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Y4 CCTs > Blood Results > Flashcards

Blood Results Flashcards

1
Q
A

Microcytic anaemia

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2
Q

What’s ferritin?

A

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

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3
Q

Causes of increased ferritin

A
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4
Q

How to check for iron overload?

A
  • 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
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5
Q

What’s transferrin?

A

Transferrin:

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6
Q

Transferrin and immune system

A
  • 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
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7
Q

What can cause an increase in transferrin levels?

A

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
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8
Q

What can cause a decrease in transferrin levels?

A

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
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9
Q

In what condition iron and ferritin levels may be decreased?

A
  • 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.

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10
Q

What’s hepcidin?

A
  • it’s produced by liver
  • it regulates iron absorption → if too much iron → hepcidin inhibits iron absorption
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11
Q

What’s the relationship between transferrin and ferritin?

A

Transferrin carries iron (e.g. from destroyed RBC) into storage (ferritin)

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12
Q

What’s TIBC?

A

TIBC = transferrin (so the protein that carries iron)

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13
Q

What’s iron saturation %?

A

Iron saturation % = transferrin saturation

% = how many receptors on the transferrin are occupied by iron

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14
Q

What’s soluble transferrin receptor saturation?

A

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

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15
Q
  • What are the abnormalities?
  • What is the diagnosis?
  • Why does she have a raised ferritin?
  • What is the future management in Anna’s case?
A
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16
Q
A

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

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17
Q

How should this unexpected finding be investigated?

A
  • FBC
  • U&E
  • Bone profile
  • ESR
  • Protein electrophoresis
  • Bence Jones protein
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18
Q

What’s working diagnosis?

A

Multiple myleoma

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19
Q
A
  • 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

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20
Q
A
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21
Q

What is the working diagnosis and what investigations would you request next?

A

NAFLD →obese, hypertensive, raised AST, ALT and GGT

Further investigations: Liver aetiology screen and ultrasound

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22
Q
A

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

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23
Q
  • What’s ANA screen for?
  • What does it test specifically for in ELISA antigen test? and what diseases it tests for?
A
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24
Q

What’s AMA?

What disease does it correspond to?

A

AMA

(Anti-mitochondrial antibodies)

Disease: Primary Biliary Cirrhosis

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25
Q

What’s ASMA?

What diseases does it correspond to?

A

ASMA

(Anti-smooth muscle antibody)

  • Autoimmune liver disease

(inc PBC and autoimmune hepatitis)

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26
Q

What’s anti-LKM?

Disease that is associated with

A

Anti - LKM

(Anti liver-kidney-microsomal)

Disease: Autoimmune hepatitis

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27
Q

What ANCA tests for?

A
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28
Q
A
29
Q
  • What are the differential diagnoses for peripheral oedema?
  • What investigations would you request and why?
A
30
Q

Diagnosis if:

PT prolonged and APTT normal

A

Deficiency of factor VII

31
Q

Diagnosis if:

PT normal and APTT prolonged

A

Deficiency of factors:

  • VIII (haemophilia A)
  • IX (haemophilia B)
  • XI
  • Lupus anticoagulant
32
Q
A

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.

33
Q

List intrinsic causes of AKI

A

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
34
Q

Post-renal causes of AKI

A
  • Prostate hypertrophy
  • retroperitoneal fibrosis
  • bladder/ prostate and cervical cancer
  • urethral strictures
  • stones
  • clots
35
Q
  • What are the differential diagnoses for acute confusion?
A

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

36
Q

What would your initial Ix be and why?

A

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

37
Q
A

Abnormalities: synovitis at MCPJs

Further Ix: FBC, CPR, aCCP, ESR

38
Q

What action should we take on the raised PSA?

A

Face to face r/v for Hx and examination

39
Q

What can raise PSA levels?

A
  • 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
40
Q

Which investigation is required?

A

TFTs

41
Q

Name the associated eye signs

A
  • Lid retraction
  • Lid lag
  • Exophthalmos
  • Ophthalmoplegia
42
Q

What TFTs will show in this case?

A

TSH low, T4 high

43
Q

Name associated conditions

A
  • T1DM
  • Pernicious anaemia
  • Vitiligo
  • Addison’s
44
Q

What Ix is required?

A

D-dimer

45
Q

•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?

A

Random venous plasma glucose

46
Q

In which situations HbA1 is not appropriate to test for?

A

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
47
Q

What results (different tests) would suggest diabetes?

A
  • HbA1c ≥ 48
  • Random venous glucose ≥ 11.1
  • Fasting Venous Glucose ≥ 7.0
48
Q

What’s likely diagnosis?

A

Cushing’s syndrome

49
Q

Features of Cushing’s syndrome

A
  • Weight gain
  • ↑BP
  • hirsutism
  • buffalo hump
  • moon shaped face
  • fatigue
  • recurrent infection
  • thin skin
  • striae
  • bruising
  • acne
  • depression
  • osteoporosis
  • myopathy
  • diabetes
50
Q

What’s that?

A

Malar rash

51
Q
  • What is the suspected diagnosis?
  • Name an investigation used to confirm this diagnosis?
  • Name the condition associated with this disease which causes thrombosis
A
  • Suspected diagnosis: SLE
  • Ix: dsDNA
  • Condition associated with this disease which causes thrombosis: Antiphospholipid syndrome
52
Q

Diagnosis?

A

Glossitis

53
Q

Name the associated type of anaemia?

What investigations would you request?

•What would you expect in the results?

A
  • Type of anaemia: Megaloblastic anaemia
  • Ix: FBC, TFT, B12 and folate
  • Expected results: ↓Hb, ↑MCV
54
Q

What’s that?

Likely diagnosis?

A

Auer Rod

AML

55
Q

Presentation of acute leukaemia

A
  • Bone pain (especially in children)
  • Symptoms of bone marrow failure e.g. anaemia, infection, thrombocytopenia,
  • Symptoms of organ infiltration e.g. lymphadenopathy, hepatosplenomegaly
56
Q

What Ix to request?

A

•Uric acid

*uric acid levels may not reflect the clinical picture

57
Q

Medications type (2) associated with Gout

A

Diuretics, chemotherapy

58
Q

What to treat with acute Gout attack?

A
  • NSAID & PPI
  • Colchicine
  • Corticosteroid
  • rest & ice
59
Q

Prevention of Gout attacks

A

Urate lowering therapy:

  • Allopurinol
  • Febuxostat
60
Q

Name that sign

Causes of it

A

Koilonychia

Causes:

  • Menorrhagia
  • Pregnancy
  • GI bleeding inc IBD and GI cancer
  • Malabsorption – Coeliac
  • CKD
  • Hookworm infection
61
Q

Causes of jaundice

(3 categories)

A
62
Q
A

Arterial Thrombosis

63
Q

Name three common heritable thrombophilias

A

Factor V Leiden

1 in 20

Protein S deficiency

1 in 300

Protein C deficiency

1 in 300

64
Q

SEs of iron supplementation

A
  • constipation
  • dark stool
  • nausea
65
Q

When to offer iron supplementation?

A
  • 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)

66
Q

Dietary changes to increase iron

A

iron-rich diet:

  • dark-green leafy vegetables
  • meat
  • iron-fortified bread (and cereals)

+ aid vitamin C to increase absorption of iron

67
Q

Elderly pt with pain the joint

What Ix would you do first?

A
  • 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
68
Q

Pathophysiology of the hepato-renal syndrome

A
  • 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
69
Q

Management of hepatorenal syndrome

A
  • vasopressin analogues (e.g. terlipressin) →work by causing vasoconstriction of the splanchnic circulation
  • volume expansion with 20% albumin
  • transjugular intrahepatic portosystemic shunt

Y4 CCTs (14 decks)

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