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Y4 SA - Oncology > Paraneoplastic and systemic effects of neoplasia > Flashcards

Paraneoplastic and systemic effects of neoplasia Flashcards

1
Q

What are paraneoplastic syndromes?

A

Paraneoplastic syndromes are a consequence of cancer but not due to the location of cancer cells

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2
Q

The systemic effects of neoplasia are due to…?

A

Consequential to the location of the tumour cells
i.e. pericardial effusion due to right atrial HSA is a systemic rather than paraneoplastic effect

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3
Q

List the 3 main effects of neoplasia on the GI system

A

Cancer cachexia and anorexia
Gastroduodenal ulceration
Protein losing enteropathy

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4
Q

Describe the mechanism of cachexia and anorexia due to neoplasia

A

Uncommon in pet cancer patients but likely indicates poor QoL
1. Anaerobic respiration due glucose utilisation and tumoural hypoxia -> increased lactate production and altered insulin sensitivity
2. Altered metabolism due cancer related cytokines and inflammation
3. Poor appetite in some patients

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5
Q

What are the main consequences of cachexia and anorexia in cancer patients?

A

Weight loss, reduced fat mass, lean muscle loss -> poor treatment tolerance

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6
Q

How can you treat cachexia and anorexia in cancer patients?

A
  • Maintain caloric intake by giving low carbohydrate high fat diet
  • Omega 3 PUFA may be beneficial in reducing inflammation related changes
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7
Q

Why is GI ulceration seen in cancer patients?

A
  1. GI tumours can -> gastric or duodenal ulceration
  2. Some tumours produce hormones / metabolites -> gastric acid -> ulceration
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8
Q

What are the consequences of gastric/duodenal ulceration?

A
  • Bleeding can lead to anaemia as a systemic effect.
  • Melena or haematoemesis occasionally seen
  • Risk of rupture
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9
Q

Which tumours produce hormone that lead to gastric ulceration?

A
  1. Dogs with MCT have elevated blood histamine -> GI signs, ulceration and bleeding
  2. Gastrinoma’s produce gastrin -> GI signs, ulceration and bleeding
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10
Q

Describe how protein losing enteropathy occurs due to neoplasia and the consequences of this

A

Systemic effect
Diffuse GI lesions can allow protein loss
- Typically low TP, globulin and albumin often accompanied by diarrhoea
- Low albumin -> ascites
- Myriad of other effects due to loss of proteins binding hormones, clotting factors etc.
Not specific for cancer but seen particularly with GI lymphoma

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11
Q

Name the 6 mechanisms of haematological effects of neoplasia

A
  1. Loss
  2. Reduced production
  3. Destruction
  4. Cytoses
  5. Mono-clonal gammopathies
  6. Coagulation disorders
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12
Q

Describe acute blood loss anaemias

A
  • If no haematemesis or melena more likely splenic than GI
  • TP drops before PCV
  • Signs of shock
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13
Q

Describe chronic blood loss anaemias

A
  • Main differentials are other GI or oral lesions
  • Clinical signs of lethargy, pallor
  • Poorly regenerative microcytic hypochromic anaemia due to iron deficiency
  • Normal or elevated platelet count
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14
Q

Reduced production cytopenia’s can be due to which 3 causes?

A
  • Anaemia of chronic inflammatory disease
  • Myelophthisis
  • Hyperoestrogenism
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15
Q

Describe the main features of anaemia of chronic inflammatory disease

A
  • Common
  • Causes include cancer, but also many other diseases.
  • Mild / moderate normochromic normocytic non-regenerative anaemia.
    Anaemia due to:
  • Disordered iron storage
  • Shortened RBC life span
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16
Q

What is Myelophthisis?

A

Crowding out of stem cells in the bone marrow by tumour cells

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17
Q

Why does Myelophthisis occur?

A

Some tumours produce suppressive cytokines
- Tumour types include lymphoma, leukaemias, multiple myeloma, rarely histiocytic sarcoma and mast cell tumour
- Prevents formation of the normal bone marrow cells

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18
Q

Describe the anaemia cause my Myelophthisis

A
  • Neutropenia then thrombocytopenia before anaemia
  • Non-regenerative normochromic normocytic anaemia
  • Diagnosis by bone marrow aspirate
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19
Q

Hoes how hyperoestrogenism cause reduced production cytopenias?

A
  • Testicular tumours: 50% of dogs with Sertoli cell tumours
  • Neutrophilia progressing to pancytopenia due to bone marrow hypoplasia
  • Other signs are feminisation and include symmetrical alopecia, pendulous prepuce, hyperpigmentation, penile atrophy, gynecomastia, prostatic metaplasia
  • Castration can reverse many signs but bone marrow changes can be slow to recover or irreversible
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20
Q

Describe the causes of destruction cytopenias

A

Paraneoplastic immune mediated anaemia and thrombocytopenia - secondary to lymphoproliferative tumours and occasionally other tumours

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21
Q

Before treating paraneoplastic immune mediated anaemia and thrombocytopenia, what must be excluded from the differentials?

A

Immune mediated haemolytic anaemia
Immune mediated thrombocytopenia

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22
Q

What is microangiopathic anaemia

A

Fragmentation and shearing of RBCs leads to anaemia
- Caused by fibrin networks
- Schistocytosis is a key indicator

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23
Q

Name 3 conditions associated with schistocytosis

A

Disseminated intravascular coagulation
Haemangiosarcoma
IMHA

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24
Q

What do polychromatophils seen on blood smears indicate?

A

Sign of regeneration

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25
Q

What are the causes of erythrocytosis

A
  • Renal tumours via increased EPO, lymphoma, nasal fibrosarcoma, TVT, hepatic tumours
  • Clinically significant erythrocytoses include PU/PD, neurological signs and seizures
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26
Q

Describe treatment for erythrocytosis

A

Phlebotomy, removal of inciting cause, hydroxyurea

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27
Q

Eosinophilia is seen due to the production of which interleukin?

A

IL-5

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28
Q

Eosinophilia is most commonly associated with which tumours?

A

Mast cell tumours
T-cell lymphoma

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29
Q

What are monoclonal gammopathies?

A

Excess production of a single immunoglobulin (antibody) by tumour cells
Elevated serum globulins on biochemistry

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30
Q

What are the clinical signs of monoclonal gammopathies?

A
  • Hyperviscosity (neurological including seizures and coma and cardiac signs)
  • Reduced immune function
  • Renal failure
  • Coagulopathies
  • Ocular disorders.
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31
Q

How are gammopathies diagnosed?

A

Electrophoresis of serum and urine (Bence-Jones proteins)

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32
Q

How would inflammation appear on electrophoresis?

A

Polyclonal gammopathy

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33
Q

How is coagulation affected by neoplasia?

A

Altered platelet function often seen in association with neoplasia
Infarcts / thromboembolism can result

34
Q

How is disseminated intravascular coagulation linked to neoplasia?

A
  • Syndrome of altered consumptive coagulation
  • Thromboembolism in small vessels and bleeding due to consumption of platelets and clotting factors
  • Multi-organ failure and death
  • Mainly in association with carcinoma and HSA
35
Q

How is DIC diagnosed on blood tests/smears?

A

Elevated APTT, PT, FDPs / D dimers, low fibrinogen, low platelet count, schistocytes

36
Q

Paraneoplastic syndrome is the case of what % of hypercalcaemia in dogs and cats?

A

2/3 canine hypercalcaemia and 1/3 feline hypercalcaemia

37
Q

List the clinical signs of paraneoplastic hypercalcaemia

A
  • PU/PD
  • Dehydration
  • GI signs: inappetence and vomiting
  • Weakness
  • Muscle fasiculations
  • Calcification of soft tissues (especially kidneys)
  • Arrythmias
  • Death
38
Q

Describe initial management of severe hypercalcaemia is an emergency

A

Rehydrate with NaCl 0.9%
3 - 4 x maintenance – also enhances calciuresis

39
Q

Once initially hydrated describe further management of severe hypercalcaemia is an emergency

A
  • Continue fluids
  • Consider furosemide: increases calciuresis by increase Na loss – moderate effect
  • Consider bisphosphonates: toxic to osteoclasts therefore slows Ca release from bone
  • Consider salmon calcitonin: short acting (a few days) but often effective
  • Consider prednisolone: only when lymphoproliferative disease diagnosed or excluded
  • Removal of inciting lesion: only effective long term treatment
40
Q

Describe the function of prednisolone in paraneoplastic hypercalcaemia cases

A

Increases calciresis also kills malignant lympho proliferative cells

41
Q

Describe the 4 functions of calcitonin in paraneoplastic hypercalcaemia cases

A
  • Inhibits Ca2+ absorption by the intestines
  • Inhibits osteoclast activity in bones
  • Stimulates osteoblastic activity in bones
  • Inhibits renal tubular cell reabsorption of Ca2+ allowing it to be excreted in the urine
42
Q

Describe a complete workup for paraneoplastic hypercalcaemic patients

A
  • Ensure rectal exam negative for anal gland tumours
  • Assess and aspirate lymph node
  • Check history for diet and toxin exposure
  • Imaging of thorax and abdomen and ultrasound neck esp. if iCa ↑ and Phos ↓
  • PTH / PTHrp / vitamin D if appropriate history of exposure
  • Bone marrow biopsy
  • Consider ACTH stim if other signs are consistent with hypoadrenocorticism
43
Q

Paraneoplastic syndrome due to an insulinoma causes which condition?

A

Hypoglycaemia

44
Q

What are the clinical signs of hypoglycaemia?

A

Weakness, disorientation, seizures, coma and death

45
Q

Describe management/treatment of paraneoplastic hypoglycaemia

A

Emergency – IV glucose + CRI glucose if necessary
Medical management – prednisolone, diazoxide, octreotide
Removal of inciting tumour

46
Q

What are some non-neoplastic DDx of hypoglycaemia?

A

Sepsis
Starvation
Liver dysfunction
Hypoadrenocorticism
Lab error
Some toxicities

47
Q

What is ectopic ACTH syndrome?

A

Rare
Reported in association with lung tumours
Clinical signs similar to hyperadrenocorticism

48
Q

How is ectopic ACTH syndrome diagnosed?

A

Positive for hyperadrenocorticism tests
+ localisable tumour
No signs of adrenal associated hyperadrenocorticism

49
Q

Name two paraneoplastic neurological sydromes?

A

Myaesthenia Gravis
Peripheral neuropathy

50
Q

Describe the clinical signs of Myaesthenia gravis

A

Secondary immune mediated disease
Weakness
Exercise intolerance
Dysphagia
Megaoesophagus and regurgitation

51
Q

When can you presume a Myaesthenia gravis diagnosis?

A

+ve ACHr antibodies and a relevant tumour

52
Q

Myaesthenia gravis is most commonly seen due to which tumour?

A

Most commonly seen with thymoma
Also reported wt osteosarcoma and lymphoma

53
Q

How is Myasthenia gravis treated?

A

Remove tumour and consider immunosuppression, manage other problems

54
Q

Which tumours have been associated with peripheral neuropathies?

A

Lung tumours, insulinoma, lymphoma, MCT, thyroid adenocarcinoma, melanoma

55
Q

How do peripheral neuropathies appear on histology?

A

Demyelination, myelin globulation and axonal degeneration

56
Q

Name some conditions caused by cutaneous paraneoplastic syndromes

A
  • Alopecia and Malassezzia associated dermatitis
  • Pancreatic associated panniculitis
  • Superficial necrolytic dermatitis (SND)
  • Paraneoplastic immune mediated disease = Pemphigus and Erythema multiforme
  • Feline Thymoma-Associated Exfoliative Dermatitis (FTAED)
  • Cutaneous flushing
  • Nodular dermatofibrosis
57
Q

Feline Paraneoplastic Alopecia (FPA) is most commonly seen in which cats?

A

Older cats (7-16 years)
No sex or breed predilection

58
Q

Describe the alopecia caused by feline paraneoplastic alopecia

A
  • Acute-onset, non-pruritic, progressive symmetrical alopecia
  • Initially affects ventral abdomen and limbs then generalises
  • Hair easily epilated
59
Q

What are the other clinical signs of feline paraneoplastic alopecia

A

Glistening skin:
- Alopecic skin inelastic and thin
- Smooth, shiny appearance
Footpad lesions: concentric scale, crusting and painful fissures affecting FPs
Malassezia dermatitis:
- Brown greasy accumulations around the eyes, nose and claw beds
- May be pruritic

60
Q

List some DDx for feline paraneoplastic alopecia

A

Dermatophytosis
Demodicosis
SIA (pruritus, psychogenic)
Telogen defluxion
Endocrinopathies
Superficial necrolytic dermatitis (SND)

61
Q

What is pancreatic panniculitis?

A

Inflammation and hydrolysis of adipose tissue
No age, breed or sex predilection

62
Q

Pancreatic panniculitis is caused by which tumours?

A

Pancreatitis and pancreatic carcinoma and adenocarcinoma

63
Q

Superficial necrolytic dermatitis (SND) can also be called?

A

Necrolytic migratory erythema
Hepatocutaneous syndrome

64
Q

Describe the main features of superficial necrolytic dermatitis

A

Dogs and cats
Hepatic disease and pancreatic neoplasia
Associated amino acid deficiency
Distinctive histo and U/S

65
Q

What are the main skin lesions seen in superficial necrolytic dermatitis?

A

Footpad hyperkeratosis - Erythema, crusting, hyperkeratosis, fissure formation
Crusting dermatitis - alopecia, erosions/ulceration, adherent crusts affecting pressure points, mucocutaneous junctions and feet

66
Q

List some other clinical signs of superficial necrolytic dermatitis

A
  • Early stages none
  • Lethargy
  • Inappetence
  • Systemic signs associated with hepatic / pancreatic disease or rarely glucagonoma
  • Some cases develop diabetes mellitus in association with hepatic disease
67
Q

What is paraneoplastic pemphigus?

A

Autoimmune-induced ulceration of the mucosae and mucocutaneous junctions
Very rare cutaneous PNS

68
Q

Describe the aetiopathogenesis of paraneoplastic pemphigus

A
  • Lymphoma, thymoma, splenic sarcoma, metastatic thymic mass
  • Primary immune mediated pemphigus also seen
  • Exact pathomechanism unknown
  • Antibodies against tumour antigens cross-react with self-antigens
69
Q

What are the cutaneous clinical signs of paraneoplastic pemphigus

A
  • Vesicles (rapidly rupture)
  • Severe ulceration of oral cavity and mucocutaneous junctions
  • Lesions often bilaterally symmetrical
  • Clawbeds and pressure points may be affected
70
Q

Describe the main features of feline Thymoma-Associated Exfoliative Dermatitis (FTAED)

A

Generalised exfoliative dermatitis
Most cases associated with thymoma
Some may be idiopathic
Older cats, no sex or breed predilection

71
Q

Describe the cutaneous clinical signs of feline Thymoma-Associated Exfoliative Dermatitis

A
  1. Exfoliative dermatitis
    - Non-pruritic
    - Diffuse erythema and skin exfoliation/scaling
    - Alopecia
    - Head and pinnae, and then generalised
  2. Kerato-sebaceous accumulations
    - Brown, keratosebaceous debris interdigital skin, claw beds and ear canals
    - Some cases associated with Malassezia dermatitis
  3. Crusting and ulceration
72
Q

What is cutaneous flushing?

A

Periodic release of vasoactive substances by tumours leads to skin colour changes
Rarely reported but reported with pheochromocytoma, lung tumours and MCT

73
Q

What is nodular dermatofibrosis

A

Nodules of well differentiated collagenous nevi mainly on limbs but also heads and trunk

74
Q

Nodular dermatofibrosis is seen in which animals?

A

Seen in middle aged GSDs with bilateral renal cysts or cyst adenocarcinoma
Inherited in autosomal dominant fashion

75
Q

What is hypertrophic osteopathy

A

Palisading periosteal proliferation along the shafts of long bones.

76
Q

What are the clinical signs of hypertrophic osteopathy?

A

Shifting lameness
Swelling / oedema
Limbs feel warm and are uncomfortable to touch

77
Q

How is hypertrophic osteopathy diagnosed?

A

Clinical signs and radiography of long bones and pelvis

78
Q

How is hypertrophic osteopathy treated?

A

Remove inciting cause
Prednisolone
Pain relief
Bisphosphonates

79
Q

What are the effects of paraneoplastic syndromes on the cardiorespiratory system?

A
  • Effusions are a systemic effect due to tumour exudation or bleeding
  • Pleural: tachypnoea and dyspnoea and restricted breathing pattern
  • Pericardial: signs of right side heart failure, collapse, pulsus paradoxus and electrical alternans
80
Q

Which 3 tumours are commonly associated with pericardial effusion?

A

Haemangiosarcoma
Chemodectoma
Mesothelioma

81
Q

What is the cause of paraneoplastic fever?

A

Sue to expression of inflammatory cytokines by or in response to the tumour
- Seen with a variety of tumours especially lymphoma, renal cancers and hepatic tumours
- Can lead to anorexia and malaise

Y4 SA - Oncology (12 decks)

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