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Surgery > General Surgery > Flashcards

General Surgery Flashcards

1
Q

What is an adhesion?

A

Scar-like tissue binding surfaces together

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2
Q

What is a fistula?

A

Abnormal connection between two epithelial surfaces

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3
Q

What is tenesmus?

A

Sensation of needing to open bowels without the ability to produce stools

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4
Q

What is an anterior resection?

A

Surgical removal of the rectum

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5
Q

What is a Hartmann’s procedure?

A

Proctosigmoidoscopy-> removal of rectosigmoid colon + closure of anorectal stump + form colostomy

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6
Q

What is a Whipple procedure?

A

Pancreaticoduodenectomy-> head of pancreas, duodenum, gallbladder and bile duct removal

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7
Q

What are the 4 criteria for a patient having capacity?

A
  • Understand information
  • Retain information
  • Weigh up the pros and cons of the decision
  • Communicate their decision
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8
Q

What is a lasting power of attourney (LPA)?

A

A person who is legally nominated to make decisions on behalf of another person if/when they lack capacity

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9
Q

What is the deprivation of liberty safeguards (DoLS)?

A

An application made from hospital/care home for a patient when they lack capacity-> means they are unable to leave the place of care

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10
Q

What does a pre-operative assessment entail?

A
  • Taking a history-> PMH, surgeries, adverse response to previous anaesthesia, medications, allergies, smoking, alcohol, possibility of pregnancy, malnourishment
  • American Society of Anaesthesiologist (ASA) grading
  • Investigations-> bloods including group + save etc
  • Looking at medications for pre-existing conditions and determining if anything needs changing
  • Assessment for VTE prophylaxis
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11
Q

What is the American Society of Anaesthesiologist (ASA) grading system and what are the different grades?

A

Assessment of physical status/fitness before surgery

  • ASA I-> normal + healthy
  • ASA II-> mild systemic disease
  • ASA III-> severe systemic disease
  • ASA IV-> severe + constant threat to life
  • ASA V-> moribund + expected to die without op
  • ASA VI-> braindead + undergoing organ donation op
  • E!-> emergency
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12
Q

What investigations may be done as part of a pre-operative assessment?

A
  • Bloods-> FBC, U+Es, clotting, HbA1c if diabetic
  • Group + save-> when lower risk of needing blood products
  • Crossmatching-> when higher risk
  • MRSA screening-> all patients
  • ABG
  • ECG
  • Echo if HF/murmurs
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13
Q

How long before operations do patients usually need to fast for and why?

A
  • 6 hours before-> no food
  • 2 hours before-> no clear fluids
  • Reduce risk of food reflux + aspiration pneumonia
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14
Q

When do contraceptives and HRT (containing oesteogen) need to be stopped pre-op?

A

4 weeks before

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15
Q

When should DOACs be stopped before surgery?

A

24-72 hours before depending on operation

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16
Q

What should be done in regards to long-term steroid therapy pre-op?

A
  • Needs adjustment to prevent adrenal crisis from stress of surgery
  • Give additional IV hydrocortisone at induction + 24 hours after op
  • Double normal dose once eating + drinking for 24-72 hours
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17
Q

What should be done in regards to insulin therapy pre-op?

A
  • Short acting should be stopped till eating and drinking
  • Continue with lower dose of long-acting insulin
  • Add variable rate infusion with glucose, sodium chloride and potassium
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18
Q

What should be done in regards to oral hypoglycaemics pre-op?

A
  • Should stop
  • Metformin-> lactic acidosis risk
  • SUs-> can cause hypo
  • SGLT2 inhibitors-> can cause DKA
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19
Q

How can a patient’s recovery be enhanced after surgery?

A
  • Early independence and mobility
  • Good nutritional support-> helps with wound healing
  • Early catheter
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20
Q

When should NSAIDs be avoided?

A

Asthma, renal impairment, heart disease, stomach ulcers

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21
Q

How does patient-controlled analgesia work?

A
  • IV infusion of strong optiate-> morphine, oxycodone or fentanyl
  • Press when pain
  • Stops responding for set time-> prevent overuse
  • Need access to naloxone (for respiratory depression) + atropine (bradycardia) + antiemetics
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22
Q

What are the risk factors for post-op nausea and vomiting?

A

Female, motion sickness history, non-smoker, opiate use post op, younger, volatile anaesthetics

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23
Q

What is used for prophylaxis of post-op nausea and vomiting?

A
  • Ondansetron-> 5HT3 antagonist + avoided in prolonged QT risk
  • Dexamethasone-> steroid, cautioned in diabetes + immunocompromised
  • Cyclizine-> H1 receptor antagonist, cautioned in elderly and heart failure
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24
Q

What is used to treat post-op nausea and vomiting?

A
  • Ondansetron-> 5HT3 antagonist + avoided in prolonged QT risk
  • Cyclizine-> H1 receptor antagonist, cautioned in elderly and heart failure
  • Prochlorperazine
  • P6 acupuncture point (inner wrist)
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25
Q

What are the types of enteral feeds?

A

By mouth, NG tube, PEG (percutaneous endoscopic gastrostomy)

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26
Q

What route is used for total parenteral nutrition?

A

IV infusion of solution

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27
Q

What are the risks of total parenteral nutrition?

A

Irritant-> thrombophlebitis

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28
Q

What are some common post-op complications?

A
  • Anaemia
  • Atelectasis-> lung collapse when under-ventilated
  • Infection
  • Wound dehiscence-> separation of wound edges
  • Ileus-> peristalsis of bowel reduces
  • Haemorrhage
  • DVT/PE
  • Shock
  • Arrythmias
  • ACS
  • CVA
  • AKI
  • urinary retention
  • Delirium
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29
Q

How might post-op anaemia be managed?

A
  • If Hb <100-> oral iron
  • Hb <70-80g/L-> transfusion
  • Remember Jehovah’s witnesses may refuse
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30
Q

What are the different compartments of fluids in the body?

A

Intracellular (2/3)

Extracellular (1/3)

  • Interstitial (80%)-> between + around cells
  • Intravascular (20%)-> in blood vessels
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31
Q

What is ‘third spacing’?

A
  • Pathological movement of fluid into spaces/cavities-> ascites, pleural effusions etc
  • Excess fluids into interstitial space at expense of intravascular space
  • May present with hypovolaemia but signs of overload
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32
Q

When should fluids be restricted?

A

Hyponatraemia, heart failure, renal failure

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33
Q

What are insensible losses?

A
  • Fluids lose due to respiration, burns, sweating etc
  • Difficult to measure
  • Can be 800ml/day+ when diarrhoea/fever
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34
Q

What are the signs of hypovolaemia?

A
  • Hypotension
  • Tachycardia
  • High CRT
  • Cold peripheries
  • High RR
  • Dry mucous membranes
  • Reduced skin turgor
  • Reduced UO
  • Sunken eyes
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35
Q

What are the signs of fluid overload?

A
  • Peripheral oedema
  • Pulmonary oedema
  • Raised JVP
  • Increased body weight
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36
Q

How much glucose is in 1L of 5% dextrose?

A

50g glucose

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37
Q

How does human albumin solution work and when is it used?

A
  • Increases plasma volume
  • Large molecules stay in intravascular space-> increases oncotic pressure to draw in and retain fluids
  • Helps correct decompensated liver disease
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38
Q

What are the major risks with giving normal saline and why?

A
  • Hypernatraemia-> 154mmol in NaCl (normal conc-> 135-145mmol/L
  • Metabolic acidosis-> 154mmol chloride in NaCl
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39
Q

What are examples of isotonic solutions?

A
  • Match osmolality of plasma ie concentration of solutes

- 0.9% saline + Hartmann’s

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40
Q

What are examples of hypotonic solutions and how do they work?

A
  • Lower concentration than plasma
  • If dilute blood then water flows from blood to interstitial space
  • 5% dextrose
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41
Q

What are examples of hypertonic solutions?

A
  • Higher concentration than plasma

- 3% saline

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42
Q

How quickly should potassium solutions be infused?

A

<10mmol/hour-> reduce risk of arrhythmia

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43
Q

What is the normal requirement of maintenance fluids per day?

A

25-30ml/kg/day

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44
Q

What is the normal requirement of sodium per day?

A

1mmol/kg/day

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45
Q

What is the normal requirement of potassium per day?

A

1mmol/kg/day

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46
Q

What is the normal requirement of chloride per day?

A

1mmol/kg/day

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47
Q

What is the normal requirement of glucose per day?

A

50-100g per day

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48
Q

What does daily monitoring for fluid levels entail?

A
  • Fluid status + balance
  • U+Es
  • Watch for anaemia + coagulopathy-> diluting blood can cause deficiencies
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49
Q

What are the potential differentials for acute generalised abdominal pain?

A

Peritonitis, obstruction, ruptured AAA, ischaemic colitis

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50
Q

What are the potential differentials for acute RUQ pain?

A

Biliary colic, acute cholecystitis, acute cholangitis

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51
Q

What are the potential differentials for acute epigastric pain?

A

Acute gastritis, peptic ulcer disease, pancreatitis, ruptured AAA

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52
Q

What are the potential differentials for acute central abdominal pain?

A

Ruptured AAA, obstruction, ischaemic colitis, early appendicitis

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53
Q

What are the potential differentials for acute RIF pain?

A

Acute appendicitis, ectopic pregnancy, ruptured ovarian cyst, ovarian torsion, Meckel’s diverticulum

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54
Q

What are the potential differentials for acute LIF pain?

A

Diverticulitis, ectopic pregnancy, ruptured ovarian cyst, ovarian torsion

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55
Q

What are the potential differentials for acute suprapubic pain?

A

Lower UTI, urinary retention, pelvic inflammatory disease, prostatitis

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56
Q

What are the potential differentials for acute loin to groin pain?

A

Renal colic, ruptured AAA, pyelonephritis

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57
Q

What are the potential differentials for acute testicular pain?

A

Testicular torsion, epididymo-orchitis

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58
Q

What are the potential signs of peritonitis on abdominal examination?

A
  • Guarding-> tensing abdominal wall on palpation
  • Rigidity-> persistent tightness
  • Rebound tenderness-> rapidly releasing pressure on abdomen creates worse pain than pressure itself
  • Coughing test-> if cough get pain in abdomen
  • Percussion tenderness
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59
Q

What is spontaneous bacterial peritonitis?

A

Infection of ascitic fluid in liver disease

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60
Q

What are the initial investigations performed in acute abdomen?

A
  • Bloods-> FBC, U+Es, LFTs, CRP, amylase, INR (synthetic liver function), serum calcium
  • Serum/urine bHCG if indicated
  • ABG-> lactate (ischaemia), pO2
  • Group and save-> before theatre
  • Blood cultures
  • AXR-> obstruction
  • CXR-> air under diaphragm in perforation
  • Abdominal US-> gallstones, BD dilatation etc
  • CT scan-> identify cause
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61
Q

How should acute abdomen by managed?

A
  • ABCDE + alert seniors
  • NBM
  • NG tube
  • IV fluids + analgesia
  • IV antibiotics if indicated
  • Medication prescription + review
  • Consultant makes plan during post-take ward round
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62
Q

What is the appendix?

A
  • Small thin tube arising from caecum
  • Where 3 teniae coli meet (longitudinal muscles of large intestine)-> single opening to appendix
  • Dead end
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63
Q

What is the pathophysiology of appendicitis?

A
  • Pathogens get trapped in appendix due to obstruction
  • Infection + inflammation-> can gangrene
  • Can rupture-> faecal contents + infective material into peritoneal cavity-> peritonitis
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64
Q

What are the signs and symptoms of appendicitis?

A
  • Starts as central abdominal pain
  • Moves to RIF + McBurney’s point within 24 hours
  • Anorexia, N+V, low grade fever
  • Signs-> guarding, rebound tenderness in RIF, percussion tenderness, Rovsing’s sign
  • Might have RIF mass-> when omentum surrounds + sticks to inflamed appendix
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65
Q

Where is McBurney’s point?

A

2/3 distance from umbilicus to ASIS

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66
Q

What is Rovsing’s sign?

A
  • LIF palpation causes RIF pain

- Present in appendicitis

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67
Q

How is appendicitis diagnosed?

A
  • Clinical presentation
  • Bloods-> inflammatory markers
  • CT scan to confirm
  • US-> in kids or to rule out gynae causes
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68
Q

How is appendicitis treated>

A

Diagnostic laparoscopy + appendicectomy

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69
Q

What are the potential complications of appendicectomy?

A

Bleeding, infection, pain, scars, damage to other organs, removal of normal appendix, VTE

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70
Q

What is Meckel’s diverticulum?

A

Malformation of distal ilium + can bleed/inflame/rupture-> volvulus or intussusception

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71
Q

What is mesenteric adenitis?

A

Inflamed abdominal lymph nodes

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72
Q

How does mesenteric adenitis present?

A

Abdominal pain + tonsilitis/URTI

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73
Q

What type of bowel obstruction is the most common?

A

Small

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74
Q

What is the pathophysiology of bowel obstruction?

A
  • Passage of food, fluids + gas blocked-> due to adhesions, hernias or malignancy etc
  • Blockage-> back pressure, vomiting + dilatation of proximal bowel
  • Fluid unable to be absorbed in bowel-> fluid loss from intravascular space into GI tract-> hypovolaemia + shock (3rd spacing)
  • Higher up-> greater fluid loss (less bowel where fluid can be absorbed)
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75
Q

What are the three main causes of bowel obstruction?

A
  • Adhesions (small)
  • Hernias (small)
  • Malignancy (large)
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76
Q

What are some of the causes of bowel obstruction?

A
  • Adhesions (small)
  • Hernias (small)
  • Malignancy (large)
  • Volvulus (large)
  • Diverticular disease
  • Strictures eg in Crohn’s
  • Intussusception in kids
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77
Q

At what age does intussusception typically present?

A

6 months to 2 years

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78
Q

What are adhesions and what can they cause?

A

Scar tissue in the abdomen binding contents together-> kink/squeeze-> obstruct (usually small bowel)

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79
Q

What can cause adhesions?

A

Abdominal/pelvic surgery, peritonitis, abdo/pelvic infections, endometriosis, congenital, secondary to radiotherapy

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80
Q

What is closed loop bowel obstruction?

A
  • 2 points of obstruction so middle section sandwiched
  • If single point in large bowel + competent ileocaecal valve-> not allow movement back to ileum-> section isolated + contents can’t flow
  • No way to drain section contents-> expansion + ischaemia-> perforation
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81
Q

How does bowel obstruction present?

A
  • Vomiting-> green/bilous or faecal
  • Abdominal distention
  • Diffuse pain
  • Constipation
  • Lack of flatulence
  • Tinkling bowel sounds
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82
Q

What are the upper limits of normal when assessing bowel diameters on an AXR?

A
  • Small-> 3cm
  • Colon-> 6cm
  • Caecum-> 9cm
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83
Q

What are the valvulae conniventes?

A

Mucosal folds that form lines for the full width of the small bowel

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84
Q

What are haustra?

A

Pouches from muscles in large bowel wall-> lines don’t extend the full width

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85
Q

What is the initial management of bowel obstruction?

A
  • ABCDE + resus
  • Bloods-> U+Es, VBG (metabolic alkalosis, lactate)
  • Drip + suck-> NBM, IV fluids, NG tube + free drainage
  • AXR or abdo CT-> see obstruction site + perforation
  • Erect CXR-> air under diaphragm in perforation
  • Conservative management if stable
  • Consider surgery
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86
Q

What are the surgical management options for bowel obstruction?

A
  • Exploratory
  • Adhesiolysis
  • Hernia repair
  • Emergency resection
  • Stents during colonoscopy-> when tumour
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87
Q

What is ileus?

A

Paralytic or adynamic temporary stopping of peristalsis in the small bowel

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88
Q

What is pseudo-obstruction?

A

Functional obstruction of the large bowel-> no cause found

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89
Q

What causes ileus?

A
  • Usually handling during surgery (post-op)

- Injury, inflammation, infection, electrical imbalance (hypokalaemia/hyponatraemia)

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90
Q

What are the signs and symptoms of ileus?

A

Vomiting (green + bilious), abdominal distention, diffuse abdominal pain, constipation, lack of flatulence, absent bowel sounds (not tinkling)

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91
Q

What might absent bowel sounds indicate?

A

Ileus

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92
Q

How is ileus managed?

A
  • Usually no treatment

- Supportive-> NBM, NG tube, IV fluids, mobilisation, TPN

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93
Q

What is volvulus?

A
  • Bowel twists around itself + mesentery it attached to
  • Where mesenteric arteries are-> supply bowel
  • Closed loop bowel obstruction-> can cut off vessels-> ischaemia + necrosis
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94
Q

What is the mesentery?

A

Membranous peritoneal tissue

  • Connects bowel to posterior abdominal wall
  • Mesenterics arteries here-> supply bowel
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95
Q

What are the two types of volvulus?

A
  • Sigmoid (most common)

- Caecal (usually younger)

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96
Q

What causes sigmoid volvulus?

A
  • Chronic constipation + lengthening of mesentery
  • Overloaded with faeces-> sink downwards + twist
  • Excess laxatives of high fibre diet can cause too
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97
Q

What are the risk factors for volvulus?

A
  • Chronic constipation
  • High fibre diet
  • Adhesions
  • Pregnancy
  • Neuropsychiatric disorder
  • Nursing home resident
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98
Q

How does volvulus present?

A

Green bilious vomiting, abdominal distention, diffuse pain, constipation, lack of flatulence

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99
Q

How is volvulus diagnosed?

A
  • Coffee bean sign on AXR-> in sigmoid volvulus

- Contrast CT-> confirm diagnosis + exclude other pathology

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100
Q

How is volvulus managed?

A
  • Same as obstruction-> NBM, NG tube, IV fluids etc
  • Endoscopic decompression for sigmoid volvulus-> tube left in place to decompress + remove later
  • Surgical-> laparotomy, Hartmann’s, ileocaecal resection, right hemicolectomy
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101
Q

What is a hernia?

A

When a weak point in a cavity wall (muscle or fascia) lets organ through

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102
Q

How does a hernia typically present?

A
  • Soft lumo
  • May have aching/pulling/dragging sensation
  • May be reducible-> can push back to normal place
  • May protrude on coughing-> high intra-abdominal pressure
  • May protrude on standing-> pulled by gravity
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103
Q

What are the potential complications of a hernia?

A
  • Incarceration-> irreducible
  • Obstruction-> blockage
  • Strangulation-> non-reducible + base tight so cut off blood supply-> ischaemia + emergency
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104
Q

What is important to comment on when examining a hernia?

A

How wide the neck/defect is-> risk assessment for strangulation

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105
Q

What is the general management for a hernia?

A
  • Conservative-> when wide neck/not good for surgery
  • Tension-free repair-> mesh over defect + suture to muscle + tissues (grow over time to support)
  • Tension repair-> suture muscles + tissue back together, rarely done as high recurrence rate
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106
Q

What are the differentials for an inguinal hernia?

A

Femoral hernia, lymph nodes, saphena varix (dilation of SFJ at junction with femoral vein), femoral aneurysm, abscess, undescended/ectopic testes

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107
Q

What is a direct inguinal hernia?

A

Weakness in the abdominal wall at Hesselbach’s triangle (not through canal/tract)

108
Q

What might you find on examination of a direct inguinal hernia?

A

Pressure over the deep inguinal ring doesn’t stop herniation-> doesn’t reduce

109
Q

What is Hesselbach’s triangle?

A

RIP

  • Rectal abdominis muscle (medial)
  • Inferior epigastric vessels (superior/lateral)
  • Poupart’s ligament (inguinal- inferior)
110
Q

What causes a femoral hernia?

A
  • Abdominal contents through femoral canal

- Opening in femoral ring (between peritoneal cavity + femoral canal)-> narrow opening so high risk

111
Q

What is the femoral triangle?

A
  • Larger area at top of thigh containing femoral canal
  • Sartoris (lateral)
  • Adductor longus (medial)
  • Inguinal ligament (superior)
  • NAVY-C contained within
112
Q

What is contained within the femoral triangle?

A

NAVY-C (lateral to medial)

  • Nerve
  • Artery
  • Vein
  • Y fronts
  • Canal-> lymph vessels + nodes
113
Q

What is an incisional hernia?

A

Weakness where muscles and tissues closed in previous surgery-> hernia

114
Q

How are incisional hernias managed?

A
  • Often left alone if large/low risk

- Can repair but difficult + high recurrence rate

115
Q

What are the different types of hernia?

A
  • Direct inguinal
  • Indirect inguinal
  • Femoral
  • Incisional
  • Hiatus
  • Umbilical
  • Epigastric
  • Spigelian-> between rectus abdominis + linea semilunaris
  • Diastasis recti-> linea alba widens + separated rectus abdominis
  • Obturator-> bottom of pelvis + irritates obturator nerve
  • Ritcher’s-> only some of bowel wall + lumen through defect so easy to strangulate
  • Maydl’s-> 2 different bowel loops in 1 hernia
116
Q

Who are umbilical hernias most common in?

A

Neonates

117
Q

What is an indirect inguinal hernia?

A

A herniation through the inguinal canal

118
Q

Where does the inguinal canal run?

A
  • Deep inguinal ring-> connects to peritoneal cavity

- Superficial inguinal ring-> to scrotum

119
Q

What is the embryological function of the inguinal canal in males?

A

Allows spermatic cord + contents from inside the peritoneal cavity through the abdominal wall to the scrotum

120
Q

What is the embryological function of the inguinal canal in females?

A

Round ligament attached to uterus + passes through deep inguinal ring-> through canal-> attach to labia majora

121
Q

How does the inguinal canal develop in utero and how can this cause hernias?

A
  • Processus vaginalis ie pouch of peritoneum from abdominal cavity through inguinal canal
  • Allows tested to descend from abdominal cavity
  • Deep inguinal ring closes after descent + PV obliterated
  • If ring patent + PV intact-> tunnel for abdominal contents-> herniate into scrotum
122
Q

What examination finding would you expect in an indirect inguinal hernia?

A

Reduce + put pressure on deep inguinal ring with 2 fingertips (between ASIS + pubic tubercle)-> remains reduced

123
Q

What is a hiatus hernia?

A

Widening in diaphragm at level of lower oesophageal sphincter-> stomach herniates up

124
Q

What are the different types of a hiatus hernia?

A
  • Type 1-> sliding ie stomach slides up with gastro-oesophageal junction
  • Type 2-> rolling ie separate portion (eg fundus) folds around + enters diaphragm opening
  • Type 3-> 1 + 2
  • Type 4-> other organs in too eg pancreas
125
Q

How does hiatus hernia present?

A

Dyspepsia, reflux, burping, halitosis

126
Q

What are the risk factors for developing a hiatus hernia?

A

Older age, obesity, pregnancy

127
Q

What are the investigations for hiatus hernia?

A
  • Might not see as intermittent
  • CXT
  • CT
  • Endoscopy
  • Barium swallow
128
Q

How are hiatus hernias treated?

A
  • Conservative-> managed GOR

- Surgical-> when high risk or symptoms eh laparoscopic fundoplication (wrap fundus around lower oesophageal sphincter)

129
Q

What are haemorrhoids?

A

Enlarged anal vascular cushions

  • Submucosal tissue with connections between arteries and veins
  • Smooth muscle and connective tissue support
  • Help with anal continence
  • Strain etc-> enlarged
130
Q

What causes haemorrhoids?

A
  • Constipation + strain
  • Pregnancy-> constipation, pressure from baby, hormones relax connective tissue
  • Obesity
  • Older age
  • Increased intra-abdominal pressure
131
Q

Where are haemorrhoids usually found?

A
  • Think of anus as clock face
  • Haemorrhoids usually at 3, 7 and 11 oclock when patient on back
  • Where cushions are
132
Q

How are haemorrhoids classified?

A
  • 1st degree-> no prolapse
  • 2nd degree-> prolapse when strain + return when relax
  • 3rd degree-> don’t return on relaxing but can push back in
  • 4th degree-> permanent prolapse
133
Q

What are the symptoms of haemorrhoids?

A
  • Asymptomatic
  • Constipation + straining
  • Sore/itchy
  • Feel a lump
  • Painless bright red bleeding not mixed with stool
134
Q

How are haemorrhoids investigated?

A
  • Inspection- can see prolapsed
  • PR exam-> may not be able to see internal ones
  • Proctoscopy-> hollow tube in cavity to inspect
135
Q

What are some differentials for haemorrhoids?

A

Fissures, diverticulosis, IBD, cancer

136
Q

How are haemorrhoids managed (non-surgical)?

A
  • Topical creams/ointments-> anusol +/- hydrocortisone, germoloids cream + lidocaine
  • Avoid constipation-> increase fibre, laxatives
  • Rubber band ligation-> cut off blood supply
  • Injection sclerotherapy
  • Infra-red coagulation-> light damages blood supply
  • Bipolar diathermy-> electric current
137
Q

How are haemorrhoids managed (surgical)?

A
  • haemorrhoid artery ligation-> suture vessel
  • Haemorrhoidectomy-> can cause faecal incontinence
  • Stapled haemorrhoidectomy-> excise tissue + add circle of staples
138
Q

What causes a thrombosed haemorrhoid?

A

Strangulation + clotting

139
Q

How does a thrombosed haemorrhoid present?

A

Purple, tender, swollen, unable to perform PR exam

140
Q

How is a thrombosed haemorrhoid treated?

A
  • Resolves with time (weeks)

- May need admission + surgery if painful

141
Q

What is diverticulosis?

A

Presence of diverticulum-> pouch/pockets in abdominal wall

142
Q

What is diverticulitis?

A

When diverticulum (pouch/pockets in abdominal wall) become infected + inflamed

143
Q

What is diverticular disease?

A

When diverticulum (pouch/pockets in abdominal wall) cause problems/symptoms

144
Q

What is the pathophysiology of diverticulosis?

A
  • Points of weakness in large intestine’s circular muscle layer where BVs penetrate
  • Increased pressure over time-> gaps + herniations through muscle layer
  • NOT in rectum as outer longitudinal muscle layer gives support
  • Areas not covered in taniae coli (3 longitudinal muscle strips) at risk
145
Q

Where is diverticulosis most common?

A

Sigmoid colon

146
Q

What are the risk factors for developing diverticulosis?

A

Older age, low fibre diet, obesity, NSAIDs

147
Q

What are the symptoms of diverticulosis?

A
  • Asymptomatic
  • Lower left abdominal pain
  • Constipation
  • Rectal bleeding
148
Q

How is diverticulosis diagnosed?

A

Often incidental on colonoscopy or CT

149
Q

How is diverticulosis treated?

A
  • Not needed when asymptomatic
  • Weight loss + diet advice
  • Bulk-forming laxatives-> isphagula husk
  • May need surgery
150
Q

How does acute diverticulitis present?

A

LIF/LUQ pain, fever, diarrhoea, N+V, rectal bleeding, palpable abdominal mass, raised inflammatory markers?

151
Q

How is uncomplicated acute diverticulitis treated?

A
  • In primary care
  • Co-amoxiclav PO 5 days
  • Analgesia-> NOT NSAIDs
  • Clear liquids + avoid solid foods
  • Review in 2 days
152
Q

How is severe acute diverticulitis managed?

A

Acute abdomen-> NBM, IV fluids, antibiotics, urgent investigations, surgery

153
Q

How are the complications of acute diverticulitis?

A

Perforation, peritonitis, peridiverticular abscess, haemorrhage, fistula, ileus, obstruction

154
Q

What is mesenteric ischaemia?

A

Lack of blood flow through mesenteric vessels-> intestinal ischaemia

155
Q

What is included in the foregut?

A

Stomach, some of the duodenum, biliary, liver pancreas, spleen

156
Q

What is included in the midgut?

A

Distal duodenum to first 1/2 of transverse colon

157
Q

What is included in the hindgut?

A

Second half of the transverse colon to the rectum

158
Q

What supplies the foregut?

A

Coeliac artery

159
Q

What supplies the midgut?

A

Superior mesenteric artery

160
Q

What supplies the hindgut?

A

Inferior mesenteric artery

161
Q

What is the pathophysiology of chronic mesenteric ischaemia?

A

Chronic intestinal angina due to narrowing of vessels by atherosclerosis-> can present as acute ischaemia

162
Q

What is the classic triad of the presentation of chronic mesenteric ischaemia?

A
  • Central colicky abdominal pain after eating
  • Weight loss due to pain (food avoidance)
  • Abdominal bruit on auscultation
  • Symptoms usually intermittent (when can’t keep up to demand
163
Q

How is chronic mesenteric ischaemia diagnosed?

A

CT angiography

164
Q

How is chronic mesenteric ischaemia managed?

A
  • Risk factors and secondary presention

- Revascularisation-> stenting, bypass

165
Q

What causes acute mesenteric ischaemia?

A
  • Rapid blockage of vessels due to thrombus or emboli

- Usually AF causing RA thrombus to aorta then superior mesenteric artery

166
Q

How does acute mesenteric ischaemia present?

A

Acute + non specific pain disproportionate to examination findings-> shock, peritonitis, sepsis

167
Q

How is acute mesenteric ischaemia diagnosed?

A
  • Contrast CT-> gold standard
  • Metabolic acidosis
  • Raised lactate
168
Q

How is acute mesenteric ischaemia managed?

A

Surgery to remove necrotic bowel + remove/bypass thrombus-> open or endovascular (stenting)

169
Q

What is the prognosis of acute mesenteric ischaemia?

A

High mortality of 50%

170
Q

Where in the bowel does cancer most commonly present?

A

Colon or rectum

171
Q

What are the risk factors for bowel cancer?

A

Family history, IBD, older age, diet, obesity, smoking, alcohol, familial adenomatous polyposis (FAP), hereditary nonpolyposis colorectal cancer (HNPCC)

172
Q

What is familial adenomatous polyposis (FAP)?

A

Autosomal dominant condition-> malfunction of APC tumour suppressor genes causing polyps (adenomas) in the large intestine-> can become cancerous

173
Q

How is familial adenomatous polyposis (FAP) managed?

A

Prophylactic panprocticolectomy-> removal of large intestine

174
Q

What is hereditary nonpolyposis colorectal cancer (HNPCC)?

A
  • Autosomal dominant-> mutation in DNA mismatch repair genes
  • High risk of cancers
  • AKA Lynch syndrome
175
Q

How does bowel cancer present?

A

Change in bowel habit, rectal bleeding, unexplained pain, iron deficiency anaemia, weight loss

176
Q

What is the 2-week wait referral criteria for bowel cancer?

A

Depends on age
40+-> abdominal pain + weight loss
50+-> unexplained PR bleeding
60+-> change in bowel habit or iron deficiency anaemia

177
Q

Who is eligible for the bowel cancer screening programme?

A
  • People aged 60-74
  • Age 50+ with weight loss
  • Age <60 with bowel habit change
  • Any age + risk factors-> FAP, HNPCC, IBD
178
Q

How does the bowel cancer screening programme work?

A
  • Faecal immunochemical test (FIT)-> look at Hb level in stool
  • If positive-> send for colonoscopy
179
Q

What investigations are done for suspected bowel cancer?

A
  • Gold standard-> colonoscopy +/- biopsy or tattoo (for surgery)
  • Sigmoidoscopy-> when only PR bleeding
  • CT colonography-> CT + bowel prep as alternative to colonoscopy
  • Staging CT-TAP
  • Carcinoembryonic antigen (CEA)-> tumour marker for relapse prediction
180
Q

What 2 methods can be used to stage bowel cancer?

A
  • TMN system

- Duke’s classification

181
Q

How does the TNM system for staging bowel cancer work?

A
  • Tx-> unable to assess
  • T1-> submucosa
  • T2-> involves muscularis propria
  • T3-> subserosa + serosa involvement
  • T4a-> through serosa
  • T4b-> reaches other tissues
  • Nx-> unable to assess
  • N0-> none
  • N1-> spread to 1-3 nodes
  • N2-> spread to 3+ nodes
  • M0-> no mets
  • M1-> mets
182
Q

How does the Duke’s Classification for bowel cancer work?

A
  • A-> mucosa + part of bowel wall muscle
  • B-> extends through muscle
  • C-> lymph node involvement
  • D-> metastases
183
Q

How is bowel cancer managed?

A
  • Depends on health + stage + histology
  • MDT involvement
  • Surgical resection-> curative/palliative, tumour or section of bowel, may need stoma or anasthamosis
  • Options for surgery-> hemicolectomy, high or low anterior resection, abdomino-perineal resection + colostomy, Hartmann’s in emergencies
  • Follow up-> every 3 years, CEA marker + CT-TAP
184
Q

What are the potential complications after bowel cancer surgery?

A

Bleeding, damage, post-op ileus, leakage/failure of anastamosis, stoma, failure to remove tumour, inciscional hernia, adhesions, low anterior resection syndrome

185
Q

What is low anterior resection syndrome?

A
  • Anastamosis between colon and rectum in surgery

- Causes urgent + frequent bowel movements and incontinence

186
Q

Where is a colostomy likely to be located?

A

Left iliac fossa

187
Q

What sort of stool does a colostomy drain?

A

More solid-> more water reabsorbed in large intestine

188
Q

Is a colostomy spouted?

A

No- flatter as less irritating to skin

189
Q

Where is an ileostomy likely to be located?

A

Right iliac fossa

190
Q

What sort of stool does an ileostomy drain?

A

More liquid-> bypasses large intestine

191
Q

Is an ileostomy spouted?

A

Yes-> more irritant to skin so no contact with skin

192
Q

Where is a gastrostomy located?

A

Between stomach and abdominal wall

193
Q

What is a percutaneous endoscopic gastrostomy?

A

Hole in stomach to allow feeding directly

194
Q

Where is a urostomy likely to be located?

A

Usually right iliac fossa

195
Q

How is a urostomy made?

A

Ileal conduit

  • Section of ileus removed and end-to-end anastamosis made
  • Ureters attached to separated section
  • Out to skin as stoma + into urostomy
196
Q

Is a urostomy spouted?

A

Yes-> irritant liquid produced so no skin contact

197
Q

Where is an end colostomy located?

A

Usually lower left abdomen

198
Q

When are end colostomies done?

A

After abdomino-perineal resection-> rectum and anus removed

199
Q

When are end ileostomies done?

A

After panproctocolectomy (eg for IBD or FAP)

200
Q

What is a J-pouch?

A

Ileo-anal anastamosis-> functions like a rectum + attached to anus

201
Q

When are loop colostomies + ileostomies done?

A

After surgery to allow healing-> 2 openings side by side with productive proximal end-> temporary

202
Q

What are the potential complications of having a stoma?

A
  • Psychosocial implications
  • Local skin irritations
  • Parastomal hernias
  • Dehydration and malnutrition
  • Constipation
  • Stenosis
  • Obstruction
  • Prolapse
  • Bleeding
  • Granulomas
203
Q

What are gallstones made of and why?

A

Cholesterol-> found in bile + concentration gets too high

204
Q

What causes symptoms in biliary colic?

A
  • Fat in digestive system causes cholecystokinin (CKK) release from duodenum
  • Stimulates gallbladder contraction-> colic when stones
205
Q

What is the anatomy of the biliary tree?

A
  • Right and left hepatic ducts leave liver + join-> common hepatic duct
  • Cystic duct from gallbladder-> joins CHD halfway along
  • Cystic duct + CHD-> CBD
  • Pancreatic duct-> joins CBD later on
  • Ampulla of Vater in duodenum-> sphincter of Oddi (ring of muscle surrounding AoV to control flow)
206
Q

What is cholestasis?

A

Blockage of bile flow

207
Q

What is cholethliasis?

A

Stones present in gallbladder

208
Q

What is choledocholithiasis?

A

Stones present in bile duct

209
Q

What is biliary colic?

A

Intermittent RUQ pain due to gallstones in the bide ducts

210
Q

What is cholecystitis?

A

Gallbladder inflammation due to cystic duct blockage and prevention of drainage

211
Q

What is cholangitis?

A

Bile duct inflammation

212
Q

What is a gallbladder empyema?

A

Pus in the gallbladder

213
Q

What are the risk factors for gallstones?

A

4Fs-> fat, fair, female, forty

214
Q

How do gallstones present?

A
  • Asymptomatic
  • Biliary colic
  • Signs of complications-> obstructive jaundice etc
215
Q

How does biliary colic present?

A

Severe colicky epigastric/RUQ pain, triggered by fatty meals, lasts 30 mins to 8 hours, associated N+V

216
Q

What can cause pale stools and dark urine?

A
  • Normally bilirubin drains through liver and bile ducts to intestines
  • Obstruction due to gallstone in BD or external mass (pancreas, cholangiocarcinoma)-> flow blocked
  • Raises serum level
217
Q

What does a raised bilirubin level indicate?

A

Obstructive jaundice eg due to gallstone in BD or external mass (pancreas, cholangiocarcinoma

218
Q

What might cause a raised alkaline phosphatase (ALP)?

A
  • A problem with the liver, biliary system or bones

- Can also be raised in pregnancy

219
Q

What might cause a raised level of aminotransferases (ALT and AST)?

A

Hepatocellular injury (as are enzymes produced by liver)

220
Q

What LFT blood results would you expect in an obstructive picture?

A

ALT + AST slightly up but higher ALP and high bilirubin

221
Q

What LFT blood results would you expect in a hepatic picture?

A

ALT + AST higher compared to ALP

222
Q

What ultrasound findings might you see in gallbladder pathology?

A
  • Stones in gallbladder or ducts
  • Bile duct dilatation
  • Acute cholecystitis-> thickened walls, fluid surrounding, stones/sludge)
  • Pancreatic duct stones
223
Q

When is magnetic resonance cholangio-pancreatography (MRCP) performed?

A
  • When US negative for gallstones

- In strictures or congenital disease

224
Q

What is Endoscopic Retrograde Cholangio-Pancreatography (ERCP)?

A
  • A procedure to clear stones in the bile duct
  • Endoscope into sphincter of Oddi + CBD
  • Take X rays and diagnose
  • Clear stones, insert stents, sphincterectomy if dysfunctional etc
  • May take biopsies
225
Q

What are the potential complications of Endoscopic Retrograde Cholangio-Pancreatography (ERCP)?

A

Excess bleeding, cholangitis, pancreatitis

226
Q

What is the management of gallbladder pathology (especially stones)?

A
  • Conservative if asymptomatic

- Laporoscopic cholecystectomy

227
Q

What are the complications of laporoscopic cholecystectomy?

A
  • Bleeding
  • Bile duct damage-> leaks + strictures
  • Other organ damage
  • Post-cholecystectomy syndrome (due to changes in bile flow)
  • VTE + anaesthetic risks
228
Q

What is post-cholecystectomy syndrome?

A
  • Complication of laporoscopic cholecystectomy
  • Changes in bile flow
  • Presents with diarrhoea, indigestion, RUQ pain, epigastric pain, intolerance of fatty food
229
Q

What is calculus cholecystitis?

A

Caused by gallstones + trapped in cystic duct of GB neck-> 95% of all acute cholecystitis

230
Q

What is acalculous acute cholecystitis?

A

Gallbladder pressure builds up as not stimulated during food emptying-> eg TPN

231
Q

How does acute cholecystitis present?

A
  • RUQ pain + can radiate to shoulder
  • Fever, N+V, tachycardia, tachypnoea, tenderness
  • Raised WBCs + inflammatory
  • Murphy’s sign positive
232
Q

What is Murphy’s sign?

A
  • RUQ pressure-> eep breath in-> acute pain + stop inspiration when gallbladder touches hand
  • Indicates acute cholecystitis
233
Q

How is acute cholecystitis managed?

A
  • Abdominal US-> thick wall, stones/sludge, fluid around GB
  • MRCP-> if CBD stone suspected but not seen on US
  • Emergency admission + conservative management
  • ERCP if stones in CBD
  • Cholecystectomy-> within 72 hours or 6-8 weeks after acute episode
234
Q

When in cholecystectomy performed in acute cholecystitis?

A

within 72 hours or 6-8 weeks after acute episode

235
Q

What are the potential complications of acute cholecystitis?

A
  • Sepsis
  • Gangrenous gallbladder
  • Perforation
  • Empyema-> infected tissue + pus collects
236
Q

What causes ascending cholangitis?

A
  • Obstruction eg CBD stones
  • Infection introduced during ERCP
  • Organisms-> E.coli, Klebsiella, Enterococcus
237
Q

How does ascending cholangitis present?

A

Charcot’s triad-> RUQ pain, fever, jaundice (raised bilirubin)

238
Q

In what condition does Charcot’s triad (RUQ pain, fever, jaundice) present?

A

ascending cholangitis

239
Q

How is ascending cholangitis managed?

A
  • Admission + treat as acute abdomen
  • Diagnose-> endoscopic US, MRCP, CT scan, abdo US
  • ERCP-> eg stone removal, dilation/stenting, biopsy
  • Percutaneous transhepatic cholangiogram-> drain through skin + liver into BDs to relieve obstruction + stent inserted
240
Q

What is cholangiocarcinoma?

A
  • Cancer originating in the bile ducts-> usually adenocarcinoma
  • Can be intra- or extra-hepatic
241
Q

What are the risk factors for cholangiocarcinoma?

A
  • Primary sclerosing cholangitis (10-20%)

- Liver flukes-> parasites

242
Q

How does cholangiocarcinoma present?

A
  • Obstructive jaundice-> pale stools, dark urine, itching
  • Weight loss
  • RUQ pain, palpable GB, hepatomegaly
243
Q

What is Courvoisier’s law?

A
  • Palpable gallbladder + jaundice is unlikely stones

- May be cholangiocarcinoma or pancreatic cancer

244
Q

How is cholangiocarcinoma investigation?

A
  • CT/MRI + biopsy for histology
  • Staging CT-TAP
  • MRCP or ERCP
  • CA19-9-> tumour marker for cholangiocarcinoma and pancreatic cancer
245
Q

How is cholangiocarcinoma managed?

A
  • Curative surgery +/- radio/chemotherapy in early cases

- Palliative-> stents, chemo, radiotherapy, end of life

246
Q

Where does pancreatic cancer commonly occur?

A

Head of pancreas-> usually adenocarcinomas

247
Q

Why does pancreatic cancer have a poor prognosis?

A
  • Spread + mets early
  • Grows large + compresses bileducts-> obstructive jaundice
  • Often presents late
  • Average survival 6 months
248
Q

How does pancreatic cancer present?

A
  • Painless obstructive jaundice
  • Yellow skin + sclera, pale stools, dark urine, itching
  • Abdominal pain, palpable epigastric mass, change in bowels, N+V
  • T2DM-> worsening or new onset
249
Q

What is the 2-week wait referral criteria for pancreatic cancer?

A
  • Age 40+ with jaundice
  • Age 60+ with weight loss + 1 of diarrhoea, back pain, abdominal pain, nausea, vomiting, constipation, new-onset diabetes
250
Q

What are the signs of pancreatic cancer?

A
  • Courvoisier’s law-> Palpable gallbladder + jaundice

- Trousseau’s sign-> migratory thrombophlebitis (different locations over time)

251
Q

What is Trousseau’s sign of malignancy and what might it indicate?

A
  • migratory thrombophlebitis (different locations over time)

- pancreatic cancer

252
Q

What are the investigations for pancreatic cancer?

A
  • Biopsy under US or CT or endoscopy
  • MRCP or ERCP
  • CA19-9 tumour marker
253
Q

How is pancreatic cancer managed?

A
  • Hepatobiliary MDT
  • Surgery when small + isolated to head-> total/distal pancreatectomy, Whipple procedure (pancreaticoduodenectomy)
  • Palliative-> stents, bypass obstruction, chemo + radiotherapy, end of life care
254
Q

What are the causes of pancreatitis?

A

I GET SMASHED

  • Idiopathic
  • Gallstones
  • Ethanol (alcohol)
  • Trauma
  • Steroids
  • Mumps
  • Autoimmune
  • Scorpion Stings
  • Hyperlipidaemia
  • ERCP (quite common)
  • Drugs-> furosemide, thiazide diuretic, azathioprine
255
Q

What can gallstones cause pancreatitis?

A
  • Stones trapped in ampulla of vater + block flow of pancreatic juices + bile
  • Reflux in pancreatic duct
  • Inflammation
256
Q

Why does alcohol cause pancreatitis?

A

Directly causes toxicity + inflammation

257
Q

How does acute pancreatitis present?

A
  • Rapid onset
  • Severe epigastric pain + radiated to back
  • Vomiting
  • Abdominal tenderness
  • Systemically unwell-> low grade fever etc
258
Q

What are the investigations for acute pancreatitis?

A
  • FBC, U+E, LFTs, calcium, CRP
  • Amylase-> 3x upper limit of normal
  • ABG
  • US for gallstones
  • CT abdomen-> monitor complications (necrosis, abscess, fluid collection)
259
Q

What is the Glasgow score for pancreatitis?

A

Assesses severity of pancreatitis-> 0-1 (mild), 2 (moderate), 3+ (severe)

  • PaO2 <8kPa
  • Age >55
  • Neutrophils ie WBC >15
  • Calcium <2
  • Urea >16
  • Enzymes ie LDH >600 or AST/ALT >200
  • Albumin <32
  • Sugar ie glucose >10
260
Q

How is acute pancreatitis managed?

A
  • Admission + supportive-> most improve within 3-7 days
  • ERCP or cholecystectomy
  • Antibiotics if indicated
261
Q

What are the complications of acute pancreatitis?

A

Necrosis, infection, abscess, peri-pancreatic fluid collections, pseudocysts, chronic pancreatitis

262
Q

What usually causes chronic pancreatitis?

A
  • Progressive and permanent deterioration-> fibrosis

- Usually alcohol

263
Q

How does chronic pancreatitis present?

A
  • Longer onset + less intense
  • Severe epigastric pain + radiated to back
  • Vomiting
  • Abdominal tenderness
264
Q

What are the complications of chronic pancreatitis?

A
  • Chronic pain
  • Loss of exocrine function-> lipase in GI tract lost
  • Loss of endocrine function-> diabetes
  • Obstruction due to damage + duct stricture
  • Pseudocysts
  • Abscess
265
Q

How is chronic pancreatitis managed?

A
  • Alcohol + smoking abstinence
  • Analgesia
  • Creon-> lipase replacement to prevent malabsoprtion of fats + steatorrhoea
  • May need-> SC insulin, ERCP + stents, surgery

Surgery (8 decks)

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