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MED 5 > Surgery/AH2 > Flashcards

Surgery/AH2 Flashcards

1
Q

AAA-definition

A

Abdominal aortic aneurysm (AAA) is a focal dilatation of the abdominal aorta to more than 1.5 times its normal diameter.

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2
Q

State some risk factors for AAA-major ones are

A 
Advanced age
Smoking (most important risk factor) 
Atherosclerosis
Hypercholesterolemia and arterial hypertension
Positive family history
Trauma
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3
Q

Best initial test to diagnose USS

A

abdominal ultrasound is the best initial and confirmatory test to diagnose AAAs and determine their extent.

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4
Q

Where is the most common location for AAA to occur at

A

Below the renal arteries- Infrarenal

Because there is less collagen in this area

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5
Q

Why do you get autonomic symptoms- sweating and feeling calmy after rupture of AAA

A

Since the celiac, sup., and inf. ganglia runs throughout the AA, a bulging aneurysm or a ruptured aneurysm causing a bleed into the peritoneal space (ant or post) will result in compression of said ganglia leading to sympathomimetic symptoms, like sweating, anxiety, anorexia, constipation.

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6
Q

Classic triad for ruptured AAA

A
  1. Hypotension/collapse
  2. Back/abdominal pain
  3. Palpable, pulsatile abdominal mass (caution
    in patients with raised BMI)
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7
Q

State some investigations you would want to order and the reason for it

A
  1. bloodwork: CBC, electrolytes, urea, creatinine, PTT, INR, type and cross
  2. abdominal U/S- screening and surveillance
  3. CT with contrast(accurate visualization, size determination, EVARplanning)
  4. peripheral arterial doppler/duplex (rule out aneurysms elsewhere, e.g. popliteal)
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8
Q

What is the medical management of AAA which is less than 5.5cm- 4 things

A

Smoking cessation (reduces rate of expansion and risk of rupture)
Improve blood pressure control
Commence statin and aspirin therapy
Weight loss and increased exercise

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9
Q

What are the indications for surgery in AAA-4 things

A
  1. Surgery should be considered for an AAA >5.5cm in diameter,
  2. AAA expanding at >1cm/year
  3. symptomatic AAA in a patient who is otherwise fit.
  4. Rupture
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10
Q

What are the mainstay treatment options for AAA repair

A

Open repair involves a midline laparotomy or long transverse incision, exposing the aorta, and clamping the aorta proximally and the iliac arteries distally, before the segment is then removed and replaced with a prosthetic graft

The endovascular repair involves introducing a graft via the femoral arteries and fixing the stent across the aneurysm –> EVAR(remember the complication is endoleaks)

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11
Q

The patient has a ruptured AAA, if the patient is stable vs unstable what do you do

A

If the patient is unstable, they will require immediate transfer to theatre for open surgical repair

If the patient is stable, they will require a CT angiogram to determine whether the aneurysm is suitable for endovascular repair*

However
Treatment: open emergency surgery (gold standard) or endoscopic treatment

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12
Q

What are some of the physical signs you may see in a pt. with a ruptured AAA which is contained

A 
Throbbing abdominal or low back pain radiating to the flank, buttocks, legs, or groin 
Grey turner sign (ecchymosis of the affected flank area)
Cullen sign (periumbilical ecchymosis)
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13
Q

Definition of a dissection

A

Dissections are a separation of the arterial wall layers caused by blood entering the intima-media space after a tear in the internal layer occurred.

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14
Q

What are the characteristic clinical features in an aortic dissection

A
  1. Sudden and severe tearing/ripping pain in the anterior chest, interscapular area, the neck, jaw or abdomen depending on the site of dissection
  2. Syncope
  3. Asymmetrical pulse and BP readings
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15
Q

What is the treatment for aortic dissection

A

A- needs help
B- conservative

Open or endovascular stent grafting repair (Stanford A dissections, which involve the ascending aorta, require immediate surgery)

Control hypertension (Stanford B dissections, which do not involve the ascending aorta, are generally treated conservatively)

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16
Q

STI and Aneurysm connection

A

Tertiary syphilis (due to obliterative endarteritis of the vasa vasorum)

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17
Q

CXR of an aortic dissection will show

A

widened mediastinum

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18
Q

What some causes of aortic dissection

A
  1. HTN
  2. Trauma
  3. Syphilis
  4. Connective tissue disease
  5. Use of amphetamines and cocaine
  6. Atherosclerosis
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19
Q

Location of aortic dissection, and its classification

A

Standford classification
Stanford A = Affects ascending aorta
Stanford B = Begins beyond brachiocephalic vessels.

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20
Q

6Ps of acute limb ischemia

A

6 Ps – all may not be present

Pain: absent in 20% of cases

Pallor: within a few hours becomes mottled cyanosis

Paresthesia: light touch lost first then sensory modalities

Paralysis/Power loss: most important, heralds impending gangrene

Polar/Poikilothermia/ Perishing cold’ Pulselessness: not re iable

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21
Q

What are the difference between embolus and thrombus causing acute limb ischemia

A

The embolus is an acute onset compared to the thrombus- which is chronic- hence there can be hx of claudication and thrombosis

examples of conditions that predispose to embolism are: arrhythmias, endocarditis, and arterial
aneurysms

existing atherosclerotic plaques (i.e. chronic PAD) can rupture causing thrombosis

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22
Q

Leriche syndrome (aortoiliac occlusive disease)-triad is

A

Pain in both legs and the buttocks
Bilaterally absent femoral, popliteal, and ankle pulses
Erectile dysfunction
Shock

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23
Q

What is the initial test for ALI and then diagnostic test,

what other tests can be done

A

Best initial test: arterial and venous Doppler
Diminished or absent Doppler flow signal distal to site of occlusion.

Confirmatory test: angiography (DSA, CTA, MRA)
Digital subtraction angiography (DSA) is the imaging modality of choice.
Should only be performed if delaying treatment for further imaging does not threaten the extremity

-can consider ECHO if embolic

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24
Q

Acute limb ischemia due to thromboembolism- treatment

  1. Leg is viable
  2. Emergency
  3. Leg is unviable
A

Acute limb ischaemia is a surgical emergency. Complete arterial occlusion will lead to irreversible tissue damage within 6 hours. Early senior surgical support is vital.

Start the patient on high-flow oxygen and ensure adequate IV access. A therapeutic dose heparin or preferably a bolus dose then heparin infusion should be initiated as soon as is practical.

Systemic anticoagulation with an IV heparin bolus followed by continuous infusion unless a contraindication is present

Viable, non-threatened limb
Urgent angiography to localize the site of the occlusion
Revascularization procedure (open or catheter-directed thrombectomy or thrombolysis) within 6–24 hours

Threatened limb: emergent revascularization procedure within 6 hours

Non-viable limb: limb amputation

Acute limb ischemia due to compartment syndrome: fasciotomy (see compartment syndrome)
Acute limb ischemia due to a dissecting aneurysm: stenting and/or surgical repair

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25
Q

Reperfusion injury (postischemic syndrome)-ALI

A

Following reperfusion, detached metabolites may trigger further complications, especially after prolonged occlusion (more than 6 h).

Possible complications
Acidosis, hyperkalemia → cardiac arrhythmia
Rhabdomyolysis → myoglobinemia → crush syndrome
Ischemia-reperfusion injury → compartment syndrome
Massive edema → hypovolemic shock
Severe complications: DIC (disseminated intravascular coagulation), multiorgan dysfunction

amputation–> if leg is not viable

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26
Q

Cold and pale limb leg

A

Acute limb ischemia

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27
Q

Hot and swollen leg

A

DVT

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28
Q

Chronic arterial insufficiency-what does that mean and characteristics features

A

chronic ischemia due to inadequate arterial supply to meet cellular metabolic demands(during walking (claudication) or at rest (limb threat/critical limb ischemia)

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29
Q

What must you if you suspect the patient has claudication

A

claudication:must differentiate vascular from neurogenic claudication or MSK

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30
Q

What is CLI

A

. includes rest pain, night pain, tissue loss (ulceration or gangrene)
. pain most commonly over the forefoot, waking person from sleep, and often relieved by hanging foot off bed

ABI <0.40

◆ pulses may be absent at some locations, bruits may be present

◆ signs of poor perfusion: hair loss, hypertrophic nails, atrophic muscle, ulcerations and infections,
slow capillary refill, prolonged pallor with elevation and rubor on dependency, venous troughing (collapse of superficial veins of foot)

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31
Q

What are the treatment options for CLI

A

1)Conservative

2) Pharmacology
- antiplatelet agents
- cilostazol

3) Surgical
- endovascular (angioplasty ± stenting)
- bypass endarterectomy
- amputation-if not suitable for revascularization, persistent serious infections/gangrene, unremitted rest pain poorly controlled with analgesics

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32
Q

Three main causes of acute limb ischemia

A

1) Emboli
2) Thrombus in-situ
3) Trauma

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33
Q

Should I do a lactate in ALI

A

Yes to assess for ischemia

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34
Q

Should I do lactate in ALI

A

Yes to assess for ischemia

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35
Q

What is the classification for CLI

A

Stage I Asymptomatic
Stage II Intermittent claudication
Stage III Ischaemic rest pain
Stage IV Ulceration or gangrene, or both

Fontaine classification of chronic leg ischaemia

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36
Q

What is Buerger’s test and angle

A

Buerger’s test involves lying the patient supine and raising their legs until they go pale and then lowering them until the colour returns (or even becoming hyperaemic). The angle at which limb goes pale is termed Buerger’s angle; an angle of less than 20 degrees indicates severe ischaemia.

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37
Q

What is the difference between chronic limb ischemia(peripheral vascular disease) and critical limb ischemia

A

Critical limb ischaemia is the advanced form of chronic limb ischaemia.

It can be clinically defined in three ways:

  1. Ischaemic rest pain for greater than 2 weeks duration, requiring opiate analgesia
  2. Presence of ischaemic lesions or gangrene objectively attributable to the arterial occlusive disease
  3. ABPI less than 0.5

On examination, the limbs may be pale and cold, with weak or absent pulses.

Other signs include limb hair loss, skin changes (atrophic skin, ulceration, or gangrene), and thickened nails.

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38
Q

What are two BIG ddx you need to exclude in chronic limb ischemia

A
  1. Spinal stenosis (‘neurogenic claudication’)
    Typically have pain from the back radiating down the lateral aspect of the leg (tensor fascia lata), often have symptoms on initial movement or symptoms that are relieved by sitting rather than standing
  2. Acute limb ischaemia
    Clinical features that are less than 14 days duration, often presenting within hours.
  3. Diabetic neuropathy is the other one- but patient needs to have T2DM
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39
Q

What assessment should be done is ALI and CLI patient

A

Cardiovascular risk assessment

-since it is basically like a heart attack of the leg

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40
Q

What is another name of peripheral vascular disease

A

chronic limb ischemia

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41
Q

What is the most important risk factor for PAD

A

smoking

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42
Q

In PAD, which artery gets most commonly blocked

A

The superficial femoral artery is commonly occluded (in the Hunters canal).

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43
Q

What are the 4 main characteristic features of chronic limb ischemia/peripheral vascular disease

A
  1. Intermittent claudication
  2. Absent or diminished pulses
  3. Trophic changes in the skin
  4. Rest pain- worse at night
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44
Q

Critical limb ischemia is indicated in PVD/Chronic limb ischemia when

A

Critical limb ischemia
The presence of any one of the following:
1.Resting pain
2.Ulcer
3.Tissue loss (gangrene)
Indicative of limb-threatening arterial occlusion

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45
Q

Fever, malaise, arthralgia
Syncope, angina pectoris
Impaired vision
15-40 Asian female

A

Takayasu’s disease

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46
Q

Migratory thrombophlebitis
Intermittent claudication, often limited to feet, calves and/or hands
Raynaud’s syndrome

A

Obliterating thromboangiitis

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47
Q

Moa of aspirin

A

Aspirin: irreversible cyclooxygenase inhibition → decreased thromboxane A2 synthesis → decreased platelet aggregation

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48
Q

MoA of clopidogrel

A

inhibition of the P2Y12 ADP receptor → decreased platelet activation and platelet-fibrin crosslinking

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49
Q

Venous ulcers

A
  • Irregular border and shallow
  • granulated base
  • venous insufficiency

Venous leg ulcers are the most common type of leg ulcer; they are prone to infection and can present with associated cellulitis

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50
Q

Ulcer is painful usually end of the day

A

Venous

Venous ulcers can be painful (particularly worse at the end of the day) and are often found in the gaiter region of the legs. Associated symptoms of chronic venous disease, such as aching, itching, or a bursting sensation, will be present often before venous leg ulcers appear.

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51
Q

What are the other associated features with venous ulcers

A 
varicose veins with ankle or leg oedema
varicose eczema
thrombophlebitis
haemosiderin skin staining
lipodermatosclerosis
 atrophie blanche.
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52
Q

Venous ulcer management

A

leg elevation and increased exercise
regular lifestyle changes

Antibiotics should only be prescribed with clinical evidence of a wound infection (most wounds are colonized, therefore swab results should only be acted upon if evidence of infection).

Multicomponent compression bandaging

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53
Q

What is the mainstay treatment for venous ulcers

A

Multicomponent compression bandaging

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54
Q

Features of arterial ulcers

A
  • small deep lesions
  • well-defined borders
  • necrotic base
  • painful
  • absent pulses
  • limbs will be cold

They most commonly occur distally at sites of trauma and in pressure areas (e.g the heel).

A patient with a suspected arterial ulcer is likely to give a preceding history of intermittent claudication (pain when they walk) or critical limb ischaemia (pain at night).

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55
Q

Where do you see arterial ulcers

A

Pressure loading points on the foot

  • toes
  • heel
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56
Q

Imaging for arterial ulcers

A

USS doppler

CT/MR angiography (CTA/MRA)

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57
Q

What are the 2 most common causes of neuropathic ulceration

A

Diabetes and vitamin b12 deficiencies

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58
Q

Features of neuropathic ulcers

A

neuropathic ulcers are variable in size and depth, with a “punched out appearance”

Painless

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59
Q

Remember a ddx for stroke is

A

Carotid artery disease

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60
Q

Varicose vein definition

A

Varicose veins are tortuous dilated segments of vein associated with valvular incompetence.

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61
Q

What is the main cause of varicose veins

A

Idiopathic(98%)

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62
Q

What are some risk factors for Varicose veins-4

A

Prolonged standing
Pregnancy
Obesity
Family Hx

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63
Q

Gold standard for varicose vein investigations is via

A

duplex ultrasound (best done by a trained technician)

assessing valve incompetence at the great/short saphenous veins and any perforators. Deep venous incompetence, occlusion (deep venous thrombosis) and stenosis must also be actively looked for.

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64
Q

What are the surgical indications for varicose veins

A

1) Symptomatic–>Worsening varicose veins may then cause pain, aching, swelling (often worse on standing or at the end of the day), or itching. Subsequent complications may include skin changes, ulceration, thrombophlebitis or bleeding.
2) Lower‑limb skin changes, such as pigmentation or eczema, thought to be caused by chronic venous insufficiency
3) Superficial vein thrombosis (characterised by the appearance of hard, painful veins) with suspected venous incompetence
4) A venous leg ulcer (a break in the skin below the knee that has not healed within 2 weeks)

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65
Q

What are the 3 surgical options for varicose veins

A

1) Vein ligation, stripping and avulsion
2) Foam sclerotherapy
3) Thermal ablation

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66
Q

In young woman, if secondary hypertension is suspected think of these 1st

A

1) Renal artery stenosis

2) Fibromuscular dysplasia

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67
Q

What is the blood supply to the GIT

A

coeliac trunk, superior mesenteric artery (SMA), and/or inferior mesenteric artery (IMA).

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68
Q

What are the watershed areas of the gut and what is the arterial supply present there

A

The splenic flexure and the rectosigmoid junction are at high risk for colonic ischemia because they are “watershed areas”.

The SMA and IMA anastomose via the marginal artery of the colon (artery of Drummond)

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69
Q

SMA supplies

A

supplies the distal duodenum, jejunum, ileum, and the right colon from the cecum to the splenic flexure

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70
Q

IMA supplies

A

supplies the left colon from the splenic flexure to the rectum

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71
Q

What is a classic presentation of a mesenteric ischemia patient

A

A classic case of ischemic colitis is a patient who presents with bloody diarrhea and severe abdominal pain after an abdominal aortic aneurysm repair!

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72
Q

What are the two conditions in the umbrella term of chronic venous disease

A
  1. Varicose veins

2. Chronic venous insufficiency:increased venous pressure resulting in alterations of the skin and veins

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73
Q

Venous ulcers are mostly found in the

A

Most frequently occur just above the ankle (gaiter region)

Shallow ulcer with irregular borders
Usually only mild pain, pruritic

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74
Q

What are causes

A

1) Hypercoagulability: increased platelet adhesion, increased clotting tendency (thrombophilia)
2) Endothelial damage: inflammatory, traumatic
3) Stasis (venous): varicosis, external pressure on the extremity, immobilization, local application of heat

To remember the three pathophysiological components of thrombus formation, think: “HE’S Virchow”: H-Hypercoagulability, E-Endothelial damage, S-Stasis.

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75
Q

What is Homan’s sign

A

Homan sign: calf pain on dorsal flexion of the foot

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76
Q

What are some of the criteria for Well’s score for DVT

-what is the cutoff for criterion

A

Active cancer
Previously documented DVT
Paralysis or recent (cast) immobilization of lower extremity
Recent bedridden or major surgery

clinical symptoms
Swelling of the entire leg
Calf swelling ≥ 3 cm compared to asymptomatic calf
Unilateral pitting edema in symptomatic leg

< 2: DVT unlikely (low risk)
≥ 2: DVT likely (high risk)

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77
Q

What is your ddx for DVT

A
  1. Muscle or soft tissue injury (i.e., posttraumatic swelling or hematoma)
  2. Lymphedema
  3. Venous insufficiency
  4. Ruptured popliteal cyst
  5. Cellulitis
  6. Compartment syndrome
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78
Q

Post-op AAA repair, what are you worried about in the abdomen

A

Acute mesenteric ischemia

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79
Q

Acute abdomen-R) shoulder or scapula

A

Biliary colic

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80
Q

Acute abdomen- to the groin

A

Renal colic

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81
Q

Acute abdomen- Periumbilical to right lower

quadrant (RLQ)

A

Appendicitis

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82
Q

What anatomical landmark differentiates upper GI bleeding vs lower GI bleeding

A

bleeding from a source proximal to the ligament of Treitz and bleeding from a source distal to the ligament of Treitz

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83
Q

What is the most common cause of UGIB

A

PUD

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5
Perfectly
84
Q

What is the most common cause of LGIB in an old person

A

Colon cancer

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85
Q

What should not be performed in LGIB

A

Barium enema

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86
Q

LGIB-what is the thing you are going to do

A

Initial management with colonoscopy to detect and potentially stop the source of bleeding

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87
Q

How do you differentiate the different types of jaundice biochemical

  • hepatocellular
  • cholestatic
  • haemolysis
A

Hepatocellular: Elevated bilirubin + elevated ALT/AST

Cholestatic Elevated bilirubin+elevated ALP/GGT ± duct dilatation upon biliary U/S

Hemolysis: decrease haptoglobin increased LDH

88
Q

What are the 5Ws of post-op fever

A

Wind POD#1-2 (pulmonary – atelectasis, pneumonia)
Water POD #3-5 (urine – UTI)
Wound POD #5-8 (wound infection - if earlier think streptococcal or clostridial infection)
Walk POD #8+ (thrombosis – DVT/PE)
Wonder drugs
POD #1+ (drug)

89
Q

7A’s of medications of surgery

A 
Analgesia
Anti-emetic
Anticoagulation
Antibiotics
Anxiolytics
Anticonstipation
All other patient meds(home meds, stress dose steroids, and β-blockers)
90
Q

What is the most common cause of post-op oliguria/anuria

-state some causes of it

A

pre-renal vs renal vs post-renal

Most common post-operative cause is prerenal ± ischemic ATN

external fluid loss: hemorrhage, dehydration, and diarrhea

internal fluid loss: third-spacing due to bowel obstruction, and pancreatitis

91
Q

The most common cause of post-op dyspnea

A

ATELECTASIS

92
Q

What is the treatment options for atelectasis in surgery

-pre and post

A

pre-operative prophylaxis
■ smoking cessation (best if >8 wk pre-operative)

• post-operative prophylaxis
■ incentive spirometry, deep breathing exercise, chest physiotherapy, and intermittent positive-
pressure breathing
■ minimize use of respiratory depressive drugs, appropriate pain control, and early ambulation

93
Q

New onset of “asthma” and wheezing in the elderly is___________ until proven otherwise

A

cardiogenic

-pulmonary edema

94
Q

Pulmonary edema-LMNOP

A 
Lasix
Morphine
Nitrates 
Oxygen
Position
95
Q

What are the common MI complications post-op

A

Common arrhythmias: supraventricular tachycardia, atrial fibrillation (secondary to fluid overload,PE, and MI)

96
Q

What are the 6S of SCC’s

A 
Smoking
Spirits (alcohol) 
Seeds (betel nut) 
Scalding (hot liquid) 
Strictures
Sack (diverticula)
97
Q

What are the CXR findings you will see with oesophageal rupture

A 
pneumothorax
pneumomediastinum
pleural effusion
subdiaphragmatic air
and 
widened mediastinum
98
Q

Barrett’s oesophagus usually precedes

-Barrett’s is a complication of ___

A

Adenocarcinoma

GERD

99
Q

What are the early and late stages of oesphgeal cancer

A

Early stages: Often asymptomatic but may present with swallowing difficulties or retrosternal discomfort

Late stages
Common
1. Progressive dysphagia (from solids to liquids) with possible odynophagia
2. Weight loss 
3. Retrosternal chest or back pain
4. Anemia

Less common

  1. Hematemesis, melena
  2. Hoarsenes
100
Q

Triad of Borehaave syndrome

A
  1. Vomiting and/or retching
  2. Severe retrosternal pain that often radiates to the back
  3. Subcutaneous or mediastinal emphysema → crepitus in the suprasternal notch or “crunching” or “crackling” sound on chest auscultation (Hamman’s sign), respectively
101
Q

What is the most common cause of esophageal perforation

A

Iatrogenic esophageal perforation: most common cause of esophageal perforation

102
Q

What is the number you should be concerned about in urine-ouput in surgical patients

A

If a patient has a urine output < 0.5 mL/kg/hour for > 6 hours: Check catheter patency.

103
Q

Post-op nausea and vomitting- state 2 causes which are procedure or treatment-related

A

Volatile general anesthetics including nitrous oxide

Perioperative opiate use

104
Q

PONV-<1 week after surgery, the cause is

A

< 1 week after surgery: self-limiting gastric or intestinal atony, or a more severe paralytic ileus

105
Q

PONV- > 1 week after surgery, the cause is

A

> 1 week after abdominal surgery: early mechanical bowel obstruction

106
Q

What are the 4 clinical features of paralytic ileus

A

Failure to pass flatus
Nausea and vomiting may be present.
Abdominal distention may be present.
Absence of bowel sounds on auscultation

107
Q

What are the main symptoms of bowel obstruction(5)

A 
nausea
vomiting
abdominal pain
 abdominal distention,
 constipation or obstipation.
108
Q

Bowel sounds are absent think

A

Paralytic ileus

109
Q

the high-pitched tinkling sound would be heard in the early phase of a

A

Mechanical sound obstruction

110
Q

What is third spacing

A

In medicine, the term is often used with regard to loss of fluid into interstitial spaces, such as with burns or edema, but it can also refer to fluid shifts into a body cavity (transcellular space), such as ascites and pleural effusions.

111
Q

In paralytic ileus, what do you see in CT/AXR- like how do you differentiate where the obstruction is

A

In paralytic ileus, findings include generalized dilatation of bowel loops with no transition point and air that is visible in the rectum.

112
Q

On MMG, what type of pattern is most common of breast cancer

A

spiculated/ star burst pattern

113
Q

Mammogram findings suspicious for

breast cancer:

A

Mass- especially spiculated (90% are maligant)
Distortion
Microcalcifications

114
Q

Concerning USS features for breast lump-5

A 
Taller than wide
Calcifications
Irregular
Invasion
Acoustic shadowing
Hypoechoic
Not compressible and not mobile
Feeding vessel or increased vascularity
115
Q

DCIS

A

Ductal carcinoma in situ (DCIS) is the presence of abnormal cells inside a milk duct in the breast. DCIS is considered the earliest form of breast cancer. DCIS is noninvasive, meaning it hasn’t spread out of the milk duct and has a low risk of becoming invasive

116
Q

What are some management options for breast cancer patients

A

1) Surgical (Breast)
◦ Breast-conserving surgery vs mastectomy
◦ Reconstruction (implant vs flaps)

2) Surgical (Axilla)
◦ Sentinel Lymph node biopsy
◦ Axillary clearance for proven involved LN

3)Radiation therapy
◦ Adjuvant or neoadjuvant

Chemotherapy
◦ Adjuvant or neoadjuvant

Hormone therapy for endocrine receptive tumours–> Herceptin for HER2 overexpression

117
Q

What are the surgical options for hernia repair

A
  • Surgical mesh repair (hernioplasty)
  • Surgical hernia repair (herniorrhaphy)

Open vs lap

118
Q

What are the different types of colorectal procedures

A

-right hemicolectomy
-left hemicolectomy
- sigmoid colectomy
- anterior resection(AR) – (for low sigmoid OR high rectal tumours)
- Abdominoperineal resection(APR) – (permanent colostomy & removal of rectum & anus)
- Hartman procedure – (surgical resection of rectal-sigmoid
colon with the closure of rectal stump & colostomy)

119
Q

small bowel is opened to the skin- what is the surgical procedure

A

ileostomy

120
Q

when the large bowels are opened to the skin-hat is the surgical procedure

A

colostomy

121
Q

What are the bowel sounds in bowel obstruction heard:

early and then late

A

High-pitched, tinkling bowel sounds (early)

Absent bowel sounds (late)

122
Q

Why is tympanic percussion seen in bowel obstruction

A

Due to gaseous distention of the bowel

123
Q

What is the conversation management of bowel obstruction

A

Fluid resuscitation, correction of electrolyte imbalance
Intestinal decompression: nasogastric tube insertion

Bowel rest (NPO)

Administration of IV analgesics and antiemetics

Gradual increase of oral intake, starting with clear fluids, can be initiated once the abdominal pain and distention subside and bowel sounds return to normal.

124
Q

Old patient, not popping, what is the cause of bowel obstruction

A

Fecal impaction, is a cause of LBO

125
Q

What are 4 indications for a surgical approach to bowel obstruction

A
  1. Suspected bowel obstruction and hemodynamic instability or features of sepsis
  2. Complete bowel obstruction with signs of ischemia/necrosis or clinical deterioration
  3. Persistent partial obstruction (> 3–5 days)
  4. Closed-loop obstruction
126
Q

The common causes of paralytic ileus can be memorized using “5 Ps”:

A

Peritonitis, Postoperative, low Potassium, Pelvic and spinal fractures, and Parturition

127
Q

What are the 2 main reasons for surgical indication any bowel obstruction-paralytic or mechanical

A

1) Sepsis

2) Haemodynamically instability

128
Q

What is the most common site of volvulus, and what is the second most common site

A

Sigmoid colon

Cecum

129
Q

What is the treatment for sigmoid volvulus

A

1)Initial resuscitation: IV fluids; acid-base and electrolyte imbalance correction; nil per oral; placement of a nasogastric tube

2) Evaluation
No signs of peritonitis: rigid/flexible sigmoidoscopic detorsion of the volvulus → inspection of the mucosa for signs of ischemia
No signs of mucosal ischemia → placement of a soft rectal tube (for bowel decompression) → semi-elective surgery within 72 hours of detorsion
Signs of mucosal ischemia → emergency surgery

Signs of peritonitis/unsuccessful endoscopic detorsion → broad-spectrum IV antibiotics and emergency surgery

3) Surgery
Sigmoid colectomy and primary anastomosis: indicated in hemodynamically stable patients with viable bowel
Hartmann’s procedure: indicated in hemodynamically unstable patients or those with ischemic/gangrenous bowel

130
Q

Why is Hartmann’s procedure done in some people

A

Hartmann’s procedure is faster to perform than sigmoid colectomy with anastomosis and is the preferred procedure in hemodynamically unstable patients. Primary anastomosis is avoided in patients with gangrenous bowel because of the high risk of anastomotic leak.

-basically if making an anastomosis is unsafe–> then you should do Hartmann

you can decide on rejoining them later

131
Q

Absent cough impulse indicates

A

An obstructed or strangulated hernia

132
Q

Congenital umbilical hernia, what is the treatment

A

Conservative: ∼ 90% will spontaneously close by 5 years of age(The likelihood of spontaneous closure decreases with increasing age and size of the umbilical hernia)

133
Q

What are some causes of anal abscess and then anal fistula(abscess become fistula over time)

A

Most common cause: flow obstruction and infection of the anal crypt glands (90% of cases)

Less common causes
Chronic inflammatory bowel disease (IBD): Crohn’s disease, ulcerative colitis (less commonly)
Acute infections of the gastrointestinal tract: e.g., complicated diverticulitis, acute appendicitis
Radiation-induced proctitis
Iatrogenic
Foreign body
Malignancy: e.g., colorectal cancer

134
Q

What are the treatment options for fistula(in general too)

A

Fistulotomy (standard approach)

Possible seton placement (enables adequate drainage and fibrosis)

Possible fibrin glue or fistula plug

135
Q

What is the treatment for anal abscess, what can you do post-op for anal abscess

A

Early surgical incision and drainage

Postoperative
Sitz baths
Analgesics and stool softeners

136
Q

bright red blood per rectum is called

A

(hematochezia)

137
Q

What is the treatment for anal fissures

A

NEED TO EXCLUDE IBD

Conservative
Dietary improvement (e.g., adequate ingestion of dietary fiber and water)
Stool softeners (e.g., docusate)
Anti‑inflammatory and analgesic creams and/or suppositories (e.g., 2% lidocaine jelly)
Sitz baths
Local anesthetic injection
Topical vasodilator therapy: calcium channel blocker gel (e.g., nifedipine) or glyceryl trinitrate ointment (GTN)

138
Q

What medication can be given for anal fissures

A

Topical vasodilator therapy: calcium channel blocker gel (e.g., nifedipine) or glyceryl trinitrate ointment (GTN)

139
Q

What are the features of rectal cancer(Which is a kind of CRC)

A 
Hematochezia
↓ Stool caliber (pencil-shaped stool)
Rectal pain
Tenesmus
Flatulence with involuntary stool loss
140
Q

Which modality of therapy is not used a treatment option for colorectal cancer

A

Radiation therapy is not a standard modality in the treatment of colon cancers!

141
Q

What are the surgical approaches for rectal cancer

A

Transanal excision–> Procedure: minimally invasive excision of small superficial tumours

Low anterior resection (LAR)

Abdominoperineal resection (APR)

142
Q

What is the 1st sign of Crohn’s Disease

A

Perianal fistulas and abscesses are often the first signs of Crohn disease!

143
Q

What is the treatment for CD- acute

  • minor
  • major
A

Acute minor–> Predsinolone PO ( for 12 to 16 weeks)

Acute severe–> Hydrocordisone IV (4-7 days and then switch to oral)

144
Q

What is the maintenance therapy for Crohn’s disease

A 
Azathioprine PO (immunosuppresant)
PLUS: Prophylactic heparin and anti-embolic stockings (due to the prothrombotic state of IBD flares).
145
Q

What is the criterion used for Ulcerative colitis to assess severity

A

Truelove and Witts’ severity index

YES eTG uses this criterion, thus Australia recognized!!

Example, Acute severe ulcerative colitis is defined (according to the Truelove and Witts criteria) by the presence of 6 or more bloody stools per day, plus at least one of the following:

temperature more than 37.8ºC
heart rate more than 90 beats/minute
haemoglobin less than 105 g/L
erythrocyte sedimentation rate more than 30 mm/hour.

146
Q

What are the 4 main intestinal symptoms of UC

A
  1. Bloody diarrhea with mucus
  2. Fecal urgency
  3. Abdominal pain and cramps
  4. Tenesmus
147
Q

If UC thinks(whats the other condition)

A

PSC

148
Q

Treatment for UC- acute

-mild-moderate

A

Oral Sulfasalazine + Mesalazine rectal

moderate to severe- Oral Azathioprine

149
Q

Treatment fo UC- a medical emergency

A 
IV Hydrocortisone(3 to 5 days) 
PLUS: Prophylactic heparin and anti-embolic stockings (due to the prothrombotic state of IBD flares).
150
Q

What is the maintenance therapy for UC

A

oral 5-aminosalicylates: Oral Sulfasalazine

151
Q 
Modified Hinchey classification of diverticulitis
I
II
III
IV
A

Stage Description
I Diverticulitis with a confined pericolic abscess
II Diverticulitis with distant abscess formation
III Perforated diverticulitis with generalized purulent peritonitis
IV Perforated diverticulitis, free communication with the peritoneum, generalized fecal peritonitis

152
Q

What investigation should not be performed in acute inflammation of diverticulitis

A

Not indicated during an acute episode → ↑ risk of perforation and exacerbating diverticulitis
Performed once the inflammation has subsided (after 6 weeks) to assess extent of diverticulitis and rule out malignancy

153
Q

What is the treatment for diverticula that is present

A

No treatment can reverse the growth of existing diverticula

154
Q

How do you guide your management of diverticulitis

A

eTG

Management depends on if complicated or un-complicated

Complicated (severe) diverticulitis refers to diverticulitis with a positive blood culture result, perforation, peritonitis, sepsis or septic shock, or an abscess larger than 5 cm in diameter. Diverticulitis without any of these features is considered uncomplicated—see Uncomplicated (nonsevere) diverticulitis

Uncomplicated Diverticulitis Management

No antibiotics required unless-

immune compromise
right-sided diverticulitis
failure to improve after 72 hours of conservative treatment (ie no antibiotic therapy)
Amoxicillin+clavulanate

Complicated Diverticulitis Management

Bowel rest, IV Anti-biotics, IV fluids and respective surgical management

Gentamicin + Metronidazole + Amoxicillin

6-8 weeks later- colonoscopy to rule out bowel cancer (no colonoscopy in the acute inflammatory stage as may lead to perforation)

155
Q

Pre-Operative Management mnemonic

A

RAPRIOP

Reassurance, Advice, Prescription, Referral, Investigations, Observations, Patient understanding and follow-up:

156
Q

Commonly stopped medications can be remembered as ‘CHOW’.

A

Clopidogrel – stopped 7 days prior to surgery due to bleeding risk. Aspirin and other anti-platelets can often be continued and minimal effect on surgical bleeding

Hypoglycaemics

Oral contraceptive pill (OCP) or Hormone Replacement Therapy (HRT) – stopped 4 weeks before surgery due to DVT risk. Advise the patient to use alternative means of contraception during this time period.

Warfarin – usually stopped 5 days prior to surgery due to bleeding risk and commenced on therapeutic dose low molecular weight heparin

Surgery will often only go ahead if the INR <1.5, so you may have to reverse the warfarinisation with PO Vitamin K if the INR remains high on the evening before

157
Q

Bowel prep required or not

-go through the different general surgery procedures

A

Upper GI, HPB, or small bowel surgery: none required

Right hemi-colectomy or extended right hemi-colectomy: none required

Left hemi-colectomy, sigmoid colectomy, or abdo-peroneal resection: Phosphate enema on the morning of surgery

Anterior resection: 2 sachets of picolax the day before or phosphate enema on the morning of surgery

158
Q

Is anorectal varices and haemorrhoids the same thing

A

NO

Hemorrhoids are not varicose veins (widening of the veins)! However, anorectal varices do exist and may occur, e.g., as a result of portal hypertension. The terms anorectal varices and hemorrhoids are often used interchangeably, but this is incorrect.

159
Q

What is the treatment for haemorrhoids and what does it depend on

A

Depends on the staging Grade I-II–> conservative management

Grade III-IV–> surgical management is warranted

160
Q

What is the procedure used for resection of cancer of the head of the pancreas

A

Whipple procedure

The most commonly used surgical technique is the pancreaticoduodenectomy (“Whipple procedure”).

161
Q

What is the treatment approach for cholangitis

A

supportive therapy, intravenous antibiotics → urgent biliary decompression → prevention of recurrence with interval cholecystectomy if there is concurrent cholelithiasis

ERCP–> therapeutic and diagnostic

ERCP is the treatment of choice, possibly in combination with Percutaneous transhepatic cholangiography (PTC) if ERCP is unsuccessful or unavailable(look if the bile ducts are consistent)

162
Q

Treatment of choice for Cholelithiasis

A

cholecystectomy

supportive therapy and dietary modifications → elective cholecystectomy only for symptomatic patients who are surgical candidates or asymptomatic patients at risk of gallbladder cancer

163
Q

Treatment of choice for choledocholithiasis

A

Endoscopic retrograde cholangiopancreatography (ERCP)

Both diagnostic and therapeutic

164
Q

Surgical approach for cholecystitis- the severity of symptoms

A

In mild cases: elective cholecystectomy within 24–72 hours

If complications are present (e.g., gangrene, perforation) or condition worsens despite conservative therapy → emergency cholecystectomy

In severe, high-risk cases: delayed elective cholecystectomy (> 2 weeks)

165
Q

On USS for cholecystitis, what will you see-4

A

Gallbladder wall thickening > 4 mm (postprandial > 5 mm)
Gallbladder wall edema (double wall sign)
Possible free fluid surrounding the gallbladder
Sonographic Murphy sign
Presence of concrement or gallstones

166
Q

Treatment of choice for cholecystitis

A

broad-spectrum antibiotics and supportive therapy → surgical management with cholecystectomy

167
Q

Fluid management- maintenance guidelines

A

Current NICE guidelines suggest the following:

Water: 25 mL/kg/day

Na+: 1.0 mmol/kg/day

K+: 1.0 mmol/kg/day

Glucose: 50g/day

168
Q

low K+, low Cl–, and alkalosis indicated

A

Diarrhea

169
Q

low K+ and acidosis

A

Vomiting

170
Q

What is the most common cause of hyperkalaemia

A

renal impairment or iatrogenic(so post-op surgery)

171
Q

Which two substances move insulin intracellular

A

1) Insulin

2) Salbutamol

172
Q

What are some ECG changes with hypokalaemia

A

1) Elongated PR interval
2) T wave flattening* or T wave inversion
3) Prominent U wave*
4) ST-segment depression

173
Q

Why should you not correct hypernatremia levels too quickly

A

Increase the risk of cerebral edema

174
Q

Most common post-op electrolyte imalance

A

Hyponatremia

175
Q

In individuals with a chronic hyponatraemia, rapid sodium correction can cause

A

Central pontine myelinolysis

176
Q

Anastomotic leak- clinical features

A

abdominal pain and fever.

They usually present between 5-7 days post-operatively. Other features* may include delirium or prolonged ileus.

177
Q

Twinkling bowel sounds

A

Mechanical bowel obs- SBO and LBO

178
Q

Absent bowel sounds

A

Functional bowel obs/paralytic ileus

179
Q

The mainstay treatment for paralytic ileus

A

The mainstay of management is NBM +/- NG tube, IV fluids, mobilisation, correct electrolyte abnormalities, and avoid bowel mobility reducing medication(pain medication)

180
Q

What is the common histological type of breast cancer, and which tissue does it arise

A

Most breast cancers are adenocarcinomas, arising from ductal tissue (80%) or lobular tissue (20%).

181
Q

What breast cancer is the most

A

Invasive ductal carcinoma

182
Q

What is Paget’s disease of the breast

A

a ductal carcinoma (usually adenocarcinoma- either in situ or invasive) that infiltrates the nipple and areola

183
Q

What are some clinical features of Paget’s disease of the breast

A

Erythematous, scaly, or vesicular rash affecting the nipple and areola

Pruritus, burning sensation, nipple retraction
The lesion eventually ulcerates → blood-tinged nipple discharge

184
Q

What ddx should be considered in Paget’s disease of the breast

A

Mamillary eczema

185
Q

Peau d’orange which cancer does it appear in

A

Inflammatory breast cancer

Erythematous and edematous (peau d’orange) skin plaques over a rapidly growing breast mass

186
Q

Inflammatory breast cancer-what is it?

A

It is a rare form of advanced, invasive carcinoma, characterized by dermal lymphatic invasion of tumor cells. Most commonly a ductal carcinoma.

187
Q

What is the most common benign condition in breast condition

A

Fibrocystic changes in the breast–> Premenstrual bilateral breast pain
Tender breast nodules

188
Q

Solitary, well-defined, non-tender, rubbery and mobile mass
Well-defined mass
Possibly popcorn-like calcifications
What do you think

A

Fibroadenoma

189
Q

Most common breast mass in women < 35 years

A

Fibroadenoma

190
Q

Bloody nipple discharge in breast condition

A

Intraductal papilloma

191
Q

Perimenopausal woman
Unilateral greenish or bloody discharge
Nipple inversion
Firm, stable, painful mass under the nipple

A

Mammary duct ectasia

192
Q

Premenstrual bilateral breast pain
Tender or non-tender breast nodules
Clear or slightly milky nipple discharge

A

Fibrocystic changes in the breast

193
Q

greenish discharge from the breast

A

Mamillary duct ectasia

194
Q

Phyllodes tumour- should we be concerned

A

Commonly benign, however, 25% can be malignant

Painless, smooth, multinodular lump in the breast
Variable growth rate: may grow slowly over many years, rapidly, or have a biphasic growth pattern
Average size 4–7 cm

195
Q

USS/Mammography

Focal mass or density with poorly defined margins
Spiculated margins
Clustered microcalcifications

Benign or malignant?

A

Malignant features :(

196
Q

A rapidly growing breast mass
Tenderness, burning sensation
Axillary lymphadenopathy
Blood-tinged

A

Inflammatory breast cancer

197
Q

Trastuzumab

A

Trastuzumab is a monoclonal antibody that inhibits tumor growth by binding to the epidermal growth factor HER2

198
Q

Triple-negative breast cancer

A

Estrogen receptor, progesterone receptor, and HER2 negative

All negative

199
Q

Paraneoplastic syndrome of breast cancer, what can you get

A

Paraneoplastic syndrome: hypercalcemia of malignancy

200
Q

What are the prognostic factors for breast cancer

A

1) Axillary lymph node status (most important prognostic factor)
2) Tumour size
3) Patient’s age
4) Receptor status (ER/PR-negative and triple-negative disease are associated with a worse prognosis)
- Histologic grade and subtype

201
Q

What are the common postoperative complications with a thyroidectomy-4

A

Postoperative complications include

  1. hematoma formation
  2. hypoparathyroidism
  3. nerve palsy (recurrent/superior laryngeal nerve)
  4. hypothyroidism.
202
Q

What are some things some the advice you can give a patient who is booked in for a thyroidectomy

-pre-op advice

A

Achieve euthyroid status preoperatively.

In hyperthyroidism to minimize the risk of thyroid storm
Thioamides
Iodides (potassium iodide)
Beta blockers (e.g., propranolol)

In hypothyroidism: thyroid hormone replacement

Preoperative oral calcium and vitamin D supplementation
Preoperative direct/indirect laryngoscopy

Just say this as well :)
The approach to surgery is very individualized. The conversation with your surgeon will include the type of operation, type of anesthesia, risks of the operation, expected length of hospitalization, and the follow up that will be necessary after your operation

203
Q

What is the most common post-op complication with thyroidectomy

A

Transient/permanent postoperative hypoparathyroidism (most common) or hypothyroidism

204
Q

Most common malignant thyroid nodule

A

Papillary carcinoma

205
Q

Which inguinal hernia are common

A

Indirect

206
Q

What is the cause of an indirect inguinal hernia

A

Congenital or acquired condition
Due to patent processus vaginalis-Outpouching of the parietal peritoneum that extends through the inguinal canal; normally obliterated by birth

207
Q

What is the main idea of surgical intervention in inguinal hernia repair

A

Main idea: reinforcement of the posterior wall of the inguinal canal with synthetic mesh or primary tissue approximation

208
Q

What are the complications of inguinal hernia surgery

A

1) Vas deferens injury
2) Spermatic vessels injury, dissection, or constriction, which may lead to testicular necrosis
3) Injury to femoral nerve, artery, or vein
4) Chronic inguinal pain
5) Bladder injury
6) General risks of surgery (see laparoscopic surgery and perioperative management)

209
Q

What is the difference between inguinal hernia and femoral hernias

A

In contrast to indirect inguinal hernias, which may occur congenitally, femoral hernias are almost always acquired.

210
Q

DDx for femoral hernia

A 
Direct or indirect inguinal hernias 
Femoral pseudohernia 
Lipoma
Lymph node enlargement
Femoral artery aneurysm 
Saphenous varix
Psoas abscess
211
Q

Treatment of femoral hernia

A

Non-complicated femoral hernia: early elective surgical repair with mesh hernioplasty (tension-free repair)

Complicated femoral hernia: herniorrhaphy (non-mesh repair)
All femoral hernias should be surgically repaired because of the high risk of complications.

212
Q

Should you reduce a strangulated femoral hernia

A

Strangulation: ischemic necrosis of contents within the hernia sac as blood flow is compromised due to incarceration
Warm, tender, and erythematous/discoloured swelling
Features of mechanical bowel obstruction

Reduction of a strangulated hernia should not be attempted because generalized peritonitis would occur following reduction of strangulated bowel loops!

A femoral hernia should be considered among 40–70-year-old women presenting with signs of mechanical bowel obstruction!

213
Q

In liver disease why does INR go up

A

INR increased due to malabsorption of Vit K

214
Q

PRESENTATIONS IN OBSTRUCTIVE JAUNDICE

A 
Pain- Probably Benign
Painless- Probably Malignant
Icterus/ Courvoisier
Cholangitis- Charcot
Dark urine and Pale Stools/ Floaters
Cachexia and weight loss
Abdominal distension
Pruritis
Depression
215
Q

Investigation of the jaundiced patient-
• Two tests central to differentiation

From these tests-what is pathognomic for obstructive jaundice

A
  1. Serum bilirubin, conjugated or not
  2. Ultrasound- Ducts dilated or not. May also suggest the diagnosis

• Thus conjugated hyperbilirubinaemia with dilated ducts, is pathognomonic of obstructive jaundice.

216
Q

Breast cancer comes back positive for these receptors

1) ER and Progesterone
2) HER-2

Which drugs can we give them
-which women gets what?

A

1) Tamoxifen or aromatase

SERM if premenopausal (e.g. tamoxifen) or aromatase inhibitors if postmenopausal (e.g.
anastrozole); optimal duration 5-10 yr

2) HER-2–> herceptin

217
Q

Why don’t you use tamoxifen in post-menopause woman

A

The side effect profile equal menopausal symptoms–> hence their menopausal symptoms get exacerbated

Endometrial cancer risk factors

MED 5 (23 decks)

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