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.
Gallstones are small, pebble-like substances that develop in the
gallbladder. The gallbladder is a small, pear-shaped sac located below
your liver in the right upper abdomen. Gallstones form when liquid
stored in the gallbladder hardens into pieces of stone-like material.
The liquid—called bile—helps the body digest fats. Bile is made in the
liver, then stored in the gallbladder until the body needs it. The
gallbladder contracts and pushes the bile into a tube—called the common
bile duct—that carries it to the small intestine, where it helps with
digestion.
Bile contains water, cholesterol, fats, bile salts, proteins, and
bilirubin—a waste product.
Bile salts break up fat, and bilirubin gives bile and stool a
yellowish-brown color. If the liquid bile contains too much cholesterol,
bile salts, or bilirubin, it can harden into gallstones.
The two types of gallstones are cholesterol stones and pigment
stones. Cholesterol stones are usually yellow-green and are made
primarily of hardened cholesterol. They account for about 80 percent of
gallstones. Pigment stones are small, dark stones made of bilirubin.
Gallstones can be as small as a grain of sand or as large as a golf
ball. The gallbladder can develop just one large stone, hundreds of tiny
stones, or a combination of the two.
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.
Gallstones are small, pebble-like substances that develop in the
gallbladder. The gallbladder is a small, pear-shaped sac located below
your liver in the right upper abdomen. Gallstones form when liquid
stored in the gallbladder hardens into pieces of stone-like material.
The liquid—called bile—helps the body digest fats. Bile is made in the
liver, then stored in the gallbladder until the body needs it. The
gallbladder contracts and pushes the bile into a tube—called the common
bile duct—that carries it to the small intestine, where it helps with
digestion.
Bile contains water, cholesterol, fats, bile salts, proteins, and
bilirubin—a waste product.
Bile salts break up fat, and bilirubin gives bile and stool a
yellowish-brown color. If the liquid bile contains too much cholesterol,
bile salts, or bilirubin, it can harden into gallstones.
The two types of gallstones are cholesterol stones and pigment
stones. Cholesterol stones are usually yellow-green and are made
primarily of hardened cholesterol. They account for about 80 percent of
gallstones. Pigment stones are small, dark stones made of bilirubin.
Gallstones can be as small as a grain of sand or as large as a golf
ball. The gallbladder can develop just one large stone, hundreds of tiny
stones, or a combination of the two.
Bile or liver problem causing yellowness
• A yellow discoloration of the skin, mucous membranes, or sclera of the eyes, jaundice indicates excessive levels of conjugated or unconjugated bilirubin in the blood.
• In fair-skinned patients, it’s most noticeable on the face, trunk, and sclera; in dark-skinned patients, on the hard palate, sclera, and conjunctiva.
Students, digital devices and success - Andreas Schleicher - 27 May 2024..pptxEduSkills OECD
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Ethnobotany and Ethnopharmacology:
Ethnobotany in herbal drug evaluation,
Impact of Ethnobotany in traditional medicine,
New development in herbals,
Bio-prospecting tools for drug discovery,
Role of Ethnopharmacology in drug evaluation,
Reverse Pharmacology.
This is a presentation by Dada Robert in a Your Skill Boost masterclass organised by the Excellence Foundation for South Sudan (EFSS) on Saturday, the 25th and Sunday, the 26th of May 2024.
He discussed the concept of quality improvement, emphasizing its applicability to various aspects of life, including personal, project, and program improvements. He defined quality as doing the right thing at the right time in the right way to achieve the best possible results and discussed the concept of the "gap" between what we know and what we do, and how this gap represents the areas we need to improve. He explained the scientific approach to quality improvement, which involves systematic performance analysis, testing and learning, and implementing change ideas. He also highlighted the importance of client focus and a team approach to quality improvement.
We all have good and bad thoughts from time to time and situation to situation. We are bombarded daily with spiraling thoughts(both negative and positive) creating all-consuming feel , making us difficult to manage with associated suffering. Good thoughts are like our Mob Signal (Positive thought) amidst noise(negative thought) in the atmosphere. Negative thoughts like noise outweigh positive thoughts. These thoughts often create unwanted confusion, trouble, stress and frustration in our mind as well as chaos in our physical world. Negative thoughts are also known as “distorted thinking”.
2024.06.01 Introducing a competency framework for languag learning materials ...Sandy Millin
http://sandymillin.wordpress.com/iateflwebinar2024
Published classroom materials form the basis of syllabuses, drive teacher professional development, and have a potentially huge influence on learners, teachers and education systems. All teachers also create their own materials, whether a few sentences on a blackboard, a highly-structured fully-realised online course, or anything in between. Despite this, the knowledge and skills needed to create effective language learning materials are rarely part of teacher training, and are mostly learnt by trial and error.
Knowledge and skills frameworks, generally called competency frameworks, for ELT teachers, trainers and managers have existed for a few years now. However, until I created one for my MA dissertation, there wasn’t one drawing together what we need to know and do to be able to effectively produce language learning materials.
This webinar will introduce you to my framework, highlighting the key competencies I identified from my research. It will also show how anybody involved in language teaching (any language, not just English!), teacher training, managing schools or developing language learning materials can benefit from using the framework.
The Art Pastor's Guide to Sabbath | Steve ThomasonSteve Thomason
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3. • Jaundice, or icterus, is a yellowish discoloration
of tissue resulting from the deposition of
bilirubin.
• The presence of scleral icterus indicates a serum
bilirubin level of at least 51 μmol/L (3 mg/dL)
4. • Yellow discoloration of skin and sclera(icterus)
and body fluid
• It may arise due to
• 1)increase bile pigment load to liver
• 2)defective conjugation
• 3)defective excretion
5.
6. The differential diagnosis for yellowing
of the skin is limited
• carotenoderma
• quinacrine
• excessive exposure to phenols
• In jaundice the yellow coloration of the skin is
uniformly distributed over the body, whereas in
carotenoderma the pigment is concentrated on the
palms, soles, forehead, and nasolabial folds.
• Carotenoderma can be distinguished from jaundice
by the sparing of the sclerae.
• Quinacrine causes a yellow discoloration of the skin
in 4–37% of patients treated with
7.
8.
9.
10.
11.
12. Types of jaundice
Pre hepatic Hepatic Post hepatic
Excessive amount of
billirubin is presented to
liver due to excess
hemolysis
Impaired cellular
uptake,defective
conjugation or abnormal
secretion of billirubin by
liver cell
Impaired excretion due
to mechanical
obstruction to bile flow
Eleveted unconjugated
billirubin in serum
Both conjugated and
uncojjugated billirubin
may be increased in
serum
Eleveted conjugated
billirubin in serum
13. Diagnostic evaluation
• History and physical examination
• Use of medications,herbal medications,recreational
drugs
• Use of alcohol
• Hepatitis risk( travel,possible parental exposure)
• History of abdominal operation,including GB surgery
• HIV status
• Exposure to toxic substances
• Other important points exposure to people with
jaundice; exposure to possibly contaminated foods;
occupational exposure to hepatotoxins; the duration of
jaundice
14. Associated symtoms
• A history of fever,perticularly when associated
with chills or right upper quadrant pain/or
history of prior billiary surgery-acute cholangitis
• Anorexia,malaise and myalgias-viral hepatitis
• Right upper quadrant pain –extrahepatic biliary
obstruction
• Acholic stool(clay colored stool)-CBD
obstruction from cancer of pancreatic head or
the duodenal ampulla
15. Physical examination
• Courvoisier sign
• Signs of liver cell failure/portal hypertension-
ascites,splenomegaly,spider angiomata and
gynecomastia
• Hyperpigmentation:in hemochromatosis
• KS ring in wilson disease
• Xanthoma in primary billiary cholangitis
• Temporal and proximal muscle wasting suggests
long-standing disease such as pancreatic cancer
or cirrhosis
16. • An enlarged left supraclavicular node (Virchow’s
node) or a periumbilical nodule (Sister Mary
Joseph’s nodule) suggests an abdominal
malignancy.
• Severe right-upper-quadrant tenderness with
respiratory arrest on inspiration (Murphy’s sign)
suggests cholecystitis.
• Ascites in the presence of jaundice suggests
either cirrhosis or malignancy with peritoneal
spread.
17. Initial laboratory test
• Normal alkaline phosphates and
aminotransferases-
• Not likely due to hepatic or biliary tract disease
• hemolysis or inherited disorders of billirubin
metabolism may be responsible
18. Some normal values
• Total billirubin: 0.2 – 1.30 mg/dl
• Conjugated billirubin: 0.0-0.3 mg/dl
• Uncongugated billirubin: 0.0-1.10
• Alkaline phosphtase: 38-126u/l
• Serum SGPT: 9-52 u/l
19. • Predominant alkaline phosphatase elevation:
• Biliary obstruction or intrahepatic cholestasis
• Also found in granulomatous liver disease such
as tuberculosis and sarcoidosis this condition
may or may not be associated with jaundice
20.
21.
22. Pre dominant aminotransferase
elevation
• Jaundice is caused by intrincic hepatocellular
disease
• Alcoholic hepatitis disproportionate elevation of
the AST(SGOT) compared with ALT(SGPT)
• AST elevation is less than eight times of upper
limitation than normal and ALT elevation less
than five times the upper limit of normal
• AST ALT ratio is greater than 2
23. • Patients with acute viral hepatitis and toxin-
related injury severe enough to produce jaundice
typically have aminotransferase levels >500
U/L, with the ALT greater than or equal to the
AST.
• While ALT and AST values <8 times normal may
be seen in either hepatocellular or cholestatic
liver disease, values 25 times normal or higher
are seen primarily in acute hepatocellular
diseases
24. Elevated INR
• Elevated INR that corrects with vitamin K
administartion –impaired intestinal absorption
of fat soluble vitamin and compatible with
obstructive jaundice
• Does not correct with vit K suggest moderate to
severe hepatocellular disease with impaired
synthetic function
25. • A low albumin level suggests a chronic process
such as cirrhosis or cancer. A normal
• albumin level is suggestive of a more acute
process such as viral hepatitis or
choledocholithiasis
26. Signs and symptoms
• Early features
yellow discolouration ( skin,sclera)
pale/clay coloured stool
dark urine
pruitis
• Late features
-xanthelmas and xanthoma
-malabsorption-
weightloss,steatorrhea,osteomalacia,incresed
bleeding tendency
27. hepatocellular obstructive Hemolytic
Abdominal pain absent present Present in crisis
pruritus transient marked Abscent
Past history a.Contact with
jaundice patient
b.drugs
a.Pain
b.Weight loss
c,.surgery
a.Of crisis
b.drugs,blood
transfusion
Examination
Tenderl iver May be present absent Absent
spleen May be present absent Present
Gall bladder Not palpable Palpable if due to
neoplasum
Not palpable
pallor absent present Present
31. General concepts
Treatment depends on underlying cause
May involve removal of offending agent
Adminstration of antibiotic,antiviral,antifungle
or anti parasitic drug
Surgery to correct blockage
Use of chemotherapy,anti inflamatory
Dietary changes
Or combination of above
Activity should be limited
32.
33.
34.
35. Case study
• 1. 24 year male suffering from malaria was put
on primaquin. He developed malaise,fatigue and
yellow discoloration of sclera and skin
• Pallor present
• Icterus present
• Febrile
• Hepatosplenomegaly +
36. Lab investigation
• Hb:5%
• Tlc: 13000
• S.billirubin: 6mg%
• Ven den berg test positive
• Urine : hemoglobin +
• Color of urine brown black
• Probable diagnosis ??
37. Case 2
• 40 year/female presents with intolerance to fatty
foods,pain in right side of abdomen,yellowing of
eyes and passage of clay color stool
• Lab investigation
• Total billirubin:20%
• Direct billirubin:16%
• Alkaline phosphates: 800 U/L
• SGPT: 90 IU/l