Erstellt von alicecartwright9
vor mehr als 8 Jahre
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Frage | Antworten |
vocal misuse | voice production behaviours that prevent the vocal mechanism form working smoothly and efficiently. |
increased tension/strain | hard glottal attack (adduction of VF before phonation) high laryngeal position anterio-posterior laryngeal squeezing |
inappropriate pitch level | puberphonia persistent glottal fry lack of pitch variability |
excessive talking | vocal fatigue |
Ventricular phonation | false VF move toward midline and cover true VF low pitch, hoarse, diplophonia |
phonotrauma/vocal abuse | harsher than normal misuse behaviours |
vocal nodules aetiology | tissue reaction to frictional trauma between VF - excessive laryngeal tension |
vocal nodules pathophysiology | small, white, protuberance on free margin of VF. junction of anterior 1/3 and posterior 2/3 of VF usually bilateral and symmetrical |
vocal nodules signs | hoarseness & breathiness habitual cough, throat clearing airflow may be increased increased subglottal pressure |
vocal nodules management and therapy | immature & nonfibrous - voice therapy fibrous - surgical removal + therapy Therapy: decrease voice usage, vocal hygiene |
vocal polyps aetiology | VF trauma due to vocal abuse secondary reaction to allergies, talking, smoking, URTI |
vocal polyps pathophysiology | sessile/broad & pedunculated usually unilateral junction anterior 1/3 and posterior 2/3 |
vocal polyps signs | diplophonia, sudden voice breaks, hoarseness, breathiness, roughness increased airflow, increased subglottal pressure |
vocal polyps management and therapy | pedunclulated & large sessile - surgical removal small sessile - therapy Therapy: similar to nodules, 2-6 months before quality improves |
Reinke's oedema AKA polypoid degeneration | build up of fluid in superficial lamina propria |
Reinke's oedema aetiology | effects women more than men VF trauma and misuse smoking gastroesophageal reflux hormonal changes |
Reinke's oedema pathophysiology | VF full of fluid full length of VF bilaterally disturbs elasticity of VF |
Reinke's oedema signs | low pitch, hoarseness, shortness of breath, increased airflow |
Chronic laryngitis | long-standing inflammation of the laryngeal mucosa secondary to phonation |
Chronic laryngitis aetiology | any long term irritation of the larynx (smoking, vocal abuse, reflux disease) |
Chronic laryngitis pathophysiology | VF red, irregular, thick, rounded rather than sharp. small dilated blood vessels on surface oedema supraglottic area |
Chronic laryngitis signs | hoarseness, high or low pitch, non-productive cough, sore throat. increased air flow and subglottal pressure |
Chronic laryngitis management and therapy | surgical stripping - if therapy unsuccessful Therapy: program to reduce vocal abuse and misuse |
Muscle tension dysphonia Aetiology | excessive muscularskeletal tension in head. and neck, intrinsic and extrinsic laryngeal muscles sensitive to emotional stress. hypercontraction of muscles |
Muscle tension dysphonia symptoms | aphonia/dysphonia breathiness, hoarseness, excessive high pitch, pain in larynx, pain in ears and chest, sensation of lump and tightness in throat, pain when pressure on larynx |
Muscle tension dysphonia physiological bases | usually normal larynx may demonstrate abnormal function secondary mucoal changes may occur |
Ventricular Dysphonia aetiology | excessive muscle tension may be substitute voice for severe deliberating disease |
Ventricular Dysphonia pathophysiology | false VF approximate and begin to vibrate increase mass VF - unable to vibrate quickly -> low pitch. |
Ventricular Dysphonia signs | low pitch, diplophonia, very hoarse. decreased range and airflow |
Ventricular Dysphonia management and therapy | medical management not used unless primary VF defect. Therapy: retrain true VF if possible. if not, compensation - improve false VF |
Psychogenic VD | Conversion VD: total or partial loss of phonation. physical symptoms not linked to anatomical or physiological disease. person convinced the problem is orgaic |
Conversion muteness | most extreme and incapacitating cough present - normal VF function |
Conversion Aphonia | involuntary whispering able to cough, laugh, cry - normal VF larynx high in neck 80% female onset sudden hoarseness -> whisper often triggered by colds acute/chronic emotional stress |
Conversion Dysphonia | varying degrees and types of hoarseness with or without strained-harsh quality falsetto breaks breathiness intermittent whispering moments of normal voice |
Psychogenic VD therapy | goal: re-establish normal VF function by re-shaping vegetative vocal functions |
Puberphonia | failure to eliminate high pitched voice structurally normal larynx mainly males |
puberphonia aetiology | psychological factors strong feelings towards feminine attachment rejects responsibilities of adulthood. Organic: endocrine disorder, severe hearing loss, URTI |
puberphonia pathophysiology | larynx high in neck and tilted down VF lax VF prevented from vibrating (arytenoids adduct tightly) thryroarytenoid muscle fails to contract (decrease VF mass, only thin edge of VF vibrate) |
puberphonia management and therapy | Therapy: goal - shape vegetative vocal production to normal voice. if therapy fails, VF augmentation is possible |
Organic VD | due to trauma associated with organic mass lesions (cancer) disorders related to endocrine disorders/changes |
Vocal process granuloma (contact ulcer) | small ulceration medial surface of vocal processes of arytenoid cartilages continued irritation in presence of bacteria |
Granuloma aetiology | repeated, forceful hyperadduction hard glottal attack, low pitch, glottal fry intubation trauma stress-related gastro-intestinal difficulties |
granuloma pathophysiology | "cup&saucer" appearance early stages - stand of mucus seen between processes |
granuloma signs | constant throat clearing, vocal fatigue breathy, hoarse discomfort, unilateral in area of thyroid cartilage increased subglottal pressure, increased airflow, increased intensity |
Granuloma management and therapy | Therapy: eliminate vocal abuse, alter voice production methods. if intensive VT fails, surgery |
Neurological VD | - laryngeal nerve paralysis SLN or RLN - spasmodic dysphonia - hypokinetic dysphonia |
SLN | innervates cricothyroid muscle tenses VF to increase pitch contributes to VF adduction vocal fatigue, hoarseness, loss of vocal range |
RLN | left lesions more common than right innervates all intrinsic muscles of larynx (not cricothyroid) lesion may be uni or bi lateral 2 types: Adductor or Abductor |
RLN paralysis | unilateral ad - VF not move to midline unilateral ab - VF remain fixed adducted bilateral ad - neither VF move to midline (phonation impossible) bilateral ab - both VF remain adducted (respiratory difficulty) |
RLN paralysis aetiology | u-RLN: intrathoracic neoplasms, aneurysms, mitral valve sternosis, neck trauma. b-RLN: thyroidectomy, neck trauma, tumours, infection |
RLN paralysis signs | u-RLN: mild breathiness, hoarseness, reduced loudness, shortness of breath. b-RLN: inhalatory stridor, voice good but both VF weakly adducted. - increased airflow, decreased subglottal pressure |
RLN paralysis management VF Medialisation (types) | injection - into/lateral to thyroarytenoid muscle, lamina propria. implantation - medial to thyroid cartilage at level of VF. arytenoid adduction - rotation of arytenoid cartilage so that tip of VP moves to midline. |
RLN paralysis management (result) & therapy | voice excellent post op deteriorates as oedema resolves improvement in one week. Therapy: techniques to reduce glottal incompetence |
Spasmodic dysphonia | strained, choked, effortful voice similar to stuttering relatively rare resistant to traditional VT |
Spasmodic dysphonia aetiology | psychology based - conversion reaction, muscularskeletal tension. neurologically based - organic/essential tremor idiopathic - unknown origin often associated with URTI, emotional stress |
Spasmodic dysphonia types | adductor abductor mixed |
Spasmodic dysphonia (ad) | true and false VF hyperadduct in intermittent and irregular spasms abrupt, vocal explosions, strained-strangled, voice breaks, harsh larynx normal at rest |
Spasmodic dysphonia (ab) | sever breathy aphonia - intermittent breaks VF episodically abduct not as common as (ad) difficult transition from voiceless consonant to vowels |
Spasmodic dysphonia (mixed) | both ad and ab laryngospasms aphonic, breathy periods and voice arrests |
Spasmodic dysphonia management | botox injections ad - thyroarytenoid/vocalis ab - psoterior cricoarytenoid causes muscle paralysis (botox is neurotoxin - blocks transmission of nerve impulse to muscle) |
Spasmodic dysphonia mx results | significant improvement (ad - 90% & ab - 70%) airflow increased and normalised reduced hyperfunction require re-injection (3-5 months) |
Spasmodic dysphonia therapy | breathy voicing elevation of pitch, easy voice onsets and artic contacts relaxation therapy co-ordination exhalation and voice onset |
Hypokinetic dysphonia aetiology | parkinson's |
Hypokinetic dysphonia pathophysiology | VF normal in structure phonation - closure incomplete unable to tense VF |
Hypokinetic dysphonia signs | monopitch, monoloudness reduced loudness reduces stress harsh, breathy increase airflow, decreased subglottal pressure |
Hypokinetic dysphonia management and therapy | drug therapy increase VF adduction increase loudness and intonation Lee Silverman Voice Treatment |
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