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Year 4 > Medicine - Gastroenterology > Flashcards

Medicine - Gastroenterology Flashcards

1
Q

Describe asparate transaminase (AST)

A
  • enzyme involved in amino acid metabolism
  • not specific to liver
  • raised with alcohol consumption as it is a mitochondrial enzyme and alcohol is metabolised mitochondrially
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2
Q

Describe alanine transaminase (ALT)

A
  • another liver enzyme, more specific to the liver than AST
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3
Q

Describe gamma glutamyl transferase (GGT)

A
  • enzyme found in many organs including the liver
  • if raised it suggests:
  • > obstruction
  • > drugs
  • > XS alcohol
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4
Q

Describe alkaline phosphatase (ALP)

A
  • dephosphorylating enzyme
  • found in the bile canaliculi system
  • raised in:
  • > bone disease
  • > adolescence
  • > obstructive liver disease
  • > pregnancy
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5
Q

Describe albumin

A
  • protein synthesised in the liver and recycled as it is needed for bilirubin movement
  • a good indicator of synthetic liver function
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6
Q

Describe prothrombin time (PT)

A
  • a measure of the time taken to convert prothrombin -> thrombin
  • a good indicator of synthetic liver function
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7
Q

What would the following LFT results suggest?

  • high AST, high ALT, low albumin
A
  • hepatocellular damage (chronic) e.g. chronic hepatitis
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8
Q

What would the following LFT results suggest?

  • high AST, high ALT, high albumin
A
  • hepatocellular damage (acute) e.g. acute hepatitis
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9
Q

What would the following LFT results suggest?

  • high ALP, high GGT
A

OBSTRUCTION
- head of pancreas cancer
PSC/PBC

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10
Q

What would the following LFT results suggest?

  • high ALP, normal GGT
A

Paget’s disease/bone disease
Pregnancy
Adolescence

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11
Q

What would the following LFT results suggest?

  • high GGT, normal ALP
    AST:ALT 2:1
A

XS alcohol consumption (AST raised as it is a mitochondrial enzyme)

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12
Q

What is acute liver failure and its causes?

A

Development of coagulopathy & encephalopathy in a patient with a previously healthy liver
Causes:
- infection
- drugs
- toxins
- vascular (Budd-Chiara syndrome, veno-occlusive disease)
- other: PBC, PSC, cancer

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13
Q

What is Budd-Chiari syndrome?

A

occlusion of hepatic vein, presents with triad of: (HAA)

  • hepatomegaly
  • ascites
  • abdominal pain
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14
Q

What are the features of acute liver failure?

A 
jaundice
fetor hepaticus
asterixis
hepatic encephalopathy
(if underlying chronic liver disease): spider navi, synthetic dysfunction, signs of portal HTN (splenomegaly, caput medusae, ascites, pancytopenia)
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15
Q

What is the pathophysiology underlying hepatic encephalopathy and how is it treated?

A

Liver fails and waste (ammonia) builds up in the blood
Reaches the brain where glutamate is converted into glutamine to clear the waste
XS glutamine = osmotic imbalance = cerebral oedema

Treatment:
Laxatives (lose NH3)
Rifaximin (an oral antibiotic that reduces the number of nitrogen forming gut bacteria)

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16
Q

What investigations should be carried out for acute liver disease?

A

Bloods: FBC (WCC, Hb), U&E, LFT, liver autoantibodies, paracetamol levels, EtOH, glucose, coag, virology, ferritin
Microbiology: blood cultures, urine culture, ascitic tap
Imaging: USS/CXR/doppler if Bud Chiari suspected

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17
Q

What is spontaneous bacterial pneumonitis

A

Infection of ascitic fluid without an apparent source

- >250/mm3 neutrophils

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18
Q

Describe how SAAG is used to analyse ascites

A

Serum ascites albumin gradient
SAAG >1.1g/dl = transudate (failures!)
SAAG <1.1g/dl = exudate (malignancy/infection)

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19
Q

How is acute liver failure treated

A

treat the cause

Monitor for complications -> sepsis, bleeding, hypoglycaemia, varices, ascites

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20
Q

How is ascites treated?

A

Low Na diet
Diuretics
Needle drainage

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21
Q

Describe acute alcohol withdrawal and the pathophysiology behind it

A

Abrupt cessation of alcohol in pts with dependence
A clinical diagnosis
Low blood alcohol triggers AWS (alcohol withdrawal syndrome)
- can occur 12-24hrs after last drink

Pathophys:
alcohol is a GABA (inhibitory) agonist
alcohol is a NMDA receptor antagonist (stops glutamate binding to NMDA receptors)
Therefore when alcohol is removed -> lack of GABA stimulation and XS glutamate signalling = XS excitatory neurotransmission

-> autonomic hyperactivity, tremor, hallucinations, seizures

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22
Q

What are the features of Wernicke’s encephalopathy

A 
Caused by thiamine deficiency (seen in alcoholics)
triad of:
- nystagmus
- ataxia
- delirium
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23
Q

What is korsakoffs syndrome?

A

chronic memory disorder due to thiamine deficiency

- severe short memory deficits and talking nonsense

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24
Q

What is delirium tremens

A

Delirium tremens (DTs) is a rapid onset of confusion usually caused by withdrawal from alcohol. When it occurs, it is often three days into the withdrawal symptoms and lasts for two to three days. Physical effects may include shaking, shivering, irregular heart rate, and sweating

25
How is acute alcohol withdrawal investigated
Good history Bloods: FBC, U&E, LFT, blood ethanol CT head CXR -> ? aspiration
26
How is AWS managed
Supportive GMAWS (guides dosing of...) Benzodiazepines Vitamin supplementation (pabrinex)
27
What questions should you ask to screen for alcohol excess?
CAGE - are you Concerned about how much you are drinking? - have you felt Annoyed by people criticising you/saying anything - do you feel Guilty about drinking? - have you ever had an Eye-opener?
28
Describe the pathophyiology of a paracetamol overdose
Paracetamol metabolised into a toxic compound called NAPQI -> causes cell apoptosis and liver/renal failure Normally at therapeutic doses NAPQI is detoxified by glutathione (but in large doses glutathione is depleted)
29
What are the features of paracetamol overdose
``` 24-48hrs: - Jaundice - Deranged LFTs >48hrs: - acute liver failure - hypoglycaemia - hepatic encephalopathy ```
30
How is paracetamol overdose treated?
- in first hour -> activated charcoal - within first 4hrs: do all bloods (including paracetamol levels - these will not be accurate if measured before 4hrs) - Use nomogram to assess risk of liver damage and if WITHIN 8hrs and high risk = IV acetyl cysteine (also called NAC parvolex) May need to contact: - psychiatry - liver transplant team
31
What are the S/Sx of opioid overdose?
Respiratory depression GI (vomiting, aspiration risk) Neuro (anywhere on a scale of confused -> comatosed)
32
How is an opioid overdose managed?
A-E (remember CXR and ABG!) | NALOXONE! (opioid antagonist) -> 400mcg given IV/IM initially, but can increase/reduce dose is needed
33
What are features of hyperbilirubinaemia?
jaundice pale fatty stools dark urine reduced synthesis of fat soluble vitamins (ADEK)
34
Name pre-hepatic causes of jaundice
``` XS haemolysis (malaria, yellow fever) Ineffective erythropoiesis (thalassaemia) ```
35
Name hepatic causes of jaundice
Drugs (can reduce UCBR uptake) Issues with conjugation (Gilberts, hypothyroid, hepatitis) Impaired CBR transport out of liver (PBC, PSC)
36
Name post-hepatic causes of jaundice
Obstruction - gallstones - HOP cancer - pancreatitis - PBS/PSC - drugs
37
What is Gilberts disease?
AD deficiency of UDP-glucoronyl transferase enzyme (converts UCBR -> CBR)
38
What is a mallory-weiss tear?
Non-variceal cause of an upper GI bleed Caused by a tear in the tissue lining the lower oesophagus Due to increased intra-thoracic pressure (coughing, wretching, straining, vomiting)
39
What is Boerhaave syndrome
Seen on CXR Pneumomediastinum Air in the mediastinum due to transmural rupture of oesophagus
40
How are ruptured oesophageal varices managed?
``` Fluids/blood transfusion Vasoactive drugs (terlipressin) Prophylactic Abx Endoscopic therapy (banding/ligation) Sengstaken tube TIPPS ```
41
Define chronic liver disease
Development of liver failure on a background of cirrhosis
42
What are the features of chronic liver disease?
``` Jaundice encephalopathy asterixis spider navi caput medusae ascites hypersplenism pancytopenia clubbing palmar erythema leukonychia dupytrens xanthelasmas gynaecomastia hair loss ```
43
Describe budd chiari syndrome
``` Hepatic vein outflow obstruction Presents with triad of: - hepatomegaly - ascites - abdominal pain ```
44
How is chronic liver disease managed?
``` Good nutrition Vitamins Avoid alcohol 6 monthly USS and APF measurements May think about liver transplant ```
45
Describe cirrhosis and its features
``` Irreversible liver damage Histologicaly: - nodular regeneration - bridging fibrosis - normal hepatic architecture ```
46
Name causes of cirrhosis
``` Alcohol Viral (HBV, HCV) Genetic disorders (Wilsons, HHC) NAFLD Autoimmune (PSC, PBC) Drugs (amiodarone, methotrexate) ```
47
What is the eradication treatment for H.pylori
Triple therapy for 7 weeks 1) PPI 2) antibiotic (clarithromycin) 3) antibiotic (amoxicillin) (use metronidazole for (3) if pen allergic)
48
Define coeliac disease and its pathophysiology
Gluten sensitive enteropathy Inappropriate t cell response to gluten causing SI villous atrophy Normally, IgA binds to the gluten component a-gliadin in the bowel so that it is targeted by immune cells and destroyed, but in coeliac disease the a-gliadin-IgA complex enters the lamina propria, TTG removes and amino acid from a-gliadin making it gliadin Then, a pro-inflammatory response is created against gliadin = disease!
49
At a histological level what are the features of coeliac disease?
Patchy mucosal inflammation Increased plasma cells and lymphocytes Loss of villous height + crypt hypertrophy (so overall intestinal thickness remains the same) Reduced SA and absorptive capacity of the bowel
50
What are the signs and symptoms of coeliac disease
``` Diarrhoea, flatulence Weight loss Fatigue Aphthous ulcers Angular stomatitis Nutritional deficiencies Anaemia (reduced Fe absorption) OP Amenorrhoea Neurological e.g. epilepsy Functional hyposplenism ```
51
How is coeliac disease investigated?
Bloods: FBC, WCC, Hb, ferritin/B12 (reduced absorption), anti-TTG antibodies Duodenal biopsies = take 4 biopsies before GFD commenced, which may show: - increased lymphocytes - villous atrophy - crypt hyperplasia
52
What criteria is used to grade coeliac disease?
MARSH, look at: - villi - crypts - no. of intraepithelial lymphocytes per 100 enterocytes
53
What are the complications of coeliac disease
EATL Refractory coeliac disease = persistent malabsorptive symptoms despite GFD for 6-12 months Type 1 = normal immunophenotype, type 2 = abnormal immunophenotype
54
Define irritable bowel syndrome and its aetiology
Mixed group of abdominal symptoms for which an organic cause cannot be found ?disrupted gut-brain axis = disordered intestinal motility and enhanced visceral perception ?microbial dysbiosis
55
What are its symptoms and how is IBS diagnosed?
``` bloating mucous urgency incomplete evacuation Diagnose if pt has recurrent abdominal pain with >2 of: - relief by defecation - altered stool form - altered bowel habit ``` (usually exacerbated by stress, menstruation, or post-infection)
56
Describe the symptoms of a patient presenting with carcinoid tumour and what this tumour secretes?
``` FAB-D Facial flushing Abdominal cramps Bronchoconstriction (wheeze) Diarrhoea ``` Due to neuroendocrine tumour secreting 5-HT (serotonin)
57
How is a carcinoid tumour investigated and treated?
Urine - look for hormone products (5-HIAA) USS/CT-guided tumour biopsy needed to confirm diagnosis ECHO - check for cardiac involvement Treatment -> resection is the only cure
58
What complication can occur when a carcinoid tumour is removed and what should you do to avoid this?
Carcinoid crisis -> sudden surge of hormone release | Give a somatostatin analogue (octreotide) to counteract this
59
Describe the King's criteria for a possible liver transplant
- High Lactate / pH <7.3 - High INR (or PT >100 seconds) - High creatinine >300umol/L - Grade 3/4 encephalopathy

Year 4 (28 decks)

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