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Pharmacology > Diabetes > Flashcards

Diabetes Flashcards

1
Q

What decreases blood glucose

A

Insulin

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2
Q

What increases blood glucose

A

T3
Glucagon
Epinephrine
Glucocorticoids

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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

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4
Q

Controlling glycemia in diabetes is goo

A

Improves survival, reduces diabetic complications, espicially in patients with type 1

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5
Q

Insulin’s

A

Rapid acting, short acting, intermediate acting, long acting

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6
Q

Rapid acting insulin

A

Aspart, lispro, glulisine

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7
Q

Short acting insulin

A

Regular insulin

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8
Q

Intermediate acting insulin

A

NPH

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9
Q

Long acting insulin

A

Detemis, glargine

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10
Q

Short acting insulin time

A

0-5 hours

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11
Q

Regular insulin time

A

0-12 hours

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12
Q

NPH

A

1-16 hours

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13
Q

Detemir

A

1-23 hours

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14
Q

Glargine

A

Kinda starts at 5 hours and goes past 24`

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15
Q

How deliver insulin

A

Standard SQ injection , portable pen, insulin pumps

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16
Q

Amylin analog

A

Amylin is a pancreatic hormone synthesized by B cells

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17
Q

Amylin MOA

A

Inhibits glucagon secretion, enhances insulin sensitivity, decreases gastric emptying (slow the rate of intestinal glucose absorption), cause satiety

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18
Q

Name amylin analog drug

A

Pramlintide

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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

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20
Q

Why incretins not a drug

A

1-2 min HL

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21
Q

Name incretin mimetic

A

Long acting GLP-1 receptor agonists

Sipeptidyl peptidase-4 inhibitors

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22
Q

Long acting GLP-1 receptor agonists

A

Exenatide, liraglutide

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23
Q

DPP4 inhibitors

A

Sitagliptin, linagliptin, zaxagliptin, alogliptin

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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

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25
Q

Katp channel blockers

A

Sulofnylurease first gen

Sulfonylureas second gen

Non sulfonylureas

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26
Q

Sulfonylureas first gen

A

Chlorpropamide

Tolbutamide

Tolazamide

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27
Q

Sulfonylureas second gen

A

Glipizide
Glyburide
Glimepiride

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28
Q

Non sulfonylureas

A

Nateglinide

Repaglinide

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29
Q

MOA Katp blockers moa

A

Binding to SUR-sulfonylurea receptor

Blocking K current through Kir6.2 inwardly rectifying k channel

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30
Q

Biguanides

A

Metformin

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31
Q

MOA biguanides

A

Amp dependent protein kinase

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32
Q

Thiazolidinediones

A

Pioglitazone

Rosiglitazone

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33
Q

MOA thiazolidinediones

A

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

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34
Q

Sodium glucose co transporter 2 inhibitors

A

Canagliflozin, dapagliflozin, empagliflozin

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35
Q

MOA sglt2 inhibits

A

Filtration complete reabsorption-> filtration partial reabsorption

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36
Q

A glycosidase inhibitors

A

Acarbose

Miglitol

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37
Q

MOA a glycosidase inhibitors

A

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

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38
Q

Describe regulation of insulin be beta cells and fold of k atp channel, l type ca channel and camp

A

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)

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39
Q

Use of insulin in hyperkalemia

A

Ok

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40
Q

AE insulin

A

Ok

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41
Q

How get hypoglycemia insulin

A

Ok

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42
Q

Hypoglycemia unawareness

A

Ok

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43
Q

Treat hypoglycemia

A

Ok

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44
Q

How amylin used to treat diabetes

A

Ok

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45
Q

Pramlintide use, AE< drug interaction

A

O

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46
Q

What are incretins and their signal transduction path

A

ok

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47
Q

How GLP1 treat diabetes

A

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

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48
Q

List DPP4 inhibitors and the MOA

A

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)

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49
Q

Use DPP4

A

Ok

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50
Q

AE DPP4 inhibitor

A

Ok

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51
Q

First vs second gen sulfonylureas

A

1st-lower potency high dose, not really used

Second gen-higher potency low dose, becoming generic

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52
Q

MOA sulfonylureas

A

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

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53
Q

AE sulfonylureas

A

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
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54
Q

Sulfonylurea drug interactions

A

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

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55
Q

Meglitinides

A

Repaglinide even, nateglinide

MOA =Katp channel inhibition

Pharm-1-1.5 hr duration 44-6 horus

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56
Q

Meglitinides MOA

A

Ok

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57
Q

Medlinitides when use

A

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

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58
Q

Meglitinides AE

A

Hypoglycemia, secondary failure, weight gain

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59
Q

Metformin MOA

A

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
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60
Q

Why metformin first line

A

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

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61
Q

AE and contraindications for metformin, explain why is should not be used in conditions predisposing to tissue hypoxia

A

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

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62
Q

List thiazolidinediones

A

Pioglitazone

Rosiglitazone

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63
Q

MOA thiazolidinedione

A

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

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64
Q

Pharmacodynamics thiazolidinedione

A

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

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65
Q

Clincial use thiazolidinedione

A

Type 2 DM alone or in combo

Delay progression from prediabetes to type 2

Euglycemic (no hypoglycemia when used alone0

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66
Q

AE thiazolidinedione

A

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

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67
Q

MOA SGLT2 inhibitors

A

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

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68
Q

When use SGLT2 inhibitso,

A

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

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69
Q

AE sglt2 inhibitors

A

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)

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70
Q

List alpha glycosidase inhibitors

A

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

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71
Q

Benefit of alpha glycosidase inhibitors

A

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

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72
Q

When use alpha glycosidase inhibitor

A

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

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73
Q

AE alpha glycosidase inhibitor

A

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

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74
Q

Rapid acting insulin

A

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

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75
Q

Short acting insulin

A

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

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76
Q

Intermediate insulin

A

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

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77
Q

Long acting insulin

A

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

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78
Q

Amylin analog

A

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

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79
Q

Insulin secretagogues

A

Incretin mimetics, Katp channel blockers

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80
Q

Incretin mimetics

A

GLP1 agonists

DPP4 inhibitors

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81
Q

GLP1 agonists

A

Exenatide, liraglutide

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82
Q

DPP4 inhibitors

A

Sitagliptin, linagliptin, saxagliptin, alogliptin

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83
Q

K channel blockers

A

Sulfonylureas

Meglitinides

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84
Q

First en sulfonylureas

A

Chlorpropamide
Tolbutamide
Tolazamide

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85
Q

Second gen sulfonylureas

A

Glipizide, glyburide, glimepiride

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86
Q

Meglitinides

A

Nateglinide

Repaglinide

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87
Q

Biguanides

A

Metformin

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88
Q

Thiazolidinediones

A

Pioglitazonerosiglitazone

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89
Q

SGLT2 inhibitos

A

Canagliflozin
Dapagliflozin
Empagliflozin

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90
Q

Inhibitors of alpha glycosidase

A

Acarbose

Miglitol

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91
Q

Receptors, signaling, hypothalmic and pituitary hormones

A

Ok

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92
Q

Growth hormone

A

Ok

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93
Q

Insulin growth factor 1 agonist

A

Ok

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94
Q

Somatostatin analogs

A

Octreotide

Lamreotide

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95
Q

GH antagonists

A

Ok

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96
Q

Gonadotropin

A

FSH analogs

  • follitropin alpha and follitropin beta
  • urofollitropin

LH
-lutropin alpha

Hcg
-choriogonadotropin alpha

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97
Q

Gnrh analogs

A

Leuprolide
Gonadorelin
Goserelin, buserelin, histrelin, nafarelin, triptorelin

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98
Q

Gnrh antagonists

A

Ganerelix, cetrorelix

Degarelix, abarelix

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99
Q

Dopamine receptor agonist

A

Bromocriptine-oral (inhibit prolactin and GH)

Cabergoline-treat high levels prolactin hormone by blocking release of prolactin from pituitary.

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100
Q

Vasopressin receptor agonists

A

Vasopressin

Desmopressin

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101
Q

Vasopressin receptor antagonists

A

Conivaptan

Tolvaptan

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102
Q

Kinase linked receptors

A

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

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103
Q

Effect of kinase receptors

A

Gene expression of suppression

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104
Q

Cytokines receptor

A

No intrinsic activity

Jak stat signaling cascade for GH and prolactin receptors

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105
Q

TGFB

A

Smad

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106
Q

Compare an contrast the overall structure of main classes of endocrine receptors

A

LOOK AT TABLE IN DSA

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107
Q

**nuclear receptors and describe the events that occur after ligand binding

A

Ok

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108
Q

Figure and table in DSA diagrams signaling et works

A

Ok

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109
Q

Somatostatin analogues

A

Ocreotide lanreotide know how and when they work

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110
Q

Gonadotropins

A

Urofollitropin

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111
Q

Bromocriptine

A

Molecular mechanism…acromegaly, infertility and galactorrhea

Inhibits prolactin and growth hormone release

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112
Q

Dopamine receptor agonists used for what

A

Acromegaly, infertility and galactorrhea

Inhibits prolactin

Inhibits growth hormone release

Bromocriptine and cabergoline (blocks release of prolactin from pituitary)

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113
Q

MOA dopamine receptor agonist

A

Inhibit growth hormone release and prolactin release

Bromocriptine, cabergoline

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114
Q

Vasopressin receptor agonists

A

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

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115
Q

Vasopressin receptor antagonists

A

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

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116
Q

Nuclear receptors

A

Regulation of transcription and protein synthesis

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117
Q

Insulin receptor

A

Effectors are Tyrosine kinase, IRS-1 to IRS-4 leading to MAP kinase , PI 3-kinase, RSK signaling pathways

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118
Q

GH somatotropin on and off

A

Somatotostatin -
GHRH -

Target organ hormone or mediator is IGF-1

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119
Q

GH another name

A

Somatotropin

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120
Q

Effector molecule DH

A

IGF-1

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121
Q

SRIF

A

Somatotropin release inhibiting factor

Somatostatin

Turns off GH

Off IGF-1

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122
Q

SRIF and growth hormone

A

Negative effect

Somatostatin turns off IGF -1

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123
Q

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

A

Urofollitropin

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124
Q

Urofollitropin

A

Males-spermatogenesis requires FSH and LH

-purified from urine of postmenopausal women and gives FSH activity

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125
Q

Desmopressin

A

Treats diabetes insipidus, bedwetting, hemophilia A, Von wiliebrand, High blood urea levels.

Antidiuretic-

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126
Q

Gonadorelin

A

GnRH agonsit used in fertility medicine and to treat amenorrhea and hypogonadism

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127
Q

Goserelin

A

Suppress production of the sex hormones (GnRH agonist)

Breast and prostate cancer…..

GnRH receptor agonist and antineoplastc by suppressing LH

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128
Q

Somatotropin

A

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

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129
Q

Indications for GH

A

Turner, chronic renal failure, prayer willi syndrome, intrauterine growth restriction, and severe idiopathic short stature

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130
Q

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

A

Oxytocin

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131
Q

Oxytocin

A

Stimulates uterine contraction and augment labor

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132
Q

Dopamine

A

Stimulant drug in the treatment of severe low blood pressure, slow heart rate and cardiac arrest.. important in new born

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133
Q

Leuprolide

A

**** 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

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134
Q

Prolactin

A

Bromocriptine and cabergoline decrease prolactin levels agonsit of the receptor

Antagonist-domperidone, metoclopramide…..haloperidol, risperidone, sulpiride INCREASE PROLACTIN LEVEL

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135
Q

vasopressin

A

SIADH

Off label-tratment of vasodilators shock, GI bleeding, ventricular tachycardia, and V fib

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136
Q

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

A

Mecasermin (downstream )

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137
Q

Mecasermin

A

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

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138
Q

Bromocriptine

A

A potent agonist at D2 receptor agonist and binds serotonin receptor, inhibits glutamate release by reversing the glutamate GLT1 transporter

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139
Q

Octreotine

A

Treat acromegaly from too much GH. It is a somatostatin analog, inhibits release of GH from pituitary glans

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140
Q

Somatropin

A

Replacement therapy when treat with exogenous GH is indicated only in limited circumstance…what are they

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141
Q

Leuprolide and ganirelix

A

Ganirelix-immediately reduces gonadotropin secretion
GnRH receptors antagonist

Leuprolide-GnRH receptor agonist
-works after a week

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142
Q

Leuprolide

A

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

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143
Q

Ganirelix

A

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

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144
Q

7 year old boy successful chemo. Now excessive thirst and urination and hypernatremia

A

Desmopressin

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145
Q

Desmopressim

A

Treat DI from vasopressin defiency

Peptide agonist of V2 and V1

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146
Q

Corticotropin

A

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

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147
Q

HGC

A

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

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148
Q

Menotropins

A

HMG

Extracted from tine postmenopausal women

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149
Q

Thyrotroph

A

TSH

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150
Q

Thyroid drugs

A

Ok

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151
Q

Thyroid hormone nuclear receptor

A

TRa,B

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152
Q

Thyroid hormone receptor mediated gene activation

A

Gene activation

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153
Q

Major hormone

A

T3

RT3 no

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154
Q

Propranolol

A

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

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155
Q

Amiodarone induced thyrotoxicosis

A

50 fold higher iodine —-> toxic!!!

Commonly prescribed for arrhythmia

Releases free iodine

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156
Q

Amiodarone

A

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

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157
Q

Methimazole

A

Anti thyroid drug used to treat hyperthyroidism -thyroid gland produces excess thyroid hormone

This amide group of medications-blocks iodide organification

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158
Q

Side effects methimazole

A

Agranulocytosis, leukopenia, thrombocytopenia, aplastic anemia, liver inflammation

Use cautioslult in patients with preexisting liver disease, a history of alcohol abuse or hepatitis

159
Q

This amide Group medication

A

PTU, methimazole, carbimazole

160
Q

Methimazole is _ times more potent than PTU

161
Q

Methimazole

A

Take before thyroid surgery
-lowers thyroid hormone levels
Minimizes the effects of thyroid manipulation

Inhibits THYROPEROXIDASE

162
Q

Potassium iodide

A

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
Q

How does K iodide protect thyroid from radiation

A

Shrinks thyroid gland
Decreases thyroid hormone production

Does not affect HR or cause irregular heartbeat

164
Q

Thyrotropin

165
Q

TSH screening test

A

Most sensitive test for hyperthyroidism and primary hypothyroidism

TSH in normal limits excludes diagnoseis

166
Q

PTU indications for use

A

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
Q

MOA PTU

A

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
Q

Levothyroxine

A

Treat thyroid hormone defiency

Manufactures from thyroid hormone->T4

169
Q

AE levothyroxine

A

Weight loss, througble tolerating heat, sweat, anxiety, trouble sleeping, tremor, fast HR,

170
Q

What drugs impair levothyroxine

A

Cholestyramine

171
Q

Radioactive iodine therapy for thyroid cancer contraindicated in

A

Pregnant women

172
Q

Atenolol for hyperthyroidism

A

Propranolol is the most widely studies and used in thyrotoxicosis

Clinical improvement of hyperthyroid

Do not alter thyroid hormone levels

173
Q

MOA bb

A

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
Q

Indication bb

A

Graves

Thyroid storm

175
Q

Perchlorate blocking agent

A

Inhibited thyroid hormone production by blocking sodium iodide symporter (NIS)

176
Q

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

A

Activates the thyroid gland TSH receptor and stimulates thyroid hormone synthesis and release

177
Q

Graves antibodies

178
Q

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

A

Preventing the addition of iodine to tyrosine residues on thyroglobulin

179
Q

Levo

A

Check T3 and T4 through out to see if up or decrease dose

180
Q

Methimazole and PTU

A

Act in thyroid cells to prevent conversion of tyrosin residues in thyroglobulin to MIT or DIT

181
Q

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

A

Agranulocytosis
-most dangerous AE of thiazides is agranulocytosis

Can also get vasculitis, hepatic damage, and hypothrombinemia

182
Q

Adrenal corticosteroid drugs

183
Q

Inner zone reticularis

A

Secretes DHEA and its sulfate derivatives DHEA-S.

Converted to DHEA in periphery by DHEA sulfatase

184
Q

Fate of DHEA in women and men

A

Converted into potent androgens in males

Converted in estrogens for females

185
Q

How do corticosteroids work

A

Ligand activated transcription factors that modulate gene expression

186
Q

Aldosterone and cortisol bind ___ with equal affinity

187
Q

Agonists corticosteroids

A

Glucocorticoids (prednisone)

Mineralocorticoids (fludrocortisone

188
Q

Antagonists corticosteroid

A

Receptor antagonists (glucocorticoid antagonists (mifepristone), mineralocorticoids antagonists (spironolactone)

Synthesis inhibitors (ketoconazole)

189
Q

What give if have agranulocytosis

190
Q

Adrenal corticosteroids

A

Receptor independent mechanisms of corticosteroid specificity

Decreased activity/inhibition of this enzyme 11B-HSD2 results in excessive activation of MR

191
Q

Known inhibitors of 11B HSD2

A

Glycyrrhizin (licorice root extract)

Carbenoxolone (UK approved for esophageal ulcers)

192
Q

Licorice

A

Increase activity of cortisol 2 MR

Leads to Na and H2O retention , K loss,

Increase in BP

193
Q

Carbohydrate metabolism

A

Gluconeogenesis

Glucose output

Glycogen synthesis

Decreased glucose uptake development of hyperglycemia

194
Q

Lipid metabolism

A

Increase lipolysis

FFA and glycerol into the gluconeogenesis pathway

Lipogenesis

Fat deposition

Change fat distribution

195
Q

Protein metabolism

A

Decrease aa uptake

Decreased protein synthesis

Dev of myopathy and msucle wasting

196
Q

Anti-insulin action of _____

A

Glucocorticoids

197
Q

Anti insulin action of glucocorticoids

A

Liver increase gluconeogenesis

Skeletal msucle
Decrease glucose intake
Decrease glycogen synthetase
Increase proteolytic

Adipose tissue
Decrease glucose uptake
Increase lipolysis

HYPERGLYCEMIA

198
Q

Effects of glucocorticoids on immune system and inflammation

A

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
Q

AE glucocorticoids and immune system and inflammation

A

Decreased inflammation and its manifestations

Immune suppression

Decreased allergic/hypersensitivity reactions

200
Q

Common clinical applications: endocrine conditions

A

Replacement therapy

-primary adrenal insuffiency (Addison’s disease)-a combination of glucocorticoid (hydrocortisone) and mineralocorticoids (fludrocortisone)

Congenital adrenal hyperplasia-hydrocortisone+ fludrocortisone

201
Q

Common NON ENDOCRINE ADRENAL APPLICATIONS

A

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
Q

Short acting glucocorticoids

A

Short to medium acting (<12 hours)

  • hydrocortisone (cortisol)
  • cortisone
  • prednisone
  • prednosolone
  • methylprednisonlone
203
Q

Intermediate acting glucocorticoids

A

12-36 horus

Triamcinolone

204
Q

Long acting glucocorticoids

A

> 36 hours

Betamethasone

Dexamethasone

205
Q

Prednisone MOA

A

Activation of GR alters gene transcription

206
Q

Clinical applications prednisone

A

Many inflammatory conditions, organ transplantation, hematologic cancers

207
Q

Pharmacokinetics prednisone

A

Duration of activity is longer than pharmacokinetic t1/2 of drug owing to gene transcription effects

208
Q

Toxicities, drug interactions prednisone

A

Adrenal suppression, growth inhibition, muscle wasting, osteoporosis, salt retention, glucose intolerance, behavioral changes

209
Q

Dosing adrenalocorrticoid drugs

A

Use lowest dose for the shortest duration possible depending on the condition
-use intermediate or short acting vs long acting drugs

210
Q

Route of adrenalocorticoid drugs

A

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
Q

When give adrenalcorticoid

A

Single in AM

Every other day-short course pulse therapy administration

212
Q

Dose tapering adrenalocorticoid

A

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
Q

AE prolonged use at high doses adrenalcorticoid /cushing disease

A

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
Q

Who should not use corticosteroid drug advisory

A

Immunocompromised (HIV/AIDS)

Diabetics

Patients with infections

Patients with peptic ulcers

Patients with cardiovascular conditions

Patients with psychiatric conditions

Patients with osteoporosis

Children

215
Q

Mifepristone MOA

A

Pharmacological antagonist of glucocorticoid and progesterone receptors

216
Q

Clinical application glucocorticoid receptor antagonist

A

Medical abortion and very rarely for cushing syndrome

217
Q

Pharmacokinetics mifepristone

218
Q

AE mifepristone

A

Vaginal bleeding in women, abdominal pain, GI upset, diarrhea, headache

219
Q

Mineralocorticoids

A

Fludrocortisone

220
Q

MOA fludrocortisone

A

Strong agonist at mineralocorticoids receptors and activation of glucocorticoid receptors

221
Q

Clinical applications mineralocorticoids

A

Adrenal insuffiency (addison)

222
Q

Pharmacokinetics fludocortisone

A

Long duration of action

223
Q

AE fludrocortisone

A

Salt and fluid retention, CHF, signs and symptoms of glucocorticoid excess

224
Q

Mineralocorticoids receptor antagonist

A

Spironolactone

225
Q

MOA spironlactone

A

Pharmacological antagonist of mineralocorticoids receptor, weak antagonism of androgen receptors

226
Q

Clinical application spironolactone

A

Aldosteronism from any cause , hypokalemia due to diuretic effect, post myocardial infarction

227
Q

Pharmacokinetics spironolactone

A

Slow onset and offset; duration 24-28 hr

228
Q

Toxicities spironolactone

A

Hyperkalemia, gynecomastia, additive interaction with other K retaining drugs

229
Q

Synthesis inhibitors

A

Ketaconazole

230
Q

MOA ketoconazole

A

Blocks fungal and mammalian CYP450 enzymes

231
Q

Clinical applications ketoconazole

A

Inhihibits mammalian steroid hormone synthesis and fungal ergosterol synthesis

232
Q

Pharmacokinetics ketaconazole

A

Oral, topical ad

233
Q

AE ketoconazole

A

Hepatic dysfunction, many drug drug CYP450 interactions

234
Q

Why are glucocorticoids given in endocrine practice

A

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
Q

What use glucocorticoids to treat

A

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
Q

Delta-4,3-keto-11-beta,17 alpha, 21 trihydroxyl configuration

A

Required for glucocorticoid activity and is present in all natural and synthetic glucocorticoids.

237
Q

Addition of a double bond between the 1 and 2 positions of hydrocortisone (cortisol) yields

A

Prednisolone, which has 4 times more glucocorticoid activity than cortisol

238
Q

Pharmacokinetics glucocorticoids

A

Bound to CBG and albumin (2/3) or circulate free (1/3)

239
Q

HL glucocorticoids

A

80 minutes-cortisol

Longer i bound

240
Q

Where is the 11 beta HS dehydrogenase type 1 enzyme found that converts inactive cortisone to cortisol

A

Many target tires

241
Q

Where is type 2 isoenzyme which converted cortisol to cortisone

A

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
Q

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

A

Protected from oxidation inactivation by the type 2 isoenzyme

243
Q

Prednisone

A

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
Q

Polymorphism in MDR-1 gene may influence the therapeutic response to steroids

A

Many glucocorticoids are both substrates for P-glycoproteins mediated efflux from cells, and inducers of P glycoproteins production

245
Q

Polymorphism in the glucocorticoid receptor gene ma increase or decrease sensitivity to glucocorticoids and, thus,

A

affect the response to both endogenous cortisol and exogenous agents

246
Q

Metabolism glucocorticoids

A

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
Q

Like cortison, which must be converted to cortisol by hepatic 11-b-HS DH, prednisone must be converted to ____ to exert any glucocorticoid action

A

Prednisolone

248
Q

Medical emergencies where use glucocorticoid

A

High doses for a few days-safe just for a few days

249
Q

Chronic therapy glucocorticoids

A

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
Q

Prednisone 5 mg/day

251
Q

When give high parenteral therapy

A

Septic shock and severe acute asthma

252
Q

IV bolus methylprednisone

A

Have been used to treat transplant rejection and some autoimmune diseases such as RA

253
Q

Pulse glucocorticoid

A

Impair cytokine generation

254
Q

High doses and membranes

A

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
Q

Oral

A

Chronic therapy

Absorbed in 30 min

256
Q

Why nonsystemic administration

A

Deliver higher local concentrations while minimizing systemic exposure .

257
Q

Intraarticular injection

A

Joint inflammation

258
Q

Inhalation therapy

259
Q

Topical application

A

Inflammatory skin disorders

260
Q

Hydrocortisone salts injected

A

IM in minutes absorbed

Esters absorbed in hour

261
Q

Cortison acetate absorption

262
Q

Triamcinolone salts and esters

263
Q

All topical and inhaled glucocorticoids problems

A

Systemic absorption potential HPA issue like cushing

264
Q

Inhaled fluticasone propionate

A

Greater systemic absorption and a greater association with adrenal suppression

265
Q

Areas of body where absorbed more

A

Intertriginous areas> forehead>scalp>face>forearm

266
Q

Why infants and kids absorb more

A

Striatum corneum much thinner

267
Q

What vehicle increases absorption

A

Urea, dimethylsulfoxide,

268
Q

Prednisone in morning why

A

Doesn’t suppress the circadian peak in cortisol secretion the next morning.

269
Q

Alternate day regimes

A

Alleviate effects

Thrice hte usual daily dose

Unsuccessful…

270
Q

Major systemic side effects glucocorticoid

A

Suppression of HPA function and Cushing

271
Q

Both exogenous and endogenous glucocorticoids exert a negative feedback control on HPA

A

Suppress CRH and ACTH

Adrenal atrophy and loss of cortisol secretory capability

272
Q

Iatrogenic cushing syndrome

A

Development of cushing syndrome depends upon the dose, timing and duration of glucocorticoid adminsitration and varies among patients

273
Q

How minimize effects

A

Exercise, calcium, VD, bisphosphonates, estrogen therapy,

274
Q

MHT

A

Menopausal hormone therapy

275
Q

Primary therapy for menopausal symptoms

A

Estrogen with/without progestin

*women with an intact uterus must also be on progestin

276
Q

AE estrogen

A

Endometrial hyperplasia/carcinoma from unopposed tissue proliferation with prolonged duration

277
Q

Benefit of MHT perimenopause-transition period(before 12 months)

A

Hormone regulation and pregnancy protection

278
Q

Estrogens

A

Estradiol

Conjugated estrogens

Esterified estrogens

Estropipate

279
Q

Estradiol

A

Acetate form and cypionate form

280
Q

Conjugated estrogens

A

Blend of at least 6 known estrogen derivatives

-derived from estrogens found in urine of pregnant mares

281
Q

Esterified estrogens

A

Combination of na estrone sulfate and na equaling sulfate

282
Q

Estropipate

A

Crystalline estrone solubilized with sulfate and stabilized with piperazine

283
Q

Progetinic

A

Medroxyprogesterone (MPA)

Methyltestosterone

Progesterone

284
Q

MPA

285
Q

Methyltestosterone

A

Alone or with EE

286
Q

Progesterone

287
Q

MO ESTROGEN

A

BIND ER A/B IN VARIOUS TISSUES, TRANSFERRED INTO NUCLEUS RESULTING IN INCREASED GENE AND PROTEIN EXPESSION

288
Q

Why women on estrogen must be on progestin if have in tact uterus

A

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
Q

Estrogen effects

A

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
Q

Women’s health initiative study

A

Examine MHT purported beneficial or preventative effects on heart disease, osteoporosis related fractures and risk of cancer

291
Q

Estrogen use alone good and bad

A

Good less breast cancer, fractures and diabetes

More dementia, gallbladder disease, stroke, venous thromboembolism, urinary incontinence

292
Q

Estrogen and progesterone good and bad

A

Good-less diabetes, fractures, colorectal cancer

Harms
Breast cancer, CAD, dementia, gallbladder disease,stroke, venous thromboembolism, urinary incontinence

293
Q

Summary WHI

A

MHT very effectively minimizes/treats vasomotor symptoms and vaginal changes

294
Q

No use MHT

A

Don’t use to prevent CVD or dementia

295
Q

Benefit on bone and colon cancer of estrogen

A

Outweighed by other risks

296
Q

When use estrogen to prevent osteoporosis

A

When at significant risk

297
Q

Should estrogen be used to treat colon cancer

A

Not solely

298
Q

For young women MHT

A

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
Q

MHT for women with vaginal symptoms

A

The preferred treatments are low doses of vaginal estrogen

300
Q

MHT for women with a uterus

A

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
Q

MHT women at risk of blood/clots/stroke

A

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
Q

MHT women at risk of breast cancer

A

An icnreased risk of breast cancer seen within 3-5 years of continuous estrogen with progestin therapy

303
Q

Risks and benefits stop ___ years after MHT is stopped

304
Q

MHT take home if therapy needed for moderate severe vasomotor symptoms

A

Use lowest dose

Treat for the shortest duration possible and re evaluate at least yearly for ongoing need for therapy

305
Q

When use vaginal estrogen

A

Vaginal dryness free of Brest cancer, endometrial cancer and hormone sensitive cancer

306
Q

Serm tsecs

A

Selective estrogen receptor modulators

Tissue selective estrogen complexes

307
Q

Serm

A

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
Q

Tsec

A

Combines the unique elements of a serm with an estrogen compound

309
Q

Serms

A

Ospemifene

Clomiphene

310
Q

Tsecs

A

Basedoxifene (only as combo with ce)

311
Q

Ospemifene indication

A

Moderate to severe dyspareunia

A symptom of vulvar and vaginal atrophy or menopause

312
Q

MOA osemifene

A

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
Q

AE ospemifene

A

Worsening of hot flashes/sweating

Estrogenic-similar effects on coagulation

Endometrial thickening and even hyperplasia

314
Q

Contraindications ospemifene

A

Unusual/abnormal vaginal bleeding

Thromboembolic diseases-CVA/MI/VTE/PE/DVT
-exercise caution in use in smokers

Estrogen related neoplasia
-uterine/ovarian/breast

315
Q

Bazedoxifene w/ce for women with intact uterus indications

A

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
Q

MOA bazedoxifene w/ ce

A

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
Q

AE bazedoxifene w/ce

A

All estrogen related effects (due to ce component

-worsening hot flashes/sweating

318
Q

Contraindication bazedoxifene

A

In all situations estrogens are…due to ce

319
Q

Anti estrogens

A

Clomiphene

320
Q

Indications for clomiphene

A

Infertility in anovulatory women

321
Q

MOA clomiphene

A

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
Q

AE clomiphene

A 
Multiple births (twins)
Ovarian cysts
-cancer with prolonged use(May limit to 3 cycles)

Hot flashes

Lateral phase dysfunction
-inadequate progesterone production

323
Q

Induction of labor/control postpartum bleeding

A

Misoprostol

Dinoprostone

Carboprost

Oxytocin

Ergot alkaloids

324
Q

Corticosteroids

A

Cortisol
Betametaons
Dexamethasons

325
Q

Delay labor (tocolysis)

A

Terbutaline

Indomethacin

Nifedipine

Mgso4

Atosiban

326
Q

Maintain pda

A

Alprostadil

327
Q

Close pda

A

Indomethacin

Ibuprofen

328
Q

Anti hypertensive preg

A

A methyldopa

Labetalol

Hydralazine

Na nitroprusside

329
Q

Misoprostol

A

Synthetic prostagladin e1 analog

330
Q

Effects misoprostol

A

Replacing PG loss in stomach during NSAID therapy

Induce uterine contraction

Maintain pda

331
Q

Indications misoprostol

A

NSAID induced gastric ulcers

Termination of intrauterine preg if <70 days with mifepristone

Off label cervical ripen labor induction

332
Q

Contraindications misoprostol

A

Preg unless abort, previous c section

333
Q

AE misoprostol

A

N/v, diarrhea, chills, pain

Tachysystole(uterine contractions rapid), prolonged uterine contractions
Fetal-hypoxia from tachysyssole or prolonged uterine contractions

334
Q

Dinoprostone

A

Prostagladins e2 analog

335
Q

Effects dinoprostone

A

Induces uterine contractions

Cervical ripen

336
Q

Indication dinoprostone

A

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
Q

AE dinoprostone

A

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
Q

Carboprost

A

Prostagladin f2a analog

339
Q

Effects carboprost

A

Induces uterine contractions, prolonged duration fo action

340
Q

Indication carboprost

A

Abortion 13-20 weeks

Post partum hemostasis

341
Q

How given carboprost

342
Q

Contraindications carboprost

A

Hypersensitivity, acute PID, cardiac, hepatic

343
Q

AE carboprost

A

HTN pulmonary edema, child shivering, dizzy gagging retching

344
Q

Oxytocin

A

Posterior pituitary hormone

345
Q

Effects oxytocin

A

Increases force, frequency, and duration of uterine contractions by binding G protein

Increase milk ejection

346
Q

Indication oxytocin

A

Labor induction

Post partum hemostasis

347
Q

Contraindications oxytocin

A

Lungs not mature

Cervix not ripe

348
Q

AE oxytocin

A

Water intoxication

349
Q

Ergot alkaloids

A

Ergonocine, ethyl ergonocine

Stimulates adrenergic ,dopaminergic, and serotonergic receptors

350
Q

Effect ergot alkaloids

A

Dose dependent on uterus causes prolonged tonic uterine contractions

Vascular construction arterioles and veins

351
Q

Indications ergot alkaloids

A

Post partum use o increase tone and decrease bleeding

Augment labor but not recommended

Migraine

352
Q

Contraindications ergot alkaloids

A

HTN, hypersensitivity

353
Q

AE ergot alkaloids

A

HTN, n/v HA

St Anthony’s fire…mania, psychosis

Dry gangrene

354
Q

Prostagladins

A

Ripen

Can cause uterine contractions any time during preg-abortion

355
Q

Oxytocin

A

During labor and delivery

Helps with post partum bleeding

356
Q

Ergot alkaloids

A

Second choice for limiting post partum bleeding

357
Q

Need time for corticosteroids to trigger surfactant productions nd brain maturation

A

Tocolytics

358
Q

<24 weeks

A

Single corticosteroid course

359
Q

24-32 weeks

A

Group b strep prophylaxis
Single corticosteroid course
Antimicrobials
Mg sulfate

360
Q

23-24 weeks

A

Group b strep prophylaxis
Single corticosteroid course
Antimicrobials to prolong latency

361
Q

> 34 weeks

A

Group b strep prophylaxis

Single corticosteroid

362
Q

Indications antenatal corticosteroids

A 
Women 24-36 weeks of gestation with 
-threatened pre term labor
Antepartum hemorrhage
Preterm rupture of membranes
Conditions requiring c section
363
Q

Betamethasone

A

Two IM injections 24 hr interval

364
Q

Dexamethasone

A

Four doses by IM injection

12 hr intervals

365
Q

Betamethasone dexamethasone

A

Induces transcription of surfactant proteins in alveolar the 2 pneumocytes

366
Q

Riot drone

A

B2 agonist tocolysis

367
Q

AE ritodrine

A

Severe hallucinations

368
Q

Mg sulfate

A

Present eclampsia seizures

Long term drug for tocolysis
-not really used

369
Q

MOA mg sulfate

A

Inhibit ach release at uterine neuromuscular junction

370
Q

AE mg sulfate

A

Skin flushing,palpitations, HA, depressed reflexes, respiratory depression, impaired cardiac conduction

Fetal-muscle relaxation, rarely cns depression

371
Q

Terbutaline

A

Increases camp, ends to K channel mediated hyperpolarization, dephosphorylation of myosin light chain

372
Q

Contraindications tertbutaline

A

Cardiac arrhythmias, poorly controlled thyroid disease or DM

373
Q

AE tertbutaline

A

Cardiac arrhythmias, pulmonary edema, MI, hypotension, sob

Baby-tachycardia, hyperinsulinism is, hyperglycemia, hypoglycemia,

374
Q

Evidence tertbutaline

A

Delays labor 2-7 days

375
Q

Nifedipine

A

Blocks ca influx through voltage gated ca channels, less ca means less contraction

376
Q

Contraindications nifedipine

A

Cardiac disease, renal disease, HTN, dont use with mg sulfate

377
Q

AE nifedipine

A

Flushing, HA, dizzy, nausea, hypotension, tachycardia

No fetal side effects

378
Q

Evidence nifedipine

A

Calcium channel blockers are preferable to other tocolytic agents compared

379
Q

Indomethacin moa

A

Blocks synthesis of PGF2a, a potent stimulator of uterine contractions

380
Q

Contraindications indomethacin

A

Renal or hepatic impairment

381
Q

AE indomethacin

A

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
Q

Evidence indomethacin

A

Insufficient

383
Q

Nitroglycerin contraindications

384
Q

AE nitroglycerin

A

HA, hypotension, neonatal hypotension.

385
Q

Atosiban moa

A

Blocks action of oxytocin,

386
Q

Contraindications atosiban

387
Q

AE atosiban

A

Ha n, allergic reaction

388
Q

Atosiban evidence

A

Doesn’t work

389
Q

Best choice for tocolytics

A

Nifedipine or indomethacin DONT COMBINE

390
Q

PDA

A

Should close in a few days from constriction caused by increased oxygen tension

Decrease circulating pge2 sue to its metabolism in lungs

391
Q

Alprostadil

A

Pge1 maintains pda

392
Q

Indications alprostadil

A

Pre term infants with congenital heart defects
-mature to cope with surgery

Heart defects need to keep open for keeping flow

393
Q

AE alprostadil

394
Q

First line htn preg

A

Methyldopa and labetalol

Pharmacology (52 decks)

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