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Module 4 - glucocorticoids Flashcards

1
Q

How do glucocorticoids differ in their molecular mechanism of action from most drugs?

A

Glucocorticoids differ in two ways: their receptors are located inside the cell rather than on the cell surface, and they modulate the production of regulatory proteins rather than affecting signaling pathways.

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2
Q

What happens when glucocorticoids penetrate the cell membrane and bind with receptors in the cytoplasm?

A

When glucocorticoids bind with receptors in the cytoplasm, they convert the receptor from an inactive form to an active form.

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3
Q

What is the next step in the molecular mechanism of glucocorticoids after the receptor becomes active in the cytoplasm?

A

After becoming active in the cytoplasm, the receptor-steroid complex migrates to the cell nucleus.

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4
Q

What does the receptor-steroid complex do in the cell nucleus?

A

In the cell nucleus, the receptor-steroid complex binds to chromatin in DNA, which alters the activity of target genes.

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5
Q

In most cases, how do glucocorticoids affect the activity of target genes?

A

In most cases, glucocorticoids increase the activity of target genes, leading to increased transcription of messenger RNA molecules for specific regulatory proteins.

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6
Q

Are there situations where glucocorticoids suppress the activity of target genes, and if so, what is the outcome?

A

Yes, in some cases, glucocorticoids suppress the activity of the target gene, leading to decreased synthesis of certain regulatory proteins.

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7
Q

How do glucocorticoids differ in their molecular mechanism of action from most drugs?

A

Glucocorticoids differ in two ways: their receptors are located inside the cell rather than on the cell surface, and they modulate the production of regulatory proteins rather than affecting signaling pathways.

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8
Q

What happens when glucocorticoids penetrate the cell membrane and bind with receptors in the cytoplasm?

A

When glucocorticoids bind with receptors in the cytoplasm, they convert the receptor from an inactive form to an active form.

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9
Q

What is the next step in the molecular mechanism of glucocorticoids after the receptor becomes active in the cytoplasm?

A

After becoming active in the cytoplasm, the receptor-steroid complex migrates to the cell nucleus.

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10
Q

What are the pharmacologic effects of glucocorticoids when administered in high doses for nonendocrine disorders?

A

High doses of glucocorticoids produce anti-inflammatory and immunosuppressive effects that are not seen at physiologic doses.

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11
Q

Are there any physiologic effects associated with high-dose glucocorticoid administration?

A

Yes, in addition to their pharmacologic effects, high doses of glucocorticoids also produce the physiologic effects observed at low doses.

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12
Q

What are the metabolic effects of high-dose glucocorticoid therapy compared to physiologic doses?

A

High-dose glucocorticoid therapy intensifies metabolic effects, including elevated glucose levels, suppressed protein synthesis, and increased mobilization of fat deposits.

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13
Q

Do most glucocorticoids have significant mineralocorticoid activity?

A

No, most glucocorticoids have very little mineralocorticoid activity, which generally results in limited sodium retention and potassium loss.

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14
Q

Is sodium retention and potassium loss completely absent with high-dose glucocorticoid therapy?

A

No, although most glucocorticoids have minimal mineralocorticoid activity, sodium retention and potassium loss can still occur in some patients and may pose risks.

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15
Q

What effect does high-dose glucocorticoid therapy have on the intestinal absorption of calcium?

A

High-dose glucocorticoid therapy can inhibit the intestinal absorption of calcium, an effect not observed at physiologic doses.

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16
Q

What are the major clinical applications of glucocorticoids primarily related to?

A

The major clinical applications of glucocorticoids stem from their ability to suppress immune responses and inflammation.

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17
Q

What are the characteristic symptoms of inflammation, and what initiates them?

A

The characteristic symptoms of inflammation are pain, swelling, redness, and warmth, initiated by chemical mediators such as prostaglandins, histamine, and leukotrienes.

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18
Q

How do prostaglandins and histamine contribute to inflammation symptoms, particularly pain and swelling?

A

Prostaglandins and histamine promote inflammation symptoms by causing vasodilation and increasing capillary permeability. They contribute to pain, with histamine directly stimulating pain receptors, and prostaglandins sensitizing pain receptors.

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19
Q

How do neutrophils and macrophages intensify inflammation, and what damage can they cause?

A

Neutrophils and macrophages heighten inflammation by releasing lysosomal enzymes that cause tissue injury.

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20
Q

What role do lymphocytes play in amplifying inflammation, and how do they do it?

A

Lymphocytes, crucial elements of the immune system, amplify inflammation by causing direct cell injury and promoting antibody formation, which helps perpetuate the inflammatory response.

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21
Q

What are the mechanisms through which glucocorticoids interrupt the inflammatory process?

A

Glucocorticoids interrupt inflammation through multiple mechanisms, including the inhibition of chemical mediator synthesis, suppression of phagocyte infiltration, and reduction of lymphocyte proliferation.

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22
Q

How do the mechanisms by which glucocorticoids suppress inflammation compare to those of nonsteroidal anti-inflammatory drugs (NSAIDs)?

A

The mechanisms by which glucocorticoids suppress inflammation are more diverse than those of NSAIDs, which primarily inhibit prostaglandin production. Glucocorticoids act through multiple pathways, resulting in more potent anti-inflammatory effects.

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23
Q

For what purpose are glucocorticoids indicated in rheumatoid arthritis?

A

Glucocorticoids are indicated for adjunctive treatment of acute exacerbations of rheumatoid arthritis.

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24
Q

What is the primary effect of glucocorticoids in rheumatoid arthritis?

A

Glucocorticoids can reduce inflammation and pain but do not alter the course of the disease.

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25
Why is prolonged systemic use of glucocorticoids in rheumatoid arthritis generally avoided?
Prolonged systemic use of glucocorticoids is avoided due to the risk of serious complications.
26
Under what circumstances may intra-articular injections of glucocorticoids be advantageous in rheumatoid arthritis?
Intra-articular injections may be advantageous when arthritis affects only a few joints.
27
What are the advantages of using local injections of glucocorticoids in rheumatoid arthritis?
Local injections can be highly effective and have less toxicity compared to systemic therapy.
28
What can be the result of intra-articular injections of glucocorticoids in terms of pain and joint mobility?
Intra-articular injections can lead to significant reductions in pain and inflammation and may prompt increased joint mobility.
29
What precaution should be given to patients who have received intra-articular glucocorticoid injections for rheumatoid arthritis?
Patients should be cautioned against excessive use of the treated joints, even if their symptoms have improved.
30
What concern is associated with the long-term use of glucocorticoids in children?
Long-term use of glucocorticoids in children can inhibit bone growth and potentially result in decreased stature.
31
How does glucocorticoid use during periods of increased bone growth in children affect the risk of osteoporosis?
Glucocorticoid use during periods of increased bone growth increases the risk of lifetime osteoporosis.
32
What are the patient care concerns regarding the use of glucocorticoids in pregnant women?
Inadequate studies in pregnant women. Teratogenic and physiologic effects observed in animal studies. Possible contribution to cleft palate if used during the first trimester. Risk of neonatal hypoadrenalism if used later in pregnancy. Benefits versus risks assessment needed. Smallest effective dose and non-systemic formulations preferred. Hydrocortisone preferred for systemic use.
33
What advice is given regarding breastfeeding for women taking glucocorticoids?
Low doses likely have minimal impact on nursing infants. High pharmacologic doses can lead to growth delay and adverse effects in nursing infants. Breastfeeding is not recommended for women taking high doses of glucocorticoids.
34
What concerns may affect older adults who use glucocorticoids long-term?
Long-term glucocorticoid use in older adults can lead to osteoporosis, adrenal insufficiency, and gastrointestinal (GI) ulceration, which may affect them disproportionately.
35
What type of doses of glucocorticoids are associated with adverse effects?
Adverse effects of glucocorticoids occur in response to pharmacologic doses, not physiologic doses.
36
How does the intensity of adverse effects change with dosage size and treatment duration?
The intensity of adverse effects increases with higher doses and longer treatment duration of glucocorticoids.
37
Are most adverse effects of glucocorticoids observed when treatment is brief (a few days or less)?
No, most adverse effects are not observed when treatment is brief, even at high doses of glucocorticoids.
38
What is a common and serious complication of prolonged systemic glucocorticoid therapy?
Osteoporosis with fractures is a common and serious complication of prolonged systemic glucocorticoid therapy.
39
Is osteoporosis a common complication when glucocorticoids are administered via inhalation or topically?
No, it is uncommon when glucocorticoids are inhaled or administered topically, even with prolonged use.
40
Which bones are most affected by glucocorticoid-induced osteoporosis?
The ribs and vertebrae are the bones most affected by glucocorticoid-induced osteoporosis.
41
How soon can vertebral compression fractures occur in some patients on high-dose glucocorticoids?
In some cases, vertebral compression fractures can occur within weeks of starting glucocorticoid therapy.
42
What should patients on glucocorticoid therapy be observed for in relation to osteoporosis?
Patients should be observed for signs of compression fractures, such as back and neck pain, and indications of fractures in other bones.
43
What are the three primary causes of glucocorticoid-induced osteoporosis?
The three primary causes are suppression of bone formation by osteoblasts, acceleration of bone resorption by osteoclasts, and reduced intestinal calcium absorption leading to hypocalcemia and increased parathyroid hormone release.
44
How do glucocorticoids affect susceptibility to infection?
Glucocorticoids can increase susceptibility to infection by suppressing host defenses.
45
What risks are associated with glucocorticoid use in relation to infections?
Increased risk of acquiring new infections. Risk of reactivating latent infections, such as tuberculosis. Potential for masking infection symptoms, leading to fulminant infections.
46
What is the role of the inflammatory response in wound healing?
The inflammatory response plays a prominent role in wound healing.
47
How can glucocorticoid therapy affect wound healing?
Glucocorticoid therapy interferes with normal inflammatory responses and can impair and delay wound healing.
48
What effect can glucocorticoids have on plasma glucose levels?
Glucocorticoids can increase plasma glucose levels, leading to hyperglycemia and glycosuria.
49
What is myopathy, and how is it related to high-dose glucocorticoid therapy?
Myopathy is characterized by weakness, and high-dose glucocorticoid therapy can cause it. Proximal muscles of the arms and legs are most affected, and severe damage can inhibit ambulation.
50
Why can glucocorticoids cause fluid and electrolyte disturbances?
Due to their mineralocorticoid activity, glucocorticoids can cause sodium and water retention and potassium loss, potentially leading to hypertension, edema, dysrhythmias, and digitalis toxicity.
51
Is serious fluid and electrolyte disturbance common with most glucocorticoids in current use?
No, most glucocorticoids in current use have minimal mineralocorticoid activity, reducing the risk of serious fluid and electrolyte disturbances.
52
How do glucocorticoids affect growth in children, and why does growth delay occur?
Glucocorticoids can suppress growth in children, likely due to reduced DNA synthesis and decreased cell division.
53
What psychologic disturbances can systemic glucocorticoids cause, and what percentage of patients experience them?
Systemic glucocorticoids can cause mild reactions like insomnia, anxiety, agitation, or irritability in about 60% of patients. Approximately 6% experience severe reactions, including delirium, hallucinations, depression, euphoria, or mania, and some may become suicidal, with up to one-third experiencing this outcome.
54
Does a history of previous psychiatric illness predispose patients to psychologic reactions caused by glucocorticoids?
No, previous psychiatric illness does not seem to predispose patients to psychologic reactions caused by glucocorticoids, and a history of good mental health does not provide protection.
55
What ocular complications can result from long-term glucocorticoid therapy?
Cataracts and open-angle glaucoma are common complications of long-term glucocorticoid therapy.
56
What factors may contribute to the development of cataracts in individuals receiving glucocorticoid therapy?
The development of cataracts may be related to factors such as age, dosage, or individual susceptibility in those receiving glucocorticoid therapy.
57
How can glucocorticoids predispose individuals to peptic ulcer disease, and what additional factors increase the risk of ulceration?
Glucocorticoids can predispose individuals to peptic ulcer disease by inhibiting prostaglandin synthesis, augmenting gastric acid and pepsin secretion, inhibiting mucus production, and reducing gastric mucosal blood flow. The risk for ulceration is increased by concurrent use of other ulcerogenic drugs, such as aspirin and NSAIDs.
58
What is iatrogenic Cushing syndrome, and what are its prominent symptoms?
Iatrogenic Cushing syndrome is induced by long-term glucocorticoid therapy and presents with symptoms identical to those of naturally occurring Cushing syndrome. Prominent symptoms include hyperglycemia, glycosuria, fluid and electrolyte disturbances, osteoporosis, muscle weakness, cutaneous striations, and lowered resistance to infection. Redistribution of fat produces central obesity, a rounded face, and a fat pad at the cervical spine characteristic of Cushing syndrome and Cushing disease.
59
What are some mild psychologic disturbances that can result from systemic glucocorticoid use, and what percentage of patients experience them?
Mild psychologic disturbances may include insomnia, anxiety, agitation, or irritability. Approximately 60% of patients experience these mild reactions.
60
What are severe psychologic disturbances that can occur due to systemic glucocorticoid use, and how common are they?
Severe psychologic disturbances may include delirium, hallucinations, depression, euphoria, or mania. These severe reactions occur in approximately 6% of patients.
61
What is the risk of suicidal tendencies in patients experiencing severe psychologic disturbances caused by glucocorticoids?
Up to one-third of patients experiencing severe psychologic disturbances may become suicidal.
62
Does a history of previous psychiatric illness increase the risk of psychologic reactions caused by glucocorticoids?
No, a history of previous psychiatric illness does not appear to predispose patients to psychologic reactions caused by glucocorticoids.
63
What complications related to the eyes can arise from long-term glucocorticoid therapy?
Long-term glucocorticoid therapy can lead to cataracts and open-angle glaucoma.
64
What factors may contribute to the development of cataracts in individuals receiving glucocorticoid therapy?
Factors such as age, dosage, or individual susceptibility may contribute to the development of cataracts in individuals receiving glucocorticoid therapy.
65
How do glucocorticoids affect the risk of peptic ulcer disease, and what can increase the risk of ulceration?
* Glucocorticoids can increase the risk of peptic ulcer disease by inhibiting prostaglandin synthesis and promoting factors that predispose to ulceration. * Concurrent use of other ulcerogenic drugs, like aspirin and NSAIDs, further increases the risk of ulceration.
66
What is iatrogenic Cushing syndrome, and what are some of its characteristic symptoms?
* Iatrogenic Cushing syndrome is a condition induced by long-term glucocorticoid therapy, presenting with symptoms identical to those of naturally occurring Cushing syndrome. * Prominent symptoms include hyperglycemia, glycosuria, fluid and electrolyte disturbances, osteoporosis, muscle weakness, cutaneous striations, and lowered resistance to infection. * Redistribution of fat leads to central obesity, a rounded face, and a fat pad at the cervical spine, characteristic of Cushing syndrome and Cushing disease.
67
What is adrenal suppression, and why is it a concerning adverse effect of long-term glucocorticoid therapy?
Adrenal suppression is the inhibition of the adrenal glands' ability to produce glucocorticoids due to the prolonged use of exogenous glucocorticoids. It is concerning because when glucocorticoid therapy is discontinued, the adrenal glands may be unable to produce glucocorticoids, leading to adrenal insufficiency.
68
How do glucocorticoids affect the release of CRH and ACTH from the hypothalamus and anterior pituitary, respectively?
Glucocorticoids suppress the release of CRH (corticotropin-releasing hormone) from the hypothalamus and ACTH (adrenocorticotropic hormone) from the anterior pituitary.
69
What happens to the adrenal glands during prolonged glucocorticoid therapy?
The adrenal glands can atrophy and lose their ability to synthesize cortisol and other glucocorticoids due to the prolonged absence of ACTH.
70
Why is adrenal insufficiency a concern when discontinuing prolonged glucocorticoid therapy, and how do patient responses vary?
Adrenal insufficiency is a concern because the adrenal glands may not immediately produce glucocorticoids when therapy is stopped, potentially leading to life-threatening situations. Patient responses to adrenal recovery are highly individualized, and the time needed for recovery can range from as short as 5 days to as long as a year.
71
What primarily determines the extent of adrenal suppression and the time required for adrenal recovery in patients receiving glucocorticoid therapy?
The duration of glucocorticoid use is the primary factor determining the extent of adrenal suppression and the time required for adrenal recovery. Dosage size is of secondary importance in this context.
72
Why is adrenal suppression concerning during periods of physiologic stress for patients on long-term glucocorticoid therapy?
Adrenal suppression can prevent the adrenal glands from secreting the larger amounts of glucocorticoids needed to cope with physiologic stress.
73
What is the significance of glucocorticoid secretion during periods of stress, such as trauma or surgery?
During stress, glucocorticoids play a crucial role in supporting the body's response and are essential for life, especially in cases of severe stress.
74
What should be done for patients on long-term glucocorticoid therapy when they face periods of physiologic stress?
Patients on long-term glucocorticoid therapy should receive increased doses during times of stress, unless they are already on very high doses.
75
Why might supplemental doses of glucocorticoids be necessary for patients even after discontinuing long-term glucocorticoid therapy during periods of stress?
After discontinuing glucocorticoid therapy, adrenal function may not have fully recovered. Thus, supplemental doses of glucocorticoids may be required during times of stress to ensure an adequate stress response.
76
Why is caution required when combining glucocorticoids with certain drugs like digoxin?
Combining glucocorticoids with digoxin can increase the risk of digoxin-induced dysrhythmias due to hypokalemia caused by glucocorticoids.
77
Which classes of diuretics should be used cautiously with glucocorticoids, and why?
Thiazide and loop diuretics should be used with caution alongside glucocorticoids because they can further deplete potassium levels, increasing the risk of hypokalemia.
78
What monitoring is advisable when glucocorticoids are used in combination with drugs like digoxin and diuretics?
Monitoring plasma potassium levels is advisable to detect and address potential hypokalemia. Additionally, healthcare providers should remain vigilant for signs and symptoms of digoxin toxicity and fluid/electrolyte imbalance.
79
Why is concurrent use of NSAIDs and glucocorticoids a concern?
Concurrent use of NSAIDs and glucocorticoids increases the risk of GI ulceration and bleeding due to their adverse effects on the GI tract.
80
How can glucocorticoid therapy affect glycemic control in diabetic patients?
Glucocorticoids can induce hyperglycemia, necessitating adjustments in the doses of glucose-lowering drugs like insulin or oral hypoglycemic agents for diabetic patients.
81
What impact can glucocorticoids have on vaccine effectiveness, and what is the concern with live virus vaccines?
Glucocorticoids possess immunosuppressant properties that can diminish antibody responses to vaccines. When live virus vaccines are administered alongside glucocorticoids, there's an increased risk of both developing and spreading viral diseases.
82
What are the contraindications for glucocorticoid use?
Glucocorticoids are contraindicated for patients with systemic fungal infections and those receiving live virus vaccines.
83
In which patient populations should glucocorticoids be used with caution?
Glucocorticoids should be used with caution in pediatric patients. Pregnant or breastfeeding women should also exercise caution when using glucocorticoids.
84
What are some medical conditions that require caution when using glucocorticoids?
Caution is necessary in patients with conditions such as hypertension, heart failure, renal impairment, esophagitis, gastritis, peptic ulcer disease, diabetes mellitus, osteoporosis, open-angle glaucoma, and infections that are resistant to treatment.
85
Why is caution required during concurrent therapy with glucocorticoids and certain medications?
Caution is needed when using glucocorticoids concurrently with potassium-depleting diuretics, digoxin, insulin, oral hypoglycemics, and NSAIDs due to potential interactions and risks associated with these combinations.
86
How should patients take glucocorticoids in terms of timing and what can they do to reduce gastrointestinal discomfort?
Patients should take glucocorticoids in the morning to mimic the natural hormone release rhythm. Taking them with milk or a snack can help reduce gastrointestinal discomfort.
87
What is the risk of abruptly discontinuing high or prolonged dosing of glucocorticoids, and what can happen during withdrawal?
Abrupt discontinuation of high or prolonged glucocorticoid dosing can lead to adrenal suppression, which can be life-threatening. Withdrawal symptoms may also occur.
88
Why is it important for patients taking glucocorticoids to carry identification like a Medic Alert bracelet?
Carrying identification ensures proper dosing during emergencies, such as trauma, where higher glucocorticoid doses may be needed to mimic the normal stress response.
89
How can glucocorticoids affect the risk of infection, and what should patients do if they suspect an infection?
Glucocorticoids can increase the risk of infection. Patients should be aware of early signs of infection, such as fever and malaise, and contact the clinic if these symptoms develop.
90
What are the signs and symptoms of fluid retention and hypokalemia, and what should patients do if they experience them?
Signs of fluid retention include weight gain and lower extremity swelling. Signs of hypokalemia include muscle weakness, irregular pulses, and cramping. Patients should notify the prescriber if these symptoms occur.
91
Why are regular eye examinations important during glucocorticoid therapy, and what should patients do if they notice changes in their vision?
Regular eye examinations help reduce the risk of cataracts and glaucoma associated with glucocorticoid use. Patients should contact the clinic if their vision becomes cloudy or blurred.
92
How can glucocorticoids potentially affect the gastrointestinal system, and what should patients do if they notice specific changes?
Glucocorticoids can increase the risk of GI bleeding. Patients should avoid over-the-counter drugs without consulting the provider and contact the clinic if they observe black, tarry stools.
93
What should patients be informed about regarding possible psychological reactions while taking glucocorticoids, and what should they do if they experience such reactions?
Patients should be informed about possible psychologic reactions and instructed to report disturbing symptoms. They should understand that dosage adjustments or other medications may be needed to manage these symptoms.
94
What lab parameters should be assessed in patients taking glucocorticoids, and when should this assessment occur?
Patients on glucocorticoids should have CBC, glucose, electrolytes, and lipids assessed. Initially, this should be done in 1 month, followed by assessments every 6 to 12 months if the patient's condition remains stable.
95
Why is it important to conduct eye exams regularly in patients taking glucocorticoids, and how often should these exams be performed?
Regular eye exams are essential to monitor for potential ocular complications associated with glucocorticoid use. These exams should be conducted every 6 months.
96
What should healthcare providers inquire about at each visit for patients on glucocorticoids, and what should they do if muscle weakness is reported?
Healthcare providers should ask about muscle weakness at each visit. If weakness is reported, they should assess the proximal muscle strength of extremities.
97
How should stools be monitored in patients taking glucocorticoids, and when should testing be performed?
Stools should be periodically tested, such as with Hemoccult. Testing should also occur as needed if there are suspicions of GI ulceration or if the patient reports GI discomfort or black or red stools.
98
How often should bone mineral density (BMD) be checked in patients on glucocorticoids, and what if it decreases from baseline?
BMD should be checked in 1 year and, if stable compared with baseline, every 2 to 3 years thereafter. If BMD decreases from baseline, it should be assessed annually.
99
What metabolic parameters should be periodically assessed in patients taking glucocorticoids, and how often should this assessment occur?
Healthcare providers should periodically assess serum glucose and the metabolic panel as guided by the patient's presentation.
100
What vital signs and measurements should be assessed at every visit for patients on glucocorticoids?
Healthcare providers should assess blood pressure (BP) and body mass index (BMI) at every visit.
101
In pediatric patients taking glucocorticoids, what specific parameter should be measured every 6 months?
In pediatric patients, healthcare providers should measure height every 6 months to monitor potential growth effects associated with glucocorticoid use.

NUR1142 (112 decks)

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