NRSG265 Principles of Nursing: Medical - Week 10 Capstone Revision - PDF

NRSG265 PRINCIPLES OF NURSING: MEDICAL Capstone and Exam Revision In recognition of Aboriginal and Torres Strait Islander peoples’ deep spiritual connection to Country, and in continuing ACU’s commitment to reconciliation, we would like to acknowledge and pay our respects to the First Peoples, the...

NRSG265 PRINCIPLES OF NURSING: MEDICAL Capstone and Exam Revision In recognition of Aboriginal and Torres Strait Islander peoples’ deep spiritual connection to Country, and in continuing ACU’s commitment to reconciliation, we would like to acknowledge and pay our respects to the First Peoples, the Traditional Custodians of the lands and waterways where ACU campuses are located. We respectfully acknowledge our Elders past and present and remember that they have passed on their wisdom to us in various ways. Let us hold this in trust as we work and serve our communities.  Revision of main concepts 3 Endocrine Disorders Type 1 vs Type 2 diabetes mellitus Type 1 Type 2 Causes Pathophysiology Signs and Symptoms Acute Hypoglycaemia complications DKA Management 6 | Pathophysiology of Type 1 DM Genetic Factors Viral infections HLA – linked genes Other damage to beta cells Immune response against beta cells Beta cell destruction Release of glucagon Lack of insulin released Liver continues to release glucose GLUT-4s are not activated Glucose unable to be taken up by cells Hyperglycaemia Type 1 diabetes 6 | 7 | Clinical Manifestations of Type 1 DM – continued Confusion Polydipsia Fatigue Tachycardia Polyphagia Polyuria Nausea, vomiting Abdominal pain Weight loss Weakness 8 | Pathophysiology – Type 2 DM Characterised by insulin resistance due to the following mechanisms: Decreased beta cell responsiveness to increased glucose levels Decreased insulin production (initial hyperinsulinaemia, then beta cell atrophy and death) Increased insulin resistance at the cell Reduction in the number of insulin binding sites Decrease in the amount of insulin binding to the receptors  RISK FACTORS AND CAUSES NON-MODIFIABLE: genetics, age, ethnicity MODIFIABLE: obesity, sedentary lifestyle, poor diet, calorie intake > energy expenditure Increased adiposity Increased insulin Beta cell dysfunction (fat tissue) resistance at the cells (liver, (pancreas) → less insulin muscle, adipose) produced Increased free fatty acids Excess glucose produced (FFAs) from liver and muscle Continued impaired Proinflammatory cytokines → glucose uptake and chronic low grade utilization inflammation of the cells HYPERGLYCAEMIA TYPE 2 DIABETES Increased reactive oxygen species (ROS) → oxidative stress → cell damage Common OHA drug classes Drug Class Biguanides (metformin) Sulphonylureas (glicazide) Mechanism of action Common adverse Nausea and vomiting effects Diarrhoea Stomach cramps Loss of appetite What is considered hypoglycaemia? BGL < ? What are 2 causes of hypoglycaemia? What are the common signs and symptoms of a hypo? Interventions for DKA and HHS – what is the rationale behind these? These are prioritised below 1. Fluid resus 2. Reverse hyperglycaemia 3. Correct acid base imbalances 4. Correct electrolyte imbalances 5. Cardiac monitoring 6. Vital obs 1/24 Respiratory Disorders Asthma Chronic respiratory condition characterised by reversible: Bronchoconstriction Oedema of airways Mucous hypersecretion Let’s review the pathophysiology of asthma, and then please list 5 clinical manifestations of this disease 15 | Pathophysiology of asthma Initial exposure to allergen (antigen) Specific IgE antibodies Minimal signs and produced to attack symptoms allergen/foreign substance Once produced, these specific IgE antibodies will Re-exposure to allergen → bind to mast cells within it will bind to IgE the lung tissue Chemical IgE activated and causes the reactions/processes will rupture of the mast cell occur → leads to s+s of asthma 16 | Allergen or irritant exposure Mast cell degranulation (injury → inflammation) within lung tissue Release of chemical mediators HISTAMINE PROSTAGLANDINS LEUKOTREINES PLATELET ACTIVATING FACTOR Vasodilation Mucous Bronchoconstriction Vascular permeability → production Oedema of airways Bronchospasms Airway obstruction COPD According to Global Initiative for Chronic Obstructive Lung Disease (GOLD,2019): “Chronic Obstructive Pulmonary Disease (COPD) is a common, preventable and treatable disease that is characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases” (p. 1). 18 | Pathophysiology of COPD Noxious stimuli Abnormal and prolonged (smoke) inflammatory response Increased neutrophils, Systemic effects: macrophages fatigue, weight loss and lymphocytes. Continuous bronchial irritation Release of and inflammation cytokines Breakdown in lung parenchyma Hypertrophy and hyperplasia of Enlargement of air spaces goblet cells Gas trapping → hyperinflation Destruction of Gas exchange abnormalities Bronchial oedema alveolar wall Airflow limitation Mucous hypersecretion Loss of elastic recoil Frequent exacerbations Airway remodeling - scarring Increased infection risk Dyspnoea Cough Hypoxaemia Hypercapnia Cor pulmonale 19 | How can cor pulmonale result from COPD? Links between PHT and cor pulmonale 20 | Asthma and COPD medications – Overview SABA (salbutamol, Relievers terbutaline) (bronchodilators) Antimuscarinic/ anticholinergic ICS Combination Preventers (fluticasone, ICS + LABA An Overview budesonide) ICS + LAMA LAMA + LABA LABA Other LAMA Oral corticosteroids Drugs used to manage respiratory conditions How do SABA drugs work to relieve the signs and symptoms of asthma and COPD? What are 2 common adverse effects?  Short acting ß2 agonists (SAßA) – salbutamol Stimulation of Adverse effects Found in due to stimulation ß2 receptors Smooth muscles of airway of ALL ß2 receptors (as well Inhibits as ß1) Bronchial smooth Tachycardia  airway diameter Palpitations muscle Tremors Produces Flushing  resistance Relaxation of airway muscles Headaches HT  gas exchange  Work of breathing Acid-base balance and ABGs 24 | Acidosis and Alkalosis – a definition Acid base imbalances generally result from Alterations to acid base balance can include: respiratory or metabolic failures RESPIRATORY ACIDOSIS ACIDOSIS RESPIRATORY ALKALOSIS Acidosis is a condition resulting from higher than normal acid levels in the blood and METABOLIC ACIDOSIS tissues. It is not a disease, but may be an METABOLIC ALKALOSIS indicator of disease ALKALOSIS What acid base imbalance can occur when a Alkalosis is a condition resulting from a patient has an opioid overdose? higher than normal level of base in the blood What about a panic attack? and tissues 25 | ABG The arterial blood gas (ABG) is a lab test used to measure the body’s acid base balance and oxygenation within the ARTERIAL blood 26 | 6 steps to ABG analysis 1. Analyse the pH 2. Analyse the PaCO2 3. Analyse the HCO3 4. Match the PaCO2 or the HCO3 with the pH 5. Does the PaCO2 or the HCO3 go in the opposite direction of the pH? (IF YES, THEN THERE IS COMPENSATION BY THAT SYSTEM) 6. Analyse the PaO2 and SaO2 Cardiac Disorders Coronary Artery Disease (CAD) Also known as coronary heart CAD disease (CHD) or ischaemic heart disease (IHD) Leads to ischaemia caused Acute Asymptomatic Chronic stable Coronary by narrowed heart (coronary) angina Syndrome arteries that supply blood to (ACS) the heart muscle. Atherosclerosis is the major Unstable ST- segment cause of CAD. It is characterised angina elevation by deposits of lipids within the Myocardial intima of the artery Non ST Infarction (MI) Most common type of CVD – segment elevation MI leading cause of morbidity and mortality 29 | Atherosclerosis – pathophysiology Atherosclerosis is the major cause of CAD. Begins as soft deposits of fat that harden with age Referred to as “hardening of arteries” Atheromas (fatty deposits) prefer coronary arteries It is characterised by deposits of lipids within the intima of the artery. Endothelial injury and inflammation play a central role in the development of atherosclerosis (Brown, Edwards, Buckley & Aiken, 2021) The stages of development in atherosclerosis are: (1) fatty streak, (2) fibrous plaque, and (3) complicated lesion. 30 | Myocardial ischaemia Imbalance between oxygen supply and demand Vasoconstriction of coronary vessel Narrowing of a major coronary artery by > 50% → ischaemia, especially during exercise Atherosclerosis most common cause Within 10 seconds of occlusion anaerobic respiration forms lactic acid Cells are then viable for approximately 20 minutes Cell death → inflammation, granulation tissue formation and scarring How is myocardial ischaemia seen on an ECG? 31 | Clinical manifestation of myocardial ischaemia Angina (chest pain) What are the signs and symptoms? anaerobic metabolism decreased nutrients and generation of ATP increased lactic acid activation of nociceptive (pain) fibres Management of angina – nitrates Aim of these drugs is to reduce cardiac workload → reduce oxygen demands NITRATES: most commonly used glyceryl nitrates (anginine, GTN) Orally inactive → adminster via sublingual, IV, nasal spray route MECHANISM OF ACTION: How do they work? Nitrates Metabolised and NO causes vasodilation of administered converted to NITRIC peripheral blood vessels → OXIDE (NO) in vessel reduces TPR walls Decreases preload and Dilates coronary arteries → Reduced cardiac afterload → Decreases SV→ increase blood flow to the workload Decreases CO → Decreases ischaemic areas of the heart O2 demands ADVERSE EFFECTS: Hypotension, Flushing, Headache, Fainting Acute coronary syndrome (ACS) When ischaemia is prolonged and not immediately reversible, acute coronary syndrome (ACS) develops: 1. unstable angina 2. non – ST-segment-elevation myocardial infarction (NSTEMI) 3. ST-segment-elevation myocardial infarction (STEMI) ACS is associated with deterioration of a once- stable atherosclerotic plaque → thrombus Partial or full occlusion Patients with suspected ACS require immediate (Brown, et al. 2021) hospitalisation. Myocardial Infarction (MI) Result of sustained ischaemia (>20 minutes), causing irreversible myocardial cell death (necrosis) 80%-90% secondary to thrombus Ischaemia starts in subendocardium Necrosis of entire thickness of myocardium takes 4 to 6 hours Loss of contractile function STEMI NSTEMI How much of the coronary artery is occluded? Degree of damage to the myocardium? Arrhythmia – what cardiac rhythm is this? This is a 6 second strip – what is the HR? What is the pathophysiology of this arrhythmia? 35 | 36 | Common cardiac drugs ACE inhibitors Beta blockers Diuretics Indications Mechanism of General MoA action Adverse effects Examples “-PRILS” “-OLOLS’’ Renal Disorders 38 | Functions of kidneys Function of the kidneys Details Regulates ion levels in Na+, Cl-, K+, Ca+2, HPO4-2 (ensures blood concentration is constant) the blood Regulates blood pH Controls both H+ and HCO3 - to regulate pH (7.35-7.45) To reduce acidosis: excretes H+ in urine, and retains HCO3 - To reduce alkalosis: excretes HCO3- in urine, and retains H+ Regulates blood volume Conserves or eliminates water in the urine Regulates blood Adjusting blood volume by increasing/decreasing water secretion in urine (through pressure (BP) aldosterone an antidiuretic hormone (ADH) Releases renin to activate the renin/angiotensin/aldosterone system (RAAS)to regulate BP Maintains blood Regulates water and solutes in the urine, maintaining a relatively constant blood osmolarity at osmolarity approximately 290 mOsm/L Produces hormones Calcitriol: an active form of vitamin D which is essential for Ca+2 uptake from GI tract Erythropoietin (EPO): stimulates the production of RBCs in the bone marrow Excretes wastes and Removal through urine including ammonia, urea, bilirubin, creatinine, uric acid, and foreign substances toxins/chemicals from the diet or drugs Regulates BGL The kidneys remove excess glucose to help maintain normal blood glucose Why does anaemia occur in a patient who has chronic kidney disease? The kidneys produce the hormone erythropoietin (EPO) → stimulates the production of RBCs in the bone marrow Pts with CKD are unable to produce adequate amounts of EPO which means they won’t produce enough RBCs → anaemia Urinary Tract Infections (UTI) UTIs include: urethritis – infection of the urethra cystitis - infection of the bladder/lower urinary tract pyelonephritis - infection of the kidney/upper urinary tract List 5 common signs and symptoms of a UTI AKI vs CKD – know the patho! Acute Kidney Injury Chronic Kidney Disease Onset Sudden Gradual, often over many years Diagnostic criteria Acute reduction in urine output *GFR < 60 ml/L/1.73 m2 for > 3 and/or Elevation in serum creatine months Kidney damage >3 months Reversibility Potentially Progressive and irreversible The primary cause of Infection Cardiovascular disease death *GFR -glomerular filtration rate Diuretics Complete the following table Drug Class Loop Diuretics Thiazide diuretics K+ sparing diuretics How strong is it? Powerful diuretics Moderately potent Low efficacy Primary mechanism of action Indications Heart failure, HT, pulmonary oedema Common adverse Hyperkalaemia effects Hyponatraemia Hypotension Nursing Strict FBC considerations Neurological Disorders 44 | Types of stroke 1. Ischaemic stroke Most common type of stroke Caused by a blocked artery from an emboli or thrombus 4 out of every 5 strokes Pathophysiology Acute ischaemic strokes result from vascular occlusion secondary to thromboembolic disease (atherosclerosis) Ischaemia causes cell hypoxia and depletion ATP → ion channels are impaired → K+ leaves the cells and Na+ and Ca2+ enter → cerebral oedema Overwhelming inflammatory response leads to further damage Further neuronal cell death and irreversible damage 45 | Types of stroke 2. Haemorrhagic stroke Caused by bleeding in the brain Long-standing high blood pressure and cerebral aneurysms 1 in every 5 strokes, but higher mortality rates Pathophysiology: Rupture of blood vessels leads to break in the wall of a blood vessel Bleeding occurs directly into brain parenchyma Can lead to damage in surrounding area due to an increased intracranial pressure 46 | Clinical manifestations - common These will vary and are dependent on the site of ischaemia Limb weakness Weakness on side of the body A sudden change in the vision of one or both eyes A severe sudden headache that cannot be explained by any injury or other cause A quick onset of dizziness, loss of coordination/balance, or other problems walking A sudden problem talking or expressing thoughts and words Sudden LOC N+V Seizures, fainting without known cause 47 | Epilepsy Epilepsy is defined as a chronic neurological disorder characterised by recurrent seizures A seizure occurs when abnormal electrical activity in the brain causes an involuntary change in body movement, sensation, awareness, or behavior There is a momentary 'imbalance' within electrical and chemical circuits in the brain; excitatory neurotransmitters (glutamate) > inhibitory neurotransmitters (GABA). 2 main types: Focal Generalised 48 | Drugs used to manage epilepsy Goal of therapy is to control recurrent seizures while minimising adverse effects and maintaining quality of life → requires frequent plasma level monitoring These drugs are able to cross the BBB, therefore have many CNS adverse effects What would be some examples of adverse effects? How can we potentially control seizure activity? Increase GABA release Decrease action of glutamate Close ion channels This all reduces excitability of neurons (reduces depolarisation)