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taz- year 3 med > GI > Flashcards

GI Flashcards

1
Q

define constipation

A

unsatisfactory infrequent stools, difficult to pass and feeling incomplete defecation

common in women, elderly and during pregnancy

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2
Q

what are the red flags of a patient with constipation

A

new onset above 50
with other symptoms such as anaemia, abdomen pain, weight loss, blood in stool

these should warrant investigation for malignancy

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3
Q

what is the conservative management of constipation

A

increased dietary fibre and fluid (may take up to 4 weeks to work)
exercise is advised

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4
Q

what is the problem of overusing laxatives

A

hypokalaemia

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5
Q

what are the different types of laxatives and when should you use them

A

1) bulk forming laxatives eg methylcellulose/sterculia
- use in adults with small hard stools
- avoid in opiod induced
- 1st line in chronic constipation

2) stimulant laxatives eg bisacodyl
- avoid in bowel obstruction as it increases gut motility

3) faecal softener eg douse sodium/glycerol

4) osmotic laxatives- increase fluid in large bowel eg lactulose
- use in opiod induced constipation

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6
Q

Describe differences in presentation between UC and crohns

A
  • C younger pts more commonly, non blood diarhoea, smoking increase risk, perianal disease (skin tags, abcesses, fistula), mouth ulcers
  • UC strong genetic link also, bloody diarrhoea, smoking protects,
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7
Q

Describe similarities in UC and crohns presentations

A

peak at 15-25 and 55-60, chronic diarrhoea with flares, colicky abdopain, urgency, tenesmus, systemic symptoms (malaise, anorexia, fever), abdo tenderness

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8
Q

Give 4 extraintestinal manifestations of crohns

A
  • clubbing
  • erythema nodosum
  • conjunctivitis
  • iritis
  • episcleritis
  • large joint arthritis
  • anklyosing spondylitis
  • fatty liver
  • granulomata of skin
  • epiglottitis
  • kidney stones
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9
Q

Is pyoderma gangrenosum associated with UC or crohns?

A

UC

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10
Q

How should IBD be investigated

A
  • bloods: FBC, LFT, U&E, LFT, ESR, CRP, haematinics, iron studies
  • stool culture and microscopy
  • faecal calprotectin
  • c diff toxin
  • colonoscopy and biospies (2 from 5 sites in distal ileum and rectum for UC)
  • AXR if toxic megacolon suspected (tender, distended abdomen)
  • pelvic MRI if perianal disease which isnt simple fistula
  • TMPT levels for azathioprine treatment
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11
Q

Describe the NICE guidelines for severity of IBD

A

Mild: <4 stools p/day, small blood in stools, no anaemia, HR<90, no fever, normal ESR and CRP
Mod: 4-6 stools, some blood, no anaemia, fever, HR<90, normal ESR and CRP
Severe: >6 stools, visible blood, systemic upset fever, high HR, anaemia, ESR or CRP up)

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12
Q

How are crohns flares managed?

A
  • pred 30-40mg
  • azathioprine added if 2nd flare in 12 months or methotrex if TPMT levels low
  • Infliximab if severe/ refractory
  • Surgery if disease limited to distal ileum
  • Antispasmodics can treat cramps if obstruction excluded
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13
Q

How is crohns remission maintained?

A

Azathioprine or mercaptopurine, infliximab if severe
Stop smoking
Lopermide can help reduce diarrhoea in remission but not acute disease

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14
Q

How is UC remission induced?

A

Aminosalicylates (mesalazine) in mild to mod disease, presnisolone if severe or this doesnt work
Azathioprine or 6MP if >1 relapse per year
CIclosporin or infliximab for rescue therapy in severe refractory colitis
Surgery last resort

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15
Q

Give 4 complications of IBD

A
  • extra intestinal manifestations (ank spond)
  • colorectal cancer, bowel cancer
  • psychosocial and sexual problems
  • osteoporosis due to steds
  • toxic megacolon (usually triggered by opiates, hypokalaemia, anticholinergics, barium enemas)
  • perforation, stricture, fistula
  • iron, folate and B12 deficiency
  • gall and renal stones
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16
Q

Define Crohns

A

Chronic inflammatory disease characterised by transmural inflammation anywhere from mouth to anus
Characterised by skip lesions and non caseating granulomas

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17
Q

What are three microscopic features of Crohns?

A

Fissuring Ulcers
Lymphoid and Neutrophil aggregates
Non caseating granulomas

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18
Q

Give 3 presentations of Crohns

A

Diarrhoea
Abdominal Pain
Weight Loss

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19
Q

Define UC

A

Chronic inflammation of mucosa and submucosa affecting the rectum and extending proximally
Continuous in nature

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20
Q

What are three microscopic features of UC?

A

Crypt Abscesses
Pseudopolyps
Hyperaemic Mucosa

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21
Q

Give three presentations of UC

A

Episodic Diarrhoea
Blood and Mucous
Cramping

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22
Q

What is faecal calprotectin and when is it raised?

A

Indicates neutrophil migration into intestinal mucosa (higher the level, the more inflammation)

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23
Q

What would you see on an Abdo Xray of IBD?

A

Mucosal Thickening
?Proximal Constipation
?Toxic Megacolon

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24
Q

What are the endoscopy options for IBD?

A

Colonoscopy - proximal large bowel disease
Flexible Sigmoidoscopy - safest if diarrhoea is bloody
Capsule Endoscopy - Small Bowel

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25
Q

When would you do an MRI in IBD?

A

For Small Bowel Crohns

For Peri-Anal disease in Crohns

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26
Q

Other than nausea, give two side effects of Azathioprine

A

Pancreatitis

Leucopenia

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27
Q

How does Infliximab work? What do you have to test for prior to prescription?

A

Prevents neutrophil aggregation and granuloma formation

Check for underlying malignancy and TB

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28
Q

what is the surgery that may be required in crohns

A

ileocaecal resection

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29
Q

Define Coeliac

A

Immune mediated inflammatory systemic disorder provoked by gluten

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30
Q

Describe the pathophysiology of Coeliac disease

A

Associated with HLA DQ2 and HLA DQ8
Lengthening of intestinal crypts
Lymphocytes infiltrate epithelium

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31
Q

Give 5 presentations of Coeliac Disease

A 
Bloating
Diarrhoea 
Weight Loss 
Steatorrhoea 
Abdo Pain
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32
Q

What blood tests would you carry out for suspected Coeliac disease?

A

Total IgA

tTG-IgA (AKA Tissue Transglutaminase IgA)

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33
Q

What other investigation (not bloods) would you carry out for suspected Coeliac disease

A

OGD and Duodenal Biopsy

Showing villous atrophy and intraepithelial lymphocytosis

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34
Q

Give four complications of Coeliac Disease

A

Small Bowel Lymphoma
Small Bowel Cancer
Osteoporosis
Neuropathy

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35
Q

how would you manage coeliac disease

A

Conservative
• Dietary removal of gluten from diet (wheat, barley, oats, rye)
◦ Rice, maize, soya, potatoes, oats and sugar are ok
• Pneumococcal vaccination –functional hyposplenism
◦ Influenza vaccine on an individual basis

Medical:
• Corticosteroids in small percentage who fail to respond to gluten-free diet

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36
Q

What are the 5 Key Questions to ask a patient presenting with Dysphagia?

A

1) Was there difficulty swallowing both solids and liquids from the start?
2) Is it difficult to initiate swallowing?
3) Is swallowing painful?
4) Is dysphagia intermittent or getting worse?
5) Does neck bulge and gargle on drinking?

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37
Q

Give two physical causes of Oesophageal Dysphagia

A

Tumour

Stricture

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38
Q

Give two neuromuscular causes of Oesophageal Dysphagia

A

Achalasia

Presbyoesophagus

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39
Q

How would you investigate Physical causes vs Neuromuscular?

A

Physical with OGD

Neuromuscular with Barium Swallow

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40
Q

What is Oropharyngeal Dysphagia?

A

Difficulty getting food to leave the mouth due to lack of coordination

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41
Q

Give a brief outlne of the four stages of Hepatic Encephalopathy

A

1 - Poor Memory and Sleep
2 - Asterixis, Agitation
3 - Drowsy
4 - Coma

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42
Q

What does a raised ALT indicate vs a raised ALP?

A

ALT - damage to hepatocytes

ALP - damage to bile ducts

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43
Q

What is Gamma GT?

A

An enzyme found in hepatocytes and biliary tract

Needs to be raised alongside ALP (as ALP can also be raised in increased bone turnover)

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44
Q

Name two autoantibodies associated with Primary Biliary Cirrhosis

A

AMA (Antimitochondrial Antibodies)

SMA (Smooth Muscle Antibodies)

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45
Q

What are the three most common causes of Chronic Liver Disease?

A

Alcoholic Liver Disease
Non Alcoholic Steatohepatitis (NASH)
Hep B&C

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46
Q

What is PBC? Give three feature?

A

Autoimmune granulomatous inflammation of intra and extrahepatic bile ducts
Associated with AMA antibody
More common in Women
Asymptomatic raised ALP

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47
Q

What is autoimmune hepatitis?

A

Autoantibodies against hepatocyte surface antigens

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48
Q

Describe the presentation of autoimmune hepatitis

A

Acute hepatitis

Jaundice

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49
Q

What is PSC? How do patients present?

A

Primary Sclerosis Cholangitis is progressive cholestasis with bile duct inflammation and strictures
Presents as pruritus with or without fatigue

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50
Q

What is the risk if a patient has IBD and PSC?

A

increased risk of colorectal malignancy

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51
Q

What is Haemachromatosis?

A

Autosomal Recessive (HFE gene) of increased iron absorption leading to deposition in skin/joints/organs

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52
Q

Why do women with Haemachromatosis present later than men?

A

Menstrual blood loss is protective

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53
Q

What is WIlson’s Disease?

A

Autosomal recessive disorder of copper excretion with deposition in liver and CNS

54
Q

Give 4 presentations of Wilson’s Disease

A

CNS Signs (Dysarthria, Dysphagia)
Slow Cognition
Decreased Libido
Kayser Fleischer Ring

55
Q

What would the serology of Wilson’s Disease show?

A

Raised LFTs
Low Serum Copper
Low Serum Ceruloplasmin
(HIGH URINARY COPPER)

56
Q

Define Cirrhosis

A

End pathology of Chronic Liver Disease implying irreversible liver damage

57
Q

Give three histological features of Cirrhosis

A

Loss of Architecture
Fibrosis
Nodular Regeneration

58
Q

Give 5 signs of Cirrhosis OE

A 
Clubbing
Palmar Erythema 
Dupuytren's Contracture 
Spider Naevi 
Gynaecomastia
59
Q

Name 3 features of Liver Failure

A

Coagulopathy (synthetic failure)
Encephalopathy (PADC)
Ascites

60
Q

What is the risk of Ascites?

A

Spontaneous Bacterial Peritonitis

61
Q

Apart from Liver Failure, give two complications of Cirrhosis?

A

Portal Hypertension

Hepatocellular Carcinoma

62
Q

What drug would you give for hepatic pruritus?

A

Colestyramine

63
Q

What medical management would you give for Hepatic Encephalopathy? How do they work?

A

Lactulose - decreases ammonia reabsorption

Rifaximin - eliminates ammonia producing bacteria

64
Q

What medical management would you give for Ascites?

A

Fluid restriction and spironolactone

65
Q

What is the MUST score?

A

Malnutrition Universal Screening Tool

Identifies adults who are malnourished or at risk of malnourishment

66
Q

What is acute liver failure?

A

Appearance of severe complications (coagulopathy and encephalopathy) rapidly after first signs of liver disease. Hyperacute is <1 week, acute= 8-28 days, subacute= 4-12 weeks.

67
Q

Give 4 causes of acute liver failure

A

Infections: viral hepatitis, yellow fever, leptospirosis
Drugs: paracetamol OD, isoniazid
Toxins: types of mushrooms
Vascular: veno- occlusive disease
Other: alcohol, fatty liver, primary billary cholangitis, haemochromatosis, autoimmune hepatitis, a1 antitrypsin deficiency, malignancy

68
Q

how does acute liver failure present?

A
  • rapid onset jaundice, weakness and ascites
  • encephalopathy: confusion, hallucinations, reduced GCS, papillodema, hypertension, bradycardia
  • Coagulopathy: prolonged PR/ INR, thrombocytopenia, bleeding, bruising, DIC
  • Signs of chronic disease: hepatic flap, caput medusa, palmer erythema, dupuytrens contracture
69
Q

How should acute liver disease be investigated?

A
  • FBC (? infection, ? GI bleed), U&E, LFT, clotting, glucose, paracetamol level, virology, CMV and EBV serology, ferritin
  • Blood culture, urine culture, asctitic tap for MC&S
  • CXR, abdo USS, doppler flow studies of portal vein
70
Q

why does encephalopathy occur in liver disease?

A

Nitrogenous waste (eg ammonia) builds up in circulation and passes to brain. Astrocytes clear it but as they do so produce excess glutamine which causes osmotic shift of fluid into cells- hence causing cerebral odema

71
Q

How is acute liver disease managed?

A
  • beware sepsis, hypos, varices bleeding, encephalopathies
  • urinary and central venous catheters to monitor fluid status
  • monitor obs
  • 10% IV glucose IV 1L/2hrs to avoid hypos
  • treat cause
  • treat malnourishment
  • treat seizures with phenytoin
  • haemodialysis if renal failure develops
  • liase with transplant service
72
Q

List 6 complications of acute liver disease and how you treat them?

A
  • cerebral odema: on ITU, 20% mannitol IV and hyperventilate
  • Ascites: fluid restriction, low salt diet, diuretics
  • upper GI bleed: vit K 10mg/d IV for 3 days, platelets, FFP + bloods as needed, endoscopy, terlipressin
  • Infection: ceftriaxone
  • Hypoglycaemia: 50 ml 50% glucose if drops <2 mmol/L
  • Encephalopathy: avoid sedatives, 20 degree head tilt, correct electrolytes, lactulose (causes colonic pH to drop so traps NH3 in colon)
73
Q

What are the five stages of MUST screening?

A

1) BMI
2) %unplanned weight loss scored via table
3) Establish acute disease effects and score
4) Add 1,2,3 and give an overall score
5) Refer to guidelines

74
Q

What would you do for ‘Low Risk’ patients following MUST screening?

A

Routine clinical care

Repeat screning

75
Q

What would you do for ‘Medium Risk’ patients following MUST screening?

A

Document dietary intake for 3 days
Adequate - continue to repeat screenings
Inadequate - follow local policy

76
Q

What would you do for ‘High Risk’ patients following MUST screening?

A

Refer to dietician or nutritional support team

77
Q

Give three reasons so many patients are malnourished

A

NBM
Increased requirements
Direct effect of treatment (N&V)

78
Q

How can you ensure an NG tube is inserted correctly?

A

test pH

CXR (especially if on PPIs)

79
Q

What can cause malnutrition?

A
  • neglect
  • poverty
  • dementia
  • severe learning dificulties and mental health problems
  • malignancy
  • renal or heart failure
  • infections (HIV, CMV, hepatitis)
80
Q

What are the 2 clinical syndromes of malnutrition?

A

marasums: inadequate protein and energy, severe muscle wasting
Kwashiorkor: fair- normal energy intake, but inadequate protein leading to odema, usually in children age 1-2

81
Q

How is malnutrition managed?

A
  • NG feeding (enteral) in those with poor intake but functional GI tract or dyspahgia
  • Parenteral nutrition (IV) is used in inadequate intake and non functional GI tract
  • treat cause
  • dietician and social services review
82
Q

What is the ROCKALL score?

A

Predicts the risk of death and rebleeding from an upper GI bleed
Done pre and post endoscopy

83
Q

Give 5 contributions to the ROCKALL score

A 
Age
Co-Morbidity 
Shock 
Source of Bleeding 
Stigmata of recent bleeding
84
Q

What is the Blatchford Score?

A

Used to predict the need for intervention in a GI bleed (intervention being transfusion or therapeutic endoscopy)

85
Q

Give 5 parameters used in the Blatchford Score

A 
Blood Urea
Systolic BP 
Malaena 
HR>100 
Syncope
86
Q

What is the most common cause of GI bleeds?

A

Peptic Ulcers

87
Q

Give a three step management plan for Variceal Bleeds

A

1) Fluid Rescucitation
2) IV Terlipressin (no IHD) and IV antibiotics
3) Urgent Endoscopy

88
Q

Describe the two endoscopy management options for a Varcieal Bleed

A 
Banding (Mechanical obstruction to flow)
Linton Tube (Tube with a single balloon)
89
Q

Describe the TIPSS procedure

A

transjugular Intrahepatic Portosystemic Shunt

Establishes communication between Hepatic Portal Vein and Hepatic Vein in an attempt to reduce portal hypertension

90
Q

How would you manage a Non Variceal bleed?

A

Most stop on their own
IV fluids, bloods
If continues do radiological embolisation

91
Q

What are the most common causes of an upper gi bleed?

A

Peptic ulcers and oesphageal varcies.
Other causes inc gastritis/ erosions, erosive duodenitis, portal hypertensive gastropathy, malignancy, mallory- weiss tear, vascular malformation

92
Q

Give 3 risk factors for peptic ulcers

A

alcohol abuse, renal failure, NSAID use, older age, anticoagulants, steroids

93
Q

Give 3 risk factors for oesphageal varices

A

advanced liver disease, continued alcohol intake, anticoagulants

94
Q

how do upper GI bleeds present?

A
  • Epigastric pain
  • haematemesis (active bleeding)
  • coffee ground vomit (bleeding has stopped or is mild)
  • malaena
  • haematochezia (profuse UGIB or colonic bleeding)
  • features of blood loss (shock, syncope, faint, dizziness, pale, cold, thready pulse, confusion, dehydration, oligourea, prolonged caprefill)
  • features of underlying disease (dyspepsia, weight loss, jaundice, ascites, spider naevi, hepatic flap)
95
Q

Describe the management of someone with an upper GI bleed who is haemodyanamicaly unstable

A
  • stop +/- reverse anticoagulants
  • activate major haemorrhage protocol (get O- blood, cross match)
  • 2x large bore cannula
  • secure airway and use suction
  • run 500ml saline over 10 mins in one and blood in other
  • platelets, FFP, vit K, prothombin complex may be needed
  • arrange urgent endoscopy
  • call 2222/ senior if severe or not improving
  • consider catheter
  • 15 mins obs until stable then hrly
  • FBC U&E, LFT, clotting, cross match
96
Q

What drug can be used if oesophageal varcies cause the upper GI bleed

A

terlipressin IV 1-2mg/ 6hr - also give IV abx

97
Q

When a pt with an upper GI bleed is haemodynamically stable, what intervention do they need?

A

Endoscopy

They also need 2x large bore cannula, cross matched blood if hb<7, terlipressin, fluids etc

98
Q

What can be done if endoscopy fails to stop an upper GI bleed

A

Surgery or emergency mesenteric angiography/ embolisation

Sengstaken- blakemore tube can be used for oesphgeal varcies

99
Q

How is H. pylori identified and treated?

A

Identified with ureas breath test

Cured with 7 day course of PPI plus amoxicillin 1g and either clarithromycin 500mg or metronidazole 400mg all TDS

100
Q

Give 4 red flags for dyspepsia

A
  • weight loss
  • fhx UGI ca
  • dysphagia
  • age >55 and new onset
  • palpable mass
  • persistant vomiting
  • UGI bleed
101
Q

Give two examples of malignant liver tumours

A

Hepatocellular carcinoma

Cholangiocarcinoma

102
Q

Give three examples of benign liver tumours

A

Cysts
Hemiangiomas
Adenomas

103
Q

What is Achalasia?

A

Impaired peristalsis of smooth muscle layer of lower oesophagus causing functional stenosis/stricture

104
Q

Give 5 presenting features of Achalasia

A 
Dysphagia (solid>liquid)
Food Bolus Impaction 
Regurgitation 
Retrosternal Chest Pain 
Heartburn
105
Q

What would a CXR of Achalasia show?

A

Vastly dilated oesophagus behind the heart (bird beak)

106
Q

Manometry is the gold standard investigation for Achalasia. What would you do before and why?

A

Barium Swallow in case of puncturing malignancy

107
Q

What would Manometry of Achalasia show?

A

High cardiac sphincter pressure with incompleterelaxation on swallowing

108
Q

What are the two management options for Achalasia?

A 
Heller Myotomy (dividing the cardiac sphincter)
Pneumatic Dilation (balloon catheter to rupture muscle without breaking mucosa)
109
Q

Give 3 drugs that are a risk factor for GORD. Why?

A

Anticholinergics
Nitrates
CCBs
Relax cardiac sphincter

110
Q

Give 3 requirements for urgent endoscopy

A

Dysphagia
Over 55
ALARM symptoms

111
Q

Describe an endoscopic grading method for GORD

A 
Savary Millar Grading
1 - Single/Multiple erosions on a single fold 
2 - Multiple erosions on multiple folds 
3 - Multiple circumferential erosions 
4 - Ulcer/Stenosis/Shortening 
5 - Barrett's Epithelium
112
Q

Give two other investigations you could do for GORD

A

Barium Swallow

24h pH monitoring

113
Q

Give 4 pharmacological treatment options for GORD

A

Antacids/Alignates
Lansopazole (30mg OD)
Ranitidine
Metacloperamide (Prokinetic)

114
Q

What are the two types of Hiatus Hernia?

A

Sliding (80%) - GOJ slides up into chest

Rolling (20%) - GOJ remains in stomach but bulge of stomach herniates either side

115
Q

Give three differences between Gastric and Duodenal ulcers

A

Pain time after eating (1-2hrs G, 2-4hrs D)
Food aggravates pain (G), Food relieves pain (D)
Vomiting common (G), Vomiting uncommon (D)

116
Q

what are the ALARMS symptoms

A

ALARMS symptoms warrant urgent endoscopy

o Anaemia (Fe deficiency)
o Loss of weight
o Anorexia
o Recent onset/progressive Sx
o Melaena/haematemesis
o Swallowing difficulty (i.e. dysphagia)
117
Q

how would you manage a peptic ulcer

A
  • lifestyle advice such as smoking cessation, weight loss and reduction in alcohol consumption plus avoidance/ cessation of NSAIDs where possible.
  • PPI for 4-8wks to reduce acid production, then reassess after this period for resolution of symptoms (“test and treat”).
  • Those pt with + H.Pylori should be started on triple therapy (PPI, clarithromycin and either amoxicillin or metronidazole).
  • If persistance of symptoms do an urgent OGD to exclude any malignancy.
  • Following this, other causes of treatment failiure an be considered such as failiure of H.Pylori eradication or Zollinger- Ellison syndrome.
  • Surgical management: rare except in emergencies such as perforation or in the management of Zollinger Ellison syndrome.
  • However in severe or relapsing disease, either partial gastrectomy or selective vagotomy may be considered.
118
Q

what is alpha 1 anti trypsin deficiency

A

• This is a rare cause of cirrhosis. Mutations in the α1-antitrypsin gene lead to reduced hepatic production of α1-AT, which normally inhibits the proteolytic enzyme, neutrophil elastase.

119
Q

how would you investigate an alpha 1 anti trypsin deficiency patient

A
  • Most patients with clinical disease develop chronic liver disease (due to accumulation of the abnormal protein within the liver) and early-onset emphysema due to proteolytic lung damage.
  • Diagnosis is made by demonstrating low serum levels of serum α1-AT and confirmed by genotype assessment.
  • On liver histology, α1-AT-containing globules are seen in hepatocytes
120
Q

how would you treat an alpha 1 anti trypsin deficiency patient

A

Treatment is for chronic lung and liver disease. Intravenous augmentation therapy with plasma-derived α1-AT is used but this not widely available. Patients should be advised to stop smoking.

121
Q

what is Budd chiari syndrome and what is the classical triad of symptoms

A
  • obstruction of the hepatitic vein by thrombosis/tumour leading to congestive schema/hepatocyte damage

1) abdo pain
2) hepatomegaly
3) ascites

portal hypertension may occur in chronic cases

122
Q

how would you treat Budd chiari syndrome

A

angioplasty/transintrahepatic portosystemic shunt may be needed

anticoagulant for life

consider liver transplant if hepatic necrosis

123
Q

what antibiotics are associated with c diff

what are some other risk factors

A

Second and third generation cephalosporinsre now the leading cause of Clostridium difficile.

• Clindamycin

risk factors other then abx
• proton pump inhibitors
• Inflammatory bowel disease
• Immunosuppression
• GI tract surgery
124
Q

how do you diagnose a c diff infection

A 
risk factors other then abx
• proton pump inhibitors
• Inflammatory bowel disease
• Immunosuppression
• GI tract surgery

Diagnosis and investigation
• Clostridium difficile antigen positivity only shows exposure to the bacteria, rather than current infection
• FBC: increased White Cell Count is characteristic
• Stool: by detecting C. diff toxin (CDT) in the stool
• Colonoscopy/Sigmoidoscopy: This has been superceded by advent of tests to detect toxins. Appearance of “pseudomembranes” is highly suggestive but not diagnostic

125
Q

how would you treat c diff

A

• first-line therapy is oral metronidazole for 10-14 days
• if severe or not responding to metronidazole then oral vancomycin may be used
• fidaxomicin may also be used for patients who are not responding , particularly those with multiple co-
• Combination for life-threatening infections: oral vancomycin + IV Metronidazole
morbidities
• for life-threatening infections a combination of oral vancomycin and intravenous metronidazole should be used

126
Q

what is a paracetamol overdose and what is the pathophysiology

A

Definition- 150mg/kg or 12g in an adult can be fatal (75mg/kg if malnourished).

A small amount of the drug is metabolized via the cytochrome P-450 pathway into NAPQI, which is extremely toxic to liver tissue, as well as being a strong biochemical oxidizer. In an average adult, only a small amount (10%) of NAPQI is produced, which is inactivated by conjugation with glutathione. When a toxic dose of paracetamol is ingested, the normal glucuronide pathway is saturated and large amounts of NAPQI are produced

127
Q

what are key questions for a suspected paracetamol overdose

A

Key questions
1. Time of the first dose
2. Time of the last dose
3. Total amount of paracetamol ingested
• the next step is to work out the serum paracetamol concentration
• 4 hours must elapse since ingesting before taking a blood sample
• Then compare this to the paracetamol poisoning treatment graph
• If the conc is above the treatment line then there is high risk of toxicity and therefore antidote is required
◦ Acetylcystine

128
Q

what is the side effect of acetylcystine

A
  • Acetylcysteine can cause an anaphylactoid reaction
  • This presents with similar features to an anaphylactic reaction (e.g. urticarial rash, nausea, tachycardia, wheeze), but it does NOT have an allergic basis (i.e. no increase mast cell tryptase)
  • If this reaction occurs, you should stop the infusion temporarily and offer symptomatic treatment with an antihistamine (e.g. chlorphenamine 10 mg IV in adults)
  • Once the patient’s symptoms are improving, you should restart acetylcysteine treatment using the next infusion in the sequence.
129
Q

which hepatitis virus have a risk of causing chronic liver disease

A

Hep B and C

Hep D with superinfection

130
Q

what is Haemolytic uraemia syndrome and how do you treat

A

its present with haemolytic anaemia, decreased platelets and AKI (due to thrombosis of glomerular capillaries)

may be caused by Ecoli as it release shiga toxin (STEC HUS)

or may be Atypical HUS caused by uncontrolled complement

can be precipitated by pregnancy

treatment:
- STEC HUS- supportive (fluid for AKI)
- A HUS- plasma infusion

ABX CONTRAINDICATED IN HUS TREATMENT EVEN WITH ECOLI

taz- year 3 med (10 decks)

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