Exam 1 (L2): Cancer/Genetics/inflammation

Question 1

neoplasm

Answer 1

-new growth

benign or malignant

Question 2

karkinoma

Answer 2

greek word crab. appendage like projection

Question 3

Cell Cycle

Answer 3

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

Question 4

Cancer cell cycle

Answer 4

No G0
Inactivates G2 (damaged cells ct)

Question 5

Stages of Carcinogenesis

Answer 5

Initiation
Promotion
Progression
Metastasis

Question 6

Initiation (carcinogenesis)

Answer 6

genes are mutated

-spontaneous or by carcinogenic agents (plastic/pollution)

Question 7

promotion (carcinogenesis)

Answer 7

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

Question 8

Progression (carcinogenesis)

Answer 8

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

Question 9

Metastasis (carcinogenesis)

Answer 9

-invasion of other organs (mets)

Question 10

Benign v Malignant categories

Answer 10

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)

Question 11

TNM System: Staging vs Grading

Answer 11

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)

Question 12

Types of cancerous gene mutation

Answer 12

1. Hereditary

2. Sporadic (from carcinogens)

Question 13

Tumor Suppressor Genes

Answer 13

• restrain cell growth (G2)

- can’t destroy/repair mutated genes when defective

Question 14

Oncogene

Answer 14

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

Question 15

Tumor Angiogenesis

Answer 15

Cancer cells secrete VEGF (vasc endothel growth factor)

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

Question 16

Para Neoplastic Syndrome

Answer 16

Unexpected disorder provoked by cancer cells.

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

Question 17

Cachexia

Answer 17

progressive loss of body fat and lean body/apetite

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

Question 18

Lung cancer

Answer 18

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

Question 19

Pathophys of Lung Cancer

Answer 19

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

Question 20

DNA

Answer 20

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

Question 21

Gene

Answer 21

fundamental unit of DNA (in chromosome)

Question 22

Chromosome

Answer 22

threadlike structure of nucleic acids that carry genetic info as genes

Question 23

Mutation

Answer 23

gene is damaged/changed, altering genetic code

-inherited or sporadic

Question 24

Human Karyotype

Answer 24

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

Question 25

Alleles

Answer 25

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

Question 26

Dominant v Recessive

Answer 26

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

Question 27

Genotype v Phenotype

Answer 27

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

Question 28

Carrier

Answer 28

Heterozygous for a recessive trait. Ie sick cell/talacemia

Question 29

Sex Linked inheritance

Answer 29

- 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

Question 30

Familial Cholesterolemia (FH)

Answer 30

-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

Question 31

Atherosclerosis

Answer 31

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

Question 32

Cystic Fibrosis

Answer 32

Lethal inherited disease (common in causasians) - from a defect in cystic fibrosis conductance regulation (CFTR) - affects pancreas/resp system

Question 33

CFTR

Answer 33

regulates flow of ions across epithelial cells--