Endocrine

Question 1

Most of the endocrine feedback loops are

Answer 1

negative feedback loops

Question 2

endocrine dysfunction is either

Answer 2

hyperfunction or hypofunction

Question 3

Endocrine disease leads to one or more of three conditions:

Answer 3

Hormone deficiency
Hormone excess
Hormone resistance

Question 4

Hormone deficiency

Answer 4

1. Autoimmune process
2. Infection
3. Inflammation
4. Infarction
5. Tumor infiltration

Example: Type I DM

Question 5

Hormone excess

Answer 5

1. Tumor growth
2. Autoimmune disease
3. Genetic mutations that cause excessive function of endocrine cells

Example: Grave’s Disease

Question 6

Hormone resistance

Answer 6

1.Genetic defects that produce dysfunctional membrane receptors.
-Hormone levels are elevated, but receptors are unable to respond.

Example: Type II DM

Question 7

Grave’s disease

Answer 7

autoantibodies form and mimic TSH- continuously stimulating the thyroid, and causing overproduction of Thyroid Hormone.

Question 8

risk factors for dysfunction

Answer 8

genetic predisposition
exposure to radiation
medication effect
environmental pollutants (BPA)

Question 9

hypothalamic-pituitary-hormonal axis

Answer 9

Hypothalamus- “coordinating center”
Consolidates signals from thought, feeling, environment, autonomic function, and peripheral endocrine feedback.
Most of the time the brain’s hypothalamic region secretes a “releasing factor” that acts on the pituitary gland.

Pituitary gland - “Master gland,” that regulates all endocrine glands in the body. Pituitary releases “tropic hormones” in response to stimulus from hypothalamus.
These tropic hormones act on specific endocrine organs, which secrete hormones that then act on the body to create a physiologic effect.

Question 10

After the endocrine gland secretes the specific hormone it was stimulated to secrete the pituitary senses the level of hormone in the bloodstream, and interprets them as being either high, low, or normal.
If low:
If high:

Answer 10

i. If low- re-releases the tropic hormone
ii. If high- ceases tropic hormone release

If the appropriate physiologic effect is not achieved, the endocrine system keeps stimulating the target organ trying to achieve it.

After the appropriate effect is achieved, the endocrine system has the ability to then shut off that effect (Negative Feedback Loop)

Question 11

Anterior Pituitary:

Answer 11

produces and secretes hormones
Thyrotropin (TSH)- Hypothyroid- low T3 & T4
Gonadotropins (FSH and LH)- low estrogen
Somatotropin (GH)- Growth delay
Corticotropin (ACTH)- Adrenal insufficiency- low cortisol
Prolactin (PRL)

Question 12

Posterior Pituitary:

Answer 12

Stores Hormones secreted by Hypothalamus
Anti-diuretic hormone (ADH)- DI
Oxytocin (OXT)
These hormones are released into circulation when needed

Question 13

Hypopituitarism

Answer 13

diminished secretion of one or more anterior pituitary hormones.
Gonadotropin deficiency Growth hormone (GH) deficiency
Thyroid-stimulating hormone (TSH) deficiency, which causes hypothyroidism
Adrenocorticotropic hormone (ACTH) deficiency, which results in adrenal hypofunction

Question 14

Hyperpituitarism

Answer 14

Excessive growth (prior to growth plate closing)= excessive height
Excessive growth (after growth plate closes)= acromegaly
Precocious puberty
DI
SIADH

Question 15

Diabetes Insipidis

Answer 15

under secretion of antidiuretic hormone (ADH), or vasopressin

Leads to:
a state of uncontrolled diuresis (polyuria) and excessive thirst and water intake (polydipsia)

Question 16

Diabetes Insipidis patient care

Answer 16

clinical manifestations:
polyuria
polydipsia

diagnosis:
water deprivation test
urine specific gravity
urine osmolality

therapeutic management:
DDAVP (synthetic vasopressin)

Question 17

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

Answer 17

hypersecretion of ADH from the posterior pituitary

Excess ADH causes most of the filtered water to be reabsorbed from the kidneys back into central circulation.

Question 18

SIADH clinical manifestations

Answer 18

fluid retention
hyponatremia
anorexia
n/v
stomach cramps
irritability
weakness
confusion/personality changes
nuerologic signs: AMS, seizure
cerebral edema

Question 19

SIADH patient labs

Answer 19

low Na
low serum osmolality (dilutional)
urine osmolality (high)

Question 20

SIADH therapeutic management

Answer 20

Usually not a chronic condition
Long term ADH antagonizing medication
Fluid restriction

Question 21

Thyroid gland

Answer 21

secretes: T3, T4, Calcitronin

Initial stimulus: thyrotropin releasing factor (TRF), excreted from hypothalmus which stimulates: thyroid stimulating hormone (TSH) release from anterior pituitary

Question 22

T3 and T4 have essentially the same function, so are collectively called “Thyroid Hormone”

The main physiologyic action of TH is to

Answer 22

regulate the basal metabolic rate and thereby control the processes of growth and tissue differentiation.

Question 23

Calcitonin helps maintain

Answer 23

blood calcium levels by decreasing the calcium concentration. Its effect is the opposite of parathyroid hormone (PTH) in that it inhibits skeletal demineralization and promotes calcium deposition in the bone.

Question 24

Juvenile hypothyroidism

Answer 24

Deficiency in Secretion of Thyroid hormone (TH)

Congenital
or
Acquired

Question 25

Congenital vs acquired juvenile hypothyroidism

Answer 25

Congenital= low levels of circulating THs and raised levels of TSH at birth Acquired= after the newborn period, may have decelerated growth from chronic deprivation of TH thyromegaly (enlargement of the thyroid). Impaired growth and development are less severe when hypothyroidism is acquired at a later age, and because brain growth is nearly complete by 2 to 3 years old, intellectual disability and neurologic sequelae are not associated with juvenile hypothyroidism.

Question 26

Clinical manifestations of hypothyroidism

Answer 26

Decelerated growth Dry skin Puffiness around eyes Sparse hair Constipation Sleepiness Mental decline

Question 27

hypothyroidism therapeutic management

Answer 27

Thyroid hormone replacement Levothyroxine

Question 28

hypothyroidism nursing interventions

Answer 28

Education Med admin Med compliance Adequate follow-up for repeat labs s/s hypothyroidism s/s hyperthyroidism

Question 29

Hyperthyroidism

Answer 29

"Graves Disease" autoantibodies to the TSH receptor causing excess secretion of TH Increased levels T3 & T4 Minimal to no TSH

Question 30

Hyperthyroidism clinical manifestations

Answer 30

Emotional lability Physical restlessness, characteristically at rest Decelerated school performance Voracious appetite with weight loss in 50% of cases Fatigue Tachycardia Widened pulse pressure Dyspnea on exertion Exophthalmos (protruding eyeballs) Wide-eyed, staring expression with eyelid lag Tremor Goiter (hypertrophy and hyperplasia) Warm, moist skin Accelerated linear growth Heat intolerance (may be severe) Hair fine and unable to hold a curl Systolic murmurs

Question 31

Thyroid storm

Answer 31

Acute onset: * Severe irritability and restlessness * Vomiting * Diarrhea * Hyperthermia * Hypertension * Severe tachycardia * Prostration May progress rapidly to: * Delirium * Coma * Death

Question 32

When affected children exhibit signs and symptoms of hyperthyroidism (e.g., increased weight loss, pulse, pulse pressure, and blood pressure), their activity should be limited to

Answer 32

classwork only. Vigorous exercise is restricted until thyroid levels are decreased to normal or near-normal values.

Question 33

hyperthyroidism therapeutic management

Answer 33

antithyroid meds subtotal thyroidectomy ablation

Question 34

Hyperthyroidism nursing interventions

Answer 34

Assessment and identification of consistent clinical manifestations Treating physical symptoms: Environmental control - Quiet, unstimulating environment to encourage rest Encouraging rest Thermoregulation - Heat intolerance= lightweight, loose, cotton clothing Education regarding diet - frequent small meals, high calorie, high protein Education regarding compliance with medication regimen Complications of medication Education related to s/s hypothyroidism Facilitate school conversation Facilitate resolution of behavioral challenges.

Question 35

Adrenal insufficiency

Answer 35

Can result from decrease ACTH from the pituitary or dysfunction of the adrenal gland. Both cause decreased cortisol secretion and decreased cortisol reserve. Long term administration of corticosteroids can cause downregulation of adrenal receptors and the gland actually atrophies. Atrophy= decreased ability of the gland to secrete cortisol This is why we have to wean steroids! If we don’t, we can place our patient into adrenal crisis!

Question 36

Central adrenal insufficiency (CAI) is

Answer 36

life threatening, involves impaired communication of hormone secretion from the pituitary or hypothalamus in the brain, and can be seen in children with genetic or malformative syndromes (Patti, Guzzeti, Di Iorgi, et al., 2018). In each case, the adrenal cortex will not secrete appropriate steroids in response to stress.

Question 37

Acute Adrenal Insufficiency clinical manifestations

Answer 37

Increased irritability Headache Diffuse abdominal pain Weakness Nausea and vomiting Diarrhea Fever (increases as condition worsens) Central nervous system (CNS) signs: Nuchal rigidity Seizures Stupor Coma Weak, rapid pulse Decreased blood pressure Shallow respirations Cold, clammy skin Cyanosis Circulatory collapse (terminal event)

Question 38

Acute Adrenal Insufficiency therapeutic management

Answer 38

Rule out sepsis, hemorrhage Administration of cortisol (hydrocortisone) Fluid resuscitation & MIVF w/glucose Electrolyte replacement Vasopressors if necessary

Question 39

Primary/Chronic Adrenal Insufficiency

Answer 39

"Addison Disease" acquired adrenal insufficiency

Question 40

Chronic Adrenal Insufficiency clinical manifestations

Answer 40

Neurologic symptoms Muscular weakness Mental fatigue Irritability, apathy, and negativism Increased sleeping, listlessness Gastrointestinal symptoms Dehydration Anorexia Weight loss Circulatory symptoms Hypotension Small heart size Dizziness Syncopal (fainting) attacks Hypoglycemia Headache Hunger Weakness Trembling Sweating Other signs (seen in some children) Recurrent, unexplained seizures Intense craving for salt Acute abdominal pain Electrolyte imbalances

Question 41

Primary/Chronic Adrenal Insufficiency therapeutic management

Answer 41

Glucocorticoids (cortisone, hydrocortisone) Dose must be increased (x2; x3) during times of stress Mineralocorticoids (aldosterone) Increased salt intake in diet

Question 42

Chronic Adrenal Insufficiency nursing interventions/education

Answer 42

Education! Medication compliance Bitter taste Always have backup supply of medication Illness especially vomiting- need to seek healthcare “Emergency dose” hydrocortisone Complications of acute & chronic steroid use

Question 43

side effects of acute steroid use

Answer 43

gastric irritation increased excitability Sleeplessness behavioral changes

Question 44

Cushing Syndrome

Answer 44

group of conditions caused by excessive circulating free cortisol Etiology: Pituitary: with adrenal hyperplasia, usually an excess of ACTH Adrenal: with hypersecretion of glucocorticoids Iatrogenic: a result of administration of large amounts of exogenous corticosteroids

Question 45

Cushing syndrome clinical manifestations

Answer 45

temporal fat ecchymoses red abdominal strae bruises weight gain poor wound healing pendulous abdomen moon face excessive hair growth hyperglycemia increased susceptibility to infection hypertension hypokalemia

Question 46

Diabetes Mellitus

Answer 46

chronic disorder of metabolism characterized by hyperglycemia and insulin resistance. most common metabolic disease.

Question 47

Type 1 DM (insulin dependent)

Answer 47

destruction of the pancreatic beta cells absolute insulin deficiency Immune mediated OR Idiopathic (rare)

Question 48

Type II DM (acquired)

Answer 48

insulin resistance in which the body fails to use insulin properly combined with relative (rather than absolute) insulin deficiency can range from predominantly insulin resistant with relative insulin deficiency to predominantly deficient in insulin secretion with some insulin resistance. typically occurs in those who are older than 45 years of age, are overweight and sedentary, and have a family history of diabetes Increasing frequency in children

Question 49

DM clinical manifestations

Answer 49

“great imitator” influenza, gastroenteritis, and appendicitis Polyphagia Polyuria Polydipsia Weight loss Enuresis or nocturia Irritability; “not himself” or “not herself” Shortened attention span Lowered frustration tolerance Dry skin Blurred vision Poor wound healing Fatigue Flushed skin Headache Frequent infections Hyperglycemia * Elevated blood glucose levels * Glucosuria Frequent UTI Diabetic ketosis * Ketones and glucose in urine * Dehydration in some cases

Question 50

DM therapeutic management

Answer 50

Insulin replacement exercise encouraged dietary considerations: Large amount concentrated sweets not ideal but no limitation Low fat is better d/t risk for atherosclerosis Increased fiber- regulates glucose No calorie restriction for growing children unless overweight

Question 51

clinical manifestations of hypoglycemia

Answer 51

tremor, pallor, rapid heart rate, palpitations, and diaphoresis weakness, dizziness, headache, drowsiness, irritability, loss of coordination, seizures, and coma (CNS glucose depletion)

Question 52

hypoglycemia quick fix

Answer 52

simple carb: table sugar, juice, jelly, candy followed by complex carb: slice of bread, crackers followed by protein: cheese stick, milk

Question 53

DKA

Answer 53

Ketones produce excessive quantities of free hydrogen ions Fall in plasma pH. Then chemical buffers in the plasma, principally bicarbonate, combine with the hydrogen ions to form carbonic acid, which readily dissociates into water and carbon dioxide. The respiratory system attempts to eliminate the excess carbon dioxide by increased depth and rate (Kussmaul respirations) Potassium is released from the cells into the bloodstream (cell death) Potassium excreted by the kidneys The total body potassium is then decreased even though the serum potassium level may be elevated as a result of the decreased fluid volume in which it circulates.

Question 54

DKA clinical manifestations

Answer 54

Kussmal respirations Lethargy Dulled sensorium/confusion Thirst Weakness Abdominal pain N/V Flushed, dehydrated skin/mucous membranes Fruity/acetone breath If untreated, progresses to acidosis, coma, and death

Question 55

DKA therapeutic management

Answer 55

NO INSULIN BOLUSES No Sodium Bicarbonate! NO FLUID BOLUSES Unable to decrease serum glucose >100mg/dL/hr Risk is cerebral edema Insulin drip initiated & runs until glucose normal and anion gap closed MIVF initiated- 0.9NS initially Dextrose added to MIVF when serum glucose = 200 Frequent labs- Q1hr glucose, Q2hr lytes Electrolyte replacement as needed- remember, total body K depleted Cardiac monitoring

Question 56

Microvascular disease develops during the first

Answer 56

30 years of diabetes neuropathy retinopathy nephropathy

Question 57

Macrovascular disease develops after

Answer 57

25 years of diabetes hypertension atherosclerotic cardiovascular disease

Question 58

Hyperglycemia appears to influence

Answer 58

thyroid function