Patho test 3[1].txt

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Patho test 3[1].txt
2012-04-03 21:07:46

nursing patho test 3 neuro
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    • author "me"
    • tags "Endocrine 17?"
    • description ""
    • fileName "Patho test 3"
    • freezingBlueDBID -1.0
    • Siadh
    • Increased adh leads to hyponatremia because:
    • Blood plasma is diluted
    • Na excreted from kidneys
  1. S/s siadh
    • Mild, moderate, severe
    • Urine is concentrated
    • Cellulare swelling=more na in cell so water is pulled into cell
    • Impaired tasted
    • Dec appetite
    • Tired
    • Altered sensation

    Severea hypona= <115, life threatening, neurological problems
  2. Treatment siadh
    • Mild=fluid restrictions
    • Mild-severe=in icu, fluid restrictions, iv lasix
    • More severe= hypertonic solution and lasix

    Also treat underlying cause
  3. Diabetes insipidus and 3 causes
    • Decreased adh
    • Neurogenic-not producing adh or its not being released from brain
    • Nephrogenic-kidneys, improper response to adh in kidneys
    • Psychogenic-psychologically related; intact of large amount of water
  4. Patho diabetes insipidus
    • dec adh leads to hypernatremia
    • Loss of water without na loss
    • Low adh leads to high diluted urine output
    • Serum osmolality increases
    • Thirst mechanism triggered, dehydrate easily
  5. S/s diabetes insipidus
    • Polyuria
    • Polydipsia
    • Nocturia
    • Thirst
    • Low urin specific gravity
    • Inc plasma osmolality
  6. Tx diabetes insipidus
    • Depends on primary cause
    • Replace adh-iv, po, intranasal
    • Strict i&o, fluid replacement
  7. Hyperthyroidism
    • Disease resulting in inc thyroid hormone, various types
    • Treatment methods include radiation of thyroid, drug therapy, and/or surgery
    • Goiter usually present
    • Tsh usually low, t4 high
    • Most common form is graves disease
  8. Graves disease
    • Autoimmune disorder
    • Autoantibodies attach to tsh receptors and dec tsh secretion
    • Tsh receptors produce t3 and t4, which dec tsh production
  9. S/s graves disease
    • Goiter
    • Nervous
    • Heat intolerance
    • Wt loss
    • Inc appetite
    • Hyperactive bowels
    • Palpitations
    • Exopthalmos
    • Thyrotoxic storm..acute crisis..hyperthermia, dysrhythmia, confused, n/v, ssent to icu
  10. Hypothyroidism
    • Decrease in th production
    • Very common, inc in women
    • Low t4, high tsh
    • Primary or secondary
  11. Primary hypothyroidism
    • Congenital defect
    • Loss of tissue after tx for hyperthyroid
    • Autoimmune (hashimoto's)
    • Antithyroid drugs
  12. Secondary
    • R/t hypothalmic or pituitary disorder
    • Will see low tsh (problem with secrection)
  13. S/s hypothyroidism
    • Weakness
    • Fatigue
    • Forgetfulness
    • Sensitivityto cold
    • Unexplained wt gain
    • Constipation
    • Myexdema** classic sign of longstanding hypothyroidism
    • Non-pitting, boggy, edema in eyes, hands, feet
  14. Alterations of adrenal function: cushings
    • Disease related to the prolonged exposure of inc level of glucocorticoids
    • Causes excessive catabolism of proteins and peripheral fat
    • Syndromes: acth dependent or independent
  15. Acth dependent
    • Caused by inc secretion of acth
    • From pituitary adenoma or lung cancer
  16. Acth independent
    • From a adrenal tumor that secretes cortisl
    • Physical or emotional stress, excessive steroids po, autoimmune disorder all put person at risk for cushings
  17. S/s cushings
    • Wt gain
    • Truncal obesity
    • Moon face
    • Buffalo hump
    • Diabetes maybe
    • Thinning of arms and legs
  18. Tx cushings
    • Depends on cause
    • Pituitary and adrenal can be removed
    • Body will be used to inc level, so will need cortisol replacement therapy after and then wean off cortisol
    • Pain, fatigue, depression
  19. Hypocortisolism-addisons disease
    • Low level of cortisol
    • Poor stimulation by acth to produce or adrenals not able to produce
  20. Patho of addisons
    Autoimmune mechanisms destroy cells leading to low level of cortisol production
  21. S/s addisons
    • Muscle weakness
    • Fatigue
    • Bronzing of skin
    • Vitiligo
    • Darkening of scars
    • Hypotension with crisis
    • Weak irregular pulse
  22. Tx and diagnosis of addisons
    • Lifelong treatment with steroids that contain cortisol
    • Diagnosis: plasma levels of cortisol
  23. Dysfunctions of pancreas
    • Diabetes
    • Type 1
    • Type 2
    • Others
    • Gestational
    • Chronic hyperglycemia
  24. Risks for pancreas dysfunction
    • Obesity
    • Inc stress
    • Pregnancy
    • Medications that antagonize insulin
    • Family history
    • Lifestyle factors
  25. Diabetes type 1 patho
    • Triggering event causes production of autoantibodies against the beta cells in the pancreas (unsure of cause)
    • Leads to decline and lack of insulin production
    • Leads to hyperglycemia and protein catabolism, also lipolysis
    • Also see excess glucagon production
  26. Cardinal s/s DM type 1
    • Polyuria
    • Polydipsia
    • Polyphagia
    • Altered fat, protein, and CHO metabolism leads to
    • --glycosuria (kidneys overloaded)
    • --wt loss (fat and pro breakdown)
    • --ketoacidosis )(breakdown of proteins and fats) ketones in urine
  27. Tx dm type1
    • Insulin replacement-avoid highs and lows
    • Meal planning- see nutritionist, diabetic diet, important to think about lipids
    • Exercise
  28. Somogyi effect
    • Period of hypoglycemia followed by rebound hyperglycemia
    • Hypoglycemia stimulates epinephrine, growth hormone, and cotricosteroids
    • These hormones produce the hyperglycemia
  29. Dm type 2 risk factors
    • Obesity
    • Bmi>25
    • Family hx
    • Racial/ethnic minority (native am, hispanics, blacks)
    • Femal gender
    • Metabolic syndrome
    • After age 40
  30. Patho dm type2
    • Insulin resistance**, obeisty key factor**
    • Also see progressive beta cell dysfunction
    • Causes may include impaired insulin secretion, peripheral insulin receptor insensitivty
    • With obesity insulin has difficult entry into cells--wt loss can reverse this effect**
  31. S/s dm type 2
    • Slower onset
    • More non specific
    • Pruritis
    • Recurrent infection
    • Visual changes
    • Parasthesias
    • Possible 3 P's
  32. Tx dm type 2
    • Lifestyle modifications: wt control
    • Maintain normal bs levels
    • Oral agents
    • Insulin may be used if orals do not control
  33. Dm acute complications
    • Hypoglycemia
    • Hyperosmolar hyperglycemic nonketotic syndrome
    • Dka
  34. Hyperosmolar hyperglycemic nonketotic syndrome
    • Uncommon, glucose >500, serum osmolality high
    • Severe dehydration and low blood volume
  35. Dka
    • Inc in glucoe and the hormones working against it, fats broken down for energy
    • Leads to metabolic acidosis due to the ketosis
    • S/s: kussmauls breathing, fruity breath
  36. Cauwe of neuropathy
    • Glucose in cells is broken down into sorbitol
    • Sorbitol pulls water into cell which causes cellular swelling
  37. Diabetic neuropathy
    • Disease process leads to nerve degeneration and delayed conduction, sensory mostly affected
    • May be reversible in some cases
    • See peripheral neurathopathy that is painful, decreased sensations often in feet
    • Assess feet ********
  38. Diabetic retinopathy
    • Vascular changes lead to ischemia of retina
    • Microaneurysms, flame hemorrhages seen
    • Can lead to retinal detachment
    • Blurred vision from sorbitol pulling water into eye
    • Eye exams important annually
  39. Diabetic nephropathy
    • Commonly seen in esrd (end stage renal disease)
    • Unknown why kidneys are damaged with dm
    • Microalbuminuria (persistent protein in urine)
    • Thickening of vessels, dec perfusion
  40. cad
    • The longer you have dm the more you are at risk
    • Those with dm at inc risk for cad
    • Factors r/t include insulin resistance high ldl's, loh hdl's, platelet abnormalities
  41. Pvd
    • Inc chance of peripheral vascular lesions leading to amputations
    • Occlusions occur b/c of inc atherosclerosis in dm
  42. Infection
    • Nueropath and visual changes
    • Dec o2 to tissues delays healing
    • Inc glucose leads to rapid growth of some pathogens
    • Vascular changes lead to dec perfusion and blood supply to area, wbc's cant get to the site
    • Wbc's function is impaired