E1--Joiner & Lindley Flashcards

1
Q

Agammaglobulinemia is caused a a defect in?

A

Bruton’s tyrosine kinase

this defect causes B cell development to stop= no immunoglobulins

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2
Q

What other, more common disease would you need to rule out before deciding an animal has agammaglobulinemia

A

Failure of passive transfer

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3
Q

A combined immunodeficiency involves which class of lymphocytes

A

B & T cells (both classes)

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4
Q

Two forms of combined immunodeficiency (CID) and which spp. they occur in

A

1) autosomal recessive (horses-Arabians, jack russells, mice)
2) X-linked; dogs

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5
Q

Autosomal recessive CID mechanism of disease

A

5 base pair microdeletion in DNA-PKcs (part of the recombinase activating gene)

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6
Q

When do clinical sign present in foals with AR CID (autosomal recessive)

A

10 days of age

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7
Q

Penumonias in foals with CID are typically _____ (name etiology)

A

Adenoviral

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8
Q

Which form of CID is associated with profound lymphopenia and decreased serum immunoglobulin levels

A

Autosomal recessive

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9
Q

With AR CID, how do the lymphoid organs look

1) grossly
2) on histopath

A

1) all lymphoid tissue is hypoplasitc

2) won’t see any lymphocytes

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10
Q

X-linked CID mechanism of disease

A

4 base pair microdeletion in the gamma-c receptor subunit

*necessary to T cell maturation, proliferation, and response to antigens

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11
Q

Dogs with X-linked CID are still able to make?

A

B lymphocytes

lack of T cells negatively impacts B cell ability to function

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12
Q

How does X-linked CID differ from AR CID:

1) on bloodwork
2) on histopath

A

1) will not have severe lymphopenia (count is made up up B cells mostly)
2) germinal centers are present (paracotical region is the same though…hypoplastic and replaced by fat)

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13
Q

Normal gradual replacement of the thymus by connective tissue and fat following puberty is referred to as?

A

Thymic involution

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14
Q

Can be a cause of early thymic involution

A

Malnutrition (via high caloric intake)

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15
Q

2 consequences of early thymic involution

A

1) higher incidence of allergic and autoimmune disease

2) abnormal DNA repair

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16
Q

Two forms of lymphatic atrophy

A

1) Senile (age associated)

2) Cachectic (malnutrition associated)

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17
Q

How does cachectic atrophy differ in the spleen and thymus

A

Occurs in the thymus due to OVER-nutrition

occurs in the spleen due to UNDER-nutrition

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18
Q

Where would you expect to find hemorrhage in the lymph node if it was drained from a local tissue?

A

Cortex & medullary sinus

*In medulla= likely started in lymph node

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19
Q

What are siderotic plaques

A

deposits of Fe & Ca in splenic connective tissues (in areas of hemosiderin accumulation)

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20
Q

Yellow encrustations present along the splenic margins and surface is indicative of?

A

Siderotic plaques

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21
Q

Describe how siderotic plaques appear on histopath

A

Ca salts & Fe encrusted on connective tissue

Swollen, hyper-refractile elastic fibers

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22
Q

3 gross findings with acute lymphadenitis

A

ln are:

1) enlarged
2) locally mobile
3) soft & hyperemic

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23
Q

Neutrophils in the following locations indicates:

1) peripheral and medullary sinuses
2) cortical areas

A

1) inflammation from drained tissue

2) hematogenous origin of infection

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24
Q

What type of lymphadenitis is common with bacterial/fungal diseases that are difficult to kill

A

Granulomatous lymphadeitis

25
Q

Lymphatic organ most commonly affected by circulatory disturbances; Name 4 potential disturbances

A

spleen;

trauma, congestion, thrombosis, torsion

26
Q

Two common causes for splenic congestion

A

1) barbiturate euthanasia

2) autoimmune hemolytic anemia

27
Q

Splenic torsion occurs most commonly with

A

GDV (large, deep chested dogs)

28
Q

What should be present on histo path with follicular hyperplasia? How is it different from follicular lymphosarcoma?

A

Hyperplasia– dense band of paracortex

LSA–atrophied paracortex

29
Q

Describe each clinical stage of LSA:

1) Stage 1
2) Stage 2
3) Stage 3
4) Stage 4
5) Stage 5

What is substaging used for?

A

1) single node involved
2) >1 node involved but on same side of diaphragm
3) generalized lymphadenopathy
4) liver and/or spleen invovlement
5) blood manifestation, bone marrows, extra nodal

*Substaging=
a–not sick
b–sick

30
Q

The 5 anatomical classifications of LSA

A
Multicentric
Alimentary
Thymic
Cutaneous
Solitary
31
Q

Classic appearance of lymph nodes with LSA

A

enlarged, pale grey-white

32
Q

Why would thymic LSA have a poorer prognosis

A

because it involves T cells

33
Q

The organ most commonly affected with the solitary form of LSA

A

Kidney

34
Q

The two forms of bovine LSA? Which is associated with BLV?

A

1) enzootic bovine LSA–BLV associated

2) Sporadic bovine LSA

35
Q

Distribution of lesions with enzootic BLSA

A

HAULS (heart, lymph nodes, abomasum, uterus, spinal cord)

Kidneys & retrobulbar space

36
Q

You necropsy a dog and see the spleen has grey/red nodules up to 2cm protruding from the cut surface;

Histopath reveals non-encapsualted aggregations of lymphocytes and compression of surrounding parenchyma

Top ddx?

A

Benign nodular hyperplasia

37
Q

On the spleen you see a well-circumscribed, red-black nodule(s); histopath reveal blood-filled vascular spaces lined by well-differentiated epithelium… top ddx?

A

Hemangioma

38
Q

T/F: the liver or spleen doesn’t look enlarged on US, there’s no need to aspirate it because it cannot have lymphoma infiltrates

A

FALSE

39
Q

Majority of canine LSA patients are what stage?

A

Stage 4 (liver/spleen involvement)

40
Q

Without treatment, what is the MST of dogs with large cell, multicentric, B-cell LSA

A

4-6 weeks

41
Q

Which chemotherapy drug protocol offers the longest MST and highest remission rates

A

CHOP-L (frontline therapy)

42
Q

Why is prolonged pre-treatment of canine LSA with steroids (i.e. pred) a negative prognostic factor?

A

Because prednisone can induce resistance to other chemotherapeutic drugs

43
Q

Most common form of LSA in cats?

A

Large cell gastrointestinal (in older, FeLV negative cats)

44
Q

LSA in cats:

1) MST
2) overall response rate compared to dogs

A

1) 6-9 months

2) Lower (50-60% compared to 85-90%)

45
Q

Two forms of leukemia

A

Lymphoproliferative

Myeloproliferative

46
Q

Which form of lymphoproliferative leukemia carries a poorer prognosis? What is its cellular classification?

A

Acute form

Large cell (or blasts) in origin

47
Q

Generally, how do acute and chronic lymphoproliferative leukemia present differently?

A

Acute form–present SICK (anorexia, PU/PD, etc); hemorrhages, markedly enlarged lns

Chronic form–SEVERE lymphocytosis but not sick , lns less enlarged

48
Q

Tx protocol for:

1) ALL
2) CLL

A

1) multi-agent; supportive

2) Chlorambucil & pred

49
Q

MST for:

1) CLL
2) ALL

A

1) 12-30 months (70% achieve remission)

2) 4 months

50
Q

Two forms of plasma cell tumors

A

Plasmacytoma

Multiple myeloma

51
Q

T/F: plasmacytomas have the potential to progress to multiple myelomas and do so very often

A

FALSE;

can progress to MM but occurs rarely

52
Q

Which findings when diagnosing multiple myleoma would be negative prognositc factors? (3)

A

Hypercalcemia
Bence jones proteinuria
Extensive bone lysis

53
Q

patients with multiple myeloma show a ___% overall response rate and have a MST of _____

A

90% overall response

MST–540days

54
Q

3 forms of histiocytic disease

A

1) histiocytoma
2) reactive processes (cutaneous and systemic)
3) malignant processes

55
Q

How are histiocytomas treated

A

They aren’t; will usually spontaneously regress (cleared by lymphocyte infiltrate)

56
Q

Two ways cutaneous and systemic histiocytosis differ

A

1) cutaneous form is responsive to steroids & non-progressive
2) systemic form can be found on mucocutaneous junctions

57
Q

Compared to histiocytic sarcoma, malignant histiocytosis is a _______ disease

A

systemic!!

histiocytic sarcoma is a solitary lesion

58
Q

Which chemo drug/protocol shows the highest remissions rate with histiocytic sarcoma

A

CCNU

MST >500days

59
Q

For malignant histiocytosis:

1) chemo drugs used
2) MST/prognosis

A

1) CCNU, doxorubicin

2) 3-4 months (poor…rapidly progressive disease)