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Year 5 Conditions > blood > Flashcards

blood Flashcards

1
Q

what causes microcytic anaemia

A

iron deficiency

thalassaemia

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2
Q

what causes normocytic anaemia

A

acute haemorrhage

anaemia of chronic disease

  • chronic inflammationa
  • chronic infection
  • malignancy
  • inc ferritein

aplastic anaemia (bone marrow failure)

  • idiopathic
  • Fanconi’s anaemia
  • hepatitis - treatment induced
  • drugs eg NSAIDs

Haemolytic anaemia

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3
Q

what causes macrocytic anaemia

A

megaloblastic (large, structurally abnor, immature cells)

  • Vit B12 deficiency
  • folate deficiency

Non-megaloblastic

  • pregnancy
  • alcohol
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4
Q

what value of MCV is microcytic anaemia

A

MCV < 80

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5
Q

what value of MCV is macrocytic anaemia

A

MCV > 100

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6
Q

defintion of anaemia?

A
  • Men  Hb < 130
  • Non-pregnant women >15 yrs old – HB < 120
  • pregnant women  HB < 110 throughout pregnancy
  • postpartum - < 100
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7
Q

aetiolgy of IDA

A
  • Dietary deficiency - really of course on its own
  • malabsorption  Coeliac disease, H pylori, achlorhydria (absence of hydrochloric acid in the stomach), pica, hiatal hernia
  • Chronic blood loss – GI loss, menstruation, UC
  • increase requirement – menstruation, pregnancy
  • Other courses : blood donation, self-harm, nosebleed and NSAIDs, aspirin, parasites, hookworms
  • Iron is absorbed in a duodenum and an upper jejunum
  • IDA is not an end diagnosis and will need further investigation
  • blood loss = most common cause of IDA
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8
Q

symptoms of IDA

A 
fatigue 
palpitations 
dyspnoea 
cognitive dysfunction 
restless leg syndrome
vertigo
tinnitus 
puritis 
score tongue 
pica - abnor dieary craving eg dirt
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9
Q

signs of IDA

A

angular cheilosis

pallor

atrophic glossitis (smooth glossy tongue)

dry rough skin and damaged hair

hair loss

koilonychia
systolic flow murmur

heart failure

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10
Q

ix for IDA

A
  • FBC  low haemoglobin
  • MCV < 80
  • MCH (mass per cell)< 27.5
  • MCHC (HB conc. per cell) – low
  • reticulocyte count (amount of youngest blood cells present)
  • blood film  microcytic + hypochromic cells
  • serum ferritin – dec (< 15 = diagnostic)
  • serum iron  low
  • total iron-binding capacity (TIBC) – inc
  • transferrin saturation (serum iron x 100/TIBC) – low
  • coeliac serology
  • H.pylori testing
  • IBD screening
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11
Q

mx of IDA

A

• address underlying cause
o Stop NSAIDs
o treat H.pylori
o treat menorrhagia
o maintain and adequate balanced intake of iron rich food – dark green vegetables, meat, apricots)
• oral ferrous sulfate 200mg table BD/TDS  continue for 3 months after iron deficiency is corrected to allow iron stores to be replenished
o SE – constipation, diarrhoea, black stool
o can also add ascorbic acid (to help absorb non-haem iron in plants and diary required asset for digestions of iron)
• consider transfusion if symptomatic at rest

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12
Q

definition of acute non-haemolytic reactions during transfusion

A

• And that first reaction to a blood transfusion which is not because of blood group incompatibility
• can be acute (24 hours) or delayed
•

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13
Q

what are the different types of acute non-haemolytic reactions during transfusion

A

o anaphylaxis
o Bacterial contamination
o Lung  Transfusion related acute lung injury (TRALI), Transfusion associated circulatory overload (TACO), Transfusion Associated Dyspnoea (TAD)
o Febrile non-haemolytic transfusion reaction

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14
Q

which type of acute non-haemolytic reactions (ANHRT) during transfusion is the most common

A

TRALI

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15
Q

pathophysiology of TRALI

A

occurs as a result of granulocyte activation in the pulmonary vasculture –> resulting in inc vascular permeability

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16
Q

clinical features of anphylactic reaction in ANHRT

A
  • Allergic reaction when patient has antibodies that react with proteins in the transfused blood
  • Occurs when a person has been previously sensitised to an allergen present in blood and on re-exposure, release immunoglobulins (IgE and IgG antibodies)
  • Occurs within 15 minutes
  • Dyspnoeic (bronchospasm and laryngeal odema), chest pain, abdominal pain and nausea, urticaria, hypotension, angioedema, tongue swelling, wheeze
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17
Q

clinical features of bacterial contamination in ANHRT

A
  • Infective shock
  • Occurs within 15 minutes
  • Acute onset hypertension or hypotension, rigors and collapse
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18
Q

clinical features of TRALI in ANHRT

A

ARDS due to donor plasma containing antibodies against patient’s leukocytes

occurs within 6 hours

sudden dyspnoea, prominent non-productive cough, hypoxia, can have frothy sputum

fever and rigors

hypotension

CXR - bilateral infiltration

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19
Q

clinical features of TACO in ANHRT

A

occurs within 6 hours

  • sudden dyspnoea
  • hypoxemia
  • raised BP/JVP
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20
Q

clinical features of TAD in ANHRT

A

breathing difficulties because of blood products - not hypertension/hypotenison

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21
Q

clinical features of febrile non-haemolytic transfusion reaction in ANHRT

A

• Fever and rigors during RBC and platelet transfusion due to platelet antibodies to transfused white cells.

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22
Q

investigation for ANHRT

A

FBC, U&Es, LFT, coag screen

first urine sample (haemoglobin)

repeat G&S

IgA level –> needs pre and post transfusion sample

serial mast cell tryptase at ime 0, 3, 24 horus

blood cultures

consider CXR if hypoxia

blood gases with hypoxia

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23
Q

mx for bacterial contamination in ANHRT

A

stop transfuison
FBC + bloodcultures

supportive measures - O2, fluid, consider ionotropic support if BP consistentialy low

  • Start broad spectrum abx + follow local SEPSIS pathway
  • Refer to haematology/ intensive care unit.
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24
Q

mx for anaphylactic reactions in ANHRT

A
  • Follow anaphylaxis guidelines
  • IM Adrenaline (epinephrine) 500 micrograms 1: 1000 intramuscularly (IM) and repeat every 5 minutes
  • 10mg IV Chlorphenamine and 200mg IV hydcortisone
  • Oxygen, fluids, salbutamol nebulisers (if required)
  • Call anaesthetist if difficulty maintaining the airway
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25
Q

mx for TRALI in ANHRT

A
  • Stop transfusion
  • Seek expert advice immediately
  • Oxygen, fluids, inotropes (as for acute respiratory distress syndrome)
  • Monitor blood gases and serial CXR
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26
Q

mx for TACO in ANHRT

A

• Assess patient and slow or stop transfusion
• Treat as for HF: Oxygen + IV furosemide
TAD

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27
Q

mx for TAD in ANHRT

A
  • Assess patient and slow or stop transfusion

* Symptomatic management.

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28
Q

mx Febrile non-haemolytic transfusion reaction for in ANHRT

A
  • Assess patient and Stopping/ slowing transfusion

* paracetamol

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29
Q

what are the 2 main types of macrocytic anaemia

A

megaloblastic
- B12 and folate deficiency

non-megaloblastic
- liver disease, alcohol, hypothyroidism

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30
Q

how is B12 absorbed in the body

A

 B12 released from food in the stomach by peptic acid  parietal cells at the gastric fundus produce intrinsic factors  intrinsic factors binds B12 to form a complex  travels to the terminal ileum  binds to transcobalamine (made in liver) blood stream

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31
Q

aetiology of Vit B12 anemia

A

pernicious anemia, HIV, diet deficiency, Crohn’s

drugs - metformin, PPI, H2 recepor antagonist, anticonvulsant

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32
Q

aetiology of folate deficiency leading to anaemia

A

malabsoprtion, dietary dificiency

drug - trimethoprim/nitrifurantoin

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33
Q

clinical features of macrocytic anaemia

A
  • Typically, asymptomatic
  • symptoms of anaemia  dyspnoea, pallor, lethargy, petechiae, glossitis, angular chilitis, cognitive impairment

• B12 (present as neuropsychiatric, peripheral neuropathy and haematological
o paraesthesia, ataxia, loss of vibration sensation
o peripheral neuropathy
o subacute degeneration of the spinal cord – triad of upgoing planters, loss of knee jerk, loss of ankle jerk
o Romberg’s test  loss of proprioception

•	Folate 
o	prolonged diarrhoea
o	headache
o	loss of appetite and weight loss 
o	tachycardia 
o	tachypnoea 
o	heart murmur 
o	signs of heart failure 
o	signs of chronic alcohol abuse
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34
Q

investigation for macrocytic anaemia

A
  • FBC  low Hb, high MCV/MCH
  • blood film  hyper-segmented, polymorphonucleated cells + oval macrocytes
  • serum B12/folate – dec
  • serum cobalamin (cobalamin = B12, diagnostic marker for Vit B12 deficiency)  dec
  • serum methylmalonic acid (inc in Vit B12 deficiency) & homocysteine (inc in B12, folate and hypothyroidism)  elevated
  • reticulocyte count  used to differentiate between B12 deficiency from haemolytic anaemia
  • intrinsic factor antibody  used to differentiate between Vit B12 deficiency or pernicious anaemia  +ve if pernicious anaemia
  • antiparietal cell antibody  used to differentiate between Vit B12 deficiency or pernicious anaemia  +ve if pernicious anaemia
  • LFT, GGT, TFT – identify causes
35
Q

management for macrocystic anaemia

A

If Neurological involvement
• Seek urgent hematology advice
• If expert advice unobtainable give hydroxocobalamin 1 mg intramuscularly on alternate days until there is no further improvement, then administer hydroxocobalamin 1 mg intramuscularly every 2 months.

No-neurological invovlment

Initial
• Initially administer hydroxocobalamin 1 mg intramuscularly 3 times a week for 2 weeks

Maintenance
• Non-diet related; administer hydroxocobalamin 1 mg intramuscularly every 2–3 months for life.
• Diet related: oral cyanocobalamin tablets 50–150 micrograms daily between meals, or have a twice-yearly hydroxocobalamin 1 mg injection. + dietary advice (eggs, meat, milk and dairy, salmon)

36
Q

complication of B12 deficiency

A

o Loss of cutaneous sensation, lots of mental and physical drive, muscle weakness, optic neuropathy, psychiatric disturbance (mild neurosis to severe dementia)

o symmetrical neuropathy affecting the legs more than the arms - usually present with ataxia or paraesthesia

o urinary or faecal incontinence

37
Q

Definition of haemolytic anaemia

A

• a number of conditions resulting to premature destruction of RBCs

38
Q

what are the different types haemolytic anaemia

A

inherited –> membrane effects, abnor HB production, enzyme defects

acquired –> immune/non-immune

39
Q

clinical features of haemolytic anaemia

A
  • Anaemia symptoms: SOB, palpitations, tachycardia, angina, pallor, fatigue, light-headedness
  • Splenomegaly: spleen becomes filled with destroyed RBC
  • Jaundice: bilirubin release from RBC destruction
  • Episodic dark urine  haemoglobinuria  suggestive of paroxysmal nocturnal haemoglobinuria
40
Q

Ix for haemolytic anaemia

A
  • FBC  low Hb & normocytic
  • MCHC  inc in spherocytes and reticulocytes
  • reticulocyte count  inc
  • blood film  identifies causes eg if spherocytosis and elliptocytosis
  • LDH  LDH inc + dec haptoglobin = 90% chance of haemolytic anaemia
  • hepatoglobin (binds to free HB)  low
  • direct coombs’ test (detect IgG or complement bound to RBC cell surface) +ve autoimmune haemolytic anaemia
  • inc bilirubin and urobilinogen
41
Q

Mx of haemolytic anaemia

A
  • administer folic acid due to risk of deficiency
  • discontinue medications that may precipitate or aggravate haemolysis.
  • Avoid transfusion unless necessary
  • Iron therapy may be indicated for intravascular causes
  • Autoimmune haemolytic therapy: corticosteroid or rituximab + intravenous immunoglobulin (IVIG)
  • Splenectomy (remove site of significant antibody production and site for RBC destruction)
  • Plasmapheresis – similar to dialysis but for the removal of antibodies in the blood.
42
Q

what cells do lymphoma affect?

A

B and T lymphocytic cells

43
Q

what cells does Hodgkin’s lymphoma affect

A

B cells only

44
Q

what cells does non- Hodgkin’s lymphoma affect

A

2 words = 2 cells

cab be B or T cells

45
Q

what can cause Burkitt lymphoma

A

EBV, HIV & malaria

46
Q

symptoms of Burkitt’s lymphoma

A

larg abdo mass and symptoms of bowel obsturction

47
Q

what can cause mucosa associated lymphoid tissue lymphoma (MALT)

A

H.pylori infection

48
Q

symptoms of MALT?

A

usually around the sotmahc

49
Q

what is the key symtpom of diffuse large B cell lymphoma

A

painless rapid growing mass in > 65

50
Q

aetiology of hodgkin lymphoma

A

unclear, EBV, glandular feer?

51
Q

aetiology of non-hodgkin lymphoma

A

o HIV, EBV, H.pylori, Hep B/C, exposure to pesticides, FHx, Herpes virus 8
o Sjogren’s syndrome, RA, SLE and coeliac disease
o immunodeficiency state eg post-organ transplant

52
Q

epidemiology of lymphoma

A
  • Hodgkin lymphoma – bimodal age distribution (20 and 75)

* Non-Hodgkin lymphoma – 5 times as common as Hodgkin lymphoma, common > 50.

53
Q

clinical features of lymphoma

A

• both Hodgkin/non-Hodgkin
o lymphadenopathy  cervical, axilla, inguinal, non-tender and rubbery often alcohol induced pain
o B symptoms  cyclic fever, weight loss, night sweats
o fatigue, itching, cough + SOB (mediastinal mass), abdo pain, recurrent infections
o splenomegaly, hepatomegaly, bone marrow infiltration
o SVC syndrome  extensive mediastinal adenopathy can compress the SVC leading to dyspnoea, cough, orthopnoea and facial and upper extremity oedema and ilated neck veins

54
Q

what staging is used for lymphoma

A

Ann arbour staging

55
Q

Ix for lymphoma

A

o FBC with differentials pancytopenia if bone marrow infiltration
o lymph node biopsy
 hodgkin’s lymphoma  Reed-sternberg cell
o blood film
 non-hodgkin lymphoma  nucleated RBC, left shift
o skin biopsy  T cells in NHL
o LFTs – LDH (raised) and albumin (low) but nonspecific
o serology for HIV, EBV, Heps virus 8
o CXR/CT/PET/MRI – stage cancer
o bone marrow biopsy – see if bone marrow infiltration took place
o ESR = prognostic factor

56
Q

mx for lymphoma

A
  • chemo +/- radiotherapy for both

* NHL  R-CHOP-21 (rituximab + cyclophosphamide+ doxorubicin + vincristine + prednisolone for 21 days)

57
Q

definition of myeloma

A

it is cancer of monoclon cells (which is a subtype of B cells that produces immunoglobulin) –> leeds to production and over-secretion of immunoglobulin into serum and urine

58
Q

what is the most common subtype of myeloma

A

IgG myeloma = most common

59
Q

RF for myeloma

A 
? 70 yrs old 
male 
black 
FHx 
obesity
60
Q

clinical features of myeloma

A

• Cancerous plasma cells invade the bone marrow.
• This leads to suppression of the development of other blood lines:
o Myeloma bone disease = bone pain

  • MM cells secrete osteoclast activating factors → This results in osteolytic lesions → subsequent pathological fractures
  • Hypercalcemia: bone resorption from osteoclasts incerasse serum calcium levels.

• Myeloma renal disease
o High levels of immunoglobulins (antibodies) can block the flow through the tubules AND Hypercalcemia hard to clear by the kidneys
o Failing kidney can’t produce EPO (anaemia – fatigue, SOB)
• Raised plasma viscosity (due to high proteins in the blood)
o Easy bruising
o Easy bleeding
• Reduced or loss of sight due to vascular disease in the eye
• Heart failure
• Stroke

61
Q

investigation of myeloma

A

FBC - normocytic, normomcgromic anaemia, low WBC, low platelets

blood films

U&Es –> kidney is affect, inc Ca2+

ALP - bone involvment

ESR - raised

plasma viscosity

serum/urine electrophoresis - paraprotein spikes (Bence-JOnes protein)

serum free light chain assy - inc conc of free light chain

serum immunoglobulins - elevated

serum albumin - elevated

skeletal survery - osteopenia, osteolytic lesion, pathological fractures

  • whole-body, low dose computed tomography (WBLD-CT)  osteolytic lesions
  • x-ray  pepper-pot skull, due to lytic lesions throughout the skull
62
Q

mx for myeloma

A 
•	MDT – oncology + haemoatology 
•	1st line  proteasome inhibitors  bortezomib 
•	stem cell transplant 
•	immunomodulatory drugs 
•	chemo 
•	monoclonal antibodies
•	symptoms control 
o	EPO transfusions 
o	VTE prophylaxis 
o	bone disease management 
	Bisphosphonates – reduce osteoclast activity (beware of jaw necrosis – must have dental review prior to starting) 
	NSAIDS 
	radio 
	orthopedi surgery 
	cement augemntations
63
Q

what is DIC

A

Disseminated Intravascular Coagulation

• A syndrome characterised by the systemic activation of blood coagulation, which generates intravascular fibrin, leading to thrombosis of small and medium sized vessels and eventually organ dysfunction. As clotting factors are exhausted haemorrhages occur.

64
Q

aetiology of DIC

A

infection
malignancy - leukaemia
trauma

pregnancy related issues –> placental abruption, amniotic fluid embolism, severe hypertension/ eclampsia and HELLP syndrome

incompatible blood group

liver disease

pancreatitis

dissecting aortic aneurysm

65
Q

clinical features. ofDIC

A 
•	bleeding from at least 3 unrelated sites is typical and likely sites incl 
o	ear, nose, throat 
o	GI tract
o	resp tract 
o	site venepuncture 
•	confusion or disorientation 
•	fever 
•	signs of haemorrhage 
•	signs of ARDS 
•	skin signs 
o	Petechiae, Purpura, Haemorrhagic bullae, Acral cyanosis, Skin necrosis, Sings of thrombosis, Localised infarction and gangrene
66
Q

ix for DIC

A
  • platelet – low
  • prothrombin time – prolonged
  • fibrinogen – dec
  • D-dimer/fibrin degradation products – elevated
67
Q

mx of DIC

A
  • A-E assessment
  • treat underling disorder
  • platelet + FFP
68
Q

pathophysiology of Sickle cell Disease

A

autosomal recessive disease - when gene codes for beta chin of HB is abnormal

69
Q

what are 4 urgent/acute diseases which can occur in Sickle Cell DIsease

A

• Vaso-occlusive crises (ribs, spine, pelvis)
o Sickle cells clogging capillaries causing distal capillaries
o Pain, dactylitis, fever, priapism (painful and persistent erection)
• Splenic sequestration crisis (MEDICAL EMERGENCY)
o Sickle cells clogging blood flow to the spleen
o Splenomegaly and painful spleen,
o Pooling of blood in the spleen leads to severe anaemia and circulatory collapse.
• Aplastic crisis
o Temporary loss of the creation of new blood cells: triggered by parvovirus B19.
o Anaemia – pallor/fatigue, tachycardia + jaundice (lemon tinge)
• Acute Chest Syndrome (MEDICAL EMERGENCY)
o Fever, chest pain, dyspnoea, tachypnoea
o New filtrates seen on chest x-ray.

70
Q

investigation for Sickle cell disease

A
  • Refer to hematology
  • Newborn help prick test at 5 days of age.
  • Blood film: sickle cells and target cells
  • ↑ bilirubin and reticulocytes
71
Q

management of chronic sickle cell disease

A
  • Avoid triggers for crises e.g. dehydration, cold, infections
  • Folic acid, Abx prophylaxis, vaccinations, hydroxycarbamide (frequent painful crisis)
72
Q

management of sickle cell crisis

A 
o	Supportive – O2
o	X match blood  - Transfusion if Hb falls quickly
o	Analgesia
o	IV fluids
o	Abx
73
Q

pathophysiology of hemophilia

A

X-linked recessive

74
Q

which factor is affected in haemophilia A

A

factor 8

75
Q

which factor is affected in haemophilia B

A

factor 9

76
Q

clinical features of haemophilia

A
  • neonatal intracranial haemorrhage  severe
  • hemarthrosis  bleeding into joint
  • IM bleed
  • excessive bruising upon learning to crawl and walk
  • epitasis
  • blood in urine
  • blood in stool
  • deep bruises
77
Q

investigation for haemophilia

A

• Activated partial Thromboplastin time (aPTT) – inc
o use to test intrinsic pathway
• Factor 8 assay or 9 – level dec
• normal prothrombin time
o use to test extrinsic and common pathway
• plasma von Willebrand factor assay – normal to exclude VWF deficiency
• other factors assay – to exclude problems elsewhere
• FBC – normal, low after bleeding
• LFT – factor deficit can be caused by liver disease
• FHx or carrier – test baby’s gender from 9 wks, if male: plan safe delivery
o can do amniocentesis or CVS to confirm diagnosis
Management

78
Q

management of ahaemophilia

A

o Avoid NSAIDs and IM injections
o Regular or prophylactic factor replacement therapy  to those with severe haemophilia
 Haemophilia A every 48hrs, for haemophilia B 2x week
 Implantable port (from 2yrs) at home
o Minor bleeding – eg minor surgery/dential extraction
 Pressure, elevation
 IV desmopressin (0.3µg/kg/12hrs over 20min) to factor 8
 desmopressin does not work in Hemophilia B
o Major bleeding (haemarthrosis etc.)
 Aim to factor 8 to 50% of normal
o Life-threatening bleeding (e.g., airway obstructing)
 Need 100% levels factor 8 (recombinant factor 8)
o PRICE

79
Q

pathophysiology of thalaessmia

A
  • autosomal recessive
  • inherited microcystic anaemia caused by mutations of the beta-globin gene leading to dec or absent synthesis of beta-globin  ineffective erythropoiesis.
80
Q

where is thalassemia most common

A

-thalassaemia most common; Southeast Asian, middle east, Mediterranean backgrounds.

81
Q

clinical features of thalassemia

A

• Severe haemolytic anaemia
• Compensatory BM hyperplasia  characteristic overgrowth of facial + skull bones
• Haemosiderosis (iron overload) + cardiomyopathy, DM + skin pigmentation due to repeated blood transfusion.
o Less common since intro of desferrioxamine
• lethargy, abdo distension, FTT, low height and weight
• pallor
• spinal changes (iron overload osteopenia)
• hepatosplenomegaly

82
Q

investigation for thalaessemia

A

• Hypochromic, microcytic anaemia in thalassaemia trait may be confused with iron def.
• Homozygous: severe hypochromic microcytic anaemia, bizarre fragmented poikilocytes and target cells.
• Diagnosis of type: Hb electrophoresis.
o ß-thalassaemia major: absence of HbA1, HbA2 + HbF
o normal ferritin

83
Q

management of thalaessemia

A

• Thalassaemia trait requires no treatment.
• Thalassemia major: regular blood transfusions to maintain Hb levels.
o Haemosiderosis (iron overload) is inevitable consequence, can minimise by use of SC/IV infusions of chelating agent desferrioxamine.
o Or PO iron chelating agents

Year 5 Conditions (19 decks)

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