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Semester 5 April > Anatomical Pathology - Leukaemia, Spleen And Lymph Nodes > Flashcards

Anatomical Pathology - Leukaemia, Spleen And Lymph Nodes Flashcards

0
Q

Defn hypersplenism

A

Peripheral blood pancytopaenia and splenomegaly (primary or secondary)

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1
Q

Congenital abnormalities of spleen

A

Accessory spleens/ splenunculi
Asplenia
Polysplenia

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2
Q

Causes of splenomegaly

A 
Congestion
Infection
Immune disorders
RBC abnormalities
1ry or metastatic neoplasms
Storage disorders
Amyloidosis
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3
Q

Causes of congestive splenomegaly

A 
Pre-hepatic = extrahepatic portal/splenic vein thrombosis
Hepatic = cirrhosis 
Post-hepatic = raised IVC pressure (RHF, pulmonary/tricuspid disease)
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4
Q

Where does pathology mainly occur in congestive splenomegaly

A

Red pulp

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5
Q

Cut surface of congestive spleen

A

Beefy red with little white pulp

Some firm brown nodules (areas of healed infarction - gamma gandy bodies)

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6
Q

Types of infection causing splenomegaly

A 
Systemic infection
Bacterial 
Viral
Chronic malarial
Granulomatous inflammation
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7
Q

What are gamma gandy bodies composed of?

A

Fibrinous and elastic tissue
Abundant haemosiderin
Dystrophic calcification

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8
Q

What organisms cause granulomatous inflammation of spleen

A

Bacterial: Tuberculosis
Fungi: histoplasmosis, cryptococcus
Protozoan: toxoplasmosis

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9
Q

Extreme bacterial splenomegaly

A

Acute septic splenitis

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10
Q

What causes splenomegaly in bacterial infection

A

Accumulation of neutrophils in sinuses and medullary cords

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11
Q

Why bacterial splenomegaly soft?

A

Proteolytic enzyme action

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12
Q

Immune causes of splenomegaly

A

Felty’s syndrome - RA and splenomegaly

SLE

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13
Q

RBC abnormalities causing splenomegaly

A

Sickle cell anemia

Hereditary spherocytosis

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14
Q

Neoplasms that cause splenomegaly

A

Hemangioma
Acute/chronic leukaemia
Myeloproliferative disorders
Hodgkin’s/ Non-Hodgkin’s lymphoma

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15
Q

Storage disorders that cause splenomegaly

A

Niemann Pick disease
Gaucher’s disease
Mucopolysaccaridoses

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16
Q

What is seen macroscopically in storage disorders

A

Red pulp expansion by macrophages (filled with abnormal storage product)

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17
Q

Causes of splenic rupture

A

Usually blunt abdo trauma (emergency splenectomy)

Spontaneous rupture - infectious mononucleosis

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18
Q

Causes of splenic infarction

A

Splenic artery occlusion due to:
Emboli
Local thrombosis (sickle cell, myeloproliferative disorders, malignant infiltrates)

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19
Q

Causes of splenic atrophy

A 
Sickle cell (infarcts)
Malabsorption disease (eg coeliac disease)
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20
Q

Slate grey spleen?

A

Malarial infection

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21
Q

Causes of infective granulomatous lymphadenitis

A

TB

Toxoplasma

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22
Q

Infective causes of necrotising lymphadenitis

A

Lymphogranuloma venereum

Cat scratch disease

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23
Q

Histological feature of necrotising lymphadenitis (infective)

A

Stellate abscesses in lymph node surrounded by palisades histiocytes

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24
Q

Cause of infective follicular hyperplasia

A

Syphilis

25
Q

Causes of infective para cortical hyperplasia

A

Infectious mononucleosis (EBV)

26
Q

Causes of non infective granulomatous lymphadenitis

A

Sarcoidosis
Crohn’s
Reaction to tumor Ag
Foreign body

27
Q

Causes of non infectious necrotising lymphadenitis

A

Kikuchi’s disease

SLE

28
Q

Non infectious causes of follicular hyperplasia

A

RA

29
Q

Non infectious causes of para cortical hyperplasia

A

Dermatopathic lymphadenopathy
Eg. Eczema, psoriasis
Cutaneous T cell lymphoma

30
Q

No infectious causes of sinus histiocytosis

A

SHML/ Rosia-Dorfman syndrome

Langerhan’s cell histiocytosis

31
Q

Defn persistent generalized lymphadenopathy syndrome

A

Persistent extrainguinal LN in two or more contiguous sites.
Greater than three months.
Unknown aetiology besides HIV.

32
Q

Distinguishing features of Hodgkin’s Disease

A

Rarely involves tonsillar area, skin, stomach, ileum.

Reed-Steenberg cells

33
Q

Reed-Steenberg cell morphology

A

Large, bi-/multi-lobulated nuclei
Large eosinophilic nucleoli
Slightly acidophilic cytoplasm

34
Q

WHO classification of non Hodgkin’s based on..

A

Type/ number of neoplastic cells
Pattern of fibrosis
Proportion of reactive lymphs to neoplastic cells

35
Q

Two main types of Hodgkin’s Disease

A

Nodular lymphocyte predominant HD

Classic HD

36
Q

Four main type of classic HD

A

Lymphocyte rich HD
Nodular sclerosing HD
Mixed cellularity HD
Lymphocyte depleted HD

37
Q

Spread of HD (?pattern)

A

Generally via lymphatics. Mostly, contiguous groups of LN are involved

38
Q

Clinical outcome of HD influenced by

A

Stage
‘‘B’’ constitutional symptoms
Disease bulk
Extent of splenic involvement

39
Q

Complications of HD

A

Infection (NB) [T cell immunity defect, splenectomy, opportunistic infections]
Cachexia
Massive organ infiltration
Complications of Rx [corticosteroids=immunosuppression, endocrine dysfunction (hypothyroid,hypogonadism), pulmonary inflammation and fibrosis, pericardial fibrosis]
Secondary malignancies

40
Q

Risk factors for NHL

A

Viruses - EBV, HTLV1

Immunodeficiency - 1ry or 2ndry

41
Q

'’B’’ symptoms of lymphoma

A

Fever
Weight loss
Night sweats

42
Q

System used to stage lymphoma

A

Ann-Arbor system

43
Q

Stage 1 lymphoma

A

Single LN region or structure

44
Q

Stage 2 lymphoma

A

2 or more LN region on same side of diaphragm

45
Q

Stage 3 lymphoma

A

LN regions on both sides of diaphragm

46
Q

Stage 4 lymphoma

A

LN region with non-contiguous extra nodal involvement

47
Q

Complications of NHL

A

Immunodeficiency (disease/ Rx)
Infection
Neutropenia, thrombocytopenia, anemia (replacement of normal bone elements by NHL, marrow damage during Rx, involvement of spleen by NHL = hypersplenism)

48
Q

Common site of extra nodal NHL

A

GIT
Thyroid, salivary glands

*no site exempt

49
Q

Extra nodal NHL may arise following

A 
H. Pylori gastritis
Autoimmune thyroiditis (Hashimoto's)
Autoimmune inflamm of salivary/lacrimal glands (Sjogren's)

Known as MALT lymphomas

50
Q

Presentation of NHL

A

Involves any LN group in body, haphazard distribution. May involve lymphoreticular tissue (spleen, BM, liver, tonsils) or extra nodal tissue. May even involve nonlymphoid tissue such as skin, brain, thyroid.
Usually painless rubbery enlarge LNs. Symptoms may occur as a result of tissue infiltration.
Fish-flesh. Loss of nodal architecture.

51
Q

Common forms of mature B cell NHL

A

Follicular
Diffuse small lymphocytic
Diffuse large cell
Burkitt’s lymphoma

52
Q

Histology of Burkitt’s lymphoma

A

Starry-sky = sheets of primitive medium sized blastic lymphoid cells and many histiocytes

53
Q

Types of Burkitt’s lymphoma

A

Endemic
Non-endemic
AIDS associated

54
Q

Types of mature T cell NHL

A

Anaplastic large cell lymphoma

Mycosis fungoides and sezary syndrome (cutaneous)

55
Q

Endemic Burkitt’s presents with

A

Enlarged jaw or ovaries.
Nodal involvement not characteristic.
Children 4-8yrs.

56
Q

Presentation of non-endemic Burkitt’s

A

Intestinal involvement common (ileum) with mesenteric LNs.

Older children.

57
Q

Causes of massive splenomegaly

A 
Chronic malaria
Gaucher's disease
CML
Myelofibrosis
Kala-azar
Infectious mononucleosis
58
Q

Three complications of splenomegaly

A

Anaemia
Thrombocytopenia
Neutropenia

59
Q

Microscopic features of granulomatous lymphadenitis

A

Cluster of epitheliod histiocytes w/wout necrosis.

Giant cells

Semester 5 April (17 decks)

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