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SUM '20 - Pharm II > Week 4 - Endocrine Drugs > Flashcards

Week 4 - Endocrine Drugs Flashcards

1
Q

Primary tx for hypothyroidism is

A

hormone replacement

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2
Q

In primary hypothyroidism what is used to monitor tx

A

TSH concentration

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3
Q

in hypothyroidism, Free T4 is what type of indicator??

what do we expect it to be normal or abnormal?

A

normal range when TSH is inhibited

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4
Q

Measurement of free T4 is warranted in

A

secondary hypothyroidism when TSH release is impaired

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5
Q

TSH release is impaired in

A

secondary hypothyroidism

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6
Q

T4 is the prohormone to?

A

T3

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7
Q

Goal of therapy for hypothyroidism: (4)

A
  • Correction of hypothyroidism to euthyroid
  • Reduction of symptoms
  • Reduction in goiter size
  • Prevention of cancer recurrence
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8
Q

when you see goiters, what are some of our concerns?

A
  • difficult airway
  • pressure on airway
  • tracheal displacement/deviation
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9
Q

In PRIMARY hypothyroidism what do we see/find?

A
  • Increase [plasma] of TSH
  • Primary defect is OF thyroid
  • Ant. Pituitary attempts to stimulate hormonal output by releasing TSH (hence the elevated TSH level)
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10
Q

In SECONDARY hypothyroidism what do we see/find?

A

Defect is at:

  • hypothalamus OR the
  • Ant. Pituitary

–> Low concentrations of both TSH and thyroid hormones circulating in plasma

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11
Q

Tx of choice for primary hypothyroidism:

A

T4: Levothyroxine (synthetic)

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12
Q

T4 half life is

A

7-10days

**allows for missing a dose for several days w/o adverse consequences.

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13
Q

IV(parenteral) T4 can be administered at what percent of patients oral dose?

A

80%

example: take 100mcg/day == 80mcg/day IV

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14
Q

An isomer of T3; supplemental T3 is:

A

Liothyronine

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15
Q

Liothyronine is ___ to ___ times as potent as levothyroxine.

A
  1. 5 to 3 times as potent

- rapid onset; short DOA

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16
Q

Is T3/Liothyronine used for long term replacement?

A

no - b/c of short doa and rapid onset

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17
Q

How do we tx HYPERthyroidism?

A
  • Anti-thyroid meds
  • radioiodine
  • and/or surgery
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18
Q

***TSH levels useful for determining diagnosis of hyperthyroidism but not for

A

degree of severity

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19
Q

Measuring free T3 and T4 is necessary to assess

in hyperthyroidism

A

the efficacy of treatment

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20
Q

Once steady state achieved, what level can be used to assess the efficacy of therapy

A

TSH

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21
Q

Compounds that interfere with synthesis of thyroid hormones or reduce amount of thyroid tissue:

A
  • Thionamides
  • Inhibitors of iodide transport mechanism
  • Iodide
  • Radioactive iodine

‘TIIR

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22
Q

examples of Thionamides:

A

Methinmazole
Propylthiouracil
Carbimazole

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23
Q

(MOA) Thionamides: exert immunosuppressive effect via a reduction in concentrations of

A

anti-thyrotropin-receptor antibodies

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24
Q

In addition to blocking hormone synthesis, Propylthiouracil also inhibits

A

the peripheral deiodination (removal of iodine) of T4 and T3.

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25
Q

anti-thyroid drugs are useful in tx before

A

elective surgery

**don’t want to have a T.Storm during surgery

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26
Q

thionamides levels peak:

A

1-2 hrs after ingestion

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27
Q

are thionamides available in parenteral form?

A

no

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28
Q

Methimazole half life is:

A

4-6 hrs and dosed every day

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29
Q

Half life of propylthiouracil is:

A

75 mins!!!

dosed several times a day

*poor compliance

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30
Q

Minor side effects of thionamide therapy are observed in ~ 5% of pts:

A
  • Urticarial
  • Macular skin rash
  • Arthralgias
  • GI discomfort
  • **Granulocytopenia and agranulocytosis are serious but rare; most likely to occur in first 3 months of anti-thyroid drug therapy
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31
Q

**Granulocytopenia and agranulocytosis are serious but rare. if to occur, when would they?

A

most likely to occur in first 3 months of anti-thyroid drug therapy

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32
Q

** what may be the earliest sign of development of agranulocytosis?

A

Pharyngitis or fever may be

Recovery is likely if the anti-thyroid drug is d/c’ed at the first signs.

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33
Q

propylthiouracil has reported toxicity of what?

A

hepatic

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34
Q

**which anti-thyroid crosses the placenta AND appears in breast milk?

A

methimazole

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35
Q

**Which anti-thyroid has limited placental crossing and is the preferred drug for use in pregnancy?

A

Propylthiouracil

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36
Q

the oldest available therapy for hyperthyroidism is:

A

iodide

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37
Q

*** Most important clinical effect of high doses of iodide is:

A

is inhibition of release of thyroid hormone.

….May reflect ability of iodide to antagonize the ability of TSH and cyclic adenosine monophosphate to stimulate hormone release

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38
Q

Iodide useful in tx before elective

A

thyroidectomy.

Combination of oral potassium iodide and propranolol is a recommended approach.

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39
Q

Combination of oral potassium iodide and propranolol is a recommended approach for :

A

tx before elective thyroidectomy.

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40
Q

Allergic reactions to iodide:

A
  • angioedema and
  • laryngeal edema:
  • life threatening.
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41
Q

therapy of choice for Grave’s hyperthyroidism

A

Radioiodine

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42
Q

** Radioactive iodide is administered after ….

A

euthyroidism is achieved via thionamides

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43
Q

____ (form of radioactive iodide) is most administered and is rapidly and efficiently trapped by thyroid gland cells and the subsequent emission of destructive Beta rays act almost exclusively on these cells with little of no surround damage

A

131-I

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44
Q

131-I can destroy thyroid gland in how many weeks?

A

6-18 weeks

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45
Q

***Iatrogenic hypothyroidism must be considered preop in any pt who has

A

previously been treated with 131-I

– b/c 10% of tx pts become hypothyroid in first yr after 131-I tx and risk increases 2-3% annually thereafter.

46
Q

1/2 to 2/3 pts are cured by how many doses of 131-I?

A

a single dose

  • remainder require 1-2 more doses
47
Q

contraindication of 131-I?

A

pregnancy (fetal thyroid will concentrate the isotope)

48
Q

Except for this cancer, most cancers accumulate little radioactivity thus 131-I is not an effective tx for ca

A

follicular cancer

49
Q

analogue of cortisol:

A

prednisolone

50
Q

mg prednisolone anti-inflammatory effect is equivalent to how many mg of cortisol?

A

5mg Prednisolone = 20 mg Cortisol

51
Q

Suitable for sole replacement of therapy in adrenocortical insufficiency b/c of the presence of glucocorticoid and mineralocorticoid effects

A

PrednisoLone

Flood pg 763-prednisone and prednisolone *

52
Q

analogue of cortisone:

A

Prednisone

53
Q

Prednisone is converted to

A

PrednisoLone after absorption in GIT

similar to prednisolone in anti-inflammatory effects

54
Q

Methyl derivative of prednisolone:

A

Methylprednisolone

55
Q

How many mg of Methylprednisolone = 20 mg of cortisol?

A

4 mg is equivalent to 20 mg of cortisol.

56
Q

Used IV for glucocorticoid effect

A

Methylprednisolone

57
Q

Fluorinated derivative of prednisolone.

A

Betamethasone:

58
Q

how many mg of Betamethasone = 20 mg of cortisol?

A

0.75mg is equivalent to 20 mg of cortisol. PO and IV available.

59
Q

Betamethason has No mineralocorticoid properties and cannot be a replacement for…

A

adrenocortical insufficiency

60
Q

Fluorinated derivative of prednisolone and isomer of betamethasone:

A

Dexamethasone:

61
Q

how many mg of Dexamethasone = 20 mg of cortisol?

A

0.75 mg is equivalent to 20 mg of cortisol.

62
Q

dexamethasone Can be used to treat certain types of

A

cerebral edema

63
Q

Triamcinolone:

A

fluorinated derivative of prednisolone:

64
Q

how many mg of Triamcinolone is = to 20 mg of cortisol?

A

4 mg is equivalent to 20 mg of cortisol.

65
Q

what drug is used often in epidural injection for tx of lumbar disc disease ?

why?

A

Triamcinolone

The hexacetonide preparation injected intra-articularly may provide therapeutic effects 3 months or longer

66
Q

**SE of Triamcinolone:

A
  • mild dieresis w/ Na loss
  • Edema (in decreased GFR)
  • *skeletal muscle weakness
  • *anorexia (vs appetite stimulation)
  • sedation (vs. euphoria)
67
Q

Unusual side effect of this drug is an increase incidence of skeletal muscle weakness; anorexia rather than appetite stimulation and sedation rather euphoria.

A

Triamcinolone

68
Q

Side Effects of Chronic Corticosteroid Therapy:

A
  • Suppression of HPA axis
  • Electrolyte and metabolic changes
  • Osteoporosis
  • PUD
  • Skeletal muscle myopathy
  • CNS dysfunctions
  • Peripheral blood changes
  • Inhibition of normal growth
69
Q

**HPA axis is responsible for

A

modulating inflammatory reactions throughout the body;

working with

  • hypothalamus,
  • pituitary gland, and
  • adrenals
70
Q

Increased susceptibility______ or

______ accompanies tx with corticosteroids

A

to bacterial or fungal infection

71
Q

corticosteroids are associated with decreasing the effectiveness of…

A

of anticoagulants

72
Q

Systemic use of corticosteroids for < 7 days even at high doses are unlikely to cause

A

adverse side effects.

73
Q

Inhaled corticosteroids are unlikely to evoke adverse

A

systemic effects

74
Q

Forms/causes of Parathyroid dependent or non-parathyroid dependent
Parathyroid: (3)

A
  1. Primary and Tertiary hyperparathyroidism
  2. Familial hypocalciuric hypercalcemia
  3. Lithium induced hypercalcemia
75
Q

Lithium may induce

A

hypercalcemia —> parathyroid

76
Q

Hypercalcemia of malignancy is usually associated with destructive bone lesions or

A

secretion of a PTH-like tumor peptide

77
Q

Hypercalcemia from parathyroid disease is associated with (

A

bone loss and osteoporosis

78
Q

management of hypercalcemia (parathyroid)

A 
Management:
IVF
Bisphosphonates
Calcitonin
Glucocorticoids
79
Q

Bisphosphonates:

Pyrophosphate analogues that lower calcium levels by inhibiting osteoclastic medicated bone

A

reabsorption

80
Q

Bisphosphonates Treat hypercalcemia in:

A
  • malignancy,
  • primary hyperparathyroidism,
  • vitamin A intoxication,
  • granulomatous disease, and
  • Paget’s disease
81
Q

***Renal injury and jaw osteonecrosis reported with

A

bisphosphonates

82
Q

***Renal injury and jaw osteonecrosis reported with bisphosphonates impacts anesthesia … how?

A

renal clearance

jaw mobility, mouth opening

83
Q

Bisphosphonates should be used early in course b/c may take …..

A

2 days to see significant results

84
Q

Glucocorticoids decrease synthesis of

A

1,25-dihydroxyvitaminD

85
Q

decreased synthesis of 1,25-dihydroxyvitaminD does what 2 things:

A
  1. ) decrease intestinal absorption of calcium and

2. )increase renal excretion of calcium

86
Q

High risk of hypocalcemia:

A 
Rhabdomyolysis
Pancreatitis
Sepsis, fat embolism
Burns, massive transfusions
Hypoalbuminema
Hypomagnesemia
Renal insufficiency
87
Q

if calcium and magnesium are low… what else may be low?

A

K+

88
Q

Most common setting for symptomatic hypocalcemia is within

A

12-24 hours after surgery,

89
Q

surgeries particularly associated with hypocalemia:

A
  • total or subtotal thyroidectomy or

- 4 gland parathyroid exploration or removal

90
Q

**Long-standing hypocalcemia with hyperphosphatemia and PTH deficiency is associated with :

A
  • calcification of the basal ganglia

- with extrapyramidal signs

91
Q

Hypocalcemia can cause:

A

Neuromuscular irritability
Arrhythmias
CHF (decreased contractility)
Hypotension

92
Q

***Acute severe hypocalcemia (with normal albumin) is a medical emergency with death from laryngeal spasm or grand mal seizures. What is the critical value?

A

Ca+ < 7.5 mg/dL

93
Q

This is indicated for acute symptomatic hypocalcemia

A

IV calcium

94
Q

10% calcium gluconate contains less elemental calcium than calcium chloride

but is less likely to cause

A

tissue necrosis during an extravasation

95
Q

1 Cause of DI

A

inadequate secretion of vasopressin by the posterior pituitary

96
Q

2

In DI- Hyper or Hypo natremia?

A

in DI - you see excessive water loss and HYPERnatremia via polyuria.

97
Q

3 Name 5 things that can cause DI

A
  1. Neurotrauma
  2. surgery of the pituitary and hypothalamus
  3. Cerebral ischemia
  4. Cerebral malignancy
  5. nephrogenic DI
98
Q

4

What is nephrogenic DI

A

results from an inability of the renal tubules to respond to adequate amts of centrally produced AVP does not respond to exogenous admin of the hormone either.

99
Q

5

What role does Vasopressin have in evaluating DI

A
  • Evaluation; administration results in a brief effect b/c of rapid enzymatic breakdown of peptides in teh tissues, especially the kidneys.
100
Q

6 What is the role of DDAVP in DI

A

administration of synthetic selective V2-R agonist, DDAVP (desmopressin), treats central DI.

DDAVP has an intense antidiuretic effect (V2) and decreased vasopressor (V1) effect.

101
Q

7

Elimination ½ life of DDAVP and side effects of DDAVP

A

1/2 time = 2.5-4.4 hours

SE (less than vasopressin): although Nausea and increases in SBP can be seen

102
Q

8

What are the routes of DDAVP

A

PO (0.3 to 0.6 mg/day)
IV (1-4 mcg/day)
Nasally (5-40 mcg/day)

103
Q

9 Why is DDAVP the drug of choice

A

d/t inadequate production of AVP by the posterior pituitary.

104
Q

10 What can DDAVP treat? What can it not treat?

A

Not effective in the tx of nephrogenic DI

  • effective in increasing vWb factor, minimize intraoperative blood loss in cardiac surgery
  • may decrease SVR leading to hypotension
105
Q

11 How does DDAVP and Von Willebrand relate

A

DDAVP causes endothelial cells to release von Willebrand factor, tissue-type plasminogen activator , and prostaglandins

106
Q

12 When does DDAVP not decrease bleeding

A

-does not decrease bleeding following cardiopulm bypass in pts who were maintained on aspirin therapy until day of surgery.

107
Q

13 Explain briefly ACE-I and perioperative hypotension

A

inhibits the renin-angiotensin system and can cause refractory hypotension after administration of anesthesia.

  • in these cases, catecholamine admin may be unsuccessful
  • vasopressin may be effective to tx hypotension from anaphylaxis and severe catecholamine deficiency after resection of a pheochromocytoma
108
Q

14 Describe Vasopressin’s role in the Refractory Cardiac Arrest

A

40U IV - was similar to epi 1 mg IV for mgmt of Vfib and PEA.

  • Vasopressin was more effective than epi for mgmt of asystole and tx of refractory cardiac arrest
  • AHA recs a single dose of 40Units considered instead of epi q 3-5mins for pts being tx for cardiac arrest.
  • vasopressin functions as a vasoconstrictor when it is administered in supraphysiologic doses which serve to displace peripheral blood vol to the central circulation w/o some of the AE’s produced by epi
109
Q

15 Describe Vasopressin’s role in esophageal varices

A

Vasopressin may serve as an adjunct in the control of bleeding E. Varices and during abd surgery in pts w/cirrhosis and portal HTN.

  • infusion of 20U over 5” results in marked decreases in hepatic BF lasting about 30mins.
  • only a moderate increase in systemic BP occurs. This effect on the portal circulation is attributable to marked splanchnic vasoconstriction. An alternative to systemic administration is the infusion of vasopressin directly into the superior mesenteric artery.

it has not been established whether selective arterial administration is after than systemic administration w/respect to cardiac and vascular side effects

110
Q

16 List 7 side effects of Vasopressin that the CRNA needs to be aware of

A
  1. vasoconstriction
  2. increased SBP
  3. increased Pulmonary artery pressures
  4. vasoconstriction of Coronary arteries/ decrease in coronary BF ==> angina
  5. stimulate gi smooth muscle
  6. Decrease in PLT count
  7. Allergic rxns from urticaria to prophylaxis
  8. prolonged use may result in antibody formation and a shortened DOA.

SUM '20 - Pharm II (30 decks)

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