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T year LOBs medicine > ALIM > Flashcards

ALIM Flashcards

1
Q

what are the symptoms of GORD?

A
  • heartburn
  • regurgitation
  • belching
  • chronic cough
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2
Q

what is the first line investigation for GORD?

A

low dose PPI challenge

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3
Q

when would you do an endoscopy for GORD?

A

Patient is over 55 with alarm symptoms

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4
Q

what is grade A in the LA classification for oesophagitis used in GORD?

A

The mucosal breaks are confined to the mucosal folds, each no longer than 5mm

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5
Q

what is grade B in the LA classification for oesophagitis used in GORD?

A

at least one mucosal break longer than 5mm confined to the mucosal folds but not continuous between two folds

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6
Q

what is grade C in the LA classification for oesophagitis used in GORD?

A

mucosal breaks that are continuous between the tops of mucosal folds but not circumferential

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7
Q

what is grade D in the LA classification for oesophagitis used in GORD?

A

Grade D: extensive mucosal breaks engaging at least 75% oesophageal circumference.

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8
Q

what lifestyle changes should be advised in a patient with GORD?

A 
Weight loss
smoking cessatation
small and regular meals
less hot drinks
reduce caffeine
less alcohol
less spicy food
don't eat at least 3 hours before going to bed
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9
Q

what is the treatment chart for GORD?

A
  1. lifestyle advice
  2. OTC antiacids
  3. PPI such as omeprezale
  4. double PPI dose and make twice daily
  5. H2 receptor antagonist
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10
Q

what are the difference in effects of magnesium vs aluminium antacids?

A

Magnesium; tend to cause diarrhoea

Aluminium; tend to cause constipation

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11
Q

what are risk factors for GORD?

A
  • obesity
  • hiatus hernia
  • pregnancy
  • delayed gastric motility
  • H.pylori
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12
Q

what drugs are a risk factor for gord?

A

anticholinergic agents
calcium channel blockers
nitrates

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13
Q

what are the two types of hiatus hernia?

A

80% sliding

15% paraoesophageal/ rolling

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14
Q

what type of hiatus hernia is more likely to cause gord?

A

sliding as the sphincter is no longer in tact

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15
Q

what is a sliding hiatus hernia?

A

The gastrooesophageal junction and part of the stomach slide up together into the chest

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16
Q

what is a rolling hiatus hernia?

A

The stomach squeezes through the hiatus landing next to the oesophagus in the chest

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17
Q

what is dyspepsia?

A

A term to describe a number of GI symptoms including heart burn, pain, nausea, belching.

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18
Q

how should you investigate dyspepsia?

A

endoscopy for patients over 55 or those with alarm symptoms

H pylori stool antigen test

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19
Q

what is the tissue change seen in Barrett’s oesophagus?

A

Squamous epithelium is replaced with metaplastic columnar mucosa

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20
Q

What is the management for low grade dysplasia in Barrett’s oesophagus?

A

repeat biopsy within 6 months. and give high dose PPI’s.

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21
Q

what is the management for high grade dysplasia in Barrett’s oesophagus?

A

High dose PPI’s are started and repeat biopsy in 3 months.

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22
Q

what is achalasia?

A

Impaired LOS relaxation causing foods and liquids to fail to reach the stomach

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23
Q

what is dysphagia?

A

Difficulty or painful swallowing often due to improper LOS function and aperistalsis

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24
Q

what are clinical features of peptic ulcers?

A

recurrent burning epigastric pain that is worse at night and when hungry

nausea

anorexia

back pain if posterior penetrating

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25
Q

how can you tell apart gastric and duodenal ulcers on clinical history?

A

Gastric: worse on eating

Duodenal: eating will relieve pain.The pain will be worse at night and vomiting is uncommon

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26
Q

what are the risk factors for peptic ulcer formation?

A
  • H.pylori
  • NSAIDS
  • steroids
  • zollinger Ellison
  • smoking
  • alcohol
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27
Q

why is H.pylori a risk factor for ulcer formation?

A

Secretes urease causing ammonia production weakening the mucosal barrier

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28
Q

why are NSAIDS a risk factor for ulcer formation?

A

inhibits COX meaning less PGE2 and PGI2

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29
Q

what is a cushings ulcer?

A

Intracranial disease causing increase in vagal stimulation leading to ulceration from increased acid secretion

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30
Q

A curling ulcer?

A

A type of duodenal ulcer due to trauma to the body such as burns

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31
Q

what possible tests are there to diagnose H.pylori?

A
  • serological antibody test
  • C urea breath test
  • stool antigen test
  • biopsy urease test
  • CLO
  • histology staining
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32
Q

how does the serological test for H pylori diagnosis work?

A

Detects IgG antibodies. Useful in diagnosis but not eradication

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33
Q

what is the C- urea breath test for H.pylori?

A

Quick and reliable
Ingest C13 urea then measure carbon dioxide levels.

sensitivity affected if taken PPIs/ antibiotics

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34
Q

what is the stool antigen test for H.pylori?

A

monoclonal antibodies are used for qualititative detection of H.pylori antigen.
Useful for both diagnosis and eradication

Patients should be off PPI’s but can continue H2 antags

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35
Q

what is the invasive biopsy urease test for H.pylori?

A

antral biopsies are added to urease and phenol red. if there is H.pylori colour change from yellow to red

cant be on antibiotics or PPI’s

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36
Q

what cancer is h.pylori infection associated with?

A
  • gastric adenocarcinoma (distal)

- B cell MALT lymphoma

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37
Q

what is often included in an eradication regime for H pylori?

A

Two antibiotics with a PPI

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38
Q

what antibiotics can be used in a H.Pylori eradication regime?

A

Metronidazole
clarithromycin
amoxicillin
tetracycline

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39
Q

what is the medical management of a peptic ulcer?

A
  • if the patient is on an NSAID stop taking it

- give a PPI

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40
Q

at what bilirubin level is jaundice detectable?

A

3mg/Dl

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41
Q

why is there jaundice in pre-hepatic causes?

A

An excess amount of bilirubin is presented to the liver due to increased haemolysis

42
Q

what levels will be in the serum of someone with pre-hepatic jaundice?

A

Elevated unconjugated bilirubin

43
Q

why is there jaundic in hepatic causes?

A

Due to impaired uptake, faulty conjugation or abnormal secretion of bilirubin by the liver cell

44
Q

what levels will be high in someone with hepatic cause of jaundice?

A

Both conjugated and unconjugated

45
Q

what is a cause of pre-hepatic jaundice?

A

Haemolysis

46
Q

what are some causes of hepatic jaundice?

A 
Viral hepatitis
Cirrhosis
Drugs
Cholangitis
Pregnancy
Cholestasis
47
Q

why is there jaundice in post hepatic causes?

A

Impaired excretion of conjugated billirubin due to mechanical obstruction

48
Q

what levels are high in the serum of someone with jaundice due to a post hepatic cause?

A

Conjugated billirubin

49
Q

what are some causes of post hepatic jaundice?

A
  • common duct stones
  • carcinoma
  • biliary sstricture
  • sclerosing cholangitis
  • pancreatic pseudocyst
50
Q

how is the urine, stool and skin change in pre- hepatic jaundice?

A

Normal urine and stool

No pruritis

51
Q

how is the urine, stool and skin change in hepatic jaundice?

A

Dark urine, normal stool and no pruritis

52
Q

how is the urine, stool and skin change in post hepatic jaundice?

A

Dark urine, acholic pale poop, pruritis

53
Q

what oher clinical signs can be seen in haemolyic (pre hepatic jaundice)?

A
  • anaemia
  • jaundice
  • splenomegaly
  • leg ulcers
54
Q

why is there high levels of unconjugated billirubin in gilberts syndrome?

A

A mutation means reduced levels of UDP glucuronosyl transferase activity. This normally conjugates billirubin

55
Q

what investigations would you do in someone with jaundice?

A
  • viral markers
  • USS
  • liver biochemistry
56
Q

when is AST raised?

A

acute phase of cellular necrosis

57
Q

what is disadvantage of suing AST for liver damage?

A

Non organ specific

58
Q

what is a raised ALP associated with?

A

biliary obstruction with cholestasis

59
Q

what liver function tests are associated with a cholestatic pattern?

A

billirubin, ALP, GGT

60
Q

what LFT’s are associated with an inflammatory pattern?

A

ALT

61
Q

what is the main route of transmission of Hep A?

A

Faecal Oral route

62
Q

what is the main route of transmission of Hep B?

A

Blood products
Sexual intercourse
Vertical transmission

63
Q

what is the main transmission of Hep C?

A

Blood products

Saliva

64
Q

what is the main route of transmission of hep D?

A

Blood products mainly

65
Q

what is the main route of transmission of hep E?

A

faeco-oral

Large water borne outbreaks

66
Q

what are complications of chronic hepatitis B or C infection?

A
  • hepatocellular caricnoma
  • liver cirrhosis
  • liver fibrosis
67
Q

what are indications for Hep B vaccination?

A
  • healthcare personnel
  • haemophilia patients
  • CKD
  • dialysis
  • long term travellers
  • MSM
  • bisexual men
  • more than 1 sexual partner
  • sex worker
  • IVDU
  • diabetics
68
Q

Why does the increased NADH in alcohol liver disease lead to increased damage?

A

Due to lactate and malate build up

69
Q

why does increased NADH in alcohol liver disease lead to an increase in lactate?

A

To use up the NADH pyruvate is converted to lactate.

70
Q

why does increased NADH in alcohol liver disease lead to an increase in malate?

A

Using up the NADH by converting oxacoacetate to malate

71
Q

why are patients with alcoholic liver disease at risk of hypoglycaemia?

A

They use up pyruvate and oxaloacetate to get rid of the NADH. This means less gluconeogenesis can take place

72
Q

why can alcooholic liver disease lead to fatty liver?

A
  • more ehtnaol means more acetate which is broken down to form malonyl CoA Which is a TG precursor

removal of NADH using DHAP leading to glycerol 3 phosphate formation

73
Q

what two TG precursors are produced in alcoholic liver disease?

A

malonyl COA

Glycerol 3 phosphate

74
Q

Why is thiamine deficiency an issue?

A

There are thiamine dependant enzymes;

  1. transketolase
  2. pyruvate dehydrogenase
  3. alpha ketogluterate
75
Q

In wernickes there is thiamine deficiency meaning pyruvate dehydrogenase can’t work what does this cause?

A

A build up of lactate

76
Q

what is the triad seen in wernickes?

A

Ataxia
Opthalmoplegia
Nystagmus

77
Q

As well as thiamine deficiency what other defieincy is often seen in alcoholics?

A

vit B3

78
Q

alcoholics can get vit B3 deficienncy how does this present?

A

Pallega
Redness and swelling of the mouth, tongue.
Skin rash
diarrhoea

79
Q

what are the stages of alcoholic liver disease?

A

Fatty iver
Alcoholic hepatitis
Alcoholic cirrhosis

80
Q

what is the pathology in alcoholic hepatitis?

A

Fatty change
infiltration of leucocytes and hepatocellular necrosis in zone 3
Mallory bodies
Giant mitochondria

81
Q

In alcoholic hepatitis mallory bodies are visible what are these?

A

dense cytoplasmic inclusions suggesting damage

82
Q

what are the clinical manifestations of fatty liver?

A

Often no symptoms

Can have nausea and vomiting

83
Q

what drugs can cause acute hepatitis?

A 
Alcohol
Rifampicin
Isoniziad
Methyldopa
Atenolol
84
Q

what drugs can cause chronic hepatitis??

A
  • methyldopa
  • nitrofurantoin
  • isoniazid
  • fenofibrate
85
Q

How does paracetomal cause acute hepatotoxicity?

A

Normally paracetomal is metabolised by glucoronidation and sulfation. Also a little by N hydroxylation forming toxic NAPQI. this is the conjugatied with glutathione to be non toxic

In OD gltathione is saturated and toxic NAPQI builds up

86
Q

what does the west haven criteria assess?

A

Impaired mental status mainly for HE

87
Q

What is your west haven criteria score based on?

A

impairment in consciousness
intellectual function
behaviour

88
Q

what is grade 1 in the west haven criteria?

A
  • trivial lack of awareness
    shortened attention span
    impaired addition
89
Q

what is grade 2 on the west haven criteria?

A

ethargy
minimal disorientation in place/time
personality change
inappropriate behaviour

90
Q

what is grade 3 in the west haven criteria?

A
  • semi stupir but can respond to verbal stimuli
    confusion
    gross disorientation
91
Q

what are the three main factors underlying the pathogenesis of ascites?

A

Low serum albumin
Portal nHypertension
Sodium and water retention

92
Q

what are causes of straw coloured ascitic fluid?

A 
malignancy
cirrhosis
TB
hepatic vein obstruction
chronic pancreatitis
constrictive pericarditis
nephrotic syndrome
93
Q

what are causes of chylous coloured ascitic fluid?

A

obstruction of the main lymphatic duct

cirrhosis

94
Q

what are causes of haemmorhagic ascites?

A

malignancy
ruptured ectopic pregnancy
abdo trauma
acute pancreatitis

95
Q

where in the bowel does crohns affect?

A

Any part from the mouth to anus

96
Q

where in the bowel does uc AFFECT?

A

Starts at the rectum and works up

97
Q

in what pattern does crohns affect tissue?

A

Patchy and discontinious

98
Q

In what pattern does uc affect tissue?

A

Continious

99
Q

What layers does inflammation in crohns affect?

A

transmural

100
Q

What layer of tissue is affected in UC?

A

just mucosal

101
Q

what is the management of UC?

A
  • Proctitis and proctosigmoiditis you give an aminosalicylate
  • corticosteroids
  • prednisolone
102
Q

what is the management of crohns?

A
  • monotherapy with prednisolone or hydrocortisone
  • can add azathioprine/ mercaptopurine
  • consider methotrexate

T year LOBs medicine (11 decks)

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