Download Endocrine Lecture

Critical Care Nursing
A Holistic Approach
Part 9
Anatomy and Physiology of the
Endocrine System
Chapter 42
Chapter 42 overview………..
• This Chapter will include information that will briefly
touch upon each gland in the Endocrine system.
• Within each gland mentioned, hormones are secreted
within that gland and will be described.
• IMP.. See table 42-1..pp 956-957. A great summary
chart….
Copyright © 2005 Lippincott Williams & Wilkins. Instructor's Resource CD-ROM to Accompany Critical Care Nursing: A Holistic Approach, eighth edition.
Purpose of Endocrine system
• A system consisting of glands throughout the body that secrete
specialized endocrine cells within each gland.
• The secretion of these specialized cells are HORMONES.
• IMP.. Hormones are either stimulatory or inhibitory!!!!!
• Each of the glands produces, synthesizes and secretes these
specialized endocrine cells called hormones into the
bloodstream to exert biochemical effects on distant sites/organs
in the body.
• Functions of HORMONES:
– help with cell growth and development.
– Electrolyte balance i.e. reabsorb NA & CA eliminate K.
– Metabolism of fats, carbs. and proteins.
– Flight or fright response = Hormones to produce
sympathetic nervous response.
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Examples: Overview
• Pituitary Gland, Anterior & Posterior: Very imp. gland
produces most of vital hormones.
• GH=growth of bones, muscles and soft tissue (anterior).
• ADH = effects the kidneys and the reabsorption of
H20.(Posterior)
• FSH & LH= reproductive function (anterior)
• Adrenal Gland, Medulla & Cortex: Adrenal medulla stores,
releases Epinephrine, Norepinephrine & Dopamine AKA
Catecholamines=emergency sympathetic nervous system
response. Adrenal Cortex stores, releases Mineralocorticoids
(Aldosterone) & Glucocorticoids (Cortisol).
• Thyroid Gland TSH, T3 and T4 = metabolic rate
• Pancreas, The Islets of Langerhauns produces insulin =
helps control glucose, glucagon=breaks down glucose
• Testes -testosterone
• Ovaries -estrogen & progesterone
• Review, table 42-1, pp. 956-957
Copyright © 2005 Lippincott Williams & Wilkins. Instructor's Resource CD-ROM to Accompany Critical Care Nursing: A Holistic Approach, eighth edition.
Copyright © 2005 Lippincott Williams & Wilkins. Instructor's Resource CD-ROM to Accompany Critical Care Nursing: A Holistic Approach, eighth edition.
Breakdown… A more in-depth look.. We
will be covering 1-4….
• 1- Hypothalamus & Pituitary Glands
– Anterior
• 4 main hormones
– Posterior
• ADH
• 2- Thyroid/Parathyroid Glands
• 3- “The Endocrine” Pancreas
• 4- Adrenal Gland………
– Medulla
– Cortex
Copyright © 2005 Lippincott Williams & Wilkins. Instructor's Resource CD-ROM to Accompany Critical Care Nursing: A Holistic Approach, eighth edition.
1-Importance of Hypothalamus & Pituitary
Glands.
• “The Gate Keepers”, the “Master Glands" work as a “UNIT”
• These 2 glands work together to have a multi system effect from the
hormones produced, secreted and circulated from the the
anterior/posterior pituitary & Hypothalamus glands.
•
Anterior Pituitary gland controls hormones that effect
–
1-Thyroid gland
–
2-Adrenal gland (will analyze Hypothalamic/ Ant. Pituitary
effect on adrenal cortex in a later slide)
–
3-Gonads
–
4- Overall Growth Hormone
• See next slide for further breakdown of numbers 1-4….
• The 2 glands together have an “Axis System” AKA “Feedback Loop”
that maintains homeostasis. How??? When one hormone is low the
release of that hormone is increased.
• Conversely, when circulating level of a hormone is high the release of
the hormone is inhibited until a lower level is reached.
Copyright © 2005 Lippincott Williams & Wilkins. Instructor's Resource CD-ROM to Accompany Critical Care Nursing: A Holistic Approach, eighth edition.
1-Importance of Hypothalamus &
Pituitary Glands (cont.)
• Feedback system works with CNS. These sensors live in the
hypothalamus.
• The following hormones from Anterior Pituitary gland and
Hypothalamus have effect on the big picture.
• Meaning the hormones stated below begin in the Pituitary then further
stimulate hormonal biochemical RXN in specific organs.
• Glands and Hormones effected. All made in anterior Pituitary
–
TSH = Metabolic function. Stimulates Thyroid gland.
–
**ACTH(Adrenocorticotropic) stimulates Adrenal cortex gland.
To then stimulate release of glucocorticoid which is cortisol.
–
FSH and LH = stimulates testes & ovaries to release testosterone
and estrogen & progesterone.
–
Growth Hormone= stimulates overall growth of bones, muscles
& organs.
• See next slide for visual of the “Feedback mechanism”, figure 42-2. pp.
958.
Copyright © 2005 Lippincott Williams & Wilkins. Instructor's Resource CD-ROM to Accompany Critical Care Nursing: A Holistic Approach, eighth edition.
Copyright © 2005 Lippincott Williams & Wilkins. Instructor's Resource CD-ROM to Accompany Critical Care Nursing: A Holistic Approach, eighth edition.
1-Hypothalamus and Pituitary Gland cont….
• Anterior pituitary (as previously stated)
– Growth hormone
– Thyroid-stimulating hormone (TSH) =Thyroid
– ACTH(Adrenocorticotropic) =Adrenal Cortex, glucocorticoid
(cortisol)
• Elevation in ACTH can be caused by Cushing's
Syndrome
• Not enough is called Addisons can be life threatening
– FSH & LH = Testes and Ovaries
• Posterior pituitary
– Antidiuretic hormone (ADH) see next slide
– Oxytocin
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Antidiuretic hormone (ADH) From
Posterior Pituitary AKA Vasporessin,
PP.960
• A hormone that decreases the production of urine by
increasing the reabsorption of H20 in the distal renal
tubules.
• ADH is released in response to decrease blood volume,
hypovolemia, body’s effort to hold on to H20.
• 3 Major Stimuli for the regulation of ADH Secretion.
– 1- Plasma Osmolality (increases initially to secrete
more ADH to hold onto more fluid)
– 2-Changes in ECF volume (increases)
– 3-Changes in arterial BP (increases)
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2-Thyroid/Parathyroid Glands
• Thyroid Gland
– T3
andT4 (thyroxine)_
responsible for generalized
metabolic rate, growth and development
• Parathyroid Gland
– Parathyroid hormone: Main function is to maintain
the body's CA levels for proper nerve and muscular
activity
Copyright © 2005 Lippincott Williams & Wilkins. Instructor's Resource CD-ROM to Accompany Critical Care Nursing: A Holistic Approach, eighth edition.
More on ADH to help understand. Review
on your own. Basic definition!!!
• ADH is a hormone stored in the posterior
pituitary gland in the brain. It is the primary
regulator of water in the body. ADH acts on
the kidneys to increase total body water. This
initially increases the plasma concentration
(Osmolality), increasing blood volume and
increasing blood pressure..
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3- Endocrine Pancreas
• Pancreas=Secretes insulin, digestive enzymes and glucagon.
Islets of Langerhauns in pancreas make insulin.
• 4 Hormones Produced in Pancreas (Islets of
Langerhauns)
• 1-Insulin
– Secreted in response to increased glucose in bloodstream.
Insulin helps transport glucose to tissue for energy.
– IDDM- decreased production of insulin
– NIDDM-Adequate production of insulin. Problem is too
much adipose tissue. Not enough insulin to cover lg.
amounts of glucose in system. Ie obesity.
– Lowers BS
• 2-Glucagon
– Stimulates the conversion glycogen to glucose in the liver.
– Major function is to elevate blood glucose levels by tapping
into protein reserves. Hence, less of a hypoglycemic RXN
between meals.
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3-Pancreas….cont
• 3-Somatostatin (stimulated by hyperglyc.)
• 4-Pancreatic polypeptide (stimulated by
hypoglyc.)
– (Review 3 and 4 on your own).
• Nice review on diagram 42-3, pp. 964
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4- Adrenal Gland……… 2 parts
1=medulla (inner) and 2=cortex (outer)
• Medullary hormones
– Dopamine
– Norepinephrine
– Epinephrine
– Catecholimine’s = all of the above released
– Sympathetic nervous response. All is elevated!!!
• Cortical hormones AKA Corticosteroids 2 types
–
1- Glucocorticoids= cortisol
• Major anti-inflammatory
• Effects glucose, protein and fat metabolism
• *** When administering a Glucocorticoids/Cortisol AKA
a steroid it increases serum glucose!!!!
• Why?? Stimulates glucagon, hence the breakdown of
glycose so more plasma glucose
– 2-Mineralocorticoids=aldosterone
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Cont. Adrenal Gland
• 2-Minereralocorticoids
•
=aldosterone
• The RENIN-ANGIOTENSIN
SYSTEM is primary
mechanism for regulating
aldosterone.
• Review: in response to Renal
ischemia, hypotension.
•
Stimulation of RENINANGIOTENSIN SYSTEM
–
Causes vasoconstriction
–
Produces aldosterone
• Know Aldostrone pp 970
• Aldosterone holds onto NA &
H20
• See next slide
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Tip: on aldosterone.
Important slide!!!
• The Renin-Angiotensin System is the primary mechanism
for regulating & secreting aldosterone.
• Renin is the initiator. Not ACTH.
• The process of the Renin-Angiotensin system consists of
many different sequential steps that lead to the
mechanism of regulating & secreting aldosterone.
• This process very complex and involves multiple
interactions between beta cells, the juxtaglomerular
apparatus & prostaglandins.
– All 3 stimulate Renin………..
– Key is that the whole system, Renin-Angiotensin
System, in its entirety, is the primary regulator of
aldosterone.
– PP. 969 and 971 and Renal Lecture
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Patient Assessment:
Endocrine System
Chapter 43
Assessment of Endocrine System,
Chapter 43
• The material of this chapter will be presented in the
following fashion:
– 5 endocrine gland’s with the applicable important
serum tests and diagnostic test for that specific
gland.
– I.e.- Thyroid Gland
• Serum studies
• Diagnostic studies
• Other applicable important physical characteristics
• Will address Hyper/hypothyroidism, Grave’s, Cushing's
Diseases etc in greater detail in Chapter 44.
– This chapter assessment & diagnostics only.
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5 Glands outlined covered in this chapter
• Again Assessment and labs in this chapter
• 1-The Hypothalamus & Pituitary Gland
• 2-The Thyroid Gland
• 3-The Parathyroid Gland
• 4-The Pancreas
• 5-The Adrenal Gland
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1-Hypothalamus/Pituitary Gland
(posterior) pp. 973
• Lab studies
– Serum antidiuretic hormone (ADH)
– Urine specific gravity
– Serum osmolality
• Diagnostic imaging
– CT
– MRI
• ??Tumors, aneurysm, traumatic brain injury
• Important to assess hydration status and related fluid
and electrolyte imbalances
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2-Thyroid Gland
pp. 976
• Thyroid hormones are regulated by
Hypothlalmus and Pituitary gland (anterior) .
• Lab studies
– Thyroid-stimulating hormones can lead to Pituitary Tumors
– Total thyroxine (T4)
– Free thyroxine and free thyroxine index
– Free triiodothyronine
(T3)
• Diagnostic imaging
– ***Thyroid scan and radioactive iodine uptake to DSG all
thyroid abnormalities, pp. 979
– Ultrasound
– Review diagram table 43-3 pp 977. Nice breakdown
• Disorder-Graves Disease (Hyperthyroid)
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Physical assessment of Graves Disease
• Graves Disease: Overactive/ increased thyroid production
causes the following physical characteristics.
– Enlarged palpable thyroid
– Exophthalmos
• See next slide
– Know S & S of Graves Disease pp 977 & 978
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3-Parathyroid Gland pp. 981
• Maintains Calcium & Phosphorus. The 4 parathyroid glands are
located behind the thyroid
• Lab studies
–
Serum calcium levels
• Ionized calcium
–
Parathyroid hormone level
• Diagnostic studies
– Plain films
– Bone scan
– MRI
• Low PTH is associated hypoparathyroidism and low
calcium. Hence muscular abnormalities i.e. Tetany
– Trousseau’s sign- carpopedal spasm
– Chvosteks sign- face twitched when touched
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4- Pancreas
• Disorders of Pancreas are characterized by chronic
hyperglycemia.
• Lab studies
– Glycosylated hemoglobin aka A1C
• Indicates how much sugar has been in a person's blood
during the past two to four months. It is used to
monitor the effectiveness of diabetes treatment.
– Fasting blood glucose level
– Glucagon
• conversion glycogen to glucose in the liver.
– Serum ketones & urine ketones
• Ketones are substances that are produced when fat
cells break down in lieu of increased cardbohydrate’s.
Ketones are acidic.
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5- Adrenal Gland pp. 984
• Again, 2 parts, outer=Cortex and inner = Medulla
• Like Thyroid, regulated by Hypothalamus & Pituitary (anterior)
• ACTH(Adrenocorticotropic) stimulates Adrenal cortex gland (see previous
slide)
• Recap:
–
Cortex/Outer-Mineralcorticoids which is aldosterone &
Glucocorticoids which is cortisol.
–
Medulla/Inner- Catecholimines, Dopa, Norepi and Epi
• Lab studies
–
Cortisol levels
–
Cortisol suppression- Given dexamethasone QHS X1 if the body
still produces ACTH and doesn’t decrease in the presence of the
drug then you have too much cortisol being produced.
Diagnoses Cushings
–
Cortisol stimulation-Injected with ACHT to see if cortisol
increases. Diagnoses Addisons
–
Urine vanillylmandelic acid, (VMA)
• Diagnostic studies
–
Adrenal scan
• DisordersCushings too much ACTH & Addison's adrenal
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insufficiency
see next slide
Addendum… Cushing's Disorder PP 984
• Disorders of Adrenal Glands - Cushing's too much
ACTH & Addison's adrenal insufficiency AKA Adrenal
Crisis covered in next Chapter.
– Cushing's Syndrome -Caused by too much
adrenocorticotropic hormone (ACTH). The ACTH is
overly stimulated in the presence of a tumor in the
Pituitary Gland.
– S & S Central obesity, thin UE and LE, moon face,
fragile skin, buffalo hump (see next slide) pp. 984
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Copyright © 2005 Lippincott Williams & Wilkins. Instructor's Resource CD-ROM to Accompany Critical Care Nursing: A Holistic Approach, eighth edition.
Common Endocrine Disorders
Chapter 44
Chapter 44 Endocrine disorders
• Disorders broken down into the following topics
– 1-Thyroid dysfunction
– 2-Adrenal Gland Dysfunction
– 3-Anti-duiretic Hormone Dysfunction
– 4-Diabetic Emergencies
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1-Thyroid Dysfunction
• Hyperthyroid – Graves’ disease, (autoimmune)
– Thyroid crisis/storm
• Hypothyroid – Myxedema
– The term myxedema is often used interchangeably with
hypothyroidism and myxedema coma.
– Myxedema coma occurs when the body's compensatory
responses to hypothyroidism are overwhelmed by a
precipitating factor such as infection, MI, CVA.
• Compare & Contrast table 44-2 pp 990 and next slide
• Know S & S.
– Hyperthyroid/Graves- pt presents with results of
being “hyper”.
• IE tachycardia, weight loss, diaphoresis,
exopthalmos
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Copyright © 2005 Lippincott Williams & Wilkins. Instructor's Resource CD-ROM to Accompany Critical Care Nursing: A Holistic Approach, eighth edition.
1- Cont………. Hyperthyroidism “Thyroid
Storm” or called “Thyroid Crisis”
• Labs: Always check TSH, T3 and free T4
– In hyperthyroidism, Graves Disease, the TSH is low
because of the overwhelming total of T4 and Free T3 and
free T4 levels.
• Treatment: Antithyroid drugs
– PTU/Propylthiouracil, block synthesis of T4 & T3
– Iodine solutions, NA Iodine (IV) & K iodine PO AKA “Lugols
Solution”.
• Iodine binds to overactive thyroid hormones.
– Dexamethasone/Decadron- a glucocorticoid, also
suppresses Thyroid
–
A Beta Blocker for tachycardia- Propanolol/Inderal
–
Sometimes Cardizem/Diltazem
– Antipyretics, cooling blankets, tepid baths for
hyperthermia symptoms
– Neuro assessments. Possibly can SZ. Have precautions
ready.
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2-Adrenal Gland Dysfunction, PP 995
• Adrenal insufficiency – Addison’s disease (autoimmune)
– Adrenal crisis- An acute, abrupt life threatening state
caused by insufficient/not enough cortisol. Dysfunction of
adrenal cortex, the outer part of the adrenals.
– S & S: headache, profound weakness, fatigue, slow,
sluggish, lethargic movement, N/V, belly pain, hypotensive
(postural), skin-color changes.
– low blood pressure secondary to decreased vascular tone
& increased HR
– Treatment: Give steroids, ABC’s, replace volume deficit.
– Recap to compare: Cushing's caused by too much ACTH
that stimulates the adrenal cortex from Pituitary Tumor
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Compare-Contrast Disorders of Adrenal
Glands
• Cushing's Syndrome Caused by too much
adrenocorticotropic hormone
(ACTH). The ACTH
is overly stimulated in the
presence of a tumor in the
Pituitary Gland.
– S & S Central obesity,
thin UE and LE, moon
face, fragile skin, buffalo
hump
• Addison’s disease- Adrenal
insufficiency (autoimmune)
• Adrenal crisis- An acute,
abrupt life threatening state
caused by insufficient/not
enough cortisol. Dysfunction
of adrenal cortex, the outer
part of the adrenals.
– S & S: headache,
profound weakness,
fatigue, slow, sluggish,
lethargic movement,
N/V, belly pain,
hypotensive
(postural),tachycardia,
skin-color changes.
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3-ADH Dysfunction
• Recap: ADH in Posterior Pituitary……….IMP!!!
• Excess of ADH (too much anti-diuretic)
– Syndrome of inappropriate antidiuretic hormone secretion
(SIADH) pp.996
• Body holding onto too much H2O. Retention & Fluid
Overload
• *Decreased serum osmolality because of over
hydration.
• Decreased UO
• Causes on Box 44-8 pp. 997
• Deficiency of ADH (Not enough anti- diuretic)
– Diabetes insipidus/& central Diabetes insipidus
– Kidneys excreting large amounts of urine. Up to 20 L.
– Can quickly lead to Hypovolemia in a pt that is not alert.
Pp 998-999
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4-Diabetic Emergencies
•
A-Diabetic Ketoacidosis
–
A critical illness that exhibits hyperglycemia, metabolic acidosis &
electrolyte imbalances.
–
DM 1-Lack of Insulin production
–
DM 2-Too much adipose tissue/glucose. Not enough insulin
–
S/S• Thirsty, frequent urination, weak, tired, dehydrated,
• Hyperventilation- Kussmauls breathing in attempt to correct
Metabolic Acidosis
• Volume depleted, dehydrated,
• CBC, Chem. 7, UA and Gases
• Treatment:
–
Fluid replacement- 1st, lots of fluids…………
–
Insulin Therapy
–
Correct electrolyte imbalances
–
Watch for Arrhythmias
–
Restore Metabolic function-Give Bi-carb???
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4-Diabetic Emergencies…cont
• B-Hyperosmolar Hyperglycemic State
– A syndrome in DM type 2 patients without ketones,
no ketoacidosis.
– Same treatment as DKA without having to treat the
acidosis.
– S/S
• Dehydrated (Most Common)
• Obtunded, can be less alert than the DKA
• No hyperventilation because no acidosis
– Treatment
• Gives fluids!!!
• Bring down glucose
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4-Diabetic Emergencies
• C- Hypoglycemia: Low BS with IDDM diabetics.
– Any stories of a hypoglycemic patient????
– How did they present??
– What did you or the nurse do???
– Do they respond quickly???
– Lets discuss…………….. Next slide
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4-Diabetic Emergencies
– How did they present??
• Change in MS, confused and increasingly
stuporous as sugar drops.
• Pale, diaphoretic, increased HR.
– What did you or the nurse do???
• Give sugar. If not alert to take PO insert IV and
give an Amp. of Dextrose 50% ASAP
– Do they respond quickly???
• Oh Ya
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