Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is a major complication of giant cell arteritis?

A

Visual loss –> optic nerve ischaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

True or False?

Polyarteritis Nodosa is not ANCA+

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is a significant complication of polyarteritis nodosa?

A

acute renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Differentiate between thrombophlebitis + phlebothrombosis

A

Thrombophlebitis = venous thrombosis formation causing inflammation and pain

Phlebothrombosis = venous thrombosis formation in absence of inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is Virchow’s Triad?

A
  1. BV injury
  2. Hypercoagulability
  3. Stasis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Clinically, what is the most common disorder of veins?

A

Varicose veins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is giant cell arteritis typically referred to as?

A

Temporal arteritis

-typically affects temporal artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the 2 large arteries?

A

Aorta & Pulmonary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Q

What are the features of malignant ulcers?

A 
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
Q

What are the causes of malignant ulcers?

A
  • UV rays

- idiopathic

27
Q

What are the features of neuropathic ulcers?

A
  • 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
Q

What is the cause of neuropathic ulcers?

A
  • due to lack of sensation (nerve fibre damage)
  • happens in regions exposed to constant pressure
  • no pain felt by patient
29
Q

What are the features of arterial leg ulcers?

A
  • 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
Q

What is etiology of arterial leg ulcers?

A
  • due to block in the artery

- ATHEROSCLEROSIS

31
Q

What are the features of venous leg ulcers?

A
  • 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
Q

What is the pathogenesis of the stasis dermatitis (woody oedema) in venous leg ulcers?

A

-due to accumulation of excretory waste products from venous pooling causing inflammation and infection to surrounding skin

33
Q

What is the etiology of venous leg ulcers?

A
  • commonest = varicose veins

- due to lack of venous drainage –> obstruction to venous flow –> stasis of blood

34
Q

True or False?

Diabetes can cause venous leg ulcers

A

False

-can only cause arterial, neuropathic and infectious ulcers

35
Q

Where are venous leg ulcers typically found?

A

COMMONEST

-gaiter region (above lateral/medial malleolus)

36
Q

What is Raynaud’s phenomenon vs. Raynaud’s disease?

A

-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
Q

What is Kaposi sarcoma?

A
  • 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
Q

What is Buerger’s disease?

A
  • thromboangitis obliterans (totally blocking arteries)
  • segmental inflammation with thrombosis of small/medium arteries
  • strong association with smoking
  • severe, painful peripheral gangrene
39
Q

What is Wegner’s granulomatosis?

A
  • rare vasculitis of small BVs
  • granulomatous inflammation around BVs
  • typically affects lung
  • antiproteinase-3
40
Q

What is polyarteritis nodosa?

A
  • 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
Q

What is giant cell arteritis?

A
  • 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
Q

What is the etiology of DVT?

A

Virchow’s Triad

43
Q

True or False?

Oral contraceptives are a risk factor for DVT

A

True

-can produce a hypercoagulable state

44
Q

What are the clinical complications of varicose veins?

A
  • stasis dermatitis

- ulcers

45
Q

What is monkeberg medial sclerosis?

A
  • medial calcific sclerosis

- intimal and media fibrosis and calcification (no obstruction)

46
Q

What is the pathogenesis of DVT?

A

Virchow’s triad factors cause thrombosis –> typically in lower legs due to increased blood stagnation –> obstruction –> stasis

47
Q

Apart from varicose veins in lower limbs, where else should it be noted for vein dilation to occur?

A
  • eosophageal varices

- haemorrhoids

48
Q

Is DVT usually unilateral or bilateral?

A

Unilateral

49
Q

What are the risk factors for DVT?

A
  • 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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions