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201 Cards in this Set
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acute and early emesis
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occurs w/i hours of chemo and last up to 24 hrs
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nausea and vomiting (acute and early) is caused by highly emitogenic drugs such as
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Cisplatin
Dacarbazine Nitrogen Mustar |
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delayed emesis
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begins or persists >24 hrs after chemotherapy
e.g. Cisplatin 2-3 days after chemotherapy |
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tx acute emsis
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metoclopramide, proclorperazine, Dexamethasone
cannabinoids (marinol) |
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what is anticipatory vomiting?
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due to prior experience. best is prevention
behavior therapy, anxiolytic |
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complications of cancer therapy
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nausea and vomiting
mucositis bone marrow suppression tumor lysis syndrome |
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mucositis
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nreakdown of mucosal baddier due to RT, chemo
allow portal of entry for bacteria recovery coincides w/ neutrophil recovery |
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causes of mucositis
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1. chemo or radiation therapy to mucosa
2. secondary infection from tx induced by myelosuppression |
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chemotherapy induced mucositis starts when
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5-7 post-chemo
last max for 10-14 days |
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tx for mucositis
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good oral hygiene
sucking on ice chips (constrict blood vessels) chlorhexidine mouth wash local lidocaine viscous and systemis analgesics (give pareneteral nutrition and morphine for the pain) |
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bone marrow suppression
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pancytopenia due to infiltration of bone marrow w/ tumor cell or damaging effect of chemo and radiation on bone marrow
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what is the neutrophil count
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neutrophil count < 500 cells/microliter
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febrile neutropenia is secondary to
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cancer and due to involvement of BM with tumor
FEVER most reliably indicate severe bacterial infection in neutropenic pts untreated gram negative bacteremia = 80% mortality rate |
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tumor lysis syndrome is due to
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rapid breakdown of cancer cells once chemo is started
most commonly seen in rapidly growing tumor and bulky tumor |
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tumor lysis syndrome is due to release of
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Uric acid
potassium and phosphates |
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neutropenic pts (bone marros suppression) should receive what tx?
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prophylactic antibiotic quinolone for prevention of febrile neutropenia
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uric A, a purine metabolite causes
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precipitation in kidney --> renal failure
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phosphate accumulation causes
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hypocalcemia and tetany
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increased K causes
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fatal arrythmias
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tx of TLS w/
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hydration
alkaline urine pH allopurinol inhibit synthesis of uric acid from xanthine and hypoxanthine Rasburinase-enzyme that degrades uric acid dialysis |
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what causes cancer cachexia
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Leptin: hormone secreted by adipocytes--> Block release of neuropeptid Y (NPY) which is a feeding regulating peptide in hypothalamus --> loss of appetite this causes decr intake and increased metabolic demand
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pts w/ cancer have inceased levels of
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1. lipid mobilizing factor
2. IL-6 3. TNF alpha which all cause wasting syndrome |
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Tumor derived factor causes
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proteolysis inducing factor --> upregulates proteasome pathway --> induce protein degradation in skeletal muscle
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how do you treat cancer cachexia?
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corticosteroids
anabolic steroids Oxandrolone Marinol medroxyprogesterone |
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cancer pain is caused by
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1. 7% directly due to tumor
2. 20% dye to anti-neoplastic therapy 3. 10% of all pain is unrelated to cancer |
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neuropathic pain
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injury to nerve
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nociceptive pain
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activation of somatic or visceral nociceptors
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tx cancer pain
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aspiring NSAID
oxycodon morphine fentanyl patch antidepressant gabapentin |
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3 approaches to pain control
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1-modify source of pain: surgery, RT, chemo, antibiotics, NSAID
2-alter central perception of pain: analgesic, anti-anxiety drugs 3- block transmission of pain to brain: nerve block and surgery |
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management of cancer pain
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step 1: mild pain--> non-opiod analgesics, limited value, good for bone pain
step 2: moderate pain, weak opioids like codeine, oxycodone step 3: severe pain, strong opiods like morphine, fentanyl patch, hydromorphone should not use long acting opioids q 12 hrs and short acting opiods for break through pain |
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cancer paraneoplastic syndrome
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most commonly assoc w/ small cell cancer
primary tumor secrete PTH-related peptide causes bone resorption and hypercalcemia tumor invade bone causing local osteolysis and hypercalcemia |
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clubbing and pulmonary osteoarthropathy - due to what cancer?
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adenocarcinoma of lung
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Cushings due to
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excessive ACTH (eg lung cancer)
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hyponatremia/SIADH 15% of cases of small call lung cancer -->
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weakness Na and osmolality w/ high urine Na in a pt with normal intravascular volume --> SIADH, fluid restriction, demeclocycline, tx underlying tumor
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hypercalcemia of malignancy
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primary tumor secret PTH-related peptide which causes bone resorption and hypercalcemia (eg lung cancer)
tumor invade bone causing local osteolysis and hypercalcemia |
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neuropathic pain
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injury to nerve
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nociceptive pain
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activation of somatic or visceral nociceptors
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tx cancer pain
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aspiring NSAID
oxycodon morphine fentanyl patch antidepressant gabapentin |
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3 approaches to pain control
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1-modify source of pain: surgery, RT, chemo, antibiotics, NSAID
2-alter central perception of pain: analgesic, anti-anxiety drugs 3- block transmission of pain to brain: nerve block and surgery |
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management of cancer pain
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step 1: mild pain--> non-opiod analgesics, limited value, good for bone pain
step 2: moderate pain, weak opioids like codeine, oxycodone step 3: severe pain, strong opiods like morphine, fentanyl patch, hydromorphone should not use long acting opioids q 12 hrs and short acting opiods for break through pain |
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cancer paraneoplastic syndrome
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most commonly assoc w/ small cell cancer
primary tumor secrete PTH-related peptide causes bone resorption and hypercalcemia tumor invade bone causing local osteolysis and hypercalcemia |
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clubbing and pulmonary osteoarthropathy - due to what cancer?
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adenocarcinoma of lung
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Cushings due to
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excessive ACTH (eg lung cancer)
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hyponatremia/SIADH 15% of cases of small call lung cancer -->
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weakness Na and osmolality w/ high urine Na in a pt with normal intravascular volume --> SIADH, fluid restriction, demeclocycline, tx underlying tumor
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hypercalcemia of malignancy
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primary tumor secret PTH-related peptide which causes bone resorption and hypercalcemia (eg lung cancer)
tumor invade bone causing local osteolysis and hypercalcemia |
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symptoms of hypercalcemia
how do you tx? |
polyurea, polydypsia, constipation, lethargy, personality changes
mental obtundation, coma and death tx: hydration, diuresis, bisphosphanate |
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acanthosis nigricans
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hyperkeratosis of epithelium
often seen in gastric and pancreatic cancer |
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CNS paraneoplastic syndrome
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1-paraneoplastic subacute cerebellar degeneration: secondary to ab to purkinje cell protein (ataxia, dysarthria, hypotonia)
2- limbic encephalopathy: dementia, hallucination, depression, agitation, and anxiety 3-subacute distal sensory neuropathy: due to anti-Hu antibody 15% of SCLC have low titer of antibody |
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symptoms of hyponatremia and SIADH
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weakness, lethargy, confusion, coma
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DX for hyponatremia and SIADH
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↓ serum Na & osmolality (<280 mOsm/kg) with a high urine osmolality (> than serum osmolality) and high urine Na (>20 mEq/L) in a patient with normal intravascular volume.
eaton-lambert syndrome or myasthenia syndrome: prox muscle weakness, pelvic girdle and thigh improves w/ activity |
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tx for hyponatremia and SIADH
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fluid restriction
demeclocycline treat underlying tumor |
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pleural effusion
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collection of fluid in the pleural cavity
mech: direct deposition of tumor or pleural surface tumor involvement of mediastinal LN |
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tumors most commonly involved are:
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breast cancer, lung cancer, lymphoma, ovarian cancer, adenocarcinoma of unknown primary
|
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sx of pleural effusion
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pain dyspnea cough
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tx of pleural effusion
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thoracentesis
cytology pleurodesis (drain fluid) |
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cardiac tamponade
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build-up of blood or other fluid in the pericardial sac puts pressure on the heart which may prevent it from pumping effectively
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malignant ascites
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collection of fluid in peritoneal cavity
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causes of malignant ascites
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ovarian cancer
GI cancer |
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sx of malignant ascites
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pain and fever
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diagnosis of malignant ascites by
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scan and paracentesis
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tx of malignant ascites
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intraperitoneal chemo
systemic chemo drainage |
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most common etiologies of pericardial effusion
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lung and breast cancer
can present w/ chest pain cytology is usually negative dyspnea is not a common symptom |
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superior vena cava syndrome is due to
Causes? |
due to compression of SVC by lymph node or tumor
causes: lung cancer, lymphoma |
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sx of SVC syndrome
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neck and facial swelling, dyspnea, cough
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tx of superior vena cava syndrome
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elevation of head of bed
diuretics radiation chemotherapy |
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39 yo small business man comes to you w/ mild difficulty in breathing, headache, mild sweeling of face and distended neck veins
reveil papillodema, the next step would be to |
biopsy the mass. this is not a medical emergency so much determine what the mass is first
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spinal cord compression is
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TRUE EMERGENCY and must be immediately recognized to prevent permanent paralysis and incontinence
in 10% may be initial presentation >90% have back pain |
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what cancers account for >50% of spinal cord compression?
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prostate cancer
breast cancer lung cancer |
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tx for spinal cord compression
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steroids
radiation surgery |
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what is the outcome of spinal cord compression?
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ambulatory at presentation will remain ambulatory
25% of nonambulatory will be able to walk and <10% of paralyzed pts will be able to walk |
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the most common site of cord compression is
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thoracic region compression
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low back pain over past 2 weeks
has NSCLC what do you do? |
give IV dexamthasone and MRI of spine
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malignancy associated hypercoagulopathy occurs in
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5-15% of pt w/ cancer
nearly 50%of pts w/ pancreatic cancers have some thromboembolic event may be due to activation of platelets by tumors and/or production of procoagulants may also be related to interference w/ protein S or C function migratory thrombophlebitis may occur (Trousseau's syndrome) myeloproliferative disorders |
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thrombosis in cancer pts occur most commonly in what cancers?
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lung
breast colorectal and prostate |
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pts with UNPROVOKED DVT have
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10% risk of developing cancer w/i 2 yrs
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incidence of cancer is highest when?
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first 6-12 months
40% will have adv disease when cancer becomes clinically evident |
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occult cancer is 3-4 times higher in pts that present with
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IDIOPATHIC DVT Instead of secondary DVT
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pts w/ cancer diagnosis at same time or w/i one yr of an episode of a DVT have a
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shorter life span than pts w cancer who do not have DVT
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why is heparin a better drug than warfarin in cancer pts?
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heparin has antitumor effects
use for at least 6 months |
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chemotherapy in pathophysiology of emesis
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stimulate
high cortical centers --> vomiting center in medulla chemoreceptor trigger zone --> vomiting center in medulla stomach and small intestine --> CTZ |
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chemoreceptor trigger zone is located in
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area postrema, 4th ventricle
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what can anti-emetic drugs?
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cannabinoids like marinol
dexamethasone proclorperazine metoclopramide |
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42 yo with stage 2 breast cancer comes to ER with severe vomiting 12 hrs after receiving chemo. what is the most effective tx?
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5-hydroxytryptamine antagonist w/ dexamethasone are most effective in tx of acute emesis
IV chemo can induce vomiting by acting on receptors in stomach and small bowel chemotherapy might induce vomiting by acting on the chemotherapy in 4th ventricles 5-Hydroxytryptamine antagonist act on chemoreceptor trigger zone as well as local receptors in stomach and small intestine |
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in addition to behavioral therapy for anticipatory vomiting, what is the best way to prevent nausea and vomiting?
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Ondranseton (anti-emetic) + dexamethasone + anxiolytic (lorazepam)
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bone marrow complication of cancer
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pancytopenia due to infiltration of BM with tumor cells and/or due to damaging effect of chemo and radiation on bone marrow
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febrile neutropenia is secondary to
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cancer tx and due to involvement of bone marrow w/ tumor
untxed gram neg bacteremia --> 80& mortality rate |
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neutropenic pts should receive prophylactic antibiotics like
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Quinolone (Cipro) for prevention of febrile neutropenia
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56 yo received chemotherapy for bladder cancer
he is febrile routine blood count shows WBC 900 w/ absolute neutrophil count of 50% |
fever in this pt is an indication of hospitalization
he is neutropenic and this is very damgerous esp with gram neg bacteremia --> 80% mortality rate |
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26 yo w/ testicular cancer who is receiving chemo comes to ER w/ temo of 102
his indwelling central venous porte shows no source of infection Chest X-ray – normal, ANC 165, urine is normal. Blood & urine culture is sent. Pt is admitted for IV ceftazidime. 3 days later temp is 100 ANC is 450; his clinical condition is otherwise stable. Blood & urine culture is neg. Repeat X-ray is normal. Repeat blood & urine culture is sent. What is the most appropriate treatment now? |
continue current antibiotic regimen
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tumor lysis syndrome
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rapid breakdown of cancer cells once chemo is started
most commonly seen in rapidly growing tumor and bulky tumor eg burkitts lymphoma, ALL damage due to release of uric A, K, phosphates |
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Treatment of TLS
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Hydration,
Alkaline urine pH Allopurinol – inhibits synthesis of Uric A from Xanthine & Hypoxanthine Rasburicase – enzyme that degrades uric acid Dialysis |
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A 28-yr-old man is evaluated for fever, soaking night sweats, wt loss, abdominal distension N, V & marked dehydration. CT of chest and abdomen revealed massive mediastinal and retroperitoneal lymphadenopathy with massive splenomegaly. BM aspirate reveal 40% replacement with Burkett’s lymphoma, an aggressive lymphoma. Uric A 18.5, S-Cr is 2.5, LDH 1050. The most appropriate next step in treatment before initiation of chemo is IV fluid plus
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iv rasburicase?
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neoplasm
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abnormal mass of tissue, the growth of which exceeds and is uncoordinate with that of normal tissues
persists in same excessive manner of cessation of stimuli which evoked the change may be benign or malignant |
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benign tumors usually end w/
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OMA
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malignant epithelial tumors called
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carcinomas
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malignant mesenchymal tumors called
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sarcomas
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more than one cell type:
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benign: fibroadenoma
malignant: carcinosarcoma |
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cancer derived from multiple germ cel layers is called
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TERATOMA
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name of benign and malignant squamous epithelium
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squamous papilloma
squamous cell carcinoma |
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name of benign and malignant
glandular epithelium |
adenoma
adenocarcinoma |
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name of benign and malignant
urothelium |
urothelial papilloma
urothelial carcinoma |
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name of benign and malignant
fibrous tissue |
fibroma
fibrosarcoma |
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name of benign and malignant
adipose tissue |
lipoma
liposarcoma |
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name of benign and malignant
cartilage |
chondroma
chondrosarcoma |
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name of benign and malignant
bone |
osteoma
osteosarcoma |
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name of benign and malignant
blood vessels |
hemangioma
angiosarcoma |
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name of benign and malignant
smooth muscle |
leiomyoma
leiomyosarcoma |
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name of benign and malignant skeletal muscle
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rhabdomyoma
rhabdomyosarcoma |
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choristoma
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ectopic normal tissue
outside of normal paremters |
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mass of disorganized but mature tissues that are normal at that site
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hamartoma
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are choristoma and harmatoma technically neoplasms?
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no bc they are developmental abnormalities and are not clonal
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list 4 basic properties that define a tumor being benign vs malignant
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1. differentiation and anaplasia
2. rate of growth: most benign tumors grow slowly and may have been present for yrs at time of diagnosis --> rate of growth usually correlates w/ degree of differentiation 3. local invasion: benign tumors are localized to their site of origin may compress but not invade surrounding structure; may be encapsulated malignant tumors not encapsulated usually usually invade into surrounding structures causing reactive inflammation and fibrosis invasion is the 2nd most important criteria after metastases |
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differentiation as it applies to neplasms and describe what loss of differentiation implies to function of tumor cells
what is high and low grade? |
extent to which tumor resembles its normal cell counterpart
benign tumors are well-differentiated malignant tumors are well, moderately, poorly, or undifferentiated (anaplstic) |
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good = well differentiated = grade
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1, low grade
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bad = moderately differentiated = grade
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2, low grade
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ugly = poorly differentiated =
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3, high grade
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ugliest = undifferentiated
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4, high grade
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anaplasia
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nuclear pleomorphism: variation in size and shape
nuclear hyperchromasia: darkly staining nuclei high nuclear/cytoplasmic ratio: Nuclei with a lot less cytoplasm than it should (immature), irregular nuclear borders large nucleoli high mitotic rate and atypical mitotic figures: tripolar, quadripolar, spindles tumor giant cells disrupted architectre |
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epithelial cell from an immature basal layer then mature towards the surface-this is called
____is loss of this maturation but without invasion of underyling stroma |
dysplasia
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full thickness dysplasia =
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carcinoma in-situ = intraepithelial neoplasia
may spontaneously regress or eventually progress to invasive cancer progression from low-->high dysplasia (loss of maturation) well worked out in some not all areas |
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3 examples of dysplasia
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squamous: uterine cervix, tracheobronchial tree: sq metaplasia fertile field for later squamous dysplasia
colon: adenomatous change dysplasia in infalmmatory bowel disease esophagus: intestinal metaplasia distal esophagus (barrett) later glandular dysplasia arising in previous metaplasia |
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implants of tumor not contiguous with primary mass is called
|
metastases
most important criteria for malignancy for all practical purpose (if a tumor has metastasized, it is malignant) almost all malignant tumors have capacity to metastasize: gliomas, most basal cell carcinomas, presence of mets is ominous sign examination of primary tumor can provide clues as to how likely the tumor is to metastasize *high risk with larger more anaplastic tumors |
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___ of cancers have already metastasized at the time of diagnosis
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30%
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describe the histologic feature which favors primary tumor from a metastatic lesion
can be difficult to determine |
transition from normal epithelium --> dysplasia-->invasive carcinoma is goodevidence for primary lesion
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what are 3 pathways by which malignant tumors often metastsize?
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lymphatic spread
hematogenous spread direct seeding of body cavities and surfaces sarcoma usually metastsize hematogenously carcinomas use all of the above routes |
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how do you predict the pattern of lymph node met?
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tumors metastasize to LN that drain the area of the primary mass
within the node, tumor emoboli follow normal route of flow subscapular sinus first--> sinusoid then disseminate throughout node |
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most nodes that contain metastatic tumor are
|
enlarged and hard
non-involved regional nodes may be enlarged due to processing of tumor antigens |
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how do you predict the pattern of hematogenous metastasis?
|
common for both sarcomas and carcinomas
venous metastasis more common then arterial tumor emboli follow normal route of drainage so tumors in portal circulation usually metastasize to liver and those in systemic circulation go to lungs first renal cell carcinoma, hepatocellular carcinoma, others invade large ceins and spread by direct extension w/ separation from primary tumor |
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what 2 tumors invade large veins and spread by direct exntesion without separation from primary mass?
|
renal cell carcinoma
heptaocellular carcinoma |
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describe seeding of body cavities as mode of metastasis?
|
occurs when a tumor breaks into body cavity and spreads along it surfaces
tumor or serosal surfaces may or may not invade into underlying stroma |
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list some potential local effects of tumors
|
benign or malignant tumors can cause local effects on function activity
impingement or destruction of surrounding structure due to expansile growth obstruction of tubular structures ulcerations secondary infection bleeding torsion, rupture, infarction |
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hormone production of endocrine and non-endocrine neoplasms
|
endocrine tumors can secrete their normal products
some nonendocrine malignant tumors can ectopically secrete hormones (paraneoplastic syndrome) |
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what is paraneoplastic syndrome?
|
not explained by local effects, metastasis, or ingenous hormone production
occur in 10% of malignant neoplasms may be the first sign of tumor can lead to significant medical problems |
|
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give 6 examples of pareneoplastic syndromes
|
1-endocrine: ectopic hormone production
2-neuromuscular: myasthenia, peripheral neuropathies and CNS disorders 3-dernatologic acanthosis nigricans, dermatomyositis, signs of Leser-Trelate 4-vascular hematologic: thrombosis, anemia, polycythemia, thrombocytosis, DIC 5-nephritic syndrome 6-clubbing: spadelike fingers, not always associated with malignancy |
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list 3 ectopic hormone production paraneoplastic syndrome along w/ neoplasms most commonly implicated :
|
Cushing syndrome, ectopic ACTH production by small cell carcinoma of lung
Syndrome of inappropriate ADH (SIADH) often due to ectopic ADH production by small cell carcinoma of lung Hypercalcemia: usually PTH-related protein secreted by SCC of lung |
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name the cytokine most directly responsible for cachexia
|
loss of body fat, lean body mass with anorexia, weakness, anemia
loss of fat due to mobilization of fatyy acids and decreased lipid synthesis anorexia due to abnormalities of taste and central appetite control not due to increase nutritional demands ot tumor Mediated through cytokine including TNF |
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degree of histological differentiation
|
GRADE
grades I-IV correlate with increasing anaplasia |
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extent of tumor size and spread
|
STAGE
stage is more clinically important than grade TNM system is most widely used |
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T =
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primary tumor T1-T4 with increasing size and effect on local structures
T0 sometimes used to indicate carcinoma in situ |
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N =
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lymph node metastasis N0-N3
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M =
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hematogenous metastasis M0-1
works best for carcinomas |
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most useful application of tumor markers
|
molecules detectable in blood or other body fluids indicative of tumor
not sensitive or specific enough for primary diagnosis of cancer used primarily to follow response to therapy |
|
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Prostate specific antigen is linked to what cancer?
|
adenocarcinoma of the prostate
|
|
|
carcinoembryonic antigen is linked to
|
colon, pancreas, somtimes stomach
|
|
|
alpha-fetoprotein (AFP):
|
hepato cellular carcinoma and yolk sac tumor
|
|
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HCG
|
choriocarcinoma
|
|
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CA-125
|
adenocarcinoma of ovary
|
|
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Prostate specific antigen is linked to what cancer?
|
adenocarcinoma of the prostate
|
|
|
primary methods of diagnosis
|
biopsy or excision
fine needle aspiration cytologic smears |
|
|
special stains of tissue section using monoclonal antibodies to detect cell-specific antigens
used for characterizing lymphomas and poorly differentiated tumors identify sources of metastatic tumor or presence of antigens of therapeutic significance |
immunohistochemistry
|
|
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carcinoembryonic antigen is linked to
|
colon, pancreas, somtimes stomach
|
|
|
detection of gene rearrangement to aid diagnosis or predict prognosis, detect minimal residual disease, detect familial predisposition to certain cancers
|
molecular pathology
|
|
|
alpha-fetoprotein (AFP):
|
hepato cellular carcinoma and yolk sac tumor
|
|
|
certain chromosomal abnormalities can aid in diagnosis or have prognostic significance
|
cytogenetics
|
|
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HCG
|
choriocarcinoma
|
|
|
uses monoclonal antibodies to detect surface or cytoplasmic cell specific antigens in aiding diagnosis especially for leukemias and lymphomas
can also be used to assess DNA ploidy |
flow cytometry
|
|
|
CA-125
|
adenocarcinoma of ovary
|
|
|
Prostate specific antigen is linked to what cancer?
|
adenocarcinoma of the prostate
|
|
|
primary methods of diagnosis
|
biopsy or excision
fine needle aspiration cytologic smears |
|
|
special stains of tissue section using monoclonal antibodies to detect cell-specific antigens
used for characterizing lymphomas and poorly differentiated tumors identify sources of metastatic tumor or presence of antigens of therapeutic significance |
immunohistochemistry
|
|
|
carcinoembryonic antigen is linked to
|
colon, pancreas, somtimes stomach
|
|
|
detection of gene rearrangement to aid diagnosis or predict prognosis, detect minimal residual disease, detect familial predisposition to certain cancers
|
molecular pathology
|
|
|
alpha-fetoprotein (AFP):
|
hepato cellular carcinoma and yolk sac tumor
|
|
|
certain chromosomal abnormalities can aid in diagnosis or have prognostic significance
|
cytogenetics
|
|
|
HCG
|
choriocarcinoma
|
|
|
uses monoclonal antibodies to detect surface or cytoplasmic cell specific antigens in aiding diagnosis especially for leukemias and lymphomas
can also be used to assess DNA ploidy |
flow cytometry
|
|
|
CA-125
|
adenocarcinoma of ovary
|
|
|
primary methods of diagnosis
|
biopsy or excision
fine needle aspiration cytologic smears |
|
|
special stains of tissue section using monoclonal antibodies to detect cell-specific antigens
used for characterizing lymphomas and poorly differentiated tumors identify sources of metastatic tumor or presence of antigens of therapeutic significance |
immunohistochemistry
|
|
|
detection of gene rearrangement to aid diagnosis or predict prognosis, detect minimal residual disease, detect familial predisposition to certain cancers
|
molecular pathology
|
|
|
certain chromosomal abnormalities can aid in diagnosis or have prognostic significance
|
cytogenetics
|
|
|
uses monoclonal antibodies to detect surface or cytoplasmic cell specific antigens in aiding diagnosis especially for leukemias and lymphomas
can also be used to assess DNA ploidy |
flow cytometry
|
|
|
mental retardation
short stature postnatal small hands and feet voracious appetite hypotonia congenital early feeding problems characteristic facies hypogonadism eyes almond-shaped upslanting strabismus narrow forehead (bifrontal) high pain threshold no vomiting, thick saliva |
Prader Willi
|
|
|
what is the chromosomal del in Prader Willi?
|
delete paternal chr 15 q11-13
|
|
|
severe mental retardation
ataxia unprovoked uncontrolled laughter seizures postnatal microcephaly flat occiput (bradycephaly) little or no speech arm held horizontal seizures paroxysms of unprovoked laughter, happy affect wide mouth, protruding tongue, prominent mandible little or no speech |
Angelman
"Happy Puppet" |
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what is the chromosomal abn of angelman?
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delete maternal chr 15 q11-13
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cleft palate
micrognathia VSD, R aorta, fallot tetraology aberrant L subclavian, "tubular" nose w/ broad, built-up bridge and narrowed tip, long face: microcephaly, dev delay/MR, psychiatric disease, long fingers, immunodeficiency, minimal --> Mild DGS |
velocardiofacial
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what is the chr abnormality of velocardiofacial and digeorge?
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Del(22)(q11.2)
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characteristic facies cleft palate heart defects thymus hypo/aplastia
cellular immunodeficiency hypocalcemia parathyroid hypo/aplasia --> hypocalcemia, CV: conotruncal heart disease truncus/tetralogy/VSD, aortic arch defects: interrupted arch, right arch micrognathia, ear anomalies, telecanthus, short palpebral fissures, short upper lip, MR, esophageal or choanal atresia, VPT, anal anomalies, early lethal frequency |
digeorge
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development disability, characteristic facies, supravalvular aortic stenosis, friendly, loquacious, hourse voice, hyperacusis, fullness around eyes and lips, medial eyebrow flare, depressed nasal bridge, epicanthal folds, irises blue w/ stellate pattern, long philtrum, supravalvar aortic stenosis, short stature, progressive tissue dysplasia, renal artery stenosis --> hypertension, joint probs, diverticulosis
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Williams
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Williams is due to what chr abn?
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Del(7)(q11.23) detected by FISH > 90% pts
1/10-20,000 maternal = paternal deletions ?more severe growth retardation w/ maternal deletions ELN(elastin) mutation |
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dwarfism, sun-sensitive butterfly rash of face, predisposition to malignancy
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Bloom syndrome
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bloom syndrome is caused by what chromosomal abn?
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high frequency of sister chromatid exchange
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short stature
radial hypoplasia anemia pancytopenia bronzing of skin predisposition to leukemia |
Fanconi anemia
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fanconi anemia chr abn?
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chromosome breakage and nonhomologous interchange
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mental retardation
macro-orchidism large ears prominant jaw high arched palate pectus excavatum, hyperextensible MP joint, hand calluses, double-jointed thumbs, single palmar crease, flat feet test individuals w/ autism or mental retardation, family history of similarly affected males |
fragile x
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what is the chr abnormality of fragile x?
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fragile site on Xq27.3
trinucleotide amplification - oonly clinically significant sytogenetically detectable fragile site |
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growth retardation, developmental delay, limb anomalies, craniofacial deformities
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robert syndrome
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what kind of chr abn in robert syndrome?
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separation of heterochromatic regions
"railroad track" sister chromatids |
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prototypic disorder for Type I immediate hypersensitivity reaction
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anaphylaxis
allergies bronchial asthma |
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immune mech of Immediate (I)
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IgE --> release of vasoactive amines --> eos
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pathologic lesions of type I
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vascular dilation, edema, SM contraction hypersecretion of mucous, tissue injury, inflammation
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antibody-mediate (II) prototypic disorder
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autoimmune, hemolytic anemia, Goodpasture anemia
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antibody-med (II) immune mech
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IgM, IgG --> bind ag on target cell or tissue --> phagocytosis or lysis; leukocyte recruitment
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pathologic lesions of antibody-mediated (II)
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phagocytosis, lysis of cells, inflammation, functional derangements without cell or tissue injury (MG)--> paralysis, graves' diseases (hyperthyroidism bc antibodies serves as ligand that turns it on)
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prototypical disorders of immune complexes (III)
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SLE
some form of glomerulonephritis serum sickness arthrus reaction |
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mech of immune complexes (III)
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Ag-Ab complexes on capillary surfaces, BM --> C' activation --> PMN--> toxicity
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pathologic lesions of immune complexes (III)
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inflammation
**Acute Necrotizing vasculitis (fibrinoid necrosis) necrosis of vessel wall intense neutrophilic infiltration necrotic tissue and deposits of immune complexes, complement, plasma protein produce a smudgy eosinophilic desposit that obscures underlying cellular detail |
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prototypic disease of cell mediate (IV)
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contact dermatitis
MS type I diabetes RA, IBD, TB |
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mech of cell mediated (IV)
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activated T cells (CD4+) --> cytokines released --> inflammation --> mac acts and CTLs
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pathologic lesions of cell mediated (IV)
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perivascular cellular infiltrates; edema, granuloma formation
cell destruction |
