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BRS 1b > gastro > Flashcards

gastro Flashcards

1
Q

what signs does vomiting during bowel obstruction show on a VBG

A

Hypochloraemia
Hypokalaemia
metabolic alkalosis

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2
Q

what signs does strangulation during bowel obstruction show on a VBG

A

metabolic alkalosis (lactic alkalosis)

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3
Q

clinical features suggesting strangulation in bowel obstruction

A

pyrexia
tachycardia
pain from colicky to constant
peritonism
raised CRP
leucocytosis
absent or reduced bowel sounds

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4
Q

most common causes of small bowel obstruction

A

adhesions
neoplasia
incarcerated hernia
crohns disease

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5
Q

bowel obstruction supportive management

A

NBM
large bore cannula
IV fluid resus
IV antiemetics
IV analgesia
correction of electrolyte imbalances
NG tube for decompression
urinary catheter

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6
Q

bowel obstructive conservative management for faecal impaction

A

stool evacuation

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7
Q

bowel obstructive conservative management for volvulus

A

rigid sigmoidoscopic decompression

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8
Q

indications for surgical management of BO

A

haemodynamic instability
sepsis
complete BO with ischaemia
complete loop obstruction
persistent obstruction of more than 2 days despite conservative treatment

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9
Q

describe the presentation of a perforated peptic ulcer

A

sudden diffuse or epigastric pain
referred shoulder pain
history of NSAIDs/steroids/recurrent epigastric pain

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10
Q

describe the presentation of a perforated diverticulum

A

LLQ pain
constipation

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11
Q

describe the presentation of a perforated appendix

A

migratory pain
anorexia
gradual worsening RLQ pain

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12
Q

describe the presentation of a perforated malignancy

A

change in bowel habits
weight loss
anorexia
PR bleeding

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13
Q

what would a VBG of GI perforation show

A

lactic acidosis

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14
Q

what would an FBC of GI perforation show

A

neutrophilic leukocytosis

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15
Q

what would a CXR/AXR show for GI perforation

A

CXR: pneumoperitoneum (free air under diaphragm)
AXR: pneumoperitoneum, free GI contents, mesenteric fat stranding

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16
Q

surgical management of GI perforation with generalised peritonitis +/- sepsis

A

explorative laparotomy/laparoscopy
upper GI (eg perforated ulcer): closure of perforation - maybe with omental patch
lower GI: resection with anastomosis and temporary stoma (to divert pressure away whilst the anastomosis heals)
obtain some intrabdomninal fluid for MC&S
do peritoneal lavage

if appendicitis do appendicectomy
if malignancy take biopsies

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17
Q

bowel ischaemia risk factors

A

age >65
cardiac arrhythmias mainly AF
atherosclerosis
vasculitis
sickle cell disease
hypercoagulation/thrombophilia
profound shock causing hypotension

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18
Q

imaging for acute appendix

A

CT - gold standard
USS - women and children
MRI - pregnant women if USS is inconclusive

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19
Q

specific clinical signs for appendicitis

A

McBurnerys sign: pain in RLQ

Blumbergs sign: rebound tenderness in RIF

Rovsing sign: pain in RLQ upon deep palpation of LLQ

Psoas sign: pain in RLQ upon flexion of right hip against resistance

Obturator sign: pain in RLQ upon passive internal rotation of the hip and flexion of knee and hip

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20
Q

steps of a laproscopic appendicectomy

A

place 3 trocars
explore RIF and identify appendix
elevate appendix
divide mesoappendix
secure base with endoloops
divide appendix
remove appendix and place in a plastic retrieval bag
do pelvic irrigation + haemostasis
remove tracers and close wound

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21
Q

2 most common causes of SBO

A

previous abdominal operation (adhesions)
external strangulated hernia (incarcerated hernia)

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22
Q

sign of LBO due to volvulus on AXR

A

bent inner tube sign / coffee bean sign

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23
Q

if you have a LBO caused by volvulus and leave it until there is necrosis/cannot salvage by rigid sigmoidoscopic decompression, what surgery do you do

A

explorative laparotomy + sigmoid colectomy + end colostomy

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24
Q

you think a pt has acute mesenteric ischaemia, what imaging should you order

A

CT Abdomen and pelvis with contrast

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25
Q

how to restore blood flow in embolic acute mesenteric ischemia

A

embolectomy of superior mesenteric artery

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26
Q

how to restore blood flow in thrombotic acute mesenteric ischemia

A

aterial bypass of superior mesenteric artery

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27
Q

brief outline of causes of acute mesenteric ischamia

A

arterial
- embolism
- thrombosis
- non occlusive
venous
- superior mesenteric vein thrombosis

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28
Q

in which patients is SMV thrombosis more likely to occur

A

patients with
portal hypertension
portal pyaemia/pyelophlebitis
sickle cell disease

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29
Q

which conditions does portal pyaemia/pyelophlebitis increase the risk of

A

intra abdominal sepsis due to
- appendicitis
- diverticulitis

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30
Q

what does portal pyaemia show on CT scan

A

air in SMV and intrahepatic portal venous system

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31
Q

4 major phyla of bacteria in the microbiota

A

bacteroidetes, firmicutes, actinobacteria, proteobacteria

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32
Q

what is the bacterial toxin TMAO linked with

A

atherosclerosis

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33
Q

what is the bacterial toxin 4-EPS linked with

A

autism

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34
Q

what is the bacterial toxin AHR ligand linked with

A

asthma, MS, rehumatoid arthiritis

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35
Q

what is an increase or decrease in SCFA’s linked with

A

increase: psychiatric syndromes, stess
decrease: IBD

36
Q

describe the composition of a MALT and where its found

A

in submucosa
lymphoid mass: aggregated lymphoid follicles surrounded by HEVs

37
Q

give examples of organised GALTs

A

peyers patches (small intestine)
caecal patches (large intestine)
isolated lymphoid follicles
mesenteric lymph nodes (encapsulated)

38
Q

give examples of non organised GALTs

A

intraepithelial lymphocytes
lamina propria lymphocytes

39
Q

describe the composition of peyers patches

A

aggregated lymphoid follicles consisting of naive T and B cells surrounded by a FAE (follicle associated epithelium)

40
Q

what 3 things does the FAE not have

A

no microvilli
no goblet cells
no secretary IgA

41
Q

what are M cells and where are they found

A

Microfold cells
found in the FAE surrounding peyers patches
have IgA receptors to take in IgA antigen complexes

42
Q

other than by M cells how else can antigens be captured

A

dendritic cells

43
Q

formation of secretory IgA

A

plasma cells secrete dimeric IgA in submucosa
dimeric IgA binds to poly-Ig receptor
receptor and dimeric IgA are taken upon into a vacuole within the epithelial cell and undergo enzymatic cleavage
are released onto the other side into lumen as secretory IgA

43
Q

formation of secretory IgA

A

plasma cells secrete dimeric IgA in submucosa
dimeric IgA binds to poly-Ig receptor
receptor and dimeric iGA are taken upon into a vacuole within the epithelial cell and undergo enzymatic cleavage
are released onto the other side into lumen as secretory IgA

44
Q

describe the process of lymphocyte homing and circulation

A

B and T cells undergo antigen presentation and activation in peyers patch

They then move to mesenteric lymph node where they undergo lymphocyte proliferation

then move into thoracic duct and then into circulation

once in circulation, can either go to peripheral immune systems eg MALTs, BALTs, skin
OR go back to lamina propria

45
Q

explain how T cells move from HEVs into lamina propria

A

alpha 4 beta 7 integrin on T cell binds two MAdCAM-1 on HEV
this activates the T cell and allows them to move into the lamina propria

46
Q

3 vaccines for cholera

A

dukoral
inactivated
oral

47
Q

treatment for cholera

A

oral rehydration

48
Q

vaccine for rotavirus

A

live attenuated vaccine: Rotarix

49
Q

most common rotavirus type in humans

A

Type A

50
Q

most common cause of diarrhoea in infants and children

A

rotavirus

51
Q

rotavirus treatment

A

oral rehydration therapy

52
Q

what type of virus is noravirus

A

RNA virus

53
Q

diagnosis for norovirus

A

sample PCR

54
Q

treatment for campylobacter

A

no treatment usually required
possibly need azithromycin

55
Q

most common cause of food poisoning

A

campylobacter

56
Q

what type of bacteria is e coli

A

gram negative intestinal bacteria

57
Q

management for C diff

A

isolate pt (as very contagious)
stop current abx
give vancomycin and metronidazole

if get lots of recurrence can do faecal microbiota transplantation

58
Q

raised CRP + WCC
new onset diarrhoea with generalised tenderness
Differential diagnoses?

A

infectious and non infectious diarrhoea

59
Q

common causes of non infectious diarrhoea

A

ischaemic colitis
microscopic colitis
Abx side effect
coeliac disease
post infectious IBS
IBD

60
Q

common causes of infectious diarrhoea

A

clostridium difficile
clostridium perfringens
klebsiella oxytoca
salmonella spp

61
Q

3 different disease categories of C diff infection

A

non severe disease (WCC<15, creatinine<150)
severe disease (WCC>15, creatinine>150)
fulminant colitis –> Hypotension, shock, toxic megacolon, ileus

62
Q

what does toxic megacolon look like on X-ray

A

dark and distended bowel

63
Q

treatment for non severe disease of C diff

A

vancomycin
fidaxomicin
metronidazole

FMT (faceal microbiota transplantation)

64
Q

what is pseudomembranous colitis

A

associated with C diff infection
severe colonic disease
formation of yellow white plaques which form pseudomembranes on mucosa

65
Q

describe mild UC

A

4 BM a day
mild symptoms
no systemic toxicity
normal CRP and ESR

66
Q

describe moderate UC

A

> 4 BM a day
mild symptoms
mild anaemia
mild systemic toxicity
nutrition maintained and no weight loss

67
Q

describe severe UC

A

> 6 BM a day
severe symptoms
systemic toxicity
raised CRP and ESR
significant anaemia
weight loss

68
Q

which scan would you do to check gall bladder/pancreas

A

MRI

69
Q

what must you alway include in the management plan for a severely vomiting patient

A

NG tube

70
Q

what scan do you do to check for gall stones

A

MRCP (MR cholangiopancreatography)

71
Q

what is a common cause of 4 quadrant tenderness peritonitis

A

perforation - leakage of contents irritates peritoneum

72
Q

describe the types of muscles of the oesophagus

A

top 1/3 - skeletal/striated
middle 1/3 - mixture of skeletal and smooth
bottom 1/3 - smooth

73
Q

what surrounds the LOS

A

diaphragm - phrenoesophageal ligament

74
Q

describe the phases of swallowing

A

phase 0: oral phase - food bolus prepared by saliva and chewing
phase 1: pharyngeal phase - pharyngeal muscles guid bolus to the UOS, which opens by reflex. LOS opens by receptive relaxation reflex (vasovagal reflex)
phase 2: upper oesophageal phase - UOS closes, superior circular muscles contract, inferior circular muscles dilate, sequential contraction of longitudinal muscles
phase 3: lower oesophageal phase - LOS opens as bolus passes through

75
Q

what is oesophageal pressure measured by

A

manometry

76
Q

resting LOS pressure

A

20 mmHg

77
Q

what is LOS resting pressure determined by

A

inhibitory NCNA neurones of myenteric plexus
(non cholinergic non adrenergic)

78
Q

pressure of peristaltic waves of oesophagus

A

40 mmHg

79
Q

regurgitation vs reflux

A

regurgitation: return of oesophageal contents from above an obstruction
reflux: passive return of gastroduodenal contents to the mouth

80
Q

pain on swallowing

A

odynophagia

81
Q

causes of achalasia (hyper motility of oesophagus)

A

due to loss of inhibitory ganglions of Aurebachs myenteric plexus and decreased activity of inhibitory NCNA neurones

primary: unkown
secondary: chagas disease
protozoa infection
oesophagitis

82
Q

risks of achalasia

A

dramatically increases risk of oesophageal cancer

83
Q

pathophysiology model of achalasia

A

genetic predisposition
environmental tigger
immune infiltrates
extracellular turnover, fibrosis, wound repair
loss of immune tolerance
apoptosis of neurones
humoural response
myenteric plexus abnormalities

84
Q

features of achalasia

A

higher LOS pressure
receptive relaxation reflex is too late
dilation of distal oesophagus as food gets stuck in
peristaltic waves can stop

85
Q

achalasia treatment

A

pneumatic dilatation
hellers myotomy with Dor fundoplication

86
Q

risk of hellers myotomy + dors fundoplication

A

oesophageal and gastruc perforation
division of vagus nerve
splenic injury

BRS 1b (10 decks)

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