Showing posts with label Haematology. Show all posts
Showing posts with label Haematology. Show all posts

Friday, May 30, 2014

Ankle Brachial Index (Mr.Foot and Mrs.Arm has different opinions on SBP)

What is Ankle Brachial Index?

The Ankle Brachial Index (ABI or ABPI) is the ratio of the blood pressure in the lower legs to the blood pressure in the arms. Compared to the arm, lower blood pressure in the leg is an indication of blocked arteries (peripheral vascular disease or PVD). The ABI is calculated by dividing the systolic blood pressure at the ankle by the systolic blood pressures in the arm.

ABPI_{Leg} = \frac { P_{Leg} }{ P_{Arm} }

risk factor for atherosclerosis:

Etiology:



Causes of Peripheral Vascular Disease:
1. Artheriosclerosis (also will develop in carotid or coronary artery, increase risk for stroke or heart attack)
Known first for pain in leg when exercising or walking(Intermittent claudication)

2. Diabetes Mellitus (There are FIVE pathway for pathogenesis of Macro and Microvascular diseases)

Treatment of PVD:
1. Cessation of smoking
2. Controlling high BP
3. Statins/Lipid level control
4. Dietary changes
5. Exercise
6. Diabetic control
7. Surgery

Pain of PVD can range from mild pain when exercise to severe pain even at rest. PVD limit the ability to exercise. Also can leads to sores and ulcers at leg that do not heal in critical limb ischemia that cause gangrene and require of amputation.

Stroke and heart attack are the most serious and common complication.

Over 5 years period, PVD sufferers
20% sustain stroke
30% fatal event

Critical Limb Ischaemia
30%- amputations
20%-dead

How to perform ABI test?
Things you need:
Doppler, Sphygmomanometer, Gel
Makes sure patient is warm and rest 10-15mins before begin
Measure all the 4 limbs SBP(posterior tibialis and brachial), take the highest reading

See here: http://www.youtube.com/watch?v=LvHeMiCaUdw

AHA ABI Interpretation:
Greater than 1.3, noncompressible arteries, obtain toe pressure
1.00-1.29, normal
0.91-0.99, appears normal, but exercise reveals low degree of obstruction
0.41-0.90, mild to moderate PAD (will experience intermittent claudication when they walk or exercise)
0.00-0.40, rest pain, failure for healing of injury to foot or toe

ABI provides 3 info:
1. Doppler sound
2. Index
3. Waveform

Normal young healthy have triphasic waveform
Biphasic: mildly abnormal
Monophasic progressive disease







People particularly at risk for PAD:
-->less than 50 years of age with DM and one other risk factor for atherosclerosis: HPT, Dyslipidemia, Smoking or Hyperhomocysteinemia

-->age 50-69, hx of diabetes or smoking

-->70 or older

-->leg symptoms upon exertion, intermittent claudication/ischemic rest pain

-->abnormal leg, ankle or foot pulse examination

-->known atherosclerotic carotid, coronary or renal artery disease

-->Psoriasis increase risk of PAD, MI or CVA

Not all people with PAD are symptomatic, only 10 percent have the classic symptoms of intermittent claudication

Adapted from:
Youtube; Vascular Hokanson Channel; How to do ABI
http://360woundcare.wordpress.com/category/uncategorized/
Netter Cardiology Images














Thursday, May 29, 2014

The Police Officer-Neutrophil (some patrol in the blood, some guard at the vessel)

Neutrophil is an amazing cell inside our body. In fact every cell is. AT first I always thought neutrophil is an agent of inflammation. Talking about inflammation made me thought of neutrophil. BUT here I read something about neutrophil today and I felt that the way it works is amazing!

Adapted from Haematology ICT WH120 H849h pg6

The blood neutrophil is the end product of an orchestrated sequence of differentiation in the myeloid cells of the bone marrow. (revise haemopoiesis!).


The mature cell has a multi-lobed nucleus and four different type of granules in the cytoplasm. (Hmm...any application of this?) They have limited lifespan of 5-6 days. Approximately half the cells are included in a normal blood count (revise what is absolute count for WBC here!), the remainder being in the marginal pool.

so, what is the marginal pool mentioned here?
Neutrophils released from the marrow enter the blood where they distribute into two compartments of approximately equal size: the circulating and the marginal pools. Neutrophils in the former compartment are freely circulating, whereas those in the marginal compartment are temporarily adherent to endothelial cells, generally in the postcapillary venules. In normal adult humans, the total of these two compartments (termed the total blood neutrophil pool) contains about 0.6 × 109 cells/kg body weight; with about one half of the cells (0.3 × 109 cells/kg) in each (circulating and marginal) pool.
In the marrow, the proportion of band to segmented neutrophils is much higher than in the blood. On that basis, it is likely that a selective release of segmented neutrophils occurs from the marrow, whereas band neutrophils generally remain behind to mature.
from this website: http://www.expertconsultbook.com/expertconsult/ob/book.do?method=display&type=bookPage&decorator=none&eid=4-u1.0-B978-1-4160-3479-7..10143-0--s0025&isbn=978-1-4160-3479-7

From CLINICAL HAEMATOLOGY, BARNARD, pg3
After about 10 days of maturation and differentiation in the marrow,the mature neutrophil polymorph has a circulating lifespan of only a few hours.The marrow storage pool of neutrophils is approx. 12 times that present in the blood. Whilst a vernous blood sample can measure the circulating neutrophil pool, there is a further marginating neutrophil pool in close proximity to blood vessel wall. the normal fate is attraction to tissue sites by inflammatory mediators or excretion in body secretions. In response to the stimulus of infection or inflammation, large no. of neutrophils maybe relesed into the circulating pool from the marrow and marginating pool to give the neutrophil leucocytosis characteristics of such states. Less mature form with unsegmented nuclei maybe prematurely liberated from the marrow to produce a 'left shift' in the differential white cell count.

That's means when released into the blood, half is circulating and half is marginating due to adhesion molecules.

Notes to come: Hypersegmented neutrophil, neutropenia, acute inflammation














Blood Group and HDN

Adapted from Haematology, an illustrated color text

The blood groups

Antigen exits on RBC membrane
Numerous blood group systems encoded by genes on different chromosomes
highly variable in their polymorphonism and clinical significance
most important is ABO system, the genes encodingis located on chromosome 9 and inherited in autosomal dominant fashion
Each antigen is a sugar residue made by a specific glucosyl transferase


This is an example of antigen H. which means no extra added residue, and this is antigen for blood group type O.




This is example of antigen A, which has added N-acetylgalactosamine to the original template antigen H. This is antigen for the blood group type A.


This is antigen B on surface of rbc blood group type B. It has another added galactos on the template antigen H.

Person who has blood group type AB is having both antigen A and antigen B on their RBC surface.

The ABO SYSTEM is crucial in blood transfusion. As the antibody against ABO antigen is naturally occuring. For example, if you are blood group type A, this means that you have antigen A on your red cell, but you do not have antigen B on your red cell, so your body will naturally have antibody against B, which we called it as anti-B.


These naturally occurring antibodies(anti-A and anti-B) are of IgM type and if the blood transfusion is not compatible, the patient serum which contains this IgM will attacks donor's red cell and will induce fatal hemolytic transfusion reaction.

So test must be done before blood transfusion. We will discuss this later on.


Another type of antigens are minor antigens. ABO is considered as major but our RBC surface might also have other antigens namely Rhesus, Duffy, Lewis, Kell etc. The antibody against these antigens are not naturally occurring, they are called 'immune antibodies' as they will only be produced when your body's immune system is sensitized by these antigens. The strongest antigen D(Rhesus), for example, can be induced through previous blood transfusion or pregnancy. In pregnancy, if the mother is Rhesus -ve but baby is Rhesus +ve(inherited from father), during first pregnancy, some of the fetal blood might leak into the mother during delivery and causes sensitization of the mother's immune system. Once mother's blood contains this antibody, the second baby which is also Rhesus +ve, the fetal antigen will be attacked by mother's developed antibody and thus develop hemolytic newborn disease(HDN). The HDN here must not be confused with Hemorrhagic Newborn Disease, which is increased risk of bleeding in newborn due to vit K deficiency which impaired the production of Factor 2, 7, 9, 10, C and S by the liver.


The reasons that being different in Rhesus grouping between mother and child has more consequences than ABO grouping is, 1) the rhesus antibody is lgG in nature and can cross placenta to reach the fetus whereas ABO antibody(IgM) can't 2) Fetus doesn't develop fully yet ABO antigen, so less likely to sensitize mother and cause an immune attack.


Notes to come: GSH, GXM, Blood Grouping, Coombs test