Unit 3 Study Guide NU 545

STI
1. Know all STIS: pathophysiology, etiology, clinical manifestations, diagnostic tests, treatment,
and complications. How is each transmitted during pregnancy to the fetus? Page 918. A pregnant woman
can transmit gonorrhea to her fetus during the birth process. The infection passes from mother to child
predominately through infected cervical and vaginal secretions. The coexistence of chlamydial infection with
gonorrhea frequently occurs. Herpes Neonatal infections can occur in utero or, more commonly, during the
intrapartum or postpartum period.
2. Know the different stages of syphilis; what organism causes each STI and is it viral, bacterial
etc.? Do you treat both partners and why page 922? Bloodborne bacteria spread to all major organ systems
during only stage II, secondary syphilis. In which stage of syphilis would the following clinical manifestations
be found: destructive skin, bone and soft tissue lesions, aneurysms, heart failure, and neurosyphilis? Tertiary.
T. pallidum organism is the only cause of syphilis. Because Treponema pallidum cannot be cultured in vitro,
early definitive diagnosis of primary or secondary syphilis depends on darkfield microscopy of a specimen
taken from a chancre, regional lymph node, or other lesion. The only secondary syphilis lesion is the
condylomata lata. Secondary syphilis is systemic, and blood-borne bacteria spread to all major organ systems.
Primary syphilis starts with a chancre and moves to regional lymph nodes. Tertiary is the most severe and
affects skin, bone, the central nervous system (CNS), and the cardiovascular system. In latent syphilis, the
infected individual has no clinical manifestations.
Primary: nonpainful chancre at site of invasion. Secondary: systemic involvement with skin rash and
lymphadenopathy. Tertiary: gummas (granuloma)

Match the Sexually Transmitted Infection with its causative agent:

Gonorrhea: Neisseria gonorrhoeae
Syphilis: Treponema pallidum
Condylomata acuminate (Warts): HPV
Pediculosis pubis (pubic lice: Sarcoptes scabiei
Lymphogranuloma: Chlamydia trachomatis
3. What age group has the greatest risk of STIs and why? Adolescent women have the highest risks
due to their immature cervix. Younger than 25.
4. Sexually transmitted diseases in teenage girls-why are they more susceptible? What unique factor
causes adolescent girls to have a high risk for sexually transmitted infections (STIs)? Immature cervix, Partly,
perhaps, because of risk-taking behavior (unprotected intercourse or selection of high-risk partners), many
adolescents have an increased risk for STI exposure and infection. The unique factor for adolescent women is that
they have a physiologically increased susceptibility to infection because of increased cervical immaturity and lack
of immunity.
CERVICAL CANCERS/ TUMORS/ PCOS, ETC
5. What causes cervical cancer page 825? Which factors are believed to increase the risk for developing
cervical cancer? Smoking, Chlamydia trachoma's infection, Human immunodeficiency viral (HIV) infection,
Human papilloma virus (HPV) infection. Cervical cancer is now established as almost exclusively caused by
the cervical HPV infection. Smoking, immunosuppression (HIV infection), and poor nutrition are cofactors. In
addition, infection with Chlamydia trachomatis has been correlated with the risk for developing cervical
cancer. Causes: Sexually transmitted human papillomavirus (HPV), early sexual activity, multiple sex partners,
smoking, poor nutrition
6. Understand the different uterine tumor types page 830. The size of benign uterine tumors, such as
leiomyomas, is thought to be caused by the influence of which hormones? Progesterone, Estrogen, Growth factors.
Leiomyomas, commonly called myomas or uterine fibroids, are benign smooth muscle tumors in the myometrium.
Type 1 uterine tumors are the most common and result from estrogen exposure leading to endometrial hyperplasia.
7. What is PCOS and what does it cause? Clinical manifestations? Treatment? Causes?
Pathophysiology? Page 810 POS is a result of a combination of conditions that include oligo-ovulation
or anovulation, elevated levels of androgens, or clinical signs of hyperandrogenism and polycystic
ovaries. Clinical manifestations of PCOS usually appear within 2 years of puberty and include
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dysfunctional bleeding or amenorrhea, hirsutism, acne, and infertility. PCOS Related to hypertension,
hyperinsulinemia, and dyslipidemia; leads to infertility, hirsutism, acne, endometrial hyperplasia,
cardiovascular disease, and diabetes mellitus
8. Etiology of cervical intraepithelial carcinoma (CIN) and cervical Ca page 827 and table 829. The
progressive neoplastic changes of cervical cells are classified from cervical intraepithelial neoplasia to cervical
carcinoma in situ to invasive carcinoma.
9. Know pathophysiology, etiology, clinical manifestations, diagnostics, treatment and
complications of endometriosis page 823. Endometrial tissue passes through the fallopian tubes and into the
peritoneal cavity and remains responsive to hormones causes endometriosis. What are the common clinical
manifestations of endometriosis? infertility and dysmenorrhea. It has been proposed that endometriosis is
caused by the implantation of endometrial cells during retrograde menstruation, during which menstrual fluids
move through the fallopian tubes and empty into the pelvic cavity (see Figure 24-16). Similar to normal
endometrial tissue, the ectopic (out of place) endometrium responds to the hormonal fluctuations of the
menstrual cycle. Endometriosis (endometrial tissue) cause: Depressed cytotoxic T cells tolerate ectopic tissues
genetics. Manifestations: Ectopic tissue respond to hormonal stimulation bleeding causes pelvic adhesions
and pain, infertility. Treatment: Drug suppression of ovulation, laparoscopic removal of ectopic implants
WOMENS REPRODUCTIVE
10. What is the difference between primary and secondary amenorrhea and what is compartment
II page 805-806? Primary amenorrhea is failure of menarche by 14 years of age. Secondary amenorrhea is the
absence of menarche for the equivalent of three cycles. Amenorrhea, galactorrhea, hirsutism, and osteoporosis
are each caused by a prolactinoma. Considering the pathophysiologic characteristics of primary amenorrhea,
what anatomic structure is involved in compartment II? Ovary. Which condition is considered a clinical
cause of amenorrhea? Failure to ovulate. Dysmenorrhea is painful menstruation; primary dysmenorrhea is
due to the release of prostaglandins in ovulatory cycles. Secondary dysmenorrhea is related to pelvic
pathologic conditions (e.g., ovarian cysts, endometriosis), which are expressed in later reproductive years
and may occur any time in the menstrual cycle. Pathologic elevated prolactin in women results in
amenorrhea.
11. What are the signs of puberty in girls 802 and boys? What delays puberty 802 girls 886 boys? In girls,
puberty begins at approximately ages 8-9 years with thelarche or breast development. Adrenarche is the increased
production of adrenal androgens. In 95% of children of delayed puberty, the problem is caused by physiologic
hormonal delays. The first sign of puberty in boys is an enlargement of the testes and a thinning of the scrotal skin.
estrogen secretion stimulates mammary growth. Full differentiation and development of breast tissue are mediated
by a variety of hormones, including estrogen, progesterone, prolactin, growth hormone, thyroid hormone, insulin,
and cortisol.
12. What is the pathophysiology behind the signs and symptoms of menopause 791 - 795? No period for 1
year. Characterized by loss of ovarian function, low estradiol and progesterone levels, high FSH and LH levels, and
decreased follicular inhibin secretion.
13. What does breast milk contain 784? The immunoglobulin IgA. Not only does breast milk composition
change over time to meet the changing digestive capabilities and nutritional requirements of the infant, but it also
contains immune cells, specific immunoglobulins, especially IgA, and nonspecific antimicrobial factors, such as
lysozymes and lactoferrin, that protect the infant against infection, allergies, and asthma. Prolactin stimulates
breast milk
14. What is the BRCA1 gene 863? Breast cancer susceptibility gene. Located on chromosome 17. Tumor
suppressor genes. 24-16 on 862.
15. Know the role of the different female hormones involved in menstruation, menopause,
ovulation, dysmenorrhea, etc 804. The absence of hypothalamic releasing or inhibiting hormones
causes the cessation of menses, impaired spermatogenesis, failure to thrive, and short stature in
children. The three phases of the menstrual cycle are • the follicular/proliferative phase, the
luteal/secretory phase, and menstruation. During menstruation, the functional layer of the endometrium
disintegrates and is discharged through the vagina. Menstruation is followed by the
follicular/proliferative phase. During this phase, the anterior pituitary gland secretes follicle-stimulating
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hormone (FSH), which causes cells of the endometrium to proliferate. By the time the ovarian follicle
is mature, the endometrial lining is restored. At this point, ovulation occurs. Ovulation marks the
beginning of • the luteal/secretory phase of the menstrual cycle. The ovarian follicle begins its
transformation into a corpus luteum. Luteinizing hormone (LH) from the anterior pituitary stimulates
the corpus luteum to secrete progesterone, which initiates the secretory phase of endometrial
development. If conception occurs, the nutrient-laden endometrium is ready for implantation. If
conception and implantation do not occur, the corpus luteum degenerates and ceases its production of
progesterone and estrogen. Without progesterone or estrogen to maintain it, the endometrium enters the
ischemic phase and disintegrates. Then, menstruation occurs, marking the beginning of another cycle.
Dysmenorrhea Excessive endometrial prostaglandin F (PGF) production causes painful menstruation,
increases myometrial contractions, and constricts blood Secondary dysmenorrheal Results from
endometriosis, pelvic adhesions, uterine fibroids, and adenomyosis.
16. Know the different parts of the female GU system and the function of each 772-775. Ovaries are not an
accessory sex organ of the female reproductive system. The region between the vaginal orifice and the anus is
called the perineum. Uterus: It sloughs compact and spongy layers of lining tissue, It is the site of embryo
implantation, Uterine muscle contraction expels the infant. The funnel-shaped, open-ended portion of the oviduct
is called the infundibulum.
17. What occurs with the fetus at each week of gestation 768? Anterior pituitary development starts
between the fourth and fifth weeks of fetal life. Anterior pituitary gland development starts between the fourth and
fifth weeks of fetal life, and the vascular connection between the hypothalamus and the pituitary is established by
the twelfth week. GnRH is produced by the hypothalamus by 10 weeks' gestation. The genital tubercle is
developed during the first 7-8 weeks' gestation. The initial reproductive structures of the male and female embryos
appear the same until between 6 and 7 weeks' gestation, the male embryo differentiates under the influence of
testes-determining factor (TDF). In the absence of testosterone, a loss of the wolffian system occurs and the two
gonads develop into ovaries at 6 to 8 weeks' gestation.
MALE REPRODUCTIVE
18. Etiology of epididymitis. Complications 785-786 and 895? Function of epididymis is to conduct sperm.
It can become inflamed from infection causing epididymitis. Pain is the main symptom of epididymitis. Pyuria or
bacteriuria and urinary symptoms may be present. Inflammation of the epididymis, generally occurs in sexually
active young males. In young men, the usual cause is a sexually transmitted microorganism. In men older than 35
years, intestinal bacteria and Pseudomonas aeruginosa, which is found in UTIs and prostatitis, may also cause
epididymitis. The pathogenic microorganism reaches the epididymis by ascending the vas deferens from an
infected urethra or bladder. Chemical epididymitis may result from inflammation caused by urine reflux into
ejaculatory ducts; it is usually self-limiting
19. Know the male GU anatomy and the function of the glands 784 788 glands. The vas deferens is a
firm, elastic fibromuscular tube that begins at the tail of the epididymis, enters the pelvic cavity within the
spermatic cord, loops up and over the bladder, and ends in the prostate gland. The prostate gland secrets prostatic
fluid, which is a thin, milky substance with an alkaline pH that helps sperm survive in the acidic environment of
the female reproductive tract. The Cowper glands secrete mucus into the urethra near the base of the penis. The
seminal vesicles are a pair of glands, each measuring approximately 4 to 6 cm long, which lie behind the urinary
bladder and in front of the rectum. Inflammation of the glans penis is called balanitis.
MALE AND FEMALE REPRODUCTIVE INFO!
The female • external genitalia collectively are called the vulva and comprise the structures externally visible: the
mons pubis, the labia majora, the labia minora, the clitoris, and the vestibule. The urethral meatus, the vaginal
opening, and two sets of glands—Skene glands and Bartholin glands—open onto the vestibule. The internal organs
of the female reproductive system are two ovaries, two fallopian tubes or uterine tubes, the uterus, and the vagina.
The ovaries are the primary female reproductive organs. They are located on both sides of the uterus and are sus-
pended and supported by ligaments. The fallopian tubes extend from the ovaries to the uterus and open into the
uterine cavity, thus providing a direct • communication between the peritoneal cavity and the uterine cavity. The
uterus lies centrally in the pelvis and is divided structurally into the body, or corpus, and the cervix. The inner
layer, the endometrium, consists of surface epithelium, glands, and connective tissue. The endometrium is shed
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during menstruation. At the lowest portion of the corpus is the internal os of the cervix. The external os is at the
lower end of the cervix. The canal of the cervix provides a direct communication from the cavity of the uterine
body through the internal os and the external os to the vagina. The vagina extends from the cervix of the uterus to
the vaginal opening. Thus, there is continuous • communication from outside the body to the peritoneal cavity
through the reproductive system structures. The male reproductive structures are the penis; the testes in the scrotal
sac; the duct system, which includes the • epididymis, the vas deferens, the ejaculatory ducts, and the urethra; and
the accessory glands, which include the seminal vesicles, the prostate, and the bulbourethral glands. The testes are
divided internally into lobules that contain the seminiferous tubules and Leydig cells. • Sperm produc-tion takes
place in the seminiferous tubules; Leydig cells secrete testosterone. On the posterior portion of each testis is a
coiled duct, the epididymis. The head of the epididymis is connected with the seminiferous tubule of the testis, and
its tail is continuous with the vas deferens. The vas deferens is the excretory duct of the testis. It extends to the
duct of the seminal vesicle and joins with it to form the ejaculatory duct. The ejaculatory duct joins the urethra,
which is the common passageway to outside the body for both sperm and urine. The accessory glands
communicate with the duct system. The prostate surrounds the neck of the bladder and the upper urethra. Its
glandular ducts open into the urethra. The bulbourethral glands, or Cowper’s glands, are located near the urethral
meatus. The penis is composed of three elongated cylindrical masses of erectile tissue, which comprise the shaft of
the penis. The inner, ventral mass is the corpus spongiosum, which contains the urethra. The two outer, dorsal,
parallel masses are the corpus cavernosa. The distal end of the penis or the glans is covered by the prepuce, or
foreskin.
GRAVES/CUSHINGS
20. What is Graves disease? Signs and symptoms? Labs 726? The pathologic features of Graves disease
indicates that normal regulatory mechanisms are overridden by abnormal immunologic mechanisms that result in
the stimulation of excessive TH. Pathologic changes associated with Graves disease include High levels of
circulating thyroid-stimulating immunoglobulins found in more than 95% of individuals. The level of thyroid-
stimulating hormone (TSH) in individuals with Graves disease is usually low; the hyperfunction of the thyroid
gland leads to suppression of TSH because of the normal negative feedback mechanism. Palpation of the neck of a
person diagnosed with Graves disease would detect a thyroid that is enlarged. Graves disease is hyperthyroidism,
associated with autoimmunity & manifested by ophthalmopathy. Graves disease, a form of type II
hypersensitivity, is the most common form of hyperthyroidism and is likely associated with autoantibodies against
the TSH receptor. The antibody binds to the plasma membrane and initiates thyroid hyperplasia of the gland
(goiter), vascularity, and hypersecretion of hormone. Ophthalmopathy is charac-terized by edema of the orbital
contents, exophthalmos, and extraocular muscle weakness that sometimes leads to diplopia and pain, lacrimation,
photophobia, and blurred vision. Treatment consists of a combination of radioac-tive iodine, surgery, or
antithyroid drugs
21. Know the pathophysiology, etiology, clinical manifestations, treatment and complications of
Cushing disease 753. A person has acne, easy bruising, thin extremities, and truncal obesity. These clinical
manifestations are indicative of Cushings disease: These symptoms are characteristic of Cushing disease and are
caused by excessive ACTH secretion. refers specifically to pituitary-dependent hypercortisolism. Cushing-like
syndrome also may develop as a result of the exogenous administration of cortisone. Elevations of pituitary ACTH
and adrenal neoplasms account for many cases of hypercorticoad renalism. Most of the clinical signs and
symptoms of Cushing are caused by hypercortisolism. The most common feature is the accumulation of adipose
tissue in the trunk, facial, and cervical areas. These have been described as “truncal obesity,” “moon face,” and
“buffalo hump.” Protein wasting is commonly observed in hypercortisolism and is caused by the catabolic effects
of cortisol on peripheral tissues. Muscle wasting is especially obvious in the muscles of the extremities. Loss of the
protein matrix in bone leads to osteoporosis and accompanying pathologic fractures, vertebral compression
fractures, bone and back pain, kyphosis, and reduced height. Loss of collagen also leads to thin, weakened
integumentary tissues through which capillaries are more visible. This accounts for the characteristic purple striae
observed in the trunk area. Loss of collagenous support around small vessels makes them susceptible to rupture
and easy bruising.
HORMONES
Hormones have specific rates and rhythms of secretion, Hormones affect only cells with appropriate receptors,
Hormones are excreted by the kidneys. Negative-feedback systems are important in maintaining hormones within
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physiologic ranges. The lack of negative-feedback inhibition on hormonal release often results in pathologic
conditions. Excessive hormone production, which is the result of the failure to turn off the system, can cause
various hormonal imbalances and related conditions. The correct option is the only accurate description of this
hormonal function.
Mineralcorticoids conserve sodium, control(s) Na+, H+, and K+ levels. Glucocorticoids are anti-inflammatory,
influence mammary response. ACTH is from adrenal cortex, Stimulates production of glucocorticoids
(gluconeogenesis, inhibits immunity, anti-inflammatory) by adrenal cortex. TSH is from thyroid gland. TRF is
adenohyphosis. Prolactin is mammary glands. Epinephrine causes fight or flight response. Gonadocorticoids act(s)
as minor sex hormone(s). Hypothalamus releasing hormone Act on anterior pituitary to stimulate release or inhibit
synthesis and release of hormones. Posterior pituitary - Antidiuretic hormone (ADH) Oxytocin causes
conservation of body water, reduces serum osmolality, may regulate CNS functions. Posterior pituitary oxytocin
Stimulates uterine contraction and lactation, has antidiuretic activity, may have a role in sperm mobility.
22. What is hypoparathyroidism 733? Renal failure is the most common cause of which type of secondary
hyperparathyroidism. The most common cause of hypoparathyroidism is damage caused during thyroid surgery
resulting in a lack of circulating PTH and causing a depressed level of serum calcium. - parathyroid gland damage.
Hyperparathyroidism causes increased osteoclastic activity. It can result in kidney stones and bone fractures from
lack of calcium uptake. Approximately 80% of primary hyperparathyroidism disorders result from a chief cell
adenoma with an increased secretion of PTH. This causes hypercalcemia and decreased serum phosphate levels.
Hypocalcemia lowers the threshold for nerve and muscle excitation. Muscle spasms, hyperreflexia, clonic-tonic
seizures, laryngeal spasms, and, in severe cases, death from asphyxiation are seen with hypocalcemia.The
treatment of hypoparathyroidism involves admin-istration of calcium and vitamin D. Hypoplastic dentition,
cataracts, bone deformities, and basal ganglia calcifica-tions do not respond to the correction of hypocalcemia, but
the other symptoms of hypocalcemia are reversible.
23. What is acromegaly 722-723? A comorbid condition of acromegaly is hypotension: Symptoms of type 2
diabetes mellitus, such as polyuria and polydipsia, may occur. Acromegaly-associated hypertension is usually
asymptomatic until symptoms of heart failure develop. Acromegaly is a disorder caused by hypersecretion of the
growth hormone (GH) in adults? Acromegaly is a term for adults who have been exposed to continuously high
levels of GH, whereas the term giantism is reserved for children and adolescents. Acromegaly is commonly caused
by GH-secreting pituitary adenoma or anterior pituitary adenoma. Acromegaly occurs in adults who are exposed to
con-tinuously excessive levels of GH. Acromegaly is uncom-mon. The most common cause of acromegaly is a
primary autonomous GH-secreting pituitary adenoma. Acromegaly occurs in adults after epiphyseal closure has
occurred and is a slowly progressive disease. In the adult, increased amounts of GH and somatomedins cause
increases in con-nective tissue and cytoplasm. If untreated, acromegaly is associated with a decreased life
expectancy because of a greater occurrence of hypertension, congestive heart failure, diabetes mellitus, and colon
or lung cancer.
24. What is the relationship between primary adenoma and thyroid and adrenal hypofunction
722? Hyperpituitarism slow growing tumors that arise from cells of the anterior pituitary most commonly
those that secrete GH and prolactin. The tumor can put pressure on surrounding functions are altered. For
example thyroid and adrenal hypo function because of the lack of TSH and ACTH and can show
symptoms of hypothyroidism and hyp0cortisolism.
25. Know the pathophysiology, etiology, clinical manifestations, treatment and complications
of syndrome of inappropriate antidiuretic hormone (SIADH) 718-719? SIADH is characterized by
high levels of ADH without normal physiologic stimuli for its release.The symptoms of SIADH
secretion are a result of dilutional hyponatremia and water retention. A diagnosis of SIADH requires a
serum sodium level of less than 135 mEq/L, serum hypoosmolality less than 280 mOsm/kg, and urine
hyperosmolarity. +Ectopic secretion of ADH most common cause (small cell adenocarcinoma in the
lungs); also common after surgery +For diagnosis, normal adrenal and thyroid function must exist
+Clinical manifestations Related to enhanced renal water retention, Hyponatremia, Hypoosmolarity.
SIADH is associated with several forms of cancer because of the ectopic secretion of ADH by tumor
cells. Tumors associated with SIADH include oat cell adeno-carcinoma of the lung, carcinoma of the
duodenum and pancreas, leukemia, lymphoma, and Hodgkin lymphoma
26. What is aldosterone and why do we need it 709, 756? It is the most potent of the naturally occurring
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mineralocorticoids and acts to conserve sodium by increasing the activity of the sodium pump of the epithelial cells
in the nephron. It maintains extracellular volume by acting on distal nephron epithelial cells to increase sodium
reabsorption and potassium and hydrogen excretion.
In the kidney, aldosterone primarily acts on the epithelial cells of the nephron-collecting duct to increase sodium
ion reabsorption. This action cannot be said of the other options. Renin and angiotensinare enzymes that promote
secretion of aldosterone and thus regulate sodium and water balance.
27. What is the role of calcitonin 701-02? If calcium levels in the blood are too high, thyrocalcit-onin
(calcitonin) concentrations in the blood should increase, thereby inhibiting osteoclasts. Calcitonin, also called
thyrocalcitonin, acts to lower serum calcium levels by inhibiting bone-resorbing osteoclasts
28. What is oxytocin? How does it relate to the pituitary gland? Where is it secreted and what are it’s
effects 699? ADH and oxytocin are synthesized in hypothalamic neurons but are stored and secreted by the
posterior pituitary. Oxytocin is responsible for the contraction of the uterus and milk ejection in lactating women
and may affect sperm motility in men. Only the posterior pituitary secretes oxytocin. Stimulates uterine
contraction and lactation, has antidiuretic activity, may have a role in sperm mobility
29. What is the role of TSH 725? Where is it secreted? Know the negative feedback loop 690.
TSH secretion is regulated by thyrotropin-releasing hormone, primarily in the hypothalamus and by negative
feedback inhibition from thyroid hormones. Increased anterior pituitary release of TSH stimulates the secretion of
thyroid hormones. TSH is inhibited by thyroxin (T4). The thyroid gland secretes calcitonin. The C cells, follicles,
and isthmus are all found in the thyroid gland. Chromophils are found in the anterior pituitary. Stimulates
production and release of thyroid hormones (growth and maturation of tissues).
Heat production begins with the hypothalamic release of thyroid-stimulating hormone (TSH) from the
anterior pituitary. The TSH causes the release of thyroxine from the thyroid gland. This hormone causes the
release of epinephrine from the adrenal medulla. Negative feedback loop: Anterior pituitary releases TSH 
stimulates synthesis of TH  thyroid hormone rises  negative-feedback effect on the HPA  inhibition of TRH
 release of TSH  decrease TH synthesis and secretion.
30. Understand the roles of epinephrine and norepinephrine 710.
Epinephine is secreted by the adrenal medulla. The TSH causes the release of thyroxine from the thyroid gland.
This hormone causes the release of epinephrine from the adrenal medulla. Epinephrine prepares the body to
act; dilates blood vessels to increase cardiac output and blood flow to the heart, brain, and skeletal muscles;
and dilates the airways to increase oxygen blood levels. Norepinephrine constricts peripheral blood vessels to
aid in the shifting of blood to the dilated vessels and increases mental alertness. Epinephrine and
norepinephrine levels are controlled by sympathetic preganglionic neurons that stimulate their secretion by the
adrenal medulla. Both increase heart rate, blood pressure, and blood glucose concentration. Epinephrine
dilates skeletal muscle blood vessels. Lymphoid tissue is innervated and, therefore, is influenced by these
substances
31. What is parathyroid hormone 732? What are the effects of PTH 702-703?
The parathyroid glands produce PTH, a regulator of serum calcium. The parathyroid glands secrete PTH. The
parathyroid glands play important role in calcium regulation. PTH is the most important regulator of calcium
(Ca++). Two pairs of parathyroid glands are normal, but the number may range from two to six pairs. They are
small and located behind the thyroid gland. The thyroid gland produces the thyroid hormone. The overall effect of
parathyroid hormone (PTH)is to increase serum calcium and to decrease serum phosphate concentration. The other
presented imbalances will not affect PTH in the de-scribed fashion. The overall effect of parathyroid hormone
(PTH)is to increase serum calcium and to decrease serum phosphate concentration. The other presented
imbalances will not affect PTH in the described fashion. An increase, not a decrease, in serum calcium inhibits
parathyroid hormone (PTH) secretion
32. Where are the target cells for each hormone located 718 Page 698 table 21-4 and 21-5. See figures at
end? Target cells for PTH Parathyroid hormone acts on its plasma membrane receptor only in the distal and
proximal tubules of the kidney's nephron. Target cells for oxytocin are in the uterus. Oxytonin causes uterine
contraction and lactation in women and may have a role in sperm motility in men.
33. Know which hormones are water soluble (table 21-1 pg 690) and which are lipid soluble.
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Peptide or protein hormones, such as insulin, pituitary, hypothalamic, and parathyroid, are wa-ter soluble and
circulate in free (unbound) forms. All the remaining options are fat-soluble hormones. Cortisol and adrenal
androgens are lipid-soluble hormones and are primarily bound to a car-rier or transport protein in circulation. The
other options are water-soluble hormones. Lipid-soluble hormone receptors are located inside the plasma
membrane and easily diffuse across the plasma membrane to bind to either cytosolic or nuclear receptors. Lipid-
soluble hormones cross by diffusion.
34. Know how protein hormones are transmitted in the blood 691.
Peptide or protein hormones, such as insulin, pituitary, hypothalamic, and parathyroid, are water soluble and
circulate in free (unbound) forms.
35. Know ADH. Where is it secreted? Where does it act 698?
ADH was originally named vasopressin because, in extremely high doses, it causes vasoconstriction and a
resulting increase in arterial blood pressure. However, significant vasoconstriction may only be achieved
pharmacologically. Once synthesized in the hypothalamus, ADH acts on the vasopressin 2 (V2) receptors of the
renal duct cells to increase their permeability. The posterior pituitary secretes ADH, which also is called
vasopressin, and oxytocin. A common cause of elevated levels of ADH secretion is ectopically produced ADH.
36. Know the relationship between calcium and phosphorus 703. Hyperphosphatemia leads to
hypocalcemia. Ca++ is considered an important second messenger that facilitates the binding of a hormone (e.g.,
norepinephrine, angiotensin II) to a surface receptor, activating the enzyme phospholipase C through a G protein
inside the plasma membrane. Calitonin lowers serum phosphate levels. Hyperphosphatemia leads to hypocalcemia
because of calcium phosphate precipitation in soft tissue and bone. Alterations in serum phosphate levels therefore
may indirectly influence PTH secretion by affecting serum calcium levels.
37. Know pituitary tumors and clinical manifestations of each 722.
The posterior pituitary secrets oxytocin. The anterior pituitary secretes TSH. If a pituitary tumor exerts sufficient
pressure, then thyroid and adrenal hypofunction may occur because of lack of thyroid-stimulating hormone (TSH)
and adrenocorticotropic hormone (ACTH). These result in the symptoms of hypothyroidism and hypocortisolism.
Visual disturbances are a result of a pituitary adenoma because of the Pressure of the tumor on the optic chiasm.
With a pituitary adenoma An individual experiences visual changes that begin in one eye but now involve the
second eye. Pituitary adenomas arise from the anterior pituitary. They are usually slow growing and benign. They
most commonly secrete GH and prolactin.
DIABETES
38. Know the pathophysiology, etiology, clinical manifestations, treatment and complications
of DM I and DM II. One of the basic pathophysiologic characteristics of type 2 diabetes is the
development of insulin-resistant tissue cells. A person diagnosed with type 1 diabetes experiences hunger,
lightheadedness, tachycardia, pallor, headache, and confusion. The most probable cause of these
symptoms is Hypoglycemia caused by increased exercise. DM is diagnosed with Fasting glucose value
greater than 126 mg/dl. Diabetes insipidus is related to an insufficiency of ADH leading to polyuria and
polydipsia. There are three forms of diabetes insipidus: a neurogenic or central form, a nephro-genic
form, and a psychogenic form. The neurogenic form of diabetes insipidus occurs when any organic lesion
of the hypothalamus, infundibular stem, or posterior pituitary interferes with ADH synthesis, transport, or
release, result-ing in too little ADH. Nephrogenic diabetes insipidus is an insensitivity of the renal tubule
to ADH, particularly the collecting tubules. This diabetes is generally related to dis-orders and drugs that
damage the renal tubules or inhibit the generation of cAMP in the tubules. The psychogenic formis
caused by an extremely large volume of fluid intake.
39. Understand the role of insulin 704 how does insulin affect potassium 706. The beta cells synthesize
insulin. Insulin facilitates the intracellular transport of potassium, phosphate, and magnesium. The alpha cells
secrete glucagon. C peptide is the bond that connects the two peptides of proinsulin. The delta cells secrete
somatostatin and gastrin. Insulin facilitates the intracellular transport of potassium (K+), phosphate, and
magnesium. Glucagon is produced by the alpha cells of the pancreas. Amylin and insulin are secreted by the beta
cells. Insulin secretion is promoted when blood levels of glucose rise.
40. Understand hypo/hyperglycemia 743-747. Hyperglycemia will inhibit glucagon release.
Glucagon is produced by the alpha cells of the pancreas. Glucagon increases blood glucose by stimulating lipolysis
Unit 3 Study Guide NU 545

and glycogenolysis. The Somogyi effect is a unique combination of hypoglycemia, followed by rebound
hyperglycemia.
41.Why do diabetic pts usually develop hyperlipidemia? 741. Intra-abdominal adipocytes or adipocyte-
associated mononuclear cells (from activated macrophages in other tissues)  release of inflammatory cytokines 
induce insulin resistance through a post-receptor mechanism  play and important role in the genesis of fatty liver,
atherosclerosis, and dyslipidemia.
42.Why do diabetic pts have CVD 747 & 751? Microvascular complications are a result of capillary
basement membranes thickening and endothelial cell hyperplasia. Macrovascular advanced glycosylated end
products attach to their receptor in the walls of blood vessels.
43.Why do diabetics develop retinopathy 747? Know microvascular complications of DM 747.
Retinopathy develops in patients with diabetes mellitus because Retinal ischemia and red blood cell aggregation
occur: Retinopathy appears to be a response to retinal ischemia and red blood cell aggregation. Stages of
retinopathy: Stage I is characterized by an increase in retinal permeability, vein dilation, microaneurysm
formation, and superficial and deep blot hemorrhages. Stage II is a progression of retinal ischemia with areas of
poor perfusion that culminate in infarcts. Stage III is the result of neurovascularization and fibrous tissue formation
within the retina or optic disc. Stage IV neurovascularization causes new abnormal and fragile blood vessels to
grow along the retina and along the surface of the clear, vitreous gel that fills the inside of the eye. If they leak
blood, severe vision loss and even blindness can result.
44.Why does polyuria and polydipsia and weight loss occur with the onset of diabetes 738 22-
7? Polyuria occurs with diabetes mellitus because of the elevation in serum glucose and Glucose
accumulates in the blood and appears in the urine as the renal threshold for glucose is exceeded,
producing an osmotic diuresis and the symptoms of polyuria and thirst.
45.Know hyperglycemic hyperosmolar syndrome (HHS) 745? Know diabetic
ketoacidosis? What’s the difference? Decreased glucose causes fatty acid use, ketogenesis,
metabolic acidosis, and osmotic diuresis, which have resulted in the symptoms listed: arterial pH
7.20; serum glucose 500 mg/dl; positive urine glucose and ketones; serum potassium (K+) 2
mEq/L; serum sodium (Na+) 130 mEq/L. The patient reports that he has been sick with the "flu"
for 1 week. When comparing the clinical manifestations of both diabetic ketoacidosis (DKA) and
hyperglycemic hyperosmolar nonketotic syndrome (HHNKS), which condition is associated with
only DKA? Kussmal respirations. Accelerated gluconeogenesis and ketogenesis are present in
DKA. DKA develops when an absolute or relative deficiency of insulin or an increase in insulin
counterregulatory hormones is present. This increase includes catecholamines, cortisol, glucagon,
and growth hormone. Emotional factors and stress, especially in children, can contribute to the
development of DKA. Profound insulin deficiency results in decreased glucose uptake, increased
fat mobilization with the release of fatty acids, and accelerated gluconeogenesis and ketogenesis. In
addition, glucose production increases, peripheral glucose use decreases, and fat mobilization
increases.
HHNKS is different from DKA in the degree of insulin deficiency and fluid deficiency. It is also
characterized by a lack of ketosis.
46. Know the pathophysiology, etiology, clinical manifestations, treatment and complications of
diabetes insipidus 719. Neurogenic and nephrogenic.
Diabetes insipidus is a result of insufficient antidiuretic hormone. The basic criteria for diagnosing DI
include a low urine-specific gravity while sodium levels are high. Neurogenic diabetes insipidus is
supported by: Electrolytes are within normal limits, but his antidiuretic hormone (ADH) level is low.
Although he has had no intake for 4 hours, no change in his polyuria level has occurred. The cause of
neurogenic diabetes insipidus (DI) is related to an organic lesion of the posterior pituitary, hypothalamus,
or pituitary stalk. Neurogenic DI is treated with ADH replacement therapy. nephrogenic DI is associated
with an insensitivity of the renal collecting tubules to ADH, Nephrogenic DI diabetic insipidus (DI) will
result if the target cells for antidiuretic hormone (ADH) in the renal collecting tubules demonstrate
insensitivity. The first laboratory test that indicates type 1 diabetes is causing the development of diabetic
nephropathy is Protein on urinalysis. Neurogenic DI is treated with ADH replacement therapy.
Unit 3 Study Guide NU 545

A 10-year-old boy was brought into the emergency room comatose, suffering from metabolic acidosis
with a blood glucose level of 800 mg/dL. The most probable disease causing his condition is type 1.
Which is/are expected during hyperinsulinism? excess insulin and epinephrine release. The neurogenic
form of diabetes insipidus occurs when a lesion of the hypothalamus, pituitary stalk, or posterior pituitary
interferes with ADH synthesis, transport, or release. Although the neurogenic form is caused by low
levels of ADH, the nephrogenic form is caused by an inadequate response of the renal tubules to available
ADH.
OBESITY/ADIPOSE/NUTRITION
47. What are the three classifications of adipose tissue ebook? Adipose tissue is classified according to
color as WAT, brown adipose tissue (BAT), and beige adipose tissue (bAT). These tissue types are found in
different locations, have different gene expression patterns, different rates of lipogenesis and lipolysis, and
different origins.
48. What hormone is linked to obesity and early puberty in females? The level of peptide YY (PYY)
decreases with increases in adiposity and decreased PYY level is associated with obesity. Cholecystokinin (CCK)
is secreted by proximal small intestinal cells following food intake. Its actions include gall bladder contraction,
release of pancreatic enzymes and insulin, satiation, and reduced food intake. The is an association between
obesity and earlier puberty in girls, perhaps from higher estrogen levels related to gonadotropin and estrogen
secretion. Girls with low body fat, reduced body weight, and intense exercise may experience delayed maturation.
Though leptin is not the trigger for puberty onset, it plays an important permissive role.
49. Know how adipose tissue provides insulation, mechanical support, and energy to the body. Adipose
tissue provides insulation and tissue support and is the body's major energy reserve, storing triglycerides and
glycerol.
50. What are the genetic, metabolic, and environmental factors that contribute to obesity? Non-Hispanic
blacks have the highest age-adjusted rate at 48.1% followed by Hispanics (42.5%), non-Hispanic whites (34.5%),
and non-Hispanic Asians (11.7%). It is projected that 42% of people in the United States will be obese by 2030.
Obesity is defined as a body mass index (BMI) that exceeds 30 kg/m2in adults and a BMI greater than or equal to
the age- and sex-specific 95th percentile of the 2000 Centers for Disease Control and Prevention growth charts in
children. Three leading causes of death in the United States are associated with obesity: cardiovascular disease,
type 2 diabetes mellitus, and cancer
51. How does the arcuate nucleus (ARC) regulate food intake and energy metabolism by
balancing the opposing effects of two sets of neurons? The arcuate nucleus (ARC) in the hypothalamus
regulates food intake and energy metabolism by balancing the opposing effects of two sets of neurons. One
set of neurons produce agouti-related protein (AgRP) and neuropeptide Y (NPY), collectively known as
AgRP/NPY neurons. These neurons promote appetite, stimulate eating, and decrease metabolism (anabolic).
52. How does obesity produce a state of chronic, low-grade inflammation in white adipose tissue
(WAT)? Most adipose tissue in the body is WAT. WAT is located in visceral (central) and subcutaneous
(peripheral) stores. WAT also is found in muscle groups providing mechanical protection and sliding of muscle
bundles, and bone marrow. Obesity produces a state of chronic, low-grade inflammation (metabolic triggered
inflammation) in WAT. Macrophages, lymphocytes (proinflammatory CD8+ T cells), neutrophils, and mast cells
infiltrate enlarged adipocytes and release inflammatory cytokines. Obesity is a state of chronic low-grade
inflammation caused by expansion of adipocyte macrophages, neutrophils, and lymphocytes that release
inflammatory mediators.
53. What are the methods of estimating or measuring the amount of adipose tissue in order to screen
for obesity. Adipose tissue has different rates of lipogenesis. Adipose tissue is found in different locations, has
different gene expression patterns, different rates of lipogenesis and lipolysis, and different origins. The only
method for directly measuring total body fat is via the DEXA scans (dual energy x-ray absorptiometry). There
are several methods for stimating or measuring the amount of adipose tissue: anthropometric measurements
including weight, height, and circumferences of various body diameters (i.e., waist-to-hip ratios and waist
circumference); skinfold thickness (measured via skinfold calipers); ultrasound to measure peripheral body fat;
and bioelectric impedance and underwater hydrostatic weighing to calculate total body fat.
54. What is the differences between malnutrition and starvation. During long-term starvation, depressed
insulin levels and increased levels of glucagon, cortisone, epinephrine, and growth hormones promote lipolysis in
adipose tissue. Malnutrition is lack of nourishment from inadequate amounts of calories, protein, vitamins, or
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minerals and is caused by improper diet, alterations in digestion or absorption, chronic disease, or a combination of
these factors. Starvation is a reduction in energy intake leading to weight loss. Short-term starvation and long-term
starvation have different effects.
55. What is anorexia of aging and what are the risk factors? The consequences of anorexia of aging
include malnutrition, physical frailty, mitochondrial dysfunction, reduced regenerative capacity, increased
oxidative stress, and imbalanced hormones. Risk factors for anorexia of aging include functional impairments and
deficiencies (e.g., loss of vision, poor dentition, inability to prepare foods); medical and psychiatric conditions
(such as malabsorption syndromes and depression); loneliness and grief; medications, including polypharmacy;
social isolation; and abuse or neglect.
Anorexia of aging is defined as a decrease in appetite or food intake in older adults, and can occur in illness-free
individuals and in the presence of an adequate food supply. The resulting undernutrition leads to adverse outcomes
and may affect up to 20% to 30% of elders.100 The anorexia of aging results from multiple age related changes,
including reduced energy needs, waning hunger, diminished senses of smell and taste, decreased production of
saliva, altered gastrointestinal satiety control mechanisms, and the presence of comorbidities.
McCance & Huether Chapters 21-27. 8th Edition McCance & Huether Chapters 21-27. 7th Edition
Chapter 21: Mechanisms of Hormonal Regulation Chapter 21: Mechanisms of Hormonal Regulation
Chapter 22: Alterations of Hormonal Regulation Chapter 22: Alterations of Hormonal Regulation
Chapter 23: Obesity and Disorders of Nutrition Chapter 23: Structure and Function of the Reproductive System
Chapter 24: Structure and Function of the Reproductive System Chapter 24: Alterations of the Female Reproductive System
Chapter 25: Alterations of the Female Reproductive System Chapter 25: Alterations of the Male Reproductive System
Chapter 26: Alterations of the Male Reproductive System Chapter 26: Sexually Transmitted Infections
Chapter 27: Sexually Transmitted Diseases Chapter 41: (Obesity and Disorders of Nutrition) Alterations of
Digestive Function