Hemotoxylin(Blue) and • Acid dyes stain basic structures:

Eosin (Pink) (proteins, membranes, and

cytoplasm). The commonest acid
dye is eosin; it is pink
• Basic dyes stain acid structures:
Nucleic acids (RNA, DNA, rER,
nuclei). The commonest basic dye is
hematoxylin; it is blue

Myelin Figures • Dead cells are replaced by whorled

phospholipid masses known as
Myelin figures(damaged cell
membrane).

Necrosis • Necrotic cells show increased

eosinophilia in H&E stained sections
due to – loss of RNA(binds the blue
dye, hematoxylin) & denaturation
of proteins(binds the red dye,
eosin).
• Cytoplasm has glassy, homogenous
appearance- loss of glycogen.
•

Councilman bodies Dead hepatocytes in viral hepatitis

Psammoma bodies  Apoptosis of a neoplastic cell with
subsequent calcification
 Psammoma bodies are seen in
 Papillary carcinoma of
thyroid
 papillary
cystadenocarcinoma of the
ovary
 meningioma

Fatty change/Steatosis • Also known as fatty metamorphosis.

• Fatty Change in Heart:
• Causes:
– Prolonged hypoxia (severe
anemia)
– Diphtheria toxin (decreased
beta oxidation of FA).
• Alcohol is the MCC of fatty change in
the liver: 3 reasons
1. Increased glycerol 3
phosphate synthesis

Differentiate between
glycogen and water
1.
Foamy Macrophages
Russell bodies (Intracellular
hyaline)
Mallory Alcoholic hyaline
(intracellular hyaline)
•
Due to increased
reduced NADH
2. Increased acetyl CoA due to
increased acetate
Increased FA synthesis
3. Decreased beta oxidation of
FA
• Other causes include:
• Kwashiorkor (Decreased Protein
intake)
1. Decreased synthesis of
apolipoproteins
• Starvation
1. Increased mobilization of FA
from adipose tissue
• CCL4 and
Reye’s syndrome: Fatty change in the liver
caused after eating aspirin by viral illness.
Stain for lipid : Oil red O and Sudan IV
Stain for glycogen : PAS
Periodic acid–Schiff–diastase (PAS-D, PASdiastase) stain is periodic acid–Schiff
(PAS)stain used in combination with diastase, an enzyme that breaks down
glycogen. PAS-D is a stain often used by pathologists as an ancillary study in
making a histologic diagnosis on paraffin-embedded tissue specimens.
*Seen in Xanthomas and hereditary
hyperlipidemic states
*Cholesterolosis (Focal accumulation of
cholesterol laden macrophages in the lamina
propria of the gall bladder)
Hyaline change seen in plasma cells.
Russell bodies are eosinophilic, large, homogenous
immunoglobulin-containing inclusions usually found in a plasma cell undergoing
excessive synthesis of immunoglobulin; the Russell body is characteristic of the
distended endoplasmic reticulum.
Plasmacytoma with
Russell bodies
 Mallory's hyaline, is an inclusion found in the cytoplasm of liver
cells. Mallory bodies are damaged intermediate filaments within

the hepatocytes.
They are a recognized feature of Wilson's disease (25%), primary
biliary cirrhosis (24%), non-alcoholic cirrhosis (24%), Hepatocellular
carcinoma (23%) and morbid obesity (8%), among other conditions
 Mallory bodies are highly eosinophilic and thus appear pink on H&E
stain. The bodies themselves are made up of intermediate
cytokeratin 8&18 filament proteins that have been ubiquinated, or
bound by other proteins such as heat shock proteins, or p62
Hyaline • Refers to arterioles that have a
arteriolosclerosis(Extracellu glassy, amorphous appearing
lar hyaline) eosinophilic material in the vessel
wall that often narrows the lumen
• Seen in small vessels in
– DM and hypertension.
Pathogenesis: increased protein is deposited in the vessel
wall that occludes the lumen
Associated conditions:
DM: nonenzymatic glycosylation of protein in the BM renders
them permeable to protein
Hypertension: increased intraluminal pressure pushes plasma
proteins into the wall of the arteriole.

Amyloid(extracellular Microscopic appearance of amyloidosis of

hyaline) kidney:
• The amorphous pink
deposits of amyloid may be found in
and around arteries, in interstitium,
or in glomeruli.

Hyaline membrane disease This is hyaline membrane disease due to

of the new prematurity and lack of surfactant
born(Extracellular hyaline) production from the immature lung. Note
the thick pink membranes lining the alveolar
spaces.

Lipofuscin Pigments • also known as Lipochrome, wear

and tear or aging pigment.
• Is un-digestible residue of
subcellular membrane.
• Not injurious to cell
• Sign of free radical injury and lipid
peroxidation.
Appearance: YELLOW BROWN, finely
granular, intracytoplasmic, often perinuclear
Purssian Blue stain Used for identifying Hemosiderin.
Mallory Body ubiquinated (marked for destruction)
masses of prekeratin filaments
Seen in hepatocytes of alcoholics
Microscopic feature of alcoholic hepatitis.
Lewy Body ubiquinated neurofilaments from
degenerated substantia nigra neurons in
Parkinson’s disease.
single or multiple, intracytoplasmic,
eosinophilic, round to elongated inclusions
with dense core surrounded by a pale halo,
composed of α-synuclein and other proteins
(neurofilament and ubiquitin)

Neurofibrillary Tangle Ubiquinated neurofilaments in brain.

Seen in old age / Alzheimer’s disease.
Langerhan Type Giant cell Seen in tuberculosis where there are
epithelioid cells.

Congo Red Stain Stains red with congo red stain used for
amyloid.

Lines of Zahn the alternating pale pink bands of platelets

with fibrin and red bands of RBC's forming a
true thrombus

Sudan Black/Oil Red O stain Used to stain Fat molecules

Schistiocytes In DIC, Peripheral smear shows

Red cell fragmentation. schistocytes
MAHA, HUS, TTP,DIC,Prosthetic heart valve
Alzhiemers type II astrocyte  It is a gray matter astrocyte with a
large nucleus (2 to 3 times larger),
pale staining central chromatin, an
intranuclear glycogen droplet, and a
prominent membrane and
nucleolus.
 It is unrelated to alzhiemers disease
 Usually occurs in patients with
hyperammonemia. Chronic liver
disease, Wilson disease and
hereditary disorders of urea cycle.

Gemistocytic Astrocyte  enlarged vesicular nucleus with

prominent nucleolus and abundant
bright pink cytoplasm-
 Most important histopathologic
finding finding.
 Giosis(astrogliosis), Hypertrophy
and hyperplasia.

Rosenthal fibres thick, elongated, bright eosinophilic protein

aggregates-bright pink eosinophilic fibres,
seen in pilocytic astrocytoma and
Alexander disease

Corpora amylacea : age related degenerative change , round,

PAS+ve, concentric lamellated polyglucosans
(5 to 50 μm).
Lafora bodies intracytoplasmic, seen in myoclonic epilepsy
Lafora bodies in grey matter in both neuronal perikarya and
neuronal processes, mostly in the subcortical grey matter
including brainstem and cerebellar nuclei
- loss of nerve cells corresponding to density of Lafora bodies
- can appear in ganglionic and bipolar cells of retina
- outside of CNS, in epithelial cells of eccrine sweat gland
ducts, skeletal muscle fibers, and cells of the PNS

Immunoperoxidase stain Glial Fibrillary acidic protein-glial filaments

relatively specific for astrocytes

β-Amyloid precursor Wide asymmetric axonal swelling, appear in

protein Stain (BAPP) hours and persist longer, best demonstrated
with silver stains or immune histochemistry

Acid Fast Bacilli Tuberculosis

Cowdry Type A intranuclear Herpes Simplex virus Type I
inclusion bodies

Owl Eye Inclusions Cytomegalovirus

Negri Bodies Seen in Rabies

JC virus/ Polyoma virus. Enlarged oligodendrocyte nuclei with
ground glass appearance (chromatin
replaced by viral inclusion)

INDIA Ink India ink stain is used to show mucoid

encapsulated yeast in CSF.

PAS, mucicarmine, silver For tissue staining of fungi we use the

stains following stains. The picture is Mucicarmine
stain of brain infected with C. neoformans

Soap Bubble Abscess Fungal capsule is characteristic for

Cryptococcus and forms "Soap bubble
abcesses”

Picture: , Whole-brain section showing the

numerous areas of tissue destruction (“soap Mucicarmine stain of cryptococci (staining red)
bubbles”) associated with the spread of in a Virchow-Robin perivascular space of the
organisms in the perivascular spaces. brain (soap-bubble lesion)

Lhermette’s sign Flexion of the neck leads to electric shock

like feeling, seen in multiple sclerosis.
Holmer Wright Rosettes Meduloblastoma

Holmer wright
psuedorosettes Neuroblastoma
Verocay Bodies • Antoni A pattern: high cellularity;
nuclear-free zones of processes
between nuclear palisading
“Verocay bodies”
Seen in schwannoma

Candle stick drippings in Tuberous sclerosis.

the ventricles Cortical hamartomas are firm areas of
cortex (likened to potatoes – “tubers”)
Microscopic Features: haphazardly arranged
cells with glial and neuronal features (large
vesicular nuclei with nucleoli like neurons,
and abundant eosinophilic cytoplasm like
gemistocytic astrocytes)
Subependymal nodules: large astrocyte-like
cells cluster beneath ventricular surface
(‘candlestick drippings’ in ventricles)

Tripehenyl Tetrazolium - If the myocardium is painted with

Triphenyl tetrazolium chloride (TTC)
non viable myocardium appears
pale due to lack of LDH

Thioridization Chronic pyelonephritis (kidneys)

Stroma ovarii (rare teratoma that contains
thyroid tissue)=
Muddy brown casts Acute tubular necrosis
Heart anamolies related 1. Trisomy 21( Downs) – endocardialcushion
defect
2. Trisomy 18, 13, Cri du Chat- VSD
3. Turners syndrome – Co-arctation of Aorta
4. Di-Georges – Truncus Arteriosus
5. Maternal rubella in 1st trimester – PDA
6. Hypoxia, ionizing radiation, alcohol ( ASD),
cigarette smoking, drugs- .
Onion skin appearance 1. Hyperplastic arteriolosclerosis
2. Primary sclerosing cholangitis-
Periductal fibrosis
Onion peel appearance
Onion skin thickening of
arterial wall
Trousseau’s sign
Trousseau’s syndrome
Holmens sign
elevated Anti Streptolysin
O syndecam chorea
( ASO) & anti DNAse
Aschoff bodies
Anitchkov cell (caterpillar
cell)
Type 4 hypersensitivity
reaction
MacCallum Plaques
Howell-Jolly bodies(nuclear
remanants)
Ewings sarcoma t(11:22)
Lyme arteritis
 Hypoparathyroidism when the hand
becomes twisted when
Migratory thrombophebitis
Deep vein thrombosis where there is pain in
the calf
Evidence of preceding strep infection then
Aschoff bodies are nodules found in
the hearts of individuals with
rheumatic fever. They result from
inflammation in the heart muscle
and are characteristic of rheumatic
heart disease. Seen in all layers of
the myocardium.
Left atrial endocardial thickeing
left atriam of the heart showing
dilated atria and maccallum plaques.
Post splenectomy, Howell–Jolly bodies are
histopathological findings of basophilic
nuclear remnants (clusters of DNA) in
circulating erythrocytes. During maturation
in the bone marrow late erythroblasts
normally expel their nuclei, but in some
cases a small portion of DNA remains. Its
presence usually signifies a damaged or
absent spleen
Target Target cells may appear in association with the
Cells/Codocyte/Mexican following conditions.
Liver disease: Lecithin—cholesterol acyltransferase
hat cell (LCAT) activity may be decreased in obstructive liver
disease. Decreased enzymatic activity increases the
cholesterol to phospholipid ratio, producing an
absolute increase in surface area of the red blood cell
membranes.
Iron deficiency: Decrease in hemoglobin content
relative to surface area is probably the reason for the
appearance of target cells. This is also seen in
Thalassemias, Hemoglobin C disease, etc.
Alpha-thalassemia and beta-thalassemia[5]
(hemoglobinopathy)
Hemoglobin C Disease
Post-splenectomy: A major function of the spleen is
the clearance of opsonized, deformed, and damaged
erythrocytes by splenic macrophages. If splenic
macrophage function is abnormal or absent because
of splenectomy, altered erythrocytes will not be
removed from the circulation efficiently. Therefore,
increased numbers of target cells may be observed.

Coin like lesions on the Pulmonary hamartoma

lungs

Singlet ring Cells Krukenberg tumors: Metastatic tumors to

ovary are uncommon, but there is one
situation in which a metastatic
adenocarcinoma to ovary appears as a large
mass and resembles a primary tumor: a so-
called "Krukenberg" tumor of ovary which
has a signet ring histologic pattern and
usually is metastatic from a primary in
gastrointestinal tract. Seen here extending
out of the pelvis at autopsy is a large right
ovarian mass. Metastases are also present in
the lower right portion of liver.

Tonofilaments Seen in epithelial tumors.

Tonofibrils are cytoplasmic protein
structures in epithelial tissues[1] that
converge at desmosomes and
hemidesmosomes.

Tonofilaments are also associated with

desmosomes (macula adherens), anchoring
them to the cytoskeleton.
arrow 5 is tonofilaments
Weibel Palade bodies Present in angiosarcoma. Weibel palade
bodies are the storage granules of
endothelial cells, the cells that form the
inner lining of the blood vessels and heart.
They store and release two principal
molecules, von Willebrand factor and P-
selectin, and thus play a dual role in
hemostasis and inflammation

Birbeck Granules Looks like a tennis racket and is Present in

histiocytic tumors and are CD1a +Ve.

Birbeck granules, also known as Birbeck

bodies, are rod shaped or "tennis-racket"
cytoplasmic organelles with a central linear
density and a striated appearance. They are
a characteristic microscopic finding in
Langerhans cell histiocytosis (Histiocytosis
X), which is one of a group of rare conditions
collectively known as histiocytosis.
Formation is induced by langerin
Mockenberg’s medial characterized by calcium deposits in
calcific stenosis muscular arteries (uterine and radial

Pink, glassy, homogenous Hyaline arteriolosclerosis

arterial wall thickening

Brassy Cough left recurrent laryngeal nerve is stretched by

the aneurysm.
Tree Barking Syphillitic aneurysm
Homan Sign pain on compression of calf or dorsiflexion
of foot

Lymphangitis  Lymphangitis presents as :

 Cluster of painful subcutaneous
red streaks along the involved
lymph channels.
 It is occasionally associated with
involvement of lymphnodes (acute
lymphadenitis) and may lead to
septicemia.

peau d’ orange appearance

(orange peel)

Cystic Hygroma Seen in turners syndrome,

String of pearls and Rosary Poly arteritis Nodosa

Sign
Bite cells G-6-PD deficiency
1. A degmacyte (aka "bite cell") is an abnormally shaped
red blood cellwith one or more semicircular portions
removed from the cell margin. These "bites" result from
the removal of denatured hemoglobin by macrophages
in the spleen.

Nuclear Dust Hypersensitivity Vasculits(microscopic

polyangitis).Neutrophilic infiltrate with
leukocytoclasis.The neutrophils undergo karyorrhexis
with formation of fragments called "nuclear dust".

Sea blue histiocytes, Zebra Niemen Pick disease, Sphingomyelinase

bodies

Balooned neurons Tay sachs disease

c
Leukoerythroblastic  Presence of immature WBC’s and nucleated
Reaction RBC’s in peripheral blood.
 Pathogenesis:
 Peripheralization of BM elements
secondary to:
Metastasis, severe bone fracture, fibrosis
Causes: Metastasis:Breast cancer most common
cause.Fibrosis:Myelofibrosis,CML, polycythemia vera

Cytoplasmic vacuolization Seen in mature neutrophils and not in band

cell neutrophils.
Toxic granules

Band form
Cytoplasmic
vacuolation

Mature neutrophil

Downey Cells/ Ballerina Seen in Ebstien Barr virus infections

Skirt appearance. (infectious mononucleosis)
EBV uses the CD21 receptors on the B-
Lymphocytes to infect the Bcells. The
cytotoxic T-Lymphocytes respond against
the infection and form atypical lymphocytes.
Paul Bunnell Reaction Basis of antibody test
Auer Rods/ Faggot Cells Seen In acute myelogenous leukemia (AML),
AML is MPO +ve and Sudan Black +ve
MPO +ve PAS +ve
Myeloblasts lymphoblasts

4-Clover leaf / flower Adult T-cell leukemia

shaped hyper lobated (CD4+ve and Tdt –ve) and since Adult T cell
leukemia releases osteoclastic factors
nucleui Hypercalcemia is seen in these patients.
Note: Immature B/T cell ALL is TdT +ve.

Smudge cells Disruped tumor cells which are often seen in

chronic lymphocytic leukemia.

Things seen in CLL: Cancer of the mature

naïve B-cell:
a) Spherocytes
b) Small lymphocytes
c) Nucleated erythroid cell
d) Smudge cells

Hairy cell leukemia Cancer of the memory B-cells

We observe pancytopenia(can be used to
differentiate from CML) and massive
sphenomegaly.
Trap +ve cells with hairy cells.

Increased succeptibility to infection by

mycobacterium aviam complex.

Excellent response to 2-
chlorodeoxyadenosine
Birbeck Granules Histiocytes X
• Proliferative disorder of immature dendritic
cells called Langerhans cell.
• Encompasses 3 conditions:
1. Eosinophilic granuloma (Single
lytic lesion)
2. Hand-Schuller Christian
disease.(Lytic lesions in the skulls,
exophthalmos & diabetes
insipidus)
 3. Letterer-Siwe syndrome(most
aggressive, eczematous rash,
multiple organ involvement &
multi focal lytic defects)
Histiocytes are:
– CD-1 positive
– On EM show presence of Birbeck
granules (tennis racket
appearance) in cytoplasm.
– Cells have a grooved nucleus 
coffee bean appearance

Reed Sternberg Cell Hodgkin Lymphoma: Unlike the non-hodgkin

lymphoma classic hodgkin lymphomas
usually arise in a single lymph node or lymph
node chain and usually spread in a
contiguous fashion, occur mostly in younger
people and have relatively few neoplastic
cells, amid a prominent mixed inflammatory
cell background. MOST of the time the cells
of origin are are B-Cells.
RS cell +ve which is CD15, 30+ve, 45-ve
1. Nodular sclerosis
2. Mixed cellularity
3. Lymphocyte predominant
4. Lymphocyte depleted

Starry sky appearance Burkitt’s lymphoma

Hall Mark cells-cells Anaplastic large cell lymphoma
resembling an embryo CD8 + cancer cells
Children & young adults
Poor outcome

Pautrier microabscess Aggregates of CD3 and CD4 +ve cells in the Pautrier microabscess
epidermis Atypical PAS positive lymphocytes in
epidermis (epidermotropism).

Aggregates of CD3 and CD 4 positive

cancer cells in epidermis called:
Pautrier micro abscesses.

What makes you suspect a cancer on

this skin biopsy?
CD4 – IHC - +ve
staining in Epidermis

Sezary cells : have same  Mycosis Fungoidis with a

characteristic leukemic phase.
 Characterized by presence of
cerebriform appearance. neoplastic cells in peripheral
blood
Popcorn cells We notice that in HL, Lymphocyte predominant type.

Seen in Lymphocyte predominance HL

Negative for CD15 & CD30
Positive for CD45

Lacunar Cells Seen in HL, Nodular sclerosis type

Heinz Bodies G-6-PD deficiency and Hb Hammersmith and β-

Thalassemia.
Hb Hammersmith: Unstable hemoglobin
• AD, Mutation in β globin-
• HBB, PHE42SER
Phe residue is one of two amino acids conserved in
all globin molecules
Functions to wedge heme into hydrophobic pocket
Ser is smaller, heme drops out of pocket
• Causes denaturation of the globin
monomer which is unstable
• Hb precipitation  inclusions (Heinz
Bodies)
• Cyanosis and Hemolysis

Ringed Sideroblasts Sideroblastic anemia:

• Are a group of anemias with a
– defect in heme synthesis in the
mitochondria.
• Are known as sideroblastic anemia because
iron accumulates in the mitochondria of
developing normoblasts in the bone
marrow and forms
– ringed sideroblasts
1. Alcoholism: most common cause
2. Pyridoxine (vitamin B6) deficiency.
3. Lead (Pb) poisoning
4. Myelodysplastic syndrome (refractory
anemia with ringed sideroblasts)
Lead poisioning
Tear Drop cells/Dacrocytes.
Myelophthisic anemia
Burr Cells/Echinocyte
Denatures ribonuclease: prevents breakdown of
ribosomes  persistence of ribosomes  coarse
basophilic stippling of RBCs
 Note: Basophillic stippling is seen in
Myelodysplastic Syndrome
 Sideroblastic anemia[2]
 Lead poisoning (normocytic anemia)[3]
 Arsenic poisoning
 Beta thalassemia (though some have
questioned this)[4]
 Alpha-thalassemia, HbH Disease
 Hereditary Pyrimidine 5'-Nucleotidase
Deficiency
 Thrombotic thrombocytopenic purpura
A dacrocyte (or dacryocyte) is a type of poikilocyte
that is shaped like a teardrop (a "teardrop cell"). A
marked increase of dacrocytes is known as
"dacrocytosis". These tear drop cells are found also in
beta thalassemia major, especially after splenectomy.
Dacrocytosis can be associated with myelophthisic
anemia, commonly caused by myelofibrosis
Leukoerythroblastic picture with immature WBC with Read up on tear drop cells
huge nucleated cells Myelophthisic anemia
nRBC Immature WBC
Leukoerythroblastic picture
BM biopsy :A must, to diagnose
13
Myelophthisic anemia
Echinocytosis is a reversible condition of red blood cells that
is often merely an artifact produced by EDTA, which is used
as an anticoagulant in sampled blood.Echinocytes can be
distinguished from acanthocytes by the shape of the
projections, which are smaller and more numerous than in
acanthocytes and are evenly spaced. Echinocytes also exhibit
central pallor, or lightening of color in the center of the cell
under Wright staining
Usually seen in :
Uremia
Pyruvate kinase deficiency
Hypomagnesemia
Hyperphosphatemia
Echinocytes, like acanthocytes, may be found in
hyperlipidemia caused by liver dysfunction, but the lipids
themselves do not integrate into the membrane. Instead, it is
speculated that cell surface receptors on the red blood cells
bind with HDL cholesterol which induces the shape change
Crew cut skull, Frontal Bone deformity- due to
bossing, Chipmonk face erythroid hyperplasias, Bone findings in severe
hemolytic anemia due to compensatory increase in
erythropoesis leading to bone distortions

Acanthocyte/ Spurr cells Have irregular spicules on their surface, can be seen
in abetalipoproteinemia,liver disese,
chorea acanthocytosis, McLeod syndrome, and several
inherited neurological disorders, such as
neuroacanthocytosis, anorexia nervosa, infantile
pyknocytosis,
hypothyroidism, idiopathic neonatal hepatitis,
alcoholism, congestive splenomegaly, Zieve syndrome,
and chronic granulomatous disease.
Pathophysiology: Acanthocytes arise from either of two
mechanisms. Alterations in membrane lipids are seen in
abetalipoproteinemia and liver dysfunction. Alteration in
membrane structural proteins are seen in
neuroacanthocytosis and McLeod syndrome. In liver
dysfunction, apolipoprotein A-II deficient lipoprotein
accumulates in plasma causing increased cholesterol in RBCs.
This causes abnormalities of membrane of RBC causing
remodeling in spleen and formation of acanthocytes.In
abetalipoproteinemia, there is deficiency of lipids and
Vitamin E causing abnormal morphology of RBCs.
Bite Cells are RBCs with bites of cytoplasm being removed by
splenic macrophages. May be seen in G6PD deficiency.

Metabisulphate test Also note: Hydroxy urea increases the fetal

Special test: Sickling test
hemoglobin level.
• Aka metabisulphite
test.
• Sodium metabisulphite
reduces oxygen
tension and induces
sickling.
• It is a screening test.

Normal RBCs Sickled RBCs

Osmotic Fragility test Special test for confirming presence of
spherocytes : ** Osmotic Fragility Test

Normal:
RBCs begin hemolysing at 0.50%
( low saline concentration)

Hereditary spherocytosis:
RBCs begin hemolysing at 0.85%
( higher saline concentration)
 Increased osmotic fragility

Treatment : Splenectomy
36

Sucrose lysis test initial screen for PNH.

Sugar water enhances complement attachment to
RBCs, leading to RBC hemolysis.
Positive Ham test Demonstrates in vitro complement induced Ham’s Test/Acidified serum test
hemolysis in acidified serum. Diagnostic test for PNH

Confirmatory test

“Pt” – patient with PNH:

“C” – control
Serum acidification →hemolysis

Hemosiderin Casts 61
In urine

Lisch Nodules Pigmented iris harmartomas: Neurofibromatosis Type

I

Brushfield Spots Brushfield spots are small, white or grayish/brown

spots on the periphery of the iris in the human eye
due to aggregation of connective tissue, a normal iris
element. These spots are normal in children
(Kunkmann-Wolffian bodies), but are also a feature of
the chromosomal disorder Down syndrome. They
occur in 35–78% of newborn infants with Down
syndrome. They are much more likely to occur in
children with Down syndrome of the Caucasian race
than children of Asian heritage with Down's
Syndrome.
They are focal areas of stromal hyperplasia,
surrounded by relative hypoplasia, and are more
common in patients with lightly pigmented irises
Lesar Trelot sign Sudden appearance of suborreheic keratosis may
indicate gastrointestinal malignancy
Boerhaave syndrome The patient ruptures esophagus after episodes of
retching. The tear appears 3-5 cm above the
gastroesophageal junction and patients display
restrosternal chest pain. Signs of the disease may
include left pneumothorax, pleural effusion,
subcutaneous or mediastinal emphysema, tachypnea
and tachycardia.
Maltese Cross Babesiosis

Porcelin Gall Bladder Carcinoma of the gall bladder: Due to calcium

deposition in the wall
Clue cell Clue cells are seen in gardenella vaginalis.Clue cells
are epithelial cells of the vagina that get their
distinctive stippled appearance by being covered with
bacteria. The etymology behind the term "clue" cell
derives from the original research article from Gardner
and Dukes describing the characteristic cells.
Treacher Collins syndrome Mandibular Hyperplasia
Schuffner Dots Appearance of multiple brick like structures in RBC.
Seen in plasmodium ovale and vivax
Methamine Silver stain is
used to identify fungi
Aschoff Bodies Aschoff bodies describe the Granulomatous
appearance and transformed macrophages seen in
acute rheumatic myocarditis.
Schaumann Bodies Laminated calcifications
Asteroid bodies Stellate giant cell cytoplasmic inclusions
Charcott Leyden Crystals Rhomboidal crystals found in allergic asthma. They
are breakdown products of eosinophills and are
found in the sputum of allergic patients.

Cruschmann spiral Curschmann's spirals refers to a finding in the

sputum of asthmatics which are spiral shaped mucus
plugs from subepithelial mucous gland ducts or
bronchioles. These may occur in several different
lung diseases
Neurotransmitters and Nucleus ceruleus Contains nor-epinephrine containing neurons
Raphae nucleus Contains serotonin releasing neurons.
Nuclei Nucleus Basalis of Contains Cholinergic neurons
Myenart
Red Nucleus Located in the anterior part of the mid-brain and its neurons
participate in the motor co-ordination of the upper extermities
Caudate Nucleus Caudate and putamen for the striatum & function in motor
activities
Substantia Niagara Contains dopaminergic neurons
Orexin Orexin, also called hypocretin, is a neuropeptide that
regulates arousal, wakefulness, and appetite.The most
common form of narcolepsy, in which the sufferer briefly
loses muscle tone (cataplexy), is caused by a lack of orexin in
the brain due to destruction of the cells that produce it.

The brain contains very few cells that produce orexin; there
 are about 10,000–20,000 orexin neurons in the human brain,
which project out of the nucleus in the lateral
hypothalamus.However, the axons from these neurons
extend throughout the entire brain and spinal cord, where
there are also receptors for orexin.
Geography associated Malaria Travel to Africa
Diseases HIV Travel to Africa & Haiti
Coccidiodes Immitis South West United
States
Blastomycosis Mississipi River valley
Histoplasmosis Ohio River valley

Cellular receptors & CMV Cellular integrins

associated Virus EBV CR2 (CD21)
HIV CD4 and CXCR4/CCR5
Rabies Nicotinic Acetylcholine
receptor
Rhinovirus ICAM1 (CD54)
Nikolsky’s Skin Skin slipping off with gentle pressure: Exfoliative
toxin in the case of staph aureus show exquisite
pathologic specificity in blistering only the superficial
epidermis. They act as proteases and cleave
desmoglein in desmosomes.

Gerstmann Syndrome Occurs as a result of a lesion of the angular gyrus.

These patients cannot comprehend written language
(alexia) nor can they write it (agraphia). They also have
acalculia (loss of ability to perform simple math),
finger agnosia (inability to recognize ones one’s
fingers), and a right-left disorientation.

Triphenyl tetrazolium If myocardium is painted with TTC then the

chloride (TTC) myocardium which is not viable will be pale due to
lack of LDH. From .5-4 hours there is no gross change
in the appearance of the myocardium. Microscopic
changes include wavy fibers.