vascular pathology Flashcards

1
Q

virchows triad

A

status of blood flow
hyperagultiantion
endothelial injury

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2
Q

thrombosis formation

A

Platelet aggregation
Localised activation of the clotting cascade Fibrin
RBCs trapped
Platelet aggregation
Localised activation of the clotting cascade Fibrin
RBCs trapped
Propagation- obstruct lumen

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3
Q

risk factors of status of blood flow

A
Burns & Trauma
Surgery
Cardiac failure- back pressure
Pregnancy
Immobility	
Long haul flights
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4
Q

cardiac thrombosis

A

Atrial
Atrial fibrillation
Mitral stenosis

Valvular
Rheumatic fever
Endocarditis

Ventricular
Dead
Myocardial infarction

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5
Q

fate of thrombus

A
  • Lysis and Resolution
  • Retraction and Re-canalisation – middle pichealing and scarirng but blood can get past
  • Organisation and Scarring- pic 3
  • Embolism
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6
Q

things that cause embolisms

A
Atheromatous debris
Vegetations on heart valves
(Infective endocarditis- bacteria and fungi at hear valve tip- causing infection)
Fat- fracture of long bone marrow
Gas (Caisson’s disease- divers) or air in blood
Amniotic fluid- embolises in birth
Tumour
Foreign material –cosmetic filler
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7
Q

how embolism can effect the lungs

A

whole branch- sudden death
end of branch -ischemia and breathlessness
parts of smaller branches- pulmonary hypertension

the biggest he embolisms the worse

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8
Q

causes of infarction

A
Atheroma
Thrombosis
Embolism
Vasculitis- inflammation of vessel
Compression
Spasm
Hyperviscosity- effecting blood content
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9
Q

mi evalution

A
<6 hours		No visible changes
				(ECG changes)
24-48 hours 	Pallor with red rim
Several days  	Pallor with red rim	Soft 
				(Haemopericardium)
Several weeks 	Grey and fibrotic
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10
Q

things that effect infarction

A
Vascular anatomy
Duration of occlusion
Metabolic requirements of tissue- brain tissue worse
General circulatory factors
	Heart failure
	Anaemia
Reperfusion injury
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11
Q

dissecting aneurysms

A

due to interval wall ruptures and vessel wall splits

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12
Q

things that can effects major arteries

A
- PAD = claudiaction- goes on rest/ not below foot/ stops when standing / Ankle-brachial pressure index < 0.9/ Blood Pressure Control
Lipids
Antiplatelets –Clopidogrel/aspirin
ACE Inhibitors
Control Diabetes 
LIFESTYLE MODIFICATION 
  • chronic ischemic disease - pain on rest/gangreen/ulcers/ dopler pressure less than 50 mmHg/ ballon angioplasty/
  • acute ishcemic - the 5 ps - 4/6hrs permanent damage/ heparin in hospital/ catheter/ embolectomy/ bypass/ amputation

aaa- over 5.5 needs treament/ ultrasounds over 65yr/ EVAR/ GRAFT

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13
Q

Internal Carotid artery stenosis

A

Causes TIA and strokes by:
embolisation usually
Or restriction of flow occasionally
If symptomatic usually intervene if stenosis > 70%
resolves within 24 hours – can affect vision, speech or limbs commonly
ENDARCHARERTMY- CLEAN AWAY PLAQUE

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14
Q

Management of angina

A

Stop and rest
GTN spray to shorten attack

Regular anti-anginal drugs:

  • Beta blockers e.g. bisoprolol
  • Nitrates e.g. isosorbide mononitrate
  • Calcium channel blockers e.g. amlodipine
  • Others – nicorandil, ivabradine, ranolazine

Percutaneous coronary intervention- ballon stretching
Coronary artery bypass graft

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15
Q

signs in clothed patients

A

General appearance – breathlessness, pallor, sweating, cyanosis
Pulse – rate(radial pulse), rhythm, volume
Blood pressure
Jugular Venous Pressure (JVP) – raised in heart failure id failed more likely on right side of heart
Peripheral oedema – ‘pitting’ indents on pressure when you put your thumb on it Chest pain – usually ischaemia/can be refered though
Breathlessness – usually heart failure
Ankle swelling – heart failure
Palpitations(abnormal awareness of heartbeat) – arrhythmia
Faintness – low blood pressure, arrhythmia

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16
Q

La adrenaline with heart issues

A

Normal adrenaline (in blood released during stress) release can increase X 20 during stress.

Recommendation: Patients with mild to moderate CVS disease can have LA containing adrenaline.

Severe CVS disease (unstable angina, recent MI, dysrythmias, severe HBP or CHF) may be considered relative contraindications to VC use

17
Q

cariac disease and when to do dental treatment

A

AMI: postpone elective Rx till 3-6 months later

Unstable angina: dental care in suitable facilities/postpone

Cardiac failure: dyspnoea (breathlessness- do not lie flat)

18
Q

monitoring high risk patients

A
Clinical signs & symptoms
BP
Pulse oximetry
ECG
not in primary care
19
Q

CCB and what oral manifestation they cause

A
Nifedipine
Amlodipine
Nicardipine
Nimodipine
Verapamil
Diltiazem

gingival hypoplasia

20
Q

management of Angiodema and the drug that causes it

A

ACE inhibitors

Stop drug and go to hospital if airway is lost due to tongue oedema can go and be intubated- rara to have surgery

21
Q

drug that causes ulceration

A
nacranavil 
a K+ channel blockers 
used for angina 
vasodilator
biopsy if worried
22
Q

rheumatic fever facts

A

can occur 2-3 weeks after a streptococcal URTI

Predominantly a childhood disorderInflammation at multiple sites

Heart		Rheumatic Heart Disease
		Endocarditis
		Myocarditis (Aschoff bodies)
		Pericarditis
Arteries	Arteritis
Joints		Flitting polyarthritis
Skin		Erythema marginatum
		Skin rashes
		Subcutaneous nodulesBacterial culture of affected tissues negative- it is a autoimmune condition 

Antibodies to streptococcal polysaccharide

Antistreptolylin O titres (ASOT) raised

Antibodies cross-react with cardiac antigens on cardiac tissues – biological accident
this can cause: vegitations/fibrous pericardium/myocardial Aschoff bodies

23
Q

sites of infective endocarditis

A

Heart valve

Mural endocardium- especially if the has been a HA

Congenital defect in heart lining

24
Q

things that predispose to ineffective endocarditis

A

-Acquired valvular heart disease with stenosis or regurgitation

-Hypertrophic cardiomyopathy- heart is enlarged
Previous infective endocarditis

  • Structural congenital heart disease, including surgically corrected or palliated structural conditions, but excluding isolated atrial septal defect, fully repaired ventricular septal defect or fully repaired patent ductus arteriosus, and closure devices that are judged to be endothelialised
  • Valve replacement.
25
Q

local effects of infective endocarditis

A

Local effects

Valve incompetence

Perforation of valve leaflets

Rupture of cordae tendineae (prolapse)

Myocarditis

Embolism to coronary vessels- can enter blood stream

26
Q

systemic effects of infective endocardiditis

A

Systemic effects

Fever, weight loss & malaise

Splenomegaly- enlargement of spleen

Embolism- lodge somewhere and cause infection here.

27
Q

infective endocardiditis symptoms

A

Embolism
Spleen abscess
Kidney abscess
Brain abscess

Skin & nail beds haemorging
Mucous membranes
Retina

Glomerulonephritis

Finger clubbing

28
Q

diagnosis and treatment of infective endocarditis

A

Embolism
Spleen abscess
Kidney abscess
Brain abscess

Skin & nail beds haemorging
Mucous membranes
Retina

Glomerulonephritis

Finger clubbingAntibiotics

Surgical removal of the valve

29
Q

pathenogensiis of thematic ever

A

Repeated episodes of rheumatic fever
Fibrosis of endocardium & valves edges
Vegetations on heart valve leaflets-composed of platelets and fibrin
Fusion of heart valve leaflets
Calcification of heart valves
60% mitral valves and stenosis and incompetence
40% aortic value stenosis and incompetence

30
Q

what is mitral valve prolapse

A

Mitral valve prolapse- cordie tenoni