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An-Najah National University

Faculty of Medicine and Health Sciences

Presented to complement the requirements


of the "clinical Practice " course

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VIRAL HEPATITIS

• Prepared by: Shama Amoudi

• Submitted to: Dr. Bayan Asem

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 OUTLINE:
 Definition of acute coronary syndrome
 Risk factors for ACS
 Presenting sign and symptoms with ACS
 Diagnosis of ACS
 Treatment of ACS
 Case report
 Recent updates

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Hepatitis
virus
infection

Chronic Acute
hepatitis hepatitis

Infection for Infection for


more than 6 less than 6
months months
HAV

 Enveloped RNA virus


 B. 24,900 new cases annually in the U.S.
 C. Person-to-person transmission
 1. Fecal-oral route
 2. Contaminated food or water
 D. Incubation period: 15-50 days (Average = 28 days)
 E. Symptoms usually last less than 2 months (but can last as long as 6
months)
 1. Abdominal pain, jaundice, pale stools, dark urine, loss of appetite
 2. Considered an acute and not chronic infection
 a. Chronic hepatitis is defined as inflammation of the liver lasting >6 months
 3. Much more severe in adults vs. children
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 F. Also can be transmitted through sex or IV drug use
Acute Coronary
Syndrome

ST-segment non-ST segment


elevation elevation acute
myocardial coronary
infarction syndromes
(STEMI) (NSTE-ACS)

non-ST segment
Unstable Angina elevation
myocardial
(UA) infarction
(NSTEMI)

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Risk factors for hepatitis A virus
Anti-HAV Total antibody (IgG + IgM)
Present or past infection
Immunity due to vaccination
Anti-HAV IgM Current, recent, or acute infection
Anti-HAV IgG Immunity to HAV from past infection or
vaccination

Total hepatitis A antibody is not useful for acute infection diagnosis


B. Diagnosis is established by the detection of serum IgM hepatitis A antibodies—
indicates whether
there is current, recent, or acute infection
1. This will be detectable at the onset of symptoms and peak during early/convalescent
phase of
the disease (remains detectable for 3-6 months)
C. IgG antibodies appear early in convalescent phase of disease and remain detectable
for decades,
which reflects lifelong protective immunity (will always remain positive if patient was
vaccinated or
previously exposed to it)
Management2
A. Self-limiting disease
B. Avoidance of acetaminophen
C. Supportive care
1. Antiemetics
2. Fluids to replete volume loss from vomiting and diarrhea
D. Fluid replacement is the most important thing to address
and to avoid anything that can be harmful
to the liver
Prevention2
A. Improved sanitary conditions
B. Safe access to water
C. Ensuring that appropriate food safety procedures are
followed
D. Vaccination is going to be the most beneficial prevention
technique
1. 2 doses given at least 6 months apart
E. Immune globulin – if exposure has occurred and no
vaccination has been given
1. Single dose
Who should be immunized against HAV3
A. All children ≥1 year of age
B. Persons with travel to areas with intermediate to high rates
of infection
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C. Men who have sex with men (MSM)


D. Illegal and injection drug users
E. Homeless
F. Persons with clotting-factor disorders
G. Persons working with HAV-infected primates or with HAV in a
research laboratory
H. Persons with chronic liver disease, including HBV- and HCV-
infected
I. Persons exposed as result of an outbreak
J. Persons who require post-exposure prophylaxis
Administration considerations5 (protective antibodies usually
develop in ~ 95% of adults after first
dose)
A. Inactivated vaccine
B. Hepatitis A vaccines considered interchangeable
C. Safe in pregnancy
D. Intramuscular (IM) injection in deltoid muscle
E. If the second dose is delayed, series does not need to be
restarted
Corticosteroid use is not recommended.
Family history: 1st
Risk Factors : Age: degree relative
men > 45 years with coronary
Smoking event before 55
women > 55
years years (men) or 65
years (women)

Hypertension Diabetes Dyslipidemia

Excessive
Chronic angina Lack of exercise
alcohol

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Presenting symptoms
:
 Chest pain (described as discomfort and pressure) lasting more than 10 minutes

 Severe dyspnea, diaphoresis, syncope and/or palpitations.

 The pain can radiate to the arms, back, neck, jaw or epigastric region.

Females, the elderly and diabetic patients are less likely to experience the classic
symptoms.

Symptoms can occur at rest, or may be precipitated by minimal exercise, cold weather,
stress or sexual intercourse.

The chest pain or discomfort is not improved or is worse five minutes after sublingual
nitroglycerin (NTG) dose every five minutes for up to three doses.

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Diagnosis:

 A 12-lead ECG should be performed and evaluated within ten minutes at


the site of first medical contact (which could be in an ambulance).

 Biochemical markers (cardiac enzymes )help establish the diagnosis.


Cardiac troponins I and T (Tnl and TnT} are the most sensitive and specific
biomarkers for ACS. They are detectable in the blood within 2 – 12 hours,
and for up to 5 - 14 days, after myocardial necrosis.

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 Levels should be obtained at presentation and 3 - 6 hours after symptom onset
in all patients with ACS symptoms. Creatine kinase myocardial isoenzyme (CK-
MB} and myoglobin are less sensitive markers but may still be monitored in
clinical practice.

UA NSTEMI
SYMPTOMS Chest pain

CARDIC ENZYMES Negative Positive

ECG changes None or transient ischemic changes – T-wave inversion


– ST depression
blockage Partial blockage

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Treatment

Medications
PCI
alone

 PCI is a coronary revascularization procedure that involves inflating a small


balloon inside a coronary artery to widen it and improve blood flow.
Usually, metal mesh, called a stent, is placed into the artery afterward to
keep the artery open.
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Initiate pharmacotherapy treatment for non st segment elevation based on patient risk :

TIMI Score:

 0-2 low risk

 3-4 intermediate risk

 5-7 high risk

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Low risk TIMI Score:

 Negative stress test : diagnosis of noncardic chest pain syndrome

 Positive stress test : coronary angiography with revascularization ( PCI OR


CABG )

Medium or high risk TIMI


Score:
 Coronary angiography with revascularization ( PCI OR CABG )

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 Lifestyle counseling should include:
- smoking cessation
- managing chronic conditions (such as HTN, DM)
- avoiding excessive alcohol intake
- encouraging physical exercise and a healthy diet.

 Regardless of the management strategy selected, acute treatment is


aimed at providing immediate relief of ischemia and preventing MI
expansion and death.

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Inhibits platelet aggregation/ clot
formation by inhibiting production of
thromboxane A2 (TXA2) via
irreversible COX1 and COX2
inhibition.

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All P2Yl2 inhibitors :

 Most drug interactions are due to additive effects with other drugs that can
increase bleeding risk. EX. NSAIDs, warfarin, SSRis and SNRis increase the
bleeding risk

 If an ACS patient experiences bleeding while on a P2Yl2 inhibitor, it should be


managed without discontinuing the P2Yl2 inhibitor, if possible.

 Stopping the P2Yl2 inhibitor (particularly within the first few months after
ACS) increase the risk of subsequent cardiovascular events.

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All P2Yl2 inhibitors :

■ Clopidogrel: avoid in combination with esomeprazole and omeprazole due

to the risk of decreased antiplatelet effect

■ Clopidogrel increases the effects of repaglinide, which can cause

hypoglycemia.

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Medications to Avoid in the
Acute Setting :

■ NSAIDs (except aspirin), whether nonselective or COX-2-selective,


should not be administered during hospitalization due to increase risk
of mortality, reinfarction, hypertension, cardiac rupture, renal
insufficiency and heart failure.

■ Immediate-release nifedipine should not be used due to increase risk


of mortality.

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Recent Updates :

1. Trimetazidine is effective in the treatment of stable angina compared with

placebo, alone or combined with conventional anti-anginal agents. Trimetazidine

may result in fewer dropouts due to adverse events. Large, long term trials

comparing trimetazidine with other anti-anginal drugs assessing clinically

relevant important outcomes are required to establish its role in clinical


https://pubmed.ncbi.nlm.nih.gov/28319269/
management.

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2. P2Y12 Inhibitor Monotherapy Combined With Colchicine Following PCI in ACS

Patients

- In ACS patients undergoing PCI, it is feasible to discontinue aspirin therapy and

administer low-dose colchicine on the day after PCI in addition to ticagrelor or

prasugrel P2Y12 inhibitors. This approach is associated with favorable platelet

function and inflammatory profiles. (Mono Antiplatelet and Colchicine Therapy


https://pubmed.ncbi.nlm.nih.gov/37587591/
[MACT]

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3. Elevated levels of plasma sLOX-1concentrations might be used as a clinical

biomarker for early recognition of NSTEMI and STEMI patients. Multicenter larger

scale studies are necessary before use in clinical practice.

https://pubmed.ncbi.nlm.nih.gov/36910399/

4. Invasive management was associated with lower risks of myocardial infarction,

MACE, and revascularization in older patients with NSTEMI, yet it may increase

the risk of major bleeding in patients aged ≥85 years.

https://pubmed.ncbi.nlm.nih.gov/37255135/

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5. The COMPASS (Cardiovascular Outcomes for People Using

Anticoagulation Strategies) trial decreased major adverse

cardiovascular events with very low-dose rivaroxaban and aspirin in

patients with coronary artery disease and peripheral artery disease.

https://pubmed.ncbi.nlm.nih.gov/36515238/

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References :

Naplex 2022 book

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