A&PII Exam (Module I)

Lipid Soluble Hormones

STEROID AND THYROID HORMONES: Can pass directly through membrane. Require a transport protein to carry them through circulation. (Ex. Estrogen, Testosterone, T3/T4)

Non-Lipid Soluble Hormone

PROTEIN HORMONES: Cannot pass through cell membrane, not lipid soluble.

Ways GH Promotes Growth

1.) Promote uptake of amino acids (to build proteins)

2.) Promote lipolysis (fat breakdown) for energy

3.) Promote glycogenolysis for energy

GH in Hypoglycemia 

GH will be secreted to increase glycogenolysis in order to release glucose into the blood stream.

GH in Hyperglycemia

Hypothalamus will release Growth Hormone Inhibiting Hormone (GHIH) to stop the secretion of GH. This will inhibit glycogenolysis so that no additional glucose will be released into the blood stream.

Acromegaly

The hypersecretion of GH during ADULTHOOD

Gigantism

The hypersecretion of GH during CHILDHOOD, prior to the epiphyseal plates closing

Diabetes Insipidous Symptoms

Hyposecretion of ADH; frequent urination, thirsty, dehydration, electrolyte loss, body cannot conserve water

Diabetes Mellitus I Symptoms

Beta cells are destroyed = cannot produce insulin, childhood on-set; weight loss, 2/3 P’s, blurred vision, thrush.

Diabetes Mellitus II Symptoms

Insulin Resistance, insulin receptors are altered or cannot receive signal; 3 P’s, weight loss, slowed healing of wounds, genital thrush, lethargic, blurred vision.

Three P’s in Diabetes

Polyuria (urine frequency), Polydipsia (thirst), Polyphagia (hunger cells unable to obtain glucose)

T3/T4 in Basal Metabolic Rate

Increase metabolism by:

1.) Promoting protein synthesis

2.) Increases number of Na/K Pumps, consuming more ATP and heat production = leading to increased body temperature.

3.) Up-regulated the number of beta receptors that bind NE/E which can increase heart rate and blood pressure

4.) Promote catabolism of glucose and fatty acids

Synthesis of T3/T4

Cells trap Iodine from the blood into lumen and begin to make TGB; enzymes within colloid attach iodine to TGB; the follicular parts of the cell (the outer edges) engulf them and fuse them with a lysosome; lysosomal enzymes form T3/T4 and diffuse it into the blood where it forms with TGB

Why does a goiter form?

There is an absence of iodine; the body continues to make enzymes and TGB, but without iodine to form T3/T4, there is no negative feedback to halt the release of TSH. The lumen/colloid continues to grow in size, swelling out into a goiter.

Hypothyroidism Symptoms

Low BMR; myxdema, collection of fluid causing facial swelling.

Hair loss, dry skin, weight gain, constipation, “Brain Fog,” slow heart rate, depression, fatigue, slowed reflexes

Hyperthyroidism Symptoms

High BMR; Graves’ Disease, autoimmune disorder where antibodies mimic TSH, thyroid is being constantly stimulating by mimic and true TSH.

High body temperature (sweaty/flushed), diarrhea, increased HR, weight loss, tired/poor sleep, increased appetite, hyperactive reflexes

Aldosterone Secretion Process

1.) Kidney detects low blood pressure/sodium/volume.

2.) Kidney releases Renin which converts Angiotensinogen into Angiotensin I 

3.) Angiotensin I goes to the lungs where it is converted into Angiotensin II by ACE (angiotensin converting enzyme)

4.) Angiotensin II triggers vasoconstriction to increase blood pressure and travels to the adrenal glands

5.) The outer zone of the adrenal cortex secretes aldosterone in response to Angiotensin II 

6.) Aldosterone tells the kidneys to keep water and water

Cortisol with Stress

Secreted by the middle zone of adrenal cortex in response to the demand for glucose; acts to maintain normal blood glucose levels by stimulating:

• Cells to break down proteins

• Lipolysis (fat break down)

• Amino acids and fats to travel through circulation to the liver to undergo gluconeogenesis (making new glucose) 

Stress Response

PATHWAY ONE (endocrine):

1.) Hypothalamus releases CRH

2.) Ant. Pituitary releases ACTH 

3.) Adrenal Cortex (middle zone) releases cortisol to increase blood glucose and provide anti-inflammatory effects to suppress injury

PATHWAY TWO (nervous):

1.) Hypothalamus triggers SNS (increase glycogenolysis, respiration, heart rate, blood pressure, etc.) 

2.) Adrenal Medulla secretes NE/E to reinforce SNS and cause resistance reaction

Male Sex Determination (XY)

SRY gene on Y chromosome encodes for TDF (testes determining factor); triggers the development of testes —> T —> secondary sex characteristics (puberty)

Female Sex Determination (XX)

Default Pathway: TDF/SRY absent from chromosome; triggers the development of female reproductive structures

Viagra Function

Inhibits erectile enzymes of corpora cavernosa from breaking down the CGMP messengers that trigger vasodilation (lowering of blood pressure/relaxing smooth muscle & arteries); increases blood flow to penis tissue

Genetic Diversity Factors

Crossing over (Prophase I) & independent assortment/alignment (Metaphase I)

Nondisjunction 

Failure of homologous pairs (MI) or sister chromatids (MII) to seperate during meiosis I or meiosis II

Monosomy

Resulting zygote has only one copy of a chromosome, lacking its pair

Trisomy

Zygote has 3 copies of a chromosome instead of 2

Trisomy 21

Down Syndrome; early autosomal have more genes, nondisjunction in later chromosomes are less likely to cause major harm/miscarriage

Turner’s Syndrome (XO)

Lacking a sex chromosome (45 total), presents as female but lacks menstruation and major secondary sex characteristics.

Klinefelter’s Syndrome (XXY)

Has an additional sex chromosome (47 total), presents as male but has less muscle mass/longer limbs, less body hair, smaller testes, and is oft less/sub/infertile

Chorionic Villi Sampling (CVS)

10-13 weeks of gestation; chorion (placenta/fetus cells) is removed and taken for chromosomal abnormalities.

Aminocentesis

14-18 weeks of gestation; amniotic fluid is taken to test cells for chromosomal abnormalities. Drawbacks: could lead to birth defects like spinal bifida (neural tube defect)

Allele

Gene expressed on chromosome

Genotype

Actual genetic make-up

Phenotype

Trait that is actually expressed

Heterozygous 

2 different alleles present in genotype

Homozygous

The same two alleles are present in genotype

Dominant Allele

An allele whose trait always shows up in the organism when the allele is present

Recessive Allele

An allele whose phenotypic effect is not observed when a dominant allele is present

Autosomal Recessive Disorders

Individual must inherit two recessive alleles to be affected (ex. Tay Sachs Disease, nonfunctional alleles are inherited from carrier-parents)

Autosomal Dominant Disorders

Individual must only posses one dominant allele to be affected (ex. Huntington Disease, dominant-carrier parent will put a 50% chance that offspring will inherit disorder)