ANXIETY DISORDERS & MANAGEMENT

A seminar on Anxiety disorders and management.

1. ANXIETY DISORDERS SILCHAR MEDICAL COLLEGE & HOSPITAL

2. PLAN OF PRESENTATION INTRODUCTION TYPES OF ANXIETY NEUROBIOLOGY OF ANXIETY DISORDERS SYMPTOMATOLOGY MANAGEMENT PHARMACOLOGICAL NON PHARMACOLOGICAL RECENT ADVANCES

3. WHAT IS ANXIETY ? ANXIETY IS A DIFFUSE, HIGHLY UNPLEASANT, OFTEN VAGUE FEELING OF APREHENSION, ACCOMPANIED BY ONE OR MORE BODILY SENSATIONS- PALPITATIONS, PERSPIRATIONS, HEADACHE ETC. PHILOSOPHERS AND THINKERS HAVE LONG WRITTEN ABOUT THE CENTRALITY OF ANXIETY IN HUMAN LIFE AND EXPERIENCES. ON THE OTHERHAND, IT IS ONE OF THE NEWEST OF SUBJECTS AS THE SCIENTISTS ARE UNDERSTANDING THE UNDERLYING PSYCHOBIOLOGY AND ITS MANAGEMENT , EFFECTIVELY ONLY FOR LAST FEW DECADES.

4. DEFINITION “Feeling of apprehension caused by anticipation of danger, which may be internal or external” “Anxiety is an emotional state commonly caused by the perception of real or perceived danger that threatens the security of an individual. It allows a person to prepare for or react to environmental changes.” This is an adaptive response, and is transient in nature.

5. ANXIETY IS A NORMAL EMOTION UNDER CIRCUMSTANCES OF THREAT AND IS THOUGHT TO BE PART OF THE EVOLUTIONARY “FIGHT OR FLIGHT” REACTION OF SURVIVAL. ANXIETY CAN PRODUCE UNCOMFORTABLE AND POTENTIALLY DEBILITATING PSYCHOLOGICAL (E.G., WORRY OR FEELING OF THREAT) AND PHYSIOLOGICAL AROUSAL (E.G., TACHYCARDIA OR SHORTNESS OF BREATH) IF IT BECOMES EXCESSIVE. SOME INDIVIDUALS EXPERIENCE PERSISTENT, SEVERE ANXIETY SYMPTOMS AND POSSESS IRRATIONAL FEARS THAT SIGNIFICANTLY IMPAIR NORMAL DAILY FUNCTIONING. THESE PERSONS OFTEN SUFFER FROM AN ANXIETY DISORDER.

6. TYPES OF ANXIETY AN INTEGRAL PART OF OUR DAY TO DAY LIFE AND HELPS THE INDIVIDUAL IN COPING WITH STRESS DEVELOPING BETTER ADAPTIVE SKILL PLANNING AHEAD BETTER PERFORMANCE INTENSED INTERNAL UNCOMFORTABLE FEELING STATE LEADS TO MALADAPTIVE BEHAVIOUR , THOUGHT AND COGNITONS AND POORER PERFORMANCE. NORMAL ANXIETY PATHOLOGICAL ANXIETY ANXIETY DISORDER

7. CLASSIFICATION OF ANXIETY DISORDER PANIC DISORDER WITHOUT AGORAPHOBIA. PANIC DISORDER WITH AGORAPHOBIA. AGORAPHOBIA WITHOUT H/O PANIC DISORDER. SPECIFIC PHOBIA. SOCIAL PHOBIA. OCD PTSD ACUTE STRESS DISORDER GENERALISED ANX- DISORDER. ANXIETY DISORDER DUE TO GENERAL MEDICAL CONDITION. SUBSTANCE INDUCED ANXIETY DISORDER. ANXIETY DIS ORDER NOS. DSM IV – TR

8. SEPARATION ANXIETY DISORDER SELECTIVE MUTISM SPECIFIC PHOBIA SOCIAL ANXIETY DISORDER PANIC DISORDER PANIC ATTACK AGORAPHOBIA GENERELIZED ANXIETY DISORDER SUBSTANCE/MEDICATION INDUCED ANXIETY DISORDER ANXIETY DISORDER DUE TO ANOTHER MEDICAL CONDITION OTHER SPECIFIED ANXIETY DISORDER UNSPECIFIED ANXIETY DISORDER DSM - V NEW !!! NEW !!! NEW !!! NEW !!! CHANGES UNLINKING OF PANIC DISORDER & AGORAPHOBIA OBSESSIVE COMPULSIVE DISORDER, PTSD & ACUTE STRESS DISORDER NO LONGER INCLUDED. PANIC ATTACK – AS A SPECIFIER

9. NEUROBIOLOGY OF ANXIETY DISORDERS

10. ALL ANXIETY DISORDERS HAVE 2 COMPONENTS TO UNDERSTAND THE NEUROBIOLOGY OF ANY ANXIETY DISORDER WE NEED TO UNDERSTAND THE NEUROBIOLOGY OF BOTH FEAR WORRY

11. FEAR - PANIC - PHOBIA WORRY - ANXIOUS MISERY - APPREHENSION - EXPECTATION - OBSESSIONS

12. LINKING ANXIETY SYMPTOMS TO CIRCUITS ANXIETY AND FEAR SYMPTOMS ARE REGULATED BY AN AMYGDALA-CENTERED CIRCUIT. WORRY, ON THE OTHER HAND, IS REGULATED BY A CORTICO-STRIATO-THALAMOCORTICAL (CSTC) LOOP. THESE CIRCUITS MAY BE INVOLVED IN ALL ANXIETY DISORDERS, WITH THE DIFFERENT PHENOTYPES REFLECTING NOT UNIQUE CIRCUITRY BUT RATHER DIVERGENT MALFUNCTIONING WITHIN THOSE CIRCUITS.

13. LOOKING AFRAID/ AFFECT OF FEAR AMYGDALA ORBITO FC ACC FEELINGS OF FEAR ARE REGULATED BY RECIPROCAL CONNECTIONS BETWEEN THE AMYGDALA AND THE ANTERIOR CINGULATE CORTEX (ACC) AND THE AMYGDALA AND THE ORBITOFRONTAL CORTEX (OFC). SPECIFICALLY, IT MAY BE THAT OVER ACTIVATION OF THESE CIRCUITS PRODUCES FEELINGS OF FEAR.

14. WHAT YOU WILL DO ? FIGHT ! FLIGHT ! FREEZE !

15. AVOIDANCE/FIGHT/FLIGHT/FREEZE MOTOR RESPONSE AMYGDALA PAG FEELINGS OF FEAR MAY BE EXPRESSED THROUGH BEHAVIORS SUCH AS AVOIDANCE, WHICH IS PARTLY REGULATED BY RECIPROCAL CONNECTIONS BETWEEN THE AMYGDALA AND THE PERIAQUEDUCTAL GRAY (PAG). AVOIDANCE IN THIS SENSE IS A MOTOR RESPONSE. OTHER MOTOR RESPONSES ARE TO FIGHT OR TO RUN AWAY (FLIGHT) IN ORDER TO SURVIVE THREATS FROM THE ENVIRONMENT .

16. HYPERVENTILATION

17. CHANGES IN RESPIRATORY RATE AMYGDALA PBN CHANGES IN RESPIRATION MAY OCCUR DURING A FEAR RESPONSE; THESE CHANGES ARE REGULATED BY ACTIVATION OF THE PARABRACHIAL NUCLEUS (PBN) VIA THE AMYGDALA. INAPPROPRIATE OR EXCESSIVE ACTIVATION OF THE PBN CAN LEAD NOT ONLY TO INCREASES IN THE RATE OF RESPIRATION BUT ALSO VARIOUS SYMPTOMS. SHORTNESS OF BREATH EXACERBATION OF ASTHMA, OR A SENSE OF BEING SMOTHERED.

18. AUTONOMIC OUTPUT OF FEAR SUDDEN DEATH ATHEROSCLEROSIS CARDIAC ISCHEMIA BLOOD PRESSURE MYOCARDIAL INFARCTION “SCARED TO DEATH” MAY NOT ALWAYS BE AN EXAGGERATION OR A FIGURE OF SPEECH!

19. AUTONOMIC OUTPUT OF FEAR AMYGDALA LC AUTONOMIC RESPONSES ARE TYPICALLY ASSOCIATED WITH FEELINGS OF FEAR. THESE INCLUDE INCREASES IN HEART RATE (HR) AND BLOOD PRESSURE (BP), WHICH ARE REGULATED BY RECIPROCAL CONNECTIONS BETWEEN THE AMYGDALA AND THE LOCUS COERULEUS (LC). LONG-TERM ACTIVATION OF THIS CIRCUIT MAY LEAD TO INCREASED RISK OF ATHEROSCLEROSIS, CARDIAC ISCHEMIA, CHANGE IN BP, DECREASED HR VARIABILITY, MYOCARDIAL INFARCTION (MI), OR EVEN SUDDEN DEATH.

20. ENDOCRINE OUTPUT OF FEAR

21. ENDOCRINE OUTPUT OF FEAR AMYGDALA HYPOTHALAMUS THE FEAR RESPONSE MAY BE CHARACTERIZED IN PART BY ENDOCRINE EFFECTS SUCH AS INCREASES IN CORTISOL, WHICH OCCUR BECAUSE OF AMYGDALA ACTIVATION OF THE HYPOTHALAMIC–PITUITARY–ADRENAL (HPA) AXIS. PROLONGED HPA ACTIVATION AND CORTISOL RELEASE CAN HAVE SIGNIFICANT HEALTH IMPLICATIONS, SUCH AS INCREASED RISK OF CORONARY ARTERY DISEASE, TYPE 2 DIABETES, AND STROKE.

22. STRESS AND THE HPA AXIS ADULT STRESSORS DISINHIBITION OF HPA AXIS BY HIPPOCAMPUS CRF RELEASE ACTH RELEASE GLUCO- CORTICOID RELEASE HIPPOCAMPAL ATROPHY ABNORMAL STRESS RESPONSE MDD ANXIETY DISORDER CRF RELEASE GLUCOCORTICOIDS INHIBIT CRF RELEASE ACTH RELEASE GLUCO- CORTICOID RELEASE NORMAL STRESS RESPONSE

23. PATHOPHYSIOLOGY DATA FROM BIOCHEMICAL AND NEUROIMAGING STUDIES INDICATE THAT THE MODULATION OF NORMAL AND PATHOLOGIC ANXIETY STATES IS ASSOCIATED WITH MULTIPLE REGIONS OF THE BRAIN AND ABNORMAL FUNCTION IN SEVERAL NEUROTRANSMITTER SYSTEMS, INCLUDING NOREPINEPHRINE (NE) SEROTONIN (5-HT) γ –AMINOBUTYRIC ACID (GABA)

24. NORADRENERGIC MODEL THIS MODEL SUGGESTS THAT THE AUTONOMIC NERVOUS SYSTEM OF ANXIOUS PATIENTS IS HYPERSENSITIVE AND OVERREACTS TO VARIOUS STIMULI. THE LOCUS CERULEUS MAY HAVE A ROLE IN REGULATING ANXIETY, AS IT ACTIVATES NOREPINEPHRINE RELEASE AND STIMULATES THE SYMPATHETIC AND PARASYMPATHETIC NERVOUS SYSTEMS. 5-HT MODEL GAD SYMPTOMS MAY REFLECT EXCESSIVE 5-HT TRANSMISSION OR OVERACTIVITY OF THE STIMULATORY 5-HT PATHWAYS. PATIENTS WITH SAD HAVE GREATER PROLACTIN RESPONSE TO BUSPIRONE CHALLENGE, INDICATING AN ENHANCED CENTRAL SEROTONERGIC RESPONSE. THE ROLE OF 5-HT IN PANIC DISORDER IS UNCLEAR, BUT IT MAY HAVE A ROLE IN DEVELOPMENT OF ANTICIPATORY ANXIETY. PRELIMINARY DATA SUGGEST THAT THE 5-HT AND 5-HT2 ANTAGONIST METACHLOROPHENYLPIPERAZINE CAUSES INCREASED ANXIETY IN PTSD PATIENTS.

25. γ- AMINOBUTYRIC ACID (GABA) RECEPTOR MODEL GABA IS THE MAJOR INHIBITORY NEUROTRANSMITTER IN THE CNS. MANY ANTIANXIETY DRUGS TARGET THE GABA RECEPTOR. BENZODIAZEPINES (BZS) ENHANCE THE INHIBITORY EFFECTS OF GABA,WHICH HAS A STRONG REGULATORY OR INHIBITORY EFFECT ON SEROTONIN (5-HT), NOREPINEPHRINE, AND DOPAMINE SYSTEMS. ANXIETY SYMPTOMS MAY BE LINKED TO UNDERACTIVITY OF GABA SYSTEMS OR DOWNREGULATED CENTRAL BZ RECEPTORS. IN PATIENTS WITH GAD, BZ BINDING IN THE LEFT TEMPORAL LOBE IS REDUCED ABNORMAL SENSITIVITY TO ANTAGONISM OF THE BZ BINDING SITE AND DECREASED BINDING WAS DEMONSTRATED IN PANIC DISORDER. ABNORMALITIES OF GABA INHIBITION MAY LEAD TO INCREASED RESPONSE TO STRESS IN PTSD PATIENTS.

26. NEUROTRANSMITTER IN CIRCUITS AMYGDALA CENTRED CIRCUIT [ FEAR LOOP ] 5HT GABA GLUTAMATE CRF/HPA NE VOLTAGE GATED ION CHANNELS. CSTC [WORRY LOOP ] 5HT GABA GLUTAMATE DA NE VOLTAGE GATED ION CHANNEL.

27. SYMPTOMS

28. GENERALIZED ANXIETY DISORDER THE DIAGNOSTIC CRITERIA FOR GAD REQUIRE PERSISTENT SYMPTOMS FOR MOST DAYS FOR AT LEAST 6 MONTHS. THE ESSENTIAL FEATURE OF GAD IS UNREALISTIC OR EXCESSIVE ANXIETY AND WORRY ABOUT A NUMBER OF EVENTS OR ACTIVITIES OR OTHER IMPORTANT AREAS OF FUNCTIONING.

29. PRESENTATION OF GENERALIZED ANXIETY DISORDER PSYCHOLOGICAL AND COGNITIVE SYMPTOMS : EXCESSIVE ANXIETY WORRIES THAT ARE DIFFICULT TO CONTROL FEELING KEYED UP OR ON EDGE POOR CONCENTRATION OR MIND GOING BLANK PHYSICAL SYMPTOMS : RESTLESSNESS FATIGUE MUSCLE TENSION SLEEP DISTURBANCE IRRITABILITY

30. PANIC DISORDER PANIC DISORDER BEGINS AS A SERIES OF UNEXPECTED (SPONTANEOUS) PANIC ATTACKS INVOLVING AN INTENSE, TERRIFYING FEAR SIMILAR TO THAT CAUSED BY LIFE-THREATENING DANGER. DURING AN ATTACK, PATIENTS OFTEN DESCRIBE AN OVERWHELMING SENSE OF DOOM, A FEAR OF DYING OR LOSING CONTROL. PANIC ATTACKS USUALLY LAST NO MORE THAN 20 TO 30 MINUTES, WITH THE PEAK INTENSITY OF SYMPTOMS WITHIN THE FIRST 10 MINUTES. SECONDARY TO THE PANIC ATTACKS, MANY PATIENTS EVENTUALLY DEVELOP AGORAPHOBIA.

31. SYMPTOMS OF A PANIC ATTACK PSYCHOLOGICAL SYMPTOMS DEPERSONALIZATION DEREALIZATION FEAR OF LOSING CONTROL FEAR OF GOING CRAZY FEAR OF DYING. PHYSICAL SYMPTOMS : ABDOMINAL DISTRESS CHEST PAIN OR DISCOMFORT CHILLS DIZZINESS OR LIGHT-HEADEDNESS FEELING OF CHOKING HOT FLUSHES PALPITATIONS NAUSEA SHORTNESS OF BREATH SWEATING TACHYCARDIA TREMBLING OR SHAKING.

32. SOCIAL ANXIETY DISORDER SAD IS CHARACTERIZED BY AN INTENSE, IRRATIONAL, AND PERSISTENT FEAR OF BEING NEGATIVELY EVALUATED OR SCRUTINIZED IN AT LEAST ONE SOCIAL OR PERFORMANCE SITUATION. EXPOSURE TO THE FEARED CIRCUMSTANCE USUALLY PROVOKES AN IMMEDIATE SITUATION-RELATED PANIC ATTACK. ADULTS WITH SAD USUALLY RECOGNIZE THEIR FEAR IS EXCESSIVE AND UNREASONABLE; HOWEVER, THEY ARE UNABLE TO OVERCOME IT WITHOUT TREATMENT. WHY CAN’T I TALK TO PEOPLE ?

33. SOCIAL ANXIETY DISORDER IN INDIVIDUALS UNDER 18 YEARS OF AGE, THE DURATION OF SYMPTOMS IS AT LEAST 6 MONTHS. THE FEAR OR AVOIDANCE IS NOT CAUSED BY A DRUG OR OTHER SUBSTANCE (E.G., COCAINE), OR A GENERAL MEDICAL OR PSYCHIATRIC DISORDER . THE MEAN AGE OF ONSET OF SAD IS DURING THE MID-TEENS. RATES OF SAD ARE SLIGHTLY HIGHER AMONG WOMEN THAN MEN AND MORE FREQUENT IN YOUNGER COHORTS. IT IS A CHRONIC DISORDER WITH A MEAN DURATION OF 20 YEARS.

34. POST TRAUMATIC STRESS DISORDER

35. POSTTRAUMATIC STRESS DISORDER (PTSD) POSTTRAUMATIC STRESS DISORDER (PTSD) IS A CONDITION MARKED BY THE DEVELOPMENT OF SYMPTOMS AFTER EXPOSURE TO TRAUMATIC LIFE EVENTS. THE PERSON REACTS TO THIS EXPERIENCE WITH FEAR AND HELPLESSNESS, PERSISTENTLY RELIVES THE EVENT, AND TRIES TO AVOID BEING REMINDED OF IT. PTSD CAN OCCUR AT ANY AGE, AND THE COURSE IS VARIABLE. ONE-THIRD OF PATIENTS WITH PTSD HAVE A POOR PROGNOSIS, AND ABOUT 80% HAVE A CONCURRENT DEPRESSION OR ANXIETY DISORDER.

36. THE HIPPOCAMPUS AND RE-EXPERIENCING AMYGDALA HIPPOCAMPUS ANXIETY CAN BE TRIGGERED NOT ONLY BY AN EXTERNAL STIMULUS BUT ALSO BY AN INDIVIDUAL’S MEMORIES. TRAUMATIC MEMORIES STORED IN THE HIPPOCAMPUS CAN ACTIVATE THE AMYGDALA, CAUSING THE AMYGDALA, IN TURN, TO ACTIVATE OTHER BRAIN REGIONS AND GENERATE A FEAR RESPONSE. THIS IS TERMED RE-EXPERIENCING, AND IT IS A PARTICULAR FEATURE OF POSTTRAUMATIC STRESS DISORDER.

37. PTSD SYMPTOMS RE-EXPERIENCING SYMPTOMS AVOIDANCE SYMPTOMS RECURRENT, INTRUSIVE DISTRESSING MEMORIES OF THE TRAUMA RECURRENT, DISTURBING DREAMS OF THE EVENT FEELING THAT THE TRAUMATIC EVENT IS RECURRING (E.G., DISSOCIATIVE FLASHBACKS) PHYSIOLOGIC REACTION TO REMINDERS OF THE TRAUMA AVOIDANCE OF CONVERSATIONS ABOUT THE TRAUMA AVOIDANCE OF THOUGHTS OR FEELINGS ABOUT THE TRAUMA, AVOIDANCE OF ACTIVITIES THAT ARE REMINDERS OF THE EVENT AVOIDANCE OF PEOPLE OR PLACES THAT AROUSE RECOLLECTIONS OF THE TRAUMA INABILITY TO RECALL AN IMPORTANT ASPECT OF THE TRAUMA ANHEDONIA RESTRICTED AFFECT SENSE OF A FORESHORTENED FUTURE (E.G., DOES NOT EXPECT TO HAVE A CAREER, MARRIAGE)

38. HYPER-AROUSAL SYMPTOMS DECREASED CONCENTRATION EASILY STARTLED HYPERVIGILANCE INSOMNIA IRRITABILITY OR ANGRY OUTBURSTS SUBTYPES ACUTE: DURATION OF SYMPTOMS IS LESS THAN 3 MONTHS CHRONIC: SYMPTOMS LAST FOR LONGER THAN 3 MONTHS WITH DELAYED ONSET: ONSET OF SYMPTOMS IS AT LEAST 6 MONTHS POSTTRAUMA

39. OBSESSIVE-COMPULSIVE DISORDER (OCD)

40. OBSESSIVE-COMPULSIVE DISORDER (OCD) OBSESSIVE-COMPULSIVE DISORDER (OCD) IS ONE OF THE TEN LEADING CAUSES OF DISABILITY. PATIENTS WITH OCD EXPERIENCE SIGNIFICANT IMPAIRMENT IN THEIR QUALITY OF LIFE (QOL), WITH REDUCTIONS IN SOCIAL, FAMILY, AND OCCUPATIONAL FUNCTIONING. BECAUSE OF THE NATURE AND POTENTIAL SEVERITY OF SIGNS AND SYMPTOMS AND THE RESULTANT NEGATIVE EFFECTS ON QOL, OCD IS CONSIDERED A MAJOR MEDICAL CONDITION.

41. NEURAL CIRCUITS OF OBSESSION/WORRY THALAMUS STRIATUM DLPFC SHOWN HERE IS A CORTICO-STRIATOTHALAMO- CORTICAL (CSTC) LOOP ORIGINATING AND ENDING IN THE DORSOLATERAL PREFRONTAL CORTEX (DLPFC). OVERACTIVATION OF THIS CIRCUIT MAY LEAD TO WORRY OR OBSESSIONS.

42. PRESENTATION OBSESSIONS REPETITIVE THOUGHTS (E.G., FEELING CONTAMINATED AFTER TOUCHING AN OBJECT, DOUBTING WHETHER THE STOVE WAS TURNED OFF) REPETITIVE IMAGES (E.G., RECURRENT SEXUALLY EXPLICIT PICTURES) REPETITIVE IMPULSES (E.G., NEED FOR SYMMETRY OR PUTTING THINGS IN SPECIFIC ORDER, IMPULSE TO SHOUT OUT OBSCENITIES IN A TEMPLE) COMPULSIONS REPETITIVE ACTIVITIES (E.G., HAND WASHING, CHECKING, ORDERING, NEED TO ASK, NEED TO CONFESS) REPETITIVE MENTAL ACTS (E.G., COUNTING, REPEATING WORDS SILENTLY, PRAYING)

43. DRUGS ASSOCIATED WITH ANXIETY SYMPTOMS ANTICONVULSANTS: CARBAMAZEPINE ANTIDEPRESSANTS: SELECTIVE SEROTONIN REUPTAKE INHIBITORS, TRICYCLIC ANTIDEPRESSANTS ANTIHYPERTENSIVES: FELODIPINE ANTIBIOTICS: QUINOLONES, ISONIAZID BRONCHODILATORS: ALBUTEROL, THEOPHYLLINE CORTICOSTEROIDS: PREDNISONE DOPA AGONISTS: LEVODOPA HERBALS: MA HUANG, GINSENG, EPHEDRA NONSTEROIDAL ANTI-INFLAMMATORY DRUGS: IBUPROFEN STIMULANTS: AMPHETAMINES, METHYLPHENIDATE, CAFFEINE, COCAINE SYMPATHOMIMETICS: PSEUDOEPHEDRINE THYROID HORMONES: LEVOTHYROXINE TOXICITY: ANTICHOLINERGICS, ANTIHISTAMINES, DIGOXIN WITHDRAWAL: ALCOHOL, SEDATIVES.

44. MEDICAL DISEASES ASSOCIATED WITH ANXIETY COMMON MEDICAL ILLNESSES ASSOCIATED WITH ANXIETY SYMPTOMS CARDIOVASCULAR : ANGINA, ARRHYTHMIAS, CONGESTIVE HEART FAILURE, ISCHEMIC HEART DISEASE, MYOCARDIAL INFARCTION ENDOCRINE AND METABOLIC : CUSHING’S DISEASE, HYPERPARATHYROIDISM, HYPERTHYROIDISM, HYPOTHYROIDISM, HYPOGLYCEMIA, HYPONATREMIA, HYPERKALEMIA, PHEOCHROMOCYTOMA, VITAMIN B12 OR FOLATE DEFICIENCIES NEUROLOGIC : DEMENTIA, MIGRAINE, PARKINSON’S DISEASE, SEIZURES, STROKE, NEOPLASMS, POOR PAIN CONTROL RESPIRATORY SYSTEM : ASTHMA, CHRONIC OBSTRUCTIVE PULMONARY DISEASE, PULMONARY EMBOLUS, PNEUMONIA OTHERS : ANEMIAS, SYSTEMIC LUPUS ERYTHEMATOSUS, VESTIBULAR DYSFUNCTION

45. MANAGEMENT

46. INVESTIGATIONS BLOOD SUGAR – T2 DM LIPID PROFILE CORTISOL LEVEL URINE DRUG SCREEN: SHOULD BE ORDERED TO RULE OUT SUSPECTED STIMULANT ABUSE TFTS: RECOMMENDED IF THE PATIENT HAS SUSPECTED THYROID DISEASE (E.G., WEIGHT LOSS, GOITRE) 24-HOUR URINE TEST FOR VANILLYLMANDELIC ACID AND METANEPHRINES: ORDERED TO RULE OUT PHAEOCHROMOCYTOMA IF CARDIAC SYMPTOMS SUCH AS TACHYCARDIA AND/OR HYPERTENSION ARE PRESENT ECG AND ECHOCARDIOGRAM: RECOMMENDED FOR PATIENTS WITH A HIGH RISK OF CARDIAC DISEASE OR EVIDENCE OF CARDIAC DISEASE PULMONARY FUNCTION TESTS: SHOULD BE CONSIDERED FOR PATIENTS WITH SHORTNESS OF BREATH AND EVIDENCE OF PULMONARY DISEASE EEG: USEFUL FOR EVALUATING PATIENTS WHERE ANXIETY IS SUSPECTED TO BE A SEIZURE PRODROMAL SYMPTOM.

47. SCALES COMMONLY USED HAMILTON’S ANXIETY RATING SCALE BECK ANXIETY INVENTORY (BAI)

48. TREATMENT PHARMACOLOGICAL NON-PHARMACOLOGICAL/ PSYCHOTHERAPY

49. PHARMACOLOGICAL

50. PHARMACOLOGICAL 3 MAJOR NEUROTRANSMITTERS ARE TARGETTED IN PHARMACOLOGICAL TREATMENT OF ANXIETY DISORDERS GABA - A. BENZODIAZEPINES SEROTONIN - B. SSRIs NOREPINEPHRIN - C. SNRIs

51. A) BENZODIAZEPINES BENZODIAZEPINES, PERHAPS THE BEST-KNOWN AND MOST WIDELY USED ANXIOLYTICS, ACT BY ENHANCING GABA ACTIONS AT THE LEVEL OF THE AMYGDALA AND AT THE LEVEL OF THE PREFRONTAL CORTEX WITHIN CSTC LOOPS TO RELIEVE ANXIETY. 3 MAJOR TYPES 1,4 BENZODIAZEPINES 1,5 BENZODIAZEPINES 2,3 BENZODIAZEPINES

52. 1,4 BENZODIAZEPINES ADVANTAGES: ANXIOLYSIS SEDATION, MUSCLE RELAXATION DISADVANTAGES COGNITIVE AND PSYCHOMOTOR IMPAIRMENT ADDICTIVENESS EG – LORAZEPAM, CLONAZEPAM, OXAZEPAM, FLUNITRAZEPAM, CHLORDIAZEPOXIDE, DIAZEPAM ETC

53. 1,5 BENZODIAZEPINE CLOBAZAM ADVANTAGES & DISADVANTAGES ANXIOLYTIC ANTIEPILEPTIC DECREASED SEDATION LOW DEPENDENCE LOW MUSCLE RELAXATION CAN BE USED IN EXECUTIVE GROUPS CAN BE CONTINUED FOR LONG PERIOD OF TIME

54. 2,3 BENZODIAZEPINES TOFISOPAM TOFISOPAM, A RACEMIC 2,3-BENZODIAZEPINE COMPRISED OF R- AND S-ENANTIOMERS, IS UNLIKE TRADITIONAL 1,4-BENZODIAZEPINES. ADVANTAGES LIKE OTHER BENZODIAZEPINES, IT POSSESSES ANXIOLYTIC PROPERTIES BUT UNLIKE OTHER BENZODIAZEPINES IT DOES NOT HAVE ANTICONVULSANT*, SEDATIVE, SKELETAL MUSCLE RELAXANT, MOTOR SKILL-IMPAIRING OR AMNESTIC PROPERTIES. * WHILE IT MAY NOT BE AN ANTICONVULSANT IN AND OF ITSELF, IT HAS BEEN SHOWN TO ENHANCE THE ANTICONVULSANT ACTION OF CLASSICAL 1,4-BENZODIAZEPINES SUCH AS DIAZEPAM. BINDS TO 2,3 BDZS SITES IN THE SUBCORTICAL AREA. IT DOES NOT BIND TO GABA-A RECEPTOR COMPLEX IN CORTICAL AREAS

55. B) SELECTIVE SEROTONIN REUPTAKE INHINITOR SEROTONIN IS A KEY NEUROTRANSMITTER THAT INNERVATES THE AMYGDALA AS WELL AS ALL THE ELEMENTS OF CSTC CIRCUITS, NAMELY, PREFRONTAL CORTEX, STRIATUM, AND THALAMUS, AND THUS IS POISED TO REGULATE BOTH FEAR AND WORRY. ANTIDEPRESSANTS THAT CAN INCREASE SEROTONIN OUTPUT BY BLOCKING THE SEROTONIN TRANSPORTER (SERT) ARE ALSO EFFECTIVE IN REDUCING SYMPTOMS OF ANXIETY AND FEAR IN EVERY ONE OF THE ANXIETY DISORDERS

56. SOME WIDELY USED SSRIs FLUOXETINE PAROXETINE ESCITALOPRAM SERTRALINE FLUVOXAMINE SIDE EFFECTS: STOMACHACHE, INCREASED ACTIVITY LEVEL, INSOMNIA, AGITATION/DISINHIBITION AT HIGHER DOSES LESS OFTEN DIARRHEA, HEADACHES, TICS, CRAMPS/TWITCHING, SEXUAL SIDE EFFECTS. START AT A LOW DOSE AND INCREASE SLOWLY BASED ON TREATMENT RESPONSE AND SIDE EFFECTS

57. C) NOREPINEPHRINE REUPTAKE INHIBITOR SYMPTOMS OF HYPERAROUSAL SUCH AS NIGHTMARES CAN BE REDUCED AND WORRY CAN BE REDUCED BY NOREPINEPHRINE REUPTAKE INHIBITORS (ALSO CALLED NET OR NOREPINEPHRINE TRANSPORTER INHIBITORS). HYPERACTIVITY OF CSTC NRI ACTION ON NE NEURONAL OUTPUT TO CSTC

58. SOME NRIs & SNRIs COMMONLY USED SEROTONIN–NOREPINEPHRINE REUPTAKE INHIBITORS (SNRIS) VENLAFAXINE DESVENLAFAXINE  DULOXETINE  MILNACIPRAN  LEVOMILNACIPRAN  NOREPINEPHRINE REUPTAKE INHIBITORS (NRIS) ATOMOXETINE  REBOXETINE  VILOXAZINE

59. OTHER COMMONLY USED DRUGS GABAPENTIN AND PREGABALIN ALSO KNOWN AS α2δ LIGANDS BIND TO THE α2δ SUBUNIT OF PRESYNAPTIC N AND P/Q VSCCS, BLOCK THE RELEASE OF EXCITATORY NEUROTRANSMITTERS SUCH AS GLUTAMATE WHEN NEUROTRANSMISSION IS EXCESSIVE. THEY HAVE DEMONSTRATED ANXIOLYTIC ACTIONS IN SOCIAL ANXIETY DISORDER AND PANIC DISORDER 5-HT1A RECEPTOR PARTIAL AGONIST - BUSPIRONE

60. OTHER COMMONLY USED DRUGS MONOAMINE OXIDASE INHIBHITORS HYDROXYZINE ANTI-PSYCHOTICS – HAS LIMITED EVIDENCE AND HIGH SIDE EFFECTS PROPRANOLOL & OXPRENOLOL- LICENSED TO TREAT ANXIETY SYMPTOMS- USED IN PTSD

61. PSYCHOTHERAPY IN ANXIETY DISORDER NUMEROUS STUDIES HAVE SHOWN THE IMPORTANCE OF COMBINING PSYCHOTHERAPY WITH PHARMACOTHERAPY IN ANXIETY DISORDERS.

62. P sychotherapy was significantly more efficacious than pharmacotherapy in obsessive-compulsive disorder (g=0.64). Furthermore, pharmacotherapy was significantly more efficacious than non-directive counseling (g=0.33), and psychotherapy was significantly more efficacious than pharmacotherapy with tricyclic antidepressants (g=0.21).

63. There was sufficient evidence that combined treatment is superior for major depression, panic disorder, and obsessive compulsive disorder (OCD). The effects of combined treatment compared with placebo only were about twice as large as those of pharmacotherapy compared with placebo only, underscoring the clinical advantage of combined treatment. The results also suggest that the effects of pharmacotherapy and those of psychotherapy are largely independent from each other, with both contributing about equally to the effects of combined treatment.

64. TYPES OF PSYCHOTHERAPY BEHAVIOUR THERAPY COGNITIVE BEHAVIOUR THERAPY PSYCHOANALYTIC PSYCHOTHERAPY

65. BEHAVIOUR THERAPY EXPOSURE AND RESPONSE PREVENTION SYSTEMATIC DESENSITIZATION IMPLOSIVE THERAPY/FLOODING ANXIETY MANAGEMENT RELAXATION TECHNIQUES – YOGA, ZEN, JPMR BIOFEEDBACK DESENSITIZATION OF THE STIMULUS EYE MOVEMENT DESENSITIZATION AND REPROCESSING SOCIAL SKILLS TRAINING

66. COGNITIVE BEHAVIOUR THERAPY CONTROL OF AUTOMATIC THOUGHTS CORRECTION OF COGNITIVE ERRORS BREAKING THE ASSOCIATION BETWEEN THE EVENTS, COGNITIVE AROUSAL AND MALADAPTIVE BEHAVIOUR

67. PSYCHOANALYTIC PSYCHOTHERAPY THE PSYCHOANALYTIC PROCESS INVOLVES BRINGING TO THE SURFACE REPRESSED MEMORIES AND FEELINGS BY MEANS OF A SCRUPULOUS UNRAVELING OF HIDDEN MEANINGS OF VERBALIZED MATERIAL AND OF THE UNWITTING WAYS IN WHICH THE PATIENT WARDS OFF UNDERLYING CONFLICTS THROUGH DEFENSIVE FORGETTING AND REPETITION OF THE PAST.

68. PSYCHOANALYTICALLY ANXIETY IS CLASSIFIED INTO 4 TYPES THE CLASSIFICATION IS BASED ON THE TYPES OF PRIMARY COMPLEX AND THE SUBSEQUENT NATURE OF ITS CONFLICT WITH THE EGO ( CONSCIOUS MIND). TRAUMATIC ANXIETY (PANIC ATTACK) – EGO BECOMES PARALYSED SEPARATION ANXIETY – SEPARATION FROM LOVED/VALUABLE OBJECTS CASTRATION ANXIETY – LOSS OF LOVED/VALUABLE OBJECT SUPEREGO ANXIETY DEPENDING ON THE TYPE OF ANXIETY PSYCHOANALYTIC METHODS ARE ADAPTED.

69. UNCONSCIOUS CONSCIOUS PRECONSCIOUS EGO CONFLICTS TRYING TO ACCESS THE CONSCIOUS MIND THROUGH PRECONSCIOUS A STRONG EGO SUPRESSES THEM

70. UNCONSCIOUS CONSCIOUS PRECONSCIOUS EGO WHEN EGO IS WEAK IT FAILS TO SUPRESS X THE CONFLICTS GAINS ACCESS TO THE CONSCIOUS MIND ANXIETY SYMPTOMS

71. ANXIETY DISORDER PHARMACY

72. GAD 1 ST LINE 2 ND LINE 3 RD LINE

73. SOCIAL ANXIETY DISORDER 1 ST LINE 2 ND LINE 3 RD LINE

74. PANIC DISORDER 1 ST LINE 2 ND LINE 3 RD LINE

75. PTSD 1 ST LINE 2 ND LINE 3 RD LINE

76. RECENT ADVANCES IN TREATMENT OF ANXIETY DISORDERS NMDA AGONIST D-CYCLOSERINE MEMANTINE

77. THANK YOU