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PATH FINAL > Haematology PATH > Flashcards

Haematology PATH Flashcards

1
Q

Hodgkin vs Non-Hodgkin lymphoma

A

Hodgkin
- Single group of nodes
- Spread by contiguity
- Mesenteric nodes and Waldeyers ring rarely involved
- Extranodal involvement uncommon
- Reed-Sternberg cells
- CD30 (no CD 20)

NHL
- Multiple group of nodes
- Non-contiguous spread
- Mesenteric nodes and Waldeyers ring involved
- Extranodal invovlement
- No RS cells
- CD20

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2
Q

Hodgkin Lymphoma
- Epi

A

40% of lymphomas.
Bimodal age peak at 25 and 75. Overall slight male predominance.

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3
Q

4 types of Hodgkin lymphoma

A
  1. Nodular sclerosis (70%)
    - common in women
    - excellent prognosis
  2. Mixed cellularity (20%)
    - EBV associated
  3. Lymphocyte-Rich (uncommon)
    - Good prognosis
  4. Lymphocyte poor
    - WORST prognosis
    - EBV positive*
  5. Lymphocyte preDOMINANCE
    - BEST prognosis
    - Popcorn cells
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4
Q

Hodgkin lymphoma risk factor ?

A
  • EBV
  • Immunosuppression
  • Connective tissue disorders
  • RA, SLE, Sarcoid, UC
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5
Q

Morphology of Hodgkin Lymphoma

A
  • RS cells in a background of non-neoplastic inflammatory cells **
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6
Q

Hodgkin lymphoma prognosis

A
  • Curable in most cases*
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7
Q

How does PTH increase serum calcium ?

A
  1. Kidney
    - increase renal absoprtion
    - increase conversion of vitamin D to active form
  2. Increase GI absoprtion
  3. Increase RANK-L expression to increase osteoclast function
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8
Q

Most common cause of hyperparathyroidism

A
  • The most common cause of primary hyperparathyroidism is a sporadic parathyroid adenoma
  • Familial syndromes are a distant second
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9
Q

How to make the diagnosis of Multiple Myeloma

A
  • Monocloncal immunoglobulin
  • Free Light chains
  • Bence-Jones proteins (directly nephrotoxic)
  • Tamm Horsfall proteins
  • Get amyloidosis AL type in kidney*
  • Rouleaux formation (high M chains)

However, 1% are non-secretors with nothing detectable in blood or urine

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10
Q

What’s the major pathological feature of Multiple Myeloma ?

A

Unregulated expression of RANKL, which activates osteoclasts.

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11
Q

Multiple myeloma
- associations

A

Urate neprhopathy

Amyloidosis

POEMS - an atypical form of myeloma – polyneuropathy, organomegaly, endocrinopathy, monoclonal gammopathy and skin changes

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12
Q

Follicular NHL features and prognosis

A
  • Indolent but incurable*
  • 40% transforms to DLBCL
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13
Q

Marginal zone lymphoma (NHL) prognosis

A

Can regress if inciting stimulus removed. Hallmark is lymphoepithelial lesion

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14
Q

Burkitt lymphoma association

A
  • EBV, HIV
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15
Q

Burkitt morphology

A

Fish flesh tumorous masses. Also a term/appearance sometimes for sarcomas.

Distribution: 60% nodal vs 40% extranodal (spleen usually)

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16
Q

What cells do you find in Parathroid hyperplasia ?

A

” Chief cell “ Hyperplasia

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17
Q

B-thalassemia or Alpha more common ? Which one more severe usually

A

B-Thalassemia more common and more severe usually

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18
Q

3 alpha gene deletion and 4 alpha gene deletion is called ?

A

3 alpha gene deletion = HbH (clinically resembles B-thalassemia intermedia)

4 alpha gene deletion = Hb Barts (Long term survival now possible with early recognition, intrauterine transfusion, stem cell transplant)

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19
Q

NF-1 or NF-2 more common?

A

NF-1 by far

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20
Q

NF-1 which chromosome mutation and gene product ?

A

Loss of Chr 17 -> decreased “neurofibromin”

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21
Q

Plexiform Neurofibroma complication ?

A
  • A plexiform neurofibroma has a lifetime risk of up to 10% of transformation into a malignant tumour
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22
Q

Main cause of death for NF-1 ?

A

Malignant peripheral nerve sheath tumor

23
Q

NF-2 epidemiology

A
  • Occurs in 1 in 40-50,000.
  • Rarely noticed prior to puberty
  • Mean age of diagnosis ~25 years
24
Q

NF-2 loss of gene on what chromosome

A
  • Loss of NF2 gene = chr22q12.
  • NF2 functions as a tumour suppressor gene (encodes for Merlin protein).
25
Q

NF-2 prognosis

A

Poor prognosis, mean age of death 36

Resection of CN8 schwannomas with hearing preservation is possible

Genetic counselling

26
Q

TS inheritance ?

A
  • Sporadic most common (60%)
  • Minority familial: AD - can skip generation due to low expressitivity
27
Q

VHL clinical presentation

A

Visual loss from retinal haemangioblastoma

28
Q

VHL complication

A

Renal cell carcinoma is a major cause of morbidity and mortality – 70% risk by age 60.

29
Q

GRANULOMATOSIS with POLYANGIITIS (Wegners)
- Pathophysiology ?
- C-ANCA positive in how many %?

A

Probably a T-cell mediated hypersensitivity response to normally “innocuous” inhaled microbial or other
environmental agents (Robbins).

C-ANCA positive in up to 95% of cases.

30
Q

Granulomatosis with Polyangiitis
- most common location ?

A

Lungs > paranasal sinuses > kidneys > joints > eye > skin

31
Q

Indications for AAA surgery

A
  • ascending aorta >5.5 cm
  • descending aorta >6.5 cm
  • growth rate >1cm/year
  • symptomatic patient
32
Q

Mycotic aneurysm cause ?

A
  • Embolisation of septic embolus (usually from infective endocarditis)
  • Extension of adjacent suppurative process or circulating organisms directly infect the arterial wall.
33
Q

Inflammatory aneurysm shape ?

A
  • Fusiform
34
Q

Adult form Coarctation of Aorta presentation ?

A
  • Presents later, often well into adulthood
  • Upper extremity hypertension with weak pulses and hypotension in the lower extremities
  • Manifestations of arterial insufficiency (ie claudication, cold legs).
  • Murmurs
35
Q

What vessels causes rib notching in Aortic Coarctation ?

A
  • intercostal and internal mammary arteries
36
Q

Aortic coarctation associations

A
  • Bisucpis aortic valve (50%)
  • VSD, ASD, mitral regurg, berry aneurysms, aortic stenosis
  • Turners
37
Q

Infantile vs Adult form Aortic coarctation

A

Infantile
- Preductal

Adult
- Postductal

38
Q

Stanford A more common or B?

A
  • A more common
39
Q

RF of aortic dissection

A
  • HTN (90%)
  • Aortic Coarctation
  • Bicuspid aortic valve
  • Connective tissue disorders
  • Cardiac catheterisation
40
Q

Morphology seen in Dissection and ANeurysm

A
  • Cystic medial degeneration
  • Intimal tear into but not beyond the media – the blood filled false lumen is usually in a plane between the middle and outer 1/3 of the media.
41
Q

Do all aortic dissection have intimal tears ?

A

No, 5-10% dont have obvious intimal tears

42
Q

Are all aortic dissection detectable on Radiology ?

A
  • No
43
Q

Atheroma development pathophysio first step

A

Endothelial injury (vascular permeability, leukocyte adhesion)

44
Q

Atheroma composition

A
  • Lipid core with fibrous cap
  • Periphery (neovascularisation).
45
Q

What are Fatty streaks

A
  • Early lesions made of lipid laden foamy macrophages in the intima that only mildly protrude into the lumen
  • Occur at any age even in kids and not all go on to become atheromatous plaques, although some do
46
Q

T-cell lymphoma high or low grade ?

A

T cell = all high grade

47
Q

Primary vs Secondary Syphilis features

A

Primary syphilis: painless chancre with nontender lymphadenopathy

Secondary: Papulosquamous, Rash skin lesions

Tertiary: gummatous lesions, neurologic or cardiovascular symptoms

48
Q

Extra-adrenal paraganglioma most common site ?

A

Approximately 85% arise below the diaphragm

49
Q

Paraganglioma more commonly maglignant if ..?

A
  • Extra-adrenal
  • Related to syndrome
50
Q

Most common parasympathetic paraganglioma ?

A
  • Carotid body paraganglioma
51
Q

Hashimoto labs ?

A
  • Lymphocytic aggregates
  • Transformed follicular cells (Askanazy/oxyphilic/Hurthle cells)
  • Anti-thyroglobulin antibodies (70%)
  • TPO (95%)
  • TSH (High)
  • Free T4 (Low)
52
Q

Hashimoto complication

A
  • Non-hodgkin lymphoma (majority)
  • Papillary thyroid cancer (1.7x increased risk)
  • Medullary thyroid cancer (2.7x increased risk)
53
Q
A

PATH FINAL (12 decks)

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