Cardiovascular conditions Flashcards

1
Q

What is the definition of hypertension?

A

Raised arterial blood pressure

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

what is the diagnosis of Hypertension?

A

Over 140/90 in clinic
stage 2 : 160/100mmhg
stage 3: 180/110mmhg

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

Epidemiology of Essential Hypertension?

A

common in men

common in black African (40-50%)

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

Primary aetiology of essential hypertension?

A

80-90% are idiopathic

Primary causes: FH , low birth weight (undernutrition = blood vessel changes)

Environmental(obesity , alcohol intake and stress)

Insulin resistance

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

Secondary aetiology of essential hypertension?

A

Cardiovascular: Aortic dissection , atherosclerosis

CKD: Haematunia 
Renal Disease(80%): polycystic kidneys , renovascular disease 

Endocrine: Conn’s disease , Adrenal hyperplasia , Cushing syndrome

Drugs: NSAID , oral contraceptive , steroids ,carbenoxolone

Pre-eclampsia

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

Pathophysiology of essential hypertension?

A

increase in cardiac output with increased pulse rate and circulating catecholamines

Resistance vessels , structural changes in HPT , leads to increase wall thickness and reduction in vessel lumen diameter.

Increase in peripheral resistance that maintain BP.
Pulse wave travels to arterial wall (each systolic contraction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what are the renal changes that occur in pathophysiology in hypertension ?

A

Reduced renal perfusion reduces GFR = reduction in sodium and water excretion. Leading to continuous production of RAAS system

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

What are the risk factors of hypertension ?

A

Age
Gender - males
Ethnicity - black African and African Caribbean
Genetics
Social deprivation - more likely to have HBP

Excessive alcohol intake
Stress and anxiety

Thyroid , Kidney and Sleep apnoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Signs and Symptoms of essential hypertension ?

A
Fatigue 
visional problems 
chest pain 
Difficulty breathing(LV hypertrophy, cardiac failure , angina)
Irregular heartbeat 
Haematuria 
Palpation of ears , chest and neck 
Weakness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Differentials for HBP?

A

Malignant hypertension
(systolic >200 and Diastolic >130)

Isolated systolic hypertension in those over 60 years >160mmg /90mmg

Postural Hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Conservative treatment for essential hypertension ?

A

Have a target BP <140/85 For diabetic patients <130/80 - use AMBPM

Lifestyle changes: Reduced alcohol and sodium intake

Increase exercise and aim to reduce weight

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pharmacological Approach of Hypertension?

A

1st line drug <55 years old and not black (ACE: end in April OR ARBS)

55years > & black - CCB : Amlodipine
If not tolerated , give thiazide like diuretics

BB not preferred choice of treatment - used in younger patients

2nd line - methyldopa
Add a third drug if needs = do not double it

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

what are the investigations for hypertension ?

A

Basic U&E , Creatinine , cholesterol , blood glucose , urine (for protein and blood )

Renal USS , Renal angiography

For secondary causes:
24 Hours - urinary metanephrines , urinary free cortisol
BP readings - 3 x both arms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Complications of hypertension ?

A

Heart attack
Aneurysm
Heart failure
torn blood vessels in the eyes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is orthostatic/Postural Hypertension ?

A

Abnormal drop in BP lower than 90/60mmhg

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

Epidemiology of postural hypertension?

A

common with increasing age , >50 years

Associated with fainting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Aetiology of postural/ orthostatic hypotension?

A
Parkinson's disease 
Anaemia 
Blood loss
Dehydration 
Medication such as: Sildenafil and BB , antidepressants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what are the conditions associated with postural hypotension?

A

MI , Diabetes , Alcohol neuropathy

Phaechromocytoma
Parkinson’s disease

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

Pathophysiology of postural hypertension?

A

Baroreceptors in the aortic arch and carotid sinus activate autonomic reflexes to rapidly return BP to normal.

The sympathetic nervous system increases heart rate and contractility and increases vasomotor tone of the capitance vessels.

pooling of the blood in lower limbs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Risk factors of orthostatic hypotension ?

A

Chronic alcohol and drug use

pregnancy(as pregnancy progresses , the volume of the circulatory system expands , BP reduces)

old age

Diabetes
smoking
Anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Symptoms and signs of orthostatic hypotension?

A

Excessive sweating

Dizziness
light-headedness

Blurred vision 
fatigue 
weakness 
palpitations 
headache 
SOB 
confusion 
Raised JVP 
Edema 
Vomitting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Differentials of orthostatic hypotension:

A

HF
MI
AF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Conservative treatment of orthostatic hypotension?

A

changes in food , reduce alcohol and drug intake
Avoid triggers e.g. high temperature
head up 20-30cm

Adequate fluid intake

Regular BP Monitoring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Pharmacological treatment of postural hypotension?

A

1st choice - Fludrocorisone (low dose)

Alpha - receptors: Midodrine is recommended for monotherapy or in combined with Fludrocortisone

Somatostatin analogue octreotide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Investigations of orthostatic hypotension:

A

Blood pressure management · Electrocardiogram (ECG) · Blood test: Glucose levels, FBC, U&E · Tilt-table testing (to confirm orthostatic hypotension · Echocardiogram – if they have an underlying cardiac problem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Complication of postural hypotension ?

A

Severe hypotension: Repeated Syncope , Stroke due to the reduced blood supply to the brain, coma. Severe postural hypotension = deprivation of oxygen to heart and brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is hypovolaemic shock ?

A

Life threatening condition when the body loss of blood volume or fluid volume (More than 1/5 of the body’s fluid or blood supply makes the heart unable to pump enough blood into the body = organs failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Epidemiology of hypovolaemic shock ?

A

Most common type in children, most commonly due to diarrheal illness in the developing world

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Aetiology of hypovolaemic shock?

A

Increasing age Comorbidities Myocardial infarction Cardiomyopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Risk factors of hypovolaemic shock ?

A

Dehydration Aneurysm rupture Heart failure Severe infection (eg. Sepsis) Renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Symptoms and signs of hypovolaemic shock

A

Shortness of breath Chest Pain Abdominal cramps

cold , pale , slate-grey

slow capillary refill , clammy Kidneys: Oliguria, anuria Brain: Drowsiness, confusion and irritability · Increased sympathetic tone Tachycardia, narrowed pulse pressure , ‘weak’ or ‘thready’ pulse Sweating Blood pressure: 25% reduction in circulating volume if the patient is young and fit = hypotension · Metabolic Acidosis Compensatory tachypnoea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

treatment of hypovolaemic shock?

A

Medical Emergency

stop fluid loss and stabilise blood volume levels

Replace lost blood volume with intravenous(IV)fluid called crystalloids.

Potentially, if high blood volume is lost, transfusion of plasma (the fluid of component of blood or RBCs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Investigations of hypovolaemic shock ?

A

Blood tests : Blood chemistry(U&E) FBC- to rule out any infections, haematocrit and haemoglobin levels Creatinine Lactic acid test • Urea nitrogen blood test, CT Scan Echocardiogram Endoscopy((to look at the bleeding source in the gastrointestinal tract) A right heart catheter to show how well the heart is pumping blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

complication of shock ?

A

Kidney failure, heart dysfunction, respiratory failure, and multiple organ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what is the definition of cardiogenic shock ?

A

Is a state of inadequate tissue perfusion primarily due to cardiac dysfunction. It may occur suddenly or after progressively worsening heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Aetiology of cardiogenic shock ?

A

The most common cause of cardiogenic shock is a heart attack

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Pathophysiology of cardiogenic shock ?

A

Low cardiac output state secondary to extensive LV infarction , development of a mechanical defect(e.g. Ventricular septal defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Risk Factors of cardiogenic shock ?

A
Elderly 
Diabetes 
History of previous infarction 
Cerebrovascular disease 
peripheral vascular disease
Multi-vessel atheroma

Anterior and RV MI are associated with an increased risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Signs and Symptoms of Cardiogenic shock ?

A

Signs of myocardial failure e.g. raised jugular venous pressure(JVP) ,

‘gallop’ rhythm , basal crackles , pulmonary oedema.

Symptoms:

Chest pain Nausea and vomiting Dyspnoea Profuse sweating Confusion/Disorientation Palpations Faintness/Syncope Signs:

Pale, mottled , cold skin with slow capillary refill and poor peripheral pulses

Hypotension Tachycardia/Bradycardia Raised JVP Peripheral Oedema Heaves , thrills or murmurs Altered mental state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Differentials of cardiogenic shock ?

A

PE
Pericardial tamponade
Tension pnuemothorax
Myocardial suppression due to sepsis

Beta blockers - suppression of myocardial contractility

metabolic disturbance e.g. hypokalaemia

thyroid storm (excessive release of thyroid hormones (THs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

treatment and management of cardiogenic shock ?

A

Treat underlying causes e.g. management of MI

ABCD
Monitor BP
Give opiate analgesia (relieve symptoms if needed)
Dopamine is given
Intra aortic balloon pump counterpulsation (increases cardic output and improves coronary artery blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Investigations of cardiogenic shock ?

A
Urine pregnancy test in women.
LFTs.
FBC to exclude anaemia.
Cardiac enzymes, including troponins.
Arterial blood gases.
Brain natriuretic peptide

ECG (may show acute MI )
CXR( Rule out pneumothorax)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Complications of cardiogenic shock ?

A

cardiopulmonary arrest
Renal failure
Stroke
Death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Definition of Phlebitis ?

A

Inflammation of a vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Definition of thrombosis ?

A

Blood clot in a vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is the definition of a thrombophlebitis ?

A

superficial thrombophlebitis is an inflammation of a vein under the skin e.g leg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Epidemiology of thrombophlebitis ?

A

Common

common with those with history of DVT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Aetiology of thrombophlebitis ?

A

Injury
Pregnancy
High dose oestrogen therapy (e.g contraceptive pill )

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Pathophysiology of thrombophlebitis ?

A

When a superficial vein , usually the long saphenous vein of the leg or its tributaries becomes inflamed and the blood within its clots

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Risk factors of thrombophlebitis?

A

Varicose veins - prone to minor injuries = inflammation

Cannulation - injures veins and triggers inflammation

IV drug abuse use 
Age(60>)
Smoking 
Obesity 
Prolonged immobilisation , trauma 
Pregnancy (6 weeks post birth)

HRT
Cancer
CHF(congestive HF)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Signs and symptoms of thrombophlebitis?

A
Pain 
Swelling 
Tenderness 
Redness 
Warmth of skin 
Vein distension in leg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Differentials of thrombophlebitis?

A

DVT
Cellulitis(acute bacterial infection of dermis)

Lymphagnitis - inflammation of lymphatic vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Management of thrombophlebitis?

A

Management

Treat pain with a simple analgesic (nonsteroidal anti-inflammatory drug – NSAID) Paracetamol Manage swellings and discomfort with compression stockings

Conservative: A warm , moist towel/flannel applied to affect limb for symptomatic relief Keep legs elevated whilst sitting- reduces swelling Keep active

Pharmacological Paracetamol NSAIDS If infected superficial thrombophlebitis(Flucloxacillin 500mg) Erythromycin Clarithromycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Investigations of thrombophlebitis ?

A

examine affected area

Special uss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Complications of thrombophlebitis ?

A

infection
blood clot can travel to upper thigh
recurrent thrombophlebitis

56
Q

what are the stages of chronic arterial occlusion ?

A

stage 1 : asymptomatic
stage 2: intermittent (relieved by rest)
stage 3 : rest pain / pain when sleeping (nocturnal pain)

57
Q

Definition of chronic arterial occlusion ?

A

when blood flood in a leg artery suddenly stops.

persistent compromise of the arterial supply to the lower limbs

58
Q

Epidemiology of chronic arterial occlusion ?

A

common

>50 years

59
Q

Aetiology of chronic arterial occlusion?

A

Atherosclerosis affecting the aorto-iliac , femoral or popliteal and calf- vessel

30% due to thromboembolus from a distant site. Association: Atrial fibrillation, acute myocardial infarction. Rarer causes: aortic dissection , trauma

60
Q

Pathophysiology of chronic arterial occlusion ?

A

Gradual atherosclerotic narrowing

61
Q

Risk factors of chronic occlusion ?

A

diabetes
hypertension
smoking
CKD

62
Q

signs and symptoms of chronic arterial occlusion ?

A

Pain Pallor(Pain appearance of the limb) Paresthesias(abnormal sensations in the limb) Pulselessness Paralysis

Chronic: thigh or calf pain brought on by exercise and relieved by rest Doppler ankle pressure <50mmHg Acute: sudden onset of pain and loss of sensation in the limb Absent pulse

63
Q

Differential Diagnoses of chronic arterial occlusion?

A

Symptoms may be confused for: Osteoarthritis hip/knee(knee pain often at rest) Venous diseases Neurospinal diseases Spinal Stenosis Fibromuscular dysplasia

64
Q

conservative treatment and management ?

A

Medical/Conservative
· Stop smoking
· Patients with diabetes mellitus need regular chiropody care and diabetic management
· Low dose aspirin reduces risks of MI and stroke · Increase exercise

65
Q

pharmacological treatment of chronic arterial occlusion

A

Pharmacological :
Cilostazol – phosphodiesterase II inhibitor –produces vasodilation and inhibits platelet aggregation (100mg dose)

Naftidrofuryl – is a vasodilator agent than inhibits vascular and platelet 5-HT2 receptors reduces lactic acid levels. Oxpentifyylline – Not recommended for patients with claudication.

66
Q

Surgical treatment of chronic arterial occlusion ?

A

Surgical Not recommended (Vascular intervention) Percutaneous transluminal angioplasty (1st option) = catheter inserted into the femoral artery In severe ischaemia with

unreconstructable arterial diseases = amputation

67
Q

Investigation of chronic arterial occlusion ?

A

Brachial / ankle pressure index (ABPI) Diagnostic Imaging:

· Digital subtraction angiography(DSA) provides arterial map , requires peripheral arterial cannulation

· Duplex ultrasound – using B-Mode ultrasound and colour.

· 3D contrast enhanced magnetic resonance angiography provides excellent imaging of both legs

68
Q

complications of chronic arterial occlusion ?

A
sores that won't heal 
ulcer 
gangrene (dead tissue)
infection 
amputation
69
Q

Definition of Acute arterial occlusion

A

sudden cessation of the arterial supply to the lower limb

70
Q

Aetiology of acute arterial occlusion ?

A

pre-existing atherosclerosis

71
Q

Risk factors of acute arterial occlusion ?

A

aortic atherosclerosis
arterial trauma
MI
Atrial fibrillation

72
Q

Symptoms and Signs of acute arterial occlusion ?

A

5p’s (pain – pallor – colour of the legs) (paraesthesia , paralysis , cold) The pain is unbearable The limb is cold with mottling and marbling of the skin. Absent pulses Reduced movement of legs

73
Q

Pharmacological treatment of acute arterial occlusion ?

A

Pharmacological Heparin People with MI – long term warfin

74
Q

Surgical Treatments of acute arterial occlusion ?

A

Embolectomy(Catheter or surgical)(thrombolysis, or bypass surgery)

75
Q

Investigation of acute arterial occlusion ?

A

Immediate angiography is required to confirm location of the occlusion Identify collateral flow and guide therapy

76
Q

what is a peripheral vascular disease ?

A

Occurs when there is significant narrowing of arteries distal to the arch of the aorta. Most often due to atherosclerosis.

77
Q

what are the epidemiology of peripheral vascular disease ?

A

Age >55

78
Q

Aetiology of PVD?

A

Atherosclerosis High blood pressure Diabetes Obesity Unhealthy diet

79
Q

Risk Factors of peripheral vascular disease ?

A

Smoking Diabetes mellitus Hypertension Hyperlipidaemia: High total cholesterol and
low density lipoprotein
Physical inactivity
Obesity

80
Q

Symptoms and Signs of peripheral vascular disease ?

A

The affected leg may be pale and cold with loss of hair and skin changes

o Weak or absent pulses, palpation of the femoral , popliteal , dorsalis pedia and posterior tibial pulses.

o Calf pain on rest or exercise o Coldness and capillary refill time reduced

o Unequal arm pressure

o Male impotence

o Walking impairment

81
Q

Differential Diagnoses of peripheral vascular disease ?

A

Spinal stenosis
Sciatica
Deep vein thrombosis Entrapment syndromes Muscle/tendon injury Cerebrovascular diseases Coronary heart diseases

82
Q

Conservative treatment of peripheral vascular disease ?

A

Conservative : Smoking cessation Regular exercises Weight control –

Hypertension control Management of diabetes

83
Q

Pharmacological treatment of peripheral vascular disease ?

A

Lipid lowering drugs – statins to reduce the risk of mortality , maintaining LDL cholesterol level ACE inhibitors(reduce CVS morbidity and mortality in patients with PAD)

Antiplatelets – clopidogrel is recommended to prevent occlusive.

Aspirin Peripheral vasodilators: Naftidrofuryl oxalate (not recommended – cilostazol , pentoxifylline and inositol nicotinate)

84
Q

Surgical treatment of peripheral vascular disease ?

A

two options: endovascular revascularisation and surgery. Bypass surgery – most common surgical approach for diffuse occlusive diseases. Amputation

85
Q

investigation of peripheral vascular disease ?

A

Full cardiovascular risk assessment :

Blood pressure(Brachial pressure indec) FBC(Anaemia will aggravate Peripheral arterial disease, thrombophilia screen
 Fasting 
blood glucose
 Lipids levels
 ECG
 Duplex ultrasonography (indicate the degree of stenosis and length of an occlusion
 MR angiography and CT angiography
86
Q

Epidemiology of Varicose veins

A

Common in females more than men

common

87
Q

Aetiology of Varicose veins

A

Most cases are primary and idiopathic (95%)
Congenital valve absence(very rare) Secondary causes include pregnancy, large fibroids and ovarian masses Obstruction(DVT)
Ovarian tumour,
constipation

88
Q

Pathophysiology of Varicose veins

A

Bloods from superficial veins of the legs passes into the deep veins via perforator veins and at the sapheno- femoral and sapheno-popliteal junctions(back of the leg).

Valves prevent bloods from passing from deep to superficial veins. If they become incompetent… venous hypertension & dilation

89
Q

Risk factor of Varicose veins

A
Prolonged standing 
Obesity 
Pregnancy
 The pill
 Family history
90
Q

Signs and symptoms of Varicose veins ?

A
Pain
 Cramps 
Tingling 
Heaviness
 Restless legs
 Signs 
Oedema 
Eczema
 Ulcers 
Hemosiderin
 Haemorrhage
 Phlebitis
 Atrophie Blanche(white scarring at the site of previous , healed ulcer) Lipodermatosclerosis- skin hardness from subcutaneous fibrosis caused by chronic inflammation and fat necrosis)
91
Q

Differential diagnoses of Varicose veins ?

A

Cellulitis
Osler-Weber rendu syndrome
Superficial phlebitis
DVT

92
Q

Investigations of Varicose veins ?

A

Patient standing 1. Inspect for: Ulcers Inspect the legs

Palpate vein for tenderness(phlebitis) and hardness(thrombosis) if ulcer is present , palpate pulses to rule out arterial disease.

Duplex Ultrasound

Combines traditional ultrasound: used for sound waves that bounce off blood vessels to create picture and the Doppler ultrasound that records sound waves reflecting off moving objects such as blood , to measure their speed.

93
Q

conservative treatment of varicose veins ?

A

Avoid prolonged standing and elevate legs when possible
Support stockings
Lose weight
Regular walks

94
Q

Surgical treatment of varicose veins ?

A
Radiofrequency ablation(VNUS Closure):
A catheter is inserted into the vein and heated at 120 degrees to destroy the endothelium , closing the vein.

Endovenous laser ablation: Similar but with a laser Injection

Sclerotherapy( either liquid or foam) Injected into multiple sites and the vein is compressed for a few weeks to avoid thrombosis) Several other options available as well(depending on the vein anatomy) :

Saphenofemoral ligation (Trendelenburg procedure), multiple avulsion(pulled out) usually done through a series of small cuts (2-4mm)

95
Q

what is Acute Rheumatic Fever?

A

Is an inflammatory disease that occurs in children and young adults(first attack normally occurs during ages 5 and 15 years) as a result of infection with group A streptococci

96
Q

Aetiology of Acute Rheumatic Fever?

A

Caused by a bacterium called group A streptococcus. This bacterium causes strep throat , scarlet fever.

97
Q

Pathophysiology of Acute Rheumatic Fever?

A

Causes the body to attack its own tissues. The reaction causes widespread inflammation throughout the body.

98
Q

Risk Factor of Acute Rheumatic Fever?

A
Overcrowding  
Poor hygiene
 Lack of access to medical services 
Age (young age) 
The heart 
Skin
Joints
99
Q

Signs and Symptoms of Acute Rheumatic Fever?

A

The disease presents suddenly with fever , joint pain and loss of appetite:

Clinical features: (Modified Jones Criteria used to identify patients with likelihood of RF)
· Changing heart murmurs , mitral and aortic regurgitation , heart failure and chest pain – caused by carditis affecting the 3 layers of the heart

· Polyarthritis – fleeting and affecting the large joints eg knees , ankles and elbows

· Skin Manifestations- erythema marginatum(pink patches on the skin) · Small non-tender subcutaneous nodules( small spots on the skin)on joints , tendons and bony prominences
· Carditis manifests (40% of patients): New/changed heart murmurs Development of cardiac enlargement cardiac failure

Appearance of pericardial effusion and ECG changes of pericarditis , myocarditis , AV block or other arrhythmias

· Non- cardiac festures: (10-30%) Fever (90%) Arthritis Acute inflammation

Sydenham’s chorea : involvement of the CNS – develops late after streptococcal infection , noticeably fidgeting and display spasmodic- impaired speech

100
Q

Investigations of Acute Rheumatic Fever?

A

Throat swabs – cultured for group A strep Blood counts shows a leucocytosis

Raised ESR(measurement of degree of inflammation in the body) and fall(sedimentation) of erythrocytes(red blood cells) and CRP(C-Reactive Protein)

Antibodies tested include ASO and Anti-DNase B, Anti-NAD(the antibodies rise during the first month of infection and then 3-6 before returning to normal levels at 6-12 Months.

ECG may show a prolonged PR Interval , Tachycardia is usual. ST Elevation suggest pericarditis.

Doppler Echocardiography

101
Q

Differential Diagnoses of Acute Rheumatic Fever?

A

Reactive Arthritis Erythema Nodosum Heart Disease: Cardiomyopathy
Infective Endocarditis
Rash: Lyme Disease

Chorea: Huntington’s disease Wilson’s disease

102
Q

management of acute rheumatic fever ?

A

Management: Eradicate the infection

Suppress the inflammation arising

103
Q

Treatment of acute rheumatic fever ?

A

Treatment : Penicillin is given , if allergic erythromycin or cephalosporin is recommended.

Other authorities recommend oral therapy first-line with a single injection of benzylpenicillin reserved for patients unlikely to complete the course.

Aspirin – to relieve arthritis within a few days , high dose is required and other NSAIDs such Naproxen is safe

104
Q

complication of acute rheumatic fever ?

A

carditis
mitral stenosis
CHD

105
Q

what is VTE?

A

venous thrombosis occurs in normal vessels – in the deep veins of the legs. Originates around the valves as red thrombi consisting of red cells and fibrin.

Propagation(spread of bacteria occurs) inducing the risk of embolization to pulmonary vessels. Chronic venous obstruction in the leg = permanent swollen legs , more prone to ulcers.

106
Q

what is a PE ?

A

PE = DVT Life threatening condition and is a blockage of an artery in the lungs by a substance that has moved from elsewhere in the body through the bloodstream(embolism) Results in blood clot in the leg that travels to the lungs

107
Q

Difference between DVT AND PE?

A

The difference between DVT and PE is that DVT is a deep vein clot which is often found in the leg , arms. Whereas a PE occurs when a DVT clot breaks free from a vein wall and travels to the lung and blocks blood supply. The blood clots originate in the thigh and travel to other parts of the body.

108
Q

Epidemiology of DVT , PE ?

A

45 >

women

109
Q

Causes of PE , DVT ?

A

Rarely, the blockage in the lung blood vessel may be caused by an embolus which is not a blood clot.

This can be: · Fatty material from the marrow of a broken bone (if a large, long bone is broken - such as the thigh bone (femur).

· Foreign material from an impure injection - for example, with drug misuse.

· Amniotic fluid from a pregnancy or childbirth (rare).

· A large air bubble in a vein (rare). · A small piece of cancerous material (tumour) that has broken off from a larger tumour in the body.

· Mycotic emboli - material from a focus of fungal infection · Major general surgery
· Major orthopaedic surgery · Multiple trauma
· Cancer – all cancers increase the risk – especially if the cancer spreads · Pregnancy and use of contraceptives

· Menopause · Age>40 higher risk
· Obesity – 2x the risk of VTE
· Immobility – long travels on the plane etc

110
Q

Pathophysiology of PE

A

A thrombus is a solid mass composed of platelets and fibrin with a few trapped red and WBC that form within a blood vessel. Hypercoagulability and obstruction =DVT As the clot propagates , proximal extension occurs and dislodges and embolises to the pulmonary arteries =

Pulmonary artery obstruction , increase in alveolar dead space and leads to redistribution of blood flow – impairing gas exchange

111
Q

Risk Factors of PE ?

A
Age
 Smoking status
 Body mass index
 History of varicose veins Congestive cardiac failure IBD 
Cancer 
COPD 
Hospital admission in the last 6 months 
Pregnancy
Oral Contraceptive
112
Q

Signs and Symptoms of DVT /PE?

A

DVT Leg pain or tenderness of the thigh or calf
Leg swelling (edema)
Skin that feels warm to touch
Reddish discoloration or red streaks

 PE: Unexplained shortness of breath
 Rapid breathing 
Chest pain underneath the ribcage
 Fast heartrate 
Light-headedness
113
Q

Differential Diagnosis of DVT/PE?

A
Muscle strain 
Skin infection (Cellulitis) Trauma
 Post-thrombotic syndrome Heart failure
 Peripheral oedema
 Venous obstruction

Septic Arthritis

114
Q

investigations of PE/DVT?

A

For DVT: Ultrasound of the leg – duplex doppler

PE: computed tomography, CT scan, CAT scan Sometimes ventilation perfusion lung scan is used.

Blood tests – INR and D-Dimers (detects clotting activity in the blood) DVT well’s score

115
Q

Treatment and management of DVT

A

Offer patients in whom DVT is suspected and with an unlikely two-level DVT Wells’ score a D-dimer test and, if the result is positive, offer either:

· A proximal leg vein ultrasound scan carried out within four hours of being requested; or

· An interim 24-hour dose of a parenteral anticoagulant (if a proximal leg vein ultrasound scan cannot be carried out within four hours) and a proximal leg vein ultrasound scan carried out within 24 hours of being requested.

116
Q

Pharmacological treatment of

A

Pharmacological · Anticoagulation – offer a choice to low molecular weight heparin or fondaparinux to patients with confirmed DVT or PE ·

Rivaroxaban, Dabigatran and Apixaban – for treatment and secondary prevention of DVT & PE

117
Q

Management of DVT/PE?

A

Assess the risk and benefits of continuing anticoagulation treatment after 3 months

Patients to carry a anticoagulants information card at all times

118
Q

Surgical treatment for DVT/PE?

A

Offer temporary inferior vena cava filters to patients with proximal DVT & PE who cannot have anti coagulation treatment, remove when eligible

119
Q

Arterial Embolism/thrombosis -

A

A sudden interruption of blood flow to an organ or body part due to an embolus.

120
Q

Pathophysiology of Arterial Embolism/thrombosis ?

A

An embolus adhering to the wall of an artery blocking the flow of blood, the major type of embolus being a blood clot.

Caused by one or more blood clots – the clots can get stuck in an artery and block blood flow. The blockage starves tissues of blood and oxygen= damage and tissue death (Necrosis)

121
Q

Aetiology of Arterial Embolism/thrombosis ?

A

High blood pressure – weakens the arterial wall, making it easier for blood to accumulate in the weakened artery and form clots:

Smoking
 Hardening of the arteries from high cholesterol Surgery that affect blood circulation
 Injuries to the arteries Heart diseases
 Atrial fibrillation (rapid/ irregular heartbeat)
 Lack of exercise Overweight
 Excessive 
amount of alcohol 
High blood pressure 
High cholesterol 
Diabetes
122
Q

signs and symptoms of Arterial Embolism/thrombosis?

A

Symptoms depends on the size of the embolus.

 In the leg or arms:
 Coldness
 Lack of pulse 
Lack of movement 
Tingling or numbness 
Pain or spasm in the muscles 
Pale skin 
A feeling of weakness Muscle pain and muscle spasm in the affected area 

The symptoms are most likely to be asymmetrical If not treated:
Ulcers
An appearance of shedding skin
Tissue
death
Blisters of the skin fed by affected artery
Skin erosion(Ulcer)

123
Q

Risk Factor of Arterial Embolism/thrombosis?

A

Atrial Fibrillation- abnormal heart rhythm Injury or damage to an artery wall
High platelet count – condition that increase blood clotting (Hypercoagulability)
Mitral stenosis
Endocarditis (infection inside of the heart)
Family history of atherosclerosis
South Asian, African or Afro-Caribbean descent

124
Q

Differentials of Arterial Embolism/thrombosis?

A

DVT

PE

125
Q

Investigations of Arterial Embolism/thrombosis?

A

Angiography of the affected extremity or organ Doppler ultrasound exam Duplex doppler
ultrasound Echocardiogram
MRI of the arm and leg Myocardial contrast echocardiography Plethysmography Transcranial doppler exam of arteries to the brain Transoesophageal echocardiography (TEE)

126
Q

Pharmacological treatment of Arterial Embolism/thrombosis?

Aim:
Requires treatment at a hospital. The goals of treatment – to control symptoms and improve the interrupted blood flow

A

Anticoagulants (e.g. warfin or heparin) can prevent new clots from forming

Antiplatelets: aspirin or clopidogrel – can prevent new clots from forming painkiller Given intravenously Thrombolytics – such as streptokinase – to dissolve the clot

127
Q

Surgical treatment of Arterial Embolism/thrombosis?

A

Bypass of the artery (arterial bypass) to create a second source of blood supply

Clot removal through a balloon catheter placed into the affected artery or through open surgery on the artery(embolectomy) Opening of the artery with a balloon catheter (angioplasty) with or without a stent

128
Q

Complications of Arterial Embolism/thrombosis?

A
Acute MI
 Infection in the affected tissue 
Septic shock Stroke Temporary or permanent decrease or loss of other organ function
 Temporary or permanent kidney failure
Tissue death and gangrene
 TIA – Transient ischaemic attack
129
Q

what is an aortic aneurysm?

A

Permanent and irreversible dilatation of a blood vessel by at least 50% of the

normal expected diameter. Aortic aneurysms are classified as abdominal (the
majority) or thoracic.

130
Q

what is an Thoracic aneurysm?

A

caused by Atherosclerosis (Atherosclerosis is a disease in which plaque builds up inside your arteries. Arteries are blood vessels that carry oxygen-rich blood to your heart and other parts of your body.

Plaque is made up of fat, cholesterol, calcium, and other substances found in the blood. Over time, plaque hardens and narrows your arteries)

131
Q

Aetiology of AAA?

A

> 70s

No specific identifiable causes

132
Q

Risk factors of AAA?

A
Mostly occurs in older people who smoke 
Genetic 
Atheroma – 
High blood pressure ,
 diabetes ,
 raised cholesterol levels , obesity
Vascular inflammation 
Male Sex 
Increasing age over 60 
Hypertension
COPD
Hyperlipidaemia 
Sedentary lifestyle 

Trauma
Infection – HIV, TB
Inflammation diseases – Bechet Diseases
Connective tissue disorder – Marfan Syndrome

133
Q

Signs and Symptoms of AAA?

A
Unruptured AAA 
Asymptomatic 
Possible Signs and Symptoms: 
Pain in the back, loin or groin:
Back pain may be due to erosion of the vertebral bodies 
Pulsatile abdominal swelling 
Distal embolization
Inflammation fibrosis e.g back pain, weight loss 

Ruptured AAA
Pain in the abdomen , loin and back
Syncope shock and collapse

134
Q

Differential diagnosis of AAA?

A

Gallstones
Acute gastritis
Myocardial infarction
Small bowel obstruction

135
Q

Investigations of AAA?

A

X-ray
Ultrasound
CT Scan of the abdomen
Abdominal MRI

136
Q

Treatment and management of AAA?

A

Surgical treatment:
- Two types:
Traditional operation: cut out the bad piece of the aorta , replace with an artificial piece of artery (a graft)
Endovascular repair : A tube is passed up from inside one of the leg blood vessels(arteries) into the area of the aneurysm = passed across the widened aneurysm and fixed to the good aorta wall using metal clips.

As there is a high risk of MI and Stroke 
Conservative: 
Healthy diet – low salt intake 
Exercise 
Smoking cessation