Brainscape's Knowledge GenomeTM

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


See full index

YEAR 3 CONDITIONS > GASTROINTESTINAL > Flashcards

GASTROINTESTINAL Flashcards

1
Q

Define Achalasia

A

Normal muscular activity of oesophagus is absent or uncoordinated.
Due to FAILURE/INCOMPLETE RELAXATION OF LOWER OESOPHAGEAL SPHINCTER.
=> delay in passage of swallowed material into stomach.

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

Aetiology of Achalasia

A

Degeneration of ganglion cells of myenteric plexus in oesophagus.
Unknown cause.

CHAGAS DISEASE

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

Epidemiology of Achalasia

A

May occur at any age
Affects both sexes equally
Annual incidence - 1/100,000

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

Presenting symptoms of Achalasia

A

INSIDIOUS onset and gradual progression of:
Intermittent dysphagia involving solids and liquids
Difficulty belching
Regurgitation (particularly at night)
Heartburn
Chest pain (atypical/cramping, retrosternal)
Weight loss (because they are eating less)

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

Signs of Achalasia on examination

A

Aspiration pneumonia
Malnutrition
Weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Investigations for Achalasia

A 
CXR:
Widened mediastinum 
Double right heart border (dilated oesophagus) 
Air-fluid level in the upper chest 
Absence of the normal gastric air bubble

Barium swallow:
Dilated oesophagus which smoothly tapers down to the sphincter (beak-shaped)

Endoscopy: exclude malignancy

Manometry:
Elevated resting LOS pressure (> 45 mm Hg).
Incomplete LOS relaxation.
Absence of peristalsis in the smooth muscle portion of the oesophagus.
Serology for antibodies against T. cruzi if CHAGAS DISEASE

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

Define Acute Cholangitis

A

Infection of the bile duct.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Aetiology of Acute Cholangitis

A

Obstruction of the gallbladder or bile duct due to stones.
ERCP.
Tumours (e.g. pancreatic, cholangiocarcinoma).
Bile duct stricture or stenosis
Parasitic infection (e.g. ascariasis).

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

Epidemiology of Acute Cholangitis

A

9% of patients admitted to hospital with gallstone disease will have acute cholangitis.
M=F.
50-60yrs.
Racial distribution = fair-skinned ppl (same as gallstone disease).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Presenting symptoms of Acute Cholangitis

A

CHARCOT’S TRIAD:
RUQ
Jaundice
Fever with rigors

Suppurative = REYNOLD’S PENTAD:
Mental confusion
Septic shock - hypotension

May complain of pruritus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Signs of Acute Cholangitis on examination

A 
Fever 
RUQ tenderness
Murphy’s sign positive
Mild hepatomegaly
Jaundice 
Mental status changes
Sepsis
Hypotension
Tachycardia
Peritonitis (uncommon - check for alternative diagnosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Investigations for Acute Cholangitis

A

Bloods:
FBC - high WCC.
CRP/ESR: possibly raised.
LFTs: typical pattern of obstructive jaundice (raised ALP + GGT).
U&Es: may be signs of renal dysfunction.
Blood cultures: check for sepsis.
Amylase: may be raised if the lower part of the common bile duct is involved.

Imaging:
X-ray KUB: for stones.
Abdominal ultrasound: for stones/dilation of common bile duct.
Contrast-enhanced CT/MRI
MRCP: to detect non-calcified stones.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Management plan for Acute Cholangitis

A

Resuscitation if in septic shock.
Broad-spectrum antibiotics: once blood cultures have been taken (select drugs that are effective against anaerobes and Gram-negative organisms: e.g. cefuroxime + metronidazole).
Endoscopic biliary drainage usually required to treat underlying obstruction.

Depends on severity:
Stage 1 (Mild)
- Antimicrobial therapy
- Percutaneous, endoscopic or operative intervention for non-responders.
Stage 2 (Moderate)
- Early percutaneous/ endoscopic drainage.
- Endoscopic biliary drainage recommended.
Stage 3 (Severe)
NOTE: severe cholangitis counts as including shock, conscious disturbance, acute lung injury, AKI, hepatic injury or DIC.
- Treatment of organ failure with ventilatory support, vasopressors etc.
- Urgent percutaneous or endoscopic drainage.
- Definitive treatment required once the clinical picture improves.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Possible complications of Acute Cholangitis

A 
Liver abscesses 
Liver failure 
Bacteraemia 
Gram-negative sepsis 
Septic shock 
AKI 
Organ dysfunction 
Percutaneous or endoscopic drainage can lead to:
Intra-abdominal or percutaneous bleeding, sepsis, fistulae and bile leakage.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Prognosis for patients with Acute Cholangitis

A

Mortality between 17-40%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Define Alcoholic Hepatitis

A

Inflammatory liver injury caused by chronic heavy intake of alcohol

17
Q

Aetiology of Alcoholic Hepatitis

A

THREE forms of liver disease caused by excessive alcohol intake:
Alcoholic fatty liver (steatosis)
Alcoholic hepatitis
Chronic cirrhosis

Severe exposure to alcohol = hepatitis (reversible with abstinence)
Repeated attacks = cirrhosis

Exposure to alcohol = steatosis (reversible with abstinence)
Continued exposure = cirrhosis

Centrilobular ballooning
Degeneration and necrosis of hepatocytes
Steatosis – fatty change
Neutrophilic inflammation
Cholestasis – condition in which bile cannot flow from liver to the duodenum
Mallory-hyaline inclusions (eosinophilic intracytoplasmic aggregates of cytokeratin intermediate filaments)
Giant mitochondria

18
Q

Epidemiology of Alcoholic Hepatitis

A

Occurs in 10-35% of heavy drinkers

19
Q

Presenting symptoms of Alcoholic Hepatitis

A 
May remain asymptomatic and undetected 
May be mild illness with:
Nausea 
Malaise 
Epigastric pain 
Right hypochondrial pain 
Low-grade fever 
More severe presenting symptoms include:
Jaundice 
Abdominal discomfort or swelling 
Swollen ankles 
GI bleeding

Long history of heavy drinking is required for development of alcoholic hepatitis (around 15-20 years)
Events may trigger the disease (e.g. aspiration pneumonia, injury)

20
Q

Signs of Alcoholic Hepatitis on examination

A 
Signs of Alcohol Excess
Malnourished 
Palmar erythema 
Dupuytren's contracture 
Facial telangiectasia – red lines appear due to widened venules 
Parotid enlargement 
Spider naevi 
Gynaecomastia 
Testicular atrophy 
Hepatomegaly 
Easy bruising
Signs of Severe Alcoholic Hepatitis
Febrile (in 50% of patients) 
Tachycardia 
Jaundice 
Bruising 
Encephalopathy (e.g. liver flap, drowsiness, disorientation) – caused by build up of ammonia in blood (which is normally removed by the liver) – crosses blood-brain barrier
Ascites 
Hepatomegaly 
Splenomegaly
21
Q

Investigations for Alcoholic Hepatitis

A 
Bloods
FBC:
Low Hb
High MCV
High WCC
Low platelets
LFTs:
High AST + ALT
High bilirubin
High ALP + GGT
Low albumin

U&Es:
Urea and K+ tend to be low

Clotting: prolonged PT is a sensitive marker for significant liver damage

Ultrasound - check for other causes of liver impairment (e.g. malignancy)

Upper GI Endoscopy - investigate varices

Liver Biopsy - can help distinguish from other causes of hepatitis

EEG - slow-wave activity indicates encephalopathy

22
Q

Management plan for Alcoholic Hepatitis

A

Acute:
Thiamine
Vitamin C and other multivitamins (can be given as Pabrinex)
Monitor and correct K+, Mg2+ and glucose
Ensure adequate urine output
Treat encephalopathy with oral lactulose/phosphate enemas – decrease ammonia generation by bacteria
Ascites - manage with diuretics (spironolactone with/without furosemide)
Therapeutic paracentesis (removing fluid)
Glypressin and N-acetylcysteine for hepatorenal syndrome

Nutrition:
Via oral or NG feeding is important
Protein restriction should be avoided unless the patient is encephalopathic
Nutritional supplementation and vitamins (B group, thiamine and folic acid) should be started parenterally initially, and continued orally

Steroid Therapy:
reduce short-term mortality for severe alcoholic hepatitis

23
Q

Possible complications of Alcoholic Hepatitis

A
  • Acute liver decompensation
  • Hepatorenal syndrome
    = cirrhosis + ascites + renal failure (if other causes of renal impairment excluded)
  • Abnormalities in blood vessel tone kidneys = vessels constrict
    because of dilatation of blood vessels in the splanchnic circulation (supplying the intestines), which is mediated by factors released by liver disease – e.g. nitric oxide, prostaglandins
    Splanchnic vasodilation = reduced effective volume of blood detected by the juxtaglomerular apparatus = activation of RAS and vasoconstriction of vessels in the kidney -> kidney failure.
    -Cirrhosis
24
Q

Prognosis for patients with Alcoholic Hepatitis

A

Mortality:
First month = 10%
First year = 40%
If alcohol intake continues, most will progress to cirrhosis within 1-3 years
Maddrey’s discriminant function/Glasgow alcoholic hepatitis score to calculate prognostic score

25
Q

Define Alcohol Withdrawal

A

The symptoms that may occur when a person has been drinking too much alcohol on a regular basis and suddenly stops drinking.

26
Q

Aetiology of Alcohol Withdrawal

A

Chronic alcohol consumption suppresses activity of glutamate (excitatory neurotransmitter) -> body compensates by increasing sensitivity to glutamate.
Alcohol consumption stops = increased glutamate activity -> excitatory symptoms

27
Q

Epidemiology of Alcohol Withdrawal

A

If untreated, 6% of alcohol-dependent patients develop symptoms
Up to 10% of them = delirium tremens

28
Q

Presenting symptoms of Alcohol Withdrawal

A 
- History of high alcohol intake 
Mild Symptoms:
Insomnia and fatigue 
Tremor 
Mild anxiety/feeling nervous 
Mild restlessness/agitation 
Nausea and vomiting 
Headache 
Sweating 
Palpitations 
Anorexia 
Depression 
Craving alcohol

More severe symptoms:
Hallucinations
Withdrawal seizures (generalised tonic-clonic)
Delirium tremens
- DEFINITION: an acute confusional state often seen as withdrawal syndrome in chronic alcoholics and caused by sudden cessation of drinking alcohol. It can be precipitated by a head injury or an acute infection causing abstinence from alcohol.
- FEATURES:
Anxiety
Tremor
Sweating
Vivid and terrifying visual and sensory HALLUCINATIONS (usually of animals and insects)
Can be FATAL

29
Q

Investigations for Alcohol Withdrawal

A

NO investigations

30
Q

Management plan for Alcohol Withdrawal

A

Chlordiazepoxide - reduces symptoms of alcohol withdrawal

Barbiturates may be used if refractory to benzodiazepines e.g. phenobarbitol

Thiamine (Pabrinex) - prevents progression to Wernicke-Korsakoff syndrome

31
Q

Possible complications of Alcohol Withdrawal

A

Can die/have seizures if left untreated

32
Q

Prognosis for Alcohol Withdrawal

A

Delirium tremens = mortality of 35% if untreated

Mortality < 2% with early detection and treatment

33
Q

Define Amyloidosis

A

Heterogenous group of diseases characterised by extracellular deposition of amyloid fibrils

34
Q

Aetiology of amyloidosis

A

Amyloid fibrils = polymers of low-molecular-weight subunit proteins.
Derived from proteins that undergo conformational changes to adopt anti-parallel beta-pleated sheet configuration.
Deposition disrupts structure and function of normal tissue.

Can be systemic or localised, e.g. in pancreatic islets of Langerhans (T2DM), cerebral cortex (Alzheimer’s), cerebral blood vessels (amyloid angiopathy), and in bones and joints.

Classified according to the fibril subunit proteins
Type AA - serum amyloid A protein aka secondary amyloidosis.
Affects kidneys, liver and spleen.

Type AL - monoclonal immunoglobulin light chains
aka primary amyloidosis
Affects kidneys, heart, nerves, gut, vascular.

Type ATTR (familial amyloid polyneuropathy) - genetic-variant transthyretin
aka familial amyloidosis
Usually causes a sensory or autonomic neuropathy +/- renal or cardiac involvement
35
Q

Epidemiology of Amyloidosis

A

AA - incidence of 1-5% amongst patients with chronic inflammatory diseases
AL - 300-600 cases in the UK per year
Hereditary Amyloidosis - accounts for 5% of patients with amyloidosis

36
Q

Presenting symptoms of Amyloidosis

A

Renal - proteinuria, nephrotic syndrome, renal failure

Cardiac - restrictive cardiomyopathy, heart failure, arrhythmia, angina

GI - macroglossia (characteristic of AL), hepatosplenomegaly, gut dysmotility, malabsorption, bleeding

Neurological - sensory and motor neuropathy, autonomic neuropathy, carpal tunnel syndrome

Skin - waxy skin and easy bruising, purpura around the eyes (characteristic of AL), plaques and nodules

Joints - painful asymmetrical large joints, enlargement of anterior shoulder

Haematological - bleeding tendency

37
Q

Investigations for Amyloidosis

A

Urine - check for proteinuria, free immunoglobulin light chains (in AL)

Bloods:

  • CRP/ESR
  • Rheumatoid factor
  • Immunoglobulin levels
  • Serum protein electrophoresis
  • LFTs
  • U&Es

SAP Scan - radiolabelled SAP will localise the deposits of amyloid

Tissue Biopsy – to diagnose amyloidosis and identify amyloid fibril protein

YEAR 3 CONDITIONS (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions