A&P Exam 4 Flashcards
Pituitary Gland Gross Anatomy
- = pea on stalk (infundibulum)
- 2 Lobes (anterior and posterior)
Anterior Pituitary Lobe
Adenohypophysis
Makes / release 6 hormones
Posterior Pituitary Lobe
-Made of Neurohypothesis infundibulum
-Makes 2 hormones
Posterior Pituitary Hormone Acquisition and release steps
- Gets hormone from hypothalamus
- Cell bodies in nucleus synthesize hormones
- Transported down axon (hypothalamic-hypophyseal tract)
- When N. fires → H releases into posterior capillaries releasing hormone
5.Releases 2 Hormones= Oxytocin and Antidiuretic Hormone
Oxytocin
Produced :
-by hypothalamic paraventricular nuclei & released from posterior pituitary
Releases:
Positive feedback for uterus and cervix
Antidiuretic Hormone
Produced:
-Hypothalamic supraoptic nuclei, released post pituitary
Target:
-Renal CD (principal cells)
Effect:
-Reabsorbs H2O= less urine and increase blood volume
Release:
-Increases blood osmolality
-Drop in blood volume
What does too much antidiuretic hormone do?
Syndrome of Inappropriate ADH Secretion (SIADH):
-Retain Water
-Edema
-increased blood pressure
-Concentrated urine
-Increase in blood osmolality
Negative Feedback Loop:
-Stimulates hypothalamus to make ADH which is released by posterior pituitary
-Causes renal collecting ducts to reabsorb H2O
-Drops blood Osmolality
What does too little antidiuretic hormone do?
Diabetes Insipidus:
-Large amt of dilute urine, Thirst, and dehydration
Alcohol:
-Inhibits inhibits it
Posterior Pituitary Hormone Acquisition and Release
Hypothalamus controls it via hypophyseal portal system (blood vessels):
-Neurons release inhibiting and releasing hormones
-Picked up by primary capillary plexus to hypophyseal portal veins to secondary
capillary plexus to pituitary cells
*Sometimes called master endocrine gland
Growth Hormone
Target:
-Almost all cells
Effect:
-Mobilizes fat as fuel
-Increases size of cells (hypertrophy)
-Spares glucose increasing plasma glucose levels
-Stimulates protein synthesis
-Induce mitosis (long bone growth/ increase muscle mass)
Regulation:
-GHRH →increase Gh
-GHIH→decreases GH
-Highest at night
Too little Growth Hormone
Child→ pituitary dwarfism
4ft , but proportional
Tx= Growth hormone
Too Much Growth Hormone in Children
Gigantism:
-Typically from tumor
Example=
Robert Wadlow
Born 1919
4ft toddler
Died at 22
8ft 11in.
439 lbs.
Too Much Growth Hormone in Adults
-Overgrowth of membranous bone on Skull, face, hands
-Diabetes mellitus
Thyroid Stimulating Hormone
Target:
-Thyroid Gland
-Tropic hormone
Effects:
-Stimulates synthesis and release of Thyroid hormones
-Stimulates development of thyroid gland
Regulation:
-Increases by low thyroid levels and TRH
-Decreases by high Thyroid Hormone
Too Much:
-Hyperthyroidism
Too Little:
-Hypothyroidism
Adrenocorticotropic Hormone
Target:
-Adrenal cortex
Effects:
-Stimulation secretion of corticosteroid hormones
Regulation:
-Increased by stress, fever, drop in glucose levels (tend to be higher in morning)
-Decreases by high levels of corticosteroid hormone
Stops hypothalamus and anterior pituitary gland
Too Much:
-Cushing’s Disease
Too Little:
Rare
Gonadotropin Types
Follicle Stimulating Hormone and luteinizing Hormone
Gonadotropins
Target:
-Gonads
Effect:
-Regulate gonadal function
In Women=Oogenesis(egg production) &
Estrogen and progesterone production
Male=Spermatogenesis & Testes make testosterone
Regulation:
-Gonadal Releasing Hormone increases it
-Estrogen, progesterone, testosterone shuts it off
Too Much:
-Decrease libido
Too little:
-Fail to mature sexually
-Infertility
-amenorrhea
Prolactin
Target:
-Breast
Effects:
-Stimulate milk production
Regulation:
-Prolactin Inhibiting Hormone= dopamine
-Prolactin Releasing Hormone= suckling and estrogen
Too Much:
-Galactorrhea
Too Little:
-Lactation failure
Melanocyte Stimulating Hormone
Target:
-Melanocytes
Effect:
-Increases melanin production
-Sot significant in humans
6 Hormones released by anterior pituitary gland
1.Growth Hormone
2.Thyroid Stimulating Hormone
3. Adrenocortropic Hormone
4.Prolactin
5.Follicle Stimulating Hormone(gonadotropin)
6.Lutenizing Hormone
Hormone Produced by middle pituitary gland
Melanocyte Stimulating Hormone
Hormones produced by thyroid gland
1.Thyroid Hormone
2.Calcitonin
Thyroid Anatomy
- 2 lobes and isthmus
- Largest purely endocrine gland
- Has good blood supply
What does the Thyroid gland arise from in embryology?
endoderm
Histology of Thyroid Gland
- Has spherical follicles full of colloid
- Surrounded by cuboidal follicular cells
- Colloid filled follicles are filled with thyroglobuline and iodine (stores enough thyroid hormone to 2-3 months)
What is thyroid hormone made of?
-Amino acid + Iodine
-Lipid soluble (needs a carrier)
Thyroid Hormone Target
all cells
4 Effects of Thyroid Hormone
1.Stimulates synthesis of enzymes that oxidize glucose
-Increases metabolic rate
2.Regulates growth and development
-Nervous system
-Skeleton
-Reproductive organs
3.Maintains BP by increasing the number of adrenergic receptors
4.Has intracellular receptor
Causes mRNA transcription
How is thyroid hormone regulated?
- Thyroid stimulating hormone releases stored TH and synthesis of New TH
- TSH increases by low levels of thyroid hormone, chronic cold exposure, and
Pregnanacy
How is thyroid hormone synthesized?
1.Follicle cells make thyroglobulin and Iodine and pump it into follicle
2.Iodine attaches to tyrosine on thyroglobulin
3.Follicle cells endocytose thyroglobulin and releases T3 and T4 into blood
4.TH transported by thyroid binding globulin (TBG)(Cells convert T4→T3)
monoiodotyrosine (MIT)
1st iodine onto tyrosine
diodotyrosine (DIT)
2nd iodine onto tyrosine
triiodotyrosine (T3)
1.most active
2.Thyroid hormone
3.3rd iodine onto tyrosine
thyroxine (T4)
1.made most
2.Thyroid hormone
3.4th iodine onto tyrosine
Hypothyroidism Symptoms
-Feel cold, weight gain, decrease metabolic rate, constipated, brain fog, dry eyes
Hypothyroidism In Adults Called
full blown →myxedema
Hypothyroidism In Kids
cretinism →jaundice, poor feeding
Hypothyroidism causes
1.Not enough iodine (can cause goiter)
2.Defective pituitary and thyroid gland
3.Decrease TSH
autoimmune= hashimoto’s
(OVERALL NOT ENOUGH THYROID HORMONE)
Tx Hypothyroidism
give thyroid hormone
Hyperthyroidism Symptoms
increase metabolic rate= increase heat, sweaty, lose weight, nervous
Hyperthyroidism Tx
Surgery to remove
Take radioactive iodine
Hyperthyroidism Causes
- Too much TSH
- Autoimmune= Grave’s Disease
-IgG antibody works against TSH Receptors–>Caucasus goiter and bulging eyes (exophthalmos)
Calcitonin
-Polypeptide
-Produced by: Parafollicular cells of the thyroid gland
-Target: Bones
Effect:
1. Stimulates uptake of calcium in bone and drop calcium levels in the blood
2. Stimulate Osteoclast activity=Increases bone density
Release: High calcium= store calcitonin
How many parathyroid glands are there?
4
Parathyroid Hormone
Target: Bones and kidney
Effect:
1.Stimulates osteoclasts(digest bone and releases calcium into blood)
2.Kidney=Reabsorb calcium from the filtrate
3.Activate vitamin D = calcitriol (causes increase calcium absorption from the gut)
Release: Decrease in blood calcium= release
Hypoparathyroidism
- too little parathyroid hormone
-Can cause hypocalcemia
-Occurs when gland is removed
-Excites neurons=Twitches, tetany, and seizures
( b/c increase resting membrane potential= easy to
depolarize)
Hyperparathyroidism
-Too much parathyroid hormone
-Can cause hypercalcemia
-Caused by:
1.Increase parathyroid hormone from gland or is ectopic
2.Lack of vit min D
3.Renal failure
Causes:
1.Leaches calcium from bones
2.Leads to fractures
3. Depresses neurons
4. Decrease reflexes
5.Weakness
(b/c membrane is hyperpolarized= harder to depolarize)
Causes Kidney Stones
Lipid Soluble Hormones (steroids)
Made from cholesterol
Made by gonads and adrenal
Can go through the pa=lasma membrane
Made to order
Long-half life in blood (days)
Need to be metabolized by the liver
Amino acid Based aka proteinaceous Hormones
Can’t cross plasma membrane
Can be stored in gland
Most hormones
Aka proteinaceous
Bits od peptide or protein
Modified amino acids→ thyroid, epinephrine, or norepinephrine
Short hald life in blood (mins)–> removed by the kidneys
How do proteinaceous hormones act?
Water soluble
Do not need a carrier
Bind to plasma membrane receptors= G protein coupled receptors which
activate 2nd messenger (cAMP)–>trigger a preprogrammed response in cell
How do fat soluble hormones act?
Need a carrier in blood
Bind to intracellular receptor
Directly activate genes
3 stimuli that control the release of hormones
1.Humoral
2.Hormonal
3.Neural
Humoral Stimulation
Ions= K and Ca
Nutrients= Glucose, amino acides
Neural Stimulation
SNS→ adrenal medulla→epi and norepinephrine
Hormonal Stimulation
Tropic hormones cause hormone release
Glands may respond to mmore than 1 hormone
Describe the different ways a hormone will interact with its target cell
- Cells need a receptor for the hormones to be able to respond to it
Hormones bind and turns on preprogrammed response - Response also depends on:
-Blood leveol hormone
-# of receptors on target cells
-Affinity of receptors for hormone
3.Target cell can change # of receptors
How hormones interact with the same target cell
Permissiveness
Synergism
Antagonism
Permissiveness
A Must be there for B to have effect
Synergism
A same effect
B has same effect
A+B increases effects
Antagonism
A opposes the effects of B
Right shift in Curve=
-Increase saturation of oxygen
-Weakens Hb and O2 bond which decreases affinity (bohr Effect)
Bohr Effect
Lower pH & increase Co2= more O2 release
External respiration
-co2 in blood→air
-deoxyhemoglobin(O2=40and CO2=45 and gets swapped) encounters
-pulmonary gas exchange and becomes oxyhemoglobin (O2=100 and CO2=40)
-driven by pressure
Internal respiration
-gas exchange that occurs with tissues
-blood has O2=100 and CO2=40 and tissue has O2-40 and CO2=45
-O2 enters and Co2 leaves tissue
What Decreases Hemoglobin saturation?
Greater temp
Lower pH
Greater Co2
What increases Hb saturation?
-Less temp
-Lower pH
-Lower CO2
-Metabolically active tissue
What happens during quiet inspiration?
Inspiration → enlarge thoracic cavity
Decreases pressure (less than atmospheric) → air moves in
Muscle:
Flattens diarphragm= increase height of the thoracic cavity
External intercoatals= lift ribs and sternum= greater diameter by a few m
Decreases pressure by 1mmHg=500ml
What happens in deep inspiration?
Mucles:
Accessory muscles →scalenes, …→ scalenes erect spine
Expiration
Muscles engaged in inspiration relax= causes passive recoil
Decreases thoracic cavity volume→ decreases volume→ increase pressure by 1mmHg
Forced Expiration
Oblique and transverse abs
Force abdominal organs against the diaphragm
Internal Intercostals
Depress rib cage further
Both of these decrease thoracic volume which increases pulmonary pressure
Adrenal Gland Anatomy
-Above kidneys
-Cushioned by fat and fibrous capsule
-2 glands:
1.Medulla
2.Cortex
Medulla (ectoderm) of the Adrenal Gland Anatomy
-knot of nervous tissue
-Part of SNS
Cortex (mesoderm) of the Adrenal Gland Anatomy
-True gland makes> 30 corticosteroids from cholesterol
-Lipid Soluble Hormones
-Made to order/not stored
-Need carrier in blood
-Use intracellular receptors/modify gene expression
Adrenal Gland Layers out to in (histology)
1.Zona Glomerulosa
2.Zona Fasciculata
3.Zona Reticularis
Zona Glomerulosa details
Mineralocorticoids
Determines mineral and water balance
Zona Fasciculata Details
Glucocorticoids
metabolism
Zona Reticularis (details)
Gonadocorticoids
Sex hormones
Mineralocorticoids
-95% are aldosterone
-produced= zona glomerulosa of adrenal cortex
-Target=kidney (distal convoluted tubule and collecting duct)
-Effect:
-Effect BP and B volume
-Stimulate production of sodium potassium pumps in the distal convoluted tubule
-reabsorption of sodium in exchange for K
-H2O follows Na
Too Much Mineralocorticoids
-aka Aldosronism
-Caused by adrenal tumor= retain water
-Edema
-Hypertension (BP increase)
-Low potassium
Too Little Mineralocorticoids
-aka Addison’s Disease
-Decrease BP and increase K
How are Mineralocorticoids Regulated
-RAAS
-has 4 paths
RAAS Path 1
- Drop in BP and volume (AKA SNS)
- Causes granular cells to release renin
- Converts angiotensinogen to angiotensin 1
- Angiotensin 1 becomes 2 by the angiotensin converting enzyme (ACE) in the lungs
- Angiotensinogen 2
Causes:
-Thirst
-ADH release
-Vasoconstriction
-Aldosterone release:
1.Increase the amount of potassium in the urine
2.Decrease the amount of sodium and water in urine
3.Increases blood volume
RAAS Path 2
Increase plasma potassium= increase aldosterone
RAAS Path 3
Increase in ACTH = increase BP and B vol
RAAS Path 4
ANP:
1.Stretch of heart increases ANP
2. Increased ANP blocks release of renin and aldosterone
3. Causes lose of water and salt and increase urine and decreas
Glucocorticoids Production, Target, and Effects
-Essential to life
Produced:
-Zona fasciculata of adrenal cortex
Target:
-Most cells
Effect:
-Maintains blood glucose levels
Glucogenesis
-Breakdown fats to glycerol and fatty acids for fuel
-Breaks down proteins to amino acids for fuel repair
-Resist stressors and depress inflammatory
-In excess = decrease inflammation and immune response
Maintains BP w/ SNS
Glucocorticoids Regulation
-Increase Stress
-Higher in the morning
-Stress is positively stimulating hypothalamus
-Hypothalamus with CRH stimulates anterior pituitary gland which causes the release of ACTH stimulating the adrenal cortex
-Adrenal cortex releases cortisol suppressing stress, hypothalamus, and anterio
Too Little Glucocorticoids
- aka Addison’s Disease
-Decrease ACTH
-Autoimmune disorder
-Destroys glands decrease production of glucocorticoids and mineralocorticoid
-Symptoms:
Decrease weight
Drop in sodium
Decrease glucose
Increase potassium
Decrease BP leading to dehydration and eventually death
Too Much Glucocorticoids
-aka Cushing’s syndrome
-Caused by to much ACTH Secretion
-Caused by tumor or adrenal damage
Symptoms:
Increase glucose= steroid diabetes
Loss of muscle mass and bone density=weakness, prone to fracture
Retain water and salt= increase BP and edema
Redistributes fat= moon face, buffalo hump
Increase in the number if infections
Gonadocorticoids
-Weak androgen
-Produced by zona reticularis and adrenal cortex
-Target= many cells
-Effect:
-Tissue converts to testosterone or estrogen
-Axillary and pubic hair growth
Too Much:
-Masculinization
-female= beard, male hair patterns
-Male= beard, sex drive
Too Little:
-unknown
Catecholamines
….
Adrenal Medulla
-Short term stress response= fight or flight
-Modified ganglionic sympathetic neurons
-hormones= catecholamines
-80% Epinephrine & 20% Norepinephrine
Adrenal Medulla Too Much and Too Little
- Too Little= no problem
- Too Much
-Tumor=pheochromocytoma
-Symptoms:
Uncontrolled sympathetic activity
Targets and Effects of the Adrenal Medulla
-Mimics SNS
1. Heart:
-Increased HR, Force, & BP
-Beta 1
2. Blood Vessels
-Constrict & Increase BP
-alpha1
3. Lungs
-Dilate bronchioles
- Beta 2
4. Liver
-Increase Blood glucose
-Beta 2
Pineal Gland
-Root of 3rd ventricle of diencephalon
-Melatonin effect= regulates sleep and wake cycle
Pancreas Anatomy
-Mixed gland
1. exocrine= acinar cells (digestive enzymes), dects (bicarbonat eand water)
2. Endocrine (pancreatic Islets)
Cells sense glucose levels in the blood
3. Alpha cells make glucagon and increase blood glucose
4. Beta cells make insulin to drop blood glucose
-arises from gut endoderm
Glucose Metabolism in Pancrease
-Burns glucose to make ATP
-Can convert glucose to fat and amino acids or glycogen (glycogenesis)
-Can make glucose from glycogen, lactose, or amino acids= glucogenesis
glycogenolysis
Glycogen → glucose
glycogenesis
Glucose→glycogen
gluconeogenesis
Pyruvic acid→glucose
glycolysis
-Glucose→pyruvic acid
-Pyruvic acid makes lactic acid and acetylCoa and water
-These release water, CO2, heat ATp, and Ketones
Lipogenesis
Glycerol +3 fatty acids –>Tryglicerides
Lipolysis
-Triglycerides → Glycerol + 3 Fatty Acids
-Fatty acids can become acetyl COa and O2 via beta oxidation
Protein can become what
amino acids and vice versa
Amino acids become what
NH3 and Keto acids and vice versa
Keto acids can become what
glucose and vice versa
Glucagon Production, Target, and Effect
- Produced: by alpha cells of pancreatic Islets
- Target (hepatocytes
- Effect:
1 molecule release 1000,000,000 glucose molecules form liver
Increase blood glucose by:
Breaking down glycogen to glucose (glycogenolysis)
Making glucose from non carbs= gluconeogenesis
glucagon release
-Decrease blood glucose, Increse SNS, and Increase amino acids
-Increases glucagon
-Increase blood glucose, growth hormone, and insulin
Decrease glucagon
Insulin Production, Target, effects
- Produced by Beta cells of pancreatic islets
- Target=Many body cells
- Effects
A. Decrease Blood glucose by
Enhancing membrane transport of glucose into muscles and fat cells
(liver , kidney, and brain cells don’t need insulin to get glucose)
-Inhibits glycogenolysis→ stimulates glycogenesis
-Inhibits gluconeogenesis→stimulates lipogenesis
-Inhibits protein breakdown→stimulates protein synthesis
B. Increase oxidation of glucose by glycolysis= ATP
Too Low Glucagon
low blood glucose
Too Much Glucagon
high blood glucose
How is Insulin Released
-Increase Blood glucose and PSNS= increase insulin
-Decrease blood glucose, SNS, growth hormone & Increase glucagon= decrease
insulin
Too Low Insulin
Diabetes Mellitus
- is low and BG high, but cells can’t use BG
1. Causes
A. SNS stimulation
-Increase glucagon–>Increase glugogenesis, Lypolysis, and glycogenolysis
B. Breaks down fat
-Too much fat in blood= heart disease
-ketones= acid/ decrease pH= ketoacidosis
C. BV’s damaged
-By osmotic effects of glucose in -blood→hands and feet
Symptoms of Diabetes Mellilitus
-Excessive hunger=polyphagia
-Pee a Lot=Polyuria
-Glucose in urine is osmotic, so it pulls water into urine
function as a diretic →dehydration→polydipsia
(always thirsty so drink a lot)
Too Much Insulin
-decreases Blood Glucose
Gonads Release What?
-Release estrogen, progesterone, and testosterone
Placenta Releases What?
-Human gonadotropic hormone, progesterone, and estrogen
Adipose Tissue Releases What?
-Leptin
-Caused from increase fat
-Decreases appetite
What do the GI Tract Enteroendocrine Cells Release?
Gastrin, secretin, Cholecystokinin
What does the skin help release?
Sun + cholesterol= cholecalciferol activated by kidney to calcitriol
What do Kidneys release?
Erythropoietin, renin
What does the thymus release?
Hormones for T cell development, thymopoietin, and thymosin
What are the 4 roles of the reproductive system?
1.Form Gametes: ova and sperm
2.Bring male and female gametes together= intercourse
3.Combine Gamet DNA= fertilization of zygote
4.Support New Life=gestation of embryo to fetus; parturition of baby
Sister chromatids
=identical part of the chromosome
Centromere
the points where two chromatids touch
Somatic Cells
Diploid: 2n = 23 pairs of homologous chromosomes
One from mom, one from dad
Carry genes for same traits
22 autosomes and 1 pair of sex chromosomes
Gametes:
Haploid: n = 23 chromosomes
Primary Reproductive organs
Gonads=Testis and Ovaries
Primary Reproductive organ Functions
-Produce gamets via Meiosis
-Make sex hormones
Female=estrogen and progesterone, males: testosterone
-Cause growth and development of reproductive organs and other organs/accesory reproductive organs
Accessory reproductive organs
-ducts, glands, external genitalia
estes
Main Male Glands
-Seminal Vesicle
-prostate
-Bulbourethral Gland
Seminal Vesicle
-60% of the semen
Yellow, viscous, alkaline, fructose
Prostate
-30% of the Semen
-Milky, acidic fluid
Bulbourethral Gland
-Thin clear mucous that lubricates penis with ejaculation
Penis Parts
-Root
-Body
-Glans
Scrotum Muscles
-has septum
-cremaster muscle
-Dartos muscle
Cremaster muscle
→ covers spermatic cord and testes
-Temperature control
-Pulls toward body when cold
Dartos Muscle
-Attaches to the fascia of scrotum skin
-Adjusts temperature
-Wrinkles
Testes
-Make testosterone
-Make sperm and fluid in seminiferous tubules
-Parts:
1.Ductus Epididymis
2.Ductus Deference
3.Spermatic Chord
Ducts Epididymis
Sperm matures and is stored
Ductus Deference
Uses peristalsis→ moves sperm out through ejaculatory duct and urethra (prostatic→ membranous→spongy)
Spermatic Chord
Inguinal canal → ductus deference→ Testicular artery→pampiniform plexus→vein
For temp regulation of
Diploid
22 pairs of autosomes
1 pair sec chromosomes
xx=female
xy=male
Gene
DNA that codes for one protein
Locus
Location of gene on chromosomes
Alleles
Different forms of the same gene
Homozygous Dominant or recessive
BB,bb
Heterozygous
Bb
Dominant
suppressive allele
Types of Traits that are dominant
Widows peaks
Dwarfism
Dimples
Freckles
astigmatism
Recessive
Repressed Allele
Types of Traits That are Recessive
Normal vision
Albinism
Cystic fibrosis
Genotype
gene= Bb, BB
Phenotype
Physical expression of genes
Independent assortment
2^n=2^23=8.5millin variations of genetic material
Variation in tetrad genetic information
Crossing over=Chromosomes exchange gene segments
-Random Fertilization
-Results=72 trillion different zygote, possible
Pattern of Inheritance
-Dominant-Recessive Inheritance
-Dominants will mask recessive
Codominance
-Both alleles are expressed
-ABO blood type=AB blood(both dominant), O recessive
Sex Linked
-X linked
-X has 25000+ genes essential to life
-Females= one x is inactive
-Barr Body
-Y has 78 genes, only 5 % are not sex related
-Traits are x linked
-Always expressed in males
-Passes mother to son
Ovary
-Follicles house oocytes
-Ligaments that attach to it
-Ovarian Ligaments= suspensory and mesovarium
-Covered by tunica albuginea
-Egg rips out of ovary (ouchy)
Cortex of Ovary
Games
Medulla of Ovary
-BVs and Nerves
Uterine Tube
-Goes from Ovary to infundibulum, ampulla, isthmus
-Smooth muscle supported by mesosalpinx
Uterus
Egg enters
Supported by cardinal, uterosacral, and round ligament
Broad Ligament:
-Mesouarium
-Mesosalpinx
-Mesometrium
Parts of Uterus from top to bottom
Fundus, body, cervix
Wall 3 layers out to in
-Perimetrium
-Myometrium (Smooth muscle)(Contracts in labor)
-Endometrium (Lines cavity)
2 layers of Endometrium
- Functional layer (Changes cyclically)(Is shed)
- Basal Layer(Stays during period)(Forms new functional layer)
Cervix
-below uteris
-secretes mucosa
-Top-internal Oz
-bottom= external oz
Vagina
-Thin walled tube below cervix
-Receives penis during sex and is a passage way for the baby to come out
Wall of Vagina in to out
-Mucosal
-Smooth Muscle=Musculans
-Adventitia
Vulva
-Mons pubis= fatty area covered with pubic hair
-Labia majora and labia minora
-Skin folds that protect vestibule
Vestibule
-Urethral opening= pee only
-Vaginal Opening
-Vestibular Glands
-Lubricate
Clitoris
Richly innervated, swells when stimulated
More nerve endings than penis
Clitoris
-Richly innervated, swells when stimulated
-More nerve endings than penis
5th week
Mesoderm–>gonadal ridges
Gonads→ cortex and medulla
Cortex→ ovary
Medullar→ testes
6th weeks
Mesonephric duct forms
Paramesonephric duct forms
7th Week
-XY makes testosterone (⅔ of level of teens)
-Paramesonephric duct→degenerates
-Seminephric tubules join -mesonephric duct→ ductus deferens, epididymis
8th week
-XX
-Mesonephric duct degenrates
-Paramesonephric duct→uterine tubes, uterus, and vagina
1. Genital tubercle
-Clitoris in female
-Penis in males
2.Genital groove
-Vestibule in females
3.Urethral folds
-Labia minora females
-Fuse into vental penis= males
4.Labial scrotal swelling
-Labia majora in females
-Scrotum in males
7th month
-Gonads are tethered to labial-scrotal swelling by gubernaculum stop growing and becomes fibrous
-As body grows→ gonads are pulled into pelvis
-Takes BVs and nerves with them
-Males=Testes will descend through the inguinal canal into the scrotum
-Takes some of the parietal peritoneum with it and forms tunica vaginalis
-Females=Ovaries descend→ stopped by broad ligament
-Gubernaculum divides in to ovarian ligament and round ligament
Describe Steps of Male Sexual Response
1.Erection
2.Ejaculation
3.Resolution
4.Final Neural Transmitter Response
Erection
-From Tactile stimulation or erotic sights, sounds, or smells causes erection
-Goes from CNS→PSNS
PSNS Reflex
-How:
Nitrous Oxide is Released →dilates arterioles→ engorges corpora cavernosa
Expansion of the corpora cavernosa compresses venous drainage
The bulbo urethral gland →lubricates penis
Ejaculation
=Propulsion of semen
-SNS spinal reflex to erection
How:
1.Bladder constricts
2.No urine goes out and no semen goes into bladder
3.Reproductive ducts and accessory glands contract
4.Semen in urethra and initiates spinal reflex→bulbospongiosus contracts and propels semen (500cm/sec aka 11mph=orgasim (intense pleasure)
Resolution
-Skeletal muscles relax
-SNS constrict arterioles feeding penis= flaccid
-refractory period=unable to achieve another orgasm (can be minutes to hours
Final Neural Transmitter Response
-Dopamine levels increase during sex
-Rewards certain behaviors
-Promotes Bonding b/w male and female
-Causes synapses in the brain to remodel so easier to have sex= good in marriage
Spermatogenesis
-Make the male gamete (sperm)
-Make 90 million sperm per day
-Body cells= 46 diploid
-haploid=23
Cells Involved in Spermatogenesis
- Basal Lamina
- Myoid Cells
- Interstitial endocrine Cells
- Sustenocytes
What Occurs in basal Lamina of Sperm Production?
-spermatogonium=sperm stem cell
Reproducing via mitosis:
1. Daughter “A” stays
2. Daughter “B” is primary spermatocyte Undergoes meiosis 1
3.Causes independent assortment
Crossing over= chiasmata
4.Forms secondary spermatocytes
5.Secondary Spermatocytes undergo Meiosis 2
6. Result = spermatids
Early spermatids can’t swim, so they are infertile
Myoid cells
Move sperm and fluid
3-5 layers
Interstitial Endocrine cells
Above myoid cells
Make testosterone
Sustenocyte (sertoli)
-produce / secrete testicular fluid
-Regulate spermatogenesis
-Phagocytize faulty sperm and excess cytoplasm
-Forms blood testis barrier=tight junctions
-Protects sperm from male immune system
b/c sperm produced at puberty)
Sperm Components
1.head
2.Mid piece
3.Tail
Sperm Tail
Flagellum
4mm/min
Sperm Mid-piece
Metabolic area
Has mitochondria
Burns fructose
Sperm Head
Has nucleus
Has acrosome
Lysosome that contains proteases that penetrate the egg
Hormone Effects of male Puberty
-Decrease sensitivity of hypothalamus to the se hormones
-This increases gondal hormones and testosterone
-Causes spermatogenesis and follicle stimulating hormone
Anabolic effects of Puberty
Reproductive organs grow 8-14yrs old
Hair in axilla, groin, face, body
Deeper voice=larynx enlarges
Skin thickens= more acne prone
Bone growth and density
Estrogen closes epiphyseal plate @ 19-21
Increase in muscle mass
Increase in basal metabolic rate
Shapes brain= arousal, sex drive
Describe how male sex hormones are released
Hypothalamus
1. Releases Gonadal Releasing Hormone Via Portal blood
2. Anterior Pituitary release FSH and LH
3. Gonads release estrogen, progesterone, Testosterone affecting Target cells
4.Estrogen, Progesterone, and Testosterone inhibit previous responses
What are hormones like before puberty in males
-Sex hormone is low
-Gonadal Releasing Hormone is Suppressed
Oogenesis and follicle development before birth
-oogonia= stem cells go through mitosis
Oogenesis and follicle development at birth
Primary oocytes–>Start meiosis and Stop at prophase 1
2 million at birth, release 500
With age, not stable
Puberty # of oocytes
-400,000 oocytes left
Cycle oogenesis and follicle development
-Secondary Oocytes + 1st polar body
-Arrests in metaphase 2
-Ovulation
-Sperm Penetrates
-Completes Meiosis 2
Main Stages of follicle development
1.Primordial Follicle
2.Primary Follicle
3.Secondary Follicle
4.Vesicular Follicle
5.Vesicular Follicle
Primordial Follicle
-Meiosis 1= suspended in prophase
-Has layer of simple squamous granular cells
-primary oocyte in the center
Primary Follicle
Stimulated by local chemicals to develop–>Granulosa Cells → cuboidal and multiply
-Layer around oocyte is formed= Zona Pellucida (glycoprotein membrane) that enables fertilization
Secondary Follicle
-Stratified layer of granulosa cells
-Make progesterone
-Convert androgen into progesterone
-Outhecal cells make andogens
Vesicular Follicles (Tertiary)
-Stimulated by FSH
-Fluid filled antrum
-2.5 cm bulge off of ovary
-Corona Radiata=Granular cells around oocyte persist
-Cumulus Ouphorus=Connects egg to wall
Ovulation is when you make what?
secondary oocyte
What occurs if oocyte is not fertilized in Ovulation
-Lost during menstrual cycle
-Corpus luteum= space after oocyte rips out
-Degenerates in 10 days
-b/cms scarred corpus albicans
What occurs if oocyte is fertilized in ovulation?
-Complete meiosis 2
-Corpus luteum persists until placenta grows and develops to take over hormone duties
-Implants at day 20 HCG= human chorionic gonadotropin
-Corpus lutenum of pregnant= grows 3x before placenta takes over
Phases of Ovarian Cycle
1.Follicular Phase
2.Ovulation Phase
3.Luteal Phase
Follicular Phase (Days 1-14)
-Vesicular follicles make estrogen
-One follicle stimulated each cycle to ovulate (most FSH sensitive)
-LH surge→meiosis1→ inflammation, weakens ovary
Ovulation
Luteal Phase
-corpusluteum forms
-progesterone is high=makes andometrium more excepting of blastocyte
-However homone released by corpus luteum suppresses FSH and LH, so it slowly dies
Uterine Phases
1.Menstrual Phase
2.Proliferative Phase
3.secretory phase
Menstrual Phase
-days1-4
-Drop in progesterone → targets arteries (spasms= pain and blood gushes out)
-Lose 20-80 ml
Proliferative Phase
-days 5-14
-Increase in estrogen= stops bleeding
-Functional layer regenerates
Secretory Phase
Day 15-28
Progesterone prepares the breasts and endometrium for implantation
What happens to ovaries in childhood before puberty
-ovaries grow because of the small amount of estrogen
What happens in female puberty?
-ages 8-13
-Hypothalamus decreases in sensitivity
(Women need fat and leptin to go into puberty)
Gonadal relaeasing Hormone increases→ increases in FSH and LH→ increases estrogen
What does the increase luteinizing hormone do in puberty?
increase in progesterone preps breasts for lactation and uteri
What does Estrogen stimulation do in female puberty?
Oogenesis and follicle growth
Development of uterus, tubes, and vagina
Breast development
Growth spurt (testosterone from theca)
Increase bone length and mass
Closes epiphyseal plate
Contributes to wider pelvic
Extra fat is given to breasts and thighs
Details about adult ovulation
Arousal in female sexual response
-PSNS
-By touch, psychological stimuli
-Structures engorge with blood: clitoris, vaginal mucosa, labia, breasts
-Secretion from vestibular glands and vaginal wall= lubrication for penis
Orgasms in female sex response
-SNS response
-Increase in muscle tension, heart rate, and blood pressure
-Rhythmic contractions of the uterus and pelvic floor muscles
-Refractory Period= None
Mechanical Methods of Birth Control
1.Abstinence=0%, avoid STI’s
2.Withdrawal=30%, cost lots of control
3.Douching= worthless=>40% failure rate
4.Unprotected=85%
Main Mechanisms of Birth Control
- Preventing development and release of oocyte
- Prevent Union of sperm and secondary oocyte
- Alter likelihood of implantation and growth
Combination pill
Pill, ring, or patch
Prevent development and release of oocyt
Suppress ovulation
Inhibits hypothalamus’ gonadal releasing hormone
Thickens cervical mucus
FR= 0.3-8%
Progesterone Only (mini pill, shot, implant)
Suppress luteinizing hormone
Thin endometrium of uterus
FR=0.5%
IUD
Prevents fertilization, but person will still ovulate
FR=0.1-2%
Mirena Implant
Progesterone only
Irregular or absent menses
Paragard
Copper
Toxic to sperm and egg
Nonhormonal
Thins endometrial lining
Thickens cervical mucus
Inhibits sperm function, transport, and fertilization
Tubal Ligation
Prevent egg and sperm from uniting
Failure rate= 0.5%
Spermicides
Cream, gell, foam, film, ect.
5-25% failure rate
Prevent egg and sperm from coming together
Vasectomy
O.01%
Prevent egg and sperm from meeting
Condoms
Prevent against sexual transmitted infection
2-15% for males
20% for females
Diaphragm
20%
Prevent union of egg and sperm
Cervical Cap
20-40% failure
Prevent union of egg and sperm
