Part 2

Anatomic findings and anatomic diagnosis of different organs

LUNGS
Anatomic Findings:
Left and Right lung weight – over all, the lung weight is unusually increased, normal lung weight is
somewhere in the range of 820gm and that would include both lungs.
Crepitant is a sign of airway obstruction causing a crackling sound may be due to patients smoking
history, COPD or related to Anatomic Diagnosis of Pneumonia.
Black Discoloration is a sign of either minor areas of congestion or anthracnosis relating to patient’s
smoking background.
Basal portion involvement and red brown color is a good indication of Pneumonia as mentioned in
Harrisons since the bacteria would settle more on the lower part of the lungs, with the discoloration that
may be indicative of the transitioning phase of Pnemonia, specifically the red hepatization phase. The
light yellow viscid materials would most likely be purulent outcome of the infection.

Microscoping findings
Interalveolar septal widening is seen in passive congestion, as indicated that hyperemia is
mostly an increased active process causing dilation, why passive congestion is dealt with widening of the
vessels but causes a reduced blood flow due to infiltrates and action of cytokines as recruitment of
inflammatory cells.

The pink coagulate is a sign of edema formation as the congestion make cause leakage of
solutes to the interstitial spaces via congestion, hemosiderin laden macrophages’ negative presence
would rule out Chronic Passive Congestion in the patient.

Anatomic Diagnosis:
Acute Bacterial Pneumonia-Community Acquired type, congestive to red hepatization phase,
basal portion in both lung fields. The most common Pneumonia related respiratory cause is from Strep.
Pnuemoniae and the involvement of the lower respiratory system is most likely a sign of bacterial origin,
as M.tb is more related to apex infection, this also may have cause the basal congestion by increase
infiltrates causing reduced out flow. (Harrisons and Robbins)

Anthracosis, right and left lungs, this would be cause by patients smoking history and/or
exposure.

Aspiration Pneumonia, this could be the root of stressor as this would be an outcome of
gastrointestinal instances, allowing the lung exposure(repeated vomiting, GERD) to an acidic
environment by chemical irritation. ( Robbins chapter 15, page 708)
LIVER

Gross Findings
The liver weighs 1800 grams with blunted edges. The capsule is delicate, smooth, tense and
wet. Cut surfaces are red-brown, and bloody

-Normally the weight of liver is around 1400-1600 grams and the edge should be is soft, sharp,
and regular with a smooth surface, unlike the result of the gross findings which is liver in
enlarged with blunted ends Bluntness or rounding of its edge, and surface irregularity are
suspicious for liver disease. Cut surface of a normal liver should be brown in color.
-Right-sided cardiac decompensation leads to passive congestion of the liver. The liver is
slightly enlarged, tense, and cyanotic, with rounded edges.
-The cut surface of the liver has a variegated mottled red appearance, representing congestion
and hemorrhage in the centrilobular regions of the parenchyma.

Microscopic Findings

The central veins and sinusoids of the centrilobular region of the hepatic lobules are distended
with blood. The portal triads are widened by accumulation of fluid.

-Microscopically there is congestion of centrilobular sinusoids. Microscopic examination, the

centrilobular region is suffused with red blood cells and atrophied hepatocytes are not
easily seen. Portal tracts and the periportal parenchyma are intact.

Anatomic Diagnosis: Acute passive congestion

SPLEEN
Gross findings
Spleen weights 350 grams with smooth and tense capsule. The cut surface is bloody.

Microscopic
The red pulp are suffused with red blood cells. The white pulp are indistinct.

Normal(from robbins):150gm
Enclosed within a think, glistening, slate-gray connective tissue capsule.
Cut surface reveals extensive red pulp dotted with gray specks which are the white pulp
follicles.

Anatomic diagnosis: acute passive congestion

(ROBBINS): Congestion is a passive process resulting from reduced outflow of blood from a
tissue. It can be systemic, as in cardiac failure, or localized, as in isolated venous obstruction.
As a result of increased hydrostatic pressures, congestion commonly leads to edema ( kaya sya
lumaki 350grams).

In chronically congested tissues, capillary rupture can also produce small hemorrhagic foci.
( reason for bloody cut surface of the spleen...i think?)

SPLEEN BECOMES ENGORGED WITH BLOOD BECAUSE OF IMPAIRED FLOW TROUGH

THE SPLENIC VEIN WHICH EMPTIES TO THE PORTAL VEIN DUE TO A LIVER DISEASE
OR CONGESTIVE HEART FAILURE.
KIDNEYS
Gross Findings
The right and left kidneys weigh 160 grams and 80 grams, respectively. Both are covered with
moderate amount of fatty tissues. The capsule of the right is stripped with ease but with slight
difficulty in the left. The surface of the right kidney is smooth with two white, firm, depressed
areas, 0.4 cm and 0.8 cm. in diameter, with a single cyst 1.4 cm in diameter at the lower pole.
The cyst is translucent with clear fluid. The inner wall is smooth and glistening. The surface of
the left kidney is with several white, firm, depressed areas ranging from 0.2 cm to 1 cm in
diameter. The cut sections of the right kidney show well-delineated cortices and medullary
pyramids with scars in the lower pole. The left kidney has a slightly distorted renal papilla and
minor calyces and several scars from upper to lower poles.
✓ Left kidney weight loss: 80g (Normal weight: 125-200g)
✓ Right kidney shows scars in the lower pole; left kidney has a slightly distorted
renal papilla and minor calyces and several scars from upper to lower poles
(scarring may be caused by infection within the kidney tissue or from a urinary
tract infection)
Microscopic Findings
Sections from the scars of both kidneys show dilated tubules filled with colloid material
associated with tubular atrophy and extensive interstitial fibrosis with few mononuclear cells,
mostly lymphocytes.
Sections from the rest of the renal tissues disclose dilated tubules, predominantly the proximal
tubules, with damaged epithelium exhibiting coagulation necrosis alternating with lining
epithelium showing cellular swelling (skip areas of necrosis). Associated with these changes are
tubules occluded by cast, interstitial edema and accumulations of neutrophils within the dilated
vasa recta. The glomeruli are unremarkable.
Section from the cyst discloses fibrous wall lined by single layer of cuboidal to flatted epithelium.

✓ Tubular atrophy and extensive interstitial fibrosis (Interstitial fibrosis and tubular
atrophy (IF/TA) describes the histologic characteristics of allograft destruction over time.
IF can be defined as the accumulation of collagen and related molecules in the
interstitium.)

Anatomic Diagnosis:
Chronic pyelonephritis, focal right kidney
· Chronic tubulointerstitial inflammation and scarring involving the calyces and pelvis
· Hallmark: coarse, discrete, corticomedullary scars overlying dilated, blunted, or deformed
calyces, flattening of the papillae
· Scars most often located in the upper and lower poles
· Atrophy in some areas; hypertrophy or dilation in others
· Dilated tubules with flattened epithelium which may be filled with casts resembling thyroid
colloid (thyroidization)
· Varying degrees of chronic interstitial inflammation and fibrosis in cortex and medulla
· Arcuate and interlobular vessels demonstrate obliterative intimal sclerosis in the scarred
areas
· (+) HPN -> hyaline arteriosclerosis seen in the entire kidney
· Glomeruli appear normal except for a variety of ischemic changes, including periglomerular
fibrosis, fibrous obliteration, and secondary changes related to hypertension
Chronic pyelonephritis, multifocal, left kidney
Ischemic acute tubular necrosis, right and left kidneys
 · Ischemia due to decreased/interrupted blood flow (malignant HPN)
· Loss of cell polarity, d/t redistribution of membrane proteins from basolateral to luminal
surface of tubular cells -> abnormal ion transport across cells, increased sodium delivery
to distal tubules
· Focal tubular epithelial necrosis, with large skip areas in between, often accompanied by
rupture of basement membrane and occlusion of tubular lumens by casts
· Eosinophilic hyaline casts common
· Interstitial edema and accumulations of leukocytes within dilated vasa recta
· Evidence of epithelial regeneration in the form of flattened epithelial cells with
hyperchromatic nuclei and mitotic figures
Simple cyst, solitary, right kidney
· Common postmortem finding without clinical significance
· Translucent, lined by gray, glistening, smooth membrane, filled with clear fluid
· Membranes composed of single layer of cuboidal or flattened cuboidal epithelium, may be
completely atrophic
· Hemorrhage into cysts -> sudden distention and pain; calcification -> bizarre
radiographic shadows
STOMACH
Gross Findings
The rugae are pale, enlarged and doughy, irregularly covered with blood clots. A solitary
ulcer 2 cm in diameter partly filled with blood clots is seen located in the lesser curvature
between the body and antrum. The blood clot was removed from the ulcer and revealed round
to oval, sharply punched-out defect with straight wall, with the mucosal margins slightly raised
with the surrounding mucosa. The mucosa in the pylorus, antrum, body and fundus are
edematous.

Microscopic Findings
Section from the ulcer shows on-going necrosis, with neutrophilic infiltrates and debris.
The base of the ulcer is located within the submucosa up to the junction with the muscularis
layer. Submucosal blood vessels contain thrombi. The mucosa adjacent to the ulcer has
mononuclear cell infiltrates, predominantly lymphocytes, found in the lining epithelium and
lamina propia, accompanied by foci of intestinal metaplasia of the lining epithelium and loss of
gastric glands as evidenced by increased stroma.

Anatomic Diagnosis: Peptic ulcer disease, with active bleeding, lesser curvature, body,
stomach

Solitary ulcer partly filled with blood clot indicates an active bleeding. Bleeding came from
damage vessels within the bae of the ulcer. Round to oval, s sharply punched-out defect with
straight wall, with the mucosal margins slightly raised with the surrounding mucosa is a very
classic indication of peptic ulcer.
Neutrophilic infiltrates and debris at the base of the ulcer is located within the submucosa up to
the junction with the muscularis layer suggest of H. pylori infection.
Presence of mononuclear cell infiltrates at the lining epithelium and lamina propia,
accompanied by foci of intestinal metaplasia loss of gastric glands is suggestive of autoimmune
gastritis.
SMALL INTESTINES

DUODENUM 1ST PART

Gross findings
• Serosal surface is pale, smooth and slightly edematous with prominent congested blood
vessels.
• The lumen contained small amount of viscid fluid.
• Plicae circulares are pale and edematous.
• The mucosa shows a solitary ulcer 1 cm. in diameter, round to oval in shape, sharply
punched-out defect with straight wall.
• The mucosal margins are slightly raised with the surrounding mucosa. The surrounding
uninvolved mucosa are edematous.
Peptic ulcers are solitary in more than 80% of patients. Lesions less than 0.3 cm in diameter
tend to be shallow while those greater than 0.6 cm are likely to be deeper. The classic peptic
ulcer is a round to oval, sharply punched-out defect. The mucosal margin may overhang the
base slightly, particularly on the upstream side, but is usually level with the surrounding mucosa.
In contrast, heaped-up margins are more characteristic of cancers.

Microscopic findings
Transmural edema
• The base of the ulcer discloses inflammatory infiltrates, predominantly neutrophils.
• Beneath is a granulation tissue infiltrated by mononuclear cells, mostly lymphocytes, and rests
on a fibrous scar.
The base of peptic ulcers is smooth and clean as a result of peptic digestion of exudate. Active
ulcers may be lined by a thin layer of fibrinoid debris underlaid by a predominantly neutrophilic
inflammatory infiltrate. Beneath this, granulation tissue infiltrated with mononuclear leukocytes
and a fibrous or collagenous scar forms the ulcer base. Vessel walls within the scarred area are
typically thickened and are occasionally thrombosed.

Anatomic diagnosis:
Peptic Ulcer, first portion, duodenum - Peptic ulcer disease (PUD) refers to chronic mucosal
ulceration affecting the duodenum or stomach. Nearly all peptic ulcers are associated with H.
pylori infection, NSAIDs, or cigarette smoking. The most common form of peptic ulcer disease
(PUD) occurs within the gastric antrum or duodenum as a result of chronic, H. pylori- induced
antral gastritis, which is associated with increased gastric acid secretion, and decreased
duodenal bicarbonate secretion. PUD results from imbalances between mucosal defense
mechanisms and damaging factors that cause chronic gastritis

Duodenum, second, third, and fourth portion

Gross findings
• Edematous plicae circulares
The mucosa and submucosa (SM) of the small intestine form distinct projecting folds called
plicae circulares which encircle or spiral around the inner circumference and are best developed
in the jejunum. These circular folds function to increase absorption along the small intestines.

Microscopic findings
• Transmural edema
Edema of the intestinal mucosa may be due to inflammation of the first portion of the small
intestine due to peptic ulcer disease. this region fails to reabsorbed fluid properly resulting to
fluid accumulation along the unaffected portion of the small intestines.

Anatomic diagnosis: the rest of the small intestines are unremarkable.

 LARGE INTESTINES

Gross findings
• Edematous plicae criculares
Edema caused by increase hydrostatic pressure, decreased colloidal pressure and increased
vascular permeability.

Micrscopic findings
• There is edema involving the mucosa and submucosa. The serosal blood vessels are
prominent and congested.
Lesions can cause inflammation and vasodilation followed by increased vascular permeability
changes vascular flow increases blood flow which may result to congestion. Elevated
hydrostatic pressure or diminished colloid osmotic pressure, disrupts the balance resulting
increase movement fluid of the vessel, sodium and water retention causing edema

Anatomic diagnosis
Transmural edema and serosal congestion

The presence of multiple delineated areas results to lesions. The ulcer progresses often
elongates and oriented into the axis of the bowel. Causing sparing of interspersed mucosa
causing a coarsely textured, cobblestone appearance which depresses the tissue below the
level of the normal mucosa may result to fissures between the mucosal folds and extends
deeply to the fistula tracts or site of perforation resulting to transmural edema, inflammation,
submucosal fibrous and hypertrophy of the muscular propria. The wall becomes thick and
rubbery .

Anatomical death:
Combined effects of alterations in host interactions with intestinal microbiota, intestinal epithelial
dysfunction, aberrant mucosal immune responses, and altered composition of the gut
microbiome. Abundant neutrophils infiltrates and damage crypt epithelium. Repeated cycles of
crypt destruction and regeneration can lead to distortion of mucosal architecture. It can also
cause epithelial metaplasia and panted cell metaplasia and noncaseating granulomas.

AORTA

Anatomic Findings
• yellow to white intimacy plaques w/o acute plaque changes in thoracic segment
(PRECLINICAL)
Fatty streaks: Lipid filled foamy macrophages beginning as multiple minute flat yellow spots
eventually coalescing into elongated 1cm long or longer.

• Several yellow plaques, ulceration, fissures, erosions, few non occlusive thrombus, some
coalesce into large masses but without significant occlusion of the lumen (CLINICAL)
Surface of atheromatous plaques exposes highly thrombogenic substances which lead to
thrombosis that may partially or completely occlude the vessel lumen

Microscopic Findings
• Intimal damage associated with acute plaque changes covered with thrombus
Rupture, erosion, hemorrhage
• Fibrous capsules fissured-eroded-ulceration covered with thrombus
plaque like that ruptured and becomes an emboli
• Calcified lipid cores
Compressed and thinned tunica media
• Vascularized Basal Portion
Neovascularization
• Microscopic findings are typical of ATHEROSCLEROSIS

Anatomical Diagnoses
Uncomplicated atherosclerosis, thoracic aorta
Uncomplicated and Complicated atherosclerosis, abdominal aorta

Underlies the pathogenesis of coronary, cerebral, and peripheral vascular disease. These cause
intimal lesions called atheromas pr atheromatous or atherosclerotic plaques that protrude into
vessel lumens. Atheromatous plaques consist of a raised lesion with a soft core of lipid (made
of cholesterol) covered by a fibrous cap. These obstruct blood flow, and may rupture causing
obstructive vascular thrombosis. Risk factors for atherosclerosis cause endothelial cell
dysfunction and influence inflammatory cell and smooth muscle cell recruitment and stimulation.
Atherosclerotic plaques develop and grow slowly over decades. Stable plaques can produce
symptoms related to chronic ischemia by narrowing vessel lines where as unstable plaques can
cause dramatic and potentially fatal ischemic complications related to acute plaque rupture,
thrombosis, or embolization

HEART

Gross findings
A. The heart weighs 580 grams and is covered with moderate amount of fatty tissues.
Explanation: Normally, the heart measures 310 grams, in this case the heart measures
more than its normal size.
B. The left ventricular free wall thickness is 2 cm. while the right ventricular free wall is 0.5 cm.
Explanation: the normal measurement of LV is around 0.6-1.1 cm, whereas in this case, the
gross finding of the LV is 2 cm which indicates that there is hypertrophy of the cardiac cells,
while the RV is normal.
Microscopic findings
A. Section from the completely occluded portion of the left anterior descending branch of the
coronary artery shows atheromatous plaque beneath a disrupted endothelium of the tunica
intima and a fissured fibrous cap covered by occlusive thrombus.
Explanation: the reason for this is there accumulation of material in the inner layer of the
wall of an artery, the material consists of mostly macrophage cells, or debris,containing lipids
and calcium.
B. Capillaries in the endomysium are compressed by the enlarged myocytes.
Explanation: since, there is hypertrophy of the myocytes, blood vessels like capillaries
tend to be compressed, thus, there would be reduced in blood flow.

Anatomic Diagnosis:
A. Myocardial infarct, transmural- refers to a myocardial infarction that involves the full
thickness of the myocardium.
B. Myocardial infarct, subendocardial- the ECG sign of subendocardial ischemia is ST
segment depression. Depression is reversible if ischemia is only transient but
depression persists if ischemia is severe enough to produce infarction.
C. Myocardial hypertrophy- as seen in this case, there is enlargement and thickening
(hypertrophy) of the walls of your heart's main pumping chamber (left ventricle). Left
 ventricular hypertrophy can develop in response to some factor such as high blood
pressure or a heart condition that causes the left ventricle to work harder.

Anatomic cause of death

Aspiration Pneumonia, this could be the root of stressor as this would be an outcome of gastrointestinal
instances, allowing the lung exposure(repeated vomiting, GERD) to an acidic environment by chemical
irritation. ( Robbins chapter 15, page 708)

Clinico-pathologic correlation

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