Cytocentrifuge

Cell Block Sections

ThinPrep (non-gyne)

Surepath (non-gyne)

Diamond Colors

Blue:

Red:

Yellow:

White:

Diamond Colors

Blue: Health

Red: Flammability

Yellow: Instability

White: Special Hazards

% ASCUS Regress?

Progress to HSIL?

%LSIL Regress?

Progress to HSIL?

% ASCUS Regress? 68%

Progress to HSIL? 7%

%LSIL Regress? 47%

Progress to HSIL? 21%

HPV genome

E6?

E7?

HPV genome

E6? : p53 binding (inhibits apoptosis)'5+3=8 even like 6'

E7? : Rb (induces S phase entry) '7 Retina TV'

flow cytometry results : mantle cell lymphoma?

CD19+, CD5+,

CD23–, CD10–

FMC7+

CD19+, CD20+

CD25+, CD11c+

CD103+

FMC7+

ACD19+, CD5+,

CD23+

CD10–, FMC7–

CD10, BCL-6,

PD-1 (CD279), and CXCL13.

+ T cell markers

Adult T-cell leukemia/lymphoma

[CD4, CD25, and FoxP3.

CD7 is almost always absent.]

follicular hyperplasia, clusters of epithelioid histiocytes, and an infiltrate of monocytoid B cells

NO NECROSIS

 Lupus erythematosus
 Vegetations covering both sides of valve
surfaces
 Fibrinoid necrosis & inflammation

 Large vessels
-- Giant cell
-- Takayasu
 Medium vessels
-- PAN
 Small vessels
-- HSP
--sle
-- cryoglobulinemia
-- Good pasture
--Wegeners
--Churg Strauss
--microscopic polyangiits

BCL-6

p53 (worse prognosis)

ANCA (antineutrophil

cytoplasmic autoantibodies)

 Antibodies against antigens in the

cytoplasm of neutrophils

 cANCA – cytoplasmic staining,

alternative leukocyte protease (3) "CP3"

 pANCA – perinuclear staining 

alternative myeloperoxidase "PM"

 Triad: upper respiratory tract,

lung, kidneys

 Necrosis, vasculitis and

granulomas

 cANCA (+) in > 90% of cases

 Closes in response to elevated oxygen tension, decreasing vascular resistance, decreasing prostaglandin E2

 May be delayed with hypoxia, prematurity, or

cardiac disease

– Clinically: Holosystolic “machinerymurmur”

 Seen in Turner’s syndrome (45 XO)

 Associated with bicuspid aortic valves

– Large VSD

– Overriding aorta

– RV outflow tract obstruction (pulmonary

stenosis/atresia)

– RV hypertrophy

 Class 1 Ab react with T and B cells

 Class 2 Ab react with B cells only

 PNH is a defect in which GPI linked

antigens (CD55, CD59) are not present on

the cell surface

 Flow assays can look for these antigens on

either RBC or neutrophils.

CD3+

CD7-

Normal follicular dendritic intact

Eosinophilia

• Females, 40 – 60 years old, assoc w HLA DR,
• Autoimmune diseases (thyroid, SS, RA, scleroderma)
• 80-95% AMA positive
• Cholestasis
• Bile duct injury
• Granulomas

• Males > Females, 25 – 60 year old
• 75% assoc with UC
• Immune attack on large bile ducts
• fibrous obliteration of bile ducts
• periductal fibrosis, ductopenia
• ↑ cholangiocarcinoma

Non-viral infectious hepatitis?

• Bacterial
– Brucellosis, salmonella (S. typhi)

• Mycobacterial
– M. tuberculosis, MAIC

• Fungal
– Coccidiomycosis

• Parasitic
– Amebiasis
– Hydatid disease

- 85% due to C282Y and/or H63D mutations
- C282Y cysteine to tyrosine substitution at
amino acid position 282
- H63D histidine to aspartate at position 63

- C282Y, highest iron overload
- H63D, lowest iron overload
- Compound heterozygotes, C282Y & H63D intermediate

paroxysmal cold hemoglobinuria, with erythrophagocytosis; the arrow points to a red cell that has been phagocytosed by
a neutrophil.

most common cause of Conn syndrome?

adrenal adenoma.

[[hyperaldosteronism (hypernatremia, hypokalemia, hypertension).]]

pituitary hormones are produced by basophilic cells

luteinizing hormone, follicle-stimulating hormone, thyroid-stimulating hormone, and adrenocorticotrophic hormone

posterior pituitary hormones

Oxytocin and ADH

anterior pituitary hormones produced by acidophils

How is an insulin tolerance test used to measure growth hormone?

creates hypoglycemia, stimulating GH production.

Resemble hepatocytes, one to two cells thick cords
Clear cell change—glycogen. No portal triads.
Naked arteries or veins.
Rare mitosis
Preserved reticulin pattern
No CD34 capillarization (focal)

Vascular lesion, arteries in fibrous stroma
Divides liver into nodules-focal cirrhosis
Cholestasis, ductures, copper, cholate stasis

Mucicarcimine +

CK7+

Hep Par Negative

In kids with
a viral illness, who were treated with aspirin,
this disease causes fatty liver and
encephalopathy. Grossly, the liver is yellow.
Histologically there liver has diffuse steatosis.
On EM, the liver cell mitochondria are
enlarged and mis-shapen.

average age of onset at age 60.

insidious onset of dyspnea.

periphery of the lung and the lower lobes.as the disease progresses, the process moves centrally, terminating in end-stage honeycombing.

-Clinically, UIP is referred to as idiopathic pulmonary fibrosis. Hyaline membranes are not a histologic hallmark of UIP.  UIP has a poor prognosis, with death typically occurring within 3-6 years of diagnosis

rare. I

-healthy immunocompetent individuals,

- rapidly progress to respiratory failure without any known cause.

- The histology is identical to diffuse alveolar damage (hence the clinical name acute interstitial pneumonia or, histologically, idiopathic diffuse alveolar damage).

The entity usually has a rapidly fatal course.

Electron microscopy of spindle cell carcinoma/carcinosarcoma reveals 2 groups?

A true carcinosarcoma demonstrates both squamous epithelial features and mesenchymal features

while sarcomatoid carcinoma demonstrates only epithelial characteristics in both the squamous and spindle cells.

Autoimmune gastritis primarily involves which part of stomach?

Mononuclear infiltrate of lamina propria and mucosa with destruction of fundic glands

Intestinal and pyloric metaplasia

Enterochromaffin cell hyperplasia positive for chromogranin

Corpus fundus

(most parietal cells)

Complete (mature) intestinal metaplasia looks like normal small intestine with straight crypts lined by absorptive cells with a brush border and goblet cells that secrete sialomucins. Paneth cells are sometimes seen, usually concentrated in the base of the glands. It is not a precancerous lesion. Incomplete (immature) intestinal metaplasia (type II) is architecturally distorted with irregular crypts, goblet cells and columnar cells with varying degrees of differentiation. Paneth cells are not seen strongly associated with subsequent development of adenocarcinoma. Incomplete (immature) intestinal metaplasia (type III) demonstrates extensive architectural distortion and is lined by undifferentiated columnar cells resembling low-grade dysplasia.

B⁺ Thalassemia?

B⁰ Thalassemia?

B⁺ Thalassemia? Reduced B globin synthesis

B⁰ Thalassemia? Absent B globin synthesis

[Normally, the two Beta chains are encoded by a SINGLE B-globin gene xsome 11. Splicing mutationsMC

The two alpha chains encoded by a identical PAIR of alpha globin genes xsome 16]

 Immune Complex Mediated
– Polyarteritis nodosa
           Secondary to SLE, Hep B

 Antibody Mediated
– Kawasaki Disease
           Necrotizing vasculitis
           Primarily pediatric disease

pANCA (Anti-Neutrophil Cytoplasmic

Antibody) may be seen

– 60-70% with Ulcerative Colitis

– 40% with Chron’s

 Anti-Saccharomyces ceriviseae Ab

(ASCA) is associated with Chron’s

 cANCA

– Usually antibody to proteinase 3

– Associated with Wegener’s (95%)

 pANCA

– Usually antibody to myeloperoxidase

– Associated with PAN or other

vasculitides

 Associated with ulcerative colitis and

Primary Sclerosing Cholangitis

 Possible antigenic targets

-  lactoferrin,

– cathepsin G

– histone H1,

– BPI (bacterial permeability increasing

protein)

 Anti-Thyroglobulin Ab in app 90%

– Thyroglobulin has >8 epitopes

 Anti-Thyroid Peroxidase (TPO)

(Microsomal) in app 95%

– Antibody is cytotoxic

 Lymphocyte Infiltrate, CD4

 HLA B8 and DR3 associated

 Anti Thyroglobulin in 50%

 Anti-TPO in 90%

 LATS Present

– Long Acting Thyroid Stimulator

– Anti-Thyroid Stimulating Hormone

 75% Female, usually adolescent

 Symptoms of other autoimmune diseases

– Hashimoto’s, PSS, diarrhea

 Type 1- Anti-Smooth muscle Ab, possibly

ANA

 Type 2- Anti-Liver Kidney Microsomes

(Cytochrome P450D2)

 10-15% have low titer AMA

 Anti-Reticulin Ab

 Anti-Gliadin Ab

 Anti- Endomysial Ab

 Anti Tissue transglutaminase

Enzyme that can deamidate gliadin

 The antigenic target of the anti-endomysial

antibody

 Mid 2000’s wisdom IgA anti TTG is the best single

test for Celiac Disease

Summary for Celiac- What

Tests are Appropriate?

 IgA Anti TTG and Anti Deamidated Gliadin

appear to be the most useful combination of

serological assays

– If the above tests are negative, and the

patient is IgA deficient, or if clinical

suspicion of Celiac is still high, then an

IgG anti TTG and IgG anti d-Gliadin is in

order

 HLA Typing- DQ2 and DQ8

 Anti-Striated muscle antibody

– Cross reacts with thymic epithelium

 Anti-Acetylcholine Receptor Ab

– Blocks neuro-muscular transmission

 Lambert-Eaton Variant

– Proximal muscle weakness

– >40 years old

– Other autoimmune disease or small cell

cancer

 CSF IgG Level

 Oligoclonal Banding

 Myelin Basic Protein level

 IgG Index

– CSF IgG/CSF Albumin

Serum IgG/Serum Albumin

Forward scatter:

Side Scatter:

Forward scatter: Size

Side Scatter: Complexity