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antipsychotics

ATYPICAL ANTIPSYCHOTIC

Atypical or second generation or novel 

Atypical or ‘2nd generation’. These medications have been used since the 1990s. These are newer types of antipsychotics.

  • These are sometimes referred to as ‘atypicals’

These are newer antipsychotic drugs on the Ugandan market and are less commonly used because they are  expensive. They are however the best antipsychotics because they control both negative and positive  symptoms of schizophrenia. These drugs are also associated with fewer side effects compared to the  typical antipsychotics. Are also called new antipsychotic drugs.

  • Some are also less likely to cause sexual side effects compared to first generation antipsychotics.

But second generation antipsychotics may be more likely to cause serious metabolic side effects. This may include rapid weight gain and changes to blood sugar levels, diabetes mellitus, hypercholesterolemia.

Mechanism of Action 

  • They block 5-HT2A-receptors with lesser degree of antagonism of D2-receptor. 
  •  Have efficacy against negative effects especially clozapine 
  •  As a result, they have fewer extrapyramidal adverse effects than the older traditional agents.
  • Atypical agents are serotonin-dopamine 2 antagonists (SDAS)
  • They are considered atypical in the way they affect dopamine and serotonin neurotransmission in the four key dopamine path way in the brain.

Classes of Atypical Antipsychotics

  •  Benzoxazoles- Risperidone 
  • Dibenzodiazepines – Clozapine  
  •  Thienobenzodiazepine- Olanzapine  
  •  Dibenzothiazepine- Quetiapine   
  •  Imidazolidinone – Sertindole 

Risperidone (Risperdal)

  • Available in regular tabs, I.M depot form and rapidly dissolving tablet.
  • Functions more like atypical antipsychotic at doses greater than 6 mg.
  • Increased extra pyramidal side effects (dose dependent) 
  • Most likely atypical to induce hyperprolactinemia. 
  • Weight gain and sedation (dose dependent) 
  • Hypotension, fatigue, abdominal pain, nausea.

Olanzapine (Zyprexa)

  • Available in regular tabs, immediate release I.M, rapidly dissolving tab, depot form. Dose 5mg-20mg/ day-OD /nocte.

Side effects

  • Sedation, weight gain, hypotension, anti cholinergic effects, changes in liver function tests.

Quetiapine (Seroquel)

  • Available in a regular tablet form only.
  • Dose: 100-400mg bid or DDD

Side effects

  • Weight gain,
  • Most likely to cause orthostatic hypotension 
  • Increase blood sugar-diabetes     

Clozapine (Clozaril) 

Available in one form-a regular tablet

  • Dose: 100-900mg bid or in  DDD

Side effects

  • Sedation , weight gain 
  • Hyper salivation

SIDE EFFECTS OF ANTI-PSYCHOTICS:

Extra pyramidal side effects:

Most of the anti-psychotic drugs may cause the imbalance of the neurotransmitters (excitatory and inhibitory) resulting into side effects known as extra pyramidal.

  1. Acute dystonia– uncontrolled muscular spasm. Muscle from spasm many part of the body, for example:
  • Oculogyric: crisis-eyes rolling upwards. 
  • Torticollis: head and neck twisted to the side

The patient may be unable to swallow or speak clearly. in extreme cases , the back may arch or the jaw dislocate.

Management: 

  • Give artane tablets or anticholinergic drugs given orally, I.M or I.V depending on the severity of symptoms.
  • Benzodiazepines like diazepam.
  • Some times change in medication, or lowering dose.
  1. Parkinsonian symptoms (pseudo-parkinsonism)
  • Tremor
  • Rigidity 
  • Bradykinesia: decreased facial expression, flat monotone voice, slow body movements, inability to initiate movement.
  • Mask like face
  • Bradyphrenia
  • Slowed thinking 
  • Salivation
  • Drooping posture.

Management 

  • Reduce the antipsychotic dose.
  • Change to atypical drug (as antipsychotic monotherapy)
  • Prescribe an anticholinergic like Artane.
  1. Akathisia (restlessness);  A subjectively unpleasant state of inner restlessness where there is a strong desire or compulsion to move.
  • Foot stamping when seated.
  • Constantly crossing or uncrossing legs.
  • Rocking from foot to foot.
  • Constantly pacing up and down.

Management

  • Reduce or lower the antipsychotic dose.
  • Give benzodiazepines like diazepam
  • Give beta blockers like propranolol 
  • Give an anti cholinergic like artane.
  1. Tardive dyskinesia (abnormal movement): It is an irreversible extrapyramidal syndrome usually common in patients who have been on anti-psychotics for long. It is characterized by persistent involuntary movement of all oral facial muscles.
  • Rabbit syndrome: lip smacking or chewing type movement as of a rabbit.
  • Tongue protrusion: fly catching.
  • Choreiform hand movements (pill rolling or piano playing)

Severe orofacial movement can lead to difficulty, speaking, eating, or breathing. Movements are worse when under stress.

Management:

  • Stop anti-cholinergic if prescribed
  • Reduce dose of anti psychotic.
  • Change to a typical drug.
  1. Neuroleptic malignant syndrome: It is rare but fatal (life threatening), occurs as a result of prolonged intake of anti psychotic drugs it is characterized by:
  • Severe mental, motor and autonomic disturbance.
  • Hyper tonicity increased muscle tone. There is an increased reflex to stimuli.
  • Generalized stiffness of the muscles affecting i.e. patient may find it unable to swallow.
  • Hyperpyrexia increased body temperature, because of that, they get profuse  sweating, this leads to fast dehydration
  •  There is increased blood pressure leading to tachycardia.

The mortality rate is 20 % as per global population. They need intensive medical and nursing.

For the above extra-pyramidal side effects, we use the following drugs to counter act them.

  • Benzhexol (artane)

We can use 2mg-4mg o.d /bid 4-5 days and then go back to PRN when acute. But otherwise, they are supposed to be given when necessary. It is under the group of anti-cholinergic drugs under the classification of drugs.

  • Benztropine mosylate (congetin)

It also falls under the group of anti-cholinergic.

Dose: 0.5-1mg to 4mg maximum o.d / PRN (orally) 

Injection: 1mg-2mg to I.m-PRN.

N.B: Children below 5yrs should not be given chlorpromazine (Largactil). Use haloperidol.

Other side effects as per systems.

Gastro intestinal tract(GIT)

  •  Dry mouth: Management: Rinsing of mouth with water (avoid candy ‘’sweetie’’ as carriers may result).
  •  Excessive salvation (sialorrhea): management give antiparkinsonian like artane or stop drug.
  •  Constipation: management: give high fibred diet, laxatives like bisacodyl
  •  Sedation: management: give smaller dose in the morning some patients can only cope with single night-time dosing. Reduce dose if necessary. 

Cardio vascular system:

  •  Postural hypotension (orthostatic hypotension): Management: advise patient to take time when standing up or change posture gradually. Reduce dose or slow down rate of increase 
  •  Cardiac arrhythmias (ECG changes): Management:  ECG monitoring, change drug.

Endocrine and metabolic system:

  •  Weight gain: Management: dietary control, exercise, change drug.
  • Galactorrhea (increased lactation): Management: change the drug
  • Amenorrhea: Management: change the drug.
  • Decreased libido: Management: reduce dose or change drug.

Haemotological.

  • Bone marrow depression.
  • Obstructive jaundice.

Ocular 

  • Blurred vision 
  • Glaucoma- increased intraocular pressure
  • Retina  pigmentation (may lead to blindness)

Genital and urinary systems.

  • Retention of urine-people can retain or pass urine 
  • Polyuria- excessive passage of urine of low specific gravity.
  • Impotence.

Allergic.

  • Photo sensitivity.
  • Skin pigmentation.
  •  Nasal congestion (thioridazine)

NURSE’S RESPONSIBILITY FOR A PATIENT RECEIVING ANTIPSYCHOTICS

  • Instruct patients the patient to take sips of water frequently to relieve dryness of mouth. Frequent mouth washes, use of chewing gum, applying glycerine on the lips are also helpful.
  • A higher fiber diet, increased fluid intake and laxatives if needed, help to reduce constipation.
  • Advise the patient to get up from the bed or chair slowly. Patient should sit on the edge of the bed for one full minute dangling his feet before standing up. Check BP before and after medication is given. This is an important measure to measure to prevent falls and other complications resulting from orthostatic hypotension.
  • Differentiate between akathisia and agitation and inform the physician. A change of drug may be necessary if side effects are severe. Administer antiparkinsonian drugs as prescribed
  • Observe the patient regularly for abnormal movements
  • Take all seizure precautions.
  • Patient should be warned about driving a car or operating machinery when first treated with antipsychotics. Giving the entire dose at bedtime usually eliminates any problem from sedation.
  • Advise the patient to use sunscreen measures (use of full sleeves, dark glasses etc) for photosensitive reactions.
  • Teach the importance of drug compliance, side-effects of drugs and reporting if too severe, and regular follow ups. Give reassurance and reduce unfounded fears and anxieties.
  • Seizure precautions should also be taken as clozapine reduces seizure threshold. The dose should be regulated carefully and the patient may also be put on anticonvulsants such as carbamazepine.

Typical Antipsychotics

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antipsychotics

Classifications of Antipsychotics.

Classification of Antipsychotics

  1. Typical (first generation)(conventional) antipsychotics.
  2. Atypical (second generation) antipsychotics.

Typical Antipsychotics or first-generation (conventional)

  • Also called typical, conventional or traditional antipsychotic agents
  • Their antipsychotic effects reflect competitive blocking of D2 receptors
  • More likely to be associated with extra pyramidal side effects (EPS) or movement disorders, such as Parkinsonism,  neck stiffness, protrusion of the tongue, upward eyeball rolling.  
  • This is most common with the highly potent drugs.
  • Primarily improve positive symptoms of schizophrenia
  • Low potency typical antipsychotics have less affinity for the D2 receptors but  tend to interact with non dopaminergic receptors resulting in more cardio toxic and anti-cholinergic adverse effects including sedation, hypotension. 

These are the most commonly used drugs in Uganda because they are cheap and available. Typical  antipsychotics are more effective in the treatment of positive symptoms than the negative symptoms.

Mechanism of Action

Predominantly block dopamine D2 receptors in the mesolimbic system of the brain.   Also blocks:  

  •  Muscarinic acetylcholine receptors  
  •  Histamine H1 receptors  
  •  Αlpha adrenoreceptors  

 The binding affinity of the typical is very strongly correlated with clinical antipsychotic and  extrapyramidal potency: the typical antipsychotic drugs must be given in sufficient doses to  achieve 60% occupancy of striatal D2 receptors 

Classes of Typical Antipsychotics

  1. Phenothiazines.
  2.  Butyrophenones.
  3. Thioxanthones.

Phenothiazines

  • Chlorpromazine (Thorazine)(Largactil)
  • Fluphenazine (Prolixin) 
  • Perphenazine (Trilafon)
  • Prochlorperazine (Compazine)
  • Thioridazine (Mellaril)
  • Trifluoperazine (Stelazine)
  • Mesoridazine
  • Promazine
  • Triflupromazine (Vesprin)
  • Levomepromazine (Nozinan)
  • Promethazine (Phenergan)

Chlorpromazine (Largactil)

 Chlorpromazine it is in a phenothiazine group. It has high sedating properties but with low extra pyramidal side effects. It is absorbed in the jejunum (in alimentary canal) and metabolized in the liver. Anti- depressants reduces metabolism of chlorpromazine. Chlorpromazine works as a competitor for relevant enzymes.

Indications

  • Schizophrenia (psychotic disorders).
  • Mania.
  • Agitation in the elders.
  • Alcohol related problems (where there are no antipsychotic drugs i.e. haloperidol and thioridazine).
  • Intractable hiccups. 
  • Nausea and  vomiting
  • It can also control spasms in small doses i.e. in tetanus.

Contra-indications:

  • Liver diseases e.g. liver cirrhosis, bone marrow depletion, in glaucoma (increased pressure in the eye.)

N.B: Chlorpromazine can induce seizures it lowers the threshold of a seizure, so a fit chart should be put to observe that.

Dosage

Orally: Depending on the severity of psychosis, dosages can range from 100mg-1500mg in daily divided doses (DDD) as per prescription. 

Injectables: This may range from 25-200mg IM. This may be given start depending on the severity of the condition. Or: It may be given continuous i.e. (continuous narcosis) i.e. 8 hourly or 12hourly, until the patient calms down, then oral treatment can be continued with.

Rectal suppository : Each suppository is of 100mg, this may be OD, BD, or TDS. It may be used in children above 5 years who cannot take drugs orally.

Syrups: This is 25mg/5mls. Suspension is also 100mg/5mls

Note: haloperidol and stelazine may be preferable in epileptic patients.  

 Piperazine e.g. Trifluoperazine (stelazine)

It is a neuroleptic of phenothiazine group. It has high extra pyramidal side effects and less sedating effects. It also has high properties of anti-hallucigenesis.

Indications:

  • Schizophrenia
  •  Mania  
  • Organic brain syndrome 
  • Mental  retardation with psychosis
  • Agitation in the elderly.
  • Severe anxiety.

Note: It’s a good drug in schizophrenic patients with negative features such as apathy, social with draw, lack of self drive.

Dosages

Oral tablets: 5-45mg in divided doses (DDD)

Injectable: 1-3mg IM. the maximum is usually 6mg, this may be given PRN.

 Piperidine e.g. Thioridazine (melleril)

It is a neuroleptics in phenothiazine group. It has moderate sedating effects and less extra pyramidal side effects, but with high anti-cholinergic effects. 

Indications:

  • Schizophrenia. 
  • Mania.
  • Agitation in the elderly (moderate side effects)

N.B: Their regular blood pressure should be monitored.

  • Behavioral disorders associated with psychosis 
  • Severe anxiety (it has also anxiolytic effect)

Contra-indications

  • As for chlorpromazine.

Dosage:

  • Give 100-1000mg in divided doses (DDD) depending on the severity of the condition.
  • Can also be given 1mg/kg body weight in children 

Butyrophenones

  • Haloperidol (Haldol) 
  • Pimozide (Orap)
  • Melperone
  • Benperidol
  • Triperidol

Haloperidol (haldol).

Generally, it has high extra pyramidal side effects but less sedating effects, 

Indications

  • Mania (drug of choice)
  • Schizophrenia
  • Alcohol related problems.
  • Organic brain syndrome of any cause 
  • Mental retardation with psychosis and agitation.
  • Nausea & vomiting 
  • Hiccup

Contra indications:

  • As for chlorpromazine.

Dosage: 5-30mg is divided doses; the maximum dose can be 60mg DDD.

It is in tablets form: 0.1, 0.5, 1mg,   5mg, and 10mg 

Injectables: 5mg-20mg IM start or continued narcosis i.e. 2hrly, 6hrly and 8hrly. 

Dosage range for children: 25-50microgram.

Trifluperidol (triperidol)

Dose: 6-8mg OD/BD or TDS

Benperidol

It is very good in patients with deviant behavior (anti-social personality disorders) 

Dose: 0.25-1.5mg OD, BD or TDS.

BLACKBOX WARNING
WARNING
See full prescribing information for complete Boxed Warning.
Increased Mortality in Elderly Patients with Dementia-Related Psychosis:
  • Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death. Analyses of seventeen placebo-controlled trials (modal duration of 10 weeks), largely in patients taking atypical antipsychotic drugs, revealed a risk of death in drug-treated patients of between 1.6 to 1.7 times the risk of death in placebo-treated patients. Over the course of a typical 10-week controlled trial, the rate of death in drug-treated patients was about 4.5%, compared to a rate of about 2.6% in the placebo group. Although the causes of death were varied, most of the deaths appeared to be either cardiovascular (e.g., heart failure, sudden death) or infectious (e.g., pneumonia) in nature. Observational studies suggest that, similar to atypical antipsychotics drugs, treatment with conventional antipsychotic drugs may increase mortality. The extent to which the findings of increased mortality in observational studies may be attributed to the antipsychotic drug as opposed to some characteristic(s) of the patients is not clear. Haloperidol is not approved for the treatment of patients with dementia-related psychosis (see WARNINGS).

Thioxanthones.

  • Chlorprothixene
  • Flupentixol (Depixol and Fluanxol)
  • Thiothixene (Navane)
  • Zuclopenthixol (Clopixol and Acuphase)

Thioxanthines are psychotropic drugs in the neuroleptics group. They were the first neuroleptics to come into use.

They are noted to have very gross side effects. With production of  new  neuroleptics drugs, the use of thioxanthines has reduced.

Indications: 

  • Schizophrenia (chronic)
  • Mania
  • And other psychotic associated conditions.

Flupentixol (depixal)

Dose: 3mg-9mg. The maximum dose can be 18mg in divided doses 

N.B: avoid giving neuroleptic injectables by I.V route for the fear of postural hypotension.

ANTIPSYCHOTIC DEPOT INJECTIONS (LONG ACTING) 

These are antipsychotics given by injection I.M. They are oily in nature and therefore, slowly released and metabolized over a period of 2 weeks up to 4 weeks.

Indications 

  • Chronic schizophrenia 
  • Cases of persistent mania 
  • Where there is total lack of oral medication compliancy in a psychotic patient. 
  • When it can be consistently be maintained. 

Give it concurrently with other oral treatment. However, it can be given alone as a maintained treatment.

Haloperidol decanoate (haldol decamate).

Dose: 50mg, 100mg-150mg (maximum) I.M. This is given monthly (4weeks).

Fluphenazine decanoate (modecate)

Initially with 12.5mg I.M stat if he is starting then 25mg-50mg for 2-4weeks

Fluspirilence (redeptin) 2mg/ml.

Give 2-4mg which is equivalent to 2mls. We can give 2mg in alternative days or weekly for one month (½) or 2months

Flupentixol decanoate (depixol)

It is very useful in patients with negative feature of schizophrenia. It has mood elevating effects.

Dose: Initially 20mg I.M, then after 10 days, increased to 40mg I.M 2-4 weekly.

Note:

  1. Give a quarter or half stated doses in elderly.
  2. After test dose, wait 4-10days before starting titration to maintenance therapy 
  3. Dose range is given in mg/week for convenience only avoid using shorter dose intervals than those recommended except in exceptional circumstances e.g. long  interval necessitates high volume ( >3-4ml) injection. 

Advice on prescribing depot injection/ medication:

  • Give a test dose.
  • Begin with the lowest therapeutic dose.
  • Administer at the longest possible licensed interval 
  • Adjust doses only after an adequate period of assessment

ATYPICAL ANTIPSYCHOTIC

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Groups, Types or Classifications of Antipsychotics. 

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Typical >>>

Atypical >>>

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Classifications of Antipsychotics. Read More »

antipsychotics

Antipsychotics

Antipsychotics

Antipsychotics are a type of psychiatric medication which are available on prescription to treat psychosis.

 Anti psychotic drugs are psychiatric drugs used in treatment of mental disorders that are  characterized by disturbance of reality and perception, impaired cognitive functioning, and diminished  mood 

They are licensed to treat certain types of mental health problem whose symptoms include psychotic experiences.

Antipsychotics, also known as neuroleptics, are a class of psychotropic medication primarily used to manage psychosis, mainly schizophrenia but also in a range of other psychotic disorders such as manic states with psychotic symptoms

They are also used together with mood stabilizers in the treatment of bipolar disorder, and they are also used in  management of other psychosis associated with depression and manic depressive illness and psychosis  associated with Alzheimer’s disease. 

Introduction to Psychosis

The term psychosis refers to a variety of mental disorders characterized by one or more of the following  symptoms:  

  1.  Diminished and distorted capacity to process information and draw logical conclusions  
  2.  Hallucinations, usually auditory or visual, but sometimes tactile or olfactory 
  3.  Delusions (false believes)  
  4.  Incoherence or marked loosening of associations  
  5.  Catatonic or disorganized behavior  
  6.  Aggression or violence 

 Antipsychotic drugs lessen these symptoms regardless of the underlying cause or causes ;

 Conditions characterized with psychosis include

  • schizophrenia,
  • mania,
  • bipolar disorder,
  • schizoaffective disorder,
  • depression,
  • alcohol withdraw syndrome,
  • and delirium. 

Factors that may lead to psychosis. 

  1.  Genetic factors 
  2.  Alcoholism 
  3.  Brain tumor 
  4.  Brain injures 
  5.  Central nervous system stimulants eg cocaine.  

Psychosis-Producing Drugs 

  1.  Levodopa 
  2.  CNS stimulants like 
  •  Cocaine  
  •  Amphetamines 
  •  Khat, cathinone, methcathinone  

     3.  Apomorphine ,Phencyclidine

Neurotransmitters 

  1. Excitatory: dopamine, adrenaline, nor adrenaline, serotonin (5-HT-5-hydroxy tryptamine)
  2. Inhibitory: Gama Amino Butyric acid (GABA)

 SCHIZOPHRENIA 

 Schizophrenia is a chronic mental disorder (psychotic) characterized by disordered thinking and loss of  touch with reality.

In other words, it is a mental disorder characterized by;

  • change in personality leading to  inability to relate to others ,
  • disturbed mood ,
  • impaired appreciation and interpretation of environment

The onset of symptoms usually occurs during adolescence and early adulthood.

Schizophrenia is thought  to be caused by excessive release of dopamine which leads to over stimulation of the brain cells resulting  into abnormal behavior. 

DOPAMINE 

  • it’s a neurotransmitter found in brain  

Effects of Dopamine 

  • Dopamine (DA) plays a critical role in initiation of movement.  
  • Controls reinforcement and cognitive function.  
  • Regulates prolactin release  
  • Plays a major role in vomiting  
  • Regulates temperature  
  • Reduces appetite  

Signs and symptoms 

Symptoms of schizophrenia are classified into two namely positive symptoms (due to distorted function)  and negative symptoms (due to diminished function).  

Positive and negative symptoms of schizophrenia 

Positive symptoms 

Negative symptoms

Hallucinations( Hearing voices, seeing things) 

Social withdrawal

Delusions( False belief) 

Emotional withdrawal

Disorganized speech 

Lack of motivation

Agitations 

Poverty of speech

 

Flat mood

 

Poor self – care

  • The positive symptons are due to stimulation. If you want to reduce these effects you would use a  depressant drug which would worsen the negative symptoms. 
  • The negative symptoms are due to depression. If you want to treat them, we would use a  stimulant drug which would potentiate the positive symptoms.  
  • The clinical phenotype varies greatly, particularly with respect to the balance between negative  and positive symptoms  
  • The positive symptoms are associated with increase in Dopamine pathway activation whereas the  negative symptoms are associated with a decrease in serotonin pathway activation.  
Key path ways affected by dopamine in the brain antipsychotics

Key path ways affected by dopamine in the Brain.

  1. Meso-cortical: – projects from the brain stem to the cerebral cortex. This path way is felt to be where the negative symptoms and cognitive disorders (lack of executive function) arise. Problem here for a psychotic patient, is too little dopamine. 
  2. Meso-limbic: – projects from the dopaminergic cell bodies in the ventral tegmentum (brain stem) to the limbic system. This pathway is where the positive symptoms come from (hallucinations, delusions and thought disorders). Problem here in a psychotic patient, there is too much dopamine.  
  3. Nigro striatal: – projects from dopaminergic cell bodies in the substantia nigra to the basal ganglia. This pathway is involved in movement regulation. Remember that dopamine suppresses acetylcholine activity. Dopamine hypo activity: can cause parkinsonian movements i.e. rigidity, brady kinesia, tremors, akathisia and dystonia
  4. Tuberoinfundibular: projects from the hypothalamus to the anterior pituitary. Remember that the dopamine release inhibits or regulates prolactin release. Blocking dopamine in this way will predispose your patient to hyper prolactinemia (gynecomastia/galactorrhea/decreased libido/ menstrual dysfunction).

General mechanisms of action antipsychotics

  • Blocking the action of dopamine receptors and path ways. Some scientists believe that some psychotic experiences are caused by the brain producing too much of a chemical called dopamine.  Dopamine is a neurotransmitter, which passes messages around the brain. Most antipsychotic drugs are known to block some of the dopamine receptors in the brain. 
  • This reduces the flow of these messages, which can help to reduce  psychotic symptoms. By blocking these pathways antipsychotics can produce both therapeutic and adverse effects.

 Blockade of dopamine and /or 5HT2 receptors in mesolimbic system.  

Blockade of 5HT2 receptor (like the α2 receptors in ANS), which allows constant release of  serotonin.  

 Many of these agents also block cholinergic, adrenergic, and histaminergic receptors. The  undesirable side effects of these agents are often a result of actions at these other receptors 

Absorption and Distribution 

  • Most antipsychotics are readily but incompletely absorbed. 
  • Significant first-pass metabolism. 
  • Bioavailability is 25-65%. 
  • Most are highly lipid soluble. 
  • Most are highly protein bound (92-98%). 
  • High volumes of distribution (>7 L/Kg). 
  • Slow elimination. 

**Duration of action longer than expected, metabolites are present and relapse occurs, weeks after  discontinuation of drug.** 

Metabolism 

  • Most antipsychotics are almost completely metabolized. 
  • Most have active metabolites, although not important in therapeutic effect, with one exception.  The metabolite of thioridazine, mesoridazine, is more potent than the parent compound and  accounts for most of the therapeutic effect. 

Excretion 

• Antipsychotics are almost completely metabolized and thus, very little is eliminated unchanged. Elimination half-life is 10-24 hrs.

Groups, Types or Classifications of Antipsychotics. 

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Psoriasis

Psoriasis

Psoriasis

Psoriasis is a chronic non contagious auto immune disease of the skin in which the epidermal cells are produced at an abnormal rate.

It results from over production of immature epidermal
cells. It affects many parts. Its cardinal sign is scaly skin that looks like silver fish which may not go away with rubbing.

Causes of Psoriasis

Psoriasis is caused by complex interactions between genetics, the immune system, and environmental factors. These include;

  •  Immune reactions.
  •  Genetic factors.
  •  Infections like strep throat, Streptococcal infections
  •  Injury to the skin such as cut or scrape.
  •  Stress.
  •  Smoking.
  •  Heavy alcohol consumption.
  •  Vitamin D deficiency.
  • Medications including high blood pressure medications and antimalarial drugs and lithium.
  • Withdrawal systems of oral or systemic corticosteroids
  • Cold weather and dry conditions

Clinical Presentations

  • A long-term history of erythematous, scaly area, which may involve. multiple areas of the body.
  • Recent streptococcal throat infection, viral infection, immunization, use of antimalarial drug, or trauma.
  • Pruritus (especially in eruptive, guttate psoriasis)
  • Red scaly, white patches
  • Small scaling spots mostly in children
  • Dry, cracked skin
  • Ocular symptoms include redness and tearing due to conjunctivitis or blepharitis
  • Pain, which has been described by patients as unpleasant, superficial, sensitive, itchy, hot, or burning.
  • High fever in erythrodermic and pustular psoriasis
  • Pitted or cracked nails, Dystrophic nails
  • Avoidance of situations requiring social interaction
  • Arthralgia: Joint pain without any visible skin findings
  • Stiff joints
  • Itching sensation
types of psoriasis

Types of Psoriasis

  1. Guttate Psoriasis; It is caused by streptococcal infection (pharyngitis or perianal). It appears as small, scaly red, tear-drop shaped called papules. It is mainly seen in children and young adults.
  2. Postular Psoriasis; Its symptoms include pustules which are yellow, pus-filled lesions. They can be Generalized pustular psoriasis (GPP) which covers many parts of the body, or Localized pustular psoriasis covering smaller areas on the palms of the hands or the soles of the feet.
  3. Plaque Psoriasis; It is the common form of psoriasis and appears as raised, inflamed, red scaly patches with a silvery-white coating at the top. It can be tender, itchy and painful. They appear on the back, elbows, knees, and scalp.
    • Affects >70 % of the body surface area

Diagnosis / Investigation

  • History, age, family history of psoriasis, past medical history from streptococcal infections, bacterial or viral infection.
  • Physical examination; Common physical examination findings of psoriasis include erythematous, scaling papules, and plaques.
  • Enzyme linked immunosorbent assay (ELISA);
    In patients with severe psoriasis, increased levels of Long Pentraxin 3 protein (PTX3) can be observed in plasma and in monocytic cultures by enzyme linked immunosorbent assay (ELISA).
  • Skin biopsy may be helpful in the diagnosis of psoriasis. Common findings include perivascular and dermal inflammatory cell infiltration, vascular dilation, and absent granular layer.
  • Blood test; blood test to rule out any other health conditions relating to the development of psoriasis.

Management of Psoriasis

Nursing management;

  •  Body hygiene; Bathing daily helps to take off scales and soothes the inflamed skin.
  • Apply moisturizers. Moisturizing the skin smooths the roughness and reduces itching and swelling.
  • Avoid psoriasis triggers; Find out what triggers your psoriasis, and take precautions to avoid them.
  •  Care for pressure areas to avoid pressure sores.
  • Avoid alcohol consumption; Drinking alcohol may make some psoriasis treatments ineffective. So avoid drinking alcohol during psoriasis treatment.
  •  Give psychological care to allay anxiety.
  • Follow a healthy lifestyle by eating nutritious food and avoiding smoking. Stay away from pollution and dirt because pollution leads to flaring up of psoriasis symptoms. Consult your dermatologists to choose the right type of shampoo or soap, that does not cause any harm to your skin.
  • Advise against exposure to sun light.
  • Physiotherapy.

Pharmacological management;
First line treatment;

Medicated creams and ointments applied directly to psoriatic lesions can help decrease inflammation, remove built-up scale, reduce skin turnover, and clear affected skin of plaques.

  •  Apply topical drugs like corticosteroids like betamethasone cream, Vitamin D analogues like calcipotriol
  • Topical betamethasone plus calcipotriene  12 hourly for 1 week.

Second line;

  •  Expose the patient to photo therapy. It has long been recognized that daily, short, non-burning exposure to sunlight can help clear or improve psoriasis.
  • Steroids; Triamcinolone topical steroid can relieve psoriasis symptoms such as itching, crusting, scaling, redness, inflammation, dryness, and discomfort. It also serves as a dental medicine (paste) to relieve the discomfort of mouth sores. 
  • Retinoids;  Oral retinoids known as Acitretin are pills to slow down the production of skin cells. Doctors prescribe Acitretin to manage severe cases of psoriasis. Its side effects are dry skin and muscle soreness. They are not allowed during pregnancy or breastfeeding.
  • Methotrexate; It is a powerful drug. Prescribed to treat adults with severe, disabling psoriasis that cannot be cured with skin medicines applied or phototherapy. Methotrexate suppresses the overactive immune system that leads to psoriasis.
  • Biologics; These are new and strong drugs. They target only that area of the immune system that is hyperactive due to psoriasis. Therefore they cause no damage to other body organs, as compared to other strong medicines.
Psoriatic arthritis

This is a form of inflammatory arthritis affecting people having psoriasis.

Causes/predisposing factors.

  • Auto immune reactions.
  • Physical trauma
  • Microbial infestation.
  • Psoriasis.
  • Family history.
  • Age; affects people with30-50 years of age though any one can suffer from it.

Signs and symptoms.

  • It can affect joints on one side or both sides of your body.
  • Symptoms almost resemble those of rheumatic arthritis. I.e. hotness, redness, tenderness, swelling, joint stiffness.

However one is most likely to develop;

  • Lower back pain.
  • Foot pain.
  • Swollen finger and toes.

Diagnosis

  • History taking.
  • Physical examination.
  • X ray.
  • MRI.
  • Rheumatic factor test.
  • Joint fluid test.

Management/treatment.

Nursing management; 

  • Apply moisturizers.
  • Use of warm compress.
  • Care for pressure areas to avoid pressure sores.
  • Ensure general hygiene to do away with funny smells.
  • Give psychological care to allay anxiety.
  • Diet; encourage taking a balanced diet.
  • Advise against exposure to sun light.
  • Physiotherapy.

 

Pharmacological management.

  • Give analgesics like paracetamol for pain.
  • NSAIDS like ibuprofen to soothe inflamation.
  • Immune suppressants like imuran, azafan, cyclosporine.
  • Biological agents like DMARDS.
  • New oral medication like apremilast to decrease the activity of the enzyme in the body that controls the activity of inflamation in the body.

Surgical treatment.

  • Joint replacement may be done.



 Complications.

  • Arthritis mutilan.( Severe painful and disability form of a disease for over time; it destroys small bones of the hands e.g. fingers).
  • Conjunctivitis.
  • Uveitis.
  • High risk of cardiovascular diseases.

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Onychomycosis

Onychomycosis

Onychomycosis

Onychomycosis means fungal infection of the nails. It represents up to 20% of all nail disorders.

Onychomycosis may affect toe- or fingernails, but toenail infections are particularly common.

  • The most common type of onychomycosis (80-90%), caused by dermatophytes, is  known as tinea unguium (tinea of the nails).

 It can result in

  • discoloration,
  • thickening,
  • chalkiness, 
  • crumbling of the nails and is often treated by powerful oral medications 
onychomycosis classifications

Classification of Onychomycosis

Onychomycosis is classified according to the clinical pattern of nail bed involvement. The main types are:

  1. Distal and lateral subungual onychomycosis (DLSO); The most common form of tinea unguium usually caused by Trichophyton rubrum, which invades the nail bed and the underside of the nail plate.
  2. Superficial white onychomycosis; Caused by fungal invasion of the superficial layers of the nail plate to form “white islands” on the plate. Accounts for only 10 percent of onychomycosis cases.
  3. Proximal subungual onychomycosis; Fungal penetration of the newly formed nail plate through the proximal nail fold. It is the least common form of tinea unguium in healthy people but found more commonly when the patient is immunocompromised.
  4. Endonyx onychomycosis; Fungal penetration through the full thickness of the nail from directly under the skin. The nail bed is not infected. Commonly found in immunocompromised conditions.
  5. Total dystrophic onychomycosis; Total destruction of the nail plate. It is the end result of any of the above four types.

Causes of Onychomycosis

  • Dermatophytes are the fungi mostly responsible for onychomycosis
  •  Trichophyton rubrum is the most common dermatophyte fungi.
  • Others include, Trichophyton interdigitale and Epidermophyton floccosum, can be causes as well.
  • The dermatophytes are identified in 90% of the toenail and 50% of fingernail onychomycosis. 
  • Candida albicans accounts for 2% of onychomycosis, occurring especially in fingernails.
  • Yeasts mainly cause fingernail onychomycosis in people whose hands are often submerged in water.

Risk Factors

  1. Age; The most common risk factor for onychomycosis is aging. Reason may be due to nail trauma, poor nail care, poor peripheral circulation e.t.c.
  2. Family history of onychomycosis
  3. Warm and moist conditions of the fingers like wearing tight fitting shoes
  4. Walking with barefoot in public places such as swimming pool, public baths and showers.
  5. Nail conditions such as tinea pedis, nail injury, nail damage, psoriasis .
  6. Conditions that are related with poor peripheral circulation such as diabetes or peripheral arterial disease.
  7. Immunodeficient conditions like cancer , post transplant care , HIV , patients on chemotherapy and radiotherapy

Clinical Presentation.

  •  Always presents with distorted nails .
  • Change in nail texture and discoloration.
  • The nail plate can have a thickened, yellow, or cloudy appearance.
  • The nails can become rough and crumbly, or can separate from the nail bed.
  • Malodor; slight foul smelling of the infected nail.

Complications.

  • Cellulitis
  • Sepsis
  • Osteomyelitis
  • Tissue damage
  • Loss of nail

Management / Treatment of Onychomycosis

Oral medications such as Oral antifungal medications such terbinafine , itraconazole and fluconazole , Treatment Options

Preferred treatment regimen: 

Terbinafine 250 mg orally OD (children <20 kg: 67.5 mg/day, 20–40 kg: 125 mg/day, >40 kg: 250 mg/day) for 6 weeks OR Itraconazole 200 mg orally O.D for 3 months OR Fluconazole 150–300 mg orally weekly for 6–12 months

Fungal laser therapy; Laser treatments aim at either stopping fungal reproduction (fungistatic) or killing fungus (fungicidal).

 

Prevention of Onychomycosis

  1. Wear appropriate fitting shoes. Both, shoes that are too tight and or too loose can cause trauma to the toenails, creating a portal of entry for fungal organisms.
  2. Avoid being barefoot in public or communal areas that are shared by other barefoot people. These areas may include public swimming pools, locker rooms, showers, and hotel rooms.
  3. Do not pick or tear at your toenails. Use clean instruments to cut the toenails straight across, avoiding rounding the edges. Trauma or aggressive cutting can create portals of entry for fungus.
  4. Thoroughly dry your feet, including between your toes after showering.
  5. Maintain dry feet throughout the day and do not wear damp shoes.
  6. If you have family members with foot or toenail fungal infections, avoid sharing common spaces barefoot.
  7. If you have diabetes or reduced blood flow to the feet, maintain foot exercises and guidelines from the healthworker.

Cummulative Exam: https://midwivesrevisionuganda.com/medicine-cumulative-test/

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Herpes zoster

Herpes zoster

Herpes zoster

Herpes zoster, also called shingles, is an infectious condition caused by varicella zoster virus (VZV), the same virus that causes varicella zoster (chickenpox).

  • The incubation period ranges from 7 to 21 days.
  • The total course of the disease is 10 days to 5 weeks from onset to full recovery.

Risk Factors

  • Older age- risk increases with age especially after age of 50
  • Suppressed immunity due to certain conditions like cancer, HIV and drugs
  • Stress due to prolonged unresolved emotional or physical stress

Pathophysiology

  • After a case of chickenpox run its course,
  • The virus lies dormant in the ganglia of the spinal nerve tracts.
  • Then the virus reactivates and travels along the peripheral nerves to the skin,
  • It then multiplies and produces painful vesicular eruptions.
  • It is most common in older adults and people who have weak immune systems.
  • Although VZV typically affects the trunk of the body,
  • It can also be noted on the buttocks or face.
  • If an ophthalmic nerve is involved, the client may potentially experience keratitis, ulceration and possibly blindness.
  • Secondary infection resulting from scratching the lesions is common.

Clinical Features

  • The initial symptom is usually a tingling sensation in the affected area.
  • Painful blisters form in the area supplied by one nerve root. This usually affects only one side of the body.
  • Pain and discomfort, which can be severe, begins about five days before the rash emerges.
  • Red papules develop into blisters, which crust over and heal within three to four weeks.
  • Malaise and fever are common and this, coupled with pain, makes shingles a debilitating condition.

Diagnosis

  • Past history of chickenpox.
  • The pain and rash of shingles is characteristically unilateral.
  • May start after a period of debility.
  • Culture and sensitivity in case of secondary infection

Assessment

Subjective Data:

  • Pain, burning
  • Numbness, tingling
  • Itching
  • Headache
  • Sensitivity to light
  • Fatigue

Objective Data:

  • Rash that develops in clusters of vesicles
  • Rash follows dermatome (nerve pathway
Nursing Management
  • Assess pain level
  • Note location and quality of pain
  • Duration
  • Non-verbal clues
  • Relieving factors
  • Severe nerve (burning) pain is the primary complaint with preceding sensations of tingling or itching.
  • Assess for signs / symptoms of bacterial infections on skin and obtain culture and sensitivity test as indicated
  • Assess for changes in vision and rash on forehead or nose

Specific Nursing care

  • Apply cool, moist dressings to pruritic lesions
  • Avoid temperature extremes, in both the air and bathwater.
  • Avoid rubbing or scratching the skin or lesion.
  • Wear loose, nonrestrictive clothing made of cotton.
  • Keep rash dry;
  • Rest, especially while malaise is a problem
  • Encourage herpes zoster vaccination
  • Explain to the patient the need for Isolation.
  • Restrict visitors
  • Keep finger nails short
  • Wear protective gears while caring for the patient

Medical Management

  • Antivirals (acyclovir, valacyclovir)  are given to decrease the severity and duration of symptoms
  • Oral analgesics (opioids) are given to treat severe pain of acute phase;
  • Antidepressants and antiepileptic medications may be given to treat post herpetic neuralgia;
  • Topical steroids provide an anti-inflammatory effect;
  • Antihistamines help with itching, especially at bedtime;
  • Topical analgesics provide pain relief
Complications
  • Ear complications such as ringing in ears, vertigo, hearing loss, one sided facial paralysis
  • Post herpes nerve pain (neuralgia) which can be very severe and persist for even years after healing
  • Eye complications such as erosion or ulceration of cornea, dryness of eyes, inflammation of optic nerve etc
Nursing Diagnosis
  1. Acute Pain or Chronic Pain related to Nerve pain (most commonly cervical, lumbar, sacral, thoracic, or ophthalmic division of trigeminal nerve) as evidenced by Alteration in muscle tone, Facial mask of pain, Reports of burning, dull, or sharp pain, Reports of pain localized to affected nerve.
  2. Deficient Knowledge related to Complexity of treatment, Herpes zoster outbreak, 
    as evidenced by Inadequate follow-up of instructions, Questioning members of healthcare team, Verbalizing inaccurate information.
  3. Risk for Infection related to Crusted-over lesions,
    Itching and scratching Skin lesions (papules, vesicles, pustules)
  4. Risk for Disturbed Body related to
    Preoccupation with changed body part and Visible skin lesions.

Nursing Interventions

1. Teach the patient about contact isolation. VZV is spread by contact with fluid from lesions containing viruses.

2. Instruct the client to avoid contact with pregnant women and immunocompromised individuals. Active lesions can be infectious, and immunosuppressed individuals are more susceptible.

3. Use universal precautions in caring for the client to prevent transmission of disease to self or other clients. VZV can be transmitted to others and cause chickenpox in a person who has not previously had the disease.

4. Suggest the use of gauze to separate the lesions in skin folds. This reduces irritation, itching, and cross-contamination.

5. Discourage the scratching of lesions. Encourage the client to trim fingernails. These measures prevent the inadvertent opening of lesions, cross-contamination, and bacterial infection.

6. Instruct the client on the use of antiviral medications, as prescribed. Antiviral agents are most effective during the first 72 hours of an outbreak when viruses are proliferating. Drugs of choice are acyclovir, famciclovir, or valacyclovir.

7. Instruct the client in the use of systemic steroids, if ordered, for anti-inflammatory effect.
The use of steroids is controversial; they are most commonly used in severe cases

8. Assist the client in articulating responses to questions from others regarding lesions and infectious risk. Clients may need some guidance in determining what to say to people who comment on the appearance of their skin. The rehearsal of set responses to anticipated questions may provide some reassurance.

9. Suggest the use of concealing clothing when lesions can be easily covered. This approach may help the client who is having problems adjusting to body image changes.

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Acne Vulgaris

Acne Vulgaris

Acne Vulgaris

Acne Vulgaris is an inflammatory skin disease caused by changes in the pilosebaceous units (skin structures comprising a hair follicle and its related sebaceous gland) of the skin.

The term acne comes from a Greek word acme meaning a skin eruption) 

Acne vulgaris is the most common cutaneous disorder affecting adolescents and young adults. Patients with acne can experience significant psychological morbidity and, rarely, mortality due to suicide.

The psychological effects of embarrassment and anxiety can impact the social lives and employment of affected individuals. 

Scars can be disfiguring and lifelong.

Acne Vulgaris Classification

Classification of Acne

It is classified as mild, moderate, or severe. 

Mild acne is defined as non-inflammatory lesions (comedones), a few inflammatory (papulopustular) lesions, or both. 

Moderate acne is defined as more inflammatory lesions, occasional nodules, or both, and mild scarring. 

Severe acne is defined as widespread inflammatory lesions, nodules, or both, and scarring, moderate acne that has not settled with 6 months of treatment, or acne of any “severity” with serious psychological upset. 

Causes of Acne Vulgaris

Acne occurs by hypersensitivity of the sebaceous glands to a normal circulating level of androgens, which are aggravated by P. acnes and inflammation.

 Causes of acne include the following:

  • Propionibacterium acnes infection, Staphylococcus epidermidis
  • Use of medications like lithium, steroids, and anticonvulsants
  • Exposure to excess sunlight
  • Use of occlusive wear like shoulder pads, headbands backpacks, and underwire brassieres
  • Endocrine disorders like polycystic ovarian syndrome and even pregnancy
  • Accumulation of dead skin cells.
  • Any medication containing halogens (iodides, chlorides, bromides), lithium, barbiturates, or androgens.
  • Conditions like Congenital adrenal hyperplasia, Cushing’s syndrome, polycystic ovary syndrome
  • Puberty
Pathophysiology of acne vulgaris

Pathophysiology of Acne

Four factors are involved:

  1. Follicular hyper keratinization .
  2. Increased sebum production .
  3. Propionic bacterium acnes (P. acnes) within the follicle. An anaerobic diphtheroid that is a normal component of skin flora.
  4. Inflammation.

During puberty, under the influence of androgens, sebum secretion is increased as 5-alpha reductase converts testosterone to more potent DHT, which binds to specific receptors in the sebaceous glands increasing sebum production. This leads to an increased hyperproliferation of follicular epidermis, so there is retention of sebum.

Distended follicles rupture and release pro-inflammatory chemicals into the dermis, stimulating inflammation.

C. acnes, Staphylococcus epidermis, and Malassezia furfur induce inflammation and induce follicular epidermal proliferation

Risk Factors

  • Role of androgens  — stimulating the growth and secretory function of sebaceous glands.
  • External factors  — Soaps, Oil-based cosmetics and facial massage, detergents,  Repetitive mechanical trauma caused by scrubbing with these agents may worsen the disorder by rupturing comedos, promoting the development of inflammatory lesions. Thus, patients with acne should refrain from rubbing their faces or picking their skin.
  • Turtlenecks, bra straps, shoulder pads, orthopedic casts, and sports helmets cause acne mechanical, in which occlusion of pilosebaceous follicles leads to comedone formation.
  • Diet  — The natural hormonal components of milk or other bioactive molecules in milk could exacerbate acne.
  • Family history  — Individuals with close family members with acne are at increased risk for the disorder. Has a more than three-fold risk among individuals with affected first-degree family members.
  • Stress  — Psychological stress can exacerbate acne. Receptors for corticotrophin releasing hormone (CRH), a hormone involved in the stress response, are present in human sebaceous glands. Severe anxiety and anger may aggravate acne, probably by stimulating stress hormones.
  • Body mass index  — There is an association between rising BMI and increased risk for acne only among females
  • Premenstruation — A premenstrual flare-up in acne seems to follow edema of the pilosebaceous duct. This occurs in 70% of female patients.

Signs and symptoms of Acne.

  • Acne vulgaris typically affects those areas of the body that have the largest, hormonally-responsive sebaceous glands, including the face, neck, chest, upper back, and upper arms.
  • Typical lesions of acne vulgaris (e.g, open comedones, closed comedones, and inflammatory lesions),
  • Scarring
  • Post inflammatory hyperpigmentation is common in patients with darker complexions, and take several months or more to resolve without treatment.
  • Adult women present with acne involving the lower face and neck that is often associated with premenstrual flares.

Management of Acne Vulgaris

Aims

  • To reduce bacterial colonies.
  • To decrease sebaceous gland activity, prevent the follicles from becoming plugged.
  • Reduce inflammation, combat secondary infection.
  • To minimize scarring and eliminate factors that predispose the person to acne.

Medical Management

  1. Topical Pharmacologic Therapy
    • Benzoyl peroxide 5% Topical bid
    • Topical antibiotics e.g. Clindamycin 1% gel 
    Systemic Pharmacologic Therapy
    • Antibiotics e.g. Doxycycline 100 mg PO bid
    • Oral Retinoids
    • Hormone Therapy,  Oral contraceptives: May help in women; estrogen decreases androgens and thereby suppresses sebum secretion.
    Surgical treatment
    • Extraction of comedo contents
    • Drainage of pustules and cysts
    • Excision of sinus tracts and cysts
    • Intralesional corticosteroids for anti-inflammatory action
    • Cryotherapy
    • Dermabrasion for scars
    • Laser resurfacing of scars
    Nursing Diagnosis
    • Impaired skin integrity
    • Deficient knowledge
    • Disturbed body image
    Nursing Management
    1. Administer prescribed medications, which may include acne products containing benzoyl peroxide (explain that these products initially cause skin redness and scaling but that the skin adjusts quickly); topical agents, such as vitamin A acid; and antibiotics such as tetracycline.
    2. Provide client and family teaching

    o    Advise the client that heat, humidity, and perspiration exacerbate acne. Explain that uncleanliness, dietary indiscretions, menstrual cycle, and other myths are not responsible for acne.

    o    Explain that it will take 4 to 6 weeks of compliance with the treatment regimen to obtain results.

    o     Instruct the client to wash his face gently (do not scrub) with mild soap twice daily.

    o    Instruct the client not to squeeze blackheads, not to prop hands on or rub the face, to wash hair daily and keep it off the face, and to use cosmetics cautiously because some may exacerbate acne.

    o    Instruct the female client to inform her health care provider if she is possibly pregnant. Some medication, such as systemic retinoic acid, have teratogenic effects, therefore a pregnancy test is required prior to treatment and strict birth-control measures are use throughout pregnancy.

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Dermatitis

Dermatitis

Dermatitis

 Dermatitis is an inflammation of the skin.

The word dermatitis is used to describe a number of different skin rashes that are caused by infections, allergies, and irritating substances.

The rashes range from mild to severe and can cause the following skin conditions depending on their cause.

Itchiness, Swelling, Painful ulcer, Reddening Thickening, Discoloration, Scaling, Crusting, Blisters, Creasing, Marking.
There are several different types. Usually all of them have in common an allergic reaction to specific allergens

Types of Dermatitis

  • Contact dermatitis. Caused by an allergen or an irritating substance. 
  • Atopic dermatitis. It presents usually with intense pruritus and is often associated with elevated levels of immunoglobulin E (IgE). Individuals who live in urban areas with low humidity are more prone to develop this type of dermatitis.
  • Dermatitis herpetiformis. Appears as a result of a gastrointestinal condition, known as celiac disease.
  • Seborrheic dermatitis. More common in infants and in individuals between 30 and 70 years old. It appears to affect primarily men and it occurs in 85% of people suffering from AIDS.
  • Nummular dermatitis. Also known as discoid dermatitis, it is characterized by round or oval-shaped itchy lesions. (The name comes from the Latin word “nummus,” which means “coin.”)
  • Stasis dermatitis. An inflammation on the lower legs which is caused by buildups of blood and fluid and it is more likely to occur in people with varicose veins.
  • Perioral dermatitis. Inflammation of the skin around the mouth 
  • Infective dermatitis. Dermatitis secondary to a skin infection
contact dermatitis of the face

Contact Dermatitis

Contact dermatitis is an acute or chronic skin inflammation that occurs when the skin comes in contact with a substance that causes a type IV delayed hypersensitivity reaction(allergic contact dermatitis) or when there is an injury to the skin’s surface (irritant contact dermatitis), or when the allergen or irritant is activated by sunlight hence Phototoxic dermatitis occurs.

Types of Contact Dermatitis
  1. Allergic dermatitis. Allergic dermatitis results from direct contact with substances called allergens, such as nickel, chlorine, presenting with; Skin reddening, Blisters that ooze, Itching which can become intense., Swelling in eyes, face and genital areas in severe cases.
  2. Irritant contact dermatitis. This is the most common form of contact dermatitis, Irritant contact dermatitis develops when your skin comes into contact with an irritating substance. Irritant contact dermatitis is either acute or chronic, according to the strength of the irritant, such as acids, kerosene. Stiff, tight feeling skin. May present with mild swelling, Dry, cracking skin, Blisters, Painful ulcers.
  3. Phototoxic contact dermatitis.  It is further divided into two categories, phototoxic and photoallergic contact dermatitis. Phototoxic contact dermatitis is a sunburn-like skin disorder resulting from direct tissue damage following the ultraviolet light-induced activation of a phototoxic agent. It is usually associated only with areas of skin which are left uncovered by clothing especially during scans and x-rays.
Causes of Contact Dermatitis

Contact dermatitis is caused by exposure to a substance that irritates your skin or triggers an allergic reaction, such irritants include;

  • Soaps. Most kinds of soaps, detergents, shampoos and other cleaning agents have harmful substances that could possibly irritate the skin.
  • Solvents. Solvents such as turpentine, kerosene, fuel, and thinners are strong substances that are harmful to the sensitive skin.
  • Extremes of temperature. There are people who are highly sensitive even when exposed to extremes of temperature and could cause contact dermatitis. 
  • Products that cause a reaction when you’re in the sun (photoallergic contact dermatitis), such as some sunscreens and cosmetics
  • Formaldehyde, which is in preservatives, cosmetics and other products
  • Personal care products, such as body washes, deodorants, hair dyes and cosmetics
  • Plants such as poison ivy and poison oak, cashew nuts, which contain a highly allergenic substance called urushiol
  • Airborne allergens, such as pollen and spray insecticides
  • Nickel, which is used in jewelry, and many other items
  • Medications, such as antibiotic creams, and there side effects such as diazepam, ceftriaxone.
  • Latex and long exposure to wet surfaces such as staying in a wet diaper for a long time.
Signs and Symptoms

Allergic dermatitis is usually affects the area where the trigger has touched the skin, while irritant dermatitis may be more widespread on the skin. Clinical features of both forms include the following:

  • Red rash. This is the commonest reaction. The rash appears immediately in irritant contact dermatitis and later in allergic.
  • Blisters or hives. Blisters and hives     may present in a pattern where skin was directly exposed to the allergen or irritant.
  • Burning skin. Irritant contact dermatitis tends to be more painful than itchy, causing swelling, burning or tenderness
  • Itching. Once the patient is exposed to an irritating substance, the patient presents with severe itching.
  • Crusting. The vesicles start to form a crust as it slowly becomes dry, cracked, and scaly skin.
  • Hyperpigmentation. Leathery patches that are darker than usual often because of scratching from irritation.
Diagnosis of Contact Dermatitis
  • Diagnosis is done by performing patch test. In this test, small samples of a chemical are placed on an area of skin to see if a rash develops.
  • Thorough history taking where the child mentions of use of certain products that are in contact with his or her skin.
  • Note; There are no tests for irritant contact dermatitis, only history of irritating substance that a child regularly come into contact with will prove that a child has irritant contact dermatitis.
Treatment of Contact dermatitis
  • The form of treatment will depend on the cause of dermatitis. Common treatments include;
  1. Cortisone-type creams. In severe cases, drugs containing cortisone may be given orally.
  2. Antihistamines. These are itching relievers.
  3. Dry skin care by use of lotions and creams.
  4. Oatmeal baths also to relieve itching.
  5. Barrier cream. These products can provide a protective layer for the skin.
  6. Avoiding the irritant. The key is to identify the substance that causes the rash so that it could be avoided.

Prevention

      For allergic contact dermatitis,

  • Avoid contact with substances that cause the skin rash.
  • Wash any child’s area that comes into contact with allergic substances.
  • Learn to recognize and remove poison oak and poison Ivy plants from playing areas of children

   For irritant contact dermatitis,

  • You can also use petroleum jelly to protect the child’s skin. Reapply the petroleum jelly two to three times a day and after washing hands.
  • Avoid contact with substances that irritate the child’s skin.
  • Use mild soaps.
  • Use hand creams frequently.

Question.

 Contact dermatitis is a type of hypersensitivity: 

A. Type I.
B. Type II.
C. Type III.
D. Type IV.

4. Answer: D. Type IV.

  • D: Type IV hypersensitivity is a delayed hypersensitivity reaction that are inflammatory in nature initiated by mononuclear leukocytes.
  • A: Type I hypersensitivity is triggered by an innocuous foreign substance (like dust, pollen or animal dander) that would cause no problems in the majority of people.
  • B: Type II hypersensitivity is the process by which IgG or IgM binds to a cell to cause injury or death (Antibody Dependent Cytotoxicity).
  • C: Type III hypersensitivity is tissue damage created by immune complexes, which are aggregations of antigen and antibodies.

Atopic Dermatitis

Atopic dermatitis, often referred to as eczema, is a chronic (long-lasting) disease that causes inflammation, redness, and irritation of the skin.

Cause
  • Unknown, idiopathic
  • Atopic dermatitis is the result of either skin barrier dysfunction
  • or immune dysregulation due to genetic defects
Clinical Features

In infancy

  • Severe pruritus: Can cause sleep disturbances in children. Red, very itchy dry patches of skin.
  • Rash on the cheeks that often begins at 2 to 6 months of age.
  • Rash oozes when scratched. Symptoms can become worse if the child scratches the rash. 
  • Chronic or relapsing skin lesions

 In adolescence and early childhood

  • Rash on creases of hands, elbows, wrists, and knees and sometimes on the feet, ankles and neck.
  • Dry, scaly, brownish grey skin rash.
  • Thickened skin with markings.
  • Skin rash may bleed and crust after scratching. 
  • Itch when sweating
Diagnosis
  • There are no reliable diagnostic laboratory findings associated with atopic dermatitis.
  • Although there is sometimes elevated total and/or allergen-specific serum IgE level.
Management of Atopic Dermatitis

Atopic dermatitis is a chronic condition which means that it can not be cured. Treatments however, are very effective in reducing the symptoms of itching and dry skin. It has also been found out that provision of prescribed lotions and oral medications can be helpful. These treatments include, corticosteroid creams and antihistamines.

  • You can also do the following to help the Child.
  • Avoid long, hot baths, which can dry the skin.
  • Use Luke warm water instead and give a spong bath to a child.
  • Apply lotion immediately after bathing while the skin is still moist. This will help trap moisture in the skin.
  • Keep the room temperature as regular as possible. Changes in room temperature and humidity can dry the skin.
  • Keep the Child dressed in a cotton. wool silk, and man made fabrics such as polyester can irritate the skin.
  • Use mild laundry soap and make sure that clothes are well rinsed.
  • Watch for skin infections. These should be dealt with immediately.
  • Avoid rubbing or scratching the rash.
  • Use moisturizers several times daily.

Nursing Diagnosis

  • Impaired skin integrity related to contact with irritants or allergens as evidenced by Inflammation
    Dry, flaky skin Erosions, excoriations, fissures, Pruritus, pain, blisters.
  • Disturbed body image related to visible skin lesions as evidenced by patient verbalizing feelings about the change in body appearance, negative feelings about the skin condition, fear of rejection or reactions from others.
  • Risk for infection related to excoriations and breaks in the skin.
  • Risk for impaired skin integrity related to frequent scratching and dry skin.

Nursing interventions

  1.  Assess skin, noting color, moisture, texture, and temperature; note erythema, edema, and tenderness. Specific types of dermatitis may have characteristic patterns of skin changes and lesions.
  2. Identify aggravating factors. Inquire about recent changes in the use of products such as soaps, laundry products, cosmetics, wool or synthetic fibers, cleaning solvents, and so forth.
    Patients may develop dermatitis in response to changes in their environment. Extremes of temperature, emotional stress, and fatigue may contribute to dermatitis.
  3. Skin care. Encourage the patient to bathe in warm water using a mild soap, then air dry the skin and gently pat to dry.
  4. Bathe or shower using lukewarm water and mild soap or non soap cleansers. Long bathing or showering in hot water causes drying of the skin and can aggravate itching through vasodilation.
  5. Topical application. Usual application of topical steroid creams and ointments is twice a day, spread thinly and sparingly.
  6. Acknowledge patient’s feelings. Allow patient to verbalize feelings regarding their skin condition.
  7. Proper hygiene. Encourage the patient to keep the skin clean, dry, and well lubricated to reduce skin trauma and risk for infection.
  8. Assist the patient in articulating responses to questions from others regarding lesions and contagiousness. Patients may need guidance in determining what to say to people who comment about the appearance of their skin. Dermatitis is not a contagious skin condition.
  9. Educate the patient about the skin condition, including triggers, treatment options, and measures to treat symptoms. Providing education regarding these topics can help patients with atopic dermatitis better understand the disease condition and manage the symptoms more effectively.
  10. Encourage the patient to engage in activities that can boost their self-esteem, such as hobbies or exercise. By engaging in enjoyable and fulfilling activities, patients can improve their self-esteem and mood, which can help them adjust with the emotional effects of the skin condition.

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Paget’s disease

Paget’s disease

Paget’s disease

Paget’s disease of bone also known as osteitis deformans is a chronic disease of the skeleton characterized by focal excessive bone remodeling. and is the second most common bone disease worldwide after osteoporosis.

Paget’s disease of bone is a disorder in which there’s a lot of bone remodeling that happens in some regions of the bone. Typically there’s excessive bone resorption followed by excessive bone growth, and that leads to skeletal deformities and potential fractures.

Pathophysiology of Paget’s Disease

In normal bone, there is a normal process called remodeling. Bone is absorbed and then reformed in response to the normal stresses on the skeleton.

  • Osteoclasts: cells that absorb bone.
  • Osteoblasts: cells that make new bone.

In Paget’s disease, osteoclasts are more active than osteoblasts. This means that there is more bone absorption than normal. The osteoblasts try to keep up by making new bone, but they overreact and make excess bone that is abnormally large and deformed.

Pathophysiology occurs in 3 stages, ie

  • Osteolytic Phase
  • Mixed Osteoclastic – Osteoblastic Phase
  • Osteoblastic Phase. 

Osteolytic phase, and as lytic mean destruction , So osteolytic phase presents with osteoclasts that destroy the bone and this destruction of bone results in formation of pits in the Bony matrix that are called resorption pits and these osteoclast will be visible as multinucleated large size cells.

Mixed (Osteoclastic – Osteoblastic) Phase, In the phase, there is both destruction as well as formation of new bone, where osteoclasts are destroying while osteoblasts are forming a new bone. Osteoblasts do not form enough bone compared to what osteoclasts are destroying.

Osteoblastic Phase. In this phase, there is excessive bone formation, and this excess quantity  is in form of mosaic pattern  of lamellar bone( jigsaw puzzle appearance)

Causes of Paget’s Disease

The causes of Paget’s disease are still unknown, idiopathic. But its thought to be a combination of environmental and genetic factors.

Risk Factors;

  • Age; common in elderly.
  • Viral; Paget’s disease may be caused by a slow virus infection, such as respiratory syncytial virus, and the measles virus.
  • Genetics. In around 15-40% of affected patients had a first-degree relative with Paget disease. 
  • Autoimmune, connective tissue, and vascular disorders are also rick factors.
signs and symptoms of paget's disease

Signs and Symptoms of Paget’s Disease

  • Bone Pain – commonly affected areas are pelvis, spine, skull, shoulders, and legs
    • is usually dull or aching pain
    • it is felt deep within the affected part of the body
    • the pain is constant and is at its worst at night
    • affected area may also feel warm
  • Joint pain, stiffness, and swelling -especially in the hips, back, and knees
  • Nerve Problems
    • pain travelling from the spine to the legs
    • pain travelling from the neck to arms and chest
    • numbness or tingling in the affected limbs
    • partial loss of movement in the affected limbs
    • problems in balance
    • loss of bladder or bowel control
  • Enlargement and bowing of femurs and lower legs
  • Enlargement of the skull around the forehead

Skull involvement may manifest these symptoms:

  • Development of hearing loss
  • Loss of vision
  • Hydrocephalus
  • Somnolence (drowsiness) due to vascular steal syndrome of the skull.

Diagnosis / Investigations.

  • X-rays – usually done to diagnose Paget’s disease. Bones may appear larger, denser, and also have a deformed shape
  • Blood tests – may reveal elevated levels of the alkaline phosphatase enzyme  with normal calcium, phosphate, and aminotransferase levels in an elderly patient are suggestive of Paget’s disease
  • Bone scan – may reveal the severity of abnormalities in the bones
  • Urine tests – Urinary Hydroxyproline is found to be elevated

Treatment and Management of Paget’s Disease

There is no cure for Paget’s disease and no way to reverse its effects on bone.

Aims;

  • To relieve bone pain and prevent the progression of the disease
  • Treatment focuses on the relief of symptoms
  • Prevention of future complications

Non-pharmacological Therapy. Physical therapy for the improvement of muscle strength and pain relief in some types of pain.

  • While there are no known ways to prevent Paget’s disease from occurring, eating a healthy diet with sufficient calcium and vitamin D, and getting regular exercise, are important components in maintaining skeletal health and joint mobility. 

Pharmacological Treatment. The medications used in the management of Paget’s disease include:

    • Biphosphonates (check more on osteoporosis)– suppress or reduce the resorption of bone by osteoclasts. Currently, there are 6 approved bisphosphonates for the treatment of Paget’s disease. Prior to the start of the therapy, patients undergo a regimen of calcium and vitamin D every day for two weeks. This is for the reduction of risk of low blood calcium after infusions. This drug is not indicated for those with low blood calcium or those with vitamin D deficiency and those with compromised renal function. Calcium supplements need to be taken with bisphosphonates to reduce the risk of hypocalcemia.
    • Calcitonins. They  decrease symptoms of bone pain, reduce inflammation over bones, improve neurological complications, and promote healing of lytic lesions. Calcitonins are used mostly by patients who cannot tolerate bisphosphonates.
  • Pain Management. Pain due to Paget’s disease may be the result of bone deformity, arthritic, or neurological complications. Acetaminophen, NSAIDs, are used for the management of pain associated with Paget’s disease.
  • Surgery. Surgical procedures used to treat fractures, malalignment, or arthritis in patients with Paget’s disease.
    • Internal fixation. This is used to treat fractures in the bone affected by the disease. In internal fixation, bone fragments are first repositioned into their normal alignment, then immobilized through the use of screws, wires, pins, or metal plates attached to the outside of the bone.
    • Osteotomy. This can help relieve pain and restore alignment to weight-bearing joints especially the hip and knee. The procedure involves the removal of a wedge of bone near the damaged joint in order to shift weight to a healthier, more stable part of the joint.
    • Total joint replacement. In this procedure, parts of a damaged or arthritic joint are removed and replaced with a metal, ceramic, or plastic device called a prosthesis. The prosthesis is designed to replicate the movement of a healthy joint.

Nursing Diagnosis

  1. : Acute pain related to joint inflammation secondary to Paget’s disease, as evidenced by pain score of 10 out of 10, guarding sign on the affected fingers, restlessness, and irritability
  2.  Activity intolerance related to joint inflammation and pain secondary to Paget’s disease, as evidenced by pain score of 8 to 10 out of 10, fatigue, disinterest in ADLs due to pain, verbalization of tiredness and generalized weakness.
  3.  Deficient Knowledge related new diagnosis of Paget’s disease, as evidenced by patient’s verbalization of “I want to know more how to manage my illness.”

Nursing Interventions.

  1. Assess the patient’s activities of daily living, as well as actual and perceived limitations to physical activity. Ask for any form of exercise that he/she used to do or wants to try.
  2. Encourage progressive activity through self-care and exercise as tolerated. Explain the need to reduce sedentary activities such as watching television and using social media in long periods. Alternate periods of physical activity with 60-90 minutes of undisturbed rest.
  3. Administer analgesics as prescribed  prior to exercise/ physical activity. Teach deep breathing exercises and relaxation techniques. Provide adequate ventilation in the room.
  4. Refer the patient to physiotherapy / occupational therapy team as required. This is to provide a more specialized care for the patient in terms of helping him/ her build confidence in increasing daily physical activity.
  5. Assess the patient’s readiness to learn, misconceptions, and blocks to learning (e.g., denial of diagnosis or poor lifestyle habits).
  6. Inform the patient the details about the prescribed medications (e.g., drug class, use, benefits, side effects, and risks) to treat acute pain. Ask the patient to repeat or demonstrate the self-administration details to you.
  7. If the patient is for surgery, explain the surgical procedure related to Paget’s to the patient and caregiver. The doctor may recommend surgery to resolve unbearable joint pain due to Paget’s disease.

Paget’s disease Read More »

Osteoporosis

Osteoporosis

Osteoporosis

Osteoporosis a musculoskeletal disorder which bones deteriorate or become brittle and fragile due to low bone mass as a result of bone
tissue loss.

 Osteoporosis occurs as a result of an imbalance between bone resorption and bone formation. Major contributing factors in the development of osteoporosis include estrogen deficiency and aging.

Classification of Osteoporosis

On the basis of etiology, osteoporosis can be classified into:

Primary Osteoporosis

Primary osteoporosis develops as a result of aging or menopause-related bone demineralization. In patients with primary osteoporosis, the bone density decreases as the age progresses. It is not merely a consequence of aging but of failure to develop optimal peak bone mass during childhood, adolescence, and young adulthood.

Secondary Osteoporosis

Secondary osteoporosis results from more severe loss of bone mass due to pathologies associated with immobilization, medications (iatrogenic), endocrine dysfunction, cancer, and chronic kidney disease.

Causes of Osteoporosis

Osteoporosis may be caused by conditions that can lead to the disturbed balance between bone formation and bone resorption.

Common causes of osteoporosis include

  •  Aging: Osteoporosis occurs at an older age, as it is believed that testosterone and estrogen are important in achieving and maintaining bone mass, so risk for osteoporosis increases with increasing age.
  • Menopause
  • Nutritional: A low calcium intake, low vitamin D intake, high phosphate intake, and inadequate calories reduce nutrients needed for bone remodeling. deficiency of calcium and vitamin D
  • Chronic renal failure
  • Immobility
  •  Hyperparathyroidism
  • Medications. Such as intake of corticosteroids, anti seizure medications, heparin, and thyroid hormone affects calcium absorption and metabolism.
  • Chronic glucocorticoid abuse.

Common risk factors

  • Age > 50
  • Menopause (lack of estrogen)
  • Family history of fracture or osteoporosis
  • History of at least two fractures
  • Alcohol consumption
  • Smoking (inhibits activity of osteoblasts)
  • Insufficient physical activity (lack of bone remodeling)
  • Glucocorticoids (steroid-induced osteoporosis)
  • Proton pump inhibitors.

Pathophysiology of Osteoporosis

Normally, The two main cells involved in bone production pathway are osteoblasts and osteoclasts.

  • Bone resorption is caused by osteoclasts, after which new bone is deposited by osteoblasts.
  • Osteoclasts determine the final outcome of bone resorption.
  • Normal balance between osteoblast and osteoclast activities within a bone is influenced by macrophages and innate adaptive immunity. This leads to the formation of a normal bone.

In Osteoporosis,  there is a disturbance of this balance leading to increased osteoclastic activity relative to osteoblastic activity, the result is resorption, and eventual bone mass loss.

  • Reduced total bone mass. Normal homeostatic bone turnover is altered; the rate of bone resorption that is maintained by osteoclasts is greater than the rate of bone formation that is maintained by osteoblasts, resulting in a reduced total bone mass.
  • Progression. The bones become porous, brittle, fragile; they fracture easily under stresses that would not break normal bone.
  •  The consequence of these changes is net loss of bone mass over time.

Role of Hormones

  • In addition to estrogen, calcium plays a significant role in bone turnover.
  • Deficiency of calcium and vitamin D leads to impaired bone deposition.
  • The parathyroid glands react to low calcium levels by secreting parathyroid hormone (parathormone, PTH) increasing bone resorption in a bid to ensure adequate calcium levels in the blood.
  • The role of calcitonin, a hormone produced by the thyroid that increases bone deposition, is less clear and probably less significant

Clinical Features of Osteoporosis

  • Fractures. The first clinical manifestation of osteoporosis may be fractures, which occur most commonly as compression fractures.
  • Kyphosis. The gradual collapse of a vertebra is asymptomatic, and is called progressive kyphosis or “dowager’s hump” associated with loss of height.
  • Decreased calcitonin. Calcitonin, which inhibits bone resorption and promotes bone formation, is decreased.
  • Decreased estrogen. Estrogen, which inhibits bone breakdown, decreases with aging.
  • Increased parathyroid hormone. Parathyroid hormone increases with aging, increasing bone turnover and resorption.

Diagnosis / Investigations

The most common test for measuring bone mineral density is;

  • Dual-energy X-ray Absorptiometry (DXA). It is a quick, painless, and noninvasive test. DXA uses low levels of x-rays as it passes a scanner over your body while you lie on a cushioned table. The test measures the BMD(bone mineral density) of your skeleton and at various sites that are prone to fracture, such as the hip and spine. Bone density measurement by DXA at the hip and spine is generally considered the most reliable way to diagnose osteoporosis.

Management of Osteoporosis

Aims

  •  To prevent further bone loss
  • To reduce your risk of bone fractures.
  •  For reduction in fracture risk with an increase in bone mass density.

Medical Management;

  1. Exercise: Exercise promotes the mineralization of bone and bone deposition particularly during growth. High impact exercise, in particular, has been shown to prevent the development of osteoporosis. However, it isn’t recommended in cases of poor nutrition, such as anorexia nervosa and celiac disease.
  2. Physical activity; Multiple studies have shown that aerobics, weight lifting, and resistance exercises can all maintain or increase BMD(bone mineral density) in postmenopausal women.
  3. Nutrition: A diet high in calcium and vitamin D prevents bone loss. Patients at risk for osteoporosis, such as persons with chronic steroid use are generally treated with vitamin D and calcium supplementation.
  4. Diet: Sufficient protein intake is necessary to maintain the function of the musculoskeletal system and to decrease the complications that occur after an osteoporotic fracture. 
  5. Smoking cessation may prevent osteoporosis. The use of tobacco products is detrimental to the skeleton as well as to overall health. 
  6. Avoiding excessive alcohol intake, or drinking only in moderation.
  7. Medications: Taking the least possible doses of certain medications associated with osteoporosis (anticonvulsants or corticosteroids).

  8. Fall prevention; by mitigating risk factors for falls are shown below:

    • Lack of assistive devices in bathrooms, by assisting with hygiene or use of hip protectors.
    • Obstacles in the walking path, Appropriate correction of visual impairment may improve mobility and reduce risk of falls.
    • Slippery conditions, by using cotton rugs and ensuring there environment is dry.

Pharmacological Management;

  • Calcium supplements with vitamin D. To ensure adequate calcium intake, a calcium supplement with vitamin D may be prescribed and taken with meals or with a beverage high in vitamin C to promote absorption, but these supplements should not be taken at the same day as bisphosphonates. • Dietary calcium 1200 ( Calcium supplement≤ 500 mg, if dietary calcium not met) mg/day and Vitamin D  800–2000 IU/day.
  • Bisphosphonates. Bisphosphonates are the first line treatment for osteoporosis. These include oral preparations of;
  1. Alendronate(70mg weekly orally.) or
  2. Risedronate(35mg weekly or 150mg monthly orally), 
  3. Ibandronate(150mg monthly orally, or 3mg every 3 months through intravenous (IV) route.), or yearly intravenous infusions of
  4. Zoledronic acid ( 5mg annually through IV route.) increase bone mass and decrease bone loss by inhibiting osteoclast function.
  • Calcitonin. Calcitonin directly inhibits osteoclasts thereby reducing bone loss and increasing bone mineral density. It is used for postmenopausal women with osteoporosis. The dosing is 100units subcutaneous daily; or 200 units intranasal daily.
  • Selective estrogen receptor modulators (SERMs). SERMs such as raloxifene which is a second line treatment, reduce the risk of osteoporosis by preserving bone mineral density without estrogenic effects on the uterus. The dosing is 60mg daily orally.

  • Parathyroid hormone: Such as Teriparatide (20mcg subcutaneous daily,) and as a recombinant PTH, it stimulates osteoblasts to build bone matrix and facilitates overall calcium absorption. Abaloparatide(80mcg subcutaneous daily) can also be used.

Surgical Management;

Surgery is not the first-line treatment option, Vertebroplasty, kyphoplasty, lordoplasty, and vesselplasty are the procedures that are usually reserved for patients with either pathological or osteoporotic vertebral fractures

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