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Para Neoplastic Syndromes in Lung Cancer

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Stelson Natalia
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Page 1: Para Neoplastic Syndromes in Lung Cancer

8/2/2019 Para Neoplastic Syndromes in Lung Cancer

http://slidepdf.com/reader/full/para-neoplastic-syndromes-in-lung-cancer 1/18

Stelson Natalia

Page 2: Para Neoplastic Syndromes in Lung Cancer

8/2/2019 Para Neoplastic Syndromes in Lung Cancer

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MANIFESTATIONOF CANCER

RECURENCE OFCANCER

Page 3: Para Neoplastic Syndromes in Lung Cancer

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Neuromuscular

Vascular

Hematological

Metabolic

Involving skeletal, muscular system and skin

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2-6% of initial tumors

8-12% during disease

51% squamosous cell carcinoma

22% adenocarcinoma

15% SCLC (small cell lung cancer)

Most patients III –IV stage or bony mts

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Anorexia

Nausea

Vomiting

Constipation

Lethargy

Polyuria

polydipsia

Dehydratation

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PTHrP (parathyroid hormon relatedprotein)

PTH ( parathormone)

Calciotriol

Cytockines ( osteoclast activatingfactors)

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- 70% structure the same as PTH +13 aminoacids onN-terminus

- Uses the same receptor with PTH

-

Has the same activity as PTH- activating of osteoclastic resorbtion,

- increasing Ca++ reabsorption,

- decreasing of P reabsorbtion

- stimulation renal 1-alpha-hydroxilase,resulting of production of 1,25-(OH)2-D3 thenincreasing of Ca++ reabsorbtion.

PTHrP cancer cell surviving factor

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80% SCLC and squamous cell carcinoma

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IL-1, IL-6, transforming growth factor (TGFalpha), tumor necrosis factor (TNF), granulocytescolony stimular factor (G-CSF)

TGF alpha + TNF = increase osteoclastic activity

TGF alpha + TNF +IL-1+IL-6 = enhancing PTHrP

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30-70% of all tumors, but most cases withoutsignificant symptoms

10% of SCLC product ADH

Symptoms – decrease Na+ and osmolarity od

blood, increase Na+ in urine

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ACTH is produced by 50% of tumors

30% of SCLC

But clinically rare

Pulmonary carcinoids produce ACTH in 35-95%

SCLC with Cushing syndrome often resistant to

the chemotherapy

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Anemia (38%) (IL-1, IL-6, IFN-gamma inhibiterytropoesis)

Leucocytosis (15%) ( G-CSF production bytumor)

Thrombocytosis (16-32%) bad prognosis

Eosinophilia (rare) bad prognosis

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Trousseau’s syndrome (superficial thrombophlebitis)

Deep venous trombosis

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Tissue factor production

Normal agent that

initiates clotting in caseof damage of tissue

(often NSCLC)

Cancer procoagulant 

is a hypothesised

protein, most likely acysteine proteaseenzyme, that occurs onlyin fetal and malignant

cells. Its activity appearsto be the activation offactor X

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Digital clubbing

Hypertrophic pulmonary osteoarthropathy

(HPO) -12% adenocarcinoma

Dermato- and polymyositis – associate 40%

SCLC

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0,01% ; exclusively SCLC; almost all caused byantibodies to the neural tissue

Lambert-Eaton myastenic syndrome (LEMS) –antibodies to the voltage gated Ca++ channels

Limbic encephalitis (encephalopathy) –antibodiesthe RNA-binding proteins

Polyneuropathy

Neuromyothonia - antibodies to the voltage gatedK + channels

Autoimmune autonomic gangliopathy -antibodies to neuronal Ach receptors

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Palmo-plantar hyperceratosis (tylosis) –canprecede of diagnosis of cancer for months or years.Poor prognosis

Akantosis nigricans ( some cases associate with

lung cancer) Acquired hypertrichosis languinosa Erythema gyratum repens Erythema multiforme

Erythroderma Exfoliative dermatitis Sweet syndrome Pruritus and urticaria

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part of the general adaptation of the body

often seen in trauma, inflammation, infection, andcancer.

proinflammatory cytokines - (TNF)-alpha,(IL)-1,IL-6, interferon (IFN)-gamma, and ciliaryneutropic factor (CNTF) have been implicated incachexia

mediators - proteolysis-inducing factor (PIF)and

lipid mobilizing factor (LMF) anorexia and metabolic alterations. Cancer patients

frequently exhibit a relative glucose intoleranceand insulin resistance


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