Module 13 Flashcards
1
Q
Important Endocrine Glands
A
Pituitary Adrenal Thyroid Parathyroid Pancreas Ovaries Testes
2
Q
Exocrine
A
secretes hormones into ducts
3
Q
Endocrine
A
secretes hormones into the blood
4
Q
What sort of gland is the Pancreas?
A
both exo and endocrine
It releases glucose and insulin into the blood, and pancreatic enzymes and bicarb through the pancreatic duct
5
Q
Main Functions of Hormones and the Endocrine System
A
Maintenance and Regulation of Vital Functions
Responses to stress and injury
Growth and development
Energy metabolism
Reproduction
Fluid, electrolyte, and acid base balance
6
Q
What is the Hypothalamic-Hypophysial Portal Systme?
A
Hypophysial = Relating to Pituitary
Portal System = Means of transporting from one place to another
Hypothalamus regulates the anterior pituitary to release hormones to a gland far away
7
Q
What occurs if there is not enough of some hormone in a far away gland?
A
the hypothalamus will release hormones down the nerve track to the anterior pituitary. Specific hormones at the ant.pit. will react to the tropic hormone signalling and release to a gland far away
8
Q
The HHP System is a ___ Tiered system of hormone release
A
3
hypothalamus hormone, ant.pit hormone, far away gland action hormone
9
Q
HPT Axis
A
Hypothalamus and Thyroid Gland Axis
10
Q
HPA Axia
A
Hypothalamus and Adrenal Gland Axis
11
Q
The Posterior Pituitary Gland releases what hormones?
A
ADH (Antidiuretic Hormone)
Oxytocin
12
Q
The Anterior Pituitary Gland releases what hormones?
A
Prolactin (LTH)
Growth Hormone (GH)
Luteinizing Hormone (LH)
Follicle Stimulating Hormone (FSH)
Adrenocorticotropic Hormone (ACTH)
Thyroid Stimulating Hormone (ZTSH)
13
Q
Adenohypophysis
A
Anterior Pituitary
14
Q
Neurohypophysis
A
Posterior Pituitary (it is called neuro since hormones go straight down nerve tracks)
15
Q
What is the “Master Gland”
A
The Pituitary Gland
16
Q
Where is the pituitary gland ?
A
Base of the brain
17
Q
What influences the pituitary gland?
A
the hypothalamus
18
Q
What does the pituitary gland do?
A
It releases hormones
Directly affects function of other endocrine glands
promotes growth of body tissues
influences water absorption by the kidney
controls sexual development and function
19
Q
Major anterior pituitary disorders?
A
Acromegaly
Giantism
Dwarfism
20
Q
Major posterior pituitary disorders?
A
Diabetes insipidus
SIADH (syndrome of inappropriate secretion of antidiuretic hormone)
21
Q
____ released by the hypothalamus inhibits GH release?
A
Somatostatin
22
Q
Tropic Hormone
A
hormone that has other endocrine glands as their target
ex: GHRH
23
Q
What causes Acromegaly
A
The HYPERsecretion of GH by the ant.pit
An ant.pit. adenoma (non cancerous) could direct GH with somatostatin being unable to counter regulate it
24
Q
When does acromegaly occur
A
in middle age after hypophyseal plates/epiphyses of long bones close
25
S/S of Acromegaly
HYPERGLYCEMIA
HYPERCALCEMIA (rare)
Headaches, Diplopia, Lethargy, Blindness, Goiters
Large Hands and Feet
Visual Problems
Deepened Voice
Thickening and Protrusion of the Jaw
Increased hair growth
Joint pain
Diaphoresis
Oily, rough skin
Menstrual Disturbances
Impotence
Potential blindness
Difficulty chewing
Gait changes
Damage to internal organs and joints
Enlarged but weak skeletal muscles
Females feel male
26
Why does hyperglycemia occur in acromegaly?
GH is responsible for high blood glc levels, so as it is an accompanying stress hormone - more glc is released in the blood
27
Why does hypercalcemia occur in acromegaly?
It is rare, but does happen in conjunction with hyperparathyroidism and hypothyroidism
28
What disease did Lou Ferigno have?
Acromegaly
29
What are the 2 types of adenoma that can cause acromegaly?
1. A toothpaste like adenoma on the pituitary that is easy to scrape off but difficult to get it all
2. A ropey one that can easily have all of it removed, but could take other tissues with it that it should not
30
What might a pituitary adenoma causing Acromegaly cause if removed?
Increased hormone release (ex: Prolactin release increasing breast size)
31
How to care/implementation for Acromegaly Patients?
Provide emotional support
Encourage client to express feelings related to altered body image
Provide frequent skin care
Provide pharmacological and nonpharmacological interventions for joint pain
Prepare client for radiation of pituitary gland is prescribed
Prepare client for hypophysectomy if planned
32
Hypophysectomy
surgical removal of the pituitary gland
33
What causes Giantism/Gigantism
HYPERsecretion of GH by the anterior pituitary gland
34
When does Giantism/Gigantism occur?
Occurs in childhood before the closure of the epiphyses of the long bones
35
What is the major different between Acromegaly and Giantism?
Acromegaly occurs in mid-age, while giantism occurs in childhood (post versus pre plate closure)
36
S/S of Giantism
Children with:
Overgrowth of long bones
Increased height in early adulthood
Deterioration of mental and physical status (GH has a negative effect on brain, muscle, and bone development so the children are huge but not necessarily smarter or stronger)
37
How to care/implementation for Giantism Patients?
Provide emotional support to client and family
Encourage client and family to express feelings related to altered body image
Prepare client for radiation of pituitary gland, if prescribed
Prepare client for hypophysectomy, if planned
38
Potential complications occurring from a Hypophysectomy
increased ICP
bleeding
rhinorrhea
meningitis
39
The first and most reliable sign of a change in ICP ...
decrease in consciousness
40
How can you tell if the post-hypophysectomy patient's drainage is CSF and not nasal?
1. The glucose content is different
| 2. CSF dries with a yellow halo
41
What to do post-operative for a hypophysectomy?
Initiate post-op care similar to craniotomy care
Monitor Vitals
Assess LOC and neurologic status
Monitor for increased ICP, bleeding, and adrenal insufficiency
Elevate HOB
Administer corticosteroids as prescribed on time
Monitor fluids and electrolyte values
Monitor for temporary diabetes insipidus due to ADH disturbances
Avoid water intoxication
Instruct client to AVOID sneezing, coughing, and blowing nose
Instruct client in administration of prescribed medications
42
Why do we give corticosteroids following a hypophysectomy?
ACTH is no longer there since Ant.Pit is gone which means cortisol (stress hormone) cannot release - and since surgery is a stressor we must administer this
43
A lot of what is needed following a hypophysectomy?
medications
44
Dwarfism
HYPOsecretion of GH by the AntPit
45
When does dwarfism occur?
In childhood
We follow a growth chart, and if they are behind we can administer GH when caught early to help prevent this
46
Is dwarfism chromosomally based?
no its hyposecretion of GH
47
S/S of Dwarfism
Retarded physical growth
Premature aging
Low intellectual development
Dry skin
Poor development of secondary sex characteristics
48
How to care/implementation for Dwarfism patients?
Provide emotional support to client and family
Encourage client and family to express feelings related to altered body image
Prepare to administer hGH (human growth hormone)
49
What is/causes Diabetes Insipidus?
PostPit issue with HYPOsecretion of antidiuretic hormone (ADH)/a deficiency in vasopressin
It causes a failure in tubular reabsorption of water in the kidneys
50
Without ADH what will happen?
a lot of water will leave as urine
tons of urinary output
51
S/S of Diabetes Insipidus
Polyuria (4-24L per day)
Polydipsia
Dehydration
Decreased skin turgor, dry mucus membranes
Inability to concentrate urine
A low urinary specific gravity of 1.006 or less (dilute urine close to water)
Fatigue
Muscle pain and weakness
Headache
Postural hypotension
Tachycardia
52
Why does tachycardia occur with diabetes insipidus?
its a compensatory mechanism for low blood pressure
53
Why does fatigue, muscle pain, weakness, headaches, etc occur with diabetes insipidus?
excessive urinary output causes electrolyte imbalances
54
Polydipsia
abnormally great thirst as part of a disease
ex: dehydration from diabetes insipidus leads to more urination and triggering thirst mechanisms causing this in patients
55
How to care/implementation for Diabetes insipidus patients?
Monitor vitals, neurological and cardiovasc status
Monitor electrolyte values
Administer vasopressin (Pitressin) or DDAVP (desmopressin) as prescribed
Monitor I and O, weight, specific gravity of urine
Instruct client to avoid foods or liquids with a diuretic type action
Maintain intake of adequate amounts of fluids
instruct client in administration of medications as prescribed
Instruct client to wear Medic-Alert bracelet
56
The best measure of fluid balance in the body is...
daily weight
57
What is/causes SIADH?
Syndrome of inappropriate secretion of ADH
PostPit disorder with CONTINUTED release of ADH
It leads to water intoxication
HYPER-ADH
58
What occurs with SIADH?
Water stays in the circulatory system and displaces into cells, which can lead to water intoxication and cerebral swelling leading to LOC changes
59
S/S of SIADH
Change in LOC
Mental status changes
weight gain
HYPERTENSION
signs of fluid volume overload
Tachycardia
Anorexia
Nausea and vomiting
HYPONATREMIA
60
Why does anorexia occur with SIADH
because the vessels around the digestive tract fill with fluid and make you not hungry
61
The cation with the greatest volume in the blood of any electrolyte is .;.
sodium (so Hyponatremia is very important to monitor)
62
SIADH symptoms can look like ...
heart failure since they have fluid buildup
63
How to care/implementation for SIADH patient?
FLUID RESTRICTION ORDERS!!!
Monitor vitals, neuro status, cardiac status
Protect client from injury
Monitor I and O
Obtain daily weights
Restrict water intake as prescribed
Monitor fluid and electrolyte balance
Administer diuretics and Iv fluids as prescribed
64
Why do we give SIADH patients 3% saline rather than the normal 0.9%?
This is considerably higher to get raw fluid back into the vascular system, and then we also give a diuretic after to eliminate fluid in urine to decrease change of fluid overload affecting the heart
65
Location of the Adrenal Glands
One per kidney, resting on top of each kidney (Add Renal - Adrenal)
66
Important functions of the Adrenal Gland
Regulate sodium and electrolyte balance
Affect carbohydrate, fat, and protein metabolism
Influences development of sexual characteristics
Sustains "fight or flight" response
67
What hormones do the adrenal glands release?
Glucocorticoids
Mineralocorticoids
Sex Hormones (Androgen, Estrogen)
EP and NEP (Catecholamines)
68
Adrenal Cortex
Outer shell of the adrenal gland
Synthesizes: glucocorticoids (cortisol), mineralocorticoids (aldosterone), and secretes small amounts of sex hormones (androgens and estrogens)
69
Adrenal medulla
Inner core of the adrenal gland working as part of the SYMPATHETIC nervous system
Produces NEP and EP
70
Disorders of the Adrenal Cortex
Addison's disease
Cushing's syndrome
Aldosteronism (Conn's Syndrome)
71
Disorder of the Adrenal Medulla
Pheochromocytoma
72
Without glucocorticoids, you will become ...
hypoglycemic (since they cause glc release)
73
Without aldosterone you will become ...
Hyponatremic, Hypovolemic, Hyperkalemic
(this holds sodium and water follows, so without you lose sodium and accompanying fluid, but also now hold onto potassium leaving dangerous hyperkalemia for the gut and heart)
74
What is/causes Addison's Disease
HYPOsecretion of adrenal cortex hormones (glucocorticoids and mineralocorticoids)
The hyposecretion can be due from various reasons
If untreated, it is fatal
75
Example of a Mineralcorticoid
aldosterone
76
Example of a Glucocorticoid
Cortisol
77
JFK had...
Addison's Disease
78
S/S of Addison's Disease
Hyponatremia
Hyperkalemia
Hypotension
Hypoglycemia
Elevated BUN
Weakness
GI disturbances
emotional disturbances
weight loss
bronze pigmentation to the skin
electrolyte imbalances
sudden death if untreated
79
Classic symptom of addisons disease is ...
Bronze pigmentation of skin from stimulation of melanocytes
80
Elevated BUN in Addisons disease indicates ...
dehydration
81
Reasons for Addison's Disease
1. Auto Immune Addisons - body attacks itself
2. TB Addison's - Tuberculosis in adrenal glands leads to hyposecretion
3. Iron overload Addisons - too much iron buildup/overload leads to malfunction
82
The typical hormonal pathway for cortisol release is ...
CRH from Hypothalamus --> ACTH from AntPit --> Cortisol from Adrenal Gland
Cortisol then negatively feedback to pituitary and CRH
83
Stimulation test
ACTH stim test where you give a dose of ACTH and try to determine whether they have primary, secondary, or tertiary insufficiency
84
ACTH is ___ ___ so you may need to give 2 doses to do the stimulation test
slow response
85
If there is an increase in cortisol following stimulation test of the second dose ...
it is a SECONDARY problem (not primary, since the adrenal gland could be stimulated by ACTH)
86
If there is no increase in cortisol following stimulation test of second dose...
There is a PRIMARY problem (since adrenal gland is not working)
87
If there is no reaction to ACTH or Cortisol at all in the stimulation test...
it is a tertiary problem with CRH and the hypothalamus
88
Most commonly, adrenal insufficiency is usually ...
primary (from adrenal gland issues)
89
How to care/implementation for Addison's Disease patients
Monitor vitals, weight, I&O, infection
Maintain fluid and electrolyte balance
Instruct client in high protein/high carb diet, to avoid stress, avoid individuals with infection, the need for lifelong corticosteroids, in over the counter med use, to avoid strenuous exercise, to wear a medic alert bracelet
Observe for Addisonian crisis secondary to stress, infection, trauma, and surgery
90
What happens to ACTH and CRH levels in primary and secondary adrenal insufficiency?
Primary: ACTH and CRH increase due to negative feedback of low cortisol
Secondary: CRH increases due to negative feedback of low cortisol and ACTH
91
Cortisol plays a vital role in ___, so its very important to consider this with ...
infection; Addison Disease patients who cannot make cortisol
(it depresses the immune system and prevents release of substances that cause inflammation during acute stress - when the stressor is resolved the immune system can resume)
92
We often get sick after finals week because ...
the cortisol levels for stress lower finally, allowing the immune system to resume
93
Addisonian Crisis
A life threatening disorder caused by acute adrenal insufficiency
It is precipitated by infection, trauma, stress or surgery on an person with Addison's Disease (anything that increases stress hormones)
94
What can (S/S) Addisonian Crisis cause?
Hyponatremia
Hyperkalemia
Hypoglycemia
Shock
Severe headache
Severe abdominal, leg, and lower back pain
Generalized weakness
Irritability and confusion
Severe hypotension
95
How to care/implementation for Addisonian crisis?
Monitor vitals
Monitor neurological status, noting irritability and confusion
Monitor I&O
Administer IV fluids as prescribed to restore electrolyte balance
Administer adrenocorticosteroids as prescribed on time schedule
Protect client from infection
Maintain bedrest and provide a quiet environment
96
What is/causes Cushing's Syndrome
HYPERsecretion of glucocorticoids from adrenal cortex
Opposite of Addison's Disease
can result from the prolonged administration of corticosteroids (exogenous administration for another disease)
97
2 Types of Hypercortisolism (Cushing's Syndrome)
ACTH Independent (Iatrogenic Cushings Syndrome)
ACTH Dependent (Cushings Disease Pituitary Adenoma)
98
Iatrogenic Cushing's Syndrome (ACTH Independent)
Independent since cortisol release/gain is separate from ACTH release
Can either be from exogenous steroid use feedback to stop the pituitary, OR a tumor that directs high cortisol levels which feedback
ACTH and Hypothalamus will release less
99
Cushing's Disease Pituitary Adenoma (ACTH Dependent)
Dependent since cortisol release/gain is dependent now on amount of ACTH
Can either be a tumor of the pituitary causing excessive ACTH which leads to cortisol release in the adrenal gland, or ectopic ACTH dependence from a lung tumor producing an ACTH like substance leading to cortisol release
100
Most common cause of Hypercortisolism (Cushings)
Dependent Pituitary Adenoma that leads to a lot of ACTH and thus a lot of cortisol
Secondary to this, a tumor can form on the adrenal gland leading to massive cortisol and aldosterone release leading to water and sodium retention indicative of bloating in Cushings disease
101
Ectopic ACTH Dependent Hypercortisolism (Cushings)
ACTH like substance comes from Lung tumor leading to cortisol release
ectopic since its coming from somewhere else but still cortisol is dependent on ACTH
102
S/S Of Cushing's Syndrome
Hypertension
Hypokalemia
Hyperglycemia
Glycosuria
Obesity with thin extremities
Moon face
buffalo hump
fragile skin that easily bruises
Hirsutism
mood swings
muscular weakness
signs of infection or osteoporosis
elevated WBC
sodium and water retention
fast gain and redistribution of fat leading to striation
Cortisol causing some osteoporosis and preventing bone formation
Suicidal tendencies from body image issues
103
How to care/implementation for Cushing's Syndrome Patients
Monitor I&O, weight, glc levels, and urinary glucose
Provide good skin care
Allow client to discuss feelings related to body appearance
Provide high protein, low calorie diet, with potassium supplements
Prepare client for adrenalectomy if prescribed
Prepare client for radiation if prescribed
Administer hormone replacement therapy as prescribed
Administer steroids as prescribed if adrenalectomy was performed
Administer chemotherapeutic agents as prescribed
Instruct client in med administration as prescribed, to avoid infection and stress, and in measure of adequate nutrition and rest
104
Why may Cushing's Syndrome patients need potassium supplements?
Na retention leads to K loss
105
What is/causes Aldosteronism (Conn's Syndrome)
Hypersecretion of aldosterone from the adrenal cortex of the adrenal gland, usually due to an adrenal lesion/tumor that is often benign
106
Why does hypertension and hypokalemia occur in conns syndrome?
Hypertension occurs from increased sodium and water retention while Hypokalemia is caused by the increased sodium retention and potassium loss
107
What is the cycle of Primary Aldosteronism?
Increased aldosterone --> increase sodium retention --> increased volume leading to high flow states to kidneys --> decreased renin needed --> repeat
108
S/S of Aldosteronism (Conn's Syndrome)
Generalized weakness
Increased thirst, nocturia, and polyuria
Edema
Weight gain
headache
Hypertension
Positive chvosteks sign
increased urinary aldosterone
HYPOKALEMIA
HYPERNATREMIA
Metabolic alkalosis
109
Chvostek Sign
when tapping the cheek it should twitch
If it is positive (no twitch) then that is a sign of hypocalcemia due to compensation for metabolic alkalsosi
110
Trusou Sign
Put a BP cuff on and observe for spasms - this is also a sign for hypocalcemia
111
How to care/implementation for a Aldosteronism (Conn's Syndrome) Patient?
Monitor vitals, weight, I&O
Assess muscular strength
Monitor for positive chvosteks sign, electrolytes, MAINTAIN SODIUM RESTRICTION AS PRESCRIBED
ADMINITER POTASSIUM SUPPLEMENTS AS PRESCRIBED
administer antihypertensive, such as aldactone as prescribed
Prep client for surgical removal of tumor if prescribed
112
How does Aldactone help Conn's Syndrome?
It is an antihypertensive that hogs aldosterone receptors so not as much potassium is lost from aldosterone binding and causing sodium retention
113
What is/causes Pheochromocytoma?
A catecholamine producing tumor is located in the adrenal gland (or potentially abdomen) causing HYPERSECRETION of hormones of the adrenal medulla and the secretion of excessive amounts of EP and NEP
114
Typically, pheochromocytoma tumors are ...
benign (< 10% malignant)
115
Primary treatment for Pheochromocytoma is
surgical excision of adrenal gland (if not possible symptomatic treatment is initiated though)
116
Pheochromocytoma tumors are usually ...
unilateral/one-sided meaning only occur on one adrenal gland
117
Pheochromocytoma is a secondary cause of ...
HTN
118
Important complications associated with pheochromocytoma include...
Hypertensive retinopathy
Nephropathy
Myocarditis
CHF
increased platelet aggregation
CVA
119
Death from pheochromocytoma can occur from ...
shock
CVA
renal failure
dysrhythmias
dissecting aortic aneurysm
120
S/S of Pheochromocytoma
NEP and EP keeps you in constant stress/anxiety state:
HTN and headaches
Hypermetabolism
Diaphoresis
Palpitation and Tachycardia
Apprehension
Emotional instability
Hyperglycemia and glycosuria
Pain in the chest or abdomen with nausea and vomiting
weight loss
fatigue and exhaustion
121
How to care/implementation for pheochromocytoma?
Monitor vitals, cardio, neuro, and renal status
Monitor for hypertensive attacks (HTN can precipitate a CVA or sudden blindness)
Keep phentolamine (Regitine) at bedside for hypertensive crisis
Prep to administer an alpha adrenergic blocking agent like Dibenzyline as prescribed to control BP
Be alert to stimuli that can precipitate paroxysm, like increased abdominal pressure, micturition, and vigorous abdominal palpation
Avoid opiates preoperatively as they can precipitate a hypertensive crisis
Monitor urine for glc and acetone
promote rest and non stressful environment
Provide a diet high in calories, vitamins, and minerals
Prohibit caffeine containing beverages and food
122
Why do we use an alpha adrenergic blocking agent with Pheochromocytoma?
The alpha receptors are responsible for EP and NEP binding as well as peripheral vasoconstriction , so by blocking these we can lower BP
123
Adrenalectomy
Surgical removal of adrenal gland
the preferred treatment for pheochromocytoma
124
What is needed if a bilateral adrenalectomy is done?
Lifelong steroid replacement
125
A unilateral adrenalectomy may require temporary steroid replacement for up to
2 years
126
What are some dangerous potential complications related to adrenalectomy?
Catecholamine levels drop as a result, so cardiovascular collapse, hypotension, and shock could occur
Hemorrhage can also occur due to high vascularity of adrenal glands
127
What should be done preoperatively for Adrenalectomy?
Prepare client for procedure
Monitor electrolytes and correct electrolyte imbalances
Assess for dysrhythmias
Monitor for hyperglycemia
Protect client from infections
Administer steroids as prescribed
(potassium is needed to prevent arrhythmia from hypokalemia, and removal drops cortisol levels which is usually protective for the stressors of surgery)
128
What should be done post-operatively for adrenalectomy?
Monitor Vitals, daily weights, electrolytes, for signs of shock and hemorrhage (particularly in first 24-48 hours)
Monito I&O, if less than 30 mL per hour notify physician as it could indicate impending shock and renal failure
Assess dressings
Monitor for paralytic ileus
Monitor kidneys due to close proximity
Administer IV fluids as prescribed to maintain blood volume
Administer pain meds as prescribed while remembering Demerol can cause hypotension
Administer steroid replacement as prescribed
instruct client in the importance of steroid therapy following surgery
129
Why is maintaining IV fluid for BP maintenance so important post-adrenalectomy?
Need to maintain circulating volume following the adrenalectomy to keep the brain and heart working
130
Where is the Thyroid Gland
anterior part of the neck
131
What does the thyroid control
rate of body metabolism and growth
132
What hormones does the thyroid gland produce
Thyroxine (T4)
Triiodothyronine (T3)
Thyrocalcitonin
133
Thyrocalcitonin
made by c cells of thyroid
Regulates calcium homeostasis
counter-regulatory to parathyroid hormone
134
What percent of iodine in the body goes to the thyroid gland?
more than 99% to produce T3 and T4
135
What cells produce T4 and T3 in the thyroid?
Follicular cells
136
What are the thyroid hormones?
T3 and T4
137
What do the thyroid hormones regulate?
Oxygen use and basal metabolic rate
cellular metabolism
growth and develoipment
138
How many atoms of iodine does T3 and T4 contain?
3 and 4 respectively (thus the names)
139
What cells produce Thyrocalcitonin to regulate calcium homeostasis in the thyroid?
Parafollicular cells (C-cells)
140
What is the pathway (HPT Axis) of thyroid hormone control?
1. Low T3 and T4 or low metabolic rate stimulate hypothalamus to release TRH (thyrotropin releasing hormone)
2. TRH enters hypophyseal portal veins to AntPit which releases TSH (thyroid stimulating hormone)
3. TSH stimulates thyroid follicular cells in almost all aspects (iodine trapping, hormone synthesis and secretion, growth of F-cells)
4. Follicular cells release T3 and T4 into blood until metabolic rate returns to normal
5. Elevated T3 inhibits release of TRH and TSH negatively
141
Increased ATP Demand from cold environment, hypoglycemia, high altitude or pregnancy leads to
increased secretion of thyroid hormones
142
What are primary, secondary, and tertiary level issues for the Thyroid?
Primary - Not enough T3/T4 or calcitonin released - Thyroid Problem
Secondary - not enough TSH - AntPit issue
Tertiary - not enough TRH - Hypothalamus issue
143
T3 and T4 have what forms
bound and unbound
Almost all T4 is bound (metabolically inactive)
Can unbind when needed and we can check levels of bound and unbound of T3 and T4
144
Initial Hyperthyroid Clinical Presentation
GOITER (initial here)
nervousness/irritability
palpitations (tachycardia)
unexplained weight loss
diarrhea
sleep disturbances (insomnia)
vision changes (exopthalmos)
amenorrhea/oligomenorrhia
so hot they wear t shirts in winter
145
Later Hyperthyroid clinical presentation
tremor
muscle weakness and fatigue
dyspnea
dependent edema
impaired mentation (confusion)
146
Incidental clinical presentations of hyperthyroidism
heat intolerance
diaphoresis
increased appetite
147
Initial Hypothyroid Clinical Presentation
Depression and loss of concentration
Dry skin (Pruritis)
cold intolerance (need layers)
Myalgias
somnolence and fatigue
menorrhagia
depressed
148
Later Hypothyroid Clinical Presentation
Goiter
unexplained weight gain
constipation
myxedema
memory loss/impairment
149
Incidental clinical presentation of hypothyroidism
Bradycardia
habitual abortion/sterility
impotence
anorexia
150
Everything is ____ ___ in hyperthyroidism, while everything is ___ ___ in hypothyroidism
ramped up, ramped down
151
Hyperthyroid Goiters occur because of ...
the thyroid gland
152
Hypothyroid Goiters occur because of ...
adrenal gland stimulation with TSH and the stimulation is not working when it is a primary problem
153
What are the altered lab findings in primary, secondary, and tertiary Hypothyroidism?
Primary (Thyroid): TRH and TSH increase, T3/4 Decrease
Secondary (Pituitary): TRH increase, TSH and T3/4 decrease
Tertiary (Hypothalamus): TRH, TSH, and T3/4 decrease
154
What are the altered lab findings in primary, secondary, and tertiary Hyperthyroidism?
Primary (thyroid): TRH and TSH decrease, T3/4 increase
Secondary (pituitary): TRH decrease, TSH and T3/4 increase
tertiary (hypothalamus): TRH, TSH, and T3/4 increase
155
What is RAI (Radioactive Iodine Uptake)?
A thyroid function test that measures the absorption of the iodine isotope to determine how the thyroid gland is functioning
156
When is the amount of radioactivity measured during an RAI
The amount of radioactivity is measured 2, 6, and 24 hours after ingestion of the capsule
157
What is a normal RAI value in 24 hours
Normal value is 5% to 35% in 24 hours
158
What things does elevated RAI values indicate
hyperthyroidism, thyrotoxicosis, decreased iodine intake, or increased iodine excretion
159
What things does decreased RAI values indicate
low T4, the use of anti thyroid medications, thyroiditis, myxedema, or hypothyroidism
160
T3 and T4 Resin Uptake Test
Blood tests for the diagnosis of thyroid disorders
161
What regulates TSH
T3 and T4 levels (negative feedback)
162
What are normal T3 levels
25 to 35%
163
What are normal T4 levels
3.8 to 11.4%
164
When might Resin Uptake show elevated T3 levels?
if there is Hyperthyroidism or T3 toxicosis
165
When might Resin Uptake show decreased T3 levels
it decreases with age
can decrease in hypothyroidism
166
When might resin uptake show elevated T4 levels?
hyperthyroidism
167
When might resin uptake show decreased T4 levels
hypothyroidism
168
The most important thing to view to diagnose a thyroid problem is ...
TSH (Thyroid Stimulating Hormone) levels in the blood
169
What occurs more, hypo or hyper thyroidism?
hypothyroidism
170
normal TSH level
0 to 6 microU/mL
171
Elevated TSH levels indicate
primary hypothyroidism
172
Decreased TSH levels indicate
hyperthyroidism or secondary hypothyroidism
173
Thyroid Scan
Test performed to ID nodules or growths in thyroid gland
Radioisotope of iodine or technetium is given prior to scan
uses ultrasounds to differentiate cystic and solid lesions
174
What should be done before a thyroid scan?
give radioisotope
check for allergies
reassure client level of radioactive meds is not dangerous to self or others
determine whether client has received radiographic contrast agents in the past 3 months as they can invalidate the scan
check with physician for discont iodine containing meds 14 days prior to test and discont thyroid meds 4-6 weeks before test
instruct client to NPO after midnight on day prior
if iodine is used, client must fast for addt 45 min after oral isotope ingestion and scan is done in 24 hours
if technetium is used, it is given via IV 30 minutes prior to scan
175
A thyroid scan is often done alongside a ...
RAI
176
What are the routes iodine and technetium is given for the thyroid scan?
Iodine - oral
Technetium - IV route
177
What occurs with needle aspiration of thyroid tissue?
Pre-op: No special prep, but do not swallow during
Aspiration occurs of thyroid tissue for cytological examination
Post op: light pressure is applied to the aspiration site after the procedure
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Disorders of Hypothyroidism
Cretinism
| Myxedema
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Disorders of Hyperthyroidism
Graves' Disease
| Thyrotoxicosis
180
Risk Factors for Thyroid Disorders
Hereditary
Congenital
Trauma
Environmental
Secondary to Other Disorders
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Typical Clinical Picture of Hypothyroidism
```
Hair Thinning
Depression
"Schizophrenia"
Irritability
Big Tongue
Croaky Voice
Dry Skin
Cold Skin
Cold Intolerance
Slowing of mind and body
Weak Heartbeat
Constipation
myxedema
Slow Reflexes
High LDL
```
182
What is the most common cause of Hypothyroidism
Primary/Autoimmune - Hashimoto's Thyroiditis - Autoimmune issue on thyroid
183
What is the 2nd most common cause of Hypothyroidism
Primary/treatment related: radioactive iodine Tx or surgery for hyperthyroidism
184
What are all the primary causes of hypothyroidism
Hashimoto's Thyroiditis - Autoimmune
Treatment Related
Iodine Deficiency
Rare Inherited Enzyme Deficiencies
185
What is Endemic Cretinism and Goiter as it relates to Iodine deficiency leading to hypothyroidism
it is the most common cause of congenital hypothyroidism in deficient areas worldwide
186
What is the major cause of mental deficiency worldwide?
Iodine deficiency
187
What is a secondary cause of hypothyroidism?
Failure of the HP axis d/t deficient TRH or TSH secretion
188
What is the difference between primary and secondary hypothyroidism?
Primary - thyroid cannot produce amount of hormones the pituitary calls for
Secondary - the thyroid isnt being stimulated by pituitary to produce hormones
189
What is/causes Cretinism
a severe thyroid HYPOfunction that results in hyposecretion of thyroid hormones in the fetus or soon after birth
190
S/S of Cretinism
Pot belly with umbilical hernia
Sensitivity to cold
Newborn Jaundice (cannot breakdown bilirubin since they lack hormones)
-Typical hypothyroidism issues:
Severe physical and mental retardation
dry skin
coarse dry brittle hair
slow teething
large tongue
poor appetite
constipation
191
Cretinism is seen more in which gender?
Female
192
How do we care/implementation for Cretinism patients
Provide emotional support
provide warmth and skin care
prevent injury
prevent constipation
encourage parents to discuss feelings regarding disorder
Administer hormone replacement of desiccated thyroid, thyroxine (synthroid), or triiodothyronine (cytomel) as prescribed
Instruct parents regarding med administration
193
When administering hormones for Cretinism, we want to give...
T4, not too much T3, since T4 converts to T3 to work
194
Myxedema
Hypothyroid state resulting from hyposecretion of thyroid hormone
condition OCCURS IN ADULTHOOD
195
When does Cretinism occur versus Myxedema?
Cretinism = Childhood/Birth
Myxedema = Adulthood
Its like Giantism and Acromegaly in that sense
196
What does the term myxedema mean in greek
mucus and swelling
197
S/S of Myxedema
Slowed rate of body metabolism
Lethargy and fatigue
Intolerance to cold
Weight gain
Dry skin and hair; loss of body hair
Bradycardia
Constipation
Generalized puffiness and nonpitting
edema
Forgetfulness and loss of memory
Menstrual disturbances
Cardiac disorders
mucopolysaccharide deposits in the fingers
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How to care for/implementation for Myxedema patients
monitor vitals and for cardiac complications
Administer & monitor thyroid replacement of desiccated thyroid, thyroxine (Synthroid) or triiodothyronine (Cytomel) as prescribed
Instruct client in low-calorie, low-cholesterol, low-saturated fat diet
Assess client for anorexia & fecal impaction
Provide roughage & fluids to prevent constipation
Provide a warm environment for the client
Avoid sedatives & narcotics due to intolerance
Monitor for overdose of thyroid
medications, characterized by tachycardia, restlessness, nervousness, & insomnia
199
Since hypothyroidism/myxedema means someone has a slower body metabolism, you should not ..
give them meds that slow things down further like narcotics and sedatives
200
Myxedema Coma
rare but serious disorder from persistent low thyroid production
can be precipitated by acute illness, rapid withdrawal of thyroid meds, anesthesia and surgery, hypothermia, and sedative/narcotic use
201
S/S of Myxedema Coma
Hypotension
Hypothermia
Hyponatremia
Hypoglycemia
Bradycardia
Mental Depression
Mood Swings
Coma
202
How to care for/implementation for Myxedema Coma
Maintain a patent airway
Monitor vital signs and LOC
Assess client’s temperature frequently
Assess blood pressure
Administer IV fluids as prescribed
Monitor electrolytes and glucose level
Administer IV glucose as prescribed
Keep client warm
Monitor for changes in mental status
Administer levothyroxine sodium IV as prescribed
Administer corticosteroids as prescribed
Avoid the use of sedatives and hypnotics
203
When treating someone with hypothyroidism, it is important not to overdose them into ___
hyperthyroidism
204
What things can cause hyperthyroidism
A tumor or adenoma of the thyroid gland itself
Secondary (ant pit) issues
Factitious (drug related) issues
Graves Disease
205
If the goiter appears initially, then what does that indicate
Hyperthyroidism
206
Typical Clinical presentation of hyperthyroidism?
Lid Lag
Neurotic Anxiety
Strong Rapid pulse
Very Active and Anxious
Brisk Reflexes
Low LDL
Diarrhea
Depression, Dementia
Osteoporosis
Atrial Fibrillation
Wide pulse pressure
207
Graves' Disease
hyperthyroid state resulting from hypersecretion of thyroid hormone
Also known as "thyrotoxicosis"
Autoimmune in nature - makes the thyroid produce too much hormone
208
What antibody is causing the autoimmune issues from Graves' Disease
Thyrotropin Receptor Antibody imitates TSH overriding negative feedback of the HPT axis and thus causing consistent overproduction of thyroid hormone
209
Graves' Disease is on the ___ level
primary (thyroid) level
210
S/S of Graves' Disease
Increased rate of body metabolism
Enlarged thyroid gland (goiter)
Cardiac dysrhythmias, such as tachycardia and palpitations
Protruding eyeballs (exophthalmos)
Hypertension
Heat intolerance
Diaphoresis
Weight loss
Smooth, soft skin and hair
Nervousness and fine tremors of hands
Personality changes
Irritability & agitation
Mood swings
211
Exopthalmos
out of socket look to eyeballs
212
Proptosis
forward displacement and entrapment of eye from behind the eyelid
213
What can untreated exophthalmos and proptosis lead to
lid failure to close while sleeping
corneal dryness
conjunctivitis in area above cornea from friction when blinking
can influence optic nerve and artery leading to blindness
214
How to care for/implementation for Graves' Disease Patients
Provide adequate rest
Administer sedatives as prescribed
Provide cool and quiet environment
Obtain daily weights
Provide a high-calorie diet
Avoid stimulants
Provide psychosocial support
Administer antithyroid medications, methimazole (Tapazole), or propylthiouracil, which blocks thyroid synthesis, as prescribed
Administer iodine preparations, Lugol's solution, saturated solution of potassium iodide (SSKI), which inhibits the release of thyroid hormone, as prescribed
Administer propranolol (Inderal) for tachycardia as prescribed
Prepare the client for radioiodine therapy as prescribed to destroy thyroid cells
Prepare client for thyroidectomy if prescribed
215
Unlike with hypothyroidism, in hyperthyroidism you should administer...
sedatives and narcotics
216
What is the danger of performing a thyroidectomy on a hyperthyroid patient, and thus is why we use antithyroid drugs first?
we need parathyroid for calcitonin and also it is highly vascularized in the area and bleeding can occur
217
How can a thyroidectomy lead to calcium issues?
it can accidentally remove the parathyroid gland leading to calcium issues and irritability in muscles --> laryngeal spasms can lead to impaired breathing as a result since the parathyroid is responsible for thyrocalcitonin
218
Thyroid Storm
an acute and fatal thyroid condition occurring from manipulation of the thyroid gland in surgery and the release of thyroid hormone into the bloodstream
can also occur from severe infection, stress, trauma, surgery, and too much exogenous hormone
"Turbo hyperthyroidism"
High mortality rate
219
S/S of Thyroid Storm
```
Fever
Diaphoresis
Dehydration
Tachycardia
Congestive heart failure and pulmonary edema
Nausea, vomiting, and diarrhea
Systolic hypertension
Tremors
Irritability, agitation, and restlessness
Delirium and coma
```
220
How to care for/implementation for thyroid storm?
Monitor vital signs
Decrease temperature, avoiding the use of salicylates as they increase free thyroid hormone levels
Avoid palpating thyroid gland
Monitor I&O
Monitor fluid and electrolyte balance
Monitor for dehydration and overhydration
Monitor pulmonary and cardiac status
Administer iodine preparations, Lugol's solution, or saturated solution of potassium iodide (SSKI), which inhibits the release of thyroid hormone, as prescribed
Administer propranolol (Inderal) for tachycardia and to reverse toxic manifestations of thyroid storm as prescribed
Administer glucocorticoids as prescribed to allay stress effects
Administer cardiac medications as prescribed to decrease heart activity
221
Why is it important to keep the body cool in thyroid storm?
we want to prevent shivering which can create heat
222
Why do we avoid giving aspirin to thyroid storm patients?
they can increase free thyroid hormone levels further (by displacing T3 and T4 from protein carriers)
223
Why is iodine preparation important for hyperthyroidism treatment
it works against thyroid function and inhibits thyroid hormone release
224
How is propranolol important for thyroid storm patients
it is a beta blocker that decreases HR and BP and reverses thyroid storm
(cardiac medicines decrease heart activity and protect the heart )
225
Thyroidectomy
removal of the thyroid gland
226
When is thyroidectomy done
performed in conditions where persistent hyperthyroidism exists
typically when cancerous, or if the tumor or goiter must be removes
227
Important Preoperative implementation for Thyroidectomy
Obtain vital signs
Obtain weight
Assess electrolyte levels
Assess for hyperglycemia and glycosuria
Assess level of consciousness
Assess for signs of thyroid storm
Administer antithyroid medications as prescribed to deplete iodine and hormones
Administer iodine as prescribed to decrease vascularity of the thyroid gland
228
Important Postoperative implementation for Thyroidectomy
Monitor for respiratory distress
Have tracheotomy set, oxygen, and suction at the bedside
Maintain semi-Fowler's position
Monitor for signs of bleeding
Check dressing anteriorly and at the back of the neck
Limit talking and assess level of hoarseness
Monitor for laryngeal nerve damage, as evidenced by respiratory obstruction, dysphonia, high-pitched voice, stridor, dysphagia, and restlessness
Monitor for signs of tetany, which can be due to trauma to the parathyroid gland
Prepare to administer calcium gluconate as prescribed for tetany
Look for signs of tetany
229
Anti thyroid drugs ___ the size of the gland
decrease
230
Iodine ___ the vascularity of the thyroid gland
decreases
231
the only way to permanently get rid of hyperthyroidism is to ...
have a thyroidectomy
232
Tetany
Hypocalcemia
involuntary spasms of muscles due to low calcium
233
What is the number 1 priority to watch for during thyroidectomy recovery?
the airway, since hypocalcemia potential exists to cause laryngospasms that could lead to tracheotomy, oxygen, and suction needed
They may also need calcium gluconate administration in emergencies
234
What are some signs of Tetany following a Thyroidectomy?
Positive Chvosteks and Trousseau Signs
Numbness of extremities and spasm of glottis
irritability
wheezing and dyspnea
visual disturbances
muscle and abdominal cramps
(KEEP AN EYE OUT FOR THESE)
235
A positive Chvostek and Trousseau sign indicates
hypocalcemia
236
Where is the parathyroid gland
located near/embedded in the thyroid
237
What does the parathyroid gland produce
PTH (parathyroid hormone)
*this controls calcium use and removal, phosphorus, and Vit D
238
What is the purpose of the parathyroid gland
control calcium and phosphorus metabolism
It pulls calcium from bones as calcium phosphate (thats how it controls both)
239
Disorders of the parathyroid gland
Hypoparathyroidism
Hyperparathyroidism
240
Hypoparathyroidism
a condition caused by hyposecretion of parathyroid hormone by the parathyroid gland
not enough calcium and high phosphorus
241
When does Hypoparathyroidism occur
following thyroidectomy from removal of parathyroid tissue
242
S/S of Hypoparathyroidism
Hypocalcemia and elevated phosphorus levels
Numbness and tingling of extremities
Cramping
Signs of tetany, such as muscular spasms, irritability, seizures, positive Trousseau’s sign, positive Chvostek’s sign, laryngospasm, and cardiac dysrhythmias
Signs of hypocalcemia, such as weakness and tingling of the extremities, painful muscle spasms, dysrhythmias, irritability, and anxiety
Increased neuromuscular irritability
Confusion
Visual problems
Depression
243
How to care for/implementation for Hypoparathyroidism
Monitor vital signs
Monitor cardiac status
Monitor for tetany and spasms
Initiate seizure precautions
Place a tracheotomy set, oxygen, and suctioning at the bedside
Provide a high-calcium, low-phosphorus diet
Provide quiet environment with no stimulus
Administer aluminum hydroxide as prescribed to decrease phosphate levels
Administer parathyroid hormone as prescribed
Prepare to administer IV calcium gluconate for hypocalcemia
Instruct client in the administration of calcium carbonate (OsCal) and vitamin D (Calciferol) as prescribed
244
What can lower phosphorus levels
Aluminum Hydroxide
245
What can protect the heart and aid in low calcium levels with hypoparathyroidism
Calcium gluconate
246
Hyperparathyroidism
condition caused by hypersecretion of parathyroid hormone by the parathyroid gland
247
S/S of Hyperparathyroidism
Bone deformities
Fractures
Calcium deposits in organs
Gastric ulcers
Nausea, vomiting, anorexia, constipation
Personality changes
Polydipsia and polyuria (chalkiness of blood makes you drink more and pee more --> higher urine osmolarity --> even more fluid in urine)
Elevated calcium and low phosphorus levels
248
How to care for/implementation for Hyperparathyroidism
Monitor cardiac function
Monitor renal status
Monitor I&O
Provide hydration
Monitor fluid and electrolyte balance
Monitor calcium and phosphorus levels
Administer furosemide (Lasix) as prescribed to lower calcium levels
Administer IV saline as prescribed to
lower calcium levels
Notify physician immediately if a precipitous drop in the calcium level occurs
Assess client for tingling and numbness in the muscles, which is caused by a sudden drop in calcium levels
Administer phosphates as prescribed, which interfere with calcium absorption
Administer calcitonin (Calcimar) as prescribed to decrease skeletal calcium release and increase renal clearance of calcium
Administer cytotoxic antibiotics as prescribed to lower calcium levels, and monitor client closely for
thrombocytopenia and renal and hepatic toxicity
Prepare client for parathyroidectomy as prescribed
Give lasix to lower calcium levels
give saline to water down blood and dilute calcium to get more circulating volume to rid of it
249
With hyperparathyroidism there is too much __ and too little ___
calcium; phosphorus
250
In hyperparathyroidism, everything ..
SLOWS DOWN - Rather than have everything be irritable and active
251
What is a precipitous drop
a drop in calcium levels going from lethargic (hyperparathyroidism) to spastic (hypoparathyroidism)
252
Parathyroidectomy
removal or one or more of the parathyroid glands
253
Preoperative Implementation for Parathyroidectomy
Monitor electrolytes, calcium, phosphate, and magnesium levels
Ensure calcium levels are decreased to near- normal (must be near normal to do this)
Inform client that talking may be painful for the first day or two postoperative
*monitoring the same stuff you did for the thyroidectomy
254
Postoperative Implementation for Parathyroidectomy
Monitor for respiratory distress!!! / Airway changes
Place a tracheotomy set, oxygen, and suctioning at the bedside
Monitor vital signs
Position client in semi-Fowler’s
Assess neck dressing for bleeding, 1 to 5 mL of serosanguineous drainage is expected
Monitor for hypocalcemic crisis, as evidenced by tingling and twitching in the extremities and face
Assess for positive Trousseau's and Chvostek’s sign, which signals the potential of tetany
Monitor for laryngeal nerve damage
Monitor for changes in voice pattern and hoarseness
Instruct client in the administration of calcium and vitamin D as prescribed
255
Following a parathyroidectomy, the patient must start taking what?
Calcium and Vitamin D supplements
256
Would a secondary level problem cause primary problems?
no it means the problem comes from the secondary level but the primary level may still be working normally
