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BRS 2 > gastro > Flashcards

gastro Flashcards

1
Q

LOS anatomical contributions?

A

left and right crux of diaphragm
phrenosophageal ligament
angle of his - prevents reflux

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2
Q

stages of swallwpoing?

A

stage 0, oral - chewing and saliva, both sphincter closefd
1 , pharyngeal - UOS open reflexively, LOS opened by vasovagal reflex (receptive relaxation reflex)
2 , UO - UOS closes, contractions of circular and long muscles
3 LO - LOS closes

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3
Q

how can oesophageal motility be measured?

A

manometry

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4
Q

normal oesophageal pressures?

A

peristaltic - 40 mmHG
LOS resting - 20 mmHG
LOS receptive relaxation - <5mmHg

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5
Q

what is receptive relaxation mediated by?

A

inhibitory noncholinergic nonadrenergic neurons of myenteric plexus

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6
Q

what do you call pain on swallowing?

A

odynophagia

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7
Q

regurg vs reflux?

A

return of oesophageal contents from above obstruction

passive return of gasproduodenal contents to mouth

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8
Q

what causes oesophageal hypermotilitiy?

A

achalasia

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9
Q

pathophysiology of achalasia?

A

loss of ganglion cells in auerbachs myenteric plexus in LOS wall → ↓ activity of inhibitory NCNA neurones (less relaxation , more contraction) → ↑ resting LOS pressure → food collects in oesphagus → ↑ pressure → dilation → peristalsis stops

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10
Q

causes of achalasia?

A

primary - unknown

secondary - chagas disease, protozoa infection, amyloid, sarcoma, eosinophilic oesophaigtiis

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11
Q

onset of achalasia?

A

insidious

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12
Q

what does acahalsia largely increase the risk of ?

A

oesophageal cancer

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13
Q

treatment options for achalasia?

A

pneumatic dilatation - weakens LOS by stretching or tearing
Hellers myotomy - removal of muscle from stomach and oesophagus
dor Fundoplication - anterior funds folded over oesophagus and sutured to right side of myotomy
peroral endoscopic myotomy

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14
Q

what causes oesophageal hypomotility?

A

scleroderma

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15
Q

pathophysiology of scleroderma?

A

neuronal defects → atrophy of oesophageal smooth muscle → distal peristalsis ceases → ↓ LOS resting pressure → GORD develops

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16
Q

causes of scleroderma?

A

autoimmune

assoicted with CREST syndrome

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17
Q

treatment options for scleroderma?

A

pro kinetics to improve peristalsis force - cisapride

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18
Q

pathophysiology of corkscrew oesophagus?

A

incoordinate contractions → dysphasia and chest pain
pressures of 400-500 mmHg
circular muscle hypertrophy
corkscrew appearance on barium swallow

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19
Q

treatment options for corkscrew oesophagus?

A

forceful pneumatic dilatation of cardia

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20
Q

2 types of vascular anomalies that can. cause dysphagia?

A

dysphagia lusoria - aberrant right subclavian artery

double aortic arch

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21
Q

3 most likely areas of oesophageal perforations?

A

cricopharangeal, aortic & bronchial, diaphragmatic constrictions

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22
Q

cause of osphaegal perforations?

A 
iatrogenic
boerhaaves
foreign body
trauma
intraoperative
malignancy
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23
Q

what procedure is oesophageal perf likely to occur?

A

OGD especially if diverticula or cancer

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24
Q

how can boerhaaves cause oesophageal perf?

A

sudden ↑ in intra oesophageal pressure w negative thoracic pressure (vomitting against closed glottis)

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25
Q

symptoms of traumatic oesophageal perf?

A

dysphagia
blood in salvia
haematemsis
surgical emphysema

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26
Q

how does oesophageal perf usually present?

A

pain, fever, dysphagia, emphysema

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27
Q

oesophageal perf investigations?

A

CXR
CT
gastrogaffin swallow
OGD

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28
Q

management of oesophageal perf?

A 
NBM, IV fluids, BS Abs & antifungals 
ITU/HDU
bloods
tertiary referal 
surgery
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29
Q

when is surgery not default management for oesophageal perf?

A

if theres minimal contamination, its contained or patient is unfit

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30
Q

surgical options for oesophageal perf?

A

vascularised pedicle flap
dor fundoplication
drains
oesophagectomy

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31
Q

what increases LOS pressure?

A

acetylcholine , a adrenergic agonists, protein food, high intraabdominal pressure → reflux inhibited

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32
Q

what decreases LOS pressure?

A

VIP, B adrenergic antagonists, dopamine, NO, chocolate, fat, smoking → promotes reflux

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33
Q

what can causes sporadic reflux?

A

pressure on full stomach
swallowing
transient sphincter opening

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34
Q

what mechanisms protect the oesophagus following reflux?

A

volume clearance - oesophageal peristalsis reflex
pH clearance - saliva
epithelium - barrier properties

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35
Q

outline the process of oesophageal protective mechanisms failing (GORD)

A

↓ sphincter pressure, ↑ transient sphincter opening. ↓ saliva production/buffering capacity, defective mucosa, hiatus hernia
→ → reflux oesphagitis → epithelial metaplasia → carinoma

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36
Q

Ixs for GORD?

A

OGD
manometry
24 hr oesophageal pH recording

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37
Q

treatment options for GORD?

A

lifestyle - wt loss, less EtOH, x smoking
PPIs
dilatation peptic strictures
laparoscopic Nissans fundoplication (wrapping funds around oesophagus)

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38
Q

areas of stomach and what they secrete?

A

cardia & pylorus - mucus
body & fundus - mucus, HCl, pepsinogen
antrum - gastrin

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39
Q

causes of erosive & haemorhagic gastritis?

A 
NSAIDS
iscahemia
trauma
alcohol
bruns
MOF
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40
Q

what doe erosive & haemorhagic gastritis lead to?

A

acute ulcer → gastric bleeding/perforation (anywhere in stomach)

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41
Q

cause of nonerosive chronic active gastritis?

A

H pylori (antrum)

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42
Q

Tx for H pylori gastritis?

A

amoxicillin. clarithromycin and pantoprazole for 7-14/7

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43
Q

pathophysiology of atrophic fundal gland gastritis?

A

autoantibodies against parts and products of parietal cells in fundus → parietal cells atrophy → ↓ acid & IF secretion (( → ↑ gastrin secretion → ECL hyperplasia → carcinoid )) ((→ pernicious anaemia)

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44
Q

what stimulates gastric secretions?

A

acetylcholine from vagus ps fibres
gastrin from antrum g cells
histamine from ECL and mast cells

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45
Q

what inhibits gastric secretions?

A

secretin in SI
somatostatin
prostaglandins, TGF-a, adenosine (decreased by NSAIDs)

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46
Q

how does the mucosa protect against acid?

A

mucus film
HCO3- secretion (requires prostaglandins)
epithelial barrier (tight junctions)
mucosal blood perfusion (will take away any H ions that get through)

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47
Q

mechanisms of repairing epithelial defects?

A

migration of epithelial cells - close gap
cell growth - stimulated by EGF, TGF-a, IGF1, gastrin
leukocytes and macrophages remove necrotic cells, angiongesis, ECM regeneration, cell division.

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48
Q

what can cause an ulcer formation?

A 
increased HCl secretion
h pylori
reduced HCO3- secretion
↓ cell formation
↓ blood perfusion
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49
Q

treatment options for ulcers?

A

PPI/H2 blocker
amoxicillin, clarithromycin, pantoprazole 7-14/7
elective sx

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50
Q

if ulcers don’t heal w medcial tretamet what do you do?

A 
should heal in 12 weeks, if not change medication
check serumgastrin (g cell hyperplasia or gastronoma)
OGD
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51
Q

when should sx be considered for ulcers?

A 
intractability of medical therapy
haemorrhage
obstrucion
perforation
relative eg. need of nsaids or steroids
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52
Q

what is riglers sign?

A

free intraperitoneal air from perforated viscus

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53
Q

what is indicative of perforated viscus on x ray?

A

free intraperitoneal and subdiaphrgamatuic air

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54
Q

most common site of ulcers in GIT?

A

first part of duodenum / pylorus

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55
Q

what criteria is used to assess acute pancreatitis?

A

modified glasgow criteria
PANCREAS
score ≥3 within 48hrs onset = severe pancreatitis
(or CRP ≥200)

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56
Q

acute pancreatitis management?

A 
fluid resus
analgesia
pancreatic rest ± nutritional support
determine cause
severe → HDU
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57
Q

level and structure at subcostal plane?

A

L3 - IMA

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58
Q

level and structure at supracristal plane?

A

l4 - bifurcation of aorta

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59
Q

foregut , midgut and hindgut locations?

A

f - distal oesophagus to 2nd part of duodenum
m - distal 2nd half of duodenum to primal 2/3 transverse colon
h - distal2/3 transverse colon to rectum

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60
Q

differences between visceral and parietal pian?

A

v - dull, crampy, burning, autonomic, embryological origin

p - sharp, ache, well-localised, somatic

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61
Q

foregut , midgut and hindgut innervation and pain site?

A

f - t5-t9, epigastrium
m - t10-t11, umbilical
h - l1-l2, suprapubic

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62
Q

constant vs colicky pian?

A

constant - inflammation, worse with movement, spleen, kidney, liver
tubular obstruction - fluctuates in severity, move to try get comfort, ureter, gallbladder, bowel

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63
Q

colicky pain that becomes constant suggests?

A

ischemia

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64
Q

what is the most potent stimulus for drinking water?

A

plasma osmolality increase

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65
Q

where does ADH act?

A

aquaporin 2 channels in CD

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66
Q

where are osmoreceptors found?

A

hypothalamus - organum vasculosum of lamina terminals and subfornical organ

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67
Q

how do osmoreceptors lead to ADH release?

A

concentrated plasma → cells shrink → ↑ proportion of cation channels → membrane depolarises & ↑ firing frequency → ↑ signals to post pitutuirary → ↑ ADH produced → fluid retention and drinking

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68
Q

what are the effects of angiotensin II?

A

vasoconstriction
↑ sympathetic activity
thirst
stimulate aldosterone release from adrenal cortex zona glomerulosa
water retention via na absorption and k excretion
adh secretion

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69
Q

structure and function of arcuate nucleus?

A

in hypothalamus
has incomplete BBB allows access to peripheral hormones
stimulatory neurons - NPY & Argp (orexigenic)
inhibitory neurons - POMC (anorexigernic)
regulation food intake by integrating central and peripheral signals

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70
Q

which neuorones does leptin stimulate and inhibit?

A

stim - POMC

inhibit - NPY & ARGP

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71
Q

what happens when POMC neurons are stimulated?

A

release a-MSH which stimulates MC4R in the paraventricular nucleus → ↓ food intake

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72
Q

what happens when ARGP neurons are stimulated?

A

MC4r in paraventrivcular nucleus is inhibited → ↑ food intake

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73
Q

what can cause morbid obesity?

A

MC4R mutations

POMC deficiency

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74
Q

what is the adipostat mechanism?

A

adipostat hormone produced from fat → detected b y hypothalamus → alters neuropeptides to increase/decrease food intake

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75
Q

what is leptin?

A

hormone made by adipocytes and circulates in plasma
acts on hypothalamus to regulate appetite and thermogenesis
eg ↑ leptin → ↓ decreased appetite & ↑ energy expenditure

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76
Q

obesity in relation to leptin?

A

obese people have ↑ leptin but also have leptin resistance so has no effect

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77
Q

what gut hormones regulate appetite?

A

ghrelin → stims appetite and gastric emptying

peptide YY → ↓ food intake

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78
Q

when are ghrelin levels highest?

A

just before meals

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79
Q

ghrelin functions?

A 
↑ gastric motility 
↑ acid secretion 
stimulate ARGP & NPY neurons
inhibit POMC neurons 
increase appetite
80
Q

where and when is PYY released?

A

terminal ileum and colon in reposing to feeding

81
Q

function of PYY?

A

↓ appetite
inhibits NPY release
stimulates POMC neurons

82
Q

what is dysbiosis?

A

when theres altered microbiota composition in the gut eg more pathobionts

83
Q

what can cause dysbiosis/

A 
infection
diet
xenobioitcs
hygiene
genetics
84
Q

what are the physical barriers to pathogens in the gut?

A

epithelial barrier
peristalis
enzymes
acidic pH

85
Q

immunological tissues of the gut?

A

Mucosa associated and gut associated lymphoid tissue

86
Q

how does the epithelial barrier defend against pathogens?

A

goblet cells produce a mucus layer
monolayer with tight junctions preventing entyr
paneth cells in crypts of Lieberkuhn → antimicrobial peptides/defensins and lysozyme

87
Q

structure and location of MALT?

A

submucosa below epithelium
lymphoid mass containing follicles surrounded by HEV post capillary venues → easy passage of lymphocytes
found in oral cavity

88
Q

what cells does GALT contain?

A

B & T lymphocytes , macrophages, APC, specific epithelial lymphocytes

89
Q

types of GALT?

A

unorganised : intraepithelial and lamina propria lymphocytes

organised : Peyers patches (SI) , caecal patches (LI), isolated lymphoid follicles, mesenteric lymph nodes

90
Q

structure and location of peyers patches? how do they facillitate antigen uptake?

A

submucosa of SI , distal ileum
aggregated lymphoid follicles covered in follicle associated epithelium
no goblet cells, microvilli or IgA
organised collecting of naive T&B cells
M cells in FAE take up antigens
M cells have IgA receptors to transfer IgA-bacteria complex into patch

91
Q

how do antigens enter peyers patches?

A

m cells have IgA receptors which can help transfer antigen-iga complex into patch
OR
transepithelial dendritic cells can take up antigens

92
Q

outline the B cell adaptive response in peyers patches?

A

T cells an epithelial cells influence B cell maturation via cytokines
naive B cells express IgM and then switch to IgA upon antigen presentation
populate lamina propria

93
Q

function of secretory IgA?

A

secreted by B cells

binds luminal antigens → prevent adhesion and invasion

94
Q

why do enterocytes have a rapid turnover?

A

~36hrs
can be directly affected by toxins in diet
turnover diminishes any negative effects

95
Q

outline pathogens is of cholera infection?

A

vibrio cholera → releases cholera enterotoxin → ↑ adenylate cyclase activity → ↑cAMP → ↑ active transport of ions into gut lumen → ↑ water secretion → diarrhoea

96
Q

symptoms of cholera?

A 
dehydration
watery diarhoea
vomiitng
nasuea
abd pain
97
Q

how is cholera diagnosed?

A

bacterial culture from stool sample on selective agar

or dipstick

98
Q

cholera treatment?

A

oral rehydration

99
Q

vaccine against cholera?

100
Q

most common cause of watery diarrhoea in children?

101
Q

vaccination against rotavirus?

102
Q

viral causes of infectious diarrhoea?

A

rotavirus

norovirus

103
Q

bacterial causes of infectious diarrhoea?

A

salmonella
e coli
Campylobacter jejuni - undercooked meat, untreated water and milk, azithromycin
clostridium difficile

104
Q

management for c diff diarrhoea?

A

isolation
stop current Abs
giver metronidazole / vancomycin
faeceal microbiota transplantation

105
Q

medical condition causes of secondary polydipsia?

A 
diabetes insipidus and mellitus 
kidney failure
conns syndrome 
Addisons disease
sickle cell anaemia
106
Q

what medications can cause secondary polydipsia?

A

laxatives
diuretics
antidepressants

107
Q

causes of primary polydipsia?

A

mental illness - schizophrenia , depression, anxiety, anorexia, drugs
brain injuries
organic brain damage

108
Q

systemic effects of polydipsia?

A 
kidney and bone damage
headache
nasuae
cramps
slow refelxes
slurred speech 
low energy
confusion
seizures
109
Q

types of eating disorders?

A 
binge eating
anorexia nervosa
bulimia nervosa
pica
rumination syndrome
avoidant/restrcitve eating
110
Q

how is anorexia staged?

A

mild BMI≥17
moderate 16-16.99
severe 15-15.99
extreme ≤15

111
Q

what neurotransmitter is involved in anorexia?

112
Q

how is obesity defined?

A

BMI ≥30
or
BMI ≥25 + comorbidity/risk factor

113
Q

when is surgical treatment indicated for people with obesity? options?

A

BMI ≥40 or ≥35 + comorbidity
gastric bypass & sleeve gastrectomy
remission of diabetes and OSA

114
Q

how does bariatric sx help with obesity?

A

reduces ghrelin → less appetite (stomach becomes full w less food)
↑ GLP1&2 (L cells) & PYY → ↑ insulin release . ↓ glucagon , ↑ satiety

115
Q

causes of non infectious diarrhoea?

A 
antibioitcs
IBD
post infectious IBS
microscopic or iscahemic colitis 
coeliac disease
haemorrhoids
116
Q

how is dirhaoea classified?

A

non-severe - WCC < 15, creatine <150
severe WCC ≥ 15, creatinine ≥150
fulminant colitis - hyoptension/shock/ileus/toxic megacolon

117
Q

antibiotics for diarhoea?

A

vancomycin
fidaxomicin
metronidazole

118
Q

how is toxic megacolon seen ion X-ray?

A

dilated small and large bowel

119
Q

when is surgery indicated for fulminant colitis?

A 
colonic perf
necrosis or full thickness ischaemia
intra abd hypertension / abd compartment syndrome 
signs of peritonitis 
end organ failure
120
Q

what is pseudomembranous colitis?

A

associated w c diff
severe colonic disease
yellow white plaques that form pseudomembranes on mucos
confirmed with endoscopy ± biopsy

121
Q

what would suggest non infectious diarrhoea instead of infectious?

A

chronicity

122
Q

ulcerative colitis management?

A

steroids
mesalazine
immunosuppressants - azathioprine, methotrexate
biologics - anti-TNF

123
Q

impacts of malnutrition?

A 
greater postoperative mortality
poorer clinical outcomes 
functional decline 
↑ hospital stay
pressure sores
re-admssions 
public health cost
124
Q

causes of malnutrition in hospital?

A 
co-morbidites
repeated NBM
mealtime inflexibility
poor dentition
dysphagia
low mood 
poly pharmacy 
disease related
125
Q

indications for nutrition support?

A

BMI < 18.5
unintentional weight loss ≥10% in last 3-6/12
BMI < 20 and unintentional weight loss ≥5% in last 3-6/12
eaten little/nothing for ≥5days
poor absorptive capacity/high nutrient losses

126
Q

types of artificial nutrition support?

A

enteral (superior)

parenteral when GI tract isnt functional/accessible

127
Q

types of enteral feeding?

A

NGT - gastric feeding possible
NDT/NJT - gastric outlet obstructions
longer than 3 months - gastrostomy/jejunostomy

128
Q

complications of enteral feeding?

A 
misplacement/blockage
hyperglycaemia
deranged electrolytes
aspitation
pian
laryngeal ulceration
vomting
diarrhoea
129
Q

why is albumin low during ↑ inflammation?

A

cytokines act on liver to down regulate production

130
Q

what is refeeding syndrome?

A

occurs in malnourished or starved patient on the reintroduction of oral, enteral, parental nutrition

starvation → glycogenolysis, gluconeogensis → protein, fat, electrolyte ↓↓ → refeeding with fluids salts nutrients → ↑ insulin → protein and glycogen synthesis → ↑ glucose and electrolyte uptake → hypokalamia, magnesaemia, phosphataemia , ↓ thiamaine, oedema

131
Q

what are the consequences of refeeding syndrome?

A 
arrhythmia 
tachycardia
heart failure
resp depression
encephalopathy 
wernickes encephalopathy
132
Q

what is an early indicator of adequate nutritional support?

A

hand grip strength

133
Q

target stoma output?

134
Q

two types of oesophageal cancers?

A

squamous cell carcinoma - upper 2/3, acetaldehyde pathways, more common in less developed world

adenocarcinoma - metaplastic columnar epithelium, lower 1/3, acid reflux, more in developed countries

135
Q

what is the progression from reflux to oesophageal cancer?

A

oesophagi’s → barret’s oesophagus (metaplsia) → low grade dysplasia → high grade dysplasia → adenocarcinoma (neoplasia)

136
Q

what are the barret’s surveillance guidelines?

A

no dysplasia → every 2-3 years
low grade dysplasia → every 6 month
high grade → intervention

137
Q

how can oesophageal cancer present→?

A

late presentation
dyspahgia
wt loss

138
Q

radical surgery option for oesophageal cancer?

A

neo-adjuvant chemo→ oesophagectomy (Ivor lewis approach)

139
Q

causes of colorectal cancer?

A

sporadic - older people
familial
hereditary syndrome , eg familial adenomatous polyposis

140
Q

how can caecal and right sided colon cancer present?

A

iron deficiency anaemia
change of bowel habit eg diarhoea
distal ileum obstruction
palpable mass

141
Q

how can sigmoid and left sided colon cancer present?

A

pr bleeding
mucus
thin stool

142
Q

rectal carcinoma presentation?

A

PR bleeding, mucus
tenesmus
anal, perineal, sacral pain

143
Q

presentations of colorectal cancer that has metastasised?

A 
jaundice, hepatomegaly 
cough, monophonic wheeze
bone pain 
regional lymph nodes
sister Mary Joseph nodule - peritoneum
144
Q

examinations of primary colorectal cancer?

A

abdominal mass
felt on DRE
rigid sigmoidoscopy
abdo tenderness and distension

145
Q

investigations for colorectal cancer?

A

faecal occult blood using faecal immnochemical test (FIT) (avoid red meat, nsaids, vit c before test)
blood tests : FBC, tumour marker (CEA useful for monitoring)
colonoscopy - can see lesions<5mm and remove small polyps
CT colonoscopy/graphy - can see lesions ≥5mm , less invasive
MRI pelvis - rectal cancer
CT chest/abdo/pelvis for staging

146
Q

colorectal cancer management?

A

right sided/transverse : resection (right hemicolectomy) and primary anastamosis

left sided : hartmanns procedure (proximal end colostomy) , primary anastomosis, palliative stent

147
Q

what is the commonest form of pancreatic cancer?

A

pancreatic ductal adenocarcinoma

148
Q

risk factors for pancreas canc er?

A

chronic pancreatitis
T2DM
smoking
family hx

149
Q

how do PDAs evolve?

A

non-invasive neoplastic precursor lesions (pancreatic intraepithelial neoplasias)
acquire genetic and epigetnic alterations

150
Q

what are the clinical presentations of carcinoma of the head of the pancreas?

A 
jaundice (invasion/compression of CBD)
palpable gallbladder (courvoisiers sign)
weight loss (malabsorption, diabetes)
pain - epigastric, can radiate to back 
persistent vomitting if duodenal obstruction 
GI bleeding
151
Q

how does carinoma of body&tail of pancreas differ to that of the head?

A

less common
at diagnosis they are often more advanced
back pain more common & marked wt loss
jaundice is uncommon

152
Q

investigations for pancreatic cancer?

A 
tumour marker CA19-9
ultrasonography
dual phase CT /MRI - mets,  respectability
MRCP
ERCP - biopsies, bilary stenting 
EUS - vascular invasion, small tumours 
laparoscopy ± US - liver & peritoneal mets
PET
153
Q

what is tumour marker CA19-9 used for and when is it unreliable?

A

pancreatic cancer

is elevated in pancreatitis, hepatic dysfunction, obstructive jaundice

154
Q

what is the primary liver cancer?

A

hepatocellular carcinoma

associated with underlying cirrhosis and aflatoxin exposure

155
Q

what is gallbladder cancer assoicted with?

A

gallstones
porcelain gall bladder calcification)
chronic typhoid infection

156
Q

aetiology of cholangiocarcinoma?

A

primary sclerosing cholangitis
ulcerative colitis
liver flukes
choledochal cyst (dilation of bile duct)

157
Q

from what cancer do secondary liver metastases come from?

A

colorectal cancer

158
Q

causes of microcytic anaemia?

A

iron deficiency anaemia
chronic disease
thallasaemia
sideroblastic

159
Q

causes of normocytic anaemia?

A 
aplastic
bkeeding
chronic disease
destruction - haemolysis
endocrine - hypothyroidism/adrenalism
160
Q

causes of macrocytic anaemia?

A 
foetus
alcohol
thyroid disorders
reticulocytosis
B12/folate deficiency 
cirrhosis
161
Q

2 GIT malignant causes of iron deficiency anaemia?

A

colonic adenocarcinoma

gastric carcinoma

162
Q

how can bowel ischaemia present?

A

sudden onset crampy abdo pain
bloody loose stool (currant jelly)
fever
signs of septic shock

163
Q

risk factors for bowel ischaemia?

A 
age≥65
arrythmias
atherosclerosis 
thrombophilia
vasculitis
sickle cell disease
shock causing hypotension
164
Q

differences between acute mesenteric iscahemia and ischaemic colitis?

A

AMI - small bowel, thromboemboli, sudden onset, abdo pain out of proportion

IC - large bowel, low flow states/atherosclerosis, mild gradual onset, moderate pain and tenderness

165
Q

what bloods would you do for bowel ischemia and what would they show?

A

FBC - neutrophilic leukocytosis

VBG - lactic acidosis

166
Q

imaging for bowel ischamia?

A

CTAP/CT angiogram

detects disrupted blood flow, vascular stenosis

167
Q

management for mild/moderate ischemic colitis?

A 
IV fluids
bowel rest/nbm
bs abx 
NG tube 
anticoagulation
serial abdo exams and repeat imaging
168
Q

what are the indication for surgery for bowel ischaemia?

A 
small bowel ischemia
peritonitis/sepsis signs
haemodynamic instability
massive bleeding
fulminant colitis with toxic megacolon
169
Q

surgical options for bowel ischemia?

A

exploratory laparotomy - resect necrotic bowel ± surgical embolectomy/mesenteric arterial bypass
endovascular revascularisation - ballon angioplasty/thrmobectomy

170
Q

presentation of acute appendicitis?

A 
periumblical pain that migrates to RLQ in 24hrs
anorexia
nausea
vomitting
low grade fever
bowel changes
171
Q

investigations for acute appendicitis and results?

A

FBC - neutrophilic leukocytosis, ↑ CRP, electrolyte imbalances
urinalysis - pyuria/haematuria

CT - gold standard
USS - child, pregnant, breastfeeding
MRI - pregnancy if US inconclusive

diagnostic laparoscopy

172
Q

what can be used to assess likeliness of appendicitis?

A

alvarado score
≤4 = unlikely
5-6 = possible
≥7 = likely

173
Q

conservative management of acute appendicitis?

A

iv fluids, analgesia, ABx
access, phlegmo, sealed perf → drainage

indicated in uncomplicated appendicitis & negative imaging

174
Q

surgical management of acute appendicitis?

A

laparoscopic appendicectomy (less pain, less infection, reduced hospital stay, better QoL)

175
Q

two types of bowel obstruction?

A

paralytic ileus

mechanical

176
Q

causes of small bowel obstruction?

A

adhesions
neoplasia
incarcerated hernia
crohns disease

177
Q

causes of large bowel obstruction?

A 
colorectal carcinoma (esp LHS)
volvulus
diverticulitis
faecal impaction
Hirschsprung disease
178
Q

difference in presentations between small and large bowel obstructions?

A

abdo pain - colicky central VS colicky/constant
vomitting - early onset, billions VS late onset, billions → faecal
constipation - late sign VS early sign
abdo distention - less significant VS early significant sign

both : dehydration, high pitched → absent bowel sound, diffuse abdo tenderness

179
Q

what suggests a strangulated bowel obstrcution?

A 
colicky to continuous pain 
tachycardia
pyrexia
peritonism
absent/reduced bowel sounds
leucocytosis
↑ CRP
180
Q

bowel =obstruction investigations?

A 
bloods - 
-↑wcc/crp = strangulation/perf
-elctorlyte imbalance
VBG
-metabloic alkalosis if vomitting
-metabolic acidosis if strangulation

erect cxr/axr - dilated bowel loops
CT abdo/pelvis

181
Q

bowel obstruction conservative management & indications?

A

no signs of iscahemia/clinical deterioration
NBM
IV fluid resus
analgesia, antiemetics, electrolyte correction
NG tube and urinary catheter

stool evacuation for faecal impaction
rigid sigmoidoscopic decompression for volvulus
oral gastrograffin for SBO

182
Q

bowel obstruction surgical management & indications?

A 
haemodynacim instability
signs of sepsis
complete BO w ischaemia
closed loop obstrcution
persistent BO despite conservative managemtn

exploratory laproscopy/laparotomy
restore intestinal transit
bowel resection with anastomosis or stoma

183
Q

presentation of a GI perforation?

A

sudden onset severe abdo pain w distention
diffuse guarding, rigidity, rebound tenderness
pain worse w movement
nausea, vomitting, constipation
fever, tachycardia, tachpnoea, hypotension
↓ / absent bowel sounds

184
Q

where does the pain from a perf peptic ulcer get referred to?

185
Q

investigations for a GI perf?

A

FBC - neutrophilic leukocytosis
VBG - lactic acidosis

erect CXR - sub diaphragmatic free air
CT abdo/pelvis - pneumoperitoneum, free gI content, localised mesenteric fat stranding

186
Q

differential diagnoses for GI perf?

A

acute pancretaitis
appendicitis
acute cholecystitis
MI

187
Q

conservative management for GI perf?

A 
NBM
NG tube
IV fluid resus
BS Abx
IV PPI
analgesia and antiemetics
urinary catheter
188
Q

surgical management for GI perf?

A

for generalised peritonitis ± sepsis

exploratory laproscopy/otomy 
primary closure of perf ± omental patch
resection w anastomosis/stoma
obtain intrabdominal fluid for cultures
peritoneal lavage
189
Q

conservative management for a sigmoid volvulus?

A

sigmoidoscope with soft rubber rectal tube → untwists volvulus

190
Q

what will be raised in acute mesenteric iscahemia?

A

serum lactate

191
Q

investigations for AMI?why?

A

CT abdo pelvis with contrast
can show thrombus in mesenteric vessels
abnormal enhancement of bowel wall
presence of embolus or infarction of other organs

192
Q

surgical management for AMI?

A

emergency exploratory laparotomy

restore SMA blood flow (embolectomy or arterial bypass) , resect nonviable bowel

193
Q

risk factors for SMV thrombosis?

A

portal htypertension
portal pyaemia
SCD

194
Q

what is portal pyaemia?

A

septic thrombophlebitis of portal venous system

can be complication of appendicitis / diverticulitis

195
Q

how can portal pyaemia present on CT?

A

air in SMV and intrahepatic portal venous system

BRS 2 (12 decks)

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