Endocrine/Nervous Flashcards
Endocrine vs. Exocrine
Ductless, secretes hormone directly into the bloodstream vs. via ducts such as sebaceous glands
Gland
An organ specializing in secretion of substances for further use in the body or excretion of substances for elimination ex. liver excretes bile pigments
Hormone
A chemical produced in one location that exerts its effect in a place far removed form the source ( via the bloodstream )
Steroid Hormones
Water insoluble, diffuse through the membrane and bind to receptors inside the cell, act directly at the level of the nucleus. Ex. androgens (testosterone), estrogen, corticosteroids.
Protein Hormones
Long chain polymers of amino acids, do not enter the cell but rather bind to cell membrane receptors and exert their effect via an intermediary (2nd messenger system) like cyclic AMP. ex. insulin; hypothalamic releasing factors.
Amine Hormones
Small molecules, do not enter the cell but rather bind to cell membrane receptors and exert their effect via an intermediary (2nd messenger system) like cyclic AMP ex. thyroxine, norepinephrine.
What is homeostasis maintained by?
The neuroendocrine control centre which is the hypothalamus by way of its control of the master gland ( pituitary gland.)
ADH
Source: Hypothalamus but stored in the post pit
Target/Action: Collecting ducts in the kidneys retain 30% more water from the filtrate= increase in BP and contraction of arteriolar smooth muscle resulting in vasoconstriction= increase in BP
ADH Patho
- Alcohol depresses ADH production from the hypothalamus and release by the post pit= increased urine volume= dehydration
- ADH deficiency may result in diabetes insipidus
Oxytocin
Source: Hypothalamus but stored in post pit
Target/Action: Promotes contraction of uterine smooth muscles during child birth=parturition and stimulates the mammary glands to letdown milk ( suckling stimulates oxytocin release) Both are positive feedback loops.
HGH
Source: Ant pit but production/release is controlled by hypothalamus’s GHRF and inhibition is controlled by the hypothalamus’s GHIF
Target: All body tissues
Action: Osteoblasts promotes deposition of bone matrix in bone tissue, protein synthesizing tissue (muscles/ tissue repair), carb catabolism (glycogen breakdown into glucose in cells causing blood glucose levels to rise)
HGH Patho
Overproduction/Hyperexcretion: pituitary giantism/acromegaly
Underproduction/Hyposecretion: pituitary dwarfism
Prolactin
Source: Ant pit but release is stimulated by PRH from the hypothalamus
Target: Mammary glands
Action: starts and maintains milk production, suckling stimulates PRH production, positive FBL
TSH
Source: Ant pit but release is controlled by TRF from hypothalamus
Target: Thyroid Gland
Action: Causes the thyroid gland to produce T3 and T4 which together make up thyroid hormone.
TH
Source: Thyroid Gland
Target: Cells
Action: Controls basal metabolic rate or cellular operations rate ( rate of aerobic cellular respiration in mitochondria resulting in things such as growth and heat production)
Thyroid Patho
- Congenital Underproduction: cretinism which is a condition where the nervous system is underdeveloped due to deficiency in thyroid hormones resulting in mental delay
- Adult Underproduction: hypothyroidism which is an autoimmune disease. S/S include: weight gain, water retention, lethargy, hypertension, decrease basal metabolic rate. treated by exogenous thyroxine.
* Goiter: thyroid enlargement usually due to lack of dietary iodine. - Adult Overproduction: hyperthyroidism which is also an autoimmune disease. S/S include: antibodies stimulate thyroid hormone release, exophthalmos or protruding eyes, thin or hyperactive dt increase basal metabolic rate, 40-50 year old females
What other hormone does the thyroid release?
Calcitonin: stimulates osteoblast activity which will overall decrease blood calcium levels
Parathyroid Glands
Parathormone: stimulates osteoclast activity which removes Ca+2 and PO4 from bones resulting in increase in blood calcium levels, also promotes calcium absorption from the small intestine and decreases calcium excretion from kidneys.
Adrenocorticotropic hormone
Source: ant pit but release is controlled by CRF from hypothalamus
Target: Adrenal Cortex
Action: Causes the adrenal cortex to release glucocorticoids, mineralocorticoids and sex hormones (gonadocorticoids) response to long term stress
Glucocorticoids
Ex. cortisol
Mobilize energy stores, protein and fat breakdown, suppress inflammatory reaction, healing and repair.
Mineralocorticosteroids
Ex. Aldosterone
Promotes Na+ retention by kidneys= increase in BP, promotes K+ and H+ secretion at DCT of kidney tubules, for example loss of blood
Sex Hormones
Steroid hormones mostly testosterone
Adrenal Medulla
Not controlled by pituitary but by the nervous system.
Hormones: Norepinephrine and epinephrine
Actions: Fight or flight response, increase in HR BP and resp. rate, bronchiolar dilation (more air in), sweat gland activity (cooling), arrestor pili contraction, pupil dilation, blood shunts from skin and gut to muscles (mobility)
Adrenal Patho
- Overproduction: esp. cortisol results in cushing syndrome S/S: buffalo hump and moon facies
General Adaptation Syndrome (GAS)
The bodies general response to unrelieved stress, cannot be diagnosed.
Three Step Response:
1. Alarm Reaction: mostly adrenal medulla hormones (fight or flight)- epinephrine, but ACTH and thyroid hormones are also released by their glands.
2. Resistance Stage: corticosteroid levels increase to deal with the long term stress
3. Exhaustion Stage: adrenal glands lose ability to cope with stressor causing collapse and death
Normally adrenal hormones feed back to the hypothalamus to inhibit further release once the stressor is relieved (negative feedback). In this case, the stressor is not relieved so the positive feedback occurs preventing normal levels of these hormones and instead relating in more Ne/epinephrine and corticosteroids to be released.
FSH and LH
Sex hormones
Melanocyte Stimulating Hormone (MSH)
From the pars intermedia
Target: Melanocytes in skin epidermis
Action: Promotes normal production of melanin (skin pigment) and acts as a neurotransmitter.
* NOT MELATONIN
Pancreas
Both exocrine and endocrine
Exocrine: acinar cells produce enzymes
Endocrine: Alpha- produces glucagon which breaks down glycogen into glucose in the liver Beta- Produces insulin which synthesizes glycogen from glucose in the liver and also promotes trans membrane movement of glucose into cells and Delta- produces somatostatin (GHIF) All three cell types are found within the islets of langerhans.
Diabetes Mellitus: Type 1 S/S
-Cause is insulin non production or insulin deficiency (Juvenile Onset) Insulin Dependant
S/S:
-Increase in blood glucose levels (hyperglycemia)
-H2O osmotically pulled from tissues
-increase in BP
-Kidneys excrete excess H2O and glucose= sugar in urine and dehydration, also electrolyte imbalances
-Cells become glucose starved therefore fats are used as an energy source=ketone bodys produced resulting in fruity smelling breath, lethargy, weight loss, and blood pH drops.
Long Term Effects of DM 1
- Atherosclerosis: increased fat transport so more fatty deposits in arteries= risk of MI, strokes, and pulmonary embolisms
- Microangiopathy: Blood capillaries become weak
- Ulceration because of poor healing due to poor vascularization and sugary blood results in infection= amputation
- Blindness due to retinal blood vessel breakage
- Glomeruli in kidneys are affected= chronic renal failure
How DM 1 Affects the Nervous System
Peripheral neuropathy: decreased or increased sensitivity to stimuli therefore decreased pain perception
Causes of Type 1 DM
- Genetic Predisposition: Inherited defect of the immune system triggered by an environmental stimulus. There are 18 genes associated with DM 1 production but some people have protector genes that would inhibit them from getting DM 1.
- Viral: Genetic defect in the immune systems on switch. The immune system does not turn on when the virus is present so the virus then attacks the beta cells destroying them.
- Autoimmune: Genetic defect in the immune systems off switch. The immune system turns on to attack the virus but does not turn off when its supposed to so it attacks the beta cells themselves.
DM 1 is and inherited defect of the immune system that interacts with environmental factors
Causes of Type 2 DM
- Genetic Predisposition: The genes that carry this trait are different from the genes that carry DM1
- Environmental Triggers: The genetic predisposition interacts with triggers such as obesity, excess calorie intake or not burning enough calories. This results in resistance to insulin
Major environmental trigger is glucotoxicity because too much glucose may be toxic to beta cells Therefore, if it goes undetected the beta cells become damaged making the body cells less responsive to glucose. = result is resistance to the action of insulin and insulin deficiency.
Treatment DM 1
Insulin injections or use of insulin pump. 10% of all cases
Treatment DM 2
Diet, exersize, oral hypoglycaemic drugs and insulin. 90% of all cases
Myelin
Fatty cell membrane coating of some axons
3 Functions of Myelin
- Insulates and protects the myelinated axons
- Allows for saltatory impulse transmission
- Acts as a tunnel for regeneration (PNS: if severed pieces are close together, CNS: generally produces molecules that inhibit regeneration
Neuroglial Cells: 4Types in CNS
Supporting cells found in CNS
- Astrocytes: star shaped, binding/ spatial organization, reabsorption of K+ and one neurotransmitters, produce scar tissue, part of blood/brain barrier-screens substances moving from blood to brain.
- Microglia: transform into phagocytes
- Oligodendrocytes: produce myelin sheath in CNS not PNS
- Ependymal Cells: Lines CNS cavities (choroid plexuses of brains ventricles) circulates CSF using cilia.
Cells in PNS
- Schwann Cells: Produce myelin sheath
2. Satellite Cells: Function like Astrocytes
Steps in Impulse Transmission Along an Axon
- Nerve cell is at resting potential which is -70mV. This is maintained by Na+/K+ pumps (3 Na out for every 2 K in to counteract the leakage of K+ gates).
- Stimulus opens both Na+ and K+ voltage gated channels. Na+ rapidly diffuses into the cell reducing cell charge difference from -70mV to +30mV= depolarization but only if the threshold potential of -40mV is reached first.
- K+ diffuse out of the nerve cells single gated K+ channels open while Na+ channels become inactivated = repolarization.
- Hyperpolarization occurs when K+ continues to diffuse out while Na+ channels are resetting because the K+ gates are leakier.
- All K and Na channels close
- Refractory period occurs when Na/K pumps re-establish resting potential so that a new impulse can be generated.
- When Na+ channels open they stimulate neighbouring Na+ channels causing impulse transmission
All or None
A neutron either fires completely or not at all. Firing only occurs if the stimulus causes depolarization to the threshold potential (minimum voltage re’q to trigger an action potential)
Saltatory Transmission
The impulse “jumps” from node of ranvier to node of ranvier because it cannot enter the nerve cell through the myelin sheath. -Very fast. De-/Re+ only occur at the nodes where Na+ and K+ gates are exposed.
Electrical Synapses
- Different from chemical synapses due to their cell to cell contact via connexons (b/w glial cells and b/w cardiac cells).
- Connexons are gap junctions that connect adjacent cells via transmembrane proteins to allow ion movement (intercalated discs).
Steps in Nerve Impulse Transmission Across a Synapse
- Action potential arrives at pre-synaptic membrane causing voltage gated Ca+2 channels to open.
- Ca diffuses into the axon bulb
- This causes neurotransmitter containing synaptic vesicles to fuse with the presynaptic membrane
- The neurotransmitter is dumped into the synaptic cleft via exocytosis
- Neurotransmitter diffuses across the synaptic cleft to the postsynaptic membrane
- When enough neurotransmitter molecules bind to specific receptor sites on post synaptic membrane, a new impulse is generated unless threshold potential is not reached.
- Stimulus termination: specific enzymes break down neurotransmitters and the presynaptic membrane reuptakes the