Abdo Pain And Jaundice Flashcards
(179 cards)
1
Q
What is inflammatory pain indicative of in the acute abdomen
A
Peritonitis - inflammation of peritoneum - gives localised pain
Constant pain, with a raised temp, pulse and leucocytosis
2
Q
What is obstructive pain indicative of in the acute abdomen
A
Colicky pain, often agitated
Pain may become constant with superimposed inflammation
3
Q
What is referred visceral pain indicative of in the acute abdomen
A
Foregut - oseophagus to D2 pain is referred to upper abdo
Midgut - D2 to transverse colon is referred to middle abdo
Hindgut pain is referred to lower abdo
4
Q
Vascular differentials of the acute abdomen
A
AAA
Mesenteric thrombosis / embolus
5
Q
Visceral differentials of the acute abdomen
A
Acute appendicitis
Meckel’s diverticulitis
Intestinal obstruction
Perforated viscus
Acute pancreatitis
Acute cholecystitis
Renal calculi
The acute scrotum
IBD
6
Q
Medical differentials of the acute abdomen
A
GORD
Referred pain from pneumonia / MI / UTI / pyelonephritis
7
Q
Gynae causes of the acute abdomen
A
Ruptured ectopic
Torted / ruptured ovarian cysts
Salpingitis
8
Q
Essential investigations for the acute abdomen
A
FBC, U&E, LFTs, CRP, lipase and blood gas
Pregnancy test
Urinalysis
Imaging
9
Q
What is a CT abdomen / pelvis used for
A
Diagnostic for most surgical pathologies
10
Q
What is an erect CXR used for
A
Useful if suspecting perforated viscus
11
Q
What is an US used for in acute abdomen
A
Most useful if suspecting gynae pathology or biliary pathology
12
Q
What is acute appendicitis
A
Occurs when the appendix lumen is obstructed by a faecolith, foreign body or lymphoid enlargement in the wall
Bacteria can then proliferate in the obstructed loop of bowel eventually leading to necrosis and perforation due to raised intraluminal pressure
Most commonly occurs in ages 10-30
13
Q
Symptoms of acute appendicitis
A
Abdo pain - starts dull and central then becomes localised and sharp in RIF
Anorexia
N&V
14
Q
Signs of acute appendicitis
A
Tachycardia
Mild fever, flushing and fetor
RIF tenderness / guarding
Rebound + percussion tenderness in RIF
Rosving’s sign (more painful in RIF than LIF when LIF pressed)
Psoas sign (pain on R hip extension: retroperitoneal retrocaecal appendix)
Obturator sign (pain on internal rotation of R hip)
15
Q
Imaging used in suspected acute appendicitis
A
In females of child bearing age US is used to try and rule out gynae pathology
In older patients CT abdo / pelvis is used to rule out alternate surgical pathology
16
Q
Management of acute appendicitis
A
ABCDE resuscitation including IV abx
Laparoscopic appendectomy
17
Q
Early / late complications of laparoscopic appendectomy
A
Early: haematoma / wound infections
Late: small bowel obstruction or incisional hernia
18
Q
Complications of acute appendicitis perforation
A
Peritonitis and sepsis
Appendiceal mass - inflamed appendix becomes covered with omentum
Appendiceal abscess - local / pelvic / subhepatic / subphrenic
Adhesions
19
Q
Pathophysiology of gallstone disease
A
Bile usually contains cholesterol, phospholipids, bile salts, water and conjugated bilirubin
Bile flows into the gallbladder if the sphincter of oddi is closed where it becomes more concentrated as water is absorbed
Presence of fatty acids or amino acids in the duodenum will lead to release of CCK which causes the gall bladder to contract and bile to be released
20
Q
What is cholelithiasis
A
Formation of stones in the gallbladder
21
Q
What are cholesterol gallstones
A
Cholesterol crystallisation within the gall bladder bile due to excess cholesterol secretion into the bile or loss of bile salt content
22
Q
Cholesterol gallstone risk factors
A
Increasing age
Obesity, high fat diet, rapid weight loss
Female sex, multiparity, pregnancy, OCP
DM
Ileal disease
Liver cirrhosis
23
Q
What are bile pigment stones
A
Both black and brown pigment gallstones contain calcium bilirubinate and form independently of cholesterol stones
- black is associated with haemolytic conditions
- brown occur due to biliary stasis / infection
24
Q
What is the difference between biliary colic and cholecystitis
A
Both are formed by cholelithiasis
Biliary colic - no associated inflammation / infection
Cholecystitis - associated inflammation / infection
25
What is choledocholithiasis
Stone impactation in the common bile duct
Can cause biliary colic if temporary or painful obstructive jaundice if more prolonged
Can also predispose to ascending cholangitis or acute pancreatitis
26
What is gallstone ileus
Uncommon
Large gallstone erodes through to the gall bladder and into adjacent duodenum
- then can produce an obstruction if it impacts in a narrow segment of bowel
27
How does gallstone ileus appear on CT / X-ray
Signs of small bowel obstruction
The gallstone may be visible and there will be air in the biliary tree
28
What is biliary colic
Associated with temporary obstruction of the gallbladder, cystic duct or common bile duct due to gallstones
29
Symptoms of biliary colic
Severe constant epigastric / RUQ pain with a crescendo characteristic
May radiate to back or right shoulder / subscapular region
N&V
Worse upon food consumption (fatty)
Systemically well
30
What is acute cholecystitis
Obstruction of gall bladder emptying (usually due to gall stone)
Leads to gall bladder distension
There is ongoing water reabsorption from the retained bile which becomes highly concentrated leading to inflammatory response in wall of gallbladder
31
Features of acute cholecystitis
- severe localised RUQ pain
- vomiting and systemic upset
- palpable gall bladder - Murphy sign positive
- rarely the gall bladder can become gangrenous and perforate leading to generalised peritonitis
32
What is ascending cholangitis
Infection of the common bile duct which usually occurs following obstruction due to choledocholithiasis
33
Symptoms of ascending cholangitis
Obstructive jaundice
High fever
RUQ pain
34
What is the key presentation of all forms of gall stone disease
RUQ pain
35
Blood results in biliary colic
Normal
36
Blood results in cholecystitis
Raised inflammatory markers (WCC / CRP)
LFTs may show marginal derangement
37
Blood results in choledocholithiasis
Normal inflammatory markers
Obstructive jaundice type picture on LFT (high bilirubin, raised ALP/ GGT)
38
Blood results in ascending cholangitis
Raised inflammatory markers
Obstructive jaundice on LFTs
39
US findings in biliary colic
Stones in gall bladder (echogenic foci and acoustic shadow)
40
US findings in cholecystitis
Thickened gall bladder wall in acute inflammation
41
US findings in choledocholithiasis / ascending cholangitis
Increased diameter of the common bile duct in obstruction
42
When is MRCP used (magnetic resonance cholangiopancreatography)
When there is diagnostic uncertainty or concern about underlying malignancy
Can visualise the biliary tree in greater detail
43
Management of asymptomatic gallstones (found incidentally)
Cholecystectomy only indicated if the patient is at significant risk of complications due to co-morbidities
- young patients also indicated as there is a long time for symptoms to develop
44
Management of biliary colic
Oral analgesia
Elective laparoscopic cholecystectomy
Low fat diet
45
Management of acute cholecystitis
Bed rest, fluids, analgesia
IV abx
Laparoscopic cholecystectomy
46
Management of choledocholithiasis
Bed rest, fluids, analgesia
Inpatient ERCP
Upper GI endoscopy with cannulation of common bile duct via sphincter of oddi
Obstructing stones broken down and removed
IV vit K to aid coagulation
Laparoscopic cholecystectomy following relief of obstruction / jaundice
47
Management of ascending cholangitis
Sepsis 6 with urgent IV abx and emergency ERCP
Patients with an infected, obstructed biliary system are high risk of rapid deterioration
48
Define acute pancreatitis
An acute inflammation of the pancreas which can be associated with significant morbidity and mortality
49
Pathology of acute pancreatitis
An initial insult to the pancreas leads to leakage of activated pancreatic enzymes into the pancreatic and peripancreatic tissue causing an acute inflammatory reaction eg gall stones damaging ampulla of vater which allows gastric contents up the pancreatic duct where they can activate pro enzymes
50
Acute pancreatitis aetiology (I GET SMASHED)
Idiopathic (20%)
Gall stones (40%)
Ethanol (35%)
Trauma (15%)
Steroids
Mumps (+CMV +EBV)
Autoimmune
Scorpion venom
Hyper / hypo lipidaemia, calcaemia, thermos
ERCP
Drugs (thiazides, sulphonamides, ACEIs, NSAIDs)
51
Symptoms of acute pancreatitis
Severe epigastric pain
Radiates to the back and may be relieved by sitting forward
N&V
52
Signs of acute pancreatitis
Tachycardia
Fever
Ileus
Jaundice
Rigid abdomen
Cullens sign (periumbilical discolouration due to peritoneal haemorrhage)
Grey-turner’s sign: flank discolouration
53
What is bruising in pancreatitis a sign of
Grave prognosis (80% mortality)
54
Investigations for acute pancreatitis
Bloods: FBC, CRP, U&E, LFT, glucose, calcium, raised serum lipase, ABG
ECG: to rule out MI
Imaging: erect CXR, RUQ US, CT abdo, MRCP
55
How to diagnose pancreatitis
Classic clinical history + raised serum lipase is enough without imaging
56
What is ALT >3x normal suggestive of
Gallstone disease
57
What is the modified Glasgow criteria for assessing severity of pancreatitis (PANCREAS)
PaO2 <8kPa
Age >55
Neutrophils: WBC >15x10^9
Calcium: <2mmol/L
Renal: urea >16mmol/L
Enzymes: LDH >600iu/L, AST >200iu/L
Albumin: <32g/L
Sugar: glucose >10mmol/L
Score of 3 or above suggest severe pancreatitis (HDU/ITU)
58
Management of pancreatitis
ABCDE for initial resuscitation
Aggressive IV fluid
Catheterise and monitor urine output
Analgesia
PPI to prevent stress ulcer
DVT prophylaxis
Urgent ERCP if due to gallstones
Withhold offending medications
59
Early complications of acute pancreatitis
- shock (hypovolemic, septic)
- ARDS
- renal failure
- DIC
- metabolic: Hypocalcaemia, hyperglycaemia, hypalbuminaemia
60
Late complications of acute pancreatitis
Abscess formation
Pancreatic pseudocysts
Intra-abdominal haemorrhage
Thrombosis of the splenic / gastroduodenal arteries
Fistulae
61
What is a pancreatic pseudocyst
A localised fluid collection rich in pancreatic enzymes with a non-epithelialised wall containing fibrous / granulation tissue
Commonly occur in pancreatitis from day 10 onwards due to disruptions of the pancreatic duct leading to extravasation of enzymes
62
How does a pancreatic pseudocyst present
Deep persistent abdominal pain +/- a mass
63
Acute pancreatitis prognosis
85% of cases settle after 3-7 days
15% require ICU admission
50% of ICU cases will end in mortality
64
Define an aneurysm
A focal dilation of an artery >150% of its normal diameter
65
What is a true aneurysm
All layers of the arterial wall are involved
66
What is a false aneurysm / pseudoaneurysm
Surrounding soft tissues lined by thrombus form the wall of the aneurysm, mainly occurring following trauma
67
AAA presentations
Mass effects: pressuring adjacent structures
Emboli events: due to development of mural thrombi
Haemorrhage: due to rupture
68
AAA causes
Atherosclerotic: eg aortic, popliteal
Developmental: berry aneurysm
Infective: mycotic in endocarditis, syphilitic in tertiary syphilis
Developmental: Marfaans / ehlers-Danlos syndrome
Trauma
69
Presentation of AAA rupture
- severe continuous / intermittent epigastric pain radiation to the back / groin
-pulsatile, expansile abdominal mass
- signs of shock
- AAA should be suspected in any male >50 presenting with renal colic
70
Management of AAA
Emergency A-E resuscitation
Transfusion for rapid blood delivery
Patient taken to theatre when stabilised
Clamp aorta bone the leak then graft
71
Prognosis of AAA
Only 50% make it to hospital
Of these 50% will not survive the operation
72
Management of AAA <5.5cm
Monitor by regular US / CT every 6-12 months
Strict control of HTN
Smoking cessation
73
What types of monitored AAA are indicated for surgery
>6cm as risk of rupture increases to 25%
AAA expanding at >1cm/year
Symptomatic
74
Which types of AAA patients are at more of a risk of rupture
Hypertension
FH of rupture
Smokers
Females
75
Describe an endovascular aneurysm repair
Use of femoral arteries to access and stent the aorta under fluoroscopic guidance
- lower mortality than conventional open operation
- lower post operative morbidity
76
Why is CKD a risk in AAA repair
The contrast used in EVAR’s is nephrotoxic
In an open procedure there is a prolonged ischaemia to the kidneys after the aorta is clamped
77
Complications of popliteal aneurysms
Acute limb ischaemia: due to rupture / thrombosis of the aneurysm or distal emboli
Chronic limb ischaemia: gradual occlusion of the aneurysm
DVT: if occluding popliteal veins
78
Investigations in popliteal aneurysms
USS to determine the size of the aneurysm
Angiography prior to the surgery to assess the distal arterial tree
79
Management of popliteal aneurysm
Femoral to distal popliteal bypass graft
Intra-vascular thrombolysis or embolectomy may occur at the time of surgery for the distal emboli
80
What is peritonitis
Inflammation of the peritoneum
Generally related to an underlying surgical pathology
81
Anatomy of the peritoneum
Is made up of the parietal peritoneum (above abdominal cavity) and visceral peritoneum (lines intraperitoneal organs)
The potential space between the 2 layers is known as the peritoneal cavity
82
What is localised peritonitis
Inflammation of the intra-abdominal organs will lead to localised inflammation of the peritoneum overlying that particular organ eg appendicitis, cholecystitis
83
What is generalised peritonitis
GI perforation (or ruptured reproductive organs / ectopic pregnancy) can cause widespread peritoneal inflammation and generalised peritonitis
- initially chemical due to the acidic nature of GI contents but infection invariably develops after 24-48 hours
84
Peritonitis presentation
Sudden onset abdominal pain - worse on movement
Generalised peritonitis - washboard rigidity
Localised peritonitis - guarding of affected area
Fever
Signs of shock (tachycardia / hypotension)
Sepsis
85
Aetiology of peritonitis
Abdo organ inflammation
Perforated GI viscus
Post surgical / post trauma
Spontaneous bacterial peritonitis - in ascitic fluid in liver failure and ascites
86
Investigations for peritonitis
CT abdomen / pelvis
87
Management of peritonitis
ABCDE resuscitation
Broad spectrum IV abx
Surgical management if underlying cause is surgical
88
What is GI perforation
Linked to peritonitis
Most commonly seen as a complication of other intra-abdominal pathologies
Requires full thickness injury of the bowel wall
89
Aetiology of GI perforation
- instrumentation (endoscopy, surgical)
- trauma
- bowel obstruction
- malignancy
- appendicitis
- PUD
- Diverticular disease
- IBD
- severe constipation
- violent vomiting
90
Describe localised GI perforation
Inflammatory response at the site of the perforation and the GI contents become walled off by the immune system leading to abscess formation
- diffuse spread of GI contents throughout the abdomen, leading to diffuse peritonitis
91
GI perforation presentation
Acute severe abdo pain
Pts who do not present with pain at the time of perforation will develop infection secondary to contamination of the abdomen and present with sepsis
92
OE of GI perforation
Guarding and rigidity
Appear toxic
Sepsis in localised
93
Investigations for GI perforation
Bloods:
- raised inflammatory markers (WCC, CRP)
- raised lactate if developing shock
- take coagulation profile and group and save as most require theatre
Imaging:
- upright CXR / AXR: pneumoperitoneum
- CT abdo / pelvis: free gas / fluid in abdo and perforated viscus
94
Management of GI perforation
ABCDE resuscitation
Broad spectrum IV abx
Usually requires surgical exploration
95
Define shock
Acute circulatory failure that compromises tissue perfusion
Can lead to irreversible organ damage and death due to cellular hypoxia
96
What is hypovolemic shock
Shock due to a lack of intravascular volume
- haemorrhage
- dehydration
97
What is distributive shock
Shock due to severe peripheral vasodilation
- sepsis
- anaphylaxis
- neurogenic shock - inhibition of spinal cord sympathetic outflow leading to vasodilation
98
What is cardiogenic shock
Shock due to intracranial causes of cardiac pump failure
- MI, arrhythmias, valve dysfunction, metabolic disturbances
99
What is obstructive shock
Shock due to extra cardiac causes of cardiac pump failure
- Massive PE, cardiac tamponade, tension pneumothorax
100
Clinical features of hypovolemic / cardiogenic shock
Patient is cold, pale, clammy with rapid threads pulse
Pulse pressure low due to vasoconstriction
101
Clinical features of septic shock
Patient is flushed, hot, sweaty, rapid bounding pulse
Pulse pressure wide due to vasodilation
102
Effect of shock on cerebral system
Autoregulation with mean arterial pressure of 50-150mmHg but below this the patient will become agitated, confused, drowsy and unresponsive
103
Effect of shock on cardiac system
Reduced diastolic pressure leads to inadequate myocardial perfusion leading to ischaemic chest pain, arrhythmias, and infarction
104
Effects of shock on respiratory system
Increased resp rate to compensate for metabolic acidosis secondary to tissue hypoperfusion
105
Effects of shock on renal system
Autoregulation with MAP of 70-170mmHg but below this there will be oliguria which leads to impaired renal function due to toxin build up
106
Effects of shock on GI system
Decreased gut motility and nutrient absorption, and decreased ability to sustain normal flora, leading to infection susceptibility
107
Effect of shock on skin
Blood supply is centralised giving cool / clammy / mottled peripheral skin
108
Define sepsis
The body’s overwhelming response to infection that can lead to tissue damage, organ failure and death
109
Pathophysiology of sepsis
Excessive cytokine release leads to a cascade of cellular changes that cause vasodilation, increased vascular permeability, immune system impairment and inappropriate activation of the coagulation cascade
110
High risk criteria for sepsis
Behaviour: objective evidence of new alteration in mental state
HR: >130 bpm
RR: >25 or new oxygen saturation requirement
SBP: <90mmHg or more than 40 below baseline
Urine output: not passed urine in previous 18 hours or less than 0.5ml/kg urine per hour in catheter
Skin: mottled appearance or cyanosis or non blanching rash
111
Moderate risk criteria for sepsis
Behaviour: new onset altered behaviour or history of acute deterioration in function
HR: 91-130bpm
RR: 21-25
SBP: 91-100 mmHg
Urine output: not passed urine in the past 12-18hrs or for catheterised patients passed 0.5-1ml/kg of urine per hour
112
Define severe sepsis
Sepsis + hypotension or evidence of end organ dysfunction
Eg oliguria, confusion, lactate >2, SpO2<94%
113
Define septic shock
Severe sepsis with hypotension not responding to fluid resuscitation
114
What are the sepsis 6 (3 in, 3 out)
1. Oxygen (in): 15ml/min via a non rebreather mask to achieve >94% sats (88-92 in COPD)
2. IV fluids (in): 500ml crystalloid stat if hypotensive or lactate >2
3. IV abx (in): local guidelines
4. Serum lactate (out): VBG or ABG. Seek urgent senior review if lactate >4
5. Blood cultures (out): ideally prior to abx. Take 2 pairs from separate sites plus from all indwelling lines
6. Catheterise (out): urine output is the most reliable measure of end organ perfusion
115
Pathophysiology of anaphylactic shock
Type I IgE mediated hypersensitivity reaction occurring in response to an angiogenesis that the body has previously been sensitised to
Degranulation of mast cells leads to release of vasoconstrictive mediators such as histamine that cause excessive vasodilation of the venous system
Compounded by bronchoconstriction and laryngeal oedema
116
Acute management of anaphylactic shock
1. Secure airway (intubation)
2. Remove cause
3. Adrenaline 0.5mg IM every 5 mins if necessary
4. Chlorphenamine 10mg IV
5. Hydrocortisone 200mg IV
6. If wheeze treat as per acute asthma
7. Raise feet of bed to help restore circulation
8. Interval bloods for serum tryptase and histamine to confirm diagnosis
117
Management of hypovolaemic shock
ABCDE
- replace any fluids being lost and titration to HR / BP / CVP / urine output
- inotropes considered if persistently hypotensive
118
Management of cardiogenic shock
ABCDE
IV diamorphine 2.5-5mg for pain / anxiety / breathlessness
Assess pulmonary oedema, don’t give fluids - furosemide infusion can provide relief
ITU / CCU for ionotropic support
119
What is pelvic inflammatory disease
Inflammatory condition involving upper genital tract in women
Can involve all of the uterus, Fallopian tubes, ovaries and neighbouring pelvic organs
120
Risk factors for PID development
Sexually active
Multiple partners
Age <25
Lack of barrier contraception
Previous STI / previous PID
IUD insertion
121
How can IUD insertion cause PID
All patients should be screened for infection prior to IUD insertion as the IUD can introduce the infection from the lower genital tract to the upper
122
Pathophysiology of PID
Endocervical canal usually forms a barrier between the vagina and upper vaginal tract
Endocervical infection can result in disruption of this barrier allowing vaginal bacteria to enter the upper genital tract
Variance between individuals can be due to immune response, oestrogen levels and cervical mucus
123
Clinical features of PID
Lower abdo pain
Dyspareunia
Abnormal uterine bleeding
Abnormal cervical or vaginal discharge
Severe disease: fever, significant abdo pain, rebound tenderness
124
OE of PID
Lower abdominal / pelvic tenderness
Purulent cervical discharge seen on speculum examination
Pelvic organ tenderness - cervical motion, uterine and adnexal tenderness
125
Investigations for PID
Bloods: raised inflammatory markers
Vaginal discharge: send for MCS + PCR to identify infective organism
Screen for pregnancy, HIV, syphilis
USS to assess for abscess / adnexal pathology
126
Management of PID
Abx 14 days
Broad spectrum due to polymicrobial nature
127
Complications of PID
Perihepatitis - inflammation of liver capsule and peritoneal surfaces
Tubo-ovarian abscess - may have palpable adnexal mass on exam
Chronic PID - low grade fever, weight loss, abdo pain
Increased future risk of ectopic pregnancy secondary to fallopian tube damage
128
Prognosis of PID
90% of cases resolve with simple abx therapy
Gonorrhoea infections are generally more severe and give higher rates of complications
129
2 types of intestinal obstruction
Small bowel or large bowel
130
How can vomiting indicate the type of intestinal obstruction
Vomiting:
- undigested food suggests gastric outlet obstruction
- bilious vomiting suggests upper SBO
- faeculent vomiting (thick / foul smelling) suggests more distal SBO / LBO
131
Symptoms of intestinal obstruction
Vomiting
Abdo pain
- intense, colicky
- worsening may represent strangulation / perforation
Constipation - inc absence of passing wind.
132
Signs of intestinal obstruction
- abdo distension
- minimal abdo tenderness (except bowel strangulation)
- tinkling bowel sounds
- dehydration - due to fluid accumulation
- central resonance to percussion
- scars : previous surgery causing adhesions
- palpable mass
133
Aetiology of SBO
Adhesions (80%)
Hernias
Crohn’s
Intussusception
134
Aetiology of LBO
Carcinoma of the colon
Diverticular disease
Sigmoid volvulus
Constipation
135
Investigations for intestinal obstruction
FBC, U&E, lipase, LFT, CRP
ABG / VBG : assess lactate - raised indicated bowel ischemia
Urinalysis / pregnancy test
CT abdo / pelvis can confirm diagnosis and indicate level of obstruction but will not show cause
136
Management of SBO
ABCDE resuscitation
NBM +NG decompression of stomach
If no signs of strangulation delay operative management by 48 hrs
Gastrograffin follow through can show level of obstruction
Abx + surgery if strangulation
137
Management of LBO
Operative (Hartmann’s)
138
What is strangulation in intestinal obstruction
Occurs when a section of the bowel is cut off from its blood supply
Most commonly occurs with a volvulus or hernia however can occur in any obstruction
Suspect if there is increasing pain / tenderness with leucocytosis and systemic upset
139
What is a volvulus
A twisting loop of bowel around its mesenteric axis resulting in obstruction +/- strangulation
140
What is a sigmoid volvulus
Most common in elderly, constipated patients
Classic coffee bean appearance on X-ray
Treatment is insertion of a long flatus tube advanced into the sigmoid which often untwists the volvulus and releases large amounts of liquid faeces / gas
If unsuccessful - emergency laparotomy
141
What is a caecal volvulus
Due to congenital malformation and gives the classic ‘embryo’ appearance of an ectopically placed caecum on an AXR
Treatment is untwisting at laparotomy
142
What is a paralytic ileus
Temporary disruption of normal peristaltic activity of the small bowel without a mechanical blockage
No bowel sounds
Identifiable cause:
- post surgery
- intra-abdominal sepsis
- electrolyte disturbances
- critically unwell patients
143
Treatment of paralytic ileus
NG tube and NBM
144
Describe the pathway of pain
A delta fibres give rise to perception of sharp immediate pain
C fibres give rise to slower onset, prolonged pain
Sensory impulses enter the cord via the dorsal root, and then ascend in the dorsal posterior column or the spinothalamic tract
Thalamic pathways to and from the cortex then mediate the emotional components of pain
145
Physiological effects of pain
Leads to catecholamines release with the resultant vasoconstriction leading to increased cardiac work and delayed healing
146
Outline the WHO pain ladder
1. Non-opioid +/- adjuvant eg paracetamol +/- NSAID
2. Weak opioid +/- non opioid +/- adjuvant eg codeine + para + NSAID
3. Strong opioid +/- non opioid +/- adjuvant eg morphine + para + NSAID
147
MOA of paracetamol
Partially unknown
Acts similarly to NSAIDs
Inhibits CNS prostaglandin synthesis
148
Properties of paracetamol
Good analgesic and antipyretic properties
Weak anti inflammatory
149
When is a 3g/day max indicated in paracetamol
Old age
Poor nutritional status
Alcoholism
150
How do NSAIDs work
Inhibit COX enzymes which normally promote production of prostaglandins and thromboxane
COX 1- expressed in most tissues with the PGs produced involved in tissue homeostasis - platelet aggregation, renal blood flow, Autoregulation and GI protection
COX 2 - induced in active inflammatory cells by IL-1 and TNF-a
Sensitises nociceptors to inflammatory mediators such as bradykinin peripherally
Sensitises afferent pain fibres in the dorsal horn centrally
151
What unwanted effects does inhibiton of COX-1 (NSAIDs) lead to
Dyspepsia and gastric ulcers
Bronchospasm
Renal insufficiency
Cardiotoxicity
Decreased platelet count
Skin reactions
152
Absolute contraindications for inhibiton of COX-1 (NSAIDs)
Severe heart failure
History of GI bleed / ulceration
153
When should NSAIDs be cautioned
Asthma
Elderly
Coagulopathies
Renal / hepatic / cardiac impairment
154
NSAID of choice for high CV risk
Naproxen
155
When is Diclofenac contraindicated
CV disease or high risk of CV events
156
Effective alternatives to oral NSAIDs
Topical NSAID gel effective for pain relief from arthritis
Topical capsaicin (chilli extract) can provide significant pain reduction if applied regularly 1-2 weeks
157
What are coxibs
COX-2 selective inhibitors
- used in RA / OA but has risk of serious adverse cardiac events
PPI should still be co-prescribed
158
How do opiates act
Act on u-opioid receptors in the CNS and throughout the body, decreasing neuro-excitability
Not effective in neuropathic pain
159
Side effects of opiates
Respiratory depression
N+V
Constipation
Sedation / depression of cough reflex
Gall bladder contraction (avoid in gall stone disease)
160
Absolute contraindications of opiates
Acute respiratory depression
Acute alcoholism
Risk of paralytic ileus
Raised ICP
Tramadol should not be used in conjunction with other serotonergic drugs
Tolerance develops within a few days - dependence may occur
161
What to do in opiate overdose
IV naloxone can rapidly reverse the toxic effects of opiates
162
What is co-prescribed for people on long term opiates
Senna
Lactulose
163
Indications of patient controlled analgesia
Post operatively or in oncology
164
Advantages of patient controlled analgesia
Allows for administration of patient controlled doses when required
Improves patient satisfaction and decreases overall doses used
165
Examples of non-drug analgesia
Splinting: very effective analgesia technique in trauma
Cold therapy: very effective around joints post surgery
TENS: electrical current applied via hand held generator to activate nerve fibres in tissues below
Acupuncture: can be effective in certain conditions
CBT
166
What is an indicator of severe disease in pancreatitis
Hypocalcaemia
167
What do raised amylase and lipase indicate
Acute pancreatitis
Amylase : 3-4x the normal range
Lipase: more of a specific marker than amylase - does not predict severity
168
What is the most sensitive blood test for diagnosis of acute pancreatitis
Serum lipase as has a longer half life whereas amylase levels can fluctuate and lead to false negative results
169
What test should be used for suspected pancreatitis presenting >24 hours after onset
Serum lipase as has a longer half life
170
How would a blockage of the cystic duct or gall bladder present
RUQ pain
No jaundice
171
Why is Crohn’s disease a risk factor for gall stones
Affects the terminal ileum which is involved in metabolism of bile salts
Excessive bile salts escape into the colon, are reabsorbed and return to the liver resulting in excessive secretion of bile pigments and the production of black stones
172
What is faecal elastase test used for in pancreatitis
Test of exocrine function of the pancreas
173
Test done to investigate obstruction with ascending cholangitis
ERCP
174
What is the name of the investigation for diagnosis and monitoring the severity of liver cirrhosis
Transient elastography
175
Which antibodies are positive in primary sclerosing cholangitis
P - ANCA
176
What cancer is there an increased risk of with primary sclerosing cholangitis
Cholangiocarcinoma
177
What is an indication of acute liver failure on blood test
Raised INR
178
Describe one of the liver signs for right sided heart failure
Firm, smooth, tender and pulsatile liver edge
179
Drugs that cause Cholestasis
COCP
Abx: fluclox, co-amoxiclav, erythromycin
Anabolic steroids, testosterone
Phenothiazines
Sulphonylureas
Fibrates
Nifedipine
