Exam 3: Endocrine disorders Flashcards
1
Q
Endocrine glans are
A
Ductless glands that affect bodily activities
2
Q
Endocrine glands release chemical messengers called
A
Hormones
3
Q
Hormones are released directly into the extracellular space to go into
A
Capillaries, then the blood, then into the target organ
4
Q
Hormones exert specific effects on
A
Target organs or tissues that have specific receptors for the hormone
5
Q
Receptors for lipid-soluble hormones
A
Inside the cell
6
Q
Receptors for water soluble hormones
A
Outside cell
7
Q
Hormones are released
A
- In response to altered cellular environment
- In order to maintain a regulated level of certain substance
8
Q
Hormone secretions are typically regulated by
A
Negative feedback control
9
Q
Negative feedback
A
Information about the effects of the hormone are fed back to the gland, which ten decreases secretion of the hormone
10
Q
Master gland
A
Pituitary gland
11
Q
Pituitary gland to attached to
A
Hypothalamus
12
Q
Anterior lobe is also called
A
Adenohypophysis
13
Q
Anterior lobe is connected to the hypothalamus via
A
blood vessels
14
Q
Posterior lobe is also called
A
Neurohypophysis
15
Q
Posterior lobe it ____ to the hypothalamus
A
Neurally connected
16
Q
Anterior and posterior lobe is separated by
A
Pars intermedia
17
Q
Regulating hormones form the hypothalamus stimulate or inhibit
A
release of hormones from adenohypophysis
18
Q
Does the posterior lobe synthesis hormones?
A
No, instead it stores and releases two hormones
19
Q
Hormones that posterior lobe stores and releases
A
ADH
Oxytocin
20
Q
Posterior lobe is connected to hypothalamus via
A
Hypothalamic-hypophyseal tract
21
Q
Hypothalamic axons terminate in the
A
Neurohypophysis
22
Q
ADH
A
Anti-diuretic hormone; vasopressin
23
Q
Major stimuli for ADH secretion
A
Under normal conditions ADH is the primary endocrine factor regulating urinary H2O balance
24
Q
Changes in plasma osmolarity sensed by osmoreceptors in hypothalamus –>
A
Stimulate or inhibit ADH -> target tissue -> fluid volume changes -> changes in osmolarity
25
Increased osmolarity =
stimulation of thirst
26
ADH also excreted via RAAS ->
Vasoconstriction & H2O retention, leading to increased BP
27
Diabetes insipidus
```
Diabetes = overflow
insipidus = tasteless
```
28
Diabetes insipidus
Disorder associated with dysfunction of neurohypophysis or interruption go the pituitary stalk
29
Hyposecretion of ADH leads to
Inability to concentrate urine, leading to increased excretion of dilute urine, dehydration, thirst, hypotension, hypernatremia
30
Normal urine output
1200 - 1500 mL/ 24 hours
31
Polyuria in diabetes insipidus
Output may be as much as 20 liters/day
32
urine specific gravity with diabetes insipidus
Decrease urine specific gravity
33
Normal urine specific gravity
1.005 - 1.030
34
Desmopressin (DDAVP)
Vasopressin analog, synthetic ADH replacement
| - Hormone replacement for Diabetes insipidus
35
Desmopressin administration
PO, IM, IV, IM, intranasal
36
Desmopressin moA
Increase permeability of renal tubular cells to water, leading to increase absorption of water INTO plasma, leading
-Decreased UP and increased uric osmolality
37
Desmopressin nursing considerations
- Monitor UO/ I&O
- Monitor urine specific gravity
- Vital signs
- Serum electrolytes
38
High levels of ADH WITHOUT normal physiologic stimuli for its release leads to
Increased renal water retention leading to dilutional hyponatremia
-- decreased UO
-- increased specific gravity
Possibly water intoxication, edema, hypertension, headache, confusion, nausea, and vomiting
39
Various causes of inappropriate ADH secretion
tumors
post-pituitary surgery
brain trauma
meningitis
40
Treatment of inappropriate ADH secretion
- Treatment of underlying medical conditions
- Diuretics
- Infuse 3% saline cautiously
41
If 3% saline is given too fast, it can cause
Neurologic issues including seizures
42
Thyroid gland
Butterfly shaped gland
| Anterior to trachea
43
Thyroid gland requires ___ for function
Iodine
44
Thyroid gland rich blood supply
80-100 mL/min
45
Thyroid gland is able to deliver
high levels or hormones if necessary
46
Thyroid gland histology
Thyroid follicles
Filled with colloid
Walls of follicles
47
Thyroid gland is filled with
colloid: glycoprotein-iodine complex
48
Walls of follicles:
Follicular cells
| Parafollicular cells produce calcitonin
49
Follicular cells
triiodothyronine (T3)
| thyroxine (T4)
50
Calcitonin
calcium hemostasis, along with actions of parathyroid
51
Key actions of thyroid glands
- Main determinant of basal metabolic rate
- Influences synthesis & degradation of carbohydrate, fat, & protein metabolism (e.g. mobilization of glycogen, gluconeogenesis)
- Increases target-cell responsiveness to catecholamines
- Increases heart rate & force of contraction
- Essential for normal growth (deficiency of thyroid hormones during fetal development, infancy, or childhood causes stunted bone growth & severe mental disability)
- Plays crucial role in normal development of nervous system
52
TSH (thyroid stimulating hormone) is regulated by
Hypothalamic pituitary thyroid feedback system
53
Decreased blood level of thyroid hormones -->
Decreased metabolic rate and body temperature, leading to
- TRH
- TSH
- --> thyroid hormones
54
Hypothyroidism
Deficient production of thyroid hormones
55
Primary hypothyroidism
Problems with thyroid gland
56
Secondary hypothyroidism
problems with pituitary or hypothalamus
57
Deficient thyroid hormone affects
ALL body systems
58
Clinical manifestations of hypothyroidism
```
Decreased BMR (basal metabolic rate)
Increased TSH levels (primary hypothyroidism)
Goiter ***
Lethargy
Fatigue
Cold intolerance
Weight gain
--> Myxedema
---> myxedema coma
```
59
Myxedema
is a characteristic sign of severe or long-standing hypothyroidism
---non-pitting, boggy edema
60
Myxedema coma is due to
Prolonged hypothyroidism
61
Myxedema coma:
```
medical emergency
Decreased LOC
Hypothermia
Hypoventilation
Hypotension
Hypoglycemia
```
62
Levothyroxine
Thyroid hormone replacement; synthetic T4
63
Levothyroxine indications
Hypothyroidism, myxedema, myxedema coma
64
Levothyroxine moA
T4 binds to thyroid receptors in cell nucleus, leading to metabolic effects via DNA transcription & protein synthesis
65
Levothyroxine administration
PO for replacement
| IV for emergencies
66
Signs and symptoms of too much Levothyroxine
S/S of hyperthyroidism
67
Levothyroxine black box warning
Do not use for weight reduction, ineffective & potentially life-threatening
68
Diseases of hyperthyroidism
Thyrotoxicosis
Graves disease
Thyrotoxic crisis (thyroid storm)
69
Thyrotoxicosis
tissues are exposed to high levels of thyroid hormone
70
Causes of thyrotoxicosis
```
Hyperactivity of thyroid gland
Graves disease
Thyroid cancer
Adenoma of thyroid
Multinodular goiter
Ingestion of excessive thyroid hormone
```
71
Clinical manifestations are related to the hypermetabolic state of thyrotoxicosis
Increase...
- oxygen consumption
- use of metabolic fuels
- sympathetic nervous system activity
```
Weight loss
Nervousness/irritability
Palpitations
SOB
Excessive sweating
```
72
Most common cause of hyperthyroidism; thyrotoxicosis
Graves disease
73
Graves disease is autoimmune caused by
Antibodies against the TSH receptor
74
in graves disease, TSI stimulates
TSH receptors but is NOT subject to negative feedback like TSH
75
in graves disease, antibodies stimulate thyroid cells to
Make high levels of thyroid hormone
76
Thyrotoxic crisis (Thyroid storm)
- Extreme, life-threatening form of thyrotoxicosis
- Death may occur within 48 hours without treatment
- Often present to ED as undiagnosed hyperthyoridism, or partially treated Graves disease; precipitated by stress, trauma, infection
77
Clinical manifestions of thyrotoxic crisis
```
Hyperthermia
Tachycardia
Tachydysrhythmias
High-output heart failure
Agitation
Delirium
N/V
Diarrhea
Dehydration
```
78
propylthiouracil drug class
Antithyroid agent
79
propylthiouracil drug class
Antithyroid agent
80
Antithyroid agent indication
Hyperthyroidism
| Thyroid storm
81
propylthiouracil moA
MOA: inhibits synthesis of thyroid hormones by blocking oxidation of iodine in thyroid gland; also prevents conversion of T4 to T3 at target tissues which decreases S/S hyperthyroidism
82
propylthiouracil black box warning
severe liver injury (some fatal) & acute liver injury have been reported
83
Adrenal glands located superior to each kidney
2 regions:
(1) adrenal cortex
(2) adrenal medulla
84
Adrenal cortex: 3 regions that have different cells that secrete different groups of steroid hormones:
(1) zona glomerulosa
(2) zona fasciculata
(3) zona reticularis
85
Adrenal medulla is innervated directly by
the sympathetic division of the ANS
86
Adrenal medulla secretes
epinephrine & norepinephrine
87
Sympathomimetic: fight or flight response
```
vasoconstriction
Increase:
-BP
-HR/force of contraction
-RR, dilate bronchioles
-Blood glucose levels
```
88
Zona glomerulosa:
mineralocorticoids
89
Zona glomerulosa: mineralocorticoids control
water & electrolyte homeostasis; primarily sodium & potassium ions
90
Primary mineralocorticoid
Aldosterone
91
Aldosterone acts on the kidneys causing
Increase reabsorption of Na
- Increase excretion of k
- Increase H2O retention
92
ACTH has
Minimal effect on aldosterone
| primarily secreted in presence of angiotensin II
93
Zona fasciculata:
Glucocorticoids
94
Zona fasciculata: Glucocorticoids
A group of hormones concerned with normal metabolism & response to stress
95
3 glucocorticoids
(1) cortisol (hydrocortisone); most abundant
(2) corticosterone
(3) cortisone
96
CRH ->
ACTH -> Cortisol
97
Functions of glucocorticoids:
- Ensure enough energy is available for metabolic needs (catabolic: mobilization of proteins & fatty acids for glucose production)
- Provide resistance to stress: glucose gives body energy to combat stresses such as fright, temperature extremes, infection, trauma, surgery
- Antiinflammatory function
98
Anti-inflammatory function of glucocorticoids
inhibit cell-mediated & humoral immunity
99
Zona reticularis
gonadocorticoids
100
Zona reticularis: gonadocorticoids hormones
Estrogens & androgens
101
Zona reticularis: gonadocorticoids;
| tumors of the adrenal glands
- virilizing adenomas in women
| - feminizing adenomas in males
102
Adrenal insufficiency Primary:
Addison’s disease
| destruction of the adrenal gland (usually autoimmune)
103
Adrenal insufficiency: Secondary
Pituitary disease
104
Adrenal insufficiency tertiary
hypothalamic dysfunction
105
Secondary adrenal insufficiency is caused by
dysfunction of the hypothalamic-pituitary axis
106
Addison's disease is an example of ____ adrenal insufficiency
Primary
107
In addition's disease, pituitary will continue to secrete
ACTH via negative feedback, BUT NO glucocorticoids are excreted by the adrenals
108
Addisons disease is a chronic metabolic disorder that requires lifelong management:
```
replacement therapy of missing hormones
regular dietary schedule
stress management
avoidance of infection
medical ID bracelet
```
109
Addisons disease clinical manifestations
- Mental lethargy
- Anorexia
- N/V
- Weight loss
- Hypoglycemia
- Decrease BP
- Decrease CO
- Hyperpigmentation (ACTH has intrinsic MSH activity)
- hypoglycemia (decrease gluconeogenesis)
- Mineralcorticoid deficiency: hypotension (SBP < 110), orthostatic hypotension, hyperkalemia, hyponatremia, hypovolemia, salt cravings
- Other: weakness, irritability, emotional lability; ♀: amenorrhea, decrease libido, sparse axillary & pubic hair
110
Adrenal crisis =
“Addisonian Crisis”
111
“Addisonian Crisis” is
Life-threatening
112
“Addisonian Crisis” is caused by
Acute lack of glucocorticoids & mineralcorticoids
113
Precipitating events (for a person with Addision’s disease or a slowly developing, previously recognized adrenal insufficiency):
- Severe infection
- Trauma
- Surgery
- Dehydration
- Profound hypoglycemia
- Shock: hypotension & vascular collapse; shock often unresponsive to vasopressors
- Coma
- Fatal if not recognized & treated promptly (0.9% NS, hydrocortisone, epinephrine, dextrose)
114
Hydrocortisone
Systemic corticosteroid
115
hydrocortisone administration
PO, IM, IV, topical
116
hydrocortisone indication
Adrenal insufficiency
Anti-inflammatory
Immunosuppressive
117
hydrocortisone cautions
- Increase incidence of secondary infections
- GI irritation
- May cause suppression of HPA axis
- may cause increase glucose; - may cause iatragenic Cushing syndrome with high doses; withdraw therapy with gradual tapering of dose
118
Hydrocortisone is used caution with patients with
renal impairment
119
Hydrocortisone can cause
iatragenic Cushing syndrome with high doses; withdraw therapy with gradual tapering of dose
120
Hydrocortisone nursing considerations
Serum glucose
Presence of infection
Gradual tapering of dose
121
Cushing Syndrome
Clinical condition resulting from chronic exposure to excessive circulating levels of glucocorticoids
122
Cushing syndrome causes
(1) excess secretion of ACTH from anterior pituitary
(2) excess secretion of glucocorticoids due to adrenal disease
(3) iatrogenic: chronic administration of glucocorticoids (e.g. hydrocortisone, prednisone)
123
Cushing syndrome; hyper secretion of adrenal glucocorticoids clinical manifestations
```
Truncal obesity
Spindly legs
Moon face
Buffalo hump
Pendulous abdomen
Poor wound healing
Hyperglycemia
Osteoporosis
Hypertension
Mood alterations
- Poor wound healing, thinning of skin, wound dehiscence following surgery
-Easy bruising
-Diabetogenic effect of glucocorticoids
```
124
Cushing syndrome can lead to
- Poor wound healing, thinning of skin, wound dehiscence following surgery (inhibition of fibroblasts & mediators of inflammation; loss of collagen by high steroid levels)
- Easy bruising (inhibition of mediators of clotting)
- Diabetogenic effect of glucocorticoids
125
Hyperthyroidism left untreated or undetected can lead to
Thyorotoxic crisis --> Thyroid storm
126
Graves disease is more common in
Women
127
T3 is known as the
Biologically active thyroid hormone
128
T4 is known as the `
Prohormone that must be converted to T3
129
Zona glomerulosa; aldosterone controls
Water and electrolyte homeostasis; primarily sodium Ions
130
Cortisol levels are influences by
Stress; acute and chronic
| Time of day
131
Alterations in adrenal function
HYPO-cortical Function (Addison Disease)
| HYPER-cortical Function (Cushing Disease, Cushing Syndrome)
132
Treatment options for Cushing syndrome
- Decrease use of corticosteroids
- Surgical removal of pituitary tumor
- Radiation to site of tumor
133
Pharmacotherapeutic options for Cushing syndrome
- Ketoconazole (Nizoral) – to control excessive production of cortisol at the adrenal gland; PO
- Pasireotide (Signifor) – works by decreasing ACTH production from a pituitary tumor; injection, BID
