Diabetes Flashcards
(394 cards)
1
Q
What decreases blood glucose
A
Insulin
2
Q
What increases blood glucose
A
T3
Glucagon
Epinephrine
Glucocorticoids
3
Q
What are the diabetes drugs
A
Insulin’s, amylin analog, insulin secretagogues (sulfonylureas, meglitinides, GLP-1 agonists, DPP4 inhibitors), biguanides, thiazolidinediones, SGLT2 inhibitor, a-glycosidases inhibitors
4
Q
Controlling glycemia in diabetes is goo
A
Improves survival, reduces diabetic complications, espicially in patients with type 1
5
Q
Insulin’s
A
Rapid acting, short acting, intermediate acting, long acting
6
Q
Rapid acting insulin
A
Aspart, lispro, glulisine
7
Q
Short acting insulin
A
Regular insulin
8
Q
Intermediate acting insulin
A
NPH
9
Q
Long acting insulin
A
Detemis, glargine
10
Q
Short acting insulin time
A
0-5 hours
11
Q
Regular insulin time
A
0-12 hours
12
Q
NPH
A
1-16 hours
13
Q
Detemir
A
1-23 hours
14
Q
Glargine
A
Kinda starts at 5 hours and goes past 24`
15
Q
How deliver insulin
A
Standard SQ injection , portable pen, insulin pumps
16
Q
Amylin analog
A
Amylin is a pancreatic hormone synthesized by B cells
17
Q
Amylin MOA
A
Inhibits glucagon secretion, enhances insulin sensitivity, decreases gastric emptying (slow the rate of intestinal glucose absorption), cause satiety
18
Q
Name amylin analog drug
A
Pramlintide
19
Q
Incretins
A
GI hormones that decrease blood glucose by GLP-1 (made in L cells)
Promotes B cell proliferation, insulin gene expression, glucose dependent insulin secretion , inhibits glucagon cause satiety, inhibits gastric emptying, short HL
20
Q
Why incretins not a drug
A
1-2 min HL
21
Q
Name incretin mimetic
A
Long acting GLP-1 receptor agonists
Sipeptidyl peptidase-4 inhibitors
22
Q
Long acting GLP-1 receptor agonists
A
Exenatide, liraglutide
23
Q
DPP4 inhibitors
A
Sitagliptin, linagliptin, zaxagliptin, alogliptin
24
Q
MOA DPP4 inhibitors
A
DPP4 is a serine protease that degreased GLP-1 and other incretins
Increase levels of GLP-1 to enhance its interactions with the cognate receptor
Effects are similar to those of GLP1 agonists
25
Katp channel blockers
Sulofnylurease first gen
Sulfonylureas second gen
Non sulfonylureas
26
Sulfonylureas first gen
Chlorpropamide
Tolbutamide
Tolazamide
27
Sulfonylureas second gen
Glipizide
Glyburide
Glimepiride
28
Non sulfonylureas
Nateglinide
| Repaglinide
29
MOA Katp blockers moa
Binding to SUR-sulfonylurea receptor
Blocking K current through Kir6.2 inwardly rectifying k channel
30
Biguanides
Metformin
31
MOA biguanides
Amp dependent protein kinase
32
Thiazolidinediones
Pioglitazone
| Rosiglitazone
33
MOA thiazolidinediones
Ligand of PPARy whihc is a nuclear receptor expressed primarily in fat, muscle, liver tissue and endothelium so get increase in glut4 in skeletal muscle and adipocytes, increase IRS-1 IRS2 and PI3K
Decrease PEPCK and NFKB and AP1
34
Sodium glucose co transporter 2 inhibitors
Canagliflozin, dapagliflozin, empagliflozin
35
MOA sglt2 inhibits
Filtration complete reabsorption-> filtration partial reabsorption
36
A glycosidase inhibitors
Acarbose
| Miglitol
37
MOA a glycosidase inhibitors
Ocmpeteive inhibiton of a glycosidase, a family of enzymes not he intestinal epithelium defer digestion and thus absorption of ingested starch and disaccharides
Lower postprandial hyperglycemia to create an insulin sparing effect
38
Describe regulation of insulin be beta cells and fold of k atp channel, l type ca channel and camp
K atp channel-closed when cell depolarized which causes ca in and insulin release
L type ca channel, (VDCC)when depolarized open and let ca into cell
Camp-gs (B2 ar agonists and GLP1 agonists)turns on ac which make camp and pka which open l type ca channel (gi inhibits this with somatostatin and a2 ar agonists)
39
Use of insulin in hyperkalemia
Ok
40
AE insulin
Ok
41
How get hypoglycemia insulin
Ok
42
Hypoglycemia unawareness
Ok
43
Treat hypoglycemia
Ok
44
How amylin used to treat diabetes
Ok
45
Pramlintide use, AE< drug interaction
O
46
What are incretins and their signal transduction path
ok
47
How GLP1 treat diabetes
Exenatide and liraglutide
GPCR turn on AC and camp and pka which upregultae insulin gene transcription and potentiation ca influx from ca channel
Exenatide-less susceptible to hydrolysis DPP4, HL 2.4 hrs
Liraglutide-rapidly absorbed lipid modified HL 11-15 hours
Use postprandial in type 2 DM who not adequately controlled with metformin, sulfonylureas, thiazolidinediones
Reduce doses of other to reduce chance of hypoglycemia
Parenteral route, improved control of hyperglycemia and induce weight loss
AE-nausea, diarrhea, anorexia. Lower risk of hypoglycemia vs pramlintide
—gluco23-6se dependent insulinotropism (ability to stimulate insulin secretion during hyperglycemia but not during hypoglycemia)
PANCREATITIS AND PANCREATIC CANCER
48
List DPP4 inhibitors and the MOA
GLIPTON
Serine protease decrease GLP1 and incretins
Increase level of GLP1
Adjunctive therap to diet and exercise in type 2 DM
Monotherapy or with metformin/sulfonylureas/tzd
Oral
AE-upper respiratory infections and nasopharyngitis, acute pancreatitis, hypoglycemia(if with insulin so adjust dose)
49
Use DPP4
Ok
50
AE DPP4 inhibitor
Ok
51
First vs second gen sulfonylureas
1st-lower potency high dose, not really used
Second gen-higher potency low dose, becoming generic
52
MOA sulfonylureas
K atp channel blockers
Bind SUR receptor block k current through kir6.2 inwardly rectifying K channel
Use for type 2 DM as monotherapy or in combination with insulin or other antidiabetic drug
53
AE sulfonylureas
Hypoglycemia, weight gain, secondary failure (respond initially later cease to respond to sulfonylureas and develop unacceptable hyperglycemia
Derm- cross reactivity with other sulfonamides
- sulfonamide antibiotics
- carbonic anhydrase inhibitors
- diuretics (thiazides, furosemide0
54
Sulfonylurea drug interactions
Enhancing their hypoglycemia effect-diasplacing from binding with plasma proteins: sulfonamides, clofibrate, salicylate
- enhancing the effect on Katp channel: ethanol
- inhibiting CYP enzymes: azole antifungals, gemfibrozil, cimetidine
Decreasing their glucose lowering effect
-inhibiting insulin secretion: beta blockers, CCBs, antagonizing their effect on Katp channel: diazoxide
Inducing hepatic CYP enzymes: phenytoin, griseofulvin, rifampin
55
Meglitinides
Repaglinide even, nateglinide
MOA =Katp channel inhibition
Pharm-1-1.5 hr duration 44-6 horus
56
Meglitinides MOA
Ok
57
Medlinitides when use
Control postprandial hyperglycemia in patients with type 2 DM
Take orally before meal
Can be used with alone or in combination with other antidiabetic drugs
58
Meglitinides AE
Hypoglycemia, secondary failure, weight gain
59
Metformin MOA
Amp dependent protein kinase activator
AMP dependent protein kinase phosphorylation a number of targets leading to
- inhibition of lipogenesis and gluconeogenesis
- increase in glucose uptake, glycolysis and FA oxidation
- lower glucose levels in hyperglycemia (but not normoglycemic) states
- increases insulin sensitivity
60
Why metformin first line
Oral agent for T2DM and 1st line
Superior or equilivent glucose lowering efficacy compared to other oral meds
Does not cause hypoglycemia
Does not cause weight gain
Taken orally
Can be used either alone or in combination with other oral agents
Decrease risk of macro and microvascular complications in diabetic patients
HL-1.5-3 horus
61
AE and contraindications for metformin, explain why is should not be used in conditions predisposing to tissue hypoxia
GI-anorexia, vomiting, nausea, diarrhea, abdominal discomfort
Decreased absorption of vitamin b12
Lactic acidosis, espicially under conditions of hypoxia, renal and hepatic insuffiency
DONT USE IN CONDITIONS PREDISPOSING TO TISSUE HYPOXIA (HF COPD) RENAL FAILURE, CHRONIC ALCOHOLISM AND CIRRHOSIS
62
List thiazolidinediones
Pioglitazone
| Rosiglitazone
63
MOA thiazolidinedione
Ligand PPARy which is nuclear receptos in fat, muscle, liver tissue and endothelium
Increase glut4 in skeletal muscle and adipocytes
Increase irs1, irs2 PI3K
Decrease PEPCK
Decrease NF-KB, AP1
64
Pharmacodynamics thiazolidinedione
Once daily oral med
Change gene expression takes 3 months and persist months after use
CYP inducing drugs decrease HL (rifampin)
Prolonged by CYP inhibiting drugs (gemfibrozil)
Safe in renal failure
65
Clincial use thiazolidinedione
Type 2 DM alone or in combo
Delay progression from prediabetes to type 2
Euglycemic (no hypoglycemia when used alone0
66
AE thiazolidinedione
Weight gain, edema (increase ENac)
Exacerbation HF due to water retention DONT USE IN CLASS III OR IV HF)
Increased Tc and LDL-c increase risk of cardiac death
Osteoporosis-bone fractures direct MSC to adipocytes differentiation , suppress differentiation of msc into osteoblasts
67
MOA SGLT2 inhibitors
Canagliflozin, dapagliflozin,
Gliflozins
Kidneys filter 160 g glucose a day which is reabsorbed by DGLT2, these drugs inhibit this transporter to increase glucose excretion and reduce hyperglycemia
-osmotic diuresis, weight loss, reduce bp, reduce uric acid, no hypoglycemia
68
When use SGLT2 inhibitso,
Adjunct to diet and exercise in adults with type 2 DM
Taken orally before the first meal once a day
In patients with hypovolemia, this condition should be corrrected before the start of therapy
69
AE sglt2 inhibitors
Hypotension, hypovolemia, orthostatic hypotension, dizzy, syncope
Genital and Uranus tract infections
Hypoglycemia if combined with insulin or insulin secretagogues
Renal function impairment
-induce a fall in gfr
Hyperkalemia 9espicially in patients with impaired renal function and those taking ACEI, ARBS, and k sparing diuretics)
70
List alpha glycosidase inhibitors
Monosaccharides absorbed from GI into blood
Competitive inhibition of a glycosidases, a family of enzymes on the intestinal epithelium defer digestion and thus absorption of ingested starch and disaccharides
Lower postprandial hyperglycemia to create an insulin sparing effect
71
Benefit of alpha glycosidase inhibitors
Monotherapy or combo in type 2 with other oral antidiabetic or insulin
Orally at mealtime
Do not cause hypoglycemia when used alone, do not cause weight gain
72
When use alpha glycosidase inhibitor
Type 2 DM as monotherapy or in combination with other oral antidiabetic agents
Orally at mealtime
Do not cause weight gain or hypoglycemia if alone
73
AE alpha glycosidase inhibitor
Malabsorption, flatulence, diarrhea, abdominal bloating
Hypoglycemia has been described when combined with insulin or insulin secretagogues
Drug interactions-decrease absorption of digoxin and propranolol and ranitidine
74
Rapid acting insulin
Aspart, lispro, glulisine
Fast absorption
Use for postprandial hyperglycemia -TAKEN BEFORE MEAL
Onset in 5 min and peaks 30 min but stop in 3 hours
75
Short acting insulin
Regular
Unmodified zinc crystals
Use for basal insulin maintenance, overnight coverage
For postprandial hyperglycemia, inject 45 min before meal (IV in emergency(
Onset in 30 min duration 10 hours and peak in 5
76
Intermediate insulin
NPH
For basal insulin maintenance and or overnight coverage
Onset 1-2 hours duration 10-12 hours
Pead4-12
Hypoglycemia-exercise induced as muscles need more glucose and hyperemic skin enhances rate of insulin absorption, delay meal or miss meal, insulin overdose
Signs-CNSconfusion bizarre behavior, seizures, coma
Sympathetic hyperactivity-tachycardia, palpitations, sweating, tremor
Parasympathetic hyperactivity: hunger, nausea
Hypoglycemic unawareness
Treat-glucose(IV if unconscious, juice, candy), diazoxide which is strong hyperglycemia agent-Katp channel opened that inhibits insulin release, glucagon
77
Long acting insulin
Detemir, glargine
Basal insulin maintenance (1-2 sc injections daily)
Onset 3-4 h
Duration 24 hours
Peak detemir 3-9 hours
Glargine peakless
AE all insulin-hypoglycemia, lipodistropy(hypertrophy of fat at site of injection, change site), resistance (gain igg antibodies that neutralize it), allergic reactions of immediate hypersensitivity, hypokalemia
78
Amylin analog
Pramlintide
Pancreatic hormone made be B cells
Inhibits glucagon secretion, enhances insulin sensitivity, decreases gastric emptying, satiety
Rapid onset duration 3 hours
Type I and type 2 DM who take mealtime insulin
SC injection before meals
AE0nausea, vomiting, diarrhea, anorexia, HPOGLYCEMIA esp is used with insulin
Drug interactions-enhances effects of anticholinergic drugs in GI
79
Insulin secretagogues
Incretin mimetics, Katp channel blockers
80
Incretin mimetics
GLP1 agonists
| DPP4 inhibitors
81
GLP1 agonists
Exenatide, liraglutide
82
DPP4 inhibitors
Sitagliptin, linagliptin, saxagliptin, alogliptin
83
K channel blockers
Sulfonylureas
| Meglitinides
84
First en sulfonylureas
Chlorpropamide
Tolbutamide
Tolazamide
85
Second gen sulfonylureas
Glipizide, glyburide, glimepiride
86
Meglitinides
Nateglinide
| Repaglinide
87
Biguanides
Metformin
88
Thiazolidinediones
Pioglitazonerosiglitazone
89
SGLT2 inhibitos
Canagliflozin
Dapagliflozin
Empagliflozin
90
Inhibitors of alpha glycosidase
Acarbose
| Miglitol
91
Receptors, signaling, hypothalmic and pituitary hormones
Ok
92
Growth hormone
Ok
93
Insulin growth factor 1 agonist
Ok
94
Somatostatin analogs
Octreotide
| Lamreotide
95
GH antagonists
Ok
96
Gonadotropin
FSH analogs
- follitropin alpha and follitropin beta
- urofollitropin
LH
-lutropin alpha
Hcg
-choriogonadotropin alpha
97
Gnrh analogs
Leuprolide
Gonadorelin
Goserelin, buserelin, histrelin, nafarelin, triptorelin
98
Gnrh antagonists
Ganerelix, cetrorelix
| Degarelix, abarelix
99
Dopamine receptor agonist
Bromocriptine-oral (inhibit prolactin and GH)
Cabergoline-treat high levels prolactin hormone by blocking release of prolactin from pituitary.
100
Vasopressin receptor agonists
Vasopressin
| Desmopressin
101
Vasopressin receptor antagonists
Conivaptan
| Tolvaptan
102
Kinase linked receptors
RTK-incorporate tyrosine kinase moiety in intracellular region that phosphorylates tyrosin resude
-insulin,
Serine/threonins kinase receptors-phosphorylation serine or throwing, TGFB
Cytokines receptors-lack enzyme activity, GH and PRL
103
Effect of kinase receptors
Gene expression of suppression
104
Cytokines receptor
No intrinsic activity
Jak stat signaling cascade for GH and prolactin receptors
105
TGFB
Smad
106
Compare an contrast the overall structure of main classes of endocrine receptors
LOOK AT TABLE IN DSA
107
**nuclear receptors and describe the events that occur after ligand binding
Ok
108
Figure and table in DSA diagrams signaling et works
Ok
109
Somatostatin analogues
Ocreotide lanreotide know how and when they work
110
Gonadotropins
Urofollitropin
111
Bromocriptine
Molecular mechanism...acromegaly, infertility and galactorrhea
Inhibits prolactin and growth hormone release
112
Dopamine receptor agonists used for what
Acromegaly, infertility and galactorrhea
Inhibits prolactin
Inhibits growth hormone release
Bromocriptine and cabergoline (blocks release of prolactin from pituitary)
113
MOA dopamine receptor agonist
Inhibit growth hormone release and prolactin release
Bromocriptine, cabergoline
114
Vasopressin receptor agonists
Vasopressin-antidiabetic actions, prevents production of dilute urine
Desmopressin
-long acting synthetic analog of vasopressin
Minimal V1 receptor activity
-antidiuretic to pressor ratio 3000 times that of vasopressin
115
Vasopressin receptor antagonists
Conivaptan
Tolvaptan
-block vasopressin receptors
Used to treat hyponatremia caused by SIADH, CHF, cirrhosis
Normally when osmolality falls, plasma vasopressin levels become low and aquaresis....in SIADH vasopressin release not fully suppressed, despite hypotonicity
Cirrhosis CHF water retention t
116
Nuclear receptors
Regulation of transcription and protein synthesis
117
Insulin receptor
Effectors are Tyrosine kinase, IRS-1 to IRS-4 leading to MAP kinase , PI 3-kinase, RSK signaling pathways
118
GH somatotropin on and off
Somatotostatin -
GHRH -
Target organ hormone or mediator is IGF-1
119
GH another name
Somatotropin
120
Effector molecule DH
IGF-1
121
SRIF
Somatotropin release inhibiting factor
Somatostatin
Turns off GH
Off IGF-1
122
SRIF and growth hormone
Negative effect
Somatostatin turns off IGF -1
123
A young couple wants to start a family. They have not conceived after 1 year of unprotected intercourse. Infertility evaluation revealed no abnormalities in the female partner and low sperm count in male. Which is a drug that is purified from the urine of postmenopausal women and is used to promote spermatogenesis in infertile men
Urofollitropin
124
Urofollitropin
Males-spermatogenesis requires FSH and LH
| -purified from urine of postmenopausal women and gives FSH activity
125
Desmopressin
Treats diabetes insipidus, bedwetting, hemophilia A, Von wiliebrand, High blood urea levels.
Antidiuretic-
126
Gonadorelin
GnRH agonsit used in fertility medicine and to treat amenorrhea and hypogonadism
127
Goserelin
Suppress production of the sex hormones (GnRH agonist)
Breast and prostate cancer.....
GnRH receptor agonist and antineoplastc by suppressing LH
128
Somatotropin
Stimulates growth, cell reproduction, and cell regeneration. Indicated only in limited circumstances
GH defiency of either childhood onset or adult onset
What causes shortness that we treat with GH-turner syndrome, chronic renal failure, prayer willi syndrome, intrauterine growth restriction and severe idiopathic short stature
129
Indications for GH
Turner, chronic renal failure, prayer willi syndrome, intrauterine growth restriction, and severe idiopathic short stature
130
29 year old 41st week of gestation has been in labor 1 hours . Although her uterine contractions had been strong a regular. They have diminished force in past hour. Which would be used to facilitate labor and delivery
Oxytocin
131
Oxytocin
Stimulates uterine contraction and augment labor
132
Dopamine
Stimulant drug in the treatment of severe low blood pressure, slow heart rate and cardiac arrest.. important in new born
133
Leuprolide
****** GnRH analogue
Acts as agonist at pituitary GnRH receptors
Treat hormone responsive cancers such as prostate cancer and breast cancer
Estrogen dependent conditions such as endometriosis or uterine fibroids
Used for precocious puberty in both males and females
Used to prevent premature ovulation in cycles of controlled ovarian stimulation for in vitro fertilization
——delay puberty in transgender youth until old enough for hormone replacement therapy
—used as alternatives to antiandrogens like spironolactone
134
Prolactin
Bromocriptine and cabergoline decrease prolactin levels agonsit of the receptor
Antagonist-domperidone, metoclopramide.....haloperidol, risperidone, sulpiride INCREASE PROLACTIN LEVEL
135
vasopressin
SIADH
Off label-tratment of vasodilators shock, GI bleeding, ventricular tachycardia, and V fib
136
3 yo boy with failure to thrive and metabolic disturbances was fund to have an inactivating mutation in the gene that encodes the GH receptor. Which of the following drugs is most likely to improve his metabolic function and promote his growth
Mecasermin (downstream )
137
Mecasermin
Child cant stimulate GH...downstream of GH main effector is IGF made in liver.
Combo of recombinant IGF_1 and binding protein that protects IGF1 from immediate destruction
Need downstream will protect it
138
Bromocriptine
A potent agonist at D2 receptor agonist and binds serotonin receptor, inhibits glutamate release by reversing the glutamate GLT1 transporter
139
Octreotine
Treat acromegaly from too much GH. It is a somatostatin analog, inhibits release of GH from pituitary glans
140
Somatropin
Replacement therapy when treat with exogenous GH is indicated only in limited circumstance...what are they
141
Leuprolide and ganirelix
Ganirelix-immediately reduces gonadotropin secretion
GnRH receptors antagonist
Leuprolide-GnRH receptor agonist
-works after a week
142
Leuprolide
Manufactured version of a hormone used to treat prostate cancer, breast cancer, endometriosis, uterine fibroids and early puberty
- GnRH analogue agonist at pituitary GnRH receptors
- initllay increase LH and FSH and testosterone and estradiol.....but bc propagation of the HOG axis is incumbent upon pulsation hypothalmic GnRH secretion, pituitary GnRH receptors become desensitized after several weeks
Protracted downregulation of GnRH receptor activity is the targeted objective of leuprorelin therapy and results in decreased LF and FSH secretion, leading to hypogonadism and thus a dramatic reduction in estradiol and testosterone levels regardless of sex
143
Ganirelix
Synthetic peptide that works as an antagonist against GnRH
Fertility treatment for women
-prevent premature ovulation in women undergoing fertility treatment involving ovarian hyperstimulation that causes the ovaries to produce multiple eggs
If premature ovulation-eggs released by the ovaries may be too immature to be used in in vitro fertilization
-ganirelix prevents ovulation until it is triggered by injecting human chorionic gonadotrophin
Competitivel blocks GnRH receptors on the pituitary gonadotroph, suppress gonadotropin secretion
Higher receptor binding than GnRH
144
7 year old boy successful chemo. Now excessive thirst and urination and hypernatremia
Desmopressin
145
Desmopressim
Treat DI from vasopressin defiency
Peptide agonist of V2 and V1
146
Corticotropin
ACTH
39 aa cleaved from MSH
Stimulated secretion of glucocorticoid steroid hormones from adrenal cortec espicially zone fasciculata
ACTH receptors
G protein coupled receptor
Increase intracellular cAMP, and activation PKA
147
HGC
Pituitary analog of hCG known as LH is produced int he pituitary gland of males and females of all ages
Final maturation induction in lieu of LH
Ovulation will happen between 38 and 40 hours after a single hCG injection
Patients that undergo IVF in general receive hCG
148
Menotropins
HMG
| Extracted from tine postmenopausal women
149
Thyrotroph
TSH
150
Thyroid drugs
Ok
151
Thyroid hormone nuclear receptor
TRa,B
152
Thyroid hormone receptor mediated gene activation
Gene activation
153
Major hormone
T3
RT3 no
154
Propranolol
Widely used to reduce HR and tremor during thyroid storm inhibits conversion of T4 to be more biologically active hormone, T3, which occurs in peripheral tissues
May help reverse reduced systemic resistance
155
Amiodarone induced thyrotoxicosis
50 fold higher iodine —-> toxic!!!
Commonly prescribed for arrhythmia
Releases free iodine
156
Amiodarone
Can cause type II amiodarone induced thyrotoxicosis
-occurs from actual thyroid tissue destruction
Patients started on amiodarone need baseline measures of TSH, T3 and T4
157
Methimazole
Anti thyroid drug used to treat hyperthyroidism -thyroid gland produces excess thyroid hormone
This amide group of medications-blocks iodide organification
158
Side effects methimazole
Agranulocytosis, leukopenia, thrombocytopenia, aplastic anemia, liver inflammation
Use cautioslult in patients with preexisting liver disease, a history of alcohol abuse or hepatitis
159
This amide Group medication
PTU, methimazole, carbimazole
160
Methimazole is _ times more potent than PTU
10
161
Methimazole
Take before thyroid surgery
-lowers thyroid hormone levels
Minimizes the effects of thyroid manipulation
Inhibits THYROPEROXIDASE
162
Potassium iodide
Treat overactive thyroid conditions (hyperthyroid) also used along with anti thyroid medicines to prepare the thyroid gland for surgical removal
Stable form of iodine
Blocks iodine uptake
Used as a treatment for hyperthyroidism
Used as a treatment for iodine defiency
163
How does K iodide protect thyroid from radiation
Shrinks thyroid gland
Decreases thyroid hormone production
Does not affect HR or cause irregular heartbeat
164
Thyrotropin
TSH
165
TSH screening test
Most sensitive test for hyperthyroidism and primary hypothyroidism
TSH in normal limits excludes diagnoseis
166
PTU indications for use
Graces, toxic multinodular goiter
- intolerant to methimazole
- surgery or radioactive iodine therapy is not an appropriate treatment option
Ameliorate symptoms of hyperthyroidism
- used in preparation for thyroidectomy
- used in radioactive iodine therapy in part it’s intolerant to methimazole
167
MOA PTU
Inhibits synthesis of thyroid hormones in hyperthyroidism
Inhibits conversion of thyroxine to triiodothyronine in peripheral tissues
Does not inactivate pre-existing T4 and T3-stored int he thyroid. Or circulation in blood
Does not interfere with he effectiveness of thyroid hormones given by month or by injection
May be an effective treatment for thyroid storm
168
Levothyroxine
Treat thyroid hormone defiency
Manufactures from thyroid hormone->T4
169
AE levothyroxine
Weight loss, througble tolerating heat, sweat, anxiety, trouble sleeping, tremor, fast HR,
170
What drugs impair levothyroxine
Cholestyramine
171
Radioactive iodine therapy for thyroid cancer contraindicated in
Pregnant women
172
Atenolol for hyperthyroidism
Propranolol is the most widely studies and used in thyrotoxicosis
Clinical improvement of hyperthyroid
Do not alter thyroid hormone levels
173
MOA bb
Membrane stabilizing action
Inhibits T4 T3 conversion
-ameliorates many disturbing symptoms and side effects of hyperthyroidism
Secondary to increased catecholamines due to blockage of beta receptors
174
Indication bb
Graves
| Thyroid storm
175
Perchlorate blocking agent
Inhibited thyroid hormone production by blocking sodium iodide symporter (NIS)
176
24 year old woman mild hyperthyroidism due to graces. She appears to be in good health otherwise. In Graves’ disease, the cause of the hyperthyroidism is the production of an antibody that does which of the following
Activates the thyroid gland TSH receptor and stimulates thyroid hormone synthesis and release
177
Graves antibodies
Mimic TSH
178
24 yo woman found to have mild HTN due to graces. She is in good health. The decision is made to begin treatment with methimazole. Methimazole reduces serum concentration of T3 primarily by which of the following mechanism
Preventing the addition of iodine to tyrosine residues on thyroglobulin
179
Levo
Check T3 and T4 through out to see if up or decrease dose
180
Methimazole and PTU
Act in thyroid cells to prevent conversion of tyrosin residues in thyroglobulin to MIT or DIT
181
24 yo woman found to have mild Hyperthyroidism due to Graves’ disease. She appears to be in good health otherwise. The decision is made to begin treatment with methimazole. Though rare, a serious toxicity associate with the thiazides is which
Agranulocytosis
-most dangerous AE of thiazides is agranulocytosis
Can also get vasculitis, hepatic damage, and hypothrombinemia
182
Adrenal corticosteroid drugs
Ok
183
Inner zone reticularis
Secretes DHEA and its sulfate derivatives DHEA-S.
Converted to DHEA in periphery by DHEA sulfatase
184
Fate of DHEA in women and men
Converted into potent androgens in males
Converted in estrogens for females
185
How do corticosteroids work
Ligand activated transcription factors that modulate gene expression
186
Aldosterone and cortisol bind ___ with equal affinity
MR
187
Agonists corticosteroids
Glucocorticoids (prednisone)
Mineralocorticoids (fludrocortisone
188
Antagonists corticosteroid
Receptor antagonists (glucocorticoid antagonists (mifepristone), mineralocorticoids antagonists (spironolactone)
Synthesis inhibitors (ketoconazole)
189
What give if have agranulocytosis
PTU
190
Adrenal corticosteroids
Receptor independent mechanisms of corticosteroid specificity
Decreased activity/inhibition of this enzyme 11B-HSD2 results in excessive activation of MR
191
Known inhibitors of 11B HSD2
Glycyrrhizin (licorice root extract)
Carbenoxolone (UK approved for esophageal ulcers)
192
Licorice
Increase activity of cortisol 2 MR
Leads to Na and H2O retention , K loss,
Increase in BP
193
Carbohydrate metabolism
Gluconeogenesis
Glucose output
Glycogen synthesis
Decreased glucose uptake development of hyperglycemia
194
Lipid metabolism
Increase lipolysis
FFA and glycerol into the gluconeogenesis pathway
Lipogenesis
Fat deposition
Change fat distribution
195
Protein metabolism
Decrease aa uptake
Decreased protein synthesis
Dev of myopathy and msucle wasting
196
Anti-insulin action of _____
Glucocorticoids
197
Anti insulin action of glucocorticoids
Liver increase gluconeogenesis
Skeletal msucle
Decrease glucose intake
Decrease glycogen synthetase
Increase proteolytic
Adipose tissue
Decrease glucose uptake
Increase lipolysis
HYPERGLYCEMIA
198
Effects of glucocorticoids on immune system and inflammation
Decrease production of prostagladins and leukotrienes
Decrease production and increased apoptosis of immune cell types
Decrease production of cytokines and their receptors
Decreased transmigration of neutrophils and macrophages from blood into tissues
Decreased expression of cell adhesion molecules
199
AE glucocorticoids and immune system and inflammation
Decreased inflammation and its manifestations
Immune suppression
Decreased allergic/hypersensitivity reactions
200
Common clinical applications: endocrine conditions
Replacement therapy
-primary adrenal insuffiency (Addison’s disease)-a combination of glucocorticoid (hydrocortisone) and mineralocorticoids (fludrocortisone)
Congenital adrenal hyperplasia-hydrocortisone+ fludrocortisone
201
Common NON ENDOCRINE ADRENAL APPLICATIONS
Immunosuppression-following oragan or bone marrow transplant, autoimmune disease, hematologic cancers (leukemia)
Inflammatory and allergic conditions-RA, IBD, asthma/COPD, allergic rhinitis, skin diseases: inflammatory dermatoses(psoriasis), hypersensitivity reactions
202
Short acting glucocorticoids
Short to medium acting (<12 hours)
- hydrocortisone (cortisol)
- cortisone
- prednisone
- prednosolone
- methylprednisonlone
203
Intermediate acting glucocorticoids
12-36 horus
Triamcinolone
204
Long acting glucocorticoids
>36 hours
Betamethasone
Dexamethasone
205
Prednisone MOA
Activation of GR alters gene transcription
206
Clinical applications prednisone
Many inflammatory conditions, organ transplantation, hematologic cancers
207
Pharmacokinetics prednisone
Duration of activity is longer than pharmacokinetic t1/2 of drug owing to gene transcription effects
208
Toxicities, drug interactions prednisone
Adrenal suppression, growth inhibition, muscle wasting, osteoporosis, salt retention, glucose intolerance, behavioral changes
209
Dosing adrenalocorrticoid drugs
Use lowest dose for the shortest duration possible depending on the condition
-use intermediate or short acting vs long acting drugs
210
Route of adrenalocorticoid drugs
Use topical inhalation routes
Ciclesonide, a prodrug activated by esterases present in bronchial epithelial cells;systemically absorbed active drug tightly bound to serum proteins
211
When give adrenalcorticoid
Single in AM
Every other day-short course pulse therapy administration
212
Dose tapering adrenalocorticoid
Rate depends on severity of condition, duration of steroid therapy and maintenance dosage
When taper doses approach physiological levels of glucocorticoids HPA axis is tested
- morning seru cortisol
- ACTH test
- CRH test
213
AE prolonged use at high doses adrenalcorticoid /cushing disease
Psychiatric-sleep disturbance/activation, mood disturbances, psychosis
Skin/soft tissue
- cushing PID appearance
- striae
- acne
- hirsutism
- edema
Neurologic
- neuropathy
- pseudomotor cerebri
Cardiovascular
-HTN
MSK
- osteoporosis
- ascetic necrosis of bone
- myopathy
Endocrine
- DM
- adrenal cortex suppression
Immunologic
- lymphocytopenia
- immunosuppression
- false negative skin test
Optho
- cataract
- narrow angle glaucoma
Developmental
-growth retardation
214
Who should not use corticosteroid drug advisory
Immunocompromised (HIV/AIDS)
Diabetics
Patients with infections
Patients with peptic ulcers
Patients with cardiovascular conditions
Patients with psychiatric conditions
Patients with osteoporosis
Children
215
Mifepristone MOA
Pharmacological antagonist of glucocorticoid and progesterone receptors
216
Clinical application glucocorticoid receptor antagonist
Medical abortion and very rarely for cushing syndrome
217
Pharmacokinetics mifepristone
Oral ad
218
AE mifepristone
Vaginal bleeding in women, abdominal pain, GI upset, diarrhea, headache
219
Mineralocorticoids
Fludrocortisone
220
MOA fludrocortisone
Strong agonist at mineralocorticoids receptors and activation of glucocorticoid receptors
221
Clinical applications mineralocorticoids
Adrenal insuffiency (addison)
222
Pharmacokinetics fludocortisone
Long duration of action
223
AE fludrocortisone
Salt and fluid retention, CHF, signs and symptoms of glucocorticoid excess
224
Mineralocorticoids receptor antagonist
Spironolactone
225
MOA spironlactone
Pharmacological antagonist of mineralocorticoids receptor, weak antagonism of androgen receptors
226
Clinical application spironolactone
Aldosteronism from any cause , hypokalemia due to diuretic effect, post myocardial infarction
227
Pharmacokinetics spironolactone
Slow onset and offset; duration 24-28 hr
228
Toxicities spironolactone
Hyperkalemia, gynecomastia, additive interaction with other K retaining drugs
229
Synthesis inhibitors
Ketaconazole
230
MOA ketoconazole
Blocks fungal and mammalian CYP450 enzymes
231
Clinical applications ketoconazole
Inhihibits mammalian steroid hormone synthesis and fungal ergosterol synthesis
232
Pharmacokinetics ketaconazole
Oral, topical ad
233
AE ketoconazole
Hepatic dysfunction, many drug drug CYP450 interactions
234
Why are glucocorticoids given in endocrine practice
Only to establish the diagnosis and cause of cushing and to treat adrenal insuffiency using physiologic replacement doses and for treatment of congenital adrenal hyperplasia, for which the dose and schedule may not be physiologic
235
What use glucocorticoids to treat
Inflammatory, allergic, and immunological disorders. If chronic, this supraphysiologic therapy has many AE, ranging from suppression oft he HPA axis and cushing syndrome to infections and changes in mental status
236
Delta-4,3-keto-11-beta,17 alpha, 21 trihydroxyl configuration
Required for glucocorticoid activity and is present in all natural and synthetic glucocorticoids.
237
Addition of a double bond between the 1 and 2 positions of hydrocortisone (cortisol) yields
Prednisolone, which has 4 times more glucocorticoid activity than cortisol
238
Pharmacokinetics glucocorticoids
Bound to CBG and albumin (2/3) or circulate free (1/3)
239
HL glucocorticoids
80 minutes-cortisol
Longer i bound
240
Where is the 11 beta HS dehydrogenase type 1 enzyme found that converts inactive cortisone to cortisol
Many target tires
241
Where is type 2 isoenzyme which converted cortisol to cortisone
Mineralocorticoid target tissues (kidney , colon, salivary glands) and int he placenta in which it protects the cell from cortisol activation of the corticosteroid type 1 (mineralocorticoid ) receptor
242
Glucocorticoids fluoridated at the 6-alpha or 9 alpha position (dexamethasone, fludrocortisone, betamethasone) or methylated at the 6 alpha position (methylprednisone), or methylozazoline at position 16, 17 (deflazacort
Protected from oxidation inactivation by the type 2 isoenzyme
243
Prednisone
More effectively oxidized by 11 beta hydroxysteroid DH type 2 than is cortisol , which may explain why prednisone has has less salt retaining activity than cortisol
244
Polymorphism in MDR-1 gene may influence the therapeutic response to steroids
Many glucocorticoids are both substrates for P-glycoproteins mediated efflux from cells, and inducers of P glycoproteins production
245
Polymorphism in the glucocorticoid receptor gene ma increase or decrease sensitivity to glucocorticoids and, thus,
affect the response to both endogenous cortisol and exogenous agents
246
Metabolism glucocorticoids
Exogenous-reduction, oxidation, hydroxylation, and conjugation reactions as endogenous steroids
Drugs(phenobarbital, phenytoin, rifampin,mitotane)-increase the metabolism of synthetic activity and natural glucocorticoids similarly, particularly by increasing hepatic 6-beta-hydroxylase activity of CyP3A4
247
Like cortison, which must be converted to cortisol by hepatic 11-b-HS DH, prednisone must be converted to ____ to exert any glucocorticoid action
Prednisolone
248
Medical emergencies where use glucocorticoid
High doses for a few days-safe just for a few days
249
Chronic therapy glucocorticoids
In less urgent circumstances
Route of administration and the disease indexes to be monitored to assess therapeutic efficacy. Glucocorticoids cat be given chronically without the risk of AE.
250
Prednisone 5 mg/day
Bone loss
251
When give high parenteral therapy
Septic shock and severe acute asthma
252
IV bolus methylprednisone
Have been used to treat transplant rejection and some autoimmune diseases such as RA
253
Pulse glucocorticoid
Impair cytokine generation
254
High doses and membranes
Dissolve cell membranes, thereby altering their physicochemical properties and the activities of membrane associated proteins, which may explain why onyl high doses are effective in treating acute exacerbations of immunologically mediated diseases
255
Oral
Chronic therapy
Absorbed in 30 min
256
Why nonsystemic administration
Deliver higher local concentrations while minimizing systemic exposure .
257
Intraarticular injection
Joint inflammation
258
Inhalation therapy
Asthma
259
Topical application
Inflammatory skin disorders
260
Hydrocortisone salts injected
IM in minutes absorbed
Esters absorbed in hour
261
Cortison acetate absorption
Slow
262
Triamcinolone salts and esters
Sloooooow
263
All topical and inhaled glucocorticoids problems
Systemic absorption potential HPA issue like cushing
264
Inhaled fluticasone propionate
Greater systemic absorption and a greater association with adrenal suppression
265
Areas of body where absorbed more
Intertriginous areas> forehead>scalp>face>forearm
266
Why infants and kids absorb more
Striatum corneum much thinner
267
What vehicle increases absorption
Urea, dimethylsulfoxide,
268
Prednisone in morning why
Doesn’t suppress the circadian peak in cortisol secretion the next morning.
269
Alternate day regimes
Alleviate effects
Thrice hte usual daily dose
Unsuccessful...
270
Major systemic side effects glucocorticoid
Suppression of HPA function and Cushing
271
Both exogenous and endogenous glucocorticoids exert a negative feedback control on HPA
Suppress CRH and ACTH
Adrenal atrophy and loss of cortisol secretory capability
272
Iatrogenic cushing syndrome
Development of cushing syndrome depends upon the dose, timing and duration of glucocorticoid adminsitration and varies among patients
273
How minimize effects
Exercise, calcium, VD, bisphosphonates, estrogen therapy,
274
MHT
Menopausal hormone therapy
275
Primary therapy for menopausal symptoms
Estrogen with/without progestin
| *women with an intact uterus must also be on progestin
276
AE estrogen
Endometrial hyperplasia/carcinoma from unopposed tissue proliferation with prolonged duration
277
Benefit of MHT perimenopause-transition period(before 12 months)
Hormone regulation and pregnancy protection
278
Estrogens
Estradiol
Conjugated estrogens
Esterified estrogens
Estropipate
279
Estradiol
Acetate form and cypionate form
280
Conjugated estrogens
Blend of at least 6 known estrogen derivatives
| -derived from estrogens found in urine of pregnant mares
281
Esterified estrogens
Combination of na estrone sulfate and na equaling sulfate
282
Estropipate
Crystalline estrone solubilized with sulfate and stabilized with piperazine
283
Progetinic
Medroxyprogesterone (MPA)
Methyltestosterone
Progesterone
284
MPA
With CE
285
Methyltestosterone
Alone or with EE
286
Progesterone
Alone
287
MO ESTROGEN
BIND ER A/B IN VARIOUS TISSUES, TRANSFERRED INTO NUCLEUS RESULTING IN INCREASED GENE AND PROTEIN EXPESSION
288
Why women on estrogen must be on progestin if have in tact uterus
Progestin oppose effects of estrogens
Women with an intact uterus must be on a progestin
Increased risk of endometrial hyperplasia/carcinoma from unopposed tissue proliferations ith prolonged duration
289
Estrogen effects
Decrease production and activity of cholesterol, antithrombin III, osteoclast is activity
Increased triglycerides and HDL-C, clotting factors, platelet aggregation, sodium/fluid retention, tBG
290
Women’s health initiative study
Examine MHT purported beneficial or preventative effects on heart disease, osteoporosis related fractures and risk of cancer
291
Estrogen use alone good and bad
Good less breast cancer, fractures and diabetes
More dementia, gallbladder disease, stroke, venous thromboembolism, urinary incontinence
292
Estrogen and progesterone good and bad
Good-less diabetes, fractures, colorectal cancer
Harms
Breast cancer, CAD, dementia, gallbladder disease,stroke, venous thromboembolism, urinary incontinence
293
Summary WHI
MHT very effectively minimizes/treats vasomotor symptoms and vaginal changes
294
No use MHT
Don’t use to prevent CVD or dementia
295
Benefit on bone and colon cancer of estrogen
Outweighed by other risks
296
When use estrogen to prevent osteoporosis
When at significant risk
297
Should estrogen be used to treat colon cancer
Not solely
298
For young women MHT
Acceptable option for treating moderate to severe menopausal symptoms in young (up to 59 or within 10 years of menopause) and health women
- individualization with risk stratification is key
- some organizations recommending patch over oral therapy
299
MHT for women with vaginal symptoms
The preferred treatments are low doses of vaginal estrogen
300
MHT for women with a uterus
Women who still have a uterus need to take a progestin along with estrogen to prevent uterine cancer
Women who have had their uterus surgically removed able to take estrogen alone
301
MHT women at risk of blood/clots/stroke
Both estrogen alone therapy and estrogen with progestin therapy increases risk of blood clots
Although risks of blood clots and strokes increase with either type of MHT, risk is less in 50-59 years
302
MHT women at risk of breast cancer
An icnreased risk of breast cancer seen within 3-5 years of continuous estrogen with progestin therapy
303
Risks and benefits stop ___ years after MHT is stopped
Stop
304
MHT take home if therapy needed for moderate severe vasomotor symptoms
Use lowest dose
| Treat for the shortest duration possible and re evaluate at least yearly for ongoing need for therapy
305
When use vaginal estrogen
Vaginal dryness free of Brest cancer, endometrial cancer and hormone sensitive cancer
306
Serm tsecs
Selective estrogen receptor modulators
Tissue selective estrogen complexes
307
Serm
Beneficial pro estrogenic (agonist) actions in select tissues with beneficial (or non harmful) anti estrogenic(antagonists0 actions in other tissues
-bone, brain, breast, endometrium
308
Tsec
Combines the unique elements of a serm with an estrogen compound
309
Serms
Ospemifene
| Clomiphene
310
Tsecs
Basedoxifene (only as combo with ce)
311
Ospemifene indication
Moderate to severe dyspareunia
| A symptom of vulvar and vaginal atrophy or menopause
312
MOA osemifene
Functions as estrogen agonist by binding to ER in vagina, but also anti estrogenic on breast
Increases superficial cell growth )on vaginal smear), increases vaginal secretions, decrease vaginal pH, reduces pain/discomfort during vaginal intercourse
Stimulators endometrial effects
-no known increased risk of endometrial cancer; yet use with caution in women with intact uterus
313
AE ospemifene
Worsening of hot flashes/sweating
Estrogenic-similar effects on coagulation
Endometrial thickening and even hyperplasia
314
Contraindications ospemifene
Unusual/abnormal vaginal bleeding
Thromboembolic diseases-CVA/MI/VTE/PE/DVT
-exercise caution in use in smokers
Estrogen related neoplasia
-uterine/ovarian/breast
315
Bazedoxifene w/ce for women with intact uterus indications
Treatment of moderate to severe vasomotor symptoms associated with menopause in women with a uterus
Prevention of post menopausal osteoporosis in women with a uterus
316
MOA bazedoxifene w/ ce
Antagonistic activity in endometrium (replaces progestin concept in women with an intact uterus) and in breast tissue; but also estrogenic (agonist) physiological effects, espicially in bone (CE)
- does not stimulate endometrial proliferation
- has been shown to destroy HER2 malignant cells, including cells resistant to tamoxifen, similar to anti estrogen drug fulcestrant
Less vaginal bleeding than ce with progestin therapy
317
AE bazedoxifene w/ce
All estrogen related effects (due to ce component
-worsening hot flashes/sweating
318
Contraindication bazedoxifene
In all situations estrogens are...due to ce
319
Anti estrogens
Clomiphene
320
Indications for clomiphene
Infertility in anovulatory women
321
MOA clomiphene
Induction of ovulation in women with amenorrhea, PCOS, and dysfunctional bleeding with anovulatory cycles
-primary blocks inhibitory actions of estrogen on hypothalamus gnrh and pituitary gonadotropin release
—increases gonadotropin secretion thereby stimulating the ovaries to develop oocyte follicles
5-9 day cycles
322
AE clomiphene
```
Multiple births (twins)
Ovarian cysts
-cancer with prolonged use(May limit to 3 cycles)
```
Hot flashes
Lateral phase dysfunction
-inadequate progesterone production
323
Induction of labor/control postpartum bleeding
Misoprostol
Dinoprostone
Carboprost
Oxytocin
Ergot alkaloids
324
Corticosteroids
Cortisol
Betametaons
Dexamethasons
325
Delay labor (tocolysis)
Terbutaline
Indomethacin
Nifedipine
Mgso4
Atosiban
326
Maintain pda
Alprostadil
327
Close pda
Indomethacin
Ibuprofen
328
Anti hypertensive preg
A methyldopa
Labetalol
Hydralazine
Na nitroprusside
329
Misoprostol
Synthetic prostagladin e1 analog
330
Effects misoprostol
Replacing PG loss in stomach during NSAID therapy
Induce uterine contraction
Maintain pda
331
Indications misoprostol
NSAID induced gastric ulcers
Termination of intrauterine preg if <70 days with mifepristone
Off label cervical ripen labor induction
332
Contraindications misoprostol
Preg unless abort, previous c section
333
AE misoprostol
N/v, diarrhea, chills, pain
Tachysystole(uterine contractions rapid), prolonged uterine contractions
Fetal-hypoxia from tachysyssole or prolonged uterine contractions
334
Dinoprostone
Prostagladins e2 analog
335
Effects dinoprostone
Induces uterine contractions
Cervical ripen
336
Indication dinoprostone
Cervical ripen at or near term who need indication for labor induction
Vaginal-continuation or cervical ripening in patients at or near term in whom there
Suppositories terminate pregnancy from 12-20 weeks of gestation
337
AE dinoprostone
Contraindications-preg, previous c section
Maternal-back pain, n/v, diarrhea, Denver, chills, ab pain, flushing, warm feeling in vagina
Abortion-fever unresponsive to nsaids
Fetal-hypoxia from tachysystole
338
Carboprost
Prostagladin f2a analog
339
Effects carboprost
Induces uterine contractions, prolonged duration fo action
340
Indication carboprost
Abortion 13-20 weeks
Post partum hemostasis
341
How given carboprost
IM
342
Contraindications carboprost
Hypersensitivity, acute PID, cardiac, hepatic
343
AE carboprost
HTN pulmonary edema, child shivering, dizzy gagging retching
344
Oxytocin
Posterior pituitary hormone
345
Effects oxytocin
Increases force, frequency, and duration of uterine contractions by binding G protein
Increase milk ejection
346
Indication oxytocin
Labor induction
Post partum hemostasis
347
Contraindications oxytocin
Lungs not mature
Cervix not ripe
348
AE oxytocin
Water intoxication
349
Ergot alkaloids
Ergonocine, ethyl ergonocine
Stimulates adrenergic ,dopaminergic, and serotonergic receptors
350
Effect ergot alkaloids
Dose dependent on uterus causes prolonged tonic uterine contractions
Vascular construction arterioles and veins
351
Indications ergot alkaloids
Post partum use o increase tone and decrease bleeding
Augment labor but not recommended
Migraine
352
Contraindications ergot alkaloids
HTN, hypersensitivity
353
AE ergot alkaloids
HTN, n/v HA
St Anthony’s fire...mania, psychosis
Dry gangrene
354
Prostagladins
Ripen
Can cause uterine contractions any time during preg-abortion
355
Oxytocin
During labor and delivery
| Helps with post partum bleeding
356
Ergot alkaloids
Second choice for limiting post partum bleeding
357
Need time for corticosteroids to trigger surfactant productions nd brain maturation
Tocolytics
358
<24 weeks
Single corticosteroid course
359
24-32 weeks
Group b strep prophylaxis
Single corticosteroid course
Antimicrobials
Mg sulfate
360
23-24 weeks
Group b strep prophylaxis
Single corticosteroid course
Antimicrobials to prolong latency
361
>34 weeks
Group b strep prophylaxis
| Single corticosteroid
362
Indications antenatal corticosteroids
```
Women 24-36 weeks of gestation with
-threatened pre term labor
Antepartum hemorrhage
Preterm rupture of membranes
Conditions requiring c section
```
363
Betamethasone
Two IM injections 24 hr interval
364
Dexamethasone
Four doses by IM injection
| 12 hr intervals
365
Betamethasone dexamethasone
Induces transcription of surfactant proteins in alveolar the 2 pneumocytes
366
Riot drone
B2 agonist tocolysis
367
AE ritodrine
Severe hallucinations
368
Mg sulfate
Present eclampsia seizures
Long term drug for tocolysis
-not really used
369
MOA mg sulfate
Inhibit ach release at uterine neuromuscular junction
370
AE mg sulfate
Skin flushing,palpitations, HA, depressed reflexes, respiratory depression, impaired cardiac conduction
Fetal-muscle relaxation, rarely cns depression
371
Terbutaline
Increases camp, ends to K channel mediated hyperpolarization, dephosphorylation of myosin light chain
372
Contraindications tertbutaline
Cardiac arrhythmias, poorly controlled thyroid disease or DM
373
AE tertbutaline
Cardiac arrhythmias, pulmonary edema, MI, hypotension, sob
Baby-tachycardia, hyperinsulinism is, hyperglycemia, hypoglycemia,
374
Evidence tertbutaline
Delays labor 2-7 days
375
Nifedipine
Blocks ca influx through voltage gated ca channels, less ca means less contraction
376
Contraindications nifedipine
Cardiac disease, renal disease, HTN, dont use with mg sulfate
377
AE nifedipine
Flushing, HA, dizzy, nausea, hypotension, tachycardia
No fetal side effects
378
Evidence nifedipine
Calcium channel blockers are preferable to other tocolytic agents compared
379
Indomethacin moa
Blocks synthesis of PGF2a, a potent stimulator of uterine contractions
380
Contraindications indomethacin
Renal or hepatic impairment
381
AE indomethacin
N, heart burn, gastritis, proctitis with hematochezia, impairment of renal function, post partum hemorrhage, ha, dizziness
Constriction of ductus arterioris, pulmonary HTN, renal issue with oligohydramnios, iv hemorrhage, hyperbilirubinemia, necrotizing enterocolitis
382
Evidence indomethacin
Insufficient
383
Nitroglycerin contraindications
HA
384
AE nitroglycerin
HA, hypotension, neonatal hypotension.
385
Atosiban moa
Blocks action of oxytocin,
386
Contraindications atosiban
Non
387
AE atosiban
Ha n, allergic reaction
388
Atosiban evidence
Doesn’t work
389
Best choice for tocolytics
Nifedipine or indomethacin DONT COMBINE
390
PDA
Should close in a few days from constriction caused by increased oxygen tension
Decrease circulating pge2 sue to its metabolism in lungs
391
Alprostadil
Pge1 maintains pda
392
Indications alprostadil
Pre term infants with congenital heart defects
-mature to cope with surgery
Heart defects need to keep open for keeping flow
393
AE alprostadil
Pyrexia
394
First line htn preg
Methyldopa and labetalol
