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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
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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
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Treatment siadh
- Mild=fluid restrictions
- Mild-severe=in icu, fluid restrictions, iv lasix
- More severe= hypertonic solution and lasix
Also treat underlying cause
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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
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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
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S/s diabetes insipidus
- Polyuria
- Polydipsia
- Nocturia
- Thirst
- Low urin specific gravity
- Inc plasma osmolality
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Tx diabetes insipidus
- Depends on primary cause
- Replace adh-iv, po, intranasal
- Strict i&o, fluid replacement
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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
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Graves disease
- Autoimmune disorder
- Autoantibodies attach to tsh receptors and dec tsh secretion
- Tsh receptors produce t3 and t4, which dec tsh production
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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
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Hypothyroidism
- Decrease in th production
- Very common, inc in women
- Low t4, high tsh
- Primary or secondary
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Primary hypothyroidism
- Congenital defect
- Loss of tissue after tx for hyperthyroid
- Autoimmune (hashimoto's)
- Antithyroid drugs
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Secondary
- R/t hypothalmic or pituitary disorder
- Will see low tsh (problem with secrection)
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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
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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
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Acth dependent
- Caused by inc secretion of acth
- From pituitary adenoma or lung cancer
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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
-
S/s cushings
- Wt gain
- Truncal obesity
- Moon face
- Buffalo hump
- Diabetes maybe
- Thinning of arms and legs
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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
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Hypocortisolism-addisons disease
- Low level of cortisol
- Poor stimulation by acth to produce or adrenals not able to produce
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Patho of addisons
Autoimmune mechanisms destroy cells leading to low level of cortisol production
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S/s addisons
- Muscle weakness
- Fatigue
- Bronzing of skin
- Vitiligo
- Darkening of scars
- Hypotension with crisis
- Weak irregular pulse
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Tx and diagnosis of addisons
- Lifelong treatment with steroids that contain cortisol
- Diagnosis: plasma levels of cortisol
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Dysfunctions of pancreas
- Diabetes
- Type 1
- Type 2
- Others
- Gestational
- Chronic hyperglycemia
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Risks for pancreas dysfunction
- Obesity
- Inc stress
- Pregnancy
- Medications that antagonize insulin
- Family history
- Lifestyle factors
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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
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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
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Tx dm type1
- Insulin replacement-avoid highs and lows
- Meal planning- see nutritionist, diabetic diet, important to think about lipids
- Exercise
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Somogyi effect
- Period of hypoglycemia followed by rebound hyperglycemia
- Hypoglycemia stimulates epinephrine, growth hormone, and cotricosteroids
- These hormones produce the hyperglycemia
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Dm type 2 risk factors
- Obesity
- Bmi>25
- Family hx
- Racial/ethnic minority (native am, hispanics, blacks)
- Femal gender
- Metabolic syndrome
- After age 40
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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**
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S/s dm type 2
- Slower onset
- More non specific
- Pruritis
- Recurrent infection
- Visual changes
- Parasthesias
- Possible 3 P's
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Tx dm type 2
- Lifestyle modifications: wt control
- Maintain normal bs levels
- Oral agents
- Insulin may be used if orals do not control
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Dm acute complications
- Hypoglycemia
- Hyperosmolar hyperglycemic nonketotic syndrome
- Dka
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Hyperosmolar hyperglycemic nonketotic syndrome
- Uncommon, glucose >500, serum osmolality high
- Severe dehydration and low blood volume
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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
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Cauwe of neuropathy
- Glucose in cells is broken down into sorbitol
- Sorbitol pulls water into cell which causes cellular swelling
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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 ********
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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
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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
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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
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Pvd
- Inc chance of peripheral vascular lesions leading to amputations
- Occlusions occur b/c of inc atherosclerosis in dm
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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
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