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Finals Revision > Gastroenterology + liver > Flashcards

Gastroenterology + liver Flashcards

1
Q

Define acute cholangitis

A

= infection and inflammation of the biliary tree, most caused by obstruction. Is a surgical emergency and has high mortality due to sepsis and septicaemia.

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2
Q

What was acute cholangitis previously called

A

ascending cholangitis

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3
Q

Causes of acute cholangitis

A
  1. Gallstones – in common bile duct, cause obstruction
  2. Infection due to ERCP procedure
  3. Benign biliary stricture e.g., from surgery
  4. Malignant obstruction – bile duct tumour, gallbladder tumour, pancreatic tumour
  5. Pancreatitis
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4
Q

Bacteria that cause acute cholangitis

A
  • Escherichia Coli
  • Klebsiella species
  • Enterococcus species
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5
Q

Risk factors for acute cholangitis

A
  • 50+ yo
  • Hx of gallstones
  • Primary or secondary sclerosing cholangitis
  • Stricture of biliary tree – benign or malignant
  • Post procedure injury of bile ducts
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6
Q

Symptoms of acute cholangitis

A 
RUQ pain
Fever
Jaundice
Hypotension 
Confusion 
Pale stools
Pruritis
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7
Q

What triad describes the symptoms of acute cholangitis?

A

CHARCOT’S TRIAD
RUQ pain
Fever
Jaundice

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8
Q

What pentad describes the symptoms of acute cholangitis?

A 
REYNOLD'S PENTAD
RUQ pain 
Fever
Jaundice
Hypotension 
Confusion
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9
Q

IX for acute cholangitis

A 
Raised inflammatory markers
Raised bilirubin 
Abdominal US
MRCP
ERCP
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10
Q

What is MRCP?

A

Magnetic resonance cholangio-pancreatography (for visualising the biliary tree)

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11
Q

What is ERCP and what can be done during ERCP?

A

Endoscopic retrograde cholangiopancreatography

o Insert an endoscope down the oesophagus, past the stomach and to the duodenum. Through the sphincter of Oddi into the common bile duct.

o Can do the following during ERCP:
 Cholangio-pancreatography – inject contrast into the duct and use x-ray to visualise the biliary system
 Sphincterotomy – cut in the sphincter to allow stones to pass
 Stone removal
 Balloon dilation for strictures
 Biliary stenting to maintain patent bile duct
 Biopsy

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12
Q

Mx for acute cholangitis

A
  • Acute management for sepsis and acute abdomen
    o NBM
    o IV fluids
    o Blood cultures
    o IV abx
    o Oxygen if required
    o Serum lactate
    o Catheterise / measure urine output
  • ERCP after 24-48 hours to relieve obstruction
  • Percutaneous transhepatic cholangiogram (PTC)
    o Radiologically guided insertion of a drain through the skin and liver into the bile ducts.
    o Drain relieves the obstruction
    o Stent can be inserted
    o For patients not suitable for ERCP or where ERCP has failed
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13
Q

What are the key features of acute pancreatitis

A

Inflammation of the pancreas. Rapid onset, after an episode of acute pancreatitis normal function usually returns.

Is mild in 80% of cases but in 20% of cases it can develop into severe life threatening disease.

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14
Q

Pathology of acute pancreatitis

A
  • Self perpetuating pancreatic enzyme mediated autodigestion

- Oedema and fluid shift ( extracellular fluid is trapped in the gut, peritoneum and retroperitoneum) = hypovolaemia

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15
Q

3 main causes of acute pancreatitis

A

Gallstones
Alcohol
Post ERCP

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16
Q

All the causes of acute pancreatitis

A

I GET SMASHED

  • I = idiopathic
  • G = gallstones
  • E = ethanol
  • T – trauma
  • S = steroids
  • M = mumps
  • A = autoimmune
  • S = scopion sting
  • H = hyperlipidaemia
  • E = ERCP
  • D = drugs e.g., furosemide, thiazide diuretics and azathioprine
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17
Q

Symptoms of acute pancreatitis

A
  • Severe epigastric pain
  • Radiating through to back
  • Sitting forwards may relieve pain
  • Associated vomiting
  • Abdominal tenderness
  • Systemically unwell – fever, tachycardia
  • Cullen’s sign = periumbilical discolouration
  • Grey-Turner’s sign = flank discolouration
  • Purtscher retinopathy = ischaemic retinopathy that can cause temporary/permanent blindness
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18
Q

Ix for acute pancreatitis

A
  1. Serum amylase
    a. >3 times upper limit of normal
    b. Levels don’t correlate with disease severity
    c. Other causes of raised amylase = pancreatic pseudocyst, mesenteric infarct, perforated viscus, acute cholecystitis, diabetic ketoacidosis
  2. Serum lipase
    a. More sensitive and specific than serum amylase
    b. Longer half life than serum amylase = can be useful for late presentations (>24 hrs)
  3. CRP
  4. Ix for Glasgow score
    a. FBC for WCC
    b. U&E for urea
    c. LFT for transaminases and albumin
    d. Calcium
    e. ABG for O2 and glucose
  5. US abdomen – to look for gallstones or biliary obstruction
  6. Contrast enhanced CT – for complications of pancreatitis
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19
Q

Scoring system for acute pancreatitis

A 
GLASGOW SCORE
-	Used to assess the severity of pancreatitis 
-	Score:
o	0-1 = mild
o	2 = moderate 
o	3+ = severe, transfer to ITU/HDU
-	One point for each of the following (PANCREAS)
P = PaO2, <8
A = age, >55
N = neutrophils, WBCs >15
C = calcium, <2
R = uRea, >16
E = enzymes, LDH >600 or AST/ALT >200
A = albumin, <32
S = sugar, Glucose >10
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20
Q

Mx for acute pancreatitis

A
  1. Acute mx:
    a. Fluid resuscitation (crystalloid)
    b. Analgesia (opioids)
    c. NBM with enteral nutrition
    d. Abx only if there is evidence of specific infection e.g. abscess or infected necrotic area
  2. ERCP for gallstone treatment
    Most improve within 3-7 days
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21
Q

Complications of acute pancreatitis

A
  1. Early complications = shock, ARDS, renal failure, DIC, sepsis
  2. Late complications (>1 week)
  3. Necrosis of the pancreas
  4. Infection of the necrotic area
  5. Abscess formation
  6. Acute peripancreatic fluid collections
  7. Pseudocysts (collections of pancreatic juice)
  8. Chronic pancreatitis
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22
Q

Chronic pancreatitis definition

A

Chronic inflammation of the pancreas that results in fibrosis and reduced function of pancreatic tissue. Affects exocrine and endocrine functions.
Similar symptoms to acute pancreatitis but less intense and longer lasting.

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23
Q

Causes of chronic pancreatitis

A
  1. Alcohol (80% of cases)
  2. Unexplained
  3. Genetic – cystic fibrosis, haemochromatosis
  4. Ductal obstruction – tumours, stones, structural abnormalities
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24
Q

Symptoms of chronic pancreatitis

A
  • Chronic epigastric pain
  • Pain worse 15 to 30 minutes after a meal
  • Steatorrhoea – develops 5 to 25 years after onset of pain (lack of pancreatic enzyme lipase that’s secreted into GI tract)
  • DM – 20 years after symptoms begin
  • Damage/strictures to duct system
  • Formation of pseudocysts or abscesses
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25
Q

Ix for chronic pancreatitis

A
  • Abdominal x-ray – pancreatic calcification
  • CT – pancreatic calcification (more sensitive and specific than x-ray)
  • Faecal elactase
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26
Q

Mx for chronic pancreatitis

A
  1. Abstinence from alcohol and smoking
  2. Analgesia
  3. Replacement pancreatic enzymes = CREON
  4. Subcutaneous insulin regime
  5. ERCP with stenting for strictures and obstruction
  6. Surgery for:
    a. Severe chronic pain – drain ducts and remove inflamed pancreatic tissue
    b. Obstruction to biliary system and pancreatic duct
    c. Pseudocysts
    d. Abscesses
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27
Q

Types of alcohol related liver disease

A

Progression of alcoholic liver disease:

  1. Alcohol related fatty liver = build up of fat in the liver, if drinking stops this process reverses in around 2 weeks
  2. Alcoholic hepatitis = inflammation of the liver. Binge drinking is associated with the same affects. Reversible with abstinence in mild cases.
  3. Cirrhosis = liver is composed of scar tissue, is irreversible. Stopping drinking can prevent further damage.
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28
Q

Screening questions for harmful alcohol drinking

A

CAGE screening questions =

  1. C = Ever thought you need to Cut down?
  2. A = Do you get Annoyed at others commenting on your drinking?
  3. G = Do you feel Guilty about drinking?
  4. E = do you need an Eye opener in the morning?

AUDIT questionnaire (alcohol use disorders identification test) – 10 questions to screen for harmful alcohol use. Score of 8+ = harmful use.

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29
Q

Complications of harmful alcohol use (6 things)

A
  1. Alcohol related liver disease
  2. Cirrhosis + hepatocellular carcinoma
  3. Alcohol dependence and withdrawal
  4. Wernicke-Korsakoff syndrome
  5. Pancreatitis
  6. Alcoholic cardiomyopathy
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30
Q

signs of liver disease

A
  1. Right upper quadrant pain
  2. Jaundice
  3. Hepatomegaly
  4. Spider naevi – cutaneous telangiectasia
  5. Palmar erythema – thenar and hypothenar eminences affects with central sparing of the palm
  6. Gynaecomastia
  7. Bruising – due to abnormal clotting
  8. Ascites – accumulation of fluid in the peritoneal cavity, causing abdominal swelling
  9. Caput medusae – engorged superficial epigastric veins
  10. Asterixis – flapping tremor in decompensated liver disease
  11. Haematemesis and melaena – due to GI bleeding (oesophageal varices, gastric irritation and coagulopathy)
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31
Q

Ix for alcohol related liver disease

A

• Bloods
o FBC – raised MCV
o LFTs – raised ALT and AST (transaminases), raised GGT, ALP raised later in disease. Low albumin. High bilirubin.
o Clotting – raised PPT
o U&Es – deranged due to hepatorenal syndrome
• US – raised echogenicity of liver e.g., fatty changes
• Endoscopy – oesophageal varices
• CT and MRI scans – fatty infiltration of liver, hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessels, ascites
• Liver biopsy – diagnosis of alcohol related hepatitis or cirrhosis (recommended before using steroid tx)

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32
Q

What is hepatorenal syndrome?

A

Hepatorenal syndrome – cirrhosis + ascites + renal failure

- Abnormal haemodynamics cause splanchnic and systemic vasodilation but renal constriction

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33
Q

Mx for alcohol related liver disease

A
  1. Stop alcohol, stop smoking, lose weight
  2. Detoxication regime
  3. Thiamine + multivitamins
  4. High protein diet
  5. Treat cirrhosis complications: portal HTN, varices, ascites (fluid restriction + diuretics), hepatic encephalopathy (lactulose, correct electrolytes, nurse with head tilted)
  6. Steroids (prednisolone) – improve short term outcomes. Need to treat any infections and GI bleeding first.
  7. Pentoxyphylline
  8. Referral for liver transplant
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34
Q

What calculation is used to see if steroids are appropriate for a patient with alcohol related liver disease?

A

Maddrey’s discriminant function used during acute episodes to decide who needs prednisolone therapy

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35
Q

Alcohol withdrawal symptoms (by hours after stopping alcohol)

A
  • 6-12hrs after stopping = sweating, tremor, headache, craving, anxiety
  • 12-24hrs after stopping = hallucinations
  • 24-48hrs after stopping = seizures
  • 24-72hrs after stopping = delirium tremens
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36
Q

Why do alcoholic patients get delirium tremens?

A

o When alcohol is removed from the system GABA under functions (GABA = relaxing effect) and glutamate over functions (glutamate/NMDA receptors = excitatory effect) = extreme excitability of the brain with excess adrenergic activity

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37
Q

Symptoms of delirium tremens

A 
	Confusion
	Agitation
	Delusions and hallucinations
	Tremor
	Tachycardia
	HTN
	Hyperthermia 
	Ataxia 
	Arrhythmias
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38
Q

Mx of delirium tremens

A

o Give chlordiazepoxide / diazepam and IV pabrinex (vitamin B)

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39
Q

What is an anal fissure?

A

longitudinal or elliptical tears in the skin of the distal anal canal characterised by pain on defecation and rectal bleeding. Acute if present for <6 weeks, chronic if present for >6 weeks.

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40
Q

Risk factors for anal fissures

A
  • Constipation
  • IBD
  • HIV, syphilis, herpes
  • Pregnancy
  • Opioid analgesia
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41
Q

Symptoms of anal fissures

A
  • Pain on defecation
  • Tearing sensation on passing stool
  • Fresh blood on stool or paper
  • Anal spasm
  • 90% occur on the posterior midline – if the fissure is elsewhere consider other underlying causes such as Crohn’s disease
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42
Q

Diagnosis of anal fissures

A

Clinical diagnosis, do PR

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43
Q

Management for anal fissures

A
  1. Soften stool – high fibre, high fluids, bulk forming laxative (ispaghula husk), 2nd line is lactulose
  2. Lubricants e.g., petroleum jelly before defecation
  3. Topical anaesthetics
  4. Analgesia
  5. Chronic anal fissure – topical GTN, surgery (sphincterotomy) or botulinum toxin
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44
Q

Name the 4 types of laxative, give examples and their indications

A
  1. Bulk forming (Fybogel, ispaghula husk) - low intake dietary fibre
  2. Stimulant (Senna, bisacodyl) - short term relief of acute constipation
  3. Osmotic (lactulose, movicol) - chronic constipation
  4. stool softener (decussate sodium) - chronic constipation
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45
Q

What is appendicitis and what’s the pathology?

A

inflammation of the vermiform appendix, most likely due to obstruction of the lumen of the appendix by faecolith, normal stool, infective agents or lymphoid hyperplasia. Inflammation of the appendix can lead to oedema and ischaemia +/- perforation (peritonitis).

Most common acute abdominal condition requiring surgery.

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46
Q

Symptoms of appendicitis

A
  • Abdominal pain – periumbilical that radiates to the right iliac fossa.
  • Worse pain on coughing/going over speed bumps. Children cant hop on R leg.
  • Tenderness at McBurney’s point
  • Loss of apetite
  • Nausea and vomiting
  • Low grade fever
  • Rovsing’s sign
  • Psoas sign
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47
Q

Where is McBurney’s point?

A

1/3rd the distance from the anterior superior iliac spine to the umbilicus

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48
Q

What is Roving’s sign?

A

palpation of L iliac fossa causes pain in R iliac fossa in acute appendicitis

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49
Q

What is Psoas sign?

A

pain on extending hip if retrocaecal appendix in acute appendicitis

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50
Q

What are the symptoms of peritonitis you may see with a ruptured appendix?

A
  • Guarding/rigidity on abdominal palpation
  • Rebound tenderness in RIF
  • Percussion tenderness
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51
Q

Differentials for acute appendicitis

A
  • Ectopic pregnancy (hCG)
  • Ovarian cysts
  • Meckel’s diverticulum (malformation of distal ileum, present in 2% of population)
  • Mesenteric adenitis in children following tonsillitis/URTI
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52
Q

Ix for appendicitis

A
  1. Mostly clinical diagnosis
  2. Raised inflammatory markers
  3. Neutrophil predominant leucocytosis
  4. Urine analysis – to rule out pregnancy, renal colic and UTI
  5. US scan – useful in females where pelvic organ pathology is suspected
  6. CT scan useful but rarely done in UK
  7. Diagnostic laparoscopy – for negative investigations but high clinical suspicion
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53
Q

Mx for appendicitis

A
  1. Appendicectomy – laparoscopic
  2. Prophylactic IV abx
  3. Perforated appendix = abdominal lavage
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54
Q

Complications of appendicitis

A
  • Ruptured appendix and peritonitis
  • Appendix mass – omentum surrounds and sticks to inflamed appendix, forming mass in RIF. Abx and supportive treatment. Appendicectomy once acute condition resolves.
  • Of appendicectomy – bleeding, infection, pain, scars, damage to bowels/bladder, removal of normal appendix, anaesthetic risks, VTE
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55
Q

What is the child-pugh score

A

Child-Pugh score

  • Used to assess severity of liver cirrhosis
  • Need to know – bilirubin, albumin, PPT, ascites, hepatic encephalopathy
  • Can get a score classed as A, B or C
  • Class B or C = listing for liver transplant
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56
Q

What are the causes of ascites without portal hypertension?

A

Hypoalbuminaemia

  • Nephrotic syndrome
  • Severe malnutrition

Malignancy
- Peritoneal carcinomatosis

Infections
- Tuberculous peritonitis

Others

  • Pancreatitis
  • Bowel obstruction
  • Biliary ascites
  • Post op lymphatic leak
  • Serositis in connective tissue disease
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57
Q

What are the causes of ascites with portal hypertension?

A

Liver disorders

  • Cirrhosis / alcoholic liver disease
  • Acute liver failure
  • Liver metastases

Cardiac

  • Right HF
  • Constrictive pericarditis

Others

  • Budd-Chiari syndrome – blood clot in hepatic veins
  • Portal vein thrombosis
  • Veno occlusive disease
  • Myxoedema
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58
Q

How do you know if someone has portal hypertension?

A

The serum ascites albumin gradient (SAAG) will be >11

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59
Q

Ix for ascites

A

aspirate ascitic fluid for cytology, culture and albumin

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60
Q

Mx for ascites

A
  1. Reduce dietary sodium
  2. Fluid restriction
  3. Aldosterone antagonist e.g. spironolactone +/- loop diuretic
  4. Drainage if tense ascites – therapeutic abdominal paracentesis. Need albumin cover to prevent circulatory dysfunction when you remove the fluid.
  5. Prophylactic abx to prevent spontaneous bacterial peritonitis
  6. Trans jugular intrahepatic portosystemic shunt (TIPS)
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61
Q

What is spontaneous bacterial peritonitis?

A

a form of peritonitis usually seen in patients with ascites secondary to liver cirrhosis

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62
Q

Symptoms of SBP

A

ascites, abdominal pain, fever

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63
Q

diagnosis of SBP

A
  • Diagnosis: paracentesis (high neutrophil count).

- Most common organism = E.coli

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64
Q

Mx for SBP

A

IV cefotaxime

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65
Q

What is cholecystitis?

A

inflammation of the gallbladder usually caused by a blockage of the cystic duct preventing the gallbladder from draining.

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66
Q

Causes of cholecystitis

A
  1. Calculous cholecystitis:
    a. Gallstones (95% of cases)
  2. Acalculous cholecystitis:
    a. Dehydration
    b. Hypoperfusion
    c. Gallbladder statis - TPN / prolonged fasting = gallbladder is not stimulated to empty so there’s a build-up of pressure
    d. Trauma
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67
Q

Symptoms of cholecystitis

A
  • RUQ pain that may radiate to R shoulder
  • Fever
  • Nausea and vomiting
  • Murphy’s sign – inspiratory arrest upon palpating the RUQ
  • Tachycardia
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68
Q

Ix for cholecystitis

A
  • Raised inflammatory markers
  • Raised WCC
  • LFTs likely normal
  • Abdo US:
    o Thickened gallbladder wall
    o Stones/sludge in gallbladder
    o Fluid around gallbladder
  • MRCP (magnetic resonance cholangiopancreatography) to visualise biliary tree if nothing is seen on US
  • HIDA scan (cholescintigraphy)
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69
Q

Mx for cholecystitis

A
  1. IV abx

2. Early laparoscopic cholecystectomy (within 1 week of diagnosis)

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70
Q

Complications of cholecystitis

A
  • Sepsis
  • Gallbladder empyema (infected tissue and pus collect in the gallbladder, need IV abx, cholecystectomy and cholecystostomy)
  • Gangrenous gallbladder
  • Perforation
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71
Q

Definition of cirrhosis

A

irreversible liver damage. Histologically there is loss of normal hepatic architecture with bridging fibrosis and nodular regeneration.

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72
Q

Causes of cirrhosis

A
  • Alcohol
  • Non-alcoholic fatty liver disease
  • Viral hepatitis – B & C
  • Haemochromatosis
  • Alpha 1 antitrypsin deficiency
  • Wilson’s disease
  • Budd-Chiari
  • Primary biliary cholangitis
  • Primary sclerosing cholangitis
  • Cystic fibrosis
  • Drugs – amiodarone, methyldopa, methotrexate, sodium valproate
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73
Q

Symptoms of cirrhosis

A
  • Jaundice – raised bilirubin
  • Hepatomegaly / shrinks
  • Splenomegaly – portal hypertension
  • Spider naevi – tenlangiectasia with a central arteriole and small vessels radiating away
  • Palmar erythema – due to hyperdynamic circulation
  • Gynaecomastia and testicular atrophy – endocrine dysfunction in males
  • Bruising – abnormal clotting
  • Ascites
  • Caput medusae – distended paraumbilical veins due to portal HTN
  • Asterixis – flapping tremor in decompensated liver disease
  • Leuconychia – white nails from hypoalbuminemia
  • Terry’s nails – white proximally but distal 1/3rd reddened by telangiectasis
  • Clubbing
  • Dupuytren’s contracture
  • Parotid enlargement
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74
Q

Ix for cirrhosis

A

• Bloods:
o Deranged LFTs
o Reduced albumin
o Increased PTT
o Hyponatraemia – fluid retention
o Urea and creatinine – deranged in hepatorenal syndrome
o Test for viral hepatitis and autoantibodies
o Alpha-fetoprotein – hepatocellular carcinoma tumour marker
o Enhanced liver fibrosis blood test – for assessing fibrosis in non alcoholic fatty liver disease.
• US liver
o Nodular surface of liver
o Corkscrew appearance to arteries with increased flow as they compensate for reduced portal flow
o Enlarged portal vein with reduced flow
o Ascites
o Splenomegaly
o Hepatocellular carcinoma
• Fibroscan (transient elastography)
o Used to check elasticity of liver, to assess the degree of cirrhosis
• Endoscopy – for oesophageal varices
• CT/MRI scans – hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessel changes, ascites
• Liver biopsy – confirms cirrhosis diagnosis

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75
Q

Two scoring systems used in liver cirrhosis

A

Do child-pugh score for cirrhosis

MELD score – for patients with compensated cirrhosis, to estimate mortality and guides transplant referral

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76
Q

Complications seen in cirrhosis

A
  1. Malnutrition
  2. Portal HTN, varices and variceal bleeding
  3. Ascites and SBP
  4. Hepatorenal syndrome
  5. Hepatic encephalopathy
  6. Hepatocellular carcinoma
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77
Q

Why do patients with cirrhosis become malnourished?

A

Cirrhosis affects the metabolism of proteins in the liver so there is reduced protein produced, therefore there’s use of muscle tissue as fuel which leads to malnutrition and muscle wasting.
The liver cant store glucose as glycogen = more use of body tissue for fuel

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78
Q

Mx for malnutrition in cirrhosis

A

o Regular meals (every 2-3 hours)
o Low sodium
o High protein, high calorie
o No alcohol

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79
Q

Why do patients with cirrhosis get portal HTN?

A

The portal vein comes from the superior mesenteric vein and the splenic vein. It delivers blood to the liver. Cirrhosis increases the resistance of blood flow into the liver so theres back pressure into the portal system.
The back pressure causes the vessels at the sites where the portal system anastomoses with the systemic venous system to become swollen and tortuous = varices.

80
Q

Where do varices occur?

A

o Gastro oesophageal junction
o Ileaocaecal junction
o Rectum
o Anterior abdominal wall via the umbilical vein (caput medusae)

81
Q

Mx for stable varices

A

o Propranolol (reduces portal HTN)
o Elastic band ligation
o Injections of sclerosant
o TIPS – trans jugular intra hepatic portosystemic shunt (connection between the hepatic vein and portal vein with a stent to relieve pressure on portal system)

82
Q

Mx for bleeding oesophageal varices

A

o Resuscitation
o Terlipressin – vasoconstriction
o Vitamin K and fresh frozen plasma (FFP) for coagulopathy
o Broad spectrum abx
o Intubation and ICU
o Urgent endoscopy – inject sclerosant into varices/elastic band ligation
o Sengstaken-Blakemore tube – inflatable tube inserted into oesophagus to tamponade bleeding

83
Q

Why do patients with cirrhosis get hepatorenal syndrome?

A

Portal hypertension leads to a loss of blood volume in the kidneys – hypoperfusion of the kidney. That activates the renin-angiotensin system and causes renal vasoconstriction.
Starvation of blood to the kidney = rapidly deteriorating kidney function.
Hepatorenal syndrome is fatal within a week without liver transplant.

84
Q

Why do patients with cirrhosis get hepatic encephalopathy?

A

Build up of ammonia in the brain. Happens as the liver calls cant metabolise the ammonia into harmless waste products and collateral vessels between the portal and systemic circulation means that ammonia bypasses the liver and goes straight into the systemic circulation.

85
Q

Symptoms of hepatic encephalopathy

A

Confusion

Reduced consciousness

86
Q

Precipitating factors for hepatic encephalopathy

A 
o	Constipation 
o	Electrolyte disturbance
o	Infection 
o	GI bleed
o	High protein diet 
o	Medications – sedatives
87
Q

Mx for hepatic encephalopathy

A 
o	Laxatives (aim for 2-3 soft motions per day)
o	Abx (rifaximin) 
o	Nutritional support
88
Q

What is coeliac disease?

A

autoimmune condition where exposure to the protein gluten causes an autoimmune reaction that causes inflammation in the small bowel. Usually develops in early childhood.

Affects 1% of the UKs population

Suspect if diarrhoea + weight loss/anaemia

89
Q

Pathology of coeliac disease and what are the 3 autoantibodies to remember?

A

T cell responses to gluten (alcohol soluble proteins in wheat, barley, rye and oats) in the small intestine that causes villous atrophy and malabsorption. Auto-antibodies are created in response to gluten that target epithelial cells of the intestine.

3 types of auto-antibody to remember:

1) Anti-tissue transglutaminase (anti-TTG)
2) Anti-endomysial (anti-SMA)
3) Deaminated gliadin peptides antibodies (anti-DGPs)

Inflammation of the small bowel (especially jejunum) – atrophy of the villi and crypt hypertrophy

90
Q

Conditions associated with coeliac disease

A
  • Dermatitis herpetiformis (vesicular, pruritic skin eruption)
  • T1DM
  • Autoimmune hepatitis
  • Thyroid disease
  • Primary biliary cirrhosis
  • Primary sclerosing cholangitis
91
Q

Genetic association with coeliac disease

A
  • HLA-DQ2

- HLA-DQ8

92
Q

risk factors for coeliac disease

A
  • HLA-DQ2 / HLA-DQ8
  • Family history
  • Immunoglobulin A deficiency
  • Other autoimmune conditions
93
Q

symptoms of coeliac disease

A 
•	Failure to thrive in young children
•	Diarrhoea
•	Fatigue
•	Weight loss
•	Mouth ulcers 
•	Recurrent cramping abdominal pain / distention 
•	Anaemia – secondary to iron, B12 or folate deficiency 
•	Dermatitis herpetiformis – itchy blistering rash typically on abdomen 
•	Rarely neurological symptoms:
o	Peripheral neuropathy
o	Cerebellar ataxia
o	Epilepsy
94
Q

complications of coeliac disease

A
  1. Anaemia – iron, folate, B12 deficiency
  2. Hyposplenism
  3. Osteoporosis, osteomalacia
  4. Lactose intolerance
  5. Enteropathy-associated T-cell lymphoma of small intestine
  6. Subfertility
  7. Ulcerative jeunitis
  8. Vitamin deficiency
  9. Non-hodgkin lymphoma
  10. Oesophageal cancer
  11. Small bowel adenocarcinoma
95
Q

diagnosis of coeliac disease

A
  1. Before testing for anti-TTG and anti-EMA antibodies – TEST FOR TOTAL IgA
    a. Both these autoantibodies are IgA
    b. Some patients with coeliac disease have IgA deficiency
    c. Therefore, if total IgA is low then the coeliac test will be negative even when they are coeliac’s
    d. If they have IgA deficiency = test for IgG version of anti-TTG or anti-EMA
  2. Do investigations while patient has gluten in their diet (need to have been eating gluten for 6 weeks prior to testing)
  3. Check coeliac specific antibodies:
    a. First line = IgA Anti-TTG antibodies – raised
    b. Anti-EMA antibodies – raised
  4. Endoscopy with biopsy (gold standard):
    a. Usually done in duodenum but jejunal biopsies performed
    b. Findings:
    i. Vilous atrophy
    ii. Crypt hyperplasia
    iii. Increased intraepithelial lymphocytes
    iv. Lamina propria infiltration with lymphocytes
96
Q

mx for coeliac disease

A
  • lifelong gluten free diet.
  • Check anti-TTG antibodies for compliance with diet and disease monitoring.
  • Immunisation against pneumococcal infection with boosters every 5 years (due to functional hyposplenism)
97
Q

Risk factors for colorectal cancer

A
  • Family hx
  • Familial adenomatous polyposis (FAP)
  • Hereditary nonpolyposis colorectal cancer (HNPCC) – LYNCH SYNDROME
  • IBD
  • Increased age
  • Diet high in red and processed meat and low in fibre
  • Obesity / sedentary lifestyle
  • Smoking
  • Alcohol
98
Q

What is familial adenomatous polyposis (FAP)?

A

o Autosomal dominant condition
o Malfunctioning of adenomatous polyposis coli (APC) genes – tumour suppressor genes
o Results in lots of polyps in the large intestine that can become cancerous (usually before 40 yo)
Risk factor for colorectal cancer

99
Q

What is hereditary non-polyposis colorectal cancer (HNPCC)?

A

Lynch syndrome
o Autosomal dominant condition
o Higher risk of number of cancers, mostly colorectal Ca. Other ca = endometrial
o Tumours develop in isolation

100
Q

Presentation for bowel cancer

A
  • Change in bowel habit – more frequent loose stools
  • Unexplained weight loss
  • Rectal bleeding
  • Unexplained abdominal pain
  • Iron deficiency anaemia (microcytic anaemia with low ferritin)
  • Abdominal or rectal mass on examination
  • Obstruction = surgical emergency
101
Q

When to refer someone you suspect has bowel cancer

A
  1. Two week wait depends on patients age and combination of symptoms
    a. >40 yo + abdominal pain + unexplained weight loss
    b. >50 yo + unexplained rectal bleeding
    c. >60+ + change in bowel habit / iron deficiency anaemia
  2. Iron deficiency anaemia with no explanation = two week wait for colonoscopy and gastroscopy
102
Q

How is bowel cancer screening done in the uk?

A
  • Faecal immunochemical tests (FIT) – look for the amount of human haemoglobin in stool
  • FIT tests can be used in general practice to assess for bowel cancer in patients who don’t meet criteria for a two week wait referral
•	FIT tests are used in the bowel cancer screening programme
o	Aged 60-74 yo
o	Can request screening if >74 yo
o	FIT test sent to homes every 2 years 
o	Positive result = colonoscopy

• Screening for patients with FAP, HNPCC or IBD = colonoscopy at regular intervals

103
Q

Ix for bowel cancer

A
  1. Colonoscopy – gold standard. Biopsy suspicious lesions
  2. Sigmoidoscopy – when theres only rectal bleeding, risk of missing cancer in the rest of the colon as you only see the rectum and sigmoid colon
  3. CT colonography – CT scan with bowel prep and contrast
  4. Staging CT scan – CT TAP (look for mets)
  5. Carcinoembyronic antigen (CEA) – tumour marker for bowel cancer
104
Q

Staging for bowel cancer

A 
Staging = TMN classification 
-	T = tumour 
o	TX – unable to assess size
o	T1 – submucosa involvement 
o	T2 – involvement of muscularis propria (muscle layer)
o	T3 – involvement of subserosa (outer layer)
o	T4 – spread through serosa 
o	T4b – reaching other tissues/organs
-	N = nodes
o	NX – unable to assess nodes
o	NO – no nodes
o	N1 – 1-3 nodes
o	N2 - 3+ nodes
-	M = metastasis 
o	M – no metastasis 
o	M1 – metastasis
105
Q

Mx for bowel cancer

A
  1. MDT meeting
  2. Surgical resection
  3. Chemotherapy
  4. Radiotherapy
  5. Palliative care
106
Q

When would you do a right hemicolectomy?

A

Cancer in the caecum, ascending colon or proximal transverse colon

107
Q

When would you do a left hemicolectomy?

A

Cancer in distal transverse or descending colon

108
Q

When would you do a high anterior resection?

A

Cancer in the sigmoid colon

109
Q

When would you do an anterior resection (TME)?

A

Cancer in the upper rectum

110
Q

When would you do a low anterior resection (low TME)?

A

Cancer in the low rectum

111
Q

When would you do an abdomino-perineal excision of the rectum?

A

Cancer in the rectum and anus

112
Q

When would you do a Hartmann’s procedure?

A

emergency procedure to remove the rectosigmoid colon and create a colostomy (can be reversed later).

Indications = acute obstruction by a tumour or significant diverticular disease.

113
Q

Complications from bowel surgery

A
  • Bleeding, infection, pain
  • Damage to nerves, bladder, ureter or bowel
  • Post operative ileus
  • Anaesthetic risks
  • Laparoscopic surgery that needs to become open surgery
  • Leakage or failure of anastomosis
  • Requirement for a stoma
  • Failure to remove tumour
  • Change in bowel habit
  • VTE
  • Incisional hernia
  • Intra-abdominal adhesions
114
Q

Follow up after bowel cancer

A
  • 3 years
  • Serum CEA
  • CT TAP
115
Q

Define constipation

A

defecation that is unsatisfactory because of infrequent stools (<3 times weekly), difficult stool passage (with staining or discomfort) or seemingly incomplete defecation.

Can be primary or secondary

116
Q

Risk factors for constipation

A
  • Female
  • > 65 yo
  • Sedentary
  • Low fibre intake
  • Inadequate fluid/calorie intake
  • Medications – opiates, calcium channel blockers, tricyclic antidepressants
117
Q

Symptoms of constipation

A
  • Infrequent stools
  • Difficult defecation
  • Sensation of incomplete evacuation
  • Excessive straining
  • Hard stools
  • Abdominal mass
118
Q

Secondary constipation causes

A
  • Neuropathy
  • Diabetes
  • Hypothyroidism
  • GI cancer
  • Neurological conditions
119
Q

Mx for chronic constipation

A
  • Diet and lifestyle advice
  • Laxatives:
    o Bulk forming: ispaghula husk
    o Stool softener: docusate sodium
    o Osmotic: lactulose
120
Q

complications of constipation

A
  • Overflow diarrhoea
  • Acute urinary retention
  • Haemorrhoids
121
Q

What is the difference between diverticulosis, diverticular disease and diverticulitis?

A

Diverticular disease = herniation of colonic mucosa through the muscular wall of the colon. Is called diverticular disease when patients experience symptoms.

Diverticulosis = the presence of diverticula, without inflammation or infection.

Diverticulitis = inflammation and infection of diverticula.

122
Q

Why do diverticula form?

A
  • Wall of the large intestine contains a layer of muscle called the circular muscle
  • Points where the muscle layer is penetrated by blood vessels = areas of weakness
  • Increased pressure in the lumen over time can cause a gap to form in these areas of circular muscle = mucosa can herniate through the muscle layer to form pouches
  • Diverticula DO NOT FORM IN THE RECTUM = outer longitudinal muscle layer that adds extra support
  • Areas of the colon not surrounded by teniae coli – vulnerable to the development of diverticula
  • Common places for diverticulosis:
    o Sigmoid colon
    o Rest of the large bowel
123
Q

Risk factors for diverticular disease

A
  • Increased age
  • Low fibre diet
  • Obesity
  • Use of NSAIDs – increased risk of diverticular haemorrhage
124
Q

Symptoms of diverticular disease

A
  • Lower left abdominal pain
  • Constipation / change in bowel habit
  • Rectal bleeding
125
Q

Diagnosis of diverticulosis

A

Incidental finding on CT or colonoscopy

126
Q

Mx of diverticular disease

A
  • No mx if asymptomatic, just advise high fibre diet and weight loss
  • Symptomatic
    o High fibre diet
    o Bulk forming laxative
    o Avoid stimulant laxatives
    o Surgery to remove affected area if significant symptoms
127
Q

Complications of diverticular disease

A
  • Diverticulitis
  • Haemorrhage
  • Development of fistula
  • Perforation and faecal peritonitis
  • Perforation and development of abscess
  • Development of diverticular phlegmon
128
Q

Symptoms of diverticulitis

A
  • Pain and tenderness in the left iliac fossa / left lower abdomen
  • Fever
  • Constipation / diarrhoea
  • Nausea and vomiting
  • Rectal bleeding
  • Palpable abdominal mass
  • Raised inflammatory markers and WCC
129
Q

Ix for diverticulitis

A
  • FBC – raised WCC
  • CRP – raised
  • Erect CXR – pneumoperitoneum in perforation
  • AXR – dilated bowel loops, obstruction, abscesses
  • CT – best way to see abscesses
  • Colonoscopy – avoid initially due to increased risk of perforation in diverticulitis
130
Q

Mx for diverticulitis

A
  1. In primary care
    a. Oral co-amoxiclav
    b. Analgesia – avoid NSAIDs
    c. Only clear liquids, avoid solid food
    d. Review in 72 hours and admit to hospital if symptoms haven’t settled
  2. Hospital admission for severe cases
    a. NBM / clear fluids only
    b. IV abx
    c. IV fluids
    d. Analgesia
    e. CT scan
    f. Urgent surgery for complications
131
Q

Complications of diverticulitis

A
  1. Perforation
  2. Peritonitis
  3. Peri diverticular abscess
  4. Large haemorrhage requiring blood transfusion
  5. Fistula e.g. between colon and the bladder or vagina
  6. Ileus / obstruction
132
Q

What are cholelithiasis?

A

Gallstones (cholelithiasis) = small stones that form within the gallbladder

133
Q

What is choledocholithiasis?

A

gallstone(s) in the bile duct

134
Q

What is cholestasis?

A

blockage to the flow of bile

135
Q

What is biliary colic?

A

severe abdominal pain resulting from obstruction of the cystic duct or the common bile duct by (most commonly) a gallstone. Pain is in the RUQ but can be poorly localised. Often occurs about 30 mins after a meal (particularly if fatty) and can last for several hours. Often vomit.

136
Q

What are the 3 types of gallstones?

A
  1. Cholesterol: yellow green stones made of hardened cholesterol
  2. Pigment: black brown stones with high bilirubin content
  3. Mixed cholesterol and pigment
137
Q

Risk factors for gallstones

A

Risk factors for gallstones (4Fs):

  • F – fat
  • F – fair
  • F – female
  • F – forty
138
Q

Symptoms of gallstones

A

• Can be asymptomatic with gallstones

• Biliary colic (caused by stones temporarily obstructing drainage of the gallbladder)
o Sever colicky epigastric/RUQ pain
o Often triggered by meals (particularly high fat meals – due to fat stimulating cholecystokinin [CCK] release from duodenum that causes contraction of the gallbladder)
o Lasts between 30 mins to 8 hours
o Nausea and vomiting

•	Can present with complications of gallstones:
o	Acute cholecystitis 
o	Acute cholangitis 
o	Obstructive jaundice
o	Pancreatitis
139
Q

Ix for gallstones

A
  1. LFTs
    a. Raised bilirubin (pale stools, dark urine)
    b. Raised ALP (can also be raised in liver/bone problems & in pregnancy from placenta)
    c. ALT and AST – slightly increased
  2. US scan – best for visualising gallstones
    a. Gallstones in gallbladder or ducts
    b. Bile duct dilation
    c. Acute cholecystitis = thickened gallbladder wall, stones or sludge in gallbladder and fluid around gallbladder
  3. MRCP – used if cant see gallstones with US scan
  4. ERCP – can clear stones from ducts
140
Q

Risks of ERCP

A

Risks of ERCP

i. Bleeding
ii. Duodenal perforation
iii. Cholangitis
iv. Pancreatitis

141
Q

Mx for gallstones

A
  • Asymptomatic = conservative management

- Cholecystectomy (laparoscopic procedure).

142
Q

Complications of cholecystectomy

A

Bleeding, infection, pain, scars
 Damage to bile duct (leaking and strictures)
 Stones left in the duct
 Damage to bowel, blood vessels or other organs
 Anaesthetic risks
 VTE
 Post cholecystectomy syndrome

143
Q

Symptoms of post cholecystectomy syndrome

A
  • Diarrhoea
  • Indigestion
  • Epigastric or RUQ pain
  • Nausea
  • Intolerance of fatty foods
  • Flatulence
144
Q

What type of cancer is gastric cancer usually?

A

Adenocarcinoma

145
Q

Risk factors for gastric cancer

A
  • 50-70yo
  • Male
  • Smoking
  • Family hx
  • Pernicious anaemia
  • Helicobacter pylori (inflammation = atrophy and intestinal metaplasia)
  • Diet high in nitrates
  • Diet low in fruit and veg
  • High salt intake
146
Q

Symptoms of gastric cancer

A
  • Epigastric pain
  • Weight loss
  • Virchow’s node – lymphadenopathy in L supraclavicular node
  • Sister mary joseph’s node – lymphadenopathy in periumbilical node
  • Irish node – lymphadenopathy in L axillary node
  • Nausea
  • Dysphagia
  • Lower GI bleeding
147
Q

Ix for gastric cancer

A
  1. Upper GI endoscopy with biopsy
    a. Signet ring cells seen
  2. Endoscopic US for staging
  3. CT TAP
  4. CXR – for prozimal gastro-oesophageal junction tumours
  5. PET scan for mets
148
Q

In what disease are signet ring cells seen on biopsy?

A

gastric cancer

149
Q

Tx for gastric cancer

A
  • Endoscopic mucosal resection
  • Gastrectomy or partial gastrectomy
  • Chemotherapy
150
Q

Define perforation

A

formation of a hole in a hollow organ

151
Q

Causes of GI perforation

A
  • Peptic ulcer disease: duodenal or gastric
  • Malignancy
  • IBD
  • Diverticulitis
  • Acute appendicitis
  • Typhoid
  • Toxic megacolon
  • Bowel obstruction
  • Penetrating trauma
  • Post ERCP
  • Foreign body ingestion
  • Radiation therapy
152
Q

Symptoms of GI perforation

A
  1. Abdominal pain and distention (acute)
  2. Nausea vomiting
  3. Fever
  4. Tachycardia
  5. Peritonitis signs
  6. Perforated peptic ulcer: referred shoulder pain
  7. Perforated diverticulosis: constipation, LLQ pain
  8. Perforated appendix: progressively worsening RLQ pain
153
Q

Ix for GI perforation

A
  • Increased WCC
  • Lactic acidosis in ischaemic perforation
  • CXR and AXR – free intraperitoneal air under the diaphragm
  • USS and CT
154
Q

Tx for GI perforation

A
  1. NBM
  2. IV abx
  3. Sepsis 6
  4. NG tube suction
  5. Explorative laparotomy – peritoneal lavage and closure of perforation
155
Q

What is GORD

A

acid from the stomach refluxes through the lower oesophageal sphincter and irritates the lining of the oesophagus.

156
Q

Risk factors for GORD

A
  • Lower oesophageal sphincter hypotension
  • Hiatus hernia
  • Oesophageal dysmobility (e.g. systemic sclerosis)
  • Obesity
  • Gastric acid hypersecretion
  • Delayed gastric emptying
  • Smoking
  • Alcohol
  • Pregnancy
  • Drugs - tricyclics, Anticholinergics, nitrates
157
Q

Symptoms of GORD

A
  1. Heartburn (burning retrosternal discomfort after meals, lying, stooping, straining and relieved by antacids)
  2. Belching
  3. Acid brash (acid or bile regurgitation)
  4. Water brash (increased salvation)
  5. Odynophagia (painful swallowing e.g. from oesophagitis or ulceration)
  6. Nocturnal cough
  7. Laryngitis (hoarseness and throat clearing)
  8. Sinusitis
158
Q

Complications of GORD

A
  • Oesophagitis
  • Ulcers
  • Benign stricture
  • Iron deficiency
  • Metaplasia > dysplasia > neoplasia (GORD may lead to Barrett’s oesophagus which can progress to oesophageal cancer)
159
Q

Ix for GORD

A
  1. Endoscopy if:
  2. Dysphagia - difficulty swallowing
  3. Over 55 yo with red flag symptoms (anaemia, loss of weight, anorexia, recent onset/progressive symptoms, melaena/haematemesis, swallowing difficulty)
  4. Treatment refractory dyspepsia
  5. 24 hr oesophageal pH monitoring - if endoscopy is normal
  6. Manometry - if endoscopy is normal
160
Q

Mx for GORD

A
  1. Lifestyle advice - Reduce caffeine and alcohol, Weight loss, Stop smoking, Small lighter meals, Avoid heavy meals before bed, Stay upright after meals
  2. Acid neutralising medication - Gaviscon, Rennie
  3. Proton pump inhibitor - Omeprazole, Lansoprazole
  4. H2 receptor antagonist- Ranitidine
  5. Surgery - Laparoscopic fundoplication
161
Q

what is H pylori?

A
  • Gram negative aerobic bacteria
  • Found in the stomach, damages the epithelial lining resulting in gastritis, ulcers and increased risk of gastric cancer
  • H. Pylori test for anyone with dyspepsia (no PPI for 2 weeks before test)
162
Q

Ix for h. pylori

A

o Urea breath test using radiolabelled carbon 13
o Stool antigen test
o Rapid urease test during endoscopy

163
Q

Eradication of h. pylori

A 
triple therapy:
o	PPI (omeprazole)
o	Amoxicillin (7 days)
o	Clarithromycin (7 days)
164
Q

What is Barrett’s oesophagus?

A
  • Reflux > metaplasia (from squamous to columnar epithelium)
  • Change to columnar epithelium = Barrett’s oesophagus
  • Barrett’s oesophagus is a premalignant condition, 3-5% develop adenocarcinoma of the oesophagus
  • Need regular endoscopy
  • Mx: PPIs, ablation treatment during endoscopy in high grade dysplasia
165
Q

What is haemochromatosis?

A

an iron storage disorder that results in excessive total body iron and deposition of iron in tissues.

166
Q

What is the genetic inheritance of haemochromatosis?

A

autosomal recessive

mutation of human haemochromatosis protein (HFE) on chromosome 6

167
Q

when do patients present with haemochromatosis?

A

usually present after 40 yo when iron overload becomes symptomatic
presents later in females who menstruate as iron is regularly eliminated

168
Q

symptoms of haemochromatosis

A

Chronic tiredness
Joint pain
Pigmentation (bronze / slate-grey discolouration)
Hair loss
Erectile dysfunction
Amenorrhoea
Cognitive symptoms (memory and mood disturbance)

169
Q

Ix for haemochromatosis

A 
Serum ferritin - high (remember its also an acute phase reactant)
Transferrin saturation - high
Low total iron binding capacity
genetic testing 
liver biopsy with pearls stain = shows iron concentration in parenchymal cells
CT abdo - increased attention in liver
MRI liver - deposits of iron
MRI heart - deposits of iron
Joint X-rays = chondrocalcinosis
170
Q

Complications associated with haemochromatosis

A

T1DM - iron affects pancreas functioning
Liver cirrhosis
Iron deposits in pituitary Galen & gonads = endocrine & sexual problems = hypogonadism, impotence, amenorrhoea and infertility
Cardiomyopathy
Hepatocellular carcinoma
Hypothyroidism (iron deposits in thyroid gland)
Chondrocalcinosis / pseudo gout (calcium deposits in joints)
Arthritis - particularly hands

171
Q

Mx of haemochromatosis

A 
Venesection - weekly
2nd line = desferrioxamine 
Monitoring of serum ferritin 
Avoid alcohol
Genetic counselling 
Monitoring and treatment of complications
172
Q

What is the special liver stain used to look for haemochromatosis?

A

Pearl’s stain

173
Q

What is Wilson’s disease?

A

An autosomal recessive disorder characterised by excessive copper deposition in the tissues

174
Q

Genetic abnormalities in Wilsons disease?

A

Autosomal recessive disorder

Defect on ATP7B gene on chromosome 13

175
Q

Pathology of Wilsons disease

A

increased copper absorption from the small intestine

decreased hepatic copper excretion

176
Q

when do patients present with wilsons disease?

A

10-25 years old
Children present with liver disease
Young adults present with neurological disease

177
Q

symptoms of wilsons disease

A

liver - hepatitis, cirrhosis

neuro -

  • basal ganglia degeneration
  • speech, behavioural and psychiatric problems
  • asterixis
  • chorea
  • dementia
  • Parkinsonism

Kayser-Fleischer rings - green/brown rings in the periphery of the iris

Renal tubular acidosis - falconi syndrome

Haemolysis

Blue mails

178
Q

Ix for wilsons disease

A

Slit lamp examination for Kayser-Fleischer rings

Reduced serum caeruloplasmin
Reduced total serum copper
Increased 24hr urinery copper excretion

Genetic analysis for ATP7B gene on chromosome 13

179
Q

Mx of wilsons disease

A

Penicillamine - chelates copper

2nd line = Tridentine hydrochloride

180
Q

What is alpha-1-antitrypsin deficiency?

A

A condition caused by an abnormality in the gene for a protease inhibitor called alpha 1 anti trypsin

181
Q

What is the genetic inheritance for alpha-1-antitrypsin?

A

Autosomal recessive

Gene defect in the gene for alpha-1-antitripsin on chromosome 14

182
Q

What is the pathology of alpha-1-antitrypsin?

A

Elastase is an enzyme secreted by neutrophils.
Elastase digests connective tissues
Alpha-1-antitrypsin is mainly produced in the liver and travels around the body offering protection by inhibiting the neutrophil elastase enzyme

183
Q

what are the main 2 organs affected by alpha-1-antitrypsin deficiency?

A

Liver

Lungs

184
Q

Symptoms of alpha-1-antitripsin deficiency

A

liver cirrhosis - mutated alpha 1 anti trypsin gets trapped in the liver, builds up and causes damage
hepatocellular carcinoma

lungs - bronchiectasis and emphysema - lack of alpha-1-antitrypsin means protease enzymes break down the connective tissue

185
Q

Diagnosis of alpha-1-antitrypsin deficiency

A

Low serum alpha-1-antitrypsin = screening test

Liver biopsy - cirrhosis & acid-Schiff positive staining globules

Genetic testing for alpha-1-antitrypsin gene

High resolution CT thorax - bronchiectasis and emphysema

186
Q

Mx of alpha-1-antitrypsin

A

Stop smoking (emphysema)
Symptomatic mx
NICE recommend against replacement alpha-1-antitrypsin
Organ transplant for end stage lung/liver disease

187
Q

What are haemorrhoids?

A

enlarged anal vascular cushions

188
Q

Risk factors for haemorrhoids

A 
Constipation
Straining 
Pregnancy
Obesity
Increased age
Increased intra-abdominal pressure - weight lifting or chronic coughing
189
Q

what are the anal cushions?

A

anal cushions = specialised submucosal tissue that contain connections between the arteries and veins so are very vascular

Anal cushions are supported by smooth muscle and connective tissue

the anal cushions are located at 3, 7 and 11 o’clock

190
Q

Classification of haemorrhoids

A

1st degree = no prolapse

2nd degree = prolapse when straining and return on relaxing

3rd degree = prolapse when straining, do not return on relaxing

4th degree = prolapsed permanently

191
Q

Symptoms of haemorrhoids

A 
Asymptomatic 
Painless bright red bleeding 
Typically blood on the toilet tissue or seen after opening the bowels 
Blood is not mixed with the stool 
Sore/itchy anus 
Feeling a lump around or inside the anus
192
Q

Examination findings for haemorrhoids

A

External, prolapsed haemorrhoid - visible swellings on inspection

Internal haemorrhoids - felt on PR exam

Can prolapse if a patient is asked to ‘bear down’ during inspection

193
Q

Ix for haemorrhoids

A

Proctoscopy - hallow tube inserted into anal cavity to visualise the mucosa

194
Q

Mx of haemorrhoids

A

Topical tx:

  • Anusol, contains chemicals to shrink haemorrhoids
  • Anusol HS, also contains hydrocortisone
  • Germoloids cream, contains lidocaine
  • Proctosedyl ointment, contains cinchoncaine and hydrocortisone

Prevention/tx:

  • Increasing dietary fibre
  • good fluid intake
  • Laxatives
  • Avoid straining

Non-surgical tx:

  • Rubber band ligation
  • Injection sclerotherapy
  • Infra-red coagulation
  • Bipolar diathermy

Surgical:

  • Haemorrhoidal artery ligation
  • Haemorrhoidectomy
  • Stapled haemorrhoidectomy
195
Q

What is a possible complication seen with haemorrhoids

A

Thrombosed haemorrhoids

196
Q

What is a thrombosed haemorrhoid?

A

caused by strangulation at the base of the haemorrhoid, resulting in thrombosis (a clot) in the haemorrhoid.

Very painful

Purple, tender swollen lumps around anus
PR exam difficult due to pain

Resolves with time, may need surgical mx

Finals Revision (18 decks)

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