356 exam Flashcards
what are the steps of the clinical reasoning cycle
- consider the patient situation
- consider cues/ information
- process information
- identify problems / issues
- establish goal/s
- take action
- evaluate outcomes
- reflect on processes and new learning
what to include in consider patient situation? ( CRS)
- List facts, people and context
what to include in collect cues/ information (CRS)
Review:
Age, gender, occupational history, chest x-ray, medical progress notes, blood gases?
Gather new information: Observations History of foreign travel? COVID risk? Blood gases?
Recall knowledge:
Anatomy and physiology of resp system
Pharmacology
Risk factors for pneumonia
What to include in process information (CRS)?
Interpret
- Look at each observation / investigations
- Within normal limits
Discriminate
- What findings can you safely disregard?
- Which obs are most relevant?
Relate
- Cluster cues together e.g. tachypnoea and SaO2
Infer / Match
- Make a decision that based on the information you have what it means
Predict
- If you don’t do something what is most likely going to happen?
- Why?
What to include in Identify problems/ issues (CRS)?
Synthesise facts and establish diagnosis
- Be able to say this is the problem because.
E.g.
hypoxic due to untreated pneumonia.
What to include in establish goals (CRS)?
Set out what you want to happen
Why not use SMART:
What to include in take action of (CRS)?
- Describe what needs to happen
- List alternative and describe rationale for choice
- Is it evidence based?
- Can you defend your chosen path?
What to include in evaluate outcomes (CRS)?
- Have the actions improved the situation?
- What is the best way of evaluating effectiveness?
What to include in Reflect on process and new learning (CRS)?
Reflect on what YOU have learned
What would you do differently?
palliative care is a philosophy of care that involves:
- holistic care
- comprehensive care
- coordinated care
Palliative care patients are cared for in:
- acute hospital settings
- community settings
- in the home
examples of life limiting conditions
Cancer Dementia/frailty Heart/vascular disease Respiratory disease Kidney disease Liver disease Neurological disease Any condition /complications that are not revisable
what is the SPICT tool?
Supportive and Palliative Care
Indicators Tool
SPICTTM tool is used to help identify people whose health is deteriorating.
Assess them for unmet supportive and palliative care needs. Plan care
SPICT indicators of poor or deteriorating health to look for
Unplanned hospital admission(s).
Performance status is poor or deteriorating, with limited reversibility.
(eg. The person stays in bed or in a chair for more than half the day.)
Depends on others for care due to increasing physical and/or mental health problems.
The person’s carer needs more help and support.
Progressive weight loss; remains underweight; low muscle mass.
Persistent symptoms despite optimal treatment of underlying condition(s).
The person (or family) asks for palliative care; chooses to reduce, stop or not have treatment; or
wishes to focus on quality of life
what is end of Life care
‘Person and family-centred care provided for a person with an active, progressive, advanced disease, who has little or no prospect of cure and who is expected to die, and for whom the primary treatment goal is to optimise the quality of life.’
how to improve Quality of Life of the palliative patient
Dying is deemed to be part of life
Needs to be cared for in the same way
Holistic care
Five domains of Holistic care
- spiritual care
- cultural care
- physical care
- social care
- emotional care
Five domains of Holistic care
- spiritual care
- cultural care
- physical care
- social care
- emotional care
How does quality of care affect the family
Not just the patient
- Family
- Friends
- Principle carer
Stressful
Emotionally/psychologically/Spiritully challenging
- Need to be
- Informed
- Educated
- Supported
Multidisciplinary team in palliative care?
- Whole team approach
- Physicians/Oncologists/ Surgeons
- Nurses
- Palliative Care Team
- Nuclear Medicine Specialists
- Physio
- OT
- Social workers
how to communicatie during palliative care
Continuous through the patient journey Involve patient, Family, Loved ones Needs to be Effective Efficient Difficult Communication Frameworks PREPARED SPIKES
What does the abbreviation PREPARED stand for in palliative care
P- Prepare for discussion
R- Relate to the person
E- elict preferences from person/ carers
P- provide information tailored to person/carers
A- Acknowledge emotions/ concerns
R- (Foster) Realistic hope
E- Encourage questions and further discussion
D- Document
What does the abbreviation spike stand for in palliative care?
S- setting up the conversation
P- Perception …Assessing the persons perception
I- Invitation.. Obtaining the persons invitation
K- Knowledge… providing knowledge and information to the person
E- Emotions…Addressing the person’s emotions with emphatic response
S- Strategy and Summary
when to begin goals of care
soon after life limiting illness
Communication expectations in goals of care during palliative care
Good communication skills essential
Listening and enquiring
Checking and Clarifying
Documentation
purpose of goals of care for palliative care patients
A way of beginning advanced care planning process
‘Our ultimate goal after all is not a good death, but a good life to the very end’
what is to be involved in palliative care plan
- Who participated in the plan
- Contact details – coordinators of care
- Clearly defined Goals & Responsibilities
- Ongoing holistic assessment (5 domains)
- Multidisciplinary involvement
- Sharing/re-evaluation details
- Links to relevant documentation
- Planning for expected evens/changes
symptoms to be managed during palliative care?
pain
dyspnoea
nausea/ dehydration
neuro deficits
hypotension
pain management in palliative patients
Pain Management
- Pain control can be achieved in 90% of palliative patients
- Stepwise Ladder Approach
- Control of breakthrough pain
what is the stepwise ladder approach to pain management in palliative care?
…
dyspnoea management in palliative care
- Positioning
- O2
- Suctioning
- Anticholergic drugs – secretions
how to optimise care during palliative care
Continuous assessment
- Physical functioning
- Social functioning
Clinical assessment
Self reporting
what are the 9 palliative care standards
1- Assessments of needs
2- developing the care plan
3- caring for carers
4- providing care
5- transitions within and between services
6- grief support
7- service culture
8- quality improvement
9- staff qualifications and training
how to care for palliative care carers
- Health care workers need care too
- End of life care
…Burnout
…Moral Distress
…Compassion fatigue - Non-Health care workers
- Stressful
…Carer Support-Assessment
…Respite Care
…Spiritual support
pharmalogical interventions for end of life care?
- Analgesics
- Nausea and Vomiting
- Hydration therapy
- Anticholergic drugs
- Administration
…Many drugs administered via pump/single doses
…Sub cutaneous via butterfly needles
Pharmacodynamics of Anticholergic drugs for palliative care?
- Blocks Transmission of acetylcholine throughout the body
- Relaxation of smooth muscle
- Drying up of secretions
- Used in end of life care for secretion management
example of Anticholergic drug
Hyoscine BUTYLbromide
what is pharmacodynamics
what a drug does to the body
what is pharmacokinetics
what our body does ADME
pharmacokinetics of Hyoscine BUTYLbromide
ADME:
Poorly absorbed in the GI tract
Does not cross the blood brain barrier – no effect on CNS
Indicationsof Hyoscine BUTYLbromide
Spasm of GI tract, renal spasm, secretion management in EOL care
adverse effects of Hyoscine BUTYLbromide
Urinary retention, dizziness, tachycardia
contraindications of Hyoscine BUTYLbromide
paralytic ileus, urinary retention, glaucoma
What makes us breathless?
Pain Exercise Trauma Obesity Genetics Smoking Allergy -Dust -Pollen -Fur -Grass Etc, etc, etc
Common respiratory conditions
Chest Infection Pneumonia Emphysema Dyspnoea Respiratory failure ARDS Asthma COPD
Aetiology meaning
The study of the causes
Acute Respiratory Distress Syndrome: Aetiology
Acute inflammatory response of the lungs
it is a form of non-cardiogenic pulmonary edema, due to diffuse alveolar injury.
Characterised by:
Hypoxemia, Decreased lung compliance, Bilateral infiltrates, Non-hydrostatic pulmonary oedema
- 10% of all ICU admissions have ARDS
- 46% mortality rate
- Most cases attributed to Pneumonia or Sepsis (40-60%)
ARDS pathophysiology
Acute Respiratory Distress Syndrome is a form of non-cardiogenic pulmonary edema, due to diffuse alveolar injury. This diffuse alveolar damage occurs secondary to an inflammatory process. The initiative of inflammation can be Direct injury to the Lung or indirect injury by systemic causes.
Non-hydrostatic pulmonary oedema – Hydrostatic pressure in the lungs is not affected – pathological processes act on the pulmonary vascular permeability result in protiens leaking from the capillaries, increasing the oncotic pressure – it exceeds that of blood and fluid is therefore drawn from the capillaries.
ARDS pathophysiology stages
Exudative phase: Injury to the alveolar capillary membrane – accumulation of protein rich fluid impairing gas exchange and release of various substances including proinflammatory cytokines which causes significant inflammatory response in the lungs – Significant ventilation-perfusion mismatch evolves causing hypoxaemia and reduced lung compliance
Proliferative phase: occurs after 1 – 2 weeks . Fibrosis and remodelling occurs. Patients have reduced alveolar ventilation, pulmonary compliance and ventilation perfusion mismatch
Fibrotic phase: Alveola become fibrotic, emphysema alterations to lungs, linked to prolonged ventilation
ARDs Management
- Treatment limited
- Treat the cause – i.e pneumonia
- Supportive care
- Ventilation – Prone!
- Fluid management
- Nutrition
What is asthma
- A chronic inflammatory disease of the airways
…Causes hyper-responsiveness, mucosal oedema and mucous production
…Allergy is the strongest predisposing factor
-Inflammation leads to cough, chest tightness, wheezing and dyspnoea
-The most common chronic disease of childhood
Can occur at any age
-Fully reversible (unlike COPD)
describe asthma in australia
-More than 2 million Australians have asthma
Most common chronic childhood disease
1 in 10 adults (usually mild)
- Children have higher rates of hospitalisations for asthma than adults
- Over 400 Australians die from asthma annually Australian Centre for Asthma Monitoring (cited in Considine, 2014)
why asthma makes it hard to breath
Parasympathetic stimulation leads to bronchoconstriction
Sympathetic stimulation leads to bronchodilation
Inflammation causes swelling of the bronchial mucosa
Inflammation causes increased mucous production
how is asthma diagnosed
Clinical manifestations
- Wheeze & chest tightness
- Dyspnoea &/or cough
- Airflow limitation/prolonged expiration
….Often recurrent & seasonal/worse nocte
Triggers:
-exercise/allergies/emotions /irritants /infections/cold air
Patient history & examination
Diagnostic testing
- Serial peak expiratory flow
- Reversibility (often with short-acting broncho-dilator)
- Various spirometry/lung function testing/exercise testing
asthma treatment/ pharmacological options
salbutamol
Ipratopium Bromide
pharmacodynamics of salbutamol
- Beta2-adrenoreceptor agonist
- Relaxes bronchial smooth muscle by acting on calcium in the cell (see p593 - Bryant et al, 2019)
Pharmacokinetics of salbutamol
Absorbed rapidly - inhalation
Metabolised by liver, excreted by kidneys
ADME – Absorption, distribution, metabolism and excretion
Absorbed rapidly – inhalation – 5-15mins peak effect within 1-2 hours
indications, adverse effects and contraindications of salbutamol
Indications – Asthma, bronchitis, emphysema
Adverse effects – tremor, palpitations, restlessness, Tachycardia
Contraindications – Beta blockers, sensitivity, hypokalaemia
pharmacodynamis of Ipratopium Bromide
- Anticholinergic drug
- Blocks the action of ACh – Bronchodilator (blocks the effects of stimulation on the parasympathetic nervous system
(see p185-186 - Bryant et al, 2019)
pharmakokinetics of Ipratopium Bromide
ADME
Absorbed rapidly - inhalation
Metabolised by liver, excreted faeces, urine and bile
Indications, adverse effects and contraindications of Ipratopium Bromide
Indications – Asthma, bronchitis, emphysema
Adverse effects – Tachycardia, arrythmias, SVT, AF, Nausea, Dry mouth/throat
Contraindications – hypersensitivity to atropine
what is asthma like for the patient
Can be challenging to treat
And very scary for the patient
different cardiovascular conditions
CHD ACS (see algorhythm, Aitken et al p285) Heart failure Cardiomyopathy Endocarditis Aneurysm
ACS algorithm
view in word
what is ACS
Umbrella term - MI - Unstable Angina .....Associated with transient or permanent thrombotic occlusion .....Leads to ischemia or infarction
acute coronary syndrome (ACS). A broad spectrum of clinical presentations, spanning ST-segment elevation myocardial infarction
through to an accelerated pa
discuss prevalence of ACS
2014-15 77,007 ACS events
> 500,000 pts present with CP annually in Au
≥ 80% of potential ACS patients do not have a Dx
Cost and resources burden (nearly $2B)
why is chest pain complex/ a problem
Multiple causes
High rates of admissions
Resource intensive: Nursing Medical Length of hospital stay Medication COST
cardiovascular causes of chest pain
Myocardial ischaemia Coronary artery spasm Myocardial infarction Pericarditis Pulmonary embolism Mitral valve prolapse Ca usually secondary cancer
non cardiovascular causes of chest pain
Dissecting Thoracic Aneurysm Herpes Zoster Oesophageal reflux Oesophageal spasm Hiatus hernia Pneumonia Pneumothorax Pleurisy Peptic ulceration Gallbladder disease Musculoskeletal pain Costochondritis
anatomy and physiology components that can cause problem in cardiovascular patients
Mechanical components
Electrical components
Vascular components
…of the heart
review diagram of the heart
- superior vena cava
- right pulmonary artery
right pulmonary vein - Opening of SVC & Pulmonary semi-lunar valve
- Right Atrium
- Opening of IVC & Tricuspid valve
- Right Ventricle
- IVC
- Aortic arch
- Ligamentum arteriosum & pulmonary artery
- Left pulmonary veins
- Left atrium
- Mitral valve & Aortic semilunar valve
- Septum & Chordae tendonae
Left ventricle
the hearts conduction system
watch video on conduction system
- The sinoatrial node, or SA node, located in the right atrium near the entrance of the superior vena cava. This is the natural pacemaker of the heart. It initiates all heartbeat and determines heart rate.
- The electrical impulses from the SA node spread throughout both the right and left atria to stimulate them for contraction.
- The atrioventricular node, or AV node, which is located between the right Atria of the Heart and RIght Ventricle serves as an electrical gateway to the ventricles. It delays the passage of weak electrical impulses to the ventricles, and if the SA node does not fire, the AV node serves as the SA Node’s backup pacemaker hence why the AV node is called the “Gatekeeper of the Heart.”
- The AV node receives signals from the SA node and passes them onto the atrioventricular bundle - AV bundle or bundle of His which divide into the right and left bundle branches that conduct the impulses toward the apex of the heart.
- The signals are then passed onto Purkinje fibers, turning upward and spreading throughout the ventricular myocardium.
- Electrical activities of the heart can be recorded in the form of an electrocardiogram, ECG, or EKG.
- The P-Q segment represents the time the signals travel from the SA node to the AV node, and the QRS complex marks the firing of the AV node and represents ventricular depolarization.
- Atrial repolarization also occurs during this time but the signal is obscured by the large QRS complex because the heart’s ventricles contract stronger than the Atria.
- The T wave represents ventricular repolarization
- The cycle repeats itself with every heartbeat.
DEPOLARIZATION= CONTRACTION REPOLARIZATION= RELAXATION
- SA node
- AV node
- right atrium and ventricle
- aortic arch
- left atrium
- Right and left bundle of His
- Left ventricles
- Perkinje fibres
what are the coronary arteries
- right coronary artery
- left coronary artery
- branch of left coronary artery
- ## branch of right coronary artery
what is atherosclerosis/ causes of CHD
Atherosclerosis- A complex and progress disorder of the arteries. Thought to involve endothelial injury or inflammation, which becomes the focal point of lipids and fibrous tissue in the form of plaques, particularly around arterial curvature and branches.
Responsible for much CHD
what are the different anginas
Stable angina
- artery spasm, closes off vessel, less o2 getting to myocardium
- Often relieved by rest alone
Unstable angina
- May come on at rest
- plaques moving through, or spasm not bought on from exertion
stable vs unstable angina process
both- plaque formation with no symptom
stable- plaque becoming more, but little blood flow is still able to flow with o2
unstable- blockage and rupture more serious
watch vid
pharmacodynamics of aspirin
Inhibits COX-1 (cyclo-oxygenase)
COX is needed to allow platelets to aggregate
see p556 - Bryant et al, 2019
pharmacokinetics of aspirin
Absorbed rapidly buccally, orally
Metabolised by liver, excreted by kidneys
indications adverse effects and contraindications of aspirin
Indications – ACS, stroke risk, fever
Adverse effects – gastritis, GI bleeding, dizzness
Contraindications – sensitivity, haemophilia, gastric ulcer…
pharmacodynamics of morphine
Opioid receptor agonist – opioid receptors ‘receive’ endorphins
Morphine mimics endorphins
Reduces pain interpretation
Pharmacokinetics of morphine
Very susceptible to 1st pass effect – if taken orally liver metabolises approx. 60% of drug
Give IV, IM in acute setting to avoid this
Morphine can actually be taken orally, intramuscularly, intravenously, subcutaneously, via
epidural, intrathecally and rectally Parenteral administration is the most ideal route due to the medication’s poor
bioavailability of 40% when taken orally (Bryant & Knight,2015) .
absorbed fast with peak concentration occurring within 60 minutes when taken
intramuscularly and within 90 minutes when taken subcutaneously.
Morphine is distributed widely throughout the body, especially to organs such as the kidney,
lung, liver and spleen. It can diffuse across the placenta.
Morphine is then metabolised in the
liver AND excreted in the urine It is because of
the first pass metabolism in the liver that oral bioavailability is so poor
indications, adverse effects, contraindications and cautions of morphine
Indications – Moderate to severe pain
Adverse effects – Nausea, constipation, respiratory depression
Contraindications – sensitivity, acute respiratory depression
Cautions – acute head injury, COPD
glyceryl trinitrate pharmacodymanics
Causes smooth muscle relaxation
Causes vasodilation – reduces cardiac preload and stroke volume
Pharmacokinetics of GTN
Metabolised by liver rapidly – short lived therapeutic effect
Indications, adverse effects, contraindications and cautions of GTN
Indications – Stable angina, ACE
Adverse effects – headache, dizziness, orthostatic hypotension
Contraindications cardiomyopathy, hypotension, hypovolaemia, raised ICP
Caution - interactions with alcohol, erectile dysfunction medication e.g. viagra
metaclopramide pharmacodynamics
Blocks (antagonises) dopamine receptors in chemoreceptor trigger zone (CTZ) in brain
CTZ relays message to vomit centres – block reduces this
Accelerates gastric emptying
metaclopramide pharmacokinetics
ADME:
Easily absorbed orally, IM, IV
Metabolised in liver
Half life 2.5 – 5 hrs
Indications, adverse effects, contraindications and cautions of metaclopramide
Indications – nausea, vomting, GORD
Adverse effects – diarrhoea, restlessness, dizziness
Contraindications – previous reaction to dopamine antagonists
Caution - patients with Parkinsons Disease
describe the brain
2% of body weight
20% of cardiac output
- Massive oxygen and glucose requirements
- Most required by neuronal activity
- …therefore maintenance of supply essential for normal neurological function
structure of the brain
review diagram - lateral ventricle - third ventricle - subarachnoid space - pia mater - skull - skin - arachnoid villi - subdural space epidural space - dura mater - arachnoid - falx cerebri
describe brain layers
The bra blancmange ... wrapped in cling film (arachnoids), ... in a paper bag (dura) ...inside a cardboard box (skull) ...wrapped in brown paper (scalp). ain is….
any of the brain layers can be damaged by
Direct impact on the box (blow),
Dropping the box (fall) or
Shaking the box (acceleration/deceleration)
what are different mechanisms of injury
Primary Injury
eg. Blow to the head
eg. The head hitting an object
eg. Acceleration-deceleration (whiplash)
…Scalp lacerations can bleed profusely and cause hypovolaemia – be aware
secondary injury from head injury examples …
From this we get: Haemorrhage Oedema Haematoma Dura tearing Structural movement Obstruction to CSF flow Hypoxia pH alterations
what is the monro kellie doctrine
the sum of volumes of brain, cerebrospinal fluid (CSF) and intracerebral blood (venous and arterial) is constant. An increase in one should cause a reciprocal decrease in either one or both of the remaining two.
what is herniation
Brain herniation occurs when something inside the skull produces pressure that moves brain tissues.
pharmacodynamics of mannitol
Osmotic Diuretic (Type of sugar)
Mannitol elevates blood plasma osmolality, resulting in enhanced flow of water from tissues, including the brain and cerebrospinal fluid, into interstitial fluid and plasma.
mannitol pharmacokinetics
ADME – Induces movement of intracellular water to extracellular and vascular spaces. Excreted from kidneys.
indications, contraindications and adverse effects of mannitol
Indications -Diuresis, >Intraocular Pressure (Glaucoma), >ICP
Contraindications - hypersensitivity, severe heart failure, pulmonary congestion, disturbance to the blood – brain barrier, dehydration
Adverse effects -nausea & vomiting, dizziness, hypotension, ARF, acidosis
tazopip pharmacodynamics
Broad spectrum semisynthetic penicillin antibiotic – contain Piperacillin and Tazobactam. Piperacillin inhibts bacterial cell wall synthesis – Tazobactam inhibits the enzyme beta-lactamase – that would normally prevent Piperacillin from working. Combining the two makes it more effective
Active against Gram-positive and Gram-negative aerobic and anaerobic bacteria
tazopip pharmacokinetics
ADME – excreted from kidneys. Caution in acute kidney injury and renal disease
indications, contraindications, adverse effects and interations of tazopip
Indications -Used for: LTI’s, UTI’s,intra abdominalinfections, skin infections, gynae infections
Contraindications - Allergic reactions to penicillin/cephalosporins & clauvalinic acid (Augmentin), jaundice
Adverse effects -nausea, vomiting,clotting problems, raised liver enzyme, resistance to therapy in prolonged use, false positives for glucose in urine
Interactions -Other antibiotics,Vecuronium, Methotrexate, Heparin and anticoagulants
what is cancer
Cancer is a genetic disorder at cellular level
Chronic disease
Uncontrolled proliferation of cells
Normal body responses:
….Cells grow and divide
….Damaged/old cells removed – replaced by new cells
Cancer
….Abnormal cells divide/replicate
…..Grow beyond normal tissue
Incidences increase with age
what can cancer be caused by
Genetic eg. oncogenes and tumor supressor genes
Environmental factors
Behavioural factors
Only >10% of cancers genetic in origin
Abnormal cell behaviour = damaged genes = mutation
theory of cellular mutations applies that Carcinogenesis causes mutation in the cellular dna
what are Oncogenes
Abnormal genes, promote cell proliferation (BRCA1, BRCA2)
what are tumour supressor genes
Encode proteins that in their normal state negatively regulate proliferation
describe carcinogenesis
view flow chart
aquired/ dna damaging agents= dna damage to normal cell= failure to repair dna ( may be caused by genetics)= mutations in somatic cell genome= altered genes causing apoptisis OR increased oncogene/ tumour supressor gene promotion= unregulated proliferaion= clonal expansion (Angiogenesis, escape from immunity and additional mutations contrubute to this)= tumour progression= malignant neoplasm= invasion and metastasis
