Adrenal, ADH and Thyroid Disorders
Lecture Prep and Study Guide
Study Guide/Objectives for after class
Adrenocortical disorders

Define Cushing Syndrome/disease and discuss the difference between primary
hyperfunction, secondary hyperfunction, and exogenous steroid excess. Cushing
syndrome is a collection of signs and symptoms associated with hypercortisolism.
Primary: disease of the adrenal cortex (Cushing’s syndrome); Secondary: disease of the
anterior pituitary (Cushing’s disease); Exogenous steroids: used in the management of
various diseases (Cushing’s Syndrome)

Discuss how each of the main clinical manifestations of Cushing Syndrome reflect a
heightened level of cortisol. Cortisol increases glucose availability so you will see glucose
intolerance and hyperglycemia. It maintains the vascular system so you will see
hypertension, capillary friability. Cortisol causes protein breakdown so you will see
muscle wasting, muscle weakness, thinning of the skin, osteoporosis and bone pain. Fat
breakdown cause redistribution of fat to the abdomen, shoulders, and face. Suppression
of immune and inflammatory responses can manifest in impaired wound healing and
immune response, and risk for infection. Cortisol also causes CNS excitability which can
cause mood swings and insomnia.

Draw a picture of what a typical patient with Cushing Syndrome might look like.
Mood swings, insomnia, libido, thinning hair, moon face and ruddy complexion,
hirsutism, buffalo hump, supraclavicular fat pad, thinning extremities with muscle
wasting and fat mobilization, truncal obesity with pendulous breasts and abdomen.

Discuss the role of drugs in the treatment of Cushing Syndrome, including the MOA,
indication, effects, and adverse effects of Aminogluthimide (Cytadren) and Ketoconazole
(Nizoral). The treatment depends on the cause. It can be caused by the pituitary or
tumor. That would need surgery or radiation.
Aminoglutethimide (Cytadren): MOA: blocks synthesis of all adrenal steroids.
Indication: temporary therapy to decrease cortisol production. Effects: reduces cortisol
levels by 50% & does not affect the underlying disease process. Adverse effects:
drowsiness, nausea, anorexia, rash
Ketoconazole (Nizoral): MOA: antifungal drug that also inhibits glucocorticoid synthesis.
Indication: adjunct therapy to surgery or radiation for Cushing syndrome. Main adverse
effect: severe liver damage. Safety issues: do not take with ETOH or other drugs that
harm liver and do not give during pregnancy.

Define Addison disease and discuss the etiology and pathogenesis, including the role
that ACTH plays in the disease process. Addison’s Disease of the adrenal cortex that
causes hyposecretion of all 3 adrenocortical hormones. The most severe effects come
from the lack of cortisol. Etiology: It can be idiopathic or autoimmune. Pathogenesis:
The adrenal gland is destroyed, and symptoms appear when it is 90% non-functional.
ACTH and MSH are secreted in large amounts.

Describe the early and late clinical manifestations of Addison disease. Early
manifestations: anorexia, weight loss, weakness, malaise, apathy, electrolyte
imbalances, skin hyperpigmentation.

Draw a picture of a patient with Addison disease.

Make a table that compares and contrasts Cushing Syndrome and Addison Disease in
terms of etiology, pathogenesis, and clinical manifestations.
o
Cushings syndrome is caused by either dysfunction of the andrenal cortex
(syndrome) or the anterior pituritary (secondary). It often results in uneven fat
distribution in the face, shoulders, and abdomen. May cause thinning of hair,
bruising, mood swings, loss of libido, and skinny extremities
o
Addisons disease is caused by the destruction of the adrenal glan resulting in
hyposecretion of: Aldosterone, Corticoids, and Androgens. It has early symptoms
of apathy, malaise, electrolyte imbalances, weakness, weight loss, and hyper
pigmentation

Discuss Addisonian (Adrenal) crisis, including the causes and clinical manifestations. This
is caused by the sudden insufficiency of serum corticosteroids. It results from sudden
loss of adrenal gland, sudden increase in chronic condition, and sudden cessation of
corticosteroid drug therapy.

Describe the role of pharmacotherapy in the treatment of Addison Disease, including
which drugs are typically given and important safety information. Adrenal insufficiency
requires lifelong corticosteroid replacement therapy. All patients require a
glucocorticoid (hydrocortisone is drug of choice, prednisone, dexamethasone). Some
patients require a mineralocorticoid: fludrocortisone. Important safety information:
dosing mimics natural release of hormones so time and small dosing is important, never
abruptly stop therapy. Dose will need to be increased during stress (example: infection,
surgery, trauma). Always maintain emergency supply, wear a medic alert bracelet!!
Adrenal medulla disorder

Define pheochromocytoma and discuss the etiology, pathogenesis, and classic clinical
manifestations. Rare tumor of the adrenal medulla that produces excessive
catecholamines (epinephrine and norepinephrine).

Discuss the role of drug therapy in the treatment of pharmacotherapy, including alpha
blockers (prototype, indication, MOA, adverse effects). The preferred treatment is
surgery. Alpha-adrenergic blockers may be used: inoperable tumors and pre-operatively
to reduce risk of acute hypertension. Phenoxybenzamine HCl (Dibenzyline). Indication:
pheochromocytoma. MOA: Lon-lasting, irreversible blockage of alpha-adrenergic
receptors. Drug effects: lowers blood pressure. Adverse effects: orthostatic
hypotension, reflex tachycardia, nasal congestion, sexual side effects in men.
Antidiuretic hormone disorders

Define and characterize SIADH. Syndrome of inappropriate antidiuretic hormone. It is an
abnormal production or sustained secretion of ADH. It is characterized by fluid
retention, serum hypoosmolality and hyponatremia, and concentrated urine.

Discuss the etiology and pathogenesis of SIADH. Malignant tumors, central nervous
system disorders, drug therapy, miscellaneous conditions.
Pathophysiology: increased antidiuretic hormone—increased water reabsorption in
renal tubules—increased intravascular fluid volume—dilutional hyponatremia and
decreased serum osmolality.

Describe what a patient with SIADH might look like clinically, including serum osmolality,
urine osmolality and specific gravity, urine output, weight changes. Serum
osmolality=low, urine osmolality and specific gravity=high, serum sodium=low, urine
output=low, weight=gain.
Describe the signs and symptoms of hyponatremia that might be seen in SIADH. Clinical
manifestations: (depend on severity and rate of onset of hyponatremia). Sx of
hyponatremia: dyspnea, fatigue. Neuro: dulled sensorium, confusion, lethargy, muscle
twitching, convulsions. GI: impaired taste, anorexia, vomiting, cramps. Severe Sx Na+
,100-115 mEq/L can result in possible irreversible neurologic damage.

Define water intoxication and describe what is happening at the cellular level.

Discuss the role of pharmacotherapy in the treatment of a patient with SIADH, including
the use of Demeclocycline (classification, drug use, MOA, and adverse effects). Drug
therapy is usually not first line. Treatment is directed at the underlying cause. For
chronic SIADH we use demeclocycline (declomycin). This is a tetracycline broadspectrum antibiotic. MOA: interferes with renal response to ADH. Adverse effects:
photosensitivity, teeth staining, nephrotoxic

Define and characterize diabetes insipidus (DI). A deficiency of ADH or a decreased renal
response to ADH. It is characterized by excessive loss of water in the urine. (Two forms
are neurogenic (central) and nephrogenic).

Differentiate between neurogenic DI and nephrogenic DI, including etiology, associated
disorders, and onset of disease. Neurogenic is caused by the hypothalamus or pituitary
gland damage. Associated disorders include stroke, TBI, brain surgery, cerebral
infections. Onset is sudden and usually this is permanent. Nephrogenic origin is renal.
The cause is loss of kidney function, or often drug related. Associated disorders include
chronic kidney disease. Onset is slow. Course of disease is progressive.

Outline the pathogenesis of DI and describe what a patient with DI might look like
clinically, including serum osmolality, urine osmolality and specific gravity, serum
sodium, urine output, weight changes, and other clinical manifestations. Pathogenesis:
Decreased antidiuretic hormone—decreased water reabsorption in renal tubules—
decreased intravascular fluid volume—increased serum osmolality (hypernatremia) &
excessive urine output.
Clinical manifestations: polyuria, polydipsia, dehydration, (based on severity: electrolyte
imbalances, hypovolemic shock—death.
Serum osmolality=high, urine osmolality and specific gravity=low, serum sodium=high,
urine output=high, weight=loss

Discuss the role of pharmacotherapy in the treatment of neurogenic DI vs. nephrogenic
DI. Include the MOA and common adverse effects of Desmopressin. Pharmacotherapy
for neurogenic DI= synthetic ADH replacement. Nephrogenic DI Tx= thiazide diuretics
used for paradoxical effect: decreases polyuria, increases urine osmolality.
Desmopressin: (DDAVP) MOA: synthetic ADH replacement therapy, anti-diuretic effects.
Delivery: nasal spray, PO, IV, SQ. Common adverse effects: small doses-none, nasal
spray-irritation, large doses: hyponatremia, water intoxication.
Diabetes Insipidus pneumonic: D-I-L-U-T-E
Dry; I+O, daily weight; Low specific gravity; urinates a lot; Treat=vasopressin, rEhydrate
Thyroid disorders


Describe the pathophysiology of hypothyroidism Insufficient levels of the thyroid
hormones t3 and t4. In primary hypothyroidism, there is an increase in release of TSH
from pituitary (release of TSH indicates a hypoactive thyroid). Hashimoto’s thyroiditis is
an autoimmune disorder and is the most common cause of hypothyroidism.
Discuss the signs and symptoms of hypothyroidism
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Early manifestations: cold intolerance, weight gain, lethargy, fatigue, memory deficits,
poor attention span, increased cholesterol, muscle cramps, raises carotene levels,
constipation, decreased fertility, puffy face, hair loss, brittle nails
Late manifestations: below normal temperature, bradycardia, weight gain, decreased
LOC, thickened skin, cardiac complications (cardiomegaly).
Explain myxedema – both types
Describe the treatment for hypothyroidism
Describe the pathophysiology of hyperthyroidism
Discuss the signs and symptoms of hyperthyroidism
Explain thyrotoxicosis and the associated manifestations
Describe the treatment for hyperthyroidism
Describe the differences between hyper and hypo disorders of the parathyroid gland
Understand the clinical manifestations for each parathyroid gland disorder
Describe the treatment for each parathyroid gland disorder
Normal A & P Review of Endocrine Function (Study questions for exam)

Describe the basic relationship between the hypothalamus and the pituitary gland.

Discuss the function of antidiuretic hormone and what causes it to be released.

Describe the adrenal glands and identify which part of the gland secretes glucocorticoids
and mineralocorticoids, and which part secretes the catecholamines.

Name the hormone that is released from the pituitary to stimulate the adrenal cortex to
release hormones.

Name the principal hormones of the gluco- and mineralocorticoids and describe how
these hormones are regulated and what their primary functions are.

Describe the basic relationship between the hypothalamus and the thyroid gland

Discuss the functions of thyroid hormones (T3 and T4)

Explain the role of the parathyroid gland
Oncology: Lecture Prep and Study Guide
Explain how cancer cells differ from normal cell characteristics. Cancer cells are constantly
moving through the cell cycle stages. No checkpoints, no DNA errors recognized, no apoptosis.
Cancer cells disregard the growth inhibitors released by neighboring cells. They grow all over as
they proliferate and can break free and metastasize in distant body sites.
Distinguish between cell proliferation and differentiation. Differentiation refers to the extent
that neoplastic cells resemble normal cells both structurally and functionally. (lack of
differentiation is called anaplasia). Proliferation is an increase in the number of cells as a result
of cell growth and cell division.
Relate the properties of cell differentiation to the development of a cancer cell line.
Discuss how cancer cells break cell rules. They don’t respect boundaries, they are not cohesive,
there is little to no communication, there is no proliferation control (meaning they can be
immortal or may die rapidly), proliferation rate is also unpredictable, “self” HLA markers are not
working, so attack may be mustered.
Explain the ways in which benign and malignant neoplasms differ.
Benign
Malignant
-Well-differentiated; resembles tissue of
origin
-Poorly differentiated; does not resemble
tissue of origin.
-Rate of growth is progressive and slow
-Rate of growth is erratic, slow to rapid
-local invasion: cohesive cells, well
demarcated tumor, often encapsulated.
-Local invasion is invasive and infiltrating,
surrounding normal tissue.
-Metastasis: none, tumor core: no necrosis
-Metastasis is frequent and tumor core can
be necrotic.
Identify the stage of cancer when given a client description (using both the staging system
and TNM systems) Malignant tumors can be graded I through III: grade I: cells are well
differentiated; grade II: cells are moderately differentiated; grade III: cells are poorly
differentiated or anaplastic cells.
TNM: T- tumor size, location, and involvement
to distant organs
N-lymph node involvement
M-Metastasis
Discuss the concept of metastasis. There is a primary tumor, and this is where the original site
started. The secondary tumor is where the cancer cell metastasized/it is a new site. The two
primary routes are lymphatic and vascular. First stop is the lymph system, cells are trapped in
the lymph nodes. Vascular spread is spread by vascular drainage. They penetrate local veins
and go through the vascular system. The first stop is often the liver and clumping, trapping, and
proliferation happens.
Describe genetic mechanisms of cancer risk.
Discuss the differences and similarities between carcinogens and promoters.
Trace the pathway for cancer spread: seeding, implantation and metastasis (vascular and
lymphatic spread).
Describe common locations for secondary tumors. Common locations for secondary tumors are
lungs, bones, liver, and brain.
State how lifestyle can contribute to the cancer risk through increased exposure to
carcinogenic agents.
Discuss the modifiable and non-modifiable risk factors of the selected types of cancer (lung,
breast, cervical, and colorectal).
Describe signs and symptoms of lung, breast, cervical, and colorectal cancers.
Lung cancer: cough, hemoptysis, wheeze or stridor, chest pain, dyspnea, weight loss, excessive
fatigue, weakness, hoarseness, obstructive accumulation of secretions in the bronchioles that
appear as pneumonia. Lung cancer is often asymptomatic, and a tumor may be an incidental
finding on a routine chest x-ray. Paraneoplastic syndrome may also be the first sign of lung
cancer.
Breast: single tumor, nontender tumor, firm tumor, irregular borders, adherence to the skin or
chest wall, upper outer quadrant of breast, nipple discharge, swelling in one breast, nipple or
skin retraction, peau d’orange (thickening of the skin that resembles an orange peel), Paget’s
disease of the breast which involves redness, crusting, pruritis, and tenderness of the nipple, is
also characteristic of a cancerous change.
Cervical: Has a long asymptomatic period before the disease becomes clinically evident.
Commonly, an abnormal pap test alerts the individual of a problem.
Colorectal: fatigue, weakness, weight loss, iron deficiency anemia, changes in bowel habits,
melena, diarrhea, constipation, lower bowel cancers can present with hematochezia and
narrowing of stool caliber.
Normal A & P Review (Study questions for exam)
Give a basic definition of the cell cycle and describe its purpose.
Differentiate between G0 and the cell cycle.
Discuss how the rate of cell division differs between different types of cells.
Describe the basic differences between stem cells, parent cells, and well-differentiated cells.
Describe the 3 basic rules of cell proliferation.
Define cell differentiation.
Chemotherapy
Study Guide
-State the goals of cancer therapy.
-Describe the barriers to successful chemotherapy related to toxicity to normal cells,
including: 100% kill, dose limiting toxic effects, late detection, poor tumor response,
drug resistance, and heterogeneity of cancer cells. 100% kill requires the use of the same dose
throughout the treatment for a 100% kill. This is hard because people can’t often tolerate the
same dose. Late detection is also a barrier because with low growth fraction, there is limited
blood supply. When the tumor has a necrotic core, it can’t get to the middle of the tumor to
destroy it. By this point, the patient is also more debilitated from the disease. Drug resistance:
cancer cells mutate constantly and natural selection-drug-resistant mutants flourish.
Heterogeneity: ongoing mutation, cells differ greatly-different responses to drugs, as tumor
ages, heterogeneity increases.
-Discuss the strategies for successful chemotherapy, including intermittent
chemotherapy,combination chemotherapy, optimizing dosing schedules, & regional drug
therapy.
-Describe the toxic effects that develop as a result of cancer chemotherapy based on
theirtargeting of high growth fraction cells. Nausea and vomiting for several days after chemo.
1-2 weeks after first round: decreased WBC’s, RBC’s, platelets. Diarrhea, alopecia, fatigue.
Three major complications: neutropenia: infection, erythrocytopenia: anemia,
thrombocytopenia: bleeding. Digestive tract injury, stomatitis, reproductive toxicities,
hyperuricemia (excessive level of uric acid in blood), extravasation, carcinogenesis, organ
damage (kidneys, lungs, CNS, heart, peripheral nervous system).
-Compare the specific differences between cell cycle-specific and cell cycle-nonspecific
antineoplastics. Cell cycle-nonspecific drugs work in any phase of the cell cycle including G0
phase. Cell cycle-specific drugs only work in one specific phase and do not work on the G0
phase. The non-specific drugs’ disadvantage is that they aren’t ass effective when cells are
active and proliferating. They are often used in combination with a cell-cycle specific agent.
-Describe the different types of anti-cancer drugs (cytotoxic agents) and give an example of
each drug.
Cytotoxic agents MOA: disrupt DNA synthesis and disrupt mitosis.
Alkylating agents: Prototype: Cyclophosphamide is a non-specific drug. It has some resistance
and usual toxicities include: vesicant, hemorrhage cystitis, sterility, and discoloration of skin and
nails.
Antimetabolites: Prototype: Methotrexate (Rhuematrex) is cell cycle specific. Resemble natural
metabolites, has some resistance. Usual toxicities: nephrotoxicity, hepatotoxicity, fetal death
and abnormalities.
Antitumor: prototype: Doxorubicin (Adriamycin) is a cell-cycle non-specific drug. Origin:
streptomyces. Usual toxicities: cardiotoxicity (sometimes fatal), acute and delayed rxn.
Mitotic inhibitors: Vinca Alkaloids: protoype: Vincristine (Vincasar), cell cycle specific, sources:
natural: periwinkle, toxicities: No bone marrow suppression in some drugs, peripheral
neuropathy, vesicant.
Antiemetic: serotonin antagonist: prototype: Ondansetron (Zofran), uses: chemo, radiation,
post-op, MOA: blocks serotonin receptors on vagal nerve and in the CTZ, efficacy is improved
with steroids, most common adverse effect: headache, diarrhea, dizziness.
-Phenergan is another antiemetic that blocks dopamine receptors in the CTZ. Major
adverse effects: respiratory depression, drowsiness, sedation, box warnings: resp. depression
<2 years old; gangrenous extravasation.
-Describe the side effects and toxic reactions associated with cytotoxic drug groups in general,
and those that are unusual and presented in class – nephrotoxicity and cardio toxicity.
Antimetabolite Methotrexate is a cell cycle specific drug that causes nephrotoxicity and
hepatotoxicity. Antitumor non-specific drug, Doxorubicin is an antibiotic that is not used as that
anymore because of high toxicity. It can cause cardiotoxicity.
-Discuss the cause and effects of the common side/adverse effects of chemotherapy.
-Discuss the MOA, therapeutic uses, and side/adverse effects of the following cytotoxic agents:
Cyclophosphamidine, Methotrexate, Doxorubicin, and Vincristine.
-State the general rule of interactions in cancer chemotherapy.
-Discuss the concept of secondary malignancy.
-Describe the use of immunotherapy in the treatment of cancer. Include the MOA and general
side effects of these treatments. Biologics MOA: uses the body’s immune system to kill cancer
cells. Types: immune checkpoint inhibitors, T-cell transfer therapy, monoclonal antibodies,
treatment vaccines, immune system modulators. Side effects: pain, swelling, flu-like symptoms,
weight gain, diarrhea, risk of infection. The use of immunotherapy is for engagement of the
immune system in hopes to get a response.
-Do you know these cancer-related terms?
-Anaplasia (Anaplastic). The loss of cellular differentiation.
-Cancer: Disease in which abnormal cells divide without control and are able to invade other
tissues. While
-Cancer in situ: Refers to preinvasive epithelial tumors of glandular or squamous cell origin.
-Carcinoma. A malignant tumor of endothelial or epithelial tissue origin
-Cell-cycle nonspecific chemotherapy:
-Cell-cycle specific chemotherapy:
-Dose-limiting side effects
-Differentiation
-Nadir
-Targeted therapy
-Tumor: Describing a new growth or neoplasm.
-Vesicant
Acid/Base & ABG
Lecture Study Guide
Topic that will be covered in class today:
1. Acid/Base
2. ABGs
Study Guide/Objectives for after class
Acid/Base:

Explain the relationship between hydrogen ion concentration and pH
Hydrogen ions increase and the pH decreases (acidic), when the hydrogen ions decrease the pH
increases (alkalotic)
Acids: more H+ ions to release (donators)
Bases: less H+ ions (accepters)

Discuss the acid/base balance in the body
PH of 7 is neutral (equal hydrogen and hydroxide(water/o2))
The body’s normal range is 7.35-7.45(BLOOD) - pH can be different throughout the body

Identify the types of acids in the body
Volatile: (can be converted into gas) Carbonic Acid(carbon dioxide and H20) excreted by the lungs
Non-volatile: ELIMINATED BY THE KIDNEYS Latic acid(metabolized in the body), acetoacetic, betahydroxybutyric, sulfuric acid, phosphoric
Describe how the body maintains acid/base homeostasis (buffers, respiratory, & renal). For the
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buffers, identify where they take place.
Buffers: Blood (accepts or releases hydrogen to maintain pH)(bicarbonate, phosphate, protein)
Resp: Lungs (body can adjust pH by changing rate and depth of breathing) ex: slow sallow not eliminating C02
= increase in C02 which decreases the pH
Renal: Kidneys (most effective pH regulator but takes days, can excrete base while preserving/producing
HC03)

Explain the bicarbonate – carbonic acid equation and how it moves back and forth
For every Carbonic acid loss in the blood, 20 HC03 ions must be eliminated
Bicarb is mostly combined with sodium

Discuss cellular compensation and the concept of electrical neutrality with acid/base balance.
Hydrogen and Potassium(in the cell) are both positively charged so when the pH is acidic hydrogen moves
into the cell pushing potassium out electrical neutrality is restored- the process will reverse when pH returns
to normal and if the kidneys are working they can excrete the excess potassium but that may lead to a
depletion

Describe the rates of correction through the various mechanisms to correct acid/base imbalance
Buffers instantaneous
Resp minutes to hours
Renal several hours to days

Identify acid-base imbalances
Acidosis: below 7.35, Alkalosis: above 7.45

Explain the compensation mechanisms in the body
Complete compensation: pH is normal, partial compensation: if the range is outside of the norm

Discuss how the respiratory system and the renal systems work to compensate
Metabolic: the respiratory system will help
Respiratory: the renal system can help
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Know the normal values of an arterial blood gas
PH: 7.35-7.45
CO2: 35-45
HCO3: 22-26
ABGs:
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Explain the components of an arterial blood gas
PH, PaCO2, HCO3
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What is the difference between a PaCO2 and a serum CO2?
PaCO2: respiratory parameter, serum C02: Measured HCO3 on chemistry panel

Discuss the differences between a primary event, a primary disorder, and compensation
mechanisms
Event: the initial issue ex: hypo/hyperventilation, vomiting, diarrhea
Disorder: results from the initial issue Ex: respiratory acidosis, metabolic alkalosis
Compensation: Lungs help the kidneys and kidneys help the lungs

Define the four types of imbalances and how to identify the imbalances
Respiratory acidosis: hypoventilation, sedatives, OD, COPD, CNS depression
Respiratory alkalosis: hyperventilation, CNS excitability, anxiety, infection
Metabolic acidosis: DKA, renal failure, cardiac arrest, shock, KUSSMALS, prolonged diarrhea
Metabolic alkalosis: vomiting, excess antacids, CNS excitability

Explain the common causes for each type of imbalance
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Discuss the clinical manifestations for each type of imbalance
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Practice identifying each imbalance and determine if it is uncompensated, partially
compensated, fully compensated, or corrected