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Surgery > random goodies > Flashcards

random goodies Flashcards

1
Q

how do you treat pseudo-obs of large bowel

A

stop ca channel blockers, anticholinergics and opiates

give neostigmine and colonoscopic decomp

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2
Q

what test should you NOT do when testing for LBO

A

Barium-messes with colonoscopy

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3
Q

how can you confirm LBO

A

Abdo X-ray

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4
Q

what does sigmoid volvulus look like on water soluble contrast enema

A

birds beak

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5
Q

right sided colonic obs Rx

A

simple

right hemicolectomy via midline lap
anastomosis

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6
Q

left sided colonic obs Rx

A

COMPLICATED-high risk anastomotic leak

3 options
1. three stage procedure
2. 2 stage procedure (colostomy and closure)
3. one stage

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7
Q

what is 1 stage

A

subtotal colectomy and ileorectal anastom, good in young patients with good sphincter tone

or

segmental colectomy with washout and primary repair A segmental colectomy

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8
Q

what is a 2 stage

A

resect obs lesion and create colostomy
then close colost.

ideal for sigmoid carcinoma

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9
Q

what is 3 stage

A

EMERGENCY MANAGEMENT because little skill required

proximal stoma created to decompress colon
obs lesion removed
stoma closed

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10
Q

alternative to surg repair

A

endoscopic stent placement (SEMS)

palliative decompression or want to recover properly then do elective

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11
Q

duration of antibiotics to treat pyogenic liver abscess

A

4-6 weeks or up to 12 weeks (multiple abscesses)

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12
Q

how to treat a pyogenic liver abscess

A

antibiotics PLUS perc drainage/catheter

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13
Q

which antibiotics are used to treat pyogenic LA

A

Ceft and Ampi

add Metronidazole if Amoebic LA is suspected

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14
Q

which organisms are involved in Pyogenic LA

A

E coli
Klebsiella
Bacteroides
Enterococcus
staph and strep from hep artery

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15
Q

first line investigation for Pyogenic LA

A

U/S then CT

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16
Q

predominant symptom in amoebic LA

A

PAIN
also get SOB and cough

chronically ill
intermittent fever

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17
Q

where is an amoebic LA usually located

A

right lobe, solitary

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18
Q

how to treat amoebic LA

A

usually metronidazole tds 800mg for 5 days is good enough

BUT

U/S guided aspiration and drainage is indicated:
1. 10cm plus
2. inadeq response to Rx
3. impending rupture into NB cavities
4. serology is negative

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19
Q

definitive host for E. granulosus

A

dog (intermediate is sheep, ingests ova from dog poo whilst grazing)

humans get it when they accidentally eat dog poo

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20
Q

how does a hydatid cyst present

A

asymp

or compression sx such as RUQ pain, enlarged liver, rupture-shock

coughing up grape skins

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21
Q

diabetic foot: features of neuropathy

A

motor-muscles weak, foot becomes deformed, pressure at weird places
autonomic-cracks, skin fissures
sensory- not aware of trauma to foot

motor-claw foot syndrome, fat creeps up, ulcer commonly at head of metatarsals or FLAT FOOT

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22
Q

what does motor neuropathy lead to

A

callus, forms at pressure points

charcot’s foot, arch of foot collapses, bone destruction, tibia and metatarsals drive pressure on mid arch of foot and ulcerates
bony deformity leads to chronic osteitis and sepsis
NOT AS COMMON AS CLAW FOOT

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23
Q

what does autonomic neuropathy lead to

A

skin fissures-allows bacteria to enter
AV shunting-leads to relative ischaemia

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24
Q

what is most common cause of diabetic foot

A

COMBO of neuro, vascular and infection predisposition

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25
Q

diabetic vascular disease tends to be more distal-true or false

A

true

also multilevel
more thigh claudication

they have popliteal trifurcation

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26
Q

how does diabetes inhibit the immune system

A

polymorphonuclear leukocyte inhibition

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27
Q

does diabetic foot have multiple pathogens or single?

A

multiple-strep and staph is most dangerous

28
Q

biggest risk factors for chronic venous disease

A

age
pregnancy

29
Q

other risk factors for chronic venous disease

A

Female sex
* Familial
* Obesity
* Caucasian Race

30
Q

are varicose veins palpable

A

yes

31
Q

telanegctasia

A

intradermal, less than 1mm

32
Q

deep blood vessels

A

below muscle fascia

iliac, femoral, popliteal and tibial veins and branches

33
Q

subcutaneous superficial blood vessels

A

long and short saphenous vein

34
Q

perforators

A

connects superficial and deep venous systems
direct and indirect(venous sinus in interrim)

35
Q

3 layers in blood vessel

A

intima, media, adventitia

veins have wider lumen, thinner media, one way valves

36
Q

which veins do not contain valves

A

central ones:
common iliac vein
IVC
Portal
Cerebral

37
Q

how is venous blood flow mediated

A

muscle pump mechanism (calves)

38
Q

Chronic Venous Disease 3 pathophysiology mechanisms

A
  1. Obstructed flow
    Intrinsic: DVT
    Extrinsic: Pregnancy
  2. Refluxing valves
    Absent valves (cong atresia)
    1 valvular incomp
    2 valvular incomp (previous DVT damage)
  3. Dysfunctional muscle pump
    neuro (spinal injury)
    muscular and joint (arthritis)
39
Q

outcome of mechanisms of CVD

A

venous insuff (entire system isnt working)
venous HPT (column of blood, increase pressure)
dilation-varicose veins
venous complications

sometimes step goes straight from venous HPT to venous complications (post-thrombotic)

40
Q

how does CVD present

A

ASYMP

or discomfort (pain, aching, throbbing, itchy, heaviness, cramping, restlessness)

cosmetic

swelling-oedema Grade 1 (below ankle), Grade 2 (above ankle), Grade 3 (above knee)

41
Q

when are symptoms worst for varicose veins

A

worse at end of day

improved by elevation and GCS (compression stockings)

examine standing and sitting

42
Q

examination of varicose veins

A

standing
sitting

distribution (greater saph vein, pelvic etc)

ankle mobility (can calf muscle pump work)

43
Q

preferred bedside exam of varicose veins

A

doppler handheld

44
Q

acute complications of varicose veins

A

varicosity related

thrombophlebitis (thrombosis and subsequent inflam)-analgesia, Ibuprofen
extensive-anticoag

bleeding-pressure and elevation

45
Q

chronic complications of varicose veins

A

venous HPT related

skin: dermatitis, hyperpig
lipodermatosclerosis (wine glass), atrophic blanche

skin ulceration, medial aspect

46
Q

how to classify CVD

A

aetiology

primary venous insuff: weak vein walls, dilated walls etc (no underlying cause)

secondary: DVT but LESS COMMON, no varicose veins, just damage inside lumen

otherwise

CEAP classification
C: clinical (4,5,6-venous insuff)
E: Etiology (cong, primary, secondary, not known)
A: Anatomy (sup, deep, perforators, not known)
P: pathophysiology (reflux, obstruction, reflux and obs, not known)

47
Q

most common CEAP

A

C2S
EP (primary)
AS (superficial)
PR

48
Q

investigations for CVD

A
  1. Duplex U/S
    looks at anatomy, physiology, causes
  2. CT venogram
    pelvic and abdo veins
    contrast and radiation drawbacks
49
Q

treatment indications for CVD

A

symptomatic

complications

cosmetic (private)

50
Q

treatment for CVD

A
  1. Obstrcution-remove obstructing object
  2. Reflux-destroy/remove vein, replace or repair valves (deep vein)
  3. Improve musc pump-physio
51
Q

dominant pathology that causes CVD

A

reflux

therefore

destroying or removing reflux vein is most common intervention

52
Q

treatment for CVD
5 types

A
  1. compression-mainstay if symp
  2. sclerotherapy-reticular, spider and perf veins
  3. transdermal laser therapy-cosmetic, retic and telangectasia
  4. endovenous ablation-cannula, stim thromb and fibrosis, stop reflux (kill blood vessel), thermal or non-thermal
  5. open surgery-minimise reflux, complications are DVT and nerve injurt
53
Q

contraindication to compression

A

mod to severe PAD

54
Q

uses of compressive therapy

A

improves symptoms
confirms venous pathology
prevents progression
prevents complications

ulcer-multilayer compressive dressings

55
Q

compressive stockings class ii

A

25-30mmHg at ankle

56
Q

what causes phlegmasia

A

extensive proximal DVT

acute complication DVT

57
Q

phlegmasia alba dolens

A

white-decreased arterial inflow but some patent venous outflow

58
Q

phlegmasia cerulea dolens

A

blue leg
deep cyanosis
sup and deep systems

59
Q

primary upper limb DVT

A

thoracic outlet syndrome

extrinsic comp of axillary vein

EFFORT THROMBOSIS

younger, active patients

needs catheter directed thrombolysis and decomp (remove 1st cerv rib)

60
Q

secondary upper limb DVT

A

CVC
surgery
cancer
trauma

older patients
PEs

61
Q

central vein filters

A

PE prevention

Lower limb: IVC
Upper limb: SVC

if anticoag contraindicated or ineffective

62
Q

gold standard for PE investigation

A

CT Pulm Angiography

63
Q

high risk dying from PE

A

BP below 90mmHg systolic more than 15 min
inotrope dependant

64
Q

medium risk dying from PE

A

Cardiac injury
RV dysfunction

65
Q

management PE

A

Anticoag

if not improving
1. thrombolysis (catheter, systemic)
2. endovascular
3. open

66
Q
A

Surgery (14 decks)

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