Tumor markers and few important details Flashcards

1
Q

CA27.29

A

Breast

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2
Q

CYFRA 21.1

A

NSCLC

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3
Q

AFP

A

Liver

Germcell tumors

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4
Q

PSA

A

Prostate

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5
Q

CEA

A

Colon

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6
Q

HCG

A

Choriocarcinoma

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7
Q

ACTH

A

Small cell carinoma

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8
Q

HE4

A

Ovary

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9
Q

Chromogranin A

A

Neuroendocine tumors

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10
Q

Colon

A

CEA

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11
Q

Ovary

A

CA15-3

HE4

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12
Q

Breast
Ovary
Pancreas

A

CA15-3

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13
Q

Breast

A

CA 27.29

CA 15-3

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14
Q

Pancreas
Bile ducts
Gastric

A

CA19-9

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15
Q

Medullary thyroid cancer

A

Calcitonin

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16
Q

Neuroendocine tumors

A

Calcitonin

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17
Q

Liver

Germ cell carcinomas

A

AFP

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18
Q

Chorinocarinoma

A

HCG

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19
Q

SCLC

A

ACTH

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20
Q

NSCLC

A

CYFRA 21.1

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21
Q

Metastasis to the brain

A

Lung
Breast
Malignant melanoma

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22
Q

Metastasis to bone

A
Lung
Breast
Thyroid 
Prostate 
Kidney
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23
Q

Metastasis to liver

A
GI 
Lung
Melanoma 
Neuroblastoma
Many more
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24
Q

Metastasis to lung

A
Breast 
Liver
Kidney
Rectum 
Germinal cell 
Sarcomas
Osteosarcoma
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25
Q

Metastasis of lung cancer to….

A

Brain
Adrenal gl
Bone

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26
Q

what is mamrantic endocarditis?

A

non-bacterial thrombotic endocarditis
deposition of fibrin, platelets and blood on the walls
occurs in the setting of hypercoagulative state

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27
Q

Ca15-3

A

Breast
Ovary
Pancreas

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28
Q

CA19-9

A

Pancreas
Bile duct
Gastric

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29
Q

Calcitonin

A

Medullary thyroid cancer

30
Q

when does Mamrantic endocarditis occur?

A

in the setting of hypercoagulative state

31
Q

what is Libmann sacks endocarditis?

A

setrile endocardidits, induced due to IC deposition

associated with SLE

32
Q

CA125

A

Ovary

33
Q

what are predisposing factors for infective endocaririds?

A
Reumathic fever
cardiac malformations
prosthetic valves
catheters 
host factors: DM, immunosuppressive, malignancy etc...
34
Q

what is a ring abscess?

A

abscess formation in infective endocardiditsn

35
Q

what is the difference between acute and subacute endocardidits?

A

acute: due to high virulence organisms (aureus)
subacute: due to low virulence organism (verdant)

36
Q

pathogenesis of rheumatic fever.

A

hypersensitive reaction against antigen of Step. pyrogens
antigen in circulation– Bcell recognise– Ig production– Ig CROSS REACT with heart tissue and others– endocarditis&GN etc

37
Q

types of myocardiopathyies

A
  1. dilated
  2. Hypertrophic
  3. Restricive
38
Q

what is a dilated myocardiopathy?

A

Due to impairment of contraction (systolic dysfunction)

caused by: Idiopathic, alcohol, myocarditis, genetic

39
Q

what is hypertrophic myocardiopathy?

A

due to impairment of compliance (diastolic problem)

caused by: GENETICS, friedreich ataxia

40
Q

what is a restrictive cardiomyopathy?

A

due to impairment of compliance (diastolic problem)

caused by: idiopathic, amyloidosis

41
Q

how are the Ejection fractions of the different cardiomyopathyies?

A

dilated: <40%
hypertrophic: 50-80%
Restrictive: 45-90%
NORMAL. 55-65%

42
Q

what is the cause for hypertrophic cardiomyopathy?

A

Genetics

point mutation in gene encoding for SACROMERIC proteins– BETA MYOSIN heavy chain…

43
Q

what is löffler endocardidits?

A

end-myocardial fibrosis with eosinophilic infiltrate (seen in restrictive cardiomyopathy)

44
Q

types of myocarditis

A
  1. lymphocytic
  2. hypersensitivity
  3. giant cel
  4. Chagas
45
Q

causes of myocarditis:

A
  1. Viral
  2. non-viral (bacterial and fungal)
  3. non infectious ( SLE)
46
Q

pathogenesis of Atheroscleoris?

A

damage to epithelium
lipids leak into intima
lipids are oxidised
oxidised lipitds are taken up by foam cells

47
Q

Risk factors for arhteroslcosis

A

Modifiable: HTN, DM, Hypercholesterolemia, smoking

non modifiable: age, gender, genetics

48
Q

types of arteriolosclerosis

A

hyalin

Hyperplastic

49
Q

causes of hyalin arteriolosclerosis

A
  1. benign HTN

2. DM

50
Q

causes for hyper plastic arteriolosclerosis

A
  1. Mallignant htn
51
Q

acitvation of neutrophils

A
  1. LTB4
  2. C5a (Mast cells)
  3. IL8
  4. Bacterial products (TLR)
52
Q

how to activate mast cells?

A
  1. IgE
  2. C5a
  3. trauma
53
Q

cardinal signs of inflammation

A
  1. redness
  2. swelling
  3. pain
  4. Fever
54
Q

what causes redness in inflammation?

A

vasodilation
histamine
PG
Bradidinin

55
Q

what causes swelling in inflammation?

A

Histamin

tissue damage

56
Q

what are the pain mediators in inflammation?

A

PGE2

Bradykinin

57
Q

what causes fever in inflammation?

A

LPS– Macrophages– IL1 and TNF

58
Q

describe the leukocyte migrations process

A
  1. rolling (P selection, E selectin)
  2. adhesion (Icam1, intergin)
  3. excavation (PECAM1 (CD31))
59
Q

vasodilators in the case of inflammation

A

PGI, PGE,PE,PGD

60
Q

vasocontritos

A

TAX2, Leukotriens

61
Q

increased vascular permeability

A

Leukotriens

62
Q

what is chronic inflammation?

A

prolonged process in which active inflammation, tissue destruction and healing occour

63
Q

what causes chronic inflammation?

A
  1. persistence infection
  2. immune reactions
  3. long exposure to toxin
64
Q

role of macrophages in chronic inflammation

A

activated by T cell via IFN

Depending on stimulatory factors, either inflammatory mediating or repair mechanism
releases substance that mediate inflammation (Proteases, ROS, NO, Eicosanoids, cytokines)

65
Q

other chronic inflammation cells

A

t lymphocytes will communicate with macrophages in a positive feedback manner
b lsmphctes will become plasma cells

66
Q

what is a granuloma?

A

accumulation of activated macrophages, can be surrounded by lymphocytes or fibrous ring

67
Q

types of granulomaouts inflammation?

A
  1. foring body granuloma
  2. immune granuloma
  3. granulomatous inflammation
68
Q

what causes frogin body granuloma?

A

due to particles that are not easily digestible.

surgical sutures

69
Q

what causes immune granuloma formation?

A

by a immune T cell mediated responds. INF actives macrophages.
example is: TB.

70
Q

what causes granulomatous inflammation?

A

inflammatory reaction with relatively few possible causes:
TB, Leprosy, syphyilis
temporal arteritis, crohns, sarcoidosis

71
Q

process of wound healing.

A

first intention (clean uninfected surgical):
1st step: homeostasis (platelets sonf fibrin)
2nd step: inflammation (neutrophils etc)
3rd step: basal cells mitotic activitiy
4th step: fibroplasia (dermis reconstruction with fibroblasts)
5th step: maturation