Pharmacology Unit 4 - Endocrine Pt. 2 Flashcards
(150 cards)
1
Q
more than ____________ of glucocorticoid therapy can cause adrenal suppression
A
2 weeks
2
Q
stress dose steroids with minor stress give _______x the dose for ____________ hours
A
2; 23-48
3
Q
stress dose steroids with severe stress (accidental trauma, major surgery), give up to ________x the normal dose for _____________ hours
A
10; 48-72
4
Q
if a patient receives stress dose steroids, it takes ____________ months for HPA function to return to normal and an additional ____________ months for cortisol levels to return to normal
A
2-12; 6-9
5
Q
corticosteroids increase pepsin and gastrin which puts patients at risk for _______________
A
peptic ulcers
6
Q
how do you treat chronic adrenocortical insufficiency (addisons disease)
A
hydrocortisone and fludrocortisone
7
Q
how do you treat acute adrenocortical insufficiency (addisons)
A
- high dose glucocorticoid therapy IV (100 mg Q8h until stable)
- correct fluid and electrolytes
- taper glucocorticoid (hydrocortisone) therapy and initiate mineralcorticoid (fludrocortisone) when stable
8
Q
describe the synthesis of thyroid hormone
A
- symporter pulls iodide from the gut and diet into thyroid gland
- in the follicular cell iodide is converted to iodine via thyroidal peroxidase (organification)
- thyroglobulin is cleaved into T3/T4
9
Q
how is iodide converted into iodine in the thyroid gland?
A
via thyroidal peroxidase (organification)
10
Q
which thyroid hormone is the most potent
A
which thyroid hormone is the most potent
T3
11
Q
T3 is ___________ x more potent/active than T4
A
2-3
12
Q
for T4 to be utilized it has to be _______________ by ______________ enzymes to T3
A
deiodinated; 5’ deiodinase (D1,D2,D3)
13
Q
what is the primary pathway for the metabolism of thyroxine (T4)
A
deiodination
14
Q
what drugs block the metabolism of T4 by blocking the three 5’deiodinase enzymes ?
A
- amiodarone
- contrast dye
- beta blockers
- corticosteroids
15
Q
_____________ and _______________ are physiologic conditions that block the three 5’ deiodinase enzymes responsible for the metabolism of T4 to t3
A
severe illness; starvation
16
Q
out of T3 and T4, which is most released from the thyroid gland
A
T4
17
Q
ratio of release T4:T3
A
5:1
18
Q
_________% of circulating T3 is d/t the metabolism of T4, and ___________% is from the direct thyroid secretion
A
80; 20
19
Q
__________ is the inactive form of thyroid hormone, and _______ is the active form
A
T4; T3
20
Q
large doses of iodine inhibit ___________________, which leads to a(n) ___________ in thyroid hormone levels
A
organification; reduction
21
Q
_______________ influences the synthesis of T3 and T4
A
iodide levels
22
Q
what conditions have a stimulatory effect on the hypothalamus to release TRH
A
- cold (hypotherm)
- acute psychosis
- circadian and pulsatile rhythm
23
Q
what inhibits the release of TRH from the hypothalamus
A
- increased T3/T4
- severe stress
24
Q
what inhibits the release of TSH from the AP
A
- somatostatin
- dopamine
- corticosteroids
- increased T3/T4
25
what stimulates the release of TSH from the AP
TRH
26
how bioavailable is T4 (thyroxine) in the body?
70-80% bioavailable
27
how bioavailable is T3 in the body?
95%
28
T4 is best absorbed where?
ileum and duodenum
29
what route is preferred for the administration of exogenous T3 and T4 ?
IV
30
____________ function is impacted by multiple drugs
thyroid function
31
Thyroid hormones are important for __________, _______________, _____________, and ___________________
optimal growth; development; function; all body tissue maintenance
32
_______________ hormones are integral to homeostasis
thyroid
33
exogenous T3 has implications in the tx of ________________, but not _____________
myxedema coma; thyroid storm
34
T/F: giving T4 will also supply T3
true; due to the T4 conversion to T3
35
what are the 3 types of anti-thyroid drugs?
1. thioamides
2. iodides
3. radioactive iodine
36
in the thioamide drugs, the ______________ group in their chemical structure is essential for antithyroid activity
thiocarbamide
37
what are your thioamide antithyroid agents ?
1. PTU
2. Methimazole
38
which antithyroid drug would you use in pregnant women in their first trimester?
PTU
39
when is PTU the appropriate anti-thyroid med to administer?
1. 1st trimester
2. thyroid storm
3. adverse reaction to methimazole
40
what is the black box warning for PTU
severe hepatitis
41
_____________________ is 10x more potent than PTU
methimazole
42
what is the thioamide drug of choice in children and adults?
methimazole
43
if a pregnant woman needs an anti-thyroid agent, which medication would you use in the 2nd and 3rd trimesters?
methimazole
44
absorption of PTU = _____________ bioavail
50-80%
45
absorption of methimazole
completely absorbed
46
both thioamide drugs are excreted in the ____________; however, ______________ is excreted slower
kidney; methimazole
47
half life of PTU
1.5 hours
48
half life of methimazole
6 hours
49
100 mg dose of PTU will inhibit _____________ by 60% for 7 hours; should be administered q _____-____h
organification; 6-8
50
30 mg dose of methimazole exerts ________________ effects for > 24 hours
anti-thyroid
51
thioamides MOA
1. prevents hormone synthesis by inhibiting thyroid peroxidase catalyzed reactions
2. blocks iodine organification
3. blocks the coupling of iodotyrosines
52
additional MOA of PTU from methimazole
inhibits the diodination of T4 and T3
53
Thoamide toxicity sx
1. maculopapular pruiritic rash
2. severe fatal hepatitis
3. agranulocytosis (granulocyte count < 500)
54
what is the most dangerous complication of thioamides
agranulocytosis
55
what is the most common adverse effect of thioamides
maculopapular pruritic rash
56
T/F: if patient has a severe adverse reaction to PTU you should switch them to methimazole
false; cross sensitivity is 50% btwn PTU and methimazole; therefore do not switch drugs in patients with severe reactions
57
PTU should be avoided in ______________
children
58
___________ is the only isotope used for tx of thyrotoxicosis
131 I (radioactive iodine)
59
MOA of radioactive iodine
rapidly accumulates in the thyroid and emits beta rays to destroy the thyroid parenchyma
60
T/F: radioactive iodine in the tx of hyperthyroidism is very painful
false; not painful
61
how is radioactive iodine administered?
orally
62
what is the most widely used B-Blocker for thyrotoxicosis
propranolol
63
what is the purpose of using adrenoceptor blocking agents in the tx of hyperthyroidic states?
tx the hypermetabolic sx (HR, BP, etc)
64
what is the most common cause of hypothyroidism in the US
hashimotos thyroiditis
65
pathogenesis of hashimotos thyroiditis
autoimmune destruction of thyroid
66
with hashimotos thyroiditis, the goiter is ____________ early and ________ later
present; absent
67
degree of hypothyroidism with hashimotos thyroiditis
mild to severe
68
which hypothyroidism causes will have the presence of a goiter?
1. early hashimotos
2. drug induced hypothyroidism
3. dyshormogogenesis
4. congenital (cretinism)
69
which causes of hypothyroidism will a goiter not be present?
1. late hashimotos
2. radiation
3. congential (cretinism)
4. secondary (TSH deficit)
70
s/sx of hypothyroidism
1. pale cool skin
2. periorbital edema, drooping eyelids
3. decreased HR
4. lethargy
5. decreased BMR
6. Stiffness and muscle fatigue, decreased DTR
71
s/sx of hyperthyroidism
1. warm, moist skin
2. periorbital edema
3. increased HR
4. dyspnea
5. increased appetite w/ wt loss
6. nervousness
7. increased BMR
72
what is the pharmacologic tx for hypothyroidism
levothyroxine
73
what foods should be avoided with levothyroxine d/t it impairing absorption
grapefruit
74
s/sx of thyroxine toxicity in children (2ndary to levothyroxine tx or hyperthyroidism)
1. restless
2. insomnia
3. accelerated bone maturation and growth
75
s/sx of thyroxine toxicity in adults (2ndary to levothyroxine tx or hyperthyroidism)
1. nervousness
2. heat intolerance
3. episodes of palpitations and tachycardia
4. unexplained weight loss
76
the _______________ is very sensitive to circulating levels of thyroxine and can lead to __________, __________
heart; a.fib; dysrhythmias
77
if a patient on levothyroxine develops dysrhythmias or angina, how should you proceed?
stope or reduce levothyroxine immediately
78
T/F: in myxedema coma, the low levels of circulating thyroid hormone is cardio protective against increased demands that could lead to angina or MI
true
79
________________ is a medical emergency and is d/t untreated hypothyroidism
myxedema coma
80
tx of myxedema coma
1. loading dose of levothyroxine (300-400 mcg IV)
2. followed by 50-100 mcg daily
3. IV T3 can also be added
81
what is the most common cause of hyperthyroidism
graves disease
82
what is the tx of choice for graves disease
thyroidectomy
83
what is the pathogenesis of graves dz?
lymphocytes secrete TSI which stimulates the TSH receptor with longer duration of stimulation, causing thyroid hormone excess
84
which Dz would present with a + TSI on labs?
graves disease
85
what is the tx of choice for Graves Dz in those over 21 years of age
radioactive iodine 131
86
Tx for graves disease
1. antithyroid drug therapy (methimazole, PTU)
2. thyroidectomy (1st line)
3. radioactive iodine
4. adjunct therapy: propranolol or metoprolol
87
the pancreas consists of approximately _________________ islets of langerhan
1 million
88
within the islets of langerhan, there are at least _____________ hormone producing cells are present
5
89
what cells secrete insulin in the pancreas
beta
90
what are the pancreatic hormones?
1. insulin
2. islet amyloid polypeptide
3. glucagon
4. somatostatin
5. pancreatic peptide
6. Ghrelin
91
what pancreatic hormone is the storage and anabolic hormone of the body
insulin
92
what is the pancreatic hormone that is the hyperglycemic factor that moblizes glycogen stores
glucagon
93
which pancreatic hormone is the universal inhibitor of secretory cells
somatostatin
94
which pancreatic hormone is a small protein that facilitates digestive processes
pancreatic peptide
95
what is the pancreatic hormone which increases GH release
Ghrelin
96
which pancreatic hormone modulates appetite, gatric empyting, glucagon, and insulin secretion
islet amyloid polypeptide (IAPP, amylin)
97
how do you confirm a dx of DM?
plasma glucose level > 126 more than once after at least 8 hours of fasting
98
what is the first line tx for DM II?
diet
99
which type of diabetes is usually seen with obesity
T2DM
100
insulin dependent diabetes that is d/t selective beta cell destruction and severe or absolute insulin deficiency
T1DM
101
insulin dependent diabetes that is d/t selective beta cell destruction and severe or absolute insulin deficiency
T1DM
102
which type of DM is immune or idiopathic
T1DM
103
which type of DM is is due to pancreatectomy, pancreatitis, nonpancreatic dz, corticosteroid therapy?
T3DM
104
which type of DM is d/t placental hormones/placenta creating an insulin resistance
T4DM
105
when does T4DM (gestational DM) typically occur
3rd trimester
106
which DM type is d/t tissue resistance to insulin action, combined with relative deficiency in insulin secretion
T2DM
107
the release of insulin requires the utilization of ____________
ATP
108
insulin in the cell --> increases _____________ use --> decrease in _________ efflux --> depolarization --> _______ influx --> opens the gate for insulin to be released via exocytosis
ATP; K; Ca
109
insulin is released from the pancreatic ____________ cells at a _____________ rate
beta; low basal
110
what causes increase in insulin release
1. increased glucose
2. B-SNS activity
3. high concentration of fatty acids
4. certain hormones (glucocorticoids, growth hormone)
5. glucagon increase
6. cholecystokinin
111
what are the causes of a decrease in insulin release?
1. increased insulin
2. leptin
3. amalyn
4. somatostatin
5. alpha-SNS activity
6. Chronic increase in glucose
7. low concentration of fatty acids
112
insulin promotes the storage of __________ & ______________
fat; glucose
113
glucocorticoids _____________ the affinity of the insulin receptor for insulin
decrease
114
which tissues have the highest expression of insulin receptors ?
1. skM
2. fat
3. liver
*those that are most sensitive to glucose
115
insulin is primarily metabolized in the __________, but 35-40% excreted in the ______________
liver; kidney
116
what are the 4 principal types of insulin preparations
1. rapid acting
2. short acting
3. intermediate acting
4. long-acting
117
with the administration of insulin, you are aiming for a serum glucose level of ________________
80 mg/dL
118
which type of insulin preparation permits more physiologic prandial insulin replacement
rapid acting
119
_____________ insulin has a fast onset and short duration of <4-5 hours
rapid-acting
120
short acting insulin onset: __________, peaks at ____________; and DOA: ___________
30 min; 2-3 hours; 5-8 hours
121
intermediate acting insulin has an onset of ____________; and a DOA of ____________
2-5 h; 4-12 h
122
long acting insulin has an onset of ___________; and a DOA of ____________
1-2 h; 11-24 h
123
________________ is a long acting insulin with a smooth background insulin level with BID dosing
detemir
124
duration of action of insulin detemir
12 hrs
125
for surgery, we only tx if BG is > ____________
200
126
what complication of DM typically occurs with T1DM?
DKA
127
which complication of DM typically occurs with T2DM
HHS
128
what is the starting dose tx of insulin for DKA
regular insulin @ 0.1 IU/kg/h IV
129
this complication of DM has profound hyperglycemia and dehydration and seen especially in the elderly
HHS
130
what is the tx for HHS
low dose insulin therapy with fluid resuscitation
131
__________________ insulin is a fast-acting preparation and is preferred in tx the abrupt onset of hyperglycemia or the appearance of DKA
regular
132
what is the dose of insulin that should be given to tx metabolic derangements of blood glucose
1-5 U IV or 0.5-2 U/h IV infusion
133
what is the most popular route of administration for insulin
SubQ
134
regular insulin can be administered ______ or ________
IV or SQ
135
what is the most common complication of insulin therapy
hypoglycemia
136
sulfonylureas bind to a sulfonylurea receptor and stimulate _____________________
insulin secretion
137
MOA of sulfonylureas
1. binds to sulfonylurea receptor --> inhibits efflux of K
2. depolarization of the cell
3. voltage gate Ca channel opens --> Ca influx
4. insulin released
138
what are your first generation sulfonylureas
"-amide"
1. Tobutamide
2. chlorpropamide
3. tolazamide
139
which oral anti-diabetic agent is the safest for elderly diabetics
tobutamide
140
what are your 2nd generation sulfonylureas
"-ide"
1. glyburide
2. glimepiride
3. glipizide
141
1st and 2nd generation sulfonylurea's are metabolized where?
liver
142
which generation of sulfonylureas are prescribed more frequently due to the decrease in adverse effects and drug interactions
2nd generation ("-ide")
143
biggest risk 2ndary to taking sulfonylureas
hypoglycemia
144
what drug is a sulfonylurea, but has no sulfur and is referred to as a meglitinide analog?
repaglinidine
145
repaglinidine is hepatically cleared via ______________
CYP3A4
146
meglitinide analogs, like repaglinidine must be taken when?
just before eating
147
an antidiabetic agent like a meglitinide analog, such as repaglinidine may be considered for those with a ____________ allergy
sulfur
148
sulfonylurea drug that is a D-phenylalanine derivative
nateglinide
149
which sulfonylurea drugs are okay for elderly with renal issues
1. repaglinidine
2. nateglinide
150
nateglinide is a sulfonylurea that is a D-phenylalanine derivative, it is hepatically cleared via ___________ & ____________
CYP2C9 ; CYP3A4
