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*year 5 > 2) GI system 1 > Flashcards

2) GI system 1 Flashcards

1
Q

ACUTE UPPER GI BLEED

  • most common causes? 5
  • other causes? 3
A

= Peptic ulcer disease (35-50%)

= gastroduodenal erosions (8-15%)

= oesophagitis (5-15%)

= mallory-weiss tear (15%)

= varices (5-10%)

  • upper GI malignancy
  • vascular malformations
  • swallowed blood (eg from facial trauma, nose bleed or haemoptysis)
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2
Q

UPPER GI BLEED

  • risk factors? 3
  • classes of drugs which increase risk? 5
A
  • alcohol dependence (all, but especially varices)
  • liver disease (same as above)
  • lots of vomiting from eg morning sickness (mallory-weiss)

(also other risk for the relevant causes - eg RFs for PUD)

DRUGS

  • anti-coagulants (LMWH, warfarin, DOAC)
  • anti-platelets (aspirin, clopidogrel)
  • NSAIDs
  • steroids
  • SSRIs
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3
Q

UPPER GI BLEED

  • name of two scores used?
  • what is each used for?
A

BLATCHFORD SCORE
- need for admission and endoscopic intervention

(0-1 = discharge w/ OP OGD)

ROCKFALL SCORE
- predicts risk of Re-bleeding and mortality post-endoscopy

(higher the score, worse the mortality)

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4
Q

UPPER GI BLEED

  • 2 presentations of blood in the vomit?
  • 2 presentation of blood in stools?
  • other clinical signs? 2
  • clinical signs and vital signs that may indicate large amount of blood loss?
A

HAEMETEMISIS

1) bright red
2) coffee ground (brown)

BACK PASSAGE

1) Melaena – tar black stools, iron smell (indicate 50-100ml blood loss)
2) Haematochezia – fresh blood or maroon (lower GI bleed)

ALSO ABDOMINAL PAIN!!!
- may also have signs of chronic alcohol abuse (jaundice etc)

Basically signs of SHOCK!

initally

  • light headed
  • SOB
  • anxious

Peripherally shut down

  • Cold
  • ↓CRT
  • ↓UO (<0.5ml/kg/hr)
  • reduced GCS

THEN
- Dyspnoea (due to anaemia) – indicates large bleed
- Tachycardic > 100bpm (compensate for ↓BP)
↓GCS
- Hypotensive <90/60 → dizzy and syncope (nb may only be postural in young people)

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5
Q

LARGE UPPER GI BLEED

  • principle of assessment + management? 1
  • bloods to take? 6 (and possible findings)
  • other things to do / give under ABC (2 do, 3 consider)
A

A-E approach

BLOODS

  • FBC (low or normal Hb, takes time to drop!)
  • U+E (raised urea out of proportion to Creat indicates massive bleed)
  • LFT
  • Clotting
  • VBG/ABG
  • cross-match OR group & save

A+B
1) airway patent and give O2 (if low)

C
2) Get IV access (ideally two) AND give fluid challenge

3) CONSIDER giving blood (O neg is immediate, type specific 20 mins, corss match 45 mins) - major haemorrhage protocol if massive!
4) CONSIDER giving vit K +/-berliplex (if active bleed on warfarin)
5) monitor urine output and CONSIDER catheterising

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6
Q

LARGE UPPER GI BLEED - DISABILITY + EXPOSURE:

  • what to make sure to do as part of abdo exam?
  • are patients allowed to eat + drink?
  • what 2 scores to calculate?
  • who to refer to? 1 (+ when to call)
A

DRE

  • essential!!
  • to see if any melaena (nb be aware of iron supplements!)

patients should be NBM (at least for 24hrs if big bleed)

calculate:

  • BLATCHFORD SCORE
  • need for admission and endoscopic intervention

ROCKFALL SCORE
- predicts risk of Re-bleeding and mortality post-endoscopy

refer to GASTRO REG

  • depnds on the size of the bleed! - if massive + active, call before even assess - if controllable, call after A-E
  • ask what drugs (if any to give and whether to give blood)

nb also call anaesthetist if struggling to protect airway

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7
Q

LARGE UPPER GI BLEED

medication to give to ALL large upper GI bleeds? 1

  • medication to consider giving if variceal cause? 2 (main CI to one of these)
A

ALL
- OMEPRAZOLE (80mg stat IV, then 8mg/h for 72hrs) - nb normally start this after OGD

VARICES

  • TERLIPRESSIN IV (decreases portal pressure, CI = IHD)
  • prophylactic ANTIBIOTICS (for SBP)

(nb don’t start these drugs until spoken to gastro reg)

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8
Q

LARGE UPPER GI BLEED

  • what intervention do all need? (+time frame)
  • purpose of this intervention
  • specificmanagement options within this intervention for variceal bleeds?
  • 2nd line management options if bleed too big?
A

need ENDOSCOPY (OGD)

  • within 4 hrs if suspect varices
  • within 12-24hrs if shocked on admission or significant co-morbidity

purpose:

1) find CAUSE of bleed
2) TREAT bleed if still active

varices = SCLEROTHERAPY (inject into varices to ‘sclerose’ them) OR banding

IF V BIG BLEED

1) balloon tamponade during OGD
2) open surgery

nb other treatment options during OGD (don’t learn off by heart):

use either mechanical (clips) w/ or w/o adrenaline; thermal coag w/ adrenaline, fibrin or thrombin w/ adrenaline, haemospray (useful for ulcers)

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9
Q

If no site of bleeing found on OGD fopllowing upper GI bleed, what could this mean? 4

A

A) Bleeding site MISSED on endoscopy

B) Bleeding site HEALED prior to endoscopy (eg mallory-weiss or dieulafoy’s)

C) blood had been SWALLOWED (so not GI bleed)

D) Site of bleeding is DISTAL to where endoscopy done (eg meckel’s diverticulum, colonic site)

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10
Q

VARICEAL BLEEDING

  • primary prevention options? 2
  • secondary prevention options?
A

PRIMARY PREVENTION

  • propranolol (mainstay!)
  • repeat endoscopic banding

don’t give propranolol acutely if bleeding as may make worse!

SECONDARY PREVENTION (ie following bleed)

  • endoscopic banding
  • TIPS (transjugular intrahepatic portosystemic shunt – joins hepatic + portal vein)
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11
Q

What complication should you observe for for all large GI bleeds?

what signs may this present with? 5

other possible complication of all GI bleeds?

A

RE-BLEED

continuous monitoring of vitals

signs of re-bleed

  • rising pulse rate
  • falling JVP
  • decreasing hourly urine output
  • further haematemesis (or melaena)
  • fall in BP (late sign) + drop in GCS

40% of patients who re-bleed will die!! - make sure monitor appropriately to catch early!

other complication = ASPIRATION pneumonia! (develops later!)

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12
Q

VARICEAL BLEEDING

  • prognosis following 1st bleed?
  • specific complication associated with variceal bleeds? 1
A

Following 1st variceal bleed – 60% re-bleed in 1st year

complications of variceal bleeds:
- Spontaneous bacterial peritonitis (SBP)

(also re-bleed + aspiration pneumonia - as with all GI bleeds)

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13
Q

TYPICAL PRESENTATION of causes of OESOPHAGEAL BLEED:

  • oesophagitis?
  • oesophageal cancer?
  • mallory-weiss tear?
  • varices?

(incl amount + appearance of blood AND associated symptoms + other features of history)

also if tend to stop spontaneously or not

A

OESOPHAGITIS
- small volume fresh red blood (often streaking vomit)
- malaena rare
- often ceases spontaneously
= usually Hx of antecedent GORD-type symptoms

OESOPHAGEAL CANCER
- usually small amounts of blood (except pre-terminal when more)
- may be recurrent until malignancy managed
= dysphagia, systemic symptoms such as weight loss

MALLORY-WEISS TEAR
- typically brisk small-moderate volume of bright red blood
- malaena rare
- usually ceases spontaneously
= Hx of repeated vomiting (treat cause of this! eg anti-emetics for morning sickness)

VARICES
- usually large volume fresh blood
- swallowed blood can -> malaena
- often associated with haemodynamic instability
- may stop spontaneously, but re-bleeds common until appropriately managed
= Hx of alcohol abuse or other liver disease

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14
Q

TYPICAL PRESENTATION of causes of GASTRIC BLEED:

  • gastric cancer?
  • dieulafoy lesion?
  • diffuse erosive gastritis?
  • gastric ulcer?

(incl amount + appearance of blood AND associated symptoms + other features of history)

also if tend to stop spontaneously or not

A

GASTRIC CANCER
- may be frank haematemesis or altered blood mixed with vomit
- amount of bleeding variable (erosion of major vessels may -> large haemorrhage)
= prodromal dyspepsia + systemic Ca symptoms

DIEULAFOY LESION
- may produce quite considerable bleeding
- may be difficult to detect endoscopically
= often no prodromal features prior to haematemesis + malaena

DIFFUSE EROSIVE GASTRITIS
- usually haematemesis (coffee ground or fresh) and epigastric discomfort
- large haemorrhage may occur with haemodynamic instability
= Hx of underlying cause: eg recent NSAID etc use, often have epigastric discomfort

GASTRIC ULCER
- small low volume bleeds more common -> iron-deficiency anaemia
- erosion into a significant vessel may -> significant haematemesis
= tend to present with symptoms (and RFs) of PUD and iron-deficiency anaemia

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15
Q

What is a DIEULAFOY LESION?

A

about 1% of all GI bleeds

condition characterized by a large tortuous arteriole most commonly in the stomach wall (submucosal) that erodes and bleeds.

it is an arteriovenous malformation

It can present in any part of the gastrointestinal tract

can be hard to detect on OGD

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16
Q

CONSTIPATION:

  • definition?
  • what criteria used to assess? (roughly describe what this consists of)
A

= 2 or fewer bowel movements a week (or fewer than normal for person)

OR

= stools passed with:

  • difficulty / straining
  • pain
  • feeling of incomplete evacuation (tenesmus)

ROME CRITERIA
“making stools glamarous”
- DON’T LEARN SPECIFIC criteria, just be aware!

constipation = persence of 2 or more features

A) straining for >25% stools
B) lumpy / hard stools for >25% stools
C) tenesmus for >25% stools
D) sensation of anorectal obstruction / blockage for >25% stools
E) manual manouveres to facilitate for >25% bowel movements
F) < 3 bowel movements a week

nb these criteria are not commonly formally used as they tend to overdiagnose - go moreon affect on QOL and any concerning features!

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17
Q

CONSTIPATION:

  • lifestyle causes / contributing factors? 3
  • situational causes / contributing factors? 5
  • functional / psych causes? 4
A

LIFESTYLE

  • poor diet
  • lack of exercise
  • not enough water

SITUATIONAL

  • old age (very common!!!)
  • post-op pain
  • dehydration
  • hospital environ (decrease privacy, have to use bed pan)
  • distant, squalid or fearsome toilets

FUNCTIONAL / PSYCH

  • IBS
  • anorexia nervosa
  • depression
  • abuse as a child
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18
Q

ORGANIC CAUSES of CONSTPIATION:

  • anorectal disease? (2 common/important, 3 rare)
  • intestinal obstruction? (4 common/important, 1 rare) - think inter + extra luminal!
  • metabolic / endocrine? (2 common/important, 3 rare)
  • neuromuscular? (1 common/important, 3 rare)

(nb medications can also cause / exacerbate constipation - see next flashcard)

A 
ANORECTAL DISEASE
(consider esp if painful!!)
= anal or colorectal Ca
= fissures, strictures (incl herpes)
- Proctalgia fugax
- rectal prolapse
- pelvic muscle dysfunction / levator ani syndrome

INTESTINAL OBSTRUCTION
= colorectal Ca
= strictures (eg crohn’s)
= pelvic mass (foetus, fibroids)
= diverticulosis (rectal bleeding more common)
- pseudo-obstruction (nb different to paralytic ileus)

METABOLIC / ENDOCRINE
= hypercalcaemia
= hypothyroidism (rarely the presenting feature though)
- hypokalaemia
- porphyria
- lead poisoning

NEUROMUSCULAR (slow transit from decreased propulsive activity)
= paralytic ileus (spinal / pelvic nerveinjury, eg surgery or trauma)
- agangliosis (hirschprungs, chagas)
- systemic sclerosis
- diabetic neuropathy

nb constipation is unlikely to be the sole symptom of a serious disease - ask re associated symptoms

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19
Q

Medications which can cause / exacerbate constipation? (2 very common, 3 common, 1 other)

(nb majority of these are classes of medication)

how to prevent constipation occuring? 2

A

= opiates
= anti-cholinergics (eg tricyclics)

  • iron
  • diuretics (eg furosemide)
  • calcium channel blockers

(- some antacids, eg w aluminium)

warn pts of this side effect - as it may affect compliance

1) dietary advice
2) co-prescribe laxatives if high risk

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20
Q

ASSOCIATED SYMPTOMS to ask about in CONSTIPATION which may indicate an ORGANIC cause (and thus need investigations):

  • GI-related? 6
  • systemic symptoms? 2
  • other specific symptoms? 2
  • what other demographic detail should be taken into account? 1

(say which condition each symptom may be suggestive of)

A

OTHER GI FEATURES

  • mucus? (Ca)
  • blood? (Ca)
  • passing wind (if not, could be obstruction!)
  • vomiting (obstruction)
  • abdo pain
  • Tenesmus (Ca)

nb if constipation alternating with diarrhoea + no other features - suspect IBS

also aways ask about diet AND medications!

SYSTEMIC

  • weight loss (Ca)
  • symptoms of anaemia (Ca)

OTHER

  • menorrhagia + other hypothyroid
  • symptoms suggestive of hypercalcaemia

AGE
- if NEW constipation >40 (esp with other signs) then investigate more!

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21
Q

POSSIBLE investigations for CONSTIPATION:

  • bedside? 1
  • bloods? 5
  • imaging if suspect obstruction? 1
  • other imaging? 2

when should you do these investigations?

A

DRE
- look for fissures etc as well as feeling for stool

BLOODS

  • FBC (for anaemia)
  • U+Es
  • ESR
  • Ca 2+
  • TFTs

if suspect obstruction = Abdo XR

sigmoidoscopy to biopsy abnormal tissue if appropriate

IF SUSPECT Ca
- colonoscopy / barium enema

Do if red flags for Ca or other organic causes or if functional is not resolving with lifestyle changes or laxatives

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22
Q

red flag symptoms for colorectal cancer? 4

A
  • change in bowel habit
  • over 40
  • weight loss
  • anaemia
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23
Q

symptomatic MANAGEMENT of CONSTIPATION (if organic cause ruled out)
- lifestyle advice? 4

A
  • reassurance
  • drink more water
  • eat more fibre (introduce slowly to avoid bloating)
  • exercise more
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24
Q

MEDICATION for symptomatic management of CONSTIPATION

  • when should this be used?
  • principles of use?
A

LAXATIVES

Use for symptomatic management of functional constipation (for a short period while changing lifestyle)

co-prescribe for drugs known to cause constipation

prescribe for organic constipation (whilst also treating underlying cause)

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25
Q

LAXATIVES:
- four different types?

for each type:

  • drug name examples (at least 2)
  • mechanism of action?
A

BULKING AGENT
= Bran powder
= ispaghula husk (eg fybogel)
- increase faecal mass, stimulating peristalsis

STIMULANT LAXATIVES
= senna
= docusate (stimulant + softening)
- increase intestinal motility

STOOL SOFTENERS
= arachis oil (can take as enema)
= docusate (stimulant + softening)
= liquid parafin
- soften stool
OSMOTIC LAXATIVES
= lactulose
= macrogel (eg movicol)
= phosphate enemas (pre-procedural)
- draw water into the bowel lumen
- movicol can cause bloating
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26
Q

BULKING AGENTS

  • drug name examples? 2
  • mechanism of action?
  • when to use?
  • how to tell pts to use?
  • contraindications? 3
A

BULKING AGENT
= Bran powder
= ispaghula husk (eg fybogel)

  • increase faecal mass, stimulating peristalsis (similar to how increased fibre works)

can use 1st line for functional constipation (alongside senna)

  • drink with lots of water, may take a few days to work

X CI: difficulty swallowing, GI obstruction or faecal impaction

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27
Q

STIMULANT LAXATIVES

  • drug name examples? 2
  • mechanism of action?
  • main side effect? 1
  • when to use?
  • contraindications? 3
A

STIMULANT LAXATIVES
= senna
= docusate (stimulant + softening)

  • increase intestinal motility (SE: abdo cramps)

short-term relief of functional constipation (often alongside bulk-forming)

X CI: intestinal obstruction, acute colitis, prolonged use (can cause colonic atony + hypokalaemia)

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28
Q

STOOL SOFTENERS

  • drug name examples? 3
  • mechanism of action?
  • when to use? 1
  • contraindications? 1
A

STOOL SOFTENERS
= arachis oil (can take as enema)
= docusate (stimulant + softening)
= liquid parafin

  • soften stool
  • particularly good for painful conditions (eg fissures)

X CI: don’t use liquid parafin for prolonged period

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29
Q

OSMOTIC LAXATIVES

  • drug name examples? 3
  • mechanism of action?
  • when to use? 3
  • main side effect? 1?
A

OSMOTIC LAXATIVES
= lactulose
= macrogel (eg movicol)
= phosphate enemas (pre-procedural)

  • draw water into the bowel lumen
  • often used for kids
  • can be 1st line for functional (if not use stimulant/bulk-forming)
  • pre-procedural as an enema
  • movicol can cause bloating
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30
Q

Who should you avoid using docusate in?

A

young people!

(only use in elderly or terminally ill)
- as long term cancer risk!

***CHECK THIS! - NOT SURE IF TRUE - THINK i’VE GOT CONFUSED WITH ANOTHER ONE

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31
Q

DIARRHOEA

  • common GI causes? 7
  • less common GI causes? 9
  • non-GI causes? 4

nb some meds also cause diarrhoea - on seperate flashcard

A

COMMON GI CAUSES

= gastroenteritis
= parasites / protazoa

= IBS

= Crohn’s
= UC
= Coeliac

= colorectal Ca

(also remember medication causes! see other flashcard)

LESS COMMON GI CAUSES

  • microscopic colitis
  • chronic pancreatitis
  • c. diff.
  • diverticular disease
  • lactose intolerance
  • laxative abuse
  • overflow diarrhoea
  • ileal / gastric rescetion
  • ischaemic colitis (high lactate)

NON-GI CAUSES

  • thyrotoxicosis
  • autonomic neuropathy
  • addison’s
  • carcinoid
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32
Q

DIARRHOEA

- broadly, what 3 things can decrease stool consistency?

A
  • water
  • fat (steatorrhoea)
  • inflammatory discharge
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33
Q

DIARHOEA

- three types of ‘watery’ diarrhoea? (and types of things that cause it)

A

OSMOTIC
- eg laxative induced

SECRETORY
- eg microscopic colitis

FUNCTIONAL
- eg IBS

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34
Q

STEATORRHOEA

  • three features?
  • three causes?
A
  • increased gas
  • offensive smell
  • floating, hard to flush stools
  • pancreatitis
  • coeliac disease
  • giardiasis
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35
Q

Inflammatory diarrhoea:

  • two most common causes?
  • two main features?
A
  • crohns
  • US
  • blood
  • frank pus
    ^in stools

nb just mucus in stools could be IBS, polyps or cancer so not that helpful…

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36
Q

Common drugs / drug classes that can cause diarrhoea? 8

nb there are many more but learn these especially

A
  • antibiotics
  • laxatives
  • PPIs
  • NSAIDs
  • propranolol
  • digoxin
  • cytotoxics
  • alcohol
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37
Q

ACUTE DIARRHOEA:

  • timeframe definition?
  • risk factors for gastroeneteritis to ask about? 4
  • systemic symptom which may point towards infective cause? 1
A

< 2 weeks = acute diarrhoea

  • medications (eg recent Abx or PPIs)
  • travel
  • contact with D&V
  • diet change (eg food intolerance or food poisoning)

systemic symptom:
- fever

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38
Q

Red flags for diarrhoea:

  • acute? 2
  • acute + chronic? 1
  • chronic? 2
A

ACUTE
- clinical dehydration
- fever
^ie systemically unwell - look for any signs of shock!

ACUTE + CHRONIC
- blood

nb if just mucus, this could be IBS

CHRONIC

  • weight loss (IBD or Ca)
  • anaemia (IBD or Ca)
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39
Q

What shoud you rule out in NEW IBS in post-menopausal women?

A

ovarian cancer

esp if accompanied weight loss!

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40
Q

DIARRHOEA

bedside test for ALL?

bedside tests for systemically unwell or chronic diarrhoea? 2 (1 for unwell, 2 for chronic)

Blood tests if systemically unwell / dehydrated with diarrhoea? (do 3, consider 1)

blood tests if chronic diarrhoea? 3

A

DRE for ALL diarrhoea (or will miss faecal impaction w overflow)

STOOL SAMPLES

  • culture + microscopy (for unwell or chronic)
  • faecal calprotectin (IBD)
  • faecal occult blood test (FOBT) (Ca)
IF SYSTEMICALLY UNWELL
- FBC (eosinophilia if parasites)
- U+E (low K if severe)
- VBG
(- blood cultures)

CHRONIC (w concerning features)

  • FBC (microcytic anaemia if coeliac or Ca, macrocytic if alcohol abuse or low B12, eg crohns or coeliac)
  • TFTs (hyperthyroid)
  • TGT (for coeliac)

nb can do CEA, but if suspect Ca should do imaging and not rely on this as only raised in some Ca’s

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41
Q

Aside from if someone who is systemically unwell with acute diarrhoea, what other features of the Hx may make you do a stool culture and microscopy for acute diarrhoea? 6 (although not necessarily urgent)

A
  • local food poisoning outbreak
  • raw seafood ingestion
  • foreign travel
  • recent Abx use
  • rectal intercourse
  • immunocompromised
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42
Q

which imaging should be considered for chronic diarrhoea if suspect:

  • crohn’s? 1
  • UC? 1
  • Bowel Ca? 1
A

crohns = flexible sigmoidoscopy

UC = colonoscopy / barium enema

Bowel cancer = colonoscopy / barium enema

nb don’t do colonoscopies / sigmoidoscopies if acute flare of IBD!!

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43
Q

Management of acute diarrhoea:

  • mainstay?
  • when should IV fluids be considered? 2
  • when to use abx? 2
  • what medications to consider? 2 (and when not to use 1)
A

ORAL rehydration FLUIDS (better than IV)

IV if:

  • very clinically dehydrated
  • bloody diarrhoea + dehydrated for >2 weeks

(nb also replace electrolytes dependent on bloods)

ABx if

  • systemically unwell with known infective diarrhoea
  • c. diff. (PO vancomycin or metronidazole)
CONSIDER:
- codeine
- loperamide 
CI: colitis (may precipitate megacolon)
^tbh rarely use for this purpose!! (rehydration salts best thing!)
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44
Q

DIARRHOEA

- advice to patients re going back to work? 2

A

48 hours after symptoms stop if viral gastroenteritis

no work until stool samples negative (if handle food - eg chefs)

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45
Q

MALNUTRITION:

- common groups of causes of malnourished patients in hospital? (also applies to out of hospital too)

A

1) INCREASED nutritional REQUIREMENTS (eg sepsis, burns, surgery, cancer)
2) INCREASED nutritional LOSSES (malabsorption, output from stoma)
3) DECREASED INTAKE (dysphagia, nausea, sedation, coma)
4) EFFECT of TREATMENT (eg nausea, diarrhoea)
5) ENFORCED STARVATION (enforced periods NBM)
6) MISSING MEALS through being whisked off (eg for investigations)
7) DIFFICULTY in FEEDING (eg lost dentures, no one to help)
8) UNAPPETISING FOOD

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46
Q

MALNUTRITION

- use of investigations in malnutrition?

A

General;ly not that helpful, but can see vitamin/electrolyte losses

low albumin is suggestive but not always (but raising albiumin is good sign of recovery!)

signs on physical exam like cachexia, falling BMI and look ing dehydrated artee more useful

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47
Q

main tools of prevention of malutrition during hospital? 3

A

1) make sure food is appetising
2) ensure that meal times are uninterrupted where possible
3) get advice from nutritionist (if someone at risk or underweight)

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48
Q

If increasing oral intake doesn’t work, what other main groups of methods of feeding can be used if patients are malnourished? 2

who must you consult before doing any of these?

if someone has been malnourished for a long time, what is an important thing to consider during management?

A

1) ENTERAL FEEDING
- NG feeding, gastrostomy etc

2) PARENTERAL FEEDING
- ie IV nutrition
- can use partial if can’t get all nutrints enterally (eg short bowel syndrome or active crohns) or use TPN if can’t take anything enterally

consult DIETICIAN before starting someone on enteral or parenteral feeding!

revent REFEEDING syndrome (ie refeed people slowly and routinely check electrolytes)

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49
Q

VITAMIN DEFICIENCY SYNDROMES:

  • vit A? 1
  • vit B1? (aka?) 2
  • vit B2? 2
  • vit B6? 1
  • vit B12? 3
  • vit C? 1
  • vit D? 2
  • vit K? 1

(describe each condition briefly)

also if there is a condition which often causes this condition then mention it too

A

VIT A
= XEROPTHALMIA
- big cause of blindness in developing world

VIT B1 (thymine)
= WERNICKE’S ENCEPHALOPATHY
- triad of: confusion, ataxia + opthalmoplegia
= BERI BERI
- heart failure w oedema (wet beri beri) or neuropathy (dry beri beri)

VIT B2
= ANGULAR STOMATIS
= CHEILITIS (aka angular stomatis)

VIT B6
= POLYNEUROPATHY

VIT B12
= MACROCYTIC ANAEMIA
= NEUROPATHY
= GLOSSITIS

VIT C
= SCURVY
- listlessness, anorexia/cachexia, gingivitis, loose teeth, halitosis, bleeding from gums, nose, hair follicles, or intro joints, bladder, gut, muscle pain/weakness, oedema

VIT D
= RICKETTS
- growth retardation, hypotonia, bow-legged or knocked knees
= OSTEOMALOACIA
- bone pain + tenderness, fractures, proximal myopathy

VIT K
= BLEEDING DISORDERS
- (basically equivalent of putting a pt on warfarin)

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50
Q

Which vitamins are fat-soluable? (and so often have malabsorption of if have steatorrhoea)

A

DAKE

= fat soluable vitamins

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51
Q

GORD

  • pathophysiology?
  • main complications it can lead to? 3
A

reflux of stomach acid + bile into oesophagus

→ if prolonged reflux →

  • oesophagitis
  • strictures
  • Barrett’s (can lead to Ca)
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52
Q

GORD:

  • specific causes? 3
  • risk factors? 4
A

CAUSES

  • Lower oesophageal sphincter defect + hypotension
  • Hiatus hernia
  • Loss of oesophageal peristaltic function or Slow Gastric emptying

Risk factors

  • Abdominal obesity
  • pregnancy
  • smoking
  • alcohol
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53
Q

GORD:

- what drug classes cause / exacerbate reflux? 2

A
  • anticholinergics (incl TCAs)

- nitrates

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54
Q

GORD:

  • oesophageal? 5
  • extra-oesophageal? 3
A

OESOPHAGEAL

  • HEART BURN (reflux) – (burning, retrosternal discomfort)
  • – Worse post-meal, lying down
  • – Relieved by anti-acids ( and PPI or H2 antag)
  • BELCHING
  • ACID BRASH
  • – acid or bile regurgitation (ask if taste acid in mouth)
  • WATER BRASH
  • – ↑↑salivation

ODYNOPHAGIA
-– painful swallowing may indicate oesophagitis or ulcers

EXTRA-OESOPHAGEAL

  • nocturnal asthma or CHRONIC COUGH (very common!)
  • LARYNGITIS
  • – hoarseness, throat clearing
  • SINUSITIS
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55
Q

GORD:
- red flag features? 6 (incl acronym!)

  • over what age is new-onset reflux also a red flag?
A

ALARMS symptoms

A = Anaemia
L = Loss of weight
A = Anorexia
R = Recent/ Refractory/progressive
M = Meleana/haematemesis
S = swallowing difficulty

NEW ONSET over 55 years = red flag

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56
Q

GORD:
- main three investigations? 3

when should you use each ?

A

A) ENDOSCOPY
– if over 55
- > 4wks
- ALARMS features

nb Stop PPI 2 weeks before scope

B) 24hr pH study ± Manometery
– if endoscopy normal

C) Barium swallow
– if screening for hiatus hernia

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57
Q

What classification system is used for GORD

A

Los Angeles Classification of GORD (1-4)

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58
Q

Conservative management of GORD:

  • dietary advice? 8
  • other lifestyle advice? 3
A

DIETARY

  • small, regular meals (avoid big)

avoid:

  • hot drinks
  • alcohol
  • fizzy drinks
  • citrus
  • spicey food
  • chocolate
  • eating < 3 hrs before bed

OTHER ADVICE

  • raise bed head
  • weight loss (reduce pressure on stomach)
  • smoking cessation
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59
Q

What medications to avoid if patient has GORD:

  • ones that damage gastric mucosa? 4
  • ones affecting gastric / oesophageal motility? 3
A

Avoid drugs that DAMAGE MUCOSA

– NSAIDs

  • steroids
  • K+ salts
  • Bisphosphonates

Avoid drugs REDUCING gastric/oesophageal MOTILITY

  • nitrates
  • calcium channel blockers
  • anti-cholinergics
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60
Q

GORD:

  • 1st line symptomatic medical management? 2
  • 2nd line medical management? 1 (+ alternative drug class = 1)
  • option if medications don’t work / very severe? 1
A

1ST LINE (if no alarms)

  • Antacids (Magnesium trisilicate mixture)
  • Alginates (Gaviscon)

2ND LINE

1) PPI (start high dose + taper down)
2) H2 antagonist (if PPI not working + ruled out alarms)

if neither working after couple of months, consider DDx (eg h.pylori)

SURGICAL OPTIONS

  • nissen fundoplication
  • stretta radiofrequency ablation of GOJ

^ consider surgeries if no other cause DDx found and refractory to drugs

(don’t both learning names of surgical options - just know they exist as last line!)

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61
Q

Possible complications of GORD? 5

A
  • Oesophagitis
  • strictures
  • ulcers
  • anaemia
  • Barrett’s oesophagus (leading to oesophageal cancer)
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62
Q

GORD differentials? (5 common/serious, 2 rare)

A

= H. pylori gastritis
= drug-induced gastritis
= Peptic ulcer disease

= gastric cancer
= oesophageal cancer

  • achalasia
  • eosinophilic oesophagitis
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63
Q

Describe pathophysiology of barret’s oesophagus?

what main risk>?

A

distal oesophagus epithelium undergoes metaplasia (squamous → columnar) → Dysplasia → oesophageal Ca (50-100 fold risk)

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64
Q

OESOPHAGEAL CANCER

- two types? (location + cell type)

A

ADENOCARCINOMA

  • lower 1/3rd
  • associated with Barrett’s
  • more common in western world

SQUAMOUS CELL CARCINOMA

  • upper 2/3rds
  • same risk factors as for head + neck cancers
  • less common in developed world
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65
Q

OESOPHAGEAL CANCER

- risk factors? 9

A

Male > F

  • obesity
  • ↓in vit.A/C
  • alcohol
  • smoking
  • achalasia
  • nitrosamine exposure
  • reflux oesophagitis
  • Barrett’s

(also increasing age)

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66
Q

OESOPHAGEAL CANCER:

  • oesophageal symptoms? 4
  • other localised symptoms? 4
  • systemic symptoms? 3
A

OESOPHAGEAL

= Dysphagia + Dyspepsia PROGRESSIVE! (First solids → soft food → liquids)

= Odynophagia

  • Regurgitation + Vomiting → Haematemesis or Melaena (small volumes)

= Retrosternal chest pain (reflux)

OTHER LOCAL

  • Hiccups
  • Lymphadenopathy
  • Hoarseness – pressure on recurrent laryngeal or larynx
  • Cough – may be paroxysmal if aspiration pneumonia

SYSTEMIC (these are LATE signs!)

  • ↓Weight
  • ↓Appetite
  • Fatigue
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67
Q

OESOPHAGEAL CANCER

  • main investigation?
  • criteria for urgent 2WW referral?
A

Referral for ENDOSCOPY 1st line

Urgent (2 wks) – if:

= dysphagia 
OR
= age ≥ 55 AND wt loss and any of: 
- upper abdo pain
- reflux
- dyspepsia

(don’t worry about learning exact referral criteria!)

Upper GI endoscopy w/ BRUSHINGS + BIOPSY

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68
Q

OESOPHAGEAL CANCER

  • staging system used?
  • imaging used to stage?
A

TNM staging

Endoscopic US or CT/MRI

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69
Q

OESOPHAGEAL CANCER

  • curative management options? 2
  • palliative management option?
A

cure = RADICAL OESOPHAGECTOMY

  • if T1/2
  • Neo-adjuvant Chemotherapy may be considered

Chemo-radiotherapy if surgery not suitable

Palliative chemo-radiotherapy to restore swallowing

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70
Q

OESOPHAGEAL CANCER

- prognosis? (5 year survival rate)

A

POOR – with or without treatment

5yr survival is 20-25% for all stages

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71
Q

HIATUS HERNIA

  • describe what happens?
  • three possible causative mechanisms? 3
  • risk factors? 6
A

Herniation of stomach through oesophageal aperture of diaphragm

POSSIBLE CAUSATIVE MECHANISMS:

1) Widening diaphragmatic hiatus
2) Oesophageal shortening pulls up the stomach
3) ↑Intra-abdominal pressure Pushes stomach up

  • Obesity
  • Pregnancy
  • Ascites
  • ↑Age
  • Trauma chest/abdo
  • skeletal deformities (scoliosis, kyphosis, pectus excarvatum)
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72
Q

HIATUS HERNIA:

  • most common type? (+ two main symptoms associated with this?
  • less common type? (+ 4 symptoms of this)

describe what’s happening in each type

A

‘SLIDING’ (80%)
= GOJ slides into thorax

  • ↑↑↑Reflux (common as LOS becomes less competent)
  • Dysphagia

‘ROLLING’ (para-oesophageal 20%)
= GOJ remains in abdo, but part of the stomach (cardia) herniates into thorax

  • Dysphagia
  • Chest pain
  • Epigastric pain or fullness
  • Nausea

(Reflux less common)

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73
Q

HIATUS HERNIA:

  • gold standard investigation?
  • other investigation that might be done? why?
  • what investigation might it be picked up incidentally on? what would you see?
A

BARIUM SWALLOW
= best diagnostic test ∆

UPPER GI ENDOSCOPY
- in any patient > 55 with new dysphagia, must exclude oesophageal cancer!!

(Stop PPI 2 weeks before scope)

CXR (may be picked up incidentally)

  • Soft tissue opacity w or w/o air fluid level
  • Retro-cardiac air-fluid level = Rolling (para-oesophageal)
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74
Q

HIATUS HERNIA:

  • symptomatic management?
  • definitive management options?
A

SYMPTOMATIC MANAGEMENT:
- Same as GORD

SURGICAL OPTIONS

1) Laparoscopic fundoplication (if refractory symptoms and risk of strangulation)
2) Gastropexy (suturing of stomach to abdominal wall)

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75
Q

PEPTIC ULCER DISEASE:

  • biggest risk factor? 1
  • other risk factors? 3
A

H. PYLORI = BIGGEST
- 95% DU, 80% GU)

  • smoking
  • NSAIDs
  • alcohol
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76
Q

PEPTIC ULCER DISEASE:

  • three symptoms + 1 sign common to both duodenal and gastric ulcers?
  • difference in presentation between the two types?
  • which type is more common?
A
  • Epigastric PAIN related to: food, hunger, time of day
  • TENDER epigastrium
  • HEART BURN (retrosternal chest pain + reflux)
  • BLOATING + Early SATIETY

DUODENAL ULCERS (80%)

  • 50% asymptomatic
  • PAIN is BEFORE meals or at NIGHT (wakes from sleep)
  • RELIEVED by EATING or milk

GASTRIC ULCERS (20%)

  • PAIN at MEALS
  • RELIEVED by ANTACID
  • also get weight LOSS
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77
Q

PEPTIC ULCER DISEASE:
- red flag features? 6 (remember acronym)

at what age is a NEW onset reflux also a red flag?

A

ALARMS symptoms

A = Anaemia
L = Loss of weight
A = Anorexia
R = Recent/ Refractory/progressive
M = Meleana/haematemesis
S = swallowing difficulty

NEW ONSET over 55 years = red flag

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78
Q

PEPTIC ULCER DISEASE

  • 1st line investigation to do?
  • other investigation to look for red flag feature?
  • 2nd line intervention if red flag features present?
A

1) Non-invasive H.Pylori test – use CARBON-13 UREA BREATH TEST

do FBC to look for LOW Hb (alarms feature -> refer)

ENDOSCOPY

  • exclude malignancy + determine extent of oesophagitis
  • only if alarms symptoms present

nb during endoscopy:

  • Multiple Biopsies (histology, H.Pylori CLO)
  • Brushings (cytology)

nb Ensure repeat endoscopy post-treatment for gastric ulcers, due to risk of malignant conversion

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79
Q

What preperation should patients always do for an elective upper GI endoscopy?

A

Stop PPI 2 wks before endoscopy

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80
Q

PEPTIC ULCER DISEASE

  • management if caused by H. Pylori? 3
  • management if caused by NSAIDs? 2
  • prognosis of both?
A

H. Pylori = TRIPLE THERAPY

  • full dose PPI
  • TWO Abx for a week (norm amox + clarithro)

(or can replace amox with metranidozole)

NSAID-induced

1) stop NSAIDs
2) PPI (ulcers should heal in 8wks)

high risk of relapse in both!!

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81
Q

PEPTIC ULCER DISEASE
- complications? 4

describe how each would present clinically

A

HAEMATEMESIS / MALAENA
- associated with erosion of large blood vessels

PERFORATION
- can cause acute abdomen w epigastric pain -> generalised rigidity (air under diaphragm on CXR)

PYLORIC STENOSIS

  • due to scarring of duodenum
  • weight loss + projectile vomiting

(projectile vomiting presents in same way as kids!)

GASTRIC CANCER
- think alarms features

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82
Q

GASTRIC CANCER:

  • PMHx risk factors? 3
  • lifestyle risk factors? 2
  • age + gender most at risk?
A
  • H. Pylori (2 fold risk)
  • pernicious anaemia
  • gastritis
  • diet low in fruit + veg
  • smoking
  • M > F
  • increased age (95% in pts >55 years)

nb gastric cancer is 5th most common cancer in UK (after the big 4)

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83
Q

GASTRIC CANCER

  • describe the typical presentation?
  • red flag symptoms? 6 (incl acronym)
A

Typical:

Dysphagia + DYSPEPSIA – progressive

Nausea + Vomiting → Haematemesis ± Melaena

Reflux

Upper abdo mass

Epigastric pain/discomfort

Weight loss, LoA, Fatigue (due to anaemia)

ALARMS symptoms

Anaemia
Loss of weight 
Anorexia – LoA 
Recent onset, refractory or progressive symptoms 
Melaena (or haematemesis)
Swallowing difficulty (dysphagia)
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84
Q

GASTRIC CANCER:

  • investigation needed for diagnosis?
  • criteria for this investigation?
  • what is name of cells that can be seen on biopsy?
  • what imaging used to stage cancer?
A

ENDOSCOPY (w biopsies + brushings)

2 wk rapid referral if: 
= Dysphagia 
OR
= Age > 55 with weight loss and 1 of: 
- upper abdo pain
- reflux
- dyspepsia

Histology (biopsy) = may show SIGNET RING CELLS (large vacuole of mucin which displaces nucleus to one side – high number of cells indicates poor prog)

(stop PPI 2 weeks before scope)

CT or EUS – stage tumour

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85
Q

GASTRIC CANCER

  • management options? 3
  • prognosis? (10 year survival)
A

GASTRECTOMY

  • if localised disease
  • plus local lymph nodes

chemo-radiotherapy

  • neo-adjuvant
  • adjuvant
  • palliative

15% 10 year survival

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86
Q

GASTRIC CANCER

- signs indicating that disease is probably incurable?

A
  • epigastric mass
  • TROISIER’s sign (enlarged left supraclavicular node – VIRCHOW’s node)
  • hepatomegaly
  • jaundice
  • ascites
  • acanthosis nigricans
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87
Q

PANCREATIC CANCER

  • are majority of tumours endo or exocrine?
  • commonest cell type?
  • commonest location in the pancreas?
A

majority of tumours are EXOCRINE

ADENOCARCINOMA (95%, poor prog)
– 60% head, 25% body, 15% tail

nb other types = Ampulla of Vater or Pancreatic islet cells – insulinoma, gastrinoma, glucagonoma (good prog)

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88
Q

PANCREATIC CANCER:

  • PMHx risk factors? 2
  • lifestyle risk factors? 4
  • age + gender most at risk?
A
  • chronic pancreatitis
  • DM (both types)
  • smoking
  • alcohol
  • abdominal obesity
  • fat / processed meat diet
  • M > F
  • over 60 = greatest risk

NB >95% have KRAS2 mutation

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89
Q

clinical presentation of PANCREATIC CANCER

  • describe features of abdo pain that may have?
  • other GI symptoms? 3
  • systemic sign? 1
  • what additional symptoms if in the head of the pancreas? 4
  • what are the classical findings on physical exam? 3 (incl name of this sign)
  • what condition can be a complication of this cancer? 1
A

Epigastric DISCOMFORT - radiating as dull backache

  • Worse supine
  • relieved sitting forward

Tumour compressing gall bladder → gastric outlet obstruction or delayed emptying → NAUSEA + VOMITING

STEATORRHOEA – secondary malabsorption (loss of exocrine func)

ANOREXIA

WEIGHT LOSS

HEAD OF PANCREAS

  • Dark urine
  • Pale stools
  • Yellow, jaundiced skin
  • Pruritis

COURVOISIER’s sign
= PALPABLE gall bladder in presence of PAINLESS, obstructive JAUNDICE
– highly indicative of pancreatic cancer 25%)

DM (common complication)

nb symptoms if in tail / body = Non-specific pain, Weight loss

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90
Q

PANCREATIC CANCER?
- bloods (1 specific, 3 general)

incl findings

A

↑CA19-9 = specific to Pancreatic Ca

FBC – normochromic anaemia or thrombocytosis (↑Plt)

LFTs – ↑Bilirubin, ↑↑ALP, ↑↑GGT (if alcohol) > ↑ALT (mild)

↑Glucose serum

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91
Q

PANCREATIC CANCER

  • 1st line imaging?
  • imaging if 1st line inconclusive?
A

ENDOSCOPIC ULTRASOUND SCAN (EUS)

  • scan liver, bile duct, pancreas
  • Pancreatic mass ± dilated biliary tree ± hepatic mets

Abdominal high resolution CT or MRI
– if EUS inconclusive and high suspicion (overlying bowel gas or fat may hide the pancreas)
- gold standard test

92
Q

PANCREATIC CANCER

  • describe management options? (including name of potentially curative surgery)
  • prognosis? (5 year survival)
A

RADICAL (resectable - rare)

  • Pancreato-duodenectomy (WHIPPLE’s) – if fit, no mets
  • Laparoscopic excision – tail lesions
  • Post-op chemo

PALLIATIVE (unresectable – common)

  • ERCP with stenting (may help obstructive jaundice + anorexia in palliative patients (frequently used))
  • Analgesia or Radiotherapy for pain

POOR prognosis – late presentation, early metastasis, poor survival

<1/5th of pts present with localised, potentially curable tumours

5 year survival is < 5%

93
Q

Complications of pancreatic cancer? 3

A

Duodenal obstruction (15-20%)

DVT or PE

secondary diabetes mellitus

94
Q

COELIAC DISEASE

  • pathophysiology?
  • risk factors? 2
  • age norm diagnosed at?
A

Immune mediated intolerance to gluten (gliadin) → causes cytotoxic T-cell inflam response in s.bowel (duodenum + jejunum) → villous atrophy + enteropathy → ↓Absorption, ↑Excretion of H2O, Ulcers, Strictures

  • PMHx of other autoimmune conditions
  • FHx of coeliac or other autoimmune conditions

bimodal distribution
- early childhood
- age 40-60
though can be diagnosed at any age!

95
Q

COELIC DISEASE

  • classic initial symptoms / groups of symptoms? 3
  • possible dermatological sign?
  • other late signs? 5
A

INITALLY:

1) Diarrhoea + FATTY STOOLS – pale, floating + foul
2) FTT + weight loss
3) ABDO DISCOMFORT, cramping or distension - ie IBS-like symptoms (in response to gluten rich food)

derm = DERMATITIS HERPETIFORMIS

  • classic skin (75%)
  • Chronic, polymorphic, pruritic, blistering skin disease
  • Elbows, knees and buttocks

LATE

  • Muscle WASTING (buttocks) + ARTHRALGIA
  • IRON (duodenum) or FOLATE (jejunum) deficiency → FATIGUE
  • DELAYED PUBERTY
  • MOUTH ULCERS
96
Q

COELIAC DISEASE

  • bloods (1 specific, 2 general)
  • gold-standard investigation? 1

(describe findings for all of these)

A

BLOODS

  • Total IgA tissue transglutaminase (tTG)
  • FBC (low Hb, microcytic anaemia)
  • low folate (sometimes low B12 too0

ENDOSCOPIC BIOPSY of s.bowel for CONFRIMATION ∆

(continue eating gluten, until biopsy is undertaken)

Jejunum (mainly – “VIC”) + Duodenum

  • diffuse Villous atrophy
  • ↑IE lymphocytes in LP
  • Crypt hyperplasia
97
Q

COELIAC DISEASE

  • management?
  • how monitor?
A

GLUTEN-FRE DIET
- Avoid wheat, rye, oats, barley.

Markers of compliance: Sx improve, histology + IgA Ab levels return to normal, -ve serology

Annual review

if presented as an infant, can do gluten challenge aged 2 to see if still have

98
Q

COELIAC DISEASE

- two possible complications?

A

COELIAC CRISIS

  • incredibly rare
  • life threatening DEHYDRATION due to diarrhoea + malabsorption

T-CELL LYMPHOMA
- ↑risk if poor adherence to diet

99
Q

COELIAC DISEASE
- two common DDx?

(especially in children)

A
  • Cows milk protein intolerance – not improved w/ gluten diet
  • Giardiasis

(also any other cause of FTT - eg heart problems)

100
Q

INGUINAL HERNIA:

  • two different types? which age gets which type?
  • gender most commonly affected?
  • other risk factors? 6
A

INDIRECT

  • go through deep AND superficial ring due to patent processus vaginalis
  • INFANTS
  • “Infants get Indirect”

DIRECT

  • goes directly through superficial inguinal ring
  • ADULTS (wth below risk factors)

MALES (8:1)
- remember, although less common, women do still get them!!

RISK FACTORS

  • obesity
  • chronic cough
  • constipation
  • urinary obstruction
  • heavy lifting
  • previous abdo surgery

nb more common on Right side

101
Q

INGUINAL HERNIA

- normal clinical presentation of uncomplicated?

A

Intermittent swelling in groin or scrotum

Firm + tender

Mass especially during coughing (↑IA pressure)

Sudden pain – unlikely to be severe

(also Vomiting + Irritability in infant)

102
Q

INGUINAL HERNIAS

  • what two examinations should you do? 2
  • what to ask pt to do during this exam? 1
  • what should you check manually?
  • what other equipment should you use in your examination? why?
  • if there is any doubt as to clinical diagnosis, what imaging can you do?
A

do abdo AND genital exam

examine and then ask patient to cough to see if lump appears / gets larger

check if hernia is reducible (if not reducible check not a scrotal lump)

also check if you can palpate above it (more likely to be scrotal lump) or not

try to transilluminate, to locate a hydrocele

can do ULTRASOUND scan if any doubt

103
Q

MANAGEMENT of INGUINAL hernias:

  • conservative? 2
  • definitive management? 1

which hernias might conservative and definitive management be appropriate?

A
  • loose weight
  • manage exacerbating factors (eg chronic cough / constipation)

definitive = SURGERY
- mesh repair commonest type

conservative if DIRECT and SMALL + NO complications

ALWAYS operate on if any complications or all INDIRECT (ie in infants)

nb don’t wait for indirect - do quickly! - undescended testes is the paeds urology surgery that you wait a few months before doing

104
Q

INGUINAL HERNIA

  • two commonest complications? (and how they occur)
  • red flags of these? 3
  • other complication that can occur in indirect (less common in direct) + how does this present?
A

Irreducible / incarcerated hernia – occurs chronically over time as hernia enlarges + fibrous adhesions form → STRANGULATION (compromises vasc supply) → SMALL BOWEL OBSTRUCTION (common complication of hernias)

  • irreducible hernia
  • very painful to touch / increasing pain
  • any signs of obstruction (vomiting, abdo distension etc)

for INDIRECT, can get HYDROCELE secondary to the patent processus vaginalis

  • get painless scrotal swelling increasing, transuillum,inates
  • norm self-limiting but surgery if still present 18-24mo
105
Q

Aside from other causes of testicular lumps (see reproductive flashcards), what else could be a DDx for an inguinal hernia?

A

Femoral hernia

swelling at top of inner thigh, under inguinal ligament

106
Q

true PERITONITIS

  • sings from end of bed? 3
  • signs on palpation / percussion? 3
  • sign on auscultation? 1
  • clinical test which will be positive? 1
A
  • lying prostrate
  • lying still
  • shocked
  • rigid abdomen (board-like)
  • guarding
  • percussion tenderness

nb don’t test rebound tenderness as this is cruel! - percussion tenderness is just as accurate and hurt as much

  • no bowel sounds

COUGH TEST
- ask pt to cough and watch face - if they wince or clutch abdomen as they do so, then positive

nb may also have symptoms like fresh blood per rectum and fever - depending on the cause of the peritonitis

nb. often confused with ‘colic’ (biliary, renal, bowel) - but pts are often restless with this and can’t sit down! - also pain waxes and wanes

107
Q

PERITONITIS

  • common causes? 6
  • what condition can present similar to this but is not actually peritonitis? 1
A
  • peptic ulcer disease (perforation)
  • gall bladder (perforation)
  • appendix (perforation)
  • diverticulitis (perforation)
  • ischaemic bowel perforation
  • spontaneous bacterial peritonitis (SBP, secondary to ascites)

so if you see true peritonitis - think perforation of somnething!!

PANCREATITIS can present exactly like peritonitis but does not require surgery - always exclude with blood tests!

108
Q

PERITONITIS:

  • bedside tests to consider? 3
  • bloods? (6 yes, 2 to consider)
  • initial imaging? 1 (and 2nd line? 1)
A
  • blood glucose
  • urine dip
  • ECG (eg pre-op)

^nb norm don’t do the top 2 if truely peritonitic

BLOODS

  • VBG
  • FBC
  • U+Es
  • LFTs
  • amylase

(- consider CRP)

  • GROUP + SAVE

(- consider clotting)

ERECT CXR = 1st line

CT abdo pelvis if this not clear (and pt stable)

109
Q
  • initial management of peritonitis? 3

- definitive management for all true peritonitis? 1

A

‘drip + suck’

  • IV fluids
  • NBM
  • analgesia (norm IV paracetamol + morphine)

need LAPAROTOMY!
- talk to surgeons about urgency (make as well enough as possible with fluids etc before surgey if time!)

110
Q

localised peritonitis:

  • how does this present?
  • common causes? 4
A

guarding at a certain area - but not all over the abdomen

  • cholecystitis
  • simple appendicitis
  • diverticulitis
  • salpingitis

nb if abscess formation is suspected (swelling, swinging fever, and raised WCC) then may need drainage (through skin or through surgery)

111
Q

Three main organs that can rupture in the abdomen? (ie ‘rupture’ causes of acute abdomen)
- main feature of presentation?

A
  • spleen
  • aorta
  • ectopic pregnancy

main feature is SHOCK!

peritonism may be mild in these conditions!

112
Q

FEMORAL HERNIA

  • main risk factor?
  • clinical presentation? (incl precise location)
A

main RF = female

HERNIATED MASS

– points DOWN leg
- in UPPER MEDIAL thigh

  • Appears or swells on coughing/straining
  • Disappears or reduces when relaxed/supine

Neck of hernia felt infero-lateral to pubic tubercle

Femoral canal boundaries: inguinal lig (anterior), lacunar lig (medially), femoral vein (lateral), pectineus/Pectineal lig (posterior)

113
Q

FEMORAL HERNIA

  • what investigations needed?
  • what often misdiagnosed as? (how to differentiate)
A

none needed, is a clinical diagnosis
- assume can use USS if unsure though…

often misdiagnosed as an inguinal hernia
- these point TOWARDS GROIN and can be felt supero-medial to pubic tubercle

google images to see difference in location!

114
Q

FEMORAL HERNIA

- management options?

A

surgically repair ALL!! (as high risk of complication if left!)

115
Q

FEMORAL HERNIA

  • main complication?
  • symptoms of this? 4
A

Strangulation (HIGH RISK 22%) → Incarceration

Mass 
– red
- tender
- tense
- irreducible

Colicky abdominal pain

Abdo distension

Vomiting

116
Q

INCISIONAL HERNIA:

  • caused by? 1
  • how common?
  • what increases risk? 1
A

Breakdown of muscle closure following abdo SURGERY

10-20% of laparotomies (much less common if laprascopic surgery)

abdominal obesity increases risk (and also makes management more difficult)

117
Q

INCISIONAL HERNIA:

  • management?
  • risk of management?
  • potential complication?
A

MESH REPAIR
- decreases recurrence, but can increase infection rates!

Like all hernias: can strangulate and cause bowel obstruction! - but rare!!

do always ask about prev abdo surgery if pt presents with bowel obstruction (or any abdo problem tbh) and examine scar sites for hernias!

118
Q

UMBILICAL HERNIA

  • how common?
  • how does it present?
  • two main groups of people who get these?
  • risk factors? 4
A

10-30% of all hernias

mass at, above or below umbilicus

INFANTS
- prematurity increases risk

ADULT

  • pregnancy
  • obesity
  • ascites
119
Q

UMBILICAL HERNIA

  • in which age group is prognosis worse?
  • management options? 2
  • who appropriate for which management?
A

INFANT

  • normally spontaneously resolves by age 4
  • operate if >1.5cm or child >4 years

ADULT

  • less likely to spontaneously resolve
  • more likely to need operation

so watch and wait OR operate

operation called MAYO REPAIR and repairs the rectus sheath

120
Q

GALLSTONES

  • pathophysiology?
  • main risk factors? 5 (way of remembering)
  • what % are symptomatic?
A

change in bile (cholesterol + bile pigment, phospholipids) concentration → formation of stones in biliary tract

  • fair
  • fat
  • female
  • fertile
  • fourty

70% asymptomatic

121
Q

GALLSTONES

  • describe biliary colic (ie socrates)
  • red flag symptoms? 2
A

Stones made in GB → symptomatic w/ cystic duct obstruction, or if passed into CBD

Sudden RUQ pain

  • collicky (gets better + worse)
  • Radiating to R.Shoulder
  • A/w nausea + vomiting
  • often following food
  • Better with analgesia

RED FLAGS

  • fever
  • jaundice

(red flags also dark urine or pale stools too - ie obstructive jaundice)

nb if vomiting makes pain better - then more likely to be colic - if little effect then more likely to be complication

122
Q

BILIARY COLIC

  • two main complications?
  • briefly describe each (incl names of signs/features)

(nb falshcards on both in ACC)

A

CHOLECYSTITIS

  • pain similar to biliary colic but more severe
  • MURPHY’s sign positive
  • may have local peritonism
  • fever

CHOLANGITIS

  • gall stone stuck in common bile duct -> obstruction
  • fever
  • jaundice
  • CHARCOT’S TRIAD = fever, jaundice, RUQ pain / tenderness

^both of thses can perforate -> full peritonism!! surgical emergency!

nb can also get chronic cholecystitis (chronic inflammation + colic that doesn’t respond to ABx, - treat surgically!)

nb can also get Acalculous cholecystitis

  • More common in T2 DM or UL disease
  • RUQ pain w/ Fever but no evidence of gall stones on US (likely due to biliary stasis or ischaemia)
  • Often presents with sepsis
123
Q

BILIARY COLIC

  • main two bloods to rule out complications? 2
  • 1st line imaging? 1
A
  • FBC (no raised WCC)
  • LFTs (not raised)

Abdo USS
- visualise stones in gallbladder

124
Q

BILIARY COLIC:

  • acute management? 3
  • definitive management? 1
A
  • analgesia
  • rehydrate
  • NBM

Elective laparoscopic cholecystectomy

125
Q

PORTAL HYPERTENSION

  • what is it?
  • pre-hepatic causes? 1
  • intra-hepatic causes? 5
  • post-hepatic causes? 4

by far most common cause in UK? 1

A

increase in the blood pressure in the portal vein, which carries the blood from the bowel and spleen to the liver

PRE-HEPATIC
- thrombus (portal or splewnic vein)

INTRAHEPATIC

= CIRRHOSIS (80% in UK)

  • schistosomiasis (commonest worldwide)
  • sarcoidosis
  • myeloproliferative diseases
  • congenital hepatic fibrosis

POST-HEPATIC

  • budd-chiari syndrome
  • right heart failure
  • constrictive pericarditis
  • veno-occlusive disease
126
Q

PORTAL HYPERTENSION:

  • clinical signs? 4
  • what can it present acutely as? 1

nb list the clinical signs caused directly as a result of portal hypertension - ie not ones as a result of liver cell death)

A
  • ascites
  • caput’s medusa (if severe)
  • ankle oedema
  • splenomegaly

(can also have anorectal varices)

often presents as: ACUTE GI BLEED (norm from varices - but can be PUD too)

also get symptoms of liver disease - eg jaundice, deranged clotting etc

127
Q

PORTAL HYPERTENSION:

- three main complications?

A
  • oesophageal variceal bleed
  • spontaneous bacterial peritonitis (SBP)
  • hepatic encephalopathy (
128
Q

Describe the pathology of cirrhosis / chronic liver disease

A

diffuse hepatic inflammation characterised by fibrosis and conversion of normal liver architecture into structurally abnormal nodules → cirrhosis often final stage of liver disease (80-90% liver parenchyma destroyed) and non-reversible (end-stage liver damage)

Fibrosis → distortion of hepatic vasculature → ↑intrahepatic resistance + portal HTN → Porto-systemic shunt

Portal HTN → oesophageal varices + hypo-perfusion of kidneys + water/salt retention (→ascites, transudative pleural effusion, splenomegaly) + ↑CO

Damage to hepatocytes → impaired liver function → ↓clotting factors + Alb (↑PT/↓Alb) and ↓ability to detoxify substances

129
Q

CLD / CIRRHOSIS

  • common causes? 4
  • less common causes? 8
A

= Alcohol abuse

= Non-alcoholic fatty liver disease (NAFLD)

= HCV (20% develop)
= HBV

Less common:

  • PBC (primary biliary cirrhosis IgM = AMA)
  • PSC (primary sclerosing cholangitis ANCA IgG)
  • Auotimmune hepatitis
  • haemochromatosis
  • methotrexate
  • biliary obstruction (CF, atresia)
  • Budd-Chiari syndrome (→venous outflow obstruction)
  • chronic heart failure
130
Q

CLD / CIRRHOSIS

  • inital vague systemic symptoms? 4
  • possible clinical signs as disease progresses? 10
  • signs of portal hypertension? 4

for clinical signs, think about doing a full GI exam and what you would find as you did it

A

Often asymptomatic (compensated) until obvious complications of liver disease (decompensated)

  • Fatigue / Malaise
  • Anorexia
  • Nausea
  • Weight loss

SIGNS
(variable depending on extent of disease)

  • Jaundice + hair loss
  • Leukonychia (↓Alb)
  • Clubbing
  • Dupuytren’s contracture, - Palmar erythema
  • Xanthelasma
  • Kayser-Fleischer ring (brown-green copper deposit – Wilson’s)
  • Hepatomegaly
  • Spider naevi (blanch and fill from centre outwards)
  • Gynaecomastia
  • Hypogonadism e.g. testicular atrophy or amenorrhoea

PORTAL HYPERTENSION

  • Ascites (can be detected clinically ≥ 1.5 litres)
  • Caput medusae
  • Splenomegaly
  • Oesophageal varices → upper GI bleed
131
Q

DECOMPENSATED LIVER DISEASE

  • aka?
  • what can it be triggered by?
  • possible features? 6
A

aka hepatic failure!

Triggered by

  • infection
  • GI bleed
  • constipation
  • opiates
  • alcohol
  • AKI
  • electrolyte disturbance

^basically can be triggered by anything that puts additional strain on body!

  • Oedema + Ascites
  • Jaundice
  • Easy bruising due to coagulopathy (↓factor II, VII, IX, X → ↑INR)
  • Oesophageal variceal rupture
  • Spontaneous bacterial peritonitis (SBP – ascetic neut > 250)
  • Hepatic encephalopathy
132
Q

Symptoms / signs of hepatic encephalopathy? 3

A
  • Liver flap
  • Confusion
  • Drowsy / ↓GCS
133
Q

Scoring system used to determine severity of liver cirrhosis?

what parameters is it based on?

what are the normal progression of these factors?

A

CHILD-PUGH SCORE
- determines severity of cirrhosis

based on:
- Albumin
- Prothrombin Time (PT)
- Bilirubin
- Ascites
- Encephalopathy 
^don't worry about knowing parameters - just know it measures severity

Nb LFTs are a poor determinant of liver failure progression, albumin and coagulation are much more sensitive

Initially: LFTs – ↑Bil ↑↑AST >↑ALT ↑ALP ↑yGT

Then, after loss of liver function - ↓Albumin ↑PT/INR

↓WCC ↓Platelets (indicate hypersplenism)

↓Clotting factors

↓Hb (may indicate occult bleeding)

Blood film – non-megaloblastic macrocytic anaemia suggests alcohol abuse

134
Q

Non-invasive liver screen (NILS):

  • purpose?
  • what investigations does it consist of?
A

work out extent AND cause of liver damage

1) LIVER USS + DUPLEX
- Look at GB/biliary tree stones,
Liver echo texture, Vasculature = portal + hepatic veinm (to detect retrograde flow and thrombus)

2) VIRAL SEROLOGY
- Hepatitis B – HBsAg, HBcAg, HBeAg, IgG/IgM
- Hepatitis C – Anti-HCV Ab, HCV RNA PCR, IgG/IgM

3) AUTOIMMUNE ANTIBODIES
- IgA = Alcohol
- IgM = AMA for primary biliary cirrhosis (PBC)
- IgG = ANA and ASA/SMA for AI Hepatitis or
- ANCA for primary sclerosing cholangitis (PSC)

4) GENETIC TESTS
- Wilson’s – ↓Serum caeruloplasmin, ↓Serum Cu, ↑24hr urinary Cu (speech + behaviour problems, Kayser Fleischer)
- Hereditary haemochromatosis - ↑Serum Ferritin > 1mg/L; Fasting Transferrin saturation > 45%; HFE gene (C282Y)
- Å1-antritrypsin – check for emphysema, liver cirrhosis or HCC; test serum a1-antritruypsin (↓a1AT < 11 umol/L)

DON’T NEED TO KNOW THIS MUCH DETAIL! - just know roughly the groups of causes and thus what looking for

135
Q

Gold-standard test for liver cirrhosis?

test done if suspect SBP?

A

GOLD STANDARD = liver biopsy

test for spontaneous bacterial peritonitis = Ascetic Tap for MC&S

136
Q

management of chronic liver disease:

  • lifestyle advice? 3
  • what nutiritional supplements to consider? 3
  • only definitive treatment? 1
A
  • stop alcohol
  • loose weight
  • exercise more

also consider stopping aggravating meds: eg NSAIDs, opiates etc

consider:

  • general nutrition
  • thiamine (esp if alcohol-related)
  • zinc?

also treat underlying cause if possible - eg anti-virals for Hep C

liver transplant is only definitive treatment

137
Q

Symptomatic management of pruritis associated with chronic liver disease? 1

A

Colestestyramine

138
Q

management of ascites:

  • conservative management? 2
  • 1st line medication to give? (how to monitor if working?)
  • 2nd line medication if poor response?
  • other two management options if severe? 2
A
  • fluid restrict (<1.5 L/day)
  • low salt diet

1st) SPIRONOLACTONE
- monitor with daily weights

2nd) FUROSEMIDE
- monitor U+Es

may require:

  • therapeutic paracentesis
  • HAS
139
Q

Complications of liver cirrhosis? 5

describe each briefly: pathophysiology + features

(don’t describe management)

A

1) HEPATIC ENCEPHALOPATHY
- large amounts of ammonia cross BBB → presents with Asterix (liver flap) w/ gentle hyper-extension of wrist → coma

2) OESOPHAGEAL VARICES
- portal hypertension -> engorged oesophageal veins -> rupture and large GI bleeds

3) HEPATOCELLULAR CARCINOMA
- painless jaundice with weight loss

4) SPONTANEOUS BACTERIAL PERITONITIS
- consider in any pt. who suddenly deteriorates; commonly E.coli, Klebsiella or Strep

5) RENAL FAILURE
- ↓Hepatic clearance of immune complex leads to accumulation in kidney → IgA nephropathy and hepatic glomerulosclerosis

140
Q

Management of hepatic encephalopathy? 1

A

lactulose - look this up!!!**

141
Q

What are the three features of hepato-renal syndrome? 3

A

Hepato-renal syndrome = Cirrhosis + Ascites + Renal failure

nb this has something like an 80% mortality rate…

142
Q

VIRAL HEPATITIS:

for each of:

  • Hep A
  • Hep B
  • Hep C

describe:

  • main method of spread?
  • acute or chronic?
A

HEP A
- faecal-oral route
= Acute

HEP B
- Blood and Babies (vertical)
= acute or chronic (if vertical, more likely chronic - 10% chronic)

HEP C
- blood
= acute -> Chronic (90%)

“A for Acute
B for Blood and Babies
C for Chronic”

143
Q

RISK FACTORS FOR:

  • Hep A? 6
  • Hep B? 3
  • Hep C? 4
A

HEP A

  • Africa
  • south America
  • travellers
  • children
  • IVDU
  • MSM

HEP B

  • +ve mothers
  • IVDU
  • sexual intercourse

HEP C

  • blood transfusion
  • IVDU
  • acupuncture
  • perinatal transmission

don’t worry if don’t get all - understand general pattern

144
Q

INTITIAL symptoms of both Hep A and Hep B? 5

  • LATER symptoms in Hep A? 4
  • OTHER symptoms in acute Hep B? 3
A

INITIAL of BOTH

  • fever (mild)
  • malaise
  • arthralgia
  • nausea
  • anorexia

LATER of HEP A

  • jaundice (rare in child)
  • tender hepatomegaly
  • lymphadenopathy
  • diarrhoea (if child)

nb can also have obstructive picture (dark urine -> pale stools)

OTHER of HEP B

  • urticaria (COMMON!)
  • jaundice
  • dark urine -> pale stools
145
Q

Complications of acute Hep B infections? 3

describe each briefly and timescale (where relevant)

A

FULMINANT HEPATITIS
= liver failure within 8 wks

DECOMPENSATED LIVER DISEASE

  • ascites
  • encephalopathy
  • GI haemorrhage

CHRONIC HEP B

  • fatigue
  • anorexia
  • nausea
  • abdo pain RUQ
146
Q

Hep C:

  • normal initial presentation?
  • other symptoms that may be present? 3
A

Early infection often mild/asymptomatic (85%)

May have similar mild systemic Sx to HBV:

  • Jaundice (20%)
  • fatigue
  • arthralgia
147
Q

Hep C:

- two biggest complications? 2

A

CIRRHOSIS
- 25% after 20 years

HEPATOCELLULAR CANCER
- highest risk of all Hep viruses

of those who get cirrhosis, 4% will get cancer

nb can also get other complications, eg:

  • glomerulonephritis
  • cryoglobinaemia
  • thyroiditis
  • autoimmune hep[atitis
  • PAN
  • polymyositis
148
Q

Hep D:

  • only risk factor? 1
  • how present?
  • blood test for? 1
A

NEEDS HBV for assembly

so HBV vaccine prevents HBD

presents similarly to Hep B! (as present simulataneously or after)

always do check ANTI-HDV ANTIBODIES (blood test) if Hep B positive

149
Q

Hep E:

  • main route of spread?
  • acute or chronic?
A

faecal-oral

?pigs in eastern europe?

almost always acute

150
Q

Hep E:

  • who most at risk of complications?
  • describe normal presentation?
A

Significant mortality in PREGNANCY

Similar presentation to Hep A

“think of as Hep A but affects pregnancy more and different geographical distribution”

151
Q

Findings on LFTS for Hep A, B and C?

A

ALT and AST both raised in all three

conjugated and unconjugated bilirubin can both be raised as well

152
Q

Two specific blood tests for Hep A? 2

what does the result of each test mean?

A

↑IgM +ve (from day 25 = acute/recent inf.)

↑IgG +ve detectable for life and indicates recovery or vaccination

153
Q

Meaning of the results of these tests in Hepatitis B:

  • HBsAg (surface antigen)
  • Anti-HBs (antibody against surface antigen)
  • Anti-HBc (antibody against core antigen)

ie which are positive/negative in:

  • vaccinated
  • past infection
  • acute infection
  • chronic infection (carrier)
A 
HBsAg 
= surface antigen
- vaccine = neg
- past inf = neg
- acute inf = POS
- chronic inf = POS
Anti-HBs 
= antibody against surface antigen
- vaccine = POS
- past inf = POS
- acute inf = POS
- chronic inf = POS
Anti-HBc 
= antibody against core antigen
- vaccine = neg
- past inf = POS
- acute inf = POS (IgM)
- chronic inf = POS (IgG)

“so if just had a vaccination then just touched the SURFACE of the condition - only get to the CORE if have/had disease”

“only detect ANTIGENS in active disease - antibodies if don’t currently have disease”

“if acute infection then IgM, if chronic IgG”

nb all of these are -ve if someone has not come into contact with virus or been vacinated!

nb there’s also an E antigen which is high in acute infection (but don’t bother remembering!)

154
Q

Aside from antibodies, antigens and LFTs, what other two tests can you do for Hepatitis B?

what test should you always do if you get a positive Heb B infection (or past infection)? 1

A

Hep B virus DNA serology (to confirm if any doubt)

liver biopsy (if complications / decompensated liver disease)

if positive, always check for anti Hep D antibodies

155
Q

HEPATITIS C investigations:

  • test to confirm exposure? 1
  • test to confirm ongoing infection/chronicity? 1
  • investigation to do if current infection to assess extent of liver damage? 1

nb also do LFTs as well!

A

confirms exposure
= anti-HCV antibodies

confirms ongoing infection / chronicity
= HCV-PCR

investigation to asssess liver damage
= liver biopsy

nb can also do hcv genotype

156
Q

Risk factors for progression of HCV to cirrhosis:

  • demographic? 2
  • lifestyle? 1
  • co-infection? 2
  • other? 1
A
  • male
  • older
  • use of alcohol
  • Hep b
  • HIV
  • higher HCV viral load
157
Q

What lifestyle management should all patients with any type of viral hepatitis be encouraged? 1

A

reduce alcohol (zero is best!)

if an acute virus, eg Hep A, stop alcohol until LFTs normalised!

158
Q

HEPATITIS A, B + E

- supportive / symptomatic treatment options in acute term? 3

A

IV fluids

anti-emetics (Metoclopramide)

Chlorphenamine (pruritis)

159
Q

1st line medical management for all viral hepatitises?

(ie in addition to supportive/symptomatic management)

additional medication required for Hep B and C?

A

Inferferon-A (an antiviral)

nb only use in Hep A and E if fulminant hepatitis occurs (rare)

basically need additional antivirals (2 or 3 in combo - don’t bother learning names!)

160
Q

which viral hepatitises need follow up with liver specialist? 3

definitive management if severe liver damage?

A

need follow up:

  • Hep B
  • Hep C
  • Hep D

liver transplant

(Hep C is leading indication for liver transplant in UK)

161
Q

Ascites:

  • most common group of causes? 1
  • second biggest group of causes? 1
  • other causes? 7
A

1)LIVER DISEASE (75%)

2) CANCER (15%)
- mainly GI tract (gastric, colonic, pancreatic, liver Ca), also Meigs syndrome (rare complication of ovarian cancer) or secondary liver mets

  • heart failure
  • kidney disease
  • TB
  • pancreatitis
  • hypothyroidism
  • protein-losing enteropathy
  • nephrotic syndrome
162
Q

Symptoms of ascites:

  • initial? 3
  • later? 3
  • clinical test for ascites? 1
A

EARLY

  • Abdominal DISTENSION (increases with time)
  • Abdominal DISCOMFORT (often mild. If severe, may be related to underlying malignancy)
  • WEIGHT GAIN (due to ↑fluid retention)

LATER

NAUSEA and ANOREXIA – due to pressure on stomach + s.bowel

DYSPNOEA – due to ↓venous return from lower limb from pressure on IVC and ↓expansion of lungs due to pressure on diaphragm

do SHIFTING DULLNESS to look for ascites

163
Q

Imaging needed for ascites? 2

other important investigation for ascites? 1 (excl bloods)

A

Abdo USS (often 1st line)

CXR – may demonstrate pleural effusion or pleural metastases or HF

Diagnostic ascetic tap or paracentesis – determines aetiology, detects cancerous cells, differentiates transudate vs. exudate, perform MC&S

164
Q

Two main complications of ascites? 2

A

HYPONATRAEMIA – diuretic effect of spironolactone or loops

HEPATORENAL SYNDROME – renal failure following liver failure (see cirrhosis notes)

165
Q

Causes of small bowel obstruction in adults? 4

which by far the most common?

A

Adhesions (60%)

Hernias (20%)

Volvulus (5%)

Gall stones (rare)

166
Q

Causes of large bowel obstruction in adults? 6

one other main cause in infants? 1

A
  • constipation
  • faecal impaction
  • stricture (eg dt diverticular / IBD)
  • volvulus (sigmoid – bowel twists upon mesentery)
  • colon Ca/malignancy,
  • hernia
  • Intussusception (infants)
167
Q

symptoms of bowel obstruction? 6

these are for both small and large bowel

A

Nausea + VOMITING

CONSTIPATION

ANOREXIA and DEHYDRATION
- (lack of colonic absorption)

Abdominal DISTENSION - ↑as obstruction progresses

Colicky ABDO PAIN
- Diffuse, central (typical)

168
Q

Different types of vomit you can get with bowel obstruction? 3

what does each indicate?

A

FAECULENT
- fermentation of intestinal contents in established obstruction

FAECAL
- colonic fistula within the proximal gut causes retrograde peristalsis

BILIOUS

  • bright green
  • indicative of small bowel
169
Q

Different types of costipation you can get with bowel obstruction? 2

what does each indicate?

A

Complete (faeces + flatus) = high obstruction

Partial (faeces)

170
Q

Main differences in presentation between large + small bowel obstruction? 3

A

LARGE BOWEL

  • distension more
  • vomiting is later
  • pain lower in abdomen and constant

SMALL BOWEL

  • vomiting is bilious + early
  • distension less
  • pain higher in abdomen
171
Q

ABDOMINAL EXAMINATION for ?OBSTRUCTION

  • clinical signs of obstruction? 3
  • what other two examinations should you do? (/body parts you should examine)
A

abdominal distension
- ↑Resonance on percussion

tender abdomen (diffuse)

Tinkling bowel sounds (LOUD)

examine

  • all hernial orrifices
  • do PR exam (ALWAYS!)
172
Q

1st line imaging for query bowel obstruction
- what does it show in small and large bowel obstruction?

what diameter (in cm) should these structures be on said imaging:

  • small bowel
  • caecum
  • large bowel

what other sign would you see if sigmoid volvulus is cause of obstruction?

A

1) ABDO X-RAY

SMALL BOWEL

  • central gas shadow
  • Valvulae Conniventes ladder like series (completely crosses lumen)
  • no gas in large bowel

LARGE BOWEL

  • peripheral gas proximal to blockage but not in rectum
  • haustra (do not fully cross lumen)
SMALL
- should be < 3cm
CAECUM
- should be < 6cm
LARGE 
- should be < 9cm

(if larger than this then suggests obstruction (or toxic megacolon etc)

COFFEE BEAN SIGN = sigmoid volvulus

173
Q

aside from abdo x-ray, what other imaging you should do? 1 (why?)

definitive imaging if obstruction confirmed? 1

A

CXR erect – determine if perforation (pneumoperitoneum)

Contrast enema CT – use to determine exact location of obstruction

174
Q

Three types of bowel obstruction?

nb this is not referring to small vs large bowel

A

Simple – one obstructing point, no vasc compromise

Closed loop – two points of obstruction, forms loop of grossly distended bowel (→ perforation typically at caecum (bowel is thin + wide))

Strangulated – blood supply compromised, patient toxic with peritonism the cardinal sign

175
Q

BOWEL OBSTRUCTION:
- 1st line supportive management for all? 2 (incl how to remember this)

definitive surgical management options?

A

“DRIP and SUCK”

  • IV fluids (and NBM)
  • NGT (ryles + food)

Also do a fluid chart

Also avoid any pro-kinetic drugs e.g. metoclopramide

EMERGENCY surgery (laparotomy) – if closed loop or strangulated or >12cm dilatation

Endoscopic stenting – useful in palliative + elderly pts.

Sigmoidoscopy + flatus tube – sigmoid volvulus

Right hemicolectomy – caecal volvulus (Rare)

DON’T LEARN specific names of surgery - just know broad different types: eg emergency laparotomy, stenting for palliative etc

176
Q

Complications of bowel obstruction?

describe signs / symptoms of each

A

STRANGULATED

  • sharp constant pain
  • local peritonism
  • fever
  • ↑WCC

PERFORATION

  • Fever
  • severe pain
  • toxic patient
177
Q

Two main DDx for bowel obstruction?

briefly describe each

ie things that present like obstruction but aren’t

A 
PSEUDO OBSTRUCTION (Ogilvie’s syndrome) – massive dilatation of colon ± s.intestine → mechanical like GI obstruction, no cause 
- basically mechanical obstruction but with no cause found

ILEUS

  • non-mechanical obstruction (ileus)
  • commonly paralytic i.e. absence of peristalsis → adynamic bowel
178
Q

ILEUS

  • what is it? (ie difference between this and obstruction)
  • iatrogenic causes? 3
  • other causes? 4
A

ILEUS = non-mechanical or functional obstruction, commonly paralytic i.e. absence of peristalsis → adynamic bowel
- ‘normal’ obstruction is actually mechanical obstruction (ie there’s something physically in the bowel!)

IATROGENIC

  • post-abdo surgery
  • Tricyclic anti-depressants
  • opioids

(nb other drugs too, but these most common)

OTHER

  • pancreatitis
  • peritonitis
  • uraemia
  • electrolyte disturbances (norm HYPOkalaemia, also ↓Mg+/↓Ca2+)
179
Q

ILEUS

  • three main symptoms / signs?
  • finding on PR exam?
A

Painless distension!

Bowel sounds absent entirely!!

No bowel movement or flatus

Large amounts of gas in rectum

180
Q

ILEUS:

  • supportive management? 2
  • definitive management?
A

“DRIP and SUCK”

  • IV fluids (and NBM)
  • NGT (ryles + food)

Also do a fluid chart

only do NG tube if vomiting etc - may be okay just with fluids and NBM

DEFINITIVE = treat underlying cause

eg just wait post-surgical, stop meds, correct electrolytes, treat pancreatitis and peritonitis

181
Q

IRRITABLE BOWEL SYNDROME (IBS)

  • what is it?
  • main demographic risk factors? 2
A

Abdo symptoms with no identifiable organic cause due to abnormal intestinal motility or ↑visceral perception

FEMALE>M (2:1)

≤ 40yo

nb also commonly have PMHx of mental health conditions

182
Q

SYMPTOMS of IRRITABLE BOWEL SYNDROME

- symptom criteria for diagnosis? 2 major 4 minor

A

Criteria for diagnosis:

ABDO PAIN relieved by defecation OR a/w altered stool form

AND > 2 of:

  • Altered stool passage (urgency, straining, incomplete evacuation)
  • Abdo bloating, distension or tension
  • Mucous PR
  • Worsening symptoms after food
183
Q

IBS

  • other non-bowel symptoms which may be present? 4
  • examination findings? 1
A
  • Lethargy
  • Nausea

Bladder symptoms - ↑freq, nocturia etc.

  • Back ache

Examination often normal
- Abdominal tenderness (general) is common

184
Q

What can often exacerbate symptoms of IBS? 3

A

Exacerbation with stress, menstruation or post-infective

185
Q

Differential diagnoses of IBS:

  • GI conditions? 7
  • other conditions? 3
  • iatrogenic? 1
A
  • crohns
  • ulcerative colitis
  • coeliac disease
  • lactose intolerance
  • diverticular disease
  • gastroenteritis (eg giardiasis)
  • colon cancer
  • endometriosis
  • ovarian tumours
  • hypo/hyperthyroid

medications, eg opioids, TCAs, calcium channel blockers

186
Q

Red flags for IBS which may indicate different diagnosis:

  • FHx? 3
  • age at presentation? 1
  • timing of symptoms? 2
  • presence of symptoms / signs? 4
  • findings on investigations? 1
A

FHx:

  • colon cancer
  • ovarian cancer
  • IBD

if >50 at presentation (GI or ovarian malignancy)

  • waking at night with pain / diarrhoea
  • timing cyclical with period (endometriosis)
  • mouth ulcers (crohn’s)
  • anorexia
  • weight loss
  • blood in stools (or on PR)

nb mucus is often present in IBS

red flags if any abnormality on bloods or other investigations

187
Q

Investigations for IBS:

  • bloods to do? (5 always, 1 to consider - when consider?)
  • bedside tests to do? (1 always, 1 consider)
  • when to refer for a colonoscopy? 3
A

Bloods – if Hx is classic IBS then:

  • FBC
  • LFT
  • ESR
  • CRP
  • TTG (Coeliac screen)

Serum CA-125 = exclude ovarian Ca (ESSENTIAL if >50yo woman, if high → urgent USS)

always do FAECAL CALPROTECTIN
- if raised, consider IBD

consider stool culture if diarrhoea prominent

Referral Colonoscopy – if > 50yo or any marker or organic disease (Blood PR, ↓Weight)

188
Q

MANAGEMENT OF IBS:

  • dietary advice?
  • other lifestyle advice? 1
  • 1st line management of constipation?
  • 1st line management of diarrhoea?
  • 1st line management of bloating / colic?
  • other 2nd line management options? 2
A

Regular meals, avoid missing meal or long gaps
8 cups fluid/d, restrict tea + coffee to 3/d, ↓fizzy drink/alc
↓high fibre food; starch; fruit (↓3/d)

encourage ↑exercise

CONSTIPATION
= Bisacodyl (stimulant) + Sodium Picosulfate (stool softener)
- (must avoid lactulose - osmotic)

DIARRHOEA
= Loperamide (take after each loose stool)

BLOATING / COLIC
= antispasmodics (eg Mebeverine, Alverine citrate)

2nd LINE

  • amitryptiline (or SSRIs)
  • CBT (if no response in 12mo)
189
Q

Rectal prolapse:

  • what is it? (describe the two different types)
  • describe common mechanism of how it occurs?
A

weak anal sphincter PLUS prolonged straining or chronic neuro/psych disorder → mucosa (partial/type 1), or all layers (complete/type 2 – more common) of rectum protrude through anus

nb can be Internal or External

190
Q

RECTAL PROLAPSE

  • biggest risk factors? 3
  • things that increase intra-abdominal pressure? 6
  • other rarer risk factors? 3
A

biggest:

  • ELDERLY
  • FEMALE
  • MULTIPAROUS

CAUSES OF ↑INTRA-ABDOMINAL PRESSURE

  • constipation
  • diarrhoea
  • BPH
  • preg
  • obesity
  • chronic cough (eg COPD, CF, Whooping cough)

OTHER RARER

  • pelvic floor dysfunction
  • parasitic infection
  • neuro disease (lumbar disc disease, cauda equine synd)
191
Q

RECTAL PROLAPSE

  • describe the features that occur as it gets worse?
  • specific associated symptoms that can also occur? 6
A

Mass protruding through anus:

1) Initially after bowel movement, retracts spontaneously
2) Then protrudes often, with straining + valsalva manoeuvres e.g. cough, sneeze
3) Late protrudes w/ normal ADL, manually replace

  • Pain
  • Constipation
  • Faecal incontinence (75% - common in external)
  • discharge of mucous
  • rectal bleeding
  • Ulceration if external
192
Q

Rectal prolapse:

  • part of abdomainal exam you always have to do if suspect? 1 (and findings)
  • other investifgations to consider? 2
A

DRE – protruding mass (w/ concentric rings of mucosa), rectal ulcers, ↓anal tone

Barium enema /Colonoscopy – evaluate colon prior to surgery to exclude other lesion

Stool microscopy/cultures – GI infection

193
Q

Conservative (ie non-surgical) management options for rectal prolapse:

  • children? 3
  • elderly? 2
A

Child

  • Use water-soluble lubricant
  • High fibre diet
  • Mild laxative

Elderly

  • Manually reduce prolapse – covering w/ sugar ↓swelling
  • Subcutaneous circumanal rubber ring
194
Q

Surgical management options for rectal prolapse?

A

RECTO-SIGMOID-ECTOMY
- if prolapse is strangulated

HAEMORRHOIDECTMY
- if simply mucosal prolapse

ABDOMINAL PROCEDURES

  • preferred and include either
  • – Marlex rectopexy (Ripstein’s), suture rectopexy, resection rectopexy (Frykman-Goldberg)

PERINEAL PROCEDURES
- ↑recurrence rate
- ↓morbidity
eg Anal encirclement (Thiersch;s wiring), Derlome’s mucosal sleeve resection (common), Altemeir’s perianal rectosigmoidoscopy

don’t learn details: just know conservative options and broadly different types of surgery

195
Q

HAEMORRHOIDS:

  • describe what they are / the pathoplogy?
  • two different types? (and the 4 degrees of one type)
A

straining, effects of gravity (erect posture) and ↑anal tone → disrupted and dilated anal cushions → piles
– vulnerable to trauma + bleeds readily

different types:

EXTERNAL (below dentate line)
– more prone to thrombosis

INTERNAL (above dentate line) grading:

  • 1st degree = remains in rectum
  • 2nd degree = prolapse through anus on defecation, spontaneously resolves
  • 3rd degree = requires digital reduction
  • 4th degree = remain persistently prolapsed, cannot be reduced

nb haemorrhoids is the Greek word for running blood

196
Q

HAEMORRHOIDS:

- risk factors? 5

A
  • Constipation
  • pelvic tumour
  • preg
  • CCF
  • portal HTN

Basically any type of congestion downstream in the blood vessels

197
Q

HAEMORRHOIDS:

  • local symptoms? 4 (which of these is most common?)
  • possible systemic symptom? 1
A

1) PAINLESS Rectal BLEED – bright red (most common)
- Often coats stools, on tissue or dripping in toilet post-defecation

  • Pruritis ani (irritation of anal region)
  • Mucous discharge
  • Rectal fullness or discomfort
  • Anaemia/fatigue due to bleed
198
Q

When are haemorrhoids painful?

A

piles are not painful (unless THROMBOSED when gripped by anal sphincter – blocking venous return)

199
Q

HAEMORRHOIDS:

- what are red flag symptoms that suggest an alternative diagnosis? 3

A
  • Weight loss
  • tenesmus
  • change in bowel habit
200
Q

HAEMORRHOIDS:

  • first thing to do if suspect?
  • other investigations to possibly consider? 3
A

Abdominal + PR exam – (1st line) palpate 3 cushions, prolapsing piles are obvious, internal haemorrhoids are not palpable

OTHER INVESTIGATIONS TO CONSIDER

FBC - if think also anaemic

Proctoscopy – visualise internal haemorrhoids + other causes for bleeding

Sigmoidoscopy – visualise high rectal pathology

201
Q

MANAGEMENT of HAEMORRHOIDS:

  • lifestyle advice for all? 2
  • 1st line medical options? 2 (eg for 1st degree)
  • 1st line non-operative option for 2nd/2rd degree? 1
  • other non-operative options? 3
  • surgical options? 2
A

LIFESTYLE

  • ↑Fluid intake
  • ↑Fibre

MEDICAL – eg for 1st degree haemorrhoids:

  • analgesia (Topical/PO analgesics + steroids)
  • Stool softener

avoid codeine (↑constipation), NSAIDs (worsens bleeds)

NON-OPERATIVE – for 2nd/3rd degree

  • RUBBER BAND LIGATION (1st line) – low recurrence rate, band is applied to base of haemorrhoid causing strangulated haemorrhoid to become necrotic and slough off

others:
- Sclerotherapy (high recurrence)
- Infra-red coag
- Cryotherapy – high complication rate
^don’t bother learning these 3 methods

SURGICAL

1) EXCISIONAL HAEMORRHOIDECTOMY – most effective Tx involves excision of piles ± ligation of vasc pedicles
2) STAPLED HAEMORRHOIDECTOMY – circular stapling gun excises haemorrhoid

202
Q

Main complication of haemoarrhoids? how does it occur?

A

Strangulation a “vicious cycle” – vascular cushions protrude through tight anus → ↑congestion + hypertrophy of cushions → ↑frequency of protrusion → ↑risk of strangulation → pain!!

203
Q

Differential diagnoses for haemorrhoids? 4

A
  • Perianal haematoma
  • anal fissure/abscess,
  • Proctalgia fugax (aka functional recurrent anorectal pain - diagnosis of exclusion)
  • rectal cancer
204
Q

ANORECTAL / PERIANAL ABSCESS:

  • most commmon causative organisms? 2
  • other causes? 2
  • most common location? 1
A

= Abscess (collection of pus) located in anal or rectal region

  • E. Coli
  • Staph Aureus

also:

  • STI
  • blocked anal glands

PERI-ANAL (45%)

Can also be Ischiorectal (<30%) or Intersphincteric (>20%)

205
Q

RISK FACTORS for ANORECTAL / PERIANAL ABSCESS:

  • GI conditions? 3
  • other medical conditions? 2
  • lifestyle factor? 1
A
  • Crohn’s disease
  • diverticulitis
  • anal / colorectal cancer
  • diabetes mellitus
  • immunocompromised
  • anal sex
206
Q

clinical presentation of ANORECTAL / PERIANAL ABSCESS:

  • how describe presentation?
  • associated symptoms? 4
A

Painful (throbbing, worse when sat down) +

Hardened tissue in peri-anal area – erythematous, swollen, tender

Lump or nodule at anus

  • Discharge of pus from rectum
  • Fever
  • Constipation
  • Pain a/w bowel movement
207
Q

investigations for ANORECTAL / PERIANAL ABSCESS:

  • bedside examination? 1
  • additional investigation to consider? (why do?)
A

DRE – usually sufficient for diagnosis

Procto-sigmoidoscopy – may be performed to exclude associated diseases / risk factros (see prev flashcard)

208
Q

management of ANORECTAL / PERIANAL ABSCESS:

  • surgical? 1
  • medical for all? 1
  • additional medical to consider? 1 (who gets?)
A

1) Surgical incision + drainage
2) Analgesia
3) Abx – not usually necessary unless a/w DM or immunosuppression

209
Q

Main complication associated with anorectal / perianal abscesses?

what % get this?

A

Fistula-in-ano – 40% of abscess pts.

210
Q

Differential diagnosis for anorectal / perianal abscess? 2

A

inflammatory bowel disease

anal / colorectal cancer

211
Q

ANAL FISSURE

  • aka?
  • what is it?
  • how common?
A

aka Fissure-in-ano

nb don’t confuse with FISTULA-in-ano

Painful tear in squamous mucosa of lower anal canal (often chronic w/ sentinel pile or mucosal tag externally)

common – 11% lifetime incidence

212
Q

ANAL FISSURE:

  • mechanical causes? 3
  • infectious causes? 2
  • GI conditions associated with? 2
A
  • constipation / hard faeces
  • spasms (→constricts rectal artery →ischaemia → ↓healing ability)
  • trauma
  • syphilis
  • herpes
  • crohn’s
  • anal cancer
213
Q

ANAL FISSURE:

  • age and gender most affected?
  • definition of timeframe of acute and chronic?
A

Common between 20-40yo

M=F

Acute < 6 wks

Chronic ≥ 6 wks

214
Q

ANAL FISSURE:
- two main symptoms?

describe the each (exacerbating features, character etc)

A

1) ANAL PAIN
- Exacerbated by defecation
- Feels like passing shards of glass
- Persists several hours post-defecation

2) BLEEDING during defecation
– FRESH, bright red

215
Q

ANAL FISSURE:

  • examination? 1
  • findings on exam? (incl features of acute vs chronic + primary vs secondary)
A

Fissure visualised on EXTERNAL exam of anus
– linear split of mucosa

Part the buttocks gently to view

Majority are posterior in midline

Acute
= clear edges, liner
Chronic
= deep, a/w external skin tag

Secondary
= tend to be multiple
Primary
= tend to be single

Do not attempt DRE – VERY PAINFUL!!!!

216
Q

ANAL FISSURE:

  • 1st line oral meds to give? 2
  • 1st line topical management to consider? 2
  • 2nd line topical management options? 2
A

1) ANALGESIA
– Paracetamol or Iburpofen
- Do not prescribe opioids (will exacerbate)

2) Bulk forming LAXATIVE – 1st line

TOPICAL

1) TOP ANAESTHETIC
– Lidocaine 5% ointment (severe pain)

2) PR GTN ointment
– if primary anal fissure with symptoms > 1 week w/o improvement

2ND LINE
- TOP Diltiazem
- TOP Botulinum toxin
(don’t bother learning this)

217
Q

Lifestyle advice to prevent future anal fissures? 3

A

Good anal hygiene,

Avoid stool holding,

Soak in shallow warm bath

218
Q

Differential diagnosis for anal fissure? 4

A

Haemorrhoids,
Abscess,

Proctitis,
Perianal sepsis

219
Q

SIGMOID VOLVULUS:

  • describe how occurs? (ie patholoogy)
  • main two complications? 2
A

chronic constipation → colon becomes distended with gas → twists on mesenteric pedicle → CLOSED LOOP OBSTRUCTION

if not treated quickly can → venous INFARCTION → PERFORATION → faecal peritonitis

220
Q

SIGMOID VOLVULUS:

  • age and gender most at risk?
  • other risk factors? 3
A
  • elderly
  • Male
  • chronic constipation or laxative use
  • crohn’s disease
  • prev abdo surgery
221
Q

SIGMOID VOLVULUS:

  • main symptoms? 3
  • late symptom? 1

how to distinguish from other causes of bowel obstruction? 2

A

Acute abdominal PAIN
– Colicky

GROSS Abdominal DISTENSION

CONSTIPATION
– Failure to pass stool OR FLATUS

Vomiting (late typically, at this point distension is severe)

how to distinguish from other causes of large bowel obstruction:

  • increased speed of onset (over a few hours)
  • increased degree of abdo distension

NB: it may present insidiously with chronic abdo distension, constipation, vague colicky pain, vomiting

222
Q

SIGMOID VOLVULUS:

  • main sign on abdo exam? 1
  • other possible signs? 2
  • add-on to do? finding? 1
A

GROSS abdo DISTENSION

  • INCREASED resonance to precussion
  • palpable mass (maybe)

DRE
– test for passage or presence of flatus or stool
- Often find EMPTY RECTAL AMPULLA

223
Q

SIGMOID VOLUVULUS:

  • main two complications?
  • symptoms / signs of these?
  • how to manage if suspect these?
A
  • bowel wall ischaemia
  • perforation (norm follows ischaemia)
  • blood-stained stool
  • peritonitis
  • shock
  • increased temp

need EMERGENCY surgery!! (norm laparotomy - if fit enough!)

224
Q

SIGMOID VOLVULUS:

  • 1st line imaging to do? 2 (SPECIFIC findings on these)
  • additional imaging to do before surgery? 1
A

AXR
– Single grossly dilated sigmoid loop > 9cm (COFFEE BEAN)
– commonly reaches xiphisternum

Erect CXR
– exclude perforation (air under diaphragm)

CT abdo – allows visualisation of volvulus and assessment of bowel wall ischaemia

225
Q

SIGMOID VOLVULUS

  • describe initial conservative management? 1
  • surgical management? 1 (incl timescale for this)
A

1) URGENT DECOMPRESSION
- Pt. lies left lateral, insert Sigmoidoscope into rectum as far as possible and pass Flatus tube alongside
- Manoeuvre into obstructed loop through twisted bowel
- Rush of liquid faeces and flatus → relieves obstruction
- Leave tube in situ for 24hrs – maintains decompression, prevents recurrence, promotes bowel’s vascular supply recovery

2) SURGICAL
- After conservative Tx, recurrences occurs therefore elective surgery is frequently required
- Resection of redundant sigmoid colon – usually a double barrel colostomy (Paul-Mikulicz)

226
Q

SIGMOID VOLUVULUS;

- main group of differential diagnoses?

A

other causes of LARGE BOWEL obstruction (eg cancer, faecal impaction, strictures, hernias etc)

also consider pseudo obstruction, ileus etc

also could be a giant sigmoid diverticulum

*year 5 (8 decks)

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