L2: Managment of DM Flashcards
(101 cards)
1
Q
Goals of TTT of DM
A
2
Q
Target of TTT in DM
A
- Normal glucose levels
- Weight Loss
- Improve blood lipid profile
- Lower blood pressure
3
Q
what are glycemic targets?
A
- HbA1C < 7 %
- Fasting blood glucose 80 - 130 mg/dL
- Postprandial blood glucose < 180 mg/dL
4
Q
Weigth target in DM
A
- Body mass index <25 kg/m2
- Waist : hip ratio men <0.95 - women <0.8
5
Q
what is Diabetes Remission?
A
Return of HbA1c <6.5%
6
Q
Characters of Diabetes Remission
A
- Spontaneously or following intervention
- Persist for 3 months
- In absence of glucose lowering pharmacotherapy
7
Q
Lipid profile targets in DM
A
8
Q
Blood Pressure target in DM
A
130/80 mmHg (but depends on age, diabetes duration, complication risk)
9
Q
Aspects of Therapeutic Lifestyle Modification in DM
A
- Weight loss (for overweight and obese patients)
- Physical Activity
- Diet
10
Q
Weight loss
(Therapeutic Lifestyle Modification)
A
Reduce by 5% to 10%
11
Q
Physical activity
(Therapeutic Lifestyle Modification)
A
150 min/week of moderate-intensity exercise (e.g., brisk walking) plus flexibility and strength training.
12
Q
Diet
(Therapeutic Lifestyle Modification)
A
13
Q
CHO eating in DM
A
healthful carbohydrates (fresh fruits and vegetables, legumes, whole grains)
14
Q
Fat Eating in DM
A
- Healthful fats → containing polyunsaturated fatty acids (nuts, avocado, certain plant oils, fish)
- Limit saturated fats → (butter, fatty red meats, tropical plant oils, fast foods) and trans fat
15
Q
Protein Eating in DM
A
- Consume protein in foods with low saturated fats (fish, egg whites, beans)
- there is → no need to avoid animal protein
- Avoid or limit processed meats
16
Q
Micronutrients in DM
A
- Routine supplementation is not necessary → a healthful eating meal plan can generally provide sufficient micronutrients
- Vitamin supplements → recommended to patients at risk of insufficiency or deficiency
However, Vit B is good for neuropathy associated with DM
17
Q
What are Categories of Oral Hypoglycemic Agents?
A
18
Q
Insulin Sensitizers
A
- Biguanides (Metformin)
- Thiazolidinedione (TZDs)
19
Q
Insulin Secretagogues
A
- Sulphonylurea ( Long acting secretagogues )
- Non-Sulphonylurea secretagogues ( Glinides ) ( Short acting secretagogues )
- Glucagon like peptide 1 receptors agonists ( GLP1 agonists ) (Injectable)
- Dipeptidyl peptidase-4 inhibitors ( DPP4 inhibitors )
20
Q
what is an example of Alpha-glucosidase inhibitors?
A
(Acarbose)
21
Q
what is the corner stone in treatment of type 2 diabetes in all guidelines?
A
Metformin
21
Q
MOA of different Oral Hypoglycemic Agents
A
22
Q
MOA of Metformin
A
22
Q
What is an example of Biguanides?
A
Metformin
23
Advantages of **Metformin**
Cheap
No weight gain
No episodes of hypoglycemia
Beneficial cardiovascular outcomes
24
SE of **Metformin**
1. Gastro-intestinal → like flatulence and diarrhea
2. Fatal lactic acidosis. → rarely
25
CI of **Metformin**
- diabetic patients with renal and/or hepatic disease
- diabetic ketoacidosis
26
Dose of **Metformin**
- Starting dose : 500 mg taken once daily with breakfast for one week
- Up-titration of the dose should be continued as required
- Maximum: 2 g per day.
27
when not to give **Metformin** (GFR)?
if the estimated glomerular filtration rate (eGFR) is <30 ml/min/1.73 m2.
28
Members of **Thiazolidinediaones**
Pioglitazone → 15- 45 mg/day & Rosiglitazone
29
MOA of **Thiazolidinediaones**
30
Advantages of **Thiazolidinediaones**
No or minimal hypoglycemia
Expected HbA1c change (%) → 0.5 – 1.4
Improves lipid profile
31
SE of **Thiazolidinediaones**
1) Weight gain
2) Edema both L.L
3) Osteoporosis especially in postmenopausal females.
32
CI of **Thiazolidinediaones**
1) Pregnancy
2) Advanced heart failure
3) Hepatic cell failure
4) Renal failure
5) Risk of bladder cancer
33
what type of secretagogues are **Sulfonylureas**?
Long acting
34
Examples of **Sulfonylureas**
35
MOA of **Sulfonylureas**
36
Advantages of **Sulfonylureas**
- Expected HbA1c change (%)→ 1.0 – 2.0 ( Effective reduction of HA1C )
- Rapidly effective
- ↓ Microvascular risk
- Not Expensive
37
SE of **Sulfonylureas**
- Hypoglycemia
- Weight gain
- Blunting of myocardial ischemia
38
CI of **Sulfonylureas**
Pregnancy
Type 1 diabetes.
Patients with acute or end-stage liver disease
Patients with end-stage renal diseases
39
what type of secretagogues are **Glinides**?
Short-Acting
40
Members of **Glinides**
Natiglinide & Mitiglinides & Repaglinide
41
what are **Glinides** Called?
They are called prandial glucose regulators as these drugs act mainly on the postprandial glucose excursions
42
MOA of **Glinides**
- Act on the same potassium channels of Sulphonylurea.
- Enhance insulin secretion
43
SE of **Glinides**
Hypoglycemia
Weight gain
44
Explain **Enteroinsular axis**
45
What are members of **GLP1 Agonists**?
Liraglutide/d
Dulaglutide/w
Semaglutide/w
Lixisinatide/d
46
Method of adminstration of **GLP1 Agonists**
Injectable
47
Advantages of **GLP1 Agonists**
1) No hypoglycemia
2) Weight loss
3) Cardiovascular & renal protection.
48
Disadvantages of **GLP1 Agonists**
Costy.
Subcutaneous injection
49
SE of **GLP1 Agonists**
- GIT upset ( Diarrhea - Nausea & vomiting )
- Acute pancreatitis
50
what are members of **DPP4 Inhibitors**?
1) Sitagliptin & Linagliptin
2) Alogliptin & Saxagliptin.
3) Vildagliptin
51
MOA of **DPP4 Inhibitors**
- ↓destruction of endogenous GLP-1 (glucagon like polypeptide 1)
- ↑↑ Incretin level which → stimulates insulin release from pancreatic B-cells in a glucose dependent manner.
52
Advantages of **DPP4 Inhibitors**
No hypoglycemia
No weight gain
Well tolerated drugs.
53
Disadvantages of **DPP4 Inhibitors**
- Costy.
- Expected HbA1c change (%)→ 0.6 – 0.9
54
SE of **DPP4 Inhibitors**
**Alter Immune function**
- Increased upper respiratory infection → nasopharyngitis, headache and nausea
- Angioedema/urticaria
55
MOA of **Alpha Glucosidase Inhibitors**
- ↓↓ The upper gastrointestinal enzymes that convert dietary starch and other
complexes into simple sugar which can be absorbed.
- Mild to moderate reduction in postprandial glucose.
56
Advantages of **Alpha Glucosidase Inhibitors**
no hypoglycemia
no weight gain
57
SE of **Alpha Glucosidase Inhibitors**
Usually cause flatulence and diarrhea
58
What are members of **Sodium Glucose Co-Transporter 2 Inhibitors**?
Canagliflozin
Dapagliflozin
Empaglifiozin
59
MOA of **SGLT2 Inhibitors**
- Inhibits glucose re-absorption from proximal convoluted tubules of the kidney
(Reduce renal glucose reabsorption by 30–50%)
- Their glycemic efficacy is dependent on glomerular filtration, and they are less
efficacious in renal impairment.
60
Advantages of **SGLT2 Inhibitors**
No hypoglycemia
Mild reduction in systolic blood pressure
Decrease body weight
↓ Albuminuria
Improve lipid profile
61
Disadvantages of **SGLT2 Inhibitors**
- Expensive drugs
- Mild to moderate reduction in A1C → 0.6 – 0.9
62
SE of **SGLT2 Inhibitors**
Urinary-tract infections
Ketoacidosis
Hypotension
Acute kidney injury
63
when not to use dapagliflozin? (GFR)
if GFR is less than 60
64
MOA of **Insulin**
65
Introduction to insulin
- Peptide hormone composed of 51 amino acids that is synthesized, packaged, and secreted in pancreatic beta cells.
66
- Insulin therapy is appropriate for patients with type 1 & type 2 diabetes.
- The absolute insulin deficiency of established type 1 diabetes can only be treated effectively with multiple daily insulin injections
..
67
Indications of **Insulin**
(CI of Sulfunylureas)
68
Insulin therapy is often used early for type 2 diabetes patients, who are: ......
- Highly symptomatic with marked catabolic state
- Newly diagnosed with very high glucose level
68
SE of **Insulin**
- Hypoglycemia & hypoglycemic coma
- Weight gain & edema
- Injection site problems
- Insulin allergy and hypersensitivity
68
Levels of Hypoglycemia
69
Clinical Manifestations in **Hypoglycemia**
70
TTT of **Hypoglycemia**
71
what causes Weight gain & edema in insulin therapy?
Due to lipogenesis and salt & water retention
72
Injection site problems in insulin
- Fat hypertrophy (“lipohypertrophy”) appears as soft lumps at the injection sites.
- Fat atrophy (“lipoatrophy”) is a loss of fat under the skin’s surface.
- Scarring of the fat (“lipodystrophy”) is caused when you inject too many times into the same site treated by frequent change of sites of injection
73
Insulin allergy and hypersensitivity
- Rare
- Result from the insulin molecule itself, and also from protamine
- Self-limited OR systemic reactions ( urticaria or anaphylaxis )
74
TTT of Insulin allergy and hypersensitivity
- Using a continuous subcutaneous pump infusion of insulin
- Switching from human insulin to insulin analogues such as aspart or lispro.
75
Def of **Insulin Resistance**
- ↑↑ daily insulin requirements > 200 IU in absence of conditions associated with ↑↑ insulin demand (infection –pregnancy…)
76
Cause of **Insulin Resistance**
- Obesity: commonest cause for mild resistance & Antibodies against insulin preparations OR receptors
77
Explain **Somogyi Effect**
**(Pseudo-insulin resistance)**
- Nocturnal hypoglycemia (known by night mare & sweating of the patient & morning headache) ------> Increased hyperglycemic hormones ----> morning hyperglycemia
78
Cause of **Somogyi Effect**
occurs due to high dose of night insulin or low amount of dinner
79
TTT of **Somogyi Effect**
**treated by reduction of night insulin**
80
Dawn Phenomenon
81
Rapid acting Insulin Preparations
82
Short acting Insulin Preparations
83
Intermediate acting Insulin Preparations
84
Long acting Insulin Preparations
85
Insulin Mixutres
86
- Humulin 70/30
- Mixtard 70/30
87
NovoMix 30
88
Routes of Adminstration of Insulin
89
How you calculate the dose of insulin?
When initiating insulin therapy, base line total daily dose is often calculated as **0.6 X body weight in kilograms**
90
Insulin regimen 1 (Twice Daily)
91
Insulin regimen 2 (Basal Bolus)
92
Selecting initial insulin regimen based on blood sugar profile
93
Initiating with Basal insulin
94
Initiating with premixed insulin
95
Initiating with prandial insulin
96
Initiating with Basal-bolus insulin
97
Done
🫡
