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Year 3 > Vascular Surgery Block > Flashcards

Vascular Surgery Block Flashcards

1
Q

When is carotid endarterectomy indicated?

A
  • A moderate (50-79%) blockage of a carotid artery and are experiencing symptoms such as stroke, mini-stroke or TIA (transient ischemic attack).

OR

  • A severe (80% or more) blockage even if you have no symptoms.
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2
Q

What are the potential side effects of carotid endarterectomy?

A
  1. Stroke (2%)
  2. Death (1%)
  3. Pain/numbness around surgical site
  4. Wound infection (<1%)
  5. Nerve damage (hoarse voice, numbness/weakness on side of face - usually temporary. Affects 4%)
  6. Narrowing of carotid artery again (restenosis; 2-4%)
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3
Q

How does the brain receive blood during a carotid endarterectomy?

A

A shunt is a small plastic tube that diverts blood around the section of the carotid artery being operated on.

The decision to use a shunt is based on surgeon preference and the results of brain blood flow monitoring during the operation.

When the surgeon has accessed the carotid artery, they’ll clamp it to stop blood flowing through it and make an opening across the length of the narrowing. If a shunt is to be used, it will be inserted now.

The surgeon will then remove the inner lining of the narrowed section of artery, along with any fatty deposits (plaque) that have built up.

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4
Q

What is a pseudo-aneurysm (false aneurysm)?

A

Involve a collection of blood in the outer layer only (adventitia) which communicates with the lumen (i.e. after trauma)

Common in IV drug users and after angiography

Present with pain + pulsatile bleeding

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5
Q

What is amaurosis fugax?

A

Temporary loss of vision due to interruption of blood flow in the retinal artery or central retinal vein

Symptoms = curtain coming down vertically into field of view. Monocular blindness/fogging/blurring of vision. Typically lasts a few seconds but can last up to hours.

Investigations = Eye + neurological examination. Carotid ultrasound or magnetic resonance angiography. Blood tests for cholesterol and blood glucose.

Prognosis = doesn’t cause permanent visual damage. Indicates atherosclerosis and an increase risk of stroke.

Treatment = Diet changes + medication (aspirin, warfarin); surgery to remove damage. Quit smoking. BP, cholesterol, glucose checks.

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6
Q

What is lupus? What are the symptoms? How is it treated?

A

Lupus is an autoimmune disease that occurs when your body’s immune system attacks your own tissues/organs. Inflammation caused by lupus can affect many different body systems — including your joints, skin, kidneys, blood cells, brain, heart and lungs.

Symptoms include (having 4+ = lupus diagnosis):

  1. Butterfly-shaped rash
  2. Raised red patches on your skin
  3. You’re sensitive to light
  4. Ulcers in your mouth or nose
  5. Arthritis in two or more joints, plus swelling or tenderness
  6. Inflammation in the lining of your heart or lungs
  7. Seizures or other nerve problems
  8. Too much protein in your urine
  9. Low blood cell counts
  10. Certain antibodies in your blood
  11. Results from a blood test called an ANA test that suggest you may have too many “antinuclear” antibodies, which could be a sign of lupus

While there’s no cure for lupus, treatments can help control symptoms.

  • NSAIDs (ibuprofen, naproxen)
  • Corticosteroids (prednisolone)
  • Antimalarials (hydroxychloroquine, chloroquine phosphate)
  • BLyS-specific inhibitors (Belimumab)
  • Immunosuppressive agents/chemotherapy
  • Anticoagulants (warfarin, heparin)
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7
Q

What is an aneurysm?

A

An artery that is dilated > 50% of its original diameter. Can be fusiform (i.e. AAA) or sac-like (i.e. Berry aneurysm)

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8
Q

What are true aneurysms?

A

Abnormal dilatations that involve all layers of the arterial wall

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9
Q

What are common causes and sites of aneurysms?

A

Causes:

  • Trauma
  • Atheroma
  • Infection (mycotic aneurysm in endocarditis; tertiary syphilis especially thoracic aneurysms)
  • Connective tissue disorders (i.e. Marfan’s, Ehlers-Danlos)
  • Inflammatory (i.e Takayasu’s aortitis)

Common sites:

  • Aorta (infrarenal most common)
  • Iliac
  • Femoral
  • Popliteal
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10
Q

At what age are people screened for aneurysms?

A

Males over 65yrs

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11
Q

What are the signs and symptoms of AAA?

A
  • Intermittent/continuous abdominal pain (radiates to back, iliac fossa, or groin)
  • Collapse
  • Expansile abdominal mass (expands + contracts unlike swellings that are purely pulsatile)
  • Shock
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12
Q

What is the definition of an unruptured AAA?

A

> 3cm across caused by degeneration of elastic lamellae and smooth muscle loss. There’s a genetic component.

Often no symptoms

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13
Q

When is rupture of AAA more common and what are the options for its treatment?

A

More common if hypertensive, smoker, female, family history

  1. Elective surgery (reserve for aneurysms ≥ 5.5cm or expanding at > 1cm/yr or symptomatic)
  2. Stenting (EVAR - endovascular stent via femoral artery; reduced mortality but higher risk of graft rejection i.e. endoleak)
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14
Q

What is the emergency management of a ruptured AAA?

A

Mortality - treated = 41%; untreated = 100%

  1. Warn theatre!
  2. Do ECG, take blood for amylase, Hb, crossmatch. Catheterize bladder
  3. Gain IV access with 2 large-bore cannula. Treat shock with O Rh- blood but keep systolic BP ≤ 100mmmHg to avoid rupturing a contained leak
  4. Take patient straight to theatre
  5. Give prophylactic antibiotics (i.e. co-amoxiclav 625mg IV)
  6. Surgery involves clamping the aorta above the leak, and inserting a Dacron graft (i.e. tube graft)
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15
Q

What is a thoracic aorta dissection?

A

Blood splits the aortic media with a sudden tearing chest pain radiating to the back.

As dissection extends, branches of the aorta occlude sequentially leading to hemiplegia (carotid artery), unequal arm pulses + BP, or acute limb schema, paraplegia (anterior spinal artery), and anuria (renal arteries)

Type A (70%) involves the ascending aorta and Type B is no involvement of the ascending aorta

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16
Q

What is the management for aortic dissection?

A
  • Crossmatch 10u blood
  • ECG + chest xray
  • CT or transoesophageal echocardiography
  • Take to ITU
  • Hypotensives: keep systolic at 100-110mmHg: labetalol or esmolol
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17
Q

What hypotensives are used commonly for aortic dissection?

A

Labetolol

Esmolol

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18
Q

What are the 6P’s of acute ischemia?

A
  1. Pallor
  2. Pulseless
  3. Painful
  4. Paralysed
  5. Paraesthetic
  6. Poikilothermia (perishingly cold)
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19
Q

What is peripheral arterial disease?

A

Occurs due to atherosclerosis causing stenosis of arteries via a multifactorial process involving modifiable and non-modifiable risk factors.

65% have cerebral/coronary artery disease

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20
Q

What is the main feature of PAD?

A

Intermittent claudication (after walking “the claudication distance” and relieved by rest)

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21
Q

What are the cardinal features of critical ischemia?

A
  1. Ulceration
  2. Gangrene
  3. Foot pain at rest (i.e. burning pain at night relieved by hanging legs over side of bed)
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22
Q

What is Leriche’s syndrome and what are the symptoms to imply Leriche’s syndrome?

A

Narrowing of iliac arteries

Buttock claudication + impotence

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23
Q

What is the Fontaine classification for PAD (4)?

A
  1. Asymptomatic
  2. Intermittent claudication
  3. Ischemic rest pain
  4. Ulceration/gangrene (critical ischemia)
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24
Q

What are signs of PAD?

A
  1. Absent femoral, popliteal, or foot pulses
  2. Cold, white legs
  3. Atrophic skin
  4. Punched out ulcers (often painful)
  5. Postural/dependent colour change
  6. Buerger’s angle (angle that leg goes pale when raised off couch) < 20º and cap refill > 15s are found in severe ischemia
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25
Q

What tests are used to diagnose PAD?

A
  1. Exclude DM, arteritis (ESR/CRP)
  2. FBC (anemia, polycythemia)
  3. U+E (renal disease)
  4. Lipids (dyslipidemia)
  5. ECG (cardiac ischemia)
  6. Thrombophilia screen + serum homocysteine if < 50y
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26
Q

What imaging is used in PAD?

A
  1. Colour duplex US (first line)

2. MR/CT angiography (if considering intervention)

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27
Q

How can risk factors be modified in PAD?

A
  1. Quit smoking
  2. Treat hypertension + high cholesterol
  3. Prescribe an antiplatelet agent to prevent progression + reduce cardiovascular risk (Clopidogrel = first line)
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28
Q

What intervention options are available for PAD?

A
  1. Percutaneous transluminal angioplasty (PTA): used for disease limited to single arterial segment (a balloon is inflated in the narrowed segment)
  2. Surgical reconstruction: If atheromatous disease is extensive but distal run-off is good consider this with a bypass graft. Autologous vein grafts are superior to prosthetic grafts (i.e. Dacron)
  3. Amputation: < 3%. May relieve pain and death from sepsis/gangrene. Knee should be preserved where possible as it improves mobility and rehab potential.
  4. Future therapies: Gene therapy (i.e. hepatocyte growth factor) in critical limb ischemia. Still undergoing clinical trials.
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29
Q

What medication is usually prescribed to treat phantom limb pain?

A

Gabapentin

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30
Q

What can cause acute limb ischemia?

A

Surgical emergency requiring revascularisation within 4-6h to save the limb!

May be due to thrombosis in situ (~40%), emboli (38%), graft/angioplasty occlusion (15%), trauma.

Thrombosis more likely in vasculopaths. Emboli are sudden (i.e. in those without previous vessel disease + can affect multiple sites + there may be a bruit).

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31
Q

How is acute limb ischemia managed?

A

Urgent open surgery/angioplasty

If the occlusion is embolic: surgical embolectomy or local thrombolyses (i.e. tissue plasminogen activator) balancing the risks of surgery with the hemorrhagic complications of thrombosis

Anticoagulate with HEPARIN after either procedure + look for the source of emboli. Be aware of possible post-op repercussion injury + subsequent compartment syndrome

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32
Q

What are varicose veins?

A

Long, tortuous and dilated veins of the superficial venous system

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33
Q

What is the pathology of varicose veins?

A

Blood from superficial veins pass into deep veins via perforator veins and at the saphenofemoral + saphenopopliteal junctions. Valves prevent blood from passing from deep to superficial veins. If they become incompetent there’s venous hypertension and dilatation of the superficial veins occurs.

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34
Q

What are risk factors to developing varicose veins?

A
  1. Prolonged standing
  2. Obesity
  3. Pregnancy
  4. Family history
  5. Contraceptive pill
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35
Q

What are the causes of varicose veins?

A
  1. Primary mechanical factors (in 95%)
  2. Secondary to obstruction (i.e. DVT, fetus, pelvic tumour)
  3. Arteriovenous malformations
  4. Overactive muscle pumps (i.e. cyclists)
  5. Rarely congenital valve absence
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36
Q

What are the symptoms of varicose veins?

A
  • Pain
  • Cramps
  • Tingling
  • Heaviness
  • Restless legs
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37
Q

What are the signs of varicose veins?

A
  • Oedema
  • Eczema
  • Ulcers
  • Hemosiderin (iron-containing, golden-brown, granular pigment derived from ferritin, the initial iron-storage protein)
  • Hemorrhage
  • Phlebitis (inflammation of a vein)
  • White scarring at the site of a previous healed ulcer (atrophie blanche)
  • Lipodermatosclerosis (skin hardness from subcutaneous fibrosis caused by chronic inflammation + fat necrosis)
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38
Q

What are the treatment options for varicose veins?

A
  1. Radiofrequency ablation: a catheter is inserted into the vein + heated to 120C destroying the endothelium + closing the vein. Results are as good as conventional surgery at 3mo
  2. Endovenous laser ablation (EVLA): similar but uses lasers. Outcomes are similar to surgical repair after 2yrs.
  3. Injection sclerotherapy: Indicated for varicosities below the knee if no gross saphenofemoral incompetence. It is injected at multiple sites and the vein is compressed for a few weeks to avoid thrombosis.
  4. Surgery: i.e. saphenofemoral ligation (Trendelenburg procedure); multiple avulsions; stripping from groin to upper calf. Post-op bandage legs tightly and elevate for 24h. Surgery is more effective than sclerotherapy in the long-term.
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39
Q

What is saphena varix?

A

Dilatation in the saphenous vein at its confluence with the femoral vein. It transmits a cough impulse and may be mistaken for an inguinal or femoral hernia, but on closer inspection it may have a bluish tinge.

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40
Q

What is gangrene?

A

Gangrene is death of tissue from poor vascular supply + is a sign of critical ischemia. Tissues are black and may slough.

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41
Q

What is the difference between dry, wet, and gas gangrene?

A

Dry gangrene: Necrosis in the absence of infection. Note a demarcation between living + dead tissue.
Treatment = Restoration of blood supply +/- amputation

Wet gangrene: Tissue death with infection (associated with discharge).
Treatment = analgesia, broad-spectrum IV antibiotics, surgical debridement +/- amputation

Gas gangrene: Subset of necrotizing myositis caused by spore-forming clostridial species. Rapid onset of myonecrosis, muscle swelling, gas production, sepsis, and severe pain.
Risk factors = diabetes, trauma, malignancy
Treatment = remove all dead tissue (i.e. amputation). Give benzylpenicillin +/- clindamycin. Hyperbaric O2 can improve survival and decrease number of debridements

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42
Q

What is necrotizing fasciitis?

A

Rapidly progressive infection of the deep fascia causing necrosis of subcutaneous tissue

There is intense pain over affected skin and underlying muscle. Group A B-hemolytic streptococci is the major cause, although infection is often polymicrobial. Fournier’s gangrene is necrotizing fasciitis localized to the scrotum and perineum

Treatment = radical debridement +/- amputaition, IV antibiotics (benzylpenicillin, clindamycin)

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43
Q

What are skin ulcers?

A

Ulcers are abnormal breaks in an epithelial surface.

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44
Q

What are common causes of skin ulcers?

A
  1. Venous disease (70% of leg ulcers)
  2. Mixed arterial + venous disease (15%)
  3. Arterial disease (2%)

Other contributing factors:

  • Neuropathy (i.e. in DM)
  • Lymphoedema
  • Vasculitis
  • Malignancy
  • Infection (i.e. TB, syphilis)
  • Trauma (i.e. pressure sores)
  • Pyoderma gangrenosum
  • Drugs (nicorandil, hydroxyurea)
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45
Q

What are the features of skin ulceration to note on examination?

A
  1. Site
    - Above medial malleolus (‘gaiter’ area) is the favourite place for venous ulcers
    - Venous hypertension leads to development of superficial varicosities and skin changes (lipodermatosclerosis = induration, pigmentation, inflammation of the skin)
    - Minimal trauma to the leg leads to ulceration which often takes many months to heal
    - Ulcers on sacrum, greater trochanter, or heel suggest pressure sores particularly if patient is bed-bound with poor nutrition
  2. Temperature
    - Ulcer + surrounding tissue = cold if ischemic ulcer
    - Skin is warm + well refused = local factors are more likely
  3. Surface Area
    - Draw a map of the area to quantify + time any healing
    - A wound > 4wks old is a chronic ulcer
  4. Shape
    - Oval, circular (cigarette burns)
    - Serpiginous (Klebsiella granulomatis)
    - Unusual morphology can be 2º to mycobacterial infection
  5. Edge
    - Shelved/sloping = healing
    - Punched out = ischemic, syphilis
    - Rolled/everted = malignant
    - Undermined = TB
  6. Base
    - Any muscle, bone, tendon destruction = malignancy, pressure sores, ischemia
    - Grey-yellow slough beneath which is a pale pink base
  7. Depth
    - Probe can be used to gauge how deep the ulceration extends
  8. Discharge
    - Culture before starting antibiotics (which usually don’t work)
    - Watery discharge = TB
    - Bleeding = malignancy
  9. Sensation
    - Decreased sensation around ulcer = neuropathy
  10. Position in phases of extension/healing
    - Healing is heralded by granulation, scar formation, and epithelialization
    - Inflamed margins = extension
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46
Q

What is slough?

A

Mixture of fibrin, cell breakdown products, serous exudate, leucocytes, and bacteria.

Doesn’t imply infection and can be part of the normal wound healing process

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47
Q

What is granulation tissue?

A

Deep pink gel-like matrix contained within a fibrous collagen network + is evidence of a healing wound

48
Q

What are the layers of an arterial blood vessel?

A

From inside to outside:

  1. Tunica intima - endothelium that lines the lumen
  2. Tunica media - smooth muscle cells + elastic fibres
  3. Tunica adventitia - collagen fibres
49
Q

On vascular examination, what indicates venous disease?

A

Look at shape, discolouration, pigmentation, swelling, varicose veins, scars, oedema, varicose eczema ulceration

50
Q

If the presence of varicose veins is known, which test do you perform and how do you do it?

A

Trendelenburg Test

With the patient supine, elevate the limb as far as comfortably possible and empty the superficial veins by “milking” the limb.
Occlude the saphenofemoral junction by pressing 3.5cm below and lateral to the pubic tubercle. Vein lies medial to the artery.
Ask the patient to stand, maintaining pressure on the saphenofemoral junction.
Observe the leg, if the varicosities refill immediately there is a leaking perforating vein further down leg. If the pressure controls the engorgement this suggests incompetence at the saphenofemoral junction.
Release the pressure, if the veins fill rapidly this confirms that the saphenofemoral junction is incompetent.

51
Q

On vascular examination, what indicates arterial disease?

A

Look at colour, hair loss, atrophic shiny skin, ulceration on peripheral pressure points, infection, necrotic and missing toes

52
Q

Where is the mid-inguinal point?

A

Half way along a line drawn between the anterior superior iliac spine and the pubic symphysis in the midline

53
Q

What is the difference between the mid-inguinal point and mid-point of the inguinal ligament?

A

Mid-inguinal point – halfway between the pubic symphysis and the anterior superior iliac spine. This is the landmark for the femoral ARTERY.

Midpoint of the inguinal ligament – halfway between the pubic tubercle and the anterior superior iliac spine (the two attachments of the inguinal ligament). This is the landmark for the femoral NERVE.

54
Q

In the presence of peripheral arterial disease, what test should you perform? How do you perform it?

A

Buerger’s Test

First assess if any pain or restriction in hips. Stand at foot of bed. Gently elevate legs towards 90º, supporting the heels and keeping legs straight. As blood empties from the legs watch for pallor (and “guttering” of the superficial veins.) In a patient with normal blood vessels the feet will go pale at this angle of 90º. In the presence of diseased vessels pallor will occur before 90º (generally 50º indicates severe ischaemia and 25º indicates critical ischaemia). After a minute ask the patient to sit up and swing legs over side of bed. Observe feet. In presence of peripheral vascular disease the feet will slowly become engorged and purple, changing to a deep red. This occurs due to a reflex vasodilation when oxygenated blood becomes available to oxygen starved tissue. (Reactive hyperaemia.) The time necessary for the “gutters” to fill up is also an indication of severity of arterial insufficiency.

55
Q

What are possible investigations to perform following a vascular examination?

A

Investigations in peripheral artery disease:
Ankle to brachial pressure index

Blood tests:
Full blood count (FBC) and ESR
Urea and electrolytes
Blood glucose
Serology for connective tissue disease

Microbiology:
Swab base of any ulcers and culture

Radiology:
Doppler ultrasound

56
Q

Discuss the quality of foot/leg pulses?

A

Triphasic = healthy. The first “phase” is accounted for by the antegrade (forward) flow in systole. The second “phase” is due to a retrograde (backwards) flow occurring in early diastole. The final “phase” is antegrade flow in diastole.

Biphasic = early atherosclerosis. Loss of retrograde signal created in early diastole.

Monophasic = Severe vascular disease. Only antegrade systolic blood flow.

No pulses = acutely ischemic limb

57
Q

What is the purpose of a suction drain after surgery?

A

Used to remove blood, pus, or other fluid from a wound site

58
Q

What’s the difference between venous and arterial clots?

A

Arterial clots -> platelet derived

Venous clots -> fibrin derived

AF -> turbulent blood flow = fibrin-derived clot
Valvular -> buildup of plaque around valve = platelet-cause of stroke

**Sometimes you can get a paradoxic embolus from venous to arterial (i.e. with patent foramen ovale)

59
Q

What causes an amaurosis fugax?

A

A clot entering the ophthalmic artery (branch of the internal carotid artery)

60
Q

What is the most common side effect of a carotid endarterectomy?

A

Hypotension

Because the baroreceptor in the carotid body has been altered from the surgery. Will readjust slowly on its own. As a result, stop any ongoing hypertensive medications.

61
Q

What are the signs of infection?

A
  • Feelings of Malaise
  • Running a Fever
  • Fluid Drainage
  • Continual or Increased Pain
  • Redness and Swelling
  • Hot Incision Site
62
Q

What is ABPI and what level is abnormal?

A

Ankle Brachial Pressure Index. It is a ratio comparing the blood pressure in the arm and ankle.

The normal ratio is between 0.9-1.2

If less than 0.9 = arterial disease

If more than 1.2 = non-compressible blood vessels

Between 0.5-0.9 = intermittent claudication

63
Q

What are the most common causes of thrombophilia and hemophilia in the patient population?

A

Thrombophilia = smoking

Hemophilia = warfarin

64
Q

What is the Virchow’s triad?

A
  1. Hypercoagulability
  2. Hemodynamic changes (stasis, turbulence)
  3. Endothelial injury/dysfunction
65
Q

What are 13 risk factors for hypercoagulability?

A
  • Hyperviscosity
  • Coagulation factor V Leiden mutation
  • Coagulation factor II G2021A mutation
  • Deficiency of antithrombin III
  • Protein C or S deficiency
  • Nephrotic syndrome
  • Changes after severe trauma or burn,
  • Cancer
  • Late pregnancy and delivery
  • Race + old age
  • Cigarette smoking
  • Hormonal contraceptives
  • Obesity
66
Q

What are the acute and chronic causes of confusion?

A

Acute:

  • Delirium
  • Urinary retention
  • Constipation
  • Dehydration
  • Infections (urine, chest, biliary, SBP - hepatic encephalopathy)
  • Medication
  • Post-operative
  • Change in environment
  • Post-seizure

Chronic:

  • Cognitive impairment
  • Dementia (Vascular, Alzheimer’s, HIV, others)
67
Q

What investigations would you do with someone that is confused?

A
  • ABG (increased CO2 = CO2 narcosis, BM, Ammonia)
  • HIV-syphilis testing
  • Ceruloplasmin (if suspecting Wilson’s disease)
  • Alcohol level in blood (red cell tranketalase - if suspecting Wernicke’s)
  • Bladder scan + exam -> urinary retention
  • PR exam -> constipation
  • Standing/seated BP -> dehydration
  • Blood cultures -> infection

Confusion Screen:

  • CT head
  • Cortisol
  • B12
  • Folate
  • TFTs
  • Ca2+
68
Q

How do you detect anemia and the type from a blood test?

A

Low hemoglobin = anemia

MCV (size of cells) = determines whether its microcytic, normocytic, or microcytic

69
Q

What are the main causes for microcytic, macrocytic, and normocytic anemias?

A

Microcytic:

  • Thalassemia
  • Sickle cell anemia
  • Iron-deficiency

Normocytic:
- Anemia of chronic disease (kidney disease, cancer, RA, thyroiditis, heart failure, liver disease)

Macrocytic:

  • Folate deficiency
  • B12 deficiency
  • Alcohol dependence
  • Myelodysplastic syndrome
  • Hypothyroidism
  • Drugs
70
Q

What are the broad categories for causes of collapse?

A
  1. Cardiogenic (arrhythmia)
  2. Vasovagal
  3. Neurological (SOL, seizure)
  4. Mechanical (fall)
71
Q

What investigations would you do on someone with collapse as their presenting complaint?

A
  • Sitting/standing BP
  • Head CT
  • ECG (24/48/72h cardiac monitor)
  • Echo
  • EEG
  • Implantable loop recorder
72
Q

Why does aortic stenosis cause syncope?

A
  1. Calcification that causes the stenosis -> calcification at the Bundle of His -> Heart block -> collapse
  2. Outflow tract obstruction reducing the amount of blood that can perfuse tissues + brain
73
Q

What are 2 conditions diabetics can develop as a result of ANS neuropathy?

A
  1. Gastroparesis

2. Hypotension

74
Q

Why does postural hypotension occur?

A
  1. Blunted catecholamine response to standing (dopamine, norepinephrine, epinephrine)
  2. Failure of lower limb vascular resistance to increase adequately.
75
Q

What is the difference between fast and slow AF? Name 4 causes of slow AF

A

Commonly AF is associated with a ventricular rate ~ 110 – 160 = Fast AF

‘Slow’ AF = ventricular rate < 60 bpm.

Causes of ‘slow’ AF include:

  1. Hypothermia
  2. Digoxin toxicity
  3. Medications
  4. Sinus node dysfunction
76
Q

Name 13 causes of AF

A
  1. Ischemic heart disease
  2. Hypertension
  3. Valvular heart disease (mitral stenosis/regurg)
  4. Acute infections
  5. Electrolyte disturbance (hypokalemia, hypomagnesemia)
  6. Thyrotoxicosis
  7. Drugs (i.e. sympathomimetics)
  8. PE
  9. Pericardial disease
  10. Acid-base disturbance
  11. Pre-excitation syndromes
  12. Cardiomyopathies: dilated, hypertrophic
  13. Pheochromocytoma
77
Q

What is the sliding scale for insulin administration?

A

The term ‘sliding scale’ refers to the increasing administration of the pre-meal insulin dose based on the blood sugar level before the meal.

78
Q

How would you describe a testicular lump?

A

SPACESPIT

Size
Position
Attachment
Consistency
Edge
Surface + Shape
Pulsation
Thrills and Bruits 
Inflammation
Transillumination
79
Q

What is inflammation of the foreskin called? Inflammation of the glans? Both?

A

Posthitis = inflammation of foreskin

Balanitis = inflammation of glans

Balanoposthitis = inflammation of both

80
Q

What is phimosis and paraphimosis?

A

Inability to retract and bring forward the foreskin respectively

81
Q

What do small firm testes suggest?

A
  1. Hypogonadism

2. Testicular atrophy

82
Q

What is hydrocele and varicocele?

A

Hydrocele = fluid filled testicles

Varicocele = an enlargement of the veins within the loose bag of skin that holds your testicles (backlog of venous system) -> disappears when patient lies down.

83
Q

If a mass is attached to a testicle what are your differentials? If separate from testicle?

A

Attached to a testicle:

  • If solid (non-translucent) -> testicular tumour
  • If cystic (translucent) -> hydrocele

Not Attached to a testicle:

  • If solid (non-translucent) -> chronic epididymitis
  • If cystic (translucent) -> epididymal cyst
84
Q

What is the most common cause of epididymo-orchitis?

A

Swelling of the epididymis and testicle most commonly caused by:

  1. UTI
  2. STI

Cleared by a course of antibiotics

85
Q

Where are the superficial and deep inguinal rings located and what is their significance?

A

The deep (internal) ring is found above the midpoint of the inguinal ligament. which is lateral to the epigastric vessels. The ring is created by the transversalis fascia, which invaginates to form a covering of the contents of the inguinal canal.

The superficial (external) ring marks the end of the inguinal canal, and lies just superior to the pubic tubercle. It is a triangle shaped opening, formed by the evagination of the external oblique, which forms another covering of the inguinal canal contents. This opening contains intercrural fibres, which run perpendicular to the aponeurosis of the external oblique and prevent the ring from widening.

86
Q

What are the contents of the inguinal canal?

A
  1. Spermatic cord (biological males only) – contains neurovascular and reproductive structures that supply and drain the testes.
  2. Round ligament (biological females only) – originates from the uterine horn and travels through the inguinal canal to attach at the labia majora.
  3. Ilioinguinal nerve – contributes towards the sensory innervation of the genitalia
    Note: only travels through part of the inguinal canal, exiting via the superficial inguinal ring (it does not pass through the deep inguinal ring). This is the nerve most at risk of damage during an inguinal hernia repair.
  4. Genital branch of the genitofemoral nerve – supplies the cremaster muscle and anterior scrotal skin in males, and the skin of the mons pubis and labia majora in females.
87
Q

Which organs are retroperitoneal?

A
  • Kidneys

- Abdominal aorta

88
Q

Name 8 surgical incision sites and an example procedure for each

A
  1. Kocher’s incision/keyhole -> cholecystectomy
  2. Midline incision -> Ruptured AAA
  3. Gridion muscle splitting/Lanz incision -> appendectomy
  4. Battle incision -> Rectum
  5. Paramedian incision -> Small intestine
  6. Transverse -> Ruptured AAA, iliac vessels
  7. Rutherfold Morrison incision -> colostomy, colon resection
  8. Pfannestiel -> Cesarian
89
Q

What are the symptoms of varicose eczema?

A
  • Itchy and swollen skin
  • Dry and flaky skin
  • Scaly or crusty skin
  • Discolouration of the skin (leaching iron pigmenting skin - hemosiderin)
  • tender/tight skin can eventually become hardened (lipodermatosclerosis)
  • small, white scars (atrophie blanche)
  • pain
  • eczema affecting other parts of the body

If not treated varicose eczema -> non-healing leg ulcers

90
Q

What is the cause of varicose eczema?

A

Varicose eczema is usually caused by increased pressure in the leg veins.

When small valves in the veins stop working properly, it’s difficult for blood to be pushed upwards against gravity and it can leak backwards.

This increases the pressure in the veins, which can cause fluid to leak into the surrounding tissue (venous HTN). It’s thought that varicose eczema may develop as a result of the immune system reacting to this fluid.

Varicose eczema is more common in people with varicose veins, as these are also often a sign that the leg veins are not working properly.

91
Q

For how many days should you stop warfarin if there’s active bleeding with a metallic heart valve in situ?

A

Intracranial bleed: 7-14d

Extracranial bleed: 48-72h

92
Q

Which nerves are commonly affected by carotid endarterectomy?

A
  • 2 lowest branches of the facial nerve (mandibular + cervical)
  • Glossopharyngeal nerve (CN 9)
  • Hypoglossal nerve (CN 12)
  • Vagus (CN 10 - which runs in carotid sheath)
93
Q

Name 2 complications of carotid endarterectomy?

A
  1. Stroke

2. Bleeding/infection (from hematoma collection)

94
Q

Name 3 causes of delayed wound healing

A

VIB

Vascular
Idiopathic
Blood sugar (diabetes)

95
Q

Which 2 conditions must be met for someone to be considered for surgical intervention?

What should be recommended to the patients if these above conditions are not met?

A
  1. Tissue loss
  2. Rest pain for more than 2 weeks
SASS:
Stop smoking
Aspirin
Statin
Supervised activity
96
Q

Discuss the differences between venous, arterial, and diabetic ulcers

A

Venous:

  • Typically on medial leg (gaiter area) or below knee
  • Shallow ulcer
  • Poorly defined edges
  • Associated with varicose eczema (itchy, hardened, scaly skin)
  • Brown/black-stained skin
  • Swelling
  • Discharge

Arterial:

  • Smaller “punched-out” ulcers
  • Well-defined edges
  • Deep ulcers
  • Typically affect the extremities + between toes
  • Painful (especially at night)
  • Cold to touch
  • Red, yellow, black sores
  • Tight, hairless skin
  • Leg reddens when dangled + pale when elevated

Diabetic:

  • Over pressure points (i.e. under big toe, balls of feet, under heel)
  • May look arterial

Arterial ulcers tend occur the tips of toes, over phalangeal heads, around the lateral malleolus, on the middle portion of the tibia, and on areas subject to trauma. These ulcers are deep, pale, and often necrotic, with minimal granulation tissue. Surrounding skin commonly is pale, cool, thin, and hairless; toenails tend to be thick. Arterial ulcers tend to be dry with minimal drainage, and often are associated with significant pain. The patient usually has diminished or absent pulses.

Venous ulcers are located on the medial lower leg, medial malleolus, and superior to the medial malleolus. You rarely see them on the foot or above the knee. They have irregular wound margins and tend to be shallow and ruddy red, although slough may be present. Venous ulcers tend to have moderate to large drainage amounts. Although they don’t usually cause a lot of pain, patients may complain of “achy” legs. Surrounding skin is scaly and weepy, possibly with hemosiderin staining and edema. The patient usually has palpable pulses.

Diabetic foot ulcers arise on the plantar aspect of the foot, over metatarsal heads, and under the heel. They have even wound margins and often are deep ulcers with red or pale granular wound beds. Slough is common. Surrounding tissue is often a callus, and cellulitis is common. A low to moderate amount of drainage is present, and foot deformities are common. The patient typically has diminished or absent sensation in the foot. Due to vessel calcifications, we don’t rely on the ankle brachial index (ABI) for these patients. Instead, we use the toe brachial pressure index (TBPI).

Even though arterial, venous, and diabetic ulcers have specific characteristics, not all individual wounds follow the rules. We may see mixed ulcers types with components of both arterial and venous assessment findings. Diabetic foot ulcers may look arterial, especially when the toe is necrotic.

97
Q

Outline the WHO analgesia ladder

A
  1. Paracetamol (15mg/kg or 1g QDS)
    - COX3 inhibitor
    - Inhibits prostaglandin synthesis
  2. NSAIDs
    - Ibuprofen (max dose 2.4g, 600mg QDS or 800mg TDS, maintenance dose = 400mg TDS)
    - Take with food to protect stomach lining
    - Aspirin (up to 900mg/day)
    - Naproxen
    - Selective COX inhibitors = ketorolac (COX1) + Celecoxib (COX2)
  3. Oral opiates
    - Codeine (240mg max; 60mg QDS)
    - Tramadol (50-100mg QDS) -> Controlled drug!
    - Oramorph (0.2-0.4mg/kg)
    - Oxycodone -> used with renal failure
  4. IV opiates
    - Morphine (0.1-0.2mg/kg; up to 60mg/day initially)
    - Fentanyl
  5. Nerve block, PCAs (pt controlled analgesia)
98
Q

How would you prescribe an opiate?

A
  1. Start PRN morphine:

5-10mg ORAMORPH 2-4º, max 60mg

  1. Give 1/6th of total daily dose for breakthrough pain
  2. Prescribe CODEINE PRN in case they need
  3. Write up regular prescription of ORAMORPH after 2d of using PRN morphine
    - Lasts 12h in body thus give BD
    - Divide daily dose by 2 -> 60mg/2 = 30mg BD
    - Keep PRN prescription for breakthrough pain
    - Check dose/change every 3D
99
Q

Name 4 antiemetics and their mechanism of action and any contraindications

A
  1. Metaclopramide -> dopamine antagonist
    - Do NOT use in PD patients. Can cause Oculogyric Crisis in young females (rare - bilateral elevation of visual gaze)
    - 10mg TDS
  2. Cyclizine -> Histamine (H1) antagonist
    - 50mg TDS
  3. Ondansetron -> 5HT3 (serotonin) antagonist
    - 4mg TDS, max 16mg

** Can prescribe any of the above 3 PO/IM/IV cause all the same dose/strength!**

  1. Procholorperazine -> antipsychotic, lots of SE
    - 12.5mg IM; 5mg PO
100
Q

Name side effects of opiates

A
  • SE tend to occur at low doses
  1. Hallucinations
  2. Confusion
  3. Fainting
  4. Dizziness
  5. Hives, rash
  6. Difficulty breathing, slow breathing
  7. Seizures
  8. N/V
  9. Swelling
  10. Hoarseness of voice
101
Q

What forms part of the pre-operative patient assessment?

A
  1. FBC
  2. Haemostasis
  3. Kidney function
  4. ECG
  5. Lung function/ABGs
  • Ensure patient has not eaten within 6h of surgery and drank any clear fluids 2h before surgery
  • For minor surgery above 5 not required unless AKI or ECG not done within 12mo; major surgery requires all of the above 5 to be assessed.
102
Q

What is the ASA score?

A

Physical status classification

Ranges from 1-6, E
5 = not expected to survive surgery
6 = brain-dead
E = emergency surgery

103
Q

What aspects of a physical examination must be performed as part of a pre-operative assessment?

A
  1. Airway assessment -> Teeth to neck
  2. Height/weight (BMI)
  3. MET tolerance -> < 4 MET’s = high risk (can the patient go up stairs?)
  4. Pacemaker -> check settings
  5. VTE assessment -> avoid TEDs with local issues in legs (I.e. bleeding, varicose veins, ulcers, infection)
104
Q

What is FEVAR and when is it used over EVAR?

A

FEVAR = Fenestrated endovascular aneurysm repair
- Used when traditional EVAR cannot be used.

EVAR is used when aneurysms are far enough away from the renal arteries which branch off the aorta that the stent can be securely attached to the aorta.

In 10% of patients with AAA, the aneurysm is too close to the renal arteries and thus FEVAR is used.
FEVAR can cover branch arteries because the graft has fenestrations that correspond to the position of branching arteries.

FEVAR is inserted into the common femoral artery and guided to the aneurysm. Fenestrations allow blood flow to continue through vessels while graft is secured. The graft is expanded within the artery with the wire frame pushing against the healthy portion of the aorta to seal the device in place.

105
Q

What are the symptoms of AAA?

A

Typically none. As size increases:

  1. Back/abdo pain
  2. Pain radiating to groin
  3. Pulsating mass in abdomen
  4. Collapse
  5. Expansile AA
106
Q

What are the risk factors for AAA?

A
  1. Increased age
  2. Male gender
  3. Smoking
  4. HTN
  5. Connective tissue disorder (Marfan’s, EDS, Loeys-Dietz syndrome)
  6. Family history of aortic aneurysms + others
107
Q

When is surgery performed on an AAA?

A

When its ≥ 5.5cm

108
Q

What is an incarcerated hernia?

A

Herniated tissue that becomes trapped and cannot be moved back into place. Can lead to bowel obstruction or strangulation.

109
Q

What are the complications of AAA open surgery and EVAR?

A

AAA Open surgery:

  • MI
  • Irregular heart rhythms
  • Bleeding
  • Injury to bowel
  • Loss of blood flow to legs/feet
  • Blood clot
  • Infection of graft
  • Lung problems
  • Kidney damage
  • Spinal cord injury

EVAR:

  • Damage to surrounding vessels/organs
  • Kidney damage
  • Loss of blood flow to legs/feet
  • Groin wound infection
  • Groin hepatoma
  • Bleeding
  • Endoleak (continuous leaking of blood out of graft + into the aneurysm sac with potential rupture)
  • Spinal cord injury
110
Q

What is a saccular aneurysm?

A

Berry aneurysm

Has a “neck” that connects the aneurysm to its main artery + larger rounded area called a dome. These aneurysms bulge on only 1 side of the artery wall.

111
Q

What are the contraindications for AAA repair (open surgery and EVAR)?

A

Open Surgery:
- Coexisting medical conditions (I.e. cardiac, pulmonary, renal dysfunction)

EVAR:

  • Adequacy of vascular access for device introduction
  • Aneurysm morphology
  • Neck length + morphology
  • Iliac artery involvement
  • Type 2 diabetes
112
Q

When describing everything you can about a condition how should you organise your answer?

A

“In A Surgeon’s Gown People Make Minor Surgical Process”

  • Incidence
  • Age
  • Sex
  • Geography
  • Predisposing Factors
  • Macroscopic features
  • Microscopic features
  • Symptoms
  • Prognosis
113
Q

When describing the causes of a condition how should you organise your answer?

A

“VITAMIN C DEF”

  • Vascular
  • Infective/inflammatory
  • Trauma
  • Autoimmune
  • Metabolic
  • Iatrogenic
  • Neoplastic
  • Congenital
  • Degenerative
  • Endocrine/environment
  • Functional
114
Q

What are the types of occlusive and functional peripheral vascular diseases?

A

Occlusive:

  1. Atherosclerosis
  2. Beurger’s Disease: chronic inflammatory condition in minor arteries of the extremities that can lead to blood clots. Tobacco use increases risk and potentially caused by an autoimmune reaction in which the body’s immune system mistakenly attacks healthy tissue.
  3. Carotid artery stenosis
  4. DVT
  5. Lymphoedema: buildup of lymph in lymphatic system

Functional:

  1. Chronic venous insufficiency: valves of veins don’t work properly
  2. Raynaud’s disease: exposure to cold temperatures or emotional upset causes a decreased blood flow to the fingers and sometimes ears, toes, nipples, knees, nose
  3. Varicose veins: caused by venous insufficiency. Pregnancy, obesity, and long periods of standing are the most common causes of this.
115
Q

What is the Fontaine Classification for peripheral vascular disease?

A

Stage 1 = asymptomatic
Stage 2 = Intermittent claudication
Stage 3 = Rest pain
Stage 4 = Ulceration or gangrene

116
Q

Other than in DVT when can D-dimer be elevated?

A
  1. Infection
  2. Post-op
  3. Malignancy
  4. Pregnancy
117
Q

What are differentials for bilateral leg swelling? Unilateral leg swelling?

A

Bilateral:

  • R heart failure
  • hypoalbuminemia (nephrotic syndrome)
  • pregnancy
  • venous insufficiency
  • vasodilator (i.e. amlodipine)
  • pelvic mass

Unilateral:

  • DVT
  • cellulitis
  • ruptured Baker’s cyst
  • insect bite/trauma
  • tumours
  • necrotising fasciitis
  • compartment syndrome

Year 3 (7 decks)

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