Test (note, sections that overlap with FA were not really put in here) Flashcards

1
Q

Why is it important to ask about ACOG integrated health medicine as a healthcare provider?

A

Because nearly 72% of patients time dont report IHM use to health care providers.

Supplements in Metabolic Disease

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2
Q

What is the purpose of the dietary supplement and health education act (DSHEA) of 1994?

A
  1. To regulate vitamins, herbs, amino acids, and others like food rather than medication.
  2. The supplements need no FDA approval
  3. FDA will only take action if product is unsafe
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3
Q

How do you tell if a supplement is higher quality?

A

It has a seal of approval from one of various companies:

Good manufacture practices (GMP)

Consumer labs (CL)

United States pharmacopeia (USP)

National sanitation foundation (NSF)

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4
Q

Which integrative health product is used frequently for primary and secondary Dyslipidemia treatment?

A

Fish oil/omega 3 FA

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5
Q

True or false:

Fish oil is effective in lowering total cholesterol levels and LDLC.

A

False:

Fish oil lowers triglyceride levels and by decreasing VLDL and apoB production

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6
Q

What is the major side effect of taking fish oil?

A

Increased risk of bleeding in combination with prescription or over the counter drugs or supplements.

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7
Q

What are two important weight loss treatment options in integrative health? Which supplement is FDA approved?

A

Ephedra and Alli.

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8
Q

Why is ephedra important to know about?

A

It once provided moderate weight loss benefits, but since the FDA has received many serious or fatal case reports, the product has been band from market.

The risk outweighs the potential benefit.

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9
Q

For whom is the weight loss drug ALLI aproved? What are the major side effects associated with this drug?

A

Patients with a BMI of 27 or more.

SE: risk of liver injury, fat soluble vitamin deficiency, and diarrhea.

Take multivitamins every day 2 hours before or after dose to prevent vitamin deficiency.

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10
Q

If the patient is taking garlic to treat hypertension, what is important for them to know before they undergo surgery?

A

They should discontinue use 2 to 3 weeks prior to surgery.

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11
Q

What are the three divisions of the anterior pituitary gland? What does each division do?

A
  1. Pars distalis: hormone screening cells
  2. Pars Intermedia: poorly developed in humans (secrete MSH)
  3. Pars tuberalis: involved in the hypothalamic portal system

Bendiak lecture

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12
Q

What does stomodeum mean?

A

Mouth opening

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13
Q

Describe the development of the adrenal gland. What primordial sturctures make the adrenal gland?

A

Mesothelium near the Urogenital ridge (cortex-mesoderm) + Sympathogonia (medulla-ectoderm)

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14
Q

What do sympathogonia develop into?

A

Chromafin cells in the medulla, which produce catecholamines.

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15
Q

What is the embryologic origin of calcitonin cells in the thyroid gland?

A

Neural crest cells that populate the ultimobranchial body. They get picked up by the thyroid gland as it descends.

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16
Q

What is the embryologic origin of thyroid follicular cells?

A

Endoderm

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17
Q

The parathyroid gland arises between wich pharyngeal pouches?

A

3rd and 4th. Much like calcitonin cells, the parathyroid gland gets picked up as the thyroid descends.

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18
Q

What are the three types of cells in the parathyroid gland? What do they do?

A
  1. Chief cells (aka PTH releasing cells)
  2. Oxyphil cells (fxn unknown)
  3. Adipose cells
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19
Q

Identifying Glands on Histology:
What do you look for to ID the Pituitary, Thyroid, Adrenal and Parathyroid glands?

A
  • Pituitary
    • Ant: acidophils/basophils, sinusoidal capillaries
    • Posterior: whispy neurons. light color.
  • Thyroid
    • Follicles with colloid
  • Adrenal
    • Capsle
  • Parathyroid
    • lots of dark circular round chief cells.
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20
Q

Look at the quiz questions from Bendiak’s lecture for histology pics.

A
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21
Q

Name the target for each of the following classes of hormones: Epi/NE

Hypothalamic Hormones

GH/PLH

Insulin

Steroids

A
  • Epi/NE
    • G proteins
  • Hypothalamic Hormones
    • G proteins
    • Somatostatin and PIF are Gi
  • GH/PLH
    • JAK/STAT (think of GH and JAK and the beanstalk)
  • Insulin
    • Tyrosine Kinase (think of the tyre-swing in insulin video)
  • Steroids
    • Transcriptional/intracellular receptors
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22
Q

True or false: A hormones that end in the letters -ine are tyrosine derivatives.

A

True

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23
Q

Which hormone increases levels of prolactin? Decreases?

A

Inc: TRH

Dec: Dopamine or PIH

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24
Q

Rapid Review from Pituitary Dysfunction Lecture:

What are the conditions associated with excess and deficiency of each of the following?

GH

Prolactin

FSH/LH

ACTH

TSH

ADH

A
  • GH:
    • Excess: Acromegaly/gigantism
    • Def: Dwarfism
  • Prolactin:
    • Excess: Hypogonadism
    • Def: No lactation
  • FSH/LH
    • Excess: rarely significant
    • Def: hypogonadism (same as Prolactin… why? Pro inhibits FSH/LH)
  • ACTH
    • Excess: Cushing (crushing amounts of cortisol)
    • Def: Adrenal insuf (addisons)
  • TSH= Hypo/hyperthyroid
  • ADH
    • Excess: SIADH
    • Def: DI
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25
Q

What is the order of hormones lost in the pituitary due to trauma?

A

Good Looking Foxes All Talk Pretty

GH=LH/FSH

ACTH/TSH

PRL

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26
Q

Which type of pituitary tumor DOES NOT primarily affect middle age adults?

A

CRANIALPHARYNGIOMA

It affects peds as well.

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27
Q

Which pituitary tumor is the most common?

A

Pituitary adenoma 85% (mostly prolactinomas if secretory)

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28
Q

How do you treat a prolactin secreting pituitary tumor?

A
DOPAMINE AGONISTS (bromocriptine,
cabergoline)!!!

Not surgery

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29
Q

What are some of the risks associated with pituitary tumor resection?

A
  • Diabetes Insipidus
  • CSF leak
  • Optic Nerve Injury
  • Injury to normal pituitary gland
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30
Q

Which drugs may be used to treat GH deficiency? Excess?

A

Def: Somatropin (GH), Mecasermin (IGF 1)

Excess: Octrotide (somatostatin) or Cabergoline and Bromocriptine (burgler with a broom)*

Or block the receptor with pegvisomant

*D2 receptors inhibit release of GH

31
Q

How do you treat hyperprolactinemia?

A

Remember the Booby Burgler with a Broom

Cabergoline, Bromocriptine

32
Q

How do you treat Central DI? What about nephrogenic DI?

A

DDAVP or Chlorpopamide

Nephrogenic: Indomethacin and hydrochlorothiazide.

33
Q

Which receptor is responsible for ADH activity? Which drugs block this? What other drug treats SIADH?

A

ADH-V2

Tolvaptan and Conivaptan (VAPTANS)

Demeclocycline

34
Q

Name 2 drugs that cause DI.

2 that cause SIADH.

A

DI: Lithium and Demeclocycline

SIADH: SSRI, TCAD, Haloperidol (think antidepressants)

35
Q

The rate limiting step in synthesis of steroids in the adrenal gland requires which enzyme?

A

P-450 enzymes or 20, 22 desmolase

36
Q

Know your hydroxylase deficiency mneumonic.

A

21

17

11

For each 1, treat it as an up arrow. The first number is Aldosterone (mineral corticoids), the second is Testosterone.

37
Q

Which adrenergic receptor decreases the amount of cAMP in the cell?

A

A2. Think of A2 as the inhibitory receptor (Gi)

For kicks, what is A1?

Gq (IP3/DAG)

38
Q

Which corticosteroid is highly antiinflammatory but has little to no salt retaining potency?

A

Dexamethasone

39
Q

Which corticosteroid has high anti-inf and mineralcorticoid effects?

A

Floudrocortisone

40
Q

Why is predinsone prescribed for GI inflamation more than cortisone?

A

Cortisone has a lower AI potencey and a higher Salt retention.

Prednisone (inactive prednisolone) is 4 : 0.3

41
Q

When i say treat addisons you say…

A

With floudrocortisone

42
Q

When i say treat Pheo you say…

A
  1. Phenocylbenzamine (Alpha 1+2 agonist) THEN
  2. B-blocker THEN
  3. Surgery
43
Q

What happens if you switch steps in pre-operative treatment of Pheos?

A

B before Alpha will produce a hypertensive crisis.

44
Q

What would each of the following imaging studies be best at detecting: Ultrasound, PET/CT, Iodine Scan

A

US: Nodules

PET/CT: METs from cancer

Iodine: Hot/Cold spots for Hyper/hypothyroidism

45
Q

What are the two major causes(subtypes) of congenital hypothyroidsm?

A
  1. Dysgenesis of gland (85%)
  2. Dyshormonogenesis (15%)
46
Q

Which genes are predominately involved in Dysgenesis of the thyroid gland?

A

PAX 8 and TITF 1 and 2

TITF= Thyroid transcription factors

47
Q

A patient has both a hypothyrodism goiter and congenital deafness. What is his syndrome called?

A

Pendrad Syndrome.

THis is a dyshormonogenesis disorder.

48
Q

Why is thyroid hormone tested 2-5 days after a baby is born and not immediately?

A

TSH levels are high during the rist few days of life.

49
Q

Thyroid studies of your pt reveal Low T3 uptake and Low T4. Whats the problem?

A

Hypothyroid

50
Q

Thyroid studies of your patient show high T3 uptake and Low T4. Whats the problem?

A

Thyroid binding globulin deficient.

51
Q

Describe the presentation of congenital hypothyroidism.

A

A baby comes in with prolonged jaundice, large tounge, hoars cry, hypotonia and umbilical hernia.

52
Q

Name 3 inhibitors of thyroid hormone synthesis

A

SCN-, CLO4- and I-

53
Q
  1. Relative to T4, T3:
  2. Has Greater oral bioavailability (95% vs 65%)
  3. Has a longer duration of action
  4. Has a greater affinity for thyroid hormone receptors
  5. Is considered a prohormone for T4
  6. Is req for most patients w hypothyroidsim
  7. Has a greater CV side effect profile
  8. IS more expensive
A

Has Greater oral bioavailability (95% vs 65%)

Has a longer duration of action

Has a greater affinity for thyroid hormone receptors

Is considered a prohormone for T4

Is req for most patients w hypothyroidsim

Has a greater CV side effect profile

IS more expensive

54
Q

What is Thyroid USP?

A

Its dessicated porcrine thyroid extract. Variable T3:T4

55
Q

Which drugs will inhibit the 5’-deiodinase which activates T4–> T3?

A

Glucocorticoids

PTU (used in hyperthyroidism)

B-blockers

56
Q

A 72-year-old woman with a long-standing history of hyperthyroidism and diabetes mellitus is brought to the emergency department comatose with a high fever, flushing, sweating, marked tachycardia, and atrial fibrillation. Her husband notes that she ran out of insulin 3 days ago and has not had a chance to refill her prescription.

In addition to insulin and supportive therapy, how would you treat her?

A

Beta Blocker

IV NaI

PTU

Hydrocortisone to protect against shock

* note thes are all the same things that inhibit T3/T4

57
Q

A 16 year old girl was brought to her pediatrician because of the absence of menarche. She has short stature, webbed neck , and Square chest. Physical examination reveals a breast buds, and female external genetalia. She also has a horseshoe kidney. Is this patient able to recieve GH treatment/

A

YES! This is Turner syndrome. Prader willi also is indicated.

58
Q

Teagan is a 2 year old boy. His dad is 67 inches tall and his mom is 62 inches tall. What is his midparental target height?

A

62+5+67/2

67 inches

59
Q

What is familial short stature?

A

Children who have normal growth velocity and height that are within normal limits for parents’ heights.

60
Q

When does constitutional growth delay manifest?

A

Growth falling off 3-6 months then normal growth velocity. Delayed puberty.

Skeltal growth delay. Late bloomer. Bone age younger than actual age.

61
Q

What tests is/are used for detecting Growth Hormone Def?

A

IGF1 or IGFBP-3 (in little people)

GH Stimulation test less than 10 (clonididne, arginine, glucagon, L-dopa)

62
Q

Which Ca supplement is better absorbed when taken with food?

CaCO3 or CaCitrate?

A

CaCO3.

CaCitrate can be taken without food.

63
Q

James D., a 53 year old man, is brought to the emergency room because of a 3 day history of nausea, vomiting and confusion. His wife states that he had been complaining of frequent urination and increased thirst since. He has lost 20 lb. during this time and has coughed up blood on several occasions. He is a smoker of 1-2 packs of cigarettes a day for the past 30 years. His physical examination reveals localized wheezing in the right upper lung field and an enlarged right supraclavicular lymph node. You request the following tests:

Serum calcium = 16.2 mg/dl (nl = 8.5 - 10.5)

Serum phosphorus = 3.4 mg/dl (nl = 2.5 - 4.5)

Serum chloride = 98 mmol/L (nl = 101 - 111)

Serum albumin = 3.2 g/dl (nl = 3.2 - 5.5)

Serum intact PTH = 2 pg/ml (nl = 11 - 54)

What is the most likely cause of his hypercalcimea?

A

Tumor secreting PTH-RP

64
Q

What is the difference between breast and lung cancer with reguards to PTH-RP?

A

Breast: Secretes PTH-RP locally and doesnt show hypercalcemia unless it has bone METs.

Lung: Secretes PTH-RP into blood.

65
Q

A patient has Low Urine Ca/Creatinine Clearance ratio, but elevated Ca in serum. Whats going on?

A

Fam Hypocalciuric Hypercalcemia

Think of this as Calcium resistance.

66
Q

A pt has elevated PTH levels, low Ca, and short 4th + 5th digits. Whats going on?

A

Pseudohypoparathyroidism

67
Q

How does treatment differ for hyperparathyroidism in the cases of adenoma vs hyperplasia?

A
  • Adenoma- remove tumor
  • Hyperplasia- remove 3.5 parathyroid glands.
    • Calcimeimetic Drug (cincalcet)
    • Antiresorptive bone drugs (bisphosphate or Denosumab)
68
Q

List five causes of hypocalcemia

A
  1. Vit D Def
  2. Hypopara
  3. Renal Failure
  4. Liver Failure
  5. Hypoproteinurea
    • low albumin (Ca carrier)
69
Q

Describe the clinical features of hypoparathyroidism.

A
  1. Paresthesias
  2. Muscle Cramps
  3. Muscle Weakness
  4. Chvostek’s Sign
    • Cheek tap elicits twitch
  5. Trousseau’s Sign
    • BP cuff leads to carpal spasm
70
Q

How is osteoporosis defined?

A

Score less than -2.5 or fractures (abnormal)

71
Q

What ligand activates osteoclast activity? Suppresses?

A

RANKL activates

Osteoprotegerin (RANKL decoy)

72
Q

What is the only drug that stimulates bone formation?

A

Teiparatide with intermittent administration.

(PTH analog)

73
Q

What is the suffix of the first line therapy for osteoporsis?

A

-dronate (bisphosphates)