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Medicine > Haematology > Flashcards

Haematology Flashcards

1
Q

Causes of macrocytic anaemia

A 
Aplastic anaemia
Myelodysplastic syndrome
Acute leukaemia (>20% blast cells)
Megaloblastic anaemia
 - Vit B12 deficiency
 - Folate deficiency
Chronic liver disease
Drugs
Hypothyroidism
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2
Q

Causes of aplastic anaemia

A 
Idiopathic
Cytotoxic drugs and radiation (cancer treatment)
Drug reaction:
 - anticonvulsants
 - antibiotics
 - NSAIDs
 - Anti-thyroids
 - Gold
Toxins
Viral (EBV, HIV)
Immune disorders (SLE, graft v host)
Miscellaneous
 - Pregnancy
 - anorexia nervosa
 - paroxysmal nocturnal haemoglobinuria
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3
Q

Diagnostic criteria for aplastic anaemia

A 
Hypocellular bone marrow with no abnormal cells or fibrosis
\+ 2 of the following:
 - Hb below 100
 - PLT below 50
 - ANC below 1.5
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4
Q

Risks of blood transfusion

A

High-moderate (1/100-1000): urticaria, fluid overload, cardiac failure
Low (1/1000-100,000): delayed haemolysis, TRALI, non-fatal acute haemolytic reaction (e.g. wrong blood)
Rare (less than 1/100000): fatal acute haemolytic reaciton, sepsis, HIV, Hep C, HTLV, malaria, syphilis

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5
Q

What is aplastic anaemia

A

Failure of bone marrow to produce enough blood cells due to reduced haematopoietic precursors due to replacement of stem cells in the marrow with fat. Leads to pancytopaenia

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6
Q

Causes of normocytic anaemia

A 
Chronic inflammatory disease
Endocrine:
 - Hypopituitarism
 - Hypothyroidism
 - Hypoadrenalism
Aplastic anaemia
Haemolytic anaemia
Acute blood loss
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7
Q

What is myelodysplastic syndrome

A

Group of haematopoietic disorders characterised by a hyper- or hypocellular marrow with impaired morphology and maturation + peripheral blood cytopaenias due to imeffective haematopoiesis - may involve all 3 lineages in myeloid haematopoiesis (RBC, PLT, PMN)
Blast cell count less than 20%

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8
Q

Presentation of myelodysplastic syndrome

A 
B symptoms: weight loss, malaise
Anaemia symptoms
Thrombocytopaenia symptoms
Neutropaenia symptoms
Symptoms of marrow failure (hyperviscosity - clots, bone pain, organ/skin infiltration, gout)
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9
Q

CBE and marrow results in myelodysplastic syndrome

A

Peripheral cytopaenias, increased MCV, dimorphic RBCs, oval shaped RBCs, hypersegmented nuclei of PMNs, hypogranular PLT
Marrow: hypercellular (usually) with dyserythropoiesis

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10
Q

Management of myelodysplastic sydnrome

A

Supportive: treat infections, transfuse PLT or RBC as needed, recombinant EPO
Cytotoxic chemo in patients with increasing myeloblasts or progression to AML

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11
Q

What is polycythaemia vera

A

It is the most common chronic myeloproliferative disorder (though still rare) characterised by predominantly raised RBCs, in addition to increased production of platelets and neutrophils.

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12
Q

Prognosis and complications of polycythaemia rubra vera

A 
Untreated: 6-18m survival
Treated: >10y
Shorter life span than general public
Complications:
 - thrombosis
 - haematological malignancy (AML, MDS)
 - non-haem malignancy
 - haemorrhage
 - post-PV myelofibrosis
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13
Q

Presentation of polycythaemia vera

A

Hyperviscosity: headache, dizziness, vertigo/tinnitus, vision disturbances, angina, intermittent claudication, major thrombotic events
H2/Cytokine prodn: peptic ulcer - abdo pain, aquagenic pruritus (40%)
Erythromelalgia (burning hands/feet + erythema/pallor/cyanosis c palpable pulses)
Early satiety (splenomegaly)
Weight loss/malaise

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14
Q

Clinical findings of polycythaemia vera

A 
Hepatomegaly
Splenomegaly
Facial plethora
Hypertension
Arthritis and gouty tophi
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15
Q

Genetic mutation associated with polycythaemia rubra vera

A

JAK2

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16
Q

Criteria for diagnosis of polycythaemia vera

A 
All of CA OR CA1+CA2+2 of CB:
Criteria A:
1. Raised total RBC mass
2. Arterial O2 >92% (not secondary to hypoxia)
3. Splenomegaly

Criteria B:

  • thrombocytosis
  • leukocytosis
  • raised ALP
  • raised Vit B
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17
Q

History of lymphoma

A 
LN enlargement - most commonly cervical nodes
B symptoms (night sweats, malaise, weight loss)
Systemic sx (pruritus, fatigue, anorexia, alcohol-induced pain at site of node)
Involvement of other organs - cough/SOB, PUD/abdo pain
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18
Q

Most common lymphomas

A

Hodgkin 3/100,000, NHL 15/100,000
HL: nodular sclerosing (70%), mixed cellularity (15%), lymphocyte-rich (5%)
NHL: 85% are B cell, 15% T-cell
DLBCL (30%), Follicular (20%), Marginal Zone [MALT] (5-10%), Mantle Cell (5%), Burkitt Cell (1-2%)

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19
Q

Histological marker of Hodgkin’s lymphoma (vs NHL)

A

Reed-Sternberg cells (“Owl-eyes” - 2 mirror image large nuclei with eosinophilic nucleolus)

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20
Q

What is Waldeyer’s ring

A

Pharyngeal/tonsillar lymphoid ring

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21
Q

International prognostic index for Non-hodgkins Lymphoma

A 
Age >60
Stage III or IV disease
Raised Serum LDH
ECOG status
>1 extranodal site
(FLIPI [follicular]: +Hb level)
(MIPI [mantle cell]: + WCC)
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22
Q

Red flags of CLL - need to refer to haem urgently

5

A
  • Rapidly rising WCC
  • Rapidly progressing lymphadenopathy or splenomegaly
  • Progressive anaemia or thrombocytopaenia
  • Recurrent life-threatening sepsis
  • Worsening constitutional symtpoms
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23
Q

What is the inheritance pattern of Glucose-6-phosphate dehydrogenase deficiency (G6PD)

A

X-linked

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24
Q

What is the role of glucose-6-phosphate dehydrogenase

A

Reduces NAPD to NAPDH which protects the cell from oxidative damage. Particularly effects RBCs because they lack other enzymes to produce NAPDH

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25
Q

What are Howell-Jolly bodies, how do you recognise them and what is the cause?

A

Remnants of the RBC nucleus. Dark round dots in the RBC cytoplasm visible without any staining. Caused by reduced splenic function

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26
Q

What are Heinz bodies, how do you recognise them and what is the cause?

A

Accumulations of denatured globin chains within the RBC, can be seen only on staining with Cresyl blue (used for reticulocyte counting)
Caused by oxidative stress, e.g. G6PD deficiency

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27
Q

Diagnostic criteria for multiple myeloma

A 
CRAB
Calcium raised
Renal insufficiency (raised creatinine)
Anaemia
Bone lesions/osteoporosis
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28
Q

Classic triad of multiple myeloma

A

Marrow plasmacytosis
Lytic bone lesions
Serum/urine M component

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29
Q

Aims for treatment in polycythemia rubra vera

A

PCV below 45%

Hb below 140

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30
Q

Cell markers for T cells

A

T helper cells: CD4

Cytotoxic T cells: CD8

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31
Q

What is produced by Th1 cells?

A

IL2 and gamma IFN

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32
Q

What is produced by Th2 cells

A

IL4, 5, and 10

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33
Q

Cause of pernicious anaemia

A

Autoimmune Disease
Anti-intrinsic factor antibodies
and
Anti parietal cell antibodies

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34
Q

Definition of sideroblastic anaemia

A

A group of inherited or acquired anaemias caused by dysfunctional metabolism of iron by the mitochondria in erythroblasts

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35
Q

Inheritance pattern of familial sideroblastic anaemia

A

X-linked

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36
Q

Causes for acquired sideroblastic anaemia

A 
Myelodysplasia
Myeloprolferative disorders
Myeloid leukaemias
Drugs (e.g. isoniazid)
Alcohol abuse
Lead
RA
Carcinoma
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37
Q

Sideroblastic anaemia on blood film

A

Excess ring sideroblasts (ring of iron granules around nucleus due to accumulation of iron in cell)

38
Q

Definition of sickle cell anaemia

A

A haemolytic anaemia caused by disorder of haemoglobin resulting from a single-base mutation: deoxygenated HbS is insoluble, thus inflexible cells - irreversible sickling due to dehydration = reduced red cell survival

39
Q

Clinical features of sickle cell anaemia

A

HbS releases O2 more readily to tissues, thus patients feel well despite being anaemic

Vaso-occlusive crises:
- dactylitis (child)
- acute pain in hands and feet
- attacks of severe bone pain (e.g. AVN)
Haemolytic anaemia
- usually stable in 60-80 range
40
Q

Cause of vaso-occlusive complications in sickle cell anaemia

A

Insoluble, rigid cells - impaired passage through microcirculation - obstruction of small vessels - tissue infarction

41
Q

Long term complications of sickle cell anaemia

A 
Reduced growth and development
 - low weight and height in childhood
- regain height by adulthood
- delayed sexual maturation
Bones:
- AVN
- compression of vertebrae
- shortening of bones
- osteomyelitis
Infections (esp. bones, lung, kidney)
Resp
- pulm HTN
- Acute chest syndrome
Leg ulcers
Cardiac
- cardiomegaly
- arrhythmias
- iron overload cardiomyopathy
- MI
Neuro:
- TIA, CVA
- seizures
- cerebral haemorrhage
Cholelithiasis
Chronic hepatomegaly and liver dysfn
Chronic tubule-interstitial nephritis
Priapism
Retinopathy
Pregnancy issues
- abortion
- IUGR
- PET
- IUFD
42
Q

Diagnosis of sickle cell aneamia

A

High reticulocyte count
Sickle cells on blood film

Hb electrophoresis: No HbA, 80-95%HbS, 2-20% HbF
Electrophoresis required for diagnosis

43
Q

Management of sickle cell anaemia

A

Hydroxyurea (increases HbF concentrations)
Inhaled NO (red. platelet function, vascular adhesion of RBCs, inc. vasodilation)
Blood transfusions (only if symptomatic e.g. CHF, TIA, aplastic crises)
Bone marrow transplantation (children under 16 with severe complications e.g. CVA, recurrent chest syndrome)

44
Q

Definition of anaemia of chronic disease

A

Anaemia caused by the insufficient release of iron from bone marrow cells to developing erythrocytes in the context of chronic inflammation

45
Q

Pathophysiology of anaemia of chronic disease

A

High levels of hepcidin expression during chronic inflammation - destroys ferroportin - reduced iron efflux from exporting tissues into plasma - reduced iron mobilisation and absorption from gut

reduced release of iron from BM to developing RBCs

46
Q

Biochemical investigations in anaemia of chronic disease

A

MCV: low normal, normal or low
Iron studies: low serum Fe, reduced total iron binding capacity, normal or increased ferritin
Bone marrow biopsy: stainable iron, iron not seen in developing erythroblasts

47
Q

Management of anaemia of chronic disease

A 
Symptomatic
Recombinant EPO (in setting of renal disease, sometimes in setting of inflammatory disease e.g. RA, IBD)
48
Q

Definition of megaloblastic anaemia

A

A macrocytic anaemia resulting from inhibition of DNA synthesis during erythropoiesis

49
Q

Causes of megaloblastic anaemia

A

VitB12 deficiency:
- vegans
- stomach pathology
- small bowel pathology
- abnormal utilisation (NO)
Folic acid deficiency
- nutritional (e.g. alcohol abuse, GI disease)
- Antifolate drugs (AEDs, MTX)
Excess utilisation
- Physiological (pregnancy, lactation, prematurity)
- Pathological (malignancy, inflammatory disease, haemodialysis, haematologic disease)
- Malabsorption
Congenital enzyme deficiencies in DNA synthesis
Drugs interfering with DNA synthesis (hydroxyurea)

50
Q

Peripheral blood smear in megaloblastic anaemia

A

Megaloblasts (large oval cells with large immature nuclei, chromatin finely dispersed and opened stippled appearance)
Polymorphs (hypersegmented 6+ lobes)
Giant metamyelocytes (2x normal size of cells, twisted nuclei)

51
Q

Management of megaloblastic anaemia

A

Transfusion not indicated
B12def:
- oral vit B12 2mg/day
- expect clinical improvement within 48h
- reticulocytosis starting after 2-3 days
- improvement of polyneuropathy over 6-12m

Folate def:
- 5mg folic acid/day

52
Q

markers of haemolysis

A 
Inc red cell production:
- reticulocytosis
- erythroid hyperplasia of marrow
Inc. red cell breakdown:
- inc. LDH
- inc. urobilinogen
- inc. plasma Hb
- Haemosiderinuria
- red. haptoglobulins
- +ve Schumm's test (methaemalbumin)
- inc K+
53
Q

Definition and types of myeloproliferative neoplasms

A

A group of disorders characterised by cellular proliferation of 1 or more haematologic cell lines in the peripheral blood, distinct from acute leukaemia

Polycythaemia vera
Essential thrombocythaemia
Primary myelofibrosis
Chronic myelogenous leukaemia

54
Q

Causes of secondary polycythaemia vera

A

EPO-ing
COPD/chronic hypoxic lung disease
high altitude`

55
Q

Management of polycythaemia vera

A

Phlebotomy
Maintenance therapy with myelosuppressive agents
- hydroxyurea, IFN a or anagrelide
- ruxolitinib (JAK1/2 inhibitor)
Prevent complications:
- daily aspirin
- allopurinol if hyperuricaemia becomes symptomatic

56
Q

Definition of essential thrombocytosis

A

A clonal disorder of unknown aetiology involving a multi-potent haematopietic progenitor cell manifested clinically by overproduction of platelets without a definable cause

57
Q

Mutations associated with essentical thrombocytosis

A

JAK2 (signalling proteins in cell)
MPL (receptor protein)
Increase activity of TPO

58
Q

Clinical features of essential thrombocytosis

A

Most often incidental finding of raised PLT on routine CBE

Haemorrhagic tendencies:
- easy bruising

Thrombotic tendencies:
- microvascular occlusions - erythromelalgia, occular migraine, TIAs

Mild splenomegaly on physical examination

59
Q

Bone marrow findings in essential thrombocytosis

A

Hypercellular marrow
Megakaryocyte hyperplasia and hypertrophy
Normal marrow reticulin - if increased, consider another diagnosis

60
Q

Complications of essential thrombocytosis

A

Intravascular stasis and thrombosis

Haemorrhage secondary to acquired Von Willebrand deficiency

61
Q

Management of essential thrombocytosis

A

Patient-based, not PLT-based
Migraine-related symptoms only respond to lowering PLT
Erythromelalgia responds to COX-1 inhibitors (aspirin, ibuprofen)
No therapy required in asymptomatic patient without CVS risk factors

Platelet reduction due to refractory symptoms on salicylates:

  • IFNa
  • Anagrelide
  • Hydroxyurea

Evolution to leukaemia is more likely to occur due to management (hydroxurea) than from the disease itself

62
Q

Definition of primary myelofibrosis

A

Clonal disorder of a multipotent haematopoietic progenitor cell characterised by marrox fibrosis, extramedullary haematopoiesis and splenomegaly

63
Q

Clinical features of primary myelofibrosis

A

Often asymptomatic, incidental discovery of splenomegaly or abnormal CBE

Night sweats
Fatigue
Weight loss
Splenomegaly
\+/- hepatomegaly
No lymphadenopaty
depending on degree of extremedullary haematopoiesis:
- ascites
- intracranial HTN
- intestinal or ureteral obstruction
- pericardial tamponade
- spinal cord compression
- skin nodules
64
Q

Peripheral blood film and biochem in myelofibrosis

A

Features of extramedullary haematopoiesis:
- teardrop-shaped RBCs
- nucleated RBCs, myelocytes and promyelocytes
+/- myeloblasts

Inc. LD
Inc. ALP

Bone marrow usually inaspirable due to fibrosis

65
Q

Management of myelofibrosis

A

No specific treatment
Allogenic bone marrow transplant is only curative treatment (consider in younger patients)
Splenectomy may be necessary if impairs feeding
Allopurinol to control hyperuricaemia
Hydroxyurea to control organomegaly
Glucocorticoids to control constitutional symptoms and AI complications
Transfusion for severe anaemia

66
Q

Complications of myelofibrosis

A

Increasing marrow failure
Shorter survival than patients with PV or ET
10% spontaneously transform to aggressive acute leukaemia

67
Q

Definition of CML

A

A myeloproliferative disease characterised by infiltration of the blood, bone marrow, and other tissues by neoplastic cells of granulocytic cell line

68
Q

Epidemiology of CML

A

20% of all adult leukaemias
85% diagnosed in chronic phase
Middle aged individuals (45-55y)
5 year survival 90% with imatinib

69
Q

Mutation associated with good prognosis in CML

A

Philadelphia chromosome

BCR-ABL1 relocation mutation from long arm of 22 to chromosome 9

70
Q

Phases of CML

A
  1. Chronic:
    - insidious onset
    - fatigue, malaise, anorexia, weight loss
    - symptoms of anaemia
    - symptoms of splenomegaly (early satiety, LUQ pain or mass)
    - vasoocclusive disease
  2. Accelerated and 3. Blastic:
    - unexplained fever
    - sig. weight loss
    - bone and joint pain
    - bleeding
    - thrombosis
    - infections

Splenomegaly
Hepatomegaly
Lymphadenopathy a poor prognostic indicator in late disease

71
Q

Confirming CML

A

CBE: inc. WCC, inc. PLT, normocytic normochromic anaemia, low leukocyte alkaline phosphatase
Film: circulating immature cells
Biopsy: hypercellular, inc Myeloid:erythroid ratio
Chromosomal studies: philadelphia chromosome (FISH)

72
Q

Management of CML

A

IMATINIB 400mg daily
- competitive inhibition at ATP-binding site of Abl-knase - inhibits tyrosine phosphorylation of proteins involved in BCR-Abl signal transduction - prevents activation of downstream pathway in cellular proliferation

S/E: fluid retention, nausea, muscle cramps, diarrhoea, skin rashes, myelosuppression

Second line (in addition to imatinib)
- Allo-HSCT
- nilotinib, dasatinib
Chemotherapy
- reserved for rapid lowering of WCC initially
- hydroxyurea
73
Q

definition of AML

A

A rapidly progressing excess of myelocytes in the blood due to an uncontrolled proliferation of leukaemic stem cells in the bone marrow. It is characterised by an excess of immature precursor cells in both the blood and the bone marrow

74
Q

Epidemiology of AML

A

most common in infants less than 1y and people over 60y
Untreated survival is less than 3m
Accounts for 70% of acute luekaemias
3/100,000

75
Q

What is a granulocytic sarcoma

A

AML as a discrete lump
Biopsy reveals many blastic neutrophils
Leukaemic cells are not in circulation, but accumulated in specific sites
Same treatment as for AML

76
Q

Clinical features of AML

A 
Bone marrow failure:
- anaemia
- neutropenia (infection)
- thrombocytopaenia (haemorrhage)
Increased WCC:
- hyperviscosity
- organ infiltration
- bone pain
- gout/hyperuricaemia
Constitutional symptoms
DIC
gum infiltration
77
Q

Peripheral blood smear in AML

A 
Granules
Auer rods (linear red composigion of crystallised  granules)
78
Q

APML blood smear

A

Multitude/bundle of auer rods (faggot bundles

79
Q

APML

A

Type of AML with high cure rates BUT high mortality in early stages - must treat very early
Associated with significant DIC

80
Q

CLL staging

A

Rai Staging system:

0: low risk - lymphocytosis ONLY
1: intermediate risk: lymphocytosis + lymphadenopathy
2: intermediate risk: lymphocytosis + hepatomegaly or splenomegaly
3: high risk: lymphocytosis + anaemia, normal platelets
4. High risk: lymphocytosis + thrombocytopaenia

Binet staging:
According to number of lymphoid tissues involved
A: less than 3 areas of enlarged lymphoid tissue
B: 3 or more areas of enlarged lymphoid tissue
C: Patients with anaemia or thrombocytopaenia regardless of lymphadenopathy

81
Q

Definition of lymphoma

A

Abnormal proliferation of the lymphoid system, occurring at any site where lymphoid tissue is found, classified as Hodgkin’s or non-Hodgkin’s based on histological appearance

82
Q

Epidemiology of Hodgkin’s lymphoma

A

Peak incidence in 20s
Male:female almost equal
3/100,000

83
Q

Prognostic factors for Hodgkin’s lymphoma

A

Hasenclever score: based on

  • serum albumin
  • Hb
  • age
  • sex
  • stage
  • leukocytosis
  • lymphopaenia
84
Q

Diagnostic investigations in multiple myeloma

A 
Urinalysis
-high protein, little albumin
- urinary light chains
- Bence jones proteins (light chains/paraproteins)
Biochemistry:
- reduced anion gap
- high Ca
- inc. BUN
- inc. Cr
- inc. uric acid
SERUM PROTEIN ELECTROPHORESIS: IgG, paraproteins
CBE: normocytic anaemia
Marrow biopsy: Plasmacytosis (over 10%)
Chest and bone XR: lytic lesions, diffuse osteopaenia
Immunoelectrophoresis: M spikes
Serum beta crosslaps: marker of bone breakdown (target in therapy less than 400)
85
Q

Management of multiple myeloma

A

Initial management:
- manage anaemia (t/f), renal failure (hydrate, dialysis), infections (ABx)
- bony lesions: analgesia, radiation, vertebroplasty, bisphosphonates
Autologous stem cell transplant
High dose CTx

86
Q

Definition of hereditary haemochromatosis

A

An inherited disorder of iron metabolism, most commonly due to a mutation in the HFE gene

87
Q

Clinical features of haemochromatosis

A 
Mostly asymptomatic
Nonspecific symptoms:
- weakness
- fatigue
- lethargy
- weight loss
Specific, organ related:
- abdominal pain
- arthralgias
- chronic liver disease stigmata
88
Q

Complications of haemochromatosis

A

Deposition in a number of different organs:

  • Liver: cirrhosis, HCC
  • Heart: CHF, cardiac arrhythmias
  • Endocrine: hypogonadism, DM, thyroid dysfunction
  • Joints: arthroplasty
89
Q

Laboratory findings in disseminated intravascular coagulation

A 
Thrombocytopaenia
Prolonged PT, APTT and TT
Increased fibrin degradation products
Reduced fibrinogen level
Fragmented RBCs
90
Q

serotonin release assay is testing for

A

heparin induced thrombocytopaenia

Medicine (12 decks)

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