Diabetes meds Flashcards

1
Q

T1DM

A

> Positive HLA-DR4, HLA-DR3 association.
weak familial predisposition
Autoimmune response that triggers the destruction of insulin producing B cells
leukocyte infiltration of islets

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2
Q

DKA

A

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.

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3
Q

T2DM

A

> 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)

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4
Q

Screening of T2DM

A

HbA1c

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5
Q

Diabetic microvascular complications

A

Diabetic Nephropathy
Diabetic Retinopathy
Diabetic Neuropathy

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6
Q

Diabetic Macrovascular Complications

A

CAD
Stroke
PAD
Monkeberg arteriosclerosis (medial calcific sclerosis)

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7
Q

Management includes

A

antihyperglycemics
statins (lipid lowering)
ACE inhibitors
ARB
aspirin (ant-platelet)

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8
Q

Sulfonylureas
DDP-4 inhibitors
SGLT-2 inhibitors
thiazolidinediones

A

NOT Licensed to be used in management of Diabetes in Children

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9
Q

Type 1 Classifications

A

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)

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10
Q

GDM

A

A1GDM = no medication required
A2GDM = REQUIRE Insulin immediately

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11
Q

MODY

A

Maturity onset of Diabetes of the Young
early onset <25 years of age
non-insulin dependent DM
Autosomal Dominant

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12
Q

MODY II

A

Single mutation leads to impaired insulin secretion due to altered Glucokinase function.

Can be managed by diet alone

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13
Q

Glucokinase

A

Glucose sensor of the B Cell

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14
Q

Bronze Diabetes

A

Due to increased iron in the body which destroy the pancreatic islets
Hemochromatosis. > Most frequent genetic dz in the white population

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15
Q

Cystic Fibrosis related diabetes

A

Pancreatic insufficiency

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16
Q

Cushing Disease

A

Glucose intolerance

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17
Q

Drug induced diabetes can be caused by

A

use of Corticosteroids

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18
Q

cleavage of Proinsulin which is a precursor of Insulin produces

A

C-Peptide

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19
Q

Congenital rubella infection
(congenital TORCH infections)

A

causes Hepatosplenomegaly

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20
Q

Insulin

A

Stimulates intracellular Potassium accumulation

Stimulates protein synthesis and uptake of AA
Inhibits Proteolysis

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21
Q

T1DM Antibodies

A

anti- GAD (anti-glutamic acid decarboxylase antibody)
anti-ICA (anti-islet cell cytoplasmic antibody)

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22
Q

T2DM Treatment

A

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

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23
Q

Contraindications to Metformin

A

> eGFR<30mL/minute/1.73m2
acute of chronic metabolic acidosis
hypersensitivity to Metformin or its components

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24
Q

GLP-1 Receptor Agonists (Incretin system mimetics)

A

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)

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25
Dipeptidyl peptidase -4 inhibitors (DPP-4 i)
>Sitagliptin >Saxagliptin (avoid in pts with HF) >Linagliptin (DPP-4 degrades GLP1, therefore DPP4 inhibitors prolong the effects of GLP1 and GIP)
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GLP secreted upon ingestion of food (incretin system) (half-life 2 - 4 mins)
Promotes satiety and reduces appetite Suppresses glucagon activity and increases glucose dependent insulin secretion
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in T2DM
Meal induced GLP-1 release is reduced
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SGLT-2 Inhibitors >Empagliflozin >Dapagliflozin reduce insulin resistance
>Recommended for CKD and eGFR 15-29mL/min / 1.73m2, >Congestive heart failure clinical ASCVD or high risk for ASCVD >Beneficial for pts who want to Lose weight or maintain their weight
29
Sulphonyl-ureas >Glimepiride >Gliclazide >Glyburide
>They inhibit ATP-sensitive potassium channels in the beta cell membrane, leading to depolarization and increased insulin release. >c/I in pts with eGFR <30mL/min) >associated with weight gain
30
Glinides ( sulfonyl-ureas analogue) >Nateglinide >Repaglinide
>Short and Rapid action >used to correct Post-prandial Hyperglycemia >Increase insulin secretion >Associated with Weight gain and renal failure
31
Thiazo-lidinedione (TZD) >Pioglitazone >Rosiglitazone
>Decrease insulin resistance and increase muscle and adipose tissue sensitivity to insulin. >Avoid in Pts with CHF, Liver pathology, and MI events > risks of # in women, >maximal clinical effect expected in a few weeks time. >associated with Weight gain, and increase LDL >Not to prescribe if risk for Bladder cancer.
32
a-Glucosidase inhibitors >Acarbose >Miglitol >Voglibose
inhibits the enzyme that degrades oligosaccharides and disaccharides in the small intestines. associated with abd discomfort and flatulence
33
Oral monotherapy lowers HbA1c levels by around 1%
every non-insulin added to metformin lowers HbA1c by an additional 0.7 -1.0%
34
Do not combine Sulfonyl-ureas and Metformin
risk of Hypoglycemia
35
if Diabetic pt undergoing surgery
avoid oral antidiabetic meds and instead insulin therapy may be initiated
36
Insulin therapy in newly diagnosed patients
if HbA1c is >10% or >300mg/dl
37
Basal insulin regimen
A type of treatment for type 2 diabetes mellitus that involves the injection of long-acting insulin (e.g., glargine) or intermediate-acting insulin combined with an antidiabetic drug. Indicated for patients with persistently elevated HbA1c levels despite noninsulin antidiabetic therapy.
38
Albumin-to-creatinine ratio Abbreviation: ACR, UACR
The ratio of urine albumin concentration to urine creatinine concentration. (proteinuria) An ACR < 30 mg/g is considered normal to mildly increased; an ACR 30-300 mg/g for more than 3 months indicates likely chronic kidney disease. An ACR > 300 mg/g is severely increased.
38
GLP-1 receptor agonists
Should be part of the treatment strategy prior to starting insulin therapy in patients with T2DM, unless they are not appropriate.
39
Screening for microvascular complications of Diabetes
>Kidney = Albumin to creatinine ration >Retinopathy >Peripheral neuropathy with focused examination of sensation (pinprick, monofilament, vibration, temperature) >autonomic neuropathy
40
Glucose handling in non-diabetic Pt
90% absorbed in the S1 section of Proximal tubule. Facilitated by SGLT-2 S3 segment (initial part of descending loop) 10% via SGLT1
40
DPP-4 inhibitor Linagliptin
Elimination via Biliary system >70% safe to use in pts reduced GFR
40
GLP-1 agonists
Proved CV safety risk of acute pancreatitis
41
SGLT-2 inhibitors
>Block glucose reabsorption therefore more is excreted in urine. (glucosuria) >potential for BP control via Na+ elimination and h2o. >CV safety >reduces risk of HF and progression to CKD >increased risks for lower UTI
42
for T2DM patients with established ASCVD or HF
GLP-1A or SGLT-2i are recommended have proved CV safety and benefit
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for T2DM patients without ASCVD but with HFrEF or CKD
SGLT2-inhibitors are recommended
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