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Notes
Acute respiratory distress syndromeRespiratory failure
Mind Maps for Medicine \ 63
62 / Chapter 2 Respi ratory: Respiratory failure
Respiratory failure
Respiratory failure occurs when gas
exchange is inadequate, resulting in
hypoxia. It is defined as a P
a
O
2
<8kPa
and classified as either type1 or
type2, based on whether there is a
high CO
2
level.
Type 1 respiratory failure
Defined as hypoxia (P
a
O
2
<8kPa) with a
normal or low P
a
CO
2
. It is caused primarily
by ventilation/perfusion mismatch.
Type2 respiratory failure
Defined as hypoxia (P
a
O
2
<8kPa) with
hypercapnia (P
a
CO
2
>6kPa). This is caused
by alveolar hypoventilation with or without
ventilation/perfusion mismatch.
Type 1 respiratory failure
• Pneumonia
•
Pulmonary oedema
•
Pulmonary embolism
•
Asthma
•
Pulmonary fibrosis
•
Pneumothorax
•
Bronchiectasis
•
Acute respiratory distress syndrome
Type 2 respiratory failure
• Obstructive pulmonary disease Asthma (severe),
COPD, obstructive sleep apnoea
•
Reduced respiratory drive Sedative drugs,
CNS tumour or trauma
•
Neuromuscular disease Cervical cord lesion,
diaphragmatic paralysis, poliomyelitis, myasthenia
gravis, Guillain–Barré syndrome
•
Thoracic wall disease Flail chest, kyphosis, scoliosis
•
Bloods: FBC, U&Es, CRP
•
ABG
•
Peak expiratory flow rate
•
Chest radiology: CXR, CT
• Microbiology: sputum and
blood cultures
• Spirometry
• ECG
Denition Classication
InvestigationsManagement Clinical features
Hypoxia
• Dyspnoea
•
Restlessness
• Agitation
• Confusion
• Central cyanosis
• Long-standing
polycythaemia,
pulmonary
hypertension, cor
pulmonale
Hypercapnia
• Headache
•
Peripheral
vasodilatation
• Tachycardia
• Bounding pulse
• Tremor/flap
• Papilloedema
• Confusion
• Drowsiness
• Coma
Type 1 respiratory failure
• Treat the underlying cause
•
Give O
2
via facemask to correct hypoxia
• Assisted ventilation if P
a
O
2
<8kPa despite 60% O
2
Type 2 respiratory failure
• Treat the underlying cause
• Controlled oxygen therapy via venturi mask; start at 24% O
2
;
O
2
therapy should be given with care but hypoxia should not
be left untreated
• Recheck the arterial blood gas after approx. 20min;
if P
a
CO
2
is steady or lower, increase O
2
concentration
in stages (see Fig.1)
• If P
a
CO
2
has risen above 1.5kPa and the patient is still hypoxic,
consider a respiratory stimulant or assisted ventilation
(e.g. NIPPV, non-invasive positive pressure ventilation)
• If improvement with NIPPV, continue and adjust settings
accordingly
• If this fails consider intubation and ventilation if appropriate
Fig. 1 Venturi masks are used to deliver
controlled percentages of O
2
in patients at
risk of type2 respiratory failure
24%
3 LMN
35%
5 LMN
Interchangeable venturi valves
31%
4 LMN
28%
4 LMN
40%
10 LMN
60%
15 LMN
Causes
https://t.me/med1917
Mind Maps for Medicine \ 65
64 / Chapter 2 Respirator y: Sarcoidosis
Sarcoidosis
A multisystem chronic inflammatory
condition characterised by the
formation of non-caseating epithelioid
granulomata at various sites in the body:
most commonly the lungs, lymph nodes,
eyes and skin. In approximately 50% of
cases the disease is detected incidentally
on routine CXR in an asymptomatic
individual.
•
It is thought that one or more unidentified antigen(s) triggers activation of
T-helper cells followed by the development of non-caseating granulomata
in genetically susceptible individuals
•
The granulomas consist of macrophages, epithelioid cells and
multinucleated giant cells surrounded by lymphocytes, monocytes, mast
cells and fibroblasts
•
The accumulation of Tlymphocytes, mononuclear phagocytic cells and
non-caseating granulomas occurs in involved organs; these granulomas
may resolve spontaneously or lead to secondary fibrosis and permanent
organ damage
• Sarcoidosis involves the lungs in >90% of cases and commonly the
lymphoreticular system, skin, eyes, muscles and joints; less commonly other
organs, including the heart, kidneys, brain and the peripheral nervous system
•
Age: occurs at all ages, although it usually develops
before the age of 50years, with the incidence peaking
at 20–39
•
Can occur in all ethnic groups but the disease is more
severe in African–Caribbeans than Caucasians
•
Family history increases risk
• HLA-B8 antigens and HLA-DRB1 and -DQB1 alleles
have been shown to confer susceptibility
•
Environmental associations: emissions from wood-
burning stoves and tree pollen, exposure to inorganic
particles, insecticides and mouldy environments have
been reported; positive associations have also been
made with service in the US Navy, metalworking,
firefighting and the handling of building supplies;
bacteria such as mycobacteria have also been linked
with sarcoidosis
Symptoms
• Constitutional symptoms Fever, night sweats, malaise, weight loss
•
Lymph nodes Commonly picked up on CXR but may be symptomatic
and affect the axillary, cervical and inguinal nodes
•
Lungs Cough (usually dry), breathlessness, wheeze, fine crackles
•
Skin Erythema nodosum (Fig. 1), lupus pernio, infiltration of scars by
granulomas
•
Eyes Uveitis (anterior and posterior), dry
eyes, glaucoma
•
Heart Arrhythmia, cardiomyopathy, heart
failure, conduction defects
•
Neurological Meningeal inflammation,
seizures, mass lesions, neuropathy,
hypothalamic pituitary infiltration
•
Hypercalcaemia Nephrolithiasis,
neuropsychiatric disturbance, abdominal
pain, bone pain
•
Liver Commonly involved but rarely clinically significant, hepatitis,
hepatosplenomegaly
• Bloods FBC (WCC usually raised), CRP/ESR (usually
raised), calcium (usually raised), LFTs (deranged if
liver involvement), ACE level raised in approx. 60% of
patients with acute disease and decreases in response
to treatment/resolution of the disease
•
CXR (see Staging)
•
ECG To check for early signs of rhythm disturbance
due to conducting system disease or effects of
hypercalcaemia
• Tuberculin test Typically negative in patients with
sarcoidosis
• CT chest Used to detect and assess the severity of
interstitial lung disease
• Lung function tests Show restrictive defect in severe,
progressive cases
•
Bronchoalveolar lavage ↑Lymphocytes, ↑CD4:CD8
ratio
•
Biopsy Transbronchial, lymph node or skin lesion
biopsies demonstrate non-caseating granulomas
• FGD PET scan Can be used to assess inflammatory
activity accurately in patients
• Gallium scan May be used to detect extrapulmonary
disease and tends to reveal a ‘lambda’ pattern
Steroids
• Oral prednisolone or IV hydrocortisone
•
Indication for steroids include:
•
CXR stageII or III who have
moderate to severe or progressive
symptoms
•
Hypercalcaemia
• Eye, heart or neuro involvement
DMARDs/biological agents
• Antimetabolites, e.g. methotrexate,
azathioprine, leflunomide and
mycophenolate, are alternatives
to steroids
•
TNF alpha inhibitors, e.g. infliximab
and adalimumab, may be prescribed
if patients not responding to
antimetabolites
Surgical
• Surgery may be considered with
severe progressive lung fibrosis,
including lung transplantation (rare)
Denition
Pathophysiology
Clinical features
Investigations
Poor prognostic factors
•
Insidious onset, symptoms
>6months
• Absence of erythema nodosum
•
Extrapulmonary manifestations
e.g. lupus pernio, splenomegaly
•
CXR: stage III–IV features
• Black ethnicity
Prognosis
Management
Staging
Syndromes associated with sarcoidosis
• Löfgren syndrome An acute form of the disease characterised by bilateral
hilar lymphadenopathy, erythema nodosum, fever and polyarthralgia; it
usually carries an excellent prognosis
•
Mikulicz syndrome Enlargement of the parotid and lacrimal glands due to
sarcoidosis, TB or lymphoma
•
Heerfordt syndrome Parotid enlargement, fever and uveitis secondary to
sarcoidosis
There are 5 stages of sarcoidosis according to CXR findings (see Fig.2)
• Stage 0 Normal CXR findings
•
Stage I Bihilar lymphadenopathy
•
Stage II Bihilar lymphadenopathy+parenchymal infiltrates
•
Stage III Parenchymal infiltrates alone
•
Stage IV Pulmonary fibrosis
Fig. 1 Erythema nodosum
Fig. 2 Stages I–IV of sarcoidosis
Stage I
(lymphadenopathy)
Stage III
(infiltrates only)
Stage II
(lymphadenopathy and infiltrates)
Stage IV
(fibrosis)
Epidemiology and risk factors
https://t.me/med1917
Mind Maps for Medicine \ 67
Gastroenterology
Chapter 3
03
Acute liver failure .........................................................................................................................................................68
Acute pancreatitis .......................................................................................................................................................70
Alpha-1 antitrypsin deciency ............................................................................................................................72
Chronic pancreatitis ...................................................................................................................................................74
Cirrhosis .............................................................................................................................................................................76
Coeliac disease ..............................................................................................................................................................80
Crohn’s disease ..............................................................................................................................................................82
Gastric cancer ................................................................................................................................................................86
Gastro-oesophageal reux disease
..................................................................................................................88
Hereditary haemochromatosis ...........................................................................................................................90
Irritable bowel syndrome .......................................................................................................................................92
Jaundice ............................................................................................................................................................................94
Oesophageal cancer and other causes of dysphagia ...........................................................................96
Peptic ulcer disease .................................................................................................................................................100
Primary biliary cholangitis ................................................................................................................................... 102
Primary sclerosing cholangitis ..........................................................................................................................104
Ulcerative colitis ........................................................................................................................................................106
Upper gastrointestinal bleed ............................................................................................................................108
Wilson’s disease..........................................................................................................................................................112
https://t.me/med1917
Notes
Acute liver failure
Mind Maps for Medicine \ 69
68 / Chapter 3 Gastroenterology: Acute liver failure
Acute liver failure (ALF) is an
uncommon but life-threatening
illness in which rapid deterioration
of the liver function results in
coagulopathy and alteration in the
mental status of a previously healthy
individual.
• Cerebral oedema
•
Hypoglycaemia
• Hypotension
•
Hepatorenal syndrome
• Sepsis
• Seizures
• Acute respiratory distress
syndrome
•
Bloods FBC, ESR, CRP, LFTs,
U&Es, glucose, ANA, AMA, SMA,
immunoglobulins, prothrombin
time/INR, hepatitis screen, EBV
and CMV serology, paracetamol
and salicylate levels
• ABG
• Ceruloplasmin and 24-h urine
copper If suspected Wilson’s
disease
•
Blood cultures
• Doppler of hepatic veins If
suspected Budd–Chiari syndrome
• CXR
• US abdomen
• Ascitic tap If ascites present
Clinical features
Acute liver failure
InvestigationsComplications
Bernau’s classication
• Fulminant hepatic failure (FHF) Liver failure takes place within
8weeks of the onset of the underlying illness
•
Subacute FHF or late-onset hepatic failure Occurs when there has
been a gap of 8–26weeks between the onset ofillness and liver failure
O’Grady’s classication
• Hyperacute Liver failure occurring <7days from disease onset
•
Acute Liver failure occurring 1–4weeks from disease onset
•
Subacute Liver failure occurring 4–12weeks from disease onset
•
Infection Viral hepatitis (mainly
hepatitisA or B, it is extremely
uncommon in hepatitisC),
leptospirosis, yellow fever, EBV,
CMV, herpes simplex virus,
dengue virus
•
Drugs Paracetamol overdose
(most common cause in
developed countries), halothane,
isoniazid, phenytoin, amiodarone,
propylthiouracil, Ecstasy, herbal
remedies, amoebic infection
•
Toxins Amanita phalloides
mushroom toxin, carbon
tetrachloride, yellow phosphorus
Supportive measures and monitoring
• Should be managed in specialised liver unit or ITU
setting with regular monitoring
• Patients who have advanced encephalopathy should
have airways protected with intubation and NG tube
inserted to avoid aspiration and remove any blood
from stomach
Treat underlying cause
• e.g. IV NAC for paracetamol overdose, stop offending
drugs, steroids for autoimmune hepatitis
Manage complications
• Treat bleeding/raised INR VitaminK e.g. 10mg IV,
platelets, fresh frozen and red cells as needed
• Treat renal failure Haemofiltration or haemodialysis
Criteria for paracetamol-induced
liver failure
• Arterial pH <7.30 (24h after ingestion)
OR all of the following:
• INR >6.5 (PT >100sec)
• Creatinine >300µmol/L
• GradeIII or IV hepatic encephalopathy
Criteria for non-paracetamol-
induced liver failure
Prothrombin time >100sec (INR >6.5)
OR any three of the following (PADDS):
• Prothrombin time >50sec (INR >3.5)
• Age <10 or >40years
• Drug-induced liver failure
• Duration of jaundice to hepatic
encephalopathy >7days
• Serum bilirubin >300µmol/L
Denition
• Manage infections Broad-spectrum
antibiotics e.g. IV ceftriaxone
•
Manage hypoglycaemia IV dextrose
• Manage ascites Restrict fluid, low-salt diet,
daily weights, diuretics
• Manage hypotension Monitor with arterial
line, fluid resuscitation
•
Manage encephalopathy Avoid sedatives,
correct electrolytes, lactulose
• Treat seizures Phenytoin
• Manage cerebral oedema Patients should
be positioned with the head elevated at 30°
in ITU; patient should have ICP monitoring;
treat with IV mannitol and hyperventilation
Emergency liver transplantation
King’s College Criteria for liver transplant
Predicts poor outcome in acute liver failure and
should prompt consideration for transplantation
Management
• Wilson’s disease
•
Autoimmune hepatitis
•
Budd–Chiari syndrome
•
Pregnancy related Acute
fatty liver of pregnancy, HELLP
syndrome
•
Reye syndrome Rare side effect
of aspirin
•
Ischaemic hepatitis e.g. From
shock or heart failure
•
Indeterminate
•
Jaundice
•
Encephalopathy (classification):
•
Grade 0 No personality or
behavioural abnormality
detected
•
Grade 1 Lack of awareness,
euphoria or anxiety,
shortened attention span,
impaired performance of
addition
•
Grade 2 Lethargy or apathy,
minimal disorientation
for time or place, subtle
personality change,
inappropriate behaviour,
impaired performance of
subtraction
•
Grade 3 Somnolence to
semi stupor but responsive
to verbal stimuli, confusion,
gross disorientation
• Grade 4 Coma
•
Fetor hepaticus
•
Asterixis/hepatic flap
•
Constructional apraxia
•
Hypoglycaemia
•
Bleeding and bruising
•
Hepatomegaly
•
Ascites
Classication
Causes
https://t.me/med1917
Notes
Acute pancreatitis
Mind Maps for Medicine \ 71
70 / Chapter 3 Gastroenterology: Acute pancreatitis
Local (the Ps)
•
Pseudocyst
•
Pancreatic abscess
• Pancreatic necrosis
• Pancreatic fistulae
• Chronic Pancreatitis
Systemic (DR SAM)
• Disseminated intravascular
coagulation
• Renal failure (acute)
• Sepsis
• Acute respiratory distress
syndrome
• Multiple organ dysfunction
Investigations
Complications
• Gallstones
•
Ethanol
•
Trauma
•
Steroids
•
Mumps (other viruses include CoxsackieB)
•
Autoimmune (e.g. polyarteritis nodosa), Ascaris
infection
•
Scorpion venom
•
Hypertriglyceridaemia, Hyperchylomicronaemia,
Hypercalcaemia, Hypothermia
•
ERCP
•
Drugs e.g. azathioprine, bendroflumethiazide,
furosemide, mesalazine, steroids, sodium valproate
•
Initially nil by mouth and resuscitation
with IV fluids
• Oxygen
•
Pain relief e.g. with opioids
•
Antibiotics (broad spectrum)
For treatment of associated cholangitis
or other acute infections; if pancreatic
necrosis is suspected, IV antibiotics should
be given
•
Severe cases should be treated in ITU or
a HDU
• Nutritional support Oral feeding can
commence in people with mild acute
pancreatitis (in absence of nausea/
vomiting, or abdominal pain); enteral
feeding is otherwise preferable and
is possible in the majority of people;
parenteral feeding is reserved for people
in whom enteral nutrition is not possible
Acute inflammation of the pancreas
causing the release of exocrine
enzymes that cause autodigestion of
the organ. There may be involvement
of local tissues and distant organs.
Management
Causes (GET SMASHED)
Glasgow Imrie criteria (PANCREAS) at 48h
after admission:
• P
a
O
2
(arterial) <8.0kPa
•
Age >55years
•
Neutrophilia White blood cells >15×10
9
/L
•
Calcium <2.0mmol/L
• Renal (serum urea) >16mmol/L
• Enzymes LDH >600IU/L
• Albumin <32g/L
•
Sugar (glucose) >10mmol/L
(≥3 points: high risk for severe pancreatitis)
Other scoring systems for prognosis include:
Ranson’s Criteria/Acute Physiology and
Chronic Health EvaluationII (APACHEII)
as well as measurement of CRP
Clinical features
Bloods
• Pancreatic enzymes: serum
amylase raised (typically ≥3×
upper limit of normal); lipase
levels are more sensitive and
more specific
• FBC, U&Es, glucose and
CRP indicate prognosis
(see Assessing severity)
• Raised bilirubin and/or serum
aminotransferase (suggest
gallstones)
• Calcium (hypocalcaemia is
relatively common and may
indicate prognosis)
Imaging
• AXR (erect) Excludes other
differentials, e.g. intestinal
obstruction and perforation, and
may show pancreatic calcification
•
CXR May show elevation of one
hemidiaphragm, infiltrates±acute
respiratory distress syndrome or
pleural effusions (in severe cases)
•
CT pancreas (contrast-enhanced)
Can identify pancreatic swelling,
fluid collection and change
in density of gland; this has
implications for prognosis and
predicts the need for surgery
• US abdomen Can show a swollen
pancreas, dilated common bile duct
and free peritoneal fluid; it is also
useful for detecting gallstones
• MRI pancreas May reveal acute
abdominal wall oedema which may
be useful in assessing severity
Acute pancreatitis
Assessing severity
Symptoms
• Acute upper abdominal pain
(may radiate to the back)
•
Nausea/vomiting
•
Anorexia
•
Pyrexia
Signs
• Fever, hypotension, tachycardia, tachypnoea
•
Epigastric tenderness, with guarding on
abdominal examination
•
Decreased bowel sounds
•
Jaundice
•
Grey Turner’s sign (ecchymosis of the
flank) and Cullen’s sign (ecchymoses in the
periumbilical region) (see Fig. 1)
Fig. 1 Cullen’s sign (A) and Grey Turner’s sign (B): signs of
retroperitoneal haemorrhage (a late clinical feature of acute
pancreatitis)
• A trigger, e.g. alcohol or any of the causes listed, is
thought to activate a common pathway leading to
marked elevation of intracellular calcium leading
to activation of intracellular proteases and release
of exocrine pancreatic enzymes
•
This results in acinar cell injury and necrosis which
promote migration of in
flammatory cells
•
This leads to local inflammatory response and
occasionally a systemic in
flammatory response,
resulting in single or multi-organ failure
By far the most common causes
Denition Pathophysiology
https://t.me/med1917
Notes
Alpha-1 antitrypsin deciency
Mind Maps for Medicine \ 73
72 / Chapter 3 Gastroenterology: Alpha-1 antitrypsin deciency
Alpha-1 antitrypsin (A1AT)
deficiency is a common inherited
condition caused by lack of the
protease inhibitor (Pi) A1AT normally
produced by the liver. It classically
causes emphysema (i.e. COPD)
in patients who are young and
non-smokers.
•
The gene for A1AT is found on
chromosome 14 and is inherited
in an autosomal recessive fashion
•
Alleles are classified by their
electrophoretic mobility: M, normal;
S, slow; and Z, very slow:
•
Normal=PiMM
•
Homozygous PiSS (50% normal
A1AT levels)
•
Homozygous PiZZ (10% normal
A1AT levels)
•
The role of A1AT is to protect cells from
enzymes such as neutrophil elastase
Conservative
• Smoking cessation
•
Pulmonary rehabilitation
Pharmacological
• Bronchodilators (see Ch2: Chronic obstructive
pulmonary disease)
• IV A1AT protein concentrates: particularly
for non-smokers with COPD attributable to
emphysema; treatment is very expensive
Surgical
Lung
• Lung volume reduction surgery
•
Lung transplantation
Liver
• Liver failure may require liver transplantation
•
Patients who manifest disease
usually have PiZZ genotype
•
If there is a deficiency of A1AT
then elastase can break down
elastin unchecked; in the lungs
this can cause destruction
of alveolar walls resulting in
emphysema
•
Some people may develop liver
disease due to congestion of
A1AT in the liver cells causing
cell destruction
Pathophysiology
Lungs
• Lung disease does not usually present
until people are in their 30s or 40s,
with smokers tending to develop
symptoms approx. 10years earlier than
non-smokers
•
COPD symptoms: dyspnoea, wheezing
and cough most common (see Ch2:
Chronic obstructive pulmonary disease)
•
There is increased risk of lung cancer
Liver
(Not everyone with A1AT deficiency will develop liver
disease)
Neonates/children
• Neonates may present with neonatal jaundice and
hepatitis
•
Older children may develop hepatitis, cirrhosis and liver
failure
Adults
• May develop hepatitis, fibrosis, cirrhosis and liver failure
•
Increased risk of hepatocellular carcinoma (due to above)
Alpha-1 antitrypsin deciency
• A1AT deficiency is one of the
most common inherited disorders
among Caucasians
•
Approx.1per 3000–5000
individuals are affected by A1AT
deficiency
•
Up to 5% of people diagnosed
with COPD are thought to have
A1AT deficiency
Epidemiology
• Serum A1AT concentrations
Reduced
• LFTs May be deranged in liver
disease
• Spirometry Obstructive picture
if emphysema present
• CXR/CT chest May show
evidence of emphysema
• Liver biopsy A1AT-containing
globules are seen in hepatocytes
Investigations
Denition
Management
Clinical features
https://t.me/med1917
Mind Maps for Medicine \ 75
74 / Chapter 3 Gastroenterology: Chronic pancreatitis
Imaging
• AXR 30% show pancreatic calcification in later stages
(seeFig.1).
• Abdominal US Reveals gallstones, duct dilatation,
pancreatic morphology
• Abdominal CT
1st-line imaging
modality for people
with a history
and symptoms
suggestiveof chronic
alcohol-related
pancreatitis
• MRCP/ERCP Useful
to look for treatable
strictures, tumours,
stones or pseudocysts
• Endoscopic US
Irregular duct walls,
duct dilatation and
cysts can be detected
Chronic pancreatitis is a chronic,
irreversible in
flammation and/or
fibrosis of the pancreas, typically
characterised by severe abdominal
pain and progressive endocrine and
exocrine insufficiency.
Common
• Malabsorption
• Diabetes mellitus
• Chronic pain
• Opioid dependency due
to chronic pain
•
Osteoporosis
• Pseudocyst formation
• Pancreatic calcification
Less common
• Duodenal/gastric outlet
obstruction
• Biliary obstruction
• Pancreatic cancer
• Fistulae
• Splenic or portal vein thrombosis
• Pseudoaneurysm
Clinical features
Chronic pancreatitis
Complications
• The underlying mechanism is unclear
•
Abnormalities of bicarbonate excretion
caused by functional defects at the level
of the cellular wall, e.g. in cystic fibrosis,
or mechanical causes e.g. trauma, can
result in pancreatic enzyme activation
•
Pancreatic enzyme activation leads to
pancreatic tissue injury and necrosis
•
Pancreatic fibrogenesis is a typical
response to injury involving a complex
interplay of growth factors, cytokines
and chemokines, leading to the deposition
of extracellular matrix
•
Alcohol causes proteins to precipitate in
the ductular structure of the pancreas;
this leads to local pancreatic dilatation
and fibrosis; there may also be direct toxic
effects of alcohol on the pancreas
• Oxidative stress seems to play an important
role in the pathogenesis of chronic
pancreatitis
Conservative measures
• Alcohol cessation
• Smoking cessation
• Dietitian support
Pain relief
• Simple analgesia initially e.g. paracetamol
and NSAIDs
• Opiates e.g. tramadol
• Coeliac plexus block via a gastric approach under
endoscopic US guidance
• ERCP may help to reduce pain by dilating
strictures of the pancreatic ducts
Managing pancreatic insuciency
• Replacement of pancreatic enzymes can help
malabsorption and also reduce pain e.g. Creon®
• Fat-soluble vitamins (A, D, E, K)
• Treat diabetes mellitus accordingly e.g. insulin
Surgery
• Cholecystectomy Clearance of
duct stones – essential if present
• Sphincterotomy Accessory papilla
in patients with pancreas divisum
•
Percutaneous or surgical
drainage (laparoscopic or open)
Pseudocyst or abscess
• Partial pancreatic resection
A Whipple’s procedure may be
necessary
• Extracorporeal shockwave
lithotripsy For adults with
pancreatic duct obstruction caused
by a dominant stone if surgery is
unsuitable
• Total pancreatectomy A last
resort for relief of intractable pain
not responding to other methods
Management
• Alcohol Approx. 70–80% of cases
•
Idiopathic Approx. 25% of cases
•
Smoking An independent risk factor
•
Congenital Pancreas divisum, annular
pancreas
•
Familial Hereditary pancreatitis,
cystic fibrosis
•
Metabolic Hypercalcaemia,
hyperlipidaemia
•
Iatrogenic e.g. ERCP, abdominal
radiotherapy
• Drugs e.g. Thiazide diuretics,
azathioprine, tetracyclines,
valproic acid and DDP-4 inhibitors
•
Trauma
•
Obstruction of the pancreatic
duct e.g. Pseudocysts, ductal
strictures, periampullary tumours,
gallstones (uncommon)
• Autoimmune disease Sjögren
syndrome, IBD and primary biliary
cirrhosis
•
Abdominal pain: classically
epigastric pain radiating into
the back
•
Nausea and vomiting
•
Decreased appetite
•
Malabsorption with weight
loss, diarrhoea, steatorrhea
and protein deficiency
•
Diabetes mellitus
(see Ch5: Diabetes mellitus)
Denition Aetiology
Bloods
Serum amylase (usually normal but
may be mildly raised in an acute on
chronic attack), albuminand clotting
studies (may be deranged in liver
disease), low calcium and B
12
(suggests
malabsorption), ALP (raised levels
suggests biliary tract obstruction
ifgamma-glutamyltransferase is
also raised), raised glucose/HbA1c
(in endocrine dysfunction), serum
trypsinogen (low)
Pathophysiology
Fig. 1 Calcification of pancreas on AXR
Investigations
Stool
• Faecal elastase (reduced if
malabsorption present)
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Mind Maps for Medicine \ 77
76 / Chapter 3 Gastroenterology: Cirrhosis
• Portal hypertension
•
Ascites
• Portosystemic encephalopathy
• Acute kidney injury (hepatorenal
syndrome)
• Hepatopulmonary syndrome
• HCC
• Bacteraemia, infection
• Malnutrition
• Osteoporosis
Clinical features
Investigations
• Alcohol Excess
•
Viral hepatitis Approx. 10% of cases (types B, C and D)
•
Non-alcoholic fatty liver disease (NAFLD)
Manage underlying cause
andslowing progression
• Alcohol abstinence
• Ensure adequate nutrition, including calorie
and protein intake
•
Treat haemochromatosis accordingly
e.g. venesection (see Ch3: Haemochromatosis)
• Treat viral hepatitis accordingly
(seeCh8: Hepatitis sections)
• Steroids for autoimmune chronic active
hepatitis
• Avoid hepatotoxic drugs
Manage complications ofcirrhosis
• Screening and management of oesophageal
varices (see Ch3: Upper gastrointestinal bleed)
• Cholestyramine to help with pruritus
• Manage hepatic encephalopathy appropriately
e.g. with oral lactulose
•
Management of ascites (see Notes)
• Screening and management of osteoporosis
(see Ch7: Osteoporosis)
Monitoring and screening
forhepatocellular carcinoma (HCC)
US liver±alpha-fetoprotein every 6months as
surveillance for HCC
Liver transplantation
The only definitive treatment for cirrhosis
Management
(Compensated cirrhosis may be asymptomatic)
Decompensated clinical features
• Jaundice
•
Signs of portal hypertension: ascites, caput medusae,
splenomegaly, variceal haemorrhage
•
Signs of hepatic encephalopathy
Features of chronic liver disease
• Nails: leuconychia, Terry’s nails, clubbing
•
Palmar erythema
•
Dupuytren’s contracture
•
Spider naevi (see Fig. 1)
•
Xanthelasma
•
Hepatomegaly
•
Gynaecomastia (see Fig. 2), atrophic testes, loss of body hair
•
Parotid enlargement
Denition Causes
Cirrhosis
Most common causes
Cirrhosis results from necrosis of liver cells followed
byfibrosis and nodule formation. This results in
impairment of liver cell function and gross distortion
ofthe liver architecture, leading to complications such
asportal hypertension.
Cirrhosis can be described as:
• Compensated The liver can still function effectively
with few or no clinical symptoms
•
Decompensated The liver is damaged to the point
that it cannot function adequately with evident
clinical complications (see Clinical features)
•
Liver fibrosis results from chronic insult
(due to causes listed) resulting in
abnormal connective tissue production
and deposition
• Cirrhosis is an advanced stage of
liver fibrosis that is accompanied
by distortion of the hepatic
architecture
• Historically, cirrhosis can be divided
into 2 types histologically:
•
Micronodular (often caused
by alcohol excess or biliary
tract disease) or
Fig. 1 Spider naevi
• Bloods:
•
FBC (occult bleeding may cause anaemia, macrocytic anaemia in alcohol
misuse, ↓WCC and platelets may indicate hypersplenism)
•
Biochemistry: LFTs (may show ↑bilirubin, ALT, AST, gamma-GT), clotting
and albumin (↓albumin and ↑INR if synthetic function affected), U&Es
(may show ↓Na
+
and renal function deranged in hepatorenal syndrome),
glucose (may be deranged)
• Specific tests for underlying cause: serum alpha-fetoprotein (↓ in
alpha-1 antitrypsin deficiency), ceruloplasmin (if suspected Wilson’s
disease); iron studies and HFE gene mutation analysis (in suspected
haemochromatosis); viral hepatitis screen (if suspected viral hepatitis
cause); enhanced liver fibrosis (ELF) test in people with NAFLD to test
for advanced liver fibrosis; autoantibodies (ANA, AMA, SMA) to rule out
autoimmune hepatitis and PBC
• US abdomen To detect cirrhosis and hepatocellular carcinoma (HCC) and
also to assess for splenomegaly and ascites
• Liver duplex To assess for hepatic venous outflow obstruction
• CT/MRI liver To detect complications of cirrhosis, such as splenomegaly,
ascites or HCC
• Ascitic tap For ascites to identify cause and rule out infection
• Liver biopsy Confirms diagnosis
• Macronodular (often seen in
chronic viral hepatitis) depending on
the size of nodules, although a mixed
picture is also seen
• The major clinical consequences of
cirrhosis are impaired hepatocyte
function, increased intrahepatic
resistance and the development
of hepatocellular carcinoma
•
Multiple circulatory abnormalities
in cirrhosis are closely linked to the
hepatic vascular alterations resulting
in portal hypertension
Pathophysiology
Complications
• Genetic:
•
Haemochromatosis
•
Alpha-1 antitrypsin deficiency
•
Wilson’s disease
•
Galactosaemia (rare)
•
Congenital tyrosinaemia
•
Glycogen storage disease typeIV
•
Cystic fibrosis
•
Autoimmune:
•
Primary biliary cholangitis (PBC)
•
Primary sclerosing cholangitis
(PSC)
•
Autoimmune hepatitis
•
Sarcoidosis
•
Hepatic venous outflow
obstruction:
•
Hepatic veno-occlusive disease
•
Budd–Chiari syndrome
•
Congestive hepatopathy (from
constrictive pericarditis)
•
Drugs e.g. Methotrexate,
amiodarone, methyldopa
Fig. 2 Gynaecomastia
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Notes
Cirrhosis
Mind Maps for Medicine \ 79
78 / Chapter 3 Gastroenterology: Cirrhosis notes
Assessing severity of cirrhosis:
Child–Pugh score (
ABCDE)
Child–Pugh score is used to assess the prognosis of chronic liver disease,
mainly cirrhosis:
•
Albumin (serum, mmol/L): <34 (1 point), 34–50 (2 points), >50
(3points)
•
Bilirubin (total, g/L): <34 (1 point), 34–50 (2 points), >50 (3 points)
•
Coagulation INR: <1.7 (1 point), 1.7–2.3 (2 points), >2.3 (3 points)
•
‘Drum’ abdomen (Ascites): none (1 point), mild (2 points), severe
(3points)
•
Encephalopathy (hepatic): none (1 point), grade I–II (2 points),
grade III–IV or refractory (3 points)
Interpretation:
•
Class A (5–6 points) = 1-year survival (100%), 2-year survival (85%)
•
Class B (7–9 points) = 1-year survival (80%), 2-year survival (60%)
•
Class C (10–15 points) = 1-year survival (45%), 2-year survival (35%)
Ascites
Denition
An abnormal accumulation of fluid within the peritoneal cavity.
Pathophysiology
• Ascitic fluid can accumulate as a transudate or an exudate
•
Broadly speaking, transudates are a result of increased pressure in the
hepatic portal vein, e.g. due to cirrhosis, while exudates are actively
secreted fluid due to infection, inflammation or malignancy
•
In cirrhosis, vasodilators are locally released due to portal hypertension;
these affect the splanchnic arteries causing reduced arterial blood
flow
and arterial pressures leading to activation of mechanisms including
the renin–angiotensin–aldosterone system, sympathetic nervous
system and ADH which results in Na
+
and water retention
•
The formation of oedema is also further exacerbated by
hypoalbuminaemia
Causes
Transudate Exudate
Portal hypertension e.g. cirrhosis Cancer: metastasis or primary
carcinomatosis
Hepatic veno-occlusive disease Infection: including peritoneal TB
Budd–Chiari syndrome Nephrotic syndrome
Cardiac failure Lymphatic obstruction
Meigs syndrome Serositis
Constrictive pericarditis
Clinical features
• Abdominal swelling/fullness
•
Shifting dullness
•
Pleural effusion and peripheral oedema may also be present
•
Other signs of underlying cause may also be present.
Diagnosis
• Bloods LFTs including serum albumin, specific tests (see above)
dependingon clinical features
•
Ascitic tap:
•
Ascitic albumin to help differentiate between transudate and
exudate (≥11g/L suggests exudate and <11g/L suggests
transudate)
•
WCC, Gram stain and culture; neutrophil count >250cells/mm
3
suggestsbacterial (usually spontaneous peritonitis)
• Cytology for malignant cells
•
Amylase to exclude pancreatitis
The serum-ascites albumin gradient (SAAG) is a formula which can further
helpto determine the cause of ascites:
SAAG=(albumin concentration of serum) – (albumin
concentration ofascitic fluid)
A high gradient (>1.1g/dL) indicates the ascites is due to portal
hypertension with 97% accuracy.
Management
• Treat underlying cause
•
Bed rest, fluid and salt restriction
•
Diuretics e.g. Spironolactone (50–100mg/day); furosemide can also
be added
• Paracentesis Used in patients with tense ascites or those who are
resistant to above treatments; provides rapid symptomatic relief; IV
infusion of albumin is administered immediately afterwards
•
Transjugular intrahepatic portosystemic shunt (TIPS) Occasionally
used for resistant ascites caused by portal hypertension
•
Treat spontaneous bacterial peritonitis accordingly with antibiotics
according to local antimicrobial guidelines after diagnostic aspiration
Cirrhosis notes
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Notes
Coeliac disease
Mind Maps for Medicine \ 81
80 / Chapter 3 Gastroenterology: Coeliac disease
Coeliac disease is an immune-
mediated, in
flammatory systemic
disorder provoked by gluten and
related prolamins in genetically
susceptible individuals. This can
result in malabsorption of nutrients
due to chronic in
flammation
and damage (villous atrophy) to
the lining of the small intestine.
Coeliac disease is associated with
dermatitis herpetiformis and other
autoimmune disorders.
Coeliac disease
• Anaemia (iron, folate and vitamin
B
12
deficiency)
• Hyposplenism
• Osteoporosis, osteomalacia
• Lactose intolerance
• Malignancy: enteropathy-associated
T-cell lymphoma of small intestine,
oesophageal cancer
• Subfertility, unfavourable pregnancy
outcomes
Complications
• Coeliac disease is strongly associated
with HLA-DQ2 (95% of patients) and
HLA-DQ8 (80%)
•
The toxin alpha-gliadin is the toxic
portion of the gluten which is contained
in wheat, rye and barley
•
Gliadin is deaminated by tissue
transglutaminase (TTG); it then interacts
with antigen-presenting cells in the
lamina propria via HLA-DQ2 and -DQ8
and activates gluten-sensitive Tcells
•
The resultant inflammatory reaction
and release of mediators causes villous
atrophy and crypt hyperplasia
(see Fig.1)
•
The following patients should be screened for coeliac
disease: autoimmune thyroid disease, dermatitis
herpetiformis, irritable bowel syndrome, type1
diabetes mellitus, 1st-degree relatives of patients with
coeliac disease
• Lifelong strict gluten-free diet (GFD)isthe only known
effective treatment
Management
• Chronic or intermittent
diarrhoea
•
Recurrent abdominal pain,
cramping or distension
•
Failure to thrive (in children)
•
Nausea and vomiting
•
Fatigue
•
Sudden or unexpected
weight loss
•
Unexplained iron-deficiency
anaemia, or other unspecified
anaemia
•
Dermatitis herpetiformis
(seeFig.2)
Clinical features
PathophysiologyDenition
Fig. 1 Lining of small bowel vs lining of small bowel with
coeliac disease
• If patient is already taking a gluten-free diet they should be asked,
if possible, to reintroduce gluten for at least 6weeks prior to testing:
• Routine bloods FBC (anaemia), iron studies (iron deficiency),
vitamin B
12
(↓), folate (↓), LFTs,calcium, albumin
•
Immunology TTG antibodies (IgA) are 1st line for diagnosis according
to NICE, endomyseal antibody (IgA), anti-gliadin antibody (IgA or IgG)
(not recommended by NICE), anti-casein antibodies are alsofound
in some patients
• Duodenal/jejunal biopsy (see Fig.3) Villous atrophy, crypthyperplasia,
↑intraepitheliallymphocytes, lamina propria infiltration with lymphocytes
• Dual energy X-ray absorptiometry (DEXA) scan Performed at diagnosis
due to increased risk ofosteoporosis
Fig. 3 Duodenal biopsy showing complete villous atrophy, marked
crypt hyperplasia, intraepithelial lymphocytosis and inflammatory
infiltrate in the lamina propria
Investigations
Normal
Damaged
Fig. 2 Dermatitis herpetiformis: itchy symmetrical eruption of vesicles and crusts over the
extensor surfaces of the body associated with coeliac disease; it is caused by deposition
ofIgAin the dermis
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