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Pathology Term 1 > Week 3 - CVS > Flashcards

Week 3 - CVS Flashcards

Leg ulcers, Vasculitis, Vein disorders

1
Q

What is the major complication of DVT

A

Pulmonary embolism
-thrombus in leg veins can get separated to form an embolus which gets carried into heart via IVC –> pulmonary circulation –> blocks major vessel –> infarction

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2
Q

What is a major complication of giant cell arteritis?

A

Visual loss –> optic nerve ischaemia

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3
Q

True or False?

Polyarteritis Nodosa is not ANCA+

A

True

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4
Q

What is a significant complication of polyarteritis nodosa?

A

acute renal failure

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5
Q

What are clinical manifestations of DVT?

A
  • oedema
  • heat
  • tenderness
  • redness
  • swelling
  • cyanosis
  • pain –> clinical exam = Homan Sign (forced dorsiflexion of foot causing pain behind knee)
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6
Q

Differentiate between thrombophlebitis + phlebothrombosis

A

Thrombophlebitis = venous thrombosis formation causing inflammation and pain

Phlebothrombosis = venous thrombosis formation in absence of inflammation

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7
Q

What is hyperhomocysteinemia? And what are common causes?

A
  • increased levels of homocysteine in the body
  • may predispose to arterial thrombosis and venous thromboembolism due to injury of vascular endothelial cells (inflammation)

*common causes = acquired deficiencies (FOLATE/B12)

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8
Q

What is Virchow’s Triad?

A
  1. BV injury
  2. Hypercoagulability
  3. Stasis
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9
Q

Why does tortuous dilation occur in superficial veins and not deep veins?

A
  • deep veins are supported by muscle/fascia, whereas superficial veins are not
  • when reversal of blood flow occurs from deep –> superficial, vessels dilate and become tortuous (VARICOSE VEINS)
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10
Q

What is the pathogenesis of varicose veins?

A
  • normally, muscles (calf) push venous blood back to heart
  • blood travels from superficial veins –> deep veins –> heart (with backflow prevented by valves)
  • in congenital valve conditions/immobilisation causing decreased muscle activity –> accumulation of blood due to lack of activity of the muscle pump –> blood falls back and pools (reversal of flow) –> this high pressure blood goes back from deep to superficial veins –> superficial vessels have no support from muscles/fascia –> develop tortuous dilatation (VARICOSE VEINS)
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11
Q

True or False?

Pulmonary embolism is a common complication of varicose veins

A

False

-v. rare as blood clot does not go back to deep then to heart due to reversal of flow in varicose veins

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12
Q

What are varicose veins?

A
  • tortuous superficial veins due to increase pressure and weak wall (reversal of flow)
  • congenital or acquired (obesity, pregnancy, long-standing jobs, immobilisation, etc.)
  • valve defect in deep veins of lower limbs
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13
Q

Clinically, what is the most common disorder of veins?

A

Varicose veins

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14
Q

What is pyogenic granuloma?

A
  • moist growth over wound resulting from excess formation of granulation tissue
  • commonly on gingiva or palmar surfaces of fingers
  • NOT a true tumour
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15
Q

What is takayasu arteritis?

A
  • similar granulomatous vasculitis to giant cell arteritis but in younger patients (<50yrs)
  • severe obstruction of major vessels –> pulseless disease
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16
Q

What is giant cell arteritis typically referred to as?

A

Temporal arteritis

-typically affects temporal artery

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17
Q

What is the commonest cause of organ ischaemia/infarction in all lifestyle disorders (i.e. DM, HTN, etc.) and its 2 types?

A

Arteriolosclerosis - microangiopathy

  1. Hyaline –> DM
    - deposition of proteins in the BV wall
  2. Hyperplastic –> HTN
    - proliferation of smooth muscle fibres
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18
Q

What is the common laboratory finding in immune-mediated vasculitis?

A

ANCA+ –> Anti-Neutrophil Cytoplasmic Antibody

-formation of Abs which react with cytoplasm of neutrophils which then cause damage to the BV

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19
Q

What are the 2 large arteries?

A

Aorta & Pulmonary artery

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20
Q

What is arteriosclerosis?

A

hardening of ANY artery

  • atherosclerosis
  • arteriolosclerosis
  • monkeberg medial sclerosis
21
Q 
True or false?
All medium (muscular) arteries are named according to location
A

True - i.e. renal, cerebral, iliac, etc

22
Q

Which arteries hold the majority of blood

A

Arterioles

  • capacitance vessels
  • function to maintain BP
23
Q

What are the features of infectious ulcers?

A
  • irregular, non-specific
  • usually multiple
  • associated with lymphadenitis
24
Q

What are the causes of infectious ulcers?

A

simple strep/staph infections –> TB, Treponema, etc

25
What are the features of malignant ulcers?
``` A-asymmetry B-border irregularity C-colour change D-diameter > 6mm E-evolving ``` - irregular, punched out, caving or with tumour - frequently painless - lymph nodes, spreading, metastasis, cancer cachexia (wt. loss, etc.)
26
What are the causes of malignant ulcers?
- UV rays | - idiopathic
27
What are the features of neuropathic ulcers?
- clean, caving, callus - punched-out ulcers, deep caving - frequently painless - absent or weak pulses - often with surrounding calluses (hyperkeratosis) - probing/debriding --> brisk bleeding (arteries still intact) - occur typically on pressure points - may have impaired sensation + diminished positional sense or 2-point discrimination --> typical of nerve damage from DM in particular
28
What is the cause of neuropathic ulcers?
- due to lack of sensation (nerve fibre damage) - happens in regions exposed to constant pressure - no pain felt by patient
29
What are the features of arterial leg ulcers?
- dry, dark, painful (gangrenous) - cold, pale, absent or weak pulses - irregular, clear border - pale granulation - does NOT bleed on touch - painful (nocturnal) --> partly relieved by dependency - skin --> shiny, loss of hair (atrophy)
30
What is etiology of arterial leg ulcers?
- due to block in the artery | - ATHEROSCLEROSIS
31
What are the features of venous leg ulcers?
- large, irregular, shallow - wet, oedematous, oozing - moist granulating base --> bleeds on touch - surrounding eczematous stasis dermatitis (woody oedema) - mild pain --> relieved by elevation (helps venous drainage) - compression bandages helpful
32
What is the pathogenesis of the stasis dermatitis (woody oedema) in venous leg ulcers?
-due to accumulation of excretory waste products from venous pooling causing inflammation and infection to surrounding skin
33
What is the etiology of venous leg ulcers?
- commonest = varicose veins | - due to lack of venous drainage --> obstruction to venous flow --> stasis of blood
34
True or False? | Diabetes can cause venous leg ulcers
False | -can only cause arterial, neuropathic and infectious ulcers
35
Where are venous leg ulcers typically found?
COMMONEST | -gaiter region (above lateral/medial malleolus)
36
What is Raynaud's phenomenon vs. Raynaud's disease?
-both are vasoconstriction of digital arteries resulting in alternating areas of pallor and cyanosis in digits Disease = primary (i.e. no other associated disorders) - hyperactive BV - cold/emotional trigger - increase in young women - normal microscopy Phenomenon = secondary to other BV disorders -immune vasculitis, SLE, Buerger's disease, atherosclerosis, etc
37
What is Kaposi sarcoma?
- malignant tumour of BVs --> angiosarcoma - common in HIV pts. --> terminal stages of AIDS - caused by HHV-8 Many types: - classic KS - endemic African KS - transplant-associated - common HIV-associated
38
What is Buerger's disease?
- thromboangitis obliterans (totally blocking arteries) - segmental inflammation with thrombosis of small/medium arteries - strong association with smoking - severe, painful peripheral gangrene
39
What is Wegner's granulomatosis?
- rare vasculitis of small BVs - granulomatous inflammation around BVs - typically affects lung - antiproteinase-3
40
What is polyarteritis nodosa?
- systemic necrotising vasculitis - renal NOT lungs - nodule formation over arteries - leads to severe gangrenous death of tissue - acute fever, myalgia, arthralgia, malaise, rash, wt. loss - neuropathy, KIDNEY FAILURE - produces necrotic ulcers (DDx. for leg ulcers)
41
What is giant cell arteritis?
- granulomatous inflammation of medium and large arteries - leads to fragmentation of internal elastic lamina with giant cells and thrombosis - clinically presents as painful, thickened, nodular temporal arteries - segmental involvement --> doesn't involve whole BV wall thickness - usually pts. >50
42
What is the etiology of DVT?
Virchow's Triad
43
True or False? | Oral contraceptives are a risk factor for DVT
True | -can produce a hypercoagulable state
44
What are the clinical complications of varicose veins?
- stasis dermatitis | - ulcers
45
What is monkeberg medial sclerosis?
- medial calcific sclerosis | - intimal and media fibrosis and calcification (no obstruction)
46
What is the pathogenesis of DVT?
Virchow's triad factors cause thrombosis --> typically in lower legs due to increased blood stagnation --> obstruction --> stasis
47
Apart from varicose veins in lower limbs, where else should it be noted for vein dilation to occur?
- eosophageal varices | - haemorrhoids
48
Is DVT usually unilateral or bilateral?
Unilateral
49
What are the risk factors for DVT?
- immobility - surgery/trauma - increased oestrogens (OCP/preg.) - medical condtions --> cancer, heart failure, nephrotic syndrome, autoimmune disorders - other --> age, varicose veins, FHx., PMHx., congenital, smoking, obesity

Pathology Term 1 (6 decks)

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