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Y2 Clinical Pathology > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is CVD

A

Cardiovascular disease
An umbrella term used to describe all conditions of the heart and blood vessels both congenital diseases and acquired conditions

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2
Q

What is ischaemic heart disease

A

Generic designation for a group of syndromes resulting from myocardial ischaemia (an imbalance between demand and supply of oxygenated blood to the heart)
Almost always caused by coronary artery atherosclerosis
Sometimes due to hypertrophy (demand)

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3
Q

What are the ischaemic heart disease syndromes

A

Myocardial infarction (duration and severity of ischaemia causes myocardial death)
Angina pectoris (ischaemia is less severe and does not cause myocardial death)
Chronic IHD with heart failure
Sudden cardiac death

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4
Q

What are the types of angina

A

Stable angina: typical angina
Prinzmetal angina: variant angina due to vasospasm rather than atherosclerosis
Unstable angina: crescendo angina

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5
Q

Where is the prevalence of IHD highest in the UK

A

Northern England and Scotland

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6
Q

What are the medical risk factors of IHD

A 
High blood pressure
High blood cholesterol (high HDL and low TC:HDL ratio)
Diabetes 
Lifestyle:
-smoking
-obesity
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7
Q

What is the pathogenesis of IHD

A

Myocardial ischaemia is a consequence of reduced blood flow in coronary arteries, due to a combination of fixed vessel narrowing and abnormal vascular tone as a result of atherosclerosis and endothelial dysfunction. This leads to an imbalance between myocardial oxygen supply and demand

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8
Q

What is myocardial infarction and what are the types

A

Death of cardiac muscle from prolonged ischaemia

Transmural vs subendocardial

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9
Q

What are the complications of myocardial infarction

A

Arrhythmias - either directly or by limited perfusion to the conduction system structures
Congestive cardiac failure - contractility dysfunction or by papillary muscle infarct sever myocardial rupture
Thromboembolism
Pericarditis
Ventricular aneurism
Cardiac tamponade
Cardiogenic shock

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10
Q

What is hypertension

A

A sustained diastolic pressure greater than 90mm Hg or sustained systolic pressure greater than 140 mm Hg

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11
Q

What causes primary hypertension

A

Majority unknown cause (90%)
Multifactorial:
-Genetics (insulin resistance- metabolic syndrome)
-Environmental (Obesity, alcohol, smoking, stress, Na+ intake)

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12
Q

How is blood pressure calculated

A

BP= cardiac output x peripheral resistance

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13
Q

What is malignant hypertension

A

BP> 180/120mmHg
Clinically signs and symptoms of organ damage
-acute hypertensive encephalopathy
-and/or nephropathy
-with retinal haemorrhages/ papilloedema
Requires urgent treatment to preserve organ function

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14
Q

What are potential hypertension complications

A

Hypertensive renal disease

Hypertensive cerebrovascular disease

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15
Q

What is systemic (left-sided) hypertensive heart disease

A

Hypertrophy of the heart is an adaptive response to pressure overload that can lead to myocardial dilation, congestive heart failure and sudden death
Left ventricular concentric hypertrophy
History or pathological evidence for hypertension

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16
Q

What is Cor Pulmonale

A

Pulmonary (right sided) hypertensive heart disease
Right ventricular hypertrophy, dilation and potentially heart failure secondary to pulmonary artery hypertension caused by disorders of the lung or pulmonary vasculature
Right ventricular hypertrophy secondary to diseases of the left side and congenital causes are generally excluded in the definition; but pulmonary venous hypertension that follows left sided diseases is quite common

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17
Q

What are aneurysms

A

A localised abnormal dilation of a blood vessel or the wall of the heart
True aneurysm - when bounded by arterial wall components or the attenuated wall of the heart
False aneurysm - (pseudoaneurysm) is a breach in the vascular wall leading to an extravascular haematoma that freely communicates with the intravascular space (pulsating haematoma)
Can rupture

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18
Q

What is an arterial dissection

A

Arises when blood enters the wall of an artery, as a haematoma dissecting between its layers
Dissections may, but do not always, arise in aneurysmal arteries
Can rupture

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19
Q

What causes aneurysms

A 
Atherosclerosis
Cystic medial degeneration
Trauma
Congenital defects
Infections (mycotic aneurysms)
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20
Q

What are risk factors for abdominal aortic aneurysm

A

Smoking
Male
Hypertension
Advanced age

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21
Q

What is heart failure/congestive cardiac failure

A

Inability of the heart to pump enough blood needed to meet the metabolic demands of the tissue
Can occur gradually or suddenly:
-Cumulative effects of chronic workload (hypertension and valve diseases) - Insidious
-Acute haemodynamic stress (fluid overload and large myocardial infarction)- sudden

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22
Q

What are the clinical effects of left sided heart failure caused by

A

Low cardiac output and hypo perfusion of tissues

Pulmonary congestion

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23
Q

How does pulmonary congestion present

A 
Dyspnea
Orthopnea
PND (paroxysmal nocturnal dyspnea)
Blood tinged sputum
Cyanosis
Elevated pulmonary "WEDGE" pressure (PCWP) (nl=2-15mmHg)
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24
Q

How does low cardiac output present

A

Reduced kidney perfusion:

  • Pre-renal azotemia
  • Renin-angiotensin-aldosterone activation
  • -salt and fluid retention ( expansion of interstitial and intravascular fluid volume

Advanced cardiac failure can lead to cerebral hypoxia - irritability, restlessness, stupor and coma

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25
Q

What are the symptoms and signs of right sided heart failure

A

Engorgement of systemic and portal venous systems results in:

  • Liver and spleen (portal congestion:
  • -Passive congestion (nutmeg liver)
  • -Congestive splenomegaly
  • -Ascites
  • -Congestion and oedema of bowel wall
  • Pleura/Pericardium (systemic venous congestion)
  • -Pleural and pericardial effusions
  • -Transudates
  • -Oedema of peripheral and dependent parts of body
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26
Q

What causes calcific aortic stenosis

A

Consequence of age-related wear and tear of either normal valve or congenital bicuspid aortic valve (which undergoes more mechanical stress and so becomes stenotic earlier)

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27
Q

What results from aortic stenosis

A 
2x gradient pressure
Left ventricular hypertrophy but no hypertension
Ischaemia
Angina
cardiac decompensation
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28
Q

What is the prognosis for aortic stenosis

A

50% die in 5 years if angina present

50% die in 2 years if congestive heart failure present

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29
Q

What is acquired aortic stenosis

A

Calcification of a deformed (congenitally bicuspid) valve
-senile calcification of anatomically normal aortic valve >70 yo
Rheumatic heart disease

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30
Q

What cause acquired mitral stenosis

A

Rheumatic heart disease

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31
Q

What is rheumatic heart disease

A 
Follows a group A strep infection, a few weeks later
Acute:
-inflammation
-Aschoff bodies
-Anitschkow cells
-Pancarditis
-Vegetations on chordae tendinae at leaflet junction
Chronic:
-thickened valves
-commisural fusion
-thick, short chordae tendinae
Mitral valves always involved
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32
Q

What is mitral valve prolapse

A

Myxomatous degeneration of the mitral valve
Unknown cause but associated with connective tissue disorders (Marfan syndrome)
Floppy valve
Easily seen on echocardiogram

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33
Q

What are the clinical features of mitral valve prolapse

A

Usually asymptomatic
Mid-systolic click
Holosystolic murmur if regurgitation present
Occasional chest pain
Dyspnea
97% no untoward effects
3% infective endocarditis, mitral insufficiency, arrhythmias, sudden death

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34
Q

What is mitral annular calcification

A

Degenerative calcification of the mitral skeleton
Usually no dysfunction
Regurgitation usually but stenosis possible
Arrhythmias and sudden death
Increased risk of infective endocarditis and embolic stork from dislodged overlying thrombi

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35
Q

What are congenital heart defects

A

Abnormalities of the heart and great vessels present from birth (may not be evident until adult life)
Faulty embryogenesis (week 3-8)
Usually Mono- morphic (single lesion)
1% of births

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36
Q

What environmental factors can result in congenital hear defects

A

Rubella (congenital rubella syndrome)
Gestational diabetes
Teratogens

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37
Q

What is ASD

A

Atrial septal defect
Abnormal fixed opening in atrial septum by incomplete tissue formation that allows communication of blood between the left and right atria
Usually asymptomatic until adulthood
Mortality is low following repair

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38
Q

How is ASD classified

A

According to location
Secundum (90%): defective fossa ovalis (near centre of atrial septum
Primum (5%): adjacent to AV valves, mitral cleft
Sinus venosus (5%): near entrance of SVC with anomalous pulmonary veins draining to SVC or RA

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39
Q

What is ventricular septal defect

A

Most common CHD defect
only 30% are isolated
Often with tetralogy of fallot
Classified according to size and location
90% involve the membranous septum (membranous VSD)
10% involve the muscular septum or lie below pulmonary valve (infundibular VSD)
If muscular septum is involved, can have multiple holes (Swiss cheese septum)
Small ones often close spontaneously
Large ones progress to pulmonary hypertension

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40
Q

Which defects shunt blood from right to left

A 
Tetralogy of Fallot
Transposition of great arteries
Truncus arteriosus
Total anomalous pulmonary venous connection
Tricuspid atresia
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41
Q

What is tetralogy of Fallot

A

Large VSD
Obstruction of RV outflow tract (subpulmonary stenosis)
Aorta overrides the VSD
RVH
Due to anterosuperior displacement of the infundibular septum during embryogenesis
Survival depends on severity of subpulmonic stenosis
Classical TOF is cyanotic congenital heart disease

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42
Q

What are the types of obstructive CHD

A

Coarctation of aorta
Pulmonary stenosis/atresia
Aortic stenosis/ atresia

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43
Q

What are the two forms of coarctation of aorta

A

Infantile form:

  • Proximal to PDA
  • Shunting of deoxygenated blood via PDA produces cyanosis in lower half of body
  • Serious

Adult form:
-Closed ductus
-Typically hypertension in the upper extremities and hypotension and weak pulses in lower extremities and features of arterial insufficiency (claudication and coldness)
Development of collateral circulation between pre-coarctation arterial branches and post-coarctation arteries though enlarged intercostal and internal mammary arteries causing visible erosions (notching) of the undersurface of the ribs

Bicuspid aortic valve 50% of the time

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44
Q

What is peripheral vascular disease

A

Atherosclerosis of arteries supplying legs or arms leading to the narrowing of the vessel lumen and restriction of blood flow

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45
Q

Who gets peripheral vascular disease

A 
Smokers
Obese people
Age>40
Family history
Men or post menopausal women
Those with a PMH:
-Diabetes
-Hypercholesterolaemia
-Hypertension
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46
Q

What is the process of atherosclerosis

A

Normal artery -> Endothelial disfunction -> Fatty streak formation -> Stable (fibrous) plaque formation -> Unstable plaque formation

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47
Q

How does peripheral vascular disease make a patient ill

A

Chronic (gradual atherosclerosis) or Acute (plaque rupture or thrombus formation) -> narrows lumen -> Reduced blood flow -> Ischaemia -> Tissue damage/death

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48
Q

What does peripheral vascular disease look like

A 
6 Ps
Pale
Pulseless
Painful
Paralysed
Paraesthetic
Perishing cold
49
Q

What is giant cell arteritis

A

Also known as temporal arteritis
Type of vasculitis affecting the large arteries in the head
Considered a medical emergency as it can lead to blindness
Most common form of vasculitis

50
Q

Who gets giant cell arteritis

A

Older individuals, very rare <50 years old
F>M
US/ Europe
PMH of polymyalgia rheumatica

51
Q

How does giant cell arteritis make the patient ill

A

Chronic granulomatous inflammation -> thickens wall of artery -> Narrows lumen -> Reduced blood flow -> Ischaemia -> tissue damage/ death

52
Q

What are the clinical features of giant cell arteritis

A

Flu like symptoms:

  • Fatigue
  • Weight loss
  • Fever

Pain:

  • Tender superficial temporal artery/ scalp
  • Jaw claudication (when eating)

Vision problems:

  • Blurred vision
  • Blindness

Stroke

53
Q

What is infective endocarditis

A

Infection and inflammation of the endocardium (lining of the heart) mainly involving the valves

54
Q

What is the epidemiology of infective endocarditis

A

Patients with:

  • Structurally abnormal valves (rheumatic heart disease, congenital heart disease, age-related valve calcification)
  • Foreign material in the heart (ICD, prosthetic valves)
  • Immunosuppression (HIV)
  • Bacteraemia (IVDU, Long term IV catheter (dialysis), colorectal cancer, dental procedures)

Can occur in healthy patients with normal hearts with virulent organisms (eg s. aureus)

55
Q

What is the aetiology of infective endocarditis

A

Bacteria (common)

  • Streptococcus
    • viridanse (dental procedures)
    • bovis (colorectal cancer)
  • Staphylococcus
    • aureus (normal hearts of healthy patients
    • epidermis (prosthetic valves

Fungi (rare)

  • Candida
  • Aspergillus
56
Q

How does infective endocarditis present clinically

A 
Splenic infarct
Splinter haemorrhages 
Janeway lesions
Oslers nodes
Roth spots
57
Q

What is pericarditis

A 
Inflammation of the pericardial sac
Acute:
-serofibrinous
-caseous
-haemorrhagic
-purylent
Chronic:
-constrictive
58
Q

What causes pericarditis

A

Infections:

  • Viruses (coxsackie B)
  • Bacteria
  • TB
  • Fungi
  • Parasites

Autoimmune:

  • Rheumatic fever
  • SLE
  • Scleroderma
  • Drug hypersensitivity
  • Post-MI (dressler’s syndrome)

Miscellaneous:

  • Uraemia
  • Radiation
  • Neoplasia
  • Trauma (including surgery)
59
Q

How does pericarditis present clinically

A

Central chest pain (exacerbated by breathing in, laying flat)
Pericardial friction rub
Fever
Pericardial effusion (may lead to cardiac tamponade)
Heart failure (with constrictive pericarditis)

60
Q

What is myocarditis

A

Inflammation of myocardium

61
Q

What causes myocarditis

A

Infections:

  • Viruses (adenovirus ‘common cold’, coxsackie A and B, ECHO, influenza, HIV, CMV)
  • Bacteria (C.diptheriae, N. meningococcus, Borrelia)
  • Fungi (candida, histoplasma)
  • Protozoa (Trypanosoma Cruzi ‘Chagas disease’)
  • Helminths (trichinosis)

Immune mediated:

  • Post group A streptococcus
  • SLE/ other autoimmune conditions
  • Drugs (methyldopa, sulphonamides)
  • Rejection of heart transplant

Other:
-Sarcoidosis

62
Q

How does myocarditis make a patient ill

A

Inflammation of myocardium -> dysfunctional myocardium -> Electrical dysfunction (arrhythmias/sudden death) or mechanical dysfunction (heart failure)

63
Q

How does myocarditis present clinically

A

Broad spectrum of changes:

  • asymptomatic
  • chest pain
  • heart failure
  • arrhythmias
  • sudden death
64
Q

What is rheumatic fever

A

A rare complication of group A streptococcal pharyngitis that affects the heart (and other parts of the body)

65
Q

Who gets rheumatic fever

A

Children
Developing countries (rare in UK now)
Often have recent history of a sore throat

66
Q

What causes rheumatic fever

A

3% of un-treated Group A streptococcus infection (streptococcus pyogenes)

67
Q

How does rheumatic fever make a patient ill

A

Group a strep infection -> antibodies made against M protein on the surface of the strep pyogenes bacteria -> antibodies also recognise proteins on surface of cells (self antigens) in the:

  • heart
  • skin
  • joints
  • CNS
68
Q

How does rheumatic fever present

A

Heart:

  • Endocarditis (mitral valve stenosis ‘fish mouth’ most common valve lesion, vegetations ‘verrucae’)
  • Myocarditis
  • Pericarditis

Skin:

  • Subcutaneous nodules
  • Erythema marginatum

Joints:
-arthritis

CNS:
-Sydenhams chorea

General symptoms:

  • Fever
  • malaise
69
Q

What is a cardiomyopathy

A

Heart muscle disease

70
Q

What are the 4 main types of cardiomyopathy

A

Dilated
Hypertrophic
Restrictive
Arrhythmogenic right ventricular cardiomyopathy

71
Q

Who gets hypertrophic cardiomyopathy and why

A

All ages and genders

Due to genetics

72
Q

How does a patient become sick with hypertrophic cardiomyopathy

A

Impaired ventricular filling
± left ventricular outflow obstruction (1/3 of cases)
Relative ischaemia

73
Q

What are the clinical features of hypertrophic cardiomyopathy

A

Heart failure
Arrhythmias and sudden death (especially in young athletes)
Mural thrombus formation ± embolisation
Chest pain (ischaemia)

74
Q

Who gets dilated cardiomyopathy and why

A 
Any age but commonly males aged 20-50yo
Cause:
-Often unknown
-Genetic ( ~50% of cases)
-Alcohol
-Catecholamines
-Pregnancy
-Haemochromatosis
-Infection 
-Lots of other causes
75
Q

What are the clinical features of dilated cardiomyopathy

A

Heart failure
Thrombus ± emboli
Arrhythmias and sudden death

76
Q

What is the pathogenesis of dilated cardiomyopathy

A

Dilated and thin walled ventricular chambers -> impaired ventricular pumping (decreased LVEF)

77
Q

What causes restrictive cardiomyopathy

A 
Idiopathic
Secondary:
-amyloidosis
-sarcoidosis
-metastatic tumours 
-deposition of metabolites (inborn errors of metabolism)
78
Q

Why does restrictive cardiomyopathy make a patient ill

A

impaired ventricular filling

79
Q

What are the clinical features of restrictive cardiomyopathy

A

Heart failure
Arrhythmias and sudden death
Mural thrombus formation ± embolisation

80
Q

What causes arrhythmogenic RV cardiomyopathy and in who

A

Genetics

Most common in young males

81
Q

How does arrhythmogenic RV cardiomyopathy make a patient ill

A

RV myocyte adhesion impaired due to mutation in desmosome proteins -> cells detach -> fibrofatty tissue forms in attempt to repair damage -> interferes with muscle contraction and electrical conduction

82
Q

What are the clinical features of arrhythmogenic RV cardiomyopathy

A 
Palpitations
Syncope
Heart failure
Thrombus ± emboli
Arrhythmias and sudden cardiac death (often exercise induced)
83
Q

What is a vascular infection

A

There is a source of infection in the heart or vascular system

84
Q

What is bacteraemia

A

Not a diagnosis but simply means bacteria have been detected in the blood

85
Q

What is a bloodstream infection

A

Bacteraemia and symptoms/ signs of infection

86
Q

What are the types of bacteraemia

A

Transient
Intermittent
Continuous

87
Q

When should CRBSI be considered as a diagnosis

A

Intravascular catheter related bloodstream infection

In any patient with an intravascular catheter and systemic signs of intection or bacteraemia or fungaemia

88
Q

What is infective endocarditis

A

Infection of the endocardium or devices within the heart

89
Q

How does infective endocarditis present

A 
Non-specific illness (lethargy, malaise, night sweats, anorexia, weight loss)
Heart failure (SOB, orthopnea, PND)
Results of extra-cardiac foci of infection (back pain from HVO, stroke, abdominal pain from splenic infarct)
90
Q

How is infective endocarditis diagnosed

A

Echocardiography (trans thoracic and trans oesophageal)

3 sets of blood cultures at different times (2 sets in severe sepsis)

91
Q

What is the non-antimicrobial management of infective endocarditis

A

Surgery:

  • replace or repair damage valves
  • remove infection when antimicrobials don’t work
  • remove infected devices
  • Prevent complications (eg stroke)
  • Drain purulent collections (eg in spleen or spine)
92
Q

What is the antimicrobial management of infective endocarditis

A
  • Antimicrobial therapy - ideally directed towards pathogens identified by blood cultures
  • 4-6 weeks treatment usually IV but some switch to oral
  • Example flucloaxacillin 2g 6 hourly IV for S.aureus
93
Q

What is a mycotic aneurysm

A

Aneurysms resulting from or secondarily infected by microorganisms

94
Q

What is the pathogenesis of mycotic aneurysm

A

Haematogenous seeding
Trauma to arterial wall and direct contamination
Extension from a contiguous infected focus
Secondary to septic microemboly

95
Q

How does mycotic aneurysm present

A

Usually systemic symptoms of infection and variable symptoms from aneurysm depending on location:

  • No localising symptoms
  • Painless swelling
  • Symptoms caused by rupture (eg intracerebral haemorrhage, collapse)
96
Q

How is a mycotic aneurysm diagnosed

A

Imaging and detection of bacteria within tissue

97
Q

How is a mycotic aneurysm managed

A

Surgical removal, stunting or coiling (depending on location) with antibiotics

98
Q

How does an infected DVT present

A

Signs and symptoms of DVT and systemic infection and/or respiratory symptoms (when infected thrombus breaks from DVT travels via the venous system to the lungs and results in pulmonary emboli)

99
Q

What is the aetiology of infected DVT

A

Depends on mechanism but commonly S. aureus, streptococci and anaerobes in IVDU

100
Q

How is infected DVT diagnosed

A

Multiple (3) blood cultures, confirmation of DVT bolus exclusion of other causes eg IE

101
Q

How is an infected DVT managed

A

Antibiotics plus anticoagulation

102
Q

What are the types of primary infections of the central nervous system

A

Meningitis
Encephalitis
Brain abscess

103
Q

What is meningitis

A

An infection of the protective membranes that surround the brain and spinal cord (meninges)
Medical emergency
Can cause life-threatening septicaemia and result in permanent damage to the brain or nerves

104
Q

What is encephalitis

A

An uncommon but serious condition in which the brain becomes inflamed (swollen)

105
Q

What is a brain abscess

A

AKA cerebral abscess
An abscess caused by inflammation and collection of infected material within the brain tissue
A focal suppurative process within the brain parenchyma (pus in the substance of the brain)

106
Q

How is meningitis classified

A

Acute pyogenic: usually bacterial meningitis
Aseptic: usually viral meningitis, lymphocytic pleocytosis
Chronic: mycobacterium tuberculosis (TBM), spirochetes (neurosyphilis), Cryptococcus neoformans

107
Q

How can infectious agents enter CNS

A

Haematogenous spread: most common, usually via arterial route, can by retrograde (veins)
Direct implantation: most often is traumatic, iatrogenic (rare), congenital (meningomyelocele)
Local extension: secondary to established infections, most often from mastoid, frontal sinuses, infected tooth etc
Along peripheral nerves: usually viruses (rabies, herpes zoster)

108
Q

What are the clinical features of meningitis

A 
Headache
Irritability
Neck stiffness
Photophobia
Fever
Vomiting
Varying levels of consciousness
Rash
109
Q

Which groups may have non specific presentations of meningitis

A

Neonates
Elderly
Immunosuppressed

110
Q

How is meningitis diagnosed in the lab

A

Blood cultures
Lumbar puncture: CSF for microscopy, gram stain, culture and biochemistry
EDTA blood for PCR

111
Q

How does viral meningitis present

A

Primarily affects children and young adults
Milder signs and symptoms
May start as respiratory or intestinal infection then viraemia
CSF shows raised lymphocyte count (50-200/cu mm); protein and sugar usually normal
Full recovery expected

112
Q

What causes viral meningitis

A 
Enteroviruses (echo, coxsackie A, B)
Paramyxovirus (mumps)
Herpes simplex, varicella zoster virus
Adenoviruses
Other: arboviruses, lymphocytic choriomeningits, HIV
113
Q

What are the symptoms of encephalitis

A 
Fever
Headache
Behavioural changes
Altered level of consciousness
Focal neurologic deficits
Seizures
114
Q

What is the incidence of encephalitis

A

3.5-7.4 per 100,000 persons per year

115
Q

What are the causes of viral encephalitis

A

Herpes viruses (HSV-1, HSV-2, Varicella Zoster virus, Cytomegalovirus, Epstein-Barr virus, Human Herpes virus 6)
Adenoviruses
Influenza A
Enteroviruses, Poliovirus
Measles, Mumps and Rubella
Rabies
Arboviruses (Japanese encephalitis; St. Louis encephalitis virus; West Nile encephalitis virus)

116
Q

What is recurrent meningits

A

> 2 episodes meningits
Symptom free intervals
Normal CSF between episodes
Must be differentiated from chronic meningitis

117
Q

How do brain abscesses present clinically

A 
Headache (most)
Focal neurological deficit (30-50%)
Fever (<50%)
Nausea, vomiting
Seizures
Neck stiffness
Papilloedema
118
Q

How are brain abscesses managed

A

Drainage is treatment of choice (but small ones can be treated with antibiotics alone):

  • Urgently reduces intracranial pressure
  • to confirm diagnosis
  • to obtain pus for microbiological investigation
  • to enhance efficacy of antibiotics
  • to avoid spread of infection into ventricles
119
Q

What are the principles in antibiotic treatment of CNS infections

A
  • Physiological properties of blood-brain barrier and blood CSF-barrier are distinct
  • Penetration of drugs into CSF and brain tissue differ
  • Ampicillin, Penicillin, Cefotaxime, Ceftazidime, and Metronidazole achieve therapeutic concentrations in intracranial pus

Y2 Clinical Pathology (11 decks)

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