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Patho 2 Exam 2 > General Endocrine > Flashcards

General Endocrine Flashcards

1
Q

Exocrine Gland

A

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

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2
Q

Endocrine Gland

A

Produces a hormone and secretes it directly into the bloodstream

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3
Q

Types of Endocrine Glands (3)

A
  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
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4
Q

Lipid Soluble Hormones

A

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

  1. Steroid hormones
  2. Thyroid hormones
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5
Q

Plasma proteins that bind to hormones (2)

A
  1. Albumin

2. Hormone-specific binding proteins

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6
Q

Albumin

A

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

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7
Q

Hormone-Specific Binding proteins (5)

A
  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
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8
Q

Hormone Effects (2)

A
  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.
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9
Q

Surface Receptor Hormones (2)

A
  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
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10
Q

Lipid-Soluble Hormone Receptors (2)

A
  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
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11
Q

Pathology at site of secretion (3)

A
  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
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12
Q

Pathology with plasma proteins

A

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

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13
Q

Pathology at sites of metabolism and excretion (3)

A
  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
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14
Q

Pathophysiology of Target Cell Sensitivity (3)

A
  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
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15
Q

Pathophysiology of the second-messenger system

A

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

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16
Q

Anterior lobe of pituitary gland

A

Where most of the mass of the pituitary gland is

  1. True endocrine structure
  2. Has endocrine cells that produce hormones
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17
Q

Posterior lobe of pituitary gland

A

an extension of the hypothalamus

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18
Q

Connecting stalk

A

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

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19
Q

PVN and SON

A

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

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20
Q

Hormones released by PVN and SON (2)

A

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
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21
Q

Relationship between hypothalamus and anterior pituitary

A

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

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22
Q

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

A

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
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23
Q

Causes of SIADH (6)

A
  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
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24
Q

Ectopic Production of ADH (6)

A
  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
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25
Q

Clinical Manifestations of SIADH (5)

A
  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)
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26
Q

Type A Osmoregularity Defect (2)

A

RANDOM

  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
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27
Q

Type B Osmoregularity Defect (4)

A

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
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28
Q

Type C Osmoregularity Defect

A

LEAK

  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
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29
Q

Type D Osmoregularity Defect (4)

A

DECREASED RENAL SENSITIVITY

  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
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30
Q

Diabetes Insipidus (5)

A
  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)
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31
Q

Central Diabetes Insipidus

A

Can’t produce ADH, primary secretory malfunction; most common

32
Q

Nephrogenic Diabetes Insipidus

A

Insensitivity to ADH at the level of the kidneys

33
Q

Non-genetic Cause of DI

A

Most common

Typical injuries include head trauma, tumor, and neurosurgical procedures. At all ages, destructive lesions of the pituitary and/or hypothalamus are the most common cause of DI
*Injury is most common cause→ can injury connecting stalk severing the hypothalamus connection to the pituitary

34
Q

Genetic Cause of DI (4 types)

A
  1. CDI with an autosomal dominant pattern inheritance is due to a mutation in the prepro-arginine vasopressin (prepro-AVP2) gene
  2. CDI with diabetes mellitus, optic atrophy, and mental retardation (Wolfram syndrome) may be inherited in an autosomal recessive pattern
  3. X-linked NDI occurs from mutations in the antidiuretic arginine vasopressin V2 receptor (AVPR2) gene, mapped to Xq28.
    * In X-linked disorders, if the male gets the X from the mother and it is affected, there is no X to fall back on, and they will get the disease
  4. NDI with an autosomal dominant or recessive pattern is due to mutations in the gene designated AQP2; this gene directs water channel formation in the distal tubule
35
Q

Treatment for Central DI

A

Desmopressin (synthetic form of ADH)

36
Q

Treatment for Nephrogenic DI

A

more complicated, paradoxical treatment, because the primary pharmacological treatment is a thiaside diuretic

*Diuretic usually would cause urine production/water loss, but the thiaside diuretic with NDI will cause a side effect of increased water reabsorption at the proximal tubule (give the drug to get the side effect); will need to monitor water intake vigilantly

37
Q

Serum ADH Levels with DI (central and nephrogenic)

A

Central DI: decreased ADH

Nephrogenic DI: normal or ADH

38
Q

Psychogenic DI (3)

A
  1. Associated with psychiatric disorders that involve acute delerium in episodes of psychosis
  2. In the course of an acute delirium, a person will have an insatiable thirst and consume large volumes of water; may appear like central DI
  3. Urinalysis is dilute, but plasma osmolarity is very dilute
39
Q

Hypopituitarism (8)

A
  1. Pituitary Tumors (Adenomas)
  2. Pan hypo-pituitarism: none of the hormones are being produced
  3. Sheehan Syndrome: can be a complication of labor and delivery
  4. Iatrogenic Hypopituitarism
  5. Trauma
  6. Infiltrative Diseases
  7. Genetic Abnormalities of Pituitary Development
  8. Growth Hormone Insensitivity (Laron Syndrome)
40
Q

Pituitary Tumors Leading to Hypopituitarism (3)

A
  1. Benign tumors that grow in the anterior pituitary; primary cause of hypo and hyperpituitarism
  2. For hyperpituitarism: pituitary overproduces hormone
  3. For hypopituitarism: the tumor grows very large and compresses the pituitary against its surrounding capsule, damaging the gland
41
Q

Sheehan Syndrome

A
  1. Can be a complication of labor and delivery
  2. The entire anterior pituitary has suffered ischemic damage and necrosis and no longer produces hormones (pan hypo-pituitary associated with post-partem hemorrage)
  3. If anterior pituitary gets enlarged (due to large hormone production), immediately after delivery a women is vulnerable to hemmorhage → when this happens, the enlarged pituitary is vulnerable to ischemic damage
42
Q

Iatrogenic Hypopituitarism

A

Usually a result of neurological surgeries that inadvertently damage connective stalk or hypothalamic sites

43
Q

Genetic Abnormalities of Pituitary Development

A

In development of the pituitary cells, some may be defective and not produce hormones

44
Q

Growth Hormone Insensitivity (Laron Syndrome)

A

Target cell insensitivity, causes laron dwarfism

45
Q

Types of Hyperpituitarism Pituitary Tumors (3)

A
  1. Acidophil – associated with oversecretion of GH
  2. Basophil – associated with oversecretion of ACTH
  3. Chromophobe – no endocrine hyperfunction
46
Q

Lactotrope Adenoma (4)

A

Prolactinomas/type of hyperpituitarism pituitary tumor

  1. Over production of prolactin
  2. Most common pituitary adenoma
  3. Are microadenomas (Adenomas less than 10mm)
  4. More common in females than males
47
Q

Female Symptoms of Lactotrope Adenoma (3)

A
  1. Amenorrhea
  2. Galactorhea (production of breastmilk)
  3. Infertility
    (all of these are normal effects of prolactin)
48
Q

Male Symptoms of Lactotrope Adenoma (4)

A
  1. Decreased libido
  2. Erectile dysfunction
  3. Gynomastea (development of breasts)
  4. Breast milk production
49
Q

Corticotrope Adenoma (2)

A

hyperpituitarism pituitary tumor

  1. Microadenomas that produces excess ACTH
  2. Cushing Syndrome: syndrome of elevated glucocorticoids
50
Q

Gonadotrope Adenoma

A

hyperpituitarism pituitary tumor

  1. Macroadenomas that secrete LH and FSH
  2. LH and FSH control gonadal function (testicular function, ovarian function)
51
Q

Thyrotrope Adenoma

A

hyperpituitarism pituitary tumor

  1. rare – over secrete TSH
  2. If above 10mm in size, can cause non-specific symptoms
52
Q

Somatotrope Adenomas (6)

A
  1. Hyperpituitarism; overproduction and hypersecretion of growth hormone
  2. Type of macroedenoma 75% of the time

Manifests in two different ways depending on onset..

  1. If onset is pre-pubescent: gigantism
  2. If onset is post-pubescent: acromegaly
  3. Increased GH and insulin-like growth factor (IGF)
  4. Will have much higher likelihood of T2DM
53
Q

Acromegaly vs. Gigantism

A

See the difference because before puberty, our long bones have epithesis and epitheseal growth plate but those growth plates are ossified after puberty and there is no more longation of the bones

A) Gigantism: very tall, long extremities

B) Acromegaly: other signs of over growth of tissue, but no extreme stature

54
Q

Metabolic Effects of Somatotrope Adenomas (2)

A
  1. Increased metabolic rate, GH inhibition of glucose uptake and increased hepatic production of glucose (hyperglycemia)
  2. Increased risk of diabetes mellitus
55
Q

Clinical Manifestations of Excess GH (3)

A
  1. Elaboration/thickening of bone and connective tissue
    * Person will start to take on stereotypical facial features with pronounced jaw line, pronounced cheek bones, pronounced brow ridge
  2. Enlarged hands and feeet
  3. Increased size of joints
56
Q

3 Varieties of Thyroid Disorders

A
  1. Hypothyroidism
  2. Hyperthyroidism
  3. Euthyroid disorders: thyroid concentration is normal but there is an abnormality in the system
57
Q

Goiter

A
  1. A common sign of thyroid disorder; enlargement of the thyroid gland
  2. Can be associated with any type of thyroid disorder
  3. Whenever you have a goiter you have a problem of either too much TSH or too much of something acting like TSH
58
Q

Non-toxic goiter (3)

A
  1. Elevated TRH, elevated TSH, but normal levels of thyroid hormone
  2. The problem is in the thyroid itself, because it is taking more TSH than normal to produce a normal level of thyroid hormone
  3. People with non-toxic goiters will either become hyper or hypothyroid if the thyroid gland dysfunction continues
59
Q

Autoimmune Hypothyroidism (Hashimoto Thyroiditis) (4)

A
  1. Most common type of primary hypothyroidism
  2. Involves production of T cells and B cells that are autoreactive to thyroid gland cells
    * They are attacking antigens on the thyroid glands and this is causing accelerated death and hypothyroidism
  3. Will see elevated TRH & TSH and low thyroid hormone
    * Because problem is at level of thyroid gland
  4. May see goiter on presentation
60
Q

Post-radioactive iodine therapy for hyperthyroidism

A

Thyroid cells pick up iodine in the body, causing hypothyroidism

61
Q

Total or subtotal thyroidectomy

A

Thyroidectomy to clear thyroid cancer, causing hypothyroidism

62
Q

Other causes of hypothyroidism (6)

A
  1. Excess iodine, which is toxic to the thyroid
  2. Radiation therapy for head and neck cancers and lymphoma
  3. Iodine deficiency
  4. Congenital disorders of thyroid hormone synthesis
  5. Certain drugs
    * Lithium
    * Interferon alpha
    * Some antiepileptic drugs
  6. Diseases of the hypothalamus
63
Q

Thyroid Hormone (3)

A
  1. Primary effect of thyroid hormone is metabolic (metabolism & heat production)
  2. Part of stimulating metabolism for cells is also stimulating growth, so thyroid hormone also promotes growth of tissue (especially in utero)
  3. It also tends to elevate blood glucose
64
Q

Hypothyroidism Clinical Manifestations (8)

A
  1. Extreme fatigue
  2. Extreme intolerance to cold (always feels cold)
  3. Skin pallor, skinseem pale and sickly
  4. Hair will be coarse and brittle
  5. Tongue may be enlarged
  6. May see puffiness around the eyes
  7. Unique edema, form of non-pitting edema caused by water that binds itself to the extracellular matrix (connective tissue)
    * This can affect CNS and cardiac tissues
    * Myxedema
    * Enlargement of the heart and CNS function
  8. Fertility problems
65
Q

Myxedema

A

neurological manifestations of hypothyroidism edema; can involve confusion or depressed cognitive function, can lead to seizures and coma

66
Q

Causes of Hyperthyroidism (3)

A
  1. Presence of abnormal thyroid stimulator (graves disease)
    * Most common
  2. Intrinsic disease if the thyroid gland (toxic multinodular goiter or functional adenoma)
  3. Excess production of TSH by anterior pituitary (rare)
67
Q

Graves Disease (5)

A
  1. Most common cause of hyperthyroidism
  2. An unusual autoimmune disorder; producing autoreactive B cells that ultimately produce antibodies that bind to the TSH receptor on the thyroid gland and then stimulate the receptor
  3. Antibody acts as a TSH agonist and produces increased thyroid secretion and hyperthyroidism
    * Thyroid stimulating immunoglobulin (TSI) = the antibody
  4. Not controlled over any negative feedback loop
    * TRH and TSH will be low, thyroid hormone will be high
  5. Will often see a goiter caused by the antibody
68
Q

Graves Disease Clinical Manifestations (10)

A
  1. Very skinny (due to high metabolic rate)
  2. Sweaty
  3. Heat intolerant
  4. Agitated: high strung, constantly moving, etc.
  5. Tachycardia
  6. Goiter
  7. Fine, thin hair
  8. Muscle wasting
  9. Ovulation problems
  10. Exothalamos: bulging of the eyes due to retro-orbital edema
69
Q

Adrenal Gland and hormones it produces (3)

A

The outside of the adrenal gland produces steroid hormones:

  1. The glucocorticoids (cortisone, cortisol, etc)
    * Typical effects: elevated blood glucose, stress-related response
  2. Mineral corticoids (aldosterone)
    * Na and Water retention, K excretion, etc.
  3. Sex hormones (estrogen, progesterone, androgens)
70
Q

Congenital Adrenal Hyperplasia (CAH) (5)

A
  1. Biosynthetic impairment of the production of glucocorticoits that occurs in utero
  2. Deficiency is usually with 21-hydroxylase, which causes the buildup of intermediates and the increased production of androgens
    * 21-hydroxylase allows for conversion into glucocorticoids and then aldosterone
  3. The result of a number of autosomal recessive enzymatic defects in the biosynthesis of cortisol from cholesterol
  4. CAH is the most common cause of ambiguous genitalia in newborn girls
  5. Infant boys may experience sexual precocity and stunted growth
71
Q

Consequences of CAH 21-Hydroxylase Deficiency (2)

A
  1. Without cortisol production, hypothalamus will be over-producing CRH on pituitary and then pituitary is over-producing ACTH (because they keep trying to produce cortisol as part of the loop)
    * So levels of CRH and ACTH in utero are very high
    * When ACTH is very high, there will be hyperplasia of the adrenal cortex
    * Babies born with CAH have HUGE ADRENAL GLANDS
  2. Instead of producing glucocorticoids, there is over-production of androgens
    * Build up of androgens causes MASCULINE EXTERNAL GENITALIA in female babies (number 1 cause of ambiguous genitalia)
    * Typical of kidneys and adrenal glands born with CAH; adrenal glands will be almost the same size of the kidney
72
Q

Adrenal Cortical Insufficiency: Addison’s Disease (4)

A
  1. Primarily autoimmune destruction of adrenal tissue
  2. Significant health problem because you can’t produce glucocorticoids and mineralcorticoids
  3. Affects both Glucocorticoids and Mineralocorticoid function
  4. Loss of aldosterone is very significant compared to loss of cortisol, because without aldosterone people are very hemodynamically unstable, can’t maintain normal BP, and are vulnerable to syncope and hypotension
73
Q

Consequences of Addison’s Disease (6)

A
  1. Hyperpigmentation, not uniform (excess ACTH on melanocytes)
  2. Progressive weakness, fatigue, poor appetite, and weight loss
  3. Dizziness with orthostasis due to hypotension occasionally may lead to syncope (volume depletion)
  4. Hyponatremia and hyperkalemia
  5. Salt craving
  6. Adrenal crisis
    * Brought about by acute stress (eg sepsis, surgical stress)
    * In absence of adrenal cortex hormones stress results in hypotension, shock, and risk of death
74
Q

Adrenal Hyperfunction: Cushing Syndrome (2)

A
  1. Cushing syndrome is caused by prolonged exposure to elevated levels of either endogenous glucocorticoids or exogenous glucocorticoids
  2. Can have increased ACTH → hyperadrenocorticism → cushing syndrome
    * Excess ACTH stimulates overproduction of the adrenal gland
75
Q

Causes of Cushing Syndrome (4)

A
  1. Exogenous steroid administration
    - Steroid therapy
    - May be for inflammation or suppression of immune system
    - Women are particularly vulnerable to steroid therapy
    - Patients with diseases that respond to steroid therapy or who have undergone organ transplants
  2. Endogenous glucocorticoid overproduction
    - ACTH-producing pituitary adenoma
  3. Primary adrenal lesions adrenal
    - Adenomas, carcinomas
  4. Ectopic ACTH production
76
Q

Clinical Manifestations of Cushing’s Syndrome (11)

A
  1. Exaggerated versions of the normal functions of cortisol
    * Cortisol impairs immune function and inflammation
    * Normally, cortisol tends to reduce subcutaneous fat on arms and legs but increases it on the face and abdomen
  2. Poor skin healing (high risk for impaired skin integrity)
    * Thin, damage-prone skin
  3. Breakdown of skeletal muscles (muscle wasting)
  4. Skinny arms and legs
  5. Large belly
    * Will occur very quickly; can see stretch marks
  6. Moon-face
  7. Osteoporosis
  8. Loss of fertility
  9. Buffalo hump (accumulation of fat below the neck & between the clavicles)
  10. Increased excitability of CNS; can cause agitation, emotional lability, mood swings
  11. Facial hair growth and flushed faces in women

Patho 2 Exam 2 (8 decks)

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