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Phase 2 mine > Cardiovascular diseases 2/haematology > Flashcards

Cardiovascular diseases 2/haematology Flashcards

1
Q

What indicates sinus rhythm?

A

P wave followed by QRS complex

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2
Q

How long should P wave be?

A

no more than 120mx / 3small squares

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3
Q

How tall should a p wave be?

A

3small squares

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4
Q

How long does a large square represent?

A

400ms

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5
Q

How can heart rate be calcuated?

A

300 by no of large squares for one beat

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6
Q

How long should PR interval be?

A

From 120ms to 200ms

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7
Q

What can cause an abnormality of axis?

A

left anterior fascicular block, left bundle branch block, left ventricular hypertrophy for left, Right axis can be caused by left posterior fascicular block, right heart hypertrophy/strain

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8
Q

Where should the direction of P waves be specific?

A

In I II V2-V6 positive and can be biphasic in V1 negative in aVR

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9
Q

What does tall p wave mean?

A

right atrium enlargment or notched broad is left atrial enlargment.

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10
Q

What is different morphology p wave show?

A

Non SA node focus

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11
Q

What can a long PR interval mean?

A

AV node disorder and conducting tissue

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12
Q

What does short PR interval mean?

A

Wolf-parkinson- white and preexcitiation or just young patients

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13
Q

What should the length of QRS be?

A

3 small squares 120ms or less

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14
Q

What might give broad QRS?

A

Ventricular conduction delay or bundle branch block or pre-excitation

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15
Q

What is a cause of small QRS?

A

obese patient pericardial effusion and infiltrative cardiac disease

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16
Q

Tall QRS complexes?

A

left ventricular hypertrophy or a thin patient

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17
Q

How should QRS change through V1-V6?

A

Negative S wave transitioning to poitive R wave by V6

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18
Q

How long shold QT interval?

A

It depends on the heart rate

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19
Q

What can cause QT change?

A

Electrolyte disturbances or drugs as well as some inherited disorders

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20
Q

What is importance of ST?

A

ST elevation or depression can be a sign of MI, early repolarisation pericarditis or endocarditis

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21
Q

What height should T be?

A

Half of QRS or less

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22
Q

where should T be positive or negative?

A

T should be inverted in aVR and III inversion in other leads can be MI strain or disease

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23
Q

Where should there be no q waves?

A

I,II, V2-V6

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24
Q

What are the types of tachycardia?

A

Atrial fibrilation, Atrial flutter, Supraventricular tachycardias, ventricular tachycardia or ventricular fibrilation

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25
Q

What are supraventricular rhythm features?

A

Narrow QRS, Can be flutter sawtooth or irregular p waves which is fibrillation

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26
Q

What shows a ventricular rhythm?

A

Doesnt use his purkije so has broad QRS complex can be regular or random fibrulation

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27
Q

What can cause bradycardias?

A

Conduction tissue fibrosis, ischaemia, inflammation of infiltration disease or drugs

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28
Q

What is first degree AV heart block?

A

When PR interval is longer than normal as conduction issues

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29
Q

What is second degree AV heart block?

A

Some P waves don’t cause QRS has ratio 2:1 3:1 etc

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30
Q

What is third degree AV block?

A

none of waves get to the ventrals so very slow rate as set by ventricular pacemaker cells

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31
Q

What is mobitx type 1 heart block?

A

type of 2nd degree gradually prolonging PR increasing then get a missed one

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32
Q

What is mobitz type 2 heart bloc?

A

2nd degree heart block where PR is same length just sometimes doesnt get conducted

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33
Q

What is the left bundle branch block?

A

The left bundle is not activating as fast and right is activated first then contraction passes from right to left passively

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34
Q

Which leads are important in bundle branch block?

A

V1 and V6

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35
Q

What shows left bundle branch block?

A

Broad QRS in v1 and v6 WiLLiam W shape in V1 M shape in V6

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36
Q

What happens in right bundle branch block?

A

The left bundle activates and the current passes passively to right bundle.

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37
Q

What does right bundle branch block look like?

A

MoRRoW V1 has M shape in QRS and V6 has W shape

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38
Q

What are signs of ischaemia or infarction?

A

T wave flattening or inversion ST segment depression followed b ST elevation and Q waves show old infarction

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39
Q

What will hyperkalaemia do to an ECG?

A

Tall tented T waves, flattening of P QRS broadening then eventually sine wave pattern

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40
Q

What will hypokalaemia do?

A

Flattenin of T wave, QT prolongation

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41
Q

What does hyper/hypocalcaemia do to ECG?

A

QT shortening for hyper and QT lengthening for Hypo

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42
Q

Where are red blood cells produced?

A

In the bone marrow

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43
Q

What are erythroblasts?

A

They are cells with a nucleus,

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44
Q

What are reticulocytes?

A

RBC without nucleuse not fully formed but do produce proteins like haemoglobin still

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45
Q

What controls erythropoeise?

A

Erythropoetin produced by kidneys also thryroid hormne testosterone and levels or iron folate and B12

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46
Q

What affects RBC production most?

A

Erythropoetin

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47
Q

What affects haemoglobin binding to oxygen/

A

Temperature 2,3 DPG, pH CO

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48
Q

What defines anaemia?

A

Levels of haemoglobin in blood for men 135-175g/L 120-160g/L for women

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49
Q

What are the types of haemoglobin?

A

Adult A and A2, foetal HbF, embryonic rtland and gower

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50
Q

When does foetal haemoglobin levels drop?

A

Just prior to birth and all by 9 months

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51
Q

Where is haemoglobin inherited from?

A

Alpha chains 4 genes from 16 and on chromosome 11 2 genes

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52
Q

What are types of haemoglobinopathies?

A

quantitative defect and qualitative

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53
Q

What are thalassaemias?

A

Common can be asymptomatic or life threatening, low or absent priduction of a chain type

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54
Q

What are the problems in thalassaemias?

A

The Haemoglobin isn’t formed properly so lots of RBC are destroyed inbone marrow or lysed in blood so haemolytic anaemia

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55
Q

What are the teypes of thalasaemias?

A

Alpha is deletion beta is mutation

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56
Q

Where are thalasaemias most common?

A

Africa and asia SEA, East mediterranian

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57
Q

What is inheritance pattern of Alpha thalassaemia?

A

Varied as need several missing to get symptoms

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58
Q

What are phenotypes and genotypes that can be inherited?

A

All four fine normal, 1 of 4 normal or minimal Hb problems, 2 on same chromosome alpha naught or one on each alpha positive homo ahve symptoms but same, 3 out of 4 is moderately sever and all for is hydrops foeatalis

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59
Q

What is worse for children aloha 0 or alpha+?

A

alpha0 with other carrier can cause significant in partner

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60
Q

What is hydrops foetalis?

A

often die in utero or shortly after birth, as when switch from foetal tey cant produce it

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61
Q

How is alpha thalasaemia diagnosed/

A

Usually blood film and PCR not needed but is diagnostic

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62
Q

What treatment is needed for alpha thalasaemia?

A

None or folic acid could need transfusion

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63
Q

What are the three types of beta thalasaemisa?

A

Thalasaemia carrier/herterozyote asymptomatic, intermedia for 2 genes less severe anaemca and don’t need transcusins. major are transfusion dependent. Genotype is not always predictive of symptoms

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64
Q

What can differentiate thalassaemia B from normal anaemia?

A

Thalasaemia B shouldnt have low iron as this is not affectd, abnormal cell shapes on blood film

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65
Q

When does beta thalassaemia major present?

A

6-12 months with failure to thrive sever symptoms, abnormal blood film, mainly Hb F should be lower,

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66
Q

What are complications of beta thalassaemia?

A

Many and wide ranging extramedullary haematopoesis and can erode through cortex and leads to bone abnormalities hepatosplenomegaly and haemochromatosis or diabetes

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67
Q

What can happen as a side effect of transfusion?

A

Iron buildup in thryroid heart adrenals pancreas ovaries testis pituitary

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68
Q

How are iron levels reduced is treatments?

A

Iron chellation

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69
Q

What is sickle cell disorders?

A

Variant in beta globin chain, produces some normal and some bad. it is recessive but not as simple

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70
Q

Where are many variants of sickle cell disease comon?

A

Where malaria is present

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71
Q

When do red blood cells insickle cell deform?

A

when low oxygen levels are present

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72
Q

What is the problem with sickle cells?

A

Vasuclar occulsions from blockage of the vessels

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73
Q

What are featurs of sickle cell acute complications?

A

wide and can be spleen problems haemolytic anaemia, painful crises dactylitis, sequestration crisese in liver pleeen, infections, acute chest syndrome, abdominal gallstones and cholangitis acute strokes

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74
Q

What can be protective in sickle cell?

A

Haemoglobin S

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75
Q

What are chronic complications of sickle cell?

A

CNS silent infarks, Eyes retinopathy bones joint replacement necrosis arthrits renal imparment recurrant priapism that can leat to erectile dysfuntion

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76
Q

How are chronic sickle cell complications managed?

A

monitoring and modiying risk factors if possible

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77
Q

How are acute sickle cell crises managed?

A

pain relief, transfusion, oxgygen

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78
Q

What is the most common membranopathy?

A

Hereditary sherocytosis leads to unstable membrane, often mild compensated haemolysis, but can be severe evidenced by splenomegaly. Suportive caure is usually enough

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79
Q

What are enzymeopathies in RBC?

A

Glycolysis enzymes are non function like Glucose 6 phosphate dehydrogenase deficiency. pyruvate kinase

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80
Q

What can cause problems for Glucose 6 phosphate dehydrogenase deficient patients?

A

Certain drugs, nitrofurantois and favabeans broad

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81
Q

Why is pyruvate kinase efficience a problem?

A

Causes build up of 2,3 DGP often precipitates it later and can often just need folic acid transfuse during severe crisis

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82
Q

How are haematological malignancies classified?

A

Acute vs Chronic and myeloid or lymphoid

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83
Q

What are malignant bone marrow pathologies?

A

Acute lineage, myeloproliferative, myelofibrosis, myelodysplaia

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84
Q

What are the treatments of haematological malignancies?

A

Supportive care Red cell transfusions, treatments of infections nausia pain, Chemotherapy, Blaket but also targeted monoclonal antibodies, radiotherapy, haemopoeitic stem cell transplantation

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85
Q

What is multiple myeloma?

A

Cancer of the differentiated B lymphocytes known as plasma cells leading to the accumulation of malignant plasma cells in the bone marrow which causes failure and paraprotein kidney failure and destructive bone disease and hypercalcaemia

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86
Q

What are the diagnostic criteria for myeloma?

A

C- calcium hyper
R- Renal failure
A- anaemia
B- bone lytic diseases

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87
Q

How can multiple myeloma be separated into separate classifications?

A

Monoclonal gammopathy of undetermined significance. no evidence of amyloid or CRAB diagnosis, smouldering myeloma, symptomatic myeloma, plasma cell leukaemia end phase when goes into blood solitary plasmacytoma, soft tissue mass of neoplastic plasma cells, AL amyloidosis

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88
Q

What investigations should be done in myeloma?

A

FBC, ESR/PV, U&E CA ALbumin, Serum and urinary electrophoresis Quantification of polyclonal lgs, XR of suspected areas or MRI CT.bone marrow aspirate

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89
Q

What are prospects in myeloma?

A

Most produce antibodies, most IgG 1/3 IgA then sometiems IgD or others often produce monoclonal free liht chainscan casues amyloidosis if do IgM could be lymphoplasmatcytic lymphoma

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90
Q

What are myeloproliferative neoplasms?

A

Haematological malignancies they are usually chronic and are an accumulation of mature blood cells in the circulation they arise from haematopotic cells,

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91
Q

What is polycythaemia Vera?

A

Too many red blood cells, haemoglobin is above normal as well. Enlarged spleen.

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92
Q

What are secondary causes of red blood cell rises?

A

Lung disease alcohol, EPO producin tumour, apparent erythrocytosis, high altitude.

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93
Q

How common is polycythemia vera?

A

qute rare 2 per 100,000

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94
Q

What is the problem with PV?

A

Clotting too much, thrombosis and can turn into acute or other poly

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95
Q

How can Polycythaemia be managed?

A

Anti clotting, cardiovascular risk reduction

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96
Q

What is essential thrombocytosis?

A

Production of platelets that are too many, but are lots of secondary causes, main problem is thrombosis riskcan turn into other conditions

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97
Q

What is myelofibrosis?

A

Bone marrow becomes filled with scar tissue and fills space. Cytopaenias, can see blast cells, anaemia, blasts, splenomegaly.

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98
Q

How to treat myelofibrosis?

A

supportive, blood transfusion, EPO, treat infection, Hydroycarbaide, Allogenic stem cell transformation. 5 year prognosis

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99
Q

What us chronic myeloid leukaemia?

A

all myeloid cells go up. genetic phillidelphia chromosime and can use ABL kinase inibitors

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100
Q

Why is knowing which multiple myeloma antibody is produced useful?

A

To see their levels of antibody as a marker of disease treatment response

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101
Q

What is Myeloma bone disease?

A

Bone disease that is a manifestation of multiple myeloma. The most common places to have issues are vertebrae, ribs, skull, shoulders, pelvis and long bones

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102
Q

What are the treatments for Myeloma bone disease?

A

clodronate zoledronic acid or pamidronate.

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103
Q

What are complications of myeloid bone disease?

A

Hypercalcaemia, spinal cord compression

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104
Q

How can myeloma be treated?

A

IMID thalidomide calss, proteosome inhibitors-velcade, corticosteroid and monoclonal antibodies for CD38

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105
Q

What is lymphoma?

A

The colonal proliferation and spread of a malignant lymphocyte. Predominantly a disease of the lymph nodes.

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106
Q

What are the main causes of lymphoma?

A

Failure of immune surveillance and regulation. impairment of immunes system and aquisition of new capabilities in malignant cells

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107
Q

What is the main cause of lymphoma?

A

Idiopathic

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108
Q

What are non-ideopathic causes of lymphoma?

A

Primary immunodeficiency. Wiscott-Aldrich syndrome, CVID, secondary immunodeficiency, HIV transplant recipients and Infection from EBV HTLV-1 Helicobacter pylori autoimmune diseases

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109
Q

How is lymphoma diagnosed?

A

Lymph node biopsy blood film or bone marrow biopsy as well.immunophenotyping, cytogenetics, molecular techniques

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110
Q

What are symptoms and signs of lymphoma?

A

Nodal disease, extranodal disease presentations, compression syndromes and systemic syndromes such as B symptoms Weight loss fever and night sweats

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111
Q

What are investigations for new case of lymphoma?

A

Bloods, CT PET-CT

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112
Q

What is performance status?

A

how well patient is in terms of in bed or not

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113
Q

How is lymphoma classified?

A

Hodgkins and non-hodgkins lymphoma, either low grade or high grade

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114
Q

What is hodgkins lymphoma?

A

painless lymphadenopathy weight loss night sweats qith reed-Sternberg cells

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115
Q

Who gets hodgkin lymphoma?

A

younger peak and older peak

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116
Q

What are the stages of hodgkin lymphoma?

A

Absence or presence of B symptoms A/B also the distribution and number of affected nodes up to stage 4

117
Q

What is prognosis for hodgekin lymphoma?

A

12-A short corse combination chemotherapy followed by radiotherapy, 90% after that 65-80%

118
Q

What is the treatment for Hodgkin lymphoma?

A

ABVD chemo treatment sometimes radio too

119
Q

What is the problem in hodgkin lymphoma?

A

The after effects of treatment are bad because they live such a long time after

120
Q

What is different about non-hodgkin lymphoma?

A

Often extranodal presentation, there are many more subtypes, there are many treatment options and varied outcomes

121
Q

What is the prognosis for low grade nonhogkins lymphoma?

A

Median survival 9-11 years incurable usually and usually advanced at presentation it is harder to treat. follicular lymphoma marginal zone lymphoma

122
Q

What are treatments for NHL indolent?

A

Watch and wait, alkylating agents, combination chemo purine analogues radiotherapy, monoclonal antibodies

123
Q

What are agressive NHL?

A

diffuse large B cell lymphoma, usually nodal presentation, usually well patient often short history

124
Q

What are early treatments of agressive NHL?

A

Short course of chemo and radiu or if its advances monoclonal antibodies as well

125
Q

What is Rituximab?

A

Monoclonal antibody for CD-20 targets B cells uaully

126
Q

What are the myeloproliferative disorders?

A

Polycythemia vera, essential thrombocytosis, myelofibrosis and chromic myeloid leukemia they are chronic conditions that evolve over years

127
Q

What are involved in haematopoesis?

A

EPO TPO signalling through JAK/STAT proteins they are involves with EPO receptors

128
Q

What is polycythemia vera?

A

Elevated RBC count may have splenomegaly, Activating mutation in JAK2 to produce RBC all the time can get itch fatigue and can transform to myelofibrosis or acute leuaemia,

129
Q

How is polycaythaemia vera treated?

A

Venesection, aspiring manage CVD risk

130
Q

What is prognosis of polycythaemia vera?

A

13 years

131
Q

What are the features of myelofibrosis?

A

cytopenia low Hb platelets and EBC marow filled with reticulin fibrosis and find blasts in circulation weight loss fatigue

132
Q

What is prgnosis of myelofibrisos?

A

can transform to acute leukaemia median 5 years (2-10)

133
Q

How can you treat Myelofibrosis?

A

usually supportive management and can have transplant or medication

134
Q

What are the “common” myeloproliferatice disorders?

A

Polycythemia, myelofibrosis, chronic myeloid leukaemia

135
Q

What is chronic myeloid leukaemia?

A

All myeloid cells go up in blood. usualy incidenatl findidns it is rare often with philladelphia chromosomes

136
Q

How is chronic myeloid leukaemia treated?

A

Imantinib to block ABL kinase

137
Q

What is chronic neutrophilic leukaemia?

A

very very rare not usually infection causes it

138
Q

What underlies a lot of myeloid diseases?

A

the Philadelphia chromosome or genetic mutations

139
Q

What is essential thrombocytosis?

A

elevated platelet cound diagnosed after secondary causes are eliminated. can cause bleeding when counts are high and can transform to acue leukaemia or myelofibrosis

140
Q

What is treatment for essential thrmbocytosis?

A

Cardiovascular risk usual life expectancy pretty much

141
Q

Where do venous thromboses usually happen?

A

In the deep veins of the leg

142
Q

What are the symptoms of DVT?

A

Swelling and pain in the legs, can get redness swelling warmth and discolouration

143
Q

What can be a complication of DVT?

A

Can cause swelling that can lead toobstruction of arteries

144
Q

What are investigations can be done to assess DVT?

A

D-dimer: normal exculdes diagnosis but can be posisitve from other causes, then ultrasound compression test in proximal veins does have issues in very early stages of thrombosis

145
Q

How are DVTs treated?

A

Low molecular weight heparin S/c of 5 days. Also antiplatelet therapy for 6 months like apixaban. Use of compression stockings and look for the cause of it

146
Q

What can cause DVTs?

A

Surgery immobility, leg fracture/POP, being on the Pill HRT pregnancy, long haul flights/ travel, or thrombophilia genetic predisposition cancers

147
Q

What is prevention of DVT?

A

Mechancal hydration early mobilisation compression stockngs and foot pumps. also low molecular weight heparin

148
Q

Who has thromboprophylaxis?

A

low risk under 40 short surgery have ….

higher risk for long surgery had

149
Q

What are Pulmonary embolisms?

A

massive and are haemodynamically significant, they are medical emergency and can be severe or not too bad

150
Q

What are symptoms of PE?

A

hypotension, cyanosis, severe dyspnoea right heart strain/failure
in less severe it is often its chest pain(pleuritic) shortness of breath may have symptoms of DVT, signs may have tachycardia and tachypnoea pleural rub

151
Q

What do you do for PE initial investigations?

A

CXR ECG Sinus tachycardia ABG type 1 respiratory failure decreased O2 CO2
D dimers CTPA wisualis segmental thrombi

152
Q

What is treatment for PE?

A

Same as DVT, low molecular weight heparin if acutely unwell could remove it with surgery

153
Q

Where are periferal arteries that can have vascular disease?

A

illiac femoro-popliteal ant tibial, Carotids, Vertebrals, coeliac mesenteric renals and subclavia/axillary

154
Q

What are the commenest vascular diseases?

A

Atherosclerosis, inflamatory and trauma

155
Q

What are complications of plaques in vessels?

A

Progression, aneurism, dissection

156
Q

What are the results of atherosclerosis?

A

Debris embolsm, aneurism, occulsion, restriction

157
Q

What are organ specific symproms?

A

Angina exercise induced.

158
Q

What is intermittent claudication?

A

moderate ischaemia, when demand increases becomes lactic acid pain, pain on exersion distal to site of atheroma often calves

159
Q

What is critical ischaemia?

A

Blood supply barely adequate for rest. get rest pain usually in distal segment, risk of gangrene or infection can be worse at night.

160
Q

What happens in acute ischaemia PVD?

A

Sudden cessation of blood supply,get 6Ps pain pallor perishing cold pulsless paresthesis paralysis

161
Q

How long to save the limb in PVD acute ischaemia?

A

4-6 hours before the limb might be lost

162
Q

What can lead to aneurism?

A

often aterosclerotic, collagen disorders Marfans, EhlersDanlos size and lcation

163
Q

What investigations should be done in PVD?

A

Risk factors for pathophysiology, Image the vessels duplex/CT/MR angiography

164
Q

What are the treatments for PVD?

A

Risk factor modification Revascualrisation in criticalischaemia otherwise amputation required

165
Q

What are surgical treatments of PVD?

A

Do bypass surgery with synthetic or real vein, or catheter stenting with a baloon

166
Q

What is carotid endarterectomy?

A

Removal of atherosclerotic tissue in the neck

167
Q

What is a stent graft?

A

Support an aneurysm with a stent over a large area

168
Q

What is chronic myeloid leukaemia?

A

uncontrolled colonal proliferation of myeloid cells usually in older patients linked with philadelphia chromosome.

169
Q

What are the symptoms of CML?

A

anaemia,

170
Q

What is acute lymphoblastic leukaemia?

A

Common in children malignancy of immature lympoid cells for T and B, commonest childhood cancer, B in children T in adilts, asscociated with downs syndrome

171
Q

What are the symptoms of acute Lymphoblastic leukaemia/

A

anaemia, infection from low WCC, bleeding, bone marrow infiltration liver spleen infiltration lymphadenopathy, CNS infiltration mediastinal masses

172
Q

What are the investigations to make diagnoses of ALL

A

FBC blood film, WCC is usually high, blast cells on film and in bone marrow, blast cells on film

173
Q

What is the difference between leukaemia and lymphoma?

A

they can cross over and mix but lymphoma is a mass in the lymph node but leukaemia is mallignant white blood cells in the blood from the bone marrow

174
Q

How to diagnose leukaemia and lymphoma?

A

Blood smear and bone marrow biopsy

175
Q

What are the types of blood disorders?

A

Proliferative diseases, haematologicla malignancies and marrow failure

176
Q

What conditions cross over PD heamatological malignancies and marrow?

A

Multile myeloma, CML

177
Q

What are classifications of leukaemia?

A

CML AML CLL ALL

178
Q

What is definition of leukaemia?

A

Malignancy arising from bone marrrow stem cells resulting imared haematopesis and celsl in peripheral blood and metastisise

179
Q

Who usually gets leukaemia?

A

Adults but ALL is children

180
Q

What divides acute and chronic leukaemia?

A

Acute younger patients blast cells in the blood cant differenciate and telad to cytopenias Chronic are cytes late block on differentiation. not many blasts and older patients

181
Q

What are the types of lymphoma?

A

Hodgkins(with reed sternberg B cells) or non-hodgkin

182
Q

What are the histological feature in AML?

A

Aure rods which are granulesperoxidase positive

183
Q

What are risk factores for acute leukaemia?

A

Genetic and environment, antuneoplastic agents ionising radiation hodkin’s lymphoma

184
Q

How are acute leukaemias cause symptoms?

A

Replace most of bone marrow so fewere other cells, enter peripheral blood, metastasize

185
Q

How to tell it is acute leukaemia?

A

Painless lymphadenopathy, bleeding, infections fatigue

186
Q

What are treatments of acute leukaemia?

A

Induction (of remission) phase, high does chemo to supresss all cells then give supportive grwoth factors later consolidation to prolongue remission

187
Q

What are chromic leukaemis ?

A

Parients older late haemopoetic stem cells, insudious onset, mature celsl smaller

188
Q

What are chromic leukaemis ?

A

Patients older late hemopoietic stem cells, insidious onset, mature celsl smaller

189
Q

What is myelodysplasia?

A

MDS is a bone marrow problem, hypercellular full of dysplastic cells with pancytopenia

190
Q

is MDS a leukeaemia?

A

it progresses into AML, dysplasia is a precursor to cancer caused by de novo mutation and environmental exposure

191
Q

Who usually gets MDS?

A

50-80 year olds

192
Q

What are the features of MDS?

A

Hypercellular marrow now proliferation No JAK mutation it is dysplasia

193
Q

What are stages of RBC production?

A

Myeloid progenitor, proerythroblast, normoblasts reticulocytes erythrocytes

194
Q

What is a reticulocyte/

A

A net like cell has rRNA giving blue cytoplasm.

195
Q

Do reticuloycyes have nuclus?

A

yes they do

196
Q

How long are reticulocytes inin the circulation?

A

24hours

197
Q

What happens in anaemia to RBC production?

A

Release and produce more reticulocytes so more are found in blood

198
Q

What is corrected reticulocyte count?

A

which compares amount of reticulocytes in relation to the amount of red blood cells

199
Q

What is RBC count?

A

Number of cells in a certain volume of blood

200
Q

What is Hb conc?

A

The amound of Hb in a certain volume of blood regardless of the number of cells

201
Q

What is haematocrit value?

A

Volume of RBC over volume of blood should be around 45 for men 40% for females

202
Q

What is MCV?

A

The average volume of a RBC in a volume small cells give low large cells give large MCV

203
Q

What is mean corpuscular haemoglobin? MCH

A

The average mass of Hb per cell

204
Q

what is mean corpuscular haemoglobin haemoglobin concentration?

A

MCHC average concentration of Hb witin each RBC

205
Q

What is Red cell distribution width?

A

RDW isused to look at type of anaemia it is the variation of the diameter of RBC

206
Q

What is anisocytosis?

A

When there is a variation of the size of cells

207
Q

What is the use of RDW?

A

When elevated indicates blood body is lacking in certain nutrients B12 folate or iron

208
Q

Why does nutritional deffieciency produce anisocytosis/

A

There isn’t enough to produce the right cell size so they decrease in size over time so there is a variation in size

209
Q

What are signs of anaemia?

A

Low total RBC mass or decreases Hb or HCT or RBC count

210
Q

What are the symptoms of anaemia?

A

Fatigue pale sometiems murmur or angina

211
Q

What are the main mechanisms for anaemia?

A

sequestration blood loss, hypoproliferative(production defects and maturation defects) and survival

212
Q

What can cakes RBC production defective?

A

Lo EPO from kidney dammage and dammage bone marrow

213
Q

What are maturation defects?

A

Cytopasmic Hb synthesis like iron deficiency or thalasaemis or nuclear DNA synthesis B12 folate and MDS

214
Q

What are survival defects in RBC?

A

intrinsiv from membrane spherocytosis defects or enzyme G^ defect or Hb itself sickle cell extrinsic by valve damage or autoimmune

215
Q

What is sequestration of RBC?

A

Spleen damages red blood cells in portal vein hypertension

216
Q

What is microcytic anaemia?

A

small RBC and decreased Hb

217
Q

Why does iron deficiency cause microcity RBC?

A

the cells shrink as they are waiting for the iron to fill them and keep shrinking so that the cell is full.

218
Q

What is the difference between iron deficiency and anaemia of chronic disease?

A

in one there is iron but can’t be used but other there isn’t much blood

219
Q

How is iron absorbed in intestines?

A

In duodenum, through enterocytes to bind to transferrin in the blood

220
Q

What are ferritin?

A

keeps iron in non toxic bound form stored in the macrophages of bone marrow

221
Q

What degrates ferritin?

A

lysosomes turn it to haemosiderin

222
Q

What is a measure of bone marrw ferritin?

A

the ferritin in blood 1mg in blood means 8 in bone marrrow

223
Q

What is iron in serum used for?

A

Reduced in iron defficiency or chronic disease anaemia, and increased iin iron overload

224
Q

What is serum total iron binding capacity?

A

The iron binding capacity of blood and refelcts iron stors it correlates with transferrin levels

225
Q

What is soluble transferrin receptor concentration

A

sTFR is increased in iron deficiency anaemia and normal in anaemia of chronic disease

226
Q

What can cause iron deficiency anaemia?

A

Decreased supply from diet or malabsorpiton, increased demand from more RBC produciton in grwoth and pregnancy or from blood loss or intravascular hemolysis

227
Q

What are symptoms or iron deficiency anaemia?

A

Tired and pale irritable cant exercise, might have a murmur, restless leg syndrome, achlorhydria coeliac disease glossitis-chelitis, koilonychia

228
Q

What are common blood results for anaemia iron deficient?

A

Low haemocrit, low MCV, low MCH low MCHC low reticulocytes often increased platelets. low serum iron, low ferritin(store) what about TIBC increased saturation % is decreased and RDW is increased sTFR is increased

229
Q

How do you diagnose iron deficiency anaemia?

A

technically biopsy but can’t do that so just treat with iron and monitor

230
Q

When do you get high WBC count with anaemia?

A

Hookworm infection

231
Q

What is treatment for anaemia?

A

Oral ferrous sulphate can give diarrhoea or constipation, usually fails from compliance, or if its from blood loss or absorption problems can give IM or IV iron if needed can have anaphylaxis

232
Q

What cell size is in thalasaemia?

A

Microcytic small cells

233
Q

What is the inheritance pattern for thalasaemia?

A

Autosomal recessive

234
Q

What does thalassaemia affect?

A

The globin chains of HbA

235
Q

What are the normal components of adult blood?

A

Small amounts of HbF alha and gamma and HbA2 alpha and delta and maily HbA alpha and beta

236
Q

What are the effects of having a thalassaemia?

A

Globin chain synthesis s unbalanced haemotetramers form that precipitate inthe RBC and leads to haemolysis and less of them are produced which leads to anaemia

237
Q

What are the levels of alpha thalassaemia?

A

Hydrops fetalis 4 deletions, 3 deletions moderately severe haemolytic anaemia major, 2 deleted asymptomatic but lowered MCV minor, 1 deletion asymptomatic trait/carrier

238
Q

What is the inheritance mechanism for alpha thalassaemia?

A

there are 2 coppies of alpha so 4 locations for deletions

239
Q

What is the problem in thalassaemia major?

A

Only beta is produced so get a tetramerform unpaied beta chains

240
Q

How are thalassaemia patients treated?

A

Give blood transfusions

241
Q

What chromosome is involved in beta thalasaemia/

A

chromosome 11

242
Q

What type of mutations happen in beta thalasaemia?

A

Slicing defiect and more severe are premature stop codon

243
Q

What are complications of beta thalasaemia major?

A

Get hepatospelnomealy as no beta globin production, also have extramedullary haematopoiesis, in skull and maxillae chipmunk facies

244
Q

What is betathalasaemia intermedia?

A

Often have alpha thalassaemia trait, qualitative effect in beta not as many haemotetramers and less haemolysis and increased HbF

245
Q

What is sideroblastic anaemia?

A

ringed sidderoblasts in bone marrow, protoporphyrin synthesis defect. caused by B6 defficience alcoholism lead poisoning MDS or X-linked

246
Q

What is macrocytic anaemia?

A

large red blood cells

247
Q

What type of anaemia do you get with B12 or folate defficiency?

A

Microplastic

248
Q

What are the divisions of macrocytic anaemia?

A

Megaloblastic for folate or deficiency and has hyper segmented neutrophils or non megaloblastic

249
Q

Why are folate and B12 deficiency macrocytic?

A

The cells don’t decrease in size to the normal size as the DNA cant regulate the size

250
Q

Which drugs can stop folate being absorbed?

A

alchol and oral contractptive pills

251
Q

What can cause folate defficiency?

A

Decreased intake, malabsorption coeliac disease, Drug inhibition, trimethoprim methotexate, or increased use in pregnancy lactation malignancy or haemolytic anaemia

252
Q

What happens with folate deficiency?

A

impared DNA sunthesis and innefective haematopoiesis pancytopenia

253
Q

How long does body have folate store?

A

4 months

254
Q

What deficiency gets neurological symptoms?

A

B12

255
Q

What are symptoms of b12 defficiency?

A

macrocytic anaemia symptoms, and glossitis, lemon yellow skin peripheral neuritis subacute combined degeneration of spine and dementia vibration proprioception,muscle weakness and ataxia

256
Q

how long does the body have stores of B12?

A

several years maybe 9

257
Q

How do B12 get absorbed?

A

Saliva adds R protein to protect from stomach acid. it is cleaved from it in dodenum then joins with intrinsic factortt and is absorbed in terminal ileum and end up in blood wit transcobalamin

258
Q

What is special about B12?

A

Methylmalonyl CoA and homocystine

259
Q

How to treat B12 deficiency?

A

IM

260
Q

What can cause non-megaloblastic anaemia?

A

liver disease, alcoholic and drugs

261
Q

What are the classes of normocytic anaemia ?

A

acute blood loss underproduction, overdestruction haemolysis

262
Q

What happens in acute blood loss?

A

loss of RBC then get more fluid in later to dilute causing anaemia can’t give saline because dilutes more

263
Q

What can cause overdestruction of RBC?

A

Extrinsic destruction, complement antibodies or membrane or enzyme defects

264
Q

What is aplastic anaemia?

A

Can give normo to macrocytic anaemia, you have pancytopenia and hypocellular marrow

265
Q

What can cause aplastic anaemia?

A

Faconi anaemia dyskeratosis, radiation drugs toxins viruses immunological ONH pregnancy, intensive chemo

266
Q

What are symptoms of pancytopenia?

A

signs of anaemia, infections if very late mucosal bleeding from pancytopenia

267
Q

What can lead to anaemia in malignancy?

A

Anaemia of crronic disease, kidney failure pain phycological, blood loss bone infiltration,

268
Q

What is paroxysmal nocturnal dyspnoea?

A

waking up in night feeling short of breath standing up relieves as fluid falls to bottom of lungs when asleep it allows you to become more hypoxic

269
Q

What are the symptoms of chronic heart failure?

A

Breathlessness cough maybe with frothy/pink sputum orthopnoea, SOB when lying down, Paroxysmal nocturnal dyspnoea oedema

270
Q

How is heart failure diagnosed?

A

clinical assessment, BNP blood test, ECho and ECG

271
Q

What can lead to chronic heart failure?

A

Ischaemic heart disease prior infarction and not, valvular heart disease hypertension and arrhythmias

272
Q

How is chronic heart failure treated?

A

BNP refere to specialist if in primary care. ABAL Ace inhibitor, Beta blocker, Aldosterona antagonist, loop diuretics add more each day (no ace in valvular disease)

273
Q

What can cause hypovolaemic shock?

A

Blood loss GI bleed, AAA rupture, Trauma, Postpartum haemmorage, Ectopic pregnancy, Haemoptysis varicies,
Non blood fluid loss, severe burns, vomiting, diarrhoea, bowel obstruction DKA, Acute pancreatitis

274
Q

What happens to signs in hypovolemic shock?

A

The BP drops, CO drops, heart rate increases,SVR increases 02 sats goes down high or low HCT depending on type of loss cyanosis, hypoxia

275
Q

How to treat hypocolaemic shock?

A

Give IV normal saline or albumin or colloid

276
Q

What can cause cardiogenic shock?

A

myocarditis, MI, valvular dysfunction, Arrhythmias, cardiomyopathies, gongenital heart diseases dialated cardiomyopathy

277
Q

What happens in cardiogenic shock?

A

Decreased in circulating volume, low BP low CO increased heart rate increased Systemic vascular resistance, increased pulmonary wedge pressure. low sats from lactic acid

278
Q

How to treat cardiogenic shock?

A

Give oxygen small amount of fluid, vasopressors to uncrease ciontractility epinephrine dobutimine

279
Q

What is obstructive cardiac failure?

A

the heart is being blocked from pumping properly. compression of the heart and compression of the great vessels.

280
Q

What are causes of obstructive shock?

A

Tension Pneumothorax, cardiac tamponade

281
Q

What can show obstructive shock?

A

Increased JVP, Low blood pressure, high heart rate, dull heart sounds distant or muffled for tamponade Massive PE low sats hypoxemic hypoxia

282
Q

What is distributiative sock?

A

Septic anaphylactic and neurogenic it is about struggling to distribute the blood rather than pumping

283
Q

What can cause septic shock?

A

Bacteraemia, endotoxins tissue dammage, leading to dialation of blood vessels and increasing vascular permeability

284
Q

What happens in septic shock?

A

The vasodilation and permeability increasing. this leads to drop in BP and reduction in peripheral resistance, can get lots of blood clots microvascular occlusions

285
Q

What are signs of septic shock?

A

Lowerd blood pressure cardiac output goes up BP goes up SVR decreases, microvascualr occlusions and acute inflammatory markers

286
Q

What can happen in anyphalactic shock?

A

Vasodilation from mast cell activation. Can lead to drop in BP increased HR redness swelling can obstruct airway. devreased SVR

287
Q

What is Neurogenic shock?

A

when the spinal heart rate and blood vessels innervation is damaged so that the control mechanisms are damaged

288
Q

What can causeneurogenic shock?

A

Acute spinal injury, stroke

289
Q

What happens in neurogenic shock?

A

Lowered peripheral resistance, vasodilated, lowered blood pressure increased

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