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Molecular Pathology > Clinical Aspects of Neoplasia > Flashcards

Clinical Aspects of Neoplasia Flashcards

1
Q

how can neoplasms lead to pressure effects or obstruction?

A

Neoplasms occupy space alongside normal tissues

Even a benign neoplasm can be life threatening

compress vital organs

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2
Q

Cancers arising within or metastatic to an endocrine gland may cause?

A

an endocrine insufficiency by destroying the gland.

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3
Q

What are the complications of Neoplasms in the gut?

A

both benign and malignant, may cause obstruction as they enlarge.

Infrequently, this may lead to intussusception

Malignant neoplasms of the gastrointestinal tract are often associated with iron deficiency anaemia.

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4
Q

what is the result of nerves being invaded?

A

pain

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5
Q

what is the result of blood vessels being invaded?

A

local haemorrhage

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6
Q

what is the result of mucosal membranes being invaded?

A

significant blood loss

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7
Q

What is Cancer Cachexia?

A

Ongoing loss of skeletal muscle mass (with or without loss of fat mass) which leads to progressive functional impairment.

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8
Q

what is the Overall % prevalence of weight loss in cancer patients?

A

may rise as high as 86% in the last 1 2 weeks of life.

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9
Q

What is the prevalence of cachexia in advanced cancer?

A

Published data reports from 60% to 80%

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10
Q

Estimates of cancer cachexia indicate that this syndrome may directly contribute to what % of cancer deaths?

A

30%

More than 50% of patients with cancer die with cachexia present

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11
Q

MECHANSIMS OF CACHEXIA?

How is Intestinal malabsorption caused in cancer patients?

A

Mechanical limitations (e.g. difficulties in swallowing, feelings of saturation, nausea)

restrict energy uptake and recovery in patients with gastrointestinal cancer.

Weight loss occurs in up to 83% of patients with upper gastrointestinal malignancy.

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12
Q

How is Cachexia due to chronic heart failure caused?

A

is thought to result from mesenteric ischemia and disturbed microcirculation of the intestine.

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13
Q

How do Chemotherapies contribute to cachexia

A

thought to contribute to the development of intestinal absorptive dysfunction.

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14
Q

how are glucose and lipid transporters involved?

A 
Alterations in expression or localization of the major intestinal glucose (SGLT1, GLUT5, GLUT2)
and lipid (CD36, NPC1L1, SRB1) transporters are likely.

Altered intestinal gluconeogenesis may further contribute to the energetic imbalance.

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15
Q

importance of gut microbiota in health?

A

Healthy energy metabolism is modulated by the amount and species of gut microbiota.

Gut microbiota influences the regulation of bile acids and cholesterol metabolism.

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16
Q

when do Gut barrier dysfunction and endotoxemia occur?

A

when the intestinal mucosal barrier leaks or breaks down.

Gut microbiota or bacterial cell wall components enter the circulation and cause an inflammatory response (cytokine production, altered levels and activation of T cells).

Increased bacterial translocation is associated with worse prognosis.

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17
Q

what is Ghrelin involved in?

A

the regulation of appetite, gut motility and gastric acid secretion.

also involves in white and brown adipose tissue function and glucose metabolism.

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18
Q

why Ghrelin may be closely linked to anorexia?

A

Ghrelin levels are elevated upon fasting

The increased ghrelin levels fail to induce appetite and energy storage (ghrelin resistance)

Other gut hormones, GLP‐1 and GIP, have less well‐defined roles.

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19
Q

The role of increased ghrelin levels in cachexia?

A

fail to induce appetite and energy storage (ghrelin resistance)

Other gut hormones, GLP‐1 and GIP, have less well‐defined roles.

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20
Q

Why are bile acids important?

A

metabolic regulators

Bile acids are not only important for digestion and fat absorption

but are also involved in the regulation of appetite and food intake.

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21
Q

Bile acids stimulates the secretion of what?

A

glucagon like peptide 1 (GLP‐1) and hormone peptide YY (PYY)

and increases the feeling of fullness

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22
Q

how do Bile acids induce energy expenditure?

A

by promoting intracellular thyroid hormone activation

via type 2 iodothyronine deiodinase (D2),

which converts inactive T4 into active T3.

proven in mice

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23
Q

The fat malabsorption seen in patients with cachexia hints toward …?

A

lower bile acid levels in wasting.

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24
Q

what are Futile cycles?

A

Mechanisms to regulate and fine‐tune metabolic processes under physiologic conditions.

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25
Q

Futile cycles in in cachectic conditions?

A

Increased and the released metabolites are involved in inter‐organ cycles.

Lactate derived from tumours is reconverted to glucose via hepatic gluconeogenesis.

Hepatic gluconeogenesis can also be fuelled by amino acids derived from muscle protein degradation.

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26
Q

Name the Cellular compartments?

A

cytosol, ER, Golgi apparatus, lysosomes, mitochondria, nucleus, and peroxisomes.

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27
Q

What does energy wasting in the liver under cachectic conditions lead to?

A

a reduction in the oxidative phosphorylation capacity of mitochondria.

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28
Q

Other hepatic involvement?

A

Decreased usage of hepatic triglyceride stores has been demonstrated in cancer cachexia.

Hepatic steatosis is a prerequisite of non alcoholic fatty liver disease and is associated with sarcopenia (muscle loss).

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29
Q

muscle role in starvation?

A

serves as a protein reserve for energy production during starvation.

Muscle accounts for up to 40% of body weight, accounting for 20 30% of total resting energy expenditure.

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30
Q

which Inflammatory mediators play a crucial role in muscle atrophy?

A

such as IL‐1b, IL‐6, and TNFα

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31
Q

role of futile cycling in muscle atrophy?

A

Futile cycling might contribute to wasting, however, it is not a major factor causing atrophy.

32
Q

Muscle atrophy in cachexia is induced by what?

A

increased protein breakdown mediated mainly by the activation of the ubiquitin‐proteasome system and the autophagic lysosomal system.

33
Q

Major role of white adipose tissue?

A

The major role is to store energy as fat,

a storage form approximately 6x more efficient than carbohydrates due to fat’s hydrophobic nature.

34
Q

how many kcal/g does Complete oxidation of fatty acids yield?

A

about 9 kcal/g

35
Q

while carbohydrates and proteins yields?

A

about 4 kcal/g.

36
Q

Elevated lipolysis is a characteristic of cachexia in both patients and rodent models,

what does this lead to?

A

adipose tissue wasting and elevated circulating free fatty acid levels.

37
Q

Lipolysis has been shown to be activated by which protien?

A

tumour‐secreted zinc‐ α2‐ glycoprotein (ZAG).

38
Q

how do Inflammatory cytokines contribute to adipose loss?

A

such as TNFα or IL‐6

both by directly activating lipolysis and by impairing insulin sensitivity.

39
Q

what complication does Glycerol released from adipose tissue during lipolysis cause?

A

can serve as a substrate for gluconeogenesis in the liver,

leading to an energy‐wasting effect as part of futile substrate cycling.

40
Q

what does Brown adipose tissue uses stored energy for?

A

heat production during thermogenesis.

41
Q

Much much brown fat do humans possess?

A

It is estimated that humans possess up to 60 g brown fat, contributing to 15 25 kcal/day.

Other studies estimate the contribution of brown adipose tissue to total basal metabolic rate
to be around 3 5%.

42
Q

What is brite tissue?

A

White adipose tissue can contain varying amounts of brite (“brown in white”) adipocytes

43
Q

the role of brite adipocytes?

A

thermogenically active.

44
Q

what is a pheochromocytoma?

A

catecholamine‐secreting tumours

45
Q

Patients with pheochromocytoma display white‐to‐brown fat conversion.

how is this seen?

A

indicated by elevated uncoupling protein 1 (UCP1) staining of the omental adipose tissue.

46
Q

Brown or brite adipose tissue thermogenesis contributes to which of the body’s abilities?

A

to defend against cold temperatures,

so more brown/brite adipose tissue would suggest elevated body temperature or cold tolerance.

47
Q

why does Cancer cachexia represents an urgent medical need?

A

due to the great impact on patients’ quality of life and the high occurrence of this condition.

48
Q

Why do Patients with cancer cachexia often associated with a poor prognosis and increased mortality?

A

are often too weak to tolerate standard doses of chemo and radiotherapy, that may be eventually interrupted.

49
Q

what are Paraneoplastic syndromes?

A

A set of signs and symptoms that is the consequence of cancer in the body,

specifically due to the production of chemical signalling molecules (such as hormones or cytokines)

by tumour cells or by an immune response against the tumour.

Sometimes, the symptoms of paraneoplastic syndromes show before the diagnosis of a malignancy.

50
Q

when are Paraneoplastic syndromes most common?

A

are typical among middle aged to older patients,

and they most commonly present with cancers of the lung, breast, ovaries or lymphatic system (a lymphoma).

Males and females are affected equally

51
Q

Paraneoplastic endocrine syndromes (PNES)

A
52
Q

treatment for paraneoplastic syndrome?

A

treat the tumour themselves is the main treatment of syndrome
but supportive therapies for symptoms of syndrome

53
Q

what is Hypercalcaemia?

A

High calcium (Ca2+) level in the blood serum.

The normal range is 2.1 2.6 mmol/L,

with levels greater than 2.6 mmol/L defined as hypercalcemia.

54
Q

when is hypercalcaemia most common?

A

Most common PNES,

it is estimated to occur in up to 30% of patients with cancer at some point during their course of disease.

55
Q

effect of developing hypercalcemia on prognosis?

A

Conveys a poor prognosis.

56
Q

Mechanisms leading to hypercalcemia

What is the most common cause?

A

Ectopic parathyroid hormone releasing peptide (PTHrP) secretion by tumours accounts (80%)

and occurs mainly with squamous cell tumours.

57
Q

how is proximal tubular reabsorption of calcium affected?

A

Increased

58
Q

how is bone resorption affected?

A

Increased

59
Q

production of RANK ligand? and what does this induce?

A

Enhances

this induces osteoclast formation and differentiation

60
Q

production of osteoprotegerin (OPG)?

A

Inhibits

61
Q

how is the secretion of 1,25 dihydroxyvitamin D affected by malignancies such as lymphoma

A

Excessive increased (< 5%)

62
Q

what is Skeletal Metastases secondary to?

A

local osteolysis and to local PTHrP secretion (15%)

63
Q

weirdly what is hypercalcemia Rarely caused by?

A

ectopic Parathyroid hormone production (<1%)

64
Q

Paraneoplastic neurological syndromes (PNNS)

What is Lambert Eaton syndrome associated with?
Which serum antibodies are detectable?

A

Lung (small cell) carcinoma

Anti VGCC

65
Q

What is Peripheral sensory neuropathy associated with?

Which serum antibodies are detectable?

A

Lung (small cell), breast and ovary lymphoma

Anti Hu, Anti Ri

66
Q

What is Cerebellar degeneration associated with?

Which serum antibodies are detectable?

A

Lung (particularly small cell) lymphoma, Ovary, uterus, Breast

Anti Yo

67
Q

What is Opsoclonus/myoclonus associated with?

Which serum antibodies are detectable?

A

Breast, lung (small cell)

Anti Ri

68
Q

What is Stiff person syndrome associated with?

Which serum antibodies are detectable?

A

Breast, lung (small cell), Thymoma, Renal cell

Anti Amphiphysin, Anti GAD65

69
Q

What is Encephalitis associated with?

Which serum antibodies are detectable?

A

Lung, Hodgkin’s disease, germ cell neoplasms (teratomas)

Anti Hu, Anti Ma2 protein, Anti Amphiphysin, Anti GAD65, Anti Tr, Anti VGKC, Anti NMDAR

70
Q

Paraneoplastic encephalitis

What is Limbic encephalitis associated with?
Which serum antibodies are detectable?

A

is seen with small cell lung cancer and testicular tumours,

and is associated with a variety of antibodies, including anti Hu and anti Ma2.

Antibodies can be detected in 60% of cases.

71
Q

how does NMDA encephalitis present?

A

as limbic encephalitis followed by coma and often status epilepticus.

Orofacial dyskinesias are characteristic.

72
Q

what type of people are affected?

A

Patients are usually younger and most have teratomas (e.g. ovarian).

73
Q

VGKC antibodies produce a variety of disorders, including … ?

A

including limbic encephalitis

with characteristic facio brachial dystonic seizures, in combination with confusion, agitation and
hyponatraemia.

74
Q

Treatment?

A

Patients may respond to immunotherapy: intravenous immunoglobulin or plasma exchange
initially, followed by steroids, rituximab or cyclophosphamide.

75
Q

Mucocutaneous paraneoplastic syndromes (MCPS)

A
76
Q

Hematologic paraneoplastic syndromes

A

Molecular Pathology (10 decks)

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