Summary SCI 225 Pathophysiology - Nightingale College
pathophysiology Midterm study guide.
Monday, February 20, 2023 9:19 AM
Homozygous ✓ the same - BB= homozygous dominant; bb homozygous
recessive Heterozygous ✓ different-Bb -
Phenotype ✓ the expression of the trait (are the eyes blue?)
Genotype✓ exact pairing of the alleles( B =blue eyes b=green eyes)
BB,bb,Bb Alleles ✓
• Recessive
• Dominant
Chromosomal disorders
• Turner syndrome→ 45 chromosomes/ missing sex chromosomes.
• cri-du - chat syndrome:→ 5 chromosomes has a deletion
• Burkitt lymphoma- translocation of chrome 8→ leads to lymph cancer
• Down syndrome- 14/21 translocation = 46 chromosomes.
• Down syndrome trisomy -Chrome 21 non disjunction= 47 chrome.
• Klinefelter syndrome=47 chrome *23 chrome non dis
junction trisomy. Chromosome mutation- duplication, deletion,
inversion, translocation
Genetic disorders can be caused by dominant allies(one parent can pass it) or by recessive alleles ( both
parents must carry it)
• Duchenne muscular dystrophy is X linked recessive - (gene dystrophen abnormality)
• Cystic fibrosis →excessive mucus in the lungs, heterozygote you have to inherit two recessive alleles
• Sickle cell anemia →The gene that codes For hemoglobin (Carrie’s oxygen to the blood) is mutated it is
recessive the makes it difficult for cells to carry oxygen because the cell shape has been affects Can be
a carrier if one patent passes the gene
• Huntington → autosomal dominant,Late onset, degenerative auto.
• Neurofibromatosis-autosomal dominant 50/50 % chance of inheriting genetic mutation (Type 1 and Type
2: cognative and dermatologic)
X linked inheritance- mom =XX ; dad=XY
22 pairs of autosomes (not sex chromosome)
hemophilia, red-green color blindness, congenital night blindness, some high blood pressure genes,
Duchenne muscular dystrophy, and also Fragile X syndrome.
mutation-change in DNA or RNA.
Gene mutations→ substitutions, interaction, deletion. Insertion and deletion are more dangerous =Frame shift mutation →
everything read Afterwards could be affected
translocation,transcription,Translation, gene splicing, Frame shift
mutation.
Necrosis → 6 types
• Fibrinoid necrosis -vessel leaking fibrin, thick pink vessel can be from hypertension or antibody deposition
• Liquidfactive necrosis -usually seen CNS from loss of blood supply. Dead leukocytes , liquify with
enzyme, bacterial infection.
• Fat necrosis white chalk fat deposits calcium, physical damage, pancreatitis enzyme damage.
• Caseous necrosis - macrophages wall off infection, granuloma, TB,
• Coagulative necrosis - ischemic decreased blood flow, dead area retains shape, cell loose nucleons
• Gangrene - black decaying extremity, chronic ischemia, diabetes, dry ischemia and wet infection.
Apoptosis natural cell death RBC live for 120 days for cell
regeneration. Autophagy- recycling cells, the cell eats its own
contents.
Alcohol on the body-
The Immune System:
Inflammatory process- vasodialation, activates clotting, vascular pemeability, mobalize defense cells, kill
pathogen and initiates repair. Inflammatory chemicals dilate blood vessels, which increase blood flow and
enhance the vessel. Anti-inflammatory.
Markers are lipids , (omega 3 fatty acids)
innate- first natural defense to any intruder, kills no matter what pathogen.
• 1st Barriers- Skin, mucosa (GI and GU), stomach acid, lactic acid (vagina), Sweat and tears.
• 2nd barrier- macrophages – white blood cells (pak-man), phagocytosis (eat the pathogens),
cytokines (cause inflammation- messengers)
• Dendrite cells- They antigens to get the specific cell response.
https://www.coursehero.com/file/196264225/pathophysiology-Midterm-study-guide-pdf/
, • Cytokines- the messenger , get the help, monocytes, neutrophils, immune system communication
1. interleukins- protein that regulate immunity and inflammation
2. Interleukins 1- go to the brain, increase temp, giving fever to fight off infection, low appetite to help
redirect energy to fight off infection.
3 . In t e r lu ki n 6 - t el ls t h e l iv e r t o m a k e o p s o n i n s
This stud y so u r c e w a s d o w n lo a d e d b y 1 0 00 0 0 8 6 6 6 0 3 8 2 1 from CourseHero.com on 08-23-2023 06:09:03
GMT -05:00
4. Interlukin 8- gets more neutrophils
https://www.coursehero.com/file/196264225/pathophysiology-Midterm-study-guide-pdf/
pathophysiology Midterm study guide.
Monday, February 20, 2023 9:19 AM
Homozygous ✓ the same - BB= homozygous dominant; bb homozygous
recessive Heterozygous ✓ different-Bb -
Phenotype ✓ the expression of the trait (are the eyes blue?)
Genotype✓ exact pairing of the alleles( B =blue eyes b=green eyes)
BB,bb,Bb Alleles ✓
• Recessive
• Dominant
Chromosomal disorders
• Turner syndrome→ 45 chromosomes/ missing sex chromosomes.
• cri-du - chat syndrome:→ 5 chromosomes has a deletion
• Burkitt lymphoma- translocation of chrome 8→ leads to lymph cancer
• Down syndrome- 14/21 translocation = 46 chromosomes.
• Down syndrome trisomy -Chrome 21 non disjunction= 47 chrome.
• Klinefelter syndrome=47 chrome *23 chrome non dis
junction trisomy. Chromosome mutation- duplication, deletion,
inversion, translocation
Genetic disorders can be caused by dominant allies(one parent can pass it) or by recessive alleles ( both
parents must carry it)
• Duchenne muscular dystrophy is X linked recessive - (gene dystrophen abnormality)
• Cystic fibrosis →excessive mucus in the lungs, heterozygote you have to inherit two recessive alleles
• Sickle cell anemia →The gene that codes For hemoglobin (Carrie’s oxygen to the blood) is mutated it is
recessive the makes it difficult for cells to carry oxygen because the cell shape has been affects Can be
a carrier if one patent passes the gene
• Huntington → autosomal dominant,Late onset, degenerative auto.
• Neurofibromatosis-autosomal dominant 50/50 % chance of inheriting genetic mutation (Type 1 and Type
2: cognative and dermatologic)
X linked inheritance- mom =XX ; dad=XY
22 pairs of autosomes (not sex chromosome)
hemophilia, red-green color blindness, congenital night blindness, some high blood pressure genes,
Duchenne muscular dystrophy, and also Fragile X syndrome.
mutation-change in DNA or RNA.
Gene mutations→ substitutions, interaction, deletion. Insertion and deletion are more dangerous =Frame shift mutation →
everything read Afterwards could be affected
translocation,transcription,Translation, gene splicing, Frame shift
mutation.
Necrosis → 6 types
• Fibrinoid necrosis -vessel leaking fibrin, thick pink vessel can be from hypertension or antibody deposition
• Liquidfactive necrosis -usually seen CNS from loss of blood supply. Dead leukocytes , liquify with
enzyme, bacterial infection.
• Fat necrosis white chalk fat deposits calcium, physical damage, pancreatitis enzyme damage.
• Caseous necrosis - macrophages wall off infection, granuloma, TB,
• Coagulative necrosis - ischemic decreased blood flow, dead area retains shape, cell loose nucleons
• Gangrene - black decaying extremity, chronic ischemia, diabetes, dry ischemia and wet infection.
Apoptosis natural cell death RBC live for 120 days for cell
regeneration. Autophagy- recycling cells, the cell eats its own
contents.
Alcohol on the body-
The Immune System:
Inflammatory process- vasodialation, activates clotting, vascular pemeability, mobalize defense cells, kill
pathogen and initiates repair. Inflammatory chemicals dilate blood vessels, which increase blood flow and
enhance the vessel. Anti-inflammatory.
Markers are lipids , (omega 3 fatty acids)
innate- first natural defense to any intruder, kills no matter what pathogen.
• 1st Barriers- Skin, mucosa (GI and GU), stomach acid, lactic acid (vagina), Sweat and tears.
• 2nd barrier- macrophages – white blood cells (pak-man), phagocytosis (eat the pathogens),
cytokines (cause inflammation- messengers)
• Dendrite cells- They antigens to get the specific cell response.
https://www.coursehero.com/file/196264225/pathophysiology-Midterm-study-guide-pdf/
, • Cytokines- the messenger , get the help, monocytes, neutrophils, immune system communication
1. interleukins- protein that regulate immunity and inflammation
2. Interleukins 1- go to the brain, increase temp, giving fever to fight off infection, low appetite to help
redirect energy to fight off infection.
3 . In t e r lu ki n 6 - t el ls t h e l iv e r t o m a k e o p s o n i n s
This stud y so u r c e w a s d o w n lo a d e d b y 1 0 00 0 0 8 6 6 6 0 3 8 2 1 from CourseHero.com on 08-23-2023 06:09:03
GMT -05:00
4. Interlukin 8- gets more neutrophils
https://www.coursehero.com/file/196264225/pathophysiology-Midterm-study-guide-pdf/
