gastro conditions Flashcards
(312 cards)
1
Q
what are haemorrhoids
A
they are vascular cushions on the anus that help the sphincters constrict
however we only say someone has haemorrhoids when these cushions become inflamed
2
Q
presentation of haemorrhoids
A
usually PAINLESS fresh blood from back passage
NOT mixed in stool
pruritus may be present!!!
3
Q
explain clock positions for pR exam and locations of haemorrhoids on this
A
clock times allocated with patient flat on back and open legs (like in surgery) and 12 is tomards belly 6 is towards back
however pr exam is not done in this position so it can be confusing
haemorrhoids in 3, 7 and 11 oclock position
4
Q
haemorrhoids 2 types
A
internal: above dentate line in anal canal- less likely to be painful
external: below dentate line: more likely to be thrombosed and painful
5
Q
haemorrhoids grades of classification
A
grade 1: do not prolapse out of the anal canal
grade 2: prolapse out of anal canal only in defecation
grade 3: prolapse out of anal canal in defecation and stay there but can be reduced
4: cannot be reduced
6
Q
haemorrhoids diagnosis
A
a rigid anoscope, proctoscope, or rectoscope
7
Q
when suspecting haemorrhoids what fo you do?
A
abdo exam and inspect rectum and PR exam to RULE OUT other pathology eg fissures or other sinister pathology
8
Q
haemorrhoids management
A
prevention: preventing constipation: high fibre, liquids and laxatives when needed
pharmacological treatment: bunch of creams and stuff you can use
non surgical treatments: BAND LIGATION: killing the supply to haemorrhoids> injection sclerotherapy
9
Q
management of acute thrombosed external haemorrhoids
A
veery painful
patients may benefit from admission if presentation within 72 hours for procedure
otherwise stool softeners ice packs and analgesia will do the trick
10
Q
colon cancer non acute presentation
A
blood in stool, unexplained weight loss, change in bowel habit (usually more lose stool),
iron def anaemia, unexplained ABDO PAIN!!!!
11
Q
screening bowel cancer programme ENgland and scotland
A
FIT test sent out to everyone 60-74 in england and 50-74 in scotland
positive fit test patients are offered a colonoscopy
12
Q
risk factors for bowel cancer
A
diet- high in meat low in fiber
obesity
13
Q
how are the genetics of bowel cancer classified
A
1) SPORADIC 95%
2- hereditary non-polyposis colorectal carcinoma 5%– isolated cancer
3- familial adenomatous polyposis 1%
14
Q
- familial adenomatous polyposis pathology and management
A
patients are full of polyps by age of 30-40 and need total proctocolectomy
15
Q
any age person single symptom indicator for FIT test
A
change in bowel habit
iron def anaemia!!!!!!
abdo mass
16
Q
over 50 single symptom FIT indicators
A
rectal bleeding
abdo pain
weight loss
17
Q
40+ 2 symptom combo FIT indicator
A
unexplained weight loss and abdominal pain,
18
Q
under 50 2 symptoms combos FIT indicators
A
rectal bleeding and either of the following unexplained symptoms:
abdominal pain
weight loss,
19
Q
60+ person (low threshold) FIT indicator
A
anaemia even if not iron def
20
Q
what symptoms can indicate direct referral even without FIT testing
A
anal mass
rectal mass and
anal ulcer
21
Q
post fit test result approach
A
if positive 2 week wait and if negative can still be considered for referral if symptoms presist and no other expl is found
22
Q
coloractal cancer management
A
palliative
chemo
surgery - palliative (symptom control) or curative intent
23
Q
what is the CEA
A
carcino embryonic antigen is a blood test used in staging and looking for reccurance of colon cacner not for screening though
24
Q
other staging investigation of colon cancer
A
CT of the chest, abdomen and pelvis
25
anal fissure presentation
bright red blood, painful with defecation
26
risk factors for anal fissure
constipation, IBD, STI!!
27
Acute management of anal fissure
dietary advice high fibre and fluids
bulk forming laxative if needed and lactulose if that doesnt work
lubricants before defecation
topical anaesthetics and analgesia
28
chronic management of anal fissure
same as acute and additional topical GTN if needed and if that doesnt work then referral for anal sphincterotomy
29
diverticular disease presentation
altered bowel habit, rectal bleeding, abdo pain
30
pathophysiology of diverticular disease
outpouchings on the bowel wall - usually happen between taenia coli where vessels pierce muscle to supply the mucosa fo rthis reason the rectum which lacks taenia is often sparred
31
complications of diverticular disease
diverticulitis
perforation
abscess
peritonitis
fistula
haemorrhage
32
diagnosis of patients presenting in clinic with suspected diverticular disease
colonoscopy or CT cologram or barium enema
33
diagnosis of patients acutely unwell with diverticular disease
plain xray will show perforation
then if needed abdo CT with IV and oral contrast to identify inflammation of bowel and local complications such as abscess formation.
34
severity classification tool for diverticular disease complications
Hinchey classificatoin
35
management of diverticular disease stable disease
high fibre and liquid diet
36
diverticulitis management
sometimes people have rescue pack AB but may need surgical involvement if recurrent acute diverticulitis attacks, if hinchley class 4: faecal peritonitis- needs resection and maybe stoma- bad prognosis
37
ulcerative colitis presentation
bloody diarrhoea, abdo pain, younger patients, left abdo pain> right
38
diagnostics for UC when stable and if diagnosis being made in flare
colonoscopy with biopsy are usually diagnostic,
raised faecal calprotectin in IBD
NO colonoscopy when flare- flexi sigmoidoscopy preferred
39
pathophysiological features of UC including histology
- red raw mucosa that easily bleeds
- only past ileocoecal valve so only large bowel
- inflammation doesnt go past submucosa (nooot all layers)
- depleted goblet cells and mucin form gland epithelium
- pseudopolyps since theres ulcerated mucosa with adjacent unaffected mucosa making it look like polyps (in lumen)
- crypt abscesses filled with neutrophils
40
most common site of UC
rectum since this is where the inflammation always starts from
41
conditions commonly associate with UC
primary sclerosing colangitis, arthritis, uveitis
42
medication used to maintain remission of UC
aminosalicylates - topical rectal for milder and oral for more severe- generally dif guidance depending on region of UC IN colon
43
vit b12 deficiency causes
1) pernicious anaemia most common
other causes: malnutrition, gastrectomy, atrophic gastritis
44
pernicious anaemia pathophysiology
autoimmune condition leading to destruction of gastric mucosa
what leads to vit b12 deficiency
1) IF antibodies
2) destruction of gastric mucosa so less production oF IF
45
presentation of pernicious anaemia
1) anaemia since b12 not produced
2) neuro symptoms since b12 is critical in myelination of neurones so tingling, confusion, concentration problems,
- other: jaundice with pallor: "lemon tinge"
atrophic glossitis
46
management of pernicious anaemia
-IM b12 3/ week initially then 1 every 3 months
-oral b12 not commonly used but may be evidence suggesting it helps maintenance of levels
-folate supplements may also be needed
47
which cancer does pernicious anaemia predispose to
gastric cancer
48
pancreatic cancer presentation
unspecific symptoms: weight loss, anorexia, epigastric pain, atypical back pain
PAINLESS!!! jaundice, abdo mass, hepatomegaly
SPECIFIC potential symptoms:
steatorrhoea due to exocrine function loss, Diabetes due to endocrine function loss
49
pancreatic cancer LFTs picture
obstructive picture (ALP> ALT)
50
pancreatic cancer diagnostics and characteristic sign
high resolution CT (double duct sign)- can also do a uss
indicates simultaneous dilatation of:
The common bile duct (CBD)
The main pancreatic duct (MPD)
suggests the presence of a mass at the head of the pancreas, which is obstructing both ducts.
51
management of pancreatic cancer
less than 20% of cases are operable at diagnosis
whipple procedure: pancreaticoduodenectomy
is performed for resectable lesions in the head of pancreas.
adjuvant chemotherapy used AFTER surgery
ERCP with stenting can be used palliatively
52
alcoholic liver disease stages
healthy-> fatty liver->hepatitis-> fibrotic liver-> cirrhosis
53
alcoholic liver disease LFT picture
AST/ ALT ration HIGH
gamma GT raised
54
management of acute alcoholic heptitis
glucocorticoid
(phentoxyphiline sometimes used but research says is not that good)
55
c dif infection most common triggers
used ot be clyndamycin now its cephalosporins
PPIs are also triggering
56
micorbiology of c dif
gram positive, anaerobic, spore forming, toxin producing, bacillus
spreads faecal oral route by spread of the spores
57
complications of c dif
toxic megacolon
58
how is c dif diagnosis made
CDT (meanig from the cc dif toxin and NOT the anitgen - that would just so exposure rather than infection
59
management of C dif
1) stop current ab is possible
2) start ORAL VANCOMYCIN
fidaxomycin- second line
vancomycin and iV mtroonidazole is third line
isolate patient in ward - hand washing!! (alcohol doesnt kill )
if reccurent infections consider microbiota transplant
60
what LFT picture does paracetamol, sodium valporate and anti TB drugs cause?
hepatocellular picture so ALT> ALP
61
What LFT picture does combined oral contraceptive pill cause
cholestasic picture so ALP> ALT
62
femoral henrnia presentation is it painful and is it reducible?
usually mildly painful and non reducible
63
complications of femoral hernia
strangulation and bowel obstruction: both are surgial emergencies
64
important DDx to exclude for femoral hernias
femoral artery aneurism
inguinal hernia
lymphadenopahty
abscess
lipoma
hydrocoele
65
Most common type of bowel cancer
Adenocarcinoma
66
meaning of incarcerated hernia
when its non reducible- stuck hernia essentially but not yet STRIANGULATED
67
how to differentiate incarcerated from striangulated hernia
PAIINNN!! incarcerated hernia is typically painless vs striangulated is painful
68
difference in management of an incarcerated vs striangulated hernia
striangulated hernia needs IMMEDIATE surgery vs incarcerated just elective
69
what advice is given to a patient while waiting to get surgery for striangulated hernia
DONT try to reduce it - can exacerbrate peritonitis
70
OTHER NAME FOR VIT B12
cobalamin
71
coeliac disease pathophysiology
the protein gluten causes villous atrophy and this in turn causes malabsorption
72
coeliac disease presentation
- chronic or intermittent diarrhoea
- Persistent or unexplained gastrointestinal symptoms including nausea and vomiting
- prolonged fatigue
- recurrent abdo pain, cramping or distension
- sudden or unexpected weight loss
- unexplained iron deficiency anaemia
- sudden or unexpected weigh loss
73
coeliac disease associated conditions
autoimmune diseases
dermatitis herpetiformis (doesnt happen much independently to coeliac disease- mostly with it)
74
diagnosis of coeliac disease
--serology - TTG!! and IgA
---and endoscopic intestinal biopsy is the golden standard!!!!!-- form duodenym> jejenum
---main findings of the biopsy: crypt hyperplasia, villous atrophy, increase in intraepithelial lymphocytes
(Also a lot of the cases are associated with HLA-DQ2 or HLA-DQ8)
75
For the endoscopic intestinal biopsy, what is true regarding the patients consumption of gluten in the 6 weeks prior?
patient needs to have been consuming gluten for at least 6 weeks prior
76
management of coeliac disease
--no gluten in diet
--this reverses the atrophy usually
-- (pasta bread, beer ect have gluten, --RICE does not, potatoes dont corn doesnt)
77
what is another important aspect of management of coeliac disease?
pneumococcal vaccine and booster every 5 years because all coeliac disease patients have a degree of functional hyposplenism
and flu vaccine on an individual basis
78
Ascending cholangitis pathophysiology and cause
ascending cholangitis is caused by a combination of outflow obstruction and infection of the billiary tree most commonly caused by e coli
79
most common predisposing factor to ascending cholanfitis
gallstone disease
80
two types of gallstone disease progression leading to ascending cholangitis
Mirizi syndrome - gallstones in gallbladder externally compress the common bile duct
or
- cholidocholithiasis- gallstones move down to the common bile duct
81
presentation of ascending cholangitis
charcot's triad: jaundice, fever, RUQ pain
if also HYPOTENSIVE and CONFUSED (think SYSTEMIC symptoms) then its reynold's pentad
82
blood results of ascending cholangitis
infective markers raised and obstructive pattern LFTs alp> alt + GGT (also raised but less) and also billirubin raised
83
diagnostic golden standard of ascending cholangitis and findings
abdo USS - stones are seen AND dilation of the bile ducts
84
crohns disease causes
generally unknown but strong genetic component
85
crohns disease ages peak incidnce
20-30 can happen in adolescence too!
86
presentation of Crohn's - most common symptom in adults and children
adults: diarrhoea (can be bloody but this is more characteristic of UC)
CHILDREN; abdo pain
other: weight loss, lethargy,
perianal disease: skin tags and ulcering
extra-intestinal features (more common in crohns colitis)
87
most common sites of Crohns
terminal ileum and colon!
ileum involvement in 80%
ileum + colon= 50%
ileum only 30%
colon only 20%
30% perianal
88
investigations for crohns
bloods:
- inflammatory markers, CRP good correlation with disease progress
- faecal calprotectin
- ANAEMIA
- DECREASED B12 AND FOLATE!
colonoscopy + biopsy for histology
89
crohns histology + colonoscopy findings
skip lesions, deep perforation till serosa, ulcers
90
what bowel loop complications are crohns patients at risk of and why
due to the lesions that are very deep (reach serosa layer) thiings like adhesions, strictures and fistulas
91
additional specific and sensitive investgations to small bowel crohns and its findings
small bowel enema
strictures: kantors string sign
proximal bowel dilation
rose thorn ulcers
fistulae
92
extra-enteral manifestations equally likely in uc and crohn's that are DEPENDEDNT on disease activity
pauciarticular arthritis asymetrical
osteoporosis
erythema nodosum
93
extra enteral manifestations of IBD unrelated to disease activity (equal in UC AND Crohns)
polyarticular arthritis -
clubbing
pyoderma gangrenosum
94
extra enteral manifestations more likely in crohns
episcleritis
95
extra-enteral manifestations more likely in UC
primary sclerosing cholangitis
uveitis
96
crohns management to induce remission (acute management)
glucocorticoids - first line!
potential additions/ alternatives
enteral feeding additionally or as an alternative where steroids will cause bad side effects eg children
5 ASA drugs - used as ALTERNATIVE to glucocorticoids but not as effective
azathiorprine used IN ADDITION to glucocorticoid
97
management of crohns to maintain remission
azathioprine or mercaptopurine is first line
methrotrexate is used second line
98
WHAT Needs to be measured before starting azathioprine or mercaptopurine?
+TPMT activity- its the liver enzyme that breaks these drugs down so if its low there is risk of toxicity
99
how common is surgery in crohns and what are some of its uses?
80% of patients with crohn's will require some form of surgery
examples:
stricturing terminal ileal disease: ileocaecal resection
segmental small bowel resections
stricturoplasty
100
crohns disease and GI cancers association
small bowel cancer (standard incidence ratio = 40)
colorectal cancer (standard incidence ratio = 2, i.e. less than the risk associated with ulcerative colitis)
101
what is trousseau's syndrome and which cancer is it most associated with
its a paraneoplastic phenomenin associated iwth pancreatic cancer causing migratory thrombophlebitis (eg red painful swellings on fingers)
102
presentation of perianal abscess
pain around the anus, worse on sitting,
may have noticed hardening tissue around anus,
puss like discharge from anus
if its long standing there may be features of systemic infection eg fever ect
103
epidemiology of perianal abscess
2:1 more men, and average age is 40
104
what is a perianal abscess
its a collection of puss in the subcutaneous tissue of the anus that has tracked from the tissue surrounding the anal sphincter.
----------------------
meaning:
The infection usually starts deeper, in the glands near the anal sphincter
From there, the infection spreads through the tissue planes until it reaches the more superficial layers (under the skin), where it forms an abscess.
105
management of perianal abscess
incision + drainage under local anaesthetic if its superficial and no involvement of sphincter or
general anaesthetic if sphincter is involved and more complicated
antibiotic only if systemic upset - hasnt been proven to hlep with healing of wound post- drainage
106
common investigations to help diagnose perianal abscess
- bloods:
-infection markers
- blood cultures
- can isually be diagnosed by inspecting hte areaor a DRE
- golden standard for anorectal abscesses is an MRI!!!!
-(other useful: transperineal USS)
-(but these are rarely used- more in complicated disease process such as underlying IBD or complications)
107
conditions commonly associated with perianal abscess
Crohn's
Diabetes mellitus due to poor wound healing
underlying malignancy
108
what bacteria commonly cause perianal abscesses
e coli if from GI tract
s. aureus if skin is the source
109
what is a Fistula
an abnormal connection between two epithelial surfaces
110
what general body area are fistulas more common in in gen surg and commonest causes of it
abdomen
crohn's and diverticular disease are common causes of it
111
general principle about resolution of fistulas?
they generally resolve spontaneously unless there is something blocking them distally
112
what are the four types of fistulae in abdomen
enterocutaneous
enterovesicular
enterovaginal
enteroenteric or enterocolic
113
characteristic of enterocutaneous
they have excretions onto skin
duodenal and jejenal have HIGHer output excretions and more acidic that may excoriate the skin compared to
colo- enteric fistulae that have more faecal secretions
114
problem with enteroenteric fistulas
overgrowth of bacteria may lead to malabsoprtion syndromes- particularly bad in IBD
115
enterovesicular fistulas presentations
frequent UTI OR PASSING GASS FROM fwhen peeing
116
management of fistula when no IBD or obstruiction
conservative as it will heal by itslef
117
management when there is Where there is skin involvement
protect the overlying skin, often using a well-fitted stoma bag- skin damage is difficult to treat
118
medicine to use in high output fistula
octreotide, this will tend to reduce the volume of pancreatic secretions.
119
when are nutritional complcations more common and how to manage in fistulas
Nutritional complications are common especially with high fistula (e.g. high jejunal or duodenal) these may necessitate the use of TPN to provide nutritional support together with the concomitant use of octreotide to reduce volume and protect skin.
120
what should surgeons avoid doing to fstulas as it worsens outcomes
probing it
121
what is THE MOST EFFECTIVE treatment For simple perianal fistulae, such as partial intersphincteric types,
fistulotomy is generally the most effective treatment.
(Deeper fistulae may be better managed with a seton drain in order to preserve continence and reduce the risk of sphincter injury)_
122
When perianal fistulae occur secondary to Crohn's disease whatis the best management
often to drain acute sepsis and maintain that drainage through the judicious use of setons whilst medical management is implemented.
123
what are some good tools to help delineate the fistula anatomy, for abscesses and fistulae that have an intraabdominal source?
barium and CT studies
124
mnemonic for viral hepatitides- order to remember them in --(which ones have vaccine? which ones are acute and which ones can be chronic? transmission routes?)
AECB(D)
"ΑΕΚ B(LOO)D"
AB- first two of alphabet have vaccine
A+E- fecal oral, only acute, very similar, difference is E HAS NO VACCINE and BAD IN PREGNANCY
C+ B- blood borne, acute AND CHRONIC (especially C)
D is like the odd one out bc you can only get it on top of a B infection- (remember-the one its next to on the mnemonic NOT in alphabet)
125
HAV + HEV serology
disease activity determined by presence of IgM ab!!!
IgG ab presence means past infection or immunity
126
Differences of HEV to HAV
hev:
very bad in preg
no vaccine!!
127
is it more common for hep C to only be acute or progress to chronic?
chronic: 55-85%
128
gold standard diagnostic for hep C
RNA test, can detect infection even very early on: 1-2 weeks sine it detects viral RNA in blood
129
How do you track whether hep C is progressing to chronic or staying acute
if RNA levels are dropping then its not developing to chronic
but if they are staying same it probably is
130
what percentage of hep B progresses to chronic hep and what is a risk factor for it
around 20% generally but young age is risk factor!
<6yo around 50% and more in even younger!
131
what is there an increased risk of in someone with chronic hep B
liver cancer
132
what are the tests to monitor and diagnose hep B
3 main antigens on hep B virus that are used:
HBsAG (SURFACE antigen) - IgG ab
HBcAG (CORE antigen) - IgM ab
E antigen - active infection
basically in hep b you go thorugh a phase called window where you can not detect the surface and igG (which are the most important to say if youll get chronic hep) and at some point either one or the other will be detected (THE AB OR ANTIGEN) and that will detemrine who "won" so id its antigen you have chronic if its antibody you are fine
133
how does hep D infect and antibodies interpretation
only in the presence of HBV and you can have either co infection- both active or superinfection: After HBV - which is worse
if IgG or igM to HDV present it means theres an active infection
134
what is the definition of volvulus
torsion of the colon around its mesenteric axis resulting in compromised blood flow and closed loop obstruction
135
most common type of volvulus
sigmoid volvulus (80%) sigmoid colon twisting on the sigmoid mesocolon (peritoneal fold)
136
in which part of the colon does a minority of volvulus happen?
in the caecum (20% of cases)- inmost people around 80% caecum is retroperitoneal so no risk of this but when this is not the case theres a risk of caecal volvulus
137
sigmoid volvulus risk factors and associations
older patients
chronic constipation
Chagas disease
neurological conditions e.g. Parkinson's disease, Duchenne muscular dystrophy
psychiatric conditions e.g. schizophrenia
138
caecal volvulus associations
all ages
adhesions
pregnancy
139
features of volvulus
constipation
abdominal bloating
abdominal pain
nausea/ vomiting
140
investigation usually used to diagnose volvulus
abdominal xray - coffee bean sign if sigmoid volvulus caecal volvulus: small bowel obstruction may be seen
141
sigmoid volvulus management
RIGID sigmoidoscopy with rectal tube insertion
142
caecal volvulus management
emergency laparotomy or laparoscopy -
if bowel is viable right hemicolectomy - (removes the redundant mobile caecum and prevents recurrence) followed by primary ileocolic anasotmosis
if bowel is non viable right hemicolectomy with stoma (end ileostomy with mucus fistula- the distal colon - remaining transverse colon is exteriorised as a mucous fistula to allow drainage of mucus)
143
most common cause of SBO and second most common
most common is adhesions sooo really notice past surgical history!!! and second is hernia
144
presentation of SBO
diffuse colicky abdo pain
distended abdo?
nausea and vomit- typically bilious vomit (accumulation of bile in the small intestine) early (late potential constipation)
"tinkling" bowel sounds!!! more common in early bowel obstruction
145
diagnosis gold standard for SBO
CT
definitive investigation and is more sensitive, particularly in early obstruction
should be done first-line - the National Confidential Enquiry into Patient Outcome and Death (NCEPOD) reports getting an abdominal x-ray first can delay treatment and may contribute to patient harm due to delayed definitive management
146
over how many cm is small bowel considered dilated?
>3cm diameter
147
initial steps in managing SBO
NBM
IV fluids
antiemetics: e.g. cyclizine – useful for general nausea; caution if bowel distension is severe due to anticholinergic effects
nasogastric tube with free drainage
148
FIRTHER MANAGEment of SBO
some patients settle with conservative management but otherwise will require surgery
149
most common cause of LBO
tumour - 60% of cases of large bowel obstruction
obstructionis the initial presenting complaint of colonic malignancy in approx 30% of cases
especially if the tumour in more distal colon since in rectum ect the diameter is smaller!
150
second and third most common causes of LBO
volvulus
diverticular disease
151
clinical presentation of LBO
as well as features suggestive of obstruction, thought should also be given to the underlying causes (e.g. any recent symptoms suggestive of colorectal cancer)
absence of passing flatus or stool
abdominal pain
abdominal distention
nausea and vomiting are late symptoms that may suggest a more proximal lesion
peritonism may be present if there is associated bowel perforation
152
INVESTIGATIONS of LBO
abdominal x-ray
still commonly used first-line
CT scan
high sensitivity and specificity for identifying obstruction (over 90% each) as well as identifying the aetiology of obstruction itself
153
what is normal diameter of large bowel
normal diameter limits are 10-12 cm for caecum, 8 cm for ascending colon, and 6.5 cm for recto-sigmoid - diameter greater than this is diagnostic of obstruction
154
initial management of LBO
NBM
IV fluids: correct dehydration and electrolyte imbalances
nasogastric tube with free drainage
IV antibiotics: if signs of perforation, ischaemia, or if surgery is planned
155
GENERALLY AS A way to remember what does definitive management of lBO depend on
presence or absence of complications (e.g. perforation, peritonitis, ischaemia)
the cause of obstruction (e.g. malignancy, volvulus, strictures)
patient’s overall fitness for surgery and prognosis
156
When is conservative management considered for LBO
(select cases)
trialled in stable patients with no signs of perforation or peritonitis
may be appropriate for:
diverticular strictures
slow-onset obstructions
close observation is essential
if no improvement within 48–72 hours, re-evaluate for intervention
157
WHICH PATIENTS require surgical management as definitive treatmemt of LBO
most patients - 75%
emergency surgery is indicated if:
clinical or radiological signs of perforation or peritonitis
evidence of ischaemic bowel
rapid deterioration despite conservative measures
158
SURGICAL methods used for A LBO
segmental resection ± primary anastomosis (if bowel is viable and patient stable)
Hartmann’s procedure (resection with end colostomy) – often used in emergency settings
subtotal or total colectomy – in cases of multiple synchronous tumours, perforation, or megacolon
stoma formation – if anastomosis is unsafe or deferred
159
when is endoscopic sttenting used for LBO management
palliative relief in patients with inoperable or metastatic colorectal cancer
bridge to surgery – allows decompression and optimisation prior to elective resection in high-risk patients
160
whay is endoscopic stent
(colonic stent)
self-expanding metallic stent (SEMS) can be inserted under endoscopic and fluoroscopic guidance
161
what is ileus
when there is reduced bowel peristalsis resulting in pseudo-obstruction.
162
most common cause of ileus and some other causes
post operative is most common but electrolyte imbalances and other neuro stuff such as parkinsons ect can be contributing/ cause
163
features of ileus
abdominal distention/bloating
abdominal pain
nausea/vomiting
inability to pass flatus
inability to tolerate an oral dietabdominal
164
when ileus is suspected what else needs to be checked since its a factor that can contribute
Deranged electrolytes can contribute to the development of postoperative ileus, so it is important to check potassium, magnesium and phosphate.
165
management of ileus
Intravenous fluid and bowel rest (nil by mouth) initially. Sips of clear fluid for comfort may be permitted
A nasogastric tube on free drainage
Avoidance of opioid analgesia
Discontinue medications known to cause ileus
Mobilisation
total parenteral nutrition occasionally required for prolonged/ severe cases
166
what is spinal cord compression caused by?
cancer metastasis to the vertebrae, so EXTRADURAL compression
167
how common is spinal cord compression amongst cancer patients
and which cancers most commonly lead to it
5% F CANCER patients get it
prostate and breast and LUNG!
168
most common and earliest sign of spinal cord compression
back pain - may be worse on lying down and coughing!!!
169
other symptoms present in spinal cord compression
lower limb weakness
sensory changes: sensory loss and numbness
neurological signs depend on the level of the lesion.
170
what are the neurological findings for spinal cord compression above L1 level
upper motor neuron signs in the legs and a sensory level.
(this means there is a clear level where sensory changes are detected due to the localised nature of pathology in spinal cord compression )
171
neurological findings in lesions of spinal cord compression below L1 level
lower motor neuron signs in the legs and perianal numbness.
172
tendon reflexes in spinal cord compression
tendon reflexes tend to be increased below the level of the lesion and absent at the level of the lesion
173
investigation for suspected spinal cord compression
urgent MRI: the 2019 NICE guidelines recommend a whole MRI spine within 24 hours of presentation
174
management of spinal cord compression
high-dose oral dexamethasone
urgent oncological assessment for consideration of radiotherapy or surgery
175
what is Disseminated intravascular coagulation
Simultaneous coagulation and haemorrhage caused by
the initial formation of thrombi which consume clotting factors (factors 5,8) and platelets,
ultimately leading to bleeding.
176
what is a critical mediator of DIC?
Tissue Factor (TF)
(released during vascular damage, exposure to cytokines, tissue factor, its also abundant in lungs brainand placenta - explains the causes of DIC...)
uppon activation it bins to coagulation factors triggering extrinsic and then intrinsic pathway of coagulation
177
causes of DIC
1) sepsis
2) trauma
3) obstetric complications e.g. aminiotic fluid embolism or hemolysis, elevated liver function tests, and low platelets (HELLP syndrome)
4) malignancy
178
WHAT IS THE blood picture in DIC
↓ platelets
↓ fibrinogen
↑ PT & APTT
↑ fibrinogen degradation products
schistocytes due to microangiopathic haemolytic anaemia
179
additionally to DIC WHAT other thing leads to prolonged APTT
heparin , but notrmal PT
180
WHAT other thing leads to prolonged BLEEDING time other than DIC
ASPIRIN
181
what other thing leads to prolonged prothrombin time other than DIC
warfarin
182
haem abnormalities caused by warfarin, heparin, aspirin, DIC
WARFARIN: prolonged PT
ASPIRIN: BLEEDING TIME
HEPARIN: APTT
DIC: APTT, PT, BLEEDING TIME
WHAD: PT, APTT, BLEEDING, ALL---- opos paei megalonei
183
what is haemochromatosis (cause and patho)
Haemochromatosis is an autosomal recessive disorder of iron absorption and metabolism resulting in iron accumulation.
caused by inheritance of mutations in the HFE gene on both copies of chromosome 6*
184
presentation of haemochromatosis
often asymptomatic in early disease and initial symptoms often non-specific: include fatigue, erectile dysfunction and arthralgia (often of the hands)
'bronze' skin pigmentation
diabetes mellitus
liver: stigmata of chronic liver disease, hepatomegaly, cirrhosis, hepatocellular deposition)
cardiac failure (2nd to dilated cardiomyopathy)
hypogonadism (2nd to cirrhosis and pituitary
dysfunction - hypogonadotrophic hypogonadism)
arthritis (especially of the hands)
185
which. features of haemochromatosis are reversible with treatment
Cardiomyopathy
Skin pigmentation
186
which features of haemochromatosis are irreversible with treatment?
Liver cirrhosis** (hepatomegaly and elevated lfts may be reversible
Diabetes mellitus
Hypogonadotrophic hypogonadism
Arthropathy
187
investigation to screen for/ diagnose haemochromatosis
general population
transferrin saturation is considered the most useful marker
ferritin should also be measured but is not usually abnormal in the early stages of iron accumulation
testing family members
genetic testing for HFE mutation
These guidelines may change as HFE gene analysis become less expensive
188
what is a typical iron study profile in patient with haemochromatosis
transferrin saturation > 55% in men or > 50% in women
raised ferritin (e.g. > 500 ug/l) and iron
low TIBC
189
further tests done in haemochromatosis once diagnosed
liver function tests
molecular genetic testing for the C282Y and H63D mutations
MRI is generally used to quantify liver and/or cardiac iron
liver biopsy is now generally only used if suspected hepatic cirrhosis
190
management of haemochromatosis
venesection is the first-line treatment
desferrioxamine may be used second-line
191
how to monitor the adequacy of venesection
monitoring adequacy of venesection: transferrin saturation should be kept below 50% and the serum ferritin concentration below 50 ug/l
192
most common organism overall in septic arthritis in adults and which group has a different one
general: s aureus
in young adults who are sexually active: neisseria gonorrhoeae - (disseminated gonococcal infection)
193
short pathophysio of septic arthritis
haematogenous spread!!!
This refers to the dissemination of bacteria through the bloodstream from a distant infectious focus, leading to seeding of the synovial membrane and joint space.
synovium is highly vascularised but lacks a basement membrane, facilitating bacterial entry once organisms are circulating in the blood.
194
most common of septic arthritis
knee
195
presentation of septic arthritis
acute, swollen joint
restricted movement in 80% of patients
examination findings: warm to touch/fluctuant
fever: present in the majority of patients
196
which is the key investigatio in septic arthritis and what does it show
synovial fluid sampling is obligatory
this should be done prior to the administration of antibiotics if necessary
may need to be done under radiographic guidance
shows a leucocytosis with neutrophil predominance
gram staining is negative in around 30-50% of cases
fluid culture is positive in patients with non-gonococcal septic arthritis
197
other investigations important in septic arthritis
blood cultures: since the most common cause of septic arthritis is hematogenous spread
joint imaging
198
Management of septic arthritis
- intravenous antibiotics which cover Gram-positive cocci are indicated. The BNF currently recommends flucloxacillin or clindamycin if penicillin allergic
--- antibiotic treatment is normally be given for several weeks (BNF states 4-6 weeks)
----- patients are typically switched to oral antibiotics after 2 weeks
needle aspiration should be used to decompress the joint
arthroscopic lavage may be required
199
2 most common symptoms of upper GI bleed + other symptoms
haematemesis and malaena (black sticky and tarry stool)
"Coffee-ground" vomiting (dark digested blood)
Lightheadedness
Syncope
Abdominal pain
Symptoms of anaemia in subacute or chronic bleeds
200
most common cause of upper GI bleed and second most common
peptic ulcer disease and thenn oesophageal varices
201
oesophageal varices pathophysiology
secondary to portal hypertension due to hepatic cirrhosis
202
other oesophageal causes of upper gi bleed
Oesophagitis: inflammation may be due to gastro-oesophageal reflux, infections (especially in immunocompromised patients), or medications such as bisphosphonates
Mallory-Weiss tear: longitudinal mucosal lacerations that occur after severe vomiting or retching
Oesophageal cancer: friable blood vessels in the tumour may cause chronic or acute bleeds
203
other gastric causes of upper gi bleed
Gastric varices:: also associated with portal hypertension
Gastritis: may be due to H. pylori infection, NSAIDs, alcohol or stress-related mucosal inflammation
Gastric cancer: tumours may ulcerate or erode blood vessels
Vascular malformations: a Dieulafoy lesion is a dilated submucosal artery that erodes the gastrointestinal mucosa resulting in massive bleeding
204
what are the two risk stratification scores used in upper gi bleed
glasgow blatchford score used BEFORE endoscopy to asses how urgently endoscopy is needed
rockal score used post endoscopy to risk stratify patients
205
what factors are taken into account for glasgow blatchford score and when can someone be discharged for outpatient OGD
haemoglobin, urea, systolic blood pressure, tachycardia, melaena, syncope, heart failure and liver disease
scoring 0 - low-risk and may be discharged for an outpatient OGD
206
some characteristic blood fingings in upper GI bleed
U&Es - classically urea is disproportionately raised due to digestion of blood
LFTs to screen for liver cirrhosis (increased risk of variceal bleeding)
207
definitive diagnostic test of upper GI bleed
Oesophago-gastroduodenoscopy (OGD)
208
what other imaging scan may be done in upper GI bleed
Chest X-ray to look for evidence of aspiration or perforation (e.g. pneumomediastinum or free air under the diaphragm)
209
what should be given before endoscopy if a variceal bleed is suspected?
terlipsessin and prophylactic antibiotics
210
how are non variceal bleeds treated?
can be treated mechanically (e.g. clipping), with thermal coagulation or with fibrin or thrombin (plus adrenaline)
211
how are oesophageal variceal bleeds treated?
band ligation
212
how are gastric variceal bleeds treated?
sclerotherapy
213
which medication do you need to be cautious to give with when it comes to upper gi bleeding and why?
Proton pump inhibitors (PPIs) should not be given prior to endoscopy
because they SHOULD NOT be given if bleed is variceal
if the OGD shows a non-variceal UGIB with stigmata of recent haemorrhage (e.g. a peptic ulcer) high-dose IV or PPIs should be started
214
what are some complicaitons of an upper gI bleed
rebleeding
aspiration of haematemesis causing pneumonia
complications of endoscopy eg perforation
death in 10% of admitted patients with an UGIB
215
what is the most common type of gastric cancer
adenocarcinoma
which originates from the glandular cells that line the stomach's mucosal layer.
216
five year survival rate of gastric cancer and hwo common
basically not that common but quite bad survuival rates
Over 7,000 new stomach cancers each year in the UK.
A full-time GP diagnose 1 person every 3-5 years.
The five-year survival rate is approximately 20%.
217
risk factors of gastric cancer
Smoking
Pernicious anaemia
H. pylori infection
High alcohol intake (> 6 units per day)
Dietary nitrosamines (found in smoked foods and gastric cancer has higher incidence in Japan)
Atrophic gastritis
Blood group A
Adenomatous polyps
Achlorhydria (as seen in Menetrier's disease)
218
is gord a risk factor for gastric cancer?
no only for oesophageal adenocarcinoma since it increases the risk of barrets oesophagus
219
signs and symptoms of gastric cacner
- Anaemia (iron deficient)
- Weight loss
- Anorexia (early satiety)
- Recent onset/progression of symptoms
- Melaena/haematemesis
- Swallowing difficulty (dysphagia)
- Lymphadenopathy - may suggest early spread
1) Left supraclavicular lymph node (Virchow's node)
2) Periumbilical nodule (Sister Mary Joseph's node)
220
diagnostic investigation of gastric cancer and characteristic finding
oesophago-gastro-duodenoscopy with biopsy
signet ring cells may be seen in gastric cancer.
They contain a large vacuole of mucin which displaces the nucleus to one side.
Higher numbers of signet ring cells are associated with a worse prognosis
221
staging investigation of gastric cancer
CT scan of the chest, abdomen, and pelvis is indicated in all patients to look for metastatic disease
other modalities they may be used for staging include endoscopic ultrasound, (FDG)-PET scanning and pre-operative staging laparoscopy
222
management of locally invasive gastric cancer
Locally invasive disease is managed with partial or total gastrectomy. Neoadjuvant chemotherapy improves outcomes for patients undergoing surgery.
223
management strategies for advanced gastric cancer
Advanced cases are managed palliatively through surgery to relieve obstruction or haemorrhage, or chemotherapy to improve quality of life.
224
(peptic ulcer disease) are dudodenal or gastric ulcers more common?
duodenal ulcers: 4x more likely than gastric
225
cause of duodenal ulcers
90% of duodenal ulcers are caused by H. Pylori infection.
others include:
NSAIDs
Chronic use of steroids
SSRIs
Increased secretion of gastric acid
Smoking
Blood group O
Accelerated gastric emptying
226
gastric ulcers risk factors
NSAIDs
H. Pylori infection
Smoking
Delayed gastric emptying
Severe stress
227
how is peptic ulcer disease sometimes classified
Peptic ulcer disease can be uncomplicated, or complicated (perforation, bleeding).
patients with complicated peptic ulcer disease may present with coffee ground vomiting (bleeding), and can be haemodynamically unstable due to perforation
228
what is a key distinguishing feature between gastric and duodenal ulcer
duodenal ulcers present with epigastric pain typically relieved on eating (closure of pyloric sphincter, less acid irritating ulcerated surface).
Symptoms of gastric ulcers on the other hand are often worsened by eating -
229
when do patients need to be referred for urgent OGD (2ww) to investigate for oesophageal and gastric cancer
if a patient > 55 with weight loss and dyspepsia should be sent for OGD to investigate for oesophageal and gastric cancer
230
what investigations do patients with suspected peptic ulcer disease need to undergo for diagnosis?
should be investigated for H.pylori infection with C-13 urea breath test
endoscopy, which allows a direct visual inspection of the ulcers. Biopsies may be taken to rule out malignancy.
231
what criteria need to be met for a C-13 urea breath test to be acurate
ensure the person has not taken a PPI in the past 2 weeks,
or antibiotics in the past 4 weeks
232
Management of H. Pylori-negative peptic ulcer disease
4-8 week course of full-dose PPI treatment in conjunction with lifestyle advice, such as:
smoking cessation
reducing alcohol intake
meals and weight and avoid NSAIDS ect
233
management of H.pylori positive with a proven gastric/duodenal ulcer which is
Associated with NSAID use
8 week PPI therapy followed by first-line eradication therapy - PPI (omeprazole/lansoperazole) + amoxicillin + clarithromycin/metronidazole for 7 days
( if pen allergic do clary AND metronidazole)
234
management of H.pylori positive with a proven gastric/duodenal ulcer which is NOT ASSOCIATED WITH nsaid USE
immediate eradication therapy with PPI (omeprazole/lansoperazole) + amoxicillin + clarithromycin/metronidazole for 7 days
235
what is done at the end of the 6-8 week PPI treatment for gastric ulcers?
a repeat endoscopy 6-8 weeks following the start of PPI treatment is recommended to ensure ulcer healing and rule out malignancy,
as well as H.pylori re-testing (C-13 urea breath test first-line, stool antigen test second line) IF THERE WAS H PYLORI
236
PERforated peptic ucer presentation
Perforated peptic ulcers present initially with localised epigastric pain which later becomes generalised and peritonitic.
237
investigations of perforated peritoneum
These patients require an AXR and erect CXR to look for pneumoperitoneum.
238
complicated peptic ulcer disease (eg perforation ) management
requires urgent surgical intervention with OGD for underunning of ulcers and haemostasis
239
causes of upper GI perforations
Oesophageal or gastric malignancies
Peptic ulcer disease
Boerhaave syndrome (oesophageal rupture secondary to forceful vomiting)
Ingestion of sharp or caustic materials
Iatrogenic e.g. during surgery or endoscopy
240
Causes of lower GI tract perforation include:
Diverticulitis
Colorectal cancer
Bowel obstruction
Colitis (e.g. inflammatory bowel disease)
Appendicitis
Infection (e.g. toxic megacolon secondary to C. difficile infection)
Iatrogenic (e.g. abdominal surgery or colonoscopy)
Mesenteric ischaemia
Invasion of the bowel by other tumours
241
symptoms of gi perforation
Abdominal pain, which is sudden in onset and severe
Nausea and vomiting
Malaise
Lethargy
242
signs of gi perforation
peritonism
Hypotension
Tachycardia
Tachypnoea
Fevers
243
diagnostic investigation for GI perforation
CT with contrast looking for free air (confirming perforation) and the site of perforation; an underlying cause may also be seen (e.g. an obstructing tumour) -
244
what does a chest xray show in GI perforation
may show air under the diaphragm (pneumoperitoneum) but is significantly less sensitive than CT
245
what may abdominal x-ray show in GI perforation
may show Rigler's sign (where gas outlines both sides of the bowel wall as it is in the peritoneal cavity as well as the lumen) - also not a first-line test due to limited sensitivity
246
management of GI perforation
Management includes resuscitation,
making the patient nil by mouth,
broad spectrum antibiotics
and analgesia.
Not all patients require surgical management (for example small perforations secondary to diverticulitis may be managed conservatively) but many do
247
surgical management of GI perforation
This usually involves a thorough washout, identifying the cause of perforation and repairing the defect
usually bowel resection and formation of a temporary stoma to protect the site of repair
248
most prevalent types of oesophageal cancer
adenocarcinoma most common in western world vs squamous cell most common globally
249
what parts of the oesophagus is adenocarcinoma and squamous cell caricnoma found in?
Adenocarcinoma typically located in the lower third of the oesophagus
Squamous cell carcinoma typically seen in the upper two-thirds of the oesophagus.
250
what is the biggest risk factor for oesophageal carcinoma and other rf?
Smoking: The most significant risk factor for both adenocarcinoma and squamous cell carcinoma.
High alcohol intake
Obesity and gastro-oesophageal reflux disease: Linked specifically to adenocarcinoma, as recurrent reflux leads to metaplastic formations of mucin-producing glandular tissue known as Barrett's oesophagus, which can further develop into neoplasia.
Achalasia
251
presentation of oesophageal carcinoma
Progressive dysphagia: Initially for solids, and later for liquids. Dysphagia typically occurs when there is obstruction of more than two-thirds of the lumen.
Weight loss: This symptom, the second most common, results from a combination of anorexia and dysphagia.
Odynophagia
Hoarseness: Can develop if there is local invasion of the recurrent laryngeal nerve.
252
when to offer 2ww urgend OGD for suspected oesophageal cancer
people with dysphagia or those aged 55 years and over with weight loss and any of the following: upper abdominal pain, reflux, or dyspepsia.
253
diagnostic investifation of oesophageal carcinoma
Upper GI endoscopy is performed to visualise and grade the tumour via biopsy.
254
staging of oesophageal carcinoma investigations
CT chest, abdomen and pelvis: Assesses the size of the tumour, local and lymph node spread, and any visceral metastases.
MRI: Identifies metastatic spread to the liver and advanced local disease.
255
primary management choice for localised disease
surgical resection
256
early stage oesophageal carcinoma management
endoscopic mucosal resection or endoscopic submucosal dissection for early-stage disease.
257
management of advanced disease in oesophageal carcinoma
Non-surgical options: Such as radiotherapy, chemotherapy or chemoradiotherapy or as neoadjuvant or adjuvant therapy with surgery.
258
causes of peritonitis
main cause is GI perforation (perf ulcer, boerhaave syndr, or secondary to cancers ect)
or infection: infections leqading to peritonitis include spontaneous bacterial peritonitis and peritoneal inf secondary to peritoneal dialysis
uncomplicated appendicitis can also cause local peritonitis
259
presentation of peritonitis
- Severe abdominal pain. Patients will often be lying completely still so as to not trigger/exacerbate pain
- Systemic signs of illness such as fever, haemodynamic instability, tachycardia
Nausea and vomiting
- Abdominal rigidity/Involuntary abdominal guarding: Involuntary tensing of the abdominal wall muscles in response to pressure on the abdomen (to protect inflamed abdominal organs).
- Rebound tenderness: Pressing on the abdomen elicits less pain than releasing the hand (as the peritoneum bounces back into place).
- Percussion tenderness
260
common cause of spontaneous bacterial peritonitis
usually seen in patients with ascites secondary to liver cirrhosis
261
investigations for peritonitis
if systemically very unwell sepsis 6
bloods for inflammatory markers and infection and LFTs and kidney function
imaging: xray ct or uss to identify fluid collections or perforations
peritoneal fluid analysis!! obtained by PARACENTESIS! can help identify causative org and guide treatment
262
diagnostic criteria for spontaneous bacterial peritonitis and most common organism found in ascitic fluid
paracentesis: neutrophil count > 250 cells/ul
the most common organism found on ascitic fluid culture is E. coli
263
management typical of spntaneous bacterial infection peritonitis
intravenous cefotaxime is usually given
264
which patients with ascites should receive prophylactic AB and what ab
patients who have had an episode of SBP
patients with fluid protein <15 g/l and either Child-Pugh score of at least 9 or hepatorenal syndrome
Offer prophylactic oral ciprofloxacin or norfloxacin
265
management principles of peritonitis
Surgical intervention: perforated viscus, appendicitis, or diverticulitis, surgical intervention is often required to control the source of infection or inflammation.
Antibiotics: Empirical antibiotic therapy should be initiated as soon as possible and then tailored according to culture results.
Supportive care: Fluid resuscitation, pain management, and monitoring of vital signs are crucial in the management of peritonitis.
266
definition of sepsis
a syndrome of life threatening organ dysfunction due to a dysregulated host response to infection
267
definition of septic shock
greater risk of death
To be classified as having septic shock: persistent hypotension requiring vasopressors to maintain a mean arterial pressure of 65 mmHg or more
AND
have a lactate of over 2 mmol/L despite adequate fluid resuscitation.
268
commonest sources (organ systems) of infection in sepsis
respiratory, genitourinary, renal and gastrointestinal
269
most common organisms identified in sepsis
Staphylococcus aureus, Escherichia coli and Pseudomonas species
In 50% of sepsis cases, no causative pathogen is identified
270
Risk factors for sepsis
Pregnancy
Recent miscarriage or abortion
Frailty
Immunocompromise due to chronic comorbidities e.g. HIV, diabetes, sickle cell disease
Immunosuppression secondary to medications e.g. chemotherapy, steroids
Recent surgery or trauma
Skin breaks or infections
Drug or alcohol misuse
Indwelling lines or catheters
271
symptoms of sepsis
General malaise
Fevers, sweats or chills
Localising signs of infection e.g. rashes, dysuria
Decreased urine output
Confusion
Breathlessness
Nausea and vomiting
Myalgia
272
On examination, signs of sepsis include:
Tachycardia
Hypotension
Pyrexia or hypothermia
Dehydration e.g. dry mucous membranes
Altered mental state including delirium
Irritability
Respiratory distress e.g. tachypnoea, accessory muscle usage
Cyanosis and hypoxia
Delayed capillary refill time
Cool extremities
Skin appears mottled or ashen
273
investigations and management of sepsis
sepsis 6- needs to be done within the HOUR of sepsis diagnosis
Blood cultures ideally prior to antibiotic administration
Lactate (i.e. a blood gas - venous or arterial)
Urine output (which may involve inserting a urinary catheter)
IV fluid resuscitation (usually a 500ml bolus over 15 minutes initially)
Supplementary oxygen to target saturations of 94-98% (88-92% if at risk of type 2 respiratory failure)
Broad-spectrum IV antibiotics (as per local guidelines)
274
what is ascites
abnormal accumulation of fluid within the peritoneal cavity.
typically associated with liver disease, particularly cirrhosis,
but can also occur due to other medical conditions affecting the heart, kidneys, or peritoneum.
275
causes of ascites related with portal venous system
The mechanism of ascites is not fully understood.
thought to involve portal hypertension causing increased hydrostatic pressure, leading to the transudation of fluid into the peritoneal cavity.
liver disorders (cirrhosis, acute liver failure, liver metastases),
cardiac causes (right heart failure)
and others such as Budd-Chiari,
Portal vein thrombosis etc. (see below).
276
ascites causes unrelated to portal venous system
reduced oncotic pressure (nephrotic syndrome, Kwashiorkor),
malignancy (peritoneal carcinomatosis,
peritoneal metastasis),
infection (increased permeability – TB),
causes of 3rd spacing (acute pancreatitis).
277
ascites signs and symptoms
Abdominal distension
Abdominal discomfort or pain
Dyspnea
Reduced mobility
Anorexia and early satiety due to pressure on the stomach
Tense abdomen
Shifting dullness
Stigmata of the underlying cause (see below)
278
primary investigation done for ascites
ascitic tap- provides information about the content of the ascitic fluid. (usually done under USS guidance)
279
what is the main analysis done to ascites fluid obtained from ascitic tap
The SAAG is calculated can help to determine the cause of ascites. (The Serum-Ascites Albumin Gradient= serum albumin- ascited fluid albumin )
if >11 this indicated portal hypertension so one of those causes mentioned earlier
if < 11 one of the non portal hypertension causes
280
initial medical management of ascites
Addressing the underlying cause
High SAAG - implementing a salt-restricted diet and fluid restriction
Administering spironolactone is first line.
Providing adjunctive diuretic therapy such as furosemide if spironolactone is insufficient.
281
next step in management for patients with ascites refractory (resistant) to medical management,
regular therapeutic paracentesis
the fluid is drained from the abdomen over a few hours.
These patients require replacement with human albumin solution (HAS) in order to avoid the ascites re-accumulating.
282
what is a serious complication of ascites and how it it identified
If the ascitic tap shows neutrophils >250mm3, this is diagnostic of spontaneous bacterial peritonitis, a serious complication of ascites. This is treated with intravenous piperacillin-tazobactam.
283
what is done for still refractory ascited in portal HT
a TIPS (transjugular intrahepatic portosystemic) shunt procedure can be considered.
284
liver cirrhosis definition
Cirrhosis refers to irreversible scarring of the liver with loss of normal hepatic architecture.
285
commonest causes of liver cirrhosis
- Alcohol
- Hepatitis B and C
- Non-alcoholic fatty liver disease (NAFLD)
286
less common causes of liver cirrhosis
Autoimmune:
Autoimmune hepatitis
Primary biliary cirrhosis
Primary sclerosis cholangitis
Sarcoid
Genetic:
Haemochromatosis
Wilson's disease
Alpha-1-antitrypsin deficiency
Drugs:
Methotrexate
Amiodarone
Isoniazid
Others:
Budd-Chiari Syndrome
Heart failure
Tertiary syphilis
287
what categories can cirrhosis be divided in clinically
clinical features of cirrhosis are broadly classified as compensated or decompensated, reflecting the severity of liver dysfunction and the presence of complications
Compensated Cirrhosis:
Characterized by a period where the liver maintains its function despite scarring, often with minimal or no noticeable symptoms.
Decompensated Cirrhosis:
Occurs when the liver scarring progresses to the point where it can no longer effectively compensate for the damage.
288
compensated cirrhosis presentation
Fatigue and anergia
Anorexia and cachexia
Nausea or abdominal pain
Spider naevi
Gynaecomastia
Finger clubbing
Leuconychia
Dupuytren's contracture (like gun fingers due to thickened tendon in ring finger vibe)
Caput medusae
Splenomegaly
289
decompensated liver cirrhosis presentation
In addition to the symptoms of compensated cirrhosis:
Ascites and oedema
Jaundice
Pruritus
Palmar erythema
Gynaecomastia and testicular atrophy
Easy bruising
Encephalopathy/confusion
Liver 'flap'
290
initial important blood tests for cirrhosis
Liver Function Tests: AST, ALT, ALP, GGT, Albumin, and Bilirubin
Full blood count to look for leucocytosis, thrombocytopaenia, and anaemia
Urea and electrolytes to establish baseline renal function and look for hepato-renal syndrome or any electrolyte abnormalities
INR to look for coagulopathy
A low platelet count, elevated aspartate aminotransferase (AST): alanine transaminase (ALT) ratio, high bilirubin, low albumin, or increased prothrombin time or
(INR) can suggest impaired liver function.
Patients can however also present with normal blood tests
291
What is transient elastography?
brand name 'Fibroscan'
uses a 50-MHz wave is passed into the liver from a small transducer on the end of an ultrasound probe
measures the 'stiffness' of the liver which is a proxy for fibrosis
292
who is transient elastography offered to
people with hepatitis C virus infection
men who drink over 50 units of alcohol per week and women who drink over 35 units of alcohol per week and have done so for several months
people diagnosed with alcohol-related liver disease
293
further investigations suggested for patients with cirrhosis
NICE recommend doing an upper endoscopy to check for varices in patient's with a new diagnosis of cirrhosis
liver ultrasound every 6 months (+/- alpha-feto protein) to check for hepatocellular cancer
294
scores used to assess mortality and severity of disease in liver cirrhosis
child- pugh score - severity of liver cirrhosis
MELD score
295
meld score factors into account and use
has been increasingly used, particularly patient's who are on a liver transplant waiting list
bilirubin, creatinine, and the international normalized ratio (INR) to predict survival.
296
score results of child pugh score interpretation
Summation of the scores allows the severity to be graded either A, B or C:
< 7 = A
7-9 = B
> 9 = C
297
management principles in liver cirrhosis
Management strategies involve nutritional guidance, medication, and possibly a liver transplant for severe cases.
medications include cholestyramine for pruritus
ascites meds
reducing recurrent episodes of encephalopathy through prophylactic lactulose and rifaximin
Using prophylactic antibiotics in patients at high-risk of spontaneous bacterial peritonitis
298
definition of liver failure (important in distinguishing it from cirrhosis)
Liver failure refers to the loss of liver function and the development of complications including coagulopathy, jaundice or encephalopathy.
299
types of liver failure
acute:
if onset of symptoms in less than 26 weeks with a previously healthy liver and subdivided into hyperacute (< 7 days), acute (8-21 days), or subacute (4-26 weeks) liver failure.
Chronic liver failure occurs on a background of liver cirrhosis.
300
acute liver failure causes
Viral Hepatitis: A, B, and E infections
Drug-Induced Liver Injury: Overdose or adverse reactions to medications
Toxic Exposures: Exposure to hepatotoxic substances
Vascular Disorders: Conditions like Budd-Chiari syndrome, characterised by hepatic vein obstruction, can result in rapid liver failure.
301
chronic liver failure causes
Alcohol Misuse:
Chronic Viral Hepatitis: infection with hepatitis B or C viruses
Non-Alcoholic Fatty Liver Disease (NAFLD):
Autoimmune Liver Diseases: .
Hereditary Conditions: Genetic disorders like haemochromatosis, Wilson's disease, and alpha-1 antitrypsin deficiency
302
presentation of LIVER FAILURE
Hepatic encephalopathy
Abnormal bleeding
Jaundice
If the cerebral oedema is severe, raised intracranial pressure may develop. This is more common in fulminant hepatic failure and has a high mortality rate.
It is important to separate the signs of liver failure from the signs of chronic liver disease. The presence of both indicates a de-compensation of chronic liver disease.
303
PATHOPHYSIOLOGY AND STAGES od hepatic encephalopathy
In liver failure, nitrogenous waste (ammonia) accumulates in the circulation.
This small molecule is able to cross the blood-brain barrier-- oedema
Four stages of hepatic encephalopathy:
1) Altered mood and behaviour, disturbance of sleep pattern and dyspraxia
2) Drowsiness, confusion, slurring of speech and personality change
3) Incoherency, restlessness, asterixis
4) Coma
304
what blood test result best reflects the synthetic function of the liver
'liver function tests' do not always accurately reflect the synthetic function of the liver.
This is best assessed by looking at the prothrombin time and albumin level.
305
criteria for the prediction of poor outcomes in acute liver failure and are therefore an indication of patients that should be considered for urgent liver transplantation.
King's College Hospital Criteria for Liver Transplant
306
King's College Hospital Criteria for Liver Transplant (non-paracetamol liver failure):
Prothrombin time >100s OR
Any three of:
Drug-induced liver failure
Age under 10 or over 40 years
1 week from 1st jaundice to encephalopathy
Prothrombin time >50s
Bilirubin ≥300µmol/L.
307
kings college hospital crit. The criteria for paracetamol induced liver failure are as follows:
Arterial pH <7.3 24h after ingestion OR
Pro-thrombin time >100s
AND creatinine >300µmol/L
AND grade III or IV encephalopathy.
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The most common complication of acute liver failure
infection.
Bacterial infection occurs in up to 80% of patients, and fungal infection in around 30%. This is thought to result from decreased phagocyte action, reduced complement levels and multiple medical interventions which are often invasive. Patients often present atypically, with no fever or raised white cell count.
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risk factors of GORD
GORD is caused by a defective lower oesophageal sphincter
obesity, alcohol use, smoking, and intake of specific foods (e.g. coffee, citrus foods, spicy foods, fat).
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Typical symptoms GORD
Dyspepsia (""heartburn"")
Sensation of acid regurgitation
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WHEN should suspected gord patients be given PPI therapy and for how long is trial therapy
For patients <40 years old who present with typical symptoms and no red flags, commence treatment with a standard-dose PPI for 4 weeks in combination with lifestyle changes.
If the patient meets criteria for urgent OGD, they should only be commenced on PPI therapy after this has been done
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complications of gord
Oesophageal ulcer
Oesophageal stricture
Barrett's oesophagus
Adenocarcinoma of the oesophagus
