This document discusses endocrine emergencies including disorders of the pancreas, pituitary, adrenal and thyroid glands. It covers the pathophysiology, manifestations, and treatment of diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS), as well as hypoglycemia, Addison's disease, and adrenal crisis. The key aspects of assessment and management are fluid resuscitation, electrolyte replacement, insulin therapy, and treatment of acidosis for DKA and HHS patients. Nursing diagnoses related to ineffective breathing, gas exchange, fluid deficits, and therapeutic management are also reviewed.

1. Endocrine
Emergencies
Doreen Graham RN,MSN, CCRN, APRN
NUR 335

2. Objectives
• Identify and explain the pathophysiology,
manifestations, and complications associated with
disorders resulting from alterations in hormones
secreted by the pancreas, pituitary, adrenal and
thyroid glands.
• Discuss diagnostic testing, medical and pharmacological
management of clients experiencing endocrine crisis.
• Discuss nursing implications and health education for
clients and/or families with alterations in endocrine
function.

3. Introduction
Endocrine system regulates
physiologic processes:
• Metabolic processes
• Energy production
• F&E balance
• Stress reactions
***Endocrine system is closely linked
with nervous system & immune
system

4. HORMONAL REGULATION:
Hypothalamus:
• Conveys information to the pituitary
Pituitary: hormonal regulation
• Response to hypothalamus
• Increased or decreased secretion of hormone
Controlled by feedback loops:
• Hormone low: stimulus to release more
• Hormone high: stimulus to limit production

5. Feedback System
 Hypothalamus: stimulates pituitary
 Pituitary gland:
- Increase/decrease
secretion of hormone
 Controlled by feedback loops
- Hormone low: stimulus to release more
- Hormone high: stimulus to limit release

6. Which hormones are regulated by the
following endocrine glands?
PANCREAS-
• alpha cells = glucagon, beta cells = insulin
ADRENAL-
• catecholamines, mineral corticosteroids, glucocorticoids
THYROID-
• TSH, t3,t4 , calcitonin (maintain blood Ca+ levels)
POSTERIOR PITUITARY-
• oxytocin
• ADH (antidiuretic hormone): key in water, glucose, and salt
regulation in blood

7. Pancreatic Disorders
 Diabetic Ketoacidosis (DKA)-
• common in type 1 diabetes
 Hyperglycemic Hyperosmolar State (HHS)
• Hyperglycemic Hyperosmolar, nonketoic coma
(HHNC)
• More in elderly and type 2 diabetes
 Hypoglycemia

8. Hyperglycemic Crises
 Reduction in circulating insulin with
elevation of counter-regulatory
hormones.
 Occurrence:
• DKA: Type 1 DM, type 2 DM on
insulin
• HHS: Type 2 DM (elderly)

9. RISK FACTORS FOR
HYPERGLYCEMIC CRISIS:
• Preexisting DM, unDX or DX.
• Relative insulin deficiency/insulin resistance.
• Comorbidities: obesity, pancreatitis, cirrhosis, hypokalemia
• Aging
• Lack of muscular activity
• Administer of Dextrose solutions, nutritional support
• Drugs:
- Thiazides
- Beta-blockers
- Exogenous catecholamines (dopamine, norepinephrine and epinephrine)
- Glucocorticoids (prednisone, hydrocortisone)
• Hyperglycemia due to ↑ gluconeogenesis, insulin
resistance, and impaired glucose tolerance.

13. DKA
Pathophysiology:
• Relative or absolute insulin deficiency.
• Increase in counter-regulatory hormones:
glucagon, cortisol, catecholamines, and growth
hormone
• Hyperglycemia: an increase in hepatic glucose
production and a decrease in peripheral utilization
• Protein stores depleted by gluconeogenesis in liver
• Breakdown of fatty acids  ketones in blood

14. DKA
 Release of free fatty metabolism:
• ↑ ketone production: impaired ketone
metabolism
• Impaired bicarbonate buffering of excess
Ketones  METABOLIC ACIDOSIS
◦ Respiratory compensation (Kussmaul’s
respirations)
◦ Osmotic fluid shifts; diuresis
◦ Electrolytes vary, often hyperkalemic

16. PATHO. OF DKA
 Altered K+ balance:
◦ Due to the fluid volumes and K+ shifts…
serum K+ values must be interpreted with caution in DKA.
◦ May also have an accumulation of lactic acid.
◦ Excess acids result in increased anion gap (8 - 16mEq/L = norm)
(Na+ + K+) – (Cl- + HCO3-)= calculation of gap
◦ ALOC r/t acidosis (CO2 buildup) & dehydration
◦ As acidosis worsens, hyperglycemia & hyperkalemia worsens.
◦ Cycle continues until coma / death occur.
Patient’s can lose up to 6L of body water!!!!!

18. DKA
In both DKA and HHS-
 high extracellular glucose levels produce an osmotic
gradient btwn. the intracellular & extracellular
spaces= OSMOTIC DIURESIS
As glycosuria and osmotic diuresis progress…
- Urinary losses of water, Na+, K+, Mg+, Ca+, and
P- occur
- This osmotic diuresis with the fluid shifts
causing worsening dehydration.
3 Main Clinical features of DKA:
Acidosis, dehydration, and hyperglycemia

20. CAUSES OF DKA:
• Infections**
• Severe stress – trauma, surgery, AMI
• Initial presentation of type 1 DM
• Missed or reduced insulin
• Nonadherence to insulin regimen
- Insulin pump failure
- Intentional omission
- Eating disorders, diet, sick days not effectively
managed
- Behavioral health issues
• Meds- Glucocorticoids
• Mismanagement of sick days
• Pregnancy in type 1 diabetes mellitus (DM)

23. Hyperglycemic Hyperosmolar State
(HHS)
Pathophysiology:
• Decreased use of glucose and/or increased
production (gluconeogenesis)
• Hyperglycemia: increased extracellular osmolality
• Osmotic diuresis
• Profound dehydration/decreased thirst mechanism
• No ketoacidosis—hyperglycemia with
hyperosmolarity blocks lipolysis

24. A client with type 1 diabetes mellitus has
diabetic ketoacidosis. Which of the
following findings has the greatest effect on
fluid loss?
1. Hypotension
2. Decreased serum potassium level
3. Rapid, deep respirations.
4. Warm, dry, skin

25. HHS
◦ Inadequate insulin secretion; usually with type 2
DM
◦ Often in geriatric patients with ↓ compensatory
mechanisms
◦ Stress response
◦ Medications:
Steroids (esp. glucocorticoids) Sympathomimetics
Beta Blockers Analgesics
Thiazide Diuretics Cimetidine
Calcium Channel Blockers Immunosuppressants
Phenytoin Diazoxide
Epinephrine Chemotherapeutic
Agents
Psychotropics (TCAs) Illicit Drugs (Cocaine,
Ecstasy)

26. DKA vs. HHS (AKA HHNC)

27. DKA & HHS: Assessment
• Based on severity of presentation
• Dehydration and hypovolemia
• N/V
• 3 Ps: Polyuria
Polyphagia
Polydipsia
• ALOC r/t…
-hypovolemic state
-loss of F&E
-CO2 buildup

28. DKA vs. HHS
 Plasma glucose > 250mg/dL
(average: 675mg/dL)
 pH < 7.30
 Bicarbonate < 15mEq/L
 Ketosis/ketones
 High anion gap
 Kussmaul’s respirations
 Acetone (fruity) breath r/t ketones
 Mortality Rate < 5%
 Develops more quickly
 Plasma glucose >DKA
(usually >1000mg/dL)
 pH more “normal” >7.30 ABG
 No Ketones
 More electrolyte imbalances
and renal dysFX
 Higher serum osmolarity than
DKA
 Tachycardia
 Higher Mortality Rate 10-40%
 Develops slower

31. DKA & HHS: Interventions
MANAGE AIRWAY
FLUID REPLACEMENT:
• 1st  0.9% NS, then 0.45% NS
• Assess VS, lung sounds, S&S of FVO
ELECTROLYTE REPLACEMENT:
• K+, phosphorus (K-Phos replacement), Mg+
• Monitor blood glucose, renal function,
UOutput
• EKG and electrolyte levels—Potassium

33.  Insulin Therapy
 Loading dose
 Continuous Regular Insulin Infusion
 Hourly glucose monitoring
WHEN GLUCOSE LEVELS APPROACH 200mg/dL…
 Decrease insulin drip rate
 Change IV to 5% dextrose with hypotonic saline
(D5 0.45% NS) to prevent hypoglycemia / cerebral
edema
DKA & HHS: Interventions

34. Treatment of Acidosis:
• Assess respiratory compensation and
LOC
• Usually corrected by fluids and insulin
• Bicarbonate only if pH < 6.9
• Patient and family education
DKA & HHS: Interventions

36. TEACHING:
• How to take blood sugar.
• How to draw up / administer insulin.
• What was the underlying cause?
-Teach pt how to manage those days in the
future.

39. Critical Thinking Question
 Which dysfunction should you
address first in a patient with
DKA?
A) Acidosis
B) Hyperkalemia
C) Hyperglycemia
D) Hypovolemia.
• Hypovolemia may be severe and
should be address first, followed by
hyperglycemia & then hyperkalemia.
• Acidosis is corrected by correcting the
other imbalances.

40. Critical Thinking
Question
 A patient withy type 1 diabetes
mellitus is admitted with DKA.
Which type of insulin should a
physician prescribe as an insulin
infusion?
A) 50/50
B) 70/30
C) NPH
D) Regular.
• Regular is the only type of insulin
that can be administered by IV route.

41. Critical Thinking
Question
 A patient is diagnosed with HHS. Which
assessment finding is expected with HHS?
A) Increase serum ketone level
B) Decrease serum sodium level
C) Decrease serum creatinine level
D) Increase serum hemoglobin levels
• HHS causes relative insulin deficiency resulting in
hyperosmolality. Serum hyperosmolality creates
osmotic diuresis which leads to dehydration.
• The serum Hgb levels increase due to
hemoconcentration.
• Serum NA+ and creatinine are elevated
• Ketones are not present in HHS.

42. Critical Thinking
Question
 A patient in the ER is admitted with HHS.
What assessment findings should a critical care
nurse expect when performing her admission
assessment?
A) Weakness, tachypnea, and hypertension
B) Bradycardia, diaphoresis, and chest pain
C) Shallow respirations, flushed skin and edema
D) Change in LOC, decrease RR, and hypotension
• HHS pts don’t typically
develop tachypnea, HTN,
Brady, diaphoresis, angina,
shallow resp, flushed skin, or
edema
• HHS is precipitated by severe dehydration
due to polyuria.
• Pt experience weakness, decrease skin turgor,
tachycardia, and decrease RR, and hypoTN.
• An altered LOC usually results from
intracerebral dehydration.

43. Critical thinking question
 You are the nurse discharging an 82yo gentleman
after having a cardiac angioplasty for CAD. The
patient is a non-insulin dependent individual taking
glyburide, metformin, and jardience at home. As the
nurse discharging the patient was are two important
issues to discuss?
A. check your blood sugars three times a day.
B. take all your medications as prescribed in the
morning and only your statin at night.
C. monitor your blood sugar closely taking your new
med metoprolol and eat regular meals and a snack.
• Patients taking BB are at a risk of decreased
awareness of hypoglycemia because of the
sympathetic NS.

44. DKA & HHS: Nursing
Diagnoses
 Ineffective breathing pattern
 Impaired gas exchange
 Deficient fluid volume
 Risk for ineffective therapeutic
management

45. Hypoglycemia
Blood glucose level (<70 mg/dL)
Causes:
• Too much insulin or oral
hypoglycemic agents
• Too little food
• Excessive physical activity
• 1st clinical sign – altered mental
status

46. MANIFESTATIONS OF
HYPOGLYCEMIA:
Early: altered mental status
Adrenergic symptoms:
• sweating, tremors, tachycardia, palpitations,
nervousness, hunger
CNS symptoms:
• inability to concentrate, headache, confusion,
memory lapses, slurred speech, numbness of lips
and tongue, irrational or combative behavior,
double vision, drowsiness
Severe hypoglycemia:
• may cause disorientation, seizures, and loss of
consciousness

48. Assessment
• Abrupt onset is and may be unexpected
• Symptoms vary from person to person
• Symptoms vary r/t the rapidity of decrease in
blood glucose and usual blood glucose range.
• Some pts may show S&S of hypoglycemia at 110.
• Decreased adrenergic response may affect
symptoms in persons who have had diabetes for
many years probably related to autonomic
neuropathy

49. Management of Hypoglycemia
 Treatment must be immediate
 Give 15 g of fast-acting, concentrated carbohydrate
• 3 or 4 glucose tablets
• 4–6 ounces of juice, regular soda (not diet soda),
milk, PB
• 6–10 hard candies
• 5-8 saltines
• 2–3 teaspoons of honey
 Retest blood glucose in 15 minutes:
• Retreat if <70 mg/dL or if symptoms last >10–15 minutes
& testing is not possible.
 Provide a snack with protein and carb unless the patient plans
to eat a meal within 30–60 minutes.

52. Emergency Measures
 If the patient cannot swallow or is
unconscious…
• SUBQ or IM glucagon = 1 mg
• 25–50 mL 50% dextrose solution IV
**Retest blood sugar within 15
mins.

54. Acute Adrenal Insufficiency:
ADDISON’S DISEASE
Primary: Destruction of adrenal glands
Secondary: Interferes with secretion of adrenal glands
***both can progress to ADRENAL CRISIS.
• Deficiency of glucocorticoids (cortisol):
-seen in primary & secondary
• Lack of mineralocorticoids (aldosterone) = primary
only

57. Lack of Cortisol/ Adrenal Crisis:
DECREASED…
• Production of glucose
• Metabolism of protein and fat
• Vascular tone
• Effect of catecholamines
• Intestinal motility  prone to ileus
• Inability to respond to stress

58. Lack of Aldosterone:
(primary only)
• Loss of Na+ and water
• ↓ retentions of Na+ and water
• ↓ circulating volume
• K+ and H+ ion retention
• Above all seen in primary adrenal
insufficiency

63. PRIMARY Acute Adrenal Insufficiency
Hypofunction of adrenal glands:
• Inadequate cortisol & aldosterone
• High K+
• Salt craving
• Autoimmune: Addison’s Disease
• Infiltration (Neoplasms)
• Hemorrhagic Destruction / Trauma
• Infection / Sepsis
• Drugs: Ketoconazole
• Tb, AIDs, HIV in endemic countries

64. ADRENAL CRISIS:
 Requires quick response, S&S vary
 In the critically ill it should be considered if pt is acutely ill with
fever, vomiting, shock, hypotension.
• CV SYSTEM: in adrenal crisis the cardiovascular S&S
are caused by hypovolemia, ↓ vascular tone, &
hyperkalemia.
Most common presentation:
• Hypotension refractory to fluids & requiring
pressors.
• Cannot get them off epi. or Levophed r/t adrenal
insufficiency.
-Need to give steroids.

66. Adrenal Crisis: Lab Values
• Hypoglycemia
• Hyponatremia
• Hyperkalemia
• Increased BUN, ↓ urine output
• Metabolic acidosis
• Nausea
• Vague abdominal pain (ileus)
We test for the cortisol level – cosyntropin stimulation test.
• Give a dose and expect a response in the level of 7-9
mcg/dl from baseline.
• Those who don’t respond are at high risk for mortality.

67. SECONDARY Acute Adrenal Insufficiency
Decrease Adrenocorticotropic Hormone (ACTH)
or suppressed normal secretion of steroids.
• Withdrawal of long-term steroid use
• Pituitary and hypothalamus disorders / tumors
• Systemic inflammatory response:
Infection/Sepsis
• Inadequate steroids in a highly stressed patient
who has received chronic steroid therapy

68. Acute Adrenal Insufficiency:
Assessment
• S&S of hypovolemia: tachycardia, hypotension (vascular
collapse), hypoglycemia  ALOC
 F&E imbalances:
◦ Postural hypotension
◦ Change in LOC
◦ Hyperkalemia, hypercalcemia, hyponatremia, hypoglycemia
 Profound Fatigue/Weakness
 GI complaints – abdominal pain, N/V/D
 ↓ renal perfusion & ↓ urine output
 Circulatory Shock  Death in Addisonian Crisis

69. Question:
 What’s an appropriate treatment
measure for a patient with Addisonian
crisis?
A) IV fluid replacement
B) IV corticosteroids
C) Blood glucose management
D) All of the above.

70. Question:
 A patient is admitted with hypotension, dehydration,
disorientation, and hyperpigmentation. Which
medication will most likely reverse this patients’
symptoms?
A) Parathormone  hypoparathyroidism
B) Liothyronine (Cytomel)  hypothyroidism
C) Prednisolone (Prelone)
D) Vasopressin (Pitressin)  D.I.
• Pt symptoms indicate Addison’s disease.
• Glucocorticoid meds (like prednisolone) are given to
prevent F&E losses, maintain blood glucose levels, and
maintain BP.

71. AI Diagnostics:
 Lab Values:
◦ Hypoglycemia
◦ Hyponatremia
◦ Hyperkalemia
◦ Eosinophilia
◦ Increased BUN
◦ Metabolic Acidosis
◦ Hypercalcemia
◦ Hyperuricemia
 Cosyntropin Stimulation Test

72. Cosyntropin Stimulation Test:
 To help DX:
• Primary adrenal insufficiency (Addison disease).
• Detect conditions affecting the pituitary gland
(secondary adrenal insufficiency).
 Pt receives an injection of cosyntropin (synthetic
portion of ACTH).
 This hormone should trigger the adrenal glands to
produce cortisol.
 Pt waits 30-60mins while body reacts to the cosyntropin
injection.
 Two blood samples are drawn — one before the test
and one after the test.

73. Cosyntropin Stimulation Test:
 Blood cortisol levels BELOW the acceptable range
following stimulation, pt may have…
• Acute adrenal crisis
• Addison’s disease (primary AI)
• Hypopituitarism.
 Blood cortisol levels ABOVE the expected range
following ACTH stimulation may be consistent with
Cushing’s syndrome.

74. Decreased cortisol levels may be seen with…
 Underactive or damaged adrenal glands (adrenal
insufficiency) that limit cortisol production:
• Primary adrenal insufficiency / Addison disease.
 An underactive pituitary gland or a pituitary gland
tumor that inhibits ACTH production:
• Secondary adrenal insufficiency.
 Treatment utilizing glucocorticoids, such as
dexamethasone and prednisone.

77. Nursing Interventions:
 Correct F&E imbalances
 Hormonal replacement
• Hydrocortisone (glucocorticoid &
mineralocorticoid properties)
• Fludrocortisone (mineralocorticoid)
 Patient & family education
• ID bracelet
• Awareness of S&S of insufficiency
• Doubling dose with minor stress

78.  D5NS until hypovolemia stabilizes- why do
we use D5NS solution?
• It corrects volume status and prevents
hypoglycemia.
• May need as much as 5L in first 12-24 hrs
 Hyperkalemia usually improves with fluids
& glucocorticoid replacement.
 We still need to monitor levels due to
hypokalemia may occur and pt may need to
have replacements.
 Acidosis is corrected with fluids &
glucocorticoid therapy.
 pH <7.1 or bicarb level >10meq…
give Sodium Bicarb

79.  Pts who are waiting for a DX of AI will receive
Decadron 4mg IV push q8h until the cosyntropin
test can be done.
• Once they have the results, they can modify
the dosage of medication.
GOLD STD. FOR REPLACEMENT:
Hydrocorticoid Sodium Succinate (solu-cortef)
• Bolus is given and titrated to a maintenance
dose based on pt status & blood levels.
• When the dose of hydrocortisone is
<100-150mg/day… fludrocortisone is added.
(oral mineralocorticoid)

82. Acute Adrenal Insufficiency:
Nursing Diagnoses
 Deficient fluid volume r/t hypovolemia, F&E
imbalances, hypoglycemia
 Ineffective tissue perfusion r/t hypovolemia
 Disturbed thought processes
 Imbalanced nutrition (less than body requirements)
 Deficient knowledge
 Activity intolerance

83. Question:
A client with Addison's disease has been admitted with a
history of nausea and vomiting for the past 3 days. The client
is receiving IV glucocorticoids (Solu-Medrol). Which of the
following interventions would the nurse implement?
A) Glucometer readings as ordered
B) Intake/output measurements
C) Sodium and potassium levels monitored
D) Daily weights
 IV glucocorticoids raise the glucose levels and often
require coverage with insulin.
 Answer B is not necessary at this time, sodium and potassium
levels would be monitored when the client is receiving
mineral corticoids, and daily weights is unnecessary.

84. Question:
Parental injections of cortisol for patients with Addison’s
disease should be injected:
A) After the patient eats
B) Deep into the deltoid
C) Deep into the gluteal muscle
D) Into the subcutaneous tissue
 Sufficient muscle mass is necessary for acute injection of
parental cortisol preparations.
 The nurse should inject them deep into the gluteal muscle.
 Cortisol should not be injected subQ bc it may cause sterile
abscess, tissue atrophy and pigmentation abnormalities.
 Steroid therapy causes GI disturbances with oral administration,
not IM injections. The patient does not have to have food in the
stomach before administration.

85. Cushing’s Syndrome
Excessive adrenocortical activity, caused by...
 Pituitary Tumors
 Adrenal Tumors
 Malignancies  ectopic production of ACTH
 Long-term use of corticosteroids.
- asthma, transplants, R.A.
 Manifestations of hypercortisolism

87. Cushing’s Syndrome:
Clinical Manifestations
 Altered fat metabolism:
◦ Protuding abdomen
◦ “Buffalo Hump”
◦ “Moon Face”
◦
 Protein Catabolism
◦ Muscle wasting  thin extremities
◦ Thin, fragile skin (loss of collagen)
◦ Striae - “Stretch marks”
◦ Osteoporosis
◦ Back Pain
CLASSIC
APPEARANCE

88. • Retention of Na+ & water:
- HTN
- Heart Failure
- Weight gain
• ↑ susceptibility to infection
- Loss of collagen, poor wound healing
• Gastric ulceration
• Virilization in women  depression r/t physical changes
- Appearance of masculine traits (ex: hirsutism)
- Recession of feminine traits
• Mood swings
Cushing’s Syndrome:
Clinical Manifestations

91. C - Central obesity, Cervical fat pads,
Collagen fiber weakness, Comedones (acne)
U– Urine: free cortisol and ↑ glucose
S - Striae, Suppressed immunity
H- Hypercortisolism, HTN, Hyperglycemia, Hirsutism
I- Iatrogenic (r/t ↑ administration of corticosteroids)
N- Noniatrogenic (r/t neoplasms)
G- Glucose intolerance, Growth retardation

92. Diagnostics:
 Dexamethasone Suppression Test: assessing the uptake overnight
 Plasma and urine cortisol levels (24hr urine)
 LABS:
• Hyperglycemia/?DM
• Hypernatremia
• Hypokalemia
• Decreased eosinophils
• Loss of lymphoid tissue
• ACTH levels
 CT / ultrasound to assess for tumors in pituitary & adrenal glands

93. 24 HOUR URINE:
 24-Hour urine for free cortisol
 Levels >80-120 mcg/day indicate Cushing syndrome.
 Low-dose dexamethasone suppression test used for
borderline results of 24-hour urine cortisol

94. DEXAMETHASONE SUPPRESSION TEST:
 Dexamethasone 1mg PO at 11pm.
 Plasma cortisol level is obtained at 8am the next morning.
HIGH CORTISOL (>5mg/dL) = CUSHINGS
 Suppression of cortisol <5mg/dl = hypothalamus-pituitary-
adrenal axis is functioning properly.
 Stress, depression, obesity, antiseizure meds, estrogen
can cause ↑ levels of dexamethasone.

95. Cortisol >5g/dL

96. ACTH LEVELS:
• Measurement of plasma ACTH by radioimmunoassay.
• Used in conjunction with the high-dose suppression test to
distinguish pituitary tumor from ectopic sites of ACTH
production.
****Important that patient gets blood work done in
the morning to get the most accurate levels.
• Later in the day the levels change.
• Times of the blood draw must be noted.
 Low ACTH with HIGH cortisol = adrenal disease.
 High ACTH and HIGH cortisol = pituitary or
hypothalamic disease

98. Cushing’s Syndrome: Medical Management
 Surgery:
• Trans-sphenoidal Hypophysectomy, Adrenalectomy
 Irradiation
 Adrenal Enzyme Inhibitors:
• Can reduce hyperadrenalism if the syndrome is caused by
ectopic ACTH secretion by a tumor that can’t be eradicated.
• ketoconazole (Nizoral) and aminoglutethimide (Cytadren).
 Reduction or tapering of corticosteroids GRADUALLY.
• Taper dose to the minimal amt needed to tx underlying cause.
• Adrenal insufficiency develops if corticosteroid dosage is
tapered rapidly.
• Indications of hypocortisolism- Vomiting, weakness,
dehydration, hypoTN

99. Trans-sphenoidal: Through mouth and nasal sinuses:
• Maintain nasal packing & reinforce if needed
• No blowing nose
• Frequent oral care
• HOB elevated to promote venous drainage from
surgical site.
Adrenalectomy:
• Can develop adrenal insufficiency within 12-48
hours after surgical intervention.
• Temporary replacement may be needed.
• If both adrenal glands have been removed,
life-time of adrenal hormones are needed

101. Cushing’s Syndrome:
Nursing Diagnoses
 Risk of injury
 Risk of infection
 Self-care deficit
 Impaired skin integrity
 Disturbed body image
 Disturbed thought processes

102. CUSHING’S VS. ADDISON’S

103. DIET: low Na+, high K+, high protein, low carb.

104. DIET: high Na+, low K+, high carbs

105. The nurse should monitor the patient with
Cushing's disease for which of the following?
1. Postprandial hypoglycemia
2. Hypokalemia.
3. Hyponatremia
4. Decreased urine calcium level
• Hypokalemia b/c Na+ retention (hypernatremia)
is accompanied by K+ depletion.
• The pt with Cushing's exhibits postprandial or
persistent hyperglycemia
Question:

106. Question:
Which client history is most significant in the
development of symptoms for a client who has
iatrogenic Cushing’s disease:
A. Long-term use of anabolic steroids.
B. Extended use of inhaled steroids for asthma.
C. History of long-term glucocorticoid use.
D. Family history if increased cortisol production.
• Iatrogenic Cushing’s disease is caused by medical
treatment --- In this case, by taking excessive steroids
resulting in the symptoms of moon face, buffalo hump, etc.

107. Following a hypophysectomy, post-op nursing care
should focus on…
A. Frequent monitoring of serum and urine osmolarity.
B. Parenteral administration of a GH-receptor
antagonist.
C. Keeping the patient in a recumbent position at all
times.
Need to monitor for DI from damage to the posterior
pituitary gland (lack of ADH)  diabetes insipidus
Question:

108. A nurse is providing discharge instructions to a client who has
Cushing’s syndrome. Which client statement indicates that
instructions related to the dietary management are understood?
A) “I can eat food that have a lot of potassium in them.”
B) “I will need to limit the amount of protein in my diet.”
C) “I am fortunate that I can eat all the salty foods I enjoy.”
D) “I am fortunate that I do not need to follow any special diet.”
• A diet low in carbs & Na+ but ample in protein and K+ is
encouraged for a client with Cushing’s syndrome.
• Such diet promotes weight loss, reduction of edema and
hypertension, control of hypokalemia, and rebuilding of wasted
tissue.
Question:

109. A nursing instructor asks a student to be describe the pathophysiology
that occurs in Cushing’s disease. Which statement by the student
indicates and accurate understanding of this disorder?
A) “Cushing’s disease results from an oversecretion of corticotropic
hormones.”
B) “Cushing’s disease results from an undersecretion of mineralocorticoid
hormones.”
C) “Cushing’s disease results from an undersecretion of mineralocorticoid
hormones.”
D) “Cushing disease results from an increased pituitary secretion of
adrenocorticotropic hormone.”
• Cushing’s disease is a metabolic disorder characterized by abnormally
increased secretion (endogenous) of cortisol, caused by increased
amounts of ACTH secreted by the pituitary gland.
• Addison’s disease is hypo-secretion of adrenal cortex hormones from
the adrenal gland.
Question:

110. A client has had a unilateral adrenalectomy to remove a tumor.
To prevent complications, the most important measurement in
the immediate post-operative period for the nurse to take is:
A) Blood pressure
B) Temperature
C) Output
D) Specific gravity
• BP is the best indicator of CV collapse in the client who has
had an adrenal gland removed.
• The remaining gland might have been suppressed due to the
tumor activity.
• Temperature would be an indicator of infection, decreased
output would be a clinical manifestation but would take
longer to occur than BP changes, and specific gravity changes
occur with other disorders.
Question:

111. Hyperthyroidism:
Thyroid Storm
Overproduction of thyroid
hormones:
 Affected by anterior
pituitary and
hypothalamus
 Positive and negative
feedback

112. Hyperthyroidism: Etiology
Toxic diffuse goiter: Most common cause
• Graves Disease (autoimmune)
• Usually occurs with unDX thyroid disease.
• Family HX, young women 30-40 y.o.
Toxic multi-nodular goiter:
• Heart failure or severe muscle weakness
• More common in older women 40-70 y.o.
Other: thyroid cancer, radiation, amiodarone (heavily iodinated,
can cause hyper- or hypo-thryoidism)

113. Thyroid Storm
• Inadequately controlled hyperthyroidism.
• Onset is abrupt, evoked by stress (trauma, surgery, infection)
• Caused by overproduction of T3 / T4
• T3/T4 produce a hyperdynamic & hypermetabolic state.
- Affects many major body functions  SNS, cardiac, and GI collapse.
- Fever, fatigue ALOC, delirium, manic, coma
- Tachycardia, atrial fib, SVT
• Medical emergency, death within 24- 48 hours without
treatment!!!  M.O.D.S.
• Mortality rate of 10%

114. Thyroid Storm: Clinical Manifestations
 High fever, heat intolerance, diaphoresis
 ↑ cardiac workload: ↑ risk for developing CHF
◦ Tachycardia out of proportion to fever,** hypotn
◦ Dysrhythmias: especially atrial (a. fib, sinus tach, SVT)
◦ ↑ O2 demands & alterations in respirations
 Tremors, muscle weakness, hyperreflexia
 Irritability, restlessness
 Visual disturbances (diplopia)
 Fear, delirium, overt psychosis, convulsions, stupor, coma
 Fatigue
 N/V/D, weight loss
 Swollen extremities

117. Thyroid Storm: Diagnostics
 Elevated T3 and T4
 Elevated T3 resin uptake
 Decreased TSH
 Electrolyte imbalances
 A-fib and SVT on EKG

119. Thyroid Storm:
Treatment Goals
 Identify underlying cause
 Antagonize peripheral effects of thyroid hormone
 Inhibit hormone biosynthesis / block TH release
 Supportive Therapy
• Tylenol (antipyretic)
• Cooling blanket, ice packs
• Oxygen
• Fluids
 Identify and treat precipitating cause
 Education

120. ADMINISTER MEDS:
• PO: propylthiouracil (PTU) and methimazole (Tapazole)
inhibit thyroid synthesis
• Take weeks to be effective.
• Iodine agents: inhibit production/release of hormones from
thyroid gland.
- ↓ vascularity & size of thyroid gland.
- Given only after PTU or methimazole has been given (1 hr).
• Meds to block effects of thyroid hormones:
• Beta-blockers (Inderal, atenolol)
• IV: works within minutes
• PO: works within an hour.
• High-dose glucocorticoids (block conversion of T4  T3 )

121. ,

122. Thyroid Storm: Interventions
• Monitor cardiovascular status
• Monitor hyperthermia
• Promote oxygenation- O2
• Fluid replacement
• Adequate nutrition, weight maintained
• Prevent injury
• Patient and family education
• Return to baseline mentation & personality
• Stable hemodynamics
• Effective breathing pattern
• Return to baseline activity

123. THYROID STORM TX:
 Antagonize peripheral effects of thyroid hormone
• Inderal, beta blocker, or reserpine.
• Inhibit hormone biosynthesis- tapazole
• Block release of TH- potassium iodide, iodide tablets
• Secondary options- lopanoic acid, lithium
• Supportive care- hydrocortisone Decadron
• High calorie / high protein diet

126. Hyperthyroidism: Nursing Diagnoses
• Altered body temperature
• Ineffective breathing
• Decreased cardiac output
• Activity intolerance
• Imbalanced nutrition (high cal/high protein diet)
• Ineffective coping
• Low self-esteem

127. Critical Thinking Question
 A patient is experiencing thyroid storm. Which
drug is contraindicated?
A) IV beta-adrenergic blockers
B) Aspirin
C) Propylthiouracil (PTU)
D) Corticosteroids
• Aspirin is contraindicated in pts
with thyroid storm.
• Blocks the binding of T3 and T4

128. The nurse is completing a health history of a
42 y.o. female with suspected Graves’ disease.
The nurse should assess this client for:
1. Anorexia
2. Tachycardia.
3. Weight gain
4. Cold skin
Critical Thinking Question

129. Myxedema Coma
Pathophysiology:
 Hypofunction of the thyroid
 Hypometabolism and hypodynamic state
• Myxedema coma can result from either primary or
secondary causes.
• Progresses gradually & slowly.
• Usually precipitated by infection, exposure to cold, or
sedative use.
• Cellular metabolism decreases to a fatal level if the patient
with myxedema is left untreated.

131. Myxedema Coma: Etiology
 Primary Disease: disorder of thyroid gland
• Hashimoto’s Disease (autoimmune)
• Surgical or radioactive treatment for Graves’ disease with
inadequate follow-up.
 Insufficient thyroid stimulation due to hypothalamus
or pituitary disease
 Exacerbation of hypothyroid state
 End stage of improperly treated or undiagnosed
hypothyroidism  death

132. Myxedema Coma: Clinical Manifestations
 Cognitive changes
◦ “Myxedema Madness,” hallucinations
◦ Dementia, delirium, psychosis, coma
◦ Slow and slurred speech
 Activity intolerance
 Cardiovascular
◦ Bradycardia, hypotension
◦ Cardiomegaly, muffled S3
◦ Decreased CO
◦ ECG changes
◦ Edema (periorbital, sacral, peripheral)
◦ Shock

134. • Pulmonary disturbances
• Hypoventilation
• CO2 retention  respiratory acidosis
• Pleural effusion
• Upper airway and tongue edema
• Hoarseness, dry mouth
• Depressed respirations
• Adventitious breath sounds
• Hypothermia
• Severe hypothermia w/o shivering
• 88.6F = grave prognosis
• Decreased DTRs and slow movements

135. Myxedema Coma:
Diagnostics
• Decreased T3 and T4
• Decreased T3 resin uptake
• Elevated TSH (primary)
• TSH is normal or low if problem in hypothalamus
or pituitary.
• Hypoglycemia
• Hyponatremia (r/t water retention)

137. Myxedema Coma: Management
Treat with replacement drugs:
 T4 – Synthroid
 T3 – Cytomel
 Combination of T3 + T4
F&E replacement:
 Thyroid replacement usually corrects Na+
Monitor respiratory status and gas exchange
 Metabolic issues, ECG changes (bradycardias)

140. Myxedema Coma:
Interventions
 Monitor cardiovascular status
 Manage hypothermia
 Protect from injury and infection
 Patient and family education

142. Myxedema Coma: Nursing Diagnoses
 Decreased cardiac output (CO)
 Ineffective breathing pattern
 Disturbed thought processes
 Hypothermia
 Excess fluid volume
 Risk for injury
 Activity intolerance
 Imbalanced nutrition
 Deficient knowledge

146. Antidiuretic hormone (ADH) disorders
Two most common:
 Diabetes Insipidus
 Syndrome of inappropriate ADH (SIADH)
Primary function of ADH=
regulation of water balance
and serum osmolyte.

148. Diabetes Insipidus:
 PRIMARY CAUSE: traumatic injury to posterior
pituitary or hypothalamus.
 Clinical presentation: abrupt onset of POLYURIA WITH
LITERS IN 24 HOURS.
 In conscious patients: they become thirsty and try to
replace the fluids
 In unconscious patients: don’t have the thirst
mechanism
 Hypovolemia, dry skin poor turgor weight loss,
tachycardia

150. Causes of DI:
 Idiopathic- familial, congenital
 Intracranial surgery
 Tumors: hypothalamus, pituitary
 Infections (endocarditis, sepsis)
 Tuberculosis sarcodosi
 Severe head injury
 Medications
 Renal diseases: polycystic kidney

152. Treatment goal of DI:
 Goal of treatment is to identify and correct
underlying cause.
 Restore normal fluid volume, osmolality, and
electrolytes
 Most common drug used in tx: DDAVP
(synthetic analog of vasopressin)
 When giving DDAVP monitor patient for
nausea, HA, HTN, hyponatremia

153. Syndrome of Inappropriate ADH
(SIADH)
• Caused by CNS disorders that stimulate the
hypothalamus or pituitary to produce EXCESS
SECRETION OF ADH.
• Head injury, infection, hemorrhage, surgery, stroke
• Inability to secrete a dilute urine, have fluid
retention, dilutional hyponatremia.
• Most important treatment is to withhold or
restrict fluids

154. Causes of SIADH
Ectopic causes:
 Lung cancer
 Prostrate cancer
 Hodgkin disease
CNS causes:
 Head trauma
 Infections- meningitis, lupus, stroke, Gillian barrè
 Drugs: amiodarone, nicotine, fentanyl, morphine, barbiturates,
cipro, Haldol

161. Critical Thinking Question
 A nurse is caring for a patient with diabetic ketoacidosis.
Urinalysis reveals proteinuria. Four days after admission, a
repeat urinalysis is also positive proteinuria. Why should this
result concern the nurse?
A) Proteinuria increases susceptibility to UTIs
B) Proteinuria is an early sign of nephropathy
C) Proteinuria stores are catabolized in the early stages of DKA
D) Proteinuria indicates the need for insulin reduction
• Proteinuria is an early sign of nephropathy. It’s caused by damage
to the glomerulus resulting from diabetes.
• Proteinuria isn’t associated with uncomplicated UTI’s, DKA or
insulin requirements

162. Critical Thinking Question
 A patient is admitted to ICU in thyrotoxic crisis.
Which findings indicated that the patient is
improving?
A) Respiratory rate increases
B) Heart rate decreases
C) Serum glucose levels increase
D) Body temperature increases
• Pt is hypermetabolic: causing tachypnea, tachycardia,
hyperglycemia, and hyperthermia.
• Reversal of any of these symptoms such as decrease in
HR indicates improvement in pt status.

163. Critical Thinking Question
 A patient with DKA is receiving NS solution for hydration and an infusion of
regular insulin at 8units/hour. His serum potassium level is 6 mEq/l. A
physician prescribes a sodium polystyrene sulfonate (Kayexalate) enema. The
patient should:
A) Receive calcium to protect his heart from negative effects of hyperkalemia
B) Receive the enema to lower his potassium level because hyperkalemia can
lead to cardiac dysfunction
C) Not receive the enema because as acidosis and dehydration are corrected
potassium will shift intra-cellular
D) Receive the enema because as acidosis and dehydration are corrected
potassium will shift out of the cell and hyperkalemia will worsen
• Initially K+ levels may be high in DKA; K+ leaves the cells and enters the
plasma as cells dehydrate.
• However, as insulin is administered, K+ moves back into the cells and the
serum K+ levels falls.
• If nurse gives Kayexalate, severe hypokalemia may occur

164. Critical Thinking Question
 A patient is diagnosed with adrenal crisis, a life threatening
deficiency of mineralocorticoid and glucocorticoid hormones. The
nurse should monitor the patient for which electrolyte imbalance
that is common with this condition?
A) Hyponatremia
B) Hyperglycemia
C) Hypernatremia
D) Hypokalemia
• One key change in adrenal crisis is deficiency in
the hormone aldosterone, a mineralocorticoid.
• Aldosterone regulates the reabsorption of Na+
and the excretion of K+ by the kidney. Deficiency
of aldosterone leads to ↓ Na+ reabsorption & ↑
Na+ retention.
• Consequently, large amounts of Na+ are excreted
in the urine.
• Chloride and water are also excreted.
• This results in hyponatremia along with depletion
of extracellular fluid volume, hyperkalemia and
mild metabolic alkalosis. Pt in adrenal crisis will
also have hypoglycemia, not hyperglycemia

165. Critical Thinking Question
 A patient with type 1 Diabetes arrives in the ER with serum glucose
level of 472 mg/dl. His ABG reveal pH 7.14, PaO2 90mm hg, PaCO2
35, HCO3- 18 mEq/l. These values suggest:
A) Compensated Respiratory Alkalosis
B) Respiratory Acidosis
C) Compensated Metabolic Alkalosis
D) Metabolic Acidosis

166. Critical Thinking Question
 A patient with a history of hypothyroidism is admitted to the ER
stuporous, hypotensive, and hypothermic. Admission labs show
serum glucose level of 67 mg/dl and serum sodium levels of 12 mEq/l.
Myxedema coma is diagnosed. Which finding indicates that treatment
for myxedema coma is effective?
A) Worsening cerebral hypoxia
B) Increase in body temperature
C) Decrease in heart rate
D) Increase PaCO2
• Myxedema coma follows severe, prolonged hypothyroidism.
• Thyroid supplement reverse the symptoms and if successful, cause the
pt’s body temp to increase.
• Increase PaCO2 levels, decrease cardiac output, and worsening
cerebral hypoxia indicate that the patient is not responding to
treatment.

167. Critical Thinking Question
 After thyroid surgery for Graves’ disease a patient
develops rapid atrial fibrillation, tremors, palpitations,
dyspnea, and anxiety. Which complications is the
patient most likely experiencing?
A) Hypocalcemic crisis
B) Addisonian crisis
C) Thyroid Storm.
D) Cushing syndrome
• After thyroid surgery the pt is at risk for thyroid
storm which ↑ metabolic rate.
• Hypocalcemia (which occurs if parathyroid glands
are accidentally removed during thyroid surgery)
causes numbness, tingling, paresthesia,
laryngospasm, and seizure.
• Addisonian crisis (which results from abrupt steroid
withdrawal or adrenalectomy) causes fatigue,
weakness, dehydration, and hyperkalemia.
• Cushing’s syndrome is caused by excessive
glucocorticoids.
• Myxedema from severe untreated hypothyroidism.