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NURS 2514 > Chapter 6 assessment > Flashcards

Chapter 6 assessment Flashcards

1
Q

Does the endocrine system have non-specific manifestations? What are the examples? (3)

A

Yes, it often has non-specific manifestations. Examples: Fatigue, altered mood, sleep pattern

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2
Q

Why is a detailed health history important?

A

Lack of clear manifestations makes patient health history useful

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3
Q

What is the function of the thyroid gland? (4)

A
  1. Major function is production, storage and release of thyroxine (T4 inactive) and triiodothyronine (T3 active)
  2. Growth
  3. Heart rate
  4. Metabolism
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4
Q

Explain the process the release of T3 in the thyroid gland (negative feedback loop)

A

Hypothalamus releases TRH, stimulating the anterior pituitary gland which then releases TSH, stimulating the thyroid which releases T4 (inactive) –> T3 (active)

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5
Q

What are the thyroid disorders on a scale? List from Hyperthyroid to Hypothyroidism

A

Thyroid storm (thyroid crisis), Hyperthyroidism, Euthyroid, Hypothyroidism, Myxedema Coma

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6
Q

What to assess during a thyroid gland assessment? (4)

A
  • Check if thyroid is palpable
  • Symmetry
  • Tenderness
  • Goitre
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7
Q

What are the hyperthyroidism symptoms? Think “FAST” (11)

A
  • Heart beat is rapid and strong, tachycardia
  • Nervous, insomnia, rapid thoughts/speech, restless, agitated, rapid speech
  • Weak
  • Increased temp. (burning lots of calories)
  • Weight loss (high metabolic rate)
  • Menstrual irregularities/infertility
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8
Q

What happens in the GI while having hyperthyroidism? (4)

A
  • Increase in secretion
  • Increase in peristalsis
  • Diarrhea
  • Hyperactive bowel sounds
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9
Q

How is hyperthyroidism diagnosed? (3)

A
  • History and physical exam
  • Blood test for TSH, T4, and if needed T3
  • RAIU (radioactive iodine uptake test)
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10
Q

Hyperthyroidism: What would you expect to see for these blood tests if the problem is with the thyroid?

A

Low TSH and High T4

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11
Q

Hyperthyroidism: What if the problem is in the pituitary or hypothalamus?

A

High TSH and High T4

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12
Q

If the patient takes a RAIU (radioactive iodine uptake test) and tested positive what does he have?

A

Grave’s disease

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13
Q

What is the treatment of Hyperthyroidism? (5)

A
  1. Methimazole “antithyroid drug”
  2. B-adrenergic blocker (propranolol often used)
  3. Radioactive iodine (RAI)
  4. Surgical - removes significant part of thyroid gland
  5. Nutritional therapy - high calorie preventing hunger and tissue breakdown, avoid caffeine, highly seasoned food, high fibre foods to decrease abdominal pain
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14
Q

What is HYPOthyroidism and what percentage of the population does it affect?

A
  • Insufficient thyroid hormone - most often autoimmune “Hashimoto’s Thyroiditis”
  • 2%
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15
Q

What are the symptoms of hypothyroidism? Think SLOW (9)

A
  • Vital signs change (Low temp. low HR, low CO, low RR)
  • Goitre
  • Fatigue
  • Lethargy
  • Constipation
  • Weight gain
  • Cold intolerance
  • Susceptibility to infection
  • Mental changes (slowing of thought, memory loss
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16
Q

When does a patient who has hypothyroidism experience symptoms?

A

Patient must have had thyroidectomy or antithyroid therapy to notice symptoms. Otherwise, it takes months to years for patient to notice.

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17
Q

How to diagnose hypothyroidism? (4)

A
  1. History and physical exam
  2. Blood test for TSH and T4
  3. May also look for TPO antibodies
  4. May have high cholesterol & triglycerides, anemia, increased creatine kinase
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18
Q

Hypothyroidism: Why should we look for TPO antibodies?

A

If TPO antibodies are present it is likely an autoimmune disease

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19
Q

Hypothyroidism: What would we expect to see for these blood tests if the problem is with the thyroid?

A

High TSH and Low T4

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20
Q

Hypothyroidism: What if the problem is in the pituitary or hypothalamus?

A

Low TSH and Low T4

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21
Q

Hypothyroidism: Why may a patient have increased creatine kinase?

A

Due to destruction of skeletal muscle

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22
Q

How is Hypothyroidism treated?(2)

A
  1. Pharmacotherapy: Levothyroxine (Synthroid)

2. Low calorie diet to promote weight loss

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23
Q

While on treatment for hypothyroidism what do we need to monitor for? (4)

A
  1. Signs of thyrotoxicosis
  2. A month to take effect
  3. Increase in insulin requirement
  4. Lifelong treatment
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24
Q

HYPERthyroid ongoing thyroid treatment: What do we assess for? (3)

A
  1. Ongoing symptoms
  2. Worsening symptoms - associated stressors
  3. Symptoms of hypothyroidism
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25
Q

HYPOthyroidism ongoing treatment: What do we assess for? (3)

A
  1. Ongoing symptoms
  2. Worsening symptoms
  3. Symptoms of hyperthyroidism
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26
Q

What do we check for health and physical exam relating to thyroid disorders for “history”? (6)

A
  1. “OPQRST” relating to current symptoms
  2. Review of systems - head to toe
  3. Reproductive/menstrual history
  4. Patient and family history - any auto immune diseases?
  5. Patient past health history - past surgery (thyroid)
  6. Meds - immigration from iodine-deficient area
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27
Q

What do we check for health and physical exam relating to thyroid disorders for “physical”? (2)

A
  1. Vital signs
  2. General head to toe - inspection, palpation, auscultation
    • Head, neck, eyes
    • Integumentary
    • Respiratory
    • Cardiovascular
    • Abdominal
    • Special assessment - thyroid gland
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28
Q

What does the medulla secrete?

A

Catecholamines

29
Q

What does the cortex secrete?

A

Cortex secretes >50 steroid hormones, collectively known as “corticosteroids”, categorized as:

  1. Glucocorticoids - Cortisol
  2. Mineralocorticoids - Aldosterone
  3. Androgens
30
Q

What controls the adrenal glands?

A

Controlled by the hypothalamus - anterior pituitary gland

31
Q

How does the adrenal gland function?

A

Hypothalamus releases CRH, which stimulates the A. Pituitary gland which then releases ACTH, which then stimulates the adrenal cortex, which in turn releases corticosteroids, resulting in biologic effects

32
Q

What is the function of glucocorticoids? (2)

A
  1. Maintaining blood glucose

2. Has anti-inflammatory action by suppressing immune system & supportive action to respond to stress

33
Q

What is the function of Mineralocorticoids (aldosterone)?

A
  1. Essential for maintenance of fluid and electrolyte balance
34
Q

What is the function of androgens? (2)

A
  1. Produced and secreted in small but significant amounts

2. Stimulate public and axillary hair growth and sex drive in females

35
Q

What dose amount is Physiological and Pharmacologic?

A

Physiological is LOW dose

Pharmacologic is HIGH dose

36
Q

What is Cushing’s syndrome?

A

High levels of circulating corticosteroids

37
Q

What causes Cushing’s syndrome to happen? (2)

A
  1. Most common - iatrogenic administration of exogenous corticosteroid in large doses for long periods of time
  2. 85% of endogenous cause for Cushing’s syndrome is a ACTH secreting tumour in pituitary (Cushing’s disease)
38
Q

What are the Cushing’s manifestations for Androgen? (3)

A
  1. Thinning of hair
  2. Acne
  3. Increased body and facial hair
39
Q

What are the manifestations of Cushing’s for Glucocorticoids? (10)

A
  1. Buffalo hump
  2. Supraclavicular fat pad
  3. Thin extremities with muscle atrophy
  4. Thin skin and subcutaneous tissue
  5. Moon face
  6. Weight gain
  7. Pendulous abdomen
  8. Ecchymosis resulting from easy bruising
  9. Purple striae
  10. Slow wound healing
40
Q

What is the manifestations of Cushing’s for Mineralocorticoids? (2)

A
  1. BP

2. Weight gain

41
Q

How is Cushing’s diagnosed? (2)

A
  1. 24 Hour urine free cortisol - Cortisol release follows a circadian rhythm so this will catch it at different times of day (very hard to do, if one time gets thrown, you will have to do it again (repeat again next day)
  2. CT or MRI of pituitary and/or adrenals for tumour localization
42
Q

What is the treatment for Cushing’s? (2) What should never be done r/t treatment? (1)

A
  1. If due to corticosteroid use (most common) –> Gradually taper off or switch to alternate-day regimen
  2. If tumour is culprit, surgical removal of gland or tumour
  3. NEVER discontinue corticosteroids abruptly
43
Q

Cushing’s Syndrome: Nursing assessment (6)

A

Monitor:

  1. Vital signs (Increase BP, increase HR, hypertension - mineral)
  2. Daily weight (mineral or gluco)
  3. Blood glucose (gluco)
  4. Signs and symptoms of infection - redness, fever, may be minimal (look for high WBC)
  5. Signs and symptoms of thromboembolic phenomena - increase risk of clotting
  6. Emotional support
44
Q

What is the cause of Addison’s disease (auto-immune)? Primary and secondary cause of adrenal insufficiency?

A

Adrenal gland is not working and lack of endogenous corticosteroids
Primary: Auto-immune (Addison), tuberculosis, CMV, adrenal tumour
Secondary: Pituitary disease, administration of exogenous corticosteroids

45
Q

What are the primary manifestations of Addison’s? (4)

A
  1. Weakness
  2. Fatigue
  3. Weight loss
  4. Anorexia
46
Q

What are the manifestations of Addison’s? (Non-primary (6)

A
  1. Insidious onset, progressive
  2. Skin hyperpigmentation (high ACTH)
  3. Reduced Aldosterone: N&V, hypotension, diarrhea (water not retained), hyponatremia, dehydration, hyperkalemia, metabolic acidosis
    4 Reduced Cortisol: Decrease blood sugar between meals, weakness & fatigue, decrease in tolerance to stress
  4. Irritability
  5. Depression
47
Q

What is the complication for Addison’s during crisis (acute adrenal insufficiency)? (10)

A
  1. Life threatening
  2. Hypotension
  3. Tachycardia
  4. Dehydration
  5. Hyponatremia
  6. Hyperkalemia
  7. Hypoglycaemia
  8. Fever
  9. Weakness
  10. Confusion - ALL lead to shock and circulatory collapse
48
Q

Addison’s is triggered by what? (4)

A
  1. Stress
  2. Sudden corticosteroid withdrawal
  3. Adrenal surgery
  4. Sudden pituitary gland destruction
49
Q

What are the GI manifestations of Addison’s? (3)

A
  1. Nausea & vomiting
  2. Diarrhea
  3. Abdominal pain
50
Q

What is the treatment for Addison’s? (3)

A
  1. Shock management
  2. Agressive hypo-cortisone replacement
  3. Increased salt in diet (due to hyponatremia)
51
Q

Serum cortisol - What would you expect to find?

A

Cortisol level is low

52
Q
  1. How is Addison’s diagnosed (4)? 2. If the rest result is low cortisol persisting, where would the problem be located? 3. If the test result is a rise in cortisol, where would the problem be located?
A
  1. ACTH stimulation test, EKG (related to arrhythmias), CT and MRI
  2. Adrenal gland
  3. Brain
53
Q

What are abnormal Addison’s lab results? (6)

A
  1. Hyperkalemia - Not excreted
  2. Hyponatremia - Excreted due to aldosterone
  3. Hypoglycaemia - Low glucocorticoids
  4. Anemia - Lack of B12 due to low intrinsic factor
  5. Increased BUN - indicates kidney injury - Kidney needs certain blood pressure, hypotension cause low blood in kidney
  6. Low urine cortisol and aldosterone
54
Q

What is the dosage for minor stress, major stress and rule for Addison’s treatment?

A
  1. Double dose - minor stress
  2. Triple dose - major stress
  3. 3X3 Rule - patient 3x dose for 3 days in terms of stress
    * *If unsure take higher dose
    * *Patient knows in long term
55
Q

Addison’s: Nursing Implementation (2)

A
  1. Frequent assessments

2. Medications: glucocorticoids, mineralocorticoids

56
Q

What are the two extremes of ADH Dysfunction (posterior pituitary)?

A
  1. Syndrome of inappropriate ADH (SIADH) - too much

2. Diabetes Insipidus (DI) - lack of ADH secretion

57
Q

What is the pathology of SIADH?

A

Recall: ADH release despite low or normal serum osmolality

  1. Increased antidiuretic hormone
  2. Increase water reabsorption in renal tubules
  3. Increased intravascular fluid volume
  4. Dilutional hyponatremia and decreased serum osmolality
    * Changes in sodium due to dilution (low sodium)
58
Q
  1. What are the manifestations of SIADH? 2. What are the symptom related to decrease in Na+ (3)?
A
  1. Fluid retention
    2A. Muscle cramps, twitching and weakness
    2B. Vomiting, abdominal cramping, anorexia
    2C. Lethargy, confusion, headache, seizure, coma
    *Unique to low sodium
    *Compare and contrast sodium symptoms
59
Q
  1. How is SIADH diagnosed? 2. What are the other two lab results?
A
  1. Simultaneous measurements of serum and urine osmolality
    1A. Serum osmolality - decreased, dilute blood
    1B. Urine osmolality - increased, very concentrated urine even tho we have high water
    2A. Decreased serum Na+ - dilution effect
    2B. Decreased Hgb and Hct - Because of dilution effect
60
Q

SIADH: What should a nurse monitor for? (4)

A
  1. Sudden weight gain (fluid retention) - Fluid retention
  2. Urine with increased concentration
  3. Change in LOC - associated with low Na+
  4. Vital signs
61
Q

What is Diabetes Insipidus (3)?

A
  • Decreased production or secretion ADH (or lack of renal response to ADH) = inability to conserve water
  • Peeing a lot
  • High sodium due to low water
62
Q

What are the 3 types of Diabetes Insipidus?

A
  1. Central (neurogenic) - interference with ADH synthesis or release
  2. Nephrogenic - inadequate renal response to ADH
  3. Primary (psychogenic) - Excessive water intake
63
Q

What is the pathophysiology of Diabetes Insipidus?

A

Decreased antidiuretic hormone –> Decreased water reabsorbtion in renal tubules –> Decreased intravascular fluid volume –> Increased serum osmolality (hypernatremia) OR Excessive urine output

64
Q

Diabetes Insipidus: What are the Manifestations? (8)

A
  1. Dying of “thirst”
  2. Polydipsia (thirsty)
  3. Abrupt polyuria
  4. Fatigue
  5. Constipation - Low water
  6. Weight loss
  7. Dehydration
  8. Decreased LOC, seizures, shock, coma - Hypernatremia
65
Q

How is Diabetes Insipidus diagnosed? (3)

A
  1. History and physical exam - may help determine origin
  2. Labs: - Urine osmolality/specific gravity - low, extremely diluted
    - Serum osmolality - high (or high-normal if
    compensating well with oral intake, very
    concentrated)
  3. Water deprivation test - stop giving for 8-10 hrs and ADH given, if no change in urine, problem is kidney
66
Q

How is diabetes insipidus treated? (3)

A
  1. Treat primary cause if possible
  2. Central DI
    2A. Acute, hypotonic IV saline to replace urine output
    2B. Vasopressin (ADH) - hormone replacement d/t lack of ADH
  3. Nephrogenic DI
    3A. Dietary measures (low sodium, <3g daily)
    3B. Thiazide diuretics - slows the GFR so theres more, time for kidneys to absorb water
67
Q 
Diabetes Insipidus(vasopressin) Nursing Considerations
Monitor (3), Assessment & Client teaching (6)
A

Monitor: Input/output, daily weights, vital signs (dehydration signs)

Assess:

  • Weight gain
  • headache
  • restlessness
  • signs of hyponatremia
  • signs of water intoxication
  • Will need decreased dose
  • increasing dilute urine - will need an increased dose
68
Q

Clinical manifestations may be

A

System wide

69
Q

What is needed for synthesis of thyroid hormones

A

Iodine

NURS 2514 (11 decks)

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