3. GROSS CLINICAL MANIFESTATION
HUMAN HYPERPLASIA
OF PROSTATE SEC.
Urinary frequency
Urinary urgency
Nocturia- Needing to get up frequently at night to
urinate
Hesitancy - Difficulty initiating the urinary stream;
interrupted, weak stream
Incomplete bladder emptying - The feeling of
persistent residual urine, regardless of the frequency
of urination
Straining - The need strain or push (Valsalva
maneuver) to initiate and maintain urination in order
to more fully empty the bladder
Decreased force of stream - The subjective loss of
force of the urinary stream over time
Dribbling - The loss of small amounts of urine due to a
poor urinary stream as well as weak urinary stream
Nodular hyperplastia results from an overgrowth of glandular and
fibromuscular tissues in the central (preurethral) region of the prostate. The
cause of hyperplasia is not exactly known, but it is probably related to the
action of dihydrotestosterone, a derivative of testosterone
5. HUMAN HYPERPLASIA
OF PROSTATE SEC.
Chapter 21: The Lower Urinary Tract and Male Genital System |
BPH (also referred to as nodular hyperplasia) is the most common
benign prostatic disease in men older than age 50 years.
Approximately 30% of white American men in that age group have
moderate to severe symptoms of BPH, and histologic evidence of
BPH is found in up to 90% of men by age 80. It is not a
premalignant lesion.
CHAPTER 21
6. GROSS CLINICAL MANIFESTATION
SQUAMOUS METAPLASIA OF
BRONCHUS SEC.
Wheezing.
Coughing up blood (hemoptysis).
Hoarseness.
Loss of appetite.
Unexplained weight loss.
Unexplained fatigue (tiredness).
The tumor surface is whitish-gray often speckled with black deposits of
anthracotic pigment. There are soft, friable areas of necrosis which
frequently cause central cavitation within the tumor.
8. SQUAMOUS METAPLASIA OF
BRONCHUS SEC.
Chapter 15: The Lung | COPD, a major public health problem, is defined by the World Health
Organization (WHO) as “a common, preventable and treatable disease that is characterized by
persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar
abnormalities caused by exposure to noxious particles or gases.” t is currently the fourth leading
cause of death in the world and is projected to rank third by 2020 due to increases in cigarette
smoking in countries such as China. There is a strong association between heavy cigarette smoking
and COPD. Overall, 35% to 50% of heavy smokers develop COPD; conversely about 80% of COPD is
attributable to smoking. Women and African Americans who smoke heavily are more susceptible
than other groups. Additional risk factors include poor lung development early in life, exposure to
environmental and occupational pollutants, airway hyperresponsiveness, and certain genetic
polymorphisms. Recognizing that emphysema and chronic bronchitis often occur together in
patients with COPD, it is still useful to discuss these patterns of lung injury and associated
functional abnormalities individually to highlight the pathophysiologic basis of different causes of
airflow obstruction. We will finish our discussion by returning to the clinical features of COPD.
CHAPTER 15
9. GROSS CLINICAL MANIFESTATION
VITREOUS DEGENERATION OF
RENAL ARTERIOLE SEC.
Sudden onset of hypertension.
Hypertension not responsive to three or
more blood pressure medications.
Increased urea (waste product excreted by
the kidneys) in the blood.
Unexplained kidney failure
Infiltration, interstitial fibrosis, and renal interstitial edema; and
renal arteriolar lesions: renal intimal thickening and vitreous
degeneration.
11. VITREOUS DEGENERATION OF
RENAL ARTERIOLE SEC.
Chapter 20: The Kidney | Chronic kidney disease (previously
called chronic renal failure) is defined as the presence of a
diminished GFR that is persistently less than 60 mL/min/1.73 m2
for at least 3 months, from any cause, and/or persistent
albuminuria. It may present with a clinically silent decline in renal
excretory function in milder forms or with prolonged symptoms
and signs of uremia in more severe cases. It is the end result of all
chronic renal parenchymal diseases.
CHAPTER 20
12. GROSS CLINICAL MANIFESTATION
HUMAN FIBRINOID
DEGENERATION SEC.
Nosebleeds
Bleeding gums
Blood in the urine
Blood in the stool
Muscle bruises
Hemorrhage of the spleen and other
organs
arteriole walls are thickened. The resulting reduced renal blood
flow causes chronic ischaemia and gradual atrophy of the tubules.
These lesions are generally not detected grossly
14. HUMAN FIBRINOID
DEGENERATION SEC.
Chapter 20: The Kidney | Chronic kidney disease (previously
called chronic renal failure) is defined as the presence of a
diminished GFR that is persistently less than 60 mL/min/1.73 m2
for at least 3 months, from any cause, and/or persistent
albuminuria. It may present with a clinically silent decline in renal
excretory function in milder forms or with prolonged symptoms
and signs of uremia in more severe cases. It is the end result of all
chronic renal parenchymal diseases.
CHAPTER 20
15. GROSS CLINICAL MANIFESTATION
HUMAN TISSUE SYSTEM
HISTIOCYTOSIS
rash on the scalp
pain in a bone
discharge from the ear
loss of appetite
fever
Abdominal area of an infant with multiple erythematous
papules covered by scale and/or crust.
17. HUMAN TISSUE SYSTEM
HISTIOCYTOSIS
CHAPTER 13: Diseases of White Blood Cells, Lymph Nodes, Spleen, and
Thymus | The term histiocytosis is an “umbrella” designation for a variety
of proliferative disorders of dendritic cells or macrophages. Some, such as
rare “histiocytic” sarcomas, are clearly malignant, whereas others, such as
reactive proliferations of macrophages in lymph nodes, are clearly benign.
Lying between these two extremes are the Langerhans cell histiocytoses, a
spectrum of clonal proliferations of a special type of immature dendritic
cell called the Langerhans cell. Because Langerhans cells are part of the
innate immune system, these tumors (as well as other clonal
histiocytoses) can be considered unusual myeloid neoplasms.
CHAPTER 13
18. GROSS CLINICAL MANIFESTATION
HUMAN BRONCHIECTASIS
SEC.
Cough and daily mucopurulent sputum
production, often lasting months to years
(classic)
Blood-streaked sputum or hemoptysis
from airway damage associated with
acute infection
Dyspnea, pleuritic chest pain, wheezing,
fever, weakness, fatigue, and weight loss
Rarely, episodic hemoptysis with little to
no sputum production (ie, dry
bronchiectasis)
focal area of dilated bronchi extending to the pleural surface, typical
of localized bronchiectasis. Bronchiectasis tends to be localized with
disease processes such as neoplasms and aspirated foreign bodies
that block a portion of the airways
20. HUMAN
BRONCHIECTASIS SEC.
Chapter 15: The Lung | Bronchiectasis is a disorder in which destruction of smooth muscle and
elastic tissue by inflammation stemming from persistent or severe infections leads to permanent
dilation of bronchi and bronchioles. Because of better control of lung infections, bronchiectasis is
now uncommon, but may still develop in association with the following: • Congenital or hereditary
conditions that predispose to chronic infections, including cystic fibrosis, intralobar
sequestration of the lung, immunodeficiency states, primary ciliary dyskinesia, and Kartagener
syndrome. • Severe necrotizing pneumonia caused by bacteria, viruses, or fungi; this may be a
single severe episode or recurrent infections. • Bronchial obstruction, due to tumor, foreign body,
or mucus impaction; in each instance the bronchiectasis is localized to the obstructed lung
segment. • Immune disorders, including rheumatoid arthritis, systemic lupus erythematosus,
inflammatory bowel disease, and the posttransplant setting (chronic rejection after lung
transplant and chronic graft-versus-host disease after hematopoietic stem cell transplantation). •
Up to 50% of cases are idiopathic, lacking the aforementioned associations, in which there
appears to be dysfunctional host immunity to infectious agents leading to chronic inflammation
CHAPTER 15
21. GROSS CLINICAL MANIFESTATION
HUMAN PATHOLOGIC
CALCIFICATION SEC.
Angina,
Congestive heart failure
Syncope
nodularity and thickening of this valve. This valve would be extremely
stiff and almost entirely immobile.
23. HUMAN PATHOLOGIC
CALCIFICATION SEC.
Chapter 2: Cell Injury, Cell Death, and Adaptations I Pathologic
calcification is the abnormal tissue deposition of calcium salts, together
with smaller amounts of iron, magnesium, and other mineral salts. There
are two forms of pathologic calcification. When the deposition occurs
locally in dying tissues, it is known as dystrophic calcification; it occurs
despite normal serum levels of calcium and in the absence of
derangements in calcium metabolism. In contrast, the deposition of
calcium salts in otherwise normal tissues is known as metastatic
calcification, and it almost always results from hypercalcemia secondary
to some disturbance in calcium metabolism.
CHAPTER 02
24. GROSS CLINICAL MANIFESTATION
HUMAN RENAL TUBULE
EPITHELIUM EDEMA SEC.
Oliguria
Edema
Fatigue
shortness of breath
confusion, nausea
seizures or coma
chest pain or pressure
Shows cellular swelling of the organ. Note that the kidney appears
pale, swollen and has a parboiled appearance. Also note the bulging
cortex
26. HUMAN RENAL TUBULE
EPITHELIUM EDEMA
SEC.
Chapter 4: Hemodynamic Disorders, Thromboembolic Disorders and Shock I
Factors influencing fluid movement across capillary walls. Normally,
hydrostatic and osmotic forces are nearly balanced so that there is little
net movement of fluid out of vessels. Many different pathologic disorders
are associated with increases in capillary hydrostatic pressure or
decreases in plasma osmotic pressure that lead to the extravasation of
fluid into tissues. Lymphatic vessels remove much of the excess fluid, but
if the capacity for lymphatic drainage is exceeded, tissue edema results.
CHAPTER 4
27. GROSS CLINICAL MANIFESTATION
HEMORRHAGIC INFARCT OF
LUNG
Dyspnea
Chest pain
Swelling or pain in unilateral
lower extremity
fever
Hemoptysis
red infarct is wedge-shaped and based on the pleura. These infarcts
are hemorrhagic because, though the pulmonary artery carrying most
of the blood and oxygen is cut off, the bronchial arteries from the
systemic circulation
29. HEMORRHAGIC
INFARCT OF LUNG SEC.
Chapter 4: Hemodynamic Disorders, Thromboembolic Disorders and Shock I
With further passage of time, infarcts resulting from arterial occlusions in
organs without a dual blood supply typically become progressively paler
and more sharply defined. In comparison, in the lung hemorrhagic infarcts
are the rule. Extravasated red cells in hemorrhagic infarcts are
phagocytosed by macrophages, which convert heme iron into hemosiderin;
small
CHAPTER 4
30. GROSS CLINICAL MANIFESTATION
RENAL ANEMIC INFARCT
Abdominal or flank pain
Nausea and vomiting
Hematuria
Fever
Note the wedge shape of this zone of coagulative necrosis resulting
from loss of blood supply with resultant tissue ischemia that
produces the pale infarct.
32. RENAL ANEMIC
INFARCT SEC.
Chapter 4: Hemodynamic Disorders, Thromboembolic Disorders and
Shock I White infarcts happens in this organ. This occur with arterial
occlusions in solid organs with end-arterial circulation (e.g., heart,
spleen, and kidney), and where tissue density limits the seepage of
blood from adjoining capillary beds into the necrotic area.
CHAPTER 4
33. GROSS CLINICAL MANIFESTATION
PULMONARY EDEMA
Coughing up blood or bloody
froth.
Difficulty breathing when lying
down (orthopnea)
Feeling of "air hunger" or
"drowning"
The reddish coloration of the tissue is due to congestion. Some
normal pink lung tissue is seen at the edges of the lungs
35. PULMONARY EDEMA
SEC.
Chapter 15: The Lung | Pulmonary edema (excessive interstitial fluid in
the alveoli) can result from hemodynamic disturbances (cardiogenic
pulmonary edema) or increased capillary permeability due to
microvascular injury (non-cardiogenic pulmonary edema) (Table 15.1). A
general consideration of edema is given in Chapter 4, and pulmonary
congestion and edema are described briefly in the context of congestive
heart failure (Chapter 12). Whatever the clinical setting, pulmonary
congestion and edema produce heavy, wet lungs. Therapy and outcome
depend on the underlying etiology.
CHAPTER 15
36. GROSS CLINICAL MANIFESTATION
PULMONARY AMNIOTIC
EMBOLISM
Pleuritic chest pain (sharp &
stabbing pain, well localised,
exacerbated by deep
inspiration)
Breathlessness
Haemoptysis
Collapse
Tachycardia
Hypotension
Gross natural color close-up of meaty cut surface with deep blue
appearance through pleura looks like diffuse alveolar damage
38. PULMONARY AMNIOTIC
EMBOLISM SEC.
Chapter 4: Hemodynamic Disorders, Thromboembolic Disease, and Shock
I Pulmonary emboli originate from DVT and are the most common form of
thromboembolic disease. PE is a common and serious disorder with an
estimated incidence of 100 to 200 cases per 100,000 people in the
United States. It is somewhat more common in males than in females. PE
causes about 100,000 deaths per year in the United States. An
estimated 20% of individuals with PE die before or shortly after a
diagnosis is made. In more than 95% of cases, PE originates from leg
DVT. Hence the risk factors for PE are the same as for DVT
CHAPTER 4
39. GROSS CLINICAL MANIFESTATION
HUMAN INFARCT OF THE
BRAIN
Sudden numbness or weakness in the
face, arm, leg, especially on one side
of the body
Confusion, trouble speaking or
difficulty understanding speech
Trouble seeing in one or both eyes
Trouble walking, dizziness, loss of
balance, or lack of coordination
Severe headache with no known
cause
edema which obscures the structures. The acutely edematous
infarcted tissue may produce a mass effect. Note the decrease in size
of the ventricle on the left with shift of the midline.
41. HUMAN INFARCT OF
THE BRAIN
Chapter 28: The Central Nervous System | Stroke” is the clinical
designation applied to these conditions and is defined as neurologic
signs and symptoms that can be explained by a vascular mechanism,
have an acute onset, and persist beyond 24 hours. Major mechanism
involves Ischemia and/or hypoxia resulting from impairment of blood
supply and oxygenation of CNS tissue. This can be either a global or
focal process, with the clinical manifestations determined by the region
of brain affected. In the brain, embolism is a more common cause of
vascular occlusion than thrombosis.
CHAPTER 28
42. GROSS CLINICAL MANIFESTATION
INTRAVENOUS THROMBI SEC.
Sudden shortness of breath
Chest pain or discomfort that
worsens when taking a deep breath
or when coughing
Lightheadedness or dizziness
Fainting
Rapid pulse
Rapid breathing
Hematemesis
dark red thrombus is apparent in the lumen . The plaques of atheroma
narrow this coronary significantly, and the thrombus occludes it
completely.
44. INTRAVENOUS
THROMBI SEC
Chapter 4: Hemodynamic Disorders, Thromboembolic Disease, and Shock
| The primary abnormalities that lead to thrombosis are (1) endothelial
injury, (2) stasis or turbulent blood flow, and (3) hypercoagulability of
the blood (the so-called Virchow triad) (Fig. 4.12). Thrombosis is one of
the scourges of modern man, because it underlies the most serious and
common forms of cardiovascular disease. Here, the focus is on its
causes and consequences; its role in cardiovascular disorders is
discussed in detail in Chapters 11 and 12
CHAPTER 4
45. GROSS CLINICAL MANIFESTATION
ADENOCARCINOMA OF LYMPH
GLAND SEC
Painless swelling of lymph nodes in
your neck, armpits or groin.
Persistent fatigue.
Fever.
Night sweats.
Shortness of breath.
Unexplained weight loss.
Itchy skin
Gross natural color obvious tumor with necrosis and anthracotic
pigment 44yo BF adenocarcinoma of lung giant cell type
47. ADENOCARCINOMA OF
LYMPH GLAND SEC
Chapter 15: The Lungs I Typical carcinoids have fewer than two mitoses
per 10 high-power fields and lack necrosis, while atypical carcinoids
have between two and 10 mitoses per 10 high-power fields and/or foci of
necrosis. Atypical carcinoids also show increased pleomorphism, have
more prominent nucleoli, and are more likely to grow in a disorganized
fashion and invade lymphatics
CHAPTER 15
48. GROSS CLINICAL MANIFESTATION
MALIGNANT LYMPHOMA SEC
Rapidly growing neck mass
Compression symptoms including
dysphagia and hoarseness
Can present with diffuse thyroid
enlargement
May be accidentally discovered
Hypothyroid manifestations may
develop
Cold nodule
Variable sized, rubbery / soft mass
White cut surface with fish flesh appearance
Necrosis could be found
50. MALIGNANT LYMPHOMA
SEC
Chapter 12: The Heart I Bronchogenic carcinoma or malignant lymphoma
can infiltrate the mediastinum extensively, causing encasement,
compression, or invasion of the superior vena cava with resultant
obstruction to blood coming from the head and upper extremities
(superior vena cava syndrome)
CHAPTER 12
51. GROSS CLINICAL MANIFESTATION
SPLENIC INFARCTION SEC
The most common presenting symptom
is left-upper-quadrant abdominal pain
(up to 70%). Additional symptoms
include fever and chills, nausea and
vomiting, pleuritic chest pain, and left
shoulder pain (Kehr sign).
splenic infarcts in a patient with infective endocarditis. Portions of
the vegetations have embolized to the spleen. These infarcts are
typical of ischemic infarcts: they are based on the capsule, pale, and
wedge-shaped. The remaining splenic parenchyma appears dark red.
53. SPLENIC INFARCTION
SEC
Chapter 13: Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus |
This splenic infarct ( ) is a consequence of systemic arterial embolization in a
patient with infective endocarditis involving either aortic or mitral valve.
Clinical findings include left upper quadrant pain and splenic enlargement.
Portions of the friable vegetations have embolized to the spleen through the
splenic artery branch from the celiac axis and then to the peripheral splenic
artery branches. Most splenic infarcts are ischemic and caused by emboli
from either vegetations on valves or mural thrombi in the heart. They are
based on the capsule, pale, and wedge shaped. The remaining splenic
parenchyma of dark red pulp has pinpoint pale malpighian corpuscles of
white pulp.
CHAPTER 13
54. GROSS CLINICAL MANIFESTATION
MYOCARDIAL INFARCTION
SEC
Chest pain or discomfort. ...
Feeling weak, light-headed, or faint
Pain or discomfort in the jaw, neck,
or back.
Pain or discomfort in one or both
arms or shoulders.
Shortness of breath.
anterior left ventricular free wall and septum in cross section. Note
that the infarction is nearly transmural. There is a yellowish center
with necrosis and inflammation surrounded by a hyperemic border.
56. MYOCARDIAL
INFARCTION SEC
Chapter 12: The Heart | MI, also commonly referred to as “heart attack,” is the death of
cardiac muscle due to prolonged ischemia. Roughly 1.5 million individuals in the United
States suffer an MI each year, causing approximately 610,000 deaths annually. The
major underlying cause of IHD is atherosclerosis; although MIs can occur at virtually
any age, 10% of MIs occur in people younger than 40 years of age, and 45% occur in
people younger than 65 years of age. Nevertheless, the frequency rises progressively
with increasing age and with increasing atherosclerotic risk factors (Chapter 11).
Through middle age, male gender increases the relative risk of MI; indeed, women are
generally protected against MI during their reproductive years. However,
postmenopausal decline in estrogen production is usually associated with accelerated
CAD, and IHD is the most common cause of death in older women. Unfortunately,
postmenopausal hormonal replacement therapy has not been shown to be protective,
and in fact, in some cases, may be detrimental.
CHAPTER 12
57. GROSS CLINICAL MANIFESTATION
LIVER ABCESS SEC
Pain right hypochondrium referred to
the right shoulder
Pyrexia (100.4 F)
Profuse sweating and rigors
Loss of weight
Earthy complexion
Gross specimen of liver tissue with an abscess (white) that formed
due to infection of the organ with Entamoeba histolytica
59. LIVER ABCESS SEC
Chapter 18: Liver and Gallbladder | More than 95% of biliary tract disease is
attributable to gallstones. Gallstones afflict 10% to 20% of adult populations
in high income countries. It is estimated that more than 20 million persons in
the United States have gallstones, totaling some 25 to 50 tons in weight,
leading to more than 700,000 cholecystectomies performed annually at a
cost of approximately $6 billion.
CHAPTER 18
60. GROSS CLINICAL MANIFESTATION
NEPHRAPOSTASIS SEC
Severe pain in your back or side that
will not go away.
Blood in your urine.
Fever and chills.
Vomiting.
Urine that smells bad or looks
cloudy.
A burning feeling when you urinate.
Tumor is typically circumscribed , and unencapsulated with a tan,
myxoid cut-surface.
62. NEPHRAPOSTASIS SEC
Chapter 8: infectious disease I Invasive candidiasis is caused by
blood-borne dissemination of organisms to various tissues or organs.
Common patterns include (1) renal abscesses, (2) myocardial
abscesses and endocarditis, (3) brain microabscesses and meningitis,
(4) endophthalmitis (virtually any eye structure can be involved), and
(5) hepatic abscesses.
CHAPTER 08
63. GROSS CLINICAL MANIFESTATION
LUNG ABSCESS
Fatigue
Loss of appetite
Sweating during the night
Fever
A cough that brings up sputum
There are adjacent areas of tan consolidation with bronchopneumonia.
Abscesses are often complications of aspiration, where they appear
more frequently in the right posterior lung.
65. LUNG ABSCESS SEC
Chapter 15: The Lung I The term pulmonary abscess describes a local
suppurative process that produces necrosis of lung tissue. Under
appropriate circumstances any bacterial pathogen can produce an
abscess; those that do so most commonly include aerobic and
anaerobic streptococci, S. aureus, and a host of gram-negative
organisms. Mixed infections often occur because of the important
causal role played by inhalation of foreign material. Anaerobic
organisms normally found in the oral cavity, including members of the
Bacteroides, Fusobacterium, and Peptococcus genera, are the
exclusive isolates in about 60% of cases.
CHAPTER 15
66. GROSS CLINICAL MANIFESTATION
CHRONIC PYELONEPHRITIS
SEC
chills.
fever.
pain in your back, side, or groin.
nausea.
vomiting.
cloudy, dark, bloody, or foul-smelling
urine.
frequent, painful urination.
The renal pelvis and ureter are markedly dilated. The calyces are
irregular and the papillae are blunted. The renal cortex and medulla
are irregular in shape and thickness, and their normal architecture is
disrupted by whitish-yellow areas of fibrosis.
68. CHRONIC
PYELONEPHRITIS SEC
Chapter 20: The Kidney | Chronic pyelonephritis is a disorder in which
chronic tubulointerstitial inflammation and scarring involve the
calyces and pelvis (Fig. 20.30). Although several diseases produce
chronic tubulointerstitial alterations (see Table 20.8), only chronic
pyelonephritis and analgesic nephropathy affect the calyces, making
pelvocalyceal damage an important diagnostic clue. Chronic
pyelonephritis at one time accounted for 10% to 20% of patients in
renal transplant or dialysis units, until predisposing conditions such
as reflux became better recognized. This condition remains an
important cause of kidney destruction in children with severe lower
urinary tract abnormalities
CHAPTER 20
69. GROSS CLINICAL MANIFESTATION
LOBSTER PNEUMONIA
Cough, which may produce greenish,
yellow or even bloody mucus.
Fever, sweating and shaking chills.
Shortness of breath.
Rapid, shallow breathing.
Sharp or stabbing chest pain that
gets worse when you breathe deeply
or cough.
Loss of appetite, low energy, and
fatigue.
This is a lobar pneumonia in which consolidation of the entire left
upper lobe has occurred
71. ADENOCARCINOMA OF
LYMPH GLAND SEC
Chapter 15: The Lungs I Typical carcinoids have fewer than two mitoses
per 10 high-power fields and lack necrosis, while atypical carcinoids
have between two and 10 mitoses per 10 high-power fields and/or foci of
necrosis. Atypical carcinoids also show increased pleomorphism, have
more prominent nucleoli, and are more likely to grow in a disorganized
fashion and invade lymphatics
CHAPTER 15
72. LOBSTER PNEUMONIA
Chapter 15: The Lungs I Pneumonia can result whenever these local defense mechanisms
are impaired or the systemic resistance of the host is lowered. Factors that impair
resistance include chronic diseases, immunologic deficiencies, treatment with
immunosuppressive agents, and leukopenia. Local pulmonary defense mechanisms may
also be compromised by many factors, including: • Loss or suppression of the cough reflex,
as a result of altered sensorium (e.g., coma), anesthesia, neuromuscular disorders, drugs,
or chest pain, any of which may lead to aspiration of gastric contents. • Dysfunction of the
mucociliary apparatus, which can be caused by cigarette smoke, inhalation of hot or
corrosive gases, viral diseases, or genetic defects of ciliary function (e.g., immotile cilia
syndrome). • Accumulation of secretions in conditions such as cystic fibrosis and
bronchial obstruction. • Interference with the phagocytic and bactericidal activities of
alveolar macrophages by alcohol, tobacco smoke, anoxia, or oxygen intoxication. •
Pulmonary congestion and edema.
CHAPTER 15
73. GROSS CLINICAL MANIFESTATION
LOBAR PNEUMONIA
grossly heavy and boggy appearing
lung tissue
diffuse congestion
vascular engorgement
accumulation of alveolar fluid rich in
infective organisms
gross appearance of a lipid pneumonia in which there is an ill-defined,
pale yellow area on the left. This yellow appearance explains the term
"golden" pneumonia.
75. LOBAR PNEUMONIA
Chapter 15: The Lung | In lobar pneumonia, four stages of the inflammatory response have
classically been described: congestion, red hepatization, gray hepatization, and resolution. In the
first stage of congestion, the lung is heavy, boggy, and red. It is characterized by vascular
engorgement, intra-alveolar edema fluid containing a few neutrophils, and the presence of
bacteria, which may be numerous. In the next stage of red hepatization, there is massive confluent
exudation, as neutrophils, red cells, and fibrin fill the alveolar spaces (Fig. 15.35A). On gross
examination, the lobe is red, firm, and airless, with a liver-like consistency, hence the name
hepatization. The third stage of gray hepatization is marked by progressive disintegration of red
cells and the persistence of a fibrinosuppurative exudate (Fig. 15.35B), resulting in a color change
to grayish-brown. In the final stage of resolution, the exudate within the alveolar spaces is broken
down by enzymatic digestion to produce granular, semifluid debris that is resorbed, ingested by
macrophages, expectorated, or organized by fibroblasts growing into it (Fig. 15.35C). Pleural
fibrinous reaction to the underlying inflammation, often present in the early stages if the
consolidation extends to the lung surface (pleuritis), may similarly resolve. More often it
undergoes organization, leaving fibrous thickening or permanent adhesions.
CHAPTER 15
76. GROSS CLINICAL MANIFESTATION
ACUTE NEPHRITIS SEC
foamy urine and edema
pain in the pelvis.
pain or a burning sensation while
urinating.
a frequent need to urinate.
cloudy urine.
atrophic kidneys with a thin cortex from a patient at autopsy with
chronic renal failure (CRF)
78. ACUTE NEPHRITIS SEC
Chapter 20: The Kidney | Manifestation of Rapidly progressive
glomerulonephritis, together with proteinuria, and acute renal failure
CHAPTER 20
79. In many of the lectures of my first half we were
being shown lots of techniques and figures of
tissues that didn't involve us using the use of
microscopes and tend to focus on a more
theoretical and academic discussion
on the second half, it is very exciting for us to actually
see tissues under the microscope. Pathologists can say
that we are approaching a new adventure of our life
time. Proper microscope use is one of the most
important skills that we should learn first and later the
most crucial part is interpreting what we see under the
microscope.
REFLECTION
ADRIAN CABALLES
ADRIAN CABALLES
