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Year 4 > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

What species causes amoebiasis

A

Entamoaeba histolytic

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2
Q

Pathophysiology of E.histolytica

A

Enter the small intestines and release active amoebic parasites (trophozoites) which invade epithelial cells of large intestines = ulcers

Then spreads to other organs through the venous system

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3
Q

What is the asymptomatic stage of E.histolytica

A

Passing the cysts through faeces

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4
Q

How long do cysts in amoebiasis last for

A

2 Months

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5
Q

What is the most common site for invasive amoebiasis

A

Liver

Can affect the lung, heart, brain and urinary tract/skin

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6
Q

Most common place to get amoebiasis

A

South and Central America, West Africa

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7
Q

Risk factors for Amoebiasis

A

MSM (oral-anal sex)
Travellers and immigrants

Usually spread faeco-oral route

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8
Q

What percentage of people with amoebiasis are asymptomatic

A

90% of infections

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9
Q

Presentation of intestinal amoebiasis

A
  1. ASYMPTOMATIC passage of cysts
  2. Abdo pain in the RIGHT or both iliac fossa but may be general and diarrhoea -> dysentry (blood and mucous in the stool)
  3. Sometimes can present without dysentry: A change in bowel habit, bloodstained stools, flatulence and colicky pain
  4. Rectal Bleeding
  5. Amoeboma
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10
Q

What is an amoeba

A

Abdominal mass in the right iliac fossa

Maybe painful and tender

Intermittent dysentry

Signs of bowel obstruction

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11
Q

What is an amoeba

A

Mass that kind of looks like colorectal carcinomas

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12
Q

What’ is fulminant colitis

A

Rare but serious form of Ulcerative Colitis

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13
Q

Risk Factors for fulminant colitis

A

Children and patients taking steroids

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14
Q

Signs of fulminant colitis

A

High-grade fever
Severe Abdominal Pain
Distention of the abdomen
Water diarrhoea

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15
Q

Signs of fulminant colitis on an X-Ray

A

Free peritoneal gas with acute gaseous dilatation of the colon

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16
Q

When does hepatic amoebiasis present

A

8 weeks to one year after initial infection

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17
Q

Signs of hepatic amoebiasis

A
  1. ANAEMIA PLUS DRY COUGH
  2. Fever starting in the evening
  3. Sweating, pyrexia and upper right quadrant pain
  4. Hepatomegaly
  5. Epigastri mass from left lobe lesion
  6. Reduced breath sounds or crepitations at the right lung base
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18
Q

Investigation for amoebiasis

A

STOOL:
1. Microscopic stool examination for trophozoites in patients with diarrhoea

  1. Repeat 3 to 6 times
  2. Specific stool E.Histolyltica testing (cultures, antigen testing or PCR)

SEROLOGY:

Antibody testing in 100% of cases of liver abscesses

USS or CT of abdomen for suspected hepatic amoebiasis

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19
Q

Management of amoebiasis

A
  1. Diloxanide Furoate for ASYMPTOMATIC individuals
  2. Metronidazole for ACUTE INVASIVE AMOEBIAC DYSENTRY

Or Tinidazole

Followed by 10 day course of diloxanide furoate to destroy remaining amoebae

Liver Amboiasis: Metronidazole + Tinidazole followed by Diloxanide Furoate for 10 days

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20
Q

When should abscess drainage be considered in amoebiasis

A

no improvement after 72 hours of treatment

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21
Q

What are the contraindications to amoebiasis drainage

A

Elderly
Frail
Septic Shock
Multilocular cysts

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22
Q

If there are contraindications to amoebiasis drainage, what should be done

A

Laparotomy (also done if ruptured)

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23
Q

Complications of amoebic colitis

A
  1. Fulminant colitis
  2. Toxic Megacolon
  3. Rectovaginal fistula
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24
Q

Is there a vaccine for amoebiasis

A

No

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25
Q

Why is ALT more specific to the liver than AST

A

ALT reside ONLY in hepatocellular cytoplasms

AST reside in cardiac and skeletal muscles as well

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26
Q

What does raised CK show

A

Muscle damage marker

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27
Q

What is the indication of ALT rising more than AST

A

Acute liver damage

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28
Q

What conditions usually have ALT over 1000 IU/L (very high

A

Drug-induced hepatitis (e.g., Paracetamol)
Acute Viral Hep A or B
Ischaremic hepatitis

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29
Q

Levels of ALT compared to AST in chronic liver disease

A

ALT > AST

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30
Q

Ratio of AST to ALT in cirrhosis

A

AST > ALT

ALT = ACUTE

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31
Q

What does a ratio of AST:ALT < 1.0 indicate

A

Non-alcoholic Liver Disease

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32
Q

Where is ALP commonly produced

A

Cells lining bile ducts

Bone

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33
Q

How can we differentiate between altered ALP from bone or from the bile duct?

A

Cholestasis = GGT PLUS ALP is elevated

Bone Disorders: ALP elevated ONLY,GGT normal

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34
Q

What investiagation can be performed to check for the source of ALP

A

Isoenzyme Analysis

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35
Q

AST:ALT ratio in alcoholic vs non-alcoholic fatty liver disease

A

AST:ALT > 1 in alcoholic

AST:ALT > 2 in non-alcoholic

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36
Q

In Acute Obstructive Hepatitis, what is the sequence of ALT/AST levels and bilirubin levels that is seen during infection

A

ALT/AST rise first

Then Bilirubin rises

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37
Q

What drugs can commonly cause liver injury

A

ACE inhibitors

Hormones: Oestrogen

Erythromycin 
Tricyclicic Antidepressants
Flucloxacillin 
COCP 
Anabolic Steroids
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38
Q

What usually causes an isolated rise in GGT

A

Alcohol Abuse or Enzyme-inducing drugs

Stopping Alcohol use for 4 weeks - FIRST LINE

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39
Q

What serum levels are prognostic for primary sclerosing cholangitis

A

NOT ALP

Serum Bilirubin Levels

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40
Q

Why can isolated abnormal ALP levels be a sign of metastatic cancers

A

Because it is a sign of invasion to the liver (e.g., sarcoidosis)

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41
Q

Name four bone conditions that have isolated raised ALP levels

A
  1. Fractures
  2. Paget’s disease of the bone
  3. Osteomalacia
  4. Bony Metastasis
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42
Q

Why can ALP be normal in myeloma or osteoporosis

A

Because it is only released in the presence of a fracture

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43
Q

How should SLIGHTLY abnormal LFT rises be managed

A

SLIGHTLY: Less than twice the upper limit of normal

Consider viral serology and ultrasound

Referral for further investigation

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44
Q

Define VERY abnormal LFTs

A

More than twice the upper limit of abnormal

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45
Q

Management of very abnormal LFTs

A
  1. Organise further blood tests and imagine
  2. Refer to outpatients urgently if cancer is suspected

HOSPITAL ADMISSION if VERY UNWELL (e.g., jaundice, ascites, encephalopathy, sepsis etc)

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46
Q

What are the role of the interstitial cells of Canal

A

Cells that form a pacemaker for intestinal musculature

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47
Q

Presentation of Achalasia

A
  1. Food impaction
  2. DYSPHAGIA
  3. Regurgitation
  4. Chest pain/Heartburn
  5. Loww of weight = malignancy
  6. Nocturnal cough
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48
Q

What is the GOLD STANDARD for achalasia

A

Manometry (high pressure in the cardiac sphincter and absent peristalsis)

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49
Q

Management of Achalasia

A

FIRST LINE: CCB and Nitrates to reduce pressure in the lower oesophageal sphincter

SURGEICAL: Heller Myotomy

If elderly, pneumatic dilatation

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50
Q

What is the main cause for acute pancreatitis

A

Gallstones by blocking the bile duct

2. Excess alcoholic conduction = periductal necrosis

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51
Q

What viruses can cause acute pancreatitis

A

Coxsackie B
Hepatitis
Mumps

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52
Q

What indicates a mumps cause of acute pancreatitis over otehrs

A

Prodromal Diarrhoea

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53
Q

What injuries can cause acute pancreatitis

A

ERCP

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54
Q

Name 5 metabolic causes of acute pancreatitis

A
  1. Hyperlipoproteniaemia
  2. Hyperparathyroidism
  3. Hypothermia
  4. Uraemia
    5, Anorexia
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55
Q

What drugs can cause acute pancreatitis

A
  1. Thiazides
  2. Valproate
  3. Azathioprine
  4. Steroids
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56
Q

Symptoms of acute pancreatitis

A
  1. Cullen sign + grey-turner sign

2. Sudden upper abode pain + vomtiing

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57
Q

What is characteristic about the pain in acute pancreatitis

A

Left UQ pain that radiates to the back

Pain decreases steadily over 72 hours

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58
Q

First Line investigation for acute pnacreatitis

A
  1. Serum Amylase levels raised

2. Plain erect Abdominal X-Ray FIRST, then CT scan which is DIAGNOSTIC

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59
Q

What blood tests indicate prognosis of acute pancreatitis

A

FBCs, U and Es and CRP

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60
Q

What metabolic finding is common in acute pancreatitis

A

Hypocalcaemia

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61
Q

Name two prognostic scores for pancreatitis

A

Glasgow Prognostic Score

Ranson’s Criteria

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62
Q

Management of acute pancreatitis

A
  1. Pain Reflief: Pethidine or Buprenorphine +/- IV BDZs

IV fluids + Nil by mouth

NG tube only for severe vomtiing

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63
Q

Why is morphine contraindicated for use in acute pancreatitis

A

Spastic effects of the sphincter of odds

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64
Q

What causes the progression of acute pancreatitis to chronic

A

Background of recurrent attacks, alcohol or smoking

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65
Q

What types of anal tumours are more common in men than women

A

Anal Margin tuomurs

Women: Anal canal tumours

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66
Q

What is the lymphatic drainage of anal carcinomas

A

Perirectal nodes

Above the dentate: Internal Pudendal nodes

Below the dentate: Inguinal, femoral and external iliac

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67
Q

What is causing an increase in rectal carcinomas

A

MSM: HPV infections

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68
Q

Risk Factors for anal carcinomas

A
  1. HPV
  2. Anal Intercourse
  3. High sexual partenrs
    4, MSM
  4. HIV
  5. Cervical cancer or CIN
  6. Smoking
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69
Q

Presentation of anal cancer

A
  1. Perianal bleeding and pain
  2. Palpable lesion
  3. Faecal incontinnence

RECTOVAGINAL FISTULAS in women

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70
Q

Through what nodes do anal margin carcinomas spread to

A

Inguinal lymph nodes

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71
Q

Through what nodes do anal canal carcinomas spread to

A

Pelvic Lymph Nodes

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72
Q

Initial investigation for anal carcnioma

A

DRE -> Biopsy -> palpate inguinal nodes

CT to stage

Check for CIN and HIV infections

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73
Q

First Line treatment for anal carcniomas

A

WELL DIFFERENTIATED: local excision

CHEMO: 5-Fluorouracil + Mitomycin C

Second line: Radiotherapy

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74
Q

Treatment of node involvement in anal cancer

A

Radiotherapy

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75
Q

What are the major prognostic factors for anal cancer

A
  1. Site, size (>4-5 cm) and lymph nodes status
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76
Q

What is the most common type of anorectal abscess

A

Perianal abscess

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77
Q

RF for anorectal abscesses

A 
Diabetes
Immunocompromised patients
MSM
IBD 
20-60 
Men more than women
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78
Q

Presentation of anorectal abscess

A 
Painful, hardened tissue in the perianal area, discharge of pus from the retcum 
Tenderness
fever
Constipation 
Dyzchezia
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79
Q

Describe the nature of the pain in an anorectal abscess

A

Constant and thrombing

WORSE WHEN SITTING DOWN

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80
Q

Investigation for Anorectal Abscess

A

A DRE

Initial Investigation: STI screens/IBD or diverticular disease

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81
Q

What is Goodsall’s rule for fistulas associated with anorectal abscesses

A

Fistulas usually open into the anal canal in the midline posteriorly

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82
Q

Management of anorectal abscesses

A 
Prompt surgical drainage 
Pain relief (NSAIDs)
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83
Q

When are antibiotics indicated for anorectal abscesses

A

ONLY with an underlying condition

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84
Q

What is Grade I ascites

A

ONLY DETECTABLE by USS

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85
Q

What is Grade 2 ascites

A

Moderate symmetrical distention of the abdomen

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86
Q

What is Grade 3 ascites

A

MARKED ABDO DISTENTION

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87
Q

What is diuretic-resistant ascites

A

Refractory to dietary sodium restriction and intensive diuretic treatment for at least one week

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88
Q

What ovarian condition can cause ascited

A

Meigs’ Syndrome + Pelural effusions - usually unilateral

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89
Q

What haematological malignancies can cause ascites

A

Hodgkin’s and Non-Hodgkin’s Lymphoma

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90
Q

What are Sister Mary Joseph nodules

A

Found in ascites, a firm nodule in the umbilicus

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91
Q

What causes Sister Mary Joseph’s nodule

A

Carcinomatosis originating from gastric, pancreatic or hepatic primaries

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92
Q

What is Virchow’s node

A

A left sided supraclavicular node

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93
Q

What does Virchow’s node indicate

A

Presence of an upper abdominal malignancy

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94
Q

What is Virchow’s triad

A
  1. venous Stasis
  2. Hypercoagulability
  3. Endothelial Injury

Causes of VTE

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95
Q

How can we monitor ascites

A
  1. Abdominal Girth

2. Weight

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96
Q

Management of ascites

A
  1. Treat underlying cuase
  2. A diet with salt intake restricted <90 mmol/day but can’t be effective in some conditions

FIRST LINE MEDICAL MANAGEMENT:
Spironolactone to increase sodium excretion and K+ absorption

Add a loop diuretic as an adjunct once maximum dose is reached

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97
Q

What initial surgical procedure can be used to relief ascites

A

Therapeutic Paracentesis, then give human albumin solution

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98
Q

What monoclonal antibody can be given to treat ascites

A

Catumaxomab

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99
Q

What major surgical procedure can be used to treat ascites

A

TIPS - more permanent than paracentesis

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100
Q

Complications of Ascites

A

Hyponateraemia from diuretics

2. Infections

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101
Q

Name 5 autoantibodies associated with autoimmune Hepatitis

A
  1. ANA (most common)
  2. ASMA (most common)
  3. anti-LKM-1
  4. Anti-SLA
  5. AMA

Antiphospholipid antibodies

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102
Q

First line investigations for autoimmune hepatitis

A
  1. Autoantibodies serum
  2. Serum protein electrophoresis

(IgG-predominant polyclonal hypergammaglobulinaemia

Raised IgG and gamma globulin

  1. AST and ALT elevated
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103
Q

GOLD STANDARD DIAGNOSTIC for AIH

A

Liver Biopsy

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104
Q

What investigation provides information on prognosis of AIH

A

Liver Biopsy

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105
Q

What autoimmune condition is particularly associated with AIH

A

Autoimmune thyroid disorders

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106
Q

Management of AIH

A
  1. Steroid induction therapy + Azathioprine for maintenance

Then a liver transplant at the terminal phases (not as commonly used)

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107
Q

How should AIH be monitored

A
  1. Test for Hep A and B immunity
  2. LFTs, glucose and FBC
  3. Calcium and Vit D supplements + DEXA scan if they’r eon steroids
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108
Q

Complication of AIH

A
  1. Hyperviscocity Syndorme

2. Carcinomas

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109
Q

What are the two types of Barrett’s Oesophagus

A

Short-Segment - <3cm

Long-Segment - >3cm

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110
Q

What kind of squamous change is seen to cause Barrett’s Oesophagus

A

Dysplasia of cells: We go from squamous to adenocarcinoma od the oesophagus

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111
Q

Risk Factors for Barrett’s Oesophagus

A 
Men
White
Increasing Age
FH 
GORD
Hiatus Hernia 
Obesity 
Smoking
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112
Q

What appears to be protective of Barrett’s Oesophagus

A

NSAIDs (blocks inflammatory cox receptors)

H. Pylori infection

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113
Q

What length Barret’s Oesophagus segment is associated with progression to Adenocarcnioma

A

> 8 cm

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114
Q

Symptoms of Barrett’s Oesophagus

A

Long History of GORD in white male, sometimes with a bit of dysphagia

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115
Q

Investigation of Barrett’s Oesophagus

A

Histology from a biopsy

Shows high grade dysplasia

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116
Q

Management of Barrett’s Oesophagus

A

LOW GRADE: Surveillance every 6 months

High-Grade: Photodynamic Therapy to downgrade dysplasia followed by radio frequency ablation

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117
Q

What is the last line surgical management of Barrett’s Oesophagus

A

Oesophagectomy

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118
Q

Life style advice for people with Barrett’s

A 
Reduce Weight 
Stop Smoking 
Reduce alcohol 
Raise head of bed at night 
Take small, regular meals
Avoid alcohol, eating and hot drinks within three hours of going to bed
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119
Q

What drugs slow down oesophageal motility

A

Nitrates
Anticholinergics
Tricyclics anti

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120
Q

What drugs damage the mucosa

A

Alendronate
Potassium Salts
NSAIDs

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121
Q

Initial drug therapy for Barrett’s

A

PPI once daily

Push up to twice daily for reisstant

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122
Q

Why is Nissen’s Fundoplication not recommended for Barrett’s Oesophagus

A

Does not prevent progression of Barrett’s Oesophagus to Oesophageal cancer

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123
Q

When should endoscopic screening be used for patients

A

Only if they hold MULTIPLE risk factors from those discussed or FH

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124
Q

What is the most common type of Benign Liver Tumour

A

hemangiomas

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125
Q

In what lobe are hemangiomas common in

A

Right lobe of the liver

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126
Q

What drug can enlarge haemngiomas

A

COCP and during pregnancy

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127
Q

How are hepatic hemangiomas managed in children

A

Regress within first two years of life

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128
Q

Presentation of hepatic hemangioas

A

R UQ pain
But usually asymptomatic and found incidentally on USS

Hepatomegaly or an arterial bruit

LArge Abdo mass
High-Output cardiac failure
Thrombocytopenia
Hypofibrinogenaemia
Microangiopathic haemolytic anaemia

ALL RARE^^

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129
Q

GOLD STANDARD for hemangiomas

A

USS

Contrast-enhanced CT

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130
Q

Management of a hemangiomas

A

Surgical resection

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131
Q

In what women are hepatic adenomas common

A

Females (15-45)

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132
Q

Signs of hepatic adenomas

A

Asymptomatic but can have slight abdo pain in the epigastrium + bloating

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133
Q

What serum levels are raise din hepatic adenoma

A

GGT
ALP

AFP

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134
Q

What conditions can cause hepatic adenomas

A
  1. Steroids
  2. Beta-thalassaemia
  3. T1 DM
  4. Glycogen storage disease
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135
Q

Management of Hepatic Adenomas

A

STOP COCP or STEROIDS

Avoid pregnancy

ANNUAL USS imaging and serum AFP levels for those who do not get resection

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136
Q

What is focal nodular hyperplasia

A

Benign nodules found on the liver - a type of benign tumour

Usually left alone, no surgical intervention

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137
Q

What is Type I Bile Malabsorption

A

Ileal Dysfunction

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138
Q

What conditions cause Types 1 BAM

A

Ileal Crohn’s disease or resection of the ileum

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139
Q

Why does Type I BAM cause bile malabsorption

A

Failure to reabsorb bile acids in the distal ileum so they spill over into the colon

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140
Q

What is Type II BAM

A

Idiopathic bile acid malabsorption, primary bilee acid diarrhoea

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141
Q

What conditions can result in BAD (Bile acid diarrhoea)

A

Ileal Crohn’s or resection

IBS-D

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142
Q

Presentation of BAM

A
  1. CHRONIC water, NO BLOOD diarrhoea
  2. Looks very IBS-like
  3. Long history of diarrhoea lasting over 10 years

Can be continuous or intermittent, nocturnal diarrhoea

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143
Q

Investigation of BAM

A

Selenium Homocholic Acid Taurine test to look for bile

  1. Serum C4 levels increased (shows increased bile acid synthesis in replacement of the bile acid lost
  2. Total stool bile acid
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144
Q

How are serum C4 levels measured

A

Requires a fasting sample

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145
Q

Management of BAD/ BAM

A

Bile Acid Binders: Colestyramine

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146
Q

Side-Effect of Cholestyramine

A

COnstipation

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147
Q

Signs of Biliary Atresia

A
  1. Normal Meconium in first few days
  2. Pale stools
  3. Normal Urine

Late Presentation: Splenomegaly from portal hypertension

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148
Q

Surgical management of Biliary Atresia

A

Kasai Portoenterostomy

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149
Q

What is Small Intestinal Bacterial Overgrowth Syndrome (Blind Loop Syndrome)

A

Where a portion of the small intestine is bypassed and cut off from the normal flow of food = malabsorption and bacterial overgrowth from stagnant food ferments

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150
Q

What conditions can be associated with small intestinal bacterial overgrowth

A

IBS
Other malabsorption syndromes (e.g., small bowel syndrome)

CF, Hypothyroidism, Coeliac’s, diverticular disease

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151
Q

How is SIBO diagnosed

A

Hydrogen breath test

GOLD: Aspiration and direct culture of jejunal aspirate

Jejunum biopsy: Crypt hyperplasia and flattened villi

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152
Q

Management of SIBO

A

Antibiotic management (TETRACYCLINES)

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153
Q

What are brebiotics

A

Alter gut bacteria by favouring growth of certain bacterial species

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154
Q

What are probiotics

A

Enhance gut barrier function, reducing inflammatory response

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155
Q

What nutrients can become deficient in SIBO

A
  1. B12 deficiency
  2. Iron deficiency
  3. Vit K decieincy
  4. Vit D deficiency
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156
Q

Presentation of SIBO

A
  1. Loss of appetite
  2. Dyspepsia
  3. Diarrhoea and steatorrhoea
  4. Bloating, Flatulence
  5. Weight Loss
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157
Q

Blood test results in SIBO

A
  1. Macrocytci anaemia from B12 deficiency
  2. Hypocalvaemia from Vit D deficiency
  3. Iron Deficiency
  4. Raised INR from Vit K deficiency
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158
Q

Management of SIBO

A
  1. Surgical correction from previous surgery

2. TETRACYCLINES

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159
Q

Where are polyps in FAP found

A

Proximal colon (these SPARE the rectum!!)

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160
Q

What investigation is done for FAP

A

Screen using flexible sigmoidoscopy for biopsy

THEN,

Colonoscopy (no sigmoidoscopy) for surveillance from 20-25 years of age annually

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161
Q

What cancers are associated with FAP

A

Colorectal cancer at the age of 40

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162
Q

What is Gardner’s Syndrome

A

Colonic polyposis with osteomalacia and soft tissue tumours

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163
Q

What is Turcot’s Syndorme

A

Colonic Polyposis and tumours of the CNS

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164
Q

At what age is FAP seen

A

15

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165
Q

What chromosome is responsible for FAP

A

5

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166
Q

At what age is FAP caused colorectal cancer seen

A

40 years old

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167
Q

Signs of FAP

A
  1. Obstruction: Constipation, vomiting and peritonitis
  2. Rectal bleeding
  3. Diarrhoea
  4. Abdo pain
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168
Q

Signs of FAP form gastric polyps

A

Epigastric pain and bleeding

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169
Q

Signs of FAP with duodenal polyps

A

Pain, bleeding or obstructive jaundice

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170
Q

Signs of FAP with polyps in the ileum

A

Obstruction

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171
Q

Where else can polyps be found in FAP

A

Thyroid, can result in thyroid carcnioma and symptoms

Dental problems: SUpernumeary teeth

Dermoid tumours

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172
Q

Investigations for FAP

A
  1. FBC

2. Carcinoembryonic Antigen testing (CEA test)

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173
Q

In what carcnioma is CEA antibodies seen

A

Colorectal carcinomas

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174
Q

What is Peutz-Jeghers Syndrome and how does this vary from FAP

A

Multiple polyps in the intestines with PIGMENTATION of the lips/hands/feet and gum buccal mucosa

Repeated bouts of abdo pain in young patient from obstruction

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175
Q

What medication is given for FAP management

A

Aspirin and Celecoxib to reduce recurrence

Sulindac or Tamoxifen

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176
Q

What surgery is used to treat FAP

A
  1. Proctocolectomoy with ileostomy

2. Total colectomy with ileo-rectal anastomosis

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177
Q

What is acute mesenteric ischaemia

A
  1. Umbrella term for obstructed blood supply to the GI tract
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178
Q

What age people are affected by acute mesenteric ischaemia

A

Over 50

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179
Q

Risk Factors for Acute Mesenteric Ischaemia

A

CONDITIONS THAT CAUSE EMBOLI:

AF
MI
Mitral Stenosis
Septic Emobil from endocarditis
Aortic aneurysms
Dissections
Arteritis
Atherosclerosis

Hypotension
Vasopressive drugs
Cocaine

Hypercoagulaility disorders (protein C and S deficiency)
Infections: Appendicitis, Diverticulitis, Cirrhosis
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180
Q

Presentation of Acute Mesenteric Ischaemia

A
  1. Colicky or constant but POORLY LOCALISED pain
  2. CHARACTERISTIC: Physical findings are very very minimal compared to the high severity of pain (no guarding or tenderness.

Later you can get signs of peritoneum

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181
Q

Investigation for Acute Mesenteric Iaschaemia

A

CT Angiography

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182
Q

Management of Acute Mesenteric Ischaemia

A
  1. Resus with IV Fluids and Oxygen FIRST
  2. NG Tube
  3. IV Broad Spectrum Antibiotics
  4. IV Unfractioned Heparin
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183
Q

When is a laparotomy indicated for patients with acute mesenteric ischaemia

A

Overt Peritonitis symptoms, to try re-establish blood supply

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184
Q

What arteries are blocked in chronic mesenteric ischaemia

A

ALL THREE ARTERIES

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185
Q

What artery supplies the transverse and descending colon

A

Marginal branches of the middle colic and left colic arteries

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186
Q

Presentation of ischaemic Colitis

A

Left iliac fossa pain
Nausea and Vomiting

Very non-specific, late stage is diarrhoea

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187
Q

What sign would indicate an alternative diagnosis to ischaemic colitis

A

Peritonism - shows full thickness ichshcaemia

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188
Q

Describe the progression of symptoms in ischaemic colitis

A

Symptoms manifest in a few hours and continue to worsen, systemic instability

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189
Q

Investigation of Ischaemic colitis

A
  1. EXLCUSION

Metabolic Acidosis
Colonoscopy: Blue, swollen mucosa SPARING the rectum

Gas on X-Ray of the abdomen

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190
Q

What characeristic sign is seen in ischaemic colitis/ mesenteric ischaemia on a barium enema

A

Thumb Printing

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191
Q

Management of ischaemic colitis

A
  1. Relief cause of hypo perfusion

2. Supportive care + Broad-spectrum antibiotics

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192
Q

When is surgery indicated for ischaemic colitis

A

If symptoms do not improve in 24-48 hours

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193
Q

What haematological conditions can cause Budd-Chiari Syndrome

A
  1. PC Vera
  2. Protein C and S deficiency
  3. APl
  4. OBestetrics
  5. COCP
  6. Sjogren’s disease, Behcet’s disease etc
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194
Q

Signs of Budd-Chiari Syndrome

A
  1. NEEDS MORE THAN ONE HEPATIC VEIN TO BE OBSTRUCTED
  2. SUDDEN RUQ pain
  3. Usually presents with gradually worsening ascites + NO JAUNDICE

Most will also have associated renal impairment

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195
Q

Signs of budd-chiari syndrome on ascitic fluid tap

A

High protein content

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196
Q

Who should be contacted if campylobacter infection is suspected

A

PHE

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197
Q

How is Campylobacter spread

A

Animal-to-Humans

Undercooked POULTRY
Pets with diarrhoea
Unpasteurised and raw milk

Southeast Asia
Occupational exposure
Contaminated water supply

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198
Q

Incubation period of campylobacter

A

2-5 days

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199
Q

Presentation of Campylobacter

A
  1. PRODROME illness of fever, headache and myalgia for 24 hours to one week.

Abdo pain with colicky, BLOODY diarrhoea
Tenesmus

Iliac fossa pain (either right or left)

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200
Q

Investigation of Campylobacter infections

A

CULTURE:

But only needed if person is systemically unwell or there are concerns in their history

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201
Q

Management of Campylobacter

A

REHYDRATION, consider hospital admission

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202
Q

What is Racecadotril

A

Intestinal antisecretory enkephalinase inhibitory, reducing hypersectrion of water and electrolytes into the intestines

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203
Q

In which adults are anti motility agents considered for acute diarrhoea

A
  1. WHO NEED TO GO BACK TO WORK OR ATTEND AN EVENT
  2. WHO CAN’t REACH THE TOILET ON TIME
  3. NEED TO TRAVEL
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204
Q

What is the first line anti motility treatment for acute diarrhoea

A

Loperamide

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205
Q

In which conditions is loperamide not given

A
  1. Dysentry
  2. E coli 0157
  3. Shigella
  4. IBD
  5. Pseudomembranous COlitis
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206
Q

What is first line treatment for campylobacter infections

A

Erythromycin for 5-7 days

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207
Q

How long should children or adults be off school for with campylobacter

A

48 Hours from last episode of diarrhoea

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208
Q

Other than Colorectal cancer, what other conditions may have raised CEA

A
  1. Breast, lung and upper GI cancers
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209
Q

What cancer tumour marker is checked for breast cancer

A

CA15-3

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210
Q

What is the triad of symptoms seen in carcinoid Syndrome

A
  1. Diarrhoea
  2. SOB
  3. Facial Flushing
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211
Q

What tumour is seen in carcinoid syndrome

A

Neuroendocrine tumours

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212
Q

Where are neuroendocrine cells found

A

Lungs and GI organs

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213
Q

What do neuroendocrine cells secrete

A

Respond to nerve cells:

Serotonin
Histamine
Bradykinin (vasodilators)
Prostaglandins (vasodilators)

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214
Q

What hormone can control the activity of neuroendocrine cells

A

Somatostatin - released by the hypothalamus

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215
Q

How does somatostatin affect the release of hormones by neuroendocrine cells

A

Inhibits the release of hormones (serotonin)

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216
Q

What is the role of serotonin in the GI system

A

Increases motility and peristalsis

Acts on platelets to constrict blood vessels

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217
Q

What is the problem with neuroendocrine tumours

A

They start hypersecreting the products previously mentioned

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218
Q

Most common site of metastiasis for neuroendocrine tumours

A

Liver - metastasis NEEDED to cause carcinoid syndrome as it stops breakdown of hormone products (e.g., serotonin)

Histamine and Bradykinin -> vasodilation -> flushing

Histamine -> itching

Serotonin -> FIBROSIS, Tricuspid regurgitation, urethral obstruction and impaired kidney function

Bronchoconstriction -> asthma and sob

Serotonin reduces tryptophan -> less niacin -> pellagra

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219
Q

How do we diagnose Carcinoid Syndrome

A

Urinalysis: Raised 5-Hydroxyindolecetic acid
CT/MRI
Octreoscan/Gallium 68 PET scan

Blood Tests: Niacin Deficiency

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220
Q

Describe the abdominal pain felt in carcinoid syndrome

A

Vague, right sided abdominal discomfort

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221
Q

Why does carcinoid syndrome result in endocardial fibrosis

A

ONLY IN LIVER involvement, as it stops to degradation of serotonin into 5-hydroxyindolecetic acid, causing more to act on platelets -> more fibrogenesis.

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222
Q

Defining characteristic of gastric carcinoid tumours

A

Cause flushing, which is pruritic and WELL-DEMARCATED

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223
Q

Characteristic signs of bronchial carcinoid tumours

A

Flushing + mental state changes

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224
Q

Baseline investigation of Carcinoid tumours

A

24-hour urinary excretion of 5-HIAA

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225
Q

What can cause false positive when investigating carcinoid syndrome

A
  1. Fruits, drugs like paracetamol, antipsychotics, caffeine, nictoine and warfarin
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226
Q

Why is octreotide given as treatment for carcinoid syndrome

A

5-HT antagonist

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227
Q

If Octreotide does not work in alleviating symptoms of carcinoid syndrome, what should be given

A

Interferon Alpha adjunct

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228
Q

What surgical technique can be used to provide short term relief of hepatic metastasis from carcinoid

A

Chemoembolism of th hepatic artery, reduces symptoms of heart failure

Or resection

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229
Q

Benefits of external beam radiotherapy

A

Relieves bone pain from metastasis

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230
Q

What is a carcinoid crisis

A
  1. Tumour outgrows its blood supply and releases lots and lots of hormones:

TRIAD:
CV collapse
Tacchycardia
Altered Mental State

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231
Q

How is a carcinoid crisis treated

A

IV octreotide and plasma

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232
Q

First line management of GORD in children

A

1-2 weeks of alienate therapy

If unsuccessful, 4 week trial of a PPI

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233
Q

What is the main type of cholangiocarcinoma

A

Ductal Adenocarcinoma

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234
Q

Inw hat location are cholangiocarcinomas commonly seen

A

In the perihilar region (bifurcation of right and left hepatic ducts)

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235
Q

Onset of cholangiocarcinomas

A

Over 60

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235
Q

Onset of cholangiocarcinomas

A

Over 60

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236
Q

What ethnicity is cholangiocarcniomas commonly seen in and why

A

Southeast Asia due to liver fluke parasitic infections

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237
Q

What chronic conditions can result in cholangiocarcniomas

A

REMEMBER:

UC -> Primary sclerosing cholangitis -> cholnagiocarcinoma

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238
Q

What live flukes can cause cholangiocarcinomas

A

Clonorchis Sinesis/ Opisthorchis viverrini and Ascaris Lumbricoides

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239
Q

What is Caroli’s Disease

A

PCKD + Intrahepatic bile duct dilation

Can realist in cholangiocarcnioma

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240
Q

Presentation of cholangiocarcinoma

A
  1. hepatomegaly
  2. Abdo pain RUQ
  3. Weight loss
  4. Pale coloured stools, dark urine and general malaise
    5
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241
Q

What is Courvoisier’s Sign

A

Palpable gallbladder felt distal to the cystic duct -> cholangiocarcinomas

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242
Q

Name two tumour markers associated with cholangiocarcniomas

A

CA 19-9 and CEA

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243
Q

What scans are needed to to diagnose cholcangiocarcniomas

A

Dilation of intrahepatic biliary trees

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244
Q

GOLD STANDARD for cholangiocarcinoma

A

ERCP to take biopsy

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245
Q

Management of Cholangiocarcinoma

A

COMPLETE surgical resection

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246
Q

Post operative treatment for cholangiocarcinoma

A

ERCP to stent the bile duct (endoscopic biliary stenting)

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247
Q

What is Reynolds’ Pentad for acute obstructive cholangitis

A
  1. Fever
  2. Jaundice
  3. RUQ Pain
  4. Mental confusion
  5. Hypotension
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248
Q

What causes cholangitis

A

When the common bile duct is obstructed, causing infection and bacteria to grow upwards into the gall bladder.

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249
Q

What surgical procedure can cause obstructive cholangitis

A

ERCP

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250
Q

Age of presentation of cholangitis

A

50-60 years

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251
Q

What parasitic infections cause cholangitis

A

Roundworm

Liver Fluke

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252
Q

What is the diagnostic criteria for cholangitis

A
  1. T >38 degrees
  2. Evidence of inflammation on lab tests
  3. Jaundice
  4. Abnormal LFTs
  5. Biliary dilation
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253
Q

What kind of jaundice is seen in cholangitis

A

Obstructive jaundice

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254
Q

If serum amylase levels are raised in cholangitis, what is the implication

A

Involvement of the lower part of the common bile duct

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255
Q

What initial imaging is done for cholangitis

A
  1. KUB Abdominal X RAY
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256
Q

What’s the GOLD STANDARD diagnostic for Cholangitis

A

Contrast-enhanced dynamic CT followed by MRI

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257
Q

Management of Cholangitis

A
  1. Vital Sign measurements
  2. RESUS
  3. IV Antibiotics after blood cultures
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258
Q

What are choledochal cysts

A

Congenital dilatation of part or the whole biliary tree

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259
Q

What are Type 1 choledochal cysts

A

Dilatations of part or all of the extra hepatic bile duct

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260
Q

What are type II choledochal cysts

A

Isolated diverticulum protruding from the wall of the common bile duct by a narrow stalk

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261
Q

What are type III choledochal cysts

A

Arise from the intraduodenal portion of the common bile duct

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262
Q

What are type IV choledochal cysst

A

Dilation of intrahepatic and extra hepatic bile ducts

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263
Q

What are type V choledochal cysts

A

Caroli’s disease - limited to intrahepatic bile ducts

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264
Q

Onset of choledochal cysst

A

10 years of age

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265
Q

Triad of choledochal cysst

A
  1. Intermittent abdo pain
  2. Jaundice
    Hepatomegaly (palpable RUQ)

But USUALLY symptomatic

Usually symptoms present because of ascending cholangitis and pancreatitis symptoms

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266
Q

GOLD STANDARD for chonedochal cysts

A

Abdominal USS

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267
Q

Management of choledochal cyssts

A

Surgical excision

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268
Q

Name two types of cholera strain

A

O1 (MOST COMMON) and O139

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269
Q

How does cholera spread

A

Contaimated water or SHELLFISH

Also person to person and faeco-oral

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270
Q

What strain of cholera has been causing recent pandemics

A

El Tor (a variant of O1)

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271
Q

RF for cholera

A

Outbreaks are common after natural disasters or populations displaced by war, due to inadequate sewage disposal and contaminated water

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272
Q

Incubation period of cholera

A

2-5 days

Asympatic shedding for 2 weeks otherwise

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273
Q

Signs of cholera

A

Profuse, watery diarrhoea with nausea and vomiting

Lose up to 20 litres a day

Signs of dehydration: Dry skin, fast but weak pulse, low BP and sunken eyes

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274
Q

Investigation for cholera

A
  1. Stool specimen testing
  2. High Hb in FBC from haemoconcentrtaino

U and E

Monitor BP

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275
Q

Management of cholera

A
  1. Oral rehydration solution
  2. If not tolerated, then IV
  3. tetracycline/doxycycline/ciprofloxacin
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276
Q

Should antidiarrhoeal drugs be given for cholera

A

No

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277
Q

What is Cholestasis

A

Where bile cannot flow from the gallbladder to the duodenum

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278
Q

Name three ways that cholestasis can happen

A
  1. Obsturctive/Extrahepatic Cholestasis -> Mechanical blockage of the duct
  2. Hepatocellular/intraheptaic -> disturbances in bile formation
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279
Q

Why are children and infants more likely to get cholestasis

A

Immaturity of the liver

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280
Q

Signs of cholestasis

A
  1. Pale stools and dark urine
  2. Abdo Pain
  3. fever from infection or cholecystitis
  4. Pruritus but no rash
  5. clubbing
  6. Hypercholestrolaemia (xanthomas)
  7. RUQ pain
    Hepatosplenomeglay
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281
Q

Management of an acutely unwell patient with suspected cholestasis (dehydration or AKI signs)

A

Hospital ADMISSION

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282
Q

Management of a patient with suspected cholestasis that is not acutely unwell

A

Organise LFTs and referral to hepatologist outpatients

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283
Q

What LFT will be deranged in cholestasis

A

ALP (+GGT)

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284
Q

What blood tests distinguish between hepatic and obstructive cholestasis

A

Obstructive: High ALP and GGT

Hepatocellular: High AST and ALT

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285
Q

How will serum albumin and globulin change in chronic disease

A

Acute: Normal

Chronic: Albumin will decrease and globulin increases

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286
Q

What does reticulocytosis in jaundice indicate

A

Prehapetic jaundice cause: Check Prothrombin Time

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287
Q

Initial Imaging for cholestasis

A

USS abdo to identify cause of obstruction

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288
Q

How to treat pruritus in cholestasis and obstruction

A

Urseodeoxycholic acid

Colestyramine

Rifampicin

Then Phototherapy

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289
Q

What condition can cholestasis present similarly to

A

Asthma type wheeze

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290
Q

When should adults with chronic diarrhoea be referred under the 2 week wait rule

A
  1. Aged 40 years+ with unexplained weight loss and abdo pain
  2. Aged 50+ with unexplained rectal bleeding
  3. Aged 60+ with iron deficiency anaemia or changes in bowel habits or face occult test is positive
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291
Q

Name two viruses that can cause chronic hepatitis

A

CMV

EBV

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292
Q

Name 5 drugs that can cause chronic hepatitis

A 
Amiodarone
Isoniazid 
Methyldopa
Methotrexate
Nitrofurantoin
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293
Q

Symptoms of chronic hepatitis

A
  1. RUQ pain
  2. Ascites
  3. Ankle Oedema
  4. Haematemesis and Melaena
  5. Pruritus (cholestasis)
  6. Breast Swelling (Gynecomastia)
  7. Testicular Atrophy
  8. Loss of Libido
  9. Amenorrhoea due to endocrine dysfunction

Encephalopathy (confusion and drowsiness)

Dupuytren’s contracture (alcoholic cirrhosis)

Xanthomas: Palmart creases

Spider Naevi

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294
Q

FBC test findings in chronic hepatitis

A
  1. Raised MCV
  2. Thrombocytopenia
  3. Anaemia
  4. Prolongued PTT
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295
Q

What immunoglobulin is raised in Autoimmune hepatitis

A

IgG

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296
Q

What immunoglobulin Is raised in primary biliary cirrhosis

A

IgM

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297
Q

How long does it take for chronic pancreatitis to present

A

5-10 years after initial acute phase

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298
Q

What can cause chronic pancreatitis

A

Obstruction of bicarbonate excretion leading to necrosis

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299
Q

Large duct pancreatitis vs small duct pancreatitis

A

Large duct pancreatitis = dilation and dysfunction of the large ducts + calcification of walls

Small duct pancreatitis = dilation of small ducts, cannot be seen on imaging, and no calcification

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300
Q

What gender usually is affected by large duct pancreatitis

A

Male

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301
Q

At what age onset is hereditary chronic pancreatitis

A

Young, with epigastric pain

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302
Q

Presentation of chronic pancreatitis

A

Abdo Pain (epigastric pain radiating to the back)

Nausea and Vomiting

Decreased Appetite

Weight loss, diarrhoea, steatorrhoea and protein deficiency

DM

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303
Q

Investigation for chronic pancreatitis

A

Serum markers
Serum Trypsinogen or Faecal Elastase test for malabsorption evidence

Secretin Stimulation Test

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304
Q

What are the most common causers of liver cirrhosis in the UK

A

Alcoholic Liver Disease

Hepatitis C

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305
Q

What is the main symptom of liver cirrhosis

A

ASYMPTOMATIC

Oedema
Ascites
Easy Bruising 
Bleeding Oesophageal Varices
Jaundice 
etc
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306
Q

What classification system is used to check for liver cirrhosis prognosis

A

Child-Pugh Classification

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307
Q

What elements are assessed in the child-push classification

A
  1. Serum Albumin
  2. Serum Bilirubin
  3. INR
  4. Ascites
  5. Encephalopathy
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308
Q

What causes oesophageal varices

A

Portal Hypertension

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309
Q

What is the primary prevention of oesophageal varices

A

Endoscopic vatical band ligation

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310
Q

What antibiotic prophylaxis should be given for ascites and liver cirrhosis

A

Prophylactic ciprofloxacin or norfloxacin

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311
Q

How should hepatocellular carcinoma be surveilled

A

Offer USS with AFP every 6 months for every cause

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312
Q

How often should upper GI endoscopy be done in people with liver cirrhosis and why is this done

A

TO detect oesophageal varices, surveillance every 3 years

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313
Q

What family members are most affected by coeliac’s

A

Twins

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314
Q

Risk Factors for coeliac’s

A 
Autoimmune disease (thyroid, T1DM)
B12 or folate deficiency 
First degree relative with coeliac's
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315
Q

What is the skin manifestation of coeliac’s disease and describe how it looks

A

Dermatitis Herpetiformis - pruritic skin disease

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316
Q

Describe neurological symptoms that can be seen in people with coeliac’s

A 
`Cerebellar ataxia 
Peripheral Neuropathy 
Epilepsy 
Dementia
Depression

GBS from positive antiganglioside antibodies

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317
Q

What is the first line investigation for coeliac’s

A

Serum Total IgA and tTg

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318
Q

What genetic testing can be done in a specialist setting for coeliac’s

A

HLA-DQ2 and DQ8

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319
Q

What is a sign of splenic atrophy

A

Howell-Jolly Bodies

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320
Q

How can deranged LFTs in coaliac’s be normalised

A

Gluten-free diet

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321
Q

If LFTs do not improve by a gluten free diet, what should be suspected

A

Autoimmune GI conditions (primary sclerosing cholangitis)

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322
Q

When is a biopsy not needed for someone with Coaliac’s

A
  1. Has IgA/tTg levels 10 times the upper limit of normal
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323
Q

Name another antibiody other than tTg that is seen in coeliac’s

A

Endomysial antibodies

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324
Q

When is a endoscopic intestinal biopsy indicated in someone with DIAGNOSED CD and why is this done

A

If serological titres remain persistently high

If symptoms are persistent

To determine whether gluten has been excluded successfully from the person’s diet

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325
Q

What is refractory CD and how is this managed

A

Refractory CD is the presence of persistent symptoms or serum antibody levels.

Refer to specialist centre first and prescribe prednisolone for the initial management while waiting for a response

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326
Q

Complications of Coeliac’s

A

Oesteoporosis
Ulcerative jejunitis
Hyposlenism (splenic atrophy is seen in most people)

Infertility

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327
Q

Risk Factors for cleft palate

A

Anticonvulsnats
BDZs
Steroids

during pregnancy

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328
Q

Risk Factors of oesophageal atresia

A

More common in twins than singletons

DOwn’s, Patau’s and Edward’s

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329
Q

What is prune belly syndrome

A

A deficiency of the abdominal wall and cryptorchidism, hydronephrosis

The gut is intact

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330
Q

First line investigation for suspected pyloric stenosis

A

Abdominal USS

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331
Q

First line surgical procedure for intestinal atresia

A

Ramstedt’s pyloromyotomy

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332
Q

Name 5 metabolic causes of constipation

A 
Hypothyroidism 
Hypercalcaemia
Hypokalaemia
Prophyria
Lead Poisoning
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333
Q

At what age in adults are further investigations for constipation indicated

A
  1. Age > 40 years
  2. A recent change in bowel habit
  3. Associated symptoms (weight loss, rectal bleeding, tenesmus)
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334
Q

What are first one investigations for constipation

A
  1. FBC
  2. U and E
  3. Ca2+
  4. TFTs

Sigmoidoscopy or biopsy later one

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335
Q

First line management of constipation in adults

A
  1. Mobilise the patient
  2. Increase fluid intake
  3. Investigate and treat the cause

Then use drugs

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336
Q

What are ‘bulk producers’

A

Increase faecal mass - stimulating peristalsis

Must be drank with plenty of fluid

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337
Q

Give an example of a bulk producer

A

Bran Poweder

Methylcellulose

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338
Q

Contraindications for bulk producers

A

Difficulty in swallowing
Obstruction
Faecal impaction

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339
Q

What are arches oil enermas

A

Stool softeners: Lubricate and soften impacted faeces

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340
Q

What are stimulant laxatives

A

Increase intestinal motility

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341
Q

Why should stimulant laxatives be avoided

A

Can cause colonic atony + hypokalaemia

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342
Q

Give some examples of stimulant laxatives

A

Senna

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343
Q

What laxative acts as a rectal stimulant

A

Glycerol suppositories

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344
Q

Name an osmotic laxative

A

Lactulose
Magnesium salts
macrogols

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345
Q

When are phosphate enemas indicate din treating conspitation

A

In addition to medications (e.g., Senna) or for rapid bowel evacuation before a procedure

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346
Q

When is pruclopride indicated in women

A

Following treatment using two laxatives at the highest dose for at least 6 months - constipation ha snot improved

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347
Q

What is pruclopride

A

A 5HT4 receptor agonist

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348
Q

What is obstructed defacation syndrome

A

An urge to defectae but can’t poo due to impaction

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349
Q

Symptoms of obstructued defecation syndrome

A

Excessive straining
Pain
Bleeding after d evacuation
Sense of incomplete emptying

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350
Q

Which gender is most affected by obstructed defamation syndrome

A

Multiparous women rather than men

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351
Q

What usually causes ODS

A
  1. Rectoceles
    Rectal prolapse
    Perineal descent
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352
Q

What is perineal descent

A

Where the perineum bulges below the bony outlet of the pelvis - a key sign of chronic constipation from chronic straining

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353
Q

Treatment of ODS

A
  1. Diet
  2. Laxatives
  3. Pelvic floor retraining
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354
Q

What is Crigler-Najjar syndrome

A

A complete deficiency of U glucoronysyl transferase enzyme (UGT) = lots of unconjugated bilirubin.

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355
Q

Complication of criggler-najjar syndrome

A

Kernicterus

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356
Q

Signs of kernicterus in children

A

HYPOTONIA
Deafness
and palsies

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357
Q

How is jaundice treated in children

A

Whole-body blue-light phototherapy to break down bilirubin

Oral calcium phosphate to aid bilirubin excretion

Liver Transplant

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358
Q

Pathophysiology of cryptosporidium

A

Oocysts attach to cells of the small bowel and invade the cells of the intestines

They survive intracellularly and secrete more oocytes to spread the infection.

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359
Q

Where are cryotosporidium infections generally found

A

Small intestiines

May spread to biliary tress in immunocompromised individuals

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360
Q

What condition can precipitate cryptosporidium infections

A

AIDS in developing countries

Acute Lymphoid Leukaemia

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361
Q

When during the year are cryptosporidium infections most prevalent

A

Spring and autumn

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362
Q

Where are cryptosporidium infections commonly acquired

A
  1. Farms or petting zoos
  2. Contact with animal dung
  3. Nurseries
  4. Waterbourne (bad water supplies)
  5. Foodbourne
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363
Q

What is the incubation period of cryptosporidium

A

5-10 days

Usually symptomatic

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364
Q

Presentation of cryptosporidium infections

A
  1. MILD fever
  2. SUDDEN Water Diarrhoea
  3. Abdominal cramps
  4. Nausea and anorexia
  5. Fatigue
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365
Q

How long does cryptosporidium infections typically last for

A

2 weeks

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366
Q

How common are relapses of cryptosporidium infections

A

33%

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367
Q

What symptoms indicate biliary spread in a cryptosporidium infection

A

RUQ pain and vomiting in HIV positive individuals

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368
Q

Investigations for suspected cryptosporidium infections

A
  1. Stool microscopy for oocytes (ONLY IF CRYPTOSPORIDIUM SPECIFICALLY IS SUSPECTED)
  2. Stool culture if not
  3. U and Es and LFTs
  4. CD4 counts etc
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369
Q

Management of cryptosporidium infetcions

A

Leave alone

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370
Q

What advice should be given to children with cryptosporidium infection

A

Stay at home for 48 hours after diarrhoea has stopped

Do not go into swimming pools for two weeks after diarrhoea has stopped

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371
Q

What is cyclical vomiting syndrome commonly associated with

A

Migraines

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372
Q

What are the four phases of the cyclical vomiting syndrome

A

Prodrome
Vomiting
Recovery
Well

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373
Q

What is the prodromal phase of CVS

A
  1. Intense sweating and nausea
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374
Q

How long can the vomiting phase of CVS last for

A

Hours to days

20 to 30 mins at a time

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375
Q

Describe the onset of episodes of vomiting in CVS

A

Same tie of the day, same length of times, same symptoms and same level of intensity

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376
Q

What can trigger CVS

A

CHOCOLATE synonym

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377
Q

How to diagnose CVS in adults

A

A minimum of three discrete episodes in one year

No nausea and vomiting between episodes

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378
Q

What gene mutation causes CF

A

CFTR gene on chromosome 7

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379
Q

At what age can dermatitis herpetiformis manifest during coeliac’s

A

30->40

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380
Q

Why is dermatitis herpetiformis underdiagnosed

A

Because only 20% of those presenting with dermatitis herpetiformis in their 30s and 40s have any symptoms of coeliac’s.

80% of DH show histopathological changes on biopsy so have co-morbiditity with coeliac’s

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381
Q

Presentation of dermatitis herpetiformis

A

Vesicular, red AND itchy rash on the extensor surfaces and abdomen

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382
Q

Where is a biopsy taken for coeliac’s

A

Duodenal biopsy

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383
Q

What drug treatment can be used for dermatitis herpetiformis

A

Gluten free diet,,

No improvement over a day or two:
Dapsone to reduce the itch

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384
Q

What is a dieulafoy lesion

A

It is a protuberant artery in the submucosa of the stomach. Has a risk of bleeding

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385
Q

Where is a diulafoy lesion commonly found

A

Proximal stomach
Small intestines
Colon
Rectum

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386
Q

Clinical presentation of a dieulafoy lesion

A

Signs of upper GI (haematemesis or Malena) bleeding

Signs of lower GI bleeding (haematochezia)

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387
Q

Investigation for a dieulafoy lesion

A

Endoscopy

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388
Q

Management of a diulafoy lesion

A

Resuscitation with fluid and bloods

Endoscopic occlusion of the vessel (sclerotherapy or laser therapy)

Adrenaline

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389
Q

Onset of a dieulafoy lesion

A

50 years old in MEN

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390
Q

What is a diverticulum

A

Herniation of the mucosa through thickened colonic muscle

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391
Q

Where are diverticula commonly found

A

Sigmoid and descending colon (so causes left flank pain)

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392
Q

Onset of diverticulitis/diverticulosis

A

85 years +

Sometimes over 40s are affected

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393
Q

Symptoms of diverticulosis

A

MAINLY asymptomatic

Usually only diagnosed after an episode of diverticulitis

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394
Q

What are the most commonbn fistulas found in diverticulosis

A

Colovesicular

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395
Q

Risk Factors of diverticulosis

A
  1. Over 50
  2. Low Fibre
  3. Obesity in younger then 40
  4. Smoking
  5. NSAIDs
  6. Paracetamol
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396
Q

Presentation of diverticulitis

A
  1. Left sided abdominal pain
  2. Pyrexia
  3. Bloating
  4. Constipation and diarrhoea
  5. Rectal bleeding
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397
Q

What exacerbates pain in diverticulitis

A

Eating

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398
Q

What relieves diverticular pain

A

Flatus

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399
Q

In what people is pain from diverticulitis found on the right side rather than the left

A

Asian patients

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400
Q

Describe the pain felt in diverticulitis

A

Intermittent/constant

Change in bowel habits

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401
Q

Can hypotension and shock be seen in diverticulitis

A

RARE

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402
Q

Examination findings in diverticulitis

A

A palpable mass, lower left quadrant

Reduced bowel sounds

A mass in rectal examinations

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403
Q

Complications of diverticulitis

A
  1. Perforation \
  2. Abscess
  3. Fistula
  4. Stircture
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404
Q

Signs of an abscess form diverticulitis

A

Persistent fever despite antibiotics being given

Signs of sepsis

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405
Q

Signs of colovesicular fistulas

A

Pneumaturia
Faecaluria

Discharge from infections

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406
Q

Describe the blood found n diverticulitis

A

Fresh, bright red and PAINLESS

Associated with mild cramps

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407
Q

INVESTIGATIONS FOR DIVERTICULAR DISEASE

A

COLONNOSCOPY - usually found on incidence when screening for colon cancer

Raised WCC so FBC, Urea and CRP

CONTRAST CT within 24 hours of hospital admission if CRP is raised

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408
Q

What is the first line investigation for haemorrhages as a presenting complaint

A

Flexible sigmoidoscopy to rule out rectosigmoid lesions

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409
Q

When should someone with diverticular disease/diverticulitis be admitted

A

Admission if significant blood loss from rectal bleeding - will need blood transfusion

Symptoms persist AFTER 24 hours 
Old or comorbidity
Pain is not being managed with paracetamol 
Hydration can't be done orally 
Antibiotics can't be given orally
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410
Q

Management of diverticulitis

A
  1. Pain relief
  2. Bulking laxatives (methylcellulose) - NOT osmotic laxatives
  3. Advise high fibre diet
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411
Q

Are osmotic laxative recommended in managing diverticular disease?

A

No

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412
Q

What oral antibiotics is first line for diverticulitis

A

Co-Amoxiclav

OR

Cefalexin + Metronidazole

OR

Trimethoprime + Metronidazole

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413
Q

What antibiotics is first line for diverticulitis in hospitals

A

IV Co-Amoxiclav

review in 48 hours

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414
Q

When is surgery indicated for diverticulitis

A
  1. Peritonitis
  2. Sepsis that is not being controlled well
  3. Obstruction
  4. Fistulas
  5. Suspected carcnioma
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415
Q

What surgery is recommended in diverticulitis

A

Primary anastomosis

OR

HARTMANN”S procedure (resecting the bowel with stoma)

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416
Q

Indications for conservative management (antibiotics and bed rest) of pericolic abscesses in diverticulitis

A

<3cm

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417
Q

WhatWhat procedure is done if pericolic abscesses are persistent

A

CT-guided percutaneous drainage

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418
Q

Surgical procedure for colovesical fistulas and colovaginal fistulas

A

Resection (single stage)

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419
Q

How can GI haemorrhages be controlled

A
  1. Immediate fluid and blood rhesus
  2. Colonoscopy to establish source of bleeding
  3. Intra-arterial vasopressin toc ontrol haemorrhage
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420
Q

What conditions can cause dry mouth

A
  1. Dehydration
  2. Drugs
  3. Anxiety
  4. Sjogren’s syndrome
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421
Q

First line management of dry mouth

A

First line:

  1. Sucking ice
  2. Sugar free sweets
  3. Petroleum jelly
Second Line:
Artificial saliva (no better than first line)
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422
Q

When are salivary stimulants (pilocarpine) recommended as treatment for dry mouth

A

If there is confirmed residual salivary gland dysfunction

Sjogren’s etc

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423
Q

What is Dupin-Johnson syndrome

A

Triad:
LFTs normal
Raised conjugated hyperbilirubinaemia
Abnormally pigmented hepatic parenchymal cells

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424
Q

What people are affected by dubin-johnson syndrome

A

Jewish and Iranian descent

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425
Q

Onset of dubin-johnson syndrome

A

Late teens or early 20s

426
Q

Clinical presentation of dubin-johnson syndrome

A

Just jaundice really

427
Q

What investigations are diagnostic of dubin-johnson synrome

A
  1. Raised conjugated bilirubin
  2. Raised urinary coproporyphryn feel (increase in C1:C3)
  3. Prolongued PTT

Laporoscopy to find pigmented liver

ABSENT GALLBLADDER on imaging

428
Q

What is rotor’s syndrome

A

Similar to dubin-johnson syndrome but has no hyperpigmentation of the liver

429
Q

Primary biliary cirrhosis vs dubin-johnson syndrome

A

PBC ansi gas pruritus

430
Q

Management of dubin-johnson syndrome

A

Re-assurance

431
Q

Presentation of dyspepsia

A
  1. Epigastric pain
  2. Bloating
  3. Flatus
  4. Nausea
  5. Fatty food intolerance
432
Q

First line Investigations for dyspepsia

A

FIRST LINE: Abdominal exam

FBC for anaemia (red flag)

H. pylori

433
Q

Indications for endoscopy referral in people with dyspepsia

A

Over 55:

  1. Persistent symptoms
  2. Raised palatelet count or nausea + vomiting
  3. Previous Barrett’s oesophagus
434
Q

When should people with dyspepsia be referred for cancer pathway

A

Chronic GI bleeding AT ANY AGE

Over 55 + weight loss

435
Q

Management of dyspepsia

A

First lien: PPI

Second Line” H2 receptor antagonist

436
Q

Management of severe oesophagi’s

A

PPI full dose for 8 weeks

Second Line: Switch to another PPI

Full dose PPI in the long term

437
Q

Name three tests used to check for H. pylori

A

C13 urea breath test
Stool Antigen test
Lab serology

438
Q

Side effects of PPIs

A 
Taste disturbances
Peripheral oedema
Photosensitivity 
Fever
Arthralgia
Myalgia
439
Q

Where are PPIs metabolised

A

Liver

440
Q

What can PPIs interfere with

A

Warfarin

441
Q

Red flag symptoms for dysphagia

A

New onset of red flags (loss of weight and worsening symptoms) + over 65

442
Q

If cancer is suspected in someone with dysphagia, what should be done

A

Referral for upper GI endoscopy within 2 weeks

443
Q

Where is ERCP indicated

A
  1. Gallstones in the bile duct
  2. Acute or chronic pancreatitis
  3. Suspected malignancy
444
Q

What is the problem with ERCP in acute pancreatitis

A

May make it worse

445
Q

What surgical procedure can cause pancreatitis

A

Cholecystecomy (causes sphincter of odds dysfunction)

446
Q

What should the patient do before getting a ERCP

A

Fast overnight
Sedated by BDZs + Analgesia
Antibiotics
Lie on their left Side

447
Q

Complication of ERCPs

A

Pancreatitis

448
Q

Onset of Eosinophilic oesphagitis

A

30-50 years

449
Q

What distinguishes GORD from EO

A

Failure to respond to proton pump inhibitors. It’s Infitration of eosinophils in the epithelium leading to GORD symptoms

450
Q

What ethnicity is affected by Eosinophilic oesophagitis

A

Caucasian men

451
Q

Symptoms of Eosinophilic oesophagitis

A

Starts off with GORD symptoms and then eventually results in dysphagia or food obstruction

452
Q

What condition is associated with eosinophilic oeosphagitis

A

Asthma and Allergic Rhinitis

453
Q

Investigation for Eosinophilic Oeosphagitis

A

Oeosophageal biopsy with microscopy showing eosinophils

454
Q

Management of eosinophilic oesophagitis

A
  1. Elemental diet (taking amino acid mixtures) for 6 weeks

First line medical management: 2. Typical Steroids: Fluticasone inhaler or Budesonide oral solution

455
Q

What’s second line medical management of eosinophilic oesophagitis

A
  1. Endoscopic balloon dilation

Usually done when strictures and oesophageal narrowing develops

456
Q

Three signs of Haemolytic Uraemic Syndrome

A
  1. Microangiopathic haemolytic anaemia
  2. Thromboyctopenia
  3. Renal Failure
457
Q

In which individuals should HUS by E.coli be suspected

A

IN children who recently visited an open farm or who have had a bout of acute bloody diarrhoea

Symptoms can be asymptomatic

458
Q

What other condition can present in E.coli 0157 infections other than HUS

A

Thrombotic Thrombocytopenia Purpura

459
Q

Describe the onset of E.coli infetcions

A

Starts as diarrhoea and abdo cramps, then become bloody after 1 day

460
Q

How does pain caused by e.coli O157 differ from other types of gastroenteritis

A

Defecation can be painful

461
Q

Diagnostic of e.coli O157 infetcions

A

Stool Sample

462
Q

How should HUS be managed

A

Supportive treatment

463
Q

How long does recovery take in HUS infections

A

1-2 weeks

464
Q

What advise should be given to children wit hHUS in regards to going to school

A

Must not go to school until after 48 hours since their normal stool

465
Q

What types of food are more likely to be carrying e.coli

A

Unwashed food
Inadequate cooking of food
Unpasteurised dairy products

466
Q

What serum level is raise din exomphalos and gastrochisis

A

AFP

467
Q

What investigation must be done in children who have suspected exomphalos and gastrochiasis

A

Karyotyping

468
Q

What is the main way we can diagnose exomphalos and agstrochisis

A

USS

469
Q

What is Beckwidth-Widemann syndrome

A
  1. Macroglossia
    Organomegaly
    Gigantism
470
Q

What pregnancy problems can result in faecal incontinence

A

Third and fourth degree tears

Rectoceles

471
Q

What risk factors can result in faecal incontinence

A
  1. Patients with urinary incontinence
  2. Frail elderly patients
  3. Stroke, MS, SPina Bifida and spinal injury
472
Q

What is the most common cause of faecal inctoninence

A

Degeneration of the smooth muscle of the internal anal sphincter from just axing

473
Q

What congenital disorders can result in fgaecal incontinence

A

Anal atresia

Hirschsprung’s disease

474
Q

How much fluid should someone with constipation aim to intake

A

1.5L

475
Q

How is straining avoided

A

Sittingo r squatting in position

476
Q

What is the first line antidiarrhoeal drug of choice

A

Loperamide hydrochloride

Second line: Codeine phosphate

477
Q

How does loperamide function

A

Acts on the u-opiioid receptors, decreasing the tone of the smooth muscles in the intestinal walls

478
Q

Management of a patient with faecal impaction

A
  1. Offer rectal laxatives over a few days

Then oral if rectal fails

479
Q

What is biofeedback therapy

A

Patients learn to control bodily processes

480
Q

What surgery is indicated in persistent faecal incontinwence

A

Sphincter repair

481
Q

If sphincter repair surgery is contraindicated, what medical treatment should be done

A

Temporary sacral nerve stimulation

Then neosphincteyr (artificial anal sphincter if unsuccessful)

482
Q

What is the last line surgical procedure for someone with faecal incontinence

A

Stoma

483
Q

What is aerophagia

A

Excess swallowing of air into the stomach -> bleching

484
Q

What physiological process causes flatulence

A

Co2, hydrogen and methane release

485
Q

What infection has belching as a key symptom

A

Giardiasis

486
Q

What medication can cause excessive belching

A

Antacids

487
Q

What lifestyle factors result n excessive belching

A

Eating too fast
Fizzy drinks
Chewing gum
Smoking

488
Q

What lifestyle can result in excessive flatulence

A

Female runners

489
Q

What is supra gastric bleching

A

Where air is sucked into and expelled form the pharynx only

490
Q

What first line lifestyle change can be used to reduce flatulence

A

Mild physical activity

Take soluble fibre to reduce flatulence

491
Q

Investigations for food allergy and intolerance

A

Food Diary

IgE mediated suspicion: Skin prick test or blood tests for antiibodies

Oral food challenge GOLD STANDARD

492
Q

What is gallstone ileus

A

The obstruction of the bowel due to impaction of one or more gallstones

493
Q

How big do gallstones have to be to cause obsturtcion

A

2.5cm

494
Q

Where is the most common site of a gallstone ileus

A

Ileum

495
Q

What is Bouveret’s syndrome

A

When the gallstone lodges in the duodenum causing gastric outlet obstruction

496
Q

In what gender is gallstone ileus more common in

A

Female

497
Q

Symptoms of gallstone ileus

A

Abdo pain -> comiting

Progressively gets worse

Colicky abdominal pain

Abso distention

Passing stools initially but stops

Vomiting hours after onset of pain

498
Q

Where is abdo pain felt in gallstone ileus

A

Periumbilical

499
Q

What is Rigler’s triad, and how does this help us to distinguish between gallstone ileus from other GI conditions

A
  1. Small bowel obstruction
  2. Presence of pneumobilia (air in the biliary tree)
  3. Gallstone in right iliac fossa on X-Ray/CT
500
Q

What is the initial management of a gallstone ileus

A

IV infusion fluids
NG tube to decompress stomach and avoid further vomiting

SURGERY - gold standard

501
Q

Why is surgery the gold standard for gallstone ileus

A

It is an abdominal emergency

502
Q

Risk Factors for gallstones

A

FFFF:

Fat 
Fair
Fertile
Female
Forty 
Others:
Age
FH
Weight loss (sudden)
Loss of bile salts (ideal resection and terminal ileitis)
Diabetes 
COCP
503
Q

What surgery may cause gallstones and cholecystitis

A

Obesity surgery, causing a sudden drop in weight

504
Q

In what disease are gallstones more common in

A

Diabetes

505
Q

Name three constituents of bile

A

Cholesterol
Bile Pigents
Phospholipids

506
Q

Why can’t cholesterol stones be seen on an X-Ray

A

They are radiolucent

507
Q

What causes black pigment stones

A

Any condition causing haemolysis (e.g., hereditary spherocytosis)

508
Q

What causes mixed stones and what do they look like

A

They are faceted

Calcium, pigment and cholesterol

509
Q

What causes brown pigment stones

A

Stasis and infetcions within the biliary system

510
Q

What species usually cause infections within the biliary system

A

E. coli and Klebsiella

511
Q

Symptoms of gallstones

A

MOSTLY ASYMPTOMATIC

Biliary colics
Acute cholecystitis

512
Q

What anatomical location causes biliary colic

A

Gallstones impacting the cystic duct or ampulla of water

513
Q

What causes acute cholecystitis

A

Distension of the gallbladder -> necrosis and ischaemia of the mucosal walls

514
Q

Describe the pain felt in biliary colics

A

Epigastric or RUQ pain that radiates to the back (scapular region)

Constant for 15 mins to 24 hours (despite its name)

515
Q

What can improve the pain of biliary colics

A

Analgesics

516
Q

What symptoms are associated with biliary colic pains

A

Nausea and vomiting

517
Q

Investigations for gallstones and cholecystitis

A

Ultrasound of the abdomen

518
Q

If an ultrasound is unable to detect a stone, what can be done

A

an ERCP

Then a CT

519
Q

Presentation of cholecystitis

A
  1. MURPHY’s SIGN positive

Epigastric/RUQ pain, vomiting, fever or a GB mass

520
Q

First line investigation for cholecystitis

A

ABdominal USS

521
Q

What is seen on an abdominal USS for cholecystitis

A

Thickened GB wall (>3mm) with pericholecystic fluid in the walls

Gallstones may not be seen

522
Q

What is the role of a Hydroxyiminodiacetic acid cholescintigraphy

A

To check for blocked cystic ducts

523
Q

What is Charcot’s triad

A
  1. RUQ
  2. Jaundice
  3. Fever
524
Q

How can gallstones cause pancreatitis

A
  1. Temporary blockage of the pancreatic duct causes premature release of pancreatic enzymes which irritate the pancreas
525
Q

Signs of Empyemas caused by gallstones

A

Fever + Leucocytosis

526
Q

Non-surgical management of symptomatic gallstones, biliary colics and cholecystitis

A
  1. PAIN RELIEF: Give opioids

IF PAIN PERSISTS FOR 24 HOURS, ADMIT.

In hospital:

IV Antibiotics

Early Laparoscopic Cholecystectomy

527
Q

When should laser lithotripsy be used for gallstones

A

When bile duct stones are proving very difficult to treat (multiple treatment efforts have been made)

528
Q

What is the risk of cholecystectomy

A

Perforation

529
Q

How should gallstones be managed if asymptomatic

A

Watch and wait

530
Q

If the gallbladder has been removed and a gallstone is causing issues, what is the first line management

A

Biliary sphincterectomy

531
Q

If the stones in biliary colics or cholecystitis are irretrievable, what is the definitive treatment

A

Biliary stenting

532
Q

Management of cholangitis

A
  1. Broad spectrum IV antibiotics

2. Surgical decompression of GB

533
Q

First line management of a biliary empyema

A

IV antibiotics + urgent decompression and Cholecystectomy

534
Q

First line treatment of gallstone ileus

A
  1. Laporotomy
535
Q

What medical treatment is given to prevent further gallstones from forming

A

Ursodeoxycholic acid

536
Q

What is dry gangrene

A

Diminshed blood supply due to vasucular issues, vasculitis

537
Q

What is wet gangrene

A

Infection of tissues by strep and staph = infection + inflammation -> blockage of blood vessels

538
Q

What is Noma

A

Gangrene of the mouth and face in immunocompromised individuals

539
Q

Wet Gangrene vs Dry Gangrene

A

Erythema vs Erythema
Black vs Brown -> Black
Discharge vs No Discharge

Dry Gangrene is also cold and pallor in the region

540
Q

Investigation of gangrene

A

Microbology swabs and peripheral blood cultures

X-Ray of affected areas

541
Q

Management of Wet Gangrene

A

Analgesia
IV Broad-spectrum antibiotics
Surgical Debridement

Amputation if not controlled

542
Q

Management of Dry Gangrene

A

Restoration of blood supply

543
Q

What is Hyperbaric Oxygen Therapy

A

Provides higher than normal oxygen to increase process of wound healing

544
Q

What is Maggot Therapy

A

Maggot eggs are applied to the gangrene area, Leads to tissue debridement and antiseptic properties

545
Q

Risk Factors for gastric cancer

A
  1. Age (75+)
  2. Men
  3. Poor socioeconomic background
  4. H pylori infection
  5. Low fruits and vegetables
  6. Preservatives
  7. Smoking
  8. Atrophic gastritis, pernicious anaemia, post-gastrectomy
  9. Hypogammaglobulinaemia
546
Q

What gene mutation increases predisposition to gastric cancer

A

E-Cadherin gene

547
Q

Presentation of gastric cancer

A
  1. Dyspepsia
  2. Weight Loss
  3. Vomiting
  4. Dysphagia
  5. Anaemia

USUALLY APPEARS BENIGN/ NON-SPECIFIC which is why patients with dyspepsia should be given Upper endoscopy

548
Q

What may lead to a delayed diagnosis of gastric cancer

A

PPIs, these appear to improve symptoms - however, does not affect survival rates

549
Q

For gastric cancer, what are the indications someone should be given upper GI endoscopy

A
  1. Dysphagia symtoms

OR

55+ with weight loss + pain/reflux/dyspepsia

550
Q

What age patient should be referred to cancer clinic with suspected dyspepsia

A

55+

551
Q

Gold STANDARD for Gastric Cancer

A

Endoscopic biopsy

552
Q

How should cancer be staged

A

CT

553
Q

What is a Krukenberg’s tuour

A

Spread of gastric carcinomas to the ovaries (BILATERAL and MUCINOUS)

Signet ring cells

554
Q

What is the main treatment of gastric cancers

A

Endoscopic surgery

555
Q

What chemotherapy agent is given for gastric cancers

A

5-Fluorouracil + -platin drug

556
Q

What is first line palliative care for gastric cancers

A

5-FU in combination with another plain drug

557
Q

What is a biomarker for gastric carcniomas

A

COX-2

558
Q

Investigation for suspected gastorenteritis

A

STOOL SAMPLE

559
Q

How is Hepatitis A spread

A

Faceo-Oral Route

560
Q

Can you be immunised for Hep A

A

Yes

561
Q

What is the biggest factor that causes death in those with HAV

A

Being over 50 (AGE)

562
Q

Incubation period for Hep A

A

2-6 weeks

563
Q

How does HAV cause hepatitis

A

Viral RNA is coated and enters hepatocytes, producing viral proteins inside cells. These assembled particles then shed through the biliary tres into faeces

564
Q

When is HAV infection spread greatest

A

2-3 weeks after infection

565
Q

What is the most common form of acute viral hepatitis worldwide

A

Hep A

566
Q

Where is Hep A most prevalent

A

Asia (india, pakistan, Bangladesh), Africa, Far East, Central America and Middle East

567
Q

Risk Factors for Hep A

A
  1. High risk areas
  2. Male homosexuality
  3. IVDU
  4. Falco-oral route
568
Q

Symptoms of Hep A

A

PRODROME: Nausea, fatigue, malaise.

NO FEVER

ICTERIC:
Dark urine 
Pale Stools 
Jaundice
Itching 
RUQ pain 
Asthralgia 
Hepatosplenomeglay
569
Q

What is the first symptom that is seen in Hep A following the prodrome

A

Dark urine

570
Q

What patients are typically asymptomatic for Hep A

A

Children (usually only get diarrhoea)

571
Q

Are fevers common in Hep A/

A

No

572
Q

First Line Investigation for Hep A

A

Serum IgM HAV

573
Q

IgM HAV vs IgG HAV

A

IgM shows acute infections (and goes away after 6 months)

IgG is lifelong and shows past infection or vaccination

574
Q

Describe the ALT:AST ratio in Hep A

A

ALT>AST

ALP rises with the rest

575
Q

What happens to PTT in hep A

A

Normal

576
Q

What happens to Bilirubin levels in Hep A

A

Rises after ALT and AST

577
Q

Management of Hep A

A
  1. Supportive

Only admit if oral rehydration etc can’t be done

578
Q

Where is Hep B prevalent

A

Sub-Saharan Africa and Asia

579
Q

Is a vaccine available for Hep B

A

yes

580
Q

Incubation period for Hep B

A

3 months

581
Q

Signs of Hep B

A 
Sudden RUQ pain
Nausea
Anorexia
MILD fever
Malaise
Slow developing obstructive jaundice

Signs of decompensated liver disease: Ascites, encephalopathy

582
Q

What antigen shows active Chronic Hep B infection

A

HBsAg for over 6 months

583
Q

What does the presence of HBeAg show

A

High rates of viral replication and infectivity with others

584
Q

What patients are at particular risk of Hep B infection

A

Neonates from mother

585
Q

Name two ways we can stage the level of liver cirrhosis

A

Transient Elastography

Liver Biopsy

586
Q

What is the only serological marker that can be detected in the first 5 weeks of HBV infection

A

HBsAg

587
Q

What serum level defines carrier status

A

HBsAg in the blood > 6 months

588
Q

What does it mean if someone is HBsAg positive but HBeAg negative

A

Lower infectivity

589
Q

What does HBcAg being present indicate

A

Implies past infection

590
Q

When ONLY HBsAg are found in the blood, what does this mean

A

Implies vaccination

591
Q

The presence of what serum titre indicates an acute infection to HBV

A

Raised IgM to HBcAg levels

592
Q

The presence of what serum levels indicate chronic Hep B infection

A

HBsAg for over 6 months

Negative IgM to HBcAg

593
Q

First line management of Hep B

A

Notify PHE + refer to hepatologist

Treatment is mainly supportive

594
Q

How can itching in Hep B be treated

A

Chlorphenamine

595
Q

What is the first line medical treatment in chronic Hep B

A

Pegylated Interferon alpha 2a

Second: Tonofovir (first line in pregnant women)

596
Q

What prophylaxis is given to people with HBV

A

6 months etacavir/tenofovir

Only if >2,000 IU/mL

597
Q

When is watchful waiting done for someone with HBV over entacavir prophylaxis

A

If HBV DNA <2,000 IU/mL

598
Q

What is watchful waiting in someone with HBV

A

Monitoring ALT every 24 weeks

599
Q

In what people whorls Hep B vaccine be avoided in

A

Those allergic to yeast

600
Q

When is Hep B serology first line investigation

A 
MSM
Sex Workers
IVDU
HIV
Sexual Assault victims
Hep B common countries
Needlestick
Workers with occupational risk (healthcare)
601
Q

How should Hep B contacts be treated

A

HB IG within 48 hours

602
Q

How should babies born to Hep B mothers be treated

A

One dose vaccine at birth

HB IG within 24 hours, 1 month and then at 6 months

603
Q

How is HCV transmitted

A 
IVDU
Blood Transfusion 
Haemodialysis
Sexual Contact 
Needlestick injuries
Perinatal transmission
604
Q

Symptoms of Acute and Chronic Hep C

A

Both are asymptomatic and usually detected on routine blood testing

605
Q

What proportion of people with acute Hep C develop chronic Hep C

A

75%

606
Q

When should serum HCV RNA be measured in healthcare staff who are initially positive

A

baseline
6 (HCV RNA)
12 (HCV RNA + anti-HCV)
24 weeks after exposure (anti-HCV)

607
Q

Symptoms of Acute HCV

A

Jaundice

Deranged liver enzymes

608
Q

How long does it take for symptoms of acute HCV to come

A

6-7 weeks after exposure

609
Q

What are the signs of Chronic HCV infection

A

Persistently elevated or fluctuating liver enzyme levels

Can go unrecognised for 20 years until LFTs are performed for blood donation

610
Q

What serum level shows active infection to Hep C

A

HCV RNA

611
Q

Why are anti-HCV levels measured at 3 months and 6 months

A

Because it can take 3 months for antibodies to become detectable

612
Q

Why are anti-HCv levels measured

A

Shows if someone has ever had HCV in the past

613
Q

What baseline investigations should be done in someone with suspected HCV

A

FBC< LFTS, U and Es, HbA1c, TFTs, ferritin

Hep A serology

Hep B serology

HIV TEST!

614
Q

What is done to diagnose cirrhosis

A

Transient Elastogrpahy

615
Q

Why is a Liver USS used in Hep C

A

Just to screen for hepatocellular cancer

616
Q

What condition predisposes HCV

A

Anything that can immunosupress:

DIABETES PARTICULARLY

Polyarteritis Nodosa
Autoimmune Hep
Thyroiditis
Lichen Planus

617
Q

First line management of HCV after taking bloods

A

Arrange SAME DAY assessment or immediate specialist referral if suspected acute or chronic Hep C

618
Q

Treatment of Hep C

A

Combination dual anticviral therapy: Ribacirin + Peginterferon alfa

619
Q

Lifestyle advice to give to Hep C

A

Stop alcohol
Stop Smoking
Advise about risk of sexual transmission

620
Q

What vaccines does everyone with Hep C need to be given

A

HEP B and A as co infection can lead to fulminant hepatitis

621
Q

When is liver transplant indicated

A

End-stage liver disease

622
Q

Why can HCV recur after transplant

A

Due to graft infection

623
Q

What o people with HCV need to be surveilled for

A

Regular Abdo USS to check for hepatic carcinoma

624
Q

Is a vaccine available for Hep C

A

No

625
Q

What serum level is raise din gilbert’s

A

Raised unconjugated bilirubin

626
Q

What is Gilbert’s syndrome

A

Causes reduction in UDP Glucoronyl Transferase enzymes

627
Q

Lab findings in Gilbert’s syndrome

A

High unconjugated bilirubin

Normal liver enzymes and everything else

628
Q

Signs of Gilbert’s syndrome

A

Intermittent episodes of non-pruritic jaundice

629
Q

What can trigger Gilbert’s syndrome

A
  1. Illness
  2. Stress
  3. fasting
  4. Dehydration
  5. Physical Exertion
  6. Insomnia
  7. Alcohol
  8. Surgery
  9. Chemotherapy and antiretrovirals
630
Q

Is fatigue felt in Gilbert’s

A

Yes but not caused by Gilbert’s itself

631
Q

Investigations for Gilberts

A

Just FBC (to ensure normal reticulocyte count) + Bilirubin levels

632
Q

What species causes Giardiasis

A

Giardia Intetsinalis

633
Q

What species causes Giardiasis

A

Giardia Intetsinalis

633
Q

What species causes Giardiasis

A

Giardia Intetsinalis

634
Q

What kind of species is Giardia Lamblia

A

Flagellated, anaerobic Protozoa

635
Q

Risk Factors for Giardiaiss

A
  1. Poor hygiene
  2. Travel to endemic areas
  3. Immunocompromise
  4. Nurseries
  5. Ano-oral sex
636
Q

Incubation period of Giardiasis

A

1-2 weeks

637
Q

Why is chlorination not enough to prevent giardiasis

A

Giardial cysts are resistant to standard chlorination

638
Q

In what people should we expect giardiasis

A
  1. Acute Diarrhoea OVER one week
  2. Traveller’s diarrhoea OVER 10 days
  3. Diarrhoea in immunocompromised patients
639
Q

Symptoms of giardiasis

A
  1. Acute or chronic diarrhoea
  2. Weight loss and failure t thrive in children
  3. Abdo pain, flatulence, bloating and nausea
640
Q

Is vomiting and fever seen in giardiasis

A

No

641
Q

Investigation for giardiasis

A

Ova, cysts and parasites (OC+P) of the stool.

642
Q

What is the problem with only checking stool microscopy for suspected giardiasis

A

Only tests for campylobacter, E coli, salmonella, shigella and cryptosporidium

643
Q

What is the string test

A

Duodenal swabs for microscopy in giardiasis

644
Q

What stain is used to check for giardiasis trophoxzoites

A

Methylene blue

645
Q

Management of Giardiasis

A
  1. Rehydration (not commonly hneeded)

METRONIDAZOLE (or Tinidazole)

646
Q

Possible complication in gairdiasis

A

Lactose Intolerance (can happen from any kind of gastroenteritis)

647
Q

What is protective against giardiaiss

A

Breast-feeding

648
Q

What is Halitosis

A

Bad Breath

649
Q

What is a big cause of halitosis in the GI system

A

H pylori infections and acid reflux

650
Q

What common problem can cause halitosis

A

Dry Mouth and alcohol

651
Q

What causes bad morning breath

A

Reduction in flow of saliva from reduced movement of the tongue, causing food residue to stagnate and bacteria overgrowth

652
Q

Management of bad breath

A
  1. Regular tongue cleaning
  2. CHlorhexidine Gluconate toothpaste
  3. treating H. pylori infection
653
Q

Name three drugs that may cause stomach ulcers

A 
NSAIDs
Doxycycline
Bisphosphonates
Tricyclic antidepressants
Anticholinergic
Nitrates
CCB
654
Q

Name some conditions that can cause GORD

A
  1. Achalasia
  2. Systemic Sclerosis
  3. Hiatus Hernia
655
Q

What are some risk factors that can cause GORD

A
  1. Smoking
  2. Alcohol
  3. Obesity
  4. Big Meals
  5. Maler
656
Q

Why do some drugs cause GORD

A

They relax the tone of the cardiac sphincter

657
Q

Why does a fatty meal cause GORD

A

Delays gastric emptying

658
Q

Can H. pylori infection cause GORD

A

No

659
Q

Clinical Presentation of GORD

A
  1. Heartburn
  2. Retrosternal discomfort
  3. Excessive salivation
  4. Odynophagia
660
Q

What causes odynophagia in GORD

A

Oesophagitis or strictures

661
Q

Name some respiratory symptoms of GORD

A
  1. Hoarse voice
  2. Chronic cough
  3. ASTHMA

Peunomnia from chronic aspiration

662
Q

What is the gold standard diagnosis of GORD

A

Endoscopy

663
Q

Why is a barium swallow not diagnostic for GORD

A

It only shows evidence of a hiatus hernia, not other problems

664
Q

When would oesophageal pH monitoring be indicated for GORD

A

To check if symptoms are ud etc acid hyper secretion

665
Q

What grading system is used to grade GORD/oesophagitis

A

Savary Miller grading system

666
Q

Describe the Savary-Miller grading system

A

Grade 1: Erosions on single fold

Grad 2: Erosions on multipl efolds

Grade 3: Multiple erosions (circumferential)

Grade 4: Ulcers and stenosis

Grade 5: Barrett’s epithelium

667
Q

When should someone presenting with GORD be referred for upper GI cancer

A

Dyspepsia in people ages over 50 + continuous symptoms or sudden onset

Weight loss + Anaemia + vomiting

Any Risk Factors

668
Q

Lifestyle advice for GORD

A

Take small, regular meals

Stop smoking

Lose Weight

669
Q

Initial management of GORD

A

One month of full dose PPI

670
Q

What should be done prior to endoscopy in patients

A

Stop medications that may precepitate or cause GORD (e.g., NSAIDs, steroids, bisphosphonates) and keep on PPI for at least two weeks

671
Q

What surgery is done for GORD

A

Nissen’s Funoplication

672
Q

If symptoms for GORD persist in patients, what should be done

A

DOuble PPI dose OR add a H2 receptor antagonist

Or extend length of treatment

673
Q

What distinguishes between internal and external haemorrhoids

A

If they’re either above or below the dentate line

674
Q

Where is the dentate line

A

2cm above the anal verge

675
Q

Describe the grades of internal haemorrhoids

A

1: Do not prolapse
2: Prolapse on striaing, reduce on its own
3: Prolapse on straining, reduced manually
4: Permenantly prolapsed

676
Q

Why are internal haemorrhoids painless

A

The upper anal canal has no pain fibres

677
Q

When can internal haemorrhoids become painful

A

If they strangulate

678
Q

What are external haemorrhoids covered by

A

Squamous epithelium

679
Q

Internal vs external haemorrhoids

A

Not painful vs painful

Can’t be seen on external examination vs can be seen

680
Q

Symptoms of harmorrhoids

A

Bright red, painless rectal bleeding with defacation

Streaks on toilet paper when wiping or blood dripping into the toilet. Not mixed in with stools

Anal itching or irritation

Feeling of incomplete evacuation

Complaining of lymphoma on the anal verge

681
Q

Examination findings in haemorrhoids

A

Asking patient to strain, can show bulging lump

682
Q

Appearance of a thromboses haemorrhoids

A

Purple and swollen

683
Q

When is a faecal immunochemical test the first line investigation in GI

A

Over 50:

Changes in bowel habit OR iron-deficiency anaemia

Over 60:
Anaemia (with or without iron deficiency)

684
Q

First line investigation for suspected haemorrhoids (ones that can’t be seen on examination)

A

Proctosocpy

685
Q

When should people be referred to specialists with a rectla bleed

A

Changes in bowel habit
Tenesmus
Abdo pain
Lower GI symptoms

686
Q

A major differential of haemorrhoids

A

Anal cancer

687
Q

First line management of haemorrhoids

A

Rubber band ligation (grade 2)

Or injection sclerotherapy/Bipolar diathermy (grade 3)

688
Q

Name a surgical management of haemorrhoids

A

Haemorrhoidectomy

689
Q

When are haemmoridectomies preferred over rubber band ligation etc

A

Grade 3 or higher who haven’t responded to treatment or recurrent

690
Q

Management of a thromboses haemorrhoids

A

Admission for excision

691
Q

Complication of haemorrhodis

A

Skin tags caused by haemorrhoid dilatation

692
Q

Main sign of h. pylori infection

A

Dyspepsia (fullness, bloating, early satiety and nausea)

693
Q

What needs tone done before a stool antigen test or urea breath test can be performed on H.pylori

A

2 week washout period with PPIs

694
Q

What test is done to monitor treatment against h. pylori

A

13C urea breath test

695
Q

What regime is given for h. pylori infections

A

Amoxicillin + Clarithromycin/metronidazole + PPI

696
Q

What is haemophilia and how can it be caused

A

Bleeding in the biliary tree, caused by liver biopsies

697
Q

Presentation of haemobilia

A

Jaundice
Biliary colics
Upper GI bleed signs

698
Q

What lab result is seen in haemobilia

A

Deranged alkaline phosphatase

699
Q

How is haemobilia diagnosed

A

Angiography

700
Q

What is hepatorenal syndrome

A

Impaired renal function can result from hepatic cirrhor=sis

701
Q

What indicated hepatorenal syndrome

A

Serum creatinine > 221 micromol/L in less than 2 weeks

Low eGFR and very poor prognosis

702
Q

What gene causes haemochromatosis

A

Chromosome 6

703
Q

Onset of haemochromatosis

A

40-60 males

After menopause in females

704
Q

Symptoms of haemochromatosis

A
  1. Fatigue
  2. Weakness
  3. Arthropathy
  4. Erectile dysfunction

Diabetes
Bronze skin
hepatomegaly
Impotence

705
Q

Where is arthropathy in haemochromatosis seen

A

Second and third metacarpoharyngela joints

706
Q

What chronic condition can be caused by haemochromatosis

A

Diabetes Mellitus

Impotence

707
Q

Name some psychiatric conditions caused by hereditary haemochromatosis

A

Depression
Irritability
Mood Swings

708
Q

What testing should be done in people with familial haemochromatoosis

A

HFE testing

709
Q

In what patients should hereditary haemochromatosis be suspected

A

Hepatocellular carcnioma
Chondrocalcinosis
T1 DM

Not recommended in people just struggling with arthritis on its own

710
Q

First Line Investigation for hereditary haemochromatosis

A
  1. Fasting transferrin saturation and serum ferritin

If transferrin saturation is raised, THEN we do an HFE test

711
Q

Why is serum ferritin the gold standard for haemochromatosis

A

Highly sensitive for iron overload. Genetic screening is not sufficient on its own

712
Q

What other conditions can result in iron overload

A

Siderblastic anaemia
Myelodysplastic syndrome
Thalassaemia

713
Q

Management of haemochromatosis

A

Phlebotomy + hydration

714
Q

What should be done before phlebotomy is conducted

A

hydration before and after treatment

715
Q

How is treatment of haemochromatosis doen

A

Using serum ferritin

716
Q

What is Hirschsprung’s’ disease

A

Loss of Auerbach plexus in submucosa causing colonic obstruction

717
Q

Signs of Hirschsprung;s disease

A

Delayed passage of the meconium

718
Q

What is the definitive diagnosis of Hirschsprung’s

A

Rectal biospy

719
Q

What is Hunter’s Syndrome

A

An accumulation of incompletely degraded glycosaminoglycans in tissues

720
Q

What glycosaminoglycans are seen in HUnter’s syndrome

A

Heparin

Dermatan Sulfate

721
Q

What causes the incomplete degradation of glycosaminoglycans in Hunter’s Syndrome

A

A loss in enzyme induronate 2-sulfatase

722
Q

Clinical presentation of Hunter’s Syndrome

A
  1. Coarse facial features
  2. LDs
  3. Thick tongue
  4. Hepatosplenomegaly
723
Q

What lesions are seen in HUnter’s Syndrome

A

Pebble-like ivory skin lesions on the pecs and abdomen

724
Q

Describe the changes in growth in Hunter’s Syndrome

A

AHort stature after the age of 3

725
Q

What is Hurler’s SYndrome

A

Similar presentation + corneal clouding

726
Q

Investigations or Huerler’s

A

Urinealysis - to check for glycosaminoglycans

727
Q

What X-Ray finding is specific to Hunter’s Syndrome

A

Dysostosis multiplex

728
Q

What complication is common in Hunter’s Sydnrome

A

Carpal Tunnel Syndrome

729
Q

What is the main cause of small intestinal obstruction

A

Adhesions
Strangulated hernias
VOluvulus
Cancers

730
Q

Where is the most common site of a volvulus

A

Sigmoid colon

731
Q

What is Ogilvie’s Syndrome

A

Intestinal pseudo-obstruction

732
Q

Name three conditions that can cause paralytic ileus

A
  1. Chest infection
  2. MI
  3. AKI
  4. Hypothyroidism
  5. DKA
733
Q

What is the first line investigation in suspected obstruction

A

Plain ABdo X-Ray

734
Q

What is the second line investigation of intestinal obstruction

A

Non-Contrast CT

735
Q

First line management of a sigmoid volvulus

A

Sigmoidoscopy

736
Q

What is Spontaneous bacterial peritonitis

A

Where patients with ascites secondary to chronic liver disease ruptures, causing peritonitis

737
Q

In which patients is spontaneous bacterial peritonitis seen in

A

Hospitalised patients

738
Q

What is secondary peritonitis

A

Where a pathology is next to the peritoneum, irritating and inflaming it

739
Q

What conditions cause localised peritonitis

A

Diverticulum or appendicitis

740
Q

Signs distinctive of intra-abdominal abscesses

A

Swinging (spiking) fevers.

There may be a mass on rectal examination

741
Q

What finding is found in FBCs during peritonitis

A

Leukocytosis

742
Q

What drugs are typically used for peritonitis

A

Cephalosporins

743
Q

What drugs are used to treat inteaabdominal abscesses

A

Two agents or cephalosporins to give broad spectrum

744
Q

What dictates prognosis in peritonitis

A

Renal dysfunction

745
Q

Name four types of intusussceptions

A
  1. Ileo-ileal
  2. Colo-colic
  3. Ileo-Colic
  4. Ileo-caecal
746
Q

What is the most common intussusception

A

Ileo-ileal (only affecting the small bowel)

747
Q

What is the main cause of intussusception in adults

A

Malignancy (lymphomas, lipomas, RCCs)

748
Q

Risk Factors for intussusception in adults

A

CF
Peutz-Jeghers Syndrome
FAP

749
Q

Clinical presentation of intussusception

A
  1. Abdominal distention
  2. Mass
  3. Reduced bowel sounds

BUT NOT OBSTRUCTION (very rare)

750
Q

Gold Standard investigation for intussusception

A

CT Abdomen to show target sign (not USS unlike in children)

751
Q

Management of intussusception

A
  1. Pneumoscopic reduction
752
Q

What is the peak incidence of IBS

A

20 and 30

753
Q

What criteria is used to classify the type of IBS

A

Rome IV

754
Q

How is IBS subtypes defined

A

If over 25% of the stools are diarrhoea or constipation

755
Q

How long do symptoms need to be present before Its can be diagnosed

A

6 months

756
Q

What is the triad of symptoms in IBS

A
  1. Abdo pain
  2. Bloating
  3. Change in bowel habits

Symptoms relieved following defacation and aggravated by eating

757
Q

What are the first line investigations for IBS

A
  1. Serum tTg and EMAs
  2. Serum CA125 for women who may have ovarian cancer
  3. Faecal Calprotectin for those with IBS
758
Q

What medication is given to people with IBS-D

A

Loperamide

759
Q

What laxative is given to those with IBS-D

A

Linaclotide (AVOID lactulose)

760
Q

What is the second line treatment for those with IBS-D

A

5-HT 3 receptor antagonists (Odansetron etc)

761
Q

What therapy should be considered in patients with IBS who do not improve after 12 months

A

CBT

762
Q

What serum level indicated acute hepatitis

A

ALT > AST

763
Q

What serum level indicates obstructive jaundice

A

Jaundice + ALT < 100

764
Q

What condition is indicated by ALT > 400

A

Acute hepatocellular damage (viral hep)

765
Q

What antibody is positive in primary biliary cholangitis

A

AMA

766
Q

Name three pregnancy conditions that can cause jaundice

A
  1. Acute fatty liver of pregnancy
  2. Intrahepatic cholestasis of pregnancy (RARE)
  3. Pre-Eclampsia (HELLP syndrome)
767
Q

At what gestation is acute fatty liver of pregnancy onset

A

35 weeks

768
Q

What is the role of lactase

A

Hydrolysis of monosaccharides, glucose and galactose in the tips of the small intestines

769
Q

What causes secondary lactase deficiency

A

Gastroenteritis
Coeliac’s
IBD
Chemotherapy

770
Q

What is the gold standard lactose intolerance test

A

Breath hydrogen test

771
Q

What is leukoplakia

A

White patch adhering to oral mucosa that can’t be removed

772
Q

What is Hairy Leukoplakia caused by (2)

A

EBV

HIV

773
Q

Management of Hairy Leukoplakia

A

Systemic antiviral therapy or topical therapy with podophyllin

774
Q

Name four contraindications to liver biopsy

A
  1. INR > 1,3
  2. Thrombocytopenia ( <60 x 10^9)
  3. Warfarin (must be stopped)
  4. Ascites
775
Q

What is fulminant hepatic failure

A

When the failure takes place WITHIN 8 weeks of the onset of the underlying illness

776
Q

Define late-onset hepatic failure

A

When hepatic failure AFTER 8 weeks (8 weeks -> 6 months)

777
Q

Define chronic decompensated hepatic failure

A

Hepatic failure > 6 months

778
Q

Name 4 Antibiotics that can cause hepatic failure

A 
Co-Amoxiclav
Ciprofloxacin 
Doxycycline
Erythromycin
Nitrofurantoin
779
Q

Name a chemotherapy drug that can cause liver cirrhosis

A

Cyclophosphamide

780
Q

What causes Reye’s Syndrome

A

Kawasaki Disease: Giving children aspirin causing fatty degeneration of the liver

781
Q

Signs of hepatic encephalopathy on an EEG

A

Shows slow waves in early stages and flattened waves later on

782
Q

What would a brain biopsy show for Reye’s syndrome

A

Cerebral oedema without inflammation

783
Q

Main complication of Reye’s Syndrome

A

Hypoglycaemia: So you need to manage Reye’s syndrome with IV 10% glucose

784
Q

What medication can cause hypomagnesia

A

PPIs

785
Q

Name some GI conditions that can cause hypo magnesia

A
  1. Acute Pancreatitis
  2. Re-feeding SYndrome
  3. IBDs + Short Bowel Syndrome
786
Q

First Line investigation for the cause of hypo magnesia

A

ECG

Renal: 24 hour urinary Mg excretion

Check Calcium, phosphate and potassium levels

787
Q

Name four changes seen on an ECG in hypomagnesia

A
  1. Wide QRD complex
  2. Prolongued QT INterval
  3. Flattened T Waves
  4. U Waves
788
Q

Symptoms of hypomagnesia

A
  1. Weakness
  2. Tremour
  3. Paraesthesia
  4. Muscle fasciculation
  5. Seizures and coma
789
Q

Management of hypomagnesia

A

Oral replacement therapy

IV Mg 10% + 0.9% NaCl

790
Q

The most common causes of hypermagnesia

A
  1. End stage kidney disease
  2. Laxatives, antacids and enemas
  3. IV nutrition
791
Q

Symptoms of hyper magnesia

A
  1. Nausea
  2. Facial flushing
  3. Hypotension
  4. Paralytic ileus
  5. Fatigue
  6. Resp depression
  7. Bradycardia
  8. Complete heart block
792
Q

If the cause of hyper magnesia is remains unexplained, what investigations should be done and why

A

TFTs and morning cortisol test

Hypothyroidism and Addison’s are rare cause of hypermagnesia

793
Q

Management of hypermagnesaemia

A

IV Calcium

794
Q

Other than vomiting, what can cause mallory-weirs tears

A

Any pulmonary conditions that result in chronic coughs (e.g., Bronchiectasis, lung cancer, bronchitis)

795
Q

Name two medications that can cause Mallory-weirs tears

A

NSAIDs and Aspirins

796
Q

What score system is used to grade an Upper GI Bleed severity

A

Rockall score

797
Q

Initial management of mallory-weirs tears

A

Endoscopy within 24 hours (as they fix up quite quickly)

OR Angiotherapy if organ ischaemia and infarction

798
Q

When does re-bleeding in mallory-weirs tears happen

A

Within 48 hours

799
Q

What is Haemachromatosis

A

People’s GI tracts end up absorbing almost 4 times the amount of iron from the intestines

800
Q

How does Haemachromatosis cause tissue damage

A

Fe3+ is reduced to Fe2+, leading to free radicals (unpaired, unstable electron atoms) -> cell damage -> cell death -> tissue fibrosis s

801
Q

Where do Multiple Endocrine Neoplasias originate from

A

Endocrine Glands:

Pituitary glands
Thyroid Glands
Parathyroid Glands
Adrenal Glands
Pancreas

Leads to OVERPRODUCTION of hormones

802
Q

What endocrine gland produces calcitonin

A

Thyroid Gland

803
Q

Role of Calcionin

A

Decreases calcium levels

804
Q

How is MEN inherited

A

Autosomal Dominant: Tumour supressor gene

805
Q

What gives rise to the different types of MEN

A

Mutations in MEN1 on Chromosome 11 - tumour supressor gene gets deactivated = TYPE 1

Mutations in RET gene coded for by MEN 1 is a protooncogene -> MEN Type 2a and 2b

806
Q

Name the three tumours seen in MEN Type 1

A

Parathyroid (MOST COMMON)
Pancreatic
Pituitary

807
Q

Signs of parathyroid tumours

A

Increased bone breakdown -> Hypercalcaemia -> calcium kidney stones

808
Q

Signs of pancreatic tumours

A

Gastrinoma (Increased gastrin = raised HCL)

PEPTIC ULCERS
ABDO PAIN
VOMITING

Insulinoma: Hypoglycaemia

Glucagonoma: Hyperglycaemia

809
Q

Signs of pituitary gland tumours

A
  1. MOST COMMON: Prolactinoma (gynecomastia and galactorrhea)

Excess Growth Hormone: Gigantism/Acromegaly

Lots of Milk leads to Giant Kids

810
Q

Most common tumour seen in MEN Type 2a

A

Thyroid Medullary Cancer from C-Cells

Secondary: Pheochromocytoma

811
Q

What do C-cells produce

A

Calcitonin

812
Q

What is Pheochromocytoma

A

Excess production of epinephrine and norepinephrine

813
Q

What syndrome is typically seen in Pancreatic endocrine tumours

A

Zollinger-Ellison syndrome

814
Q

Other than the pancreas, where else can MEN type 1 tumours be found in the GI system

A

Duodenal microgastrinomas

815
Q

What skin symptoms are seen in MEN Type 1 and are indications of the disease

A

Multiple angiofibromas (spots)

816
Q

Surgical management of MEN Type 1

A

Resection of affected organ usually

817
Q

What is a bolus NG Tube

A

Uses gravity to push food down the tube

818
Q

Define Intermittent NG TUbes

A

By Gravity or Pump

819
Q

Define continuous NG Tube

A

By Pump

820
Q

What type of NG Tube increases the risk of GI symptoms

A

Anything by gravity

821
Q

What are contraindications for NG Tube feeding

A
  1. High risk of aspiration
  2. GORD
  3. Gastric Stasis
  4. Upper GI Strictures
  5. Nasal Injuries
  6. Basilar skull fracture
822
Q

How should a patient bed at in the insertion of an NG Tube

A

Semi Upright position (at an angle)

823
Q

Two ways we check the position of an NG TUbe

A
  1. Testing pH of apirate

2. X-Ray to confirm

824
Q

What receptors in the Gut are responsible for vomiting in infections, drugs or radiotherapy treatment

A

5-HT3

825
Q

Which receptors are triggered by mechanoreceptors in the gut (from mechanical distortion)

A

H1 and ACh

826
Q

What receptors are involved in the chemoreceptor trigger zome

A

5-HT3 and D2 receptors

827
Q

Name three ways that the mechanoreceptors in the gut can be stimulated and trigger vomiting

A 
Pelvic or abdominal tumours
Bowel obstruction secondary to malignancy 
Gastric Stasis (peptic ulcers, hepatomegaly, drugs)
828
Q

What metabolic condition can trigger the chemoreceptor trigger zone

A

Hypercalcaemia

829
Q

What drugs trigger the chemoreceptor trigger zone

A

Anti-epileptics
Opioids
Antibiotics
Digoxin

830
Q

When should hypercalcaemia be the suspected pathology relating to vomiting

A

IF it is accompanied by drowsiness

831
Q

Management of vomiting caused by irritation or stretching of the meninges

A
  1. High-Dose IV Dexamethasone + Oral Cyclizine
832
Q

How should vomiting caused by pelvic or abdominal tumours be treated

A

First Line: Oral or SC Cyclizine

^ first line even with aggravated by movement

Second Line: Add Dexamethasone

833
Q

How does Cyclizine stop vomiting

A

Blocks ACh and H1 receptors

834
Q

First Line management of vomiting caused by PARTIAL malignant bowel obstruction

A

STOP OSMOTIC AND STIMULANT LAXATIVES + PLACE ON DOCUSATE (Poo-softening)

AS LONG AS THERE IS NO COLIC:
Then place on metoclopramide or domperidone

835
Q

What type of drugs are metoclopramide and domperidone

A

Prokinetics

836
Q

How do pro kinetics work

A

Block D2 receptor activity in the gut

837
Q

What drug is contraindicated in pro kinetic drugs

A

Antimuscarinic (Cyclizine) as they are competitively blocked by them

838
Q

Second line management of partial bowel obstruction

A

AS LONG AS NO COLICS (Just flatus):

Olanzapine

839
Q

First line management of Complete Bowel Obstruction

A

Cyclizine

840
Q

Second Line anti-emetic in complete bowel obstrutcion

A

Levomepromazine if Cyclizine fails to work

841
Q

If vomiting persists in complete bowel obstruction, what should be done

A

Refer for stent emplacement to overcome obstruction OR start corticosteroids

842
Q

First line management of vomiting induced by gastric stasis

A

Metoclopramide or Domperidone

843
Q

IF Metaclopramide or domperidone (pro kinetics) fail to stop vomiting, what should be given

A

Ranitidine or Octreotide (which reduce gastric secretions)

844
Q

First line Management of chemically/metabolically induced nausea (Opioid induced, kidney disease and hypercalcaemia)

A

Haloperidol

845
Q

What else should be given to people with hypercalcaemia, alongside haloperidol

A

Bisphosphonates

846
Q

What is the first line medical management of nausea secondary to cytotoxic therapy or radiotherapy

A

Haloperidol

847
Q

IF haloperidol fails to manage nausea from cytotoxic or radiotherapy, what should be given

A

Levomepromazine

848
Q

If Haloperidol and levopromazine fail to control chemically/metabolically induced nausea, what should be given as an alternative

A

5-HT3 antagonists (Odansetron/Palonosteron etc)

849
Q

What is the first line medication given for vomiting associated with cisplatin chemotherapy

A

Aprepitant + 5-HT3 antagonist + Dexamethasone

It is becoming increasingly common to use this combination as standard therapy in emetogenic chemotherapy management

850
Q

First lIne management of motion-induced nausea

A

Cyclizine EVERY 8 hours or Hyoscine Hydrobromide

851
Q

If the origin of nausea and vomiting is uncertain, what medication should be given as first line

A

Levomepromazine as it blocks5-HT2, H1 and ACh receptors

852
Q

Name some nematodes (roundworms) that can cause infections in people

A

Ascaris Lumbricoides
Hookworm
Threadworm

853
Q

When should a transcutaneous bilirubinometer be used in babies

A

Born after the 35 weeks gestation and after 24 hours

854
Q

Where are norovirus strains typically concentrated in

A

Shellfish
Oysters
Plankton

855
Q

When does norovirus particularly affect the UK

A

November -> April

856
Q

Symptoms of Norovirus

A

Nausea + Vomiting
WATER Diarrhoea

Fever

857
Q

How long doe sit take for people to make a full recovery

A

1-2 days

858
Q

Complication of Norovirus in some people

A

Seizures

Dehydration (similar to gastroenteritis but the diarrhoea is watery)

859
Q

First line investigation for suspected norovirus

A

PCR stool sample

860
Q

Management of Norovirus

A

Oral rehydration and then IV

861
Q

Should anti-emetics or antidiarrhoeals be used in Norovirus?

A

No as it can cause C.difficile infections

862
Q

How is norovirus spread

A

Falco-oral route

863
Q

How long should a person isolate/stay at home for with norovirus

A

48 Hours

864
Q

What causes oesophageal spasms

A

When waves that push food through th oesophagus can’t progress normally

865
Q

Diffuse vs Nutcracker oesophageal spasms

A

Uncordinated contractions (some contract at once) vs Co-ordinated but with excessive amplitude

866
Q

Symptoms of Oesophageal spasms

A

Centralised, severe, crushing and retrosternal pain

Can be gripping or stabbing and radiate to the neck, back or upper arms

Dysphagia and Reflux symptoms

867
Q

First Line Investigation for oesophageal Spasms

A

CARDIAC investigations are indicated first

868
Q

Onset of oesophageal cancer

A

75+

869
Q

Risk Factors of Oesophageal Caners

A 
Tobacco
Alcohol
Barrett's Oesophagus
Chronic inflammation 
Achalasia
Obesity 
FH of hiatus Hernia
870
Q

Name two types of oesophageal cancers

A

Sqamous cell carcnioma

Adenocarcinoma

871
Q

Name the three layers in the mucosa of the oesophageal wall

A

Stratified Squamous Epithelium
Lamina Propria (connective ‘anchoring’ tissue)
Muscular Mucosa

872
Q

What is the gastroosopheageal junction

A

Squamous Epithelium of the oesophagus

Columnar Epithelium of the stomach

873
Q

What is the most common type of oesophageal cancer

A

Squamous cell carcinoma

874
Q

Where is squamous cell carcinoma of the oesophagus usually found

A

Upper 2/3rds of the oesophagus

875
Q

Risk Factors for Squamous Cell Carcinoma

A

Smoking
Hot Fluids
Smoking
STRICTURES

Damages the squamous cells = more likely to mutate

876
Q

Where are adenocarcinomas commonly found

A

Lower 1/3rd of the oesophagus

877
Q

What can cause Adenocarcinomas

A

GORD -> Barrett’s Oesophagus (type of metaplasia)

878
Q

Name two conditions that increase the risk of oesophageal cancer

A

Plummer-Vinson Syndrome

Palmoplantar Keratoderma

879
Q

What is Plummer-Vinson Syndrome

A

Iron Deficiency Anaemia
Glossitis
Cheilosis (cracking of the mouth)
Oesophageal rings causing difficulty swallowing

880
Q

What is Palmoplantar Keratoderma

A

Thick patches of skin on the hands and feet

881
Q

Symptoms of Oesophageal Cancer

A

Initially Asympatomatic

Progressive Dysphagia
Odynophagia
Heartburn
Vomiting
Pain in the chest, radiating to the back
Irretractable Hiccups
Meana
Hoarseness
Lymphadenopathy
882
Q

When should people be referred for urgent Upper GI Endosocpy

A

Dysphagia

OR
55+ and Abdo pain OR Reflux OR Dyspepsia

883
Q

When should people be referred for non-urgent GI Endoscopy for oesophageal cancer

A

Haematamesis

884
Q

When should people over 55 be referred for Upper GI NON URGENT GI Endoscopy

A

Treatment resistant dyspepsia
UPper Abdo pain + low haemorrhage levels
Raised platelet count + nausea/vomiting/weightloss/reflux

885
Q

First line investigation of Oesophageal Cancer

A

Bloods

URGENT ENDOSCOPY for biopsy

886
Q

How can we stage oesophageal cancer

A

FDG-PET scan + CT of the chest and upper abdomen

887
Q

Management of T1b oesophageal adenocarcinomas tumours

A

Endoscopic mucosal resection or remaining Barrett’s mucosa

888
Q

Management of T1b SCC oesophageal carcinomas

A

Chemoradiotherapy OR Resection

889
Q

Why should HER2 testing be done in people with oesophagi-gastric adenocarcinomas

A

Cmmon cause of cancer sin that junction, especially metastatic. Must treat with adjuvant Trastuzumab and Cisplatin

890
Q

What is the first line management of dysphagia at palliative level

A

Stenting

891
Q

Risk Factors of Oesophageal strictures

A

Barret;s
GORD
Benign peptic strictures

892
Q

What rheumatic disease can cause oesophageal strictures

A

Rheumatoid Arthritis

Stevens-Johnson syndrome

893
Q

What autoimmune conditions can cause oesophageal strictures

A

Thyroid Disease

Perniciouss Anaemia

894
Q

What would a CXR show for Oesophageal strictures

A

Gross dilatation of achalasia - CXR is FIRST LINE

895
Q

Why is Endoscopy not ideal for oesophageal strictures

A

Can perforate the oesophagues

896
Q

What is an Oesophageal web

A

Smooth extension of oesophageal tissue containing only the mucosa and submucosa

897
Q

Where are oesophageal webs commonly found

A

IN the upper area of the oeosphagus

898
Q

What sign is commonly associated with oesophageal webs

A

Iron Deficiency: Comes with iron deficiency anaemia symptoms) in women

899
Q

What syndrome commonly has oesophageal webs

A

Plummer-Vinson - however, most webs are not associated with the condition

900
Q

What are oesophageal rings

A

Concentric extensions of the tissue: Muscoa, submucosa AND muscles

901
Q

Symptom of oesophageal rings

A

Nothing - Asymptomatic

902
Q

Management of benign oesophageal strictures and rings

A

Oeosphageal dilatation at endoscopy

903
Q

Pre-hepatic causes of oesophageal varcies

A

Portal Vein thrombosis

904
Q

Intrahepatic causes of oesophageal varices

A

Cirrhosis
Portal hypertension
Acute Hepatitis
Schistosomiasis

905
Q

Poste hepatic causes of oesophageal varcies

A

Tumour compression
Budd-Chiari Syndrome
Constrictive pericarditis

906
Q

Symptoms of oesophageal varices

A

Haematemesis and Melaena

Pallor, hypotension, reduced urine output from loss of blood

907
Q

Management of Oesophageal varices

A

URGENT ENDOSCOPY

Terlipresisn in an active bleed for 5 days or after haematosis is achieved + Antibiotics

908
Q

First line management of non-bleeding varicies

A

Band ligation

Second Line: Emergency Sclerotherapy

909
Q

How should Gastric Varices be treated

A

N-butyl-2-cyanoacrylate or TIPS

910
Q

What is N-Butyl-2-Cyanoacrylate

A

Glue like substance that embolisms varices

911
Q

When is TIPS indicated for an oesophageal varcies

A

If a vatical haemorrhage is UNCONTROLLED

A temporary balloon tamponade is placed while we wait for TIPS operation

912
Q

Prophylaxis to prevent bleeding in oesophageal varices

A

Beta Blockers + Nitrates

913
Q

IF beta blockers are contraindicated to varices, what is the next intervention

A

Vatical band ligation

914
Q

Name three times organs are donated

A
  1. Donation after brainstem death
  2. Donation after circulatory death
  3. Living organ donation
915
Q

Can someone under 16 donate an organ?

A

Yes

916
Q

Under what circumstances should we prepare to donate someone’s organs (Criteria)

A
  1. Receiving end of life care
  2. Catastrophic brain injury
  3. Absence of one or more cranial nerve reflees

AND GCS < 4

OR life sustaining treatment being stopped would cause circulatory death

917
Q

What patients are prioritised for donations over others

A

Children whoa re then prioritised by waiting time

918
Q

What is Osler-Weber-Rendu SYndrome

A

Hereditary haemorrhage telangiectasia

919
Q

What can cause pancreatitis

A

GET SMASHED:

G- Gallstones
E - Ethanol 
T - Trauma
S - Steroids
M - Mumps
A. Autoimmune
S - Scorpion Stings
H - Hypertriglyceridaemia, hypercalcaemia, hyperparathyroidism
E- ERCP
D - Drugs (valproate, azathioprine and slufonamides)
920
Q

What cell in th epancrease produces somatostatin

A

Delat Cells

921
Q

What is the role of somatostatin

A

Inhibits secretion of pancreatic hormones

922
Q

Role of Amylin and what cell in the pancreas produces it

A

Beta Cells

Slows gastric emptying to stop spikes in glucose levels

923
Q

Name three enzymes produced by the exocrine pancrease

A

Proteases (trypsinogen)

Lipase
Amylase (starch and maltose degradation)

Elastases

924
Q

Role of CCK

A

Stimulates bile secretion via the gallbladder contraction

925
Q

What are the most common cancers of the pancreas

A

Adenocarcinomas of the exocrine pancreas

926
Q

How can distal adenocarcinomas cause pancreatitis

A

Disrupts and blocs the secretion of exocrine enzymes, causing them to be secreted into the pancreas instead of the duodenum. Food in the duodenum remains undigested

927
Q

Risk Factors for pancreatic cancer

A
  1. Smoking
  2. Diet
  3. Hereditary pancreatitis
  4. Chronic Pancreatitis
  5. FH of pancreatic cancer
  6. Genetic cancers
  7. IBD
  8. Peptic Ulcer Disease
928
Q

What genetic risk factors cause pancreatic cancer

A
  1. BRCA1 + BRCA2
  2. FAP
  3. Peutz-jeugher’s Syndrome
  4. Lynch Syndrome
  5. von Hippel-Lindau Syndrome
  6. MEN 1
  7. Gardner’s Syndrome
929
Q

Onset of symptoms of pancreatic cancer

A

Happen late, until it’s too late for surgery

930
Q

Early presentations of pancreatic cancer

A
  1. VAGUE: Epigastric pain and dull backache
931
Q

Where are most pancreatic cancers found

A

Head of the pancreas, usually cause obstructive jaundice

932
Q

Symptoms of pancreatic symptoms

A
  1. Abdo pain
  2. Jaundice
  3. Acute Pancreatitis
  4. Weight loss
  5. Steatorrhoea
  6. Palpable gallbladder (Courvoisier’s sign positive)
  7. Nausea and vomiting
933
Q

What causes nausea and vomtiing in pancreatic cancer

A

Compression of the pancreatic head on the duodenum = GOO

934
Q

What is Courvoisier’s sign

A

A palpable gallbladder + painless jaundice

935
Q

Describe abdominal pain in pancreatic exocrine tumours

A

Back pain is dull and worse lying supine, better sit forwards

936
Q

First line investigation for suspected pancreatic cancer

A
  1. FBC
  2. LFTs to confirm jaundice
  3. Serum glucose
937
Q

What is the tumour marker for pancreatic cancer

A

CA19-9

938
Q

What does serum glucose look like in pancreatic cancer

A

Hyperglycaemia

939
Q

What is the first line investigation for people suspected pancreatic cancer following blood tests

A

Pancreatic protocol CT Scan -> draining the bile duct

940
Q

If pancreatic cancer has not been diagnosed by pancreatic CT scan, what should be done

A

FDG-PET or Endoscopic US-guided tissue biopsy

941
Q

Investigation for pancreatic cysts

A

MRCP

942
Q

Criteria for pancreatic resection

A
  1. Obstructive jaundice with cystic lesions in pancreatic head
  2. Enhancing solid components in the cyst
  3. Pancreatic duct > 10mm
943
Q

How can pancreatic cancers be staged

A

CT

Then an FDG-PET/CT scan

944
Q

When is an MRI indicated for pancreatic cancers

A

If liver metastases is indicated

945
Q

What adjuvant therapy is used for pancreatic exocrine tumours

A

Gemcitabine + Cepcitabine following resection

946
Q

How to treat unresectable pancreati cancers

A

Chemotherapy.

Second-Line if not tolerated: Gemcitabine

947
Q

What is the role of capecitabine

A

Raidosensitiser, makes chemotherapy more receptive

948
Q

First line treatment of metastatic pancreatic cancer

A

Folfirinox

949
Q

What prophylaxis is given to people with pancreatic cancer who are receiving chemotherapy

A

LMWH

950
Q

What nutritional intervention is given in pancreatic cancers

A

Pancreatin (enteric)

951
Q

When should pancreatic resection be prioritised over biliary drainage in pancreatic cancer

A

Those who have biliary obstruction

952
Q

surgical intervention for duodenal obstruction in unresectable pancreatic resection

A

Gastrojejunostomy

953
Q

How is nausea and vomiting treated in pancreatic cancer

A

Prokinetics

954
Q

What drugs can cause peptic ulcers

A

NSAIDs

Steroids

955
Q

What should happen to NSAIDs that have caused peptic ulcer disease

A

Stopped immediately

956
Q

First line management of duodenal ulcers

A

PPIs

957
Q

First line drug to prevent duodenal ulcers

A

Misoprostal

958
Q

What is the preferred NSAID to give to patients who are susceptible to peptic ulcers

A

low dose aspirin + full dose naproxen

959
Q

IF a patient has a peptic ulcer with no known origin, what should be done

A

Assess if any over the counter medication they use has aspirin or NSAID traces

960
Q

First line management of bleeding ulcers

A

Endoscopic ablation

961
Q

What should be done if a gastric ulcer persists

A

Refer to secondary care for repeat endoscopy

962
Q

When should a patient with peptic ulcer be hospitalised

A

Haematemesis or Melaena as this only happens with a large blood vessel rupture

963
Q

Side-effects of misprostol

A

Diarrhoea and abdo pain

964
Q

What is the first line imaging for Renal colics

A

KUB X-Ray

965
Q

What film is ordered for suspected intestinal obstruction

A

Erect and Supine f=X-Rays

966
Q

What imaging is used to diagnose appendicitis

A

Abdominal CT

967
Q

Symptoms of Plummer-Vinson Syndrome

A

Painless, intermittent dysphagia (as it causes oesophageal rings and webs)

968
Q

Main cause of portal hypertension

A

Hepatic cirrhosis

969
Q

Two roles of the portal venous system

A

Contains nutrients absorbed by the GI (mesenteric and splenic portal veins)

Liver metabolites (toxins) -> kidneys for excretion

970
Q

Name three junctions that the hepatic portal system connects to the systemic system at

A

Inferior portion of the oesophagus (oesophageal varices)

Superior portion of anal canal

Round Ligament of liver

971
Q

How does the round ligament form

A

Umbilical cord is shut

Umbilical vein closes -> round ligament

972
Q

What causes portal hypertension physiologically

A

Blocked exit to the IVC causes increase in pressure of the portal veins

973
Q

What defines portal hypertension

A

Pressure rise of 5-10 mmHg

974
Q

What compound is deranged in liver failure

A

Ammonia (very elevated()

975
Q

What causes hepatic encephalopathy

A

Toxins pass through the BBB

976
Q

What causes caput medusae

A

Blockage of the hepatic portal system causes abdominal veins to dilate as the round ligament becomes patent from high pressure

977
Q

Result of portal hypertension in the splenic portal vein

A

Splenomegaly

978
Q

Why do we get anaemia, leukopenia and thrombocytopenia in portal hypertension/ Liver Cirrhosis

A

Because of splenomegaly from a dilated splenic vein

979
Q

How does portal hypertension and liver cirrhosis result in ascites

A

Endothelial cells release NO to combat hypertension

Arteries dilate

BP drops

Aldosterone secreted causing more water and sodium uptake

Fluid moves into tissues causing ascites

980
Q

What is a pre-hepatic obstruction causing portal hypertension

A

Thrombus occluding the portal vein

981
Q

Three causes of intra hepatic portal hypertension

A

Cirrhosis

Schistosomiasis

Sarcoidosis

982
Q

Post-hepatic causes of liver failure

A

RHF
Constrictive pericarditis
Budd-Chiari Syndrome

983
Q

What’s BUdd-Chiari syndrome

A

Where a thrombus or tumour inside the venous veins stops flow upwards into the IVC

984
Q

What first line investigation should be done for portal hypertension

A

LFTs, U and Es, glucose, FBC, clotting

Ferritin (for haemochromatosis)
Hepatitis Serology
Autoantibodies
Alpha-1 antitrypsin 
Serum Caeruloplasmin levels
985
Q

What is the first line scan for Portal Hypertension

A

Abdo USS

986
Q

If abdo USS is inconclusive for portal hypertension, what is the next investigation

A

CT SCan

987
Q

What are normal Hepatic Venous Pressure Gradient

A

<5mmHg

988
Q

How is portal hypertension treated

A

Non-Selective Betablockers + Nitrates

TIPS

Salt Restriction

989
Q

What is the prophylaxis of oesophageal varices

A

Non selective beta blockers (ie., Propranolol or Carvedilol)

990
Q

Whenis TIPS the indicated intervention for Ascites

A

In those getting frequent paracentesis

991
Q

How are rectal varices managed

A

Similar to Oesophageal

992
Q

Complication of ascites

A

Spontaneous bacterial peritonitis

993
Q

What is Hepatic Hydrothorax

A

The presence of pleural effusion in a patient with cirrhosis and all other causes have been terminated

994
Q

What cells are destroyed in primary biliary cholangitis

A

Small interlobular bile ducts

995
Q

Onset of primary biliary cholangitis

A

65

996
Q

What conditions can cause primary biliary cholangitis

A

AUTOIMMUNE

Thyroid
Systemic Sclerosis
Coeliac’s
Cholelithiasis

997
Q

What lab result is seen commonly among most patients with primary biliary cholangitis

A

Hyperlipidaemia

998
Q

Bilirubin levels in primary biliary cholangitis

A

INITIALLY NORMAL (as are PTT and albumin)

999
Q

IgM levels in primary biliary cholangitis

A

Raised

1000
Q

What is the definitive treatment of Primary Biliary Cholangitis

A

Liver Transplant

1001
Q

Primary Biliary Cholangitis vs Primary Sclerosing Cholangitis

A

Primary Biliary Cholangitis is usually in women (hence, thyroid issues) vs Men (Crohn’s and UC) for sclerosing

PBC = AMA positive

1002
Q

What is Proctalgia Fugax

A

Sudden cramping pain in the rectum

1003
Q

First line investigation for proctalgia (anal pain)

A

Anoscopy or proctoscopy

1004
Q

Treatment of proctalgia fugax

A

Re-assurance

1005
Q

First line management of symptomatic pruritus ani

A

Soothing ointment (bismuth or zinc oxide)

Topical corticosteroids

Antihistamines to help sleep

1006
Q

When should anyone with pruritus ani be referred to colorectal surgeon or dermatologist

A

4 weeks and symptoms persist

1007
Q

What bacteria causes pseudomembranous colitis

A

C. difficile

1008
Q

How is C. difficile diagnosed

A

Stool toxin EIA

1009
Q

When is a sigmoidoscopy used to diagnose Clostridium Difficile infections

A

If a patient is asymptomatic (stool culture is not clinically useful

1010
Q

What is the first line antibiotic for C. difficile infection

A

Vancomycin

1011
Q

What is the second line antibiotic for Clostridium Difficile

A

Fidaxomicin

1012
Q

When is Metronidazole given for Pseudomembranous colitis

A

Third Line: Stepped up vancomycin with or without metronidazole

1013
Q

First line antibiotic for a re-infetcion for C. difficile (12 weeks after symptoms resolve)

A

Fidaxomicin

1014
Q

First line intervention for life-threatening C.difficile Infection

A

Vancomycin + Metronidazole

1015
Q

When should someone with pseudomembranous colitis be referred for surgery

A

Acute SEVERE colitis:

So,
WCC: 15 x 09 per litre
50% increase in creatinine concentration
Fever over 38.5 degrees

1016
Q

What is the first line management of someone with an unexplained anal mass or ulcer

A

Referral at 2-week pathway IMMEIDATELY

1017
Q

Management of an irreducible rectal prolapse

A

Prompt surgical referral to prevent strangulation or gangrene

1018
Q

What is the most common cause of gastroenteritis in children

A

Rotavirus

1019
Q

Where does salmonella infetcions typically originate from

A

Beef
Chicken
UNPASTEURISED milk or Eggs

Vegetables, any food really as well.

1020
Q

Is Salmonella always associated with bloody diarrhoea

A

Usually but not always

1021
Q

How long does salmonella fever last for

A

48 hours

1022
Q

GOLD STANDARD for salmonella gastroentersitis

A

PCR testing

1023
Q

Management of salmonella gastroenteristi

A

Rehydration

Racecadotril to prevent dehydration

1024
Q

When can antibiotics be used for salmonella infection

A

> 50 years old
Immunocompromised
CVD
<6 months

1025
Q

What antibiotic is given for salmonella if indicated

A

Ciprofloxacin

1026
Q

How long should people stay off from school for with salmonella

A

48 hours from last episode of DNV

1027
Q

Onset of Sarcoidosis

A

20-40

1028
Q

Signs of sarcoidosis in the GI system

A

Deranged LFTs (bout it)

Splenomegaly and hepatomegaly sometimes

1029
Q

When is regular screening for colorectal cancer done

A

50 to 74 every 2 years

1030
Q

What is the screening for colorectal cancer

A

Faecal Immunochemical test

1031
Q

What Endocrinological condition is at high risk of colorectal cancer

A

Acromgealy

1032
Q

When should someone with acromegaly be offering colonosocpic screening

A

After 40

1033
Q

How often should people with a history of HNPCC or Lynch syndrome undergo a colonoscopy

A

Every 2 years after the age of 25

1034
Q

Management of FAP

A

Prophylactic colectomy from 16 to 25

Endosocpcy three yearly from 30

1035
Q

What bacteria causes dysentry

A

Shigella

1036
Q

How is shigella spread

A

Faec oral
Travel
Daycare
Nursing homes

1037
Q

How are most cases of shigellosis acquired in the UK

A

Travel

There has been an increase among MSM

Swimming in infected waters

1038
Q

How does dehydration affect haematocrit levels

A

Raises them

1039
Q

What vitamin deficiency causes Night Blidness and Xeropthlamia (conjunctivitis)

A

Vitamin A

1040
Q

What vitamin deficiencies can cause paraesthesia (not B12 and folate)

A

D and E

Magnesium

1041
Q

What vitamin deficiency can cause tetany

A

D and E

Calcium

Magnesium

1042
Q

What vitamin deficiency causes Ataxia and retinopathy

A

Vit E

1043
Q

What vitamins can cause dyspnoea and fatigue

A

Iron
Folic acid
B12

1044
Q

What is characteristic of Vit D Deficiency

A

Bowing of the anterior knees

1045
Q

How is Short Bowel Syndrome managed

A

Total Parenteral Nutrition

1046
Q

How is a sigmoid volvulus managed

A

Decompression and untwisting using a sigmoidoscopy

If this doesn’t work, Resection of the redundant sigmoid colon

1047
Q

What causes fatty liver

A

Accumulation of triglycerides and lipids in hepatocytes causeing inflammation

1048
Q

What medications can cause steatohepatitis

A 
Amiodarone
Tamoxifen
Steroids
Tetracyclines
Oestrogens
Methotrexate
1049
Q

What medically caused conditions can lead to steatohepatitis

A

Short Bowel Syndrome and Refeeding Syndrome

Rapid Weight Loss

1050
Q

What Gyne condition can cause steatoheaptitis

A

PCOS

1051
Q

What metabolic disorder can lead to steatohepatiitis

A

Wilson’s

1052
Q

Gold standard to diagnose steatohepatitis

A

Liver Biopsy

1053
Q

LFT findings in steatohepatitis

A

ALT raises FIRST and then falls under AST.

Can sometimes be normal

1054
Q

What liver enzyme is raised from alcoholism

A

GGT

1055
Q

USS finding in steatohepatitis

A

Hyperechogenic liver on USS

1056
Q

What is the mainstay treatment of steatohepatitis

A

Weight Loss and treat comordibities

1057
Q

What is the tumour marker for colorectal cancer

A

CEA

1058
Q

What markers are used to check breast cancer therapy monitoring

A

CA15-3 or CA27.29

1059
Q

What two cancers can CA19-9 be a tumour marker for

A

Biliary tree

Pancreatic cancer

1060
Q

How can medullary thyroid cancer be monitored

A

Calcitonin levels

1061
Q

What is the tumour marker for follicular or papillary thyroid cancer

A

Thyroglobulin

Year 4 (16 decks)

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