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INTERPRETING BLOOD RESULTS Anya Olsen 1 DIFFERENT BLOODTESTS • Full Blood Count (FBC) • IncWhite Blood Cell (WBC) • Coagulation tests • Thyroid FunctionTest (TFT) • Liver FunctionTest (LFT) • U&E 2FULL BLOOD COUNT 3 COMPONENTS OF A FBC • Red cell tests • Haemoglobin (Hb) • Haematocrit (Hct) • Mean corpuscular volume (MCV) • Red cell distribution width (RDW) • Red cell count (RCC) • Reticulocyte count • Mean corpuscular haemoglobin (MCH) • Mean corpuscular haemoglobin concentrate (MCHC) 4 COMPONENTS OF A FBC • White cell tests • White blood cell count (WBC/WCC) • Breakdown ofWBC into different types of cells • Platelet tests • Platelet count • Mean platelet volume (MPV) • Platelet distribution width (PDW) 5 RED BLOOD CELLS Hb Amount of Hb in whole blood Men 130-180 g/L Women 115165 g/L Hct Percentage of blood sample made up of RBC Men 0.4-0.54 L/L Women 0.370.47 L/L MCV Average size of RBC in blood 80-100 fL RDW Range from largest to smallest RBC RCC Number of RBC present per unit volume Reticulocyte count Number of immature RBC 0.2-2% MCH Amount of Hb per RBC 27-32 pg/cell MCHC Average conc. of Hb in a given volume of blood 6 ANAEMIA Amount of Hb MCV Causes Macrocytic Low Increased B12,folate deficiency,alcohol,liver disease,hypothyroid, pregnancy, reticulocytosis, myelodysplasia, cytotoxic drugs Microcytic Low Reduced Thalassaemia/haemoglobinopathies,Anaemia of chronic disease/inflammation,Iron deficiency anaemia,Lead poisoning, Sideroblastic anaemia (TAILS) Normocytic Low Normal Anaemia of chronic disease,chronic kidney disease,aplastic anaemia,haemolytic anaemia,blood loss,hypersplenism 7 MEGALOBLASTICVS NORMOBLASTIC Megaloblastic = bone marrow produces large, structurally abnormal, immature RBC. Due to impaired DNA synthesis. Normoblastic = normal Megaloblastic Normoblastic Macrocytic B12,folate deficiency Alcohol,liver disease,hypothyroid,pregnancy, reticulocytosis, myelodysplasia, cytotoxic drugs 8 RETICULOCYTE COUNT Raisedin context of anaemia Functioning to produce new cells but RBC being destroyed Low Problem with bone marrow not producing enough cells. Nutritional deficiencies or bone marrow disorder Raisedin absence of anaemia Compensating for blood loss or haemolysis. Could be due to increased oxygen demand 9 HAEMATINICS • Serum ferritin • Direct correlation between serum ferritin and overall iron stores • Also, an acute phase protein • Increased in inflammatory states such as chronic kidney disease,liver disease, malignancy • <15ug/l indicates iron deficiency • <150ug/l potential iron deficiency alongside inflammatory condition or renal impairment • >150ug/l iron deficiency unlikely 10 HAEMATINICS • Total Iron Binding Capacity (TIBC) • Measurement of total iron concentration in the sample when fully saturated • Transferrin • Iron transporter molecule- can rise in iron deficiency • Negative acutephase protein so decreases in inflammatory states • Transferrin saturations • Ratio of total serum iron to transferrin • <16% supports diagnosis of iron deficiency 11 WHITE BLOOD CELLS Neutrophils RISE IN BACTERIAL INFECTIONS Lymphocytes RISE INVIRAL INFECTIONS . May be also increase in haematological malignancy Monocytes Increase in bacterial infection,autoimmune disease, steroid use Eosinophils HELMINTH INFECTIONS Basophils Role in parasitic infections and allergies Blasts Immature cells normally in bone marrow.If in blood this could be leukaemia 12 PLATELET COUNT Cause Low Acute: consumption,viral infection,medications,DIC,heparin induced thrombocytopenia,ITP,pre-eclampsia Chronic: hypersplenism, cirrhosis, alcohol excess, medications, ITP, autoimmune disease,B12/Folate deficiency,iron deficiency,HIV,Hep B/C,haematological disease,bone marrow failure High Reactive,myeloproliferative disorders,iron deficiency, hyposplenism/post splenectomy,underlying malignancy 13a. Iron deficiency anaemia b.Hereditary haemochromotosis c. Anaemia of chronic disease d.Sideroblastic anaemia e.Haemolytic anaemia 14 a. Iron deficiency anaemia b.Hereditary haemochromotosis c.Anaemia of chronic disease d.Sideroblastic anaemia e.Haemolytic anaemia This is due to the Low Hb indicatesanaemia MCV is normal This generally shows that it has been going on for a while. If it was if the MCV was low then this would be iron deficiency 15a. Anaemia of chronic disease b.Folate deficiency c. Hypothyroidism d.Iron deficiency e.Vitamin B12 deficiency 16 a. Anaemia of chronic disease b.Folate deficiency c. Hypothyroidism d.Iron deficiency e.Vitamin B12 deficiency Ileocaecal resection may result in vitamin B12 deficiencyis is due to the lack of terminal ileum which is the main site of absorption for B12 17COAGULATION SCREEN 18 PROTHROMBIN (PT/INR) • 12-13 seconds • Time taken for blood to clot via the extrinsic pathway • Internationalnormalisedratio (INR) is commonly used for patients on warfarin • Only factor in the pathway isVII • Measures overall clotting factor synthesis or consumption • Can be affected by DIC,Vit K def, warfarin levels or liver disease PT – Play Tennis OUTSIDE therefore PT is extrinsic 19The intrinsic, extrinsic and common pathways of the coagulation... | Download Scientific Diagram (researchgate.net) 20 ACTIVATED PARTIAL THROMBOPLASTIC TIME (APTT) • 35-45 seconds • Time taken for blood to clot via the intrinsic pathway • Similarly to PT,it will be affected by clotting factor synthesis or consumption • Can be affected by factorsVIIv,WF, IX and XI • HaemophiliaA (VIII- X linked recessive) • HaemophiliaB (IX– X linked recessive) • HaemophiliaC (XI– autosomal recessive) • VonWillebrandsdisease (vWF pairs up withVIII) APTT – Play Table Tennis INSIDE therefore APTT is intrinsic 21The intrinsic, extrinsic and common pathways of the coagulation... | Download Scientific Diagram (researchgate.net) 22 BLEEDINGTIME Condition PT/INR APTT Platelet Notes count Vit K def/Warfarin High High - INR range varies dependent on condition HaemophiliaA/B/C - High - Symptoms of clotting disorders: haemarthrosis, muscle haematomas,prolonged bleeding after dental surgery vWF disease - -/High - Symptoms of platelet disorders:petechiae,bruising,contact bleeding (e.g.gums),menorrhagia DIC High High Low Total coagulopathy, treat primary cause, give platelets and clotting factors ITP/TTP/HUS - - Low Lack of PT/APTT derangement is differentiator from DIC. NEVER give platelets to these patients ITP = immune thrombocytopenic purpura TTP = Thrombotic thrombocytopenic purpura HUS = haemolyticuraemicsyndome 23 DIRECTVS INDIRECT COOMBSTEST • Used to find out if an individual has haemolytic anaemia • Direct • More frequently performed • Checks for antibodies or complement proteins on surface of RBC • Used to identify autoimmune haemolytic anaemia • Can occur due to lupus, leukaemia, mononucleosis, medications • Indirect • Checks for antibodies against foreign blood cells in the serum • Used to prior to a blood transfusion or to check if mother has Rh antibodies during pregnancy https://study.com/learn/lesson/direct-vs-indirect-coombs-test-examples.html 24a. EMA binding assay b.Direct Coombs test c. Indirect Coombs test d.Serum haptoglobin e.Hepatitis viral screen 25 a. EMA binding assay b.Direct Coombs test c. Indirect Coombs test d.Serum haptoglobin e.Hepatitis viral screen The jaundice has been caused due to excesshaemolysis Her Hb is showing as low and bilirubin significantly raised. There are no issues with ALP, ALT, GGT, albumin. Her blood smear also shows spherocytosis indicating that some of the blood cells are mishapenand this could be due to autoimmune haemolyticanaemia which would be proven by a Direct Coombs test 26a. Platelet count low,PT reduced,APTT reduced,bleeding time reduced b. Platelet count high,PT prolonged,APTT prolonged,bleeding time prolonged c. Platelet count low,PT normal,APTT normal,bleeding time prolonged d. Platelet count low,PT prolonged,APTT,prolonged,bleeding time prolonged e. Platelet count normal,PT prolonged,APTT prolonged,bleeding time prolonged 27 a. Platelet count low,PT reduced,APTT reduced,bleeding time reduced b. Platelet count high,PT prolonged,APTT prolonged,bleeding time prolonged c. Platelet count low,PT normal,APTT normal,bleeding time prolonged d. Platelet count low, PT prolonged,APTT, prolonged, bleeding time prolonged e. Platelet count normal,PT prolonged,APTT prolonged,bleeding time prolonged Tissue factor can be released in excess during sepsis, this leads to increased fibrin deposition in microcirculation. As DIC progresses, the platelets and coagulation factors are used up and therefore this leads to a long PT, APTT and bleeding time. You need to correct the underlying issue which is causing DIC, thm isacor ld be trauma, organ destruction, sepsis or severe infection (including severe coronavirus disease 2019 [COVID-19] infection), severe obstetric disorders, some malignancies, major vascular disorders, and severe toxic or immunological reactions. They will also need a platelet transfusion and coagulating factors. This will likely be Fresh Frozen plasma (FFP) and a platelet transfusion if bleeding is acute and active. Disseminated intravascular coagulation- Symptoms, diagnosis and treatment | BMJ Best Practice 28Normal ranges Platelets 150-400 *10^9/l PT 10-14 secs APTT 25-35 secs a. Antithrombin III deficiency b.Von Willebrand’s disease c. Antiphospholipid syndrome d.Haemophilia A e.Haemophilia B 29 Normal ranges Platelets 150-400 *10^9/l PT 10-14 secs APTT 25-35 secs a. Antithrombin III deficiency b.Von Willebrand’s disease c. Antiphospholipid syndrome d.Haemophilia A e.Haemophilia B A grossly elevated APTT may be caused by heparin therapy, haemophilia or antiphospholipid syndrome. A normal factorVIIIc activity points to a diagnosis of haemophilia B (lack of factor IX). Antiphospholipid syndrome is a prothrombotic condition 30The intrinsic, extrinsic and common pathways of the coagulation... | Download Scientific Diagram (researchgate.net) 31THYROID FUNCTIONTESTS 32 TFTS • TRH • Thyroid releasing hormone released from the hypothalamus stimulates the pituitary to release... • TSH • Thyroid stimulating hormone from the pituitary causes the thyroid to releaseT3 andT4 • T4 • T3.the inactive version ofT3,this needs to be altered by removal of part of the molecule to form • T4 is generally used in theinterpretation ofTFTs • T3 • Is the active form of the thyroid hormones.This is what affects all the cells and organs in your body These organs can alter from T3 to T4 Liver. Kidneys. Muscles. Thyroid. Pituitary gland. Brown adipose (fat) tissue(This type of fat produces heat to help maintain your body temperature in cold conditions). Centralnervous system. 33 TFTS • TRH • Thyroid releasing hormone released from the hypothalamus stimulates the pituitary to release... • TSH • Thyroid stimulating hormone from the pituitary causes the thyroid to releaseT3 andT4 • T4 • T3.the inactive version ofT3,this needs to be altered by removal of part of the molecule to form • T4 is generally used in theinterpretation ofTFTs • T3 • Is the active form of the thyroid hormones.This is what affects all the cells and organs in your body These organs can alter from T3 to T4 Liver. Kidneys. Muscles. Thyroid. Pituitary gland. Brown adipose (fat) tissue(This type of fat produces heat to help maintain your body temperature in cold conditions). Centralnervous system. 34TFTS 35 TFTS TSH T4 HYPO Primary HI LO Secondary NORM LO Subclinical HI NORM HYPER Primary LO HI Secondary NORM/HI HI Subclinical LO NORM 36 AUTOIMMUNE THYROID • Graves’ • Shows a hyperthyroid picture • TSH receptor stimulating antibodies aiyroid peroxidase (TPO) antibodies are present • Hashimoto’s • Shows a hypothyroid picture • Anti-thyroid peroxidase (TPO) and/or ant-thyroglobulin (Tg) antibodies 37What is the most likely diagnosis? a. Graves disease b. Hashimoto’s c. Hyperthyroid d. Hypothyroid e. Subacute thyroiditis 38 What is the most likely diagnosis? a. Graves disease b. Hashimoto’s c. Hyperthyroid d. Hypothyroid e. Subacute thyroiditis This is due to the hyperthyroid picture and being TSH receptor stimulating antibody positive 39What further finding would support the likely diagnosis? a. Multinodulargoitre b. Pretibialmyxoedema c. Smooth enlarged tendergoitre d. Thinning of hair e. Weight gain 40 What further finding would support the likely diagnosis? a. Multinodulargoitre b. Pretibialmyxoedema c. Smooth enlarged tendergoitre d. Thinning of hair e. Weight gain • eye signs (30% of patients) • exophthalmos • ophthalmoplegia • pretibialmyxoedema • thyroid acropachy, a triad of: • digital clubbing • soft tissue swelling of the hands and feet • periosteal new bone formation 41Normal ranges TSH 0.5-5.5 mu/l T4 9-18 pmol/l HbWomen: 11160 g/l Plt 150-400 * 10/l WBC4.0-11.0 * 10/l a. Sick thyroid syndrome b. Acute bacterial thyroiditis ESRWomen: < ((age + 10) / 2h)r mm/ c. Hashimoto’s thyroiditis d. Subacute thyroiditis e. Toxic multinodguit r 42Normal ranges TSH 0.5-5.5 mu/l T4 9-18 pmol/l HbWomen: 11160 g/l Plt 150-400 * 10/l WBC4.0-11.0 * 10/l a. Sick thyroid syndrome b. Acute bacterial thyroiditis ESRWomen: < ((age + 10) / 2h)r mm/ c. Hashimoto’s thyroiditis d. Subacute thyroiditis e. Toxic multinodguit r 43a. Graves disease b. Sick thyroid syndrome c. De Quervain’sthyroiditis (subacute thyroiditis) d. Hashimoto’s thyroiditis e. Toxic multinoduitae 44a. Graves disease b. Sick thyroid syndrome c.De Quervain’sthyroiditis (subacute thyroiditis) d. Hashimoto’s thyroiditis e. Toxic multinoduitae 45LIVER FUNCTIONTESTS 46 LFTS Bilirubin • Hyperbilirubinaemiacauses jaundice • Normal urine + stools = pr-eepatic • Dark urine + normal stools = hepatic • Dark urine + pale stools = poshepatic (obstructive) Unconjugatedhyperbilirubinaemi auses • Haemolysis,impaired hepatic uptake,impaired conjugation Conjugatedhyperbilirubinaemi auses • Hepatocellular injury, cholestasis Isolated bilirubin rise • Gilbert's syndrome,haemolysis https://geekymedics.com/interpretatio- f-liver-function-tests-lfts/ https://teachmesurgery.com /hpb/presentations/jaundice/ 47 LFTS ALT vs ALP • ALT – hepaTocellularinjury • More thanTENfold increase inAL indicates hepatocellular injury • ALP – cholestasis(P for Pause) • More thanTHREEfold increase inAL indicates cholestasis • Only ALP rise = bony metastases, vit D deficiency, recent bone fracture,renal osteodystrophy https://geekymedics.com/interpretatio- f-liver-function-tests-lfts/ 48 LFTS GGT • If rise inALP,check GGT as can suggest biliary epithelial damage and bile flow obstruction. • Can be raise due to alcohol and drugs e.g. phenytoin • Markedly raised ALP with raised GGT = cholestasis (normally) https://geekymedics.com/interpretatio- f-liver-function-tests-lfts/ 49A.Ascending cholangitis B.Autoimmune hepatitis C.Common bile duct gallstones D.Pancreatic cancer E. Primary biliary cholangitis 50 A.Ascending cholangitis B.Autoimmune hepatitis C.Common bile duct gallstones D.Pancreatic cancer E. Primary biliary cholangitis Gallstones may be present in the CBD causing ongoing jaundice and pain after cholecystectomy Even though this patient has had a cholecystectomy, gallstones can still be present in the common bile duct. This can cause biliary colic and obstructive jaundice after cholecystectomy. Therefore common bile duct stones are the most likely diagnosis. Ascending cholangitis can present with jaundice and right upper quadrant pain. However the patient usually pyrexial and has a raised white cell count which is not the case in this patient. The pattern of the patient's LFTs is typical of cholestasis. Therefore autoimmune hepatitis is unlikely to be the diagnosis. Pancreatic cancer affecting the head of the pancreas can cause obstructive jaundice. However this is typically painless and therefore is unlikely to be the diagnosis. Primary biliary cholangitis can cause cholestasis. However, typically this would feature painless obstructive jaundice and so is unlikely to be the diagnosis. 51A.Alcoholic hepatitis B.Gallstones C.Haemochromatosis D.Non-alcoholic fatty liver disease E. Primary biliary cholangitis 52 A.Alcoholic hepatitis B.Gallstones C.Haemochromatosis D.Non-alcoholic fatty liver disease E. Primary biliary cholangitis Obesity with abnormal LFTs- ? non-alcoholic fatty liver disease Raised transaminases in an obese individual who does not have a history of excessive alcohol consumption should raise the suspicion of non -alcoholic fatty liver disease (NAFLD). This disease is also closely linked to insulin resistance, hence her history of pre-diabetes is a further risk factor. Alcoholic hepatitis is unlikely given her level of alcohol intake. NICE guidelines state that consumption of less than 20g (2.5 units) per day in women, and less than 30g (3.75 units) per day in men, is used as the cutoff to diagnose NAFLD. Gallstones in isolation do not tend to cause raised transaminases unless associated with complications such as acute cholecystitis or ascending cholangitis. This patient is not exhibiting such symptoms. While it is important to arrange further investigations (including autoantibodies) to check for other liver pathology, there is little indication of primary biliary cholangitis in this patient. This usually manifests either in symptoms of pruritus, or an incidental finding of a raised ALP in an asymptomatic patient. 53While haemochromatosis can certainly manifest in abnormal liver function tests with a raised ferritin, the transferrin saturation- calculated as (iron / TIBC) x 100 - is well below the 40% threshold for females (based on British Society oHf aematology guidelines) which would prompt consideration of iron overload. Furthermore we would normally expect ferritin to be even higher (>1000 ug/L) in haemochromatosis. Note that milder elevations of serum ferritin is commonly seen in NAFLD, as seen here. 53Most likely diagnosis? A. Biliary colic B. Alcoholic fatty liver disease C. Alcohol induced liver cirrhosis D. Acute alcoholic hepatitis E.Hepatic encephalopathy 54 Most likely diagnosis? A. Biliary colic B. Alcoholic fatty liver disease C. Alcohol induced liver cirrhosis D. Acute alcoholic hepatitis E.Hepatic encephalopathy Acute alcoholic hepatitis It is hepatitis and not just cirrhosis due to the tender hepatomegaly, increased WBC and raised CRP. 55UREAAND ELECTROLYTES 56 U&E • Sodium • Potassium • eGFR • Urea • Creatinine 57 CAUSES OF DERANGED SODIUM Fluid depleted Normovolaemic Fluid overloaded • Diuretic therapy • SIADH • Cardiac failure HypoNAtraemia Hypoadrenalism • Hypothyroidism • Liver failure • Volume depletion • Psychogenic polydipsia • Renal failure (nephrotic (vomiting/diarrhoea and other syndrome especially) large vol loss e.g.burns,fistula, • Hypoalbuminaemia haemorrhage) HyperNAtraemia • Diabetes insipidus • Poor water intake • Administration of excess sodium in IV fluids • Administration of drugs containing high concentrations of sodium 58 CAUSES OF DERANGED POTASSIUM HypoKalaemia • Drugs – diuretic therapy • Intestinal losses – excess vomiting,profuse diarrhoea,high stoma or fistula output • Renal tubular disease – renal tubular acidosis, drug induced tubular damage • Endocrine causes – Cushing’s and Conn’s • Metabolic alkalosis HyperKalaemia • Drugs – excess K+ supplementation,K+ sparing diuretics,combination of drugs e.g. ACE and diuretic • Rhabdomyolysis • Endocrine diseases –Addison’s • Diabetic Ketoacidosis 59 RENAL FUNCTION • eGFR • This measures kidney function and can help to determine stages of CKD/AKI • Urea • Levels indicate both production and elimination • Poor dietary intake can lead to low urea • High urea can be due to renal failure and GI b– protein)stion of blood • Creatinine • This is waste product from muscles • Can be used to help stageAKIs and used in the eGFR calculation https://books.google.co.uk/books?id=PeFgZTdfs3oC&pg=PA43&lpg=PA43&dq=interpr eting+u%26e&source=bl&ots=78W- YRDuRV&sig=ACfU3U0sWf1THyTeIb44FBNos5EOKtpB3A&hl=en&sa=X&ved=2ahUKE win_7K_hO_6AhV1nVwKHckyDRQQ6AF6BAghEAM#v=onepage&q=interpreting%20u %26e&f=false 60ANY QUESTIONS? 61FEEDBACK 62
