Explanation of what splenomegaly is in relation to its dimension deviation from normal spleen.Classification of splenomegaly according to it's size in adult and pediatric. The causes of splenomegaly along with the symptom that would manifest as a result of this anomaly. Lastly, diagnosis of splenomegaly
Anemia Causes, Types, Symptoms, Diet, and Treatment Dr Medical
https://userupload.net/0gv9ijneu7hf
Anemia is a condition that develops when your blood lacks enough healthy red blood cells or hemoglobin. Hemoglobin is a main part of red blood cells and binds oxygen. If you have too few or abnormal red blood cells, or your hemoglobin is abnormal or low, the cells in your body will not get enough oxygen.
It is characterized by a yellow appearance of the (1) Skin (2) Mucous membranes and (3) Sclera caused by bilirubin deposition. It is the most specific clinical manifestation of Hepatic dysfunction.
Jaundice is usually present clinically when the plasma bilirubin concentration reaches 2 to 3 mg/dl.
When bilirubin clearance from the Liver to the Intestinal tract is impaired (as in acute hepatitis and bile duct obstruction) it may be accompanied by alcoholic (Gray coloured) stools.Solubility increases in water , soluble conjugated bilirubin leads to Tea coloured urine.
Explanation of what splenomegaly is in relation to its dimension deviation from normal spleen.Classification of splenomegaly according to it's size in adult and pediatric. The causes of splenomegaly along with the symptom that would manifest as a result of this anomaly. Lastly, diagnosis of splenomegaly
Anemia Causes, Types, Symptoms, Diet, and Treatment Dr Medical
https://userupload.net/0gv9ijneu7hf
Anemia is a condition that develops when your blood lacks enough healthy red blood cells or hemoglobin. Hemoglobin is a main part of red blood cells and binds oxygen. If you have too few or abnormal red blood cells, or your hemoglobin is abnormal or low, the cells in your body will not get enough oxygen.
It is characterized by a yellow appearance of the (1) Skin (2) Mucous membranes and (3) Sclera caused by bilirubin deposition. It is the most specific clinical manifestation of Hepatic dysfunction.
Jaundice is usually present clinically when the plasma bilirubin concentration reaches 2 to 3 mg/dl.
When bilirubin clearance from the Liver to the Intestinal tract is impaired (as in acute hepatitis and bile duct obstruction) it may be accompanied by alcoholic (Gray coloured) stools.Solubility increases in water , soluble conjugated bilirubin leads to Tea coloured urine.
Daily bilirubin production - 250-300mg%
85% heme moiety of aged RBC
5% RBC precursors destroyed in bone marrow ( ineffective
erythropoiesis),Catabolism of some heme proteins – myoglobin,
cytochrome, peroxidase
the following document contains various diagnostic test for screening liver function. and interpretation of results, which may confirm the presence of a disease or disorder
INTERPRETATION OF COMMON BIOCHEMICAL TESTS INCLUDING LFT & RFT.pptxDr Debasish Mohapatra
Biochemical tests are commonly used in day-to-day practices for diagnosis of diseases. Liver function test and renal function tests are common tests done.
Liver function tests and interpretation is a very important topic for students of medical and allied fields. It is essential for efficient practice of clinical and laboratory medicine.
Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
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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.
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
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.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
It’s work is regulated by androgens which are responsible for male sex characteristics
Generalised disease of the prostate due to hormonal derangement which leads to non malignant enlargement of the gland (increase in the number of epithelial cells and stromal tissue)to cause compression of the urethra leading to symptoms (LUTS
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.
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
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
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NYSORA Guideline
2 Case Reports of Gastric Ultrasound
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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
2. I T I S T H E Y E L L O W I S H D I S C O L O R A T I O N O F T H E
T I S S U E S D U E T O D E P O S I T I O N O F B I L I R U B I N
W H I C H O C C U R S I N P R E S E N C E O F
H Y P E R B I L I R U B I N E M I A
JAUNDICE
4. Clinically jaundice is evident when serum bilirubin
crosses 3 mg/DL
Jaundice is latent I.e., clinically non evident (only
detected by serum analysis) when serum bilirubin
is in between 1 - 3 mg/DL.
Unconjugated hyperbilirubinemia – when direct
bilirubin level is less than 15% of total serum
bilirubin.
Conjugated hyperbilirubinemia – when direct
bilirubin level is greater than 15%
5. Sites to be examined
Upper bulbar conjuctiva (contains elastin which
has hisj affinity for bilirubin)
Base of tongue
Mucous membrane of palate (specially soft palate)
Palms and soles
General skin surface
6. Differential diagnosis
Carotenoderma (discoloration is limited to palms,
sole, forehead, nasolabial fold with sparing of
sclera)
intake of drug quinacrine (only skin, urine and eyes
are yellow)
excessive exposure to phenols.
11. Hemolytic Jaundice/Pre hepatic Jaundice
Excess production of
bilirubin due to excess
breakdown of hemoglobin
Indirect bilirubin
(insoluble in water since
unconjugated).
12. Causes of pre hepatic jaundice
HEMOLYTIC DISORDERS
1. Inherited
a. Spherocytosis, elliptocytosis- Hereditary condition, with defect or
absence of RBC membrane protiens.
b. glucose 6 phosphate dehydrogenase- Most common cause of enzyme
deficiency hemolysis.
- autosomal recessive condition
triggered by certain certain food,
drugs, etc. Avoiding such triggers
is advised.
c. pyruvate kinase deficiency- second most common cause of enzyme
deficiency hemolysis.
b. sickle cell anemia- Abnormal haemoglobin synthesis leading to
sickeling under low oxygen condition. Incresed hemolysis.
13. 2. Acquired
a. Microangiopathic haemolytic anemias
b. Paroxysmal nocturnal hematuria.
c. Spur cell anemia.
d. Immune haemolysis.
e. Parasitic infections-
- Malaria- patient presents with fever chills rigor, hepatosplenomegaly
- Babesiosis
14. INEFFECTIVE ERYTHROPOIESIS
1. Cobalamin, Folate deficiency- Megaloblastic anemia
2. severe iron deficiencies- Microcytic hypochromic anemia
3. Thalassemia
• INCREASED BILIRUBIN PRODUCTION
1. Massive blood transfusion
2. Resorption of hematoma.
• DRUGS
1. Rifampicin, ribavirin, Probenecid.
15. Hepatic Jaundice
Liver’s ability to conjugate or
excrete bilirubin is affected
Increased level of conjugated
and unconjugated bilirubin
present
16. Causes of hepatic jaundice
VIRAL HEPATITIS
features HAV HBV HCV HDV HEV
transmission Feco-
oral
Parentral
,sexual,
perinatal
parentral Parentral,
sexual,
perinatal
Feco oral
Carrier none .1-30% 1.5-3.2% variable none
chronicity none occasional common common none
cancer none + + +- none
prognosis excellent Worsen with
age
moderate Acute-good
Chronic-poor
good
• Other viruses- Epstein barr, CMV, HSV
17. • ALCOHOLIC HEPATITIS- Balloon degeneration, fibrosis of
parenchymal tissue.
- 160g/day for 10-20yrs(women are more
susceptible)
• DRUG TOXICITY
1. Acetaminophen- Predictable, Dose dependent
2. Isoniazid- Unpredictable, Idiosyncratic.
• ENVIRONMENTAL TOXINS
- Vinyl chloride, Jamaica bush tea-pyrrolizidine
alkaloids , kava kava, Wild mushrooms.
18. WILSON’S DISEASE- hepato lenticular degeneration
due to copper accumulation in liver tissue.
AUTOIMMUNE HEPATITIS
INHERITED CONDITIONS-
Indirect hyperbilirubinemia
- Gilbert syndrome- Enzyme(UDP glucoronyl transferase) deficiency- 10-33%
activity only.
- Crigler-najjar syndrome type 1- Enzyme – absent
type2- enzyme activity- 0-10%
Direct hyperbilirubinemia
- Dubin Johnson syndrome- mutation in MRP2 gene. Defect in canalicular
transport of organic anions
- Rotor syndrome- defect in bilirubin storage.
19. Obstructive Jaundice
Bilirubin formation rate is
normal
Conjugation is normal =
direct bilirubin
Any intrahepatic or
extrahepatic condition leading
Obstruction to the flow of bile.
20. Causes of post hepatic / obstructive jaundice
INTRAHEPATIC CAUSES
1. Viral hepatitis-
a. Fibrosing cholestatic hepatitis- hep.B and C
b. hep A, Epstein barr, cytomegalovirus infection.
2. Alcoholic hepatitis
3. Drug Toxicity-
a. Pure cholestasis- anabolic and contraceptive steroids
b. Choleststic hepatitis- chlorpromazine, erythromycin estolate
c. Chronic cholestasis- prochlorperazine and chlorpromazine
26. Investigation
Depends on aetiology –that can be concluded by :-1.history, 2.C/F, 3.Clinical Ex.
Jaundice- cause by rise in blood plasma of bilirubin
Normal= <1 mg/dL---------- 1. Unconjugated/Indirect= 0.2-0.7 mg/dL
2.Conjugated/Direct =0.1-0.4 mg/dL
If bilirubin value is– 1. >1mg/dL, -Hyperbilirubinemia
2. >2-2.5mg/dL, -Start diffusing into tissues
3. ~3mg/dL, -Clinically jaundice detectable
The typical investigation will include blood levels of enzymes found primarily from the
liver, such as the aminotransferases (ALT, AST), and alkaline phosphatase (ALP);
bilirubin (which causes the jaundice); and protein levels, specifically, total protein and
albumin. Other primary lab tests for liver function include gamma glutamyl
transpeptidase (GGT) and prothrombin time (PT)
27. Pre-hepatic Jaundice
Cause- Mainly by haemolysis of RBC
Detoxification Function Test –
- Serum:- Increase unconjugated bilirubin
-Urine:- Bilirubin= Absent (unconjugated bilirubin is not water soluble)
-Urobilinogen= Increases (Increase in 6x function of Normal liver
to cope with load of unconjugated bilirubin)
Stool:- Fecal Urobilinogen increases
Rest of parameter usually remains normal.
28. Hepatocellular Jaundice
Detoxification Function Test:-
1. Serum bilirubin- conjugated and unconjugated both increased
2. Urine -Bilirubin – Present (Conjugated Bilirubin is water soluble)
Urobilinogen- decreased
3. Fecal stercobilinogen/Fecal Urobilinogen- decreased
Enzymatic test:-
1. AST,ALT – highly raised (due to lysis of liver parenchymatic cells)
2. ALP, GGT – is slightly raised
AST and ALT rise is significantly higher than the ALP and GGT rise
Plasma albumin level is low but plasma globulins are raised due to an increased
formation of antibodies
30. Post Hepatic/Obstructive Jaundice
Detoxification test
1. Serum bilirubin – Direct(conjugated)– increased
2. Urine – Bilirubin- Present
- Urobilinogen – absent
3. fecal stercobilinogen- trace to absent
Enzymatic Test
1. AST,ALT – Slightly increase
2. ALP, GGT- Highly Incresed
If the ALP (10–45 IU/L) and GGT (18–85) levels rise
proportionately about as high as the AST (12–38 IU/L) and
ALT (10–45 IU/L) levels, this indicates a cholestatic
problem
32. Radiological Investigation
Plain radiographs -are of limited utility as Frequently,
calculi are not visualized because few are radiopaque.
Ultrasonography (USG)- most sensitive technique for
visualizing the biliary system, particularly the gallbladder.
Procedure of choice for the initial evaluation of cholestasis
and for helping differentiate extrahepatic from
intrahepatic causes of jaundice
CT Scan -helps visualize liver structures more consistently
than USG. CT scan has limited value in helping diagnose
CBD stones because many of them are radiolucent and CT
scan can only image calcified stones ( in such situation CT
cholangiography by the helical CT technique is used)
33. Radiological Investigation-Continue
MRI- MRCP (Magnetic resonance cholangiopancreatography)
type is used to visualize the hepatobiliary tree.
It helps in detecting biliary and pancreatic duct stones, strictures,
or dilatations within the biliary system. It is also sensitive for
helping detect cancer. MRCP combined with conventional MR
imaging of the abdomen can also provide information about the
surrounding structures (eg, pseudocysts, masses).
Biopsy
• Usually done at last in series of investigation to establish the cause of
Jaundice.
• In patients with apparent intrahepatic cholestasis, the diagnosis is often
made by serologic testing in combination with percutaneous liver biopsy.
• to assess the condition of the liver tissue if it may have been damaged by a
condition such as cirrhosis or liver cancer.
37. Treatment of pre hepatic causes
• G6PD deficiency - mostly people recover on their own
o if progresses to hemolytic anaemia, oxygen therapy or
blood transfusion may be required.
• Spherocytosis
o These infants should be treated with phototherapy
and/or exchange transfusion as clinically indicated.
o Folic acid is required to sustain erythropoiesis.
o Patients with HS are instructed to take supplementary
folic acid for life in order to prevent a megaloblastic
crisis.
o Splenectomy is the definitive treatment for HS
38. • Sickle cell anaemia
o Treatments may include medications to reduce pain and
prevent complications, blood transfusions and supplemental
oxygen, as well as a bone marrow transplant.
o Antibiotics -Children with sickle cell anemia may begin taking
the antibiotic penicillin when they're about 2 months of age and
continue taking it until they're at least 5 years old.
• Immune related hemolysis – corticosteroids, folic acid is
main line of treatment
• Parasitic Infections like malaria are treated with
antimalarial drugs like chloroquine, artesunate,
lumefantrine,amodiaquine
• Ineffective erythropoiesis- iron and folic acid
supplementation, vit B12 tablets given and repeated blood
transfusions
39. Treatment of hepatic causes
• Viral hepatitis
Hepatitis A is mostly self limiting no treatment is
required, but in some cases 0.02 ml/kg administration
of anti-HAV Ig can be given.
Hepatitis B treated with combination of HBIG and Hep
b vaccines.
Recombivax and Engerix-B are 2 vaccines for
hepatitis B
Hepatitis C is treated with interferons.
• Other Viral infections like EBV, CMV, HSV are treated
with Antiviral medications like acyclovir , ganciclovir
and foscarnet.
41. Discriminant function - determines the prognosis of the person suffering from
alcoholic liver disease. Given by Maddrey.
It is calculated by a simple formula:
(4.6 x (PT test - control))+ S.Bilirubin in mg/dl
A value more than 32 implies poor outcome.
MELD – model for end stage liver disease
scoring system for assessing the severity of chronic liver disease
MELD uses the patient's values for serum bilirubin, serum creatinine, and the
international normalized ratio for prothrombin time (INR) to predict survival.
42. • Wilsons disease- pharmacologic
treatment with chelating agents such as
D-penicillamine and Other agents
include sodium dimercaptosuccinate,
dimercaptosuccinic acid
44. SUPPORTIVE MANAGEMENT
Preoperative biliary decompression (ERCP or PTC)
Intravenous admistration of 5% dextrose saline followed by 10%mannitol
or loop diuretics to prevent hepatorenal syndrome/ renal failure(12 to 24
hours prior to surgery)
catheterization to monitor output
Broad spectrum antibiotic prophylaxis with 3rd generation cephalosporins
Parenteral vitamin K +/- fresh frozen plasma
Need careful fluid balance to correct dehydration
Correction of hypokalemia and other electrolyte imbalance.
Cholestyramine and antihistamine for symptomatic relief of pruritis
44
45. Definitive treatment depends upon the
cause-
• Choledocholithiasis- cholecystectomy is done
• Carcinoma of head of pancreas- whipple resection
done
• Ca gall bladder- whipple resection done but if
unoperable radiological stenting is done.
• Choledochal cyst- excision of the cyst with
reconstruction of extrahepatic biliary tree.
• Stricture- endoscopic stenting. Standard care is
surgery by roux-en-y choledocojejunostomy.