Chapter 13: Altered Hormonal and Metabolic Regulation (Nursing 2450)

Hormones

Chemicals made by cells that affect growth or function of other targeted tissues/organs
involved in metabolism, growth, sexual dev, stress, etc

Endocrine system

Collective group of cells capable of secreting hormones

Can only cells of endocrine system release hormones?

No (immune system cells release cytokines, neurons release NT)

Characteristics of hormones: Control is regulated via __?

Hypothalamic-pituitary axis

Characteristics of hormones: Feedback

modification or control of a process or system by its results or effects
hypothalamus receives input in form of NT, chem mediators, etc
can be neg or pos

Characteristics of hormones: when a hormone binds to a receptor, what are the two outcomes that may happen?

Act on target organ to achieve effect
Act on gland to produce another hormone

What are the releasing hormones produced by the hypothalamus?

Growth hormone (GH)
Thyrotropin
Corticotropin
Gonadotropin
(All have -releasing hormone to the end of them)

What are the inhibiting hormones produced by the hypothalamus?

Dopamine (inhbits prolactin)
Somatosin (inhibits GH and TSH)

Anterior pituitary gland function

Receives signal from hypothalamus via circulation
under neg feedback regulation

Posterior Pituitary gland function

Direct neural connection (axons)
not under neg feedback regulation

What hormones does the APG release?

luteinizing hormone
Adrenocorticotropin
Prolactin
GH
Thyroid stimulating (TSH)
Follicle stimulating (FSH)

Corticotropin releasing hormone (CRH)

Released by hypothalamus and acts on anterior pituitary to release adrenocorticotropic hormone

Adrenocorticotropic hormone (ACTH)

Released by anterior pituitary gland (from CRH binding)
acts on adrenal cortex
stimulates release of hormones (Aldosterone and cortisol)

Gonadotropin releasing hormone (GnRH)

Released by hypothalamus and acts on anterior pituitary gland to release LH (leutinizing hormone) and FSH (follicle stimulating hormone)

follicle stimulating hormone (FSH)

Released from anterior pituitary gland (from GnRH binding)
targets reproductive organs and stimulates sexual reproduction (ovulation in women; sperm production in men)

Growth hormone releasing hormone (GHRH)

released by hypothalamus and acts on pituitary gland to release growth hormone

Growth hormone (GH)

Released by anterior pituitary (when GHRH binds)
Targets bones, muscles, tissues
stimulates growth

Thyrotropin releasing hormone (TRH)

released by hypothalamus and acts on anterior pituitary gland to release thyroid stimulating hormone

Thyroid stimulating hormone (TSH)

Released by the anterior pituitary (When TRH binds)
Acts on thyroid gland to produce secretion of thyroid hormones (T3 and T4)

Positive feedback loop

presence of hormone stimulates increased production of hormone until cycle interrupted
less common (Example: oxytocin released during labor; stretching happens)

Negative feedback loop: what are the two mechanisms

Low levels of hormones stimulates release of more hormones
High levels of hormones inhibit release of hormones

dirunal patterns of secretion

Daily

What must hormones bind to in order to elicit a response?

Receptor

Cell to cell communication: Paracrine

Hormone cell communicating to nearby cell

Cell to cell communication: Autocrine

Hormone cell communicating to self

Cell to cell communication: Endocrine

Hormone cell communicating with capillary (helps with far distance)

Cell to cell communication: Synaptic

Hormone cell (neuron) communicating via neuron to neuron (axon/terminal to dendrites)

Cell to cell communication: Neuroendocrine

Hormone cell (neuron) communicating with capillary

What did Dr. Hans Selye do?

Discovered new sex hormone
Injected ovarian extract into rats

What is stress?

Threat to homeostasis
Can be real or perceived
can be good or bad

Stage I of stress

Stimuli from senses sent to brain

Stage II of stress

Brain deciphers stimulus as threat or non threat

Stage III of stress

Body stays activated until threat gone

Stage IV of stress

Body returns to homeostasis
threat gone

Stress hormones: Catecholamines

Norepinephrine (released from presynaptic neurons)
Epinephrine (secreted by adrenal medulla)

Stress hormones: Glucocorticoids (steroid hormone)

Cortisol (secreted by adrenal cortex)

Immune system effects in response to stress

Decreased resistance to infection
alteration of immune response

Selye's General Adaptation Syndrome: alarm stage

Stressor triggers hypothalamic-pituitary-adrenal axis (HPA)

Selye's General Adaptation Syndrome: Resistance (adaption) stage

Begins with action of adrenal hormones (cortisol, (nor)epinephrine)

Selye's General Adaptation Syndrome: Exhaustion stage

Occurs only if stress continues and adaption is not successful

Altered hormone function

Impairment of endocrine gland
Lack of/excessive hormone synthesis
Impaired receptor binding
Impaired feedback mechanisms
Impaired cell response to hormones

Hypopituitarism

not enough hormones via pituitary gland
Results in fatigue, dry skin, growth impairment, anorexia,etc

Diagnosing altered hormone function

History and physical examination
Lab tests (serum and hormone levels)
Imaging
Genetic test

Altered hormone function treatment

Removal of tumor releasing hormone
medication that replaces hormone deficiency

Syndrome of inappropriate antidiuretic hormone (SIADH) pathophysiology

Excessive production and release of ADH (usually caused by tumor secretion)
water accumulates in cells
Sodium diluted in extracellulat space

What is the result of Syndrome of inappropriate antidiuretic hormone (SIADH)?

Hypotonic hyponatremia

Syndrome of inappropriate antidiuretic hormone (SIADH) Clinical manifestations

Decreased urine output
Anorexia
nausea
psychosis
coma
seizure
(depends on serum sodium levels)

Syndrome of inappropriate antidiuretic hormone (SIADH) diagnostic criteria

hyponatremia
Hypotonicity
Decreased urine volume
concentrated urine (high sodium)

Syndrome of inappropriate antidiuretic hormone (SIADH) treatment

Remove cause
water restriction
Isotonic or hypertonic IV fluid
pharmacologic treatment

diabetes insipidus (DI) pathophysiology

Insufficient ADH
inability to retain water

diabetes insipidus (DI) clinical manifestations

Polyuria
Excessive thirst
Dehydration
Shock

diabetes insipidus (DI) diagnostic criteria

ADH levels
Serum solute concentration
Urine specific gravity

diabetes insipidus (DI) treatment

Treat cause
hydration
Desmopressin (Anti diuretic)

another name for hyperthyroidism?

Grave's disease

Hyperthyroidism (Graves disease) pathophysiology

Excessive thyroid hormone due to excess stimulation of thyroid gland, disease of thyroid gland, or excess production of TSH

What type of hypersensitivity is Grave's Disease

Type II
IgG binds to TSH receptors

Hyperthyroidism (Graves disease) clinical manifestations

Goiter
Weight loss (fast metabolism(
Tremors
Sweating
Weakness
Exopthalmos (Excessive inflammation)

Hyperthyroidism (Graves disease) diagnostic criteria

Sertum TSH (Low)
Serum T3/T4 (High)

Hyperthyroidism (Graves disease) treatment

meds that block T3/T4 production
Surgical removal of gland (requires thyroid HRT after)

Hypothyroidism pathophysiology

Deficiency of thyroid hormone (T3/T4)
happens due to lack of thyroid development, deficient synthesis of TH, impaired secretion of TSH or TRH

Hypothyroidism clinical manifestations

Fatigue
cold intolerance
constipation
Goiter
weight gain

Hypothyroidism diagnostic criteria

TSH levels (high)
total T3 and T4 uptake

Hypothyroidism treatment

lifelong thyroid HRT

Cushing syndrome pathophysiology

Excess glucocorticoids secreted from adrenal cortex

Cushing syndrome clinical manifestations

Metabolic alteration
obesity of trunk, face, and upper back
Glucose intolerance
Suppression of immunity/inflammation
impaired stress response

Cushing syndrome diagnostic criteria

Cortisol levels in 24 hoururine
imaging studies (detect tumor that may be secreting)

Cushing syndrome treatment

Remove cause of excess cause of cortisol secretion

Addisions disease pathophysiology

Autoimmune destruction of adrenal cortex
glucocorticoid deficiency
ACTH levels increase to make up for deficiency

Addisions disease clinical manifestations (glucocorticoid deficiency)

Darker pigmentation of skin (from high ACTH)
Hypoglycemia
Weakness
weight loss
personality changes

Addisions disease clinical manifestations (mineralocorticoid deficiency)

dehydration
hyponatremia
hyperkalemia
hypotension
Shock

Addisions disease diagnostic criteria

Hyponatremia
hyperkalemia
Corticosteriod levels low after ACTH administered

Addisions disease treatment

Fluid replacement
Oral glucocorticoid and mineralocorticoid replacment

A patient with a "buffalo hump" and a "moon face" enters the primary care clinic. Which diagnosis is most likely for this patient?

Cushings syndrome