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Satia's MRCS copied decks > MRCS part A- Principles of surgical oncology and breast and endocrine > Flashcards

MRCS part A- Principles of surgical oncology and breast and endocrine Flashcards

1
Q

Define Chordoma

A

Bone tumour

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2
Q

What is the origin of Chordoma?

A

Remnants of notochord

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3
Q

What is the clinical picture of Chordoma?

A

I)Slow-growing tumour II)Location (a)anywhere from the skull base to the sacrum (b)the two most common locations are: -skull base -sacrum III)Histological types: (a)classical(conventional) -lobulated tumour -composed of group of cells -the cells have: +nuclei-(1)small (2)round +cytoplasm-(1)abundant (2)vacuolated (b)Chondroid -Shows features of both Chordoma and chondrosarcoma -Indolent clinical course (c)De-differentiated

Never in rib

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4
Q

What is the incidence of Chordoma?

A

Rare

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5
Q

What is the characteristic feature of the Chordoma?

A

Slow-growing bone tumour

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6
Q

What is the location of the chondroma?

A

(1) anywhere from the skull base to the sacrum
(2) the 2 most common locations are
- skull base
- sacrum

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7
Q

What are the histological types of chondroma?

A

a)classical(conventional)
-lobulated tumour
-composed of group of cells
-the cells have:
+nuclei-(1)small
(2)round
+cytoplasm(1)abundant
(2)vacuolated
(b)Chondroid-Shows features of both chondroma and chondrosarcoma
-Indolent clinical course
(c)De-differentiated

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8
Q

What is the other name for classical Chordoma?

A

Conventional

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9
Q

Discuss classical Chordoma

A

-lobulated tumour
-composed of group of cells
-the cells have:
The cells have small round nuclei and abundant vacuolated cytoplasm

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10
Q

Discuss chondroid chordoma

A

-Shows features of both chondroma and
chondrosarcoma
-Indolent clinical course

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11
Q

Discuss treatment of Chordoma

A

Complete surgical resection followed by radiotherapy
+Advantages-offers the best chance of long term control
+Disadvantages-
(a)For surgery
Proximity to the spine compromises resection margins
(b)For radiotherapy
-Problem:(1)Chordomas are radio resistant requiring high doses of radiation to be controlled
(2)Proximity of Chordomas to vital neurological structures such as the brain stem and nerves
limits the dose of radiotherapy
-Solution:Highly focused radiation
.e.g.,-proton therapy
-carbon ion therapy
.more effective than conventional X-ray radiation

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12
Q

What is the specific treatment of Chordoma?

A

Complete surgical resection followed by radiotherapy

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13
Q

What is the advantage of both surgery and radiotherapy for Chordoma?

A

Offers the best chance of long term control

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14
Q

What are the disadvantages of surgery and radiotherapy for Chordoma?

A

(a)For surgery
Proximity to the spine compromises resection margins
(b)For radiotherapy
-Problem:(1)Chordomas are radio resistant requiring high doses of radiation to be controlled
(2)Proximity of Chordomas to vital neurological structures such as the brain stem and nerves
limits the dose of radiotherapy
-Solution:Highly focused radiation
.e.g.,-proton therapy
-carbon ion therapy
.more effective than conventional X-ray radiation

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15
Q

What is the disadvantage of surgery for Chordoma?

A

Proximity to the spine compromises resection margins

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16
Q

What are the disadvantages of radiotherapy for Chordoma?

A

-Problem:(1)Chordomas are radio resistant requiring high doses of radiation to be controlled
(2)Proximity of Chordomas to vital neurological structures such as the brain stem and
nerves limits the dose of radiotherapy
-Solution:Highly focused radiation
.e.g.,-proton therapy
-carbon ion therapy
.more effective than conventional X-ray radiation

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17
Q

What is the origin of colorectal cancer?

A

Adenomatous polyp

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18
Q

What is the advantage of colorectal cancer screening?

A

Reduce mortality by 12%

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19
Q

Discuss the NHS screening programmes

A
  • Most cancers develop from adenomatous polyps. Screening for colorectal cancer has been shown to reduce mortality by 16%
  • The NHS now has a national screening programme offering screening every 2 years to all men and women aged 60 to 69 years. Patients aged over 70 years may request screening
  • Eligible patients are sent faecal occult blood (FOB) tests through the post. This is being replaced by FIT testing.
  • Patients with abnormal results are offered a colonoscopy
  • The NHS BOSS flexible sigmoidoscopy screening comprises a single flexible sigmoidoscopy to patients aged 55 years
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20
Q

What is the method for national screening programme?

A

Faecal occult blood:(1)sent through the post

(2) replaced by FIT testing
(3) If abnormal results-colonoscopy

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21
Q

Discuss NHS BOSS single sigmoidoscopy

A

+Features-At colonoscopy,approximately:
(1)5 out of 10 have normal exam (2)4 out of 10 have polyps which may be removed due to premalignant potential
(3)1 out of 10 have cancer
+Method-Single flexible sigmoidoscopy for patients aged 55 years

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22
Q

What is the method for NHS BOSS single sigmoidoscopy?

A

Single flexible sigmoidoscopy for patients aged 55 years

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23
Q

Discuss the diagnosis of colorectal cancer

A

.Essentials-The following patients need referral:(1)Altered bowel habits >6 weeks

  • (Mnemonic;ART)**_ (2)New onset _**Rectal bleeding
    (3) *_T_    enesmus

.Method-I)Colonoscopy:Is the GOLD STANDARD,provided it is complete and good mucosal visualisation is achieved
II)Other options:(1)Double contrast barium enema
(2)CT colonograpy
III)Tumour marker:Carcinoembryonic antigen(CAE)
-the main tumour marker in colorectal cancer
-used routinely in follow ups
-correlates roughly with disease burden
-not all tumours secret it
-may be raised in conditions such as IBD

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24
Q

Enumerate the conditions that necessitate referral of patients with colorectal cancer

A

Mnemonic;ART

(1) Altered bowel habits
(2) New onset Rectal bleeding
(3) Tenesmus

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25
Q

What are the methods used to diagnose colorectal cancer?

A

I)Colonoscopy:Is the GOLD STANDARD,provided it is complete and good mucosal visualisation is achieved
II)Other options:(1)Double contrast barium enema
(2)CT colonograpy
III)Tumour marker:Carcinoembryonic antigen(CAE)
-the main tumour marker in colorectal cancer
-used routinely in follow ups
-correlates roughly with disease burden
-not all tumours secret it
-may be raised in conditions such as IBD

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26
Q

Discuss staging of colorectal cancer

A

I)chest/abdomen/pelvis CT
II)Pelvic MRI-for patients with rectal cancer to evaluate mesorectum
III)Dukes and TNM classification systems
-for examination purposes
-Dukes:

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27
Q

What is the purpose of the Dukes classification?

A

Gives the extent of spread of colorectal cancer

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28
Q

What is Dukes A in colorectal cancer?

A
  • Tumour confined to the bowel but not extending beyond it.
  • without nodal metastasis.
  • 5 year survival 95%
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29
Q

What is the 5 year survival rate for Dukes classification?

A

95%

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30
Q

What is Dukes B in colorectal cancer?

A

Tumour invading bowel wall
Without nodal metastasis
5 year survival 75%

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31
Q

What is the 5 year survival of Dukes B in colorectal cancer?

A

75%

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32
Q

What is Dukes C in colorectal cancer?

A

Lymph node metastasis
5 year survival 50%

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33
Q

What is the 5 year survival of Dukes C in colorectal cancer?

A

50%

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34
Q

What is Dukes D in colorectal cancer?

A

Distant metastasis
5 year survival 6%(25% if respectable)

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35
Q

What is the incidence of extravasation injury?

A

6%

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36
Q

What is the aetiology of extravasation injury?

A

Chemotherapy with:(1)Doxorubicin

(2) Vincristine
(3) Vinblastine
(4) Cisplatin
(5) Mitomycin
(6) Mithramycin

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37
Q

What is the complication of extravasation injury?

A

Ulceration in 30%

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38
Q

What is the incidence of ulceration in extravasation injury?

A

30%

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39
Q

What is the treatment of extravasation injury?

A

I)stop infusion
II)infusing device aspirated
III)elevate the extremity
IV)compression-(1)cold compression:for doxorubicin ulceration
(2)warm compression:for extravasation of vinca alkaloids
V)Drugs-(1)Dimethylsulfoxide:within 5 hours
(2)Corticosteroids:no evidence to support their use in extravasation injury
(3)Sodium bicarbonate:no evidence to support their use of extravasation injury
(4)Hyaluronidase:for extravasation of total parentral nutrition(TPN)

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40
Q

What is the cold compression used for in extravasation injury?

A

for doxorubicin ulceration

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41
Q

What is the warm compression used for in extravasation injury?

A

for extravasation of vinca alkaloids

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42
Q

What are the drugs used to treat extravasation injury?

A

(1) Dimethylsulfoxide:within 5 hours
(2) Corticosteroids:no evidence to support their use in extravasation injury
(3) Sodium bicarbonate:no evidence to support their use of extravasation injury
(4) Hyaluronidase:for extravasation of total parentral nutrition(TPN)

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43
Q

What is the timing of use of dimethylsulfoxide?

A

Within 5 hours

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44
Q

What is the evidence of use of extravasation?

A

No evidence to support their use extravasation injury

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45
Q

What is the evidence of use of sodium bicarbonate in extravasation injury?

A

No evidence to support their use in extravasation injury

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46
Q

What is the use of hyaluronidase in extravasation injury?

A

For extravasation of total parentral nutrition(TPN)

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47
Q

What is the management of non small cell lung cancer?

A

(1) Surgery
(2) Mediastinoscopy
(3) Radiotherapy
(4) Chemotherapy

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48
Q

What is the incidence of surgery in the management of non small cell lung cancer?

A

Only 20% suitable for surgery

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49
Q

What are the contraindications for surgery in the management of non small cell lung cancer?

A

Mnemonic;ASF/MTVS

(1) Assess general health
(2) Stage IIIb or IV(i.e.,metastasis)
(3) FEV1-(a)<1.5L is a general cut off point
(b) some authorities may advocate further lung function tests as operation may still go ahead based on the results if:
- FEV1<1.5L for lobectomy
- FEV1<2L for pneumonectomy
(4) Malignant pleural effusion
(5) Tumour near the hilum
(6) Vocal cord paralysis
(7) Superior vena cava(SVC)obstruction

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50
Q

What should be done for the patient with non small cell lung cancer before surgery?

A

Assess general health

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51
Q

What is the stage of non small cell lung cancer that forbids surgery?

A

Stage IIIb or V(i.e.,metastasis)

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52
Q

What do stage IIIb or V mean?

A

Metastasis

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53
Q

Discuss FEV1 as a contraindication of surgery in non small cell lung cancer

A

(a) <1.5L is a general cut off point
(b) some authorities may advocate further lung function tests as operation may still go ahead based on the results if:
- FEV1<1.5L for lobectomy
- FEV1<2L for pneumonectomy

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54
Q

What is the general cut off point which is considered as a contraindication for surgery in non small cell lung cancer?

A

FEV1<1.5L

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55
Q

What is the indication of lobectomy in non small cell lung?

A

FEV<1.5L

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56
Q

What is the indication of pneumonectomy in non small cell lung cancer?

A

FEV<2L

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57
Q

What is the indication of mediastinoscopy in non small cell lung cancer?

A

Prior to surgery as CT does not always show mediastinal lymph nodes involvement

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58
Q

What is the type of radiotherapy in non small cell lung cancer?

A

(1) Palliative
(2) Curative

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59
Q

What is the feature of the chemotherapy in non small cell lung cancer?

A

Poor response

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60
Q

What if the general health is bad in a patient with non small cell lung cancer?

A

The surgery is contraindicated

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61
Q

What are the SIGN guidelines on control of pain in adults?

A

I)The breakthrough dose of morphine=1/6 the daily dose of morphine
II)All patients with opioids should receive laxatives
III)Opioids should be used with caution in CKD,these are preferred-(1)Alfentanil
(2)Buprenorphine
(3)Fentanyl

IV)Metastatic bone pain may respond to-(1)NSAID
(2)Bisphosphonate
(3)Radiotherapy
V)When increasing the dose of opioids the next dose should be increased by 30-50%

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62
Q

What is the breakthrough dose of morphine on palliative care for control of pain in adults?

A

1/6th daily dose of morphine

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63
Q

What should be given to all patients administering opioids?

A

Laxatives

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64
Q

Discuss opioids and CKD

A

Opioids should be used with caution in CKD

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65
Q

What are the preferred drugs for CKD instead of opioids?

A

(1) Alfentanil
(2) Buprenorphine
(3) Fentanyl

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66
Q

What should be given to a metastatic bone disease?

A

(1) NSAIDs
(2) Bisphosphonate
(3) Radiotherapy

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67
Q

How much is the increasing dose of opioids the next time the dose needs to increased?

A

Should be increased by 30%-50%

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68
Q

Discuss conversion between opioids

A
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69
Q

How to convert oral codeine to oral morphine?

A

Divide by 10

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70
Q

How to convert oral tramadol to oral morphine?

A

Divide by 5

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71
Q

How to convert oral morphine to oral oxycodone?

A

Divide by 2

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72
Q

How to convert oral morphine to subcutaneous diamorphine?

A

Divide by 3

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73
Q

How to convert oral oxycodone to subcutaneous diamorphine?

A

Divide by 1.5

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74
Q

What are the typical tumours that spread to bone?

A

(1) Thyroid
(2) Bronchus

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75
Q

What are the commonest bone sites affected in secondary malignant tumour of bone?

A

(1) Skull
(2) Sternum
(3) Ribs
(4) Vertebrae(usually thoracic)
(5) Pelvis
(6) Proximal femur

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76
Q

What is the incidence of 2ry(metastatic) and 1ry bone tumours?

A

Metastatic(2ry) lesions affecting bone are more common than 1ry bone tumours

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77
Q

What are the causes of pathological fracture?

A

Mnemonic;OUT

(1) Osteolytic lesions-are the greatest risk for pathological fracture
(2) Under loading(Harrington)-when the lesion occupy 50% or less of the bone
(3) Torsion about a bony fulcrum-when 75% of the bone is affected

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78
Q

Discuss Harrington criteria for pathological fractures

A
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79
Q

Discuss Mirel’s criteria for pathological fracture

A

.Uses-help determine the risk of fracture.
.Feature-more systematic than the Harrington system

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80
Q

What is the use of Mirel’s system in treatment of pathological fracture?

A

Help determine the risk of fracture

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81
Q

What is the feature of the Mirel’s scoring system in management of pathological fracture?

A

More systematic than Harrington scoring system

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82
Q

What should be done for isolated metastatic bone deposit?

A

Consideration should be given to excision and reconstruction as the outcome is better

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83
Q

What is the non operative treatment?

A

I)Hypercalcaemia,treat with-(a)rehydration
(b)bisphosphonate
II)Pain-(a)opiate analgesics
(b)radiotherapy
III)Some tumours such as breast and prostate-(a)chemotherapy
(b)hormonal agents

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84
Q

According to what conditions biopsy modalities vary?

A

Mnemonic;SET

(1) Site
(2) Experience
(3) Subsequent planned Therapeutic outcome

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85
Q

What are the modalities of tissue sampling?

A
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86
Q

Discuss fine needle aspiration cytology(FNAC)

A

+Technique

(1) passing a needle through a lesion whilst suction is applied to a syringe
(2) the material obtained is expressed onto a slide and sent for cytology

+Drawbacks

(1) operator dependent-limited by operator inexperience
(2) may or may not be image guided
(3) limited by the lack of histological architectural information(e.g.,follicular carcinoma of the thyroid)
(4) if discharge(e.,nipple discharge),information may be meaningless

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87
Q

What is the technique for fine needle aspiration cytology?

A

(1) passing a needle through a lesion whilst suction is applied to a syringe
(2) the material obtained is expressed onto a slide and sent for cytology

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88
Q

What are the drawbacks of the fine needle aspiration cytology?

A

(1) operator dependent-limited by operator inexperience
(2) may or may not be image guided
(3) limited by the lack of histological architectural information(e.g.,follicular carcinoma of the thyroid)
(4) if discharge(e.,nipple discharge),information may be meaningless

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89
Q

How do we obtain tissue samples?

A

Tissue samples may obtained by.
1st/Core biopsy
obtained by use of spring loaded gun with a needle passing quickly through the lesion of interest

2nd/True cut biopsy

  • achieves the same objective as core biopsy but the needle moved by hand
  • image guidance may be desirable(e.g.,in breast lesions)
  • consider any planned surgical resection as it may be necessary to resect the biopsy along with the specimen(e.g.,in sarcoma surgery)

3rd/For superficial lesions

  • complete excision or excision biopsy
  • e.g.,malignant melanoma-needs more radical surgical approach after excision biopsy than would be the case in basal cell carcinoma

4th/Punch biopsy

  • unclear skin lesions
  • e.g.,whether a skin lesion is vasculitic or not
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90
Q

Discuss core biopsy

A

obtained by use of spring loaded gun with a needle passing quickly through the lesion of interest

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91
Q

Discuss true cut biopsy

A
  • achieves the same objective as core biopsy but the needle moved by hand
  • image guidance may be desirable(e.g.,in breast lesions)
  • consider any planned surgical resection as it may be necessary to resect the biopsy along with the specimen(e.g.,in sarcoma surgery)
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92
Q

How do obtain tissue samples for superficial lesions?

A
  • complete excision or excision biopsy
  • e.g.,malignant melanoma-needs more radical surgical approach after excision biopsy than would be the case in basal cell carcinoma
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93
Q

Discuss punch biopsy

A
  • unclear skin lesions
  • e.g.,whether a skin lesion is vasculitic or not
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94
Q

What is the incidence of fibroadenoma?

A

(1) 12-13% of all palpable breast lesions
(2) 60% of all breast lesions in 18-25 years of age

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95
Q

What is the classification of the fibroadenoma?

A
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96
Q

What is the size of the fibroadenoma?

A

(1) <3 cm-watchful waiting without biopsy
(2) >3-4cm-core biopsy:to exclude a phylloides tumour,but if phylloides tumour
(a) wide excision
(b) mastectomy if lesion is large
- surgical excision

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97
Q

What should be done for <3 cm fibroadenoma?

A

watchful waiting without biopsy

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98
Q

What should be done to >3-4 cm fibroadenoma?

A

-core biopsy:to exclude a phylloides tumour,but if phylloides tumour
(a)wide excision
​ (b)mastectomy if lesion is large
-surgical excision

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99
Q

Discuss pathogenesis of fibroadenoma

A

(1) <25 years,breast is classified undergoing development
(2) Develop from a whole
(3) Lobular units are being formed
(4) Dense stroma is formed within the breast tissue
(5) Development of fibroadenoma

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100
Q

What is the clinical picture of fibroadenoma?

A

Breast lump
+clinical history-(1)mobile
(2)firm
+natural history-size;(1)10% increase in size
(2)30% gets smaller over 2 years
(3)the remainder stay the same
(4)in pregnancy and lactation they increase in size and sequester milk
-no risk of malignancy

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101
Q

What is the single most common clinical feature of fibroadenoma?

A

Breast lump

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102
Q

What is the clinical history of breast lump in fibroadenoma?

A

(1) mobile
(2) firm

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103
Q

What is the natural history of breast lump in fibroadenoma?

A
  • size;(1)10% increase in size
    (2) 30% gets smaller over 2 years
    (3) the remainder stay the same
    (4) in pregnancy and lactation they increase in size and sequester milk
  • no risk of malignancy
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104
Q

What is the incidence of fibroadenoma increasing in size?

A

10%

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105
Q

What is the incidence of fibroadenoma getting smaller and in what duration?

A

30% over 2 years

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106
Q

What happens to fibroadenoma in pregnancy and lactation?

A

They increase in size and sequester milk

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107
Q

What is the risk of malignancy in fibroadenoma?

A

No risk of malignancy

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108
Q

What is the treatment of fibroadenoma?

A

(1) Circumareolar incision-especially if the patient wishes
(2) Mammotome-for smaller incision

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109
Q

Enumerate causes of hyperthyroidism

A

(1) Graves disease(difuse toxic goitre)
(2) Toxic nodular goitre
(3) Toxic nodule
(4) Rare causes

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110
Q

Discuss Graves’ disease

A

.Features

(1) Diffuse vascular goitre
(2) Appears at the same time as the clinical manifestations of hyperthyroidism

.Incidence
commoner in younger females

.Aetiology

(1) Autoimmune disorder(50%)
(2) Glandular hypertrophy and hyperplasia occur as a result of the thyroid stimulating effect of TSH receptor antibodies(95%)

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111
Q

What are the features of the Graves’ disease?

A

(1) Diffuse vascular goitre
(2) Appears at the same time as the clinical manifestations of hyperthyroidism

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112
Q

What is the incidence of Graves’ disease?

A

Commoner in younger females

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113
Q

What is the aetiology of Graves’ disease?

A

(1)Autoimmune disorder(50%)

(2)Glandular hypertrophy and hyperplasia occur as a result of the thyroid stimulating effect of TSH receptor antibodies(95%)

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114
Q

What is the other name for Graves’ disease?

A

Diffuse toxic goitre

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115
Q

What is the incidence of autoimmune disorder in the aetiology of Graves’ disease?

A

50%

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116
Q

What is the chance of finding TSH receptor antibodies in Graves’ disease?

A

95%

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117
Q

Discuss toxic nodular goitre

A

(1) In this disorder the goitre is present for long time before clinical symptoms
(2) Inactive nodules-in most cases
(3) Internodular tissue-responsible for hyperthyroidism

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118
Q

Discuss toxic nodule

A

.Definition
Nodule-(1)overactive
(2)autonomously functioning

.Types

(1) as part of generalised nodularity
(2) true toxic adenoma

.Signs and symptoms mnemonic;
symptoms-LEH/WEP
signs-TAHET/L

.Diagnosis

(1) Plasma T3:(a)the most sensitive test for diagnosing hyperthyroidism
(b) which is raised
(2) TSH:(a)<0.5 U/L suggests hyperthyroidism
(b) TSH level is low as the autonomously functioning thyroid tissue exerts negative feedback
(c) TSH receptor antibodies tested for Graves’ disease(95%)
(d) TSH and T4 are sensitive tests for hypothyroidism

.Treatment

(1) Block and replaced regime-Advantages:(a)The 1st line medical treatment for Graves’ disease
(b) The favoured option
- Drugs:(a)Carbimazole-administered at higher doses
(b) Thyroxine-administered orally
- Duration:(a)6-12 months
(b) then wean off medication
(2) On relapse-(1)Ongoing medical therapy
(2) Radiation
(3) Surgery

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119
Q

Define toxic nodule

A

Nodule-(1)overactive
(2)autonomously functioning

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120
Q

What are the types of toxic nodule?

A

(1) as part of generalised nodularity
(2) true toxic adenoma

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121
Q

What are the symptoms and signs of Hyperthyroidism?

A

Signs and symptoms mnemonic;
symptoms-LEH/WEP
signs-TAHET/L

122
Q

Discuss diagnosis of toxic nodule

A

(1) Plasma T3:(a)the most sensitive test for diagnosing hyperthyroidism
(b) which is raised
(2) TSH:(a)<0.5 U/L suggests hyperthyroidism
(b) TSH level is low as the autonomously functioning thyroid tissue exerts negative feedback
(c) TSH receptor antibodies tested for Graves’ disease(95%)
(d) TSH and T4 are sensitive tests for hypothyroidism

123
Q

What is the significance of plasma T3 in diagnosis of thyroid disease?

A

(a) the most sensitive test for diagnosing hyperthyroidism
(b) which is raised

124
Q

What is the significance of TSH in thyroid disease?

A

(a) <0.5 U/L suggests hyperthyroidism
(b) TSH level is low as the autonomously functioning thyroid tissue exerts negative feedback
(c) TSH receptor antibodies tested for Graves’ disease(95%)
(d) TSH and T4 are sensitive tests for hypothyroidism

125
Q

What is the treatment of toxic nodule?

A

(1) Block and replaced regime-Advantages:(a)The 1st line medical treatment for Graves’ disease
(b) The favoured option
- Drugs:(a)Carbimazole-administered at higher doses
(b) Thyroxine-administered orally
- Duration:(a)6-12 months
(b) then wean off medication
(2) On relapse-(1)Ongoing medical therapy
(2) Radiation
(3) Surgery

126
Q

Discuss block and replacement regime in treatment of toxic nodule

A
  • Advantages:(a)The 1st line medical treatment for Graves’ disease
    (b) The favoured option
  • Drugs:(a)Carbimazole-administered at higher doses
    (b) Thyroxine-administered orally
  • Duration:(a)6-12 months
    (b) then wean off medication
127
Q

What are the advantages of block and replacement regime in treatment of toxic nodule?

A

(a) The 1st line medical treatment for Graves’ disease
(b) The favoured option

128
Q

What are the drugs used for treatment in toxic nodule as block and replacement regime?

A

(a) Carbimazole-administered at higher doses
(b) Thyroxine-administered orally

129
Q

What is the duration of the block and replacement regime in treatment of toxic nodule?
OR
What is what duration of treatment of toxic nodule?

A

(a) 6-12 months
(b) then wean off medication

130
Q

Discuss thyroid function test

131
Q

Interpret the following values

(1) low TSH
(2) high or normal free T4
(3) normal T3

A

Thyrotoxicosis(e.g.,Graves disease)

132
Q

What are the values of thyroid function test in thyrotoxicosis(e.g.,Graves disease)?

A

(1)low TSH
​(2) high or normal free T4
(3)normal T3

133
Q

Interpret the following values
(1)high TSH
​(2)low free T4

A

Primary hypothyroidism(primary atrophic hypothyroidism)

134
Q

What is the results of thyroid function test in primary hypothyroidism(primary atrophic hypothyroidism)?

A

(1)high TSH
​(2)low free T4

135
Q

Interpret the following values

(1) low TSH
(2) low free T4

A

Secondry hypothyroidism

136
Q

What should be done for secondary hypothyroidism?

A

Replacement steroid therapy is required prior to thyroxine

137
Q

Interpret the following values
(1)low or normal TSH
​(2) low free T4

A

Sick euthyroid syndrome

138
Q

Discuss sick euthyroid syndrome

A
  • referred to as non thyroidal illness
  • common in hospital inpatients
  • TFT:(1)low or normal TSH (2)low free T4
139
Q

What is the other name for sick euthyroid syndrome?

A

Non thyroidal illness

140
Q

What is the incidence of sick euthyroid syndrome?

A

Common in hospital inpatients

141
Q

What is the thyroid function test result in sick euthyroid syndrome?

A

(1)low or normal TSH
​(2)low free T4

142
Q

Interpret the following values
(1)high TSH
​(2) high or normal free T4

A

Poor compliance with thyroxine

143
Q

What is the thyroid function test in poor compliance with thyroxine?

A

(1)high TSH
​(2)normal or high free T4

144
Q

Interpret the following values

(1) low TSH
(2) normal free T4

A

Steroid therapy

145
Q

What is the thyroid function test in steroid therapy?

A

(1)low TSH
​(2)normal free T4

146
Q

What is the correlation of the thyroid peroxidase(microsomal)antibodies?

A

Autoimmune disease of thyroid,e.g:

(1) Hashimoto’s thyroiditis(100%)
(2) Graves disease(70%)

147
Q

What is the assay associated with Hashimoto’s thyroiditis?

A

Thyroid peroxidase(microsomal)antibodies

148
Q

What is the assay associated with Graves’ disease?

A

Thyroid peroxidase(microsomal)antibodies(70%)

149
Q

What is the incidence of correlation between Hashimoto’s thyroiditis and thyroid peroxidase(microsomal) antibodies?

150
Q

What is the incidence of correlation between Graves’ disease and thyroid peroxidase(microsomal) antibodies?

151
Q

What is the correlation of the TSH receptor antibodies?

A

Graves’ disease(95%)

152
Q

What is the correlation of the thyroglobulin?

A

(1) not useful in distinguishing between thyroid diseases
(2) used as part of thyroid cancer follow up

153
Q

What is the correlation of calcitonin in thyroid disease?

A

(1) released from parafollicular cells
(2) found in medullary carcinoma of the thyroid

154
Q

Treatment of large multi nodular goitre

A

Total thyroidectomy

(1) the treatment of choice for large multi nodular goitre
(2) for pressure symptoms

155
Q

Treatment of toxic nodule

A

Hemithyroidectomy

156
Q

Treatment of follicular lesion(THY 3f)

A

Hemithyroidectomy to establish diagnosis

157
Q

Treatment of papillary thyroid cancer

A

(1)Total thyroidectomy

(2)Central compartment nodal dissection(extended lymphadenectomy as required)

158
Q

Treatment of follicular thyroid cancer

A

Total thyroidectomy(usually completion as already had hemithyroidectomy)

159
Q

Treatment of anaplastic thyroid cancer

A

Palliative radiotherapy

160
Q

Treatment of medullary thyroid cancer

A

(1) Total thyroidectomy
(2) Screen for other MEN tumours

161
Q

Treatment of lymphoma of the thyroid

A

Core biopsy

162
Q

Treatment of persistent refilling cysts

A

(1) Injection sclerotherapy
(2) Surgery if this fails

163
Q

Treatment of Graves’ disease

A

(1) with eye signs-total thyroidectomy
(2) without eye signs-patient choice radioiodine vs surgery

164
Q

Treatment of Graves’ disease with significant eye signs

A

Total thyroidectomy

165
Q

Treatment of Graves’ disease without eye signs

A

Patient choice radioiodine vs surgery

166
Q

Indication of hemithyroidectomy

A

(1)Toxic nodule

(2)Follicular lesion(THY 3f)

167
Q

Indication of total thyroidectomy

A

Mnemonic;Lastly Papa Found Mama’s Graves

(1) Large multi nodular goitre
(2) Papillary thyroid cancer
(3) Follicular thyroid cancer
(4) Medullary thyroid cancer
(5) Graves disease with significant eye signs

168
Q

Discuss management of thyroid disease

169
Q

What are the general manifestations of thyroid disease?

A

(1) euthyroid(a symptomatic)
(2) clinical signs of thyroid dysfunction
(3) mass or not

170
Q

How to assess thyroid disease?

A

(1) History
(2) Examination including USS
(3) If nodule-image guided fine needle aspiration
(4) Radionucleotide scanning is of limited use

171
Q

What are the types of the thyroid tumours?

A

(1) Papillary carcinoma
(2) Follicular thyroid carcinoma
(3) Anaplastic thyroid carcinoma
(4) Medullary thyroid carcinoma
(5) Lymphomas

172
Q

Discuss multi nodular goitre

A

.Incidence
One of the most common reasons for presentation

.Manifestations

(1) Euthyroid and asymptomatic+no discrete nodules-reassurance
(2) Copressive symptoms-total thyroidectomy

173
Q

What is the incidence of multi nodular goitre?

A

One of the most common reasons for presentation

174
Q

What are the manifestations ,and their treatment,of the multi nodular goitre?

A

(1) Euthyroid and asymptomatic-reassurance
(2) Compressive symptoms-total thyroidectomy
(3) Subtotal thyroidectomy-results in recurrent disease that requires a difficult revisional resection

175
Q

Discuss endocrine dysfunction

A

I)managed by physicians initially
II)indications of surgery
(1)surgery offered alongside radioiodine
(2)for patients with Graves’ disease that fails with medical management
(3)for patients who prefer no radiation(e.g.,pregnant women)
III)Hypothyroidism
(1) not offered thyroidectomy
(2)if offered resection that would be during early phase of Hashimoto’s thyroiditis and with time toxic phase passes and
thyroxine can be given

176
Q

What are the complications following surgery in endocrine dysfunction?

A

(1) recurrent laryngeal nerve damage
(2) bleeding-due to CONFINED SPACE HAEMATOMA which may cause respiratory distress because of laryngeal oedema
(3) Hypocalcamia-due to damage to parathyroid gland

177
Q

What is the cause of bleeding in thyroid dysfunction surgery?

A

due to CONFINED SPACE HAEMATOMA which may cause respiratory distress because of laryngeal oedema

178
Q

What is the cause of respiratory distress in thyroidectomy?

A

Bleeding owing to the CONFINED SPACE HAEMATOMA’S may rapidly lead to respiratory compromise due to laryngeal oedema

179
Q

What is the cause of hypocalcaemia in thyroidectomy?

A

damage to the parathyroid glands

180
Q

What is the other name of subacute thyroiditis?

A

De Quervain’s thyroiditis

181
Q

Define subacute thyroiditis

A

thought to occur following viral infection and typically presents with hyperthyroidism

182
Q

What is the cause of subacute thyroiditis?

A

viral infection

183
Q

What are the features of subacute thyroiditis?

A

(1)Hyperthyroidism (2)Painful goitre (3)Raised ESR (4)Globally reduced uptake on iodine-131 scan

184
Q

What is the management of subacute thyroiditis?

A

Mnemonic;SAS

(1)Self limiting do not require treatment (2)Aspirin or other NSAID for thyroid pain (3)Steroids-in more severe cases esp.if hypothyroidism develops

185
Q

Define Hashimoto’s thyroiditis

A

an immunological disorder in which lymphocytes become sensitised to thyroidal antigens

186
Q

What are the three most important antibodies in Hashimoto’s thyroiditis?

A

(1)Thyroglobulin-early in Hashimoto’s,thyroglobulin antibody is markedly elevated and then declines (2)TPO (3)TSH-R

187
Q

What are the features of Hashimoto’s thyroiditis?

A

(1)Goitre and either euthyroid or mild hypothyroidism (2)Progressive hypothyroidism and associated symptoms

188
Q

What is the treatment of Hashimoto’s thyroiditis?

A

(1)B blockers-to manage symptoms during hyperthyroid phase of illness (2)Thyroxine-for hypothyroidism

189
Q

What is the single most common complication for Hashimoto’s thyroiditis?

A

Hypothyroidism

190
Q

What happens to the thyroglobulin in Hashimoto’s thyroiditis?

A

During the early phase of Hashimoto’s the thyroglobulin antibody is markedly elavted then declines

191
Q

Why we give B blockers in Hashimoto’s thyroiditis?

A

to manage symptoms during the hyperthyroid phase of illness

192
Q

Why we give thyroxine in Hashimoto’s thyroiditis?

A

For hypothyroidism

193
Q

Define insulinoma

A

Insulin producing tumours of the pancreatic B cells

194
Q

What is the incidence of insulinoma?

A

1/1000000/year

195
Q

What is the size of insulinoma?

196
Q

What is the incidence of benign lesions or tumours in insulinoma?

197
Q

What is the incidence of MEN type 1 in insulinoma?

198
Q

What is the incidence of pancreatic islet cell tumours in patients with MEN1?

199
Q

What are the typical features of insulinoma?

A

(1) Symptomatic hypoglycaemia during fasting
(2) Concomitant blood glucose < 3 mmol/L
(3) Relief of hypoglycaemia by use of glucose

200
Q

What are the investigations of insulinoma?

A

When neuroglycopenic symptoms occur blood is taken for:-

(1) serum insulin levels-plasma insulin concentration is > 10 micro U/ml in this disorder
(2) serum glucose
(3) C-peptide concentration
(4) pro-insulin concentration

201
Q

How insulinoma tumours are localised and what is the accuracy of each test?

A

(1) USS(25% accuracy)
(2) Endoscopic USS(75% accuracy)
(3) CT scanning(40% accuracy)
(4) Somatostatin receptor scintigraphy(50 % accuracy)
(5) MRI(100% accuracy) for larger malignant insulinomas

202
Q

What is the accuracy of USS in localisation of insulinoma tumours?

203
Q

What is the accuracy of endoscopic USS in localisation of insulinoma tumours?

204
Q

What is the accuracy of CT scanning(pancreatic protocol)in localisation of insulinoma tumours?

205
Q

What is the accuracy of somatostatin receptor scintigraphy in localisation of insulinoma tumours?

206
Q

What is the accuracy of MRI in localisation of insulinoma tumours?

207
Q

What is the treatment of insulinoma?

A

(1)Blind segmental resection of the pancreas(e.g.,Whipples)
-can not be justified since the majority of insulinoma tumours are benign(90%)
-acceptable for malignant tumours
(2)Laparotomy
-the best approach at laparotomy is to corroborate preoperative imaging with intraoperarive USS to identify the lesion
-tumours may be close to the pancreatic duct and this must be appreciated by the operating surgeon
(3)Octreotide
The perioperative use of octreotide reduces the amount of pancreatic drainage,but not overall complications

208
Q

Discuss the use of blind segmental resection of the pancreas(e.g.,Whipples)

A
  • can not be justified since the majority of insulinoma tumours are benign(90%)
  • acceptable for malignant tumours
209
Q

Discuss the use of laparotomy in the treatment of insulinoma

A
  • the best approach at laparotomy is to corroborate preoperative imaging with intraoperarive USS to identify the lesion
  • tumours may be close to the pancreatic duct and this must be appreciated by the operating surgeon
210
Q

Discuss the use of octreotide in the treatment of insulinoma?

A

The perioperative use of octreotide reduces the amount of pancreatic drainage,but not overall complications

211
Q

What is the origin of glucagonoma?

A

Alpha 2 cells of pancreas

212
Q

What is the cause of symptoms in glucagonoma?

A

Hormone overproduction

213
Q

What are the symptoms of glucagonoma?

A

(1) Diabetes
(2) Hypoaminoacidaemia
(3) Normochromic normocytic anaemia
(4) Necrolytic migratory erythema(NME)-the most characteristic clinical sign(as opposed to symptom)of this pathology

214
Q

What are the investigations of glucagonoma?

A

(1) Serum glucagon levels > 1000pg/ml is diagnostic
(2) CT chest/abdomen/pelvis
(3) Endoscopic USS
(4) Combined CT/MRI-accurately localise the lesion in 95% of cases

215
Q

What is the diagnostic test for glucagonoma?

A

(1) Serum glucagon levels > 1000pg/ml is diagnostic
(2) CT chest/abdomen/pelvis
(3) Endoscopic USS
(4) Combined CT/MRI-accurately localise the lesion in 95% of cases

216
Q

What is the diagnostic level of glucagon for diagnosis of glucagonoma?

A

>1000pg/ml

217
Q

How to localise glucagonoma?

A

Combined CT/MRI-accurately localise the lesion in 95% of cases

218
Q

What is the accuracy of combined CT/MRI in localising glucagonoma?

219
Q

What is the treatment of glucagonoma?

A

(I)Chemotherapy
-with:(1)Doxorubicin and 5FU
(2)Sunitinib-a biological agent
-for metastatic glucagonoma
(II)Resection
-for small tumours
-similar to the resections for adenocarcinoma

220
Q

Define somatostatinoma

A

Neuroendocrine tumours

221
Q

What is the incidence of somatostatinoma?

222
Q

What is the origin of the somatostatinoma?

A

Pancreas or the GIT

223
Q

What is the incidence somatostatinoma?

A

(1) Rare with an approximate incidence of 1/40 million
(2) Sporadic(over 90%)
(3) Most are malignant(85% of patients have metastasis)

224
Q

What is the general incidence of somatostatinoma?

A

Rare(1/40 million)

225
Q

What is the incidence of sporadic somatostatinoma?

226
Q

What is the incidence of malignant somatostatinoma?

A

Most are malignant and 85% of patients have metastasis

227
Q

What is the incidence of metastasis of somatostatinoma?

228
Q

What are the features of somatostatinoma?

A

(1) Excessive secretion of somatostatin hormone by tumour cells of D-cell origin
(2) Slow growing

230
Q

What is the clinical picture of somatostatinoma?

A

They are frequently associated with a classical clinical pentad:-

(1) D.M
(2) Cholelithiasis
(3) Weight loss
(4) Steatorrhoea
(5) Dirrhoea
(6) Hypochlorhydria and achlorhydria

231
Q

What is the clinical pentad of somatostatinoma?

A

They are frequently associated with a classical clinical pentad:-

(1) D.M
(2) Cholelithiasis
(3) Weight loss
(4) Steatorrhoea
(5) Dirrhoea
(6) Hypochlorhydria and achlorhydria

232
Q

What are the investigations to diagnose somatostatinoma?

A

(1)Serum somatostatin
(2)CT
(3)MRI
(4)Endoscopic USS
(4)Biopsy-as with all pancreatic malignancies,biopsy is not routinely performed unless the patient is not going to have
a definitive resection

233
Q

What biopsy is used for in somatostatinoma?

A

as with all pancreatic malignancies,biopsy is not routinely performed unless the patient is not going to have a definitive resection

234
Q

What is the treatment of somatostatinoma?

A

Chemotherapy with doxorubicin and 5FU as typically agents of choice

235
Q

What is the prognosis of somatostatinoma?

A

The tumours are,however,slow growing so reasonable 5 year survival figures are seen even when metastatic disease is present.
5 year survival rate in those resected without metastasis is 100%

236
Q

What is the figure of 5 year survival rate in somatostatinoma and what its condition?

A
  • Figure:100%
  • Condition:in those resected without metastasis
237
Q

What is the figure of 5 year survival rate in somatostatinoma?

238
Q

What is the condition for the figure(100%) of 5 year survival rate?

A

In those resected without metastasis

239
Q

Define gastrinoma?

A

Tumours of borderline biological behaviour but do progress over time

240
Q

What is the location of gastrinoma?

A

Typically located near the head of the pancreas

241
Q

What is the association of gastrinoma?

A

They are typically associated with Zollinger Ellison syndrome(think ulcers refractory to PPI=check gastrin levels)

242
Q

What is the treatment of gastrinoma?

A

Surgical excision

243
Q

What are the causes of primary hyperparathyroidism?

A

Mnemonic;SHMMCشمس

(1) Solitary adenoma(80%)
(2) Hyperplasia(15%)
(3) Multifocal disease(10-15%)
(4) Multiple adenoma(4%)
(5) Carcinoma(1% or less)

244
Q

What are the clinical features of primary hyperparathyoidism?

A

I)Elderly females-In exams primary hyperparathyroidism is stereotypically seen in elderly females with an:-
(1)unquenchable thirst
(2)inappropriately normal or raised parathyroid hormone level
II)Bones,stones,abdominal groans and psychic moans
(1)Bone pain/fracture
(2)Renal stones and renal colic
(3)Recurrent abdominal pain due to peptic ulceration/constipation/pancreatitis
(4)Depression and changes to emotional and cognitive state
(5)Polydepsia,polyuria
(6)Hypertension

245
Q

What are the conditions associated with primary hyperparathyroidism?

A

(1) Hypertension
(2) Multiple endocrine neoplasia;MEN I and MEN II

246
Q

What are the investigations of primary hyperparathyroidism?

A

(1) Calcium-raised
(2) PTH-may be raised or normal
(3) Urine calcium/Creatinine clearance ratio > 0.01
(4) Technetium-MIBI subtraction scan

247
Q

What is the level of calcium in primary hyperparathyroidism?

248
Q

What is the level of PTH in primary hyperparathyroidism?

249
Q

What is the level of Urine calcium/Creatinine clearance ratio in primary hyperparathyroidism?

250
Q

What is the type of MEN in primary hyperparathyroidism?

A

MEN I and II

251
Q

What is the treatment of primary hyperparathyroidism?

252
Q

What are the indications of surgery in primary hyperparathyroidism?

253
Q

What are the investigations of secondary(renal)hyperparathyroidism?

254
Q

What is the level of PTH in secondary(renal)hyperparathyroidism?

255
Q

What is the level of calcium in secondary(renal) hyperparathyroidism?

A

Low or normal

256
Q

What is the level of phosphate in secondary(renal) hyperparathyroidism?

257
Q

What is the level of vitamin D in secondary(renal) hyperparathyroidism?

258
Q

What is the other name for secondary hyperparathyroidism?

A

Renal hyperparathyroidism

259
Q

What is the cause of secondary(renal) hyperparathyroidism?

A

Parathyroid gland hyperplasia as a result of low calcium,almost always in a setting of chronic renal failure

260
Q

What are the clinical features of the secondary(renal)hyperparathyroidism?

A
  • May have few symptoms
  • Eventually may develop
    (1) bone disease
    (2) osteitis fibrosa cystica
    (3) soft tissue calcifications
261
Q

What is the treatment or management of secondary(renal)hyperparathyroidism?

262
Q

What are the indications of secondary(renal) hyperparathyroidism?

263
Q

What is the level of calcium that indicates surgery in primary hyperparathyroidism?

A

> 1mg/dl above normal

264
Q

What is the prerequisite of hypercalcaemia to have surgery done in primary hyperparathyroidism?

A

Episode of life threatening hypercalcaemia

265
Q

What is the level of urine calcium that make surgery necessarily done in primary hyperparathyroidism?

A

Hypercalciuria > 400 mg/day

266
Q

What is the level of creatinine clearance that make surgery necessarily done in primary hyperparathyroidism?

A

< 30% compared with normal

267
Q

What is the age that make surgery necessarily done in primary hyperparathyroidism?

A

< 50 years

268
Q

What is the level of bone mineral density that make surgery necessarily done in primary hyperparathyroidism and what are the sites?

269
Q

What is the T score that make surgery necessarily done in primary hyperparathyroidism?

A

Lower than -2.5

270
Q

What is the cause of tertiary hyperparathyroidism?

A

(1) Hyperplasia of parathyroid glands after correction of underlying renal disorder
(2) Hyperplasia of all 4 glands is usually the cause

271
Q

What is the clinical picture of tertiary hyperparathyroidism?

A

(1) Metastatic calcification
(2) Bone pain and or fracture
(3) Nephrolithiasis
(4) Pancreatitis

272
Q

What are the investigations of tertiary hyperparathyroidism?

A

(1) PTH-raised
(2) Calcium-high or normal
(3) Phosphate-low or normal
(4) Vitamin D-low or normal
(5) Alkaline phosphatase-raised

273
Q

What is the level of PTH in tertiary hyperparathyroidism?

274
Q

What is the level of calcium in tertiary hyperparathyroidism?

A

High or normal

275
Q

What is the level of phosphate in tertiary hyperparathyroidism?

A

Low or normal

276
Q

What is the level of vitamin D in tertiary hyperparathyroidism?

A

Low or normal

277
Q

What is the level of alkaline phosphatase in tertiary hyperparathyroidism?

278
Q

What are the indications of surgery in tertiary hyperparathyroidism?

A

.Principle
Allow 12 months to elapse following transplant as many cases will resolve

  • .*Indication
    (1) autonomously functioning parathyroid gland
    (2) if the culprit gland can be identified then it should be excised

.Method
Total parathyroidectomy and reimplantation of the gland

279
Q

Discuss benign familial hypocalciuric hypercalcaemia

A

.Definition
relativlely benign condition

.Incidence
rare

.Aetiology
autosomal dominant genetic disorder

  • *.Diagnosis(investigations)**
    (1) genetic testing
    (2) concordant biochemistry-urine calcium:creatinine clearance ratio < 0.01-distinguished from primary hyperparathyroidism
280
Q

Define benign familial hypocalciuric hypercalcaemia

A

relativlely benign condition

281
Q

What is the incidence of benign familial hypocalciuric hypercalcaemia?

282
Q

What is the cause of benign familial hypocalciuric hypercalcaemia?

A

Autosomal dominant genetic disorder

283
Q

What are the investigations(diagnosis)of benign familial hypocalciuric hypercalcaemia?

A

(1) genetic testing
(2) concordant biochemistry-urine calcium:creatinine clearance ratio < 0.01-distinguished from primary hyperparathyroidism

284
Q

How to distinguish between benign hypocalciuric hypercalcaemia and primary hyperparathyroidism?

A

urine calcium:creatinine clearance ratio < 0.01-distinguished from primary hyperparathyroidism

285
Q

What is the differential diagnosis of hyperparathyroidism?

A

Benign familial hypocalciuric hypercalcaemia

286
Q

Define phaeochromocytoma

A

Neuroendocrine tumour of the chromaffin cells of the adrenal medulla

287
Q

What is the rule of 10 in phaeochromocytoma?

A

(1) 10% of cases are bilateral,although most tumours are bilateral(often right sided)
(2) 10% occur in children
(3) 11% are malignant(higher when tumour is located outside the adrenal)
(4) 10% will not be hypertensive
(5) smaller than 10 cm

288
Q

What are the clinical features of phaeochromocytoma?

A

(1) Labile hypertension
(2) Hyperglycaemia
(3) Familial cases are usually linked to the multiple endocrine neoplasia syndromes(considered under its own heading)

289
Q

What is the diagnosis(investigations) of phaeochromocytoma?

A

(1) Urine analysis of vanillymandelic acid(VMA)-false +ve may occur e.g.,in patients eating vanilla ice cream
(2) Plasma metanephrine levels
(3) CT and MRI scanning to localise the lesion

290
Q

How to localise phaeochromocytoma?

A

CT and MRI scanning

291
Q

Discuss treatment of phaeochromocytoma

A

1st/medical treatment first
I)Alpha adrenoreceptor blocker:(1)Irreversible-should be given
(2)Reversible-minority may prefer it
II)Beta blocker:(1)e.g.,Labetalol-coadministered for cardiac chronotropic control
(2)Isolated beta blockade-should not be considered as it causes unapposed alpha activity
III)Moderate volumes of IV normal saline perioperatively-because patients are often volume depleted

2nd/Laparoscopic adrenalectomy
.Indication-once medically optimised
.Complications-(1)Catastrophic haemorrhage in the inexperienced hands-because adrenals are highly vascularised
-this is particularly true of the right sided resections
where IVC is perilously close
(2)IVC damage-repaired by laparotomy
-the defect is enclosed within a Satinsky style vascular clamp as using any other instrument
results in vascular trauma
-the defect is closed with prolene sutures

292
Q

Discuss medical treatment of phaeochromocytoma

A

I)Alpha adrenoreceptor blocker:(1)Irreversible-should be given
(2)Reversible-minority may prefer it
II)Beta blocker:(1)e.g.,Labetalol-coadministered for cardiac chronotropic control
(2)Isolated beta blockade-should not be considered as it causes unapposed alpha activity
III)Moderate volumes of IV normal saline perioperatively-because patients are often volume depleted

293
Q

Why we should not give patients with phaeochromocytoma beta blockers?

A

As it causes unopposed alpha activity

294
Q

Why we should give IV fluids to patients with phaeochromocytoma and what is the type of these fluids?

A

Moderate volumes of IV normal saline perioperatively-because patients are often volume depleted

295
Q

What is the surgical treatment of phaeochromocytoma?

A

Laparoscopic adrenalectomy
.Indication-once medically optimised
.Complications-(1)Catastrophic haemorrhage in the inexperienced hands-because adrenals are highly vascularised
-this is particularly true of the right sided resections
where IVC is perilously close
(2)IVC damage-repaired by laparotomy
-the defect is enclosed within a Satinsky style vascular clamp as using any other instrument
results in vascular trauma
-the defect is closed with prolene sutures

296
Q

What is the indication of laparoscopic adrenalectomy for the treatment of phaeochromocytoma?

A

once medically optimised

297
Q

What are the complications of laparoscopic adrenalectomy for the treatment of phaeochromocytoma?

A

(1)Catastrophic haemorrhage in the inexperienced hands-because adrenals are highly vascularised
-this is particularly true of the right sided resections
where IVC is perilously close
(2)IVC damage-repaired by laparotomy
-the defect is enclosed within a Satinsky style vascular clamp as using any other instrument results in vascular
trauma
-the defect is closed with prolene sutures

298
Q

What is the cause haemorrhage in laparoscopic adrenalectomy for the treatment of phaeochromocytoma?

A

(1) inexperienced hands
(2) highly vascularised adrenal glands

299
Q

What is the most common side for occurrence of complications of adrenalectomy and why?

A

Rt side where the IVC is perilously close

300
Q

How is the IVC damage is repaired during adrenalectomy?

A

IVC damage-repaired by laparotomy
-the defect is enclosed within a Satinsky style vascular clamp as using any other instrument results in vascular
trauma
-the defect is closed with prolene sutures

301
Q

Discuss incidental adrenal lesions(incidentaloma)

302
Q

Compare different types of hyperparathyroidism

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