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Flashcards in General Endocrine Deck (76)
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Exocrine Gland

Secretes the chemical messenger or product onto the surface of an organ
*Mammary gland, sweat glands, etc.


Endocrine Gland

Produces a hormone and secretes it directly into the bloodstream


Types of Endocrine Glands (3)

1. CNS: Pineal gland, hypothalamus, pituitary gland
*Central endocrine glands

2. Outside of CNS: thyroid gland, adrenal gland, pancreas (pancreas is both endocrine and exocrine)
*Peripheral endocrine glands

3. Organs: kidney, heart


Lipid Soluble Hormones

Required to be bound to a plasma protein when released into the bloodstream

1. Steroid hormones
2. Thyroid hormones


Plasma proteins that bind to hormones (2)

1. Albumin
2. Hormone-specific binding proteins



Anything lipid soluble can bind to this; it has a very low affinity for hormones
*It binds and unbinds freely but binds long enough for hormones to travel using it


Hormone-Specific Binding proteins (5)

1. Testosterone binding hormones, estrogen binding hormones, etc.

2. The hormone is usually lipid soluble but doesn’t have to be, because the purpose of these proteins is to maintain a stable concentration of the hormone in the bloodstream

3. High affinity for the protein

4. Helps extend the half-life of a hormone in the bloodstream, because if they are bound to the protein they can’t be excreted, metabolized, or act on the target cells

5. Acts as a moving storage and maintenance of a stable concentration


Hormone Effects (2)

1. Dependent on the amount of free hormone in the plasma (equivalent or related to plasma concentration)

2. Non-bound form of hormones are available for metabolism, secretion, actions on target cells, etc.


Surface Receptor Hormones (2)

1. Water soluble hormones, because they can’t diffuse across the membrane

2. Activation of these receptors will trigger a second messenger system in order to bring about a response


Lipid-Soluble Hormone Receptors (2)

1. For fat-soluble hormones, because they can diffuse across the membrane

2. Usually found within the nucleus, which allows the hormone to affect gene expression
*The gene tends to lead to a physiological response


Pathology at site of secretion (3)

1. A gland can over produce or under produce a hormone for some reason

2. Result of over secretion: too much of the physiological response

3. Under-secretion: not enough of the physiological response


Pathology with plasma proteins

If you are under-expressing/not producing enough albumin, it affects the amount of hormone that can travel in the blood
*Same with hormone specific binding proteins


Pathology at sites of metabolism and excretion (3)

1. There are times when there is reduced renal or liver function, so that the rate of metabolism and excretion is impaired

2. If we turn down metabolism and excretion, there will be a higher plasma level of the hormone
*This is because rate of removal is going down

3. Will have the effect of too much physiological response of the hormone


Pathophysiology of Target Cell Sensitivity (3)

1. May have target cell problems that include receptors (not enough or defective receptors)

2. If receptors are defective, this will seem as under-production of the hormone (hypo) because the hormone may be there but it is unable to create the effect
LEADING TO........
3. Without the physiological response, there will be no negative feedback, so the endocrine gland gets the constant signal that there is not enough of the hormone and then over-produces the hormone
*Blood concentration of the hormone will be high
*Could lead to the gland eventually burning out
*Seen with type 2 diabetes and the pancreas


Pathophysiology of the second-messenger system

If a second messenger system is always switched on, it can look like a hyper problem
*Get too much physiological response, and endocrine secretion will go down because of the negative feedback


Anterior lobe of pituitary gland

Where most of the mass of the pituitary gland is
1. True endocrine structure
2. Has endocrine cells that produce hormones


Posterior lobe of pituitary gland

an extension of the hypothalamus


Connecting stalk

Connects hypothalamus and pituitary gland; any damage to this can cause serious endocrine system problems



Neurosecretory hormones in the hypothalamus, which produce two different hormones that get shuttled down the axon then stored in axon terminals located in posterior pituitary
*When stimulated, the hypothalamus releases the hormones in the posterior pituitary and then into the bloodstream


Hormones released by PVN and SON (2)

Oxytocin and Vasopressin

1. Oxytocin: part of female reproductive system, important in labor and delivery for uterine contractions
*Also important during breastfeeding (ejection of milk)
*When a woman is not in labor or nursing, oxytocin functions in men & women for social bonding
*Also part of female stress response

2. Vasopressin: ADH hormone


Relationship between hypothalamus and anterior pituitary

1st: Hypothalamus releases hypothalamic hormones that act on cells in the anterior pituitary controlling the release of anterior pituitary hormones

2nd: The anterior pituitary hormones enter general circulation and act on a third endocrine gland
*Several anterior pituitary hormones get released via control by the hypothalamus


Syndrome of Inappropriate ADH secretion (SIADH or hyper-ADH) (4)

The over-release of ADH

1. See it when people are experiencing intense injury, infection, activation of a stress response

2. ADH causes water retention when blood osmolarity is low/dilute
*Producing very concentrated urine

3. There is too much ADH release, and the release is being triggered by something other than plasma concentration/osmolarity

4. If your blood is dilute and urine is concentrated or if blood is concentrated and urine is dilute, it means something is wrong with ADH
*Because if ADH were normal and you had dilute (too much water) blood, your kidneys would be trying to get rid of water → so dilute blood would be along with dilute urine
*If you had concentrated blood, then kidneys would be trying to conserve it and urine would be concentrated


Causes of SIADH (6)

1. Increased hypothalamic production due to infections of the CNS, neoplasms, or drug induced (chemotherapeutics or antipyretics)
*Neoplasms: Abnormal growth of cells in the CNS, affecting the hypothalamus

2. Pulmonary Diseases that may cause hypoxia or hypoxemia (Pneumonia, Tuberculosis, ARF, Asthma)

3. Severe nausea and/or pain

4. Ectopic Production of ADH

5. Drug-induced potentiation of ADH

6. Idiopathic


Ectopic Production of ADH (6)

1. Ectopic cells are produced when there is a tumor, and they switch on the gene to produce hormone

2. Some cancers, especially lung and duodenal cancer, are associated with ectopic hormone production
*Common hormones that are over produced in this way: ADH, aldosterone

3. Oat cell carcinoma of lung

4. Bronchogenic carcinoma

5. Carcinoma of duodenum

6. The ectopic production of ADH is the least predictable and most difficult to control, because the ectopic production of the hormone doesn’t respond to negative feedback, so it produces hormone at whatever rate/times it wants


Clinical Manifestations of SIADH (5)

1. Serum hypoosmolarity and hyponatremia
*Dilute blood

2. Urine hyperosolarity
*Concentrated urine

3. Urine sodium excretion that matches sodium intake
*Check Na to rule out other problems

4. Normal adrenal and thyroid function

5. Absence of conditions that can alter volume status (like congestive heart failure, renal insufficiency, etc)


Type A Osmoregularity Defect (2)


1. Observed in 20%, large and unrelated fluctuations in AVP occur unrelated to the rise in plasma osmolality (usually occurs in association with tumors )

2. If you look at the relationship between blood osmolarity and ADH concentration, there is no relationship; random fluctuations, doesn’t coincide with one another; matches the ectopic production
*Normally there is a linear relationship and as blood osmolarity increases, ADH increases, and a blood osmolarity below a threshold will shut off ADH secretion


Type B Osmoregularity Defect (4)

RESET OSMOSTAT; Changing of the set-point

1. Observed in about 35%, a prompt and parallel rise in AVP with plasma osmolality, but a significant lowering of the threshold for release is present.

2. Pattern is consistent with an osmoreceptor reset at a lower-than-normal level. (pulmonary disorders)

3. There is a resetting of the osmo-stat; so instead of it being at 280, it may have moved down to 275, etc. but the relationship between the rise in osmolarity and release slope has stayed the same, but the line has just moved over
*The normal threshold for ADH secretion is 280 mOsm, so if someone is at 275 then there ADH release will be 0
*Blood has to have at least 280 blood concentration for there to be any ADH release

4. Typical of pulmonary disorder problems


Type C Osmoregularity Defect


1. Observed in 35%, AVP is persistently elevated at low and normal plasma osmolality; however, above the threshold for AVP release, plasma AVP increases normally. This pattern is observed with meningitis or head injuries.

2. No matter where you are (even if you are below threshold) you always have a little leaking of ADH

3. Very typical of hypothalamic problems (meningitis, encephalitis); the hypothalamus is leaking


Type D Osmoregularity Defect (4)


1. Observed in 10%, plasma AVP is appropriately suppressed under hypotonic conditions and does not rise until plasma osmolality reaches the normal threshold level; it does not result in maximal urinary dilution. Pattern is consistent with an increased renal sensitivity to vasopressin.

2. Absolute ADH concentration may be normal, but the body seems to be over-responding to it, so you get increased renal sensitivity

3. The person can never really achieve maximal urinary dilution (urine osmolarity of 100) because their kidneys are still responding to ADH

4. Typical of drugs that potentiate the affects of ADH


Diabetes Insipidus (5)

1. A problem of not enough ADH; either you aren’t producing enough or the kidneys aren’t sensitive to it
*A failure to secrete central ADH

2. Too much urine production causing dehydration and extreme thirst
*Characterized by the excretion of large volumes of dilute urine

3. Urine output can be anywhere from 4-8L/day or 8-12L/day

4. High urinary volume will make the person extremely thirsty, so they will consume high amounts of water but still be extremely thirsty (polyuria and polydipsia)

5. Plasma osmolarity is very high (while urine osmolarity is very low)