Section 6 Flashcards
leading cause of death in the US
cardiovascular disease
pancreas exocrine cell
acini cells
secrete pancreatic juice for digestion
pancreas endocrine cells
- alpha cells(20%) produce glucagon
stimulus: low blood sugar
action: stimulates liver to breakdown glycogen and release glucose into the blood - beta cells(75%) produce insulin
stimulus: high blood sugar
action: allows glucose to get into cells, glycogen production in the liver
Diabetes Mellitus Type 1
Cause: autoimmune
Pathology: destruction of beta cells
Result: No or little insulin is produced
Diabetes Mellitus Type 2
Formerly known as adult onset
Pathology: insulin resistance
Result: need more insulin release
Diabetes Mellitus Gestational Diabetes
Insulin resistance during pregnancy
A form of type 2
Goes away after delivery (most of the time)
2-10% of US pregnancies
Type 1 diabetes consequences
Ketone bodies: formed by the liver in times of starvation; used in the brain, heart, and liver
– Consequence: lower pH (they are acidic) metabolic acidosis
Dehydration
– Glucose reabsorption in the kidneys is at capacity – Glucose is lost in urine brings water with it
– Excess urine (polyuria) and excess thirst (polydipsia)
Diabetic coma:
– Loss of consciousness due to
• Hyperventilation: due to acidosis (death in 24-48 hours)
• Very low blood sugar: due to too much insulin (death in 1-2 hours)
• Severe dehydration: due to hyperglycemia
Type1 Diabetes treatment
insulin injections
diet regulation
exercise
Type 2 diabetes risk factors
genetics 15%-60%
physical inactivity
obesity
Type 2 Diabetes disease progression
Cellular response to insulin becomes impaired
– Takes more insulin to get the same amount of glucose out of the blood progressively more and more
– Onset of elevated blood glucose
– Pancreatic beta cells become damaged (worn out)
– Lower insulin production and release
Type 2 diabetes diagnosis
Fasting glucose>126mg/dl or HbA1C>6.5%
Pre-diabetes glucose > 100 or HbA1C 6-6.5%
Insulin resistance was present long before
Type 2 Diabetes consequences
cardiovascular disease
kidney failure
vision problem
type 2 diabetes treatment
diet modification exercise weight loss insulin sensitizing drugs(metformin) insulin injections(later stage)
3 main factors responsible for controlling blood glucose levels
impaired insulin secretion
decreased glucose uptake
increase HGP
cardiovascular disease pathology
atherosclerosis: hardening of arteries, plaque build up causing narrowing, clot formation
first sign of cardiovascular disease
endothelial disfunction
cardiovascular disease risk factors
genetics obesity(especially abdominal) high saturated fat diet physical inactivity diabetes
endothelial cells do what?
line arteries
respond to shear stress and release nitric oxide(NO) into smooth muscle to cause vasodilation
what produces nitric oxide(NO)
eNOS(endothelium derived nitric oxide synthase)
what does nitric oxide(NO) do
Blocks macrophages from entering endothelium
Inhibits platelet aggregation on vessel walls
endothelial dysfunction results from
eNOS producing free radicals or reactive oxygen species instead of functional nitric oxide(NO)
progression of artherosclerosis
- Endothelial dysfunction (low NO release):
– Low NO monocytes start to migrate into vessel wall
2.Immune Activation and Cell Aggregation:
– Macrophages engulf oxidized LDL become foam cells
– T-Cells become activated by macrophages inflammation
– Platelets aggregate on endothelial cells
– Smooth muscle cells migrate to intima layer - Plaque formation:
– Platelets in lumen build up, smooth muscle cells build up form fibrous cap
– Foam cells die create necrotic core - Angiogenesis and plaque rupture
– Plaque builds up it’s own blood supply
– Macrophages release chemicals that weaken plaque
– Plaque ruptures coagulation process blocks blood flow locally or clot dislodges and blocks blood flow where ever it stops - Blocked blood flow causes heart attack or stroke
connections between type 2 diabetes and cardiovascular disease
- High blood glucose leads to glycation (glucose binds to it) of eNOS which leads to more free radical production and endothelial dysfunction
- Insulin signaling in cells normally leads to eNOS activation and formation of NO
• Insulin resistance blocks this mechanism leading to lower NO levels and endothelial dysfunction
gregor mendel
Austrian monk from the mid 1800’s
principle of segregation
During fertilization each parent passes on 1 of their alleles for each trait
ex. punnet square
principle of independent assortment
Each allele is sorted independently of all other alleles
ex. eye color and vision
gamete
sex cells that carry traits (sperm and eggs)
gene
region of a chromosome that determines a particular characteristic or trait
allele
any one of alternative forms of a specified gene (trait)
dominant
an allele that only needs 1 to show its effect
– Denoted by a capital letter
recessive
an allele that needs 2 to show its effect
– Denoted by a lowercase letter
genotype
genetic make up of an individual-which alleles
are present
phenotype
appearance of an individual-how genes are expressed
homozygous
identical alleles for a certain trait
– Can be dominant or recessive
heterozygous
different alleles for a certain trait
codominance
Two different alleles show their effect even if only one copy is present
ex. blood type
incomplete dominance
Heterozygous organisms show a phenotype intermediate between the two alleles
ex. sickle cell anemia
multiple alleles
More than 2 alternative alleles
ex. blood type
polygenic inheritance
Most traits depend on simultaneous inheritance and expression of more than 1 gene.
ex. height, hair color, skin color
dominant-recessive inheritance
dominant: only 1 allele needed to express trait
recessive: 2 alleles are needed to express trait
differences between mitosis and meiosis
mitosis -somatic cells -genetically identical -same number of chromosomes parent vs. daughter -end with 2 diploid cells -purpose: cell growth and repair meiosis -sex cells -not identical -half number of chromosomes parent vs. daughter -end with 4 haploid cells -purpose: reproduction
cell division
interphase -Centrioles replicate -Preparation for mitosis prophase -cell division already duplicated metaphase -chromosomes line up at center of cell anaphase spindles pull chromatids apart telophase -nuclear membrane starts to form
crossing over
Homologous chromosomes paired together
occurs in prophase I
protein synthesis
DNA -> RNA -> Amino Acids -> proteins
– 3 DNA ->3 RNA -> 1 Amino Acid
silent mutation
change in DNA structure -> different RNA -> still codes for the same AA -> protein is the same
ex. CGC -> CGA -> arginine
missense mutation
change in DNA structure -> different RNA -> different AA -> protein is different ex. sickle cell anemia DNA: CTC -> CAC RNA: GAG -> GUG AA: Glutamine -> Valine
nonsense mutation
change in DNA -> change in RNA -> stop codon
ex. blue eyes
mutation causes
– Mistake during DNA replication that was not caught
– UV light
– Radiation
– Chemicals
changes in chromosome number
Down Syndrome(Trisomy 21) -extra copy of chromosome 21 Turner's Syndrome -loss of a sex chromosome -XO female Klinefelter’s syndrome -XXY male
