Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Medicine > Gastrointestinal > Flashcards

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the steps in the metabolism of alcohol?

A
  1. Alcohol –> acetaldehyde.
    ENZYMES: alcohol dehydrogenase, CYP2E1, Catalase.
  2. Acetaldehyde –> acetic acid.
    ENZYME: aldehyde dehydrogenase.
  3. Acetic acid –> acetyl Co A into the Krebs Cycle.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the mechanisms of alcohol toxicity?

A
  1. Toxic metabolites - e.g. acetaldehyde.
  2. Metabolism causes NAD –> NADH. Altered NAD:NADH ratio stimulates excess triglyceride production in the liver –> steatosis.
  3. CYP2E1 causes production of ROS –> inflammation and fibrosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the main MOA of alcohol?

A

Increased action of GABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the cause of Wernicke-Korsakoff syndrome?

A

Thiamine deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Explain the stages of alcoholic liver disease.

A
  1. Steatosis = fatty build-up
  2. Steatohepatitis = fatty + inflammation
  3. Fibrosis and cirrhosis = + scarring and nodularity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

List 5 symptoms of alcoholic liver disease.

A 
RUQ pain
Jaundice
Nausea and vomiting
Anorexia
Weight loss
Fatigue
GI bleeding
Abdominal distention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How would you treat alcohol use disorder?

A
  1. Brief intervention/ 5As/ motivational interviewing.
  2. Psychosocial support - CBT, AA
  3. Pharmacotherapy:
    1st line: naltrexone or acamprosate.
    2nd line: disulfiram
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

MOA of NALTREXONE.

CI

A

Opioid receptor antagonist.
Decreases pleasure from alcohol use and potentially decreases cravings.
CI = opioid use, liver failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

MOA of ACAMPROSATE

CI

A

Modulates glutamate transmission.

CI = ESKD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

DDX of upper GI bleeding

A 
VARICES: oesophageal or gastric
EROSION/ ULCER: oesophageal or gastric
MALLORY-WEISS TEAR
BOERHAAVE SYNDROME
AVM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the clinical features of Mallory-Weiss tears?

A

Primary symptom is haematemesis.

+/-
Pain
Hypovolemia –> vital sign abnormalities
Lower GI bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How would you manage a patient:

(1) with cirrhosis, to prevent varices?
(2) with known varices, to prevent a first variceal bleed?

A

(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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How would you treat a patient with ascites?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

List causes of abdominal distention and ascites.

A 
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
Q

What tests would you order on ascitic fluid?

How would you interpret?

A

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
Q

What are the complications of GORD?

A 
Oesophagitis
Upper GI bleeding
Barrett's oesophagus
Stricture
Adenocarcinoma
Respiratory disorders - e.g. worsening of asthma
30
Q

What is your approach to diagnosing GORD?

A
  • 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
Q

List red flags for GORD.

A 
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
Q

How would you manage Barrett’s oesophagus?

A

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
Q

What are the complications of H pylori infection?

A

Gastritis
Peptic ulcer disease
Gastric adenocarcinoma
Gastric lymphoma

34
Q

Helicobacter pylori
Indications for testing?
Types of investigations

A

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
Q

Explain the physiology of gastric acid secretion.

A

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
Q

HIATUS HERNIA
What are the 2 types of hiatus hernia?
How do the present?
What are their complications?

A

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
Q

How would you diagnose a hiatus hernia?

A

Usually:

  • CXR –> air-fluid level in thorax (paraoesophageal) OR
  • Upper endoscopy OR
  • Barium swallow
38
Q

How would you treat a hiatus hernia:
Sliding?
Paraoesophageal?

A 
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
Q

PROTON PUMP INHIBITOR
Use
How to use
UE

A

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
Q

DDX for dysphagia

A
  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
  1. EXTRINSIC COMPRESSION
    - Neck abscess
    - Goiter
  2. NEUROLOGICAL
    - Stroke
    - Parkinson’s
    - MS
    - MND
    - Muscular dystrophy
41
Q

Achalasia

  • Cause?
  • Pathology?
  • Investigations and findings?
  • Treatment?
A

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
Q

Explain the aetiology and pathophysiology of anal fissures.

A

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
Q

What are the classical clinical features of anal fissures?

A

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
Q

How would you investigate/diagnose an anal fissure?

A 
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
Q

How would you treat an anal fissure?

A

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
Q

Explain the pathophysiology of PUD.

A

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
Q

List complications of PUD.

A 
Erodes into/through structures -- 
- GI bleeding
- Perforation
- Fistula
Chronic inflammation and scarring - 
- Stricture -- Gastric outlet obstruction
48
Q

What is the first line therapy for H. pylori-induced PUD?

A

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
Q

What are the clinical features of hepatitis?

A 
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
Q

How is Hepatitis A transmitted?

List risk factors for hepatitis A infection.

A

Faecal-oral transmission.

RISK:

  • Travel to endemic area
  • Ingestion of contaminated foods
  • Not immunised for hepatitis A
  • MSM
  • Occupational exposure - HCW, day-care
51
Q

What are the possible consequences of hepatitis A infection?

A

Does NOT cause chronic hepatitis.

Can rarely result in fulminant hepatitis.

52
Q

How would you confirm the diagnosis of suspected hepatitis A infection?

A

LFTs - raised esp ALT & AST (hepatitic)

IgM anti-HAV +

53
Q

How is hepatitis A treated?

A

Supportive care
Self-limited condition
Vaccination

54
Q

What is the most common cause of:

  • viral gastroenteritis?
  • viral gastroenteritis in children?
A

Norovirus is overall the most common cause of viral gastroenteritis.
In children, rotavirus is the most common cause.

55
Q

List risk factors for gastroenteritis.

A

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
Q

What is your work-up of acute gastroenteritis?

A 
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
Q

How would you approach the treatment of gastroenteritis?

A 
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
  6. Prevention -
    - Proper hand hygiene
    - Avoid undercooked foods, dirty water
    - Vaccination: rotavirus (cholera and typhoid for travel to endemic areas)
58
Q

How is Hepatitis B transmitted?

A
  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
Q

How often does HBV become chronic?

A

Risk of chronic HBV depends on the age of the patient.
Perinatal infection = 90% risk
Children = 20-50%
Adult = <5%

60
Q

How does HBV replicate?

A

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
Q

What serology is ordered for HBV infection?

Explain the interpretation.

A 
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
Q

What is indicated by:
HBsAg positive
anti-HBs negative
anti-HBc IgM positive

A

Active HBV infection

63
Q

What is indicated by:
HBsAg positive
Anti-HBs negative
Anti-HBc IgG positive

A

Chronic HBV infection

64
Q

What is indicated by
HBsAg Negative
Anti-HBs positive
Anti-HBc IgG positive

A

Immune after resolved HBV infection

65
Q

What is indicated by
HBsAg Negative
Anti-HBs Positive
Anti-HBc IgG negative

A

Vaccinated to HBV

66
Q

How do you treat acute hepatitis B infection?

A

Supportive care
Cease substance use
Cease hepatotoxic substances

67
Q

How do you treat chronic HBV infection?

A

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

Medicine (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions