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