Case 14: extra and anaemia Flashcards

1
Q

Questions to ask with allergy symptoms during weaning

A
  • What foods have they tried?
  • Which formulas have they been given?
  • Has they tried lactose free milk?
  • Has they had any medications for eczema?
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2
Q

Allergy tests- when they may be inaccurate

A
  • Specific IgE testing: can be falsely negative if high total IgE levels (eczema, atopy)
  • Allergy testing should be 4-6 weeks after symptoms i.e. anaphylaxis or severe allergic response
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3
Q

Management for weaning child with food allergies

A
  • Cows milk allergy: stop formula milks & change to eHF and subsequent amino acid formula. In non IgE reactions a ‘milk ladder’ can be used to reintroduce dairy back in the diet
  • Allergen free diet
  • Iron, vitamin D and calcium supplements
  • Food challenge/feed
  • Optimise eczema management with emollients, steroid creams, skinnies and garments
  • Children can grow out of allergies and are offered periodic investigation (IgE testing and food challenge). >16 have it life long
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4
Q

Why are drug allergy histories difficult

A
  • Patients may have no first hand recollection of an allergic response if the reaction occurred at a young age or under anaesthesia
  • In the acutely ill patient many drugs may have been administered together making identification of the culprit drug difficult
  • Infection is a potent trigger for urticaria and angioedema
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5
Q

Types of drug reactions

A
  • Immediate: includes urticaria, angiodema, rhinitis, bronchospasm, N+V and anaphylaxis. Occurs within 6 hours of administration. Typically first hours
  • Non-immediate drug reactions: includes maculopapular rashes, Steven Johnson syndrome, toxic epidermal necrolysis, serum sickness, drug fevers, pneumonitis and nephritis. Occurs within 8-12+ hrs post administration
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6
Q

Drug allergy: history

A
  • Description of reaction
  • Symptoms sequence and duration
  • Treatment provided
  • Outcome
  • Timing in relation to drug administration
  • How long had the drug been taken before the onset of the reaction
  • When was drug stopped and what was the effect
  • Photograph of reaction illness for which drug was taken (illness may be cause)
  • Other medications which being taken at the time
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7
Q

Management of Drug allergies

A
  • Add an allergy alert to avoid certain medications to the patients records
  • Drug allergy testing is not indicated if other medication choices available
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8
Q

Drug reactions with Eosinophilia and Systemic Symptoms (DRESS)

A
  • Typically begins three weeks after starting medication
  • Involved: skin rash, fever, enlarged lymph nodes, and involvement of internal organs
  • Eosinophilia
  • Caused by: anticonvulsants (such as phenytoin, carbamazepine), allopurinol (used for gout), sulfa antibiotics, and some antiviral medications
  • Manged conservatively by stopping meds and systemic corticosteroids
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9
Q

Pollen count

A
  • Tree pollens counts are high between March and April
  • Grass pollen from May through to August
  • Weeds from June – September.
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10
Q

How to use nasal sprays

A

head forward looking at the feet with the nozzle pointed away from the midline.

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11
Q

Conjunctivitis

A

Inflammation go the outermost layer of the white of eye and inner surface of eyelid. When the small blood vessels in the conjunctiva become inflamed, they are more visible.

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12
Q

Season allergic rhino conjunctivitis (Hay fever)

A
  • Investigations: skin prick testing, specific IgE testing
  • Medications: Over-the-counter or prescription antihistamines (Cetirizine, Fexofenidine), decongestants, nasal corticosteroids (don’t use Kenalog), or eye drops (Cromoglicate, nedocromil) can help relieve symptoms. If poor control offer short course of oral prednisolone.
  • Immunotherapy: for severe allergy
  • Typical management: Antihistamine (Flexofenandine), nasal steroids (Avamys- Flucticasone) and eye drops (olopatadine)
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13
Q

Desensitisation therapy for Allergic rhinoconjunctivits

A
  • offered if triple therapy (Antihistamine, nasal corticosteroids and eye drops) doesn’t work and oral steroids are required.
  • Reduces symptom burden though some medication may still be required
  • Done for a minimum of 3 years. Treatment can wear off and may need to be repeated
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14
Q

Causes of non allergic rhinitis

A
  • Infection: Usually self -resolving
  • Environmental triggers: Smoke, perfume, paint fumes, changes in weather / temperature, alcohol, spicy food, stress
  • Medicines and recreational drugs: ACE inhibitors, beta blockers, NSAIDs, cocaine
  • Overuse of nasal decongestants: Reduce swelling of the blood vessels. If used for >5-7 days then rebound symptoms
  • Hormone changes: Pregnancy, puberty, HRT, OCP, Hypothyroidism
  • Structural nasal problems: **Deviated nasal septum; polyps
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15
Q

Anaemia

A
  • Haemoglobin concentration of blood below normal range for age and sex: Adult male <130, Adult female <115
  • Causes tissue hypoxia
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16
Q

RBC cycle

A
  • Erythropoiesis: Megakaryocyte Erythroid Progenitor → Erythroblast -) Nucleus extrusion (nucleus expelled) → Reticulocyte → RBC
  • Low blood levels stimulate kidney to produce erythropoietin
  • Erythropoietin (EPO)stimulates Erythropoiesis on the bone marrow: takes 3 weeks
  • Old RBC’s (after 3 months) are phagocytised in the spleen/liver
  • Haemoglobin is broken down and either re-used in the body i.e. iron or excreted i.e. bilirubin
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17
Q

Causes of reduced RBC production

A
  • Reduced EPO response: kidney disease (low EPO production) or chronic inflammation (reduced response)
  • Iron, B12 or folate deficiency: poor dietary intake, malabsorption, chronic inflammation
  • Reduced bone marrow production: Malignancy, infection, aplastic anaemia, Myelosuppressive drugs (chloramphenicol, alcohol) and Myelosuppressive infection (parvovirus or HIV)
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18
Q

Causes of anaemia

A
  • Reduced RBC production
  • Increased demand: Pregnancy and lactation. Can get folate deficiency as erythropoiesis increases
  • Blood loss: acute or chronic
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19
Q

Causes of increased RBC destruction

A
  • Haemolytic anaemias (autoimmune, drug induced, Hereditary spherocytosis)
  • Haemoglobinopathies (Thalassaemia, sickle cell disease),
  • Hypersplenism when RBC are pooled in the spleen (Portal hypertension i.e. liver disease)
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20
Q

Clinical assessment of anaemia history

A

Anaemia symptoms: lethargy, lightheaded, SOB, palpitations, angina

Clinical Assessment of anaemia history
- Bleeding history
- Features of cancer/infection: weight loss, change in bowel habit, fever
- Symptoms of specific anaemias: fluctuating jaundice in haemolytic anaemias. Memory loss/paraesthesis in severe B12 deficiency
- Dietary history
- Menstrual history
- PMH: CKD, cancer
- past surgical: bariatric or GI

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21
Q

Medications which can cause anaemia

A
  • NSAIDs, anticoagulation (increased risk of bleeding)
  • Dapsone (haemolysis)
  • Chloramphenicol (marrow suppression
22
Q

Clinical signs of anaemia

A
  • Angular cheilitis: Iron deficient
  • Koilonychia
  • Enlarged tongue: B12 deficiency
  • Pallor, jaundice
  • Hair thinning
  • Consider rectal/vaginal exam
23
Q

Microcytic hypochromic anaemia

A
  • MCV <80, MCH <27
  • Causes: Iron deficiency, Haemoglobinopathies (Thalassaemia), Lead poisoning (rare), Sideroblastic anaemia (rare)
  • Investigations: Ferritin
24
Q

Further investigations in microcytic anaemia

A
  • Ferritin can rise in inflammation. Look at CRP and consider measuring serum iron and TIBC (TIBC is raised in iron deficiency and low in anaemia of chronic disease)
  • If microcytic anaemia with normal ferritin: Haemoglobinopathy screen
25
Q

Normocytic normochromic anaemia

A
  • MCV: 80-95, MCV >27
  • Causes: anaemia of chronic disease, after acute blood loss, renal disease, Mixed deficiencies (both iron and folate)
  • Investigations: Blood film, Reticulocytes, U&E’s, LFT’s, CRP, ferritin, B12, folate, HIV
26
Q

Reticulocyte count and bone biopsy

A

Reticulocyte count
- Low: poor bone marrow production
- High: haemolysis

Bone biopsy: significant anaemia, unknown cause

27
Q

Macrocytic anaemia

A
  • MCV >95
  • Megaloblastic: Vitamin B12 deficiency, folate deficiency
  • Non-megaloblastic: Alcohol, Liver disease, Haemolytic anaemia, Aplastic anaemia, Myelodysplasia, Myeloma etc
  • Investigations: Blood film, Reticulocytes, B12, folate, LFT’s, U&E, LDH, DAT, Myeloma screen HIV
28
Q

B12 deficiency

A
  • Assess for subacute combined degeneration of the spinal cord
  • Consider endoscopy as associated risk of gastric cancer
  • Test for pernicious anaemia: intrinsic factor and parietal cell antibodies
29
Q

Mechanism of low platelets

A
  • Decreased production
  • Increased destruction/consumption
  • Over-storage (splenic sequestration)
30
Q

Causes of low platelets

A
  • Consumptive: Sepsis, Hypersplenism, Liver disease, DIC, TTP
  • Immune: Viral infections (HIV, Hep B and C), medications, Autoimmune
  • Underproduction: B12/folate, Alcohol, Myelodysplasia/aplastic anaemia, Bone marrow infiltration (malignancy, infection). Drugs including chemo, anti-epileptics, psych drugs
  • Dilutional: massive transfusion, pregnancy
  • Destruction: ITP, autoimmune
  • Overstorage in the spleen: Hypersplenism due to portal
31
Q

Thrombocytopaenia clinical context

A

Thrombocytopaenia is only really significant if platelets <100. Main causes of low platelets is alcohol or acute illness. Other causes: Liver failure or B12/folate deficiency. More concerned about acute change.

32
Q

Thrombocytopaenia investigations

A
  • First line: Blood film (a low platelet count may be wrong if they are clumping together probably a lab issue), B12/folate, LFT’s, U&E, clotting, HIV, Hep
  • Clinical info: alcohol (Liver cirrhosis and portal hypertension cause increased destruction and polling in the spleen), medication, acute illness
  • Exclude serious things: TTP/MAHA, acute leukaemia (detected on blood film), DIC with bleeding, HIT (Heparin Induced Thrombocytopaenia use the 4T score)
33
Q

DIC coag screen

A
  • high PT/ APTT
  • low fibrinogen
  • high fibrin degradation products
34
Q

Thrombocytopaenia: when to contact haematology

A
  • Acute and platelets <50 without cause or between 50-100 and chronic
  • Bleeding
  • Abnormal blood film
  • Concern about HIT or TTP
35
Q

Transfusing platelets

A

Unlikely to spontaneously bleed with platelets >20 so if well and not bleeding don’t transfuse. Unless planned invasive procedure

36
Q

Causes of different haematological cancers

A

Immature Haematopoietic stem cells which are cancerous cause acute leukaemia

Matures Haematopoietic stem cells which are cancerous cause chronic leukaemia

Myelodysplastic disease’s are all cancer which affects stem cells in the bone marrow but progress is slower

37
Q

Myelodysplastic syndrome (MDS)

A
  • Disease of the elderly
  • Progressive bone marrow failure due to production of dysfunctional blood cells
  • One type of cell or single lineage i.e. red cells causing anaemia
  • All cell lineages causing pancytopenia
  • Affects Myeloid lineage
38
Q

MDS spectrum

A
  • Mildly low count in one cell line: refractory anaemia
  • Low counts in multiple cell lines: Refractory cytopenia with multi-lineage dysplasia (RCMD)
  • Production of Leukaemia cells (blasts): Refractory anaemia with excess blasts (RAEB) which will lead to acute Myeloid Leukaemia
39
Q

MDS symptoms and investigations

A
  • Symptoms of marrow failure- anaemia: fatigue, SOB, pallor
  • Low WCC: fever, infection
  • low platelets: bruising, bleeding
  • Investigations: FBC, blood film, bone marrow biopsy
40
Q

Bone marrow contents

A

Leukaemia: condition of bone marrow failure secondary to accumulation of malignant blasts.

Bone marrow typically contains 50% fat cells and 50% cellular activity.

41
Q

MDS diagnosis

A
  • FBC: Macrocytic anaemia, cytopenia
  • Blood film: irregular abnormal cells (dyplasic)
  • Bone marrow biopsy: Hypercellular, abnormal maturation
42
Q

Leukaemia diagnosis

A
  • FBC: Cytopenia, high WBC
  • Blood film: blasts
  • Bone marrow biopsy: Hypercellular, blasts
43
Q

Acute and definitive treatment for Leukaemia

A
  • Acute: treat infection with broad spectrum Abx, Transfuse blood and platelets
  • Definitive: Chemo, bone marrow transplantation
44
Q

Management of MDS

A
  • Transfusion support
  • Growth factors i.e. EPO
  • Disease modifying chemotherapy: not curative
  • Curative is bone marrow transplant but rarely indicated at MDS patients are elderly
45
Q

Acute lymphoblastic Leukaemia

A
  • Most common childhood malignancy: peak incidence 1-5
  • Malignancy of pre-cursor lymphocytes, most common is B-cells
  • Typical symptoms: persistent fever, pallor, unusual bleeding, lymphadenopathy and/or organomegaly
46
Q

Risk factors for ALL

A
  • Genetics: including trisomy 21 (Downs syndrome), Klinefeters syndrome and fanconi anaemia
  • Viral exposure
  • Environment: smoking or radiation exposure
  • Philadelphia (T 9,22): associated with worse prognosis, more commonly seen in adults
  • Younger adults have better prognosis then adults
  • High WBC at diagnosis is worse prognosis
  • T cell ALL has worse prognosis then B-cell ALL
47
Q

Classification of ALL

A
  • B cell lineage (85% of cases)
  • T cell lineage (10-15% cases)
  • Rare cases of NK cell lineage (<1% of cases)
48
Q

Characteristics of B-ALL

A
  • Philadelphia chromosome (Ph+)
  • Hyperdiploid B-ALL/LBL
  • Hypodiploid B-ALL/LBL
  • T(v;11q23.3);KMT2A-rearranged
  • T (12;21): genetic abnormality associated with kids ALL
49
Q

Clinical features of ALL

A
  • Organomegaly: Hepatomegaly or Splenomegaly. Can present with weight loss, abdo pain or distension
  • Fever: persistent, recurrent or refractory. Can cause night sweats
  • Lymphadenopathy: painless firm lymph node
  • Bone pain: limp or refusal to weight bear
  • Unusual bleeding/bruising or a petechial rashis a common result of Thrombocytopaenia
  • Anaemia can cause pallor, persistent fatigue or syncope.
50
Q

NICE guidelines Leukaemia

A

Afull blood countwithin 48 hours for patients with suspected leukaemia. They recommend children or young people withpetechiaeorhepatosplenomegalyare sent for immediate specialist assessment.