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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
Q

How is acute alcohol withdrawal investigated

A

Good history
Bloods: FBC, U&E, LFT, blood ethanol
CT head
CXR -> ? aspiration

26
Q

How is AWS managed

A

Supportive
GMAWS (guides dosing of…)
Benzodiazepines
Vitamin supplementation (pabrinex)

27
Q

What questions should you ask to screen for alcohol excess?

A

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
Q

Describe the pathophyiology of a paracetamol overdose

A

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
Q

What are the features of paracetamol overdose

A 
24-48hrs:
- Jaundice
- Deranged LFTs
>48hrs: 
- acute liver failure
- hypoglycaemia
- hepatic encephalopathy
30
Q

How is paracetamol overdose treated?

A
  • 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
Q

What are the S/Sx of opioid overdose?

A

Respiratory depression
GI (vomiting, aspiration risk)
Neuro (anywhere on a scale of confused -> comatosed)

32
Q

How is an opioid overdose managed?

A

A-E (remember CXR and ABG!)

NALOXONE! (opioid antagonist) -> 400mcg given IV/IM initially, but can increase/reduce dose is needed

33
Q

What are features of hyperbilirubinaemia?

A

jaundice
pale fatty stools
dark urine
reduced synthesis of fat soluble vitamins (ADEK)

34
Q

Name pre-hepatic causes of jaundice

A 
XS haemolysis (malaria, yellow fever)
Ineffective erythropoiesis (thalassaemia)
35
Q

Name hepatic causes of jaundice

A

Drugs (can reduce UCBR uptake)
Issues with conjugation (Gilberts, hypothyroid, hepatitis)
Impaired CBR transport out of liver (PBC, PSC)

36
Q

Name post-hepatic causes of jaundice

A

Obstruction

  • gallstones
  • HOP cancer
  • pancreatitis
  • PBS/PSC
  • drugs
37
Q

What is Gilberts disease?

A

AD deficiency of UDP-glucoronyl transferase enzyme (converts UCBR -> CBR)

38
Q

What is a mallory-weiss tear?

A

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
Q

What is Boerhaave syndrome

A

Seen on CXR
Pneumomediastinum
Air in the mediastinum due to transmural rupture of oesophagus

40
Q

How are ruptured oesophageal varices managed?

A 
Fluids/blood transfusion
Vasoactive drugs (terlipressin)
Prophylactic Abx
Endoscopic therapy (banding/ligation)
Sengstaken tube
TIPPS
41
Q

Define chronic liver disease

A

Development of liver failure on a background of cirrhosis

42
Q

What are the features of chronic liver disease?

A 
Jaundice
encephalopathy
asterixis
spider navi
caput medusae
ascites
hypersplenism
pancytopenia
clubbing
palmar erythema
leukonychia
dupytrens
xanthelasmas
gynaecomastia
hair loss
43
Q

Describe budd chiari syndrome

A 
Hepatic vein outflow obstruction
Presents with triad of:
- hepatomegaly
- ascites
- abdominal pain
44
Q

How is chronic liver disease managed?

A 
Good nutrition
Vitamins
Avoid alcohol
6 monthly USS and APF measurements
May think about liver transplant
45
Q

Describe cirrhosis and its features

A 
Irreversible liver damage
Histologicaly:
- nodular regeneration
- bridging fibrosis
- normal hepatic architecture
46
Q

Name causes of cirrhosis

A 
Alcohol
Viral (HBV, HCV)
Genetic disorders (Wilsons, HHC)
NAFLD
Autoimmune (PSC, PBC)
Drugs (amiodarone, methotrexate)
47
Q

What is the eradication treatment for H.pylori

A

Triple therapy for 7 weeks

1) PPI
2) antibiotic (clarithromycin)
3) antibiotic (amoxicillin)

(use metronidazole for (3) if pen allergic)

48
Q

Define coeliac disease and its pathophysiology

A

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
Q

At a histological level what are the features of coeliac disease?

A

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
Q

What are the signs and symptoms of coeliac disease

A 
Diarrhoea, flatulence
Weight loss
Fatigue
Aphthous ulcers
Angular stomatitis
Nutritional deficiencies
Anaemia (reduced Fe absorption)
OP
Amenorrhoea
Neurological e.g. epilepsy
Functional hyposplenism
51
Q

How is coeliac disease investigated?

A

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
Q

What criteria is used to grade coeliac disease?

A

MARSH, look at:

  • villi
  • crypts
  • no. of intraepithelial lymphocytes per 100 enterocytes
53
Q

What are the complications of coeliac disease

A

EATL
Refractory coeliac disease = persistent malabsorptive symptoms despite GFD for 6-12 months
Type 1 = normal immunophenotype, type 2 = abnormal immunophenotype

54
Q

Define irritable bowel syndrome and its aetiology

A

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
Q

What are its symptoms and how is IBS diagnosed?

A 
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
Q

Describe the symptoms of a patient presenting with carcinoid tumour and what this tumour secretes?

A 
FAB-D
Facial flushing
Abdominal cramps
Bronchoconstriction (wheeze)
Diarrhoea

Due to neuroendocrine tumour secreting 5-HT (serotonin)

57
Q

How is a carcinoid tumour investigated and treated?

A

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
Q

What complication can occur when a carcinoid tumour is removed and what should you do to avoid this?

A

Carcinoid crisis -> sudden surge of hormone release

Give a somatostatin analogue (octreotide) to counteract this

59
Q

Describe the King’s criteria for a possible liver transplant

A
  • 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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