Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Renal Exam III > Renal Cell Carcinoma fs > Flashcards

Renal Cell Carcinoma fs Flashcards

1
Q

Renal cell carcinoma overview

A

CarcinomaAdenocarcinoma of the kidney
-50,000 new cases in US/yr
12,000 deaths
2:1 male preponderance…70 yrsold
-Tobacco…cigarettes…obesity ,HT ,estrogen therapy
-4% familial (Autosomal dominant form)
-Associated with Von Hippel–Lindausyndrome(VHL gene chromosome 3)Clinical-Usually Silent… costovertebralpain, palpable mass, hematuria
fever……weight loss………weakness………METASTASES in 25% at presentation
ParaneoplasticSyndromes….polycythemia, hypercalcemia, Cushing syndrome… ect.

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

renal tumor numbers

A

51000 cases diagnosed and 12900 deaths annually

3% of adult malignancy

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

sporadic papillary genomics

A

trisomy 7,16,17

mutated, activated MET>PRCC oncogenes

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

Hereditary papillary genomics

A

Trisomy 7

mutated activated MET

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

Sporadic Clear cell genomics

A

Translocations 3:6, 3:8, 2:11 and deletions on chromosome 3

loss of vhl
inactivated mutated vhl
hypermethylation of vhl

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

Hereditary clear cell

A

Translocations 3:6, 3:8, 2:11 and deletions on chromosome 3

loss of vhl
inactivated mutated vhl
hypermethylation of vhl

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

RCC

cell of origin
most common appearance
second most common apperaacne

A

tubule epithelial cell

clear cell carcinoma

papillary carcinoma

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

VHL syndrome

A

von Hippel-Lindau (VHL) disease, or von Hippel-Lindau syndrome, is a rare genetic disorder characterized by visceral cysts and benign tumors in multiple organ systems that have subsequent potential for malignant change.

usually vascular tumors

cysts are seen that have become malignant for rcc

visceral cysts and benign tumors in multiple organ systems that have subsequent potential for malignant change.

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

Where is the VHL gene located?

A

Cytogenetic Location: 3p25.3

Molecular Location on chromosome 3: base pairs 10,141,634 to 10,153,669

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

other malignancies in vhl

A 
retinal agniomata
pulmonary hemangiomas
liver hamangiomas
multiple pancreatic cysts
epididymal cysts
cerebellar hemangioblastoma
pheochromocytoma
rcc and cysts
cystadenomas of broad ligament
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

vhl proteins

A

when vhl protein is notmal it binds to hifa and it is destroyed if it doesnt bind hifa binds hifb these products are created and you get a lot of vascularization

vegf pdgfb tgfa epo

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

what causes rcc to appear clear

A

lipids and glycogen

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

Renal Cell Carcinoma (RCC)(Hypernephroma) Major Clinical Characteristics

A

Classic triad of most common presenting signs/symptoms
Hematuria(60%)
Costovertebral pain(40%)
Palpable flank mass(30-40%)
All 3 present only in 10% of RCC patients

Important Characteristic
Tendency widespread metastasis before local signs/symptoms

25% RCC patients have radiologic evidence of metastatic disease at time of their initial diagnosis.

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

Type: conventional clear cell

% Total RCC

% 5-year Survival

A

70 -75%

70% without mets (with mets 45%-with renal vein or perinephric fat invasion-15%)

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

Type: papillary

% Total RCC

% 5-year Survival

A

15 -20%

86%

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

Type: chromophobe

% Total RCC

% 5-year Survival

A

7%

95%

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

Type: RCC unclassified

% Total RCC

% 5-year Survival

A

5%

18%

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

Major Factors in Prognosisof Renal Cell Carcinoma

A

Stage(particularly size of tumor)
The bigger the tumor,
the worse the prognosis

Histologic Type

Mode of Spread
Hematogenous -not lymphatic

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

Renal Carcinoma staging

Stage I

A

5 year survival 96%

Tumor

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

Renal Carcinoma staging

Stage II

A

5 year survival 82%

tumore>7cm in greatest dimension and limited to kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Renal Carcinoma staging

Stage III

A

5 yr survival 64% tumor in major veins adrenal gland or perinephric tissue and or 1 regional lymph node involved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Renal Carcinoma staging

Stage IV

A

5 year survival 23%

tumor beyond gerotas fascia

more than 1 lymph node involved and more than 1 distant metastasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

cannon ball mets

A

rcc spread to lung

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

erythematous-violaceious lobulated mass on skin

A

rcc spread to skin

25
Q

bone mets

A

rcc spread to bone

26
Q

Rcc clinical presentation second card

A

silent for most of course

classic triad 5-10% of pts
flank pain
hematuria
palapable abdominal mass

hematuria present 40% of pts

systemic symptoms
   anaemia
   fatigue
   cachexia
   wt loss
   hypercalcemia
   hepatic dysfunction

paraneoplastic syndrome
parathyroid like hormones epo renin gonadotropins palacenal lactogen prolactin enteroglucagon insulin like homrones adrenocorticotropic hormone and prostaglandins identified in rcc pt

27
Q

RCC Diagnostic workup

A

General - history pe

lab studies - cbc lfts alkaline phosphatase bun creatinine ua

radiographic studies

28
Q

RCC radiographic studies

A

xray kub region

ultrasound - distinguish cysts from solid masses

iv urography - starting point for hematuria avaluations and function of contralateral kidney

ct - provide an excellent assessment of the parenchyma and nodal status

mri - excellent demonstration of solid renal masses and is image test of choice to demonstrate extent of vena caval involvement with tumor, useful in patients with renal insufficiency

29
Q

general concept of interstitial space

A

Fluid filters and diffuses (O2) out of blood capillaries and enters into the interstitial space

Starling’s Equation

Fluid is drained from the interstitial space by absorption into lymphatic capillaries.
Oncotic/hydrostatic pressures, valves and contractions move the fluid along.

30
Q

Lymphovascular invasion and metastasis:

A

Tumor metastasis involves a coordinated series of complex events that include promotion of angiogenesis and lymphangiogenesis, detachment of malignant cells from the primary tumor, microinvasion of the surrounding stroma, blood and/or lymphatic vessel invasion, survival of the malignant cells in the blood and/or lymphatic flow, and extravasion and growth in secondary sites. Because the large lymphatic vessels reenter the blood vascular system, malignant cells spread via the lymphatic system to the regional lymph nodes and, from this point, to distant organs (Fig. 3). Follow-up data have shown that 80% of the tumors, mainly those of epithelial origin, disseminate through the lymphatic vasculature; the remaining 20% use the blood circulation to colonize secondary organs.
The blood vessels are not the best route for the success of malignant dissemination. Although their disorganized structure may contribute to the intravasion of malignant cells or emboli, in the bloodstream these cells experience serum toxicity, high shear stresses and mechanical deformation. Consequently, the viability of the tumor cells is seriously compromised. Conversely, the success rate of lymphogenous spread is high. As previously referred, the structure and function of the lymphatic capillaries facilitates intravasion of tumor cells or emboli. On the other hand, the composition of the lymph is similar to interstitial fluid, which provides an optimal medium for the survival of malignant cells. In collecting lymphatic vessels, muscle fibers assure lymph propulsion, that flows slowly, and valves prevent its backflow. Lymph nodes are areas of flow stagnation that represent ideal “incubators” for malignant cells’ growth. Some cells exit the lymph node through the efferent channels or high endothelial venules. Other cells may remain mechanically entrapped for long periods of time, originating micrometastases. Martens and colleagues described the expression of a gene signature of scavenger and lectin-like receptors in the lymph node sinus, which are known mediators of tumour cell adhesion and, therefore, can contribute to selective metastasis in an organ-specific context. Probably, tumor-cell-specific characteristics, microenvironmental factors and crosstalk between tumor and host cells have a pivotal role in determining survival and growth of micrometastasis. Moreover, lymph node lymphangiogenesis may provide an additional mechanism to facilitate further metastatic spread throughout the lymphatic system. The occurrence of lymphangiogenesis prior to arrival of tumor cells indicates that signals derived from the primary tumor are transported to the draining lymph nodes.
Pathways of dissemination of malignant cells:
Different tumors metastasize preferentially to different organs, suggesting that tumor spread is a guided process. It has been reported that malignant cells may use chemokine receptor ligand interactions to guide the colonization of target organs. Chemokines are a family of chemoattractant cytokines that bind to G protein-coupled receptors expressed on target cells, namely malignant cells . For instance, breast cancer cells, that normally choose regional lymph nodes, bone marrow, lung and liver as their first sites of destination, overexpress CCR7 (chemokine, CC motif, receptor 7) and CXCR4 (chemokine, CXC motif, receptor 4). Their ligands, SLC/CCL2 (secondary lymphoid chemokine / CC- type chemokine ligand 21) and SDF-1 CXCL12/ (stromal cell-derived factor 1 / chemokine, CXC motif, ligand 12) are expressed at high levels by isolated lymphatic endothelial cells and lymphatic endothelium from vessels present in the preferred sites of metastasis. This guides chemoattraction and migration of tumor cells, and characterizes lymphatic vessel invasion as an active event.

31
Q

new way to track malignancy

A

tumor dna and rna in blood

32
Q

Clinical presentations of neoplasms

Local effects

A

mass effect (eg leiomyoma>menorrhagia)

invasion (eg SCC of cervix>renal failure secondary to ureteric obstruction)

33
Q

Clinical presentations of neoplasms

metastases

A

Mesothelial surface (eg ovarian serious carcinoma>malignant ascites)

lymph node (eg pancreatic adenoca>lymphadenopathy(virchows node)

organ
Liver, lung, bone, cns

34
Q

Clinical presentations of neoplasms

Paranelioplastic syndromes

Endocrine

A

Epo>polycythemia (rcc, hepatocellular Ca)

siadh>hyponatremia (small cell ca lung)

acth> cushing (small cell ca lung, scc lung)

PTHrp and pth>hyercalcemia (myeloma, breast, lymphomas)

Insulin>hypoglycemia (islet cell tumors) also IGF2 (other tumors)

Serotonin>carcinoid syndrome (mid-gutwith metastasis to liver)

Catecholamines>episodic sympathetic system (pheochromocytomas)

35
Q

Clinical presentations of neoplasms

Paraneoplastic syndromes

Migratory Thrombphlebitis

A

(pancreatic adenocarcinoma)

36
Q

Clinical presentations of neoplasms

Paraneoplastic syndromes

Neruologic (onconeural antibodies)

A

Myasthenia gravis (thymoma)

eaton-lambers mg (multiple)

CNS, PNS, ANS (multiple)

37
Q

Clinical presentations of neoplasms

Paraneoplastic syndromes

skin and joints

A

acanthosis nigricans

dermatomyositis

38
Q

Clinical presentations of neoplasms

Paraneoplastic syndromes

kidney

A

membranous glomerulopathy

39
Q

Low grade papillary urothelial

papillomas

A
  • Exophytic or endophytic (inverted)

* Benign, cured by resection

40
Q

low grade papillary urothelial

carcinoma

A

–PAPILLARY UROTHELIAL NEOPLASMS OF LOW MALIGNANT POTENTIAL
–LOW GRADE PAPILLARY UROTHELIAL CARCINOMA
•Larger than papillomas, thicker epithelium,
•Recur after resection, but don’t become high grade or invade
•Orderly architecture; mildly atypical cytology, few mitoses
•Recur but only invade infrequently
•Treat by TURBT; 98% 10 year survival

41
Q

urothelial low grade tumors

A

hyperplasia>fgfr3/raas activation>papillary carcinoma ta

42
Q

urothelial muscle-invasive tumors

A

dysplasia>p53 signaling pathway>CIS invasive carcinoma T2, metastasis

43
Q

Progression of carcinoma: a schema

Precancer (dysplasia)

A

squamous metaplasia:

low grade papillary TCC - mild
high grade papillary - moderate
CIS - severe

44
Q

Progression of carcinoma: a schema

Carcinoma

A

Squamas metaplasia:

invasive urothelial carcinoma (invasion, LVI)

45
Q

Progression of carcinoma: a schema

Metastasis

A

Squamos metaplasia:

Perivesicle nodes

(sentinel lymph node, regional lymph nodes, systemic)

46
Q

normal urothelium

A

umbrella cell

47
Q

cis

A

full thickness abnormalities

48
Q

non-invasive in-situ cancer

A

No lymphatic vessels or blood vessels in mucosa

49
Q

invasive in situ cancer

A

Tumor cells have access to lymphatic channel as soon as the tumor has invaded through the basement membrane.

50
Q

Staging: superficial

A

Stage:ois, os, I
TNM: tis, ta, t1
L nodes:
5 year survival: 90%

51
Q

Staging infiltrating

A

Stage: II, III
TNM: t2, t3a, t3b,
L nodes: 26, 50
5 year survival: 70%

52
Q

Staging invasion of adjacent structures

A

Stage: III, IV
TNM: t4a, t4b
L nodes: 70
5 year survival: 10-20%

53
Q

Staging lymph node invasion

A

Stage: IV
TNM: N+
L nodes: 100%
5 year survival: 10-20%

54
Q

staging distant extension

A

Stage: IV
TNM: M+
L nodes: 100%
5 year survival:10-20%

55
Q

Tissue biopsy

A

sample of cells form the body

56
Q

liquid biopsy is useful when there is

A

not enough tissue sample available

note enough tumor tissue in the sample

a hard to reach tumor

need for regular monitoring

57
Q

liquid biopsy steps

A

free circulating nucleic acids come mainly from dead cells and ncan contain cancer related mutations

rna from exosomes, microvesicles that are used to transport genetic instructions between cells

circulating tumor cells result from cancers that shed cells from the primary tumor into the blood stream

58
Q

liquid biopsy potential applications

A

monitoring treatment response, drug resistance, disease recurrence

detection of genomic mutations to guide treatment decisions, various tumors of an earlier stage

Renal Exam III (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions