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Pharm 2 > Exam #3 Liver, Gallbladder, Pancreas > Flashcards

Exam #3 Liver, Gallbladder, Pancreas Flashcards

1
Q

Ammonia

A

Turns into urea. Ammonia is created with the breakdown of proteins. It is highly toxic to the brain if it accumulates into the blood, which is why the liver turns it into urea.
Lab level: 15-45 mcg/dl
- In high levels, causes a mental status change

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2
Q

Liver Facts

A
  1. Largest solid organ in the body
  2. Located in RUQ
  3. Not normally felt on palpation
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3
Q

ALT Lab

A

7-56 U/L

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4
Q

AST Lab

A

10-40 U/L

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5
Q

Bilirubin is…

A

The final product in the destruction of RBC. degradation of heme from the natural destruction of RBC.
- Normal lab level: Below 1; if it is higher its a sign that either your RBC are breaking down at a high rate or that your liver is not breaking down waste.

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6
Q

Jaundice

A

Yellowing of the skin and sclerae of the eyes

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7
Q

Cholestasis

A

Systemic retention of excess bilirubin and other bile solutes

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8
Q

2 forms of bilirubin in bloodstream?

A
  1. Unconjugated bilirubin: Is insoluble in water. Can travel in the blood stream. Pigment before reaching liver. Requires transport proteins. Cannot be excreted.
  2. Conjugated bilirubin: Is water soluble. Does not require transport proteins. Can be excreted from body. (Non-Toxic)
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9
Q

Cirrhosis Steps

A

Characterized by widespread fibrotic ( scarred ) bands of connective tissue.
- Leads to increased vessel pressure.
- Inflammation caused by either toxins or disease resulting in extensive degermation and destruction of hepatocytes
- Tissue becomes nodular.
- At first the liver enlarges ( hepatomegaly ) then liver shrinks in size and hardens.
- Elevated liver enzymes

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10
Q

Cirrhosis Causes

A
  • Obesity
  • Hep C
  • Alcoholic Cirrhosis
  • Biliary Cirrhosis
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11
Q

Cirrhosis Assessment

A

Fatigue, weight gain, GI symptoms, abdominal pain, fector hepaticus ( bad breath, fruity, musky ) , asterixis ( course tremor, hand flapping ) , ascites, spider angioma, jaundice
1. Hepatomegaly: Early on, you can feel liver upon palpation
2. Splenomegaly: Late stages

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12
Q

Cirrhosis Complications

A
  • Fluid Overload: Ascites
  • Potential for hemorrhage; due to Poral Hypertension
  • Acute confusion
  • Pruritis; due to excess bilirubin, jaundice
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13
Q

Cirrhosis Interventions

A
  • Low sodium diet ( early stages )
  • IV Vitamin supplements ( needed in late stages )
  • *Diuretics
  • Oral and IV supplement
  • *Beta blockers; to prevent hemorrhage
  • TIPS procedure
  • *Lactulose; to treat high ammonia levels
  • Non-absorbable antibiotics; Neomycin
  • Manage itching; moisturize
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14
Q

Complication of Cirrhosis
Portal HTN

A

: Increased portal venous pressure, pressure over 5 mmHg. Increased resistance to blood flow.
Problems- Hyperdynamic circulation, esophageal varices and hemorrhage, rectal varies, splenomegaly

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15
Q

Transjugular Intrahepatic Portosystemic Shunt
( TIPS )

A

Is used to treat portal hypertension.
- Connects portal vein to hepatic vein in the liver.
- Reduces internal bleeding in the stomach and esophagus in patients with cirrhosis and may also reduce stomach accumulation ( ascites )

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16
Q

Ascites

A

The abnormal collection of excess fluid in the abdominal cavity
- Complication of cirrhosis
- Hypovolemia can occur
- Can affect RAAS system

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17
Q

Ascites S/S

A
  • Increased abdominal girth
  • Weight gain
  • Decreased appetite
  • Abdominal discomfort
  • Dyspnea
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18
Q

Ascites Treatment

A
  • Diuretics; Sprinalactone, furesomide
  • Sodium restriction less than 2000 mg
  • Electro and creatinine monitoring
  • TIPS procedure
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19
Q

Paracentesis

A

Removing fluid!
- Done when someone has a swollen abdomen, pain or problems breathing because there is too much fluid
( Ascites )

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20
Q

Esophageal Varices

A

Develop as a result of increased portal hypertension
- Increased pressure in blood vessels, risk of bleeding increases, decreased prothrombin
S/S: Melena, bright red rectal bleeding, decreased H/H, fatigue
Treatment: Vasoconstrictors, Venodilators, esophageal band, blood transfusion, TIPS procedure

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21
Q

Biliary Obstruction

A

Production of bile in the liver is decreased
- Fat soluble vitamins absorption is decreased
- Without Vit K; clotting factors are not produced

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22
Q

Hepatocellular

A

Liver cannot effectively excrete bilirubin resulting in excessive amounts of circulating bilirubin

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23
Q

Intrahepatic obstructive

A

Edema, fibrosis, scarring of hepatic channels and bile ducts

24
Q

Hepatic Encephalopathy

A

Enlarged liver due to / Ammonia build up!
S/S: anxiety, irritability, cognitive impairment, confused, flapping hand motion ( asterixis ) , muscle twitches
Interventions: HOB elevation, frequent neuro checks, simple carb, moderate protein and fat diet.
Med: Lactulose to stop ammonia build up!

25
Q

Lactulose

A

Works by decreasing the amount of ammonia in the blood of patients with liver disease. Draws ammonia into colon where it is removed as stool.
- Diarrhea is expected
- No more than 2-3 BM a day! Monitor

26
Q

Prodromal Phase

A

Begins about 2 weeks after exposure
- Highly contagious
- Nonspecific symptoms
- N/V, anorexia, coughing, low fever

27
Q

Icterus Phase

A

2 weeks after prodromal phase
- Can last 6 weeks
- Jaundice, tea colored urine, clay covered stools, enlarged liver, prolonged PT/INR

28
Q

Convalescent Phase

A

Begins as jaundice resolves, usually 6-8 weeks after exposure
- Enlarged liver may continue
- Usually resolves within 12 weeks after onset of jaundice

29
Q

Hep A

A

Transmission: Fecal Oral from contaminated food/water
-Acute Infection
-With Hep A the patient can be contagious 2 weeks before the s/s appear and 1-3 weeks from when the symptoms appear.
Diagnosed:
1. anti-HAV ( IgM and IgG )
2. anti-HAV igM = active infection
3. anti-HAV IgG = past infection
Prevention: Hand washing, vaccine, ( 2 doses, 6 mon apart )

30
Q

Hep B

A

Transmission: Blood and other bodily fluids like semen, saliva, vaginal fluid
Diagnosed:
1. HBsAg
2. Anti- HB’s = past infection
Treatment:
Acute= None just supportive care
Chronic= Antiviral medications or interferon ( Children at most risk )
Prevention: Vaccine for all infants, hand washing, following sharp precautions
( 3-4 doses, 6-18 months )

31
Q

Hep C

A

Transmission: Blood and bodily fluids through skin or mucosal route, not casual contact
- Intravenous drugs most common, sharps
- Leading cause of end stage liver disease!
-Most chronic cases
Diagnosed: presence of anti-HCV for chronic infections
Treatment: antiviral medications
Prevention: No hand washing, no vaccine

32
Q

Hep D

A

Only infects people when they have Hep B

33
Q

Hep E

A

Fecal oral; HEV antibodies, no chronic form, hand washing

34
Q

Hep A and E

A

Similar!
- Fecal oral
- Only cause acute infections
- Supportive and rest for treatment

35
Q

Hep B,C,D

A

Similar!
- Via blood/ bodily fluids
- All acute/ chronic
- Only Hep B has vaccine

36
Q

Cholecystitis

A

-Is a redness and swelling (inflammation) of the gallbladder. It happens when a digestive juice called bile gets trapped in your gallbladder. The gallbladder is a small organ under your liver. It stores bile which is made in the liver.
Causes: Gallbladder stone, gallstones impacted in cystic duct, bacteria, alterations in F&E, bile stasis

37
Q

Clinical Manifestations of Cholecystitis

A
  • Epigastric heaviness, RUQ pain
  • Symptoms occur after eating
  • Pain can radiate to right shoulder or scapula
    ( Murphys Sign )
  • Steatorrhea
  • Leukocytosis: High WBC
  • Fever / chills
  • Jaundice
38
Q

Cholecystitis Interventions

A
  • IV Therapy; prevent dehydration
  • Opioids: pain
  • Ketorolac; NSAID: For inflammation

Surgical:
- Cholecystectomy; removing gallbladder
- ERCP; visualizes the biliary tree by cannulation of the common bile duct through the duodenum

39
Q

Cholecystitis Interventions Cont

A
  • Low fat diet
  • Fruits and veggies
  • Whole grains
  • No high fat foods
40
Q

Cholelithiasis

A

Gallbladder stone formation ( gallstones )
- Biliary colic = most common symptom
- Can be cause by abnormal metabolism

41
Q

Risk factors for Cholecystitis

A

Five F’s
1. Female
2. Fair
3. Fat
4. Fertile
5. Forty

Other: changes in metabolism, biliary stasis, D.M, sedentary lifestyle, family history

42
Q

Four Major Processes for Acute Pancreatitis

A
  1. Lipolysis: Fat necrosis of endocrine and exocrine cells, fatty acids released, hypocalcemia occurs
  2. Proteolysis: Splitting of proteins hydrolysis of peptide bond to smaller polypeptides, may lead to thrombosis and gangrene of pancreas
  3. Necrosis of blood vessels; elastase is activated by trypsin and causes elastic fibers of the blood vessels and duct to dissolve, generalized hemorrhage occurs
  4. Inflammation; Leukocytes cluster around the hemorrhage and necrotic areas of the pancreas
43
Q

Acute Pancreatitis Assessment

A

History: Ask about alcohol usage and medical problems
Physical:
-Severe abdominal pain, LUQ. relief w fetal position.
-Can radiate to right shoulder / scapula ( Murphys Sign ) -Jaundice
gray blue discoloration of the abdomen ( Grey Turners Sign )

44
Q

Acute Pancreatitis Labs and Diagnostics

A
  • Lipase = ELEVATED
  • Amylase = ELEVATED
  • Glucose = ELEVATED
  • PT and apTT = ELEVATED
  • WBC = ELEVATED
  • Bilirubin = ELEVATED

Diagnostics;
1. Ultrasound
2. ERCP

45
Q

Acute Pancreatitis Complications

A
  • Coagulation Defects; DIC, creates many small blood clots. Because your body has used up the proteins and platelets that make your blood clot, DIC can cause excessive external bleeding
  • ARDS; respiratory distress from massive inflammation
  • Peritonitis ( fever, rebound tenderness )
  • Jaundice
  • Shock
  • Pancreatic pseudocyst ( collection of leaked pancreatic fluid )
46
Q

Acute Pancreatitis Interventions

A
  • IV Med: Hydromorphone for acute pain
  • NPO: once pain starts to resolve, start on clears
  • NG tube for suctioning
  • IV Fluid and Electro replacement
  • Monitor Blood Glucose
  • Acid reducers and PPI
  • Surgical: ERCP

After discharge…
- Low fat, low sugar
- Add enzymes with meals

47
Q

Chronic Pancreatitis

A
  • ETOH most common risk factor
48
Q

Chronic Pancreatitis Assessment

A
  • Abdominal pain
  • Ascites
  • Respiratory compromise
  • Steatorrhea
  • Weight loss
  • Jaundice
  • Dark urine
  • Polyuria, polydipsia, polyphagia
  • Assess: Amylase, lipase, bilirubin, ERCP, Ultrasound or CT
49
Q

Chronic Pancreatitis Intervention

A
  • Opioid Analgesic
  • PERT ( pancreatic enzyme replacement therapy )
  • H2 or PPI
  • Alcohol cessation

Surgical: Whipple Procedure

50
Q

Pancreatic Cancer

A
  • Head of pancreas is the most common site!
51
Q

Pancreatic Cancer Risk Factors

A
  • Cig smoking
  • Obesity
  • DM
  • Diet
  • Chronic pancreatitis
  • Genetic
52
Q

Pancreatic Cancer Assessment

A
  • Slow, vague presentation
  • Jaundice ( Late stages )
  • Weight loss
  • Anorexia, N/V
  • ERCP: Diagnosis
53
Q

Pancreatic Cancer Interventions

A
  • Chemo + Radiation: Shrink tumor
  • Opioids

Surgery: Whipple
- Also known as pancreaticoduodenectomy: it removes the head of the pancreas, the first part of the small intestine ( duodenum ) , the gallbladder and bile duct

54
Q

Cullen Sign

A

Cullen’s sign is described as superficial oedema with bruising in the subcutaneous fatty tissue around the peri-umbilical region.

55
Q

Turner Sign

A

Grey Turner sign is an uncommon subcutaneous manifestation of intra-abdominal hemorrhage that manifests as ecchymosis or discoloration of the flank. [1][2] This sign is classically associated with severe acute necrotizing pancreatitis, which can be associated with the Cullen sign (periumbilical ecchymosis)

Pharm 2 (10 decks)

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