Exam #4 Flashcards

1
Q

Anterior Pituitary

A
  • adenohypophysis
  • vascular
  • produces hormones:
  • ACHT: increases cortisol
  • TSH: increase T4/T3
  • FSH: gonads
  • LH: gonads
  • GH
  • excessive GH is almost always due to a tumor
  • overproduction of GH = acromegaly
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2
Q

Posterior Pituitary

A
  • neurohypophysis
  • neural
  • collects, stores and releases hormones based on signals received
  • vasopressin (ADH): reabsorbs water
  • oxytocin: lactation
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3
Q

Acromegaly

A
  • anterior pituitary issue with GH
  • excess of growth hormone after the epiphyseal plate closure: no growth in height but hands, feet and face. Big tongue, deep voice, thickened vocal chords
  • generally affects middle-aged adults
  • starts gradually: 7-9 yrs between onset and final dx
  • causes: pituitary adenoma (tumor on ant pit)
  • life expectancy reduced 5-10 years: excess circulating glucose, triglycerides
  • if untreated these patients are likely to have cardiac (atherosclerosis), respiratory (tightening of throat), diabetes (increased circulating glucose, GH inhibits insulin) and cancers (increased tissue growth from GH)
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4
Q

S/S of Acromegaly

A
  • thickening of hands, feet, nose, and mouth
  • usualyl what leads to dx with CT scan and they visualize tumor
  • speech issues: thickening of tongue, deepening voice, hypertrophy of vocal chords
  • slepe apnea: upper airway narrowing
  • peripheral neuropathy: result of nerve damage, pain generally to hands and feet, excess tissue increases pressure on nerves
  • muscle weakness
  • visual changes/headache (tumor)
  • Labs: increased GH, increased IGF1, increased glucose
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5
Q

IGF1

A

look up

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6
Q

DX of acromegaly

A
  • MRI, CT to assess pituitary tumor
  • ophthalmic exam: tumor may put pressure on optic nerve
  • diagnosis often promted by headaches and/or visual changes
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7
Q

TX of acromegaly

A
  • hypophysectomy: removal of pituitary tumor
    ~ done transphenoid
    ~ incision is made just unde the inner, upper lip
    ~ immediate reduction in GH levels followed by a drop in IGF1 levels, will be seen in just a few weeks post removal
  • radiation: if surgery fails
    ~ goal is complete remission
    ~ done in combination with drugs
  • medications: octreotide reduces GH, SQ 3 x week
  • sandostatin and lareotide: longer acting, IM every 2-4 weeks, GH inhibitor
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8
Q

Trans-sphenoidal Hypophysectomy

A
  • HOB 30 degrees
  • decrease pressure on the sell turnica (where pituitary is located) and decreases headaches
  • assess neuro changes
  • instruct pt to avoid: vigorous coughing, sneezing, straining, blowing nose
  • prevent CSF leakage: relax, bedrest,
  • glucose level > 30 = CSF leak
  • pt at risk for meninngitis if CSF leak
  • if pt complains of consistent supraorbital headache, may indicated CSF leak: bedrest, tyelinol for headache
  • CSF leak usually resolves within 72 hours and if it doesnt may need surgery
  • mouth care q 4 hours
  • avoid brushing teeth for 10 days
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9
Q

SIADH

A
  • overproduction of ADH from posterior pituitary with low sodium in ECF which causes intracellular swelling
  • due to a tumor in the post pit
  • S/S SIADH
    ~ hyponatremia (norm 135-145)
    ~ hypo-osmolality (285-295)
    ~ headache: sodium issues, neuro issues
    ~ muscle cramps, muscle twitching
    ~ weakness, vomiting, abdominal cramps
    ~ fluid retention and concentrated urine with normal kidney function
  • increaesd urine osmolarity, decreased ECF osmolarity
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10
Q

how does SIADH happen?

A
  • ADH causes sodium retention, thereby holds in water
  • inappropriate ADH causes too much water to be retained
  • bronchogenic small cell cancer (oat cell ca): synthesizes and releases ADH, secretes its own synthetic ADH
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11
Q

TX of SIADH

A
  • serum sodium
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12
Q

Diabetes Insipidus

A
  • vast quantities of dilute urine
  • deficiency of production or secretion of ADH
    (1) central DI: pituitary issue, lack of ADH production or release
  • brain injury, CNS infarction, brain tumor or head surgery (all increase ICP)
  • leasts for 10-14 days
  • dilantin can give you DI
    (2) nephrogenic DI: adequate amounts of ADH but kidneys dont respond
  • renal damage or lithium (blocks ADH at kidney level)
    (3) psychogenic DI: from excessive water intake
  • lesios in the thirst center or by psychiatric problem
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13
Q

S/S of DI

A
  • massive diuresis, urine output of 4-30L a day
  • low urine specific gravity
  • low urine osmolarity and high serum osmolatity
  • increased thirst
  • generalized weakness
  • weight loss
  • constipation
  • poor skin turgor
  • hypotensions
  • tachycardia
  • shock
  • increased sodium in serum
  • cells shrink, neuro issues, agitation, muscle issue
  • decreased ADH, high na, high serum osmo, increased urine output
  • urine specific gravity
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14
Q

DI TX

A

(1) central DI
- DDAVP - IV, SQ, nasal: synthetic for of ADH taht causes reabsoprtion of water decreases the amount of urine, pt not to drink more than 3 L a day, weights daily
- DSW IVF titrate to replace urine output: hypotonic solution to decrease serum osmo

(2) nephrogenic DI
- low sodium diet
- thiazide diuretics
- serial labs: sodium, osmolality
- strict I&Os
- daily weights

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15
Q

Thyroid Gland

A
  • thyroxine (T4) and Tri-iodothyronine (T3) regulate energy metabolism , growth, and development
  • Goiter: hypertrophy and enlargment of thyroid gland
  • hyper/hypothyroidism or normal thyroid funtion (too mch T3/T4)
  • goiter can be found in graves disease
  • most often a goiter is found with lack of iodine in diet
  • malignant nodules needs to be removed: radiation can be used, palpable deformity of the thyroid gland
  • thyroiditis: inflammation of thyroid, pain around ear down to thyroi. palpate and listen to bruit near thyroid
  • viral or bacterial or autoimmune in nature
  • TX: bacterial abx, hypothyroid needs thyroid replacement
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16
Q

hyperthyroidism

A
  • excess circulating levels of T3/T4
  • increased cellular metabolism
  • effects women more than men
  • primary ages effects 20-40yrs
  • Grave’s Disease: autoimmune disease unknown etiology marked by thyroid enlargement and excess TSH
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17
Q

Grave’s Disease

A
  • autoimmune disease
  • thyroid enlargement and excess TSH
  • initially: increased T3/T4 which causes no TSH in ant pit
  • later: decreased T3/T4 and increased TSH in ant pit
  • patient develops antibodies to TSH receptors: antibodies bind to receptors causing stimulation of the thyroid gland and releasing T3 and T4
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18
Q

S/S hyperthyroidism

A
  • HTN
  • increased HR and bounding pulse
    systolic murmor: r/t hypervolemia ad hypertension
  • dysrhythmias: increased myocardial oxygen consumption
  • palpitations
  • exophthalmos: protrusion of eyeballs (fluid buildup behing eyes, eyelid forced open)
  • increased cell metabolism all otgether
  • increased appetite
  • weight loss
  • diarrhea
  • hair loss
  • thinning nails
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19
Q

thyroid storm, thyroid crisis

A
  • don’t know you have it then exposed to a stressor and it happens all of a suddent
  • hyperthyroidism untreated may lead to a thyroid storm
  • all hyperthyroid manifestations are heightened
  • critical illness lasts 7-10 days, potentially lethal
  • thought to be caused by several stressors: infection, trauma, surgery, heart and nerve tissue become more sensitive
  • S/S = r/t increased tissue sensitivity to thyroid horomones: severe tachy, heart failure, high temp, shock, restlessness, agitaiton, seizures, abdominal pain, nauseam, vomiting, diarrhea, delirium, coma
  • labs: low TSH and increased thyroxine
  • TX: antithyroid drugs, iodine, beta adrenergic blockers, prophylthiouracil (PTU) and methimzole (tapazole) inhibit synthesis of thyroid hormones
  • iodine inhibits synthesis of T3 and T4 (only when given in very large doses it inhibits production), beta blockers treat symotims of slow heart rate
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20
Q

Hyperthyroidism, diagnostic testing

A
  • hyperthyroidism: Low TSH level, elevated free T4
  • normal TSH levels: 0.3-5.4
  • normal T4 levels: 5-12
  • these tests along with s/s and history will confirm diagnostics
  • how to differentiate grave’s disease from other hyperthyroidisms: RAIU (radioactive iodine uptake test) – graves = 35-95%, thyroiditis =
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21
Q

treatment for hyperthyroidism

A
  • antithyroid drugs: propylthiouracil (PTU) and methimazole (tapazole): antithyroid drugs blocks the synthesis of thyroid hormones. PTU also blocks conversion of T4 to T3
  • PTU only orally absorbed
  • can take 1-2 weeks to work
  • may be used long term 6-15 months
  • iodine: used with other antithyroid drugs to prepare patient for thyroidectomy or for treatment of thyrotoxic crisis
  • not used long term
  • large doses of iodine inhibit synthesis of T3 and T4
  • beta adrenergic blockers utilized to treat symptoms caused by tissue responses to catecholamine
  • RAI destroys thyroid tissue thus limiting the secretion of thyroid horomone: maximal effet is seen in 2-3 months, pt remain on therapy until maximal effects seen from RAL
  • surgical therapy utilized when patient is unresponsive to other forms of therapy, also used with removal of a large goiter that is presing on the throat or thyroid
  • subtotal thyroidectomy: surgery of choice, significant portion of thyroid removal
  • total thyroidectomy: 90% of thyroid removed
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22
Q

concerns with hyprethyroid treatment

A
  • can make pt hypothyroid due to removal of too much thyroid tissue
  • post operatively: N/v, oxygen levels, comfort
  • watch site for swelling of the net and tissues, hemorrhage, hematoma laryngeal stridor
  • trachestomy tray in the room always in case of emergency
  • take frequent vitals, frequent oxygen checks HOB up to decrease swelling
  • watch for signs of tetany d/t hypoparathyroidism
  • trousseaus sign: sign of Tetnay, bp cuff inflated and wrist flexes
  • chevostek’s sign: cheek flinches, sign of tetany
    • tetany = a condition marked by intermittent muscular spasms, caused by malfunction of the parathyroid glands and a consequent deficiency of calcium.
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23
Q

dangers after thyroid surgery

A
  • airway swelling
  • n/v
  • HOB elevated
  • watch for s/s of tetany (can be caused by nicking the parathyroid during surgery)
  • tetany: proximity to parathyroid, chvosetek’s sign and trousseau’s sign
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24
Q

hypothyroidism

A
  • insufficient cirrculating thyroid hormone r/t destruction of thyroid tissue, defective hormone synthesis (lithium, amiodarone), iodine deficiency
  • may be transient: from thyroiditis, discontinuation of thyroid therapy (if you stop synthroid and your body isnt used to making its own thyroid hormone then it will be slow at making it at first)
  • iatrogenic: can be the result of a thyroid removal of tissue removal
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25
Q

patho of hypothyroidism

A
  • decreased protein synthesis: may lead to absent RBC and amino acid production
  • Incomplete fat & carbohydrate metabolism: inadequate gluconeogenesis
  • ineffective lipolysis: high cholesterol levels, cant break down fat so leads to high cholesterol
  • hyaluronic acid: gel like substance, in interstitial tissues - puffy face and eyes, accumulates in muscles, esp heart, tongue, pharynx, esophagus
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26
Q

s/s hypothyroidism

A
  • fatigue, lethargy
  • personality changes: depression, somnelence
  • impaired memory, slowed speech
  • depressed appearance about them
  • disruptive sleep patterns
  • SOB, exercise intolerance
  • constipation
  • hair loss, brittle nails, weight gain
  • myexedema: gel like distribution in face, mask-like
  • symptoms depend on severity: some may have no symptoms, periorbital edema, puffy skin, prominant tongue
  • decreased cardiac output and contractility
  • anemia is a common problem due to decreased protein levels and increased o2 consumption (high cellular metabolism)
  • Gi motility slowed
  • intolerant of cold, cant shiver to keep themselves warm
  • respiratory: muscles weak, increased PaCO2, decreased PaO2, decreased RR
  • kidneys: decreased GFR, increased ADH secretion, inabikity to maintain body heat
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27
Q

myxedema coma

A
  • mental slugglishness can lead to coma
  • this is a medical emergency
  • subnormal temperature
  • hypotension, decreased CO
  • hypoventilation, decreased RR
  • patient needs: IV thyroid replacement thearpy, vital organ support (in ICU)
  • ICU with warming blanket, IV warming fluids, ventilator, meds to help with BP
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28
Q

hypothyroidism diagnostic tests

A
  • serum level TSH can be indicative of cause of hypothyroidism
  • TSH high = defect originated in the thyroid
  • TSH low = defect originates in pituitary or hypothalamus
  • low T4
  • elevated cholesterol, triglycerides, creatinine kinase
  • pt may be anemic, poor RBC synthesis
  • decreased erythropoietin and RBC production
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29
Q

treatment of hypothyroidism

A
  • slowly replace hormone to decrease risk of CV system issues
  • avoid shifting from hypo to hyper
  • older patients require smaller doses and need closer monitoring
  • medications: levothyroxine (synthroid) improvement takes time (2-14 days). lifelong medications. educate patient
  • most pts can be treated on an outpatient basis except myxedema pts
  • educate pt: must take apical pulse before med admin, if tachy call MD asap, don’t stop taking meds, give meds in the morning because they speed up metabolism and may cause insomnia
30
Q

hyperparathyroid

A
  • increase in secretion of PTH
  • PTH regulates calcium and phosphate levels
  • calcitonin inhibits PTH
31
Q

types of hyperparathyroidism

A
  • primary: increase in seretion of PTH leading to disorders of calcium, phosphate and bone metabolism. Common cause is adenoma
  • secondary: compensatory response to a disease that induces hypocalcemia (chronic renal failure, vitamin D, deficiency)
  • tertiary: hyperplasia of parathyroid gland and loss of negative feedback, similar to secondary
32
Q

S/s hyperparathyroidism

A
  • dysrhythmias - calcium issues
  • hypertension
  • anorexia and weight loss
  • nausea and vomiting
  • constipation
  • bone pain/bone fractures - demineralization of bones
  • emotional disturbances: irritability, memory problems, depression, confusion, delirium, coma
  • increased calcium –> decreased cell excitability
  • osteoporosis: calcium drawn out of bones, breaking down
  • emotional disturbances: full range from confusion to coma
  • poor coordination
  • headache
  • hypercalcuria (increase ca in urine)
33
Q

hyperparathyroidism diagnostic testing

A
  • PTH elevated
  • calcium levels elevated: exceed 10
  • phosphorous levels low: usually less than 3
  • test for presence of bone disease, bone density measures
34
Q

treatment for hyperparathyroidism

A
  • for primary and secondary = surgical intervention
  • partial or complete removal of the parathyroid gland with autotransplantation of the normal parathyroid tissue in the sternocleidomastoid muscle
  • remove excess tissue then replant it somewhere else to still stimulate PTH but decrease mass in throat
  • nonsurgical due to being elderly or multiple comorbidities that sugery may not be an option –> encourage mobikity, dietary changes, moderate calciium intake, increased fluid intake (decrease calcium stones)
  • medications that can decrease serum and urine calcium levels - biphosphonates (inhibits osteoclastic activity)
35
Q

post op surgical care hyperparathyroid sugery

A
  • monitor airway: swelling, stridor
  • watch for hemorrhage
  • fluid and electrolyte disturbances: calcium levels, tetany, laryngeal stridor
  • tetany from sudden decrease in calcium levels as evidenced by chvostek’s and trousseau’s
36
Q

hypoparathyoridism

A
  • very uncommon
  • caused by genetic defect
  • accidental removal of the parathyroid gland or damage to the vascular supply of the glands during neck surgery (typically iatrogenic causes, surgery)
  • inadequate amount of circulating PTH
  • characterized by hypocalcemia resulting from lack of PTh to maintain serum calcium levels
37
Q

S/S of hypoparathyroidism

A

anxious/apprehensive

  • decrease in calcium levels causing tetany
  • muscle tension resulting in paresthesias and stiffness
  • positive trousseau’s – BP on arm
  • positive chvotek’s – cheek, it stays in
  • respiratory function may be compromised by: accessory muscle spasm, laryngeal induced airway obstruction
  • hypoparathyroid diagnostic tests: labs = low PTH, low calcium, high serum phosphate
38
Q

treatment of hypoparathyroidism

A
  • PTH replacements are not recommended due to expense and parenteral administration
  • calcium replacements: important to increase calcium and vit D in the diet
  • treat symptoms: IV calcium gluconate if PT is passed out
  • nutrition: diet high in calcium and vitamin D
39
Q

Cushing Syndrome

A
  • too much glucocorticodids, increased ACTH
  • 85% by ACTH secreting pituitary tumor
  • prolonged use of high dose corticosteroids
40
Q

s/s of cushing syndrome

A
  • weight gain: due to increased cortisol, reabsorption of sodium and water and ridding of potassium in the urine; increased glucose levels
  • accumulation of adipose tissue in the trunk, face, cervical spine “moonface”
  • transient weight gain fro water and sodium retention
  • hyperglycemia/hypokalemia
  • protein wasting
  • muscle wasting/muscle weakness: fat in trunk, skinny in limbs
  • catabolic state
  • osteoporosis: catabolic state
  • skin is thin fragile with purplish/red striae, wound healing is delayed: androgens secreted
  • mood changes: irritabile, anxious, irrational euphoria
  • HTN
  • menstrual disorders: too much aldosterone
  • gynecomastia/impotence
41
Q

cushings syndrome diagnostic tests

A
  • 24 hour urine for free cortisol levels” 50-100 a day is indicative of cushing’s, borderline could be a false positive (illness, excitement, stress)
  • CT scan of pituitary and adrenal gland (determines where the excess cortisol is coming from)
  • MRI of pituitary and adrenal gland
42
Q

treatment of cushing syndrome

A
  • normalize hormone secretion
  • treat underlying cause
  • high dose prolonged use of steroids: consider gradual taper to D/C, adjust dose
  • steroids cause low levels of ACTH produced from antitary pituitary (if you stop steroids fast then you wont have enough ACTH {releases cortisol})
  • pituitary/adrenal tumor surgical removal
  • mitotane: supresses production and metabolism of cortisol
  • metyrapone, ketoconzaole and aminoglutethimide: used to inhibit cortisol synthesis
43
Q

care of cushings patient post op

A
  • risk for hemorrhage
  • manipulation of tissue may cause release of excess hormones into circulation
  • closelet watch BP, F&Es
  • high dose corticosteroids are given to help pt with recover from stress
  • pt should avoid severe temp, infections, emotional distrubances
  • lifetime corticosteroid replacement required by many patients
44
Q

Addison’s Disease

A
  • *** LOOK UP- adrenal insufficiency, can result from adrenal removal
  • glucocorticoids, mineralcorticoids, androgens = all decreased
  • most common cause is an autoimmune resoonse
45
Q

S/S Addison’s Diease

A
  • anorexia, weight loss, n/v
  • smoky/bonzed hyperpigmentation of face, neck, hands: due to hypersecretion of ACTH, affects melanocytes
  • hypotension: cant reabsorb na and h2o
  • weakness
  • anemia
  • low sodium, low volume, dehydration, hyperkalemia
46
Q

Addison’s Crisis

A
  • life threatening emergency caused by insufficient adrenocortical hormones
  • addisons’s crisis triggered by sharp decrease in hormones: infection, surgery, trauma, hemorrhage (results from stress with improper hormone response)
  • s/s severe hypotension, hypotnatermia, hyperkalemia, hypoglycemia, fever, weakness, confusion, severe vomiting and diarrhea, severe pain
  • patients at high risk for shock, treat low BP with high volume IEVFs
47
Q

Addison’s disease treatment

A
  • hydrocortisone replacement lifelong med replacement
  • monitor vital signs: hypo and hypertension
  • I&Os
  • daily weights
  • protect from infection
  • protect from stressors: difficult time dealing with any stressors d/t lack of ability to priduce corticosteroids
  • lots of pt education: dosing with stress recognizing corticosteroid deficiency
  • corticosteroid comolications and side effects: hypokalemia, peptic ulcer disease, muscle atrophy and weakness, mood and behavior changes, weakens bones
  • predisposition to diabetes high glucose levels increase BP
  • susceptible to infection
48
Q

hyperaldosteronism

A
  • caused by adrenal adenoma: excessive aldosterone secretion causing sodium retention and potassium excretion, patient presents with high blood pressure and low potassium, headache, fatigue, cardiac dysrhythmias
  • DX: MRI and CT to find tumors
  • TX: surgical removal, low sodium diet and potassium sparing diuretics, watch BP
49
Q

pheochromocytoma

A
  • caused by tumor in the adrenal medulla producing excessive cathecholamines (increased norepi and epi, increased BP)
  • profound episodic symptomatic HTN: H/A, tachycardia, palpitations, anxiety, chest pain
  • diagnostic: 24 hr urine collection for catecholamine metabolites, CT/MRI for tumor location
  • tx: removal of tumor
50
Q

kidney disease

A
  • Acute Kidney Injury (AKI): suddent onset, acute decrease in urine output and/or increase in creatinine, potentially reversible, motrality 60%, usually die from infection
  • Chronic Kidney Disease (CKD): gradual onset, GRF
51
Q

Acute Kidney Injury (AKI)

A
  • rapid loss of kidney function with a rise in serum creatinine (azotemia) and/or decrease in urine output
  • Azotemia: accumulation of nitrogenous waste products (urea, nitrogen, creatinine) in the blood
  • ranges from very slight deterioration to sever impairment in kidney function
  • potentially reversible but high mortality rate
  • most commonly occurs after severe, prolonged hypotension or hypovolemia or exposure to nephrotoxins
52
Q

AKI causes

A
  • prerenal causes: external to the kidney, sudden reduction in blood flow to the kidneys –> dehydration, blood loss, severe cardiac disease, usually resolves quickly with correction of cause, HTN can lead to intrarenal issues
  • Intranrenal Causes: infections, toxins, nephrotoxic drugs, or direct trauma, actue tubular necrosis, recent blood transfusions (clogs up kidneys), recent use of contrast
  • postrenal causes: urinary tract obstructions, stones, BPH, cancer of bladder or prostate, usually resolve quickly with correction of cause
53
Q

AKI clinical course

A
  • if prerenal or postrenal, resolves with tx of the cause
  • if intrarenal (or damage to the kidney occurs), usually follows three phases:
    1) oliguric
    2) diuretic
    3) recovery
  • if recovery doesnt occur then the patient develops chronic kidney disease
54
Q

AKI, Oliguric Phase

A
  • develops 1-7 days after the incident or 24 hours of the ischemic event (MI), lasts 10-14 days
  • urine output less than 400ml/day
  • UA with casts, RBCs, WBCs, specific gravity fixed at 1.010, urine osmo of 300, may have proteinurea
  • fluid retention: Aldosterone and ADH (retain sodium and water)
  • metabolic acidosis
  • sodium imbalance: diluted blood, put on low sodium diet
  • potassium increase: backs up from low GFR
  • infection: immunocompromised state with back up of waste products in blood
  • waste product accumulation (increase creatinine): musculoskeletal issues
  • neuro disorders (acidosis)
55
Q

AKI, Diuretic Phase

A
  • can last 1-3 weeks
  • daily urine output 1-5L: massive dump of water and electrolytes
  • nephrons still not fully functional
  • kidneys can excrete waste, but still can’t concentrate the urine
  • hypovolemia
  • hypotension
  • hyponatremia
  • hypokalemia
56
Q

AKI, recovery phase

A
  • may last 12 months
  • begins when GFR increases
  • BUN and creatinine plateau, then decrease
  • If pt doesn’t recover, they will progress to chronic kidney disease
57
Q

AKI diagnostic studies

A
  • thorough history to determine cause
  • urine output
  • serum creatinine (build up = not urinating it out)
  • UA: helps determine cause
  • kidney ultrasound and renal scan: finds lesions, masses, blockages, ureters
  • CT
  • renal biopsy: best if intrarenal cause (scarring)
  • no contrast media can further damage kidneys (can cause rare lethal kidney problem)
58
Q

AKI TX

A
  • # 1 goal is to ensure adequate cardiac output and intravascular volume
  • IV fluids
  • low dose diuretics
  • careful monitoring of I/Os, check weights
  • prevent hyperkalemia: flat P wave, peaked T wave
  • use RRT (renal replacement therapy) only if needed
  • nutritional management: enough calories to prevent ketosis and protein breakdown, low sodium and potassium, increased fat (to prevent ketoacidosis)
59
Q

AKI prevention of hyperkalemia

A
  • regular insulin IV (with IV glucose)
  • sodium bicarbonate: helps with acidosis
  • calcium gluconate IV: increases heart threshold to prevent cardiac dysrhythmias due to increased k+
  • hemodialysis: poop out K+, check bowels to make sure they are present to prevent a GI rupture before giving
  • dietary restrictions: low potassium and sodium
60
Q

AKI treatment

A
  • prevention
  • avoid exposure to contrast media
  • prevent hypotension and hypovolemia
  • close watch of I/Os and F/E status
  • watch for nephrotoxic drugs and contrast dye
  • be careful with ACE inhibitors
  • acute care
  • meticulous aspetic technique
  • meticulous skin care: increased BUN will push urea out to the skin (BUN 200+) and make it really itchy
  • meticulous mouth care: urea pushed through mouth membranes, urea ordor breath, blisters and ulcerations in mouth
  • strict I/Os, daily weight, closely watch F&E, promote good nutrition
61
Q

gerontologic considerations with AKI

A
  • more susceptible
  • not as likely to recover
  • dehydration is big risk factor
  • more likely to already have CV disease and/or diabetes
  • kidneys can’t compensate well w/ dehydration: thin skin, decreased amount of fluids, lean muscle mass, increased adipose tissue
62
Q

chronic kidney disease (CKD)

A
  • progressive, irreversible loss of kidney function
  • many causes, but diabetes and HTN are most common
  • CKD is much more common that acute kidney injury (AKI)
  • african americans have highest rate of CKD (4x whites)
  • 1 in 9 americans has CKD, often asymptomatic
  • 5 stages, can never get better or go backwards
63
Q

CKD manifestations

A
  • anxiety, depression
  • HTN, heart failure, CAD, pericarditis
  • anorexia, n/v, GI bleeding
  • carbohydrate intolerance, hyperlipidemia
  • anemia, bleeding, infection
  • fatigue, headache, sleep disturbances
  • pulmonary edema, pneumonia
  • pruritis, ecchymosis
  • vascular and soft tissue calcifications, osteomalacia
  • paresthesias
64
Q

CKD manifestations by system

A
  • urinary system: no changes in urine output in early stages, may even have polyuria, as it progresses have fluid retention, may develop anuria after on dialysis for a while (body becomes more dependent on dialysis)
  • metabolic problems: waste product accumulation (n/v, lethargy, fatigue), impaired thought processes, altered cardohydrate metabolism, diabetic may require less insulin, elevated triglycerides (high VLDLs, high LDLs, low HDLs, most CKD pts die from CV disease)
  • electrolyte and acid-base imbalances: hyperkalemia, sodium, magnesium can be high, metabolic acidosis
  • hematologic system: anemia, bleeding tendencies, infection
  • Cardio system: most common cause of death for CKD pts (CAD, MI, HTN, stroke, PAD, HF, dysrhythmias, uremic pericarditis), vascular calcification, arterial stiffness (from bone breakdown and excess calcium)
  • respiratory system: dyspnea, pulmonary edema, pleuritis, resp infections
  • GI system: stomatitis, metallic taste in mouth, uremic fetor (urea breath), anorexia, n/v, weight loss, malnutrition, GI bleeding, constipation
  • neuro: nitro waste build up causes changes in LOC, lethargy apathy, fatigue, irriability, altered mental status, peripheral neuropathy, muscle twitching
  • musculoskeletal: mineral and bone disorder, osteomalacia, vascular calcifications, uremic red eye (body picks up on low ca, increases PTH, bone breakdown, increased ca in blood, body cant use it without calcitriol, increase ca stays in blood and causes stones all over
  • integumentary: prutitis, uremic frost
  • reproductive: infertility, decreased libido, amenorrhea, anovulation, impotence
  • psychologic changes: personality hehavior changes, emotional lability, withdrawn, depressed
65
Q

CKD diagnostic studies

A
  • dipstick for protein or microalbuminuria in urine
  • urine for albumin-to-creatining ratio which estimates protein and albumin excretion rate
  • UA can detect RBCs, WBCs, protein, casts, glucose
  • ultrasound of kidneys
  • GFR is preferred method to determine kidney function
  • renal biopsy can give a definitive diagnosis
66
Q

CKD treatment

A
  • focus is on prevention and early identification to deter the progression
  • preserve existing kidney function
  • treat CV disease: can increase risk of dying from CKD
  • prevent complications
  • control HTN, hyperparathyroid, anemia, hyperglycemia, dyslipidemia
  • dialysis or transplant will be needed for stage 5
  • tx for hyperkalemia: restrict potassium in diet and drugs. IV glucose/insulin or IV calcium gluconate (drives k into cells and out of blood), sodium polystyrene sulfonate (kayexelate)
  • tx for hypertension: target BP
67
Q

CKD nutritional therapy

A
  • protein restriction: not needed if doing dialysis, but may be beneficial in earlier stages of CKD
  • discourage high protein diets and supplements
  • those doing peritoneal dialysis need higher doses of protein
  • if malnourished can take a supplement high in protein but low in sodium and potassium (nepro)
  • fluid restriction: not restricted in early stages, food liquid at room temperature count as fluid, limit intake to 1-3kg between dialysis tx
  • sodium and potassium restriction: 2g-4g/day, avoid cured meats, pickled foods, canned soups, hotdogs, cold cuts, soy sauce, salad dressing, salt substitutes, oranges, bananas, melons, tomatoes, prunes, raisins, deep green/yellow veggies, beans, legumes
68
Q

CKD nursing care

A
  • avoid antacids, NSAIDs, decongestants, antihistamines that contain pseudephedrine (builds up in blood and causes issues/damage)
  • monitor BUN and creatinine if pt must take a nephrotoxic drug
  • teach pt to take daily BPs
  • teach to identify s/s of fluid overload, hyperkalemia, other electrolyte imbalances
  • measure I and Os
  • avoid IV pyelograms and contrast dye
  • best circumstance is to receive transplant before starting dialysis
  • most pts will require dialysis
69
Q

normal BUN

A

= 7-20

70
Q

normal creatinine

A

= 0.7-1.3

71
Q

Renal Replacement Therapy (RRT)

A
  • indicated for: volume overload resulting in compromised cardiac or pulmonary function, elevated serum potassium levels, metabolic acidosis, BUN > 120, significant change in mental status, pericarditis or cardiac tamponade
  • for pts who do not respond to dietary adjustements and drug therapy
  • CCRT: goes 24 hours a day and can go for 30-40 days
  • hemodialysis
72
Q

normal GFR

A

above 90 is best

below 60 for 3+ months = chronic kidney disease