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.
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.
10.
11.
12.
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
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!!!!!
17.
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
19.
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)
21.
22.
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)
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
35.
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.
37.
38.
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.
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
47.
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.
50.
51.
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.
53.
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
55.
56.
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
59.
60.
61.
62.
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.
65.
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.
75.
76.
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)
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
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
89.
90.
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.
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
97.
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
100.
101. Cushing’s Syndrome:
Nursing Diagnoses
Risk of injury
Risk of infection
Self-care deficit
Impaired skin integrity
Disturbed body image
Disturbed thought processes
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:
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
115.
116.
117. Thyroid Storm: Diagnostics
Elevated T3 and T4
Elevated T3 resin uptake
Decreased TSH
Electrolyte imbalances
A-fib and SVT on EKG
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 )
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.
130.
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
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)
136.
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)
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.
147.
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
149.
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
151.
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
155.
156.
157.
158.
159.
160.
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.
Editor's Notes
Endocrine system effects almost every cell, organ, and function of the body
The endocrine system is closely linked with the nervous system and the immune system
Hypothalamus and pituitary gland play a major role in hormonal regulations
Hypothalamus manufactures and secretes several releasing and inhibiting hormones that are conveyed to the pituitary.
The pituitary responds to these hormones by increasing or decreasing hormone secretions, thus regulating circulating hormone levels.
When hormones are low there is a positive feedback loop to stimulate more hormone release
A negative feedback loop is when there is too much hormones circulating it inhibits the production of more hormones.
Posterior Pituitary: oxytocin (female reproduction) and anti-diuretic hormone ADH- aka vasopressin- increase peripheral vascular resistance which increases arterial blood pressure. Key role in homeostasis and regulation of water, glucose and salt in the blood.
Thyroid:T3, T4 (cellular metabolism), calcitonin (maintain blood calcium levels)
Adrenal: adrenal medulla- catecholamines (flight or fight), adrenal cortex 3 area produce 1)mineralocorticoids, primary aldosterone 2) glucocorticoids (hydrocortisone), cortisone, corticosterone, sex hormones androgen and estrogen 3) glucocorticoids
Pancreas- alpha cells produce glucagon, beta cells produce insulin and delta cells produce somatostatin
Where are these located? Adrenal think add-renal because they are added to the renal organs (kidneys), pancreas behind the stomach extending to the spleen within the duodenal curve
What are some risk factors for developing Hyperglycemia in patients who are critically ill?
Preexisting DM, undiagnosed or diagnosed
Cormorbities like obesity, pancreatitis, cirrhosis, hypokalemia
Aging
Lack of muscular activity
Relative insulin deficiency/insulin resistance
Administer of Dextrose solutions, nutritional support
Drugs: thiazides, beta-blockers
Administer of exogenous catecholamines (dopamine, norepinephrine and epinephrine), glucocorticoids (prednisone, hydrocortisone)
Hyperglycemia due to increase gluconeogenesis, insulin resistance, and impaired glucose tolerance.
Arrow SymbolArrow TypeAlt Code
The liver responds to the lack of fuel (glucose) in the cell by converting glycogen to glucose for release into the blood stream.
Excessive glucose molecules in the serum trigger osmosis and fluid shifts occur.
Usually r/t infectious processes (pna, UTIs, surgical wounds, trauma, pancreatitis, alcohol abuse, thiazide corticosteroids)
Without endogenous insulin, the body breaks down fats for energy. In the process fatty acids develop too fast and are converted to ketones, resulting in the severe metabolic acidosis.
With the breakdown of fatty acids causes a starvation state which accompanies DKA
Kussmaul’s's: type of hyperventilation -metabolic acidosis, breathing is first rapid and shallow, but as acidosis worsens, breathing gradually becomes deep, slow, labored and gasping. The patient looks air hungry. Seen in only severe acidotic states and is rarely seen.
Osmotic diuresis due to the high glucose level pulling the fluid out of the cells. This causes a fluid loss of up to 6l of water. This then impairs insulin secretions and promotes further insulin resistance. This makes the glucose levels high due to dehydration which then continues the osmotic diuresis.
We see the altered mental status of these patients due to the cellular dehydration and hyperosmolar state.
Acidosis also affects the potassium level. For every 0.1 change in pH there ‘s a reciprocal 0.6 change in potassium. As acidosis worsens blood glucose levels increase and hyperkalemia worsens. This cycle continues until coma or death occur.
3 Main Clinical features of DKA are: Acidosis, dehydration and hyperglycemia
NML VALUES: Na (135 – 145), K+ (3.5 – 5.0), Cl- (98 – 108), HCO3 (22 – 30)
CLOSE GAP by giving IVF and insulin.
Unrelieved thirst, increased hunger, weight loss
Ketones, fluid shifts, diuresis, weight loss
Vomiting, abdominal pain (abdominal pain disappears with IVF and insulin)
Caused by an absence of or inadequate amount of insulin resulting in abnormal metabolism of carbohydrate, protein, and fat
TX: IVF, insulin drips (regular only), electrolyte replacement (K+ and bicarb to control metabolic acidosis)
Assess pt response: lactic acid levels, is gap closing, are ketones disappearing?
HYPERGLYCEMIC HYPEROSMOLAR NON-KETOTIC COMA
Hyperglycemia causes osmotic diuresis with loss of water and electrolytes; hypernatremia, and increased osmolality occur.
Hyperosmolality and hyperglycemia occur due to lack of effective insulin. Ketosis is minimal or absent.
Don’t see lipolysis and the increase of fatty acid production which means it does not convert to ketones like in DKA
Onset is gradual and patient my not notice they are in it. So when they do come in to see an MD they are really dehydrated.
Patients can loss up to 9 liters of total body water
Answer is 3, due to rapid respirations patients lose fluids from lungs and skin, by vaporization usually up to 900cc is lost through vaporization
Hyperventilation: losing moisture, more effect on fluid loss than K+ levels
High mortality rate
Happens with high calorie parenteral nutrition feedings that exceed the patient’s ability to metabolize glucose can induce HHS
HHS: no abdominal pain, no ketones, more neuro symptoms (tremors / seizures), fever, S&S of hypovolemic shock r/t massive fluid losses.
-occurs due to lack of effective insulin
-more osmotic diuresis, inc. loss of water & electrolytes
-onset is gradual, may not notice they are in it until severe dehydration occurs
DKA: absent insulin, sudden onset, ketones, abdominal pain
Dehydration > with HHS
Polyuria= excessive urine production
Polyphagia= eating too much
Polydipsia= excessive thirst
What was the underlying cause?
Electrolytes vary according to water loss and level of hydration
DKA develops quick, HHs is more insidious
DKA: hyperkalemia initially then hypokalemia as glucose levels normalize, metabolic acidosis, mild hyponatremia, rapid onset
HHS: No breath odor, BS are very elevated, hypernatremia, normal potassium levels, lack of acidosis, slower onset
Electrolytes imbalances due to severe dehydration
DKA: rehydration leads to increased plasma volume and decreased K+, insulin enhances the movement of K+ from extracellular fluid into the cells
Monitor:
Blood glucose and renal function/UO
EKG and electrolyte levels—Potassium
VS, lung assessments, signs of fluid overload
Prevention for DKA:
“Sick day rules”
Assess for underlying causes
Diagnosis and proper management of diabetes
Why do we change the fluids to have dextrose??? Prevent hypoglycemia and cerebral edema
As Blood glucose levels normalize the sodium levels normalize as well
Assess K+ levels (esp. in DKA)
Caution when giving bicarb because studies have shown it is not beneficial to the patient and may cause problems with cerebral function.
D) Hypovolemia may be severe and should be address first, followed by hyperglycemia and then hyperkalemia. Acidosis is corrected by correcting the other imbalances.
D-Regular is the only type of insulin that can be administered by IV route. The 70/30 and 50/50 insulin are combination of regular and NPH insulin and are not given IV.
D-HHS causes relative insulin deficiency resulting in hyperosmolality. Serum hyperosmolality creates osmotic diuresis which leads to dehydration. The serum hemoglobin level increases due to hemoconcentration. Serum NA and creatinine are elevated and not ketones
D- HHS is precipitated by severe dehydration due to polyuria. Pt experience weakness, decrease skin turgor, tachycardia, and decrease RR, and hypotension. An altered LOC usually results from intracerebral dehydration. HHS pts don’t typically develop tachypnea, HTN, Brady, diaphoresis, CP, shallow Resp, flushed skin, or edema
c. Patients taking beta blockers are at a risk of decreased awareness of hypoglycemia because of the sympathetic nervous system
Assess the pts normal… 110 may be their 70.
Stroke alert… first assess sugar! Altered mental status can be caused by hypoglycemia
Milk, 5-6 saltines, ½ roll of lifesavers 5-6 hard candies
Uncommon disorder and occurs in all ages of people and both sexes. Both primary and secondary Addison’s disease can progress to adrenal crisis. Hypofunction of the adrenal glands which is creates deficiency in glucocorticoids and mineralocorticoids levels.
Acute Adrenal Insufficiency AKA Addison’s Disease
This can cause profound shock
Potassium retention = Hyperkalemia
Treatment is solucortef is the drug of choice
Profound hypotension, hypoglycemia, neurologic changes (HA, confusion, lethargy, apathy, emotional labiality), hyponatremia, Hypercalcemia, tachycardia, hyperpigmentation
Most serious complication of Addison’s disease: Addisonian crisis which can occur gradually or suddenly:
Seen in Crisis: Na and water loss with K retention, arrhythmias & decrease Cardiac output, tachycardia and oliguria
First: hypotension, due to vascular collapse. Standard vasopressor therapy is difficult to regulate because the response to catecholamines by the patient is unpredictable.
Second: blood glucose plummets and coma and death ensues if immediate treatment isn’t available.
D) All the therapies indicated are first line treatment during Addisonian crisis.
C- Pt symptoms indicate Addison’s disease. Glucocorticoid med like prednisolone are given to prevent fluid and lyte loss, maintain blood glucose levels and maintain BP. Parathormone is used to treat hypoparathyoidism. Liothyronine is used to treat hypothyroidism. Vasopressin is used to treat Diabetes insipidus.
This test is used to diagnose or exclude primary and secondary adrenal insufficiency, Addison's disease and related conditions.
D5NS until hypovolemia stabilizes- why do we use D5NS solution? It corrects volume status and prevents hypoglycemia.
How many liters may be required for therapy in the first 12 to 24 hrs? as much as 5L
Hyperkalemia usually improves with fluid replacement and glucocorticoid replacement. We still need to monitor levels due to hypokalemia may occur and pt may need to have replacements.
Acidosis is correct with fluid and glucocorticoid therapy. If pH is less than 7.1 or bicarb level are less than 10meq what can we give the patient? Sodium Bicarb
Patient who they are waiting for a diagnosis of adrenal insufficiency they will receive Decadron 4mg IV push every 8 hours until the cosyntropin test can be done. Once they have the results then they can modify the dosage of medication
Gold standard for replacement is hydrocorticoid sodium succinate (solu-cortef). Bolus is given and titrated to a maintenance dose based on patients status and blood levels.
When the dose of hydrocortisone is < 100-150mg/day then fludrocortisone is added (oral mineralocorticoid)
PT education?
ID braclet
Awareness of S/S of insuffiency
Doubling dose with minor stress
These tumors increase hormone secretion
Commonly caused by steroid use- What patient population do we need to be aware of that might be at risk for this? Asthma, transplant patients, rheumatoid arthritis,
Virilization is characterized by the appearance of masculine traits and the recession of feminine traits
Women are 5 times more likely to get this than men
Depression very big- due to big physical changes
Suppression Test: Dexamethasone 1mg is administered orally at 11pm and a plasma cortisol level is obtained at 8am the next morning. Suppression of cortisol to less than 5mg/dl indicated that hypothalamus-pituitary-adrenal axis is functioning properly.
Stress, obesity, depression and medications like antiseizure and estrogen can elevate levels.
24 hour urinary free cortisol level can be used as well
Measurement of plasma ACTH by radioimmunoassay is used in conjunction with the high dose suppression test to distinguish pituitary tumor from ectopic sites of ACTH production. Low ACTH with a high cortisol level indicates adrenal disease. Elevated ACTH and cortisol indicate pituitary or hypothalamic disease
Important that patient gets blood work done during the morning to get the most accurate levels. Later in the day the levels change. Times of the blood draw must be noted.
Use CT scans or ultrasounds to view adrenal glands and look for tumors.
Through mouth and nasal sinuses:
RN care: maintain nasal packing an reinforce if needed, no blowing nose, frequent oral care, HOB to promote venous drainage from surgical site 80% success rate
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
Adrenal Enzymes inhibitors can be used to reduce hyperadrenalism if the syndrome is caused by ectopic ACTH secretion by a tumor that cannot be eradicated
If caused by medications than tapering the dose to the minimal needed to treat underlying cause
Risk for infection is a priority because….
Diet low in salt high in protein- NOT fresh fruit and vegetables, high carbohydrates and potassium, of high sodium and calories
Answer is 2. hypokalemia because sodium retention is accompanied by potassium depletion causing hypokalemia. The individual with crushing's exhibits postprandial or persistent hyperglycemia, patients with Cushing's have hypernatremia
Usually occurs with undiagnosed thyroid disease
Graves seen more in young woman 30-40 years old. Positive family history
Toxic multinodular goiter is more common in women however they are older 40-70 years old
Other causes: secondary to radiation, thyroid cancer
Amiodarone is heavily iodinated compound can cause hyper or hypothyroid
What cardiac event can occur due to hyperthyroidism??? A fib
Onset is abrupt and evoked by a stressful event such as trauma, surgery, or infection
Due to overproduction of T3 and T4 increases adrenergic activity and severe hypermetabolism results. This can rapidly lead to cardiac, sympathetic nervous system and GI collapse.
Irritability, restlessness, visual disturbances such as diplopia (double vision), swollen extremities
Due to the increased cardiac workload the patient is at risk for developing heart failure
Sinus tach / SVT… assess t3/t4, tsh … need thyroid hormones balanced.
Exophthalmos
Decrease TSH why? Due to the negative feedback
Ltye: sodium, calcium
Supportive therapy: Tylenol (antipyretic), cooling blankets, ice packs, oxygen, fluid intake
Pt and family education-long term to identify and treat precipitating causes.
Steroids, BB to control HR
PTU and tapazole can take weeks to see effects, no IV dose only oral
Iodine agents inhibits release of thryoid hormones form the thyroid gland, inhibit thyroid hormone production and decrease the vascularity and size of the thyroid gland.
Beta-blockers to block the effects of thyroid hormones (inderal, atenolol). Results should be seen within how long? Minutes using the IV route and 1 hour after oral route. High doses of glucocortiods given to block the conversion of T4 to T3 and thereby decreasing the effects of thyroid hormones on peripheral tissue.
Patient outcomes:
Temp WDL
Return to baseline mentation and personality
Stable hemodynamic within normal limits
Effective breathing pattern
Nutritional needs met and weight maintained
Return to baseline activity
Verbalize understanding of illness, treatment and potential complications
Ensure adequate nutrition & adequate volume
High cal / high protein diets
Answer is 2. increase in metabolic rate generates heat and produces tachycardia, you have anorexia in hypothyroid, loss of weight despite having a good and adequate appetite is hyperthyroid
slowed
The end stage of improperly treated, neglected or undiagnosed hypothyroidism. Life threatening with a mortality rate of 50%
2 classifications: primary-originates as a disorder of the thyroid gland. Second is caused by a failure to stimulates normal thyroid function or an inability to synthesize thyroid hormones due to an iodine deficiency or use of antithyroid medication.
Myxedema coma can result from either primary or secondary and progresses gradually and 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.
Madness--Dementia, delirium, hallucinations, coma or psychosis
Periorbital edema, dry flaky rough skin, thick brittle nails, and sacral or peripheral edema.
Cardiac: muffled S3
Decrease mental ability (slight mental slowing to sever obtundation)
slow and slurred speech
Severe hypothermia without shivering. Body temp??? 88.6F which they have a grave prognosis. If pt has a temp of 98.6 or higher suspect infection.
Decrease deep tendon reflexes
Thick dry tongue
Hoarsness
Significant depressed respirations and adventitious breath sounds
Hyponatremia from what? Water retention
Maybe vented if pt in coma
IV synthroid
IV fluids
Warming devices
Maintenance thyroid replacement
Assess LOC and ability to maintain airway
Monitor respiratory status, ABGs, Oxygen
VS and cardiac arrhythmias
Monitor temp
Medications as ordered. Sedatives are contraindicated
Administer IV fluids as ordered and monitor fluid balance status, serum lytes, and blood glucose
Assess possible source of infection- provide meticulous skin care
Need very good skin care (not moving much, dry and flaky skin)
Injury is from head injury or surgery
More in your textbook
Ddavp synthetic doesn’t have the vasopressor properties of the aquous or lysine vasopressin
May give 3% sodium iv, needs to be on a pump, monitor vitals lung sounds, monitor serum sodium levels ,I&o. not to infuse greater than 50 cc hr.
Small cell lung ca
B- 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
B-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
C- Initally K+ levels may be high in DKA; K+ leaves the cells and enters the plasma as cells dehydrate. However, as insulin is administered potassium moves back into the cells and the serum potassium levels falls. If nurse gives Kayexalate severe hypokalemia may occur
A- one key change in adrenal crisis is deficiency in the hormone aldosterone, a mineralocorticoid. Aldosterone regulates the reabsorption of sodium and the excretion of potassium by the kidney. Deficiency of aldosterone leads to decrease sodium reasborption in the distal tubules of the kidneys and increased sodium retention. Consequently, large amounts of sodium 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
D- low ph and low bicarb level indicate metabolic acidosis, which is common with elevated glucose levels. With insulin deficiency, the body breaks down fat, releasing free fatty acids. The pt bicarb levels are low because bicarb buffers the acids. Compensated respiratory alkalosis may have normal pH, PaO2 below 35 mmHG and a low bicarb level. Resp acidosis has low pH and PaO2 exceeds 45 mm hg. Compensated metabolic alkalosis has normal pH and PaO2 and bicarb elevated
B- 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.
C- after thyroid surgery the pt is at risk for thyroid storm which increases 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 and myxedema from severe untreated hypothyroidism