Done by: Ayana - sara qhatani – sara dhahry – elham Lama – alaa – kholud - eilaf. Objective. At the end of this session, students will be able to: Identify differential diagnosis of a case presented with the symptoms of polyuria and polydipsia.
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Ayana - sara qhatani – sara dhahry – elham
Lama – alaa – kholud - eilaf
weight is 98 kg.
apart from being obese.
DM DI Psychological
check blood check ADH ask about
sugar level level water intake
NEED TO BE TESTED
It is a condition characterized by excessive thirstand polyuriasecondary to
deficiency of ADH (cranial DI)
or kidneydoes not respond to ADH (nephrogenic DI) .
- No hyperglycemia or glucose in urine in case of diabetes insipidus.
causes poluria via a process called osmotic diuresis due to the high blood sugar leaking into the urine and taking excess water along with it.
Pt complain of poluria ,polydipsia ,weakness
have 2 risk factor : obesity & sedentary lifestyle
DM more common than DI.
Pt Systematic examination is normal
usually come with other symptom
( dehydration, fever , vomiting ,diarrhea)
DI less common than DM
hyperglycemia and abnormalities in carbohydrate,
fat, and protein metabolism. It results from defects in insulin secretion, insulin sensitivity, or both.
1) C .O :
How can I help you?
2) HPI :
When did the symptoms start?
e.g. loss of appetite , decrease vision
Social Hx :
Occupation, education , smoking , alcohol , marital state , living condition .
Family Hx :
Dm , hypertension , Tb , asthma
Any other diseases ?
Surgical Hx .
1_ family history of DM
2_ sex and age
3_ life style include diet & physical activity.
4_ Symptoms & when did they start.
Study of WHO in 2004 :
From Ann Saudi Med. 2011 Jan:
Occur in childhood or early adulthood.
develops when the body’s immune system destroys pancreatic beta cells, causing absolute insulin deficiency.
Risk factors for type 1 diabetes may include autoimmune, genetic, and environmental factors.
There is a long preclinical period (up to 9 to 13 years) marked by the presence of immune markers.
Hyperglycemia occurs when 80% to 90% of β- cells are destroyed.
Individuals with type 1 DM are often thin and are prone to develop diabetic ketoacidosis if insulin is withheld or under conditions of severe stress.
Latent Autoimmune Diabetes in Adults (LADA) is a form of autoimmune (type 1 diabetes) which is diagnosed in individuals who are older than the usual age of onset of type 1 diabetes ( > 25 year ) .
Often, patients with LADA are mistakenly thought to have type 2 diabetes, based on their age at the time of diagnosis
caused by mutations in a number of different genes defects of insulin secretion.
Occur in late childhood, adolescence, or early adulthood.
diagnosis of MODY is based on presence of :
- non-ketotic hyperglycemia
in conjunction with a family history of diabetes. -
DM accounts for as many as 90% of DM cases marked by the presence of immune markers.
This is the most common form of diabetes mellitus and is highly associated with a family history of diabetes, older age, obesity and lack of exercise, history of gestational diabetes, impaired glucose metabolism.
It usually begins as insulin resistance, where the cells do not use insulin properly.
As the need for insulin rises, the pancreas gradually loses its ability to produce insulin.
F marked by the presence of immune markers.orm of glucose intolerance diagnosed
in pregnant women.
occurs more frequently among African Americans, obese women and women with a family history of diabetes.
requires treatment >>> normalize maternal blood glucose levels to avoid complications in the fetus.
Women who had GDM have a 20% to 50% chance of developing diabetes
Uncommon causes of diabetes (1% to 2% of cases) include:
- Endocrine disorders (e.g. acromegaly, Cushing’s
- Exocrine pancreas (e.g. pancreatitis)
- medications (e.g. glucocorticoids, pentamidine, niacin, and α- interferon).
Urine test: marked by the presence of immune markers.
- For Pregnant diabetic woman to check adequate nutrition and glycemic control
Pre- diabetic marked by the presence of immune markers.
It’s a state of abnormal glucose homeostasis characterized by the presence of
impaired FPG, GTT , or both.
It is often described as the “gray area” between normal blood sugar and diabetic levels
Diagnosed by: marked by the presence of immune markers.
1) signs or symptoms: 2) lab investigation
- Constant hunger . - FPG 100-125 mg/dl
- Blurred vision. - 2hPG 140-199 mg/dl
- weakness. - HbA1c 5.7-6.4 %
- Unexplained weight loss.
important clinically because: marked by the presence of immune markers.
When lifestyle changes such as
- eating healthy foods
- physical activity in daily routine
- maintaining a healthy weight
may be able to bring your blood sugar level back to normal and prevent development DM 2 .
important lab investigation for a patient who is presenting with DM as follow up :
HbA1c at least twice a year in patients meeting treatment goals on a stable therapeutic regimen.
Screening for type 2 DM should be performed every 3 years beginning at the age of 45.
But considered at an earlier age and more frequently in individuals with risk factors .
Pregnant women should be assessed for GDM at their first prenatal visit and proceed with glucose testing if at high risk.
The recommended screening test is : with DM as follow up :
fasting plasma glucose (FPG)
Normal FPG is less than 100 mg/dL
Or less than (5.6 mmol/L).
blood pressure control.
Regular insulin given subcutaneously, requiring injection 30 minutes prior to meals.
Lispro, aspart, and glulisine insulins have shorter durations of action than regular insulin, injection 10 minutes prior to meals.
Neutral protamine hagedorn (NPH) with DM as follow up :is intermediate-acting. contribute to a labile glucose response, nocturnal hypoglycemia, and fasting hyperglycemia.
Glargine and Detemir are long-acting “peakless” human insulin analogs that result in less nocturnal hypoglycemia than NPH insulin when given at bedtime
Symptomatic patients may initially require insulin or combination oral therapy to reduce glucose toxicity (which may reduce β-cell insulin secretion and worsen insulin resistance).
Sulfonylureas with DM as follow up :: stimulating insulin secretion .
Meglitinides:stimulating insulin secretion in presence of glucose.
Biguanides (metformin) : enhances insulin sensitivity of both hepatic and peripheral (muscle) tissues.
Thiazolidinediones (Glitazones) : enhance insulin sensitivity in muscle, liver, and fat tissues indirectly. Insulin must be present in significant quantities for these actions to occur.
Insulinfor patient who doesn't maintain good control of blood sugar with drugs.
studies included people with IGT and other high-risk characteristics for developing diabetes.
They found that lifestyle changes can prevent or delay the onset of type 2 diabetes among high-risk adults.
In the Diabetes Prevention Program, a large prevention study of people at high risk for diabetes, the development of diabetes was reduced 58% over 3 years .
The major organs and body systems involved in diabetes complications are the:
heart and blood vessels
Eye Problems: with DM as follow up :
Cataracts, Retinopathy, glucoma
To prevent :
Keep blood pressure and blood sugar levels in check .
make sure the eyes are examined on the schedule prescribed by the doctor
Kidney Disease (Diabetic Nephropathy) with DM as follow up :
High blood sugar can damage the blood vessels in the kidneys.
maintain good blood sugar control by following the diabetes treatment plan.
regular blood pressure and urine albumin tests checks up.
Nerve Damage (Diabetic Neuropathy) with DM as follow up :
can involve nerves in many different parts of the body. The most common early symptoms are numbness, tingling, or sharp pains in the feet or lower legs.
controlling blood sugar levels with diet, exercise, and diabetes medications will help reduce risk.
Heart and Blood Vessel Diseases with DM as follow up :
heart attack ,stroke and blockage of blood vessels in the legs and feet, which can lead to foot ulcers.
maintain a healthy weight.
check blood lipid and blood pressure regularly to be sure they're in a healthy range.
- Kumar & Clark's Clinical Medicine (Saunders, 2009).
-Pharmacotherapy: A PathophysiologicApproach, 8th Edition [JosephDiPiro]
-Davidson's Principles and Practice of Medicine