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Module 17 > Approach to Cancer Patient > Flashcards

Approach to Cancer Patient Flashcards

1
Q

what breeds are predispoed to osteosarcomas

A

giant/large breeds

great dane, deerhound, lurcher, rottweiler

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2
Q

what breeds are predisposed to histiocytic sarcoma

A

bernese mountain dogs

flat coated retriever

rottweiler

min schnauzer

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3
Q

what breeds are predisposed to lymphoma

A

boxer

golden retreiver

lab

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4
Q

what breeds are predisposed to mast cell tumours

A

boxer

pug

sharpei

weimeraner

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5
Q

what breeds are predisposed to bladder transitional cell carcinomas

A

scottish terriers

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6
Q

what breeds are predisposed to CNS tumours

A

brachycephalic dogs – glioma

dolicocephalic – meningioma

boxer

g retreiver

french bull dog

boston terrier

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7
Q

what breeds are predisposed to nasal tumours

A

dolicocephalic breeds

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8
Q

what breeds are predisposed to hemangiosarcoma

A

german shepherd dog

golden retriever

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9
Q

what are the tumour incidences in male cats

A
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10
Q

what are the tumour incidences in female cats

A
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11
Q

what are the tumour incidence in male dogs

A
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12
Q

what are the tumour incidences in female dogs

A
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13
Q

what are the presentations of cancer patients

A
  1. superficial mass/lump
  2. non-specific clinical signs as direct effect of internal tumour – ex. obstruction, compression
    - vomiting

diarrhea

weight loss/wasting (GI mass)

dyspnea, weight loss (thoracic mass)

  1. non-specific clinical signs/medical presentation due to indirect effect of internal tumour due to secreted peptide/cytokine/hormone
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14
Q

what is a paraneoplastic syndrome

A

systemic, metabolic and endocrinological effects associated with some tumour types

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15
Q

what are endocrine disease paraneoplastic syndromes

A
  1. hyperthyroidism (thyroid adenoma in the cat)
  2. hyperadrenocorticism (pituitary adenoma ACTH/adrenal tumour)
  3. acromegaly (pituitary adenoma GH in cats)
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16
Q

what is the most common paraneoplastic syndrome

A

hypercalcemia

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17
Q

what are other paraneoplastic syndromes (9)

A
  1. hypercalcemia
  2. hyperhistaminemia (MCT)
  3. hypoglycemia
  4. hyperestrogenemia (feminization)
  5. hypergastrinemia - rare
  6. immune mediated syndromes
  7. hyperviscosity syndrome
  8. hypertrophic osteopathy
  9. cachexia syndrome
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18
Q

what are normal controllers of serum calcium

A

PTH, 1,25 vitD3 increase

Calcitonin decreases

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19
Q

what are cancer increasers of seurm calcium

A

PTH, PTH-rP (PTH related protein 70% sequence homology to PTH)

Local factors/cytokines (IL1, IL6, TNF)

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20
Q

describe how hypercalcemia occurs

A
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21
Q

what are hypercalcemia of malignancy (5)

A
  1. lymphoma/leukaemia - most common cause of hyperca (PTHrp induced)
  2. apocrine gland adenocarcinoma of the anal sac (25-55% of cases)
  3. bone tumours/multiple myeloma (local osteolysis)
  4. other malignant tumours (mammary, thryoid, lung, thymoma)
  5. parathyroid adenoma (bening) – PTH induced
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22
Q

what are non neoplastic causes of hyperca (5)

A
  1. endocrine: hypoadrenocorticism (parathyroid adenoma)
  2. renal: severe primary renal failure
  3. poisoning: vit D toxicity (rodenticides, diet)
  4. inflammatory: infections/granulomatous inflammatory disorders (osteomyelitis, osteoporosis, blasto or coccidiomycosis)
  5. lab error: lipemia, hemolysis, hemoconcentration, hyperproteinemia
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23
Q

how do hyperca patients present (4)

A

Hypercalcemia may cause numerous clinical sign —> together they form a syndrome to suggest underlying hypercalcemia:

  1. Renal: PUPD
  2. Gastrointestinal: anorexia, vomiting, constipation
  3. Neuromuscular: muscle weakness, tumours, lethargy
  4. Cardiovascular: hypovolemia, bradycardia, dysrhythmias
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24
Q

what is the normal serum calcium in the dog and what would be considered hyperca

A

Normal serum calcium (doh) = 2.34-3.0 mmol/l

Hypercalcemia > 3mmol/l

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25
Q

what is the normal ionized calcium in the dog and what would be considered ionized hyperca

A

Ionized calcium (active form) (dog) = 1.2-1.4 mmol/l

Ionized hypercalcemia > 1.4 mmol/l

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26
Q

what is the main ddx of hypercalcemia in the dog

A

cancer

~2/3 in dogs

~1/3 in cat

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27
Q

what is the approach to to hyperca (3)

A
  1. is the hyperca real? (repeat the test to exclude lab error, is it affected by protein levels/hemoconcentration, check ionized calcium is elevated, check age of animal – young, growing?)
  2. rule out non-neoplastic causes – blood results (ACTH, renal), access to poisons, dietary supplements
  3. hunt for a tumour
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28
Q

how do you hunt for the tumour in hyperca patients in your clinical exam (5)

A
  1. lymphoma most common –> check lymph nodes enlarged
  2. apocrine adenocarcinoma of the anal sac –> rectal exam
  3. parathyroid tumour/adenoma –> US neck/PTH gland
  4. multiple myeloma –> bone pain, ocular changes
  5. metastatic bone tumours –> bone pain
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29
Q

what diagnostics can you use to find the tumour in hyperca patient (5)

A
  1. chest rads: 3 views, LNs/lung mets/masses
  2. abdominal ultrasound (check internal LNs, organs)
  3. limb and spine rads (bone lysis/lesions)
  4. routine bloods (any clues to organ involvement)
  5. bone marrow biopsy (tumour cells)
30
Q

are PTH and PTHrp useful in hypercalcemia patients to diagnose cancer?

A
31
Q

what is the issue with testing PTH and PTHrp levels

A

EDTA sample needs to be frozen immediately and sent on dry ice to lab

$$$ and time delay for result but can help in some cases with no obv causes of hyperca

32
Q

what are the signs of hypogylcemia syndrome

A
  1. episodic collapse/weakness
  2. low blood glucose
33
Q

what are tumour causes of hypogylcemia

A
  1. insulinoma (high insulin)
  2. hepatic neoplasia (altered glucose metabolism, consumption)
34
Q

what are non-tumour causes of hypogylcemia (3)

A
  1. sepsis, pregnancy toxemia
  2. liver diseases – shunts, cirrhosis, storage diseases
  3. hypoadrenocorticism
35
Q

what are syndromes of feminization (4)

A
  1. gynacomastia
  2. bilaterally symmetrical alopecia
  3. reduced libido
  4. pendulous prepuce
36
Q

what are estrogen producing tumours (3)

A
  1. sertoli cell tumour (testicle)
  2. increased plasma E2
  3. lower plasma testosterone
37
Q

what are the signs of a sertoli cell tumour

A
  1. anemia: pallor, weakness
  2. thrombocytopenia: petechiae
  3. neutropenia: sepsis, pyrexia
38
Q

what are other systemic tumour effects that can occur (3)

A
  1. cachexia: lymphoma, any extensive systemic or metastatic tumour (altered metabolism by tumour –> weight loss, emaciation)
  2. hypertrophic pulmonay osteopathy (marie’s disease): primary lung mass or metastatic disease –> periosteal new bone growth (long bones), painful limbs, lameness
  3. dermatological changes (rare): glucagon producing tumours – hepatocutaneous syndrome
39
Q

what are neuropathies

A

LSA, any tumour type

immune mediated nerve changes

neurological deficits, muscle wastage

40
Q

what is myasthenia gravis and what tumours does it occur with

A

thymoma

antibody production to acetyl choline receptors

muscle weakness, collapse at exercise

41
Q

what are hematological immune mediated syndromes

A

immune mediated hemolytic anemia

immune mediated thrombocytopenia

pallor, petechiae, hemorrhage

42
Q

what other hematological effects can occur with cancer (5)

A
  1. anemia of chronic disease
  2. vasculitis
  3. DIC or other coagulopathies
  4. decreased or increased cell #s (neutrophilic leukocytosis, eosinophilia, thrombocytosis, lymphopenia)

pallor, petechiae, hemorrhage, edema

43
Q

what is hyperviscosity syndrome

A

thick viscous blood

44
Q

what causes hyperviscosity syndrome (2)

A
  1. increased # of RBCs (polycythemia vera (neoplastic), secondary polycythemia)
  2. increased protein in blood: overproduction of Ig by plasma cells (multiple myeloma) or other B cell tumours
45
Q

what are the options to diagnose a tumour

A
  1. biopsy
  2. FNA
46
Q

what does a biopsy provide

A

tissue architecture and tumour grade

most accurate and definitive diagnosis

47
Q

what is needed for a biopsy

A

sedation/local or GA

more expensive

time consuming

48
Q

what does an FNA provide

A

quick easy cheap no GA

can diagnose sarcoma, carcinoma, LSA, MCT

but no tissue architecture (no grade) and can be unrepresentative

49
Q

what are the types of biopsy tools (4)

A
  1. tru cut
  2. grab forceps
  3. jamshidi needle
  4. punch
50
Q

what are the two types of biopsy

A
  1. incisional (wedge)
  2. excisional (whole mass)
51
Q

what are the criteria to determine tumour grade (6)

A
  1. cellular differentation, pleomorphism
  2. mitotix index (per 10hpf)
  3. invasiveness
  4. amount of necrosis
  5. overall cellularity
  6. stromal/inflammatory reaction
52
Q

how are soft tissue sarcomas graded

A

low grade (grade I)

high grade (III)

intermediate grade (II)

53
Q

how were soft tissue sarcomas originally graded and now how are they graded

A

traditionally attempted to define sarcomas by cell lineage and behaviour was predicted from this

  1. hemangiopericytoma, PNST, fibrosarcoma
  2. myxosarcoma, rhabdomyosarcoma
  3. lymphangiosarcoma, leiomyosarcoma
  4. synovial sarcoma, histiocytic sarcoma
  5. hemangiosarcoma

but more recently call everything soft tissue sarcomas and use defined criteria to assign grade

54
Q

how are mast cell tumours graded

A

patnaik scheme

based on histopathology not cytology

3 tier system

55
Q

what is the grading criteria for dermal MCT tumours in the patnaik scheme (4)

A
  1. cell morphology and differentiation
  2. mitotic index
  3. extent of tissue involvement
  4. cellularity and stromal reaction
56
Q

what are the features of well differentiated MCT grade I (6)

A
  1. well differentiated mast cells
  2. no tissue invasion (dermis only)
  3. no mitotic figures
  4. minimal stromal reaction
  5. low histological grade/benign nature
  6. low risk of metastasis

prognosis good following surgery >90% long term survival

57
Q

what are the features of poorly differentiated MCT (grade III) (7)

A
  1. poorly differentiated, pleomorphic mast cells (few/no granules), binucleate or multinucleated cells
  2. very cellular
  3. 3-6 mitoses per hpf
  4. extend into subcutis and tissues
  5. hemorrhage, edema, necrosis
  6. aggressive, locally invasive tumours
  7. high rate of distant metastasis

poor prognosis, very few long term survivors (>6 months)

58
Q

what are the features of intermediate grade MCT (grade II) (5)

A
  1. moderately differentiated/pleiomorphic mast cells
  2. some local tissue invasion - lower dermis, subcutis and occasionally deeper
  3. 0-2 mitoses per hpf
  4. some areas of edema, necrosis
  5. variable behaviour

40-75% long term survival

prognosis variable

good (wide) surgery improves prognosis

59
Q

what are the problems with the patnaik scheme

A
  1. difficult to apply: MCT with some mitoses – low grade? MCT in subcut tissues – low grade?
  2. >50% of MCT called grade 2 tumours
  3. grade 2 tumours have 50:50 chance of long survival so not helpful
60
Q

what is the kiupel scheme used for MCT tumour grading

A

2 tier classification system

low and high grade only

high grade criteria (focuses on morphology, not invasion)

high grade MCT habe shorter time to metastasis or new tumour development and shorter survival (<4 months compared to >2 years for low grade)

61
Q

what is tumour staging

A

defining the anatomical extent of the tumour in terms of primary site and distant spread determined by a clinician = clinical assessment

62
Q

how are tumours staged

A

using the TNM system

T = primary tumour

N = node

M = metastasis

63
Q

how is the primary tumour assessed (2)

A
  1. measure its dimensions with ruler or calipers (important for staging and tumour response)
  2. assess whether there is local invasion (physical exam - palpation, radiography, US, CT/MRI)
64
Q

how are the lymph nodes assessed (N) (4)

A

assess the sentinel LNs/anatomical drainage LNs to see if they are enlarged due to tumour infiltration

  1. palpate (enlarged, hard, fixed?)
  2. image
  3. aspirate
  4. biopsy/excise
65
Q

how are distant metastases assed (4)

A
  1. physical exam: for external mets ex. skin lesions
  2. imaging: for internal mets xray/CT, chest, US abdomen
  3. lab evaluation: organ function may be altered
  4. FNA/biopsy if possible to confirm suspicious lesions
66
Q

why do staging?

A
  1. to decide whether treatment/what treatment is feasible (combined with grade information)
  2. helps predicts clinical behaviour/prognosis
  3. provides a precise record of the tumour extent in the body at that time (anatomical staging)
  4. to monitor how tumour changes with time (response to treatment – shrinks (CR/PR), progressive (PD), static (SD)
67
Q

how would you clinically stage an oral tumour using TNM

A
68
Q

what tumours have their own staging system because they do not follow the TNM path of metasasis

A
  1. lymphoma: disseminated disease affecting multiple lymph nodes (own vet system I-V)
  2. mast cell tumour: can become disseminated (own vet system I-IV)
  3. thymoma: human (masaoka) staging system
69
Q

describe the staging system of lymphoma (I-V)

A
70
Q

describe the staging system of MCT (I-IV)

A

Module 17 (31 decks)

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