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!Final Year > Gastrointestinal (3) > Flashcards

Gastrointestinal (3) Flashcards

1
Q

What is Portal Hypertension?

A

Increase in the pressure within the portal vein (carries blood from the bowel to the liver)

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2
Q

What is the aetiology of Portal Hypertension?

A
  1. Most common cause is liver cirrhosis where the scar (fibrotic) tissue blocks the flow of blood through the liver
  2. Other causes include thromboembolic events, schistosomiasis and HIV related conditions
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3
Q

What is the epidemiology of Portal Hypertension?

A

Common complication of cirrhosis, can result in liver failure

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4
Q

What are the presenting symptoms and signs of Portal Hypertension?

A
  1. Abdominal swelling: ascites
  2. Haematemesis
  3. PR bleeding or melaena
  4. Signs of encephalopathy
  5. Caput medusae (dilated superficial abdominal veins)
    Splenomegaly
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5
Q

What are the appropriate investigations for Portal Hypertension?

A
  1. Clinical diagnosis based on the presence of ascites or of dilated veins (caput medusae) or varices
  2. Others:
    a. FBC: thrombocytopaenia ± anaemia, leukopaenia
    b. LFTs: deranged (low albumin, raised others, pronged prothrombin time)
    c. Endoscsopy (oeshgeal varices)
    d. Imaging: CT scan
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6
Q

What is the management of Portal Hypertension?

A
  1. B-Blockers and endoscopic banding of varices if present
  2. Transjugular intrahepatic portosystemic shunt (TIPS): radiological procedure whereby a vascular tract is created in the liver from hepatic to portal veins allowing decompression of portal hypertension
  3. Ascites: Diuretics (spironolactone ± furosemide), dietary sodium restriction (2g/day), therapeutic paracentesis
  4. Liver transplantation is the only curative measure for cirrhosis
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7
Q

What are the complications of Portal Hypertension?

A

Complications of liver cirrhosis:
1. Jaundice
2. hepatic encephalopathy
3. Ascites, risk of SBP
4. Variceal bleeding
5. Hepatocellular carcinoma

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8
Q

What is Primary biliary cholangits?

A
  1. Previously referred to as primary biliary cirrhosis
  2. A chronic liver disorder typically seen in middle-aged females (female:male ratio of 9:1)
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9
Q

What is the pathophysiology of primary biliary cholangitis?

A
  1. Not fully understood although it is thought to be an autoimmune condition
  2. Interlobular bile ducts become damaged by a chronic inflammatory process causing progressive cholestasis which may eventually progress to cirrhosis
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10
Q

What is the epidemiology of primary biliary cholangitis?

A

Middle aged females

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11
Q

What are the associated conditions of primary biliary cholangitis?

A
  1. Sjogren’s syndrome (seen in up to 80% of patients)
  2. Rheumatoid arthritis
  3. Systemic sclerosis
  4. Thyroid disease
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12
Q

What are the antibodies involved in primary biliary cholangitis?

A

Anti-mitochondrial antibodies

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13
Q

What is the main presenting symptom of primary biliary cholangitis?

A

Itching (pruritus)

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14
Q

What are the early features of primary biliary cholangitis?

A
  1. May be asymptomatic (e.g. raised ALP on routine LFTs)
  2. Fatigue
  3. Pruritus
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15
Q

What are the clinical features of primary biliary cholangitis?

A
  1. Pruritus
  2. Cholestatic jaundice
  3. Hyperpigmentation, especially over pressure points
  4. RUQ pain (10%)
  5. Aanthelasmas, xanthomata
  6. Clubbing
  7. Hepatosplenomegaly
  8. May have symptoms of associated disease e.g. dry eyes and dry mouth
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16
Q

What is a late feature of primary biliary cholangitis?

A

Acute liver failure

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17
Q

How is primary biliary cholangitis diagnosed?

A
  1. Immunology:
    a. Anti-mitochondrial antibodies (AMA) M2, 98% of patients and are highly specific
    b. Smooth muscle antibodies in 30% of patients
    c. Raised serum IgM
  2. Imaging:
    a. Required before diagnosis to exclude an extrahepatic biliary obstruction
    b. This is typically a RUQ ultrasound or MRCP
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18
Q

What is the first line management of primary biliary cholangitis?

A

Ursodeoxycholic acid: slows disease progression and improves symptoms

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19
Q

What is the management of primary biliary cholangitis?

A
  1. Ursodeoxycholic acid
  2. For pruritus: cholestyramine
  3. Fat-soluble vitamin supplementation
  4. Liver transplantation
    e.g. if bilirubin > 100 (PBC is a major indication), recurrence in graft can occur but is not usually a problem
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20
Q

What are the complications of primary biliary cholangitis?

A
  1. Cirrhosis → portal hypertension → ascites, variceal haemorrhage
  2. Osteomalacia and osteoporosis
  3. Significantly increased risk of hepatocellular carcinoma (20-fold increased risk)
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21
Q

What condition is associated with a 20x increased risk of hepatocellular cancer?

A

Primary biliary cholangitis

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22
Q

What is primary sclerosing cholangitis?

A

A biliary disease of unknown aetiology characterised by inflammation and fibrosis of intra and extra-hepatic bile ducts

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23
Q

What condition is closely associated with primary sclerosing cholangitis?

A

Ulcerative colitis: 4% of patients with UC have PSC, 80% of patients with PSC have UC

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24
Q

What other conditions are associated with primary sclerosing cholangitis?

A
  1. Crohn’s (much less common association than UC)
  2. HIV
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25
Q

What are the features of primary sclerosing cholangitis?

A
  1. Cholestasis:
    a. jaundice, pruritus
    b. raised bilirubin + ALP
  2. Right upper quadrant pain
  3. Fatigue
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26
Q

What are the standard investigations for primary sclerosing cholangitis?

A

ERCP/ MRCP: showing multiple biliary strictures giving a ‘beaded’ appearance

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27
Q

What are the investigations for primary sclerosing cholangitis?

A
  1. ERCP/ MRCP
  2. p-ANCA may be positive
  3. Bloods: LFTs show raised bilirubin and ALP
  4. Limited role of liver biopsy: may show fibrous, obliterative cholangitis often described as ‘onion skin’
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28
Q

What are the complications of primary sclerosing cholangitis?

A
  1. Cholangiocarcinoma (in 10%)
  2. Increased risk of colorectal cancer
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29
Q

What cancers are associated with PBC and PSC?

A

PBC: hepatocellular carcinoma
PSC: cholangiocarcinoma

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30
Q

What is Rectal Prolapse?

A

The abnormal protrusion of the full thickness (or only the mucosal layer) of the rectum through the anus

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31
Q

What is the aetiology of Rectal Prolapse?

A

Triggered by:
1. Pregnancy
2. Constipation or chronic straining
3. Diarrhoea (15%)
4. Chronic cough (COPD, CF)
5. Neurological conditions: MS, cauda equina syndrome

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32
Q

What are the different types of Rectal Prolapse?

A
  1. Full-thickness: The full thickness of the wall of the rectum sticks out through the anus, can be a partial or complete protrusion (most common)
  2. Mucosal: Only the lining of the anus (known as the mucosa) sticks out through the anus
  3. Internal: The rectum folds in on itself but does not stick out through the anus
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33
Q

What is the epidemiology of Rectal Prolapse?

A
  1. More common in adults than children, and it is particularly prevalent in women aged 50 years or older
  2. In older women, rectal prolapse will often occur at the same time as a prolapsed uterus or bladder because of general weakness in the pelvic floor muscles
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34
Q

What are the presenting symptoms/signs of Rectal Prolapse?

A
  1. Patients may notice a mass protruding which is associated with defection (initially this is reducible however overtime it becomes permanent)
  2. Usually does not cause pain
  3. Faecal incontinence (75%)
  4. PR mucus or bleeding
  5. Discomfort
  6. Further constipation
  7. Symptoms of complication:
    a. Strangulated prolapse: ischaemia of the rectum which can become gangrenous (can become ulcerated or necrotic)
    b. Reduced anal sphincter tone
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35
Q

What are the appropriate investigations for a Rectal Prolapse?

A
  1. Proctography: A type of X-ray that shows the rectum and anal canal during a bowel movement
  2. Colonoscopy/sigmoidoscopy
  3. Endoanal ultrasound: A thin ultrasound probe looks at the muscles used to control the bowels
  4. Can consider anal manometry: to assess anal sphincter tone
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36
Q

What is the management of a rectal prolapse?

A
  1. Conservative: pelvic floor exercises, methods to empty bowel comfortably
  2. Rectal irrigation
  3. Surgery:
    a. Ventral mesh rectopexy
    b. Perineal repair
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37
Q

What is rectal prolapse repair?

A
  1. Perineal repair (Delorme’s operation or Altemeier procedure)
  2. During surgery, the lining of the bowel, or the section of bowel that has prolapsed, is removed and stitched back together
  3. Under spinal or general anaesthetic.
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38
Q

What are the risks of a perineal repair in the management of a rectal prolapse?

A
  1. Bleeding from the rectum
  2. Narrowing of the anal canal
  3. Bowel incontinence
  4. Leak from the anastomosis (most severe and life threatening complication)
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39
Q

What are the indications of a splenectomy?

A
  1. Trauma: 1/4 are iatrogenic
  2. Spontaneous rupture: EBV
  3. Hypersplenism: hereditary spherocytosis or elliptocytosis
  4. Malignancy: lymphoma or leukaemia
  5. Splenic cysts, hydatid cysts, splenic abscesses
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40
Q

When is an elective splenectomy indicated?

A
  1. Spleen is often large: splenomegaly
  2. Most cases can be performed laparoscopically
  3. The spleen will often be macerated inside a specimen bag to facilitate extraction
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41
Q

What are the complications of a splenectomy?

A
  1. Haemorrhage (may be early and either from short gastrics or splenic hilar vessels)
  2. Pancreatic fistula (from iatrogenic damage to pancreatic tail)
  3. Thrombocytosis: give prophylactic aspirin
  4. Encapsulated bacteria infection e.g. Strep. pneumoniae, Haemophilus influenzae and Neisseria meningitidis
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42
Q

What can encaspulated infections lead to in a patient with a splenectomy?

A

Post-splenectomy sepsis (therefore requires vaccination and prophylactic antibiotics)

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43
Q

What vaccinations should patients receive following a splenectomy?

A

If elective, should be done 2 weeks prior to operation:
1. Hib, meningitis A & C
2. Annual influenza vaccination
3. Pneumococcal vaccine every 5 years

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44
Q

What antibiotics should patients receive prophylactically following a splenectomy?

A

Penicillin V:
1. Penicillin should be continued for at least 2 years and at least until the patient is 16 years of age
2. Although the majority of patients are usually put on antibiotic prophylaxis for life

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45
Q

What are the post-splenectomy changes?

A
  1. Platelets will rise first (therefore in ITP should be given after splenic artery clamped)
  2. Blood film will change over following weeks, Howell-Jolly bodies will appear
  3. Other blood film changes include target cells and Pappenheimer bodies
  4. Increased risk of post-splenectomy sepsis, therefore prophylactic antibiotics and pneumococcal vaccine should be given
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46
Q

What is Ulcerative Colitis?

A

A type of chronic relapsing and remitting inflammatory bowel disease that characteristically involves the rectum and xtends proximally to affect a variable length of the colon (large bowel)

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47
Q

What is the aetiology of Ulcerative Colitis?

A
  1. Seems to occur in genetically susceptible people in response to environmental triggers (HLA-B27)
  2. Thought to be autoimmune, strong association with elevated serum pANCA (anti-neutrophil cytoplasmic autoantibodies) and primary sclerosing cholangitis
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48
Q

What is the pathophysiology of UC?

A

Inflammation starts at rectum (hence it is the most common site for UC), never spreads beyond ileocaecal valve and is continuous

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49
Q

What is the epidemiology of UC?

A

Peak incidence of ulcerative colitis is in people aged 15-25 years and in those aged 55-65 years

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50
Q

What are the presenting features of UC?

A

Insidious and intermittent symptoms:
1. Bloody diarrhoea
2. Urgency
3. Tenesmus
4. Abdominal pain, particularly in the left lower quadrant
5. Extra-intestinal features: uveitis, arthritis, Pyoderma gangrenosum

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51
Q

How is UC generally diagnosed?

A
  1. Routine investigations include bloods, faecal calprotectin, stool culture
  2. Colonoscopy + biopsy (flexible sigmoidoscopy is preferred due to risk of perforation)
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52
Q

What are the typical findings on colonoscopy and biopsy of UC?

A
  1. Red, raw mucosa, bleeds easily
  2. No inflammation beyond submucosa (unless fulminant disease)
  3. Widespread ulceration with preservation of adjacent mucosa which has the appearance of polyps (‘pseudopolyps’)
  4. Inflammatory cell infiltrate in lamina propria
  5. Neutrophils migrate through the walls of glands to form crypt abscesses
  6. Depletion of goblet cells and mucin from gland epithelium
  7. Granulomas are infrequent
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53
Q

What are the main differences between UC and Crohn’s disease?

A

UC: rectum and extends proximally, continuous, no inflammation beyond submucosa, greater risk of colorectal cancer
Crohn’s: mouth to anus involvement, skip lesions, inflammation is transmural (affects all layers), includes goblet cells and granulomas

54
Q

What are the features of UC on barium enema?

A
  1. Loss of haustrations
  2. Superficial ulceration, ‘pseudopolyps’
  3. Long standing disease: colon is narrow and short -‘drainpipe colon’
55
Q

What is the classification of UC?

A
  1. Mild: < 4 stools/day, only a small amount of blood
  2. Moderate: 4-6 stools/day, varying amounts of blood, no systemic upset
  3. Severe: >6 bloody stools per day + features of systemic upset (pyrexia, tachycardia, anaemia, raised inflammatory markers)
56
Q

How is the management of UC divided?

A

Inducing remission and maintenance

57
Q

What is involved in inducing remission in mild to moderate UC?

A
  1. Proctitis
    a. Topical (rectal) aminosalicylate: for distal colitis rectal mesalazine
    b. If remission is not achieved within 4 weeks: add an oral aminosalicylate
    c. If remission still not achieved: add topical or oral corticosteroid
  2. Proctosigmoiditis and left-sided UC:
    a. Topical (rectal) aminosalicylate
    b. If remission is not achieved within 4 weeks: add a high-dose oral aminosalicylate OR switch to a high-dose oral aminosalicylate and a topical corticosteroid
    c. If remission still not achieved stop topical treatments and offer an oral aminosalicylate and an oral corticosteroid
  3. Extensive disease
    a. Topical (rectal) aminosalicylate and a high-dose oral aminosalicylate
    b. If remission is not achieved within 4 weeks: stop topical treatments and offer a high-dose oral aminosalicylate and an oral corticosteroid
58
Q

What is involved in inducing remission in severe UC?

A
  1. Should be treated in hospital
  2. First line: IV steroids
  3. IV ciclosporin may be used if steroid are contraindicated
  4. If after 72 hours there has been no improvement: consider adding intravenous ciclosporin to intravenous corticosteroids or consider surgery
59
Q

What is involved in maintaining remission in mild to moderate UC?

A
  1. Proctitis and proctosigmoiditis:
    a. topical (rectal) aminosalicylate alone (daily or intermittent) or
    b. an oral aminosalicylate plus a topical (rectal) aminosalicylate (daily or intermittent) or
    c. an oral aminosalicylate by itself: this may not be effective as the other two options
  2. Left-sided and extensive UC:
    low maintenance dose of an oral aminosalicylate
60
Q

What is the maintenance remission management of UC following a severe relapse or >=2 exacerbations in the past year?

A

Oral azathioprine or oral mercaptopurine

61
Q

What can lead to a UC flare?

A
  1. Can have no identifiable trigger
  2. Stress
  3. Medications: NSAIDs, antibiotics
  4. Cessation of smoking
62
Q

What are the possible complications of Ulcerative Colitis?

A

From high to low risk:
1. Inflammatory pseudopolyps
2. Primary sclerosing cholangitis
3. Benign stricture
4. Colonic adenocarcinoma
5. Massive lower GI bleed (haemorrhage)
6. Infection
7. Perforation
8. Toxic megacolon

63
Q

What is the prognosis of Ulcerative Colitis?

A
  1. Overall mortality does not appear to be increased in patients with UC compared with the general population, however it is more in patients with associated complications
  2. The most common cause of death remains toxic megacolon
  3. Colonic adenocarcinoma develops in 3% to 5% of patients
64
Q

What is viral hepatitis?

A

An infection with the RNA viruses, hepatitis A (HAV) or hepatitis E virus (HEV), that is not associated with chronic liver disease

65
Q

What are the main risk factors for viral hepatitis?

A
  1. Recent travel (Hep A)
  2. IV drug use (Hep E)
66
Q

What are the common symptoms of viral hepatitis?

A
  1. Nausea and vomiting, anorexia
  2. Myalgia
  3. Lethargy
  4. Right upper quadrant (RUQ) pain
67
Q

What are the signs of Viral hepatitis on physical examination?

A
  1. Pyrexia
  2. Jaundice
  3. Tender hepatomegaly- spleen may be palpable (20%)
  4. Absence of stigmata of chronic liver disease, although a few spider naevi may appear, transiently
68
Q

What is Hepatitis A?

A
  1. Typically a benign, self-limiting disease, with a serious outcome being very rare
  2. Transmission is by faecal-oral spread, often in institutions
  3. Doesn’t cause chronic disease
69
Q

What are the features of Hepatitis A?

A
  1. Flu-like prodrome
  2. Abdominal pain: typically right upper quadrant
  3. Tender hepatomegaly
  4. Jaundice
  5. Deranged liver function tests
70
Q

What is the immunisation of Hepatitis A?

A
  1. An effective vaccine is available
  2. After the initial dose a booster dose should be given 6-12 months later
71
Q

Who should receive Hepatitis A immunisation?

A
  1. People travelling to or going to reside in areas of high or intermediate prevalence, if aged > 1 year old
  2. People with chronic liver disease
  3. Patients with haemophilia
  4. Men who have sex with men
  5. Injecting drug users
  6. Individuals at occupational risk: laboratory worker; staff of large residential institutions; sewage workers; people who work with primates
72
Q

What is Hepatitis B?

A
  1. Spread through exposure to infected blood or body fluids, including vertical transmission from mother to child
  2. The incubation period is 6-20 weeks
  3. ds-DNA virus
73
Q

What are the features of Hepatitis B?

A

Fever, jaundice and elevated liver transaminases

74
Q

What are the complications of Hepatitis B?

A
  1. Chronic hepatitis (5-10%). ‘Ground-glass’ hepatocytes may be seen on light microscopy
  2. Fulminant liver failure (1%)
  3. *Hepatocellular carcinoma
  4. Glomerulonephritis
  5. Polyarteritis nodosa
75
Q

What is the management of Hepatitis B?

A
  1. Pegylated interferon-alpha used to be the only treatment available: reduces viral replication in up to 30% of chronic carriers
  2. Other antiviral medications are increasingly used with an aim to suppress viral replication: e.g. tenofovir
76
Q

What is hepatitis B serology?

A
  1. Surface antigen (HBsAg):
    a. Marker of active infection
    b. Normally implies acute disease (present for 1-6 months)
    c. If present for > 6 months then this implies chronic disease (i.e. Infective)
  2. HBsAb: antibody immunity
    a. Can be through either past infection or immunisation
  3. Anti-HBc implies previous (or current) infection
  4. HBcIgM: appears during acute or recent hepatitis
  5. HbeAg: results from breakdown of core antigen from infected liver cells as is, therefore, a marker of infectivity
77
Q

What is the Hepatitis B serology for someone who has been immunised?

A

anti-HBs positive, all others negative

78
Q

Which factor in serology is a marker of active infection (and therefore a carrier)?

A

HBsAg (surface antigen)

79
Q

What is Hepatitis C?

A
  1. Most common Hepatitis in Europe: can lead to hepatocellular carcinoma
  2. At risk groups include intravenous drug users
80
Q

How is Hepatitis C transmitted?

A
  1. Risk during a needle stick injury is about 2%
  2. Vertical transmission rate from mother to child is about 6%. (higher if there is coexistent HIV)
  3. Breastfeeding is not contraindicated in mothers with hepatitis C
  4. Risk of transmitting the virus during sexual intercourse is probably less than 5%
  5. No vaccine for hepatitis C
81
Q

What are the features of Hepatitis C?

A

Only around 30% of patients will develop features such as:
1. A transient rise in serum aminotransferases / jaundice
2. Fatigue
3. Arthralgia

82
Q

What is the investigation of choice for Hepatitis C?

A

HCV RNA

83
Q

What is chronic Hepatitis C?

A

Defined as the persistence of HCV RNA in the blood for 6 months

84
Q

What are the complications of chronic Hep C?

A
  1. Rheumatological problems: arthralgia, arthritis
  2. Eye problems: Sjogren’s syndrome
  3. Cirrhosis (5-20% of those with chronic disease)
  4. Hepatocellular cancer
  5. Membranoproliferative glomerulonephritis
85
Q

What is the management of Hep C?

A
  1. Treatment depends on the viral genotype - this should be tested prior to treatment
  2. Currently a combination of protease inhibitors (e.g. daclatasvir + sofosbuvir or sofosbuvir + simeprevir) with or without ribavirin are used
  3. Ribavirin:
    a. Tertaogenic
    b. Side-effects: haemolytic anaemia, cough
86
Q

What is Hep D?

A
  1. Transmitted parenterally
  2. It is an incomplete RNA virus that requires hepatitis B surface antigen to complete its replication and transmission cycle
87
Q

What other hepatitis is needed for Hep D infection?

A

Hepatitis B:
1. Co-infection: Hepatitis B and Hepatitis D infection at the same time
2. Superinfection: A hepatitis B surface antigen positive patient subsequently develops a hepatitis D infection

88
Q

What is Hepatitis E?

A
  1. RNA hepevirus
  2. Spread by the faecal-oral route, with an incubation period: 3-8 weeks
  3. Common in Central and South-East Asia, North and West Africa, and in Mexico
89
Q

What is the main difference between Hep A and Hep E?

A

Whilst it causes a similar disease to hepatitis A, it carries a significant mortality (about 20%) during pregnancy

90
Q

What are the prevention measures for Viral hepatitis?

A

For Hep A and E:
1. Public health: Safe water, sanitation, food hygiene standards
2. Both are notifiable diseases
3. Immunization (HAV only)
For Hep B and C:
1. High risk groups are IVDU
2. Serology in mothers who are at high risk
3. Hep B vaccine

91
Q

What is Vitamin B12 deficiency?

A

A common condition that can manifest with neurological, psychiatric, and haematological disorders

92
Q

What is the epidemiology of Vitamin B12 deficiency?

A
  1. Prevalence increases with advancing age
  2. May be more prevalent in vegans and strict vegetarians who don’t get enough dietary supplementation
93
Q

What are the presenting symptoms of Vitamin B12 deficiency?

A
  1. Symptoms of anaemia: dyspnoea, fatigue
  2. Paraesthesias: tingling, early and subtle symptom of neurological damage, may have decreased vibration sense
94
Q

What are the appropriate investigations for Vitamin B12 deficiency?

A
  1. Bloods:
    a. Serum Vitamin B12: <148 picomols/L (<200 picograms/mL) indicates probable vitamin B12 deficiency
    b. FBC: elevated MCV, low haematocrit, low Hb
    c. Reticulocyte count: Low reticulocyte index indicates decreased production
  2. Blood film: megalocytes, hypersegmented polymorphonucleated cells- causing megaloblastic anaemia
95
Q

What is Folate deficiency?

A

Classically presents as megaloblastic anaemia, with absence of neurological signs

96
Q

What is the aetiology of Folate deficiency?

A
  1. Can be due to decreased intake or intestinal malabsorption of folate (such as coeliac disease)
  2. Increased demand in pregnancy, lactation, and prematurity can lead to folate deficiency
97
Q

What is the epidemiology of Folate deficiency?

A

The primary age groups affected:
a. Pre-school children
b. Pregnant women
c. Older people
Thought to be a low prevalence in high income countries and high in low income countries

98
Q

What are the presenting symptoms of Folate deficiency?

A
  1. Symptoms of anaemia: dyspnoea, fatigue
  2. Prolonged diarrhoea
  3. Headache
  4. Loss of appetite
  5. Weight loss
    (No paraesthesia as opposed to B12 deficiency)
99
Q

What are the appropriate investigations for Folate deficiency?

A
  1. Bloods:
    aFBC: low Hb, elevated MCV and MCH
    b. Reticulocytes: low corrected reticulocyte count (decreased production)
    c. Serum folate: low
    d. Red blood cell folate: Low-better indicator of tissue folate status than serum folate
    e. Serum Vitamin B12: IMPORTANT TO EXCLUDE (can co-exist)
  2. Blood film: Macrocytic anaemia, macrocytosis, anisocytosis, poikilocytosis, hypersegmented neutrophils
100
Q

What can Vitamin A deficiency cause?

A

Xerophthalmia is a progressive eye disease where there is abnormal dryness of the conjunctiva and cornea of the eye, with inflammation and ridge formation

101
Q

What are the presenting symptoms and signs of Vitamin A deficiency?

A
  1. Initially presents with with night blindness (may cause injuries)
  2. As diseases progresses, cornea becomes hazy and can develop erosions which can lead to its destruction- complete blindness (dry conjunctiva):
    a. Bitots spots on conjunctiva
    b. Corneal xerosis – cornea appears dry and dull
    c. Corneal ulcerations
    d. Keratomalacia – last stage of xerophthalmia - softening of cornea, followed by perforation of eyeball and blindness
102
Q

What are the appropriate investigations for Vitamin A deficiency?

A
  1. Check sight in darkness
  2. Serum retinol binding protein
  3. Zinc levels – zinc deficiency can interfere with production of retinol-binding protein
  4. Iron studies – can affect metabolism of vitamin A, FBC: for anaemia or infection
103
Q

What is Vitamin B1 deficiency?

A
  1. Known as thiamine deficiency, severe and chronic form is known as beriberi
  2. Can lead to Wernicke’s encephalopathy
104
Q

What are the aetiology and epidemiology of Vitamin B1 deficiency?

A
  1. Dry Beriberi:
    a. Thiamine deficiency with nervous system involvement
    b. Usually occurs with poor caloric intake and physical inactivity
    c. Involves peripheral neuropathy
    d. Wernicke encephalopathy and Korsakoff syndrome are forms of dry beriberi
  2. Wet Beriberi:
    a. Thiamine deficiency with cardiovascular involvement
    b. High cardiac workload results in heart failure with general oedema
    c. Common in alcoholics and in developing countries due to malnutrition
105
Q

What are the presenting symptoms and signs of Vitamin B1 deficiency?

A

Dry:
a. numbness of peripheries
b. confusion
c. trouble moving legs
d. pain
Wet:
a. palpitations
b. SOB
c. leg swelling (oedema)
d. tachycardia

106
Q

What can Vitamin C deficiency lead to?

A

Scurvy (severe deficiency)

107
Q

What are the aetiology and epidemiology of Vitamin C deficiency?

A
  1. Vitamin C is important for wound healing and immune function and iron absorption
  2. Usually due to inadequate diet or increased demand such as in pregnancy
108
Q

What are the presenting symptoms and signs of Vitamin C deficiency?

A
  1. Fatigue
  2. Depression
  3. Rash
  4. Internal bleeding, Petechiae
  5. Gingivitis, loose teeth, foul breath
  6. Impaired wound healing
  7. Bleeding from gums, nose, hair follciles or into joints
  8. In children, bone growth may be impaired
  9. Muscle pain and weakness
109
Q

What are the aetiology and epidemiology of Vitamin E deficiency?

A
  1. Can be caused by cystic fibrosis affecting absorption, abetalipoproteinaemia, chronic cholestatic hepatobiliary disease, short bowel syndrome
  2. Causes haemolysis and neurological deficit
  3. Very rare
110
Q

What are the presenting symptoms and signs of Vitamin E deficiency?

A
  1. Weakness (distal muscle)
  2. Loss of vibration sense
  3. Decline in visual field/ retinopathy
  4. Hyporeflexia
  5. Decreaed proprioception
  6. Ataxia
  7. Dysarthria
111
Q

What are the aetiology and epidemiology of Vitamin K deficiency?

A
  1. Vitamin K is important for coagulopathy so main symptom is excessive bleeding
  2. Risk Factors:
    a. Anticoagulants
    b. Lack of vitamin K in diet
    c. Antibiotics which interfere with vitamin K absorption
    d. Fat malabsorption e.g. in coeliac disease, CF
  3. Rare in adults, more common in infants
112
Q

What are the presenting symptoms and signs of Vitamin K deficiency?

A
  1. Easily bruising
  2. Dark black, tar like stool
  3. Nose bleeds (epistaxis- haemorrhage)
113
Q

What is the management of Vitamin deficiency (A, B, C, D, E, K)?

A
  1. Vitamin A:
    a. Supplements
    b. Re-educate and monitor diet: chicken, eggs, leafy green veg
  2. Vitamin B1:
    a. Thiamine (Pabrinex) IV
    b. Oral supplementation to continue after IV
    c. If there is coexisting hypoglycaemia, ensure thiamine given before glucose
  3. Vitamin C:
    a. Dietary education
    b. Ascorbic acid >250mg/24h oral
  4. Vitamin D:
    a. Vitamin D and calcium replacement
    b. Monitor 24 hr urinary calcium, serum calcium, Phosphate, ALP, PTH, Vitamin D levels
    c. Treat the underlying cause
  5. Vitamin E: supplements
  6. Vitamin K: Vitamin K supplement
114
Q

What are the possible complications of Vitamin deficiency (A, B, C, D, E, K)?

A
  1. Vitamin A: Blindness and respiratory infections
  2. Vitamin B: Wernicke’s encephalopathy and Korsakoff’s psychosis
  3. Vitamin C: Scurvy; easy bruising, easy bleeding and joint and muscle pains
  4. Vitamin D:
    a. Bone deformities
    b. Depression
    c. Hypocalcaemia symptoms = CATs go NUMB: Convulsions, Arrhythmias, Tetany, NUMBness/paraesthesia
  5. Vitamin K: Excessive bleeding and anaemia
115
Q

What is the prognosis of Vitamin deficiency (A, B, C, D, E, K)?

A
  1. Generally good if treated early
  2. Korsakoff psychosis is chronic
  3. Bone deformities in children are permanent
116
Q

What is Volvulus?

A

Defined as torsion of the colon around it’s mesenteric axis resulting in compromised blood flow and closed loop obstruction

117
Q

What are the most common sites for Volvulus?

A
  1. Sigmoid volvulus:
    a. Around 80% of cases
    b. Describes large bowel obstruction caused by the sigmoid colon twisting on the sigmoid mesocolon
  2. Caecum:
    a. 20% of cases
    b. Usually a retroperitoneal structure hence why only 20%
118
Q

What is associated with sigmoid volulus?

A
  1. Older patients
    2.Chronic constipation
  2. Chagas disease
  3. Neurological conditions e.g. Parkinson’s disease, Duchenne muscular dystrophy
  4. Psychiatric conditions e.g. schizophrenia
119
Q

What is associated with Caecal volvulus?

A
  1. All ages
  2. Adhesions
  3. Pregnancy
120
Q

What are the features of volvulus?

A
  1. Constipation
  2. Abdominal bloating
  3. Abdominal pain
  4. Nausea/vomiting
121
Q

What is the first line investigation for volvulus?

A

Usually abdominal film:
1. Sigmoid volvulus: large bowel obstruction (large, dilated loop of colon, often with air-fluid levels) + coffee bean sign
2. Caecal volvulus: small bowel obstruction may be seen

122
Q

What is the best investigation for volvulus?

A

CT scan: because volvulus usually presents as large bowel obstruction (if sigmoid) or small bowel (if caecal)

123
Q

What is the management of volvulus?

A
  1. Sigmoid volvulus: rigid sigmoidoscopy with rectal tube insertion
  2. Caecal volvulus: management is usually operative, right hemicolectomy is often needed
124
Q

What is Wilson’s disease?

A

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

125
Q

What is the aetiology of Wilson’s disease?

A
  1. Caused by a defect in the ATP7B gene located on chromosome 13
  2. As a result metabolic abnormalities arise, including increased copper absorption from the small intestine and decreased hepatic copper excretion
126
Q

What are the main features of Wilson’s disease?

A

Result from excessive copper deposition in the tissues, especially the brain, liver and cornea:
1. Liver: hepatitis, cirrhosis
2. Neurological:
a. basal ganglia degeneration
b. speech, behavioural and psychiatric problems (often the first manifestations)
c. also: asterixis, chorea, dementia, parkinsonism
3. Kayser-Fleischer rings:
a. green-brown rings in the periphery of the iris
b. due to copper accumulation in Descemet membrane
c. Often a sign of neurological involvement

127
Q

What are the other features of Wilson’s disease aside from Liver, brain and cornea involvement?

A
  1. Renal tubular acidosis (esp. Fanconi syndrome)
  2. Haemolysis
  3. Blue nails
128
Q

What are the investigations for Wilson’s disease?

A
  1. Slit lamp examination for Kayser-Fleischer rings
  2. Reduced serum caeruloplasmin
  3. Reduced total serum copper (counter-intuitive, but 95% of plasma copper is carried by ceruloplasmin): free (non-ceruloplasmin-bound) serum copper is increased
  4. Increased 24hr urinary copper excretion
  5. Diagnosis is confirmed by genetic analysis of the ATP7B gene
129
Q

What is the management of Wilson’s disease?

A
  1. Penicillamine (chelates copper) has been the traditional first-line treatment
  2. Trientine hydrochloride is an alternative chelating agent which may become first-line treatment in the future
130
Q

What can penicillamine (copper chelating agent) increase the risk of?

A
  1. Membranous glomerulonephritis
  2. May exacerbate an myasthenia crisis

!Final Year (26 decks)

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