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PATHO/PHARM II > Conditions Effecting the Endocrine System and PharmacotherapyPart Three: Hypothalamus & Pituitary > Flashcards

Conditions Effecting the Endocrine System and PharmacotherapyPart Three: Hypothalamus & Pituitary Flashcards

Exam 3

1
Q

Hypothalamus: Where is it located?

A

Located at the base of the brain

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2
Q

Hypothalamus: what is it connected to and how?

A

Connected to the pituitary gland by pituitary stalk

Connected to anterior pituitary through blood vessel network

Connected to posterior pit. via a nerve tract

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3
Q

Hypothalamus: What does it produce?

A

Produces releasing and inhibiting hormones that work on the anterior pituitary

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4
Q

Hypothalamus: What does it produce (having to do with water)?

A

It produces antidiuretic hormone (ADH), which is stored in the posterior pituitary until it is needed.

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5
Q

Regulation by Hypothalamus:

What type of hormones does it release?

A

Growth hormone–releasing hormone

Thyrotropin-releasing hormone

Gonadotropin-releasing hormone

Corticotropin-releasing hormone

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6
Q

Regulation by Hypothalamus:

Negative feedback loop having to do with hypothalamus?

A

Hypothalamus: Releasing factor X –> pituitary: hormone A –>

Target organ get stimulated, causing release of hormone B –> Produces biologic effect

Hormone B –> hypothalamus & pituitary to suppress further release of factor X & hormone A, suppressing further release of hormone B

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7
Q

Hypopituitarism

A

Insufficient amounts/absence of anterior pituitary hormones

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8
Q

Panhypopituitarism

A

Is a rare condition that involves a lack of all the hormones your pituitary gland makes.

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9
Q

Hypopituitarism:

What is the most common cause of this?

A

Pituitary infarction or space-occupying lesions (most common)

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10
Q

Hypopituitarism:

Causes are: Pituitary infarction or space-occupying lesions (most common) what are examples?

A

Pit tumors, adenomas, aneurysms, significant blood loss

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11
Q

Hypopituitarism:

Causes include:

A

Pit infarction or space-occupying lesions (most common)

Congenital defects

Cerebral or pituitary trauma

Autoimmune conditions

Infections of brain & supporting tissues

Traumatic brain injury

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12
Q

Hypopituitarism:

Caused by: Congenital defects like what?

A

Pituitary hypoplasia, or aplasia

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13
Q

Hypopituitarism:

Caused by: Cerebral or pituitary trauma
such as?

A

Surgery,

infections,

stroke,

radiation,

injury

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14
Q

Hypopituitarism:

Cause by: Autoimmune conditions like?

A

Hypophysitis (inflamed pituitary)

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15
Q

Hypopituitarism:

Patho: How is the pituitary?

A

Pituitary highly vascular

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16
Q

Hypopituitarism:

Patho: What does the pituitary heavily rely on?

A

Relies heavily on blood from the hypothalamus

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17
Q

Hypopituitarism:

Patho: What does this make you vulnerable to? What does that lead to?

A

Vulnerable to ischemia & infarction –> tissue necrosis, edema, fibrosis –> sx of hypopituitarism

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18
Q

Hypopituitarism:

Patho: What may compress pituitary cells? What does that lead to?

A

Adenomas & aneurysms may compress pit cells –> compromised hormonal output

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19
Q

Hypopituitarism: Clinical Presentation/Tx - What does it depend on?

A

Depends on which hormones affected

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20
Q

Hypopituitarism: Clinical Presentation/Tx

Depends on which hormones affected
What are examples?

A

E.g. ACTH, TSH, FSH, LH, Growth hormone deficiency

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21
Q

Hypopituitarism: Clinical Presentation/Tx

What is evaluation and treatment?

A

Levels of pituitary hormones
Imaging – MRI, CT

Replacement of target hormones

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22
Q

Hyperpituitarism: Patho

What is it?

A

Hypersecretion of ant pit hormones

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23
Q

Hyperpituitarism:

Patho
What is caused by?

A

Commonly caused by a benign, slow-growing pituitary adenoma

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24
Q

Hyperpituitarism:

Patho
What does it do to nerves? What does that lead to?

A

Impingement on nerves: Visual & cranial nerve disturbances

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25
Q

Hyperpituitarism:

Patho: Because it is an extension to hypothalamus, what else is effected?

A

Extension to hypothalamus disturbs controls of wakefulness, thirst, appetite, & temp

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26
Q

Hyperpituitarism: Patho- Can be caused by what else?

A

Hypersecretion from tumor

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27
Q

Hyperpituitarism: Patho-Hypersecretion from tumor

Why does this occur?

A

Adenomatous tissue secretes hormones of the cell type from which it arose

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28
Q

Hyperpituitarism: Patho

How may HYPOpituitarism occur from this?

A

Hypopituitarism may occur from pressure exerted by tumor

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29
Q

Hyperpituitarism: Clinical Manifestations

What occurs?

A

Increased section of growth hormone from tumor

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30
Q

Hyperpituitarism: Clinical Manifestations

If tumor exerts enough pressure on surrounding pituitary cells what occurs?

A

Hypothyroid

Adrenal hypofunction

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31
Q

Hyperpituitarism: Clinical Manifestations

If tumor exerts enough pressure on surrounding pituitary cells hypothyroid occurs-why?

A

Hypothyroid-Because of lack of TSH

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32
Q

Hyperpituitarism: Clinical Manifestations

If tumor exerts enough pressure on surrounding pituitary cells adrenal hypofunction occurs-why?

A

Adrenal hypofunction
Low ACTH –> hypocortisolism

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33
Q

Hyperpituitarism: Clinical Manifestations

What are they related to?

A

Related to tumor growth & hyper or hyposecretion

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34
Q

Hyperpituitarism: Clinical Manifestations

What manifestations occur?

A

Visual changes, impairment –> blindness

Increased tumor size

Cranial nerves –> neuromuscular function

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35
Q

Hyperpituitarism: Clinical Manifestations

Increased tumor size leads to?

A

Increased tumor size –> headache, fatigue, neck pain, seizures

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36
Q

Acromegaly- what is it?

A

Is an increase in growth hormone which leads to grow huge bones

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37
Q

Patho of acromegaly:

How does production of too much growth hormone occur?

A

Cells produce too much growth hormone that is released into the bloodstream

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38
Q

Patho of acromegaly:

Cells produce too much growth hormone that is released into the bloodstream- What does this do to the liver?

A

Caused the liver to release a hormone called insulin growth factor-1 (IGF-1)

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39
Q

Patho of acromegaly:

Cells produce too much growth hormone that is released into the bloodstream- What does this do to the bones and soft tissue?

A

Causes the bones and soft tissue to grow

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40
Q

Patho of acromegaly
When is it diagnosed?

A

Usually dx’d adults aged 40-59

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41
Q

Patho of acromegaly

What occurs in children?

A

Peds – gigantism

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42
Q

Patho of acromegaly

Peds – gigantism

How does it occur?

A

Children & adolescents

Growth plates have not yet closed

Excessive skeletal growth ≈ 8-9ft

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43
Q

Patho of acromegaly

What are results of this?

A

overgrowth of bones and soft tissue (especially in the face, hand, and feet),

joints become enlarged, thicker, wider and arthritic

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44
Q

Patho of acromegaly:

Results:
What kind of issues occur?

A

cardiac disease,

arthritis,

carpal tunnel syndrome,

cardiomegaly,

sleep apnea, diabetes,

and hypertension,

hyperglycemia

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45
Q

Patho of acromegaly:

What are signs and symptoms?

A

Thicker eyelids,

widened nose,

protruding mandible and brow,

thicker lips,

widening of space btwn teeth

Secondary diabetes mellitus

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46
Q

Patho of acromegaly:

Signs and symptoms: Why does Secondary diabetes mellitus occur?

A

GH antagonizes insulin

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47
Q

Acromegaly Management:

What diagnostic tests are done?

A

PMH
PE
Serum hormone levels
Brain CT
Pituitary MRI
Vision testing
X-rays

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48
Q

Acromegaly Management:

Diagnostic tests done: How do serum hormone levels appear for acromegaly?

A

Acromegaly - ↑’d IGF-1 & GH

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49
Q

Acromegaly Management:

Treatment strategies: How to treat?

A

Underlying etiology & hormone affected

Somatostatin analogues (Octreotide)

GH receptor antagonists

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50
Q

Acromegaly Management:

Treatment strategies: How to treat tumors?

A

Tumors, often reoccurring:

SX
Radiation
Chemo

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51
Q

Acromegaly Management: What do Somatostatin analogues (Octreotide) do?

A

Inhibit GH production

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52
Q

Antidiuretic Hormone:

What is it known as?

A

ADH (also known as vasopressin)

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53
Q

Antidiuretic Hormone:

What does it promote?

A

Promotes renal conservation of water

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54
Q

Antidiuretic Hormone: What does it work on?

A

Works on the collecting ducts of the kidney to increase their permeability to water

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55
Q

Antidiuretic Hormone: Where does the water come from?

A

H2O withdrawn from the tubular urine back into extracellular space

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56
Q

Antidiuretic Hormone:

What does water reabsorption lead to?

A

Reabsorption (conservation) of H2O leads to very concentrated urine by the time it leaves the body

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57
Q

Antidiuretic Hormone:

What factors promoting/stimulating ~

A

controlled via hypothalamus

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58
Q

Antidiuretic Hormone:

Factors promoting/stimulating ~ controlled via hypothalamus

A

High blood osmolality sensed by hypothalamus –> ADH gets released from posterior pituitary to reabsorb water to dilute body fluids

Hypotension

Decrease in plasma volume

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59
Q

Diabetes Insipidus- What is it?

A

Deficiency of ADH

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60
Q

Diabetes Insipidus- What is it?

A

Excessive fluid excretion

DI= “Dry Inside”

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61
Q

Diabetes Insipidus- What do the kidneys do?

A

Kidneys unable to conserve water

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62
Q

What is DI deficit in?

A

While both have excess urine output, DI is from a deficit of antidiuretic hormone.

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63
Q

Diabetes Insipidus: What is it?

A

Partial or complete deficiency of ADH

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64
Q

Diabetes Insipidus:

What is it a diagnosis of?

A

DX of inability to produce concentrated urine

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65
Q

Diabetes Insipidus:

What area is diseased?

A

Disease of posterior pituitary

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66
Q

Diabetes Insipidus:

Patho: What does insufficient ADH lead to?

A

Insufficient ADH –> Large volumes of dilute urine, increased plasma osmolality

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67
Q

Diabetes Insipidus: What are the two types?

A

Central (neurogenic) DI (hypothalamus/pituitary is the cause)

Nephrogenic DI (kidneys are at fault)

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68
Q

Diabetes Insipidus:

What are examples of Central (neurogenic) DI (hypothalamus/pituitary is the cause)?

A

Examples:

Brain tumor,

head injury,

brain surgery,

CNS infections,

TBI,

thrombosis,

infections

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69
Q

Diabetes Insipidus:

Central (neurogenic) DI (hypothalamus/pituitary is the cause): How does it?

A

Pressure to the posterior pituitary from inflammation in the brain or a growth

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70
Q

Diabetes Insipidus:

Central (neurogenic) DI (hypothalamus/pituitary is the cause): How is the onset?

A

Abrupt onset

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71
Q

Diabetes Insipidus:

Nephrogenic DI (kidneys are at fault):

What occurs?

A

Adequate amount of vasopressin secreted by the posterior pituitary, but kidneys fail to respond because of other abnormalities

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72
Q

Diabetes Insipidus:

Nephrogenic DI (kidneys are at fault):

Why does it occur?

A

Genetic mutation

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73
Q

Diabetes Insipidus:

Nephrogenic DI (kidneys are at fault):

How is onset?

A

Gradual onset

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74
Q

Diabetes Insipidus: Nephrogenic DI (kidneys are at fault)

What are examples?

A

Examples: renal damage,

meds (eg loop diuretics, colchicine, lithium),

pyelonephritis,

uropathy,

polycystic kidney disease

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75
Q

Diabetes Insipidus: How is ADH secretion in Central (neurogenic) DI?

A

Decreased antidiuretic hormone

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76
Q

Diabetes Insipidus: Central (neurogenic) DI leads to decreased ADH. What does that cause?

A

Decreased water reabsorption in renal tubules

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77
Q

Diabetes Insipidus: Nephrogenic DI -how does it effect ADH?

A

Adequate ADH released

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78
Q

Diabetes Insipidus: Nephrogenic DI -causes adequate ADH released what does that lead to?

A

Decreased response of collecting ducts to ADH

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79
Q

Diabetes Insipidus: What does Central (nephrogenic) DI and Nephrogenic DI both lead to?

A

Increases excessive urine loss (polyuria)

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80
Q

Diabetes Insipidus: Central (nephrogenic) DI and Nephrogenic DI both lead to Increases excessive urine loss (polyuria): What does this cause?

A

Decreases intravascular fluid volume

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81
Q

Clinical Manifestations of Diabetes Insipidus include:

A

Polyuria

Polydipsia

Nocturia

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82
Q

Clinical Manifestations of Diabetes Insipidus: Why does polyuria occur?

A

kidneys excrete excessive dilute urine

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83
Q

Clinical Manifestations of Diabetes Insipidus: How much urine is lost with polyuria?

A

Can lose up to 8 to 12L/day (normal output 1-2L/day)

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84
Q

Clinical Manifestations of Diabetes Insipidus: Polyuria- What is the quality of the urine?

A

Low urine osmolality

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85
Q

Clinical Manifestations of Diabetes Insipidus:

Polydipsia- Why is this common?

A

Excessive thirst common due to quickly excreted water causing dehydration

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86
Q

Clinical Manifestations of Diabetes Insipidus:

What is thirst a compensation for?

A

Thirst is a compensation reaction for the loss of hydration

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87
Q

Clinical Manifestations of Diabetes Insipidus:

Complications

A

Hypernatremia

Severe dehydration

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88
Q

Clinical Manifestations of Diabetes Insipidus:

Hypernatremia: Why does this occur?

A

Hypernatremia - ADH primarily affects water reabsorption, not electrolytes; thus, sodium is retained in the body

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89
Q

Clinical Manifestations of Diabetes Insipidus:

Why does severe dehydration occur?

A

Severe dehydration - Excessive fluid loss through urine leads to intravascular fluid loss

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90
Q

Diabetes Insipidus: What is the treatment?

A

Fluid replacement – oral or IV

Eliminate causes

ADH replacement

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91
Q

Diabetes Insipidus Treatment:

What does ADH replacement consist of?

A

Vasopressin

DesmopressinDDAVP

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92
Q

Diabetes Insipidus Treatment:

ADH replacement - Vasopressin:

What is Vasopressin identical to?

A

Identical to naturally occurring ADH

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93
Q

Diabetes Insipidus Treatment:

ADH replacement - Vasopressin:

What kind of actions does it have?

A

Has powerful vasoconstrictive actions

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94
Q

Diabetes Insipidus Treatment:

Vasopressin:
Has powerful vasoconstrictive actions: What does it cause?

A

Can cause CV events, ischemia

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95
Q

Diabetes Insipidus Treatment:

Desmopressin DDAVP : What is it?

A

Structural analogue

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96
Q

Diabetes Insipidus Treatment:

DesmopressinDDAVP: How fast is response?

A

Response is rapid

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97
Q

Diabetes Insipidus Treatment:

DesmopressinDDAVP: How is urine levels?

A

Urine volume quickly drops to normal

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98
Q

Diabetes Insipidus Treatment:

DesmopressinDDAVP: How long is treatment?

A

Tx may be lifelong

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99
Q

Diabetes Insipidus Treatment:

DesmopressinDDAVP: How is the medication administered?

A

Adm PO, Sq, IV or nasal spray

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100
Q

Diabetes Insipidus Treatment:

What are adverse effects?

A

Water Intoxication

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101
Q

Diabetes Insipidus Treatment:

How does water intoxication occur?

A

Occurs from excessive water retention

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102
Q

Diabetes Insipidus Treatment:

Adverse Effects:
How does water intoxication present?

A

Preceding drowsiness, listlessness, HA

Severe –> convulsions, terminal coma

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103
Q

Diabetes Insipidus Treatment:

Adverse Effects: Water intoxification

What is treatment?

A

Tx: diuretic tx/fluid restriction

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104
Q

Diabetes Insipidus Treatment:

Adverse Effects: Water intoxification

How to prevent water intoxication?

A

Prevent with reduction of fluid intake @ TX start

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105
Q

Diabetes Insipidus Treatment:

Adverse Effects: Water intoxication

What does water intoxication cause an increased risk for?

A

↑ risk with renal impairment

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106
Q

Syndrome of Inappropriate ADH (SIADH): In basic terms, what is it

A

Excessive ADH

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107
Q

Syndrome of Inappropriate ADH (SIADH): What happens to renal water retention?

A

Increased renal water retention Siadh = “Soaked Inside”

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108
Q

SIADH: How is ADH?

A

Too much ADH is secreted from the pituitary or kidney’s response to it is excessive

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109
Q

SIADH:

What does ADH cause the body to do in general (not related to disease)?

A

ADH causes the kidney to reabsorb H2O so urine production decrease

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110
Q

SIADH: When does excessive ADH occur?

A

Increases after spinal surgery, with traumatic brain injuries, and certain drugs

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111
Q

SIADH: Who is it common in?

A

More common in older adults and hospitalized patients

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112
Q

SIADH: How is urine concentration?

A

Urine inappropriately concentrated because H2O reabsorbed that normally would be excreted.

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113
Q

SIADH: Patho

What effect does SIADH have on salt levels of the body?

A

Patho:Dilutional hyponatremia (hypoosmolality)

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114
Q

SIADH: What are causes of this?

A

Meds

Cancers

Pulmonary disorders

GI fluid losses

Fluid loss replaced only with D5W

CNS disorders

Self-induced water intoxication

Adrenal insufficiency (lack of aldosterone)

Post op

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115
Q

SIADH: Causes of SIADH

What meds could cause SIADH?

A

Meds:

Thiazides diuretics,

Chemo,

antidepressants,

antipsychotics,

narcs,

anesthetics,

NSAIDs,

thiazides

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116
Q

SIADH: Causes of SIADH

How could cancers cause SIADH?

A

*Cancers: ectopic production of ADH by solid tumors

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117
Q

SIADH: Causes of SIADH

What pulmonary disorders can cause SIADH?

A

Pulmonary disorders:

pneumonia,

TB,

CF,

resp failure

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118
Q

SIADH: Causes of SIADH

What *CNS disorders can cause SIADH?

A

brain tumors,

head injury,

meningitis,

intracranial hemorrhages,

stroke

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119
Q

SIADH:

Why would SIADH occur post op?

A

Postop: ADH released in response to stress of surgery, anesthesia, pain, nausea

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120
Q

Patho of SIADH:

What are the steps to SIADH?

(4 steps)

A
  1. ADH is released despite normal or low plasma osmolarity
  2. Increases water reabsorption in renal tubules
  3. Decreases urine production (oliguria)
  4. Increases intravascular fluid volume
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121
Q

Clinical Manifestations of SIADH include:

A

Fluid Retention and Weight Gain

Oliguria, Hyponatremia, Muscle Cramping, Weakness, GI sx

Mental Confusion, Lethargy, Muscle twitches, Irritability, Seizures, Coma

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122
Q

Clinical Manifestations of SIADH:

Why does fluid retention occur?

A

Water is reabsorbed back into circulation due to an increase in permeability of the renal distal tubule and collecting ducts caused by increased ADH.

123
Q

Clinical Manifestations of SIADH:

Why does weight gain occur?

A

Weight gain is from retained fluids, not excess fat

124
Q

Clinical Manifestations of SIADH:

Why does weight gain occur but no edema present?

A

Since most fluids are located intravascularly, fluid is retained leading to weight gain but usually no edema is present (no peripheral edema).

125
Q

Clinical Manifestations of SIADH:

Why does Hyponatremia occur?

A

The reabsorption of water increases intravascular fluid volume which dilutes sodium in the blood (dilutional hyponatremia).

126
Q

Clinical Manifestations of SIADH:

Why does Oliguria occur?

A

Reabsorption of water also causes a decrease in urine output.

127
Q

Clinical Manifestations of SIADH:

Why does Oliguria, Hyponatremia, Muscle Cramping, Weakness, GI sx
occur?

A

Hyponatremia affects normal functioning of nerve and muscle tissue causing cramping and weakness.

128
Q

Clinical Manifestations of SIADH:

Why does Mental Confusion, Lethargy, Muscle twitches, Irritability, Seizures, Coma occur?

A

Cerebral edema due to declining plasma osmolality and serum sodium levels.

129
Q

Clinical Manifestations of SIADH:

Why does swelling of brain cells occur?

A

Swelling of brain cells and neuron occurs due to hyponatremia from dilution of the excess fluid.

130
Q

Clinical Manifestations of SIADH:

Why does Mental Confusion, Lethargy, Muscle twitches, Irritability, Seizures, Coma occur?

A

Hyponatremia affects normal nerve synapses in the brain causing confusion and irritability and even seizure and coma.

131
Q

SIADH: How is it diagnosed?

A

Serum hypoosmolality

Hyponatremia

Urine hyperosmolarity

132
Q

SIADH:

What is treatment?

A

Correct the cause

Fluid restriction because of hyponatremia

Monitor neuro status

For Na loss – replacement

Administration of vasopressin (ADH) receptor antagonists – the vaptans

133
Q

SIADH:

What is treatment if Na loss is severe?

A

If severe: cautious administration of hypertonic saline to prevent damage to myelin sheath & injury & death to nerve cells in CNS

134
Q

SIADH:

Treatment: Administration of vasopressin (ADH) receptor antagonists – the vaptans

What are the examples?

A

Conivaptan

135
Q

SIADH:

Conivaptan Treatment: What does Conivaptan do?

A

Conivaptan – blocks vasopressin (V2) receptors in renal collecting ducts, thus promoting renal excretion of free water, leaving Na behind for reabsorption into blood which leads to increase in Na+ in blood

136
Q

SIADH:

Conivaptan Treatment: What is this a treatment for specifically?

A

Tx of hyponatremia/hypervolemia

137
Q

SIADH:

Conivaptan Treatment: What are Adverse Drug Reactions to this?

A

ADRs: hypokalemia,

headache,

fever,

constipation,

diarrhea,

vomiting,

thirst,

dry mouth,

polyuira

138
Q

S/sx of DI & SIADH:

How are daily weights for DI?

A

Decreases

139
Q

S/sx of DI & SIADH:

How are daily weights for SIADH?

A

Increases without edema

140
Q

S/sx of DI & SIADH:

What are mental changes related to that occur with DI?

What happens to cells and neurons

A

Related to electrolyte imbalance and hypotension

Cells and neurons shrink

141
Q

S/sx of DI & SIADH:

What are mental changes related to that occur with SIADH?

What happens to cells and neurons?

A

Related to degree of hyponatremia

Cells and neurons swell

142
Q

Adrenal Glands: Where are they located?

A

Located on each kidney

143
Q

Adrenal Glands:

What is the medulla? What does it produce?

A

Medulla: inner portion (of kidney), produces epinephrine and norepinephrine

144
Q

Adrenal Glands:

Medulla: inner portion (of kidney), produces epinephrine and norepinephrine

What is this involved in?

A

fight-or-flight stress response

145
Q

Adrenal Glands:

What is the cortex? What does it produce?

A

Cortex: outer portion that produces steroids, cortisol

146
Q

Adrenal Glands:

What steroids and stuff does the cortex produce?

A

Mineralocorticoids

Glucocorticoids

Gonadocorticoids

147
Q

Adrenal Glands:

Mineralocorticoids: What are they primarily?

A

Primarily aldosterone, which acts to conserve sodium and water

148
Q

Adrenal Glands:

Mineralocorticoids: What electrolytes do they effect? How?

A

Sodium retention, potassium & hydrogen loss

149
Q

Adrenal Glands:

What is the most potent mineralcorticoid?

A

Aldosterone is most potent naturally occurring MC & conserves Na

150
Q

Adrenal Glands:

Glucocorticoids: What do they primarily control?

A

Primarily cortisol

151
Q

Adrenal Glands:

Glucocorticoids: What is it needed for?

A

Needed to maintain life

Protect body from stress

152
Q

Adrenal Glands:

Glucocorticoids: What do they have an influence over?

A

Influence carbohydrate metabolism

153
Q

Adrenal Glands:

Gonadocorticoids are also called?

A

Gonadocorticoids, or sex hormones

154
Q

Adrenal Glands:

Gonadocorticoids are involved in what?

A

Male & female sexual characteristics

155
Q

Adrenal Glands:

Hypothalamus produces ______ to stimulate pituitary to release ______.

A

Hypothalamus produces CRH to stimulate pituitary to release ACTH

156
Q

Adrenal Glands: What does ACTH alert the adrenals to do?

A

ACTH alerts adrenals to produce cortisol

157
Q

What is the most important glucocorticoid?

A

Cortisol

158
Q

Physiological Effects of Glucocorticoids include effects on:

A

Carbohydrate metabolism

Protein metabolism

Fat metabolism

Stress

CV system

Water & Electrolytes

159
Q

Physiological Effects of Glucocorticoids:

Carbohydrate metabolism: What do glucocorticoids do for this?

A

Elevation of glucose & increase its availability to ensure brain has adequate supply

160
Q

Physiological Effects of Glucocorticoids:

Carbohydrate metabolism: Elevation of glucose & increase its availability to ensure brain has adequate supply- How does it do this?

A

Stimulates gluconeogenesis

Reduction of peripheral glucose uptake by muscle & adipose tissue

161
Q

Physiological Effects of Glucocorticoids:

Protein metabolism: What effect does glucocorticoids have on this?

A

Catabolism (breakdown) –> can cause muscle wasting & skin thinning @ high levels for prolonged time

162
Q

Physiological Effects of Glucocorticoids:

Protein metabolism: What is glucocorticoids the opposite of?

A

Opposite of insulin

163
Q

Physiological Effects of Glucocorticoids:

Fat metabolism: What do glucocorticoids have to do with fat metabolism?

A

Promote fat breakdown –> can cause fat redistribution

164
Q

Physiological Effects of Glucocorticoids:

Fat metabolism: When glucocorticoids are used for a long time what can occur?

A

When present for long time – potbelly, moon face, buffalo hump

165
Q

Physiological Effects of Glucocorticoids:

Stress: Effect of glucocorticoids on stress?

A

Adrenals secrete large amts of cortisol (during stress?)

166
Q

Physiological Effects of Glucocorticoids:

Stress: Effect of glucocorticoids on stress (bp and blood glucose)

A

Maintain BP & blood glucose.

167
Q

Physiological Effects of Glucocorticoids: What will happen with severe deficiency of cortisol?

A

In severe deficiency –> circulatory collapse & death

168
Q

Physiological Effects of Glucocorticoids:

CV system: Effect of glucocorticoids on this?

A

Maintains vascular system integrity, BP, perfusion to muscles

169
Q

Physiological Effects of Glucocorticoids:

CV system: Effect of decreased glucocorticoids on this?

A

Decreased GCs –> capillaries more permeable, vessels less able to constrict –> hypotension

170
Q

Physiological Effects of Glucocorticoids:

CV system: effect of glucocorticoids on rbcs and hgb?

A

Increased RBC, Hgb

171
Q

Physiological Effects of Glucocorticoids:

Water & Electrolytes: What does glucocorticoids work similar to?

A

Similar actions to aldosterone

172
Q

Physiological Effects of Glucocorticoids:

Water & Electrolytes: What does glucocorticoids to with these?

A

Retention of sodium & water

Excretion of potassium

173
Q

Pharmacologic Effects of Glucocorticoids:

What happens when there are high doses taken?

A

At high doses effects more intense

174
Q

Pharmacologic Effects of Glucocorticoids:

At high doses, what are the intense effects that occur?

A

Glucose levels rise

Protein synthesis suppressed

Fat deposits mobilized

Inhibits intestinal absorption of calcium

Some pts experience mineralocorticoid activity

Anti-inflammatory/immunosuppressant effects

175
Q

Pharmacologic Effects of Glucocorticoids:

Some pts experience mineralocorticoid activity: Like what?

A

Na+ retention, K+ loss

176
Q

Pharmacologic Effects of Glucocorticoids:

Anti-inflammatory/immunosuppressant effects: What happens to chemical mediators?

A

Inhibit synthesis of chemical mediators (PGs, leukotrienes, histamine)

177
Q

Pharmacologic Effects of Glucocorticoids:

Anti-inflammatory/immunosuppressant effects: What is it used for?

A

Reduce pain, swelling, warmth, redness, pain

178
Q

Pharmacologic Effects of Glucocorticoids:

Anti-inflammatory/immunosuppressant effects : How does it do this?

A

Suppress infiltration of phagocytes & suppress lymphocytes, reducing the immune component of inflammation

179
Q

Pharmacologic Effects of Glucocorticoids:

ADRs:

A

Adrenal insufficiency

Iatrogenic Cushing’s syndrome

Osteoporosis

Infection

Elevated WBC (leukocytosis)

Glucose intolerance

Myopathy (muscle injury)/weakness

Psychological agitation

PUD

Cataract/Glaucoma

Fluid & Electrolyte disturbance

180
Q

Pharmacologic Effects of Glucocorticoids:

Fluid & Electrolyte disturbance lead to?

A

Na/H2O retention –> htn, edema

181
Q

Pharmacologic Effects of Glucocorticoids:

Cataract/Glaucoma is caused by:

A

Ocular htn

182
Q

Mineralocorticoids: What do they influence?

A

Influence renal processing of sodium, potassium, and hydrogen

183
Q

Mineralocorticoids: What is an example?

A

Aldosterone

184
Q

Mineralocorticoids:

Aldosterone- what does it promote?

A

Promotes sodium and potassium hemostasis

185
Q

Mineralocorticoids:

Aldosterone- how does it promote sodium and potassium hemostasis?

A

Acts on collecting ducts of nephron to reabsorb Na+ & secrete K+ and H+

186
Q

Mineralocorticoids:

Aldosterone- what does it maintain?

A

Maintains intravascular volume

187
Q

Mineralocorticoids:

Aldosterone- what kind of effects does it have on high levels?

A

Has harmful cardiovascular effects at high levels

188
Q

Mineralocorticoids:

Aldosterone-Has harmful cardiovascular effects at high levels- like what?

A

Myocardial remodeling impairing pumping cardiac activity,

myocardial/vascular stiffening,

SNS activation,

stimulation of cardiac activity

189
Q

Mineralocorticoids:

Aldosterone-Has harmful cardiovascular effects at high levels-how is it regulated?

A

Regulated by renin-angiotensin-aldosterone system (RAAS)

190
Q

Patho of Cushing’s: What is Cushing’s caused by?

A

Excessive cortisol

191
Q

Patho of Cushing’s:

What is Cushing’s syndrome?

A

Cushing syndrome – clinical manifestations resulting from chronic exposure to excess cortisol in the body, regardless of cause

192
Q

Patho of Cushing’s:

Cushing’s syndrome causes can include what?

A

Can include iatrogenic steroids tx, over-secretion of cortisol from adrenals, over-secretion of adrenal glands by ACTH-secreting tumor in pituitary, ectopic ACTH-secreting tumor

193
Q

Patho of Cushing’s:

Cushing’s disease (specific case) –

A

excess endogenous secretion of ACTH caused by an ACTH-producing pituitary tumor

194
Q

Cushing’s Syndrome/Disease:

What are predisposing factors?

A

Adrenal adenoma: Cushing’s syndrome

Pituitary adenoma/carcinoma: Cushing’s disease

An ectopic carcinoma

Iatrogenic (caused by medical treatment)

195
Q

Cushing’s Syndrome/Disease:

Predisposing factors: Adrenal adenoma: Cushing’s syndrome- What is it?

A

Hypersecretion of corticosteroids (rare, benign)

196
Q

Cushing’s Syndrome/Disease:

Predisposing factors: Adrenal adenoma: Cushing’s syndrome- Who is it common in?

A

More common in children

197
Q

Cushing’s Syndrome/Disease:

Pituitary adenoma/carcinoma: Cushing’s disease

A

Hypersection ACTH from pituitary over-stimulates adrenals

198
Q

Cushing’s Syndrome/Disease:

An ectopic carcinoma-

A

An ectopic carcinoma causing paraneoplastic syndrome from a substance produced by a tumor (eg small cell cancer of lung)

199
Q

Cushing’s Syndrome/Disease:

Iatrogenic (caused by medical treatment) conditions:

A

Treatment with large amounts of exogenous glucocorticoids
Cushing-like syndrome

200
Q

Cushing’s Syndrome/Disease:

Pituitary adenoma/carcinoma:
What does a pituitary tumor do? What does it lead to? (Having to do with ACTH)

A

Pituitary tumor causes overproduction of the hormones ACTH and cortisol.

Loss of feedback control of ACTH.

201
Q

Cushing’s Syndrome/Disease:

Adrenal adenoma:
What does a adrenal cortex tumor cause? What does it lead to? (Having to do with ACTH)

A

Adrenal cortex tumor causes increased production of cortisol, which inhibits ACTH secretion due to negative feedback.

202
Q

Cushing’s Syndrome/Disease:

What does paraneoplastic syndrome arise from? (Having to do with ACTH)

A

Paraneoplastic syndrome (cancer) arises from tumor secretion of hormones that increases ACTH, resulting in excessive cortisol production

203
Q

Cushing’s Syndrome/Disease:

What do Iatrogenic conditions do (having to do with ACTH)

A

Iatrogenic conditions inhibit ACTH secretion and give a false elevated cortisol reading.

Administration of large amounts of oral steroids.

Steroid abuse is also a possibility.

204
Q

Effects of Cushing’s Syndrome/Disease:

A

Excessive amounts of glucocorticoids (primarily cortisol) are released from hyperplastic, thickened adrenal cortex.

205
Q

Cushing’s Clinical Manifestations cont’d:

What are symptoms of face and body?

A

Moon face (round and puffy)

Buffalo hump (fat pad back of neck)

206
Q

Cushing’s Clinical Manifestations cont’d:

Why does moon face and buffalo hump occur?

A

Excess cortisol redistributes body fat

207
Q

Cushing’s Clinical Manifestations cont’d:

How is stress response?

A

Poor stress response

208
Q

Cushing’s Clinical Manifestations cont’d:

Why is there poor stress response?

A

Hyperfunctioning adrenals overwhelmed by additional stress

209
Q

Cushing’s Clinical Manifestations cont’d:

How is hair and wound healing?

A

Thinning hair & delayed wound healing

210
Q

Cushing’s Clinical Manifestations cont’d:

Why is there thinning hair and delayed wound healing?

A

Protein synthesis is decreased

211
Q

Cushing’s Clinical Manifestations cont’d:

Why does weight gain occur?

A

Adipose tissue accumulates and fluid retention occurs

212
Q

Cushing’s Clinical Manifestations cont’d:

What happens with weight?

A

Weight gain

213
Q

Cushing’s Clinical Manifestations cont’d:

What happens to muscle and what else happens?

A

Wasting of muscle in the limbs with truncal obesity

214
Q

Cushing’s Clinical Manifestations cont’d:

Why does Wasting of muscle in the limbs with truncal obesity occur?

A

Muscles atrophy from excess cortisol

215
Q

Cushing’s Clinical Manifestations cont’d:

How is skin?

A

Thin, fragile skin with red or purple streaks, bruising

216
Q

Cushing’s Clinical Manifestations cont’d:

How is hair GROWTH?

A

Hirsutism (excessive hair growth) on chin, chest

217
Q

Cushing’s Clinical Manifestations cont’d:

Why is there Hirsutism?

A

Excess androgens (sex hormones) are secreted

218
Q

Cushing’s Clinical Manifestations cont’d:

How is emotional state?

A

Emotional liability and euphoria (mood swings)

219
Q

Cushing’s Clinical Manifestations cont’d:

Why is there Emotional liability and euphoria (mood swings)?

A

Altered metabolism of glucose, need it for brain

220
Q

Cushing’s Clinical Manifestations cont’d:

How are bones?

A

Osteoporosis

221
Q

Cushing’s Clinical Manifestations cont’d: Why is there osteoporosis?

A

Catabolic effects of bone matrix develops from excess cortisol

222
Q

Cushing’s Clinical Manifestations cont’d: How is glucose?

A

Glucose intolerance, possibly resulting in secondary diabetes

223
Q

Cushing’s Clinical Manifestations cont’d: Glucose intolerance, possibly resulting in secondary diabetes- why?

A

Gluconeogenesis and insulin resistance increase from cortisol excess

224
Q

Cushing’s Clinical Manifestations cont’d:

How is bp and electrolytes?

A

Hypertension, edema, and hypokalemia (decreased serum potassium)

225
Q

Cushing’s Clinical Manifestations cont’d:
Why is there Hypertension, edema, and hypokalemia (decreased serum potassium)?

A

Mineralocorticoid (aldosterone) effect is increased, retaining sodium and water, high cortisol can also act on mineralocorticoid receptors

226
Q

Cushing’s Clinical Manifestations cont’d:

What are people prone to?

A

Prone to infections

227
Q

Cushing’s Clinical Manifestations cont’d:

Why are they prone to infections?

A

Immune & inflammatory response suppressed

228
Q

Cushing’s Clinical Manifestations:

What are labs?

A

Mineralocorticoid effects:

Hyperglycemia

Metabolic alkalosis

Serum & urine cortisol, ACTH levels

229
Q

Cushing’s Clinical Manifestations:

Evaluation
Labs: What are Mineralocorticoid effects?

A

Mineralocorticoid effects:

Hypokalemia & Hypernatremia (Na & H2O retention)

230
Q

Cushing’s Clinical Manifestations:
Evaluation- How is Cushing’s evaluated?

A

Dexamethasone Suppression Test (ACTH suppression test; Cortisol suppression test)

231
Q

Read slide 45 when time

A
232
Q

Treatment: For Adrenal adenoma/carcinoma – ?

A

surgical removal adrenal gland

Bilateral adrenalectomy –

233
Q

Treatment: For Adrenal adenoma/carcinoma – What is needed for a Bilateral adrenalectomy?

A

– need replacement with GCs & mineralocorticoids

234
Q

Treatment:If inoperable adrenal carcinoma – What is needed?

A

If inoperable adrenal carcinoma – Mitotane

235
Q

Treatment: What is Mitotane? What does it do?

A

anticancer drug – destroys adrenocortical cells

236
Q

Cushing’s Clinical Manifestations cont’d:

Treatment:

Pituitary adenoma: How to treat? If first treatment not successful, what should be done?

A

Partial removal of pituitary may be enough lower ACTH

If partial removal unsuccessful –> may need full removal

237
Q

Cushing’s Clinical Manifestations cont’d

Treatment: What does Ketoconazole do?

A

Blocks GC synthesis & inhibits enzymes for cortisol synthesis

238
Q

Cushing’s Clinical Manifestations cont’d

Treatment: How is Ketoconazole used?

A

Off-label

used as adjunct to radiation & surgery

239
Q

Cushing’s Clinical Manifestations cont’d

Treatment: What is Ketoconazole considered?

A

Anti-androgenic

240
Q

Cushing’s Clinical Manifestations cont’d

Treatment: Ketoconazole can effect what?

A

Can cause significant liver function

241
Q

Addison Disease- What is it?

A

Adrenal Hormone Insufficiency

242
Q

Adrenal Hormone Insufficiency: What is it hypofunction of?

A

Adrenocortical hypofunction (hypocortisolism)

243
Q

Adrenal Hormone Insufficiency:

Adrenocortical hypofunction (hypocortisolism)- What is an example disease?

A

Addison disease (Primary adrenal insufficiency)

244
Q

Adrenal Hormone Insufficiency:

Addison disease (Primary adrenal insufficiency): What is it a pathology of?

A

Pathology of one or both adrenal glands

245
Q

Adrenal Hormone Insufficiency:

Addison disease (Primary adrenal insufficiency): How does it effect synthesis of steroids?

A

Inadequate corticosteroid & mineralcorticoid synthesis

246
Q

Adrenal Hormone Insufficiency:

Adrenocortical hypofunction (hypocortisolism)= Addison disease (Primary adrenal insufficiency): What happens to ACTH levels?

A

Elevated ACTH (loss of neg feedback) – no cortisol to stop ACTH

247
Q

Adrenal Hormone Insufficiency:

Adrenocortical hypofunction (hypocortisolism)= Addison disease (Primary adrenal insufficiency)- Who is it common in?

A

Most common in adults 30-60 years old, both genders affected

248
Q

Adrenal Hormone Insufficiency:

Adrenocortical hypofunction (hypocortisolism)= Addison disease (Primary adrenal insufficiency)- What are causes?

A

Causes: Genetics, other autoimmune diseases, chronic infections

249
Q

Adrenal Hormone Insufficiency:

Adrenocortical hypofunction (hypocortisolism)= Addison disease (Primary adrenal insufficiency)- How does T cells work?

A

AutoAbs & T cells attack the adrenal cortical cells

250
Q

Adrenal Hormone Insufficiency:

Adrenocortical hypofunction (hypocortisolism): Addison disease (Primary adrenal insufficiency)-

What is Addisonian Crisis?

A

Addisonian crisis—hypotension leading to vascular collapse and shock

251
Q

Adrenal Hormone Insufficiency:

Adrenocortical hypofunction (hypocortisolism)
Addison disease (Primary adrenal insufficiency): What two hormones are effected? Why?

A

Both cortisol & aldosterone affected because adrenal gland itself fails

252
Q

Adrenal Hormone Insufficiency:

Secondary hypocortisolism: What is it?

A

Adrenal atrophy

253
Q

Adrenal Hormone Insufficiency:

Secondary hypocortisolism: What does it result from?

A

Often results from prolonged exposure to exogenous glucocorticoids (steroids)

254
Q

Adrenal Hormone Insufficiency

Secondary hypocortisolism: What is the role of GCs?

A

GCs suppress ACTH secretion –> adrenal atrophy –> inadequate corticoid steroid synthesis once exogenous GCs withdrawn – never withdraw steroids, taper!

255
Q

Adrenal Hormone Insufficiency:

Secondary hypocortisolism: SLIDE NO MAKE SENSE TO MEEEE!

A

Pit infarction, pit tumors that compress ACTH-secreting cells or removal of pit gland (Decreased ACTH)
Low ACTH —> adrenal atrophy occurs & adrenal steroid synthesis depressed

256
Q

Pathophysiology of Addison’s Disease: Why does this disease occur?

A

Adrenocortical insufficiency.

257
Q

Pathophysiology of Addison’s Disease:

What happens to adrenal tissue?

A

Adrenal tissue is destroyed by autoantibodies against adrenal cortex.

258
Q

Pathophysiology of Addison’s Disease:

What does adrenal gland atrophy lead to?

A

Adrenal gland atrophy decreases production of all the adrenocortical secretions: glucocorticoids (cortisol and cortisone), mineralocorticoids (aldosterone), and androgens (sex hormones).

259
Q

Addison’s: Clinical Manifestations:

Symptoms occur based on what fact?

A

Sx of hypocortisolism & hypoaldosteronism

260
Q

Addison’s: Clinical Manifestations:

What are symptoms?

A

Weakness & easily fatigued

Skin changes – hyperpigmentation

Anorexia, n/v

Salt craving, mood changes, depression

Hyperkalemia, Hyponatremia, Hypoglycemia

261
Q

Addison’s: Clinical Manifestations:

How are electrolytes?

A

Hyperkalemia, Hyponatremia, Hypoglycemia

262
Q

Addisons’s Clinical Manifestations:

What occurs with Adrenal crisis/Addisonian crisis? (bp, water levels)

A

Hypotension –> complete vascular collapse & shock

Dehydration, lethargy, GI sx

263
Q

Addisons’s Clinical Manifestations:

When does Adrenal crisis/Addisonian crisis occur? (in who)

A

Developed in the undiagnosed & under physiologic stress

264
Q

Addison’s Clinical Manifestations cont’d:

Why does Hypoglycemia, hyponatremia, hyperkalemia occur?

A

Impaired gluconeogenesis & decreased mineralocorticoid (aldosterone activity)

265
Q

Addison’s Clinical Manifestations cont’d: How is body hair?

A

Decreased body hair

266
Q

Addison’s Clinical Manifestations cont’d:

Why is there decreased body hair?

A

Decreased androgens

267
Q

Addison’s Clinical Manifestations cont’d:

How is skin?

A

Hyperpigmentation (bronze color) in extremities, skin creases, buccal mucosa, and tongue

268
Q

Addison’s Clinical Manifestations cont’d:

Why does hyperpigmentation occur?

A

Increased ACTH, resulting from low cortisol secretion, stimulates melanocytes (skin pigmentation cells)

269
Q

Addison’s Clinical Manifestations cont’d:

What happens with blood volume?

A

Decreased blood volume

270
Q

Addison’s Clinical Manifestations cont’d:

Why is there decreased blood volume?

A

Decreased mineralocorticoid (aldosterone) activity results in fluid loss through the urine

271
Q

Addison’s Clinical Manifestations cont’d:

What happens to bp- and what does that lead to?

A

Hypotension, syncope

272
Q

Addison’s Clinical Manifestations cont’d:

Why does hypotension and syncope occur?

A

Decreased effectiveness of epinephrine and norepinephrine to vasoconstrict vessels from lack of cortisol; secondary to decreased blood volume

273
Q

Addison’s Clinical Manifestations cont’d:

How is weight?

A

Fatigue, weight loss

274
Q

Addison’s Clinical Manifestations cont’d:

Why is there weight loss?

A

Hypoglycemia

275
Q

Addison’s Clinical Manifestations cont’d:

Why are there personality changes?

A

Altered emotional stability from decreased glucocorticoids; brain needs glucose to function

276
Q

Addison’s Clinical Manifestations cont’d:

Why is there poor stress response?

A

Overwhelmed and underfunctioning adrenals: Cannot produce enough hormones for the additional stress; can lead to an Addisonian crisis (all the symptoms happen quickly and severely), a life-threatening situation

277
Q

Adrenal Crisis: What are symptoms of this?

A

Hypotension,

dehydration,

weakness,

lethargy,

GI sx

278
Q

Adrenal Crisis: What happens if it is left untreated?

A

Left untreated –> shock, death

279
Q

Adrenal Crisis:

Causes

A

Adrenal or pituitary failure

Undiagnosed disease

Failure to provide pts receiving replacement therapy with adequate GC doses

Adrenal crisis may also be triggered by abrupt withdrawal from chronic high-dose GC therapy

280
Q

Adrenal Crisis: What is treatment?

A

Rapid replacement of fluid, salt, GCs, glucose for energy

Hydrocortisone 100mg IV bolus followed by 50mg every 8 hrs

NS with dextrose

281
Q

Adrenal Crisis: Evaluation of Labs?

A

Hyponatremia & hyperkalemia

Depressed serum & urine levels of cortisol

Dehydration –> elevated BUN

Hypoglycemia

282
Q

Adrenal Crisis: Evaluation of Labs?

What does increased ACTH indicate?

A

ACTH increased – primary adrenal insufficiency

283
Q

Adrenal Crisis: Evaluation of Labs?

What does decreased ACTH indicate?

A

Decreased ACTH – pituitary infarction or tumor-compressing ACTH-secreting cells

284
Q

Slide 53- Cosyntropin

A
285
Q

Agents for Replacement Therapy in Adrenocortical Insufficiency:

What is required?

A

Replacement therapy with corticosteroids/Glucocorticoids required

286
Q

Agents for Replacement Therapy in Adrenocortical Insufficiency:

In addition to Replacement therapy with corticosteroids/Glucocorticoids required, what else may some people need?

A

Some patients also require a mineralocorticoid (eg fludrocortisone)

287
Q

Agents for Replacement Therapy in Adrenocortical Insufficiency:

What is the only mineralocorticoid available?

A

Fludrocortisone is the only mineralocorticoid available

288
Q

Agents for Replacement Therapy in Adrenocortical Insufficiency:

What are the principal glucocorticoids used?

A

Principal glucocorticoids used are hydrocortisone, dexamethasone, and prednisone

289
Q

Agents for Replacement Therapy in Adrenocortical Insufficiency:

What does chronic insufficiency require?

A

Chronic insufficiency requires LIFELONg tx (pt education a must!!!)

290
Q

Agents for Replacement Therapy in Adrenocortical Insufficiency:

What must be done in times of stress?

A

At times of stress (infections, surgery, trauma) pts MUST increase GC dose. Failure to do so could be fatal.

Take 3x the usual dose for 3 days

291
Q

Agents for Replacement Therapy in Adrenocortical Insufficiency: How is it given?

A

Oral for chronic replacement of glucocorticoids

292
Q

Agents for Replacement Therapy in Adrenocortical Insufficiency: How is the oral for chronic replacement of glucocorticoids taken?

A

Take entire dose upon awakening since levels of GCs normally peak in the AM or take ⅔ in the morning and ⅓ in the afternoon

293
Q

Agents for Replacement Therapy in Adrenocortical Insufficiency:

How are mineralcorticoids taken?

A

Mineralocorticoids taken daily

294
Q

Hydrocortisone: What is it and what is it similar to?

A

Synthetic steroid with a structure identical to that of cortisol

295
Q

Hydrocortisone: What is it used for?

A

Used for replacement therapy in adrenocortical insufficiency

296
Q

Hydrocortisone : When is oral used?

A

Oral is used for chronic therapy

297
Q

Hydrocortisone: What kind of action does it have?

A

Has both glucocorticoid & mineralocorticoid actions

298
Q

Hydrocortisone: When would parental administration occur?

A

Parental administration for acute insufficiency & to supplement oral therapy in times of stress

299
Q

Hydrocortisone: Adverse effects

A

Low dose, devoid of adverse effects

Large doses, chronic – highly toxic

300
Q

Hydrocortisone:

What are large doses for?

A

Adrenal suppression and promotion Cushing’s syndrome

301
Q

Nursing Implications of Hydrocortisone : Read slide 59

A
302
Q

What is a potent mineralcorticoid?

A

Fludrocortisone

303
Q

Fludrocortisone: What can it be used with?

A

In most cases, used in combination with hydrocortisone

304
Q

Fludrocortisone:

ADRs

A

If dose too high: Na & H2O retained, K+ is lost

Expansion of blood volume, htn , edema, cardiac enlargement

Monitor for weight gain, swelling of lower exts, irregular heartbeat, hypertension, hypoK

If these changes occur, d/c med temporarily

PATHO/PHARM II (27 decks)

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