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| How does motion sickness trigger vomitting? | Disturbances of the semi-circular canals or the vestibule will send electrical signals to the vestibular nuclei in the brain to stimulate histamine and muscarinic receptors via the vestibular/cochlea nerve (VIII- 8) , signal gets passed on to the CTZ then to the vomiting centre to trigger vomiting reflex |
| How does cerebral stimulation work to induce vomitting? (smells, sight, pain) | Stimuli are processed through the higher brain centre (cerebral cortex) and electrical impulses are sent to the vomiting centre via stimulation of the muscarinic receptors |
| How does gastric stimulation trigger the vomitting reflex? | Gastric epithelial lining consists of rugae containing microscopic gastric pits – lined by cells called. The enterochromaffin (EC) cell is an enteroendocrine cell subtype the cells that Release serotonin in response to cytotoxic agents - Stimulates serotonin receptors on Vagus nerve to bring sensations to the vomiting centre to trigger the vomiting reflex |
| What are the indicators of increased lilkihood of PONV? | Female Non smoker( protective mechanism) Use of post op opioids History of PONV |
| What are the 3 phases of chemotherapy induced nausea and vomitting? | • Acute – occurring within a few minutes to hours • Delayed – occurring 24 hours after drug administration. • Anticipatory – occurring before drug administration, a conditioned response (psychological response – negative experiences to chemo drugs) |
| What are the causation theories in nausea and vomitting during pregnancy? | Increased amount of hormones protective mechanism to protect the embryo from harmful substances |
| What is the nursing management of caring for someone experiencing nausea and vomitting? | Prevention of nausea and vomiting if possible (goal of care – prevent before it happens) Must be managed if it is affecting nutrient and fluid intake or if it delays essential treatments Assess the cause Administer medications by a route that is likely to be effective Minimise the distressing experience of nausea and vomiting |
| What is Ondansetron - 5HT3 Serotonin receptor antagonists used for and its mode of action? | Chemo and post op nausea and vomitting - It reduces the vomiting reflex by blocking serotonin at 5HT3 receptors both peripherally in the gastro-intestinal tract and centrally in the chemoreceptor trigger zone |
| What are the common side effects of ondansetron? | Headache and constipation |
| What is cyclizine - Histamine – H1 receptor antagonists used for and its mode of action? | Motion sickness - blocks the action of histamine and mucuranic receptors reducing the stimulation of the CTZ |
| What are the side effects of cyclizine ? | Anti muscuranic – drowsiness , dry mouth , constipation |
| What is the mode of action of metoclopramide - dopamine 2 receptor antagonist? | It stimulates gastrointestinal peristalsis (accelerating gastric emptying and intestinal transit time), lowers oesophageal sphincter pressure, and antagonises dopamine receptors in the chemoreceptor trigger zone. |
| What are the side effects of metoclopramide? | Extra pyramidal – drowsiness nausea bowel disturbances |
| Nursing management of nausea and vomitting? | Assess the cause give appropriate antiemetic remove bad smells maintain fluid intake position patient upright during and after eating oral hygiene |
| Implications of non management of nausea and vomitting ? | Exhaustion Ability to manage pain (pain threshold decreases) Surgical implications – wound site rupture(severe vomiting can rupture sutures – increase in abdominal pressure) distress |
| Diagnostic criteria for major depressive disorder? | 5 more more depressive symptoms ongoing for more than 2 weeks that doesnt get better - The symptoms cause significant distress or impairment in social,work, family |
| Nursing considerations for depression? | Develop a therapeutic rapport Encourage client to express feelings encourage goal setting Structure the day – gently support client to become involved in regular brief social and recreational activities Encourage regular meals and activities of daily living (sleep, exercise and mindfulness). |
| Difference between bipolar 1 and 2? | Bipolar 1 : A person with bipolar 1 disorder may or may not have a major depressive episode. The symptoms of a manic episode may be so severe that you require hospital care. Bipolar 2 : involves a major depressive episode lasting at least two weeks and at least one hypomanic episode (a period that’s less severe than a full-blown manic episode). |
| What is mania in bipolar disorder? | Persistently elevated mood, which may be one of elation or irritability; increased activity; and poor judgement |
| What is hypomania in bipolar disorder? | Mild form of mania – less severe no psychotic episodes • No significant impairment in social or occupational function |
| What are some symptoms of a manic episode? | Racing thoughts decreased need for sleep increased activity exaggerated sense of self confidence loss of touch with reality |
| Nursing considerations for manic episode? | Safety – prevent person from hurting themselves or others. Provide a low-stimulus environment – quiet rooms with limited activities or stimuli set boundaries and simple instructions - do not argue |
| Interventions and treatment for mood disorders? | Recovery Planning (awareness of triggers) Lifestyle medicine (exercise, diet, sleep) Talking therapies CBT Cognitive behaviour therapy Music, Art therapy Mindfulness/relaxation techniques Antidepressant/Mood stabilsing medication |
| Causation theories of mood disorders? | Hormonal factors – excess cortisol Genetic links trauma neurochemical - monoamine hypothesis stress during pregnancy and after birth |
| What are the four classes of anti depressants? | SSRIs (e.g. fluoxetine or citalopram), SNRIs serotonin and noradrenaline reuptake inhibitors (e.g. venlafaxine ) TCA tricyclic antidepressants (e.g. amitriptyline) and Monoamine oxidase inhibitors (MAOIs) (phenelzine) |
| What is the mode of action of SSRI'S - sertraline? | Inhibit the reuptake of serotonin at the pre synaptic cleft making it more available in the synapse |
| Side effects of SSRIS? | Headache weight gain insomnia sexual dysfunction excessive sweats |
| Nursing considerations for anti depressents? | Suicide risk serotonin syndrome - educate patient will not immediately work - takes time to see therapeutic effect need to ween off medication - educate on discontinuation syndrome must not be used with other anti depressents |
| Mode of action of serotonin noradrenaline reuptake inhibitor? | Inhibits the reuptake of serotonin and noradrenaline at the pre-synaptic cleft making it more available in the synapse |
| Mode of action of TCA tricyclic antidepressants (e.g. amitriptyline ? | Inhibits reuptake of serotonin and noradrenaline by blocking the serotonin transporter and the norepinephrine transporter enhancing neurotransmission |
| What is the mode of action of monoamine oxidase inhibitors? | Used when other medication hasn’t worked. Inhibits the action of monoamine oxidase which is responsible for the breakdowns of amines. This increases the concentration of neurotransmitters across the synapse. |
| What are the effects of serotonin syndrome? | Tachycardia hyperthermia tremors confusion |
| What are the effects of discontinuation sydrome? | Imbalance flu like symptoms anxiety electric shocks in the brain |
| What is the mode of action of lithium? | Lithium displaces K+ & Na+, possibly Ca+2 to occupy sites making it harder for the action potential to be relayed through neurons - Inhibits excitatory neurotransmitters such as dopamine and glutamate and promotes GABA-mediated neurotransmission |
| Side effects of lithium? | GI effects: nausea, vomiting, diarrhoea, dyspepsia, weight loss or weight gain CNS changes: lethargy, sedation, tremor |
| Nursing considerations for lithium? | Monitor for lithium toxicity • Be careful with dehydration- hydration is important to balance the extra salts daily blood tests to monitor serum levels |
| Why is a neurological assessment needed? | As part of an initial assessment to establish baseline recordings Determine changes Deterioration Stability Improvement |
| What might affect LOC? | Hypoxia intracranial pressure sedating drugs electrolyte imbalances |
| Late signs of raised ICP? | Hemiparesis raised blood pressure sweating seizures |
| Whats involved with a neurological assessment? | Level of consciousness motor function pupillary function respiratory function vital signs |
| Why is assessing pupil movement important ? | If the eyes move together into all six fields, extraocular movements are intact |
| What is Cushing's triad a sign of? | Raised ICP - Increased systolic BP Decreased heart rate Irregular/ decreased respiration |
| What is the glascow coma scale ? | Used to assess a wide variety of conditions where consciousness levels are in question Assesses: Eye responses : Scores1- 4 Verbal response: Scores1 -5 Best motor response : Scores1-6 |
| Observations when a patient is on a PCA - patient controlled analgesia? | Normal Post Operative vital sign checks Pain Intensity rest/movement Level of Consciousness Respiration rate regular checks |
| How to opioids work with nociception? | Transmission phase of Nociception help stop transmission from the periphery to the spinal cord Perception phase by altering the limbic system (important in terms of perception) Modulation phase by helping in the activation of the descending inhibitory pathways that then modulate transmission in the spinal cord. |
| Side effects of opioids? | Respiratory depression (major concern) Nausea and vomiting (common) antiemetics charted too Constipation (can lead to bowel obstruction) sedation hypotension - falls risk |
| What is some patient teaching around PCA use? | Educate the patient pre op or pre use about how the PCA works Explain that the is very effective as analgesia maintenance once pain is well controlled. It is always best to teach the patient to push for pain relief before the pain is severe. Patients need reassurance that the PCA has safety mechanisms such as the total hourly dose that mean ‘overdose’ is unlikely Only the patient can press their button ie not for relatives and friends to push |
| Possible problems with PCA analgesia? | Need to have cognitive awareness to use, physical dexterity to use, and need to know if the patient is opioid naïve There may be equipment problems Prescription errors |
| What is an epidural? | Method of pain relief and anesthetic injected into the epidural space around the spinal cord - Local anesthetics and Opioids: Morphine, Fentanyl |
| Nursing considerations for an epidura? | BP, P, Temp post op observations for the organisation ie ½ hrly for 2 hours, 1 hrly four hours, then 2 , 4 hrly Resp rate 1/24 for 24 hours Pain assessment Dermatome levels: 2hrly-4hrly, or if there is a change in rate of the epidural infusion |
| Complications of epidural? | Tubing and pumps need to be clearly marked displacement of catheter infection urinary retention - numb bladder resp depression |
| What are nerve blocks? | Long-acting local anesthetics, such as bupivacaine or ropivacaine Nerve blocks interrupt all afferent and efferent transmission to the area Interrupt transduction and transmission - inhibit action potential |
| Possible complications of nerve blocks? | LA Systemic toxicity is a potential complication haematoma is another potential complication of RS block secondary to vascular injury during needle or catheter placement nerve injury allergic reaction Infection Increased risk of falls with some blocks ie a femoral nerve block |
| What is the mode of action of opioids? | Binds to opiate receptors in the brain resulting in inhibition of the ascending pain pathways thus altering the perception and response to pain |
| What is pychosis? | A cluster of symptoms comprising one or more of the following: Hallucinations Delusions Disorganised thoughts and behaviour disconnection from reality |
| What is schizophrenia? | A mental disorder that effects perception, thoughts and behavior - characterized by phsycosis episodes |
| What are the causation theories of schizophrenia? | Diathesis Stress Model (predisposition of vulnerability and stress) Childhood Trauma Genetics Prenatal Factors Dopamine Hypothesis (increased dopamine Drug use ( recreational drug use – cocaine, cannabis etc . Triggers psychotic disorders with underlining predispositions |
| What are the three stages of schizophrenia? | Prodromal, acute, residual |
| The prodromal phase can often go on for 2 years - what are three symptoms? | Worsening of usual work or school performance Worsening intellectual and organisational functioning Social withdrawal |
| What are the positive symptoms of schizophrenia? | Hallucinations (mainly auditory) Delusional thinking Disorganised or bizarre behaviour, movement disorders - catatonia |
| What are the negative symptoms of schizophrenia? | Anhedonia (lack of feelings) Blunt affect (lack of expression) Avolition (lack of motivation) Poverty of speech/thought Social withdrawal Insomnia |
| What is schizoaffective disorder? | Thought disorder that includes both psychotic features and mood symptoms |
| What are some impacts of phycosis? | Impacting on the person’s sense of self, experience of life and the world, and relationships. |
| Nursing considerations for physcosis? | Mental state exam - BATOMI gain rapport and trust engage person to reality orientated activities involving connection and contact explore impacts of both negative and positive symptoms focus on recovery - acknowledge their views and needs encourage person to understand meaning of their phycosis |
| What is the mode of action of typical antipsychotics (haloperidole)? | Block D2 receptors in brain reducing dopaminergic transmission - usually treat positive symptoms |
| What are the side effects for typical antipsychotics? | Can cause extra pyramidal symptoms sedation postural hypotension sexual dysfunction |
| What is the mode of action of Atypical antipsychotics? | Block D2 and serotonin receptors reducing transmission - works well for positive and negative symptoms - balances serotonin - dopamine |
| What are the side effects of Atypical antipsychotics (Risperidone)? | Hypertension postural hypotension metabolic disorders sedation risk of neuroleptic malignant syndrome in all antipsychotics |
| Clozapine is a Atypical antipsychotic, what are some important factors about this drug? | Used for treatment-resistant people who dont respond to other meds Advice patient of flu like symptoms (fever and sore throat) risk of Agranulocytosis (low WBC) Blood tests weekly for first 18 weeks and then 4 weekly (FBC; looking for drop in baseline WBC or absolute neutrophil count (ANC) |
| What are extra pyramidal symptoms (ADPT) | Akathisia – restlessness Dystonia – involuntary facial movement Pseudo-parkinsonisms – symptoms of Parkinson's disease induced by medication: Rigidity, tremor, shuffling gait Tardive Dyskinesia – involuntary movements of the tongue, lip smacking/chewing/sucking, face & limbs |
| What is the meaning of intellectual disability? | Problems with mental abilities such as learning, problem solving, judgement) adaptive functioning (activities of daily life such as communication and independent living) |
| How is ID diagnosed? | Long process, requires input from different health professionals - Family History e.g. some chromosomal micro-deletions can occur in family members e.g., 15q11.2 microdeletion Alcohol, drug misuse/abuse e.g. Fetal alcohol syndrome [FAS] (common cause of ID Detailed history e.g. seizure disorders, attentional difficulties, sleep disturbances, behavioral disorders MRI/CT IQ test |
| What may a diagnoses of ID support for the child and family? | Access to information about the symptoms Obtain information about what can be done to help the child Determine specifically where and how to help the child funding |
| What are the types of intellectual disabilities? | Trisomy 21 (downs syndrome) fetal alcohol spectrum disorder autism |
| What are the characteristics of downs? | Short stature ID Language is delayed Short and long-term memory is affected Heart defects, GI defects, visual and hearing defects |
| How is downs diagnosed? | Prenatal screening • Chorionic villus sampling (CVS) (invasive – sample of tissue from placenta • Amniocentesis – sample of amniotic fluid containing foetal tissues from the amniotic sac surrounding foetus |
| What is fetal alcohol spectrum disorder? | Ethanol and its metabolite acetaldehyde can alter fetal development by disrupting cellular differentiation and growth, disrupting DNA and protein synthesis and inhibiting cell migration |
| What are the poor life outcomes associated with FASD? | At increased risk of child abuse and neglect Poor educational outcomes Mental health and substance abuse issues |
| How is early identification achieved in intellectual disabilities? | Comprehensive developmental checks (e.g. plunket, B4 school checks) so deviations from normal development are recognised addressing parental concerns about their child’s development prompt referral and access to diagnostic services Treatment: MDT approach to providing specific therapies |
| What can cause ID? | Trauma – before and after birth Alcohol Infection Environment Chromosome abnormalities Metabolic issues Substance abuse |
| Nursing considerations for ID? | Person centered approach that promotes client participation and provides opportunities to make choices Self-determination – support and encouragement Encouragement and praise – developing independence, self esteem, confidence think about external support use non verbal cues |
| Under the Disability Act 2005 people with disabilities are entitled to? | Have their needs assessed • Have individual service statements drawn up, setting out what services they should get • Access independent complaints and appeals procedures • Access public buildings and public service employment |
| The vision of the nz disability strategy is to? | New Zealand is a non-disabling society – a place where disabled people have an equal opportunity to achieve their goals and aspirations, and all of New Zealand works together to make this happen |
| What is a peak flow meter used for? | Used for the diagnosis, monitoring and assessment of the severity of respiratory compromise, particularly in patients with asthma measures forced expiratory volume - peak expiratory flow rate |
| What is allergic rhinitis(hayfever)? | Exsposure to an allergen - can be early or late reaction watery rhinorrhea (runny nose) nasal obstruction nasal itching Sneezing |
| What is asthma? | A chronic inflammatory disorder of the lungs that are hypersensitive with recurrent episodes of wheezing, coughing, tightness of the chest, and shortness of breath, irritable cough |
| What are predisposing factors of asthma? | Family history of: Hypersensitivity Allergies atopy, smoking during pregnancy, exposure to pollution past medical history of allergies |
| How does an acute flare up of asthma happen? | Of IgE occurs – binds to inflammatory cells Initiates B-lymphocyte activation IgE binds to cells and causes release of inflammatory mediators: inflammatory process causing airway inflammation, mucus production (goblet cells), bronchospasm and bronchoconstriction |
| How is asthma diagnosed? | Health history asthma symptom diary peak flow spirometry listen to lungs |
| How is asthma managed? | Accurate diagnosis – pharmalogical treatment Assess control of symptoms Pharmacological treatment Complete an asthma action/management plan Assess risk of severe exacerbations |
| What is COPD? | Chronic obstructive irreversible progressive disease of the lungs |
| COPD is an umbrella term for which conditions? | Chronic bronchitis emphysema irreversible asthma |
| What is chronic bronchitis? | Inflammation causes chronic bronchial secretions and narrowing of the bronchi(main culpurt) -excess secretion of goblet cells causes narrowing of airways |
| What is emphysema? | A permanent destructive enlargement of the airspaces within the lung)break down of walls of alveloli – gas echange is reduced air becomes trapped – permanent |
| What is irreversible asthma? | Poorly controlled childhood asthma, multiple acute exacerbations = remodeling, structural and chronic inflammatory changes cause partial or no reversibility in lung function |
| What are the predisposing factors for COPD? | Smoking pollution chemical exposure childhood asthma thats uncontrolled |
| Symptoms of chronic bronchitis? | Productive cough Wheezing and/or rhonchi, are universal features Progressive dyspnea on exertion Repeated purulent respiratory infections |
| Non pharmalogical interventions for COPD? | Smoking cessation low exercise - maintain lung function pulmonary rehabilitation immunization - prevent infections management plan |