Endocrine Flashcards
1
Q
Hormone circulation
A
- Released from granules in the glands into bloodstream
- Hormone must not be bound to protein to leave circulation (measure both free and bound)
- Hormones may be activated or inactivated after gland release
2
Q
Endocrine regulation
A
- Direct vs indirect: is there an intermediary hormone or other mechanism involved? (indirect)
- Feedback vs feedforward: is response to a change after the change occurred (feedback) or before it occurred in anticipation for the change (feedforward)
- Controlling vs permissive: acutely causing the effect (controlling) or requires other machinery to have an effect (permissive)
3
Q
Endocrine dysfunction
A
- If hormone A is controlled by hormone B, and hormone A level is abnormal, there could be 2 possibilities
- Either hormone B (effector hormone) level is abnormal and resulting in the abnormal A level (inappropriate relationship)
- If the effector hormone (B) is responding accordingly to the abnormal level of A, then it is a primary dysfunction
4
Q
Measuring hormone amount
A
-Bioassay: measuring the effect of a crude extract
-Physiochemical assays: to detect unique physical and/or chemical properties of the hormone
Binding assays: immunodilution, immunocapture, fluorescence resonance energy transfer (FRET) all use Abs and hormone receptor analogs
-Immunodilution: add tagged hormone to assay (fixed receptors) then out-compete them w/ standard, measure amount needed to add
-Immunocapture: add hormone to assay, wash, then add tagged Ab for hormone to assay and measure how much Ab must be added
-Sandwich (FRET): Use 2 different Abs (both bind to hormone), one that requires 433nm to fluoresce (gives off 500nm) and one that fluoresces at 525nm but requires a different wavelength. When both are bound to hormone, the complex will use the 433nm and give off 525nm
-Things that can affect these tests: mutated hormones, degraded hormones, mutated/degraded binding proteins/Abs
5
Q
Measure rates of hormone production
A
- Measure venous-arterial difference in concentration across the gland
- Measure plasma turnover (using tracer)
- Measure urinary excretion product
6
Q
Contributions to obesity
A
- Difference btwn composition of fuel and the composition of food
- Relative amount of fat burned is less than the relative amount in food
- An RQ (respiratory quotient) greater than FQ (food quotient) can lead to obesity (quotients are amount of CO2 produced per O2 used)
- Thus a higher RQ means more glucose is being utilized as energy and not fat (RQ of glc = 1, RQ of fat = .7)
7
Q
Feeding cycles
A
- During the absorptive state carbs are the major source of energy. Proteins and glycogen are synthesized. Triglycerides are stored in adipose using G-3-P to make TAGs (either glucose or glycogen used to make G3P b/c adipose lack glycerol kinase)
- During this state carbs and AAs can be used to make fats via “anaerobic” glycolysis (thru AcCoA)
- Postabsorptive state: FAs are used for energy (glc is spared) except in nervous tissue and RBCs. Net release of FAs from adipose. Glc made in liver via GNG and glycogenolysis. Proteins are degraded and AAs converted into glc
- Starvation: Glc stores only sufficient for one day, fat stores can last over a month. Brain converts to ketone bodies
8
Q
Insulin in absorptive state
A
- Promotes glc uptake in muscle, reduces utilization of fat
- Promotes glycogen synthesis
- Promotes AA uptake and protein synthesis
- Promotes TAG storage in adipose (increased glc entry and inhibition of HSL)
- Hyperinsulemia can be a cause of obesity
9
Q
Regulation of insulin release
A
- Parasympathetic nerves from vagus, also release of incretins from GI distinguishes glc rise from food from a glc rise from hepatic output
- Sympathetic nerves inhibit insulin release, also epinephrine binds to mostly alpha adrenergic receptors (different from most tissues, which usually express more beta adrenergics)
10
Q
Insulin resistance
A
- For insulin to work it must be pulsatile; constant activation leads to desensitization
- Hyperinsulemia leads to insulin resistance
11
Q
Glucagon in the post absorptive state
A
- Fall of glc causes release of glucagon, which promotes FA release from adipose, and promotes glc release from liver (opposes insulin)
- Control: epinephrine promotes secretion
- Epinephrine also acts on muscle to increase glycogenolysis and lactate efflux. It promotes blood flow through adipose, lipolysis, and FA efflux
- Lack of epinephrine can lead to hypoglycemia
12
Q
Signals to CNS about food
A
- Ghrelin is released from the stomach containing an O-linked octanoyl side group, which is required for action on its CNS receptor
- Lesions to lateral hypothalamus cause anorexia, lesions to the ventromedial hypothalamus cause voracious overeating and obesity
- CNS controls adipose tissue in part by vagal control of insulin release
- Leptin is a protein that makes you want to eat less. Animals w/ leptin deficiency or mutated leptin receptors eat much more and are obese (works on the CNS)
- Leptin is from white adipose, leptin deficiency or resistance can lead to obesity
13
Q
Hypothalamus regulates endocrine functions
A
- Does so by portal system to pituitary (anterior only, posterior thru neurons)
- Releasing hormones released by hypothalamus cause pituitary to release effector hormones, which act on certain organs (peripheral glands). These glands in turn release other hormones which have activity throughout the body
- Negative feedback loops regulate endocrine activity (both to hypothalamus and pituitary)
- Releasing hormones from hypothalamus have ultra short loop (inhibit release of releasing hormones from the hypothalamus)
- Pituitary hormones have short loop and inhibit releasing hormone release from hypothal
- Peripheral gland hormones have long loops and act on both releasing hormones in hypothal and effector hormones from pituitary
14
Q
Dysregulation of endocrine signaling
A
- Can be primary dysfunction (only the peripheral gland is abnormal). In this case both the pituitary and the thypothal hormones will be compensating by changing levels appropriately
- Can be secondary dysfunction (either @ hypothal or pituitary). Distinction depends on the abnormalities of the other levels
- If the hypothal is abnormal, both down stream targets (pituitary effector hormones and peripheral gland hormones) will have abnormal values
- If pituitary is abnormal only the peripheral gland hormones will be abnormal, but the hypothal releasing hormone will change accordingly in an attempt to compensate (this is an inappropriate relationship)
15
Q
Organization of the adrenal gland
A
- Outer 80% is cortex, which synthesizes steroids (aldosterone, cortisol, androgens)
- Inner 20% is medulla which synthesizes catecholamines (epinephrine, norepinephrine)
- Sympathetic activation of gland results in synthesis and release of catecholamines
16
Q
Effects of epinephrine
A
- Epinphrine binds to both alpha and beta adrenergic receptors, but binds better to beta
- The effect of epinephrine on a tissue depends on: the ratio of a/B receptors and the concentration of epinephrine
17
Q
Examples of different effects of epinephrine
A
- In the pancreas there are much more alpha receptors than B receptors. Thus epinephrine mostly binds to the a receptors, causing decrease in both glucagon and insulin release
- In blood vessels a receptors lead to vasoconstriction and B receptors lead to vasodilation
- There are many more a receptors in peripheral CVS, so @ high concentrations of epinephrine most of the receptors bound are a and vasoconstriction results
- But at low concentrations of epinephrine, most of it is bound to B receptors due to the higher affinity, and vasodilation results
18
Q
Tumors of the adrenal medulla
A
-Pheochromocytoma leads to excessive release of epinephrine, which can lead to other problems like hypertension
19
Q
Regulation of steroid hormones synthesis
A
- Steroids are synthesized from cholesterol (C21 and C19 steroids). These are not stored but made upon activation of cAMP
- Steroid hormones are glucocorticoids (cortisol), mineral corticoids (aldosterone), androgenic (the C19 hormones, no role in men due to testosterone from testes)
- Androgenic hormones are converted to testosterone by peripheral tissues and has effects only in women. Made in the cortex in zone reticularis
20
Q
Adrenal mineralcorticoids
A
- Made in cortex, zona glomerulosa
- Acts on kidneys to retain Na and water
- Kidneys sense decrease in blood volume and release renin, which activates angiotensin I into active form, angiotensin II
- Angiotensin II stimulates release of aldosterone from adrenal glands
- Aldosterone promotes Na and water retention, K excretion
- Adrenal adenomas can constitutively secrete aldosterone, leading to depressed renin levels
