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Clinical Medicine 4 > Lecture 2 (GI)- Exam 1 > Flashcards

Lecture 2 (GI)- Exam 1 Flashcards

1
Q

Fatty Liver diseases:
* What are the three types?

A
  • Alcoholic Fatty Liver Disease AKA Alcoholic steatosis
  • Non-Alcoholic Fatty Liver Disease (NAFLD)
  • Non-Alcoholic Steatohepatitis (NASH)
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2
Q
  • What does non Non-Alcoholic Fatty Liver Disease stem from?
  • What is Non-Alcoholic Steatohepatitis (NASH)?
A

Non-Alcoholic Fatty Liver Disease (NAFLD)
* Stem from Metabolic Syndrome: Obesity & DM type II
* Pregnancy

Non-Alcoholic Steatohepatitis (NASH)
* Type of NAFLD: inflammation and fatty liver disease

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3
Q

Fatty Liver Diseases
* How does it appear on US?
* What can damage and help fatty liver?

A
  • On US – see hypo-echoic appearance on the liver. Bx – see fat globules.
  • High fructose corn suryp is damaging to the liver.
  • Metformin can reduce fatty liver.
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4
Q

Autoimmune Hepatitis
* Usually seen in who?
* Presents as what?
* Can be due to what?

A
  • Usually seen in young-middle aged women
  • Presents as chronic hepatitis – elevated LFT’s, multiple spider nevi, acne, hepatomegaly, hirsutism (cortisol problem). Amenorrhea may be a presenting symptom.
  • Can be due to Hx of Hashimoto Thyroiditis – predisposes.
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5
Q

Autoimmune Hepatitis
* What are the markers?
* What is the treatment? (2)

A

(+) ANA and/or (+) Smooth muscle antibodies are detected in the serum

Treatment:
* Prednisone with or without azathioprine (Imuran)
* Liver transplant for treatment failure

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6
Q

Alcoholic Liver Disease
* Predisposed?
* Only 20% of alcoholics develop what?
* What increases chances?
* Most common cause of what?
* Will potentiate what?

A
  • Genetically predisposed.
  • Only 20% of alcoholics develop liver disease
  • Poor nutrition increases chances, female sex too
  • Most common cause of liver disease in certain areas
  • Will potentiate other causes, always investigate other etiologies
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7
Q

Alcoholic Liver Disease
* Best treatment is when?
* There is a great degree of what?
* What is the Expected clinical picture?(3)

A
  • Best treatment is early intervention and counseling.
  • There is a great degree of reversibility if alcohol stopped. Less chance after first alcoholic hepatitis episode (fibrosis will not be reversed)
  • Expected clinical picture: AST>ALT, Macrocytic anemia, electrolyte abnormalities (decreased Vit B-thiamine)
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8
Q

Wilson’s disease
* What type of disorder?
* Inadequate what? What is low and high?

A

Autosomal recessive disorder

Inadequate hepatic secretion of copper
* Low concentration or defect of ceruloplasm (copper binding enzyme) in the serum
* Excessive copper accumulation in the LIVER and BRAIN and EYES

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9
Q

Wilson’s disease
* What happens to liver?
* What can be abnormal?
* What type of ring?

A

In addition to liver complications ->cirrhosis

Neuro-Psychiatric abnormalities
* Movement disorder
* Psychiatric disorders

Kayser-Fleischer ring (pathognomonic)

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10
Q

What is this?

A

Kayser-Fleischer Ring in Wilson’s Disease
* Outside of cornea (grayish ring)

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11
Q

Wilson’s Disease: Dx
* Increased what?
* Elevated what?
* Low what?
* What do you need to do?

A
  • Increased urinary copper excretion (>100 mcg/24hr)
  • Elevated hepatic copper concentration (>250 mgc/g)
  • Low serum ceruloplasmin levels (<20 mcg/dL)
  • Liver biopsy – acute or chronic hepatitis or cirrhosis
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12
Q

Wilson’s Disease: Txt
* Restiction of what?
* Oral what? What does that cause?
* Liver transplant for who?

A
  • Restriction of dietary copper (shellfish, organ foods, legumes)
  • Oral Penicillamine chelation enhances urinary excretion of copper (give with supplementation pyridoxine 50mg/week)
  • Liver transplantation for fulminant hepatic failure or end-stage cirrhosis.
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13
Q

Hemochromatosis Pathophysiology
* Abnormal what?
* What type of disease?

A
  • Abnormal absorption of Normal Iron Intake
  • Autosomal Recessive disease caused by a mutation in the HFE gene on chromosome 6
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14
Q

Hemochromatosis Pathophysiology
* What does it lead to?
* Also accumulates where?

A
  • This leads to increased iron absorption from the intestine -> hepatic iron overload -> hepatic insufficiency, hepatomegaly -> cirrhosis.
  • Also accumulates in gonads, heart and liver
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15
Q

Hemochromatosis – signs and symptoms
* What happens to skin, liver, heart?
* What may be present?

A
  • Bronzed skin/Skin pigmentation
  • Hepatomegaly
  • Cardiomegaly w/ or w/o heart failure or conduction defects
  • Restrictive cardiomyopathy and can have conduction defects on EKG
  • Diabetes may be present->Bronze DM
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16
Q

Laboratory Findings in Hemochromatosis
* What is elevated? (4)

A
  • Elevated LFTs
  • Elevated serum iron
  • Fasting Elevated Transferrin Saturation >50% (test for iron overload)
  • Elevated Ferritin

TIBC is low, serum iron is high. Opposite to iron def.

Transferrin Saturation (%) = ( serum iron/ TIBC) x 100%

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17
Q

Laboratory Findings in Hemochromatosis
* Diagnosis is confirmed via what? (2)

A
  • Genetic testing for hemochromatosis.
  • Liver biopsy will also show excessive iron deposition
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18
Q

Hemochromatosis Treatment
* Avoid what?
* Phlebotomy for who?
* Chelating agent deferoxamine may be used in patients with what?

A
  • Avoid foods high in iron
  • Phlebotomy 1-2 U of blood for symptomatic patients and patients with ferritin level >1000mcg, for 2-3 years until ferritin saturation is <50% and ferritin level is <50 mcg/L. Then periodic phlebotomy every 2-4 months.
  • Chelating agent deferoxamine may be used in patients with hemochromatosis and anemia) who cannot tolerate phlebotomies
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19
Q

Alpha 1 Antitrypsin Deficiency
* What is it? What does it not do?
* High associated with what?

A

Genetic (codominant) mutation in alpha 1 antitrypsin protein
* Which no longer protects lungs and liver against irritants

High association of Chronic Lung Disease (Emphysema) and Cirrhosis

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20
Q

Alpha 1 Antitrypsin Deficiency
* Also see what?
* A child will have what? What are the test?
* What is the txt? (3)

A

Also see panniculitis and vasculitis

A child with elevated LFT’s and Lung problems or chronic allergies should be tested
* AAT blood test or genetic testing

Tx: augmentation of donated AAT
* Lung/Liver transplant
* Steroids

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21
Q
A

Global elevation=hepatic failure

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22
Q

Which of the following lab findings is crucial in determining how sick this patient is?
A. PT
B. LDH and haptoglobin
C. Total bilirubin
D. The elevation of ALT
E. Elevation of Alk Phos

A

A. PT

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23
Q

Which finding on physical exam is crucial in determining how sick this patient is?
A. Number of spider nevi
B. Presence of Splenomegaly
C. Neurologic examination

A

C. Neurologic examination

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24
Q

Acute/Fulminant Liver Failure
* Acute-more progressive how?
* Presence of what?
* Fulminate hepatitis happens how?
* Etiologies?

A
  • Acute – more progressive over period of time
    * Presence of coagulopathy, and progressive encephalopathy within 4-8 weeks of presentation of elevated LFT’s. Presentation may be quicker.
  • Fulminant hepatitis: much more rapid (Lightning fast) failure within days of initial injury
  • Common etiologies; medication induced, infectious ( Hep B and A ). Autoimmune.
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25
Q

Fulminant Hepatic Failure
* What will severe acute liver injury show?(3)

A
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26
Q

Fulminant Hepatic Failure
* What are the typical clinical symptoms?

A
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27
Q

What is the DDX of FHF? (ABC’s)-9

A
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28
Q

What are drugs and toxins associated with FHF? (a lot lol)

A
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29
Q

FHF-Prognosis
* What are the predictors of worst outcomes? (4)

A
  • Increased degree of encephalopathy
  • Elevation of Prothrombin Time (PT/INR)
  • Age >40 or <10
  • Bilirubin level
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30
Q

FHF - Prognosis
* What tends to have a better prognosis?
* What etiologies rarely survive without liver transplant?

A
  • Acetaminophen overdose & Viral hepatitis A, B, and D tend to have a better prognosis
  • FHF secondary to other drugs, Wilson’s Disease or idiopathic etiologies rarely survive without liver transplant
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31
Q

FHF-Management
* Search for what?
* What do you need to monitor and treat?
* Check what levels? What do you give?

A

Search for etiology and treat the cause

Treat complications
* Monitor glucose levels and treat hypoglycemia (gluconeogenesis)
* Check NH3 levels in serum-> Give Lactulose (for constipation) for encephalopathy

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32
Q

FHF management:
* When is FFP given?
* What do you do for those who do not recover?

A
  • Fresh Frozen Plasma (FFP) if clinically significant bleeding or before any procedures (including central line placement)
  • Liver transplant for those who do not recover
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33
Q

Common Etiologies & Treatment of ACUTE FHF
* Fill in and also what is the mcc?

A

Maximum dose of Tylenol/Acetaminophen is 3(newer recommendation) -4 grams a day in a person weighing at least 150lbs

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34
Q

What are major causes of cirrhosis?

A
  • Alcohol
  • Hepatitis C
  • Hepatitis B (in developing countries)
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35
Q

What are other causes of cirrhosis (a lot lol)

A
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36
Q

Alcoholic Cirrhosis
* May be seen with what? What is the lab?
* What may be seen in severe alcoholism? What is the empiric txt?
* What is common?
* What is the txt?

A
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37
Q

Major Complications of Cirrhosis
* What are the two main issues?
* What are the sxs? (5)

A
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38
Q

Common Portal Hypertension Findings (not specific)
* What are a lot of the sxs?

A
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39
Q

fill in for child’s classification

A

Class A has better prognosis than Class C.

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40
Q

Complication of Portal HTN - Esophageal Varices
* May appear when?
* What is the most serious complication of portal HTN?
* What is the screening?

A
  • May appear when portal vein pressures rise above 10mmHg
  • Variceal hemorrhage is the most serious complication of portal HTN
  • Screening: EGD->ALL patients with portal HTN - screen for esophageal varices
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41
Q

Complication of Portal HTN - Esophageal Varices
* What is the prevention?

A

Prevention of initial or recurrent variceal bleeding – Beta-Blockers (reduce portal pressures by decreasing cardiac output and splanchnic vasoconstriction) Propranolol or Nadolol
* Decrease in HR by 25%, but no lower than 55 bpm

Propranolol – not selectiv.

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42
Q

Practice Guidelines – Acute episode of Variceal hemorrhage
* Maintain what and how?
* Short term use of what?
* What should be started as soon as possible when variceal hemorrhage is suspected?

A
  • Intravascular volume support and blood transfusions - maintain a hemoglobin of ∼8 g/dL
  • Short-term (maximum 7 days) antibiotic prophylaxis should be instituted in any patient with cirrhosis and GI Hemorrhage (fluoroquinolones) to prevent bacterial peritonitis-> SE QT prolongation
  • Pharmacological therapy (somatostatin or its analogues octreotide and vapreotide; terlipressin) should be initiated as soon as variceal hemorrhage is suspected and continued for 3–5 days after diagnosis is confirmed
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43
Q

Practice Guidelines – Acute episode of Variceal hemorrhage
* What should br performed within 12 hours?
* TIPS is indicated in who?
* Balloon tamponade should be used when?

A
  • EGD, performed within 12 hours, should be used to make the diagnosis and to treat variceal hemorrhage, either with endoscopic variceal ligation or sclerotherapy
  • TIPS is indicated in patients in whom hemorrhage from esophageal varices cannot be controlled or in whom bleeding recurs despite combined pharmacological and endoscopic therapy
  • Balloon tamponade should be used as a temporizing measure (maximum 24 hours) in patients with uncontrollable bleeding for whom a more definitive therapy
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44
Q

Esophageal Varices Interventional Treatment
* What is TIPS?

A

TIPS (transjugular intrahepatic portosystemic shunt procedure)

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45
Q

How can ascites be present by?

A

Present by physical examination &/or Abdominal Ultrasound

46
Q

Ascites Evaluation
* What should be performed and when?

A

Abdominal paracentesis in LLQ
* should be performed and ascitic fluid should be obtained from patients with new-onset ascites

47
Q

Ascites
* What do you need to look for/ calculate ?
* (3)

A
  • Ascitic fluid cell count and differential
  • Ascitic fluid total protein
  • Calculate serum Ascites Albumin Gradient (SAAG)
  • Ascitic fluid cultures if infection is suspected (fever, abdominal pain, or unexplained encephalopathy)
48
Q

How do you calculate SAAG? What do the numbers mean

A

SAAG (g/dL) = (Serum Albumin - Ascites Albumin)
* SAAG >1.1 g/dL = Portal HTN (other less common causes causes = CHF, myxedema, budd-chiari syndrome)
* SAAG <1.1g/dL = pancreatic ascites, nephrotic syndrome, peritoneal TB, bowel obstruction, biliary ascites

49
Q

What does SAAG stand for?
* Ascites is either made where?
* What is the hepatic sinusoid designed for?
* The diseased hepatic sinusoid becomes what?

A
50
Q

What is going with when there is high SAAG?

A
51
Q

What is going on when the SAAG is low?

A
52
Q

Ascites management
* What needs to be restricted?
* What is given in terms of medication? (2)

A

Dietary sodium restriction (2000 mg per day [88 mmol per day])

Oral diuretics to increase urinary sodium excretion
* Spironolactone and Furosemide – titrate as needed.

53
Q

Ascites management:
* What do you do for refractory ascites?
* What do you need to calculate/give for ascites evaculation?

A

Refractory ascites
* Therapeutic Paracentesis
* Referral for liver transplant

Ascites evacuation
* If drain more than 5L of Ascites, must replace 5g of albumin per each L above 5L

Supplementing 5 g of albumin per each liter over 5 L of ascitic fluid removed decreases complications of paracentesis, such as electrolyte imbalances and increases in serum creatinine levels secondary to large shifts of intravascular volume.

54
Q

Spontaneous Bacterial Peritontitis (SBP)
* What are the sxs?
* How do you dx it?

A
  • Symptoms – fever, abdominal pain/tenderness in a patient with cirrhosis
  • Diagnosis - positive ascitic fluid bacterial culture and an elevated ascitic fluid absolute PMN count without an evident intra-abdominal or surgical source of infection.
55
Q

Spontaneous Bacterial Peritontitis (SBP)
* How do you tx it?
* How do you prohylaxis it?

A

TX
* IV cefotaxime (3rd generation cephalosporin) .
* PO Ofloxacin may be used in pts without vomiting, shock, hepatic encephalopathy, or serum creatinine greater than3 mg/dL.

Prophylaxis
* Short term norfloxacin or Sulfa drugs (Bactrim) in patients with cirrhosis and gastrointestinal hemorrhage
* Long term Bactrim in patients with previous SBP infection

56
Q

Hepatorenal Syndrome
* What is it?

A

Advanced chronic or acute liver failure with portal hypertension & serum creatinine greater than 1.5 mg/dL or 24-hour creatinine clearance less than 40 mL per minute w/ no sustained improvement in renal function.

57
Q

Hepatorenal Syndrome
* What is the patho behind it?

A

Sodium Retention -> Renal vasoconstriction -> Reduced renal blood flow

Just a poor liver. Need transplant.

58
Q

Hepatic Encephalopathy
* What are the psych sxs? (5)

A
  • Sleep disturbance
  • Disorientation
  • Somnolence
  • Confusion
  • Unconsciousness
59
Q

Hepatic Encephalopathy
* What are the neuro sxs (5)

A
  • Asterixis
  • Ataxia
  • Loss of reflexes
  • Nystagmus
  • Coma
60
Q

Hepatic Encephalopathy
* Acute hepatic encephalopathy associated with what?
* Chronic hepatic encephalopathy occurs in who?

A
  • Acute hepatic encephalopathy associated with marked cerebral edema is seen in patients with the acute onset of hepatic failure
  • Chronic hepatic encephalopathy occurs in subjects with chronic liver disease and portosystemic shutting of blood
61
Q

Hepatic Encephalopathy
* What is the patho?

A

The pathophysiology of hepatic encephalopathy is multifactorial, and increased ammonia concentration, false neurotransmitters, endogenous benzodiazepine-like substances, abnormal fatty acid metabolism, free radical damage, cerebral edema, and increased mercaptans all have been implicated

62
Q

Hepatic Encephalopathy
* Cerebral edema is found in 80%of patients with what?

A

Cerebral edema is found in 80%of patients with acute hepatic encephalopathy and is due to both cytotoxic edema and increased permeability of the blood-brain barrier

63
Q

Hepatic Encephalopathy Management
* What do you need to check?

A

Check blood ammonia level if hepatic encephalopathy is suspected
* Note: level of elevation may not always correlate with clinical symptoms and levels may fluctuate

64
Q

Hepatic Encephalopathy Management
* How do you treat it?

A

Lactulose (converts NH3 to unabsorbed NH4 – creating diarrhea) until diarrhea, then 15-30mL TID-QID prn 2-3 loose stools a day.
* PO or Enema (if unconscious or unable to take PO)

65
Q

General Treatment of Cirrhosis
* Avoid what? (2)
* Vaccinate against what?

A
  • Avoid ETOH!!!
  • Avoid hepatotoxic medications ->Tylenol max 2g/day
  • Vaccinate against Hep A and B (Twinrix)
66
Q

General Treatment of Cirrhosis
* how do you treat the complications of portal HTN?

A

Esophageal Varices: propranolol.

Ascites: spironolactone +/- Loop diuretic.
* Spontaneous Bacterial Peritonitis - ABX

Hepatic Encephalopathy: Lactulose

67
Q

General Treatment of Cirrhosis
* What and how do you screen?

A

FREQUENT screening for Hepatocellular Carcinoma
* AFP marker and RUQ US ~every 6-12 months

68
Q

Hepatocellular Carcinoma/Malignant Hepatoma
* What is it?
* 80% are associated with that?

A
  • Malignant neoplasm of the liver that arises from parenchymal cells
  • 80% are associated with Cirrhosis
69
Q

Hepatocellular Carcinoma/Malignant Hepatoma
* What are the sxs? (4)

A
  • Cachexia, weakness, weight loss
  • Ascites – may be bloody (suggesting portal or hepatic vein thrombosis from a tumor or bleeding from the necrotic tumor)
  • Tender hepatomegaly w/ a palpable mass
  • Auscultation may reveal a bruit or friction rub over the tumor
70
Q

Diagnosis of Hepatocellular Carcinoma
* What is the preffered imaging studies to determine location and vasculature?
* What is diagnostic?
* What marker can you use?

A
  • CT and MRI are the preferred imaging studies to determine the location and vasculature of the tumor (US is useful for screening purposes)
  • Liver biopsy is diagnostic
  • AFP (alpha-fetoprotein) >1000 ng/mL is presumptive of hepatocellular carcinoma (without biopsy).
71
Q

Hepatocellular Carcinoma: txt
* What may result in cure? In who?
* Who has a 75% 5-year survival rate?

A
  • Surgical resection of solitary hepatocellular carcinomas may result in cure if liver function is preserved (Child’s class A)
  • Liver transplant w/ small unresectable tumors in patients with advanced cirrhosis may have a 75% 5-year survival rate.
72
Q

Hepatocellular Carcinoma: txt
* What do you do for patients who are not candidates for resection?

A
  • Chemoembolization via the hepatic artery is palliative and may prolong survival in some patients
  • Small Tumors: Injection of absolute ethanol, radiofrequency ablation, cryotherapy
73
Q

Indications for Liver Biopsy
* What are the indications (a lot lol)

A
74
Q

What are the indications for liver transplant? (3)

A
  • Chronic, irreveversible liver disease or fulminant hepatic failure when no alternative therapy is available
  • Correct certain congenital enzyme deficiencies & inborn errors of metabolism
  • Fulminant hepatic failure consider for grade III-IV coma (before cerebral edema develops)
75
Q

Liver Transplantation
* What are the guidelines? (7)

A
  • Expected death in 2 years
  • Preferably in anticipation of major complication(variceal bleeding, irreversible encephalopathy, severe malnutrition, and incapacitating weakness, hepatorenal syndrome)
  • Refractory ascites, intractable coagulopathy, hepatopulmonary syndrome
  • Bili > 10-20 mg/dL
  • Albumin < 2 g/dL
  • Worsening coagulopathy
  • Poor quality of life
76
Q

Liver Transplantation
* What are the absolute contraindications? (4)

A
  • Extrahepatobiliary sepsis or malignancy
  • Severe cardiopulmonary disease
  • Preexisting advanced CV or pulmonary disease
  • Active alcoholism or drug abuse
77
Q

Liver Transplantation
* What are the relative contraindications? (4)

A
  • Age > 70
  • HIV infection
  • Extensive abdominal surgery
  • Portal & superior mesenteric vein thrombosis
78
Q

Liver imaging studies: US
* Useful to dx what? ( what is normal and abnormal)
* Distinguishes what?

A

Useful to diagnose biliary obstruction (dilatation of common bile ducts)
* Normal is 4mm
* >7mm is suggestive of obstruction (tumor/stone/stricture)

Distinguishes normal liver architecture from abnormal.

Usually first step
Hard to do if lots of gas or big patient.

79
Q

Liver imaging studies: CT and MRI
* Detecting what?
* Assessing what?
* ID what?
* Early dx of what?
* ID what?
* Detection of what?

A
  • Detecting mass lesions in the liver and pancreas
  • Assessing hepatic fat content
  • Identifying idiopathic hemochromatosis
  • Early diagnosis of Budd-Chiari Syndrome
  • Identifying Dilation of intrahepatic bile ducts
  • Detection of splenomegaly

MRI is most sensitive

80
Q

Liver studies: Endoscopic Ultrasound (EUS)
* What is it used for? (3)

A
  • Biopsy & DX of esophagus, stomach, lung, pancreas, and rectal cancers.
  • Evaluating chronic pancreatitis and other masses or cysts of the pancreas.
  • Studying bile duct abnormalities including stones in the bile duct or gallbladder, or bile duct, gallbladder, or liver tumors.
81
Q

What is the most sensitive and specific diagnostic test for pancreatic cancer?

A

Endoscopic Ultrasound (EUS)

82
Q

Liver studies: Endoscopic Retrograde Cholangiopancreatography (ERCP)
* Gold standard for what? What can it see? (3)
* In addition to imaging, a variety of what?

A

“Gold standard” for diagnosing Biliary Obstruction
* Periampullar carcinoma
* Common Duct Stones
* Primary Sclerosing Cholangitis

In addition to imaging, a variety of tools are available for treatment

83
Q

Endoscopic Retrograde Cholangiopancreatography (ERCP)
* What are the complications? (3)

A
  • Pancreatitis (3 out of 5 pts)
  • Bleeding &/or perforation
  • Aspiration (decreased risk if NPO 6-8 hrs prior to procedure)
84
Q

Liver studies: Magnetic Resonance Cholangiopancreatography (MRCP)
* What is it?
* What is the limitations?

A

Non-invasive test of Biliary Disease/Biliary Obstruction

Limitations
* MRCP is NOT a therapeutic procedure

MRCP – cant do any intervention. Not therapeutic, lower risk. Just to image.

85
Q

What is this? What does it do?

A

A normal gallbladder is shown here with a velvety dark green mucosa and a thin wall.
* Collect generated bile and cont. it (responsive to cholecyticine and signals the need for contraction after fatty foods)

86
Q

Gallbladder Common Problems
* Cholelithiasis:
* Cholecystitis:

A
  • Cholelithiasis: natural hx of asymptomatic vs symptomatic. Sonogram is best study for diagnosis. Identify complications such as choledocholithiasis. Need for therapeutic ERCP.
  • Cholecystitis: inflammation due to gallstones. Diagnosis through cholecystogram or sonogram. Treatment is surgical
87
Q

Gallbladder Common Problems
* Acalculous cholecystitis:? test?
* Tumors:

A
  • Acalculous cholecystitis: low albumin states, chronic diseases, outpatient population. Need HIDA scan for diagnosis
  • Tumors; usually at late age (>65yo)->Adenocarcinoma most common
88
Q

Etiology of Gallstones
* Balance between what?
* Presence of what?
* Other situations that can alter balance? (5)
* Race?

A
  • Balance between bile components; lecithin, bile acids and cholesterol.
  • Presence of diseases that can alter that balance (i.e. hemolysis, lithogenic cholesterol, supersaturated bile )
  • Other situations that can alter balance: TPN, pregnancy, vagotomy (via decrease in CCK), ileal resection, medications.
  • Race: American Indians, Hispanics.
89
Q

Cholelithiasis
* What are the three main types of gallstones?

A

Three major types of gallstones
* Cholesterol – most common in the US
* Pigment
* Mixed

90
Q

Cholelithiasis
* what do mixed and cholesterol gallstones contain?
* Pigment stones have what?
* In U.S., 80% of stones are what?

A
  • Mixed & cholesterol gallstones contain > 70% cholesterol monohydrate
  • Pigment stones have < 10% cholesterol & are composed primarily of calcium bilirubinate
  • In U.S., 80% of stones are cholesterol or mixed, 20% pigment
91
Q

What does this show?

A
92
Q

Predisposing Factors for Cholelithiasis ? (11)

A

5 F’s
Female, fair, fertile, fat, 40

93
Q

Cholelithiasis
* What are the sxs?

A
  • Many gallstones are “silent”, present in asymptomatic pts
  • Symptoms occur when stones produce inflammation or obstruction of cystic or CBD’s
94
Q

Cholelithiasis
* What is the txt?

A

Asymptomatic – no treatment needed

Symptomatic – cholecystectomy
* Ursodial may be used in patients who are expected to form stones (bariatric surgery or rapid weight loss (Ozempic))
* If sxs but no inflammation/stones on imaging then can do outpt surgery within 2 weeks

95
Q

Cholelithiasis Complications
* What are the complications? (4)

A
  • Choledocholithiasis
  • Cholecystitis
  • Cholangitis
  • Pancreatitis
96
Q

Lithiasis in Biliary Tract
* Biliary tract lithiasis most often begins how?
* A small enough calculus may become what?
* Stone may travel further down into where?
* Stone may travel further down &, near ampulla, obstruct what?
* Stone may pass through what?

A
97
Q

Acute Cholecystitis
* What is it?

A

Acute inflammation of the gallbladder generally secondary to gallstones (>95% of cases)

98
Q

Acute Acalculous Cholecystitis(10%)
* Associated with what?
* What are the associations? (7)

A

Associated with higher complication rate

Associations
* Prolonged acute illness
* Fasting
* Hyperalimentation leading to GB stasis
* Vasculitis
* Cancer of GB
* CBD stone
* GB infections (Leptospira, Streptococcus, parasite)

99
Q

Acute Cholecystitis
* What are the sxs? (6)

A
  • Attack of biliary colic that worsens
  • Nausea, vomiting & anorexia
  • Fever
  • Exam typically reveals RUQ tenderness
  • Palpable RUQ mass found in 20% of pts
  • Murphy’s sign is present when deep inspiration or cough during palpation of RUQ produces increased pain or inspiratory arrest
100
Q

Acute Cholecystitis
* What do the labs show?

A

Mild leukocytosis

Bilirubin, alkaline phosphatase, ALT & AST may be mildly
elevated.
* Bilirubin elevation > 4mg/dl is unusual and suggests choledocholithiasis (not just cholecystitis)

Elevation of amylase/lipase (consider biliary pancreatitis due to stone if >500 U)

101
Q

Acute Cholecystitis
* What imaging needs to be done? (2) What sign is present?

A

RUQ US useful for demonstrating gallstones & occasionally a phlegmonous mass surrounding GB
* Sonographic Murphy’s sign (the presence of maximal tenderness elicited by direct pressure of the transducer over a sonographically localized gallbladder) seen in >95% of patients

HIDA Scan (nuclear imaging) may show an obstruction of the cystic or common hepatic duct.
* More sensitive test than US.

102
Q

Acute Cholecystitis
* What are the complications? (7)
* What is the txt?

A

Complications
* Empyema
* Hydrops – big dilation
* Gangrene
* Perforation
* Fistulization – to bowel or somewhere else
* Gallstone ileus
* Porcelain Gallbladder – very hard and looks like porcelain

All Treated with Surgery and ABX if indicated

103
Q

Acute Cholecystitis
* What is the txt? What is needed for high risk surgical patients?
* For Chronic or Subacute cholecystitis, what should be done?

A
104
Q

Choledocholithiasis/Cholangitis
* What is the etiology? (2)

A
  • In pts with cholelithiasis, passage of gallstones into CBD occurs in 10-15%; increases with age
  • At cholecystectomy, undetected stones are left behind in 1-5% of pts
105
Q

Choledocholithiasis/Cholangitis
* What are the sxs?

A
  • Choledocholithiasis- may present as an incidental finding, biliary colic, obstructive jaundice, cholangitis, or pancreatitis
  • Cholangitis usually presents as fever, RUQ pain, and jaundice (Charcot’s triad)
106
Q

Choledocholithiasis/Cholangitis
* What do the labs show? (4)

A
  • Elevations in serum bilirubin, alkaline phosphatase, & aminotransferases
  • Leukocytosis usually accompanies cholangitis
  • Blood cultures frequently positive
  • Amylase is elevated in 15% of cases
107
Q

Choledocholithiasis/Cholangitis
* What imaging needs to be done? What does it show?

A
  • Diagnosis usually made by cholangiography either preoperatively by ERCP or intraoperatively at time of cholecystectomy
  • US may reveal dilated bile ducts but is not sensitive for detecting common duct stones

DO ERCP first and remove stone and then refer for cholecystectomy.

108
Q

Choledocholithiasis
* What is the txt? What about high risk or elderly?

A
  • Laparoscopic cholecystectomy & ERCP have decreased need for choledocholithotomy & T-tube drainage of bile ducts
  • Endoscopic biliary sphincterotomy followed by spontaneous passage or stone extraction is the treatment of choice in elderly or high-risk pts.
109
Q

Choledocholithiasis
* Preoperative ERCP is indicated in gallstone patients with what? (3)

A

(1) history of jaundice or pancreatitis
(2) abnormal LFTs
and
(3) US evidence of a dilated common bile duct or stones in the duct

110
Q

Cholangitis
* What is the txt?(5)

A
  • IV antibiotics
  • NPO
  • Hydration
  • Analgesia
  • Stones should be removed surgically or endoscopically (ERCP)

Clinical Medicine 4 (13 decks)

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