Lecture ILO’s Flashcards

Question

Management of sickle cell crisis

Answer 1

● EMERGENCY: A - E approach! Low threshold for admission ● If known SCD, often have a personalised management plan ● Treat any infection ● Manage pain with analgesia ● Keep warm ● Keep hydrated (IV Fluids may be needed) ● Penile aspiration in priapism ● Distraction techniques ● Avoid any other potential triggers ● Blood transfusions

Answer 2

• Severe pain that isn’t controlled by simple analgesia or low dose opioids • Dehydration caused by severe vomiting or diarrhoea • Signs of sepsis • Symptoms or signs of acute chest syndrome: e.g raised RR, hypoxia, signs of lung consolidation • New neurological signs or symptoms • Symptoms or signs of acute fall in haemoglobin • Acute enlargement of spleen or liver over 24 hours • Marked increase in jaundice • Haematuria • Priapism lasting more than 2 hours or worsening of recurrent episodes

Answer 3

Thalassemia ● All pregnant women are offered a test, typically at 10 weeks ● If the woman is a carrier, father will be tested ● Can have further testing if dad is a carrier e.g chorionic villous sampling, amniocentesis to determine whether baby has thalassemia

Answer 4

Sickle Cell Disease ● Not all women are offered a test ● Those from high risk groups and in areas with a higher prevalence of haemoglobin diseases are offered a test ● Can use family origin questionnaires if unsure whether to consider offering a test ● If the woman is a carrier, father will be tested ● Can have further testing if dad is a carrier e.g chorionic villous sampling, amniocentesis to determine whether baby has SCD ● SCD carries increased risk of miscarriage, prematurity, pre-eclampsia, vaso-occlusion, chest crisis and anaemia

Answer 5

Microcytic anaemia: Iron deficient anaemia Anaemia of chronic disease Thalassaemia SCD Normocytic anemia: Folate + iron deficiency Macrocytic anaemia: B12 deficiency Folate deficiency Alcohol Pregnancy Chronic liver disease Haemolytic Bone marrow failure

Answer 6

• Fe2+ = Ferrous State • Fe3+ = Ferric State • Haem= Porphyrin ring containing iron in ferrous state • Iron is either absorbed as haem or as free iron ions • Free iron in ferric state requires reduction to ferrous state for absorption by – Acidic conditions of stomach acid – Ascorbic Acid (Vitamin C) also reduces to ferrous state – Duodenal cytochrome b ferric reductase (found on brush border of duodenal enterocytes) • Absorbed mostly in proximal small intestine (duodenum)

Answer 7

Red blood cells White blood cells Platelets Plasma Centrifuge the blood: Plasma (55% of the blood at the top) Leukocytes and platelets (<1% in the middle) Erythrocytes (45% at the bottom)

Answer 8

Formation of blood cellular components which are all derived from haematopoietic stem cells

Answer 9

Erythropoiesis is the process which produces red blood cells, which is the development from erythropoietic stem cell to mature red blood cell.

Answer 10

Platelets 9-10 days Erythrocytes 120 days Leukocytes a few days to a few years

Answer 11

Foetus 0-2 months yolk sac Foetus 2-7 months lover, spleen Foetus 5-9 months bone marrow Infant bone marrow (practically all bones) Adults vertebrae, ribs, sternum, skull, sacrum, pelvis, proximal end of femur

Answer 12

Located within all bones Red marrow and yellow marrow At birth all bone marrow is red In adults half is red Red marrow: haematopoietic tissue Yellow marrow: fat cells Micro environment- stormal cells - fibroblasts, fat cells, endothelial cells, macrophages Express adhesion molecules and secrete growth factors Stromal matrix - physical support for haematopoietic cells

Answer 13

Blood stem cell Myeloid stem cell (CFU-GEMM) Proerythroblast Early erythroblast Late erythroblast Normoblast Reticulocyte Erythrocyte

Answer 14

Biconcaved disk shape Central area of pallor Production: Erythropoiesis Growth factor: erythropoietin Lifespan: 120days No organelles Oxygen and carbon dioxide transporters

Answer 15

Blood stem cells -> Myeloid stem cell -> megakaryoblast -> promegakaryocyte -> megakaryocytes -> platelets

Answer 16

Blood stem cell Myeloid stem cell Monoblast Promonocyte Monocytes Wandering macrophage (monocytes migrate to tissues and mature into macrophages)

Answer 17

Formed from granulopoiesis Approx 14days for myeloblasts to form mature cells which are released into peripheral blood Most abundant white blood cell (50-70%) 1st line defence to bacteria Average life span in circulation is 5 days and then further 1-2 days in tissues

Answer 18

Formed from granulopoiesis 1-4% of circulating leukocytes Provide protection against parasites Involved in allergic responses 8-12 hours lifespan in circulation and further 8-12 days in tissue

Answer 19

Lymphocyte production T lymphocyte B lymphocyte Plasma cells Natural killer cells

Answer 20

• Koilonychia (spoon shaped nails) • Atrophic glossitis (inflamed tongue) • Angular Chelitis (chapped lips) • Post-cricoid webs (Plummer Vinson Syndrome): Causes dysphagia (thin membranes in back of throat)

Answer 21

• Blood Loss – GI Blood loss • NSAIDs, Peptic ulcer, Cancer (oesophageal, gastric, colo-rectal) – Mennorhagia – Blood donation – Haematuria (blood in urine) – Epistaxis (nose bleeds) • Pregnancy – Higher iron demand – Also risk of B12 and folate deficiency – If MCV normal in pregnancy:think of mixed iron with B12 or Folate (or both) deficiency • Malabsorption – Coeliacs Disease(villous atrophy in duodenum/jejenum) – Bowel resection e.g.Gastrectomy • Dietary deficiency (very uncommon in developed countries) – High concentrations of iron found in red meat,cereals,spinach,beans

Answer 22

• FBC: Microcytic anaemia – MCV (mean cell volume): <76 fL – TIBC (Total iron binding capacity)= Increased (Microscope) – Blood film: Microcytic (small), hypochromic (pale due to lack of iron which is red) red cells – Ferritin: Low • Acute phase protein (ie. Involved in inflammation), thus may be increased in states of inflammation – Iron: Low (less sensitive than ferritin)

Answer 23

Colon cancer and gastric cancer and coeliac disease are common causes for IDA • All patients should have coeliac serology testing • All men and post-menopausal women should have URGENT upper and lower GI endoscopy unless obvious other cause of blood loss • Only if advanced coeliac or gastric cancer on OGD should negate the need for colonoscopy • Pre-menopausal women should be screened for coeliac disease but only need endoscopies if >50years, GI symptoms or strong family history of colo-rectal cancer • Small bowel investigations only required if: suspect pathology or iron deficiency refractory to treatment

Answer 24

– Acquired: • Immune Mediated (Coombs Test Positive) – Autoimmune- warm and cold – Drugs – Paroxysmal cold haemoglobinuria • Coombs Test negative • Microangiopathic • Infection(Malaria) • Paroxysmal nocturnal haemoglobinuria – Hereditary: • RBC Metabolism Defects- G6PD deficiency, Pyruvate kinase def. • RBC Membrane Defects- Hereditary spherocytosis, ellipocytosis • Haemaglobinopathies- Sickle Cell Anaemia, Thalassaemia

Answer 25

Excessive destruction of red blood cells faster than rate of erythropoesis leads to HA • Usual RBC lasts 120 days, this is significantly reduced in HA • RBCs are either destroyed in: – Blood vessels (intra-vascular) – Reticulo-endothelial System (extra-vascular) • Ie. Macrophages of the spleen, liver, bone marrow • Various mechanisms: – Acquired or inherited abnormality to RBC structure...therefore body removes RBCs – Antibodies directed against the RBC...lead to removal of RBC

Answer 26

• Normal or raised MCV • Raised unconjugated (indirect) bilirubin – Bilirubin= breakdown product of haem • Raised urinary urobilinogen (dipstick test) • Raised lactate dehydrogense(LDH) – Product of metabolism • Increased reticulocyte count – Normal- 0.5-2% – Pre-cursor of mature erythrocyte in bone marrow – Larger than RBC with DNA/RNA remnants (appears blue on blood film)

Answer 27

Acquired 1)Immune mediated (Direct Anitglobulin Test Positive) Drug induced Autoimmune haemolytic anaemia Paroxysmal cold haemoglobinuria Direct Anti-globulin test negative Microangiopathic haemolytic anaemia Infection Paroxysmal nocturnal haemaglobinuria

Answer 28

Hereditary 1) EnzymeDefects - Glucose-6-phosphate dehydrogenase (G6PD) deficiency - Pyruvate kinase deficiency 2) MembraneDefects - Hereditary spherocytosis - Hereditary elliptocytosis 3) Haemoglobinopathies - Sickle Cell Anaemia - Thalassaemia

Answer 29

Treatment • Steroids/immunosupressents • Splenectomy • Keep warm (in cold AIHA)

Answer 30

• Clinical Features – Anaemia and haemolytic crisis – Jaundice – Splenomegaly – Legulcers – Aplastic Crisis (usually precipitated by infection especially parvovirus b19) • Investigations – FBC, blood film and other markers of haemolysis – Negative Coombs Test – Osmotic fragility test (used in diagnosis of any cell membrane defect ) • RBCs placed in hypotonic solutions (as RBCS take up water they swell and eventually lyze) • Spherocytes tolerate less better and lysis occurs earlier • Treatment – Splenectomy(usually delayed until after child hood to avoid severe infection) – Folate replacement (all conditions where high turn over of RBCs cause folate deficiency) (folate makes DNA)

Answer 31

Activation of the clotting pathway (intrinsic or extrinsic pathway) causes lots of clotting factors leading to the release of prothrombin, and then thrombin which converts fibrinogen to fibrin. Fibrin then causes the clot. Spectrum disorder, the clot can be in any vein- central vein would be bad or if the clot breaks off and travels to the lung (PE) that would be bad Equal in males and females Can affect all ages (child trauma) but more likely in over 50’s

Answer 32

Simple ultrasound/ duplex sonography Do a WELLS score of likelihood of clot D dimer test (detects breakdown of fibrin) to see if clot is present (non specific)

Answer 33

Wells score result If high- do an ultrasound If low- do a D-dimer If negative low chance of DVT If positive high chance of DVT- do an ultrasound

Answer 34

MCV- mean corpuscular volume (average size of RBC) PCV- packed cell volume (mainly RBC volume) MCH- mean corpuscular haemoglobin (average amount of Hb per RBC) looking at the colour MCHC- mean corpuscular Hb concentration

Answer 35

Haemorrhage - lost too much blood - hypovalemic shock n Lie flat if not already n Continue high flow oxygen n biggest cannula- Grey/ green cannula x2, antecubital fossae n U&E, LFT, FBC, clotting, glucose, cross-match n ? G&S already done n Give N Saline/ gelofusin stat n Monitor vital signs closely

Answer 36

Rh positive

Answer 37

Group & Save This test consists of 3 processes: 1. ABO and RhD group of the patient's blood - if the patient has not been grouped before then the initial sample is grouped using 2 different reagents. 2. Antibody screen of patient's plasma - this is to check whether the patient has acquired atypical antibodies as a result of a previous transfusion or pregnancy. Though it can identify the presence of these atypical antibodies, if they are detected then further testing is required on that sample to determine the specific types. 3. Separate and save the plasma by storing at -30°C, and retain the red cells at 4°C, in case the patient has a future transfusion and has problems which necessitate re-examining the patient's original sample. The length of time that a sample can be stored and be viable for future release of blood is determined by National Guidelines.

Answer 38

Blood can be released almost immediately with valid G&S Emergencies without prior G&S ̈ Blood required immediately 2 units O Neg Blood required within 10 minutes ABO and RhD compatible ̈ Blood required within 20 + minutes Await full cross-match

Answer 39

Activation of coagulation cascade due to endothelial damage and/or release of pro-coagulation factors Widespread generation of fibrin and fibrin degradation products (FDP’s) leading to initial thrombosis Consumption of coagulation factors leading to bleeding n Platelet aggregation leading to thrombocytopaenia Treat with FFP, cryoprecipitate, PRC, platelets FFP is also often required in massive transfusion to replace clotting factors not present in PRC ̈ Not the same as DIC

Answer 40

Bacterial infections (gram positive sepsis) Viral Fungus Parasitic (malaria) Malignancy- haematologic (acute myelocytic leukaemia) Obstretic- placental abduction, eclampsia Trauma- burns, MVA Transfusions- haemolytic reactions

Answer 41

Packed red cells (PRC) Platelets Fresh Frozen Plasma (FFP) ̈ Contains all coagulation factors in plasma Cryoprecipitate ̈ Derived from FFP ̈ High concentrations of VIII:C, vWB factor and fibrinogen ̈ Useful for DIC Prothrombin Complex Concentrate (PCC) ̈ Derived from FFP ̈ High concentrations of II, VIII, IX, X, Protein S and C ̈ Used to reverse warfarin when INR>8 and haemorrhage

Answer 42

Factors in blood which from one person wouldn’t be therapeutically beneficial Coagulation factor concentrates ̈Superseded by recombinant factors VIII, IX, XII in inherited haemophilias Human albumin solution (4.5% or 20%) ̈Nephrotic syndrome / liver disease Immunoglobulins ̈Normal – generalised immunodeficiency ̈Specific – eg. Anti-D

Answer 43

Haemolytic transfusion reaction ̈ Most serious complication ̈ Usually due to ABO incompatibility ̈ Avoid with meticulous attention to paperwork 4 patient identifiers (Name, DOB, Hosp No., Address) ̈ Rigors, fever, lumbar pain, dyspnoea, hypotension, renal failure, DIC ̈ Stop transfusion immediately and initiate emergency treatment ̈ May result in death

Answer 44

How much of mums blood has gone into the baby if mum is rh neg and baby is rh positive

Answer 45

Treatment Routine anti-D prophylaxis given to all RH negative mothers after delivery and at susceptible times during pregnancy Untreated can lead to mild fetal haemolytic anaemia through to fatal hydrops fetalis Treat with phototherapy for neonatal jaundice through to intra-uterine transfusion if severe Coombs test on cord blood to determine degree of fetal haemolysis Kleihauer test on maternal blood to determine dose of anti-D required post-delivery

Answer 46

Pernicious anaemia caused by B12 deficiency n Autoimmune condition n Atrophy of gastric mucosa n Destruction of parietal cells which produce intrinsic factor n Intrinsic factor required for B12 absorption in terminal ileum n Check parietal cell antibodies and intrinsic factor antibodies n Particular association with autoimmune thyroid disease n Schilling test to differentiate between intrinsic factor deficiency and terminal ileum absorption problem n Treat with injected B12 supplements, rarely oral.

Answer 47

Vitamin B12 deficiency Pernicious anaemia (autoimmune) Rarely dietary Disease of terminal ileum Folic acid deficiency Dietary Alcohol Drugs – methotrexate, trimethoprim, phenytoin

Answer 48

Polycythemia - high Hb Usually secondary - Bert’s COPD Hypoxia induces production of erythropoetin (EPO) which stimulates increased red cell production to enhance oxygen carrying capacity of blood Complications include thrombosis and cardiac failure due to increased blood viscosity

Answer 49

Reduction in all major cell lines Usually due to decreased healthy marrow production Aplastic anaemia Autoimmune Drugs eg. cytotoxics Infection eg. parvovirus Irradiation ̈ Treat with immunosuppressants if autoimmune, and blood component transfusions to support blood count ̈ Young patients may benefit from bone marrow transplant n Infiltration due to malignancy ̈ Myelodysplastic syndrome, haematological malignancy (leukaemia, lymphoma, myeloma), metastatic spread Myelofibrosis (rare variant of myelody splastic syndrome)

Answer 50

Being septic with very little functioning immune system Most serious type of infection - Medical emergency Patients succumb quickly to overwhelming sepsis without prompt treatment U&E, FBC, LFT, clotting, CRP, fibrinogen, blood cultures x3, MSU, CXR Aim to give IV antibiotics and IV fluids within 1 hour (Reserved for most serious infections) Tazosin, gentamicin, teicoplanin, vancomycin, ceftazidime, metronidazole used Follow hospital protocol Will present with very low neutrophils as low immune system

Answer 51

Platelet disorder Immune Thrombocytopaenia Purpura (ITP) ̈ Anti-platelet auto antibodies ̈ Acute in children approx 2 weeks following infection ̈ Chronic in adults (mainly women) Presents with purpura, easy bleeding, epistaxis, menorrhagia May require no treatment if platelets >20 Treat initially with prednisolone If relapse, immunosuppressant regime + splenectomy Other causes of decreased platelets include systemic lupus erythromatosis (SLE), thrombotic thrombocytopaenia purpura (TTP) and haemolytic ureamic syndrome (HUS) Causes of increased platelets include essential thrombocytosis (premalignant) and transient response to infection/ inflammation

Answer 52

An object from another part of the body that obstructs blood flow. Most typically it is a blood clot (thrombus) that becomes and an embolus. Common sites- brain, heart, lungs

Answer 53

• Achilles tendinitis • Achilles tendon rupture • Ankylosing spondylitis • ACL injury • Baker's cyst • Bone cancer • Broken leg • Bursitis • Cellulitis • Chronic exertional compartment syndrome • Claudication • Deep vein thrombosis • Gout • Growing pains • Growth plate fractures • Hamstring injury • Herniated disk • Infection • Juvenile rheumatoid arthritis • Knee bursitis • Legg-Calve-Perthes disease • Meralgia paresthetica • Muscle cramp • Muscle strain • Night leg cramps • Osgood-Schlatter disease • Osteoarthritis • Osteochondritis dissecans •Osteomyelitis •Paget's disease of bone • Patellar tendinitis • Patellofemoral pain syndrome • Peripheral artery disease • Psoriatic arthritis • Reactive arthritis • Rheumatoid arthritis • Sacroiliitis • Septic arthritis • Sciatica • Shin splints • Spinal stenosis • Sprains and strains • Stress fractures • Tendinitis • Thrombophlebitis • Torn meniscus • Varicose veins • Peripheral neuropathy • Posterior cruciate ligament injury • Pseudogout

Answer 54

• Sudden, severe pain in the calf • Signs of acute limb ischaemia (coolness, pallor, pulse deficits, delayed capillary refill) • Dyspnoea, Chest pain, and or sweating associated with leg pain • Signs of systemic toxicity (delirium, tachycardia, shock, pallor) • Crepitation, tenseness, foul discharge, bullae, necrosis • Positive risk factors for deep venous thrombosis (DVT) • Any neurologic deficits and abnormalities in the lower limbs.

Answer 55

• DeepVeinThrombosis • VaricoseVeins • Peripheralartery Disease (PAD) • MuscleCramps • Stenosis of spinal canal

Answer 56

• A history of DVT. • Cancer (known or undiagnosed). • Age over 60 years. • Being overweight or obese. • Male sex. • Heart failure. • Medical illness, for example acute infection. • Acquired or familial thrombophilia. • Inflammatory disorders (for example, vasculitis, inflammatory bowel disease). • Varicose veins. • Smoking.

Answer 57

Risk factors that temporarily raise the likelihood of DVT • Recent major surgery. • Recent hospitilisation. • Recent trauma. • Chemotherapy. • Significant immobility (bedbound, unable to walk unaided or likely to spend a substantial portion of the day in bed or in a chair). • Prolonged travel (for more than 4 hours). • Significant trauma or direct trauma to a vein (for example intravenous catheter). • Hormone treatment (for example oestrogen- containing contraception or hormone replacement therapy). • Pregnancy and the postpartum period. • Dehydration.

Answer 58

Warning signs of pulmonary embolism include – Shortage of breath Chest pain or discomfort that worsens when patient takes a deep breath or when patient coughs Feeling lightheaded, dizzy or fainting. Rapid Pulse Coughing up blood

Answer 59

• Refer immediately for same-day assessment and management, if deep vein thrombosis (DVT) is suspected in a woman who is pregnant or has given birth within the past 6 weeks. • For all other people with suspected DVT, use the two-level DVT Wells score to assess the probability of a DVT on an individual basis. Don’t do a d-dimer on pregnant women as it will automatically be raised

Answer 60

Active cancer (treatment ongoing, within the last 6 months, or palliative) 1 Paralysis, paresis, or recent plaster immobilization of the legs. 1 Recently bedridden for 3 days or more, or major surgery within the last 12 weeks requiring general or regional anaesthesia. 1 Localized tenderness along the distribution of the deep venous system (such as the back of the calf). 1 Entire leg is swollen. 1 Calf swelling by more than 3 cm compared with the asymptomatic leg 1 Pitting oedema confined to the symptomatic leg. 1 Collateral superficial veins (non-varicose) 1 Previously documented DVT 1 Subtract two points if an alternative cause is considered at least as likely as DVT. -2

Answer 61

A common complication that occurs after A DVT is postthrombotic syndrome (this condition is also known as postphlebetic syndrome). • Interestingly the symptoms may not appear until a few years after the dvt. • Signs and symptoms include leg pain, skin discoloration, and skin sores. • This syndrome is caused by damage to the veins from the blood clot which reduces blood flow in the affected areas. • Chronic venous hypertension causing limb pain, swelling, hyperpigmentation, dermatitis, ulcers, venous gangrene, and lipodermatosclerosis. • It affects up to 50% of people usually within 2 years of dvt of the lower limbs and can be debilitating with significant impact on quality of life.

Answer 62

• Cellulitis is a non-necrotizing inflammation of the dermis caused by invasion of bacteria • In immunocompetent patients usual infection is with staph. Aureus • Often follows a break in the skin (cut, fissure, laceration, insect bite or puncture wound). • Increased likelihood with patients with athletes foot, lymphatic obstruction, venous insufficiency and obesity. • Recurrent cellulitis may be due streptococci invasion particularly those with chronic lymphoedema • Different possible pathogen involves using other antibiotics or combinations of antibiotics

Answer 63

• Localised pain, swelling & tenderness generally present • The leg is usually red and hot, but also swollen and tender on examination • Fever and malaise are common in cases of cellulitis • Management involves raising the leg (above the level of the heart) • Oral antibiotics are given for mild infections (usually flucloxacillin for staph. Aureus) • IV antibiotics are given for more severe cases and those who are immunocompromised • These are usually given in OPAT clinics if the patient is clinically stable to be treated at home.

Answer 64

• Dependent Oedema is a condition in which there an accumulation of fluid underneath the skin causes abnormal swelling. • This usually occurs in areas of the body that are lower than the heart. • Most common sites are arms, legs and ankles. • One of the most common cause is congestive heart failure. • This is a condition where the heart muscles become too weak to effectively pump blood throughout the body.

Answer 65

Congestive heart failure Kidney damage Extremely low levels of albumin in the blood (hypoalbuminemia)

Answer 66

• Varicose Veins are visible on the surface of the skin and are unsightly as they occur more commonly in women. (increase when taking HRT) • They appear to be twisted, dark blue or purple veins, and are caused by weak valves and walls of the veins. • The valves in veins become weak allowing blood that should be moving towards the heart is allowed to flow backwards. • Blood pools in the veins and enlarge and become varicose. • The veins appear blue because they contain deoxygenated blood. • Complications include the development of varicose ulcers around the ankles and the potential formation of blood clots where the leg swells suddenly (this called thrombophlebitis).

Answer 67

• Painful cramping in the legs trigged by walking or climbing stairs • Leg numbness or weakness • Coldness in lower leg or foot, especially compared to opposite leg. • Sores on the toes ,feet or legs. • A change in colour of the legs • Hair loss or slower hair growth on feet and legs • Slower growth of toenails • Shiny skin on the legs • If PAD progresses pain may occur at rest which is described as Ischaemic rest pain.

Answer 68

• PAD happens when the arteries in the leg become narrowed & blocked resulting in a reduced blood flow to the extremities. • This can cause the lower leg to cramp and feel pain when the patient walks, climbs stair or do other types of exercise, because muscles aren’t getting enough blood. (angina of the leg!) • If the arteries become severely narrowed or blocked, the pain persists even at rest. • More likely to see this condition if the patient has diabetes, high BP high cholesterol or they smoke or are obese. • More likely if the patient has a history of other sites of occlusive vascular disease in heart or brain(describe the patient as known arteriopath)

Answer 69

– Pain—constantly present and persistent. – Pulseless—ankle pulses are always absent. – Pallor(or cyanosis or mottling). – power loss or paralysis. – Paraesthesia or reduced sensation or numbness. – Perishing with cold. If there is ischaemia due to an embolus: – Onset is acute. – The limb appears white (because there is no collateral circulation). – Vascular examination in the other leg is usually normal. If there is ischaemia due to thrombosis: – Onset is more gradual. – The leg may not be white and symptoms may be less severe (due to collateral circulation, which is often well-developed in people with chronic peripheral vascular disease). – Presentation is usually with worsening claudication and rest pain. Pulses in the other leg may also be absent.

Answer 70

• Achillestendinitis • ShinSplints • Stressfracture • Compartment syndrome • Baker’scyst • Tennisleg

Answer 71

Blood Glucose<3.5mmol/L Triggers? • Infection • Overexercise • Undereating,missedmeals, delayed meals • Gastroparesis • Hypoglycaemicunawareness • Toomuchinsulin(selfharm, administration error) • Lipohypertrophy • Renalfailure • Medications:Sulphonylurea+ others Signs and Symptoms?

Answer 72

Autonomic: (warning signs) Sweating Paraesthesia (pins and needles) Feeling hot Shakiness Anxiety Palpitations Pallor Neuroglycopaenic: Difficulty speaking Loss of concentration Drowsiness Dizziness Hemiplegia Fits Coms

Answer 73

Retinopathy Nephropthy Neuropathy

Answer 74

Background diabetic retinopathy Pre-proliferative diabetic retinopathy Proliferative diabetic retinopathy Advanced diabetic retinopathy

Answer 75

• Damage to the blood vessels in the retina due to hyperglycaemia • Commonest cause of blindness in under 60’s in the UK • Asymptomatic • Screening at least yearly • Pregnancy can accelerate the progression due to growth factors, so should be screened in 1st and 3rd trimester • More regular follow if evidence of retinopathy

Answer 76

Dots (micro-aneurysms) & Blots (small intraretinal haemorrhages) Hard exudates (lipid exudates that often form in a circle around a leaking blood vessel

Answer 77

Cotton wool spots (fluffy white areas that result from retinal ischemia Clusters of irregular branched vessels within the retina

Answer 78

New vessel formation

Answer 79

Background retinopathy that occurs within one disc diameter of the macula

Answer 80

Lens swelling Not diabetic retinopathy as usually takes about 5 years after diagnosis

Answer 81

• Cataracts • Glaucoma • Diabetic retinopathy • Cranial nerve palsy • Retinal detachment • Retinal or vitreous haemorrhage

Answer 82

Maculopathy - 1-3 months Pre- proliferative - 1 month Proliferative - 1-2 weeks Sudden loos of vision - same day Retinal detachment - same day Cataract - non urgent

Answer 83

As a result of poor uncontrolled glycemic control Yearly eye screening Optimise glycaemic control Mange BP Pro-proliferative, Maculopathy: •Laser photocoagulation •Intra-vitreal anti-VEGF for macular oedema Prevent patient progressing into proliferative Visual aids Driving regulations

Answer 84

• Very common cause of Chronic Kidney Disease • Diabetic nephroathy accounts for 20-44% of new patients requiring renal replacement therapy •First sigh is micoralbuminuria (higher level of albumin (protein) in the urine than normal) Complications/Associations: • Significant increase in cardiac mortality if nephropathy • CV disease risk increased 2-3 fold if microalbuminaemia • CV disease risk increased 10 fold if frank proteinuria • Proteinuria->Nephrotic Syndrome • CKD and Hypertension

Answer 85

Yearly eGFR estimation and urinary albumin excretion (first-pass morning urine specimen) • Early morning urine Albumin:Creatinine Ratio >3mg/mol • eGFR<60 • Tests show be consistently raised for >3months (at least 2-3 samples)