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N3523 Adult and Older Adult Health Care II > Exam 4 - Study Material (liver) > Flashcards

Exam 4 - Study Material (liver) Flashcards

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
Q

What are the clinical manifestations of cirrhosis?

A
  • —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
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26
Q

What would be used to diagnose a patient with cirrhosis?

A
  • —CBC; serum electrolytes
  • —Serum albumin
  • —Liver function tests
  • —Prothrombin times
  • —Stool for occult blood
  • —Esophagogastroduodenoscopy (EGD)
  • —Liver biopsy
  • —Liver scan
  • —Liver ultrasound
  • —Angiography
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27
Q

How would you manage a patient with cirrhosis?

A
  • —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.
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28
Q

What are some complications with cirrhosis?

A
  • —Upper GI bleed
  • —Infections
  • —Hypokalemia
  • —Azotemia
  • —Drug side effects
  • —Too high protein ingestion
  • —Constipation
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29
Q

What are some characteristics of variceal hemorrhage?

A
  • —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
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30
Q

How would you manage a patient with variceal hemorrhage?

A
  • —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.
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31
Q

What are the clinical manifestations of a Hepatocellular Carcinoma?

A
  • —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
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32
Q

What are some riskfactors for cholelithiasis?

A
  • —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
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33
Q

What are the manifestations of a choleliathiasis (gall stones)? – uncomplicated

A
  • —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
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34
Q

What are they atypical syptoms of cholelithiasis?

A
  • —Chest pain
  • —Nonspecific abdominal pain
  • —Belching, fullness after meals; early satiety
  • —Abdominal distention/bloating
  • —Epigastric or retrosternal burning
  • —N/V without biliary colic
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35
Q

What are the manifestations of a complicated cholelithiasis

A
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36
Q

What causes cholecystitis?

A

—Causes:

  • —With obstruction; without obstruction (acalculous cholecystitis)
  • —Bacterial –> ecoili
  • —Neoplasms
  • —Anesthesia
  • —Opioids
  • —Inflammation
  • —Extensive fibrotic tissue
  • —
  • —
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37
Q

What are the manifestations of choleystitis?

A
  • —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
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38
Q

What are some diagnostic tests done for choloecystitis?

A
  • —CBC; WBC with differential
  • —Liver function tests; total bilirubin
  • —Serum amylase – they want to rule out any pancreatitis
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39
Q

How would you manage a patient with cholelithiasis?

A

—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:

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40
Q

What are some nursing interventios for patients with biliary disorders?

A
  • —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
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41
Q

What are some nursing interventions for post-op care with biliary disorders?

A
  • —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
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42
Q

What causes acute pancreatits?

A

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

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43
Q

How is a patient diagnosed with acute pancreatitis?

A

—Diagnostic criteria - ≥ 2 of the following:

  • —Typical abdominal pain
  • —Amylase/lipase > 3x UL
  • —Confirmatory findings on US/CT imaging
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44
Q

What are the clinical manifestations of acute pancreatitis?

A
  • —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
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45
Q

What are some laboratory diagnostic tests for acute pancreatitis?

A
  • —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
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46
Q

How would you manage a patient with acute pancreatitis?

A
  • —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
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47
Q

What kind of nutrition plan will a patient with acute pancreatitis be on?

A
  • —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
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48
Q

What are some medications used for acute pancreatitis?

A
  • —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
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49
Q

What are the 2 types of chronic pancreatitis?

A
  1. —Chronic obstructive pancreatitis
  2. —Chronic calcifying pancreatitis/alcohol induced
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50
Q

What are the clinical manifestations of chronic pancreatitis?

A
  • —Two primary symptoms – abdominal pain & pancreatic insufficiency
  • —Abdominal pain
  • —Pancreatic insufficiency
  • —Malabsorption
  • —Pancreatic diabetes
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51
Q

How would you manage a patient with chronic pancreatitis?

A
  • —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
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52
Q

What are the manifestations of a pseudocyst?

A
  • —Most asymptomatic
  • —Abdominal pain, duodenal or biliary obstruction
  • —Vascular occlusion or fistula formation
  • Spontaneous infection with abscess formation
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53
Q

How would you manage a patient with a psuedocyst?

A
  • —If small – follow up one year until cyst becomes about 12 cms
  • —Drainage & stenting if indicated
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54
Q

What are some disorders of the anterior pituitary gland?

A
  • 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
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55
Q

What are some disorders asssociated with the posterior pituitary gland?

A
  • SIADH
  • Diabetes insipidus
56
Q

What are some clinical findings associated with pituitary tumors?

A
  • 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
Q

What is hypopituitarism?

A
  • 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
Q

What causes hypopituitarism (anterior pituitary)?

A

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
Q

What are the manifestations of a patient with hypopituitarism?

A

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
Q

What is hyperpituitarism (anterior) and what causes it?

A
  • 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
Q

What is prolactin hypersecetion?

A
  • 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
Q

What are the signs and symptoms of prolactin hypersecretion?

A
  • galactorrhea
  • amenorrhea
  • decreased libido
  • erectile dysfunction
63
Q

What is the treament for hyperpituitarism?

A
  • 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
Q

What is acromegaly?

A
  • 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
Q

What are the signs and symptoms of acromegaly?

A
  • 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
Q

What are the long term effects of acromegaly?

A
  • 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
Q

How would you treat acromegaly?

A
  • 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
Q

What is SIADH and what does it result in?

A
  • Occurs despite normal or low plasma osmolarity
  • Results in fluid retention, serum hypoosmolality, dilutional hyponatremia, hypochloremia, concentrated urine with normal renal function
69
Q

What are the manifestations of SIADH?

A
  • 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
Q

What are the nursing interventions for patients iwth SIADH?

A
  • 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
Q

What is diabetes insipidus and what causes it?

A
  • 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
Q

What causes central DI?

A

linfections of meninges, head injury, surgery of the Hypothalamus- pituitary, amyloidosis, TB

73
Q

What causes Nephrogenic DI?

A

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
Q

What are the signs and symptoms of DI?

A
75
Q

What are some lab findings for DI?

A

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
Q

How would you manage a patient with DI?

A
  • 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
Q

Describe fluid therapy for DI patients?

A
  • 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
Q

What 3 hormones does the thyroid secrete?

A
  • 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
Q

What is hyperthyroidism and what causes it?

A
  • 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
Q

What is grave’s disease

A
  • Most common cause of hyperthyroidism
  • Autoimmune disorder
  • Affects women more than men
  • Characterized by:
    • diffuse goiter
    • hyperthyroidism
    • infiltrative ophthalmopathy
    • infiltrative dermaopathy
81
Q

What is plummer’s disease?

A
  • Presents with multiple nodules and a milder form of hyperthyroidism
  • More common in persons over 40 yrs.
  • Not autoimmune
82
Q

What is thyroiditis and what causes it?

A
  • inflammation of the thyroid gland.
  • Can lead to release of excess amounts of thyroid hormones
    *
83
Q

What are some characteristics of hyperthyroidism?

A
  • 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
Q

What are the clinical manifestations of hyperhyyroidism?

A
  • 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
Q

What are the symptoms of thyrotoxicosis?

A
  • nervousness, hyperexcitable, irritable, apprehensive
  • Palpitations
  • Heat intolerant - perspire freely
  • skin flushed continuously
  • fine tremor of hands
  • startled facial expression (exophthalmos)
86
Q

How can you diagnose a patient with hyperthyroidism?

A
  • 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
Q

How do you treat patients with hyperthyroidism?

A
  • 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
Q

What are some nursing diagnoses associated with hyperthyroidism?

A
  • 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
Q

What is hypothyroidism and what causes it?

A
  • 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
Q

What is hashimoto’s thyroiditis?

A
  • 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
91
Q

What are the signs and symptoms of hypothyroidism?

A
  • 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
92
Q

What are some nursing diagnoses associated with hypothyroidism?

A
  • 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
93
Q

How would you diagnose hypothyroidism and how would you treat it?

A
  • §Primary – Increased TSH level
  • lDecreased free T4 level
  • lIncreased cholesterol, LDL, triglycerides
  • l
  • §Levothyroxine (synthroid) = DOC
  • lOlder patients – need to know their cardiac status
94
Q

What is hyperparathyroidism and what causes it?

A
95
Q

What are the signs and symptoms of hyperparathyroidism?

A
  • muscle weakness
  • Loss of appetite
  • Fatigue
  • Constipation
  • Emotional disorders
  • Shortened attention span
  • Osteoporosis, fractures, kidney stones
96
Q

How would you diagnose hyperparathyroidism?

A
  • Bone x-rays
  • Lab tests to measure calcium & parathyroid hormone levels
97
Q

How would you treat hyperparathyroidism?

A
  • 1st priority - control elevated calcium levels –> give bisphosphonates
  • Removal of gland
  • Low calcium diet
98
Q

What is hypoparathyroidism?

A
  • 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.
99
Q

What are the signs and symptoms associated with hypoparathyroidism?

A

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)
100
Q

What is chovstek’s sign?

A
  • Elicited by tapping the patient’s face lightly over the facial nerve.
  • Facial muscle twitching indicates a positive finding.
  • Indicates hypocalcemia & occurs with hypomagnesia
101
Q

What is trousseau’s sign?

A
  • 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
102
Q

What are the treatments for hypoparathyroidism?

A

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
103
Q

Describe the care for a hypophysectomy

A
  • 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
104
Q

Describe post op care for hypothysectomy

A

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.
105
Q

How would you care a patient having a thyroidectomy pre op?

A
106
Q

What are some nursing interventions post op for a patient with a thyroidectomy regarding ineffective breathing patterns?

A
  • 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
107
Q

What is acute thyrotoxicosis and what causes it?

A

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
108
Q

What is the primary focus with acute thyrotoxicosis?

A

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.
109
Q

What are some nursing interventions for acute thyrotoxicosis?

A
  • 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.
110
Q

What is a myxedema coma, and what are some problems that develop because of it?

A

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
111
Q

What hormones does the adrenal cortex secrete?

A
  • glucocorticoids (cortisol)
  • mineralcorticoids (aldosterone)
  • sex steroid hormones
112
Q

What hormones does the adrenal medulla secrete?

A
  • NE
    Epinephrine
113
Q

What is addison’s disease and what causes it?

A

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
114
Q

What are some characteristics of addison’s disease?

A
  • Clinically rare disease
  • Seen in persons 30-50 years old
  • More common in women
115
Q

What are the manifestations of addison’s disease?

A

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
116
Q

What are some nursing interventions for hypoaldosteronism?

A
  • Vital signs frequently- monitor for
    • hypotension, tachycardia, tachypnea
  • Fluid volume deficit
    • watch uop and report < 30cc/hr
    • fluid replacement
117
Q

How would you treat hypoaldosteronism?

A

cortisol replacement- life long replacement

  • Fludrocortisone (Florinef) - mineralocorticoid
    • promotes inc. reabsorption of Na+ and loss of K+, H2O, H+ from distal renal tubules
118
Q

What would you teach a patient with hypoaldosteronism regarding their medications?

A
  • 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
Q

What is Adrenocortical hyperfunction (Cushing syndrome & Cushing disease)?

A
  • 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
120
Q

What are the effects of prolonged increases in Cortisol levels?

A
  • ↓ 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
121
Q

What are the clinical manifestations of Cushing syndrome/disease?

A
  • Bone effects
  • Weight gain
  • Glucose intolerance
  • Protein wasting
122
Q

Describe the bone effects of cushing’s disease/syndrome

A
  • ↑ bone resorption
  • ↓ bone formation & ↓ Ca++ absorption (intestine)
  • ↑ renal Ca++ excretion (hypercalciuria → kidney stones)

All of these factors contribute to osteoporosis

123
Q

Describe the effects of cushing’s disease/syndrome on weight

A

Weight gain – fat deposition & transient Na+ & H2O
retention (from mineralcorticoid effects of high cortisol)
 Facial (moon face)
 Cervical (buffalo hump)
 Truncal (central obesity)

124
Q

Describe the glucose intolerance associated with cushing’s disease/syndrome

A
  • Cortisol-induced insulin resistance
  • ↑ gluconeogenesis & glycogen storage by liver
125
Q

Describe the protein wasting associated with cushing’s disease/syndrome

A

Catabolic effects of high cortisol on peripheral tissues leads to muscle wasting

126
Q

What are the complications associated with cushings disease/syndrome?

A
  • ↑ 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
127
Q

Who is at risk for cushings disease / syndrome?

A
  • 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
128
Q

How would you manage patients with cushing’s syndrome?

A
  • 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
129
Q

What are some nursing interventions for patient’s with cushing syndrome?

A
  • 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
Q

What causes Hyperaldosteronism?

A
  • 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
131
Q

What are the manifestations of hyperaldosteronism?

A
  • HTN, hypokalemia, Hypernatermia
  • ↑ Na+,
  • hypervolemia
  • metabolic syndrome (HTN, obesity, dyslipidemia, hyperglycemia),
  • metabolic alkalosis,
  • ↑ urinary K+,
  • No edema – Na+ excretion rate “reset”
132
Q

What are the clinical signs and symptoms of hyperaldosteronism?

A
  • headache
  • fatigue
  • muscle weakness
  • nocturia
  • loss of stamina
  • Paresthesias may occur if K+ depletion
  • Dysrhythmias
  • Metabolic alkalosis (tetany)
133
Q

How would you manage patient’s with hyperaldosteronism?

A
  • 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
Q

What is pheochromocytoma?

A

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
135
Q

What effect does the tumor have with a patient with pheochromocytoma?

A

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
136
Q

What are the clinical manifestations of pheochromocytoma and how would you diagnosis it?

A

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. +

137
Q

How would you manage patients with pheochromocytoma?

A

§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

N3523 Adult and Older Adult Health Care II (9 decks)

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