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Hepatitis
Hepatitis = inflammation of the liver
Causes of Hepatitis
Hepatitis can be caused by:
Infectious agents
Viruses
Bacteria
Fungi
Drugs/medications
Alcohol
Food intoxication → example: poisonous mushrooms
Obesity
Autoimmune diseases
Viral Hepatitis
Almost any virus can potentially cause liver inflammation, but usually the virus causes other symptoms/clinical manifestations too.
There are 5 viruses that specifically target the liver:
Hepatitis A, B, C, D, and E
HAV = Hepatitis A
HBV = Hepatitis B
HCV = Hepatitis C
HDV = Hepatitis D
HEV = Hepatitis E
Easy way to remember:
Hepatitis = inflamed liver
A → B → C → D → E = the major hepatitis viruses that target the liver.
Acute hepatitis
Acute hepatitis = sudden liver damage/inflammation that develops over days to weeks.
1. Incubation Period
Usually 2–12 weeks
The virus is present, but symptoms may not appear yet.
2. Preicteric Stage (~1 week)
Preicteric = before jaundice
Symptoms are usually nonspecific, meaning they can look like many other illnesses:
Fever
Nausea/vomiting
Myalgia → muscle/body aches
Headache
Fatigue
Pain in the upper right abdomen
Liver enlargement (hepatomegaly)
3. Icteric Stage
Icteric = jaundice develops
Jaundice → yellow skin and eyes
Choluria → dark urine
Acholia → pale/white-colored stool
Duration can vary.
4. Convalescence Stage
Convalescence = recovery
Symptoms gradually improve.
Duration varies depending on the person and type of hepatitis.
Easy sequence to remember:
Incubation → Preicteric → Icteric → Convalescence
Think:
Nothing → Sick → Yellow → Recover
Important:
Preicteric = before jaundice
Icteric = jaundice
Bilirubin metabolism
Bilirubin comes from the breakdown of old RBCs.
1. RBC breakdown
Old RBCs are broken down by macrophages.
This produces heme.
Heme → unconjugated bilirubin
Unconjugated bilirubin = NOT water-soluble
2. Liver processes bilirubin
Unconjugated bilirubin travels to the liver.
Liver cells (hepatocytes) add glucuronic acid.
This is called conjugation.
Unconjugated → conjugated bilirubin
Conjugated bilirubin = water-soluble
3. Bilirubin leaves the body
Conjugated bilirubin is released into bile.
Bile carries it to the intestine.
Gut bacteria convert it to urobilinogen.
From there:
Most urobilinogen → stercobilin → feces
Small amount → kidneys → urine
Super simple pathway
Old RBC → Heme → Unconjugated bilirubin → Liver → Conjugated bilirubin → Bile → Intestine → Urobilinogen
Mostly → feces
Small amount → urine
What you REALLY need to know
Unconjugated = before the liver = not water-soluble
Conjugated = after the liver = water-soluble
This becomes important when you learn why hepatitis can cause jaundice, dark urine, and pale stools.
Acute hepatitis: Laboratory
Acute hepatitis → liver cells are damaged → liver enzymes increase in the blood.
1. Increased liver enzymes
Blood tests may show increased:
ALT (alanine transaminase)
AST (aspartate transaminase)
Alkaline phosphatase (ALP)
Lactate dehydrogenase (LDH)
These increases indicate liver injury/damage.
2. Increased bilirubin
If the liver isn't working properly:
Direct (conjugated) bilirubin ↑
Indirect (unconjugated) bilirubin ↑
Increased bilirubin can lead to jaundice (yellow skin/eyes).
3. Urine findings
Urine may contain urobilinogen, a metabolite produced during bilirubin breakdown.
Easy way to remember:
Hepatitis = liver damage →
Liver enzymes ↑
ALT + AST + ALP + LDH
Bilirubin ↑
Direct + Indirect
Urine → urobilinogen
Big picture:
Damaged liver → enzymes leak into blood + bilirubin builds up → jaundice.
Fulminating hepatitis
Fulminant hepatitis = massive, rapid destruction of liver tissue → severe liver dysfunction.
What happens?
1. Liver can't clear toxins
A damaged liver cannot properly remove toxins from the blood.
Toxins build up → acute encephalopathy (brain dysfunction)
Possible symptoms:
Asterixis → “flapping” movement of the hands
Confusion
Disorientation
Agitation
Coma in severe cases
2. Coagulopathy
The damaged liver cannot make enough clotting factors.
Blood takes longer to clot → increased bleeding
Can lead to:
Prolonged coagulation time
Bleeding
Disseminated intravascular coagulation (DIC)
Easy way to remember:
Fulminant hepatitis = Liver destruction → 2 major problems
Toxins → brain problems
confusion → coma
Less clotting factors → bleeding problems
coagulopathy → DIC
BIG IDEA: The liver is failing rapidly and severely, affecting both the brain 🧠 and blood clotting.
Fulminating hepatitis: Laboratory
Fulminant hepatitis = massive liver destruction → severe liver dysfunction.
1. Liver enzymes increase
There is a major increase in:
ALT
AST
Alkaline phosphatase (ALP)
Lactate dehydrogenase (LDH)
Important: In very late stages, these enzyme levels may drop.
Why? A severe drop does not necessarily mean the liver is recovering—there may be fewer functioning liver cells left to release enzymes.
2. Bilirubin increases
Because the liver is not functioning properly:
Direct (conjugated) bilirubin ↑
Indirect (unconjugated) bilirubin ↑
Can cause jaundice.
3. Coagulopathy
The damaged liver cannot make enough clotting factors.
Prothrombin time (PT) ↑ → blood takes longer to clot
Increased risk of bleeding
4. Thrombocytopenia
Platelet count ↓
Further increases the risk of bleeding
Easy way to remember:
Fulminant hepatitis =
Enzymes ↑
Bilirubin ↑
PT ↑
Platelets ↓
Most important:
Late-stage enzyme drop ≠ improvement. It can indicate massive liver cell destruction.
Chronic hepatitis
Chronic hepatitis = long-term inflammation/damage of the liver lasting months to years.
Important points
Can occur with or without a previous episode of acute hepatitis.
Causes ongoing liver damage and inflammation.
Can lead to poor liver function.
Complications
1. Cirrhosis
Long-term liver damage → scarring of the liver
Scarring can interfere with normal liver function.
2. Hepatocarcinoma
Chronic infection + inflammation can increase the risk of liver cancer.
Late-stage chronic hepatitis
Ascites → buildup of fluid in the abdomen
Hepatic encephalopathy → brain dysfunction caused by liver failure/toxin buildup
Can start mildly and become more severe.
Easy way to remember:
Chronic hepatitis = months/years → ongoing damage → complications
Chronic inflammation → Cirrhosis → Liver cancer
Late stage:
Ascites + Encephalopathy
Acute vs. Chronic:
Acute | Chronic |
|---|---|
Days–weeks | Months–years |
Sudden liver damage | Long-term liver damage |
Can recover | Can progress to cirrhosis |
— | Increased risk of liver cancer |
— | Ascites + encephalopathy in late stages |
Chronic hepatitis: Laboratory
Chronic hepatitis → long-term liver damage → abnormal liver tests.
1. Liver enzymes increase
ALT ↑
AST ↑
Alkaline phosphatase ↑
LDH ↑
The increase is usually lower than in acute hepatitis because the damage is occurring more slowly over a long period.
2. Signs of poor liver function
Bilirubin ↑
Direct (conjugated) bilirubin ↑
Indirect (unconjugated) bilirubin ↑
Can contribute to jaundice.
Albumin ↓
The liver normally makes albumin.
Damaged liver → less albumin production → low blood albumin.
Coagulopathy
Liver makes many clotting factors.
Liver damage → fewer clotting factors → increased bleeding risk.
3. Urine
Urine may contain urobilinogen, a metabolite of bilirubin.
Easy way to remember:
Chronic hepatitis =
ALT, AST, ALP, LDH ↑ (but lower than acute)
Bilirubin ↑
Albumin ↓
Coagulopathy
Urobilinogen in urine
Key difference from acute hepatitis
Acute: enzymes can become very high because of sudden liver cell injury.
Chronic: enzymes are persistently elevated but usually lower, while signs of poor liver function become more important.
Hepatitis A - HAV
Definition: Hepatitis A is an RNA virus and a common cause of acute hepatitis.
1. Characteristics
RNA virus
Incubation period: about 4 weeks
Causes acute hepatitis
Does NOT become chronic
Rarely causes fulminant/fulminating hepatitis (severe liver failure)
2. Transmission
Fecal–oral route
Usually spread through contaminated:
Food
Water
Hands
3. Treatment
No specific antiviral treatment
Usually treated with supportive care while the body clears the infection.
4. Prevention
Vaccine-preventable
Easy way to remember:
Hepatitis A = Acute + fecal-oral + no chronic infection + vaccine
Feature | Hepatitis A |
|---|---|
Virus | RNA |
Incubation | ~4 weeks |
Transmission | Fecal-oral |
Chronic? | No |
Fulminant hepatitis | Rare |
Specific treatment | No |
Vaccine | Yes |
Hepatitis B - HBV
Definition: Hepatitis B is a DNA virus that can cause acute or chronic liver infection.
1. Characteristics
DNA virus
Can cause:
Acute hepatitis → may look similar to Hepatitis A
Asymptomatic acute infection → person may have no symptoms
About 10–15% of adults develop chronic hepatitis
2. Transmission
HBV is transmitted through:
Blood
Sexual contact
3. Chronic Infection
If chronic HBV is untreated for years or decades, it can lead to:
Cirrhosis → permanent liver scarring
Liver cancer (hepatocellular carcinoma)
Important: Chronic HBV is a major risk for cirrhosis + liver cancer.
4. Prevention & Treatment
Vaccine: highly effective
Specific treatment: available to control chronic infection
A complete cure can be difficult
Easy way to remember:
Hepatitis B = Blood + Sex + DNA + Chronic risk
Feature | Hepatitis B |
|---|---|
Virus | DNA |
Transmission | Blood + sexual |
Acute infection | Yes |
Chronic infection | ~10–15% of adults |
Cirrhosis | Can occur |
Liver cancer | Can occur |
Vaccine | Highly effective |
Treatment | Controls infection, cure is difficult |
Hepatitis B: Diagnosis
HBV diagnosis is based on blood tests that detect viral antigens and antibodies.
1. HBsAg — Hepatitis B surface antigen
Appears early after infection
Means HBV is currently present
If it stays positive for a long time → suggests chronic infection
2. Anti-HBc
There are two types:
IgM anti-HBc
Appears during recent/acute infection
Helps indicate a new infection
IgG anti-HBc
Appears later
Can remain for life
Shows the person has been infected with HBV at some point
3. Anti-HBs
Appears after the person clears the virus
Indicates immunity
Can also appear after vaccination
4. HBV DNA
PCR can detect HBV DNA
Used to detect/measure the amount of virus in the blood.
Easy way to remember
HBsAg = virus is present
IgM anti-HBc = recent infection
IgG anti-HBc = past/current infection
Anti-HBs = immunity
HBV DNA = viral genetic material
Big exam point: Anti-HBs = immunity, while HBsAg = active infection.
Hepatitis C - HCV
Definition: Hepatitis C is an RNA virus that is mainly spread through blood and has a high chance of becoming chronic.
1. Characteristics
RNA virus
Discovered in the late 1980s
Acute hepatitis can occur, but it is usually mild
Up to 80% of infections become chronic
2. Transmission
Mainly bloodborne
Sexual transmission is rare
Common in:
People who received blood products before the 1990s
People who inject drugs
3. Chronic Hepatitis C
Chronic HCV can eventually cause:
Cirrhosis → liver scarring
Liver cancer
Important: HCV has a very high risk of becoming chronic compared with Hepatitis A or B.
4. Diagnosis
Step 1: Anti-HCV antibody test
Used as a screening test
Positive = the person has been exposed to HCV
It does NOT prove the virus is still present because antibodies can remain even after the person clears the infection.
Step 2: PCR-HCV
Confirms whether HCV is currently present
Detects HCV RNA
5. Treatment
New, highly effective specific antiviral drugs have been developed.
Most cases respond well to treatment.
Easy way to remember:
Hepatitis C = Blood + Chronic + PCR + Curable
Feature | Hepatitis C |
|---|---|
Virus | RNA |
Main transmission | Blood |
Sexual transmission | Rare |
Acute infection | Usually mild |
Chronic infection | Up to 80% ⚠ |
Cirrhosis | Can occur |
Liver cancer | Can occur |
Screening | Anti-HCV |
Confirmation | PCR-HCV |
Treatment | Highly effective |
Hepatitis D (Delta) - HDV
Definition: Hepatitis D is an RNA virus that cannot replicate on its own. It needs Hepatitis B (HBV) to reproduce.
1. Characteristics
RNA virus
Needs the HBV envelope to replicate
Therefore, HDV only occurs with HBV
You cannot have Hepatitis D without Hepatitis B.
2. Severity
Occurs as Hepatitis B + D
Causes more severe hepatitis than HBV alone
Increases the risk of serious liver disease.
3. Treatment
Specific treatment is available
However, treatment is not very effective.
Easy way to remember:
Hepatitis D = Dependent on B
D needs B
B + D = worse hepatitis
Feature | Hepatitis D |
|---|---|
Virus | RNA |
Needs HBV? | Yes |
Can occur alone? | No |
Severity | Worse than HBV alone |
Treatment | Available, but not very effective |
EXAM TIP: If you see “RNA virus that requires HBV” → Hepatitis D.
Hepatitis E - HEV
Definition: Hepatitis E is an RNA virus that is very similar to Hepatitis A and usually causes acute hepatitis.
1. Characteristics
RNA virus
Causes acute hepatitis
Incubation period: about 4 weeks
Usually does not become chronic
2. Transmission
Fecal–oral route
Often associated with travel to less developed regions of the world
Can spread through contaminated food or water
3. Important Complication
Can cause fulminant/fulminating hepatitis, especially in pregnant individuals.
This is a major difference from Hepatitis A.
4. Diagnosis
Two main options:
PCR-HEV → detects HEV RNA
IgM for HEV → indicates recent infection
5. Treatment & Prevention
Can be treated with antiviral medications
No vaccine available (according to your lecture)
Easy way to remember:
Hepatitis E = “A-like” but dangerous in pregnancy
E = RNA + fecal-oral + 4 weeks + acute
Pregnancy → risk of fulminant hepatitis ⚠
Feature | Hepatitis E |
|---|---|
Virus | RNA |
Incubation | ~4 weeks |
Transmission | Fecal-oral |
Disease | Acute hepatitis |
Fulminant hepatitis | Especially pregnancy |
Vaccine | No |
Diagnosis | PCR-HEV or IgM |
Treatment | Antivirals |
STIs or STDs?
Both are used, but STI (sexually transmitted infection) is generally preferred today.
STI = sexually transmitted infection
A person can have an infection without having symptoms or disease.
STD = sexually transmitted disease
Usually implies the infection has caused symptoms or illness.
Easy way to remember:
STI = infection, with or without symptoms
STD = infection that has caused disease
For your Infectious Diseases class, I'd use STI unless your professor specifically uses STD.
Urethritis
Definition: Urethritis is inflammation of the urethra, often caused by an STI.
1. Signs
Purulent urethral discharge → pus-like discharge
Pyuria → white blood cells (WBCs) in urine
Erythema of the meatus → redness around the urethral opening
2. Symptoms
Pain and discomfort
Dysuria → burning/pain when urinating
3. Most Common Pathogens
The two most common causes are:
Neisseria gonorrhoeae → gonorrhea
Chlamydia trachomatis → chlamydia
Important: The symptoms usually cannot reliably tell you whether it is gonorrhea or chlamydia.
4. Diagnosis & Treatment
Laboratory testing is needed to distinguish between the two.
If laboratory testing is not available, treatment should cover both:
N. gonorrhoeae
C. trachomatis\
Easy way to remember:
Urethritis = Urethra inflammation → discharge + burning
Gonorrhea + Chlamydia = the big 2 causes
Feature | Urethritis |
|---|---|
Definition | Inflammation of urethra |
Main symptoms | Pain + dysuria |
Signs | Discharge + pyuria + redness |
Common pathogens | N. gonorrhoeae + C. trachomatis |
Can symptoms distinguish them? | Not reliably |
Lab testing | Needed |
If testing unavailable | Treat for both |
Urethritis: Diagnosis
1. Urinalysis
↑ WBCs in urine → pyuria
Positive leukocyte esterase → indicates WBC activity/inflammation
2. NAAT — Main Diagnostic Test
Nucleic Acid Amplification Tests (NAATs), such as PCR, are commonly used.
>90% sensitive and specific
Can use:
Urine
Genital swabs
Rectal swabs
Throat swabs
Can detect asymptomatic infections
Easy: NAAT/PCR = highly accurate + can find infections without symptoms.
3. Gram Stain for Gonorrhea
A Gram stain of urethral discharge can show:
Gram-negative intracellular diplococci (GNID)
>95% sensitive
>99% specific
Strong evidence for Neisseria gonorrhoeae.
Remember:
Gonorrhea = Gram-negative intracellular diplococci
4. Culture
Culture of urethral discharge can be technically difficult.
Can be useful when treatment isn't working or drug-resistant gonorrhea is suspected.
Helps determine which antibiotics will work.
Quick Review
Test | What it tells you |
|---|---|
Urinalysis | Pyuria + leukocyte esterase |
NAAT/PCR | Highly accurate; detects symptomatic & asymptomatic infection |
Gram stain | GN intracellular diplococci → gonorrhea |
Culture | Helpful for suspected antibiotic resistance |
Urethritis: Treatment
1. Gonococcal Urethritis (GU)
Caused by Neisseria gonorrhoeae.
Treated with a single dose of an IM antibiotic 💉
2. Non-Gonococcal Urethritis (NGU)
Usually caused by organisms such as Chlamydia trachomatis.
Treated with oral antibiotics
Treatment can be:
Single dose
7-day course
3. When You're Not Sure
If chlamydia cannot be excluded → treat for both gonorrhea + chlamydia
If you cannot distinguish GU from NGU → treat for both
Easy rule:
Can't tell? → Treat both.
4. Partner Treatment
Notify and treat sexual partners
Important because it:
Prevents reinfection
Helps prevent continued spread of the infection
Quick Review
Type | Treatment |
|---|---|
GU (gonorrhea) | Single-dose IM antibiotic 💉 |
NGU | Oral antibiotics |
Chlamydia can't be excluded | Treat both |
GU vs NGU unclear | Treat both |
Sexual partners | Notify + treat |
Pelvic Inflammatory Disease (PID)
Definition: PID is a bacterial infection that causes inflammation of the female reproductive organs, including the uterus, fallopian tubes, and ovaries.
1. Causes
Can occur after an untreated chlamydia and/or gonorrhea infection.
However, PID does not always follow an STI.
Often polymicrobial → caused by multiple types of bacteria.
2. Risk Factors
Risk is increased with:
Young age
Multiple sexual partners
Condomless sex
Previous STIs
Previous episodes of PID
Easy way to remember:
PID = Pelvic organs become inflamed because of bacterial infection.
Big point:
Chlamydia + Gonorrhea → common causes, but PID can involve multiple bacteria.
Feature | PID |
|---|---|
Type | Bacterial infection |
Organs affected | Uterus, fallopian tubes, ovaries |
Common STI causes | Chlamydia + Gonorrhea |
Infection type | Often polymicrobial |
Major risk factors | Young age, multiple partners, condomless sex, previous STIs/PID |
Pelvic Inflammatory Disease (PID)
1. Clinical Presentation
Common signs and symptoms include:
Lower abdominal/pelvic pain
Often more tender during a pelvic exam
Vaginal discharge
Vaginal bleeding
Fever
Other signs of systemic inflammation
Easy way to remember:
PID = pelvic pain + discharge/bleeding + fever
2. Diagnosis
There is no single specific diagnostic test for PID.
Tests may show:
Signs of systemic inflammation
Fluid collection in the abdomen/pelvis
Diagnosis is mainly based on the clinical presentation because laboratory tests are not specific.
3. Treatment
Requires prolonged courses of combined antibiotics
Antibiotics may be given IV, especially in more severe cases.
Surgery may be needed if complications occur, such as an abscess.
4. Complications
Untreated or severe PID can cause:
Sepsis
Infertility
Increased risk of ectopic pregnancy
Chronic pelvic pain
Big Picture
Untreated infection → PID → inflammation → possible permanent reproductive damage
Category | PID |
|---|---|
Main symptom | Lower abdominal/pelvic pain |
Other symptoms | Discharge, bleeding, fever |
Diagnosis | No specific test |
Treatment | Prolonged combination antibiotics |
Severe cases | IV antibiotics ± surgery |
Complications | Sepsis, infertility, ectopic pregnancy, chronic pelvic pain |
Genital ulcers
Definition: Genital ulcers are open sores that occur on the skin or mucous membranes of the genital area.
1. What are ulcers?
Ulcer = open sore on the skin or mucosa.
Genital ulcers can be caused by different infections, including some STIs.
2. Condom Protection
Genital ulcers may occur in areas not covered by a condom.
Therefore, sexual transmission can still occur even when condoms are used.
Easy way to remember:
Genital ulcer = open sore → may be outside the condom-covered area → transmission is still possible.
Important: Condoms reduce the risk of STI transmission but do not provide 100% protection against infections spread by skin-to-skin contact.
Syphilis: Clinical presentation
Definition: Syphilis is a bacterial STI that progresses through different stages if untreated.
1. Primary Syphilis — 2–4 weeks
The bacteria enters through the skin or mucous membrane.
Causes an ulcer (open sore) called a chancre.
Usually occurs on the genitals, but can occur elsewhere.
The ulcer may heal even without treatment.
2. Secondary Syphilis — 4–8 weeks
The infection spreads into the bloodstream.
Causes a rash.
Other systemic symptoms may occur.
3. Latent Syphilis — Months to years
The rash disappears.
The bacteria remains in the body but is dormant.
The person may have no symptoms.
4. Tertiary Syphilis — Usually years later
Can cause serious damage to multiple organs.
Possible complications include:
Neurological problems
Psychiatric problems
Cardiovascular problems
Orthopedic/bone problems
Easy way to remember:
Primary → Secondary → Latent → Tertiary
Sore → Rash → Silent → Organ damage
Stage | Timing | Main feature |
|---|---|---|
Primary | 2–4 weeks | Ulcer/chancre |
Secondary | 4–8 weeks | Rash |
Latent | Months–years | No symptoms |
Tertiary | Usually years | Organ damage |
Syphilis: Diagnosis and Treatment
1. Diagnosis — Immunological Tests
There are 2 main types of blood tests:
Nontreponemal tests: VDRL or RPR
Lower specificity → can have false positives.
Results can be quantified (measured by a titer).
Useful for checking response to treatment.
If the titer decreases after treatment → treatment is working.
Treponemal test: FTA-Abs
Higher specificity → more specific for syphilis.
Usually remains positive after infection.
Does not tell you how active the disease is.
Easy way to remember:
RPR/VDRL = Response → useful for monitoring treatment.
FTA-Abs = Fingerprint → more specific for syphilis.
2. Treatment
Penicillin is the main treatment.
Can be given:
IM injection
IV infusion
The treatment depends on the stage of disease.
More advanced disease → longer antibiotic treatment.
3. Prevention
No vaccine is available.
Condom use can reduce transmission.
Frequent STI testing helps detect infections early.
DoxyPEP may be used for some people at increased risk to help prevent certain bacterial STIs.
Quick Review
Test/Approach | Main purpose |
|---|---|
VDRL/RPR | Lower specificity; monitor treatment response |
FTA-Abs | Higher specificity; confirms exposure/infection |
Penicillin | Main treatment |
Vaccine | None |
Condoms + testing | Prevention |
DoxyPEP | Prevention for certain high-risk individuals |
Genital herpes
Definition: Genital herpes is a lifelong viral STI caused mainly by HSV-2, but it can also be caused by HSV-1.
1. Cause
Most cases → HSV-2
Sometimes → HSV-1 (the virus commonly associated with cold sores)
Infection is lifelong.
Recurrences are common because the virus remains in the body.
2. Ulcers
Genital herpes ulcers are typically:
Shallow
Multiple
Clustered together
Painful
Easy way to remember:
Herpes = painful, shallow, clustered sores
3. Diagnosis
If ulcers are present:
NAAT/PCR from the wound → helpful for detecting HSV.
If there are no ulcers:
Serology (blood test) can detect HSV-2 antibodies.
Positive antibodies mean the person has been infected at some point.
It does not necessarily mean there is an active infection right now.
Test results should always be interpreted together with the clinical presentation.
4. Treatment
Genital herpes is treated with antiviral medications.
Antivirals help control symptoms and outbreaks, but they do not eliminate the lifelong infection.
Quick Review
Feature | Genital Herpes |
|---|---|
Main cause | HSV-2 |
Sometimes | HSV-1 |
Ulcers | Shallow, multiple, clustered, painful |
Infection | Lifelong |
Recurrence | Common |
Ulcers present | NAAT/PCR of wound |
No ulcers | Serology |
Treatment | Antivirals |
Cure | No cure |
Genital ulcers: Comparative
This is a high-yield distinction for genital ulcers:
Feature | Syphilis | Herpes (HSV-2) |
|---|---|---|
Number | Few | Multiple |
Appearance | Larger ulcers | Small, clustered ulcers |
Border | Clear/sharp border | Clean base with redness around ulcers |
Pain | Usually not painful | Painful/tender |
Lymph nodes | Enlarged, usually not painful | Enlarged and tender/painful |
Easy way to remember:
Syphilis = Single-ish + Silent
→ Few, larger, painless ulcer
Herpes = Hurt + Huddled
→ Multiple, small, clustered, painful ulcers
Exam clue:
Painless genital ulcer → think syphilis
Painful clustered genital ulcers → think HSV-2
Doxy PEP
Definition: DoxyPEP = taking doxycycline after condomless sex to help prevent certain bacterial STIs.
What can it reduce?
Studies have shown that DoxyPEP can reduce the incidence of:
Gonorrhea
Chlamydia
Syphilis
Who?
Your lecture specifically states benefits among:
Cisgender men who have sex with men
Transgender women who have sex with men
Easy way to remember:
DoxyPEP = Doxycycline AFTER sex → prevents some bacterial STIs
Important: DoxyPEP is for prevention, not treatment of an existing STI, and it does not prevent viral STIs like herpes or HIV.
Anogenital warts (HPV)
Definition: Anogenital warts are raised, cauliflower-like skin lesions caused by human papillomavirus (HPV).
1. Warts
Can occur in the:
Genital area
Anal area
Perineal area
Warts themselves are usually not dangerous.
They can be removed:
Chemically
Surgically
2. HPV & Cancer
Some types of HPV are high-risk/carcinogenic and can cause:
Cervical cancer
Rectal/anal cancer
Throat cancer
Not all HPV types cause cancer. Some mainly cause warts, while others are associated with cancer.
3. Prevention & Screening
HPV vaccines include protection against the most important cancer-causing HPV types.
Regular Pap smears help detect abnormal cervical cells/lesions early.
Easy way to remember:
HPV = Warts + Cancer risk
Low-risk HPV → warts
High-risk HPV → cancer risk
Vaccine + Pap screening → prevention/early detection
Feature | Anogenital Warts (HPV) |
|---|---|
Appearance | Raised, cauliflower-like |
Location | Genital, anal, perineal |
Cause | HPV |
Warts dangerous? | Usually |
Treatment | Chemical or surgical removal |
Cancer risk | Some HPV types → cervical, anal/rectal, throat cancer |
Prevention | HPV vaccine |
Screening | Regular Pap smear |