DM Flashcards

1
Q

کامپلیکیشن هایی که به دنبال هایپرگلایسمی رخ میدن هر کدوم در چه استیجی از بیماری رخ میدن؟

A

those secondary to acute hyperglycemia may occur at any stage of the disease, whereas those related to chronic hyperglycemia typically begin to appear during the second decade

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2
Q

در Hx کسی که تشحیص دیابت گذاشتیم چیارو باید جتما بپرسیم؟ 8

A

A complete medical history should be obtained with special empha- sis on DM-relevant aspects such as
1-current weight as well as any recent changes in weight,
2-family history of DM and its complications,
3-sleep history, 🛌😴
4-risk factors for cardiovascular disease,
5-exercise, 🚴🏻‍♀️🤸🏻‍♀️🏋🏻‍♀️
6-smoking status, 🚬🚬
7-history of pancreatic disease,
8-and ethanol use. 🍺🍷

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3
Q

علائم هایپرگلایسمی که تو هیستوری میگه بهمون ؟ ۸

A
1-polyuria, 
2-polydipsia,
3- weight loss, 
4-fatigue, 
5-weakness, 
6-blurry vision, 
7-frequent superficial infections (vaginitis, fungal skin infections),
8- and slow healing of skin lesions after minor trauma. 

Blurred vision results from changes in the water content of the lens and resolves as hyperglycemia is controlled.

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4
Q

چه metabolic derangements ای به دنبال DM ایجاد میشه؟

علتش چبه؟

A

Metabolic derangements relate mostly to hyperglycemia (osmotic diuresis)

and to the catabolic state of the patient
(urinary loss of glucose and calories, muscle breakdown due to protein degradation and decreased protein synthesis).

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5
Q

بیمار دیابتی که new نیست، در هیستوری ش تاکیدمون رو چیه؟

A

In a patient with established DM, the initial assessment should include a review of symptoms at the time of the initial diabetes diagnosis. This is an essential part of the history that can help define whether the correct type of DM has been diagnosed.

2-prior diabetes care, including types of thera- pies tried,
3-the nature of any intolerance to previous therapies,
4-prior HbA1c levels,
5- self-monitoring blood glucose results,
6-frequency of hypoglycemia (<3.0 mmol/L, <54 mg/dL),
7- presence of DM-specific complications,
8-and assessment of the patient’s knowledge about diabetes, exercise, nutrition, and sleep history.

8-the presence of DM-related comorbidities should be established (cardiovascular disease, hypertension, dyslipidemia).

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6
Q

هیپوگلایسمی یعنی زیر چند؟

A

۵۴ گرم بر dl

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7
Q

خانومی که دیابت داره و میخواد بچه دار باشه، چه شزایطی باید داشته باشه که اوکی بده؟

A

all women of childbearing age be counseled about the importance of tight glycemic control (HbA1c <6.5%) prior to conception.

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8
Q

در دیابت چه نکاتی در معاینه خیلی مهمه برامون؟

A
1-weight
2- and BMI
3, retinal examination
4, orthostatic blood pressure
5, foot examination
6, peripheral pulses
7, and insulin injection sites. 
8-BP
9-Because periodontal disease is more frequent in DM, the teeth and gums should also be examined.
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9
Q

در دیابتی ها فشار چند باشه HTN محسوب میشه؟

A

Blood pressure >130/80 mmHg is considered hypertension in individuals with diabetes.

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10
Q

معاینه سالانه پای دیابتی چجوری انجام میشه؟

A

An annual foot examination should
(1) assess blood flow (pedal pulses), sensation (vibratory sensation [128-MHz tuning fork at the base of the great toe], the ability to sense touch with a monofilament [5.07, 10-g monofilament], pinprick sensation, ankle reflexes, and nail care;

(2) look for the presence of foot deformities such as hammer or claw toes and Charcot foot; and
(3) identify sites of potential ulceration.

The ADA recommends annual screening for distal symmetric polyneuropathy beginning with the initial diagnosis of diabetes and annual screening for autonomic neuropathy 5 years after diagnosis of type 1 DM and at the time of diagnosis of type 2 DM. This testing is aimed at detecting loss of protective sensation (LOPS) caused by diabetic neuropathy

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11
Q

مشخصات charecteristic، دیابت تایپ ۱؟ 5

A

Individuals with type 1 DM tend to have the following characteristics:

(1) onset of disease prior to age 30 years
(2) lean body habitus
(3) requirement of insulin as the initial therapy;
(4) tendency to develop ketoacidosis
(5) an increased risk of other autoimmune disorders such as autoimmune thyroid disease, adrenal insufficiency, pernicious anemia, celiac disease, and vitiligo.

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12
Q

مشخصات charecteristic، دیابت تایپ ۲ ؟

A

(1) diabetes onset after the age of 30 years
(2) are usually obese (80% are obese, but elderly individuals may be lean);
(3) may not require insulin therapy initially;
(4) may have associated conditions such as insulin resistance, hypertension, cardiovascular disease, dyslipidemia, or polycystic ovarian syndrome.

In type 2 DM, insulin resistance is often associated with abdominal obesity (as opposed to hip and thigh obesity) and hypertriglyceridemia.

Although most individuals diagnosed with type 2 DM are older, the age of diagnosis is declin- ing, and there is a marked increase among overweight children and adolescents.

Some individuals with phenotypic type 2 DM present with diabetic ketoacidosis but lack autoimmune markers and may be later treated with oral glucose-lowering agents rather than insulin (this clinical picture is sometimes referred to as ketosis-prone type 2 DM).

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13
Q

What is latent autoimmune diabetes of the adult?

این بیماران چه مشخصاتی دارن؟

A

some individuals (5–10%) with the phenotypic appearance of type 2 DM do not have absolute insulin deficiency but have autoimmune markers (GAD and other ICA autoantibodies) suggestive of type 1 DM (termed latent autoimmune diabetes of the adult).

Such individuals are more likely to be <50 years of age, thinner, and have a personal or family history of other autoimmune disease than individuals with type 2 DM.

They are much more likely to require insulin treatment within 5 years.

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14
Q

مشخصات دیابت های مونوژنیک؟ 4

A

Monogenic forms of diabetes should be considered in

1-those with diabetes onset in childhood or early adulthood and especially those diagnosed within the first 6 months of life

2-an autosomal pattern of diabetes inheritance

3-diabetes without typical features of type 1 or 2 diabetes

4-and stable mild fasting hyperglycemia

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15
Q

چه لب تست هایی رو برای بیمار دیابتی چک میکنیم؟

A

1-The laboratory assessment should first determine whether the patient meets the diagnostic criteria for DM

2-and then assess the degree of glycemic control.

3-the patient should be screened for DM-associated conditions (e.g., albuminuria, dyslipidemia, thyroid dysfunction).

4- Serum insulin or C-peptide measurements may be useful, but should always be interpreted with a concurrent blood glucose level. A low C-peptide in the setting of an elevated blood glucose level may confirm a patient’s need for insulin.

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16
Q

گول درمانی ما در دیابت چیه؟

A

The goals of therapy for type 1 or type 2 diabetes mellitus (DM) are to
(1) eliminate symptoms related to hyperglycemia

(2) reduce or eliminate the long-term microvascular and macrovascular complications of DM
(3) allow the patient to achieve as normal a lifestyle as possible.

To reach these goals, the physician should identify a target level of glycemic control for each patient, provide the patient with the educational and pharmacologic resources necessary to reach this level, and monitor/treat DM-related complications.

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17
Q

گلوکز پلاسما ب چند برسه علایم رفع میشه؟

A

Symptoms of diabetes usually resolve when the plasma glucose is 200 mg/dL, and thus most DM treatment focuses on achieving the second and third goals.

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18
Q

Guidelines for Ongoing, Comprehensive Medical Care for Patients with Diabetes?

A
  • Individualized glycemic goal and therapeutic plan
  • Self-monitoring of blood glucose (individualized frequency)
  • HbA1c testing (2–4 times/year)
  • Lifestyle management in the care of diabetes, including:
    • Diabetes-self-management education and support
    • Nutrition therapy
    • Physical activity
    • Psychosocial care, including evaluation for depression, anxiety

• Detection, prevention, or management of diabetes-related complications, including:
• Diabetes-related eye examination (annual or biannual)
• Diabetes-related foot examination (1–2 times/year by provider; daily by
patient)
• Diabetes-related neuropathy examination (annual)
• Diabetes-related kidney disease testing (annual)

  • Manage or treat diabetes-relevant conditions, including:
  • Blood pressure (assess quarterly;)
  • Lipids (annual)
  • Consider antiplatelet therapy
  • I nfluenza/pneumococcal/hepatitis B immunizations
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19
Q

چه مواردی هست که باید به بیمار دیابتی یاد بدیم که خودش انجام بده؟

Self management

A

1-self-monitoring of blood glucose (SMBG);

2-urine ketone monitoring (type 1 DM);

3-insulin administration;

4-guidelines for diabetes management during illnesses;

5-prevention and management of hypoglycemia

6-foot and skin care;

7-diabetes management before, during, and after exercise;

8-and risk factor-modifying activities.

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20
Q

ورزشی که با هدف افزایش insulin sensitivity و پایین اوردن قند انجام شه چقدر باید باشه؟

A

In patients with diabetes, the ADA recommends 150 min/week (distributed over at least 3 days) of moderate aerobic physical activity with no gaps longer than 2 days.

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21
Q

بیماران دیابتی چه‌ نوع ورزشی براشون ضرر داره؟
چرا؟
چی میشن؟

A

Despite its benefits, exercise presents challenges for individuals with DM because they lack the normal glucoregulatory mechanisms (nor- mally, insulin falls and glucagon rises during exercise).

Skeletal muscle is a major site for metabolic fuel consumption in the resting state, and the increased muscle activity during vigorous, aerobic exercise greatly increases fuel requirements.

Individuals with type 1 DM are prone to either hyperglycemia or hypoglycemia during exercise,

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22
Q

اینکه به دنبال ورزش هایپر گلایسمی ایجاد شه یا هیپوگلایسمی به چی بستگی داره؟

A

1-depending on the preexercise plasma glucose
2-the circulating insulin level
3-and the level of exercise induced catecholamines.

🔹If the insulin level is too low, the rise in catecholamines may increase the plasma glucose excessively, promote ketone body formation, and possibly lead to ketoacidosis.

🔹Conversely, if the circulating insulin level is excessive, this relative hyperinsulinemia may reduce hepatic glucose production (decreased glycogenolysis, decreased gluconeogenesis) and increase glucose entry into muscle, leading to hypoglycemia.

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23
Q

چجوری میشه جلوی هایپو/ هایپرگلایسمی به دنبال ورزش در دیابتی هارو گرفت؟

A

(1) monitor blood glucose before, during, and after exercise
(2) delay exercise if blood glucose is >14 mmol/L (250 mg/dL) and ketones are present;
(3) if the blood glucose is <5.6 mmol/L (100 mg/dL), ingest carbohydrate before exercising;
(4) monitor glucose during exercise and ingest carbohydrate to prevent hypoglycemia;
(5) decrease insulin doses (based on previous experience) before and after exercise and inject insulin into a nonexercising area;
(6) learn individual glucose responses to different types of exercise.

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24
Q

کدوم دیابتی ها ورزش براشون ممنوعه؟

A

Untreated proliferative retinopathy is a relative contraindication to vigorous exercise, because this may lead to vitreous hemorrhage or retinal detachment.

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25
Q

از چه اندکس هایی Glycaemic control را متوجه میشیم؟

A

the patient’s measurements provide a picture of short-term glycemic control, whereas the HbA1c reflects average glycemic control over the previous 2–3 months.

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26
Q

بیماران دیابتی چند بار در روز باید قندشونو چک‌کنن؟

چه زمانی از روز؟

A

🍇Individuals with type 1 DM or individuals with type 2 DM taking multiple insulin injections each day should routinely measure their plasma glucose three or more times per day (some measure >10 times/day) to estimate and select mealtime boluses of short-acting insulin and to modify long-acting insulin doses.

🍇Most individuals with type 2 DM require less frequent monitoring, although the optimal frequency of SMBG has not been clearly defined.

🍇Individuals with type 2 DM who are taking insulin should use SMBG more frequently than those on oral agents.

🍇Individuals with type 2 DM who are on oral medications should use SMBG as a means of assessing the efficacy of their medication and the impact of dietary choices and exercise. Because plasma glucose levels fluctuate less in these individuals, one or fewer SMBG measurements per day may be sufficient.

🍇Most measurements in individuals with type 1 or type 2 DM should be performed prior to a meal and supplemented with postprandial measurements to assist in reaching postprandial glucose targets

27
Q

چرا هموگلوبین A1c رو اندازه میگیریم؟

چی مبگه به ما

A

When plasma glucose is consistently elevated, there is an increase in nonenzymatic glycation of hemoglobin; this alteration reflects the glycemic history over the previous 2–3 months, because erythrocytes have an average life span of 120 days

28
Q

چرا در مورد بیمار دیابتی ای تو خونه قندشو چک کنه لازمه هر چند وخ یبار HbA1c هم چک شه؟

هر چند وخ یبار لازمه که چک شه؟

A

postprandial and nocturnal hyperglycemia may not be detected by the SMBG of fasting and preprandial capillary plasma glucose but will be reflected in the HbA1c.

🥕In patients achieving their glycemic goal, the ADA recommends measurement of the HbA1c at least twice per year.

🥕More frequent testing (every 3 months) is warranted when glycemic control is inadequate or when therapy has changed.

29
Q

در بیماری که سطح HbA1c ش نرمال نیس چه مواردی ممکنه مخدوشگر باشن؟ 5

A
Clinical conditions leading to abnormal RBC parameters such as 1-hemoglobinopathies, 
2-anemias, 
3-reticulocytosis, 
4-transfusions, 
5-and uremia may alter the HbA1c result.
30
Q

رر

A

Ff

31
Q

زمانی که HbA1c مخدوش شده و دقبق نیست، جایگزینش برای کنترل گلایسمیک چیه؟

A

The degree of glycation of other proteins, such as albumin, or measurement of 1,5-anhydroglucitol can be used as an alternative indicator of glycemic control when the HbA1c is inaccurate.

The fructosamine assay (measuring glycated albumin) reflects the glycemic status over the prior 2 weeks.

32
Q

وقتی میخوایم درمان دارویی رو برا دیابت شروع کنیم اولین قدم چیه؟

A

The initial step is to select an individualized, glycemic goal for the patient.

33
Q

تارگت گلایسمیک کنترل هر فرد بر چه اساسی تعیین میشه؟ ۷

A

Important factors to consider include :
🌻the patient’s age and ability to understand and implement a complex treatment regimen,

🌻presence and severity of complications of diabetes,

🌻known CVD,

🌻ability to recognize hypoglycemic symptoms,

🌻presence of other medical conditions or treatments that might affect survival or the response to therapy,

🌻lifestyle and occupation (e.g., possible consequences of experiencing hypoglycemia on the job),

🌻and level of support available from family and friend.

34
Q

تارگت HbA1c چنده؟

A

In general, the ADA suggests that the goal is to achieve an HbA1c as close to normal as possible without significant hypoglycemia.

In most individuals, the target HbA1c should be <7% with a more stringent target ≤6.5% for some patients

35
Q

در کدوم دسته از بیماران تارگت گلایسمیک رو میذاریم رو زیر ۸-۸/۵؟ 4

A

it may still be appropriate to set a higher HbA1c target <7.5 or 8%
1-for patients with impaired awareness of hypoglycemia.

2-A higher HbA1c goal may also be appropriate for the very young or old
3-or in individuals with limited life span
4-or comorbid conditions.

For example, an appropriate HbA1c goal in elderly individuals with multiple, chronic illnesses and impaired activities of daily living might be 8.0 or 8.5%.

36
Q

در بیماران دیابتی که ریسک CVD دارند،،چه cautionsی رو برای گلایسمیک کنترل باید مد نظر قرار بدیم؟

A

(1) early in the course of type 2 diabetes when the CVD risk is lower, improved glycemic control likely leads to improved cardiovascular outcome, but this benefit may occur more than a decade after the period of improved glycemic control;
(2) intense glycemic control in individuals with established CVD or at high risk for CVD is not advantageous, and may be deleterious, over a follow-up of 3–5 years;
(3) hypoglycemia in such high-risk populations (elderly, CVD) should be avoided;
(4) improved glycemic control reduces microvascular complications of diabetes even if it does not improve macrovascular complications like CVD.

37
Q

بر اساس مکانیسم برای DM2 چه glu lowering agents ای داریم ؟ 5

A

glucose-lowering agents are subdivided into agents that :

1-increase insulin secretion,

2-reduce glucose production,

3-increase insulin sensitivity,

4-enhance GLP-1 action,

5- promote urinary excretion of glucose

38
Q

مکانیسم بایگوانیدها در پایین اوردن گلوکز؟

اثرات کلینیالش روی بیمار؟

A

Metformin, representative of this class of agents, reduces hepatic glucose production and improves peripheral glucose utilization slightly

Metformin
1- reduces fasting plasma glucose (FPG) 
2-and insulin levels, 
3-improves the lipid profile, 
4-and promotes modest weight loss.
39
Q

دوز متفورمین و دوز ماکسیممش؟

A

An extended-release form is available and may have fewer GI side effects (diarrhea, anorexia, nausea, metallic taste).

Because of its relatively slow onset of action and GI symptoms with higher doses, the initial dose should be low and then escalated every 1–2 weeks based on SMBG measurements to a maximally tolerated dose of 2000 mg daily.

40
Q

بنفیت های لانگ ترم متفورمین؟

A

Long-term use is associated with reduced micro- and probably macrovascular complications, but the data are less conclusive for macrovascular complications.

41
Q

علایم Toxicity of metformin?

چجوری میشه پیشگیری کرد؟

A

The major toxicity of metformin, lactic acidosis, is very rare and can be prevented by careful patient selection.

Vitamin B12 levels are lower during metformin treatment and should be monitored.

42
Q

What are the contraindications of metformin? 5

A

Metformin should not be used in patients with :

1-moderate renal insufficiency (glomerular filtration rate [GFR] <45 mL/min), metformin may be safe at a GFR >30 mL/min, with a reduced dose when the GFR is <45 mL/min.

2-any form of acidosis,

3-unstable congestive heart failure (CHF),

4-liver disease,

5-severe hypoxemia.

43
Q

در چه بیمارانی ما متفورمین رو قطع میکنیم و به جاش انسولین میدیم؟ 3

A

1-Hospitalised patients

2-in patients who can take nothing orally

3-in those receiving radiographic contrast material

44
Q

داروهای محرک ترشح انسولین در کدوم بیماران بیشتر مناسبن؟

A

These drugs are most effective in individuals with type 2 DM of relatively recent onset (<5 years) who have residual endogenous insulin production.

45
Q

کدوم نسل Sulfonylureas در درمان دیابت حایگاه داره؟
چه اثراتی داره؟
دوزش چجوریه؟
چه زمانی ار روز باید خورده شه؟

A

Second-generation sulfonylureas have a more rapid onset of action and better coverage of the postprandial glucose rise, but the shorter half-life of some agents may require more than once-a-day dosing.

Sulfonylureas reduce both fasting and postprandial glucose and should be initiated at low doses and increased at 1- to 2-week intervals based on SMBG.

In general, sulfonylureas increase insulin acutely and thus should be taken shortly before a meal; with chronic therapy, though, the insulin release is more sustained.

Long-term use is associated with reduced micro- and macrovascular complications.

46
Q

در بین سولفونیل اوره ها کدوم ارجحه در افراد مسن؟

A

Glimepiride and glipizide can be given in a single daily dose and are preferred over glyburide, especially in the elderly.

47
Q

در مورد repaglinide:
مکانیزم؟
Advantages and disadvantages?
Contra indications?

A

Insulin secretionافرایش
ATP sensitive potassium channel

Short onset of action : نیمه عمرشونم کوتاه و باید بلافاصله قبل غذا مصرف سه
lower post-prandial glucose

hypoglycaemia

renal or liver disease

48
Q

عوارض جانبی داروهای محرک‌ ترشح انسولین؟

ریسک فاکتور هاش در بیماران دیابتی؟

A

Insulin secretagogues, especially the longer acting ones, have the potential to cause hypoglycemia, especially in elderly individuals.

Hypoglycemia is usually related to delayed meals, increased physical activity, alcohol intake, or renal insufficiency.

49
Q

بنفیت های داروهای GLP agonists?

A

Exenatide
Liraglutide : Long acting

1-Weight loss وAppetite suppression: به چاقا دوس داریم بدیمش
Higher doses of liraglutide than used for glucose-lowering effects have been approved for weight loss therapy for obesity.

2-do not cause hypoglycaemia

3-Liraglutide treatment has also been associated with a decrease in CVD events in patients with type 2 DM and established CVD and
4-with lower rates of diabetic kidney disease.

50
Q

What are the contraindications of GLP 1 Agonist? 5

A

1-renal disease

2-agents that slow GI motility

3-medullary carcinoma of tyroid

4-pancreatic disease

5-Multiple endocrine neoplasia

51
Q

چرا exenatide و liraglutide هیپوگلایسمی نمیدن؟

در چه صورتی ممکنه بدن؟

A

Agents in this class do not cause hypoglycemia because of the glucose-dependent nature of incretin-stimulated insulin secretion (unless there is concomitant use of an agent that can lead to hypoglycemia— sulfonylureas, etc.).

یعنی وقتی گلوکز پایینه سبب ترشح انسولین نمیشن نمیدن که هیپوگلایسمی بده

52
Q

مگانیسم های GLP 1 agonist زد كاهش قند خون؟ ۴

A

افرایش ترشح انسولین
کاهش ترشح گلوکاگون
کاهش سرعت تخلیه معده
ایجاد احساس سیری و کاهش اشتها

53
Q

What are the side effects of GLP 1?

A

The major side effects are nausea, vomiting, and diarrhea.

Some formulations carry a black box warning from the FDA because of an increased risk of thyroid C-cell tumors in rodents and are contraindicated in individuals with medullary carcinoma of the thyroid, multiple endocrine neoplasia, or pancreatic disease.

Because GLP-1 receptor agonists slow gastric emptying, they may influence the absorption of other drugs.

54
Q
درمورد DPP iv Inhibitors:
چه داروهایی؟
مکانیسم؟
مشکلات؟
کنترا اندیکیشن؟
A

Linagliptin
Sitagliptin
Vildagliptin
🧡🧡🧡🧡🧡

افرایش انسولین ، کاهش گلوکاگون
💚💚💚💚💚
Angioedema 
urticaria and immune-mediated dermatologic 
effects
❤️❤️❤️❤️❤️
Renal  disease
باید دوز رو کاهش داد
55
Q

عوارض جانبی DDP iv i ها؟

به کیا نباید بدیم با توجه به این عارضه؟

A

There is conflicting evidence concerning a potentially increased risk for acute pancreatitis with GLP-1 receptor agonists and DPP-IV inhibitors, although initial concerns about possible premalignant lesions appear to be unfounded.

For now, it is reasonable to avoid these agents in patients with pancreatic disease or with other significant risk factors for acute pancreatitis (e.g., heavy alcohol use, severely elevated serum triglycerides, hypercalcemia).

56
Q

بنفیت DDIVp Inhibitors

A

هیپوگلایسمی نمیدن
افزایش وزن نمیدن
Well tolerated

57
Q

مکانیسم اثر acarbose در پایین اوردن قند حون؟

با توجه به مکانیسم چه زمانی از روز باید مصرف شن؟

A

Glucosidase inhibitors reduce postprandial hyperglycemia by delaying glucose absorption; they do not affect glucose utilization or insulin secretion.

This class of agents is not as potent as other oral agents in lowering the HbA1c but is unique because it reduces the postprandial glucose rise.

These drugs, taken just before each meal, reduce glucose absorption by inhibiting the enzyme that cleaves oligosaccharides into simple sugars in the intestinal lumen.

58
Q

اکاربوز رو در چه بیمارانی یا با چه داروهایی همزمان نباید داد؟

A

α-Glucosidase inhibitors may increase levels of sulfonylureas and increase the incidence of hypoglycemia.

Simultaneous treatment with bile acid resins and antacids should be avoided.

These agents should not be used in individuals with inflammatory bowel disease,
gastroparesis,
or a serum creatinine 2 mg/dL.

59
Q

عوارض جانبی آکاربوز؟

میشه کمش کرد؟

A

Therapy should be initiated at
a low dose with the evening meal and increased to a maximal dose over weeks to months.

The major side effects (diarrhea, flatulence, abdominal distention) are related to increased delivery of oligosaccharides to the large bowel and can be reduced somewhat by gradual upward dose titration.

60
Q

اگر هیپوگلایسمی رخ بده در زژیم درمانی ای که توش آکاربوز هست بیمار باید چیکار کنه؟

A

the patient should consume glucose because the degradation and absorption of complex carbohydrates will be retarded.

61
Q

What are the side effects of thiazolidinediones?

A

Peripheral edema

CHF

weight gain : 2-3kg

fractures : in postmenopausal women taking these agents.

Macular edema

small reduction in the hematocrit, and a mild increase in plasma volume.

have been shown to induce ovulation in premenopausal women with polycystic ovary syndrome. Women should be warned about the risk of pregnancy because the safety of thiazolidinediones in pregnancy is not established.

pioglitazone may be associated with an increased risk of bladder cancer.

62
Q

مکانیسم Pioglitazone?

A

کاهش مقاومت به انسولین
افزایش Glucose Utilization

The PPAR-γ receptor is found at highest levels in adipocytes but is expressed at lower levels in many other tissues. Agonists of this receptor regulate a large number of genes, promote adi- pocyte differentiation, reduce hepatic fat accumulation, and promote fatty acid storage.

63
Q

اثرات پیوگلیتازون بر چربی ها و پروفایل چربی؟

A

Thiazolidinediones promote a redistribution of fat from central to peripheral locations.

 The prototype of this class of drugs, troglitazone, was withdrawn from the U.S. market after reports of hepatotoxicity and an association with an idiosyncratic liver reaction that sometimes led to hepatic failure. Although rosiglitazone and pioglitazone do not appear to induce the liver abnormalities seen with troglitazone,
Rosiglitazone raises low-density lipoprotein (LDL), high-density lipoprotein (HDL), and triglycerides slightly. 

Pioglitazone raises HDL to a greater degree and LDL a lesser degree but lowers triglycerides.

64
Q

چه W/U هایی لازمه قبل شروع پیوگلیتازون؟

A

the FDA recommends measurement of liver function tests prior to initiating therapy.

Modestly increased transaminase levels related to underlying fatty liver disease should not preclude treatment as these levels may improve with thiazolidinediones due to a reduction in hepatic fat content.