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N351: Pathophysiology I > Module 13 > Flashcards

Module 13 Flashcards

1
Q

Important Endocrine Glands

A

Pituitary
Adrenal
Thyroid
Parathyroid
Pancreas
Ovaries
Testes

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2
Q

Exocrine

A

secretes hormones into ducts

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3
Q

Endocrine

A

secretes hormones into the blood

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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

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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

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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

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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

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8
Q

The HHP System is a ___ Tiered system of hormone release

A

3

(hypothalamus hormone, ant.pit hormone, far away gland action hormone)

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9
Q

HPT Axis

A

Hypothalamus and Thyroid Gland Axis

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10
Q

HPA Axia

A

Hypothalamus and Adrenal Gland Axis

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11
Q

The Posterior Pituitary Gland releases what hormones?

A

ADH (Antidiuretic Hormone)
Oxytocin

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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)

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13
Q

Adenohypophysis

A

Anterior Pituitary

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14
Q

Neurohypophysis

A

Posterior Pituitary (it is called neuro since hormones go straight down nerve tracks)

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15
Q

What is the “Master Gland”

A

The Pituitary Gland

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16
Q

Where is the pituitary gland ?

A

Base of the brain

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17
Q

What influences the pituitary gland?

A

the hypothalamus

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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

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19
Q

Major anterior pituitary disorders?

A

Acromegaly
Giantism
Dwarfism

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20
Q

Major posterior pituitary disorders?

A

Diabetes insipidus

SIADH (syndrome of inappropriate secretion of antidiuretic hormone)

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21
Q

____ released by the hypothalamus inhibits GH release?

A

Somatostatin

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22
Q

Tropic Hormone

A

hormone that has other endocrine glands as their target

(ex: GHRH)

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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

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24
Q

When does acromegaly occur

A

in middle age after hypophyseal plates/epiphyses of long bones close

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25
Q

S/S of Acromegaly

A

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

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26
Q

Why does hyperglycemia occur in acromegaly?

A

GH is responsible for high blood glc levels, so as it is an accompanying stress hormone - more glc is released in the blood

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27
Q

Why does hypercalcemia occur in acromegaly?

A

It is rare, but does happen in conjunction with hyperparathyroidism and hypothyroidism

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28
Q

What disease did Lou Ferigno have?

A

Acromegaly

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29
Q

What are the 2 types of adenoma that can cause acromegaly?

A
  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
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30
Q

What might a pituitary adenoma causing Acromegaly cause if removed?

A

Increased hormone release (ex: Prolactin release increasing breast size)

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31
Q

How to care/implementation for Acromegaly Patients?

A

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

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32
Q

Hypophysectomy

A

surgical removal of the pituitary gland

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33
Q

What causes Giantism/Gigantism

A

HYPERsecretion of GH by the anterior pituitary gland

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34
Q

When does Giantism/Gigantism occur?

A

Occurs in childhood before the closure of the epiphyses of the long bones

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35
Q

What is the major different between Acromegaly and Giantism?

A

Acromegaly occurs in mid-age, while giantism occurs in childhood (post versus pre plate closure)

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36
Q

S/S of Giantism

A

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)

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37
Q

How to care/implementation for Giantism Patients?

A

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

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38
Q

Potential complications occurring from a Hypophysectomy

A

increased ICP

bleeding

rhinorrhea

meningitis

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39
Q

The first and most reliable sign of a change in ICP …

A

decrease in consciousness

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40
Q

How can you tell if the post-hypophysectomy patient’s drainage is CSF and not nasal?

A
  1. The glucose content is different
  2. CSF dries with a yellow halo
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41
Q

What to do post-operative for a hypophysectomy?

A

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

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42
Q

Why do we give corticosteroids following a hypophysectomy?

A

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

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43
Q

A lot of what is needed following a hypophysectomy?

A

medications

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44
Q

Dwarfism

A

HYPOsecretion of GH by the AntPit

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45
Q

When does dwarfism occur?

A

In childhood

We follow a growth chart, and if they are behind we can administer GH when caught early to help prevent this

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46
Q

Is dwarfism chromosomally based?

A

no its hyposecretion of GH

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47
Q

S/S of Dwarfism

A

Retarded physical growth

Premature aging

Low intellectual development

Dry skin

Poor development of secondary sex characteristics

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48
Q

How to care/implementation for Dwarfism patients?

A

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)

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49
Q

What is/causes Diabetes Insipidus?

A

PostPit issue with HYPOsecretion of antidiuretic hormone (ADH)/a deficiency in vasopressin

It causes a failure in tubular reabsorption of water in the kidneys

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50
Q

Without ADH what will happen?

A

a lot of water will leave as urine

tons of urinary output

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51
Q

S/S of Diabetes Insipidus

A

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

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52
Q

Why does tachycardia occur with diabetes insipidus?

A

its a compensatory mechanism for low blood pressure

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53
Q

Why does fatigue, muscle pain, weakness, headaches, etc occur with diabetes insipidus?

A

excessive urinary output causes electrolyte imbalances

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54
Q

Polydipsia

A

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

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55
Q

How to care/implementation for Diabetes insipidus patients?

A

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

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56
Q

The best measure of fluid balance in the body is…

A

daily weight

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57
Q

What is/causes SIADH?

A

Syndrome of inappropriate secretion of ADH

PostPit disorder with CONTINUTED release of ADH

It leads to water intoxication

HYPER-ADH

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58
Q

What occurs with SIADH?

A

Water stays in the circulatory system and displaces into cells, which can lead to water intoxication and cerebral swelling leading to LOC changes

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59
Q

S/S of SIADH

A

Change in LOC

Mental status changes

weight gain

HYPERTENSION

signs of fluid volume overload

Tachycardia

Anorexia

Nausea and vomiting

HYPONATREMIA

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60
Q

Why does anorexia occur with SIADH

A

because the vessels around the digestive tract fill with fluid and make you not hungry

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61
Q

The cation with the greatest volume in the blood of any electrolyte is .;.

A

sodium (so Hyponatremia is very important to monitor)

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62
Q

SIADH symptoms can look like …

A

heart failure since they have fluid buildup

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63
Q

How to care/implementation for SIADH patient?

A

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

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64
Q

Why do we give SIADH patients 3% saline rather than the normal 0.9%?

A

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

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65
Q

Location of the Adrenal Glands

A

One per kidney, resting on top of each kidney (Add Renal - Adrenal)

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66
Q

Important functions of the Adrenal Gland

A

Regulate sodium and electrolyte balance

Affect carbohydrate, fat, and protein metabolism

Influences development of sexual characteristics

Sustains “fight or flight” response

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67
Q

What hormones do the adrenal glands release?

A

Glucocorticoids
Mineralocorticoids
Sex Hormones (Androgen, Estrogen)
EP and NEP (Catecholamines)

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68
Q

Adrenal Cortex

A

Outer shell of the adrenal gland

Synthesizes: glucocorticoids (cortisol), mineralocorticoids (aldosterone), and secretes small amounts of sex hormones (androgens and estrogens)

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69
Q

Adrenal medulla

A

Inner core of the adrenal gland working as part of the SYMPATHETIC nervous system

Produces NEP and EP

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70
Q

Disorders of the Adrenal Cortex

A

Addison’s disease

Cushing’s syndrome

Aldosteronism (Conn’s Syndrome)

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71
Q

Disorder of the Adrenal Medulla

A

Pheochromocytoma

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72
Q

Without glucocorticoids, you will become …

A

hypoglycemic (since they cause glc release)

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73
Q

Without aldosterone you will become …

A

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)

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74
Q

What is/causes Addison’s Disease

A

HYPOsecretion of adrenal cortex hormones (glucocorticoids and mineralocorticoids)

The hyposecretion can be due from various reasons

If untreated, it is fatal

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75
Q

Example of a Mineralcorticoid

A

aldosterone

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76
Q

Example of a Glucocorticoid

A

Cortisol

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77
Q

JFK had…

A

Addison’s Disease

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78
Q

S/S of Addison’s Disease

A

Hyponatremia
Hyperkalemia
Hypotension
Hypoglycemia

Elevated BUN

Weakness

GI disturbances

emotional disturbances

weight loss

bronze pigmentation to the skin

electrolyte imbalances

sudden death if untreated

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79
Q

Classic symptom of addisons disease is …

A

Bronze pigmentation of skin from stimulation of melanocytes

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80
Q

Elevated BUN in Addisons disease indicates …

A

dehydration

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81
Q

Reasons for Addison’s Disease

A
  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
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82
Q

The typical hormonal pathway for cortisol release is …

A

CRH from Hypothalamus –> ACTH from AntPit –> Cortisol from Adrenal Gland

Cortisol then negatively feedback to pituitary and CRH

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83
Q

Stimulation test

A

ACTH stim test where you give a dose of ACTH and try to determine whether they have primary, secondary, or tertiary insufficiency

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84
Q

ACTH is ___ ___ so you may need to give 2 doses to do the stimulation test

A

slow response

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85
Q

If there is an increase in cortisol following stimulation test of the second dose …

A

it is a SECONDARY problem (not primary, since the adrenal gland could be stimulated by ACTH)

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86
Q

If there is no increase in cortisol following stimulation test of second dose…

A

There is a PRIMARY problem (since adrenal gland is not working)

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87
Q

If there is no reaction to ACTH or Cortisol at all in the stimulation test…

A

it is a tertiary problem with CRH and the hypothalamus

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88
Q

Most commonly, adrenal insufficiency is usually …

A

primary (from adrenal gland issues)

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89
Q

How to care/implementation for Addison’s Disease patients

A

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

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90
Q

What happens to ACTH and CRH levels in primary and secondary adrenal insufficiency?

A

Primary: ACTH and CRH increase due to negative feedback of low cortisol

Secondary: CRH increases due to negative feedback of low cortisol and ACTH

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91
Q

Cortisol plays a vital role in ___, so its very important to consider this with …

A

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)

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92
Q

We often get sick after finals week because …

A

the cortisol levels for stress lower finally, allowing the immune system to resume

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93
Q

Addisonian Crisis

A

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)

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94
Q

What can (S/S) Addisonian Crisis cause?

A

Hyponatremia
Hyperkalemia
Hypoglycemia

Shock

Severe headache

Severe abdominal, leg, and lower back pain

Generalized weakness

Irritability and confusion

Severe hypotension

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95
Q

How to care/implementation for Addisonian crisis?

A

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

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96
Q

What is/causes Cushing’s Syndrome

A

HYPERsecretion of glucocorticoids from adrenal cortex

Opposite of Addison’s Disease

can result from the prolonged administration of corticosteroids (exogenous administration for another disease)

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97
Q

2 Types of Hypercortisolism (Cushing’s Syndrome)

A

ACTH Independent (Iatrogenic Cushings Syndrome)

ACTH Dependent (Cushings Disease Pituitary Adenoma)

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98
Q

Iatrogenic Cushing’s Syndrome (ACTH Independent)

A

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

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99
Q

Cushing’s Disease Pituitary Adenoma (ACTH Dependent)

A

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

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100
Q

Most common cause of Hypercortisolism (Cushings)

A

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

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101
Q

Ectopic ACTH Dependent Hypercortisolism (Cushings)

A

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

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102
Q

S/S Of Cushing’s Syndrome

A

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

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103
Q

How to care/implementation for Cushing’s Syndrome Patients

A

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
Q

Why may Cushing’s Syndrome patients need potassium supplements?

A

Na retention leads to K loss

105
Q

What is/causes Aldosteronism (Conn’s Syndrome)

A

Hypersecretion of aldosterone from the adrenal cortex of the adrenal gland, usually due to an adrenal lesion/tumor that is often benign

106
Q

Why does hypertension and hypokalemia occur in conns syndrome?

A

Hypertension occurs from increased sodium and water retention while Hypokalemia is caused by the increased sodium retention and potassium loss

107
Q

What is the cycle of Primary Aldosteronism?

A

Increased aldosterone –> increase sodium retention –> increased volume leading to high flow states to kidneys –> decreased renin needed –> repeat

108
Q

S/S of Aldosteronism (Conn’s Syndrome)

A

Generalized weakness

Increased thirst, nocturia, and polyuria

Edema

Weight gain

headache

Hypertension

Positive chvosteks sign

increased urinary aldosterone

HYPOKALEMIA

HYPERNATREMIA

Metabolic alkalosis

109
Q

Chvostek Sign

A

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
Q

Trusou Sign

A

Put a BP cuff on and observe for spasms - this is also a sign for hypocalcemia

111
Q

How to care/implementation for a Aldosteronism (Conn’s Syndrome) Patient?

A

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
Q

How does Aldactone help Conn’s Syndrome?

A

It is an antihypertensive that hogs aldosterone receptors so not as much potassium is lost from aldosterone binding and causing sodium retention

113
Q

What is/causes Pheochromocytoma?

A

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
Q

Typically, pheochromocytoma tumors are …

A

benign (< 10% malignant)

115
Q

Primary treatment for Pheochromocytoma is

A

surgical excision of adrenal gland (if not possible symptomatic treatment is initiated though)

116
Q

Pheochromocytoma tumors are usually …

A

unilateral/one-sided meaning only occur on one adrenal gland

117
Q

Pheochromocytoma is a secondary cause of …

A

HTN

118
Q

Important complications associated with pheochromocytoma include…

A

Hypertensive retinopathy

Nephropathy

Myocarditis

CHF

increased platelet aggregation

CVA

119
Q

Death from pheochromocytoma can occur from …

A

shock

CVA

renal failure

dysrhythmias

dissecting aortic aneurysm

120
Q

S/S of Pheochromocytoma

A

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
Q

How to care/implementation for pheochromocytoma?

A

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
Q

Why do we use an alpha adrenergic blocking agent with Pheochromocytoma?

A

The alpha receptors are responsible for EP and NEP binding as well as peripheral vasoconstriction , so by blocking these we can lower BP

123
Q

Adrenalectomy

A

Surgical removal of adrenal gland

the preferred treatment for pheochromocytoma

124
Q

What is needed if a bilateral adrenalectomy is done?

A

Lifelong steroid replacement

125
Q

A unilateral adrenalectomy may require temporary steroid replacement for up to

A

2 years

126
Q

What are some dangerous potential complications related to adrenalectomy?

A

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
Q

What should be done preoperatively for Adrenalectomy?

A

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
Q

What should be done post-operatively for adrenalectomy?

A

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
Q

Why is maintaining IV fluid for BP maintenance so important post-adrenalectomy?

A

Need to maintain circulating volume following the adrenalectomy to keep the brain and heart working

130
Q

Where is the Thyroid Gland

A

anterior part of the neck

131
Q

What does the thyroid control

A

rate of body metabolism and growth

132
Q

What hormones does the thyroid gland produce

A

Thyroxine (T4)

Triiodothyronine (T3)

Thyrocalcitonin

133
Q

Thyrocalcitonin

A

made by c cells of thyroid

Regulates calcium homeostasis

counter-regulatory to parathyroid hormone

134
Q

What percent of iodine in the body goes to the thyroid gland?

A

more than 99% to produce T3 and T4

135
Q

What cells produce T4 and T3 in the thyroid?

A

Follicular cells

136
Q

What are the thyroid hormones?

A

T3 and T4

137
Q

What do the thyroid hormones regulate?

A

Oxygen use and basal metabolic rate

cellular metabolism

growth and develoipment

138
Q

How many atoms of iodine does T3 and T4 contain?

A

3 and 4 respectively (thus the names)

139
Q

What cells produce Thyrocalcitonin to regulate calcium homeostasis in the thyroid?

A

Parafollicular cells (C-cells)

140
Q

What is the pathway (HPT Axis) of thyroid hormone control?

A
  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
Q

Increased ATP Demand from cold environment, hypoglycemia, high altitude or pregnancy leads to

A

increased secretion of thyroid hormones

142
Q

What are primary, secondary, and tertiary level issues for the Thyroid?

A

Primary - Not enough T3/T4 or calcitonin released - Thyroid Problem

Secondary - not enough TSH - AntPit issue

Tertiary - not enough TRH - Hypothalamus issue

143
Q

T3 and T4 have what forms

A

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
Q

Initial Hyperthyroid Clinical Presentation

A

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
Q

Later Hyperthyroid clinical presentation

A

tremor

muscle weakness and fatigue

dyspnea

dependent edema

impaired mentation (confusion)

146
Q

Incidental clinical presentations of hyperthyroidism

A

heat intolerance

diaphoresis

increased appetite

147
Q

Initial Hypothyroid Clinical Presentation

A

Depression and loss of concentration

Dry skin (Pruritis)

cold intolerance (need layers)

Myalgias

somnolence and fatigue

menorrhagia

depressed

148
Q

Later Hypothyroid Clinical Presentation

A

Goiter

unexplained weight gain

constipation

myxedema

memory loss/impairment

149
Q

Incidental clinical presentation of hypothyroidism

A

Bradycardia

habitual abortion/sterility

impotence

anorexia

150
Q

Everything is ____ ___ in hyperthyroidism, while everything is ___ ___ in hypothyroidism

A

ramped up, ramped down

151
Q

Hyperthyroid Goiters occur because of …

A

the thyroid gland

152
Q

Hypothyroid Goiters occur because of …

A

adrenal gland stimulation with TSH and the stimulation is not working when it is a primary problem

153
Q

What are the altered lab findings in primary, secondary, and tertiary Hypothyroidism?

A

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
Q

What are the altered lab findings in primary, secondary, and tertiary Hyperthyroidism?

A

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
Q

What is RAI (Radioactive Iodine Uptake)?

A

A thyroid function test that measures the absorption of the iodine isotope to determine how the thyroid gland is functioning

156
Q

When is the amount of radioactivity measured during an RAI

A

The amount of radioactivity is measured 2, 6, and 24 hours after ingestion of the capsule

157
Q

What is a normal RAI value in 24 hours

A

Normal value is 5% to 35% in 24 hours

158
Q

What things does elevated RAI values indicate

A

hyperthyroidism, thyrotoxicosis, decreased iodine intake, or increased iodine excretion

159
Q

What things does decreased RAI values indicate

A

low T4, the use of anti thyroid medications, thyroiditis, myxedema, or hypothyroidism

160
Q

T3 and T4 Resin Uptake Test

A

Blood tests for the diagnosis of thyroid disorders

161
Q

What regulates TSH

A

T3 and T4 levels (negative feedback)

162
Q

What are normal T3 levels

A

25 to 35%

163
Q

What are normal T4 levels

A

3.8 to 11.4%

164
Q

When might Resin Uptake show elevated T3 levels?

A

if there is Hyperthyroidism or T3 toxicosis

165
Q

When might Resin Uptake show decreased T3 levels

A

it decreases with age

can decrease in hypothyroidism

166
Q

When might resin uptake show elevated T4 levels?

A

hyperthyroidism

167
Q

When might resin uptake show decreased T4 levels

A

hypothyroidism

168
Q

The most important thing to view to diagnose a thyroid problem is …

A

TSH (Thyroid Stimulating Hormone) levels in the blood

169
Q

What occurs more, hypo or hyper thyroidism?

A

hypothyroidism

170
Q

normal TSH level

A

0 to 6 microU/mL

171
Q

Elevated TSH levels indicate

A

primary hypothyroidism

172
Q

Decreased TSH levels indicate

A

hyperthyroidism or secondary hypothyroidism

173
Q

Thyroid Scan

A

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
Q

What should be done before a thyroid scan?

A

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
Q

A thyroid scan is often done alongside a …

A

RAI

176
Q

What are the routes iodine and technetium is given for the thyroid scan?

A

Iodine - oral

Technetium - IV route

177
Q

What occurs with needle aspiration of thyroid tissue?

A

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

178
Q

Disorders of Hypothyroidism

A

Cretinism
Myxedema

179
Q

Disorders of Hyperthyroidism

A

Graves’ Disease
Thyrotoxicosis

180
Q

Risk Factors for Thyroid Disorders

A

Hereditary

Congenital

Trauma

Environmental

Secondary to Other Disorders

181
Q

Typical Clinical Picture of Hypothyroidism

A

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
Q

What is the most common cause of Hypothyroidism

A

Primary/Autoimmune - Hashimoto’s Thyroiditis - Autoimmune issue on thyroid

183
Q

What is the 2nd most common cause of Hypothyroidism

A

Primary/treatment related: radioactive iodine Tx or surgery for hyperthyroidism

184
Q

What are all the primary causes of hypothyroidism

A

Hashimoto’s Thyroiditis - Autoimmune
Treatment Related
Iodine Deficiency
Rare Inherited Enzyme Deficiencies

185
Q

What is Endemic Cretinism and Goiter as it relates to Iodine deficiency leading to hypothyroidism

A

it is the most common cause of congenital hypothyroidism in deficient areas worldwide

186
Q

What is the major cause of mental deficiency worldwide?

A

Iodine deficiency

187
Q

What is a secondary cause of hypothyroidism?

A

Failure of the HP axis d/t deficient TRH or TSH secretion

188
Q

What is the difference between primary and secondary hypothyroidism?

A

Primary - thyroid cannot produce amount of hormones the pituitary calls for

Secondary - the thyroid isnt being stimulated by pituitary to produce hormones

189
Q

What is/causes Cretinism

A

a severe thyroid HYPOfunction that results in hyposecretion of thyroid hormones in the fetus or soon after birth

190
Q

S/S of Cretinism

A

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
Q

Cretinism is seen more in which gender?

A

Female

192
Q

How do we care/implementation for Cretinism patients

A

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
Q

When administering hormones for Cretinism, we want to give…

A

T4, not too much T3, since T4 converts to T3 to work

194
Q

Myxedema

A

Hypothyroid state resulting from hyposecretion of thyroid hormone

condition OCCURS IN ADULTHOOD

195
Q

When does Cretinism occur versus Myxedema?

A

Cretinism = Childhood/Birth

Myxedema = Adulthood

Its like Giantism and Acromegaly in that sense

196
Q

What does the term myxedema mean in greek

A

mucus and swelling

197
Q

S/S of Myxedema

A

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

198
Q

How to care for/implementation for Myxedema patients

A

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
Q

Since hypothyroidism/myxedema means someone has a slower body metabolism, you should not ..

A

give them meds that slow things down further like narcotics and sedatives

200
Q

Myxedema Coma

A

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
Q

S/S of Myxedema Coma

A

Hypotension
Hypothermia
Hyponatremia
Hypoglycemia

Bradycardia

Mental Depression

Mood Swings

Coma

202
Q

How to care for/implementation for Myxedema Coma

A

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
Q

When treating someone with hypothyroidism, it is important not to overdose them into ___

A

hyperthyroidism

204
Q

What things can cause hyperthyroidism

A

A tumor or adenoma of the thyroid gland itself

Secondary (ant pit) issues

Factitious (drug related) issues

Graves Disease

205
Q

If the goiter appears initially, then what does that indicate

A

Hyperthyroidism

206
Q

Typical Clinical presentation of hyperthyroidism?

A

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
Q

Graves’ Disease

A

hyperthyroid state resulting from hypersecretion of thyroid hormone

Also known as “thyrotoxicosis”

Autoimmune in nature - makes the thyroid produce too much hormone

208
Q

What antibody is causing the autoimmune issues from Graves’ Disease

A

Thyrotropin Receptor Antibody imitates TSH overriding negative feedback of the HPT axis and thus causing consistent overproduction of thyroid hormone

209
Q

Graves’ Disease is on the ___ level

A

primary (thyroid) level

210
Q

S/S of Graves’ Disease

A

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
Q

Exopthalmos

A

out of socket look to eyeballs

212
Q

Proptosis

A

forward displacement and entrapment of eye from behind the eyelid

213
Q

What can untreated exophthalmos and proptosis lead to

A

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
Q

How to care for/implementation for Graves’ Disease Patients

A

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
Q

Unlike with hypothyroidism, in hyperthyroidism you should administer…

A

sedatives and narcotics

216
Q

What is the danger of performing a thyroidectomy on a hyperthyroid patient, and thus is why we use antithyroid drugs first?

A

we need parathyroid for calcitonin and also it is highly vascularized in the area and bleeding can occur

217
Q

How can a thyroidectomy lead to calcium issues?

A

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
Q

Thyroid Storm

A

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
Q

S/S of Thyroid Storm

A

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
Q

How to care for/implementation for thyroid storm?

A

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
Q

Why is it important to keep the body cool in thyroid storm?

A

we want to prevent shivering which can create heat

222
Q

Why do we avoid giving aspirin to thyroid storm patients?

A

they can increase free thyroid hormone levels further (by displacing T3 and T4 from protein carriers)

223
Q

Why is iodine preparation important for hyperthyroidism treatment

A

it works against thyroid function and inhibits thyroid hormone release

224
Q

How is propranolol important for thyroid storm patients

A

it is a beta blocker that decreases HR and BP and reverses thyroid storm

(cardiac medicines decrease heart activity and protect the heart )

225
Q

Thyroidectomy

A

removal of the thyroid gland

226
Q

When is thyroidectomy done

A

performed in conditions where persistent hyperthyroidism exists

typically when cancerous, or if the tumor or goiter must be removes

227
Q

Important Preoperative implementation for Thyroidectomy

A

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
Q

Important Postoperative implementation for Thyroidectomy

A

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
Q

Anti thyroid drugs ___ the size of the gland

A

decrease

230
Q

Iodine ___ the vascularity of the thyroid gland

A

decreases

231
Q

the only way to permanently get rid of hyperthyroidism is to …

A

have a thyroidectomy

232
Q

Tetany

A

Hypocalcemia

involuntary spasms of muscles due to low calcium

233
Q

What is the number 1 priority to watch for during thyroidectomy recovery?

A

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
Q

What are some signs of Tetany following a Thyroidectomy?

A

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
Q

A positive Chvostek and Trousseau sign indicates

A

hypocalcemia

236
Q

Where is the parathyroid gland

A

located near/embedded in the thyroid

237
Q

What does the parathyroid gland produce

A

PTH (parathyroid hormone)

*this controls calcium use and removal, phosphorus, and Vit D

238
Q

What is the purpose of the parathyroid gland

A

control calcium and phosphorus metabolism

It pulls calcium from bones as calcium phosphate (thats how it controls both)

239
Q

Disorders of the parathyroid gland

A

Hypoparathyroidism

Hyperparathyroidism

240
Q

Hypoparathyroidism

A

a condition caused by hyposecretion of parathyroid hormone by the parathyroid gland

not enough calcium and high phosphorus

241
Q

When does Hypoparathyroidism occur

A

following thyroidectomy from removal of parathyroid tissue

242
Q

S/S of Hypoparathyroidism

A

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
Q

How to care for/implementation for Hypoparathyroidism

A

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
Q

What can lower phosphorus levels

A

Aluminum Hydroxide

245
Q

What can protect the heart and aid in low calcium levels with hypoparathyroidism

A

Calcium gluconate

246
Q

Hyperparathyroidism

A

condition caused by hypersecretion of parathyroid hormone by the parathyroid gland

247
Q

S/S of Hyperparathyroidism

A

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
Q

How to care for/implementation for Hyperparathyroidism

A

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
Q

With hyperparathyroidism there is too much __ and too little ___

A

calcium; phosphorus

250
Q

In hyperparathyroidism, everything ..

A

SLOWS DOWN - Rather than have everything be irritable and active

251
Q

What is a precipitous drop

A

a drop in calcium levels going from lethargic (hyperparathyroidism) to spastic (hypoparathyroidism)

252
Q

Parathyroidectomy

A

removal or one or more of the parathyroid glands

253
Q

Preoperative Implementation for Parathyroidectomy

A

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
Q

Postoperative Implementation for Parathyroidectomy

A

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
Q

Following a parathyroidectomy, the patient must start taking what?

A

Calcium and Vitamin D supplements

256
Q

Would a secondary level problem cause primary problems?

A

no it means the problem comes from the secondary level but the primary level may still be working normally

N351: Pathophysiology I (11 decks)

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