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GI Flashcards

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USMLE® Step 1 flashcards
1
Q

risk factors for oral malignancy

A

Tobacco, alcohol, HPV, cannabis

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2
Q

High risk sites for oral malignancy

A

ventral and lateral tongue

floor of mouth

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3
Q

signs/symptoms of oral malignancy

A 
Erythroplakia
Leukoplakia 
Erythroleukoplakia
ulcer
number feeling
change in voice
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4
Q

GORD (reflux) and causes

A

Inflammation of oesophagus due to refluxed low pH gastric content and squamous epithieum

  1. defective sphincter mechanism +/-hiatus hernia
  2. Abnormal oesophageal motility
  3. Increased intra-abdominal pressure
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5
Q

Management of GORD

A 
Lifestyle modifications
Antacids - symptomatic relief
H2 antagonists e.g. ranitidine 
PPI: Omeprazole and lansoprazole - superior  
surgery: nissen fundoplication
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6
Q

Barrett’s oesophagus

A

Replacement of stratified squamous epithelium by columnar epithelium in the oesophagus

typical improvement in reflux symptoms

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7
Q

investigations and management barrets

A

endoscope and biopsy (Columnar lined mucosa with intestinal metaplasia)

  • Optimise PPI
  • endoscopic mucosal resection
  • radiofrequency ablation
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8
Q

Allergic oesophagitis

A

Personal/family history of allergy and Asthma

  • Increased eosinophils
  • negative ph for reflux
  • endoscope - corrugated
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9
Q

allergic oesophagus management

A

steroids/ chromoglycate/ montelukast

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10
Q

Squamous cell carcinoma of oesophagus

A

Malignant Oesophageal tumours in upper 1/3rd of oesophagus

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11
Q

Squamous cell carcinoma of oesophagus Mx

A

Endoscopic Mucosal resection: Option instead of an oesophagectomy if oesophageal cancer is diagnosed very early on. It involves cutting out the tumour using a loop of wire at the end of a thin flexible tube.

radiofrequency ablation (RFA): radiowaves

Radiotherapy – quite successful – before

Surgery: If T1-T2 localised disease: radical curative transthoracic esophagectomy

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12
Q

Adenocarcinoma of oesophagus

A

lower 1/3rd oesophagus

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13
Q

Achalasia

A

Coordinated peristalsis and lower oesophageal sphincter fails to relax (degeneration of the myenteric plexus)

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14
Q

Achalasia management

A

Endoscopic balloon dilation or Hellers cardiomyopathy then PPIs

Botulinum toxin

Calcium channel blockers and nitrates to help relax the sphincter

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15
Q

Peptic ulceration

A

breach in the gastrointestinal mucosa as a result of acid and pepsin attack. edges are clear cut and punched

can be gastric or duodenal

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16
Q

peptic ulceration: pathology of protective layer destruction

A 
Medications: steriods or NSAIDs
Helicobacter pylori (exposes gastric mucosa to acid and ammonia to which directly damages cells)
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17
Q

peptic ulceration signs/symptoms

A

epigastric discomfort, bleeding, nausea and vomiting

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18
Q

Eating improves the pain of

A

duodenal ulcers

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19
Q

eating worsens pain of

A

gastric ulcers

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20
Q

rapid urease test for?

A

H. Pylori

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21
Q

eradication of H. Pylori therapy

A

Antacids (Gaviscon)

PPI + amoxcillin 1g bd + clarithromycin 500mg bd

PPI + metronidazole 400mg bd + clarithromycin 250mg bd

Endoscope:

DU: uncomplicated DU requires no f/u and only if ongoing symptoms

GU: f/u endoscopy at 6-8 weeks and ensure healing and no malignancy

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22
Q

Gastric adenocarcinoma location and pathology

A

In UK proximal tumours of cardia/GOJ increasing and distal and gastric body tumours decreasing

H.pylori infection  chronic gastritis  intestinal metaplasia/atrophy  dysplasia  carcinoma

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23
Q

gastric adenocarcinoma types

A

intestinal (better prognosis and diffuse (infiltrates stomach wall) e.g. signet cell cancer

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24
Q

virchow’s node?

A

gastric adenocarcinoma

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25
Q

gastric adenocarcinoma management

A

Early gastric cancer: endoscopic mucosal resection

Partial gastrectomy – advanced distal tumours

Total gastrectomy – proximal tumours

Combination chemotherapy: epirubicin, cisplatin & fluorouracil) to increase survival in advanced disease

Neo-adjuvant chemotherapy before surgery – improve survival

Surgical palliation: obstruction, pain or haemorrhage

Trastuzumab for HER-2 positive cancers

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26
Q

Gastric lymphoma

A

Derived from mucosa associated lymphoid tissue (MALT): B, T cells, Plasma cells and macrophages

associated with H. Pylori. Continuous inflammation induces an evolution into a clonal B-cell proliferation: low grade lymphoma. If unchecked evolves into a high grade B-cell lymphoma

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27
Q

Gastric lymphoma management

A

May regress with H. Pylori eradication (triple therapy)

Rituximab

Chemotherapy and radiotherapy

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28
Q

GIST tumour and management

A

soft tissue sarcoma from interstitial cells of cajal

surgery and KI (Imatibib and sunitinib)

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29
Q

Gastroparesis

A

delayed gastric emptying

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30
Q

Gastroparesis management

A

Removal of precipitating factors e.g. drugs

Liquid / sloppy diet

Eat little and often

Promotility agents

Gastric pacemaker

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31
Q

Acute mesenteric ischaemia

A

Involves the small bowel and may follow the superior mesenteric artery thrombosis, thromboembolism from heart (e.g. A.Fib) and mesenteric vein thrombosis

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32
Q

Pathology of acute mesenteric ischaemia

A

Mucosal infarct (regeneration/resolution: mucosal integrity restored)

Mural Infarct (Repair and regeneration: fibrous stricture, chronic ischaemia, ‘mesenteric angina’ and obstruction)

Transmural infarct (Gangrene: perforation, peritonitis, sepsis and death if not resected)

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33
Q

acute mesenteric ischaemia signs/symptoms

A

severe abdominal pain
constant, central and around RIF
Clinical signs are out of proportion to pain/degree of illness

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34
Q

acute mesenteric diagnosis

A

Arterial blood gases: Persistent metabolic acidosis (high lactate)

Abdominal X-ray: gasless abdomen

CT/MRI: evidence of ischaemia with CT/MRI angiography or formal arteriography if doubt remains

Laparotomy: nasty, necrotic bowel at laparotomy

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35
Q

acute mesenteric management

A

Resuscitation with fluid, antibiotics (piperacillin/tazobactam) and LMWH/heparin

Thrombolysis with angiography

Surgery: resect, renastomose and planned return if fitter

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36
Q

Meckel’s diverticulum

A

Outpouching or bulge in the lower part of the small intestine.

The bulge is congenital (present at birth) and is a result of incomplete regression of vitello-intestinal duct (leftover of the umbilical cord)

Tubular structure, 2 inches long, 2 foot above IC valve in 2% of people

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37
Q

Meckel’s diverticulum management

A

surgery

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38
Q

Appendicitis signs/symptoms

A

central abdominal pain, moves to RIF and becomes localised there

Tender in McBurneys point (1/3 distance from ASIS to umbilicus)

N&V

Rovsings sign (palpate in LIF, pain in RIF)

Rebound tenderness

WCC, pyrexia, tachycardia

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39
Q

appendicitis investigations

A

Ultrasound and CT scan

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40
Q

appendicitis management

A

analgesia, antibiotics, appendicectomy

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41
Q

appendix mass?

A

An appendix mass occurs when the omentum surrounds and sticks to the inflamed appendix, forming a mass in the right iliac fossa.

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42
Q

appendix management

A

supportive therapy: antibiotics

surgery when acute situation has resolved

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43
Q

mesenteric adenitis

A

inflamed abdominal lymph nodes.

presents with abdominal pain, usually in younger children. This is often associated with tonsillitis or an upper respiratory tract infection.

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44
Q

neoplasms of appendix

A

adenocarcinoma of the caecum

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45
Q

Lymphomas of small bowel and management

A

Non-Hodgkin’s lymphoma

Enteropathy associated T-cell lymphomas

Maltomas (B-cell) derived

chemotherapy, surgical resection and autologous stem cell transplant

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46
Q

Carcinoid tumours of small bowel

A

Diverse group of tumours of enterochromaffin cell (neural crest) origin capable of producing 5HT (serotonin). Commonest site is the appendix

can cause appendicitis, inteussusception, obstruction, paraneoplastic syndrome

mets to liver: carcinoid syndrome: flushing, diarrhoea and RUQ

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47
Q

Carcinoma of small bowel

A

associated with crohns and coeliac disease

adenocarcinoma: starts in cells of the bowel (epithelial cells): duodenum

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48
Q

risk factors for colorectal carcinoma (genetic)

A

familial adenomatous polyposis: a rare condition where an inherited faulty gene makes many polyps develop on the bowel lining

Lynch syndrome (Hereditary non-polyposis colorectal cancer or HNPCC): a gene fault that increases the risk of several different types of cancer at a younger age

Peutz Jeghers syndrome: an inherited condition where benign (non cancerous) polyps form in the bowel.

Crohn’s
Coeliac disease

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49
Q

signs/symptoms of carcinoma of small bowel

A 
•	pain or lump in your tummy (abdomen)
•	weight loss
•	feeling and being sick
•	diarrhoea
•	tiredness
•	dark black poo, due to bleeding in the small bowel
•	blockage in the bowel
anaemia
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50
Q

management of small bowel cancer?

A

surgery with adjuvant chemo if not spread and fit enough

e.g. top of duodenum: pancreaticoduodenectomy

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51
Q

Whipples disease

A

GI malabsorption that affects middle age white males. Caused by Tropheryma whipplei

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52
Q

Whipples disease management

A

• IV ceftriaxone (or penicillin + streptomycin) for 2 weeks then oral co-trimoxazole for 1 year

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53
Q

Coeliac disease - foods

A

wheat, barley and rye

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54
Q

coeliac disease signs/symptoms

A

o Failure to thrive in young children
o Diarrhoea, excess flatus and discomfort
o Fatigue
o Weight loss
o Mouth ulcers
o Anaemia secondary to iron, B12 or folate deficiency
o Dermatitis herpetiformis (an itchy blistering skin rash typically on the abdomen)
o Vitamin deficiencies
malabsorption: steatorrhea
gallstones

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55
Q

coeliac diagnosis

A

check IgA levels for IgA deficiency

anti-TTG or anti-EMA antibodies

duodenal biopsy

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56
Q

Types of intestinal failure

A

Type 1 - short term - post op, obstruction, chemo/radiotherapy

Type 2 - septic patients, abdominal fistulae, post surgery awaiting reconstruction

type 3 - chronic intestinal failure

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57
Q

short bowel syndrome

A

<200cm

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58
Q

Common viral gastroenteritis

A

rotavirus, norovirus and adenovirus

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59
Q

E.COLI 0157 spread

A

It is spread through contact with infected faeces, unwashed salads, beef (raw milk/water) but wide range

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60
Q

signs/symptoms of e.coli 0157

A

• This causes abdominal cramps, bloody diarrhoea and vomiting

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61
Q

what to not give in e.coli 0157

A

use of antibiotics increases the risk of haemolytic uraemic syndrome therefore antibiotics should be avoided if E. coli gastroenteritis is considered.
• No anti-motility drugs or NSAIDs

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62
Q

e.coli 0157 cause and symptoms/signs of it

A

HUS

abdomen pain, fever, pallor, petechiae, oliguria

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63
Q

e.coli 0157 diagnosis

A 
•	High white cells
•	Low platelets
•	Low HB
•	Red cell fragments
•	LDH>1.5 x normal
•	Stool culture
•	PCR enzyme immunoassay  
incubation 1-14
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64
Q

Most common cause of travellers diarrhoea

A

Campylobacter jejuni

  • raw or improperly cooked poultry
  • untreated water
  • unpasteurised milk

Incubation 2-5 days

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65
Q

campylobacter symptoms

A
  • Abdominal cramps/pain
  • headache
  • Diarrhoea often with blood
  • Vomiting
  • Fever
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66
Q

Shigella spread? Incubation?

A

spread by faeces contaminating drinking water, swimming pools and food.

1-2 days

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67
Q

shigella signs/symptoms

A

bloody diarrhoea, abdominal cramps, fever, tenesmus

can cause HUS

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68
Q

salmonella spread and incubation

A

raw eggs, poultry and food contaminated with infected faeces of small animals

12 hours to 3 days

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69
Q

salmonella signs/symptoms

A
  • Watery diarrhoea that can be associated with mucus or blood
  • Abdominal pain
  • Vomiting
  • Fever (12-36 hours of exposure)
  • Headache
  • Invasive infection: bacteraemia, sepsis, meningitis, osteomyelitis & septic arthritis
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70
Q

Fried rice and abdominal cramping and profuse vomiting within 5 hours of ingestion

A

bacillus cereus

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71
Q

bacillus cereus

A

water diarrhoea

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72
Q

Yersinia Enterocolitica

A

gram negative bacillus

raw or undercooked pork can cause infection.

spread through contamination with the urine or faeces of other mammal such as rat and rabbits.
incubation 4-7 days

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73
Q

YE

A

affects chihldren - watery/bloody diarrhoea

older children - mesenteric lymphadenitis

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74
Q

Unpasteurised milk products & deli counter e.g. cheese products (9-48 hours)

A

listeria monocytogenes

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75
Q

listeria - high risk groups

A

immunosuppression and pregnancy

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76
Q

listeria management

A

Ampicillin plus gentamicin for systemic disease

Co-trimoxazole (CNS disease)

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77
Q

C diff toxins and colonoscope findings

A

Toxin A and B

Severe = patchy pseudomembranous colitis

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78
Q

C diff management

A

Non-severe: Oral Metronidazole 400mg (10 days)

Severe: Oral/NG Vancomycin 125mg qds ± IV metronidazole (10 days)

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79
Q

Amoebiasis, what is it? route? complication?

A
  • Entamoeba histolytica: a protozoa
  • Faecal-oral spread, strong association with poor sanitation
  • Amoebic liver abscess: Incubation period 8-20 weeks & More common in men
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80
Q

Amoebic management

A

Metronidazole/tinidazole for amoebic dysentery and invasive disease

Diloxamode furoate: luminal agent to destroy gut cysts (10 days)

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81
Q

Giardiasis

A

microscopic flagellated protozoa

Invades duodenum and proximal jejunum

These mammals may be pets, farmyard animals or humans. It releases cysts in the stools of infected mammals. These cysts then contaminate food or water and are eaten to infect a new host. This is called faecal-oral transmission.
• Incubation usually around 7 days

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82
Q

Giardiasis management

A

metronidazole or Tinidazole (7days)

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83
Q

Diverticula

A

Mucosal herniation through muscle coat (pouches in bowel wall: 0.5-1cm)

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84
Q

Diverticulosis

A

small, bulging pouches (diverticula) develop in your digestive tract without symptoms.

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85
Q

diverticulitis

A

• When one or more of these pouches become inflamed or infected,

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86
Q

diverticulitis investigations

A

barium enema, sigmoid/colonoscopy, CT scan

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87
Q

diverticulitis management

A

uncomplication: high fibre diet and weight loss
diverticulitis: admit, antibiotics, analgesia and fluid resus

complex diverticulitis: surgical resection, percutaneous drainage and hartmann’s drainage

88
Q

ischaemic colitis causes

A

arterial: AF
venous: dvt

89
Q

Collagenous colitis

A

thickened basement

chronic watery, non-bloody diarrhoea or loose stool, often between 3 and 20 times daily

90
Q

Lymphocytic colitis

A

No chronic architectural changes in crypts

Intraepithelial lymphocytes are raised

No thickening of BM

91
Q

microscopic colitis

A

both lymphocytic colitis and collagenous colitis.

92
Q

Upper small bowel obstruction

A

acute (Hours): large volumes of gastric, pancreatic and bilary secretions

93
Q

distal small bowel obstruction

A

colicky abdominal pain and vomiting faecal origin

94
Q

ileo-caecal valve remains competent ?

A

caecum progressively distends with swallowed air and eventually may rupture: ‘closed loop obstruction’

95
Q

ileo-caecal valve remains incompetent ?

A

small bowel distends, delaying the onset of symptoms.

96
Q

Volvulus types

A

sigmoid: twists on mesentery (anti-clockwise)
caecal: counter clocker

97
Q

volvulus investigations

A

axr and ct scan

98
Q

volvulus management

A

endoscopic decompression

Laparotomy (Hartmann’s for sigmoid) and (right hemicolectomy for caecal)

99
Q

IBS management (1st line ….

A

loperamide for IBS-D
Laxatives for IBS-C
Anti-spasmodic for IBS-Cramps - buscopan

100
Q

Crohn’s disease

A

Chronic inflammatory and ulcerating condition of the GI tract with exacerbations and remissions that can affect anywhere from the mouth to the anus (segmental disease)

101
Q

crohn’s diagnosis

A

Bloods: anaemia, B12 & ferritin, infection (WCC, CRP, ESR), TFTs, U&E and LFTs
Faecal calprotectin
Ultrasound, CT and MRI
Endoscope and biopsy

102
Q

Crohn’s inducing remission

A

1st line: steroids

add in immunosuppressant (Azathioprine, methotrexate)

Anti-TNF therapy: infliximab and adalimumab

103
Q

Crohns - maintaining remission

A

First line: Azathioprine or Mercaptopurine

Alternatives: Methotrexate

Anti-TNF: Infliximab or Adalimumab

104
Q

Crohn’s surgery

A

Emergency: Failure to respond to medical therapy, small bowel obstruction, abscess, fistulae

Elective: Failure to respond to medical therapy and dysplasia of colon mucosa

105
Q

Ulcerative colitis

A

Chronic inflammatory disorder confined to colon and rectum with unknown aetiology

Continuous and confluent extending proximally from rectum for varying lengths

106
Q

UC: Truelove and Witt criteria

A

> 6 bloody stools/24 hour + 1 or more of

Fever (>37.8°C)

Tachycardia (>90/min)

Anaemia (Haemoglobin <10.5g/dl)

Elevated ESR (>30mm/hr) – now look at CRP and albumin (low – not responding to treatment)

107
Q

UC inducing remission

A

IV fluids and GI rest

Mild to moderate

  • aminosalicylate (5-ASAs): mesalazine (double in acute relapse)
  • steroids

severe
-IV corticosteroids
2nd line: IV ciclosporin
Anti-TNF therapy

108
Q

maintaining remission in UC

A

Aminosalicyate e.g. mesalazine
Azathioprine and meractopurine
- methotrexate (alternative)

Anti-TNF: Infliximab or Adalimunmab

109
Q

surgery UC

A

Pan proctocolectomy

- permanent ileostomy or ileo-anal anastomosis (J pouch)

110
Q

Emergency surgery UC

A

subtotal colectomy

111
Q

Toxic megacolon

A

acute or acute on chronic fulminant colitis

Transverse >5.5cm and Caecum >9cm

112
Q

colorectal carcinoma

A

adenocarcinoma: rectum and sigmoid

113
Q

Genetic predisposition for colorectal carcinoma

A

Heriditary Non Polyposis Coli (HNPCC): <100 polyps: right sided

Familial adenomatous polyposis (FAP): > 100 polyps: throughout colon

114
Q

Colorectal carcinoma investigations

A

Bloods: FBC (microcytic anaemia), LFT

Faecal occult blood: blood in faeces
Colonoscopy/sigmoidoscopy
CT scan and CT colonography

CT Chest for staging and MRI for rectal cancers and liver mets

115
Q

Colorectal bowel screening

A

Scotland (50-72) and England (60-72): every 2 years: stool sample, if positive, offered colonoscopy

116
Q

Causes of upper GI bleed

A
  1. Oesophageal varices
  2. Mallory Weiss tear
  3. Gastric/duodenal ulcer
  4. Cancers of stomach or duodenum
117
Q

Rockall and Glasgow-Blatchford Score

A

Rockall - rebleed after endo

Glasgow: scoring system for suspected upper GI bleed (remember drop in Hb, rise in urea)

118
Q

General management of haematemesis

A

A - ABCDE
B- Bloods (FBC, coag, U&E, LFTs, group, save and crossmatch
T - transfuse (fresh frozen plasma, platelets, prothrombin complex concentrate)
E - Endoscopy
D - Drugs
E- endoscopy

119
Q

Endoscopic treatment of peptic ulcers

A
  1. Injection: adrenaline causes tamponade affect, causes vasoconstriction and tip into clot formation
  2. Heater probe coagulation: electric current passed through it and clot it
  3. Combinations: need to do duel therapy for highest rate of haemostasis e.g. adrenaline and heater probe
  4. Clips
  5. Haemospray
  6. Acid suppression
120
Q

Endoscopic treatment of stable varices

A

Propranolol reduces portal hypertension by acting as a non-selective beta blocker

Elastic band ligation of varices

Injection of sclerosant (less effective than band ligation)

TIPS

121
Q

Endoscopic treatment of bleeding oesophageal varices

A
  1. Terlipressin (vasopressin analogue)
  2. Endoscopic variceal ligation (banding)
  3. Sclerotherapy
  4. Sengstaken-Blakemore balloon
  5. TIPS
  6. Propranolol infusion
122
Q

indirect inguinal hernia

A

frequent in males
through the deep and superficial ring
lateral to the epigastric. Above and medial to the pubic tubercle

123
Q

direct inguinal hernia

A

weakness in the abdominal wall around Hasselbach’s triangle. protrudes directly through abdominal wall

124
Q

femoral hernia

A

lateral and below pubic tubercle

125
Q

epigastric hernia

A

fascia defect in the linea alba between the xiphoid process and the umbilicus

126
Q

paraumbilical hernia

A

factors include stretching of the abdominal wall by obesity, multiple pregnancy and ascites

127
Q

umbilical hernia

A

results from persistent elevation of intraabdominal pressure. Part of the intestine or fatty tissue bulges through the muscle near the belly button (navel, umbilicus).

128
Q

Incisional hernias

A

Iatrogenic: bigger the incision – the bigger the risk

Commonest complication of a laparotomy (exploration of the abdomen)

Due to inadequate closure of the muscle and tissues after the incision

129
Q

Spigelian hernia

A

hernia through the Spigelian fascia, which is the aponeurotic layer between the rectus abdominis muscle medially, and the semilunar line laterally.

130
Q

Haemorrhoids

A

venous “vascular cushions” that have become enlarged due to increased pressure (e.g. secondary to straining in constipation)
o 1st degree: no prolapse
o 2nd degree: prolapse when straining and return on relaxing
o 3rd degree: prolapse when straining, do not return on relaxing but can be pushed back
o 4th degree: prolapsed permanently

131
Q

Haemorrhoids management

A 
anusol cream and LA
Sclerosation therapy
rubber band ligation 
Open haemorrhoidetcomy 
stapled haemorrhoidectomy 
HALO/THD procedure
132
Q

Anal fissure

A

Tear in the anal margin due to passage of a constipated stool.

Glass passing through back passage

133
Q

Anal fissure management

A

dietary advice and stool softeners

Pharmacological sphincterotomy: GTN - Dilate vessels helps to heal quicker

Lateral Sphincterotomy: cut the lower part of the internal sphincter muscle. This will relieve the spasm in the sphincter, allowing a better blood supply to heal the fissure.

Botox injection

134
Q

Alcoholic Liver Disease Pathology

A

2-3 days: Fatty liver: Reversible in around 2 weeks

4-6 weeks: Hepatitis: Reversible with permanent abstinence

Mths-yrs: Fibrosis: Irreversible

Years: Cirrhosis: Irreversible

Healthy - steatosis - hepatitis

135
Q

ALD Signs/symptoms

A
  • Jaundice
  • Hepatomegaly
  • Spider Naevi
  • Palmar Erythema
  • Gynaecomastia
  • Bruising – due to abnormal clotting
  • Ascites
  • Caput Medusae – engorged superficial epigastric veins
  • Asterixis – “flapping tremor” in decompensated liver disease
136
Q

ALD investigations

A 
AUDIT questionnaire 
Bloods: FBC (raised MCV), LFTS (ALT/AST, GT, bilirubin), U&E (hepatorenal syndrome), clotting (PR prolonged), low albumin 
Ultrasound 
Fibroscan
Endoscopy: oesophageal varices 
CT/MRI
137
Q

ALD management

A

14 units, detox, B1 (THiamine), steriods (short term), complication of cirrhosis

138
Q

AL withdrawal

A

o 6-12 hours: tremor, sweating, headache, craving and anxiety
o 12-24 hours: hallucinations
o 24-48 hours: seizures
o 24-72 hours: “delirium tremens”

139
Q

Delirium tremens

A

Chronic alcohol user results in the GABA system becoming up-regulated and the glutamate system being down-regulated to balance the effects of alcohol.

When alcohol is removed from the system, GABA under-functions and glutamate over-functions causing an extreme excitability of the brain with excess adrenergic activity.

140
Q

DT signs/symptoms

A

Acute confusion, severe agitation, Delusions and hallucinations, Tremor, Tachycardia

Hypertension, Hyperthermia, Ataxia (difficulties with coordinated movements) & Arrhythmias

141
Q

Management of Alcohol withdrawal

A

Chlordiazepoxide and IV B1

142
Q

Wernicke’s encephalopathy signs/symptoms

A

confusion
oculomotor disturbances
ataxia

143
Q

Korsakoffs syndrome

A

memory impairment (retro and anterogreade)

144
Q

NAFLD

A

• Non-alcoholic fatty liver disease (NAFLD) forms part of the “metabolic syndrome” group of chronic health conditions (diabetes, obesity, hyperlipidaemia) relating to processing and storing energy that increase risk of heart disease, stroke and diabetes.

145
Q

signs/symptoms of liver cirrhosis

A

Jaundice – caused by raised bilirubin
Hepatomegaly
Splenomegaly – due to portal hypertension
Spider Naevi – these are telangiectasia with a central arteriole and small vessels radiating away
Palmar Erythema – caused by hyperdynamic circulation
Gynaecomastia and testicular atrophy in males due to endocrine dysfunction
Bruising – due to abnormal clotting
Ascites
clubbing
Caput Medusae – distended paraumbilical veins due to portal hypertension
Asterixis – “flapping tremor” in decompensated liver disease

146
Q

Ascites

A

fluid in the peritoneal cavity. The increased pressure in the portal system causes fluid to leak out of the capillaries in the liver and bowel and into the peritoneal cavity.

147
Q

Ascites management

A

improve underlying liver disease, low Na diet and no NSAIDs

Prophylactic antibiotics against SBP e.g. ciprofloxacin

Spironolactone

Paracentsis or drain

TIPS or transplant in refractory

148
Q

SBP organisms

A

E. Coli, klebsiella and staph/enterococcus

149
Q

SBP diagnosis

A

culture and neutrophils over 250

150
Q

SBP management

A

IV cephalosporin such as cefotaxime

• Vascular instability: Terlipressin

151
Q

Hepatic encephalopathy

A

o The functional impairment of the liver cells prevents them metabolising the ammonia into harmless waste products.

Collateral vessels between the portal and systemic circulation mean that the ammonia bypasses liver altogether and enters the systemic system directly.

152
Q

HE management

A

laxatives e.g. lactulose: excretion of ammonia

antibiotics e.g. rifaximin

153
Q

Hep A

A

RNA virus, faecal oral route

cholestasis (slowing of bile flow through the biliary system) with dark urine and pale stools

154
Q

Hep B

A

DNA virus, direct contact with blood/bodily fluids, sex, sharing needles and vertical transmission

155
Q

Hep B viral markers

A

Surface antigen (HBsAg) – active infection

E antigen (HBeAg) – marker of viral replication and implies high infectivity

Core antibodies (HBcAb) – implies past or current infection

Surface antibody (HBsAb) – implies vaccination or past or current infection

Hepatitis B virus DNA (HBV DNA) – this is a direct count of the viral load

156
Q

Acute Hep B management

A

• No antivirals given
• Monitor for encephalopathy and monitor for resolution
o of Hep B or Hep C, or Hep E if immunocompromised
• Notify Public Health
• Immunisation of contacts
• Test for other infections if at risk

157
Q

Chronic Hep B Mx

A

• OPTION 1 – more widely used
o Suppressive antiviral drug (5 licensed to date) e.g. entecavir, tenofovir
• OPTION 2 – you can identify the patients that may benefits from these
o Peginterferon alone

158
Q

Hep C

A

RNA virus, blood and body fluids

159
Q

Hep C antibody tests

A
  • Hepatitis C antibody is the screening test. If positive test for…
  • Hepatitis C RNA testing (PCR) is used to confirm the diagnosis of hepatitis C, calculate viral load and assess for the individual genotype
  • IgG positive (antibody), RNA negative = past infection (may still get re-infected if still injecting), will not get liver disease due to HCV unless they get re-infected
  • IgG positive (antibody), RNA positive = active infection (usually chronic)
160
Q

Hep C management (actual medical)

A

Antiviral treatment with direct acting antivirals (DAAs) is tailored to the specific viral genotype

They are typically taken for 8 to 12 weeks e.g., sofosbuvir, simeprevir, ledipasvir, voxilaprevir

Response defined by loss of HCV RNA in blood sustained to 6 months after end of therapy. Virological cure known as Sustained Virological Response or SVR

161
Q

Hep D

A

RNA virus but requires Hep B (attaches to HBsAg)

162
Q

Hep E

A

RNA virus, tropics, faecal oral route

163
Q

Autoimmune hepatitis types

A

Type 1 (adults: women in late 40s or early 50s). menopause - fatigue and features of liver disease on exam

Type 2: children or teenagers or early 20s: acute hepatitis with high alt/ast and jaundice

164
Q

Autoantibodies for AH

A

Type 1 Autoantibodies:
Anti-nuclear antibodies (ANA), Anti-smooth muscle antibodies (anti-actin) and Anti-soluble liver antigen (anti-SLA/LP)

Type 2 Autoantibodies:
Anti-liver kidney microsomes-1 (anti-LKM1), Anti-liver cytosol antigen type 1 (anti-LC1) and AMA

165
Q

autoimmune hep management

A

prednisolone (tapered), azathioprine (immunosuppressant) and liver transplant

166
Q

Primary Biliary Cirrhosis

A

condition where the immune system attacks the small bile ducts within the liver (unknown aetiology). INtralobular bile ducts back up, fibrosis and cirrhosis - liver failure

167
Q

PBC signs/symptoms

A

fatigue, itching without rash (bile acids), jaundice, pale stools and dark urine, xanthelasma

168
Q

PBC diagnosis

A

ALP raised, AMA, ANA

169
Q

PBC management

A

Ursodeoxycholic acid reduces the intestinal absorption of cholesterol

Colestyramine (or obeticholic acid) is a bile acid sequestrate in that it binds to bile acids to prevent absorption in the gut and can help with pruritus due to raised bile acids

Liver transplant

Immunosuppression (e.g. with steroids) is considered in some patients

Fat soluble vitamin deficiency may occur in PSC and PBC. Monitor levels and supplement if necessary.

170
Q

Primary Sclerosing Cholangitis

A

large and medium sized intrahepatic or extrahepatic ducts become strictured and fibrotic

171
Q

PSC diagnosis

A

ALP
p-ANCA, ANA, aCL
MRCP
Biopsy

172
Q

PSC management

A

• Liver transplant
• ERCP can be used to dilate and stent any strictures (use x-rays)
• Ursodeoxycholic acid is used and may slow disease progression
• Colestyramine (bile acid sequestrate): binds to bile acids to prevent absorption in the gut and can help with pruritus due to raised bile acids
• Monitoring for complications
Fat soluble vitamin deficiency may occur in PSC and PBC

173
Q

Haemochromatosis

A

excessive total body iron and deposition of iron in tissues (autosomal recessive gene: chromosome 6)

secondary: iron overload from diet, iron therapy and transfusions

174
Q

Haemochromatosis signs/symptoms

A
  • Type 1 Diabetes (iron affects the functioning of the pancreas)
  • Liver Cirrhosis
  • Iron deposits in the pituitary and gonads lead to endocrine and sexual problems (hypogonadism, impotence, amenorrhea, infertility)
  • Cardiomyopathy (iron deposits in the heart)
  • Hepatocellular Carcinoma
  • Hypothyroidism (iron deposits in the thyroid)
  • Chrondocalcinosis / pseudogout (calcium deposits in joints) causing arthritis
175
Q

Haemochromatosis management

A

venesection, monitor serum ferritin, avoid alcohol

176
Q

Wilson’s disease

A

excessive accumulation of copper in the body and tissues. AR and chromosome 13

177
Q

Wilsons disease investigations

A

Low serum caeruloplasmin
Liver biopsy for liver copper content
24-hour urine copper assay

178
Q

Wilsons management

A

copper chelation using: Penicillamine and Trientene

179
Q

Alpha-1-antitrypsin deficiency

A

autosomal recessive deficiency of a protease inhibitor called alpha 1 antitrypsin. excessive protease enzymes attacking liver and lung

180
Q

Budd chiari

A

Thrombosis of the hepatic veins

181
Q

Haemangioma

A

commonest, • Hypervascular tumour and usually single small well demarcated capsule. No treatment

182
Q

Focal Nodular Hyperplasia (FNH)

A

Benign nodule formation of normal liver tissue. Congenital vascular anomaly

183
Q

Hepatocellular adenoma

A

Benign neoplasm composed of normal hepatocytes: no portal tract, central veins or bile ducts. Maligant transformation higher in males

184
Q

management of hepatocellular adenoma

A 
stop hormones, wt loss
excise for males
Females: 
o	<5cm or reducing in size - annual MRI 
o	>5cm or increase in size - for surgical excision
185
Q

Hepatocellular carcinoma signs/symptoms

A

Weight loss and RUQ pain (most common) and mass
• Worsening of pre-existing chronic liver disease
• Acute liver failure and ascites
• Signs of cirrhosis
• Hard enlarged RUQ mass

186
Q

Hepatocellular management

A 
Liver transplantation (Best available treatment): Removes tumour and liver
  o Only if single tumour less than 5cm or less than 3 tumours less than 3cm each

Resection: Feasible for small tumours with preserved liver function (no jaundice or portal HTN): <3cm

Local ablation: For non resectable and patients with advanced liver cirrhosis

Chemoembolisation: TransArterial ChemoEmbolization - TACE

Systemic therapy: sorafenib

187
Q

Cholelithiasis

A

Gallstones form when there is an imbalance between the ratio of cholesterol to bile salts disrupting micelle formation

This can cause cholestasis: blockage to the flow of bile

188
Q

Cholelithiasis risk factors

A

fair, fat, female and forty

189
Q

Biliary colic

A

Stone impacts in cystic duct temporally. Intermittent right upper quadrant pain caused by gallstones irritating bile ducts (cystic duct obstruction)

190
Q

Biliary colic signs/symptoms

A

• Gradual build-up pain in RUQ and may last between 2-6 hours
• Radiates to back / shoulder
• Associated with indigestion / nausea – after we eat
`

191
Q

Biliary colic investigations

A

ALP, ultrasound, CT scan (if USS doesn’t show ductal stones), ERCP

192
Q

Biliary colic management

A
  • Analgesia and rehydrate
  • Low fat diet / lose weight if obese and observe 3-6 months
  • If recurrent episodes pain / colic consider / refer for laparoscopic cholecystectomy
  • Unfit – Ursodeoxycholic acid 10mg/kg/day
193
Q

Acute cholecystitis

A

Inflammation of the wall of the gallbladder. Majority caused by gallstones (calculous cholecystitis) that impacts at the neck of the gallbladder (cystic duct)

194
Q

acute cholecystitis signs/symptoms

A

• Murphy’s sign:
o RUQ tenderness exacerbated by deep inspiration
o Place hand in RUQ and apply pressure
o Ask patient to take deep breath in
o Gallbladder will move downwards under your hand and cause pain
• Continuous epigastric or RUQ pain (referred to right shoulder)
• Vomiting, nausea, fever and local peritonism

195
Q

Acute cholecystitis Mx

A
  • IV antibiotics and IV fluids: amoxicillin, gentamicin and metronidazole i.e. triple therapy
  • Nil by mouth
  • Urgent Laparoscopic cholecystectomy (Open surgery if there is GB perforation)
196
Q

Cholangitis

A

Bile duct infection (biliary obstruction)

RUQ pain, jaundice and rigors (Charcots triad). Swinging fever

197
Q

cholangitis Mx

A

antibiotics (triple therapy), sepsis protocol and ERCP

198
Q

Gallstone ileus

A

Fistula between gallbladder and duodenum causing large gallstone to pass into small intestine (stone erodes through GB into duodenum and obstructs ileum)

199
Q

Gallstone ileus management

A

urgent laparotomy and interval cholecystectomy (3 months)

200
Q

Carcinoma of gallbladder

A

Adenocarcinoma and associated with gallstones. PSC high risk factor

201
Q

Cholangiocarcinoma

A

Adenocarcinoma: slow growing and mostly distal extra hepatic or perihilar : bile duct cancer. UC and PSC

202
Q

Cholangiocarcinoma signs/symptoms

A

obstructive jaundice, weight loss, malaise

203
Q

cholangiocarcinoma investigations

A

ALP, Bilirubin, FBC
US
CT/MRI, ERCP/MRCP
Biopsy

204
Q

cholangiocarcinoma management

A
  • Surgical resection: Only chance of cure
  • Bile duct and liver resection (major hepatectomy + extrahepatic bile duct excision + caudate lobe resection
  • Palliation: Biliary stent – ERC/PTC insertion
205
Q

Acute pancreatitis causes

A

• Causes (I GET SMASHED)
Iatrogenic (post ERCP), Gallstones, Ethanol, Trauma, Steroids, Mumps, autoimmune, scorpion venom, hyperlipidaemia (+ hypotension and hypercalcemia), ERCP and drugs

Main common ones: Alcohol, gallstones and post ERCP

206
Q

acute pancreatitis signs/symptoms

A
  • Sudden onset severe abdominal pain
  • Cause epigastric pain radiating to the back
  • Patients may be severely shocked
  • Vomiting prominent
  • Tachycardia, fever, jaundice, shock, ileus, rigid abdomen, tenderness
  • Periumbilical bruising (Cullen’s sign) and flank bruising (grey turners sign): blood vessel autodigestion and retroperitoneal haemorrhage
207
Q

acute pancreatitis Iv

A 
Bloods: lipase, amylase and CRP
AXR
ABG
Erect CXR
CT: Complications
US: Gallstones
208
Q

acute pancreatitis management

A
  • Nil by mouth (consider NJ feeding to decrease pancreatic enzyme stimulation)
  • IV fluids (crystalloid) and Careful monitoring
  • Escalate care according to Glasgow score
  • Urinary catheter and consider CVP monitoring
  • Analgesia: Pethidine or morphine (might cause sphincter of oddi to contract)
  • Endoscopic drainage of large pseudocysts
  • ERCP: gallstone and progressive jaundice
  • Antibiotics only if evidence of infected pancreatic necrosis Surgery to remove infected pancreatic necrosis
209
Q

Acute pancreatitis complications

A
  • Pancreatitic necrosis and Pseudocysts (fluid in lesser sac): fever, a mass ± persistent increase in amylase/LFT: resolve or need drainage
  • Abscess: drainage
  • Bleeding: elastase eroding major vessel (splenic artery): embolization
  • Thrombosis: colic branches of SMA or gastroduodenal/splenic arteries
  • Fistulae
  • Infection in necrotic areas
  • Chronic pancreatitis
210
Q

Chronic pancreatitis

A

• Relapsing disorder may develop insidiously or following bouts of acute pancreatitis

Progressive and irreversible damage (loss of exocrine and endocrine function)

211
Q

Chronic pancreatitis Iv

A
  • Amylase may not rise in and acute exacerbation of chronic pancreatitis because the pancreas has lost it’s ability to produce the enzyme
  • Ultrasound ± CT: pancreatic calcifications
  • MRCP
  • AXR: Speckled calcification
  • Faecal elastase
212
Q

chronic pancreatitis management

A

analgesia
creon: enzyme replacement and fat soluble vitamins
insulin

213
Q

pancreatic cancer

A

90% are adenocarcinomas of the head of the pancreas (ductal).

Invades duodenal wall: constrict common bile duct. direct invasion of spleen

214
Q

Courvoisiers law?

A

Painless jaundice plus a non-tender palpable gallbladder is pancreatic cancer until proven otherwise

215
Q

signs/symptoms of pancreatic cancer

A
  • Non-specific upper abdominal/back pain
  • Painless obstructive jaundice
  • Unintentional weight loss
  • Pale stools (due to lack of bile)
  • Steatorrhoea (greasy stools due to malabsorption due to lack of bile)
  • Dark urine (due to obstructive jaundice)
  • Palpable mass in epigastric region
216
Q

Pancreatic cancer management

A

whipples or total pancreatectomy

Medical Diseases (18 decks)

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