WEEK 1: Tuberculosis immunology Flashcards
Your patient, who is receiving Pyrazinamide, report stiffness and extreme pain in the right big toe. The site is extremely red, swollen, and warm. You notify the physician and as the nurse you anticipated the doctor will order?
A. Calcium level
B. Vitamin B6 level
C. Uric acid level
D. Amylase level
c
You note your patient’s sweat and urine is orange. You reassure the patient and educate him that which medication below is causing this finding?
A. Ethambutol
B. Streptomycin
C. Isoniazid
D. Rifampin
D
A patient with active tuberculosis is taking Ethambutol. As the nurse you make it priority to assess the patient’s?
A. hearing
B. mental status
C. vitamin B6 level
D. vision
The answer is D. This medication can cause inflammation of the optic nerve. Therefore, it is very important the nurse asks the patient about their vision. If the patient has blurred vision or reports a change in colors, the MD must be notified immediately.
A patient taking Isoniazid (INH) should be monitored for what deficiency?
A. Vitamin C
B. Calcium
C. Vitamin B6
D. Potassium
The answer is C. This medication can lead to low Vitamin B6 levels. Most patients will take a supplement of B6 while taking this medication.
. A patient is taking Streptomycin. Which finding below requires the nurse to notify the physician?
A. Patient reports a change in vision.
B. Patient reports a metallic taste in the mouth.
C. The patient has ringing in their ears.
D. The patient has a persistent dry cough.
The answer is C. This medication can be very toxic to the ears (cranial nerve 8). Therefore, it is alarming if the patient reports ringing in their ears, which could represent ototoxicity.
Outline TB treatment drugs.
First-line anti-tuberculosis drugs: 6-8/12 treatment
Isoniazid (H) Bactericidal
Rifampin (R) Bactericidal
Streptomycin (S) Bactericidal
Ethambutol (E) Bactericidal
Pyrazinamide (Z) Bactericidal
Second-line anti-tuberculosis drugs: MDR-TB
Fluroquinolones (ofloxacin, ciprofloxacin): Bactericidal
Thioamides(ethinoamide,prothionamide): Bacteristatic
Cycloserine Bacteristatic
Paraminosalicylic acid (PAS) Bacteristatic
Thiacetazone Bacteristatic
Kanamycin/amikacin Bactericidal
Compare MDR-TB (Multidrug-Resistant Tuberculosis) and XDR-TB (Extensively Drug-Resistant Tuberculosis).
MDR-TB (Multidrug-Resistant Tuberculosis):
Definition: MDR-TB is tuberculosis that is resistant to at least two of the most powerful first-line anti-TB drugs, isoniazid and rifampicin.
Causes: MDR-TB arises due to improper use of anti-TB medications, including incomplete treatment regimens, incorrect dosages, or use of poor-quality drugs. It can also result from transmission of drug-resistant strains from person to person.
Treatment Challenges: MDR-TB requires treatment with second-line drugs, which are less effective, more toxic, and often more expensive than first-line drugs. Treatment regimens for MDR-TB are longer (typically lasting 9-24 months) and have a lower success rate compared to drug-susceptible TB.
Control Measures: To prevent the emergence and spread of MDR-TB, it is crucial to ensure proper management of TB cases, including accurate diagnosis, appropriate treatment, and measures to prevent transmission in healthcare settings and communities.
XDR-TB (Extensively Drug-Resistant Tuberculosis):
Definition: XDR-TB is a form of MDR-TB that is additionally resistant to fluoroquinolones and at least one of three injectable second-line drugs (amikacin, kanamycin, or capreomycin).
Causes: XDR-TB develops when MDR-TB strains acquire additional resistance to second-line drugs, often due to inadequate treatment regimens, poor adherence to treatment, or transmission of resistant strains.
Treatment Challenges: Treatment options for XDR-TB are limited and often less effective due to the high level of resistance. XDR-TB is associated with poorer treatment outcomes, higher rates of treatment failure, and increased mortality compared to MDR-TB.
Control Measures: Preventing the emergence and spread of XDR-TB requires robust TB control programs, including prompt detection of drug resistance, access to quality-assured diagnostic tests, appropriate treatment regimens, infection control measures, and public health interventions to limit transmission.
Describe type I hypersensitivity (Anaphylactic)
Type 1 hypersensitivity is caused when an antigen binds to IgE molecules attached to receptors on the surfaces of tissue mast cells and circulating basophils.
If the antigen cross-links these receptors it causes the cells to degranulate releasing their contents, primarily histamine. The cells also release prostaglandins and leukotrienes and a variety of cytokines which continue the response after the effects of histamine have diminished.
Histamine is a vasoactive amine – it produces an inflammatory reaction, often including localised oedema as blood vessels become leaky, secretion of mucus, and effects on smooth muscle.
This response is part of the normal immune response to parasite infection, but it can also be produced in response to innocuous environmental antigens (allergens) like grass pollen, animal dander etc., when it becomes a hypersensitivity.
Type 1 hypersensitivity can be localized where it gives rise to asthma, hay fever, eczema etc.
Or it can be systemic, leading to anaphylactic shock a potentially fatal hypersensitivity response to normally innocuous stimuli such as an antibiotic, food material, or insect bite or sting.
Describe type II hypersensitivity (Cytotoxic Hypersensitivity)
This arises when antibodies directed against cell surface antigens cause destruction of the cell by a complement mediated reaction or by antibody- dependant cell mediated cytotoxicity (ADCC).
Because complement activation and ADCC are only produced by IgG and IgM type antibodies this is mediated by IgG and IgM.
The mechanism involved here is the normal immune response to pathogen cells in the blood and intracellular fluids. It becomes a hypersensitivity when it is directed against the body’s own cells or cells administered therapeutically.
Transfusion reactions, hemolytic disease of the newborn, and drug induced hemolytic anaemia are examples of type 2 hypersensitivity, but it also plays a part in destruction of tissue by autoimmune reactions.
Describe type III hypersensitivity (immune complex mediated hypersensitivity)
When a soluble antigen is recognised and bound by an antibody, it forms an immune complex. Normally this complex is picked up and cleared by phagocytes, but if large amounts of antigen enter the blood or body fluid they may be formed in amounts too large to be cleared quickly.
These complexes deposit in areas where blood capillary constriction occurs or where plasma filtration takes place. The complexes activate complement, which generates small peptide fragments which are anaphylotoxins ie. they activate mast cells and generate a local inflammatory response.
Type 3 complex formation can be localised, or it can be generalised. The generalised form gives rise to serum sickness, most commonly produced by therapeutic use of large amounts of pre-formed antibody, such as horse antibodies used as snake bite anti-venom, or anti-rabies serum.
Symtoms include fever, weakness, rashes, oedema and erythema, and lymphadenopathy. Glomerular nephritis occurs when complexes lodge in glomeruli, and reactive arthritis occurs when complex deposition occurs in synovial joints.
Describe type IV hypersensitivity (Delayed type Hypersensitivity).
Delayed type hypersensitivity is caused when micro-organisms engulfed by macrophages are able to resist the macrophage digestive enzymes and live within the endocytotic vesicles of the cells.
The immune system combats this by displaying proteins derived from the engulfed micro-organisms on the cell surface attached to type 2 major histocompatibility antigens.
These foreign peptides are recognised by CD4 +ve T-cells (Th cells) .
Th 1 cells are cloned and recognise infected macrophages. They respond by secreting cytokines which activate the macrophages – they generate cytotoxic molecules usually containing oxygen or nitrogen free radicles (species with unpaired electrons, which are extremely reactive and damaging to tissue).
The cytokines also attract more macrophages to the area.
This is a normal immune response which is self limiting if it controls the organism, but if it fails to control the organism it becomes chronic and causes tissue damage.
This is the cause of tuberculosis and a number of other infective diseases, including leprosy.
Describe Type V (Stimulatory Hypersensitivity)
Stimulatory hypersensitivity is not part of the original Gell and Coombs classification, but it is often included as an extra type.
It arises when an antibody is raised against a receptor, and instead of producing a type 2 cytotoxic reaction which destroys the cell, it stimulates the receptor producing the same effect as the cognate ligand.
The most common example of type 5 hypersensitivity is Graves’ disease, a form of hyperthyroidism caused by an autoantibody which binds to the thyroid stimulating hormone receptor on thyroid cells.
In Graves’ disease levels of both thyroid hormones, T3 and T4, are raised but the level of thyroid stimulating hormone (TSH) is very low. This is because the binding of antibody to TSH receptor stimulates release of thyroid hormones in the same way that the cognate ligand, TSH would.
The elevated levels of T3 and T4 have a feedback inhibitory effect on TSH release.
What is the infective dose for mtb?
The infective dose is probably <100 bacillae.
