1. Most pts with disseminated cancers are hypercoagulable, meaning that they have a tendency for forming clots. Classic Example: a pt with painless jaundice, left
supraclavicular node (this is a distracter), had light color stools, lesions that jump from one part of body to next – trousseau’s sign: a superficial migratory thrombophlebitis due to carcinoma of the head of the pancreas). Pancreatic cancers can ALSO mets to left supraclavicular node (virchow’s node), and often describe trousseau’s sign, which is a vascular problem in the veins that jumps from one place to the next.
2. Another common thing seen is disseminated cancers is thrombocytosis – an elevated platelet count. Other causes of thrombocytosis: Fe def, splenectomy (ie see scar on abdomen), TB, anemias. If you cannot find any obvious cause of thrombocytosis then the cause is cancer.
40% of disseminated cancers are thrombocytosis Or a do a stool guaic for colon cancer
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D. MCC fever in malignancy = gram neg. infection. An E. coli if you have an indwelling catheter; Pseudomonas if you have a respirator, staph aureus can also be the cause from an indwelling catheter, but this is gram “+”.
MCC death in cancer = infection XV. Paraneoplastic syndromes
These are signs and sometimes symptoms saying that you may have an underlying cancer present. Its important b/c when you recognize the signs and symptoms, then you can catch the cancer before it metastasize.
MC Paraneoplastic syndrome = hypercalcemia
2 mechanism for hypercalcemia in malignancy:
1) mets to bone, produce a chemical (IL-1, PGE2, both of which activate osteoclasts) that produces lytic lesions in bone, and you get hypercalcemia
2) renal adenocarcinoma or squamous carcinoma of mainstem bronchus that sits there and makes PTH-like peptide and causes hypercalcemia b/c it acts like PTH and breaks down bone.
This is Paraneoplastic, but it’s not the most common one.
Example: 2 black lesions – both are markers for gastric adenocarcinoma; usually under the arm – called acanthosis nigricans, and other is called seborrheic keratosis (these are not
neoplasms); however, when these suddenly develop overnight, you get multiple outcroppings (lesserr tree-ar sign), and the outcroppings is a phenotypic marker for gastroadenocarcinoma;
this is easy to remember b/c 2 black lesions are markers from gastroadenocarcinoma.
44. Acanthosis nigricans
45. Seborrheic keratosis (Leser Trelat) Example: clubbing – inflammation beneath on the bone called periostitis; inflamm of underlying bone causes proliferation of the soft tissue around it, which leads to clubbing (called
hypertrophic osteoarthropathy). Clubbing is not always assoc with cancer; also assoc with bronchiectasis, IBS. But, if it’s a malignancy, it is due to primary lung dz.
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43. Hypertrophic osteo-arthropathy Example: least common collagen vascular dz, but the most often assoc with a certain cancer.
They have an elevation of serum CK; this is dermatomyositis; raccoon eyes, so you see inflammation of skin and muscle; high assoc with leukemias, lymphomas and lung cancer.
Patches of knuckles – goltrin’s patches (seen in dermatomyositis).
Example: vegetations (sterile) on the mitral valve – assoc with mucous producing cancers such as colon cancer; this is called marantic endocarditis-aka nonbacterial thrombotic endocarditis;
they are not infections and these marantic vegetations are assoc with mucous secreting colon cancers. Can they embolize? Yes. You will need history to separate from rheumatic fever, but history will relate more to colon cancer (ie polyarthritis)
46. Marantic endocarditis
Example: hyponatremia or Cushing’s – cancer in the lung = small cell carcinoma, which is secreting either ADH or ACTH; also, for small cell, they are aput tumors,
S-100 Ag positive, neural crest origin, neural secretory granules.
54. Small cell carcinoma of lung
Example: Hypercalcemia or secondary polycythemia: renal adenocarcinoma (can make PTH like peptide and/or EPO).
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Example: Hypoglycemia or secondary polycythemia: Hepatocellular carcinoma (they can make EPO or insulin-like factor).
71. Hepatocellular carcinoma
Example: Hypocalcemia or Cushing’s: auto dominant, and the rare tumor marker that can be converted to amyloid (calcitonin) – medullary carcinoma of the thyroid.
XVI. Tumor markers
A. 2 markers associated with Testicular cancer – alpha feto protein (AFP) (which is really the albumin of a fetus) and HCG. AFP is a maker for–yolk sac tumor (endodermal sinus tumor). So the tumors in kids are yolk sac tumors (alpha feto protein)
AFP is also assoc with Hepatocellular carcinoma, increased in neural tube defects (must be on folate while pregnant to prevent neural tube defects). In Down’s syndrome AFP is decreased.
Marker for malignancy in bone, assoc with monoclonal spike: Bence Jones Proteins (light chain Ig), assoc with Multiple Myeloma.
Tumor marker for prostate cancer: PSA; not sp for cancer b/c it can be also increased in
hyperplasia; it is sensitive but not specific. If you do a rectal exam, it is not increased. PSA is NOT an enzyme; it is an Ag and is within the actual cell. It will not increase with a rectal exam.
Breast cancer (surface derived) – 15, 3.
CEA–125: Ovarian cancer
CEA –Ag for colon cancer; and sometimes used for small cell, and breast ca. CEA can be a part of an immune complex, and will get CEA: anti-CEA immune complexes which deposit in the kidney, and lead to nephrotic syndrome – this is diffuse membranous glomerulonephritis = MC overall cause of nephrotic syndrome. Many of these are related to malignancy b/c CEA can be the Ag that is deposits in the glomeruli.
woman with a trophoblastic mole, what would you get? Beta HCG
What is MC primary tumor of the brain in kids? Cerebellar cystic astrocytoma (B9). It’s not medulloblastoma. All astrocytomas are B9 (if asked what is the most common malignant primary tumor, and then the answer is medulloblastoma, which derives from cerebellum). MC actual tumor of the brain – cerebellar tumor derived from astrocytes;
MC childhood cancer = ALL leukemia (other childhood tumors include CNS tumors,
neuroblastomas (in the adrenal medulla), Burkitts, Ewing’s (tumor of bone with onion skinning), embryonal rhabdomyosarcoma.)
Adults: incidence:
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in woman: breast, lung, colon In men: prostate, lung, and colon
Killers: lung is #1 in both (followed by prostate/breast and colon) 2nd MC cancer and cancer killer in men and women combined = colon
Therefore, from age 50 and on, you should get a rectal exam and a stool guaic.
After 50, MCC cancer of “+” stool guaic is colon cancer.
MC gyn cancer: endometrial (#2 is ovarian, and #3 is cervix)
Cervix is least common b/c Pap smear. When you do a cervical pap, picking up cervical dysplasia, not cervical cancer (therefore the ‘incidence’ isn’t the highest).
B/c cervical pap smears; the incidence of cervical cancer has gone down significantly b/c the detection of the precursor lesion, cervical dysplasia. So, b/c cervical Pap smear, incidence of cervical cancer has gone down dramatically (picking up the precursor lesion); with mammography, the incidence of breast cancer decreases, same with PSA.
MC Gyn cancer killer: ovarian (#2 = cervical, #3 = endometrial); therefore to remember, the MC has the best prognosis – endometrial is MC and has the best prognosis.
What is the only known existing tumor vaccine? HBV …why?
MC infection transmitted by accidental needle stick in the hospital = Hepatitis B B/c viral burden of Hepatitis B is greater than any infection, even more so than HIV.
So, with the Hepatitis B vaccine, you won’t get three things (1) Hepatitis B, (2) Hepatitis D (requires Hep B), and (3) hepatocellular carcinoma (related to Hepatitis B related cirrhosis).
How do you eradicate hepatocellular carcinoma? Vaccination (ie in the Far East).
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CHAPTER 6. HEMATOLOGY: RBC