Long term conditions Flashcards
Vit D def risk factors
Pigmented skin • Use of sun cream/concealing clothes • Old age • Nursing home • Malabsorption • Short bowel • Renal disease • Cholestatic liver disease • Drugs (anticonvulsants, rifampicin, HAART)
Vit D présentation
- Proximal muscle weakness/pain (osteomalacia may be asymptomatic)
- ↓ bone density on DEXA or osteopenia on plain x-ray may indicate vitamin D deficiency
- Severe vitamin D deficiency causes hypocalcaemia, tetany, seizures
- Rickets in children presents with deformities (knock knees, bowed legs) and impaired growth
Investigations for Vitamin D Deficiency
- ↓ serum 25-hydroxy-D3
- <25mmol/Linosteomalacia
- 25-50mmol/LinvitaminDinsufficiency
- ↑ ALP, PTH
- ↓/normal phosphate and calcium
- X-ray shows characteristic defective mineralisation and Looser’s pseudofractures (low density bands running perpendicular to the cortex, commonest in femur/pelvis)
Management of Vitamin D Deficiency
Vitamin D supplementation
• Initial loading dose stage and subsequent maintenance
phase (oral/IM)
• Supplementary calcium (1000-1200mg/day)
• e.g. Cholecalciferol / calcichew
RA presentation
- Insidious onset of pain, early morning stiffness (>30 mins)
- Symmetrical swelling of proximal joints of hands/feet
- PIPJs affected, but DIPJs not affected
- Ulnar deviation, MCP/PIPJ swelling, Z-shaped thumb, Boutonniere deformity, Swan-neck deformity
- May also involve wrists, elbows, shoulders, cervical spine, knees, ankles, feet
joints for RA
• PIPJs affected
MCP/PIPJ swelling, Z-shaped thumb, Boutonniere deformity, Swan-neck deformity
Investigation for RA
Investigations for Rheumatoid Arthritis
• FBC: Normochromic, normocytic anaemia; thrombocytosis
• ESR, CRP raised in proportion with inflammatory activity
• Rheumatoid Factor (RhF) not specific for RA
• Anti-CCP
• X-ray
• Synovial fluid: sterile, raised neutrophils
Management of Rheumatoid Arthritis
• NSAIDs and Coxibs (± Paracetamol, codine)
• Relieve pain but do not slow disease progression
• Corticosteroids
• Suppress disease activity but require high doses (short-term use)
• Disease Modifying Anti-Rheumatic Drugs (DMARDs); start <6 weeks from first presentation
• Methotrexate (mouth ulcers, diarrhoea, liver fibrosis, pulmonary fibrosis, renal impairment,
teratogenic)
• Sulfasalazine (mouth ulcers, hepatitis, reversible male infertility)
• Leflunomide (diarrhoea, hypertension, hepatitis, alopecia)
• Biologics
• TNF-α blockers (CXR before starting; immunosuppression risks latent TB)
• Stop smoking
Clinical Features of Psoriatic Arthritis
Peripheral arthritis
• Absence of RhF or Anti-CCP (“seronegative”)
• DIPJ swelling
• Dactylitis (“sausage fingers”)
• Arthritis mutilans is a severe form with destruction of small bones in hands and feet
Investigations for Psoriatic Arthritis
Routine bloods, ESR normal
• RhF, anti-CCP negative
• X-ray: “pencil-in-cup” deformity in IPJs
Management of Psoriatic Arthritis
- NSAIDs ± paracetamol
- Intra-articular corticosteroid injections
- If severe, methotrexate/TNF-α blockers
- Emollients for skin disease
Parathyroid hormone (PTH)
Kidney→increased calcium resorption and reduced reabsorption of phosphate convert vitamin D to active form
Bone→release of calcium
Small intestine→increased absorption of dietary calcium
Primary Hyperparathyroidism causes
Primary = Hypersecretion of PTH Causes:
• 85% isolated parathyroid adenoma
• 15% diffuse parathyroid hyperplasia
• <1% parathyroid carcinoma
Primary Hyperparathyroidism presentation
PTH - raised
Calcium - increased
phosphate decreased
2ndary Hyperparathyroidsim causes
Causes:
• Chronic kidney disease
• Vitamin D deficiency
2ndary Hyperparathyroidsim presentation
PTH - raised
Calcium - low or normal
phosphate increased or decreased
Hypercalcaemia presentation
Thirst • Increased urination • Constipation • Bone pain • Fatigue • Depression • Confusion • Kidney stones • Palpitations
Hypoparathyroidism = Reduced or absent PTH
PTH low
Calcium decreased
Phosphate increased
Clinical Features of Paget’s Disease of bone
Common sites: pelvis, femur, lumbar spine, skull, tibia
• Most cases asymptomatic
• Pain in bone/nearby joint (cartilage/adjacent bone damage)
• Deformities: enlargement of skull, bowing of tibia
• Complications: nerve compression (deafness, paraparesis), pathological fractures, high output heart failure, osteosarcoma
Investigations for Paget’s Disease
- ↑ ALP (reflects level of bone formation) • Often >1000 u/L
- Normal Ca2+, PO43-
- Urine hydroxyproline excretion ↑
- X-ray shows localised bony enlargement and distortion, sclerotic changes (↑ density) and osteolytic areas (loss of bone and ↓ density)
- Radionucleotide bone scan shows ↑ uptake of bone- seeking radionucleotides
Management of Paget’s Disease
- Bisphosphonates (zoledronate IV)
- Inhibitboneresorptionby↓osteoclasticactivity
- Indicated in symptomatic patients and asymptomatic patients at risk of complications
- Disease activity monitored by serum ALP or urinary hydroxyproline
Osteoporosis vs Osteopenia
Osteoporosis = bone mineral density >2.5 SD below young adult mean value (T-score ≤ –2.5) •Osteopenia = T-score –1 to –2.5
Risk Factors for Osteoporosis
- ↑ age
- Previous fragility fracture • Family history of #NOF
- ↓ BMI
- Smoking
- Alcohol abuse
- Glucocorticoid therapy
- ↑ bone turnover
- ↑ risk of falls
- Rheumatoid arthritis
Clinical Features of Osteoporosis
- Symptoms result from fractures, typically • Thoracicvertebrae
- Lumbarvertebrae
- Proximalfemur
- Distal radius (Colles’ fracture)
- Thoracic vertebral fractures may lead to kyphosis and loss of height (“widow’s stoop”)
Osteoporosis tests
X-rays detect fractures but are insensitive for osteopenia
• Dual Energy X-ray Absorptiometry (DEXA)
• Gold standard measurement of bone mineral density
• Indicated in radiographic osteopenia, previous fragility
fracture (<75 years), glucocorticoid therapy (<65 years), BMI <19, maternal history #NOF, BMD-dependent risk factors
• FRAX assessment tool
• Estimates 10 year probability of osteoporotic fracture for
untreated patient aged 40-90
Management of Osteoporosis
• New vertebral fractures require bed rest for 1-2 weeks and strong analgesia
• Muscle relaxants (e.g. diazepam), calcitonin SC, pamidronate IV
• Non-spinal fractures treated by orthopaedics
• Stop smoking, ↓ alcohol, adequate dietary
calcium/vitamin D, regular weightbearing exercises
• Elderly: physiotherapy, assessment of home safety to ↓ risk of falls, hip protectors as required
medical
• Bisphosphonates (e.g. alendronate, risedronate, zoledronate); inhibit osteoclasts, ↑ bone mass at hip/spine, ↓ fracture incidence
• Denosumab (monoclonal Ab to RANKL) SC 6 monthly; anti- resorptive agent, ↑ bone mineral density, ↓ fracture incidence
• Selective oestrogen-receptor modulators (SERMs, e.g. raloxifene, bazedoxifene); activate bone oestrogen receptors (not endometrial oestrogen receptors)
• Recombinant human parathyroid peptide 1-34 (teriparatide); stimulate bone formation, indicated in severe/refractory osteoporosis
• Oestrogen therapy (e.g. HRT); early post-menopausal women
• Testosterone; men with evidence of hypogonadism
Microbial keratitis causes
Microbial keratitis
Infection of the cornea causing an epithelial breach with underlying stromal involvement
Broad range of causes:
• Bacterial – most common
• Protozoan (acanthoemeba) – uncommon but severe
• Fungus – rare in UK (common elsewhere)
• Viral – HSV, VZV
Bacterial keratitis: organisms
Common organisms:
Pseudomonas Aeruginosa
Staphylococcus Aureus Streptococci (pyogenes, pneumonia) Neisseria Gonorrhoeae
Bacterial keratitis: risk factors
Risk factors: *Contact lens wear* • Extended wear • Poor hygiene • Swimming/shower/sleeping Trauma Ocular surface disease Immunosuppression/diabetes/vit A def
microbial keratitis symtoms
Symptoms and signs:
Painful red eye, watering and photopobia
White infiltrate on the cornea with overlying epithelial defect
Bacterial keratitis management
Rx: Topical antibiotics (moxifloxacin). Stop contact lens wear for now
fungal keratitis symtoms
Symptoms and signs:
Gradual onset of pain, blurred vision, watery, red eye and photophobia.
White fluffy lesion on cornea, filamentary or satellite lesions +/- hypopyon (white blood cells)
fungal keratitis management
Rx: topical amphotericin/natamycin + antibacterial drops.
Slower recovery, long treatment duration
Acanthamoeba keratitis:
Ubiquitous protozoa in soil, water and upper respiratory tract Cystic, highly resilient Risk factors: *Contact lens wear* • Extended wear • Poor hygiene • Swimming/shower/sleeping Trauma
Acanthamoeba keratitis: symtoms
Symptoms: Blurred vision, red eye and severe disproportionate pain
Signs: Early subtle signs such as white lines and later circular ring infiltrate
Acanthamoeba keratitis: treatment
Treatment: topical amoebicides (polyhexamethylene biguanide PHMB +/- chlorhexidine)
Later corneal transplant if scarring
Viral keratitis:
Common organisms: Herpes simplex Herpes zoster
Risk factors:
History of cold sores or other herpetic rashes
History of trauma Atopy/ocular surface disease Poor sanitation Immunosuppression/diabetes
Viral keratitis: symtoms
Symptoms: mild discomfort, red eye, watering, photophobia and blurred vision
Signs: Red eye with dendritic corneal ulcer staining with fluorescein. Reduced corneal sensation.
Viral keratitis treatment
Treatment: topical antiviral (acyclovir or ganciclovir) 5 x day for around 2 weeks
keratitis tests
Not always enough to recognize aetiology clinically so will need lab diagnosis via corneal scrape
Empirical cover with hourly topical antibiotic with 48 hour review Contact lens education important
gout what is this - things that cause this
Impaired renal excretion of uric acid
• Drugs (e.g. thiazide diuretics, low-dose aspirin)
• Hypertension
• Hypothyroidism
• Primary hyperparathyroidism
• Increased lactic acid production (e.g. alcohol, exercise, starvation)
gout investigations
- Serum uric acid – raised
- RhF, anti-CCP negative
- Synovial aspiration
- Negatively birefringent needle-shaped sodium urate crystals = normal gout
gout management
• NSAIDs
• Colchicine; high dose for 24 hours, tapered doses for 1
week
• Weight loss, reduce alcohol, rationalise diuretics
• Low purine diet (spinach, shellfish, offal)
• Allopurinol (start 2 weeks after acute gout) or febuxostat
gout aspiration
Negatively birefringent needle-shaped sodium urate crystals = normal gout
red flags in back pain
RED FLAG SYMPTOMS: • Extremes of age <20 or >55 years • Acute onset pain • History of malignancy • History of trauma • Immunocompromised- HIV, long term steroids • Systemic symptoms: fever, night sweats, loss of weight • Thoracic pain • Pain at rest or night pain • Focal or progressive neurological deficit • Urinary or bowel disturbance • Disturbed gait, saddle anaesthesia
back pain ddx
Mechanical back pain: • Spondylosis • Spondylolithesis • Intervertebral disc prolapse • Spinal stenosis (claudication pain) • Apophyseal joint disease • Musculoskeletal • Non specific back pain
Referred back pain:
• Aortic aneurysm
• Pyelonephritis, renal calculus
• Pancreatitis, duodenal ulcer
Sinister causes: • Infection (discitis/ epidural abscess) • Malignancy (primary spinal or bony metastases) • Cauda equina or metastatic compression of the spinal cord • Multiple myeloma • Traumatic spinal fracture • Osteoporotic crush fracture • Paget’s disease
Inflammatory -
Rheumatoid arthritis Seronegative spondyloarthritides
Psoriatic
Ankylosing spondylitis Reiter’s syndrome Enteropathic
Investigations back pain
Pathway for investigating back pain
• XR of the spine +/- CXR (for ?malignancy)
• FBC and ESR (elevated in sinister causes)
• Biochemical profile (calcium, ALP and phosphate)
• Immunoglobulins, protein electrophoresis, Bence jones protein and urine protein electrophoresis (myeloma)
• PSA (prostate)
managment back pain
Management:
Analgesia, rest, exercises, physiotherapy, appropriate referral to a specialist if findings from investigation or not improving after 2-3 weeks
Clinical Features of Ankylosing Spondylitis
Clinical Features of Ankylosing Spondylitis
• Asymmetrical peripheral arthritis
• Absence of RhF or Anti-CCP (“seronegative”)
• Loss of lumbar lordosis and increased kyphosis
• Limitation of lumbar spine mobility in both sagittal and coronal planes
• Abnormal Schober’s test
Investigations for Ankylosing Spondylitis
Investigations for Ankylosing Spondylitis • ESR, CRP raised • RhF, anti-CCP negative • X-ray: bamboo spine (or normal) • MRI: sacroilitis
Management of Ankylosing Spondylitis
Management of Ankylosing Spondylitis • Morning exercises • NSAIDs; slow release, taken at night • Methotrexate (helps peripheral arthritis, not spinal disease) • TNF-α blockers
6 associated A’s of Ankylosing Spondylitis
6 associated A’s of Ankylosing Spondylitis
- Apical pulmonary fibrosis
- Anterior uveitis
- Aortic regurgitation
- Achilles’ tendonitis
- AV node block
- Amyloidosis
Pesudogout associated conditions
haemochromatosis, hyperparathyroidism, Wilson’s disease, alkaptonuria
Acute CPP crystal arthritis (“Pseudogout”) presentation
- Acute CPP crystal arthritis (“Pseudogout”)
- Mono-/oligo-arthritis
- Most commonly affects knees; also wrists, shoulders, ankles, hands, feet
- Joint pain and swelling
- Mayhaveassociatedfever
Chronic CPP crystal inflammatory arthritis presentation
Chronic CPP crystal inflammatory arthritis
• Destructive changes (similar to osteoarthritis)
• Progressive destruction may lead to neuropathic joint
• Usuallyaffectsknees,wrists,shoulders,hips
pseudogout cystals
Positively birefringent rhomboidal calcium pyrophosphate crystals
management of Pesudogout
Management of Pesudogout
• NSAIDs
• Colchicine; high dose for 24 hours, tapered doses for 1
week
• Local corticosteroids – must exclude septic arthritis
red flags in chronic pain
Age less than 20 greater than 55 Neurological symptoms/signs Trauma Thoracic back pain History of cancer Weight loss Systemic symptoms Pain incapacitating/worsening Deformity
Yellow flags - Psychosocial risk factors for chronic pain
Belief that back pain is potentially severely disabling
Fear avoidance behaviour
Low mood and social withdrawal
Expectation of passive treatment rather than the belief that active participation will help
There is no rationale for using strong opioids in chronic pain use?
gabapentin
amitriptyline
AST:ALT
chronic liver disease
<1 (i.e. more ALT) suggests chronic liver disease/non-alcoholic; >1 suggests cirrhosis; >2 suggests alcoholic disease
cholestasis LFT’s
Increased ALP raised GGT
ALP increase more than ALT
extrahepatic problem – usually obstruction e.g. gall stones; can be seen also in primary biliary cirrhosis and primary sclerosing cholangitis
Indicators of liver damage
ALT
AST
ALP
GGT – useful to discern if raised ALP is due to liver or bone (or rarely another) pathology
Indicators of liver synthetic function
Bilirubin
Albumin
INR
LFT’s
Obstructive aka Cholestatic Pattern
High bilirubin
High ALP
Normal ALT
LFTs
Hepatitic Pattern –
Very high ALT – between 200- 2000 U/L
Varying bilirubin – the higher the level, the greater the degree of damage
Slightly raised ALP – should be no higher than 2x normal.
Increased prothrombin time – usually will be slightly raised. In cases of severe liver failure it may exceed 25 seconds
hepatocellular injury.
A greater than 10-fold increase in ALT and a less than 3-fold increase in ALP
cholestasis.
less than 10-fold increase in ALT and a more than 3-fold increase in ALP
cause of jaundice:
Normal urine + normal stools = pre-hepatic cause
Dark urine + normal stools = hepatic cause
Dark urine + pale stools = post-hepatic cause (obstructive)
Common causes of acute hepatocellular injury
Poisoning (paracetamol overdose)
Infection (Hepatitis A and B)
Liver ischaemia
Common causes of chronic hepatocellular injury
Alcoholic fatty liver disease
Non-alcoholic fatty liver disease
Chronic infection (Hepatitis B or C)
Primary biliary cirrhosis
monitoring requirements
Statins
LFTs at baseline, 3 months and 12 months
monitoring requirements
Ace inhibitors
U&E prior to treatment
U&E after increasing dose
U&E at least annually
Amiodarone
monitoring requirements
TFT, LFT, U&E, CXR prior to treatment
TFT, LFT every 6 months
Azathioprine
monitoring requirements
FBC, LFT before treatment
FBC weekly for the first 4 weeks
FBC, LFT every 3 months
Lithium
moitoring requirements
TFT, U&E prior to treatment
Lithium levels weekly until stabilised then every 3 months
TFT, U&E every 6 months
Sodium valproate
monitoring requirements
LFT, FBC before treatment
LFT ‘periodically’ during first 6 months
!st line depression
Selective serotonin reuptake inhibitors (SSRIs) are considered first-line treatment for the majority of patients with depression
citalopram and fluoxetine are currently the preferred SSRIs
sertraline is useful post myocardial infarction as there is more evidence for its safe use in this situation than other antidepressants
SSRIs should be used with caution in children and adolescents. Fluoxetine is the drug of choice when an antidepressant is indicated.
Adverse effects of SSRI’s
dverse effects
gastrointestinal symptoms are the most common side-effect
there is an increased risk of gastrointestinal bleeding in patients taking SSRIs. A proton pump inhibitor should be prescribed if a patient is also taking a NSAID
patients should be counselled to be vigilant for increased anxiety and agitation after starting a SSRI
fluoxetine and paroxetine have a higher propensity for drug interactions
Citalopram and the QT interval
it advised that citalopram and escitalopram are associated with dose-dependent QT interval prolongation and should not be used in those with: congenital long QT syndrome; known pre-existing QT interval prolongation; or in combination with other medicines that prolong the QT interval
the maximum daily dose is now 40 mg for adults; 20 mg for patients older than 65 years; and 20 mg for those with hepatic impairment
SSRI’s interactions
Interactions
NSAIDs: NICE guidelines advise ‘do not normally offer SSRIs’, but if given co-prescribe a proton pump inhibitor
warfarin / heparin: NICE guidelines recommend avoiding SSRIs and considering mirtazapine
aspirin: see above
triptans - increased risk of serotonin syndrome
monoamine oxidase inhibitors (MAOIs) - increased risk of serotonin syndrome
SSRI discontinuation
When stopping a SSRI the dose should be gradually reduced over a 4 week period (this is not necessary with fluoxetine). Paroxetine has a higher incidence of discontinuation symptoms.
Discontinuation symptoms increased mood change restlessness difficulty sleeping unsteadiness sweating gastrointestinal symptoms: pain, cramping, diarrhoea, vomiting paraesthesia
SSRI’s and pregnancy
SSRIs and pregnancy
- BNF says to weigh up benefits and risk when deciding whether to use in pregnancy.
- Use during the first trimester gives a small increased risk of congenital heart defects
- Use during the third trimester can result in persistent pulmonary hypertension of the newborn
- Paroxetine has an increased risk of congenital malformations, particularly in the first trimester
Lithium use and Mode of action
Lithium is mood stabilising drug used most commonly prophylactically in bipolar disorder but also as an adjunct in refractory depression. It has a very narrow therapeutic range (0.4-1.0 mmol/L) and a long plasma half-life being excreted primarily by the kidneys.
Mechanism of action - not fully understood, two theories:
interferes with inositol triphosphate formation
interferes with cAMP formation
Lithium adverse effects
nausea/vomiting, diarrhoea
fine tremor
nephrotoxicity: polyuria, secondary to nephrogenic diabetes insipidus
thyroid enlargement, may lead to hypothyroidism
ECG: T wave flattening/inversion
weight gain
idiopathic intracranial hypertension
leucocytosis
hyperparathyroidism and resultant hypercalcaemia
lithium moitoring
when checking lithium levels, the sample should be taken 12 hours post-dose
after starting lithium levels should be performed weekly and after each dose change until concentrations are stable
once established, lithium blood level should ‘normally’ be checked every 3 months
after a change in dose, lithium levels should be taken a week later and weekly until the levels are stable.
thyroid and renal function should be checked every 6 months
patients should be issued with an information booklet, alert card and record book
Olanzapine specific side effects
dyslipidemia and weight gain, and is also associated with diabetes and sedation.
Quetiapine specific side effects
weight gain and dyslipidemia.
posteural hypertension
Clozapine specific side effects
f agranulocytosis and full blood count monitoring is therefore essential during treatment
reduced seizure threshold - can induce seizures in up to 3% of patients
constipation
myocarditis: a baseline ECG should be taken before starting treatment
hypersalivation
Risperidone specific side effects
extrapyramidal side effects, as well as cause postural hypotension and sexual dysfunction.
Symptoms of mania in primary care:
Urgent referral to CMHT
Duloxetine mechanism of action
serotonin and noradrenaline reuptake inhibitor
OCD associations
Associations depression (30%) schizophrenia (3%) Sydenham's chorea Tourette's syndrome anorexia nervosa
reverse dystonia which may be induced by haloperidol.
procyclidine
Extrapyramidal side-effects (EPSEs) of antipsychotics
Parkinsonism
acute dystonia: sustained muscle contraction (e.g. torticollis, oculogyric crisis)
akathisia (severe restlessness)
tardive dyskinesia (late onset of choreoathetoid movements, abnormal, involuntary, may occur in 40% of patients, may be irreversible, most common is chewing and pouting of jaw)
EPSEs may be managed with procyclidine
diagnosis of depression over dementia
short history, rapid onset
biological symptoms e.g. weight loss, sleep disturbance
patient worried about poor memory
reluctant to take tests, disappointed with results
mini-mental test score: variable
global memory loss (dementia characteristically causes recent memory loss)
Alcohol withdrawal timeline
symptoms: 6-12 hours
seizures: 36 hours
delirium tremens: 72 hours
Alcohol withdrawa
Management
patients with a history of complex withdrawals from alcohol (i.e. delirium tremens, seizures, blackouts) should be admitted to hospital for monitoring until withdrawals stabilised
first-line: benzodiazepines e.g. chlordiazepoxide. Lorazepam may be preferable in patients with hepatic failure. Typically given as part of a reducing dose protocol
carbamazepine also effective in treatment of alcohol withdrawal
phenytoin is said not to be as effective in the treatment of alcohol withdrawal seizures
Management of generalised anxiety disorder (GAD)
NICE suggest a step-wise approach:
step 1: education about GAD + active monitoring
step 2: low intensity psychological interventions (individual non-facilitated self-help or individual guided self-help or psychoeducational groups)
step 3: high intensity psychological interventions (cognitive behavioural therapy or applied relaxation) or drug treatment. See drug treatment below for more information
step 4: highly specialist input e.g. Multi agency teams
Drug treatment
generalised anxiety disorder (GAD)
NICE suggest sertraline should be considered the first-line SSRI
if sertraline is ineffective, offer an alternative SSRI or a serotonin–noradrenaline reuptake inhibitor (SNRI)
examples of SNRIs include duloxetine and venlafaxine
If the person cannot tolerate SSRIs or SNRIs, consider offering pregabalin
interestingly for patients under the age of 30 years NICE recommend you warn patients of the increased risk of suicidal thinking and self-harm. Weekly follow-up is recommended for the first month
panic disorder drug treatment
Treatment in primary care
NICE recommend either cognitive behavioural therapy or drug treatment
SSRIs are first-line. If contraindicated or no response after 12 weeks then imipramine or clomipramine should be offere
Schizoid personality disorder is characterized by at least 3 of the following:
Few, if any, activities, provide pleasure;
Emotional coldness, detachment or flattened affectivity;
Limited capacity to express either warm, tender feelings or anger towards others;
Apparent indifference to either praise or criticism;
Little interest in having sexual experiences with another person (taking into account age);
Almost invariable preference for solitary activities;
Excessive preoccupation with fantasy and introspection;
Lack of close friends or confiding relationships (or having only one) and of desire for such relationships;
Marked insensitivity to prevailing social norms and conventions.
mirtazapine,
works by blocking alpha2-adrenergic receptors, which increases the release of neurotransmitters.
Two side effects of mirtazapine, sedation and an increased appetite, can be beneficial in older people that are suffering from insomnia and poor appetite.
