Term
| glomerulosa layer of the adrenal gland |
|
Definition
| Just underneath the capsule, the glomerulosa “layer” produces the mineralocorticoid, aldosterone, the hormone required for salt balance. |
|
|
Term
| fasiculata layer of the adrenal gland |
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Definition
| produces the glucocorticoid, cortisol, one of the key stress hormones. Some adrenal androgens also may be manufactured there. |
|
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Term
| Reticularis layer of the adrenal gland |
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Definition
| May synthesize some adrenal androgens, also potentially some cortisol. |
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Term
| Layers of the adrenal cortex |
|
Definition
| Just underneath the capsule, the glomerulosa “layer” produces the mineralocorticoid, aldosterone, the hormone required for salt balance. The next “layer” down (fasciculata) produces the glucocorticoid, cortisol, one of the key stress hormones. Some adrenal androgens also may be manufactured there, though they mostly come from the third later, the reticularis, which also may synthesize some cortisol. These three layers comprise the adrenal cortex. |
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Term
|
Definition
| Located in the innermost part of each adrenal gland is a different endocrine gland, the adrenal medulla. This really is an extension of the Autonomic Nervous system. Its primary secretion is epinephrine (ca 80%) with norepinephrine making up the balance. |
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Term
| What is important about the the vasculature and flow direction through the adrenal gland? |
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Definition
| Some of the blood traversing the outer layers, most particularly the fasiculata layer making cortisol next passes through the adrenal medulla. The consequence is that cortisol coming from the cortex immediately baths the medulla. Key here is that cortisol induces / activates the enzymes responsible for making epinephrine. This is just one reason the secretion of these two stress hormones often is so tightly coupled. |
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Term
| What else is found in the reticularis layer of the adrenal gland, other than glucocorticoid production (cortisol)? |
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Definition
| Here we find the necessary enzymes for its synthesis from a cholesterol precursor. Here, too, are located surface receptors for the hormonal signal governing cortisol production, Adrenocorticotropic Hormone, or ACTH. |
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Term
| What are some characteristics of people who hyper-secretion of cortisol? |
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Definition
| Overweight. A major cause of this is increased food intake. The fat burden primarily is located axially, along the trunk. Hence the characteristic “moon face” and “buffalo hump” at the back of the neck. |
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Term
| Individuals with high levels of cortisol have a much higher incidence of what disease? |
|
Definition
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|
Term
| What is the effect of excess cortisol on bones? |
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Definition
| The bones are degraded. The reason for this basically is the same as for the skin purple striae: cortisol in this case is destroying the connective tissue elements of bone in / on which bone mineral is deposited. |
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Term
| What is the physiological purpose of cortisol? |
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Definition
| A key stress hormone needed for the body to respond to any kind of stress from running a marathon to taking an HSF exam. It MUST be present in order for the body and its organs to respond to any kind of homeostatic challenge. Its level does not necessarily have to rise, but it MUST be there. |
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Term
| What happens to the cardiovascular system, kidneys, and liver if cortisol is absent? |
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Definition
| If cortisol is absent, the cardiovascular system cannot adapt to exercise, which will cause collapse. The kidney cannot adjust its output of urine after the afflicted individual has become severely dehydrated or has drunken too much water (or beer). The liver responds poorly when called upon by epinephrine to release glucose. For these homeostatic challenges to be handled appropriately, cortisol must be present. |
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|
Term
| What is cortisol's effect upon glucose? |
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Definition
| exerts a glucose sparing action, just as you should recall Growth Hormone does. This helps assure a supply of glucose for the brain and, as for Growth Hormone, has a lot to do with increased fat products in the blood (due to over-eating). |
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Term
| How is cortisol an energy provider? |
|
Definition
|
|
Term
| What is the negative feedback loop for cortisol? |
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Definition
| Very similar to the system for the thyroid. Cortisol is the key negative feedback signal, again, exerting its effect on the pituitary by regulating the number of CRH receptors. |
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Term
| What are the general effects of exess cortisol? |
|
Definition
1. Suppression of Immune and inflammatory reactions.
2. Breakdown of Connective Tissue and Bone.
3. Metabolism (see below): increased incidence of Diabetes Mellitus.
4. Excess can have mineralocorticoid effects on electrolytes (due to structural similarities between cortisol and aldosterone). |
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Term
| What are the general effects of exess cortisol on foodstuff metabolism? |
|
Definition
Protein
Increased muscle protein breakdown: muscle wasting
Increased synthesis of liver gluconeogenic enzymes
(e.g. transaminases)
Carbohydrate
Increased gluconeogenesis from protein
Reduced glucose uptake by muscle
Increased appetite
Fat
Peripheral mobilization
Central (“axial”) deposition
Increased appetite (“Buffalo Hump”)
Increased appetite: body weight/
Fat increases |
|
|
Term
| Androgenic hormones from the adrenal cortex are regulated in part by what key hormone? |
|
Definition
| Adrenocorticotropic hormone (ACTH) |
|
|
Term
| Mature ACTH still retains what type of enzymatic activity? |
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Definition
| The sequence for a skin tanning hormone, melanocyte stimulating hormone (MSH) is present in the cortisol sequence. Cortisol retains some of this activity. |
|
|
Term
| What is the diurnal rhythym of cortisol? |
|
Definition
| There is a very pronounced diurnal rhythm, driven by the CNS set-point. Cortisol levels are relatively high in the morning and very much lower in the evening. This is somewhat analogous to having a day-night thermostat in your home, such that the temperature (setpoint) automatically is lowered in the evening and then raised in the morning (though don’t take the analogy too far). It is critical, therefore, that the diagnostician know exactly when a blood sample was taken for measurement of cortisol (or ACTH). One of the problems of changing time zones is the problem of moving the timing of the morning cortisol secretory peak. |
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|
Term
| What is the "episodic" release of ACTH? |
|
Definition
| It is very much episodic. This, in turn, reflects episodic release of the releasing hormone for ACTH coming from the hypothalamus (CRH). Episodic release is critical to proper function of this endocrine feedback loop. You first learned of this concept in CMB where the importance of FM signaling was discussed, as compared with AM signaling. As you may also recall, and as you will hear again in the reproduction section of HSF, episodic / FM signaling is required for the reproductive control system to work. |
|
|
Term
| What are the qualities of visceral fat? |
|
Definition
High Concentration of
Cortisol Receptors
Can make Cortisol
Cortisol has selective effects on
visceral fat
- Promotes fat cell
differentiation
Visceral fat is a hugely important
endocrine organ |
|
|
Term
| What is the key hormone for managing salt balance? |
|
Definition
| The mineralcorticoid, aldosterone, as synthesized by the glomerulosa. |
|
|
Term
| What are the effects of aldosterone deficit? |
|
Definition
- Sodium loss
- Potassium retention
- Death |
|
|
Term
| What are the effects of aldosterone excess? |
|
Definition
- Sodium retention
- Potassium loss
- Hypertension |
|
|
Term
| What are the key effects of aldosterone? |
|
Definition
- Blood Volume control
- Sodium Retention
- Potassium Loss |
|
|
Term
| What electrolyte generally determines blood volume? |
|
Definition
| With rare exception, it is sodium, by its osmotic properties that determines blood volume. Where sodium goes, water also must go. So high blood levels of sodium mean / cause high blood volume. Low sodium levels mean / cause low blood volume. |
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|
Term
| What is the most general form of the aldosterone secretion feedback loop? |
|
Definition
The juxtaglomerular apparatus is right where blood coming into the working part of the kidney, the nephron, is filtered. The cells of the juxtaglomerular apparatus respond to changes in blood volume. Abnormally low blood volume distorts the cells in such a way as to cause them to release a key substance, renin. That means the JGA is sensitive to sodium levels in the blood.
Low sodium means low volume which calls forth renin. This ultimately will cause aldosterone release which will cause sodium retention by the kidney, correcting the problem. |
|
|
Term
| How is the liver involved in the aldosterone secretion feedback loop? |
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Definition
| The normal liver is producing a precursor hormone constantly. Known as angiotensinogen, this molecule, once modified will have the capacity to elicit aldosterone release from the kidney. Renin has proteolytic activity and converts the angiotensinogen to angiotensin-I (A-I). A second enzyme, Angiotensin Converting Enzyme (ACE) must convert A-I to Angiotensin-II (A-II). ACE is located in the blood vessel endothelium, especially in the lung, a logical place as all blood passes through the lung in one complete pass of the circulation. It is A-II that drives aldosterone release. The result will be a rise in blood sodium and, therefore, blood volume. |
|
|
Term
| How is angiotensin involved in regulating blood volume? |
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Definition
| Though normal regulation of vascular tone is the province of other regulatory mechanisms primarily involving the ANS, angiotensin can be called upon in emergencies. As blood volume falls, so does blood pressure, unless A-II vasoconstriction is accomplished. Additional roles of the hormone include regulation of thirst, cardiac hypertrophy and vascular remodeling. |
|
|
Term
| What is the second stimulus for aldosterone secretion (other than sodium levels)? |
|
Definition
A second stimulus for aldosterone secretion is potassium. This is a direct action on the adrenal gland. In fact the aldosterone secreting cell is considerably more sensitive to changes in potassium than sodium. You recently have learned (cardiovascular section of HSF) that changes in blood potassium have devastating effects on the heart.
Finally, an important input to the JGA renin-secreting cell is input from the ANS via β-receptors. This is an important additional mechanism for preserving blood volume. |
|
|
Term
| How is the regulation of angiotesin-II receptors special? |
|
Definition
| Most surface acting hormones DOWN-regulate their surface receptors: recall CMB and the reminder about this in the Endocrine Introduction lecture. The angiotensin receptor is different. It is so important to restore blood pressure / volume that the angiotensin receptor is a locus of positive feedback: increasing levels of angiotensin in the blood UP-regulate the number of functional angiotensin receptors. |
|
|
Term
| What is aldosterone's mechanism of action? |
|
Definition
| Aldosterone works a number of ways on the kidney to assure proper sodium recovery. It increases the amount and activity of a sodium-potassium exchange pump the moves sodium out of and potassium into the forming urine. It also increases the amount and activity of the sodium-potassium ATPase enzyme necessary to continue sodium on its way back into the circulation. |
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|
Term
| What are the key "fight or flight" effects of EP/NE? |
|
Definition
1. Cardiovascular System: heart -- increased force and rate of contraction; redistribution of blood flow away from skin, GI tract, kidney by vasoconstriction.
2. Lung: increased rate and depth of breathing; bronchiolar dilatation.
3. Sweating.
4. Anxiety.
5. Increased overall metabolism: increased oxygen consumption. |
|
|
Term
| What are the key metabolic effects of EP/NE? |
|
Definition
Carbohydrate:
Liver Glycogen mobilization, gluconeogenesis
Muscle glycogen mobilization
Fat:
Increased lipolysis: mobilization
Protein:
Little or no effect |
|
|
Term
| What key hormones are synthesized in the adrenal medulla? |
|
Definition
| Epinephrine and norepinephrine |
|
|
Term
| How is the release of EP and NE from the adrenal medulla controlled? |
|
Definition
| By the hypothalamus via the splanchnic nerve |
|
|
Term
| What are the KEY effects of epinephrine? |
|
Definition
Lipolysis
Glycogenolysis
Gluconeogenesis
Breakdown of glycogen in the liver and muscle occurs within minutes. Glycogenolysis delivers glucose to the blood in terms of liver output and provides glucose endogenously to muscle for energy.
If epinephrine levels remain elevated, there will be an increase in gluconeogenesis by the liver. This especially is possible if cortisol also is elevated (almost always the case) so that cortisol can engineer the delivery of amino acids from muscle protein breakdown to the liver to serve as the gluconeogenic precursor.
A second key arm of epinephrine action is to cause mobilization of adipose tissue fat reserves. This provides additional energy substrate for muscle and lever, in the case of the liver the energy from fat metabolism being used to drive energy-consuming gluconeogenesis. |
|
|
Term
|
Definition
- post. pituitary
- Hypothalamus sends messages via neurons to posterior pituitary gland (neurohypophysis)
- ADH (vasopressin) and oxytocin formed in nuclei in hypothalamus and sends to neurohypophysis |
|
|
Term
|
Definition
- Anterior part or pituitary
- Hypothalamic neurons have short axons that terminate on vascular portal (hypothalamic-hypophysial) system that directly connects hypothalamus and adenohypophysis
- Endocrine nature of signaling
- Releasing hormones travel this way to cause release of pituitary hormones known as trophic (or tropic) hormones |
|
|
Term
| Embryologic origin of pituitary |
|
Definition
- Posterior: neural tissues
- Anterior: from tissue in roof of the developing mouth |
|
|
Term
| Location of pituitary and clinical implications |
|
Definition
- Resides in sella turcica in head
- The bony cavity leaves little room for over-sized tissue and several other important nerves (some cranial, including optic) and circulatory pathways (carotids) are close by.
- Optic tracts are nearby so can lose visual acuity |
|
|
Term
|
Definition
- Released from neurophypophysis
- Antidiuretic hormone
Key to regulation of blood tonicity, though can play an emergency role in regulation of vascular tone |
|
|
Term
|
Definition
- From neurohypophysis
- Important in milk production at birth |
|
|
Term
|
Definition
1. Thyroid hormones
Adrenal gland hormones |
|
|
Term
| Negative releasing hormones |
|
Definition
- Come from hypothalamus (set point) as well as the releasing hormones
- Turn off pituitary (thermostat/feedback) as a consequence of build-up of the hormones (negative feedback mechanism) |
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|
Term
| Pituitary and feedback control (from beginning) |
|
Definition
Ex: thyroid hormone
1. CNS sends neurotransmitters to trigger hyoothalamus
2. Hypothalamus sends releasing hormones
3. Certain cells in pituitary give off TSH (appropriate trophic hormone)
4. Thyroid releases thyroid hormone
5. Thyroid hormone circulates and is ultra-specific feedback signal onto pituitary
6. In presence of excess hormone the pituitary decreases the receptors for releasing hormone (TRH)
7. Thryoid gland shuts down (less signal saying to release thyroid hormone) |
|
|
Term
|
Definition
- Of anterior pituitary
- Small proteins or glycoproteins
- Thought to come from unique cell type (except 2 for reproductive system - FSH and LH may come from same cell) |
|
|
Term
|
Definition
- Not ultra-specific
- Also locally produced elsewhere in body and subserve all sorts of interesting functions |
|
|
Term
|
Definition
- one of several key hormones responsible for overall body growth (only causes lengthening in children with active epiphyseal plates)
- also important in regulation of
carbohydrate and fat metabolism
1. growth promoter
2. fat mobilizer
3. glucose sparer |
|
|
Term
|
Definition
- widening of bones in adulthood
- widening of bones and lengthening in childhood
- many acquire diabetes mellitus |
|
|
Term
| Growth hormone release and action |
|
Definition
1. hypothalamus releases GHRH (growth hormone releasing hormone) or GHRIH( AKA somatostatin)
2. anterior pituitary regulates secretion of GH depending on hypothalamus signals
3. GH then acts on liver to produce signal molecules called somatomedins (insulin-like growth factors - IGFs) which go to skeletal muscle and cause growth effects of hormone
4. GH also directly effects fat and carbohydrate metabolism |
|
|
Term
| Negative feedback of growth hormone system |
|
Definition
- exerted by somatomedin/IGF levels as well as blood levels of foodstuffs (esp blood glucose that are affected by GH)
** GH itself is not the feedback regulator |
|
|
Term
| Factors affecting GH secretion |
|
Definition
1. sleep increases GH
2. exercise increases
3. amino acid consumption increases GH
4. Hypoglycemia increases
5. Somatomedins (IGFs) INHIBIT
6. Fatty acids INHIBIT
7. Hyperglycemia INHIBITS |
|
|
Term
|
Definition
- agents of GH for the growth process
- produced in the liver and then circulate to skeletal tissue to cause their growth |
|
|
Term
|
Definition
- local, organ-specific growth
- ex: needed when part of an organ has been removed
- not from liver
- never reach general circulation ut rather act in paracrine fashion to cause local organ growth |
|
|
Term
| Fasting and IGF secretion |
|
Definition
| - liver decreases output of IGF when GH levels are elevated |
|
|
Term
| Longitudinal bone growth in adults with high GH levels |
|
Definition
| - only in ribs, the rest of the bones are restricted by calcified epiphyseal plates |
|
|
Term
|
Definition
- causes changes in carb metabolism
- blocks glucose uptake by muscle (specifically insulin-sensitive)so it is spared for other purposes/organs
- thus causes tendency toward
- hyperglycemia
- causes mobilization of fat stores to fuel the body while sparing glucose (muscle actually prefers fat energy to glucose)
- fat products in blood also block glucose uptake by muscles by themselves by blocking insulin action |
|
|
Term
| Relationship of fat insulin and growth hormone |
|
Definition
- antagonists
- also insulin and insulin are synergists for growth: GH increases protein synthesis while insulin mostly reduces protein breakdown |
|
|
Term
| How does growth hormone work |
|
Definition
1. tyrosine kinase-associated receptor binds GH
2. the receptor becomes associated with a membrane-located tyrosine kinase (JAK) leadig to activation of signal molecules like STAT |
|
|
Term
| Diagnosing thyroid disorders |
|
Definition
- inject radio-iodide and it should accumulate in the thyroid gland because the thyroid gland is excellet at taking up iodide from blood and make thyroid hormone
- then scan to see if the lobes are symmetrical, if there are hotspots etc |
|
|
Term
|
Definition
- abnormality, even tumor in thyroid, but the the rest of the thyroid that is still functioning is able to maintain proper thyroid hormone levels
- patient may just present for the cosmetic problem of an enlarged neck |
|
|
Term
| Signs of excess thyroid hormone (T3, T4) |
|
Definition
1. heat intolerance
2. CNS changes
3. Sweating
4. Hyperglycemis
5. Muscle catabolism
6. exopthalmos (possibly due to TSH)
7. Cardiovascular axis activity (increased but efficiency decreased)
8. BMR increased |
|
|
Term
| Signs of decreased thryoid hormone (T3, T4) |
|
Definition
1. lipemia
2. cholesterolemia
3. cold intolerance
4. myxedema
5. obesity
6. slow speech
7. poor cardiovascular axis function |
|
|
Term
| Key functions of thyroid hormone |
|
Definition
1. development (Brain)
2. BMR
3. Synergy with the ANS |
|
|
Term
| Thyroid hormone release/control steps |
|
Definition
1. Higher CNS give pos or neg stimulus to hypothalamus
2. hypthalamus releases TRH to adenohypophysis to stimulate and ST (somatostatin)to inhibit
3. Adenohypophysis releases TSH (thyroid stimulating hormone) to thyroid gland
4. thyroid gland releases T4 (thyroxine) and T3 (triiodothyronine)
5. T3 is a negative feedback molecule on adenohypophysis
6. T4 also gives off more T3 and rT3 (reverse T3) |
|
|
Term
| Thyroid stimulating hormone |
|
Definition
- from adenohypophysis
- causes growth (for more release of hormone) of thyroid gland and release of T4 and T3
- DETERMINES SIZE OF THYROID GLANDS |
|
|
Term
|
Definition
- T4 because each molecule has 4 iodides attached to it
- biologically inactive
- has the ability to convert to active T3 as well as rT3 in peripheral tissues |
|
|
Term
|
Definition
- T3 because it has 3 iodides
- biologically active
- negative feedback on pituitary |
|
|
Term
|
Definition
- rT3
- an iodide has been removed in the wrong place to create a biologically inactive molecule
- happens regularly when T4 goes to rT3 the tissues decide whether they get T3 (active) or rT3 |
|
|
Term
|
Definition
- circular structures in thyroid gland
- filled with thyroiglobulin |
|
|
Term
|
Definition
- on basal surface of epithelial cells in thyroid gland
- concentrates iodide in the epithelial cell some 20x over that in general circulation |
|
|
Term
|
Definition
- TG
- on rough endoplasmic reticulum of epithelial cells on thyroid follicles
- will be secreted
- high content of tyrosine which makes T4 and T3 |
|
|
Term
| Thyroid peroxidase enzyme |
|
Definition
- at apical surface of epithelial cell helps iodide covalently link with tyrosine residues on thyroglobulin molecule
- creates mono-iodotyrosine (MIT) or di-iodotyrosine (DIT)
- then the tyrosine can bind to another tyrosine
- if both tyrosines are DIT then together they form T4, MIT and DIT form T3 |
|
|
Term
| Storage of thyroid hormones |
|
Definition
- unique storage of up to a several week supply of potential throid hormone
- T3, T4 exocytosed into follicular space |
|
|
Term
| Release of stored thyroid hormones |
|
Definition
1. some TG with MIT, DIT, T4, and T3 within its structure is endocytosed at apical surface of epithelial cell
2. endosome then fuses with lysosomes so all peptide bonds in thyroglobulin are hydrolyzed leaving free MIT, DIT, T4, and T3
4. T4 and T3 are diffuse out of cell and MIT and DIT are recycled to capture idodide |
|
|
Term
| Defects in MIT and DIT recycling pathway |
|
Definition
- known to cause hypothyroid disease
** important to iodide management by thyroid epithelial cell |
|
|
Term
|
Definition
- well-known sign of thyroid deficiency during embryonic development
- key defect is lack of normal nerve myelination |
|
|
Term
|
Definition
- maintains normal BMR in adults
- controls levels by regulating the rate of movemet of energy substrates through their respective metabolic pathways
- increased thyroid hormone speeds up synthesis and degradative pathways (deg. more)
- increased demand for ATP and thus more heat production
- degradative pathway sped up the most so when TH elevated one loses stores of carbs, fat, and protein (to make the ATP) and wastes away |
|
|
Term
| Why do blood levels of lipids fall in hyperthyroid disease? |
|
Definition
| - there is an increased mobilization of lipids from fat stores, but the metabolism is using them up faster than they are being mobilized |
|
|
Term
| Cannot force feed metabolism |
|
Definition
- in hyperthyroidism the metabolic rate is increased and it requires more ATP
- ATP cannot be produced by increasing calories, but depends on the ADP concentration, the energy charge of the cell
- utilize fat, carb, and proteins to make the ATP |
|
|
Term
| Thyroid hormone and Na+/K+ -ATPase |
|
Definition
- regulates the level of this in plasma membrane
- this enzyme alone may be responsible for upwards of 30% of the ATP used in normal living |
|
|
Term
| Thyroid hormone and body temperature |
|
Definition
- primarily ANS and blood control not thyroid hormone
- plays a role in extreme temperatures like adjusting after being born or cooling children's bodies for surgery to extremem temps |
|
|
Term
***EXAM QUESTION***
Why do individuals with thyroid hormone disorders respond with more or less sensitivity to epinephrine than healthy individuals? |
|
Definition
- epinephrine works via adenylyl cyclase second messenger system
- here beta receptor activation turns on Gs which leads to a rise in cyclic-AMP
- GI is the cyclase inhibitory pathway
- increased thyroid hormone leads to a fall in Gi removing the normal braking force for beta receptor activation |
|
|
Term
| Assessing a feedback control system |
|
Definition
1. acquire accurate and complete history
2. measure key elements of endocrine system for thyroid: T3 and TSH (TRH is not in systemic circulation only in hypo-pituitary portal system
3. challenge system to see if it responds appropriately. Ex: give TSH and see what happens to T3 or give T3 and see what happens to TSH, or give TRH and look at TSH, o radio-active iodide |
|
|
Term
|
Definition
| - due to thyroid gland itself |
|
|
Term
|
Definition
| - due to the pituitary gland |
|
|
Term
|
Definition
1. critical role in digestion and later assimilation and use by body
2. delivery of bicarbonate to neutralize stomach acid coming into the small intestine
3. produces digestive enzymes |
|
|
Term
| Consequences of lack of insulin |
|
Definition
1. acidosis
2. dehydration
3. electrolyte loss leading to coma and death
- all due to reduced glucose uptake, principally in muscle also from mobilization of fat stores increasing blood sugar levels |
|
|
Term
| Blood glucose and kidneys |
|
Definition
- kidney's job is to reabsorb all glucose so it is not excreted
- reliant on special glucose transporter in epitherlium and it has a finite capacity
- when blood sugar is high (when defective insulin for ex) it cannot all be recovered and some is in urine
- gluose is osmotically active: traps water and electrolytes and brings them out in the urine dehydrating the body
- loss of energy also makes one hungry like loss of insulin does directly |
|
|
Term
| Cosequences of mobilization of fat stores during insulin deficiency |
|
Definition
- build-up of acid products in blood causing acidosis
- lung tries to compensate by blowing off CO2
- increased rate and depth of respiration is a sign of poorly controlled disease |
|
|
Term
| Muscle wasting from insulin deficiency |
|
Definition
| - protein can be used as energy source causing rapid muscle wasting |
|
|
Term
| Insulin counter-regulatory homones when low insulin |
|
Definition
| - although they should stop being produced the mechanisms sensing glucose in blood do not work and even though blood glucose levels are high these hormones are released causing further elevation |
|
|
Term
| Hormones that cause a rise in blood sugar |
|
Definition
1. glucagon
2. growth hormone
3. cortisol
4. epiephrine |
|
|
Term
| Principal targets of insulin |
|
Definition
1. Liver
2. adipose
3. muscle |
|
|
Term
|
Definition
1. hypoglycemia
2. convulsions
3. coma |
|
|
Term
| Insulin-dependent diabetes mellitus |
|
Definition
- Type I
- pancreas stops making insulin
- at some point in childhood beta cells begin to be recognized as foreign and are destroyed
- genetic predisposition
- accounts ofr 5% of diabetes mellitus in the world |
|
|
Term
| Non-insulin dependent diabetes mellitis |
|
Definition
- type II diabetes
- reduced ability of body to respond to insulin, followed by pancreas losing ability to synthesize and secrete it
- some small genetic predisposition, but main cause is obesity |
|
|
Term
| Insulin as storage hormone |
|
Definition
| - as a storage hormone it promotes utilization and storage of incoming carbs, fat and protein |
|
|
Term
| Insulin's effect on glucose and the Liver |
|
Definition
- free transport in, no insulin needed
- insulin promotes conversion of glucose to glycogen and prevents glycogen breakdown in liver
- also prevents synthesis of glucose from amino acids in liver |
|
|
Term
| Mechanism by which insulin increases glucose uptake |
|
Definition
| - does not increase transporters but causes re-location of current transporters to surface of muscle (and fat) cell |
|
|
Term
| Insulin and fat deposition |
|
Definition
- key hormone for fat deposition promotes uptake of triglycerides by fat tissue but also blocks their release
- In order to cross plasma membrane of fat cells, triglycerides must be broken down by an endothelial cell lipase into their building blocks: glycerol and fatty acids
- once in fat cell the building blocks are re-synthesized into triglyceride
- insulin stimulates endothelial cell lipase and inhibits intracellar lipase (used to export triglycerides from fat cells) |
|
|
Term
| Insulin as growth hormone |
|
Definition
- required for optimal deposition of protein
- most prominent effect here is to block muscle protein degradation |
|
|
Term
| Long-term consequences of diabetes mellitus |
|
Definition
1. serious neuropathies
2. impaired vision
3. kidney failure
- due to small vessel disease and poorly mannaged blood glucose |
|
|
Term
|
Definition
- most prominent feedback signal is glucose (negative feedback loop)
- amino acids also play a role
- the ANS also fine-tunes insulin
- epinephrine blocks insulin release through alpha receptors (don't wnat to store calories at a time when stress demands their use)
- gastointestinal hormones released as part of digestions process reinforce insulin release |
|
|
Term
| Insulin's effect on plasma membrane ion pumps |
|
Definition
1. very rapidly causes uptake of potassium into many cells of body accompanied by sodium release
- acts like aldosterone causing kidney to retain sodium and dump potassium |
|
|
Term
| Aldosterone and insulin deficiency rescue |
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Definition
- aldosterone would help with the potassium loss, but it would take a couple of hours because it works via intracellualr receptors and nuclear transcription
- the potassium loss is disastrous on heart
- it's why you need to inject insulin (to treat hyperkalemia) |
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Term
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Definition
- tyrosine kinase
- need to be phosphorylated (both kinase receptor and key signal molecules that bind it) to be effective |
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Term
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Definition
- fastest of all known hormones causing liver glycogenolysis delivering molecules of glucose to blood in seconds
- also helps boost ability of the liver to oxidize fatty acids, especially in absence of insulin
- acts through plasma membrane receptors, specifically on cyclic-AMP second messenger system
- inositol phosphatide pathway also affected by glucagon |
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