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Finals > Surgery > Flashcards

Surgery Flashcards

1
Q

What is the Modified Glasgow Score?

A

tool to assess severity of acute pancreatitis

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2
Q

In the Modified Glasgow Score, what score indicates severe pancreatitis

A

> =3 within 48hrs onset

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3
Q

What is the tumour marker for pancreatic cancer?

A

Ca 19-9

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4
Q

What is the tumour marker for ovarian cancer?

A

CA 125

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5
Q

What is the tumour marker for hepatocellular carcinoma

A

AFP - alpha-feto protein

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6
Q

What is the tumour marker for colorectal cancer?

A

CEA - carcinoembryonic antigen

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7
Q

What are the key features of Crohn’s disease (macroscopic and microscopic)

A 
macroscopic:
mouth to anus
skip lesions
transmural
mucosal oedema

Microscopic:
epitheloid granulomas`

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8
Q

Which part of the bowel does Crohn’s most commonly affect?

A

terminal ileum

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9
Q

What kind of perianal disease can occur in crohn’s

A 
fistulae
fissure
abscess
skin tags
ulcers
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10
Q

What skin changes can occur in crohn’s

A

erythema nodosum

pyoderma granulosum

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11
Q

What investigations should be carried out in suspected crohn’s

A

FBC, U+E, ESR, CRP, LFT, B12, folate
stool mc+s, c diff toxin
Colonoscopy with biopsies, small bowel enema, capsule endoscopy

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12
Q

What are the expected blood results in chron;s

A

anaemia

raised inflammatory markers

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13
Q

What is the management of crohn’s to induce remission

A

supportive: IV fluids, nutrition

  1. corticosteroids eg IV hydrocortisone
  2. 5-ASA eg. mesalazine
  3. add on mercaptopurine, azathioprine or methotrexate
  4. if no response, consider infliximab or adalimumab
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14
Q

What is the management of crohn’s to maintain remission

A
  1. mercaptopurine or azathioprine
  2. methotrexate
  3. mesalazine
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15
Q

What are indications for surgery in Crohn’s

A 
peritonitis
obstruction
abscess
fistula
not responding to medical therapy
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16
Q

What are the aims of surgery in crohn’s

A

resect worst areas

defunction distal disease

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17
Q

What are the compications of crohn’s

A 
strictures
fistulae
osteoporosis
anaemia
renal stones
gallstones
primary sclerosing cholangitis
cholangiocarcinoma
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18
Q

What age is crohn’s most common

A

15-30

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19
Q

What age is UC most common

A

15-25

55-65

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20
Q

Describe the typical macroscopic and microscopic features of UC

A 
macro:
rectum up
continuous
mucosal
pseudopolyps

micro:
crypt abscesses
reduced goblet cells

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21
Q

What investigations should be done in suspected UC

A

FBC, U+E, LFTs, CRP, ANCA, p-ANCA, ANSA
stool culture and CDT
AXR, erect CXR
colonoscopy

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22
Q

How is the severity of UC classified?

A

mild - <4 stools per day, little blood

moderate - 4-6 stools per day, no systemic upset

severe - >6 stools per day, systemic upset (raised HR, raised inflammatory markers, anaemia, pyrexia)

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23
Q

What is the treatment for UC to induce remission

A

mild/moderate

  1. oral or rectal mesalazine or sulfasalazine
  2. oral or rectal prednisolone

severe
1. IV steroids - hydrocortisone

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24
Q

What is the treatment for UC to maintain remission

A
  1. oral/rectal mesalazine or sulfasalazine (aminosalicylates)
  2. azathioprine or mercaptopurine
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25
Q

What are the complications of UC

A

toxic megacolon
VTE
depression and anxiety
primary sclerosing cholangitis

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26
Q

State seven differences between crohn’s and UC

A 
transmural, mucosal
mouth to anus, rectum up
skip lesions, continuous
granulomas, crypt abscesses
strictures and fistulae, no
smoking increases risk, smoking decreases risk
ulcers and perianal disease, no
no, increased risk colorectal cancer
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27
Q

State some mechanical ways of preventing VTE in post op patients

A

Early ambulation after surgery
Compression stockings
Intermittent pneumatic compression devices

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28
Q

State some ways of preventing VTE in post op patients with medications

A

stop the pill 4 weeks prior to surgery
LMWH, unfractionated heparin if patient in renal failure or fondaparinux
continued for 5-7days post op or until mobile
major cancer or hip/knee replacement for 28days+

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29
Q

What is chronic liver disease?

A

progressive inflammation and destruction of liver parenchyma leading to fibrosis and cirrhosis

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30
Q

What are the causes of chronic liver disease

A 
alcohol
hep B/C
non-alcoholic fatty liver disease
genetic - Wilson's, haemochromatosis
autoimmune - primary biliary sclerosis
drugs - methotrexate,isoniazid, amiodarone, sodium valproate
vascular - Budd-Chiari
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31
Q

What is haemochromatosis

A

autosomal recessive mutations in HFE gene - leading to increased iron uptake and deposition in tissue

leads to cirrhosis, heart failure and diabetes
hypogonadism

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32
Q

How is haemochromatosis treated

A

venesection

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33
Q

What is Wilson’s disease

A

autosomal recessive condition causing increased uptake and decreased excretion of copper, leading to increased Cu2+ in blood and deposition in tissues

deposition in liver, brain, cornea

leading to cirrhosis, psychiatric problems

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34
Q

How is wilson’s treated

A

penicillamine - chelates copper

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35
Q

What is Budd-Chiari syndrome

A

hepatic vein thrombosis

venous congestion causes hepatomegaly
if hypoxia of tissues, necrosis occurs

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36
Q

What is metabolic syndrome

A

presence of 3/5 of

T2DM
obesity
HTN
hypertriglyceridamia
hyperlipidaemia
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37
Q

What non-alcoholic fatty liver disease

A

in presence of metabolic syndrome

insulin resistance leads to increased fat deposition and reduced fatty acid oxidation, increased synthesis fatty acids.
leads to steatosis
inflammation due to hepatocyte cell death leads to steatohepatitis
stellate cells lay down fibrotic tissue leading to cirrhosis

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38
Q

define steatosis

A

abnormal fatty depositis in hepatocytes

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39
Q

define steatohepatitis

A

steatosis plus inflammation causes by hepatocyte necrosis

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40
Q

define cirrhosis

A

degeneration of cells, inflammation, and fibrous thickening of tissue in liver
nodules of regenerating hepatocytes surrounded by collagen

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41
Q

Why does alcohol cause cirrhosis

A

alcohol broken down by alcohol dehydrogenase forming acetaldehyde
uses NAD+ (decreasing B oxidation of fa) giving NADH (increases fatty acid synthesis)
leads to steatosis

acetaldehyde is toxic, as are ROS produced by reaction
leads to inflammation
therefore, steatohepatitis

nodular regeneration and fibrosis by stellate cells
scar tissue starts to form around veins
= cirrhosis!

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42
Q

What is a key histological finding in steatohepatitis of alcoholic liver disease

A

Mallory bodies in cytoplasm of hepatocytes

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43
Q

Which hepatitis increased the risk of hepatocellular carcinoma

A

HBV

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44
Q

What are the key serology findings in HBV

A

HBsAg - presence of disease
anti HBs - immune
anti HBc - have been exposed to virus

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45
Q

What is the treatment for HBV

A

acute: peginterferon alfa
chronic: entecavir

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46
Q

What is the treatment for HCV

A

ribavirin + peginterferon alfa

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47
Q

What are the symptoms of chronic liver disease

A 
lethargy
N+V
anorexia
pain in RUQ
fever
easy bruising
blood in stools
haematemesis
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48
Q

What are the signs of chronic liver disease

A 
jaundice 
palmar erythema
hepatic flap
spider naevi
caput medusae
gynacomastea 
testicular atrophy
loss of body hair
ascites
hepatomegaly
splenomegaly
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49
Q

What are the complications of chronic liver disease

A

oesophageal varices
hepatic encephalopathy
HCC
spontaenojus bacterial peritonitis

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50
Q

Describe how you would investigate a patient with presumed chronic liver disease

A

urinalysis
FBC, clotting, U+E, LFTs, albumin, viral serology, iron, ferritin, copper
USS, endoscopy, transient elastography

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51
Q

What are the signs of hepatic encephalopathy

A

confusion
cognitive impairment
constructional apraxia
liver flap

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52
Q

State the stages of hepatic encephalopathy

A

I - irritability, sleep disturbance, dyspraxia
II - confusion, inappropriate behaviour, liver flap
III - incoherent, restless, liver flap, stupor
IV - coma

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53
Q

What causes ascites in cirrhosis

A

reduced albumin - reduced oncotic pressure

portal hypertension - increased hydrostatic pressure (RAAS activation due to sphlancnic vasodilation)

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54
Q

How is ascites treated

A

fluid restriction
spironolactone
low salt diet

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55
Q

How is encephalopathy treated

A

referral to ITU
manage airway - intubation
lactulose

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56
Q

What long term monitoring is needed in cirrhosis

A

6m USS liver and alpha fetoprotein for HCC

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57
Q

what causes varicose veins

A

valvular insufficiency in superficial veins, leading to dilation.
tortuous veins

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58
Q

what are the risk factors for varicose veins

A 
female
pregnancies
standing up for prolonged time
family history
obesity
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59
Q

What are the symptoms of varicose veins

A 
purely cosmetic
pain (after prolonged standing)
itching
aching
swelling of legs
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60
Q

What are the signs of varicose veins

A

tortuous veins along small and great saphenous veins

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61
Q

What is deep venous insufficiency?

A

failure of the venous system, characterised by valvular reflux, venous hypertension and obstruction

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62
Q

what are the signs of chronic venous insufficiency

A 
peripheral oedema
venous eczema
lipodermatoclerosis
haemosiderin deposition
atrophie blanche
venous ulcers
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63
Q

Where are venous ulcers most commonly found

A

medial malleolus

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64
Q

describe the course of the great saphenous vein

A

dorsal venous arch
anterior to medial malleolus
posterior to medial condyle of knee
inserts into femoral vein inferior to inguinal ligament

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65
Q

describe the course of the small saphenous vein

A

dorsal venous arch
posterior to lateral malleolus
inbetween heads of gastrocnemius
into popliteal vein

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66
Q

What investigations need to be done when investigating varicose veins

A

FBC, U+E, LFTs, BNP,

duplex ultrasound of veins, ABPI

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67
Q

What is the conservative management of varicose vein

A

elevation
weight loss
not standing for prolonged periods of time
compression stocking

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68
Q

what are the surgical options for treatment of varicose veins

A

laser ablation
foam sclerotherapy
ligation, stripping and avulsion

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69
Q

What is a saphena varix

A

dilatation at the top of the long saphenous vein due to valvular incompetence.

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70
Q

How is a saphena varix tested for?

A

cough impulse at saphenofemoral junction

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71
Q

What is trendelenberg’s test for varicose veins

A

raise leg to 45 degrees
milk veins
tourniquet around thigh
lower leg
varicose veins return = incompetency below level of tourniquet
varicose veins do not return = incompetency above level of tourniquet

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72
Q

What is MEN1

A

inherited

parathyroid
pancreas - gastrinoma or insulinoma
anterior pituitary

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73
Q

describe MEN2

A

2A - phaeochromocytoma, parathyroid, medullary thyroid cancer

2B - MTC, phaeochromocytoma, neuromas, Marfan’s

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74
Q

Define acute hepatic failure

A

liver failure occuring suddenly in a previously healthy liver

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75
Q

define acute on chronic liver failure

A

decompensation of chronic liver disease

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76
Q

define fulminant hepatic failure

A

acute liver failure + encephalopathy

due to mass necrosis of liver cells leading to severe impairment of function

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77
Q

Define hyperacute, acute and subacute fulminant hepatic failure

A

hyperacute - less than seven days sinnce onset of jaundice
acute - 7-28d
subacute - 5-26 weeks

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78
Q

Which hepatitis viruses cause acute liver failure

A

Hep A and E

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79
Q

What are the signs of acute liver failure

A 
jaundice
RUQ pain
fever
nausea
anorexia
fatigue
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80
Q

What are the signs of fulminant hepatic failure

A 
hepatic encephalopathy - confusion, constructional apraxia, altered mental state
ascites
asterixis
acidosis
hypoglycaemia
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81
Q

State some investigations you would want to do in acute liver failure

A

FBC, U+E, LFTs, clotting, albumin, iron studies, viral serology, paracetemol level
blood cultures
liver USS
ascitic tap - MC+S

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82
Q

What are the indications for liver transplantation in paracetamol overdose

A

Arterial pH < 7.3, 24 hours after ingestion

or all of the following:
prothrombin time > 100 seconds
creatinine > 300 µmol/l
grade III or IV encephalopathy

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83
Q

What are gallstones formed from?

A

cholesterol
bile pigments
calcium

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84
Q

Define biliary colic

A

intermittent pain due to movement of gallstones into cystic duct causing transient obstruction

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85
Q

define cholecystitis

A

infection and inflammation of gall bladder due to obstruction of cystic duct

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86
Q

define cholangitis

A

inflammation and infection of common bile duct due to gallstone present in common bile duct

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87
Q

What are the symptoms of biliary colic

A

intermittent RUQ pain
worse after meal or at night
spontaneous resolution

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88
Q

What are the signs and symptoms of cholecystitis

A

pain in RUQ
fever
+ve Murphy’s sign
nausea and vomiting

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89
Q

What are the signs and symptoms of cholangitis

A 
fever
RUQ pain
jaundice
hypotension
confusion
deranged LFTs
90
Q

What investigations should be done is gallstone pathology

A

FBC, U+E, LFTs, CRP, amylase

USS, MRCP if USS not diagnostic

91
Q

What are the findings on USS for gallstones

A

presence of stones
thickened gallbladder wall
dilated ducts

92
Q

What is the management of biliary colic

A

analgesia

elective cholecystectomy

93
Q

What is the management of cholecystitis

A

IV analgesia and fluids
broad spectrum antibiotics
cholecystectomy within 1 week

94
Q

What is the management of cholangitis

A 
IV fluids
analgesia
Abx
ERCP for removal of stones from CBD within 48hours
cholecystectomy
95
Q

What is the treatment for empyema of gall bladder

A

cholecystectomy

percutaneous cholecystotomy if not fit for surgery (followed by cholecystectomy if possible at later date)

96
Q

What are the complications of cholecystectomy

A

may need to convert to open surgery
leakage of bile
bleeding
injury to CBD

97
Q

What are the complications of gallstones

A

pancreatitis
gallstone ileus
empyema
perforation of gall bladder

98
Q

Why does biliary colic occur after fatty meals?

A

presence of fatty acids stimulates enteroendocrine cells to release CCK
CCK causes contraction of gall bladder

99
Q

Describe the pathophysiology of acute pancreatitis

A

inflammation of the pancreas due to injury of the acinar (exocrine cells). leads to enzymatic spillage, inflammatory cascade activation and localized oedema

100
Q

What are the symptoms of acute pancreatitis

A

nausea and vomiting

pain! - radiating to back

101
Q

What are the causes of acute pancreatitis

A 
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion bites
Hypercalcaemia
ERCP
Drugs - azothioprine, thiazides, loop diuretics
102
Q

What are the signs of acute pancreatitis

A 
tachycardia
fever
Grey-Turner's/Cullen's
epigastric tenderness
abdominal distension
jaundice
103
Q

What is the cause of Grey-Turner’s/Cullen’s signs

A

retroperitoneal bleeding due to haemorrhage from necrotic pancreas

104
Q

What investigations should be done in suspected pancreatitis

A

ECG
FBC, U+E, LFTs, amylase, lipase, calcium, ABG, CRP
USS, AXR, erect CXR

105
Q

What can causes a raised amylase

A 
pancreatitis
mesenteric ischaemia
ectopic pregnancy
perforation
DKA
cholecystitis
106
Q

What sign is seen on AXR in pancreatitis

A

sentinel loop = dilated proximal jejunal loop due to local inflammation of pancreas

107
Q

What is the differential diagnosis in acute pancreatitis

A

AAA rupture
bowel perforation
aortic dissection
duodenal ulcer

108
Q

State the management of acute pancreatitis

A

oxygen - maintain above 95% sats
IV fluids
analgesia
catheter to monitor urine output

109
Q

What are some of the systemic complications of acute pancreatitis

A

DIC
Acute Respiratory Distress Syndrome (ARDS)
Hypocalcaemia
Hyperglycaemia - secondary to disturbances of insulin metabolism
Hypovolemic shock and multiorgan failure

110
Q

What are some of the local complications of acute pancreatitis

A

pancreatic necrosis
pancreatic pseudocyst
pancreatic abscess

111
Q

Describe how pancreatic necrosis occurs

A

Ongoing inflammation eventually leads to ischaemic infarction of the pancreatic tissue, often 7-10 days after the onset of pancreatitis. Any suspected pancreatic necrosis should be confirmed by

112
Q

How is suspected pancreatic necrosis investigated and treated

A

CT scan,
sterile - conservative
?pancreatic necrosectomy (open or endoscopic)

113
Q

What is a pancreatic pseudocyst

A

pancreatic fluid surrounded by fibrous/granulation tissue often occur 4 weeks after acute pancreatitis

114
Q

What is the treatment for a pancreatic pseudocyst

A

most resolve spontaneously.

if not: surgical debridement or endoscopic drainage (often into the stomach)

115
Q

In IDDM with well controlled diabetes,what is the perioperative insulin management for a patient undergoing a minor procedure

A

day before: normal doses

day of: reduced once daily long acting to 80% normal dose. continue other short acting doses

116
Q

In IDDM with poorly controlled diabetes or a major operation, what is the insulin management perioperativly

A

day before: 80% dose once daily long acting insulin

day of: 
80% dose once daily long acting insulin
omit other short acting doses
start variable rate IV insulin infusion
monitor blood glucose hourly - target 6-10mmol/L

once stable eating and drinking:
convert back to SC insulin

117
Q

during variable rate IV insulin infusion intraoperatively, what should be done if the blood glucose falls below 6mmol/L

A

give IV glucose 20% to prevent drop below 4mmol/L

118
Q

What is the perioperative insulin regimen in emergency surgery?

A

check blood glucose, ketones, HCO3- and U+Es

if no ketosis, start variable rate IV insulin infusion

119
Q

Which diabetic drugs can be continued intraoperatively

A

pioglitazones, DDP-4 inhibitors, GLP-1 agonists

120
Q

Whcih diabetic drugs need to be stopped on the fay of surgery?

A

metformin (if at risk of AKI or pt going to miss more than 1 meal)
sulfonylureas
SGLT-2 inhibitors

121
Q

Why is metformin stopped pre-op in diabetics?

A

risk of lactic acidosis

122
Q

Why are sulfonylureas stopped pre-op in diabetics?

A

risk of hypoglycaemia

123
Q

Why are SGLT-2 inhibitors stopped pre-op in diabetics?

A

risk of DKA

124
Q

Which antibiotics are given as prophylaxis in musculoskeletal surgery?

A

IV co-amoxiclav 1.2g in induction room and then 8 and 16 hours later

IV gentamicin and teicoplanin in induction room

125
Q

Describe the pathophysiology of chronic pancreatitis

A

chronic fibro-inflammatory disease of the pancreas, with progressive and irreversible damage to the pancreatic parenchyma. Calcification of parenchyma
there is recurrent and persistent evidence of exocrine and endocrine insufficiency

126
Q

What are the causes of chronic pancreatitis

A 
alcohol
idiopathic
hypercalcaemia
CF
obstruction pancreatic duct - neoplasm?
127
Q

What are the symptoms of chronic pancreatitis

A 
pain in epigastrium radiating to back - relived with sitting forwards/hot water bottle
N+V
weight loss
steatorrhoea
narcotic abuse
128
Q

What are hte signs of chronic pancreatitis

A

epigastric tenderness

erythema ab igne

129
Q

What investigations should be done in chronic pancreatitis?

A

urinalysis
FBC, U+E, blood glucose, amylase, lipase, LFTs
faecal elastase
USS

130
Q

What are important differentials to consider in chronic pancreatitis

A

acute cholecystitis,
peptic ulcer disease,
acute hepatitis

131
Q

What is the management of chronic pancreatitis

A 
analgesia!!!
stop alcohol
pancreatic enzyme replacement
insulin
steroids if cause autoimmune
surgery: pancreaticoduodenectomy, Whipple'a
132
Q

Which vitamins are those with chronic pancreatitis at risk of becoming deficient in?

A

ADEK

133
Q

What is a Whipple’s procedure?

A

removal of the head of the pancreas, first and second parts of the duodenum, the pyloric antrum, the gallbladder and the bile duct.

tail of pancreas anastamosed with duodenum and body of stomach anastamosed with distal duodenum

134
Q

What are hte complications of chronic pancreatitis

A 
exocrine insufficiency - malabsorption
endocrine insufficiency - diabetes
pancreatic cancer
pseudocyst
biliary obstruction
135
Q

What is the pathophysiology of colorectal cancer

A

adenoma-carcinoma sequence
stepwise pattern of mutational activation of oncogenes (e.g. K-ras) and inactivation of tumour suppressor genes (e.g. p53) that results in cancer.
epithelium to abnoramal epithelium to adenoma to adenocarcinoma

136
Q

what proportion of adenomas will progress to adenocarcinomas

A

10%

137
Q

What are the risk factors for colorectal carcinoma

A 
sporadic!
alcohol
smoking
high in processed meats diet
age (>60yrs),
family history,
inflammatory bowel disease, 
low fibre diet,
138
Q

What are the symptoms of colorectal cancer

A 
change in bowel habits
weight loss
abdominal pain
blood in stools
tiredness
139
Q

what are the signs of colorectal carcinoma

A

pale conjunctiva
mass in abdomen
mass on PR

140
Q

What are the differential diagnoses for colorectal cancer

A 
diverticular disease
haemorrhoids
anal fissure
IBD
diverticulitis
141
Q

What investigations should be done in suspected colorectal carcinoma

A

FBC, LFTs, U+Es, CEA, clotting
stool culture
colonoscopy + biopsy

142
Q

Describe the process of colorectal cancer screening

A

60-75y FOB home testing every 2 years

if +ve invited for colonoscopy

143
Q

What is the most common location for colorectal carcinioma

A

rectum

sigmoid colon

144
Q

State the Duke’s staging of colorectal carcinoma

A

I - confined beneath muscularis mucosa
II - extension through muscularis mucosa
III - nearby lymph nodes
IV - distant metastasis

145
Q

Describe a right hemicolectomy and what it is used for

A

ileocolic, right colic, and right branch of the middle colic vessels (branches of the SMA) are divided and removed with their mesenteries.
removal of caecum, ascending colon and hepatic flexure

right sided cancers

146
Q

Describe a left hemicolectomy

A

left branch of the middle colic vessels (branch of SMA/SMV), the inferior mesenteric vein, and the left colic vessels (branches of the IMA/IMV) are divided and removed with their mesenteries.
removal of splenic flexure and descending colon

left sided cancers

147
Q

Describe a sigmoid colectomy

A

the IMA is fully dissected out
removal of sigmoid

sigmoid cancers

148
Q

Describe an anterior resection

A

removal of sigmoid and rectum, formation of anastamosis between descending colon and remaining rectum. leaves the rectal sphincter intact

a defunctioning loop ileostomy is performed to protect the anastomosis and reduce complications in the event of an anastomotic leak. This is then reversed electively approximately four to six months later.

high rectal cancer

149
Q

Describe an abdominoperineal resection

A

removal of the distal colon, rectum and anal sphincters, resulting in a permanent colostomy.

low rectal tumours

150
Q

Why is laparoscopic surgery preferred to open?

A

faster recovery times,
reduced surgical site infection risk,
reduced post-operative pain,

151
Q

Describe a Hartmann’s procedure

A

This operation involves the removal of the sigmoid colon and a variable portion of the upper rectum and left colon

colon brought out through the abdominal wall to form colostomy. rectum is closed off with stitches or staples and returned to the pelvis. The procedure is usually reversible by surgery

152
Q

What investigations should be done after the initial diagnosis of colerctal cancer has been made

A

CTCAP - look for metastasis and local invasion

153
Q

What is neo-adjuvant chemotherapy?

A

chemotherapy before surgery

Reduction of tumor mass decreases the extent and invasiveness of a surgery and makes it easier for the surgeon to distinguish between normal and cancerous tissue

154
Q

What is adjuvant chemotherapy?

A

chemotherapy after surgery

155
Q

What treatments can be used in palliative care for colorectal cancer

A

endoluminal stenting - to relieve/prevent obstruction

stoma

156
Q

What are the heriditary causes of colorectal carcinoma?

A

HNPCC - hereditary non-polyposis colorectal carcinoma

FAP - familial adenomatous polyposis

157
Q

What factors need to be present for an anastamosis to heal

A

adequate blood supply,
mucosal apposition
no tissue tension.

158
Q

What is bowel obstruction?

A

structural block of passage of bowel contents through the bowel due to a mechanical obstruction

159
Q

What is paralytic ileus?

A

bowel contents not moving due to lack of peristalsis

160
Q

What can cause paralytic ileus

A 
post operative
chest infections, 
myocardial infarction, 
stroke 
acute kidney injury.
161
Q

What are the key differences in examination between true bowel obstruction and paralytic ielus

A

obstruction - tinkling bowel sounds

paralytic ileus - no bowel sounds

162
Q

How is paralytic ileus managed>?

A

Daily U&Es
Encourage mobilisation
Reduce opiate analgesia and any other bowel mobility reducing medication

Prolonged cases may warrant insertion of a nasogastric (NG) tube on free drainage and catheterising with a fluid balance chart

163
Q

What are some extramural causes of bowel obstruction

A

external compression by mass
adhesions
hernias
volvulus

164
Q

What are some mural causes of bowel obstruction

A 
strictures
carcinoma
intussception
diverticular strictures
Meckel's diverticulum
165
Q

What are some intraluminal causes of bowel obstruction

A

faecal impaction
foreign bodies - bezoars
gallstone ileus

166
Q

What are the most common causes of obstruction in the small bowel?

A

adhesions

hernias

167
Q

What are the most common causes of obstruction in the large bowel?

A

tumours
diverticular disease
volvulus

168
Q

What are the symptoms of bowel obstruction

A

vomiting - starts gastric contents, then bilious fluids, then faeculant
absolute constipation
abdominal pain - colicky
abdominal distension

169
Q

DEscribe the pathophysiology of bowel obstruction

A

gross dilatation of the proximal limb of bowel,
results in increased peristalsis of the bowel.
leads to secretion of large volumes of electrolyte rich fluid into the bowel (sometimes termed ‘third spacing’).

170
Q

Why might vomiting not be present in bowel obstruction

A

closed-loop obstruction eg. volvulus or large bowel obstruction with competent ileocaecal valve

171
Q

What might you find on examination in bowel obstruction?

A 
distended abdomen
patient in pain!
scars from previous surgery
tinkling bowel sounds
hernias
cachexia - cancer?
discomfort on palpation
172
Q

What signs might be present on examination if bowel obstruction has lead to bowel ischaemua

A

focal tenderness - rebound tenderness/guarding

173
Q

What tests should be done in suspected bowel obstruction

A 
ECG
FBC, U+E, G+S, clotting, ABG
AXR, erect CXR
CT abdomen
contrast fluoroscopy
174
Q

Why is a CT abdomen more useful than AXR in bowel obstruction

A

(1) more sensitive for bowel obstruction;
(2) can differentiate between mechanical obstruction and pseudo-obstruction;
(3) can demonstrate the site and cause of obstruction
(4) may demonstrate the presence of metastases if caused by a malignancy

175
Q

What are the signs on AXR in small bowel obstruction

A

> 3cm dilation
valvulae conniventes - whole width bowel wall
central location

176
Q

What are the signs on AXR in large bowel obstuction

A

> 6cm dilation
haustra - not whole width bowel
peripheral location

177
Q

How is sigmoid volvulus seen on AXR

A

‘coffee bean’ appearance

thick ‘inner wall’ represents the double wall thickness of opposed loops of bowel, with thinner outer walls due single thickness.

178
Q

How does bowel obstruction lead to bowel ischaemia

A

as the bowel distends, the intramural vessels become stretched and the blood supply is compromised, leading to ischaemia, necrosis and perforation

179
Q

How is bowel obstruction treated conservatively?

A 
NBM and insert wide bore NG tube to decompress the bowel 
IV fluids  - 4-5 litres in first 24h
correct any electrolyte disturbances 
Urinary catheter and fluid balance.
Analgesia
180
Q

What proportion of obstruction due to adhesions resolves with conservative management?

A

60-70%

181
Q

Why would bowel obstruction need to be managed surgically?

A

Suspicion of intestinal ischaemia
closed loop bowel obstruction
Small bowel obstruction in a patient with a virgin abdomen (no prev abdo surgery)
A cause that requires surgical correction (e.g. a strangulated hernia or obstructing tumour)
If patients fail to improve with conservative measures (typically after ≥48 hours)

182
Q

How can sigmoid volvulus be treated?

A

colonoscopy! deflates it

90% resolve!

183
Q

How is volvulus defined?

A

torsion of the colon around it’s mesenteric axis resulting in compromised blood flow and closed loop obstruction.

184
Q

Describe the pathophysiology of peripheral arterial disease

A

progressive narrowing of the arteries (by atherosclerosis) leading to symptomatic redeced blood supply to the limbs

185
Q

What are the risk factors for peripheral vascular disease?

A 
IHD
obesity
diabetes
age
HTN
hyperlipidaemia
FH
186
Q

What are the symptoms of PVD

A

pain on walking in calf/buttock/thigh, relieved by rest

187
Q

What are the signs of PVD

A

pale limb
prolonged capillary refill
lack of peripheral pulses
arterial ulcers

188
Q

What are the key differentials in PVD

A

acute limb ischaemia

spinal stenosis

189
Q

What are the key differences between PVD and spinal stenosis

A

PVD - pain on walking, relieved within by rest

stenosis- pain on walking or standing, relieved by sitting down

190
Q

Define the stages of chronic limb ischaemia

A

Stage I Asymptomatic
Stage II Intermittent claudication
Stage III Ischaemic rest pain
Stage IV Ulceration or gangrene, or both

191
Q

What investigations should be carried out in suspected PVD

A

ABPI, doppler ultrasound, ECG, BP

FBC, lipids, glucose

192
Q

What is ABPI

A

ankle brachial pressure index

ratio of the systolic blood pressure in the lower leg to that in the arms.

193
Q

What do the findings of the ABPI mean?

A

> 1.2 Abnormally hard vessel (e.g. calcified due to diabetes)
1.0-1.2 Normal
0.8-0.9 Mild arterial disease: mild claudication
0.5-0.79 Moderate arterial disease: severe claudication
<0.5 Severe arterial disease: rest pain, ulceration and gangrene (critical ischaemia)

194
Q

Describe the medical management of PVD

A 
risk factor modification:
stop smoking
exercise
weight loss
diabetic control 
HTN control
lipid lowering
antiplatelets - statin/clopidogrel
195
Q

What are the options in surgical management of chronic limb ischaemia

A

revascularisation = angioplasty. used for single lesions

venous graft bypass - used for diffuse disease

196
Q

Which patients with PVD should be considered for surgery?

A

risk factor modification has been discussed; and supervised exercise has failed to improve symptoms.

Any patients with critical limb ischaemia

197
Q

How is critical limb ischaemia defined?

A

Ischaemic rest pain for greater than 2 weeks duration, requiring opiate analgesia

Presence of ischaemic lesions or gangrene objectively attributable to the arterial occlusive disease

ABPI less than 0.5

198
Q

What are the signs on examination of critical limb ischaemia

A 
pale and cold limb
weak or absent pulses. 
hair loss, 
atrophic skin, 
ulceration
gangrene
thickened nails
199
Q

define acute limb ischaemia

A

sudden decrease in perfusion to a limb hat threatens the viability of the limb

200
Q

What are the causes of acute limb ischaemia

A

thrombosis - rupture of atherosclerotic plaque
embolus
trauma

201
Q

Where could be the source of the embolus in acute limb ischaemia

A

AF,
post-MI mural-thrombus,
abdominal aortic aneurysm
prosthetic heart valves.

202
Q

What are the signs and symptoms of acute limb ischaemia

A 
acute onset of:
Pain
Pallor
Pulselessness
Paresthesia
Perishingly cold
Paralysis
203
Q

Describe the characteristics of a class I acute limb ischaemia

A

no sensory loss
no motor loss
arterial and venous doppler present
no threat to limb viability

204
Q

Describe the characteristics of a class IIa acute limb ischaemia

A 
minor sensory loss
no motor loss
arterial doppler not present
venous doppler presnt
salvageable
205
Q

Describe the characteristics of a class IIb acute limb ischaemia

A 
moderate sensory loss - more than toes
mild motor loss
arterial doppler not present
venous doppler present
salveagable if immediately revascularised
206
Q

Describe the characteristics of a class III acute limb ischaemia

A 
sensory loss
motor loss
arterial doppler not present
venous doppler not present
not salvagable - permanant tissue damage inevitable
207
Q

What is the differential diagnosis for acute limb ischaemia

A

critical chronic limb ischaemia,
acute DVT
spinal cord compression
peripheral nerve compression

208
Q

What investigations should be carried out in acute limb iscahemia

A

ECG, doppler ultrasound, ABPI
FBC, thrombophilia screen, serum lactate
CT angiogram, USS abdo

209
Q

How long does it take for acute limb ischaemia to develop into irreversible tissue damage

A

6 hours

210
Q

What is the initial management of acue limb ischaemia

A

IV heparin infusion

if embolic, the options are:
Embolectomy
Local intra-arterial thrombolysis
Bypass surgery

If thrombotic disease, the options are:
Local intra-arterial thrombolysis
Angioplasty
Bypass surgery

211
Q

What are the signs of irreversible limb ischaemia

A

mottled non-blanching appearance

hard woody muscles

212
Q

What is the management for irreversible limb ischaemia

A

urgent amputation

213
Q

What is the long term management of acute limb ischaemia after reperfusion

A 
modification of risk factors
stop smoking
weight loss
exercise 
antiplatelet'
control HTN
statin
control diabetes
control source of embolus
214
Q

What are the complications after reperfusion in acute limb ischaemia

A

compartment syndrome
hyperkalaemia - K+ released from cells
AKI from rhabdomyolysis

215
Q

What are the causes of constipation

A

Post-operative ileus
Physiological – low fibre diet or poor fluid intake.
Iatrogenic – opioid analgesia, anticonvulsants, or antihistamines.
Functional – mainly painful defecation (such as anal fissures).
Pathological - bowel obstruction, hypercalcaemia, or hypothyroidism).

216
Q

What examination and investigations need to happen in constipation

A

DRE
abdominal examination - for signs of obstruction or peritonism
if no obvious cause or signs of obstruction etc: Ca2+, TFT, AXR

217
Q

Name the four types of laxative

A

bulk forming
osmotic
stimulant
faecal softeners

218
Q

Which types of laxative are used for hard stools?

A

bulk forming

osmotic

219
Q

Which types of laxative are used for soft stools?

A

stimulants

220
Q

Name some bulk forming laxatives

A

isphagula husk

methylcellulose

221
Q

What is the mechanism of action of bulk forming laxatives

A

increase bulk and fibre, absorb water

leads to stimulation as the bowel is stretched

222
Q

How long does it take bulk forming laxatives to act

A

72hrs

Finals (32 decks)

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