Endo 2

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maps504
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248931
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Endo 2
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2013-11-25 00:08:25
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  1. Adrenal Cortex: hormones/functions
    • 1.      glucocorticoids – glucose
    • metabolism, role in response to stress

    • a.       inc conversion of
    • protein/fat to glucose

    b.      inc breakdown of protein

    c.       inc use of fatty acids

    d.      dec immune response

    • 2.      mineralocorticoids – fluid
    • and e-lyte balance – aldosterone = sodium and water reabsorption and K
    • excretion.

      3.  androgens – sex steroids
  2. Cushings
    Syndrome
    • 1. 
    • Definition:  excess corticosteroids.  Most common cause is ACTH secreting pituitary
    • tumor.  Other- adrenal tumor, ectopic
    • ACTH producing tumor

     

      2.  Pathophysiology:  no regulation, inc hormones

     

    • 1.      Clinical
    • Manifestations: 

    a.       glucocorticoids:

    1.      wt gain

    2.      glucose intolerance

    3.      protein wasting

    • 4.      easy bruising, purple striae
    • in abdomen

    5.      bronze skin

    6.      delayed wound healing

    7.      mood disturbances

     

    b.      mineralocorticoids:

    1.      water, Na retention

    2.      HTN

     

    c.       androgens:

    1.      acne

    2.      women – virilization

    3.      men - feminization

     

      4.  Diagnostic Tests:

                a.  ACTH level

                b.  serum cortisol

                c.  urine cortisol

                d.  blood glucose

     

      5.  Treatment:

    a.       surgery

    b.      meds to suppress cortisol
  3. Hyperaldosteronism
    • Definition:  excess secretion of
    • aldosterone

     

    •   2.  Pathophysiology:  excess leads to inc Na and water reabsorption
    • = hypervolemia.  Also inc in secretion of
    • K = hypokalemia

     

      3.  Clinical Manifestations

    a.       HTN

    b.      hypokalemia

     

      4.  Diagnostic Tests:

                a.  serum Na

                b.  serum K

                c.  serum aldosterone 

                d.  aldosterone suppression test

     

     5.  Treatment:

    a.       surgery

    • b.      meds to control HTN,
    • hypokalemia

     

    • D.  Addisons
    • Disease 

    •   1.  Definition: 
    • insufficent function, all corticosteroids are dec.  Etiology: autoimmune reaction

     

    •   2.  Pathophysiology:  elevated serum ACTH with inadequate
    • corticosteroid synthesis.  Adrenal tissue
    • destroyed by antibodies against adrenal cortex

     

      3.  Clinical Manifestations:  dec levels

    a.       glucocorticoids

    • 1.      dec in gluconeogenesis –
    • hypoglycemia

    2.      weakness, fatigue

    3.      n/v

    4.      wt loss

    b.      mineralocorticoids

    1.      inc Na and water loss

    2.      K retention

    c.       androgens

    1. dec axillary/pubic hair

     

      4.  Diagnostic Tests:

    •             a. 
    • serum cortisol and aldosterone

                b.  urine cortisol and aldosterone

                c.  ACTH

                d.  serum K

                e.  glucose

                f.  ACTH stimulation tests

     

     

     

     5.  Treatment

    a.       treat cause

    b.      replacement steroids

    c.       diet – in Na
  4. Pancreas - Diabetes Mellitus: definition
    Definition

    •             Lack
    • or dec in insulin production by B-cells of pancreas or the insulin produced is
    • ineffective.   Metabolic problems:

                1.  dec utilization of glucose:

     

                2.  increased fat mobilization:

     

                3.  increased protein utilization:
  5. Types of DM
    Type I - IDDM  

    •             Insulin production dec or completely
    • absent due to dec in number of B-cells in pancreas. <40 yrs old.  Onset, progression of symptoms rapid

     

    •             Patho:  a. 
    • genetic factors.,  Human leukocyte
    • antigens (HLAs)

    •                          b. 
    • autoimmune reaction.

    . Type II - NIDDM

    •             80%
    • of cases.   >40 yrs.   Amount of insulin produced may be normal,
    • inc or dec.  Problem -> insulin unable
    • to bind with cell receptor sites.  Due to
    • a defect at receptor sites, dec # of sites or problem with postreceptor sites
    • (inside cell).  Onset of symptoms occur
    • over a long period, able to adjust.

     

                Patho:  genetic influence, obesity, age
  6. CM for Type 1 IDDM
    • a.  three P's
    • - polyuria, polydipsia and polyphagia.

                            b.  weight loss or underweight status

                            c.  ketosis
  7. CM for type 2 NIDDM
    Onset gradual.

                            a.  three P's may or may not be present

                            b.  obesity
  8. Dignosis test and treatment
    • .  blood
    • glucose (sugar) level:  (80-160)

      2.  fasting blood sugar:  (70-110)

      3.  oral glucose tolerance test

     

    E.  Treatment

      1.  Diet
  9. Activity/excercise: Benefits
    • a.  lowers
    • blood sugar

                            b.  improves insulin sensitivity

                            c.  facilitates weight loss

                            d.  reduces cholesterol and triglyceride levels
  10. Meds for DM
    Type I:  Insulin

               

    •            Type II: Oral hypoglycemic
    • agents  (OHAs)

    •                         a.  lower blood sugar by stimulating B-cells to
    • release insulin

    •                         b.  make target tissues more sensitive to effects
    • of insulin by inc # of                                                           receptor sites

                            c.  enhance insulin's activity at post-receptor sites

    •                         d.  dec glucose production in liver
    • (gluconeogenesis)
  11. .  Acute
    Complication
    1.  DKA:   Type I

    • Glucose accumulates, use fat and protein
    • stores.  Fat -> ketones.  Ketones -> metabolic acidosis and H2O
    • loss.  Protein metabolism -> further
    • hyperglycemia.  Hyperglycemia causes
    • osmotic diuresis -> dehydration, hypovolemia and hyperosmolarity.   Electrolyte imbalances - K

    •             S&S:  n/v, hypotension, change in MS, Kussmauls
    • resp.

                Treatment:


                            a.  fluid

                            b.  insulin

                            c.  electrolytes

     

    •   2.  HHNK:  
    • NIDDMs.   like DKA except no
    • ketosis.  Severe hyperglycemia ->
    • fluid and e-lyte loss -> 
    • hyperosmolarity, hypovolemia.

                S&S:  similar to DKA except no acidosis or ketosis

                Treatment:  same as DKA

               

      3.  Hypoglycemia:.  BS<50 symptoms

                mild:  tremors, palpitations, diaphoresis

    •             moderate:  impaired CNS function, HA, inability to
    • concentrate, drowsiness

                severe:  disorientation, unconsciousness, seizures
  12. Treatment for Acute complication
    • a.  quick
    • acting carbo

                                        b.  glucagon injection

                                        c.  high dextrose solution IV
  13. Chronic Complications/Prevention
    • 1.  Retinopathy   deterioration of the blood vessels in the
    • retina.

               

     

     

    •   2.  Nephropathy   damage to capillaries that supply
    • glomerulus. destruction of glomeruli and nephron damage -> renal failure

               

     

    •   3.  Neuropathy          70% of diabetics.  
    • dec in nerve conduction

    •             a.  peripheral neuropathy:  burning, aching, painful at times.   muscle weakness, sensory loss, loss of fine
    • motor skills, problems with ambulation. 
    • Potential for injury or undetected injury

                b.  autonomic neuropathy:

    •             GI:  gastroparesis - delayed emptying of gastric
    • contents.

    •             GU:  neurogenic bladder - urinary retention,
    • frequent UTIs, overflow inc.

                            impotence

     

      4.  Macrovascular Disease

    •             atherosclerosis
    • – CAD, stroke, peripheral vascular disease

     

      5.  Infection 

    a.       sensory changes

    b.      hypoxia

    c.       pathogens

    d.      blood supply

                e.   WBC

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