Exam II material Flashcards
The endocrine system provides ______ of many tissues
Broadcast regulation
The specificity of the endocrine system is due to:
Receptors
Compared to the nervous system, the responses of the endocrine system are:
Slower but longer lasting
Where does the endocrine system release hormones into?
The blood
List the three functions of hormones:
- Maintenance of Homeostasis
- Growth & Differentiation
- Reproduction
Endocrine organs can be divided into what two categories:
- Major endocrine glands
- Organs containing endocrine cells
Primary function is to make a hormone & release it when the stimuli for release are present:
Major endocrine gland
Organs that happen to have endocrine cells within them, allowing them to release a hormone although their primary function is NOT endocrine regulation:
Organs containing endocrine cells
List the specialized endocrine glands (Major endocrine glands)
- Parathyroid gland
- Thyroid gland
- Pituitary gland
- Adrenal gland
- Pineal gland
List some organs that contain endocrine cells, but their primary function is NOT endocrine regulation:
- Hypothalamus
- Skin
- Adipose tissue
- Thymus
- Heart
- Liver
- Stomach
- Pancreas
- Small intestine
- Kidneys
- Gonads
A hormone that causes secretion of a hormone by an endocrine gland
Tropic hormone
How do we classify hormones?
Based on their strucutre
What are the three classifications of hormones?
- Proteins & polypeptides
- Steroids
- Tyrosine derivatives
Describe the time period in which protein/polypeptide hormones are made and released:
Made in advance & stored in vesicles until signaled for release
Protein/polypeptide hormones are synthesized first as:
Preprohormones
The preprohormone will be converted into a:
Prohormone
In protein/polypeptide hormones, what is packed into vesicles in the endocrine cell prior to secretion?
Prohormone
After the prohormone is cleaved, it is now:
Active hormone
The pneumonic for protein/polypeptide hormones:
Protein/Polypeptide = Pre & Pro hormone (all begin with Ps)
In addition to the active hormone, what is released when the prohormone is cleaved?
Inactive fragments
What is the first thing to be cleaved from preproinsulin?
Signal peptide
After the signal peptide is cleaved from preproinsulin what occurs?
Protein folding
Following cleavage of the signal peptide from preproinsulin & protein folding, what results:
Proinsulin
Proinsulin is stored in:
Vesicles
Upon receiving a signal for release into the bloodstream, what is cleaved from proinsulin to convert it to active insulin?
C-peptide
Along with insulin release into the bloodstream, what is also released?
C-peptide
If you wanted to measure someones baseline endogenous production & release of insulin you could measure the:
C-peptide levels in the bloodstream
Protein & polypeptide hormones are often made as an:
Inactive precursor
The inactive precursor of protein & polypeptide hormones:
Preprohormone
What does the signal peptide in insulin serve as?
A marker that tells the cell that insulin needs to undergo exocytosis
Where are the receptors located for protein/polypeptide hormones?
In the plasma membrane
Describe the time period in which steroid hormones are made & released:
Made & released on demand
Where are the receptors located for steroid hormones?
Located inside the cell
Why are steroid hormone receptors located inside the cell?
Because steroid hormones can cross the plasma membrane & bind to internal receptors on target cells
Hormones from the hypothalamus, anterior pituitary, posterior pituitary & pancreas:
Protein/polypeptide
Hormones from the adrenal cortex, ovaries & testes:
Steroid hormones
Steroid hormones are synthesized from:
(derivatives of)
Cholesterol
What are two hormones that are derived from cholesterol that are STRUCTURALLY very similar?
Aldosterone & Cortisol
DHEA, Androstenedione, Testosterone & Estradiol are all steroid hormones involved in:
Reproduction
What determines what steroid hormone will be produced from the precursor cholesterol?
The complement of enzymes present
Describe the time period present in which amine hormones are made & released:
Made early and stored until secreted
Amine hormones are derived from:
Amino acid Tyrosine
Thyroid hormone, Epinephrine & Norepinephrine are all:
Amine hormones
Epinephrine & Norepinephrine are both:
Adrenal medullary neurohormones
Thyroid hormones bind to the protein:
Thyroglobulin
Epinephrine & Norepinephrine are stored in vesicles & released via:
Exocytosis
Structurally what is the difference between T3 & T4:
The number of iodide atoms attached
What is the precursor to Epinephrine & Norepinephrine?
Dopine
Hormones released into circulation can either circulate ____ or ________
Freely or with binding proteins
The majority of ____, ____ & ____ hormones circulate in their free form:
Amines, Peptide/Protein hormone
What is the exception to most amines circulating in their free form & why?
Thyroid hormone
Its double ring structure makes it soluble enough to where it needs help getting through the plasma
Describe the solubility of amines and peptide/proteins hormones:
Water soluble
_____ & ____ hormones circulate bound to specific transport proteins
Steroid & Thyroid
Some binding proteins are specific for a given hormone, but some plasma proteins such as ___ & ____ can bind to many hormones
Globulin & Albumin
Prevalent protein in the plasma that functions as transportation for a lot of different things such as lipid soluble hormones & fatty acids
Albumin
Most binding proteins are synthesized in the:
Liver
Patients with a compromised/dysfunctional liver may show signs of:
Endocrine deficiencies
Why might a patient with a compromised liver show endocrine deficiencies?
Because most binding proteins are synthesized in the liver & if you can’t make your binding proteins you can’t get enough hormone into the blood
It is always the ______ version of the hormone that binds to receptors & affects the target cell:
Free version (binding protein stays in blood vessel)
The constitutive level of plasma hormones
Basal level
The stimulated level of plasma hormones
Peak levels
The variable pattern of hormone release (peaks & troughs) is determined by the interaction & integration of multiple control mechanisms which include: (4)
Hormonal
Neural
Nutritional
Environmental
When a hormone is constantly secreted in small amounts at a time:
Tonic release
Hormone fluctuations that happen dependent on the time of day
Circadian rhythm
Give an example of a hormone that follows circadian rhythm release:
Cortisol
When does cortisol levels spike?
In the early morning hours
What can work in addition to circadian rhythm release to regulate the release of hormones:
Stimuli
Growth hormone is released during sleep making it following a circadian rhythm release pattern but also displays:
Pulsatile secretion
Secreted in pulses (secretes, stops, secretes, stops)
Pulsatile secretion
The location of the hormone receptor depends on the ______ properties of the hormone
Chemical
The chemical properties of the hormone that determine the location of the hormone receptor can be:
Lipophobic & Liphophillic
Ligand/Receptor binding demonstrates:
- Specificity
- Affinity
- Saturation
Which classes of hormones bind to plasma membrane receptors?
Polypeptide/Protein hormones
Amine hormones*
What amine hormone does not bind to plasma membrane receptors? (except to the rule)
Thyroid hormone
Which class of hormones binds to nuclear receptors?
Steroid hormones + thyroid hormone
Which amine hormones bind to plasma membrane receptors?
Epinephrine & Norepinpehrine
What type of receptors would the following hormones bind to & why?
- Glucagon
- Angiotensin
- GnRH
- SS
- GHRH
- FSH
- LH
- TSH
- ACTH
Plasma membrane receptors- they are peptide/protein hormones
In general many of the receptors that proteins/peptide hormones & amine hormone bind to in the plasma membrane are:
G-protein coupled receptors (GPCRs)
Involved in turning on or off a protein that is already in the cell:
Plasma membrane receptors
What class of hormone receptors are involved in causing a change in gene expression to get a biological response?
Nuclear receptors
Class of hormone receptors involved in making new proteins:
Nuclear receptors
Thyroid hormone & steroid hormones bind to receptors located in:
Either the cytoplasm or the nucleus
Once the steroid hormone or thyroid hormone binds to the receptor located in the nucleus or cytoplasm what occurs next?
Transformation of receptor to expose DNA-binding domain
Following binding of the steroid hormone or thyroid hormone to the receptor & transformation of the receptor to expose the DNA-binding domain what next occurs?
Binding to enhancer-like element in DNA
Examples of plasma membrane hormone receptors:
- GPCR
- Tyrosin kinase
Why do plasma membrane hormone receptor numbers vary greatly in different target tissues:
Provides a way to achieve specific tissues activation
What are two examples of plasma membrane hormone receptors that are more distributed:
- Thyroid hormone receptors
- Insulin receptors
Why are thyroid hormone receptors & insulin receptors more sidled distributed?
Because their actions are something that most cells participate in
How do IGF-1 & Insulin work?
By activating a tyrosine kinase receptor
If it is plasma membrane receptor generally it will activate or inhibit _____ to ______
An existing protein to yield a faster response
Where are nuclear hormone receptors located?
Cytoplasm or nucleus
Nuclear hormone receptors typically leads to:
Formation of new proteins
Nuclear hormone receptors all act to:
Increase or decrease gene expression
In a nuclear hormone receptor, the hormone receptor complex binds to a ______ in the _____ region of the gene which leads to either the activation or repression of ______
Hormone responsive element
Promotor region
Gene transcription
Because nuclear hormone receptors binding a hormone leads to the formation of a new protein, describe the timeline involved:
It takes a little bit longer to get the response & the response will last a bit longer
Hormones that bind to nuclear receptors (thyroid hormone & steroid hormones) undergo _____ to get through the plasma membrane
SImple diffusion
The body often releases multiple hormones:
At the same time
What are the effects of combined hormone actions: (4)
- Antagonism
- Additive
- Synergistic
- Permissiveness
When two hormones change one variable in opposite directions:
Antagonsim
When the response of hormone is equal to the two portions that each hormone provide (2+3=5)
Additive
When the combined hormone response is greater than the individual responses of each hormone added together (2+3=10)
Synergistic
The presence of one hormone is necessary for another hormone’s maximum affect:
Permissiveness
Determine which hormone interaction is being described in the following situation:
Parathyroid increases plasma calcium levels; Calcitonin decreases plasma calcium levels:
Antagonism
Determine which hormone interaction is being described in the following situation:
Glucagon, cortisol & epinephrin all increase blood glucose more than the sum of their individual effects:
Synergism
Determine which hormone interaction is being described in the following situation:
Thyroid hormone causes expression of B adrenergic receptors in bronchiolar smooth muscle:
Permissive
What determines whether the negative feedback will be short loop or long loop?
The location of the hormone that acts as negative feedback in the system
When the last hormone in the pathway inhibits the system upstream
Long loop negative feedback
When an intermediate hormone in the pathway inhibits the system upstream
Short loop negative feedback
Feedback where the hormonal product or an intermediate hormone enhances the hormone secretion:
Positive feedback
Causes an endocrine gland to secrete a hormone
Tropic hormone
Stabilizes the system & prevents over-secretion:
Negative feedback
Hormones that have other endocrine glands as there targets:
Tropic hormones
A tropic hormone from the hypothalamus that acts on the anterior pituitary to release TSH
Thyroid releasing hormone (TRH)
Thyroid releasing hormone (TRH) comes from:
The hypothalamus
TRH acts on the:
Anterior pituitary
TSH (Thyroid stimulating hormone) is released from:
The anterior pituitary
TSH is released from the anterior pituitary & acts on:
The thyroid gland
In the regulation of thyroid hormone, a stimulus causes the hypothalamus to secrete ____ which acts on the ______
TRH
Anterior pituitary
In the regulation of thyroid hormone, _____ cells in the anterior pituitary release _____
Thyrotropic cells
Thyroid stimulating hormone
In the regulation of thyroid hormone, TSH stimulates _____ cells of the thyroid gland to release _____
Follicular cells
Thyroid hormone (TH)
Thyroid hormone produces effects in the body that include:
- Increase in metabolic activity
- Increase in body temperature
In the regulation of thyroid hormone, thyroid hormone stimulates target cells to increase ____ activities resulting in an increase in basal body temperature
Metabolic activities
In the regulation of thyroid hormone, increased body temperature is detected by the hypothalamus & the secretion of _____ by the hypothalamus is ____
TRH
Inhibited
In the regulation of thyroid hormone, thyroid hormone also blocks TRH receptors on thyroid cells inhibiting synthesis & release of ____. Both effects indirectly dampen _____ production in the thyroid
TSH
TH
Thyroid hormone working to negatively feedback is an example of:
Long loop negative feedback
If hormone levels are NOT kept in balance via negative feedback mechanisms what occurs?
Endocrine disorders/Pathologies
Enlargement of the thyroid due to increased or decreased thyroid hormone levels:
Thyroid goiter
Disease characterized by increased cortisol levels:
Cushings disease
Abnormality in the last endocrine organ secreting the hormone leading to either hypo- or hyper-secretion:
Primary endocrine disorder
List the causes of primary hyposecretion:
- Partial destruction of the gland
- Dietary deficiency
- Enzyme deficiency required for hormone synthesis
List the causes of primary hypersecretion:
- Endocrine gland tumor
Abnormality in tropic hormone leading to either hypo- or hyper-secretion:
Secondary endocrine disorder
List the causes of secondary hyposecretion:
A lack of sufficient tropic hormone
List the causes of secondary hypersecretion:
A tumor (either in an endocrine gland that secretes tropic hormones or in a non-endocrine tissues that secretes hormones)
When you see an endocrine hormone disturbance as a result of cancer:
Paraneoplastic endocrine syndrome
When you think of primary endocrine dysfunction you should think:
LAST gland in pathway
Type of diagnostic endocrine function test in which you give something to make hormone levels go up to see if hormone levels actually go up:
Type of diagnostic endocrine function test in which you give something to inhibit the hormone levels in question & look to see if that actual works:
Stimulation test
Suppression test
Suppression test would be used to detect what type of endocrine dysfunction:
Hyperfunction
List the types of diagnostic test used to examine endocrine function (7):
- Plasma hormone levels
- Autoantibodies
- Urine hormone/hormone metabolite levels
- Stimulation tests by administration of tropic or stimulating hormone
- Suppression tests when hyperfunction of endocrine organ is suspected
- Measurement of hormone receptor presence , number & affinity
- Imaging
Stimulation tests work by administering a ____ hormone:
tropic or stimulating
An example of measuring hormone receptor presence as an endocrine diagnostic function test:
Estrogen receptors in breast tumors
What autoantibodies might be tested when doing diagnostic tests of endocrine function:
- Hashiomoto thyroiditis
- Type I DM
- Graves disease
- Addison disease
- Autoimmune hypoparathyroidism
Glucagon, Angiotensin, Gonadotropin releasing hormone (GnRH), Somatostatin (SS), Growth hormone releasing hormone (GHRH), Follicle stimulating hormone (FSH), Lutenizing hormone (LH), Thyroid stimulating hormone (TSH), Adrenocorticotropin hormone (ACTH)
Are all ____ hormones
When are they made?
Polypeptide/protein hormones
Made in advance & stored until use
Epinephrine & norepinephrine are ____ hormones
When are they made?
Amine hormones
Made in advance and then stored
Thyroid hormone (TH) is a ____ hormone
When is it made?
Exception: amine hormone
Made in advance and then stored but does bind to nuclear receptors
Aldosterone, Cortisol, Estradiol, testosterone, also mineralocorticoids, glucocorticoids, and androgens are all _____ hormones
When are they made?
Steroid hormones
Made on demand
List things that stimulate growth hormone (GH) release:
GHRH
Dopamine
Catecholamines (in times of stress & exercise)
Excitatory amino acids
Thyroid hormone
Fasting (Hypoglycemia)
List things that inhibits growth hormone (GH) release:
Somatostatin (SS)
IGF-1 (because of negative feedback)
Glucose (at high levels- hyperglycemia)
Free fatty acids
GHRH, Dopamine, Catecholamines, excitatory amino acids and thyroid hormone would cause ______ of growth hormone release
Stimulation
Portion of the pituitary that is truly filled with endocrine cells- a true endocrine gland:
Adenohypophysis
Adenohypophysis is referring to what portion of the pituitary gland:
Anterior pituitary
Portion of the pituitary that contains axon terminals of hypothalamic neurons:
Neurohypophysis
Neurohypophysis is referring to what portion of the pituitary gland:
Posterior pituitary
The pituitary gland is locked in the ______ ventral to the ______
Sella turcica
Diaphragma sella
List the hormones secreted by the anterior pituitary: (6)
- FSH
- LH
- Adrenocorticotropin
- Thyroid-stimulating hormone
- Prolactin
- Growth hormone
List the hormones secreted by the posterior pituitary: (2)
- ADH/Vasopressin
- Oxytocin
The pituitary gland secretes _____ hormones
Peptide hormones
What are the most prevalent cells in the anterior pituitary & what do they secrete?
Somatotrophs
Growth hormone
What percentage of cells in the anterior pituitary do somatotrophs comprise?
30-40%
What is the second most prevalent type of cell in the anterior pituitary & what do they secrete?
Corticotrophs
ACTH
What percentage of cells in the anterior pituitary do corticotrophs comprise?
20%
Aside from corticotrophs & somatotrophs, what types of cells makeup the anterior pituitary & what do they secrete?
Thyrotrophs - TSH
Gonadotrophs- LH & FSH
Mammaotrophs- Prolactin
Adenomas involving somatotropin cells can cause _____ if occurring in children before the closing of long bones (epiphyseal plates) or _____ in adults with musculoskeletal, neurologic, and other medical consequences
Gigantism
Acromegaly
Benign tumor of epithelial cells that makes hormones:
Adenoma
Endocrine cells are derived from:
Epithelial cells
If a benign tumor is involved in somatotropic cells this would cause over secretion of:
Growth hormone
Majority of cells in the anterior pituitary are devoted to making _____ & _____
GH & ACTH
Neurons in the hypothalamus synthesize & secrete ______ hormones that control endocrine cells in the ______
Hypothalamic releasing/inhibiting hormones
Anterior pituitary
The hypothalamic hormones are released into the ______ in the ______ (in the hypothalamus)
Primary capillary plexus
Median eminence
Responsible for carrying the hypothalamic hormones to the sinuses of the anterior pituitary gland:
Hypothalamic-hypophyseal portal blood vessels
Hypothalamic-hypophyseal portal blood vessels carry the hypothalamic hormones to the ______ of the anterior pituitary gland
Sinuses
Regulation of anterior pituitary secretion
- ______ releases hormones that enter into the blood
- Hormones travel through the ________
- Hormones will continue down through the capillary bed to the ______ wire they can leave the blood & regulate activity of the endocrine cells
- Hypothalamus
- primary capillary plexus
- Sinus
Two capillary beds in series
Portal system
The hypothalamic-hypophyseal portal vessel is comprised of:
Primary capillary plexus + sinus
The hypothalamic hypophyseal portal allows for:
Communication from the hypothalamus to the anterior pituitary
Where do releasing hormones come from?
Hypothalamus
Where do stimulating hormones cone from?
Anterior pituitary
The hypothalamic regulatory hormones bind to_____ in the various endocrine cells of the anterior pituitary
G-proteins coupled receptors
Following the binding of the hypothalamic hormones to the G-protein coupled receptors in the anterior pituitary, what is responsible for stimulating or inhibiting anterior pituitary hormone secretion?
Second messengers (cAMP via Adenylate cyclase, IPs & DAG via Phospholipase C)
Growth hormone inhibiting hormone (GHIH) =
Somatostatin
Prolactin inhibiting hormone (PIH) =
Dopamine
Growth hormone is secreted by somatotrophs in the anterior pituitary. The releasing hormone (secreted by hypothalamus) would be _____ (gas) while the inhibiting hormone would be ______ (breaks)
GHRH
GHIH
GH, a peptide hormone acts _____ on target tissues and as a ______ to the liver
Directly
Tropic hormone
GH, a peptide hormone acts directly on target tissues ad as a tropic hormone to the _____ which releases _____
Liver
IGF1
In what situation might growth hormone significantly increase and quickly?
Prolonged starvation/fasting
Growth hormone acts tropically on the liver to activate _____ a cell signaling pathway that causes the release of _____
JAKSTAT
IGF1
A cell signaling pathway in the liver activated by GH that responds by release of IGF1
JAKSTAT
What are some target tissues of growth hormone? (6)
- Liver
- Chondrocytes
- Muscle cells
- Adipose cells
- Anterior pituitary (short loop negative feedback)
- Hypothalamus (long loop negative feedback)
If GH acts on chondrocytes what results?
- increased amino acid uptake
- Increased protein synthesis
GH acting on chondrocytes to increase amino acid uptake as well as protein synthesis is ultimately necessary for:
Linear growth
In addition to growth hormone acting on chrondocytes being necessary for linear growth what is also necessary for linear growth:
IGF1
GH can act on muscles to:
Increase protein synthesis
In addition to growth hormone acting on muscle to increase protein synthesis what is also necessary for protein synthesis:
IGF1
In excess how does growth hormone affect adipose tissue?
Anti-insulin action
What are two locations of negative feedback of growth hormone:
- Directly feeding back to anterior pituitary (short loop)
- Feeding back to hypothalamus (long loop)
If negative feedback via growth hormone occurs on the hypothalamus what hormone may be released:
Somatostatin
Describe the secretion of growth hormone:
Pulsatile secretion; lower concentration during day with highest levels a few hours after sleep
When is growth hormone secreted at the highest levels:
A few hours following sleep
GH secretion can be stimulated by: (5)
- Starvation (protein deficiency)
- Fasting (hypoglycemia)
- Acute stress
- Exercise
- Excitement
The secretion of GH during the neonatal period can be described as:
The secretion of GH during childhood can be described as:
The secretion of GH during puberty can be described as:
The secretion of GH during adulthood can be described as:
- High secretion
- Decreased secretion
- Peak levels of secretion
- Decreased secretion with age
Stimulation of GH release: (5)
- GHRH
- Dopamine
- Catecholamines
- Excitatory amino acids
- Thyroid hormone
Inhibition of GH release: (4)
- Somatostatin
- IGF1 (due to negative feedback)
- High levels of glucose
- High levels of free fatty acids
Many of the growth & metabolic effects of GH are mainly produced by:
IGFs
IGFs may also be called:
Somatomedins
IGF1 is produced in most tissues and acts on neighboring cells in a ____ manner
Paracrine
The major site of IGF1 synthesis:
The liver
How many IGF binding proteins are there?
6
_____ in adults is one of the main growth promoting insulin-like growth factors:
IGF1
Osteocytes responding to mechanical sensors can release:
IGF1
Osteocytes responding to _____ can release IGF1:
Mechanical sensors
After osteocytes release IGF1 what happens?
IGF1 binds to receptors on osteoblasts to enhance bone formation
Mechanisms of actions of GH & IGF1:
Growth in nearly all tissues of the body, mainly IGF1 occurs through what mechanisms:
- increased cell size
- mitosis
- Differentiation of bone & muscle cells
Mechanisms of actions of GH & IGF1:
What are the overall outcomes of the affects of GH & IGF1 causing growth in nearly all tissues in the body:
- increased organ size
- increased organ function
- increased linear growth
- increased lean body mass
Mechanisms of actions of GH & IGF1:
Effect of increased amino acid uptake and protein synthesis result in:
Increased lean body mass
Mechanisms of actions of GH & IGF1:
How does this effect glucose?
Reduced glucose utilization
Mechanisms of actions of GH & IGF1:
Reduced glucose utilization is due to:
- decreased cellular uptake
- increased hepatic glucose production
- increased insulin secretion
Mechanisms of actions of GH & IGF1:
The reduced glucose utilization can lead to:
Insulin resistance; diabetogenic
Mechanisms of actions of GH & IGF1:
Describe the effects on fatty acids:
Mobilization of fatty acids from adipose tissue (lipolysis)
The mobilization of fatty acids from adipose tissue:
lipolysis
Mechanisms of actions of GH & IGF1:
Lipolysis results in:
Increased FFA in blood and use of FFA for energy
Before fusion of the epiphyseal plates, GH & IGF1 stimulate:
- Chondrogenesis
- Widening of the epiphyseal plates
Following GH and IGF1 stimulating chondrogenesis & widening of the epiphyseal plates, what occurs:
Bone matrix deposition stimulating linear growth
In adults, GH and IGF1 play a role in regulating the normal physiology of:
Bone formation
In adults, how do GH & IGF1 play a role in regulating normal physiology of bone formation?
By increasing bone turnover
How do GH and IGF1 stimulate the increase in bone turnover (thereby regulating bone formation):
- activation of osteoblasts (mainly)
- Increase bone resorption via osteoclasts (lesser extent)
Kids: GH & IGF1 =
Adults: GH & IGF1 =
Chondrogenesis
Increased bone turnover
Osteoblast are of what origin?
Mesenchymal precursor cells
What is responsible for the formation of active osteoblasts from the osteoblasts precursors?
IGF1
Gigantism occurs in ____
Acromegaly occurs in _____
Children
Adults
Excess growth hormone in children leading to gigantism is typically caused by:
Pituitary tumor (90%)
What areas are commonly involved in pituitary tumors that give rise to gigantism?
Sella & cavernous sinus
Tumor causing excessive growth hormone release:
Somatotropin adenoma of pituitary
Describe the facial features that may be associated with gigantism/acromegaly: (4)
Coarse facial features
Large fleshy nose
Frontal bossing
Jaw malocclusion
Coarse facial features including a large fleshy nose, frontal bossing & jaw malocclusion are collectively reffered to as:
Acromegalic facies
What issue with the thyroid may occur with gigantism/acromegaly?
Goiter
Describe the potential effects on the heart & what conditions may result due to gigantism/acromegaly
Cardiomegaly
Hypertension
Coronary heart disease
Describe the chest & spine in individuals effected by acromegaly/gigantistm:
Barrel chest
Kyphosis & hyperostosis
The abnormal glucose tolerance & secondary insulin resistance in an acromegaly/gigantism effected individual may result in:
Diabetes Mellitus
Growth hormone shifts the body from using ___ to ____ for metabolism
Carbs to fats
Describe the reproductive consequences on individuals with acromegaly/gigantism:
Male sexual dysfunction & menstrual disorders
Describe what can occur due to the thicken skin & hypertrophy of sebaceous & sweat glands in gigantism/acromegaly:
Hyperhidrosis & oily skin
Hyperhidrosis & oily skin in acromegaly/gigantism can occur due to:
Thickened skin (hypertrophy of sebaceous & sweat glands)
What can occur in the joints of individuals with gigantism/acromegaly:
Degenerative arthritis
Describe the neuronal effects caused by gigantism/acromegaly:
Parathesias due to peripheral neuropathy
What is a potential treatment for pituitary micro adenoma:
Adenectomy via transphenoidal approach followed by medication
Oral manifestations of GH excess: (7)
- Thick rubbery skin, enlarged nose, thick lips
- Macrocephaly
- Macrognathia
- Disproportionate mandibular growth
- Anterior bite & malocclusion
- Macroglossia, Dyspnea, Dysphagia, Dysphonia, Sialorrhea
- Hypertrophy of pharyngeal & laryngeal tissues
Enlarged head=
Enlarged jaw=
Macrocephaly
Macrognathia
The disproportionate mandibular growth cause by excess GH includes:
Mandibular prognathism- jaw gets forward
Generalized diastemata- teeth separation
The anterior open bites & malocclusion caused by excess GH is due to:
Combination of macrognathia & tooth migration
Define each:
Macroglossia
Dyspnea
Dysphagia
Dysphonia
Sialorrhea
Enlarged tongue
Difficulty breathing
Difficulty swallowing
Difficulty speaking
Slobbering/droolinh
The hypertrophy of the pharyngeal & laryngeal tissues due to excess GH can lead to ________ & how?
Sleep apnea due to the increased growth of pharyngeal & laryngeal tissues obstructing the airway
What are the causes of growth hormone deficiency: (5)
- Hypothalamic disorders
- Mutations
- Combined pituitary deficiencies
- Radiation
- Psychosocial deprivation
Combined pituitary hormone deficiencies:
Panhypopituitarism
What type of mutations may lead to GH deficiency:
GHRH receptor
GH gene
GH receptor
IGF1 receptor
A decrease in GHRH or an increased in GHIH can lead to
Growth hormone deficiency
What depends on the time of onset & severity of hormone deficiency:
(talking about growth hormone)
Clinical manifestations
The clinical manifestations caused by complete growth deficiency include: (4)
- Slow linear growth rates (shorter stature)
- Normal skeletal proportions
- Pudgy, youthful appearance (decreased lipolysis)
- In the setting of cortisol deficiency hypoglycemia
The most common form of dwarfism that is caused by an autosomal dominant conditions that results from a mutation in the FGF-3 receptor in cartilage & brain:
Achondroplasia
Mutation in the FGF-3 receptor in the cartilage & brain makes the receptor overly active and it inhibits cartilage growth at growth plates so:
Limb growth is reduced (growth of trunk is not impacted)
Mutated receptor involved in achondroplasia:
FGF-3
Oral manifestations of GH deficiency include:
- Disproportionate delayed growth of the _____ & ____ = ____ facial appearance
- _____ & ____ of the ___ regions of the jaws are abnormal & may be disproportionately smaller than adjacent structures
- Solitary _____
- Eruption of primary & secondary dentition & shedding of deciduous teeth are ______
- Skull & facial skeleton; small
- Tooth formation & growth; alveolar
- Median maxillary central incisor
- Delayed
How are the oral manifestations of GH deficiency managed:
Correction of dental & skeletal malocclusions
Incisor defects in a child with GH deficiency occurs in both:
Primary & permanent dentition
Oral manifestations of GH deficiency includes tooth formation & growth of alveolar regions of the jaw are abnormal & may be disproportionately smaller than adjacent anatomic structures this can cause:
- Tooth crowding & malocclusion
- Plaque accumulation
- Poor oral hygiene
- Gingivitis & perio disease
The posterior pituitary contains ~100,000 _________ whose cell bodies are in the_______
Unmyelinated axons of neurons
hypothalamus
Areas of concentrated neuronal cell bodies in the hypothalamus that have axons that go through the infundibulum with their synaptic terminals located in the posterior pituitary gland
Paraventricular nucleus & Supraoptic nucleus
The paraventricular nucleus produces ______
Oxytocin
The supraoptic nucleus produces _____
ADH
List all at the names for the abbreviation ADH:
- Antidiuretic hormone
- Arginine Vasopressin (AVP)
Both ADH and Oxytocin are classified as:
Neurohormones
Both ADH and oxytocin are neurohormones made of:
Polypeptides of nine amino acids
While the paraventricular nucleus secretes Oxytocin, and the supraoptic nucleus secretes ADH, they both have the ability to:
Secrete some of the other neurohormone
Describe the similarities between ADH & oxytocin
VERY SIMILAR STRUCTURE & both amine hormones
What are the two primary functions of ADH
- Vasoconstriction (smooth muscle & blood vessels)
- Antidiuretic (holds on to water)
ADH/AVP mechanism of action:
- Contraction of vascular smooth muscle via _____
V1 Receptors
When ADH causes contraction of vascular smooth muscle through V1 receptors what results?
Increases blood pressure
V1 stands for:
Vasopressin-1 receptor
When ADH acts on V1 receptors what occurs?
Contraction of vascular smooth muscle (blood vessels) leading to increase in BP
ADH/AVP mechanism of action:
Functions in the renal renal tubules via:
V2 Receptors
Where are the V2 receptors (for ADH) located?
Late distal tubule & collecting duct
What results when ADH binds to V2 in the last distal tubule & collecting duct?
AQP-2 proteins are inserted into the apical membrane of tubular epithelial cells
Where is aquaporin-2 inserted following ADH binding to V2 receptors?
The apical membrane of tubular epithelial cells
Following ADH binding to V2 receptors in the renal tubules and AQP-2 being inserted into the apical membrane of tubular epithelial cells what results?
This allows for water reabsorption (in accordance with AQP3 & AQP4 on the basolateral membrane
For water reabsorption to occur through AQP2 what also has to be present?
AQP3 & APQ4 on the basolateral membrane
V2 receptors in the late distal tubule and collecting duct are _____ receptors
GPCR
Although water can go through the apical membrane via simple diffusion, the aquaporins allow for:
Water channels so a lot more reabsorption can occur
_____ allows for water to enter the apical membrane
_____ are always on the basolateral membrane and allow for the continuation of the water
AQP-2
AQP-3 & AQP-4
Stimuli for ADH secretion (3)
- Decreased blood volume
- Increased osmolarity
- Decreased BP
In regard to ADH secretion, decreased blood volume is considered:
Isotonic
In regard to ADH secretion, increased osmolarity is considered:
Isovolemic
The most potent stimulator for ADH release is:
Increased osmolarity (linear on a graph)
If blood volume goes down, ADH will function to _______ to resolve the issue
Keep water
If the osmolarity of plasma is too high, ADH will function to ____ in order to ______
Keep water
Dilute it
If your blood pressure is too low, ADH will function to _____ in order to ____-
Keep water
Raise it
ADH working to keep water in the body will resolve what three issues:
- High osmolarity
- Low BP
- Decreased blood volume
Decreased or absent feeling of thirst:
Hypodipsia
Hypodipsia may result in ______ which can cause ______
Reduced intake of water
Hypernatremia
A common problems in elderly people, but is also associated with lesions in the thirst center of the hypothalamus, head trauma, occult hydrocephalus or subarachnoid hemorrhage
Hypodipsia
List causes of hypodypsia: (5)
- Eldery people
- Lesions in hypothalamus (thirst center)
- Head trauma
- Occult hydrocephalus
- Subarachnoid hemorrhage
Diabetes insipidus is a caused by caused by:
ADH imbalance
What are the two types of diabetes insipidus:
Neurogenic (Central)
Nephrogenic (Peripheral)
What do DI and DM have in common?
Large urine output
If you have increased osmolarity you would feel:
Thirst (normal conditions)
Disease caused by inability to produce & secrete ADH:
Neurogenic/Central Diabetes Insipidus
Describe the ADH levels in an individual with Neurogenic/Central DI:
Low levels of ADH (they are unable to produce/secrete it)
Treatment for a patient with neurogenic/central DI would be:
To supplement ADH (likely in the form of medication)
Person with a tumor near the posterior pituitary gland has surgical removal of the tumor, causing damage to supraoptic nucleus in the posterior pituitary.
What are they unable to to produce, what disease would this result in?
ADH
Neurogenic/Central DI
Lacking a response to ADH (like a resistance)
Nephrogenic/Peripheral DI
Nephrogenic/Peripheral DI occurs in the:
Kidneys
When ADH is present but the kidneys either do not respond at all, or response inappropriately to the hormone:
Nephrogenic/Peripheral DI
Describe the levels of ADH an individuals with nephrogenic/peripheral DI would have and why:
High levels off ADH because they can produce ADH but the stimulus causing secretion is never satisfied
Uncharacteristically, really high levels of ADH secretion & NOT becaue it is needed (Oversecretion of ADH)
Syndrome of inappropriate ADH (SIADH)
A patient with diabetes insipidus may present with:
Polyuria
Excretion of large volumes of urine
Polyuria
Describe the urine in a patient with Diabetes Insipidus:
Hypotonic/tasteless (insipid)
Other causes of polyuria (not DI) may include: (2)
- Primary ingestion of excess fluid
- Inreased metabolism of ADH (pregnancy)
Primary ingestion of excess fluid:
Primary polydipsia
Increased and uncontrolled secretion of ADH that causes volume expansion & hyponatremia:
Syndrome of Inappropriate ADH (SIADH)
In the case of a patient with SIADH what would the increased secretion of ADH cause: (2)
- Volume expansion
- Hyponatremia
Relative to a dentist, what can cause excessive ADH release?
Surgery, pain, stress
Why do pregnant women have to pee more?
During pregnancy, ADH metabolism is increased so less water is reabsorbed causing her to pee more
What hormone causes milk ejection from the breast in lactation?
Oxytocin
What hormone stimulates the contraction of the uterus towards the end of gestation:
Oxytocin
Where is oxytocin released from?
Posterior pituitary
Describe the feedback of oxytocin release:
Positive feedback
Describe the relationship between Oxytocin & Prolactin:
Permissive
Where is prolactin released from?
Anterior pituitary
What does prolactin cause?
Milk production in breasts
What causes milk secretion in the breast (mechanism)
Myoepithelial cell contraction
What causes uterine contraction (mechanism)
Stretch of cervix at the end of pregnancy
Objective evidence of a disease that can be seen or measured:
Sign
Enlarged hands, polyuria & tachycardia are all examples of:
A sign
Cannot be measured (they are subjective) but are reported by person:
A symptom
Headache & numbness are both examples of:
A symptom
Plasma Membrane Hormone receptors:
List the four plasma membrane hormone receptors:
- G-protein coupled
- Tyrosine-Kinase
- Serine Kinase
- Cytokine
Plasma Membrane Hormone receptors:
What are our two types of GPCRs?
Gs & Gq
Plasma Membrane Hormone receptors:
Elaborate on the types of Gs coupled receptors: (6)
What second messenger do they produce?
- Beta-Adrenergic
- Calcitonin
- ACTH
- Glucagon
- TSH
- Vasopressin
They produce the second messenger cAMP
Plasma Membrane Hormone receptors:
Elaborate on the types of Gq coupled receptors: (3)
What second messenger do they produce?
- Alpha-adrenergic
- Angiotensin-II
- TRH
They produced the second messengers IP3, DAG, Ca2+
What type of plasma membrane hormone receptor would insulin and IGF-1 bind to?
Tyrosine-kinase
What type of plasma membrane hormone receptor would growth factor bind to?
Tyrosine-kinase
After cytokine binds to its plasma membrane hormone receptor (leptin) what second messenger does it activate?
JAK/STAT
Why would some receptors such as the receptors for insulin and thyroid hormone be more widely distributed?
Because the effects of these hormones is something that we want a lot of cells to respond to
About 93% of the active hormones secreted by the thyroid gland is:
T4
About 7% of the active hormone secreted by the thyroid gland is:
T3
T4=
T3=
Thyroxine
Triiodothyronine
What thyroid hormone is more potent?
T3
Thyroid hormone impact _____ & _____ and also have a _____ action on ______
Metabolism & growth/development
Permissive
Catecholamines
What thyroid cells are involved in making thyroid hormone?
T thyrocyte cells
What is stored in the colloid of a follicle?
Thyroglobulin
Parafollicular cells secrete:
Calcitonin
What is the action of calcitonin?
Tone down plasma calcium (decrease)
In the middle of the thyroid follicle=
Colloid
Where is thyroid hormone made & stored until it is time to be released?
Colloid
What is required for thyroid hormone synthesis?
Iodine (I2)
Thyroid hormone requires iodine (I2) because this is needed for:
Thyroid follicular cells to actively transport Iodide (I-) obtained from the diet
Iodine synthesis steps:
- Thyroid hormone synthesis requires _____
- ____ comes from the diet
- Thyroid cells have a transporter called:
- The follicular cells will:
- The iodide gets into the cell and a second transporter called ___ removes ___ and brings ____ into the colloid of the follicular cell
- Once inside the colloid Iodide gets concentrated into ______
- Iodine (I2)
- Iodide (I-)
- NA+/I- symporter (NIS)
- Concentrate the iodide
- Pendrin; chloride; iodide (I-)
- Iodine
The Na+/I- transporter is a ____
Symporter
The Na+/I- symporter is a _____ transporter
Secondary active
Iodide must exit the _____ across the ____ to accesse the _____ where the initial steps of thyroid hormones synthesis occur:
thyrocyte
apical membrane
colloid
What enzyme works in the iodination & coupling process:
Peroxidase
What is a general term we give for anion exchangers?
Pendrin
Pendrin is a ______ that exchanges ____ for ____ bringing ____ in and ____ out in the process of thyroid hormone synthesis
Anion exchanger
Cl-/I-
I-
Cl-
Pendrin is ALWAYS moving:
Two negatively charged substances in opposite directions
T3 & T4 are produced in the colloid & complexed with:
Thyroglobulin (TG)
The enzyme involved in all of the production steps in the formation of thyroid hormone:
(Tyrosine, Monoiodotyrosine, Diiodotyrosine, T3, RT3, T4)
Peroxidase
Thyroglobulin is made of:
A bunch of tyrosine amino acids
Which works first in making T3 & T4 (pendrin or peroxidase???)
Pendrin then peroxidase
T3 & T4 secretion into the blood:
- ____ is internalized by endocytosis
- The vesicles fuse with ____ in the cell
- ____ cleaves T3 & T4 from ____
- T3 & T4 diffuse out of the cell & into the ___
- Colloid
- Lysosomes
- Protease; thyroglobulin
- Capillaries
Colloid is a ____ of thyroid hormones
Reservoir
Majority if not all of T3 & T4 bind with ____ for transport:
Plasma proteins
What are the plasma proteins that T3 & T4 bind to?
Thyroxine-binding globulin (TBG)
Transthyretin (TTR)
Albumin
What causes the long half-life of T4?
The strength of its binding to the transport protein
Because T3 doesn’t bind as tightly to the transport protein its half life is:
2-3 days
For T3 & T4 to be secreted into the blood:
Colloid is taken into the follicular cell via:
Pinocytosis
For T3 & T4 to be secreted into the blood:
T3 & T4 undergo ____ to be secreted into the blood
Simple diffusion
Target cells make active T3 by using enzymes called ____ that remove an Iodine from T4
Deiodinases/Iodinases
Individual target cells can alter their exposure to T3 by regulating:
Their tissue Deiodinase synthesis
What are the three different Deiodinases?
D1, D2, D3
All three of the deiodinases contain a rare amino acid called:
Selenocysteine
In selenocysteine there is a ___ molecule in the place of _____ which is essential for their enzymatic activity
Selenium in the place of sulfur
What are various conditions that inhibit deiodinase activity?
- Selenium deficiency
- Burns
- Trauma
- Advanced cancer
- Cirrhosis
- Chronic kidneys disease
- MI
- Febrile states
- Fasting
- Stress
If someone has a condition that inhibits deiodinase activity they could show signs of:
Why?
Hypothyroidism
Because they are not able to convert T4 to T3
T3 actions occur ____ compared to T4
Sooner
When does the maximum activity of T3 hormone occur?
Around 2-3 days
Compare the activity of T4 to T3:
T4 has a slower onset but a longer duration of action (can last until about 40 days)
A variety of genes have the thyroid hormone response element which can lead to:
Gene transcription & synthesis of new proteins
The synthesis of new proteins due to the action of T3 & T4 can lead to what five main responses?
- Metabolism
- Cardiovascular response
- CNS development
- Growth
- Many other system responses
A big effect of the thyroid hormone is on metabolism, what effects can be seen due to T3 & T4 synthesizing new proteins that effect metabolism: (9)
- Increased BMR
- Increased glucose absorption
- Increased gluconeogenesis
- Increased glycogenolysis
- Increased lipolysis
- Increased protein synthesis
- Increased O2 consumption
- Increased mitochondria
- Increased Na+/K+ ATPase activity
Background amount of oxygen utilized by cells; a basic indicator of metabolism
BMR
A big effect of the thyroid hormone is on the cardiovascular system, what are some effects relating to this?
- Increased cardiac output
- Increased tissue blood flow
- Increased heart rate
- Increased heart strength
- Increased respiration
The cardiovascular effects of thyroid hormone are caused by an increase in ____ which is a ____ effect
Beta-receptors; permissive effect
The negative feedback of the thyroid hormone is mainly at the level of ____ but can also occur _____
Anterior pituitary
Hypothalamus
It is T4 that is the circulating form of thyroid hormone that is able to caused the feedback inhibition, but it gets converted into T3 in the _____ & ___ so its actually the T3 that inhibits the secretion of ____ & ____
Anterior pituitary & hypothalamus
TSH & TRH
What actually causes the feedback inhibition of thyroid hormone:
The anterior pituitary and hypothalamus express deiodinase so when T4 levels in the tissues increases they readily convert it (via deiodinase) to T3 which actually causes the inhibition
Describe the secretion of TSH:
Pulsatile with increases in evening hours & peak around midnight
Describe the secretion of thyroid hormone:
Thyroid hormone secretion mirrors TSH (pulsatile with increase in evening hours & peak around midnight) but also tonically secreted (small amounts)
Thyroid hormone stimulates _____ by most metabolically active tissues:
Oxygen consumption
How does thyroid hormone effect the BMR?
Increases it
Thyroid hormone stimulates ____ metabolism:
Carbohydrate
Thyroid hormone stimulate carbohydrate metabolism by:
- Uptake of glucose by cells
- Enhances glycolysis & gluconeogenesis
- Increases CHO absorption from GI tract
Describe the effects of thyroid hormone on metabolism relating to proteins:
Stimulate proteins catabolism & synthesis (but mostly catabolism)
Describe the effects of thyroid hormone relating to fat:
Stimulates fat metabolism
Thyroid hormone stimulates fat metabolism by:
Increasing lipid mobilization & oxidation of fatty acids
Thyroid hormone is required to convert _____ to_____, which is why hypothyroid patients may exhibit yellow skin
Beta carotene to vitamin A
Vitamin is important in:
Wound healing
Thyroid hormone is responsible for decreasing circulating ____ levels.
A person with hyperthyroidism may have ______ due to this
Cholesterol
Hyperlipidemia
With no thyroid hormone at all, what would the BMR look like?
BMR levels would be around 45-50% of normal rate
Thyroid hormone is needed for _____ regarding the nervous system:
Needed for normal development
Thyroid hormone impacts ____, so someone with hypothyroidism may have have prolonged _____
Reflex time
Prolonged reflex time
In someone with hyperthyroidism, due to the increased reactivity of neuronal synapses they may experience:
Muscle tremors
If someone feels tired but has difficulty sleeping, and anxiety, worry & paranoia they may have:
(relating to thyroid hormone effect on NS)
Hyperthyroidism
Hyperthyroidism effects on cardiovascular system include:
- increased expression of beta-adrenergic receptors
- increased blood flow, HR and heart contractility
Describe the permissive effect of thyroid hormone on the cardiovascular system. What might this cause?
Thyroid hormone increases expression of beta-adrenergic receptors and this would lead to an increased SNS response
Thyroid hormone effects on the endocrine system:
Increased ___ consumption that results in increased secretion of ____ needed to maintain ____ levels
Glucose
Insulin
Blood glucose
Thyroid hormone effects on the endocrine system:
Thyroid hormone causes activation of bone formation so this causes a need for increased:
PTH secretion
Thyroid hormone effects on the endocrine system:
Thyroid hormone causes increased inactivation of ___ which leads to more ____ release by the _____
Glucocorticoids; ACTH; anterior pituitary
Thyroid hormone effects on the GI system:
Thyroid hormone causes in increase _____ & ____ intake
Appetite
Food
Thyroid hormone effects on the GI system:
Thyroid hormone causes increased rate of ____ & _____ of GI tract
Individuals with hyperthyroidism may have ____ due to this
Individuals with hypothyroidism may have ____ to this
Secretion & motility of GI tract
Diarrhea
Constipation
Enlarged thyroid gland=
Goiter
Goiter is an enlarged thyroid gland that:
DOES NOT indicate functional status
Goiter can be seen in:
Hypothyroidism, Hyperthyroidism & Euthyroidism
Normal levels of thyroid hormones
Euthyrodism
Goiter can be caused by:
Excessive amounts of TSH secretion
High TSH stimulate thyroid to secrete large amounts of _____ into ____ resulting in gland enlargement /goiter
Thyroglobin colloid
Follicles
The most common of hyperthyroidism
Graves disease
Although graves disease is the most common form of hyperthyroidism, hyperthyroidism can also occur due to:
Thyroid adenoma
Graves disease is an ____ disease
Explain how:
Autoimmune
Antibodies to the TSH receptor called thyroid stimulating immunoglobulins are produced and they stimulate the thyroid gland directly to produce too much thyroid hormone (T3 & T4)
Describe the category of disorder that Graves Disease is, and how the hypothalamus & anterior pituitary are effected:
Primary Endocrine disorder- because issue is at level of thyroid gland
Strong negative feedback causes TSH & TRH levels to be reduced
Graves disease is more common in:
The girlies
List the signs & symptoms of Graves Disease:
(10)
- Sweating/heat intolerance
- Increased metabolism
- Increased appetite
- Weight lose
- Fine hair/proteins synthesis
- Increased NS response (Emo instability, insomnia, nervy, restlessness)
- Fine tremor
- Goiter
- Exophthalmus (bug eyes)
- Pretibial myxedema
Treatment of thyroid disease:
Radioactive iodine to ablate thyroid gland followed by L-thyroxine (T4) to prevent hypothyroidism
Antithyroid drugs
Beta-blockers to block permissive effect of thyroid hormone
(Surgery rarely indicated)
Oral symptoms of hyperthyroidism may include:
- Burning mouth syndrome
- Gum disease
- Excessove salivation
- Weakening of mandible
- Increased caries risk
Elevated thyroid hormone with stressful event or serious illness causing fever, tachycardia, elevated BP, nausea, vomitting, diarrhea, breathing problems:
Thyroid storm (thyrotoxicosis)
What can bring on a thyroid storm/thyrotoxicosis?
Trauma, surgery, infection, DKA or MI
Overall a thyroid storm can be described as:
Exaggerated sympathetic response
In patients with hyperthyroidism or those that exhibit signs/symptoms of it what is extremely important?
Administration of epinephrine is CONTRAINDICATED & elective dental care should be deferred
Autoimmune reaction against the thy gland that destroys it rather than stimulating it:
Hashimoto’s thyroiditis
What is the most common cause of hypothyroidisim:
Hashimoto’s thyroiditis
Prior to diagnosis of Hashimoto’s thyroiditis, most patient first exhibit:
Autoimmune thyroiditis
In Hashimoto’s thyroiditis, inflammation leads to ____ of the thyroid resulting in ____
Fibrosis
Decreased secretion of thyroid hormone
What is the target of the antibodies in Hashimoto’s thyroiditis?
Peroxidase
What class of disorder is Hashimoto’s characterized by?
Primary endocrine disorder
Another form of hypothyroidism (not Hashimoto’s) can be due to:
Low iodine
Hypothyroidism due to low iodine is classified as:
Primary endocrine disorder
In the absence of iodine describe the levels of T3, T4, TSH, & TRH:
Low T3 & T4
Elevated TRH & TSH
In hypothyroid state, goiter is due to _____ while no goiter is due to _____
Iodine deficiency
TSH deficiency
Hypothyroidism due to iodine deficiency= _____ = _____ deficiency
Hypothyroidism due to TSH deficiency= _____ = _____ deficiency
Goiter, Primary
No goiter, Secondary
Symptoms of hypothyroidism may include:
- Weight gain
- Constipation
- Cold/diminished perspiration
- Lethargy
- Impaired memory
- Lack of NS stimulation
- Coarse, dry brittle hair
- Hairloss
- Loss of lateral eyebrows
- Slow pulse (bc decreased number of beta receptors)
- Enlarged heart
- Facial edema
- Periperhal edema (hands & feet)
Unique symptom seen in sever cases of hypothyroidism:
Myxedema
In hyperthyroidism patients where does the myxedema occur?
In hypothyroidism patients where does the myxedema occur?
Hyper= Pretibial myxedema
Hypo= face
Myxedema occurs due to increased quantities of ____ & ____ bound with protein plus water that accumulates in the skin
Hyaluronic acid & Chondroitin sulfate
Dull expressionless facies with puffiness of eyelids, swollen, cool waxy dry, coarse & pale skin, with lots of creases describes a patient effected with ______ and the treatment would be _____
Myxedema
L-thyroxine (T4)
Required for postnatal brain maturation
Thyroid hormones
Results from congenital absence of thyroid gland:
Congenital cretinism
Results from iodine deficient diet; most common cause worldwide:
Endemic cretinism
Cretinism can cause ____ of neonates.
Skeletal growth is more inhibited than soft tissue growth resulting in:
Physical & mental retardation
Obese, stocky & short with large protruding tongue
Cretinism can cause a lack of development of the:
Nervous system
List the hypothyroidism oral manifestations: (6)
- Macroglossia
- Dysgeusia
- Delayed tooth eruption
- Poor wound healing
- Increased periodontal disease
- Salivary gland enlargement
The poor wound healing and increased risk of infection in a hypothyroidism patient is due to:
Decreased activity of fibroblasts
Patients with hypothyroidism are sensitive to:
Central nervous system depressants or barbituates
85% of the body’s phosphate is stored in the ___
14-15% of the body’s phosphate is stored in the ___
Less than 1% of the body’s phosphate is stored in the ___
Bones
Cells
ECF
Only 0.1% of the bodies calcium is found in the _____
1% of the bodies calcium is found in the _____
The rest of the bodies calcium is stored in the ____
ECF
Cells & organelle
Bones
When levels of calcium are too low:
Neuronal hyper-excitability (tetany due to extra NA+ influx)
When levels of calcium are too high:
Neuronal depression (Blocks Na+ influx)
Carpal spasms can be due to:
HYPOcalcemia
Control points for calcium & phosphate include:
- Absorption- via intestines
- Excretion- via urine (calcium & phosphate) & feces (calcium only)
- Temporary storage- via bone (hydroxyapatite)
Ca10(PO4)6(OH)2
Hydroxyapatite
What are the hormones that regulate plasma calcium?
PTH, Calcitriol, Calcitonin
How does PTH regulate plasma calcium & phosphate?
Increases plasma calcium
Decreases plasma phosphate
How does PTH work to raise plasma calcium & lower plasma phosphate?
- Mobilizes calcium from bone
- Enhances renal reabsorption of calcium
- Increases intestinal absorption of calcium (indirectly)
How does calcitriol regulate plasma calcium & phosphate?
Increases plasma calcium
Increases plasma phosphate
How calcitriol work to raise plasma calcium & phosphate?
Calcitriol is the primary hormone that enhances intestinal absorption of calcium & it also causes absorption of phosphate
The primary hormone that enhances intestinal absorption of calcium and also causes absorption of phosphate
Calcitriol
What are the other names for calcitriol?
1,25-dihydroxyxholecaliferol
Vitamin D3
Calcitriol acts on the intestines ____ to enhance absorption of calcium & also phosphate, while PTH acts on the intestines _____ to enhance absorption of calcium
Directly
Indirectly
Calcitonin comes from:
Parafollicular cells of the thyroid gland
How does calcitonin regulate plasma calcium & phosphate?
Decreases plasma calcium
Decreases plasma phosphate
How does calcitonin work to decrease plasma calcium & phosphate?
By simulating bone formation
What hormones stimulate bone formation?
- Calcitonin
- Insulin
- Growth hormone
- IGF-1
- Estrogen
- Testosterone
______ & _____ stimulate bone matrix resorption which functions to increase plasma calcium
Calcitriol
PTH
Calcitriol & PTH stimulate bone matrix ___
How does this effect plasma calcium?
Resorption
Increases plasma calcium
Bone resorption:
- Osteoblasts release _____
- _____ binds to the ____ on preosteoclasts and this leads to the activation of ______
- RANKL
- RANKL; Rank receptors; osteclasts
What is the goal of bone resorption?
To increase plasma calcium levels
What type of cell is activated during bone resorption?
What activates this type of cell?
Osteoclasts
RANKL binding to its receptor on preosteoclasts
Factors that stimulate bone matrix resorption:
(4)
- PTH
- Excessive levels of calcitriol
- Prolactin
- Corticosteroids
What is the goal of bone deposition?
To form bone- put calcium into bone from the blood
_____ stimulates bone matrix deposition and inhbits osteoclasts
Calcitonin
Calcitonin stimulates bone matrix deposition and inhibits osteoclasts which ultimately does what to plasma calcium?
Decreases
If calcium levels in the blood are sufficient we dont need to:
Breakdown bone
Anabolic or anti-resorptive factors (for bone)=
- Estrogens
- Calcitonin
- Testostserone
- Calcium
- BMP
In order to avoid RANKL further activating osteoclasts ____ will bind to it so it cannot bind to its receptor
OPG
OPG binding to RANKL ultimately leads to:
Apoptotic osteoclasts
Osteoclast that do NOT function to break down bone:
Apoptotic osteoclasts
Affects almost 10 million individuals in the US, though only a small proportion are diagnosed & treated. Occurs when there is an imbalance in bone resorption & bone formation
Osteoporosis
Risk factors for osteoporosis: (superficial)
- Vitamin D deficiency
- Inadequate calcium intake
- Glucocorticoid medications
- Reduced physical activity
- Estrogen deficiency
- Cigarette smoking
- Alcohol
Describe why vitamin D deficiency can lead to osteoporosis:
Because this can lead to really high PTH levels (secondary hyperparathyroidism) which leads to excessive bone breakdown
Describe why inadequate calcium intake can lead to osteoporosis:
Because this can lead to really high levels of PTH (secondary hyperparathyroidism) which leads to excessive bone breakdown
Describe why glucocorticoid medications can lead to osteoporosis:
They suppress the immune response leading to the risk of weak & brittle bones
Describe why post-menopausal estrogen deficiency can lead to osteoporosis:
Estrogen stimulates the process of bone matrix deposition so the lack of estrogen would throw the balance off
Treatments for osteoporosis include:
- Excerise
- PT
- Estrogen replacement
- Calcium
- Vitamin D
- Bisphosphonates
When giving vitamin D to an osteoporosis patient you must make sure ____ levels do not get too high
PTH
Four pea-sized glands on the posterior surface of the thyroid glands:
Parathyroid glands
PTH is secreted by:
Chief cells
What are the effect of PTH & how?
Increased plasma calcium by: indirectly increasing intestinal absorption, decreasing renal excretion & increasing bone resorption
How does PTH decrease plasma phsophate?
By increasing renal excretion
Describe the renal effects of calcium & phosphate by PTH:
Increases renal excretion for phosphate
Decreases renal excretion for calcium
Why is PTH’s effect on the intestinal absorption of calcium considered indirect?
Because it causes more synthesis of vitamin D which in turn causes increased intestinal absorption of calcium
When PTF is secreted due to decreased ECF calcium this leads to:
Hypertrophy of Parathyroid gland
How would a decrease in ECF calcium concentration effect the rate of PTH secretion?
Increase
What conditions would lead to hypertrophy of the parathyroid gland?
Chronic cases- pregnancy, rickets, lactation
Chronically if you hypertrophy the parathyroid gland, it becomes:
Even better at secreting PTH
An increased ECF concentration of calcium leads to ___ of the parathyroid gland
Decreased activity
If the parathyroid gland has a decrease in activity, it will have a ____ in size
Decrease
What conditions can cause a decrease in activity & size of the parathyroid gland?
- Increased vitamin D intake at excessive levels
- Excess quantities of calcium in diet
- Bone resorption caused by factors other than PTH
Describe the effect on plasma calcium:
Bone resorption
Increases
Describe the effect on plasma calcium:
Reabsorption of calcium by renal tubules:
Increases plasma calcium
Describe the effect on plasma calcium:
Conversion of 25-hydroxycholecalciferol to 1, 25-dihydroxycholecalciferol:
Increases plasma calcium
Describe the effect on plasma phosphate:
Decreased reabsorption by renal tubules:
Decreases plasma phosphate
Where do we get Cholecalciferol (vitamin D3) from?
Skin from sun
In the process of calcitriol synthesis:
Cholecalciferol is converted to ____ by what organ?
25-Hydroxycholecalcierfol
Liver
In the process of calcitriol synthesis:
25-Hydroxycalciferol is coverted to _____ by what organ?
1,25-dihydroxycholecalciferol (calcitriol)
Kidney
In the process of calcitriol synthesis:
What tells the kidney to do the conversion of 25-dihydroxycholecalciferol to the active form?
Parathyroid hormone
Where is the main effect of Calcitriol?
Intestine- absorption of Ca & Phosphate from diet
Where can calciferol act although not the main effect?
Kidneys- reduced excretion of Ca & Phosphate
Bones- bone deposition (indirectly)
Vitamin D3 can be stored in the liver for:
Several months
Describe the regulation of calcitriol levels:
Tightly regulated- if someone takes excess vitamin D3 the liver will still only convert so much into the 25-hydroxycholecalciferol
Someone with compromised liver and kidney function may exhibit:
Vitamin D deficiency
Peptide hormone secreted by parafollicular cells:
Calcitonin
Parafollicilar cells reside in the ____ and may also be called ____
Thyroid gland
C cells
Calcitonin is released in response to:
Elevated free plasma calcium
Calcitonin decreases the levels of plasma calcium by decreasing the activity of ___ thus decreasing ____
Osteoclasts
Bone resporption
Not a major controlled of calcium in humans:
Calcitonin
What two systems does calcitonin act on?
Bone & kidneys
Excess PTH secretion due to a parathyroid gland tumor would be classified as:
Primary hyperparathyroidism
Primary hyperparathyroidism can lead to extreme ____ activity in bones causing _____, more specifically _____
Osteoclastic activity
Cystic bone disease
Osteitis fibrosa cystica
Such excessive bone breakdown that we see scar tissue & fibrosis in bones:
Cystic bone disease (Osteitis fibrosa cystica) (caused by primary hyperparathyroidism)
Primary hyperparathyroidism can cause hypercalcemia leading to: (in relation to urine)
Polyuria & Calciuria
What phosphate levels and why in patients with primary hyperparathyroidsim?
Low phosphate due to increased renal excretion
Describe why someone with primary hyperparathyroidism would exhibit muscle weakness and easy fatigability:
Too much calcium- blocks sodium influx leading to neuronal depression (impedes signaling by neurons)
Primary hyperparathyroidism signs and symptoms include:
Stones, bones, abdominal groans & psychic moans
Describe the stone component of primary hyperparathyroidism:
- Renal stones
- Nephrocalcinosis
- Polyuria
- Polydipsia
- Uremia
Describe the bones component of primary hyperparathyroidism:
- Cystic bone disease
- Osteomalacia/rickets
- Arthritis
Describe the abdominal groans component of primary hyperparathyroidism:
- Constipation
- Indigestion
- Nausea
- Vomiting
- Peptic ulcers
- Pancreatitis
Describe the psychic moans component of primary hyperparathyroidism:
- Lethargy/fatigue
- Depression
- Memory loss
- Paranoia
- Personality change
- Confusion, stupor, coma
Other symptoms, not included in stones, bones, moans and groans from primary parahyperthyroidism include:
- Proximal muscle weakness
- Keratitis
- Conjunctivitis
- Hypertension
- Itching
High PTH levels that occur as compensation for hypocalcemia & NOT due to an issue with the parathyroid gland:
Secondary Hyperparathyroidism
What are the two causes of hypocalcemia that lead to secondary hyperparathyroidism?
- Vitamin D deficiency
- Chronic renal disease- cannot synthesize Vit D3
What disease are you at risk for with high levels of PTH?
Osteoporosis
Disease that would results from accidental surgical parathyroid gland removal (not common):
Primary Hypoparathyroidism
What increases membrane Na+ permeability leading to neuromuscular excitability & muscle spasma
Hypocalcemia
What is the condition for the wonky ass hand:
Carpal spasm
How many adrenal glands do we have?
Where are they located?
Two adrenal glands
One ontop of each kidney
Describe the structure of an adrenal gland:
Outer cortex + inner medulla
What portion of the adrenal gland is essential for life?
Adrenal cortex
The adrenal cortex secretes:
- Corticosteroids
- Mineralcorticoids
- Sex hormones
Is the adrenal medulla essential for life?
No
The adrenal _____ is a true endocrine organ
Cortex
Although it is not essential for life, the adrenal medulla is important in:
Secreting epinephrine & norepinephrine in response to sympathetic nervous system stimulation
The adrenal medulla hormones are NOT essential for life but help an individual deal with:
Emergencies
The adrenal cortex secretes several hormones that are made from:
Cholesterol
What are the three layers of the adrenal cortex?
Zona Glomerulosa
Zona Fasciculata
Zona Reticularis
The largest zone of the of the adrenal cortex:
Zona Fasciculata
The Zona Glomerulosa secretes _____ and is regulated by ______
Mineralcorticoids
RAAS
RAAS stands for:
Renin-angiotensin-aldosterone system
The Zona Fasciculata secretes ____ and is regulated by _____
Glucocorticoids
HPA (CRH, ACTH)
HPA stands for:
Hypothalamic-pituitary-adrenal axis
The Zona Reticularis secretes ____ and is regulated by _____
Androgens
HPA
The adrenal medulla is related to the _______ & secretes ____
Sympathetic nervous system; catecholamines
What type of cells secrete catecholamines?
Chromaffin cells
The do the chromaffin cells of the adrenal medulla secrete Epi & NE?
Directly into the blood
What are the three tissues involved in the HPA?
Hypothalamus, pituitary, adrenal gland
Why does the zona glomerulosa secrete so much aldosterone?
Bc enzymes involved in the formation of aldosterone from cholesterol are highly expressed in the zona glomerulosa
What enzyme is responsible for the conversion of cortisol to cortisone?
11HSD Beta 2
What enzyme is responsible for the conversion of cortisone to cortisol?
11HSD Beta 1
The reactions that occur for the synthesis of steroid hormones in the adrenal cortex take place in the ______ or the _____
Mitochondria
Endoplasmic reticulum
Describe the activity of cortisone at cortisol receptors:
Reduced activity
Can be used to make testosterone & androgens:
Androstenedione
Aldosterone is classified as a:
Mineralcorticoid
Aldosterone functions in the kidneys to:
- Increase renal reabsorption of sodium
- Increase renal secretion of Potassium
Aldosterone working to increase renal reabsorption of Na+ and increasing renal secretion of K+ results in:
Increase in ECF volume and mean arterial pressure
What stimulates aldosterone secretion?
- Angiotensin II
- Increased levels of K+
- Decreased levels of Na+
Aldosterone has effects on:
- Kidney
- Sweat glands
- Salivary glands
What portion of the adrenal cortex is responsible for aldosterone secretion?
Zona Glomerulosa
What are the main functions of angiotensin-II
- Vasoconstriction
- Release of aldosterone
What function of angiotensin-II is interrelated to the sympathetic nervous system:
Release of aldosterone
Since aldosterone causes increased tubular reabsorption of sodium, ultimately raising blood sodium levels what happens to water?
Water retention occurs because where sodium goes water follows
The effects of aldosterone on sweat glands is important to:
Conserve body salt in hot environments
The effects of aldosterone on the salivary gland is important in:
Conservation of sodium during high rates of salivary secretion
In addition to hyperkalemia ______ causes secretion of aldosterol
Angiotensin II
An enzyme release by the cells in the kidneys in response to a variety of stimuli (Example: SNS)
Renin
Angiotensin converting enzyme (ACE) is produced by the:
Endothelium
List the steps of the RAAS:
Angiotensinogen gets converted to Angiotnesin I by the enzyme Renin
Angiotensin I gets converted to Angiotensin II by the enzyme ACE
Angiotensin II ultimately causes the secretion of _____ but also does ____, ____ & _____
Ultimately aldosterone secretion but also ADH secretion, thirst stimulation & vasoconstriction
What do vasoconstriction, aldosterone secretion, ADH secretion & thirst stimulation all have in common?
These all work to raise BP
In RAAS, the nonactive precursor made by the liver and found in the plasma:
Angiotensinogen
Where is large amounts of ACE found?
In the lungs
Alot of _____ medications target RAAS:
HTN
How do ACE inhibitors work?
If you inhibit ACE you will make less angiotensin II= lower BP
Primary hyperaldosteronism may also be called:
Conn’s syndrome
In primary hyperaldosteronism where is the problem?
The adrenal gland
What are the causes of primary hyperaldosteronism?
- Adrenal adenoma (benign)
- Adrenal hyperplasia
- Adrenal carcinoma (malignant)
Describe the levels involved in primary hyperaldosteronism (Conn’s syndrome):
Low levels of renin
Signs & symptoms of primary hyperaldosteronism (Conn’s syndrome) include:
Hypertension
Hypernatremia
Hypokalemia
Headaches
Weakness
Fatigue
Polyuria
HYPOKALEMIC ALKALOSIS
LOW PLASMA RENIN
Explain why someone with primary hyperaldosteronism would have low levels of plasma renin?
Due to so much aldosterone production we will have strong negative feedback
A byproduct of cells trying to regulate the K+ levels in the case of primary hyperaldosteronism (Conn’s)
Hypokalemic alkalosis
In hypokalemic alkalosis the cells attempt to regulate K+ levels leads to an absence of:
H+ in the ECF
Treatment options for primary hyperaldosteronism (Conn’s) include:
Surgical removal of tumor or most of the adrenal tissue when hyperplasia is present
Mineralcorticoid receptor antagonist
Disease caused by decreased blood flow and pressure in the renal artery- in which the kidney thinks BP is low and secretes renin excessively
Secondary hyperaldosteronism
Describe the levels of renin in secondary hyperaldosteronism:
High levels of renin
What are causes of secondary hyperaldosteronism?
- CHF
- Renal artery stenosis
How might CHF lead to secondary hyperaldosteronism?
Pumping function of heart is declined, leading to low BP, and aldosterone levels will rise to compensate
How might renal artery stenosis lead to secondary hyperaldosteronism?
Renal artery pumps blood to kidney and there can be an atherosclerotic plaque in the vessels resulting in decreased blood flow to kidney. Kidney now thinks BP is low and secretes excessive renin to try to compensate for the “low BP.” Extra renin leads to extra angiotensin II which leads to extra aldosterone secretion
The other kidney is working just fine
Signs & symptoms of secondary hyperaldosteronism include:
- High plasma renin
- Hypernatremia w/extracellular volume expansion
- Edema
- Decreased cardiac output
- Similar clinical findings to primary hyperaldosteronism (EXCEPT RENIN LEVEL)
Hormone that functions in the mobilization of energy stores & suppresses the immune system:
Cortisol
What hormone is secreted in response to stress?
Cortisol
Cortisol is categorized as a _____ and comes from the ______ of the adrenal cortex
Glucocorticoid
Zona fasciculata
More cells in the adrenal cortex make ____ than any other cells because of the size of the Zona Fasciculata
Cortisol
What are some examples of stressors that may cause cortisol secretion?
Heat
Cold
Hypo/Hyperglycemia
(Not just psychological stress)
Cortisol says “there is a stressful situation, let me throw a bunch of nutrients in the blood” but a consequence of cortisol is that:
It suppresses the immune system
When does cortisol levels spike? What hormone is opposite of this?
Early morning hours; Growth hormone
Cortisol feeds back and inhibits:
- ACTH secretion from anterior pituitary
- CRH secretoin from hypothalamus
Describe what type of feedback is seen through cortisol:
Long loop only
What are the four main actions of cortisol?
- Gluconeogenesis
- Protein mobilization
- Fat mobilization
- Stabilizes lysosomes
The action of cortisol leads to the suppression of immune function?
Stabilizing lysosomes
Why are other hormones secreted when ACTH is secreted?
Because the gene for ACTH forms a larger protein (a preprohormone)
What is the name of the preprohormone that ACTH is derived from?
Proopriomelanocortin (POMC)
In addition to ACTH being synthesized from POMC what else is secreted?
- Melanocyte stimulating hormone (MSH)
- Beta-endorphin
- Beta-lipotrophin
A clinical sign of elevated ACTH pathologically is:
Increased skin pigmentation from melanocytes)
What is a byproduct of ACTH production?
MSH
Cortisol has a similar affinity for the ____ receptor as _____
Mineralcorticoid receptor (MR)
Aldosterone
What is found at higher circulating concentrations, aldosterone or cortisol?
Cortisol
Since cortisol is able to bind to the MR receptor, why doesn’t it cause a mineralcorticoid effect?
11B2HSD enzyme converts cortisol to cortisone in aldosterone responsive tissues making sure the aldosterone binds to the MR receptor, not cortisol
____ does not bind to GC or MR receptors with as high of an affinity as _____
Cortisone; Cortisol
A genetic deficieny of 11B2-HSD that leads to the syndrome:
AME (apparent mineralocorticoid excess)
______ is a compound found in licorice that inhibits the activity of _____
Clycerhetininc acid
11B2-HSD
What do we expect under normal conditions when the adolsterone binds the mineralocorticoid receptor in the epithelial cells of the kidney:
Increased sodium reabsorption
Increased potassium secretion
Where would we find 11B2HSD receptors?
Where would we find 11B1HSD receptors?
Kidneys, Salivary gland & Sweat glands
Skin
High circulating cortisol levels such as in Cushing’s syndrome can:
Overwhelm the 11HSDB2 receptor
Both AME syndrome & high circulating cortisol levels will ultimately cause:
High blood pressure
Effects of Cortisol on metabolism:
Stimulation of ____ & _____ in the liver resulting in ______
gluconeogenesis & glycogenolysis
Increases plasma glucose
Effects of Cortisol on metabolism:
____ action resulting in decreased glucose uptake in the muscle & fat but not the brain & heart
Anti-insulin
Effects of Cortisol on metabolism:
Makes _____ worse by increasing ____ levels, ____ levels, & ____ formation & ____ secretion
Diabetes
Glucose, lipid
Ketone body
Insulin
Describe what two hormones are antagonists when dealing with the carbohydrate effect of cortisol on metabolism:
Cortisol & insulin are antagonist
Describe what can happen with a diabetic that is scared of the dentist due to cortisol:
They come in, they get stressed out, their cortisol levels rise and in turn their blood sugar rises (bc cortisol stimulates gluconeogenesis & glycogenolysis)
Effects of cortisol on metabolism:
Inhibits ____ synthesis & increases ______ especially in skeletal muscle
Protein; proteolysis (provides a source of AA for glycoenogenesis)
Effects of cortisol on metabolism:
Cortisol excess leads to ____ weakness, pain, ___ skin and abdominal ___ due to the protein catabolic effect
Muscle
Thin
Abdominal striae
Effects of cortisol on metabolism:
Promotes ____, and shifts the energy system to utilization of ____ to ____ in times of stress
Lipolysis
Glucose to fatty acids
Effects of cortisol on metabolism:
Causes ____ deposition in certain areas (abdomen, interscapular “buffalo hump” and a rounded “moon face”
Lipid
95% of the glucocorticoid activity is due to the secretion of:
Cortisol
Absence of cortisol contributes to _____ due to the loss of _____ of _____ on blood vessels
Circulatory failure
Permissive action
Catecholamines
Lack of cortisol prevents mobilization of ______ (glucose & free fatty acids) during stress & can result in _____
Energy sources
Fatal hypoglycemia
Vasoconstriction of blood vessels occurs via:
Alpha 1 receptors
Describe the effect cortisol has on catecholamines (Alpha1 receptor) on blood vessels:
Permissive effect- the presence of cortisol allows the alpha 1 receptors effect to be maximized
Why would BP decrease when cortisol levels are low:
The presence of cortisol allows the alpha1 receptors response to be maximized, so without the maximum response BP would be lower
How does cortisol effect the immune system?
Suppresses immune system
What are a few ways that cortisol suppresses the immune system?
- Stabilizes lysosomal membrane
- Opposes inflammation (by decreasing WBC migration & phagocytosis)
- Suppresses T lymphocytes
What property of glucocorticoids allows them to be used in treatment of patients with diseases/conditions involving exaggerated inflammatory response?
Their anti-inflammatory action
How can treatment with glucocorticoids cause osteoporosis?
Because cortisol stimulates bone resorption via an increase in RANKL expression by osteoblast
Treatment with glucocorticoid promotes apoptosis of _____ & ____ which can further lead to osteoporosis
Osteoblasts & Osteocytes
The zona reticularis is responsible for the secretion of:
androgens
The zona reticularis begins secreting adrenal androgrens around age _____, peaking around age _____ & ______ with age
8; 20; decreasing
Adrenal androgens secreted by the zona reticularis include:
DHEA/DHEAS
Androstenedione
Testosterone
Estrogens
Describe the effects of adrenal androgens in males versus females:
Adrenal androgens have only weak effects in males but contribute ~50% of active androgens in females
Describe the effects of adrenal androgens in females:
Growth of pubic hair, axillary hair & libido
A condition resulting from excess androgen production in pre-pubertal boys:
Precocious pseudopuberty
Normally puberty in boys is stimulated by _____ which leads to the secretion of FSH and LH
But if the adrenal gland is oversecreting androgens it can lead to:
Hypothalamus secreting GRH
Early puberty NOT due to the hypothalamic pituitary axis
If boys are effected by precocious pseudopuberty brought on by excessive androgen secretion from the adrenal gland this can cause:
Early development of secondary sexual characteristics (under age 8)
______ deficiency can result in virilization in newborn females & pseudo-hermaphroditism
21-hydroxylase deficiency
21-Hydroxylase deficiency leads to an overproductionof:
Androgens (DHEA, DHEAS, Androstendione)
Androgen secreting tumors producing excess androgen result in: (in females)
Virilization & precocious pseudopuberty in females
Precocius pseudopuberty:
Early puberty not caused by HPA secreting GRH, but instead due to adrenal androgens in excess
21-hydroxylase is an enzyme critical for making ___ & ____ and in the absence of this enzyme there is buildup of excessive amounts of _____ & _____ precursors resulting in excessive production of ______
Aldosterone & cortisol
Aldosterone & cortisol precursors
Androgen precursors (DHEA, DHEAS, Andrestenedione)
Androstenedione is a precursor to:
Testosterone
5-Dihydrotestosterone
Estrogenes
Although androstenedione is not the precursor made in the greatest amounts compared to DHEA & DHEAS, it is the precursor with the:
Greatest effect
Why does the precursor androstenedione have the greatest effect (compared to DHEA & DHEAS)
Because it is more readily convertied peripherally to testosterone & estrogens
In adults, hormonally active, benign adrenal adenomas usually secrete _____ or ____
Aldosterone or cortisol
Virilizing tumors in women are more likely to be caused by:
Ovarian tumors
Virilizing adrenal tumors are ____ and virilization is usually due to ______
Rare; hypersecretion of adrenal androgens
List some signs & symptoms of virilization:
Male-pattern baldness
Male muscularture
Clitoromegaly
Increased libido
Rapid linear growth with advanced bone age
Primary adrenal insufficiency
Addison’s
Addison’s disease can be caused by primary atrophy or injury to the _____
adrenal cortex
In about 80% of Addison’s atrophy occurs due to ____ of all cortical zones
autoimmune destruction
Describe the level of ACTH in addison’s disease:
High levels of ACTH
Describe the levels of corticosteroid production in addison’s disease:
Low corticosteroids
Addison’s disease can be characterized by a loss of:
Glucocorticoid, mineralcorticoid, & androgen secretion
Secondary adrenal insufficiency is due to low levels of:
ACTH
If the pituitary gland is unable to secrete enough ACTH this would restult in:
Low cortisol production (secondary adrenal insufficiency)
Often latrogenic due to abrupt cessation of steroid therapy
Secondary adrenal insufficiency
What is affected in primary adrenal insufficiency that is NOT affected in secondary adrenal insufficiency:
Mineralcorticoid secretion
Would signs and symptoms of glucocorticoid deficiency be seen in primary or secondary adrenal insufficiency or both?
Would signs and symptoms of mineralcorticoid deficiency be seen in primary or secondary adrenal insufficiency or both?
Would signs and symptoms of androgen deficiency be seen in primary secondary adrenal insufficiency or both?
Glucocorticoid deficiency= both- both have lack of cortisol production
Mineralcorticoid deficiency= primary only
Androgen deficiency= Both- In addisons there is a loss of androgen & in secondary there is low ACTH leading to low androgen production (bc ACTH stimulates androgen production)
Two important symptoms of glucocorticoid deficiency include:
Hypoglycemia- because cortisol normally raises blood glucose
Low BP- due to the lack of alpha1 receptor permissive effect
Hyperpigmentation in primary adrenal insufficiency is due to excess of ______
POMC
Cushing’s disease is a _____ disorder its characterized by _____
Cushing’s sydnrome is a _____ disorder characterized by ____
Secondary- occurs due to brain- high ACTH
Primary- occurs due adrenal cortex- low levels of ACTH
Both cushings disease/syndrome is characterized by:
High cortisol levels
Cushings Disease or Syndrome?
- Secondary disorder
- Primary disorder
- Due to adrenal cortex
- Due to brain
- Oversecretion of ACTH leads to excessive cortisol level
- Overproduction of cortisol leads to low levels of ACTH
- Disease
- Syndrome
- Syndrome
- Disease
- Disease
- Syndrome
To distinguish between Cushing’s disease & syndrome, what hormone levels would you look at?
ACTH
Conn’s syndrome is an issue with _____
Cushing’s syndrome is an issue with _____
Pheochromoyctomoa is an issue with ______
Mineralcorticoids
Glucocorticoids
Catecholamines
Sudden release of hormone causing sudden “attack” due to chromaffin cell in the adrenal medulla resulting in excessive secretion of epi & norepi
Pheochromocytoma
What cells are involved in pheochromocytoma?
Chromafin cells
Can be characterized by an exaggerated sympathetic response:
Pheochromocytoma
What hormones are invovled in pheochromocytoma:
Epi & Norepi
Entire length of thick filament (some overlapping thin filament)
A-band
Includes ONLY thin filaments
I-band
Includes only thick filaments
H-zone
Where thin filaments are anchored
Z-line
Link the central regions of thick filaments
M-line
When a sarcomere shortens during contraction, what happens to the zone of overlap
Increases
When a sarcomere shortens during contraction , what happens to the I-band?
Decreases
When the sarcomere shortens during contraction, what happens to the A-band?
THE A-BAND DOES NOT CHANGE IN LENGTH
Dark band:
Light band:
A-band
I-band
In muscle, functions as an ATPase enzyme:
Myosin
When myosin binds to ATP what happens?
It hydrolyzes the ATP
What regulate when contraction can happen?
Troponin & tropomyosin
Protein that connects thin filaments to glycoproteins in the sarcolemma:
Dystrophin
Provides scaffolding for sarcomeres:
Dystrophin-glycoprotein complex
What is the difference between Duchenne & Beckers muscular dystophy?
Duchennes= more severe, low levels of dystrophin if any at all
Beckers= makes some dystrophin but not enough, because of this muscle cells weaken and, better prognosis
List some types of muscular dystrophy:
Duchenne
Beckers
Myotonic
Oculopharyngeal
Limb girdle
