Paraneoplastic Flashcards

1
Q

• Disorders that accompany benign or malignant

diseases but are not directly related to mass effects or invasion

A

PARANEOPLASTIC SYNDROME:

ENDOCRINE/HEMATOLOGIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Tumors of neuroendocrine origin, such as small
cell lung carcinoma (SCLC) and carcinoids,
produce a wide array of ____ and are
common causes of paraneoplastic syndromes.

A

peptide hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

(expression of a hormone from its normal
tissue of origin)
o For example, ACTH of the pituitary

A

eutopic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q
hormone production from an atypical 
tissue source
-For example, the squamous lung CA
o Conveys abnormal physiology 
associated with neoplastic hormone 
production
o Not fully understood
A

Ectopic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q
is often 
characterized by abnormal regulation of 
hormone production (e.g., defective 
feedback control) and peptide 
processing.
A

Ectopic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

• Occurs in up to 20% of patients with cancer.
• Most common in cancers of lung, head and neck,
skin, esophagus, breast, genitourinary, multiple
myeloma, lymphomas
• PTHrP production probably cause osteolysis and
hypercalcemia

A

HUMORAL HYPERCALCEMIA OF MALIGNANCY (HMM)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Another cause of HHM is excess production of

A

1,25- dihydroxyvitamin D

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

o Structurally related to PTH and binds to the
PTH receptor, explaining the similar
biochemical features of HHM and
hyperparathyroidism
o Plays a key role in skeletal development and
regulates cellular proliferation and
differentiation in other tissues, including skin,
bone marrow, breast, and hair follicles

A

PTHrP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

HMM is stimulated by:

A
  • Hedgehog pathways
  • Gli transcription factors
  • TGF-ß
  • Ras oncogene
  • Loss of p53
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

HMM clinical manifestations:

A

Hypercalcemia, fatigue, mental status changes, dehydration, symptoms of nephrolithiasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

is the initial presenting

feature of malignancy

A

Hypercalcemic
o With a Calcium level of >3.5 mmol/L
(>14 mg/dL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

HMM: Elevated _________ confirms the diagnosis

A

PTHrP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

HMM treatment: Oral phosphorous (250 mg po 3-4x daily) until
serum phosphorus _____

A

> 1mmol/L (>3 mg/dL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Saline rehydration to dilute serum calcium and

promote _______

A

calciuresis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Used for acute management of life thereatening hypercalcemia

A

Furosemide (loop diuretic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Used for chronic management of life thereatening hypercalcemia

A

Bisphosphonates used for chronic treatment;
o Pamidronate 30-90 mg IV
o Zolendronate 4-8 mg IV
o Etidronate 7.5 mg/kg/day po for 3-7 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

o 2-8 U/kg sc every 12 hrs)

o Severe hypercalcemia

A

Calcitonin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

for patients with;
o Lymphoma
o Multiple myeloma
o Leukemia

A

Glucocorticoids (prednisone 40-100 mg po in 4

divided doses)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Tumor-Association SIADH compensatory mechanisms:

A

decreased thirst,
suppression of aldosterone, production of atrial
natriuretic peptide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Examples of tumors causing SIADH are

A

Small Cell

Lung CA and carcinoids (most common)

21
Q

SIADH clinical manifestations

A
• Asymptomatic
• Hyponatremia
• Weakness, lethargy, nausea, 
confusion, depressed mental status, seizures
• Suppressed thirst mechanism
22
Q

SIADH DIAGNOSIS

A
  • Hyponatremia
  • Decreased serum osmolality
  • Normal or increased urine osmolality
23
Q

o Inhibit vasopressin action along the renal
distal tubule
o Slow onset of action (1-2 weeks)

A

Demeclocycline (150-300 mg 3-4x daily)

24
Q
Hypertonic saline (3%) or NSS plus furosemide for 
severe hyponatremia (< 115 meq) - treatment for:\_\_\_\_
A

SIADH

25
Q

• Slow Na correction (0.5-1 meq/L per hr)

o to prevent_________

A

central pontine

myelinolysis

26
Q

• 10-20% of cases
• Neuroendocrine tumors
• Increased expression of the
proopiomelanocortin (POMC) gene.

A

Cushing’s Syndrome

27
Q

is the most

common cause of ectopic ACTH

A

Small Cell Lung CA (>50%)

28
Q

Cushing’s syndrome clinical manifestations:

A

-Less marked weight gain (centripetal fat
distribution)
• Fluid retention, hypertension, hypokalemia,
metabolic alkalosis, glucose intolerance, steroid
psychosis
• Increased skin pigmentation
• Marked skin fragility, easy bruising (due to
increased glucocorticoids)
• Severe hypokalemia
• Depression or personality changes
• Diabetes mellitus
• Poor wound healing
• Opportunistic infections (P. carinii, mycotic)

29
Q

Cushing’s syndrome diagnosis: Urine free cortisol levels

A

> 2-4x normal

30
Q

Cushing’s syndrome diagnosis: Plasma ACTH level

A

> 22 pmol/L (> 100pg/mL)

31
Q

High dose ______ (8mg per orem)
suppresses 8:00 am serum cortisol (50%
decrease from baseline) in 80% of pituitary
ACTH-producing adenomas

A

dexamethasone

32
Q

CUSHING SYNDROME TREATMENTS:

A
KMMG
• Ketoconazole (200-400 mg bid po)
• Metyrapone (250-500 mg q 6 hrs)
• Mitotane 3-6 g po in 4 divided doses
• Glucocorticoids (to avoid adrenal
insufficiency
33
Q

Hmm calcium level

A

> 3.5mmol (14md/dL)

34
Q

Tumor-induced hypoglycemia:excess production of IGF-II

A
  • Mesenchymal tumors
  • Hemangiopericytomas
  • Hepatocellular tumors
  • Adrenal carcinomas
35
Q

Erythrocytosis

A

Renal CA, hepatocarcinoma, cerebellar hemangioblastomas

36
Q

granulocytosis

A

Lung Ca, GIT ca, Ovarian ca

37
Q

Thrombocytosis

A

Lung CA, git, breast, ovarian CA

38
Q

The most significant risk factor for cancer overall is

A

AGE (2/3 over 65 y.o)

39
Q

NINE MODIFIABLE RISK FACTORS FOR

MORE THAN ONE-THIRD OF CANCERS WORLDWIDE

A
  1. Smoking
  2. Alcohol consumption
  3. Obesity
  4. Physical inactivity
  5. Low fruit and vegetable consumption
  6. Unsafe sex
  7. Air pollution
  8. Indoor smoke from household fuels
  9. Contaminated injections – HIV
40
Q

The first priority in patient management after the diagnosis of cancer is established and shared with the
patient

A

staging

41
Q

is an anatomically based system
that categorizes the tumor on the basis of the size of
the primary tumor lesion, the presence of nodal
involvement, and the presence of metastatic disease

A

TNM classification (most widely used)

42
Q

are the ones with bad prognosis, tumor has involved other organs.

A

T3, N2, N3, M1

43
Q

second major determinant of treatment outcome is

the

A

physiologic reserve of the patient

44
Q

Instead,

surrogate markers for physiologic reserve are used, such as

A

the patient’s age or Karnofsky
performance status or Eastern Cooperative
Oncology Group (ECOG) performance status.

45
Q

Older patients and those with a Karnofsky
performance status ___ or ECOG __ have a poor prognosis unless the poor
performance is a reversible consequence of the
tumor.

A

<70, ≥3

46
Q

chemotherapy or

chemotherapy plus radiation therapy delivered before the use of definitive surgical treatment

A

Neo adjvant therapy

47
Q

The most common side effects of treatment are:

A

o nausea and vomiting
o febrile neutropenia
o Myelosuppression

48
Q

Delayed emesis tx

A

cisplatin