q.
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iii
TABLE OF CONTENTS
TOPICS
PAGES
I.
DISEASES OF THE HEART
1-8
II.
DISEASES OF THE LUNGS
9 - 16
III.
DISEASES OF THE GASTROINTESTINAL TRACT
17 - 23
IV.
DISEASES OF THE LIVER
AND GALLBLADDER
24 - 30
V.
DISEASES OF THE KIDNEY
31 – 36
VI.
DISEASES OF THE LOWER URINARY
TRACT AND MALE GENITALIA
37 - 43
VII.
DISEASES OF THE FEMALE GENITALIA
44 – 51
VIII.
DISEASES OF THE BREAST AND SKIN
52 - 58
IX.
DISEASES OF THE ENDOCRINE SYSTEM
AND THE EXOCRINE PANCREAS
59 – 68
X.
DISEASES OF THE BONES, JOINTS AND
SOFT TISSUES
69 - 75
XI.
DISEASES OF THE CNS
76 - 81
XII.
DISEASES OF THE HEAD, NECK AND EYES
82 - 85
APPENDICES
86+
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iv
I. DISEASES OF THE HEART
Slides:
# 184 Myocardial Hemorrhage
# 39 Subacute Bacterial Endocarditis
DEMO Rheumatic Heart Disease
Gross : Rheumatic Heart Disease
Tetralogy of Fallot
Subacute Bacterial Endocarditis
Patent Ductus Arteriosus
Introduction:
Cardiovascular disease tops the cause of death in the world. The
developing countries account for about 80% of the burden. In the Phillipines, the
2016 DOH statistics place Ischemic heart disease as the number cause of death
causing 12.7% death but if Hypertensive diseases (5.3%) and other Heart
diseases (4.5%) are included the total death rate goes up to 22.5%. The major
categories of heart diseases include congenital heart, ischemic heart,
hypertensive heart, valvular, and primary myocardial diseases.
CONGENITAL HEART DISEASES
Congenital heart disease refers to cardiovascular abnormalities that one is
born with. Most of these disorders arise from errors in embryogenesis during the
third to eight weeks of gestation, when major cardiovascular structures start to
form and to function.
Congenital heart diseases are mainly caused by sporadic genetic
abnormalities such as single gene mutations, small chromosomal deletions, and
monosomies and trisomies. The most common genetic cause of congenital heart
disease is trisomy 21 (Down Syndrome) where 40% of the patients have one or
more heart defects. Most affected patients have no identifiable genetic factors
such that environmental factors, alone or in combination with genetic factors may
also contribute to congenital heart disease. In some cases, environmental factors
(toxin or infection) may be the primary cause, e.g., congenital rubella infection,
gestational diabetes, and exposure to teratogens. Nutritional factors may also
modify risk of congenital heart disease. The major categories of congenital heart
disease include malformations causing:
- left-to-right shunt (Atrial Septal Defect, Ventricular Septal Defect and
Patent Ductus Arteriosus)
- right-to-left shunt (Tetralogy of Fallot, Transposition of Great Arteries,
and Tricuspid Atresia
- obstruction (Coarctation of the aorta, pulmonary stenosis and atresia and
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-1-
1. PATENT DUCTUS ARTERIOSUS: p 535
1.1 Definition: PDA is persistence after birth of the normal communication
between the pulmonary arterial system and the aorta of the fetus. About
90% occurs as an isolated anomaly and 10% in association with VSD,
coarctation of the aorta or pulmonary or aortic stenosis. PDA normally
constricts and closed functionally 1 – 2 days after birth.
1.2 History: An intrauterine fetal death baby, 37 – 38 weeks, was delivered
in the hospital. History revealed mother had viral infection during the first
trimester of pregnancy. P.E. revealed a macerated fetus. Autopsy showed
the presence of multiple congenital abnormalities in the heart including a
patent ductus arteriosus.
Draw and label completely.
pulmonary artery
aorta
patent ductus arteriosus.
Which of the following word/set of words are responsible for the persistence of
ductus arteriosus? Choose and put a check on your three (3) correct answers.
( ) declining local levels of prostaglandin E2
( ) decreased pulmonary vascular resistance
(x) hypoxia
( ) increased arterial oxygenation
(x) in association with VSD
When does preservation of a PDA become life- saving?
________________________________________________________________
________________________________________________________________
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-2-
2. TETRALOGY OF FALLOT: p 535
2.1 TOF represents the most common cyanotic congenital heart disease.
The four cardinal features of TOF are ventricular septal defect,
subpulmonic stenosis, overriding of the aorta, and hypertrophy of the right
ventricle. The clinical consequences of TOF depend primarily on the
severity of subpulmonic stenosis.
2.2 History: A 2 year old child was admitted because of difficulty of
breathing and cyanosis. History revealed that cyanosis has been noted
since birth and most prominent when the child is crying.
Draw and label completely.
VSD
subpulmonic stenosis
overriding of the aorta
right ventricular hypertrophy
Why is the heart of patient’s with TOF “booth-shaped”?
________________________________________________________________
________________________________________________________________
Explain why patient’s with TOF rarely develop right ventricular failure?
________________________________________________________________
________________________________________________________________
4b,c Classic TOF
3. HEMORRHAGE, HEART: p 540
3.1 Definition: Presence of red blood cells outside of the blood vessel
lumen
3.2 Etiology: Hemorrhage of the heart may have one of the following
causes:
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-3-
3.2.1. Necrosis of blood vessels, like infarction
3.2.2 Penetrating chest trauma
3.2.3. Infiltration of tumor into the myocardium
3.3 History: A 35 year old male, heavy cigarette smoker, marketing
director of an appliance store was admitted because of severe,
constricting pain over the anterior chest of 2 hours duration accompanied
by cold, clammy perspiration, and hypotension. He died in the intensive
care unit 24 hours after admission. Autopsy was done.
3.4 Examine the slide. Focus the slide under LPO and examine the
interstitium. Label completely the myocardial fibers, abundant interstitial
red blood cells, hypereosinophilic cytoplasm of necrotic myocardial fibers.
Examine the specimen. Draw and label completely.
myocardial fibers
interstitial red blood cells
.
Which of the following words/set of words is/are responsible for the development
of this lesion? Choose and put a check on your 4 best answers.
(
(
(
(
) Platelet dysfunction
) Vasospasm
) Thrombosis
) Embolism
( ) Vasculitis
( ) Atherosclerosis
( ) Thrombophilia
What is the difference between a STEMI and a NSTEMI?.
___________________________________________________________
___________________________________________________________
___________________________________________________________
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-4-
VALVULAR HEART DISEASE
Introduction:
The heart valves, lined by endothelial cells, work to keep blood flow
in the heart in one direction. The valves should be mobile, pliable and with
structural integrity. The aortic and pulmonic valve should open during
systole to allow blood to go to the aorta and systemic circulation and the
lungs for gas exchange, respectively. While the mitral and tricuspid valve
should close during systole to prevent backflow of blood to the left and
right atrium, respectively. The functional disturbances produced by
valvular disease are stenosis and insufficiency. Stenosis leads to failure of
a valve to open completely, thus impeding forward flow. Insufficiency or
regurgitation, on the other hand, is the failure of a valve to close
completely, thus allowing backward flow.
4. RHEUMATIC HEART DISEASE: p 557
4.1 Definition: RHD is the long-term result of active rheumatic carditis
presenting clinically as valvular heart disease
4.2 Etiology: Recurrent rheumatic fever caused by β-hemolytic
streptococcus. The antibodies and CD4+ T lymphocytes formed against
the M-protein of the bacteria cross-react with the self-antigens of the
heart.
4.3 History: A 20 year old female complained of chest pain accompanied
by joint pain, subcutaneous nodules and fever. Patient had a history of
recurrent pharyngitis since childhood. Pertinent P.E. showed grade III
pansytolic murmur best heard at the right parasternal border.
4.4 Examine the slide and gross specimen of RHD. Label completely the
following gross features: commissural fusion, verrucae, hypertrophic
papillary muscles, thickened and fused chordae tendinae, thickened and
retracted valvular leaflets, left ventricular hypertrophy.
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-5-
Draw and label completely.
GROSS:
commissural fusion
hypertrophic papillary muscles
thickened & fused chordae tendinae
left ventricular hypertrophy
MICROSCOPIC.
Cardiac muscles
Aschoff bodies
Anitschkow cells
Lymphoplasmacytic infiltrates
Which of the following words/set of words comprise the major criteria for
Rheumatic fever? Choose and put a check on the five (5) correct answers.
(
(
(
(
(
) elevated acute phase reactants
) migratory polyarthritis
) erythema marginatum
) fever
) tonsillitis
(
(
(
(
(
) pancarditis
) arthralgia
) subcutaneous nodules
) Syndenham chorea
) pharyngitis
Why is pharyngeal culture negative in patients with rheumatic fever? What
laboratory examination can be used for its diagnosis?
________________________________________________________________
________________________________________________________________
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-6-
5. SUBACUTE INFECTIVE ENDOCARDITIS (SBE): p 559
5.1 Definition and Etiology: One of the most serious of all infections is
characterized by colonization or invasion of heart valves, mural
endocardium, or other cardiovascular sites by a microbiologic agent,
leading to the formation of bulky, friable vegetations composed of
thrombotic debris and organisms often associated with destruction of the
underlying cardiac tissues. Infective endocarditis is classified into acute
and subacute forms. Acute endocarditis is characterized by destructive,
tumultuous infection, frequently of a previously normal heart valve by a
highly pathogenic organism, like S. aureus, leading to death within days to
weeks of more than 50% of patients despite antibiotics and surgery. SBE
is caused by low virulent organisms, like S. viridans, in a previously
abnormal heart especially on deformed valves, appear insidiously, pursue
a protracted course for weeks to months, and patients recover after
appropriate antibiotic treatment.
5.2 History: A 25 years old, known RHD patient was admitted because of
fever, easy fatigability, loss of weight, and flu-like symptoms. P.E.
revealed presence of changing murmur over the mitral area and petechial
and subungual hemorrhages.
Examine the slide. Draw and label completely.
Valvular cusp
Bacterial colonies
Dystrophic calcifications
Granulation tissue
Fibrosis
Match the type of endocarditis in column I with the cause in column II.
I
II
___1. Acute infectious endocarditis
B
A. Hypercoagulability
___2. Libman-Sack endocarditis
A
B. Staphylococcus aureus
___3. Nonbacterial thrombotic endcarditis D C. Streptococcus viridans
___4. Rheumatic heart disease
E
D. Systemic lupus erythematosus
___5. Subacute infectious endocarditis C
E.Post-streptococcal endocarditis
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-7-
CASE ANALYSIS:
A 67 y/o, male chronic hypertensive, diabetics, 40 pack year smoker
sought admission because of difficulty of breathing on exertion, grade III
pitting pedal edema and paroxysmal nocturnal dyspnea. Pertinent
Physical examination findings include: BP - 180/100 mm Hg; T - 37.3oC;
HR - 87/min; RR - 40/min. There is displacement of the PMI at the 6 th
ICSLAAL. Occasional crackles are heard over the lung bases. The liver is
palpable 3 fingers breadth below the RSCL.
What is the complete diagnosis of the case? What are your bases?
Diagnosis:________________________________________________________
Bases:___________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
What is paroxysmal nocturnal dyspnea? What causes it?
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
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-8-
II. DISEASES OF THE LUNGS
Slides:
# 46
# 100
# 101
# 48
DEMO
Atelectasis
Bronchopneumonia
Lobar pneumonia
Abscess, lungs
Bronchiectasis
Gross :
Bronchiectasis
Bronchogenic carcinoma
Introduction:
The cardinal function of the lung is to facilitate gas exchange between
blood and inspired air. The respiratory system arises as an outgrowth from the
ventral wall of the foregut. From the trachea, the left and right main stem bronchi
arise. The bronchi further divides into bronchioles leading to the terminal
bronchioles and the acinus. An acinus is made up of respiratory bronchiole,
alveolar ducts and alveolar sacs. Microscopically, the entire respiratory tree is
lined by pseudostratified columnar epithelium, except for the vocal cords which
are lined by squamous epithelium.
1. ATELECTASIS p 670
1.1 Definition: incomplete expansion (neonatal atelectasis) or collapsed of
a previously inflated lung leading to an “airless” parenchyma
Forms
A. Resorption atelectasis
Etiology
complete airway obstruction with
resorption of air in dependent areas
causing collapse and shift of
mediastinum towards atelectatic lung
B. Compression atelectasis
pleural cavity is partially or completely
filled with blood, air, fluid exudate or
tumor causing a shift of mediastinum
away from involved lung
C. Contraction atelectasis
local or generalized fibrotic changes in
the lung or pleura
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-9-
Examine the slide. Draw and label completely.
Collapsed, slit like alveoli
Congested blood vessels
Which of the following words/set of words cause/s resorption atelectasis?
Choose and put a check on the correct answers.
( ) fibrosis
( x) exudates within smaller bronchial
( ) pleural effusion
( x) excessive secretions
(x ) foreign body aspiration
( ) hemothorax
2. BRONCHIECTASIS p 683
2.1 Definition : disease characterized by irreversible dilatation of bronchi
and bronchioles caused by muscle and elastic tissue
destruction seen in chronic infections associated with
necrosis
2.2 Etiology : Congenital or hereditary conditions like primary ciliary
dyskinesia
Post infectious like necrotizing pneumonia
Bronchial obstruction as in the presence of foreign body
Other conditions : autoimmune diseases, posttransplantation
Idiopathic
2.3 Morphology :
Gross :
usually affects the lower lobes
Dilated airways, sometimes up to 4x the normal size and can
be followed almost to the pleural surfaces
Cut surface – transected dilated bronchi appear as cysts
filled with mucopurulent exudate
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Microscopic features : may vary with the activity and chronicity of the
disease
- Intense acute and chronic inflammatory exudation
within the walls of the bronchi and bronchioles
- Desquamation of the lining epithelium and
extensive areas of necrotizing ulceration
- Pseudostratification of the columnar cells or
squamous metaplasia of the remaining epithelium
- Areas of liquefaction necrosis (abscess) may be
present
- In chronic cases – fibrosis of the bronchial and
bronchiolar walls leading to partial or total lumen
occlusion.
Examine the slide. Draw and label completely.
Markedly dilated bronchus
Inflammatory cells
Desquamated lining epithelium
Fibrosis
Necrotic cartilage
Which of the following manifestations is/are seen in bronchiectasis? Choose and
put a check on the five (5) correct answers.
( x) dyspnea
( ) chest pain
(x ) hemoptysis
(x ) cyanosis
( ) wheezing
( ) nocturnal dyspnea
( x) foul smelling sputum
( x) orthopnea
( ) clubbing of fingers
(x ) severe, persistent cough
Which of the following complications is/are seen in bronchiectasis? Choose and
put a check on the three (3) correct answers.
( x) cor pulmonale
( ) pleural effusion
( ) malignancy
(x ) brain abscess
( x) amyloidosis
( ) arrhythmia
( ) sepsis
( ) pneumothorax
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-11-
PULMONARY INFECTIONS
Infection of the lung parenchyma of any cause is called pneumonia.
Pneumonia occurs whenever there is impairment of the local defense
mechanism of the lungs or in the presence of immunosuppression..
Two patterns of anatomic distribution in bacterial pneumonia :
a. Patchy consolidation characteristic of bronchopneumonia
b. Fibrinosuppurative consolidation of an entire lobe or a large portion of
a lobe is characteristic of lobar pneumonia
Common Etiologic agents :
Streptococcus pneumonia
Haemophilus influenza
Moraxella catarrhalis
Staphylococcus aureus
Klebsiella pneumonia
Pseudomonas aeruginosa
Legionella pneumophilia
3. BRONCHOPNEUMONIA pp 702 - 705
3.1 Microscopic features: suppurative inflammation predominantly
composed of neutrophils that fill up the bronchi, bronchioles, and adjacent
alveolar spaces
Examine the slide. Draw and label completely.
bronchus with exudate
lung parenchyma with neutrophils
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Which of the following feature/s are seen in bronchopneumonia? Choose and put
a check on the our (4) correct answers.
(
(
(
(
) patchy
) widened alveolar septae
) neutrophilic infiltrates
) lymphocytic infiltrates
4. LOBAR PNEUMONIA
(
(
(
(
) lobular
) fibrosis
) hyaline membrane
) catarrhal exudates
pp 702 - 705
4.1 Four stages of inflammatory response:
a. Congestion
Gross:
red, heavy, boggy
Microscopic: vascular engorgement, intra-alveolar fluid with
few neutrophils, numerous bacteria
b. Red Hepatization
Gross:
red, firm, airless with liver-like consistency
Microscopic: massive confluent exudation with neutrophils,
red cells and fibrin filling up the alveolar spaces
c. Gray hepatization
Gross:
gray brown, dry surface , liver-like consistency
Microscopic: progressive disintegration of red cells and
persistence of fibrinosuppurative exudates
d. Resolution
Microscopic: progressive dissolution of exudates within the
alveolar spaces granular semi fluid debris
ingested by macrophages
4.2 Examine the slide of lobar pneumonia. What is the stage of
inflammatory response? Label completely the following : neutrophilic infiltrates,
fibrin, congested blood vessel.
Examine the slide. Draw and label completely.
Fibrinosuppurative exudates filling up
the alveolar spaces
Congested blood vessels
Stage: ____________________
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-13-
Which of the following are complications of bacterial pneumonia? Choose and
put a check on the (3) correct answers.
( x) Abscess formation
( ) pneumothorax
( x) Bacteremic dissemination
( ) cor pulmonale
( x) Empyema
( ) diffuse alveolar damage
5. LUNG ABSCESS p 708
5.1 Definition: focal liquefaction necrosis within the lung, characterized by
dissolution of lung tissue and replacement by suppurative exudate
5.2 Etiologic agents: Streptococci sp., S. aureus, gram negative organisms
Associated factors in the pathogenesis :
a. Aspiration of infectious agent – most frequent cause
b. Complication of primary lung infection ( post pneumonic
abscess)
c. Septic emboli
d. Postobstructive pneumonia secondary to lung tumor
e. Penetrating lung injury
f. Direct spread of infection from adjacent organs
g. Hematogenous spread
5.3 Morphology:
Gross: single or multiple - varying in size from few mm to
large cavities of 5 to 6 cm
Microscopic: Cardinal histologic feature is suppurative
destruction of the lung parenchyma within the central area of
cavitation.
Examine the slide. Draw and label completely.
abscess
cellular debris and fibrin
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What are the manifestations of lung abscess? Choose and put a check on the
five (5) correct answers.
(x ) chest pain
( x) cough
( ) crackles
( ) cyanosis
( ) dyspnea
( x) fever
( x) foul-smelling sputum
( ) orthopnea
( x) weight loss
( ) wheezes
Case Analysis:
A 25 year old Mexican – African woman had multiple pigmented lesions
on the skin. CXR was done as part of routine testing and there is prominent
bilateral hilar lymphadenopathy. The patient is also complaining of blurring of
vision.
Laboratory studies reveal polyclonal hypergammaglobulinemia,
hypercalcemia and increased serum angiotensin – converting enzyme. What is
the most likely disease of the patient?
_____________________________________________________
What are the characteristic histologic findings associated with this disease if a
lung and skin biopsy will be performed?
_____________________________________________________
_____________________________________________________
TUMORS OF THE LUNG
Tumors in the lung are often malignant (90 – 95% are carcinomas). Histologic
variants of the majority of the lung tumors are as follows :
A.
B.
C.
D.
Gross :
Adenocarcinoma
Squamous cell carcinoma
Small cell carcinoma
Large cell carcinoma
arise most often in and about the hilus of the lung emerging from
the main stem bronchi (central location) or can also be
found on the periphery
fungating mass into the bronchial lumen causing obstruction
direct extension into the peribronchial tissue and lung parenchyma
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6. BRONCHOGENIC CARCINOMA (Adenocarcinoma) p 712
6.1 Micoscopic: pseudostratified columnar ciliated epithelium, malignant glands
and the normal alveoli.
Examine the specimen. Draw and label completely.
Bronchus
Malignant glands
Match the clinical feature with the pathologic basis of lung cancer:
I
II
___ 1. Cough
G
A. recurrent laryngeal nerve invasion
___ 2. diaphragm paralysis
D
B. pericardial involvement
___ 3. Hoarseness
A
C. chest wall invasion
___ 4. Horner syndrome
S
D. phrenic nerve invasion
___ 5.cardiac tamponade
B
E.sympathetic ganglia invasion
F. airway obstruction by tumor
G. involvement of central airways
Case Analysis :
A 67 year old female with significant smoking history presents with cough and
shortness of breath. CT scan shows a central mass near the right mainstem
bronchus. Based on the location of the mass, what are the histologic variants of
lung cancer that you will include as your differential diagnosis? Why?
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
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III. DISEASES OF THE GASTROINTESTINAL TRACT
Slides :
DEMO
# 43
# 113
# 141
# 94
# 225
Typhoid ileitis
Acute Appendicitis
Adenocarcinoma, stomach
Amoebic colitis
Adenocarcinoma, colon
Hemorrhoids, anus
Introduction:
The small and the large intestines are involved in many similar conditions,
etiologically and morphologically, and the only difference may lie in the clinical
features because of the difference in function performed by these segments of
the GIT and their anatomic characteristics.
1. TYPHOID ILEITIS p 789
1.1 Definition: also known as Typhoid fever or Enteric fever
Clinically presenting with loss of appetite, pain in the
abdomen, loose stools with blood, vomiting and nausea
followed by a short asymptomatic phase then bacteremia
with fever and flu-like symptoms
Etiology:
Salmonella typhi (endemic), Salmonella paratyphi (travelers)
Morphology:
Gross: ileum - plateau-like mucosal elevations which may reach
8.0 cm diameter
Microscopic: Enlargement and hyperplasia of Payer’s patches
Mucosal oval ulcers oriented along the axis of the
ileum
Neutrophils and mononuclears cells on the stroma
Examine the slide. Draw and label completely.
Denuded mucosa
Hyperplastic Peyer patch
Hypertrophic macrophages
Erythrophagocytosis
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4
-17-an6
7
2
9
What organ may be colonized by S. typhi and what significance are associated
with this colonization?
________________________________________________________________
________________________________________________________________
What extraintestinal complications are seen in typhoid fever? Choose and put a
check on the five (5) correct answers.
( ) endocarditis
( ) meningitis
( ) myocarditis
( ) myocardial infarction
( ) myositis
( ) encephalopathy
( ) arthritis
( ) seizures
2. ACUTE APPENDICITIS p 816
Definition:
Inflammation of the appendix associated with slow increase
in intraluminal pressure compromising venous drainage
Etiology:
Luminal obstruction by fecalith, gallstone, neoplasm or mass
of oxyuriasis vermicularis worms
Morphology:
Microscopic: HALLMARK is presence of neutrophils in the
muscularis propia
Mucosal neutrophils and focal superficial mucosal
ulceration
Early Acute Appendicitis: congestion of subserosal vessels with scattered
perivascular neutrophilic infiltrates within all layers of the wall.
Acute Suppurative Appendicitis - with areas of liquefaction necrosis
Acute Gangrenous Appendicitis - hemorrhagic ulceration and gangrenous
necrosis that extends into the serosa
Examine the slide. Draw and label completely.
Neutrophilic infiltrates in muscularis propia
Congested blood vessels
Luminal and serosal exudates
Interstitial edema
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Choose from among the words/group of words the complication/s of acute
appendicitis. Put a check on the correct answer/s.
( x ) perforation
( ) pneumonia
( ) carcinoma
(x ) liver abscess
( ) short bowel syndrome
( ) Reiter syndrome
(x ) pyelophlebitis
( x) portal venous thrombosis
( ) obstruction
( x ) bacteremia
Case Analysis:
A 58 year old male presents with vomiting of blood, black tarry stool,
stools positive for guaiac and signs of circulatory collapse. He has a 15 year
history of burning midepigastric abdominal pain and tenderness relieved by food
intake and NSAIDS. Esophagogastroduodenoscopy revealed a peptic ulcer in
the upper duodenum. What organism is associated with this disease?
__________________________________________________________
If a tissue biopsy will be obtained, what are the histologic findings / layers of
peptic ulcer lesion?
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
3. ADENOCARCINOMA, STOMACH p 771
Definition: Adenocarcinoma is regarded as the most common malignancy
of the stomach mostly involving the gastric antrum.
Morphology:
Gross: bulky tumors as polypoid , exophytic masses protruding
into the lumen or infiltrative growth pattern causing wall
thickening
Microscopic patterns:
1. Intestinal type: assuming a glandular configuration lined
by malignant columnar cells often with apical mucin
vacuoles or intraluminal mucin
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2. Diffuse type: discohesive malignant cells that do not form
glands but exhibit large mucin vacuole that expand the
cytoplasm and push the nuclei to the periphery creating a
“signet-ring” appearance. Mucin lakes may be present.
Examine the slide. Draw and label completely.
Malignant glands
Choose from among the following words/group of words the most important
prognostic indicators for gastric cancer. Put a check on the two (2) correct
answers.
( ) depth of invasion
( ) histologic type
( ) nodal metastasis
( ) histologic grade
CASE ANALYSIS :
A 64 year old Caucasian female with a 7 year old history of GERD presents with
heartburn and regurgitation of acidic nature. Esophagogastroduodenoscopy was
performed and the lesion seen is suggestive of Barrett esophagus.
Discuss how GERD can give rise to gastric adenocarcinoma.
________________________________________________________________
________________________________________________________________
________________________________________________________________
2
4. AMOEBIC COLITIS p 794
Definition: Amebiasis is a protozoan infection most frequently affecting
the cecum and ascending colon and presenting as dysentery.
Etiology: Entamoeba histolytica which attaches to intestinal crypts and
burrows creating a flask shaped ulcer.
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Morphology: flask shaped ulcer exhibits narrow neck and broad base with
neutrophils; organisms with ingested red blood cells
Examine the slide. Draw and label completely.
Mucosa
Necrosis
Trophozoites
Inflammatory cells
From among the list of words/group of words below, choose the segments of the
gastrointestinal tract which may be involved in amebiasis. Put a check on the five
(5) correct answers.
( ) appendix
( ) Ileum
( ) ascending colon
(x) rectum
( ) cecum
( ) transverse colon
( ) descending colon
( ) sigmoid colon
( ) duodenum
( ) stomach
5. ADENOCARCINOMA, COLON p 810
Definition: Gland forming tumor and regarded as the most common
malignancy of the GI tract
Morphology:
Gross:
polypoid , exophytic masses causing lumen obstruction
(right-sided) or annular lesions creating “napkin-ring”
constriction (left-sided colon carcinoma)
Microscopic:
Well / moderate / poorly differentiated malignant glandular
structures lined by columnar cells exhibiting nuclear atypia
invading the desmoplastic stroma and infiltrating the wall of
the intestine. Signet ring cells may be present.
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Examine the slide. Draw and label completely.
Regular appearing colonic glands
Malignant glands
Muscularis propia
What is the role of Aspirin and other NSAIDS in the pathogenesis of colon
cancer?
________________________________________________________________
________________________________________________________________
________________________________________________________________
Guide Questions: Tabulate the characteristic features of right-and left-sided colon
adenocarcinoma.
Features
Gross findings
Right-sided
Left-sided
Microscopic findings
Clinical manifestations
6. HEMORRHOIDS, ANUS p 815
Definition:
abnormally dilated hemorrhoidal plexus in the anal canal
presenting as intraluminal protrusion brought about by prolonged
increased pressure
Etiology: almost always related to constipation and venous stasis of
pregnancy and also portal hypertension in liver cirrhosis
Morphology : dilated, varying shapes and sizes, thin walled, endothelial
lined vascular channels; may exhibit thrombosis; inflammatory cells
scattered on the stroma
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External hemorrhoids – collateral vessels located within the
inferior hemorrhoidal plexus ; located below the anorectal
line ; histologically lined by squamous epithelium
Internal hemorrhoids
- dilatation of the superior
hemorrhoidal plexus within the distal rectum ; histologically
lined by mucin secreting glands
Mixed (internal and external) hemorrhoids : lined by
squamous and mucin secreting epithelium.
Examine the slide. Draw and label completely.
dilated blood vessels
hemorrhage
thrombus
Trace how the hemorrhoidal plexus of veins serve as a collateral circulation in
patients with cirrhosis. Number the vessels below to reflect this with cirrhosis as
first event and .return of blood to the right side of the heart as last event.
1. cirrhosis
internal pudendal vein
portal vein
common iliac vein
middle hemorrhoidal plexus
11. right side of the heart
inferior vena cava
inferior hemorrhoidal plexus
internal iliac vein
superior hemorrhoidal plexus
Inferior mesenteric veins
CASE ANALYSIS :
A 28 year old, female presents with weight loss, fatigue, low grade fever,
episodes of abdominal pain and diarrhea. Endoscopy showed thickening of the
terminal ileum with narrowed lumen and mucosa appears “cobblestone-like”.
What is your diagnosis?
________________________________________________________________
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IV. DISEASES OF THE LIVER AND THE BILIARY SYSTEM
Slides on:
# 111
# 159
# 174
# 212
# 107
# 151
CPC, liver
Post-necrotic cirrhosis ( plus gross )
Parasitic cirrhosis
Tuberculosis, liver
Cholangiocarcinoma
Chronic cholecystitis
Introduction:
The normal adult liver weighs 1,400 to 1,600 gm. It is supplied by the
portal vein (60 – 70%) and the hepatic artery (30 – 40%). The liver has been
divided into metabolic lobules (hexagonal) or acini. The acini are triangular areas
with apices at the terminal hepatic venules or central veins and bases at the
portal tracts. The acinus is further subdivided into zones 1, 2, and 3. Zone 3 is
located around the central vein whereas zone 1 is around the portal triad. Many
forms of hepatic injury exhibit a zonal distribution. Review the histology of the
liver. See the relative locations of the hepatocytes, sinusoids, bile canaliculi,
Kupffer cells, Ito cells, limiting plates, and portal triads.
1. CHRONIC PASSIVE CONGESTION, LIVER: p 864
Definition: Accumulation of blood in the vascular system due to obstruction
to flow.
Etiology: Acute and chronic passive congestion of the liver usually reflects
acute or slowly developing cardiac decompensation, most commonly
right – sided heart failure. But because there is an element of
preterminal circulatory failure in every death, congestive hepatic
changes are commonplace at autopsy.
History – A 76 year old male was admitted because of dyspnea,
wheezing and a a grade 3 pitting pedal edema. He is a 50-pack year
cigarette smoker, barrel-chested and breaths through pursed lips.
He died one month after admission because of right-sided heart
failure. An autopsy was done which showed a right ventricular
hypertrophy and hepatomegaly.
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Microscopic: dilated central vein, atrophic liver cords, dilated sinusoids
filled with red blood cells and centrilobular necrosis.
Dilated central vein
Atrophic hepatocytes
Dilated sinusoids
Centrilobular necrosis
1.4 Guide Questions:
1.4.1 Describe the liver grossly in CPC, liver.
___________________________________________________________
___________________________________________________________
1.4.2What are the manifestations of patients with impaired blood
inflow.to the liver?
___________________________________________________________
___________________________________________________________
2.POST-NECROTIC CIRRHOSIS:
22.1 Definition: Liver Is characterized by irregularly sized nodules
separated by variable but mostly broad scars.
2.2 Etiology: Commonly caused by viral hepatitis, autoimmune
hepatitis, hepatotoxins, pharmaceutical drugs, and even alcohol. In
about 20% of cases, the inciting cause of the cirrhosis cannot be
determined and labeled as “cryptogenic cirrhosis”.
2.3 History: A 65 years old female has been receiving blood
transfusion for several years now due to thalassemia. She developed
on and off jaundice for the last 15 years. She succumbed to sepsis and
an autopsy was done which showed a small coarsely nodular liver.
Examine the slide of post-necrotic cirrhosis and label the following:
portal triad, fibrosis, regenerating nodules (pseudolobules), and
mononuclear cells.
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Draw and label completely.
MICROSCOPIC:
:
Fibrosis
Regenerating nodules
Mononuclear cells
Portal triad
GROSS
Micronodules
Macronodules
2.4 From among the list of etiology of liver disease, choose the leading
causes of chronic liver failure. Put a check on the four (4) correct
answers.
( ) Hemochromatosis
( x ) Chronic HCV infection
( ) HAV Infection
( x ) Non-alcoholic fatty liver disease
( x ) Chronic HBV infection
( ) Hepatoma
( ) Biliary cirrhosis
( x ) Alcoholic liver disease
3. SCHISTOSOMIASIS, LIVER:
3.1 Definition and Etiology: Schistosomiasis is the most important
helminthic disease infecting 200 million and killing 250,000 annually.
Most of the mortality is due to hepatic granulomas and fibrosis, caused
by S. mansoni, S. japonicum, and S. mekongi depending upon the
geographic location. In the Philippines, S. japonicum is endemic in
certain areas particularly in the Bicol region.
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3.2 History – A 65 year diabetic from Sorsogon died from sepsis.
Incidental findings include presence of Schistosoma eggs in the liver
and the ovary.
3.3 Examine the slide of Schistosomiasis, liver. Draw and label
completely the Schistosoma eggs, surrounding granuloma, and areas
of fibrosis.
________________________
________________________
________________________
3.4 Guide Questions:
3.4.1 What is “pipe – stem” fibrosis?
________________________________________________
________________________________________________
________________________________________________
4.TUBERCULOSIS, LIVER:
4.1 Definition and Etiology: Tuberculosis is caused by mycobacterium
tuberculosis. Most infections are acquired by person to person
transmission of airborne organisms from an active case to a susceptible
host. The liver is involved in systemic miliary tuberculosis. It occurs when
spread of bacteria disseminate through the systemic arterial system.
Other areas may be involved to include bone marrow, spleen, adrenals,
meninges, kidneys, fallopian tubes, and epididymis.
4.2 History – A 47 y/o, male underwent an exploratory laparotomy due to a
mass in the liver.
4.3 Draw and label the components of granuloma in the liver: epithelioid
cells, lymphocytes, foreign body giant cells, Langhan giant cells, fibrosis
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Draw and label completely
MICROSCOPIC:
granuloma
epithelioid cells
lymphocytes
fibrosis
multinucleated giant cells
From among the list of organs below, choose the ones that are usually resistant
to tuberculosis. Put a check on the four (4) correct answers.
(x ) cervical lymph nodes
( ) thyroid
( x ) testes
( x ) ovary
( x ) adrenal
( x ) meninges
( ) myocardium
( ) skeletal muscle
( ) pancreas
( x ) colon
5. CHOLANGIOCARCINOMA:
5.1 Definition and Etiology: Cholangiocarcinoma is second most common
hepatic malignant tumor after hepatoma. It arises from the biliary tree,
the bile ducts within and outside of the liver. The risk factors are
associated with chronic inflammation which causes mutations or
epigenetic alterations in ductal epithelium.
5.2 History – A 48 year old female sought admission because of severe
jaundice of one week duration associated with loss of weight, 30%,
anorexia, and flatulence. An ultrasound of the hepatobiliary tree and
abdomen disclosed the presence of a mass in the perihilar area. Patient
refused surgical intervention. She was discharged and readmitted after 4
months because of difficulty of breathing. She died 3 days later.
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Examine the slide. Draw and label completely.
MICROSCOPIC:
Hepatocytes
Malignant glands
From among the list of predisposing factors, choose the ones that predispose to
the development of cholangiocarcinoma. Put a check on the five (5) correct
answer/s.
(x
(x
(
(x
(
) infestation by liver flukes
) primary sclerosing cholangitis
) Alcoholic liver cirrhosis
) HBC infection
) cigarette smoking
( ) activation of WNT signalling
( ) aflatoxins
( x ) HBV infection
( ) α-1-antitrypsin deficiency
(x ) Hepatolithiasis
6. CHRONIC CHOLECYSTITIS
6.1 Definition and Etiology: Chronic cholecystitis may be a sequel to
repeated bouts of mild-to- severe acute cholecystitis although in many
instances it arises without apparent antecedent acute attacks. In more
than 90% of the cases, it is associated with cholelithiasis.
6.2 History – A 40 year old female, obese patient was admitted because of
recurrent, colicky, right hypochondriac pain of 2 weeks duration .
Pertinent P.E. findings disclosed tenderness over the right
hypochondriac area. An ultrasound of the hepatobiliary tree disclosed
the presence of stone in the common bile duct with consequent
dilatation of the more proximal segments. A laparoscopic
cholecystectomy was done and the gall bladder submitted for
histopathologic examination.
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Examine the slide. Draw and label completely.
Tall columnar epithelium
Fibrosis
Lymphocytic infiltrates
Rokitansky-Aschoff sinuses
The following are risk factors for gallstone formation. Put a check for four (4) risk
factors of pigment stone.
( ) advancing age
( x ) Asians
( ) Europeans
( x ) Chronic hemolytic syndromes
( ) gallbladder stasis
( x ) biliary infection
( x ) ileal disease
( ) obesity
CASE ANALYSIS:
A 25-year-old, female hemophiliac developed jaundice of one week duration. She
has been receiving blood transfusion for the last 10 years. Pertinent physical
examination include: T - 37.8oC; BP- 130/80 mm Hg; HR - 78/min; RR - 26/min;
yellowish sclerae; liver - palpable 2 fb beneath the RSCAMCL, tender. Liver
profile showed: HBsAg, HBV-DNA , HBeAg, and IgM-anti-HBc - reactive; anti HBs and anti-HBe - non-reactive; ALT - 1500 units; ALP - 200 units.
Guide questions:
1 What is your complete diagnosis?
________________________________________________________
2 What is this patient chance of developing hepatocellular carcinoma?
__________________________________________________________
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V. DISEASES OF THE KIDNEY
Slides :
DEMO
Acute proliferative glomerulonephritis
# 68
Tuberculosis, kidney
# 223
Chronic pyelonephritis
# 222
Renal cell carcinoma
# 213
Acute tubular necrosis
Gross:
Polycystic kidney disease
Introduction:
The kidneys are paired retroperitoneal organs that converts approximately 1700
liters of blood per day into urine. It is involved in the elimination of waste products
of metabolism (like BUN and Creatinine), regulation of water and salts, acid-base
balance, and hormone secretion (Ex: prostaglandin, renin and erythropoietin).
1. ACUTE PROLIFERATIVE GLOMERULONEPHRITIS
Definition: also called as Poststreptococcal or Postinfectious is
characterized by diffuse proliferation of granular cells accompanied by
inflammatory infiltrates
Etiology: immune complexes deposition – incited by an exogenous (poststreptococcal infection of the pharynx or skin) or endogenous antigen
(nephritis in SLE)
Morphology: Microscopic features:
CLASSIC diagnostic feature : enlarged hypercellular glomeruli due to
infiltration by leukocytes both neutrophils and monocytes
proliferation of mesangial and endothelial cells (crescents
may be formed)
Diffuse proliferation and leucocyte infiltration involving all
lobules
Interstitial edema and inflammation
Tubules may contain red blood cell casts
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Examine the slide. Draw and label completely.
hypercellular glomeruli
red blood cell casts
inflammatory cells
Describe the immunofluorescence and electron microscopic findings
EM : _____________________________________________
IF : _____________________________________________
CASE ANALYSIS:
A 7 year old girl was diagnosed to have pharyngitis. After two weeks, she
presented with tea colored urine, periorbital swelling, body malaise, nausea and
headache
1. What laboratory examinations can be done?
_________________________________________________________
2. Enumerate the streptococcal antigenic components responsible for the
immune reaction.
_________________________________________________________
****************
2. TUBERCULOSIS, KIDNEY
Definition: A disease which occurs when the bacilli disseminate through
the systemic arterial system in case of systemic military tuberculosis. It
may also be an isolated organ involvement of the kidney after
hematogenous dissemination.
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Morphology:
Chronic caseating granulomatous inflammation
Tubercles often exhibit central area of caseation
Granulomatous / fibrocollagenous wall with scattered
mononuclear inflammatory cells, epithelioid cells and giant
cells (foreign body or langhans giant cells)
Draw and Label completely.
caseation necrosis
epithelioid cells
lymphocytes
fibrosis
multinucleated giant cells
Enumerate other diseases that may manifest with granulomatous type of
inflammation
________________________________________________________________
________________________________________________________________
3. CHRONIC PYELONEPHRITIS
Definition: The disease is characterized by chronic tubulointerstitial
inflammation and renal scarring leading to damage of the pelvocalyceal
system. There are two forms of the disease:
a. reflux nephropathy – vesicoureteral reflux
b. chronic obstructive pyelonephritis
Morphology :
Microscopic features :
Tubular atrophy or hypertrophy and dilation in some areas
Tubules may dilate with flattened epithelium containing colloid casts
Chronic interstitial inflammation and fibrosis which may be
interspersed by neutrophils
Obliterative intimal sclerosis of blood vessels
Glomeruli may appear normal or exhibit fibrosis
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Examine the slide. Draw and label completely.
Fibrosis
Lymphocytic infiltrates
Glomerulus
Thyroidization
What are the routes by which the bacteria reach the kidney?
________________________________________________________________
________________________________________________________________
CASE ANALYSIS:
A 56 year old man with prostatic nodular hyperplasia was found to have chronic
pyelonephritis. What are characteristic gross findings of the kidney.
________________________________________________________________
________________________________________________________________
4. RENAL CELL CARCINOMA
Definition: Malignant tumor of the kidney with smoking as the most
significant risk factor. The most common type is the Clear Cell variant
accounting to 70-80% of cases.
Morphology:
Microscopic features:
malignant tumor cells are arrange from solid to trabecular or tubular
individual tumor cells have rounded, polygonal shape and
abundant, clear or granular cytoplasm, delicate branching
vasculature, may exhibit cystic, as well as, solid areas
some tumor cells may show marked nuclear atypia
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Examine the slide. Draw and label completely.
Malignant cells with clear cytoplasm
Tubules
Enumerate the major types of renal cell carcinoma
________________________________________________________________
________________________________________________________________
5. GROSS : POLYCYSTIC KIDNEY DISEASE
Definition: A disorder in which multiple cystic structures are seen
embedded on the renal parenchyma. There are many types of cystic
lesions of the kidney. It may be a single cyst or multiloculated.
Morphology: usually bilaterally enlarged and heavy (may reach up to 4kg
each kidney); External surface exhibits multiple cysts, usually 3 to 4cm in
diameter
Draw and Label completely.
multiple cysts
Describe the difference between autosomal dominant and autosomal recessive
polycystic kidney disease
______________________________________________________________
______________________________________________________________
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CONCEPT MAP: Using the phrases below, make a concept map on the
pathogenesis of acute proliferative glomerulonephritis in a 3 y/o male patient
nephrotoxigenic Streptococcus
pharyngitis
immune complex deposition
proliferation of endothelial cells
proliferation of mesangial cells
hematuria1
hypertension
tea-colored urine
influx of leucocytes
increase BUN / Creatinine
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VI. DISEASES OF MALE GENITALIA AND LOWER URINARY TRACT
Slides:
# 217
# 66
# 221
# 200
# 201
# 216
Atrophy, testis
Seminoma, testis
Chronic prostatitis
Benign prostatic hyperplasia or Nodular hyperplasia
Adenocarcinoma, prostate gland
Transitional cell carcinoma, urinary bladder
INTRODUCTION:
The diseases of the male genital tract includes the penis, testis,
epididymis and the prostate. The components of the lower urinary tract shares
morphologic similarities. The seminal vesicles and prostate lie close to each
other. The enlargement of the prostate leads to urinary tract obstruction.
1. ATROPHY, TESTIS
Definition : Decrease in size resulting from regressive changes
Causes :
atherosclerotic narrowing of blood supply, inflammation –
orchitis, cryptorchidism, hypopituitarism, malnutrition –
cachexia, irradiation, treatment regimen – anti androgen
medications, exhaustion atrophy – high levels of circulating
FSH
Morphology : tubules are small
absence or decreased spermatogenesis
thickened basement membrane
interstitial tissue shows varying degrees of fibrosis
increased number of interstitial cells of Leydig
Examine the slide. Draw and label completely.
Absence of mature sperm cells
Sertoli cells
Thickened basement membrane
Increased Leydig cells
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What are the parameters that needs to be requested in the evaluation of
infertile male ?
___________________________________________________________
___________________________________________________________
Enumerate possible causes of male infertility. Give examples of pretesticular, testicular and post-testicular causes
___________________________________________________________
___________________________________________________________
___________________________________________________________
___________________________________________________________
2. SEMINOMA, TESTIS
Definition:
two
It is the most common type of germ cell tumor, divided into
major categories : classic and spermatocytic
Morphology: “classical” or “typical” seminomas
Gross: homogenous, gray white lobulated cut surface usually with
no areas of hemorrhage or necrosis.
Microscopic :
sheets of seminoma cells composed of uniform cells
divided into delicate lobules by fibrous septa
individual cells is large and round to polyhedral with
distinct cell membrane, clear or watery appearing
cytoplasm, large central nuclei with one or two prominent
nucleoli
moderate amount of lymphocytes on the stroma
syncitiotrophoblasts may be present
Examine the slide. Draw and label completely.
Seminoma cells
Thin fibrous septae
Lymphocytes
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-38-
Enumerate and describe briefly the other types of germ cell tumors
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
3. CHRONIC PROSTATITIS
Definition : Prostatitis are of several types, namely: acute and chronic
bacterial prostatitis, chronic abacterial prostatitis, and granulomatous
prostatitis.
Chronic prostatitis is inflammation of the prostate gland often
presenting with history of low back pain, dysuria, perineal and
suprapubic discomfort.
Chronic bacterial prostatitis : history of recurrent UTI
with positive bacterial cultures and demonstration of
leucocytosis on expressed prostatic secretions.
Chronic abacterial prostatitis : most common form of
prostatitis with no history of recurrent urinary tract
infection, the secretions of the prostate often contains 10
leucocytes per HPF, and, bacterial culture are uniformly
negative
Morphology : Prostatic glands are scattered lined by a basal layer of low
cuboidal epithelium and covered by a layer of columnar
secretory cells.
Fibromuscular stroma with scattered mononuclear
inflammatory infiltrates composed of admixture of
lymphocytes & macrophages
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-39- permission. All rights reserved.
For personal use only. No other uses without
Examine the slide. Draw and label completely.
fibrosis
lymphocytes
prostatic glands
What is / are the laboratory examination/s and expected results that can be
done among patients with prostatitis?
________________________________________________________________
________________________________________________________________
________________________________________________________________
4. BENIGN PROSTATIC HYPERPLASIA OR NODULAR HYPERPLASIA
Definition: This is a benign disease causing urinary obstruction,
sometimes requiring surgical intervention. It involves hyperplasia of glandular
and / or stromal components.
Morphology: Hallmark is nodular appearance – the composition of the
nodules ranges from purely stromal fibromuscular nodules or
fibroepithelial nodules with predominance of glandular
component; small clusters of lymphocytes in the interstititium
and around the ducts; Glandular proliferation is characterized by
aggregations of small to large to cystically dilated glands lined
outer cuboidal flattened epithelium and inner columnar cells
Draw and Label completely.
cystically dilated glands
corpora amylacea
hyperplastic columnar cells
fibromuscular stroma
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-40-
Describe briefly the pathogenesis of benign prostatic hyperplasia
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
Enumerate the clinical manifestations
________________________________________________________________
________________________________________________________________
________________________________________________________________
5. ADENOCARCINOMA, PROSTATE
Definition: A malignant tumor usually seen among men 65 or older. It is
known to
be associated to hormonal factors. Genetics linkage was also seen
in few cases.
High grade prostatic intraepithelial neoplasia (PIN) is
considered as a precursor lesion of prostatic adenocarcinoma.
Morphology: Most of the lesions are composed of well defined, glandular
patterns that appear crowded, lack the outer basal layer and the
cytoplasm ranges from pale-clear to amphophilic cytoplasm. The
nuclei is enlarged with one or more prominent nucleoli.
Gleason grading system is based on the glandular architecture and
the nuclear atypia is not evaluated. It defines five histologic patterns or
grades with decreasing differentiation.
Grade 1:
Grade 2:
Grade 3:
Grade 4:
Grade 5:
well differentiated tumors with neoplastic glands that are
uniform and round in appearance packed into well
circumscribed nodules ; back-to-back uniform–sized
malignant glands.
majority of the glands are of the uniform in size
and exhibit crowding with focal areas wherein the glands are
of variable size and slightly dispersed.
variably sized, more widely dispersed moderately
differentiated glands
partial loss of polarity of the glands with few luminal
differentiation
no glandular differentiation and the tumor cells infiltrate
the stroma in he form of cords, sheets and nests ; almost
total loss of the polarity of the glands
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The primary and secondary pattern are added to obtain the Gleason
score or sum. The most well differentiated tumors have a Gleason score of 2 (1 +
1) and the least differentiated have a score of 10 (5 + 5).
Examine the slide. Draw and completely label.
malignant glands
Gleason’s score: __________
What are the parameters that needs to be assessed in the staging of prostatic
adenocarcinoma
_____________________________________________________________
_____________________________________________________________
Enumerate the laboratory examinations that are often part of the diagnostic workup among patients with prostatic adenocarcinoma
____________________________________________________________
____________________________________________________________
6. TRANSITIONAL ( UROTHELIAL) CARCINOMA, URINARY BLADDER
Definition : A malignant tumor that classically presents with painless
hematuria.
Morphology:
Papillary urothelial neoplasms of low malignant potential (PUNLMPs)
Papillae projects from a fibrovascular stalk covered by thicker
layer of urothelium or exhibits diffuse nuclear enlargement
Mitotic figures are rare
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Examine the slide. Label the malignant cells.. Determine the type of urothelial
carcinoma.
malignant cells
WHO grade : __________________
Describe briefly the following :
(a) Papillomas
_____________________________________________________________
_____________________________________________________________
(b) PUNLMPs
_______________ _____________________________________________
_____________________________________________________________
(c) Low Grade Papillary Urothelial Carcinoma
_____________________________________________________________
_____________________________________________________________
(d) High Grade Papillary Urothelial Carcinoma
____________________________________________________________
____________________________________________________________
-43-
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VII. DISEASES OF THE FEMALE GENITAL TRACT
Slides:
# 24
# 120
# 144
# 226
Chronic cervicitis with squamous metaplasia and nabothian cyst
Simple hyperplasia without atypia, endometrium
Ectopic pregnancy, fallopian tube
Mucinous cystadenoma, ovary
Gross:
Hydatidiform mole, uterus
Dermoid cyst, ovary
Introduction:
Diseases of the female genital tract are common in clinical practice. It
also includes complications of pregnancy, inflammations, tumors and hormonally
induced effects.
1. CHRONIC CERVICITIS WITH SQUAMOUS METAPLASIA & NABOTHIAN
CYST
Definition:
Marked inflammation produces reparative / reactive changes
of the epithelium which can lead to shedding of atypical
squamous
cells. Squamous metaplasia refers to focal or
extensive
replacement of the mucin-secreting
glandular epithelium by
stratified
squamous
epithelial cells. Chronic cervicitis preferentially
affects the squamocolumnar junction and endocervix. It
usually
presents as edema, hyperemia, fibrosis and
metaplastic changes.
The etiology is variable.
Morphology:
Landmarks are as follows:
Ectocervix – lined by squamous epithelium exhibiting maturation
Squamocolumnar junction – transition of squamous to columnar
epithelium (squamo-columnar junction)
Endocervix – lined by columnar epithelium with glands lined by
single layer of mucin secreting epithelium with basally oriented
nuclei
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Histomorphologic features to look for are as follows:
Areas of METAPLASIA: endocervical glands or endocervical
epithelium wherein there is a change
from columnar to squamous epithelium
Mononuclear inflammatory cells on the stroma
Dilated endocervical glands – lining epithelium may range from
columnar to low cuboidal to flattened,
sometimes with intraluminal eosinophilic
material – Nabothian cyst/s
Examine the slide. Draw and Label completely.
endocervical glands
inflammatory infiltrates
squamous metaplasia
nabothian cyst
Differentiate LSIL from HSIL
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
Enumerate and describe briefly the different types of cervical intraepithelial
neoplasia
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
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-45-
2. SIMPLE HYPERPLASIA, ENDOMETRIUM
Definition:
Prolonged unremitting estrogen stimulation leads to
endometrial hyperplasia. WHO classification takes into account both the
architectural and cytologic features, dividing it into categories as simple
and complex (on the basis of architecture), and subdividing each into
typical and atypical (on the basis of cytology).
Morphology of Simple hyperplasia:
increased number of glands of varying shapes and sizes with
cystic dilatation
areas of glandular crowding with little intervening stroma
lining epithelium of the glands may be columnar with no atypia
(without atypia) or exhibits nuclear atypia (with atypia)
Examine the slide. Draw and Label completely.
Cystically dilated endometrial glands
dense stroma
columnar epithelium w/o atypia
What are the microscopic features favoring carcinoma over hyperplasia
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
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-46-
3. MUCINOUS CYSTADENOMA, OVARY
Definition:
Ovarian mucinous tumors have been categorized as benign
(mucinous cystadenoma0, borderline, and malignant (mucinous
adenocarcinoma and cystadenocarcinoma).
Morphology: Gross: unilocular or multiloculated cystic mass containing
sticky gelatinous fluid; smooth inner lining of the cavity wall;
usually no solid areas protruding into the cavity lumen.
Microscopic: tumor lined by tall columnar epithelial cells with
apical mucin and basal nuclei; no nuclear atypia or
stratification.
Examine the slide. Draw and Label completely.
single layer of columnar epithelium
apical mucin
basally oriented nuclei
Describe morphologically the different benign surface epithelial tumors (serous,
mucinous, endometrioid, transitional).
Gross
Microscopic
Serous
Mucinous
Endometrioid
Transitional
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-47For personal use only. No other uses
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3.2. Enumerate and describe briefly the Germ Cell tumors
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
4. DERMOID CYST, OVARY
Definition:
Dermoid cysts are mostly benign teratomas that appear
cystic. It is usually seen in the young during active reproductive years.
Morphology: usually unilateral, sometimes bilateral (10-15% of cases)
characteristically unilocular cyst filled with hair and yellow
sebaceous material
may have a small solid foci called dermal protuberance
tooth / teeth may be present
Examine the specimen. Draw and Label completely.
strands of hair
tooth
cyst wall
Enumerate and differentiate the types of teratoma:
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
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-48-
5. GROSS: HYDATIDIFORM MOLE, UTERUS
Definition: Included in the category of gestational trophoblastic diseases
characterized by proliferation of placental tissue, either villous or
trophoblastic. H-mole is associated with invasive mole or choriocarcinoma.
The risk of development is higher at the far ends of reproductive life: teens
and between 40 – 50 y/o.
Morphology: delicate, friable, cystic structures with thin translucent walls
often fluid filled (assuming “grape-like” structures)
Examine the specimen. Draw and Label completely.
uterine wall
cluster of cystic structures
Differentiate complete versus partial mole.
Feature
Karyotype
Complete Mole
Partial Mole
Villous edema
Trophoblast proliferation
Atypia
Serum hCG
What is choriocarcinoma? What conditions precedes its development (state the
chances)?
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
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-49-
6. ECTOPIC PREGNANCY, FALLOPIAN TUBE, p. 1036
Definition: Implantation of the fetus to the fallopian tube instead of
intrauterine location.
The fallopian tube is the most common site of ectopic pregnancy leading
to hematosalpinx. Dilatation of the tube can eventually lead to rupture and
pelvic hemorrhage.
Morphology: Dilated lumen of the fallopian tube containing placental
tissues composed of immature chorionic villi and trophoblasts on a
background of hemorrhage, fibrin and inflammatory cells.
Examine the slide. Draw and Label completely.
wall of fallopian tube
chorionic villi
hemorrhage
Activity:
Fill the spaces in the puzzle (next page).
1. predisposing condition leading to tubal pregnancy
2. manifestation of ectopic pregnancy
3. complication of tubal pregnancy
4. implantation of placenta in the lower uterine segment
5. characterized by hypertension, proteinuria and edema
6. inflammation of the umbilical cord
7. endometrial glands and stroma in the myometrium
8. distinct cytologic change in the mature cells seen in condyloma acuminatum
9. uncommon vaginal tumor frequently seen in infants and children <5 years old
10. most common benign tumor
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-50- Medical Foundation.
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6
9
3
2
8
1
5
10
4
7
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-51-
DISEASES OF THE BREAST AND SKIN
Slides:
# 205
# 122
# 202
# 025
# 062
# 069
Fibrocystic disease
Invasive Ductal Carcinoma
Phyllodes Tumor
Molluscum contagiosum
Verruca vulgaris
Basal cell carcinoma
Introduction:
Breast lesions are more common in females than in males. The most
common breast lesion is fibrocystic change and fibroadenoma is the most
common breast tumor.
1. FIBROCYSTIC CHANGE
Definition: Fibrocystic change is a benign cystic lesion of the breast and is the
most common cause of palpable breast mass. There are 3 patterns of
morphologic changes which are cyst formation, fibrosis, and adenosis.
Morphology: Cystic lesion lined by atrophic cells in a background of
fibrocollagenous stroma. Areas exhibiting proliferation of acini are noted.
Apocrine metaplasia and calcifications may also be seen.
Examine the slide. Draw and Label completely.
cysts
adenosis
fibrosis
Enumerate the common clinical symptoms of breast diseases
________________________________________________________________
________________________________________________________________
________________________________________________________________
Differentiate atypical ductal hyperplasia from atypical lobular hyperplasia
________________________________________________________________________
________________________________________________________________________
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-52-
2. INVASIVE DUCTAL CARCINOMA
Invasive ductal carcinomas of the breast are further classified into several
types. Invasive ductal carcinoma, no specific type (NST) is the most
common and accounts for 2/3 of all invasive ductal carcinomas. Other
types are medullary carcinoma, mucinous carcinoma, tubular carcinoma,
and invasive papillary carcinoma.
Morphology: Malignant ductal cells disposed in clusters, cords and in
sheets with intervening scanty stroma some exhibiting desmoplasia.
Examine the slide. Draw and Label completely.
malignant cells
benign ducts/lobules
fibrosis
Activity:
2.1 Create a concept map using the following key words.
1. mutation in BRCA2
5. ductal carcinoma in situ
2. 16q loss
6. PIK3CA mutations
3. invasive ductal carcinoma
7. atypical ductal hyperplasia
4. lung metastases
8. ER-positive tumor cells
2.2 What are the components of Scarf Bloom Richardson in tumor grading and
how is it scored?
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
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________________________________________________________________
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________________________________________________________________
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-53-
3. PHYLLODES TUMOR
Phyllodes tumors are stromal tumor arising from intralobular stroma. Can
occur at any age but mostly present in the sixth decade. These should be
excised with wide margins to avoid recurrences.
Morphology: The tumors vary in size, larger lesions have “leaf like” pattern
owing to bulbous protrusions of the proliferating stroma into the lumen.
These tumors compared to fibroadenoma have increased stromal
cellularity, cytologic atypia, and stromal overgrowth.
Examine the slide. Draw and Label completely.
bulbous protrusion of stroma
cellular stroma
compressed lumen
Describe other benign stromal lesions
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
Give examples of malignant stromal tumors
________________________________________________________________
________________________________________________________________
________________________________________________________________
SKIN
Introduction: Diseases of the skin and diseases manifesting as a skin lesion may
have similar appearances. It is important to be able to describe morphologically
(Gross and Microscopic) the different skin lesion.
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-54-
Macroscopic (Gross) appearance:
Excoriation: Traumatic lesion breaking the epidermis and causing a raw
linear area
Lichenification: Thickened, rough skin; usually the result of repeated
rubbing
Macule, Patch: Circumscribed, flat lesion distinguished from surrounding
skin by color. Macules are < 5mm, patches are > 5mm
Onycholysis: Separation of nail plate from nail bed
Papule, Nodule: Elevated dome-shaped or flat-topped lesion. Papules are
< 5mm, nodules are > 5mm
Plaque: Elevated flat-topped lesion, usually >5mm across
Pustule: Discrete, pus filled, raised lesion
Scale: Dry, horny, plate-like excrescence; usually the result of imperfect
conification
Vesicle, Bulla, Blister: Fluid filled raised lesion <5mm across (vesicle) or >5mm
across (bulla). Blister is the most common term for either.
Wheal: Itchy, transient, elevated lesion with variable blanching and erythema
formed as the result of dermal edema
Microscopic Lesions
Acanthosis
Dyskeratosis
Erosion
Exocytosis
Hydropic swelling
Hypergranulosis
Hyperkeratosis
Lentiginous
Papillomatosis
Parakeratosis
Spongiosis
Ulceration
Vacuolization
Definition
Activity: Complete the Microscopic definitions.
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-55-
4. MOLLUSCUM CONTAGIOSUM
Molluscum contagiosum is a common, self-limited viral disease of the skin
caused by a poxvirus. Infection is usually spread by direct contact,
particularly among children and young adults.
Morphology: firm, pruritic, pink nodule with central umbilication
cup-like lesion filled with verrucous epithelial hyperplasia
with molluscum bodies.
Examine the slide. Draw and Label completely.
skin
cup-like lesion
molluscum bodies
Activity:
4.1 In which layers of the skin do you look for the molluscum bodies?
________________________________________________________________
________________________________________________________________
4.2 Describe the poxvirus causing molluscum contagiosum.
________________________________________________________________
________________________________________________________________
5. VERRUCA VULGARIS
Verruca vulgaris is the most common type of wart. These lesions are
found most commonly on the hands appearing gray white to tan, flat to
convex lesions with rough surface. Human papilloma virus causes this
type of lesion.
Case: History: A 25 year old male has multiple rough papule submitted for
histopath excised the dorsal aspect of his right hand.
Morphology: Skin lesion exhibiting papillomatosis, hyperkeratosis,
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is downloaded
Timothy Sam M.granules.
Valdez (20190107101)
acanthosis,
koilocytosis,
andforkeratohyaline
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-56-
Examine the slide. Draw and Label completely.
hyperkeratosis
papillomatosis
acanthosis
koilocytosis
Activity:
5.1 What are the HPV subtypes associated with this lesion? How is it
transmitted?
________________________________________________________________
________________________________________________________________
5.2 What other terminologies are used for verruca in the following areas?
Dorsal surface of the hand
Sole
Palm
Genital area
6. BASAL CELL CARCINOMA
Basal cell carcinoma is the most common invasive cancer in humans.
These are slow growing tumors that rarely metastasize, may present as
Nevoid basal cell carcinoma syndrome (Gorlin syndrome or basal cell
nevus) which is an autosomal dominant disorder characterized by multiple
basal cell carcinoma.
History: A 60 year old, mestizo sought consult because of a pearly,
telangiectatic nodule in the right cheek. A wide excision biopsy was done
and submitted for histopathologic examination.
Morphology: Nests of atypical basaloid cells in the dermis, with peripheral
palisading of malignant cells, and surrounded by clefts.
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Examine the slide. Draw and Label completely.
nests of basaloid cells
peripheral palisading
clefts
Activity:
6.1 Discuss the role of PTCH gene in the pathogenesis of basal cell carcinoma.
________________________________________________________________
________________________________________________________________
________________________________________________________________
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IX. DISEASES OF THE ENDOCRINE SYSTEM AND EXOCRINE
PANCREAS
Slides:
# 054
# 056
# 130
# 146
# 125
# 175
# 40
Hurthle cell adenoma
Follicular adenoma
Hashimoto’s thyroiditis
Papillary carcinoma, thyroid
Parathyroid adenoma
Adrenal hemorrhage
Acute hemorrhagic pancreatitis
DISEASES OF THE THYROID GLAND
Introduction:
The thyroid gland is one of the most responsive organs in the body. Free
T3 and T4 act through specific nuclear receptors to modulate cell growth and
functional activity of all kinds. The gland responds to many stimuli and is in
constant state of adaptation.
Diseases of the thyroid are of great importance because most are
amenable to medical or surgical management. They present principally as
thyrotoxicosis (hyperthyroidism), hypothyroidism, and as a focal or diffuse
enlargement of the gland (goiter).
1. HURTHLE CELL ADENOMA: pp. 1093-1094
Adenomas of the thyroid are typically discrete, solitary masses derived
from follicular epithelium, and hence are also known as follicular
adenomas. In general, follicular adenomas are not forerunner to
carcinomas but share genetic alterations. Hurthle cell adenomas are
composed of follicular cells with abundant granular, eosinophilic
cytoplasm, are well-encapsulated, and have a distinct growth pattern from
the adjacent non-neoplastic thyroid tissues.
History – A 36 year old female from was admitted because of an rightsided anterior neck mass of 1 year duration. On radionuclide scanning, the
mass took up less radioactive iodine than the normal thyroid parenchyma
(cold nodules). A subtotal thyroidectomy was performed and specimen
submitted for histopathologic examination.
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-59-
Examine the slide. Draw and Label completely.
thyroid follicles
fibrous capsule
hurtle cell change
Activity:
1.1 Differentiate a Hurthle cell adenoma from a Hurthle cell carcinoma.
________________________________________________________________
________________________________________________________________
1.2 Describe Hurtle cell change.
________________________________________________________________
________________ ________________________________________________
2. FOLLICULAR ADENOMA: pp. 1093-1094
Adenomas of the thyroid are typically discrete, solitary masses derived
from follicular epithelium, and hence are also known as follicular
adenomas. The vast majority of adenomas are nonfunctional although a
small proportion produces thyroid hormones which is independent of TSH
stimulation (thyroid autonomy) and causes clinically apparent
thyrotoxicosis.
.
History: A 32 year old female was admitted because of a right-sided
anterior neck. A partial right thyroidectomy was performed specimen
submitted for histopathological examination.
Examine the slide. Draw and Label completely.
neoplastic cells
fibrous capsule
surrounding regular thyroid follicles
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-60-
Activity:
2.1 Why is a definitive diagnosis of follicular adenoma made only after careful
histologic examination of resected specimen?
________________________________________________________________
________________________________________________________________
________________________________________________________________
2.2 How is an adenoma differentiated from a multinodular goiter with dominant
nodule?
________________________________________________________________
________________________________________________________________
3. HASHIMOTO’S THYROIDITIS : pp. 1086-1088
Also referred to as struma lymphomatosa, is marked by intense infiltrate of
lymphocytes admixed with plasma cells that virtually replace the thyroid
parenchyma. It is the most common cause of hypothyroidism in regions
that have sufficient iodine and a major cause of nonendemic goiter in
children. Hashimoto’s thyroiditis is an organ-specific, autoimmune disease
caused primarily by a defect in T-cells. B cells from thyroid tissues of
patient with Hashimoto’s disease
are
activated
and
secrete
autoantibodies directed against thyroid antigens (TSH receptor, iodine
transporter, thyroglobulin, and thyroid peroxidase).
History- A 50 year old woman was admitted because of an anterior neck
mass of 3 months duration associated with lethargy easy fatigability, and
cold intolerance. Patient also
noticed slow mental process and speech.
Pertinent P.E. findings: T=37.2oC, HR= 60/min; BP=90/60 mm Hg; mass
at the anterior neck measuring 4x3 cm.; firm, movable, well-delineated
borders, and moves with deglutition. Grade II nonpitting pedal edema;
TSH=increased, T3 and T4 = decreased. A subtotal thyroidectomy was
performed and specimen submitted for histopathological examination.
Biopsy revealed normal thyroid follicles with colloid, dense lymphocytic
infiltrates, atrophic thyroid follicles, lymphoid follicles with germinal center
formation, and Hurthle cells.
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-61-
Examine the slide. Draw and Label completely.
atrophic thyroid follicles
lymphoid follicles w/ germinal center
hurtle cell change
inflammatory infiltrates
Activity:
3.1 What is “hashitoxicosis”?
________________________________________________________________
3.2 Explain briefly the pathogenesis of Hashimoto’s thyroiditis.
________________________________________________________________
________________________________________________________________
________________________________________________________________
4. PAPILLARY CARCINOMA, THYROID : pp. 1094-1097
Papillary Carcinoma is the most common morphologic variant of thyroid
carcinoma (85%). Irradiation of the head and neck area during the first two
decades of life is particularly carcinogenic to the thyroid. Some variants
are associated with activation of Papillary thyroid carcinoma (PTC)
oncogene in combination with RET proto-oncogene in chromosome 10
(RET/PRC).
History: A 24 year old female sought admission because of an anterior
neck mass of two years duration not relieved by medications. Patient is
generally well. Laboratory examinations were with in normal limits. The
only significant finding is the presence of a “cold” nodule within the
thyroid. A fine needle aspiration biopsy of the nodule revealed “negative
for malignant cells” so a subtotal thyroidectomy with frozen section biopsy
was contemplated which was released as “malignant”. A total
thyroidectomy was performed.
Morphology: normal thyroid follicles, the tree-branching pattern, “Orphan
Annie eyes” appearance of nuclei, nuclear grooving, and
pseudoinclusions. Psammoma bodies may be seen.
This material is downloaded for Timothy Sam M. Valdez (20190107101)
at FEU Dr. Nicanor Reyes Medical Foundation.
For personal use only. No other uses without permission. All rights reserved.
-62-
Examine the slide. Draw and Label completely.
papillary excrescences
optically clear nuclei
nuclear groove
thyroid follicles
Activity:
4.1 Make a concept map using the following key words.
1. follicular variant
6. dysphagia
2. Orphan Annie eye nuclei
7. NTRK1 mutation
3. BRAF mutation
8. nuclear groove
4. hoarseness
9. RAS mutation
5. papillary excresences
10. ionizing radiation exposure
____, ____
DISEASES OF THE PARATHYROID GLAND
Introduction:
The parathyroid glands (4) lie in close proximity to the upper and lower
poles of the thyroid. It consists mostly of chief cells which are polygonal cells that
contain the parathormone. The activity of the pathyroid gland is controlled by the
level of ionized (free) calcium in the blood. Decreased level of free calcium
stimulate the synthesis and secretion of PTH and increased free calcium level
serves as a negative feed-back loop to PTH secretion.
1. PARATHYROID ADENOMA pp. 1101-1103
Parathyroid adenoma causes 85-95% of primary hyperparathyroidism
which leads to hypercalcemia . Other causes include Primary hyperplasia,
5-10%, and Parathyroid carcinoma less 1%. The adenomas are almost
always solitary, weighs from 0.5 to 5gm., soft, tan, well-circumscribed and
covered by a delicate capsule. Microscopically, it is composed
This material is
for Timothy
Sam M.chief
Valdez
(20190107101)
predominantly
ofdownloaded
fairly uniform,
polygonal
cells
with small, centrally
at
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Dr.
Nicanor
Reyes
Medical
Foundation.
located nuclei with few nests of larger oxyphil cells.
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-63-
History: A 40 year old male underwent an executive check-up and was
found to have elevation of ionized calcium in the blood. A plain KUB
revealed stones in the right kidney. Other findings include beginning
osteoporosis of the vertebral bones. The PTH level was likewise
increased. A parathyroidectomy was done which showed an adenoma
having normal parathyroid tissues, delicate capsule, and proliferating
chief cells
Examine the slide. Draw and Label completely.
proliferating chief cells
capsule
Activity:
1.1 How would you differentiate parathyroid adenoma from primary hyperplasia
microscopically?
________________________________________________________________
________________________________________________________________
1.2 Describe osteitis fibrosa 71ystic. Explain the evolution of this lesion.
________________________________________________________________
________________________________________________________________
1.3 What are the causes of hypercalcemia in relation to level of parathyroid
hormone?
Raised PTH
Decreased PTH
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-64-
DISEASES OF THE ADRENAL GLANDS
Introduction:
The adrenal glands are paired endocrine organs consist of a cortex and a
medulla. The normal gland weighs about 4 gm but may be decreased with acute
stress due to lipid depletion and increased due to hypertrophy and hyperplasia in
chronic stress. The adrenal cortex secretes glucocorticoids, mainly cortisol (zona
fasciculata); mineralocorticoids, most important is aldosterone (zona
glomerulosa); and sex steroids (zona reticularis). The adrenal medulla
synthesizes and secretes catecholamines (mainly epinephrine).
1. ADRENAL HEMORRHAGE
Massive adrenal hemorrhage may destroy sufficient adrenal cortex to
cause acute adrenocortical insufficiency. This may occur among newborns
following a prolonged and difficult delivery, in patients maintained on
anticoagulant therapy, postsurgical patients who developed DIC and as a
complication of bacteria (Waterhouse-Friderichsen Syndrome).
History – A 2 year old child was admitted because of high grade fever,
vomiting , and delirium. PPE: T – 39.8 0C; rigidity; (+) Babinski and
Brudzinski sign, (+) ankle clonus; widespread purpuric rashes which do
not disappear on pressure. Patient died on the second day after
admission and an autopsy was done.
Examine the slide. Draw and Label completely.
adrenal tissue
red blood cells
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at FEU Dr. Nicanor Reyes Medical Foundation.
For personal use only. No other uses without permission. All rights reserved.
-65-
Activity:
1.1 What are the components of Waterhouse-Friderichsen Syndrome?
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
1.2 What are the causes of Addison disease?
________________________________________________________________
________________________________________________________________
________________________________________________________________
1.3 What is the histologic appearance of pheochromocytoma?
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
DISEASES OF THE EXOCRINE PANCREAS
Introduction
Adult pancreas is a transversely oriented retroperitoneal organ in the area
of duodenum. The exocrine pancreas consists of 80-85% of the organ and is
composed of acinar cells that secretes variety of proenzymes such as
trypsinogen,
chymotrypsinogen,
procarboxypeptidase,
proelastase,
kallikreinogen and prophospholipase A & B.
1. ACUTE HEMORRAHGIC PANCREATITIS pp 884-887
Acute pancreatitis is a relatively common disorder characterized by acute
onset of abdominal pain due to enzymatic necrosis and inflammation of
the pancreas. About 80% of the disease is associated with biliary tract
disease and alcoholism.
History: A 45 years old, male, chronic alcoholics was brought to the
emergency room because of severe abdominal pain of one hour duration.
He had just had a drinking spree in a friend’s birthday party and had
barely slept when he was awakened by severe abdominal pain and
vomiting. Pertinent P.E. findings include BP = 80/50 mm Hg; T = 38.5 oC;
HR = 115/min with cold, clammy perspiration. Emergency treatment was
given but patient succumbed 16 hours after admission. A partial autopsy
was done. The pancreas weighed 180 gm, reddish-brown, with areas of
This material
is downloaded
for Timothy Sam
Valdez
(20190107101) chalky fat
blue-black
hemorrhage
interspersed
withM.foci
of yellow-white,
at
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Nicanor
Reyes
Medical
Foundation.
necrosis. One hundred ml of serous, slightly turbid, brown-tinged fluid was
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recovered from the peritoneal cavity (Chicken-broth).
-66-
Morphology: Necrotic acini, areas of hemorrhage, necrotic fat cells, saponified
fat, interstitial edema and neutrophilic infiltrates
Examine the slide. Draw and Label completely.
_________________
_________________
_________________
_________________
_________________
Activity:
1.1 What are the two most common predisposing factors associated with acute
pancreatitis?
________________________________________________________________
________________________________________________________________
1.2 What are the important elevated enzymes associated with acute pancreatitis?
________________________________________________________________
________________________________________________________________
1.3 What are the complications and sequelae of acute pancreatitis?
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
CASE ANALYSIS:
1. A 30 y/o male from Cordillera sought admission because of an anterior neck
mass of 1 year duration. The mass measures 4x4 cm, non-tender, and moves
with deglution. Patient is euthyroid.
1.1 What is your most probable diagnosis?
________________________________________________________________
1.2 Describe your expected histologic findings.
________________________________________________________________
________________________________________________________________
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________________________________________________________________
at FEU Dr. Nicanor Reyes Medical Foundation.
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-67-
2. A 68 y/o type II diabetic patient was admitted because of severe pallor and
markedly decreased urine output. He is a known hypertensive with poor
compliance. Hemoglobin – 70 g/L; Serum creatinine is 1200 umol/L.
2.1 What is your main diagnosis?
________________________________________________________________
________________________________________________________________
2.2 What morphologic findings do you expect in the kidneys?
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
2.3 Explain the pathogenesis of the anemia in this patient.
________________________________________________________________
___________________________________________________________ _____
________________________________________________________________
________________________________________________________________
This material is downloaded for Timothy Sam M. Valdez (20190107101)
at FEU Dr. Nicanor Reyes
Medical Foundation.
-68For personal use only. No other uses without permission. All rights reserved.
X. DISEASES OF BONES, JOINTS, AND SOFT TISSUES
Slides:
# 85
# 053
# 180
# 177
# 20
# 052
Osteosarcoma
Chondrosarcoma
Giant cell tumor of bone
Fibrous dysplasia, bone
Gout, subcutaneous tissue
Liposarcoma
Introduction:
Bone is a type of connective tissue and is unique because it undergoes
mineralization. Biochemically it is defined by its special blend of organic (35%),
cells and proteins matrix and inorganic (65%) elements, calcium hydroxyapatite.
Joints are constructed to provide both mobility and mechanical support. Joints
are of two types: solid joints (synarthroses) and cavitated (synovial) joints.
Hyaline cartilage is present in the articular surfaces and serves as an elastic
shock absorber and wear-resistant surface.
1. OSTEOSARCOMA: pp 1198 – 1200
Osteosarcoma is a malignant mesenchymal tumor in which the
malignant cells produce bone matrix. It is the most common primary
malignant
tumor of the bone (20%), exclusive of myeloma and
lymphoma. Bimodal age distribution is noted in osteosarcoma, 75%
occurs in those less than 20 years old and smaller second peak in the
elderly. Most common site is distal femur and proximal tibia (60%).
History: A 24 year old male was admitted because of fracture sustained
during a game of basketball. X-ray of the lower right leg showed fracture
of the tibia in an area of lytic and blastic mass that has permeative
margins. A surgery was performed with frozen section of the lesion.
Morphology: vary sized tumor cells with large hyperchromatic nuclei,
bizarre tumor giant cells, extensive necrosis and lace-like pattern of
neoplastic bone.
Examine the slide. Draw and Label completely.
neoplastic cells w/ large hyperchromatic nuclei
tumor giant cells
neoplastic bone
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-69-
Activity:
1.1 What is the characteristic radiologic appearance of ostesarcoma? Describe
the appearance.
________________________________________________________________
________________________________________________________________
1.2 What are the age groups frequently associated with high incidence of
osteosarcoma?
________________________________________________________________
________________________________________________________________
2. CHONDROSARCOMA: pp 1202 – 1203
Chondrosarcoma are tumors that produce neoplastic cartilage. They are
half as frequent as osteosarcoma and the second most common
malignant matrix-producing tumor of the bone. Chondrosarcomas most
commonly arises from the central portions of the skeleton, including the
pelvis, shoulders and ribs and rarely involves the distal extremities.
History – A 47 year male was admitted because of painful swelling over
the right shoulder which was noted 4 months prior to consultation. He took
mefenamic acid and piroxicam which only temporarily relieved the pain
and swelling. X-ray revealed endosteal scalloping with foci of flocculent
density in the adjacent bone. A biopsy was done and submitted for
histopathologic examination.
Morphology: malignant chondrocytes and areas of necrosis.
Examine the slide. Draw and Label completely.
malignant chondrocytes
Activity:
2.1 What are the different histologic types of chondrosarcoma? Which of these
has the best prognosis and why?
This material is downloaded for Timothy Sam M. Valdez (20190107101)
________________________________________________________________
at FEU Dr. Nicanor Reyes Medical Foundation.
________________________________________________________________
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________________________________________________________________
-70-
2.2 What is the usual presentation of chondrosarcoma? What are the 5 year
survival rates for grade 1 and 3 chondrosarcoma?
________________________________________________________________
________________________________________________________________
3. GIANT CELL TUMOR (OSTEOCLASTOMA) pp 1203 -1204
Giant cell tumor contains a mixture of mononuclear cells and a profusion
of multinucleated osteoclast-type giant cells. It is a relatively uncommon
but locally aggressive neoplasm.
History: A 30 y/o male sought consult because of a painfull mass around
the left knee. An X-ray showed a tumor which eroded into the subchondral
bone plate destroys the overlying cortex, producing a bulging soft-tissue
mass delineated by a thin shell of reactive bone. Curettage of the
involved bone was done.
Morphology:
sheets of uniform mononuclear cells and numerous
osteoclast-type giant cells.
Examine the slide. Draw and Label completely.
multinucleated giant cells
Activity:
3.1 What are the common locations of osteoclastoma?
________________________________________________________________
________________________________________________________________
3.2 What is the pathogenesis of giant cell tumor?
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
This material is downloaded for Timothy Sam M. Valdez (20190107101)
________________________________________________________________
at FEU Dr. Nicanor Reyes Medical Foundation.
________________________________________________________________
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-71-
4. FIBROUS DYSPLASIA, BONE: pp 1206 – 1207
Fibrous dysplasia is a benign tumor-like lesion of bone best characterized
as a localized developmental arrest. All the components of a normal bone
is present but they failed to differentiate into their normal structures.
History: A 15 year old girl was brought for consultation because of
distortion with widening of her 6th right rib. A biopsy was done.
Morphology: Examine the slide of fibrous dysplasia. Look for areas which
show curvilinear trabeculae of woven bone surrounded by moderately
cellular fibroblastic proliferation.
Draw and Label completely.
fibroblastic proliferation
curvilinear trabeculae of woven bone
Activity:
4.1 What are the different clinical patterns of fibrous dysplasia? Describe each
pattern briefly.
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
4.2 Describe the characteristic radiologic finding in fibrous dysplasia.
________________________________________________________________
________________________________________________________________
5. GOUT, SUBCUTANEOUS TISSUE: pp 1214 – 1217
Gout is the common endpoint of disorders that produce hyperuricemia. It
is marked by transient attacks of acute arthritis due to crystallization of
urates within and about the joints leading eventually to chronic gouty
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is downloaded
Timothy Sam
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arthritis
with deposition
offormasses
of urates
in (20190107101)
joints and other sites
at
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creating tophi.
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-72-
History – A 65 year female sought consultation because of on and off
swelling with pain of the big toes and ankles of 15 years duration. A biopsy
of the ankle mass was done.
Examine the slide of Gout. Look for areas with urate crystal deposition
surrounded by macrophages, lymphocytes and Foreign Body giant cells.
Draw and Label completely.
urate deposits
foreign body multinucleated giant cells
inflammatory cells
Activity:
5.1 Make a concept map using the following keywords.
1. tophaceous gout
6. URAT1 & GLUT9 abnormality
2. monosodium urate deposits
7. heavy alcohol consumtion
3. obesity
8. partial deficiency of HGPRT
4. hyperuricemia
9. acute arthritis
5. gouty nephropathy
10. asymptomatic intercritical period
_____, _____, _____, _____
5.2 What is the histologic hallmark of gout? What are the components of this
histologic hallmark?
________________________________________________________________
________________________________________________________________
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________________________________________________________________
at FEU Dr. Nicanor Reyes Medical Foundation.
________________________________________________________________
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-73-
6. LIPOSARCOMA, SUBCUTANEOUS TISSUE p1220 -1221
Liposarcomas are one of the most common sarcomas of adulthood and
appear between the ages of 50 and 60. It usually arise in the deep soft
tissues of the proximal extremities and retroperitoneum and are notorious
for developing into large tumors.
History: A 55 y/o female sought consult because of a rapidly growing
mass in the left arm. A biopsy was done and submitted for histopathologic
examination.
Examine the slide of liposarcoma. Note for the presence of adipocytes,
lipoblasts, myxoid stroma, and round tumor cells.
Draw and Label completely.
lipoblasts
myxoid stroma
round tumor cells
Activity:
6.1 What are the different types of liposarcoma? What type of liposarcoma is
present in your slide? Explain.
________________________________________________________________
________________________________________________________________
________________________________________________________________
6.2 What genetic abnormality is associated with liposarcoma?
________________________________________________________________
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-74-
CASE ANALYSIS:
1. An 18 year old boy sought admission because of a mass in the areas of the
left knee of 2 months duration. X-ray of the knee showed a large destructive,
mixed lytic and blastic mass with infiltrative margins. The tumor has broken
through the cortex and lifts the periosteum.
1.1 What is the most probable diagnosis?
________________________________________________________________
1.2 Among the elderly, what bones and the specific areas of the bone are
commonly involved?
________________________________________________________________
________________________________________________________________
________________________________________________________________
1.3 What are the different histologic subtypes for this kind of neoplasm?
________________________________________________________________
________________________________________________________________
________________________________________________________________
This material is downloaded for Timothy Sam M. Valdez (20190107101)
at FEU Dr. Nicanor Reyes Medical Foundation.
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-75-
XI. DISEASES OF THE CENTRAL NERVOUS SYSTEM
Slides :
# 115
# 003
# 31
# 117
# 162
T.B. meningitis
Viral encephalitis
Malaria, brain
Astrocytoma, brain
Meningioma
Introduction:
The functional properties of the CNS are topographically localized so that
diseases in the CNS are also geographically distributed. Thus their topographics
serve to individualize them and to facilitate their recognition. Examples:
Caudate nuclei
Huntington’s disease
Substantiate nigra
Parkinsonism
Motor neurons of spinal cord, brain
Amyotrophic lateral sclerosis
stem & cerebrum
Anterior horn cells of the spinal cord
Poliomyelitis
and motor nuclei of brain stem
Temporal lobe of cerebrum
Herpes simplex
Medulla
Rabies
Brain stem and cerebellum
Gliomas (childhood)
Cerebrum
Gliomas (adult)
The rate of evolution of the disease process and the age of the patient
likewise give some clues as to the diagnosis and etiology of lesion.
1. TUBERCULOUS MENINGITIS: pp. 1274
Tuberculous meningitis may occur as a part of a systemic disease or as
an isolated end-organ disease from a silent, usually pulmonary lesion.
During hematogenous dissemination, T.B. bacilli may seed distant organ
systems, including the meninges where the organism are destroyed in all
organs but persist only in the meninges to cause tuberculous meningitis.
The brain may also be involved to cause a diffuse meningoencephalitis.
History: A 29 year old female was admitted because of severe
frontal headache and vomiting of food previously taken of 2 days duration.
This started as body malaise, anorexia, and low grade fever of one week.
Because of the increasing severity of the headache and persistence of
vomiting, patient consulted and subsequently admitted. Pertinent P.E.
findings include: T = 380C; BP = 120/80 mm Hg; HR = 88/min; (+)
neck rigidity; (+) Babinski and Brudzinski’s sign. CSF examination
revealed pleocystosis, predominantly lymphocytes, increased protein, and
a slightly decreased sugar. Peripheral blood examination revealed
This material is downloaded for Timothy Sam M. Valdez (20190107101)
leukocytosis with
lymphocytosis.
Patient
developed
at FEU
Dr. Nicanor Reyes
Medical
Foundation.change in sensorium.
rd
0nFor
thepersonal
3 hospital
day
from uncal
herniation
onreserved.
the 5th hospital
use only.
No and
other died
uses without
permission.
All rights
day.
-76-
Examine the slide of tuberculous meningitis. Look for the
necrosis, mononuclear cell infiltrates, Langhan giant cells,
normal brain parenchyma.
caseation
fibrosis, and
Draw and Label completely.
granuloma
epithelioid cells
caseation necrosis
inflammatory cells
fibrosis
meninges
Activity:
1.1 Make a concept map using the following key words.
1. primary TB
6. secondary TB
2. caseation necrosis
7. tuberculous meningitis
3. activated macrophages
8. latent infection
4. hemoptysis
9. miliary TB
5. pulmonary cavitation
10. progressive primary TB
2. VIRAL ENCEPHALITIS: pp. 1275 -1278
Viral encephalitis or encephalomyelitis is a parenchymal infection of the
brain almost invariably associated with meningeal inflammation. The
degree of tropism exhibited by some viruses is particularly striking
in the nervous system. Some viruses infect specific cell types; others are
restricted to particular areas of the brain. Direct indication of viral infection
is the presence of inclusion bodies and, most importantly the identification
of the virus by ultrastructural, immunocytochemical and molecular
methods.
History: An 18 year old female was admitted because of convulsions
few minutes prior to admission. The present illness started 4 weeks prior
to admission as upper respiratory tract infection of one week duration
followed by lethargy and body weakness. She consulted a private
This material
for Timothy
Valdez
(20190107101)
physician,
wasis downloaded
given vitamins
but Sam
wasM.not
improved.
A week PTA,
at
FEU
Dr.
Nicanor
Reyes
Medical
Foundation.
behavioral changes was noted for which she was brought to a hospital
For personal use only. No other uses without permission. All rights reserved.
where she was given anti-depressant. The patient was still taking the
medications when she had seizures thus subsequently admitted.
-77-
Pertinent P.E. findings include: T = 37.3oC, BP = 120/70 mm Hg; stiff
neck, hyperactive deep tendon reflexes; CSF examination revealed
pleocytosis with lymphocytic predominance, increased protein, and
normal sugar. The patient stayed in the ward for 10 days but died from
complicating bronchopneumonia.
Examine the slide of viral encephalitis. Look for the
perivascular and
parenchymal mononuclear cell infiltrates neuronophagia, glial nodules and
congested blood vessels.
Draw and Label completely.
perivascular cuffing
inflammatory infiltrates
congested blood vessels
neuronophagia
Activity:
2.1 Explain the pathogenetic basis for viral tropism in the CNS.
________________________________________________________________
________________________________________________________________
2.2 Identify the disease process where the following inclusion bodies are found:
a. Negri bodies:
____________________________________
b. Cowdry bodies:
____________________________________
c. Cytomegalic cells intranuclear and intracytoplasmic inclusions bodies:
____________________________________
3. MALARIA, BRAIN; pp: 390 – 392; 1280
Cerebral involvement by P. falciparum, which causes as many as 80%
deaths among children, is due to adhesion of the parasite to endothelial
cells with in the brain. Patients with cerebral malaria have increased
amounts of ICAM-1, thrombospondin receptor, and CD46 receptor on their
This material
is downloaded
Timothy
M. Valdez
(20190107101)
cerebral
endothelial
cells to for
which
theSam
malaria
– infected
red cells bind.
at FEU Dr. Nicanor Reyes Medical Foundation.
For personal use only. No other uses without permission. All rights reserved.
History: An infant born to a P. falciparum infected mother developed
congenital malaria and died one month after birth.
-78-
Morphology: Examine the slide of malaria, brain. Note for the brain
parenchyma, blood vessels with red blood cells containing hemozoin
pigments, and ring hemorrhages.
Draw and Label completely.
congested blood vessels
hemozoin pigments
Activity:
3.1 What are the features of P. falciparum which accounts for its greater
pathogenicity?
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
3.2 What is the role of Duffy antigen and Sickle cell anemia in the pathogenesis
of malaria?
________________________________________________________________
________________________________________________________________
4. ASTROCYTOMA: pp 1306 – 1309
Tumors of the glial cells (Gliomas) include astrocytomas,
oligodendrogliomas, and ependymomas. Fibrillary astrocytomas accounts
for 80% of adult primary brain tumors. It is usually found in the cerebral
hemispheres but may occur in the cerebellum, brain stem, or spinal cord.
The highest grade lesions are characterized by a mixture of firm, white
areas and softer, yellow foci of necrosis as well as cystic change and
hemorrhage (GLIOBLASTOMA).
History: A 34 year old male was admitted because of recurrent, severe
headache of 8 weeks duration initially relieved by mefenamic acid. One
day PTA, the patient noted weakness of the left upper extremity. Few
minutes PTA, he had seizures thus consulted and subsequently admitted.
This material is downloaded for Timothy Sam M. Valdez (20190107101)
CT scan revealed
a mass over the right cerebral hemisphere. A
at FEU Dr. Nicanor Reyes Medical Foundation.
craniotomy
excision
of the
done and
specimen
submitted
For personalwith
use only.
No other
usesmass
withoutwas
permission.
All rights
reserved.
for histopathologic examination.
-79-
Examine the slide of Astrocytoma. Draw and label completely the brain
parenchyma and malignant astrocytes.
malignant astrocytes
Activity:
4.1 What are the four molecular subtypes of astrocytoma? Discuss each subtype
briefly.
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
4.2 What are the characteristic histologic changes present in Glioblastoma
multiforme that are not seen in other grades of astrocytoma?
________________________________________________________________
________________________________________________________________
5. MENINGIOMA, BRAIN: pp 1314 – 1315
Meningiomas are predominantly benign tumors of adults, attached to the
dura, and arise from the meningothelial cells of the arachnoid. They may
be found along the external surfaces of the brain or within the ventricular
system arising from the stromal arachnoid cells of he choroid plexus.
History: A 35 years old female sought consult because of recurrent
headache of increasing severity. The headache was temporarily relieved
by paracetamol. A CT-scan showed a mass over the left parietal convexity
compressing the underlying brain parenchyma. A craniotomy was done
with excision of the mass which was submitted for histopathologic
examination.
This material is downloaded for Timothy Sam M. Valdez (20190107101)
Morphology: Examine
the slide of meningioma. Look for the whorled
at FEU Dr. Nicanor Reyes Medical Foundation.
sheets
of neoplastic
cells,
psammoma
bodies,
and fibrous
For personal
use only. meningothelial
No other uses without
permission.
All rights
reserved.
tissues.
-80-
Draw and Label completely.
neoplastic meningothelial cells
psammoma bodies
fibrous tissue
Activity:
5.1 What are the various histologic patterns of meningioma? Describe each
pattern briefly.
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
________________________________________________________________
5.2 What is the significance of the presence of multiple lesions in meningioma?
________________________________________________________________
________________________________________________________________
________________________________________________________________
********************************************************************************************
CASE ANALYSIS:
1. An 80 y/o male was brought to the hospital because of alterations in mood
and forgetfulness. He has forgotten his children’s names and some fine motor
function. He gives excess change to clients in their grocery. Her answers to
some questions are irrelevant.
1.1 What is your most probable diagnosis?
___________________________________________________________
1.2 What CNS histologic findings do you expect to see?
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___________________________________________________________
at FEU Dr. Nicanor Reyes Medical Foundation.
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-81-
XII. DISEASES OF THE HEAD AND NECK AND EYES
Slides:
# 218
# 220
# 219
# 227
Phthisis bulbi
Pleomorphic adenoma
Warthin’s tumor
Mucoepidermoid carcinoma
1. PHTHISIS BULBI: p 1342
Phthisis bulbi is a small and internally disorganized eye which can be
brought about by intra-ocular inflammation, trauma, chronic renal
detachment and other conditions.
Morphology:
Ciliochoroidal effusion
Cyclitic membrane
presence of exudates between the
ciliary body and sclera and the choroid
and sclera
presence of membrane extending from
one aspect of the ciliary body to the
other
Chronic retinal detachment
Optic nerve atrophy
Presence of intra-ocular bone (osseous
metaplasia)
Thickening of the sclera
Draw and Label completely.
ciliochoroidal effusion
retinal detachment
optic nerve atrophy
thickened sclera
Activity:
1.1 What is sympathetic ophthalmia?
________________________________________________________________
________________________________________________________________
1.2 What is retinoblastoma? Give the histologic features of this lesion.
This material is downloaded for Timothy Sam M. Valdez (20190107101)
________________________________________________________________
at FEU Dr. Nicanor Reyes Medical Foundation.
________________________________________________________________
For personal use only. No other uses without permission. All rights reserved.
-82-
2. PLEOMORPHIC ADENOMA: pp. 744-745
Pleomorphic adenoma is also known as mixed tumor and represent 60%
of the tumors in the parotid gland exhibiting both epithelial and
mesenchymal differentiation. It presents as painless, slow growing, mobile
masses within the parotid or submandibular or buccal cavity.
Morphology:
Epithelial elements disperse throughout the matrix along with
varying degrees of myxoid, hyaline, chondroid and even osseous
tissue
Epithelial element resemble ductal cells or myoepithelial cells
arranged in duct formation, irregular tubules, strands, acini or
sheets of cells
Mesenchyme – like background composed of loose myxoid tissue
Draw and Label completely.
epithelial elements
loose myxoid stroma
salivary glands
Activity:
2.1 What is the reason for the high recurrence rate of pleomorphic adenoma?
________________________________________________________________
________________________________________________________________
2.2 What is the incidence of malignant transformation in pleomorphic adenoma?
________________________________________________________________
________________________________________________________________
2.3 From the list, choose the characteristic/s that best describe the most common
lesion of salivary glands.
( ) chromosomal rearrangements involving PLAG1
( ) gray white cut surface with myxoid and blue transluscent areas
( ) 60% of tumors in the parotid
( ) blockage or rupture of salivary gland duct
3. WARTHIN TUMOR (PAPILLARY CYSTADENOMA LYMPHOMATOSUM): p. 745
Warthin tumor is a benign tumor that arises almost exclusively in the
This gland.
material is downloaded for Timothy Sam M. Valdez (20190107101)
parotid
at FEU Dr. Nicanor Reyes Medical Foundation.
For personal use only. No other uses without permission. All rights reserved.
-83-
Morphology :
Cystic or cleft-like spaces lined by a double layer of palisading
neoplastic epithelial cells resting on a lymphoid stroma
Double layer lining consists of a surface of columnar cells with
abundant, finely granular, eosinophilic cytoplasm giving an
oncocytic appearance which rests on a layer of cuboidal to
polygonal cells
Lymphoid stroma may exhibit prominent germinal centers
Occasionally foci of squamous metaplasia may be seen.
Draw and Label completely.
double layer of palisading neoplastic cells
lymphoid stroma
germinal center
Activity:
3.1 Arrange the following salivary glands according to likelihood of a salivary
gland tumor being malignant.
A. parotid
B. sublingual
____ > ____ > ____
C. submandibular
3.2 From the list, choose the characteristic/s that best describe Warthin tumor.
( ) increased risk with smokers
( ) males > female
( ) common in 20 to 30 years old
( ) 4% recurrence rate after excision
( ) 10% are bilateral
( ) similar tumor arises in the lacrimal gland
3.3 What is the characteristic appearance of the neoplastic cells?
______________________________________________________________
______________________________________________________________
______________________________________________________________
______________________________________________________________
4. MUCOEPIDERMOID CARCINOMA: pp. 745-746
Definition: Most common primary malignant tumor of salivary gland.
This material is downloaded for Timothy Sam M. Valdez (20190107101)
at FEU Dr. Nicanor Reyes Medical Foundation.
For personal use only. No other uses without permission. All rights reserved.
-84-
Morphology: Grossly appearing as large mass lacking well defined capsule
with infiltrative margins. Cut section shows pale and gray-white cut surface
most often having small mucin containing cysts. Microscopically composed of
cords, sheets or cystic configurations of squamous, mucous or intermediate
cells.
Examine the slide. Draw and label completely.
Squamous cells
Mucous cells
Intermediate cells
Cysts
Activity:
5.1 What is the chromosomal abnormality associated with Mucoepidermoid
carcinoma?
______________________________________________________________
______________________________________________________________
5.2 What are the survival rates in relation to low grade and high grade
Mucoepidermoid carcinoma?
______________________________________________________________
______________________________________________________________
This material is downloaded for Timothy Sam M. Valdez (20190107101)
at FEU Dr. Nicanor Reyes Medical Foundation.
For personal use only. No other uses without permission. All rights reserved.
-85-
APPENDIX A
Instructional Learning Outcomes in Pathology B
INSTRUCTIONAL LEARNING OUTCOMES FOR HEART DISEASES
Instructional Learning Outcomes (ILOs)
Learning Content
1.Describe important normal morphologic
features of the heart
2. Enumerate heart changes in the elderly
3. Discuss in general pathogenesis of heart
impairment
4. Describe heart failure
4.1 forward and backward
4.2 right and left sided
5. Discuss common congenital heart diseases
including:
5.1 etiology & pathogenesis
5.2 conditions with left to right shunt
5.3 conditions with right to left shunt
5.4 obstructive congenital anomalies
6. Discuss ischemic heart disease
6.1 pathogenesis
6.2 ischemic syndrome
6.2.1 angina
6.2.2 myocardial infarction
6.2.3 chronic heart disease
6.2.4 sudden cardiac death
7. Discuss Hypertensive heart disease
7.1 Systemic (Left) hypertensive heart
disease
7.2 Pulmonary (Right) hypertensive
heart disease (Cor pulmonale)
8.Discuss valvular heart disease
8.1 calcific valve diseases
8.2 mitral valve prolapse
8.3 rheumatic heart disease
8.4 infective endocarditis
8.5 non-infective endocarditis
8.6 carcinoid heart disease
9. Discuss cardiomyopathies such as
9.1 dilated cardiomyopathy
9.2 hypertrophic cardiomyopathy
9.3 restrictive cardiomyopathies
9.4 myocarditis
10. Discuss pericardial diseases
10.1 Pericardial effusions
10.2 Hemopericardium
10.3 Pericarditis
11. Discuss benign and malignant neoplasia
of the heart
Assessment/
Evaluation
Normal heart features
Changes in aging heart
Five principal mechanisms
impairment
Right and left sided heart failure
of
heart
Dev of abnormalities
PDA, VSD, ASD tetralogy of Fallot, RV atresia,
persistent truncus
Cardiac blood supply
Production of ischemia
Ischemic syndrome
Systemic (Left) hypertensive heart
disease Pulmonary (Right) hypertensive heart
disease
Action of heart valves
Differentiate valve conditions
RHD, IE, NTE, carcinoid HD
Features of CMP
Dilated. hypertrophic, restrictive etiology of
specific CMP
Pericardial effusions, Hemopericardium,
Pericarditis (Acute and chronic inflammation)
Myxoma, metastatic tumors, effect of tumors
outside the heart
This material is downloaded for Timothy Sam M. Valdez (20190107101)
at FEU Dr. Nicanor Reyes Medical Foundation.
For personal use only. No other uses without permission. All rights reserved.
Student able to
score 75% or
more
in
a
written
objective test;
Student able to
identify 75% or
more of slides
in
move
practical
examination
Student able to
contribute/part
icipate
adequately in
the
clinicopathologic
discussion.
INSTRUCTIONAL LEARNING OUTCOMES FOR DISEASES OF THE LUNGS
Instructional Learning Outcomes (ILOs)
Learning Content
1. Explain the anatomy, histology and
physiology of the lung
2. Classify the congenital lung diseases
3. Explain atelectasis and differentiate the
types
4. Classify pulmonary edema as to causes
5. Describe the features of acute lung injury
6. Categorize diffuse pulmonary diseases
7. Explain the mechanisms of asthma,
emphysema,
chronic
bronchitis
and
bronchiectassis
8. Classify emphysema as to anatomic
distribution
9. Differentiate emphysema from chronic
bronchitis
10. Categorize the chronic diffuse interstitial
diseases
11. Classify pneumoconiosis
12. Explain mechanism of granulomatous
disease like sarcoidosis
13.Differentiate
hypersensitivity
pneumonitis from pulmonary eosinophilia
14.Explain pulmonary alveolar proteinosis
15. Classify lung diseases of vascular origin
16. Differentiate pneumonia from abscess
17. Classify pneumonia as to cause
18. Describe the stages of lobar pneumonia
19. Categorize lung tumors
20. Explain the mechanism of lung cancer
and differentiate the histologic types
21.Classify paraneoplastic syndromes
21. Classify diseases of the pleura
22. Differentiate adenocarcinoma
malignant mesothelioma
from
Respiratory tree, pulmonary acinus and
lobule, pneumocytes, air exchange
Agenesis, hypoplasia, cysts
Resorption, compression, contraction
Hemodynamic, microvascular injury
Profound dyspnea refractory to oxygen
therapy, endothelial and alveolar epithelial
damage, hyaline membrane
Obstructive vs. Restrictive
Asthma-bronchoconstriction,
emphysemaloss of elastic recoil, chronic bronchitismucous gland hyperplasia hypertrophy
Centriacinar, panacinar, distal acinar,
irregular
Emphysema-low elastic recoil, chronic
bronchitis-normal
Fibrosing
diseases,
pneumoconiosis,
granulomatous disease
Coal workers pneumoconiosis, asbestosis,
silicosis
Systemic autoimmune
Hypersensitivity pneumoniis-immunologically
mediated, pulmonary eosinophilic-may be
secondary
Congenital or acquired
Pulmonary hypertension, thromboembolism
Abscess-liquefactive necrosis, pneumonia –
lung infection
Bacterial, primary atypical
Congestion, red & gray hepatisation,
resolution
Carcinomas, carcinoids, mesenchymal
Cigarette smoke-mutation of K-RAS, p53, RB
gene, Adenocarcinoma, small cell, squamous,
large cell
Cushings, carcinoid, SIADH
Fluid-effusions,
primary of metastatic
tumors
CEA, TTF1 + = adenocarcinoma calretenin + =
mesothelioma
This material is downloaded for Timothy Sam M. Valdez (20190107101)
at FEU Dr. Nicanor Reyes Medical Foundation.
For personal use only. No other uses without permission. All rights reserved.
Assessment/
Evaluation
Student able to
score 75% or
more
in
a
written
objective test;
Student able to
identify 75% or
more of slides
in
move
practical
examination
Student able to
contribute/part
icipate
adequately in
the
clinicopathologic
discussion.
INSTRUCTIONAL LEARNING OUTCOMES FOR GIT DISEASES
Instructional Learning Outcomes (ILOs)
1.Enumerate the general signs and
symptoms produced by
1.1esophageal diseases
1.2 Gastric diseases
1.3 Intestinal diseases
1.4 Colonic diseases
2. Discuss briefly the different
gastrointestinal diseases under the
following categories based on etiology,
pathogenesis, morphology & clinical
features.
Learning Content
Assessment/
Evaluation
1. General signs and symptoms of diseases
involving:
Esophagus, stomach, small intestines, colon
Student able to
score 75% or
more
in
a
written
objective test;
Atresia, fistula, and duplications, Ectopia,
Meckel
diverticula,
Pyloric
stenosis,
Hirschsprung disease
Esophagitis, Barrett esophagus, Acute & Chronic
gastritis, Peptic ulcer, Infectious enterocolitis
(Cholera,
Campylobacter
entrocolitis,
Shigellosis,
Salmonellosis,Typhoid
fever,
Yersinia, Escherichia coli, Pseudomembranous
colitis, Whipple disease, viral enterocolitis,
Entameba
histolytica,
Giardia
lamblia,
Cryptosporidium), Crohn disease & Ulcerative
colitis, Achalasia, Esophageal webs, Schatzki
ring, Hernia,Adhesion, Volvulus,Intussusception
Benign tumors
Inflammatory, Hyperplastic, Fundic gland
polyps, Hamartomatous, Peutz-Jeghers Synd.,
Cowden Synd.,
Bannayan- Ruvalcaba-Riley
Synd., Cronkhite-Canada Synd.
Esophageal Adenocarcinoma, Squamous cell
carcinoma,
Gastric
carcinoma,
Gastric
lymphoma, Carcinoid tumor, GIST
Colonic adenocarcinoma, Squamous cell
carcinoma, Cloacogenic carcinoma, Basaloid
carcinoma
Menetrier’s disease, Zollinger-Ellison S.
Esopahgeal Varix, Ischemic bowel disease,
Infarction, Angiodys[plasia, Hemorrhoids
Malabsorption syndrome, Cystic fibrosis, Celiac
disease,
Tropical
sprue,
Autoimmune
enteropathy,
Lactase
deficiency,
Abetalipoproteinemia,
Irritable
bowel
syndrome, Zenker, Traction, Epiphrenic, Meckel
Sigmoid diverticula, Acute appendicitis, Tumors
of the appendix, Diseases of the peritoneal
cavity,
Peritoneal
infection,
Sclerosing
retroperitonitis, Cysts, Mesothelioma
Student able to
identify 75% or
more of slides
in
move
practical
examination
This material is downloaded for Timothy Sam M. Valdez (20190107101)
at FEU Dr. Nicanor Reyes Medical Foundation.
For personal use only. No other uses without permission. All rights reserved.
Student able to
contribute/part
icipate
adequately in
the
clinicopathologic
discussion
INSTRUCTIONAL LEARNING OUTCOMES FOR LIVER AND BILIARY TRACT DISEASES
Instructional Learning Outcomes (ILOs)
Learning Content
1. Describe the normal liver
2. Describe the major patterns of hepatic
injury
3. Explain the different types of liver
failure
4. Discuss liver cirrhosis based on
etiology, pathogenesis, morphology &
clinical features.
5. Explain the different consequences of
portal hypertension
6. Discuss the function of bile, bilirubin
metabolism and associated diseases
7. Discuss different disorders of the liver
based on etiology, pathogenesis,
morphology & clinical features.
8. Discuss different disorders of the
gallbladder based on:
8.1 Etiology
8.2 Pathogenesis
8.3 Morphology
8.4 Clinical features
Assessment/
Evaluation
Architecture, physiology, and blood supply of
the normal liver
Feathery
and
ballooning
degeneration;
Apoptosis; Necrosis
Acute & Chronic liver failure
Student able to
score 75% or
more
in
a
written
objective test;
Cirrhosis:
Student able to
identify 75% or
more of slides
in
move
practical
examination
Jaundice; Ascites; Portosystemic shunts;
Hyperammonemia; Hypoalbuminemia
Bile functions; Bilirubin metabolism, Jaundice,
cholestasis, hereditary hyperbilirubinemia
Infectious disorders, Autoimmune hepatitis
Drug and Toxin induced liver diseases
Alcoholic liver disease, Hemochromatosis
Wilson disease, alpha1-AT deficiency
Neonatal cholestasis, Intrahepatic biliary tract
disease, preeclampsia and eclampsia
acute fatty liver of pregnancy
intrahepatic cholestasis of pregnancy
drug toxicity after bone marrow transplantation
graft-versus-host disease and liver rejection
nonimmunologic damage to liver allografts
nodular hyperplasias; benign neoplasms;
malignant tumors
Congenital anomalies of the gallbladder
Cholelithiasis:
Acute and Chronic cholecystitis
Chledocholithiasis and ascending cholangitis;
Biliary atresia; Choledochal cysts
Carcinoma of gallbladder & extrahepatic ducts
This material is downloaded for Timothy Sam M. Valdez (20190107101)
at FEU Dr. Nicanor Reyes Medical Foundation.
For personal use only. No other uses without permission. All rights reserved.
Student able to
contribute/part
icipate
adequately in
the
clinicopathologic
discussion.
PATHOLOGY B: INSTRUCTIONAL LEARNING OUTCOMES FOR HEAD AND NECK AND EYES
Instructional Learning Outcomes
Learning Content
1. Discuss some of the common diseases
Dental caries; Gingivitis; Periodontitis
in the oral cavity and diseases presenting
Fibrous proliferative lesions; Apthous ulcers;
as oral cavity lesion based on etiology,
glossitis
pathogenesis, morphology & clinical
HSV and other viral infections;
features.
Oral Candidiasis and other fungal infections
Leukoplakia and Erythroplakia;
Squamous cell carcinoma
2. Discuss some of the common diseases
Inflammatory process:
in the upper airways as to:
Rhinitis; Sinusitis; Pharyngitis; Tonsillitis; Croup
2.1 Etiology
New Growth:
2.2 Pathogenesis
Nasal polyp; Sinonasal papilloma; Angiofibroma;
2.3 Morphology
Olfactory neuroblastoma; Nasopharyngeal
2.4 Clinical Features
carcinoma; Laryngeal nodule; Carcinoma of the
larynx
Discuss some of the common diseases in
Otitis media; Cholesteatoma; Otosclerosis;
the ears based on etiology, pathogenesis,
Basal cell carcinoma; Squamous cell carcinoma
morphology & clinical features.
4. Discuss some of the common diseases
Branchial cyst; Thyroglossal duct cyst;
in the neck based on etiology,
paraganglioma
pathogenesis, morphology & clinical
features.
5. Discuss some of the common diseases
Xerostomia; Sialadenitis
in the salivary glands based on etiology,
pathogenesis, morphology & clinical
Pleomorphic adenoma; Warthin tumor;
features.
Mucoepidermoid carcinoma; Adenoid cystic CA,
Acinic cell tumor
6. Describe the anatomy of the orbit.
Anatomy of the orbit
Discuss some of common diseases of the
Cellulitis, Fungal infection, Inflammatory
orbit based on etiology, pathogenesis,
Pseudotumor & Posterior Scleritis
morphology & clinical features.
Grave’s disease, Hemangioma, Lymphangioma,
Lymphoma, metastatic tumor
7. Describe the anatomy of the eyelid.
Anatomy of the eyelid
8. Discuss some of common diseases of
Hordeolum, Chalazion, Blepharitis
the eyelid based on etiology,
Basal cell CA, sebaceous CA, squamous cell CA
pathogenesis, morphology & clinical
Kaposi sarcoma
features.
9. Describe the anatomy of the
Anatomy of the conjunctiva.
conjunctiva.
10. Discuss some of common diseases of
Inflammation, Pinguecula & pterygium
the conjunctivae based on etiology,
squamous cell CA, melanoma, nevus
pathogenesis, morphology & clinical
and mucoepidermoid CA
features.
11. Describe the anatomy of the sclera.
Anatomy of sclera
12. Discuss the common diseases of the
Scleritis, staphyloma
sclera based on etiology, pathogenesis,
osteogenesis imperfecta
morphology & clinical features.
congenital melanosis oculi
13. Describe the anatomy of the cornea
Anatomy of the cornea
14. Discuss the common diseases of the
calcific band keratopathy, actinic band,
cornea based on etiology, pathogenesis,
keratopathy, keratoconus
morphology &This
clinical
features.
Fuch’s,
Macular,
Granular
& Avelino
material is downloaded for
Timothy
SamLattice,
M. Valdez
(20190107101)
15. Describe the anatomy ofatthe
anterior
Anatomy
the anterior
segment.
FEU
Dr. Nicanor
ReyesofMedical
Foundation.
segment. For personal use only. No other uses without permission. All rights reserved.
16. Discuss the common diseases of the
Cataract
anterior segment based on etiology,
Glaucoma
pathogenesis, morphology & clinical
endophthamitis and panophthalmitis
features.
Assessment
Student must
be able to get
75% written
objective test.
Student must
be able to
identify 75% of
slides in a
practical exam.
Student must
be able to
participate in
slide cases and
CPC case with
journal
discussion.
17. Describe the anatomy of the uvea.
18. Discuss the common diseases of the
uvea based on etiology, pathogenesis,
morphology & clinical features.
19. Describe the anatomy of the retina
and vitreous
20. Discuss the common diseases of the
retina based on etiology, pathogenesis,
morphology & clinical features.
21. Discuss the common diseases of the
optic nerve based on etiology,
pathogenesis, morphology & clinical
features.
22. Enumerate the changes associated
with end stage eye
Anatomy of the uvea
Uveitis, sympathetic ophthalmia, melanoma,
nevus
Anatomy of retina and vitreous
Retinal detachment, hypertension, diabetes
mellitus, Retinopathy of prematurity, sickle cell
retinopathy, retinal, radiation retinopathy,
Retinal artery & vein occlusions, age related
macular degeneration, Retinitis pigmentosa,
retinitis, retinoblastoma, lymphoma
Anterior ischemic optic neuropathy
papilledema
glaucomatous optic nerve damage
other optic neuropathy
a. Leber hereditary optic neuropathy
optic neuritis
ciliochoroidal effusion, cyclitic membrane,
retinal detachment, optic nerve atrophy & bone
metaplasia
INTRUCTIONAL LEARNING OUTCOMES FOR DISEASES OF THE PANCREAS
Instructional Learning Outcomes (ILOs)
Learning Content
1.Describe morphology of pancreas
2. Discuss the congenital anomalies of
pancreas.
3. Discuss pancreatitis based on etiology,
pathogenesis,
morphology,
clinical
features:
4. Discuss nonneoplastic lesion of the
pancreas
based
on
etiology,
pathogenesis,
morphology,
clinical
features:
5. Discuss neoplasms of the pancreas
based on etiology, pathogenesis,
morphology, clinical features:
Morphology of pancreas
Pancreas divisum, Annular pancreas, Ectopic
pancreas, Agenesis
Acute pancreatitis
Chronic pancreatitis
Congenital cyst
Pseudocyst
Cystic neoplasm
Pancreatic Carcinoma
Acinar cell carcinoma
Pancreatoblastoma
This material is downloaded for Timothy Sam M. Valdez (20190107101)
at FEU Dr. Nicanor Reyes Medical Foundation.
For personal use only. No other uses without permission. All rights reserved.
Assessment/
Evaluation
Student able
to score 75%
or more in a
written
objective test;
Student able
to
identify
75% or more
of slides in
move practical
examination
Student able
to
contribute/par
ticipate
adequately in
the
clinicopathologic
discussion.
INSTRUCTIONAL LEARNING OUTCOMES FOR KIDNEY DISEASES
Instructional Learning Outcomes (ILOs)
Learning Content
1.Describe the clinical manifestations of
renal diseases:
Clinical manifestations of nephritic syndrome,
nephrotic syndrome, asymptomatic hematuria/
proteinuria, acute kidney injury, chronic kidney
disease, end stage renal disease, renal tubular
defects, urinary tract infection, nephrolithiasis,
urinary tract obstruction and renal tumors
Structure of glomerulus
Pathologic responses of glomerulus to injury
Pathogenesis of glomerular injury
Mechanism of progression of glomerular
diseases
2. Discuss the different glomerular
Nephritic syndrome
diseases based on etiology, pathogenesis,
Acute proliferative glomerulonephritis
morphology & clinical features.
Poststreptococcal
Nonstreptococcal
Rapidly progressive glomerulonephritis
Nephrotic syndrome
Membranous nephropathy
Minimal change diasease
Focal segmental glomerulosclerosis
HIV associated nephropathy
Membranoproliferative glomerulonephritis
Isolated glomerular abnormalities
IgA nephropathy
Hereditary nephritis
Alport syndrome & Benign Familial
Hematuria
Chronic glomerulonephritis
Glomerular Lesions associated with systemic
disease
Lupus nephritis
Henoch-Schonlein purpura
Diabetic nephropathy
Other systemic disorders
3. Discuss the tubular and interstitial Acute Tubular Injury/Necrosis
diseases based on:
Tubulointerstitial Nephritis
3.1 etiology
Pyelonephritis and UTI
3.2 pathogenesis
acute pyelonephritis
3.3 morphology
chronic pyelonephritis
3.4 clinical features
Tubulointerstitial Nephritis Induced by drugs
& toxin
acute drug induced interstitial nephritis
nephropathy associated with NSAID’s
Other tubulointerstitial diseases
Urate nphropathy
Hypercalcemia and Nephrocalcinosis
Acute Phosphate Nephropathy
Light Chain cast Nephropathy
Bile cast nephropathy
This material is downloaded for Timothy Sam M. Valdez (20190107101)
4. Discuss the different vascular
diseases
Nephrosclerosis
at FEU Dr. Nicanor Reyes Medical Foundation.
affecting theFor
kidney
baseduse
on: only. No other uses
Benign
and malignant
personal
without
permission. All rights reserved.
4.1 etiology
Renal artery stenosis
4.2 pathogenesis
Thrombotic microanglopathies
4.3 morphology
Other vascular disorders
4.4 clinical features
Atherosclerotic vascular dso.
Assessment/
Evaluation
Student able to
score 75% or
more
in
a
written
objective test;
Student able to
identify 75% or
more of slides
in
move
practical
examination
Student able to
contribute/part
icipate
adequately in
the
clinicopathologic
discussion.
5. Discuss congenital and developmental
anomalies
6. Discuss cystic diseases of the kidney
based
on
etiology,
pathogenesis,
morphology & clinical features.
7. Discuss urinary tract obstruction based
on etiology, pathogenesis, morphology &
clinical features.
8. Discuss renal tumors based on etiology,
pathogenesis, morphology & clinical
features.
Atheroembolic renal dse.
Sickle cell nephropathy
Diffuse cortical necrosis
Renal infarcts
Agenesis of the kidney, Hypoplasia, Ectopic
kidneys and Horseshoe kidneys
Autosomal dominant polycystic kidney disease
Autosomal recessive polycystic kidney disease
Cystic diseases of the renal medulla
Multicystic Renal dysplasia
Acquired (dialysis associated) cystic disease
Simple cyst
Urinary
tract
obstruction,
etiology,
pathogenesis, morphology and clinical course
Urolithiasis
Renal papillary adenoma, Angiomyolipoma,
Oncocytoma,
Renal
cell
carcinoma,
Urothelial carcinoma of the renal pelvis
INSTRUCTIONAL LEARNING OUTCOMES FOR DISEASES OF LUT AND MALE GENITAL SYSTEM
Instructional Learning Outcomes
Learning Contents
1.Discuss the diseases of the ureter based
on etiology, pathogenesis, morphology &
clinical features.
2.Discuss the diseases of the urinary
bladder based on etiology, pathogenesis,
morphology & clinical features.
3. Discuss the diseases of the urethra
based on etiology, pathogenesis,
morphology & clinical features.
4. Discuss the diseases of the penis based
on etiology, pathogenesis, morphology &
clinical features.
5.Discuss the diseases of testis &
epididymis based on etiology,
pathogenesis, morphology & clinical
features.
6.Discuss diseases of the prostate based
on etiology, pathogenesis, morphology &
clinical features.
congenital anomalies, inflammation,tumors &
tumor like lesions
congenital anomalies, acute & chronic cystitis
& special forms of cystitis, metaplastic lesion,
urothelial tumors, mesenchymal tumors,
secondary tumors, obstruction
Inflammation, tumors & tumor like lesions
hypospadias, epispadias, phimosis
inflammation, benign and malignant tumors
Cryptochidism, atrophy, non specific
epididymitis & orchitis, granulomatous orchitis,
specific inflammations, torsion, germ cell
tumors: seminoma, embryonal carcinoma, yolk
sac tumor, teratoma & choriocarcinoma, leydig
& Sertoli cell tumo, gonadoblastoma,lymphoma
benign prostatic hyperplasia
prostatic adenocarcinoma, other tumors &
tumor-like lesions
This material is downloaded for Timothy Sam M. Valdez (20190107101)
at FEU Dr. Nicanor Reyes Medical Foundation.
For personal use only. No other uses without permission. All rights reserved.
Assessment/
Evaluation
Student able to
get 75% in a
written
objective test;
Student able to
identify 75% of
slides in a
Practical
examination
Student able to
contribute/
participate
adequately in
the clinicopathologic
discussion
INSTRUCTIONAL LEARNING OUTCOMES FOR DISEASES OF FEMALE GENITAL TRACT
Instructional Learning Outcomes (ILOs)
Learning Content
1. Describe the embryology of the female Embryology of the female genital tract
genital tract
2. Describe the common infections of the Gardnerella vaginalis, Herpes simplex virus,
lower genital tract
Candida albicans, Trichomonas vaginalis
2.1 clinical features
2.2 morphology
3. Describe the common infections of the PID: gonococcal vs puerperal infection
lower and upper genital tract
3.1 clinical features
3.2 morphology
4. Describe the benign lesions of the vulva Bartholin’s cyst, Lichen sclerosus, Squamous
4.1 clinical features
hyperplasia,
Polyps,
Condyloma
lata,
4.2 morphology
Condyloma acuminata
5. Describe the premalignant and VIN, Basaloid & Warty CA, Keratinizing SCCA
malignant lesions of the vulva based on Papillary hidradenoma, Extra-mammary Paget’s
etiology, pathogenesis, morphology & dse & Melanoma
clinical features.
6. Describe the premalignant and Squamous
cell
carcinoma,
Vaginal
malignant lesions of the vagina based on intraepithelial neoplasia, adenocarcinoma,
etiology, pathogenesis, morphology & embryonal rhabdomyosarcoma
clinical features.
7. Describe the inflammatory lesions of Acute cervicitis, Chronic cervicitis
the
cervix
based
on
etiology,
pathogenesis, morphology & clinical
features.
8. Describe the benign lesions of the cervix Endocervical polyp, Condyloma acuminate
as to based on etiology, pathogenesis,
morphology & clinical features.
9. Describe the malignant lesions of the
cervix based on etiology, pathogenesis, CIN, Pap smear, SCCA
morphology & clinical features.
10. Discuss briefly the normal cyclic Normal endometrial cycle
changes in the endometrium
11. Describe functional endometrial Anoovulatory cycle, Inadequate luteal phasse,
disorder based on etiology, pathogenesis, Oral
contraceptives,
menopausal
&
morphology & clinical features.
postmenopausal changes
12. Describe the inflammatory disorders of Acute endometritis & Chronic endometritis
the endometrium based on etiology,
pathogenesis, morphology & clinical
features.
13. Describe and Differentiate adenomysis Adenomyosis & Endometriosis
and endometriosis based on etiology,
pathogenesis, morphology & clinical
features.
14. Describe and differentiate the various Hyperplasia: Simple w/o atypia; Simple w/
forms of hyperplasia based on etiology, atypia; Complex w/o atypia; Complex w/ atypia
pathogenesis, morphology & clinical
features.
15. Describe the common tumor of the Endometrial polyp, Adenocarcinoma
This material is downloaded for Timothy Sam M. Valdez (20190107101)
uterus based on etiology,atpathogenesis,
Leiomyoma,
Leiomyosarcoma,
Mullerian tumor
FEU Dr. Nicanor
Reyes Medical
Foundation.
morphologyFor
& clinical
features.
personal use only. No other uses without permission. All rights reserved.
16. Describe the common lesions of the Tuberculous salpingitis, Suppurative salpingitis
fallopian tube
& Tumor & cysts
17. Describe the common non-neoplastic Follicle & Luteal cysts, Polycystic dse & Stromal
lesions of the ovary based on etiology, hyperthecosis
Assessment/
Evaluation
Student able to
score 75% or
more
in
a
written
objective test;
Student able to
identify 75% or
more of slides
in
move
practical
examination
Student able to
contribute/part
icipate
adequately in
the
clinicopathologic
discussion.
pathogenesis, morphology & clinical
features.
18. Describe the common ovarian tumors
based
on
etiology,
pathogenesis,
morphology & clinical features.
19. Describe common disorders of
pregnancy based on etiology,
pathogenesis, morphology & clinical
features.
20. Describe common gestational
trophoblastic diseases based on
etiology, pathogenesis, morphology &
clinical features.
Serous, Mucinous, Endometrioid, Clear cell,
Transitional
cell
tumor,
Teratomas,
Dysgerminoma,
Yolk
Sac
tumor,
Choriocarcinoma, Granulosa Cell tumor,
Fibromas, Thecomas, Fibrothecomas, Sertoli
Leydig tumor, Metastatic tumors
Spontaneous abortion, Ectopic pregnancy, Twin
placenta,
Abnormalities
of
placental
Implantation, Placental infections, Preeclampsia
and Eclampsia
Hydatidiform mole (Complete vs partial),
Invasive mole, Choriocarcinoma, Placental Site
trophoblastic tumor
INSTRUCTIONAL LEARNING OUTCOMES FOR DISEASES OF THE BREAST
Instructional Learning Outcomes
Learning Contents
1. Discuss the disorders of breast
development based on etiology
& clinical significance
2. Discuss the clinical presentation
of breast diseases
3. Enumerate the different
categories of breast diseases
4.Discuss the different diseases
under each category based on
etiology, pathogenesis,
morphology & clinical features.
Milkline remnants, Accessory axillary breast tissue
Congenital nipple inversion
Pain, Palpable masses, Nipple discharge
Mammographic screening: Densities & Calcifications
Inflammatory disorders, Benign epithelial lesions,
Carcinoma of the breast, Stromal breast tumors, Other
malignant tumors of the breast, Gynecomastia and
Carcinoma
acute mastitis, periductal mastitis, mammary duct
ectasia, fat necrosis, lymphocytic mastopathy,
granulomatous mastitis, nonproliferative breast
changes, proliferative diseases without atypia,
proliferative diseases with atypia, Carcinoma In Situ,
Invasive ductal carcinoma, Invasive lobular carcinoma,
Medullary carcinoma, Mucinous carcinoma, Tubular
carcinoma, Invasive papillary carcinoma, Metaplastic
carcinoma, Fibroadenoma, Phyllodes tumor, Benign
stromal lesions, Malignant stromal tumors
Gynecomastia, Carcinoma in male
This material is downloaded for Timothy Sam M. Valdez (20190107101)
at FEU Dr. Nicanor Reyes Medical Foundation.
For personal use only. No other uses without permission. All rights reserved.
Assessment/
Evaluation
Students able
to answer
correctly 75%
of questions in
a written
objective test
Students able
to diagnose
75% of
pathologic skin
and breast
lesions of gross
specimens and
slides
Students able
to do clinicopathologic
correlation of
diseases of the
skin and breast
INTRUCTIONAL LEARNING OUTCOMES FOR ENDOCRINE DISEASES
Instructional Learning Outcomes (ILOs)
Learning Content
1.Enumerate the different endocrine
organs
2. Discuss the normal morphology of the
endocrine organs.
3. Tabulate the hormones produced by
the endocrine glands by organs as to:
3.1 cell/s producing the hormone
3.2 physiologic effects of the hormone
3.3 causes & effects of hypersecretion
3.4 causes & effects of hyposecretion
4.Discuss the following diseases based on
etiology, pathogenesis, morphology,
clinical features:
Pituitary gland, thyroid gland, , parathyroid
glands, endocrine pancreas, adrenal glands and
pineal gland
Normal histology of the endocrine organs
Hormones secreted by the endocrine glands,
source, and effects of normal secretion, oversecretion, and hormone deficiency
Pituitary
Anterior pituitary adenomas, Posterior pituitary
adenomas, Hypothalamic suprasellar tumors,
Thyroid
Grave disease, Cretinism, Myxedema, Hashimoto
thyroiditis, Subacute thyroiditis, Subacute
lymphocytic thyroiditis, Diffuse nontoxic goiter,
Multinodular goiter, Thyroid adenoma,Papillary
carcinoma,
Follicular carcinoma, Medullary
carcinoma, Anaplastic carcinoma
Parathyroid glands
Primary
hyperpara-thyroidism,
Secondary
hyperpara-thyroidism,
Pseudohypoparathyroidism
Endocrine pancreas
Diabetes mellitus, ,Insulinoma, Gastrinomas
Adrenal glands
Primary hyperaldosteronism
Adrenogenital syndromes, Primary acute adrenal
insufficiency, Waterhouse-Friderichsen syndrome
Primary chronic adrenocortical insufficiency
Secondary adrenocortical insufficiency
Adrenocortical neoplasms, Pheochromocytoma
Tumors of extra-adrenal paraganglia
Multiple Endocrine Neoplasia syndrome
Pinealomas
This material is downloaded for Timothy Sam M. Valdez (20190107101)
at FEU Dr. Nicanor Reyes Medical Foundation.
For personal use only. No other uses without permission. All rights reserved.
Assessment/
Evaluation
Student able
to score 75%
or more in a
written
objective test;
Student able
to
identify
75% or more
of slides in
move practical
examination
Student able
to
contribute/par
ticipate
adequately in
the
clinicopathologic
discussion.
INSTRUCTIONAL LEARNING OUTCOMES FOR DISEASES OF THE SKIN
Instructional Learning
Learning Contents
Outcomes
1.Describe the functions of
the different structures in
the skin
2.Define the different
macroscopic and microscopic
terms used to describe skin
pathology
3.Enumerate the different
categories of skin disorders
4.Discuss the different
diseases under each
categories based on:
4.1 etiology
4.2 pathogenesis
4.3 morphology
4.4 clinical course
Functions of: Squamous epithelial cells, Melanocytes,
Dendritic cells, Lymphocytes, Neural end organs and axonal
processes, Adnexal components
Macroscopic terms: Excoriation, Lichenification, Macule,
Onycholysis, Papule, Scale, Vesicle, Wheal
Microscopic terms: Acantholysis, Acanthosis, Dyskeratosis,
Erosion, Exocytosis, Hydropicswelling,
Hypergranuloperkeratosis, Lentiginous, Papillomatosis,
Parakeratosis
Disorders of pigmentation and melanocytes, Benign epithelial
tumors, Premalignant and malignant epidermal tumors,
Tumors of the dermis, Tumors of cellular migrants to the skin,
Disorders of epidermal maturation, Acute inflammatory
dermatosis, Chronic inflammatory dermatosis, Blistering
(Bullous) Diseases, Disorders of epidermal appendages,
Infection
1. Disorders of pigmentation and melanocytes: freckle,
lentigo, melanocytic nevus, dysplastic nevus, melanoma
2. Benign epithelial tumors: seborrheic keratosis, acanthosis
nigricans, fibroepithelial polyp, epithelial cyst, adnexal tumors
3. Premalignant and malignant epidermal tumors: actinic
keratosis, squamous cell carcinoma, basal cell carcinoma
4. Tumors of the dermis: benign fibrous histiocytoma,
dermatofibrosarcoma protruberans
5. Tumors of cellular migrants to the skin: mycosis fungoides,
mastocytosis
6.Disorders of epidermal maturation:Ichthyosis
7. Acute inflammatory dermatosis: Urticaria, Acute
eczematous dermatitis, erythema multiforme
8. Chronic inflammatory dermatoses: psoriasis, seborrheic
dermatitis, lichen planus
9.Blistering Diseases:
9.1 inflammatory blistering disorders: pemphigus, bullous
pemphigoid, dermatitis herpetiformis
9.2 noninflammatory blistering disorders: epidermolysis
bullos, porphyria
10. Disorders of epidermal appendages: acne vulgaris, rosacea
11.Panniculitis: erythema nodosum, erythema induratum
12. Infection: verrucae (warts), molluscum contagiosum,
impetigo, superficial fungal infection
This material is downloaded for Timothy Sam M. Valdez (20190107101)
at FEU Dr. Nicanor Reyes Medical Foundation.
For personal use only. No other uses without permission. All rights reserved.
EVALUATION
Students able
to answer
correctly 75%
of questions in
a written
objective test
Students able
to diagnose
75% of
pathologic skin
and breast
lesions of
gross
specimens and
slides
Students able
to do clinicopathologic
correlation of
diseases of the
skin and
breast
INSTRUCTIONAL LEARNING OUTCOMES FOR DISEASES OF THE BONES, JOINTS AND SOFT TISSUES
Instructional Learning
Learning Content
Assessment/
Outcomes (ILOs)
Evaluation
1. Discuss the normal
anatomy of Bone
1.1 Appearance
1.2 Function
2. Developmental and
Acquired Abnormalities in
Bone cells, Matrix and
Structure
3. Discuss Fractures &
Osteonecrosis
4. Describe Osteomyelitis
5. Discuss Bone Tumors and
Tumor-like lesions
based on
etiology, pathogenesis,
morphology & clinical
features.
6. Discuss the normal
anatomy of joints
7. Discuss diseases of the
joints based on
etiology, pathogenesis,
morphology & clinical
features
8. Discuss Tumor and Tumorlike lesions of the joints
based on
etiology, pathogenesis,
morphology & clinical
features
9. Discuss Soft Tissue Tumor
and Tumor-like lesions
based on
etiology, pathogenesis,
morphology & clinical
features
Skeletal system; components of bone; Functions of bone;
Growth & Development; Bone modeling and remodeling
Type 1 collagen disease; Type 2, 10 & 11 collagen disease;
Mucopolysaccharidoses; Osteopetrosis; Osteoporosis; Paget
disease; Rickets & Osteomalacia; Hyperparathyroidism; Renal
Osteodystrophy
Type; Healing process; Factors influencing healing;
osteonecrosis
Pyogenic; Tuberculous; Syphilis
Bone forming tumors
Osteoma; Osteiod Osteoma; Osteoblastoma
Cartilage forming tumors
Osteochondroma; Chondromas; Chondroblastoma;
Chondromyxoid fibroma; Chondrosarcoma
Fibrous and Fibro-Osseus Tumors
Fibrous cortical defect & non-ossifying fibroma;
Fibrous dysplasia; Fibrosarcoma & MFH
Other Tumors of the bone
Ewing Sarcoma; Giant cell tumor; Primitive
Neuroectodermal tumor; Aneurysmal bone cyst
Review: types, components, function
Osteoarthritis; Rheumatoid arthritis; Juvenile rheumatoid
arthritis; Seronegative Spondyloarthropathies; Infectious
arthritis; Gout and gouty arthritis
Ganglion and Synovial cyst; Giant cell tumor of Tendon sheath
Fatty Tumors
Lipoma; Liposarcoma
Fibrous tumors
Nodular fasciitis; Myositis Ossificans
Superficial & deep seated fibromatoses
Fibrohistiocytic tumors
BFH; MFH
Tumors of Skeletal muscle
Rhabdomyosarcoma
Tumors of Smooth muscle
Leiomyoma; Leiomyosarcoma
Synovial Sarcoma
This material is downloaded for Timothy Sam M. Valdez (20190107101)
at FEU Dr. Nicanor Reyes Medical Foundation.
For personal use only. No other uses without permission. All rights reserved.
Student able
to score 75%
or more in a
written
objective test;
Student able
to identify
75% or more
of slides in
move practical
examination
Student able
to
contribute/par
ticipate
adequately in
the clinicopathologic
discussion.
INTRUCTIONAL LEARNING OUTCOMES FOR CNS DISEASES
Instructional Learning Outcomes
Learning Content
(ILOs)
1.Explain the reactions of different
brain cells to injury
2. Classify cerebral edema as to
principal types
3. Explain the development of
hydrocephalus and differentiate
types
4. Categorize brain herniation
5. Classify malformations and
developmental diseases
6. Explain perinatal brain injury
7. Categorize brain trauma
8. Classify parenchymal brain injuries
9. Differentiate traumatic vascular
injuries
10. Classify spinal cord trauma
11.
Categorize
cerebrovascular
diseases
12. Differentiate thrombotic from
embolic brain injuries
13.
Classify
intracranial
haemorrhages
14. Explain the routes of brain
infection
15. Categorize brain infection
16. Classify meningitis base on CSF
findings
17. Differentiate demyelinating from
degenerative brain disease
18. Explain toxic and acquired
metabolic diseases
19. Classify brain tumors
20. Differentiate types of gliomas
21. Categorize
familial tumor
syndromes
Red neuron, inclusions, neuronophagia, microglial
nodule, gliosis
Vasogenic & cytotoxic
Decreased
resorption,
increased
production,
communicating, non-communicating, ex vacuo
Transtentorial, subfalcine, tonsillar
Neural tube defects, forebrain and posterior fossa
anomalies
Cerebral palsy, periventricular leukomalacia
Skull fracture, parenchymal and traumatic vascular
injuries
Contusion, concussion, laceration
Epidural and subdural hematoma
Above c4, below c4, thoracic
Atherosclerotic, thrombosis, embolism, infarction,
intracranial
hemorrhage,
hypertensive
cerebrovascular disease
Thrombotic-pale infarct, embolic-red/hemorrhagic
infarct
Spontaneous intracerebral hemorrhage, subarachnoid
hemorrhage
Hematogenous, local extension, direct implantation,
peripheral nerves
Bacterial, viral, fungal protozoan, prion disease
Acute bacterial, viral, fungal, tuberculous
Multiple sclerosis, Alzheimer disease, Pick, Parkinson
disease
Ethanol,
methanol,
radiation,
hypoglycaemia,
hyperglycemia, hepatic encephalopathy,
Vit. B
deficiency
Gliomas,
neuronal,
poorly
differentiated,
meningiomas, peripheral nerve sheath
Astrocytoma, oligodendroglioma, ependymoma
Neurofibromatosis types 1 & 2. , Von -Hippel Lindau,
This material is downloaded for Timothy Sam M. Valdez (20190107101)
at FEU Dr. Nicanor Reyes Medical Foundation.
For personal use only. No other uses without permission. All rights reserved.
Assessment/
Evaluation
Student able
to score 75%
or more in a
written
objective test;
Student able
to
identify
75% or more
of slides in
move practical
examination
Student able
to
contribute/par
ticipate
adequately in
the
clinicopathologic
discussion.
INSTRUCTIONAL LEARNING OUTCOME FOR DISEASES OF THE PERIPHERAL NERVE & SKELETAL MUSCLE
Instructional Learning
Learning Contents
Assessment/
Outcomes
Evaluation
1. Discuss the general reactions
of the motor unit to injury
2. Differentiate type 1 from
type 2 muscle fibers
3. Enumerate the major
categories of peripheral nerve
diseases.
4. Discuss the different diseases
of the peripheral nerve under
each category based on
etiology,
pathogenesis,
morphology & clinical features
5. Discuss the different diseases
of the neuromuscular junction
based
on
etiology,
pathogenesis, morphology &
clinical features
6. Enumerate the different
categories of diseases of the
skeletal muscles
7. Discuss the different diseases
of the skeletal muscle under
each category based on
etiology,
pathogenesis,
morphology & clinical features
Segmental demyelination, axonal degeneration & muscle
fiber atrophy, nerve regeneration & reinnervation of
muscle, reactions of the muscle
Characteristics of type 1 and type 2 muscle fibers
Inflammatory neuropathies, Infectious polyneuropathies,
Hereditary neuropathies, acquired metabolic & toxic
neuropathies, traumatic neuropathies
Guillain-Barre
syndrome,
Chronic
Inflammatory
Demyelinating polyradiculopathy, Leprosy, Varicella zoster
Diphtheria, Hereditary motor and sensory neuropathies,
Diabetes, Toxic neuropathies, Neuropathies associated with
malignancy, Traumatic neuropathies, Schwannomas,
Neurofibromas, Malignant Peripheral Nerve Sheath Tumor
Neurofibromatosis Type 1 and Type 2
Myasthenia Gravis, Lambert-Eaton Myasthenic syndrome
other diseases of NMJ
Skeletal Muscular Atrophy, Neurogenic and Myopathic
changes in skeletal muscle, Inflammatory myopathies, Toxic
myopathies, Inherited diseases of skeletal muscle
Skeletal Muscular Atrophy, Inflammatory myopathies
Dermatomyositis, Polymyositis, Inclusion body myositis
Infectious myositis, Toxic myopathies, Inherited diseases of
Skeletal muscle, Congenital myopathies, Duchenne and
Becker muscular dystrophy, Myotonic dystrophy, EmeryDreifuss Muscular dystrophy, Fascioscapulohumeral
dystrophy, Limb-Girdle Muscular dystrophy, Diseases of
Lipid or Glycogen metabolism, Mitochondrial myopathies
Spinal Muscular atrophy and differential diagnosis of a
hypotonic infant, Ion Channel Myopathies
This material is downloaded for Timothy Sam M. Valdez (20190107101)
at FEU Dr. Nicanor Reyes Medical Foundation.
For personal use only. No other uses without permission. All rights reserved.
Student able
to score 75%
or more in a
written
objective test;
Student able
to
identify
75% or more
of slides in
move practical
examination
Student able
to
contribute/par
ticipate
adequately in
the
clinicopathologic
discussion.
APPENDIX B
DEPARTMENT OF PATHOLOGY
GUIDELINES AND POLICIES IN PATHOLOGY B
Revised July 2020 for ONLINE course
TEXTBOOK
Robbins and Cotran Pathologic Basis of Diseases, Kumar, Abbas & Aster 10th edition
REFERENCE BOOKS
Wheater’s Basic Histopathology, Stevens, Lowe, Young 5th edition
Curran’s Atlas of Histopathology, 4th edition
REQUIREMENTS
Laboratory manual, to be purchased at the FEU-NRMF Bookstore
Lap Top/Smart phone/Tablet with provision for internet connectivity, preferably at least
2mbps.
Profile picture and Full Name in different platforms (Zoom, Telegram, Moodle, Zimbra)
ATTENDANCE
Will be checked during lecture and laboratory sessions
You will be marked LATE if you enter the chat room within 16-30 minutes of the
scheduled start of classes. You will be marked ABSENT if you enter the chat room 30
minutes after the scheduled start of classes.
If three absences are incurred, the re-admission slip needs to be secured from the
Department Chairman. An accumulated more than three absences (>20% of the total
number of subject hours), can be given a grade of “unauthorized widrawal”. This will
likewise be reported to the Office of the Dean.
LECTURE
Lectures will be conducted using ZOOM.
Instructional learning objectives per topic will be uploaded via Moodle.
LABORATORY
Images of the tissues will be provided by the subject coordinator one week prior to slide
orientation.
Each student will be assigned to prepare a report (etiology, pathogenesis, gross and
microscopic appearance, clinical features). The report will be graded accordingly
equivalent to one quiz. For lesions that were previously tackled, the presentation need
not be repeated again.
Activities during the laboratory: orientation of new slides, drawing and labeling of the
various lesions and answering guide questions in your manual. The camera needs to be
on as the Zoom classes are ongoing to show that the students are answering the
manuals after the reporting is conducted. Manuals will be submitted at the end of the
session.
SMALL GROUP DISCUSSION
SGD session will be conducted using ZOOM.
Three clinicopathologic (CPC) cases will be discussed during the semester. The case
protocol will be uploaded via Moodle
Each case will be discussed for three weeks:
o The first and third cases will be discussed in the following order:
1st week – Clinical discussion : During this session the student is
This material is downloaded for Timothy Sam M. Valdez (20190107101)
expected
toNicanor
know the
following
main clinical diagnosis, differential
at FEU Dr.
Reyes
Medical: Foundation.
diagnosis,
other
diseases
that may
be present,
clinicalreserved.
cause of death
For personal use
only. No
other
uses without
permission.
All rights
2nd week – Anatomic discussion : During this session, the student is
expected to enumerate the anatomic diagnosis per organ and the basis.
The diagnosis per organ will then be categorized as follows :
o
o
o
I : Disease causing death directly
II: Disease/s contributing or related to death by cause or effect
III: Significant disease/s not related to death but significant
enough to contribute to the death of the patient
IV: Incidental disease/s
V: Anatomic cause of death
3rd week – correlation of clinical and anatomic findings.
In the second case, the anatomic discussion will be conducted first before the
clinical discussion (reverse CPC).
Pretest will be given with MOODLE as platform
The class will be divided into small groups with delegated faculty proctor. The
students can volunteer to participate or the proctor may call the students
randomly. The participation in the discussion will be graded accordingly.
Correlation of Clinical and Anatomic Findings :
A type written flow chart will be conceptualized showing the sequence of events based
on the autopsy findings. The relationship of the autopsy findings with the clinical
presentation is established. The pathophysiology needs to be explained. The ancillary
procedures will also be discussed in correlation to the clinical and autopsy findings. This
is an individual work and needs to be uploaded as an assignment using Moodle.
Flow chart example:
65 year old male, smoker, known
hypertensive for 10 years
Renal Cortical Cyst
Left Ventricular Hypertrophy
Renal Cell Carcinoma
Necrosis, erosion of capsular
blood vessel distention
tumor growth in the upper
pole of the right kidney
tumor embolus
hematuria
costovertebral pain
abdominal mass
Massive Lung metastases
tumor cells obstruct flow of
air in the alveolar ducts
rales
flaring of ala nasi
accessory muscles of respiration
destruction of lung
contracts to help propel air in &
parenchyma
out of lungs
(decreased gas exchange)
intercostals & subcostal retractions
Peripheral respiratory failure
not enough oxygenated blood
goes to vital organs
Deathfor Timothy Sam M. Valdez (20190107101)
This material is downloaded
at FEU Dr. Nicanor Reyes Medical Foundation.
For personal use only. No other uses without permission. All rights reserved.
*Include supporting physical examination findings, laboratory results and autopsy findings
Categorization example:
I- Renal cell carcinoma with massive metastasis to the lung
II- Renal cell carcinoma metastatic to the liver and lung; bronchopneumonia
III- LVH
IV- Renal cortical cyst
V- Peripheral Respiratory Failure secondary to massive lung metastases of renal cell carcinoma
and a superimposed bronchopneumonia
EXAMINATIONS
Chapter exam (platings) on lecture topics will be given every Mondays
Preliminary examination will be composed of theoretical (90%) and laboratory (10%)
questions. Laboratory questions will be in the form of “objective structured projection
exam”.
The fault tolerant system will be used. You are expected to be online 15 minutes prior to
the start of examination.
Manuals must be uploaded before the start of the long exam via Moodle . Late
submission will have corresponding deductions.
Coverage of long examinations will be uploaded via Moodle.
Complete uniform (or white top with sleeves) must be worn. The laptop is the
recommended gadget to use in taking the examination. Other gadgets that are opened
which are caught on camera, or, images uploaded via telegram will be interpreted as an
act of cheating. Academic dishonesty in any form, such as follows: attempt to cheat,
assisting others to cheat or participating or engaging in such improper conduct is a
serious violation. This will result in nullification of the student’s exam and administrative
process will be initiated. Penalty for cheating/ attempt to cheat is dismissal from the
medical foundation (FEU-NRMF revised student code of conduct 2015). Examples of
improper conduct: looking at or copying from other student’s exam; using mechanical
aid that is not permitted; allowing other student to copy your answer; communicating
with another student during the exam; using unauthorized gadgets during the exam.
Use Telegram for any questions and clarification and the proctor/IT will assist you.
Make up of plating/s (excused) and long examination/s will be given within one week
after submission of e-mail addressed to the department chairman, through the subject
coordinator via Zimbra. Make-up examination may be in any format (essay,
identification, matching, etc.).
Answer key to examinations (short and long exam) will be made available via Moddle
after all students have submitted. The key can be challenged within twenty-four (24)
hours.
Moodle count is final.
GRADING
1st prelim
20%
Passing
> 75%
2nd prelim
20%
Removal
> 70 to < 75%
Finals
24%
Failure
< 70%
Platings
20%
Manual checking
2%
This
material is downloaded
for Timothy Sam M. Valdez (20190107101)
Lab Q
in plating
5%
at FEU Dr. Nicanor Reyes Medical Foundation.
CPC
9%
For personal use only. No other uses without permission. All rights reserved.
100%
Prepared by:
RONALD C. DY QUIANGCO, MD
Coordinator, Pathology B
Noted by:
Approved by:
ROGELDA G. BONGAT, MD, MHPEd, FPSP
Vice Chairman for Academic Affairs
MARI KARR A. ESGUERRA, MD, FPSP, MSPH
Department Chairman
---------------------------------------------------------------------------------------------------------------------------
AGREEMENT:
Date: __________________
I have read, explained to me, understood and will comply with the Pathology Department
Guidelines and Policies for Pathology B (revised July 2020).
PRINT the complete Name:
Student No.:
Signature: ______________________________ Section:_______Semester:______SY:_________
This material is downloaded for Timothy Sam M. Valdez (20190107101)
at FEU Dr. Nicanor Reyes Medical Foundation.
For personal use only. No other uses without permission. All rights reserved.