L3 Hepatobiliary and Pancreatic problem

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Description and Tags

p.5-10, 12-13, 30-34 physiology skipped

Last updated 7:40 AM on 9/22/26
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53 Terms

1
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Which gallbladder disease does the following description refers to ?

  • Steady RUQ/epigastric pain;

  • no fever/infection.


Biliary Colic

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What is the primary mechanism of Biliary Colic

Transient blockage of the cystic duct by a stone.

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Which gallbladder disease does the following description refers to ?

  • Persistent RUQ pain, fever,

  • positive Murphy’s sign.

  1. Assess RUQ pain / tenderness

  2. Press your fingertips under the liver border at the right costal margin

  3. Ask the client to inhale deeply

  4. Note the degree of tenderness

+ve Murphy’s sign: Sharp pain that causes the client to hold the breath (inspiratory arrest 吸氣停止)

Cholecystitis

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What is the primary mechanism of Cholecystitis

Prolonged blockage of the cystic duct; gallbladder becomes inflamed/infected.

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Which gallbladder disease does the following description refers to ?

  • Pain + Jaundice


Choledocholithiasis

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What is the primary mechanism of Choledocholithiasis

Stone in the Common Bile Duct (CBD).

<p><span>Stone in the Common Bile Duct (CBD). </span></p>
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Which gallbladder disease does the following description refers to ?

  • Charcot’s Triad:

    • Fever, Jaundice, RUQ pain.


Cholangitis

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What is the primary mechanism of Cholangitis

Infected obstruction of the CBD.

<p>Infected obstruction of the CBD. </p>
9
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Which gallbladder disease does the following description refers to ?

  • Severe epigastric pain radiating to back; elevated pancreatic enzymes.


Biliary Pancreatitis

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What is the primary mechanism of Biliary Pancreatitis

Stone blocks the pancreatic duct outflow.

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Which gallbladder disease is a clinical emergency (Life-threatening)

Cholangitis

  • Infected obstruction of the CBD.

  • Charcot’s Triad:

    • Fever, Jaundice, RUQ pain.


12
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In LFT, what does the marker “ Bilirubin” indicates ?

  • a marker of haem catabolism

    • The level of conjugated (direct) bilirubin reflects biliary obstruction,

    • unconjugated (indirect) bilirubin is a reflection of haemolysis


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In LFT, what is “ Albumin, prothrombn” ?

markers of protein synthesis.

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In LFT, what does the marker “Bilirubin” (total ± direct) indicates / reflect?

jaundice severity (production, processing, or drainage problem)

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In LFT, what does the marker “Albumin + INR (PT)” indicates / reflect?

synthetic liver function (severity/chronicity)

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In LFT, what does the marker “ Transaminases” refers to & indicates?

Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT)

  • markers of hepatocellular damage

  • “cell leak” enzymes


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In LFT, what does the marker “ ALP, GGT” indicates ?

Hepatic alkaline phosphatase (ALP) and γ-glutaryl transpeptidase levels (GGT)

  • reflect cholestasis / bile duct obstruction (bile flow problem)

  • ALP could also be raised in bone disease


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In LFT, what does the marker “Urea and anmmonia” indicates?

markers of protein catabolism

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In LFT, what does the marker “Haemoglobin” indicates? (2)

  • anaemia associated with chronic bleeding from oesophageal varices;

  • macrocytosis associated with abnormal lipid synthesis, which occurs in alcoholism


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In LFT, what does the marker “Cholesterol & triglycerides” indicates?

reflect abnormal lipid metabolism

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In LFT, what does the marker “Immunoglobulins” indicates?

  • raised concentrations reflect the reduced phagocytosis of absorbed antigen by Kupffer cells

    • Kupffer cells phagocytose and catalyze bacterial and other antigens absorbed from the GI tract

  • resulting in increased activity at other antibody-producing sites


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In LFT, what does the marker “alpha 1 antitrypsin” indicates?

deficiency associated with cirrhosis


a protective protein made by the liver that travels through the bloodstream to shield the lungs from destructive inflammatory enzymes

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In LFT, what does the marker “Alpha fetoprotein” indicates?

marker of hepatocellular carcinoma

24
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In LFT, what is the purpose of checking drug half-life

sometimes measured where drug metabolism is compromised

25
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A patient has jaundice and pruritus.
Which lab pattern most strongly suggests biliary obstruction?

ALP ↑↑ + GGT ↑↑ with direct (conjugated) bilirubin ↑, ALT/AST mild–moderate ↑

26
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First nursing priority in a cirrhotic patient with confusion:

Perform an ABCD assessment, check vital signs + capillary blood glucose, and assess for immediate deterioration



  • Airway: Is the patient protecting it? Aspiration risk? GCS trend

    • if drowsy/vomiting → side position, suction ready,

      consider NBM.

  • Breathing: RR, SpO2, work of breathing; give O2 if needed.

  • Circulation: BP, HR, perfusion, temperature; consider sepsis screening.

  • Disability: Capillary blood glucose (fast, reversible), GCS/AVPU, pupils.

  • Exposure: Look for bleeding, infection sources, trauma, needle marks

Put on monitoring: SpO2, ECG, BP cycling, temperature

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What will you suspect / think about if the patient show confusion ?

  • Hypoxia, hypotension/shock, sepsis, hypoglycaemia, drug toxicity,

    intracranial event, or HE.

    • Stabilize and rule out immediately reversible threats first


28
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When assessing the airway, if GCS is = / < 7, what will we consider ?

Intubation

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What is the nursing priority for a cirrhosis patent with confusion after performing the ABCDE assessment ?

Establish IV access and prepare fluid

  • because hypotension will become more difficult to set up IV HB


30
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What is the purpose of giving lactulose in manageing a cirrhotic patient with confusion ? Suggest whether it is appropriate to be the first priority decision/

  • Lactulose is appropriate if hepatic encephalopathy is likely, but after initial stabilization

  • if reduced consciousness or aspiration risk

    →oral lactulose may be unsafe without airway assessment

  • If severe HE, may need NG administration under appropriate precautions


31
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Explain the use of lactulose in treating hepatic encephalopathy

  • Non-absorbable disaccharide that acidifies the colon, converting ammonia (NH3) to ammonium (NH4+) and reducing absorption

  • Dose: 20–30 mL orally every 1–2 hours until 2–3 soft stools/day

  • Rectal enema: For Grade III/IV HE or when oral route not possible


32
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What is the purpose of urgent CT brain in manageing a cirrhotic patient with confusion ? Suggest whether it is appropriate to be the first priority decision/

  • Consider CT if: head trauma/fall, focal neurology, anticoagulation, sudden severe headache, seizure etc..

  • Still: stabilize first (ABCD) before transport/imaging.


33
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What is the purpose of start rifaximin in manageing a cirrhotic patient with confusion ? Suggest whether it is appropriate to be the first priority decision/

  • adjunct, not first-line in acute moment

  • It is usually add-on for recurrent HE or after lactulose.

  • Not an immediate “first priority” action in an unstable/confused patient.


34
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Explain the use of rifaximin in treating hepatic encephalopathy

  • Antibiotic with minimal absorption in the gastrointestinal tract

    • resulting in high concentrations within the intestines

  • reduce ammonia production by targeting and eliminating ammonia-producing

    bacteria in the colon

    • works by binding to bacterial DNA-dependent RNA polymerase, inhibiting bacterial RNA synthesis

  • often considered for patients who do not respond to lactulose / those who

    experience intolerance


35
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Describe the pathophysiology of Hepatic Encephalopathy

  • Ammonia that results from bacterial and enzymatic deamination

    of amino acids in the intestines normally goes to the liver via

    the portal circulation where it is converted to urea, and to be excreted by the kidney

  • When blood is shunted past the liver via the collateral vessels or the

    liver is so damaged that it is unable to convert ammonia to urea

  • Ammonia levels in the systemic circulation increase & accumulate

  • The ammonia crosses the blood-brain barrier and produces neurologic manifestations.

    • neurotoxic effects of ammonia includes: abnormal

      neurotransmission, astrocyte swelling, and inflammatory cytokines


36
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List & explain the risk factors of Hepatic Encephalopathy (10)

Cerebral depressants (e.g., opioids)

↓ Metabolism by liver, causing ↑ drug levels and cerebral depression

Constipation

↑ Ammonia production from bacterial action on feces

Dehydration / diuretic overuse

Potentiates ammonia toxicity

GI bleeding

↑ Ammonia in GI tract

Hypokalemia

Potassium needed by brain to metabolize ammonia

Hypovolemia

↑ Ammonia because of hepatic hypoxia
Impaired cerebral, liver, and renal function because of ↓ blood flow

Infection

↑ Metabolic rate and cerebral sensitivity to toxins

Metabolic alkalosis

Facilitate transport of ammonia across blood-brain barrier , ↑ Renal production of ammonia

↑ Metabolism

↑ Workload of liver

Uremia (renal failure)

Retention of nitrogenous metabolites


37
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List the nursing management after administrating lactulose in treating hepatic encephalopathy (4)

  • LOC and mental status

  • Bowel frequency (target 2–3/day)

  • Electrolyte imbalances (especially potassium)

  • Signs of dehydration


38
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Suggest the s/s for Grade II Hepatic Encephalopathy

Confusion, lethargy, disorientation to time, and presence of asterixis (flapping tremor)

39
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List the nutritional nursing management for hepatic encephalopathy (2)

  • NO NEED protein intake restriction

    • should maintain protein intake at around 1.2 to 1.5 gm/kg/d.

  • Small meals throughout the day to prevent fasting, which can increase ammonia production


40
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<p>Suggest the best diagnosis base on the following assessment findings: (+ explain why not the others conditions)</p>

Suggest the best diagnosis base on the following assessment findings: (+ explain why not the others conditions)

Acute Biliary Pancreatitis (most likely)

  • Gallstones + dilated CBD + elevated enzymes


Acute Cholangitis

  • Jaundice + fever (though no fever yet)

Peptic Ulcer Perforation

  • Less likely, no peritoneal signs

Hepatitis

  • Unlikely with high lipase/amylase


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