6.006 pathophysiology revision.pptx
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Kāwhe break Reading BNU6.006 This Photo by Unknown Author is licensed under CC BY-SA Lets do some Pathophysiology This is a summary to the pathophysiolo...
Kāwhe break Reading BNU6.006 This Photo by Unknown Author is licensed under CC BY-SA Lets do some Pathophysiology This is a summary to the pathophysiology Of many conditions we covered in the BNU6.006 Block course. It is not a complete study guide, But it is a good place to start. Chest radiograph retrieved 10/12/18 from https://en.wikipedia.org/wiki/Chest_radiograph Remember to use the group work PPTs that you did on moodle as part Of your study. And to look after your own wellbeing During your study time. Hope you find this helpful. Review of terminology From the Greek word meaning “to give a reason for” Aetiology A study of the causes, origins and reasons for disease process A study of the functional changes that Pathophysiology occur within an individual due to a disease or pathologic state Tuberculous Respiratory Asthma This Photo by Unknown Author is licensed under CC BY-SA Pulmonary Emboli Chronic Bronchitis Emphysema Chronic Obstructive Pulmonary Disease Progressive chronic disease characterised by irreversible Emphysem airway obstruction, hindering a expiratory flow Umbrella term encompassing emphysema, chronic bronchitis Chronic and asthma Asthma* Bronchitis Each has their own pathophysiology but all contribute to airway inflammation initiated by a noxious irritant Emphysema Destruction of elastin in alveoli https://pxhere.com/en/photo/1376780 Macrophages Neutrophils release Irritant recruited, inflammatory releasing mediators elastase Other proteases Elastase breaks T-lymphocytes cause tissue down elastin cause further damage to causing tissue damage alveolar wall destruction of elastic fibres Pulmonary Alveolar walls lose elasticity, Cell apoptosis capillary bed reduced, increasing (death) compliance (too increasing pressure in stretchy) pulmonary artery Loss of elasticity allows the alveoli to expand with inspiration, but reduces its ability to recoil in expiration Results in CO2 being ‘trapped’ increasing the alveolar PCO2 *Bronchiole constriction also contributes to air/gas ‘trapping’ A rise in alveolar PCO2 means CO2 cannot diffuse readily from pulmonary capillaries, causing a build up in arterial blood = hypercapnia Accumulation of damage causes large air spaces to develop Surface area is reduced, reducing gas exchange between alveoli and pulmonary capillaries = hypoxaemia and hypercapnia Direct contact of alveoli with capillary beds is reduced, reducing gas exchange When administering a drug as a registered nurse you will need to be aware of the following… Oxygen should be prescribed and administered to a target: for chronic ventilatory failure (COPD) SpO2 88-92% Oxygen (O2) Medical Gas is appropriate; for most other medical Adverse effects patients 92-96% is appropriate. Toxicity with Treatment of hypoxaemia by increasing alveolar prolonged Patients should be exposure to high oxygen tension. The aim is achieve a normal or monitored for improvement in work O2 concentrations; near-normal oxygen saturation for an individual of breathing and decreased affinity patient. increased PaO2 to of Hb for CO2 in Pharmacokinetics CO2 retainers Pharmacodynamics indicate efficacy. Oxygen is largely inhaled into the (Haldane effect) Oxygen therapy improves alveoli and diffuses into the capillary effective cellular oxygenation. It bed. Oxygen combines with Patient Precautions acts to restore normal cellular haemoglobin, with a small amount being dissolved in the plasma. education Oxygen therapy activity at the mitochondrial Oxygen is metabolised in the tissues should include devices should not level and reduce metabolic almost entirely in the mitochondria, be used near an acidosis. where oxidative enzymes reduce the correct oxygen in the formation of adenosine administration open flame due to triphosphate (ATP). Excretion of its’ high and use of combustibility oxygen metabolites (CO2 and H2O) is oxygen delivery via the lung and renal system. devices. When administering a drug as a registered nurse you will need to be aware of the following… Monitoring Peak flow measurements Salbutamol short-acting β2 adrenergic agonist (SABA) before and after administration Bronchodilator – relief of symptoms during can help Adverse effects maintenance treatment of asthma and COPD; determine Tachycardia, effectiveness headache, nervous prevention or treatment of exercise/allergen induced tension, fine hand bronchospasm. tremor, hypotension Hyper/hypokalaemia (which may cause Pharmacodynamics Pharmacokinetics weakness, fatigue, Salbutamol is a β2-adrenergic Onset by inhalation is rapid (5- tremors, muscle agonist and stimulates β2- spasm) 15 mins). Peak effect reached in Patient adrenergic receptors. Binding to 1-2 hours. Metabolised in liver Contraindication these receptors in the lungs and excreted in kidneys. education results in relaxation of bronchial s What common side smooth muscles effects to expect Caution with CVD, diabetes and HTN Appropriate delivery of inhaler (including Inhaler may contain spacer, mouth care) lactose Asthma & COPD action plans https://www.asthmafo undation.org.nz/resou rces/asthma-action-pl ans Keep hydrated ………… it helps you to retain information. Arthrosclerosis Cardiac Kidney injury Acute Kidney Injury Acute kidney injury (AKI) occurs when the kidneys are unable to remove the body's metabolic waste or perform their seven regulatory functions - Acid- base balance / Water balance /Toxin removal /Erythropoietin production (RBC production in the bone marrow) /Vitamin D activation / maintenance of BP and electrolyte regulation These metabolic wastes build up in the body. GFR falls as the disease progresses Rapid loss of renal function due to kidney damage – can be life threatening Pre-renal causes – low cardiac output, low BP, severe vomiting Intrarenal (intrinsic) causes - damage to renal tissue, nephrotoxins, NSAIDS Post-renal causes – obstruction, renal calculi, How does AKI differ from CKD? AKI – is a condition that is often associated with acute illness and occurs within a short period (days/hours) 20% of AKI is associated with medication AKI may develop into CKD CKD has a poorer prognosis Chronic Kidney Disease(CKD) Characterised by the gradual loss of renal function CKD - kidney damage or a decrease in eGFR for at least 3/12 Individuals with CKD are at an increased risk of CVD Some people with CKD go onto to develop end stage renal failure (ESRF) Diabetes was the most common reason for someone starting renal replacement therapy (RRT) dialysis or transplantation Early detection is very important to slow or stop progression of the disease Clinical Manifestations of Chronic Kidney Disease CORONARY ARTERY DISEASE Coronary artery Ischaemia vasospasm but no pain Ischaemic heart disease Results from narrowed coronary arteries – atherosclerotic plague Obstruction reduces flow of oxygenated blood to heart muscle =Angina Chest, jaw, arm or back pain/discomfort / Shortness of breath/ Dizziness, feeling faint / Panic/ anxiety Can lead to Acute MI/ cardiac arrest if thrombis develops, dislodges and obstructs a Coronory artery. Two types of MI – NSTEMI and STEMI Atrial fibrillation A common arrythmia effecting the upper chambers of the heart (atria). In AF, the hearts electrical signal that initiates the beat becomes irregular, firing from multiple foci in atrium instead of just the SA node. This causes the atria to twitch rather than contract fully. This irregular electrical activity can lead to ineffective emptying of blood from Atria into the ventricles. Blood gets trapped and Pools in atrium developing clots. These clots can be transferred throught The heart into the lungs (PE) to the Brain (CVA). Prolonged AF can stress the myocardium and contribute to CAD and risk of MI. Heart Failure When administering GTN as a registered nurse you will need to be aware of the following… H Monitoring requirement GTN/ Glyceryl Trinitrate Antianginal s B/P HR Side effects: Flushing Headache Indications for Dizzyness Rare -Dry use: chest Pharmacodynamics Patient education mouth Contra- pain/anginaPharmacokinetics Antagonises NO receptors = relaxes indications smooth muscle. Sublinugual, dermal, Sit down rapidly metabolised VIAGRA Dilates veins and Stand up ETOH arteries. short duration slowly Reduces B/P HR < 50 When administering Morphine as a registered nurse you will need to be aware of the following… H Monitorin Morphine Sulfate, names g requireme include: Morphine Sulfate (IV) nts Oxynorm, Sevredol, MS Contin RR B/P Side-effects: HR Sedation Dizzyness Indications for use: Nausea Constipation Hallucinations Pharmacodynamic Patient education Contra- analgesia/sedation s Pharmacokinetics Opioid mu-receptor Careful mobilising. indications: antagonist. Oral, IM, IV, PR Avoid ETOH resp. depression, Targets CNS opiate Short half life & other severe asthma, receptors. Depresses opiates. TBI, acute abdo CNS, RR, GI. pain Vasodilation. When administering a drug as a registered nurse you will need to be aware of the following… Monitoring requirement Atorvastatin / Lipitor: s Liver Common side HMG CoA reductase inhibitors effects function dyspepsia, nausea, flatulence, Indications for use-reduce the risk of diarrhoea, muscle heart attack and stroke by lowering total pain, tenderness or weakness cholesterol and low-density lipoprotein cholesterol Pharmacodynami Pharmacokinetics Patient education cs PO Avoid grapefruit lowers plasma juice Contraindicatio cholesterol and Mean elimination Minimal alcohol ns lipoprotein levels half-life values range Can be taken at avoid in from 11 to 24 hours any time of the pregnancy the liver is the day-with or care in liver primary site of without food disease action When administering a drug as a registered nurse you will need to be aware of the following… Monitorin g requireme Metoprolol – Beta-blocker nts BP Side effects - dizziness, HR nausea, fatigue, bradycardia Indications for use: hypertension, Patient angina, heart failure, arrhythmias, post- education Contraindicatio myocardial infarction, migraine ns avoid in Do not stop patients with a Pharmacodynamic prophylaxis abruptly- history of asthma s Pharmacokinetics Modified –can precipitate bronchospasm ß1-selective ß- PO, IV release tablets can Do not confuse blocker; reduces or Mean elimination be halved or immediate inhibits the agonistic half-life of metoprolol release and effect of swallowed modified release. in plasma is 3.5 whole with a catecholamines on hours glass of the heart water - do not crush or chew. When administering ace inhibitors such as acupril you will need to be aware of the following… Monitoring requiremen ts Maintain B/P and HR Cilazapril, enalapril / Fluid balance & weight ACE inhibitors documentati Common on side effects Dehydration, Indications for use: for Watch urine hyperkalaemi treatment of fluid volume excess in output Pharmacodynamic Patient a, dry cough heart failure s & HTN Pharmacokinetics education Contraindicati PO, IV Prevents angiotensin Take same ons I converting to Binds to tissue & time. Have Significant drug angiotensin II. plasma protein. regular B/P interactions, Prevents constriction Often by glomerular checks. precautions of blood vessels & kidney function, filtration, absorbed Avoid prevents angiotensin & eliminated rapidly. alcohol. Will rash, liver impairment. I secreting B/P↓ HR ↓ Urine need blood aldosterone. output↑ checks Promotes diuresis. Copyright Ara 2016 When administering Frusemide as a registered nurse you will need to be aware of the following… Monitorin g Frusemide (Frusid, Lasix) requireme nts Weight, Blood pressure, – Loop diuretic Pulse, electrolytes Side effects , fluid Electrolyte balance disturbance, Indications for use – treatment of dizziness, Patient postural oedema associated with heart failure, education hypotension, cirrhosis, renal impairment and take with ototoxicity nephrotic syndrome Pharmacokinetics food, ? Pharmacodynamic possible Interacts with s inhibits PO, IV potassium several drugs reabsorption of supplements, including highly protein Aminoglycoside sodium & chloride in bound, oral half life report ringing in ears, abdo antibiotics, the loop of Henle 1-2hrs, peak effect anticonvulsants pain, muscle , antidiabetics 1hr, IV peak effect weakness & etc. 30mins cramps When administering a drug as a registered nurse you will need to be aware of the following… Monitorin g requireme nts – monitor for signs of increased bleeding, Low Dose Aspirin peptic ulcer disease (Acetylsalicylic Acid) - Patient education NSAID Indications for use: Anti- Common adverse effects GI – do not Bleeding, take if you have a Acute renal insufficiency platelet history of Pharmacodynamics peptic ulcer Impedes clotting by Pharmacokinetics disease, Contra- blocking prostaglandin indications PO, IV, PR asthma or synthesis preventing uncontrolle Asthma, GI formation of platelet- rapidly absorbed, d high bleeding, aggregating substance peak serum levels peptic ulcer thromboxane A2- works 60 minutes blood for lifespan of platelet pressure, take with food Remember to eat well To support your Neurology And study ….. Neurology ‘Normal’ Brain Autonomic Dysreflexia Dermatomes Parkinsons Disease Spinal Cord Injury Mechanical disruption to the structure & function of the spinal cord & spinal nerve pathways. Can be a traumatic or non traumatic injury Symptoms depend on degree of paralysis & potential for rehabilitation depends on the level of lesion. PATHOPHYSIOLOGY: Process leading to spinal cord ischaemia and hypoxia of secondary injury Spinal Shock: Areflexia (sudden depression reflex activity) < level injury Muscles paralysed, flaccid and without sensation below level of injury Bowel and bladder function lost Gastric stasis Paralytic ileus Neurogenic shock (caused by Spinal Cord Injury) Loss of autonomic control leads to: ↓ BP, ↓ HR Peripheral venous pooling Priapism Loss of temperature control Lack of perspiration below level of injury Autonomic Dysreflexia Occurs after spinal shock has resolved in persons with SCI above T6 Stimulus causes sympathetic nerves to become overactive to a noxious stimuli (ie; bladder / infection / ingrown toenail), causes widespread vasoconstriction and excessive hypertension the parasympathetic response can’t compensate with vasodilation below the injury level and drops HR excessively to compensate instead. Can be fatal if untreated Stroke Cerebral vascular accident (CVA) The World Health Organisation (WHO) defines stroke as a clinical syndrome: Rapidly developing clinical signs of focal(or global in case of coma) disturbance of cerebral function Lasting more than 24 hours or leading to death No apparent cause other than a vascular origin Hypertension contributes to over 12.7 million strokes annually Two main types of stroke Ischaemic stroke Haemorrhagic stroke 85% of all strokes are ischaemic Intracerebral (ICH) and subarachnoid haemorrhage (SAH) Cerebral embolism is a blood A burst blood vessel will cause blood to clot or debris formed elsewhere leak into brain tissue and surrounding in the body which travels to the structures, causing a rise in intracranial brain. If it cannot pass through pressure and damage to brain tissue the lumen it will occlude the vessel, interrupting blood flow Ascension Michigan (2012). Embolic stroke [screenshot]. Retrieved January causing tissue ischaemia. 22, 2019, from https://www.youtube.com/watch?v=B95O WQlj_mQ Cerebral thrombosis is a narrowing of the cerebral arteries caused by plaque build- up. A clot then forms on the plaque, occluding the vessel lumen and restricting blood flow Blooms the Chemist (2015). Thrombotic stroke [screenshot]. Retrieved January 22, to an area of the brain. Tissue Cook Children’s Health Care System (2018). Hemorrhagic stroke animation [screenshot]. Retrieved January 22, 2019, from 2019, from https://www.youtube.com/watch?v=K8VMaSJ ischaemia results if not https://www.youtube.com/watch?v=e9_9oWBsjAc URV8 thrombolysed. Contralateral symptoms Right Brain Injury Left Brain Injury Paralysed left side Paralysed right side Special perceptual Speech and language deficits deficits Quick, impulsive Slow, cautious behavioural style behavioural style Memory deficits Memory deficits R L Wikipedia (2019). Body outline jpeg. Retrieved January 23, 2019, from https://commons.wikimedia.org/wiki/File:Body_Outline.jpg Treatments Ischaemic/TIA Haemorrhagic Thrombolytic agents (t-PA) Surgical evacuation of haematoma via stimulates fibrinolysis of craniectomy atherosclerotic lesion (clot buster) Relief of raised intracranial pressure using surgical removal or placement of Needs to be administered within external ventricular drains 3 hours of symptoms Clipping or endovascular coiling of cerebral aneurysm to prevent re- Carotid endarterectomy (removal bleeding of plaque from extra cranial cerebral arteries) Hypoxic Brain Injury Insufficient oxygen and glucose supply to brain tissue caused by: Smoke inhalation Carbon monoxide poisoning Cardiac arrest Strangulation Drowning Drug overdose Traumatic birth Stroke Electrocution Traumatic Brain Injury (TBI) Closed (blunt) brain injury Basilar skull fracture Open brain Injury Concussion Contusion Diffuse axonal injury (DAI) Focal injury https://commons.wikimedia.org/wiki/ File:Bilateral_periorbital_ecchymosis_(raccoon_eyes).jpg Localised vs diffuse brain injury Widespread/diffuse Localised/focal Coup = direct impact Contrecoup = secondary damage away from injury site Diffuse axonal injury(brain stem, closed head injury)coma, mortality 33-50% Meningitis Meningitis is an inflammation of the protective membranes covering the brain and spinal cord, known as the Meninges, which can be caused by vial, bacterial, or other types of infections. Parkinsons Dopamine neurons play a crucial role in the movement and transmission of afferent motor neurons that help coordinate and regulate muscle activity. Patients with Parkinsons disease have a depletion of dopaminergic neurons in the substantia nigra is essentially halved, resulting in physiological changes and symptoms such as tremors rigidity, postural impairment and bradykinesia. There are both motor and non-motor signs and symptoms associated with Parkinson's Disease that effect an individual's quality of life. Epilepsy Seizures occur due to an imbalance of excitatory and inhibitory drive at synaptic level and excessive firing of neurons and impulses in the brain. Cushing’s Triad Pathophysiology of raised Intra-cranial pressure(ICP) Rise in ICP greater than CPP Parasympathetic response causes reduced blood flow to Cerebral ischaemia stimulates a sympathetic response initiated by ↑ BP is detected the brain. Reduced blood flow by baroreceptors. This results means less O2/glucose (adrenaline release to ↑BP & HR) in order to increase blood in an attempt to reduce BP by delivery to tissue causing ↓ HR cerebral ischaemia. flow and therefore O2 delivery Ongoing ↑ BP causes further Breakdown of Na+/K+ pump rise in ICP and further causes water to enter the cell, restriction of blood flow. A ↑S resulting in cell death. BP switch of aerobic cellular respiration to anaerobic As cerebral oedema worsens, the brainstem is compressed DEATH respiration results in ↓ ATP production for cellular causing irregular respirations before death is imminent ↓H ↓R function (cerebral ischaemia) R R BRAIN DEATH Profound unconscious state with NO reaction to outside stimuli. Excluded all other potential causes including drugs, Healthy live hypthermia, severe hypothyroidism brain. Heartbeat and respirations can only be maintained by invasive support. Clear evidence needed that serious brain injury has occured. Brain swelling, MRI and CT and that it is not curable. loss of grey white matter Needs 2 Drs for diagnosis and beside tests. TESTS PERRLA pupil check Eye sensitivity to dry cotton wool ball pressure or painful stimuli attempt to trigger gag reflex apnoea test - disconnect from ventilator Take a walk and Relax ……. This Photo by Unknown Author is licensed under CC BY-NC-ND Peri-Op / Triage & Trauma / Diabetes MVA trauma patient awaiting C-spine clearance Crohns Disease Pain “An unpleasant sensory and emotional experience associated with actual and potential tissue damage”……(International Association for the Study of Pain, 1979). Pain is always subjective. Each individual learns the application of the word through experiences related to injury in early life. Essentially: ‘Pain is what the person says it is’ but sometimes the person doesn't say !!! 1: Acute pain is “normal” pain, it is felt when hurting a toe, breaking a bone, having a tooth ache or walking after an operation. Predictable beginning and end. 2: Chronic pain is a “pain illness”, it is felt day after day, month after month & seems impossible to heal.“never ending story”. Unpredictable beginning and ending. 3: Chronic pain syndrome = constellation of behaviours related to persistent pain. (CRPS) represents significant life role disruption. This slide will help you think about what effect these medications have on the processing of pain(refer back to your worksheet) Think about the effects medication targeted at these areas may have on the patient and write them down. (eg. Physiological signs and symtoms) Opioids Brain Tricyclic antidepressants Alpha agonists Opioid Dorsal Local anaesthetics horn Tricyclic anti depressants NMDA antagonists Of the spinal cord Anticonvulsants Local anaesthetics Peripheries Non steroidal anti inflammatory Pharmacological treatment options….. Paracetamol and ibuprophen – block formation of prostaglandins that stimulate nociceptors. Novocaine/ropivicaine/bupivacaine( local anaesthetics) – blocks conduction of nerve impulses along pain fibers. Morphine/Oxycodone/fentanyl - bind to opioid receptor sites and ↓the perception of pain to the brain. Anticonvulsants and antidepressants. are often used to help treat chronic pain- may block some neurotransmitters. Eg. gabapentin Amitriptyline Tramadol. Interferes with reuptake of serotonin and noradrenaline and has a weak opiate effect. In clinical practice you will become familiar with these more commonly prescribed analgesics. Its good to know about the effects/side effects, route, duration of action. As Registered Nurses it is expected you will know before administering! Opioid ( eg morphine/fentanyl oxycodone) side effects Nausea and vomiting: Pruritus: common common. Not an allergy. -- Antihistamines Hydration,(IV or oral) Urinary retention: not common. Antiemetic's regularly often associated with Change of opiate if severe. epidural/spinal anaesthesia. Constipation: common. Monitor.--May need urinary catheter. Prevention better than cure. Hallucinations: uncommon regular bowel regime. Disturbing--- Change of opiate Monitoring. Regular management. Reassurance, aperients. education Respiratory depression is a major side effect of opioid overdose. When administering opioids Nurses are expected to be alert to the expected signs and symptoms associated with opioid induced respiratory depression. And have the antidote Diseases/disorders of the gastrointestinal tract(G.I) are many and varied and may result from … Bleeding, trauma, perforation, obstruction. Inflammation, infections, infestations. Cancers benign and malignant Congenital disorders. Circulatory and nervous system faults. Aging. Disorders of the Gastrointestinal Oesophagitis: tract Gastroesophageal reflux Gastritis (GORD) Inflammation of stomach Acid reflux. mucosa. Gastric acid, pepsin and bile irritate Mucous membrane becomes the squamous epithelium. oedematous, hyperaemic Resulting in inflammation, erosion (congested with fluid and blood). and ulceration of the oesophageal Chronic gastritis may occur due to mucosa. helicobacter pylori or Symptoms : pain(burning ulceration. (Farrell, 2017 p 978) sensation in the oesophagus). Symptoms: heart burn, bloating, Dyspepsia (indigestion) sour taste in mouth nausea, Regurgitation, hyper salivation. vomiting. Be aware the pain symptoms may mimic cardiac pain. Cholecystitis: gall bladder 56 inflammation. Associated with: Sludge (mixture of particulate solids precipitated from bile. consists of cholesterol crystals, calcium bilirubinate pigment, and other calcium salts) Gallstones( may be asymptomatic). Incidence higher in females >40yrs. Acute cholycystitis: Pain + rigidity of upper abdomen. pain radiates to mid sternum or right shoulder region. Associated with nausea and vomiting. If the Common bile duct becomes obstructed = jaundice.(yellow tinge to the skin associated with itchiness). Appendicitis: 57 can occur at any age more commonly in young adults and children. Inflammation of appendix. Resulting from kinking or occlusion by faecalith.(hardened mass of faecal matter). Pain periumbilical progressing to RT lower quadrant at McBurney’s point. Rebound tenderness on palpation. Low grade fever/nausea vomiting Complications Peritonitis or localised abscess can occur within 24 hours after onset of pain. Sourced: Crisp: Evolve resources for Potter& Perry’s Fundamentals of nursing. Australian version 4th ed 58IRRITABLE BOWEL SYNDROME: results from functional disorder of intestinal motility. Symptoms are present for at least 3 days a month. Chronic Intermittent & recurrent abdominal pain. Irregular bowel habit Diarrhoea, constipation, abdominal distension, flatulence, bloating. Continual defecation urge, urgency, feeling of incomplete evacuation. Click on the link below for further explanation of this syndrome (HINT open up in slide show first) irritable bowel syndrome 59 DIVERTICULOSIS: Diverticula + inflammation = Diverticulitis Found in 50% of people over age 60 Development of sac like mucosal projections –outpouches (diverticula) in large bowel. Develops as a result of food/bacteria being retained in a OUT POUCHES diverticulum. Infection /inflammation results and leads to abscess or Brown& Edwards: evolve resources for perforation. Lewis’s medical surgical nursing 4th Ed. Commonly found in the sigmoid colon. Inflammatory bowel disease: group of chronic disorders characterised by exacerbations & remissions. Crohn’s disease: Common in young adults/adolescents. Ulcerative colitis More common in women and older More common in Caucasian and population 50-80 years.(Farrell,M (2017 p 1011) people of Jewish descent. peak incidence between 30-50 years 5% Subacute ,chronic inflammation of all patients may go on to develop colon layers of colon(transmural). cancer.( Farrell,M ,2017, p 1013) Oedema and thickening progressing Affects superficial mucosa rectum to ulceration of mucosa. and colon Skip lesions separated by normal multiple ulcerations, tissue. desquamation of epithelium, abscesses form infiltrating Scar tissue and formation of granulomas interfere with normal submucosa layers. colon function. Bowel narrows, shortens presence of fistulas. Hernias 61 A protrusion of a viscus through an abnormal opening or a weakened area eg. Bowel ( inguinal Usually occurs in abdomen Examples May be reducible or irreducible. Complications: Incarcerated e.g. intestines slide into the hernia and cannot be pushed back into abdomen. Pain and discomfort. Strangulated. Blood is unable to flow to intestines which are incarcerated in the hernia. Pain ++ ++ urgent surgery is required. Sourced from: Lewis's medical –surgical nursing.(2015) 4 th ed Australian version. Mosby Elsevier Volvulus 62 Latin word - rolled up, twisted Twisting of part of intestine around itself = obstruction Frequently in colon, but can occur in stomach and small bowel. Can lead to: gangrene, obstruction, perforation, peritonitis & death. Sourced from: Lewis's medical –surgical nursing. (2015) 4th ed Australian version. Mosby Elsevier Colorectal 63 surgery for Colorectal Ca - Colectomy Partial Removal of the colon or removal of the entire colon is one of the most common forms of Colorectal surgery Name of the procedure describes the extent of the surgery eg Hemicolectomy part of the ascending or descending colon Usually for colorectal cancers 2nd most common cancer & 2nd most common cause of death from cancer Rates & mortality declining NZ has a lower rate of early stage diagnosis Each year 2500 – 3000 diagnosed with colorectal cancer 1100 – 1200 die each year as a result of colorectal cancer Risk factors –Obesity / Smoking /Excess ETOH /High fat and/or Low fiber diet and / or red meat(?) Gender ↑males /Age > 55 Family history, familial adenomatous polyposis (FAP) / Colorectal polyps / http://www.wecareindia.com/minimally-invasive/ Inflammatory bowel disease (IBD) sigmoid-colectomy-surgery.html 64 Left hemi colectomyRemoval of diseased area of bowel and length of normal bowel either side of it. Removal of any potentially diseased areas. Two ends of healthy bowel are anastomosed (joined together by stitching or stapling the ends together). Wound closed with clips or stitches. Commonly performed laparoscopically or may start this way and proceed to open surgery. +/- stoma / ostomy (ileostomy, transverse, sigmoid) Temporary – loop, double barrelled, Hartman's pouch OSTOMY stoma An ostomy is a surgical opening A stoma (Greek word for mouth or that opening). connects an organ or underlying The end of the organ or structure structure on the skin surface. directly to the skin. Bowel types Colostomy’ There are different types of Illeostomy ostomies created for different purposes to maintain normal body function. They are named after the organ or structure they connect to. e.g Urinary types. Tracheostomy is an opening through Urostomy the neck connecting the trachea Illeal conduit’ allowing the patient to breathe. UTEROSTOMY Sourced from: Crisp: Evolve Resources for Potter & Perry's Fundamentals of Nursing Australian Version, 4th Edition TX for GORD or gastritis may include administration of Omeprazole. 66 When administering a drug as a registered nurse you will need to be aware of the following… Monitoring requirements – Watch for worsening symptoms of Omeprazole (Losec) underlying Common adverse condition effects abdominal pain, constipation, diarrhoea, Patient education – take flatulence, nausea and vomiting along Proton Pump Inhibitor missed dose as soon as with headaches (PPI). Pharmacodynamics Pharmacokinetics remembered. Significant drug Suppress gastric acid PO half-life interactions, somewhere between DO NOT double diazepam, secretion by inhibiting the dose! Store < ketoconazole, hydrogen-potassium 30mins and 2 hours 25C. Iitraconazole and adenosine triphosphatase with the duration of digoxin (ATPase) enzyme system at action Rebound effect the secretory surface of may occur. 3-5 days the gastric parietal cells Trauma Call Criteria https://youtu.be/QvB4dyx-rVk Penetrating injury / high speed mechanism of injury Intubated Respiratory distress (↑RR, ↓SpO2) Shock ↓BP ↓LOC Penetrating injuries to head, neck, torso, & extremities proximal to elbow or knee If a patient scores greater than two of these – a trauma call will be initiated. Chest wall instability or deformity (e.g. flail chest) Two or more proximal long-bone fractures Paediatrics: >3 m or 2 X height of child High speed vehicle crash Paediatric Burns Type 2 Diabetes Mellitus T2DM accounts for approximately 90% of Pathology of T1DM patients with diabetes mellitus An autoimmune disease in which the immune Genetic pre-disposition. Increased incidence with advancing age but system has destroyed the insulin-producing beta cells in the pancreas recently more common in young adults /children. Incidence rises with increased waistline measurement including childhood obesity. No insulin is produced so glucose cannot Approximately 90% of patients with T2DM are enter cells -- hunger (polyphagia) & lethargy obese. Can go undiagnosised After a meal the blood glucose rises. Associated with sedentary lifestyle. More common in Pacific Island & Maori glucose hyper-concentrated in bloodstream exceeds the renal threshold & is excreted in the urine Similar symptoms as Type 1 DM. Water follows by osmosis so the urine output Some may be diet controlled, on oral increases –Polyuria & Polydipsia (Excessive hypoglycaemics or require Insulin. Thirst) Stores of triglycerides are catabolised for Gestational diabetes is glucose intolerance that energy causing weight loss. occurs during pregnancy in some women with – acidic ketones are produced as waste additional demands on the woman’s body. products of the lipid breakdown If a woman has glucose intolerance pre-natal it may develop into gestational diabetes. Insulin injections are needed. Once baby is born the woman may regain normal but at risk of T2DM in future. Hormones that regulate blood glucose The blood glucose is lowered by insulin The blood glucose is raised by Glucagon but also by Adrenaline (so that glucose is available for an emergency) Growth hormone (by stimulating lipolysis so lipids are available for growth leaving glucose to be available for the brain) Cortisol (which makes additional glucose available to deal with stress situations) So any condition that triggers these hormones will raise a diabetics BGL – but they don’t have insulin to control it. Hyperglycaemic Hyperosmolar non- Ketoacidosis in ketotic T1DM syndrome (HHNS) Diabetic ketoacidosis is a complication of T1DM which More common in Type 2 DM develops over a few days when (and older people). there is increased demand for insulin Persistent hyperglycaemia – Severe stress results in osmotic diuresis – Infection Loss of water and electrolytes The extra demand for glucose Differs from DKA in that causes increased breakdown of ketoacidosis is prevented by lipids & excessive amounts of ketones are produced as waste. the secretion of endogenous insulin As ketones accumulate in the blood the pH falls. – The patient develops metabolic acidosis – Untreated this progresses to coma & death. + Insulin -All persons with type 1 diabetes require regular insulin Persons with type 2 diabetes may eventually require regular insulin due to disease progression Acute conditions that result in hyperglycaemia that require short term insulin therapy Surgery, stress, infection, pregnancy. Consider the patient who is NBM. Insulin formulations differ in: Time of onset Peak effect Duration of action https://clinicalkeymeded.elsevier.com/#/books/9780729542753/cfi/6/108!/ ………. And study. This Photo by Unknown Author is licensed under CC BY Long Term conditions / Cancer Radiotherapy. Impairments are what individuals have. They may be physical, sensory, neurological, psychiatric, intellectual or other impairments. Disability is the process which happens when one group of people create barriers by designing a world only for their way of living, taking no account of the impairments other people have (The New Zealand Disability Strategy 2013) Long Term Conditions are chronic conditions people live with often for the rest of their life. Such as Asthma , COPD, Type 2 Diabe tes, Chronic Kidney disease, Irritable Bowel Syndrome, or Chrons disease Heart Failure, Stroke ,Angina and many more. Venous ulcers Arterial Ulcers -Gaiter area of the leg or affect the dorsum of the foot. Feet, heels and toes, often over bony prominences. -Wound bed covered with a fibrinous layer mixed -The ulcer appears punched out with well with marked edges. granulation tissue. -Painful -Pitting oedema -Non granulating often with a necrotic base. -Surrounding skin dusky or pale. -An irregular edge -Cool extremities with reduced capillary return. -Brown pigmentation of the surrounding skin. - Skin hairless thin and brittle with a shiny texture. -Often painless unless infected. -toenails thick and become opaque they may be lost. - May be copious exudate. - Reduced or absent peripheral pulses Pressure Injuries (PI) Pressure injuries(PI)usually develop over bony parts of the body They can result from continued pressure or shear and/or friction Decreased mobility and altered sensation increase the risk of PI Equipment such as O2 tubing and IDC tubing can also cause PI Most pressure injuries are preventable – so preventing them before they develop or progress is really important. 2 hourly turns. Cancer is …………. Cancer is the name given to a group of disorders that causes cells to escape normal controls on cell division Meaning that it is a disease that occurs at a genetic level. Changes occur to the genes that control cell function Can be inherited from our parents Or develop over a persons lifetime e.g. damage to DNA related to environmental exposure or errors that occur as a cell divides Chemotherapy Chemotherapy acts on rapidly reproducing/dividing cells in the body Different chemotherapies work on differing parts of the cell cycle to cause cell death 5 phases of a cell cycle G0 = Resting stage (cells are in this most of the time) G1 = RNA and Protien Synthesis (18-30 hours) S = DNA Synthesis – chromosomes containing DNA are copied(18 – 20 hours) G2 = Construction of Mitotic phase – just before cell splits into 2 M – Mitosis – cell splits into 2 new cells What is Radiation Therapy? Radiation is produced from the linear accelerator Shaped and delivered according to someone's treatment plan Interacts with the cells in a patients body Result directly in breaking the bonds in DNA or Interacts with oxygen within cells and produce something called Free radicals
