Factors that Improve Effective Communication with Patients

What are the factors known to improve effective communication?

The following is a list of the factors that contribute to effective communication with patients during clinical assessment. 

Use Minimal Prompts

Interrupting your patient during a clinical assessment prohibits them from explaining their concerns. Points that are important for you as a clinician are often less important for the patient.  Knowing whatever is important to the patients and addressing their concerns is immensely important from a holistic and biopsychosocial model of health care. Using minimal prompts helps patients to communicate their concerns so you can address them. 

1. Sit squarely in relation to the patient
2. Open body position in relation to the patient
3. Leaning slightly towards the client
4. Eye contact maintained
5. Relax while listening
6. Listen to the message content
7. Listen for feelings
8. Respond to feelings
9. Note all non-verbal cues

Risk factors for Parkinsonism

The following are some risk factors for Parkinson's disease. 

1. Pesticide exposure
2. Head injury
3. Drinking well water
4. Agricultural occupation
5. Use of beta-blockers.

Development in the first year of life summarised

Development in the first year of life summarised

1. Smiling starts at 3 weeks. 
2. Selective smiling starts at 6 months. 
3. Fear of strangers starts at 8 months, while separation anxiety starts later to that. 
4. At the end of the first year, children also learn a few simple words like mama, dada, etc. 
5. Weaning starts at around 6 months and should have completed by the end of the year. 
6. An ordered sleep-wake cycle has also got established, Children learn to point at objects in the first year of life.

Types of Personality Disorder

It is classified into three clusters as:

Suspicious:

which include

Antisocial

Paranoid

Schizoid

Schizotypal

Emotional and impulsive:

Borderline

Histrionic

Narcissitic

Anxious:

Avoidant

Dependent

Obsessive compulsive

Another way to classify them is Mad, Bad and Sad respectively for the suspicious, impulsive and anxious clusters. Remember there are no clusters in ICD11 anymore, The individual personality disorders have been eliminated from ICD11.

What is Neuroleptic malignant syndrome (NMS) ?

How do we define NMS?

It is an acute disorder of thermoregulation and neuromotor control that occurs because of exposure to dopaminergic drugs.

What drugs or medications can cause NMS?

Antipsychotics, especially the ones with high anti-dopaminergic potency. But also dopaminergic agonist withdrawal e.g. withdrawal from levodopa.

The Gene associated with antisocial behaviour

Criminal behavior, lack of guilt, and irritability are typical features of antisocial personality disorder. Evidence suggests that a low-activity variant of the MAO-A gene predisposes to adult antisocial behavior in men, especially in those who faced early adversity^1–4. Catechol-O-methyltransferase enzyme metabolizes dopamine and other monoamines. Its gene, the COMT-gene, occurs in two forms: a high-activity form and a low-activity form. They associate these variants with differential abilities of the prefrontal cortex, especially working memory. People with low-activity form may have a more efficient prefrontal cortex, likely because of the greater dopamine level in the synaptic space^5,6. We have associated serotonin transporter gene variants with neuroticism and a predisposition to depression. The variants may also influence individual response to SSRIs8. APOE4 gene is a risk factor for Alzheimer’s disease (compared to APOE2 and APOE3).

 COLLEGE OF PHYSICIANS & SURGEONS PAKISTAN

27th February 2019

MCPS

UBJECT: PSYCHIATRY

ANSWER ALL QUESTIONS (TOTAL QUESTIONS: 10)

USE SEPARATE ANSWER BOOK FOR EACH QUESTION

PAPER:

TIME ALLOWED

3 HOURS

2.4 A young unmarried male of 25-year was diagnosed as a case of schizophrenia. There is family history of psychiatric illness in the family. He developed the disease acutely with prominent positive features. He taq responded to treatment within two months and was well supported by his family, however, his family is still very cautious, inquisitive and worried excessively as the patient has adopted a lonely lifestyle.

a) What are the factors ointing towards good and bad prognosis in this

patient? b) What are the characteristic features of "high expressed emotions

family?stilette 1481 ellipse, c) What family interventions can be done in patients with schizophrenia?

CHA

Q.5 A 31-year-old male presents with history of episodes of sudden onset of palpitation, trembling of body and fear of losing control which lasts for about 15-30 minutes. а вече стан реаги

Cats

Porse

pluche

a) What is the most likely diagnosis? b) What is the DSM 5 diagnostic criteria of your likely diagnosis.

(ICD-10) Almost

c) Outline the management of this patient.

wei- Pig Hardecs, kreativer, pmE, CeT, helf bax.

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Q.6 A young well-dressed girl of about 23-year presents to your psychiatric OPD with complaints of aphonia and difficulty in swallowing. Relevant examination and investigations do not reveal any significant pathology. On history you detect some major stressors in her life during the period of last 06 months.

a) What is the most probable diagnosis (keeping in view the classifications of ICD-10 and DSM-5)?

b) How is this disorder classified in DSM?

c) Enlist the biological factors implicated in the etiology of this disorder

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athy

Most common Methods of Suicide

Men

1. hanging


2. drug overdose


3. self poisoning by car exhaust fumes


4. drowning and jumping

Women

1. drug overdose


2. hanging


3. drowning

(UK- Wasserman 2009)

Opioid Epidemiology in Pakistan

Nationwide, one per cent of the population –over one million people– were estimated to be regular opiate (heroin or opium) users. The majority (80 per cent) use heroin, while one-third (33 per cent) use opium. Opium users were slightly older (mean age 38.2, standard deviation 10.1 years) than heroin users (mean age 33.8, standard deviation 9.4 years), and more likely to live in rural environments whereas heroin users live in cities. Two-thirds of opium users and one- third of heroin users were married, and while opium users mostly live in a home (84 per cent), nearly forty per cent of heroin users living in a park/road, shrine, or a location other than a home.

A daily heroin habit in Pakistan is estimated to cost between 1.50 and 3.00 USD, yet only 6.5 per cent of heroin users are employed full time. To earn money, one-third report donating/selling blood, and forty per cent report exchanging sex for drugs or money. Opiate users also often beg for money in the streets or perform tasks for daily wages such as selling rubbish. A small number (7 out of 3,330) reported working as professional injectors who inject other users, and one-quarter of users receive financial support from family or friends.

The average number of years of opiate use among respondents was 16 (15 among heroin users and nineteen for opium users), evidence of the long-term nature common for opioid use. Poly-drug use is also quite common among opiate users, whereas 74 per cent also used other psychotropic substances in the past year. The majority also use cannabis (67 per cent), but a considerable proportion also uses tranquillizers or sedatives (26 per cent) and various other substances such as prescription opiates (7 per cent) and/or cough syrups (4 per cent).

IMPORTANT MOOD DISORDER TOPICS LEARN FOR THE FCPS-2 EXAM

1. Learn the differential diagnosis of depression, dysthymia, stupor,  psychotic depression.  

2. Outline the assessment and treatment of these conditions.  Assess treatment resistance 

3. Enlist or identify risk factors (dysthymia, depression)  Investigate stupor, depression with organic findings Treatment options for refractory depression 

4. Use of lithium in depression 

5. Relevant guidelines, recommendations for depression Patient education about depression and antidepressants Antidepressant response 

6. Association of depression with medical conditions Depression in pregnancy 

7. Lithium (extensively tested from several aspects including risks and benefits used in pregnancy and lactation, predictors of response, efficacy in various conditions, mechanisms/causes of loss of efficacy in the long-term, etc. Take-home message >> wherever you see a line, a para, a topic about lithium READ IT)  

8. (Postnatal) manic episode management and diagnosis Psychosocial interventions for bipolar affective disorder.

9. Genetic Epidemiology of bipolar affective disorder.

BEHAVIORAL TREATMENTS FOR PTSD

Behavioural Treatments For PTSD 

Prolonged Exposure 

Introduction

Prolonged exposure is a manual-guided CBT comprising ten, sixty-to-ninety-minute weekly individual therapy sessions. We can explain the central therapeutic component of prolonged exposure on "Pavlovian learning theory." 

Approach

The treatment involves repeatedly presenting a conditioned stimulus (e.g., a trauma reminder) in the absence of an unconditioned stimulus (e.g., the traumatic event). They do this through imaginal exposure during therapy sessions and through in vivo exposure in the environment. 

Evidence

On average, prolonged exposure proves robust symptom severity improvement. 

Cognitive Processing 

Introduction

Another manual-guided cognitive behavioural modality that has received strong empirical support to treat PTSD is cognitive processing therapy. 

Approach

Cognitive processing therapy comprises twelve weekly, 60-minute individual sessions. 

This therapy involves 

1. Imagining and reviewing written narratives 
1. these depict the thoughts and emotions about the traumatic event.
2. Participants receive homework assignments 
• Designed to identify and challenge the maladaptive thought patterns that maintain the symptoms. 

Modified Group-Therapy Cognitive Therapy

A modified group-therapy version of cognitive processing therapy has promising results. 

Cognitive-Only therapy

Evidence also supports the effectiveness of cognitive-only cognitive processing therapy.

It includes: 

1. Psychoeducation
2. Cognitive skill-building 
3. Cognitive restructuring skills. 

The cognitive-only therapy does not employ written narratives, and the most recent treatment manual recommends cognitive-only therapy as the first-line version, with written narratives as an optional modification. 

Eye Movement Desensitization and Reprocessing

Introduction

Eye movement desensitisation and reprocessing is one of the three most-studied treatments for PTSD. 

Approach

This therapy incorporates a variety of techniques, including prolonged exposure and cognitive restructuring, but it differs in that it applies these techniques in conjunction with guided eye movement exercises. 

Narrative Exposure

Narrative exposure therapy is a manual-guided psychotherapy developed to treat PTSD among individuals seeking asylum from political or organized violence. 

Approach

In this technique, which also includes psychoeducation about PTSD, participants narrate their relevant developmental memories in chronological order and narrate details of their trauma exposures as they were experienced over time. Typically, the sessions are 60 to 120 minutes, once a week for 4 to 10 weeks. 

Present-Centered Therapy

Present-centered therapy is a time-limited intervention that includes a psychoeducation component, skill development to manage daily stressors and challenges, and homework to solidify the new skills developed in sessions., This therapy has demonstrated efficacy in a variety of populations and is commonly used in randomized controlled trials as a comparator for new or adapted PTSD treatments. 

Cognitive Behavioral Conjoint Therapy

Cognitive behavioral conjoint therapy for PTSD is a manual-guided, 15-session CBT. This intervention is designed to improve PTSD symptoms and relationships at the same time. 

Evidence

Research in this area is critical, as dyadic distress and dysfunction are saliently associated with poor individual PTSD treatment outcomes. 

Approach

Cognitive behavioral conjoint therapy involves psychoeducation on PTSD and relationships, learning communication skills to address avoidance related to PTSD and relationship problems, and challenging trauma-related beliefs. 

Other Interventions

The empirical literature on other interventions is limited, but the research shows promising findings. These integrate cognitive behavioral and other therapeutic approaches. 

• Emotion-focused therapy

• Brief eclectic psychotherapy. 

Protocol for Lithium

Step 1: First obtain a complete history (to confirm that lithium is indicated and suitable, there is no contraindication, identify whether the patient is taking any medications that interact with lithium, likely to adhere to treatment and the protocol)

Step 2: Physical examination especially blood pressure, pulse, weight, BMI, and thyroid examination

Step 3: Laboratory investigations especially TFTs, eGFR, ECG if needed, and in women of childbearing age, a pregnancy test. Serum calcium is also desirable.

Step 4: Education of the patient about the effects, side effects, the need for strict adherence, the risk of toxicity, signs of toxicity, and conditions that increase the risk of toxicity (in a way that generates a realistic and balanced view of the risks and advantages). Provide written materials Step 5: Start lithium OD200mg or 400mg. Aim for a plasma level of 0.4 to 0.8 mmol/L initially.

Step 6: Check plasma level after a week, then every two weeks until the plasma level is stable (target levels of about 0.4-0.8 mmol/dl). Step 7: If there is a suboptimal response, target a plasma level of up to 1mmol/L. Once a steady-state has been achieved, check every 6 weeks for some time. If no serious issues arise early then, check plasma lithium every 6 months

Step 8: Monitor for side effects history(esp. weight gain and fatigue) and lab investigations( Serum calcium, TFTs, and RFTs including eGFR) every six months.

Step 9: When planning to stop lithium, taper off gradually at a rate not more than 0.2mmol/L (plasma level)weekly.

ICD 10 Multiaxial System

In multi-axial diagnosis, a patient’s problems are viewed within a broader context, which includes clinical diagnosis, assessment of disability, and psychosocial factors. In ICD-10, multi-axial diagnoses are made along three axes, as follows:

Axis I: clinical diagnoses

This includes all disorders, both psychiatric and physical, including learning disability and personality disorders. 

Axis II: disabilities

Conceptualized in line with WHO definitions of impairments, disabilities, and handicaps, this covers a number of specific areas of functioning that are rated on a scale of 0–5 (‘no disability’ to ‘gross disability’):

Personal care: personal hygiene, dressing, feeding, etc.

Occupation: expected functioning in paid activities, studying, homemaking, etc.

Family and household: participation in family life.

Functioning in a broader social context: participation in the wider community, including contact with friends, leisure, and other social activities. 

Axis III: contextual factors

The factors considered to contribute to the occurrence, presentation, course, outcome, or treatment of the present Axis I disorder(s). They include problems related to:

Negative events in childhood.

Education and literacy.

Primary support group, including family circumstances.

Social environment.

Housing or economic circumstances.

(Un)employment.

Physical environment.

Certain psychosocial circumstances.

Legal circumstances.

Family history of disease or disabilities.

Lifestyle or life-management difficulties.

Neurotransmitters Involved in the Aetiology of Depression

Neurotransmitters Impairments in Depression

Depression involves impairments in the following neurotransmitters:

Serotonin: It has reduced levels in synaptic space.
Glutamate: it has decreased levels in the anterior brain region.
Dopamine: there are complex changes in dopaminergic neurotransmitters; we may say it impairs dopaminergic neurotransmitters. 

What does the Monoamine Hypothesis of Depression posit?
It posits an imbalance in the monoamine neurotransmitters causes depression. 
What kind of monoamine neurotransmitter imbalance causes depression?
A decrease
What are the monoamine neurotransmitters impairments in patients with depression?
Nor-adrenaline, serotonin, dopamine
What was noticed in the 1950s?
Drugs that decreased monoamine neurotransmitters caused symptoms like depressive disorder
What are the characteristics associated with nor-adrenaline?
Sleeping, energy, motivation, emotion
Characteristics of serotonin?
Mood control, sleeping, hunger
What other job does serotonin do?
Regulates adrenaline
What happens if there is a low level of serotonin?
Low level of adrenaline, lack of motivation and pleasure
Characteristics of dopamine?
Emotion, addiction, pleasure, and cog function
What does a decreased amount of dopamine explain?
Diminished interest and lack of pleasure
How many weeks might drugs take to work?
6 weeks
Why do drugs not work straight away?
Because of a neuro-circulatory change in the brain
What type of neuro-circulatory changes occur?
Because of the low levels, an up-regulation in the sensitivity occurs on receptor sites of post-synaptic neuron
What happens when the neurotransmitter suddenly become available through drugs?
A down-regulation occurs in the sensitivity, causes post-synaptic neuron receptors sites to desensitise
What did Lilmeck find? (strength)
He compared the brain of fifteen dead patients with and without depressive disorder found that there were differences in the part of the brain that produces noradrenaline showing that nd is involved
What did McNeal and cimbolic find? (strength)
Depressives show a lower level of 5hiaa which is produced when serotonin is broken down
What does another biological explanation suggest that goes against this one?
Suggests that part of the nervous system is involved, and that increased cortisol is associated with depressive disorder, incomplete
What do MRI scans show about the theory?
There have been differences in those with and without the depressive disorder, specifically a smaller hippocampus, so it is structural and biochemical
What is Monoamine Oxidase-A?
A chemical that removes monoamine neurotransmitter from the synapse when they are not needed
What does too much moa-a mean?
That too much of the neurotransmitter are being taken away producing symptoms of depressive disorder