Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Y3R5: Medicine I 🩺 > L2: Managment of DM > Flashcards

L2: Managment of DM Flashcards

1
Q

Goals of TTT of DM

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Target of TTT in DM

A
  • Normal glucose levels
  • Weight Loss
  • Improve blood lipid profile
  • Lower blood pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are glycemic targets?

A
  • HbA1C < 7 %
  • Fasting blood glucose 80 - 130 mg/dL
  • Postprandial blood glucose < 180 mg/dL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Weigth target in DM

A
  • Body mass index <25 kg/m2
  • Waist : hip ratio men <0.95 - women <0.8
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is Diabetes Remission?

A

Return of HbA1c <6.5%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Characters of Diabetes Remission

A
  • Spontaneously or following intervention
  • Persist for 3 months
  • In absence of glucose lowering pharmacotherapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Lipid profile targets in DM

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Blood Pressure target in DM

A

130/80 mmHg (but depends on age, diabetes duration, complication risk)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Aspects of Therapeutic Lifestyle Modification in DM

A
  • Weight loss (for overweight and obese patients)
  • Physical Activity
  • Diet
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Weight loss
(Therapeutic Lifestyle Modification)

A

Reduce by 5% to 10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Physical activity
(Therapeutic Lifestyle Modification)

A

150 min/week of moderate-intensity exercise (e.g., brisk walking) plus flexibility and strength training.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Diet

(Therapeutic Lifestyle Modification)

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

CHO eating in DM

A

healthful carbohydrates (fresh fruits and vegetables, legumes, whole grains)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are Categories of Oral Hypoglycemic Agents?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Insulin Sensitizers

A
  • Biguanides (Metformin)
  • Thiazolidinedione (TZDs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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 )
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is an example of Alpha-glucosidase inhibitors?

A

(Acarbose)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is the corner stone in treatment of type 2 diabetes in all guidelines?

A

Metformin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

MOA of different Oral Hypoglycemic Agents

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

MOA of Metformin

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is an example of Biguanides?

A

Metformin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Advantages of Metformin

A

 Cheap
 No weight gain
 No episodes of hypoglycemia
 Beneficial cardiovascular outcomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

SE of Metformin

A
  1. Gastro-intestinal → like flatulence and diarrhea
  2. Fatal lactic acidosis. → rarely
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

CI of Metformin

A
  • diabetic patients with renal and/or hepatic disease
  • diabetic ketoacidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Dose of Metformin

A
  • 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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

when not to give Metformin (GFR)?

A

if the estimated glomerular filtration rate (eGFR) is <30 ml/min/1.73 m2.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Members of Thiazolidinediaones

A

Pioglitazone → 15- 45 mg/day & Rosiglitazone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

MOA of Thiazolidinediaones

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Advantages of Thiazolidinediaones

A

 No or minimal hypoglycemia
 Expected HbA1c change (%) → 0.5 – 1.4
 Improves lipid profile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

SE of Thiazolidinediaones

A

1) Weight gain
2) Edema both L.L
3) Osteoporosis especially in postmenopausal females.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

CI of Thiazolidinediaones

A

1) Pregnancy
2) Advanced heart failure
3) Hepatic cell failure
4) Renal failure
5) Risk of bladder cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what type of secretagogues are Sulfonylureas?

A

Long acting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Examples of Sulfonylureas

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

MOA of Sulfonylureas

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Advantages of Sulfonylureas

A
  • Expected HbA1c change (%)→ 1.0 – 2.0 ( Effective reduction of HA1C )
  • Rapidly effective
  • ↓ Microvascular risk
  • Not Expensive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

SE of Sulfonylureas

A
  • Hypoglycemia
  • Weight gain
  • Blunting of myocardial ischemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

CI of Sulfonylureas

A

 Pregnancy
 Type 1 diabetes.
 Patients with acute or end-stage liver disease
 Patients with end-stage renal diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what type of secretagogues are Glinides?

A

Short-Acting

40
Q

Members of Glinides

A

Natiglinide & Mitiglinides & Repaglinide

41
Q

what are Glinides Called?

A

They are called prandial glucose regulators as these drugs act mainly on the postprandial glucose excursions

42
Q

MOA of Glinides

A
  • Act on the same potassium channels of Sulphonylurea.
  • Enhance insulin secretion
43
Q

SE of Glinides

A

 Hypoglycemia
 Weight gain

44
Q

Explain Enteroinsular axis

A
45
Q

What are members of GLP1 Agonists?

A

 Liraglutide/d
 Dulaglutide/w
 Semaglutide/w
 Lixisinatide/d

46
Q

Method of adminstration of GLP1 Agonists

A

Injectable

47
Q

Advantages of GLP1 Agonists

A

1) No hypoglycemia
2) Weight loss
3) Cardiovascular & renal protection.

48
Q

Disadvantages of GLP1 Agonists

A

 Costy.
 Subcutaneous injection

49
Q

SE of GLP1 Agonists

A
  • GIT upset ( Diarrhea - Nausea & vomiting )
  • Acute pancreatitis
50
Q

what are members of DPP4 Inhibitors?

A

1) Sitagliptin & Linagliptin
2) Alogliptin & Saxagliptin.
3) Vildagliptin

51
Q

MOA of DPP4 Inhibitors

A
  • ↓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
Q

Advantages of DPP4 Inhibitors

A

 No hypoglycemia
 No weight gain
 Well tolerated drugs.

53
Q

Disadvantages of DPP4 Inhibitors

A
  • Costy.
  • Expected HbA1c change (%)→ 0.6 – 0.9
54
Q

SE of DPP4 Inhibitors

A

Alter Immune function

  • Increased upper respiratory infection → nasopharyngitis, headache and nausea
  • Angioedema/urticaria
55
Q

MOA of Alpha Glucosidase Inhibitors

A
  • ↓↓ 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
Q

Advantages of Alpha Glucosidase Inhibitors

A

 no hypoglycemia
 no weight gain

57
Q

SE of Alpha Glucosidase Inhibitors

A

Usually cause flatulence and diarrhea

58
Q

What are members of Sodium Glucose Co-Transporter 2 Inhibitors?

A

 Canagliflozin
 Dapagliflozin
 Empaglifiozin

59
Q

MOA of SGLT2 Inhibitors

A
  • 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
Q

Advantages of SGLT2 Inhibitors

A

 No hypoglycemia
 Mild reduction in systolic blood pressure
 Decrease body weight
 ↓ Albuminuria
 Improve lipid profile

61
Q

Disadvantages of SGLT2 Inhibitors

A
  • Expensive drugs
  • Mild to moderate reduction in A1C → 0.6 – 0.9
62
Q

SE of SGLT2 Inhibitors

A

 Urinary-tract infections
 Ketoacidosis
 Hypotension
 Acute kidney injury

63
Q

when not to use dapagliflozin? (GFR)

A

if GFR is less than 60

64
Q

MOA of Insulin

A
65
Q

Introduction to insulin

A
  • Peptide hormone composed of 51 amino acids that is synthesized, packaged, and secreted in pancreatic beta cells.
66
Q
  • 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
A

..

67
Q

Indications of Insulin

(CI of Sulfunylureas)

A
68
Q

Insulin therapy is often used early for type 2 diabetes patients, who are: ……

A
  • Highly symptomatic with marked catabolic state
  • Newly diagnosed with very high glucose level
68
Q

SE of Insulin

A
  • Hypoglycemia & hypoglycemic coma
  • Weight gain & edema
  • Injection site problems
  • Insulin allergy and hypersensitivity
68
Q

Levels of Hypoglycemia

A
69
Q

Clinical Manifestations in Hypoglycemia

A
70
Q

TTT of Hypoglycemia

A
71
Q

what causes Weight gain & edema in insulin therapy?

A

Due to lipogenesis and salt & water retention

72
Q

Injection site problems in insulin

A
  • 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
Q

Insulin allergy and hypersensitivity

A
  • Rare
  • Result from the insulin molecule itself, and also from protamine
  • Self-limited OR systemic reactions ( urticaria or anaphylaxis )
74
Q

TTT of Insulin allergy and hypersensitivity

A
  • Using a continuous subcutaneous pump infusion of insulin
  • Switching from human insulin to insulin analogues such as aspart or lispro.
75
Q

Def of Insulin Resistance

A
  • ↑↑ daily insulin requirements > 200 IU in absence of conditions associated with ↑↑ insulin demand (infection –pregnancy…)
76
Q

Cause of Insulin Resistance

A
  • Obesity: commonest cause for mild resistance & Antibodies against insulin preparations OR receptors
77
Q

Explain Somogyi Effect

A

(Pseudo-insulin resistance)

  • Nocturnal hypoglycemia (known by night mare & sweating of the patient & morning headache) ——> Increased hyperglycemic hormones —-> morning hyperglycemia
78
Q

Cause of Somogyi Effect

A

occurs due to high dose of night insulin or low amount of dinner

79
Q

TTT of Somogyi Effect

A

treated by reduction of night insulin

80
Q

Dawn Phenomenon

A
81
Q

Rapid acting Insulin Preparations

A
82
Q

Short acting Insulin Preparations

A
83
Q

Intermediate acting Insulin Preparations

A
84
Q

Long acting Insulin Preparations

A
85
Q

Insulin Mixutres

A
86
Q
  • Humulin 70/30
  • Mixtard 70/30
A
87
Q

NovoMix 30

A
88
Q

Routes of Adminstration of Insulin

A
89
Q

How you calculate the dose of insulin?

A

When initiating insulin therapy, base line total daily dose is often calculated as 0.6 X body weight in kilograms

90
Q

Insulin regimen 1 (Twice Daily)

A
91
Q

Insulin regimen 2 (Basal Bolus)

A
92
Q

Selecting initial insulin regimen based on blood sugar profile

A
93
Q

Initiating with Basal insulin

A
94
Q

Initiating with premixed insulin

A
95
Q

Initiating with prandial insulin

A
96
Q

Initiating with Basal-bolus insulin

A
97
Q

Done

A

🫡

Y3R5: Medicine I 🩺 (39 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions