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General Surgery > Part Two - general > Flashcards

Part Two - general Flashcards

0
Q

Breslow thickness

A

Tumour depth - Approximate five year survival

< 1mm - 95-100%
1-2mm - 80-96%
2.1-4mm - 60-75%
> 4mm - 50%

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1
Q

Dukes classification

A

Dukes’ A = invasion into but not through bowel wall - 90% five year survival
Dukes’ B = invasion through the bowel wall but not involving nodes - 70%
Dukes’ C = involvement of lymph nodes - 30%
Dukes’ D = distant metastases - <15%

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2
Q

Submandibular space

A

Anterior upper neck
Above investing layer of deep cervical fascia
Between hyoid and mandible to mucous membrane of floor of mouth

Contains:

  • Mylohyoid muscle
  • Sublingual gland above mylohyoid muscle
  • Submandibular gland hooking around posterior border of mylohyoid

Cellulitis here = LUDWIG’S ANGINA

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3
Q

MAGIC trial

A

United Kingdom Research Council MAGIC Trial
503 patients with potentially resectable gastric (74%), distal oesophageal (11%) or OGJ adenocarcinomas (15%)
Surgery alone or surgery plus perioperative chemotherapy
Three preop and three post op cycles of epirubicin, cisplatin and infusional 5-fluorouracil
T2+ disease with no distant metastases or locally advanced inoperable disease as per CT, USS and laparoscopy
Only 42% could complete treatment
Five year survival improved from 23% to 36%
Problem - more T1/T2 tumours in chemotherapy group

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4
Q

CA 125

Cancer antigen 125

A

Large transmembrane glycoproteins derived from both coelomic (pericardium, pleura, peritoneum) and müllerian ( fallopian tubes, endometrium, endocervical) epithelia.

Elevated in malignant conditions:

  • Ovarian carcinoma
  • Fallopian tube carcinoma
  • Primary serous peritoneal carcinoma
  • Endometrial carcinoma
  • Endocervical adenocarcinoma
  • Pancreatic carcinoma
  • Breast carcinoma
  • Lymphoma
  • Lung carcinoma
  • Colorectal carcinoma

Elevated in benign conditions

  • Endometriosis
  • Cirrhosis
  • Acute peritonitis
  • Acute pancreatitis
  • Acute PID
  • First trimester of pregnancy
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5
Q

Describe Strasberg classification oh bile duct injury

A

Type A - Bile leak from cystic duct or minor hepatic ducts draining liver bed
Type B - Occlusion injury of aberrant right hepatic duct
Type C - Transection without ligation of proximal aberrant right hepatic duct
Type D - lateral injury to major bile duct
Type E - Transection of main duct
* E1 / Bismuth 1 - Injury >2cm from confluence
* E2 / Bismuth 2 - Injury <2cm from confluence
* E3 / Bismuth 3 - Injury at confluence, confluence intact
* E4 / Bismuth 4 - Destruction of biliary confluence
* E5 / Bismuth 5 - Injury to aberrant right hepatic duct and main duct

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7
Q

Define SIRS

A

SIRS = systemic inflammatory response syndrome

Clinically defined by two or more of:

  • Temperature > 38 or < 36
  • Pulse rate > 90
  • WCC > 12 or < 4 x 10*9/L
  • Respiratory rate > 20/min or PaCO2 <32 mmHg
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8
Q

Daily water turnover in the gut

A 
Ingested 2.0L
Endogenous secretions 7.0L
- Salivary glands 1.2L
- Stomach 2.5L
- Bile 0.5L
- Pancreas 1.5L
- Intestine 1.0L
Reabsorbed 8.8L
- Jejunum absorbs > ileum > colon
Faeces 0.2L
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9
Q

Define harmatoma

A

Disorganised but benign-appearing mass composed of cells indigenous to particular site

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10
Q

Define pseudopolyp

A

Inflammatory pseudo polyps are irregularly shaped islands of residual intact mucosa resultant from ulceration and regeneration in IBD.

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11
Q

How large do lymph nodes need to be on CT to suggest LN metastases?

A

Thorax & abdomen - 1cm in short axis
Supraclavicular - 0.5cm in short axis
Retrocrural - 0.6cm in short axis

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12
Q

What is metaplasia?

A

The reversible replacement of one differentiated cell type with another mature differentiated cell type

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13
Q

Subclavian artery

A 
Divided into three parts by saclenus anterior
1st part medial with three branches
- Vertebral artery
- Internal thoracic artery
- Thyrocervical trunk
     - Inferior thyroid artery
     - Inferior laryngeal artery
     - Ascending cervical artery
     - Superficial cervical artery
     - Suprascapular artery
2nd part behind muscle with two branches
- Costocervical trunk
     - Deep cervical
     - Superior intercostal
- Dorsal scapular artery
3rd part lateral to muscle with no branches
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14
Q

Axillary artery

A

Continuation from SCA beginning lateral border 1st rib and terminating lower border terries major
Divided into three parts by pec minor
1st part medial to muscle with one branch
- Superior thoracic artery
2nd part behind muscle with two branches
- Thoracoacromial trunk - CHAP branches
- Lateral thoracic artery
3rd part lateral to muscle with three branches
- Subscapular -> thoracodorsal & circumflex scao
- Anterior circumflex humeral
- Posterior circumflex humeral

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15
Q

Indications for the open abdomen

A

1 - prevention or treatment of ACS
2- damage control for life-threatening intra-abdominal bleeding
3 - management of severe intra-abdominal sepsis

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16
Q

Define abdominal hypertension

A

Sustained pathologic increase in intra-abdominal pressure greater than or equal to 12mmHg

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17
Q

Define abdominal compartment syndrome

A

Sustained pathologic increase in intra-abdominal pressure greater than 20mmHg that is associated with new organs dysfunction/failure

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18
Q

What is abdominal perfusion pressure (APP)?

A

= MAP - IAP

Is a measure of the net pressure available for perfusion of intra-abdominal organs

Target APP associated with appropriate perfusion is 60mmHg

Analogous to cerebral perfusion pressure

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19
Q

Principles of managing IAP

A
  1. Serial monitory of IAP
  2. Optimisation of systemic perfusion and organ function in the patient with increased IAP
  3. Institution of specific medical procedures to reduce IAP
  4. Prompt surgical decompression for refractory IAH
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20
Q

Risk factors for IAH/ACS

A

Four categories of risk factors:

  1. Diminished abdominal wall compliance
  2. Increased intraluminal content
  3. Increased abdominal contents
  4. Capillary leak / fluid resuscitation

Specific examples:

  • > 5L crystalloid within 24 hours
  • > 10U packed red cells within 24 hours
  • Hypothermia < 33
  • Acidosis with BE < -14 and/or pH 30
  • Burns:
    • TBSA > 30% risk factor for IAH
    • TBSA >50% risk factor for ACS
    • Inhalation risk factor for ACS
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21
Q

How do you measure intra-abdominal pressure?

A

Bladder pressures. Instill 25mL saline via a foley catheter attacher to a pressure transducer zeroed at the MAL in the supine position. Take the reading at end-expiration.

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22
Q

How does warfarin work?

A

Coumarin derivative with structure similar to vitamin K. It causes the production of inactive vitamin K dependent coagulation factors - II, VII, IX and X.

23
Q

How is warfarin reversed?

A 
Cease for 5 days
Vitamin K 1-10mg
Prothrombinex 50IU/kg
FFP 30ml/kg
Recombinant factor VIIa 15-90units/kg
24
Q

What is Prothrombinex?

A

Sterile, freeze-dried powder containing purified human coagulation factors II, IX and X and low levels of factors V and VII.

25
Q

What is dabigatran?

A

A direct thrombin inhibitor that is renal excreted and difficult to reverse. Only known effective measure for reducing effect is haemodyalysis

26
Q

How do you test the effect of dabigatran?

A

HEMOCLOT and ecarin clotting time are specific assays but not generally available.
If TCT and aPTT are normal there is probably no significant drug presence but if they are elevated they do not correlate well with affect

27
Q

How do you reverse dabigatran?

A

Haemodialysis only method.
Support measures may include:
- Keep good UO as renal excreted
- Platelets if 80 or less and/or on anti-platelet agent
- Oral charcoal if ingested within two hours
- Replace calcium if low
- Tranexamic acid IV (15-30mg/kg) +/- continuous infusion (1mg/kg/hr)
- Consider Prothrombinex +/- rFVII

28
Q

How does heparin work?

A

It is an indirect thrombin inhibitor which increases the efficacy of antithrombin III such that thrombin is aggressively inactivated. Also inactivates factors IIa, IXa, Xa, XIa, XIIa.
Enoaxaparin just inhibits Xa.

29
Q

How is heparin reversed?

A 
Because of short half life, just ceasing administration may be enough. 
Else protamine:
- 1mg per 100mg UFH within 3 hours
-------fully reversed
- 1mg per 1mg LMWH with 8 hours
-------up to 80% reversed
30
Q

What defines massive blood loss?

A
  • Loss of entire blood volume within 24 hours
    • Loss of 50% within 3 hours
    • Ongoing blood loss of 150ml/min
    • Ongoing blood loss of a.5ml/kg/min
    • Rapid blood loss leading to circulatory failure
31
Q

Define shock

A

Inability of the body to maintain adequate end organ perfusion

32
Q

How is haemorrhagic shock classified?

A

Into four classes based on amount of blood lost, HR, BP, PP, RR, UO and CNS.

15/30/40/>40
140

33
Q

Define massive transfusion

A

10+ PRBCs within a 24 hour period

34
Q

Damage control resuscitation strategies

A

For patients with overwhelming injury burden and massive blood loss

Includes:
Permissive hypotension
Aggressive 1:1:1 ratio transfusion
Selective use of haemostatic adjuncts

35
Q

What is permissive hypotension?

A

With-hold of minimise fluids as long as cerebral perfusion is evidence and SBP remains above a threshold value of 70-80mmHg

36
Q

What are massive transfusion protocols?

A

Institution based protocols activated in appropriate patients that standardise replacement of platelets and clotting factors in an optimum ratio to PRBCs and increases transfusion efficiency. Adjuncts of tranexamic acid, Prothrombinex and rFVIIa included

37
Q

How do local anaesthetics work?

A

Drugs that prevent pain by reversible blockade of conduction along nerve fibres by sodium channel blockade. Small diameter fibres like pain fibres are the most sensitive

38
Q

Lignocaine

A

Reversible sodium channel blocker
Acts rapidly 5 mins
Duration 2 hours
5 mg/kg without or 7mg/kg with adrenaline
Toxic dose 300mg without or 500mg with adrenaline

39
Q

Bupivacaine

A

Reversible sodium channel blocker
Acts within 10mins
Duration 4 hours
2mg/kg without or 3mg/kg with adrenaline
Toxic dose 175mg without or 225mg with adrenaline
35ml without or 45ml with adrenaline in 0.5% mix

40
Q

What is the risk of malignancy with CT?

A

1/200

1/400 fatal

41
Q

How do you diagnose a chyle leak?

A

Increased drain output with enteral nutrition
Change in drain output from serous to milky
Triglyceride level >110mg/dL
Presence of chylomicrons

42
Q

Treatment of chyle leak

A

Diagnosis then STEPWISE approach
NBM or high protein-low far oral diet with MCT supplements +/- somatostatin/ocreotide - 50% success
If no response within 5-14 days - ligation - 90% success
Consider early ligation if:
- Drain > 1L/day
- Younger adult patients at low risk of further complications
- After resection of a malignancy as less likely to respond to conservative management as leaking from collaterals that seldom heal spontaneously

43
Q

Good technique for closure

A

Nonabsorbable monofilament
Continuous stitch
Suture length-to-incision ratio of 4:1 = 1cm of tissue at 1 cm intervals

44
Q

WHO criteria for screening

A

RAIN ESCAPES

R = recognisable early stage of disease
A = ability for continuous screening, not a one off
I = important problem
N = natural history known
E = evidence that early treatment beneficial
S = sensitive, specific, simple, acceptable screening test
C = cost effective
A = adequate resources
P = no psychological harm
E = effective, safe, acceptable treatment
S = strategy to identify those who should be screened
45
Q

Explain the hypokalaemic hypochloraemia metabolic alkalosis with paradoxical aciduria

A

Vomit out HCl and KCl to a lesser extent-> alkalosis
K + exchanges for H+ -> exacerbating hypokalaemia
DT favours Na+/H+ over Na/K+ -> aciduria
Thereby aggravating the metabolic alkalosis in GOO

46
Q

ABCs of non-surgical management

A 
A - analgesia & antibiotics
B - breathing optimisation
C - catheter & consent
D - DVT prophylaxis & drain
E - electrolytes & emesis treatment
F - fluids, food & ferrous
G - gastric protection & glucose
47
Q

ARDS

A

Clinical syndrome of pulmonary dysfunction resulting from infection, inflammation, tissue injury or cellular shock

48
Q

Criteria for diagnosis of ARDS

A
  1. Hypoxaemia
  2. Bilateral pulmonary infiltrates
  3. Exclusion of heart failure
  4. Acute onset
49
Q

Pathophysiology of ARDS

A
  1. Exudative phase - fucked type II pneumocytes
  2. Fibroproliferative phase - mesochymal cells = fibrosis
  3. Resolution phase - type II recover and fix fuckedness
50
Q

Treatment ARDS

A 
Supportive
Prophylaxis
Identify & treat underlying cause
Omega three fatty acids
Lung protective ventilation
Prone positioning
51
Q

Cardiopulmonary exercise testing

A

Accurate way to assess exercise tolerance which is the best predictor of post-operative complications.
Measures maximal oxygen consumption (VO2 max) which is a measure of level of work achieved on a static bike with increasing resistance via ECG and gas analyser.
>20ml/kg/min –> OK for surgery
not for surgery

52
Q

Arista

A

MPH = microporous polysaccharde hemispheres derived from purified plant starch. Puff powered. Works in minutes and absorbs in 24 hours.

Controls capillary, venous and arteriolar bleeding when pressure, ligature and other conventional methods of haemostats are ineffective or impractical.

Eg - presacral vein bleeding, liver trauma

53
Q

Surgicel

A

Absorbable haemostatic agent ORC = oxidised regenerated cellulose. Provides a matrix for platelet adhesion and aggregation. Absorbs in 7-14 days. Has anti-bacterial properties.

54
Q

Proceed mesh

A

ORC, PDS, polypropylene.

Soft polypropylene mesh encapsulated by PDS

General Surgery (25 decks)

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