Gastrointestinal Flashcards
1
Q
What is the recommended healthy level of alcohol intake in Australia?
A
No more than 4 drinks on any occasion. No more than 10 drinks/ week.
2
Q
What are the steps in the metabolism of alcohol?
A
- Alcohol –> acetaldehyde.
ENZYMES: alcohol dehydrogenase, CYP2E1, Catalase. - Acetaldehyde –> acetic acid.
ENZYME: aldehyde dehydrogenase. - Acetic acid –> acetyl Co A into the Krebs Cycle.
3
Q
What are the mechanisms of alcohol toxicity?
A
- Toxic metabolites - e.g. acetaldehyde.
- Metabolism causes NAD –> NADH. Altered NAD:NADH ratio stimulates excess triglyceride production in the liver –> steatosis.
- CYP2E1 causes production of ROS –> inflammation and fibrosis.
4
Q
What is the main MOA of alcohol?
A
Increased action of GABA
5
Q
List 6 acute effects of alcohol.
A
NEUROPSYCH: - euphoria - decreased inhibition - emotional lability - impaired judgement - respiratory depression - decreased LOC RENAL: - inhibition of ADH --> diuresis CV: - cutaneous vasodilatation --> flushing GIT: - Nausea and vomiting
6
Q
List 10 long-term complications of excessive alcohol use.
A
GIT: - inflammation: oesophagitis, gastritis, pancreatitis - PUD - oesophageal varices - alcoholic liver disease, cirrhosis CANCER: - oral - pharynx/ larynx - oesophageal - breast - CRC - HCC NEURO: - dementia - Wernicke-Korsakoff syndrome CARDIAC: - Dilated cardiomyopathy IMMUNOSUPPRESSION --> infection ACCIDENTS/ TRAUMA UROLOGY: - Erectile dysfunction - Decreased libido - Testicular atrophy - Infertility
7
Q
What is the cause of Wernicke-Korsakoff syndrome?
A
Thiamine deficiency
8
Q
What are the features of Wernicke-Korsakoff syndrome?
A
WERNICKE = triad:
1. Encephalopathy –> disorientation, memory problems, unable to sustain attention
2. Eyes –> nystagmus, gaze palsy
3. Ataxic gait –> wide based, short steps
KORSAKOFF = amnesia
9
Q
Explain the stages of alcoholic liver disease.
A
- Steatosis = fatty build-up
- Steatohepatitis = fatty + inflammation
- Fibrosis and cirrhosis = + scarring and nodularity
10
Q
List 5 symptoms of alcoholic liver disease.
A
RUQ pain Jaundice Nausea and vomiting Anorexia Weight loss Fatigue GI bleeding Abdominal distention
11
Q
What bloods would you order to investigate suspected alcoholic liver disease? What results would you expect to see?
A
LFTs: raised GGT, raised AST and ALT, with AST:ALT > 2.
Albumin: low
FBC: megaloblastic anaemia
EUC: possibly increased creatinine - hepatorenal syndrome
Coags: raised PT and INR
12
Q
What are the DDX for alcoholic liver disease - what tests would you order to differentiate?
A
Viral hepatitis = serology
Hemochromatosis = iron studies
Wilson’s disease = ceruloplasmin
Primary biliary cirrhosis = anti-mitochondrial antibody (AMA)
Autoimmune hepatitis = ANA, anti-smooth muscle antibody (ASMA)
Alpha-1-antitrypsin deficiency
13
Q
What are principles of managing alcoholic hepatitis?
A
Supportive care. Abstinence from alcohol. Nutrition - address malnutrition, deficiencies. Hepatitis A and B immunisation. Consider prednisolone. Treat cirrhosis/ complications.
14
Q
What are the clinical features of alcohol withdrawal?
A
NEUROPSYCH: - anxiety, agitation - confusion - insomnia, fatigue - seizures - visual hallucinations AUTONOMIC INSTABILITY: - sweating - tremor - tachycardia - palpitations - hypertension
15
Q
How would you treat alcohol use disorder?
A
- Brief intervention/ 5As/ motivational interviewing.
- Psychosocial support - CBT, AA
- Pharmacotherapy:
1st line: naltrexone or acamprosate.
2nd line: disulfiram
16
Q
MOA of NALTREXONE.
CI
A
Opioid receptor antagonist.
Decreases pleasure from alcohol use and potentially decreases cravings.
CI = opioid use, liver failure
17
Q
MOA of ACAMPROSATE
CI
A
Modulates glutamate transmission.
CI = ESKD
18
Q
MOA of DISULFIRAM.
What is the effect of alcohol + disulfiram combination?
CI?
A
Altered alcohol metabolism –> build-up of acetaldehyde.
Alcohol use –> flushing, palpitations, sweating, headache, N&V.
Do not start within 24 hours of alcohol use.
CI = heart disease, psychotic disorders
19
Q
DDX of upper GI bleeding
A
VARICES: oesophageal or gastric EROSION/ ULCER: oesophageal or gastric MALLORY-WEISS TEAR BOERHAAVE SYNDROME AVM
20
Q
How would you investigate upper GI bleeding?
A
Labs:
FBC, coags, EUC (creatinine often elevated in hypovolemia/ AKI), LFTs, BUN (BUN often increased in upper GI bleed)
Imaging:
For Boerhaave syndrome –> confirm with CXR or CT chest and abdo using water soluble contrast (e.g. Gastrografin)
Endoscopy:
Upper GI endoscopy is diagnostic method of choice
21
Q
Explain your approach to treating upper GI bleeding.
A
Support:
- DRSABCD
- Monitor vitals
- Large bore IV cannula x 2
- Oxygen to maintain sats
- Analgesia if required
Avoid:
- NSAIDS
- Anticoagulants, aspirin
Replace:
- IV fluids
- Blood type and crossmatch –> Transfusion of appropriate blood product: RBCs, platelets, FFP
Treat underlying cause:
VARICEAL –>
- Antibiotic
- Octreotide
- Upper endoscopy with variceal ligation
- If bleeding uncontrolled –> balloon tamponade
- If bleeding still uncontrolled –> TIPS
NON-VARICEAL –>
- PPI
- Endoscopic therapy - coagulation therapy, adrenaline injection, clips
- If uncontrolled –> Interventional radiology w/ arterial embolization
- If still uncontrolled –> laparotomy
22
Q
How would you treat Boerhaave syndrome?
A
- Admit - requires ICU and close monitoring
- Stabilise - DRSABCD
Decide on non-operative versus surgical management:
- Can consider non-operative management in certain populations (stable, minimal mediastinal contamination, no infection) –>
- – Secure the airway
- – NBM for 7 days + TPN
- – NG tube with suction
- – Analgesia
- – IV broad spectrum ABX
- – PPI
- – Repeat imaging at 7 days prior to initiating oral intake
If not suitable for conservative management –> operate:
- Prepare for surgery
- – NBM, IV cannulae, FBC, Coags, blood group and hold/ crossmatch
- – Close the oesophageal leak and drain fluid collection
- – IV broad spectrum ABX
23
Q
What are the clinical features of oesophageal rupture?
A
SYMPTOMS:
- PAIN - SEVERE!!!
- Recent retching/ vomiting (if spontaneous rupture i.e. Boerhaave syndrome)
Context - can be spontaneous (vomiting) or iatrogenic (endoscopy, balloon dilatation, TOE), blunt trauma or swallowed foreign body
SIGNS:
- Distressed
- Vital sign abnormalities - fever, tachycardia, tachypnoea, hypotension
- Subcutaneous emphysema
- Hamman sign (systolic crunch at cardia apex)
24
Q
What are the clinical features of Mallory-Weiss tears?
A
Primary symptom is haematemesis.
+/-
Pain
Hypovolemia –> vital sign abnormalities
Lower GI bleeding
25
How would you manage a patient:
(1) with cirrhosis, to prevent varices?
(2) with known varices, to prevent a first variceal bleed?
(1)
Upper endoscopy performed on every patient at time of diagnosis of cirrhosis.
Prevent further hepatic injury - treat hepatitis, stop drinking, lose weight etc.
Monitor with endoscopy every 2-3 years
(2)
Non-selective B blocker - e.g. propranolol OR
Endoscopic variceal ligation
Monitor with endoscopy every 1-2 years
26
How would you treat a patient with ascites?
Non-Pharmacological:
- Sodium and fluid restriction
- Avoid NSAIDs, ACE-I and ARBs
Moderate volume ascites - Diuretics: spironolactone PLUS frusemide
Large volume ascites - Paracentesis + albumin
ABX prophylaxis for SBP
Consider TIPS, consider liver transplantation
27
List causes of abdominal distention and ascites.
```
Causes of abdominal distention are:
Fat
Foetus
Flatus
Fluid
Faeces
Filthy big tumour
```
Causes of ascites are:
PORTAL HYPERTENSION
- Cirrhosis: alcoholic liver disease, hepatitis, NAFLD
- Non-cirrhotic portal hypertension: Budd-Chiari, portal vein thrombosis, splenic vein thrombosis
HYPOALBUMINEMIA
- Nephrotic syndrome
- Protein losing enteropathy
MALIGNANT
- Ovarian cancer
- Peritoneal carcinomatosis
INFECTION
- Peritoneal TB
28
What tests would you order on ascitic fluid?
| How would you interpret?
Order:
- Cell count and differential
- Albumin and total protein
- Gram stain and culture
Plus bloods: FBC, EUC, LFTs, albumin
Interpretation:
Neutrophil count: > 250 /mm^3 = diagnostic of SBP
Gram stain and culture: + in infection
Serum to ascites albumin gradient = serum albumin minus ascites albumin -->
> 11 g/L --> likely portal htn; < 11 g/L --> likely not portal htn
29
What are the complications of GORD?
```
Oesophagitis
Upper GI bleeding
Barrett's oesophagus
Stricture
Adenocarcinoma
Respiratory disorders - e.g. worsening of asthma
```
30
What is your approach to diagnosing GORD?
- Can usually make a clinical diagnosis and confirm with PPI trial
- Investigations performed if features are atypical, red flags present or 60+ years:
1. Upper endoscopy with biopsy
2. If OGD is non-diagnostic you may:
- - Ambulatory pH monitoring
- - Barium swallow and/or manometry if dysphagia
H pylori testing not recommended for GORD.
31
List red flags for GORD.
```
VITAL SIGN ABNORMALITY
SYSTEMIC SYMPTOMS: fatigue, weight loss, night sweats
PATIENT fx: 60+ years
COMPLAINT fx:
- Swallow: odynophagia, dysphagia
- Anaemia or GI bleeding
- Early satiety
FAMILY hx: of GI cancer esp oesophageal
```
32
How would you manage Barrett's oesophagus?
Treatment depends on presence of dysplasia
(Barrett's is metaplasia --> progresses to dysplasia: low grade to high grade --> adenocarcinoma)
Non-dysplastic -->
Lifestyle + PPI + surveillance endoscopy every 3-5 years
Low-grade dysplasia --> somewhat controversial
Lifestyle + PPI + surveillance endoscopy every 6-12 mo OR
endoscopic mucosal resection + radiofrequency ablation
High-grade dysplasia -->
PPI + endoscopic mucosal resection + radiofrequency ablation
33
What are the complications of H pylori infection?
Gastritis
Peptic ulcer disease
Gastric adenocarcinoma
Gastric lymphoma
34
Helicobacter pylori
Indications for testing?
Types of investigations
Workup is indicated if PUD and to confirm eradication of H pylori 4-6 wks after treatment completion.
NON-INVASIVE TESTING:
1. urea breath testing (urea labelled with radioactive carbon given PO --> if H pylori infection, bacterial urease cleaves urea --> releasing labelled C --> breath out labelled CO2, which is detected)
2. stool antigen testing
3. serology
```
INVASIVE TESTING:
endoscopy + biopsy with
1. urease testing (biopsy sample --> placed in solution containing urea and pH indicator --> if urease present in sample, urea converted by bacterial urease to ammonia --> pH change --> colour change)
2. culture
3. histology - i.e. microscopy
```
- Serology not recommended as unable to distinguish between current infection and past infection that has resolved.
- Urea breath test and urease testing can be false-neg if taking ABX or PPI/H2 receptor antagonist
35
Explain the physiology of gastric acid secretion.
Parietal cell stimulation --> H/K-ATPase pumps fuse with cell membrane --> H+ secreted into lumen of stomach (in exchange for K+).
Stimulation of parietal cell is by:
1. Acetylcholine
2. Histamine
3. Gastrin
ACH and gastrin also stimulate ECL cells to produce histamine.
Inhibition is by somatostatin (from D cells).
36
HIATUS HERNIA
What are the 2 types of hiatus hernia?
How do the present?
What are their complications?
TYPE 1 = sliding (90% of hiatal hernias)
- -> most are asymptomatic
- -> if symptomatic --> reflux sx
Complications -->
- Oesophagitis
- Barrett's oesophagus
- GI bleeding from ulcer
TYPE 2 = rolling/ para-oesophageal (10%)
Epigastric pain
Nausea
Postprandial fullness
Complications -->
- Volvulus --> strangulation -->
- -- Gastric outlet obstruction
- -- Perforation
- -- Death
37
How would you diagnose a hiatus hernia?
Usually:
- CXR --> air-fluid level in thorax (paraoesophageal) OR
- Upper endoscopy OR
- Barium swallow
38
How would you treat a hiatus hernia:
Sliding?
Paraoesophageal?
```
SLIDING:
Asymptomatic --> not required
Symptomatic --> as for GORD
- Lifestyle
- PPI
- Laparoscopic fundoplication
```
PARAOESOPHAGEAL:
Asymptomatic --> often surgical repair (depends on patient age and comorbidities)
Symptomatic --> surgical repair (reduce herniated viscus, excise the hernia sac, and repair diaphragmatic defect)
39
PROTON PUMP INHIBITOR
Use
How to use
UE
Indication: GORD - frequent or severe symptoms
Start with 4-8 week course of PPI
e.g. omeprazole 40mg daily PO 0.5hr before meal
If symptoms NOT controlled --> upper endoscopy
If symptoms controlled -->
After course, titrate down slowly - either continuing at the lowest dose that gives relief or stopping.
If symptoms recur on stopping, return to the lowest dose of PPI that provided effective control.
UE:
- Interstitial NEPHRITIS
- increased risk of PNEUMONIA
- INFECTION: gastroenteritis, C difficile
- impaired NUTRIENT absorption - e.g. iron deficiency anaemia
- FRACTURE risk
40
DDX for dysphagia
1. OESOPHAGEAL PROBLEM:
```
DYSMOTILITY
- Achalasia
- Diffuse oesophageal spasm
- Nutcracker oesophagus
INFLAMMATION/ INFECTION
- Oesophagitis: reflux, eosinophilic, pill-induced, caustic ingestion
CANCER
ANATOMICAL
- Hiatus hernia
- Foreign body
- Diverticulum
- Rings
- Webs
AUTOIMMUNE
- Scleroderma
- Sjogren's syndrome
```
2. EXTRINSIC COMPRESSION
- Neck abscess
- Goiter
3. NEUROLOGICAL
- Stroke
- Parkinson's
- MS
- MND
- Muscular dystrophy
41
Achalasia
- Cause?
- Pathology?
- Investigations and findings?
- Treatment?
Cause: primary (unknown cause) or secondary: Chagas disease (Trypanosoma cruzi), infiltrative disease (sarcoidosis, amyloidosis)
Pathology:
Degeneration of cells in the myenteric plexus -->
failure of peristalsis + failure of relaxation of LOS
Symptoms:
Dysphagia - BOTH solids and liquids from onset
IX:
Manometry -->
- LOS: elevated resting pressure + incomplete relaxation
- Aperistalsis
Barium swallow -->
- Dilated oesophagus
- Bird beak narrowing at LOS
- Aperistalsis
- Delayed emptying of barium into stomach
Treatment:
Good surgical candidate --> pneumatic dilation
Poor surgical candidate --> pharmacotherapy with calcium channel blocker or nitrates
42
Explain the aetiology and pathophysiology of anal fissures.
Most anal fissures are primary - caused by local trauma from: hard stool, anal sex.
Secondary can also occur from: Crohn disease, STI.
Typically
- trauma causes tear in anoderm
(usually posterior midline - this area is particularly susceptible due relative ischemia)
--> pain leads to spasm of anal sphincter --> ischemia --> delay in healing.
43
What are the classical clinical features of anal fissures?
SYMPTOMS:
1. Pain!!!
- onset usually associated with passage of hard stool
- severe and sharp, like passing knife/glass
- exacerbated by defecation
2. Rectal bleeding
- usually bright red blood, coating stool or on wiping
SIGNS
1. obvious fissure - tear in anoderm
2. sentinel pile
44
How would you investigate/diagnose an anal fissure?
```
Mainstay = physical examination
NO DRE - too painful
+/- examination under anaesthesia
+/- endoscopy
+/- manometry if considering surgery and need to investigate anal tone - determines which operation should be performed
```
45
How would you treat an anal fissure?
Acute fissure - usually respond to conservative management.
- relieve constipation: fiber, stool softener, fluid intake
- Sitz bath
- topical analgesic e.g. lidocaine gel (Pain relief --> stop internal sphincter spasm --> improved blood flow --> healing)
- topical vasodilator (topical GTN or topical calcium channel blocker to relieve spasm and promote blood flow)
Try conservative treatment for 6-8 weeks (>50% will heal with this approach) --> if not successful, referral to colorectal surgeon.
Chronic (>8weeks) fissure - may require surgical management. Surgery is more effective than conservative tx, but has risk of incontinence.
Gold standard surgery = lateral internal sphincterotomy
If high risk of faecal incontinence (e.g. women with prior obstetric injury, IBD, prior anal sphincter injury) --> perform botox injection or fissurectomy instead
Secondary fissure --> treat the underlying disease
46
Explain the pathophysiology of PUD.
PUs arise when factors that damage the mucosa > factors that protect it.
Protective factors:
1. Mucous-bicarbonate layer (physical barrier + maintains neutral pH at epithelial surface)
2. Tight junctions
3. Restitution - epithelial cell migrate into erosions
Damaging factors:
1. Stomach acid
2. Pepsin
3. H pylori
4. NSAIDs
H pylori virulence factors = urease (splits urea to form ammonium - neutralizes gastric acid surrounding the bacterium); motility - has flagella; adhesins - attach to stomach epithelium. H pylori causes (1) inflammation and (2) possibly hypersecretion of gastric acid (impairs somatostatin so HCl release isn't turned off by low pH)
NSAIDs --> inhibition of COX --> decreased production of prostaglandins. Some PGs are protective in the stomach -->
- Stimulate secretion of mucin and bicarbonate --> maintain the protective barrier.
- Decrease acid secretion
- Enhance mucosal blood flow
- Enhance epithelial cell proliferation and restitution
47
List complications of PUD.
```
Erodes into/through structures --
- GI bleeding
- Perforation
- Fistula
Chronic inflammation and scarring -
- Stricture -- Gastric outlet obstruction
```
48
What is the first line therapy for H. pylori-induced PUD?
Triple therapy:
1. Esomeprazole 20mg PO BD for 7 days
2. Amoxicillin 1g PO BD for 7 days
3. Clarithromycin 500mg PO BD for 7 days
49
What are the clinical features of hepatitis?
```
SYMPTOMS:
Vital signs: fever
General systemic fx of viral infection: fatigue, malaise, myalgias, headache
GIT fx:
- anorexia, n&v
- RUQ pain
- jaundice, pruritus
- pale stools, dark urine
```
```
SIGNS:
Vital signs: fever
GIT:
Inspection - jaundice, scleral icterus
Palpation - RUQ tenderness, hepatosplenomegaly
```
50
How is Hepatitis A transmitted?
| List risk factors for hepatitis A infection.
Faecal-oral transmission.
RISK:
- Travel to endemic area
- Ingestion of contaminated foods
- Not immunised for hepatitis A
- MSM
- Occupational exposure - HCW, day-care
51
What are the possible consequences of hepatitis A infection?
Does NOT cause chronic hepatitis.
| Can rarely result in fulminant hepatitis.
52
How would you confirm the diagnosis of suspected hepatitis A infection?
LFTs - raised esp ALT & AST (hepatitic)
| IgM anti-HAV +
53
How is hepatitis A treated?
Supportive care
Self-limited condition
Vaccination
54
What is the most common cause of:
- viral gastroenteritis?
- viral gastroenteritis in children?
Norovirus is overall the most common cause of viral gastroenteritis.
In children, rotavirus is the most common cause.
55
List risk factors for gastroenteritis.
Age: very young (< 5 years) and old (>65 years)
Travel to developing country
Ingestion of contaminated foods/ undercooked foods
Crowded living condition
Reduced gastric acid - e.g. PPI
Recent ABX
MSM
Immunocompromise - e.g. HIV, DM, corticosteroid, chemotherapy
56
What is your work-up of acute gastroenteritis?
```
Usually dx is clinical.
Further testing indicated for:
SEVERE DISEASE:
- Vital sign abnormality - e.g. fever
- Blood or mucous in stools
- Severe abdominal pain
- Complications - e.g. sepsis
AT RISK PATIENT:
- Immunocompromise
PUBLIC HEALTH ISSUE:
- Suspected outbreak
```
STOOL --> common tests:
- Stool MCS (culture is neg in viral gastroenteritis)
- Assay for Shiga toxin
- Assay for C difficile toxin
BLOODS -->
FBC (leukocytosis = bacterial cause, is absent in viral gastro; eosinophilia suggests parasitic infection; decreased platelets in HUS or TTP complicating E coli infection)
EUC (check for electrolyte disturbance due to vomiting and diarrhoea)
+ blood culture if septic
57
How would you approach the treatment of gastroenteritis?
```
Consider admission for:
SEVERE DISEASE
-- high fever
-- severe symptoms
-- sepsis
RISK IF SENT HOME:
-- insufficient oral intake to maintain hydration
```
1. Maintain hydration/ rehydrate
- oral rehydration if possible - including replacement of electrolytes
- IV hydration if the above is insufficient
2. Control symptoms
- Loperamide: anti-motility agent - use with caution, do NOT use if bloody stools or fever (increased risk of prolonging bacterial gastroenteritis + increased risk of HUS with E coli infection)
3. Consider antibiotics
- Do not use for bloody diarrhoea (increase the risk of HUS)
- Do not use if no fever (more likely viral)
4. Monitor
5. Infection control measures
- single room
- PPE
5. Prevention -
- Proper hand hygiene
- Avoid undercooked foods, dirty water
- Vaccination: rotavirus (cholera and typhoid for travel to endemic areas)
58
How is Hepatitis B transmitted?
1. Blood
- IVDU
- Contaminated blood products
2. Body fluids - semen, saliva
- Sexual contact
3. Vertical
The most common route depends on the prevalence of HBV:
Low prevalence areas --> IVDU most common, then sexual contact
High prevalence areas --> vertical
59
How often does HBV become chronic?
Risk of chronic HBV depends on the age of the patient.
Perinatal infection = 90% risk
Children = 20-50%
Adult = <5%
60
How does HBV replicate?
HBV is a circular DNA virus (incomplete, only partially double-stranded).
HBV enters the hepatocyte --> uncoated --> moves to nucleus --> viral DNA polymerase synthesises missing DNA to make it a complete circular dsDNA molecule -->
cell's RNA polymerase makes mRNA positive strand -->
this strand is then used to make a negative mRNA strand -->
viral DNA replicated from the negative RNA by virally-encoded reverse transcriptase -
i.e. there is RNA-dependent DNA synthesis.
61
What serology is ordered for HBV infection?
| Explain the interpretation.
```
Serology that can be ordered is:
Surface = HBsAg, anti-HBs
Core = anti-HBc
E = HBeAg and anti-HBe
HBV DNA
```
Generally, screening is first performed with HBsAg and anti-HBc IgM --> if positive perform full serology
HBsAg is + in ACTIVE INFECTION (both acute and chronic)
Anti-HBs + when the patient is IMMUNE (from past infection or vaccination)
Anti-HBc IgM + in an ACUTE INFECTION
Anti-HBc IgG + in CHRONIC or PAST infection.
HBe + = HIGHLY INFECTIOUS, assoc with high HBV viral load
In an acute infection -->
First, HBsAg becomes +
Then anti-HBc IgM becomes +
Then HBsAg disappears
If infection resolves -->
anti-HBs +
anti-HBc IgG +
In a chronic infection,
HBsAg +
HBeAg +
62
What is indicated by:
HBsAg positive
anti-HBs negative
anti-HBc IgM positive
Active HBV infection
63
What is indicated by:
HBsAg positive
Anti-HBs negative
Anti-HBc IgG positive
Chronic HBV infection
64
What is indicated by
HBsAg Negative
Anti-HBs positive
Anti-HBc IgG positive
Immune after resolved HBV infection
65
What is indicated by
HBsAg Negative
Anti-HBs Positive
Anti-HBc IgG negative
Vaccinated to HBV
66
How do you treat acute hepatitis B infection?
Supportive care
Cease substance use
Cease hepatotoxic substances
67
How do you treat chronic HBV infection?
Ultimate goal is seroconversion - i.e. HBsAg becomes anti-HBs - this is infrequently achieved, so practically the intent is suppression of HBV DNA to non-detectable levels --> reduces progression to liver failure and reduces risk of HCC.
```
2 classes of drugs used:
(1) Interferon: peginterferon alfa
Immune modulator
Time-limited treatment (48 weeks)
But more UE than direct antivirals
```
(2) Direct antiviral drugs: entecavir, tenofovir (nucleoside/ nucleotide analogues)
Inhibit HBV polymerase --> decreased viral replication
Long-term therapy required, often life-long
Generally well tolerated
