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272 Pathophysiology > Exam 1 (L2): Cancer/Genetics/inflammation > Flashcards

Exam 1 (L2): Cancer/Genetics/inflammation Flashcards

1
Q

neoplasm

A

-new growth

benign or malignant

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2
Q

karkinoma

A

greek word crab. appendage like projection

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3
Q

Cell Cycle

A 
G0 (rest
G1 (prep-duplicates all)
S (synthesis, DNA rep)
G2 (Check point- looking for damage- repair/apoptosis)
M: (Mitosis: 2 daughter cells)
Cytokinesis: divides cytoplasm
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4
Q

Cancer cell cycle

A 
No G0
Inactivates G2 (damaged cells ct)
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5
Q

Stages of Carcinogenesis

A

Initiation
Promotion
Progression
Metastasis

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6
Q

Initiation (carcinogenesis)

A

genes are mutated

-spontaneous or by carcinogenic agents (plastic/pollution)

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7
Q

promotion (carcinogenesis)

A
  • time for early screening: breast/prostate exams
  • lengthy but reversible here
  • preneoplastic cells (metaplstic) are proliferating
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8
Q

Progression (carcinogenesis)

A
  • btw pre malignant lesions and actual cancer cells
  • rapid inc in size
  • maybe further mutation
  • maybe invade other organs
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9
Q

Metastasis (carcinogenesis)

A

-invasion of other organs (mets)

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10
Q

Benign v Malignant categories

A
  1. Differentiation (B: well diff, M: poorly (anaplasia))
  2. Growth Rate (B: slow/progressive. M: erratic)
  3. Metastasis (M: frequent. cells travel via blood/lymph)
  4. Invasiveness (B: cohesive, M: invasive and infiltrating)
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11
Q

TNM System: Staging vs Grading

A

When growth is considered malignant

Staging:

  • Tumor: Tx-3
  • Nodes (Nx,0,1-3)
  • Metastasized (Mx, M0, M1) can’t be assessed, no, yes

Grading: differentiation

  • well-differentiated (B)
  • moderately (B/M)
  • poorly (M)
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12
Q

Types of cancerous gene mutation

A
  1. Hereditary

2. Sporadic (from carcinogens)

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13
Q

Tumor Suppressor Genes

A
  • restrain cell growth (G2)

- can’t destroy/repair mutated genes when defective

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14
Q

Oncogene

A

Proto-oncogene: stimulates cell movement through cell cycle (G0)
becomes Oncogene: no more G0 (unrestrained growth)

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15
Q

Tumor Angiogenesis

A

Cancer cells secrete VEGF (vasc endothel growth factor)

  • cancer cells get more nutrients
  • starve out other cells
  • -angiogenesis (path)
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16
Q

Para Neoplastic Syndrome

A

Unexpected disorder provoked by cancer cells.

ie. luncg canger inc production ADH
- breast cancer -> hypercalcemia

17
Q

Cachexia

A

progressive loss of body fat and lean body/apetite

  • cytokines released by WBC to fight tumor (breaks down muscle and fats)
  • cancer related
18
Q

Lung cancer

A

-leading cancer related death
Etiology:
-Cigs/asbestos/family history/radon exposure (arsenic/xrays)

19
Q

Pathophys of Lung Cancer

A
  1. toxins paralyze cilia of resp tract
  2. further accum of toxins/carcinogens
  3. Cells undergo change (hyperplasia/metaplasia)
  4. Activation of oncogenes. Deact Tumor suppressors
  5. Uncheck growth
  6. Hemoptysis (coughing blood)- eroded lining of epithelium
  7. Lesion enlarges-> mass-> dyspnea (diff breathing)
  8. Now unable to perform exchange of gas (hypoxia)
  9. Mass to pleural surface-> pleural effusion (fluid)=dyspnea/chest pain
  10. mass=obstruction= high secretions -> pneumonia (lung inflammation)

other: weight loss, fatiguability, mets to bone/brain

20
Q

DNA

A
  • carries genetic info
  • Nucleotides: phosphates, sugar, nitrogen base
  • -sequencing must be perfect
21
Q

Gene

A

fundamental unit of DNA (in chromosome)

22
Q

Chromosome

A

threadlike structure of nucleic acids that carry genetic info as genes

23
Q

Mutation

A

gene is damaged/changed, altering genetic code

-inherited or sporadic

24
Q

Human Karyotype

A

-23 pairs of chroms
- 1=sex
XX-female
XY=male

25
Q

Alleles

A

Ea chromosome in a pair has correponging genes. (alleles)
-can be homo or heterozygous
Hetereozygous: alleles have dif codes
Homosygous: same codes

26
Q

Dominant v Recessive

A

Dominant: visible in heterozygous people
Recessive: does not manifest in the presence of a dominant trait.
–many diseases are recessive (beware inbreeding)

27
Q

Genotype v Phenotype

A

G: technical genetic make
P: How the genetic trait manifests in an individual (what is seen)

28
Q

Carrier

A

Heterozygous for a recessive trait. Ie sick cell/talacemia

29
Q

Sex Linked inheritance

A
  • gene of a particular trait is located on X chromosomes
  • X allele is dominant over Y
  • So many offspring (XY) X allele will always manifest
  • ex) hemophilia/colorblindness
30
Q

Familial Cholesterolemia (FH)

A

-Autosomal dominant disorder
-Absence/dysfunctional LDL (low density lipro) receptor.
What should happen?
1. Hepatocytes take LDL (from food)-> suppress liver synthesis of cholesterol (- feedback)
FH
1. no receptors. So LDL not taken by hepatocytes. So LDL stays in blood. Body thinks it needs synth of LDL/cholesterol-> hepatic synth of LDL NOT suppressed -> make too much cholesterol.
–Result: w/o treatment: widespread atherosclerosis
–Treatment: cholesterol lowering drugs, low fat diet, exercise

31
Q

Atherosclerosis

A

Formation of fatty plaques in blood. (presensts in FH)

32
Q

Cystic Fibrosis

A

Lethal inherited disease (common in causasians)

  • from a defect in cystic fibrosis conductance regulation (CFTR)
  • affects pancreas/resp system
33
Q

CFTR

A

regulates flow of ions across epithelial cells–

272 Pathophysiology (4 decks)

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