Dr. D.'s Overhead Lecture Notes                                Section 4 - REPLACE PAGE NUMBERS WITH PAGES FROM SIXTH EDITION4
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Page index for Sec04
Kidney Functions
Kidney Operations
Kidney Regulation
    1. Renin-angiotensin mechanism
    2. ADH mechanism
Renal Failure
        - stages
        - types
Glomerulonephritis
Acute poststreptococcal glomerulonephritis  (APSGN)
Rapidly progressive glomerulonephritis
Chronic glomerulonephritis
Pyelonephritis
Acute pyelonephritis
Chronic pyelonephritis
Hypertensive Kidney
Polycystic Kidney
Hydronephrosis
Nephrotic Syndrome
End stage kidney
Uremic Syndrome
    Chemical imbalances
    Consequences
   Treatment strategies
Acute Renal Failure
    Causes
    Pathogenesis
    Consequences
   Treatment strategies
Endocrine System Notes
1. Treatment strategies
Diabetes mellitus
1. Major types of diabetes mellitus
2. Contributing factors
A. Effects of high blood glucose
    1. Kidney tubules
    2. Blood vessels
    3. Blood
    4. Connective tissue
    5. Nervous system
    6. Eyes
    7. Bacteria
B. Effects of high ketoacids
Treatment Goals
Treatment Strategies

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Kidney Functions - for homeostasis (p. 659)

        1. Normal adult kidney, gross
        2. Normal adult kidney, cross section, gross [IVP]
        84. Normal glomerulus, microscopic *

    1. regulate blood osmotic pressure (2.85mOsm)
    2. regulate concentration of each mineral salt
    3. regulate pH (7.35 - 7.45)
    4. regulate blood pressure
    5. eliminate nitrogen wastes
    6. regulate RBC production
    7. activate vitamin D

Kidney Operations and urine formation - for functions 1-5 above

    1. filtration (pp. 657, 658, 662)(sketch)
         - in glomerulus
         - separates small molecules from large molecules and cells -> filtrate
    2. reabsorption (pp. 657, 662, 667)(sketch)
         - PCT (proximal convoluted tubule)
              - bulk reabsorption
              - not much regulation (some by aldosterone)
         - loop of Henle
              - Na⁺ (sodium ions)
              - not regulated
         - DCT (distal convoluted tubule)
              - small amount reabsorbed
              - well regulated (by aldosterone)
         - collecting duct
              - water
              - well regulated (by ADH)
    3. secretion (pp. 657, 662, 667)(sketch)
         - PCT, DCT, and collecting duct
              - H⁺, N, K⁺, PO^-3, uric acid, others

Kidney Regulation

    1. Renin-angiotensin mechanism (p. 671)

        With decr. BP (sketch)
 

decr. BP  or  change in filtrate Na+ conc.  -> incr. renin  ->   incr. angiotensin
yields                                           yields
systemic vasoconstriction	incr.aldosterone (from adrenal cortex)
yields	yields
	incr. Na+ and H2O reabsorption
	yields
	incr. blood volume
yields
incr. BP (homeostasis)

        With incr. BP (sketch)

    2. ADH mechanism(p. 670)

        With decr. BP(sketch)
 

        With incr. BP(sketch)

Renal Failure

    acute renal failure
    chronic renal failure
        - may start in glomeruli, tubules, or vessels
        - all parts finally damaged ->
           - end stage kidney  (ESK) (structural) (p. 706)
                      43. End stage renal disease, gross
                      44. End stage renal disease, microscopic *
          -  renal failure (inadequate function) (pp. 692, 724)
          -  uremic syndrome (certain S&S) (p. 724)

    - stages based on % nephrons and presence of S&S
            - decreased renal reserve
                - 1%-75% of nephrons gone  =  99%-25% of nephrons left
                - S&S only under stress conditions
            - renal insufficiency
                - 75%-90% of nephrons gone  =  25%-10% of nephrons left
                - S&S always present
            - renal failure ( =  end stage kidney  = uremic syndrome)
                - 90%-100% of nephrons gone  =   10%-0% of nephrons left
                - severe S&S (uremic syndrome) and loss of homeostasis

    - types (p. 696)

            - glomerulonephritis  =  (glomeruli affected first)
              84. Normal glomerulus, microscopic *
            - pyelonephritis  =  (tubules affected first)
            - hypertensive kidney  =  5% of cases (vessels affected first)
            - polycystic kidney  =  5% of cases (all parts affected) (p. 712)
            - other causes
                (1) diabetes mellitus (p. 714)
                (2) renal artery stenosis (pp. 687, 710)
                (3) systemic connective tissue autoimmune diseases (p. 711)
                (4) toxins (phenacetin, lead, certain medications, etc.)

Glomerulonephritis

Acute poststreptococcal glomerulonephritis  (APSGN) (p. 704)

    causes
          infection someplace other than the urinary system

    pathogenesis
        84. Normal glomerulus, microscopic *
        41. Nodular glomerulosclerosis, microscopic *
        42. Nodular glomerulosclerosis and hyaline arteriolosclerosis, microscopic, PAS stain *
        88. Focal segmental glomerulosclerosis (FSGS), microscopic *
        89. Focal segmental glomerulosclerosis (FSGS), microscopic, Trichrome stain *
        90. Post-streptococcal glomerulonephritis, low power microscopic *
        91. Post-streptococcal glomerulonephritis, high power microscopic *
        92. Post-streptococcal glomerulonephritis, granular immune deposits, immunofluorescence microscopy *
        93. Post-streptococcal glomerulonephritis, electron micrograph *
        94. Membranous glomerulonephritis, microscopic *
 (sketch)

infection in body  ->  immune response  ->  Ag-Ab complexes
yields  (1) & (2)
(1) clogged glomeruli  (pp. 159, 703) ->	decr. GFR  ->	oliguria, azotemia, edema, incr. BP
	yields
	incr. renin (p. 671)  -> incr. H2O retention
	yields
	incr.incr. oliguria,  incr. incr. edema,  incr. incr. BP
(2) inflamed glomeruli (pp. 159, 703) -> large pores  -> protein leakage  -> proteinuria, casts, hematuria

        NOTE: edema from
                        1. decr. GFR
                        2. renin mechanism

 - 85% cases resolve, some cases ->  permanent damage, 2%-5% cases -> ESK

Rapidly progressive glomerulonephritis (RPGN) (p. 705)

        causes
        autoimmiune attack on kidneys

    pathogenesis

        98. Rapidly progressive glomerulonephritis with crescents, microscopic *
        99. Rapidly progressive glomerulonephritis with crescents, microscopic *
        100. Rapidly progressive glomerulonephritis with crescents, fluorescence microscopy *

Chronic glomerulonephritis (CGN)  2-40 years to reach ESK (p. 705)

    pathogenesis(sketch)
 

idiopathic (possibly infection in body & Ag-Ab complexes) -> (1) & (2)

(1) clogged glomeruli  ->  like APSGN with renin  ->  incr. incr. edema etc.

(2) very inflamed glomeruli  ->  very large pores  ->  incr. incr.. protein leakage (p. 708) (nephrotic syndrome) -> decr. COP  -> (a) decr.  fluid return & (b) hyperlipidemia

yields

a. ->  incr. incr. incr.  edema

a. -> decr. blood volume -> incr. ADH (p. 670)  ->  incr. incr. H2O retention  -> incr. incr. incr. incr.  edema (not incr. BP)

and

b. -> atherosclerosis  -> more kidney problems

      finally  ->  tubule and vessel damage -> ESK, renal failure, uremic syndrome
           44. End stage renal disease, microscopic *

        NOTE: edema from
                        1. decr. GFR
                        2. renin mechanism
                        3. decr. COP
                        4. ADH mechanism

Pyelonephritis

Acute pyelonephritis
    causes
        infection in kidney, toxins
    pathogenesis(sketch)

    infection in kidney or toxins -> injured and inflamed tubules (p.699c) -> decr. amount and  decr. control of reabsorption and secretion  -> decr. homeostasis (osmotic pressure, conc. of salts, pH, BP)

       infection from
           blocked urine flow from -
                - strictures(sketch)
                - calculi (sketch)
                              1.Synovial fluid with sodium urate crystals, polarized light with red compensator, microscopic. *
                              7. GIF animation of urinary tract lithiasis
                - neoplasms (sketch)
                - prostatic hypertrophy (sketch)
                              18. Bladder hypertrophy and calculus with obstruction from nodular hyperplasia of prostate, gross
                - neurogenic bladder
           introduction from -
                - sexual activity (especially from shorter urethra in women)
                - cystoscopy
                - catheters
                  decr. resistance from -
                - stress
            refluxing from -
                - faulty ureter/bladder connection (sketch)

    systemic S&S (leucocytosis, fever, chills, back pain, voiding pain)
    urine S&S (polyuria, proteinuria, bacteria, pyuria, casts (pp. 684, 700), WBCs)

Chronic pyelonephritis (p. 700)

    causes
        chronic infection in kidneys, chronic toxins

    pathogenesis

    infection in kidney, chronic toxins  ->  chronic tubule inflammation  -> injured and scarred tubules (p. 706)  -> decr. amount and  decr. control of reabsorption and secretion  -> decr. homeostasis (osmotic pressure, conc. of salts, pH, BP)
    - finally  ->  glomeruli and vessel damage  ->
                             ESK (p. 706)
                             renal failure
                             uremic syndrome

    S&S =
            polyuria
            nocturia
            low urine specific gravity (dilute urine) (p. 682)
           dehydration (p. 682)
           salt loss (p. 682)
           incr. or  decr. pH (p. 683)
           incr. renin (attempts to retain Na⁺ and H₂O)

Hypertensive Kidney
    causes
          high blood pressure
    pathogenesis

        37. Benign nephrosclerosis, gross
        38. Malignant nephrosclerosis, gross
        39. Malignant nephrosclerosis with fibrinoid necrosis, microscopic *
        40. Hyperplastic arteriolitis with hypertension, microscopic *

    chronic incr. BP -> kidney vessel damage -> fibrosis  ->  ischemia  ->  glomeruli and tubule damage  -> decr. GFR ->   incr. renin  ->  incr.incr. BP -> more vessel damage  -> -> ->
             ESK (p. 709)
             renal failure
             uremic syndrome

    S&S =
              incr. BP
              proteinuria
              hematuria
              azotemia

Polycystic Kidney  (p. 712)
    causes
        genetic (inherited)
    pathogenesis (sketch)

        62. Dominant polycystic kidney disease, gross
        63. Dominant polycystic kidney disease, gross
        64. Dominant polycystic kidney disease, gross [CT]
        67. Multiple simple renal cysts, gross
        62.Dominant polycystic kidney disease with polycystic liver, gross [CT]
        62. Dominant polycystic kidney disease with polycystic liver, gross [CT]

    abnormal gene  ->  cyst formation  ->  damaged nephrons  ->  renal failure & uremic syndrome

Hydronephrosis
    causes
        chronic partial urine obstruction, urine refluxing
    pathogenesis (sketch)

    (1) chronic partial obstruction (stricture, calculi, neoplasms, prostatic hypertrophy, neurogenic bladder)  ->
        or
    (2) refluxing  ->

          urine retention  ->  pressure in kidney  ->  tubule and vessel damage

      S&S = oliguria followed by polyuria, azotemia, acidosis, kidney atrophy

      finally  ->  glomerular damage  ->
                          ESK
                          renal failure
                          uremic syndrome
            calculi
           1.Synovial fluid with sodium urate crystals, polarized light with red compensator, microscopic. *
           7. GIF animation of urinary tract lithiasis
           10. Hydronephrosis with calculus at ureteropelvic junction, gross
           9. Hydronephrosis, severe, gross [CT]
           8. Hydronephrosis from obstruction by calculus, gross
           11. Hydroureter and hydronephrosis, gross [XRAY]
            prostatic hypertrophy
           18. Bladder hypertrophy and calculus with obstruction from nodular hyperplasia of prostate, gross
    S&S  =  oliguria followed by polyuria, azotemia, acidosis, kidney atrophy

Nephrotic Syndrome (p. 708)
    causes
        massive protein loss in urine (severe proteinuria)
   pathogenesis
 

very inflamed glomeruli  ->  very large pores  ->  incr. incr. protein leakage (nephrotic syndrome) -> decr. COP (hypoalbumemia) -> (a) decr.  fluid return & (b) hyperlipidemia (from liver metabolism)

yields (a. decr. COP & b. hyperlipidemia)

a. decr. COP ->  1. incr. incr. incr. EDEMA

a. decr. COP ->  decr. fluid return  ->  decr. blood volume -> incr. ADH  ->  incr. incr. H2O retention  -> incr. incr. incr. incr. edema & decr. BP -> (2, 3, & 4)

2. decr. GFR  ->  H2O retention  ->  incr. incr. EDEMA

3.  incr. renin  ->  H2O retention  ->  incr. incr. EDEMA

4.  incr. ADH  ->  H2O retention  ->  incr. incr. EDEMA

b. hyperlipidemia  -> atherosclerosis  -> more kidney problems, etc.

        NOTE: edema from
                        1. decr. GFR
                        2. renin mechanism
                        3. decr. COP (occurs first)
                        4. ADH mechanism

End Stage Kidney  (pp. 700, 706, 709, 714)

              43. End stage renal disease, gross
              44. End stage renal disease, microscopic *
    - glomeruli  - solidified (hyalinized)
    - tubules  - few, small, distorted
    - vessels  - few, small, distorted
    - much scar tissue (fibrosis)

Uremic Syndrome

  Chemical imbalances
        1. water (regulated and variable reabsorption)
            - excess retention  ->  osmotic problems,  incr. BP, edema, CHF
            - excess elimination  ->  osmotic problems,  decr. BP
            - no regulation by kidney  ->  urine specific gravity of 1.010 = renal failure = ESK
        2.  sodium (regulated and variable reabsorbed - most is reabsorbed)
            - excess retention (common)  ->  edema,  incr. BP, CHF
            - excess elimination (rare)  ->  nerve and muscle malfunction
        3.  potassium (regulated and variable reabsorption and secretion)
            - excess retention (usual) or elimination  ->  arrhythmias
        4.  pH (regulated and variable secretion)
            - excess retention (usual) or elimination  ->  enzyme malfunction  -> cell malfunction, cell injury, cell death
        5. nitrogen wastes (eliminated by filtration - ex. urea, creatinine)
            - excess retention  ->  toxicity  ->  cell injury/cell death
        6. uric acid (eliminated by filtration and secretion)
            - excess retention  ->  crystals  ->  inflammation (ex. gout)
        7. blood proteins (usually retained)
            - excess loss (damaged glomeruli or tubules)  ->
                 (1) casts  ->  blocked tubules and urine flow
                 (2) decr. COP  ->  edema, nephrotic syndrome

Consequences(pp. 724, 727, 729, 731)
        - multiple organ and system malfunctions

Treatment strategies (p. 735)
        1. substitute regulation
               - conservative
                    a. regulate input (diet = foods and beverages)
                    b. regulate production (e.g., exercise)
                    c. regulate output (e.g., temperature, medications, exercise)
               - extreme
                    d. dialysis (pp. 742, 744)
                    e. transplant (p. 746)
        2. check for and treat complications (ex. infection, circulatory problems, bone degeneration, gout)

Acute Renal Failure

  Causes(p. 756)
          1. ischemia (pre-renal)
          2. toxins (tubular necrosis)
          3. obstruction (post-renal)

Pathogenesis(p. 759)

        1. ischemia  -> decr. GFR  -> (sketch)
                   oliguria             ->          relief  ->  recovery
                   (low GFR)
                             or  yields
                   polyuria            ->          relief  ->  recovery
                   (damaged tubules)
                            or  yields
                   renal failure (uremic syndrome)

        2. toxins  ->  tubule injury  ->
           32. Acute tubular necrosis with ethylene glycol poisoning, microscopic*
                    oliguria            ->          relief  ->  recovery
                    (casts block)
                           or  yields
                     polyuria          ->          relief  ->  recovery
                     (damaged tubules)
                          or  yields
                     renal failure (uremic syndrome)

        3. obstruction  ->
                    oliguria          ->          relief  ->  recovery
                    (partial obstruction)
                          or  yields
                     polyuria       ->           relief  ->  recovery
                    (damaged tubules)
                         or  yields
                     renal failure (uremic syndrome)

Consequences(pp. 724)
      - multiple organ and system malfunctions

Treatment strategies (pp. 735, 742, 744, 746)
        - same as for above for uremic syndrome

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Endocrine System Lecture Notes
        Endocrine System Lecture Notes

Chapter 58
1. Treatment strategies
    - reduce hormone excesses (e.g., remove part or all of endocrine gland)
    - augment deficient hormone (e.g., administer hormone injections)

Chapter 63 - Diabetes mellitus = DM = a disease involving loss of ability to regulate blood glucose levels and resulting in a decrease in tolerance of carbohydrate input (i.e., glucose levels rise above normal)

    Normal islets of Langerhans, with immunoperoxidase stains (right, insulin and left, glucagon), microscopic
    Islet of Langerhans, insulitis, microscopic
    Islet of Langerhans, deposition of amyloid, microscopic

1. Major types of diabetes mellitus
    - Insulin dependent diabetes mellitus = IDDM
        - insulin supplements required for survival
        - also called Type I diabetes mellitus
        - also called juvenile onset (most cases develop during youth)
        - also called ketosis-prone (most cases show high levels of ketones in the urine - ketones come from fat breakdown)
        - represents 5% - 10% of cases of DM

    - Non-insulin dependent diabetes mellitus = NIDDM
        - survival possible without insulin supplements
        - also called Type II diabetes mellitus
        - also called maturity onset diabetes mellitus (most cases develop after age 40)
        - also called non-ketosis prone (few cases show excess ketone levels in the urine)
        - represent 90% - 95% of cases of DM

    - other types are from other causes (e.g., pregnancy = gestational DM, pancreatitis or cancer or other disorders = secondary DM)

2. Contributing factors (a - g)

    a. Genes, especially for NIDDM
        - environmental factors (e.g., virus, obesity) may trigger genes to decrease insulin production

    b. Sedentary lifestyle
        - low muscle activity decreases sensitivity of muscle cells to insulin and therefore more insulin is needed to get the same effect
(sketch)

    c. Obesity, especially from high carbohydrate diet
        - obesity decreases sensitivity of cells to insulin and therefore more insulin is needed to get the same effect
(sketch)

    d. Stress (e.g., infection, emotions)
        - stress -> increase in glucocorticoids and norepinephrine, which antagonize insulin and raise blood glucose levels

    e. Pregnancy
        - estrogen antagonizes insulin

    f. Autoimmune response
        - autoimmune attack on the pancreas destroys insulin-producing cells
        - major cause of IDDM

    g. Medications
        -various medications antagonize insulin (e.g., corticosteroids used as anti-inflammatory agents)
 

3. Normal regulation of  blood glucose

    - pancreatic hormones
        - main regulators
            - insulin
                - from beta cells in pancreas
                - cause decr. blood glucose
            - glucagon
                - from alpha cells in pancreas
                - causes incr. blood glucose
        - other hormones
            - (e.g., norepinephrine, growth hormone, glucocorticoids, sex hormones, etc.)
    - maintain homeostasis of blood glucose in spite of input (diet) and use (metabolism)
        - normal range  =  70 - 120 mg% in blood
    - mechanisms of normal control
        - liver cells (+ or -), fat cells (+ or -), and muscle cells (- only) are main cells involved

    Normal (sketch)
 

incr. blood glucose ->	incr. insulin     &           ->   decr. glucagon	1. incr. gluc. into cells                        ->	-> decr. blood glucose       (homeostasis)
		2. incr. gluc. stored as          glycogen ->
		3. incr. gluc. stored as           fat ->
		4. incr. gluc. used for            proteins ->

(sketch)  (graph)                                                     (cell)

   Normally:

        glucose + O₂  ->  CO₂ + H₂O + energy

        fats + O₂  ->  (needs some glucose for reactions) ->
                                        CO₂ + H₂O + energy

4. "Regulation" of blood glucose with diabetes mellitus (sketch)
 

incr. blood glucose -> (but little glucose in pancreas cells)	"no" insulin     &           ->   incr. glucagon	1. decr. gluc. into cells        ->	-> incr.incr.     blood glucose   (not homeostasis)   (still little glucose      in pancreas cells)
		2. gluc. made from      glycogen     leaves cells ->
		3. gluc. made from      fat  leaves cells ->
		4. decr. gluc. used for      proteins ->

"no" insulin       &             -> incr. incr. glucagon   (still little glucose in pancreas cells)	1. decr. gluc. into cells        ->	-> incr. incr. blood  glucose      (not homeostasis)      (still little glucose in pancreas cells)
	2. gluc. made from      glycogen     leaves cells ->
	3. gluc. made from      fat  leaves cells ->
	4. decr. gluc. used for      proteins ->

(sketch) (graph)                                                     (cell)

   Note:  incr. blood glucose -> incr. incr. blood glucose ->
                incr. incr.incr. blood glucose -> etc.

                1. high blood glucose
                     AND in severe cases
                2. high blood ketoacids (sketch)

A. Effects of high blood glucose
    1. Kidney tubules (regulate osmotic pressure, salts, BP) (sketch)

                a. glycosuria -> energy loss -> polyphagia
                        (and weight loss when severe)
        Renal glomerulus, nodular glomerulosclerosis, microscopic
        Renal glomerulus, nodular glomerulosclerosis, hyaline arteriolosclerosis, PAS stain, microscopic

                b. polyuria -> (1, 2)
                        1. dehydration -> thirst -> polydipsia
                        2. osmotic problems, decr. BP (sketch)

                c. salt loss -> salt imbalance -> malfunctions (sketch)
                        (e.g., heart, brain) -> coma, death

    2. Blood vessels (glycoproteins)

        a. capillaries
                thick basement membranes -> (1, 2) (sketch)
                    1. decr. capillary exchange -> cell malfunctions
                    2. clogged glomeruli -> decr. GFR -> -> -> ESK
                 84. Normal glomerulus, microscopic *
                 41. Nodular glomerulosclerosis, microscopic *
                 42. Nodular glomerulosclerosis and hyaline arteriolosclerosis, microscopic, PAS stain *

        b. arterioles
                vessel wall injury -> kidney vessel damage -> -> ESK (like hypertensive kidney)
                 42. Nodular glomerulosclerosis and hyaline arteriolosclerosis, microscopic, PAS stain *

        c. arteries
                atherosclerosis -> M.I.s, strokes, peripheral vascular disease -> poor healing, infections, gangrene
           Left anterior descending coronary artery, advanced atherosclerosis, gross
           Left anterior descending coronary artery, recent thrombus, microscopic
           Interventricular septum, recent myocardial infarction, gross
           Aortic atherosclerosis demonstrated in three aortas, gross
           Foot with previous healed transmetatarsal amputation and recent ulcer, gross
           Gangrenous necrosis and ulceration, lower extremity, gross

    3. Blood (glycoproteins)
            glycoproteins ->  (a, b, & c)

                a. thrombus formation -> ischemia -> cell injury
                b. decr. O₂ on Hb -> decr. O₂ supply -> cell injury
                c. decr. WBC functioning -> incr. infections

    4. Connective tissue (glycoproteins) (sketch)
            linked fibers ->  (a & b)

                a. decr. diffusion -> decr. servicing of cells -> cell injury/cell death (ex. dermis)

                b. stiffness -> difficulty moving

    5. Nervous system (sorbitol)
            sorbitol in neurons & myelin -> neuron malfunction -> decr. sensory and motor functioning -> (a-d)

                a. decr. sensations
                b. decr. muscle strength -> increased injury and infections
                c. decr. muscle reflexes
                d. decr. autonomic reflexes -> (1-3)
                      1. decr. sweating -> incr. hyperthermia
                      2. abnormal G.I. peristalsis -> indigestion and maldigestion
                      3. fecal and urinary incontinence

     6. Eyes (sorbitol) (sketch)

              in lens -> cataracts -> blindness
           Normal appearance, retina on funduscopic examination
           Cataract of the crystalline lens, gross
            Cataract, gross
              in retina -> diabetic retinopathy -> blindness (sketch)
           Diabetic retinopathy on funduscopic examination
           Proliferative diabetic retinopathy on funduscopic examination
           Glaucoma, cupping of the optic disk on funduscopic examination
           Glaucoma with excavation of the optic cup, microscopic

    7. Bacteria (glucose)

         incr. glucose -> incr. bacterial growth -> incr. infections
              Kidney, acute pyelonephritis, microscopic
              Renal pelvis, infection with Candida albicans, PAS stain, microscopic

B. Effects of high ketoacids

        ketoacids -> (1, 2, & 3)

            1. decr. pH (acidity) -> cell malfunction
                    (ex. brain -> coma, death)
            2. salt loss in urine -> cell malfunction (sketch)
                    (ex. brain -> coma, death)
            3. incr risk of infection
           Nasopharynx, mucormycosis (zygomycosis), H and E stain, microscopic

Treatment Goals  (1, 2, & 3)
    1. maintain glucose homeostasis
    2. prevent ketoacidosis
    3. prevent complications

Treatment Strategies  (1 - 6)
        1. substitute regulation
                a. regulate input (diet = foods and beverages, CHOs) (regulates glucose levels)
                b. regulate use (e.g., exercise) (alters glucose use and insulin sensitivity)
                c. avoid obesity (alters insulin sensitivity)
                d. insulin therapy (regulates glucose levels)
                e. medications (regulate insulin production and glucose levels)
        2. check for and treat complications (e.g., see above)

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