Endocrine Patho Part 1 - Disorders of the Pituitary Gland, Growth, Thyroid, and Adrenal Flashcards

1
Q

What is a gland?

A

aggregation of cells which secrete substances not related to their ordinary metabolic needs

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2
Q

What does an endocrine gland do?

A

secrete hormones into the circulation

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3
Q

What are hormones?

A

Chemical messengers that exert action on specific targets, either singe or multiple. Their actions are determined by the amount of free hormones in the blood, along with the number of receptors available for binding

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4
Q

Which hormones does the hypothalamus release?

A

Corticotropin releasing(CRH), Thyrotropin releasing(TRH), growth hormone(GHRH), gonadotropin releasing (GRH)

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5
Q

Which hormones does the anterior pituitary gland release?

A

growth hormone(GH), adenocorticotropic(ACTH), thyroid stimulating (TSH), Follicle stimulating (FSH), Luteinizing(LH), Prolactin

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6
Q

Which hormones does the poterior pituitary gland release?

A

antidiuretic

oxytocin

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7
Q

Which hormones does the adrenal cortex release?

A

mineralicorticoids - aldosterone

glucocorticoids - cortisol

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8
Q

Which hormones does the adrenal medulla release?

A

epinepherine

norepinephrine

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9
Q

Which hormones does the thyroid release?

A

T3 & T4

Calcitonin

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10
Q

Which hormones does the Parathyroid release?

A

parathyroid hormone

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11
Q

Which hormones do the pancreatic islet cells release?

A

insulin

glucagon

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12
Q

Which hormones does the kidney release?

A

Vitamin D

calcitriol

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13
Q

Which hormones do the ovaries release?

A

estrogen

progesterone

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14
Q

Which hormones do the testes release?

A

testosterone

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15
Q

What happens in endocrine primary disorder?

A

problem occurring in the gland responsible for producing the hormone

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16
Q

What happens in the endocrine secondary disorder?

A

problem in the gland sending messages (pituitary)

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17
Q

What happens in tertiary disorder?

A

problem in the hypothalamus

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18
Q

What happens in the Hypothalamic/ Pituitary Axis?

A

hypothalamus senses low hormone in blood then sends the paracrine message to the pituitary. The pituitary sends hormones to glands and then the glad produces hormones and releases into the blood. The hypothalamus sense and turns off message

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19
Q

Pituitary Gland

A
  • Pea sized gland at the base of the brain
  • connected to the hypothalamus by the infundibulum
  • 2 lobes
    • posterior lobe
    • anterior lobe
  • master gland
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20
Q

Posterior Pituitary

hormones released and pathologies

A

releases Oxytocin and ADH
-ADH responds to input from osmoreceptors, barorecpetors, and stress to increase water reabsorption in the kidneys

Pathologies

  • Syndrome of Inappropriate ADH
    • urine output decreases, more water reabsorption, increased BP and edema
  • Disbetes Insipidus
    - a lot of urine, decreased bp, show signs of dehydration
  • most often found in patients with head injuries
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21
Q

Anterior Pituitary

hormones

A

GH, TSH, ACTH, FSH, LH

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22
Q

What is Pituitary Dysfunction caused by?

A

Pituitary tumors
trauma
dysfunction of hypothalamus

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23
Q

What causes Hypopituitarism?

A

causes decrease in the release of pituitary hormones which affects many other part of the endocrine system
growth hormone is usually lost first, followed by FSH/LH
ACTH is usually lost last
can be life threatening, especially with a decrease in ACTH which causes adrenal insufficiency

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24
Q

What is Hypopituitarism caused by?

A

either congenital or acquired

caused by tumors, radiation to the brain, ischemia/infarction, or traumatic brain injury

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25
When do problems become evident in hypopituitarism?
When 70-90% of the anterior pituitary is destroyed
26
What is the treatment for hypopituitarism?
hormone replacement | ex. cortisol for decrease in ACTH
27
What hormones are necessary for normal growth?
``` Growth hormone from pituitary Insulin-like growth factors (liver) Thyroid hormone Insulin Androgens (testosterone) -women, adrenal cortex, men, testes ```
28
Where and when is the growth hormone released? | What is it needed for?
Released throughout life by pituitary Stimulated by: Hypothalamic GH-releasing Factor (GHRF) Release greatest in stage IV sleep, first 1-4 hours of sleep Needed for growth and to regulate metabolic functions (fluids, glucose)
29
What are some effects of GH?
Acts through insulin-like growth factors (IGFs) produced by the liver Cartilage growth & bone growth Linear growth on epiphyseal growth plates Visceral and endocrine organs Cardiac and skeletal muscle growth Facilitates protein synthesis in cells Increases fatty acids Increases serum glucose by causing insulin resistance
30
What are some causes of short stature in children?
Variants of normal- short parents Low birth wt –intrauterine growth retardation Life time consequence, small throughout life Chromosomal abnormalities – Turner’s syndrome ( X chromosome) Hypothyroidism Pan-hypopituitarism Protein calorie malnutrition Chronic kidney disease Poorly controlled diabetes Excess glucocorticoids – Cushings / iatrogenic Malabsorption syndromes like celiac disease Psychosocial dwarfism Neglect or abuse will have poor growth, take them out and they will catch up Environment plays a huge role in health IGF-1 deficiency (Laron-type) Skeletal abnormalities (achondroplasia) Most common cause, IGF is release but the bones do not have enough of the receptor GH deficiency
31
What happens with congenital GH deficiency?
Slow growth -(nml IQ, obesity, immature facial features, delay in skeletal maturity & puberty) Hypoglycemia and seizures Obesity - no signal to break down fatty acids
32
What happens in a growth hormone deficiency in adults?
``` either present since childhood or developed later, such as hypopituitarism from a tumor symptoms: fatigue, malaise decrease in lean body mass increased abdominal obesity increased cardiovascular disease ```
33
What causes tall stature in children?
normal variant - genetic genetic or chromosomal disorder- Marfan or XYY Excess GH - gigantism (children) acromegaly (adults)
34
When must gigantism occur? What does it cause? How can you treat it?
before epiphyseal plate fusion it may cause hypertrophy in the heart or hypertension in the veins possible treatment is sex hormones to cause epiphyseal fusion
35
What is acromegaly caused by? What are some signs and symptoms? What is the treatment?
``` usually caused by pituitary adenoma S/S increased bone width not length soft tissue increases pain in joints coarse skin and body hair accelerated atherosclerosis hypertension sleep apnea elevated glucose headaches Tx normalizing IGF-1 or tumor removal ```
36
What happens in the feedback mechanism for secretion of TRH and
Hypothalamus recognizes low thyroxine (T4) in blood Releases TRH (thyrotropin releasing hormone) Stimulates Thyroid Stimulating Hormone (TSH) from anterior pituitary Causes thyroid to produce thyroid hormone Increased thyroid hormone suppresses TRH & thus TSH Note: Cold temperatures also increase TRH and thyroid hormone release
37
How do you test for Thyroid function?
Serum Thyroid Stimulating Hormone (TSH) level From pituitary gland Serum Free T3, T4 – amount available to enter cells From thyroid gland
38
What are the functions of the thyroid hormone function?
Increases cellular metabolism and protein synthesis Growth and development of children, including sexual maturity Control of metabolic rate - ↑ metabolism of glucose, fat, protein Affects blood lipid levels CV function: increases oxygen consumption, blood flow, cardiac output GI function: ↑secretions, ↑motility, ↑appetite, ↓wt Neuro function: ↑ muscle activity and tremor (not at normal, but if there’s too much)
39
What is the difference between the primary, secondary, tertiary, and Goiter Thyroid Disorders?
``` Primary: problems in thyroid Secondary: pituitary problems Tertiary: hypothalamus problems Goiter (enlarged thyroid gland) can occur in hypo- or hyper-thyroidism Wont know which until you look at other signs and symptoms ```
40
What happens in hypothyroidism? In primary, secondary, and tertiary?
``` Decreased T3 & T4 from thyroid Primary Increased TSH as pituitary tries to increase production Low thyroxine (T3 & T4 ) Secondary High TRH Low TSH: no messages being sent to thyroid Low T3 and T4 Tertiary Low TRH, Low TSH, Low T3/T4 ```
41
What happens in congenital hypothyroidism?
Lack of gland / or abnormal synthesis of hormone or deficient TSH secretion Symptoms appear after birth because of maternal hormone in utero Cretinism: s/s associated with UNTREATED congenital hypothyroidism Routine screen at birth Treat with thyroxine
42
What are the signs and symptoms of cretinism?
``` Longer physiologic jaundice Hoarse cry/ enlarged tongue Choking with feeding Enlarged abdomen and umbilical hernia Sluggish – feeding Lack of interest and somnulence Mental retardation and impaired growth if not treated ```
43
What happens in acquired primary hypothyroidism?
``` Primary hypothyroidism: destruction of thyroid gland – most common Secondary (lack of TSH) and tertiary (lack of TRH) less common Causes of Primary Acquired Hypothyroidism: Hashimoto thyroiditis Most common cause Autoimmune (Hype 2 antibodies) Iodine deficiency Idiopathic causes Postpartum thyroiditis Temp inflammation of thyroid Thyroidectomy Damage from radiation Medications: Lithium, antithyroid drugs, amiodarone * Everything sloes down, metabolism, weakness, fatigue, cold intolerance, weight gain ```
44
What are the symptoms of hypothyroidism?
Slowed metabolism Weakness, fatigue, lethargy, mental dullness, cold intolerance Weight gain, decreased appetite Yellow skin (problem with metabolism carotene) Constipation Slow reflexes Elevated serum cholesterol – not using fatty acids for fuel Bradycardia Cold intolerance Myxedema: accumulation of fluid due to altered metabolism mucopolysaccharides (sugars) * when sugar sits in tissue, it draws fluids in Puffy face and tongue, legs Carpal tunnel/nerve compression – because tissue is swollen Effusions (pericardial, pleural) – build up of fluid in spaces Lab: Low T4, elevated TSH, thyroid antibodies to diagnose Hashimoto
45
What happens in Myxedema Coma?
``` Progression of all the hypothyroid signs May be precipitated by acute illness or narcotics/sedative (overuse) Decreased/change LOC Hypothermia without shivering Hypoventilation – slow, shallow BR Bradycardia Hypotension Hypoglycemia, lactic acidosis ```
46
What happens in hyperthyroidism?
``` Characterized by increased metabolism Increased thyroxine (T3, T4) from thyroid gland Low TSH if primary High TSH if secondary or Increased TRH if tertiary Types of Primary Hyperthyroidism Graves disease – autoimmune Antibodies binding to receptors on the thyroid and trigger release of T3 and T4 Adenoma of thyroid Thyroiditis Excess ingestion of thyroxine ```
47
What happens in Graves Disease?
``` Most prevalent hyperthyroidism Onset 20-40 years old Genetic predisposition – HLA class Autoimmune hyperthyroidism Abnormal stimulation of thyroid by thyroid stimulating hormone receptor antibodies Act through normal receptors ```
48
S/s of hyperthyroidism?
``` Opthalmopathy (exophthalmos) Lid lag- sclera shows above iris Protrusion beyond orbit Dermopathy (myxedema) Goiter Increased SNS sensitivity Increased blood pressure / pulse, RR, palpitations Nervousness, restlessness, tremor Heat intolerance – sweating Fatigue Weight loss despite inc. appetite Thin skin Moist (velvety) skin – increased perspiration Hair loss- fine, silky hair Muscle cramps Decreased menstruation Heat intolerance Atrial fibrillation – elderly Abnormal electrical stimulus ```
49
Tx of hyperthyroidism?
``` Destruction of part of thyroid gland Radioactive Iodine Surgical removal of part Medication to stop thyroxine production Propylthiouracil (PTU) Methimazole (Tapazole) Treatment of SNS sx with beta blockers ```
50
Thyroid Storm/ Thyrotoxic Crisis
Excessive amounts of thyroxine (T4) – life threatening (T4 usually above 7 ng/dL ( .7-1.8 ng/dL) Persons with hyperthyroidism not treated Or having severe stress reaction S/S thyrotoxic crisis High body temperature Extreme CV effects (tachycardia, AF, CHF, angina) Extreme CNS effects (delirium, agitation) Tx: cool patient, remove thyroid hormone by pheresis, etc. Beta blockers to block CNS stimulation
51
What does Aldosterone do?
``` Stimulates Na+/K+ pump in renal tubule Na reabsorbed into blood Water follows K moves out to kidney filtrate Triggers: RAAS Renin ( decreased glomerular filtration rate) High K+ Low Na+ Stress ```
52
What controls the release of glucocorticoids (cortisol)?
``` Bursts in early morning, 6-8AM Declines as day progresses Diurnal pattern reversed in night shift workers Also released in stress, depression Cortisol goes up in depression ```
53
Actions of Cortisol?
``` Glucose metabolism effects Gluconeogenesis Insulin resistance Protein metabolism effects Breaks down proteins to amino acids Increasing serum amino acids Fat metabolism Mobilization of fatty acids Use of fats for energy Altered fat distribution Influences emotional behavior Suppression immune/inflammatory response ```
54
Addison Disease (primary adrenal insufficiency)
Lack of all the adrenal cortical hormones Mineralocorticoids (Aldosterone) Glucocorticoids Androgens (testes still produce testosterone) Life-time replacement is necessary Adrenal cortex destruction (90% destroyed before sx). Causes: Autoimmune Infection (TB, histoplasmosis, cytomegalovirus, HIV, etc) Cancer of adrenal glands Bilateral hemorrhage (anticoagulants) Drugs (ketoconazole)
55
Addisons Pathophysiology
Aldosterone, cortisol, and androgens all decreased ACTH level high as it tries to stimulate the adrenal cortex to produce hormones Aldosterone Deficiency Excessive urinary losses of Na+, Cl- and water Increased retention of K+ Dehydration Decreased blood pressure Decreased cardiac output Weakness, fatigue, possible circulatory shock
56
Addison Disease
Glucocorticoid Deficiency Hypoglycemia – can’t control glucose levels w/o cortisol Lethargy & weakness Anorexia, nausea/vomiting Weight loss Androgen deficiency Males; no symptoms (testes still produce testerone) Females: sparse pubic/axillary hair Darkened pigmentation due to ACTH- bronze skin, blue/black mucous membranes
57
Treatment of Addison Disease
``` Lifetime hormone replacement Can give just cortisol somtimes Daily PO hydrocortisone or Fludrocortisone (Florinef) Has both the mineralcorticoid and glucocorticoid effects Need increased doses during stress ```
58
What are some causes of adrenal insufficiency? | Secondary and Tertiary
``` Secondary: Hypopituitarism Low ACTH No trigger for adrenal glands to produce Tertiary: Hypothalamic damage No CRH Long term steroid therapy – iatrogenic cause ```
59
Acute Adrenal (Addisonian) Crisis
``` Life threatening May occur in: Person with Addison’s disease if exposed to a stressor Children with congenital disease Deficiency of adrenal hormones leads to: Severe hypotension due to water loss Vascular collapse Tx: replacement of sodium, fluids, sugar, steroid (cortisol) ```
60
Cushing Syndrome: Glucocorticoid Excess
Pituitary form –Cushings Disease Excessive ACTH Pituitary tumor producing ACTH Adrenal form- tumor on adrenal gland Ectopic form –nonpituitary tumor that secretes ACTH (small cell lung cancer) Also: Iatrogenic Cushing Syndrome from exogenous steroids
61
What happens with glucocorticoid Excess?
Glucocorticoids possess some mineralcorticoid (aldosterone) activity thus excess Result in hypokalemia HTN from water, Na+ retention Excess cortisol effects Excess androgen effects Females: Hirsuitism (male pattern hair growth), acne, menstrual irregularity
62
Cushing's S/s, dx, and rx
Weight gain - “buffalo hump”, “moon face”, “truncal obesity” Muscle weakness - Muscle wasting Thin skin on forearms and legs Purple striae – breasts, thighs, abdomen Glucose intolerance/hyperglycemia Diabetes 20% Osteoporosis (due to decrease in bone building) Depressed immune / inflammation Gastric ulcers Irritability, depression Dx: Find cause of hypersecretion of cortisol Hormone suppression and stimulation tests Imaging to look for pituitary or other tumor Rx: Iatrogenic – taper, decrease steroid dose