HistoPATHOLOGY Flashcards
Asthma
There are 2 types of asthma: intrinsic (30%) which is triggered by non-immune stimuli and extrinsic (70%)-> type 1 hypersensitivity reaction.
The reaction is confined to the bronchi (nothing in the alveoli), and we can observe a reduction in the bronchial diameter due to bronchospasm, mucosal edema and excessive mucus production.
The lumen in plugged with mucus, in some parts the epithelium is missing, in the wall there is mix inflammatory infiltration -> should see eosinophils
The muscle might be hyperthropied
APC -> TH2
- IL-4 -> B cell -> IgE
- IL-5 -> Eosinophils
- IL-13 -> Epithelial cells mucus secretion
Purulent meningitis
In the central nervous system pyogenic bacteria most often cause purulent inflammation of the leptomeninges and of the subarachnoid space. Among the causal organisms are E. Coli, H. influenza and N. meningitides.
The leptomeninx is markedly wider over the cerebral cortex. It is infiltrated by neutrophils and eosinophilic fibrin material. This exudate fills the subarachnoid space. The blood vessels are dilated and congested. The wall of the vein might also be infiltrated with lympthocytes.
Thrombi in femoral artery
identify lines of Zahn
Lobar pneumonia
This type is an inflammation that affects an entire lobe. Most typically due to pneumococci
Morphologically:
Lung is swollen, the pleura is covered by fibrinous or purulent exudate
The affected lobe is not aerated -> alveoli are not filled with air
HEPATIZATION: the consistency is firm, as in the liver!
There are 3 stages of hepatization:
- 1st: lung is flooded with blood -> red hepatization (rubra)
- 2nd: fibrin infiltration -> gray hepatization (grisea)
- 3rd: invasion of the fibrin by leukocytes -> they have a function is fibrin degradation -> yellow hepatization (flava)
- If the patient survives the 6th day (crisis) -> survival
On the slide: the stage is b/w the gray and the yellow: the alveoli are filled with fibrin and neutrophils
fat embolism in the kidney
deposition in glomeruli
oil red O - Specific staining for fat.
The fat filling up the hilum is red.
Fat emboli, stained red by this type of staining
PTIC: small capillaries b/w the tubules are filled with the fat which can close them.
Also seen in the glomeruli capillaries.
Carcinoid appendix
Carcinoid is a neuroendocrine cell tumor (NET). In this case it is benign, but there are malignant types as well (NEC)
Neuroendocrine tumors arise from cells of the endocrine and nervous system.
They are normally found in the stomach, small intestine, appendix, lung and pancreas.
Cells form trabecular structures. Have a “salt and pepper” nuclei (nuclei that demonstrates granular chromatin).
in this slide, we perform immunohistochemistry (Antibody against a specific protein) against the following markers:
- chromogranin A
- synaptophysin
- CD56
The immunohistochemistry is done for at least 2 markers, as it is not obligatory to have all the 3. A brown colour means positive result.
Together with the tumor, acute appendicitis can be observed.
APC benign polyp
Benign neoplastic polyps of the colonic mucosa (in this case: tubular adenoma)
Pseudostratified columnar epithelium
Goblet cells are almost absent in the specimen -> the cells have a bluish cytoplasm, the nuclei (which normally is thin in the goblet cell and is found in the periphery) is larger, vesicular and have prominent nucleoli. So the features that can be described are:
- crowded cells
- mucin secretion is decreased
- bluish colour
- inflammatory cells in the lamina propria
There are several types of adenoma:
- AT: adenoma tubulare
- ATV: adenoma tubulovillosum
According to severity:
- AT -> ATV -> cancer
Has a stalk which is an extension of the normal mucosa and submucosa
Might be related to familial polyposis coli
Have a chance to become malignant
Ductal breast carcinoma (Breast carcinoma)
Apoptosis
Cell membrane remain intact -> no inflammation.
We can see nuclear changes: karyopyknosis, karyorrhexis (nuclei breaks into pieces). We can see leakage of apoptotic bodies.
In can be a physiological process, when there is no need for a cell (embryogenesis, hormone-dependent tissue, inflammatory cells) but is can be pathological, after DNA damage, accumulation of misfolded proteins or viral infection)
Nutmeg liver
focal fatty degeneration
Spotted, not diffused
Right sided heart failure exist in those patients -> stasis of the blood because no proper pumping -> pressure increases in the venous side -> O2 saturation drops
In the central veins of the liver, the pressure increases and the O2 drops, thus the hepatocytes in the immediate vicinity goes through fatty changes (because no fatty acid oxidation). The rest remains viable due to the supply from the arteries.
*Fatty liver (steatosis) Degeneration adiposa hepatis*
diffuse fatty globules
A mechanism of reversible cell injury.
Occurs due to starvation, hypoxia, toxins/alcohol, protein malnutrition, obesity.
The FA, instead of being incorporated into TAG, are catabolized into phsopholipids, CH-E, ketone bodies
The hepatocytes contain lipid vacuols: microvesicular and macrovesicular. They coalesce to larger ones, thus, we see that the nucleus is found in the periphery.
The fat is dissolved in the staining procedure -> we see empty vacuoles.
fatty necrosis-acute pancreatitis
fatty saponification
Is the result of release of pancreatic enzymes, mainly lipase, from the acinar cells. it might happen due to stone in the common bile duct -> bile passes instead to the pancreas -> activation of the enzymes
The lipase digests the TAG into FFA. The FFA react with Ca -> chalky white area. It might cause drop of the Ca In the circulation -> tetany.
The lipase might travel in the circulation into other area.
Look at the fat necrotic spots -> normal structure is gone. No nuclei. Hematoxyphil staining due to Ca
*Wilms tumor - Nephrobalstoma*
This is the most common primary tumor of the kidney in young children (usually appears at the age of 2-5). Frequently associated with chromosomal abnormalities.
The tumor has a triphasic appearance:
- blastemal: closely packed undifferentiated cells (small round cells)
- stromal: loose connective tissue (pinkish area)
- epithelial: tubular structures
The proportions of those components are variable
encephalomalacia
liquefactive necrosis of the brain
Is due to marked reduction or cessation of flow.
At the necrotic area we can see eosinophillic necrotic cells. at the rim of the uninvolved brain one can find mononuclear cells. some might contain hemosiderin. The uninvolved adjacent brain is edematous (contains vacuoles)
At a later stage there is glial proliferation around the infarct followed by formation of their fillaments -> gliotic scar is formed.
Breast cancer
HER2 immunohistochemistry
prostate hyperplasia
hormonal defect between androgenes (decrease) and eostrogen (increase)
Enlargement of the prostate is a common finding in men over 50 years of age, probably due to an imbalance in the regulation of androgen and estrogen. The changes begin in the periurethral glands.
3 changes can be seen:
- Adenomatous hyperplasia: an increase in the glandular component
- Fibromuscular hyperplasia: an increase in the smooth muscle and fibrous stroma
- Atrophic parts
Some glands are dilated, they are lined by low cuboidal epithelium.
The glands have an outer 2 layers of myoepithelial cells. this is normal. If we see only one layer of myoepithelial cell it indicates cancerous state (not the case here!)
Some glands contain corpora amylacea
The connective tissue septa between the lobules is widened.
Carcinoma planocellulare cutis
(squamous cell carcinoma of the skin)
Carcinoma: malignant tumor of epithelial origin
An invasive tumor
Epithelium is thick with too long papilla.
Inflammatory reaction: lymphocytes (and some giant cells) surround the tumor
Keratinization deep in the dermis -> keratin pearls
Hyperkeratinization of the surface -> parakeratosis: nuclei are seen in the stratum corneum
AMI
Look at the pinkish area. Observe several features:
- nuclei are missing->karyolysis
- cant see striations. Fine structure of the cytoplasm is missing
- leukocytes infilatration, frequently on the border
This infarct is more than 24 hours old. We can see RBCs in the vicinity -> there was an attempt to reperfuse the area. However, without reperfusion, AMI is an anemic type.
SLE - diffuse glomerulonephritis
granulomas foreign body
adenocarcinoma coli
Adenocarcinoma is a malignant tumor originating from the epithelial lining of ducts or glands.
The epithelium penetrates deep. In this case it reaches the submucosa (at that level it can spread via the lymphatics)
Usually develops from ATV (adenoma tubulovillosum)
Microscopic findings:
- Usually form polypoid mass
- Usually found in association with intestinal metaplasia and dysplasia of adjacent mucosa.
- The tumor forms cribriform structure: islands of cancer cells with an abnormal lumen
- (in some cases: the lumen might be absent)
- Many mitotic figures
- Less mucus secretion, crowded cells with vesicular nuclei and visible nucleoli
pulmonary abscess
circumscribed pus in a non preformed cavity
This is a form of purulent inflammation in which the exudate is termed pus and is rich of:
- Neutrophils, edema fluid, necrotic cells
It Is caused by an infection of streptococci, pneumococci, staphylococci.
Types according to location:
- abscess: pus in a non-preformed body cavity
- empyema: pus in a pre-formed body cavity
- phlegmone: no sharp borders
This slide contains an abscesa (bluish-circled structure) in the lung. we know it is an abscess b/c it is in the middle of the lung parenchyma
Structure:
- Central necrotic zone
- Surrounded by a pyogenic membrane: blue layer of PMNI
- Surrounded by a granulation tissue: fibrin (with some bluish spots termed “bacterial clouds”)
Induratio brunea pulmoni
heart failure cells
(show left heart failure staning prussian blue)
In Hg: Fe2+
Here Fe3+ -> the dye finds to this -> blue staining of the hemosiderin in the HFCs
The anthracosis remains black
pulmonary edema
acute phase of left heart failure
The alveoli of the lungs are filled up with transudate that impairs the gas exchange. It can be due to increased hydrostatic pressure in the pulmonary capillaries (left ventricular failure, renal disease, shock).
Alveoli are filled up with faintly eosinophilic material
The capillaries are extremely dilated ->
The congestion is seen as dilated capillaries. can be judged by the number of RBCs filling the lumen -> in normal cases only 1 should be seen. Here -> several
The increased hydrostatic pressure leads to transudation of plasma fluid -> oedema
severe allergic nasal polyps
glands dilated filled with mucus
Structures protruding from the surface = polyps. Can be tumor, inflammatory reaction. In this case it is due to allergy. It occupies the space that should be used for breathing.
In the slide we can see an extremely dilated structures filled with eosinophilic material -> they used to be the nasal glands, and they became dilated due to the excessive mucus production. The connective tissue between the gland is filled with scattered inflammatory cells (look for the eosinophils which are the classical sign of the hypersensitivity reaction)
DIC - Disseminated intravascular coagulation
fibrin thrombi in glomeruli PTAH staining (fibrin staining)
DIC is a thrombohemorrhagic disorder caused by systemic activation of the coagulation pathway, leading to formation of thrombi throught the microcirculation. The widespread thrombosis leads to 2 phenomena:
- microthrombi -> hypoxia -> microinfarcts
- depletion of platelets and coagulation factors + activation of fibrinolysis -> bleeding disorder.
DIC is initiated by endothelial injury, with the resultant exposure of ECM and TF
Such phenomena can be fetus mortus, severe burning, neoplastic disease etc.
The slide is taken from the kidney and is stained with fibrin staining.
The fibrin is seen in the glomeruli as dark blue
The lighter blue color represents the RBCs
Tuberculosis
actinomyces
sulfur PAS
A chronic purulent disease. Its causative agent is actinomyces israelii, a gram positive bacteria. It is part of the normal flora of the mouth and can become pathogenic after local trauma, operation or immunosuppression.
The process occurs in the subcutaneous tissue and usually leads to the formation of an abscess. Later the pus breaks to the surface of the skin or mucosa by the formation of fistula. Macroscopically, the pus contains yellow granules which are the colonies of the bacteria.
On the slide we see a darkened area: this is an abscess cavity surrounded by a granulation tissue (neutrophils, fibroblasts and macrophages). The pathogen in the cavity seems as an oval granules and from the periphery filamentous structures are radiating.
Retinoblastoma
Flexner wintersteiner rosette cuboidal cells around central lumen (no neuropil)
Chronic Gastritis
Slide: biopsy of the stomach
There are 3 types of chronic gastritis
- autoimmune type: affects primarily the body of the stomach. We see atrophy of the gastric gland with loss of parietal cells. there is an atrophy of the gastric gland and intestinal metaplasia -> the epithelial cells are replaced with goblet cells and columnar absorptive epithelium typical for the small intestine. Small round cell infiltration in the lamina propria.
- B.bacterial gastritis: most commonly caused by Helicobacter Pylori. It usually affects the mucosa of the stomach antrum. Intestinal metaplasia is commonly seen in this type of gastritis -> some glands resemble the crypts of Lieberkuhn of the small intestine. The small round cell infiltration is seen in the lamina propria
- C.chemical (alcohol, non-steroid): mainly inflammation of the superficial mucosa, few cells infiltrating the lamina propria. The neck of the gastric glands show hyperplasia and the lamina propria is edematous.
This biopsy is probably of the 2nd type, but the bacteria should be demonstrated
It is typical to see some neutrophils infiltrating the epithelium of the gastric glands (-> “sign of activity in the chronic gastritis”).
Look for the presence of plasma cells which have round eccentric nucleus.
Fibrinous pericarditis
We can see the normal myocardium and the subpericardial fatty tissue.
The pericardial surface is covered by a thick layer of eosinophilic fibrin.
We can see dilated and congested blood vessels and infiltration with lymphocytes.
Coagulative hemorhagic necrosis of the lung (dual circulation)
A pulmonary embolus will cause infarction only if the there is compromised bronchial circulation of cardiac function (as in the case of congestive heart failure)
At the necrotic area the nucleus cannot be seen. The alveoli are flooded with blood. An infiltration with neutrophils is seen at the edge of the necrotic area.
Embolus usually from DVT.
cervix carcinoma
CIN = cervical intraepithelial neoplasia, is a precancerous state -> the basement membrane remains intact.
in the cervix there is the squamo-columnar junction.
Layers: basement membrane-basal layer-polygonal layer-planocellular. The basal cells are undifferentiated cells which are the progenitors of the other layers. This cells start to increase and replace more and more area of the epithelium.
It is HPV related -> indicated by cells called Koilocytes which are seen vacculated with enlarged nucleus
carcinoma basocellular (basal cell carcinoma)
The tumor arises from the basal lager of stratifies squamous epithelium
Frequently occur on the face
It is a semimalignant tumor: grow locally in an invasive pattern (usually till to the dermis), frequently reoccur but DOES NOT give metastasis.
Microscopic findings: the tumor form cell groups that extend deep into the dermis in a finger-like manner.
the tumor cells stain darkly. Mitosis are rare.
The cells at the periphery of the tumor clump are arranged in a palisade pattern whereas the central cells are haphazardly arranged
Adjacent to the tumor we can see lymphocyte infiltrate.
As the tumor grows under the normal epidermis, it results its necrosis and ulceration -> also called “ulcus rodens”
Cystic fibrosis - bowel + pancreas
-most common lethal genetic disease
-autosomal recessive
- 80% have the same genetic defect
- “mucovicidosis”: lesion in several organs but most severe is in the lung
- GI: meconium ileus -> the slide shows that the entire lumen is filled with the mucus
- pancreas: it contains a lot of connective disuse (ducts are totally plugged -> exocrine gland becomes atrophied -> replaced by fibrosis)
Due to inability to remove the mucus -> chronic inflammation=chronic pancreatitis -> see lymphocytes in the surrounding
The ducts seem dilated and are filled with the mucus!
-advantage of the mutation: provides some protection from TB
Caseus necrosis from tuberculosis
expand in lymph node of the lung most probably
Caseous necrosis is a combination of coagulative and liquifactive necrosis which is usually associated with a foci of TB infection. The coagulation dominated but the outlines of the tissue is not preserved.
The center of the tubercle has eosinophilic caseous necrosis surrounded by Langhans cells and epitheloid cells. the later have elongated shape, pale staining and oval nuclei. The epitheloid cells are surrounded by lymphocytes.
*the importance of necrosis: things can be released from the necrotic cell: enzymesuse them as a marker. However, ions can be released as well such as K and this is dangerous
Bronchopneumonia
In this case the infection + inflammation spreads along the bronchial tree into the lung parenchyma
In contrast to lober pneumonia, in which the entire lobe is involved, in this case there are focal lesions: we are able to see parts in which there is a normal lung structure but in other parts the normal tissue structure is absent: the alveoli are not filled with air but neutrophils are there.
Each focus contains a bronchus or bronchioles (look for anthracosis in its wall)
Problems with this situation:
- no air -> no gas exchange -> hypoxia
- difficult to pump out the blood -> right heart is decompensated
- fever -> tachycardia
glomerular-kidney amyloidosis
Congo red – amyloidosis renis
Beta pleated sheat -> congo red -> metachromasia -> red becomes green with polarized light
Rheumatic nodule
cholestasis
stasis of bile flow in the liver because of gall stone
A disturbance in the normal bile secretory mechanisms accompanied by accumulation of bile in the liver. The serum levels of bile pigments become elevated and cause jaundice.
Intrahepatic cholestasis = hepatocellular jaundice
The accumulated bile forms yellow to green granules in the cytoplasm of hepatocytes and kupffer cells. bile canaliculi are also dilated due to the bile.
It can also be a result of mechanical obstruction of the extrahepatic bile duct, but then the changes are seen in the portal areas.
Neuroblastoma
homer Wright pseudorosette
small blue blastema tumor cells
slide of adrenal gland
the most common childhood malignant tumors:
- neuroblastoma: tumor of peripheral nerve tissue, mostly in the sympathetic ganglia and in the adrenal medulla. Occurs at an age<5 years. Usually differentiate to ganglio-neuro-blastoma
- meduloblastoma: tumor of the brain (mainly the cerebellum)
- wilms tumor
All the aforementioned tumors are called “small round cells tumors”
- tumor cells have the same size, spherical nuclei, deeply stained. They completely fill the medulla
- Rossette formation: this structures are characteristic for blastoma in general: the tumor cells are arranged in circular formation with fibrillary cytoplasmic extensions fill up the central area -> called neuropil
Papilloma laryngis
papilloma refers to a benign epithelial tumor growing exophytically (outwardly projecting) in finger-like fronds and is of proven viral etiology.
The papilloma has a tree-like branching fibrovascular core.
The surface of the papilloma is covered with squamous epithelium with regular stratification.
Acanthosis: the stratum spinosum is wider!!
Basement membrane is intact
Lots of mitotic figures
Sjorgen disease glands
Also called sicca syndrome. An autoimmune mediated destruction of the lacrimal and salivary glands -> the target are the ductal epithelial cells. ANA, RF and antibodies against RNP are present.
Lacrimal gland destruction -> lack of tears -> drying of the corneal epithelium -> inflammation, erosion, ulceration (keratoconjuctivitis)
In the oral cavity the process leads to xerostomia.
Much more common in women
Slide**: salivary gland. there is a significant damage to the gland parenchyma.
There is an infiltration of lymphocytes are in some areas we can see groups of surviving epithelial cells which forms epimyoepithelial islands.
The lymphocytes might proliferate and form tumors.
acute appendicitis
Don’t confuse the presence of the normal lymphatic follicles with inflammatory process!
We see an area where the mucosa is absent -> this is an ulcer, which is the earliest stage of acute appendicitis. The mucosa in this area is replaced by fibropurulent exudate (fibrin + neutrophils)
The ulcer deepens until perforation of the appendix
On the outer surface (serosa) we can see redish material -> it contains fibrin and neutrophils (purulent inflammation of the surface)
Carcinoma metastaticum lymph nodi
pleuritis carcinomatosa
tumor cells in pleural effusion
(pleural carcinomatosis)
Tuberculosis Ziehl Neelsen saininig
With this staining, the bacilli seems as thin, long, straight rods which stain red in a pale blue background.
Look for it in the rim of the tubercle
Hypertrophy of the myocardium
acute rejection of kidney transplant - tubulitis
Transplantation requires life-long immunosuppression. The immunosuppression can cause infectious diseases, malignant tumor -> give as little as possible. Without immunosuppression, rejection occurs.
There are 3 types of rejection:
- hyperacute rejectionis occurs within minutes or hours after transplantation and mediated by a pre-formed antibodies found in the receipient against the graft endothelium.
Characteristics:
* **Arteritis and arteriolitis,** thrombosis fibrinoid necrosis in the vessel wall which leads to precipitation of fibrin and cellular debris (further occlusion). 2. **acute rejection:** within weeks or month after transplantation * _a.acute cellular rejection:_ related with **tubulitis**. There is an interstitial infiltration of CD4, CD8 T cells and mononuclear cells, all cause edema formation and parenchymal damage. * _b.acute humoral rejection_: related with **vasculitis** which is caused by antidonor antibody.
3. chronic rejection: developes within years and doesn’t respond to standard immunosuppression regiments. Characterized by:
- vascular changes: (mainly in the arteries and arterioles) Intimal smooth muscle proliferationfibrosisgeneral ischemia in the organ
A sign for kidney rejection is decreased urine amount. The acute type is treated with increased dose of immunosuppressant.
this slide is a kidney biopsy (->see the glomeruli), and it is an acute rejection. An acute rejection is a combination of cellular and humeral reaction.
There are areas which are full with inflammatory cells: eosinophils, plasma cells lymphocytes->mixed type inflammation -> sign for acute rejection. However, the pure sign for acute rejection is tubulitis: lymphocytes in the basement membrane.
In the tubules the infiltration is not as extensive as the interstitium.
Humeral component of the acute type: when we see endothelial cells infiltrated by lymphocytes, but this is not present here. In order to prove humeral component, we should apply immunohistochemistry. Humeral rejection is more intense and requires higher dose of immunosuppression.
Gaucher disease
mutation in the gene encoding glucosylceramidase
gene product is responsible for cleaving glucose residues from ceramide -> accumulation of glucosylceramide in the phagocytic cells -> transform into Gaucher cells (large, cytoplasm is described as “wrinkled tissue paper”). Macrophages become activated and release large amounts of cytokines.
There are 3 variants:
- Type 1: 99% of the cases. no CNS involvement, hepatosplenomegaly and bone involvement.
- Compatible with life. Type 2 and 3 have CNS involvement.
Therapy: enzyme replacement or reducing the substrate glucosylceramide by inhibiting its synthesise.
IRDS
Idiopathic respiratory distress syndrome IRDS
Risk factors: early delivery (prematurity), cesarean section, DM of the mother
There is a deficiency or a total lack of surfactant which is produced by type 2 pneumocytes
The impedence of the lung increases -> as ductus arteriosus is still open, the blood passes from the right heart side to the aorta instead of reaching the lung for oxygenation -> hypoxia
different from ARDS by etiology: in the adult type the cause might be viral infection, shock, drug, hypersensitivity reactions
the lungs are atelectatic but some alveoli are aerated. Some of the later are lined by hyaline membrane: homogeneous eosinophilic material composed of proteins + necrotic cell debris
the lumen contain alveolar macrophage and type 2 pneumocytes
the lung can recover but a bronchopulmonry dysplasia developes
Myocarditis in Rheumatic fever
Aschoff body
Rheymatic myocarditis is a manifestation of rheumatic fever, which is a post-streptococcal disease (type A streptococci). It is caused by antibodies which are produced against the bacteria but cross react with heart antigens. All three layers of the heart are involved (pancarditis)
Slide:
Fibrinous pericarditis -> pinkish area without nuclei
Myocardium: look at the interstitium, at the the perivascular area (between the myocytes):
We can see a small granuloma called “Aschoff body”: its center is acellular, eosinophilic and necrotic and is surrounded by lymphocytes, fibroblasts and Anitschkow cells which are mesenchymal cells with elongated nuclei and central band of chromatin.
Other cells are Aschoff giant cells (aschoff myocyt)
Lung Metaplasia
respiratory epithelium → squamous (stronga)
Nuclei in the epithelium with different sizes -> pleomorphism.
Sometimes seen like stratified squamous epithelium but there is not real difference b/w the layers -> dysplasia, an increased rate of cell division which is coupled with incomplete maturation of the cell. In some parts it infiltrates the tissue.
Metaplasia: the change to other cell type (squamous). It develops b/c the respiratory epithelium cannot cope with the smoking -> epithelium changes to squamous b/c it and deal better -> If smoking continuous it becomes cancerours.
Sarcoidosis
This is an example for a non-infectious immune granuloma.
Sarcoidosis is a multisystem disease of unknown etiology characterized by non-caseating granuloma (in contrast to TB) in many tissues and organs. It is supposed that it is a disease of disordered immune regulation in genetically predisposed individuals which are exposed to environmental agents.
The non-caseating granuloma is composed of a collection of epitheloid cells (with an abundant eosinophilic cytoplasm and vesicular nuclei) rimmed by an outer zone of CD4 T cells. fibroblasts are found in the periphery of the granuloma and they lay down the collagen that replaces the granuloma with a scar.
Giant cells might be present, and in their cytoplasm we can sometimes find:
- Schaumann bodies: laminated calcified concentrations
- astreoid bodies: eosinophilic star shaped.
- Their presence is not required for the diagnosis of sarcoidosis.
