Diabetes meds Flashcards
T1DM
> Positive HLA-DR4, HLA-DR3 association.
weak familial predisposition
Autoimmune response that triggers the destruction of insulin producing B cells
leukocyte infiltration of islets
DKA
Primarily seen in pts with T1DM.
Insufficient insulin levels often secondary to an acute infection
Manifests as hyperglycemia 300 -600mg/dl, polyuria, polydispsia, nausea, vomiting, volume depletion ( dry oral mucosa), mental status changes and coma
Ketones, Sweet smelling breathe, mentation change, acidosis.
T2DM
> Has a strong genetic component
NO HLA association
There is insulin resistance and or impaired secretion due to B cell dysfunction.
Amyloid polypeptide deposits in islets (IAPP)
Screening of T2DM
HbA1c
Diabetic microvascular complications
Diabetic Nephropathy
Diabetic Retinopathy
Diabetic Neuropathy
Diabetic Macrovascular Complications
CAD
Stroke
PAD
Monkeberg arteriosclerosis (medial calcific sclerosis)
Management includes
antihyperglycemics
statins (lipid lowering)
ACE inhibitors
ARB
aspirin (ant-platelet)
Sulfonylureas
DDP-4 inhibitors
SGLT-2 inhibitors
thiazolidinediones
NOT Licensed to be used in management of Diabetes in Children
Type 1 Classifications
Type 1A = Insulin dependent
LADA = Latent autoimmune diabetes in adults (late onset of type 1 diabetes in adults) often mistaken for T2DM
Type 1B = idiopathic (strong hereditary component, no auto antibodies detected)
GDM
A1GDM = no medication required
A2GDM = REQUIRE Insulin immediately
MODY
Maturity onset of Diabetes of the Young
early onset <25 years of age
non-insulin dependent DM
Autosomal Dominant
MODY II
Single mutation leads to impaired insulin secretion due to altered Glucokinase function.
Can be managed by diet alone
Glucokinase
Glucose sensor of the B Cell
Bronze Diabetes
Due to increased iron in the body which destroy the pancreatic islets
Hemochromatosis. > Most frequent genetic dz in the white population
Cystic Fibrosis related diabetes
Pancreatic insufficiency
Cushing Disease
Glucose intolerance
Drug induced diabetes can be caused by
use of Corticosteroids
cleavage of Proinsulin which is a precursor of Insulin produces
C-Peptide
Congenital rubella infection
(congenital TORCH infections)
causes Hepatosplenomegaly
Insulin
Stimulates intracellular Potassium accumulation
Stimulates protein synthesis and uptake of AA
Inhibits Proteolysis
T1DM Antibodies
anti- GAD (anti-glutamic acid decarboxylase antibody)
anti-ICA (anti-islet cell cytoplasmic antibody)
T2DM Treatment
Biguanides - Metformin is the first line initial treatment
increase peripheral glucose uptake by tissues and muscle.
s/e diarrhea and Abd. discomfort,
Vit B12 def. > diabetic neuropathy worsens
Contraindications to Metformin
> eGFR<30mL/minute/1.73m2
acute of chronic metabolic acidosis
hypersensitivity to Metformin or its components
GLP-1 Receptor Agonists (Incretin system mimetics)
Recommended for pts with eGFR<30ml/min), clinical ASCVD, or high risk of ASCVD
>Semaglutide (oral or injectable)
>Liraglutide (daily SQ )
>Dulaglutide (weekly SQ)
> Exenatide
Albiglutide
Lixisenatide
(((Tirzepatide))(look up latest studies)