Cardiovascular diseases 2/haematology Flashcards
1
Q
What indicates sinus rhythm?
A
P wave followed by QRS complex
2
Q
How long should P wave be?
A
no more than 120mx / 3small squares
3
Q
How tall should a p wave be?
A
3small squares
4
Q
How long does a large square represent?
A
400ms
5
Q
How can heart rate be calcuated?
A
300 by no of large squares for one beat
6
Q
How long should PR interval be?
A
From 120ms to 200ms
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
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
9
Q
What does tall p wave mean?
A
right atrium enlargment or notched broad is left atrial enlargment.
10
Q
What is different morphology p wave show?
A
Non SA node focus
11
Q
What can a long PR interval mean?
A
AV node disorder and conducting tissue
12
Q
What does short PR interval mean?
A
Wolf-parkinson- white and preexcitiation or just young patients
13
Q
What should the length of QRS be?
A
3 small squares 120ms or less
14
Q
What might give broad QRS?
A
Ventricular conduction delay or bundle branch block or pre-excitation
15
Q
What is a cause of small QRS?
A
obese patient pericardial effusion and infiltrative cardiac disease
16
Q
Tall QRS complexes?
A
left ventricular hypertrophy or a thin patient
17
Q
How should QRS change through V1-V6?
A
Negative S wave transitioning to poitive R wave by V6
18
Q
How long shold QT interval?
A
It depends on the heart rate
19
Q
What can cause QT change?
A
Electrolyte disturbances or drugs as well as some inherited disorders
20
Q
What is importance of ST?
A
ST elevation or depression can be a sign of MI, early repolarisation pericarditis or endocarditis
21
Q
What height should T be?
A
Half of QRS or less
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
23
Q
Where should there be no q waves?
A
I,II, V2-V6
24
Q
What are the types of tachycardia?
A
Atrial fibrilation, Atrial flutter, Supraventricular tachycardias, ventricular tachycardia or ventricular fibrilation
25
What are supraventricular rhythm features?
Narrow QRS, Can be flutter sawtooth or irregular p waves which is fibrillation
26
What shows a ventricular rhythm?
Doesnt use his purkije so has broad QRS complex can be regular or random fibrulation
27
What can cause bradycardias?
Conduction tissue fibrosis, ischaemia, inflammation of infiltration disease or drugs
28
What is first degree AV heart block?
When PR interval is longer than normal as conduction issues
29
What is second degree AV heart block?
Some P waves don't cause QRS has ratio 2:1 3:1 etc
30
What is third degree AV block?
none of waves get to the ventrals so very slow rate as set by ventricular pacemaker cells
31
What is mobitx type 1 heart block?
type of 2nd degree gradually prolonging PR increasing then get a missed one
32
What is mobitz type 2 heart bloc?
2nd degree heart block where PR is same length just sometimes doesnt get conducted
33
What is the left bundle branch block?
The left bundle is not activating as fast and right is activated first then contraction passes from right to left passively
34
Which leads are important in bundle branch block?
V1 and V6
35
What shows left bundle branch block?
Broad QRS in v1 and v6 WiLLiam W shape in V1 M shape in V6
36
What happens in right bundle branch block?
The left bundle activates and the current passes passively to right bundle.
37
What does right bundle branch block look like?
MoRRoW V1 has M shape in QRS and V6 has W shape
38
What are signs of ischaemia or infarction?
T wave flattening or inversion ST segment depression followed b ST elevation and Q waves show old infarction
39
What will hyperkalaemia do to an ECG?
Tall tented T waves, flattening of P QRS broadening then eventually sine wave pattern
40
What will hypokalaemia do?
Flattenin of T wave, QT prolongation
41
What does hyper/hypocalcaemia do to ECG?
QT shortening for hyper and QT lengthening for Hypo
42
Where are red blood cells produced?
In the bone marrow
43
What are erythroblasts?
They are cells with a nucleus,
44
What are reticulocytes?
RBC without nucleuse not fully formed but do produce proteins like haemoglobin still
45
What controls erythropoeise?
Erythropoetin produced by kidneys also thryroid hormne testosterone and levels or iron folate and B12
46
What affects RBC production most?
Erythropoetin
47
What affects haemoglobin binding to oxygen/
Temperature 2,3 DPG, pH CO
48
What defines anaemia?
Levels of haemoglobin in blood for men 135-175g/L 120-160g/L for women
49
What are the types of haemoglobin?
Adult A and A2, foetal HbF, embryonic rtland and gower
50
When does foetal haemoglobin levels drop?
Just prior to birth and all by 9 months
51
Where is haemoglobin inherited from?
Alpha chains 4 genes from 16 and on chromosome 11 2 genes
52
What are types of haemoglobinopathies?
quantitative defect and qualitative
53
What are thalassaemias?
Common can be asymptomatic or life threatening, low or absent priduction of a chain type
54
What are the problems in thalassaemias?
The Haemoglobin isn't formed properly so lots of RBC are destroyed inbone marrow or lysed in blood so haemolytic anaemia
55
What are the teypes of thalasaemias?
Alpha is deletion beta is mutation
56
Where are thalasaemias most common?
Africa and asia SEA, East mediterranian
57
What is inheritance pattern of Alpha thalassaemia?
Varied as need several missing to get symptoms
58
What are phenotypes and genotypes that can be inherited?
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
59
What is worse for children aloha 0 or alpha+?
alpha0 with other carrier can cause significant in partner
60
What is hydrops foetalis?
often die in utero or shortly after birth, as when switch from foetal tey cant produce it
61
How is alpha thalasaemia diagnosed/
Usually blood film and PCR not needed but is diagnostic
62
What treatment is needed for alpha thalasaemia?
None or folic acid could need transfusion
63
What are the three types of beta thalasaemisa?
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
64
What can differentiate thalassaemia B from normal anaemia?
Thalasaemia B shouldnt have low iron as this is not affectd, abnormal cell shapes on blood film
65
When does beta thalassaemia major present?
6-12 months with failure to thrive sever symptoms, abnormal blood film, mainly Hb F should be lower,
66
What are complications of beta thalassaemia?
Many and wide ranging extramedullary haematopoesis and can erode through cortex and leads to bone abnormalities hepatosplenomegaly and haemochromatosis or diabetes
67
What can happen as a side effect of transfusion?
Iron buildup in thryroid heart adrenals pancreas ovaries testis pituitary
68
How are iron levels reduced is treatments?
Iron chellation
69
What is sickle cell disorders?
Variant in beta globin chain, produces some normal and some bad. it is recessive but not as simple
70
Where are many variants of sickle cell disease comon?
Where malaria is present
71
When do red blood cells insickle cell deform?
when low oxygen levels are present
72
What is the problem with sickle cells?
Vasuclar occulsions from blockage of the vessels
73
What are featurs of sickle cell acute complications?
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
74
What can be protective in sickle cell?
Haemoglobin S
75
What are chronic complications of sickle cell?
CNS silent infarks, Eyes retinopathy bones joint replacement necrosis arthrits renal imparment recurrant priapism that can leat to erectile dysfuntion
76
How are chronic sickle cell complications managed?
monitoring and modiying risk factors if possible
77
How are acute sickle cell crises managed?
pain relief, transfusion, oxgygen
78
What is the most common membranopathy?
Hereditary sherocytosis leads to unstable membrane, often mild compensated haemolysis, but can be severe evidenced by splenomegaly. Suportive caure is usually enough
79
What are enzymeopathies in RBC?
Glycolysis enzymes are non function like Glucose 6 phosphate dehydrogenase deficiency. pyruvate kinase
80
What can cause problems for Glucose 6 phosphate dehydrogenase deficient patients?
Certain drugs, nitrofurantois and favabeans broad
81
Why is pyruvate kinase efficience a problem?
Causes build up of 2,3 DGP often precipitates it later and can often just need folic acid transfuse during severe crisis
82
How are haematological malignancies classified?
Acute vs Chronic and myeloid or lymphoid
83
What are malignant bone marrow pathologies?
Acute lineage, myeloproliferative, myelofibrosis, myelodysplaia
84
What are the treatments of haematological malignancies?
Supportive care Red cell transfusions, treatments of infections nausia pain, Chemotherapy, Blaket but also targeted monoclonal antibodies, radiotherapy, haemopoeitic stem cell transplantation
85
What is multiple myeloma?
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
86
What are the diagnostic criteria for myeloma?
C- calcium hyper
R- Renal failure
A- anaemia
B- bone lytic diseases
87
How can multiple myeloma be separated into separate classifications?
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
88
What investigations should be done in myeloma?
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
89
What are prospects in myeloma?
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
90
What are myeloproliferative neoplasms?
Haematological malignancies they are usually chronic and are an accumulation of mature blood cells in the circulation they arise from haematopotic cells,
91
What is polycythaemia Vera?
Too many red blood cells, haemoglobin is above normal as well. Enlarged spleen.
92
What are secondary causes of red blood cell rises?
Lung disease alcohol, EPO producin tumour, apparent erythrocytosis, high altitude.
93
How common is polycythemia vera?
qute rare 2 per 100,000
94
What is the problem with PV?
Clotting too much, thrombosis and can turn into acute or other poly
95
How can Polycythaemia be managed?
Anti clotting, cardiovascular risk reduction
96
What is essential thrombocytosis?
Production of platelets that are too many, but are lots of secondary causes, main problem is thrombosis riskcan turn into other conditions
97
What is myelofibrosis?
Bone marrow becomes filled with scar tissue and fills space. Cytopaenias, can see blast cells, anaemia, blasts, splenomegaly.
98
How to treat myelofibrosis?
supportive, blood transfusion, EPO, treat infection, Hydroycarbaide, Allogenic stem cell transformation. 5 year prognosis
99
What us chronic myeloid leukaemia?
all myeloid cells go up. genetic phillidelphia chromosime and can use ABL kinase inibitors
100
Why is knowing which multiple myeloma antibody is produced useful?
To see their levels of antibody as a marker of disease treatment response
101
What is Myeloma bone disease?
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
102
What are the treatments for Myeloma bone disease?
clodronate zoledronic acid or pamidronate.
103
What are complications of myeloid bone disease?
Hypercalcaemia, spinal cord compression
104
How can myeloma be treated?
IMID thalidomide calss, proteosome inhibitors-velcade, corticosteroid and monoclonal antibodies for CD38
105
What is lymphoma?
The colonal proliferation and spread of a malignant lymphocyte. Predominantly a disease of the lymph nodes.
106
What are the main causes of lymphoma?
Failure of immune surveillance and regulation. impairment of immunes system and aquisition of new capabilities in malignant cells
107
What is the main cause of lymphoma?
Idiopathic
108
What are non-ideopathic causes of lymphoma?
Primary immunodeficiency. Wiscott-Aldrich syndrome, CVID, secondary immunodeficiency, HIV transplant recipients and Infection from EBV HTLV-1 Helicobacter pylori autoimmune diseases
109
How is lymphoma diagnosed?
Lymph node biopsy blood film or bone marrow biopsy as well.immunophenotyping, cytogenetics, molecular techniques
110
What are symptoms and signs of lymphoma?
Nodal disease, extranodal disease presentations, compression syndromes and systemic syndromes such as B symptoms Weight loss fever and night sweats
111
What are investigations for new case of lymphoma?
Bloods, CT PET-CT
112
What is performance status?
how well patient is in terms of in bed or not
113
How is lymphoma classified?
Hodgkins and non-hodgkins lymphoma, either low grade or high grade
114
What is hodgkins lymphoma?
painless lymphadenopathy weight loss night sweats qith reed-Sternberg cells
115
Who gets hodgkin lymphoma?
younger peak and older peak
116
What are the stages of hodgkin lymphoma?
Absence or presence of B symptoms A/B also the distribution and number of affected nodes up to stage 4
117
What is prognosis for hodgekin lymphoma?
12-A short corse combination chemotherapy followed by radiotherapy, 90% after that 65-80%
118
What is the treatment for Hodgkin lymphoma?
ABVD chemo treatment sometimes radio too
119
What is the problem in hodgkin lymphoma?
The after effects of treatment are bad because they live such a long time after
120
What is different about non-hodgkin lymphoma?
Often extranodal presentation, there are many more subtypes, there are many treatment options and varied outcomes
121
What is the prognosis for low grade nonhogkins lymphoma?
Median survival 9-11 years incurable usually and usually advanced at presentation it is harder to treat. follicular lymphoma marginal zone lymphoma
122
What are treatments for NHL indolent?
Watch and wait, alkylating agents, combination chemo purine analogues radiotherapy, monoclonal antibodies
123
What are agressive NHL?
diffuse large B cell lymphoma, usually nodal presentation, usually well patient often short history
124
What are early treatments of agressive NHL?
Short course of chemo and radiu or if its advances monoclonal antibodies as well
125
What is Rituximab?
Monoclonal antibody for CD-20 targets B cells uaully
126
What are the myeloproliferative disorders?
Polycythemia vera, essential thrombocytosis, myelofibrosis and chromic myeloid leukemia they are chronic conditions that evolve over years
127
What are involved in haematopoesis?
EPO TPO signalling through JAK/STAT proteins they are involves with EPO receptors
128
What is polycythemia vera?
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
How is polycaythaemia vera treated?
Venesection, aspiring manage CVD risk
130
What is prognosis of polycythaemia vera?
13 years
131
What are the features of myelofibrosis?
cytopenia low Hb platelets and EBC marow filled with reticulin fibrosis and find blasts in circulation weight loss fatigue
132
What is prgnosis of myelofibrisos?
can transform to acute leukaemia median 5 years (2-10)
133
How can you treat Myelofibrosis?
usually supportive management and can have transplant or medication
134
What are the "common" myeloproliferatice disorders?
Polycythemia, myelofibrosis, chronic myeloid leukaemia
135
What is chronic myeloid leukaemia?
All myeloid cells go up in blood. usualy incidenatl findidns it is rare often with philladelphia chromosomes
136
How is chronic myeloid leukaemia treated?
Imantinib to block ABL kinase
137
What is chronic neutrophilic leukaemia?
very very rare not usually infection causes it
138
What underlies a lot of myeloid diseases?
the Philadelphia chromosome or genetic mutations
139
What is essential thrombocytosis?
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
What is treatment for essential thrmbocytosis?
Cardiovascular risk usual life expectancy pretty much
141
Where do venous thromboses usually happen?
In the deep veins of the leg
142
What are the symptoms of DVT?
Swelling and pain in the legs, can get redness swelling warmth and discolouration
143
What can be a complication of DVT?
Can cause swelling that can lead toobstruction of arteries
144
What are investigations can be done to assess DVT?
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
How are DVTs treated?
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
What can cause DVTs?
Surgery immobility, leg fracture/POP, being on the Pill HRT pregnancy, long haul flights/ travel, or thrombophilia genetic predisposition cancers
147
What is prevention of DVT?
Mechancal hydration early mobilisation compression stockngs and foot pumps. also low molecular weight heparin
148
Who has thromboprophylaxis?
low risk under 40 short surgery have ....
| higher risk for long surgery had
149
What are Pulmonary embolisms?
massive and are haemodynamically significant, they are medical emergency and can be severe or not too bad
150
What are symptoms of PE?
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
What do you do for PE initial investigations?
CXR ECG Sinus tachycardia ABG type 1 respiratory failure decreased O2 CO2
D dimers CTPA wisualis segmental thrombi
152
What is treatment for PE?
Same as DVT, low molecular weight heparin if acutely unwell could remove it with surgery
153
Where are periferal arteries that can have vascular disease?
illiac femoro-popliteal ant tibial, Carotids, Vertebrals, coeliac mesenteric renals and subclavia/axillary
154
What are the commenest vascular diseases?
Atherosclerosis, inflamatory and trauma
155
What are complications of plaques in vessels?
Progression, aneurism, dissection
156
What are the results of atherosclerosis?
Debris embolsm, aneurism, occulsion, restriction
157
What are organ specific symproms?
Angina exercise induced.
158
What is intermittent claudication?
moderate ischaemia, when demand increases becomes lactic acid pain, pain on exersion distal to site of atheroma often calves
159
What is critical ischaemia?
Blood supply barely adequate for rest. get rest pain usually in distal segment, risk of gangrene or infection can be worse at night.
160
What happens in acute ischaemia PVD?
Sudden cessation of blood supply,get 6Ps pain pallor perishing cold pulsless paresthesis paralysis
161
How long to save the limb in PVD acute ischaemia?
4-6 hours before the limb might be lost
162
What can lead to aneurism?
often aterosclerotic, collagen disorders Marfans, EhlersDanlos size and lcation
163
What investigations should be done in PVD?
Risk factors for pathophysiology, Image the vessels duplex/CT/MR angiography
164
What are the treatments for PVD?
Risk factor modification Revascualrisation in criticalischaemia otherwise amputation required
165
What are surgical treatments of PVD?
Do bypass surgery with synthetic or real vein, or catheter stenting with a baloon
166
What is carotid endarterectomy?
Removal of atherosclerotic tissue in the neck
167
What is a stent graft?
Support an aneurysm with a stent over a large area
168
What is chronic myeloid leukaemia?
uncontrolled colonal proliferation of myeloid cells usually in older patients linked with philadelphia chromosome.
169
What are the symptoms of CML?
anaemia,
170
What is acute lymphoblastic leukaemia?
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
What are the symptoms of acute Lymphoblastic leukaemia/
anaemia, infection from low WCC, bleeding, bone marrow infiltration liver spleen infiltration lymphadenopathy, CNS infiltration mediastinal masses
172
What are the investigations to make diagnoses of ALL
FBC blood film, WCC is usually high, blast cells on film and in bone marrow, blast cells on film
173
What is the difference between leukaemia and lymphoma?
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
How to diagnose leukaemia and lymphoma?
Blood smear and bone marrow biopsy
175
What are the types of blood disorders?
Proliferative diseases, haematologicla malignancies and marrow failure
176
What conditions cross over PD heamatological malignancies and marrow?
Multile myeloma, CML
177
What are classifications of leukaemia?
CML AML CLL ALL
178
What is definition of leukaemia?
Malignancy arising from bone marrrow stem cells resulting imared haematopesis and celsl in peripheral blood and metastisise
179
Who usually gets leukaemia?
Adults but ALL is children
180
What divides acute and chronic leukaemia?
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
What are the types of lymphoma?
Hodgkins(with reed sternberg B cells) or non-hodgkin
182
What are the histological feature in AML?
Aure rods which are granulesperoxidase positive
183
What are risk factores for acute leukaemia?
Genetic and environment, antuneoplastic agents ionising radiation hodkin's lymphoma
184
How are acute leukaemias cause symptoms?
Replace most of bone marrow so fewere other cells, enter peripheral blood, metastasize
185
How to tell it is acute leukaemia?
Painless lymphadenopathy, bleeding, infections fatigue
186
What are treatments of acute leukaemia?
Induction (of remission) phase, high does chemo to supresss all cells then give supportive grwoth factors later consolidation to prolongue remission
187
What are chromic leukaemis ?
Parients older late haemopoetic stem cells, insudious onset, mature celsl smaller
188
What are chromic leukaemis ?
Patients older late hemopoietic stem cells, insidious onset, mature celsl smaller
189
What is myelodysplasia?
MDS is a bone marrow problem, hypercellular full of dysplastic cells with pancytopenia
190
is MDS a leukeaemia?
it progresses into AML, dysplasia is a precursor to cancer caused by de novo mutation and environmental exposure
191
Who usually gets MDS?
50-80 year olds
192
What are the features of MDS?
Hypercellular marrow now proliferation No JAK mutation it is dysplasia
193
What are stages of RBC production?
Myeloid progenitor, proerythroblast, normoblasts reticulocytes erythrocytes
194
What is a reticulocyte/
A net like cell has rRNA giving blue cytoplasm.
195
Do reticuloycyes have nuclus?
yes they do
196
How long are reticulocytes inin the circulation?
24hours
197
What happens in anaemia to RBC production?
Release and produce more reticulocytes so more are found in blood
198
What is corrected reticulocyte count?
which compares amount of reticulocytes in relation to the amount of red blood cells
199
What is RBC count?
Number of cells in a certain volume of blood
200
What is Hb conc?
The amound of Hb in a certain volume of blood regardless of the number of cells
201
What is haematocrit value?
Volume of RBC over volume of blood should be around 45 for men 40% for females
202
What is MCV?
The average volume of a RBC in a volume small cells give low large cells give large MCV
203
What is mean corpuscular haemoglobin? MCH
The average mass of Hb per cell
204
what is mean corpuscular haemoglobin haemoglobin concentration?
MCHC average concentration of Hb witin each RBC
205
What is Red cell distribution width?
RDW isused to look at type of anaemia it is the variation of the diameter of RBC
206
What is anisocytosis?
When there is a variation of the size of cells
207
What is the use of RDW?
When elevated indicates blood body is lacking in certain nutrients B12 folate or iron
208
Why does nutritional deffieciency produce anisocytosis/
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
What are signs of anaemia?
Low total RBC mass or decreases Hb or HCT or RBC count
210
What are the symptoms of anaemia?
Fatigue pale sometiems murmur or angina
211
What are the main mechanisms for anaemia?
sequestration blood loss, hypoproliferative(production defects and maturation defects) and survival
212
What can cakes RBC production defective?
Lo EPO from kidney dammage and dammage bone marrow
213
What are maturation defects?
Cytopasmic Hb synthesis like iron deficiency or thalasaemis or nuclear DNA synthesis B12 folate and MDS
214
What are survival defects in RBC?
intrinsiv from membrane spherocytosis defects or enzyme G^ defect or Hb itself sickle cell extrinsic by valve damage or autoimmune
215
What is sequestration of RBC?
Spleen damages red blood cells in portal vein hypertension
216
What is microcytic anaemia?
small RBC and decreased Hb
217
Why does iron deficiency cause microcity RBC?
the cells shrink as they are waiting for the iron to fill them and keep shrinking so that the cell is full.
218
What is the difference between iron deficiency and anaemia of chronic disease?
in one there is iron but can't be used but other there isn't much blood
219
How is iron absorbed in intestines?
In duodenum, through enterocytes to bind to transferrin in the blood
220
What are ferritin?
keeps iron in non toxic bound form stored in the macrophages of bone marrow
221
What degrates ferritin?
lysosomes turn it to haemosiderin
222
What is a measure of bone marrw ferritin?
the ferritin in blood 1mg in blood means 8 in bone marrrow
223
What is iron in serum used for?
Reduced in iron defficiency or chronic disease anaemia, and increased iin iron overload
224
What is serum total iron binding capacity?
The iron binding capacity of blood and refelcts iron stors it correlates with transferrin levels
225
What is soluble transferrin receptor concentration
sTFR is increased in iron deficiency anaemia and normal in anaemia of chronic disease
226
What can cause iron deficiency anaemia?
Decreased supply from diet or malabsorpiton, increased demand from more RBC produciton in grwoth and pregnancy or from blood loss or intravascular hemolysis
227
What are symptoms or iron deficiency anaemia?
Tired and pale irritable cant exercise, might have a murmur, restless leg syndrome, achlorhydria coeliac disease glossitis-chelitis, koilonychia
228
What are common blood results for anaemia iron deficient?
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
How do you diagnose iron deficiency anaemia?
technically biopsy but can't do that so just treat with iron and monitor
230
When do you get high WBC count with anaemia?
Hookworm infection
231
What is treatment for anaemia?
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
What cell size is in thalasaemia?
Microcytic small cells
233
What is the inheritance pattern for thalasaemia?
Autosomal recessive
234
What does thalassaemia affect?
The globin chains of HbA
235
What are the normal components of adult blood?
Small amounts of HbF alha and gamma and HbA2 alpha and delta and maily HbA alpha and beta
236
What are the effects of having a thalassaemia?
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
What are the levels of alpha thalassaemia?
Hydrops fetalis 4 deletions, 3 deletions moderately severe haemolytic anaemia major, 2 deleted asymptomatic but lowered MCV minor, 1 deletion asymptomatic trait/carrier
238
What is the inheritance mechanism for alpha thalassaemia?
there are 2 coppies of alpha so 4 locations for deletions
239
What is the problem in thalassaemia major?
Only beta is produced so get a tetramerform unpaied beta chains
240
How are thalassaemia patients treated?
Give blood transfusions
241
What chromosome is involved in beta thalasaemia/
chromosome 11
242
What type of mutations happen in beta thalasaemia?
Slicing defiect and more severe are premature stop codon
243
What are complications of beta thalasaemia major?
Get hepatospelnomealy as no beta globin production, also have extramedullary haematopoiesis, in skull and maxillae chipmunk facies
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What is betathalasaemia intermedia?
Often have alpha thalassaemia trait, qualitative effect in beta not as many haemotetramers and less haemolysis and increased HbF
245
What is sideroblastic anaemia?
ringed sidderoblasts in bone marrow, protoporphyrin synthesis defect. caused by B6 defficience alcoholism lead poisoning MDS or X-linked
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What is macrocytic anaemia?
large red blood cells
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What type of anaemia do you get with B12 or folate defficiency?
Microplastic
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What are the divisions of macrocytic anaemia?
Megaloblastic for folate or deficiency and has hyper segmented neutrophils or non megaloblastic
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Why are folate and B12 deficiency macrocytic?
The cells don't decrease in size to the normal size as the DNA cant regulate the size
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Which drugs can stop folate being absorbed?
alchol and oral contractptive pills
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What can cause folate defficiency?
Decreased intake, malabsorption coeliac disease, Drug inhibition, trimethoprim methotexate, or increased use in pregnancy lactation malignancy or haemolytic anaemia
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What happens with folate deficiency?
impared DNA sunthesis and innefective haematopoiesis pancytopenia
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How long does body have folate store?
4 months
254
What deficiency gets neurological symptoms?
B12
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What are symptoms of b12 defficiency?
macrocytic anaemia symptoms, and glossitis, lemon yellow skin peripheral neuritis subacute combined degeneration of spine and dementia vibration proprioception,muscle weakness and ataxia
256
how long does the body have stores of B12?
several years maybe 9
257
How do B12 get absorbed?
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
What is special about B12?
Methylmalonyl CoA and homocystine
259
How to treat B12 deficiency?
IM
260
What can cause non-megaloblastic anaemia?
liver disease, alcoholic and drugs
261
What are the classes of normocytic anaemia ?
acute blood loss underproduction, overdestruction haemolysis
262
What happens in acute blood loss?
loss of RBC then get more fluid in later to dilute causing anaemia can't give saline because dilutes more
263
What can cause overdestruction of RBC?
Extrinsic destruction, complement antibodies or membrane or enzyme defects
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What is aplastic anaemia?
Can give normo to macrocytic anaemia, you have pancytopenia and hypocellular marrow
265
What can cause aplastic anaemia?
Faconi anaemia dyskeratosis, radiation drugs toxins viruses immunological ONH pregnancy, intensive chemo
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What are symptoms of pancytopenia?
signs of anaemia, infections if very late mucosal bleeding from pancytopenia
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What can lead to anaemia in malignancy?
Anaemia of crronic disease, kidney failure pain phycological, blood loss bone infiltration,
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What is paroxysmal nocturnal dyspnoea?
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
What are the symptoms of chronic heart failure?
Breathlessness cough maybe with frothy/pink sputum orthopnoea, SOB when lying down, Paroxysmal nocturnal dyspnoea oedema
270
How is heart failure diagnosed?
clinical assessment, BNP blood test, ECho and ECG
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What can lead to chronic heart failure?
Ischaemic heart disease prior infarction and not, valvular heart disease hypertension and arrhythmias
272
How is chronic heart failure treated?
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
What can cause hypovolaemic shock?
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
What happens to signs in hypovolemic shock?
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
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How to treat hypocolaemic shock?
Give IV normal saline or albumin or colloid
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What can cause cardiogenic shock?
myocarditis, MI, valvular dysfunction, Arrhythmias, cardiomyopathies, gongenital heart diseases dialated cardiomyopathy
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What happens in cardiogenic shock?
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
How to treat cardiogenic shock?
Give oxygen small amount of fluid, vasopressors to uncrease ciontractility epinephrine dobutimine
279
What is obstructive cardiac failure?
the heart is being blocked from pumping properly. compression of the heart and compression of the great vessels.
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What are causes of obstructive shock?
Tension Pneumothorax, cardiac tamponade
281
What can show obstructive shock?
Increased JVP, Low blood pressure, high heart rate, dull heart sounds distant or muffled for tamponade Massive PE low sats hypoxemic hypoxia
282
What is distributiative sock?
Septic anaphylactic and neurogenic it is about struggling to distribute the blood rather than pumping
283
What can cause septic shock?
Bacteraemia, endotoxins tissue dammage, leading to dialation of blood vessels and increasing vascular permeability
284
What happens in septic shock?
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
What are signs of septic shock?
Lowerd blood pressure cardiac output goes up BP goes up SVR decreases, microvascualr occlusions and acute inflammatory markers
286
What can happen in anyphalactic shock?
Vasodilation from mast cell activation. Can lead to drop in BP increased HR redness swelling can obstruct airway. devreased SVR
287
What is Neurogenic shock?
when the spinal heart rate and blood vessels innervation is damaged so that the control mechanisms are damaged
288
What can causeneurogenic shock?
Acute spinal injury, stroke
289
What happens in neurogenic shock?
Lowered peripheral resistance, vasodilated, lowered blood pressure increased
