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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
diabetic vascular disease tends to be more distal-true or false
true also multilevel more thigh claudication they have popliteal trifurcation
26
how does diabetes inhibit the immune system
polymorphonuclear leukocyte inhibition
27
does diabetic foot have multiple pathogens or single?
multiple-strep and staph is most dangerous
28
biggest risk factors for chronic venous disease
age pregnancy
29
other risk factors for chronic venous disease
Female sex * Familial * Obesity * Caucasian Race
30
are varicose veins palpable
yes
31
telanegctasia
intradermal, less than 1mm
32
deep blood vessels
below muscle fascia iliac, femoral, popliteal and tibial veins and branches
33
subcutaneous superficial blood vessels
long and short saphenous vein
34
perforators
connects superficial and deep venous systems direct and indirect(venous sinus in interrim)
35
3 layers in blood vessel
intima, media, adventitia veins have wider lumen, thinner media, one way valves
36
which veins do not contain valves
central ones: common iliac vein IVC Portal Cerebral
37
how is venous blood flow mediated
muscle pump mechanism (calves)
38
Chronic Venous Disease 3 pathophysiology mechanisms
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
outcome of mechanisms of CVD
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
how does CVD present
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
when are symptoms worst for varicose veins
worse at end of day improved by elevation and GCS (compression stockings) examine standing and sitting
42
examination of varicose veins
standing sitting distribution (greater saph vein, pelvic etc) ankle mobility (can calf muscle pump work)
43
preferred bedside exam of varicose veins
doppler handheld
44
acute complications of varicose veins
varicosity related thrombophlebitis (thrombosis and subsequent inflam)-analgesia, Ibuprofen extensive-anticoag bleeding-pressure and elevation
45
chronic complications of varicose veins
venous HPT related skin: dermatitis, hyperpig lipodermatosclerosis (wine glass), atrophic blanche skin ulceration, medial aspect
46
how to classify CVD
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
most common CEAP
C2S EP (primary) AS (superficial) PR
48
investigations for CVD
1. Duplex U/S looks at anatomy, physiology, causes 2. CT venogram pelvic and abdo veins contrast and radiation drawbacks
49
treatment indications for CVD
symptomatic complications cosmetic (private)
50
treatment for CVD
1. Obstrcution-remove obstructing object 2. Reflux-destroy/remove vein, replace or repair valves (deep vein) 3. Improve musc pump-physio
51
dominant pathology that causes CVD
reflux therefore destroying or removing reflux vein is most common intervention
52
treatment for CVD 5 types
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
contraindication to compression
mod to severe PAD
54
uses of compressive therapy
improves symptoms confirms venous pathology prevents progression prevents complications ulcer-multilayer compressive dressings
55
compressive stockings class ii
25-30mmHg at ankle
56
what causes phlegmasia
extensive proximal DVT acute complication DVT
57
phlegmasia alba dolens
white-decreased arterial inflow but some patent venous outflow
58
phlegmasia cerulea dolens
blue leg deep cyanosis sup and deep systems
59
primary upper limb DVT
thoracic outlet syndrome extrinsic comp of axillary vein EFFORT THROMBOSIS younger, active patients needs catheter directed thrombolysis and decomp (remove 1st cerv rib)
60
secondary upper limb DVT
CVC surgery cancer trauma older patients PEs
61
central vein filters
PE prevention Lower limb: IVC Upper limb: SVC if anticoag contraindicated or ineffective
62
gold standard for PE investigation
CT Pulm Angiography
63
high risk dying from PE
BP below 90mmHg systolic more than 15 min inotrope dependant
64
medium risk dying from PE
Cardiac injury RV dysfunction
65
management PE
Anticoag if not improving 1. thrombolysis (catheter, systemic) 2. endovascular 3. open
66

Surgery (14 decks)

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