CTF Tutorials PDF

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Tutorials from Medicine placement at QEUH...

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CTF Tutorials

Arterial Blood Gas and Respiratory Failure Respiratory failure is a failure in the respiratory process, causing hypoxia within the body. This is detrimental to the health of a patient as hypoxic conditions lead to ischaemic tissues, and organ failure. There are two types of respiratory failure: - Type 1 respiratory failure is Hypoxaemia (PaO2 < 8 kPa) with normal (or lowered) CO2 levels. This is caused through a failure of oxygenation, commonly due to pneumonia or asthma o This can be managed through the administration of high-flow oxygen in order to reach desirable sats:  Ward Oxygen  Nasal Cannula  2-4L/min  Venturi Mask  2-10L/min  Trauma Mask  15L/min  Nasal high flow  Optiflow / respiflow  NIV  CPAP - Type 2 respiratory failure is Hypoxaemia (PaO2 < 8 kPa) AND Hypercapnia (PaCO2> 6kPa). This is a result of failure of oxygenation and ventilation, commonly caused through COPD, drugs or neuromuscular diseases such as MND. o The management of type 2 respiratory failure is not as straight forward as the administration of oxygen can potentially cause failure of the patient’s respiratory drive. This is common in COPD patients where instead of their respiratory drive being driven by hypercapnia, as with the rest of us, chronic retention of CO 2 causes adaptation to their respiratory drive being driven by hypoxia. Therefore, administration of long-term oxygen eliminates this, leaving no respiratory drive. ABGs can help us to determine respiratory failure, and any metabolic abnormalities within an acutely unwell patient. To assess these, we need to look at things in the following order: - Is the patient Hypoxic? o Normal values on room air are 10-13kPa, which needs to be adjusted for inspired oxygen concentration - What is the pH/H+ concentration? o pH < 7.35 (or H+ > 45)  Acidosis o pH > 7.45 (or H+ < 35)  Alkalosis - What is the paCO2? o >6.0kPa suggests retention of CO2, suggesting type 2 respiratory failure  If this is coupled with an acidotic picture, this is respiratory acidosis o e.g. Venous return, end diastolic volume Afterload is effectively aortic impedance --> e.g. systemic vascular resistance Contractility is the force generated at any given end-diastolic volume

The rest of this tutorial was gash so best practice it is. Inflammatory Bowel Disease

Jaundice Jaundice, also known as icterus, is caused by high levels of circulating bilirubin, resulting in the deposition of it in tissues. This leads firstly to yellowing of the sclera, and then the skin. Associated symptoms also include an itch, pale stools, dark urine and other symptoms specific to the cause of the jaundice. As jaundice results due to an increase in deposition of bilirubin, there must be an underlying mechanism to the excess production of this mechanism. Bilirubin is usually metabolised in the following way:

LFTs Pre-Hepatic Hepatocellular Post-Hepatic Bilirubin Increased Increased Increased AST Neutral Greatly Increased Neutral or Increased ALT Neutral Greatly Increased Neutral or Increased Alk Phos Neutral Neutral or Increased Greatly Increased  Urinalysis --> can help differentiate between causes also: Urinalysis Pre-Hepatic Hepatocellular PostHepatic Bilirubin None Present Present Urobilinogen Moderately Increased Moderately Increased None  Imaging may be used to differentiate causes --> Ultrasound, MRCP, CT Gastro Case Presentation This case focused on a patient who present with haematemesis and melena, probably due to excessive alcohol abuse. The main points to take away are the Glasgow-Blatchford score, a scoring system used to establish the likelihood of patients with an upper GI bleed will need intervention such

as transfusion or endoscopy. Scores of 6 or more were associated with a greater than 50% risk of needing an intervention:

Another scoring system to know about regarding upper GI bleeding is the Rockall score, a scoring system used to identify patients at risk of adverse outcome following acute upper gastrointestinal bleeding. It is interpreted by simple addition, with a score less than 3 carrying good prognosis, and a score more than 8 carrying a high risk of mortality:

Headache

Seizures

GCS

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Movement Disorders

Hot Swollen Joint

Connective Tissue Diseases

DME Tutorial

Renal Tutorial Acute Kidney Injury

Chronic Kidney Disease

Renal Replacement Therapy Indications for acute dialysis can be remembered through AEIOU: o Acid-base disorders  acidaemia o Electrolyte disturbances  hyperkalaemia o Intoxication  common intoxicants can be remembered through SLIME:  Salicylic acid  aspirin  Lithium  Isopropanol  hand-sanitiser  Magnesium  laxatives can contain these  Ethylene glycol  anti-freeze o Overload of fluid  peripheral or pulmonary oedema o Uraemic syndromes  Uraemic encephalopathy or Pericarditis Glomerulonephritis This is a term used to cover a variety of conditions which affect the glomerular apparatus, and therefore the function of the kidney. They can be divided as follows:  Non-proliferative – These present as nephrotic syndrome (Proteinuria + Hyperlipidaemia + Hypoalbuminaemia + peripheral oedema) o Minimal change GN  This presents will basically no change other than the abnormal podocytes seen on electron microscopy

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Treatment is with supportive care plus addition of steroid (Prednisolone)  Most patients will respond well to treatment o Focal Segmental Glomerulosclerosis  This is where segments of the glomeruli develop sclerosis  Genetic causes have been identified  Steroids are often ineffective, with 50% of patients progressing to renal failure o Membranous GN  This is the production of a thickened GBM, usually idiopathic  Third have chronic membranous GN  Third go into remission  Third will progress to renal failure  Proliferative – These present with nephritic syndrome (HTN + haematuria + Oliguria) o IgA Nephropathy  This is the most common cause of GN in adults  Presents with macroscopic haematuria  Presents 24-48 hours after URTI/GI infection  IgA deposits can be seen in the matrix o Rapidly Progressive GN (Crescenteric)  Vascultic Disorders  Wegener’s Granulomatosis o This is a vasculitis affecting the lungs, kidneys and other organs o c-ANCA is found to be positive o Treat with steroids + Cyclophosphamide  Microscopic Polyangitis o This is a small vessel vasculitis o p-ANCA is found to be positive o Treat with long-term steroids +/- cytotoxic agents  Goodpastures Syndrome  This is an auto-immune condition with anti-GBM antibodies  The glomerulus and the lung are affected  haematuria + haemoptysis  Treat with steroids +/- steroid sparing agents o Membranoproliferative GN  This can be primary (immune-mediated) or secondary (e.g. SLE or Hepatitis)  Usually progresses to ESRF o Post-infectious GN  This usually occurs weeks after an URTI, usually Step Pyogenes  Supportive treatment is given, resolving over 2-4 weeks A GN screen can be done in suspicion of GN to identify the underlying cause in order to tailor treatment accordingly. This involves:  Anti-Streptolysin O (ASLO)  this is produced against a specific streptococcal bacteria, commonly indicating rheumatic or scarlet fever  ANCA  associated with small vessel vascultic disorders such as Wegener’s or microscopic Polyangitis  Anti-GBM  Goodpasture’s Syndrome  Complement levels  measure immune-mediated GNs

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Antinuclear antibodies (ANA)  there are many subtypes of these, but they point to conditions such as Lupus, autoimmune hepatitis, Sjorgen’s syndrome, scleroderma and other connective tissue disorders

Anaemia Anaemia is defined as a reduced amount of haemoglobin or RBcs within the blood. It is however, not a diagnosis, but rather a presentation of symptoms, which usually arrive due to inadeqwuate oxygen transport: o Symptoms:  Fatigue  SOB  Palpitations  Feeling faint o Signs  Pallor  Tachycardia  Koilonychia  IDA  Jaundice  haemolytic  If severe may have flow murmur Causes of anaemia are based around the process od production opf RBCs:  Decreased Production  Increased Destruction  Blood loss Haematological Malignancies To understand haematological malignancies, we need to remember basics of haematopoiesis:  Stem cells differentiate into: o Common myeloid progenitors differentiate into  Erythrocytes  Megakaryocytes  Platelets  Myeloblasts, which in turn differentiates into  Basophil  Neutrophil  Eosinophil  Monocyte o Common lymphoid progenitor differentiates into  Lymphoblast, which differentiates into lymphocytes:  T Lymphocyte  B Lymphocyte Malignancies arise when there is a genetic mutation affecting these progenitor cells in the bone marrow, affecting all cells in the cell line. This then disrupts the differentiation and maturation of the cells, resulting in leukaemias and myeloproliferative disorders Leukaemia Leukaemias can be acute or chronic, and can affect both the myeloid and lymphoid cell lines. Acute Leukaemias have large numbers of undifferentiated cells in the bone marrow and peripheral

blood, with >20% being diagnostic of an acute leukaemia. These cells crowd the bone marrow and then spill out into the peripheral blood, preventing adequate differentiation in other cell lines, thus presenting with clinical features following bone marrow failure. It requires highly aggressive and urgent treatment as can be fatal within a few weeks. Symptoms include:  Anaemia  lethargy, SOB, chest pain, dizziness  Thrombocytopenia  bruising, bleeding, purpura  Leukopenia  recurrent infections  Bone pain  Lymphadenopathy Acute Lymphoid Leukaemia is more common in children aged 2-4, or in older adults, with it being slightly more common in males. It usually affects the B-Lymphocytes, but can sometimes also affect T-Lymphocytes also. It has a poor prognosis for males, older than 4, CNS involvement and chromosomal abnormalities, but can still be treated:  Chemotherapy is the mainstay of treatment: o Remission induction  this rapidly kills most tumour cells, aiming for less than 5% remaining in bone marrow. Agents used include prednisolone, vincristine and daunorubicin o Consolidation  high doses of multi-drug chemo is used to further reduce the tumour burden, with intrathecal treatment (methotrexate) also possibly required at this time Drugs used for this stage include Cyclophosphamide, Cytarabine, Daunorubicin and Vincristine. o Maintenance  a final high blast dose is giving to destroy any remaining malignant cells and reduce the risk of relapse. Drugs for this include Mercaptopurine, Methotrexate or a once a month 5-day course of Vincristine.  Radiotherapy can be used for bone pain, areas of high burden disease, or as preparation for bone marrow transplant  Stem cell or bone marrow transplant may be required and is the ideal treatment but can be difficult to organise for specific matching and patient suitability Acute Myeloid leukaemia can occur at any age, but is more common in older people, and is highly associated with Down Syndrome. There are 8 subtypes (M0-M7), based on the cell type the leukaemia has developed from. They have a better prognosis when found in younger patients, with 35-40% of people under 60 cured, compared to 5-15% of those over 60. Myelodysplasia or myeloproliferative disorders can transform into AML, but it can be treated as mentioned. Treatment usually is aimed at inducing remission with chemotherapy, usually with Cytarabine and an Anthracycline. However, haematopoietic stem cell transplant is often needed in relapsed AML. Myeloma This is a cancer which affects the plasma cells, which are the cells responsible for the production of immunoglobulins and antibodies. An abnormal number of plasma cells are produced, filling the bone marrow and therefore inhibiting the production of the other cell lines, hence the symptoms they present with (CRAB):  HyperCalcaemia  Renal Failure  Anaemia  Bone pain  Hyperviscosity  high risk of VTE  Spinal cord compression  Immune paresis  recurrent infections

 Confusion  Constipation  Nausea  Weight loss Myeloma cells can usually only produce one type of abnormal immunoglobulin, called the paraprotein. These are excreted in the urine (Bence-Jones Protein), causing renal failure. They are non-functioning immunoglobulins, so the patient is immunosuppressed. The bone pane and lytic lesions comes due to the destruction of bone from the plasma cells. Investigation and management in patients who present with the above symptoms, suspecting myeloma should concentrate on the following:  Investigations o Bloods  FBC  anaemia, thrombocytopenia, leukopenia  Calcium  elevated  U&Es  renal failure o Immunoglobulins and Serum protein electrophoresis o Urine  Bence Jones protein o Skeletal survey of skull, chest, spine, pelvis and femur  Lytic lesions o Bone marrow  aspiration and possible removal of some  Management o Depends on age:  Intensive management should be done if under 65 with minimal comorbidities. The aim is to reduce the bulk of the disease, before stem cell transplantation  Non-intensive management should be done in those over the age of 7- or in those with co-morbidities o Drugs: 1. Steroid  Dexamethasone or Prednisolone 2. Chemo agent  Melphalan or Cyclophosphamide 3. Thalidomide or Bortezomib o Bisphosphonates should be given for bone disease and hypercalcaemia Lymphoma These are caused by a malignant proliferation of lymphocytes, accumulating in the lymph nodes, peripheral blood or in the organs. Investigations should therefore include FBC, U&Es, blood film, urate, LDH, CT CAP, biopsy of lymph node and bone marrow, and possibly a lumbar puncture. Staging of lymphomas is commonly done through the Ann-Arbor System, which influences the prognosis of the cancer: I. Confined to a single lymph node region II. Involvement of 2 or more nodal areas on the same side of the diaphragm III. Involvement of nodes on both sides of the diaphragm IV. Spread to liver or bone marrow (Each stage is then subdivided into A or B, depending on whether B symptoms (Weight loss >10%, unexplained persistent or recurrent fever, drenching night sweats) are featured within past 6 months)

 Hodgkin’s Lymphoma is indicated due to the pr3esence of Reed-Sternberg cells on the blood film o The peak incidence is between 20 and 40 years’ old o Associated with Epstein-Barr Virus

Presentation:  Enlarged, painless ‘rubbery’ lymph nodes  Fever  Weight loss  Night sweats  Anaemia  Hepato/Splenomegaly o Types include:  Lymphocyte predominant  Nodular Sclerosing  Mixed  Lymphocyte deplete o Treatment:  Chemotherapy (ABVD)  Adriamycin, Bleomycin, Vinblastine, Dacarbazine  Radiotherapy  Supportive treatments  blood/platelet transfusion, early treatment of infections  Stem cell transplant o Prognosis dependent on subtype  e.g. >95% 5-year survival rate in lymphocyte predominant with favourable prognostic factors  Non-Hodgkin’s lymphoma is a very diverse group of diseases o Can be divided into classifications:  Indolent / Low grade  relatively mature cells with low turnover, so can therefore ‘watch and wait’ until there is organ involvement before initiating treatment.  Examples include: o Follicular lymphoma o Marginal zone lymphoma  Treated with Rituximab or Chlorambucil, or with localised radiotherapy  High grade  immature cells with high turnover, meaning rapidly progressive disease without treatment  Examples include: o Burkitt’s o Diffuse large B cell lymphoma o Lymphoblastic lymphoma  Presents usually with rapidly enlarging lymphadenopathy, B symptoms and symptoms of bone marrow failure  Treatment is with R-CHOP chemotherapy:  Rituximab  Cyclophosphamide  Hydroxydaunorubicin  Oncovin  Vincristine  Prednisolone o...