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Stage 4 > Malignancy > Flashcards

Malignancy Flashcards

1
Q

Clubbing with central cyanosis = 2 things

A

Fibrosing alveolitis

Eisonhower syndrome

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2
Q

Skin manifestations indicate stage what NSCLC & SCLC?

A

4

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3
Q 
Small cell carcinoma - LIQUID Smoke
Aetiology
Behaviour
Location
Key features - All but PTH neoplastic syndromes

No clubbing?

A

Neuroendocrine “oat” cells (APUD cells) start central then metastasise quickly like LIQUID but rapid response to Rx

4 syndromes:
1. SVC obstruction > Central hilar location with obstruction of right upper lobe >

  1. ADH > SIADH
  2. ACTH > Cushing’s syndrome
  3. Eaton-Lambert syndrome - limb muscle weakness due to antibodies against Ca channel > reduced AcH. Unline myasthenia gravis bulbar muscles are NOT affected (swallowing). Diagnose with EMG. Steroids

“Oat cell” - flat cell shape and scanty cytoplasm

SMOKING association

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4
Q 
Non small cell: Squamous 
Aetiology
Behaviour
Location
Key features
A

Slow central cavitation

Lung collapse, pneumonia or pleural effusion

PTH > Hypercalcemia = Short QT

Hypertrophic Pulmonary Osteoarthropathy (HPOA)

SMOKING association

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5
Q 
Non small cell: Adenocarcinoma
Aetiology
Behaviour
Location
Key features
A

Peripheral mucus glands > diffuse > brain and bone mets

Associated with ASBESTOS (AA) NOT smoking!

Pink frothy sputum + sharp pleuritic pain

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6
Q 
Non small cell: Large cell
Aetiology
Behaviour
Location
Key features
A

Begin anywhere and grow quickly

Large peripheral mass on CXR with mediastinal lymphadenopathy

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7
Q

Two lung cancers most associated with smoking

A

Small cell
Squamous
S.S.S

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8
Q

Malingnant Mesothelioma

A

Surface serosal cells of pleura > thickened pleural rim > pleural effusion

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9
Q

General Lung Cancer
Sx
Ix
Mx

A

Haemoptysis, nicotine stain, clubbing (NSCLC), lymphadenopathy, SVC obstruction (dusky skin + raised nonpulsatile JVP), pleural effusion, weight loss

Dysphagia can occur if tumour compresses

Hoarse voice can occur if recurrent laryngeal nerve compressed by tumour (usually inoperable)

Pancoasts syndrome - apical tumour invades wall and interrupts sympathetic chain = Pain in T1 distribution + horners (meiosis, ptosis, anhydrosis)

  1. CXR, FBC, biochem, PFTs
  2. Contrast CT - staging
  3. Bronchoscopy + biopsy

NSCLC often suitable for surgery if no mets
V/Q scan to see if whole lung can be removed

Surgery - lobectomy if localised
Radiotherapy
Chemotherapy in those with good performance status
Pleural drain for effusions, stent for SVC obstruction, opiates

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10
Q 
General Lung Cancer
Complications
Mechanism
Sx
Ix
Mx
A

General:
Dermamyositis, Anemia, Acanthosis nigricans in lung and gastric ca (black stain on skin)

Non small cell:
Hypercalcemia due to PTHrP - True paraneoplastic hypercalcemia doesnt have bony mets
Stones, bones, groans, thrones, moans
Short QT
High Ca and undetectable PTH
Saline! -> IV bisphosphonates

Small cell:
SVC Obstruction - External pressure from tumour/blood clot/or lymphoma
Non-pulsatile JVP, dilated veins, flushed face, reduced mental function
CXR: Superior mediastinal widening, pleural effusion and right hilar mass -> CT
Stenting

Ectopic ACTH - released from tumour
Cushings = truncal obesity, HTN, proximal weakness, hirsutism, hypokalemic acidosis, hyperpigmentation, hyperglycemia
Increased 24hr urinary cortisol + plasma ACTH
NO RESPONSE to dexamethasone suppression test

SIADH - Increased water reabsoprtion from kidney via aquaporins > dilutional hyponatremia
Asymptomatic, cerebral oedema, reduced GCS
Urine osmolality > serum osmolality, high urinary
Fluid restrict

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11
Q

Peripheral vs Central lung cancers

A

Peripheral: Adenocarcinoma, large cell

Central: Small cell, squamous

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12
Q

Prognosis depends on what 3 factors

A
  1. Performance status (most important)
  2. Metastasis
  3. Increased LDH
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13
Q

Neutropenic sepsis
Definition
Mx

A

Pyrexia >38 / >37.5 on 2 readings OR rigor/ hypotension/ tachycardia
+ <1 neutrophils

Occurs after chemo thus loss of immune repsonse = no fever, normal CXR

Black/green infection sites

Infection screen/cultures > IV ABx
AVOID paracetmaol, PR + PV exam

The other post cancer Rx condition is = Radiation pneumonitis - 9 week lag + alveoli oedema + hyperaemia = STEROIDS

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14
Q

Calcium + albumin + hydrogen

A

Calcium is either bound to albumin or free/ionised/active.

When albumin is low (nephrotic syndrome, liver disease) then a higher proportion of calcium is free as opposed to bound to albumin thus although calcium may appear normal the level of active calcium is actually much higher.

Corrected calcium levels take this into account and bump up the calcium lab test level.

Hydrogen also bind to albumin so when there is alkalosis H+ leaves albumin to join the serum, this then leaves albumin free for calcium to bind to thus decreasing level of free/active calcium = hypocalcemia

High Na, Low K, alkalosis (lose H in exchange for K), H leaves albumin to join serum, calcium binds to albumin (hypocalcemia)

Low Na, High K, acidosis (K is lost in exchange for H), more H in serum binds to albumin, less calcium can bind to albumin = hypercalcemia

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15
Q

What cancer causes hypocalcemia

A

Medullary carcinoma of thyroid > calcitonin = hypocalcemia (Calcitonin production from C cells of thyroid)

Lytic bony mets

Bisphosphonate use

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16
Q

Cause and cancer

  1. Tobacco and asbestos
  2. UV
  3. EBV
  4. Hepatitis
  5. Schistosoma haem
  6. Schistosoma jap
  7. Malaria
A
  1. Malignant mesothelioma
  2. Xeroderma pigmentosum - ARecessive defect in NERepair enzyme = reduced NER = Less UV damage repaired
  3. Lymphoma
  4. Hepatocellular ca
  5. Bladder
  6. Liver and colon
  7. Burkitts lymphoma
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17
Q

Basal cell carcinoma suspected, how to assess the lesion?

And if it was fungal?

A

Perform a full thickness biopsy at the edge of the lesion (proliferative area rather than necrotic centre)

Scrapings and culture from the base of the ulcer

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18
Q 
Germ cell cancer general
Behaviour
Risk factors
Sx
Ix
Mx
A

Short doubling time = susceptible to chemo

FH, testicular maldescent, Klinefelters, down syndrome, infertility

Testicular cancer: Painless solid mass in scotum, back pain, dragging sensation, gynaecomastia due to high hHCG, sore nipples
Ovarian cancer: Grow rapidly, abdo pain/distension,
Headache, blurred vision, dyspnea if brain/lung mets

Diagnostic: Testicular mass + aFP + bHCG!
US balls
CXR cannoball mets

Orchidectomy + implant
CT/MRI for mets/staging

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19
Q 
Seminoma vs Non-seminoma
Definition/Histology
Tumour markers
Spread
Prognosis
Surveillance
Complications
A 
Seminoma = Uniform cells
Non-seminoma = Everything else (Mature teratoma, teratocarcinoma, embryonal, yolk sac, choriocarcinoma
Seminoma = bHCG in 10%
Non-seminoma = Yolk sac - AFP (yAF saP), Choriocarcinoma - bHCG (fastest growing tumour like a bab)
All = LDH - poor prognosis/tumour bulk marker

Seminoma: Para-aortic nodes. Slow and haem is rare
Non-seminoma: haem

Infertility, avoid pregnancy for 2 years
Rx: Acute - neutropenia, alopecia, fatigue etc
Chronic - Pulmonary fibrosis, HTN

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20
Q

False positive for hCG

A

Cannabis

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21
Q 
Tumour lysis syndrome
Pathophysiology
Adverse effects
Risk factors
Prevention
Mx
A

Death and breakdown of a large number of tumour cells into toxic components which induce renal AKI

Hyperuricemia (nucleic acid breakdown)
Hyperkalemia (K from dead cells)
Hyperphosphatemia (dead cells)
Hypocalcemia (opposite to phosphate and renal failure)

AKI due to urate/uric acid
Arrhythmias due to metabolites

High LDH or chemo sensitive tumours - BURKITTS, leukemia, small cell, germ cell

Hydrate, correct elctrolytes and ALLOPURINOL / Rasburicase

22
Q 
Breast cancer
Risk factors
Sx
Complications
Prevention
A

High estrogen - early menarche, late menopause, nulliparous, HRT, obesity AND alcohol and RADIATION

Painless breast lump (cyclical pain = less likely to be cancer, fibrocystic disease)
Lymph nodes, nipple discharge/retraction, discolouration, PEAU D’ORANGE, eryhtmea, ulceration, thickening, loss of symmetry, lung mets

Pagets disease = Bloody nipple discharge + Eczematoid erythematous change in nipple

Bone mets:
MRI to Dx

Spinal cord compression:
MRI to Dx
Bilateral UMN signs +- new back pain/motor dysfunction

Mastectomy
Ovarian ablation
MRI + Mammography screening 47-73

23
Q

Familial breast cancer

A

Multiple affected relatives at YOUNGER age, bilateral breasts and male

BRCA12, Li-Fraumeni, Cowden’s

Worse histological features = aneuploidy, higher grade and proliferation

Often triple hormone negative - hormone Rx unlikely to work

24
Q

Breast cancer Ix

A

US - solid or cyst?
Cyst?
1. Aspirate/FNA if cystic and if keeps producing blood then could be cystic breast ca (very rare)
Fibrodenoma will be hypoechoic

Solid?

  1. Mammography - malignant features = Asymmetry, microcalcifications, a mass, architectural distortion
  2. Use MRI if younger/dense breast tissue
  3. FNA - cytology
  4. Biopsy - excisional gives definitive diagnosis as whole mass removed

Non-palpable mass?
Biopsy or MRI

CA15.3 only used to assess Rx

Assess for hormone receptor targets: HercepTest + FISH
Triple negative = hereditary cancer syndrome

Radioisotope bone scan (doesnt capture myeloma) for bony mets but MRI is better

25
Q

Breast cancer Ix

A

US - solid or cyst?
Cyst?
1. Aspirate/FNA if cystic and if keeps producing blood then could be cystic breast ca (very rare)
Fibrodenoma will be hypoechoic

Solid?

  1. Mammography - malignant features = Asymmetry, microcalcifications, a mass, architectural distortion
  2. Use MRI if younger/dense breast tissue
  3. FNA - cytology
  4. Biopsy - excisional gives definitive diagnosis as whole mass removed

Non-palpable mass?
Biopsy or MRI

CA15.3 only used to assess Rx

Assess for hormone receptor targets: HercepTest + FISH
Triple negative = hereditary cancer syndrome

Radioisotope bone scan (doesnt capture myeloma) for bony mets but MRI is better

26
Q 
Ovarian cancer
Risk factors
Sx
Spread
Ix
A

Postmenopausal women
More ovulations = Higher risk - low parity and infertility increase risk as ovulations continue, lots of babies and COCP decreases ovulations
FH + talc

Associated with BRCA1 - less aggressive course + better response to chemo

Abdo pain/swelling > ascites
Early satiety
Bladder/rectal Sx from mass +-PV bleeding
Meig’s syndrome: Ascites + pleural effusion + benign pleural effusion

Transcoelemic spread via paracolic gutter

CA-125 (better for surveillance not Dx) - doubling from upper limit normal = relapse - look at serial steep curve not snapshot
CEA + in younger hCG, AFP, LDH for germ cell tumours

  1. US
  2. Consider CT/MRI
    Dx. Explorative laparotomy + biopsy
RMI = UxMxCA-125 =  >200 = referral
M= menopause status
U= Ultrasound
27
Q
  1. Ionising radiation seen in ? and causes ?
  2. Non-ionising is?
  3. EBV linked with ?
  4. Hepatitis linked with ?
  5. Malaria linked with ?
  6. Liver fluke ?
  7. Breast ?
  8. Ovary ?
  9. Cervical ?
  10. Endometrial ?
  11. Anabolic steroids ?
A
  1. Xrays > BM ,breast, thyroid
  2. UVB
  3. Burkitts lymphoma, Hodgkins lymphoma
  4. Liver ca
  5. Burkitts lymphoma
  6. Cholangiocarcinoma
  7. Estrogen exposure
  8. Number of ovulations - COCP reduces
  9. HPV + maybe more sex = more use COCP
  10. Unopposed estrogen
  11. Liver ca
28
Q 
Autosomal dominant inherited cancer syndromes - gene and Sx
Li-Fraumeni
Lynch syndrome 
Familial Adenomatous Polyposis
Breast/Ovarian syndrome 
MEN
Cowdens syndrome
Neurofibromatosis
RB1 mutation
A

Li-Fraumeni: TS p53 gene on chromosome 17 = childhood cancers + premenopausal breast ca

Lynch syndrome: aka HNPCC DNA mismatch repair (TS) genes MLH MSH = Colon + endometrial ca

FAP: TS APC gene = Colon polyps on very young > colon ca

BRCA1/2: TS repairs dsDNA breaks = Breast, ovarian, prostate, pancreas

MEN: MEN gene is TS. RET (REKT) is ONCOGENE. 3P, 2P 1M, 1P 2M

Cowdens syndrome: TS PTEN = breast + mucocutaneous overgrowth. PTENding to be a COW w/ breast + mucocutaneous lesions

Neurofibromatosis: TS NF1/2 = NEurofibrosarcomas, optic glioma, axillary freckling!

RB1: TS RB1 = Retinoblastoma - no red light reflex

29
Q

Oncogenes (rest are TS)

A

myc (malaria induces)
HER-2
K-ras
RET

30
Q

You risk over diagnosing but you want cancer screening tests to be very ?

A

Sensitive!

Specific aint so important

31
Q

Lead time bias? (early = longer survival)

Length time bias? (benign-ish detected = longer survival)

A

Lead time bias: When you detect tumours earlier of course the cancer survival time increases as it has an early start date

Length time bias: More indolent tumours are detected which have better survival anyway

32
Q

Screening programmes
Breast
Colorectal
Cervical

A

3 yearly mammography (microcalcification+soft tissue density) from 47-73

Look for faecal occult blood in over 50s

Smear: 3 yearly 25-49 then 5 yearly 50-64
DOESN’T detect adenocarcinoma
Abnormal = Colposcopy + biopsy

33
Q

Epitrochlear + splenomegaly = ?

A

CLL

CLL and over 70 = better prognosis than no CLL

34
Q

What can we do when we find a tumour that is not the primary site of cancer?

A

Biopsy then immunohistochemistry

35
Q

PTH secretion can be from?
Low aFP means what with regards to HCC?
CA-125 is for more than ovarian ca?
CEA not specific to one cancer but good for ?

A

NSCLC
Ruled out
Peritoneal/pleural irritation
Monitoring Rx

36
Q 
Tumour markers
aFP
CA125
CA19-9
Calcitonin
CEA
b-HCG
Ca15-3
A 
Non-seminoma + liver
Ovarian - never diagnostic
Pancreas
Medullary cell carcinoma of thyroid
Colorectal - monitor every 6 months
Choriocarcinoma + non-seminomas + 10% seminoma
Breast
37
Q

Tumour markers which can be diagnostic in ANY patient presenting with a carcinoma of unknown primary?

A

AFP
b-HCG
PSA

38
Q

This patient has a malignancy that is widely metastatic and incurable. What is the best approach to treatment?

A

Chemotherapy

39
Q

When is TTF-1 positive?

A

NSCLC

40
Q

Colon cancer sounding Sx. First and Dx investigation

A

AXR
Colonscopy
Stage with CT

41
Q

Most common metabolic complication of malignancy?

A

Hypercalcemia - multiple myeloma, breast, lung

Test corrected Ca

42
Q

Approach to unknown cancer origin

A
  1. Search for primary site
  2. Rule out potentially trwatable/curable tumours
  3. Characterise pathological entitiy
    Favourable > curative
    Unfavourable > palliative
43
Q

Carcinogenesis

Example of proliferative signalling

A

PDGF being secreted by glioblastomas that also have PDGF receptors - AUTOCRINE loop

HER2/NEU (ERBB2) receptor is amplified in some breast ca. Blocking this receptor can treat the cancer/stop proliferation. HER/NEU2 receptor blockage – trastuzumab – AKA Herceptin.

RAS and BRAF are signal-transducing ONCOGENES. BRAF = melanoma = Vemurafenib

44
Q

Carcinogenesis

Example of evading growth suppressors

A

In Rb there is always two hits (tumour suppressor recessive). Either:

  1. Germline + somatic = familial
  2. Somatic + somatic = sporadic
45
Q

Carcinogenesis

Example of avoiding immune destruction

A

Alter microenvironment OR release proteins that inhibit immune cell function

HIV = HHV8/Kaposi sarcoma

46
Q

Carcinogenesis

Example of immortality

A

Cancer cells can regenerate their telomeres via telomerase. This leads to limitless replicative potential.

47
Q

Carcinogenesis
Examples of inflammation causing tumours AND protein where defect causes invasion AND therapeutic target to block invasion/mets

A

H.pylori > barrets
Hep > HCC
UC > Colon ca

CADHERIN

C-met

48
Q

Carcinogenesis

Angiogenesis

A

Hypoxia inducible factor > VEGF

Von hippel lindau inhibits HIF but not in some cancers

Target VEGF with bevacizumab

49
Q

Carcinogenesis

Example of DNA repair cancer genes

A

BRCA1/2

MLH etc Lynch syndrome HNPCC

50
Q

Carcinogenesis

Example of resisting cell death

A

B cell lymphomas – carry a characteristic BCL2 translocation which protects the cells from apoptosis and signals to keep the cell alive.

51
Q

Germline vs Somatic

Oncogene vs TS

A

Germline – mutations present at embyrogenesis – affect all cells and gametes.

Somatic - mutation only present in affected cell and its descendants. Non inheritable

Oncogenes:
A mutated gene – gain of function – that causes cancer
= Dominant – only need one mutation to cause cancer

Tumour suppressor genes:
Loss of function – disabling inbuilt codes that are there to stop excessive proliferation.
= Recessive – two hit hypothesis – need two allelic mutations to cause cancer

52
Q

Carcinogenesis

Example of deregulating cellular energetics

A

Normal cells use ATP by exudative phosphorylation with OXYGEN

Cancer cells don’t need oxygen as they use aerobic glycolysis / WARBURG EFFECT > used when rapid growth required

Stage 4 (12 decks)

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