Brainscape's Knowledge GenomeTM

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


See full index

Pathology > Meningitis tutorial > Flashcards

Meningitis tutorial Flashcards

1
Q

What are the routes of CNS infection?

A
  • Haematogenous
  • Direct inoculation (trauma, neurosurgery)
  • Local extension (sinusitus, osteomyelitis)
  • Iatrogenic
  • Along nerves (rabies, herpes zoster)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the meninges?

A

They are a protective covering of the brain, comprising the Dura, Arachnoid and Pia

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

Where does cerebrospinal fluid originate, and where does it circulate?

A

It originates in the choroid plexus within the ventricles and circulates in the subarachnoid space which is between the arachnoid and the pia mater

When the CSF becomes inflamed, meningitis occurs

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

What is meningitis?

A

Meningitis is the inflamation of the meninges (inflammation of the arachnoid, pia and cerebrospinal fluid within the subarachnoid space

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

What are the 3 groupings for meningitis?

A
  • Septic - The subarachnoid space contains an acute inflammatory exudate.
  • Aseptic - Viral meningitis is grouped in here as no orgnaisms found on gram staining. The CSF will also contain mononuclear cells.
  • Chemical or non-infectious
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are some common causative agents in the following age groups

  • Neonates:
  • Infants:
  • Adolescents:
  • Elderly:
A
  • Neonates: E. coli, group B streptococci, mycobacterium tuberculosis
  • Infants: Haemophilus influenzae
  • Adolescents: Neisseria meningitidis
  • Elderly: Streptococcus pneumoniae, listeria monocytogenes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Descirbe Neisseria meningitidis

A

Its a capsulated (assists virulence) Gram -ve diplococcus.

N. Meningitidis is spread by droplets, and is a common coloniser of the oropharynx. It’s usually eliminated by an immune response.

Infection follows exposure to strains that we’ve not encountered before (e.g. some other peoples N. Meningitidis rather than our own)

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

Describe mycobacterium tuberculosis, how we can identify it, and what occurs on the 1st and secondary infection

A

It’s a slender aerobic rod bacteria, which can be identified with a Ziehl Neelsen or auramine fluorescent staining or with PCR

First infection causes an adaptive immune response with the activation of T cells. The secondary infection causes type 4 hypersensitivity and host tissue damage occurs.

It gains access to the meninges when the host defenses have failed and it builds up in the blood, this is called miliary TB

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

What occurs in the secondary infection with Mycobacterium tuberculosis? And what are the CSF findings?

A

Type 4 hypersensitivity occurs, and this leads to the formation of granulomas and fibrosis. This causes thickening of the meninges and obstruction to the flow of CSF.

The CSF has low sugar, as organisms use it as an energy source, and there are increased proteins (mainly in chronic, not much in acute). There are also lymphocytes and monocytes/macrophages present. Since this is chronic inflammation there is not as many WBC’s as an acute infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why do granulomas form?

A

Granulomas form due to the immune response to TB as monocytes are activated by cytokines from lymphocytes to form epthelioid cells (activated macrophages resembeling epithelial cells)

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

What are some viruses, fungi and protozoan that can cause meningitis?

A

Viruses: Entreroviruses, Herpes simplex type 2, Varicella zoster, Mumps

Fungi: Cryptococci, candida

Protozoan: Plasmodium

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

What are symptoms and signs of acute meningitis?

Also, what about for chronic?

A

Acute

  • Headache
  • Stiff neck
  • Positive Kernig’s sign - straight leg raising results in pain due to stretching of the meninges
  • Fever
  • Anorexia - later nausea and vomiting
  • Later - confusion and loss of consciousness (due to raised intracranial pressure)
    • Chronic: less dramatic with headache, feeling unwell, confusion and vomiting
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the Brudzinski’s neck sign?

A

Its a test for neck rigidity

Passive flexion of the neck causes flexion of both legs and thighs

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

What is Kernig’s sign?

A

When the patient is supine, with hip flexed 90 degrees, and the knee can’t be fully extended without extreme pain

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

Fill in the missing info for a normal CSF from a lumbar puncture

Colour:

Pressure:

Cells:

Protein:

Glucose:

A

Colour: Crystal clear

Pressure: 6-18 cm H2O

Cells:0-6 cells/ml csf. Usually mononuclear cells, 75% lymphocytes

Protein: 0.2-04 g/L

Glucose: Approx. 1/3 of serum glucose

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

What is the following info for csf from an LP from someone with acute bacterial meningitis?

Colour:

Pressure:

Cells:

Protein:

Glucose:

A

Colour/turbidity: Creamy colour, due to increased cells and protein. It is quite purulent.

Pressure: increased

Cells: Cell count is high

Protein: Increased due to inflammatory exudate

Glucose: Decreased as neutrophils and organisms use as energy source.

Gram stain: Organisms are identified

17
Q

Fill in the following for the csf from an LP from someone with Aseptic meningitis

Colour/Turbidity:

Pressure:

Cells:

Protein:

Glucose:

Gram stain:

A

Colour/Turbidity: Clear to cloudy

Pressure: Mild to moderate

Cells:Increased, mainly mononuclear

Protein: Moderate increase

Glucose: Normal range

Gram stain: Negative

18
Q

Fill in the following for the csf from someone with meningitis due to Chronic Tuberculosis

Colour/Turbidity:

Pressure:

Cells:

Protein:

Glucose:

Gram stain:

A

Colour/Turbidity: Cloudy, not purulent

Pressure: Mild to moderate

Cells: Increased, mainly mononuclear

Protein: Mild increase

Glucose: Mild to moderate decrease

Gram stain: Negative (can be identified by PCR and/or grown on special medium (slow process).

19
Q

What do we use to identify organisms from csf?

What can we use for suspected unusual organisms?

A

Routinely csf specimens would have: Gram stain, culture, protein and glucose assesment

For suspected unusualy organims: Ziehl Nielsen staining, PCR/latex agglutination detect microbial antigens

20
Q

What is the pathophysiology of meningitis?

A

Organisms first enter the csf, and this results in the release of cytolines from astrocytes and microglia.

The changes to the blood/brain barrier due to cytokines released results in increased permeability leading to vasogenic oedema and brain swelling - this causes raised intracranial pressure and the changes in consciousness and vomiting often seen.

There will be an acute inflammatory exudate thats forms in the subarachnoid space

21
Q

From the gross appearance, what can be seen in a brain thats had menigitis?

A

The brain is swollen, there is marked vasocongestion and dilation of the vessels, and there is also pus in the subarachnoid space especially around the brain stem and cerebellum.

22
Q

If treatment for meningitis is delayed, what can occur?

A

The exudate may become organised leading to fibrosis within the subarachnoid space.

Fibrous bands form around cranial nerves leading to palsies, and the blockage of csf flow may lead to hydrocephalus. And vasculitis of vessels the outer surface of cortex leads to cortical infarction. And epileptic fits begin to occur.

23
Q

What is bacteremia?

A

Bacteremia is when there is a non propagating organism in the blood. There are minimal to no mediators or toxins. There is also minimal or no endothelial tissue damage and coagulation. DIC is not possible in bacteremia.

24
Q

What is septicaemia?

A

Septicaemia is when there is a propagating bacteria present in blood which are producing toxins. There are maximal mediators and toxins, and maximal endothelial & tissue damage & coagulation. DIC is possible.

25
Q

What is DIC, and how does it occur?

A

Scattered, diffuse, exaggerated thrombosis in microcirculation.

It occurs due to the blood being to exposed sub-endothelial collagen, and due to the release of thromboplastin (tissue damage)

26
Q

What are the types of shock?

A
  • Cardiogenic
  • Hypovolemic
  • Neurogenic
  • Anaphylactic
  • Septic - especially due to Gram +ve bacteria
27
Q

Memorise this flow chart of septic shock from Gram negative organisms

A
28
Q

Understand (not memorise) this flow chart for pathogenesis of septic shock

A
29
Q

When gram -ve organisms enter the blood, what occurs with neutrophils and macrophages?

A

Gram -ve organisms bind and activate neutrophils and macrophages with release of cytokines IL-1, 6, 8 & TNF-a plus NO and platelet activating factor

the clinical condition that results in proportional to the amount of cytokines released

30
Q

How do gram +ve organisms cause septic shock?

A

The exotoxins on the cell surface or that are released bind to MHCll on Antigen presenting cells and T cells (can cause up to 10% of T cells to become acitvated), and this results in massive quanities of cytokines to be released, leading to septic shock

31
Q

What occurs to the physiology of the body during septic shock/septicaemia

A
  • There is vasodilation leading to low peripheral resistance, causing a decrease in blood pressure
  • There is a decrease in myocardial contractilty, leading to decreased BP
  • Endothelial damage, due to endotoxins, cytokine or decreased perfusion leakage results in decreased volume, and decreased blood pressure
  • DIC occurs, especially in microcirculation - results in microthrombi, decreasing perfusion
32
Q

Flow chart for DIC

A
33
Q

What id Disseminated intravascular coagulation?

A

It is the activation of both the clotting cascade and the fibrinolytic system at the same time. This leads to exhaustion of clotting factors, platelets, fibrinogen and Protein C with production of D-dimers from fibrin breakdown.

The affected patients bleed from drip sites, areas of trauma and areas of necrosis.

34
Q

How is DIC treated?

A
  • We remove the underlying cause, and replace the coagulation products.
  • In septic shock we use antibiotic therapy, fresh fozen plasma, coagulation products and packed red cells.
35
Q

What is Waterhouse-Friederichsen Syndrome?

A

Acute adrenal insufficiency due to massive haemorrhage into the adrenal glands. It is associated with septic shock which is caused by N. Meningitidis, pneumococcus and haemophilis influenzae

Pathology (6 decks)

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