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Endocrine.DM

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					In Capsule Series
                            Endocrine


                       Diabetes mellitus

Def. :
         It’s a clinical syndrome in which there is an error of CHO
          metabolism ; due to : insulin deficiency, resistance or both,
          ending in : chronic hyperglycemia ± glucosuria,
                     vasculopathy & neuropathy.

Etiology :         ☺      ( 1ry →    95% &        2ry    →    5% )

           I. Primary :              ( includes 3 types : )

                a. Type 1 : ( previously called insulin-dependant DM or
                             juvenile-onset DM ).
                b. Type 2 : (previously called non insulin-dependant DM
                             or adult-onset DM ).
                c. MODY : mature onset diabetes in young patient.
                             - intermediate ( ) type 1 & type 2.
                             - occurs in young patient.
                             - ttt by oral anti-diabetic drugs.

    N.B. :   The old classification of insulin dependant & non-insulin
             dependant DM is misleading because many patient é type 2
             DM eventually require insulin for control hyperglycemia.

          II. Secondary D.M. :
                a. Pancreatic causes :
                       i. Chronic pancreatitis.
                      ii. Pacreatectomy.
                b. Endocrinal :
                       i. Cushing : cortisone.
                      ii. Acromegaly : GH.
                     iii. Thyrotoxicosis.
                c. Drugs :
                       i. Cortisone.
                      ii. Thiazide.
                     iii. Contra-ceptive pills.
                d. Others :
                       i. Gestational diabetes.
                      ii. DIDMOAD syndrome.
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Pathogenesis :
      Type 1 :      10%.
                  An autoimmune destruction of i pancreatic islet β-cells
                  leads to insulin deficiency.
                  Genetic predisposition alone does not seem to be
                  sufficient, perhaps viral infection may play a role.
                  without insulin, these patients are prone to develop
                  ketoacidosis.
                  Although typically diagnosed before age 30, it can
                  present at any age due to variability in rate of β-cell
                  destruction.

      Type 2 :
                  It’s characterized by peripheral insulin resistance, so
                  hyperglycemia develops despite above average level of
                  insulin.
                  In addition, it may be due to abnormal structure of insulin
                  or anti-insulin hormones esp. glucagons.
                  Factors that may play a role in pathogenesis include :
                  genetic predisposition & obesity.

                                    Type 1                         Type 2
Incidence :                          10 %                             85%
Pathogenesis :              Insulin deficiency due to         Insulin resistance.
                               damage of β-cells.
Insulin level :                        ↓↓                     Normal or even ↑↑
Age if onset :             Younger (usually < 30y).         Older (usually > 30y).
Body weight :                         Thin.                 Obese (usually 80 %).
Hereditary :                - 30% in identical twins - Near 100%
                            - usually no family history. - strong family history.
C/P:
  - Severity :                     Sever.                    Mild or moderate.
  - Ketoacidosis :               Common.                   Rare, need ppt factors.
  - Complication :             More common.                    Less common.
TTT :
 -Oral hypoglycemic :         Ineffective.                       Effective.
 - Insulin :             Necessary (essential for life )    Usually not required
          N.B : In type 2 we may need insulin when B cells fail after years.
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Stages of DM :
        I. Pre diabetes     :        (impaired glucose tolerance)
            a.   It refers to a group of people who have glucose values
                 too high to be considered normal but not fit i criteria
                 for i diagnosis of DM.
            b.   It’s intermediate category ( ) normal & DM.
            c.   There is risk factor for future diabetes & CVS diseases.
            d.   This group includes :                 ‫ت‬      ٤
                       i. +ve family history.
                      ii. obesity.
                     iii. ♀ é bad obstetric history → macrosomia.
                     iv. renal glucosuria.

        II. Latent diabetes       :
                   Diabetes appear only on exposure to stress &
                   disappears after removal of stress e.g. : pregnancy.

       III. Chemical diabetes :
                   Raised blood glucose é no symptoms.

       IV. Clinical diabetes      :
            a. Uncomplicated :
                      Classic triad of symptoms :         3p
                       polyuria : due to osmotic diuresis.
                       polydepsia : due to loss of fluid.
                       polyphagia weight loss : as a result of ↓ insulin
                          → no glucose can enter satiety center
                          → ↑↑ of satiety center.
            b. Complicated :
                  i. May be I 1st presentation.
                 ii. Symptoms of complications ……. see later.

         N.B. : ● DD of polyuria        :
                      - sever  polyuria       → DI.
                      - moderate ~            → DM.
                      - mild     ~            → CRF.
                 ● DD of polyphagia é weight loss :
                      - Thyrotoxicosis
                      - DM             -    Ascaris

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Investigations of DM :
        I. Blood      :
             1. Blood sugar tests :
                   i. Fasting blood glucose :
                            70 - 110 mg % →normal.
                            > 126 mg %    →DM.
                            110 - 126 mg % →impaired glucose
                            tolerance.
    N.B. : fasting is defined as no caloric intake for at least 8 hours.
                   ii. 2 h. post-prandial : ( after ingestion of 75 mg
                       glucose).
                             < 140 mg %          →     normal.
                             > 200 mg %          →     DM.
                             140 - 200 mg % →          impaired glucose
                                                       tolerance.
                  iii. Random ( casual ) glucose level :
                                it means glucose level during any time of
                                day é out regard to last meal.
                                Symptoms of diabetes ( 3p ) + casual
                                blood glucose > 200 mg%. →        DM.
             2. Oral glucose tolerance test : ( OGTT )
                    i. Patient should be fasting over night.
                   ii. Fasting bl. sugar is done.
                  iii. The patient is fed 75 gm glucose orally.
                 iv. Take bl. & urine samples every 1/2 h. for 2 h.
                  v. Diagnosis of diabetes is done acc. To i above
                       mentioned criteria.
                                Normal curve : 3 criteria :
                                1) Fasting : 70-110.
                                2) Reach maximal point in 1h. but still
                                    under 180 mg %.
                                3) Return to normal within 2 h.
             3. Cortisone glucose tolerance test :
                    i. Dexamethazone 3 mg is given before OGTT.
                   ii. It will induce hyperglycemia in latent & pre-
                       diabetic.
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        II. Urine     :
             1. Glucosuria : occurs when glucose serum level exceeds
                180 mg % ( renal threshold ); but it's not a good
                indicator for DM diagnosis.
             2. Ketonuria : for diagnosis of diabetic ketoacidosis.
        III. Monitoring of ttt     :        ( to assess ttt efficacy )
             1. Plasma glucose monitoring.
             2. Glycosylated hemoglobin ( HBA1c )
                     i. ( HBA1c ) is an indicator of glycemic control.
                    ii. Normally it's less than 7 % of total HB, & if > 12% →
                        poor glycemic control in the past 3 months.
                   iii. It can differentiate ( ) stress induced
                        hyperglycemia from DM.
       IV. Investigations for complication            :
             1. Plasma lipids.
             2. Urine analysis & renal function tests.
             3. ECG.
             4. Chest X-ray from TB.
        V. Investigations for i cause :
                      If 2ry diabetes is suspected < 5 %.

     N.B. : New WHO diagnostic criteria :
                2 of these 3 criteria :
                   1- Fasting plasma glucose      > 126 mg %.
                   2- Random plasma glucose       > 200 mg %.
                   3- Classic triad of diabetic symptoms ( 3p ).

Pathogenesis of diabetic complications :
     glycosylation      :                    ←         ‫ا م‬         ‫آ ز‬
     sorbitol pathway :           ‫ا‬           ←
         1. Glycosylation :
                This may lead to thickness of basement membrane of
                capillaries with narrowing of their lumen affecting
                 → retinal blood vessels, renal glomeruli & vasa nervosa
                 → leading to vasculopathy.
         2. Sorbitol pathway        :
                Glucose is reduced to sorbitol by aldole reductase of
                ATPase activity & cell energy → leading to neuropathy.
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Complications of DM :
  I. Cutaneous :
      1.   Infection :        carbuncle &        recurrent abscess.
      2.   Pruritis     :     pruritis vulvae.
      3.   Delayed healing of wound.
      4.   Xanthelasma ; due to hyperlipidemia.
      5.   Necrobiosis lipoidica diabeticorum :
              a. painless papule with central yellowish area surrounded
                   by brownish border.
              b. usually over i ant. surface of i legs.
              c. due to cutaneous bl. vessels occlusion.
      6.   Vasculopathy       :      leads to gangrene.

  II. Cardiovascular :

      1.   Microangiopathy     :
             a. diabetic retinopathy                  →   retina.
             b.   ~      nephropathy                  →   glomeruli.
             c.   ~      neuropathy                   →   vasa nervosa.

      2.   Macroangiopathy        :
             a. cerebral :        thrombosis &    ischemia.
             b. coronary :        angina     &    MI ( C.H.D. ).
             c. peripheral :      gangrene & intermittent cludication.
             d. renal      :      reno-vascular HTN.

      3.   Cardiomyopathy         :     due to microangiopathy.

      4.   Blood pressure :
              a. systemic hypertension.
              b. postural hypotension due to autonomic neuropathy.

     N.B. :     Causes of HTN in diabetic patient :
                  1-   diabetic nephropathy.
                  2-   obesity.
                  3-   Insulin    →    retention of Na.
                  4-   2ry diabetes : Cushing      &    acromegaly.

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 III. Chest :
       1.  Recurrent chest infection esp. T.B.
                 ( T.B. follows DM as its shadow ).
N.B. : Characteristically T.B. is apical lesion except in diabetes it’s basal.
        2. Kussmaul respiration ( air hunger ) & acetone smell in DKA.

 IV. Gastrointestinal :
                         Diabetes never have a normal bowel habits.
       1.    Diarrhea : due to :
                a. Sympathetic neuropathy      → parasympathetic
                   dominance → nocturnal diarrhea.
                b. Vasculopathy.
                c. Infection.
       2.    Constipation       :    due to vagal neuropathy.
       3.    Liver →     fatty liver →    hepatomegaly.

  V. Genital :
       1.    In ♂ :      impotence            →      psychological.
                                              →      neuropathy.
                                              →      vasculopathy.
       2.    In ♀ :         infections &      pruritis vulvae.
       3.    Effects of DM on pregnancy :
                a. On mother :
                         i. Eclampsia.
                        ii. post. Partum hge.
                       iii. puerperal sepsis.
                b. On fetus :
                         i. High birth weight.
                        ii. Hypoglycemic baby.
                       iii. Congenital anomalies.
                      iv. Respiratory distress syndrome.
       4.    Effects of pregnancy on DM :
                a. ↑ needs for insulin        due to       ↑ anti-insulin :
                                              estrogen &         progesterone.
                b. ↓ renal threshold for glucose.
                c. ↑ incidence of complications.

 VI. Eye :
       1.    Infection   :      chalazion.
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        2.    Repeated error of refraction, because i lens may be
              affected by reversible osmotic changes in patients é acute
              hyperglycemia.
        3.    New vessels formation in iris ( rubeosis iridis )
        4.    Optic neuritis.
        5.    Cranial nerve palsy ( 3,4 & 6 cranial nerves).

        6.    Diabetic retinopathy :
                 a. It’s I most characteristic form of diabetic eye diseases.
                 b. Especially in type 1 DM of long duration.
                 c. It’s of 2 types :
                         i. Non proliferative : micro-aneurysm, hge,
                            exudates ( benign form)
                        ii. Proliferative : neovascularization, this type must
                            be treated as early as possible by
                            photocoagulation by laser.
     N.B. :            without ttt 50% of proliferative patients become blind
                       within 5 – 10 years.

 VII. Diabetic foot :
        1.    Def. :       Trophic changes in foot of diabetic patients (
                    ulcers, falling of hair & gangrene ).
        2.    Ae. : vasculopathy, neuropathy & infection combine to
                    produce tissue necrosis.
        3.    TTT :
                 a. Control of diabetes.
                 b. Careful foot cleaning &         careful nail cutting.
                 c. For infection :     strong antibiotic & drainage of pus.
                 d. For ischemia :      revascularization & amputation in
                    gangrene.
     N.B. :            50% of all lower limbs amputation are performed in
                       people é diabetes.

 VIII. Renal :
              The kidney may be damaged by diabetes in 3 main ways :
                      Glomerular damage.
                      Ischemia resulting in narrowing of afferent &
                      efferent arterioles.
                      Ascending infection.


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     1.   Pyelonephritis :
                In usual pyelonephritis triad ( ∆ ) of
                                                   Fever.
                                                   Pain.
                                                   Dysuria.
          But, DM modify pyelonephritis through :
          → necrosis of tip of papillae ( acute necrotizing papillitis ).
          → fever, pain, dysuria + heamaturia & anuria may occur.

     2.   Diabetic nephropathy :
             a. Ae. : long standing DM ( type1 > type2 ), onset within
                    15 years.
              b. Pathology :         Glomerular sclerosis :
                   i. Thickening of basement membrane of glomeruli.
                  ii. Deposition of glyco-protein.
                 iii. Hyalinization of afferent & efferent arterioles.
    N.B. : DM affects efferent more than afferent.
           So ; there is more narrowing in eff. than in aff., this ↑↑ intra-
           glomerular pressure .
           So ; there is progressive leak of large molecules ( esp.
           protein) into urine.
              c. Types :
                  i. Diffuse : 80 %.
                 ii. Nodular : 20 % ( Kimmelestiel-Wilson’s syndrome ).
              d. C/P :                                    ٤
                   i. Long standing DM ( 10 – 20 years ).
                  ii. Proteinurea :
                         1. micro-albuminuria.     followed by
                         2. macro-albuminuria.     followed by
                         3. heavy proteinurea & nephrotic syndrome.
                 iii. Lately, CRF &      HTN.
                iv. Diabetic retinopathy & neuropathy are usually
                      present.
   N.B.
          :      CRF normal sized kidney in sonar :
                               DM.
                               Amyloidosis.
                 CRF big sized kidney in sonar :

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                                              Polycystic kidney.
                                 CRF small sized kidney in sonar :
                                              Chronic glumerulo-nephritis.                          ( GN )
                                              Chronic pyelonephritis.




          IX. Neurological :
                   1. Diabetic macroangiopathy.
                   2. Diabetic neuropathy.
                   3. Diabetic comas.
-----------------------------------------------------------------------------------------------------------------
                  1. Diabetic macroangiopathy                              : due to atherosclerosis :
                                     a.   Stroke.
                                     b.   Hge.
                                     c.   Thrombosis.
                                     d.   Ischemia.

                  2. Diabetic neuropathy                          :
                     i. Pathogenesis              :

                             unknown but there are 4 important theories :
                             1. Hypovitaminosis : polyuria washes water soluble B
                                complex.
                             2. Microangiopathy of vasa nervosa.
                             3. Metabolic ketosis : toxic effect of keton bodies.
                             4. Transformation of glucose to sorbitol by aldose
                                reductase enzyme.                      (‫ا ط‬      )

                    ii. C/P :
                          1. Feature of polyneuropathy may precede the
                                discovery of DM.
                             2. Starts as mono-neuropathy or mono-neuropathy
                                multiplex, affecting
                                   a. Peripheral nerves :  sciatica  ,    femoral,
                                                           ulnar     &    median.
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                                        :
                         b. Cranial nerves   III , VI              or     VII.
                3. Frank diabetes → polyneuropathy.
                         a. Symmetrical mainly sensory with pain & parasthesia
                            esp. in L.L., followed by superficial sensory of stock &
                            glove type.
                         b. Early loss of deep sensations, resulting in loss of deep
                            reflexes & sensory ataxia.
                         c. Motor weakness is late.


                4. Autonomic neuropathy :
                         a. CVS :
                                 i. Postural hypotension.
                                ii. Silent myocardial infarction
                               iii. At 1st tachycardia then fixed H.R.
                         b. Chest          :
                                1- Respiratory arrest ( unknown ).
                         c. GIT :
                                 i. Delayed gastric empting.
                                ii. Early nocturnal diarrhea, late constipation.
                         d. Genitor-urinary :
                                 i. Impotence
                                ii. Sensory, motor or autonomic bladder.
                         e. Skin :
                                    Hyperhydrosis then anhydrosis.
                         f. Trophic changes :
                                 i. Ulcers.
                                ii. Loss of hair.
                               iii. Rough nail.

     iii. TTT        :
                1.   Strict control of DM : diet, oral hypoglycemic or insulin.
                2.   Reassurance may be all that needed.
                3.   Physiotherapy if motor weakness is present.
                4.   Drugs :
                         a. Analgesics of neurotic pain
                         b. Vit. B complex ( TRI B ) & ATP ( adenoplex ).
                         c. Capillary modulators : Ca diabetes ( Doxium )
                         d. Aldose reductase inhibitor : sorbinil.
                         e. Cerebrolysin.(nerve growth factor)


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        3. Diabetic comas          :
             1.   Hypoglycemic coma. ( insulin reaction )
             2.   Diabetic ketoacidosis.    ( DKA )
             3.   Hyperglycemic hyperosmolar non ketotic coma.
             4.   Diabetic lactic acidosis.
             5.   Other causes of coma : uremic, hepatic, ………




   1.    Hypoglycemic coma :
           a. Ae.        :
                  May occur in all diabetics who are on drug ttt esp.
                  insulin due to :
                            • Missed meal.
                            • Over dose of insulin.
                            • Unexpected exercise.
                  it’s a major cause of anxiety for diabetic patients.
           b. C/P         :
                    Diabetic patients typically develop symptoms of
                    hypoglycemia when blood glucose values fall below
                    50 mg % but severity of symptoms can vary with the
                    individual.
                    Symptoms of hypoglycemia are divided into :
                                Adrenergic symptoms :
                                     due to ↑↑ catecholamines.
                                CNS ( neuro-glycemic )       :
                                     due to cerebral dysfunction.
                  i. Adrenergic symptoms :             ‫ت‬       ٥
                             1- Tachycardia ( palpitation ).
                             2- Sweating.
                             3- Tremors.
                             4- Anxiety.
                             5- Hunger pain.
              ii. CNS symptoms                :            ‫ت‬      ٥
                       1- Headache.
                       2- Blurring of vision.
                       3- Lack of concentration.
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                                 4- Convulsion may occur.
                                 5- Coma.
    N.B.        :      Hypoglycemic unawareness : means hypoglycemia
                       that occurs unnoticed by i patient because it’s not
                       associated with any adrenergic symptoms.
            Ae. :
                                      During night.
                                      β-blocker.
                                      Old age.
                                      Recurrent hypoglycemia.


            c. Investigation :
                          Low blood glucose < 50 mg % & absent in urine.
            d. TTT           :
                      i. If patient is conscious       :
                              oral glucose in i form of candy.
                     ii. If patient is comatosed       :
                              50 cc glucose 25 - 50 % IV followed by saline
                              infusion.
   N.B.     :            Recovery is very rapid except in irreversible brain
                         damage.

   2.     Diabetic ketoacidosis “ DKA ” :
            a. Def.          :
                         DKA is an extremely serious metabolic complication
                    of DM due to sever insulin deficiency, it’s ch’ by i triad of :
                          - Acidosis.
                          - Ketosis.
                          - Hyperglycemia.
            b. Ae.           :
                       • Occurs mainly in type 1 DM, due to sever insulin
                         deficiency, it’s usually seen in the following
                         conditions :
                                            Previously un diagnosed DM
                                            Missed insulin ( neglected ttt ).
                       • PPT. factors :
                                            Infection.
                                            Stress : surgery,M.I .
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N.B. :   In type 1 DM      : DKA occurs with or without ppt factors.
         In type 2 DM      : DKA occurs with ppt factors only.
         c. Pathogenesis & C/P :
                 sever insulin deficiency leads to :    ‫ت‬      ٥

             i. Glucose can’t enter cells     →     hyperglycemia
                                                    > 250 mg %.
              ii. ↑↑ lipolysis   → ↑ production of keton bodies
         ( β-hydroxy-buteric acid, acetoacetic acid & acetone )
                       → ketoacidosis ( PH < 7.3 ).

            iii. Effects of ketosis : gradual onset :   ‫ت‬      ٥

                 1- Muscles :
                               a. generalized weakness.
                               b. muscle pain.
                 2- Kidney :
                     ketonuria together with glucosuria lead to sever
                               a. polyuria.
                               b. polydepsia.
                               c. dehydration.
                 3- GIT :
                               a. anorexia.
                               b. nausea.
                               c. vomiting.
                               d. abdominal pain.
                 4- Respiration :
                               a. Kussmaul respiration ( deep rapid )
                               b. acetone odour of breath.
                 5- CVS :
                               a. depressed contractility.
                               b. rapid weak pulse.
                               c. low BL.P.
            iv. Shift of K outside cells in absence of insulin.
             v. End stage :       coma due to combined effect of
                               1. ketone bodies.
                               2. acidosis.
                               3. dehydration.
                               4. electrolyte disturbance.

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      d. Investigations :
          i. Blood :
                              1.   ↑ glucose.
                              2.   ↑ ketone bodies.
                              3.   ↑ FFA.
                              4.   ↓ HCO3.
                              5.   ↓↓ Na ( pesdohyponatremia due to polyuria).
                              6.   ↑↑ K due to extra-cellular shift of K
                                   seen with insulin deficiency.
         ii. Urine       :
                              1. glucosuria.
                              2. ketonuria.



      e. TTT      :
          i. Insulin :
                         short acting insulin.
                         low dose of insulin therapy 5 – 10 u/ h
                         infusion.
                         when blood glucose < 250 mg /dl →
                         reduce insulin to 2 – 4 u/ h.

         ii. Fluid therapy :
                        6 – 8 L is usually required.
                        at first saline is given, then change to
                        glucose 5% when bl. glucose < 250 mg/dl.

         iii. K therapy :
                             hypokalemia occurs é insulin ttt due to
                             intracellular shift, so ad ( 20 – 40 m. eq )
                             to each 1 L of fluid.

         iv. Na bicarbonate :
                       in sever acidosis [ PH < 7.1 ]


         v. Broad spectrum antibiotics.




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                   Hypoglycemic coma                      DKA
 Patient :           - follow ttt.               - neglect ttt.

 Onset :             - acute.                    - gradual.

 Pulse :             - tachycardia.              - weak.
                     - good volume.              - rapid.

 Bl.P. :             - ↑                         - ↓
 Skin :              - Sweaty.                   - dry.

 Pupils :            - dilated.                  - not dilated.

 Breath :            - normal.                   - acetone odour.

 Urine :             - no sugar.                  - +ve sugar & acetone.

 Coma :              - Irritable.                 - not irritable.

 IV glucose :         - rapid recovery.           - no effect.




      3.     Hyperglycemic-hyperosmolar non ketotic coma : ( HHNK )
              • There is minimal insulin level which is not enough to inhibit
                hyperglycemia but enough to ↓↓ ketogenesis , so there is
                hyperglycemia without ketosis.
              • It occurs in old type 2 DM.
              • Patients typically having sever hyperglycemia ( > 600
                mg/dl ), sever dehydration & plasma osmolarity ( > 340
                mg/dl ) is the landmark of this condition.
               N.B. :
                - sever dehydration may lead to renal failure.
                - sever hyperosmolarity may lead to neurological
                    symptoms ( convulsions & coma ).
              • TTT :
                        o Aggressive fluid replacement.
                        o Insulin.
                        o Low molecular weight heparin to prevent
                           thrombotic complications.

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              4.    Lactic acid coma :
                      • There is sever metabolic acidosis without significant
                        hyperglycemia or ketosis.
                      • It’s due to tissue hypoxia ( e.g. : high dose of biguanids ) →
                        anaerobic glycolysis → lactic acid.
                      • TTT        :      NaHCO3

           X. Diabetic infections :
                    1.   skin                     :       staph          &       candiasis.
                    2.   GB                       :       cholecystitis.
                    3.   urinary tract            :       pyelonephritis & perinephric abscess.
                    4.   lung                     :       T.B.           &       pneumonia.

                    N.B. :
                             1- Acute diabetic complications :
                                         =     diabetic coma +                             infections.
                             2- Micro-vascular complications :
                                         =     diabetic triopathy.
                             3- Hyperglycemic coma :
                                     =   DKA        +     HHNK.


        TTT of D.M. :
              I. General measures.
             II. Diet.
            III. Oral hypoglycemic.
           IV. Insulin.
            V. TTT of complication.
-----------------------------------------------------------------------------------------------------------------

            I. General measures                   :
                    a. Reassurance.
                    b. Education about nutrition & lifestyle modifications.
                    c. Exercise.
           II. Diet              :
                    a. It’s an important item in ttt of D.M.
                    b. Diet alone can control mild cases of type II D.M.
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              c. Total calories/day :
                         depending on weight & physical activity :
                      i. mild       activity               → 1500 cal /d.
                     ii. moderate     ~                    → 2500 cal /d.
                    iii. sever        ~ & pregnancy        → 3500 cal /d.
              d. Food components :
                      i. CHO        :     50%.
                                 - avoid simple sugars.
                                 - artificial sweeteners may be used.
                     ii. fat        :     30%.
                                 - avoid saturated fat.
                    iii. protein    :     20%.
                   iv. vitamins     :     B-complex        &     vit.A.
                    v. ↑↑ fibers    :     ↑ satiety.
              e. Number of meals :
                         3 main meals + 2 snacks in between,
                         to avoid hyperglycemia or hypoglycemia with ttt.
       III. Oral hypoglycemic :
              a. Sulphonylureas         :
                    i. mech. of action :
                         1. ↑↑ release of insulin from pancreas.
                         2. ↑↑ peripheral action of insulin.
                         3. ↓↓ hepatic production of glucose.


                    ii. preparations :
Drug                  Trade name           Dose ( mg/d )    Duration of
                                                            action
       1st generation :
- Cholropropamide         Pamidine            100 - 500         long acting
 - Acetoheamide            Dimelor            250 - 750        intermediate
  - Tolbutamide            Diamol             500 - 2000            short
       2nd generation :
 - Glibenclamide            Doanil.            2.5 - 15         long acting
   - Glimepiride           Amaryl.              1-6             long acting
    - Gliclazide          Diamicron.           40 - 240        intermediate
     - Glipizide           Minidiab            2.5 - 30             short



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               iii. indication :
                              type II DM not controlled by diet alone esp.
                              in non obese patients.
             iv. side effect :
                     1. allergy.
                     2. hypoglycemia.
                     3. GIT upset & cholestatic jaundice.
        b. Biguonides               :
               i. mech. of action :
                     1. ↑ anaerobic glycolysis.
                     2. ↓↓ glucose absorption.
                     3. ↓↓ appetite.
              ii. preparations :
                        Metformin ( Glucophage        –    Cidophage )
                                   - 500 mg t.d.s.   - 850 mg t.d.s.
              iii. indications :
                      1. type II DM not controlled by diet alone esp. if in
                         obese patients.
                      2. combined with suphonylurea or insulin to
                         achieve control.
             iv. side effects :
                      1. GIT irritation.
                      2. lactic acidosis.
        c. Recent drugs :
                i. Glucosidase inhibitors : ( Glucobay ) 50 mg t.d.s.
                   breakdown of CHO in intestine glucose absorption.
               ii. Repaglinide ( Novonorm ) insulin production at meal.


 IV. Insulin      :
        a. Action :
              i. Rapid action : ↑↑ entery of glucose, K & a.a. into i
                 cells.
             ii. Gradual action :
                    1. CHO           :           hypoglycemia:
                           a. ↑ glycogensis.
                           b. ↓ gluconeogenesis.
                           c. ↑ peripheral utilization of glucose.
                    2. fat           :
                           a. ↑↑ lipogenesis.
                           b. ↓↓ lipolysis.                      ‫ و‬fat‫ال‬
                                                                       - 81 -
 In Capsule Series
                                Endocrine

                        3. protein       :             anabolic.
            b. Preparations : was discovered in 1921.

       Type                      Trade names              Duration of action
1- Short-acting :          - Insulin Actarapid.         Onset    : < ½ h.
   ( soluble,              - Humulin R                  Peak     : 2 – 4 h.
   crystalline )           • Each 1ml = 20 units        Duration : 6 – 8 h.
2- Intermediate :          -    Insulin NPH             Onset    : 2 h.
                           -    Humulin N               Peak     : 6 – 8 h.
                           -    Monotard                Duration : 12 – 24 h.
                           -    Lente
                           •    Each 1 ml = 40 units
3- Long-acting :           -    Ultralente           Onset    : 6 – 8 h.
                           -    Ultratard            Peak     : 12 – 24 h.
                           -    Humulin L            Duration : up to 36 h.
                            •   Each 1 ml= 40 units.
4- Insulin mixture :                30% short + 70% NPH      ( mixtard )

            c. Indications :                              ‫ت‬      ٧
                    i. Type 1 DM.
                   ii. Type 2 DM not controlled é diet & oral hypoglycemic.
                  iii. During pregnancy, infection & surgery.
                 iv. DKA & HHNK ( critical episodes of type 2 DM ).
                  v. ↑↑ K ( Hyperkalemia ).
                 vi. Insulin stimulation test for GH assessment.
                 vii. Insulin stimulation test in pan-hpypopituitarism.


            d. Dose :          trial &     error.      ( s. c. )
                     i. Start é 20 u ( ½ cm )/d mixtard → non obese patient&
                        start é 30 u ( ¾ cm )/d mixtard → obese patient.
                    ii. The dose is gradually ( 5 u ) until control is achieved.
                   iii. 2/3 of dose in i morning & 1/3 of dose in i evening.
            N.B. :      1 cm mixtard = 40 u.
                 :      If mixtard is not available → 1/3 crystalline insulin + 2/3
               NPH can be mixed in i syringe & injected as rapid as you can.
            e. Administration :
                  i. S.C.
                 ii. Insulin pump.
                                                                              - 82 -
In Capsule Series
                          Endocrine

              iii. Insulin pens.
       N.B. :      Oral insulin →   under trial.
       f. Complications :                                  ‫ت‬  ٧
              i. Hypoglycemia & hypoglycemic coma.
             ii. Allergy : use human insulin.
            iii. Insulin resistance :
                    1. obesity → mild resistance.
                    2. antibodies against insulin.
           iv. Insulin lipodystrophy : atrophy or hypertrophy of s.c.
                 fatty tissue at i site of insulin injection.
            v. Insulin edema : Na & H2O retention.
           vi. Weight gain.
           vii. Pseudo insulin resistance ( Somogi effect ) : nocturnal
                 hypoglycemia due to over insulin dose → ↑↑ anti-insulin
                 hormones → rebound hyperglycemia in I morning.

       N.B. :    the ideal goals for glycemic control in patient with DM
          (Q : criteria for good diabetic control ?)
                         Lab. :
                                - Fasting plasma glucose ( 90 - 130 ) mg/dl
                                - Post prandial plasma glucose : < 180 mg/dl.
                                - HbA1c < 7%.
                         Clinical :
                                - No symptoms of DM.
                                - No symptoms of hypoglycemia.

  V. TTT of complication      :
                              See complications.




                                                                      - 83 -
    In Capsule Series
                                    Endocrine

      Scheme of ttt of DM :

                             Diabetic patient




         Type 1                                          Type 2


      Diet & insulin                                       Diet




                        controlled                         uncontrolled


                                                    Oral hypoglycemic



                         obese                            Non obese


                       Biguanides                       sulfonylurea



uncontrolled              controlled       controlled                  uncontrolled



    Add sulfonylurea                                         Add biguanides

                                     Uncontrolled



                                       Insulin


                                                                            - 64 -

				
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