Diabetes Mellitus Type 2: Medical History

Medical history (history of illness) is an important component in the diagnosis of type 2 diabetes mellitus. Family History

  • Are there any conditions in your family that are common, such as obesity, hypertension, diabetes mellitus, dyslipidemia, myocardial infarction, stroke, early mortality, amputation?
  • Are there any hereditary diseases in your family?

Social anamnesis

Current medical history/systemic medical history (somatic and psychological complaints).

  • Do you have increased thirst?
  • Do you need to urinate very frequently? How often?
  • Do you often feel tired, exhausted?
  • Do you suffer from visual disturbances?
  • Have you noticed any skin changes? Boils? Itching? Delayed wound healing?
  • Skin lesions such as furunculosis (inflammation of multiple hair follicles).

Vegetative anamnesis including nutritional anamnesis.

  • Are you overweight? Please tell us your body weight (in kg) and height (in cm).
  • Do you smoke? If so, how many cigarettes, cigars or pipes per day?
  • Do you drink alcohol? If yes, what drink(s) and how many glasses per day?
  • Do you use drugs? If yes, what drugs and how often per day or per week?

Self history incl. medication history.

Medications (with potential diabetogenic effects).

  • 5-alpha-reductase inhibitors (dutasteride, finasteride).
  • Alloxan
  • Alpha blockers, centrally acting
  • Antiarrhythmics
  • Antibiotics
    • Gyrase inhibitors (1st generation) – nalidixic acid.
    • Rifampicin
  • Antidepressants* *
    • Tricyclic antidepressants [insulin resistance ↑, weight gain]
  • Antiepileptic drugs
    • Phenytoin
  • Antihypertensives
    • Imidazolines (clonidine)
  • Antiprotozoal agents (pentamidine* , pentacarinate) [beta cell toxic effects].
  • Antipsychotics (neuroleptics)* * [insulin resistance ↑, weight gain]
  • Antiretroviral therapeutics
  • Arsenic trioxide
  • Benzothiadiazine derivatives (e.g., diazoxide) and analogues* * [→ potassium losses → insulin secretion ↓; effect is delayed, usually weeks to months after therapy).
  • Beta-blockers* * [increase in insulin resistance as a result of weight gain; inhibition of insulin secretion from beta cell and/or decreased muscle blood flow]
    • Nonselective beta blockers (eg, carvedilol, propranolol, soltalol) [inhibition of insulin secretion; more potent than selective beta blockers]
    • Selective beta-blockers (e.g., atenolol, bisoprolol, metoprolol).
  • Betamimetics (synonyms: β2-sympathomimetics, also β2-adrenoceptor agonists) – fenoterol, formoterol, hexoprenaline, indaceterol, olodaterol, ritodrine, salbutamol, salmeterol, terbutalinehyperglycemia.
  • Chemotherapeutic agents/immunosuppressants.
    • Cycosporine A
    • Sirolimus (rapamycin)
    • Tacrolism
  • Dilantin*
  • Diuretics (risk increase approximately 23%).
  • H2 antihistamines (H2 receptor antagonists, H2 antagonists, histamine H2 receptor anatgonists) – cimetidine, famotidine, lafutidine, nizatidine, ranitidine, roxatidine.
  • Hormones and hormonally active substances
    • ACTH
    • Glucagon
    • Glucocorticoids* – betamethasone, budesonide, cortisone, fluticasone, prednisolone [insulin resistance ↑; altered cellular glucose metabolism]
    • Catecholamines
    • Prolactin
    • Thyroid hormones* – thyroxine
    • Sex steroids
    • Tokolytics
    • Growth hormone* (WH; somatropin; Engl.: somatrophin) and analogues
  • HIV therapy* *
    • Nucleoside analogue (didanosine) [pancreatitis.]
    • Protease inhibitors (indinavir, nelfinavir, ritonavir, etc.) [insulin secretion ↓, insulin resistance ↑; centripetal obesity with hypertriglyceridemia]
  • Indomethacin
  • Immunosuppressants* * [insulin secretion↓]
  • Interferon-α* / alpha-interferon [induction of organospecific autoimmune disease/type 1 diabetes]
  • Lipid-lowering agents (risk increase approximately 32%); risk increase for menopausal women (hazard ratio [HR] 1.71, 95% CI, 1.61-1.83)
  • Morphine
  • MTOR inhibitors (everolimus, temsirolimus)
  • Nicotinic acid*
  • Psychoactive substances
    • Haloperidol
    • Imipramine
    • Lithium
    • Phenothiazide and derivatives
  • Streptozotocin [beta cell toxic effects.]
  • Sympathomimetics
    • Α-adrenergic agonists
    • Β-adrenergic agonists
  • Theophylline
  • Vacor* (pyrinuron, pyriminil; rodenticide) [beta cell toxic effects].
  • Vasodilators (diazoxide).
  • Cytostatics
    • Alkylants (cyclophosphamide)
    • L-asparaginase

* Directly diabetogenic * * Indirectly diabetogenic

Environmental exposure – intoxications (poisonings).

  • Bisphenol A (BPA) as well as bisphenol S (BPS) and bisphenol F (BPF).
  • Air pollutants
    • Particulate matter: long-term exposure to particulate matter in children (for every 10.6 µg/m³ of additional airborne nitrogen dioxide (NO2), the incidence of insulin resistance increased by 17%. For airborne particulate matter (up to 10 µm in diameter), there was a 19% increase in insulin resistance per 6 µg/m³).
  • Organic phosphates (OP) in insecticides: e.g., chlorpyrifos, dichlorvos (DDVP), fenthion, phoxim, parathion (E 605) and its ethyl and methyl derivatives, and bladane.
  • Pesticides