Blood Results Flashcards
Microcytic anaemia
What’s ferritin?
Ferritin:
- intracellular protein → binds iron and stores it to be released in a controlled fashion at sites where iron is required
- acute phase protein → may be synthesised in increased quantities in situations where inflammatory activity is ongoing
* Falsely elevated results may therefore be encountered clinically and need to be taken in the context of the clinical picture and blood results
Causes of increased ferritin
How to check for iron overload?
- The best test to see whether iron overload is present is transferrin saturation
- Typically, normal values of < 45% in females and < 50% in males exclude iron overload
What’s transferrin?
Transferrin:
- iron-binding blood plasma glycoproteins
- control the level of free iron (Fe) in biological fluids
- produced in the liver
Transferrin and immune system
- innate immune system → transferrin binds iron, → creating an environment low in free iron that stops bacterial survival (iron withholding) → the level of transferrin decreases in inflammation
What can cause an increase in transferrin levels?
Increased plasma transferrin level:
- often seen in patients suffering from iron deficiency anemia, during pregnancy, and with the use of oral contraceptives → as increase in transferrin protein expression
- When plasma transferrin levels rise, there is a reciprocal decrease in percent transferrin iron saturation → increase in total iron binding capacity in iron deficient states
What can cause a decrease in transferrin levels?
A decreased plasma transferrin can occur in:
- iron overload diseases
- protein malnutrition
- an absence of transferrin→ a rare genetic disorder atransferrinemia
- *a* condition characterized by anemia and hemosiderosis in the heart and liver that leads to heart failure and many other complications
In what condition iron and ferritin levels may be decreased?
- iron and ferritin are bound the total body ferritin levels may be decreased in cases of iron deficiency anaemia
Measurement of serum ferritin levels can be useful in determining whether an apparently low haemoglobin and microcytosis is truly caused by an iron deficiency state.
What’s hepcidin?
- it’s produced by liver
- it regulates iron absorption → if too much iron → hepcidin inhibits iron absorption
What’s the relationship between transferrin and ferritin?
Transferrin carries iron (e.g. from destroyed RBC) into storage (ferritin)
What’s TIBC?
TIBC = transferrin (so the protein that carries iron)
What’s iron saturation %?
Iron saturation % = transferrin saturation
% = how many receptors on the transferrin are occupied by iron
What’s soluble transferrin receptor saturation?
sTFR
It’s to differentiate iron deficiency anaemia from anaemia of chronic disease
- Anaemia of chronic disease → sTFR is normal
- Iron deficiency anaemia → sTFR is increased
*think about it as TIBC
- What are the abnormalities?
- What is the diagnosis?
- Why does she have a raised ferritin?
- What is the future management in Anna’s case?
Working diagnosis: Primary hyperparathyroidism
Further investigation for raised calcium:
FBC
Anaemia – multiple myeloma
ESR
Raised ESR – multiple myeloma
UE
Impaired renal function – secondary/ tertiary hyperparathyroidism
LFTs
Raised Alkaline phosphatase – bony metastases
Parathyroid hormone
Raised in Primary/ Secondary/ Tertiary hyperparathyroidism, Suppressed in malignant causes.
Vitamin D
Must be normal before diagnosing Primary Hyperparathyroidism
Also:
ACE
Sarcoidosis
TFTs
Thyrotoxicosis
Cortisol
Adrenal insufficiency
How should this unexpected finding be investigated?
- FBC
- U&E
- Bone profile
- ESR
- Protein electrophoresis
- Bence Jones protein
What’s working diagnosis?
Multiple myleoma
- Abnormality: jaundice
- What information do you require from the history?
Presence of dark urine
History of foreign travel
Presence of pale stool
Previous episodes of jaundice - Gilbert’s
History of blood transfusion
Medication history
Alcohol and drug history inc IVDU
Sexual history
History of medical treatment abroad
Contacts with jaundice –viral hepatitis
Occupation- sewage workers Hepatitis A
Family history of jaundice- Gilbert’s
Known autoimmune disease- autoimmune hepatitis
Pregnancy
Presence of tattoos
Previous malignancy
- List your initial investigations and reasons why?
FBC
Anaemia- malignancy, raised WBC/neuts – infection, low plts- etoh/portal hypertension
UE
Hepato-renal failure – often cirrhosis
LFT
Investigate the pattern of jaundice, Albumin –indicates synthetic liver function
What is the working diagnosis and what investigations would you request next?
NAFLD →obese, hypertensive, raised AST, ALT and GGT
Further investigations: Liver aetiology screen and ultrasound
Questions to ask:
- Type of bleeding: mucocutaneous – often seen in platelet defects and Von Willebrand disease, haemarthrosis/ muscle haematomas – often seen in coagulation factor deficiencies.
- Severity of bleeding: anaemia, blood transfusion
- Previous tests of the haemostatic system – operations, dental extractions, trauma, childbirth.
- Age of onset
- Family history
- Other medical problems e.g. liver disease, Cushing’s – purpura, HSP
- Drugs: aspirin, NSAIDs, Warfarin, DOACs
Further Ix in primary care: FBC and coagulation screen
- What’s ANA screen for?
- What does it test specifically for in ELISA antigen test? and what diseases it tests for?
What’s AMA?
What disease does it correspond to?
AMA
(Anti-mitochondrial antibodies)
Disease: Primary Biliary Cirrhosis
What’s ASMA?
What diseases does it correspond to?
ASMA
(Anti-smooth muscle antibody)
- Autoimmune liver disease
(inc PBC and autoimmune hepatitis)
What’s anti-LKM?
Disease that is associated with
Anti - LKM
(Anti liver-kidney-microsomal)
Disease: Autoimmune hepatitis
What ANCA tests for?
- What are the differential diagnoses for peripheral oedema?
- What investigations would you request and why?
Diagnosis if:
PT prolonged and APTT normal
Deficiency of factor VII
Diagnosis if:
PT normal and APTT prolonged
Deficiency of factors:
- VIII (haemophilia A)
- IX (haemophilia B)
- XI
- Lupus anticoagulant
Working diagnosis: Nephritic syndrome due to post infective glomerulonephritis (likely streptococcal). Nephritic syndrome – hypertension, fluid retention, blood and protein in the urine with renal impairment.
Next: Acute referral to medicine for management of hyperkalaemia.
List intrinsic causes of AKI
Intrinsic:
- Glomerular → glomerulonephritis
- Interstitial → medication, infection, systemic disease e.g. sarcoid, lupus
- Tubular → ischaemia secondary to prolonged hypotension, nephrotoxic e.g. contrast, aminoglycosides, rhabdomyolysis, myeloma and tumour lysis
- Vascular → thrombosis, infraction, vasculitis
Post-renal causes of AKI
- Prostate hypertrophy
- retroperitoneal fibrosis
- bladder/ prostate and cervical cancer
- urethral strictures
- stones
- clots
- What are the differential diagnoses for acute confusion?
V
Vascular
Ischaemic stroke, haemorrhagic stroke, vasculitis, TIA, MI
I
Infection
UTI, LRTI, Meningitis, Encephalitis, Cellulitis- ulceration, Brain abscess
T
Trauma
Subdural haemorrhage
A
Autoimmune
Vasculitis, SLE
M
Metabolic
Hypo/ Hyperglycaemia, Hypercalcaemia, Hypo/ Hypernatraemia, Thyroid dysfunction, Hypoxia, Raised CO2, Renal failure, Liver failure, adrenal crisis
I
Iatrogenic & other
Medication- opiates, sedatives, tricyclics,
Constipation
Urinary retention
Post ictal
N
Neoplasm
Intracranial lesions, other locations causing metabolic disturbance
S
Substances
Alcohol
What would your initial Ix be and why?
FBC
WBC- infection
Neuts- bacterial infection
Lymphs- viral infection
U&E
Hypo/ hyper natraemia
Raised urea and creatinine – renal failure
Bone profile
Hypercalcaemia
Glucose
Hypo/ hyper glycaemia
LFTs
Deranged LFTs- liver failure
TFTs
Hypo/ hyper thryoidism
CRP
Infection
Abnormalities: synovitis at MCPJs
Further Ix: FBC, CPR, aCCP, ESR
What action should we take on the raised PSA?
Face to face r/v for Hx and examination
What can raise PSA levels?
- benign prostatic hyperplasia (BPH)
- prostatitis and urinary tract infection (NICE recommend to postpone the PSA test for at least 1 month after treatment)
- ejaculation (ideally not in the previous 48 hours)
- vigorous exercise (ideally not in the previous 48 hours)
- urinary retention
- instrumentation of the urinary tract
Which investigation is required?
TFTs
Name the associated eye signs
- Lid retraction
- Lid lag
- Exophthalmos
- Ophthalmoplegia
What TFTs will show in this case?
TSH low, T4 high
Name associated conditions
- T1DM
- Pernicious anaemia
- Vitiligo
- Addison’s
What Ix is required?
D-dimer
•16yr old Joe presents to his GP with a six week history of weight loss, thirst and polyuria. He is referred to secondary care with suspected T1DM. Which test should be requested?
Random venous plasma glucose
In which situations HbA1 is not appropriate to test for?
HbA1c is not appropriate in the following situations:
- Age <18
- Patients with sudden onset of symptoms <2/12
- Pregnancy
- Acutely unwell
- Patient’s taking medications which may cause rapid increases in glucose e.g. steroids
- Presence of genetic/ haematological factors that influence HbA1c
What results (different tests) would suggest diabetes?
- HbA1c ≥ 48
- Random venous glucose ≥ 11.1
- Fasting Venous Glucose ≥ 7.0
What’s likely diagnosis?
Cushing’s syndrome
Features of Cushing’s syndrome
- Weight gain
- ↑BP
- hirsutism
- buffalo hump
- moon shaped face
- fatigue
- recurrent infection
- thin skin
- striae
- bruising
- acne
- depression
- osteoporosis
- myopathy
- diabetes
What’s that?
Malar rash
- What is the suspected diagnosis?
- Name an investigation used to confirm this diagnosis?
- Name the condition associated with this disease which causes thrombosis
- Suspected diagnosis: SLE
- Ix: dsDNA
- Condition associated with this disease which causes thrombosis: Antiphospholipid syndrome
Diagnosis?
Glossitis
Name the associated type of anaemia?
What investigations would you request?
•What would you expect in the results?
- Type of anaemia: Megaloblastic anaemia
- Ix: FBC, TFT, B12 and folate
- Expected results: ↓Hb, ↑MCV
What’s that?
Likely diagnosis?
Auer Rod
AML
Presentation of acute leukaemia
- Bone pain (especially in children)
- Symptoms of bone marrow failure e.g. anaemia, infection, thrombocytopenia,
- Symptoms of organ infiltration e.g. lymphadenopathy, hepatosplenomegaly
What Ix to request?
•Uric acid
*uric acid levels may not reflect the clinical picture
Medications type (2) associated with Gout
Diuretics, chemotherapy
What to treat with acute Gout attack?
- NSAID & PPI
- Colchicine
- Corticosteroid
- rest & ice
Prevention of Gout attacks
Urate lowering therapy:
- Allopurinol
- Febuxostat
Name that sign
Causes of it
Koilonychia
Causes:
- Menorrhagia
- Pregnancy
- GI bleeding inc IBD and GI cancer
- Malabsorption – Coeliac
- CKD
- Hookworm infection
Causes of jaundice
(3 categories)
Arterial Thrombosis
Name three common heritable thrombophilias
Factor V Leiden
1 in 20
Protein S deficiency
1 in 300
Protein C deficiency
1 in 300
SEs of iron supplementation
- constipation
- dark stool
- nausea
When to offer iron supplementation?
- When Hb is below 100 → offer iron supplementation with ferrous sulphate
- When Hb is below 80 → blood transfusion
(if Hb over 100 - first encourage dietary changes)
Dietary changes to increase iron
iron-rich diet:
- dark-green leafy vegetables
- meat
- iron-fortified bread (and cereals)
+ aid vitamin C to increase absorption of iron
Elderly pt with pain the joint
What Ix would you do first?
- ESR and bone profile → to ensure it’s normal (e.g. increased ESR in Multiple myeloma)
*if any of above result abnormal do MM screen
- We do not do X-ray as first - line and as often as in the elderly patient with OA it won’t change management
Pathophysiology of the hepato-renal syndrome
- Vasoactive mediators → splanchnic vasodilation → which reduces the systemic vascular resistance → ‘underfilling’ of the kidneys
- The above (underfilling) is sensed by the juxtaglomerular apparatus which then activates RAAS renal → vasoconstriction which is not enough to counterbalance the effects of the splanchnic vasodilation
Management of hepatorenal syndrome
- vasopressin analogues (e.g. terlipressin) →work by causing vasoconstriction of the splanchnic circulation
- volume expansion with 20% albumin
- transjugular intrahepatic portosystemic shunt
