Exam 4 - Study Material (liver) Flashcards

(137 cards)

1
Q

What are the functions of the liver?

A
  • —Storage of nutrients
  • —Breakdown of erythrocytes
  • —Bile formation & secretion
  • —Synthesis of plasma proteins; cholesterol
  • —Immunity – Kupffer cells
  • —Conversion of ammonia into urea
  • —Inactivation - various substances (ammonia, toxins, steroids, other hormones)
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2
Q

What are some changes to the liver with aging?

A
  • —Decrease in size, weight
  • —Decreased portal blood flow
  • —Decreased metabolism of some medications
  • —Increased prevalence of gallstones
  • —Atypical presentation of biliary tract disorders
  • —Liver function test values remain unchanged
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3
Q

How is hepatitis A transmitted and what are the manifestations of hepatitis A?

A
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4
Q

How would you diagnose a patient with hepatitis A?

A
  • —Gold standard: clinical picture & Serum IgM anti-HAV
    • —+ at onset
    • —Peaks during acute/early convalescence
    • —Positive - 4-6 months
  • —Serum IgG anti-HAV:
    • —Early convalescence
    • —Detectable for decades
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5
Q

What are the risk factors for hepatitis B?

A
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6
Q

What are the manifestations of heptitis B? (viral)

A
  • 70% are subclinical – asymptomatic
  • Flu like symptoms
    *
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7
Q

How would you diagnose a patient with heptitis B?

A
  • —HBsAg – Hallmark serologic marker of HBV:
    • —1-10 weeks after acute exposure
    • —Detectable up to 6 months
  • —Anti-HBs (hepatitis B surface antibody):
    • —Appears – life-time immunity—
  • —If “window period” (no HBsAg or Anti-HBs) – may be diagnosed by detecting IgM antibodies against HB core antigens
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8
Q

What are some risk factors for heptitis C?

A
  • **—Most common blood-borne infection **
  • —Most asymptomatic; not detected
  • —Incubation period 60-160 days
  • —IV drug users; blood transfusions
  • —HIV infection
  • —High-risk sexual behavior
  • —Hemodialysis
  • —Occupational exposure
  • —Perinatal transmission—
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9
Q

What are the manifestations of a heptitis C infection?

A

—elevated liver function tests, perhaps jaundice

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10
Q

How would you diagnose a patient with hepitis C?

A
  • —Anti-HCV antibodies
  • —Acute:
    • —If HCV-RNA with detectable replicating virus – needs Rx
    • —If HCV-RNA not detectable & no replications – no Rx
  • —Immunosuppressed; hemodialysis
    • —HCV RNA test even if anti-HCV negative
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11
Q

What are some characteristics of Hepatitis D?

A
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12
Q

What drugs can cause drug/toxin induced hepatitis?

A
  • —Acetominophen
  • —Some - Anesthetic agents; antidepressants; antibiotics, anti-metabolities
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13
Q

What are the acute and later symptoms of drug/toxin induced hepatitis?

A
  • —Acute: abrupt; chills, fever, rash, pruritis, anorexia, nausea, fatigue, anorexia, abdominal discomfort, headache
  • —Later: jaundice, dark urine, hepatomegely
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14
Q

What are the acute clinical manifestations of hepatitis?

A
  • —Hepatomegaly; splenomegaly
  • —Lymphadenopathy
  • —Jaundice
  • —Dark urine; light/clay-colored stools (because of lack of bile)
  • —Pruritus (itching –> scratching)
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15
Q

How would you treat drug/toxin induced hepatitis?

A

—Rx: stop drug! S&S may slowly diminish; may need liver transplant.

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16
Q

Describe the convalescent phase associated with hepatitis A

A
  • —Major complaints: malaise, fatigue, hepatomegaly
  • —Almost all cases of HVA resolve
    • —Acute illness – 2-3 weeks
    • —Lab recovery -9 weeks
  • —Complications – rare:
    • —Fulminant hepatic failure
    • —Chronic hepatitis
    • —Cirrhosis of the liver
    • Hepatocellular carcinoma
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17
Q

How would you manage patients with hepatitis A?

A
  • —Bed rest & nutritious diet – then progressive ambulation
    • —Small frequent feedings
    • —Low-fat option, high protein; adequate fluids
  • —For those with more severe hepatitis infections – enteral feedings may need to be considered
  • —No alcohol for at least 6 months following recovery
  • —Serial liver function studies monitors recovery
  • —Medications – avoid those that affect liver function
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18
Q

What medications will be given to a patient with hepatitis B?

A
  • —Not all respond to current therapeutic regimens
  • —A-interferon
  • —Antiviral agents
    • —Lamivudine (Epivir)
    • —Adefovir ( Hepsera)
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19
Q

How would you prevent hepatitis A transmission?

A
  • —Good hygiene, hand washing & sanitation
  • —Vaccination for travel to foreign countries with high incidence
  • —Hepatitis A vaccine
  • —Immune globulin (IG) if contact
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20
Q

How would you prevent transmission of hepatitis B?

A
  • —Standard precautions/infection control measures
  • —Screening of blood products
  • —Immunization:
    • —Series – 3 injections – 0,1 & 6 months
    • —Hepatitis B immune globulin (HBIG)
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21
Q

How would you prevent hepatitis C?

A
  • —No vaccine available
  • —Screening - blood products
  • —Prevention - needle sticks
  • —Reduce infection spread
  • —Avoid high risk behaviors
  • —Use barrier precautions when in contact with blood or body fluids
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22
Q

What would you teach a patient with hepatitis A,B, or C?

A
  • —Hepatitis A & B
    • —Education – re infection
    • —Vaccinations available
    • —Hygiene practices
  • —Hepatitis C
    • —Education – re infection
    • —Infection control measures
    • —Modification of high risk behaviors
    • —Treatment protocols
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23
Q

What is cirrhosis?

A

—Chronic disorder; normal hepatocytes replaced with diffuse hepatic fibrosis (Scarring of the liver)

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24
Q

What can cause cirrhosis?

A
  • —Chronic alcohol consumption
  • —Hepatitis – C & B
  • —Primary biliary
  • —Non-alcoholic fatty liver
  • —Environmental factors; exposure to chemicals
  • —Predisposition regardless of alcohol intake or diet
  • —Alpha 1-antitryptsen deficiency (it maintains surfactant)
  • —Repeated episodes of heart failure (congestion and backing up of blood)
  • —Autoimmune
  • —Cause may not be known
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25
What are the clinical manifestations of cirrhosis?
* —**Asymptomatic for long periods** * —Systemic – fever, weakness, fever, weight loss * —GI disturbances * —Abdominal pain * —Amenorrhea * —Erectile dysfunction; gynecomastia * —**Portal hypertension →hepatomegaly; splenomegaly → developing ascites** * —Infection; spontaneous bacterial peritonitis * —Vitamin deficiencies * —Jaundice * —Hematologic * —Skin lesions * —Encephalopathy - subclinical * —Anemia * —Malnutrition * —Hematologic * —Neurologic changes * —Hepatic encephalopathy * —Day-night reversal; asterixis; tremor * —Delirium, drowsiness, coma * —Asterixis * —Fetor hepaticus -- must smell from all of the urea
26
What would be used to diagnose a patient with cirrhosis?
* —CBC; serum electrolytes * —Serum albumin * —Liver function tests * —Prothrombin times * —Stool for occult blood * —Esophagogastroduodenoscopy (EGD) * —Liver biopsy * —Liver scan * —Liver ultrasound * —Angiography
27
How would you manage a patient with cirrhosis?
* —Rest – depends upon stage & S&S * —Nutrition * —Skin care * —Reduce risks for injury * —Monitor for bleeding * —B complex, folate acid; ferrous sulfate * —Vitamins – especially K * **—Avoid: alcohol, aspirin, NSAIDs, acetaminophen** * **—For ascites – Na+ restricted to 400-800 mg/day** * **—If poor response to Na+ restriction** * **—Spironolactone (Aldoctone) spares K+ & Furosemide (Lasix) wastes K+** * May restrict protein initially * —Re-introduce protein; daily 1.2 gm/kg/day * —Small frequent meals - high carbohydrate, low Na+ & protein; bedtime snack * —**Medications: lactulose (helps get rid of ammonia and fluid); oral antibiotics** * —Discontinue sedatives, analgesics, tranquilizers * Monitor for complications & infections.
28
What are some complications with cirrhosis?
* **—Upper GI bleed** * —Infections * —Hypokalemia * —Azotemia * —Drug side effects * —Too high protein ingestion * —Constipation
29
What are some characteristics of variceal hemorrhage?
* —1/3 of persons with varicies * —1st bleeding episode – mortality of 30-50% * —Manifestations: * —Hematemesis * —Melena * —Hypovolemic shock * —Avoid alcohol, aspirin, irritating foods * —Report chronic coughing & URIs for Rx * Rx - endocsopic sclerotherapy or banding
30
How would you manage a patient with variceal hemorrhage?
* —Needs intensive care setting * —Hemodynamic support * —Balloon tamponade * —NG tube & gastric decompression * —02, IV fluids, electrolytes, volume expanders * —Blood; blood products * —Medications: * —Somatostatin (Octretide) – preferred, causes vasoconstriction of the splenic vessels * —Vasopressin * —Monitor: * —Hemodynamic function * —Patient condition; associated symptoms * —Treatments including tube care & GI suction * —Oral care; I & O * —Implement measures to reduce anxiety & agitation * —Quiet calm environment; reassurance * —Education & support – family & pt.
31
What are the clinical manifestations of a Hepatocellular Carcinoma?
* —May be asymptomatic * —Abdominal pain * —Anorexia, weight loss * —Weakness/malaise * —Anemia * —Jaundice * —Enlarged; irregular liver * —Cirrhosis symptoms * —Hepatomegaly * —Abdominal bruits * —Ascites * —Splenomegaly * —Weight loss; muscle wasting * —Fever * —Chronic liver disease signs
32
What are some riskfactors for cholelithiasis?
* **—High:** * —Multiparous women \> age 40 * —Obesity * —Native Americans * —**Others: ** * —Estrogen therapy * —Diabetes mellitus * —Cirrhosis, hemolysis * —Infections of biliary tract * **—Rapid weight loss; frequent weight changes**
33
What are the manifestations of a choleliathiasis (gall stones)? -- uncomplicated
* —Most asymptomatic * —If symptomatic: * —**Pain following fatty meal – ½ hr. – 6 hrs.** * —N/V; diaphoresis * —_Not_ exacerbated by movement; squatting, bowel movements or passage of flatus * —Several attacks before seeking medical attention * May have refered pain in the shoulder
34
What are they atypical syptoms of cholelithiasis?
* —Chest pain * —Nonspecific abdominal pain * —Belching, fullness after meals; early satiety * —Abdominal distention/bloating * —Epigastric or retrosternal burning * —N/V without biliary colic
35
What are the manifestations of a complicated cholelithiasis
36
What causes cholecystitis?
—Causes: * —With obstruction; without obstruction (acalculous cholecystitis) * —Bacterial --\> ecoili * —Neoplasms * —Anesthesia * —Opioids * —Inflammation * —Extensive fibrotic tissue * — * —
37
What are the manifestations of choleystitis?
* —Fatty food ingestion 1 hr. + before initial pain onset * —Nausea/vomiting; diaphoresis * —Fever, tachycardia * —RUQ abdominal tenderness * —**Possible + Murphy’s sign** * —Guarding; rebound * —Jaundice (25%) * —May resolve in 7-10 days without treatment * —Possible complications
38
What are some diagnostic tests done for choloecystitis?
* —CBC; WBC with differential * —Liver function tests; total bilirubin * —Serum amylase – they want to rule out any pancreatitis
39
How would you manage a patient with cholelithiasis?
—Diet - ↓ fat, ↑protein, ↑carbohyrates —Medical dissolution therapy * —Ursodeoxycholic acid (UDCA) * —Ursodiol (actigall) * —Chenodeoxycholic acid (CDCA or Chenix) —Other dissolving options: * —Methyl tertiary terbutyl ether (MTBE) * —Oral drugs - bile salts —Nonsurgical removal: * —Endoscopic sphincterotomy ( ERCP) — * Intracorporal – mechanical shock waves Extracorporal shock wave lithotripsy (ESWl) — Surgical removal:
40
What are some nursing interventios for patients with biliary disorders?
* —Assess and manage pain * —Oral care – especially if N/V * —Interventions for pruritis * —Personal hygiene as needed * —Intake & output * —Monitor for hemorrhage * —Assess; monitor for infection * —Assess – signs of obstruction
41
What are some nursing interventions for post-op care with biliary disorders?
* —Low Fowler’s position * —NG tube to suction; IV fluids; I & O * —NPO; then soft, low-fat, high carbohydrate diet * —Maintain skin integrity; assess & promote biliary drainage if T-tube in place. * —Analgesics for pain; assess pain relief * —Encourage coughing & deep breathing * —Progressive ambulation * —Monitor & evaluate potential complications
42
What causes acute pancreatits?
**Major causes:—** * **Gallstone - ~45%** * —Chronic alcohol abuse - ~30% * —Hyper-triglycerides – 3rd most common cause 1000mg/dl + Other causes: * —Endoscopic retrograde cholangiopancreatography (ERCP) * —Trauma * —Postoperative * —Drugs —Sphincter of Oddi dysfunction
43
How is a patient diagnosed with acute pancreatitis?
**—Diagnostic criteria - ≥ 2 of the following:** * —Typical abdominal pain * —Amylase/lipase \> 3x UL * —Confirmatory findings on US/CT imaging
44
What are the clinical manifestations of acute pancreatitis?
* —Onset - abrupt * —Pain * —Systemic: Fever, tachycardia, hypotension, pallor, diaphoresis, N&V, weakness * —Abdomen – tender, most often no guarding, rigidity or rebound; distention, no bowel sounds * —Anxious— * —Looks acutely ill; may sit with trunk flexed & knees flexed * —N/V; diaphoresis; fever * —Hypotension; shock * —Abdominal wall discoloration – Gray Turner’s; Cullen’s sign * —Diminished or absent bowel sounds * —Dyspnea; hypoxia * —Jaundice * —Renal failure * —Confusion &/or agitation
45
What are some laboratory diagnostic tests for acute pancreatitis?
* —CBC with differential; * —Electrolytes * —Ca++ * —Lipids, BUN, Sr. Creatinine, LFTS * —Prothrombin; other coagulation tests * **—Serum amylase (20-110 U/L)** * **—Serum lipase (0-160 U/L)** * —Blood glucose * —Arterial Pa02 – hypoxemia
46
How would you manage a patient with acute pancreatitis?
* —Fluid replacement; electrolytes -- use calloids * —Frequent hemodynamic monitoring * —Analgesia with parenteral opioids * —**Maintain/monitor urine output \>0.5cc/kg/h** * **—Bedrest**, NPO, frequent oral care; skin care * —I & O * —Position – for comfort & respiratory effort * —Manage & stabilize metabolic complications * —Monitor for possible complications
47
What kind of nutrition plan will a patient with acute pancreatitis be on?
* —NPO – initially; begin PO intake when no pain, no N/V, + bowel sounds, pt. hungry * —Bland - small, frequent feedings – ↑ protein; ↑ carbohydrate, ↓fat – solid preferred if at all possible. * —Supplemental fat soluble vitamins; nutritional drinks * —Nasograstric feedings if unable to take PO * **—No caffeine or alcohol**
48
What are some medications used for acute pancreatitis?
* —Analgesia – morphine, dilaudid * —Antibiotics – only with infections * —Others medications tried – H2 blockers, glucagon, antacids, have not proven to be effective * —PPIs may still prescribed to prevent stress ulcers * —Most recently, NSAIDs via the rectal route has been proven to be most beneficial following ERCP
49
What are the 2 types of chronic pancreatitis?
1. —Chronic obstructive pancreatitis 2. —Chronic calcifying pancreatitis/alcohol induced
50
What are the clinical manifestations of chronic pancreatitis?
* —Two primary symptoms – abdominal pain & pancreatic insufficiency * —Abdominal pain * —Pancreatic insufficiency * —Malabsorption * —Pancreatic diabetes
51
How would you manage a patient with chronic pancreatitis?
* —Prevent further attacks * —**No alcohol!** * —Pain relief * —Diet – bland, ↓ fat, ↑ carbohydrate; protein * —Endocrine insufficiency may result from islet cell destruction which leads to diabetes * —Periodic blood glucose assessments; insulin may be required * —**Exocrine insufficiency typically manifests as weight loss and steatorrhea** * —If steatorrhea present, a trypsinogen level \< 10 is diagnostic for chronic pancreatitis * —Manage with low-fat diet and pancreatic enzyme supplements (Pancrease, Creon) with meals & with a PPI
52
What are the manifestations of a pseudocyst?
* —Most asymptomatic * —Abdominal pain, duodenal or biliary obstruction * —Vascular occlusion or fistula formation * Spontaneous infection with abscess formation
53
How would you manage a patient with a psuedocyst?
* —If small – follow up one year until cyst becomes about 12 cms * —Drainage & stenting if indicated
54
What are some disorders of the anterior pituitary gland?
* Disorders * Tumors are the most common cause of primary anterior pituitary disorders * Usually benign * Produce symptoms of hypersecretion of 1 or more hormones * #1 prolactin * #2 Growth hormone * Growing mass can produce neuro symptoms from increased ICP
55
What are some disorders asssociated with the posterior pituitary gland?
* SIADH * Diabetes insipidus
56
What are some clinical findings associated with pituitary tumors?
* Headache * hemianopia * loss of visual acuity * blindness due to pressure exerted on the dura and optic chiasm * Disorder of target organ (ie, cushing’s syndrome)
57
What is hypopituitarism?
* Is a partial or complete loss of the anterior lobe’s function. * Affects the function of endocrine glands that are stimulated by anterior pituitary hormones. * Can be deficit of one hormone or all * Deficient in LH & FSH
58
What causes hypopituitarism (anterior pituitary)?
**Primary:** * pituitary tumors * inadequate blood supply to the pituitary * infections or inflammatory diseases * sarcoidosis or amyloidosis * irradiation * surgical removal of pituituary tissue * Sheehan syndrome * autoimmune disease **Secondary:** * tumors of the hypothalamus surgical damage to pituitary * inflammatory diseases * **head injuries**
59
What are the manifestations of a patient with hypopituitarism?
**Manifests two ways:** * Hyposecretion of the target organ * S/S of a growing pituitary tumor **•Headaches** **•Visual changes (either peripheral or central vision)** * Anosmia * Seizures
60
What is hyperpituitarism (anterior) and what causes it?
* An oversecretion generally of prolactin or growth hormone. * Most commonly caused by a benign tumor such as adenoma * In adults - begins between ages 30-50 which is after the end plates of the bones have closed. * Bones become deformed rather than enlongated.
61
What is prolactin hypersecetion?
* Prolactin Hypersecretion - most common endocrine abnormality caused by hypothalamus- pituitary disorders. * Most common cause are pituitary adenomas * Prolactin - necessary for lactation. * Causes: physiological, pathological, pharmacological
62
What are the signs and symptoms of prolactin hypersecretion?
* galactorrhea * amenorrhea * decreased libido * erectile dysfunction
63
What is the treament for hyperpituitarism?
* Surgery - outcomes based on size of tumor & basal prolactin level. * Medical tx * Bromocriptine or Cabergoline- dopamine agonist that stimulates dopamine receptors and affects both the hypothalamus and pituitary levels. Works by inhibiting PRL secretion by tumor.
64
What is acromegaly?
* Occurs in pituitary gland produces excess growth hormone in the adult. * Occurs after the epiphyseal plates have closed. * First noticed in hands and feet (excessive growth of soft tissue) * **Gigantism in children**
65
What are the signs and symptoms of acromegaly?
* Swelling of feet and hands * Facial features coarse as bones grow * increased perspiration * protruding jaw * voice deepens * enlarged lips, nose, & tongue * thickened ribs (barrel chest) * joint pain * Degenerative arthritis * enlarged heart * enlargement of other organs * Peripheral neuropathies * Proximal muscle weakness * **Snoring/ sleep apnea -- because of the growth of the tounge** * fatigue & weakness * headaches * loss of vision * irregular menstrual cycles * breast milk production in women * impotence in men
66
What are the long term effects of acromegaly?
* Joint pain - leads to crippling degenerative arthritis * Heart enlarged and impaired - leads to failure * Tissue compresses on nerves - pain, loss of visual fields * Headaches
67
How would you treat acromegaly?
* Surgery to remove the tumor - hypophysectomy **(1st line)** * Radiation * Drug therapy- octreotide (Sandostatin) – reduces GH levels * Given SC 3Xs weekly * Diet - may dev. DM or carbohydrate intolerance * CHF - salt restriction
68
What is SIADH and what does it result in?
* Occurs despite normal or low plasma osmolarity * Results in fluid retention, serum hypoosmolality, dilutional hyponatremia, hypochloremia, concentrated urine with normal renal function
69
What are the manifestations of SIADH?
* Decreased Na+ and Cl- levels * Muscle cramping, pain, weakness, risk for seizures * **Na+ (\< 120 mEq severe vomiting, abdominal cramps, muscle twitching seizures)** * Stimulation of thirst, DOE, fatigue * Decreased urine output and weight gain * Decreased plasma osmolality **– can lead to cerebral edema --\> increased ICP** * Diagnostic – sodium level, urine and serum osmolality, urine specific gravity (\> 1.005)
70
What are the nursing interventions for patients iwth SIADH?
* Frequent vital signs, LOC * **Daily weights, assess heart & lungs** * **Assess S/S hyponatremia,** * **Seizure precautions** * Position HOB flat or \< 10degree elevation * **Frequent oral hygiene - because they are going to feel thirsty** * **Maintain fluid restriction (800-1000ml per day)**, strict I & O * If sodium is \< 120, they will give a hypertonic fluid
71
What is diabetes insipidus and what causes it?
* DI is a syndrome of altered water balance in which ADH is deficient or there is a renal resistance to its effects. * **Caused primarily by inadequate secretion of ADH.** * Neurogenic or central DI * Nephrogenic or renal DI
72
What causes central DI?
linfections of meninges, head injury, surgery of the Hypothalamus- pituitary, amyloidosis, TB
73
What causes Nephrogenic DI?
**Physiologic:** * familia, sarcoma, multiple myeloma, SCD, CF, electrolye disturbances such as hypercalcemia or hypokalemia **Drugs:** * aminoglycosides, foscarnet, lithium, amphotericin B, cisplatinum, **demeclocycline (helps treat SIADH)**, rifampin
74
What are the signs and symptoms of DI?
75
What are some lab findings for DI?
Serum chemistry * Increased serum osmolality _\>_ 295 mOsm/kg * Increased serum sodium _\>_ 148 mEq/L Urinalysis * Decreased urine osmolality 50-100 mOsm/kg * Decreased urine sodium _\>_ 20 mEq/L * Specific gravity 1.005 * Urine volume - _\>_ 6 liters per day
76
How would you manage a patient with DI?
* Correct underlying cause * Medications * Desmopressin (DDAVP) intranasally. * Aqueous vasopressin (Pitressin) SC or IM * short acting agent (4-6 hours) * Diabinese, **tegretol** can be tried * Nephrogenic DI – low-sodium diet, thiazide diuretics, indomethacin
77
Describe fluid therapy for DI patients?
* Hypotonic saline such as 1/4 or 1/2 strength saline. * Titrated to hourly uop. * Titration may be 500 ml uop for 1 hour is replaced by 500 ml of IV fluid bolus the next hour.
78
What 3 hormones does the thyroid secrete?
* Thyroxine (T4) - regulate cell metabolism & energy production, influence growth & development, & affect cell differentiation in the fetus. * Triiodothronine (T3) * Calcitonin - increases calcium deposits in bones, decrease serum calcium levels.
79
What is hyperthyroidism and what causes it?
* An increased production and secretion of thyroid hormone from thyroid gland. * **Causes:** * Grave’s disease (most common, 60-90%) * Plummer’s disease (toxic multinodular goiter) * Thyroiditis
80
What is grave's disease
* **Most common cause of hyperthyroidism** * Autoimmune disorder * Affects women more than men * **Characterized by:** * diffuse goiter * hyperthyroidism * infiltrative ophthalmopathy * infiltrative dermaopathy
81
What is plummer's disease?
* Presents with multiple nodules and a milder form of hyperthyroidism * More common in persons over 40 yrs. * Not autoimmune
82
What is thyroiditis and what causes it?
* inflammation of the thyroid gland. * Can lead to release of excess amounts of thyroid hormones *
83
What are some characteristics of hyperthyroidism?
* Increased metabolic rate, heat production, O2, peripheral vasodilation * Altered CHO, protein, & fat metabolism * **Increased body temp., Intolerance to heat, Warm & moist skin, increased appetite, metabolic fatigue, weight loss, muscle weakness** * **Blood glucose elev, decreased triglycerides, and cholesterol, hepatic dysfunction, increased # of stools** * They will develop hyperglycemia * Diarrhea * Altered CV functioning - hypermetabolic and adrenergic state * Increased myocardial oxygen consumption, shortened systolic interval, increased cardiac output * Tachycardia, palpitations, increased blood pressure, dyspnea, angina, atrial fib, CHF * Nervousness, restlessness, decreased attention span, insomnia, emotional lability
84
What are the clinical manifestations of hyperhyyroidism?
* Feeling nervous, irritable, & excitable * Increase appetite with progressive weight loss * Heat intolerance with frequent perspiration * Exophthalmos (bulging eyes) from decreased venous drainage * Enlarged thyroid or goiter * Dyspnea * Insomnia * Amenorrhea * Tachycardia (90-160 beats/min) * Increase in systolic BP
85
What are the symptoms of thyrotoxicosis?
* nervousness, hyperexcitable, irritable, apprehensive * Palpitations * Heat intolerant - perspire freely * skin flushed continuously * fine tremor of hands * startled facial expression (exophthalmos)
86
How can you diagnose a patient with hyperthyroidism?
* Decreased TSH levels (becuase the thyroid is producing too much) * **Elevated free T4 levels** * Radio active iodine to differentiate Graves disease from other forms of thyroiditis
87
How do you treat patients with hyperthyroidism?
* **Anti-thyroid drugs - Propulthiouracil (PTU) or methimazole.** * Usually will control problem within a few weeks. * Radioactive iodine - most widely recommended permanent treatment of hyperthyroidism. * Acts relatively quickly * If they take this they will be on life long synthroid (**DON'T TAKE VITAMINS WITH THIS DRUG)** * Surgical removal * Symptom management - beta blockers
88
What are some nursing diagnoses associated with hyperthyroidism?
* Altered nutrition RT exaggerated metabolic rate, excessive appetite, & increased GI activity * Avoid giving anything that can cause diarrhea * Avoid caffiene * * Ineffective coping RT irritability, hyperexcitability * Altered body temperature * Disturbance in self-esteem RT to changes in appearance, excessive appetite, & weight loss
89
What is hypothyroidism and what causes it?
* A decrease in the secretion of thryoid hormone. * May be caused by an interference with thyroid hormone production or a reduction in thyroid mass.
90
What is hashimoto's thyroiditis?
* An autoimmune process where the thyroid enlarges and becomes inefficient in converting iodine into thyroid hormone and compensates by enlarging. * TSH levels will be high * T4 levels low * Thyroid antibodies in 95% of patients
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What are the signs and symptoms of hypothyroidism?
* Fatigue * Weight gain * Anorexia * Intolerance to cold * Constipation * Dry skin & brittle nails * Swollen eyelids * Coarse, dry hair * Decreased libido * Memory loss * Irritability * Abnormal menstrual cycles
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What are some nursing diagnoses associated with hypothyroidism?
* Activity intolerance RT fatigue & depressed cognitive process * Altered body temperature * Constipation RT depressed GI function * Altered thought process RT depressed metabolism & altered CV and respiratory status
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How would you diagnose hypothyroidism and how would you treat it?
* §Primary – Increased TSH level * lDecreased free T4 level * lIncreased cholesterol, LDL, triglycerides * l * §Levothyroxine (synthroid) = DOC * lOlder patients – need to know their cardiac status
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What is hyperparathyroidism and what causes it?
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What are the signs and symptoms of hyperparathyroidism?
* muscle weakness * Loss of appetite * Fatigue * Constipation * Emotional disorders * Shortened attention span * Osteoporosis, fractures, kidney stones
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How would you diagnose hyperparathyroidism?
* Bone x-rays * Lab tests to measure calcium & parathyroid hormone levels
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How would you treat hyperparathyroidism?
* 1st priority - control elevated calcium levels --\> give bisphosphonates * Removal of gland * Low calcium diet
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What is hypoparathyroidism?
* Characterized by too little parathyroid hormone production * Leads to decreased levels of calcium (hypocalcemia) & increased levels of phosphorus (hyperphosphatemia) * Very rare condition * usually caused because of loss of active tissue following thyroid or parathyroid surgery.
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What are the signs and symptoms associated with hypoparathyroidism?
Clinical signs 2nd to hypocalcemia * neuromuscular excitability, irritability, & muscle cramping (tingling in hands, fingers, & around mouth; severe - tetany) Other symptoms * Nausea, vomiting, diarrhea, & abdominal cramping * Acute - can cause tetany (tonic spasms in the upper and lower extremities accompanied by pain)
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What is chovstek's sign?
* Elicited by tapping the patient’s face lightly over the facial nerve. * Facial muscle twitching indicates a positive finding. * Indicates hypocalcemia & occurs with hypomagnesia
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What is trousseau's sign?
* Elicited by grasping the patient’s wrist or inflating the blood pressure cuff on the upper arm to constrict the circulation for a few minutes. * Palmar flexion is a positive finding. * Indicative of hypocalcemia & hypomagnesia
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What are the treatments for hypoparathyroidism?
Treatment * Replacement of Calcium & vitamin D * Calcium supplementation of 1.5-3 g/day * Vitamin D – preferred preparations (Calcatrol) * Diet – high in Ca++ * lTofu, dark green vegetables, soybeans * **Acute tetany - calcium gluconate IVP**
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Describe the care for a hypophysectomy
* Transsphenoidal approach used * avoids disturbing the cranium * incision is performed in upper gum line * Pre-operative care * sinuses are cleansed and antibiotic spray applied * Cortisol given to tolerate stress * After gland removed - muscle graft from anterior thigh used to pack dura and prevent leakage of CSF. * Nasal packing inserted after incision closed * Mustache dressing applied
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Describe post op care for hypothysectomy
Neurological assessment * Assess for s/s of target gland deficiences * •**Diabetes insipidus (DI), Addison’s disease, hypothyroidism** * **Avoid coughing, sneezing, or blowing nose - CSF leak** * **•encourage deep breath instead** * Strict I & O * Oral hygiene * NO toothbrush for 2 weeks * •provide oral rinses and dental floss * **Assess for meningitis (HA, Inc. temp, nuchal rigidity)** * After packing removed- observe for rhinorrhea * Monitor nasal drip for glucose (\> 30 mg/dL) * Avoid bending at the waist * Prevent constipation * Elevate HOB (at least 30 degrees at all times) * Teach patient he may have anosmia for 3-4 months * Lifelong replacement of cortisol (if total) or vasopressin for DI.
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How would you care a patient having a thyroidectomy pre op?
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What are some nursing interventions post op for a patient with a thyroidectomy regarding ineffective breathing patterns?
* Assess respiratory status * Observe for bleeding * Record amount/type of wound drainage * Monitor proper functioning of drains * Monitor patient’s neck for enlarging mass * Assess cough, swallowing, and aspiration * Maintain tracheostomy tray readily available
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What is acute thyrotoxicosis and what causes it?
**It is severe manifestations of hyperthyroidism, with symptoms of:** * elevated temperature * increased tachycardia * onset of dysrhythmias * worsening tremors * worsening mental status * Abdominal pain * (Delirium) **Causes:** * Grave’s disease * nonadherence to prescribed therapy
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What is the primary focus with acute thyrotoxicosis?
**The Primary focus is fever (ie, 105 F) & cardiovascular changes:** **Maintain cardiac output:** * Monitor CV status q 1hr * Report changes such as tachycardia, dysrhythmias, s/s of CHF linitially see atrial fibrillation * Decrease cardiac workload by decreasing physical & emotional stressors. **Maintain normothermia:** * Monitor temperature q 1 hr. * use external cooling devices. * Maintain room temp in cool range. * **DO NOT give salicylates (aspirin). Only Tylenol.**
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What are some nursing interventions for acute thyrotoxicosis?
* Administer oral propylthiouracil (PTU) as ordered. * Administer iodine preps as ordered - maybe IV or PO. * Administer dexamethasone as ordered. * Administer propranolol as ordered. * Other supportive therapy: O2, cardiac glycosides, etc.
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What is a myxedema coma, and what are some problems that develop because of it?
**It is a severe form of hypothyroidism that leads to:** * Develop respiratory problems (usually cause of death) * function impaired by large tongue and sleep apnea * respiratory effort decreased by hypoxic & hypercapneic ventiatory drives and respiratory mm weakness. * Develop cardiac problems * cardiac output low because of bradycardia & low stroke volume; may develop CHF * Treatment: supportive * Administer L-thyroxine (thyroid hormone) IV
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What hormones does the adrenal cortex secrete?
* glucocorticoids (cortisol) * mineralcorticoids (aldosterone) * sex steroid hormones
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What hormones does the adrenal medulla secrete?
* NE Epinephrine
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What is addison's disease and what causes it?
**It is a disorder characterized by decreased:** * mineralocorticoids * glucocorticoids * androgen secretion **Autoimmune process responsible for 80% of all cases - results in atrophy of gland.** * 90% of adrenal cortex destroyed before see manifestations * Most significant deficiencies are cortisol & aldosterone
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What are some characteristics of addison's disease?
* Clinically rare disease * Seen in persons 30-50 years old * **More common in women**
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What are the manifestations of addison's disease?
**Hyperkalemia - K+ levels of more than 7 meq/L** * aldosterone deficiency affects the ability of the distal tubules of the nephrons to conserve Na+, therefore Na+ is lost, and K+ is retained. * Leads to arrhythmias and possibly cardiac arrest. **Hypotension, decreased cardiac output, tachycardia, decreased heart size:** * Na+ & water excreted - leads to- dehydration - which leads to - hypotension * Decreased heart size - microcardia diminished workload of heart. Can lead to circulatory collapse, shock and death. **Decrease in glucocorticoids:** * Metabolic disturbances - glucocorticoids have an “anti-insulin” effect. * Gluconeogenesis - decreases with resultant hypoglycemia & liver glycogen deficiency. * Client grows weak, exhausted, and suffers from anorexia, wt. Loss, and N/V * Decreased resistance to stress **Increased ACTH leads to Increased MSH:** * stimulates the epidermal melanocytes - which- increases skin pigmentation and mucus membranes * Have a tanned or bronze appearance * Mood changes - delusional thinking, difficulty with stress, lethargic, apathetic, depressed, forgetful, emotionally labile
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What are some nursing interventions for hypoaldosteronism?
* Vital signs frequently- monitor for * hypotension, tachycardia, tachypnea * Fluid volume deficit * watch uop and report \< 30cc/hr * fluid replacement
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How would you treat hypoaldosteronism?
**cortisol replacement- life long replacement** * Fludrocortisone (Florinef) - mineralocorticoid * promotes inc. reabsorption of Na+ and loss of K+, H2O, H+ from distal renal tubules
118
What would you teach a patient with hypoaldosteronism regarding their medications?
* **Take daily glucocorticoid in divided doses (2/3 on awakening in AM & 1/3 late afternoon)** * take medication with snack or meal * increase dose as directed for increased physical stress * never skip a dose; if sick notify MD * always wear Medic-Alert bracelet * learn how to administer emergency IM injections of hydrocortiosone
119
What is Adrenocortical hyperfunction (Cushing syndrome & Cushing disease)?
* Cushing syndrome occurs from chronic over exposure to excess cortisol. ↓ feedback inhibition by cortisol on CRH & ACTH secretion * Cushing disease occurs from over production of pituitary ACTH by a pituitary adenoma. * Can also be caused by hyperaldosteronism
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What are the effects of prolonged increases in Cortisol levels?
* ↓ feedback inhibition by cortisol on CRH & ACTH release which leads to low levels of ACTH which leads to adrenal cortex atrophy which leads to ↓ cortisol secriton * Loss of diurnal variation in cortisol secretion
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What are the clinical manifestations of Cushing syndrome/disease?
* Bone effects * Weight gain * Glucose intolerance * Protein wasting
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Describe the bone effects of cushing's disease/syndrome ## Footnote
* ↑ bone resorption * ↓ bone formation & ↓ Ca++ absorption (intestine) * ↑ renal Ca++ excretion (hypercalciuria → kidney stones) **All of these factors contribute to osteoporosis**
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Describe the effects of cushing's disease/syndrome on weight
Weight gain – fat deposition & transient Na+ & H2O retention (from mineralcorticoid effects of high cortisol)  Facial (moon face)  Cervical (buffalo hump)  Truncal (central obesity)
124
Describe the glucose intolerance associated with cushing's disease/syndrome
* Cortisol-induced insulin resistance * ↑ gluconeogenesis & glycogen storage by liver
125
Describe the protein wasting associated with cushing's disease/syndrome
Catabolic effects of high cortisol on peripheral tissues leads to muscle wasting
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What are the complications associated with cushings disease/syndrome?
* ↑ cortisol → ↑ vascular sensitivity to catecholamines → vasoconstriction/↑ BP * Metabolic syndrome (central obesity, hypertension, glucose intolerance, dyslipidemias) * Infections from immune system suppression * Altered mental status (irritability, depression, psychiatric disorders) from cortisol effects on hippocampal neurons * Hyperglycemia, glycosuria, hypokalemia, metabolic alkalosis
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Who is at risk for cushings disease / syndrome?
* Take glucocorticoids more often than once every other day * Have been taking glucocorticoids for longer than 3 weeks. * Use long acting meds. such as dexamethasone * Take parenteral preps of steroids * take doses above what is needed * Take doses after 4 pm
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How would you manage patients with cushing's syndrome?
* Fluid restriction Intake & output * Medications that interfere with ACTH production may be used for palliation. * If cause is a pituitary adenoma * use surgery (hypophysectomy) or radiation * If adrenal adenoma or carcinoma * adrenalectomy
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What are some nursing interventions for patient's with cushing syndrome?
* Decrease controllable stressors * Monitor physiological coping ability * Monitor VS q 2-4 h especially for HTN and Inc. HR * Monitor blood sugars **Control fluid volume excess** * Restrict fluids as prescribed; distribute fluids over 24 h.; use ice chips to prevent thirst. * Provide low sodium diet * Provide K+ supplement as required. * Monitor daily weight, I & O, daily labs (Na+, K+, pH). **Prevent falls & infection** * Temperature q 4h * assess mouth, lungs, skin, GU tract for s/s infection * Limit staff & visitors with s/s of URI * preventive measures - TCDB, oral hygiene q 2h, etc
130
What causes Hyperaldosteronism?
* Adrenal tumor, excessive cortex stimulation (angiotensin II, ACTH, ↑ K+), mineralcorticoid excess, adrenal hyperplasia * Primary (adrenal cortex) * Secondary (extra-adrenal, e.g., ↑ renin release/activation of angiotensin II, diuretic use) * continuous excessive secretion of aldosterone leads to higher levels of angiotensin II * mechanical obstruction of renal vessels (renal stenosis) * renin-secreting tumors
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What are the manifestations of hyperaldosteronism?
* HTN, **hypokalemia, Hypernatermia** * ↑ Na+, * hypervolemia * metabolic syndrome (HTN, obesity, dyslipidemia, hyperglycemia), * metabolic alkalosis, * ↑ urinary K+, * No edema – Na+ excretion rate “reset”
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What are the clinical signs and symptoms of hyperaldosteronism?
* headache * fatigue * muscle weakness * nocturia * loss of stamina * Paresthesias may occur if K+ depletion * Dysrhythmias * Metabolic alkalosis (tetany)
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How would you manage patient's with hyperaldosteronism?
* surgery * adrenalectomy which may be unilateral or bilateral * Must get K+ in normal range * –give K+ sparing agent (spironolactone) * –drug is aldosterone antagonist to promote fluid balance * Low sodium diet * glucocorticoids replacement with surgery
134
What is pheochromocytoma?
**Is a catecholamine-producing tumor that arises in chromaffin cells.** * Most common are unilateral & on right side. * Must benign; 10% malignant. * Accounts for 0.1% of HTN * Women, 40-60
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What effect does the tumor have with a patient with pheochromocytoma?
**Tumor synthesizes epinephrine & norepinephrine. Excessive catecholamines stimulate alpha & beta receptors and can have a wide range of adverse effects.** * Tachycardia * Peripheral vasodilation * Bronchodilation * Increased myocardial contractility * Glycogenolysis * Free fatty acid secretion
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What are the clinical manifestations of pheochromocytoma and how would you diagnosis it?
**Presents with:** * severe headaches * palpitations * profuse diaphoresis * flushing * apprehension or feeling of impending doom * Pain in the chest N/V Diagnosis: 24 hr urine collection of metanephrines -a byproduct of catecholamine metabolism – 95% pts. +
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How would you manage patients with pheochromocytoma?
§Management lSurgery is the treatment of choice. Postoperative care is like patient who undergoes an adrenalectomy. •Short-acting alpha-adrenergic blocking drug used to control HTN during surgery lPreoperative * Goals: adequate tissue perfusion, nutritional needs, comfort * Hypertension is the hallmark - take regular BP lying & sitting –avoid smoking, caffeine, do not change position quickly-effect BP –Alpha-adrenergic blocking drugs used to bring HTN under control before surgery