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Diabetes drug classes (8) MOA insulin

Rapid-acting insulin Biguanides


Short-acting insulin Biguanides MOA
Intermediate-acting
insulin
Clinical use of biguanides
Long-acting insulin Biguanide toxicity
1a
Bind insulin receptor --> Tyr kinase
-->
Liver: Glycogenesis
Muscle: Increases glycogen and
protein synthesis + K uptake
Fat: aids TG storage
Insulin, biguanides, sulfonylureas,
Glitazones/ thiazolidinediones,
alpha-glucosidase inhibitors, amylin
analogs, GLP-1 analogs, DPP-4
inhibitors
Metformin Lispro, Aspart, Glulisine
Overall decreases gluconeogenesis,
and increases insulin
sensitivity (=> increased
peripheral glucose uptake =>
increased glycolysis)
Regular insulin
Oral
DOC in T2D
Can be used in pts w/o
islet function
NPH
Lactic acidosis - CI in
renal failure
Gi upset
Glargine, Setermir
1b
Sulfonylureas: first-gen
Glitazones/
thiazolidinediones
Sulfonylureas: second-gen
Glitazones/
thiazolidinediones: MOA
Sulfonylureas: MOA
Glitazones/
thiazolidinediones
toxicities
Sulfonylureas: Clinical
use
Alpha-glucosidase
inhibitors
Sulfonylureas: toxicity
Alpha-glucosidase
inhibitors: MOA
2a
-"glitazone"
Tolbutamide,
Chlorpropramide
Bind and activa PPAR-y (nuclear
transcription regulator) --> increased
levels of adiponectin + increased insulin
sensitivity in peripheral tissues
Note: genes activated by PPARy regulate
fatty acid storage and glucose metabolism
Glyburide, Glimepiride,
Glipizide
Weight gain, edema
Hepatotoxic
Heart failure
Close K channels in beta-
cells --> cell depolarizes --
> triggers insulin release
via Ca influx
Acarbose
Miglitol
T2D: stimulate release of
endogenous insulin
T1D: useless (bc require
some islet function)
Inhibit brush-border alpha-
glucosidases => delayed sugar
hydrolysis and glucose
absorption --> decreased post-
prandial hyperglycemia
1st-gen: disulfiram-
like effects
2b
Amylin analogs DPP-4 inhibitors: MOA
GLP-1 analogs
PTU or methimazole:
MOA
GLP-1 analogs: MOA
PTU or methimazole:
clinical use
GLP-1 analogs: toxicity
PTU or methimazole:
Toxicity
DPP-4 inhibitors
Levothyroxine/
triiodothyronine: MOA
3a
Increase insulin, decrease
glucagon
Pramlintide
Block TPO => no organification of
iodide, no coupling of thyroid
hormine synthesis
PTU also blocks 5'deiodinase =>
decreased peripheral conversion of
T4 to T3
Exenatide, Liraglutide
Hyperthyroidism
Increase insulin, decrease
glucagon
Aplastic anemia
Hepatotoxic (PTU)
Teratogen (Methimazole)
Pancreatitis
Thyroxine replacement -"gliptin"
3b
Levothyroxine/
triiodothyronine: clinical
use
Toxicity of demeclocycline
Clinical use of GH Glucocorticoids
Clinical use of
somatostatin (octreotide)
Glucocorticoids MOA
Clinical use of Oxytocin
Glucocorticoids clinical
use
Clinical use of
demeclocyline
Glucocorticoids toxicity
4a
Nephrogenic DI
Photosensitivity
Bone/ teeth abnormalities
Hypothyroidism
Myxedema
-"sone"
Triamcinolone
GH deficiency
Turner syndrome
Decreased LT and PG
production by blocking
PLA2 and COX
expression
Acromegaly
Carcinoid, Gastrinoma
Glucagonoma
Esophageas varicies
Addison's
Inflammation
Immune suppression
Asthma
Stimulate labour (uterine
contractions)
Milk let-down
Prevents uterine hemorrhage
Iatrogenic Cushing's syndrome (see
FA13 p 305 for details)
Adrenal insufficiency if stopped after
chronic use (bc adrenals stopped making
endogenous steroids when exogenous
were being provided)
SIADH (bc ADH
antagonist, part of
tetracycline family)
4b

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