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Pathophysiology - Diseases > Diseases and disorders of Endocrine system > Flashcards

Diseases and disorders of Endocrine system Flashcards

1
Q

What is the endocrine system function?

A

compromisesa number of glands and glandular tissue that secrete chemical messengers called hormone into blood

include pituary gland, thyroid gland, parathyroid glands, adrenal glands, endocrine pancreas, and gonads

accessory endocrine tissue found in heart, stomach, intestines, kidney and thymus

conrtoled by pituary (master gland) which is controlled by hypotalamus

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2
Q

what do the endocrine hormones affect?

A

many aspects of body functions including:
growth
development
energy metabolism
muscle and fat ditribution
sex development
fluid and electrolytre balance
inflammation and immune responses

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3
Q

What are hormones composed of?

A

either proteins (ex: insulin) or chains of amino acids (ex: epinephrine), others r steroids or fatty substances derived from cholesterol

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4
Q

neg feed back mechanism of hormones?

A

if level of hormone is adequte its further release is stopped

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5
Q

What is the pituary gland?

A

pea-sized organs located at base of brain

aka hypophsyis, made of anterior lobe (adenohypophysis) and posterior lobe (neurohypophysis)

stalk called infundibulum connects pituary to floor of hypothalamuus connect

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6
Q

6 hormones produced by anterior pituary?

A

are called tropic hormones (menas they control function of other endocrine glans):

  1. prolactin
  2. growth hormone (GH)
  3. adrenocorticootropic hormone (ACTH)
  4. luteinizing hormone (LH)
  5. Follicle-stimulating hormone (FSH)
  6. Thyroid-stimulating hormone (TSH)
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7
Q

hormones of posterior pituary gland

A

antidiuretic hormone (ADH) and oxytocin

r produced in hypothalamus and r stored posterior pituary gland

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8
Q

What is Growth Hormone (GH)?

A

aka somatotropin

affects all parts of body by promoting growth of tissue and bone

before puberty GH stimulates growth of long bones = mroe height (also increases size of soft tissues like liver, heart and kidney)

after adolescne GH is secreted less but is continued to promote tissue replacement and repiare

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9
Q

What is thryroid-stimulating hormone?

A

Controls hormone secretion by thyroid gland (no TSH = no thyroid function)

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10
Q

What is adrenocorticotropic hormone?

A

stimulates release of adrenal cortex hormones (adrenal glands have inter part - adrenal medulla - and outer part - adrenal cortex)

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11
Q

What are gonadotropins?

A

regulates sexual development and function

include FSH (stimulates egg amd sperm production) and LH (stimulates ovaries to produce estrogen and progesterone and stimulates testes to produce testosterone)

surge in LH = signal for ovulation

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12
Q

What is prolactin?

A

stimulates breast development and formation of milk during pregnancy and after delivery

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13
Q

What is antidiuretic hormone?

A

AKA VASOPRESSIN, STIMULATES WATER ABSOPRTION IN KIDNEY AND HAS ANTIDIEURTEIC EFFECT

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14
Q

What is oxytocin?

A

target is smooth muscle of uterus (stimulates uterine contractions, mammary glands (suckling it = release of milk from breasts) and prostate (cause ejaculation of prostate gland secretion)

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15
Q

What is the thyroid gland?

A

located in neck region, 1 lobe on either side of trachea

connecting strip (isthmus) anterior to trachea connect the lobes

produces thyroid hormone (TH) (is actually 2 iodine -containing hormones: thyroxine (T4) and triiodothronine (T3)

T4 is primary thryoid hormone (most t3 is created by conversion of T4 to T3)

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16
Q

Effect of thryoid hormone on diff parts of body (Basal metabolic rate/temperature regulation,Carbohydrate/lipid/protein metabolism,
Nervous system,
Cardiovascular system,
Muscular system,
Skeletal system,
Gastrointestinal system,
Reproductive system,
Integumentary system)?

A

Basal metabolic rate/temperature regulation - Increases basal metabolic rate and body heat production
Carbohydrate/lipid/protein metabolism - Promotes glucose catabolism; mobilizes fats; essential for protein synthesis; enhances the synthesis of cholesterol by the liver
Nervous system - Promotes normal development of the nervous system in fetus and infants; promotes normal nervous system function in adults
Cardiovascular system - Promotes normal functioning of the heart
Muscular system - Promotes normal muscular development and function
Skeletal system - Promotes normal growth and maturation of the skeleton
Gastrointestinal system - Promotes normal gastrointestinal motility; increases secretion of digestive juices
Reproductive system - Promotes normal reproductive function in females
Integumentary system - Promotes normal hydration and secretory activity of skin

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17
Q

What is the paratyroid gland?

A

4 tiny glands located psoterior to the thyroid gland

(sometimes repmoved with tyroidectomy before funciton was understood)

secretes parathyroid hormone (PTH) aka parathormone

reguilates levels of circulating calcium and phosphate

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18
Q

percent of calcium in body?

A

99% is in the bones

1% is elsewehere and is essential to blood-clotting along with nervous conduction and increase heart muscle tone and is imprtant ot muscle contraction

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19
Q

What does PTH?

A

increases concetration of calcium in blood by having kidney reabsorb calcium and not secrete into urine

also increases absoprtion of calcium in intestines and increases citivty of osteroclasts (break down bone and release calcium into the bloodstream)

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20
Q

What is the adrenal glands?

A

located at top of each kidney

each gland has 2 parts = an outer adrenal cortex and inner adrenal medulla

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21
Q

What does the adrenal cortex do?

A

is stimulated by ACTH

secretes many corticoids (corticosteriods)
which can be divided into mineralocorticoids (regulate salt balance, main is aldosterone), glucocorticoids (regulate carb, lipid and protein metabolism, main is cortisol or hydrocortisone), and sex hormones (androgens and estrogen)

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22
Q

What does adrenal medulla do?

A

secretes epinephrine (adrenalin) and norepinephrine which are secreted in stress situatiosn where additional energy and strength r needed

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23
Q

What does aldosterone do?

A

causes sodium retention and potassium secretion by kidneys

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24
Q

What does epinephrine and norepinephrine?

A

epinephrine - vasodilation, increases heart rate, bp, and respiration

norepinephrine - vasoconstriction

together they help shint blood to vital organs when needed

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25
Q

What is the endocrine pancreas?

A

fish shaped organ in middle of abd cavity, below stomach

divided into head, body, and tail w/ head neartest to duodenum and opening of pancreatic duct

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26
Q

functions of endocrine pancrease?

A

synthesis, storage, release of insulin (secreted by beta cells located in patches of tissue called islets of langerhans aka pancreatic islets), glucagon (secreted by alpha cells of islets) and somatostatin (delta cells, inhibits secretion of glucagon and insulin)

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27
Q

Insulin and glucagon relationship?

A

antagonistic to each other to maintian normal blood glucose of 80-120 mg/dl

insulin lower blood glucose, glucagon elevates it by stimulating liver to release glycogen in form of glucose

after meal blood sugar increases = insulin which moves sugar into blood and tissues to be converted to glycogen which is converted into glucagon when blood sugar levels drop

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28
Q

What do the gonads do?

A

overies and testes

function is endocrine gland + source of ova and sperm

ova secretes estrogen and progesterone (sexual development, secondary sex characterisitcs and reproductive cycle)

testes secerte testosterone (sexual development, secondary sex characterisitcs)

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29
Q

What endocrine organs can be physically examined?

A

thyroid and testes

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30
Q

How to measure hormone levels?

A

in blood or urine samples via enzyme-linked immunosorbant assay (ELISA), and radioimmunoassay (RIA)

in these tests labeled hormone (antigen) competes with unlabed hrmone for binding sites on an antibody

if v. high concentration of hormone in blood or urine sample most of resulting antigen-antibody complexes will be unlabeled

v. low concentration of hormone in blood or urine sample, most of the antigened-antibody complexes will be labled

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31
Q

What is anterior pituary hyposecretion?

A

is result of inherited disorders, malignant tumors, inadequate secretion of hormones, inflammation, and vascular changes of pituary gland

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32
Q

What is pituitary dwarfism?

A

due to inadequate secretion of growth hormone by pitaury gland (adult height reachign only 4 ft 10)

only known risk factor is injury or trauma to pituitary gland

cause is mostly idiopathic, other causes may include genetics, congenital, cranial tumor in pituary gland interfering with hormone production, trauma to the gland or radiation treatment to the head

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33
Q

estimated _______________ ppl have pituary dwarfism

in us pituary dwarfism affects fewer than _________ ppl

A

1 in 14,000 to 1 in 27,000

200,000

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34
Q

s/s of pituitary dwarfism?

A

children w/ pituitary dwarfism r proportionately small

  • slowed growth before age of 5 years
  • absent or delay sexual development
  • short stature and height for age
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35
Q

How to diagnose and treat pituitary dwarfism?

A

diagnose - physical exam, secondary tooth eruption is delayed, fat deposits in lower trunk area blood test confirming low GH and imaging tests

treat - GH replacement therapy until child reaches 5 ft, replacement thyroid and adrena hormones when multiple hormone deficines r found (as they approach puberty, sex hormoens r adminstered if needed)

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36
Q

What is gigantism?

A

result of hypersecretion of GH (somatotropin) in children = abn and accelerated growth, typically of long bones bc epiphyseal closure has not begun

100 cases of gigantism reported to date

no known risk factors for gigantism

most common cause is benign tumor of the pituary gland that leads to excessive secretion of GH

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37
Q

s/s of gigantism?

A
  • facial features may thicken
  • hands & ft may be disproportionately enlarged,
  • headaches may develop along with excess sweating
  • late onset of puberty
  • joint problems
  • CV weakness and myoptahy
  • shorter life expenctancy
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38
Q

how to diagnose and treat gigantism?

A

diagnose - physical exam, imaging tests, biopsy, elevated levels of GH, age-reference norms for insulin-like growth factor 1 (IGF-1) r best indicators of endogeounous secretion of GH), pituary MRI or CT, bone radiographs show thickening of cranium, enlargement of jaws and elongation of long bones, and blood test

treat - depends on etiology (if well-defined tumors then surgery), radiation therapy, med to reduce growth hormone secretion, if surgery than transsphenodial apprach

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39
Q

What is acromegaly?

A

result of excess GH secretion in adulthood

4,676 cases per million people

no known risk factors for acromegaly

slow but harmful onset, s/s are usually present for a number of yr before diagnosis

caused by benign tumor of pituitary gland or adenoma that leads to excessive seretion of GH

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40
Q

s/s of acromegaly

A

grwith plates of long bones r clsoed to long bones dont increase in length
- enlargemetn of hands, feet and head
- soft-tissue thickening of palms of head and soles of ft
- enlargemetn of forehead
- enlargement of the jaw to cause teeth to spread
- enlargement of tongue
- arthritis

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41
Q

How to diangose and treat Acromegaly?

A

diagnose - med history, physical exam, blood test for high GH and IGF-1, glucose tolerance tests bc increased glucose levels = failure of suppression of GH levels, MRI and CT, and biopsy

treatment - focuses on correcting metabolic abn, improving cliical features and correcting underlying cause (surgical removal of tumors through transsphenoidal approach), med to decrease GH secretion prior to surgery or when surgery isn’t possible, radiation

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42
Q

What is diabetes insipidus?

A

distrurbance of water metabolism, resulting in extreme thrist and excessive secretion of dilute urine due to results from decreased secretion or action of ADH (vasopressin) (may be hereditary, head trauma, cerebral eema, intracranial lesion, renal tubular resistance, more common in men, childhood or early adulthood)

occur in 3 in 100,000

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43
Q

risk factors for diabetes inspidus?

A

head injury, brain surgery, kidney disease, pregnancy, taking certain meds (lithium, amphotercin B, demeclocycline)

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44
Q

s/s of diabetes insipidus?

A

polyuria
polydipsia
disturbed sleep due to bedwetting
daytime fatigue
fever, headaches
wt loss
low bp
dry mucous membranes
hypotension
dizziness
poor skin turgor

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45
Q

2 types of DI?

A

Central DI - damage to pituary gland from surgery, tumor, illness (ex: meningitis), inflammation or head injury

Nephrogenic DI - defect in kidney tubules, making kidneys unable to properly respond to ADH (can be bc genetic disorder, chronic kidney disorder, drugs like lithium and emecloycline)

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46
Q

how to diagnose and treat diabetes insipidus?

A

diagnose - med history, physical exam, urinalysis (shows colorless urine w/ low specific gravity (<1.005)) and water restriction test (when urine concentration is stable on consecutive measurements or blood osmolality is above normal, vasopressin is administered)

treat - removing the primary cause and treating symptoms to prevent dehydration, may be controlled with vasopressin (nasal spray or tablet), vasopressin is ineffective for nephrogenic DI so treatment is compensatory fluid intake with effort to correct underlying etiology, thiazide dieuretic by inducing mild volume depletion (kidney transplant may be needed)

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47
Q

what is water restriction test?

A

used to treat DI

urine of DI pt is colorless and has v. low specific gravity (diluted urine)

limits pt water intake for few hours while measuring urine output, bp, and urine concentration, after several hrs pt is given vasopressin meds (med decrease urine output and increase urine concentration)

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48
Q

What is hypothyroidism?

A

below-normal production of T4 by thyroid gland

is in 1-2% of population

caused by autoimmune diseases (hashimotos’s disease), family tendecy, surgery to remove all or part of thyroid, radiation treatment, treatment for hyperthyroidism, certain meds (lithium, interferon)

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49
Q

risk factors for hypothyroidism?

A

being female
over 50
having autoimmune disorder
having close relative with thyroid disease or an autoimmune disease
use of radioactive iodine
surgical removal of thyroid gland
radiation to head or neck
antithyroid med
pregnancy
some meds (lithium, interferon)

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50
Q

s/s of hypothyroidism?

A

vary and depend on severity of deficiency

unexplained wt gain
dry skin
hair loss
swollen face, hands legs, ankles or ft
increased sensitivity to cold
aches and pains in muscles or joints
hoarse or raspy voice
constipation
heavy or irregular periods
fatigue
slower thinking
trouble remembering things
slower speech
depression
enlarged thyroid
changes in blood cholesterol levels
slow heart rate
infertility

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51
Q

Diagnose and treat hypothyroidism

A

diagnose - med history, s/s, blood test confirming low T4 and T3 and high TSH, autoantibody testing, and imaging tests

treat - thyroid hormone replacement therapy

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52
Q

What is congenital hypothyroidism

A

aka cretinism, occurs in 1 in 4,000 newborns

no known risk factors

most often result of hypoplasia (underdevelopment), aplasia (absence of development) and failure of thyroid gland to migrate to its normal anatomical position

maternal factors like iodine deficiency and ingestion of antithyroid meds during pregnancy can cause hypothyroidism in both mother and fetus

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53
Q

s/s of congenital hypothyroidism

A

intellectual development disorder
umbilical hernia
protruding abd
reduced level of activity and generalized lethargy
continuous wt gain even with physical feeding habits
small stature
retardation of physical growth
developmental delay
swelling in eyelids, enlarged tongue and coarse facial features

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54
Q

how to diagnose and treat cretinism?

A

diagnose - blood test confirming low levels of T3 and T4 and high TSH usually within first 10 days of birth, thyroid scan confirming absence of thyroid tissue

treat - adequate treatment with thyroid hormone supplements as soon as possible

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55
Q

What is hypertyroidism?

A

excess thyroid hormone

graves’ disease is most common form of hyperthyroidism (occurs in 0.4% of the population) (entire thyroid gland hypertrophies, resulting in diffuse goither and overproduction of thyroid hormones)

more common in women than men

onset is btwn 20 and 40 yrs

associated with autoimmune disease such as diabetes mellitus and rheumatoid arthritis

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56
Q

risk factors of Graves’ diease?

A

being female
family history
stress
smoking

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57
Q

s/s of Graves’ disease

A

increased metabolism
multisystem changes
exitability
profuse perspiration and war, moist skin
muscle weakness
nail change (onycholysis)
enlargement of thyroid
nervousness
irritability
heat intolerance
increased sweating
insomnia
rapid or irregular heartbeat
fatigue
diarrhea
wt loss
1/2 of ppl with Graves’ disease have Graves’ ophthalmopathy (bulging eyes)
sudden increase in severity may signal thyrotoxicosis (thyroid storm) from v high levels of thyroid hormone levels

58
Q

how to diagnose Graves’ disease?

A

diagnose - family history, physical exam, s/s, blood test confirming high T3 and T4, and low TSH, and imaging

59
Q

How to treat Grave’s disease?

A

depends on severity, etiology, presence of complication, goal is to bring metabolic rate to normal with minimal complications

administration of antithyroid drugs such as propylthiouracil and methimaole (tapazxole) to block synthesis of thyroid hormone

b-blockers such as propranolol hydrochloride (inderal) and atenolol (Tenormin) r given to treat tachycardia

radioactive iodine therapy or surgery (thyroidectomy)

60
Q

What is cause of Graves’ disease?

A

abnormal immune system response that causes the thyroid gland to produce too much thyroid hormone

(immune system releases abn antibodies that mimic TSH, and thereby thyroid hormone is increased

61
Q

What is simple goiter?

A

enlargement of thyroid gland usually evident by swelling in neck

may be caused by iodine deficiency (iodine is needed to produce T3 and T4 which = thyroid hormone, and inadequate blood thyroid hormone levels = increased secretion of TSH = thyroid gland increasing in size), eating large amt of goiter-producing foods (soy, peanuts, peaches, spinach, turnips, brussel sprouts, seaweed, cabbage) that inhibit TH production, certain meds (immunosuppressants, antiretrovirals, lithium) or may be idiopathic

62
Q

risk factors of simple goiter?

A

being female, over 40, family history of goiter

63
Q

s/s of simple goiter?

A

thryoid gland can compress trachea or esophagus, causing diff breathing or swallowing, dizziness and syncope
- wt loss despite hearty appetite
- heat intolerance
- tachycardia
- anxiety
- increased sweating may be reported by pt when there is excessive production of thyroid hormones

64
Q

how to diagnose and treat simple goiter?

A

diagnose - medical history, physical exam, blood test to measure levels of decreased TH and increased TSH, measurement of radioactive iodine uptake by thyroid, thyroid ultrasonography and imaging tests

treatment - administer 1 drop per wk of saturated solution of potassium iodide,thyroid hormone replacement pills if goiter is bc underactive thyroid, small doses of iodine if goiter is bc lack of iodine, radiation therapy to shrink gland if bc thyroid is producing too much TH, surgery to remove all or part of gland

65
Q

prevent simple goiter?

A

adequate intake of dietary iodine (150-300 ug) and monitoring intake of goiter-producing foods and medication

66
Q

What is thyroid cancer?

A

priamry cancer that starts in the thyroid glands

secondary metastases from breast, colon, kidney, skin cancer to thyroid gland

commonly diagnosed at a younger age than most other adult cancers

women 3x r more likely

67
Q

The American Cancer Society estimates in 2013 there will be ________ new cases of thyroid cancer and ___________ deaths due to thyroid cancer.

Nearly ____ out of _______ cases are found in people
younger than ____ years of age.

A

60,220

1,850

two out of three

55

68
Q

Risk factors for thyroid cancer?

A

being female
diet low in iodine
exposure to radiation (esp in early childhod0

69
Q

s/s of thyroid cncer?

A

no s/s early in disease

as tumor grows s/s like lump in neck, voice hoarseness, difficulty swallowing, pain in neck and throat, swollen lymph nodes in neck, dysphagia, hoarseness resulting from compression of upper aerodigestive tract,

70
Q

how to diagnose and treat thyroid cancer?

A

diagnose - medical history, physical exam, blood tests to measure levels of TSH and TH, imaging tests and biopsy, fine needle aspiration and histologic exam, check for carcinoembryonic antigen (CEA) which can serve as tumor marker as they r secreted by medullary carcinomas along w/ calcitonin

treat - surgery, radioactive iodine treatment, thyroid hormone therapy, radiation therapy, chemo, and targeted therapy

71
Q

What is hyperparathyroidism + age/gender and primary + secondary?

A

results from excessive secretion of parathyroid hormone by parathyroid glands

caused by benign tumors of parathyroid, causing oversecretion of pTH (size of tumor is often correlated with amt of parathyroid hormone secreted in blood)

most frequently in ppl over 40, at 2x more common in women

secondary is caused by low levels of serum calcium or serum vitamin D from renal disease

72
Q

The overall prevalence of hyperparathyroidism in the general population is about __ in 1,000 but may be up to ____ in 1,000 in postmenopausal women.

A

3

21

73
Q

Risk factors of hyperparathyroidism?

A

postmenopausal

chronic vitamin D deficiency

neck area radiation

lithium therapy

74
Q

What does hyper parathyroid cause?

A

excess parathyroid hormone = increased levels of circulating calcium (hypercalcemia) which comes from bone reabsorption so as calcium levels rise phosopate levels fall, bones weaken, bend, and fracture

giant cell tumor, cysts of the bone, kidney stones made of calcium, and calcium deposits in stomach, lungs and walls of blood vessels (making them hard) may form

75
Q

s/s of hyperparathyroidism?

A
  • pain in bones sometimes confused with arthritis
  • increased breakdown of bone from skeletal system (demineralization)
  • hypercalcemia
  • nervous system is depressed
  • muscles lose their tone and weaken
  • heart muscle is affected
  • pulse slow
    GI disturbance (from deposition of calcium in mucosa in GI tract)
  • abd pain
  • vomiting
  • constipation
    calcium deposit in eyes can cause irritation and excessive tearing
76
Q

how to diagnose and treat hyperparathyroidism?

A

diagnose - blood tests to confirm high PTH and calcium and low phosphorous, urinalysis to confirm increased calcium, alkaline phosphatase elves tend to be icnreased, urine calcium is high, low bone mineral density, esp in sites richer in cortical bone, and imaging tests

treat - depends on etiology, surgery to remove tumor if adenoma or parathyroid glands, if hyperlasia then 3 out of 4 parathroid glands r removed, diuerteics to increase urine output (increase calcium exertion) and limiting intake of calcium, treatment is aimed at lowing serum calcium levels)

77
Q

What is hypoparathyroidism?

A

result of decrease in secretion of parathyroid hormone by parathyroid glands
commonly caused by surgical removal of thyroid gland

prevalence in US in 4 in 1000

78
Q

risk factors of hypoparathyroidism?

A

damage to glands from heavy metals (copper or iron)
immune disorders (Addison’s disease)
a family history of hyperparathyroidism
some infections

79
Q

s/s of hypoparathyroidism

A

principal manifestation is tetany (sustained muscular contraction)
muscles of hands and feet contract in a characteristic fashion
- circulating levels of calcium r reduced = hypocalcemia w/ occasional possibilty of excessive deposits of calcium into tissue = hyperexcitable nervous system - overstimulation of skeletal muscle
- numbness and tingling of fingertips, toes, ears, or nose
- emotional changes, confusion, irritabilty
- laryngospasm
- arrhythmias
- respiratory paralysis

80
Q

how to diagnose and treat hypoparathyroidism?

A

diagnose - physical exam, neuromuscular hyperexcitability aong w/ hisotry of possible insult to parathyroid glands, presence of Trousseau phenomenon is sure indication of hypocalcemia, blood test confirming low PTH and calcium and high phosphate, ECG, and imaging test

treat - calcium and vitamin D

81
Q

What is hypoadrenalism?

A

aka primary adrenal insufficiency or Addison’s disease

partial or complete failure of adrenocortical function

result of undersecretion of hormones by adrenal cortex

first described in 1855 by THomas Addison (described symptoms associated with destruction of adrenal glands)

occurs in 1 in 1000 ppl

more common in female (female to male ratio is 2:1)

usually diagnosed in 30s-50s

82
Q

risk factors of Addison’s disease?

A

having other autoimmune problems such as Graves’ disease, hypopituitarism. and vitilgo

83
Q

What are the s/s of Addison’s disease?

A

lack of cortisol, aldosterone and adrenal androgens

wt loss, fatigue, and anorexia from deficiency in cortisol

bronze skin color

cardiovascular difficulties such as irregular pulse, reduced cardiac output, orthostatic hypotension

depression, anxiety and emotional distress

most distinctive sign is hyperpigmentation in non-sun-exposed areas like gingvia tissue and creases of hands

GI signs r anorexia or loss of appetite, and discomfort, vomiting and diarrhea

fluid loss from these symptoms is associated with hypotension, dizziness, lack of blood sodium and syncope (fainting )

84
Q

Causes of Addison’s disease?

A

any disease that damages the entire adrenal cortex

75-80% of all cases are due to autoimmune

other causes are infectious diseases like tuberculosis, fungal disease, opportunistic infection associated with AIDS, certain cancers, and hemorrhage of adrenal gland after anticoagulation med

85
Q

how to diagnose and treat Addison’s disease?

A

diagnose - med history, physical exam, blod test confirming low cortisol and high ACTH, ACTH stimulation tests that measure level of crtisol before and after injection of synthetic ACTH, and imaging tests

treat - lifelong replacement of both glucocorticoids and mineralocorticods, may need additional meds like hydrocortisone during stress

86
Q

what can addison’s disease cause?

A

cane cause acute adrenal insufficiency (life-threatening, esp in pt with chronic adrenal insufficiency who a;also have another acute illness like infection, trauma or severe physical stress like surgery)

s/s r rapid and include N&V, and pain and severe hypotension, death from shock and CV collapse

treated with immediate rehydration with salt solutions and IV glucocorticoid replacement

87
Q

What is hyperadrenalism?

A

can be due to overproduction of cortisol (Cushing’s syndrome) or overproduction of aldosterone (Conn’s sudnrome)

88
Q

What is Cushing’s disease

A

condition of chronic hypersecretion of adrenal cortex = excessive circulating cortisol levels

prevalence is 1 in 500,000 ppl

etiology is most often benign pituitary tumor, adrenal tumor resutling in excessive secretion of cortisol (prolonged admin of large doseses of cortisone will also cause Cushing’s syndrome), excessive secretion of corticotropin from pituariy gland, production of corticotropin in another organ, iatrogenic factors such as prolonged administration or large doses of glucocorticoids

risk factors r having adrenal tumor or corticosteroid therapy

89
Q

s/s of Cushing syndrome?

A

fat accumulation behind the shoulders (buffalo hump) and in trunk = protruding abd
round “moon-shaped” face
salt and water retention
hyperlipidemia
hyperglycemia
osteoprosis
atherosclerosos
changes in mood and cognition and decerased short-term memory
fatigue
weakness
impaired wound healing
hypertension
wt gain
stretch marks on skin
excessive hair growth
amenorrhea and impotence

90
Q

How to diagnose and treat Cushing’s disease?

A

diagnose - physical appearance, blood and urine test to confirm high levels of cortisol and imaging tests

treatment - goal is to correct hypersecretion of adrenal hormones (removal of pituary tumors through surgery or radiation, med to block synthesis of corticosteroids r useful in pt who cant have surgery)

91
Q

What is Conn’s syndrome + gender?

A

etiology is benign tumor of adrenal cortex

prevalence of Conn’s syndrome is 0.05-2.0%

women r 2x moe likely to suffer from Conn’s sudrome

incidence increases with age

no known risk factors

92
Q

s/s of Conn’s syndrome

A

only symptom is hypertension which may cause headaches, blurred vision and dizziness

some pt with hyperaldosteronism have normal K levels, others have low K levels, leading to fatigue, numbness, increased urination, increased thirst, muscle crampls and muscle weakness

93
Q

How to diagnose and treat Conn’s syndrome?

A

diagnose - blood test to confirm high level of aldosterone and low or undetectable level of rennin which is produced by kidney and imaging tests

treat - surgery, antihypertensive meds and aldosterone blockers

94
Q

What is diabetes mellitus (DM)

A

endocrine disease of impaired glucose regulation and hyperglycemia caused by genetics, environ factors, and lifestyle choices

chronic disorder of carb, fat and protein metabolism caused by inadequate production of insulin by pancrease or faulty use of insulin by cells

factors that contribute is absolute insulin deficiency, reduction in insulin secretion, decreased glucose utilization and increased glucose production

prevalence of DM is 8.3%

95
Q

What is type 1 diabetes?

A

little or no insulin production

5-10% of all diabetes causes

formerly known as juvenile-onset diabetes bc peak is 10-14

risk factors r genetics, family history of T1DM, certain viral infections, being Caucasian, living in a northern climate and having other autoimmune diseases

96
Q

s/s of T1DM?

A

polyuria, polydipsia, polyphagia

bc water movement by concentration grade water is lost through kidnets as glucose concentration rises so pt drink a lot of water to compensate

excess glucose but body cant take it in bc lack of insulin = very hunger by losing weight

97
Q

When does T1DM occur?

A

when an autoimmune process develops in indv where immune system attacks and destroys beta cells (ver several months usually but sometimes very quickly or for yrs)

once 80% or more of beta cell function is destroyed pt no longer have sufficient insulin capacity to control blood glucose = hyperglycemia

98
Q

How to diagnose and treat T1DM?

A

diagnose - urine test to show presence or absence of glucose in urine, fasting blood glucose levels, glucose tolerance testing and glycosylated hemoglobin testing to monitor and diagnose diabetes

treat - insulin, regular exercise, maintaining healthy wt, healthy diet and monitoring blood sugar

99
Q

what is glucose tolerance testing?

A

challenges body’s ability to secrete and use insulin

after 10hr fast

pt drinks standard glucose solution and blood and urine samples are taken and analyzed for next 3 hrs

no gluse in urine, blood glucose shouldn’t exceed 170 mg/dL

100
Q

What is glycosylated hemoglobin determination?

A

monitor long term control of diabetes

indicates avg blood glucose level over past 6 days

normal values should be below 6 and for diabetics is should be less than 7

101
Q

What is glycosylated hemoglobin determination?

A

monitor long term control of diabetes

indicates avg blood glucose level over past 6 days

normal values should be below 6 and for diabetics is should be less than 7

102
Q

What is type 2 diabetes?

A

body resists the effect of insulin or doesn’t produce enough insulin to maintain glucose levels

90-95% of diabetic cases

risk factors r family history, 45+, obesity, history of gestational diabetes, sedentary lifestyle, history of high bp, high cholesterol or hyperlipidemia

103
Q

s/s of type 2 diabetes?

A

polyuria, polydipsia, polyphagia, wt loss, fatigue, blurred vision, numbness or tinglingin hands or feet ad slow wound healing

104
Q

How to diagnose and treat type 2 diabetes?

A

diagnose - urine testing and blood glucose testing

treatment - blood sugar monitoring, healthy eating, regular exercise, possible diabetes medication (increase body’s sensitivity to insulin and lower glucose production in liver or stimulate pancreas to produce and release more insulin_ or insulin therapy

105
Q

What is gestational dabetes?

A

diabetes developed during pregnancy where resistance to effects of insulin is related to metabolic changes of pregnancy bc increased need for insulin

4% of pregnancies

hormones produced by placenta during pregancanct lead to higher blood glucose levels, usually mother’s pancreas is able to make more insulin to overcome effects of pregnancy hormones on blood sugar levels but if mom cant then blood sugar levels rise, =gestational diabetes

increased destruction of insulin by placenta, reduced effectiveness of maternal insulin durign pregnancy

106
Q

risk factors of gestational diabetes?

A
  • over 25
  • family history of T2DM
  • personal history (prediabetes, gestational diabetes, giving birth to baby weighing more than 9 lb, unexpected stillbirth) and being overweight
107
Q

s/s of gestational diabetes

A

mostly doesn’t cause s/s

rarely causes polydipsia, polyphagia, polyuria

108
Q

how to diagnose and treat gestational diabetes?

A

diagnose - oral glucose tolerance test (2-hr postprandial), fasting blood flucose, glucose tolerance test, and glycated hemoglobin test

treat - monioring blood sugar, healthy diet, regular physical activity, possibly diabetes meds or insulin therapy, hypoglycemic agents (most women revert to normal glucose tolerance after pregnancy but have big risk for diabetes later in life)

109
Q

Ketones and diabetes

A

when body doesn’t get enough sugar it uses protein and fat as energy source, produces ketones (in blood, breath and urine its called ketosis, aka ketoacidosis ) which are acidic so these produce acidosis or low pH in tissue

110
Q

complications of type 1 diabetes?

A

diabetic coma and insulin hsock

result of improper insulin administration (too much or too little)

diabetic coma - no enough insulin or too many carbs
s/s r polyuria, polydipsia dehydration and ketoacidosis (person becomes lethargic and falls into coma)

insulin shock - too much insulin, not enough food, excessive exercise (s/s r quick and include low blood sugar, sweating, lightheadness and trembling, if not treat person becomes confused and coma) - needs IV glucose and emergency med treatment

111
Q

What is hyperosmolar hyperglycemic state?

A

occurs in older, debiliated pt with type 2 diabetes

similar to DKA, associated with acute stress from infection, medical illness or surgery

no ketone formation but hyperglycemia in ranges of 250400 mg/dL

treatment aimed at rehtdration, correction of hyperglycemia and electrolyte distrubance (Aggresive IV fluid and electrolyte replacement as pt can loose 10 L or 2.5 G of fluid in short time)

112
Q

What are some chronic complications of diabetes?

A

due to chronic pathological insult to microvasculature (small bv) and microvasculature (large bv)

microvascular disease - primarily in eyes, kidneys and nerves, damages endothelial cell lining of bv, resulting in progressive narrowing and occlusion of large and small vessels, cells die when vessel occlusion cuts off blood supply

macrovascular disease - leads to CV disease, leading cause of death in pt with diabetes

113
Q

What is microvascular disease for diabetes?

A

includes retinopathy, nephropathy and neuropathy

diabetic retinopathy is leading cause of blidnenss among adults age 20-74

diabetic nephropathy occus in approx 20-30% of pt with diabetes (leading cause of end-stage kidney disease)

60-70% of diabetic pts have nerve damage or neuropathy (s/s of neuropathy is numbness or tingling in hands and ft, severe, burning muscle aches, loss of sensation in ft and poor circulation can lead to sever infections ad requiring amputations)

MOre than 60% of nontraumatic limb amputation in US occur annually in ppl with diabetes

114
Q

What is hypergonadism?

A

result of increased hormone production before puberty by gonads = precocious puberty (age 9 in guys and age 8 in girls)

precocious puberty currently affects 1 in 5000 ppl and 10x more likely in girls

115
Q

what are risk factors of hypergonadism?

A
  • being a girl
  • obesity
  • being exposed to sex hormones
  • having other medical conditions (congenital adrenal hyperplasia, hypothyroidism)
116
Q

s/s of precocious puberty

A

Both
- pubic or underarm hair
- rapid growth
- acne
- adult body odor
Women
- breast developments
- first menstruation
Men
- enlarged testicles and penis
- facial hair
- voice deepening
- spermatogenesis
- sebaceous gland activity increases

117
Q

causes of precocious puberty?

A

Girls:
- mostly idiopathic
- encephalopathy
- meningitis
- endocrine disorders
- ovarian and adrenal tumors
- hypersecretion of ovarian hormones in females r rare bc negative-feedback stimulation of gonadotropic hormone stops ovarian hormone secretion

Boys:
- caused by tumor in testes or pituitary gland
- inadvertent ignestion of sex steroids through therapeutic meds or deliberate ingestion of sex steroids

118
Q

how to diagnose and treat hypergonadism?

A

diagnose - child’s and family’s medical history, physical exam, and blood tests to confirm elevated levels of sex hormones, MRI, brain scan, skull and bone radiographic studies, chromosomal karyotype studies (for girls, test for FSH, LH, sex steroids in normal adult range)

treat - remove cause of precocious puberty, removal or radiation of tumors and meds to suppress or counteract sex hormones, gonadotropin-releasing romone (GnRH) agonists, meds that inhibit androgen action (spironolactone), inhibit androgen synthesis (ketoconazole), block the coneversion of androgens

119
Q

Growth hormone and age

A

growth hormone levels decreases with age (in men thi maifests after 30 as decrease in lean body mass and decrease in thickness and strength of bone matrix)

body fat increase = growth hormone level decrease

increased body fat correlated with greater risk of diabetes, heart disease, and cancer.

Decreased bone density makes bones more
susceptible to fracture.

120
Q

thyroid, kidney, pancrease with age

A

decrease in t3:T4 ratios with age decrease metabolic rate

incidence of autoimmune disease of the thyroid
among females increases with age.

age-related decline in the kidneys’ sensitivity to aldosterone occurs, accompanied by a diminishing capacity of the kidneys
to secrete renin when needed.

The body is less able to deal with the stress of changes in bp, dehydration, and disease in general.

increased incidence of abnormalities in bp, sodium and potassium levels,
acid-base balances, and osmotic pressure.

The pancreas retains the ability to secrete
insulin at normal levels with age, but tissue responsiveness to insulin decreases. Insulin resistance leads to a greater incidence of T2DM.

121
Q

T2DM with aging

A

It is estimated that T2DM occurs in 10% of those over age 56

in 20% of those between
45 and 76, and in 40% of people over age 85.

Although T1DM is somewhat less common than
T2DM, and its occurrence is unrelated to aging,
it remains among the 10 leading causes of death
among people over age 65.

Androgen and estrogen levels drop with age, although this is considered a normal process of aging.

122
Q

common s/s of endocrine disorders:

A
  • growth abn
  • emotional distrubrances or psychiatric problems
  • skin, hair and nail changes
  • edema
  • hypertension or hypotension
  • arrhythmia
  • changes in urine output
  • muscle weakness and atrophy
  • menstrual irregularity or amenhorrhea
  • impotence or changes in libido
  • sterility
  • changes in energy level
123
Q

diagnostic procedures for endocrine disorders?

A
  • blood serum or plasma which is collected by phelobtomy method
  • blood spot testing (requires capillary blood)
  • urien and saliva testing
  • radioimmunoassay or immunometric assay methodology and occasionally 24 hr urine test
  • CT, ultrasonogrpahy, MRI and biopsy
124
Q

What is hypopituatarism?

A
  • condition caused by deficiency or absnece of any of the pituary hormones produced by anterior pituary lobe
  • pituary tumor, hypothalamus tumor, congential deficiency, some r acquires (ex: hypopituatarism resulting from damage to pituary gland caused by radiaiton or surgical removal or from ischemia of gland caused by infarct, tumor, or basilar skull fracture), destruction of entire anterior lobe (panhypopituitarism)
125
Q

s/s of hypopituatarism

A
  • metabolic dysfunction
  • sexual immaturity
  • delayed growth
  • atrophy of glands (bc pituary fglands stimulates other endocrine glands)
  • when thyrotropin secretion is reduced function of thyroid is affected = hypothyroidism
  • secretion of corticotropin is reduced = salt balance, nutrient metabolism r affected
  • secretion of gonadotropin = impaired sexual functions includign sexual development, menustration and libido
  • delayed goewths in kids
126
Q

how to diagnose hypopituatarism

A
  • complete medical evaluation
  • history of head trauma
  • previous radiation
  • surgical procudure to gland or nearby tissue
  • plasma levels of all or some itiaury hormone r low
  • radiographic films of skull, cranial CT and MRI
127
Q

treatmetn of hypopituatarism

A
  • if neoplasia is uase then removal of tumor
  • replacement therapy w/ hormonal supplements includign thyroxine (t4), cortisone, sex hormones, somatropin (hH)
128
Q

What is hashimoto thyroiditis?

A
  • chronic lymphocytic thyroiditis is chronic disease of immune system that attack thyroid gland
  • heredity play prominent role
  • antibody appear to destroy thyroid tissue
  • gland enlarges as result of inflammatory process w/ infiltration by lymphocyte and plasma cells
  • gland tissue is replaced by fibrous tissue and signficant number of pt w/ hashimoto become hypothyroid
129
Q

s/s of hashimoto thyroiditis

A
  • occurs in women 8x more likely
  • common btwn 45 and 65
  • leadign cause of goiter and hypothyroidism
  • gradual and painless lumpy enlargement of thyroid gland which cause feeling of pressure in neck and may result in difficulty wit hswallowing
  • sensitivty to cold, wt gain, fatigue, depression, mental apathy
130
Q

how to diagnose and treat Hashimoto thyroiditis

A

diagnose - serum TSH levels r elevated, autoantibodes against thyroid tissue such as thyroid peroxidase antibodies (TPOs), characteristic chagnes can be seen in thyroid gland through needle boipsy and exam of gland tissue, radioactive idoine uptake will show low uptake

treat - lifelong replacement of thyroid hormones in t w/ hypothyroidism

131
Q

What is myxedema and myxedema coma?

A
  • myxedema (hypothyroidism) is a disease charcteized by clinical manifestiations associated w/ low metabolic rate caused by thyroid hormone deficiency
  • myxedem coma is result of severe untreated hypothyroidism exacerbated by an acute event such as MI, infection or use of sedatves
  • result of thyroid gland’s inabiluty to synthesize T4 being impaired as a result of reduced amt of thyrotropin, radiation destruction of thyroid gland, surgical removal of gland w/o t4 replacement therapy, tumor, failure of thyroid gland, Hashmito thyroiditis, failure of pituary to produce thyrotropin
132
Q

s/s of myxedema?

A
  • slowing function in multiple organs
  • excessive fatigue
  • musclular weakness
  • loss of hair
  • wt gain
  • constipation
  • intolerance to cold r common symptoms
  • skin is dry and scaly
  • puffiness of hands and face
  • enlarged tongue
  • severe hypothyroidism
  • hypothermia
  • altered mental status (slurred speech and drowsiness, followed by profound lethargy or even unconsciousness)
133
Q

diagnose and treat myxedema?

A

diagnose - clnical features, low levels of thyroid hormones and significantly elevated TSH levels

treat - achieve normla thyroid function w/ lowest possible dose, treat myxedema coma w/ levothyroxine sodium orally or intravenously

134
Q

types of thyroid cancer?

A
  • papullary (small nipplelike proejctions) (most common - 30-60 y/os)
  • follicular (saclike ball of cells) (most common - 30-60 y/os)
  • medullary (Affecting interior poriton of gland) (80% of cases r sporadic, some r genetic, resulting in multiple endocrine neoplasia (MEN) type 2, mostly in 3rd decade of life)
  • anaplastic (loss of differntiation of cells) (rare, mainly 60+)
135
Q

prognosis for thyroid cancer?

A
  • over 5 yr survival rate for ppl diagnosed 2008-2014 is greater than 99% for papullary, follicular and medullary and 30% for anaplastic
  • regional thyroid cancer if spread to other iorgans or tissues close to thyroid gland (follicular - 96%, papillary - 99%, medullary - 91%, anaplastic - 13%)
  • if metastic papillary - 78%, follicular - 56%, medullary - 37%, anaplastic - 3%
136
Q

what are untreated or poorly managed diabetes complications

A
  • retinopathy = blindness
  • neuropathy
  • renal failure
  • atherosclerosis = myocardial infarction
  • cerebrovascular accident
  • hyperglycemia = delayed healing and impaired resistance to infection
137
Q

drugs to treat type 2 diabetes

A
  • sulfonylureas
  • meglitinide drugs (oral hypoglycemic drugs) such as glipizide (Glucotrol0, glyburide (DiaBeta or Micronase), repaglinide (Prandin), and nateglinide (Starlix) stimulide pancrease to produce insulin
  • Meformin (Glucophage) prevents liver fro m producign hepatic glucose and helps enchance behefits of avaiable insulin)
  • acarbose (Precose) delays digestion of carbs
  • Rosiglitazone (avandia) and pioglitazone (actos) beling to thiaz0olidinedione class of drugs = insulin sensitizer by binding to peroxisome proliferator-activated receptor (PPARs) of cells
  • pramlintide (symlin) resembles human amylin produced by pancrease
  • pramlintide (Symlin) increases production of insulin right after eating
  • incretion hrmones
  • DPP IV inhibitors inhibit DPP IV wich breaks down incretin hormones that regulate gluvose levels (Sitagliptin (Januvia), saxagliptin (Onglyza), linagliption (Tradjenta) and alogliptin (Nesina)
  • Bromocriptine (Cycloset) increases dopamine receptor
  • sodium-glucose linked transporter 2 inhibitor = reduction of blood glucose (Canagluflozin (Invokana) and dapagliflozin (Farxiga))
138
Q

what is lactic acidosis?

A
  • rare side effect from metformine and is seen in pt w/ renal failure, liver failure and congestive heart failure
  • weakness, fatigue, unusual muscle pain, dyspnea, unusual stomach discomfort, dizziness or lightheadness, bradycardia or cardiac arrhythmias
139
Q

What is metabolic syndrome?

A

0 aka syndrome X
- may increase indv risk for type 2 diabetes and CV disease
5 components:
1. Central obesity (waist circumference of greater than 35 in)
2. increased blood pressure (130/85 mm Hg)
3. abn triglyceride levels above 150 mg/dL
4. abn HDL cholesterol levels below 40 mg/dL
5. fasting glucose levels above 100 mg/dL

140
Q

What is hypoglycemia?

A
  • abn low glucose levels in blood
  • ,ajor cause is insulin overdose
  • failure to eat menal or excessive exercise
  • elevated blood alcholo level
  • sulfonylureas
  • fasting, delayed or excessive secretion of insulin by pancrease, adenoma or carcinoma of pancreas, GI disorder, various hereditary or endocrine disorders
141
Q

s/s of hypoglycemia?

A
  • occurs when excessive insulin enters bloodstream or when glucose relase rate falls below tissue demands
  • may occyyr despute adequate food intake
  • sweating, nervousness, weakness, hunger, dizziness, trembling, headache, palpitations, confusion, visual distruvrances, behavior that may mistaken for drunkeness, stupor, coma and seizures,
142
Q

diagnosis and treatment of hypoglycemia?

A

diagnose - glucometer, glucose tolerance test (lower than 50 mg/dL), s/s that resolve w/ administration of glucose

treat - IV infusion of glucose, hormone glucagon, complex carb and protein snack is given, if tumor then surgery, diet is modified to correct herreditary fructose intoleramce or gastrointestinal condition

Pathophysiology - Diseases (22 decks)

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