Part 1

A 25-year-old junior nurse presents to a physician with a 2-3-week history of fatigue, loss of
appetite, and right upper quadrant discomfort. During the past week, she has noticed yellow
discoloration of her eyes. She was previously healthy and has no chronic medical problems.
She enjoys alcoholic drinks when meeting up with friends. Three months ago, she suffered a
needle-stick injury while attending to a trauma patient. She did not seek medical care
immediately due to the patient’s critical condition but suspected that the patient might be an IV
drug user

Discussion

1. What differential diagnoses should be considered for a young adult presenting with
fatigue, loss of appetite, and right upper quadrant discomfort?
1. Hepatitis
2. Jaundice
3. HIV

2. What are the risk factors/ causes/ factors leads to needle stick injury?

- Maybe Lack of Coordination (overlooked)

- Prevention? -> never recap ur needle
- Complications
- Transmission of diseases
- Blood Borne Disease (HIV, HBV, HCV)
- Bacterial Infections
- Management
- Report and then Blood Test.

3. What are the potential implications of yellow discoloration of the eyes in the absence of other
chronic medical problems?

- Jaundice
- Hepatitis
- Gallstones
- Tumores
- Genetics - Gilbert’s Syndrome
- Alcoholic Drinks
- G6PD

4.How might social habits, such as alcohol consumption, contribute to her symptoms?

5. History Taking (which Questions)

 Family History

Vaccinations

Past Medical history

Medications

6. Physical Examinations

- GI examinations (look for tenderness)

- Edema

7. Lab Examinations

- LFTs (albumin, ALP, ALT)

Part 2

On physical examination, she has jaundice, right upper quadrant tenderness and hepatomegaly

(liver span of 16 cm). She has no stigmata of a chronic liver disease.

Difficult Words

- Stigmata = scar, pain, wound (stigmata of chronic liver disease, which includes spider
nevi, palmar erythema, gynecomastia, caput medusae, Dupuytren contractures, parotid
gland enlargement, and testicular atrophy).
-

1. Acute Vs Chronic Liver Diseases

2. What type of Hepatitis is this Patient having?
3. Lab Results.
4. Stigmata of Chronic Liver DIsease?
5. How to rule out Hepatitis B and C?
a. Hepatitis B - Mom to Baby, more stable outside body
b. Hepatitis C - Needles, More likely to cause acute symptoms, less stable (cannot
survive long outside body).
INR: The international normalised ratio (INR) blood test tells you how long it takes for your blood
to clot.

AST, ALT, ALP?

Antibodies Indicators

Vaccinations

Diagn

osis- Hepatitis C

Urine Bilirubin and Urobilinogen (+) → ?

Different Types of Jaundice?

Learning outcomes:

1. ANATOMY OF LIVER (brief!) (Pyae)

a. Microscopic / gross findings
2. FUNCTION AND PHYSIOLOGY OF LIVER (ishka,joyce, max)
a. Bilirubin and Metabolism of Bilirubin
b. Liver function test
i. Significance
ii. Interpretation
iii. Importance
3. Jaundice (Azlina)
a. Pathophysiology
b. Classification
4. Hepatitis C [ yuxuan (a,b,c,d), pinhui (e,f,g,h) ]
a. Etiology/ risk factors
b. Epidemiology
c. Pathogenesis
d. Signs and Symptoms
e. Complication
f. Diagnosis
i. Physical examination
ii. Lab Results interpretation
g. Treatment
h. Management & Prevention
5. Needle Stick Injury ( basyirah and sw)
a. Standard Protocol and Management
b. Epidemiology
c. Psychological aspects
Learning Outcomes

6. ANATOMY OF LIVER (brief!) (Pyae)

a. Microscopic / gross findings
b. Blood supply
 Hepatic Portal Vein - 70% of liver blood supply

Hepatic Artery - 30% of liver blood supply

c. Lymphatic drainage
i. Periportal lymphatic vessels: surround the portal triads and
hepatic lobules. They collect lymph fluid from the periportal space,
which is the area between the hepatocytes (liver cells) and the
sinusoids (capillaries).
ii. Sublobular lymphatic vessels: Located along the hepatic veins,
these vessels drain lymph from the central and sublobular regions
of the liver lobule.
 d. Capsular lymphatic vessels: lie on the surface of the liver, beneath the
Glisson's capsule (connective tissue capsule surrounding the liver).
They drain lymph from the capsule itself and the upper zones of the liver
lobules.

Lymph Nodes

Doesn’t have a lymph node itself..Drains into nearby lymph nodes.

● Right and left hepatic lymph nodes
● Celiac lymph nodes
● Gastric lymph nodes
● Superior mesenteric lymph nodes
● Splenic lymph nodes

7.
LO2

The liver is a vital organ located in the upper right-hand portion of the abdominal cavity.
It performs over 500 essential functions, including the regulation of chemical levels in
the blood and the excretion of bile, which helps carry away waste products1. The liver
processes blood from the stomach and intestines, breaking down nutrients and
metabolizing drugs into forms that are easier for the body to use or that are

non-toxic1.

Bilirubin Metabolism: Bilirubin is a yellow bile pigment produced through the breakdown
of red blood cells in a process known as hemolysis. The metabolism of bilirubin
involves several steps:
 1. Creation of Bilirubin: Reticuloendothelial cells (macrophages) in the blood take
up red blood cells and metabolize the hemoglobin into its components—heme
and globin. Heme is then broken down into iron and biliverdin, which is
subsequently reduced to create unconjugated bilirubin2.
2. Bilirubin Conjugation: Unconjugated bilirubin travels in the bloodstream bound to
3. albumin to the liver. In the liver, it is conjugated with glucuronic acid by the
enzyme glucuronyl transferase, forming water-soluble conjugated bilirubin2.
4. Bilirubin Excretion: Conjugated bilirubin is excreted into the duodenum in bile. In
the colon, bacteria deconjugate bilirubin and convert it into urobilinogen. Most
urobilinogen is further oxidized to stercobilin and excreted through feces, giving
them their color. A small portion is reabsorbed into the bloodstream and excreted
in the urine as urobilin2.
Jaundice can occur if there is an accumulation of bilirubin, leading to a yellow
discoloration of the skin and eyes. This can be due to various reasons, including
increased hemolysis or issues with liver function affecting bilirubin processing2.

https://www.hopkinsmedicine.org/health/conditions-and-diseases/liver-anatomy-and-functions
https://teachmephysiology.com/gastrointestinal-system/liver/bilirubin-metabolism/

Function and Physiology of the Liver: The liver, the largest internal organ, plays a crucial
role in numerous bodily functions. It is responsible for:

● Metabolism: The liver metabolizes carbohydrates, proteins, and lipids to maintain

homeostasis. It converts excess glucose into glycogen for storage and releases
it back into the bloodstream when needed.
● Detoxification: It detoxifies various metabolites, synthesizes proteins, and
produces biochemicals necessary for digestion.
● Bile Production: Bile, essential for the digestion of fats, is produced by the liver
and stored in the gallbladder.
● Synthesis of Blood Proteins: It produces albumin (the main protein of blood
plasma), clotting factors, and other vital proteins1.
● Storage of Vitamins and Minerals: The liver stores vitamins A, D, E, K, and B12,
and the minerals iron and copper.
● Blood Filtration: It filters and clears the blood of drugs and other harmful
substances.
● Immune Function: The liver is part of the immune system; it contains Kupffer
cells that digest pathogens and old blood cells.
Types of Liver Function Tests:
 ● Alanine transaminase (ALT): An enzyme found mainly in the liver. High levels
may indicate liver damage.
● Aspartate aminotransferase (AST): An enzyme found in the liver and other
tissues. Elevated AST levels can also suggest liver damage.
● Alkaline phosphatase (ALP): An enzyme related to the bile ducts; high levels can
indicate bile duct problems.
● Gamma-glutamyl transferase (GGT): An enzyme that, when elevated, can
indicate bile duct damage or alcohol abuse.
● Total bilirubin: Measures the amount of bilirubin in the blood. High levels can
lead to jaundice and suggest liver dysfunction.
● Albumin: The main protein made by the liver. Low levels can indicate chronic liver
disease.
● Total protein: This test measures the total amount of protein in the blood and can
help diagnose liver disease.
● Lactate dehydrogenase (LDH): An enzyme that, when elevated, can suggest liver
damage.
● Prothrombin time (PT): Measures how long it takes blood to clot. Prolonged PT
can indicate liver disease.
Purpose of Liver Function Tests: LFTs are used to:

● Screen for liver infections, such as hepatitis.

● Monitor the progression of a disease, such as cirrhosis.
● Monitor how well a treatment is working.
● Check the severity of liver damage.
● Monitor side effects of certain medications.
Results Interpretation:

● Normal Results: Indicate a well-functioning liver.

● Abnormal Results: Can suggest a variety of issues, such as liver inflammation,
damage, infection, or bile flow blockages.
Follow-Up: Abnormal results typically lead to further testing to pinpoint the exact cause
of the liver issue. This may include imaging tests like an ultrasound or CT scan, and
sometimes a liver biopsy.
Importance of Liver Function Tests: LFTs are crucial in the early detection and
management of liver disease. They help in:

● Diagnosing liver conditions early, which can lead to better outcomes.

● Guiding treatment decisions and monitoring their effectiveness.
● Adjusting medications that may be causing liver-related side effects.
LO3: Jaundice

What is Jaundice?

· It is not a disease, but it is a clinical presentation characterised by yellow discoloration of skin, sclera
and mucous membrane

Why this happens?

· Due to increased levels of bilirubin in the blood

· Billirubin a yellow-orange pigment derived from the breakdown of heme, which is released during the
destruction of red blood cells.

Pathophysiology

Under normal circumstances, bilirubin undergoes conjugation within the liver, making

it water-soluble. It is then excreted via the bile into the GI tract, the majority of which

is egested in the faeces as urobilinogen and stercobilin (the metabolic breakdown

product of urobilingoen). Around 10% of urobilinogen is reabsorbed into the

bloodstream and excreted through the kidneys. Jaundice occurs when this pathway

is disrupted, when there is an elevation of serum bilirubin. This can be caused by

prehepatic, intrahepatic, or post hepatic defects.

The types of jaundice

1. Prehepatic Jaundice (Haemolytic Jaundice):

 ○ Pathophysiology: Prehepatic jaundice occurs due to an increased breakdown of red
blood cells (hemolysis), leading to an excess production of unconjugated bilirubin. The
rate of bilirubin production exceeds the liver's capacity to conjugate and excrete it.
○ Causes: Conditions that cause hemolysis of red blood cells, such as hemolytic anemias
(sickle cell anemia, thalassemia), transfusion reactions, certain infections (malaria), and
hereditary disorders affecting red blood cell metabolism, result in prehepatic jaundice.
2. Hepatocellular Jaundice:
○ Pathophysiology: Hepatocellular jaundice results from liver cell damage or dysfunction,
impairing the liver's ability to process bilirubin. Damage to hepatocytes disrupts bilirubin
uptake, conjugation, or excretion processes.
○ Causes: Hepatocellular jaundice can be caused by various liver diseases and conditions,
including viral hepatitis (hepatitis A, B, C), alcoholic liver disease, drug-induced liver
injury (medications, toxins, alcohol), cirrhosis, fatty liver disease (non-alcoholic
steatohepatitis), and liver tumors.
3. Posthepatic Jaundice (Obstructive Jaundice):
○ Pathophysiology: Posthepatic jaundice occurs when there is a blockage in the bile
ducts, hindering the flow of bile and bilirubin from the liver into the intestines. This leads
to a buildup of conjugated bilirubin in the bloodstream.
○ Causes: Obstruction of the bile ducts can be caused by gallstones (cholelithiasis)
blocking the common bile duct, tumors (pancreatic cancer, bile duct cancer), bile duct
strictures (inflammation, scarring), congenital abnormalities of the biliary tract, and
parasitic infections (liver flukes).
4. Neonatal Jaundice:
○ Pathophysiology: Neonatal jaundice in newborns occurs due to an imbalance between
bilirubin production and elimination. Newborns have an increased rate of red blood cell
breakdown, coupled with immature liver function, leading to elevated bilirubin levels.
○ Causes: Neonatal jaundice can result from physiological factors such as immature liver
function, breastfeeding jaundice (inadequate milk intake), breast milk jaundice
(substances in breast milk inhibiting bilirubin elimination), blood group incompatibilities
(Rh or ABO incompatibility), and certain underlying medical conditions affecting bilirubin
metabolism.
LO4: Hepatitis C
Hepatitis C is an infection caused by the hepatitis C virus (HCV), which attacks liver cells and
causes liver inflammation. HCV is a bloodborne pathogen commonly transmitted through
needlestick injuries in health care settings or through shared drug-injection needles.
Screening plays a central role in detecting HCV infection because most infected individuals are
asymptomatic or mildly symptomatic. Approximately 85% of individuals with an acute infection
that is not recognized and treated will develop chronic hepatitis C, which is associated with
cirrhosis, hepatocellular carcinoma, and increased mortality. The presence of HCV antibodies
and HCV RNA confirm the diagnosis. HCV infection can be safely and effectively treated with
direct-acting antivirals (DAAs), which have cure rates of over 95%. Simplified algorithms for the
use of DAAs in treatment-naive patients without decompensated cirrhosis reduce the need for
specialist-guided care.

Aetiology of Hepatitis C
Hepatitis C infection is caused by the hepatitis C virus (HCV).

You can catch hepatitis C if the blood of someone who has HCV
enters your body. Exposure may occur:

● After a needlestick or sharps injury

● If blood from someone who has HCV contacts a cut
on your skin or contacts your eyes or mouth
● While injecting street drugs

People at risk for HCV are those who:

● Inject street drugs or share a needle with someone who has HCV
● Have been on long-term kidney dialysis
● Have regular contact with blood at work (such as a health care worker)
● Have unprotected sexual contact with a person who has HCV
● Were born to a mother who had HCV
● Received a tattoo or acupuncture with needles that were not disinfected properly after
being used on another person (risk is very low with practitioners who have a tattoo
license or permit or an acupuncture license)
● Received an organ transplant from a donor who has HCV
● Share personal items, such as toothbrushes and razors, with someone who has HCV
(less common)
● Received a blood transfusion (rare in the United States since blood screening became
available in 1992)
Epidemiology of Hepatitis C

The hepatitis C virus (HCV) has a significant global impact, with 58 million people chronically
infected and about 1.5 million new infections occurring per year.2 There remains considerable
global variation within these figures. In high-income countries, the prevalence is generally below
2%, with people who inject drugs (PWID) being disproportionately affected, while countries with
low-middle incomes have the highest prevalence (see Table 1). WHO also estimated that in
2019 approximately 290,000 people died from hepatitis C, mostly from cirrhosis and
hepatocellular carcinoma.2

​ Table 1. Countries with the highest prevalence of hepatitis C globally, and

comparison with the UK prevalence
Egypt: 4.4–15%
​ Gabon: 4.9–11.2%
​ Uzbekistan: 11.3%
​ Cameroon: 4.9–13.8%
​ Mongolia 9.6–10.8%
​ Pakistan: 6.8%
​ Nigeria: 3.1–8.4%
​ Georgia: 6.7%
​ (UK: 0.4%)

In England in 2020, around 81,000 people were living with chronic HCV infection.1 However,
this represents a significant reduction from earlier years, thanks to the introduction of very
effective treatments, which will be explored further in part 2 of this series. For example, by 2020,
the prevalence of HCV in England had fallen by 37% compared to the 2015 baseline (see
Figure 1) and HCV mortality decreased by 35%.1
Figure 1
Estimated prevalence of chronic hepatitis C virus (HCV) infection in England, 2010–2020 (with
95% credible intervals)1

Early diagnosis of HCV infection is essential for the most effective treatment and care. However,
from a global perspective, only 19% (13.1 million) of people living with hepatitis C know their
status. In England in 2020, 40.4% of PWID surveyed were aware of their HCV antibody-positive
status,1 but this does not necessarily link successfully to treatment services.

In malaysia:
We organized a cross-sectional study at the end of 2020 across Malaysia. We used a two-stage
stratified random sampling technique to select representative community dwelling individuals
aged ≥15 years. The optimum size sample required was 5000 based on the single proportion
sample size formula, adjusted for design effect and non-response. We obtained written
consents and assent (if ≤ 18 years) and conducted face-to-face interviews to collect
sociodemographic characteristics and HCV status. We collected blood samples and extracted
serum to test for HCV antibodies. A positive sample (denotes HCV infection) would be tested
further for HCV core antigen. Positive results on both tests denote chronic infection.4 We used
SPSS v26 to perform descriptive analysis and apply weights in complex sampling analysis to
obtain representative prevalence and their 95% Confidence Interval (CI)
Out of 5957 eligible individuals, test results were available for 4076 (response rate 68.4%).
Their mean age was 41.2 ± 17.3 years. The weighted prevalence of HCV infection in Malaysia
was 0.4% (95% CI 0.2–0.7) amounting to an estimated 90,119 infected “population age ≥15
years. More than half of them (≈51,675) are chronically infected with a prevalence of 0.2% (95%
CI 0.1 -- 0.4).

https://www.thelancet.com/journals/lanwpc/article/PIIS2666-6065(23)00120-7/fulltext#:~:text=Th
e%20weighted%20prevalence%20of%20HCV,population%20age%20%E2%89%A515%20year
s.

Pathogenesis of Acute Hepatitis C Infection

In

1. Viral Entry: Hepatitis C virus (HCV) enters hepatocytes via attachment and fusion to
the cell membrane.

2. Replication: Inside the hepatocytes, HCV RNA genome is released. Virus begins to
replicate using the host cell machinery.

3. Immune Response: Immune system recognizes the presence of the virus → initiates an
immune response. CD4+ and CD8+ T cells, as well as B cells are to control the infection.
 4. Inflammation: The immune response results in inflammation of the liver, which can
cause liver damage and dysfunction.

5. Resolution or Chronic Infection:

Two possible scenarios:
a. Immune system is able to clear the virus, and the infection resolves within 6
months, OR
b. virus persists and leads to chronic hepatitis C infection, which can cause cirrhosis
and hepatocellular carcinoma over time

Clinical Features of Acute Hepatitis C Infection

1. Fatigue & malaise General feelings of tiredness, weakness and
lack of energy

2. Loss of appetite Decreased appetite and weight loss

3. Nausea & vomiting

4. Abdominal pain Pain @ RUQ may occur due to inflammation

of liver

5. Jaundice Yellowing of the skin and sclera

6. Dark urine Urine may appear dark or brown

7. Clay-colored stools Stools may appear pale or clay-colored

*people with acute hepatitis C may experience joint pain, fever, and itching
Complications
Approximately 85% of individuals with an acute infection that is not recognized and treated will
develop chronic hepatitis C, which is associated with cirrhosis, hepatocellular carcinoma,
and increased mortality.

a. Cirrhosis and cirrhosis-related sequelae (ie, esophageal varices)

■ 10% to 20% of patients with hepatitis C will develop cirrhosis
b. Hepatic failure
■ Develops in 3% to 6% of patients with chronic hepatitis C and cirrhosis
per year
c. Hepatocellular cancer
■ Incidence of 1% to 5% per year among patients with chronic hepatitis C
and cirrhosis
■ Successful treatment with direct-acting antivirals is associated with a 70%
reduction in risk of hepatocellular carcinoma; however, ongoing
surveillance is still required for patients with cirrhosis
d. Extrahepatic complications
■ Cryoglobulinemia occurs in up to 35% of hepatitis C cases and may be
associated with vasculitis and glomerulonephritis
■ Increased risk for non-Hodgkin lymphoma
■ Increased risk for type 2 diabetes mellitus
​
Diagnosis
● Physical examination
● Lab Results interpretation

Clinical Presentation

History
● Most people with hepatitis C are asymptomatic
● Acute hepatitis C symptoms, present in a minority of patients, subside after a few
weeks. These are usually nonspecific and include the following:
○ Fever
○ Fatigue, malaise, or weakness
○ Anorexia
○ Nausea or vomiting
○ Abdominal pain
○ Arthralgia or myalgia
● Manifestations of excess bilirubin occur in a small percentage of patients with
hepatitis C, and they suggest a diagnosis of hepatitis. The manifestations are:
○ Dark or concentrated urine
○ Clay-colored bowel movements
○ Jaundice
○ Pruritus
● Chronic hepatitis C is largely asymptomatic; symptoms associated with cirrhosis may
appear after years of silent infection
○ Abdominal distention
○ Peripheral edema
○ Bleeding or bruising easily

Physical examination
● Acute hepatitis C
○ Fever
○ Scleral icterus
○ Jaundice
○ Right upper quadrant tenderness
○ Palpable liver edge
● Chronic hepatitis C is undetectable by examination until there are signs of cirrhosis,
which are as follows:
○ Cachexia
○ Scleral icterus
○ Jaundice
○ Gynecomastia
○ Large, firm, nodular liver
 ○ Ascites
○ Peripheral edema
○ Ecchymoses
○ Spider angiomata

Hepatitis C lab tests

● Anti-HCV antibodies (EIA/ELISA immunoassay): initial test for immunocompetent
individuals who are HCV naïve
● HCV RNA (qualitative PCR)
○ If anti-HCV antibody test is positive
○ Alternatively, as the initial test in patients with the following
■ Prior HCV infection
■ Immunocompromised

Interpretation of hepatitis C tests

Additional evaluations

Laboratory studies
● Viral load determination: quantitative PCR for HCV RNA
● Routine studies
○ CBC, BMP (Basic metabolic panel)
○ Hepatocellular enzymes
■ Normal or ↑ transaminases (10–20 × ULN)
 ● Transaminases: Enzymes involved in amino acid metabolism,
e.g., alanine aminotransferase (ALT) and aspartate
aminotransferase (AST), which are used clinically as parameters
of hepatocellular injury.
■ Fluctuating ALT peaks indicate acute HCV infection
● (ALT) Alanine aminotransferase: An enzyme involved in amino
acid metabolism that catalyzes the transfer of an alpha-amino
group between glutamate and alanine. Primarily found in
hepatocytes; thus, serum concentrations are used to monitor for
hepatocellular damage.
○ Cholestasis parameters (The laboratory values that indicate that bile cannot flow
from the liver to the duodenum)
■ ↑ GGT
● Gamma-glutamyl transferase: A membrane-bound enzyme of
glutathione metabolism and amino acid transport. The most
sensitive parameter for diseases of the liver and/or biliary tract.
However, it is not very specific, as it is found in many tissues.
■ ↑ Alkaline phosphatase
● A group of enzymes found throughout the body but produced
predominantly in the liver, bones, placenta, and small intestine.
Common causes of elevated serum ALP include cholestasis, bone
disease (e.g., bone metastases, Paget's disease,
hyperparathyroidism), and pregnancy. The normal reference range
is 20–70 U/L.
■ ↑ Bilirubin
● A hemoglobin breakdown product and parameter of cholestasis.
Serum total bilirubin consists of unconjugated bilirubin and
conjugated bilirubin.
○ Liver synthetic function tests (alterations suggest cirrhosis)
■ ↓ Albumin
● A protein whose functions include maintenance of colloid osmotic
pressure and transportation of enzymes and degradation
products. Produced exclusively by the liver and comprises the
majority of total plasma proteins (~60%). Levels decrease with
decreased hepatic synthesis, urinary protein loss, and
malnutrition.
■ ↓ Total protein
■ ↑ PT/INR
● PT (prothrombin time): An assay that evaluates the extrinsic and
common pathways of the coagulation cascade (measures activity
of factors I, II, V, VII, and X). Used to evaluate coagulation
 disorders and to monitor the effect of warfarin. Normal range is
11–15 seconds.
● INR: The ratio of an individual's prothrombin time (PT) relative to
the PT of a control sample. Common causes of elevation include
vitamin K deficiency and warfarin therapy. Used to monitor the
effectiveness of the latter.
● Evaluation of coinfection
○ HIV testing
○ Hepatitis B serology
○ Hepatitis A serology
● Serum pregnancy test (if applicable): ideally performed directly before initiating treatment

Liver biopsy
● Consider when:
○ Etiology of hepatitis is unknown
○ Accurate liver fibrosis staging would alter treatment

Treatment
Not all hepatitis infected individuals require therapy.

General principles
● The goal of treatment is sustained virologic response (SVR).
○ SVR: The absence of hepatitis C virus RNA after 12 weeks of therapy with
direct-acting antivirals. A patient in this state is considered to be cured of
hepatitis C virus infection.
● Refer patients with end-stage liver disease for liver transplantation evaluation.

Antiviral therapy
HCV infection is always treated with a multidrug approach (no antivirals are approved as
monotherapy).
● Direct-acting antivirals (DAAs)
○ Antivirals target and inhibit HCV-encoded proteins that are essential for the
HCV replication cycle.
○ Example regimens
■ Glecaprevir PLUS pibrentasvir (all 6 genotypes)
■ Sofosbuvir PLUS velpatasvir (all 6 genotypes)
■ Ledipasvir PLUS sofosbuvir (genotypes 1, 4, 5, and 6)
■ (genotypes refer to the different strains of HCV)
 ● Interferon PLUS ribavirin
○ Was the preferred treatment before the development of DAAs
○ Associated with severe adverse effects (e.g., arthralgias, thrombocytopenia,
leukopenia, depression, anemia) and teratogenicity
○ Contraindicated in patients with decompensated cirrhosis (high risk of worsening
cirrhosis decompensation)

DAAs have superior efficacy and safety profiles compared with interferon or ribavirin-based
regimens and are thus preferred.
Acute and chronic HCV are treated with the same antiviral regimens.

Supportive care/ management

● All individuals with HCV
○ Avoid hepatotoxic drugs (e.g., acetaminophen) and alcohol use.
○ Counsel about HIV and hepatitis B prevention.
○ Counsel regarding adherence, reinfection prevention, and medication risks.
● Hepatitis A and B seronegative individuals: Offer hepatitis A vaccination and/or
hepatitis B vaccination.
● People who inject drugs
○ Counsel on harm reduction strategies.
○ Refer for treatment of substance use disorder.
Monitor for complications of HCV infection in individuals who decline antiviral treatment or do
not achieve SVR.

Prevention
● Currently, no effective vaccine or postexposure prophylaxis exists
● Public programs encourage safe needle disposal and discourage needle sharing
among people who inject drugs
● Avoidance of high-risk behaviors
○ Safe sexual practices, including use of barrier contraception, are imperative to
reduce transmission by sexual contact for patients with multiple sexual partners if
either partner is HIV positive or at risk for other sexually transmitted infections
○ Advise patients that transmission of hepatitis C occurs through contact with
blood, and therefore, they should avoid sharing razor blades, toothbrushes,
or nail clippers
○ Transmission between long-term monogamous but HCV-discordant couples is
uncommon
● Universal precautions by health care workers
● Sterilization of medical equipment
 ● Avoidance of breastfeeding by hepatitis C–infected adults with cracked or bleeding
nipples

Screening tests
● HCV-antibody testing with reflex HCV-RNA polymerase chain reaction testing is the
initial screening test
○ Quantitative HCV-RNA testing is performed for a positive anti-HCV test result;
document the baseline viremia before antiviral treatment
● Patients exposed to hepatitis C virus within the 6 months preceding a negative
HCV-antibody test are recommended to have HCV-RNA or repeat HCV-antibody testing
after 6 months or more have elapsed
● Health care workers with occupational exposure
○ Determine hepatitis C status of source patient; no further testing is required if
source patient is HCV negative
○ If source patient is positive for HCV or status is unknown, obtain baseline
anti-HCV antibody test within 48 hours of exposure
○ If baseline anti-HCV test result is negative, test for HCV-RNA 4 weeks after
exposure or test for anti-HCV 4 to 6 months after exposure
● Perinatally exposed children
○ Antibody-based testing is recommended at or after age 18 months; testing earlier
may detect maternal antibody
● Testing with an HCV-RNA assay can be considered as early as age 2 months

,8. Needle Stick Injury

a. Standard Protocol and Management

b. Epidemiology
i. NSIs are common among healthcare workers worldwide, occurring in
various healthcare settings.
ii. The risk of becoming infected with a blood-borne virus after NSI is highest
for hepatitis B, followed by hepatitis C, and then HIV. For every 1,000
NSIs from an infected patient, 300 HCWs will become infected with HBV
iii. Underreporting of NSIs is widespread globally due to
1. fear of repercussions
2. lack of awareness about reporting procedures
3. perceptions of NSIs as a routine hazard.
iv. Risk Factors
1. inadequate training
2. lack of access to safety devices
3. high patient volume
4. long working hours
5. understaffing
6. inadequate safety culture
7. workplace distractions.
v. Prevention Strategies
1. implementing safer work practices
2. providing comprehensive training on sharps safety
3. promoting the use of safety-engineered devices (e.g., retractable
needles, needleless systems)
4. ensuring access to personal protective equipment
5. establishing protocols for reporting and managing NSIs
6. fostering a culture of safety in healthcare settings
 c. Psychological aspects

​ -Fear and Anxiety

​ Needle stick injuries often provoke immediate fear and anxiety, particularly due to
concerns about potential exposure to infectious diseases such as HIV, hepatitis B, and
hepatitis C. The uncertainty surrounding the health implications can lead to heightened
stress levels.]
​
​ -Guilt and Shame
​ Individuals who experience needle stick injuries may feel guilty or ashamed, especially if
they believe the incident was preventable or if they perceive themselves as having made
a mistake that led to the injury.
​
​ -Stigma and Social Isolation
​ Some individuals may face stigma or social isolation following a needle stick injury,
particularly in healthcare or other occupational settings. Fear of judgment or
discrimination from colleagues or supervisors can exacerbate feelings of shame and
isolation.
​
​ -Post-Traumatic Stress Symptoms
​ In some cases, needle stick injuries can lead to symptoms associated with
post-traumatic stress disorder (PTSD), such as intrusive thoughts, nightmares, and
hyperarousal. This can occur particularly if the individual perceives the event as
traumatic or if they have a history of trauma.
​
​ -Depression and Mood Disturbances
​ Needle stick injuries can trigger or exacerbate symptoms of depression and other mood
disturbances. The uncertainty about health outcomes, along with the potential disruption
to work or personal life, can contribute to feelings of sadness, hopelessness, and
irritability.
​
​ -Coping Mechanisms
​ Individuals may adopt various coping mechanisms to deal with the psychological impact
of needle stick injuries. This can include seeking social support from friends, family, or
colleagues, engaging in relaxation techniques or mindfulness practices, or seeking
professional mental health support.
​
​ -Risk Perception
​ Needle stick injuries can alter an individual's perception of risk, particularly in healthcare
settings. They may become hypervigilant about safety protocols and procedures, or they
may develop heightened anxiety or avoidance behaviors related to certain tasks or
procedures.
​
​ -Work-related Stress
​ For healthcare workers, needle stick injuries can contribute to overall work-related
stress. Concerns about health outcomes, potential repercussions from supervisors, and
the need to undergo testing and follow-up procedures can all add to the stress of an
already demanding job.
​
​ -Long-term Effects
​ Even after the physical wounds of a needle stick injury have healed, individuals may
continue to experience psychological effects, including anxiety or fear related to future
needle-related procedures or situations.