A 45-year-old male presented with jaundice, abdominal distension, and pain. Imaging found intrahepatic biliary radical dilatation and lymphadenopathy. Liver biopsy was recommended to determine the underlying cause of cholestatic jaundice and evaluate for possible malignancy given concerning findings on CT scan and clinical presentation.
Obstructive jaundice is one of the important surgical topics. In this playlist I have discussed the introduction, choledocholithiasis, Carcinoma Pancreas and biliary atresia. If you watch all these videos together you will become confident in Managing obstructive jaundice.
Obstructive jaundice is one of the important surgical topics. In this playlist I have discussed the introduction, choledocholithiasis, Carcinoma Pancreas and biliary atresia. If you watch all these videos together you will become confident in Managing obstructive jaundice.
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
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Pulmonary Thromboembolism - etilogy, types, medical- Surgical and nursing man...VarunMahajani
Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
New Directions in Targeted Therapeutic Approaches for Older Adults With Mantl...i3 Health
i3 Health is pleased to make the speaker slides from this activity available for use as a non-accredited self-study or teaching resource.
This slide deck presented by Dr. Kami Maddocks, Professor-Clinical in the Division of Hematology and
Associate Division Director for Ambulatory Operations
The Ohio State University Comprehensive Cancer Center, will provide insight into new directions in targeted therapeutic approaches for older adults with mantle cell lymphoma.
STATEMENT OF NEED
Mantle cell lymphoma (MCL) is a rare, aggressive B-cell non-Hodgkin lymphoma (NHL) accounting for 5% to 7% of all lymphomas. Its prognosis ranges from indolent disease that does not require treatment for years to very aggressive disease, which is associated with poor survival (Silkenstedt et al, 2021). Typically, MCL is diagnosed at advanced stage and in older patients who cannot tolerate intensive therapy (NCCN, 2022). Although recent advances have slightly increased remission rates, recurrence and relapse remain very common, leading to a median overall survival between 3 and 6 years (LLS, 2021). Though there are several effective options, progress is still needed towards establishing an accepted frontline approach for MCL (Castellino et al, 2022). Treatment selection and management of MCL are complicated by the heterogeneity of prognosis, advanced age and comorbidities of patients, and lack of an established standard approach for treatment, making it vital that clinicians be familiar with the latest research and advances in this area. In this activity chaired by Michael Wang, MD, Professor in the Department of Lymphoma & Myeloma at MD Anderson Cancer Center, expert faculty will discuss prognostic factors informing treatment, the promising results of recent trials in new therapeutic approaches, and the implications of treatment resistance in therapeutic selection for MCL.
Target Audience
Hematology/oncology fellows, attending faculty, and other health care professionals involved in the treatment of patients with mantle cell lymphoma (MCL).
Learning Objectives
1.) Identify clinical and biological prognostic factors that can guide treatment decision making for older adults with MCL
2.) Evaluate emerging data on targeted therapeutic approaches for treatment-naive and relapsed/refractory MCL and their applicability to older adults
3.) Assess mechanisms of resistance to targeted therapies for MCL and their implications for treatment selection
Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
2. • A 45-year-old male ….
• C/O –
Yellowish discoloration of eyes, itching & lowgrade intermittent fever since 3 months.
Swelling over the feet, abdominal distension and
abdominal pain since last month.
• Past alcoholic but had stopped since one year.
• Denied any high-risk sexual behavior.
Jaundice
4. CholestasisDefinition –
Conjugated hyperbilirubinemia due to :
I. Impaired bile formation (hepatocytes)
II. Impaired bile flow (bile ducts/ductules)
Consequences• Secondary liver damage
I. Bile acid-induced hepatocyte injury
II. Secondary biliary cirrhosis
• Failure of substances secreted in bile to reach intestine
I.
II.
Bile acid deficiency in gut
Fat malabsorption/fat-soluble vitamin malabsorption
5. Towards central hepatic vein
Biliary canaliculus
Liver cell
Obstruction
C
Bilirubin,
Bile salts, &
Phospholipids
Endoplasmic reticulum
N
Sinusoidal blood
Towards Interlobular Bile duct
Screening tests that suggest cholestasis –
Color change in skin/sclera/stool/urine
Biochemical tests (Alkaline Phosphatase , Bilirubin)
6. Clinically-
Histologically-
Bile plugs (bilirubinostasis),
Feathery degeneration of
hepatocytes (cholate stasis),
Small-bile-duct destruction,
Peri cholangitis,
Portal edema,
Bile lakes and infarcts
(typically with extrahepatic
obstruction),
Finally , biliary cirrhosis.
Pruritus,
Fatigue,
Xanthomas,
Hepatic Osteodystrophy:
back pain from
osteoporosis,
Pale stools, or
steatorrhea
Evidence of fat-soluble
vitamin deficiency.
Enlarged liver with a
firm smooth non-tender
edge.
After 3–5 yrs of jaundice , liver cell failure indicated by deep jaundice, ascites, edema and
a lowered serum albumin develops. Pruritus lessens and the bleeding is not controlled by
vitamin K. Hepatic encephalopathy is terminal.
8. EVALUATION OF CHOLESTATIC JAUNDICE
• The first question -whether the cholestasis is
from intrahepatic or extrahepatic process.
CLUES TO EXTRAHEPATIC
OBSTRUCTIONS –
•Abdominal pain,
•Palpable GB or
upper abdominal mass,
•Evidence of cholangitis, and
•H/O- past biliary surgery.
CLUES TO INTRAHEPATIC
CHOLESTASIS-
Pruritus, as in primary
biliary cirrhosis (PBC)
and primary sclerosing
cholangitis (PSC) patient
9. Extrahepatic causes of cholestatic jaundice
Benign
Choledocholithiasis
Postoperative biliary
strictures
Primary sclerosing
cholangitis
Chronic Pancreatitis
AIDS cholangiopathy
Mirizzi’s Syndrome
Parasitic Disease
(Ascariasis)
Malignant
Cholangiocarcinoma
Pancreatic cancer
Gall Bladder Cancer
Ampullary Cancer
Malignant involvement
of the porta hepatis
lymph nodes
10. Intrahepatic causes of cholestatic jaundice
1) Viral Hepatitis
A. Fibrosing cholestatic hepatitis – Hep. B
&C
B. Hep.A, EBV, CMV
2) Alcoholic Hepatitis
3) Drug toxicity
A. Pure cholestasis- Anabolic &
contraceptive steroids
B. Cholestatic hepatitis- chlorpromazine,
erythromycin, Amoxiclav
C. Chronic cholestasis- chlorpromazine &
prochloperazine
4) Primary Biliary cirrhosis
5) Primary Sclerosing cholangitis
6) Vanishing Bile duct Syndrome
A. Chronic rejection of liver transplant
B. Sarcoidosis
C. Drugs
7) Non hepatobiliary Sepsis
8) Benign post-operative cholestasis
9) Para neoplastic Syndrome
10) Veno-occlusive disease
11) GVHD
12) Inherited
A. Progressive familial
intrahepatic cholestasis
B. Benign recurrent cholestasis
13) Cholestasis of pregnancy
14) Total Parenteral Nutrition
15) Infiltrative diseases
A. TB
B. Lymphoma
C. Amyloidosis
16) Infections
A. Malaria
B. Leptospirosis
11. • Risk factors1.
2.
3.
4.
5.
6.
Alcohol intake,
Medications,
Pregnancy
Sexual contact, drug abuse, needle punctures.
ICU – Sepsis, shock liver & TPN .
After BM transplantation- Veno occlusive disease or GVHD
• family history –
Benign recurrent intrahepatic cholestasis (BRIC).
• Details –
Onset, duration,
Intermittent or progressive,
Associated symptoms like dark urine, acholic stools, arthralgia,
rash, wt loss, fever, chills, and pain in RHC.
12. Clinical History & cause of cholestasis
1. Pain - duct stones, tumor or gallbladder disease.
2. Arthralgia , myalgia predating jaundice -hepatitis (viral/drug related)
3. Fever and rigors- cholangitis d/t duct stone or traumatic stricture
(Charcot’s intermittent biliary fever). Or systemic infection
4. Contaminated foods, /alcohol consumption.
5. H/O hepato-toxins - Drugs /chemicals/ occupational
6. Parenteral exposures (Bl. Transfusions, drug abuse/ tattoos, sexual
activity)
7. H/o Ulcerative colitis - ? PSC
13. Physical Examination –
1) S/o chronic liver disease, temporal & proximal muscle weakness.
2) S/o Cholesterol deposition (Xanthomas, xanthelasmas) flat or slightly raised, yellow
and soft , usually around the eyes, in the Palmar creases, below the breast and on the neck, chest or back.
3) Anemia – GI blood loss, nutritional deficiency, hypersplenism
4) Itching marks, clubbing, and lymphadenopathy.
5) Virchow’s node or sister Mary Joseph's nodule- abdominal malignancy.
6) Jugular venous distension – hepatic congestion.
7) S/o Fat soluble vitamin deficiency –
1)
2)
3)
4)
Vit.D (osteomalacia, Demineralized bone, Kyphosis, Fractures),
Vit.E (cerebellar ataxia, posterior column dysfunction, peripheral neuropathy),
Vit.K(Puncture hematoma, Spontaneous bruising )
Vit.A(night blindness, thick skin)
8) S/O Hepatic Osteoarthropathy – loss of height, back pain, collapsed
vertebrae & fractures particularly of ribs with minimal trauma.
16. Abdominal Examination
1.
Hepatomegaly
Alcoholic liver disease, primary or secondary hepatic neoplasm,
infiltrative disease, and primary biliary cirrhosis.
2.
Enlarged tender liverViral ,alcoholic hepatitis, infiltrative process, or chronic passive
congestion of liver.
3.
Murphy’s Sign –
Cholecystitis, Ascending cholangitis
4.
Enlarged gallbladder –
Non- calculous biliary obstruction
5.
Hard & nodular hepatomegaly –
? metastatic malignancy.
6.
Other abdominal masses –
Primary ca stomach or colon.
17. • Ascites + Jaundice - Cirrhosis or malignancy with peritoneal spread.
• Rectal examination and sigmoidoscopy may indicate carcinoma.
• Marked splenomegaly- Cirrhosis + portal HTN or lymphoproliferative
disease
• Stools - loose, pale, bulky and offensive , sticky to the pan & non
flushable
-Our Case –
O/E –
Pallor +, icteric , B/L pedal edema.
1 x 1 cm firm lymph node in left
axilla.
P/A –
Tender hepatomegaly - 3 cm with
a smooth surface.
-Investigations –
Total bilirubin 10 mg% (D= 4.2).
ALP (1923 IU/L) & GGT 85 IU/L- raised.
AST and ALT normal.
Albumin of 2.4 gm%.
PT INR 1.7 corrected by Vit.K suppl.
Hb 10 gm/dl .Normal PBS
Urine positive for BS & BP
18. Laboratory work up
• CBC –
Anaemia - infection, blood loss or malignant disease.
PMN leucocytosis - cholangitis or underlying neoplasm.
• LFTs1.
2.
3.
4.
Alkaline Phosphate out of proportion to ALT/AST
Albumin linked Bilirubin (δ Fraction / biliprotein)
Low albumin - chronic process (cirrhosis/ cancer)
Normal Albumin - acute process ( viral
choledocholithiasis)
5. Elevated PT – Vit K Deficiency
• RFTs- Sepsis , HRS, malignancy .
hepatitis/
19. Enzymes raised in cholestasis
1) Alkaline Phosphatase (ALP), gamma-glutamyl
transpeptidase (GGT) & 5’-nucleotidase (5’NT).
2) ALP isoenzymes are also present in bone &
placenta.
3) Increase in ALP, GGT & 5’NT hepatobiliary
origin.
4) GGT levels – Fatty liver, alcoholic liver disease.
20. Proteins:
Albumin:
Decreased – advanced cirrhosis
& signify severe hepatic dysfunction.
Usually normal - acute hepatitis
Globulins:
Non-specific elevation – Chronic liver disease.
Disproportionate elevation
1) IgG in autoimmune hepatitis,
2) IgM in PBC &
3) IgA in alcoholic liver disease.
21. Prothrombin time (PT) & (INR)
An increasing INR/PT - hepatocellular dysfunction.
May be deranged in cholestasis,
1. But due to the malabsorption of Vit. K
Rapidly corrected by Parenteral administration of Vit K.
22. Other tests:
• Serological/ replicative markers –
specific diagnosis of acute or chronic viral hepatitis.
• Anti mitochondrial antibody (AMA) for PBC (90%)
• P-ANCA in PSC (65%)
• Antinuclear factor (ANA),
• Anti-smooth muscle antibody (ASMA) &
• Anti-liver kidney microsome (LKM) antibody
• Alpha- feto protein, which is raised in HCC &
• Other Malignancies – CEA, CA19.9, PSA
• S. Ceruloplasmin for Wilson disease.
seen in
autoimmune
hepatitis;
23. • Serum drug levels
• Urine dipstic test (Ictotest) Conjugated bilirubin +ve.
• X rays- changes of
osteomalacia
• Bone mineral density
by dual energy x-ray
absorptiometry (DEXA).
24. Imaging
RUQ Ultrasound
CT scan
ERCP
PTC
Endoscopic Ultrasound
Endoscopic CT
MR cholangiography
USG abdomen –
Normal size liver & echo pattern
With intrahepatic biliary radical
dilatation (IHBRD) in left lobe,
splenomegaly (18 cm),
Normal CBD and gallbladder.
Minimal free fluid.
No focal lesions
USG
Dilated bile
ducts
Non- dilated
bile ducts
? Intra hepatic
cholestasis
CT/MRCP/
ERCP/PTC
Serologic studies
AMA
Hepatitis serologies
Hep -A, CMV, EBV
Review drugs
Negative
MRCP/ liver biopsy
AMA
Positive
Liver Biopsy
25. Imaging
USG
Limitations
First-line imaging
Inexpensive
No ionizing radiation
GB stones readily
detected.
5. Absence of biliary
dilatation suggests
intrahepatic cholestasis &
oppositely extrahepatic
cholestasis
1) Distal CBD, bowel gas,
Obesity
2) False negative – Partial
obstruction,
cirrhosis,
scarring d/t PSC
3) Except mass lesion in the
head of the pancreas, USG
usually does not identify
the type of obstruction.
1.
2.
3.
4.
27. Our Case
Other tests –
1)
2)
3)
4)
5)
Viral serologies – Ve for HIV, HBV and HCV .
Blood culture sterile.
Sputum AFB , CXR - NAD.
Weil-felix, Paul-Bunnel and Brucella serologies negative.
Ascitic fluid - Transudative no cells & negative ADA.
Provisional diagnosisAlcoholic liver disease with ? Biliary malignancy
A contrast CT abdomen –
Multiple ill-defined nonenhancing lesions in the
liver, largest 1.4 cm x 1.0 x 1.0 cm rounded lesion (? necrotic lymph node)
at the porta hepatis with IHBRD seen above this level in left lobe. Multiple
small para-aortic, periportal and mesenteric lymph nodes present.
28. CT Scan
1) Localizes level of the
obstruction, in about
90% cases.
2) First choice in
lymphoma,
for retroperitoneal
lymph node
involvement
Gallbladder
Dilated bile
ducts
Mass in
head of
the
pancreas
Dilated bile ducts and gallbladder
29. When clinical suspicion is supported by CT or USG,
1) MRCP
Noninvasive screening ,rapid and comfortable.
Failed or incomplete conventional ERCP.
Variant biliary duct anatomy/ congenital duct abnormalities.
Post operative anatomy where ERCP would be difficult.
Evaluating changes of chronic pancreatitis or sclerosing cholangitis.
Distal CBD Stone
PSC
30. Direct cholangiography (PTC and ERCP)
Direct visualization
99% sensitivity & specificity.
Therapeutic interventions .
ERCP is the procedure of choice in suspected
ampullary or duodenal lesions in ca pancreas & when
gallstone
obstruction
is
suspected,
where
sphincterotomy & stone extraction can be
implemented.
34. Biliary stricture due to
cholangiocarcinoma
Alk phos = 669 IU Bili = 17.5 mg/dl
AST =
68 IU
ALT = 38 IU
Bile duct obstruction
from chronic pancreatitis
35. • PTC is preferred when obstructing lesion is high
• C/I- Marked ascites and coagulopathy.
• PTC and ERCP may be used together across a difficult
obstruction.
• Sometimes hepatobiliary scintigraphy, may help
evaluating biliary leaks & congenital malformations.
• Endoscopic CT & MRCP –
Biliary obstruction, specially
transplantation.
in
setting
of
in
liver
37. Liver Biopsy
Major indications –
Contraindications –
1)
2)
3)
4)
1) Bleeding tendencies,
chronic hepatitis,
cirrhosis,
Unexplained abnormal LFT,
hepatosplenomegaly of
unknown etiology,
5) suspected infiltrative /
Granulomatous disease
Complications
1) Minor – Prolonged RHC pain,
(6%).
2) Major - intra-abdominal
bleeding, mortality ( 0.01%).
2) INR>1.5 or PT >3 sec
above the control,
3) Severe thrombocytopenia
4) Marked ascites .
Transjugular liver biopsy
or no biopsy at all are
alternatives.
38. Cholestatic liver disease is broadly categorized as
extra-hepatic or intrahepatic.
Common
hepatic duct
Liver
Gallbladder
Intrahepatic
Perihilar
Distal
extrahepatic
Common
bile duct
Ampulla
Of Vater
Duodenum
39. CHOLEDOCHOLITHIASIS
• Mechanism of jaundice –
i. Impaction & edema of the common duct (Mirizzi syndrome)
ii. Direct inflammation of porta hepatis.
• CBD stones retained after cholecystectomy may produce jaundice
in the immediate postoperative period or even several years later .
• Pain (biliary colic or from acute pancreatitis).
• Rapid rise & rapid decline within 72 hours in aminotransferases .
• If Cholangitis in choledocholithiasis –
Fever with chills, abdominal pain, & jaundice. ( Charcot’s triad )
40. BENIGN STRICTURES OF THE BILE DUCTS
• In adults most common after surgery.
• PSC -multiple or diffuse strictures.
• Chronic alcoholic pancreatitis- a long stricture in the
intrapancreatic portion of the common duct.
• Ampullary stenosis - trauma during passage of a stone
& AIDS.
• Cholangitis - frequent in benign than in malignant one.
41. NEOPLASTIC OBSTRUCTION
• Pancreatic carcinoma commonest
• Other tumors Cholangiocarcinoma, ampullary
tumors, and carcinoma of GB
• Abdominal pain
• Loss of appetite and weight ,
• Progressive deep & painless
jaundice.
• Klatskin’s tumor
Macro cystic adenocarcinoma of
the pancreatic head.
42. • Tumors producing complete obstruction of CBD may be
accompanied by marked, palpable dilatation of the gallbladder
(Courvoisier’s law).
• Ampullary tumors produce intermittent jaundice because of
sloughing and partial relief of the block.
• Highest surgical cure of all tumors presenting as painless jaundice.
• Metastatic cancer may obstruct the bile duct, as may lymphoma.
• Hepatocellular carcinoma rupture into the biliary system throwing
tumor emboli obstructing common duct.
• Compression by adjacent tumor/ peribiliary lymph node
infiltrated by lymphoma, or metastatic ca breast.
• Direct infiltration by lymphoma.
43.
44. UNCOMMON CAUSES OF OBSTRUCTIVE JAUNDICE
• Choledochal cyst .
• Duodenal diverticulum
• Hemobilia, (biliary colic, jaundice & GI bleeding).
• Ascaris ,liver flukes (Fasciola, Clonorchis or Opisthorchis).
• Secondary sclerosing cholangitis
infections in immunodeficiency.
d/t
opportunistic
• Cryptosporidium parvum, cytomegalovirus (CMV), and
Microsporidia most frequently found.
46. Drug-induced cholestasis.
Direct hepato-toxic
Idiosyncratic
• Clinically mimic viral hepatitis or biliary tract disease.
• Serum-sickness-like features (rash , arthralgia,& eosinophilia)
• Only practical approach is to eliminate the drug and monitor.
Antimicrobial agents
Augmentin , cloxacillin,
erythromycin, ethambutol,
dapsone, fluconazole,
griseofulvin, ketoconazole
Cardiovascular agents
Disopyramide β-blockers,
ACE inhibitors, ticlopidine,
warfarin, methyldopa
Endocrine agents
Sulfonylureas, estrogens,
tamoxifen, androgens,
niacin, OCPs, anabolic
steroids
HAART-
Immunosuppressive agents –
Azathioprine, cyclosporine,
gold salts, NSAIDs
Psychopharmacologic
agents
Tricyclic
antidepressants, BZDs,
Phenothiazines,
Phenytoin, halothane
Zidovudine,
Protease Inhibitors
( Indinavir, Ritonavir)
47. Alcoholic hepatitis.
Marked tender hepatomegaly & e/o liver cell
failure .
Viral hepatitis.
Acute phase of viral hepatitis;
Most commonly hepatitis A, Hepatitis C, and
hepatitis E.
Though jaundice may be profound up to 6
months, complete recovery is the rule.
48. AIDS related cholangiopathy
• Cryptosporidium most frequent .
• Rarely
Microsporidia,
CMV,
Mycobacterium avium complex, and
Cyclospora
• Papillary stenosis if CD4 <100
• Elevated ALP (mean 800 IU/L).
• Jaundice unusual, If present, suggests
other disorders, like drug, alcohol
abuse or neoplasm
49. Primary biliary cirrhosis.
Autoimmune chronic non- suppurative cholangitis
AMA positivity in 95% & ANA 30% cases.
Progressive destruction of interlobular bile ducts(medium & small).
Elevated ALP, IgM, and cholesterol & later on bilirubin.
Predominantly middle aged female.
Fatigue, pruritus, hyper pigmentation, Xanthomas.
Majority have associated autoimmune disorders
(Sjögren’s syndrome, scleroderma, and arthritis).
Biopsy is diagnostic .
UDCA- only drug, prolongs survival & improves biochemical
abnormalities.
53. Idiopathic adulthood ductopenia.
Rare and defined by the presence of ductopenia (decrease of bile
ducts in >50% of the portal triads) and cholestasis in the absence of
known cholestatic liver disease. A diagnosis of exclusion.
Histology similar to primary biliary cirrhosis.
UDCA may result in biochemical improvement.
Autoimmune hepatitis.
Females (70%)
Anti LKM 1 , ANA and ASMA & hyper gammaglobulinemia in 80%.
Associated autoimmune disorders include arthritis, rash, thyroiditis,
Sjögren’s syndrome, and ulcerative colitis.
55. Decompensated chronic liver disease.
Jaundice may occur in chronic hepatitis or cirrhosis.
Other evidence of severe liver cell dysfunction is
present & jaundice is prognostically a grave sign.
Lymphoma.
3% and 10% cases of lymphoma develop jaundice .
Fatty liver.
Middle aged women with obesity, diabetes, and Hyper
lipidemia and a variety of other medical problems.
Cholestasis seen in about 5% cases.
56. Granulomatous hepatitis.
• Common cause of cholestatic liver disease.
• Sarcoidosis, infection (TB and fungal, esp. histoplasmosis),
hypersensitivity reaction, malignancies, IBDs, and as a feature of
other chronic liver disease.
• Pathologically,
Granulomas are nodular infiltrates consisting of aggregates of
epithelioid cells or macrophages with a rim of mononuclear cells/
Giant cells .
• Clinically, often asymptomatic, or Nonspecific symptoms .
• Routine bacterial & fungal blood culture, may be required.
• Benign course, with spontaneous recovery in most .
58. Sarcoidosis.
Systemic disease characterized by non- caseating
granuloma of multiple organs.
70% have hepatic granulomas. Portal granuloma result in
cholestasis & destruction of interlobular bile ducts.
Elevated alkaline phosphatase most characteristic
abnormality & reduced with corticosteroids.
Concomitant intrathoracic disease, pulmonary symptoms,
and significant anemia/ leucopenia.
59. Bacterial infection (sepsis)
• Most commonly gram-negative bacteria,
• also Staphylococcus aureus
streptococcal pneumonia.
in
TSS
&
• Rarely leptospira, clostridium & borrelia.
• Massive ductular dilatation & retained bile at
the interface of hepatic parenchyma & portal
tracts, (cholangitis lenta).
60. Total parental nutrition.
• When >60% calories as carbohydrates given > 3-4 weeks.
• Gallbladder stasis is almost universal & thereby gall stones.
• No oral feeding
that stimulate bile flow
Diminished release of hormones
Diminished bile flow
• Direct oxidant stress to the liver.
• If TPN cannot be discontinued, it should be cycled around
10 hrs/day. Keeping glucose <6 g/kg/day and lipid <2
g/kg/day.
• Recently UDCA is found helpful.
61. Benign recurrent intrahepatic cholestasis (BRIC).
• Characterized by...
Recurrent epi. of jaundice & pruritus,+ Symptom-free intervals.
Biochemical signs of cholestasis.
Histologically- canalicular stasis, normal bile ducts and absence of
inflammation and fibrosis.
• Sporadic or familial forms (chromosome 18)- Progressive familial
intrahepatic cholestasis (PFIC types 1-3) .
• GGT is normal with high alkaline phosphatase.
• Cholestatic episodes may last for many months.
• The episodes in BRIC eventually resolve without morphological
sequelae
62. Cholestasis of pregnancy.
Recurrently in 2nd & 3rd trimester of pregnancy &
resolves after delivery.
? inherited & Contraceptive drugs are a risk factor.
Biochemical cholestasis with pruritus, & jaundice.
Histologically similar to BRIC.
Increased risk of premature delivery or stillbirths.
UDCA has been used with success.
63. Sickle cell anemia.
Causes of jaundice –
Viral hepatitis,
Choledocholithiasis,
Hepatic sickle cell crisis
Hepatic sickle cell crisisSevere RUQ pain, fever,
leukocytosis, jaundice, tender
hepatomegaly, and moderate
elevation of alkaline
phosphatase.
Resolution followed by persistent
cholestatic jaundice for several
weeks
Postoperative jaundice.
• Prevalence - 17%
• Causes –
1.
2.
3.
4.
Sepsis,
Drugs or anesthetic-induced
hepatitis,
Obstruction from
pancreatitis,
choledocholithiasis,
Or direct injury to the biliary
tree.
• “Benign postoperative
cholestatic jaundice”
occurs between post op
day 1 to 10.
64. OTHER INTRAHEPATIC CAUSES OF
CHRONIC CHOLESTASIS
•
•
•
•
•
•
•
•
•
Nodular regenerative hyperplasia (NRH),
Bone marrow transplant (BMT),
Connective tissue diseases (CTD),
Felty’s syndrome,
Mastocytosis,
Hypereosinophilic syndrome,
Hyperthyroidism,
Space occupying lesions.
Para neoplastic syndromes of Hodgkin’s, Medullary thyroid
Ca, RCC, Renal sarcoma, T cell lymphoma, Prostate Ca, Many
GI malignancies.
• Stauffer’s Syndrome – Intrahepatic cholestasis in RCC
65. SUMMARY
EVALUATION OF CHOLESTASIS AND/OR JAUNDICE
1) Suspect cholestasis on history, physical exam, lab.
1) Look for clues to mechanical obstruction of ducts
and/or mass lesions (radiologic studies).
1) Visualize, diagnose and treat mechanical obstruction.
Consider intrahepatic cholestasis, obtain liver biopsy.
66. What happened to our patient…
Histopathology of lymph node - caseating granulomatous lymphadenitis.
Liver biopsy - consistent with tuberculosis, with periportal epitheloid
granulomas.
The patient was started on AKT.
He became afebrile on ATT with regression of jaundice and
constitutional symptoms.
After completing six months of AKT, complete resolution of jaundice.
Repeat ultrasound showed normal liver with no IHBRD or focal lesions.
67. Treatment of cholestatic jaundice …
Medical management:
Obstructive Jaundice :
• UDCA
Key Principle is Decompression
• DietMCT, Fat soluble vitamin
supplementations & calcium
• Pruritus –
Cholestyramine, antihistaminic, phenobarbitone
• Bone disease –
Vit.D, Bisphopshonates
1)
When cholangitis IVF, Antibiotics,
Decompression
2)
Stones Remove stones vs. stent vs
Drainage (ERCP /PTC/ surgery)
3)
Benign stricture Endoscopic dilatation/ stent vs
drainage catheter
4)
Cancer Stent vs drainage +/- resection