Endocrine

Front 1

treatment of type I diabetes

Back 1

low-sugar diet, insulin replacement

Front 2

type II diabetes

Back 2

dietary modification, exercise, wl, oral hypoglycemics and insulin replacement

Front 3

insulin lispro

Back 3

rapid acting
Action: Bind insulin receptor (tyrosine kinase activity).
Liver: increase glucose stored as
glycogen.
Muscle: increase glycogen and
protein synthesis, K+uptake.
Fat: aids TG storage.

Clinical use:
Type I DM, type 2 DM , gestational diabetes, Iife-threatening hyperkalemia, and stress-induced hyperglycemia.

Toxicities: hypoglycemia, hypersensitivity reaction (very rare)

Front 4

insulin aspart

Back 4

rapid-acting
Action: Bind insulin receptor (tyrosine kinase activity).
Liver: increase glucose stored as
glycogen.
Muscle: increase glycogen and
protein synthesis, K+uptake.
Fat: aids TG storage.

Clinical use:
Type I DM, type 2 DM , gestational diabetes, Iife-threatening hyperkalemia, and stress-induced hyperglycemia.

Toxicities: hypoglycemia, hypersensitivity reaction (very rare)

Front 5

regular insulin

Back 5

rapid-acting
Action: Bind insulin receptor (tyrosine kinase activity).
Liver: increase glucose stored as
glycogen.
Muscle: increase glycogen and
protein synthesis, K+uptake.
Fat: aids TG storage.

Clinical use:
Type I DM, type 2 DM , gestational diabetes, Iife-threatening hyperkalemia, and stress-induced hyperglycemia.

Toxicities: hypoglycemia, hypersensitivity reaction (very rare)

Front 6

NPH insulin

Back 6

intermediate acting
Action: Bind insulin receptor (tyrosine kinase activity).
Liver: increase glucose stored as
glycogen.
Muscle: increase glycogen and
protein synthesis, K+uptake.
Fat: aids TG storage.

Clinical use:
Type I DM, type 2 DM , gestational diabetes, Iife-threatening hyperkalemia, and stress-induced hyperglycemia.

Toxicities: hypoglycemia, hypersensitivity reaction (very rare)

Front 7

insulin glargine

Back 7

long-acting
Action: Bind insulin receptor (tyrosine kinase activity).
Liver: increase glucose stored as
glycogen.
Muscle: increase glycogen and
protein synthesis, K+uptake.
Fat: aids TG storage.

Clinical use:
Type I DM, type 2 DM , gestational diabetes, Iife-threatening hyperkalemia, and stress-induced hyperglycemia.

Toxicities: hypoglycemia, hypersensitivity reaction (very rare)

Front 8

insulin detemir

Back 8

long-acting
Action: Bind insulin receptor (tyrosine kinase activity).
Liver: increase glucose stored as
glycogen.
Muscle: increase glycogen and
protein synthesis, K+uptake.
Fat: aids TG storage.

Clinical use:
Type I DM, type 2 DM , gestational diabetes, Iife-threatening hyperkalemia, and stress-induced hyperglycemia.

Toxicities: hypoglycemia, hypersensitivity reaction (very rare)

Front 9

tolbutamide

Back 9

Sulfonylurea; first generation
Action: Close K+ channel in B-cell membrane, so cell depolarizes --> triggering of insulin release vie increased Ca2+ influx

Clinical use:
Stimulate release of endogenous insulin in type 2 DM. Requires some islet function, so USELESS IN TYPE I DM.

Toxicities: disulfiram like effects

Front 10

chlorpropamide

Back 10

Sulfonylurea; first generation
Action: Close K+ channel in B-cell membrane, so cell depolarizes --> triggering of insulin release vie increased Ca2+ influx

Clinical use:
Stimulate release of endogenous insulin in type 2 DM. Requires some islet function, so USELESS IN TYPE I DM.

Toxicities: disulfiram like effects

Front 11

Glyburide

Back 11

Sulfonylurea, Second generation
Action: Close K+ channel in B-cell membrane, so cell depolarizes --> triggering of insulin release vie increased Ca2+ influx

Clinical use:
Stimulate release of endogenous insulin in type 2 DM. Requires some islet function, so USELESS IN TYPE I DM.

Toxicities: hypoglycemia

Front 12

Glimepiride

Back 12

Sullfonylurea, Second generation
Action: Close K+ channel in B-cell membrane, so cell depolarizes --> triggering of insulin release vie increased Ca2+ influx

Clinical use:
Stimulate release of endogenous insulin in type 2 DM. Requires some islet function, so USELESS IN TYPE I DM.

Toxicities: hypoglycemia

Front 13

Glipizide

Back 13

Sulfonylurea, Second generation
Action: Close K+ channel in B-cell membrane, so cell depolarizes --> triggering of insulin release vie increased Ca2+ influx

Clinical use:
Stimulate release of endogenous insulin in type 2 DM. Requires some islet function, so USELESS IN TYPE I DM.

Toxicities: hypoglycemia

Front 14

Metformin

Back 14

Biguanide
Action: Exact mechanism is unknown. decreased gluconeogenesis, increased glycolysis, increased peripheral glucose uptake (insulin sensitivity).

Clinical use:
Oral
can be used in patients WITHOUT islet function

Toxicities: Most grave adverse effect is lactic acidosis (CI in renal failure) - lactate is taken up into liver for gluconeogenesis, which is inhibited by metformin, therefore it builds up in the blood.

Front 15

Pioglitazone

Back 15

glitazones/thiazolidinediones
Action: Increase insulin sensitivity in peripheral tissues (by causing a release of adipnectin from adipocytes). Binds to PPAR-gamma nuclear transcription regulator.
Overall decreased gluconeogenesis and increased uptake in muscle.

Clinical use: Used as monotherapy in type 2 DM or combined with other agents.

toxicity: weight gain, edema, hepatotoxic. CI in class III/IV HF

Front 16

Rosiglitazone

Back 16

glitazones/thiazolidinediones
Action: Increase insulin sensitivity in peripheral tissues (by causing a release of adipnectin from adipocytes). Binds to PPAR-gamma nuclear transcription regulator.
Overall decreased gluconeogenesis and increased uptake in muscle.

Clinical use: Used as monotherapy in type 2 DM or combined with other agents.

toxicity: weight gain, edema, hepatotoxic. CI in class III/IV HF

Front 17

Acarbose

Back 17

alpha-glucosidase inhibitors
Action: Inhibit intestinal brush border alpha-glucosidases. Delayed sugar hydrolysis and glucose absorption leads to DECREASED postprandial hyperglycemia.

Clinical use: used as a monotherapy in type 2 DM or in combo.

toxicity: GI disturbances

Front 18

Miglitol

Back 18

alpha-glucosidase inhibitors
Action: Inhibit intestinal brush border alpha-glucosidases. Delayed sugar hydrolysis and glucose absorption leads to DECREASED postprandial hyperglycemia.

Clinical use: used as a monotherapy in type 2 DM or in combo.

toxicity: GI disturbances

Front 19

Pramlintide

Back 19

amylin mimetic
Action: decreases release of glucagon
Clinical use: type 2 DM
toxicities: hypoglycemia, nausea, diarrhea

Front 20

Exenatide

Back 20

GLP-1 analog
Action: increases insulin by stimulating release from beta cells
decreases glucagon release
slows gastric emptying

clinical use: type 2 DM

toxicities: nausea, vomiting, pancreatitis

Front 21

propylthiouracil

Back 21

Mechanism: inhibit organification of iodide (I- --> I) and coupling (iodination) of thyroid hormone synthesis.
Also decreases peripheral conversion of T4 to T3 (methimazole does not)
Clinical use: hyperthyroidism
Toxicity: skin rash, agranulocytosis (rare severe and dangerous leukopenia), aplastic anemia

Front 22

methimazole

Back 22

Mechanism: inhibit organification of iodide (I- --> I) and coupling (iodination) of thyroid hormone synthesis.
Clinical use: hyperthyroidism
Toxicity: skin rash, agranulocytosis (rare severe and dangerous leukopenia), aplastic anemia
Possible teratogen (PTU is not)

Front 23

levothyroxine

Back 23

T4
Mechanism: thyroxine replacement
Clinical use: hypothyroidism, myxedema
Toxicity: tachycardia, heat intolerance, tremors, arrhythmias

Front 24

triiodothyronine

Back 24

T3
Mechanism: thyroxine replacement
Clinical use: hypothyroidism, myxedema
Toxicity: tachycardia, heat intolerance, tremors, arrhythmias

Front 25

GH

Back 25

GH deficiency
Turner's

Front 26

Somatostatin (octreotide)

Back 26

acromegaly
carcinoid
gastrinoma
glucagonoma

Front 27

oxytocin

Back 27

stimulates labor
uterine contractions
milk let-down
controls uterine hemorrhage

Front 28

ADH (desmopressin)

Back 28

pituitary (central) DI

Front 29

Demeclocycline

Back 29

Mechanism: ADH antagonist (a tetracycline antibiotic)
clinical use: SIADH
toxicity: nephrogenic DI, photosensitivity, abnormalities of bone and teeth

conivaptan also used to treat SIADH

Front 30

Hydrocortisone
Prednisone
Triamcinolone
dexamethasone
beclomethasone

Back 30

Mechanism: decrease the production of leukotrienes and prostaglandins by inhibiting PLA2 and expression of COX2.
Clinical use: Addison's disease, inflammation, immune suppression, asthma.
Toxicity: Iatrogenic Cushing's syndrome - buffalo hump, moon facies, truncal obesity, muscle
wasting, thin skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes (if chronic - GCs are primarily catabolic; also increase the enzymes for gluconeogenesis and glycogen synthesis, thereby antagonizing insulin, leading to hyperglycemia).
Adrenal insufficiency when drug stopped after chronic use.