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Adv. Med Surg > HEPATIC DISORDERS > Flashcards

HEPATIC DISORDERS Flashcards

1
Q

ANATOMY OF LIVER

A
  • largest gland of the body
  • Located in the upper right abdomen
    * A very vascular organ that receives
    blood from GI tract via the portal vein and from the hepatic artery
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2
Q

Physical examination of Liver (7)

A
  • Pallor, jaundice
  • Petechiae, erythema, angiomas
  • Gynecomastia
  • Neurologic status
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3
Q

Health Assessments of Liver (6)

A

Past medical history
Family history
Physical exam
Medication history → if liver enzymes are ↑ → stop drinking, Tylenol, herbs
Lifestyle behaviors → hepatitis d/t drug/sex
Travel history → 3rd world countries ↑ r/o hep A d/t sanitation

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4
Q

FUNCTION OF LIVER (8)

A
  • Glucose metabolism
  • Ammonia conversion (stomach/gut)
  • Protein metabolism (albumin/globulin)
  • Fat metabolism
  • Vitamin and iron storage
  • Bile formation, Bilirubin excretion
  • Drug metabolism
  • Hormone metabolism
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5
Q

LIVER Function Studies/LFTs (5)

Liver Diagnostics (4)

A

LIVER FUNCTION TESTS [LFTs]

  1. Serum Aminotransferase: AST, ALT, GGT, GGTP, LDH (alcoholics) (chronic patients) [HIGH]
  2. Serum alkaline phosphatase/Serum ammonia; Cholesterol* -> Hepatic Encephalopathy [HIGH]
  3. Bilirubin test associated w/ jaundice [HIGH]
  4. Prothrombin Time [PT/PTT/INR] (increased clotting time)(coagulation panel) [HIGH]
    • Serum protein studies *: Low Albumin (<3.5)-> low Ca + low platelets [LOW]

Diagnostic Tools:
LIVER BIOPSY

**Ultrasonography;

CT

MRI

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6
Q

LIVER BIOPSY
[PRE-DURING-POST PROCEDURE]

A
  • Preprocedure:
    informed consent, AM NPO,
    *Coagulation test [pre: PTT/PT → post: CBC (bleeding)], hx of meds, sedation, local anesthesia
  • During procedure:
    supine or left lateral with right arm above head, breathing- exhale and hold
    (complications in Bx→ ↓diaphragm → PNA)
  • Postprocedure:*
    ***turn on to the right side with a pillow under the costal margin x several hours (prevents bleeding)
  • no coughing or straining,
  • no heavy lifting or strenuous exercise x 1 week**
    *post labs: CBC (for bleeding)
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7
Q

CLINICAL MANIFESTATIONS AND COMPLICATIONS OF CIRRHOSIS
(Hepatocyte Dysfunction) (7)

Cirrhosis is a late stage of scarring (fibrosis) of the liver caused by many forms of liver diseases and conditions, such as hepatitis and chronic alcoholism.

A

A= ↓ Albumin
B= ↑ Bile → ↑ Bilirubin (Jaundice) + ↑ Cholesterol (CVD)
C= ↑Clotting factors [PT/PPT/INR] → bleeding (bruising)

** 1. Jaundice d/t increase bile
2. Bleeding (bruising) d/t coagulation defect (lack of clotting factors) [PT/PPT/INR]**

**3. Portal hypertension, leading to 4+5
4. ascites (fluid in peritoneal cavity),
5. varices (collateral circulation) **

6. Hepatic encephalopathy or coma-mental changes d/t high ammonia levels -PRIORITY (CHANGE OF LOC)

7. Hepatorenal syndrome – sudden ↓ UO, ↑BUN/CRE → ↓ renal function (hypovolemia)
(D/t edema, decreased intravascular volume, renal blood flow and glomerular filtration are decreased)

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8
Q

WHAT IS JAUNDICE?

A

Yellow- or green-tinged sclera and
skin caused by increased serum
↑ bilirubin levels

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9
Q

WHAT ARE THE TYPES OF JAUNDICE? (4)

A
  • Hemolytic
  • Hepatocellular (HEPATITIS, CIRRHOSIS)
  • Obstructive (STONES,TUMOR)
  • Hereditary hyperbilirubinemia

Hepatocellular and obstructive jaundice are most associated with liver disease

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10
Q

HEPATOCEULLAR JAUNDICE
MANIFESTATIONS

A

Hepatocellular:* hepatitis, cirrhosis*
* May appear mildly or severely ill
* Lack of appetite, nausea, weight loss
* Malaise, fatigue, weakness
* Headache, chills, and fever if infectious in origin

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11
Q

MANIFESTATIONS OF OBSTRUCTIVE JAUNDICE

A

Obstructive: stones, tumor
Dark orange-brown urine and
light clay-colored stools
* Dyspepsia and intolerance of fats, impaired digestion; Pruritus-severe itching of skin (seen w/ cirrhosis d/t ↑bile salts in skin)

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12
Q

WHAT IS PORTAL HYPERTENSION?

A
  • OBSTRUCTED BLOOD FLOW through the LIVER resulting in back flow and
    ↑ increased pressure throughout the portal venous system
  • Portal hypertension is characterized by →
    ↑ VENOUS PRESSURE in the portal circulation, as well as splenomegaly, ascites, and gastric varices and esophageal varices.
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13
Q

PORTAL HYPERTENSION MANIFESTATIONS (7)

A

** 1.↑ Venous Pressure in the portal circulation d/t back flow in blood leading to Collateral circulation develops** in an
attempt to↓ high portal vein pressure and also to ↓ the increased plasma volume and lymphatic flow.
2. Splenomegaly d/t splenic vein unable to drain into portal vein
3. Ascites- increased fluids in peritoneal cavity
** (Varices) 4. Esophageal varices and 5. gastric varices** d/t collateral circulation
6. caput medusae (ring of varices around the umbilicus), d/t collateral circulation
7. hemorrhoids d/t collateral circulation

Portal HTN resulting in increased capillary pressure and obstruction of venous blood flow
* Proteins shift from the blood vessels via the larger pores of the sinusoids (capillaries) into the lymph space. When the lymphatic system is unable to carry off the excess proteins and water , they leak through the liver capsule into the peritoneal cavity.
* The osmotic pressure of the proteins pulls additional fluid into the peritoneal cavity (↓albumin)

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14
Q

WHAT IS ASCITES AND WHAT ARE THE 5 CAUSES OF IT?

A

Ascites is the fluid in peritoneal cavity d/t:

**1. Portal hypertension ** → ↑ capillary filtration pressure from cirrhosis → ASCITES

2. Hepatocyte Failure (type of jaundice [cirrhosis/hepatitis]) → Decreased ↓ synthesis of albumin →
↓ serum oncotic pressure* (EDEMA) → water shifts to the peritoneal cavity→ leakage of plasma out of vascular space → ASCITES

3. Hepatocyte Failure → Hyperaldosteronism↑d/t (altered metabolism from hepatocyte failure): occurs when aldosterone is not metabolized by damaged hepatocytes → altered metabolism in RAAS) → ↑Aldosterone (↑Renin) → increased ↑ sodium reabsorption by the renal tubules → dehydration leading to ↓BP (hypovolemia) → ASCITES

  1. Hyperaldosterone ( Renin) also d/t PAV (Peripheral Arterial Vasodilation → to↓plasma volume causing leakage of plasma to vascular space → Ascites
  2. Bacterial peritonitis → ↑ capillary permeability → loss of plasma → Ascites

Hypokalemia is common → excessive secretion of potassium caused by hyperaldosteronism↑

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15
Q

INTERVENTIONS OF ASCITES
(4/8)

A

***1. Record abdominal girth and weight daily **
* Patient may have striae, distended veins, and umbilical hernia *
**2. Monitor VS and for potential fluid and electrolyte imbalances * **
**3. Relief of dyspnea →
*Semi- or high Fowler’s position **
*4. Skin care (Risk of skin breakdown)
* Special mattress (pressure-relieving mattress)
5. Turning schedule, at least every 2 hours **
* 6. ROM exercises
* 7. Coughing/deep breathing exercises
8. Elevate lower extremities/scrotum
** Because of alterations in immune function associated with cirrhosis, patients with ascites are at RISK FOR SPONTANEOUS BACTERIAL PERITONITIS (ENLARGED BOARD-LIKE STOMACH)(FEVER) (Monitor temp)

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16
Q

TREATMENTS FOR ASCITES (3)

A

Low-sodium diet (2 g sodium); severe
ascites may need to* restrict their sodium
intake to 250 to 500 mg/day. * also decrease protein*

Diuretics : Spironolactone (Aldactone)
* A high-potency loop diuretic, such as
furosemide (Lasix), is frequently used in combination with a
potassium-sparing drug.

*Paracentesis: (last resort) Removal of fluids from peritoneal cavity

17
Q

PROCEDURES FOR PARACENTESIS
[PRE AND POST]

A

Indications: Severe Ascites and abdominal fluid (Refractory to diuretics) [Last Resort from tx]

[PRE-] Immediately before a paracentesis, have the patient void to prevent a puncture of the bladder.

[POST] When a paracentesis is done, **the patient sits on the side of the bed or is placed in high Fowler’s position.
**
[POST] Following the procedure, monitor VS+ for
hypovolemia and electrolyte imbalances, and check the dressing for bleeding and leakage

Monitor abdominal girth and weight daily

18
Q

ESOPHAGEAL VARICES
MANIFESTATIONS (4) [HMGS]

A

MANIFESTATIONS
* hematemesis
* melena
* general deterioration
* Shock

  • Occurs in about 1/3 of patients with
    cirrhosis and varices, mortality of
    30-50%
19
Q

PREVENTIONS FOR ESOPHAGEAL VARICES (5)

A

* screening endoscopy q 2 years
avoid alcohol, ASA, & NSAIDs
* Propranolol and nadolol
(nonselective β-blocker)
to ↓ portal pressure- to ↓ risk of hemorrhage

best indicator for B-BLOCKER effectiveness →
Stools test negative for occult blood → (lack of blood in the stools)

20
Q

MANAGEMENT/INTERVENTIONS FOR
ESOPHAGEAL VARICES

A

* If an acute bleeding occurs: stabilize patient,
manage airway, provide IV therapy and blood

**Drug therapy combinations and endoscopic therapy **

Vasopressin (Terlipressin) or Octretide (Sandostatin) to ↓ bleeding with vasoconstriction effect

Nitroglycerin may be used in w/ vasopressin to
↓ coronary vasoconstriction

-Varices can rupture with severe cough, rough food, very fragile
-H2-receptor blockers (-tidine) prevent irritation and bleeding from the varices caused by GERD
-No NG Tube and Avoid Valsalva Meneuver

21
Q

NI for Balloon Tamponade: Sengstaken–Blakemore Tube

A
  • Nursing alert:
  • Monitor for complications (i.e., aspiration PNA)
  • Scissors at bedside
  • Semi-Fowler’s position
  • Oral/nasal care-The patient is unable to swallow saliva
  • Inflate gastric portion of balloon with 100 -200 ml of air
  • If bleeding continues inflate esophageal balloon 25 -40 mmHg → check q 2hrs for right pressure
    If no bleeding is noted, you can deflate the balloon
  • Esophageal balloon is deflated q8-12 hrs to avoid necrosis but if the gastric balloon is deflated, the esophageal balloon may occlude the airway.
22
Q

SURGERIES FOR ESOPHAGEAL VARICES
(5)

A

Endoscopic Sclerotherapy

Esophageal Banding

Esophageal variceal ligation (EVL):

TIPS & Portal Systemic Shunts: Transjugular Intrahepatic
Portosystemic Shunt (TIPS) (Risk for hepatic encephalopathy &
accelerated liver failure)

Balloon Tamponade: Sengstaken–Blakemore Tube
* Nursing alert:
* Monitor for complications (i.e., aspiration PNA)
* Scissors at bedside
* Semi-Fowler’s position
* Oral/nasal care-The patient is unable to swallow saliva

23
Q

The client is now with decompensated cirrhosis. Appropriate nursing actions (+/-)

A

Respiratory
o Initiate continuous pulse oximetry monitoring. (+)
o Administer oxygen therapy via nasal cannula. (+)
o Use incentive spirometry every 2 hours (-)
o Elevating the head of bed >30 degrees (+)

Gastrointestinal
o Limiting protein intake (-)
o Managing nausea and vomiting (+)
o Provide high calories with high carbohydrate diet (+)
o Increase fluids intake (-)

Neurological
o Perform neurological checks every 2 hours (+)
o Maintain safe environment (+)
o Place the client a room far from the nursing station (-)
o Administer sedatives to calm the client (-)

24
Q

Hepatic Encephalopathy and Coma

A

A life-threatening complication of liver
disease. May result form the
accumulation of ammonia and other
toxic metabolites in the blood
* Inability to detoxify
Portal hypertension – *portal blood
enters systemic circulation directly (ammonia produced by bacterial digestion of dietary)
* Ammonia crosses blood-brain barrier

25
Q

CLINICAL MANIFESTATIONS OF
Hepatic Encephalopathy and Coma (5)

A

**1. Impaired consciousness (disoriented), and/or inappropriate behavior, ranging from
2. sleep disturbances to lethargy to deep coma. **

**3. Asterixis (flapping tremor of the hand): impending coma - NI: Hand movement w/ arms extended in front of the client → if flapping w/ extension then that is bad

4. Fetor hepaticus: sweet, slightly fecal odor – this odor is from the accumulation of digestive by-products that the liver is unable to degrade.

5. Apraxia- inability to perform a simple figure/action d/t brain damage

26
Q

MANAGEMENT of
Hepatic Encephalopathy and Coma (5)

A

** Maintain safe environment
-Perform neurologic assessment q 2 h **

* Lactulose to reduce serum ammonia levels
(PO, NG tube, or enema) : acidic & sugar –
priority care*

* Diet (for patient without complications):
↑ CAL (3000 cal/day) with ↑ Carb;
Moderate to low fat;
Protein restriction [limit protein→ limit ammonia
-Protein restriction may be appropriate
in some patients immediately following
a severe flare of symptoms (i.e. episodic hepatic encephalopathy)

***Discontinue sedatives analgesics and
tranquilizers **

* Monitor VS and promptly treat
complications and infections

27
Q

Lactulose management (4)

A

Lactulose 1. (laxative) to
2. reduce serum ammonia levels
*(PO, NG tube, or enema) : acidic & sugar –priority care

  • traps ammonia in the gut & the laxative effect of the drug expels the ammonia from the colon;
  • Constipation should be prevented (should have good bowel movements 2-3x soft stools/day)
    1. Maintain about 2-3 x soft stool → if not ↑Fluids/water
    1. Oral ATB (neomycin, flagyl, rifaximin ) to reduce ammonia-forming bacteria in the colon; particularly in patients who do not respond to lactulose
  • if ↑ Ammonia → LOC altered tx. w/ Lactulose
  • ↓ K+ (hypokolemia) d/t loose stools
28
Q

Hepatitis A (HAV)
S/S
Complications
Prevention

A

INFECTIOUS HEPATITIS
FECAL-ORAL transmission
-Incubation: 15–50 days; Illness may last 4–8 weeks

May occur with or without symptoms; flu-like illness
Preicteric phase: Headache, malaise, fatigue, anorexia, fever
Icteric phase(acute): Dark urine, jaundice of sclera and skin, tender liver
Antibodies (HAV+IgM) acute phase
Antibodies (HAV+IgG) indicate past infections and lifelong immunity

29
Q

HEP A (HAV)
COMPLICATIONS

HEP A & HEP E SIMILAR

A

Complication: Fulminant hepatitis

→ Fulminant hepatic failure: sudden severely impaired liver function in a previously healthy person
* Develop within 8 weeks after the first symptoms of jaundice *

** S/S: Preicteric (before jaundice; highly contagious)= Headache, malaise, fatigue, anorexia, fever
*Icteric (increased bilirubin signs)= Dark urine, jaundice of sclera and skin, tender liver**

30
Q

HEP A RISK FACTORS (5/8)

A
  • young children, institutionalized individuals, health care personnel,
    **day care workers, food handlers,
    sanitation workers, laundry workers,
    travelers to underdeveloped countries **
31
Q

HEP A PREVENTION/INTERVENTIONS

A

Good hand washing [MOST IMPORTANT
safe water, education on food, proper sewage disposal, hygiene

Vaccine [2 x (NOW + 6 months]
* Natural active: Hep A exposure naturally —> develop antibodies = lifelong immunity (IgG)
* Artificial active: Vaccine
* Natural passive: Breastfeeding
* Artificial passive: immunoglobulin
Passive: already has antibodies
**Active: needs to produce antibodies **
Antibodies (HAV+IgM) acute (icteric) phase
Antibodies (HAV+IgG) indicate past infections and lifelong immunity

Immunoglobulin for contacts to provide
passive immunity within 2 weeks (antibodies)

***Bed rest during acute stage **

Well-balanced diet
* ↑ calorie, Vit supps
**Avoid alcohol & drugs **

32
Q

HEP B (HBV)
TRANSMITTED VIA?
S/S + COMPLICATIONS

A

SERUM HEPATITIS
Transmitted through blood found in blood, saliva, semen, and vaginal secretions, sexually transmitted, *transmitted to infant at the time of birth;

May occur without symptoms;
May develop arthralgias, rash
May be severe. Carrier state possible.
Increased risk of chronic hepatitis, cirrhosis, and hepatic (LIVER) cancer. - MAJOR WORLDWIDE CAUSE
-Screen for liver cancer q6-12 months
- Long incubation period; 1–6 months

**Complication: Fulminant hepatitis **

33
Q

HEP B (HBV)
PREVENTIONS

A

*Hand washing
Avoid unprotected sexual intercourse.
** Vaccine:** for persons at high risk, routine vaccination of infants
Three series- now, 1mo, and 6 mo.**Check for yeast allergy **

  • Passive immunization [hepatitis B immune globulin (HBIG)] for those exposed;
  • TX hepatitis B immune globulin (HBIg) contains antibodies to hepatitis B virus (HBV)(anti-Hbs) marker of positive response to vaccine.
    HBIg temporarily increases the clients resistance to hepatitis; short-lived protection/immunity being an example of passive immunity. Give HBIg before hep B vaccine to provide passive immunity.

Standard precautions/infection control measures
* Screening of blood and blood products

**Bed Rest*

Nutritional support during acute stage [ HBsAg, anti-HBc, HBeAg]
IMPROVE APETITIE/maintaining adequate intake

Medications for chronic hepatitis B
include alpha interferon and antiviral
agents: lamividine (Epivir), adefovir (Hepsera)

34
Q

HEP C (HCV)

A

Non-A, Non-B Hepatitis

***Transmitted by blood and sexual contract, including needle sticks and sharing of needles **
Most common form from alcohol-induced

A cause of 1/3 of cases of LIVER CANCER
most common reason for liver transplant

  • Incubation period is variable;

**Symptoms are usually mild; same as HBV but less severe and anicteric (jaundice) **

Chronic carrier state frequently occurs and LIVER CANCER

35
Q

HEP C (HCV)
PREVENTION/RISK/TX

A

** Prevention:** public health programs to decrease needle sharing among drug users
* Screening of blood/hx of IV drugs

  • Standard precautions/Prevention of
    needle sticks for health care workers/Barrier precautions with contact of blood or bodily fluids
  • Treatment: Antiviral agents: interferon
    and ribavirin (Rebetol) → Monitor WBC (leukopenia)
36
Q

HEP D (HDV)

A

**Only people w/ hepatitis B are at risk for hep D **
* Hepatitis B vaccine also prevents HDV
* Transmission is through blood and sexual contact
* Symptoms and treatment are similar to hepatitis B but more likely to develop fulminant liver failure and chronic active
hepatitis and cirrhosis

  • Complication: Fulminant hepatitis
37
Q

Physical examination of Liver (7)

A
  • Pallor, jaundice
  • Petechiae, erythema, angiomas
  • Gynecomastia
  • Neurologic status

Adv. Med Surg (8 decks)

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