[PHARMA] ANTI-DIABETICS Flashcards by Aseel Maher

1st line therapy in T2DM

Metformin + lifestyle modifications

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secretagogues

sulfonylureas
non-sulfonylureas

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sensitizers

metformin
Tzds (Pioglitazone)

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α-glucosidase inhibitor

acarbose

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SGLT2 inhibitors

canagliflozin

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DPP4 inhibitors

Sitagliptin

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GLP1 agonists

Liraglutide

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Sulfonylureas chronic use leads to

↓Glucagon

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sulfonylureas mechanism of action

↑insulin secretion via
binds to β-cell receptors–> (-) ATP-sensitive K+channels=↓K+ efflux=depolarization=Ca++ influx via voltage gated channels= INSULIN RELEASE

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sulfonylureas indications

T2DM
(if initial therapy fails/ metformin is CI)

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sulfonylureas 1st generation disadvantage

↑PPB= ↑ adverse effects + drug interaction

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sulfonylureas 2nd generation advantages

-↑receptor affinity= 150x more potent
-less adverse effects & interactions

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sulfonylureas CI (5)

1-T1DM
2-DM w/ pregnancy & lactation
3-DM w/ stress
4-DM w/ renal or liver disease
5-past history of sulfa allergy

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sulfonylureas CI in pregnancy & lactation because

cross placenta & excreted in milk—>hypoglycemia in fetus

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sulfonylureas CI in T1DM because

needs functioning Beta-cells

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sulfonylureas CI in DM w/ stress because (3)

-ineffective
-stress ↑ insulin requirements
-ketoacidosis liable to occur

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sulfonylureas CI in liver & renal diseases

-metabolized by liver & excreted by kidney so
prolonged action—> ↑hypoglycemia risk

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sulfonylureas adverse effects (3)

Hypoglycemia
Hypersensitivity (skin rash)
Heavy weight

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hypoglycemia is increased w/ sulfonylurea use in cases of

-preparation w/ long t1/2
-impaired elimination (old age, renal/liver disease)

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nonsulfonylureas mechanism of action

-↑ insulin secretion via:
binds to β-cell receptors= (-) ATP-sensitive K+ channels= ↓K+ efflux= depol=Ca++ influx=INSULIN RELEASE

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nonsulfonylureas advantages (4)

1-rapid onset, short duration
2- ↓ early hyperglycemia
3- ↓ late hyperglycemia
4-used in patients w/ sulfa allergy

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nonsulfonylureas disadvantages (3)

1-frequent dosing (3times/day)
2-mild hypoglycemia
3-weight gain

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Nonsulfonylureas used cautiously in

liver impairement

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DOC in patient w/ sulfa allergy

nonsulfonylurea secretagogues

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peak effect of sulfonylureas

after 2-3 hours so give before main meal

euglycemics

sensitizers; metformin Pioglitazone (Tzds) acarbose

drugs causing weight gain

1-secretagogues; sulfonylureas & nonsulfonylureas 2- Tzds

drugs NOT causing weight gain

metformin

metformin mechanism of action

(-) Hepatic gluconeogenesis (+) Glycolysis in SKM & adipose tissue= ↑uptake of blood glucose + ↑ lactic acid ↓intestinal absorption=mild anorectic effect

metformin advantages (3)

1-NO hypoglycemia 2-NO weight gain (so↓ insulin resistance) 3- NO drug interactions

metformin doesn't lead to drug interactions due to

-NO PPB -NO hepatic metabolism

metformin indications

T2DM w/ lifestyle modifications & diet

metformin adverse effects

1-GIT upset 2-Lactic acidosis

GIT symptoms of metformin can be managed by

starting w/ low dose and gradually increasing it

GIT symptoms of metformin (4)

1-metallic taste 2-anorexia 3-dyspepsia 4-diarrhea

metformin CI in (3)

1-RF 2-Liver failure 3-HF, MI, pneumonia, alcoholics ⤷(severe hypoxia)

Pioglitazone (Tzd) mechanism of action

-* (+) PPAR-γ receptors (msc,liver,fat) (+) adipocytes synthesis & differentiation -↑new insulin-sensitive fat cells - ↑ FFA uptake - (-) intracellular lipolysis= ↓FA mobilization to blood - ↓ insulin resistance= ↑ glucose uptake - (-) hepatic gluconeogenesis= ↓ blood glucose

Tzd indications

-T2DM monotherapy (if met/sulfa are CI) -combination

Tzds adverse effects

1-fluid retention & edema 2-weight gain 3-fractures

Tzds CI in

1-HF 2-Liver impairement

Tzds must be monitored for

liver injury

Acarbose mechanism of action

(-) α-glucosidase enzyme= ↓intestinal glucose absorption

drugs altering gene regulation

Tzds

drug w/ insulin sparing effect

acarbose

acarbose advantages

1-limits postprandial glucose increase 2-NO hypoglycemia

acarbose adverse effects

GIT= flatulence, abdominal pain, diarrhea due to fermentation

acarbose indications

T2DM, metformin intolerance: adjuvant to sulfonylurea

SGLT2 inhibitors mechanism of action

(-) SGLT2 in PCT ↓ glucose reabsorption ↑excretion ↓ HbA1c, weight, BP

SGLT2 inhibitors indications

monotherapy/combined w/ metformin & Tzfd

SGLT2i adverse effects (3)

1-genitourinary infections 2-mild hypoglycemia 3-fractures

SGLT2i precaution

adequate renal function is necessary

SGLT2 advantages

1-given orally once/day= compliance 2-useful in DKD

DPP4i mechanism of action

(-) DPP4= ↑incretins ↑glucose-dependent insulin release ↓glucagon ↓ hyperglycemia

DPP4i indications

T2DM: monotherapy/ combo w/ metformin or Tzds

DPP4i adverse effects (3)

1-nasopharyngitis 2-URTI 3-joint pain

GLP-1 agonists mechanism of action

↑ glucose-dependent insulin release ↑ β-cell responsiveness ↓ inappropiate postprandial glucagon ↓gastric emptying = ↓food intake

GLP-1 agonists compared to natural GLP1

more stable than natural GLP1

GLP1 agonists adverse effects

1-Nausea w/ high doses 2-pancreatitis 3-medullary thyroid carcinoma

amylin analogues mechanism of action

↓ inappropriate postprandial glucagon ↓gastric emptying improves satiety

incretin mimetic

liraglutide

GLP-1 route of admin? dose?

SC once/day

drug chosen in obesity

liraglutide

drugs causing hypoglycemia

sulfa nonsulfa SGLT2 amylin analogues

amylin analogue indication

T1DM & T2DM Prior to meal adjunct to insulin

amylin analogues adverse effects

1-hypoglycema 2-NV 3-anorexia

causes Na+ retention

insulin Tzds

neutral

metformin Sitagliptin

unfavorable CVS effects

sulfonylureas Tzds (in HF)

induces lactic acidosis in HF & RF

metformin

beneficial in patients w/ DM & HF

SGLT2i

beneficial for patients w/ CVS events

GLP-1 agonists (Liraglutide )

drugs causing bone fractures

Tzds SGLT2

(+) glucose dependent insulin release

DPP4i GLP-1 agonists

drugs NOT causing hypoglycemia

metformin acarbose

DKA coma management

fluid replacement Insulin KCL Bicarbonate TTT of underlying cause

most important step in management of DKA coma

fluid replacement

DKA coma: fluid replacement

3-5L -isotonic saline followed by half tonic solution (IF ↑Na+) -5% glucose if glucose falls to 250mg/dl (to prevent brain edema due to ↓plasma osmolality)

DKA coma: insulin therapy

-regular insulin IV/ IM until blood acetone disappears -↓ IV dose by half if glucose falls to 250mg/dl -once patient is stable--> SC 4times/day

DKA coma: K+ replacement

KCl according to K+ level -20mmol if normokalemic -40mmol if hypokalemic

mild acidosis is corrected by

insulin spontaneously

DKA coma: Bicarbonate

when pH <7.1 stop when pH= 7.2

DKA coma: underlying cause

infections give broad spectrum Ab